Textbook of Oral Surgery - Balaji 3rd Edition

Textbook of Oral
and Maxillofacial
Surgery
THIRD EDITION
S.M. Balaji MDS, PhD, DSc (Hans)

Director and Consultant Oral and Maxillofacial Surgeon
Balaji Dental, Craniofacial Hospital and Research Centre, Chennai, Tamil Nadu,
India
Member, Dental Council, Government of India
Dr B C Roy National Awardee, lv[edical Council of India
Diplomate, International Council of Implantology, USA
Former Member of Senate, The Tamil NaduGovt. Dr MGR Medical University,
Chennai, Tamil Nadu, India
Former Member of Senate and Syndicate, Annamalai University, Chidambaram,
Tamil Nadu, India.
Former Executive Member, Dental Council, Government of India
Consultant Maxillofacial Surgeon
IndiraGandhi Memorial Hospital, Male, Republic of Maldives
Victoria Hospital, Mahe, Republic of Seychelles
Govt. Jawaharlal Nehru Hospital, Port Louis, Republic of Mauritius
Formerly Apollo Hospital, Colombo, Sri Lanka
Padma Preetha Balaji BDS, MDS
Consultant Oral and Maxillofacial Surgeon
Balaji Dental, Craniofacial Hospital and Research Centre
Chennai, Tamil Nadu, India
Table of Contents
Cover
Title page
Copyright
Dedication
Foreword
Preface to the Third Edition
Preface to the First Edition
Section I: Definition and Scope of Oral Surgery
Chapter 1: Definition and Scope of Oral Surgery
Dentistry (ADA Definition)
Purpose of specialisation
What a graduate should know

Section II: Diagnosis
Chapter 2: History Taking and Clinical Examination
History taking
Clinical examination
Examination of ulcer
Examination of a swelling
Chapter 3: Radiodiagnosis
Diagnostic tools
Plain X-rays
Digital imaging
Tomography
Magnetic resonance imaging
Nuclear medicine
Ultrasonography
Chapter 4: Diagnostic Aid—Haematological, Biochemical and Microbiological

Investigations
Haematological investigations
Biochemical investigations
Microbiologic tests
Chapter 5: Histopathological Investigation
Biopsy
Cytology
Immunohistochemistry
Section III: Medical Management in Oral Surgery
Chapter 6: Management of Medically Compromised
Hypertension
Diabetes mellitus
Hypoglycaemia
Dysrhythmia
Angina pectoris
Myocardial infarction
Congestive heart failure
Infective endocarditis
Asthma
Chronic obstructive pulmonary disease
Renal disorders
Adrenal insufficiency
Hyperthyroidism
Haematologic diseases
Congenital coagulation defects
Bleeding disorders
Platelet disorders
Neurological disorder
Pregnancy
Infectious diseases
Hepatitis B
Chapter 7: Medical Emergencies and their Management
Chapter 8: Therapeutics in Oral Surgery
Antimicrobials
Analgesics
Anti-inflammatory
Antioedematous substances
Antiallergic
Local anaesthesia
Sedatives and hypnotics
Muscle relaxants
Dressings to protect wounds and relieve pain
Stimulants for circulatory failure, syncope and collapse
Section IV: Anaesthesia in Oral Surgery
Chapter 9: Local Anaesthesia
Electrophysiology of nerve conduction (Fig. 9.1)
Classification
Basic injection techniques
Intraoral techniques (Fig. 9.7)
Extraoral techniques
Block anaesthesia for the mandible
Complication of local anaesthesia
Chapter 10: General Anaesthesia
Preanaesthetic evaluation
General examination
Delivery of anaesthetic gases and vapours
Managing the airway
Anaesthetic drugs
Induction of anaesthesia
Maintenance of anaesthesia: inhalational (volatile) agents and intravenous

infusions
Muscle relaxation during anaesthesia: neuromuscular blocking drugs and

their antagonism
Conscious sedation
Section V: Principles of Practising Oral Surgery
Chapter 11: Armamentarium
Airway maintenance/anaesthesia
Presurgical asepsis and draping
Soft tissue handling armamentarium
Instruments used for reflecting the mucoperiosteal flap

Hard tissue handling instrument
Instruments used for management of fractures
Miscellaneous instruments
Diathermy (electrocautery)
Chapter 12: Sterilisation and Disinfection
Cleansing of instruments
Methods of sterilisation
Operating room decorum
Infection control
Chapter 13: Incisions and Flaps
Incision
Principles of wound incision
Principles and guidelines for flap designs
Intraoral incisions
Extraoral incisions
Extraoral flap designs in oral surgery
Skin grafts (Fig. 13.20−13.22)
Chapter 14: Suturing Materials and Techniques
Classification
Absorbable suture materials
Non-absorbable suture materials
Needles
Principles of suturing
Suture methods
Knot
Staples
Wound closure tapes
Chapter 15: Haemorrhage and Shock
Haemorrhage
Haemostasis
Shock
Chapter 16: Wound Care
Surgical drains
Section VI: Minor Oral Surgery
Chapter 17: Exodontia
Indications for extraction
Contraindications for extraction
Assessment of teeth for extraction
Preoperative radiographs
Surgical Plan
Anaesthesia
Techniques of extraction of teeth
Principles of tooth removal

Complications of extraction
Chapter 18: Impaction
Maxillary third molars
Impacted cuspids
Surgical technique
Chapter 19: Endodontic Surgery
Classification of endodontic surgery
Chapter 20: Preprosthetic Surgery
Hard tissue surgeries
Soft tissue procedures
Repositioning of inferior alveolar nerve (IAN) (Fig. 20.48)
Chapter 21: Dental Implantology
Implant treatment protocol
Surgical complication of implant therapy
Section VII: Space Infections
Chapter 22: Head and Neck Space Infections, Part -I
Chapter 23: Head and Neck Space Infections, Part -II
Chapter 24: Head and Neck Space Infections, Part -III
Potential spaces
Classification of fascial spaces
Primary fascial spaces
Buccal space
Infratemporal space
Submental space
Submandibular space
Sublingual space
Secondary fascial spaces (Fig. 24.15)
Parotid space infection
Submasseteric space
Pterygomandibular space
Lateral pharyngeal space
Retropharyngeal space
Peritonsillar abscess (quinsy)
Life threatening complication of orofacial infections
Ludwig’s angina
Clinical features
Carotid space infection (Fig. 24.25)
Chapter 25: Osteomyelitis, Osteoradionecrosis and Osteochemonecrosis
Osteomyelitis
Osteoradionecrosis
Osteochemonecrosis
Treatment of medication-related osteonecrosis of the jaw

Section VIII: Maxillofacial Pathologies
Chapter 26: Cysts of the Oral Cavity
Odontogenic and nonodontogenic cyst derivatives
Pathogenesis of cyst formation
Prognostic factors
Chapter 27: Odontogenic Tumours
Benign tumours
Malignant tumours
Chapter 28: Nonodontogenic Tumours
Osteoma
Fibro-osseous lesions
Chapter 29: Oral Cancer
Staging and grading of oral cancer
Aetiopathogenesis
Squamous cell carcinoma
Histologic variants of squamous cell carcinoma
Basal (Rodent ulcer)
Ewing’s sarcoma (endothelial myeloma, round cell sarcoma)
Osteosarcoma (osteogenic sarcoma)
Multiple myeloma (plasma cell myeloma, plasmacytoma)
Chapter 30: Management of Head and Neck Tumours

Surgical management
Radiotherapy
Radiosensitisers
Radioprotectors
Radiation mitigator
Chemotherapy
Chapter 31: Salivary Gland Pathologies
Classification of salivary gland diseases
Chapter 32: Maxillary Sinus and its Implications
Maxillary sinus
Advances in the management of maxillary sinus disease
Chapter 33: Orofacial Cleft
Prevalence
Evolution of theories of cleft embryo pathogenesis
Development of cleft lip and palate
Aetiology of oral cleft (OC)
Pathological anatomy
Problems faced by cleft children and their management
Management of patients with cleft lip and palate
Primary correction
Lip repair
Secondary corrections
Closure of alveolar cleft
Chapter 34: Orofacial Neuropathy
Anatomy of the peripheral nerve
Classification of disorders of the nerve
Section IX: Dentofacial Deformities
Chapter 35: Orthognathic Surgery
Diagnosis and treatment planning
Chapter 36: Distraction Osteogenesis
History of development of craniofacial distraction
Stages of distraction
Classification of distraction
Distractor device
Devices
Biologic aspect of distraction osteogenesis
Imaging of callus and its radiographic stages
Section X: TMJ
Chapter 37: Anatomy of TMJ
Embryology
Joint anatomy
Chapter 38: TMJ Disorders
Classification of TMJ disorders
Temporomandibular joint disorders classification
Structural and developmental disorders of the condyle (Flowchart 38.1)
I. Functional disorders
Surgical management
Chapter 39: TMJ Ankylosis
Aetiology
Pathophysiology of TMJ ankylosis
Classification of ankylosis
Clinical presentation
Radiologic assessment
Management
False ankylosis
Chapter 40: Internal Derangements and Condylar Dislocation
Physiologic movements of the TMJ
Internal derangement
Condylar dislocation (Condylar dislocation, Subluxation, Hypermobility of

TMJ)
Section XI: Maxillofacial Trauma
Chapter 41: Emergency Management and Preliminary Examination of a

Trauma Patient
Chapter 42: Basic Principles of Management of Maxillofacial Trauma
Principles in managing panfacial fractures
Chapter 43: Dentoalveolar Fracture
Chapter 44: Fractures of the Mandible
Classification of mandibular fracture (Box 44.2 and Box 44.3)
Condylar fractures
Edentulous mandible fracture
Chapter 45: Maxillary Fractures
Chapter 46: Orbitozygomatic Complex
Anatomy
Mechanism of zygomatico-orbital fractures
Orbital fractures
Clinical finding
Timing of repair
Principles of treatment of ZMC fractures
Fracture reduction
Fixation technique
Zygomatic arch fractures
Orbital floor reconstruction
Chapter 47: Naso-Orbito-Ethmoid Fracture
Anatomy of naso-orbito-ethmoid region

Nasal bone fracture
Chapter 48: Frontal Bone Fractures
Surgical anatomy
Applied anatomy
Biomechanics of frontal sinus injury
Types of frontal sinus fractures
Evaluation of frontal sinus injury
Management of frontal sinus fracture
Complications of frontal bone fracture
Section XII: Miscellaneous
Chapter 49: Medicolegal Considerations in Dentistry
Chapter 50: Recent Advances
Bone substitutes
Bioresorbable plates
Lasers in oral surgery
Piezoelectric surgery
Robotic surgery
Index
Copyright
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Textbook of Oral and Maxillofacial Surgery, 3e SM Balaji, Padma Preetha

Balaji
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Dedication
To
my mother for her incessant prayers
my father for making me what I am
Prof US Nayak for honing my skills
my wife for being my strength
my children, all the reasons of my life
Foreword
It has been said that somethings never change. That can be said about many
areas in oral and maxillofacial surgery. However, it is also true that it is still a
dynamic specialty and somethings are constantly changing, and new and
unique concepts and procedures are being added. Therefore, it is essential that
these changes be carefully documented so that those entering the profession of
dentistry or those studying to become oral and maxillofacial surgeons, as well
as those already practicing in the specialty, have an appropriate reference
source for these information.
It has been nearly 5 years since the last edition of this book and this new
edition still maintains that solid basis of material that forms the foundation of
the specialty, presented in a unique and easily understandable manner.
However, it also reflects the numerous changes that have occurred during this
period. Thus, there have been significant modifications and additions to many
of the 50 chapters. These include those on radiographic diagnosis,
armamentarium, preprosthetic surgery, cysts of the oral cavity, salivary gland
pathology, orthognathic surgery and temporomandibular joint anatomy. As in
the past editions, Professor Balaji has continued to supplement the descriptive
material with flowcharts and tables to help the readers better understand the
key issues. In addition to the many clinical images and colour illustrations
already contained in the book, numerous new images, flowcharts and
summary tables have been added.
Over time not only does information change and need to be updated, but
methods of learning also change. This is particularly true for the new
generation of students and residents. To accommodate these changes,
Professor Balaji has introduced an extensive series of online video notes into
parts of the book to help young students with limited exposure to complex
clinical scenarios better understand these areas. While of major importance for
the latter generation, experienced oral and maxillofacial surgeons should also
find this addition of considerable interest.
In writing the Foreword for the second edition of this book, I complemented
Professor Balaji for his efforts in producing this outstanding and
comprehensive textbook. He is again to be commended for his continued
unique and visionary approach to documenting the scope of oral and
maxillofacial surgery.
Daniel M. Laskin, DDS, MS, DSc
Professor and Chairman Emeritus
Department of Oral and Maxillofacial Surgery
Schools of Dentistry and Medicine
Virginia Commonwealth University
Richmond, VA, USA
Preface to the Third
Edition
We have a great pleasure in presenting this third edition of Textbook of Oral
and Maxillofacial Surgery following the huge success of the second edition of
our textbook since 5 years. Continuous compliments and approbation from the
students, teachers and professors all over the world for our previous editions
have motivated us to publish this third edition in a more advanced and
comprehensive way. Also, the art and science of oral and maxillofacial surgery
has advanced since the last edition of the book. This edition has been designed
to include all such remarkable advances.
This edition has been designed to equip the students with as much
knowledge on all topics as desirable from the point of view of brilliant success
in both theory and practical examinations as well as to face real-life clinical
scenarios. With the involvement of a young surgeon in this edition, the
mindset of the 21st century dentist is being included in the thought process of
understanding, conceiving and executing the student-centric book for oral and
maxillofacial surgery. The book since its first edition more than a decade ago
has always been for imbibing advances, simplifications and making it more
student-friendly without compromising the quality or quantity of knowledge.
In all meetings and conferences, after the release of the second edition of this
book, dental students never ceased to amuse me during impromptu
interactions. Students posed interesting questions and challenges, as a result of
which we need to constantly improvise the approach to the expression,
teaching, explanation and making the concept and skill easy to teach in the
book.
The style of presentation, pedagogical approach, organisation and writing
style has been retained as in the previous edition as it was widely appreciated.
In addition to the revised and updated text, this edition has an extensive series
of 15 online videos. This has been arranged to make reading and
comprehension better while studying, mostly at the request of young students
with limited exposure to complex clinical scenarios. Such specific links are
marked with a unique AR code at the end of image captions. I hope the young
dental students would be exposed to more complex clinical scenarios beyond
their regular clinical exposure.
We are in an era of antibiotic resistance and world bodies have called for the
rational use of antibiotics. Among dentistry, still oral surgery is known to be
using antibiotics regularly. In an effort to aid the awareness of antibiotic
resistance in the oral microbial flora, a holistic approach for increasing
awareness has been made. The chapter on space infection is now reorganised
in a better way as Part I–III with additional illustrations and flowcharts. This
would be helpful for the students to effectively choose their antibiotics and
minimise antibiotic resistance.
Large-scale additions and modifications are done in the following chapters:
Radiodiagnosis, Armamentarium, Preprosthetic Surgery, Cysts of the Oral Cavity,
Salivary Gland Pathologies, Orthognathic Surgery, Anatomy of TMJ and Recent
Advances.
In addition to the previous 2500 clinical images and 400 colour illustrations,
nearly 200 more images have been added along with new flowcharts and
tables for better understanding of the topics.
Efforts have been made to make maxillofacial surgery more interesting and
understandable for the undergraduate students with inclusion of contents,
which are must-know for postgraduates. We are sure that this book marks the
shelf of all undergraduate and postgraduate students, not excluding the
professionals.
S.M. Balaji
Padma Preetha Balaji
Preface to the First
Edition
As an Oral and Maxillofacial Surgeon, I have explored that our students still
lack a practical and concise textbook on oral and maxillofacial surgery and
need to refer several textbooks to learn each aspect of Oral Surgery. When I
was a student I found that there were no Indian authors for any book of oral
and maxillofacial surgery. All these had motivated me to frame a specialised,
aphoristic and updated book, based on my clinical and surgical experience for
the past 18 years in the field of oral and maxillofacial surgery and that of my
colleagues, accepted and published by peer reviewed journals. I intend to
provide a lucid and comprehensive package of the pathologies encountered in
the oral cavity demanding surgical treatment, their clinical detection, the use
of modern technological advancement in the diagnosis, the various treatment
options available, their advantages and limitations, the recent advances,
application of the results of the research work undertaken and the possible
vistas of improvements in the future. I have tried to present my knowledge in
the subject adhering to the contemporary, accepted standards of proficiency
and competence.
The line diagrams are an expressive interpretation of our surgical pictures
which are worked upon and simplified to render them more comprehensible
and comparable with the real photographs. Therefore, these illustrations are
easy to remember and reproduce during examination. The practical and
pictographic explanation of the procedures has an edge over the conventional
method of learning.
The emphasis is laid upon the language that is simple, understandable and
exclusively designed for the students whilst maintaining its international
standards. Therefore I believe that this book would be very useful from
examination point of view for both undergraduate and postgraduate students.
My objective was to present this area of expertise of oral and maxillofacial
surgery in its fullest scope by accumulating as inclusive a text as possible. I
have made my first attempt and I hope that this text serves the requirements
of the students. In the future I assure of enhanced endeavour to present an
even broader scope of this field.
S.M. Balaji
SECTION I
Definition and Scope of
Oral Surgery
Chapter 1: Definition and Scope of Oral Surgery

CHAPTER 1
Definition and Scope of

Oral Surgery


The evaluation, diagnosis, prevention, and/or treatment (nonsurgical, surgical
or related procedures) of diseases, disorders, and/or conditions of the oral
cavity, maxillofacial area and/or the adjacent and associated structures and
their impact on the human body; provided by a dentist, within the scope of
his/her education, training and experience, in accordance with the ethics of the
profession and the applicable law.
The dentist act 1948

Scope of dentistry has been defined by the Dental Council of India (DCI),
which, in turn, has been empowered by the Parliament to structure a course
aimed at preventing, diagnosing, and treating diseases of the mouth and teeth.
According to the Dentist Act (1948), ‘Dentistry’ includes:
1. The performance of any operation on and the treatment on any disease,

deficiency or lesion of the human teeth or jaws and the performance of
radiography or in connection with human teeth or jaws or the oral
cavity;
2. The giving of any anesthetic in connection with any such operation or
treatment;
3. The mechanical construction or the renewal of artificial dentures, or
restorative dental appliances;
4. The performance of any operation on, or the giving of any treatment,
advice or attendance to any person preparatory to, or for the purpose
of, or in connection with the fitting, inserting, fixing, constructing,
repairing or renewing of artificial dentures or restorative dental
appliances, and the performance of any such operation and the giving
of any such treatment, advice or attendance, as is usually performed or
given by dentists.
The Dentist Act is clear in its mandate and has entrusted approved
universities all over the India to run courses to qualify individuals in the art
and science of dentistry. With advances in the field of dentistry, postgraduate
programmes were also started to develop focus in certain areas of dentistry,
thus paving the way for specialists such as orthodontists, periodontists,
prosthodontists, maxillofacial surgeons and so on.
The specialists are expected by implication to focus on their unique areas so
as to impart concentrated information to dental students. The graduate dentist
is therefore expected to fully evolve out of the united endeavour of many
specialists who teach him/her the respective subjects.
Oral surgery
The word ‘Surgery’ is derived from the Greek word chir meaning hand and
ergos meaning work. Therefore, theoretically surgery means any work done
with the hands; but the usage is generally limited to practical therapies such as
those involving cutting, repairing and dressing living tissues.
Therefore, ‘Oral Surgery’ deals with the diagnosis and treatment of oral
conditions of the jaw and mouth structures that require surgical intervention.
This dental speciality is limited to the surgical removal of teeth and the
treatment of diseases, deformities and defects of the jaws and associated
structures.
Setting rigid limits to any speciality is likely to stifle development and
enterprise and cannot satisfactorily account for variation in interest and ability
among its practitioners. So, although oral surgery could be said to be an area
of practice within dentistry, its limits are not well defined and it spreads
somewhat toward other aspects of surgery. ‘Maxillofacial surgery’ is a term
that implies a greater scope of surgical interest. ‘Craniofacial surgery’, on the
other hand, it is a more specific term relating to the specialised area dealing
with disorders that affect both the cranial and the facial skeleton.
Oral and maxillofacial surgery

Oral and maxillofacial surgery is a speciality of dentistry concerned with the
diagnosis and surgical treatment of congenital or acquired diseases,
dysfunction, defects or injuries of the mouth, jaws, face, neck and adjacent
craniofacial regions.
Scope of practice of a dentist and oral and

maxillofacial surgeon
The word ‘scope’ is, as the Webster’s dictionary would have it, ‘the range of
one’s awareness, thoughts or actions’. The general dental practitioner, who
acquires a registration to practice on finishing his/her undergraduate degree
and 1 year of internship, is required to undertake surgical treatments beyond
the tooth and its supporting ligament as well as to diagnose a range of
disorders that may benefit from a surgical solution or may have to be
distinguished from those that require surgery.
The scope of practice of a dentist and a maxillofacial surgeon are widely
different. A postgraduate maxillofacial surgeon is trained to treat more
complex disorders of the teeth and the facial structures. There is also an
important distinction to be drawn between those conditions that a dentist
should treat in the practice and those that are better treated by a specialist or in
a hospital setting. Further distinction must be made between what is common
practice in one country and what is not accepted in another. Some of these
differences are cultural and some historical.
Oral surgical procedures performed by a general

practitioner
• Extraction and simple impactions
• Management of complications arising due to minor surgical problems
• Endodontic surgeries
• Incision and drainage of abscess
• Alveoloplasty
• Traumatic injuries not involving severe bone fractures
• Management of pathological conditions of the oral mucosa and bone
Procedures that should be performed only by

specialists
• Roots displaced into the maxillary sinus
• Orthognathic surgery
• Transplantation of tissues
• Oral oncology
• Complicated maxillofacial surgeries and space infections
• Difficult impactions, such as, distoangular impactions
• Temporomandibular joint problems
• Congenital malformations of the orofacial region
• Preprosthetic surgeries
Specialisation would essentially serve to equip one with a sharper focus on
one of the areas within a broad speciality. It is also expected (though not
mandated) that the specialist will not dilute his skills by performing general
dental work. They may be considered as an authority in their subject with
skills far beyond the requirement of legal competence. They would, as
mandated by the Dental Council of India, be qualified to teach the subject in
recognised dental institutions.
Over many decades dentistry and medicine have undergone a series of
specialisations. The development of dentistry itself could be seen as a
specialisation within medicine. The advantage of specialisation is increased
skill among practitioners in that area of practice. The disadvantage is loss of
some general and widely applicable abilities.
Relationship of oral surgery with other dental

specialities
Orthodontics are required for the correction of malocclusion and jaw
deformities in cleft or other craniofacial defects. Preprosthetic surgery
performed by the oral surgeon sometimes becomes mandatory for the better
functioning of the prosthesis. The practice of conservative dentistry and
periodontics requires application of oral surgery for the treatment of periapical
pathology. Management of medically compromised patients and medical
emergencies necessitates the understanding of medicine and physiology. The
speciality also has a very close association with other branches of dentistry like
oral medicine and radiology, oral pathology and forensic odontology.
The relationship of oral surgery with plastic surgery, ENT and orthopaedic
surgery is well known in the treatment of various maxillofacial and
craniofacial deformities. Each speciality substantiates its validity in fruitful
coexistence, therefore, it is difficult to limit the professional interests of the
specialities.
The curriculum
Undergraduate curriculum in oral and maxillofacial surgery is designed,
based on its objectives, to expose students to the speciality and help them
develop the knowledge, skills and values to become competent in performing
minor oral surgery. The educational programme rests on two central elements:
(1) a rigorous didactic programme that combines lectures with small-group
learning and (2) a clinical programme that imparts proficiency in the basics of
oral surgical practice. Beyond core surgical competencies, students completing
the course should come away with a good understanding of the evaluation,
diagnosis and perioperative management of the surgical patient. The blending
of critical thinking and a humanistic approach to patient care with the latest
techniques of surgical practice is a pervasive theme throughout the
curriculum. The curriculum provides the students with a solid foundation that
they will use for the rest of their professional lives, whether or not surgery is a
career goal.
The 1-year senior internship programme is a period of expanded clinical
experience in oral surgery. It gives ample exposure to a variety of minor oral
surgical procedures. The internship is a demanding and time-intensive period
in a student’s professional education, but one that serves as a building block
for acquisition of advanced knowledge in the field of surgery, regardless of a
student’s ultimate career goals.

• Assess the general condition of the patients, be able to manage patients
with medical illness in the general practice and make appropriate
specialty referral.
• Appropriately assess and diagnose oral and maxillofacial surgery
conditions, order the proper investigations necessary at the general
practice level and then to treat or refer the case.
• Control pain and anxiety.
• Basic surgical skills including exodontias, raising mucoperiosteal flaps,
removal of retained roots and roots broken during extraction and
simple removal of impacted wisdom teeth.
• Assess facial fractures, oral neoplastic lesions, craniomaxillofacial
deformities and facial infections.
• Manage intraoperative and postoperative complications arising in a
clinical practice, including medical and surgical complications and to
provide necessary life saving and airway maintenance procedures.
Dual degree qualification

In India practice of oral and maxillofacial surgery as a clinical speciality
requires a Masters in Dental Surgery (maxillofacial surgery) alone. But of late,
in the United States and other nations, there has been an increased inclination
toward making this speciality a dual degree one. There has been a rise of the
dual degree (DDS/MD) programmes among American OMS residencies. Dual
degree programmes have been embraced by about 40% of the existing OMS
programmes in the United States.
Oral and maxillofacial surgery has a unique position, straddling the dental
and medical professions, creating controversy over whether dual medical and
dental qualifications are necessary.
Oral surgeons are the products of a unique style of hybrid professional
education that includes areas of both dentistry and medicine. We are the
‘surgeons’ to our dental colleagues and the ‘dentists’ to our medical
colleagues.
As the scope of oral and maxillofacial surgery continues to expand into
areas that have traditionally been medical specialities, the educational and
political advantages of membership in the medical fraternity will be
important, as the number of dual qualified surgeons will continue to increase.
At the same time, the scope of practice for OMS is not an issue of single or
dual degree but must be related to the surgeon being trained to competence in
the procedures performed. Future evolution will be based on continual
advancements in the speciality and related areas, as well as the development
of new techniques. While medical education may improve a core fund of
general knowledge, surgical residency is the determinant of surgical
competence and the scope of practice.
Pros and cons of the speciality

Rapid growth and development of the speciality provide a wide range of
opportunities for the students and increase the scope of the speciality.
Unfortunately, due to the overlapping of the speciality with other
specialities like ENT, ophthalmology and likewise, we are unable to achieve
any kind of generalisation, which the other surgeons have achieved.
The goal of oral surgery is to provide the highest level of training in the full
scope of oral and maxillofacial surgery and to ensure the development of
skilled surgeons capable of providing continued comprehensive care. The
curriculum should have a strong academic flavour with a high priority given
to research.
SECTION II
Diagnosis
Chapter 2: History Taking and Clinical Examination

Chapter 3: Radiodiagnosis
Chapter 4: Diagnostic Aid—Haematological, Biochemical and
Microbiological Investigations
Chapter 5: Histopathological Investigation
CHAPTER 2
History Taking and

Clinical Examination
History taking
Chief complaints
History of present illness
Past medical history
Past surgical history
Past dental history
Family history
Social and occupational history
Personal history
General examination
Local examination
Extraoral examination
Intraoral examination
History
Duration
Mode of onset
Pain
Discharge
Inspection
• Number
• Position
• Site
• Size and shape
• Floor
• Edge
• Discharge
• Surrounding area
Palpation
• Tenderness
• Edge and surrounding tissue
• Base
• Mobility
• Bleeding
History taking
Duration
Mode of onset
Site/shape
Pain
Similar swelling
Inspection
• Number
• Site
• Size and Shape
• Colour
• Surface
• Edge
• Base
• Skin over the swelling
Palpation
• Local temperature
• Tenderness (pain on pressure)
• Position, size and extent
• Surface
• Edges or margins
• Consistency
• Fluctuation
• Translucency
• Reducibility
• Anatomical plane and fixity
Auscultation
Examination for pressure effects
Aspiration
Symptom: Any sensation or change in the body function that is expressed only
by the patient and is associated with particular disease.
Sign: Any objective evidence of disease. It can be recognised by the patient,
dental surgeon or others.
Swelling: Swelling refers to a localised or generalised enlargement.
Ulcer: A local defect or excavation of the surface of an organ or tissue produced
by the sloughing of necrotic inflammatory tissue.
Growth: Proliferation of tissue.
Percussion: Listening to the sounds produced by tapping with a finger or
percussing with a hammer.
Fistula: An abnormal passage leading from a suppurative cavity to the body
surface.
Abscess: An abscess is a pathological thick walled tissue cavity filled with
necrotic tissue, bacteria and leucocytes caused by localised collections of
purulent inflammatory tissue and suppuration from infection in a buried
tissue, organ or confined space.
Aneurysm: This is a localised dilatation or ballooning of a blood vessel.
Bruit: A sound reflecting turbulence of flow, especially an abnormal sound.
Edge: It indicates the margin of the lesion.
Floor of ulcer: Exposed surface of the ulcer.
Macule: Focal area of colour change which is not elevated or depressed in
relation to its surroundings.
Papule: Solid, raised lesion which is less than 5 mm in diameter.
Nodule: Solid, raised lesion which is greater than 5 mm in diameter.
Sessile: Describing a growth whose base is the widest part of the lesion.
Pedunculated: Describing a growth whose base is narrower than the widest
part of the lesion.
Verrucous: Describing a growth exhibiting a rough, warty surface.
Vesicle: Superficial blister, 5 mm or less in diameter and filled with clear fluid.
Bulla: Large blister, greater than 5 mm in diameter.
Pustule: Blister filled with purulent discharge.
Fissure: Narrow slit-like ulceration or groove.
Plaque: Lesion that is slightly elevated and is flat on its surface.
Petechiae: Round pinpoint haemorrhage.
Ecchymosis: Nonelevated area of haemorrhage larger than petechiae.
Telangiectasia: Vascular lesion caused by dilatation of small, superficial blood
vessel.
An integral aspect of patient evaluation and management is the development

of a clinical differential diagnosis. It applies the knowledge of various
pathologic entities that involve the region, information obtained from the
history, physical examination and initial radiographs (for lesions of bone).
The diagnosis should be done in the sequential manner:
• Complete history
• Clinical examination
• Radiographic and other laboratory investigations
• Diagnosis
History taking
Name
Name is mandatory for identification purposes.
Age
The occurrence of disease definitely has predilection for different age groups.
For example:
Congenital abnormalities
Cleft lip, cleft palate (Fig. 2.1A, B)
Infants
Epstein pearls and Bohn nodules, melanotic neuroectodermal tumour of
infancy
Children
Haemangiomas, eruption haematoma
Young adults
Fibrous dysplasia, some sarcomas
Middle and old age
Ameloblastoma, carcinoma, Paget disease
FIGURE 2.1 (A) Cleft lip and palate. (B) Isolated cleft palate.
Address
The knowledge of geographical distribution of diseases is important. In the
hospital record, the full postal address of the patient should be recorded for
future correspondence and follow-up
Sex
Certain diseases affect one sex exclusively or preferentially
Haemophilia
Affects males only although the disease is transmitted through females
Pregnancy tumour
Exclusively in females
Chief complaints
• Patient is asked to describe the problem or the reason for seeking
treatment along with duration
• Should be recorded in patient’s own words
History of present illness

• Site along with the duration of the complaint
• Onset progress of the problem
Lesions present at/from birth : Congenital, developmental
Slowly growing (months to : Reactive hyperplasia, cysts, benign tumours
years)
Moderately growing masses (few : Chronic infections, cysts, malignant tumours
weeks to 2 months)
Rapidly growing masses (hours : Abscesses, infected cysts, aneurysms, salivary
to days) extravasation/retention phenomena, haematomas
Swelling recurring only during : Sialolithiasis
eating
Swelling associated with fever : Infection, lymphomas
• Whether associated with pain

• Any history of associated fever or rigors, if any how long
• Whether the symptom is recurrent in nature
• Whether associated with tooth
• Any associated discharge or secondary changes
Purulent : Infected cyst, abscess

Serous : Parotid fistula
Serosanguineous : Carcinomatous ulcers
Bluish black discharge with granules : Actinomycosis
• Whether the patient has received consultation or undergone any

treatment
• Similar symptom in any other part of the body

An elaborate past medical history should be elicited.
For example:
CVS
Myocardial infarction, angina pectoris, congestive cardiac failure, rheumatic
heart disease, congenital heart diseases, valvular disease, infective
endocarditis and hypertension
RS
Bronchial asthma, bronchitis, chronic obstructive pulmonary disorder (COPD)
GI
Peptic ulcer, gastritis, cirrhosis, jaundice, hepatitis
GU
Pregnancy, postpartum, lactation, periodicity of menstrual cycle, use of
contraceptives, renal failure
Endocrine
Hyperthyroidism, diabetes mellitus, Addison disease, Cushing syndrome,
hyperparathyroidism (Fig. 2.2)
FIGURE 2.2 Brown tumour of bilateral nasomaxillary complex in a

known case of hyperparathyroidism.
CNS
Seizures, hemiplegia, previous head injury, psychiatric disorders
Bleeding/clotting disorders
Haemophilia, anti-coagulant therapy, ITP
Infectious disease
Tuberculosis, acquired immunodeficiency syndrome (AIDS), herpes, hepatitis
Allergy to pharmacotherapeutic agents or other allergies.
Any medication being taken like nonsteroidal antiinflammatory drugs
(NSAIDs), corticosteroids, anticoagulants, antiepileptic drug, antidepressants.
• Liver disorders: Cirrhosis, jaundice, hepatitis

• Bleeding disorders: Haemophilia, anticoagulant therapy
• Respiratory disorders: Bronchial asthma, chronic obstructive lung disease
• Neurological disorders: Seizures, hemiplegia, history of head injury
• Renal disorders: Renal failure, dialysis
• Reproductive system: Pregnancy, postpartum, lactation, periodicity of
menstrual cycle, use of oral contraceptives
• Gastric disorders: Peptic ulcer, diarrhoea, vomiting
• Endocrine disorders: Hyperthyroidism, diabetes
• Allergy to pharmacotherapeutic agents or other allergies
• Any medication being taken: Like NSAIDs, corticosteroids, anticoagulants,
antiepileptic drugs
Past surgical history

Detailed past surgical history with diagnosis, procedure and postsurgical
details is mandatory.
Any history of blood transfusions, allergies, complications due to general
anaesthetics/muscle relaxants/reversing agents used need to be elicited.
Any history of treatment of facial bone fractures and usage of rigid fixation
implants.
Past dental history

History of past dental treatments undertaken should be elicited.
• History of extraction, scaling, filling, root canal treatments, minor

surgical procedures
• History of any implants, prosthesis used
• History of allergy, complication due to local anaesthetics
• Eventful/uneventful postextraction period
Any history of dental extractions, conservative treatment and any prosthetic

appliance should be noted .
Family history
• Age and health status of parents, siblings and children
• Cause of death of deceased family members
• History of parental consanguinity
• Any history suggestive of hypertension, diabetes, neoplasia, bleeding
disorders, facial deformities, infectious diseases
• History of similar defect or disorder in the parent or immediate
relative indicating inheritance (Fig. 2.3)
FIGURE 2.3 Treacher Collins syndrome —father and son.
Social and occupational history

• Identify the psychosomatic disturbances
• History of recent travel
Occupation
Physical and environmental factors with emotional strains and stresses may be
reflected in the oral cavity.
• Silicosis, berylliosis : Glass factory workers
• Hepatitis and HIV risk : Commercial sex workers, health care workers and surgeons
• Leukaemia : Radiologists
Personal history
Diet
Vegetarian or nonvegetarian
Brushing habits
Tobacco abuse
Which form of tobacco consumption, duration of habit and frequency of use
Alcohol abuse
Duration, quantity and frequency
In females
Menstrual history, pregnancy, lactation
General examination
Examination of the patient represents the second stage of diagnostic
procedure:
• Level of consciousness
• Ambulatory or nonambulatory
• Gait disturbances
• Built—well built/moderately built/poorly built
• Nourishment—well nourished/undernourished
• Structural deformities or alterations—for example syndactyly,
kyphosis, scoliosis and so on
• Psychological status
• Patient’s general state of mind, whether calm and quite or any
discomfort, restlessness
• Built of the individual
• Nourishment of the individual—whether undernourished or
malnourished
• Structural deformities and alterations, if any, should be observed
Vital signs
• Temperature
• Pulse rate
• Respiratory rate
• Blood pressure
Peripheral signs
• Anaemia
• Cyanosis
• Jaundice
• Clubbing
• Pedal oedema
Systemic examination
A systematic examination of the general body systems including
cardiovascular, gastrointestinal, central nervous and genitourinary systems is
carried out. Any relevant abnormalities are documented.
Local examination
Extraoral
• Inspection
▪ Facial symmetry
♦ Soft tissue symmetry
♦ Symmetry of movement of soft tissues (nerve)
♦ Skeletal symmetry
♦ Symmetry of movement of hard tissues (joint)
▪ Facial proportions
▪ Facial profile
▪ Skull form
▪ Skin and soft tissue
♦ Eye
♦ External ear
♦ Nose
♦ Lips
• Palpation
▪ TMJ examination
▪ Lymph node examination
▪ Salivary gland examination
Intraoral
• Jaw movements and mouth opening

• Teeth
• Gingiva
• Alveolar mucosa
• Labial mucosa and lip
• Buccal mucosa
• Palate and fauces
• Tongue
• Floor of the mouth
Inspection
A close observation of the abnormal area (lesion) is made. Then the site of the
lesion is carefully observed and compared to the normal architecture of the
structure giving consideration for age, gender and site. The spectrum of the
change can range from complete absence as in aplasias to extensive
overgrowth (neoplastic). Based upon these deviations, the time, magnitude,
direction and the degree of response of the tissue to the aetiological agent
(causative factor) are determined. This comparison of abnormal or anomalous
areas to the supposed or normal tissues should be carefully performed taking
into account the principles of facial growth, bone remodelling, development of
facial musculatures, as well as the extent of muscle activity.
The structural alteration could be as a result of:
a. Congenital anomalies (agenesis/hypoplasia/hyperplasia)

b. Developmental anomalies (hypotrophic/hypertrophic)
c. Traumatic (abrasion/erosion/ulceration/laceration/simple, compound,
comminuted or greenstick fractures/avulsive/denervation)
d. Neoplastic (nodular/ulcerative/papillomatous/proliferative)
e. Infective (swelling/redness/loss of function)
1. Facial symmetry (Fig. 2.4A–T)

Symmetry of the face depends on:
• Soft tissue symmetry

• Symmetry of movement of soft tissue (nerve)
• Skeletal symmetry
• Symmetry of movement of hard tissue (joint)
FIGURE 2.4 ( A ) Hemifacial atrophy (Parry Romberg syndrome) .

( B) Hemifacial microsomia (OMENS). (C) Plexiform
neurofibromatosis. (D) Postburn scar . ( E-H) Congenital facial
lipomatosis involving left -side face progressive with age . (I) Left
canine space infection with orbital cellulitis. (J ) Haemangioma .
(K) Ulceroproliferative lesion—squamous cell carcinoma.
(L) Complete facial palsy. Right lower motor neuron lesion (LMNL).
(M) Ptosis of right upper eyelid. (N) Postsurgical ablation—loss of
hard tissue induced facial asymmetry. (O) Loss of hard tissue
posttrauma. (P) Cementifying fibroma of right maxilla—
superolateral displacement of right orbital contents.
(Q) Hemimandibular elongation—left side. (R) Unilateral TMJ
ankylosis with secondary deformity. (S) Left orofacial cleft.
(T) Facial asymmetry from left mandibular osteoma.
Soft tissue symmetry

Quantum of the soft tissue defect or excess and the texture or morphology
change are observed as asymmetries of the soft tissue. Colour change, texture
change, as well as size change are noted.
For example
• Defect—hemifacial atrophy, hemifacial microsomia

• Excess—masseter hypertrophy, neoplasm, neurofibromatosis, facial
lipomatosis, abscess, cellulitis
• Colour change—haemangiomas, inflammatory swellings
• Texture change—ulcer, sinus opening
Symmetry of soft tissue movement

Eliciting motor functions of the facial musculature (7th) and ocular muscles
(3rd, 4th, 6th) cranial nerves will display the underlying asymmetry of the face
in function.
For example
Asymmetric smile, inability to close the eye and lift the eyebrow—facial palsy.
Skeletal symmetry
Though confirmation of skeletal symmetry can be done only through
radiographic examination, measurement of deviation of the structure from the
midline/original size is considered.
For example
• Loss of hard tissue (postsurgical/trauma)

• Bony enlargement (jaw tumours)
• Dentofacial deformities (hemimandibular elongation or hypoplasia)
Symmetry of hard tissue movement
Asymmetry on opening and closing the mouth (deviation on mouth opening)
signifies a TMJ ankylosis.
For example
• Traumatic: Condylar fracture, internal derangement

• Congenital: Hemifacial microsomia
Detailed examination of each structure or lesion are described in detail in

the relevant chapters.
2. Facial proportions
Relation between upper, middle and lower third face. This is mainly measured
for orthognathic surgery and for details refer to Chapter 35.
3. Facial profile
The profile of the patient is generally classified as orthognathic, concave or
convex. Details about the same can be found in the Chapter 35.
4. Skull form (Fig. 2.5A–L)

Skull form is determined by early sutural synostosis.
a. Scaphocephaly (boat shaped): Sagittal suture synostosis

b. Brachycephaly: Bilateral coronal suture synostosis
c. Plagiocephaly: Unilateral coronal suture synostosis
d. Trigonocephaly: Metopic suture synostosis
e. Turricephaly (tower skull): Bilateral coronal along with multiple suture
synostosis
f. Oxycephaly: Bicoronal and multiple suture synostosis
g. Clover leaf skull (Kleeblattschadel anomaly): Bitemporal synostosis
FIGURE 2.5 (A–D) Scaphocephaly–premature sagittal synostosis.
(E–H) Turricephaly–tower head deformity–premature synostosis of
bicoronal with other sutures. (I, J) Trigonocephaly–premature
metopic suture synostosis. (K) Plagiocephaly showing flattened left
forehead. (L) Premature fusion of left coronal suture.
5. Skin and soft tissue (Fig. 2.6A–D)

Changes in the colour, texture of the skin/surrounding structures as well as the
anomalous shape of the structure are noted in the soft tissue examination.
FIGURE 2.6 (A) Albinism. (B) Haemangioma. (C) Cafe au lait
spots in neurofibromatosis. (D) Hairy naevus.
Pallor—anaemia, vitiligo, albinism

Discolouration—inflammation, haemangioma, SLE, ecchymosis, naevi,
melanoma, Addison disease, cafe au lait spots, psoriasis, telangiectasia—
numerous inherited or congenital conditions display cutaneous telangiectasia.
• Osler–Weber–Rendu syndrome
• Sturge–Weber syndrome
• Ataxia telangiectasia
• Texture-proliferative lesion like squamous cell carcinoma
I. Eye (Fig. 2.7A–I)
• Though ophthalmic examination needs to be performed by a specialist,

certain basic findings need to be elicited before arriving at a
provisional diagnosis
• Presence/absence of structures of the eye
• Visual acuity/field of vision
• Intercanthal distance: Increased hypertelorism, decreased
hypotelorism
• Interorbital distance
• Interpupillary distance
• Eye movements: Extraocular muscles
• Asymmetry in movement/and at rest: Strabismus
• Cleft (craniofacial clefts)
• Coloboma: Congenital craniofacial deformities
• Proptosis, exophthalmos: Hyperthyroidism
• Subconjuctival haemorrhage: Circumorbital oedema, enophthalmos
FIGURE 2.7 (A) Anophthalmia. (B) Increase in intercanthal

distance—traumatic telecanthus (interpupillary and interorbital
distance normal). (C) Increased interorbital distance—
hypertelorism (increased interpupillary and interorbital distance).
(D) Orbital hypertelorism with epicanthal folds and bilateral nasal
cleft. (E) Unilateral orbital hypertelorism with dystopia.
(F) Strabismus. (G) Goldenhar syndrome—mandibular hypoplasia,
epibulbar dermoid with ear deformity. (H) Subconjunctival
haemorrhage, circumorbital oedema, swelling due to trauma with
abrasion. (I) Exophthalmos—Crouzon’s syndrome.
II. External ear (Pinna) (Fig. 2.8A–F)
• Anotia: Complete absence of external ear

• Positional changes: Low set ears
• Change in morphology: For example, microtia, bat ears, cupped ears
• Preauricular skin tags: Hemifacial microsomia
• Preauricular sinus: For example first arch syndrome
• Ear bleed: For example, condylar fracture
• Discharge: For example, middle ear infection
FIGURE 2.8 (A) Anotia–absence of external ear. (B) Microtia. (C)

Bat ear deformity. (D) Cup ear deformity. (E) Low set ear with pre-
auricular skin tags. (F) First branchial cleft sinus.
III. Nose (Fig. 2.9A–F)

Changes in size, shape, symmetry of the nasal structures, such as the ala,
columella, septum, dorsum and the nasion, should be examined and
documented. Congenital deformities like the cleft, hemirhinia, hypertelorism,
encephalocele are accompanied by nasal deformities pathognomonic to the
nature of the lesion.
• Asymmetric ala, septum and dorsum: Unilateral cleft lip nose

• Depressed nasal bridge, shortened columella and broad nasal base:
Bilateral cleft lip nose
• Discharge from the nose: Epistaxis, CSF rhinorrhoea (trauma)
• Regurgitation of fluids: Oronasal fistula
• Septal deviation
FIGURE 2.9 (A) Arhinia. (B) Asymmetric ala, septum and dorsum
associated with unilateral cleft lip (operated). (C, D) Depressed
nasal bridge, shortened columella and broad nasal base—bilateral
cleft lip. (E) Deviated nasal septum. (F) Bilateral cleft ala.
IV. Lips (Fig. 2.10A–C)

The colour, contour, size, shape and symmetry of the lip are examined.
FIGURE 2.10 (A) Lip pits–lower lip. (B) Macrostomia. (C) Lateral
facial cleft.
• Colour change: Vitiligo, cheilitis, smoker’s melanosis, haemangiomas

• Contour: Cleft, lip pits, tumours
• Size: Macrostomia
• Asymmetry: Facial palsy
Palpation
Confirmation of inspectory findings. Palpation of each lesion is described in
detail in the following sections.
1. Temporomandibular joint (TMJ)
The TMJ is examined bilaterally in the preauricular area. Palpate directly over
the joint with index finger when the mandibular movements are made. The
joints can be palpable by two methods:
i. Intraaural (finger through the external auditory meatus)

ii. Preauricular (anterior to tragus).
The joint may also be auscultated for crepitus or popping sounds. Detailed
description on examination and diagnosis of TMJ disorders has been
explained in the Chapter 38.
2. Lymph node examination (Fig. 2.11)

The body has approximately 600 lymph nodes but only those in the
submandibular axillary or inguinal regions may be normally palpable in
healthy people. Lymphadenopathy refers to nodes that are abnormal in size,
consistency or number. If lymph nodes are enlarged in two or more
noncontiguous sites it is termed generalised and localised if only one area is
involved.
FIGURE 2.11 Lymph nodes of head and neck.
If lymph nodes are detected, the following characteristics should be noted

and examined (Table 2.1).
Table 2.1
Lymph nodes in the neck (Fig. 2.11)

Level Nodes Anatomic boundaries
I Submental Nodal tissues between anterior belly of digastric muscles and
cephalad to hyoid bone
Submandibular Nodal tissues in the triangular area bounded by anterior and posterior
bellies of digastric and inferior border of body of mandible
II Upper jugular Nodal tissues around upper portion of internal jugular vein (IJV) and
group upper part of spinal accessory nerve, extending from base of the skull
(jugulodigastric) up to bifurcation of carotid artery or hyoid bone. Posterior limit—
anterior border of sternocleidomastoid muscle. Anterior border—
lateral limit of sternohyoid muscle
III Midjugular group Nodal tissue around upper portion of IJV from inferior border of level
(juguloomohyoid) II up to the omohyoid muscle or cricothyroid membrane
IV Lower jugular Nodal tissue around lower third of IJV from inferior border of level III
group up to clavicle
(supraclavicular)
V Posterior triangle Nodal tissue around lower portion of spinal accessory nerve and
group along transverse cervical vessels and bounded by triangle formed by
clavicle, posterior border of sternocleidomastoid and outer border of
trapezius
Size
Nodes are generally considered to be normal if they are up to 1 cm in diameter
and become palpable only when enlarged.
Pain/tenderness
When a lymph node increases in size, its capsule stretches and causes pain.
Pain is usually the result of any inflammatory process or suppuration, but may
also result from haemorrhage into the necrotic centre of a malignant node. The
presence or absence of tenderness does not reliably differentiate benign from
malignant conditions.
Consistency
Stony hard
Carcinoma usually metastatic
Firm rubbery nodes

Lymphoma
Soft nodes
Infections or inflammatory conditions
Suppurant nodes
Fluctuant
Shotty nodes
Refers to small nodes that feel like buckshot under the skin, as found in the
cervical nodes of children with viral illness
Matted nodes
A group of nodes that are instead of feel connected and seem to move as a
unit. Nodes that are matted could be benign like in tuberculosis, sarcoidosis,
lymphogranuloma venereum or malignant like metastatic carcinoma.
Location
Localised lymphadenopathy is based on the infection or lesion in the node per
se or in its drainage area.
For example
• Oral infection: Submandibular/submental

• Tonsilitis: Upper jugular nodes
3. Salivary glands examination (Fig. 2.12A, B)
Parotid gland
Parotid gland swelling typically presents as preauricular swelling elevating
the ear lobule.
FIGURE 2.12 (A) Examination of parotid gland swelling. (B)

Bimanual palpation.
In case of glandular swelling the location, size and shape of the swelling are
assessed as for any other swelling. Motor nerve function of facial or ipsilateral
side should be assessed to rule out nerve compression or involvement.
Intraorally, any inflammation of the duct opening or pus discharge from the
opening is noted.
Sublingual and submandibular glands

Bimanual palpation of the gland is done with index fingers, one intraorally
and the other extraorally medial to lower border of the mandible.
Intraorally, the openings of the duct are identified and any inflammation,
quality of salivary flow and pus discharge are noted.
A. Jaw movements and mouth opening (Fig. 2.13A, B)
• Mouth opening: It is assessed as maximal interincisal distance

measured from maxillary to mandibular central incisors. In case of
edentulous patient alveolar ridge of both jaws.
• Protrusion, retrusion and lateral movements are assessed to detect any
deviation from midline.
FIGURE 2.13 (A) Deviation on mouth opening due to TMJ internal

derangement. (B) Limitation in mouth opening—trismus.
B. Teeth (Fig. 2.14A, B)
• Number
• Size and shape
• Colour
• Root stumps
• Dental caries
• Missing teeth
• Occlusion
• Occlusal plane parallelism to the pupillary plane
FIGURE 2.14 (A ) Yellowish discolouration of the teeth. ( B) Dental

caries of upper anterior teeth.
C. Gingiva (Fig. 2.15A–F)
• Size
• Shape
• Contour
• Colour
• Bleeding
• Ulceration
• Abnormal growth
• Pockets
FIGURE 2.15 (A) Haemangioma—right retromolar region. (B)

Bleeding on provocation. (C) Epulis. (D) Pyogenic granuloma.
(E) Malignant melanoma. (F) Gingival fibromatosis.
D. Alveolar mucosa
• Colour
• Contour
• Consistency
FIGURE 2.16 Buccal mucosa showing alterations associated with
submucous fibrosis.
E. Labial mucosa (Fig. 2.16)
• Labial mucosa and lip

• Assess for any alteration in:
▪ Colour
▪ Texture
▪ Vermilion border
FIGURE 2.17 Buccal mucosa showing altered texture in a white
lesion.
F. Buccal mucosa (Fig. 2.17)
• Colour
• Contour
• Consistency
G. Palate and fauces (Fig. 2.18A, B)
• Colour
• Contour
• Consistency
• Tonsils—enlargement, infection and lith
• Soft palate—movements
FIGURE 2.18 (A) Intraoral examination—palatal fistula. (B) Palatal
abscess due to fractured 22 (left lateral incisor).
Oropharynx (palatine and pharyngeal tonsils, posterior pharyngeal wall,

uvula, anterior and posterior pillars)
Any enlargement of tonsil, deviation of uvula or swelling are noted.
H. Tongue (Fig. 2.19A–I)
• Size
• Shape
• Protrusion
• Retraction
• Lateral movements
FIGURE 2.19 (A) Macroglossia. (B) Beckwith–Wiedemann
syndrome—macroglossia. (C) Tongue enlargement—
haemangioma. (D) Lymphangioma. (E) Sublingual dermoid. (F)
Sublingual lymphangioma. (G) Cystic swelling within the
musculature of the tongue. (H, I) MRI with contrast showing an
intralingual cystic mass.
I. Floor of the mouth
• Colour
• Swelling/ulcer
• Ductal opening—dilatation, inflammation, sialolith
History
Duration
• Short (less than 2 weeks): Acute ulcer

• Long (more than 2 weeks): Chronic ulcer
Mode of onset
• Traumatic ulcer: Primary healing/secondary healing

• Delay in healing: Specific (healing may delayed in case of diabetes,
tuberculosis, syphilis or some neurological disease) infection/general
disease in background
• Tuberculous lymph nodes: Nodule or lump precedes the ulcer
Pain
• Syphilitic/trophic ulcer: Painless

• Tuberculous/aphthous ulcer: Painful
• Carcinomatous ulcer: Complete absence of pain in early stages, painful if
secondarily infected
Discharge
• Nature of discharge: Serum/pus/blood
Inspection (Fig. 2.20A–C)
I. Number
FIGURE 2.20 (A) Ulceration on the right lateral border of the

tongue. (B) Squamous cell carcinoma—ulceroproliferative lesion
with secondary changes in the surrounding skin. (C) Basal cell
carcinoma in the right inner canthus of eye.
Single: Tumour (basal cell carcinoma, squamous cell carcinoma)
Multiple: Aphthous ulcer
Herpetic ulcer
Allergic stomatitis
Pemphigus
II. Position
Rodent ulcer (BCC): Common in the face, 80% above the line joining the
corner of the mouth to the ear lobule
Herpetic ulcer: Angle of mouth and around lips
III. Site
• Herpetic ulcer: Attached mucosa

• Aphthous ulcer: Mobile mucosa
• Minor salivary gland tumour: Posterior hard palate
• Tuberculous ulcer: Tip of tongue and neck
IV. Size and shape
• Carcinomatous ulcer: Irregular

• Tuberculous ulcer: Oval but coalescence may give them irregular border
V. Floor
Look for presence of any slough or membrane.
• Healthy and healing: Red and florid granulation tissue

• Slow healing: Pale and smooth granulation
• Gummatous ulcer: Wash leather slough (pathognomonic)
• Squamous cell carcinoma: Fungation or cauliflower appearance
• Malignant melanoma: Ulcerated black mass
VI. Edge
• Spreading ulcer: Inflamed and oedematous

• Healing ulcer: Red granulation tissue in the centre followed by blue
zone, white zone in the periphery
• Tuberculous ulcer: Undermined and blue
• Gummatous ulcer: Thick, perpendicular and clearly punched out
• Squamous cell carcinoma: Raised and rolled out
• Rodent ulcer: Raised and have pearly white beaded
• Carcinomatous ulcer: Exhibits growth in excess of destruction (especially
at the edges)
• Basal cell ulcer: Everted edges
VII. Discharge
Character, amount and smell should be noted.
• Normal healing: Little and serous discharge

• Spreading ulcer: Copious and purulent discharge
VIII. Surrounding area
• Acute inflamed ulcer: Red, glossy and oedematous.
Palpation
I. Tenderness
Extremely painful: Acutely inflamed ulcer

Non-tender/painless: Chronic nonhealing ulcer
II. Edge and surrounding tissue
SCC (carcinomatous ulcer): Marked induration

Cellulitis: Cardboard-like consistency
III. Base
Acute ulcer: Soft

SCC: Marked induration
IV. Mobility
Carcinomatous ulcer: Fixed
V. Bleeding
Malignant ulcer and healthy granulation tissue bleeding during palpation.
History taking
Duration
• Birth: Congenital epulis, congenital neurofibroma, cystic hygroma

• Short duration: Inflammatory swelling
• Long duration: Neoplastic (benign)
Mode of onset
• Immediately after trauma: Haematoma

• Spontaneous and grow rapidly: Inflammation
• Rapid onset: Malignant swellings especially sarcomas
• Spontaneous and steady growth: Benign
• From burn scar/ulcer/vaccination/pricking of ear/keloid
Site/shape
• Midline swelling: Dermoid cyst, thyroid swelling, thyroglossal cyst

• Lateral swelling: Submandibular swelling, carotid body tumour,
parapharyngeal tumour
• Dumbell shape: Temporal and infratemporal space infection
• Hemispherical: Swelling ranula
Pain
• Site: Localised/generalised/referred
• Character: Throbbing/dull
• Throbbing: Inflammatory lesion tending to suppurate
• Lancinating: Abscess
• Dull: Non-specific
• Painless: Benign and early carcinomas
Similar swelling
Enquire about similar swelling elsewhere in the body, for example Hodgkin
lymphoma, neurofibroma.
A. Inspection (Fig. 2.21A, B)
I. Number
Whether single or multiple.
Single: Isolated swelling like thyroglossal cyst

Multiple: Generalised swellings as in neurofibromas, lipomas (Dercum’s
disease)
FIGURE 2.21 (A) Proliferative growth in the right lateral border of

the tongue (squamous cell carcinoma). (B) Swelling in left
masseteric region.
II. Site
Dermoid cyst occurs in the areas of embryological fusion (above the outer
canthus of the eye, midline).
III. Size and shape

Whether ovoid, spherical, pyriform or irregular.
IV. Colour
Haemangioma: Red or purple

Ranula/mucocele: Blue
V. Surface
Whether smooth, lobulated or irregular.
Smooth: Cyst
Rough or irregular: Carcinoma
Ulceroproliferative: Squamous cell carcinoma
Cauliflower-like appearance: Verrucous carcinoma, papilloma
VI. Edge
Whether well defined, ill-defined or diffuse.
VII. Base
Pedunculated or sessile.
VIII. Skin over the swelling

Smooth or any discharge or changes such as fistula, sinus, ulceration and
punctum (sebaceous cyst).
• Engorged vein or visible pulsation

• Pigmentation
• Any scar formation
• Inflammation—red and oedematous
• Sarcoma—tense, glossy and often red in which subcutaneous veins
become characteristically dilated and engorged, owing to increased
vascularity
• Carcinoma infiltrating towards the skin—peculiar oedema of the cutis
—peau d’orange is often seen
• Scar—postoperative (linear scar with suture marks), injury (irregular
scar) or suppuration (broad, depressed and puckered scar).
B. Palpation
I. Local temperature
Local temperature is always raised in all acute inflammatory swellings, but
some rise of local temperature is quite common in sarcoma, especially that of
bone, on account of increased vascularity.
II. Tenderness (pain on pressure)

As opposed to pain, which is a symptom, tenderness is a sign. Tenderness is
more marked in inflammatory conditions than in new growths.
III. Position, size and extent

The position, size and extent of the lesion in relation to the underlying
anatomic structures is of significance in diagnosis (e.g. a midline swelling in
neck that moves with deglutition and tongue protrusion is indicative of
thyroglossal cyst).
IV. Surface
• Smooth: Cyst
• Lobular: Lipoma
V. Edges or margins
• Rough and irregular: Carcinoma

• Well defined, smooth: Benign growth
• Well defined, irregular and rough: Malignant growth and chronic
inflammation
• Well defined, when pressed upon its slips away under the examining
finger: Subcutaneous lipoma
• Well defined but yield to the palpating finger—cyst
VI. Consistency
• Soft: Lipoma
• Cystic: Cyst and chronic abscess
• Firm: Fibroma
• Hard but yielding: Chondroma
• Stony hard: Secondary carcinoma of lymph nodes
• Bony hard: Osteoma and osteoclastoma
• Gaseous swelling: Surgical emphysema, gas gangrene. Gaseous
swellings (e.g. surgical emphysema, gas gangrene) give a peculiar
crepitus on gentle palpation. Soft or cystic swelling suggests fluid in it
Some sebaceous and dermoid cysts in which the contents are pultaceous or
putty-like. Such cysts, when pressed upon, can be moulded into different
shapes.
VII. Fluctuation
Fluctuation is characteristic of cystic swellings, that is swellings which contain
fluid. Fluctuation is usually a reliable sign though it is occasionally absent in a
tense cyst.
VIII. Translucency
Swelling that contains clear fluid appears translucent, for example ranula
(bluish translucent mass in the floor of the mouth due to submandibular gland
duct obstruction).
IX. Reducibility
Compress the swelling and note the degree of reducibility. Swellings, for
example haemangioma, lymphangioma, are reducible either partially or
completely.
X. Anatomical plane and fixity
Fixity to the skin: Swellings arising from the skin, for example papilloma,
cutaneous wart, sebaceous cyst, epithelioma and so on, move with the
movement of the skin. When the skin is fixed, it can neither be moved
nor be pinched up. This occurs in inflammatory conditions and
carcinoma. The skin over a rapidly growing mass as sarcomas may be
stretched making it immobile though not fixed. Tumours in the
subcutaneous tissue are free from the skin and move freely over the
contracted muscle, for example lipomas.
Fixity to the muscle: To test the relation of a tumour to the adjacent
muscle, the patient is made to contract the muscle and observe
whether the swelling:
▪ Diminished in size—mass lies under the muscle
▪ Remains unaltered—mass is incorporated in the muscle.
▪ Becomes prominent—mass is superficial to the muscle and is
pushed forwards by the underlying taut muscle.
Fixity to vessels and nerves: Tumours in connection with vessels and nerves
can be moved across (i.e. at right angles to their axes) but not along the
direction of their axes.
Thrill is palpable murmur commonly found in arteriovenous malformation.
C. Auscultation
All pulsatile swellings as aneurysms or AV malformations should be
auscultated.
D. Examination for pressure effects

Mandibular swelling compresses the inferior alveolar canal and can cause
paraesthesia of the inferior alveolar nerve dermatome (e.g. ameloblastoma).
Parotid swelling compressing or involving the facial nerve can cause facial
paresis or palsy, for example malignant pleomorphic adenoma.
E. Aspiration
Aspiration is the last part of examination of the swelling as it is invasive.
Aspiration is done only in cystic and fluid filled masses. It is should be
performed only with large wide bore (18 gauge) needle. The aspirated content
may contribute for the diagnosis of the lesion. In suspected vascular lesions
aspiration is contraindicated.
• Straw coloured fluid: Dentigerous cyst, periapical cyst

• Curdy white: Odontogenic keratocyst
• Frank pus: Abscess or infected cyst
• Negative aspiration: Stafne bone cyst (traumatic bone cyst)
• Blood: AV malformations, haemangioma
Ulcerative conditions
Syphilis Primary
• Initially the disease begins with a chancre on the skin
• Commonly affected sites are mouth, rectum and genitals
• Chancre is firm, round and not tender to touch
• The chancre heals after 2–6 weeks
Secondary
• The rash is reddish brown in colour, not itchy and is widespread
• Lymph node swelling is common
• All symptoms of this stage will disappear within 3 weeks–9 months
Latent
• This stage lasts up to few years
• However, a man in latent stage is still infected and can be diagnosed by
blood test
Tertiary
• Symptoms include painful, nonhealing skin ulcers, bone pain, liver
disease and anaemia
• Many vital organs will be affected
Behchet syndrome Genital ulcers, oral ulcers, uveitis
Reiter syndrome Arthritis, conjunctivitis, urethritis and oral ulcers
Cyclic neutropaenia Oral ulcers, adenopathy, periodontal problems
Carcinoma of Ulcers in the palate, sinusitis, malocclusion
maxillary sinus
Gonorrhoea In male
• A yellow, green or white discharge from penis
• Tender or swollen opening of the penis
• Tender testicles
• Sore throat
In female
• Vaginal discharge
• Pain or burning sensation while urinating
• Fever
• Sore throat
• Pain in the abdomen
Tubercular ulcer • Ulcers with shallow base and rolled out margins are present
• These ulcers are very painful in nature
Leprosy • Infiltration, reddish yellow nodules, perforation, ulceration are seen in
the soft palate
• Superficial erosions and loss of papilla are seen on the dorsal surface of
the tongue
Actinomycosis • Sinus with pus discharge is seen in the mandible on the involved side
• The pus contains yellow sulphur granules which is a characteristic
feature of actinomycosis
Noma • Ulcers are present on the gums and the cheeks
• Foul smelling drainage is present causing bad breath
• Destruction of the bone causes facial deformity
Aphthous ulcers • These ulcers usually occur on tongue, lips and floor of the mouth
• They are round or oval in shape usually measuring about 2–4 mm in
diameter
• They usually occur in groups and reoccur at intervals of 1–4 months
Erythema • Vesicles and blisters are seen (BULLAE)
multiforme • Commonly involves face and lips
• It has the characteristic bull’s eye appearance because the central core is
surrounded by red rings
Squamous cell • Non-healing ulcer with rolled out edges
carcinoma • Lymph node involvement is present
• May occur on lips, tongue, alveolar bone, buccal mucosa, floor of the
mouth
Lupus • Chronic autoimmune disease
erythematosus • Malar rash (butterfly shaped erythema over cheeks and nasal bridge)
• Raynaud phenomenon (discolouration of the fingers/toes after
temperature change or emotional events)
• Fatigue, fever and arthralgia
• Ulcers/mucocutaneous involvement, renal involvement
Wegener’s • It is a type of vasculitis or inflammation of the blood vessels
granulomatosis • Fever, skin sores, frequent sinusitis, haemoptysis
• Joint pain and weakness
Red blue lesions

Haemangioma • It is a red or a blue lesion which usually occurs on skin, lips, tongue and
buccal mucosa
• Blanching when pressure applied over it
Pyogenic • It is a red, pink or a purple lesion may be lobulated or smooth
granuloma • They bleed profusely on trauma
• Females are more commonly affected than males
Erythroplakia • It is a fiery red velvety patch
• Usually found on the retromolar area or in the floor of the mouth
• It occurs between 50 and 70 years of age
Kaposi sarcoma • It is a bluish or a reddish malignant lesion of the skin usually found in
AIDS patients
Median rhomboid • Oval or rhomboid shaped area present in the midline on the dorsum of the
glossitis tongue
• The lesion is erythematous and depapillated with a smooth shiny surface
Geographic • This condition is characterised by the presence of smooth depapillated
tongue areas on the tongue thus giving it a map-like appearance
• Burning sensation and soreness of the tongue is present
Anaemia • Loss of papilla on the dorsal surface of the tongue thus giving it a shiny
glossy surface
• Females are more commonly affected than males
• Angular cheilitis is also present
Scarlet fever • Rashes are present all over the body
• Fever, chills, nausea and vomiting are present
• Strawberry tongue is a characteristic feature of scarlet fever
Psoriasis • This disease is characterised by presence of thick red skin with flaky silver
white patches
• Burning and itching sensation of the skin
Vitamin B • Symptoms include sore throat, cheilitis, photophobia, glossitis and fissure
deficiency tongue
Plasma cell • Diffuse reddening and swelling of the gums is present
gingivitis
Blood dyscrasia • Haemorrhagic patches are present (petechiae, ecchymosis)
Peripheral giant • It occurs due to continuous irritation from a trauma
cell granuloma • It is usually bluish purple in colour
• It can be sessile or pedunculated and measures about 2 cm in size
Pigmentations of oral and perioral tissues

Physiologic • This pigmentation is due to increased production of melanin
pigmentation • Most common pigmentation in dark skinned people
• Appears since childhood
Smoking • Brownish and blackish pigmentations are commonly present on the lower lip
associated and the palate
melanosis • Oral melanotic macules are present
Amalgam • It is an iatrogenic pigmentation which is caused by the dentist to the patient
tattoo either during filling, extraction or while preparing a crown for an amalgam
filled tooth
• Usually found on the palate and buccal mucosa
Heavy metal • These are pigmentations caused due to heavy metals like bismuth, mercury,
pigmentation lead and platinum
• These pigmentations commonly involve the marginal gingiva
Melanoma • Melanomas are of two kinds
– Skin melanoma
– Oral melanoma
• Skin melanomas are mainly due to UV rays
• Oral melanomas have poor prognosis
• Most commonly affected area is the palate
Verrucous papillary lesions

Papillary hyperplasia • Red cobblestone lesion, commonly seen in the denture wearers
• It is similar to condyloma latum
Squamous papilloma • White painless cauliflower-like lesion, commonly seen in tongue, floor
of mouth and palate
• Commonly seen in adults
Focal epithelial • Usually appears as multiple painless nodules
hyperplasia • Commonly seen in the tongue, buccal mucosa and floor of mouth
Keratoacanthoma • Firm, well circumscribed, elevated lesion
• Commonly affects skin and nails
Verrucous carcinoma • Indurated malignant lesion, usually white in colour with a rough
surface
Pyostomatitis • Multiple small pustules seen
vegetans • Buccal mucosa commonly affected
Vesiculobullous conditions
Herpes simplex • Initially vesicles with fluid are formed
• These vesicles rupture and form ulcers that are extremely painful
Varicella zoster • Painful ulcers and vesicles are present
• Commonly affects trunk and face
Measles • Koplik spots—clustred, white lesions on the buccal mucosa near each
Stensen duct (pathognomonic for measles)
• Fever, malaise, rashes are other symptoms
Pemphigus • Multiple painful ulcers after the formation of bullae are seen
vulgaris • Nikolsky sign is a characteristic feature
Herpetiformis • Vesicles and pustules are present on the skin and in the oral cavity
dermatitis
Epidermolysis • Bullae followed by the appearance of ulcers
bullosa • May cause scarring
• Nikolsky sign is positive
Herpes zoster • Multiple ulcers along the course of the nerve
• Very painful
• Trunk, head and neck are involved
Hand foot and • Painful lesions present on oral mucosa, hands and feet
mouth disease
Herpangina • Multiple ulcers present in the posterior part of the oral cavity and in the
pharynx
• Children are commonly affected
Cicatricial • Painful bullae are present
pemphigoid • Involves the oral cavity, eyes and the genitals
White lesions
Leukoedema • Grey or white appearance of the mucosa
• Usually bilateral
White sponge naevus • White keratotic macules and papules are present in the
buccal mucosa
• Usually painless
Frictional hyperkeratosis • It is a painless white patch
• Usually involves the edentulous ridge, buccal mucosa and
tongue
Fordyce granules • They are small yellowish or white raised spots seen usually
on the buccal mucosa
• Ectopic sebaceous glands in the oral cavity
Candidiasis • Creamy white patches are present in the oral cavity
• These patches are scrapable
• Sometimes accompanied by painful cracks in the corners of
the mouth
Lichen planus • Bilaterally white striae are present
• Usually asymptomatic
• Papules and lesions are also present
• Lacy white streaks are present on the buccal mucosa called
Wickham striae
Hairy tongue • Elongation of filliform papilla of the tongue
• Usually painless
Hereditary benign intra-epithelial • Painless white lesions, commonly involves the buccal
dyskeratosis mucosa
• Usually it is asymptomatic
Solar cheilitis • Epithelium becomes atrophic, commonly affects the lower
lip
CHAPTER 3
Radiodiagnosis
Plain X-rays
Intraoral radiographs
• Intraoral periapical (IOPA) radiograph
• Occlusal radiograph
Types of mandibular occlusal projections
Types of maxillary occlusal projections
Extraoral radiographs
• Orthopantomogram
• Lateral view skull/cephalogram
• PA view skull/cephalogram
• Occipitomental view
• Waters’ view
• Submentovertex view (SMV)
• Reverse Townes’ view
• Oblique lateral—body
• Oblique lateral—ramus
Digital imaging
Tomography
• Conventional tomography
• Computed tomography
• Cone beam CT
Nuclear medicine
• Radioisotope imaging
Ultrasonography
Diagnosis is defined as the identification of disease after clinical examination

and proper investigation of the clinical signs and symptoms. The process of
eliciting the history of the illness and examining the diseased site using visual
and tactile senses has been explained in detail in Chapter 2. Though diagnosis
can be arrived at using clinical examination alone, some diseases require
further investigation using special aids.
Diagnosis is arrived at by a hypothetico-deductive process, which is refined
in every stage of investigation performed on the patient. When the patient
presents with a complaint, the clinician elicits the history and performs the
preliminary clinical examination to arrive at a ‘provisional diagnosis’ and
‘differential diagnosis’. Based on this provisional diagnosis, relevant
investigations are advised to confirm the diagnosis. While an array of
diagnostic tools is now available to the clinician, these investigative tools are
expensive and sometimes invasive. Therefore, a good provisional diagnosis
based on history and clinical examination will reduce the risk and economic
burden.
Sometimes definitive diagnosis may not precede treatment too. In many
cases, the final diagnosis or ‘definitive diagnosis’ can only be arrived after
removal of the lesion and by examining it under a microscope to determine its
histopathology.
Diagnostic tools
The most commonly used diagnostic tools are broadly classified in this
textbook for ease of explanation (Box 3.1) is as follows:
• Radiological Examination
• Haematological Investigation
• Biochemical Investigation
• Microbiological Investigation
• Salivary diagnostics
• Histopathological Examination
Box 3.1 Diagnostic tools

A. Radiological Examination
1. Plain film/digital X-rays

a. Intraoral
i. IOPA
ii. Occlusal view radiographs
b. Extraoral
i. Orthopantomogram (OPG)
ii. Lateral view skull/lateral cephalogram
iii. PA view skull/PA cephalogram
iv. Occipitomental view
v. Waters’ view or paranasal sinus view (PNS)
vi. Submentovertex view (SMV) or jug-handle view
vii. Reverse Townes’ view
viii. Oblique lateral view mandibular body
ix. Oblique lateral view mandibular ramus
2. Tomography
a. Computed tomography (CT)
b. Cone beam CT (CBCT)
c. Denta scan
3. Magnetic resonance imaging (MRI)
4. Radionucleotide imaging—
a. Scintigraphy or Bone scan
b. Single Photon Emission Computed Tomography (SPECT)
c. Positron Emission Tomography (PET)
5. Bone density scan—DEXA scan
6. Contrast enhanced radiological investigations
a. Sialography
b. Arthrography
c. Angiography
7. Ultrasonography
B. Haematological investigation (Chapter 4)
1. Complete blood count

2. Erythrocyte sedimentation rate (ESR)
3. Coagulation profile
C. Biochemical investigation
1. Liver function tests

2. Kidney function tests
D. Microbiological examination (Chapter 4)
1. Culture and sensitivity tests

2. HIV tests
3. Hepatitis tests
4. Tuberculosis tests
E. Histopathological examination(Chapter 5)
1. Cytological biopsy
a. Exfoliative cytology
b. Brush biopsy
c. Aspiration biopsy
d. FNAC
2. Tissue biopsy
a. Incisional biopsy
b. Excisional biopsy
c. Frozen section
3. Special diagnostic stains
a. Supra vital stains
b. Chemiluminescence
c. Vizilite
d. Microlux
Plain X-rays
X-rays or radiographs are the most commonly employed diagnostic tools since
they are ubiquitous. They are usually available at the dental chair side or
hospital itself. They are also faster, easy to acquire and much cheaper than the
other diagnostic tools. The electromagnetic rays that are generated by the X-
ray machine are collimated and focussed at specific angulations at the patient.
While bone blocks the rays, soft tissue lets them penetrate at varying degrees
depending on the density of the soft tissue. The rays are then captured in a
film or a sensor. By processing the film or the sensor, a two-dimensional image
of the structures through which the X-rays passed through can be obtained as
a radiographic film or a digital image in the computer, which can be later
printed out in any media as per requirement.
The radiodensity of the image is determined by the amount the X-ray beam
attenuated (stopped) by the structure:
• The radiopaque or white parts of the image show the dense structures,
which have completely stopped the X-ray beam. Example: bone,
metallic objects, such as implants, plates, embedded foreign particles,
bullets, etc.
• The radiolucent or black parts of the image show the areas where the
X-ray beam has passed through the object without any hindrance.
Example: air filled maxillary sinus.
• The grey parts show areas where the X-ray beam has been hindered to
a varying degree. Example: soft tissues, such as fat, muscle and glands
having vary radiodensities. Cartilage is more radiodense than fat but
less than bone.
The radiodensity of the image obtained also depends on the intensity of the
X-rays used, possibility of superimposition, distance from the X-ray source
and sensitivity of the film. Depending on the placement of the film, the plain X-
rays that are used in maxillofacial surgery are classified as intraoral and
extraoral (Table 3.1) and of standard sizes.
Table 3.1
Radiographic film—size
Film Film size

Intraoral–periapical radiograph Size 0: 22 × 35 mm—children
(IOPA) Size 1: 24 × 40 mm—anterior, adult
Size 2: 31 × 41 mm—standard size (anterior and posterior)
adult
Bitewing Size 0: 22 × 35 mm—anterior, children
Size 1: 24 × 40 mm—posterior, children anterior, adults
Size 2: 31 × 41 mm—posterior, adults (standard size)
Size 3: 27 × 54 mm—posterior, adults (all posterior teeth are
seen in 1 film)
Occlusal view Size 4: 57 × 76 mm—(4 times larger than standard periapical
film)
Panoramic film 5 × 12 in., 6 × 12 in.
Cephalometric film 5 × 7 in., 8 × 10 in.
Intraoral radiographs
The size of the film or the sensor is reduced, in order to accommodate it easily
within the mouth. The X-ray generator and the film are held close to the area
being investigated. Since there is minimal superimposition and a small area
alone is targeted, the X-rays are clearer and they involve lesser radiation.
Depending upon the site of placement they are classified as intraoral–
periapical (IOPA), occlusal or bitewing. IOPA and occlusal radiographs are
widely employed in oral and maxillofacial surgery. Bitewing radiograph is
used for detection of decay and periodontal lesions.
Advantages
• Best spatial resolution,

• Minimal distortion,
• Midline structures can be best visualized without superimposition,
• Chair side availability—need not to shift the patient.
Disadvantages
• Cannot be used in patients with restricted mouth opening

• Not useful for viewing large lesions
Intraoral periapical (IOPA) radiograph

The film is held in relation to the long axis of the tooth. Best image can be
obtained if the film is placed parallel to the long axis of the tooth, in close
proximity and the rays are perfectly perpendicular to the tooth and the film.
However, the shape of the arch and the space constrain in the mouth can
prevent such ideal placement. To overcome this technical problem, the angle
of the cone and the X-ray are varied to get the best possible image with
minimal distortion.
Techniques
Parallel cone technique
Cone
Long cone to obtain parallel, nondivergent X-rays.
Film
Placed in a holder parallel to the long axis of the tooth, perpendicular to the X-
rays.
Holder
A (Rinn) holder with a bite plane and a ring to direct the X-ray perpendicular
to the film.
Bisecting cone technique
Film
The film packet is placed as close to the tooth as possible without bending the
film (Fig. 3.1).
FIGURE 3.1 Bisecting angle technique.
Cone
The angle formed between the long axis of the tooth and the long axis of the
film packet is assessed and imaginarily bisected. The X-ray tube is placed at
right angles to this bisecting line with the central ray of the X-ray beam aimed
through the long axis of tooth. Using the geometrical principle of Cieszynski’s
rule of isometry the actual length of the tooth in the mouth will be equal to the
length of the image of the tooth on the film.
Structures viewed
Teeth, periapical area, lamina dura, periodontal ligament space, alveolar bone,
floor of maxillary sinus adjacent to the roots of the maxillary teeth.
Indications
• For detection and assessment of dental caries, periodontal lesions,

alveolar fracture, periapical lesions, retained root fragments, foreign
body and impacted teeth.
• Evaluation of root apex formation.
• During endodontic treatment.
• Detecting fracture of teeth.
• Study of crown and root length and their morphology.
Advantages
• Better visibility of periapical region and their pathology compared to

other views.
• Evaluation of integrity of lamina dura and periodontal ligament space
is best done using an IOPA radiograph only.
Disadvantages
• Cannot be taken in case of patients with limited mouth opening.

• Difficult to detect any large pathology involving the jaws beyond the
periapical region.
• Multiple radiographs have to be taken for the evaluation of the entire
arch.
• Increased risk of exposure to radiation in case of entire arch evaluation.
• Cannot be used in patients with an exaggerated gag reflex.
IOPA radiograph is an integral armamentarium of dental and oral surgery.

It is used for basic investigations where lesions are small and the patient is
able to open the mouth adequately. A digital version of the same is called
radiovisuography (RVG). When IOPA radiograph is not possible, an OPG is
advised.
Occlusal radiograph
Occlusal radiographs are those intraoral radiographs taken placing the film in
the occlusal plane. The films are usually of size 5.7 × 7.6 cm.
Types of mandibular occlusal projections
Anterior mandibular occlusal projection
Film
Place the receptor in the mouth with the long axis perpendicular to the sagittal
plane and push it posteriorly until it touches the rami.
Central beam
Orient the central ray with—10-degree angulation through the point of the
chin toward the middle of the receptor; this gives the ray—55 degree of
angulation to the plane of the receptor.
Point of entry
The point of entry of the central ray is in the midline and through the tip of the
chin.
Cross-sectional mandibular occlusal projection
Film
The anterior border of the receptor should be approximately 1 cm beyond the
mandibular central incisors.
Central beam
Direct the central ray at the midline through the floor of the mouth
approximately 3 cm below the chin, at right angles to the centre of the
receptor.
Point of entry
Point of entry of the central ray is in the midline through the floor of the
mouth approximately 3 cm below the chin.
Lateral mandibular occlusal projection
Film
Place the receptor as far posterior as possible, then shift the long axis buccally
(right or left) so that the lateral border of the receptor is parallel with the
buccal surfaces of the posterior teeth and extends laterally approximately
1 cm.
Central beam
Direct the central ray perpendicular to the centre of the receptor through a
point beneath the chin, approximately 3 cm posterior to the point of the chin
and 3 cm lateral to the midline.
Point of entry
Point of entry of the central ray is beneath the chin, approximately 3 cm
posterior to the chin and approximately 3 cm lateral to the midline.
Structures viewed
Mandibular dental arch, floor of the mouth, buccolingual borders of the
mandible and calcifications on the floor of the mouth.
Indications
• Sialolith/radiopaque calculi in the submandibular ducts.

• Buccolingual position of the unerupted mandibular teeth.
• Buccolingual expansion of the body of the mandible by cysts, tumours
or osteodystrophies.
• Assessment of displacement of fractures of the anterior mandible in the
horizontal plane.
Advantages
• Identify the submandibular dust calculi

• Differentiate the buccal or lingual positioning of impacted tooth
Types of maxillary occlusal projections
Anterior maxillary occlusal projection
Film
Place the receptor in the mouth with the exposure side toward the maxilla, the
posterior border touching the rami, and the long dimension of the receptor
perpendicular to the sagittal plane.
Central beam
Middle of the receptor with approximately +45 degree vertical angulation and
0 degree horizontal angulation
Point of entry
The central ray enters the patient’s face approximately through the tip of the
nose.
Cross-sectional maxillary occlusal projection
Film
Long dimension perpendicular to the sagittal plane, crosswise in the mouth.
Gently push the receptor backward until it comes in contact with the anterior
border of the mandibular rami.
Central beam
Middle of the receptor with vertical angulation of +65 degree and a horizontal
angulation of 0 degree.
Point of entry
Central ray enters the patient’s face through the bridge of the nose.
Lateral maxillary occlusal projection
Film
Place the receptor with its long axis parallel to the sagittal plane and on the
side of interest. Push the receptor posteriorly until it touches the ramus.
Position the lateral border parallel with the buccal surfaces of the posterior
teeth, extending laterally approximately 1 cm past the buccal cusps.
Central beam
Vertical angulation of +60 degree, to a point 2 cm below the lateral canthus of
the eye, directed towards the centre of the receptor.
Point of entry
Central ray enters at a point approximately 2 cm below the lateral canthus of
the eye.
Structures viewed
Maxillary dental arch, hard palate, greater palatine foramina and buccal cortex
of the maxilla.
Indications for prescription
• Unerupted canines, supernumeraries and odontome

• Cleft alveolus and palatal swellings
• As midline view, to determine the buccopalatal position of unerupted
canines.
• Evaluation of size and extent of lesion, such as cyst and tumours in the
anterior maxilla/palate.
• Assessment of fracture of the anterior teeth and alveolar bone.
Advantages
Periapical assessment of the maxillary anterior teeth, especially in children but
also in adult unable to tolerate periapical films.
Extraoral radiographs
Extraoral radiographs are most commonly used for detection of maxillofacial
fractures and large lesions of the jaws. However, unlike long bones, facial
bones cannot be viewed without superimposition. Therefore, several
angulations have been standardised to view specific anatomic units of the
maxillofacial skeleton. The structures that can be viewed and the indications
for prescription have been enumerated in Table 3.2.
Table 3.2
Comparison of extraoral radiographs
Extraoral radiograph Structures viewed Indications

Lateral view Craniofacial bones, paranasal • Cephalometric radiograph is
skull/cephalogram air sinuses especially used for growth studies and
Film placed parallel to sphenoid sinus, frontal sinus, orthodontics
midsagittal plane; beam sella turcica, pterygopalatine • True lateral skull radiograph
perpendicular to film fossa, maxillary antrum can be used to investigate
(difference between true fractures of skull base and
lateral skull and true cranium, middle third
cephalometric lateral fractures, frontal, sphenoid,
skull is that the true maxillary sinuses, conditions
lateral skull is not affecting the skull vault, sella
standardised or turcica (tumour of pituitary
reproducible) gland)
• Asymmetry of the mandibular
ramus and body can also be
investigated
PA view Skull vault, orbit, frontal bone • Investigation of frontal sinuses,
skull/cephalogram and the frontal sinus, nasal fractures of skull vault
Canthomeatal line at 10 cavity, nasal septum, condylar • Conditions affecting the
degree to film; beam neck, ramus and angle of the cranium (Paget disease,
perpendicular to film mandible, facial skeleton multiple myeloma, Brown’s
tumour)
• Intracranial calcifications
• Facial asymmetry
Standard occipitomental Frontal sinus, orbits, nasal • Investigation of maxillary
view—0 degree OM bones, nasal septum, maxilla, antrum, ethmoid and frontal
Film placed zygoma, mandible, sinuses
perpendicular to sagittal sphenoidal sinus • Detecting Le Fort I, Le Fort II,
plane with canthomeatal Le Fort III, zygomatic complex,
line 45 degree to the film; nasoethmoidal complex, orbital
beam centred through blow out, coronoid process
occiput at horizontal (0 fractures
degree) • Investigation of sphenoidal
sinus (X-ray needs to be taken
with open mouth)
Waters’ view Orbits, maxillary sinus, To diagnose the infections and
(30 degree occipitomental zygoma, frontal sinus, nasal pathologies of paranasal
view) Same as standard cavity, nasal septum, sinuses.
except that beam directed zygomatic arches, frontal, To view orbitozygomatic
30 degree to horizontal maxillary, temporal process of fractures
from above the head zygoma, zygomaticofrontal
suture, condylar and coronoid
process of mandible
Submentovertex view Base of mandible, base of • Destructive/expansive lesions
Canthomeatal line skull, lateral wall of orbit, affecting the palate, pterygoid
parallel to film; beam foramen magnum, region or base of skull
perpendicular to film condylar head, lateral • Investigation of sphenoid sinus
pterygoid plate, articular • Assessment of mandibular
eminence, zygomatic width, fractures of zygomatic
arch, sphenoidal sinus arches (taken with reduced
Submentovertex view is exposure)
of two types:
• Base of skull projection
• Zygomatic arch projection
Zygomatic arch
projection:
Zygomatic arch projection
is also called as the jug-
handle view.
This radiograph is
essentially similar to the
base of the skull
projection with the
exception that the
radiation exposure is less
Reverse Townes’ view Condylar heads and necks • High fractures of condylar neck
Canthomeatal line at 30 • Intracapsular fractures of the
degree to film; beam TMJ
perpendicular to film; • Investigation of the articular
mouth open surfaces of condylar heads in
TMD, condylar hyper-
/hypoplasia
Oblique lateral—body Teeth, alveolar ridge and • Assessment of the
Film in contact with cheek body of the mandible presence/position of the
at molar area; beam aims impacted teeth
at molar-premolar area • Detect fractures of mandible
oblique to the sagittal • Osseous lesions of mandible
plane of the patient
Oblique lateral—ramus Third molar–retromolar area, To diagnose the pathologies and
Film in contact with cheek angle, ramus, condyle and fractures of the mandibular
at the ramus area; beam coronoid process of the ramus and condyle
aims at ramus area mandible
Advantages
• Superior spatial resolution

• Low cost
Disadvantages
• Two-dimensional (2D) image of 3D structure

• Superimposition of structures
Orthopantomogram
Structures viewed
Teeth, orbit, nasal cavity, nasal septum, inferior nasal concha, incisive
foramen, nasal spine, maxillary sinus, palate, maxillary tuberosity, pterygoid
processes, pterygopalatine fossa, zygomatic bone, articular tubercle, coronoid
process, condyle, joint space, mandible, mandibular canal, mental foramen
and hyoid bone (Fig. 3.2).
FIGURE 3.2 OPG showing normal anatomical landmarks.
Indications
• Screening for pathologies as cysts, tumours, fractures, impacted teeth

in mandible.
• Dental caries, periodontal and periapical lesions of maxillary and
mandibular dentition.
• Screening for osteoporosis.
• TMJ ankylosis.
• TMJ disorders and lesions.
• Explain status of teeth.
Advantages
• Evaluation of maxilla and mandible in one film.

• Useful in case of patients with the complaint of limited mouth opening,
extreme gag reflex, fearful or uncooperative children.
• Less time is required to do OPG survey than intra-oral survey.
• Aids in patient education and case presentation. Conditions, such as
impactions, eruption pattern of teeth, growth and development, need
for replacement of missing teeth and fractures are more easily
illustrated on panoramic views.
• Reduces the risk of multiple exposures to radiation when compared
with conventional full mouth intraoral radiography.
• Relatively simple procedure to perform.
• Requires minimal patient cooperation (patients are only required to
stand still for 15–20 s of exposure).
Disadvantages
Image quality
Tomograms inherently show magnification, geometric distortion and poor
definition.
Less effective in detecting early inter proximal or recurrent caries,
disruptions in lamina dura, loss of crestal alveolar bone and thickened
periodontal membrane.
Overlap
OPG units have a tendency to produce overlapping of teeth images, most
particularly in the premolar area.
Superimposition
There is often superimposition of the vertebral column on the anterior portion
of the OPG (incisors region).
Distortion
The amount of horizontal and vertical distortion varies from one part of the
film to another. This results in an uneven magnification of the image. Some
structures and spaces may be seen larger than actual size.
Overuse
The ease and convenience in obtaining the OPG might lead to carelessness by
substitution for other projection that might be adequate. This is one of the
prime concerns in regard to patient dosage.
Lateral view skull/cephalogram

Film
Parallel to mid-sagittal plane (Figs. 3.3–3.6);
FIGURE 3.3 Technique of taking lateral view of skull.

FIGURE 3.4 Technique of taking lateral cephalogram, using
cephalostat and standardised beam distance.
FIGURE 3.5 True lateral cephalogram, anatomical landmarks
showing 1. Frontal sinus, 2. Nasion, 3. Nasal bone, 4. Sphenoid
sinus, 5. Sella, 6. External auditory meatus, 7. Mastoid, 8. Anterior
nasal bone, 9. Hard palate, 10. Pterygoid, 11. Soft palate, 12.
Dorsum of tongue, 13. Hyoid, 14. Trachea, 15. Atlas, 16. Posterior
wall of pharynx.
FIGURE 3.6 True lateral cephalogram showing cephalometric
landmarks. 1. Nasion (N), 2. Sella (S), 3. Orbitale (Or), 4. Porion
(Po), 5. Anterior nasal spine (ANS), 6. Point A, 7. Posterior nasal
spine (PNS), 8. Point B, 9. Pogonion (Pog), 10. Gnathion (Gn), 11.
Menton (Me), 12. Gonion (Go).
X-ray beam
Perpendicular to film
(Difference between true lateral skull and true cephalometric lateral skull is that the
true lateral skull is not standardised or reproducible).
Structures viewed
Skull, facial bones, paranasal air sinuses especially sphenoid sinus, frontal
sinus, sella turcica, pterygo-palatine fossa, maxillary antrum, nasal bones.
Indications
• Cephalometric radiograph is used for growth studies and
orthodontics.
• True lateral skull radiograph can be used to investigate fractures of
skull base and cranium, middle third fractures, frontal, sphenoidal,
maxillary sinuses, conditions affecting the skull vault (multiple
myeloma, Paget’s disease, hyperparathyroidism), sella turcica (tumour
of pituitary gland).
• Symmetries of the mandibular ramus and body can also be
investigated (Figs. 3.7 and 3.8).
FIGURE 3.7 Lateral view skull—Paget’s disease.

FIGURE 3.8 Lateral view skull—multiple myeloma.
PA view skull/cephalogram
X ray beam
Perpendicular to film (Figs. 3.9–3.11),
FIGURE 3.9 Technique of PA view.
FIGURE 3.10 PA skull showing anatomical landmarks. 1. Frontal
sinus, 2. Frontal bone, 3. Orbit, 4. Linea temporalis, 5. Sphenoid, 6.
Ethmoid air cells, 7. Nasal septum, 8. Mastoid, 9. Coronoid, 10.
Inferior turbinate, 11. Maxillary sinus, 12. Nasal cavity, 13.
Condyle, 14. Transverse process of atlas, 15. Angle of mandible.
FIGURE 3.11 PA view showing bicondylar fracture. 1. Frontal
sinus, 2. Cribriform ethmoid/with crista galli, 3. Greater wing of
sphenoid, 4. Sphenoidal sinus, 5. Nasal septum, 6. Mastoid
process, 7. Inferior turbinate, 8. Fractured condyle, 9. Coronoid
process, 10. Dens of axis vertebra, 11. Angle of mandible.
Patient position
Canthomeatal line 90 degree to film; head tipped forward with forehead and
nose touching the film (forehead nose position).
Structures viewed
Skull vault, orbit, the frontal bones and frontal sinus, nasal cavity, nasal
septum, angle, ramus condyle of the mandible and the facial skeleton.
Indications
• Investigation of frontal sinuses, fractures of skull vault, conditions

affecting the cranium (Paget’s disease, multiple myeloma and Brown’s
tumour).
• Intracranial calcifications.
• Facial asymmetry.
Occipitomental view—0 degree standard

Patient position
Patient is positioned facing the film with the head tipped back so the
radiographic baseline is at 45 degree to the film, the so-called nose–chin position
(Figs. 3.12 and 3.13).
FIGURE 3.12 Technique of standard occipitomental view.

FIGURE 3.13 Standard occipitomental view.1.Frontal sinus,
2. Orbit, 3. Zygoma, 4. Zygomatic arch, 5. Nasal bone, 6. Nasal
septum, 7. Maxillary sinus, 8. Coronoid process, 9. Condyle, 10.
Anterior arch of atlas, 11. Foramen magnum, 12. Dens,
13. Posterior arch of atlas.
X ray
Tube-head is positioned with the central ray horizontal (0 degree) centred
through the occiput
Structures viewed
Frontal sinus, orbits, nasal bones, nasal septum, maxilla, zygoma, mandible
and sphenoidal sinus.
Indications
• Investigation of maxillary antrum, ethmoid and frontal sinuses.

• Detecting Le Fort I, Le Fort II, Le Fort III, zygomatic complex,
nasoethmoidal complex, orbital blow out and coronoid process
fractures.
• Investigation of sphenoidal sinus (radiograph to be taken with open
mouth).
Waters’ view (30 degree occipitomental view)

Other name: Paranasal sinus view (PNS view) (Figs. 3.14 and 3.15).
FIGURE 3.14 Technique of 30 degree occipitomental view.

FIGURE 3.15 PNS view (Waters’ projection). 1.Frontal sinuses, 2.
Linea temporalis, 3. Orbit, 4. Zygomatic frontal suture, 5. Nasal
septum, 6. Zygoma, 7. Maxillary sinus, 8. Zygomatic arch, 9.
Coronoid, 10. Condyle.
Patient position: Patient is positioned facing the film with the head tipped
back so the radiographic baseline is at 45 degree to the film, the so-called nose–
chin position.
X ray: Tube-head is aimed downward from above the head, with the central
ray at 30 degree to the horizontal, centred through the lower border of the
orbit.
Structures viewed
Orbits, frontal sinus, maxillary sinus, nasal cavity, nasal septum, zygoma,
zygomatic arches, frontal, maxillary, temporal process of zygoma, zygomatico-
frontal suture, condylar and coronoid process of mandible.
Indications
• To diagnose the infections and pathologies of para-nasal sinuses.

• To view orbitozygomatic fractures.
Advantage
This projection is very useful in the diagnosis of maxillary sinusitis, Le Fort II
and Le Fort III fractures, orbitozygomatic fractures and sinus pathologies.
Submentovertex view (SMV)

Patient position: Canthomeatal line parallel to film. The head is tipped
backward as far as is possible, to ensure that the vertex of the skull touches the
film (Figs. 3.16–3.17).
FIGURE 3.16 Technique of submentovertex view.

FIGURE 3.17 True submentovertex view—basal view. 1. Nasal
septum, 2. Medial wall of orbit, 3. Anterior wall of maxilla, 4. Nasal
septum (vomer), 5. Lateral wall of orbit, 6. Zygomatic arch, 7.
Coronoid process, 8. Ramus of mandible, 9. Sphenoid sinus, 10.
Foramen ovale, 11. Condyle, 12. Foramen spinosum, 13. Anterior
arch of atlas, 14. Angle of mandible, 15. Dens, 16. Foramen
magnum.
X-ray: Beam aimed upward at 5 degree to the horizontal.
Structures viewed
Base of mandible, base of skull, lateral wall of orbit, foramen magnum,
condylar head, lateral pterygoid plate, articular eminence, zygomatic arch and
sphenoidal sinus.
SMV is of two types:
Zygomatic arch projection is also called as the jug-handle view. This

radiograph is essentially similar to base of the skull projection with the
exception that the radiation exposure is less.
Submentovertex view is of two types:

Jug-handle view:
Zygomatic arch projection is also called as the jug-handle view. This

radiograph is essentially similar to base of the skull projection with the
exception that the radiation exposure is reduced to one third.
Indications
• Destructive/expansive lesions affecting the palate, pterygoid region or

base of skull,
• Identify the position of the condyle, and evaluate fractures of the
zygomatic arch (taken with reduced exposure).
• Also demonstrates the sphenoid, ethmoid sinuses, and lateral wall of
maxillary sinus.
Advantage
The SMV helps to identify the position of the condyle, visualize base of the
skull and evaluate fractures of the zygomatic arch. This projection also
demonstrates the sphenoid, ethmoid sinuses, and lateral wall of maxillary
sinus.
Disadvantage
Contraindicated in neck injuries, vertigo since this projection requires neck
extension.
Reverse townes’ view

Positioning similar to PA skull except mouth open position is maintained
(Figs. 3.18 and 3.19).
FIGURE 3.18 Technique of Reverse Towne’s view.
FIGURE 3.19 Reverse Townes’ projection. 1. Arch of atlas,
2. Foramen magnum, 3. Condyle, 4. Zygomatic arch, 5. Neck of
condyle, 6. Orbit, 7. Middle turbinate, 8. Nasal septum, 9. Inferior
turbinate.
Condylar heads come out of the glenoid fossae on opening the mouth,
thereby making them visible.
Structures viewed
Bilateral condylar head and neck
Indications
• High fractures of condylar neck, intracapsular fractures of the TMJ.

• Investigation of the quality of the articular surfaces of condylar heads
in temporomandibular disorder (TMD) and condylar
hyper/hypoplasia.
Oblique lateral—body
Film: In contact with cheek at molar area (Fig. 3.20);
FIGURE 3.20 Oblique lateral projection of mandibular body.
Beam: Aims at molar–premolar area oblique to the sagittal plane of the

patient.
Structures viewed
Teeth, alveolar ridge and body of the mandible.
Indications
• Assessment of the presence/position of impacted teeth

• Detection of fractures of mandible and osseous lesions of mandible
This radiograph is very useful in the diagnosis of fracture or any pathology

in patients with restricted mouth opening.
Advantage
Lateral jaw projection is useful to examine the mandibular posterior region.
This radiograph is very useful in the diagnosis of fracture or any pathology in
patients with restricted mouth opening.
Oblique lateral—ramus
Film: In contact with cheek at the ramus area (Fig. 3.21);
FIGURE 3.21 Oblique lateral projection of mandibular ramus.
Beam: Aims at ramus area.
Structures viewed
Third molar–retromolar area, angle of the mandible, ramus, condyle neck and
coronoid process.
Indications
To diagnose the pathologies and fractures of the mandibular ramus and
condyle.
Digital imaging
Digital images are acquired either directly by using a sensor or imaging plate
or indirectly by scanning and digitalising a film-captured image. Digital
imaging systems are divided into two types:
1. Solid-state technology or corded (direct)

2. Photo-stimulable phosphor-storage plate or cordless (indirect)
Solid-state technology
These systems employ conventional X-ray generating equipment while the
conventional film is replaced by either a CCD (charged coupled device) or a
complementary metal oxide semiconductor (CMOS) sensor, which is connected to
the computer via a cable (or cord).
These detectors have in common certain physical properties and the ability
to generate a digital image in the computer without any other external device.
In medicine, the use of solid-state detectors is referred to as digital
radiography. In dentistry, intraoral solid-state detectors are often called
sensors.
Solid-state detectors collect the charge generated by X-rays in a solid
semiconducting material. The key clinical feature of these detectors is the
rapid availability of the image after exposure. The X-ray photons that reach the
sensor get converted to light, by an intensifying or scintillation screen, which
in turn is picked by the CCD/CMOS and converted into an electrical charge.
This charge gets relayed to the computer to produce an almost instantaneous
digital image on the monitor (hence, the term real-time). Different sized
intraoral, as well as panoramic, sensors are available.
Specially designed intraoral sensor holders (with and without beam aiming
devices) have been developed which are similar to those used for conventional
film. For infection control the sensors need to be covered with a protective
plastic barrier envelope.
Photo-stimulable phosphor imaging or cordless systems

Films have been replaced by reusable photo-stimulable phosphor-imaging
plates (PSPP) in this system. The plates contain a layer of barium fluorohalide
phosphor. The phosphor layer absorbs and stores the X-ray energy which has
not been attenuated by the patient. The image plate is then placed in a reader
where a laser beam scans it. The stored X-ray energy in the phosphor layer is
released as light. A photomultiplier detects it. Now, the information is relayed
to the computer which gets displayed on the monitor as a digital image.
The size of the plate and the system used determines the time taken to read
the plate. It usually varies between 1 and 5 min. Extraoral plates for panoramic
and skull radiography is also available. Radiographic techniques are identical
to those using conventional film. Conventional film holders are used to carry
the intraoral plates placed in protective barrier envelopes. Upon removal of
the intensifying screens, the extraoral plates are placed in conventional
cassettes.
Tomography
Tomography can be utilised to section or slice the object and thereby eliminate
undesirable overlap. It is achieved by simultaneous movement of the X-ray
tube and the film. The movement occurs around a point or fulcrum as the tube
and the film are connected. The objects closest to the point or fulcrum are seen
most sharply and the objects farthest away from the point of rotation are
almost completely blurred. Thus, an image layer within the body is produced
while the blurring makes the images of structures above and below that layer
invisible. This technique is also called body section radiography. Types of
tomography are:
1. Conventional tomography
2. Computed tomography (CT)
Conventional tomography
Also called tomography, planography and body-section radiography.
Conventional tomography employs different types of motion of the X-ray tube
and the film. They are linear, circular, trispiral, elliptical and hypocycloidal;
the simplest of the motions being linear. The more complex the motion, the
sharper the image.
Computed tomography
In CT the images are produced by an ionising radiation, which allows
visualization of greater variety of tissue structures; beyond the four basic
densities (air, bone, soft tissue and fat) seen on the conventional radiograph.
In conventional radiograph, one projection is used to form an image while
CT uses multiple small projections across the body and combines the
information to form an image. A section or axial ‘slices’ refers to each
individual picture of CT (Figs. 3.22–3.30).
FIGURE 3.22 (A and B) CT scanner.

FIGURE 3.23 CT scan with 3D reconstruction showing right TMJ
ankylotic mass.
FIGURE 3.24 Axial section showing right TMJ ankylotic mass.
FIGURE 3.25 Sagittal section.
FIGURE 3.26 Coronal section.
FIGURE 3.27 (A and B) Axial image.

FIGURE 3.28 (A and B) Sagittal image.
FIGURE 3.29 (A and B) Coronal image.

FIGURE 3.30 (A−C) Transaxial image.
The entire CT process is divided into three segments:
1. Data acquisition
2. Image reconstruction
3. Image display
Equipment and theory

To acquire data, a generator, a gantry, and a table are necessary. The X-ray
tube, data acquisition system, collimators and detectors are housed in the
gantry. Commonly used detectors are either solid-state crystals or pressurized
xenon gas. Raw data include all measurements obtained from the detector
array. Some of these raw data are used in the creation of image data. An image
is reconstructed only after the raw data are averaged and each pixel is
assigned a Hounsfield number (quantified measurement of density). To verify
the proper head alignment view, a preliminary image is taken of the selected
jaw and is referred to by many names (e.g. topogram, scout and scanogram).
Each axial CT image is about 1.5 mm thick. The maxilla usually requires about
20–30 axial sections, whereas the mandible requires about 30–35 sections.
Hounsfield units
Hounsfield units (HU) or CT numbers are named after Sir Godfrey Newbold
Hounsfield. It is a quantitative scale used to describe radiodensity.
HU denotes the amount of the X-ray beam that a particular voxel of tissue
attenuates. In CT scan, Hounsfield Unit is proportional to the degree of X-ray
attenuation. It is allocated to each pixel (picture element) to represent the
density of the tissue.
3D reconstruction of CT images (Fig. 3.23)

The original 2D slices are used to create 3D images. No additional scanning or
radiation exposure is needed. Artefacts may be produced in the reformation
process but there is no new information in the images. Despite this, the
reconstructed 3D images assist in the visualization of large comminuted,
displaced and complex fractures involving multiple planes, easy to diagnose
expansile lesions, useful in planning surgery, in the fabrication of
stereolithographic models and patient education.
Indications of head and neck CT scan
• Investigation of intracranial disease including tumours, haemorrhage,

and infarcts.
• Assessment of fractures involving faciomaxillary skeleton.
• In tumour diagnosis and staging.
• Investigation of bone and soft tissue pathologies of head and neck.
• Malformations of skull.
• Pathologies of paranasal sinuses.
• Aneurysm, arteriovenous malformations or vascular pathology (CT
angiography).
Advantages
• Detailed imaging of intracranial lesions.

• Imaging of hard and soft tissues simultaneously.
• Excellent differentiation between different types of tissues, both
normal and diseased.
• Reconstructed images can be obtained.
• Images can be enhanced by the use of IV contrast media and providing
additional information.
• Linear measurements, area, volume of structures can be calculated
using built-in or added software.
Disadvantages
• The equipment is very expensive.

• Very thin, contiguous or overlapping slices may result in a generally
high dose investigation.
• Metallic objects, such as stainless steel mini-plate and stainless steel
crown may produce marked artefacts like streak or star across the CT
image.
• Inherent risks associated with IV contrast agents.
Tissue Intensity value [HU]

Bone 1000
Liver 40–60
White matter in brain 46
Grey matter in brain 43
Blood 40
Muscle 10–40
Kidney 30
Cerebrospinal fluid 15
Water 0
Fat −50–100
Air −1000
Cone beam CT (CBCT)
It is one of the latest revolutionary cutting edge technologies in dental and
maxillofacial imaging. The scanner rotates 360 degree around the patient’s
head (Figs. 3.23 and 3.24). It enables quick, fast, easy visualisation of patient’s
craniofacial structure with unparallel precision of 3D. It provides undistorted
dimensional images of the jaws in cross-sectional, axial, coronal, sagittal,
panoramic and 3D images (Figs. 3.25–3.29). Cone beam CT utilizes a cone
shaped X-ray beam directed toward the patient’s head, whereas a fan-shaped
X-ray beam is used by traditional medical CT (Figs. 3.31–3.37).
FIGURE 3.31 Cone beam CT scanner used for imaging in a patient

in standing posture.
FIGURE 3.32 CBCT scanner rotating 360 degree around the
patient’s head during scanning.
FIGURE 3.33 Axial section showing hypodense lesion in left
mandible body.
FIGURE 3.34 Coronal section.
FIGURE 3.35 Sagittal section.
FIGURE 3.36 Coronal section showing the lesion.

FIGURE 3.37 CBCT 3D reconstruction.
Multiple two-dimensional projection images are acquired for a field of view

selected according to the region of interest (ROI) in CBCT. The degree of X-ray
attenuation is shown by grey scale (voxel value) in CBCT while in CT it is
measured in pixels.
Principles of CBCT image formation
• The object is placed between the source and the detector mechanism.
• The X-ray imaging unit rotates around the object at a continuous rate.
• X-ray source produces cone-shaped beam that radiates the patient’s
mouth and jaw as the arm rotates.
• CMOS flat panel contains caesium iodide scintillator that converts X-
rays into visible light.
• Photosensitive pixels convert scintillator light into electric signals.
Electric signals are converted into digital output by on chip circuitry
system.
• The images of the object are taken at a rate of 5–10 per second for about
30 s.
• After 360 degree rotation the image data is converted by a computer
into 3D images.
Indications
CT CBCT
• Investigation of intracranial disease including tumours, • Oral and maxillofacial implants.
haemorrhage and infarcts. • Impacted teeth, cystic, and
• Assessment of fractures involving faciomaxillary skeleton. neoplastic lesions.
• In tumour diagnosis and staging. • Maxillofacial trauma.
• Investigation of bone and soft tissue pathologies of head • Orthodontic treatment planning
and neck. and implant.
• Malformations of skull. • Anchorage.
• Pathologies of paranasal sinuses. • Endodontic pathology.
• Aneurysm, arteriovenous malformations or vascular • Temporomandibular joint (TMJ)
pathology (CT angiography). analysis.
• Airway studies (sleep apnoea).
Advantages
CT CBCT
• Detailed imaging of intracranial lesions. • Low radiation than
• Imaging of hard and soft tissues simultaneously. CT scan
• Excellent differentiation between different types of tissues, both • Unlimited 3D views
normal and diseased. • Less discomfort
• Reconstructed images can be obtained. • Can be taken in
• Images can be enhanced by the use of IV contrast media, providing sitting posture
additional information.
• Linear measurements, area, volume of structures can be calculated
using built-in or added software.
Disadvantages
CT CBCT
• Expensive equipment. • High-speed scans (less than
• Very thin, contiguous or overlapping slices may result in a 30 s)
generally high dose investigation. • Compact/Reduced size—
• Metallic objects, such as stainless steel mini-plate and stainless feasible for use in dental
steel crown may produce marked streak or star artefacts across office
the CT image. • High-spatial resolution
• Inherent risks associated with IV contrast agents. applicable for maxillofacial
diagnosis
• Low-radiation exposure (10
times lesser than the regular
CT scanner)
• Cost effective
• Safe for children
Entity CT CBCT
Technology Uses fan shape beam Uses cone shape beam
Patient CT makes use of a supine machine with a Sitting up/standing machine of
positioning large gantry smaller dimensions
Machine size Size of a conventional CT scanner precludes Same size as a OPG machine—
its installation and usage in dental surgery compact and easy to install
Radiation Radiation exposure ranges from 100–300 Radiation exposure for both
microsieverts (µSv) for maxilla and 200–500 maxilla and mandible ranges
(µSv) for the mandible from 34–102 (µSv)
Artefacts Artefacts arising from metal are severe Not that severe
Less motion artefact when compared to More motion
CT
Image quality Greater contrast resolution and more Poor soft tissue contrast when
discrimination between different tissue types compared to CT
(bone, teeth and soft tissue)
Denta scan
The technique of Dental CT was developed by Schwarz et al in 1987. They
used curved multiplanar reconstruction of jaw. Dental CT involves the
acquisition of axial scans of the jaw with the highest possible resolution with
curved and orthogonal multiplanar reconstructions.
Best useful for dental implant procedure.
Reduced metal artefact when compared to CT.
Allows accurate display of the vertical and buccolingual dimensions of the
jaw in actual 1:1 life size.
Indication
Implant-bone estimation (height and width).

Another recently developed imaging modality is MRI. It is based on the
behaviour of protons (positively charged nuclear particles) in a magnetic field
(Fig. 3.30). Hydrogen, the simplest atom consists of one proton in the nucleus
and one orbiting electron. These hydrogen protons are used to create the MR
image.
Indications
• Soft tissue neoplasia—tongue, cheek, neck, etc.

• TMJ—integrity and position of the disc.
• Malignant involvement of the lymph nodes.
• Perineural invasion by malignant neoplasia.
• Soft tissue swelling—space infections, masseter hypertrophy, space
occupying lesion, etc.
Contraindications
• Ferromagnetic or electronically operated active devices, such as

automatic cardioverter defibrillators.
• Cardiac pacemakers and other pacemakers, e.g. for the carotid sinus.
• Metallic splinters in the eye.
• Ferromagnetic haemostatic clips in the central nervous system (CNS).
• Cochlear implants.
• Insulin pumps and nerve stimulators.
• Prosthetic heart valves (in high fields, if dehiscence is suspected).
• Haemostatic clips (body).
• Non-ferromagnetic stapedial implants.
• Claustrophobia.
• Intraocular ferrous foreign bodies.
• Bullets, pellets and shrapnel.
• Orthopaedic implants, materials and devices.
Advantages
• Noninvasive
• Uses nonionising radiation
• Produces high quality images of soft tissue resolution in any imaging
planes.
Disadvantages
• Bone cannot be captured by MRI as bone does not give any MR signal;
a signal is only obtainable from bone marrow, although this is of less
importance.
• Long scanning time and thus demanding on the patient.
• Contraindicated in patients with surgical clips, cardiac pacemakers,
and cochlear implants and in the first trimester of pregnancy.
• Equipment tends to be claustrophobic and noisy.
• Equipment is very expensive.
• Differentiation is difficult as bone, teeth, air and metallic objects all
appear dark.
Nuclear medicine
Nuclear medicine refers to the branch of medicine that uses radioactive
substances in diagnosis and therapy. It consists of pharmaceutical substances
labelled with radioisotopes ‘radiopharmaceuticals’. They consist of chemical
molecule, which determines the behaviour of the radiopharmaceutical in the
body. The radiation emitted by the radionuclide may be detected from outside
the body by a radionuclide-imaging device (a gamma camera) or may be
detected in a sample of a body fluid (e.g. plasma or urine).
Radioisotopes
Radioisotopes are isotopes with unstable nuclei which undergo radioactive
disintegration. This disintegration is often accompanied by the emission of
radioactive particles or radiation (Table 3.3).
Table 3.3
Common isotopes used in head and neck region imaging

Radionuclide Half life Target areas
(t1/2)
99mTc-MDP (technetium-99m methylene 6h • Salivary glands, thyroid,
diphosphonate) bone
• Blood, liver, lung and heart
Gallium (67Ga) 78 h Tumours and inflammation
Iodine (131I or123I) 8 days Thyroid
The important emissions are:
• Alpha particles
• Beta – (electron) and beta + (positron) particles
• Gamma radiation
Gamma camera
It is an electronic device used in medical diagnosis for imaging the distribution
of radioactive compounds in the tissues (after injection) (Fig 3.38).
FIGURE 3.38 Gamma camera.
Radioisotope imaging
Radionuclide imaging is also called functional imaging. It assesses physiologic
changes which is a direct result of biochemical alteration.
Procedure
Radioactive compounds that have an affinity for particular tissues. Hence, the
so-called target tissues are injected intravenously. The radioactive compounds
get concentrated in the target tissue and their radiation emissions are then
detected and imaged, usually using a stationary gamma camera. It allows the
function of the target tissue to be examined under both static and dynamic
conditions.
Indications
• Tumour staging—assessment of the sites and extent of bone metastasis.

• Assessment of continued growth in condylar hyperplasia.
• Investigation of salivary gland function, particularly in Sjogren
syndrome.
• Evaluation of bone grafts.
• Evaluation in osteomyelitis of maxillofacial bones.
• Investigation of the thyroid abnormalities.
Advantages Disadvantages
• Assessment of function of the target • Poor image resolution: minimal information about
tissue target tissue anatomy
• During one bone scan the whole • High radiation dose
skeleton can be imaged • Images are not usually disease-specific
• Results can be enhanced • Some investigations take several hours
• Facilities are not widely available
Imaging methods
• Static
• Dynamic
• Whole body
• SPECT
• PET
Static
1. A ‘snapshot’ of the radiopharmaceutical distribution within a part of

the body.
2. Example: lung scans; spot bone scans images and thyroid images.
3. Static images of the organ or structure are usually obtained in various
orientations, anterior, posterior and oblique.
Whole body imaging
1. Uses a specially designed moving detector system to produce and

image of the entire body or a large body section.
2. The gamma camera collects data as it passes over the body.
3. Example: whole-body bone scans, tumour or abscess imaging.
Dynamic imaging
1. Display the distribution of a particular radiopharmaceutical over a

specific period.
2. ‘Flow’ study of a particular structure is generally used to evaluate
blood perfusion to the tissue time-lapse images.
3. Example: cardiac, hepatobiliary, and gastric emptying studies.
SPECT
1. Produces image similar to CT and MRI in that a computer creates thin

slices through a particular organ.
2. Example: cardiac perfusion, brain, liver and bone studies.
PET
1. Uses positron emission from particular radionuclides to produce

detailed functional images within the body.
2. PET is unique in that its images are of blood flow or metabolic
processes at the cellular level rather than the more conventional
anatomic image produced by X-ray, CT, MRI or even SPECT.
BONE SCAN
Bone scintigraphy is a diagnostic study used to evaluate the distribution of
active bone formation in the body. Phosphate analogues can be labelled with
99mTc and are used for bone imaging because of their good localization in the
skeleton and rapid clearance from soft tissue. 99mTc-MDP (Tc-99m methylene
di-phosphonate) uptake depends on osteoblast and osteoclast activity.
Increased uptake denotes osteoblastic activity and decreased uptake signifies
pure lytic lesion, osteoclast activity (Fig. 3.39).
FIGURE 3.39 Normal bone scan.
Abnormality in a bone scan is seen either as increase or decrease in

radionuclide accumulation described as hot spot or cold spot.
A hot spot is an area that appears black because bone growth is more active
with increased accumulation of radionuclide (e.g. increased vascularity, bone
formation, metastasis, new bone formation/growth, bone graft with positive
vascularity). A cold spot is an area that appears lighter or white because bone
growth (metabolic activity) is less active (e.g. malignant tumours like lung and
breast, bone ischaemia and necrosis, haemangiomas, radiation therapy and
infection).
Three phase bone scan

It is done to see if there is soft tissue hyperaemia.
First phase: It is the perfusion phase or vascular phase.
Second phase: It is the blood pooling phase or soft tissue phase.
Third phase: It is the bony phase.
First phase
30–60 dynamic images are usually obtained over 1 minute immediately after
injection. This is radionuclide angiography and gives an idea about the local
vasculature. During the 1st min after injection, injected dose is still
intravascular.
Second phase
Static image is obtained in 5 minutes after dose injection.
Within 5 min post injection, radiopharmaceutical moves from intravascular
space to extravascular space (soft tissue). It gives idea about soft tissue
oedema.
Third phase
It is the bony phase image obtained in 2–4 h post-injection.
It is same as whole body bone scan.
SPECT
The photons (gamma rays) are emitted from the patient and detected by a
gamma camera rotating around the patient. A cross-sectional image or SPECT
scan shows the distribution of radioactivity, thereby enabling the exact
anatomical site of the source of the emissions to be determined (Figs. 3.40 and
3.41).
FIGURE 3.40 SPECT machine.
FIGURE 3.41 SPECT image.
PET
PET–CT is an advanced imaging modality, which depicts the metabolic or
biochemical activity in the body correlated with anatomic imaging by CT scan
(Figs. 3.42 and 3.43).
FIGURE 3.42 PET machine.
FIGURE 3.43 PET imaging. (1) CT image showing no significant

neck mass. (2) PET imaging shows two lumpy abnormal
radioactive concentration shadows on the right side of the neck (3)
PET/CT imaging shows two abnormal fluorodeoxyglucose
hypermetabolism areas in the sternocleidomastoid region of the
right side of the neck, which were considered lymph node
metastases.
Useful in diagnosis of regions of increased metabolic activity as:
• Malignancies and distant metastasis

• Osteomyelitis of jaw
• Metastatic masses of unknown origin
• Acute inflammatory lesions
DEXA SCAN
Bone density scanning, also called dual-energy X-ray absorptiometry (DEXA) or
bone densitometry. It is an enhanced form of X-ray technology that is used to
measure bone loss/bone mineral density (Fig. 3.44).
FIGURE 3.44 Bone density test.

DEXA is most often done on the lower spine and hips.
It is used primarily in the diagnosis and management of osteoporosis and
other disease states characterized by abnormal bone metabolism disorder.
WHO osteoporosis classification
T score:
Normal: >−1
Osteopenia (low bone mass): −1 to −2.5
Osteoporosis: <−2.5
Severe osteoporosis <−2.5 plus fragility fractures
Arthrography
Arthrography involves injection of a radiopaque contrast material into the
joint spaces. The space occupied by the disc can then be visualized lying
between the layers of contrast material. Arthrography provides information
regarding the soft tissue components, specifically the shape and position of the
articular disc (Figs. 3.45 and 3.46).
FIGURE 3.45 Arthrography—insertion of needle into the joint

space.
FIGURE 3.46 Arthrographic image.
Types of arthrography
1. Single contrast arthrography
2. Double contrast radiography
Complications
• Joint sepsis
• Allergic reaction to the iodinated contrast medium
• Haemarthrosis
• Pain during and after the procedure
• Extravasation of the contrast medium
• Disc perforation
• Transient facial paralysis
Ultrasonography
Ultrasonography (USG) is a diagnostic tool that is widely available, relatively
inexpensive, noninvasive and easily reproducible. It is valuable in identifying
various orofacial swellings, such as inflammatory swellings due to dental or
skin infections, diseases of the salivary glands, lymph node pathologies, soft
tissue cysts and neoplasms.
Transducers with very high-pulsed frequencies (3.5–10 MHz) are used in
ultrasonography to generate electrical impulses that are transmitted into the
tissues being examined.
As the sound passes through the tissues of different acoustic impedances, it
is partly transferred to particles within the medium (as vibrational energy),
part of it continues to penetrate, and part of it is reflected back toward the
transducer.
The reflected echoes are reconverted into electrical energy, amplified,
processed and displayed on a screen. The echoes of the sonographic images
are termed as hypoechoic, hyperechoic and isoechoic images.
Hypoechoic
A mass is hypoechoic if its intensity is lower than that of the adjacent tissue.
Hypoechoic masses are darker.
Hyperechoic
A mass is hyperechoic if its intensity is higher than that of the adjacent tissue.
Hyperechoic masses are brighter.
Isoechoic
A mass is isoechoic if its intensity is similar to that of the adjacent tissue. The
appearances of isoechoic masses are also bright.
A calcified mass appears hyperechoic and a clear fluid or blood appears
anechoic (free of echoic masses).
Limitations
Limited use in hard tissue lesions.
(The ultrasonography wave must be capable to travel through the tissue to
return to the transducer. If the tissue absorbs it, no image will result. Since air,
bone and other calcified materials absorb nearly the entire ultrasonography
beam; its limited use is in diagnosing hard tissue lesions).
Advantages
• Sound waves are not ionising radiation.

• No known harmful effects on any tissues by the present energies and
doses used in diagnostic ultrasonography.
• Images show good differentiation between different soft tissues and
are very sensitive to detect focal disease in the salivary glands.
• Technique is widely available and inexpensive. To assess the
continuity of distracted soft callus before the commencement of
consolidation period (distraction osteogenesis).
Disadvantages
• Ultrasonography has limited use in the head and neck region because
sound waves are absorbed by bone. Its use is therefore restricted to the
superficial structures. Technique is operator dependent.
• Images can be difficult to interpret for inexperienced operators because
image resolution is often poor.
• Real-time imaging as the radiologist must be present during the
investigation.
Recent advances in imaging
• Digital sensors
• Digital subtraction radiography
• CT
• CBCT
• Denta scan
• MRI
• Ultrasound—3D and 4D, colour Doppler
• Nuclear imaging
▪ SPECT
▪ PET
▪ DEXA scan
CHAPTER 4
Diagnostic Aid—
Haematological,
Biochemical and
Microbiological
Investigations
Complete blood count
• Peripheral blood smear
• Haematocrit/packed cell volume
• Haemoglobin
• Platelet count (thrombocyte count)
• Red blood cell count
• Red blood cell indices
• White blood cell count and differential count
Erythrocyte sedimentation rate
• Methods of performing the ESR
Coagulation profile
• Bleeding time
• Capillary fragility test
• Clotting time
• Prothrombin time
• Partial thromboplastin time/activated partial
thromboplastin time
• Coagulation factors
Liver function test
• Bilirubin
• Alkaline phosphatase
• Gamma glutamyl transferase
• SGPT and SGOT
Renal function tests
Microbiologic tests
Nonculture methods
Culture methods
Culture media
• Laboratory aids in the selection of antimicrobial
therapy
Molecular diagnostics
• Nucleic acid probe test
• Polymerase chain reaction
Immunological methods
Most lesions of the oral and maxillofacial region can be diagnosed using
clinical and radiological investigation alone. However, when the cause of the
lesion is beyond the oral cavity, like an oral manifestation of a systemic
disease, investigations need to be broadened to assess the general health of the
patient. This is usually performed by a ‘haematological’ or ‘biochemical’
analysis of the blood and other body fluids like urine. In the same way, in
cases where the cause is microbial, investigation of the causative organism and
its antibiotic sensitivity helps us in treating the disease more effectively rather
than resorting to empirical antibiotics. Therefore, haematological, biochemical
and microbiological investigations form a main part of the ‘diagnostic’ aids.
Haematologists analyse and record the appearance of red blood cells (RBCs),
white blood cells (WBCs) and platelets, to predict, detect and diagnose
diseases. These tests are essential in the diagnosis of oral diseases since
conditions as severe as leukaemia can first manifest as an inflamed gingival
lesion. While abnormalities in clotting and bleeding time may pinpoint a
disease, it is also one of the mandatory presurgical tests for ensuring
preparation of the oral surgeon to provide uneventful postsurgical
complications.
For example, patients on anticoagulant therapy should have their INR
(international normalised ratio) checked before any surgical procedure is
undertaken. The Sickledex test is used to screen sickle cell anaemia prior to
general anaesthesia in populations (Gudalur Adivasi, Tamil Nadu) prone to
the disease.
The haematological tests that are commonly done to elicit disease, as well as
for presurgical assessment of the patient are:
I. Complete blood count with differential count

1. Peripheral blood smear
2. Haematocrit/Packed cell volume (PCV)
3. Haemoglobin (Hb)
4. Platelet count
5. Red blood cell count
6. Red blood cell indices
i. Mean corpuscular volume (MCV)
ii. Mean corpuscular haemoglobin (MCH)
iii. Mean corpuscular haemoglobin concentration
(MCHC)
7. White blood cell count and differential
i. Neutrophils
ii. Lymphocytes monocytes
iii. Eosinophils
iv. Basophils
II. Erythrocyte sedimentation rate (ESR)
III. Coagulation profile
1. Clotting time (CT)
2. Bleeding time (BT)
3. Prothrombin time (PT) and International normalised ratio
(INR)
4. Activated partial thromboplastin time (APTT)
5. Clotting factors
I. Complete blood count

It is the most commonly performed test. The test consists of several individual
tests of significance in understanding the patient's circulatory, immune and
cardiovascular system (Fig. 4.1).
FIGURE 4.1 Automated haematology analyser and result.
1. Peripheral blood smear

Blood smear is a qualitative measure of the blood cells that involves the
preparation of a smear of peripheral blood drop on a slide. The smear is then
microscopically examined to observe the morphology of RBCs, WBCs and
platelets. Size, shape, colour and structure of the RBC are observed. WBC is
measured for number and distribution. Number and appearance of platelets
are observed for thrombocytopathy.
Abnormal RBC can be
i. Hyperchromic: Highly coloured may indicate dehydration, e.g.

megaloblastic anaemia.
ii. Hypochromic: Pale cells due to low haemoglobin content as seen in iron
deficiency anaemia.
iii. Anisocytes: Variable sizes of cells seen in vitamin B12 deficiency.
iv. Macrocytes: Large cells—seen in pernicious anaemia, folic acid
deficiency, increased erythropoiesis and postsplenectomy anaemia
(macrocytic anaemia).
v. Microcytes: Small cells—seen in iron deficiency anaemia and
thalassaemia major (microcytic anaemia).
vi. Sickle cells: Haemoglobin S (HbS) found in sickle cell anaemia causes
the cells to be crescent shaped.
vii. Target cells: Thin cells with less haemoglobin C disease, thalassaemia
major, iron deficiency, liver disease, postsplenectomy.
viii. Ovalocytes/elliptocytes: Oval or elliptical cells seen in microcytic
anaemias, megaloblastic anaemias and haemoglobinopathies.
ix. Poikilocytes: Irregular in shape—anaemia.
x. Schistocytes: Fragmented RBC in usual helmet, spiral, triangular shapes
—seen in haemolytic anaemia, prosthetic valves, severe valvular
disease and burns.
xi. Heinz–Ehrlich bodies: Denatured haemoglobin attached to cell
membrane—seen in glucose-6-phosphate dehydrogenase deficiency,
drug-induced haemolytic anaemias, unstable haemoglobin deficiency
and unstable haemoglobin after splenectomy.
xii. Howell–Jolly bodies: Dark purple spherical remnants of nuclear material
—seen in severe haemolytic anaemia, pernicious anaemia, leukaemia,
thalassaemia, myelodysplasias and in postsplenectomy.
xiii. Rouleaux formation: Sticking together of the RBC—seen in
cryoglobulinemia, giant cell arteritis, macroglobulinaemia and multiple
myeloma.
xiv. Basophilic stippling: Dark spots caused by defective haemoglobin
synthesis, seen in lead or heavy metal poisoning and thalassaemia.
xv. Stomatocytes: Slit like areas of pallor producing a mouth-like
appearance—seen in acute alcoholism, congenital stomatocytosis,
drugs like phe-nothiazines, hepatobiliary, cardiovascular and
neoplastic diseases.
2. Haematocrit/packed cell volume
• Haematocrit is the proportion of RBC to plasma within a sample of

blood. The collected sample is centrifuged to estimate the RBC
sediment by their weight.
• Blood volume is compensated by the body by shifting the intracellular
and interstitial fluid to intra-vascular compartments. However, loss of
RBC takes sometimes to compensate, indicated by a drop in
haematocrit.
• Haematocrit also measures hydration level.
• Haematocrit is approximately three times haemoglobin. It may be 5%–
10% higher when capillary blood is used rather than venous blood.
• Haematocrit and haemoglobin may be serially assessed to evaluate for
blood loss.
• It can be used to assess blood loss. A 3% drop indicates one unit blood
loss approximately, though this does not become apparent
immediately since equivalent amount of RBC and plasma is lost
during a bleed.
Normal values
Female: 37%–48%
Male: 42%–52%
Pregnancy: Decreased due to haemodilution
Elderly: Slightly decreased
Newborn: Increased
Abnormal increase in burns, cardiovascular disease, chronic lung disease,

congenital cardiac defects, Cushing disease, dehydration, polycythaemia vera,
liver cancer and shock.
Abnormal decrease in anaemia, haemorrhage, chronic infection, bone marrow
suppression, leukaemia, malnutrition, lymphoma, multiple myeloma,
cirrhosis, rheumatic fever and hypothyroidism.
3. Haemoglobin
Haemoglobin concentration determines the oxygen carrying capacity of blood.
When the patient's hydration status is normal, the haemoglobin is
approximately one-third of the haematocrit value.
Normal values
Female: 12–16 g/dL

Male: 13–18 g/dL
Pregnancy: Decreased by haemodilution
Elderly: Slightly decreased
Newborn: Increased
Haematocrit and haemoglobin indicates oxygen carrying capacity of the

blood. Haemoglobin is used as an indicator for the determination of necessity
of blood or packed cell transfusion after blood loss. A fall in haemoglobin
concentration below 10 g/dL is considered low. A fall in haemoglobin below
6 g/dL in a young individual indicates need for packed cell transfusion.
Determination of whether or not an individual with Hb level of 6–10 g/dL
requires blood transfusion depends on the patient's intravascular volume
status and the risk factors of inadequate oxygenation.
4. Platelet count (thrombocyte count)

Platelets, which are formed from the megakaryocytes in the bone marrow,
circulate in the blood stream with a life span of 8–12 days. They are removed
from circulation by the spleen. When the wall of a blood vessel is broken,
platelets aggregate to form a plug to stop bleeding. They release
phospholipids that are required by the intrinsic coagulation pathway (Refer
Chapter 15 on Haemostasis in Oral Surgery). Therefore, they are essential for
haemostasis.
Normal values
1,50,000–4,00,000 cells per cubic mm.
Normally increased by: High altitudes, cold temperatures, exercise,
excitement, drugs (cephalosporins, clindamycin, clozapine, corticosteroids,
danazol, dipyridamole, donepezil, eptoin, gemfibrozil, lithium and oral
contraceptives).
Normally decreased by: Hormones prior to menstruation, drugs (ACE
inhibitors, acetaminophen, allopurinol, antiarrhythmics, barbiturates,
chemotherapeutic agents, diuretics, donepezil, infliximab, NSAIDs and
phenothiazines).
Thrombocytosis (increased number of platelets) can occur in acute infections,
posthaemorrhagic anaemia, chronic leukaemia, asphyxiation, iron deficiency
anaemia, rheumatoid arthritis, cirrhosis, heart diseases, myeloproliferative
disorders, etc.
This condition predisposes to thrombosis (hyper-coagulability).
Thrombocytopaenia (decreased number of platelets) can occur in dengue, acute
leukaemia, AIDS, SLE, idio-pathic thrombocytopaenic purpura, aplastic
anaemia, clostridial infection, lymphoproliferative disease, disseminated
intravascular coagulation, radiation, splenomegaly, prosthetic heart valve, etc.
This condition predisposes to bleeding and hypo-coagulability.
• Low 50,000–1,50,000 per cubic mm—no signs of spontaneous bleeding

• Very low 20,000–50,000 per cubic mm—prolonged bleeding
• High risk less than 20,000 per cubic mm—spontaneous bleeding
5. Red blood cell count

RBC count measures the number of RBC (erythrocytes) per cubic millimetre of
blood. Life span of RBC is 80–120 days. Erythropoietin, a hormone secreted by
the kidney stimulates RBC production. Age, altitude, exercise, posture and
pregnancy are the factors influencing RBC count.
Normal values
Adult male: 4.7–6.1 × 106/mm3

Female: 4.2–5.4 × 106/mm3
Newborn: 3.5–5.1 × 106/mm3
1–2 years: 3.6–5.2 × 106/mm3
3–7 years: 4.1–5.5 × 106/mm3
8–12 years: 4.0–5.4 × 106/mm3
People living in high altitudes may have higher count since the oxygen
concentration of air is lower in high altitudes.
False low: Presence of agglutinins, haemolysis of sample, pregnancy

False high: Dehydration
Abnormal increase (Polycythaemia): In smoking, polycythaemia vera,

cardiovascular diseases, chronic hypoxia, chronic lung disease, Cushing
disease, hepatic cancer, drugs (corticosteroids, danazol, gen-tamicin, thiazide
diuretics).
Abnormal decrease in anaemias, haemorrhage, vitamin B deficiency,
leukaemia, multiple myeloma, alcohol abuse, bone marrow suppression,
chronic infection, renal failure, haemodilution, SLE (subacute bacterial
endocarditis), drugs (acetaminophen, aciclovir, allopurinol, amitriptyline,
antimalarials, MAO inhibitors, phenytoin, captopril, chemotherapy).
6. Red blood cell indices

Tissue oxygenation depends on the number and function of RBCs and the
concentration of haemoglobin. RBC indices are used to measure if the RBCs
are normal in size and have the appropriate amount of haemoglobin.
i. Mean corpuscular volume (MCV): Measurement of RBC size.
Normal values
Male: 78–100 fL
Female: 78–102 fL
Increase in MCV: Large (macrocytic) RBC—macrocytic anaemia as in

vitamin B12 or folic acid deficiency.
Decrease in MCV: Smaller (microcytic) RBC—iron deficiency and
thalassaemia.
ii. Mean corpuscular haemoglobin (MCH): Measure of the amount of
haemoglobin contained within the RBC.
Normal: 26–33 pg/cell
iii. Mean corpuscular haemoglobin concentration (MCHC) is the haemoglobin

content relative to the size of the cell (haemoglobin concentration) per
RBC.
Normal: 32–36 pg/cell
RBC's can not hold more than 37 g/dL of haemoglobin.

Increase in MCHC: Hyperchromic RBC—hereditary spherocytosis.
Decrease in MCHC: Hypochromic RBC—iron deficiency and thalassaemia.
Diagnosis of anaemia using RBC indices

Normocytic, normochromic MCV, MCHC normal, e.g. haemolytic anaemia and anaemia of
anaemia chronic disease
Microcytic/ hypochromic MCV ↓
anaemia MCHC ↓
e.g. iron deficiency anaemia,
thalassaemia, lead poisoning
Macrocytic/ normochromic MCV ↓
anaemia MCHC—normal, e.g. anaemia of folate deficiency and
vitamin B12 deficiency
7. White blood cell count and differential count

The WBC being of different types and properties, increases and decreases in
different conditions, their count can reveal the ongoing pathology. A moderate
increase in the same indicates infection and a decrease can be a compromise to
the immune system. A significant increase in WBC especially the immature
form indicates leukaemia.
Normal values
White blood cell count: Total number of blood cells in 1 mm3 of blood
Adult: 4,500–10,500/mm3
Child 6–12 years: 4,500–13,500/mm3
Child 2–6 years: 5,000–15,500/mm3
Child <2 weeks: 5,000–21,000/mm3
Newborn: 9,000–30,000/mm3
Differential percentages and absolute counts

Percentage of cells within a sample of 100 WBC
Neutrophils 40%–60%: 3000–7000 cells/mm3

Basophils 0.5%–1%: 15–100 cells/mm3
Eosinophils 1%–4%: < 450 cells/mm3
Lymphocytes 20%–40%: 1000–4000 cells/mm3
Monocytes 2%–8%: < 850 cells/mm3
II. Erythrocyte sedimentation rate

The erythrocyte sedimentation rate (ESR) is a simple, frequently performed
haematology test, often referred to as the ‘sedimentation rate’, which measures
the speed at which RBCs sediments in 1 h in a vertical column of
anticoagulated blood under the influence of gravity (Fig. 4.2). Rate of
sedimentation of the RBCs varies according to the difference in the quantity of
fibrinogen in the blood. Thus, the ESR, expressed in mm/h, would be increased
in inflammatory and necrotic conditions. Conditions that elevate fibrinogen in
blood, namely, pregnancy, diabetes mellitus, end-stage renal failure, heart
disease, collagen vascular disease and malignancy increase the sedimentation
rate of the RBCs. A decreased ESR is associated with conditions in which the
erythrocytes have a smaller, irregular shape like sickle cell anaemia,
polycythaemia, etc. ESR is therefore not a specific test for diagnosis of
pathology (except a few like polymyalgia rheumatica, temporal arteritis and
rheumatoid arthritis) but an indicator of sickness.
FIGURE 4.2 ESR analyser. (A) ESR analysis—Wintrobe method.
(B) Fully automated ESR analyser.
Normal values:
Age below 50 years:

Men 0–15 mm/h
Women 0–20 mm/h
Age above 50 years:
Men 0–20 mm/h
Women 0–30 mm/h
Methods of performing the ESR
There are several methods of measuring the ESR, each with advantages,
disadvantages and different levels of sensitivity. Each method has its own set
of reference values because the methods differ in technique and the equipment
used.
Manual methods
• Wintrobe
• Westergren (modified)
Wintrobe method
The Wintrobe ESR method is performed using a Wintrobe tube graduated
from 0–100 mm (0–10 cm) and with a capacity of 1 mL of blood. The Wintrobe
tube is placed in the sedimentation rack and is filled to the 0 mark with 1 mL
of well-mixed anticoagulated blood and left undisturbed vertically on a rack.
At the end of 1 h, the distance at which the erythrocytes have sedimented at
the bottom of the tube in the blood sample is measured using the markings on
the ESR tube. The distance is recorded in millimetre. The advantages of the
Wintrobe method are its simplicity and the lack of expensive equipment.
However, this method is not as sensitive as the Westergren ESR method.
Westergren method
The Westergren ESR method is performed using a Westergren tube (or
pipette) which is graduated from 0 to 200 mm, 30 cm long with a bore of
2.5 mm, open at both ends and a Westergren rack for holding the tubes. 1.6 mL
of blood is diluted with 0.4 mL of 3.8% sodium citrate solution. The pipette is
then filled to 0 level and left in the special stand for 1 h and readings marked
after 1/2 h and 1 h. The test has been modified in recent years and most
laboratories now perform the Modified Westergren method.
Modified Westergren kits are available that have closed systems with self-
filling disposable tubes and premeasured diluents. These kits eliminate the
bio-hazard risks present in the original Westergren method and also provide
accurate filling of the tube.
Conditions in which the ESR may be increased or decreased in the following

diseases:
Increased erythrocyte
Decreased erythrocyte sedimentation rate
sedimentation rate
Pregnancy (after 12th Sickle cell anaemia
week) Polycythaemia vera
Anaemia Spherocytosis
Polymyalgia rheumatical Increased plasma viscosity
Rheumatoid arthritis Microcytosis
Temporal (giant cell) Congestive cardiac failure
arteritis Factor V deficiency
Tissue injury/necrosis Hyperalbuminaemia
Macrocytosis Poikilocytosis
Inflammatory diseases Chronic lymphocytic leukaemia (elevated WBC)
Malignancy Hypofibrinogenaemia, hypergammaglobulinemia
Acute and chronic associated with dysproteinaemia and hyperviscosity
infections Drugs like: albumin, aspirin, corticotrophin, cortisone,
Multiple myeloma lecithin, steroids
Increased plasma
fibrinogen
Increased plasma
globulins
Coccidiodomycosis
Crohn disease
Menstruation
Drugs like: dextran,
heparin, oral
contraceptives
False increased rate False decreased rate
Tube tilted (not vertical) Low temperature of blood
Vibration of tube during Air bubbles in tube
test Improper blood dilution
Improper blood dilution Improper mixing of blood
Improper mixing of blood Room temperature <20°C
Room temperature >25°C
After mixing, the Westergren tube is inserted into the vial with a twisting
motion until the tube reaches the bottom of the vial. The blood column will
automatically show zero and any extra blood will overflow into the sealed
reservoir. The vial containing the tube is placed in the sedimentation rack for
exactly 1 h. At the end of the hour, the distance the erythrocytes have
sedimented and are measured in millimetres per hour.
III. Coagulation profile

Prolonged bleeding after a minor surgical procedure most commonly is due to
a local cause or tissue injury, but it is also the most common signs of
haemorrhagic disease and may develop into a haemorrhagic emergency.
Sometimes investigations performed after encountering prolonged bleeding
after dental procedure may be the way by which the disease is first recognised.
Flowchart 4.1 depicts the way a bleeding disorder should be investigated
and diagnosed.
FLOWCHART 4.1 Bleeding disorder investigations.
The following tests are therefore, essential parts of the coagulation profile:
1. Bleeding time (BT)

2. Capillary fragility test
3. Clotting time (CT)
4. Prothrombin time (PT) and International normalised ratio (INR)
5. Activated partial thromboplastin time (APTT)
6. Clotting factors
1. Bleeding time
Bleeding time is the measure of the duration of bleeding after an injury,
namely, a skin puncture. Bleeding time is a screening test for diagnosis of
platelet function and for vascular (peripheral capillary) defects. Therefore
evaluation of bleeding time is used to determine whether the function of
platelets is adequate. Prolonged bleeding time with normal platelet count
prompts further investigation of the clotting sequence or deficiency in platelet
function. Bleeding time can be determined by either Duke or lvy method.
Normal bleeding time by Ivy method is 2–9 min and by Duke's method is 1–
3 min. Bleeding time is usually normal in most coagulation disorders. The test
is useful to differentiate von Willebrand disease from haemophilia.
Haemophilic subjects and haemophilic carriers, who are deficient in factor VIII
activity, usually have a normal bleeding time, normal platelet adhesiveness
and normal ristocetin test. In contrast to patient with von Willebrand disease
factor VIII-related antigen (von Willebrand factor) is normal or slightly
increased and their ratio of factor VIII activity to factor VIII-related antigen is
significantly reduced.
2. Capillary fragility test

The capillary fragility or tourniquet test is based on the incidence of petechiae
(small red bleeding spots) formation produced by an inflated blood pressure
cuff over a 5-min period. It is also called as Hess test or Rumpel–Leede test.
Procedure
Take the patient's blood pressure and record it, for example, 100/70. Inflate
the cuff to a point midway between systolic blood pressure and diastolic blood
pressure and maintain for 5 min. Reduce and wait 2 min. Count the number of
petechiae in a 5 cm diameter circle of the area under pressure in the
antecubital fossa.
Normally less than 15 petechiae are seen. Fifteen or more petechiae indicate
capillary fragility, which occurs due to poor platelet function, bleeding
diathesis or thrombocytopenia, and can be seen in cases of scurvy, and dengue
fever.
The most common cause of abnormalities in vascular function and platelet
adhesion tests is thrombocytopenia. Dextran, penicillin G, nonsteroidal
antiinflammatory drugs (NSAIDs) and streptokinase streptodornase may
cause a prolonged bleeding time.
3. Clotting time
Clotting time (CT) is measured as the time taken for the blood to form fibrin
bands or thrombus. The venous blood drawn is filled immediately into
capillary tubes and the formation of bands checked by breaking the tubes at
regular intervals and checking the formation of the strings of fibrin. In the
Lee–White procedure, the coagulation time of whole blood is determined in
regular or silicone tubes.
Anticoagulants and tetracyclines may cause increased clotting time whereas
corticosteroids and epinephrine cause decreased values. Prolonged
coagulation times are associated with haemophilia, hypo-fibrinogenemia and
factor IX deficiency. Abnormalities in any of these tests indicate the
requirements for further coagulation studies.
4. Prothrombin time
• Prothrombin time (PT) is used to assess efficient functioning of the

coagulation process.
• This test is used in identifying bleeding disorders caused by either
deficiency or inefficiency of coagulation factors that constitute the
extrinsic system.
• These factors include fibrinogen (factor I), pro-thrombin (factor II),
factor V, factor VII and factor X.
• PT is also an index of the capacity of plasma to form thrombin. The PT
measures the amount of time it takes for a fibrin-clot to form in a
plasma sample added with calcium and tissue thromboplastin.
• Results are compared with a normal plasma control and the
prothrombin time is reported either in seconds or as the percent of
prothrombin calculated from a standard activity curve.
• If the patient's blood is deficient in one of the II, V, VII, X factors then
the patient's PT in seconds will be higher than the control PT in
seconds (or less than the control if using percentages). A modification
of this technique (the prothrombin–proconvertin procedure) using a
1:10 dilution of both patient and control plasma in the presence of
prothrombin-free-plasma as a source of factors I and V, is a more
sensitive index of specific deficiencies in pro-thrombin, factor VII, IX
and X.
• The PT is also used to monitor the effectiveness of anticoagulant
therapy with warfarin sodium which interferes with the production of
vitamin K-dependent clotting factors, such as prothrombin.
• A normal range for PT is 8.8–11.6 s, but varies according to the norms
established by individual laboratories.
• Oral anticoagulant therapy aims to maintain the PT at 1.5–2 times the
control value (in seconds). Thus, a therapeutic goal, if receiving an
anticoagulant, would be a PT of 24 s or 25% of normal activity.
• If the PT is greater than 30 s, the patient is at risk for spontaneous
haemorrhage.
• PT may be increased in vitamin K deficiency, defici-ency of factors I, II,
V, VII, X, acute leukaemia, chronic pancreatitis, liver disorders,
hypofibrinogenaemia. Diarrhoea, vomiting and alcohol ingestion may
increase PT results. High fat diet may decrease PT value. Besides
warfarin, mefenamic acid, antibiotics, aspirin, glucagon, phenytoin,
vitamin A, MAO inhibitors increase PT value. Steroids, antacids,
antihistamines, caffeine, oral contraceptives, ascorbic acid,
theophylline, rifampicin and diuretics may decrease PT value.
INR: To provide standardisation of PT reporting among different

laboratories, the WHO recommends the use of the international normalised
ratio (INR) to express the intensity of therapy. Most laboratories now report
both the PT and the INR. Maintaining an INR of 2.0–3.0 is advised for
prophylaxis/treatment of venous thrombosis and thromboembolic
complications associated with a trial fibrillation, for pulmonary embolism, for
prophylaxis of systemic embolism after myocardial infarction and for
prosthetic cardiac valves. A higher INR of 2.5–3.5 is recommended for cardiac
valve replacement which involves mechanical valves and antiphospholipid
antibody syndrome.
5. Partial thromboplastin time/activated partial thromboplastin time
• The partial thromboplastin time (PTT) is used to appraise the proper

functioning of the coagulation cascade by measuring the time taken for
a clot to form in a plasma sample to which calcium and partial
thromboplastin have been added.
• If addition chemicals are added to standardise and accelerate the test,
the result is reported as an activated partial thromboplastin time
(APTT).
• This test is helpful for diagnosing bleeding disorders that occur due to
deficient or defective coagulation factors I, II, III, V, IX, X, XI and XII
that form the intrinsic system.
• APTTs may infer normal clotting function but moderate single factor
deficiencies may be present which will not decrease the APTT until
their concentration or function is below 30%–40% of normal.
• The PTT is also used to monitor heparin therapy.
• Normal range for PTT is 60–90 s; APTT is 25–35 s.
• Heparin is commonly administered intravenously in thromboembolic
conditions. The therapeutic level of PTT for a patient receiving heparin
is 1.5–2.5 times the control value. If the value falls below the
therapeutic level for a patient on heparin, an increase in anticoagulant
dosage is warranted. If the APTT is higher than 100 s, the patient is at
high risk for spontaneous bleeding therefore the dosage needs to be
tapered.
6. Coagulation factors
Coagulation factor assay is performed to diagnose congenital or acquired
deficiency of haemostasis like haemophilia, von Willebrand disease, vitamin K
deficiency, etc. For example, tests of factor VIII-related antigen are used in the
differential diagnosis of classic haemophilia and von Willebrand disease in
cases in which there is no family history of bleeding and bleeding times are
borderline or abnormal. A test for ristocetin cofactor is done to help diagnose
von Willebrand disease by determining the degree or rate of platelet
aggregation that is taking place.
Clinical implications of deficiencies in clotting factors
1. Inherited deficiencies
• Any of the specific factors—I, II, V, VII, VIII, IX, X, XI, XII and XIII—
may be deficient on a familial (congenital) basis.
• Factor VII is decreased in hypoproconvertinaemia (autosomal
recessive).
• Factor VIII is decreased in classic haemophilia A and von Willebrand
disease (inherited autosomally).
• Factor IX is decreased in Christmas disease or haemophilia B (sex-
linked recessive).
• Factor XI is decreased in haemophilia C (autosomal dominant).
Acquired condition
• Factor I (Fibrinogen) is decreased in disseminated intravascular

coagulation (DIC), fibrinolysis, liver disease.
• Factor II (Prothrombin) is decreased in liver disease, vitamin K
deficiency.
• Factor V (Labile factor/Proaccelerin) is decreased in deep vein thrombosis
(DVT), DIC, fibrinolysis, liver disease, pulmonary embolism.
• Factor VII (Stable factor/Proconvertin) is decreased in haemorrhagic
disease of the newborn, kwashiorkor, liver disease, vitamin K
deficiency.
• Factor VIII (Antihaemophilic globulin) is decreased in haemophilia A, von
Willebrand disease, autoimmune disease, fibrinolysis, DIC, post
partum.
• Increased in coronary artery disease, Cushing syndrome,
hyperthyroidism, hypoglycaemia, inflammation, late pregnancy,
macroglobulinaemia, myeloma, postoperative period, progesterone
use, rebound activity after sudden cessation of warfarin,
thromboembolic conditions.
• Factor IX (Christmas factor) is decreased in haemophilia B (Christmas
disease), vitamin K deficiency, haemorrhagic disease of newborn, liver
disease like cirrhosis, congenital deficiency, disseminated
intravascular coagulation, nephrotic syndrome.
• Factor X (Stuart–Prower factor) is decreased in vitamin K deficiency,
DIC, liver disease, amyloidosis increased in pregnancy.
• Factor XI (Plasma thromboplastin antecedent) is decreased in intestinal
malabsorption of vitamin K, haemophilia C, liver disease, stress,
normal newborn and congenital heart disease.
• Factor XII (Hageman factor) is decreased in nephritic syndrome, normal
newborn and pregnancy.
• Factor XIII (Fibrin stabilising factor) is decreased in postoperative period,
pernicious anaemia, myeloma agammaglobulinemia,
hyperfibrinogenaemia, lead poisoning, liver disease.
Many diseases have a biochemical basis and therefore a biochemical analysis
of the readily accessible body fluids reveals the pathology in progress
(Fig. 4.3). In the dental surgical practice, oral manifestation of a systemic
disease can be diagnosed by biochemical tests. For example, cotton wool,
multifocal radiodense conglomerates seen in osteitis deformans (Paget disease)
may also be encountered in florid cement-osseous dysplasia and Gardner
syndrome; however an elevation of alkaline phosphatase occurs only in Paget
disease. Elevated serum calcium can indicate hyperparathyroidism (Brown
tumour) and can differentiate a giant cell granuloma from Brown tumour.
Impaired liver function may also indicate a bleeding disorder; therefore
biochemical tests are important.
FIGURE 4.3 Automated biochemistry analyser.
The biochemical analyses that are commonly used by an oral surgeon for
diagnosis and for presurgical evaluation are:
I. Liver function tests

a. Bilirubin
b. Alkaline phosphatase (ALP)
c. Gamma glutamyl transferase (GGT)
d. Alanine aminotransferase/serum glutamic pyruvic
transaminase (ALT/SGPT)
e. Aspartate aminotransferase/serum glutamic oxaloacetic
transaminase (AST/SGOT)
f. Albumin
g. Prothrombin time
h. Lactate dehydrogenase (LDH)
II. Renal function tests
a. Serum uric acid
b. Serum creatinine
c. Creatinine clearance
d. Blood urea nitrogen
e. Blood osmolality
f. Uric acid, urine
g. Osmolality, urine
1. Liver function test
a. Bilirubin
Normal values
Total bilirubin 0.3–1.0 mg/dL

Direct (conjugated) bilirubin 0.0–0.4 mg/dL
Indirect (unconjugated) bilirubin 0.1–1.0 mg/dL
• It is one of the components of bile that is secreted by the liver into the
gastrointestinal (GI) tract.
• Bilirubin is formed as a result of haemoglobin breakdown, after
destruction of RBC.
Types of bilirubin
There are two types of bilirubin
i. Direct (conjugated):
▪ In normal body, liver secretes bilirubin into the GI via bile
which is excreted via faeces, as direct or conjugated bilirubin
with only minimal amounts being reabsorbed into the
bloodstream.
▪ Level of direct bilirubin rises in the blood when there is an
obstruction in the bile flow from liver termed obstructive
jaundice (as from gallstones) or hepatic jaundice. In such
cases, because the bilirubin is unable to reach the intestines for
excretion and instead, enters the bloodstream for excretion by
the kidneys (urobilinogen).
▪ It was named ‘direct’ bilirubin because this water soluble type
of bilirubin reacts directly with the reagents added to the
blood sample.
▪ Direct bilirubin is the only type of bilirubin able to cross the
glomerular filter; thus it is the only type of bilirubin that can
be found in the urine.
▪ If conjugated hyperbilirubinaemia is present, the presence of
concomitant alkaline phosphatase elevations must be assessed
and biliary obstruction should be excluded.
ii. Indirect (unconjugated):
▪ Indirect bilirubin, also known as free or unconjugated bilirubin,
is normally found in the bloodstream.
▪ Its name is derived from the fact that this non-water soluble
bilirubin does not directly react with reagents added to a
blood sample. Alcohol must be added for the reaction to
occur.
▪ Indirect bilirubin rises in haemolytic jaundice, when the
breakdown of haemoglobin results in a higher than normal
level of indirect bilirubin being present in the bloodstream.
▪ Therefore this is the type of bilirubin elevated in cases of
hepatocellular dysfunction, such as hepatitis. Asymptomatic
adult patients with an isolated, mild unconjugated
hyperbilirubinaemia should be evaluated for Gilbert
syndrome, haemolysis and medication induced
hyperbilirubinaemia.
▪ Total bilirubin is composed of the direct bilirubin plus the
indirect bilirubin. The total bilirubin level increases with any
type of jaundice.
b. Alkaline phosphatase
Normal values
Female: 30–100 U/L

Male: 45–115 U/L
ALT:AST 1:1
• ALP is an enzyme found in the cells lining the biliary tract and in the
osteoblasts involved in the formation of new bone and also in liver,
bone, placenta, intestine and kidneys.
• ALP is excreted from the liver in the bile.
• Increased ALP levels are found most commonly during periods of
bone growth (as in children), in various types of liver disease and in
biliary obstruction.
• ALP is also a tumour marker that increases in the case of osteogenic
sarcoma and in breast or prostate cancer that has metastasised to the
bone.
c. Gamma glutamyl transferase
Normal values
Female: 5–29 U/L

Male: 5–38 U/L
Child: 3–30 U/L
Newborn: 5 times child normal value
• GGT is an enzyme that is found in the liver and biliary tract and to a
lesser degree in the heart, kidneys, pancreas, prostate gland and
spleen.
• Its function is to assist in amino acid transport across cell membranes.
• GGT is often measured in conjunction with ALP to determine whether
the ALP is increased due to liver disease. While ALP may be increased
with either hepatobiliary or bone disorders, the GGT is more specific
for hepatobiliary problems like alcoholic cirrhosis or hepatic
carcinoma.
• GGT is more sensitive than ALP, the transaminases (ALT, AST) and
leucine aminopeptidase in detecting obstructive jaundice, cholangitis
and cholecystitits.
d. SGPT and SGOT

SGPT refers to ALT and (SGOT) refers to AST.
SGPT/ALT SGOT/AST
Female: 7–30 U/L Female: 7–30 U/L
Male: 10–55 U/L Male: 10–55 U/L
Elderly: slightly high
Children: 2–3 times adult normal values
• ALT is an enzyme found mainly in the liver but also in the kidneys,
heart and skeletal muscle tissue.
• It functions as a catalyst for amino acid production.
• ALT value is used mainly in the diagnosis of liver disease and to
monitor the effects of hepatotoxic drugs.
• ALT is assessed along with AST in monitoring liver damage.
• AST is an enzyme present in the heart, liver and muscle. It is released
into the circulation subsequent to damage or death of cells.
• AST levels usually increase within 12 h of the injury and remain
elevated for 5 days. Thus, this test is performed along with creatine
kinase (CK) isoenzymes, LDH, LD and troponin when there has been
damage to the cardiac muscle, as in myocardial infarction.
• These two values normally exist in an approximately 1:1 ratio.
Enzymes Normal value Elevated/decreased

Bilirubin Total bilirubin: Drugs that increase total bilirubin: Allopurinol, steroids,
0.3–1.0 mg/dL MAO inhibitors, oral contraceptives
Drugs that decrease total bilirubin: Barbiturates, caffeine,
penicillin
Direct Elevated direct bilirubin: Biliary obstruction (e.g.
(conjugated) choledocholithiasis), cirrhosis, pregnancy
bilirubin: 0.0–
0.4 mg/dL
Indirect Increased indirect bilirubin: Increased haemolysis, decreased
(unconjugated) hepatic uptake/conjugation (e.g. Gilbert syndrome), cirrhosis,
bilirubin: 0.1– erythroblastosis fetalis, malaria
1.0 mg/dL
Prothrombin 10–14 s Elevated: Strong prognostic indicator of poor outcome and need
time for liver transplantation in acute liver failure, acetaminophen
overdose
Albumin 3.5–5.0 g/dL Decreased: Malnutrition, severe illness, renal losses (e.g. nephritic
syndrome) and gut losses (protein-losing enteropathy)
AST or Female: 7– Increased in: Acute hepatocyte injury due to drugs (e.g.
SGOT 30 U/L acetaminophen overdose), viruses (e.g. hepatitis A, hepatitis
Male: 10– B), or ischaemia (e.g. myocardial infarction)
55 U/L AST >× 2 higher than ALT characteristic of alcoholic liver
disease; also in cirrhosis, hepatitis, pancreatitis, liver CA
Elderly: Decreased in: Beriberi, diabetic ketoacidosis, haemolysis,
Slightly high pregnancy, uraemia
Children: 2–3 Drugs that increase: Acetaminophen, allopurinol, antibiotics,
times adult chlorpropamide, cholinergics, methyldopa, vitamin A
normal values Drugs that decrease: Metronidazole
ALT:AST = 1:1
ALT or Female: 7– Increased in: Hepatitis, cirrhosis, liver cancer, biliary
SGPT 30 U/L obstruction (cholestasis), bone metastasis, congestive heart
Male: 10– failure, muscle inflammation, infectious mononucleosis,
55 U/L shock, trauma
Drugs that increase: ACE inhibitors, acetaminophen,
ALT:AST = 1:1 anticonvulsants, antibiotics, heparin, NSAIDs
ALP Female: Increased in: Biliary obstruction, bone metastasis, calcium
30–100 deficiency, CA pancreas, cirrhosis, eclampsia, fracture,
U/L hepatitis, high fat intake, hyperparathyroidism, infectious
Male: 45– mononucleosis, leukaemia, CA liver, osteogenic sarcoma,
115 U/L osteomalacia, Paget's disease, pancreatitis, pregnancy, RA,
Elderly: rickets, vitamin D deficiency
Slightly Decreased in: Cystic fibrosis, excessive vitamin D intake,
high hypophosphataemia, perinicious anaemia, celiac disease,
Children: chronic nephritis, scurvy
1–3 times Drugs that increase: ACE inhibitors, anticonvulsants,
adult heparin, NSAIDs, oestrogens
Puberty: Drugs that decrease: Fluorides, propranolol
5–6 times
adult
norms
GGT Female: 5– Increased in: Acute pancreatitis, alcoholism, biliary
29 U/L obstruction, cholecystitis, cholelithiasis, cirrhosis, hepatitis,
Male: 5–38 MI, renal cancer, SLE GGT is a sensitive marker of alcohol
U/L ingestion and certain hepatotoxic (liver toxic) drugs
Child: 3– Marker of cholestasis, but may be due to alcohol and other
30 U/L drugs through enzyme induction
Newborn: Drugs that increase: Aminoglycosides, barbiturates, NSAIDs,
5 times phenobarbital, phenytoin
child Drugs that decrease: Oral contraceptives
normal
value
2. Renal function tests

Test Related physiology
BUN (blood The end product of protein metabolism is urea, which is excreted entirely by the
urea kidneys; therefore, the BUN is an indication of liver and kidney function
nitrogen)
Serum Creatinine is formed when creatinine phosphate is used in skeletal muscle
creatinine contractions, which is entirely excreted by the kidneys; therefore, the serum
creatinine levels are an indication for renal function. The creatinine level is not
affected by hepatic function so it is a more precise indication of renal function than
is the BUN. A 50% reduction in glomerular filtration rate (GFR) doubles the
creatinine level
24-h urine Measures GFR and is dependent upon renal artery perfusion and glomerular
collection filtration (GF)
for
creatinine
clearance
Urinalysis Cloudy, foul smelling, WBCs—urinary tract infection (UTI)
Dark yellow—dehydration
Acetone odour—diabetic ketoacidosis
Presence of protein—injured glomerular membrane
Glucose—diabetes mellitus
Ketones—fatty acid metabolism
Crystals—renal stone formation possible
Many hyaline casts—proteinuria
Cellular casts—nephrotic syndrome
Intravenous IV-administered, radiopaque dye allows the visualisation of the kidneys, renal
pyelogram pelvis, ureters and bladder
(IVP)
Prostatic PSA is a glycoprotein found in all prostatic epithelial cells. An increase may be
specific indicative of prostatic enlargement, thus this test is used to screen for prostatic
antigen cancer and as an indicator of treatment success/failure
(PSA)
▪ AST > ALT infers alcohol-induced hepatitis, cirrhosis and metastatic

cancer of the liver.
▪ ALT > AST infers viral or drug-induced hepatitis and hepatic
obstruction other than malignancy.
▪ Twofold increase is suggestive of an obstructive problem that may need
surgical intervention.
▪ 10-fold increase of ALT and AST occurs in hepatitis.
Microbiologic tests
All diagnostic tests must be sensitive, specific and accurate should have a
positive predictive value and high likelihood ratio. Diagnostic medical
microbiology deals with the detection of the microbial aetiological agent of an
infection. The microbe causing the infection in a host body can be identified by
inducing the specimen taken from the host body to a number of laboratory
procedures. They can be:
I. Nonculture methods
II. Culture method
III. Culture media
IV. Molecular diagnostics
V. Immunologic methods
I. Nonculture methods
a. Light microscopic identification
i. Bright field or standard microscopy (Fig. 4.4): Organisms from a specimen

or colonies can be identified by the microscopic morphological features
as viewed under microscope.
ii. Dark ground microscopy: The specimen is illuminated obliquely by a
special condenser so that the light rays do not enter the objective
directly. The organisms look bright against a dark background, e.g.
Treponema pallidum.
iii. Fluorescence microscopy: Bacteria or cells are stained with fluorescent
dyes, such as auramine to detect microbial antigens in a specimen. The
latter is ‘stained’ with specific antibodies tagged with fluorescent dyes.
For example, QBC Malaria test tubes are internally coated with
acridine orange stain and anticoagulant with specific antibodies tagged
with fluorescent dyes. The specimen is collected in the tube and
centrifuged, then examined under special fluorescence microscopes to
detect the parasite. Direct immuno-fluorescence stain is a combination
of serology with fluorescence microscopy where the pathogen is
viewed by using antibody labelled with fluorescent dyes, e.g.
fluorescein isothiocynate, lissamine, rhodamine, specific antigen can be
detected and based on which infecting bacterium can be identified. In
addition, fluorescence microscopy is used for tubercle bacilli.
FIGURE 4.4 Binocular bright field microscope.
b. Electron microscopy
In electron microscopy, light waves are replaced by a beam of electrons, which
allows resolution of extremely small organisms, such as virions. Electron
microscopy can be used in diagnostic virology, like direct examination of
specimens.
II. Culture methods

The pathogen is multiplied in a conducive environment and identified by
viewing them under a light or electron microscope. Their virulence and
sensitivity to antibiotics can also be tested after their colonies are grown.
a. Solid or liquid media are used for bacterial and fungal growth (Fig. 4.5).
b. Cultured cells from animals/human beings are used for viral growth.
c. Bacteria can be identified by its morphological, physiological and
biochemical characteristics as:
1. Morphology of the bacteria and its colonial characteristics: Size, shape,
elevation (flat, convex, umbonate), margin (entire, undulate,
filamentous), colour, smell and texture; effect on blood (alpha, beta or
non haemolytic) (Fig. 4.6).
2. Stains: Gram stain and Ziehl–Neelsen staining technique are used to
identify bacteria by subjecting them to coloured dyes. Gram stain is
performed routinely to reveal the shape and size of bacteria and to
classify organisms into four categories: Gram-positive cocci, Gram-
positive bacilli, Gram-negative cocci, Gram-negative bacilli. Gram stain
gives clue to plan further diagnostic techniques and therapy. Ziehl–
Neelsen stain is performed on specimens including sputum, urine, pus,
when infections by mycobacteria are suspected. Similarly, Indian ink
(negative staining) is used for capsulated bacteria. Albert and Neisser
stain can identify Corynebacterium diphtheriae. Spore staining is a
technique for detecting sporulating bacteria.
3. Aerobic/anaerobic Bacteria can be identified depending on their growth
in the presence or absence of air in the culture period. They are
differentiated as aerobic, anaerobic, capnophilic (i.e. grows well in
carbon dioxide excess) based on their growth requirements.
4. Biochemical tests
• Biochemical reactions of the bacteria are used to identify them.
• Sugar fermentation reactions, the fermentation of glucose,
lactose, sucrose, mannitol and other sugars by pure culture
are checked for the production of acid and gas or both.
• This test identifies a host of bacteria.
• Other biochemical tests are: Indole production test, Methyl red
test, Voges–Proskaur test, Citrate utilisation test, H2S
production test, Oxidase test, Catalase test, Urease production
test, Phenylalanine deaminase test, Nitrate reduction test,
Gelatin liquefaction test, Amino acid decarboxylase test, etc.
5. Enzyme profile: The organism is incubated with an appropriate, known
enzyme substrate. If the enzyme is secreted by the organism, then this
will -react with the substrate and cause a colour change. Some bacteria
can be identified primarily by production of a characteristic enzyme,
e.g. coagulase produced by Staphylococcus aureus, lecithinase produced
by Clostridium perfringens.
6. Other methods for identification are:
• Study of antigenic characters
• Study of growth factor requirements
• Study of toxin production
• Study of metabolic end products by gas liquid
chromatography
FIGURE 4.5 Blood agar streaked with bacterial inoculum.
FIGURE 4.6 Gold colour—growth of Staphylococcus aureus, white
colour—Staphylococcus albus in agar.
Obtaining sample for culture and detection

When a patient is diagnosed with an infection, the clinician further attempts to
identify the pathogen through laboratory tests conducted by a microbiologist.
To achieve an accurate result and to interpret it clinically, following points
should be considered while collecting the sample for culture and sensitivity:
1. The clinician must provisionally diagnose the infection and request for
the correct test. All pathogens (virus, bacterium, fungus or other
parasite) cannot be isolated by a single test.
2. The specimen collected should be of good quality and before the
commencement of antimicrobial therapy. Contamination by the normal
microbiota of the surrounding areas misleads the diagnosis. For
example, pus should be collected from the depth of the lesion not the
surface.
3. Adequate quantity of specimen should be collected.
4. Vitality of the organism till it reaches the laboratory should be ensured
and cross-contamination strictly avoided.
5. The timing of collection should be ideal (acute infectious phase).
6. Label the specimen with at least two information about the patient.
7. Treatment should not be deferred until identification of pathogen since
growth of pathogen in the culture may be delayed.
Disease Specimen Commonly isolated pathogens
Odontogenic Pus Polymicrobial,
infection Group A β-haemolytic streptococci, S.
aureus
Anaerobes: Bacteroides melaninogenicus,
Eikinella corrodens
Cellulitis of Punch biopsy Group A β-haemolytic streptococci, S. aureus
skin
Impetigo Swab Group A β-haemolytic streptococci, S. aureus;
rarely, Corynebacterium diphtheriae
Ulcers Punch biopsy; deep tissue Mixed flora
aspirate or biopsy
Perioral Pus Mixed flora of mouth and pharynx
abscess Klebsiella pneumoniae, Streptococcus sp.,
Staphylococcus sp.
Osteomyelitis Pus or bone specimen obtained Multiple; often
by aspiration or surgery S. aureus
Diagnosis of infection by anatomic site

Wounds, tissues, bone, abscesses, fluids
• The pus in closed, undrained soft tissue abscesses, osteomyelitis:

mostly contains only one organism as the infecting agent; most
commonly staphylococci, streptococci or enteric Gram-negative rods.
Anaerobic bacteria (bacteroides, peptostreptococci) sometimes play an
essential causative role and mixtures of anaerobes are often present
therefore anaerobic culture must be performed.
• Acute osteomyelitis: organisms can often be cultured from blood
before the infection has become chronic.
• Open wounds, mucosal surfaces: Multiple micro-organisms.
• Deep suppurating lesions, such as chronic osteomyelitis draining into
exterior surfaces through a sinus or fistula: The flora of the surface
through which the lesion drains must not be mistaken for that of the
deep lesion. Instead, specimens should be aspirated from the primary
infection through uninfected tissue.
• Eroded skin and mucous membranes: Yeast or fungus infections.
Candida, Aspergillus and other yeasts or fungi can be seen
microscopically in smears or scrapings from suspicious areas and can
be grown in cultures. Treatment of a specimen with KOH and
calcofluor white greatly enhances the observation of yeasts and
moulds in the specimen.
III. Culture media

Majority of pathogenic bacteria grow on solid media, nutrient agar or blood
agar (the most widely used culture media). Routinely specimen is inoculated
on blood agar and MacConkey agar. The culture media in which the bacteria
are cultured or grown are chosen as per the organism under consideration.
• Blood agar is a solid nutrient agar with 5%–10% horse or sheep blood,
the most commonly used culture media.
• Chocolate agar, which is the heated blood agar, is used for isolation of
Haemophilus influenzae, Neisseria species.
• Cysteine-lactose-electrolyte deficient (CLED) agar which contains
Peptone, L-cysteine, lactose, etc. is used to culture coliform bacteria.
• Peptone and semisynthetic media are used for antibiotic sensitivity
tests.
• Deoxycholate citrate agar, selenite F broth are used for culturing
Salmonella and Shigellla species.
• Thiosulphate-citrate-bile salts-sucrose (TCBS) agar for Vibrio cholerae.
• Wilson and Blair's medium for Salmonella species.
• Thayer–Martin medium for Neisseria species.
• Lowenstein–Jensen (LJ) medium for Mycobacteria.
• Robertson's cooked meat liquid medium is used mainly to culture
anaerobes.
• Liquid media containing peptone, sodium chloride and water is used
as base for sugar fermentation tests.
• Liquid nutrient broth with meat extract is used for general culture.
• Many types of yeast will grow on blood agar. Biphasic and mycelia
phase fungi grow better on media designed specifically for fungi.
Brain–heart infusion agar, with and without antibiotics and inhibitory
mould agar have largely replaced the traditional use of Sabouraud
dextrose agar to grow fungi. Media made with plant and vegetable
materials, the natural habitats for many fungi, also grow many fungi
that cause infections. Cultures for fungi are commonly done in paired
sets, one set incubated at 25–30 °C and the other at 35–37 °C. Staining
agents that are used for identifying fungal mycelium are KOH
preparation, Indian ink preparation and calcofluor white stain.
Candida albicans
Even though many strains of Candida can colonise the oral mucosa, the most
frequently occurring oral fungal infection is Candida albicans. It is highly
infective due of its higher level of pathogenicity and adherence properties. C.
albicans is a normal inhabitant in 40%–65% of healthy adult oral cavity. The
papillated dorsal surface of the tongue and palatal mucosa underneath a
maxillary denture are the usual reservoir sites. An immunocompromised
patient is more susceptible to oral candidal infection. The
immunocompromise may be local or systemic. Local factors include denture
wearing and decreased flow of saliva (Sjogren). Systemic factors include
diabetes mellitus, pernicious anaemia, AIDS and organ-transplanted patients
under immune suppressing drugs. Additionally, the C. albicans infection itself
can suppress the immune system.
Clinical forms are:
1. Pseudomembranous
2. Erythematous
3. Hyperplastic
4. Denture erythematous
5. Median rhomboid glossitis may also be regarded as a form of chronic
oral candidiasis
6. Angular cheilitis may be preceded by monilial infection
Diagnosis
The microscopic demonstration of fungal hyphae is highly diagnostic of the
candidal infection.
1. PAS smear (Periodic acid–Schiff stain)

2. Incision biopsy.
Because C. albicans is an oral commensal, confirmation of diagnosis of
infection is often done by the resolution of lesions in response to
antifungal medications.
Treatment
1. Nystatin: Used as a topical agent in rinse or pastille forms; safe

2. Clotrimazole: Topical agent in lozenge form; may cause liver enzyme
changes
3. Ketoconazole: Systemic prescription; may cause liver changes
4. Fluconazole
5. Chlorhexidine can be used as an oral rinse or as a disinfectant for
dentures
Laboratory aids in the selection of antimicrobial therapy
Test for antibiotic susceptibility
1. The specimen is inoculted in two agar plates for culturing under

aerobic and anaerobic conditions (Primary plates).
2. The blood agar is then incubated for 2–3 days at 37 °C for 18 h.
3. The plates are inspected for bacterial growth. The shapes and sizes of
the colonies are identified. If the infections are monomicrobial, they are
identified and can be cultured further for antibiotic sensitivity. If they
are polymicrobial, the putative pathogens are isolated and subcultured
on fresh blood agar plates to obtain single organism cultures and
incubate it at 37 °C for 24–48 h.
4. The pure culture is harvested and identified using biochemical
reactions, selective media or specific antibody reactions.
5. A filter paper disc impregnated with different antibiotics is applied
onto a lawn of the organism seeded on an agar plate. After overnight
incubation, the growth pattern of the colonies around the impregnated
antibiotics shows the susceptibility of the organism to the antibiotic.
The zones of growth indicate resistance and zones of inhibition
indicate susceptibility.
Disc diffusion susceptibility test (Figs. 4.7, 4.8)
Interpretation
a. The disc test measures the ability of drugs in inhibiting the growth of
bacteria. The results correlate well with therapeutic response in those
disease processes where body defences can frequently eliminate
infectious microorganisms.
b. The commonly performed disc diffusion susceptibility test must be
interpreted shrewdly and used prudently since the drugs included are
not comprehensive. In general, only one member of each major class of
drugs is represented. For Staphylococci, penicillin G, oxacillin, cefazolin,
erythromycin, gentamicin and vancomycin are used. For Gram-
negative rods, ampicillin, piperacillin, cefazolin, second- and third-
generation cephalosporins and other ‘antipseudomonal penicillins’,
trimethoprim-sulphamethoxazole, fluoroquinolones and the
aminoglycosides (amikacin, tobramycin, gentamicin) are included. The
choice of drugs to be included in a routine susceptibility test battery
should be based on the susceptibility patterns of isolates in the
laboratory, the type of infection (community acquired or nosocomial)
and cost efficacy analysis for the patient population.
c. The diameter of zones of growth inhibition of one drug being larger than
that of drug acting on the same organism does not mean higher
susceptibility since the sizes depend on molecular size and diffusability
of the drug and not on inhibitory action. Each drug has a specific and
different minimum diameter of inhibition zone that denotes
‘susceptibility’ of an isolate by the disc diffusion technique.
FIGURE 4.7 Disc diffusion susceptibility test.
FIGURE 4.8 Interpretation of disc diffusion susceptibility test.
IV. Molecular diagnostics

Molecular diagnostics has two modalities:
• Nucleic acid probe test

• PCR (polymerase chain reaction)
1. Nucleic acid probe test

It uses gene probes (cloned fragments of DNA) that recognise complimentary
sequences of nucleic acid of microorganisms, based on which the infecting
organism is identified. The test can be used for diagnosis of mycobacterial,
chlamydial, neisserial and other bacterial infections.
Gene identification probes (Fig. 4.9)

Every identified species of microbe has a unique DNA or RNA sequence
somewhere on its genome that differentiates it from another species. In
diagnostic microbiology, this character is used to detect microbes in the
clinical samples from the infected patient by detecting the DNA sequence. The
advantage of gene identification is that the swab samples could be simply sent
by post to distant laboratories for identification, even in paper points, without
the fear of death of organisms and the associated cumbersome culture
procedures or transport media. Gene identification is done using probes. A
few examples are:
i. DNA gene probes are pieces of DNA that are labelled radioactively or
with a chemiluminescent marker. The probes carry a single strand of
DNA analogous to the pathogen that is sought in the clinical sample.
ii. Oligonucleotide probes are based on the variable region of the 16 s
ribosomal RNA genes. The nucleotide sequences of the latter gene of a
number of microbes have been well characterised and are known to be
well preserved across species, except for several small variable regions.
This property is helpful in the construction of specific oligonucleotide
probes of about 18–30 bases, which are much more specific than the
DNA probes.
iii. Ribosomal RNA (rRNA) is highly species-specific and this property is
used to produce RNA probes that are useful for both diagnostic
microbiology and taxonomic studies. The most commonly used are the
5, 16 and 23 S probes.
FIGURE 4.9 Construction of a DNA fingerprint of microbes from
clinical specimen.
2. Polymerase chain reaction
It uses the ability of DNA polymerase enzyme to synthesise a large amount of
specific DNA from a single piece of DNA. These tests are highly sensitive and
are particularly important in the identification of organisms that are difficult
or slow to grow (e.g. Mycobacterium, Neisseria, Chlamydia).
Polymerase chain reaction is a simple technique in which a region of a DNA
molecule, even as small as a single gene, can be copied repetitiously using a
DNA polymerase enzyme. This technique is used to identify bacteria that
cannot be cultured.
Methods
1. A region of the DNA molecule with known nucleotide sequences of the

borders is chosen. It is necessary to know the border sequence since the
short oligonucleotides must hybridise with both ends of the strand of
the double helix of the DNA molecule, for the PCR to begin.
2. Denaturation step: The double strand of the DNA molecule is
denatured by heat (90–95 °C) and split to single strands.
3. Hybridisation step: The oligonucleotides, now acting as primers,
hybridise to the region next to the target DNA sequence, which is then
copied, multiplied (several times) and amplified (55 °C).
4. Synthesis step: PCR uses a thermostable DNA polymerase to produce a
twofold amplification of target DNA with each temperature cycle. The
DNA -polymerase enzyme, Taq polymerase, a heat-stable enzyme from
Thermus aquaticus (Taq), a thermophile bacterium from hot springs and
the nucleotides (deoxyribonucleoside 5′-triphosphate (dNTP): adenine,
guanine, cytosine, thymine) are added to the primed template DNA
and incubated at 72 °C for synthesis of new complementary strands or
-amplicons.
5. The mixture is subjected to heat (94 °C) in order to dissociate the newly
synthesised complementary strands (amplicons) from the template.
6. On being cooled to 45–60 °C, more primers hybridise once again at their
respective positions, including positions on the newly synthesised
strands and a second cycle of DNA synthesis occurs.
7. This three-step PCR cycle of denaturation-hybridisation-synthesis can
be repeated, usually 25–40 times in a thermocycler, which results in
exponential accumulation of several million copies of the amplified
fragment amplicons.
8. After staining with ethidium bromide, a sample of the amplified
fragments is subjected to electrophoresis system in agar gel to visualise
the product, which manifests as a discrete band.
9. The last step is now precluded in advanced variations of PCR, such as
real-time PCR where the amplicon can be identified using labelled
probes and labelled fluorophores.
Types of PCR
The basic PCR methodology is now improved to provide microbiological
analytical tools. The three commonly used variations of PCR are: nested,
multiplex and real-time PCR.
Nested PCR To increase the sensitivity of the conventional PCR, two
different sets of primers are used: one to begin the amplification primarily and
the other to anneal with the internal sequence of the amplion in a more specific
manner to obtain much more specific multiples.
Multiplex PCR To further increase the specificity, instead of one, multiple
loci of the nucleotide are amplified simultaneously to save time, resources and
to diagnose more accurately.
Real-time PCR Usage of gel electrophoresis is obviated. Probes or labelled
fluoroprobes are used to identify the target sequence in real-time. Real-time
PCR enables: (1) analysis of multiple amplicons at specific time sequences
during a reaction period; (2) semiquantitative estimation of the yield and (3)
multiplex evaluation of the products.
Advantages
• In cases where the clinical specimen is insufficient the pathogen can be

identified using PCR techniques. Even a single DNA molecule can be
used for an amplification reaction.
• PCR results can be obtained in hours while conventional culture
methods would take days to obtain. Amplification of viral DNA in a
patient sample could be made within hours, even before the onset of
symptoms.
• It can be used even for RNA viruses. After the RNA molecule is
converted into single-strand complementary DNA (cDNA) with an
enzyme called reverse transcriptase which transcribes the RNA code
into DNA in a reverse manner, the PCR primers and Taq polymerase
are added, followed by standard PCR techniques to obtain results.
Disadvantages
PCR reactions may yield nonspecific data and hence sensible selection of
primers and careful conduct of the assays is important to prevent
contaminants giving rise to false-positive results. But with new advances, such
as microarray technology this problem has been overcome.
V. Immunological methods
a. Antigen testing: The microbe's antigenic property can be used for its
detection.
i. Latex agglutination test—used for detection of soluble
antigen (Ag) in specimens such as urine, CSF, serum, etc. in
infections due to H. influenzae, streptococci (Group A and B),
Neisseria, etc.
ii. Coagglutination test—detection of Ag in streptococcal,
pneumococcal, neisserial, salmonella, H. influenzae and other
infections.
iii. Enzyme-linked immunosorbent assay (ELISA)—detection
of Ag in various bacterial infections.
iv. Slide agglutination test—used for identification and
confirmation of bacteria grown in culture.
v. Commercial kits are available to detect antigenic property of
many viruses, herpes simplex I and II, influenza A and B,
CMV, etc.
vi. The advantages of these procedures are that they allow
detection of viruses that do not readily grow in cell culture
(e.g. rotaviruses, hepatitis A virus) or that grow very slowly
(e.g. cytomegalovirus). In general, the antigen detection
assays for viruses are less sensitive than the viral culture and
nucleic acid amplification methods.
b. Antibody testing: Identification of antibody or cell-mediated immune
responses to the microbe in the host body. Serological tests are used in
the diagnosis of infections in which causative agent is difficult to
culture, e.g. Treponema pallidum, Mycoplasma pneumoniae, Chlamydiae,
etc. Diagnosis is done on the basis of detection of specific antibody to
the infectious agent. Active infection is diagnosed by demonstrating
specific IgM or a fourfold increase in IgG antibodies in paired sera
taken 10–14 days apart.
The commonly used serological tests in different bacterial infections are:
i. Agglutination test, e.g. Widal test in enteric fever, Brucella
agglutination test in bruellosis. In latex agglutination test,
an antigen-specific antibody (either polyclonal or
monoclonal) is fixed to latex beads. When the clinical
specimen is added to a suspension of the latex beads, the
antibodies bind to the antigens on the microorganism
forming a lattice structure and agglutination of the beads
occurs. Coagglutination is similar to latex agglutination
except that Staphylococci rich in protein A are used instead of
latex particles. Co-agglutination is less useful for antigen
detection compared with latex agglutination but is helpful
when applied to identification of bacteria in cultures.
ii. Indirect Coombs test—for demonstration of incomplete
antibodies in serum, e.g. brucellosis.
iii. Complement fixation test—for diagnosis of Q fever, syphilis,
etc.
iv. Flocculation test: e.g. VDRL test for syphilis
v. Indirect immunofluorescence test—for antibody detection in
syphilis, Legionella, Mycoplasma, Borrelia and other
infections.
vi. Enzyme-linked immunosorbent assay (ELISA) and
radioimmunoassay (RIA) tests are used for detection of
antibodies in a number of bacterial infections.
vii. Immune electron microscopy (IEM): Viruses not detectable by
conventional techniques may be observed by immune
electron microscopy (IEM). Antigen–antibody complexes or
aggregates formed between virus particles in suspension are
caused by the presence of antibodies in added antiserum
and are detected more readily and with greater assurance
than individual virus particles. IEM is used to detect viruses
that cause enteritis and diarrhoea; these viruses generally
cannot be cultured by routine virus culture.
Enzyme-linked immunosorbent assay systems involving use of antigens,

haptens or antibodies labelled with an enzyme for measurement of substances
in biological fluids. These assay systems have been given various names:
enzyme-, enzymic-, enzymatic- and enzyme-immunoassay (EIA), enzyme-
linked immunoassay, enzyme-labelled immunoassay, enzyme-coupled
immunoassay, immunoenzymatic assay and enzyme-linked immunosorbent
assay (ELISA). There are many types of EIAs to detect antigens. A capture
antibody specific to the antigen in question is bound to the wells of plastic
micro-dilution trays. Then the clinical specimen suspected to contain the
microbe and therefore the antigen is incubated in the wells. The wells are then
washed. A second antibody for the antigen, labelled with enzyme, is used to
detect the antigen. The antigen is then detected colorimetrically by adding the
substrate for the enzyme.
Western blot: Another form of EIA, to detect antibody, is immunoblotting
(Western blot), whereby defined antigens are placed on strips of nitrocellulose
paper. Following incubation with the test antibody-containing specimen, the
strip is further treated with an enzyme-labelled antibody, usually from
another animal, against the test antibody. Addition of the substrate for the
enzyme allows detection of the antigen-specific bound antibody by
colorimetric reaction. Western blot tests are used as the confirmatory tests for
antibodies in HIV infection and Lyme disease.
ELISA and Western blot are diagnostic tests for HIV. (Refer to Chapter 7
Management of Medically Compromised for further details).
Immunochromatography: A significant modification of EIAs is the
development of immunochromatographic membrane formats for antigen
detection. In this format, a nitrocellulose membrane is used to absorb the
antigen from a specimen. A coloured reaction appears directly on the
membrane with sequential addition of conjugate followed by substrate. In
some formats, the antigen is captured by bound antibody directed against the
antigen. These assays have the advantage of being rapid and also frequently
include a built-in positive control.
Relation of stage of illness to presence of virus in test materials and to

appearance of specific antibody.
Stage or period of illness Virus detectable in test materials Specific antibody demonstrable*
Incubation Rarely No
Prodrome Occasionally No
Onset Frequently Occasionally
Acute phase Frequently Frequently
Recovery Rarely Usually
Convalescence Very rarely Usually
*
Antibody may be detected very early in previously vaccinated persons.
Syndrome and virus Specimen Detecting system

Infectious mononucleosis Epstein–Barr (EB) virus
Cytomegalovirus Blood, Lymphoid cell culture, PCR;
Hepatitis A virus nasopharyngeal swab serologic testing
Hepatitis B virus Blood, urine, throat Cell culture; shell vial culture,
Hepatitis C virus swab antigen detection, PCR
Hepatitis D virus Serum, faeces IEM, EIA, RT-PCR
Serum EIA, PCR
Serum EIA, PCR
Serum EIA
Exanthemas
Varicella-zoster virus Vesicle fluid Cell culture. Direct fluorescent
Measles (rubeola) virus Nasopharyngeal antibody is most sensitive
Rubella virus swab, blood, urine Cell culture. Direct fluorescent
Herpes simplex virus Nasopharyngeal antibody
swab, blood, urine Cell culture
Vesicles, usually oral Cell culture
or genital
AIDS (acquired immunodeficiency syndrome)
Human Blood, particularly Cell culture
immunodeficiency virus leukocytes
(HIV)
Measuring the immune response to virus infection
A viral infection elicits both cellular and humoral immune responses.
Measurement of either may be used to diagnose and quantify a viral infection.
Cellular immunity
This can be assessed by:
i. Dermal hypersensitivity: When available, tests for dermal

hypersensitivity to measure cellular immune responses offer certain
advantages in easily and quickly determining prior exposure to
infectious agents. The mumps skin test is often used (along with the
candida skin test) as a positive control when tuberculin skin tests are
applied. Most people have had mumps or mumps vaccine and those
with normal immunologic systems have positive skin tests. The skin
test may lead to an increase in antibodies, e.g. in the complement
fixation test.
ii. Lymphocyte transformation.
iii. Cytotoxicity tests.
Humoral immunity
a. IgM appears initially and are followed by IgG antibodies.

b. IgM antibodies disappear in several weeks.
c. IgG antibodies persist for many years.
d. Diagnosis of a viral infection is done serologically by demonstrating a
rise in antibody titre to the virus or by demonstrating antiviral
antibodies of the IgM class.
e. The methods used include:
i. The neutralisation (Nt) test
ii. The complement fixation (CF) test
iii. The haemagglutination inhibition (HI) test
iv. The immunofluorescence (IF) test (Fig. 4.10)
v. Passive haemagglutination
vi. Immunodiffusion
FIGURE 4.10 Immunofluorescence test.
CHAPTER 5
Histopathological
Investigation
Biopsy
Indications for biopsy
Types of biopsy
Incision biopsy
• Punch biopsy
• Wedge biopsy
Excision biopsy
• Shave biopsy
Needle biopsy
• Core needle biopsy—Trucut biopsy
Image/CT-guided biopsy
Vacuum-assisted biopsy
Bone marrow biopsy
Biopsy procedure
Steps of biopsy
Cytology
Exfoliative cytology
Brush biopsy
Needle biopsy
• Aspiration biopsy
• Fine needle aspiration biopsy
Basic principle and procedure
Application
Advances in histopathological evidences
Endoscopic/arthroscopic biopsy
Sentinel node biopsy
Frozen section
Chemiluminescence (reflective tissue fluorescence)
Anaplasia/anaplastic
Any difference in the form or the arrangement of cells evident by the
appearance of immature cells resulting from failure of differentiation.
Anaplasia is the hallmark of malignant transformation.
Apoptosis
Programmed cell death. A type of cell death occurring in a cell causing cell
shrinkage, chromatin condensation and cell fragmentation which is removed
by phagocytosis.
Atypia
Atypia is a nonspecific term referring to any change in a cell form that may be
due to inflammation, precancerous condition or malignancy.
Biopsy
Biopsy is a method of removal of tissues from the living organism to
determine the presence or extent of the disease. The tissues are analysed
microscopically and chemically.
Cytopathology
Cytopathology is the study of cells under the microscope to analyse the
features of the underlying disease.
Desmoplasia/desmoplastic
As the malignant cells penetrate the adjacent tissues, a connective tissue
barrier of new collagen is formed as a host response in an effort to control the
malignant cells. This host response is called desmoplasia and it is the
characteristic feature of invasion and malignancy.
Differentiation
Described as the degree of resemblance of the malignant cells to their normal
counterparts.
Well differentiated
Malignant cells that almost appear like normal cells of the tissue are termed as
well differentiated. They do not advance aggressively.
Moderately differentiated
Intermediate in aggressiveness. Poorly differentiated or undifferentiated—the
malignant cells whose appearance is primitive or bizarre. It advances
aggressively.
Dysplasia
Irregularly arranged cellular variations that appear in epithelium but shows
no malignant growth. Although nonmalignant, it is recognised as an
important risk factor for the development of malignancy.
Extravasation
Describes the process by which the cellular components of blood such as red
or white blood cells evades the walls of the blood vessel and enters the
adjacent tissues.
Grade/grading
Grading is a measure of prognosis that generally depends on the extent of
differentiation of the cancerous cells.
• Low-grade cancer—well differentiated.

• High-grade cancer—poorly differentiated.
Each cancer has a specific grading system and standards. Numerical grading
system is usually followed for most of the cancer.
They are specified as grade I-well differentiated cancer to grade III–IV, high
grade poorly differentiated cancers. Usually, low-grade cancers are slow
progressive, while the high-grade cancers are highly aggressive.
Hydropic degeneration
Blebbing of cells usually found in cell injury.
Hyperchromatic
Describes the dark staining of cell nucleus with routine H and E staining. It
indicates the active growth phase, such as in cancer cells.
It is the process of identifying specific antigens from the samples which
comprises of immunology (study of the immune response) and histology
(study of the microscopic anatomy and chemistry).
Inflammation
It is the host response of the tissues to harmful stimuli, such as irritation,
injury or infection. The cardinal signs are pain, heat, redness, swelling and
sometimes loss of function.
Invasion
One of the characteristic features of malignant tumour, describing growth
pattern of cancer cell, invading the basement membrane and infiltrating the
adjacent tissue.
Karyorrhexis
Describes the rupture and breakdown of a cell nucleus during cell death or
necrosis.
Mesenchymal
Usually refers to soft tissue. The mesenchymal derivatives are collagen
connective tissue, neural tissue, smooth and skeletal muscle, cartilage and
sometimes bone.
Mitogen
Chemical substance that triggers mitosis in the cells.
Multifocal
Arising independently in several different places.
Myofibroblast
A variant fibroblast, which has the structural feature of both fibroblast and
smooth muscle cell. It consists of a highly irregular nucleus, large amount of
rough endoplasmic reticulum and a dense cluster of filaments which enable
the muscle to contract.
Oncogene
A gene which is capable of causing cancer.
Oncoprotein
A protein which is related to cancer, either due to the decrease or increase the
chance or virulence of a tumour. Oncoprotiens are synthesised when the
oncogene is expressed.
Perineural invasion
Cancer cells penetrating in and around nerves, e.g. adenoid cystic carcinoma.
Pleomorphic, pleomorphism
Alteration in size and shape of cell and/or their nuclei.
Stage/staging
A qualitative assessment of cancer prognosis. The four components of staging
are tumour size, nodal status, grade and metastasis.
Stroma
Described as the connective tissue supporting matrix which acts as a
framework.
Vascular invasion/lymphatic invasion

Cancer cells penetrating into and localised within the blood or lymphatic
vessels.
Biopsy
Biopsy is a surgical procedure to obtain tissue from a living organism for its
microscopical examination, usually to perform a diagnosis.
In maxillofacial surgical practice at times, a biopsy may be the only way to
confirm the diagnosis of a lesion. There are various methods of obtaining the
biopsy. Irrespective of the method used, the main objective is to give a
sufficient amount of ideal sample for the pathologist to interpret. An improper
uncharacteristic sample cannot be interpreted and should be avoided, because
the patient is unnecessarily subjected to an additional biopsy.
Indications for biopsy

A biopsy is mandatory for:
• Idiopathic lesion of more than 2 weeks duration.

• Any inflammatory lesion that does not respond to topical treatment for
2 weeks.
• Any persistent tumescence (swelling), either visible or palpable
beneath relatively normal tissue without any clear diagnosis.
• Lesions that is suggestive of malignancy.
• Bone lesions that cannot be exclusively based on their radiographic
appearance.
Types of biopsy
Incision biopsy
• It is the excision of a precise portion of the oral lesion for microscopic

examination.
• It is employed on large, diffuse lesions often above the size of 2 cm in
its maximum dimension.
• It is also employed on lesions with suspected malignant potential.
• The aim of the procedure will be to remove a portion of the lesional
tissue in question along with a sample of normal adjacent tissue for
comparison.
• A wedge biopsy is made by a wedge shaped incision, begins 2–3 mm
from the normal tissue and penetrates into the region surrounding the
abnormal tissue. It is always better to incise tissue narrow and deep
than broad and shallow.
• A punch biopsy is a type of incisional biopsy that is done using a
surgical punch of diameter (usually 4/8/10 mm in diameter). This type
of biopsy is usually done in mass screening programmes from
representative areas.
Advantage
Incision biopsy is minimally invasive and generally very safe.
i. Punch biopsy (Fig. 5.1A, B)
• A small cylindrical punch is applied into the lesion through the full
thickness of the skin and a plug of tissue is removed.
• A small cylindrical punch is removed from the lesion the punch
comprises the full thickness of skin and the plug of tissue.
• The plug of tissue comprises of cone-shaped core of tissue with its
widest diameter at the skin surface and narrowest at the biopsy base.
• It is the widely accepted procedure for diagnostic skin biopsy or
removing small lesions (Flowchart 5.1).
FIGURE 5.1 (A–B) Punch biopsy.
FLOWCHART 5.1 Histopathological investigations.
Indications
• It is the method of choice for many flat lesions.

• Interpretation of skin tumours like basal cell carcinoma or Kaposi’s
sarcoma.
• Diagnosis of bullous kind of lesions like Pemphigus vulgaris.
• Diagnosis of inflammatory skin disorders like Discoid lupus
erythematoses.
• Removal of small skin lesions, such as intradermal naevi.
• Diagnosis of a typical appearing lesion like a typical mycobacterial
infections.
• Evaluation of the lesions of uncertain origin.
• Used to confirm or exclude the presence of malignancy.
Advantages
• Simple procedure.
• Can be expertised by the physician.
• Time conserving.
• Low incidence of infection, bleeding or nonhealing.
• Scarring is insignificant, hence it is cosmetic.
Disadvantage
Punch biopsy less than 3 mm heal by secondary intention. Punch biopsy
greater than 3 mm need one or two sutures to prevent unacceptable scarring.
ii. Wedge biopsy
• An incisional biopsy in which a lesion is removed, with a wedge of

normal surrounding tissue.
• Elliptical skin incision is made using the scalpel.
• A large wedge biopsy may require two layered closure.
Indications
• Vesicular or bullous lesion

• Ulcerative lesion
Excision Biopsy
Usually, excisional biopsy is done for small minor lesions that are clinically
benign (Fig. 5.2A–C).
FIGURE 5.2 (A–C) Excisional biopsy.
The entire lesion is removed for examination and diagnosis. Hence, it is

diagnostic, as well as curative.
Application
These are performed for lesions that require complete removal for diagnostic
or therapeutic purposes. Indicated for lesions diagnosed as benign, requiring
complete removal. Generally, lesions less than 2 cm in the greatest dimension
are least likely to be malignant.
Advantages
• An excisional biopsy allows for histopathologic examination of an

entire lesion.
• Another advantage of an excisional biopsy is the amount of tissue that
can be removed from one biopsy site, ensuring adequate samples for
various studies, such as culture, histopathology, immuno-fluorescence
and electron microscopy.
Disadvantages
• If the tumour is highly infiltrative the margin of excision cannot be

exactly elicited, further surgery will be needed.
• Furthermore, cancerous cells actively multiply at the tumour margins,
debulking of the mass may result in residual cancerous cells left
behind.
• Excision needs greater precision and skill of the surgeon.
Shave biopsy (Fig. 5.3)
• A scalpel or razor blade is used to shave off a thin layer of the lesion
parallel to the skin.
• Shave biopsies will normally provide information only about the
epidermis and high dermis.
• It may be both diagnostic and curative in case of keratoses, plane warts
and benign pigmented lesions.
• The shave biopsy may also be used to sample tumours, such as basal
and squamous cell carcinoma.
• Indications for shave biopsies include lesions elevated above the skin,
pathology confined to the epidermis.
• Examples include seborrhoeic or actinic keratoses, skin tags, warts and
superficial basal or squamous cell carcinomas.
FIGURE 5.3 Shave biopsy.
Performing a shave biopsy

Shave biopsies are classified into superficial and deep (Table 5.1).
Table 5.1
Difference between superficial and deep shave biopsy

Superficial shave biopsy Deep shave biopsy
Superficial shave biopsies are done across or The deeper shave biopsy (also known as
nearly parallel to the skin surface and extend ‘saucerisation’ biopsy) facilitates sampling of
into the epidermis and superficial dermis, e.g. dermis and epidermis which is important for
removal of skin tags and other small exophytic assessing carcinomas, e.g. basal cell and
growths squamous cell carcinoma
Advantage
Shave biopsies are time conserving, need only little expertise and heal without
the need of sutures.
Disadvantage
Shave biopsies should not be used for pigmented lesions; since if unsuspected
melanoma is partially removed, it cannot be properly staged.
Needle biopsy
Needle biopsy may be of:
• Core needle biopsy.

• Aspiration biopsy (explained under cytology).
• Fine needle aspiration cytology (explained under cytology).
Core needle biopsy—Trucut biopsy (Fig. 5.4)

Core needle biopsy involves the removal of a core of deep tissue usually using
a Trucut needle.
FIGURE 5.4 Core needle biospy—trucut needle biopsy.
Advantages
• CNB allows for accurate diagnosis because of the large quantity of tissue
that can be obtained.
• The type and grade of the tumour, its invasiveness, as well as hormone
receptor status can be assessed. This is an advantage over FNAC,
particularly in case of patients with large masses suggestive of cancer.
Image/CT-guided biopsy
• The procedure is comparable to core biopsy; it is conducted with a

larger needle with assisted CT scan equipment.
• The simultaneous CT scan allows identification and visualisation of the
exact site of the tumour on the computer screen.
• This advanced technology enables the operator to directly guide the
needle into the tumour and obtain several samples of tissue. The tissue
samples are later examined by the pathologist.
Vacuum-assisted biopsy
It is a variant of the core biopsy an automated suction device is attached to the
lateral side of the needle. It increases the amount of fluid and cells aspirated
through the needle. This ensures larger tissue sample and reduces the need for
repuncture.
Bone marrow biopsy (Fig. 5.5)
• Bone marrow is a spongy substance present in the core of large bones

where blood cells are formed.
• Bone marrow biopsy is indicated in patients with abnormal blood
counts, as in case of unexplained anaemia, high white cell count, low
platelet count.
• Bone marrow is obtained from the red marrow of pelvic bone mainly
posterior superior iliac spine.
FIGURE 5.5 Bone marrow biopsy.
Biopsy procedure
Steps of biopsy
• Selection of the area of biopsy

• Preparation of the surgical field
• Local anaesthesia
• The incision
• Tissue handling
• Suturing of the resulting wound
1. Selection of area of biopsy (Table 5.2)
• Biopsy is generally avoided in an infected site; however, a biopsy is

indicated to rule out infection.
• Preferentially, the area of advancing inflammatory changes of the
lesion is desirable for biopsy. This is because pathological changes take
place over a period of time hence a too early biopsy may be
nonspecific.
• The vesicles and blisters which have appeared in the last 48 h are
chosen for biopsy.
• Older lesions showing secondary changes like crusts, fissures, erosions,
excoriations and ulcerations are avoided since the characteristic
feature of disease may not be clearly distinguished.
• For larger lesions, the edge, the thickest portion or the area with
abnormal colouration should be biopsied, because these sites will most
likely contain the distinctive pathology.
• Vesicles should preferably be biopsied intact with adjacent normal
appearing skin, because disruption makes histological interpretation
more difficult.
• Bulla should be biopsied at their edges, keeping the blister roof
attached.
• If the differential diagnosis is broad, taking biopsy from several sites
can minimise sampling error. Important cosmetic areas, such as the
face should be approached with caution, and areas with poor healing
characteristics should be avoided if other sites are available for biopsy.
• An excisional biopsy is done in small sized lesions.
• Incisional biopsy is done in the most definitive area of the lesion.
• In case of doubtful malignant character of the lesion, the following aids
can be used as an adjunct to select representative areas:
▪ Toluidine blue
▪ VELscope
▪ Vizilite plus
▪ Microlux DL
▪ Oral CDx
Table 5.2
Lesions and their biopsy sites

Pathological Selection of area for biopsy
lesion
Vesicles Newest vesicles (usually within 48 h of their appearance) biopsied intact with
adjacent normal appearing skin
Bulla At their edge, keeping the blister roof intact
Non-bullous Maximal lesional skin and minimal normal skin
lesion
Larger lesion Edge, the thickest portion or the area with abnormal colouration
Toluidine blue
Toluidine blue is a metachromatic vital dye of the thiazine group that
increases visual detection of oral precancer and cancer lesion after negative
clinical examination. It is effectively used as a nuclear stain because of its
ability of DNA binding.
Mechanism
• The dysplastic and malignant cells contain quantitatively abundant

nucleic acid as compared to normal cells. Since the toluidine blue stain
is basically a nuclear dye, it stains these abnormal cells specifically and
thus helps in diagnosis.
• Actively growing tissues contains high level of sulphated
mucopolysaccharides, hence the dyes will bind to the actively growing
tissues like tumours which is rich in sulphated mucopolysaccharides.
• Toluidine blue also binds to negatively charged mitochondrial
membranes, which occurs more prominently in dysplastic and
malignant cells.
Composition
100 mL of 1% toluidine blue consists of
• 1 g Toluidine blue powder,

• 10 mL of 1% acetic acid,
• 4.19 mL absolute alcohol and
• 86 mL distilled water
Procedure
The patient is asked to rinse with
1. Water for 20 s to remove debris

2. 1% acetic acid for 20 s
3. 1% Toluidine blue water solution for high risk areas for 20 s
4. Mouth wash with 1% acetic acid should be applied, to clear
mechanically retained stain and
5. A final rinse with water
The sample should include healthy tissue at the margin of the lesion.
Advantages
• Vital stain with toluidine blue has been helpful in early diagnosis and
treatment.
• It is used to confirm clinical impressions regarding tissues at the risk of
malignancy.
• Helps in deciding the area of biopsy site within suspected lesions and
surgical margins.
Disadvantage
False positive result may occur in case of dye retention by filiform papillae,
ulcerations and mechanically in fissures.
Lugol’s iodine
Lugol’s iodine staining based on the principle of higher amount of glycogen in
the normal mucosa compared to abnormal mucosa.
Composition
• Iodine
• Potassium iodide
• Distilled water
Lugol’s iodine is retained in the normal squamous epithelial cells than in the
dysplastic cells. Dysplastic or cancer cells have lower glycogen content owing
to proliferation when compared to normal cells.
Lugol’s iodine produces brown black staining.
Light-based detection systems
VEL scope (narrow emission tissue fluorescence)
• Approximately 30 years ago, it was discovered that cancer can be

detected by using the autofluorescence property of tissues.
• Consecutively, the technology concerning fluorescence imaging and
spectroscopy in cancer screening for a number of anatomic sites
including the oral cavity has improved.
• In fluorescence spectroscopy, the tissues are exposed to various
excitation wavelengths so that subtle differences between normal and
abnormal tissues are noted.
• The fluorescence imaging involves the exposure of tissue to a specific
wavelength of light, which results in the autofluorescence of cellular
fluorophores after excitation.
• When there is morphological alteration in the cells, the concentration
of fluorophores is altered which affects the scattering and absorption
of light in the tissue. This leads to change in colour which is observed
visually.
• VEL scope is a portable tool used for direct visualisation of the oral
cavity. It is available for commercial use for screening oral cancer.
• The unit emits intense blue excitation light (400–460 nm), a pale green
autofluorescence is emitted by the normal mucosa, this is seen through
the selective (narrow-band) filter incorporated within the instrument
handpiece.
• Filtration of the normal light beam is essential so that the narrow range
of reflected blue-white light needed to cause autofluorescent signal is
visualised.
• The areas of abnormal or suspected tissues are darker than the adjacent
normal tissue due to decreased amounts of normal autofluorescence.
2. Preparation of the surgical field
• Common skin antiseptics such as isopropyl alcohol, povidone iodine

or chlorhexidine gluconate can be used to prepare the biopsy site.
• Mark the intended lesion with a surgical marker as it may be
temporarily obliterated following injection of the anaesthetic solution.
3. Local anaesthesia
An amide-type local anaesthetic with vasoconstrictor is used. Infiltration
should be given 1 cm away from the area to be biopsied.
4. The incision
• A well defined, delicate incision is made to remove a portion of the

tissue during an incisional biopsy.
• Soft tissue incisions are elliptical in shape, thus a V-wedged tissue
comprising both the lesion and the healthy margins are obtained.
• In case of more than one lesion in the oral cavity, multiple biopsies are
necessary.
5. Tissue handling
• The specimen should be meticulously handled to avoid crushing of

tissues and placed in the fixing solution.
• Wash the specimen with copious running saline to remove traces of
blood.
• 10% formalin is the widely used fixing agent, it causes minimal
histological alterations in the samples. Other reagents such as
isopropyl or methyl alcohol, saline or distilled water should never be
used as it severely alters the microstructures leading to misdiagnosis.
• Surplus amount of fixing agent should be used about 10- to 20-fold the
volume of the sample is used.
• For immunofluorescence or immunostaining, the specimens should
not be fixed and should be sent immediately to the laboratory for
freezing or placed in Michel’s solution (Michel’s transport media is not
a fixative, it is merely a solution that maintains isotonicity and pH of a
tissue (7.0–7.2). It effectively stabilises proteins for
immunofluorescence. This solution is made up of citric acid,
ammonium sulphate, N-ethylmaleimide and magnesium sulphate.
• The specimen is sent to the pathologist, it should also carry a summary
containing identification of the patient, clinical records, clinical signs,
radiographic features (if applicable), a provisional diagnosis and the
orientation of the sample.
6. Suture
• The suture should achieve good haemostasis, facilitate healing and

should be removed after 6–8 days.
• Contraindications to suturing include biopsies in infected or poorly
healing skin; these wounds heal better by secondary intention. It is
also contraindicated in susceptible cancerous lesion to avoid cell
seeding in healthy tissue.
Cytology
Cytology refers to a branch of pathology that deals with making diagnosis of
diseases and conditions through the examination of tissue samples from the
body. The cells of tissue are studied using this technique. Only cellular
architecture can be studied using this technique. Relationship between cells is
not possible with this technique. Cytologic examinations may be performed on
body fluids (e.g. are blood, urine and cerebrospinal fluid) or on material that is
aspirated (drawn out via suction into a syringe) from any parts of the body.
Difference between biopsy and cytology is depicted in Table 5.3.
Table 5.3
Difference between biopsy and cytology
Biopsy Cytology
A biopsy is the process by which tissue Cytopathology is the branch of pathology dealing
is obtained for microscopic or other with diagnosis of disease at the cellular level
investigation
Biopsy may be diagnostic or therapeutic Cytology tests may be used for diagnosis or for
screening
Advantages: Advantages:
• It is easy to tell the difference between • There is better microscopic detail of the cells
carcinoma in situ and invasive • It is often more convenient and less expensive than
carcinoma biopsy techniques
• Additional sections can be cut from the • A fine needle can reach anatomical areas where
paraffin block and used for special biopsy would be difficult— the head of the pancreas,
stains, or immuno-histochemistry retroperitoneum, the periphery of the lung
• Complete cure in case of excisional • Not as uncomfortable as a biopsy
biopsy • The diagnosis may be available within a few
minutes (histologic diagnosis, other than frozen
section diagnosis, normally takes 1 day)
Disadvantages: Disadvantages:
• Invasive • It is difficult to diagnose whether the malignancy is
• Patient discomfort in situ or invasive
• Cytology preparations do not lend themselves to
good immuno-histochemistry (with some
exceptions)
Exfoliative cytology
• Using an orange woods patula or a sterile plastic spatula, the

superficial mucosal lesions are scrapped by a single powerful stroke.
• The collected material is placed on glass slides and a thin smear is
made.
• The cells thus collected are then fixed using absolute alcohol or
standard fixatives.
• Ideally performed to identify suspected premalignant lesions,
candidiasis, herpes zoster and very rarely for certain mucocutaneous
lesions.
• The lesions are reported as:
▪ Class I (Normal)—Only normal cells were observed.
▪ Class II (Atypical)—Presence of minor atypia, but no evidence
of malignancy.
▪ Class III (Intermediate)—The cells display wide atypia that may
be suggestive of malignancy, precancerous lesions or
carcinoma in situ.
▪ Class IV (Suggestive of cancer)—A few epithelial cells with
malignant characteristics or cells with borderline
characteristics.
▪ Class V—Positive cancer cells, that are obviously malignant.
• Class I and II need not be followed upon a periodic basis depending on
degree of clinical suspicion. However, for class III an incisional biopsy
is suggested while for class IV and V a definitive biopsy is indicated.
Brush biopsy (Fig. 5.6)
• Brush biopsy is an easy, affordable and noninvasive technique of

biopsy.
• The purpose of the oral brush biopsy is to identify lesions that are
clinically innocuous though histologically may the function of exhibit
atypical cells, dysplasia or frank carcinoma.
• This is the latest diagnostic procedure that utilises a computer-assisted
method of analysis developed by Oral CDx (Oral Scan Laboratories,
Suffern, NY). It is a main tool in clinical assessment of oral lesions.
• The Oral CDx is a diagnostic system that combines a painless oral
brush biopsy (full transepithelial oral biopsy), which is taken in the
dental office, with advanced computer analysis.
• A brush biopsy kit, supplied from the manufacturer contains a brush
biopsy instrument (round stiff nylon brush), a bar-coded glass slide,
alcohol-based fixative and a protective plastic case for mailing and
instruction sheet.
• The nylon brush is designed to collect cells from all layers of
epithelium including basal cell layer.
• This method of collection is in contrast to traditional exfoliative
cytology where only superficial epithelial cells are usually collected
and evaluated.
• The procedure includes applying firm pressure on the lesion and
rotating the brush 5–10 times.
• Pinpoint bleeding or exposure of pinkish-red mucosa usually signals
that an adequate and successful sample collection.
• Following cell extraction, the nylon brush is manipulated over the
glass slide so that more cells are distributed evenly across the slide.
• The slide is treated with the alcohol fixative in the kit. The slide is
dried, transferred to a plastic container and mailed.
• It is analysed by computerised programmes specifically designed for
pathological review.
• Results are given as negative, a typical or positive (Table 5.4).
• A biopsy returned with a result of a typical or positive requires an
incisional or excisional biopsy to microscopically review the
histological architecture of the lesion for definitive diagnosis.
FIGURE 5.6 Brush biopsy.
Table 5.4
Classification of oral CDx specimen

Categories Interpretation
Negative No epithelial abnormality
Atypical Abnormal epithelial changes of uncertain diagnostic significance
Positive Definite evidence of dysplasia or carcinoma
Inadequate Incomplete transepithelial biopsy
Advantages of oral CDx, brush biopsy over exfoliative cytology
• The dysplastic or cancerous cells that are located deep to the keratin
layer are included in the biopsy.
• The procedure consists of microscopic screening of the cytological
smear consisting of 1000s of normal cells to identify abnormal cells
because the exfoliating normal cells are in enormous numbers because
of epithelial turnover.
Advantages
• Helps in case of diagnosis of recurrent tumour in previous cancer site.

• Noninvasive procedure compared to surgical biopsy.
• Local anaesthesia is not required.
• Reduced chair side time.
• Simple procedure which is easy to master.
• Can be used as a screening tool for oral cancer.
Indications
• Precancerous lesions • Herpes simplex virus infection
• Oral squamous cell carcinoma • Human papilloma virus infection
• Candidiasis • P. vulgaris
Needle biopsy
Needle biopsy can be aspiration biopsy, FNAC and core needle biopsy.
i. Aspiration biopsy
• Needle aspiration biopsy refers to procedure of removing contents of a

lesion, usually a swelling for the purpose of analysis or quick
observation by the clinician (Table 5.5).
• Aspiration biopsy is typically used to rule out the possibility of a
vascular lesion.
• A 18-gauge needle and syringe injected into the exact area.
• The needle may be subsequently read just so that it is placed within the
centre of the lesion.
• Negative pressure (pulling back on the plunger) is brought in the
syringe to acquire positive aspiration.
• If it is difficult to aspirate, the lesion is most likely solid and a different
type of biopsy may be needed.
• If a purulent aspirate is observed as frank pus, possibility of an
infection (abscess) is almost confirmatory.
• If a straw-like fluid is obtained, cyst should be suspected.
• The presence of blood on aspiration indicates vascular lesion; however,
it may also suggest the presence of a bleeding lesion.
Table 5.5
Pathological lesions and their suspected aspirate content

Aspirate Suspected lesion
Air Traumatic bone cyst, paranasal sinuses
Purulent (frank pus) Abscess, infected cyst or lesions
Straw coloured fluid Cyst
Frank blood Vascular lesion/bleeding lesion
Curdy white or cheesy white Odontogenic keratocyst (OKC)
ii. Fine needle aspiration biopsy (Figs. 5.7 and 5.8)
• After inserting the needle into the swelling, clumps of cell aggregates
are aspirated into the syringe.
• These are smeared on a slide, stained and visualised under a
microscope by the pathologist.
FIGURE 5.7 Fine needle aspiration biopsy.

FIGURE 5.8 Direct immunofluorescence.
Indications
• Initial method of diagnosis for almost all solid/swelling of head and

neck region (Fig. 5.9).
• Part of initial diagnostic work-up of lymphadenopathy, metastatic
lesion or lymphomas.
• Indicated in distinguishing benign from malignant and cystic lesions
from inflammatory lesions.
• Part of initial evaluation of swelling of major salivary gland.
• Helps in distinguishing salivary gland neoplasm, soft tissue neoplasm,
parotid lymph nodes, lymphoepithelial cells, sialadenitis with
sensitivity and specificity.
• Used for definitive diagnosis of odontogenic tumours like
ameloblastoma, OKC, etc.
FIGURE 5.9 Indirect immunofluorescence.
Advantages
• Minimally invasive.
• Safe, fast and cost-effective method.
• Less time consuming.
• They do not spread the tumours or disrupt the field for surgical
dissection.
• Helps in differentiating benign and malignant lesions, thus helping in
presurgical planning.
Histochemistry: The process where a variety of ‘special stains’ are used to
enable cell recognition and diagnosis depending on chemical reactions of cell
and tissue components in frozen section.
Immunohistochemistry: (IHC) This is a special staining process where both
immunologic, histologic and biochemical techniques are used to detect antigen
in tissues.
Many diseases and disease subtypes are mostly identical in their cellular
patterns. They can be accurately differentiated by detecting the specific
molecules in the cells. These specific molecules are called markers.
Immunohistochemistry is the immunological process of localising proteins
in cells of a tissue section using the principle of antibody–antigen binding in
biological tissues.
Distribution and localisation of specific cellular components within a cell or
tissue is best visualised by IHC.
Basic principle and procedure

• The basic critical principle of IHC, as with any other special staining
method, is the binding of the specific antibody to the target
immunogen, followed by the amplification and visualisation of the
antigen–antibody link. Cytoplasmic, nuclear, cell membrane, lipids
and proteins are the target cellular antigens in immunohistochemistry.
• Immunohistochemical staining is done with the antibodies that
identify the target protein (Table 5.6).
• Antibodies are highly specific, binds only with the target protein in the
tissue section.
• IHC can be carried out on different types of cell and tissue preparation
including routine formalin fixed; paraffin wax embedded material,
frozen section and cytological preparations.
• The tissue should be immediately transferred to the laboratory for
freezing or put in Michel’s solution.
• The target ‘immunogen’ may be physically hidden by the antibody
because of the protein folding caused during fixation.
• The pretreatment or antigen retrieval is done after the deparaffinising and
rehydrating the section, where enzyme (trypsin/proteases) or heat is
used to remodel the protein structure making the antigen accessible.
• Immunohistochemical staining—application of primary antibody
followed by enzyme conjugated secondary antibody (monoclonal or
polyclonal, Table 5.7).
• The antibody–antigen interaction is then observed using either
chromogenic detection or fluorescent detection.
• Chromogenic detection—a coloured precipitate is formed at the location
of the protein when the enzyme-conjugated antibody cleaves the
substrate.
• Fluorescent detection—after conjugation with the antibody, fluorophore
can be seen under fluorescence microscopy (direct and indirect
immunofluorescence, Table 5.8).
Table 5.6
Cell types and their molecular staining

Cell type Tumour Molecular staining
Epithelial Papillomas, adenomas, carcinomas Cytokeratin, epithelial membrane antigen
(squamous cell carcinoma, basal cell (EMA)
carcinoma, adenocarcinoma)
Plasma Plasmacytomas Monoclonal immunoglobulin light or
cells heavy chains; plasma cell-associated
antigens (PCA, PC, CD 38); EMA
Langerhans Langerhans cell histiocytosis (e.g. S-100 protein; CD—1a
histiocytes eosinophilic granuloma)
Table 5.7
Polyclonal and monoclonal antibodies
Polyclonal antibodies Monoclonal antibodies

• Polyclonal—a mixture of antibodies • Monoclonal—only one type of
▪ Will recognise multiple epitopes and provide robust antibody
detection ▪ Highly specific, as a primary
▪ Tolerant to changes in antigen, can work with antibody
denatured proteins ▪ Vulnerable to loss of epitope
▪ Can be used when the antigen is not fully characterised ▪ Will attach to one antigen in a
▪ Produced from intact living animals mixture
▪ Less ‘background’ response
▪ Produced from animals cell in
culture
Table 5.8
Direct and indirect immunofluorescence
Direct immunofluorescence (Fig. 5.8) Indirect immunofluorescence (Fig. 5.9)

• Choose an antibody that attaches to the • A second antibody is attached to the complex
molecule of interest composed of the antigen and the primary
antibody
• A fluorochrome is chemically attached to the • The fluorochrome is attached to the
antibody to form a ‘conjugate’ secondary antibody
• The molecule of interest is considered to exist • The secondary antibody must be generated
wherever fluorescence from the attached against the immunoglobulins of the primary
fluorochrome is detected antibody source
• Advantage: Simplicity • Advantage: Can result in greater fluorescence
• Disadvantages: if more than one secondary antibody sticks to
▪ Expensive a primary antibody
▪ The fluorescent signal could be too weak
requiring amplification
Application
• Immunohistochemistry have been used in field of cell and tissue
biology, embryology and diagnostic pathology.
• Location of replicating, apoptotic and signalling cells.
• Identification of activation states and different types of cells in tissues.
• Examination of cytoskeletal structures.
Advances in histopathological evidences

Endoscopic/arthroscopic biopsy
The endoscope or arthroscope can be used to view the TMJ and a biopsy of
any joint lesion can be effectively done.
Advantage
It is possible to visualise the lesion directly and to take tissue samples through
the scope for further analysis.
Disadvantages
• Expensive.
• Difficult to master.
Sentinel lymph node biopsy

A sentinel lymph node is defined as the first lymph node to which cancer cells
are most likely to spread from a primary tumour. Sometimes, there can be
more than one sentinel lymph node.
A sentinel lymph node biopsy (SLNB) is a procedure in which the sentinel
lymph node is identified, removed, and examined to determine whether
cancer cells are present. This is done by injecting a radioactive substance, a
blue dye, or both near the tumour to locate the position of the sentinel lymph
node. Once the sentinel lymph node is located, the surgeon makes a small
incision (about 1/2 inch) in the overlying skin and removes the node.
SLNB may help in avoiding more extensive lymph node surgery. Removing
additional nearby lymph nodes to look for cancer cells may not be necessary if
the sentinel node is negative for cancer.
Frozen section
• During resection of malignant and huge benign tumours, it is required

that the surgical margins are made free of tumour cells.
• Hence, during surgery, bits of tissues along the surgical margin are taken
and sent for rapid microscopic examination and opinion.
• The bits of tissue are processed in a special instrument called cryostat,
which is a microtome (a laboratory instrument used to cut the tissue into
thin slices of thickness 1 micrometer) inside a freezer.
• The tissue is loaded on a metallic cassette, it is stabilised and rapidly
frozen to −20 to −300°C.
• The specimen is blocked in gel like medium usually a mixture of
polyethylene glycol and polyvinyl alcohol.
• Consecutively, it is cut frozen with the microtome. The sections are placed
on a glass slide, stained with haemotoxylin and eosin. This technique is
quicker than the conventional histology technique.
Chemiluminescence (reflective tissue fluorescence)
• Chemiluminescence is usually used as an aid in the diagnosis of cervical

mucosa for ‘ace white’ premalignant and malignant lesions.
• Nowadays, the same technology is adapted for use in oral cavity and
marketed as ViziLite Plus and MicroLux DL.
• These systems aim for easy identification of oral mucosal abnormalities.
The systems are used similarly; patient should first rinse mouth with a 1%
acetic acid solution, and the oral cavity is directly visualised by a blue-
white light source.
• A disposable chemiluminescent light packet is present in Vizilite Plus,
while a reusable, battery powered light source is present in MicroLux DL.
• 1% Acetic acid wash removes surface debris, due to the mild cellular
dehydration; visibility of epithelial cell nuclei is increased.
• Normal epithelium is lightly bluish while abnormal epithelium is
distinctly white (acetowhite) under blue-white illumination.
• The tolonium chloride solution in the Vizilite Plus (TBlue) labels the ace
white lesion such that it is visible under normal light, thus, aids in further
biopsy procedures.
• Various studies have suggested that chemiluminescence is a dependable
oral cancer screening aid.
SECTION III
Medical Management in
Oral Surgery
Chapter 6: Management of Medically Compromised

Chapter 7: Medical Emergencies and their Management
Chapter 8: Therapeutics in Oral Surgery
CHAPTER 6
Management of
Medically Compromised
Hypertension
Diabetes mellitus
Hypoglycaemia
Dysrhythmia
Angina pectoris
• Aggravating factors
• Management
• Major and minor criteria
• Dental aspects
Asthma
Renal disorders
Hyperthyroidism
Haemophilia A
Christmas disease (Haemophilia B)
Bleeding disorders
von Willebrand disease
Platelet disorders
Thrombocytopaenia
Idiopathic thrombocytopaenic purpura
Neurologic disorder
Seizure
Pregnancy
Infectious diseases
Tuberculosis
Human immunodeficiency virus
• Clinical stages
• Investigations
• Assays for anti-HIV antibodies
• Assays to directly detect HIV infection
• Monitoring CD4 T cell counts
• Prognostic tests and treatment monitoring
• Clinical manifestations in HIV based on CD4 count
• Clinical staging of HIV based on CD4 count
Hepatitis B
The key to successful dental management of a medically compromised patient

is mainly accomplished by detailed history taking, including past health
condition, drugs and medications taken by the patient. All of this information
should be applied to assess the risk of problems related to specific conditions
identified in the evaluation. Certain conditions have a direct bearing on the
management and treatment of these patients, which may have to be altered or
modified as a result. Thus, the treatment plan may have to be modified for the
patient’s safety and the management of these patients should be taken with
utmost care.
Hypertension
Hypertension refers to blood pressure that is consistently above 140/90 mmHg
(for more than 6 months). Hypertension may have no cause (essential or
idiopathic) or may be associated with any primary disease (secondary
hypertension).
Dental aspects
Treatment modifications
• The blood pressure should be controlled before elective dental

treatment or the opinion of a physician should be sought first (Tables
6.1 and 6.2).
• Patients with stable hypertension may receive dental care in short,
minimally stressful appointments.
• It is essential to avoid anxiety and pain, since endogenous epinephrine
released in response to pain or fear may induce dysrhythmias. Dental
management can be complicated, sometimes the blood pressure rises
even before a visit for dental care.
• Patients are best treated in the late morning. Endogenous epinephrine
levels peak during morning hours and adverse cardiac events are most
likely in the early morning.
• Continuous blood pressure monitoring is indicated.
• Raising the patient suddenly from the supine position may cause
postural hypotension and loss of consciousness if the patient is using
antihypertensive drugs such as thiazides, furosemide or a calcium-
channel blocker.
• The management of hypertensive patients may also be complicated by
disease such as cardiac or renal failure.
• Systemic corticosteroids may raise the blood pressure and
antihypertensive treatment may have to be adjusted accordingly.
• Some nonsteroidal anti-inflammatory drugs (indometacin, ibuprofen
and naproxen) can reduce the efficacy of antihypertensive agents.
Thus, potential drug interactions should be assessed.
Table 6.1
Dental management based on blood pressure

Blood Management Procedure
pressure
(mmHg)
140/90 No special precaution needed —
142/92– Depending on the dental procedure and • Epinephrine containing local

200/110 patient’s level of anxiety, consider some type anaesthesia should be used
of sedation or delay elective treatment until cautiously. The epinephrine should
blood pressure is controlled not exceed 0.04 mg during a single
visit
• Use stress reduction protocol
• Avoid sodium containing IV
solution and rapid posture changes
>200/110 Wait until the situation is under control Avoid extraction until the BP is under
control
Table 6.2
Hypertension; ASA (American Society of Anaesthesiologists) grading
and dental management
Local anaesthesia
• Adequate analgesia and anaesthesia must be provided.

• An aspirating syringe should be used to give a local anaesthetic, since
epinephrine (adrenaline) in the anaesthetic given intravenously may
(theoretically) increase hypertension and precipitate dysrhythmias.
Blood pressure tends to rise during oral surgery under local
anaesthesia and epinephrine (adrenaline) can contribute to this.
• Epinephrine in combination with local anaesthetics is contraindicated
in an hypertensive patient with systolic pressure of more than
200 mmHg and/or diastolic pressure of more than 115 mmHg.
• Epinephrine-containing local anaesthetics should not be given in large
doses to patients taking nonselective beta-blockers, since interactions
between epinephrine and the beta-blocking agent may induce
hypertension and cardiovascular complications.
• Conscious sedation may be advisable to control anxiety.
General anaesthesia
• All antihypertensive drugs are potentiated by general anaesthetic

agents and can induce hypotension. This is especially the case with
barbiturates and opioids.
• Intravenous barbiturates in particular can be dangerous in patients on
antihypertensive therapy, but halothane, enflurane and isoflurane may
also cause hypotension in patients on beta-blockers.
• However, antihypertensive drugs should not be stopped, since
rebound hypertension can result.
• Hypertension may be a contraindication to general anaesthesia if
complicated by:
▪ Cardiac failure
▪ Coronary or cerebral artery insufficiency
▪ Renal insufficiency
• Chronic administration of some diuretics such as furosemide may lead
to potassium deficiency, which should, therefore, be checked
preoperatively as it may result in intraoperative complications such as
dysrhythmia, increased sensitivity to muscle relaxants such as curare.
Diabetes mellitus
The clinical diagnosis of diabetes is often indicated by the presence of
symptoms such as polyuria, polydypsia and unexplained weight loss.
Diabetes mellitus is commonly divided into two types:
• Type I diabetes (insulin-dependent diabetes mellitus—IDDM) is an

autoimmune disease resulting in the loss of pancreatic insulin-
producing beta cells with absolute lack of insulin and is associated
with episodes of ketoacidosis. The condition usually begins at an early
age and insulin has to be administered from an outside source.
• Type II diabetes (non-insulin dependent diabetes mellitus—
NIDDM) is a condition where pancreatic beta cells continue to
produce insulin, but glucose level in the blood remains high because of
decreased insulin activity, insulin receptors resistance or both. Long-
term complications include autonomic and peripheral neuropathies, as
well as ocular, renal and cardiovascular manifestations. Acute
complications include hypoglycaemia and coma from either
ketoacidosis or a non-ketotic hyperglycaemic hyperosmolar state.
General consideration
The patients with diabetes are more prone to infections hence pre- and
postoperative antibiotics are necessary for prevention of infection.
Also, in case of long standing diabetics they may have additional systemic
complications like renal failure, cardiac disorders, ophthalmic problems and
vascular diseases.
ASA physical Treatment considerations

status
II • Eat normal breakfast and take usual insulin dose in the morning
• Avoid missing meals before and after surgery
• If missing meal is unavoidable, consult physician or ↓ insulin dose by half
III • Monitor blood glucose levels more frequently for several days following
surgery and modify insulin accordingly
• Consider medical consultation
IV • Consult physician before treatment
Investigations
• Urine analysis for sugar and acetone

• Oral glucose tolerance test (GTT)
• Fasting blood glucose
• Random plasma glucose
• Renal profile: blood urea nitrogen, serum creatinine, serum electrolyte
Prevention
Prevention of patient going to ketoacidosis or hypoglycaemia.
Signs of diabetic ketoacidosis

Vomiting, tachypnea, kussmaul breathing (deep, rapid breathing at regular
intervals), dehydration, circulatory collapse.
Management of diabetic ketoacidosis includes administration of insulin to
normalise body metabolism and restoration of body fluids and electrolytes.
Sugar levels and insulin doses

Sugar level (mg%) Insulin dose
80–120 Plain 5% dextrose
120–180 4 units in 5% dextrose
300 and above 14 units in normal saline
Hypoglycaemia
Management of hypoglycaemia in the dental office presents more dramatic
results than does management of hyperglycaemia because most individuals
will experience a dramatic remission of symptoms in a short period of time.
Choice of management is based on the patient’s level of consciousness.
Clinical findings
• Weakness, dizziness
• Pale, moist skin
• Shallow respirations
• Headache
• Altered level of consciousness
Conscious patient (Flowchart 6.1)

Step 1: Recognise hypoglycaemia. Altered behaviour (in the absence of alcohol
on the patient’s breath) and other clinical signs of possible glucose
insufficiency should lead suspicion of hypoglycaemia in both diabetic and
nondiabetic individuals. Question regarding their last meal and insulin dose.
FLOWCHART 6.1 Management of hypoglycaemia in a conscious
patient.
Step 2: Terminate the dental procedure.

Step 3: Position the patient. As with any conscious individual in an
emergency situation, position of the patient will be predicated upon comfort.
In most situations the patient will prefer an upright position.
Step 4: Basic life support, as indicated. Assess the adequacy of the airway,
breathing and circulation and implement any step considered necessary. This
patient is conscious and will have adequate control over airway, breathing and
circulation.
Step 5: Administer oral carbohydrates. If the patient is conscious and
cooperative but still demonstrating clinical symptoms of hypoglycaemia, the
therapy of choice is oral carbohydrate. The emergency kit contains sugar,
which can be dissolved and ingested by the patient. Other available items
might include orange juice, cola beverages and candy bars.
Step 6: Permit patient to recover. The patient should be observed for
approximately 1 h before being permitted to leave the dental office. Determine
if the patient has eaten before the dental appointment and reaffirm the
importance of the patient’s eating shortly before the next dental visit.
If the patient has no response to oral glucose or will not cooperate by taking
oral glucose, the doctor should take the following steps.
Step 7: Summon medical assistance. When oral carbohydrates have proved
ineffective, additional treatment is needed. Coincident with the consideration
of additional therapy, outside medical assistance should be summoned.
Step 8: Administer parenteral carbohydrate. Should the administration of
oral carbohydrate prove ineffective in reversing the signs and symptoms of
hypoglycaemia or should the patient be uncooperative and refuse to take oral
carbohydrate, the parenteral administration of drugs should be considered.
Glucagon, 1 mg, may be administered intramuscularly over 2–3 min.
The patient will usually respond within 10–15 min after intramuscular
injection of glucagon and within 5 min following intravenous 50% dextrose. Oral
carbohydrates should be started as soon as they can be tolerated by the
patient. Small amounts of honey, syrup or decorative icing can be placed into
the buccal fold if parenteral administration is unavailable and if the patient
will cooperate.
Step 9: Monitor the patient. Vital signs should be monitored at least every 5
min during the incident until medical assistance becomes available.
Medical personnel will provide definitive care to the patient either in the
dental office or after transport to a hospital facility. In most instances this
patient will be hospitalised, at least until the blood sugar levels are corrected.
Prior to subsequent dental care, seek methods of preventing its recurrence
during later treatment.
Unconscious patient (Flowchart 6.2)

Step 1: Terminate the dental procedure.
FLOWCHART 6.2 Management of hypoglycaemia in an
unconscious patient.
Step 2: Position the patient. The unconscious patient is placed into the
supine position with the legs elevated slightly.
Step 3: Basic life support, as indicated. If the diabetic patient loses
consciousness, then quickly implement the steps of basic life support
(positioning checking airway, breathing and vital signs). These steps ensure
adequate oxygenation and cerebral blood flow. However, this patient will
remain unconscious until the underlying metabolic cause (e.g. hypoglycaemia)
has been corrected. It is most probable that the only steps of basic life support
required for hypoglycaemia or insulin shock will be management of the
patient’s airway. Breathing will be spontaneous and adequate circulation will
be present.
Step 4: Summon medical assistance. If the unconscious patient fails to
respond to the steps of basic life support, medical assistance should be sought.
Step 5: Definitive management. An unconscious person with a prior history
of diabetes mellitus must always be presumed to be hypoglycaemic unless
proved otherwise. Definitive management of the unconscious diabetic entails
the administration of carbohydrate by the most effective route available. In
most instances this will be an intravenous injection of a 50% dextrose solution
or an intramuscular injection of 1 mg glucagon.
Glucagon (1 mg IM or IV) leads to an elevation of blood glucose via the
breakdown of glycogen stores in the liver. The response of glucagon is
variable, with an onset of action of approximately 10–20 min and a peak
response in 30–60 min. If neither glucagon nor 50% dextrose are available, a
0.5 mg dose of a 1:1000 concentration of epinephrine may be administered
subcutaneously or intramuscularly and repeated every 15 min as needed.
Epinephrine increases blood glucose levels. It should be used with extreme
caution in patients with known cardiovascular disease. Once consciousness is
restored, these patients should receive oral carbohydrates.
Transmucosal application of sugar. In the absence of the parenteral route or
of parenteral drugs, maintain basic life support until medical assistance
arrives. Although it is important that liquids never be placed in the mouth of
an unconscious or stupor patient—the risk of aspiration or airway obstruction
is too great—a thick paste of concentrated glucose can be used with a high
degree of safety. Recommendations include the placement of a small amount
of honey or syrup into the buccal fold. The rectal administration of honey or
syrup (30 mL per 500 mL of warm water), the so-called ‘honey bear enema’, has
been found effective.
Step 6: Recovery and discharge. The unconscious hypoglycaemic will
recover consciousness when the blood glucose level has been elevated, as long
as no additional damage has occurred (e.g. from hypoxia or other causes).
Once conscious, oral forms of carbohydrate, such as soft drinks, may be
administered.
It must be noted that severe hypoglycaemia can be associated with the
development of seizures of a generalised tonic-clonic nature. Management of
these seizures will follow the guidelines discussed in the section on seizure
disorders.
Drugs used in management. Conscious patient: oral forms of sugar.
Unconscious patient: 50% dextrose (IV), glucagon (IM or IV), sugar paste
(transmucosal), syrup or honey (rectal).
Management
• Postpone the treatment until the diabetes is under control

• Give early morning appointments
• Follow stress reduction protocol
• If the patient is allowed to eat normal diet after surgery, ask him/her to
take his/her regular diet and regular insulin
• If the patient is not allowed to eat normal diet after surgery, then he/she
should take only half the regular dose of insulin
• Any infection should be treated promptly, i.e. with antibiotics
Dysrhythmia
Dysrhythmia refers to an abnormality in rate, regularity and sequence of
cardiac activation due to disturbance in cardiac impulse generation or
conduction. It is commonly seen in patients with a history of ischaemic heart
disease or myocardial infarction.
Management
• Limit the administration of epinephrine to 0.04 mg.

• If the patient’s arrhythmia is controlled, no special precautions are
necessary.
• If the patient has an arrhythmia, dental treatment should be delayed. If
it occurs in the middle of the treatment, treatment must be terminated
until the heart rhythm stabilises (requires hospitalisation).
• If angina pectoris occurs, stop the treatment, administer oxygen,
minimise stress and wait till the pain resolves.
Stress reduction protocol
Stress reduction protocol: normal, healthy, anxious patient (ASA I)
1. Recognise the patient’s level of anxiety

2. Premedicate the evening before the dental appointment, as needed
3. Premedicate immediately before the dental appointment, as needed
4. Schedule the appointment in the morning
5. Minimise the patient’s waiting time
6. Use psychosedation during therapy
7. Use adequate pain control during therapy
8. Follow up with postoperative pain/anxiety control
Stress reduction protocol: medical risk patient (ASA II, III, IV)
1. Recognise the patient’s degree of medical risk

2. Complete medical consultation before dental therapy, as needed
3. Schedule the patient’s appointment in the morning
4. Monitor and record preoperative and postoperative vital signs
5. Use psychosedation during therapy, as needed
6. Use adequate pain control during therapy
7. Length of appointment—variable; do not exceed the patient’s limits of
tolerance
8. Follow up with postoperative pain/anxiety control
Dental aspects
• Dysrhythmias can be induced, particularly in the elderly and patients

with coronary artery disease or aortic stenosis, by:
▪ Manipulation of the neck, carotid sinus or eyes (vagal reflex)
▪ Rarely by local anaesthetics: supraventricular or ventricular
ectopics may develop during dental extractions or minor pre-
prosthetic surgery but are rarely significant
▪ General anaesthetic agents especially halothane (isoflurane is
safer)
▪ Preoperative digitalisation
▪ Erythromycin or azole antifungal drugs, in patients taking
terfenadine, cisapride or astemizole
Local anaesthesia
• An aspirating syringe is advised. Epinephrine accidentally entering the

blood may (theoretically) increase hypertension and precipitate
dysrhythmias. Blood pressure tends to rise during oral surgery under
local anaesthesia and epinephrine (adrenaline) theoretically can
contribute to this.
• Adequate analgesia is essential. Pain can cause dangerous increase of
endogenous epinephrine than that of anaesthesia.
• Epinephrine-containing local anaesthetics should not be given in large
doses to patients taking beta-blocking agent. It may induce
hypertension and cardiovascular complications. Mepivacaine 3% is
preferable to lidocaine.
• Intraosseous or intraligamental injections with local anaesthetic agents
containing a vasoconstrictor should usually be avoided to prevent
excessive systemic absorption.
• Gingival retraction cords containing epinephrine should be avoided.
• Cardiac pacemakers usually now have two (bipolar) electrode leads
and present few problems for dental treatment.
• In patients with pacemakers, magnetic resonance imaging, electro surgery,
diathermy and transcutaneous nerve stimulation are contraindicated.
• Pacemaker single beat inhibition of little consequence may occasionally
be caused by dental equipment such as piezoelectric ultrasonic scalers
and ultrasonic baths, older ferromagnetic ultrasonic scalers, pulp
testers, electronic apex locators, dental induction casting machines,
belt-driven motors in dental chairs and older X-ray machines. Modern
piezoelectric scalers have no significant effect, but some devices may
exhibit faster pacing rates.
• The only safe procedure under such circumstances is to avoid the use
of all such equipment whenever a patient with a pacemaker is being
treated, as it is difficult to assess the level of risk in any individual
patient. Patients should be treated in the supine position, electrical
equipment kept over 30 cm away and rapid, repetitive switching of
electrical instruments avoided.
• Diagnostic radiation and ultrasonography have no effect on
pacemakers.
• Unless a cardiac valve lesion is also present, patients with permanent
pacemakers do not require antibiotic prophylaxis.
Angina pectoris
Angina is a symptom of ischaemic heart disease produced when myocardial
blood supply cannot be increased to meet the increased oxygen requirement as
a result of coronary artery disease.
Signs and symptoms

If the myocardium becomes ischaemic, it produces heavy pressure or
squeezing sensation in the substernal region that can radiate to the left
shoulder, arm and the submandibular region. Once the myocardial work
requirements are lowered or oxygen supply to the heart muscle is increased,
the discomfort disappears.
Dental aspects
• Preoperative glyceryl trinitrate and sometimes oral sedation (e.g.

Temazepam) are advised.
• Dental care should be carried out with minimal anxiety, oxygen
saturation, blood pressure and pulse monitoring.
• Effective local anaesthesia is essential.
• Ready access to medical help, oxygen and nitroglycerine is crucial.
Stable angina
Before dental treatment, patients with stable angina should be reassured and
possibly sedated with oral diazepam.
Prophylactic administration of 0.3–0.6 mg glyceryl trinitrate may be
indicated if the patient has angina more than once a week.
Unstable angina
Elective dental care should be deferred because of the risk of infarction.
Preoperative 0.5 mg glyceryl trinitrate sublingually or by inhalation should be
given, together with relative analgesia monitored by pulse oximetry and local
analgesia, but such patients are best cared for in a hospital, as intravenous
nitrates may be indicated.
Post-angioplasty
Elective dental care should be deferred for 6 months; emergency dental care
should be in a hospital setting.
Patients with bypass grafts

These patients do not require antibiotic cover against infective endocarditis.
Patients should not receive an epinephrine containing local anaesthetics,
since it may possibly precipitate dysrhythmias.
Patients with vascular stents that are successfully engrafted

It may be prudent to provide antibiotic coverage if emergency dental
treatment is required during the first 6 weeks postoperatively. Elective dental
care should be deferred. Patients usually require long-term anticoagulant
medication. Appropriate action is done to deal with potential bleeding
tendency by altering the drug intake.
Oral aspects
Angina during the dental procedure: refer to Chapter 7 Medical Emergencies and
their Management.
Myocardial infarction (MI) is cellular death of the myocardium due to
ischaemia resulting from discrepancy in the oxygen demand and supply.
Precautions
• In case of patients with past MI, careful history should be taken

concerning their cardiovascular system to avoid any complication.
• History should be elicited regarding medications, since most patients
receive anticoagulants to decrease coronary thrombogenesis after
infarction.
Management
• Elective oral surgical procedures should be postponed for 6 months after

MI.
• Emergency oral surgical procedures within the period of 6 months require
hospitalisation.
• Surgery in either of the above-mentioned cases require:
▪ Clearance from the patient’s physician
▪ Proper history of previous or current medication
▪ Prophylactic antibiotics
▪ Easy availability of nitroglycerine, oxygen and medical help
Dental treatment should be stopped immediately if the following signs

persist:
• Chest pain
• Dyspnoea
• Rise in heart rate
• Rise in blood pressure
• Dysrhythmias
• Patients within 6 months of an MI (recent MI) have been considered at

greatest risk of further MI. Chest pain or dysrhythmias or other
complications have generally been classified as ASA Class IV. A level
of reinfarction of 50% has been reported in major surgery done during
this period. Therefore, in recent MI:
▪ Higher risk procedures such as elective surgery should be
deferred.
▪ Elective dental care should be deferred.
▪ Simple emergency dental treatment under LA may be given
during the first 6 months after an MI but the opinion of a
physician should be sought first.
• Asymptomatic patients with previous older MI (more than 6 months
and below 12 months) can normally have elective dental care carried
out safely under stress reduction protocol. Higher risk procedures
such as elective surgery may need to be deferred.
• Symptomatic previous but older MI (more than 12 months) patients
can normally have elective dental care carried out safely under stress
reduction protocol.
• Anxiety and pain must be minimised and the physician may advocate
preoperative use of glyceryl trinitrate.
• Effective local analgesia and monitoring of blood pressure,
electrocardiograph, pulse and oxygen saturation are indicated.

In congestive heart failure (CHF), the cardiac output is insufficient to meet the
demands of the body.
Due to the reduction in cardiac output, patient suffers from generalised
weakness and vascular overload due to impaired renal clearance. It is
manifested by paroxysmal nocturnal dyspnoea, orthopnoea and pedal
oedema.
Management
• Postpone the treatment until the patient is medically fit.

• Avoid supine position. Changes in position should be done slowly.
• Follow stress reduction protocol.
• General anaesthesia is contraindicated in uncontrolled CHF.
• Bupivacaine is contraindicated as it is cardiotoxic.
• Epinephrine should be used minimally.
Dental aspects
• The dental chair should be kept in a partially reclining or erect position

and avoid supine position due to risk of severe dyspnoea.
Normal, healthy, but anxious patient (ASA I) Medical risk patient (ASA II, III, IV)
1. Patient reassurance
1. Patient reassurance 2. Medical consultation before treatment, as
needed
2. Premedication to be given the night before 3. Morning appointments
the scheduled appointment 4. Preoperative and postoperative monitoring
3. Premedication immediately before the of vital signs
scheduled appointment 5. Psychosedation during treatment, as
4. Morning appointments needed
5. Minimise waiting time 6. Adequate pain control during treatment
6. Psychosedation during treatment, as 7. Length of appointment variable, according
needed to patient’s limits of tolerance
7. Adequate pain control during treatment 8. Postoperative pain and anxiety control
8. Flexible length of appointment
9. Postoperative pain and anxiety control

9. Postoperative pain and anxiety control
• Dental treatment may precipitate dysrhythmias, angina or heart

failure.
• In patients with mild controlled cardiac failure, routine dental care can
be provided with adequate stress reduction protocol and analgesia.
▪ Medical attention should be obtained before any dental
treatment.
▪ Elective dental treatment should be delayed until the
condition has been stabilised medically.
▪ Emergency dental care should be conservative, principally
with analgesics and antibiotics.
• Appointments should be short.
• Patients are best treated in the late morning (endogenous epinephrine
levels peak during morning hours and cardiac complications are most
likely in the early morning).
• An aspirating syringe should be used to give a local anaesthetic.
Epinephrine may, theoretically, increase hypertension and precipitate
dysrhythmias. Blood pressure tends to rise during oral surgery under
local anaesthesia.
• Bupivacaine should be avoided as it is cardiotoxic. Otherwise, local
anaesthesia can be used safely.
• Interactions between excessive doses of the local anaesthetic and
nonselective beta-blockers should be assessed.
• Cardiac monitoring may be desirable.
• Medication such as diuretics may cause orthostatic hypotension and
therefore patients should be raised slowly to the upright position.
• Nonsteroidal anti-inflammatory drugs (NSAIDs) other than aspirin
should be avoided in those patients taking ACE inhibitors, since they
increase the risk of renal damage.
• Erythromycin and tetracycline should be avoided in patients treated
with digoxin as they may induce digitalis toxicity by impairing gut
flora metabolism of the digitalis.
• General anaesthesia is contraindicated in cardiac failure until it is
under control. Care should be taken after general anaesthesia, since
there is a predisposition to venous thrombosis and pulmonary
embolism.
Infective endocarditis (IE) is an infection of the lining of heart chambers and
heart valves caused by bacteria, viruses, fungi or other infectious agents. The
infection may be bacteraemic (bacteria in the blood), which is common during
dental and surgical procedures. The infection can cause growths on the heart
valves, lining of the heart or lining of the blood vessels that can dislodge
forming emboli to the brain, lungs, kidneys or spleen. Streptococcus viridans, an
organism commonly found in the mouth, is responsible for approximately half
of all bacterial endocarditis. Other common organisms include Staphylococcus
and Enterococcus.
Aggravating factors
Pre-existing conditions that increase the likelihood of developing endocarditis
include
• Congenital heart disease (atrial septal defect, patent ductus arteriosus

and others)
• Rheumatic heart disease
• Cardiac valve anomalies (such as mitral insufficiency)
• Prosthetic heart valve
• Scar tissue or prosthetic coverings in the cardiovascular system.
The purpose of prophylactic antibiotic is to prevent the colonisation of

bacteria in these areas of susceptibility. Gram-positive cocci, which
predominates the oral aerobic microflora, are implicated in most cases of
bacterial endocarditis.
Management
Prophylactic antibiotics must be prescribed for patients with degenerative
cardiac or atherosclerotic valvular defects as dental procedures likely to
produce a bacteraemia.
Bacteraemic dental procedures
Higher incidence
• Extractions
• Periodontal procedures including subgingival placement of antibiotic
strips, scaling, root planing and probing
Major and minor criteria
Major criteria
1. Positive blood culture for IE
Isolation of microorganism known to cause IE from two separate blood
cultures, e.g. viridans streptococci, S. bovis, S. aureus, S. epidermidis,
enterococci, Haemophilus sp., Actinobacillus sp., etc. Persistently positive
blood culture—defined as recovery of a microorganism consistent with
endocarditis from:
a. Atleast two blood cultures drawn more than 12 h apart or
b. All of three or a majority of four or more separate blood
cultures, with first and last drawn at least 1 h apart
2. Evidence of endocardial involvement
Positive echocardiogram for IE:
a. Mobile intracardiac mass on valve or supporting structures or
in path of regurgitant jet or on implanted material without any
alternative anatomical explanation
b. Abscess
c. New partial dehiscence of prosthetic valve or new valve
regurgitation
3. Clinical evidence of new valvular regurgitation
4. Positive serology for Q-fever or other causes of culture-negative
endocarditis such as Bartonella spp. and Chlamydia psittaci.
5. Positive identification of a microorganism from blood culture or
excised tissue using molecular biology methods.
Minor criteria
Predisposition: Predisposing heart condition or IV drug abuse.
Fever: >38°C.
Vascular phenomena: Major arterial emboli, septic pulmonary infarcts,
mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage,
Janeway lesions, newly diagnosed clubbing, splinter haemorrhages,
splenomegaly.*
Immunological phenomena: Glomerulonephritis, Osler’s nodes, Roth spots,
+ve rheumatoid factor, high ESR (>1.5 times upper limit of normal), high C-
reactive protein level (>100 mg/L).*
Microbiological evidence: Positive blood culture, but not meeting major
criteria as defined above.
*
Additional modifications to the Duke criteria appear to improve diagnostic
sensitivity while retaining specificity.
• Dental implant placement and replantation of avulsed teeth

• Endodontic (root canal) instrumentation or surgery only beyond the
apex
• Initial placement of orthodontic bands but not brackets
• Intraligamentary and intraosseous local anaesthetic injections
• Prophylactic cleaning of teeth or implants where bleeding is
anticipated
• Subgingival placement of antibiotic fibres or strips
Lower incidence
• Restorative dentistry (operative and prosthodontic) with or without

retraction cord. This includes restoration of carious (decayed) or
missing teeth
• Local anaesthetic injections (non-intraligamentary and non-
intraosseous)
• Intracanal endodontic treatment; postplacement and core build up
• Placement of rubber dam, postoperative suture removal, taking
impressions, fluoride treatments
• Placement of removable prosthodontic/orthodontic appliances and
their adjustment
• Taking of oral radiographs
Suggested antibiotic prophylaxis regimens
Local anaesthesia
• Amoxicillin—2 g orally 1 h prior to the dental procedure.

• If allergic to or received penicillin in the last month—clindamycin orally
600 mg 1 h prior to the dental procedure.
General anaesthesia
• Amoxicillin IV + amoxicillin orally—1 g at induction and 0.5 g 6 h later.

• If allergic to penicillin, vancomycin IV (1 g over hour before the
procedure) + gentamicin IV (120 mg over 1 h).
Dental aspects
• From the purely dental standpoint, it is obligatory to prevent the onset

of infective endocarditis in view of the high morbidity and mortality.
This depends on:
▪ Identification of patients at risk
▪ Planned preventive dental care
▪ Deciding which treatments require antimicrobial cover
▪ Giving the appropriate antibiotic(s) at the appropriate time
• Identification of patients at high risk for infective endocarditis—these
include mainly those with:
▪ Previous endocarditis
▪ Prosthetic cardiac valves
Asthma
An asthmatic attack involves narrowing of the smaller airways, wheezing and
dyspnoea. It may be triggered by immunological, chemical, infections or
emotional causes.
Proper medical history should be taken regarding precipitating factors,
frequency and severity of the attacks, medication used, etc.
Management
• Postpone the treatment until the disease is well controlled

• Use stress reduction protocol
• Check for any wheezing at the time of surgery
• A bronchodilator inhaler should be easily available
• Adrenal insufficiency should be considered in patients on corticosteroid
therapy
• Avoid NSAIDs
• Ask patient to continue the medication
Dental aspects
• Asthmatic patients should be asked to bring their usual medication

with them when coming for dental treatment.
• Elective dental care should be deferred in severe asthmatics until they
are in a better phase.
• Interactions of theophylline with epinephrine, erythromycin,
clindamycin, azithromycin, clarithromycin or ciprofloxacin may result
in dangerously high levels of theophylline.
• Patients on leukotriene—modifying drugs may have a prolonged INR
and bleeding tendency because of impaired liver metabolism.
• Patients on systemic corticosteroid treatment—risks associated with
steroid complications and operations are dangerous on such patients
without adequate preparation.
• Occasionally, patients with asthma may react to the sulphites present
as preservatives in vasoconstrictor-containing local anaesthetics. It
may be better, where possible, to avoid solutions containing
vasoconstrictors.
• Conscious sedation:
▪ Relative analgesia with nitrous oxide and oxygen is preferable
to intravenous sedation and gives more immediate control of
the asthmatic patient.
▪ Sedatives in general are better avoided as, in an acute
asthmatic attack, even benzodiazepines can precipitate
respiratory failure.
• General anaesthesia is best avoided. General anaesthesia may be
complicated by hypoxia and hypercapnia, which can cause pulmonary
oedema even if cardiac function is normal and cardiac failure if there is
cardiac disease. The risk of postoperative collapse of the lung or
pneumothorax is also increased. Halothane or better enflurane,
isoflurane, desflurane or sevoflurane are the preferred anaesthetics,
but ketamine may be useful in children. An asthmatic attack may be
precipitated by drugs causing histamine release directly; therefore,
morphine, methohexitone, thiopentone, suxamethonium, tubocurarine
and pancuronium should, therefore, be avoided.
• The use of corticosteroid inhalers occasionally causes oral or
pharyngeal thrush
▪ Beta2-agonists and ipratropium bromide can cause a dry
mouth. Antiasthmatic drugs may lower the salivary pH.
Periodontal inflammation is greater in asthmatics than in
those without respiratory disease.
▪ Gastro-oesphageal reflux is common, with occasional tooth
erosion.

Chronic obstructive pulmonary disease (COPD) is a progressive pulmonary
disease caused by excessive smoking leading to the loss of elastic properties of
the airway, mucosal oedema, excessive secretion and bronchospasm. All these
result in obstruction to air-flow, frequent infection, alteration in gas exchange
chronic hypoxemia and subsequent hypercarbia. Patients usually have barrel
chest, cough with expectorations and wheezing during breathing. Two variant
forms seen are ‘blue bloaters’ and ‘pink puffers’.
Precautions
• Postpone the treatment till the lung function has improved.

• Avoid using sedation, hypnotics or narcotics that depresses
respiration.
• Seat the patient in an upright position in the dental chair.
• Use stress reduction protocol.
• Do not supply oxygen to the patient without consulting the patient’s
physician because the patient is used to breathing with a high arterial
CO2 level and depressed O2 level. When suddenly the arterial O2 is
increased through O2 administration, the hypoxia based respiratory
stimulation is jeopardised and the rate of respiration becomes very
low.
• Adrenal insufficiency should be considered in patients under chronic
steroid therapy.
• Monitor respiratory and heart rate.
Dental aspects
• Patient with COPD is best treated in the upright position as they are
commonly orthopneic.
• Interactions of theophylline with drugs such as epinephrine,
erythromycin, clindamycin, azithromycin, clarithromycin or
ciprofloxacin may result in dangerously high levels of theophylline.
• Relative analgesia is given only if absolutely necessary and only in
hospitals after full preoperative assessment. Diazepam and midazolam
are mild respiratory depressants and should be avoided.
• General anaesthesia should be used only if necessary and only after
full preoperative assessment. Intravenous barbiturates are totally
contraindicated.
Renal disorders
Most patients with end-stage renal disease (ESRD) require periodic dialysis
and suffer concurrent heart disease, hypertension and/or diabetes. They are
usually classified under American Society of Anesthesiologist (ASA III).
Impairment in renal function can cause disturbances in acid base balance,
serum calcium and phosphorus levels, electrolyte imbalance and fluid
retention. It can also cause disturbances in drug metabolism.
Preoperative preparations
• Medications like anticoagulants are reviewed

• Acid base and electrolyte abnormalities should be corrected before
surgery
• Prophylactic antibiotic should be given to patients using renal shunt to
prevent any infection
• Dental treatment is usually done on the day following the dialysis
• Alter the dosage when using drugs eliminated by the kidney
• Avoid using nephrotoxic drugs
• Monitor blood pressure and heart rate
Dental aspects
• The main management problems in patients of chronic renal failure

(CRF) include
▪ Bleeding tendencies: Careful haemostasis should be ensured if
oral surgical procedures are necessary. Dental treatment is
best carried out on the day after dialysis, when there has been
maximal benefit from the dialysis and the effect of the
heparin has worn off. In case of uncontrolled prolonged
bleeding, desmopression (DDAVP) may provide haemostasis
for up to 4 h. If this fails, cryoprecipitate may be effective; this
has peak effect at 4–12 h and lasts up to 36 h. Conjugated
oestrogens may aid haemostasis; the effect takes 2–5 days to
develop, but persists for 30 days.
▪ Infections: Infections are poorly controlled in patients with
CRF, especially if immunosuppressed and tends to spread
locally followed by septicaemia. They also accelerate tissue
catabolism, causing clinical deterioration. Infections can be
difficult to recognise as signs of inflammation are masked.
Haemodialysis predisposes to blood-borne infections such as
hepatitis and extra pulmonary tuberculosis. Odontogenic
infections should be treated vigorously.
• Erythromycin and cloxacillin can be given in
standard dosage.
• Penicillin, metronidazole and cephaloridine should
be given in lower doses, since very high serum
levels can be toxic to the central nervous system.
Benzylpenicillin has significant potassium content
and may be neurotoxic hence contraindicated.
• Tetracyclines can worsen nitrogen retention and acidosis in CRF.
• Patients who should be considered for antimicrobial prophylaxis
before extractions, scaling or periodontal surgery include
▪ Polycystic kidneys (who may also have mitral valve prolapse).
▪ On peritoneal dialysis, since bacteraemia can result in
peritonitis.
▪ On haemodialysis, vascular access infections are usually
caused by skin organisms such as S. aureus and only rarely by
oral microorganisms. Patients with most arteriovenous
fistulae are therefore not considered at risk from infection
during dental treatment. However, those with prosthetic
bridge grafts of polytetrafluorethylene or tunnelled cuffed
catheters may need to be managed with precautions similar
to those at risk from infective endocarditis. An alternative is
to give 400 mg teicoplanin IV during dialysis, which gives
cover for at least a day. Antibiotic prophylaxis may also be
indicated if there is uraemia-related chemical trauma of heart
valves, placing the patient at possible long-term risk of
endocarditis.
▪ Renal transplanted patients: Drug modification
• Drugs that are directly nephrotoxic must be
avoided.
• Drugs excreted mainly by the kidney may have
undesirably, enhanced or prolonged activity if
doses are not lowered. Drug therapy may need to
be adjusted, depending on the degree of renal
failure, the patient’s dialysis schedule or the
presence of a transplant.
• Aspirin and other nonsteroidal anti-inflammatory
analgesics should be avoided, since they aggravate
gastrointestinal irritation and bleeding associated
with CRF.
• Antihistamines or drugs with antimuscarinic side
effects may cause dry mouth or urinary retention.
• Fluorides can usually safely be given topically for
caries prophylaxis. Systemic fluorides should not
be given because of possible fluoride excretion by
damaged kidneys.
• Antacids containing magnesium salts should not be
given as there may be magnesium retention.
Antacids containing calcium or aluminium bases
may impair absorption of penicillin V and
sulphonamides.
• Many renal patients are on antihypertensive therapy, digoxin and
diuretics, which may also complicate management.
• Postoperative complications: Major surgical procedures may be
complicated by hyperkalaemia as a result of tissue damage, acidaemia
and blood transfusion. Hyperkalaemia predisposes to dysrhythmias
and may cause cardiac arrest. Dialysis is deferred postoperatively if
possible, since heparinisation is required.
Local anaesthesia and conscious sedation

Local anaesthesia is safe unless there is a severe bleeding tendency.
Conscious sedation
Relative analgesia may be used. The veins of the forearms and the saphenous
veins are lifelines for patients on regular haemodialysis. If it is necessary to
give intravenous sedation or take blood, other veins such as those at or above
the elbow should be used because of the risk of consequent fistula infection or
thrombophlebitis. Midazolam is preferable to diazepam because of the lower
risk of thrombophlebitis.
Adrenal insufficiency can be classified as primary or secondary.
Primary adrenal insufficiency occurs when the adrenal gland itself is
dysfunctional. Secondary adrenal insufficiency, also termed central adrenal
insufficiency, occurs when there is lack of adrenocorticotropic hormone
(ACTH) secretion from the pituitary gland, which is responsible for
hypofunction of the adrenal cortex.
The most common cause for secondary adrenal insufficiency is chronic
therapeutic corticosteroid administration.
To combat stress in case of surgical procedures, steroid coverage should be
considered in patients under corticosteroid therapy. The physiological
rationale for steroid cover is that long-term corticosteroid therapy for
autoimmune or inflammatory disease (such as rheumatoid arthritis, ulcerative
colitis or asthma) suppresses the hypothalamic-pituitary-adrenal (HPA) axis.
In normal patients, severe illness, trauma, stress and surgery are accompanied
by activation of the HPA axis. Patients with HPA axis suppression from long-
term corticosteroid therapy may be unable to produce this physiological
response to stress. Therefore, these patients usually require steroid
supplementation by administering double the usual dose.
Management
• Monitor vital signs and strictly follow anxiety reduction protocol.

• If the patient is under corticosteroid therapy, the patient should double
the dose on the day of, day before and the day after surgery.
• If the patient is currently not on steroids but had taken 20 mg or more
of hydrocortisone (or its equivalent) for more than 2 weeks within the
past 1 year, then:
▪ Day before surgery—60 mg IM or IV
▪ Day of surgery—60 mg IM or IV
▪ 2 days after surgery—40 mg IM or IV
▪ 3 days after surgery—20 mg IM or IV
Acute adrenal insufficiency is a life-threatening situation. Refer to Chapter 7

Medical Emergencies and their Management.
Hyperthyroidism
Thyrotoxicosis refers to the hypermetabolic clinical syndrome resulting from
serum elevation of thyroid hormone levels, especially free thyroxine (T4),
triiodothyronine (T3) or both.
Hyperthyroidism is a type of thyrotoxicosis in which increased thyroid
synthesis and secretion by the thyroid gland produces thyrotoxicosis. Causes
of thyrotoxicosis include autoimmune diseases like Graves’ disease,
lymphocytic thyroiditis, toxic multi-nodular goiter and subacute thyroiditis.
Clinical features
Tremor, eyelid lag, warm, moist and hyperpigmented skin, weight loss,
palpitation, tachycardia, excessive sweating and sometimes exophthalmos.
Management
To prevent thyroid storm

(Thyroid crisis or thyroid storm is an acute worsening or exaggeration of the
symptoms of hyperthyroidism that may occur due to infection or stress.)
• Postpone the treatment until hyperthyroidism is well controlled

• Avoid using atropine and excessive epinephrine
• Monitor vital signs
Dental aspects
• Patients with uncontrolled hyperthyroidism can sometimes be difficult

to manage, as a result of heightened anxiety, hyperexcitability and
excessive sympathetic activity. Conscious sedation may, therefore, be
particularly desirable.
• An aspirating syringe should be used to give a local anaesthetic.
• Local anaesthetics containing epinephrine should in theory be avoided
because of the possible risk of dangerous dysrhythmias. However,
there seems little clinical evidence for this and the risk is probably only
real if an overdose is given.
• Effective analgesia must be provided.
• Benzodiazepines may potentiate antithyroid drugs and therefore
nitrous oxide, which is more rapidly controllable, is probably safer.
• Povidone iodine and similar compounds are best avoided.
• Carbimazole occasionally causes agranulocytosis, which may cause
oral or oropharyngeal ulceration.
All patients should be asked about any history of bleeding disorders, since
most of them may be aware about their coagulopathies.
Haemorrhage is alarming to the patient and may be an emergency. An
adequate history is the single most important part of the evaluation; physical
examination is also necessary and laboratory tests are needed to confirm the
diagnosis (Tables 6.3 and 6.4).
Table 6.3
Laboratory findings in clotting disorders
APTT, Activated partial thromboplastin time (or KPTT); FDP, fibrin-degradation
products; FL, fibrinogen level; PT, prothrombin time; TT, thrombin time.
Table 6.4
Severity of haemophilia
Degree Factor VIII in blood (%)
Severe <1
Moderate 1–5
Mild >5–25
Normal >25

Haemophilia A
• Haemophilia A is the most common clotting 10 times as common as
haemophilia B.
• Inherited as a sex-linked recessive trait, haemophilia affects males.
• Haemophilia A is due to defective factor VIII (anti-haemophilia factor,
AHF). This is a glycoprotein of several components, including factor
VIII C (procoagulant that participates in the clotting cascade), VIII
R:Ag (von Willebrand factor, which binds to platelets and is the carrier
for factor VIII C) and VIIIR:RCo (ristocetin cofactor, which supports
platelet aggregation). In haemophilia A only factor VIII C is reduced.
• Haemophilia typically becomes apparent in childhood when bleeding
into muscles or joints (haemarthroses) occurs following injuries.
• Haemarthroses can cause joint damage and cripple the patient, but
bleeding after dental extractions is sometimes the first or only sign of
mild disease.
• Dental extractions or deep lacerations are followed by persistent
oozing for days or weeks and can be fatal as the haemorrhage cannot
be controlled by pressure or local measures.
• The characteristic feature of bleeding in haemophilia is that it seems to
stop immediately after the injury (as a result of normal vascular and
platelet response) but, after an hour or more, intractable oozing or
rapid blood loss starts and persists.
Investigations
In suspected cases, the following tests should be done:
• Bleeding time
• Platelet count
• PTT
• PT
• Evaluation of clotting factors and time
Diagnosis and management of haemophilia A

The typical findings in haemophilia can be summarised as follows:
1. Prolonged activated partial thromboplastin time (APTT)

2. Normal prothrombin time (PT)
3. Normal bleeding time
4. Low factor VIII C but normal VIII R: Ag (von Willebrand factor) and
VIIIR:RCo (ristocetin cofactor)
• Factor VIII assay is required as even the APTT may be normal
in mild haemophilia.
• If bleeding starts or is expected, treatment consists of
replacement of the missing clotting factor, rest and often the
use of antifibrinolytic agents.
• Rarely, von Willebrand disease may mimic haemophilia. The
history may help to distinguish them (Table 6.5) but
laboratory testing is essential.
• Factor VIII must be replaced to a level adequate to ensure
haemostasis.
• The use of fresh plasma or fresh frozen plasma,
cryoprecipitate or fractionated human factor concentrates
obtained from pooled blood sources have been tried, but they
have the disadvantage of potential to carry blood-borne
pathogens such as hepatitis viruses, HIV and various herpes
viruses.
• Porcine factor VIII and genetically engineered factor VIII
considerably replaced them with desmopressin and tranexamic
acid.
Table 6.5
Haemophilia A and von Willebrand disease

Haemophilia A von Willebrand disease
Inheritance Sex-linked recessive Autosomal dominant
Haemarthroses/deep Common Rare
haematomas
Epistaxis Uncommon Common
Gastrointestinal Uncommon Common
bleeding
Haematuria Common Uncommon
Menorrhagia Common Common
Postextraction bleeding Starts 1–24 h after trauma, Starts immediately
lasts 3–40 days Lasts 24–48 h and is often
Not controlled by pressure controlled by pressure
Bleeding time Normal Prolonged
Factor VIII coagulant Reduced Reduced
activity
Factor VIIIR:RCo Normal Reduced
Replacement therapy
• Human freeze-dried factor VIII concentrate (factor VIII fraction, dried)

is used when the deficiency is sufficiently severe. This preparation is
stable for one year at 4°C but once reconstituted should be used
without delay.
• New recombinant factor VIII can also be used as replacement agent.
• In milder cases (factor VIII levels within 5%–25% of normal)
desmopressin and tranexamic acid may be used satisfactory.
• Once the clot has been formed, instruct the patient not to do any
activity like blowing, gargling, etc., which would result in
dislodgement of the clot.
• Avoid prescription of NSAIDs which can prolong bleeding.
• Avoid drugs that may cause drug interactions and inhibit warfarin
metabolism.
Injections
• Local anaesthesia should be avoided in the absence of factor VIII

replacement.
• Regional (inferior dental or posterior superior alveolar) blocks or
injections in the floor of the mouth must not be used, since they can
cause haemorrhage into tissue spaces causing airway obstruction.
• Submucosal infiltrations have caused widespread haematoma
formation, but intraligamentary injections may be safe.
• Infiltration anaesthesia may be used with caution and is adequate for
conservation work in children, but lingual infiltration must be
avoided.
• If factor replacement therapy has been given, regional anaesthesia can
be used, provided the factor VIII level is maintained above 30%, but
infiltration is preferable.
• Intravenous midazolam or relative analgesia can be used.
• Intramuscular injections should be avoided unless replacement
therapy is being given, as they can cause large haematomas.
Minor surgery
• Endotracheal intubation for general anaesthesia may cause bleeding

from nasal trauma and is dangerous in unprepared patients, since
replacement therapy has to be given for the surgical procedure,
intubation can be carried out.
• An oral latex cuffed endotracheal tube is recommended to minimise
trauma to the nasal and tracheal lining.
• A factor VIII level of between 50% and 75% is required for dental
extractions.
• Antihaemophilic factor (AHF) may also need to be given postoperatively
but many patients can be managed with antifibrinolytic agents given
during the subsequent 10 days. If oral bleeding recurs postoperatively,
factor VIII must be given.
• Antifibrinolytics significantly reduce factor VIII requirements.
• Tranexamic acid is used in a dose of 1 g (30 mg/kg) orally, 4 times daily
starting 24 h preoperatively.
• Tranexamic acid used topically significantly reduces bleeding. Ten
millilitres of a 5% solution used as a mouth rinse for 2 min, 4 times
daily for 7 days, is recommended. This solution can be made up by
diluting 10% tranexamic acid solution with sterile water.
• Desmopressin (deamino-8-D arginine vasopressin: DDAVP) is a
synthetic analogue of vasopressin which induces the release of factor
VIII C, von Willebrand factor (vWF) and tissue plasminogen activator
(tPA) from storage sites in endothelium.
• Given as an intravenous infusion (0.3–0.5 µg/kg just before surgery
and repeated 12 hourly if necessary for up to 4 days), desmopressin
can temporarily correct the haemostatic defect in mild haemophilia.
• Desmopressin may cause facial flushing and slight tachycardia, but the
chief adverse effect is tachyphylaxis—declining response on repeated
injection.
• The buccal approach to lower third molars is therefore safer. Minimal
bone should be removed and the teeth should be sectioned for
removal where possible.
• The packing of extraction sockets is unnecessary if replacement
therapy has been adequate but the packing of the small amount of
oxidised cellulose soaked in tranexamic acid into the depths of the
sockets will give better result.
• Acrylic protective splints are rarely used because of their liability to
cause mucosal trauma and to promote sepsis, but they may be needed
in certain sites such as the palate.
• Local haemostasis can be aided by collagen, Gelfoam or Surgicel
inserted into extraction sockets and by cyanoacrylate or fibrin glues.
• Infection induces fibrinolysis, so to avoid secondary haemorrhage,
appropriate antibiotic is administered.
• Postoperatively a diet of cold liquid and minced solids should be taken
for up to 10 days.
• Care should be taken to detect haematoma formation which may
manifest itself by swelling, dysphagia or hoarseness. The patency of
the airway must always be ensured.
*
Factor VIII dose in units = weight in kg × 25 given 1 h preoperatively (for dental
extraction).
†
Factor VIII dose in units = weight in kg × 50 given 1 h preoperatively (for maxillofacial
surgery).
Christmas disease (haemophilia B)

Christmas disease (Factor IX deficiency) is clinically identical to haemophilia A
and inherited in the same way.
Dental management
• Human dried factor IX concentrate is supplied as a powder to be

reconstituted with sterile distilled water for intravenous
administration.
• A dose of 20 units factor IX per kg body weight is used intravenously 1
h preoperatively.
• The standard preparation may also contain factors II, VII and X. Factor
IX is more stable than factor VIII. Its half-life is often up to 2 days, so
that replacement therapy can sometimes be given at longer intervals
than in haemophilia A.
Bleeding disorders
Von Willebrand disease
von Willebrand disease (pseudohaemophilia) is the most common inherited
bleeding disorder that affects about 1% of the population. It is caused by a
deficiency of or defect in, von Willebrand factor (vWF). The vWF, synthesised
in endothelium and megakaryocytes, normally acts as a carrier for factor VIII
protecting it from proteolytic degradation. A deficiency in vWF thus leads to a
low factor VIII concentration in the blood. vWF also bridges between platelets
and damaged endothelium. Thus, the bleeding tendency in von Willebrand
disease results both from a clotting defect and a defect in platelet function.
• von Willebrand disease affects females as well as males and clinical

presentation usually differ from haemophilia A (Table 6.5).
• The common pattern is bleeding from mucous membranes, with
purpura of mucous membranes and the skin.
• Gingival haemorrhage is more common than in haemophilia.
• The low level of vWF results in poor platelet adhesion after trauma.
Platelets usually fail to aggregate in the presence of ristocetin so that,
unlike haemophilia, purpura is common and the bleeding time is
prolonged but the best assay is the ristocetin cofactor assay.
• von Willebrand disease is characterised by a prolonged bleeding time,
usually a prolonged APTT, low levels of vWF (Factor VIIIR:Ag) and
low factor VIII C and VIIIR:RCo (ristocetin cofactor) levels.
• It is usually inherited as an autosomal dominant, but a severe form of
the disease may be inherited as a sex-linked recessive trait like true
haemophilia. Rarely, von Willebrand disease may be acquired,
particularly in patients with autoimmune or lymphoproliferative
diseases.
• Types of von Willebrand disease—Type I, Type II A and II B, Type
III.
Dental management
• Aspirin and NSAIDs should be avoided.

• Desmopressin: In most patients with von Willebrand disease, the
haemostatic defect can be controlled with desmopressin, via a nasal
spray.
• Type IIB disease, stimulates release of dysfunctional vWF which leads,
in turn, to platelet aggregation and severe but transient
thrombocytopaenia. Second, it is also contraindicated in Type III
disease, where so little vWF is formed that essentially the same
management is required as for haemophilia A. However, since factor
VIII has a prolonged half-life, less frequent infusions may be required.
• Thus, Type I von Willebrand disease can be treated with desmopressin
but Type II and III require clotting factor replacement.
Platelet disorders
Platelet function may be impaired by many diseases or drugs, but deficiencies
of platelets (thrombocytopaenias) are the most clinically important cause
(Table 6.6).
Table 6.6
Drugs that may impair platelets or their functions
• Nonsteroidal anti-inflammatory drugs

Aspirin
Diclofenac
Diflunisal
Ibuprofen
Mefenamic acid
• Beta-lactam antibiotics
Ampicillin and derivatives
Methicillin
Penicillin G (benzyl penicillin)
Cephalosporins (some)
Gentamicin
Rifampicin
Sulphonamides
Trimethoprim
• General anaesthetic agents
Halothane
• Cytotoxic agents
Asparaginase
Carmustine
Daunorubicin
Vincristine
• Psychoactive agents
Antihistamines (some)
Diazepam
Tricyclic antidepressants
Chlorpromazine
Haloperidol
Valproate
• Diuretics
Acetazolamide
Chlorothiazide
Furosemide
• Antidiabetics
Chlorpropamide
Tolbutamide
• Cardiovascular drugs
Digitoxin
Quinine
Oxprenolol
Heparin
Methyldopa
Thrombocytopaenia
Causes
• Drugs such as heparin, chemotherapeutic agents, alcohol

• Leukaemia, lymphoma or bone marrow tumours
• HIV, mumps, rubeolla or parvovirus infections
• Sequestration of the platelets by an enlarged spleen
• Acute or chronic liver disease
▪ Autoimmune destruction of the platelets by IgG antibodies,
causing idiopathic thrombocytopaenic purpura (ITP)
Idiopathic thrombocytopaenic purpura

Thrombocytopaenia exists when the platelet count falls below
100,000 cells/mm3 presenting as petechiae, ecchymoses, haematomas,
epistaxis, haematuria, mucocutaneous bleeding and, occasionally,
haemorrhage into tissues. Oral manifestations include spontaneous gingival
bleeding, petechiae or haematomas of the mucosa, tongue or palate. There are
many causes of thrombocytopaenia but ITP, an autoimmune disorder is one of
the most common (Table 6.7).
Table 6.7
Manifestations of thrombocytopaenia and management of surgery
Dental management
The main complication in dental treatment is haemorrhage. In patients with
ITP, the bleeding tendency is sometimes effectively controlled by
corticosteroids.
• Regional anaesthetic block injections are contraindicated if the platelet

levels are below 30,000 cells/mm3
ITP steroid treatment protocol

Initial steroid treatment protocol for ITP: Initial steroid treatment protocol
1 mg/kg/day prednisone, PO for 2–6 weeks.
Subsequent steroid treatment protocol for ITP: Prednisone dose is
individualised for every patient. Usually the dose of prednisone is tapered to
less than 10 mg/day for 3 months and then withdrawn. Splenectomy is done if
discontinuation of prednisone causes a relapse.
• Follow the ‘rule of twos’ for major dental treatment and provide extra
steroids prior to surgery if the patient is currently on steroids or has
used steroids for 2 weeks longer within the past 2 years.
Minor surgery
• Haemostasis after minor surgery is usually adequate if platelet levels

are above 50,000 cells/mm3.
• Platelets can be replaced or supplemented by platelet transfusions,
though sequestration of platelets occurs rapidly.
• Platelet transfusion is indicated for established thrombocytopaenic
bleeding.
• When given prophylactically, platelets should be given half before
surgery to control capillary bleeding and half at the end of the
operation to facilitate the placement of adequate sutures.
• Platelets should be used within 6–24 h after collection and suitable
preparations include platelet-rich plasma (PRP), which contains about
90% of the platelets from a unit of fresh blood and platelet-rich
concentrate (PRC), which contains about 50% of the platelets from a
unit of fresh whole blood.
• PRC is thus the best source of platelets. Platelet infusions carry the risk
of isoimmunisation, infection with blood-borne viruses and, rarely,
graft-versus-host disease.
• Where there is immune destruction of platelets (e.g. in ITP), platelet
infusions are less effective.
• The need for platelet transfusions can be reduced by local haemostatic
measures and the use of desmopressin or tranexamic acid or topical
administration of platelet concentrates.
• Absorbable haemostatic agents such as oxidised regenerated cellulose
(Surgicel), synthetic collagen (Instat) or microcrystalline collagen
(Avitene) may be put in the socket to assist clotting in postextraction
socket.
• Drugs that affect platelet function, such as gentamicin, antihistamines
and aspirin, should be avoided.
Major surgery
For major surgery, platelet levels over 75,000 cells/mm3 are desirable.
Features of bleeding disorders

Platelet defects Purpuras Coagulation defects
Gender affected Females more than Males
males
Family history Rarely Positive
Nature of bleeding Immediately Delayed after trauma
after trauma Persistent
Relatively short-
lived
Effect of locally applied pressure May cause bleeding Bleeding recurs when
to cease pressure removed
Spontaneous bleeding into skin or mucosa Common Uncommon
or from mucosa
Bleeding from minor superficial injuries, Common Uncommon
e.g. needle prick
Deep haemorrhages or haemarthroses Rare Common
Bleeding time Prolonged Normal
Tourniquet test Positive Negative
Hess test
Platelet count Often reduced Normal
Clotting function Normal Abnormal
Neurological disorder
Seizure
In patients with known seizure disorders, questions about the type of seizure,
stimuli for the seizure, pre-seizure and the frequency and type of medication
should be questioned.
Management
• Schedule early morning appointments.
• Patients are instructed to take their medication properly for several
days prior to the dental appointment.
• Avoid stress and follow anxiety reduction protocol.
Factors precipitating attacks should be avoided as:
1. Withdrawal of anticonvulsant medications

2. Epileptogenic drugs
3. Fatigue, starvations or stress
4. Infection
5. Flickering lights (television; strobe lights)
Dental aspects
• When carrying out dental treatment in a known epileptic, a strong

mouth prop should be kept in position and the oral cavity kept as free
as possible of debris. As much apparatus as possible should be kept
away from the area around the patient.
• Drugs which are epileptogenic or interfere with anticonvulsants are
contraindicated.
• Aspirin, azoles and metronidazole can interfere with phenytoin.
• Propoxyphene and erythromycin can interfere with carbamazepine.
• Benzodiazepines are antiepileptogenic, but nitrous oxide can increase
the central nervous system (CNS) depression in patients on
anticonvulsants.
• Avoid electronic dental analgesia.
Pregnancy
Dental management
• First trimester: No dental treatment except in emergencies.

• Second trimester: This is the appropriate time for all dental procedures.
• Third trimester: No dental treatment except in emergencies. Due to
risk of supine hypotensive syndrome in the third trimester, the patient
is turned to one side (left lateral position) during treatment.
• In all the cases avoid unnecessary exposure to radiation and use proper
protection.
• Avoid using drugs with teratogenic potential.
Postpartum
Avoid administering drugs secreted in breast milk.
Infectious diseases
Tuberculosis
Tuberculosis (TB) is caused by Mycobacterium tuberculosis, M. bovis or M.
africanum. TB spreads via airborne particles which are aerosolised when an
infected patient coughs, sneezes or speaks. These particles can remain in air
circulation for extended periods of time.
A person can get infected when these particles are inhaled into the lung. The
development of infection is facilitated by an increased concentration of
infectious droplets in the air, inadequate ventilation and recirculation of
infected air.
High-speed dental instrumentation creates an aerosol of water, saliva and
potentially infectious droplets through the air/water irrigation systems
necessary to prevent pulpal overheating during dental preparation. For this
reason, it is appropriate to always have eye and face protection and adequate
suction when using high-speed rotary instrumentation.
Dental management
• No elective treatment is rendered until the patient gets a clearance

from his/her physician.
• It is appropriate to perform emergency and palliative procedures;
however, routine dentistry should be deferred until the patient is on
appropriate drug therapy and the infective period has lapsed.
• If emergency treatment is necessary, the patient should be treated
following all universal protocols in a level 3 infection control facility
with high efficiency particulate air (HEPA) filters (filters that remove
most particles larger than 0.3 µm in diameter) and laminar airflow
cabinet. These cabinets sterilise the air that flows over the infectious
material as well as the air to be exhausted. The air flows in sheets
which serves as a barrier to particles from outside the cabinet and
direct the flow of contaminated air into the HEPA filters. These
cabinets are known as laminar flow biological safety cabinets.
Human immunodeficiency virus

Human immunodeficiency virus (HIV) is a human retrovirus which depends
upon the enzyme reverse transcriptase (RNA-directed DNA polymerase) to
replicate itself within the host cells. HIV has a short latency period, after which
clinical symptoms become evident, with eventual progression to acquired
immunodeficiency syndrome (AIDS). HIV is transmitted via direct absorption
(by needle puncture or break in the skin or mucous membrane) of body fluids,
including blood, semen, vaginal secretions, cerebrospinal fluid, synovial fluid,
pleural fluid, pericardial fluid, peritoneal fluid, saliva, as well as unfixed
tissues. Patients with positive HIV serology and CD4 count below 200 cells/µl
are considered to have AIDS. Compared with other health care providers,
dental professionals have a lower risk of being infected with HIV, due to the
decreased amount of viral load in saliva. Pure saliva does not contain viruses
unless contaminated by blood. It has been estimated that the risk of
transmission from patients to health care providers is higher than transmission
from health care providers to patients.
HIV-1 occurs worldwide, while HIV-2 occurs principally in West Africa and
a few other geographic areas. Due to the social stigma attached to the
infection, the laboratory diagnosis must be established precisely, with no
possibility whatsoever of a falsely positive result. The structure of HIV,
replication and its immune response to infection must be understood for
charting the diagnostic tests.
HIV-1 and HIV-2 are retroviruses. These are enveloped and have single
strands of positive-sense RNA. Through the use of the viral enzyme reverse
transcriptase, the RNA is transcribed into DNA, which is integrated into the
host cell genome.
Factors which increase the risk for HIV transmission include
• Donor source from a patient with terminal AIDS

• Injury with a sharp device with visible blood
• Injury with hollow bore needles—has higher rate of transmission of
disease, since it contains an inoculums of blood and virus.
Clinical stages
The WHO system for adults classifies patients into one of the four hierarchical
clinical stages ranging from stage 1 (asymptomatic) to stage 4 (AIDS). The
demonstration of even one clinical condition in that stage’s criteria determines
the clinical stage of the patient.
Stage 1
Patients who are asymptomatic or have persistent generalised
lymphadenopathy (lymphadenopathy of at least two sites [not including
inguinal] for longer than 6 months) are categorised as being in stage 1, where
they may remain for several years.
Stage 2
Even in early HIV infection, patients may demonstrate several clinical
manifestations.
Clinical findings included in stage 2 (mildly symptomatic stage) are as
follows:
• Unexplained weight loss of less than 10% of total body weight.

• Recurrent respiratory infections (such as sinusitis, bronchitis, otitis
media and pharyngitis).
• Range of dermatological conditions including herpes zoster flares,
angular cheilitis, recurrent oral ulcerations, papular pruritic eruptions,
seborrhoeic dermatitis and fungal nail infections.
Stage 3
Clinical stage 3 (the moderately symptomatic stage) category is as follows:
• Weight loss of greater than 10% of total body weight.

• Prolonged (more than 1 month) unexplained diarrhoea.
• Pulmonary tuberculosis.
• Severe systemic bacterial infections including pneumonia,
pyelonephritis, empyema, pyomyositis, meningitis, bone and joint
infections and bacteraemia.
• Mucocutaneous conditions, including recurrent oral candidiasis, oral
hairy leukoplakia and acute necrotizing ulcerative stomatitis,
gingivitis or periodontitis, may also occur at this stage.
Stage 4
The WHO clinical stage 4 (the severely symptomatic stage) designation
includes all of the AIDS-defining illnesses.
Clinical manifestations for stage 4 disease that allow presumptive diagnosis
of AIDS to be made based on clinical findings alone are as follows:
• HIV wasting syndrome

• Pneumocystis carinii pneumonia (PCP)
• Recurrent severe or radiological bacterial pneumonia
• Extrapulmonary tuberculosis
• HIV encephalopathy
• CNS toxoplasmosis
• Chronic (more than 1 month) or orolabial herpes simplex infection
• Oesophageal candidiasis
• Kaposi’s sarcoma.
Other conditions that should arouse suspicion that a patient is in clinical
stage include:
• Cytomegaloviral (CMV) infections (CMV retinitis or infection of

organs other than the liver, spleen or lymph nodes)
• Extrapulmonary cryptococcosis
• Disseminated endemic mycoses (e.g. coccidiomycosis, penicilliosis,
histoplasmosis)
• Cryptosporidiosis, isosporiasis
• Disseminated nontuberculous mycobacteria infection
• Tracheal, bronchial or pulmonary Candida infection
• Visceral herpes simplex infection
• Acquired HIV-associated rectal fistula
• Cerebral or B cell non-Hodgkin lymphoma
• Progressive multifocal leukoencephalopathy (PML)
• HIV-associated cardiomyopathy or nephropathy
The presence of these conditions unaccompanied by the AIDS-defining

illnesses, however, should prompt confirmatory testing.
Investigations
The viral protein that is most commonly assayed directly is p24. Antibody
responses can be found against a variety of other HIV gene products: env
products (envolpe), glycoprotein (gp) 160 (gp160, gp120, gp41); gag (core
proteins), p24, p17, p9, p7 and pol (polymerase), p66, p51, p32, p11.
Two to 6 weeks after infection, 50% or more of patients develop an
infectious mononucleosis-like syndrome. At this time there are high levels of
HIV-1 in the blood, which can be detected by culture or by reverse
transcriptase polymerase chain reaction (PCR). Antibodies to HIV-1 proteins
become detectable 2–8 weeks after infection. There is an IgM response to gag
gene products, which gradually shifts to an IgG response. Generally, IgG
responses to p24 and gp120 occur initially followed by responses to gp41 and
other proteins. Viraemia and blood p24 levels fall with the antibody response
and may be undetectable during the asymptomatic period of infection, while
p24 antibody levels remain high. Late in the course of the disease, the p24
antibody levels decrease while the p24 antigen increases. During the time soon
after infection, when high levels of HIV-1 viraemia occur, the CD4 T cell count
decreases. Early in the asymptomatic period, it returns towards normal only to
decrease gradually over time and more rapidly during the late stages of AIDS.
The tests used to diagnose HIV-1 infection are commercially available
products that are highly developed and standardised. Several kits may be
available for the same type of tests. These are outlined in a generic manner
below.
Assays for anti-HIV antibodies
A. Enzyme-linked immunosorbent assay (enzyme immunoassay) (ELISA)

Enzyme-linked immunosorbent assay (ELISA) or enzyme immunoassay (EIA)
is the primary screening test for diagnosis of HIV-1 infection. Generally, HIV-1
antigens are immobilised on a solid surface, commonly plastic wells or beads.
The patient’s serum and appropriate reagents are added. HIV-1 antibodies
bound to the immobilised HIV-1 antigens are then detected with an enzyme
labelled antihuman IgG and a calorimetric reaction. The amount of colour is
proportionately higher with higher HIV-1 antibody concentrations. Colour
above a certain cutoff point is considered a positive test. ELISA for HIV-1 is
more than 99% sensitive and 99% specific. Infants born to HIV-1-infected
mothers generally have positive ELISAs for HIV-1 because of transplacental
transfer of antibodies. The test will gradually become negative if the infant is
not truly infected with HIV-1.
The necessity to rapidly detect individuals who may be HIV positive and to
do so while they are still on-site in a clinic environment has led to several
improvements in EIA testing. An assay has been developed to test oral
secretions. In addition, several rapid immunoassays for use with whole blood
and serum have also been approved for use. All rapid tests should be treated
in the same fashion as conventional assays. Positive results should be
confirmed by Western blot and a negative test in a person with strong clinical
suspicion should have a repeat test if clinically indicated.
B. Western blot
The Western blot test is used as a measure of specific HIV-1 antibodies to
confirm a positive ELISA result. In the Western blot test, HIV-1 proteins are
electrophoretically separated on a nitrocellulose strip. The strip is incubated
with the patient’s serum. The specific HIV-1 antibodies are subsequently
detected using an enzyme-linked antihuman IgG. A positive calorimetric
reaction forms bands on the nitrocellulose paper corresponding to the position
of specific HIV-1 antigens.
The criteria for a positive test are any two bands corresponding to p24, gp41
and gp 120/160. The absence of bands is a negative result, while the presence
of bands that do not meet the criterion for a positive test is an indeterminate
result. False-positive and false-negative results are relatively uncommon.
Patients with positive ELISAs and indeterminate Western blots need repeated
testing and clinical evaluation. An infant born to an HIV-1-infected mother
may have a positive Western blot, but this will gradually become negative if
the infant is not truly infected with HIV-1.
Assays to directly detect HIV infection
C. Detection of p24 antigen

ELISA is used to detect p24 antigen. Anti-p24 antibodies are immobilised on a
solid surface and incubated with the patient’s serum. The amount of p24 is
detected using enzyme-linked anti-HIV-1 IgG and a calorimetric reaction. The
p24 antigen is detectable during the acute viraemic stage of infection and in
the late stages of AIDS. A very small percentage of asymptomatic persons with
HIV-1 infection are p24 antigen-positive.
D. Detection of HIV-1 RNA

A variety of commercial assays are available to detect and to quantitative HIV-
1 RNA. These include PCR, nucleic acid sequence-based amplification
(NASBA) and branched DNA (bDNA) assays for both detection and
quantitation of HIV-1. These assays can be used to detect HIV-1 infection prior
to the time following infection when antibody tests become positive. They are
also used to follow the effectiveness of anti-HIV-1 therapy.
E. Detection of HIV-1 proviral DNA

DNA is extracted from mononuclear cells obtained from anticoagulated
peripheral blood. Oligonucleotide primers specific to segments of the
integrated HIV-1 proviral DNA are used in a PCR assay. This type of assay can
be used for an antibody-positive infant born to an HIV-1 infected mother to
determine if the infant also infected. This is the preferred test for the infant
younger than 18 months of age.
HIV-1 culture
Tissue culture was the first test developed to diagnose HIV-1 infection. It was
used to establish HIV-1 as the cause of AIDS. Peripheral blood mononuclear
cells from a potentially infected patient are cocultured with peripheral blood
mononuclear cells from an uninfected person that have been stimulated with
phytohaemagglutinin and interleukin-2. The cultures are observed for
formation of multinucleated giant cells, for HIV-1 reverse transcriptase activity
or for HIV-1 p24 antigen production. Quantitative cell culture and quantitative
plasma culture can be performed as well. HIV-1 culture has a sensitivity of
95%–99%. HIV-1 culture is time-consuming and expensive, and thus not cost-
effective for routine use.
Monitoring CD4 T cell counts

Absolute CD4 T cell counts are widely used to monitor the patient’s HIV-1
infection status. The counts generally are obtained using whole blood cells
stained with anti-CD4 antibodies labelled with a fluorescent dye. The red
blood cells are lysed and the CD4 cells counted using flow cytometry.
Prognostic tests and treatment monitoring

A high viral load as measured by high HIV-1 RNA levels implies a poor
prognosis. Similarly, a low CD4 T cell count indicates risk for an opportunistic
infection and thus a poorer prognosis. Both the viral load and the CD4 T cell
count are used to monitor the effectiveness of anti-HIV-1 drug therapy.
Genotyping assays use the reverse transcriptase polymerase chain reaction to
amplify HIV-1 RNA that codes for viral enzymes targeted by antiretroviral
drugs. Analysis of the amplified sequences allows determination of mutations
that code for resistance to the drugs. Such resistance testing is recommended
in the settings of first-regimen or multiple-regimen failure or in pregnancy.
CDC definition of AIDS in patients with laboratory evidence of HIV

A definite diagnosis of:
1. Bacterial infections, multiple or recurrent in a child <13 years
2. Disseminated coccidioidomycosis
3. HIV encephalopathy (HIV dementia or subacute encephalitis)
4. Disseminated histoplasmosis
5. Diarrhoea for >1 month
6. Kaposi’s sarcoma
7. Lymphoma of the brain (primary)
8. Non-Hodgkin’s lymphoma of B cell or unknown immunological phenotype and one of several
specified types
9. Disseminated mycobacterial disease (other than mycobacterium tuberculosis)
10. Extrapulmonary mycobacterium tuberculosis involving at least one site outside the lungs
11. Recurrent Salmonella (nontyphoid) septicaemia
12. HIV wasting syndrome
Or, a presumptive diagnosis of:
1. Candidosis of the oesophagus
2. Cytomegalovirus retinitis with loss of vision
3. Kaposi’s sarcoma
4. Lymphoid interstitial pneumonia and/or pulmonary lymphoid hyperplasia in a child of 13
years of age
5. Disseminated mycobacterial disease
6. Pneumocystis carinii pneumonia
7. Toxoplasmosis of the brain in a patient of 1 month of age
The following conditions, in the presence of HIV infection, have been added to the definition
of AIDS:
1. Cervical cancer
2. Two episodes of bacterial pneumonia in 12 months
3. Pulmonary tuberculosis
CDC/WHO laboratory classification of HIV infection
CD4 cells/µl Total lymphocyte count/µl
1. >500 >2000
2. 200–499 1000–1999
3. <0.2 <1000
Clinical manifestations in HIV based on CD4 count
CD4 count Clinical finding
>500/mm3 Persistent generalised lymphadenopathy
Aseptic meningitis
Polymyositis
Guillain–Barre syndrome
200–500/mm3 Pneumococcal pneumonia
Pulmonary tuberculosis
Thrush
Kaposi’s sarcoma
Anaemia
Idiopathic thrombocytopaenia purpura
Oral hairy leukoplakia
B cell lymphoma
Cervical intraepithelial neoplasia
<200/mm3 Disseminated or chronic herpes simplex
Military or intrapulmonary tuberculosis
Candidal oesophagitis
Peripheral neuropathy
HIV-associated dementia
Coccidiodomycosis
<50/mm3 Disseminated M. avium
Cytomegalovirus retinitis
Clinical staging of HIV based on CD4 count
Clinical stage CD4 count Duration

Acute infection 1000–750 1–4 weeks
Asymptomatic 750–200 2–15 years
Early symptomatic 500–100 1–5 years
Late symptomatic 50–200 1–4 years
Advanced disease 50–0 0–2 years
Protocol for dental management of HIV positive individuals (for both

asymptomatic and symptomatic individuals):
1. An annual routine dental check up

2. Oral prophylaxis (plaque control, supra/subgingival scaling) every 6–
12 months
3. Annual radiographic assessment
4. Institute an appropriate treatment schedule based on the patient’s
requirements
a. Identify, diagnose and manage fungal, bacterial, viral and
other oral lesions (biopsy may be taken if considered
appropriate)
b. Manage xerostomia: Patients should be instructed to avoid
tobacco and alcohol, greater liquid intake is recommended,
xylitol chewing gum can be prescribed to stimulate
salivation
c. Cellulitis and osteomyelitis can be treated with penicillin V
2 g/day for 5–10 days + metronidazole 400 mg at 8 h
intervals
d. Periodontal treatment: Scaling, root planing, periodontal
surgery if indicated. (Irrigate with 0.1% chlorhexidine
gluconate.) Complex periodontal surgeries (bone
regenerative procedures) can be postponed in individuals
with CD4 count less than 200
e. Conservative and endodontic treatment: Regular fluoride
applications, caries removal and restoration. Asymptomatic
and symptomatic periapical lesions should be treated with
endodontic treatment and periapical surgery (if indicated)
f. Prosthodontic treatment: Complex prosthodontic
rehabilitation (fixed denture prosthesis, implants) can be
planned in individuals with CD4 count more than 200.
Simple prosthodontic work such as removable partial
dentures or complete denture can be planned for patients
with CD4 count. Patients can be instructed to clean their
removable dentures with 0.1% chlorhexidine gluconate or
with 1 part benzal chloride in 7.5 parts of water + antiseptic
soap + 1% hypochloride.
Oral surgical procedures: Assess the risk of septicemia (institute antibiotic

prophylaxis if appropriate). Estimate the haemostasis status (in the event of
history of thrombocytopaenia purpura or hepatic problems postpone the
surgery). Estimate CD4, CD8 counts, platelets and red blood cell counts.
Major antiretroviral therapeutic agents and their common side effects

Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs)
Zidovudine (AZT)
Didanosine (ddI)
Tenofovir (TDF)
Emtricitabine (FTC)
Zalcitabine (ddC)
Stavudine (d4T)
Lamivudine (3TC)
Abacavir (ABC)
Common side effects associated with NRTIs:
Lactic acidosis AZT, ddI, ddC, d4T
Lipoatrophy AZT, ddC, d4T
Peripheral neuropathy ddI, ddC, d4T
Pancreatitis ddI, ddC
Anaemia, neutropaenia AZT
Nephrotoxicity TDF
Hypersensitivity ABC
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Efavirenz, nevirapine, delavirdine
Common side effects associated with NNRTIs:
Rash All NNRTIs
Elevated AST, ALT All NNRTIs
CNS symptoms, teratogenic Efavirenz
Protease inhibitors (PIs)
Indinavir (IDV)
Ritonavir (RTV)
Saquinavir (SQV)
Nelfinavir(NLV)
Tipranavir (TPV)
Lopinavir (LPV)
Atazanavir (ATV)
Fosamprenavir (FPV)
Common side effects associated with PIs
Fat accumulation All (PIs)
Insulin resistance All (PIs)
Hyperlipidaemia All (PIs)
Nephrolithiasis IDV
Diarrhoea RTV, LPV, TPV
Fusion inhibitors
Enfuvirtide (ENF)
Common side effects associated with fusion inhibitors:
Local pain Enfuvirtide (ENF)
Management of occupational exposure and postexposure prophylaxis:
• Basic regimen
▪ Zidovudin 300 mg twice a day for 4 weeks
▪ Lamivudine 150 mg for 4 weeks
• Extended regimen
▪ Basic regimen + Indinavir 500 mg/thrice
▪ Basic regimen + Protease inhibitor
Hepatitis B
Exposed health care workers are at risk for main types of viral hepatitis like
hepatitis B. The chance of transmitting hepatitis B virus (HBV) is about 30%
per encounter. The risk of transmission is directly related to the extent of
contact with contaminated body fluids.
HBV is a highly infectious agent capable of being transmitted sexually,
perinatally and parenterally. Transmission usually occurs via blood and blood
products in volumes of even less than 0.0001 mL. Risk groups for HBV include
parenteral drug users, health care workers who have frequent exposure to
blood, haemodialysis patients and infants born to infected mothers. Risk of
hepatitis B in health care workers is high due to high carrier state (unknown)
in the patients.
Immunisation against hepatitis B is acquired via recombinant and yeast-
derived vaccinations, which are very effective. Poor responders to vaccinations
are patients on haemodialysis, immunosuppressed patients, elderly and obese
patients, smokers and those with HIV-related disease. All health care workers
should be immunised against hepatitis B.
Universal precautions
The infection control for patients with tuberculosis, hepatitis and HIV should
strictly adhere to the currently promulgated standards and guidelines, called
universal precautions. They are called so because they are to be applied for all
patients with these hazardous infectious diseases and to all treatment
procedures. It is essential for all dental care providers to recognise these
guidelines and render safe care to their patients.
• All personnel in the dental office should be vaccinated against hepatitis B

virus.
• Hands must be washed carefully with an antiseptic solution every time
the gloves are removed, to remove the build-up of bacteria beneath the
gloves.
• Gloves should be changed for each patient whenever they are damaged,
torn and in procedures which exceed more than 1 h.
• The gloves should be covered with an overglove if it is necessary to
temporarily leave the field of operation.
• Cross-contamination can be prevented by avoiding touching items which
are not in the field of operation like the eyewear, face mask, radiograph,
etc., with gloved hands.
• Mask with minimum 95% filtration efficiency for particles 3–5 mm should
be used and changed for each patient.
• When dealing with tuberculosis patients, masks with greater filtration
capacity should be used.
• A protective eyewear should be used by all dental care providers during
the delivery of treatment. The eyewear should have side shields on either
side. Nowadays chin-length face shields are available which can be used
along with the mask for better protection against splatter particles.
• Proper clinical attire should be worn to protect the exposed skin and
street clothings. These clinical attires should be worn only during the
delivery of treatment and should be laundered after the completion of
treatment.
• To prevent hair from coming in contact with the dental equipment or the
operating field, the dental care provider should wear disposable caps.
• All the instruments used should be properly cleaned and appropriately
sterilised.
• In the operating room the extraneous items should be removed because
the bacterial aerosol and the splatter which occurs constantly during the
procedure might settle on the items. The bulk storage containers should
be substituted with unit storage package.
• Restorative material should not be kept open in cardboard boxes.
Whenever needed they should be brought from the central supply area
and should be handled with freshly gloved hands.
• Single use disposable burs should be used or the burs require for
treatment procedures should be packaged and sterilised in a small bur
block.
• When recapping the needles one-handed swoop technique should be
used where the point of the needle is put inside the cap, then the syringe
is raised in the vertical position and the cap is allowed to settle down over
the needle.
Waste control
Needles and other sharp instruments should be disposed in a hard-walled
puncture-proof container. Other infectious wastes like gauze, cotton rolls,
towels, etc., should be sterilised and then disposed of appropriately.
Management of these patients should be based on universal precautions

CHAPTER 7
Medical Emergencies
and their Management
Importance of medical history

ASA physical status classification system
Emergency equipment
• Emergency drugs
Emergency management of an unconscious patient— BLS/CPR
• Danger
• Responsiveness
• Summon
• Circulation
Chest compression (C)
Airway (A)
• Needle cricothyrotomy
• Surgical cricothyrotomy
• Tracheostomy
Breathing (B)
Medical emergencies in dental practice
Vasovagal syncope
• Pathophysiology of vasovagal syncope
• Dental consideration
Postural hypotension
• Predisposing factors
• Pathophysiology
• Clinical features
• Management
Hyperventilation
• Manifestations of hyperventilation
• Management
Asthma
• Management
Angina pectoris
• Types
• Management
• Predisposing factors
Epilepsy
• Causes of seizures in dental office
• Triggering factors
• Clinical manifestations
• Dental consideration of an epileptic patient
• Management
Hypoglycaemia
• Management
Acute adrenal insufficiency
• Prevention of acute adrenal insufficiency
• Management
Anaphylaxis
• Pathophysiology
• Management
LA toxicity
Needle breakage
Foreign body aspiration
• Prevention
• Management
Haemorrhage
Haematoma
Surgical emphysema
Oral surgical procedures being elective and outpatient procedures are not
prone to many emergency situations. However, if encountered, the patient
would anticipate the practitioner to be equipped to handle the same. Some life-
threatening emergencies require split-second decisions and immediate
treatment. A delay may prove fatal. This chapter discusses the most common
emergencies that may be encountered, the equipment and the medications that
must be readily accessible, basic life support measures and means of
anticipating (and avoiding) such situations.
Importance of medical history

Knowledge of medical and drug history of the patient would prepare the oral
surgeon to handle an exacerbation of the medical problem. The procedure may
be duly modified to suit the patient. Scoring systems like the one designed by
American Society of Anesthesiologists (ASA) assess a patient at risk of such
emergencies.
ASA (American Society of Anesthesiologists) physical status classification

system
ASA physical status 1—A normal healthy patient.
ASA physical status 2—A patient with mild systemic disease.
ASA physical status 3—A patient with severe systemic disease that limits
activity and is not incapacitating.
ASA physical status 4—A patient with incapacitating severe systemic
disease that is a constant threat to life.
ASA physical status 5—A moribund patient who is not expected to survive
without an operation.
ASA physical status 6—A declared brain-dead patient whose organs may
be removed for donor purposes.
• The classification of the patient helps us decide if the patient can be

treated as an outpatient.
• A patient with a higher risk of medical emergencies must be treated in
a hospital with adequate facilities to handle emergencies.
• If the patient is under treatment for a systemic disease, is pregnant, has
undergone a recent surgery or has undergone an immunity modifying
treatment, due opinion, concurrence and consent should be obtained
from the treating specialist before embarking on any oral surgery.
Emergency equipment
The following equipment must be available and accessible in oral surgical
practices:
• Oxygen cylinder with regulator suitable for delivering high flow

oxygen
• Bag-mask device with oxygen reservoir
• Basic airway adjuncts (LMA oropharyngeal and nasopharyngeal
airways)
• Equipment for recording blood pressure
• Spacer device to deliver salbutamol or any bronchodilator
• Paper bag
Emergency drugs (Table 7.1, Fig. 7.1A–E)
1. In outpatient clinics
• Oxygen
• Adrenaline/epinephrine (1:1000, 1:10,000)
• Glyceryltrinitrate (nitroglycerine)
• Aspirin tablets
• Salbutamol inhaler
• Prednisone tablets
• Hydrocortisone IV
• Chlorpheniramine tablets
• Pheniramine maleate IV
Table 7.1
Emergency drugs to be kept in the operatory
Parenteral preparations
1. Anticonvulsant Diazepam, midazolam
2. Antihistamine Diphenhydramine
Chlorpheniramine
3. Antihypoglycaemic 30% Dextrose in water, glucagon
4. Corticosteroid Methylprednisolone
Dexamethasone
Hydrocortisone
5. Narcotic antagonist Naloxone
6. Vagolytic Atropine
7. Sympathomimetic Epinephrine
8. Hydrating agent Normal saline
Oral preparations
1. Antihistamine Diphenhydramine
2. Antihypoglycaemic Candy, sugar, glucose powder
3. Vasodilator Nitroglycerine
4. Antiplatelet aggregator Aspirin
5. Steroid Prednisolone
Inhaled preparations
1. Bronchodilator Epinephrine bitartrate, salbutamol
2. Respiratory stimulant Aromatic ammonia
3. Oxygen
FIGURE 7.1 (A–E) Emergency drugs.

2. In hospital-based practices
• Dextrose 50%
• Glucagon
• Normal saline
• Haemaccel
• Promethazine
• Midazolam
• If equipped with defibrillator: amiodarone and atropine
• Morphine (with due narcotic drug license)
• Sodium bicarbonate
• Calcium gluconate
• Potassium chloride
• IV Lignocaine
• Diazepam
• Theophylline
Emergency management of an unconscious patient

—basic life support (BLS)/cardiopulmonary
resuscitation (CPR)
The most commonly encountered emergency in oral surgical practice is the
patient fainting. Unconsciousness or syncope can be caused by a myriad of
reasons ranging from fear to a complication caused by an existing medical
condition. An oral surgeon can also be called to handle an emergency on the
roadside or at a community. In such instances emergency management
precedes diagnosis of the condition. The diagnosis of the condition can follow
next. No other aspect of emergency care is as important.
I. Danger
Make sure that you are safe and then ensure the safety of the patient. The
patient must be moved to a safer place where he may not injure himself or be
injured by any other external factors. The dental chair may be surrounded by
sharp, rotary instruments that can potentially harm the patient. It might be
safer to shift the patient to the floor in case there is a chance he/she may roll or
fall from the chair. The supine position is preferred.
II. Responsiveness
Responsiveness of the patient will determine the mental alertness of the
patient. A verbal response will ensure the patency of airway. Responsiveness
of the patient may be classified as follows:
AVPU
A = Alert
V = Response to verbal stimulus
P = Response to pain
U = Unresponsive
III. Summon
Summon medical assistance (ambulance).
IV. Circulation
If there is no pulse, chest compressions should be started immediately. If there
is a bleeding and loss of blood volume, direct compression may be employed
to arrest the bleeding as well as CPR should be initiated at the earliest.
CPR: 2010 American Heart Association cardiopulmonary resuscitation (CPR) and
emergency cardiac care (ECC):
• In 1960 Kouwenhoven, Knickerbocker and Jude documented 14

patients who survived cardiac arrest with the application of closed
chest cardiac massage. That same year, at the meeting of the Maryland
Medical Society in Ocean City, MD, the combination of chest
compressions and rescue breathing was introduced. Two years later,
in 1962, direct-current, monophasic waveform defibrillation was
described. In 1966 the American Heart Association (AHA) developed
the first cardiopulmonary resuscitation (CPR) guidelines, which have
been followed by periodic updates.
• Basic life support (BLS) is the foundation for saving lives following
cardiac arrest. Fundamental aspects of adult BLS include immediate
recognition of sudden cardiac arrest and activation of the emergency
response system, early performance of high quality.
• However, the conventional teaching for many years was:
A. Airway
B. Breathing
C. Circulation
Initiating the effort to maintain a patent airway and ventilation was the
priority.
• The newest development in the 2010 AHA Guidelines for CPR and ECC
is a change in the basic life support (BLS) sequence of steps from ‘A-B-
C’ (Airway, Breathing, Chest compressions) to ‘C-A-B’ (Chest
compressions, Airway, Breathing) for adults and paediatric patients
(children and infants, excluding newborns).
Chest compression (C) (Fig. 7.2A–G)

Chest compressions before giving rescue breaths (C-A-B rather than A-B-C).
Chest compressions can be started immediately, whereas positioning the head,
attaining a seal for mouth-to-mouth rescue breathing or obtaining or
assembling a bag-mask device for rescue breathing all take time.
• Heel of one hand to be positioned over the junction of the lower and
middle third of the sternum, between the nipples and the other hand is
placed on top of the fist.
• Chest to be compressed hard and fast at a rate of 100 per minute.
• Depth of compression should be 2 inches (5 cm) at least. Wait for chest
recoil.
• Release pressure and repeat cycles of 30 compressions, followed by
two attempted rescue breaths (ratio of compressions:breaths = 30:2).
• By changing the sequence to C-A-B, chest compressions will be
initiated sooner and ventilation only minimally delayed until
completion of the first cycle of chest compressions (30 compressions
should be accomplished in approximately 18 s).
• For a victim of asphyxial arrest, the priority would be to provide about
five cycles (about 2 min) of conventional CPR (including rescue
breathing) before activating the emergency response system. Also, in
newly born infants, arrest is more likely to be of a respiratory aetiology
and resuscitation should be attempted with the A-B-C sequence unless
there is a known cardiac aetiology.
• ‘Look, listen and feel’ has been removed from the algorithm.
Performance of these steps has been considered inconsistent and time
consuming.
• The recommended compression-ventilation ratio is 3:1 in infants
because ventilation is critical to reversal of newborn asphyxial arrest
and higher ratio may decrease minute ventilation. If the arrest is
known to be of cardiac aetiology, a higher ratio (15:2) should be
considered. If no circulation is present, if you are unsure or in infants if
the pulse rate is less than 60 per minute, start external chest
compressions at the rate of 100 compressions per minute.
• Minimise interruptions in effective chest compressions until return of
spontaneous circulation (ROSC) or termination of resuscitative efforts.
Any unnecessary interruptions in chest compressions (including
longer than necessary pauses for rescue breathing) decreases CPR
effectiveness.
FIGURE 7.2 (A) Patient made to lie on a flat surface away from
danger. (B) Check for carotid pulse. (C) Anatomical landmarks of
the chest—sternum, ribs, heart within the rib cage. (D, E) The heal
of one hand is placed over the junction of middle and lower third of
sternum between the nipples. The other hand is placed on top of
the fist. (F) Compression is made to a depth of 2 inches (5 cm).
(G) Chest compression is done with the arm unflexed at elbow.
Electrical therapies (defibrillators) (Fig. 7.3A–C)
• To give the victim the best chance of survival, three actions must occur
within the first moments of a cardiac arrest: activation of the
emergency medical services (EMS) system, provision of CPR and
operation of a defibrillator.
• Rescuers should minimise the interval between stopping compressions
and delivering shocks and should resume CPR immediately after
shock delivery.
• If more than two rescuers are present, CPR should be performed while
a defibrillator is being obtained and readied for use.
• When two rescuers are present, the rescuer operating the automated
external defibrillator (AED) should be prepared to deliver a shock as
soon as the compressor removes his or her hands from the victim’s
chest and all rescuers are ‘clear’ of contact with the victim. Rescue
breathing prior to the shock will increase the time from compression to
shock and thus it is reasonable to proceed immediately to shock
without rescue breathing.
• Cardioversion of adult atrial flutter and other supraventricular
tachycardias generally requires less energy; an initial energy of 50–
100 J is often sufficient. If the initial shock fails, providers should
increase the dose in a stepwise fashion.
• After shock delivery, the rescuer should not delay resumption of chest
compressions to recheck the rhythm or pulse. After about five cycles of
CPR (about 2 min, although this time is not firm), ideally ending with
compressions, the AED should then analyse the cardiac rhythm and
deliver another shock if indicated.
FIGURE 7.3 (A–C) Defibrillator.
Airway (A) (Fig. 7.4A–D)
a. In an unconscious patient, without an external agent blocking the

airway (as in case of an aspirated object), the tongue could be
posteriorly displaced causing a partial or total airway block at the level
of the larynx. To prevent hypoxia, airway needs to be cleared,
obstruction removed and free flow of air to lungs ensured. If required,
ensuring a patent airway is followed by oxygenation with rescuer
(mouth-to-mouth respiration/rescuer exhaled air), ambu bag
(atmospheric air) (Fig. 7.5) or 100% oxygen if available.
b. Head tilt/chin lift procedure:
i. Patient should be in supine position.
ii. Lift the chin forward to move the mandible anteriorly while
tilting the head backwards.
iii. Neck is hyperextended.
c. Jaw thrust/chin lift manoeuvre (for neck injury patients)
i. Jaw thrust manoeuvre: Lift the mandible forward with your
index fingers while pushing against the zygomatic arches
with your thumbs. Your thumbs provide the
counterpressure to prevent movement of the head when the
mandible is pushed forward.
ii. Chin lift manoeuvre: Place one hand on the forehead to
stabilise the head and neck. Grab the mandible between the
thumb and the index finger of the other hand. Lift the
mandible forward.
iii. Hold the head to keep the head and neck still and in
alignment with the rest of the body.
iv. Cannot be used in mandibular fracture or dislocation
patients.
FIGURE 7.4 Head tilt manoeuvre.

(A) Patient at rest. (B) Pressure at forehead tilting the head and
extending the neck creating a patent straight airway. Head tilt chin
lift manoeuvre.
(C) Patient at rest. (D) Head tilted at forehead. Extending the neck
with chin lifted opening the jaw and hence a patent airway.
FIGURE 7.5 Oxygenation using ambu bag.
Means of securing airway (refer to Chapter 10 General Anaesthesia)
• Supraglottic devices
▪ Oropharyngeal airway (Fig. 7.6A–C)
▪ Nasopharyngeal airway
▪ Laryngeal mask airway
• Intubation-endotracheal tube
• Cricothyrotomy
▪ Needle cricothyrotomy
▪ Surgical cricothyrotomy
Needle cricothyrotomy (Fig. 7.7A, B)

The cricothyroid membrane is identified and punctured using a large-bore
cannula (12–14 gauges) attached to a syringe. Aspiration of air confirms that
the cannula lies within the trachea. The cannula is then angled to about 45
degrees caudally and advanced off the needle into the trachea. A high flow
oxygen supply is then attached to the cannula and insufflated for 1 s followed
by a 4 s rest. Expiration occurs via the upper airway as normal. This
techn]ique only oxygenates the patient and does not eliminate carbon dioxide.
It is therefore limited to about 30-min use while a definitive airway is
created.
Surgical cricothyrotomy
This involves making an incision through the cricothyroid membrane with a
scalpel to allow the introduction of a small-diameter tracheostomy tube or
tracheal tube (5–6 mm).
It is more difficult to perform and often results in significantly more
bleeding than the needle cricothyroidotomy. The advantage, however, is that
once a tube of this diameter has been inserted, the patient can be adequately
ventilated, thereby ensuring oxygenation and elimination of carbon dioxide
and the airway suctioned to remove any blood or debris.
Tracheostomy (Fig. 7.8A–F)
Tracheostomy or tracheotomy (though different procedures, terms used
interchangeable) refers to surgical/nonsurgical (percutaneous) entry into
trachea through the anterior wall to secure airway for oxygenation. The
surgical tracheostomy techniques were standardised in 1909 by Chevalier
Jackson.
Recently, due to increased complications and morbidity of surgical
tracheostomy, percutaneous tracheostomy or cricothyrotomy is preferred.
Indications of tracheostomy
• To secure and clear the airway in upper respiratory tract obstruction

(actual or potential).
• To secure and maintain a safe airway in patients with injuries to the face,
head or neck and following certain types of surgery to the head and neck
in unstable cervical spine fracture.
• To facilitate the removal of bronchial secretions where there is poor cough
effort with sputum retention.
• To protect the airway of patients who are at high risk of aspiration, that is
patients with incompetent laryngeal and tongue movement on
swallowing, e.g. neuromuscular disorders, unconsciousness, head
injuries, stroke, etc.
• To enable long-term mechanical ventilation of patients, either in an acute
ICU setting or sometimes chronically in hospitals.
• To facilitate weaning from artificial ventilation in acute respiratory failure
and prolonged ventilation.
• In paediatric age group (controversial).
• Facilitate long-term airway management.
Contraindications
There is no absolute contraindications existing since it is an emergency life
saving procedure.
1. Children under 5 years of age. Tracheostomy is the preferred emergency
airway procedure in young patients, though needle cricothyroidotomy
is more desirable.
2. Pre-existing pathology of larynx—e.g. carcinoma, epiglottitis.
3. Lack of experience and knowledge of cricothyoidotomy.
4. Cervical trauma.
Classification of tracheostomy
1. Depending on the method of initial insertion—either surgical or

percutaneous (needle).
2. Depending on the intended duration.
Temporary tracheostomy when the patient requires long-/short-term
respiratory support or cannot maintain the patency of their airway due
to existent or anticipated upper airway obstruction. These tubes will be
removed when the patient recovers.
Long-term/permanent tracheostomy is usually performed due to carcinoma
of the naso-oropharynx or larynx. Dependent on the stage of the disease
either a tracheostomy or a laryngectomy will be performed.
3. Depending on the situation demanding the procedure as
Emergent tracheostomy This is performed within 2–3 min in an emergency

situation when patient is anoxic and requires immediate oxygenation
and verification to avoid cerebral hypoxia.
Urgent tracheostomy or timely tracheostomy This procedure is performed in
5–10 min where patient is not severely anoxic may be from partial
upper airway obstruction but has high potential to become completely
anoxic in short duration.
Elective tracheostomy This is performed in the operating room with
adequate equipment, assistance, hyperextended neck as planned earlier.
Surgical tracheostomy: procedure

Step 1 The skin from the chin to below the clavicles is sterilely prepared.
Step 2 Local anaesthesia with a vasoconstrictor is usually infiltrated into the
skin and deeper tissues to reduce the amount of bleeding during the
procedure.
Steps 1 and 2 Will not be performed in emergency and urgent tracheostomy.
Step 3 The skin of the neck over the 2nd tracheal ring is identified and a
vertical incision about 2–3 cm in length is created. This is applicable in
emergency where
a. If incision is placed superior or inferior to intended location, it can be

extended accordingly without wasting time.
b. Though incision crosses the aesthetic Langer’s line of tension with
potential unaesthetic scar, aesthetics is not a consideration in
emergency.
For elective tracheostomy, incision is placed horizontally along natural

cervical skin crease.
Step 4 Sharp dissection following the skin incision is done to cut across the
platysma muscle.
Step 5 Blunt dissection parallel to the long axis of the trachea is done to
spread the submuscular tissues (sternohyoid, sternothyroid and other strap
muscles until the thyroid isthmus is identified. If the gland lies superior to the
third tracheal ring, it can be bluntly undermined and retracted superiorly to
gain access to the trachea. If the isthmus overlies the second and third ring of
the trachea, either the gland is mobilised or complete transection of the
isthmus must be made.
Step 6 A cricoid hook engages the space between cricoids and first tracheal
ring pulling the trachea upward. Blunt dissection is continued longitudinally
through the pretracheal fascia.
Step 7 Entry into trachea.
Linear incision A linear incision is the simplest choice and least traumatic to
the cartilage. Typically, it is made through the interspace between the second
and third tracheal rings. This can also be done as vertical with guide sutures
placed on either sides.
Tracheal window removes the midportion of the third or fourth tracheal ring
to create a window. This minimises trauma to the remaining cartilage
resulting from passage of the tracheostomy tube.
Bjork flap An inferiorly based U-shaped flap that incorporates the ring
below the tracheal incision is raised and sutured to the skin at the inferior
margin of the tracheotomy. This helps to keep the tracheal incision close to the
skin edge and facilitates tube replacement if the tube is accidentally
dislodged. During removal of tube, the flap can be resutured. This fistula is
truly a ‘stoma’ with tracheal mucosa approximated to the skin. The stability of
this tract is believed to be superior to the ring resection-removal technique.
Step 8 Placement of the tube and securing to the neck. The tube is inserted
vertically downward into the trachea avoiding damage to the tracheal mucosa
of posterior wall. The tube is secured by suturing the flanges to the neck skin.
This is followed by tying the flanges of tube with thread encircling the neck
taking care to avoid strangulation.
Percutaneous tracheostomy
This is the most commonly used technique in critical care as it is simple and
quick. It can be performed at the bedside using anaesthetic sedation and local
anaesthetic and therefore is often the technique of choice in the critically ill.
The procedure involves the insertion of a needle through the neck into the
trachea followed by a guide wire through the needle. The needle is removed
and the tract made gradually larger by inserting a series of progressively
larger dilators over the wire until the stoma is large enough to fit a suitable
tube (Seldinger technique). This is then secured by cloth ties or a holder.
Complications of tracheostomy
Complications can be divided into those associated with insertion of the
tracheostomy (surgical or percutaneous) or those which arise following the
procedure. These complications are grouped as follows:
1. Immediate complications (perioperative period)

• Haemorrhage (usually minor, can be severe if thyroid or blood
vessels damaged).
• Misplacement of tube—within tissues around trachea or to
main bronchus.
• Pneumothorax.
• Tube occlusion.
• Surgical emphysema.
• Loss of the upper airway.
2. Delayed complications (postoperative period <7 days)
• Tube blockage with secretions or blood. May be sudden or
gradual.
• Partial or complete tube displacement.
• Infection of the stoma site.
• Infection of the bronchial tree (pneumonia).
• Ulceration and/or necrosis of trachea.
• Mucosal ulceration by tube migration (due to loose tapes or
patient intervention).
• Risk of occlusion of the tracheostomy tube in obese or fatigued
patients who have difficulty extending their neck.
• Tracheoesophageal fistula formation.
• Haemorrhage (local tissue trauma or erosion through blood
vessels).
3. Late complications (late postoperative period >7 days)
• Granulomata of the trachea may cause respiratory difficulty
when the tracheostomy tube is removed.
• Tracheal dilation, stenosis, persistent sinus or collapse
(tracheomalacia).
• Scar formation requiring revision.
• Blocked tubes may occur at any time, especially if secretions
become thick, the secretions are not managed appropriately
(suction) and humidification is not used.
• Haemorrhage.
FIGURE 7.6 (A, B) Oropharyngeal airway insertion just before

extubation. (C) Oropharyngeal airway in place. Through the
anterior flange, suction is introduced to clear upper airway or
oropharynx.
FIGURE 7.7 (A) Anatomical landmarks of the neck—lower border

of mandible, hyoid bone, thyroid cartilage, cricothyroid membrane,
cricoid cartilage, tracheal rings, clavicle and sternum. (B) Location
and position of the needle for cricothyrotomy.
FIGURE 7.8 (A) Anatomical landmarks of the neck—lower border

of mandible, hyoid bone, thyroid cartilage, cricothyroid membrane,
cricoid cartilage, tracheal rings, clavicle and sternum.
(B) Horizontal incision for elective tracheostomy. (C) Vertical
incision for emergency tracheostomy. (D) Entry into the trachea—
tracheal window. (E) Entry into the trachea—Bjork flap.
(F) Tracheostomy tube in-situ in a child with potential upper airway
compromise.
Breathing (B)
• To give breaths to an infant, use a mouth-to-mouth and mouth-to-nose

technique.
• To give breaths to a child, use a mouth-to-mouth technique.
• Make sure the breaths are effective (i.e. the chest rises). Each breath
should take about 1 s. If the chest does not rise, then reposition the
head, make a better seal and try again.
• It may be necessary to move the child’s head through a range of
positions to provide optimal airway patency and effective rescue
breathing.
• In an infant, if there is difficulty making an effective seal over the
mouth and nose, then try either mouth-to-mouth or mouth-to-nose
ventilation. When the mouth-to-mouth technique is used, pinch the
nose closed. When using the mouth-to-nose technique, close the
mouth.
• In either case make sure the chest rises when you give a breath. In case
of one rescuer, provide two effective ventilations using as short a
pause in chest compressions as possible after each set of 30
compressions.
• One cycle of CPR consists of 30 compressions and 2 breaths. When
compressions are delivered at a rate of about 100 per minute, five
cycles of CPR should take roughly 2 min (range: about 1.5–3 min).
• In case of two rescuers 15 compressions 1 breath per rescuers.

Emergencies encountered can be
I. Due to anxiety
a. Syncope (most commonly vasovagal syncope)/postural
hypotension
b. Hyperventilation
II. Due to the prior medical condition of the patient
a. Status asthmaticus
b. Cardiac emergencies
i. Angina pectoris
ii. Acute myocardial infarction and cardiac arrest
c. Status epilepticus
d. Diabetic complications
i. Hypoglycaemia
ii. Hyperglycaemia
e. Adrenal crisis
f. Haemorrhagic disorders (dealt in Chapter 15 Haemostasis and
Shock)
III. Due to the anaesthetic/drugs used by the oral surgeon
a. Anaphylaxis
b. LA toxicity (refer to Chapter 9 Local Anaesthesia)
IV. An accident during the procedure
a. Needle breakage (refer to Chapter 9 Local Anaesthesia)
b. Choking and aspiration
V. Postsurgical sequelae
a. Haemorrhage (refer Chapter 15 Haemostasis and Shock)
b. Haematoma (refer to Chapter 9 Local Anaesthesia)
c. Surgical emphysema (refer to Chapter 10 General Anaesthesia)
Vasovagal syncope
Vasovagal syncope is usually defined as a transient loss of consciousness due
to cerebral ischaemia caused by a reduction in blood supply to the brain.
Vasodilatation causes pooling of blood in peripheries and vagal stimulation
causes slowing of the heart; this combination causes a dramatic fall in blood
pressure.

Vasovagal syncope (three phases)
• Presyncope
• Syncope
• Postsyncope
Causes
• Psychologic factor—pain or fear

• Postural changes
• Anoxia
• Carotid sinus syndrome
Pathophysiology of vasovagal syncope (Tables 7.2–7.3,

Flowchart 7.1)
Anxiety causes increased release of catecholamines, which cause decreased
peripheral vascular resistance, resulting in pooling of blood in the peripheries
and fall in arterial blood pressure. Compensatory mechanisms come into play
and cause increased heart rate, rapid breathing, pallor and perspiration.
Decompensation occurs soon which results in hypotension and reduced
cerebral blood flow and eventually syncope.
Table 7.2
Clinical finding and pathophysiology of syncope

Presyncope
Clinical finding Pathophysiology
E A Feeling of warmth in the Fear/pain: Release of catecholamines
R neck and face
L Pallor and BP decreased Decreased peripheral vascular resistance, pooling of blood in
Y peripheries (skeletal muscles), decreased cardiac return
HR increased Compensatory carotid and aortic reflex
Perspiration (forehead) Fatigue
Patient complains of Decreased vascular perfusion to brain (normotensive patient
feeling dizzy or requires diastolic of 50 mmHg at upright position and
nauseous 30 mmHg in supine position to maintain cerebral perfusion)
L A Yawning Cerebral hypoxia
T Coldness of hand and Compensatory peripheral vasoconstriction
E feet
HR decreased Reflex bradycardia
Dilated pupils Decreased cerebral perfusion
Disturbed vision
Loss of consciousness BP falls by 30/15 mmHg
Syncope
Breathing irregular, jerky, CNS depression
gasping/quiet shallow barely
perceptible/apnoea
Dilated pupils
Convulsive twitching
HR decreased < 50 per minute Reflex bradycardia
pulse weak and thread, Severe
cases: ventricular asystole
Incontinence Muscle relaxation
Airway obstruction Tongue fall back
If not recovered within 5 min with proper management—it is not just a vasovagal syncope
Postsyncope (recovery)
Consciousness regained Increase in BP after proper positioning
Consciousness regained by increase in BP after change of
posture
Pallor, nausea, weakness, Can persist up to 24 h due to autonomic disturbances
sweating
HR, BP normalises Restored cerebral perfusion
Table 7.3
Differentiating clinical findings between syncope and seizure

Symptom or sign Syncope Seizure
Tongue biting Anterior tongue Lateral tongue
Duration <5 min >5 min
Aura No Yes
Postictal state Seconds Minutes or longer
Incontinence No Yes
Tonic–clonic jerks Occasional Frequent
Metabolic acidosis Occasional Frequent
FLOWCHART 7.1 Syncope—pathogenesis.
Dental consideration
Follow anxiety reduction protocol (Box 7.1). Follow adequate postoperative
pain and anxiety control technique.
Box 7.1 Stress reduction protocol
• Premedicate the patient with hypnotics for a relaxed sleep the night
before the surgery
• Premedicate the patient with sedatives on the day of surgery
• Schedule the surgery in the morning
• Minimise the patient waiting time
• Consider psychosedation during surgery
• Administer adequate pain control measures during surgery
• Reduce the length of the appointment
• Avoid any anxiety during surgery
• Follow-up postoperative pain and anxiety control
• Effective postoperative analgesics
Management
Stop all the treatment; make the patient supine with legs raised. Give
supplemental oxygen. Monitor vital signs, check for breathing. Perform basic
life support (BLS) if breathing is absent and summon for medical assistance. If
breathing is present, then hold some ammonia salts under the patient’s nose to
revive consciousness. Have the patient escorted home.
Postural hypotension
Postural hypotension or orthostatic hypotension is defined as a disorder of the
autonomic nervous syndrome in which syncope occurs when patient assumes
an upright position. Orthostatic (postural) hypotension differs from
vasodepressor syncope in that there is only reduction in the blood pressure
whereas in syncope peripheral circulatory failure is also present.
Predisposing factors
• Chances of postural hypotension increase with age.

• If we suddenly change the position of the dental chair after a long
period of recumbency to upright position, the risk of postural
hypotension increases.
• It is more common in pregnant women in the first and third trimester.
• Patients who are receiving drugs that produce vasodilatation
(antihypertensives, narcotics and many psychiatric drugs) have a
predisposition to orthostatic hypotension.
Pathophysiology
Due to the failure of one or more normal adaptive mechanisms, body’s
response to gravity is inadequate in case of postural hypotension. When the
patient moves into upright position, the systolic pressure drops to less than
60 mmHg. However, the heart rate changes slightly or remains the same. The
combination of rapid decrease in BP, but no change in heart rate is
pathognomonic of postural hypotension. When the cerebral blood flow drops
below the critical level of approximately 30 mL of blood per minute per
100 mg of brain, the patient loses consciousness.
Clinical features
Patient usually complains of palpitations and generalised weakness.
Patients undergoing treatment in supine or semi-supine position should not
rise rapidly. By changing the patient’s chair position 2–3 times within minute
or by uprighting the chair position gradually after the treatment, postural
hypotension can be prevented.
Management
The unconscious patients should be placed in a supine position with the legs
elevated. This helps in cerebral perfusion. If the patient does not regain
consciousness, treat patient as for syncope.
Hyperventilation
Hyperventilation is often caused by anxiety which is most commonly seen in
patients in their adolescence and early adulthood and can frequently be
prevented through anxiety control. Males are often affected.
Hyperventilation may lead to profound metabolic changes that include a fall
in arterial CO2 concentration. This causes cerebral vasoconstriction and
respiratory alkalosis resulting in loss of consciousness.
The patient may notice tingling of fingers or lips, muscular tremor, tetanic
spasm of the peripheries and dizziness. These symptoms tend to increase
anxiety, respiratory rate and depth. Eventually the patient will become
unconscious due to cerebral hypoxia. The patient may be apnoeic for a period
due to reduced respiratory drive with low arterial CO2 concentration. As the
arterial CO2 level rises and cerebral vasoconstriction reverses, the patient starts
breathing and regains consciousness. Hyperventilation recommences and the
cycle continues with further loss of consciousness.
Manifestations of hyperventilation
Manifestations of hyperventilation are depicted in Table 7.4.
Table 7.4
Hyperventilation manifestations
Dizziness
Weakness
Disturbed consciousness
Tingling or numbness of fingers, toes and lips
Increased rate and depth of breathing
Shortness of breath
Angina
Xerostomia
Palpitations
Tachycardia
Myalgia
Tremor
Tetanic spasm
Extreme anxiety
Management
Stop the treatment as soon as you notice the symptoms and reassure the
patient. Make the patient lie in semi-erect position. If the patient is conscious,
ask him/her to re-breath into paper bags to increase inspired CO2 and to
overcome alkalisation. If the patient is unconscious, maintain proper airway
until he/she regains consciousness. This condition is a self-limiting one and
eventually the patient will settle. If the previously discussed steps fail to
terminate an episode of hyperventilation, parenteral drugs may have to be
administered to reduce the patient’s anxiety and to slow the rate of breathing.
The drugs of choice in this situation are parenteral (IV) diazepam or
midazolam. Diazepam 10–15 or 3–5 mg midazolam for the average adult or
titrated until the patient exhibits clinical recovery.
Asthma
Asthma described by American Thoracic Society is a disease characterised by
an increased responsiveness of the trachea and bronchus to various stimuli
and is manifested by undispersed narrowing of the airways that changes in
severity either spontaneously or as a result of therapy. In case of asthmatic
patients, respiratory problems are easily triggered by emotional stress or
through a variety of pharmacological agents. So, it is a challenge to manage
these patients safely if there is no known history of asthma. But in most cases,
patient will give a history of asthma and would be carrying medications for
the same.
Clinical features
• Respiratory distress (patient will complain of shortness of breath and

want to sit erect—orthopnoea)
• Audible wheezing
• Coughing
• Dyspnoea
• Tachycardia
• Difficulty with expiration
If the patient has severe bronchospasm, he/she might become cyanotic and
hypoxic with eventual loss of consciousness.
By strictly adhering to anxiety reduction protocol, acute episodes of asthma
precipitated by emotional stress can be minimised or eliminated. Patients
should be asked to bring their regular medication with them. Care should be
taken while administering LA with vasodepressors due to sulpha containing
agents (preservative) which can trigger. Barbiturates, opioids and NSAIDs
should not be used since these groups increase the risk of bronchospasm by
histamine release.
Management
• Terminate all dental treatment and position the patient in an erect or

semi-erect position. Before proceeding further we should assess the
severity of asthma.
• If the patient is in acute severe phase, he/she cannot speak in complete
sentences. His/her pulse rate will be greater than 110 per minute,
respiratory rate will be greater than 45 per minute.
• If the patient has severe life-threatening asthma, then he/she will have
a silent chest, cyanosis, sweating, hypercarbic flush, bradycardia,
confusion and agitation.
• Administer the antiasthmatic drug normally used by the patient
followed immediately by hydrocortisone 200 mg intravenously along
with oxygen.
• If there is no response within 2–3 min, give salbutamol or terbutaline
by slow intravenous injection or 1 mL of 1 in 1000 adrenaline
intramuscularly. Summon for medical assistance.
Angina pectoris
Angina is a Latin word describing a spasmodic, cramp like, choking and
suffocating pain in the chest. Angina indicates the presence of significant
degree of coronary artery disease or ischaemic heart disease. The discomfort
from cardiac ischaemia is described as squeezing sensation, which begins in
the retrosternal location radiating to the left shoulder and arm.
Types
The two types of angina are stable and unstable angina.
Stable angina
Stable angina occurs only on exertion and is relieved by rest with no changes
in precipitating factors within the previous 60 days.
Unstable angina
Unstable angina describes a syndrome that is intermediate between stable
angina and myocardial infarction. There are changes in the pattern, frequency
and duration of precipitating factors. Sudden onset is considered unstable.
Management
If patient complains of chest pain,
• Stop the dental procedure (remove all foreign body including

cotton/gauze).
• Change chair position to patient’s comfort (mostly upright).
• Administer 0.5 mg glyceryl trinitrate (GTN) sublingually.
• Monitor vitals.
• If pain relieved in 2–3 min and vitals remain stable, postpone the
dental treatment.
• If no pain relief, medical management and hospital care is required.
Myocardial infarction (MI) is a clinical condition caused by necrosis of a region
of myocardium due to decrease in the coronary artery blood supply. This
condition is usually characterised by severe and prolonged substernal pain
which simulates angina pectoris but is of more intense and of longer duration.
Similar to that of angina pectoris.
Clinical features
The patient complains of severe pain, usually described as pressing,
squeezing, bursting, burning, choking or crushing sensation within the chest
not relieved by rest or nitroglycerine and can persist for a long time. It is most
commonly located over the middle to upper third of the sternum.
Signs and symptoms
• Cold sweat
• Levine sign (characterised by the patient’s fist clenched over the
sternum describing the discomfort)
• Dyspnoea
• Orthopnoea
• Nausea
• Vomiting
• Giddiness
• Light-headedness
Signs include pale appearance of face and mucous membranes, peripheral

cyanosis, very rapid heart and respiratory rate. The patient is usually very
restless with cool, pale and moist skin.
Patients with recent episode of MI within 6 months are usually on oral
anticoagulant and are at increased risk of another episode. Delay any dental
treatment for 6 months post MI is advisable. The risk:benefit ratio of
temporarily stopping the anticoagulant is assessed before initiating the dental
treatment (invasive).
Patient with an episode of MI >6 months earlier
• Anxiety reduction protocol should be followed.

• Proper history should be taken for evaluation and identification of the
patients who are at an increased risk of another episode.
• Dental treatment should be carried out with effective LA, less anxiety
and oxygen saturation, pulse and BP monitoring. The dose of LA
should be limited. Gingival retraction cords containing adrenaline
should be avoided.
An episode of MI on dental chair
• Terminate all dental treatment and position the patient in a semi-

reclined posture if he/she is unconscious.
• If the patient is conscious and breathless, reassure and change posture
to sitting posture.
• Give glyceryl trinitrate tablets or spray under the tongue.
Repeat this after 5 min if pain is not relieved, patient requires emergency
hospital care.
Epilepsy
Epilepsy is a group of disorders of brain function causing episodic
disturbances of consciousness and motor or sensory function. There are
several types of epilepsies. In major seizures, there is a sudden spasm of
muscles producing rigidity (tonic phase). Jerky movements of the head, arms
and legs may occur (tonic–clonic phase). The victim becomes unconscious,
may have noisy or spasmodic breathing, salivation and urinary incontinence.
Status epilepticus refers to a type of seizure that continues for more than 5
min or a repeated seizure that begins before the individual recovers from the
initial episode and is a true medical emergency. A common precipitating
factor for status epilepticus is failure of the epileptic patients to take
antiepileptic drugs, other factors being trauma and tumour.
Causes of seizures in dental office
1. Hypoxia secondary to syncope

2. Hypoglycaemia
3. Local anaesthetic overdose
4. Failure of epileptic patients to take antiepileptic drugs
5. Head injury
Triggering factors
1. Flashing lights
2. Alcohol ingestion
3. Physical or emotional stress
4. Decreased physical health
5. Missed meal
6. Infection
7. Epileptogenic drugs
8. Withdrawal of anticonvulsant medication
Clinical manifestations
There may be involuntary movement of one part of the body before the loss of
consciousness or a generalised convulsion. This is known as aura. The aura
consists of mood changes, irritability, brief hallucination or headaches. Clinical
manifestations are characterised by sudden loss of consciousness, continued
spasm of respiratory muscles which makes breathing impossible. The skin
colour and mucous membrane become dusty or cyanotic. Bladder and bowel
control may be lost.
Dental consideration of an epileptic patient
• Adequate history regarding the disease should be obtained with

specific reference to its duration and predisposing factors, types of
drugs taken and duration of medication.
• Treatment should be undertaken only if the patient is under good
control, with no recent episodes.
• Premedication with antianxiety drugs and stress reduction protocol
should be followed.
• Optimal dosage of local anaesthesia.
Management
• Terminate the dental treatment: Place the patient in the supine

position, loosen any tight clothes and avoid restraining the patient.
The mouth should not be forced open nor attempts made to insert any
object into the mouth. Turn the victim into a stable side position as
soon the seizures stops, open and maintain clear airway to avoid
aspiration and check for breathing.
• If the patient is conscious after the seizure, monitor vital signs,
administer oxygen and consult a physician. Have the patient escorted
home by his/her relative or attendant.
• If the patient is unconscious with no response to management get
medical assistance as early as possible, maintain airway, monitor vital
signs, initiate basic life support (if necessary) and transfer the patient
to hospital care facility.
• If the seizure lasts for more than 5 min (status epilepticus) or if
repeated seizure occurs, then the following protocol must be followed:
▪ Administer diazepam 5 mg per minute IV (up to 10 mg) or
midazolam 3 mg per minute IV/IM (up to 6 mg) titrate until
seizure stops. Once the seizure stops monitor the vital signs,
administer oxygen and transport to emergency care facility.
Hypoglycaemia
A common emergency situation encountered in a diabetic patient is
hypoglycaemia resulting from mismatch of insulin dose and serum glucose.
Usually it results from failure to take food or over dosage of insulin,
hypoglycaemic drugs or alcohol.
Hypoglycaemia is of rapid onset; inability with varied clinical presentation as,
lethargy, sweating, tachycardia, nausea, anxiety, irritability, disorientation,
unconsciousness, hypotension, hypothermia and seizure.
1. Stress reduction protocol is of paramount importance in managing

these patients.
2. Appointments should be of short duration and early in the morning.
3. Routine dental procedures and minor surgical procedures under local
anaesthesia can be carried out just after a meal (preferably breakfast)
and routine antidiabetic medication with no special precautions.
4. Glucose drinks should be available in the dental clinic while dealing
with diabetic patients.
5. It is advisable to use local anaesthesia without epinephrine because
minimal doses of epinephrine have been shown to elevate blood
glucose concentration. However, it has also been shown that the dose
used in dental local anaesthetic solution is unlikely to cause any
danger. The use of appropriate local anaesthetic of shorter duration
minimises the complication.
6. Antibiotic cover prior to dental surgery is advised to prevent infection.
7. Complicated oral surgical procedures should be avoided in such
patients until blood glucose levels are stabilised.
Management
• In case of known diabetic, when the patient loses consciousness or

altered level of consciousness, the first suspicion of hypoglycaemia is
made, unless otherwise proven.
• If conscious, oral sugar sources as candy or glucose solutions can be
given.
• If patient is unconscious, 20 mL of 50% dextrose IV or 1 mg glucagon
IM can be given.
Acute adrenal insufficiency

A rarely encountered factor, which may result in unconsciousness, is adrenal
crisis or acute adrenal insufficiency. Cortisol is considered to be the most
important hormone of the adrenal cortex, which helps the body to adapt to
stress and is essential for survival. Primary adrenal insufficiency owing to
destruction of adrenal cortex is extremely rare. Adrenal insufficiency
secondary to exogenous corticosteroid administration is becoming relatively
common due to the extensive use of therapeutic corticosteroids. Most
significant complication of long-term corticosteroid therapy is suppression of
adrenocorticotropic hormone (ACTH) secretion leading to adrenal atrophy
and failure to respond to stress.
Prevention of acute adrenal insufficiency

Based on history and questionnaire, acute adrenal insufficiency can be
prevented. Adrenocortical suppression should be considered if the patient has
had glucocorticosteroid therapy:
• In a dose of 20 mg or more of cortisone

• Via oral or parenteral route for a continuous period of 2 weeks or
longer
• Within 2 years of dental therapy
Nausea, fatigue, vomiting, hypotension, mental confusion, pain in the back,
abdomen, legs, which may ultimately lead to coma and death.
Acute adrenal insufficiency patients are unable to adapt to stress, therefore
their blood steroid level should be increased by administration of exogenous
steroids. Stress reduction protocol should be strictly followed. Minor
operations under LA may be performed by giving steroids (double the usual
dose) 2 h pre- and postoperatively. Aspirin and other NSAIDs should be
avoided as they may increase the risk of peptic ulceration in those on
corticosteroids. Susceptibility to infection is increased by systemic steroid use;
no prophylactic antibiotic may be indicated.
Management (Flowcharts 7.2 and 7.3)

• Terminate all dental procedures
• Monitor vital signs
• Summon medical assistance
• Administer glucocorticoid (200 mg hydrocortisone IV)
• Provide basic life support (BLS)
• Transport to hospital for emergency medical care
• Check blood level for glucose and give glucose (oral or IV) if
hypoglycaemic. Repeat 200 mg hydro cortisone at 4–6 h interval as
required and monitor BP.
FLOWCHART 7.2 Management protocol for conscious patient.

FLOWCHART 7.3 Management protocol for unconscious patient.
Step 1: Terminate dental therapy

As soon as signs and symptoms of possible acute adrenal insufficiency are
noted, dental treatment must be interrupted immediately. Acute adrenal
insufficiency should be suspected in patients who develop symptoms of
mental confusion, nausea, vomiting and abdominal pain and who are
currently receiving glucocorticosteroids or have received 20 mg or more of
cortisone (or its equivalent) by oral or parenteral administration for a period of
2 weeks or longer within the past 2 years.
Criteria for determining adrenal insufficiency
1. History of current or recent long-term steroid use

2. Mental confusion
3. Nausea and vomiting
4. Abdominal pain
5. Hypotension
Management of adrenal insufficiency

Step 2: Position the patient
If the patient appears mentally confused, wet, the patient is placed in supine
position with the legs elevated slightly or in a comfortable position.
Step 3: Monitor vital signs

Blood pressure and heart rate should be monitored every 5 min during the
episode. Hypertension and tachycardia are common.
Step 4: Summon medical assistance

Medical assistance with emergency kit and oxygen should be summoned as
early as possible. Oxygen may be administered by means of a full face mask or
nasal hood. A flow of approximately 5–10 L/min will be adequate.
Step 5: Administer glucocorticosteroid
Step 6
In a patient known to have chronic adrenal insufficiency, the immediate
administration of 100 mg of hydrocortisone sodium succinate is suggested and
should be re-administered every 6–8 h.
If possible, the 100 mg of hydrocortisone should be administered
intravenously over 30 s. The intramuscular route may be employed instead of
intravenous administration, with 100 mg (2 mL) injected into the vastus
lateralis or mid-deltoid area.
Step 7: Additional management

Additional drugs include intravenous fluids to counteract the volume
depletion and hypotension that are usually present. An Addisonian patient
may be up to 20% volume depleted. Hypoglycaemia is also treated
immediately and aggressively with intravenous administration of glucose 50%
dextrose or 1–2 mg glucagon administered IM.
Anaphylaxis
Anaphylaxis is a potentially life-threatening immune reaction. Anaphylactic
reactions may occur after a single and first-time exposure to certain substances
such as drugs. Anaphylaxis is a clinical syndrome of severe hypersensitivity
reaction characterised by cardiovascular system (CVS) collapse, respiratory
system depression, skin reactions and smooth muscle contractions.
Pathophysiology
Whenever a foreign body (antigen) enters into the host, defence mechanism
comes into play, like phagocytes and nonspecific clinical substance assisting
the removal of the foreign substance. The combination of antigen with
circulating antibody on sensitised cells apparently results in the release of
histamine which causes the spasmodic contraction of smooth muscles of
bronchioles, pulmonary arteries and GI tract. Increased capillary permeability
with resulting oedema occurs, particularly in the tracheolaryngeal mucosa,
which is life-threatening and a common cause of death in anaphylaxis.
Clinical features
Cutaneous manifestations
• Pruritus
• Urticaria
• Angioedema
• Generalised erythema
Respiratory manifestations
• Wheezing
• Coughing
• Stridor
• Dyspnoea
• Laryngeal oedema
• Respiratory arrest
CVS manifestations
• Tachycardia
• Shock
• Hypotension
• Cardiac dysrhythmia
• Cardiac arrest
GIT manifestations
• Nausea
• Vomiting
• Abdominal cramps
• Urinary incontinence
• Diarrhoea
• Tenesmus
A proper history should be taken and patient should be questioned about the
drugs to which he/she is allergic and manifestations of the allergies. When a
drug allergy is suspected, precaution must be taken to prevent the
administration of the drug and alternative should be considered. In a patient
with a history of allergy, LA is avoided and pain is controlled through the
administration of oral analgesics. Equipment, drugs and assistance needed for
the management of anaphylaxis should always be available when allergy
testing is carried out. If the allergy is confirmed, the patient should be sent to
physician for hypersensitivity testing and information should be recorded
permanently in his/her case sheet.
Management
• Terminate the dental treatment.

• If the allergic reaction is confined to the skin, an antihistamine is
administered either intravenously or intramuscularly.
• If respiratory involvement is seen, position the patient in supine
position with the legs elevated, ensure a clear upper airway and give
oxygen; administer 0.5 mL of 1:1000 epinephrine by establishing
intramuscular access. Adrenaline should be followed by an
antihistamine like chlorpheniramine 10 mg IV and 20 mg IV of
hydrocortisone.
• Repeat this every 5 min, if needed as guided by BP, pulse, until the
patient gets better. Continue oxygen at the rate of 5–6 L/min.
Adrenaline is given IM and not IV unless the patient is severely ill or
has no pulse.
In case of bronchospasm, administer salbutamol, initiate BLS and monitor

vital signs. Consider cricothyrotomy by specialist if the laryngospasm is not
relieved with epinephrine. Prepare the patient for transport to emergency care.
LA toxicity
Refer to Chapter 9 Local Anaesthesia.
Needle breakage
Foreign body aspiration

During oral surgical procedures, aspiration of foreign bodies into the airway is
always a serious problem, which might cause severe airway obstruction. This
is much more common if the patient is positioned in a supine or semi-erect
position or when there is absence of gag reflex (when the patient is sedated).
The aspirated foreign body can either obstruct the airway or might be
swallowed and pass through the gastrointestinal tract harmlessly. However,
this should be confirmed by a chest radiograph to rule out foreign body in the
respiratory tract. When a foreign body is aspirated into the larynx, violent
coughing may try to expel the aspirated material if it is small, but in case of
larger objects it might obstruct the airway and coughing cannot expel the
aspirated material. Small materials like burs, reamers, files, inlays, tooth
structure, etc. may dislodge into the oropharynx of patients who may swallow
or aspirate them. Objects swallowed into the GI tract can produce peritoneal
abscess, perforation and peritonitis. Objects aspirated into the bronchus can
produce lung abscess, pneumonia, atelectasis and infection.
Prevention
A rubber dam is very effective during any operative procedure in preventing
the swallowing of objects. Therefore, it is recommended for most procedures
except for periodontics and oral surgery where it is not feasible to use a rubber
dam. Oral packing using gauze creates a pharyngeal curtain, which effectively
prevents the entry of small instruments or fluids like blood into the airway
(under GA).
Clinical features
• Coughing
• Choking sensation
• Dyspnoea
• Stridorous breathing
• Cyanosis
Management (Table 7.5, Flowchart 7.4)

• Once a foreign body aspiration is suspected, stop the dental procedure.
• Ask the patient to cough out the obstruction.
• If the patient is unable to cough out the object, becomes apprehensive
and gasps for breath, perform Heimlich manoeuvre (Box 7.2).
• If patient losses conscious during these unsuccessful attempts, shift the
patient to the floor and perform the Heimlich manoeuvre again and
inspect the oral cavity for object. Perform ‘finger sweep’ or use Magill
forceps to remove the object if visible.
• If successful in retrieval, BLS is done based on vitals.
• If unsuccessful in retrieval, then look, listen and feel for breathing. If
the patient is breathing with adequate ventilation, then monitor vitals
and shift for hospital care.
• If the patient shows no signs of breathing it is indicative of airway
obstruction, emergency airway management should be initiated
followed by hospital-based care.
Table 7.5
Management of foreign body obstruction
Type of obstruction Management

1. Partial-adequate air exchange Encourage patient of cough and clear the airway
2. Partial-inadequate exchange Treated similar to complete obstruction
3. Complete conscious Heimlich manoeuvre-4 thrusts
Repeat till object dislodged
4. Complete unconscious Open airway ventilate-4 manual thrusts-2 finger sweeps
In case unable to ventilate reposition airway and retry
Repeat sequence till needed
FLOWCHART 7.4 Foreign body management.
Box 7.2 Method of performing Heimlich manoeuvre

(Fig. 7.9A–E)
D&E is Heimlich
Approach the patient from behind and keep your hands on the patient’s
abdomen just below the rib cage. Hands are then quickly pulled into the
abdominal area attempting to remove the residual air in the lungs which in
turn dislodges any obstruction in the airway.
FIGURE 7.9 (A) Patient choking of upper airway obstruction
typically showing distress signal of hand over the chest. (B) Back
blows performed on an adult as part of initial obstructed airway
management. (C) Note the patient is still in distress.
(D, E) Heimlich manoeuvre in a conscious patient. (F) Heimlich
manoeuvre in an unconscious patient.
Haemorrhage
Refer Chapter 15 Haemorrhage and Shock.
Haematoma
Refer Chapter 9 Local Anaesthesia.
Surgical emphysema
Refer Chapter 10 General Anaesthesia.
Comparison of various medical emergencies and their treatment
response
CHAPTER 8
Therapeutics in Oral
Surgery
Antimicrobials
Antibiotics
Classification of antibiotics
Consideration before administration of antibiotics
Factors involved in therapeutic effectiveness
Aetiologic agents of orodental infections
Properties of an ideal antibiotic
Commonly used antibiotic drugs
Penicillin
Cephalosporins
Macrolides
Clindamycin
Tetracycline
Antibiotics for special dental indications
Metronidazole
Fluoroquinolones
Prophylactic use of antibiotics
American Heart Association (Aha) guidelines—May 2007
Antifungal agents
Nystatin
Clotrimazole
Ketoconazole
Fluconazole
Bacitracin
Neomycin
Polymyxin B
Kanamycin
Antiviral agents
Analgesics
Nonsteroidal anti-inflammatory drugs
Ibuprofen
Acetyl salicylic acid (aspirin)
Phenylbutazone and oxyphenbutazone
Naproxen
Acetaminophen (paracetamol)
Centrally acting analgesics—opioids
Morphine
Codeine
Pethidine
Pentazocine
Propoxyphene
Anti-inflammatory
Steroidal anti-inflammatory drugs
Corticosteroids
Nonsteroids
Hyaluronidase
Streptokinase
Serratiopeptidase
Antiallergic
Diphenhydramine
Tripelennamine hydrochloride
Hydrocortisone
Local anaesthesia
Barbiturates
Pentobarbital sodium
Phenobarbital
Nonbarbiturate sedatives
Benzodiazepines
Diazepam
Midazolam
Lorazepam
Ethinamate
Meprobamate
Promethazine hydrochloride
Muscle relaxants
Chlorzoxazone
Dressings to protect wounds and relieve pain
Tincture of benzoin
Balsam of Peru
Surgical cement
Butyl cyanoacrylate spray
Xylocaine ointment
Triamcinolone acetonide emollient paste
White head varnish
Stimulants for circulatory failure, syncope and collapse
Ammonium carbonate
Aromatic spirits of ammonia
Amyl nitrite
Oxygen
Newer drugs
Drugs are of utmost significance in the control of infections, pain and

postoperative consequences. With trends towards increasing outpatient care,
an increasing number of medically compromised patients can be expected to
be seen in a typical dental clinic.
The mechanism of action and potential interactions of various commonly
used drugs are important to the clinician treating the medically compromised
patient to provide optimal care and prevent iatrogenic damages.
This chapter comprises a brief description of the antibiotics, anti-
inflammatory, antiallergic, analgesics, corticosteroids, sedatives and hypnotics
used in day-to-day practice.
Therapeutics in Oral Surgery
• Antimicrobial
▪ Antibiotic
▪ Antifungal
▪ Antiviral
• Analgesics
▪ NSAID (nonopioid)
▪ Opioid
• Anti-inflammatory
▪ Steroidal
▪ Nonsteroidal
• Antioedematous
• Local anaesthetics (Refer to Chapter 9 Local Anaesthesia)
• Sedatives and hypnotics
▪ Barbiturates
▪ Nonbarbiturates
• Antiallergic
▪ Antihistamine
▪ Steroidal
• Muscle relaxants
• Dressings to protect wounds and relieve pain
• Stimulants for circulatory failure, syncope and collapse
Antimicrobials
Drugs used to prevent or treat infections caused by pathogenic (disease
producing) microorganisms. This includes antibacterial (antibiotic), antiviral,
antifungal.
Antibiotics
Antibiotics are chemical substances which either kill or inhibit the growth of
microorganisms. One of the most difficult problems to manage in dentistry is
an odontogenic infection. These infections may range from low grade, well-
localised infections requiring minimal treatment to a severe, life-threatening
facial space infection. Antibiotics are used for three reasons in dentistry:
1. To treat infections of the oral cavity,
2. As preoperative prophylaxis to prevent bacterial, endocarditis and
other systemic complications in susceptible patients due to bacteraemia
caused by dental procedures
3. To prevent postoperative infection and improve healing at the
operative site.
Antibiotics are classified on the basis of chemical structure, effect, type of
organism and spectrum of activity (Table 8.1).
Table 8.1
On the basis of the chemical structure

• Sulphonamides • Quinolones
• β-lactam antibiotics • Tetracyclines
• Aminoglycosides • Macrolides
• Imidazole derivatives • Polyene antibiotics
• Polypeptide antibiotics • Nitrobenzene derivatives
• Diaminopyrimidines
On the basis of effect
• Bacteriostatic: Tetracyclines, chloramphenicol, erythromycin,ethambutol, sulphonamides
• Bactericidal: Penicillins, aminoglycosides, ciprofloxacin, rifampin, cotrimoxazole, polypeptides,
cephalosporins, vancomycin, nalidixic acid
On the basis of action against the type of organism
• Antibacterial • Antifungal
• Antiviral • Antiprotozoal
• Antihelmintic
On the basis of spectrum of activity
• Narrow-spectrum: Penicillin, erythromycin, streptomycin
• Broad-spectrum: Tetracyclines, chloramphenicol
On the basis of origin
• From fungi: Cephalosporin, griseofulvin, penicillin
• From bacteria: Bacitracin, polymyxin B, colistin
• From actinomycetes: Aminoglycosides, tetracyclines, chloramphenicol, macrolides, polyenes
Mechanisms of action
• Inhibition of cell wall synthesis: Penicillins, cephalosporins, bacitracin, vancomycin
• Destruction of cell membrane: Colistin, bacitracin, amphotericin, polymyxins
• Inhibition of protein synthesis: Chloramphenicol, erythromycin, clindamycin, tetracyclines
• Interfere with DNA functioning: Rifampicin, metronidazole
• Interfere with DNA synthesis: Acyclovir, zidovudine
• Interfere with DNA gyrase: Ciprofloxacin
• Interfere with RNA functioning: Streptomycin, gentamycin
• Antimetabolite: Sulphonamides, ethambutol, trimethoprim, pyrimethamine
Consideration before administration of antibiotics
Some of the things to be considered when antibiotics are given are efficacy,
toxicity, cost and dosage, route of administration, duration of antibiotic
treatment and the use of combination therapy. When discussing efficacy of the
drug, it is important to understand absorption, distribution and excretion
characteristics of the selected antibiotics.
Aetiology of the underlying disease

The underlying aetiology of the disease should be confirmed as being
microbial.
Culture sensitivity
Whenever possible the pus, blood, saliva, urine or other secretions should be
collected for the microorganism culture and should be tested against different
antibiotics for maximum sensitivity.
Efficiency
If the drug can reach the site of infection and be active against the pathogenic
organisms, it has good efficacy.
Toxicity
This relates to idiosyncratic reactions and dose-dependent organ damage. The
antibiotics should maintain broad effect of antimicrobial action with minimal
risk to the patient.
Age of the patient

Certain drugs are not recommended for infants like chloramphenicol which
can cause ‘grey baby syndrome’.
Pregnancy
Certain drugs are considered to be teratogenic and should not be administered
in pregnant women.
Drug resistance
Drug resistance refers to the emergence of resistant strains of bacteria. It most
commonly results due to mutation. These resistant strains survive in spite of
the antibiotic therapy. The first step mutants are usually of low resistance
whereas their descendants, i.e. the second step mutants are of higher
resistance.
Drug resistance can be minimised through the following precautions

• By using large doses in the beginning of treatment in order to inhibit
the growth of the organisms and the first step mutants.
• The antibiotic treatment should be continued for a period that is long
enough to substantially reduce the viable organisms. Therefore,
antibiotics are prescribed for a period of more than 3 days.
• Combination therapy involving use of two drugs (which does not
show any crossresistance) with synergistic or additive action helps in
reducing the development of resistant strains.
Drug allergy
If the patient gives a history of allergy to any particular drug, an alternative
should be considered.
Agents that inhibit cell wall synthesis

Antibiotics require growing cells (cells synthesising new cell wall material) to
exert a bactericidal effect. Likewise, if little growth is occurring a bacteriostatic
agent has little to affect (e.g. penicillins and cephalosporins).
Cost
This involves price of the agent, frequency of the doses and duration of
treatment. Newer drugs may be available in the market which may be more
costly but not necessarily more effective.
Dosages
This should maintain serum levels within wide or narrow margins between
therapeutic and toxic levels. Usually drugs with narrow margins of safety are
calculated on the basis of the patient’s condition and severity of the infection.
Oral therapy is indicated for low to moderate-grade infections whereas
parenteral therapy should be considered in compromised patients or in more
serious infections as blood serum and tissue levels are achieved more rapidly.
Duration of treatment is dependent on type and severity of infection, organism
sensitivity, patient’s clinical improvement and is typically continued for 5–
14 days.
Combination therapy
This is usually indicated for more severe life-threatening infections to achieve
appropriate antibiotic therapy. The advantage of multiple antibiotic therapy
results from the synergistic nature among antibiotics. Combinations of
antibiotics are indicated in infections caused by Pseudomonas, enterococcal
group D streptococci, resistant pathogens and life-threatening infections.
Advantages
• It helps in achieving additive synergistic activity of the antibiotics.
• Due to synergistic combination, the doses of individual drug are
reduced which, in turn, reduces adverse effects of the individual drug.
• It reduces the development of drug resistance.
• It widens the spectrum of activity of the drugs and hence can be used
against many mixed infections and in other infections where the
bacterial diagnosis is unknown.
Disadvantages
• Increased cost of therapy.

• Increased risk of adverse effects when both the drugs have adverse
effects.
• Increased risk of super infection by the resistant organisms.
• Alteration of the normal flora.
Factors involved in therapeutic effectiveness
Incision and drainage of abscesses
• The avascular nature of the abscess hinders the distribution of an

antibiotic to the centre of the infectious foci.
• Abscesses are usually caused by anaerobic bacteria which grow slowly
and produce an infection that is difficult to treat.
• Proper incision and drainage helps in removing a number of causative
bacteria; it allows the killing of strict anaerobes by exposure to oxygen.
Age and extent of infection

Chronic and well-established abscess consists mainly of a large number of
slowly growing bacteria against which both bactericidal and bacteriostatic
agents may be relatively ineffective. A higher concentration of antibiotic may
be required for an infection with a large number of bacteria.
Bactericidal vs. bacteriostatic antibiotics

In a patient with impaired immune function, a bactericidal antibiotic is
preferable to a bacteriostatic agent. By killing the bacteria, less reliance is
placed on host defence processes, which are ultimately responsible for the
eradication of the infection.
Antibacterial spectrum
Narrow-spectrum antibiotics are preferred if the antibacterial activity includes
the aetiologic agents, because: (1) they are often more effective when
compared to broad-spectrum agents against a specific group of
microorganisms and (2) the likelihood of superinfection is reduced as they
have less effect on the normal microflora.
Route of administration and timing of dosage

Most antibiotics are given orally and usually on an empty stomach, to prevent
destruction by gastric acidity.
Dosage regimen
Adequate concentration of the antibiotic must be attained at the infection site
as inadequate concentration leads to destruction of less susceptible bacteria
and the development of a resistant infection. An average of 5–7 days of
therapy is required; however, with severe infections or lowered host
resistance, a longer duration may be required.
Distribution of antibiotic in the body

In order to be effective, an antibiotic must gain access to the infected site,
whether it is in bone, soft tissue or an area with a poor blood supply. Most
antibiotics gain ready access to oral soft tissues.
Metabolism and excretion of antibiotics

When choosing an antibiotic, the dentist should have a thorough knowledge of
the patient’s medical history, such as in case of a renal insufficiency, avoid a
drug that is excreted by the kidney or at least mandate a reduction in dosage.
Patient factors (pregnancy) (Tables 8.2–8.3)

The use of antimicrobial agents during pregnancy is associated with varying
degrees of risk; utmost care is required when antibiotic administration is
contemplated, especially during the first trimester:
• Streptomycin, one of the first drugs to be linked to fetotoxicity, has

been associated with damage to the cranial nerve VIII and skeletal
defects.
• Tetracyclines used during the last trimester of pregnancy cause
hypoplasia of teeth and bones of the foetus and have been associated
with the occurrence of congenital cataracts.
• Maternal hepatic toxicity can be caused with tetracycline use during
pregnancy.
• Other antibiotics like sulphonamides and chloramphenicol cross the
placenta and are contraindicated.
• Some antibiotics are secreted into milk and may present problems for
the nursing infant.
Table 8.2
Drug usage in the pregnant patient
Table 8.3
Drugs to avoid in the nursing mother

Drug Effect on nursing infant
Metronidazole Potential for tumorigenicity. Nursing may be resumed 48 h after drug has been
stopped
Antihistamines Newborns and infants have increased sensitivity to antihistamines
Benzodiazepines These drugs can cause sedation in infants
Aetiologic agents of orodental infections

Orodental infections are generally caused by various Gram-positive aerobes, a
few Gram-negative aerobes (rarely found) and an array of Gram-positive and
Gram-negative anaerobes. Infections that are characterised by cellulitis tend to
contain more aerobic bacteria, whereas an abscess is predominately anaerobic
in nature. Often, orodental infections include a complex mix of both anaerobic
and aerobic bacteria in which the anaerobic species predominate by about a 2:1
ratio.
The types of microorganisms present in orodental infections include (in
decreasing number of isolates):
• Bacteroides (including Prevotella and Porphyromonas species)

• Alpha-haemolytic streptococci
• Peptococci
• Peptostreptococci
• Fusobacterium
• Eubacterium
• Unspecified streptococci
• Actinomyces
• Veillonella
• Beta-haemolytic streptococci
• Staphylococcus aureus
• Propioni bacterium
The most commonly isolated aerobic species were alpha-haemolytic

streptococci. The most commonly isolated anaerobes were bacteroides and
species previously grouped in that genus, such as Prevotella melaninogenica.
The mixture of bacteria seen in orodental infections may increase
pathogenicity through a type of bacterial synergism. For example, P.
melaninogenica is not usually pathogenic; however when added to other
bacterial species, pathogenic mixtures can form, producing an orodental
infection. It may be that the other bacteria supply the vitamin K needed for the
growth of P. melaninogenica, which in turn, provides the infection with its
destructive component, because of its ability to produce proteolytic enzymes
such as collagenase.
Properties of an ideal antibiotic
• It should be bactericidal, yet exhibit the narrowest antibacterial

spectrum to minimise superinfections
• Should not induce bacterial resistance
• Should be absorbed well orally
• Should be acid stable
• Should have uniform distribution into bone as well as soft tissue. It
should achieve a tissue concentrations, well above the minimum lethal
concentration (MLC) for the causative microorganisms and at
reasonable doses
• Should possess reasonable half-life so that not more than 3 times a day
dosing is required
• Should not be toxic to the patient
• Should not exhibit side effects or drug interactions in the patient
• Should be readily excreted
Commonly used antibiotic drugs

Penicillin
Penicillin remains the first-choice antibiotic for the initial treatment of most
acute odontogenic infections. Penicillin compounds may be divided into two
groups:
i. Natural penicillins
ii. Semisynthetic penicillins
Naturally occurring penicillins

Among these, penicillin G and penicillin V are the most commonly used.
Semisynthetic penicillins
These penicillins are produced by chemically combining specific side chains or
by incorporating specific precursors in the mould cultures.
In this category are some compounds that are not inactivated by
staphylococcal penicillinase. These are used in the management of ‘resistant’
staphylococcal infections. They are oxacillin and methicillin.
Oxacillin and methicillin have relatively narrow ranges of antibacterial
activity, but are effective against Staphylococci resistant to the other types of
penicillin. Now strains resistant to methicillin (MRSA-methicillin resistant S.
aureus) and Vancomycin (VRSA-vancomycin resistant S. aureus) being treated
by Linezolid, quinupristine/dalftopristin and daptomycin.
Penicillin V
Spectrum
The antibacterial spectrum of penicillin V includes:
• Gram-positive cocci (streptococci, some nonresistant staphylococci and

pneumococci).
• Gram-positive rods (Bacillus, Coryne bacterium, Clostridium and other
genera).
• Most oral anaerobes such as Bacteroides, Porphy-romonas, Prevotella,
peptococci, peptostreptococci, Actinomyces, Veillonella, Eubacterium,
Eikenella, Capnocytophaga, Campylobacter, Fusobacterium and others.
• Penicillin V also is effective against Treponema pallidum and some other
spirochetes.
Many of the microorganisms listed in this paragraph are involved in
odontogenic infections. The semisynthetic compounds are effective against
many strains of penicillinase-producing staphylococci and their use generally
should be confined to this area.
Action
They are bactericidal in action. They are effective only against organisms that
are actively reproducing.
Dosage
The average adult dosage is 600,000 to 1,200,000 units daily. When necessary,
much larger doses may be given with little danger of toxicity. The average
adult dosage of phenoxymethyl penicillin (penicillin V) is 125–250 mg 4 times
daily. This dosage also applies to the semi-synthetic penicillins.
Administration
Penicillin may be administered orally, intramuscularly or intravenously.
Adequate blood levels can be achieved with penicillin V via the oral route. For
most patients who are not critically ill, this is probably the most desirable
method of administration.
Precautions
Penicillin is the antibiotic most frequently involved in untoward reactions.
1. Avoid penicillins in patients with a history of allergy or one who has

ever reacted unfavourably to the drug. Patients with a history of
asthma, hay fever or other allergy are more prone to have a sensitivity
reaction to penicillin. Patients may have cross-sensitivity to penicillin.
2. Injectable penicillinase may be used to neutralise penicillin. This must
be used with care, since some severe allergic responses have been
reported to penicillinase itself. Theoretically, penicillinase will have no
neutralising effect on the semi-synthetic penicillin compounds.
Adverse effects
These include allergic reactions of all kinds and gastrointestinal disturbances.
Patients allergic to one penicillin derivative should be considered allergic to all
derivatives unless proved otherwise.
Semisynthetic penicillin
Amoxicillin
• It is effective against Gram-negative bacteria as well as Gram-positive
bacteria and most oral anaerobes.
• It is slightly less active than penicillin V against Gram-positive cocci,
except enterococci for which it is more active.
• Amoxicillin has been shown to be active in vitro against Actinobacillus
actinomycetemcomitans.
• Its broader spectrum has advantages in those situations where
extended-spectrum penicillin is important.
• Amoxicillin yields effective concentration that are higher than
equivalent dose of penicillin V, because of its better oral absorption
and lower binding to plasma protein (20% for amoxicillin versus 80%
for penicillin V).
• Amoxicillin, infact, would be the drug of choice for treatment of
orodental infection.
• It has greater potential to produce superinfection of the gastrointestinal
tract and vagina (because of its broader spectrum of activity against
Gram-negative aerobes) and its tendency to produce skin rash (9%), a
possible consequence of allergic reactions to the 6-amino side chain of
amoxicillin.
• Amoxicillin is currently indicated for the treatment of mixed Gram-
positive and Gram-negative aerobic infections (e.g. some periodontal
infections).
• It may also be useful in treating early onset periodontitis and refractory
periodontitis.
• Lastly, amoxicillin may retain clinical efficacy against infections
involving streptococci or other species resistant to penicillin V by a
mechanism other than beta-lactamase production.
Dosage
500 mg 8 hourly—oral.
Amoxicillin with clavulanic acid (Augmentin)
• The addition of clavulanic acid which has essentially no antibacterial

activity of its own but beta-lactamase enzymes makes amoxicillin
more effective against many bacteria (e.g. Bacteroides, Haemophilus,
Peptococcus, Peptostreptococcus and Staphylococcus) that have become
resistant to amoxicillin by elaboration of beta-lactamase enzymes.
• When treating infection where beta-lactamase production is a problem,
amoxicillin with clavulanic acid may be a useful choice while awaiting
culture and sensitivity tests (it should be noted again that both
anaerobic, as well as aerobic culture and sensitivity tests should be
obtained).
Dosage
Available in dosages as 375 mg (Amox 250 mg + Clauv 125 mg), 625 mg
(Amox 500 mg + Clauv 125 mg), 1 g (Amox 875 mg + Clauv 125 mg). Used
according to the severity and the site of the infection.
Cloxacillin and dicloxacillin
• These are penicillin derivatives which are not in-activated by beta-

lactamase enzymes.
• They are less effective than penicillin V against most Gram-positive
cocci and their use is reserved for the treatment of infections caused by
nonmethicillin-resistant, penicillinase-producing S. aureus.
• Since S.aureus exists in 1% or less of the isolates causing orodental
infection, it is unlikely that the use of dicloxacillin or cloxacillin in
dentistry will often be needed.
Ampicillin
Ampicillin is active against both Gram-positive and Gram-negative organisms,
including Escherichia coli.
Carbenicillin
It is active against Pseudomonas; these agents have very specific usage
indications and should not be substituted for the natural penicillins.
Cephalosporins
• The cephalosporins comprise a group of beta-lactamase antibiotics that

structurally resemble the penicillins.
Classification
First-generation cephalosporins
• Cefadroxil
• Cephalexin
• Cephaloridine
• Cephalothin
• Cephapirin
• Cefazolin
• Cephradine
Second-generation cephalosporins
• Cefaclor
• Cefoxitin
• Cefprozil
• Cefuroxime
Third-generation cephalosporins
• Cefdinir
• Cefixime
• Cefpodoxime Ceftibuten
• Ceftriaxone
• Cefotaxime
Fourth-generation cephalosporins
• Cefepime
• Cefluprenam
• Cefozopran
• Cefpirome
• Cefquinome
• There are more than 20 cephalosporins, of which 8 can be given orally.

• The mechanism of action of cephalosporins is almost identical to that
of the penicillins.
• Of the orally active cephalosporins only cefaclor, cefuroxime and
cefprozil (second generation) have significant activity against
anaerobes Gram-positive and Gram-negative organisms and are
therefore preferred for orodental infections.
• Some first-generation cephalosporins, despite poor anaerobic activity,
are used to treat dental infections such as dentoalveolar abscess.
• Their clinical effectiveness may be due to their activity in killing
aerobes that deplete oxygen in the local environment and facilitate the
growth of anaerobes.
• The major problem with resistance has been with staphylococci, which
are rarely present as aetiologic agent in orodental infections but are
important contaminants of surgical or traumatic skin wounds.
• A number of cephalosporins may reach therapeutic concentrations in
osseous tissues (bone concentrations) after administration of usual
doses and are useful for bone and joint infections caused by
susceptible microorganisms (e.g. cephalexin, cefoperazone, has been
shown in alveolar bone and is active against various Gram-positive
aerobic bacteria found in dental infections).
• The bactericidal action of cephalosporins is beneficial for patients with
a compromised immune system.
• The restricted activity of the orally active first-generation and second-
generation cephalosporins against anaerobes limits their usefulness in
treating orodental infections of anaerobic aetiology (e.g. periapical
abscesses).
• It is imperative to note; however, that cephalosporins can be cross-
allergenic with the penicillins. They may be used cautiously only if the
patient’s reaction to penicillin was not of the immediate type.
Cephalosporins cannot be used in patients who have exhibited
anaphylactic reactions to any penicillin derivative.
• It is noteworthy that these orally active second-generation
cephalosporins are considerably more expensive than erythromycin or
clindamycin, which usually would be effective in treating such
anaerobic orodental infections.
• Third and fourth-generation cephalosporins have antipseudomonal
activity, extended activity against Gram-negative and anaerobes than
first and second generations.
• All third and fourth generation cephalosporins cross the blood brain
barrier except cefoperazone.
Dosage
• Cefaclor 250 mg 8 hourly—oral

• Cefuroxime 500 mg 12 hourly—oral
• Ceproxil 500 mg 24 hourly—oral
Macrolides
• The macrolide antibiotics appropriate for treating dental infections are

erythromycin (various dosage formulations), clarithromycin and
azithromycin.
• The use of erythromycin for treatment of common orodental infections
of bacterial origin is second only to that of the penicillin derivatives,
but it should be borne in mind that resistance develops rapidly.
• Therefore, patient compliance, adequate dosage and duration of
therapy are essential and minimum inhibitory concentrations should
be maintained at the site of infection.
• Erythromycin occupies a secondary position to penicillin because:
1. It is usually bacteriostatic rather than bactericidal
2. Resistance can develop quickly to erythromycin
3. It is slightly inferior to the penicillins in eradicating most
orodental infections. However, erythromycin is an excellent
alternative drug for treating infections in patients allergic to
penicillin.
• Erythromycin is effective against most of the aerobic Gram-positive
microorganisms that cause orodental infections and it also exhibits
good activity against many oral anaerobic bacteria.
• The drug has been used successfully for treating oral infections, such
as pericoronitis, periapical abscesses, periodontal abscesses, cellulitis,
infected cysts, purulent osteitis, various forms of infectious stomatitis
and necrotising ulcerative gingivitis (NUG).
• The average adult dose is 250 mg every 6 h. Some cases of
gastrointestinal disturbance have been observed, but these occur very
rarely.
• Clarithromycin and azithromycin, although more expensive than
erythromycin, may be of value in treating susceptible orodental
infections in patients in whom erythromycin causes gastrointestinal
disturbances.
• Clarithromycin is also more active than erythromycin (2–4 times)
against streptococci, staphylococci and anaerobic bacteria. There may
be cross-resistance between erythromycin and new macrolides,
particularly among streptococci and staphylococci.
Clindamycin
• Clindamycin is well suited to treat certain orodental infections.

• Its spectrum encompasses most aerobic and anaerobic microorganisms
encountered in orodental infections, but its antibacterial spectrum is
not so broad as to cause significant superinfections.
• An important exception is pseudomembranous colitis caused by
overgrowth of Clostridium difficile.
• Clindamycin is bacteriostatic.
• However, it may achieve bactericidal concentrations for certain
bacteria.
• It is well absorbed after oral administration, has minimal adverse
effects (except diarrhoea and pseudomembranous colitis), gives high
active concentrations in bone and soft tissues and exhibits few
problems of resistance development by microorganisms.
• Clindamycin is usually taken orally, but can also be given parenteral if
patients cannot tolerate oral administration. It should be considered as
an alternative for treatment of orodental infections caused by
susceptible Gram-positive cocci or Gram-positive or Gram-negative
anaerobes.
• Clindamycin is indicated for purulent osteitis or other bone infection and
infections caused by anaerobic organisms, such as Bacteroides species or by
other pathogens that cannot be eradicated by penicillin or one of the
macrolide antibiotics.
• Clindamycin is useful in treating dentoalveolar abscesses and chronic
infections.
Tetracycline
The broad-spectrum bacteriostatic tetracycline antibiotics have been employed
extensively in the treatment of infections. Their widespread use and often
misuse, has resulted in the appearance of a number of resistant bacterial
strains, a fact that has reduced their clinical usefulness. Tetracyclines used for
treatment of orodental infections are tetracycline, minocycline and
doxycycline.
• At best, the tetracyclines are fifth-choice antibiotics, behind the penicillins,

macrolides, cephalosporins and clindamycin in the treatment of acute
orodental infections.
• Tetracyclines may be useful in treating certain types of periodontal
disease. A 2-week course of tetracycline therapy has been found to be
effective in patients with advanced periodontitis unresponsive to
conventional therapy alone.
• Tetracyclines are also useful in treating juvenile periodontitis and early
onset periodontitis.
• Higher concentration of tetracyclines, especially minocycline, in
gingival fluids, may help eradicate bacteria resistant to concentrations
that can normally be achieved in the plasma.
• Studies of tetracycline and doxycycline have indicated enhanced repair
and tissue regeneration of the periodontium and prevention of
recurrent periodontitis in high-risk patients. The tissue collagenase-
inhibiting effect of the tetracyclines, is relatively marked in the
gingival crevice because the drugs are concentrated several folds in
sulcular fluid.
• Although tetracyclines should not be used as a penicillin substitute for
prophylaxis against bacterial endocarditis, since many of the causative
organisms are resistant, they may have a role in preventing
endocarditis after dental therapy.
Dosage
Tetracycline: 250–500 mg 4 times daily.
Doxycycline
50–100 mg once or twice daily.
Antibiotics for special dental indications

There are several antibiotics that are frequently used in medicine but are only
occasionally indicated for dentistry. These include metronidazole for strict
anaerobic infections, ciprofloxacin for oral treatment of Pseudomonas infection and
penicillinase-resistant penicillins for infections caused by penicillinase-producing
strains of Staphylococcus.
Metronidazole
• Metronidazole is active only against obligate anaerobic bacteria, but

within this range it is highly efficacious against the groups most
responsible for clinical diseases: Bacteroides, Prevotella,
Porphyromonas, Eubacterium, Fusobacterium, Veillonella,
Campylobacter, Capnocytophaga, Clostridium, Treponema,
Peptococcus and Peptostreptococcus.
• Metronidazole has been shown to be an effective drug for the
treatment of NUG, but its use in the majority of dental infections, at
least as a single agent, will probably be limited by which lack of
effectiveness against aerobic and facultative bacteria.
• When given along with alcohol, it produces a disulfiram like reaction.
Dosage
400–800 mg 8 hourly depending on disease severity.
Fluoroquinolones
• Ciprofloxacin and ofloxacin are of potential use in dentistry.

• At present, the only therapeutic application for ciprofloxacin is as an
orally active agent for an orodental infection caused by a susceptible
species of Pseudomonas.
• Nevertheless, the drug is active against a variety of aerobic and
facultative organisms implicated in infections involving oral structures
and its use is being explored.
• Because ofloxacin has a broader spectrum of activity against oral
anaerobes, it may be preferred for orodental infections
Antibiotic drug interactions
Antiobiotic Drugs interacting Reaction
with antibiotic
Penicillins Erythromycin, Bacteriostatic drugs will inhibit protein synthesis
tetracycline antagonising the effect of penicillins
Amoxicillin Oral If given concomitantly will reduce the effectiveness of the
contraceptives contraceptives resulting in breakthrough bleeding and risk of
ovulation
Clindamycin Oral If given concomitantly will reduce the effectiveness of the
(Cleocin) contraceptives contraceptives resulting in breakthrough bleeding and risk of
ovulation
Erythromycin Cyclosporine Increases the serum level of both medications
Phenytoin Increased levels of both medications. Phenytoin (dilantin)
level should be monitored to avoid toxicity
Oral Same as in penicillin
contraceptives
Theophylline Erythromycin is associated with increases in theophylline
serum levels that could lead to toxicity due to competitive
binding to a specific enzyme that is responsible for
metabolising theophylline
Warfarin Increases activity of warfarin. Increased INR
Metronidazole Alcohol Absolutely contraindicated, could cause flushes, nausea,
vomiting, headaches and chest pain
Cimetidine Decrease in plasma clearance of metronidazole
Phenobarbital and Reduces metroindazole serum levels, half-life time and
phenytoin effectiveness
Warfarin sodium Potentiation of anticoagulation effect
Ciprofloxacin Antacids All if given concomitantly with ciprofloxacin could interfere
with its absorption
Aminophylline, Could cause severe and fatal reactions including cardiac
Aminophylline, Could cause severe and fatal reactions including cardiac
dyphylline, arrest, seizures, respiratory failure and status epilepticus
theophylline and
all its products
Caffeine Its clearance is decreased by ciprofloxacin and the t1/2 is
increased
Cyclosporine Increased nephrotoxicity of cyclosporine
Phenytoin Potential reduction in phenytoin levels and triggering of
seizure activity
Warfarin sodium Enhanced anticoagulation effect
Tetracycline Antacids Impairs the absorption of tetracycline and thus reduces the
serum concentration and efficiency of the antibiotic
Iron Iron pills will decrease the effectiveness of tetracycline
Oral Depressed plasma level of prothrombin activity
anticoagulants
Oral Reduced efficiency and increased incidence of breakthrough
contraceptives bleeding and risk of ovulation
Penicillins Interference with bactericidal action of penicillins
Dosage
400 mg 8 hourly.
Prophylactic use of antibiotics

• Infective endocarditis
• Cerebrospinal rhinorrhoea
• Compound facial or skull fractures
• Major oral and maxillofacial surgery (e.g. osteotomies or tumour
resection)
• In surgery of immunocompromised or debilitated patients or following
radiotherapy to the jaws.
Many dental procedures cause a transient bacteraemia and as a result

certain categories of patients may be placed at risk of developing bacterial
endocarditis or other systemic infections. Prophylactic use of antibiotics has
been shown to protect patients.
1. At risk of bacterial endocarditis or endarteritis.

2. With a history of nephrotic syndrome.
3. At risk of infection due to impaired host defence mechanisms because
of disease state.
4. At risk of infection because of drugs they are taking (e.g.
corticosteroids).
5. From infection following oral or maxillofacial therapy due to severe
traumatic injuries (e.g. fracture of the mandible) to the head and neck
regions.
6. In patients with prosthetic heart valves, a controversial category of
patients for whom antibiotic coverage is sometimes recommended in
those with prosthetic knees, hips and elbows.
Prophylaxis against wound infection
• Routine use of antibiotics is not generally indicated as most dental

procedures, including exodontia and simple periodontal surgery, are
not associated with a high-risk of infection.
• However, for orthognathic surgery, prophylactic antibiotics are often
used. This is to avoid the risk associated with the extensive soft tissue
and bone involvement in the surgery.
• Placement of endosseous implants also presents a significant risk of
infection and antibiotic prophylaxis should be considered.
• Placement of tetracycline impregnated in an absorbable dressing has
been reported to be associated with a reduced incidence of dry socket.
The tetracycline is well tolerated and is often combined with a topical-
glucocorticoid to reduce postoperative discomfort. Presumably, the
antibiotic reduces bacterial growth in the socket, thus minimising
microbial fibrinolytic activity and preserving clot integrity.
• In clinical practice, more difficult the case the more likely an antibiotic
will be prescribed or used by the surgeon. Difficulty may be estimated
by such measures as length of procedure, degree of instrumentation
and amount of bone removed. In addition, the presence of local
infection (e.g. pericoronitis) increases the risk of postoperative
complications.
• In general, for patients not at special risk, prohylactic antibiotic use for
dental or simple oral surgical procedures is not indicated and should
be discouraged.
There are numerous medical conditions which predispose patients to

bacteraemia-induced infections. Because it is not possible to predict when a
susceptible patient will develop an infection, prophylactic antibiotics are
recommended. These prophylactic antibiotics are administered when these
patients undergo procedures that are at risk for producing bacteraemia
(Table 8.4). This guideline is intended to help practitioners make decisions
regarding antibiotic prophylaxis for dental patients at risk. An effective
antibiotic regimen should be directed against the most likely infecting
organism, with antibiotics administered shortly before the procedure. When
procedures involve infected tissues or are performed on a patient with a
compromised host response, additional doses or a prescribed postoperative
regimen of antibiotics may be necessary.
Table 8.4
Regimens for a dental procedure
IM, Intramuscular; IV, intravenous.

a
Or other first- or second-generation cephalosporin in equivalent adult or paediatric
dosage.
b
Cephalosporins should not be used in an individual with a history of anaphylaxis,
angioedema or urticaria with penicillins or ampicillin.
Dental procedures and endocarditis prophylaxis
1. Standard general prophylaxis for patients at risk: Amoxicillin: Adults,

2.0 g (Children, 50 mg/kg) given orally 1 h before procedure.
2. Unable to take oral medications:
Ampicillin: Adults, 2.0 g (Children, 50 mg/kg) given IM or IV within
30 min before procedure.
3. Amoxicillin/Ampicillin/Penicillin—Allergic patients:
Clindamycin: Adults, 600 mg (Children, 20 mg/ kg) given orally 1 h before
procedure.
Or
Azithromycin or clarithromycin: Adults, 500 mg (Children, 15 mg/kg)
orally 1 h before procedure.
4. Amoxicilin/Ampicillin/Penicillin—Allergic patients unable to take oral
medications: Within 30 min before the procedure.
Or
Cefazolin: Adults, 1.0 g (Children, 25 mg/kg) IM or IV 30 min before
procedure.
Endocarditis prophylaxis recommended
• Dental extractions
• Periodontal procedures including surgery, scaling and root planing,
probing and recall maintenance
• Dental implant placement and reimplantation of avulsed teeth
• Endodontic (root canal) instrumentation or surgery only beyond the
apex
• Subgingival placement of antibiotic fibres or strips
• Initial placement of orthodontic bands but not brackets
• Intraligamentary local anaesthetic injections
• Prophylactic cleaning of teeth or implants where bleeding is
anticipated
Endocarditis prophylaxis not recommended
• Restorative dentistry (operative and prosthodontic) with or without

retraction cord
• Local anaesthetic injections (nonintraligamentary)
• Intracanal endodontic treatment; postplacement and build up
• Placement of rubber dams
• Postoperative suture removal
• Placement or removal prosthodontic or orthodontic appliances
• Taking of oral impressions
• Fluoride treatments
• Taking of oral radiographs
• Orthodontic appliance adjustment
• Shedding of primary teeth
American heart association (Aha) guidelines—May 2007

Conditions of highest risk
Included
• Prosthetic heart valves

• Prior endocarditis
• Cyanotic heart disease
▪ Unrepaired
▪ Repaired congenital heart disease with prosthetic material or
device within 6 months
▪ Repaired with residual defects
• Heart transplant with ‘valvulopathy’
Not included
• Bicuspid aortic valve

• Acquired aortic or mitral valve disease
▪ MVP with regurgitation
▪ Prior valve repair
• Hypertrophic cardiomyopathy with latent or resting obstruction
Dental procedures
All dental procedures that involve manipulation of gingival tissue, periapical
region of the teeth or perforation of the oral mucosa.
• Dental extractions
• Periodontal procedures
• Endodontic instrumentation
• Prophylactic cleaning
• Initial placement of orthodontic bands (not brackets)
Indications for prophylaxis
• Unrepaired cyanotic congenital heart disease, including palliative shunts

and conduits
• Completely repaired congenital heart defect with prosthetic material or
device, whether placed by surgery or by catheter intervention, during the
first 6 months after the procedure
• Repaired congenital heart disease with residual defects at the site or
adjacent to the site of a prosthetic patch or prosthetic device
Antifungal agents
Nystatin
• Topical nystatin is historically the most commonly used drug for

treatment of candidal infections of the oral cavity (oral moniliasis,
thrush, denture stomatitis).
• The adult dosage is 3 mL (300,000 units) of suspension in each side of
the mouth (600,000 units), which is swished and held in the mouth for
5 min before swallowing.
• This treatment should be repeated every 4 h for at least 10 days or 48 h
after disappearance of all clinical symptoms.
• For nystatin pastilles (200,000 units each), one or two may be dissolved
in the mouth 4–5 times daily.
• Denture stomatitis may be treated by lining the tissue surface of the
denture with the ointment form (100,000 units/g).
Clotrimazole
• Clotrimazole is a highly effective, more palatable alternative to

nystatin that is administered topically for treatment of oral candidias is
in the form of a troche (lozenge).
• Slow dissolution allows binding to the oral mucosa from which it is
gradually released to exert its anti-fungal activity.
• The swallowed drug is variably but poorly absorbed, therefore it is
considered a topically applied antifungal agent.
• Clotrimazole is not used systemically.
• The dosage regimen is a 10 mg troche dissolved in the mouth, 5 times
daily, for at least 14 days.
• 1% cream or lotion is available for cutaneous candidiasis and
dermatophytoses.
Ketoconazole
• Ketoconazole is useful in treating chronic mucocutaneous candidiasis.

• Although very effective against oral candidiasis, it should be reserved
for cases refractory to other antifungal agents.
• Ketoconazole given orally interacts with a number of drugs, including
terfenadine and astemizole (may cause serious cardiac arrhythmias).
• When ketoconazole is given systemically, the daily dosage regimen is
200–400 mg orally; it is also applied topically as a 2% cream.
Fluconazole
• Fluconazole is the drug of choice for systemic management of

candidiasis.
• Studies have shown a 96% and 79% cure rate in oropharyngeal
candidal infections with fluconazole and clotrimazole, respectively.
• Drug interactions are less of a problem than with ketoconazole;
however, fluconazole can inhibit the metabolism of cyclosporine,
phenytoin, oral anticoagulants, sulphonylureas and zidovudine.
• The daily dose of fluconazole is 100–200 mg orally.
Bacitracin
• It is bactericidal and effective against Gram-positive organisms when

given at the dosage of 500 units per gram of soluble base.
• The route of choice is topical.
• The drug may also be administered intramuscularly but renal damage
has been reported.
Neomycin
• Bactericidal.
• Effective against Gram-positive and Gram-negative organisms at the
dosage of 5 mg per gram of soluble base.
• The route of choice is topical.
• The drug may also be administered orally and intramuscularly.
• Systemic administration may cause renal damage and possible damage
to the cranial nerve VIII.
Polymyxin B
• Bactericidal
• Effective against Gram-negative organisms and bacilli
• The usual dose is 0.1%–0.25% in aqueous solution
• The route of choice is topical
• The drug may also be administered intramuscularly and orally
• Systemic administration may cause renal damage and damage to the
nervous system
Kanamycin
• Effective against many forms of staphylococci that may be resistant to

other agents.
• Daily dosage should not exceed 2 g given in 2–4 divided doses.
• The drug should be given intramuscularly.
• It may be given orally in preparation for surgery of the gastrointestinal
tract.
• The drug is nephrotoxic and may also cause deafness because of its
toxic effect on the cranial nerve VIII.
• These newer antibiotics seem to be active against many strains of
resistant staphylococci.
• Their chief field of usefulness is in this area.
• They are not recommended for treatment of the more common
conditions caused by susceptible organisms.
Antiviral agents
• Idoxuridine has been used for herpetic lesions in the mouth.
• Some success has been claimed when the drug is applied
iontophoretically to the lesions.
• Acyclovir is available for topical or systemic (oral) administration.
• In the patient with a normal immune system, neither the ointment nor
systemically used drug appears to have a major effect on the severity
or duration of herpes labialis.
• Otherwise, the agent is used topically and/or systemically in
immunocompromised patients for treatment of initial or recurrent
mucocutaneous herpetic lesions.
• Oral therapy is also effective in preventing reactivation of herpes
simplex virus in immunocompromised patients.
Analgesics
Analgesics are the drugs that relieve pain regardless of its source and type.
Control of postoperative pain following oral surgery involves choosing the
analgesic regime that is appropriate for each patient. Analgesics can be
divided into two groups based on their site of action:
i. Peripherally acting analgesics—nonsteroidal anti-inflammatory drugs

(NSAIDs)
ii. Centrally acting analgesics—opioid
Non-steroidal anti-inflammatory drugs

Management of acute postsurgical pain is essential to adequately treat oral
and maxillofacial surgery patients. Postsurgical pain can be managed
effectively by using specific treatment methods that are well justified by
current research. These methods include:
• Comprehensive presurgical consultation

• Consideration of the use of sedation or general anaesthesia
• Use of long-acting local anaesthesia
• Administration of an oral analgesic prior to the time of surgery
• Meticulous and careful surgery
• Administration of a perioperative glucocorticoid
• Postoperative convalescence
• A regularly administered analgesic for 48–72 h
• Consideration of rescue medications
• Return for evaluation of unusual or unexpected pain, as necessary.
Use of such strategies gives the clinician the greatest probability of effective
pain management. Pain control by the use of opioids and NSAIDs are the most
common therapies.
Mechanism of action
NSAIDs interfere with the production of prostaglandins in the surgical
wound. Specifically, the conversion of arachidonic acid into prostaglandins by
cyclooxygenase (COX) is inhibited. Prostaglandins are nociceptive compounds
that enhance pain by sensitising primary afferent nerves, i.e. they reduce the
threshold at which these nerves are activated to send pain signals to the
central nervous system (CNS). Reduction of prostaglandins in the surgical
wound results in a diminished intensity of pain by essentially elevating the
threshold at which pain afferent nerves discharge.
Advantages associated with use of NSAIDs
• NSAIDs are effective and useful analgesics for postsurgical pain and
can be administered in a variety of formulations (oral, tablet and
liquid) and dosages.
• A major advantage to the use of these agents is that there is no risk of
addiction and abuse potential is low.
• The adverse effects associated with NSAIDs occurs, especially when
the patient is monitored post surgically for unanticipated or
continuing pain.
• Moreover, the cyclooxygenase-2 pathway inhibitors may prove to have
fewer adverse effects.
• Current preliminary data have shown that NSAIDs have a topical
effect when applied to a surgical wound and a local effect when
injected in or around an area of wounded tissue. If this route of
administration proves to be feasible, it is possible that many of the
adverse effects associated with NSAIDs might be avoided.
Adverse drug reaction

NSAIDs are administered orally in most situations. Although side effects
occur infrequently when they are administered judiciously, they do act
systemically, thereby contributing to potential adverse effects. Additionally,
recent data have shown that pharmacologically induced reduction of
nociceptive neuropeptides may have an adverse effect on fibroblast
proliferation as part of the reparative healing process.
• NSAIDs inhibit COX, they also decrease the production of

thromboxane A2, a potent platelet aggregating agent, thus increasing
the potential for bleeding.
• Inhibition of the gastric prostaglandins, especially prostaglandin E2
and prostacyclin, has an adverse effect on the gastrointestinal (GI)
mucosa, which also increases the potential for bleeding.
• The greatest risk with the use of NSAIDs is spontaneous GI
haemorrhage.
• If an NSAID is administered concomitantly with an anticoagulant, the
potential for bleeding increases markedly.
• NSAIDs also have an adverse effect on the genito-urinary system. A
decrease in renal blood flow and the rate of glomerular filtration has
been observed in patients with chronic renal disease. For this reason,
NSAIDs may be contraindicated in patients taking diuretics and are
certainly contraindicated in patients with severe renal disease.
NSAIDs are also associated with nephrotoxicity when taken
chronically or in combination. Additional GI side effects include
dyspepsia, peptic ulcer, dysphagia and abdominal pain. To minimise
the possibility of these adverse events, NSAIDs should be taken after
meals or with food. Patients predisposed to GI disease should take
NSAIDs with caution. In patients with a history of alcohol abuse or
peptic ulcer disease, extra caution should be used.
Aspirin and NSAIDs have significant risk potential for severe allergic
reactions or anaphylaxis. This phenomenon has been attributed to
prostaglandin synthesis inhibition, driving the inflammatory mediator
pathway towards lipoxygenase metabolism, thereby increasing wound
concentrations of the slow-releasing substance of anaphylaxis.
Patients with a history of aspirin sensitivity, allergic reactions to multiple
medications or asthma are at particular risk. Other potential adverse effects,
such as cardiovascular (tachycardia, oedema), CNS (dizziness, headache) and
hepatic (increased liver enzymes) have been reported, but occur less
frequently.
Ibuprofen
Mode of action
Nonsteroidal anti-inflammatory agent which reduces prostaglandin activity by
inhibiting prostaglandin synthesis.
Indications
Control postsurgical pain. Peak blood levels obtained within 1–2 h stays active
as an analgesic for 4–6 h.
Side effects
Gastrointestinal problems like nausea, dyspepsia, heartburn, vomiting and
abdominal pain can occur. More severe problems such as gastric ulceration
and bleeding can occur in patients using ibuprofen for prolonged period of up
to 1 year. Changes in vision, tinnitus, aseptic meningitis, increased fluid
retention and skin disorders have also rarely been reported with ibuprofen.
Contraindications
History of allergic reactions to ibuprofen, other NSAIDs and aspirin. Not
recommended for pregnant or nursing women.
Precautions
Ibuprofen inhibits platelet aggregation but this effect usually causes small
changes in bleeding time in normal patients. This is less than that seen with
aspirin. Patients on anticoagulant therapy or with intrinsic bleeding disorders
can be at risk for haemostatic problems with the concurrent use of ibuprofen.
Patients with decreased renal or liver function, heart failure or under
diuretic therapy can be at risk for liver dysfunction, renal failure and fluid
retention while taking ibuprofen.
Dosage
200–400 mg; 4–6 hourly.
Acetyl salicylic acid (aspirin)

Mode of action
Its analgesic action is explained by synergism between prostaglandins and
pain producing substances like Bradykinins released by the inflammatory
process. The inhibition of prostaglandin synthesis leads to analgesia by raising
the threshold of pain. The antipyretic action results from inhibition of
prostaglandin synthesis in hypothalamus.
Anti-inflammatory effects are also derived from their ability to inhibit
prostaglandin synthesis. Since prostaglandins are potent vasodilator agents,
aspirin provides symptomatic relief from inflammatory effects.
Indication
It is an effective analgesic for mild to moderate degrees of pain.
Side effects
Sensitive reactions may manifest as rashes, swelling, asthma and rarely
anaphylaxis. Ingestion can promote nausea, vomiting, bronchospasm and
gastrointestinal bleeding due to erosion of mucous membrane.
Precautions
Young children are highly susceptible to aspirin poisoning (therapeutic
overdose).
Dosage
325–650 mg 4–6 hourly as an analgesic
Phenylbutazone and oxyphenbutazone

Mode of action
Same as aspirin.
Indication
These drugs are potent antiinflammtory and poor analgesics.
Side effects
These drugs have been proved to cause a granulocytosis, leukopaenia. They
are also known for causing gastric irritation.
Precautions
Retention of sodium and water may aggravate hypertension and congestive
cardiac failure.
Precautions to be taken for any dental procedure if the patient is in aspirin.
However, their judicious use is advocated for the pronounced anti-
inflammatory effect.
Naproxen
Mode of action
Nonsteroidal anti-inflammatory agent which reduces prostaglandin activity. It
has anti-inflammatory analgesic and some antipyretic activity.
Contraindication
History of allergic reactions to naproxen, other NSAIDs and aspirin.
Precautions
Naproxen inhibits platelet aggregation but this effect usually causes small
changes in bleeding time in normal patients. This is less than that seen with
aspirin.
Patients on anticoagulant therapy or with intrinsic bleeding disorders can be
at risk for haemostatic problems with the concurrent use of naproxen. Patients
with decreased renal or liver function, heart failure or under diuretic therapy
can be at risk for liver dysfunction, renal failure and fluid retention while
taking naproxen.
Dosage
500 mg 8 hourly.
Acetaminophen (paracetamol)
Mode of action
Peripheral and centrally active analgesic and antipyretic, minimal anti-
inflammatory activity. Hence, it is not categorised as NSAIDs.
Indications
Control of postsurgical pain. Peak blood levels obtained within 30 min to 1 h
stays active as an analgesic for 4–6 h.
Side effects
Minimal side effects.
Contraindication
History of allergic reaction to acetaminophen.
Dosage
500 mg 8 hourly, maximum of 4 g/day.
Centrally acting analgesics—opioids

Centrally acting analgesics include the opiates (morphine and codeine) and
opiate like analgesics (methadone and meperidine). Here, the exact site and
mechanism of analgesia are not certain but it is clear that these drugs produce
their analgesic action by affecting the CNS and not by peripheral actions.
Advantages
• Opioids have been used as analgesic medications widely and are the
cornerstone for the management of moderate to severe acute pain.
• They have effects on specific opioid receptors (κ and µ) in neural
tissues, substituting or enhancing the effect of chemically similar
endogenous compounds, specifically, endorphins and enkephalins.
• Opioid receptors are present in the CNS, but have also been discovered
in peripheral primary afferent nerve fibres.
• Opioids can be administered via many more routes than NSAIDs,
including transdermal, oral, intramuscular, intravenous, transmucosal,
intranasal and other routes.
• As a medication to control acute pain caused by oral and maxillofacial
surgical procedures, opioids are prescribed in combination with
acetaminophen or NSAIDs (including aspirin) administered orally.
• In a hospital setting, parenterally administered opioids are more
common, with novel methods of delivery; patient controlled analgesia
has been used frequently and has proved to be efficacious.
Risks associated with the use of opioids

The effects that opioids exert on opioid receptors are also responsible for their
adverse effects. As with the NSAIDs, the adverse effects of opioids are caused
by systemic interactions.
Drug interactions with commonly used pain medications

Pain control Drugs interacting Reaction
medication
Aspirin Aluminium carbonate, Concurrent administration delays the rate of
aluminium hydroxide, absorption as aspirin.
sodium bicarbonate,
magnesium oxide
Oral hypoglycaemic May cause hypoglycaemia by competing with the
hypoglycaemic agent for binding sites in the
plasma causing an increased level of the free
hypoglycaemic agent available in the circulation.
Warfarin/oral Aspirin will potentiate the anticoagulation effects
anticoagulants by inhibiting platelet clumping and by displacing
oral anticoagulants from plasma protein to
increase its activity in preventing synthesis of pro-
thrombin.
Acetaminophen Rifampin—barbiturates Decreases the analgesic effect of acetaminophen.
Increased risk of acetaminophen induced
hepatotoxicity
Chronic use of ETOH Increased potential for hepatotoxicity even with
normal doses of acetaminophen.
Oxycodone CNS depressants, Increased CNS depression.
Hydrocodeine anxiolytic hypnotics,
Codeine narcotic analgesics,
sedatives, MAO inhibitors,
tricyclic antidepressants
Ibuprofen Aspirin Potential net decrease in anti-inflammatory
activity.
Increased risk of GI irritation.
Thiazides Reduced natriuretic effect
Oral anticoagulants Potential increased risk of bleeding.
Naproxen Aspirin Aspirin displaces naproxen sodium from its
sodium binding sites causing an increased rate of excretion
of naproxen sodium thus shortening its
therapeutic time.
ACE inhibitors and beta- May decrease the antihypertensive effect of the
blockers ACE inhibitor.
Oral anticoagulants Prothrombin time may be affected. Bleeding time
may be increased.
Furosemide Natriuretic effect is inhibited.
Glipiside, glyburide, Increased potential for drug toxicity.
sulphonamides,
anticonvulsants
Warfarin Increase in bleeding time.
• Universal fear of patient abuse and dependence.

• However, studies have shown that opioids used for pain relief in
patients without a history of opioid dependence do not produce drug-
related behaviour that would be suggestive of drug dependence or
abuse.
• Opioids when used in the management of postoperative pain have
been associated with nausea and vomiting.
• Gastric intolerance is a significant adverse drug reaction to the use of
opioid medications.
• The additional GI side effect of constipation has been more often
associated with parenteral in-hospital use than it has with short-term
administration as a combination analgesic.
• Because of the respiratory depressive effect associated with opioids,
they are contraindicated in patients with chronic respiratory
impairment, e.g. chronic bronchitis or chronic obstructive pulmonary
disease (COPD), head injury.
• Other adverse effects have been reported to involve the genitourinary
system (urine retention), the CNS (hallucinations, psychomimetic
effect) and the GI system (hepatic toxicity). These adverse effects are
seen infrequently with short-term use for acute postoperative oral and
maxillofacial surgical pain.
Morphine
Mode of action
Depresses the cerebral cortex and raises the threshold to afferent pain stimuli.
Indications
Pain relief, sedation sleep and as preanaesthetic medication.
Side effects
Nausea, vomiting and constipation.
Contraindications
Morphine releases histamine from the tissues, resulting in mucosal oedema,
bronchospasm and consequently difficulty in breathing. So, it is
contraindicated in patients with respiratory distress, acute head injury.
Precautions
• Because of its depressant action on respiratory centre and pupillary

constriction, it should not be administered in head injuries and lung
diseases.
• Due to the drug dependence, withdrawal symptoms begin with a
sense of craving for this drug. Later, the patient develops anxiety,
agitation, restlessness followed by depression.
Codeine
• Codeine is the methyl ether of morphine.
• This is a naturally occurring analgesic.
• It is considerably more potent than the antipyretic analgesics.
• It is nonaddictive.
• Produces no disturbing side effects except constipation and dryness of
mouth.
Pethidine
• Pethidine is a major synthetic analgesic.

• Its pharmacologic action is similar to morphine.
• Unlike morphine, respiration is not depressed.
• Euphoria, addiction, dependence and sedation are similar to morphine.
• It is particularly useful when short duration of analgesic action is
required and as preanaesthetic medication.
• Contraindications are similar to that of morphine.
Pentazocine
• This benzomorphine derivative has a potent analgesic and a weak

opioid antagonist activity.
• It does not cause euphoria.
• As an analgesic it is half as effective as morphine and can cause
respiratory depression.
• It has a shorter duration of action than morphine hence is not
recommended in myocardial infarction.
Propoxyphene
• Propoxyphene is a less potent analgesic; side effects are similar to

codeine, the abuse potential is less than Methidine.
• The potential for sedative side effects (especially among patients taking
CNS depressants, barbiturates, hypnotics, alcohol and other opioids) is
concern.
• However, this CNS side effect may, in many instances, be considered
an advantage, because opioids are widely used to induce sedation and
relieve anxiety, in addition to producing analgesia.
Anti-inflammatory
Steroidal anti-inflammatory drugs
Corticosteroids
Corticosteroids are naturally occurring substances produced by the adrenal
cortex. Synthetic corticosteroids are used extensively in all aspects of clinical
medicine as they possess potent anti-inflammatory and immunosuppressive
properties.
Perioperative use of corticosteroids has been advocated for reduction of
pain, oedema and trismus following oral surgical procedures. Short-acting
products such as hydrocortisone are the least potent. Prednisolone and
methylprednisolone, which are intermediate-acting products, are 4–5 times
more potent than hydrocortisone. Dexamethasone is a long-acting, systemic
corticosteroid; its potency is about 25 times greater than the short-acting
products.
Systemic steroids can be used as adjuvant analgesics in the treatment of
neuropathic and cancer-related pain.
Classification
Duration of action
Short-acting
Cortisol (hydrocortisone)
Cortisone
Prednisone
Prednisolone
Methyl prednisolone
Intermediate-acting
Triamcinolone
Long-acting
Betamethasone
Dexamethasone
Anti-inflammatory action of corticosteroids
• Corticosteroids inhibit many of the processes associated with

inflammation, which include decreased production of prostanoids
owing to decreased expression of cycloxygenase-2, decreased
generation of cytokines [interleukin (IL)-1 to IL-8 and tumour necrosis
factor-alpha (TNF-α)], reduction in the concentration of complement
proteins in the plasma, decreased histamine release from mast cells.
• At the cellular level, corticosteroids reduce poly-morphonuclear

leukocyte (PMN) chemotaxis and phagocytosis.
Hydrocortisone
Uses
The anti-inflammatory and immunosuppressive effects of hydrocortisone are
utilises in the treatment of:
1. Inflammatory ocular, dermatological and bowel conditions

2. Asthma
3. Allergic reactions and shock
4. Rheumatoid diseases
5. Immunosuppression and organ transplantation
6. Malignancies, particularly leukaemias
7. Cerebral oedema.
Hydrocortisone can also be used as replacement therapy in:
1. Adrenal insufficiency
2. Congenital adrenal hyperplasia.
Mechanism of action
• Hydrocortisone is the endogenous glucocorticoid cortisol, which is

released at times of stress and disease.
• Hydrocortisone increases the synthesis of lipocortin-1, which in turn
inhibits the activity of phospholipase A2, leading to a decrease in
synthesis of prostaglandins, thromboxane and leukotrienes.
• This is essential for preparation of the body for assault, as well as
dampening the immune response to disease which can be potentially
self-destructive in the absence of cortisol.
• Hydrocortisone exerts its effects by regulating gene expression in
target tissues, which generally leads to a delay of hours between its
administration and any observed clinical effects.
• Anti-inflammatory and immunosuppressive properties of
hydrocortisone are very complex and are brought about by effect on
blood vessels, inflammatory cells (lymphocytes, monocytes and
granulocytes) and inflammatory mediators.
• Hydrocortisone decreases the synthesis of vasoactive chemicals such as
histamine, cytokines, lysosomal enzymes and various components of
the complement system.
• The exact mechanism by which this inhabitation takes place may
involve the inhibition of arachidonic acid release.
Perioperative corticosteroid use

• Perioperative use of corticosteroids has been advocated for reduction
of pain, oedema and trismus following oral surgical procedures.
• Corticosteroids reduce the amount of inflammation associated with
oral surgery, especially oedema.
• Corticosteroid doses ranging from 80 to 625 mg hydrocortisone
equivalent anti-inflammatory dosage. No significant adverse reactions
were noted.
• The potential for complications induced by perioperative corticosteroid
use, such as adrenal suppression and delayed wound healing, should
also be considered.
• In patients with prolonged steroid therapy the adrenocortical activity

is suppressed; in such patients supplementary hydrocortisone should
be given.
• Prolonged presence of steroid in blood results in decreased output of
ACTH. This results in decreased function and atrophy of the adrenal
cortex. Rapid withdrawal of hydrocortisone results in adrenal crisis.
• For the routine activity, level of secretion may be sufficient. But in case
of stress as in any minor or major dental surgical procedure, the
adrenal cortex may be unable to secrete more to cope up with the
stress.
• Even minor surgery may prove disastrous. Therefore, such patients
should be hospitalised and supplemented with double the usual dose
2 days before surgery and 2 days after surgery. Later on the dose is
gradually tapered.
Implications in dentistry
• Recurrent oral ulceration may be treated with topical steroids, but
maintaining long enough contact between the steroid and the oral
lesion is often difficult.
• Severe oral lesions like pemphigus, erosive lichen planus, etc. need to
be treated with systemic corticosteroids.
• Intrarticular hydrocortisone may be injected in the temporomandibular
joint to relieve refractory pain and stiffness from joint inflammation.
• Sometimes, acorticosteroid is needed to suppress pain and swelling
due to dental surgery (e.g. impacted third molar extraction).
• In case of patients who are/have been in recent past on long-term
corticosteroid therapy, consideration has to be given to the need for
supplementary prophylactic corticosteroid to cover a dental
procedure.
• In general, simple extractions and other mildly traumatic surgeries do
not warrant additional steroid dose.
• For traumatic procedures and those to be performed under general
anaesthesia, supplementary steroids may be needed, particularly if the
dose and duration of steroid therapy are such as to have caused
significant adrenal suppression or the patient is excessively anxious.
Anti-inflammatory actions of corticosteroids applicable to dentistry
Oral ulceration and oral mucosal lesion
• Corticosteroids are widely used in the treatment of recurrent aphthous

ulceration and other oral mucosal lesions such as lichen planus,
mucous membrane, pemphigoid and pemphigus.
• Many of these conditions are treated by topical applications and
examples of such preparations include hydrocortisone sodium
succinate oromucosal tables (2.5 mg), triamcinolone acetonide 0.1% in
an adhesive base (Orabase), betamethasone spray (50–100 µg) and
betamethasone soluble tablets (500 µg) dissolved in water and used as
a mouthwash.
• Applying any topical medication to the oral mucosa is difficult and
often the best results are achieved when there is maximal contact time
between the lesion and the medication.
• For severe cases of oral ulceration, systemic corticosteroids may be
necessary and the drug of choice is prednisolone.
Bell’s palsy
• This is unilateral facial paralysis affecting one or more branches of the

facial nerve.
• Bell’s palsy is of unknown aetiology, but may be subsequent to a viral
infection.
• Systemic prednisolone is the treatment of choice and therapy must be
started within 5–6 days of onset of the paralysis.
• It is usual to start off treatment with prednisolone with a high dose,
reducing this over a period of 10 days.
Postoperative pain and swelling after dental surgery
• There has been much interest in the use of systemic corticosteroids to

reduce pain and swelling after removal of impacted lower third
molars and after orthognathic surgery.
• Methyl prednisolone and betamethasone are the corticosteroids used
for this purpose, usually administered intramuscularly just before
surgery or dexamethasone intravenously.
• The efficacy of corticosteroids for reducing post-operative pain after
dental surgical procedures remains uncertain and such pain may
respond better to an NSAID.
Steroid drug and anti-inflammatory dosage
Cortisol (hydrocortisone)—100 mg
Prednisolone—5 to 10 mg for postoperative swelling, used up to 30 mg
tapering dosage in case of acute neural inflammation as in Bell palsy
Methyl prednisolone—4 to 48 mg/day orally (adult dose).
Intermediate-acting
Triamcinolone—topical
Long-acting
Betamethasone—Adult: 0.5–5 mg daily

Dexamethasone—8 mg b.d. or t.d.s. according to the need
Nonsteroids
Refer to NSAIDs on page 154.
For the prevention of traumatic oedema and the treatment of postoperative
and traumatic oedema, certain enzymes and antihistamines may be used.
Hyaluronidase
Hyaluronidase is an enzyme prepared from mammalian testes and acts by
depolymerising hyaluronic acid an essential component of intracellular
ground substance which determines the permeability of tissues.
Mechanism of action
It causes breakdown of the intercellular cement by hydrolysing hyaluronic
acid, mucoitin acid and chondroitic sulphuric acid, leading to the permeability
of connective tissues.
Hyaluronidase should not be injected locally if infection is present without
the adequate coverage of an antibiotic to which the organisms involved are
sensitive. It should not be injected directly into an abscess but around it.
Injections can be made intraorally or extraorally.
Hyaluronidase helps in:
• Resorption of persistent swellings from injuries or operative

procedures
• Elimination of muscular trismus
• Providing better nutrition to flaps and skin grafts
• Treatment of temporomandibular joint disturbances.
The injection of a few drops of a local anaesthetic into the surface is

recommended, but deep infiltration should be avoided since epinephrine
constricts the blood vessels. Pressure applied after the injection is beneficial.
Inserting a gauze pack intraorally or an ice bandage to apply a pressure pack
extraorally can accomplish this. No pain or other untoward effects should
result. Hyaluronidase (for injection)—Vial contains 150 turbidity reducing
units (TRU). Dissolve in 1–5 mL sterile saline solution.
Streptokinase
Streptokinase tablets contain 10,000 units of streptokinase and at least 2500
units of streptodornase, a concentrated combination of enzymes elaborated by
haemolytic streptococci.
Mechanism of action
• Streptokinase brings about lysis by removing the barrier and limiting

membrane in areas of oedema.
• It improves circulation, which facilitates the action of body defence
and the effect of antibiotics.
• It activates plasminogen, a component of blood plasmin is formed,
which acts on the fibrin present in large amounts in oedema fluids
which prevents ecchymosis.
Steroids Interacting Reaction

drug
All Antacids Decreased absorption of orally administered corticosteroids.
glucocorticoids
Anticoagulants Corticosteroids may oppose anticoagulation action.
(oral)
Barbiturates, Decreased effects of corticosteroids.
carbamazepine
Contraceptives Decreased corticosteroid clearance. (Increase t1/2), thus
(oral) increasing the therapeutic dosing time with increased
therapeutic effects.
Digitalis Increased risk of digitalis toxicity associated with
hypokalaemia.
Diuretics Increased risk of hypokalaemia.
Hydantoins Increased corticosteroid clearance, thus decreasing therapeutic
effects.
Isoniazid Decreased the serum concentration of isoniazid making it less
effective.
Macrolides Decreased methyl prednisolone clearance.
Salicylates Decreased serum salicylate levels, thus decreasing the
effectiveness of the salicylate.
Theophylline Alterations in the activity of theophylline may occur.
Theophylline levels should be monitored.
Uses
• Anti-inflammatory effect
• Postoperative oedema
• Swelling
• Abscesses
• Haematomas associated with fractures or operative procedures
• Prevent ecchymosis caused by extravasation of blood
The tablets are placed into the buccal pouch and allowed to dissolve slowly
so that absorption can take place from the mucosa. The swallowed enzymes
are destroyed by gastric acidity. Results are obtained in 24–48 h. In case of
infections, antibiotics should be given simultaneously.
Dose
Streptokinase tablets use one quarterly (6 h).
Serratiopeptidase
• Serratiopeptidase is a proteolytic enzyme.

• It hydrolyses Bradykinin, histamine and serotonin responsible for
oedematic status.
• It reduces swelling, improves microcirculation, etc.
It has anti-inflammatory, antioedemic and fibrinolytic activity and acts

rapidly on localised inflammation. It acts by binding to alpha-2-macroglobulin
in the blood in the ratio of 1:1, which helps to mask its antigenicity but retains
its enzymatic activity and is slowly, transferred to site of inflammation.
Serratio-peptidase when consumed in unprotected form is destroyed by acid
in the stomach.
However, enteric coated granules enable the enzyme to pass through the
stomach unchanged and be absorbed in the intestine. It is found negligibly in
urine suggesting that it is transported directly from the intestine into the blood
stream.
Adverse effects
Hypersensitivity reactions, such as rash or redness, may infrequently occur.
Anorexia, gastric discomfort, nausea or vomiting may infrequently occur.
These can be minimised if the tablets are taken after meals.
Dose
10–20 mg one quarterly (6 h).
Antiallergic
Adrenalin
• Adrenalin is the drug of choice for anaphylactic shock from any cause
in addition to oxygen, which should be administered promptly.
• This drug is important in the treatment of allergic diseases since it will
quickly relieve the patient in acute attacks of angioneurotic oedema
and urticaria.
• Other types of allergic reactions are overcome by direct competitive
action with histamine due to a physiologic antagonism.
• It is administered through the subcutaneous route because through its
local vasoconstrictor action it is absorbed so slowly that excessive
action is avoided.
• Intravenous injections are used in emergency only. 0.15 mL of a 1:1000
solution is drawn into the syringe and is diluted with water to make
1 mL.
• 0.05 mL of the diluted solution is injected slowly. Repeat at the rate of
0.1 mL every 30 s until the syringe is empty. In severe emergency as
much as 1–2 mL of adrenalin 1:1000 may have to be administered.
Diphenhydramine
Diphenhydramine is considered one of the best anti-histamines. It also acts as a
sedative and causes some drowsiness and is also used for motion sickness. It is
the second drug of choice often used in the management of emergency as
anaphylaxis for controlling the uncontrolled histamine release from mast cell
de-granulation.
Allergic emergency dosage: 1 mg/kg IV (up to 50 mg).
Tripelennamine hydrochloride
This drug also has excellent antihistamine action. It is a sedative. It is used in
conjunction with penicillin (q.v.) to eliminate allergic reactions frequently
caused by penicillin.
Dose
Tripelennamine hydrochloride, 25 mg, PO quarterly 4 h after meals.
Hydrocortisone
Classification
Corticosteroid (short-acting)
Hydrocortisone (Cortisol) is a steroid of the glucocorticoid class. Its anti-
inflammatory and immunosuppression property is used in emergency
management of allergies as anaphylaxis. It is the second drug of choice to
adrenaline. It mainly acts by:
1. Anti-inflammatory—decreases laryngeal oedema thereby life saving

2. Bronchodilation
3. Immunosuppression.
Emergency indications and actions
• To prevent further deterioration in patients severely affected by an

anaphylactic reaction.
• Acute asthma exacerbations.
• Acute adrenal crisis.
• Life-threatening reactions require large doses of hydrocortisone as
well. Inj. hydrocortisone takes several hours to exert its effect.
• Naturally it is not so useful in acute anaphylactic reactions but it can
prevent the relapse of symptoms when the effect of adrenaline is over
(Table 8.5).
• In acute asthma exacerbations or status asthmatics, patients cannot
inhale inhalational glucocorticoids properly. These patients may
require IV hydrocortisone along with other measures like O2
inhalation, IV fluid therapy and nebulised or SC salbutamol, etc.
• Hydrocortisone inhibits the synthesis of prostaglandins and
leukotrienes and reduces the inflammation or bronchial tree and
alveoli.
Table 8.5
Emergency drugs and their effects
Drug Use
Adrenaline Restores blood pressure
Antihistamine, e.g. chlorphenamine Reduces effects of histamine (vasodilation and oedema)
Hydrocortisone Reduces oedema and inflammation
Salbutamol Bronchodilation
Atropine Restores heart rate in bradycardia
Aminophylline Bronchodilation
Dosage
In anaphylactic reaction, inj. hydrocortisone sodium succinate (100–200 mg) is
administered IV after adrenaline.
In asthma exacerbations, 200 mg (children 100 mg) is administered IV every
6 h.
Intravenous therapy with hydrocortisone is soon replaced by oral
prednisolone once clinical improvement is evident.
Adult: 100–500 mg IV
Paediatric: 1–2 mg/kg IV
Contraindications
Hydrocortisone should not be used in patients with active untreated infections
or in patients with known alcohol or bisulphate hypersensitivity.
Precautions
Chronic treatment may lead to adrenal suppression. Therefore, the lowest dose
for the shortest period of time must be used. Hydrocortisone should be used
with caution in patients with hypothyroidism or cirrhosis.
Adverse reactions and side effects

Adverse reactions and side effects are more common when hydrocortisone is
used at high doses and for long-term therapy.
CVS: hypertension
CNS: headache, restlessness, depression, personality changes
ENT: increased intraocular pressure
GI: anorexia, nausea, vomiting, peptic ulcer formation
Drug interactions
Hydrocortisone may cause an increased risk of hypokalaemia with the use of
diuretics. Hypokalaemia may increase the risk of digoxin toxicity.
Hydrocortisone may increase the risk of GI effects with the concurrent use
with NSAIDs, including aspirin.
Local anaesthesia

Goals of sedatives and hypnotics in oral surgery
• Alleviate patient’s fear and anxiety

• Sedate and calm the patient intraoperatively
• Minimises pontaneous movements intraoperatively
• Alter patient’s recall (anterograde amnesia)
• Maintain protective reflexes (conscious sedation)
• Allow rapid and complete recovery in outpatient settings
• Achieve safe and effective pain and anxiety control (intraoperatively
and postoperatively)
Barbiturates
These drugs are derived from barbituric acid. They are used for simple
insomnia, neurosis and hysteria. They are also used to prevent excitation,
convulsions and sometimes after local anaesthesia and postoperative
struggling, nausea and vomiting.
Pentobarbital sodium
Pentobarbital sodium is a sedative. Its action is of relatively short duration.
However, it has a more prolonged hypnotic effect. It is used orally as
premedication the night before an operation to assure the patient of a good
night’s rest and shortly before an anaesthetic is used.
Dose
For sedation
Pentobarbital sodium, 0.1 g per orally. If deep hypnosis is desired, a double
dose may be given—0.2 g per orally.
Phenobarbital
Phenobarbital is the slowest acting barbiturate. Phenobarbital sodium, which
has a greater solubility, acts more rapidly. Used orally before an operation
under local anaesthesia, it gives excellent sedation.
Dose
Sedation
Phenobarbital sodium, 0.03 g PO
Hypnosis
Phenobarbital, 0.1 g PO
Nonbarbiturate sedatives
These are recent drugs that are nonhabit forming and have none of the
disadvantages of barbiturates, which in large doses produce depression and
coma.
These are excellent for the management of neurotic, refractory patients and
nervous and apprehensive children.
Benzodiazepines
These are well suited for moderate and deep sedation because of their
anxiolytic, amnesic and sedative properties. These drugs provide sedation and
retrograde amnesia with minimal effect on cardiovascular and respiratory
systems in healthy patients. They do not provide analgesia.
Commonly used drugs are:
• Midazolam (Versed)
• Diazepam (Valium)
• Lorazepam (Ativan)
Mechanism of action
They act by facilitating the gamma aminobutyric acid (GABA) receptors in
brain. GABA is the chief inhibitory neuropeptide in brain. They are highly
lipid soluble and rapidly enters the CNS and binds to GABA receptors. This
results in the opening of the chloride channels and hence reduces excitability.
Clinical effects
• Moderate to deep sedation

• Anxiolysis
• Hypnosis
• Anterograde amnesia
• Anticonvulsant
• Spinal cord mediated skeletal muscle relaxation
The clinical effects of each benzodiazepine are due to binding to GABA

receptors at different sites.
Adverse effects
• Cardiovascular, haemodynamic changes and respiratory depression

becomes more significant when given in combination with steroid.
• Longer elimination and greater anxiety in elder patients.
• Venoirritation may occur in case of diazepam and lorazepam.
Diazepam
• Water insoluble and highly lipid soluble and hence enter the brain
rapidly
• Used as sedative, anxiolytics, amnesic and anti-convulsant drug
• Highly protein bound
• Metabolised in liver producing oxazepam and dimethyl diazepam as
two active metabolite
Dosage
Adult—2.5–10 mg slowly over 2 min, Titrate: 2–5 mg every 5–10 min,
maximum—20 mg Paediatric—0.1–0.3 mg/kg increment over minimum of
3 min, maximum 0.6 mg/kg
Premedication oral dose—0.2–0.4 mg/kg.
Contraindications
Decreased albumin concentrations like burns, malnutrition, liver disease,
sepsis and renal dysfunction may increases its effects.
Side effects
• Painful on injection—(since it is dissolved in propylene glycol and

sodium benzoate)
• Withdrawal effect—(due to abrupt discontinuation of drug after
prolonged use) causing anxiety, hyperexcitability and seizures
Midazolam
• Short-acting
• Water-soluble benzodiazepines
• Used as sedative, anxiolytics, amnesic and anticonvulsant drug
• 2–3 times more potent than diazepam commonly used in procedural
sedation
• Bound strongly to plasma proteins
• Metabolism is by hydroxylation in liver
• Excretion is by kidney after conjugation
Dosage
Adult—0.5–2.5 mg slowly over 2 min, titrate 0.5 mg increments, maximum
5 mg.
Paediatric—0.05–0.1 mg/kg, titrate 0.25 mg/kg every 5 min, maximum
0.2 mg/kg
Premedication oral dose—0.5 mg/kg.
Contraindication
Obese patient—due to increase volume of distribution and prolonged half-life
of drug.
Lorazepam
• Long-acting benzodiazepines
• Similar properties of midazolam and diazepam
• Potent amnesic property
• Metabolised in liver to inactive metabolites
• Slower onset of action with slower metabolic clearance compared to
midazolam
• Used for longer procedures requiring amnesia, sedation and anxiolysis
Dosage
Adult—0.02–0.05 mg/kg slowly over 2 min, may repeat 1/2 dose every 10–15
min, maximum 2 mg
Paediatric—0.05 mg/kg over 2 min, may repeat 1/2 dose every 10–15 min,
maximum 2 mg
Premedication oral dose—0.05 mg/kg.
Ethinamate
Ethinamate is a nonbarbiturate compound recommended for preoperative
sedation of ambulatory patients. It is a sedative hypnotic, which produces
CNS depression. It produces sedation in a relatively short time and the
duration of its effect is shorter than that of other oral hypnotics. There are no
known contraindications to its use. In the usual dosage, it has no specific effect
on blood pressure, pulse or respiration.
Dose
Ethinamate, 500 mg, PO for premedication.
Meprobamate
Meprobamate is an interneural blocking agent, in which effects resemble the
barbiturates. It is effective in anxiety states; it lessens tension, reduces
irritability and restlessness and has muscle-relaxing properties. It has a
prolonged action and is useful in conditions in which emotional stress is a
factor.
Dose
Meprobamate, 400 mg, 1 tablet, PO t.i.d.
For dental procedures

1 tablet once a day, 1 tablet 1/2 to 1 h before appointment; then 1 tablet t.i.d.
(children, 1/2 tablet only).
Promethazine hydrochloride
Promethazine hydrochloride (Phenergan) is a mild sedative. It can be injected
intravenously to relieve apprehension and to produce light sleep. It may also
be administered orally, 25 mg, the evening before operation and
intramuscularly, 50 mg, 1 h before the operation. If used as a preoperative
sedative, it also prevents postoperative nausea and vomiting, especially if
repeated at 2–4 h intervals, if indicated.
It is also one of the most potent antihistaminic drugs. It prevents
bronchospasm and has been used to protect against allergic reaction. It
counteracts anaphylactic shock.
Dose
Promethazine, 25–50 mg, PO, Promethazine, 1 mL (25 mg), IV.
Muscle relaxants
The following drugs are used mostly for muscle hyperactivity and muscle
spasm which occur as a secondary phenomenon in association with musculo-
skeletal pain.
• Carisoprodol
• Cyclobenzaprine
• Methocarbamol
• Chlorzoxazone
Chlorzoxazone
Chlorzoxazone is a centrally-acting agent for painful musculoskeletal
conditions.
Mechanism of action
• Chlorzoxazone acts primarily at the level of the spinal cord and

subcortical areas of the brain.
• It inhibits multisynaptic reflex arcs involved in producing and
maintaining skeletal muscle spasm of varied aetiology.
Uses
• It helps in reduction of the skeletal muscle spasm with relief of pain

and increased mobility of the involved muscles.
• Chlorzoxazone tablets are indicated as an adjunct to rest, physical
therapy and other measures for the relief of discomfort associated with
acute, painful musculoskeletal conditions (Trismus).
Dosage
250–750 mg 3–4 times a day.
Metabolism
Chlorzoxazone is rapidly metabolised and is excreted in the urine, primarily in
a conjugated form as the glucuronide.
Adverse reaction
• Gastrointestinal bleeding
• Drowsiness
• Dizziness
• Malaise
• Overstimulation
• Allergic-type skin rashes
• Petechiae or ecchymoses
• Angioneurotic oedema or anaphylactic reactions that are extremely
rare
• Discoloration of the urine resulting from aphenolic metabolite of
chlorzoxazone in some patients
Dressings to protect wounds and relieve

pain
Oral wounds have to be dressed to protect bare bone or to prevent food from
contaminating the wound and causing pain. Such dressings are generally
applied on iodoform tape or in case of large wounds, iodoform gauze, which
does not unfurl as easily.
Tincture of benzoin
• Benzoin, 20% in alcohol, is a protective and soothing agent.

• Iodoform gauze is saturated with it and applied as needed to fill a
wound or cover it.
• Benzoin is used as an antiseptic treatment for dry, cracked skin and as
an expectorant for respiratory conditions such as severe bronchitis.
Balsam of Peru
• Balsam of Peru is a resin extracted from the bark of the Peruvian

balsam tree.
• It is an antiseptic that combats bacteria, promotes wound healing and
kills parasites, especially scabies.
• Balsam of Peru is used externally for infected and poorly healing
wounds, burns, dry socket, bedsores, frostbite, leg ulcers, bruises
caused by artificial limbs and haemorrhoids.
• It is a dark brown, viscid liquid, which has an agreeable odour.
• It is not sticky and does not harden.
• Saturated gauze may be placed intraorally into a resection wound, on
the denuded hard palate or into a bone cavity to protect the wound,
prevent pain and allow granulation to take place beneath. It may be
left for several days.
Surgical cement
• Ward surgical cement is very useful in periodontal surgery.

• The cement consists of a powder (zinc oxide, powdered pine resin,
talcum and asbestos) and a liquid (isopropyl alcohol 10%, clove oil,
pine resin, pine oil, peanut oil, camphor and colouring material).
• The powder and the liquid are mixed to the proper consistency and
applied around the teeth to protect gingival wounds.
• It may be admixed with tannic acid powder for its astringent
haemostatic action.
• The liquid is an excellent anodyne that may be applied alone into tooth
sockets on iodoform gauze.
Butyl cyanoacrylate spray
• Butyl cyanoacrylate spray had been developed for intraoral use by

Bhaskar et al. (1966).
• It is an adhesive spray to cover wounds in the mucosa and has
haemostatic and bacteriostatic properties, decreasing the healing time.
Xylocaine ointment
This ointment, containing 5% xylocaine, may be applied to the skin or oral
mucosa to relieve pain or pruritus.
Triamcinolone acetonide emollient paste
• Kenalogin Orabase is a preparation used for the treatment of acute and

chronic lesions of the oral mucosa.
• It is recommended for use in ulcerative stomatitis, erosive lichen
planus, denture stomatitis, desquamative gingivitis and aphthous
stomatitis.
• It contains a highly effective topical corticosteroid in a new adhesive,
emollient vehicle.
• It has a marked anti-inflammatory action and the Orabase assures
longer duration in situ.
Dose
Kenalog in Orabase, 5 g tubes.
Apply 2 to 3 times per day.
White head varnish

Composition
• Benzoine—200 g
• Iodoform—200 g
• Balsam of tolu—100 g
• Storax—150 g
• Ether—2l g
Uses
• It is the only solution which remains uninfected till the stabilisation
process is complete
• Mainly for the treatment of dry socket
• Dressing bony cavities after surgery (maxillary antrum)
Advantage
• Waterproof solution
Disadvantage
• It contains iodoform and the patient may be sensitive to this.
Stimulants for circulatory failure, syncope

and collapse
Ammonium carbonate
• Ammonium carbonate is freely soluble in water.

• It is used as aromatic spirits of ammonia, 100 mL of which contains
3.5–4.5 g of ammonium carbonate with some free ammonia and
aromatic oils in a mixture of distilled water and alcohol.
• In case of syncope, it is a useful reflex stimulant when inhaled; also,
slow slipping of the slightly diluted drug will stimulate circulation.
Aromatic spirits of ammonia
• Use by inhalation.
• Repeat after 15 min.
• Aromatic spirits of ammonia, 2 mL diluted in 3 parts of water.
Administer in small sips to cause irritation of the pharynx.
Amyl nitrite
• Amyl nitrite is a clear, yellowish, volatile liquid, soluble in alcohol and

ether but not in water.
• It is available as pearls, which contain 0.2 mL of the compound.
• The pearls are broken and the fumes inhaled from gauze or a
handkerchief.
• It is used as a vasodilator and antispasmodic and is especially useful in
anginal seizures.
Dose
Amyl nitrite pearls, 0.2 mL, by inhalation.
Oxygen
• The most important use of oxygen is for the prevention and treatment
of anoxia caused by inadequate oxygenation of the blood passing
through the lungs.
• In oral surgery, hyperbaric oxygen is used for the treatment of
osteomyelitis. Refer to Chapter 25 Osteomyelitis, Osteradionecrosis and
Osteochemonecrosis.
Newer drugs
Daptomycin
Linezolid
Tigecyclin (Tetracyclines group)
Dalfopristin–Quinupristin
Newer fluorquinolones (Trovafloxacin)
Newer beta lactum antibiotics
• Cephalosporins—Ceftaroline, ceftabiprole
Newer Macrolides
• Fidaxomicin
SECTION IV
Anaesthesia in Oral
Surgery
Chapter 9: Local Anaesthesia

Chapter 10: General Anaesthesia
CHAPTER 9
Local Anaesthesia
Electrophysiology of Nerve Conduction

Theories for mode of action of local anaesthesia
Acetylcholine theory
Calcium displacement theory
Surface charge theory
Membrane expansion theory
Specific receptor hypothesis
Mechanism of action
Classification
Systemic effects of local anaesthetic solution
Ideal properties of a local anaesthetic
Composition of local anaesthetics
Vasoconstrictors
• Systemic effects of vasoconstrictors
Applied anatomy
Nerve block
Field block
Local infiltration
Auxiliary technique
Intrapulpal injection
Intra-ligamentary technique
Intraosseous injection
Intraseptal injection
Topical local anaesthesia
Block anaesthesia for the maxilla
Intraoral techniques
Posterior superior alveolar nerve block
Middle superior alveolar nerve block
Anterior middle superior alveolar nerve block
Anterior superior alveolar nerve block
Palatal anaesthesia
Greater palatine nerve block
Nasopalatine nerve block
Maxillary nerve block
Infraorbital block
Intraoral techniques
Inferior alveolar nerve block
Direct technique (Halstead approach)
Indirect technique (Fischer 1-2-3 technique)
Gow-Gates technique
Vazirani–Akinosi’s closed-mouth mandibular block
Mental nerve block
Buccal nerve block
Lingual nerve block
Mental nerve block
Mandibular nerve block
Complications of local anaesthesia
Complications occurring due to injection technique
Needle breakage
Trismus
Haematoma
Facial nerve paralysis
Diplopia
Paraesthesia
Oedema
Postanaesthetic intraoral lesions
Infection
Complications occurring due to anaesthetic solution
Toxicity of the drug
Allergy to the drug
Burning sensation
Local anaesthetics are the drugs that on coming in contact with the nerve fibre
interrupt the propagation of the nerve impulse in a prolonged and reversible
manner. Niemann isolated an alkaloid, cocaine, from coca leaves which was
later introduced as a local anaesthetic in 1884 Köller, an ophthalmologist, who
also noticed the local vasoconstrictive and ischaemic action of this drug. In
1905, Procaine was synthesised by Einhorm as first local synthetic anaesthetics.
This was used until the discovery of lidocaine by Löfgren in 1943.
‘Local anaesthesia is defined as a transient and completely reversible loss of

sensation in a circumscribed area of the body caused by a depression of
excitation in nerve endings or an inhibition of the conduction process in
peripheral nerves.’
Electrophysiology of nerve conduction

(Fig. 9.1)
Nociception (pain awareness) is mediated by nerve ending receptors called
nociceptors in the peripheral tissues. The stimuli are transmitted by the
nociceptors are transmitted to the CNS by intramembranous transfer of
particles like sodium and potassium. The constant change in the membranous
potential allow the impulses to be conducted through the nerves. The resting
potential inside the nerve is usually −70 mV, the impulse initiations that fail to
reach the threshold potential (−55 mV) dies without progressing.
FIGURE 9.1 (A) The graph depicts the Steps 1 to 4 of Nerve
Conduction. (B) The sequence of events that occur in Steps 1 to 4
of nerve conduction.
STEP 1: Slow depolarization is the development of the potential to reach

threshold potential (–55mV). A few Na+ ions move into the nerve membrane
at this stage to increase the membrane potential.
STEP 2: The threshold potential is a critical level to which a membrane
potential must be depolarised it is usually between −50 to −55mV. At this
threshold potential, the cell’s voltage-gated sodium channels open to begin a
cascade of events involving other ion channels for conduction of nerve
impulse.
STEP 3: A sudden sodium influx occurs inside the membrane is called as
Rapid Depolarization. The potential reaches a maximum of +40 mV which is
called peak action potential.
STEP 4: After which Repolarization occurs due to potassium efflux. Steps 1–
4 takes 1 millisecond to complete and reach resting potential. Hyperpolarization
is the event of an undershoot of the membrane potential below the resting
potential up to –90 mV (Fig. 9.1A–B).
Methods to induce local anaesthesia

1. Mechanical trauma
2. Low temperature Anoxia
3. Chemical irritants
4. Neurolytic agents such as alcohol and phenol
5. Chemical agents such as local anaesthetics
Theories for mode of action of local anaesthesia

1. Acetylcholine theory
Acetylcholine is involved in nerve conduction together with its role as a
neurotransmitter at nerve synapses. But there is no evidence of involvement of
acetylcholine in neural transmission along the body of the neuron.
2. Calcium displacement theory

According to this theory, displacement of calcium from certain membrane sites
that controls the permeability to sodium prevents depolarisation. Altering the
concentration of calcium ions has no effect on local anaesthetic activity.
3. Surface charge theory

Local anaesthetics bind to the nerve membrane and change the electrical
potential at the membrane surface. LA molecules carrying net positive charge
make the electrical potential at the membrane surface more positive, thereby
increasing the threshold potential. Recent evidence shows that there is no
alteration in the resting potential by local anaesthetics and they act within the
nerve membrane channels rather than at the surface.
4. Membrane expansion theory

Local anaesthetics diffuse to hydrophobic regions and expand the membrane
preventing the sodium permeability. Lipid soluble molecules alter the
lipoprotein matrix of the nerve membrane and decrease the diameter of
sodium channels. There is no direct evidence to support this theory.
5. Specific receptor hypothesis

Specific receptor hypothesis is the most favoured theory. Local anaesthetics act
by attaching themselves to specific receptors in the nerve membrane. The local
anaesthetic receptor is located at or near the sodium channel in the nerve
membrane either on its external surface or on the internal axoplasmic surface.
Once the receptors access is gained, sodium ion permeability is decreased or
eliminated and nerve conduction interrupted.
Mechanism of action
Local anaesthesia primarily acts by decreasing the permeability of the nerve
membrane to sodium ions. They have insignificant effect on potassium
conductance. Calcium ions present within the cell membrane control the
conductance of the sodium ion across the membranes. The release of calcium
ion from this cell membrane results in an increased sodium permeability of the
nerve membrane. This is the first step in nerve membrane depolarisation. The
local anaesthetic molecules act by competitive antagonism with calcium for the
same site on the nerve membrane.
Classification
Pharmacodynamics and pharmacokinetics
Local anaesthetic solutions can be classified into ester or amide type
depending on their chemical linkage (Tables 9.1–9.4). Ester-linked local
anaesthetics are readily hydrolysed in aqueous solution whereas amide-linked
local anaesthetics are relatively resistant to hydrolysis.
Table 9.1
Classification of local anaesthetics based on chemistry
Esters Amides Quinoline

• Benzoic acid esters
Butacaine Prilocaine Centbucridine
Cocaine Bupivacaine
Benzocaine Mepivacaine
Hexylcaine Etidocaine
Piperocaine Articaine
Tetracaine Lidocaine
• Para aminobenzoic acid esters
Procaine
Chloroprocaine
Propoxycaine
Table 9.2
Classification of local anaesthetics according to biologic site and mode of action

Class Agent acting at receptor site—external surface of nerve membrane
A
Class Agent acts at receptor site—internal surface of nerve membrane
B
Class Agent acts by a receptor independent—Benzocaine
C
Class Combination of physiochemical receptors and receptor independent mechanism (most LA
D e.g. Lignocaine, mepivacaine)
Table 9.3
Classification of local anaesthetics according to duration of action

Duration: pulpal Duration: soft tissue LA
Ultrashort (10–15) 30–45 Lignocaine 2% (plain)
Mepivacaine 3% (plain)
Prilocaine 4% (infiltration)
Short (45–60) 120–180 Procaine
Chloroprocaine
Intermediate (60–90) 180–270 Lignocaine Prilocaine (block)
Mepivacaine
Long (>90) >270 Bupivacaine
Etidocaine
Tetracaine
Table 9.4
Classification of LA based on mode of administration
I. Injectable
a. Low potency, short duration
i. Procaine
ii. Chloroprocaine
b. Intermediate potency and duration
i. Lidocaine
ii. Prilocaine
c. High potency, long duration
i. Tetracaine
ii. Bupivacaine
iii. Ropivacaine
iv. Dibucaine
II. Surface anaesthetic
a. Soluble
i. Cocaine
ii. Lidocaine
iii. Tetracaine
b. Insoluble
i. Benzocaine
ii. Butyl aminobenzoate
iii. Oxethazaine
The ester type anaesthetics are metabolised by the hepatic

pseudocholinesterases and plasmatic esterases, producing para-amino benzoic
acid (PABA), which are excreted in urine. The ester type is 100% metabolised
and the amide type is 90% metabolised, the remainder being unmetabolised
anaesthetic.
Factors affecting activity of local anaesthesia

• Purely basic forms of local anaesthetics are not stable and dissolve
poorly in water. However, weakly basic forms of local anaesthetic
drug readily combine with acids to form local anaesthetic salt. This salt
is stable and is soluble in water. Therefore, the local anaesthetic
solutions are available as salts, commonly hydrochloric salt dissolved
in distilled water and used for injections.
• The effectiveness of the local anaesthesia is decreased by the
acidification of the tissues. Therefore, poor anaesthesia results when
anaesthetic solution is injected into an inflamed area.
• Local anaesthesia without epinephrine is more active than the same
agent with epinephrine because the pH of solutions with epinephrine
is less (3.3) when compared to the pH of solutions without epinephrine
(5.5).
• Alkalisation of local anaesthesia increases its effectiveness and speeds
up the action but since local anaesthesia is very unstable in its basic
form, it cannot be used for clinical purposes.
• Local anaesthetic agents are vasodilators. This results in increased and
fast absorption of the solution into the bloodstream thereby increasing
its toxicity. The duration of local anaesthetic activity is also decreased
and bleeding at the site of administration is increased. The addition of
epinephrine in the local anaesthetic agent overcomes all these
drawbacks as it causes vasoconstriction of the local blood vessels.
Systemic effects of local anaesthetic solution

1. Cardiovascular system
Local anaesthetic decreases electrical excitability of the myocardium,
conduction rate and force of contraction. All these factors together result in
myocardial depression (but not at a dose attained after intraoral injection of
one or two dental cartridges). At a dose of 1.5–5 µg/mL it has antiarrhythmic
activity. It can be used as a potent drug for ventricular tachycardia, ventricular
premature contractions and in cardiac arrest from ventricular fibrillation.
2. Blood vessels
Local anaesthetics cause vasodilatation of the blood vessels except for cocaine
which produces vasoconstriction. It primarily produces hypotension (at a level
approaching overdose) due to depression of the myocardium and smooth
muscle relaxation of the vessel wall. At lethal levels it causes cardiovascular
collapse.
3. Central nervous system

At low level there is no significant effect. Lidocaine causes CNS depression at
toxic levels.
At 0.5–4 mg/mL—anticonvulsive action

Due to their depressant action on the CNS, local anaesthetics raise the seizure
threshold by decreasing the hyperexcitability of the cortical neurons from
where the convulsive episodes originate.
At 4.5–7 mg/mL—preseizure signs and symptoms

Preseizure signs and symptoms include slurred speech, shivering, tremor,
warm flushed feeling of the skin, light headedness, dizziness, drowsiness,
visual disturbance, auditory disturbance, etc.
At 7.5–10 mg/mL—convulsive action
At this dose, lidocaine causes tonic–clonic seizure. Seizure continues as long as
the drug is present in the blood. The duration of presence of local anaesthesia
in blood is further increased by the increased blood flow to the brain.
Increased cerebral metabolism also leads to progressive metabolic acidosis
which prolongs the seizure activity.
Further increase in the dose causes CNS depression and respiratory arrest as
a result of respiratory depression.
4. Respiratory system
At nonoverdose levels, it has a relaxant effect on bronchial smooth muscles.
Overdose leads to respiratory arrest as a result of respiratory centre depression
(CNS depression).
Ideal properties of a local anaesthetic

1. It should be nonirritant to the tissue to which it is applied.
2. It should not cause any permanent alteration of nerve structure.
3. Systemic toxicity should be low.
4. It must be effective in parenteral, as well as topical application.
5. Time of onset should be as short as possible.
6. Duration of action should be adequate to complete the procedure as
well as comfortable recovery.
7. It should be stable in solution and should readily undergo
biotransformation in the body.
8. It should be sterile or should be capable of undergoing sterilisation by
heat without deterioration.
Composition of local anaesthetics

Table 9.5 depicts composition and function of local anaesthetics.
Table 9.5
Composition and function of local anaesthetics

Composition Function
Lignocaine hydrochloride— Local anaesthetic agent
2% (20 mg/mL)
Sodium meta-bisulphite— Reducing agent
(0.5 mg)
Methylparaben—0.1% (1 mg) Preservative
Distilled water Diluting agent
Thymol Fungicide
Sodium chloride or Ringer’s Isotonic solution
solution—6 mg
Adrenaline—1:80,000 Vasoconstrictor
(0.012 mg)
Sodium hydroxide To adjust pH
Nitrogen bubble—1.2 mm in Present oxygen from being trapping in the catridge and
diameter potentially destroying the vasopressor
In search of greater effectiveness for LA, vasoconstrictor agents are usually

added to the anaesthetic solutions. This combination has constituted a real
advance in the field of stomatology, improving the dental operation.
2 mL of 2% lidocaine contains 36 mg of lidocaine hydrochloride. In solutions
at 1:80,000 concentration of epinephrine contains 0.0125 mg/mL and 1:1,00,000
concentration contains 0.01 mg/mL of epinephrine.
Safety levels of local anaesthetics

The toxic dose for lignocaine varies depending on whether it is injected with a
vasoconstrictor or not. Without a vasoconstrictor the toxic level is put at 3–
4.4 mg/kg. When a vasoconstrictor is added to the solution the toxic level is
raised to 7 mg/kg. The difference is due to the more rapid uptake of lignocaine
when not used with a vasoconstrictor and is not accurate when the injection is
given intra-vascularly.
Absolute contraindications to local anaesthesia
1. Myocardial infarction within 6 months

2. Recent hepatitis A or hepatitis B
3. Jaundice
4. Local infections or sepsis
5. Hypersensitivity to lidocaine
Relative contraindications to local anaesthesia
1. Chronic renal failure

2. Hyperthyroidism
3. Atypical plasma cholinesterase
4. Pregnancy—during the first trimester
5. Hypertension
6. Malignant hyperthermia
7. Congenital methaemoglobinaemia
Vasoconstrictors
Vasoconstrictors used in local anaesthetics can be clarified based on chemical
structure and mode of action (Tables 9.6–9.7).
Table 9.6
Classification of vasoconstrictors based on chemical structure

Catecholamines Noncatecholamines
Epinephrine (natural) Amphetamine
Norepinephrine (natural) Methamphetamine
Levonordefrin (synthetic) Ephedrine
Isoproterenol (synthetic) Mephentermine
Dopamine (natural) Hydroxyamphetamine, Metaraminol, Methoxamine, Phenylephrine
Table 9.7
Classification of vasoconstrictors based on mode of action

Direct-acting drugs Indirect-acting drugs Mixed-acting drugs
Epinephrine Tyramine Metaraminol
Norepinephrine Amphetamine Ephedrine
Levonordefrin Methamphetamine
Isoproterenol Hydroxyamphetamine
Dopamine
Methoxamine
Phenylephrine
Systemic effects of vasoconstrictors
1. Cardiovascular system
Increases cardiac output, stroke volume, systolic and diastolic blood pressure,
heart rate, myocardial oxygen consumption and force of myocardial
contraction. All these factors together result in decreased cardiac efficiency.
2. Blood vessels
They have vasoconstrictive properties on small capillaries which contain alpha
receptors. However, in large blood vessels supplying skeletal muscles (which
contain both alpha and beta receptors), beta-2-receptor activity predominates
in small doses and alpha receptor activity predominates in larger doses.
3. Respiratory system
It causes bronchodilatation of smooth muscles of the bronchioles (beta 2
effect).
4. Central nervous system

In therapeutic doses, epinephrine has no effect on the CNS. In excessive dose,
it acts as a CNS stimulant.
5. Metabolism
It stimulates glycogenolysis in the liver and skeletal muscles, thereby
increasing blood sugar level. It increases oxygen consumption in the tissues.
Applied anatomy
The trigeminal nerve (Figs. 9.2–9.3)
The trigeminal or fifth cranial nerve is the sensory nerve of face and consists
largely of somatic afferent fibres but it also contains motor afferent fibres. It is
the nerve of the first branchial arch and is the largest of the cranial nerves.
FIGURE 9.2 The anatomy of the mandibular nerve and its
branches.
FIGURE 9.3 (A) Course and distribution of trigeminal nerve. (B)
Ophthalmic (V1) Maxillary (V2) and mandibular (V3) division of
trigeminal nerve dermatome.
The larger sensory and smaller motor root of this nerve leaves the bone
about half way up its ventrolateral surface. The cell bodies of the sensory root
form the gasserian (trigeminal or semilunar) ganglion which lies in an
invagination of the dura mater near the apex of petrous temporal bone. The
three divisions of the nerve leave the ganglion and exit the skull via the
superior orbital fissure, foramen rotundum and foramen ovale. The
innervation of the maxillary teeth and adjacent soft tissues comes from the
following branches of the second division, i.e. the maxillary nerve.
a. The posterior superior alveolar (or dental) nerves, usually two or three in
number, leave the maxillary nerve in the pterygopalatine fossa to
course downwards on the surface of the maxillary tuberosity which
they enter through small foramina to supply the roots of all molar teeth
except the mesiobuccal root of first molar.
b. The middle superior alveolar nerve arises from the infraorbital nerve and
supplies premolar teeth and the mesiobuccal root of first molar.
c. The anterior superior alveolar nerve arises further anterior in the
infraorbital canal and supplies the anterior teeth.
d. The greater palatine nerve travels via the greater palatine canal from the
sphenopalatine ganglion to the hard palate. It supplies tissues on the
palate posterior to the canine teeth.
e. The long sphenopalatine nerve, after leaving the sphenopalatine ganglion
passes medially through the sphenopalatine foramen, crosses the root
of nose to travel along the nasal septum and enter the oral cavity via
incisive canal. It supplies palatal tissues adjacent to the anterior teeth
and anastomoses with greater palatine nerve in region of the canine
tooth.
These branches may be seen as describing two nerve loops: (1) the outer
loop lies deep to the cortical bone of the maxilla and consists of the superior
alveolar nerves and their parent nerve (the maxillary infra-orbital nerve) and
(2) the inner loop consists of the greater palatine nerve only and the long
sphenopalatine nerve, which leave the sphenopalatine ganglion and
anastomose near the maxillary canine tooth.
The motor root runs with the third or mandibular division and supplies four
masticatory muscles, two tensors (tympani and palati), anterior belly of the
digastric and mylohyoid.
The innervation of the mandibular teeth and contiguous tissues arises from
following branches of the third division:
a. The inferior alveolar nerve which enters the mandible at the mandibular
foramen and together with its terminal branches and incisive nerve,
supplies all the teeth.
b. The mylohyoid nerve a branch of inferior alveolar nerve, runs
downwards and forwards in mylohyoid groove on medial surface of
the ramus of mandible to innervate the mylohyoid muscle.
c. The lingual nerve which on its way to supply the anterior two-third of
the tongue also supplies the lingual gingival tissues.
d. The mental nerve innervates the gingiva anterior to the mental foramen,
as well as the skin and mucous membrane of the lower lip and chin
approximately to the midline.
Depending upon the site of injecting the local anaesthetic solutions in relation
to the nerve, there are three major technique of LA as,
• Nerve block
• Field block
• Local infiltration
There are other auxiliary injection techniques as,
1. Intrapulpal injection
2. Intra-ligamentary technique
3. Intraosseous injection
4. Intraseptal injection
5. Topical analgesia
Nerve block
Nerve block is the method by which regional anaesthesia is secured by
depositing the anaesthetic solution within close proximity to a main nerve
trunk. This will prevent the afferent impulses travelling centrally beyond this
point.
Field block
Field block is the method by which regional anaesthesia is secured by
depositing the local anaesthetic solution in proximity to larger terminal nerve
branches. This will make the area to be anaesthetised walled off or
circumscribed to prevent the central passage of afferent impulses.
Local infiltration (supraperiosteal) (Fig. 9.4)

In this technique, small terminal nerve endings in the area of surgery are
flooded with anaesthetic solution so that the area becomes insensible to pain
or prevent them from becoming stimulated and creating an impulse.
FIGURE 9.4 Local infiltration.
Auxiliary technique
Intrapulpal injection (Fig. 9.5)
This technique is utilised in procedures which require direct instrumentation
of the pulpal tissue. Intrapulpal injection can adequately control pain arising
from pulpal exposure.
FIGURE 9.5 Intrapulpal injection.
A 25-gauge needle is inserted into the pulp chamber; firmly wedging the
needle into the chamber or canal. Considerable amount of resistance might be
encountered; therefore, the solution is injected under pressure.
Intra-ligamentary technique (periodontal ligament injection)

(Fig. 9.6)
Here the anaesthetic solution is deposited forcefully under pressure into the
periodontal ligament (PDL) of the tooth which has to be anaesthetised. This
technique is useful for anaesthetising only one tooth of maxillary or
mandibular arch. It may be necessary to repeat the PDL injection on all four
sides of the tooth. This technique is mostly used in restorative dentistry
whenever isolated areas of inadequate anaesthesia are present.
FIGURE 9.6 Intra-ligamentary injection.
A 27-gauge short needle is placed between the periodontal ligament and the
tooth in such a way that bevel of the needle faces the tooth to be anaesthetised.
The needle may need to be bent for gaining access. A 0.2 mL of the local
anaesthetic is deposited under pressure.
Intraosseous Injection
Local anaesthetic solution is deposited into the cancellous bone adjacent to the
tooth to be anaesthetised. It is used when other methods have failed.
The soft tissues are anaesthetised using a local infiltration. A small incision
is made in the apical region of the tooth to be anaesthetised and a hole is
drilled through the dense cortical plate to reach the cancellous bone. A 25-
gauge needle is inserted to this hole and approximately 1 mL of local
anaesthetic solution is deposited under pressure.
Intraseptal injection
The intraseptal injection is a variation of the intraosseous and PDL injections.
This injection may be effective where the condition of the periodontal tissues
in the gingival sulcus precludes the use of PDL injection. It is useful in
achieving osseous soft tissue anaesthesia and haemostasis for periodontal
curettage and surgical flap procedures.
The soft tissue over the area is anaesthetised through local infiltration and a
27-gauge short needle is inserted distal to the tooth in the porous intraseptal
bone. 0.2 mL of the local anaesthetic is deposited under pressure. This
technique is more effective in children and younger adults.
Topical local anaesthesia
Topical local anaesthesia renders the free nerve endings in accessible
structures incapable of stimulation by application of a suitable solution
directly over the surface.
Block anaesthesia for the maxilla

The various injections are as follows:
1. The posterior superior alveolar nerve block (tuberosity block)

2. The anterior or middle superior alveolar nerve block (the infraorbital
nerve block)
3. The greater palatine nerve block
4. The nasopalatine or long sphenopalatine nerve block (the incisive canal
block)
5. The maxillary nerve block:
a. Via the pterygomaxillary fissure
b. Via the greater palatine canal
c. By an external approach

Posterior superior alveolar nerve (PSA block)
Other names: Tuberosity block, zygomatic block.
FIGURE 9.7 (A–C) The different areas anaesthetised and intraoral
nerve block techniques and supraperiosteal infiltration are shown
in the illustrations.
( Scan to play Maxillary Local Anesthesia techniques)
Areas anaesthetised
In this technique, the area supplied by the posterior superior alveolar nerve is
anaesthetised. They are: pulpal anaesthesia of third, second and first maxillary
molars (with the exception of the mesiobuccal root of the maxillary first molar)
buccal periodontium and bone overlying these teeth.
Landmarks
Mucobuccal fold, maxillary tuberosity and zygomatic process of maxilla.
Technique (Figs. 9.8–9.10)

Position the patient so that his maxillary occlusal plane is at 45 degree angle to
the floor. A 25-gauge short needle is used. The needle should be inserted at the
height of the mucobuccal fold in the region distal to the maxillary second
molar. The target area is the posterior superior alveolar nerve as it enters the
posterior surface of the maxilla. This requires that the patient’s mouth be
opened only to a comfortable extent, as excessive opening brings the coronoid
process of the mandible forwards and prevents the needle from being
advanced from the lateral aspect. This nerve is located posterosuperior and
medial to the maxillary tuberosity.
FIGURE 9.8 Anatomical landmarks for PSA block shown in a skull.
FIGURE 9.9 Demonstration of PSA block in a skull.

FIGURE 9.10 Clinical demonstration of PSA block-needle placed
distal to second molar and directed 45 degree to the sagittal and
occlusal plane with the buttress as a guide.
The index finger is placed in the mucobuccal fold of the bicuspid area and
moved posteriorly until the prominence of the zygomatic buttress is reached.
This is approximately in the region above the first molar area. Here the
fingertip is rotated so that the finger nail is facing the attached gingiva. The
finger is passed posteriorly over this buttress until it dips in a sulcus posterior
to the buttress. The finger is kept such that it is at an angle of 90 degree to the
occlusal surface of the maxillary teeth and at an angle of 45 degree to the
sagittal plane. The needle is positioned in the depth of the sulcus close to the
pterygomaxillary fissure, high in the mucobuccal fold above the distobuccal
root of the second molar, bisecting the fingernail.
Middle superior alveolar nerve block (Fig. 9.11A–B)

Middle superior aveolar nerve is not always present when absent the posterior
superior alveolar nerve supplies the molars and premolars.
FIGURE 9.11 (A–B) The needle is inserted at the height of the
mucobuccal fold above the maxillary second premolar with the
orientation of the bevel towards the bone.
Nerves anaesthetised
Middle superior alveolar nerve and terminal branches
Area anaesthetised
Maxillary first and second premolars with mesiobuccal root of the first molar
with the adjacent buccal mucosa and bone over the tooth.
Indications
It is given when ASA nerve block fails to anaesthetise the first and second
premolar and PSA nerve block fails to anaesthetise mesiobuccal root of first
molar.
Technique
The upper lip is retracted to make the tissue taut and to gain visibility, a 27-
gauge needle is inserted at the height of the mucobuccal fold above the
maxillary second premolar with the orientation of the bevel towards the bone.
The needle is penetrated till the needle tip is located above the apex of the
second premolar. After negative aspiration 0.9–1.2 mL of solution is deposited
over 30–40 s.
Anterior middle superior alveolar nerve block

(Fig. 9.12)
Area anaesthetised
The anterior and middle superior alveolar (AMSA) nerve block, achieves
pulpal anaesthesia from the central incisor to second premolar through palatal
approach with a single injection. The palatal mucosa from midline raphe to the
cervical region of the maxillary teeth and the gingival and buccal mucosa of all
the maxillary teeth of the corresponding side.
FIGURE 9.12 (A–C) (A) Anterior middle superior alveolar foramen

through which the corresponding nerve exits to supply the palatal
soft tissue, buccal gingival tissue and the pulps of the incisors,
canines, premolars and the mesiobuccal root of the first molar. (B)
The site of deposition of the anaesthetic agent into the foramen by
a computer-controlled local anaesthetic delivery (C-CLAD) (C) C-
CLAD system.
Technique
This technique was first reported by Freidman and Hochman in 1997 with the
development of CCLAD system, it provides pulpal anaesthesia to multiple
teeth from a single injection site. The site of penetration with C-CLAD on the
palatal side of the premolars at the intersection of the horizontal and vertical
aspects of the palate opposite the apices of the premolars, a point midway
between the gingival crest bisecting the premolars and the median palatine
raphe.
Disadvantage
This technique has an unpredictable anaesthetic success of the teeth and
variable duration of action for clinical use as the first choice when compared to
the other techniques that have greater efficacy in the maxilla.
Advantage
In the maxilla most dental procedures require multiple injections that
anesthetise facial structures and affect the smile line. Anaesthetizing the teeth
without numbing the facial muscles is usually useful in restorative dentistry.
Anterior superior alveolar nerve block

Other names: Infraorbital nerve block.
Infraorbital nerve block

Other names: Anterior superior and middle superior alveolar nerve block.
Areas anaesthetised
In this technique, the areas supplied by the anterior superior alveolar nerve,
middle superior alveolar nerve, infraorbital nerve along with its branches, the
lateral nasal nerve, inferior palpebral nerve and superior labial nerves are
anaesthetised. Areas anaesthetised are maxillary incisors, canine, premolars
and mesiobuccal root of maxillary first molar on the injected side, buccal
periodontium and bone of the same teeth, lower eyelid along with lateral
aspect of nose and the upper lip.
Landmarks
Supraorbital notch, infraorbital notch, pupil of the eye, infraorbital foramen,
bicuspid teeth and mental foramen.
Techniques (Figs. 9.13–9.17)

There are basically three techniques for infraorbital nerve block:
i. Bicuspid approach
ii. Central incisor approach
iii. Extraoral approach
FIGURE 9.13 Surface anatomical landmarks. A vertical imaginary
line connecting pupil, infraorbital rim, notch, infraorbital foramen
and mental foramen.
FIGURE 9.14 Bicuspid approach demonstration in a skull.
FIGURE 9.15 (A–B) Bicuspid approach. Needle oriented parallel to

the bicuspids towards the infraorbital foramen with the index finger
over the infraorbital rim acting as the guide.
FIGURE 9.16 Demonstration of central incisor approach in a skull.
FIGURE 9.17 Central incisor approach—needle bisects the central
incisor from mesial to distal penetrating the vestibular mucosa with
the index finger over the infraorbital rim.
Patient is positioned in such a way that his/her maxillary occlusal plane is at

an angle of 45 degree to the floor. The target is determined by palpating the
supraorbital and infraorbital notches. A vertical imaginary line is drawn
through these landmarks which will pass through pupil of the eye, infraorbital
foramen, bicuspid teeth and mental foramen. After palpating the infraorbital
margin, the finger is moved downwards from it where a concavity will be felt.
This is the infraorbital depression and the infraorbital foramen is in its deepest
part. Maintaining the index finger on this foramen externally, retract the lip
using the thumb to expose the mucobuccal fold or vice versa.
Bicuspid approach
In the bicuspid approach, the needle is held parallel to the bicuspid teeth. The
puncture is made over the first premolar at the height of the mucobuccal fold
which allows the needle to be advanced between the levatorlabii superioris
above and the levator anguli oris below. The penetration of the needle should
be between 16 to 20 mm; 0.9 to 1.2 mL of solution should be deposited and the
overlying tissues gently massaged to aid penetration of the solution into the
canal.
Central incisor approach

In the central incisor approach, the needle is directed such that it bisects the
crown of central incisor of the same side to the mesioincisal angle to the
distoincisal angle. The needle is inserted for about 5 mm from the mucobuccal
fold and 0.9 to 1.2 mL of anaesthetic solution deposited.
Extraoral approach
A 27 or 30 gauge needle is used to approach infra-orbital foramen
percutaneously by injecting between ala of nose and upper part of nasolabial
fold directing needle laterally towards infraorbital foramen.
Palatal anaesthesia
Palatal injection proves to be a very traumatic experience for many dental
patients.
Greater palatine nerve block

Other names: Anterior palatine nerve block.
Anterior palatine nerve.
Areas anaesthetised
Posterior portion of hard palate and its overlying soft tissues, anteriorly upto
the first premolar and medially to midline.
Area of insertion
Soft tissues slightly anterior to the greater palatine foramen.
Landmarks
Greater palatine foramen and junction of maxillary alveolar process and
palatine bone.

The greater palatine foramen is located about 4 mm anterior to the termination
of the hard palate so that it is normally situated opposite the second molar
about half way between the gingival margin and midline. A 27- or 25-gauge
needle is used. The greater palatine foramen is approached from opposite side
at a right angle to the curvature of the palatal bone. The needle is inserted
anterior to the foramen half way between the palatal aspect of the gingival
margin of the second molar and the midline of the palate. Approximately
0.25 mL of solution is deposited here.
FIGURE 9.18 Landmarks in the skull.

FIGURE 9.19 Surface anatomical landmarks. Mid-palatine raphe,
palatal gingival margin of second molar and the half way between
the two landmarks is the greater palatine foramen.
FIGURE 9.20 Demonstration of greater palatine nerve block in a
skull.
FIGURE 9.21 Clinical demonstration of greater palatine nerve block
—needle directed from opposite site just anterior to the foramen
located 1 cm medial to the palatal gingival margin of 2nd molar.
Nasopalatine nerve block

Other names: Incisive canal nerve block, sphenopalatine nerve block.
Right and left nasopalatine nerves.
Areas anaesthetised
Hard and soft tissues in the area between canine to canine.
Area of insertion
Tissue lateral to incisive papilla.
Target area
Incisive foramen located beneath incisive papilla.
Landmark
Central incisors and incisive papilla.
This procedure is extremely painful therefore a preparatory anaesthesia is
secured before insertion of the needle into the incisive papilla.
FIGURE 9.22 Surface anatomy in a skull—nasopalatine foramen in

a severely resorbed maxilla.
FIGURE 9.23 Demonstration of nasopalatine nerve block in skull.
FIGURE 9.24 Clinical demonstration of nasopalatine nerve block—
needle insertion into the incisive papilla directed parallel to the
inclination of the central incisors.
Preparatory anaesthesia
0.25 mL of local anaesthetic solution is deposited by inserting the needle at a
right angle to the labial plate into the labial intraseptal tissues in between the
two maxillary central incisors.
Procedure
The position of the nasopalatine canal is marked by the papilla situated just
behind the central incisors. The needle is withdrawn and reinserted slowly
into the groove surrounding the papilla. The bevel is best placed so that it
faces distally and the needle is advanced through the canal. Up to 0.25 mL of
anaesthetic solution is deposited.

Maxillary nerve block is useful for profound anaesthesia of the maxilla. Two
approaches are usually employed: (1) greater palatine canal approach—
difficulty in locating and negotiating the canal and (2) high tuberosity
approach—higher incidence of haematoma.
Other names: Second division nerve block, V2 nerve block.
Areas anaesthetised
1. Pulpal anaesthesia of maxillary teeth on the side of nerve block (central
incisor to last molar)
2. Buccal periodontium and bone overlying these teeth
3. Soft tissues and bone of hard palate and part of soft palate medial to the
midline
4. Skin of lower eyelid, side of nose, cheek and upper lip
Techniques
Maxillary nerve block via the greater palatine canal (Figs. 9.25–9.26)
The puncture point for this injection is about 4–5 mm anterior to the greater
palatine foramen, the needle having to pass through soft tissue before entering
the foramen. The foramen opens into the greater palatine canal, which is
situated between the second and third maxillary molars about 1 cm towards
midline of the palate from the palatal gingival margin.
FIGURE 9.25 Maxillary nerve block through greater palatine

approach demonstration in skull.
FIGURE 9.26 (A–B) Note the needle inserted into greater palatine
foramen ends in the pterygopalatine fossa anaesthetising the trunk
of maxillary branch of trigeminal nerve (V2). Greater palatine
foramen in the horizontal plate of palatine bone continues as a
canal that opens into pterygopalatine fossa.
Occasionally, a slight depression may be noted overlying the foramen. A

42 mm needle is passed upwards and backwards about 45–60 degree to the
upper occlusal plane and slightly laterally (less than 10 degree) to almost its
full depth.
About 2 mL of solution is deposited and this usually diffuses adequately
through the superior end of the canal to reach the maxillary nerve. The
patient’s head is tilted back with wide mouth opening to give good access and
possibility. Aspirate immediately as the needle enters a tissue space, as
inadvertent penetration into the nasopharynx may be demonstrated by
aspiration of air.
Maxillary nerve block via the pterygomaxillary fissure/high tuberosity

approach (Fig. 9.27)
A 25-gauge long needle is inserted high on the mucobuccal fold above the
distal aspect of maxillary second molar. The bevel should be oriented towards
the bone. To make this task easier, the patient is asked to open his/her mouth
partially and the mandible is retracted towards the side of injection. Advance
the needle slowly in an upward, inward and backward direction for
approximately 30 mm. No resistance should be felt for advancing the needle;
the presence of any resistance indicates that the angle of the needle towards
midline is too great. The tip of the needle is now in the pterygopalatine fossa
in proximity of maxillary nerve. About 2 mL of solution is deposited following
negative aspiration.
FIGURE 9.27 (A–B) The needle inserted at the height of the
mucobuccal fold distal to the maxillary second molar ends in the
pterygopalatine fossa anaesthetising the trunk of maxillary branch
of trigeminal nerve (V2). (B) A 42 mm needle is used for both
techniques.
Infraorbital block (Figs. 9.28–9.31)
FIGURE 9.28 Illustration of infraorbital nerve dermatome.
FIGURE 9.29 Surface anatomical landmarks for infraorbital nerve
block. Nasolabial fold, infraorbital rim, vertical imaginary line
through pupil connecting infraorbital foramen and mental foramen,
as a straight line.
FIGURE 9.30 Surface anatomy of infraorbital foramen in a skull
showing the orientation of needle. Note the foramen opens
inferiorly and medially.
FIGURE 9.31 Clinical demonstration of infraorbital nerve block
(extraoral)—needle directed towards infraorbital foramen just
lateral to the nasolabial fold directed superiorly and mediolaterally.
This direction is in accordance with the infraorbital foramen which
opens inferomedially.
Nerves Anaesthetised
• Infraorbital nerve and its branches: inferior palpebral, lateral nasal and
superior labial
• Anterior middle and superior alveolar nerve
Areas anaesthetised
Incisors and bicuspids on the injected side, alveolar bone and overlying
tissues, upper lip, side of the nose, lower eyelid.
Landmarks
Pupil of the eye, infraorbital notch, infraorbital ridge, infraorbital depression.
Technique
The infraorbital foramen is located by using the landmarks as mentioned for
the intraoral approach and the foramen is marked. The overlying skin and
subcutaneous tissues are anaesthetised by local infiltration. A 27-gauge needle
is inserted through the marked area between ala of nose and upper part of the
nasolabial fold and directed slightly upward and laterally and entered into the
foramen. It should not exceed a depth of 0.3 mm into the foramen. After
negative aspiration 1 mL of anaesthetic solution is deposited slowly.
Maxillary nerve block (Figs. 9.32–9.36)
Maxillary teeth, hard and soft palate, tonsils, maxillary alveolar bone and
overlying tissues, nasal septum and floor of the nose, anterior cheek, upper lip,
side of the nose, lower eyelid, anterior temporal and zygomatic regions.
FIGURE 9.32 Surface anatomical landmarks for extraoral maxillary
nerve block—sigmoid notch, inferior border of zygomatic arch.
FIGURE 9.33 Demonstration in skull—position I.
FIGURE 9.34 Clinical demonstration—position I: needle penetrates

perpendicular to the skin through the centre of the sigmoid notch
and hits the lateral pterygoid plate.
FIGURE 9.35 Demonstration of position II in skull.
FIGURE 9.36 Clinical demonstration—position II. Needle
withdrawn slightly and redirected anteriorly to the pterygo maxillary
fissure.
Technique
The midpoint of the zygomatic process and the depression in its inferior
surface are marked. A 22-gauge needle of 4.5 cm is marked with a rubber
marker. The syringe is directed perpendicular to the sagittal plane until it
contacts the lateral pterygoid plate. The insertion of the needle should not
exceed the rubber marker. Now the needle is withdrawn and redirected in a
slightly forward direction and anaesthetic solution is slowly deposited.

The nerves which supply the teeth and associated tissues of the mandible are
the inferior alveolar nerve, with its mental and incisive branches, the lingual
nerve and the long buccal nerve. The inferior alveolar nerve and its two
branches can be blocked at the mandibular and mental foramina respectively.
The lingual and long buccal nerves are blocked at very definite locations
(Fig. 9.37).
Following block injections will be described:
1. Inferior alveolar nerve block

2. Lingual nerve block
3. Mental injection
4. Long buccal nerve block
Inferior alveolar nerve block (Fig. 9.38)
Alternative name: Mandibular block
FIGURE 9.37 (A–B) The different areas anaesthetised by intraoral

and extraoral nerve block techniques are shown in the illustrations.
( Scan to play Mandibular Local Anesthesia techniques)
FIGURE 9.38 (A–D) (A) Osseous anatomy of the medial aspect of

the mandible, this is the site where the local anaesthetic drug is
deposited. (B) Anatomy of the inferior alveolar nerve, lingual nerve
and long buccal nerve. The inferior alveolar nerve enters the
inferior alveolar canal, the lingual nerve originating at the
mandibular foramen and coursing posteromedial to the last molar
has been demonstrated. (C) Soft tissue anatomy and point of
insertion of the needle has been marked. (D) The
pterygomandibular space consisting the inferior alveolar nerve and
vessels, this is the site where the local anaesthetic solution is
deposited for an Inferior alvelolar nerve block. The space is
bounded medially by the medial pterygoidand laterally the ramus of
the mandible.
1. Inferior alveolar nerve

2. Incisive nerve
3. Mental nerve
4. Lingual nerve
5. Long buccal (occasionally)
Areas anaesthetised
1. Mandibular teeth to midline

2. Body of mandible
3. Inferior portion of ramus
4. Buccal mucoperiosteum and mucous membrane anterior to mandibular
first molar
5. Lingual soft tissues and periosteum
6. Anterior two-third of tongue and floor of oral cavity
7. External and internal oblique ridge
Landmarks
1. External oblique ridge

2. Coronoid notch
3. Buccal pad of fat
4. Pterygomandibular raphe
5. Pterygotemporal depression
6. Pterygomandibular space
Technique
There are basically two techniques for anaesthetising the inferior alveolar
nerve.
• Direct technique: Inferior alveolar nerve is anaesthetised first, hence it is

known as direct technique (Halstead approach).
• Indirect technique: Inferior alveolar nerve is anaesthetised in the third
position, hence it is known as indirect technique or ‘Fischer 1-2-3
technique’.
Direct technique (Halstead approach) (Figs. 9.39–9.43)
Needle position
• 1st positon: Inferior alveolar nerve is anaesthetised from the opposite

side.
• 2nd position: Lingual nerve is anaesthetised from the opposite side.
• 3rd position: Long buccal nerve is anaesthetised separate
FIGURE 9.39 Demonstration of direct inferior alveolar nerve block

—position 1 in skull. Needle is directed from the contra-lateral
premolars just behind the lingual anaesthetising the inferior
alveolar nerve directly.
FIGURE 9.40 Clinical demonstration—position 1: anaesthetising
inferior alveolar nerve. Note the index finger placed along the
deepest portion of anterior ascending ramus and needle bisecting
it.
FIGURE 9.41 Demonstration of position 2 in skull: needle is

withdrawn from Position 1 along the same direction with
simultaneous injection of LA to anaesthetise the lingual nerve.

lingual nerve.

long buccal nerve.
Technique (Fig. 9.38)
Patient is seated in the dental chair in supine or semisupine position with
mouth wide open such that his/her mandibular plane is parallel to the floor.
Using index finger or thumb of the left hand palpate the external oblique ridge
and move the finger posteriorly till the coronoid notch (greatest depth of the
anterior border of the ramus of mandible) is contacted. The palpating finger is
moved across the retromolar triangle and onto the internal oblique;
pterygomandibular raphe and pterygotemporal depression can be seen
clearly. Now place the index finger or thumb behind the mandible extraorally
to assess the width of the mandible. A 25-gauge needle is inserted from the
opposite side parallel to mandibular plane bisecting the thumb or index finger
up to half the distance between the palpating finger intraorally and the finger
behind the ramus of the mandible extraorally until the needle contacts the
bone. After negative aspiration, 1.8 mL of solution is deposited slowly. The
needle is now withdrawn about half the inserted depth and the remaining
local anaesthetic solution injected to anaesthetise the lingual nerve. The long
buccal nerve is anaesthetised using a separate insertion between the external
and internal oblique ridges.
The tissue in the mucobuccal fold is entered with the help of a 25-gauge
needle at an angle of 45 degree to the body of mandible just distal to the most
posterior tooth.
Indirect technique (Fischer 1-2-3 technique) (Figs. 9.44–9.49)
Needle position
• 1st position: Long buccal nerve is anaesthetised from the opposite side.
• 2nd position: Lingual nerve is anaesthetised from the same side.
• 3rd position: Inferior alveolar nerve is anaesthetised from the opposite
side.
FIGURE 9.44 Demonstration of indirect (Fischer 1, 2, 3) technique
—position 1: needle directed from contralateral premolars bisecting
the index finger for surface anaesthesia.
FIGURE 9.45 (A) Site of needle penetration. (B) Clinical

demonstration of Position 1.
FIGURE 9.46 Demonstration in skull—position 2. Without
withdrawing the needle, the syringe is repositioned to the same
side and LA injected anaesthetising lingual nerve.

lingual nerve from ipsilateral side.
FIGURE 9.48 Demonstration in skull—position 3: anaesthetising
inferior alveolar nerve.
inferior alveolar nerve from contralateral side bicuspids.
Technique
The position of the patient and identification of landmarks are similar to that
for the direct technique.
1st position (long buccal nerve)

Once the tip of the finger is on the internal oblique ridge the patient is asked to
open his/her mouth wide and a 15/8 inch needle is held in pen grasp and
inserted from the opposite side bicuspid area into the mucous membrane
bisecting the index finger nail. The clinician should not attempt to contact the
bone. 6 mm of the needle should have penetrated the tissues. 0.5 mL of local
anaesthetic drug is deposited here to anaesthetise the long buccal nerve but
usually this nerve does not get anaesthetised.
2nd position (lingual nerve)

The syringe is withdrawn slightly and shifted on the same side so that it glides
over the temporalis tendon on the internal oblique ridge. Here the needle is
further advanced to a depth of 6–9 mm and 0.5 mL of local anaesthesia should
be deposited.
3rd position (inferior alveolar nerve)

The syringe is again returned to the opposite side and further advanced to a
distance of 12–15 mm until bony resistance is felt. After negative aspiration
1.8 mL of the solution is deposited slowly to anaesthetise the inferior alveolar
nerve.
A tingling sensation in the lower lip and one half of the tongue indicates the
effects of the anaesthesia.
Gow-Gates technique
Devised by Dr. George Gow-Gates, a general practitioner of dentistry, in
Australia in 1973. This technique has an advantage of higher success rate than
inferior alveolar nerve block.

2. Mental nerve
3. Incisive nerve
4. Lingual nerve
5. Mylohyoid nerve
6. Auriculotemporal nerve
7. Buccal nerve
Areas anaesthetised
Same as inferior alveolar nerve block along with skin over zygoma, posterior
portion of cheek and temporal regions.
Target area
Lateral region of condyle neck, just below the insertion of lateral pterygoid
muscle.
Landmarks
Extraoral
Lower border of tragus of ear, which corresponds to the centre of external
auditory meatus and corner of the patient’s mouth.
Intraoral
Tip of the needle is placed just below mesiopalatal cusp of maxillary second
molar.

Patient is positioned in supine posture with neck extended and mouth wide
open. This position facilitates the injection by moving the condyle anteriorly.
Now palpate the anterior border of the ramus of the mandible and identify the
tendon of temporalis muscle. Penetrate the needle gently into tissues just distal
to maxillary second molar tooth at the height of mesiopalatal cusp of second
molar. The needle should be just medial to the temporal tendon and directed
in the direction parallel to an imaginary line drawn from the corner of the
mouth to the intertragic notch of the ear and advanced until the fovea region
of the condylar neck is contacted. With negative aspiration, deposit 1.8 mL of
solution over 60–90 s. The patient is asked to keep the mouth wide open for
20–30 s after the injection to allow bathing of the nerve with the solution.
FIGURE 9.50 Demonstration of Gow-Gates technique in skull.
FIGURE 9.51 Clinical demonstration of Gow-Gates technique:
mouth wide open and needle is directed parallel to the inter-tragic
notch line drawn from the corner of the mouth to inter-tragic notch.
FIGURE 9.52 The needle is angulated parallel to the divergence of

ear to face.
Vazirani–Akinosi’s closed-mouth mandibular block

This technique was originally proposed by Dr. Joseph Akinosi in 1977, which
later on gained importance since the landmarks are easily identified and the
technique is simple to master (Figs. 9.53–9.55).
FIGURE 9.53 (A–B) Demonstration of Akinosi’s technique in skull.

Note the needle in contact with the green wire (indicating inferior
alveolar nerve).
FIGURE 9.54 Illustration depicting the site of needle insertion in

Vazirani–Akinosi technique.
FIGURE 9.55 Clinical demonstration of Vazirani–Akinosi’s
technique: needle insertion medial to ramus at the height of
maxillary molar mucogingival junction.

2. Mental nerve
3. Incisive nerve
4. Lingual nerve
5. Buccinator
6. Mylohyoid nerve
Areas anaesthetised
Same as inferior alveolar nerve block.
Target area
• Soft tissue on the medial border of ramus of mandible in the region of

inferior alveolar nerve, lingual and mylohyoid nerves.
• Height of injection is below that of Gow-Gates technique.
Landmarks
1. Mucogingival junction of maxillary third or second molar

2. Maxillary tuberosity
3. Coronoid notch on ramus of mandible
Technique
Patient is positioned in the supine posture with the teeth occluded.
Retract the lip to expose the maxillary and mandibular teeth. The syringe is
directed parallel to the occlusal and sagittal planes at the level of mucogingival
junction of maxillary molars. Penetrate the needle just medial to the ramus of
mandible 25–30 mm into the tissues. Now the tip of needle lies in mid portion
of pterygomandibular space, close to the branches of mandibular nerve. With
negative aspiration 1.5–1.8 mL of anaesthetic solution is deposited.
Mental nerve block

Mental nerve and terminal branch of inferior alveolar nerve.
Areas anaesthetised
Buccal mucous membrane anterior to the mental foramen, i.e. from first molar
to midline, lower lip and skin of chin.
Target area
Mental nerve when it exits from the mental foramen, located between the
apices of the first and second premolars.

The apices of the two premolars are estimated and a 1 inch, 25-gauge needle is
used to puncture at a point just behind the mental foramen and somewhat
lateral to the depth of the labial sulcus (the cheek being retracted) so that about
1 cm of tissue is penetrated. The needle is advanced to a position beneath the
fingertip where gentle palpation should allow the foramen to be found. The
needle travels mainly downwards but also slightly anteriorly and medially
until the periosteum of the mandible is gently contacted. About 0.5–1 mL of
solution is deposited and the fingertip is used to help massage it into the canal.
FIGURE 9.56 Surface anatomy of mental foramen in a skull at the
apex of premolars directed posterosuperiorly.
FIGURE 9.57 Illustration of mental nerve block dermatome.
FIGURE 9.58 Demonstration of mental block in a skull—note the
direction of needle anteroinferiorly in accordance with the foramen
anatomy.
FIGURE 9.59 Clinical demonstration of mental nerve block.
Buccal nerve block

Alternative names: Long buccal nerve block, buccinator nerve block.
Target area
Buccal nerve as it passes over the anterior border of ramus.
Landmarks
Mandibular molars and mucobuccal fold.
1. Buccal soft tissue is retracted with the index finger of left hand.
2. Syringe is directed towards injection site parallel to the occlusal plane
on the side of injection.
3. Penetrate needle distal and buccal to last molar.
4. With negative aspiration, deposit 0.2–0.5 mL of solution.
Lingual nerve block (Fig. 9.60)

The lingual nerve is usually blocked in the pterygo-mandibular space where it
lies anteromedial to the inferior alveolar nerve, about 1 cm or slightly less from
the mucosal surface. It is possible to inject this nerve either before or after the
inferior alveolar nerve is anaesthetised.
FIGURE 9.60 Demonstration of lingual nerve block in a skull. Note

the nerve can be anaesthetised anywhere along its course.
The lingual nerve can be blocked at a site posteroin-ferior to the third molar
by a submucosal injection or anaesthetised by infiltration at the site of surgery
in the lingual sulcus. Up to 0.5 mL of the solution is used for blocked side. An
aspiration test is normally not necessary.
Mental nerve block
Mental nerve, incisive nerve.
Areas anaesthetised
Lower lip, mandible and overlying structures anterior to the mental foramen,
mandibular teeth anterior to the mental foramen.
Landmarks
Bicuspid teeth, lower border of the mandible, supra-orbital notch, infraorbital
notch, pupil of the eye.
Techniques
The supraorbital and infraorbital notches are located by palpation. An
imaginary line is drawn through supraorbital notch, pupil of the eye,
infraorbital notch which continues down to pass through mental foramen. A
point which is midway between the lower border of the mandible and gingival
margin is estimated and marked on the imaginary line to locate the mental
foramen. A 22-gauge needle is directed slightly anteroinferiorly towards the
mental foramen that opens in a posterosuperior direction. After negative
aspiration 1 mL of anaesthetic solution is deposited slowly into the foramen.
Mandibular nerve block (Figs. 9.61–9.67)

Mandibular nerve and its subdivision.
FIGURE 9.61 Surface anatomical landmarks for extraoral
mandibular nerve block—sigmoid notch, inferior zygomatic arch,
lateral pterygoid plate. Note the mandibular nerve exiting the
foramen ovale directed towards the mandibular foramen.
FIGURE 9.62 Note the mandibular nerve (V3) exiting the foramen
ovale posterior to the lateral pterygoid plate.
FIGURE 9.63 Demonstration in skull—position 1. Needle directed
perpendicular through the sigmoid notch hitting the lateral
pterygoid plate.
FIGURE 9.64 Demonstration of same in skull.

FIGURE 9.65 Clinical demonstration—position 1. Needle
penetrates perpendicular to the skin through the centre of the
sigmoid notch.
FIGURE 9.66 Demonstration in skull—position 2. Needle

withdrawn slightly and directed posterior to the lateral pterygoid
plate and LA deposited close to the mandibular nerve (V3).
FIGURE 9.67 Clinical demonstration of position 2 of mandibular
nerve block.
Areas anaesthetised
Temporal region, auricle of the ear, external auditory meatus,
temporomandibular joint, salivary glands and lower portion of the face except
the angle of the jaw.
Landmarks
Same as that for extraoral maxillary nerve block.
Technique
The technique is same as that for maxillary nerve block with the exception that
the marker is placed at 5 cm on the needle. When the needle contacts the
pterygoid plate it is withdrawn and redirected slightly upwards and posterior,
so that it passes posterior to the lateral pterygoid plate.
Complication of local anaesthesia

1. Complications occurring due to injection technique
• Needle breakage
• Trismus
• Haematoma
• Facial nerve paralysis
• Diplopia
• Paraesthesia
• Oedema
• Postanaesthetic intraoral lesions
• Infection
2. Complications occurring due to anaesthetic solution
• Toxicity of the drug

• Allergy to the drug
• Burning sensation
Complications occurring due to injection technique

Needle breakage (Fig. 9.68)
Causes
• Sudden and unexpected movement by the patient in the opposite

direction of the needle insertion when the needle penetrates the soft
palate
• Reuse of the needle
• Defective manufacturing
FIGURE 9.68 Needle breakage. Broken needle in the

pterygomandibular space (inferior alveolar nerve block).
Prevention
• Use larger gauge needles

• Use longer needles
• Do not insert the needle till its hub
• Do not redirect the needle in multiple directions inside the tissues.
Management
• Remove the needle if it is visible, with the help of a haemostat.

• If not visible, take appropriate radiographs of the region. Localise the
needle and if in accessible region removal can be done surgically.
• If the needle is lost into the tissue spaces, e.g. pterygomandibular
space, infratemporal space, assure the patient and review regularly.
Unless complicated by pain or infection, fibrous capsule forms and the
foreign body, requires no management.
Trismus
Muscle spasm resulting in defective mouth opening.
Causes
• Trauma to the muscles and blood vessels in the infratemporal space.

• Trauma to the muscle caused by repeated needle insertion especially
medial pterygoid in inferior alveolar nerve block.
• Low grade infection
• Excessive haemorrhage or haematoma which produces irritation of the
tissues and muscle dysfunction.
• Solutions which contain alcohol or other cold sterilising solutions
irritate the tissues and produce trismus.
Prevention
• Use sharp, sterile, disposable needles as the trauma and infection

caused by them is less
• Do not use contaminated needles
• The injection technique should cause as less trauma as possible
• Clean the area of needle insertion with an antiseptic solution before
injection
• Avoid repeated insertion
• Avoid using barbed needle that results when needle hits the bone
• Change needle for every new insertions made.
Management
• Moist heat therapy where in hot towels are applied for 20 min an hour
• Analgesics for managing pain
• Physiotherapy involving dynamic jaw exercise.
Haematoma (Fig. 9.69)

Haematoma is defined as effusion into the extravascular space. It is rare in the
palatal region due to the close adherence of the palatal mucoperiosteum to the
bone.
FIGURE 9.69 Figure illustrating needle penetration into the

pterygoid venous plexus, damage to which can cause haematoma.
This commonly occurs during the high tuberosity nerve block.
Cause
Damage blood vessel by the needle during penetration of soft tissues.
Prevention
• The surgeon should use an appropriate technique according to the
anatomic structures.
• The number of needle penetrations should be as low as possible.
• The surgeon should follow injection techniques with structures a lesser
risk of haematoma.
• The surgeon should use shorter needles for posterior superior alveolar
nerve block.
Management
• Apply direct pressure over the bleeding site for a few minutes
• Apply ice locally
• Prescribe analgesics, antibiotics and muscle relaxants.
Facial nerve paralysis (Figs. 9.70–9.71)

Usually occurs in inferior alveolar nerve block. Facial nerve is the motor
supply to muscles of facial expression. Loss of motor action of the muscles of
facial expression produced by local anaesthesia lasts for one to several hours.
The patient suffers unilateral paralysis of the facial muscles.
FIGURE 9.70 Transient facial palsy of right side at rest.
FIGURE 9.71 Transient facial palsy of right side during action.
Cause
Injection of local anaesthetic agents in the parotid capsule or within the
substance of the parotid gland.
Prevention
Ensure that the needle tip contact the bone before the solution is injected.
Management
• Reassure the patient and explain that it is transient

• Remove contact lenses if the patient is wearing
• Avoid further dental therapy and reassess for recovery
Diplopia (Fig. 9.72)

Diplopia refers to double vision.
FIGURE 9.72 Diplopia—due to paralysis of lateral rectus muscle

(abducent nerve).
Cause
It is caused by the paralysis of the lateral rectus due to diffusion of anaesthetic
solution directly from the pterygomaxillary fossa inferior orbital tissue to the
orbit. This will, in turn, affect the ciliary ganglion located between the optic
nerve and the lateral rectus muscle of the eye.
Prevention
Proper injection technique.
Management
Reassure the patient by explaining the situation. The diplopia lasts only for a
few hours and will resolve without any residual effect.
Paraesthesia
It refers to altered sensation in the area of skin or mucosa.
Causes
• Trauma to the nerve by inadvertent needle penetration.

• Injection of local anaesthetic solution with alcohol or cold sterilising
solution near a nerve produces irritation and oedema of the tissues
and subsequent pressure on the nerve
• Haemorrhage around the neural sheath also causes pressure on the
nerve, leading to paraesthesia.
Prevention
Proper injection technique.
Management
• Most cases resolve within 8 weeks

• Reassurance to the patient
• Review regularly to check for Tinel’s sign
• If it persists for more than 1 year, it requires neurosurgical
intervention.
• If no recovery after 1 year, microneurosurgery may be advocated.
Oedema
Oedema (also known as dropsy or fluid retention) is swelling caused by the
accumulation of abnormally large amounts of fluid in the spaces between the
body’s cells or in the circulatory system.
Causes
• Trauma
• Allergy (angioedema is most common)
• Haemorrhage
• Infection
• Injection of irritating solution
Prevention
• Asepsis: Avoid injecting into abscess or infection site and reinjecting—

area of the oral cavity
• Use atraumatic techniques and gentle handling of tissues
• Proper medical history of the patient
Management
• Assess the type of oedema, cause and check for airway (no risk of
obstruction) and vital signs
• Traumatic oedema resulting from inflammation resolves in 1–3 days
with antiinflammatory drugs.
• Allergic oedema: Requires immediate assessment to avoid risk of
anaphylaxis: treated with antihistaminics and steroidal
antiinflammatory drugs.
Postanaesthetic intraoral lesions
• Recurrent aphthous ulcer or herpes simplex sometimes develops after

intraoral injection of local anaesthetics.
• Herpes simplex develops on oral mucosa attached to the bone, e.g.
palate, attached gingiva
• Recurrent aphthous stomatitis develops on oral mucosa not attached to
the bone, e.g. buccal mucosa
• Pain is the major symptom and may last for 7–10 days.
Cause
Trauma to the oral tissues caused by the needle or any other instrument
reactivates the dormant disease.
Prevention
Gentle handling of tissues.
Management
• Topical anaesthetics
• Reassurance to the patient
• Avoid steroidal antiinflammatory drugs
Infection
Use of unsterilised, contaminated needles can induce infection.
Cause
Commonly involved pathogens include Pseudomonas, Escherichia coli,
Staphylococcus aureus, Mycobacterium.
Prevention
• Use of disposable syringes and needles

• Use of appropriately sterilised needles
• Avoid crosscontamination between different sites within the oral
cavity
Management
Treat the infection with appropriate antibiotics.
Complications occurring due to anaesthetic

solution
Toxicity of the drug
This refers to symptoms manifested as a result of over dosage or excessive
administration of a drug. The blood level of the drug necessary to produce a
toxic effect may differ for the same drug from one individual to the other and
in the same individual from day to day. Clinically, the patient demonstrates
talkativeness, excitability, restlessness, lethargy, increased blood pressure,
tachypnoea, unconsciousness, etc. which are clinical presentation of extended
systemic effects.
Causes
• Accidental intravascular injection

• High dosage
• Rapid absorption into the blood stream
Prevention
• A thorough medical history of the patient prior to administration of

LA
• Administration of minimal effective volume of drug sufficient to
achieve the desired anaesthesia
• Aspiration should be done before depositing the solution
• Slow administration of the anaesthetic solution
Management
• Treatment should be symptomatic

• Discontinue any further administration of the LA
• Adequate ventilation must be maintained
• BLS is performed if required
Allergy to the drug

Allergy is defined as a hypersensitive state acquired through exposure to a
particular allergen. Some patients may be allergic to the LA solution. The
clinical manifestations may vary from case to case and includes angioedema,
urticaria, dermatitis, fever, asthma, rhinitis and anaphylaxis.
Cause
Specific antigen–antibody reaction in a patient who has been previously
sensitised to a particular drug or chemical derivative.
Prevention
• Intradermal test dose

• No drugs should be administered if the patient gives a history of
allergy.
Management
Depending on the degree of clinical presentation, it is treated by:
• Antihistamine agents
• Oxygen
• Steroids
• BLS administration if required
• In case of anaphylaxis, management varies (refer to Chapter 7 Medical
Emergencies and their Management.)
Burning sensation
This is not an uncommon complication during injection of local anaesthetics.
Causes
• Decreased pH of the injected solution

• Rapid injection
• Contamination of local anaesthetic cartridges
Prevention
• Slow administration of LA
• Use of sterile cartridges
Management
In the majority of cases, the patient may not even be aware of the sensation
and since it lasts for only a few seconds, no management is required.
CHAPTER 10
General Anaesthesia
History
Previous anaesthetics history
Airway assessment
Risk assessment
Premedication
Anxiolysis
Amnesia
Antiemetic
Antacid
Antiautonomic
Analgesia
Delivery of gases to the operating theatre
PMGV System
Role of the anaesthetic machine
Anaesthetic breathing systems
The circle system
Soda lime
Mechanical ventilation
Principles of mechanical ventilation
Managing the airway
• Face masks
• Oropharyngeal airway
• Nasopharyngeal airway
Laryngeal mask airway (supraglottic airway)
Tracheal intubation
Indications for tracheal intubation
Equipment for tracheal intubation
Technique of oral intubation
Complications of tracheal intubation
Intravenous anaesthetic (induction) agents
• Sodium thiopentone
• Propofol
• Ketamine
• Midazolam
Inhalational induction
Maintenance of anaesthesia: inhalational (volatile) agents and

intravenous infusions
Nitrous oxide
Halothane
Isoflurane
Sevoflurane
Propofol (2,6-di-isopropylphenol)
Ether (diethyl ether)
Muscle relaxation during anaesthesia: neuromuscular blocking drugs
and their antagonism
Normal neuromuscular transmission
Non-depolarising muscle relaxants
Tubocurarine
Alcuronium
Pancuronium
Atracurium
Vecuronium
Mivacurium
Depolarising muscle relaxants
Suxamethonium chloride (succinylcholine—Sch)
Pseudocholinesterase deficiency
Prolongation of neuromuscular blockade
Monitoring neuromuscular blockade
Clinical monitoring
Peripheral nerve stimulation
Anticholinesterases
Neostigmine
Conscious sedation
Features of conscious sedation
Techniques currently accepted for routine use in
dentistry
Clinical effects
Objectives of conscious sedation
Commonly used pharmacological agents for conscious
sedation
General anaesthesia
A drug induced reversible loss of consciousness during which patients are not
arousable, even by painful stimulation. The ability to independently maintain
ventilatory function is often impaired. Patients require assistance in
maintaining a patent airway and positive pressure ventilation may be
required because of depressed spontaneous ventilation or drug induced
depression of neuromuscular functions.
Preanaesthetic evaluation consists of the consideration of information from
multiple sources that may include the patient’s medical records, interview,
physical examination, and findings from medical tests and evaluations.
History
To avoid any complications it is mandatory to elicit the required history from
the patient.
Current medical/systemic/surgical problems
The aspects relating to the cardiovascular and respiratory systems are the most
important in a patients’ medical history. The questions and details required
will vary depending upon the disease present, its severity, anticipated
anaesthesia and the planned operation.
Previous anaesthetics history
• History of any difficulties with previous anaesthetics, for e.g. nausea,

vomiting, dreams, awareness, postoperative jaundice. The records of
previous anaesthetic exposure is noted to rule out or clarify problems
like difficulties with intubation, drugs administered or adverse drug
reactions.
• Idiosyncratic Hepatic Injury may result from repeated exposure to
halothane. Hence to avoid this risk, the approximate date of previous
administration of anaesthetics, particularly if recent, is noted.
Drugs and allergies

Dose and duration of medication, prescribed as well as over the counter self-
medication, herbal products, natural supplement, etc.
Compared to any other group, the geriatric population consumes more
systemic medications. Special attention must be paid to drug interactions and
complications that arise in this population.
Except some adjustment in dosage which may be required (e.g.
antihypertensives, insulin), administration of most drugs is continued
including the morning of operation.
Preoperatively some drugs need to be discontinued. Due to the risk of
interactions with drugs used during anaesthesia, the monoamine oxidase
inhibitors should be withdrawn 2–3 weeks before surgery.
Due to the increased risk of venous thrombosis, the oral contraceptive pill
should be discontinued at least 6 weeks before elective surgery.
Patients should discontinue their herbal supplements at least 2 weeks prior
to surgery as per recent studies by the American Society of Anesthesiologists
(ASA) on herbal supplements and the potentially harmful drug interactions
that may occur with their continued use preoperatively.
To avoid excessive bleeding, aspirin should be discontinued 7–10 days
before surgery and thienopyridines (such as clopidogrel) for 2 weeks before
surgery. As selective cyclooxygenase-2 (COX-2) inhibitors do not potentiate
bleeding they can be continued until surgery. 4–5 days prior to invasive
procedures oral anticoagulants should be stopped, allowing INR to reach a
level of 1.5 prior to surgery
History of previous blood transfusions is important.
Family history
A history of prolonged apnoea after anaesthesia may suggest
pseudocholinesterase deficiency. History of any inherited or ‘family’ diseases,
e.g. sickle cell disease, porphyria, malignant hyperpyrexia. Malignant
hyperthermia is a rare inherited disorder with high mortality rate that occurs
following GA administration.
Social history
Smoking
Avoiding smoking for 8 weeks improves the airways, for 2 weeks reduces
their irritability and for as little as 24 h prior to anaesthesia decreases
carboxyhaemoglobin levels.
Alcohol
Induction of liver enzymes and tolerance to anaesthetic drugs results from
excessive consumption of alcohol. Alcohol withdrawal syndrome
postoperatively is the risk that should be considered.
Drugs
The use of drugs for recreational purposes needs to be determined specifically
including type, frequency and route of administration. These groups of
patients are at risk of infection with hepatitis B and human immunodeficiency
virus (HIV). In patients using an intravenous route due to widespread
thrombosis of veins, there can be difficulty with venous access.
Pregnancy
In all women of childbearing age, the date of the last menstrual period (LMP)
should be noted. In early pregnancy the risk of inducing a spontaneous
abortion is increased by anaesthesia, while in late pregnancy the risk of
regurgitation and aspiration is increased.
Review of systems
A complete review of systems to look for undiagnosed disease or inadequately
controlled chronic disease should be includeed in the history. The most
relevant in respect of fitness for anaesthesia and surgery are the diseases of the
cardiovascular and respiratory systems.
Cardiovascular system
Specific enquiries must be made about:
• Angina: its incidence, precipitating factors, duration, use of antiangina
medications as glyceryl trinitrate (GTN) tablets or spray.
• Previous myocardial infarction and subsequent medical care.
• History of palpitations, cough, shortness of breathe and syncope.
• History of orthopnoea, paroxysmal nocturnal dyspnoea, ankle
swelling.
• Patients with a history of ischaemic heart disease (IHD), myocardial
infarction (MI), hypertension, heart failure and valvular heart disease
are important to be identified.
• Greater risk of perioperative reinfarction, the incidence of which is
related to the time interval between infarct and surgery in patients
with a proven history of myocardial infarction.
• Exaggerated cardiovascular responses during aesthesia may result
from untreated or poorly controlled hypertension (diastolic
consistently > 110 mmHg). The risk of myocardial ischaemia is
increased by both hypertension and hypotension. Blood Pressure
should not exceed 180/110 mmHg before general anaesthesia.
• Anaesthetic drugs have depressant effects on the heart which will
worsen heart failure, thereby impairing the perfusion of vital organs.
• Anticoagulants may be taken by patients with valvular heart disease or
prosthetic valves. Prior to surgery they may need to be discontinued or
changed. During certain types of surgery, antibiotic prophylaxis will
be required.
Assessing cardiovascular risk

The American College of Cardiology (ACC) and the American Heart
Association (AHA) published a task force report on Guidelines for
Perioperative Cardiovascular Evaluation for Noncardiac Surgery (Table 10.1)
Table 10.1
Guidelines for perioperative cardiovascular evaluation for noncardiac surgery
Major clinical predictors (markers of unstable coronary artery disease)

Myocardial infarction <6 weeks Unstable or severe angina (class III–IV)
Decompensated congestive heart failure
Significant arrhythmias (e.g., causing hemodynamic instability)
Severe valvular disease (e.g., aortic or mitral stenosis with valve area <1.0 cm2) CABG or
PTCA <6 weeks
Intermediate clinical predictors (markers of stable coronary artery disease)
Previous myocardial infarction <6 weeks and <3 months (<3 months if complicated) based on
the history or the presence of pathologic Q wavesMild angina (class I-II)
Silent ischaemia (Holter monitoring)
Compensated congestive heart failure, ejection fraction <0.35
Post CABG or PTCA <6 weeks and <3 months, or <6 years, or with antianginal therapy
Diabetes mellitus Renal insufficiency
Minor clinical predictors (increased probability of coronary artery disease)
Familial history of coronary artery disease Age >70 years
ECG abnormalities (arrhythmia, LVH, left bundle branch block)
Low functional capacity History of stroke
Uncontrolled systemic hypertension
Hypercholesterolemia
Smoking
Post infarction (>3 months), asymptomatic without treatment
Post CABG or PTCA <3 months and <6 yr, and no symptoms of angina nor antianginal
therapy
CABG = coronary artery bypass grafting. PTCA= percutaneous transluminal coronary
angioplasty, LVH=left ventricular hypertrophy
Patient-Related Predictors for Risk of Perioperative Cardiac Complications
(Table 10.2)
Table 10.2
Patient-related predictors for risk of perioperative cardiac complications
High risk procedures (cardiac complication rate >5%)

Emergency surgery
Aortic and major vascular surgery
Prolonged surgical procedures with large fluid shifts or blood lossUnstable hemodynamic
situations
Intermediate risk procedures (cardiac complication rate 1%–5%)
Abdominal or thoracic surgery
Neurosurgery
ENT procedures
Minor vascular surgery, including carotid endarterectomy
Orthopedic surgery
Prostatectomy
Low risk procedures (cardiac complication rate <1%)
Breast surgery Superficial surgery Eye surgery
Endoscopic and reconstructive surgery Ambulatory surgery
Diabetes mellitus is included in intermediate category because it is

frequently associated with silent ischaemia and represents an independent risk
factor for perioperative mortality.
Surgery-Related Predictors for Risk of Perioperative Cardiac Complications
Previous MI
Elective anaesthesia and surgery were previously considered to be
contraindication for MI within 6 months of proposed surgery. The risk after a
previous infarction is relatively less to the age of the infarction than to the
functional status of the ventricles and to the amount of myocardium at risk from
further ischaemia have been recently proved.
The myocardium needs a period of 6 weeks to heal after an infarction and
for the thrombosis to resolve. Therefore, for coronary revascularised patients
only vital or emergency surgical procedures should be considered and all
elective operations should be postponed.
The period of intermediate risk ranges from 6 weeks to 3 months; but in
cases of arrhythmias, ventricular dysfunction or continued medical therapy, it
should be extended beyond 3 months.
Delaying surgery more than 3 months after an ischaemic accident has
demonstrated no benefit in uncomplicated cases.
Therefore, before performing noncardiac surgery after myocardial infarction
or revascularisation a 3-month minimum delay is indicated.
Recent studies, have demonstrated a marked benefit of reduced cardiac
complication rate by operating under the protection of β1-adrenergic
antagonism.
Perioperative cardiac complications

Major perioperative cardiac complications are myocardial infarction,
pulmonary oedema, ventricular fibrillation, primary cardiac arrest, or
complete heart block.
Perioperative MI: carries a high mortality. It occurs within the first 2 days of
surgery and usually presents atypically (without chest pain).
The ACC/AHA Guidelines for Perioperative Cardiovascular Evaluation for
Noncardiac Surgery offer recommendations for a patient suffering a
perioperative MI includes consideration for prompt angioplasty, aspirin, beta-
blockade and possible angiotensin converting enzyme inhibitor therapy.
Respiratory system
Enquire specifically about these symptoms:
• Cough and production of sputum (volume and colour)

• Dyspnoea
• Wheeze (and precipitating factors)
• Identify patients who have a history of chronic obstructive pulmonary
disease (COPD), emphysema, bronchiectasis and asthma.
• Patients with preexisting lung disease, particularly if they are also
obese, are more prone to positive chest infections. Unless it is for a life-
threatening condition, a patient with an acute upper respiratory tract
infection should have anaesthesia and surgery postponed.
• A very useful indication of both cardiac and respiratory reserve is the
patient’s ability to perform everyday physical activities before having
to stop because of symptoms (e.g. chest pain, shortness of breath).
Other conditions that are important if identified in the medical history
Diabetes
When a diabetic patient needs surgery, neglect of the long-term complications do
more harm than short-term control of blood glucose levels. The majority of long-
standing diabetics develop compromise in one or more organs. Careful
preoperative assessment of symptoms and signs of peripheral vascular,
cerebrovascular and coronary disease is essential in a diabetic patient planned
for elective surgery. It is important to identify and manage the coexisting
pathologies perioperatively.
Postoperatively patients may develop hypoglycaemia [glucose level
<50 mg/dL (2.8 mmol/L) in adults and <40 mg/dL (2.2 mmol/L) in children]
due to residual effects of long-acting oral hypoglycemic agents or insulin
preparations given preoperatively, in addition to perioperative fasting.
Anaesthetics, analgesics, sedatives and sympatholytics agents alter the usual
presenting symptoms of hypoglycaemia thereby delaying the recognition of
hypoglycaemia in the perioperative period. In addition, blunting of the
adrenergic symptoms associated with hypoglycaemia is found in diabetics
with autonomic neuropathy. Confusion, irritability, fatigue, headache and
somnolence are the initial symptoms which may progress to seizures, focal
neurologic deficits, coma and death.
Generally, in diabetic patients there is an increased incidence of IHD, renal
dysfunction, postoperative infection, autonomic and peripheral neuropathy.
Incidence of intra- and postoperative complications increases.
Neuromuscular disorders
In these patients care must be taken when administering muscle relaxants, care
must be taken.
Chronic renal failure

Anaemia, electrolyte abnormalities and altered drug excretion are some of
problems seen in these patients. The choice of anaesthetic agents is restricted
due to altered drug excretion.
Jaundice
This is usually indicative of infective or obstructive liver disease. Alteration in
drug metabolism may be present. Preoperatively, patient’s coagulation must
be checked.
Epilepsy
Perioperaively, in patients with a history of well-controlled epilepsy, measures
should be taken to avoid disruption of antiepileptic medication. On the
morning of surgery, regular medications should be continued and regular
dosing should be reestablished as early as possible after surgery.
In case of day case surgeries, if a single dose is missed, it should be taken as
soon as possible after surgery. Antiepileptic drugs (AEDs) should be
administered parenterally when multiple doses are likely to be missed. I.V.
forms of phenytoin, sodium valproate, and levetiracetam are available (where
i.v. doses are equivalent to oral doses) and carbamazepine is available as a
suppository.
Serum concentrations of phenytoin are checked daily in patients admitted to
ICU. It serves as a guide for adjusting the dose.
General examination
Physical examination
Vital signs
Airways
Examination of airway is important as various causes related to dental,
mandible or cervical spine may cause difficulty during endotracheal
intubation. Especially in case of trauma, cervical spine examination is
mandatory. Various causes related to difficult laryngoscope mentioned in
Box 10.1
Box 10.1 Anatomical causes associated with difficult

laryngoscope
• Proclined incisors
• Long and high arched palate
• Retrognathic mandible
• Restricted mandibular movement
• Decreased atlanto-occipital distance (cause reduced neck extension)
• Short muscular neck
• Gross obesity
• Large breast in females
Conditions associated with difficult laryngoscope

Congential deformities
Down syndrome, Pierre Robin syndrome, Treachercollins syndrome, Marfan’s
syndrome [associated with small mouth/large tongue/cleft palate
Trauma and infection
Dental abscess, fracture of mandible [causes reflex spasm of masseter and
medial perygoid relieved by anaesthesia]
TMJ ankylosis
Restricted/Immobility of mandible [not relieved after anaesthesia]
Soft tissue oedema/swelling/mass
Infections, trauma, tumours
Miscellaneous:
• Foreign bodies, scarring after infection/radiotherapy/burns
Airway assessment
Assessment is often made in three stages: (1) observation of patient’s
anatomy, (2) simple bedside tests and (3) X-rays.
1. Observation of the patient’s anatomy
• Amount of mouth opening (interincisal distance) A receding mandible

• Teeth: position, number and health
• Tongue size
• Soft tissue swellings of the neck
• Deviated larynx or trachea
• Mobility of the cervical spine in both flexion and extension.
2. Simple bedside test

a. Wilson score
Five factors are assessed and scored based on a set of criteria. A score greater
than five suggests difficult intubation. Rarely used now.
b. Mallampati criteria
The patient is asked to open the mouth and maximally protrude the tongue
while sitting upright. The view of the pharyngeal structures is noted and
graded I–IV. Grades III and IV suggest difficult intubation (Fig. 10.1,
Table 10.1).
c. Thyromental distance
With the head fully extended; on the neck, the distance between the bony
point of the chin and the prominence of the thyroid cartilage is measured. A
distance less than 7 cm indicate difficult intubation (Fig. 10.2).
Thyromental distance (Patil’s test)

Tip of the thyroid to menton distance Difficulty level
6.5 mm No problem for laryngoscope
6–6.5 mm Difficult, but laryngoscope possible
< 6 mm Very difficult/impossible laryngoscope
Hb, Haemoglobin; ECG, electrocardiograph.
3. X-rays [not used routinely]

Measurements can be made on a lateral X-ray of the head and neck, which can
be used to help predict an impaired view at laryngoscopy. These include a
decreased distance between the occiput and the spinous process of C1 (< 5
mm) and an increase in the posterior depth of the mandible (>2.5 cm).
Allowance for any magnification should be taken into account for X-ray.
FIGURE 10.1 Pharyngeal structures seen during Mallampati

assessment.
FIGURE 10.2 Thyromental distance.
Arrhythmias, e.g. atrial fibrillation need to be determined. Auscultation
should be done to rule out valvular heart disease which may need further
investigations. The patient’s blood pressure should be taken. Finally, any
potential problem with intravenous access can be identified by inspecting the
peripheral veins.
Respiratory system
Identify signs like dyspnoea, wheezing, signs of collapse, consolidation and
effusion. The presence and degree of pulsus paradoxus serves as a useful
indicator of the severity of airway obstruction.
Nervous system
Identify chronic disease of the peripheral and central nervous systems and
record any evidence of motor or sensory impairment.
Musculoskeletal system
Restriction of movement and deformities are seen in patients with connective
tissue disorders. Patient’s cervical and temporomandibular joints need specific
attention Table 10.3.
Table 10.3
Modified Mallampati classification

Grade Structures visualised
Grade I Posterior pharyngeal wall, soft palate and uvula, faucial pillars, tongue base
Soft palate, uvula, fauces, pillars
Grade II Soft palate and uvula, faucial pillars, tongue base
Soft palate, uvula, fauces
Grade III Soft palate, faucial pillars, tongue base
Soft palate, base of uvula
Grade IV Hard palate and tongue base
Only hard palate visible
Special investigations
In patients with no evidence of concurrent disease, investigations can be
limited (Table 10.4).
Table 10.4
Baseline investigations for otherwise healthy patients

Age Sex Investigations
< 40 Male Nil
Female Hb and haematocrit values
41–60 Male ECG, blood sugar, serum creatinine Hb,
Female ECG, blood sugar, creatinine
> 61 Both Hb, ECG, blood sugar, creatinine
Hb, Haemoglobin; ECG, electrocardiograph.
Additional investigations
Ultimately, the need for investigations is dictated by the presence of other
disease processes. The following are a guide to those commonly investigated.
Investigations depend on type of surgery, comorbid illness, and patient’s
present medical condition
CBC, HB, HCT: History of increased bleeding, haematologic disorders,
renal disease, chemotherapy or radiation treatment
1. Urea and electrolytes
a. Patients taking digoxin, diuretics, steroids

b. Those with diabetes mellitus, renal disease, vomiting, diarrhoea,
Hypertension
2. Liver function tests
a. Patients with known hepatic disease

b. A history of a high alcohol intake (>50 units/week)
c. Evidence of malnutrition
d. Patients with metastatic disease
3. Blood sugar
a. Diabetes mellitus
b. Patients with severe peripheral arterial disease
c. Patients taking long-term steroids
4. ECG
a. Patients known to be or found to be hypertensive or with the history of

CAD, MI, diabetes, congestive heart failure, chest pain, palpitations,
murmurs, peripheral oedema, syncope, dizziness, dyspnea, shortness
of breath, stroke
b. Those patients with symptoms or signs of heart disease
5. Chest X-ray
a. History or signs of cardiac or respiratory disease

b. Patients with suspected or known malignancy
c. Patients from areas of endemic tuberculosis who have not had a chest
X-ray in the previous year.
6. Pulmonary function tests

Patients with dyspnoea on mild exertion or asthmatics require measurement
of peak expiratory flow rate (PEFR); forced expiratory volume in 1 s (FEV 1);
forced vital capacity (FVC).
Factors prompting preoperative pulmonary evaluation:
• Age >70
• Morbid obesity
• Thoracic surgery
• Upper abdominal surgery
• History of smoking, cough
• Any pulmonary disease
7. Coagulation screening
a. Patients with history of bleeding diathesis or patients on anticoagulants

or previous excessive intraoperative bleeding, hepatic disease, poor
nutritional status
b. Those with known history of liver disease or jaundice
8. Sickle cell screen (Sickle dex)
a. Patients with a family history of sickle cell disease

b. Patients whose ethnic origin has risk of sickle cell disease. If positive,
electrophoresis may be required for definitive diagnosis.
9. Cervical spine X-ray
a. Patients with rheumatoid arthritis

b. Patients with a history of major trauma or surgery to the neck
10. Echocardiograph
a. Presence of any congenital disease, abnormal ECG, poor functional

reserve, history or signs of cardiac disease
b. History of cardiac illness in the family
Risk assessment
1. Special indicators of risk
One system used to predict the risk of a cardiac event is the Goldman index.
Points are awarded as shown in Table 10.5.
Table 10.5
Goldman index
History Points
> 70 years 5
Myocardial infarction in prior 6 months 10
Examination
Third heart sound (gallop rhythm) or raised jugular venous pressure (JVP) 11
Significant stenosis 3
ECG
Rhythm other than sinus or presence of premature atriawl complexes 7
More than five ventricular ectopics per minute 7
General
PaO2 < 60 mmHg; PaCO2 > 50 mmHg
K’< 3 mmol/L
Urea > 8.5 mmol/L; creatinine > 200 mmol/L
Chronic liver disease
Bedridden for noncardiac disease for one or more criteria 3
Operation
Intrathoracic, intraperitoneal or aortic operation 3
Emergency surgery 4
Goldman index point scale showing risk of associated cardiac event or death
Points % Risk cardiac event % Risk death
0–5 0.7 0.2
6–12 5.0 2.0
13–25 11.0 2.0
> 26 22.0 56.0
2. General indicators of risk (Tables 10.6–10.8) not used routinely
Table 10.6
Factors associated with increased risk of Mortality

Increasing age: > 60 years
Sex: male > female
Worsening physical status
Increasing number of concurrent medical conditions, in particular;
myocardial infarction
diabetes mellitus
renal disease
Increasing complexity of surgery
Intracranial
major vascular
Intrathoracic
Increasing length of surgery (>2 h)
Emergency operations
Table 10.7
ASA physical status scale

ASA Physical Status Classification System
ASA Physical Status 1—A normal healthy patient
ASA Physical Status 2—A patient with mild systemic disease
ASA Physical Status 3—A patient with severe systemic disease that limits activity and is not
incapacitating
ASA Physical Status 4—A patient with incapacitating severe systemic disease that is a constant
threat to life
ASA Physical Status 5—A moribund patient who is not expected to survive with or without an
operation
ASA Physical Status 6—A declared brain-dead patient whose organs may be removed for donor
purposes
ASA Class E—Added as a suffix for emergency operation
E—Emergency operation of any variety (used to modify one of the above classifications (I–
IV), i.e ASA III–E)
• The classification of the patient helps us decide if the patient can be treated as an
outpatient.
• A patient with a higher risk of medical emergencies must be treated in a hospital with
adequate facilities to handle emergencies.
• If the patient is under treatment for a systemic disease, is pregnant, has undergone a recent
surgery or has undergone an immunity modifying treatment, due opinion, concurrence
and consent should be obtained from the treating specialist before embarking on any oral
surgery.
Table 10.8
Relationship between ASA status and postoperative mortality

ASA class Absolute mortality (%) Guide mortality per 10000 anaesthetics
I 0.1 7.2
II 0.2 19.7
III 1.8 115.1
IV 7.8 766.2
V 9.4 3358.0
ASA, American Society of Anesthesiologist.
Premedication
Premedication originally referred to those drugs administered to facilitate the
induction and maintenance of anaesthesia, literally preliminary medication.
The 6 A’s of premedication
1. Anxiolysis
2. Amnesia
3. Antiemetic
4. Antacid
5. Antiautonomic
6. Analgesic
1. Anxiolysis
Many patients awaiting surgery are anxious. Benzodiazepines is the most
commonly prescribed among the anaesthetic drugs. A degree of sedation and
amnesia is produced. Orally administered 45–90 min preoperatively as well-
absorbed from the gastrointestinal tract.
Large doses may cause hypnosis and unconsciousness. It may cause
moderate depression of circulation and respiration also cause
agitation/restlessness.
Those most commonly used include:
• Temazepam 20–30 mg
• Diazepam 10–20 mg
• Lorazepam 2–4 mg
Other agents that are useful as anxiolytics are Barbiturates, Butyrophenones

(Droperidol), phenothiazines (promethazine, trimeprazine,
Diphenhydramine). In addition, they produce sedation and are mildly
antiemetic. Sometimes, phenothiazines are associated with extrapyramidal
symptoms and hypotension, secondary to their a-blocking actions. b-blockers
may occasionally be of use in patients who with excessive somatic
manifestations of anxiety, e.g. tachycardia.
Diazepam: It is considered as the “gold standard” drug with excellent
anxiolytic, amnestic and sedative effect. It is dissolved in organic solvents
hence it causes pain on IV and IM. It has long duration of action hence not
suitable for day care surgical procedures. Pre administration of diazepam is
given on the night before surgery for anxiolysis. It is contraindicated in
cirrhosis, liver and renal dysfunction patients.
Midazolam: It is a rapidly metabolising drug with sedative, anxiolytic and
excellent amnestic agent. Rapid onset of action and more potent than
diazepam. Major advantage is that it does not cause phlebitis as it is water
soluble.
Barbiturates: It is previously used for preoperative sedation before
benzodiazepines. They do not produce analgesia sometimes may cause
antianalgesic effects. They also cause cardiovascular and respiratory
depression. It is contraindicated in porphyria patients. Due to its various side
effects it is largely replaced by benzodiazepines
2. Amnesia
Should provides anterograde amnesia and also by reducing risk of awareness
during surgery.
E.g.: Lorazepam, Midazolam
3. Antiemetic
Antiemetic drugs are often used as part of the premedication in an attempt to
reduce the nausea and vomiting induced by the administration of opioids. A
wide variety of drugs have antiemetic properties and many of these are used
for premedication:
• Dopamine antagonists, e.g. metoclopramide, domperidone, droperidol

• Antihistamines, e.g. cyclizine, promethazine
• Anticholinergics, e.g. atropine, hyoscine
• Phenothiazines, e.g. promazine
• 5-Hydroxytryptamine antagonists, e.g. ondansetron
Most commonly used drugs are metoclopramide and ondansetron

4. Antacid
To reduce the risk of regurgitation and aspiration of gastric acid, patients who
are about to be anaesthetised must have an empty stomach. This is usually
achieved by a period of starvation preoperatively. It may be difficult to
guarantee in patients who have hiatus hernias and those who are very
anxious. Delayed gastric emptying is seen in patients who have received
opiates preoperatively or present as emergencies, particularly if in pain. To
increase the pH and reduce the volume a variety of drug combinations are
used:
• Oral sodium citrate: chemically neutralises residual acid

• Cimetidine, ranitidine (H2 antagonists): reduce acid secretion
• Metoclopramide: increases gastric emptying and lower oesophageal
sphincter tone. Potential for regurgitation is reduced.
An alternative is using a naso- or orogastric tube for aspiration of gastric

contents: only in pregnant or full stomach cases in emergency.
Oral or intravenous formulations of ranitidine, pantaprazole are used
preoperativley in mostly full stomach patients
5. Antiautonomic
Parasympathetic reflexes
Profound bradycardia resulting from excessive vagal activity, may be seen
following the use of certain anaesthetic agents:
• Use of Halothane, especially for induction

• Repeated doses of suxamethonium
• Techniques using alfentanil, particularly if combined with vecuronium.
Surgical stimuli also have the same effect:
• During traction on the extraocular muscles (squint corrections)—

occulomotor reflex
• Elevation of a fractured zygoma
• Periorbital surgery
In Neonates and Infants Atropine is given preoperatively before induction to

prevent Bradycardia intra-operatively
Bradycardia is prevented by administration of anticholinergic agents like
atropine and glycopyrrolate. Though used preoperatively, they are most
effective when administered intravenously at induction.
In conjunction with hyoscine, they also prevent excessive secretion of saliva
induced by the presence of objects in the mouth, e.g. an oropharyngeal airway
or the use of the anaesthetic agents ketamine and ether.
Sympathetic reflexes
Tachycardia and hypertension at the time of intubation indicates increased
sympathetic activity. This is undesirable in certain patients, e.g. ischaemic
heart disease or raised intracranial pressure and hypertensive patients.
Attenuation of these responses can be done by the use of b-blockers. They can
be administered either orally preoperatively (atenolol, propranolol) or
intravenously at induction (esmolol).
Administration of potent analgesics at induction of anaesthesia (fentanyl,
alfentanil) serves as an alternative.
6. Analgesia
Although the oldest form of premedication, now generally reserved for
patients in pain preoperatively. Intramuscular form is the best route of
administration. The most commonly used are:
• Morphine
• Pethidine
• Fentanyl
Morphine and pethidine (and papaveretum) were widely used due to their
sedative effects but are relatively poor as anxiolytics. Benzodiazepines have
largely replaced them. In addition, opiates have side effects like nausea,
vomiting, respiratory depression and delayed gastric emptying.
In patients receiving opioids preoperatively, these drugs may be continued
with watch on respiration. In patients with acute pain, paracetamol and
NSAIDS are recommended as these are nonsedating and don’t cause
respiratory depression.
Miscellaneous
Pre-medicants are a variety of other drugs that are commonly administered
prophylactically prior to anaesthesia and surgery. The following are the most
common:
Steroids:
to patients on long-term treatment or who have received them within the past
3 months.
Antibiotic prophylaxis:
to patients with prosthetic or diseased heart valves.
Anticoagulants:
as prophylaxis against deep venous thrombosis.
Transdermal GTN:
administered as patch or a paste (percutol) in patients with ischaemic heart
disease to reduce the risk of coronary ischaemia.
EMLA:
a topically applied local anaesthetic cream. It is used to reduce the pain of
inserting an intravenous cannula.

Intravenous anaesthetic injection is used for induction and then gases and
vapours are administered for maintenance Tables 10.9–10.10.
Table 10.9
Medications that may have an interaction with anaesthetic agents

Drug group Comments
Angiotensin Potent vasodilators; synergistic with the effects of anaesthetics causing
converting hypotension
enzyme (ACE)
inhibitors:
i. Captopril
ii. Enalapril
Antibiotics: Duration of block is prolonged due to synergistic effect with
i. Aminoglycosides neuromuscular blocking drugs; Renal toxicity with long-term therapy or
ii. Polymyxins combination with some diuretics
Anticoagulants: During intubation, insertion of central lines, local/regional anaesthesia,
Oral: surgery, insertion of a nasogastric tube there is increased risk of
i. Warfarin, haemorrhage
ii. Nicoumalone
iii. Intravenous:
heparin
Anticonvulsants Potent inducers of hepatic enzymes, increased doses of induction agents
i. Barbiturates and opioids may be required.
ii. Phenytoin
iii. Carbamazepine
Benzodiazepines Wide variety of drugs with varying half-lives; tolerance common; additive
effect with others CNS depressants. Flumazenil (a specific
benzodiazepine) can precipitate a withdrawal syndrome
β-blockers: Hypotension may result from negative inotropic effects combined with
i. Atenolol vasodilatation by anaesthetic agents. Intraoperative blood loss cannot be
ii. Metoprolol determined by pulse rate.
iii. Oxyprenolol
iv. Propranolol
v. Sotalol
Calcium Nonspecific calcium antagonists: Isoflurane, enflurane and halothane
antagonists: Additive effects producing hypotension
i. Diltiazem Bradycardia secondary to decreased atrioventricular conduction by
ii. Nifedipine Verapamil
iii. Verapamil Toxicity common, predisposing to arrhythmias, potentiated by
iv. Digoxin suxamethonium
Diuretics: Dysrhythmias and prolonging neuromuscular blockade resulting from
i. Thiazides hypokalaemia
ii. Loop diuretics Hyponatraemia
Lithium Effects of non-depolarising neuromuscular-blocking drugs is prolonged
Monoamine Uncommon but potentially fatal interactions with opioids, particularly
oxidase pethidine and all sympathomimetics. Must be stopped at least two weeks
inhibitors prior to surgery
(MAO):
i. Isocarboxazid
ii. Phenelzine
iii. Tranylcypromine
Steroids Hypotension at induction of anaesthesia
Due to adreno-cortical suppression, supplementary doses required for
patients on long-term treatment or if taken in
the past 3 months
Tricyclic Potentiates the effects of exogenous catecholamines causing arrhythmias,
antidepressants for example adrenaline, used as a vasoconstrictor in local anaesthetics or
to reduce bleeding
Table 10.10
Relationship between saturated vapour pressures (SVP) and vapour
concentration for volatile agents
Delivery of gases to the operating theatre
This is achieved either by piped distribution (along with medical vacuum)
known as ‘piped medical gas and vacuum’ (PMGV), from bulk storage of the
gas or by the use of small cylinders attached directly to the anaesthetic
machine (Fig. 10.3).
FIGURE 10.3 Atlanto occipital extension.
PMGV System (Fig. 10.4)

This is used for the delivery of oxygen, nitrous oxide and vacuum. The gases
are delivered via specially made system with copper piping (to reduce
degradation), which carries labels at regular intervals. These pipelines end in
outlets, which serve as self-closing sockets, each specifically coloured and
labelled for one gas. The gases are delivered at a pressure of 4 bar [400 kPa, 60
pounds per square inch (psi)], except for medical air, which is delivered at
7 bar (700 kPa, 75 psi) to power medical tools. Flexible, reinforced hoses and
colour-coded throughout their length are used for onward delivery to the
anaesthetic machine.
FIGURE 10.4 PMGV system.
Oxygen
A liquid oxygen reserve supplies the oxygen. It is the most often and most
economical means to supply it. It is stored under pressure (10–12 bar,
1200 kPa) at approximately –180°C, in what is effectively a thermos flask or
more correctly a vacuum insulated evaporator (VIE). From the VIE to the
pipeline system, the gas is warmed to ambient air temperature.
To manage the possible failures of the main system a reserve bank of
cylinders of compressed oxygen is present.
Nitrous oxide and medical air

These are supplied from large cylinders bank is formed by joining several
cylinders and attached to a common manifold. There are usually two banks:
one that is running (duty bank) with all cylinders turned on and a second or
reserve bank. An additional small emergency supply is available. Switching
between banks is carried out automatically and accompanied by audible and
visual signals to indicate that replacement is required.
Compressor is used to supply medical air, which delivers air to a central
reservoir. To meet the desired quality before distribution at the necessary
pressure, it is dried and filtered here.
Vacuum
Two pumps are connected to a system capable of generating a vacuum of at
least 400 mmHg below atmospheric pressure. It is delivered to the anaesthetic
rooms, operating theatre and other appropriate sites. Bacterial filters are
present at several stages between the outlets and the pumps in order to
prevent contamination by aspirated fluids.
Role of the anaesthetic machine

This is more often referred to as the Boyle’s machine after HEG Boyle who
commissioned the first British machine in 1917 having seen one in the USA.
Its main functions are:
• To reduce the pressure of the gases from the pipelines or cylinders to a

safe level to be used in patients
• For the accurate delivery of varying flows of gases to a patient’s
breathing system
• To permit additional anaesthetic vapours to be added to the gas stream
(Fig. 10.5).
FIGURE 10.5 Boyle’s apparatus.
Although, there are probably still many models and variations of the Boyle’s
machine in use, the following description will concentrate on a typical,
modern version.
Anaesthetic breathing systems
In a spontaneously breathing patient, delivery of gases to the patient is
achieved by using what is commonly referred to as an anaesthetic circuit. It is
technically more accurate to call them anaesthetic breathing systems. Only one
true circuit is in common use, the ‘circle system’. There are five systems
available and they are classified by Mapleson as Mapleson A, B, C, D or E.
Final delivery of gas to the patient is via a facemask or by attaching the system
to a laryngeal mask or tracheal tube. It is becoming increasingly common to
place a low-resistance, disposable, bacterial filter at the patient end of the
system because several patients in succession may breathe through the same
system. In order to reduce the risk of cross-infection this is changed between
patients.
Components of a breathing system
A connection for fresh gas input

On the anaesthetic machine this may be direct connection to the common gas
outlet.
A reservoir bag (usually of 2-l capacity)

As its name suggests, this acts as a gas reservoir. Its presence overcomes the
problems of having a constant flow from the machine and using relatively low
flows. During expiration, fresh gas flow is diverted into the bag, which is then
used to meet the patient’s peak inspiratory flow (30–40 l/min), which exceeds
the flow rate used for anaesthesia (usually <10 l/min). The reservoir can also be
used to monitor ventilation by watching its movements and, by compressing it
the patient can be manually ventilated. Finally, the bag acts as a safety device
where should an obstruction develop distally, it easily distends to
accommodate the flow of fresh gas while maintaining a low pressure. This
protects the lungs against barotrauma.
An expiratory valve
An expiratory valve is one which opens during expiration to allow the
elimination of gas containing carbon dioxide and prevent its accumulation
within the system.
The circle system

The anaesthetic breathing systems relied on a combination of the opening of
an expiratory valve and the inflow of fresh anaesthetic gas to eliminate carbon
dioxide, before the advent of circle system. Even the most efficient system is
still not effective as, in addition to carbon dioxide, the expired gas contains
oxygen and anaesthetic agents. Furthermore, much of the heat and
humidification, added to these gases as they are inspired, are also lost.
The circle system overcomes these inefficiencies; they are passed through a
container of soda lime (the absorber), which chemically removes carbon
dioxide, instead of dumping the expired gases. The patient re-breathes the
supplementary oxygen and anaesthetic agents that are added to maintain the
required concentrations.
In an ideal system only enough oxygen and anaesthetic agent would be
added to replace what is removed. This would consist of 250–300 mL oxygen,
the body’s basal requirement and the amount of anaesthetic required. More of
both oxygen and agent be required initially, gradually reducing as the tissues
became saturated. In such a system, the volume of gas would remain constant.
This is referred to as a closed system. In practice, such low flows are difficult
to achieve and are potentially dangerous as hypoxia can rapidly occur.
Consequently, totally closed systems are not commonly used and more often,
the circle is used with an excess fresh gas flow to allow for any leaks and to
ensure adequate concentrations of oxygen and anaesthetic.
Soda lime
Soda lime consists of a mixture of calcium hydroxide (90%), sodium hydroxide
(5%) and potassium hydroxide (1%). Water is also present in the granules.
Sodium carbonate is produced as a result of reaction between carbon dioxide
and sodium hydroxide. This in turn reacts with calcium hydroxide to form
calcium carbonate. Important by-products of the reactions are water and heat.
As a result, the gases within the circle are heated and humidified which help
prevent their loss from the patient. The granules of soda lime are carefully
sized to have a large surface area but present little resistance to ventilation.
Eventually the soda lime will become exhausted and unable to absorb any
more carbon dioxide. This is indicated by an increasing inspired carbon
dioxide concentration as it fails to be absorbed and due to the incorporation of
an indicator it results in a change in the colour of the granules. Transition from
pink to white is seen in one of the commonly used preparations.
Mechanical ventilation
When a patient is rendered apnoeic, he/she becomes dependent upon the
anaesthetist to support his/her ventilation. Apnoea is usually a deliberate
occurrence following the administration of a muscle relaxant or occasionally
the use of the potent opioid analgesics. Ventilation of the lungs with oxygen
and anaesthetic gases is achieved using a mechanical ventilator in conjunction
with tracheal intubation. In the short term, ventilation can be (and frequently
is) achieved by closing the expiratory valve and ‘squeezing the bag’ to increase
the pressure in an anaesthetic breathing system, thereby forcing gas into the
lungs. Such a technique is inefficient for all but a short period of time and can
lead to hypoxaemia and hypercarbia. It is most commonly used after the use of
non-depolarising relaxant to maintain oxygenation via a face mask prior to
intubation or following intubation using suxamethonium while waiting for the
return of spontaneous ventilation. Whenever mechanical ventilation is
employed as part of the anaesthetic technique, a gas-tight system is required to
ensure that the lungs are ventilated and this is usually provided by the use of a
cuffed tracheal tube. The patient is totally dependent upon the function of the
ventilator and close clinical observation of the patient is essential coupled with
monitoring of, at least, expired volume, inspired oxygen concentration, airway
pressure and pulse oximetry. Because of the risk of accidental disconnection at
many places, a dedicated alarm capable of detecting this should also be used.
Principles of mechanical ventilation

During spontaneous ventilation, descent of the diaphragm and expansion of
the chest wall causes the intrapulmonary pressure to fall 1–2 cm H2O below
atmospheric pressure. Air flows into the lungs and at the end of inspiration
the pressure in the alveoli is atmospheric. Intermittent positive pressure
ventilation (IPPV) is the technique where during mechanical ventilation, a
positive pressure is applied to the anaesthetic gas by the ventilator so that it
flows into the lungs. As these ventilators are very powerful and capable of
generating high inspiratory pressures, they are usually pressure limited to
reduce the risk of pulmonary barotrauma.
Managing the airway

An essential prerequisite for safe and successful conduct of anaesthesia is
maintenance of the patient’s airway. During resuscitation, patients often have
an obstructed airway either as the cause or result of their loss of consciousness.
Basic techniques
In anaesthesia, basic techniques are used to maintain the airway when the
patient is breathing spontaneously, with the anaesthetic gases delivered to the
patient’s airway via a face mask or when ventilating a patient prior to
intubation.
Loss of the airway as a result of anaesthesia is most easily restored by a
combination of the head tilt and a jaw thrust. The jaw thrust is provided by the
anaesthetist’s fourth and fifth fingers (of one or both hands) lifting the angle of
the mandible. Patient’s mandible is ‘lifted’ into the mask rather than the mask
being pushed into the face achieving the desired effect.
Face masks
In adults, anatomical face mask is the most commonly used (Fig. 10.6).
Leakage of anaesthetic gases is prevented by its design which fits the facial
contours with minimal pressure. An air-filled cuff around the edge facilitates
this. Different sizes of the mask are available. The smallest size provides a
good seal and should be used (dead space that occurs is minimised by it).
Ambu face mask is an alternative, with a transparent body, permitting easy
identification of vomit, thereby making it popular for use in resuscitation. In
between uses all masks must be disinfected adequately.
FIGURE 10.6 Adult anatomical face mask.
Simple adjuncts
These are often used to help maintain the airway in conjunction with the
techniques described above. After the induction of anaesthesia most
commonly used airway adjuncts like the oropharyngeal (Guedel) and
nasopharyngeal airways, are inserted to prevent stimulation of reflex activity,
e.g. coughing, vomiting or laryngeal spasm.
Oropharyngeal airway
Oropharyngeal airway is a curved plastic tube, flattened in cross-section and
flanged at the oral end. The tongue is prevented from falling back by the
design of the oropharyngeal airways which lie over the tongue, preventing it
from falling back into the pharynx. The sizes range from neonates to large
adults. By comparing the airway length to the vertical distance from the corner
of the patient’s mouth to the angle of the mandible the correct size is
determined. In adults, the most common sizes are 2–4, for small to large adults
respectively (Fig. 10.7).
FIGURE 10.7 (A–B) Oropharyngeal airway insertion just before
extubation. (C) Oropharyngeal airway in place, through the anterior
flange suction is introduced to clear upper airway or oropharynx.
The oropharyngeal airway is inserted ‘upside down’ as far as the back of the
hard palate. It is then rotated through 180 degrees and fully inserted until the
flange lies in front of the teeth (or gums in an edentulous patient). This
technique is used to try and reduce the risk of pushing the tongue back into
the pharynx and causing obstruction.
Nasopharyngeal airway
Nasopharyngeal airway is an alternative to the oro-pharyngeal airway and as
the name suggests, it is inserted via the nose. They are round, malleable plastic
tubes, bevelled at the pharyngeal end and flanged at the nasal end. They are
sized on their internal diameter in millimetres, the length increasing with
diameter. The most common sizes in adults are 6–8 mm, for small to large
adults respectively (Fig. 10.8).
FIGURE 10.8 Insertion of nasopharyngeal airway. (Size of
nasopharyngeal airway is measured from tip of nose to tragus).
The patency of the both nostirls should be checked and the airway
lubricated prior to inserting a nasopharyngeal airway (usually the right). The
airway is then inserted using a twisting action with the bevel facing medially
to avoid traumatising the turbinates, along the floor of the nose. The tip should
lie in the pharynx and the flange at the nostril when it is fully inserted. To
prevent inhalation of the airway a large safety pin may be inserted through the
flange. Force should not be used if obstruction is encountered, as severe
bleeding may be provoked. The other nostril can instead be tried.
Submental intubation (Fig. 10.9)

When both oral and nasal intubations are deemed unsuitable, control of the
airway can be achieved by submental intubation. Major advantage is that it
eliminates the risk associated with complication of tracheostomy.
FIGURE 10.9 (A–B) Submental intubation.
Signs of airway obstruction

Indications that the methods above are failing to maintain the airway are:
• Snoring sounds, usually as a result of the tongue partially obstructing

the pharynx secondary to the mandible falling back.
• In-drawing of the supraclavicular, suprasternal and intercostal spaces
during obstructed inspiration.
• Use of the accessory muscles; sternomastoid and scalene in an attempt
to try and overcome the obstruction.
• Paradoxical respiratory movement (seesaw respiration); in-drawing of
the thorax and expansion of the abdomen as the diaphragm contracts
vigorously, usually in the face of complete obstruction.
Common problems arising using these techniques along with a face mask
during anaesthesia are:
• Absence of a good seal between the patient’s face and the mask,
particularly in patients without teeth
• For prolonged periods, fatigue when holding the mask
• Due to the loss of upper airway reflexes, the risk of aspiration remains
Traditionally these problems were overcome by resorting to tracheal

intubation. However, there is now an intermediate alternative, the laryngeal
mask airway.
Laryngeal mask airway (supraglottic airway)

Introduced in 1987, the laryngeal mask airway (LMA) has substantially
changed airway management in anaesthetic practice. Over the laryngeal
opening a mask is present. An inflatable cuff on the perimeter of the mask
creates a seal and helps to stabilise it. A tube is attached to the mask which
protrudes from the mouth and directly connects to the anaesthetic breathing
system. The LMA is available in a variety of sizes suitable for all patients. It
ranges from neonates to adults. Sizes 3 and 4 are the most commonly used in
female and male respectively. Although, it was designed to be used in
spontaneously breathing patients, the LMA can be used to ventilate patients
too. High inflation pressure must be avoided, else leakage occurs past the cuff,
which reduces the ventilation and may cause gastric inflation. The version
with a reinforced tube is also available.
Technique for insertion

To prevent coughing or laryngospasm the patient’s reflexes must be
suppressed to a level similar to that needed for the insertion of an
oropharyngeal airway.
• Deflate the cuff and lubricate the mask lightly.

• A head tilt is performed, the patient’s mouth is opened fully and the
tip of the mask inserted along the hard palate with the open side
facing but not touching the tongue.
• Using the index finger, the mask is then further inserted to provide
support for the tube. Eventually, the tip of the mask lies at the upper
oesophageal sphincter where resistance is felt.
• Now the cuff is fully inflated using an air-filled syringe attached to the
valve at the end of the pilot tube.
• Either by a length of bandage or adhesive strapping attached to the
protruding tube, the laryngeal mask is secured.
• Some of the problems of the previous techniques are overcome by
laryngeal mask. It is unaffected by the shape of the patient’s face or the
absence of teeth and provides a good seal. It avoids fatigue and other
associated problems by not requiring the anaesthetist to hold it in
position. Finally, it does not eliminate the risk of aspiration of
regurgitated gastric contents (Fig. 10.10).
FIGURE 10.10 Insertion of laryngeal mask airway.
Relative contraindication to use LMA is in case of increased risk of

regurgitation e.g. in emergency cases, pregnancy.
Recently, the laryngeal mask has been found to be useful in two other areas:
• Allows maintenance of the airway in a difficult tracheal intubation.

Alternatively via the LMA, a small-diameter tracheal tube or
introducer can be passed into the larynx.
• LMA can be inserted more rapidly and successfully during
cardiopulmonary resuscitation by non-anaesthetists than a tracheal
tube and can achieve more effective ventilation than by using a self-
inflating bag and face mask. In the future, the LMA will find a role in
airway management during resuscitation.
Unlike most modern equipment, the LMA is reusable if it is sterilised

between patients.
Tracheal intubation
The best method of providing and securing a clear airway in the anaesthetised
patient and during resuscitation is the tracheal intubation. However,
compared to the other methods it requires more training, equipment, skill and
practice for its achievement. Basically, the technique consists of inserting a
tube via mouth (oral) or nose, through the larynx, so that the tip lies in the
upper trachea, usually facilitated by direct laryngoscopy. In addition, abolition
of the laryngeal reflexes is required and this is achieved in anaesthesia most
commonly by the administration of muscle relaxants. It is important to
remember that at this point, the patient will also become apnoeic and
dependent upon the anaesthetist to maintain ventilation and oxygenation.
Alternatively, the laryngeal reflexes may be abolished by:
• Deep inhalational anaesthesia

• Local anaesthesia of the larynx, usually in an awake-patient.
These techniques are reserved for use in patients with anticipated difficult
intubation, when problems in ventilating the patient after the administration
of a muscle relaxant, e.g. airway tumours, facial trauma, immobility of the
cervical spine, TMJ ankylosis and trismus.
Indications for tracheal intubation
• Use of muscle relaxants as a part of the anaesthetic technique, thereby

necessitating the use of mechanical ventilation.
• In patients with a full stomach, usually those requiring emergency
surgery, the presence of a cuffed tracheal tube protects from aspiration
of regurgitated gastric contents.
• Patient position which makes maintenance of the airway difficult, e.g.
the lateral or prone position.
• During surgeries on the head and neck, to secure the airway, tracheal
intubation protects against the aspiration of blood into the lungs.
• Ventilation with 100% oxygen without leaks
• Suction clearance of inhaled debris
• A route for drug administration.
Equipment for tracheal intubation
The following is a list of the basic needs for adult oral intubation:
• Laryngoscope with a curved blade (Macintosh)

• Tracheal tubes, inflated and cuffed, available in a variety of sizes. The
most important details are the internal diameter expressed in
millimetres and the length in centimetres diameter, 22–24 cm length.
a. For males: 7.5–8.0 MM internal cardiopulmonary
resuscitation when intubation allows:
b. For females: 7.0–7.5 MM internal diameter, 20–22 cm
length.
• Once the tube is in place, use syringe to inflate the cuff.
• Connect the tube to the anaesthetic system or ventilator tubing with a
catheter mount or ‘elbow’.
• Suction to remove excess secretions. For emergency patients it must be
switched on and kept ready for conditions where the patient vomits or
regurgitates.
• Listening for breath sounds during ventilation via stethoscope to check
correct placement of the tube.
• Accessories: A semirigid introducer (gum elastic bougie—60 cm) to
assist with intubation; Magill’s forceps, designed to remove debris or
direct the tip of a tube; a length of bandage or tape to secure the tube
by its reach into the pharynx.
Laryngoscopes
The laryngoscope was designed to allow direct visualisation of the larynx to
facilitate the insertion of a tracheal tube and consists of a handle and blade.
The blade is placed into the mouth to sweep the tongue to the left and elevate
the epiglottis to reveal the larynx. Illumination is provided by a light source
close to the tip, powered by batteries situated within the handle. The most
popular design in use today is the curved blade developed by Sir Robert
Macintosh which bears his name.
There is a wide selection of laryngoscopes available for use in paediatric
anaesthesia, which carries the names of their inventors, e.g. Soper, Seward,
Miller, Robert Shaw, Sheila Anderson.
Tracheal tubes
These were earlier manufactured from red rubber and could be sterilised for
reuse. They have now been largely superseded by disposable plastic (PVC)
ones. Apart from eliminating the risk of cross-infection, plastic tubes are
chemically less irritating to the larynx, less likely to kink and require a lower
pressure in the cuff to achieve a seal. Tracheal tube sizes are according to their
internal diameter in millimetres and manufactured in 0.5 mm intervals. A
standard 15 mm connector permits connection to the breathing system.
A tracheal tube with an inflatable cuff is used for anaesthesic procedures in
adults. This is necessary because once past the narrowest part of the airway
(vocal cords), the tube lies in the trachea that has a much larger diameter. A
seal prevents leakage of anaesthetic gases back past the tube when positive-
pressure ventilation is provided. The cuff also helps prevent the risk of any
foreign material, e.g. gastric acid, food or blood being aspirated into the lungs.
A syringe is used to inflate the cuff by injecting air, which runs part way
either within or attached to the tracheal tube. At the distal end of the tube is a
one-way valve in order to prevent deflation and a small pilot balloon
indicating the cuff is inflated. Caution to ensure that the cuff is not over-
inflated as high pressure can be generated which may compress the tracheal
mucosa, rendering it ischaemic. During positive-pressure ventilation, the cuff
is slowly inflated until there is no audible evidence of a leak.
Tracheal tubes are connected to the appropriate breathing system or
ventilator tubing via a catheter mount. This is simply a short piece of
corrugated tubing with a 15 mm connection at one end and 22 mm connection
at the other.
Technique of oral intubation

Abolition of the laryngeal reflexes is required in intubation requires as already
described and during the procedure the patient must be monitored
appropriately.
Positioning
Patient’s neck flexed and the head extended at the atlanto occipital joint is the
optimal position for intubation. With the help of index finger and thumb of the
right hand in a scissor-action, the patient’s mouth is then fully opened.
Laryngoscopy
The left hand is used to hold the laryngoscope and the blade is introduced into
the mouth along the right-hand side of the tongue, displacing it to the left. The
blade is advanced until the tip lies in the vallecula, gap between the base of the
tongue and the epiglottis. In the direction of the handle of the laryngoscope is
pointing the force is then applied. Force is applied such that the effort comes
from the upper arm, not the wrist. The larynx gets exposed by lifting the
tongue and epiglottis. This should be seen as a triangular opening, with the
apex anteriorly and the true cords laterally. (Refer 11.1–11.5)
Intubation (Figs. 10.11–10.12)

In the right side of the mouth the tracheal tube is introduced. It is then
advanced and seen to pass through the cords. Until the cuff lies just below the
cords, it is further advanced. Right hand firmly holds the tube and the
laryngoscope are carefully removed. To prevent any leak during ventilation
the cuff is inflated sufficiently. Finally, by listening for breath sounds in both
axillae the position of the tube is confirmed and it is then secured in place.
FIGURE 10.11 Steps in oral intubation in a paediatric patient.

FIGURE 10.12 Step by step demonstration of intubation in an adult
patient. ( Scan to play An Overview of General Anesthesia)
Five-point auscultation is done:
• Epigastrium to rule out oesophageal intubation,

• Apex of lung on both sides,
• Base of lung on both sides
For nasotracheal intubation, through the right nostril along the floor of the
nose with the bevel pointing medially, a well-lubricated tube is introduced to
avoid damage to the turbinate. In the manner described above it is visualised
using a laryngoscope after advancing into the pharynx. By pressure on the
proximal end it can either be advanced directly into the larynx or the tip
picked up with Magill’s forceps (designed not to impair the view of the larynx)
and directed into the larynx. As for oral intubation the procedure is continued.
Difficult intubation
As the larynx cannot be visualised, usually tracheal intubation is not
straightforward. This can be predicted at the preoperative assessment or may
remain unexpected. Many different techniques have been described to help
solve this problem.
These include:
• Pressure by an assistant in a downward and upward direction during

the manipulation of the thyroid cartilage to try and bring the larynx or
the posterior aspect into view.
• A 60 cm long gum-elastic bougie is inserted into the trachea and over
this a tracheal tube is ‘railroaded’ into place.
• A fibre optic bronchoscope is introduced into the trachea via either the
mouth or nose. It is used as a guide over which a tube can be passed
into the trachea. It can be used in both anaesthetised and awake
patients hence, is advantageous.
During difficult intubation, whether predicted or not, hypoxia must be

prevented. The LMA can be used as a temporary measure and if intubation is
essential, then a tracheostomy may have to be performed. If the patient cannot
be oxygenated via the upper airway, then it may be necessary to resort to the
creation of a surgical airway.
Complications of tracheal intubation
Hypoxia
Hypoxia can result from many causes.
1. Unrecognised oesophageal intubation: Oxygen and anaesthetic gases are

delivered into the stomach. The best method for detecting this is to
measure the carbon dioxide in expired gas; less than 0.2% is indicative
of oesophageal intubation. The most reliable indicator is the
monitoring of ET CO2 monitoring.
Other less reliable signs are:
• Burping sounds as gas escapes
• Large volume of air required to fill the cuff
• On auscultation, diminished breath sounds are heard
• On ventilation, decreased chest movements are seen
• Over the epigastrium, gurgling sounds are heard
An alternative is to withdraw the plunger rapidly of a 50 mL bladder
syringe attached to the tracheal tube. If the tracheal tube is in the
oesophagus, the walls collapse over the end of the tube, resistance is
felt and air cannot be aspirated (Wee’s oesophageal detector). If the
patient has been preoxygenated then pulse oximetry shows changes at
a later stage. The tube should be removed and the patient ventilated
via a face mask if the position of the tube is doubtful.
2. Failed intubation and inability to ventilate the patient using a facemask. This
results from abnormal anatomy or airway pathology. During the
preoperative assessment most cases are predictable. Some anaesthetists
advocate attempting ventilation by mask after induction in all patients
about to receive muscle relaxants.
3. Failed ventilation, as a result of kinking of the tube, disconnected or
inserted too far and passing into one main bronchus.
4. Blockage of the airway directly resulting from aspiration of
regurgitated gastric contents or secondary to laryngeal spasm and
bronchospasm. To reduce the risk of regurgitation cricoid pressure can
be used in the period between loss of consciousness and insertion of a
cuffed tube into the trachea to protect the airway (see below).
Trauma
Although often regarded as a minor event, it is a common cause for complaint
by patients postoperatively. During laryngoscopy and insertion of the tube to
the lips, teeth, tongue, pharynx, larynx, trachea, nose and nasopharynx during
nasal intubation, damage can occur. This usually causes soft tissue swelling or
bleeding. Indirect damage like mandible (dislocation) and the cervical spine
and cord, particularly where there is preexisting degenerative disease or
trauma can occur.
Reflex activity
• Laryngoscopy and intubation are frequently accompanied by

disturbances in cardiac rhythm and hypertension, which may
jeopardise patients with coronary artery disease, aortic or intracranial
aneurysms. These responses are exaggerated in hypertensive patients.
These events may also cause a rise in intracranial pressure secondary
to increased cerebral blood flow. Specific action is usually taken to
reduce the hypertensive response in patients at risk, e.g. pretreatment
with β-blockers, potent analgesics (fentanyl, alfentanil) or lignocaine.
• In patients who are inadequately anaesthetised, vomiting may be
stimulated when laryngoscopy is attempted. This is more likely to
occur when there is material in the stomach, e.g. in emergencies if the
patient is not starved, in patients with intestinal obstruction; or in
delayed gastric emptying, as after opiate analgesics or following
trauma.
• Stimulation of the epiglottis or larynx leads to reflex adduction of the
cords called as laryngeal spasm. It is abolished by deepening the level
of anaesthesia while maintaining oxygenation.
Anaesthetic drugs
Phases of general anaesthesia
• Induction
• Maintenance
• Recovery
Induction
Induction time begins with the onset of administration of general anaesthesia
to the development of surgical anaesthesia.
Maintenance
Sustaining the state of general anaesthesia
Recovery
Administration of anaesthetic agent is stopped and consciousness is regained.
Intravenous anaesthetic (induction) agents
Induction agents are those drugs, which are used to start (induce) anaesthesia.
Generally, consciousness is regained as these drugs are redistributed from the
brain to other tissues. Alternatively, anaesthesia can be induced by the
inhalation of an increasing concentration of a volatile agent. Of the IV agents
currently in use, only propofol is used subsequently to maintain anaesthesia
(Flowchart 10.1).
FLOWCHART 10.1 Classification of general anaesthesia.
1. Sodium thiopentone
Sodium thiopentone is most commonly used water soluble barbiturate
induction agent. It is a yellow powder with a faint smell of garlic due to the
presence of sulphur in the molecule. It is dissolved in water to make a 0.5%
solution (500 mg in 20 mL), which is very alkaline (pH 10.5) and inhibits
bacterial growth. The ampoules contain a small amount of sodium carbonate
to maintain solubility. Thiopentone is incompatible with any other drug and
precipitation follows mixing.
Induction
• Dose:2–7 mg/kg
• Dose varies according to age: for Adults 3–4 mg/kg
• Induction of anaesthesia is rapid and smooth
• Consciousness usually returns after 4–10 min
Systemic effects
Central nervous system
• Sedation, loss of consciousness and anaesthesia

• Potent anticonvulsant property
• Hypotension
• Fall in cardiac output
• Venodilatation
Respiratory system
A short period of breath-holding, hypercapnia and ultimately apnoea.
Miscellaneous
• Muscle relaxation
• Hepatic enzymes are induced and urine output reduced.
Advantages
Induction is rapid with minimal excitation effects and good initial recovery. It
is painless on IV injection.
Disadvantages
• Alkaline solution is an irritant to tissues and can cause necrosis if the

injection extravasates. Respiratory depression and loss of protective
laryngeal reflexes can both lead to the development of hypoxia and
can cause hypotension and circulatory collapse in overdose.
• Accidental intraarterial injection causes acute, severe pain with loss of
the distal circulation due to intense vascular spasm. If untreated, this
can cause gas gangrene.
2. Propofol
Propofol is an IV anaesthetic agent, a phenolic derivative, which is not water
soluble. It is prepared as an emulsion (hence white in colour) in soybean oil
and egg phosphatide. Ampoules contain a 1% solution (200 mg in 20 mL) with
no bactericidal agent. Once opened, the contents must either be used or
discarded.
Induction
• Dose is usually between 1.5 and 2.5 mg/kg.

• Either pain or a burning sensation on injection can occur.
• Induction of anaesthesia is rapid.
• After 4–7 min, there is a rapid, full recovery of consciousness.
Systemic effects
• Sedation
• Loss of consciousness and anaesthesia
• May reduce the seizure threshold in epileptic patients
• Hypotension
• Vasodilatation
• Inhibits baroreceptor reflex, hence no reflex tachycardia occurs
Respiratory system
• Apnoea
• Ventilation and the response to carbon dioxide are depressed.
Miscellaneous
Muscle relaxation is more pronounced after propofol.
Advantages
• Quality of recovery following propofol is better than any other agent,

which has made it the drug of choice for day-care surgery.
• Significant reduction in postoperative nausea and vomiting
• Nonirritant to veins
• Hypersensitivity and allergic reactions are uncommon.
• Allergies can occur to propofol
Disadvantage
The discomfort on injection can be minimised by either adding a small amount
of lignocaine to propofol (2 mL of 1%) or by preinjection of a similar volume of
local anaesthetic.
Not used in < 1 year age
3. Ketamine
Although, less used now, this is a versatile induction agent. It is a
phencyclidine derivative, presented as a clear, water soluble solution in three
different concentrations: 10, 50 and 100 mg/mL. The multidose ampoules have
a long shelf-life. Unlike other agents it can be administered either
intravenously or intramuscularly to induce anaesthesia.
Induction
• Intravenous (IV) dose is 1–2 mg/kg.

• The intramuscular (IM) dose is 5–10 mg/kg and it may take 8–10 min to
lose consciousness and the subsequent duration of action is variable.
Systemic effects

Ketamine produces ‘dissociative anaesthesia’, the most important features of
which are anterograde amnesia and intense analgesia. Intracranial pressure
may be increased due to increased cerebral blood flow. It is strongly associated
with vivid hallucinations during recovery.
• Tachycardia
• Increase in both systolic and diastolic blood pressure
• Increase in cardiac output
• High doses cause direct cardiac depression
Respiratory system
• Ventilation is minimally depression of and the response to carbon

dioxide is maintained
• Bronchodilatation
Miscellaneous
• Increased muscle tone

• Increase in salivation
Advantages
• In cases of difficult venous access, intramuscular injections are useful.

• Used in repeated minor painful procedures especially in children e.g.
burns dressings.
Disadvantages
• Hallucinations and unpleasant dreaming during recovery, particularly

in females.
• The increase in intracranial pressure makes it potentially dangerous for
use in patients with head injuries.
• May exacerbate preexisting hypertension.
• Hallucinations can be minimised by the use of benzodiazepines, either
as premedication or given concurrently and by allowing a quiet, slow
recovery.
Miscellaneous
Midazolam
Occasionally, the IV administration of a benzodiazepine is used to induce
anaesthesia. The most commonly used is midazolam. It does not produce a
rapid loss of consciousness hence, not a true induction agent.
Inhalational induction
Under certain circumstances, IV induction of anaesthesia may not be practical,
e.g. in uncooperative child or a patient with absence of suitable veins.
Furthermore, inhalational induction is the safe technique in a patient with
airway compromise, as following the administration of an IV agent, the patient
may become apnoeic, the airway may be lost with ventilation and oxygenation
becoming impossible. The alternative (apart from the very rare use of IM
ketamine) is to use one of the inhalational agents, normally used to maintain
anaesthesia.
The patient is allowed to breathe in oxygen an increasing concentration of
an inhalational agent (if there is airway compromise) or in a mixture of oxygen
and nitrous oxide. Unlike when using the IV agents, anaesthesia is induced
more slowly and respiration is preserved.
Earlier with the use of ether, four stages of anaesthesia (Guedel stages) were
recognised. But this staging is not applicable to the present day general
anaesthesia. (Fig. 10.13)
FIGURE 10.13 Stages of GA (especially with ether).
Stage I (stage of analgesia or disorientation)

From the beginning of induction of general anaesthesia to loss of
consciousness.
Stage II (stage of excitement or delirium)
From loss of consciousness to onset of automatic breathing. Only eyelash
reflex disappears while other reflexes remain intact and coughing, vomiting
and struggling may occur; respiration can be irregular with breath-holding.
Stage III (stage of surgical anaesthesia)

From onset of automatic respiration to respiratory paralysis. It is divided into
four planes:
Plane I
—from onset of automatic respiration to cessation of eyeball movements.
Eyelid reflex is lost, swallowing reflex disappears, marked eyeball movement
may occur but conjunctival reflex is lost at the bottom of the plane.
Plane II
—from cessation of eye ball movements to beginning of paralysis of
intercostals muscles. Laryngeal reflex is lost although inflammation of the
upper respiratory tract increases reflex irritability, corneal reflex disappears,
secretion of tears increases (a useful sign of light anaesthesia), respiration is
automatic and regular, movement and deep breathing as a response to skin
stimulation disappears.
Plane III
—from beginning to completion of intercostal muscle paralysis.
Diaphragmatic respiration persists but there is progressive intercostal
paralysis, pupils dilated and light reflex is abolished. The laryngeal reflex lost
in plane It can still be initiated by painful stimuli arising from the dilatation of
anus or cervix. This was the desired plane for surgery when muscle relaxants
were not used.
Plane IV
—from complete intercostals paralysis to diaphragmatic paralysis (apnoea).
Stage IV
From stoppage of respiration till death. Anaesthetic overdose causes
medullary paralysis with respiratory arrest and vasomotor collapse. Pupils are
widely dilated and muscles are relaxed.
Maintenance of anaesthesia: inhalational

(volatile) agents and intravenous infusions
After induction, anaesthesia is most commonly maintained by the
administration of a combination of nitrous oxide and an anaesthetic vapour in
oxygen, which the patient breathes spontaneously or which is delivered to the
lungs by a ventilator. The amount of anaesthetic delivered is expressed as the
percentage by volume, the concentration usually reflecting the potency of the
agent used. An inspired concentration of 1%–2% of the halogenated agents
will anaesthetise most patients, whereas 70% nitrous oxide alone may not be
sufficient to guarantee unconsciousness.
Nitrous oxide
• Colourless, inorganic gas

• Sweet smelling
• Nonirritant gas
• Neither flammable nor explosive
• Supports combustion
• Available in cylinders coloured French blue.
Anaesthesia
• Good analgesic but a poor anaesthetic.

• 70% is the maximum safe concentration administered as an inspired
oxygen concentration of 30% is required to provide adequate
oxygenation during anaesthesia.
• Mainly serves as the vehicle for the other potent volatile agents, at the
same time reducing the concentration of volatile agent required.
Systemic effects
• Increasing cerebral blood flow

• Raises the intracranial pressure
Cardiac output or blood pressure is effected mildly.
Can increase catecholamine levels and causes epinephrine induced
arrhythmias, cardiac output and blood pressure is slightly elevated or
unchanged
Respiratory system
• Cause a decrease in the tidal volume and slight increase in the
respiratory rate
• No muscle relaxation with nitrous oxide
Advantages
• Good analgesic
• Nitrous oxide has an excellent long-term record.
Disadvantages
• Nitrous oxide diffuses rapidly into air-filled cavities and causes a rise
in pressure where expansion cannot take place, e.g. in the middle ear
or within the skull (pneumocephalus).
• Rapid excretion of nitrous oxide into the alveoli dilutes remaining
oxygen present, thereby producing a transient hypoxia called as
diffusion hypoxia or Fink effect at the end of anaesthesia
• Bone marrow suppression by interfering with the production of factors
necessary for DNA synthesis.
Halothane
• Colourless, volatile
• Pleasant odour
• Nonflammable and nonexplosive at clinical concentrations, even when
mixed with oxygen.
• Decomposition occurs on exposure to light and this is retarded by
storing it in amber bottles with the addition of 0.01% thymol.
Anaesthesia
• Very potent anaesthetic

• It is administered via a calibrated vapouriser to prevent overdose.
Induction can be achieved with 2%–4%.
• Maintenance with 0.5%–1.5% inspired concentration when
administered with 70% nitrous oxide and 30% oxygen.
• No analgesic action
• In spontaneously breathing patients it is commonly used with nitrous
oxide and oxygen or in the same combination as part of a balanced
technique along with a muscle relaxant and an analgesic in a
ventilated patient.
Systemic effects

Cerebral blood flow is increased causing a rise in the intracranial pressure.
• Cardiac output and blood pressure falls

• Myocardial depression and vasodilatation
• Dysrhythmias
• Sinus bradycardia
• Increased vagal tone
• Ventricular extrasystoles are associated with increased circulating
levels of adrenaline.
Respiratory system
Respiratory depressant
Metabolism
Significant amount of halothane is metabolised in the liver (> 20%) and gets
excreted over many days.
Advantages
• Potent anaesthetic
• Rapid induction and recovery
• Recovery is slower with halothane as compared to other inhalational
agents
• Potentiates the effects of non-depolarising muscle relaxants
Disadvantages
• Significant rise in cerebral blood flow raising intra-cranial pressure

• Is one of the more potent triggers of malignant hyperthermia
• Hepatotoxicity
• Halothane hepatitis
• Has no analgesic action
Isoflurane
• A colourless liquid
• Nonflammable at clinical concentrations
• Pungent smell
• Mildly irritant to breathe
• Isoflurane is a very stable molecule and hence does not require any
preservative and has a long shelf-life.
Anaesthesia
• More potent than halothane

• It is the least soluble, allowing very rapid changes in the depth of
anaesthesia and recovery. Its use as an induction agent is limited by its
pungency and tendency to cause coughing.
• It does not have least solubility: Desflurane is least soluble
• 5% is required for induction
• 1%–1.5% for maintenance of anaesthesia when used with 70% nitrous
oxide and 30% oxygen.
Systemic effects

Isoflurane causes dose-dependent depression, with cerebral blood flow being
affected minimally and intracranial pressure at low concentrations.
• Fall in blood pressure mainly due to peripheral vasodilatation

• Minimal myocardial depression
• Tachycardia in young patients due to maintenance of the baroreceptor
reflexes
Respiratory system
• Depression of ventilation
• Tidal volume is affected greater than respiratory rate
• Response to hypoxia and hypercarbia is also reduced
• Good relaxation of skeletal muscle
Advantages
• Rapid recovery
• Minimal hangover effects
• Popularly used in day-care surgery
• No apparent renal or hepatic toxicity and isoflurane can be repeated at
short intervals.
Widely used during operations requiring induced hypotension, as this effect

is achieved mainly by vasodilatation rather than myocardial depression.
Isoflurane is a preferred maintenance inhalation agent because it is cheaper
and more cardio stable than halothane
Disadvantages
• Pungency of isoflurane limits its use for inhalation induction of

anaesthesia
• May worsen myocardial ischaemia in patients with severe coronary
artery stenosis.
Sevoflurane
• Latest inhalational agent

• Fluorinated derivative of methyl isopropyl ether
• Colourless liquid
• Nonflammable at clinical concentrations
Anaesthesia
• Relatively weak anaesthetic agent (MAC 2.5% in oxygen, 1.2% in 70%

nitrous oxide).
• Induction, changes in depth and recovery from anaesthesia is
facilitated by low solubility.
• Less irritant to the respiratory tract than isoflurane and halothane.
• Allows rapid induction and rapid recovery.
Systemic effects

Depression of the central nervous system.
Due to peripheral vasodilatation, the blood pressure decreases in a dose-
related manner.
Respiratory system
With decrease in ventilator response to carbon dioxide, ventilatory depression
occurs. It causes reversal of bronchospasm.
Miscellaneous
• The effects of non-depolarising relaxants are potentiated.

• Minimal release of fluoride ions (which can cause renal damage above
a certain concentration) and the levels quickly fall at the end of
anaesthesia due to the rapid exhalation of sevoflurane as a result of its
insolubility.
Advantages
Ease of inhalation and lack of solubility make sevoflurane useful in short
cases, e.g. anaesthesia for day-care surgery, at the end of anaesthesia, rapid
exhalation of sevoflurane with minimal release of fluoride ion (nephrotoxic
above certain level).
Disadvantages
Contact between sevoflurane and carbondioxide absorbing agents, e.g.
sodalime in a circle system, results in the formation of a number of toxic
compounds including formaldehyde, hydrofluoric acid and an alkene, termed
Compound A. Initial investigations suggest that the concentrations produced
in the clinical situation are below the level causing renal damage in humans.
The slow induction and recovery, frequent nausea and vomiting and
profuse salivation requiring the use of an anticholinergic premedicant, are the
main clinical disadvantages.
Ether predispose to an unacceptable risk of fires and explosions due to its
flammability considering the increasing use of electrical apparatus in the
modern operating theatre.
Propofol (2,6-di-isopropylphenol)
The rate of infusion of propofol will vary between patients and will depend
upon the concurrent administration of other drugs, e.g. opioids or nitrous
oxide, used in conjunction to provide analgesia and help prevent the risk of
awareness. A typical infusion regimen in conjunction with oxygen-enriched
air and an intravenous analgesic (alfentanil) would be:
Dose: 50–150 µg/kg/min with nitrous oxide or an opiate is recommended
Advantages
• Total avoidance of all inhalational agents

• Risks such as malignant hyperpyrexia, hepatitis and the problems
associated with nitrous oxide, particularly during long procedures can
be eliminated.
Disadvantages
If an inadequate rate of infusion was used in a patient given muscle relaxants,
it could potentially lead to them being conscious and paralysed (it must be
remembered that this situation is not unique to infusions, the same can still
happen if inadequate concentrations of an inhalational agent are used).
Accurate devices are also required to deliver constant infusions (e.g. electronic
syringe pumps), a situation analogous to the vaporisers required for
inhalational agents.
Ether (diethyl ether)
• Ether was the first agent used successfully to produce surgical

anaesthesia
• Rarely used nowadays
• Inflammable
Anaesthesia
• Moderately potent anaesthetic agent

• Irritant, causing coughing, breath-holding and laryngeal spasm if the
inspired concentration is increased rapidly.
• High concentrations need to be given if ether is used for induction
(15%–25%), with 3%–5% required for maintenance, increasing to 10%–
12% for muscle relaxation.
Advantages
• In contrast to other volatile agents, ether causes a degree of respiratory

and cardiovascular stimulation, until deep levels of anaesthesia are
produced.
• Muscle tone is reduced in proportion to the depth of anaesthesia,
bronchial smooth muscle tone useful in asthmatics.
Disadvantages
The slow induction and recovery, frequent nausea and vomiting and profuse
salivation requiring the use of an anticholinergic premedicant are the main
clinical disadvantages. However, unacceptable risk of fires and explosions due
to the increasing use of electrical apparatus in the modern operating theatre.
Muscle relaxation during anaesthesia:

neuromuscular blocking drugs and their
antagonism
Before the introduction of neuromuscular blocking drugs, high concentrations
of inhalational anaesthetic agents or by regional anaesthesia was used to
achieve relaxation of skeletal muscles to facilitate surgical access. Both
techniques are associated with a variety of problems including hypotension,
respiratory depression and delayed recovery. Muscle relaxation could be
achieved with administration of less anaesthetics by the introduction of curare
in 1942 (Flowchart 10.2).
FLOWCHART 10.2 Classification of skeletal muscle relaxants.
Normal neuromuscular transmission

• Under normal circumstances, a nerve impulse travels as a wave of
depolarisation to arrive at the axonal terminal.
• Depolarisation of the nerve terminal results in the release of the
neurotransmitter acetylcholine, which diffuses across the gap between
the nerve terminal and the adjacent muscle membrane or motor end
plate (also called the synaptic or junctional cleft).
• At this site, the muscle membrane contains large numbers of
acetylcholine receptors, which on combination with the
neurotransmitter cause the opening of specialised ion channels.
• If sufficient acetylcholine is released and enough ion channels open,
this ultimately leads to the generation of a muscle action potential,
which is
• Propagated along the muscle membrane and eventually results in
muscle contraction.
• In order to ensure that muscle contraction occurs, acetylcholine is
released in far greater quantities than required.
• The action of acetylcholine on the receptors is terminated by the
presence of an enzyme, acetylcholinesterase, present in the synaptic
cleft.
• The neuromuscular blocking drugs or muscle relaxants work by
interfering with the normal action of acetylcholine by blocking the
receptors on the postsynaptic muscle membrane.
• They are divided into two groups, the names of which are based on
their mode of action.
Classification of skeletal muscle relaxant

Muscle relaxants are classified based on the mode of action, duration of action
and their site of action.
Peripherally acting muscle relaxant

Drugs acting peripherally at neuromuscular junction by causing non-
depolarisation or depolarisation block.
Drugs causing non-depolarising block (competitive)
Long acting
D-Tubocurarine, metocurine, alkuronium chloride, pancuronium bromide,
gallamine triethiodide, pipercuronium chloride, doxacurium hydrochloride.
Intermediate acting
Vecuronium bromide, atracurium besylate, cisatracurium besylate,
rocuronium bromide.
Short acting
Mivacurium chloride, rapacuronium bromide.
Drugs causing depolarising block
• Decamethonium
• Succinyl choline (suxamethonium chloride)
Centrally acting muscle relaxant
Barbiturates
Phenobarbitone
Glycerol ethers
Mephenesin, carisoprodol, metho-carbamol, chlormezanone, chlorzoxazone
Benzodiazepines
Diazepam
GABA derivatives
Baclofen
Drugs acting directly on muscle
• Dantrolene sodium
• Quinine
Non-depolarising muscle relaxants

These drugs compete with acetylcholine and block its access to the
postsynaptic receptor sites on the muscle but do not cause depolarisation. As
increasing the concentration of acetylcholine will overcome their action, they
are sometimes referred to as competitive relaxants.
All of the non-depolarising relaxants are administered intravenously and
the time of onset to maximum effect is relatively slow (1.5–3 min).
Nondepolarising relaxants are used in two ways: along with
suxamethonium in order to maintain relaxation during surgery or as the sole
agent to provide relaxation for tracheal intubation and surgery.
Although, recovery of normal neuromuscular function occurs
spontaneously after the use of these drugs, it is usually accelerated by the
administration of an anticholinesterase.
Curare, alcuronium and pancuronium were the predominant non-
depolarising relaxants until the 1980s, but were rapidly superseded by the
arrival of atracurium and vecuronium. Mivacurium and rocuronium are the
latest additions to the range of muscle relaxants. All these drugs vary in their
potency, duration of action and side effects.
Tubocurarine
Tubocurarine or more commonly curare was the first non-depolarising relaxant
to be used in clinical practice. It is often referred to as a long acting relaxant
(along with alcuronium and pancuronium). Curare is obtained from the plant
Chondrodendron tomentosum, which cultivates in the Amazon area and is used
by the local Indians traditionally as an arrow poison.
Clinical uses
• The initial dose of 0.5 mg/kg takes approximately 3 min to provide
sufficient relaxation to allow intubation.
• Adequate relaxation is provided for surgery for 30–40 min. This is
slightly prolonged when inhalational agents are used.
• Supplementary doses of 0.15 mg/kg can be administered to extend the
duration of block. It is supplied in 1.5 mL ampoules containing
10 mg/mL.
Alcuronium
Alcuronium is synthesised from a curare alkaloid and therefore has properties
similar to curare. It is supplied in 2 mL ampoules containing 5 mg/mL. The
amber-coloured ampoules deteriorate on exposure to sunlight.
Pancuronium
A synthetic muscle relaxant, pancuronium was the first one introduced into
clinical practice, with a chemical structure based upon the steroid ring nucleus.
Clinical use
In patients with renal failure it is not recommended for use.
Atracurium
First of the modern generation of intermediate duration non-depolarising
relaxants, stored at 4°C to reduce the rate of spontaneous degradation.
Clinical uses
• Profound relaxation is produced by an initial dose of 0.5 mg/kg

allowing intubation after 1.5–2 min. This lasts for 20–25 min and once
spontaneous recovery starts, it proceeds very rapidly.
• When used during prolonged procedures, the administration of an
infusion (0.5 mg/kg/h) is preferable to intermittent increments in order
to maintain a steady degree of relaxation.
• In patients with either renal or hepatic dysfunction, it is the relaxant of
choice. In hypothermic patients its actions will be prolonged, e.g.
during cardiac surgery.
Vecuronium
Vecuronium is related to pancuronium in that it has a steroid ring nucleus. It
is supplied as a white, freeze-dried powder (10 mg), which is reconstituted for
use with 5 mL of sterile water to give a solution containing 2 mg/mL.
Clinical uses
• Profound relaxation results with an initial dose of 0.1 mg/kg in 1.5–

2 min. This will provide adequate relaxation for 15–20 min. This can be
extended by increasing the dose to 0.15–0.2 mg/kg with few side
effects.
• More common to use an infusion of 50–80 µg/kg/h in case of longer
procedures.
• As with a tracurium, recovery is rapid once it commences.
Mivacurium
The first of the two newest relaxants, mivacurium is structurally related to
atracurium. It is regarded as a short acting non-depolarising relaxant. It is
supplied in solution containing 2 mg/mL.
Clinical uses
• The initial dose of 0.15 mg/kg provides relaxation, allowing intubation

in 2 min. However, the duration of action is only 10–15 min, after
which time recovery is sufficiently rapid does not require the routine
administration of an anticholinesterase.
• Although it can be used to maintain relaxation, its use in day-care
surgery for short procedures serves great advantage.
Depolarising muscle relaxants

As their name suggests, following administration, they cause depolarisation of
the motor end plate. Currently, only suxamethonium is in regular clinical use.
Suxamethonium chloride (succinylcholine—Sch)

A quaternary amine ester, suxamethonium consists of two molecules of
acetylcholine joined together ‘back-to-back’ (via their non-quaternary ends).
On administration, it mimicks the action of acetylcholine at the receptors on
the motor end plate producing depolarisation of the muscle membrane
followed by uncoordinated muscle contractions. Depolarisation continues for
several minutes, thereby preventing further muscle activity, as
suxamethonium is not broken down by acetyl cholinesterase. Ultimately,
plasma cholinesterase hydrolyses it with the restoration of normal
neuromuscular transmission.
Suxamethonium is available in 2 mL ampoules, containing 50 mg/mL. It
hydrolyses at room temperature and therefore has to be stored at 4°C.
Clinical uses
• Suxamethonium can be administered intravenously, intramuscularly

or subcutaneously.
• Profound relaxation in 40–60 s, lasting 4–6 min is achieved with the
dose of 1.5 mg/kg in adults.
• Infants and neonates require a slightly higher dose, 1.5–2 mg
respectively.
Advantages
Suxamethonium produces profound, short-lived muscle relaxation that is
more rapid in onset than any of the other currently available relaxants.
Facilitation of tracheal intubation in an emergency makes it the drug of choice,
e.g. in a patient likely to regurgitate and aspirate.
Disadvantages
• Suxamethonium has to be stored at 4°C to prevent breakdown.

• Administration may cause:
▪ Hyperkalaemia
▪ Malignant hyperpyrexia in susceptible patients
▪ Loss of vitreous exacerbating the damage in penetrating eye
injuries may result from increased intraocular pressure
▪ Muscular pain around the limb girdles, which is most
common 24 h after administration in young adults due the
fasciculations damaging muscle fibres.
▪ Prolonged apnoea in patients with pseudocholinesterase
deficiency, which may be secondary to liver dysfunction. Of
greater importance is the presence, in the population, of
individuals with genetically determined
pseudocholinesterase deficiency, e.g. Arya Vysya Chettiars of
South India.
Pseudocholinesterase deficiency
A variety of genes have been identified which are involved in
pseudocholinesterase production. The most significant of these are:
• Normal homozygotes with sufficient enzyme: Hydrolyse suxamethonium

in 4–6 min (950 per 1000 population)
• A typical homozygote with slightly reduced enzyme levels: Suxamethonium
lasts 10–20 min (50 per 1000)
• A typical homozygote with marked deficiency of enzyme: This group is
apnoeic for up to 2 h after suxamethonium (<1 per 1000).
Treatment of this group consists of ventilatory support with maintenance of

anaesthesia or sedation until recovery occurs. The patient should subsequently
be warned, given a card with details and, because of its inherited nature, the
remainder of the family should be examined appropriately.
Prolongation of neuromuscular blockade

• Occasionally certain factors may prolong the effects of these drugs. For
non-depolarising relaxants, this involves concurrent use of those drugs
that affect calcium flux, most notably verapamil, nifedipine (calcium
antagonists and also aminoglycoside antibiotics (e.g. gentamicin).
• A part from the pseudocholinesterase deficiency, the length of action of
suxamethonium will be prolonged in patients with liver failure, in the
puerperium (reduced plasma cholinesterase) and in those using
echothiophate eye drops, an anticholinesterase, for the management of
glaucoma.
• Monitoring the degree of neuromuscular blockade in these patients
and adjusting the dose of drug accordingly will overcome any
potential problems of unanticipated prolonged paralysis.
Monitoring neuromuscular blockade

This can be done either clinically or by the use of a peripheral nerve
stimulator.
Clinical monitoring
• This method relies on having a conscious, cooperative patient and is

therefore limited in its application to those patients recovering from
anaesthesia. The neuromuscular junction in certain muscle groups is
stressed by asking the patient to perform a sustained activity, in other
words, to produce a tetanic contraction.
• Commonly used tests include:
▪ Lift the head off the pillow for 5 s
▪ A hand grip for 5 s
▪ The ability to produce avital capacity breath, >10 mL/kg
• In the patient who has not completely recovered from anaesthesia and
has a reduced level of consciousness, residual neuromuscular block
can be indicated by the presence of ‘see-sawing’ or paradoxical
respiration.
Peripheral nerve stimulation

One of the most common arrangements is stimulation of the ulnar nerve at the
wrist while monitoring the contractions of the adductor pollicis.
Anticholinesterases
• The administration of these drugs blocks the actions of the enzyme
acetylcholinesterase, which destroys acetylcholine at cholinergic
synapses and results in an increase in its concentration. This action is
used to reverse neuromuscular block induced by the administration of
non-depolarising relaxants.
• The speed of action of these drugs in reversing neuromuscular block
depends upon the intensity of the block when they are administered;
the more the intensity of the block, the slower the reversal.
• Anticholinesterases will work at the neuromuscular junction to
increase acetylcholine levels (nicotinic effects) and also at
parasympathetic nerve endings (muscarinic effects) to cause
bradycardia, spasm of the bowel, bladder and bronchi, increased
bronchial secretions, etc. Therefore, they are always administered with
a suitable dose of atropine or glycopyrrolate, to block the unwanted
muscarinic effects.
Neostigmine
This is the most commonly used anticholinesterase and a fixed dose of 2.5 mg
intravenously is used in adults to reverse residual neuromuscular block. After
approximately 5 min its maximal effect is seen and lasts for 20–30 min. It is
usually administered concurrently with either atropine 1.2 mg or
glycopyrrolate 0.5 mg. An ampoule containing 2.5 mg neostigmine premixed
with 0.5 mg glycopyrrolate is available.
Conscious sedation
Conscious sedation is defined as ‘minimally depressed level of consciousness
that retains the patient’s ability to independently and continuously maintain
an airway and respond appropriately to physical stimulation or verbal
command and that is produced by a pharmacological or non-pharmacological
method or a combination’.
Features of conscious sedation
• Retains the patient’s ability to maintain a patent airway independently

and continuously
• Permits appropriate response by the patient to physical stimulation or
verbal command
• Maintains protective reflexes
Techniques currently accepted for routine use in dentistry
1. IV sedation or deep conscious sedation is a type of sedation involving

administration of medications directly into the bloodstream through
intravenous route. The greatest advantage of IV sedation is that the
surgeon or anaesthesiologist has complete control of the entire
procedure. In case of inadequate sedation, patient can be fully sedated
or reversed. The drugs used for IV sedation are more effective than the
same drugs taken orally. There is a more profound amnesia associated
with this technique.
2. Enteral conscious sedation ‘orally administered sedation’, sometimes
called ‘sedation dentistry’ is administered by taking an oral sedation.
All body functions remain normal and the person is able to breathe on
their own. The patient will often fall asleep. Some degree of amnesia is
common. The disadvantage with this method of sedation is that the
level of sedation for each person is not predictable.
3. Inhalation conscious sedation, nitrous oxide/ oxygen sedation also
known as ‘laughing gas’. This is the most frequently used sedation
method in dentistry. All bodily functions remain normal and the
person is able to breathe on their own. The patient will often sleep and
experience some degree of amnesia of the dental appointment.
Clinical effects
• For 20–30 min acute detachment and later a state of relaxation.

• Anterograde amnesia (loss of memory following administration of the
drug) for the same period.
• Cardiovascular depression is minimal (the relative hypotension and
bradycardia due to the relief of hypertension and tachycardia caused
by anxiety).
• In most cases, minimal respiratory depression is seen. The exception is
in patients with impaired respiratory function or in those who have
taken other depressants such as opiates, alcohol, where the effect may
be more marked. However, excessively rapid intravenous injections
have the potential to cause respiratory depression leading to apnoea
and respiratory arrest, which is life-threatening if not diagnosed and
treated promptly.
• Additional properties of benzodiazepines:
▪ Muscle relaxant
▪ Anticonvulsant (used to treat status epilepticus).
Objectives of conscious sedation

The need for conscious sedation are as follows:
• To allay apprehension, anxiety or fear

• To decrease stress associated with traumatic or prolonged procedures
• To control gagging
• To stabilise the blood pressure for patients with hypertension or a
history of cardiovascular disease.
While administering conscious sedation, it is imperative to have access to all

resuscitative measures, as certain catastropic complications may arise.
Commonly used pharmacological agents for conscious

sedation
1. Benzodiazepines
Benzodiazepines have antianxiety, anticonvulsant, sedative, muscle relaxant
and amnesic properties. Midazolam and diazepam are the medications used in
the dental operating set-up.
2. Midazolam
Midazolam is a short acting benzodiazepine CNS depressant. Conscious
sedation prior to short diagnostic or surgical procedures is an indication,
either alone or with a narcotic:
• Water soluble
• Nonirritating to veins
• Faster and shorter acting
• Three times more potent than diazepam
• It may be administered IV, IM, PO, rectally or nasally. The most
common route of administration is IV.
Midazolam is a potent sedative agent that should be administered slowly

over 2 min for a single large bolus dose. Rapid or excessive IV doses may
result in respiratory depression or arrest. If not recognised and treated
promptly, death or hypoxic encephalopathy may result.
The initial IV dose may be as little as 0.5–1.0 mg, but should not exceed
2.5 mg in a healthy adult. It should be titrated to the desired effect. An
excellent indicator of an adequate dose is slurred speech. For patients over
60 years of age, debilitated patients or patients receiving narcotics, lower doses
should be used.
Onset of sedation after IV injection is achieved within 3–5 min. The duration
of effect ranges from 1 to 6 h after IV injection, but patients should not do any
activity that require fine motor or cognition skills (i.e. driving, cooking). The
half-life ranges from 1.2 to 12.3 h.
Midazolam should not be used on patients with known benzodiazepine
hypersensitivity or acute narrow-angle glaucoma. Adverse reactions from IV
administration include hiccups, nausea, vomiting, over sedation, headache,
coughing and pain at the injection site.
3. Diazepam
Diazepam has been replaced for the most part by midazolam but is still used
occasionally for conscious sedation and as a premedication for nonpainful
procedures. Like midazolam, diazepam is indicated for conscious sedation
prior to short diagnostic or surgical procedures, either alone or with a narcotic.
It may be administered IV, IM or PO, although IM administration is very
painful and hence not recommended. A large vein should be used to inject
diazepam. It cannot be mixed with other medications or diluted as it carries
the risk of precipitation.
Adverse reactions
• Extremely irritating to the tissues

• Venous thrombosis
• Phlebitis
• Apnoea
• Hypotension
• Diazepam can be given orally as a premedication prior to many
nonpainful surgical procedures.
• Effective anxiolytic
4. Fentanyl
Fentanyl is a synthetic opioid. It is indicated for analgesic action short duration
procedures. If given alone, dosage should begin at 1–2 µg/kg, which is about
75–150 µg for an average size adult. If given in conjunction with a
benzodiazepine a smaller dose should be used. The average patient usually
requires 50–100 µg. Fentanyl has an immediate response and effective
excellent analgesia. It has a half-life of 2–4 h, but patients should not do any
activities that require fine motor or cognition skills (i.e. driving, cooking).
Rapid IV administration can lead to a rigid chest wall and difficulty in
breathing. This effect may be reversed with naloxone (Narcan) or may require
a depolarising muscle relaxant and intubation.
This short acting (30–50 min) potent opioid analgesic related to pethidine is
generally given IV at the beginning of painful surgical procedures. Reflex
effects of painful stimuli are abolished.
Dose: 2–4 mg/kg

After IV fentanyl, the patient becomes drowsy yet conscious and his/her
cooperation can be commanded. Respiratory depression is marked, but
predictable; patient may be encouraged to breathe and assistance may be
provided.
Supplemental doses of fentanyl are needed every 30 min or so, but recovery
is prolonged after repeated doses.
1. Fentanyl is used effectively as sedation, adjunct to regional/local

anaesthetics. It is also used as supplement anaesthetics in balanced
anaesthesia. This permits use of lower anaesthetic concentrations with
better hemodynamic stability.
2. Combined with benzodiazepines, it can obviate the need for inhaled
anaesthetics for diagnostic, endoscopic, angiographic and other minor
procedures in poor risk patients, as well as for burn dressing.
5. Ketamine
Ketamine is a nonbarbiturate hypnotic with very high margin of safety. It
has good tissue compatibility (no irritation to veins). Ketamine produces a
so-called ‘dissociative anaesthesia’—profound analgesia, immobility, amnesia
with light sleep and feelings of dissociation from one’s own body and the
surroundings.
Dose
A dose of 1–3 mg/kg IV (average 1.5 mg/kg) or 6.5–13 mg/kg IM (average
10 mg/kg).
Ketamine produces the above effects within a minute and recovery starts
after 10–15 min, but patient remains amnesic for 1–2 h. It does not cause
relaxation of tongue so doesn’t interfere with airways thus making it ideal for
dentistry.
Emergence delirium, hallucinations and involuntary movements occur in up
to 50% patients.
1. Ketamine is effective for short procedures as operations on head and
neck especially in asthmatics
2. It is also useful for repeated use particularly for burn dressings
3. Combined with diazepam, it is useful in angiography, cardiac
catheterisation and trauma surgery.
4. Avoided in hypertensive and ischaemic heart disease patients.
5. Major disadvantage is increased intracranial and intraocular pressure
with increased occurrence of nausea and vomiting.
6. Propofol
It is the recent IV anaesthetic agent, used for induction/maintenance of
anaesthesia and also for sedation during short dental procedures done under
LA. Major advantage of propofol is rapid recovery irrespective of the duration
of infusion.
Dose
1–2 mg/kg/min (for sedation)
• Possess significant antiemetic property at low doses

• Rapid recovery without hangover effect
• Full orientation returns within 5–10 min
SECTION V
Principles of Practising
Oral Surgery
Chapter 11: Armamentarium

Chapter 12: Sterilisation and Disinfection
Chapter 13: Incisions and Flaps
Chapter 14: Suturing Materials and Techniques
Chapter 15: Haemorrhage and Shock
Chapter 16: Wound Care
C H A P T E R 11
Armamentarium
Laryngoscope
Face mask
Oropharyngeal airway
Nasopharyngeal airway
Laryngeal mask airway (LMA)
Tracheal (endo) tube
Tracheostomy tube
Swab holder
Towel clip
Scalpel
Scissors
Dissecting forceps
Tissue forceps
Allis forceps
Haemostat
Needle holder
Retractors
Tongue and cheek retractors
Langenbeck retractor
Austin’s retractor
Cat’s paw retractor
Obwegeser’s coronoid/ramus retractor notched right-
angle retractor
Skin hook
Channel retractor
Alar retractor
Nasal speculum
Tongue depressor
Retractors with light source
Mechanical devices
Lister’s sinus forceps
Periosteal elevator
Chisel
Pterygoid chisel
Osteotome
Mallet
Rongeurs
Bone File
Bone Gouge
Surgical curettes
Bone scoop
Smith’s bone spreader
Rotary and power drill instrument
• Microsaws
• Burs
Instruments used for management of fractures
Hayton-William Forceps
Rowe’s disimpaction forceps
Rowe’s zygomatic elevators
Walsham’s forceps
Asch forceps
Awl
Long (Obwegeser zygomatic arch awl)
Short (Kelsey−Fry bone awl)
Wire pushers
Wires, wire twisters and wire cutters
Mouth gag
Mouth prop
Trocar
Surgical suction apparatus
Foley’s catheter
Ryles’ tube
Surgical loupes
Operating microscope
The advancements in oral and maxillofacial surgery and the refinements in

surgical technique have complimented the evolution of the surgical
armamentarium. Armamentaria have evolved to ease surgery, shortening on-
table time, widening the surgical field, increasing visibility, minimising
trauma to surgical area, etc. A surgical instrument is a specially designed tool
or device for performing specific actions and carrying out desired effects
during a surgery or operation. Most of the surgical instruments are made of
high-grade steel, either stainless steel, tungsten carbide or chrome-plated. Each
instrument has a particular purpose and should be handled accordingly.
Inclusion of rotary and power-driven tools in bone cutting procedures has
greatly influenced the hard tissue surgeries.
Objectives
The major objectives of the armamentarium used in the oral and maxillofacial
surgery are:
• To provide an optimal surgical field

• For optimal visibility
• To decrease physical strain of the surgeon
• To enable patient comfort
• To protect vital structures
Armamentarium used in oral and maxillofacial surgery can be categorised

as depicted in Table 11.1.
Table 11.1
Armamentarium in oral and maxillofacial surgery

1. Laryngoscope
• Rigid
• Fibreoptic
2. Face mask
3. Oral/nasal pharyngeal airway
4. Laryngeal mask airway
5. Endotracheal tube
• Oral
• Nasal
6. Tracheostomy tube
Instruments used for handling sterile instruments:
1. Cheatle sterilizer forceps
2. Cheatle forceps container
Presurgical draping and asepsis
1. Swab holder
2. Towel clips
• Pinchter type towel clip
• Beckhaus towel clips
Soft tissue handling instruments
1. Scalpel
Blade handle
Blades
2. Scissor
3. Dissecting forceps
• Toothed forceps
• Non-toothed forceps
4. Tissue forceps
• Allis forceps
• Babcock’s forceps
• Lane’s forceps
• Kocher’s forceps
• Haemostat (artery forceps)
5. Instruments used for reflecting the mucoperiosteal flap
• Moon’s probe
• Periosteal elevators
• Cleft palate raspatory
6. Needle holders
7. Retractors
• Cheek retractor
• Langenbeck’s retractor
• Austins retractor
• Cat’s paw retractor
• Obwegeser’s ramus retractor
▪ Long (obwegeser)
▪ Short
• Obwegeser’s chin retractor
• Weider’s retractor
• Seldin’s retractor
• Minnesota retractor
• Copper Malleable retractor
• Skin hook
• Channel retractor
• Sigmoid notch retractor
• Alar retractor
• Nasal Speculum
• Tongue depressor
• Retractors with light source
8. Mechanical Devices
• Haemostatic clips
• Stapling devices
9. Lister’s sinus forceps
Hard tissue handling instruments
1. Periosteal elevator
2. Chisel
3. Pterygoid chisel
4. Osteotome
5. Mallet
6. Bone rongeur
• Jensen Middleton ronguers
• Miller and colburn bone file
7. Bone file
8. Nasal rasp
9. Bone gouge
10. Surgical curette
11. Volkmann Bone scoop
12. Bone Grasping forceps
• Crocodile bone holding forceps
• Sequestrum holding forceps
13. Smith’s bone spreader
14. Gigli saw
15. Rotary and power devices
• Microsaws
• Burs
Special instruments in fracture management
• Hayton−William forceps
• Rowe’s maxillary disimpaction forceps
• Rowe’s zygomatic elevator
• Walsham’s forceps
• Asch forceps
• Awl
▪ Long
▪ Short
• Wire pusher
• Wire twister
• Wire Cutter
• Bone plates
• Plate holder
• Screw driver and holder
• Plate bender and cutter
• Erich’s arch bar
• Mouth gag
▪ Fergusson
▪ Heister
▪ Dott−Kilner
▪ Dingman
• Mouth prop
• Trocar and cannula
• Suction tips
• Suction apparatus
• Foley’s self-retaining catheter
• Ryle’s tube
• Surgical drain
• Surgical loupes
• Operating microscope
• Diathermy
Laryngoscope (Figs. 11.1–11.5)
Rigid laryngoscope
A laryngoscope is a device used to view the larynx and adjacent structures,
most commonly used for securing the airway with a tube (endotracheal).
FIGURE 11.1 Rigid laryngoscope—handle with curved blades of
three different sizes for adults.
FIGURE 11.2 Laryngoscope in inactivated position—blade

attached to the handle.
FIGURE 11.3 Laryngoscope in working position. Note the

illumination provided by light bulb.
FIGURE 11.4 Paediatric rigid laryngoscope with short blades and
long handle.
FIGURE 11.5 Rigid paediatric laryngoscope in use to visualise
vocal cords before intubation.
Parts
• Detachable blade
• Handle unit with light source
Blade
• Rigid component inserted into mouth.

• Available in several sizes, with the numbers increasing with size.
• Blade has a base, heel, tongue flange, web, tip and light source.
• Blade has a lamp (bulb) that transmits light with source in the handle.
• Base of the blade has a slot to engage the handle.
• Blade may be straight, e.g. Guedel blade or curved, e.g. Macintosh.
Handle
• Compound that is held in hand with a rough surface for traction.

• Designed to accept blades
• When the blade and handle are in working position, an electric circuit
is completed thus activating the light bulb.
Flexible fibreoptic endoscope (Figs. 11.6–11.13)

The fibreoptic endoscope is a flexible endoscope composed of the following
parts:
FIGURE 11.6 Fibreoptic endoscope.

FIGURE 11.7 Fibreoptic endoscope with the light source connected
—external xenon light source.
FIGURE 11.8 Handle with the working channel port, tip control
knob connected to the light source.
FIGURE 11.9 Eye piece and focusing ring.
FIGURE 11.10 Fibreoptic endoscope with the endotracheal tube

passed over the insertion portion.
FIGURE 11.11 Fibreoptic cable from the xenon light source
illuminating the endoscope tip. Note the tip can be angulated
according to the need.
FIGURE 11.12 Accessories connected (suction).

FIGURE 11.13 Under fibreoptic guidance nasotracheal intubation
done.
Light source
• High intensity xenon light source is provided with a fibreoptic cable

(light cord) connected to handle.
• Alternative light source—halogen light source or handle with batteries.
Handle
• Handle or body is the part held in hand

• Handle includes an:
▪ Eyepiece
▪ Focusing ring
▪ Working channel port
▪ Tip control knob or lever (bending or angulations controls).
Insertion portion or tube

The portion of endoscope over which the tracheal tube is passed during
intubation. It contains an image transmitting bundle and light conducting
bundles.
Accessories
Suction
Face mask (Figs. 11.14–11.15)

Face mask or piece allows administration of gases from external breathing
system. It consists of mask body, face seal and a connector.
FIGURE 11.14 Facemask of adult and paediatric sizes with

adaptor.
FIGURE 11.15 Preoxygenation using face mask prior to
endotracheal intubation. Insert—note the jaw thrust manoeuvre.
Oropharyngeal airway (Fig. 11.16)

Oropharyngeal airway is a rubber or plastic device that extends from the lip to
the pharynx with the bite portion between teeth and flanges outside lips. It
helps to maintain an open airway, prevent patient biting and occluding the
tracheal tube, protect tongue from biting and facilitate suctioning, e.g. Guedel
airway.
FIGURE 11.16 Oropharyngeal airway.
Nasopharyngeal airway (Fig. 11.17)

A nasopharyngeal airway is also called nasal airway or nasal trumpet. It
resembles a shortened tracheal tube with flanged end made of rubber or
plastic. It is used as an alternative to oral airway, e.g. Bardex nasopharyngeal
airway.
FIGURE 11.17 Nasopharyngeal and oropharyngeal airways.

Laryngeal mask airway (LMA) (Fig. 11.18)
Laryngeal mask is an alternative to both face mask and tracheal tube, used to
secure the airway by a low-pressure seal around laryngeal inlet; using
inflatable cuff. It is also called brain mask, laryngeal mask airway or brain
mask airway (BMA).
FIGURE 11.18 Laryngeal mask airway device for ventilation. Note

2 tubes—for ventilation and suction. Silicon mask with inflatable
cuff.
Tracheal (endo) tube (Figs. 11.19–11.20)

This tube is inserted into the trachea and used to conduct gases and vapours to
and from the lungs.
FIGURE 11.19 PVC endotracheal tubes: 1. Inflated cuffed Ring
Adair Elwyn (RAE) nasal tube. 2. Noninflated cuffed RAE oral tube.
3. Inflated cuffed flexometallic tube. 4. Uncuffed paediatric oral
tube.
FIGURE 11.20 Endotracheal intubation (oral).
RAE (Ring Adair Elwyn) preformed tracheal tube

These are plastic tubes which are longer than other tubes. Nasal and oral
version of the tube with a preformed bend either cuffed or uncuffed is
available. The curvature facilitates the tube to be directed over the patient’s
forehead and reduces pressure on nares.
Flexometallic (spiral embedded) tube

These tubes have a metal or nylon spiral reinforcing wire that is covered both
internally and externally by rubber, latex or polyvinylchloride (PVC). It is
resistant to kinking and compression.
Tracheostomy tube (Fig. 11.21)

This is the miniature form of the endotracheal tube that may be cuffed or
uncuffed. It is designed to be placed transtracheally to secure airway and
ventilation. Though mostly used in case of emergency airway management it
is sometimes used electively, e.g. post-laryngectomy. Refer to Chapter 7 on
Medical Emergencies and their Management.
FIGURE 11.21 Single use disposable tracheostomy tube.
Cheatle forceps and container (Fig. 11.22)

Cheatle Sterilizer Forceps is a long instrument having a curved shaft without a
lock, used to remove sponges, gauze pieces or other sterilized instruments
from boilers and formalin cabinets. This ensures that each item is removed and
the others are not infected. The forceps are placed in a container of methylated
spirits when not in use.
FIGURE 11.22 Cheatle forceps and container.

Swab holder (Figs. 11.23–11.24)
The swab holder has a ratchet and two long blades which has fenestrations
and serrations at the operating end. The jaw of the forceps is usually rounded
and to be able to use the instrument for delicate and fragile operations, the tips
may even be elongated. It is used to hold the swab and paint the surgical area
with an antiseptic preoperatively. It can also be used by the surgeons to hold
soft tissue without causing much damage to the tissues.
FIGURE 11.23 Swab holder.

FIGURE 11.24 Swab holder being used for holding the betadine
soaked swab as a part of preoperative asepsis.
Towel clip (Fig. 11.25)

The towel clips can be of forceps type (Backhaus towel clip) or Pincher type.
The difference lies in the joints. The Backhaus towel clip has a box joint and
the Pincher type has spring joint. The working ends may have either sharp
points or blunt flat tips that overlap in the closed position.
FIGURE 11.25 Towel clips.
Uses
• Towel clips are used to maintain surgical towels and drapes in the
correct position during an operation thereby creating a sterile surgical
field.
• To stabilise suction tubes, motor cables and other cables to the sterile
field.

Scalpel (Figs. 11.26–11.27)
(Scalpere = to cut, Latin)
The scalpel is the traditional instrument of surgeons used to make incision or
excise soft tissues. Scalpels are composed of a handle and a disposable blade.
FIGURE 11.26 Scalpel handles (Bard−Parker).
FIGURE 11.27 Bard−Parker blades.
Blade handles
The two commonly used surgical scalpel handles are the number 3 and beaver
style. Each handle uses a different kind of blade and attachment method. The
handle has a receiving slot for the blade. The No. 3 handle is short and wide; it
uses a slotted blade that slides onto the handle. Controlled pen grasp with the
dominant hand is the common technique followed in placing incisions, though
palm and thumb grasp may be used sometimes.
Blades
The most commonly used blades are Bard−Parker blades (BP).
The blades come in presterilised packages and should be discarded after
using once. They are attached and removed from the handles with haemostatic
forceps. This prevents accidental cuts and any possible infection. The four
blades most often used with this handle are the no.10, no.11, no.12 and no.15.
Blades no.10 and no.15 have similar working ends. The difference is that the
no.10 blade is longer. The cutting edge on both the blades is on the curved part
of the blade.
Uses of the different blades
• No. 10—for making skin incisions

• No. 11—for making stab incisions as in case of draining pus from an
abscess cavity and drain placement
• No. 12 and 15—for carrying out surgeries in the mucogingival areas
and other areas of the oral cavity.
Scissors (Fig. 11.28)

(Latincisorium = a cutting instrument)
Scissors are cutting instruments used primarily for cutting soft tissues,
dissecting through the tissue planes, excision of soft tissue and for cutting
suture material. It may be straight, curved or angled; blunt or sharp tipped.
Choosing the correct scissors for the task is crucial in performing the
procedure (e.g.) Mayo, Goldman fox, Iris.
FIGURE 11.28 Straight and curved surgical scissors.
Dissecting forceps (Figs. 11.29–11.31)

Dissecting forceps or thumb forceps are the forceps that grip when
compressed between thumb and fingers while the blades separate on
releasing, as they are made of springing steel. They are excellent multipurpose
instrument.
• As a rule, they are to be held like a pen.

• They have no locking mechanism, as they intend to provide temporary
grip to hold tissues.
• Commonest types are toothed and non-toothed, available in various
shapes.
FIGURE 11.29 Dissecting forceps Adson—toothed and non-

toothed (2).
FIGURE 11.30 Dissecting forceps Adson—toothed and non-
toothed (2).
FIGURE 11.31 Adson toothed forceps used for suturing following

partial glossectomy.
Toothed forceps
They have one tooth on one tips interdigitates with two teeth on opposing tip.
The teeth puncture the tissue surface, tether and prevent it from slippage,
rather than crushing it from compression of holding. It is best used to hold
tough tissue as skin, fascia, cartilage and bone, e.g. Adson tissue holding
forceps.
Non-toothed forceps
They exert the grip through serrations on opposing tips. They are used to
manipulate delicate tissue as small ducts, blood vessels and for suture
removal. Sometimes round nosed non-tooth forceps make excellent dissecting
tool.
Tissue forceps
These forceps are instruments to grasp tissues that rely on the shape and
opposing surfaces of the blades for grip. They are indicated for use in
conditions where:
• A traction suture or hook may cut out

• Tissues tend to slip with smooth retractors.
Types of tissue forceps

Grasping instruments
• Tissue holding forceps
a. Allis forceps (Figs. 11.32–11.33)

These are toothed tissue holding forceps with locking handle and a ratchet
with triangular expansion at the tip where serrations are present. It is
indicated for use to hold or grasp tough tissue and where fibrous tissue layers
are planned for excision. It cannot be used on small excisions of
histopathological importance as the sharp teeth can cause damage.
FIGURE 11.32 Allis tissue holding forceps.
FIGURE 11.33 Working portion of the Allis tissue holding forceps

with teethed serrations to hold tough tissues.
b. Other forceps
Lanes forceps, Babcock forceps, Ring forceps, Kocher’s (Ochsner’s artery
forceps): They are used to grasp heavy tissue and may be used as clamp. They
may have straight or curved jaws.
Babcock’s tissue holding forcep (Fig. 11.34)

It causes less trauma than the all is forceps as they are non-perforating forceps
used to grasp soft tissue. It has a ratchet and triangular expansion with
fenestrations at the end without teeth. It is used during head and neck
dissection surgeries to hold thick flaps and the thyroid gland.
FIGURE 11.34 Babcock’s tissue holding forcep.
Lane’s tissue holding forceps (Fig. 11.35)

Lane Tissue Forceps are non-ratcheted thumb forceps. The tip is broad and
expanded with a wide opening. It is used for holding tough tissue such as
fascia and cartilage.
FIGURE 11.35 Lane’s tissue holding forceps.
Kocher’s Forceps−Ochsner’s Artery Forceps (Figs.

11.36–11.37)
The Kocher’s Forceps is named after Emil Theodor Kocher, a Swiss surgeon
who was awarded Nobel Prize in 1909. The Kocher’s is a hemostatic forceps. It is
specifically designed to catch the bleeder that are deep within tissue hence it is
ideally used on tough structures like fascia, salivary gland and to divide strap
muscles during thyroidectomy or tracheostomy. The forceps can also be used
to catch the structure that is bleeding causing the bleeders to clog and provide
haemostasis. The toothed-tip grips the structure firmly, so that it will not slip.
FIGURE 11.36 Kocher’s toothed heavy artery forceps—straight.

FIGURE 11.37 Kocher’s toothed heavy artery forceps—curved.
Haemostat (Figs. 11.38–11.39)

(Haema—blood, stasis—stoppage—Greek)
A haemostat, also called a haemostatic clamp, is a surgical tool which
resembles a set of scissors with a locking clamp replacing the blade. There are
many types of haemostats namely Kelly, Crile and Halstead. A haemostat is
commonly used to control bleeding, especially from a torn or punctured blood
vessel, until the bleeding can be repaired by sutures or other surgical
techniques. The handle has a lock and thus the vessel may be held clamped.
Small vessels may simply be crushed to attain haemostasis whereas larger
vessels have to be ligated or cauterised.
FIGURE 11.38 Straight artery forceps (haemostat). Insert showing

horizontal serrations.
FIGURE 11.39 Curved artery forceps.
Instruments used for reflecting the

mucoperiosteal flap
Moon’s probe (Fig. 11.40)
It is a right angled probe with a narrow working edge, flat handle and blade
which is blunt and a rounded tip. It helps in retracting the mucosa without
traumatisation and used for elevation of the mucoperiosteum prior to
extraction.
FIGURE 11.40 Moon’s probe.

Periosteal elevator (Figs. 11.41–11.42)
This is a double-ended instrument with a broad end (raspatory) and a sharp
end (rugine end). The sharp end should be maintained sharp to prevent
shredding of the flap. Commonest in use are No: 9 Molt and No: 23 Seldin and
Howarth periosteal elevator. This instrument is used to expose the bone
elevating the periosteum off the bone as a mucoperiosteal flap (intraorally) or
separately (e.g. harvesting a rib graft). The sharp end is also used in tooth
extraction to initially elevate the gingiva (prying motion) as well as aid in
extraction by wedge principle. The raspatory end is used to gently elevate the
soft tissue flaps from the underlying bone without tearing. It is used to retract
flaps to visualize the area of interest during multiple extractions and surgical
procedures. Periosteal elevators are mainly used to lift full thickness soft tissue
flaps.
FIGURE 11.41 Molt periosteal elevator.
FIGURE 11.42 Cleft palate raspatory.
Needle holder (Figs. 11.43–11.45)

Needle holders are forceps with locking mechanism to hold needles during
suturing procedures. The typical needle holder has two short, rather blunt,
serrated beaks with a distinct groove in each beak. The grooves provide space
for the placement and retention of the needle. At the end of handles, there is a
graduated, notched-locking device that lets the surgeon secure the suture
needle in the desired position as if the needle were an extension of the needle
holder. A modification of this is Gillie’s needle holder that is a combination of
needle holder and scissors.
FIGURE 11.43 Needle holder. Note the crisscross serrations with

the groove in the centre for holding needle. Working portion of the
needle holder is comparatively smaller than the haemostat.
FIGURE 11.44 Needle holder holding the needle at three-fourth of
its length from the tip.
FIGURE 11.45 Needle holder in use.
Retractors
Retracting and exposing instruments are used to hold back or retract organs or
tissue to gain exposure to the operative site. They are either ‘self-retaining’
(stay open on their own) or ‘manual’ (held by hand). While identifying
retractors, look at the blade not the handle. There are different kinds of
retractors, but the purpose is the same for each. Retractors are also used to
hold back structures in the oral cavity.
In oral surgery, tissue retractors hold tissues and flaps away from the
surgical field to provide better visibility. Some retractors have blunt fork-like
prongs that effectively allow handling of the tissues without causing excessive
damage.
Tongue and cheek retractors (Figs. 11.46–11.47)

These retractors are designed to hold and retract the cheeks, tongue or a
portion of the mucosa during surgical procedures. The retractors are made of
metal or plastic and may be large, curved or angled.
FIGURE 11.46 Cheek retractor.
FIGURE 11.47 (A and B) Metal cheek retractor.
Langenbeck retractor (Fig. 11.48)

These are used for retraction of soft tissues and incision edges to have a better
visibility of deeper structures. This is the most commonly used retractor in oral
surgery which has a long handle and an L-shaped blade on one or both the
ends. They are available in various sizes of blade width.
FIGURE 11.48 Langenbeck retractors—large, medium, small and
reverse (from below).
Austin’s retractor (Fig. 11.49)

This is the most commonly used instrument in the removal of impacted third
molars. It is a short right angled instrument which is helpful in retracting the
mucoperiosteal flap and to a lesser extent the cheek.
FIGURE 11.49 Austin retractor used in retracting buccal flap in

bilateral sagittal split osteotomy (BSSO) procedure.
Cat’s paw retractor (Fig. 11.50)

The retractor end resembles a cat’s paw. It is most commonly used for gentle
retraction of soft tissues. Care should be taken not to apply excessive force
which might lead to soft tissue damage.
FIGURE 11.50 Cat’s paw retractor.
Obwegeser’s coronoid/ramus retractor notched right-angle

retractor (Figs. 11.51–11.54)
This retractor is similar to Langenbeck retractor in all aspects except that it has
a V-shaped notch on the retracting end which is helpful to engage the anterior
border of the ramus and to retract the soft tissues. It is used in retraction of the
soft tissues and in surgeries involving the anterior border of the ramus of
mandible (like sagittal split osteotomy, coronoidectomy, angle fracture fixation
etc.).
FIGURE 11.51 Obwegeser’s coronoid ramus retractor notched
right-angle retractor.
FIGURE 11.52 Obwegeser’sright-angle retractor designed to

engage anterior border of ramus and coronoid process retracting
soft tissues.
FIGURE 11.53 Demonstration of using coronoid retractor in
mandible.
FIGURE 11.54 Demonstration of using coronoid retractor in
mandible, engaging anterior border of mandibular ramus.
Obwegeser’s chin retractor
Weider’s tongue retractor (Fig. 11.55)

Wieder Retractor has a right-angled serrated blade, specifically designed to
protect the tongue during lower jaw procedures, where the tongue must be
removed from covering the occlusal surface of the teeth. It is available in two
sizes. The end of the handle is curved for better control. Weider Tongue
Retractor is designed to hold mucoperiosteal flaps, cheeks, lips and tongue
away from the surgical area.
FIGURE 11.55 Weider’s tongue retractor.
Seldin’s retractor (Fig. 11.56)

It is a straight instrument with broad tip and a flat handle, the larger end is
slightly curved designed for reflecting and retracting the mucoperiosteum
after incisions of the gingival tissue. It is a non cutting blade.
FIGURE 11.56 Seldin’s retractor.
Minnesota retractor (Fig. 11.57)

Both Austin’s and Minnesota retractors are used to retract cheek and the
mucoperiosteum simultaneously. It consists of a handle and a rounded and
slightly pointed working part. It is used for holding and retracting the lip or
cheek. It is suitable for retracting tissue edges and opening the cheek wide and
can also be used as a lip retractor during an oral procedure.
FIGURE 11.57 Minnesota retractor.
Copper Malleable retractor (Fig. 11.58)

Copper Malleable Retractor is a flattened instrument that can be bent to the
desired direction. It is used in bicoronal flap and craniosynostosis surgeries, to
retract the parenchyma while doing craniotomies and also to retract the
eyeball during orbital floor reconstruction surgeries.
FIGURE 11.58 Copper Malleable retractor.
Available sizes
Length (mm) Width (mm)

305 13
305 25
305 38
305 51
Skin hook (Figs. 11.59–11.60)

Skin hook is a long narrow instrument with a curved tip to engage soft tissues.
It is used for retracting skin following the incision placement.
FIGURE 11.59 Skin hook.

FIGURE 11.60 Skin hook in use during primary cleft lip repair.
Channel retractor (Figs. 11.61–11.63)

It is an effective lower border retractor useful in sagittal split osteotomy,
mandibular body osteotomies.
FIGURE 11.61 Channel retractor.
FIGURE 11.62 Demonstration of using channel retractor in
mandible.
FIGURE 11.63 Demonstration of using channel retractor in

mandible engaging mandibular lower border.
Sigmoid notch retractor: (Fig. 11.64 A−B)

It is a curved mandibular retractor used in vertical subsigmoid (vertical
ramus) osteotomy. Retraction of the masseter muscle during vertical ramus
osteotomy (VRO) by inserting a sigmoid notch retractor into the sigmoid
notch. Another type of sigmoid notch retractor is called Bauer’s retractor
which is used in VRO and bilateral sagittal split osteotomy, it is placed to
protect the contents of the sigmoid notch.
FIGURE 11.64 (A−B) Sigmoid notch retractor.
Alar retractor (Fig. 11.65)

Alar retractor as the name suggest is a simple instrument used to retract the
ala of the nose during rhinoplasty.
FIGURE 11.65 Alar retractor—in use during rhinoplasty.
Nasal speculum (Fig. 11.66)

Speculum is an instrument used to widen an opening to look within a passage
or a cavity. Nasal speculum is used to widen the nasal cavity and to examine
the nasal and internal structures and is widely used in rhinoplasties. It has two
long blades for ease of insertion into the nostrils which are separated by a
spring in between them when the handle is compressed.
FIGURE 11.66 Nasal speculum.
Tongue depressor (Figs. 11.67–11.68)

It is a retractor used for depressing the tongue for better examination of the
oral cavity and in case of surgeries of posterior oral cavity and oropharynx
that effectively displace tongue from the field of view of surgery. It is a single
L-shaped blade-like instrument.
FIGURE 11.67 Tongue depressor.
FIGURE 11.68 Tongue depressor in use.
Retractors with light source (Figs. 11.69–11.74)

Some retractors are designed to be enabled with external light source that
facilitate good visual field and illumination, e.g. Langenbeck, nasal speculum,
etc.
FIGURE 11.69 Channel retractor with external light source.
FIGURE 11.70 Channel retractor with light source.

FIGURE 11.71 Depiction of the usage of channel retractor with
external light source.
FIGURE 11.72 Lower border retractor with light source to illuminate

the site of surgery.
FIGURE 11.73 Nasal speculum with external light source and a
depiction of its use to visualise posterior nasopharynx.
FIGURE 11.74 Retractor with light source being used for placement
of mandibular ramal distractor.
Mechanical devices
These are time saving devices that facilitate difficult procedures.
Haemostatic clips
These are metal clips that can be applied across blood vessel and ducts to
occlude by special forceps.
Stapling devices (Figs. 11.75–11.76)

These are devices similar to paper stapling machines used for skin
approximation instead of sutures.
FIGURE 11.75 Stapling device.

FIGURE 11.76 Wound closure using staples.
Lister’s sinus forceps (Fig. 11.77)

Lister’s sinus forceps are used for probing and forcing an entry into an abscess
sac (cavity) or for creating an opening into an abscess by Hilton’s operation.
Forceps has gripping surfaces which are long and thin with slightly bulbous
points. This helps in draining of the abscess. This involves entering the sinus
with jaw closed and exiting with the forceps opened. This enlarges the wound,
facilitates, drainage as well as avoids damage to the vital structures if any.
FIGURE 11.77 (A–B) Lister sinus forceps—long beaks with no

ratchet.

Periosteal elevator (Figs. 11.41, 11.78)
This is a double-ended instrument with a broad end (raspatory) and a sharp
end (rugine end). The sharp end should be maintained sharp to prevent
shredding of the flap. Commonest in use are No: 9 Molt and No: 23 Seldin and
Howarth periosteal elevator. This instrument is used to expose the bone
elevating the periosteum off the bone as a mucoperiosteal flap (intraorally) or
separately (e.g. harvesting a rib graft). The sharp end is also used in tooth
extraction to initially elevate the gingiva (prying motion) as well as aid in
extraction by wedge principle. The raspatory end is used to gently elevate the
soft tissue flaps from the underlying bone without tearing.
FIGURE 11.78 Howarth periosteal elevator.
Chisel (Figs. 11.79–11.80)

Chisel is a mono-bevelled instrument used for removal of bone. It has a heavy
metal or fibre handle. The bevel has to be sharp for efficient chipping or
cutting of bone. For cutting or removal of the bone, the bevel is placed facing
away from the bone or the bevel towards the bone to be removed. The major
advantage of the chisel is that the clear cut is created with no bone dust. The
disadvantages are:
• Risk of uncontrolled force delivery that can be dangerous

• Uncomfortable to use in awake patient (under LA).
FIGURE 11.79 Chisels of varying sizes, shapes and design.
FIGURE 11.80 Chisel—mono-bevelled instrument.
Pterygoid chisel (Figs. 11.81–11.83)

This is an angled chisel available in sizes of 8 mm, 10 mm and 12 mm. The
handle is usually long and made of heavy metal or fibre. It is specifically
indicated for pterygomaxillary dysjunction in Le Fort osteotomies of maxilla.
FIGURE 11.81 Pterygoid chisel—long heavy handle with curvature.
FIGURE 11.82 Demonstration (in a dry skull) of application of

pterygoid chisel for pterygomaxillary dysjunction. Note the index
finger placed in palatal aspect to determine dysjunction.
FIGURE 11.83 Pterygoid chisel directed 45˚ anterior and medial to
the pterygomaxillary fissure.
Osteotome (Figs. 11.84–11.86)

Osteotome is similar to chisel, but it is bi-bevelled and is used for splitting of
the bone as well as tooth (odontectomy).
FIGURE 11.84 Straight osteotomes of varying sizes.
FIGURE 11.85 Straight osteotome—bi-bevelled instrument.
FIGURE 11.86 Curved osteotomes—curved bi-bevelled instrument.
Mallet (Fig. 11.87)

The mallet is made of wood, rubber, nylon or stainless steel. Stainless steel
mallets are preferred because they can be sterilised which reduces the risk of
infection and prolongs its use. The mallet is designed to weigh 8 ounces for
delivering controlled force on the chisel and the osteotome, e.g. Gardner’s
mallet.
FIGURE 11.87 Stainless steel mallet.

Rongeurs (Figs. 11.88–11.91)
Rongeur forceps are used to trim irregular, uneven or overhanging bone
(alveolectomy, alveoloplasty), usually after multiple extractions and to trim
harvested bone graft. The blades are sharp and are brought together by the
handles for cutting the bone. It has a steel spring spreader, which opens the
beaks when pressure is released. The Jensen Middleton Rongeur, traditionally
used in removal of pathological nasal turbinate has double pivot points that
makes the instrument longer, this allows to access more posterior areas in the
oral cavity. The spring action allows repeated cuts of the bone without much
effort to reopen the instrument.
FIGURE 11.88 Jensen Middleton ronguers.

FIGURE 11.89 Bone rongeur.
FIGURE 11.90 Tip cutting (blu Bone rongeur—sharp beaks for

cutting bone and central concavity for collecting the bone chips.
FIGURE 11.91 Rongeur in clinical use.
Uses
• To remove sharp bony projections during alveoloplasty and after

extraction.
• To trim harvested bone graft.
Bone File (Figs. 11.92–11.93)

Bone file is used for smoothening of bone after extraction or during
alveoloplasty. Another instrument that is similar to the bone file is the nasal
rasp used in Rhinoplasty. It is a double-ended instrument where one end is
large and other end is small. The serrations in the bone file can remove bone
by pull stroke.
FIGURE 11.92 Miller and colburn bone file.

FIGURE 11.93 Bone file.
Bone Gouge (Fig. 11.94)

A hollow chisel used for cutting or channelling cortical bone and scooping
soft, cancellous bone used in bone graft.
FIGURE 11.94 Bone gouge.
Uses
• To remove sharp bony projections during alveoloplasty and after

extraction.
• To trim harvested bone graft.
Surgical curettes (Fig. 11.95)
Curettes are sharp, spoon-shaped instruments used to debride infected
cavities in bone from the tooth sockets. They come in many sizes that may be
straight or angled. The type used depends on the nature of socket, curvature of
roots that were in the socket and location of the cavity. The single-ended Molt
curettes have large handles. They are the straight number 2 and number 4; the
paired, angled number 5L and number 6R (L for left and R for right). Other
curettes in dental surgery may be double-ended and have slender handles.
FIGURE 11.95 Surgical curette—spoon-shaped instrument.
Uses
• To remove debris from the extraction site, e.g. Periapical granuloma.

• To remove granulation tissues from the periapical lesions in
apicoectomy.
• To removes equestrum which develops in non-healing sockets.
• To debride small periapical cyst and other cysts.
Bone scoop (Figs. 11.96–11.99)

Bone scoop has a working end similar to that of curette (e.g. Volkmann’s
scoop). It is primarily used for debriding contents from an intraosseous
abscess cavity or cyst. Since it has sharper margins it can also be used to scoop
out periphery of the cavity bone. It is also used to harvest cancellous bone
during bone grafting, e.g. Iliac.
FIGURE 11.96 Bone scoops of varying sizes and designs.
FIGURE 11.97 Bone scoop—working end.
FIGURE 11.98 (A–B) Bone grasping forceps.
FIGURE 11.99 Sequestrum holding forceps—straight.
Smith’s bone spreader (Figs. 11.100–11.104)

Spreader is an instrument with three blades. It is activated by a spring
mechanism. The blades are separated when the handle is squeezed (2 blades in
one direction and 1 blade in opposite direction).
FIGURE 11.100 Smith spreader—3 blades.

FIGURE 11.101 Smith spreader in closed position.
FIGURE 11.102 Smith spreader in open position.

FIGURE 11.103 Smith spreader used to separate osteotomised
segments in BSSO—positioned between the segments to be
osteotomised.
FIGURE 11.104 Smith spreader used to separate osteotomised

segments in BSSO—note the separation of the fragments.
It is mainly used to separate the osteotomised fragments as in case of sagittal

split osteotomy (e.g. smith spreader).
Gigli saw (Fig. 11.105)
A gigli’s saw is a flexible wire with a handled handles used in the cutting of
bone manually. It is generally used in segmental resection of the mandible and
in craniotomies. The bone cuts were smoother and predictable than the used of
chisel and mallet.
FIGURE 11.105 (A–B) Gigli saw.

Rotary and power drill instrument (Figs.
11.106–11.108)
Handpiece and burs are rotary instruments that remove bone most efficiently
and quickly. The burs are available in various sizes and shapes and made up
of carbide or stainless steel. The bur is attached to the head of the handpiece
which has a cartridge driven by air pressure. This drilling instrument is used
for making osteotomy cuts, removing bone (osteotomy), smoothening of bone
(osteoplasty), splitting of teeth (odontectomy) or drilling a hole in the bone for
wiring or plate fixation.
FIGURE 11.106 Micromotor with straight handpiece.

FIGURE 11.107 Rotary power drill instruments—stainless steel and
tungsten carbide burs.
FIGURE 11.108 Microdrill and saws.

Microsaws
The microsaws are instruments used to cut bone. Due to their high speed and
thin blade design they help in quick cutting of bone with minimal bone loss.
They are especially useful in maxillary and mandibular osteotomies. There are
different types in microsaws based on the direction of movement of the
handpiece. The main three types are oscillating, reciprocating and sagittal.
Each model has different types of blades in varying sizes and shapes.
Burs
These are stainless steel or tungsten carbide rotary cutting instruments used
extensively in hard tissue surgeries as osteotomy, fracture fixation, etc.
Instruments used for management of

fractures
Hayton−William Forceps
Hayton−William forceps has two curved beaks that are widely divergent
which engage behind the tuberosity of the maxilla. It is used to hold both
maxillae (R&L) as single segment before initiating disimpaction with Rowe’s
forceps.
Rowe’s disimpaction forceps (Fig. 11.109)

This instrument is used in pairs for the reduction of maxilla in Le Fort
fractures where the maxilla is impacted. It has two blades—straight and
curved. The straight one is padded and used to pass through the nostrils. The
curved one is unpadded and is used to pass into the oral cavity to grip the
palate. The paired instruments are always used together along with Hayton
−William forceps in case of mid-palatal split to disimpact the maxilla in
downward and forward direction.
FIGURE 11.109 (A) Rowe’s disimpaction forceps. R: Right; L: Left;
P: Palatal; N: Nasal. (B) Demonstration of application of Rowe’s
disimpaction forceps (in a dry skull).
Rowe’s zygomatic elevators (Figs. 11.110–11.112)

Rowe’s zygomatic elevators are used to reduce the fractured zygoma through
the Gillies temporal approach. They work by 3rd order of lever principle with
fulcrum at one end.
FIGURE 11.110 Rowe’s zygoma elevator.

FIGURE 11.111 Rowe’s zygoma elevator to reduce fractured
zygoma. Demonstration in a dry skull model.
FIGURE 11.112 Position of the working end of Rowe’s zygomatic
elevator, posterior to the buttress.
Walsham’s forceps
This paired forceps is used for the reduction of nasal fractures. It has two
curved blades—one is padded and the other unpadded. The padded blade is
inserted internally into the nostril and the unpadded blade is placed externally
over the nasal bone and manipulated for the reduction of the nasal fracture.
Asch forceps
These forceps are used for reduction of nasal fractures and also to align the
nasal septum. When reducing the nasal septum, both the blades are inserted
internally one on each side of the septum. In case of nasal bone fracture
reduction, one blade is inserted internally and the other is placed externally to
hold the nasal bone laterally and medially respectively.
Awl (Figs. 11.113–11.114)

Awls are long slender instruments provided with an eyelet at the tip through
which the wire or suture material is passed.
FIGURE 11.113 Awl—long (Obwegeser) and short rigid.
FIGURE 11.114 Awl for circum zygomatic static suspension in

facial palsy using tensor fascia lata. (A) Awl introduced medial to
the arch. Insert showing securing of harvested fascia lata to the
eyelet of the awl. (B) Fascia lata guided medial to the zygomatic
arch using the awl. (C) Checking for the length of the fascia lata
before guiding it lateral to the zygomatic arch using the awl.
Long (Obwegeser zygomatic arch awl)
Used in
• Circum-zygomatic suspension of Le Fort II fracture of maxilla

• Adam wire suspension for Le Fort III
• Circum-zygomatic static suspension for facial palsy
Short (Kelsey−Fry bone awl)
Used in
Per alveolar wiring by boring action on the alveolar ridge in circum
mandibular wire for cap splint or gunning splint placement. Kelsey−Fry bone
awl is available as a straight type or in a curved pattern which is used in
Obwegeser’s method of circum mandibular wiring.
Wire pushers (Figs. 11.115–11.116)

These instruments are used to push the wire into the interdental space during
intermaxillary fixation. They are also useful in adapting the wires tightly
around the teeth.
FIGURE 11.115 Wire pusher.
FIGURE 11.116 Wire pusher being used for adapting the

interdental wire.
Wires, wire twisters and wire cutters (Figs.

11.117–11.118)
Thin stainless steel wires (26 gauge) are used in oral surgery for the fixation of
fractures, osteotomy cuts and the intermaxillary fixation. These wires are
available in different lengths and sizes. The 26 gauge wires are most
commonly used for maxillofacial trauma. A wire twister is an instrument used
to hold the wire as well as for twisting it. They have a design similar to a
needle holder but with shorter broader blades and cross wire grooves that
avoid wire slippage. Wire-cutters are used to cut off the excess wires after
securing the wiring in place.
FIGURE 11.117 Wire twister, note the short broad blades with
crisscross grooves to prevent wire slippage.
FIGURE 11.118 Stainless steel wire, Erich arch bar and wire cutter.
Plates—titanium and stainless steel

Bone plates and screws used to surgically fix the bone fractures, osteotomies,
maxillary and mandibular reconstruction with on lay grafts. It is made up of
titanium or stainless steel (Figs. 11.119–11.121).
FIGURE 11.119 Plate holder.
FIGURE 11.120 (A–B) Plates—titanium and stainless steel.
FIGURE 11.121 (A–B) Screw carrier and driver with 703 and 701
burs.
Mouth gag (Fig.11.122)
Ferguson mouth gag
This is a ratchet type gag with a long handle and box joint. It is used to
improve mouth opening in patients with acute onset trismus, e.g. post surgery
and infections.
FIGURE 11.122 Ferguson mouth gag—ratchet type gag with long

handles and box joint.
Heister mouth gag (Figs. 11.123–11.124)

It is a T-shaped mouth gag with 2 blades separated by a adjustable knob at the
joint similar to Ferguson mouth gag.
FIGURE 11.123 Heister mouth gag—T-shaped gag with adjustable
knob.
FIGURE 11.124 Heister jaw opener in clinical use—postgap
arthroplasty physiotherapy.
Dingman (Figs. 11.125–11.126)

In 1960, Dingman designed the mouth gag. This mouth gag has a transverse
bar with a rectangular frame on which an adjustable tongue retractor is
mounted in the centre. It has two clamps on either side for adjusting the
opposite pair of alveolar retractors. These alveolar retractors coact with the
tongue retractors to retain the jaws in desired open position. The alveolar
retractors can be adjusted both for axial rotation and longitudinal sliding. In
addition it has two self-retractory cheek retractors on either side to retract
cheek).
FIGURE 11.125 Dingman mouth gag.
FIGURE 11.126 Dingman mouth gag for cleft surgery.
Dott−Kilner (Figs. 11.127–11.129)

This is similar to Dingman except that it lacks cheek retractors and has a C-
shaped frame.
FIGURE 11.127 Dott−Kilner mouth gag.
FIGURE 11.128 Dott−Kilner mouth gag C-shaped frame and
tongue blades of different sizes. Note the tongue blade is designed
to accommodate the oroendotracheal tube.
FIGURE 11.129 Dott−Kilner retractor used as mouth gag for cleft
palate repair.
Mouth prop (Fig. 11.130)

A mouth prop is a device for maintaining the maxilla and mandible apart
during the surgical procedure. It consists of a vertical rubber block having a
concave surface on either of its ends to fit the maxillary and mandibular teeth.
Blocks of different sizes are available attached to a chain and the operator can
choose the required amount of mouth opening.
FIGURE 11.130 Mouth prop.
Trocar (Fig. 11.131)

A trocar is a sharp cylinder pointed instrument with a sleeve or a cannula. It is
used to gain entry into the surgical site through a stab incision on the skin to
avoid an incision, wide opening or scar. In oral surgery, it is used for
transbuccal approach to the ramus of the mandible.
FIGURE 11.131 (A–B) Trocar and cannula.
Surgical suction apparatus (Fig. 11.132)

Components
• Hose (tubing)
• Handle
• Tips
FIGURE 11.132 (A) Suction apparatus and suction tip. (B)
Disposable suction tips.
Hose
The hose is used to connect the handle to the suction apparatus and has sterile
tubing that is available in various lengths. It can be made up of rubber or
silicone polymer.
Handle
The handle has a bulbous portion on one end and a chuck on the other end.
The bulbous portion is slipped into one end of the hose and the chuck holds
the tip.
Tips
The tips are introduced into the surgical field to remove away blood,
secretions, cystic fluid, etc. and create a clear visual field for surgery. The tips
may be straight or angulated. Sometimes styles are provided along with the
tips to remove any debris if it gets lodged in the lumen. There are several tips
available based on length and diameter.
Foley’s catheter (Fig. 11.133)

Foley’s catheter is a self-retaining disposable tube placed through the urethra
into the bladder for continuous urine drainage. A self-retaining catheter is one
which can remain in the bladder and is held in by a balloon which prevents it
from displacement.
• In its basic form it has two interior channels, one wider channel for
drainage and one for the balloon inflation. To inflate this type of
catheter, the clip on the inflation channel is released once the catheter
is in position and the balloon inflates.
• The catheter is passed through the urethra and position is confirmed
by the free passage of urine through the wider tube. Now the balloon
is inflated via the smaller tube by injecting water. Similarly, when the
catheter is to be withdrawn the water in it is aspirated through the
narrower tube.
FIGURE 11.133 Foley catheter.
Ryles’ tube (Figs. 11.134–11.135)

• Ryles’ tube is a specially designed tube made up of red rubber or
nontoxic, nonirritant polyvinyl chloride (PVC) for nasogastric
introduction of nutrition and aspiration of intestinal secretion. It
measures about 105 cm. It may have three lead shots in the tip, which
appears radiopaque in radiographic examination and assists the
passage of tubing during intubation. Super smooth low friction surface
facilitates easy intubation is provided with an X-ray opaque strip
throughout the length.
FIGURE 11.134 Ryles’ tube in a patient on MMF
(maxillomandibular fixation).
FIGURE 11.135 Ryles’ tube—infant feeding.

The NG tube must be measured from the tip of the patient’s nose, looping
around the ear and then down approximately 5 cm below the xiphoid process
to mark the level of insertion. The standard depth markings are 40 cm (at the
level of gastrooesophageal junction), 50 cm (level of the body of the stomach),
60 cm (level of pylorus) and 65 cm (level of duodenum) from distal end. The
end of the tube is lubricated with local anaesthetic, (2% xylocaine gel) and
inserted into one of the patient’s anterior nares. The tube should be directed
posteriorly as it moves through the nasopharynx and oropharynx. It then
glides down the posterior pharyngeal wall. Now the patient is asked to mimic
swallowing to past the pharynx and enters the oesophagus and into the
stomach. The tube must then be secured in place to prevent it from moving.
Care must be taken to ensure that the tube has not entered the trachea. The
reliable method to determine the position of the tube is to aspirate some fluid
with a syringe and subject it on a pH paper which determines the acidity of
the fluid. Other methods commonly practiced are introducing a small quantity
of a fast gush of air into the tube through a 10 mL syringe and auscultation for
a bubbling sound over epigastrium, but a recent study proved this method
unreliable. However, an abdominal radiograph is considered the “gold
standard” for determining the position of the NG tube. If feeding is required
for a longer period of time, other options, such as placement of a PEG tube,
Uses
• For the purpose of feeding debilitated patients for long-term

gastrointestinal feeding in patients who cannot take oral feed, for
aspiration of intestinal secretions and for gastric lavage in case of
poisoning.
Infant feeding tube

Infant feeding tubes often incorporates a 1 cm depth markings used in infants
with faciomaxillary injuries and anorexia.
Surgical drain (Fig. 11.136)

Surgical drain is a channel or tube used to remove pus, blood or other fluids
from a wound.
FIGURE 11.136 Surgical drain is a channel or tube used to remove
pus, blood or other fluids from a wound.
Indications
1. To help eliminate dead space.

2. To evacuate existing accumulation of fluid, to remove pus, blood,
serous exudates.
3. To prevent the potential accumulation of fluid
4. Decrease infection rate.
Classification
1. Open and closed drain

2. Active and passive drain
Open drain
Open drain generally include corrugated rubber drain. The drain is generally
collected in gauze pad or stoma bag.
Corrugated rubber drain

It is made up of red rubber or PVC and is an open passive drain. The
corrugations on both surfaces of the drain prevent closure of the wound and
allow fluid to drain out freely by capillary action and gravity. It is stabilized to
the skin by an anchoring stitch. It is used post operatively for superficial
parotidectomy, for abscess collected in soft tissue spaces and Ludwig’s angina.
Disadvantages
The rate of infection is higher in open drain as it may lead to wound soakage
that would require repeated dressings due to the risk of infection.
Closed drain
The tube is connected to a sterile bag with or without a one-way valve.
Advantages: the rate of infection is reduced.
Tube drains
It is made of red rubber or PVC and has multiple side holes near its tip for free
drainage. It is put in the most dependent part of the wound and taken out
through a separate stab incision using the shortest possible route. Types of
tube drains are closed and connected to a sterile bag under negative pressure.
Hemovac drain
Hemovac drain has a fine tube with many holes at the end, which is attached
to an evacuated glass bottle or a large bellow chamber of 600 mL providing
suction. It is used to drain blood under the skin. It is used for efficient
postoperative drainage of closed internal wounds to prevent infection or
haematoma. It can be used for prolong suctioning.
It has curved needles that help in creating a stab incision on the skin for the
drain tubes and clamps to contain the continued suction effect while removing
the collected fluid from the bellow chamber. The drain is sterilized by ethylene
oxide before packing.
Advantages
Since it is a closed system, there is no chances of soakage and does not require
repeated dressings. The exact amount of drainage of fluid can be measured. It
can be kept for a longer time as there is minimal chance of infection from
outside. Removal of the drain is easier and the patient is more comfortable.
Disadvantages
The drawback is that holes may be blocked by blood clots, debris or
surrounding tissues.
Surgical loupes (Fig. 11.137)
Surgical loupes are optical magnification system used widely in surgical
procedures requiring fineness.
• Loupes are two monocular microscopes with side-by-side lenses

converging to focus on the operative field.
• Magnified image is formed by the convergent lenses of the convergent
lens system (Keplerian optical system).
• These loupes may be simple, compound or prism type.
• Most maxillofacial, dental and periodontal procedures can be done
with more preciseness with either compound or prism loupes of ×4 to
×5 magnification.
FIGURE 11.137 Surgical loupe.
Advantages
1. Increased surgical quality

2. Less tissue trauma—a traumatic tissue management
3. Accurate wound closure
4. Coaxial lighting with the loupes efficiently reduces the surgeon’s eye
strain, increases visualisation and surgeon comfort
5. Improved documentation (video recording).
Disadvantages
1. Increased surgical time

2. Need for practice learning curve
3. Long adjustment period for clinical efficiency
4. High cost
5. Limited depth of field and field access
6. Fixed focal length limits mobility of the operator or surgeon
7. Field of vision is limited restricting visualisation to a narrow surgical
field.
Operating microscope (Fig. 11.138)

The surgical operating microscope is more versatile and advantageous than
magnifying loupes. The microscope offers multiple flexibilities, magnification
optics and comfort. Surgical operating microscopes are used mainly during
microsurgeries. A compact optical unit delivers clear and sharply focused
images. The magnification typically ranges from 4× to 40×.
FIGURE 11.138 Surgical operating microscope.
Advantages
• Photographs of the surgical procedures can be taken without

disturbing the surgeon’s surgical field.
• Excellent video documentation is also available through the operating
microscope using a video beam splitter attachment.
• The video of surgical procedures can be documented for the
educational and documentation purpose.
They provide high resolution and good contrast stereoscopic vision. A

surgical microscope must have manoeuvre ability, stability and an adequate
working distance for instrumentation.
Diathermy (electrocautery)
Surgical Diathermy is electrically induced generation of local heat in body
tissues by high-frequency electromagnetic currents been used in medical,
dental surgeries for decades.
Types
Based on type of current used:
• Unipolar cautery
• Bipolar cautery
Unipolar cautery Bipolar cautery

Causes tissue cutting and coagulation Cause tissue coagulation
only
Conduction pale should be used on the patient Conduction plate is not
required
Adjacent tissues get damaged easily No damage happens to
the adjacent tissues
Should not be used in patients with Artificial valves and used Can be used
cautiously in presence of other vascular prosthesis
Based on type of action:
• Coagulation cautery: causes haemostasis by tissue coagulation. 100º

• Cutting cautery: causes disintegration of the subjected tissue. 1000º
• Blended cautery: combination of coagulation and cutting
Uses
• To achieve haemostasis by thermal or electrical methods

• To cut through the tissues in a avascular surgical field
• To reduce blood loss in procedures where blood loss is caused due to
surgical dissection.
• Used to remove small cutaneous lesions
CHAPTER 12
Sterilisation and
Disinfection
Physical agents
Sunlight
Drying
Heat
• Flaming
• Incineration
• Hot air oven
Moist heat
• Boiling
• Pasteurisation of milk
• Steam under pressure/ autoclaving
Tests for efficiency for heat sterilisation
Filtration
Radiation
• Nonionising radiation
• Ionising radiation
Ultrasonic and sonic vibration
Glass beads steriliser
Chemical agents
Disinfectants
Alcohols
Aldehydes
• Formaldehyde
• Glutaraldehyde
Biguanides
Halogens
Gas
• Formaldehyde gas
• Beta propiolactone (BPL)
Testing of disinfectants
Operator’s preparation
Infection control
Aseptic precautions in the operating room
High speed evacuation
Handling and disposal of sharp instruments
Barrier technique
Sterilisation in dentistry
Sterilisation of dental equipment
Prevention of biofilms
Sterilisation procedures
Protective measures
• Needle stick injury
• Disposal of waste
The first step in asepsis is cleanliness, a concept already adopted by

Hippocrates. Modern concept of asepsis evolved in the 19th century. Ignaz
Semmelweis showed that washing the hands prior to delivery reduced
puerperal fever. After the suggestion by Louis Pasteur, Lister introduced the
use of carbolic acid as antiseptic and reduced surgical infection rates. Trend
went from antiseptics to asepsis, introducing principles and practices that have
remained valid unto this day. Von Bremann introduced the autoclave, a device
used for sterilisation of surgical instruments.
Asepsis
Asepsis is the practice to reduce or eliminate contaminants (such as bacteria,
viruses, fungi and parasites) from entering the operating field in surgery to
prevent infection. Ideally, a sterile field means free of contaminants, which is
difficult to attain. However, the goal is elimination of infection, not sterility.
Antiseptic
A chemical that is applied to living tissues such as skin or mucous membrane
to prevent infection by inhibiting the growth of bacteria.
Disinfectant
A chemical used on nonvital objects to kill surface vegetative pathogenic
organisms, but not spores or viruses.
Disinfection
The destruction or removal of all pathogenic organisms or organisms capable
of giving rise to infection.
Sterilisation
A process by which an article, surface or medium is free of all microorganisms
either in the vegetative or spore state.
Cleaning of instruments is a very important critical preparatory step for
effective sterilisation.
Without adequate cleaning, many disinfection and sterilisation processes are
ineffective. Cleaning is critical in removal of gross debris, prevention of cross-
contamination and protection of the health care worker (HCW) in the
processing area. Cleaning is considered to be the removal of visible dirt, soil,
organic matter or other foreign material from an instrument or object.
Cleaning generally means the removal of, rather than the killing of,
microorganisms.
Soaps and detergents are used for cleaning purposes. They reduce the
surface tension along the instrument surface allowing emulsification of the
contaminants which are then removed by rinsing. Other solvents like acetone,
ether and xylene are used for cleaning.
• Choose a detergent compatible with the type of the surgical

instrument.
• Hand cleaning of dental instruments should be carried out using warm
water and detergent using puncture resistant latex gloves.
• Dried fat or protein sediments and debris over the instrument surface
may require an enzyme detergent soak.
• Cleaning of instruments can also be done using ultrasonic bath. The
liquid in the ultrasonic bath should be changed at least twice each day
as often it becomes heavily contaminated. At the end of each day, the
ultrasonic bath should be emptied, cleaned and dried.
• After ultrasonic cleaning, the instruments should be thoroughly rinsed
with water to remove the cleaning solution and examined for any
residual debris; if any is found, it should be removed manually.
• Cavitation is a process in which microscopic bubbles rapidly form and
then collapse on the instrument surfaces creating suction that removes
the debris. Ultrasonic cleaning is achieved by cavitation. To minimise
organic build-up or reduce bioburden on the instruments, best
practices in the preoperative setting would include keeping the
instruments as free as possible of blood and organic debris during the
surgical procedure.
• Lumens of suction or cannulae should be flushed with water to remove
blood/fluids, which may dry and adhere to the surface.
• A nonfibrous sponge should be used to wipe off microsurgical and
other delicate tips.
• Once the procedure has ended, hinged instruments should be opened
and placed in a splash basin of sterile water to soak.
• Sharp, cutting, delicate or power instruments are managed separately
to avoid damage to the surgical tools.
• Instruments that are too large to be contained in a basin may be
covered with a towel soaked in water to keep the organic debris and
blood from drying on the instrument surface.
Removal of debris from instruments in the field
• Reduce the number of microorganisms on the device.

• Reduce the nutrient material that might support pathogenic growth.
• Minimise the risk of environmental exposure from aerosolisation or
spillage.
• Decrease the possibility of device damage from organic debris: blood,
saline, iodine or radiologic dyes.
• Decreases the need to vigorously clean a device to remove encrusted
debris.
Sterilisation is a process by which an object, surface or medium is freed of all
microorganisms either in the vegetative or spore state.
The agents used in sterilisation are classified as:
Physical agents
• Sunlight
• Drying
• Dry heat: flaming, incineration, hot air
• Moist heat: pasteurisation, boiling, steam under normal pressure, steam
under pressure
• Filtration: candles, asbestos pads, membranes
• Radiation
• Ultrasonic and sonic vibration
• Glass beads steriliser
Chemical agents
• Alcohols: ethyl, isopropyl, trichlorobutanol

• Aldehydes: formaldehyde, glutaraldehyde
• Dyes
• Halogens
• Phenols
• Surface-active agents
• Metallic salts
• Gases: ethylene oxide, formaldehyde, beta-propiolactone
Physical agents
Sunlight
Sunlight possesses appreciable bactericidal activity and plays an important
role in the spontaneous sterilisation that occurs under natural conditions. The
action is primarily due to its content of ultraviolet rays.
Drying
Moisture is an essential prerequisite for bacterial growth. Drying creates an
environment unsuitable for bacterial growth. But this method is unreliable and
has no effect on spores.
Heat
The lethal effect of heat on microorganisms has long been known. Heat is fast,
reliable and relatively inexpensive. Above maximum growth temperatures,
biochemical changes in the cell’s organic molecules result in its death. These
changes arise from alterations in enzyme molecules or chemical breakdowns
of structural molecules, especially in cell membranes. Heat also evaporates
water and since all organisms depend on water, this loss may be fatal.
Types of heat
Two types of heat are: (1) dry heat and (2) moist heat.
Dry heat
The lethal effect of dry heat is due to protein denaturation and coagulation,
oxidative damage and the toxic effect of elevated levels of electrolytes.
Instruments with a sharp cutting edge, such as chisels are preferably
sterilised by exposure to dry heat at 160°C for 1 h since autoclaving might
reduce their sharpness and promote rusting.
Application of dry heat
Flaming (Fig. 12.1A−B)

The flame of the Bunsen burner is employed for a few seconds to sterilise the
bacteriological loop before removing a sample from a culture tube and after
preparing a smear. Flaming the tip of the tube also destroys organisms that
happen to contact the tip, while burning away lint and dust. Scalpels and
needles could be passed a few times through the Bunsen flame without
allowing them to become red hot.
FIGURE 12.1 (A−B) Sterilisation by dry heat method: flaming.
Incineration
Incineration is an excellent method for rapidly destroying materials such as
soiled dressings, animal carcasses, bedding and pathological material.
Disposable hospital gowns and certain plastics are examples of materials that
may be incinerated. Incineration is a high-temperature dry oxidation process
that reduces organic and combustible waste to inorganic, incombustible matter
and results in a significant reduction of waste volume and weight. This
process is usually selected to treat wastes that cannot be recycled, reused or
disposed off in a landfill site.
The combustion of organic compounds produces mainly gaseous emissions,
including steam, carbon dioxide, nitrogen oxide, certain toxic substances (e.g.
metals, halogenic acids) and particulate matter, plus solid residues in the form
of ashes.
Hot air oven (Fig. 12.2A−B)

The hot air oven utilises radiating dry heat for sterilisation. This type of energy
does not penetrate materials easily and therefore, long periods of exposure to
high temperatures are necessary. For example, at a temperature of 160°C
(320°F), a period of 2 h is required for the destruction of bacterial spores.
Higher temperatures are not recommended because the wrapping used for
equipment tends to char at 180°C. The hot air method is useful for sterilising
dry powders and water-free oily substances, as well as for many types of
glassware, such as pipettes, flasks, forceps, scissors, scalpels and glass
syringes. Dry heat neither corrodes sharp instruments as steam often does, nor
does it erode the ground glass surfaces of nondisposable syringes.
FIGURE 12.2 (A−B) Hot air oven.
Placing instruments inside the hot air oven

The material should be arranged so as to allow free circulation of air in
between the objects. Glassware should be perfectly dry before being placed in
the oven. Cutting instruments should ideally be sterilised for 2 h at 150°C. The
oven must be allowed to cool slowly for about 2 h before the door is opened,
since the glassware may crack due to sudden or uneven cooling.
Effect on microorganisms
The effect of dry heat on microorganisms is equivalent to that of baking. The
heat changes microbial proteins by oxidation reactions and creates an arid
internal environment, thereby burning microorganisms slowly. It is essential
that organic matter such as oil or grease films be removed from the materials,
because organic matter insulates against dry heat. Moreover, the time required
for heat to reach sterilising temperatures varies according to the materials.
This factor must be considered in determining the total exposure time.
Moist heat
Moist heat kills microorganisms by denaturing their proteins. Denaturation is
a change in the chemical or physical property of a protein. It includes
structural alterations due to destruction of the chemical bonds holding
proteins in a three-dimensional form. As proteins revert to a two-dimensional
structure, they coagulate (denature) and become nonfunctional. The
coagulation of proteins requires less energy than oxidation and, therefore, less
heat needs to be applied. Moist heat can penetrate better than dry heat, hence
kills the microorganisms rapidly at a lower temperature than dry heat.
Application of moist heat
Boiling
Immersion in boiling water is the first of several moist heat methods that shall
be considered. Moist heat penetrates materials much more rapidly than dry
heat because water molecules conduct heat better than air. Lower
temperatures and a shorter exposure time are therefore required than for dry
heat.
Boiling water is not considered a sterilising agent because the destruction of
bacterial spores and the inactivation of viruses cannot always be assured. If it
is imperative that boiling water be used for sterilisation, the instruments must
be thoroughly cleaned to remove traces of organic matter, such as blood or
faeces. The minimum exposure period should be 30 min, except at high
altitudes, where it should be increased to compensate for the lower boiling
point of water. Washing soda may be added at a 2% concentration to increase
the efficiency of the process.
Vegetative bacteria are killed at 90 to 100°C but sporing bacteria require
prolonged periods of boiling. Cutting instruments become dull by repeated
boiling. In addition to instruments, rubber gloves, catheters and syringes may
be boiled.
Pasteurisation of milk
Pasteurisation is not the same as sterilisation. Its purpose is to reduce the
bacterial population of a liquid such as milk and to destroy organisms that
may cause spoilage and human disease. Spores are not affected by
pasteurisation.
One method for milk pasteurisation, called the holding method, involves
heating at 62.9°C for 30 min. Although thermophilic bacteria thrive at this
temperature, they are of little consequence because they cannot grow at body
temperature. For decades, pasteurisation has been aimed at destroying
Mycobacterium tuberculosis, long considered the most heat-resistant bacterium.
More recently, however, attention has shifted to destruction of Coxiella burnetii,
the agent of Q fever, because this organism has a higher resistance to heat.
Since both organisms are eliminated by pasteurisation, dairy microbiologists
assume that other pathogenic bacteria are also destroyed.
Two other methods of pasteurisation are the flash pasteurisation method at
71.6°C for 15 s and the ultra-pasteurisation method at 82°C for 3 s followed by
cooling quickly to 13°C or lower. These processes destroy all non-sporing
pathogens, such as mycobacteria, brucellae and salmonellae.
Steam under pressure/autoclaving

Moist heat in the form of pressurised steam is regarded as the most
dependable method for the destruction of all microbes, including bacterial
spores. This principle is incorporated into a device called the autoclave.
Mechanism of action (Fig. 12.3)

A basic principle of chemistry is that when the pressure of a gas increases, its
temperature increases proportionally. Because steam is a gas, increasing its
pressure in a closed system increases its temperature. As the water molecules
in steam become more energised, their penetration increases substantially.
Sterilisation by steam under pressure is best carried at temperatures between
108 and 147°C. A variety of materials like dressings, instruments, culture,
media and pharmaceutical products can be sterilised by steam under pressure.
The appropriate temperature for sterilising aqueous solutions is between 108
and 126°C.
FIGURE 12.3 Autoclave: mechanism of action.
Types of steam sterilisers (Fig. 12.4A–D):
1. Laboratory autoclaves
2. Hospital dressing sterilisers
3. Bowl and instrument sterilisers
4. Rapid cooling sterilisers
FIGURE 12.4 (A) Vertical autoclave. (B−C) Horizontal autoclave.
(D) Digital monitor in automated autoclave.
Even the domestic pressure cooker can be used as a steriliser.

In its simplest form, the laboratory autoclave consists of a vertical or
horizontal cylinder of gun metal or stainless steel, in a supporting sheet iron
case. The lid or door is fastened by screw clamps and made airtight by an
asbestos washer. The autoclave has on its lid or upper side a discharge tap for
air and steam, a pressure gauge and a safety valve that can be set to blow off at
any desired pressure. Heating is by gas or electricity.
• Sufficient water is put in the cylinder, the material to be sterilised is

placed on the tray and the autoclave is heated.
• The lid is screwed tight with the discharge tap open.
• The safety valve is adjusted to the required pressure.
• The steam-air mixture is allowed to escape freely till all the air has
been displaced. This can be tested by leading the escaping steam into a
bucket of water through rubber tubing.
• When no more air-bubbles come out in the bucket the discharge tap is
closed.
• The steam pressure rises inside and when it reaches the desired set
level, the safety valves open and the excess steam escapes.
• From this point, the holding period is calculated. When the holding
period is over, the heater is turned off and the autoclave is allowed to
cool till the pressure gauge indicates that the pressure inside is equal
to the atmospheric pressure.
• The discharge tap is opened slowly and air is let into the autoclave.
• If the tap is opened when the pressure inside is high, liquid media will
tend to boil violently and spill from their containers and sometimes an
explosion may occur.
• If opened after the pressure inside has fallen below atmospheric
pressure, an excessive amount of water would have evaporated and
lost from the media.
• Most autoclaves contain a sterilising chamber into which articles are
placed and a steam jacket where steam is maintained.
• Instruments and materials for sterilising in the autoclave are usually
enclosed in muslin wrappers as surgical packs. These packages must
be porous to allow steam to penetrate and reach the instruments
(Fig. 12.5A−B).
• Packing of instruments is done in double thickness and each surgical
pack is marked as to the contents and date of sterilisation.
• As steam flows from the steam jacket into the sterilising chamber, cool
air is forced out and a special valve increases the pressure to
15 pounds/square inch (lb/in2) above normal atmospheric pressure.
• The temperature rises to 121.5°C and the superheated water molecules
rapidly conduct heat into the microorganisms. The time for
destruction of the most resistant bacteria spore is now reduced to
about 15 min.
• For denser objects, up to 30 min of exposure may be required.
• A detachable handle is then fitted to the sterilising tray so that the
instrument can be carried to the operative site without danger of
dropping or contamination.
• The autoclave is used to control microorganisms in both hospitals and
laboratories. It is employed for blankets, bedding, instruments,
intravenous solutions and a wide variety of other objects.
• Autoclave can also be used to sterilise bacteriological media and
destroy pathogenic cultures.
• The glassware and metal sterilised instruments should remain
wrapped until next used not more than 2−3 days.
FIGURE 12.5 (A) Biohazard bags used for autoclaves. (B)
Instruments in surgical pack after autoclave.
To gauge the success of sterilisation, a strip containing spores of a (Bacillus

stearothermophilus) is included with the objects treated. At the conclusion of the
cycle, the strip is placed in nutrient broth medium and incubated. If the
sterilisation process has been successful, no growth will occur, but growth
indicates failure.
In recent years a new form of autoclave, called the prevacuum autoclave has
been developed for sterilisation procedures. This machine draws air out of the
sterilising chamber at the beginning of the cycle. Saturated steam is then used
at a temperature of 132−134°C at a pressure of 28 to 30 lb/in2. The time for
sterilisation is now reduced to as little as 4 min. A vacuum pump operates at
the end of the cycle to remove the steam and dry the load. The major
advantages of the prevacuum autoclave are the minimal exposure time for
sterilisation and the reduced time to complete the cycle (Table 12.1).
Table 12.1
Comparison of various methods of sterilisation
I Autoclaving
Advantages 1. Economical
2. Good penetration
3. Short cycle time
4. Easily monitored
5. No special chemicals or exhaust required
Disadvantages 1. Carbon steel gets damaged
2. Moisture retention
II Hot air oven
Advantages 1. Economical
2. Does not rust metals
3. Easily monitored
4. Used for anhydrous oils and powders
Disadvantages 1. Difficult to control temperature
2. Slow penetration
3. Photos, textiles, rubber or metal solder
joints cannot be used
III Chemiclaving
Advantages 1. Short time cycles
2. Limits rust on high carbon steel
3. Easily monitored
Disadvantages 1. Instruments must be dry
2. Damages textiles and liquids
3. Costly
4. Unpleasant odour
5. Good ventilation required
Tests for efficiency for heat sterilisation
Thermocouple
Thermocouple is a thermometric testing and a reliable gauge of efficiency. One
recording is taken from a thermocouple placed inside a test pack of towels and
a second one from the chamber drain. Comparison between the two
recordings gives a good guide regarding the speed at which the steam
penetrates the load.
Brown’s test
These are ampoules that contain a chemical indicator which changes its colour
from red through amber to green at a specific temperature.
Autoclave tape (Fig. 12.6A−B)

This is a tape printed with sensitive ink that undergoes a colour change at a
specific temperature. This test forms the basis of the Bowie−Dick test for high
vacuum autoclaves. Two pieces of strips are struck onto a piece of square
paper and placed in the middle of the test pack. With the application of
temperature of 134°C for 3.5 min, there is a uniform development of bars
throughout the length of the strips. This shows that the steam has passed
freely and rapidly to the centre of the load.
FIGURE 12.6 (A) Autoclave tape. (B) Autoclave tape—before and

after sterilisation. Note the colour change.
Filtration
The filter is a mechanical device for removing microorganisms from a solution.
As fluid passes through the filter, organisms are trapped in the pores of the
filtering material. The solution that drips into the receiving container is
decontaminated or, in some cases, sterilised. Filters are used to purify
beverages, intravenous solutions, bacteriological media, toxoids and many
pharmaceuticals.
Several types of filters are available for use in the microbiology laboratory:
Inorganic filters
are typified by the Seitz filter, which consists of a pad of porcelain or ground
glass mounted in a filter flask.
Organic filters
are advantageous because the organic molecules of the filter attract organic
components in microorganisms. One example, the Berkefeld filter, utilises a
substance called diatomaceous earth.
Membrane filter
is a third type of filter that has received broad acceptance. It consists of a pad
of organic compounds such as cellulose acetate or polycarbonate, mounted in
a holding device.
Air can also be filtered to remove microorganisms. The filter generally used
is a high-efficiency particu-late air (HEPA) filter. This apparatus can remove
over 99% of all particles, including microorganisms with a diameter larger
than 0.3 µm. The air entering surgical units and specialised treatment facilities,
such as burn units, are filtered to exclude microorganisms. In some hospital
wards, as pulmonary wards and in certain pharmaceutical filling rooms, the
air is recirculated through HEPA filters to ensure its purity.
Radiation
Two types of radiation are used for sterilising purposes: (1) nonionising and
(2) ionising.
Infrared and ultraviolet rays are of the nonionising low energy type while γ
rays and high-energy electrons are of the high energy ionising type.
Nonionising radiation
In nonionising radiation, electromagnetic rays with wavelengths longer than
those of visible light are used and these are to a large extent absorbed as heat.
Infrared radiation
can be considered as a form of hot air sterilisation. Infrared radiation is used
for rapid mass sterilisation of syringes. It can also be used to purify air.
Ultraviolet radiation
is used for disinfecting enclosed areas such as entryways, hospital wards,
operation rooms and virus research laboratories. When microorganisms are
subjected to UV light, cellular DNA absorbs the energy and undergoes
molecular changes. This affects the synthesis of proteins through mRNA
essential for survival. Moreover, replication of the chromosome by binary
fission is impaired. Ultraviolet light effectively reduces the microbial
population where direct exposure takes place. It is used to limit air borne or
surface contamination in a hospital room, morgue, pharmacy, toilet facility or
food service operation. It is noteworthy that ultraviolet light from the sun may
be an important factor in controlling micro organisms in the air and upper
layers of the soil, but it may not be effective against all bacterial spores.
Ionising radiation
The spectrum of energies includes two forms of radiation useful for destroying
microorganisms. These are: (1) X-ray and (2) γ-rays.
Both have wavelengths shorter than the wavelength of ultraviolet light. X-
rays, γ-rays and cosmic rays are highly lethal to DNA and other vital cell
constituents. They have very high penetrative power. As X-rays and γ-rays
pass through microbial molecules, they force electrons out of their shells,
thereby creating ions. For this reason, radiations are called ionising radiations.
The ions quickly combine with and destroy proteins and nucleic acids such as
DNA, causing death. Gram-positive bacteria are more sensitive to ionising
radiations than Gram-negative bacteria. Ionising radiations are currently used
to sterilise heat-sensitive pharmaceuticals as vitamins, hormones and
antibiotics, as well as certain plastics and suture materials. Large commercial
plants use gamma radiation for sterilising swabs, culture plates, catheters and
various types of rubber, cardboard, oils, greases, fabrics and metal foils.
Ultrasonic and sonic vibration (Fig. 12.7A−B)

Ultrasonic and sonic waves are credited with bactericidal powers but the
results are variable. Microorganisms vary in their sensitivity to them and
survivors are found after such treatment. Hence, this method is of no practical
value in sterilisation and disinfection.
FIGURE 12.7 (A) Digital ultrasonic cleaner. (B) Ultrasonic cleaning

of Implant drills.
Glass beads steriliser

This method employs a heat transfer device. The media used are glass beads,
molten metal and salt. The temperature achieved is 425–475°F or 218–246°C.
The method employs submersion of small instruments, such as endodontic
files and burs, into the beads; they are sterilised in 10 s provided they are
clean.
Chemical agents
Disinfectants
The physical agents for controlling microorganisms are generally intended to
achieve sterilisation, the destruction of all forms of life, especially bacterial
spores. Chemical agents, by contrast, rarely achieve sterilisation. Instead, they
are only expected to destroy the pathogenic organisms in an object. The
process of destroying pathogens is called disinfection; the object is said to be
disinfected. If the object is lifeless, such as a tabletop, the chemical agent is
known as a disinfectant. However, if the object is living, such as a tissue of the
human body, the chemical is called an antiseptic.
Antiseptics and disinfectants are usually bactericidal, but occasionally they
may be bacteriostatic. A bactericidal agent kills microorganisms, while a
bacteriostatic agent temporarily prevents their further multiplication without
necessarily killing them.
None of the chemicals used for cold sterilisation satisfactorily meets all of
the requirements for true sterilisation. Alcohol is expensive; it evaporates
readily and also rusts instruments. The widely used ben-zalkonium chloride
1:1,000 solution requires an anti rust additive (sodium nitrate) and long
periods of immersion (18 h). The more recently introduced cold sterilising
chemicals employ hexachlorophene compounds as the active base. These
chemicals claim adequate sterilisation of heat-sensitive instruments in 3 h.
Fundamentally, most of the cold sterilising media that may be safely used
probably kill vegetative bacteria, but there is doubt of their effectiveness
against spores and fungus.
Alcohols
Alcohols are effective skin antiseptics and valuable disinfectants for medical
instruments. For practical use, the preferred alcohol is ethyl alcohol. Ethyl
alcohol is active against vegetative bacterial cells, including the tubercle
bacillus, but it has no effect on spores. It denatures proteins and dissolves
lipids, an action that may lead to cell membrane disintegration. Ethyl alcohol
also is a strong dehydrating agent.
Because ethyl alcohol reacts readily with any organic matter, medical
instruments and thermometers must be thoroughly cleaned before exposure.
Usually, a 50% to 80% alcohol solution is recommended because water
prevents rapid evaporation and assists penetration into the tissues. A 10-min
immersion in 70% ethyl alcohol is generally sufficient to disinfect a
thermometer or delicate instrument. Ethyl alcohol is used in many popular
hand sanitisers.
Alcohol is the commonest skin antiseptic used before a venipuncture or
injection. It mechanically removes bacteria from the skin and dissolves lipids.
Isopropyl alcohol or rubbing alcohol, has high bactericidal activity in
concentrations as high as 99%. Methyl alcohol is toxic to the tissues and is
never used as antiseptic, though may be used as disinfectants for cabinets and
incubators.
Aldehydes
Formaldehyde (Fig. 12.8A–C)

Formaldehyde is a gas at high temperatures and a solid at room temperatures.
When 37 g of the solid are suspended in 100 mL of water, a solution called
formalin results.
FIGURE 12.8 (A) Fumigators—formaldehyde for sterilising

operating theatres and closed chambers. (B−C) Formalin chamber.
In the gaseous form, formaldehyde is expelled into a closed chamber where

it is a sterilising agent for surgical equipment, hospital gowns and medical
instruments. However, penetration is poor and the surface must be exposed to
the gas for up to 12 h for effective sterilisation. Instruments can be sterilised by
placing them in a 20% solution of formaldehyde in 70% alcohol for 18 h.
Formaldehyde, however, leaves a residue and instruments must be rinsed
before use. It is used to preserve anatomical specimens and for destroying
anthrax spores in hair and wool. Ten percent formalin containing half percent
sodium tetraborate is used to sterilise clean metal instruments. Under properly
controlled conditions, clothing, bedding, furniture and books can be
satisfactorily disinfected.
Formaldehyde (HCHO) is active against the amino group in the protein
molecule. In aqueous solutions, it is markedly bactericidal and sporicidal and
also has a lethal effect on viruses.
The gas is irritant and toxic when inhaled. Surfaces, which have been
disinfected by this agent, may give an irritant vapour for some time after
disinfection and this can be nullified by exposure to ammonia vapour when
disinfection has been completed. Formaldehyde has been widely used for
fumigating operating theatres. It is also available in tablet form.
Glutaraldehyde (Fig. 12.9A−B)

Glutaraldehyde is one of the most effective chemical liquids for sterilisation
purposes that can destroy vegetative cells within 10−30 min and spores in 10 h.
Glutaraldehyde is an alkylating agent, usually employed as a 2% solution. To
use it for sterilisation purposes, materials have to be precleaned, immersed for
10 h, rinsed thoroughly with sterile water, dried in a special cabinet with
sterile air and stored in a sterile container to ensure that the material remains
sterile. If any of these parameters is altered, the materials may be disinfected
but may not be considered sterile. It is especially effective against tubercle
bacilli, fungi and viruses. It can be safely used to treat corrugated rubber,
anaesthetic tubes, plastic endotracheal tubes, metal instruments and polythene
tubing.
FIGURE 12.9 (A−B) Glutraldehyde 2% solution.

Biguanides
Chlorhexidine is active against a number of bacteria. It can be prepared in
alcohol or with cetrimide 0.5% + 70% of alcohol or chlorhexidine with
cetrimide or 4% solution with detergent can be used as preoperative scrub.
Halogens
The halogens are a group of highly reactive elements. Two halogens, chlorine
and iodine, are commonly used for disinfection.
Chlorine is available in a gaseous form and as both organic and inorganic
compounds. It is widely used in municipal water supplies, where it keeps
bacterial populations at low levels.
The chloramines, such as chloramines-T, are organic compounds that
contain chlorine. They are valuable for general wound antisepsis and root
canal therapy.
Chlorine is effective against a broad variety of organisms, including most
Gram-positive, Gram-negative bacteria and many viruses, fungi and protozoa.
However, it is not sporicidal. The halogen is believed to cause the release of
atomic oxygen, which then combines with and inactivates certain cytoplasmic
proteins, such as enzymes. Another theory is that chlorine changes the
structure of cell membranes, thus leading to leakage.
Iodine atom is slightly larger than the chlorine atom, is more reactive and
more germicidal. Iodine acts by halogenating tyrosine portions of protein
molecules.
Tincture of iodine, a commonly used antiseptic for wounds, consists of 2%
iodine and sodium iodide dissolved in ethyl alcohol.
Gas
Formaldehyde gas
Formaldehyde gas is widely used in operation theatres and other rooms. After
sealing the windows and other outlets, formaldehyde gas is generated by
adding 150 g of KMnO4 to 280 mL formalin for every 1000 cu ft (28.3 cu m) of
room volume. The reaction produces considerable heat; therefore, heat
resistant vessels should be used. After starting generation of formaldehyde
vapour, the doors should be sealed and left unopened for 48 h.
Beta propiolactone (BPL)

Beta propiolactone is a condensation product of ketane and formaldehyde
with a boiling point of 163°C. It is said to be more efficient for fumigating
purposes than formaldehyde. It has a rapid biocide action, but unfortunately
has carcinogenic activity.
Testing of disinfectants
In the Rideal−Walker test, suspensions containing equal numbers of typhoid
bacilli are submitted to the action of varying concentrations of phenol and of
the disinfectant to be tested. The dilution of the test disinfectant, that sterilises
the suspension in a given time, divided by the corresponding dilution of
phenol, is stated as the phenol coefficient (phenol = 1) of the disinfectant. This
test does not reflect natural conditions as the bacteria and the disinfectant react
directly without any organic matter being present. Modifications have
therefore been suggested. In the Chick−Martin test, the disinfectant acts in the
presence of organic matter. Even this modification falls short of simulating
natural conditions. Various other modifications have been introduced, but no
test is entirely satisfactory.

Attainment of complete asepsis in surgery may never be fully possible. The air
contamination of wounds is a ubiquitous problem.
• The ceiling, walls and floors should be disinfected on a regular basis

• Admission inside the operating room must be restricted to operating
personnels
• Contemporary operating rooms are built with conductive flooring
• Autoclavable sterile light handles disposable nasal cannulae, nasal
mask should be used to avoid cross-contamination
Operator’s preparation
1. Conductive footwear
Operating room personnel and visitors must wear conductive footwear.
2. Scrub suit
Street clothes are replaced with a scrub suit. The scrub suit comprises a pair of
clean linen trousers and a short-sleeved shirt.
3. Surgical head cap

A surgical cap is used to cover the hair completely. A head covering or cap
protects the hair and head against splashes from the patient’s vomit, blood or
other body fluids. Use disposable or cotton caps.
4. Eyewear
Protective clear eyeglasses or nonfogging goggles are used to protect the eyes
from splashes or spills of infectious body fluids.
5. Mask
A mask is used to cover the nose and mouth of the surgeon. It can be HEPA-
filter mask or surgical mask.
HEPA-filter or biosafety mask

A HEPA-filter mask filters the air to prevent breathing in small particles and
harmful microorganisms. It provides protection from air borne transmission of
microorganisms. A HEPA-filter or biosafety mask is light weight and easy to
use. It can be reused by the same health care worker as long as it continues to
fit comfortably and the mask does not become contaminated, crushed or
splattered with body fluids.
Surgical masks
will not filter out small particles, but they will protect the health care worker
from droplets or splashing of body fluids. A surgical mask consists of three
layers: (1) inner layer facing the wearer absorbs water, (2) middle layer is the
cotton filter and (3) outer layer is water resistant. Wearing surgical mask is a
way to prevent the spread of droplet and respiratory tract infections.
• The surgical mask should fit snugly over the face.

• The folds should face downward on the outside, with metallic strip
uppermost.
• Tie all the strings that keep the surgical mask in place or fix the rubber
bands of the surgical mask round the ears properly.
• The surgical mask should fully cover the nose, mouth as well as the
chin.
• The metallic wire part of the surgical mask should be moulded
securely to the bridge of the nose and along both sides of the face
beneath the eyes to prevent leakage.
• Once in position, one should not fiddle with the mask as this could
transfer any contamination from the hands to the face.
• Always wash hands before and after taking off the mask.
6. Hand scrub technique (Fig. 12.10A–D)

The surgeon’s hands should be appropriately scrubbed. The suitable
preparations for hand scrub are 4% chlorhexidine gluconate and 7.5%
povidone iodine (Betadine). Presently, highly detergent soaps containing
hexachlorophene are commonly utilised in prescribed scrub techniques. Nails
should be cut short and all jewellery removed before washing and the nails
should be scrubbed first, thoroughly with a brush.
FIGURE 12.10 (A–D) Hand scrub technique.
The surgical scrubbing is done in the following manner. Brush, soap (or
hexachlorophene detergents) and water are used to scrub the hands and
forearms till the elbows. A 2-min scrub between operations is acceptable. The
fingernails must be adequately cleansed. Sterile orangewood sticks are
conveniently provided for this purpose. If non-detergent soap is used for the
scrub, a longer scrub period is required and a post-scrub rinse with a low-
surface tension antiseptic such as alcohol or hexachlorophene is
recommended.
After the scrub, hands are dried in the operating room with a sterile hand
towel. At this stage, the hands are considered surgically clean but not sterile.
7. Surgical gown (Fig. 12.11)

Surgical gowns are available in disposable forms and as surgical cotton gowns.
The surgeon’s back as well as the gown below the level of the waist are
considered unsterile.
FIGURE 12.11 Donning of surgical gown.
8. Gloves (Fig. 12.12)

Gloves are manufactured with natural rubber latex or synthetic rubber
materials, like vinyl, neoprene, nitrile, polyurethane or other synthetic
compounds. Surgical gloves are generally latex gloves only, though synthetic
ones are also available. Latex surgical gloves or sterile gloves are used to
prevent cross-infection during surgery. They are flexible, durable and allow
the required sensitivity during the procedures.
FIGURE 12.12 Gloving.
While selecting the type of examination glove, the material properties

should be taken into consideration. Vinyl gloves can be used for short
duration tasks where the stress on the gloves and exposure to body fluids is
less. On the contrary, latex gloves can be used when the exposure to the body
fluids is more.
Apart from their categorisation as natural latex or synthetic, they are further
classified as specific use or speciality gloves. The choice is based on personal
preference and procedure:
• Powdered surgical gloves

• Powder-free surgical gloves
• Synthetic surgical gloves.
These are available in different sizes, as:
• Small, medium, large or extra large.
• Number coded (e.g. 6, 6½ and 7)
Ideally a glove should be
• Soft
• Comfortable
• Elastic
• Sensitive
• Resistant to tearing or puncture
• Less allergenic potential
• Low levels of residual process chemicals
• Low levels of latex proteins
During the gloving technique only the interior of the glove should be
touched by hands because the exterior surface is considered as sterile. The
hand to glove and glove to glove technique of donning is used. Double
gloving provides extra protection but reduced sensitivity, dexterity and
possible discomfort.
Modified starch powder has replaced talcum as the dusting agent of choice.
However, sterile creams are being used for this purpose more than dusting
agents.
Infection control
Infection
The lodgement and multiplication of a parasite in or on the tissues of a host
constitutes infection.
Infectious disease
Infectious disease or communicable disease is a disease caused by a biological
agent such as by a virus, bacterium or parasite.
Primary infection
Initial infection with a parasite in a host is termed as primary infection.
Reinfection
Subsequent infections by the same parasite in the host are termed reinfection.
Secondary infection
When resistance of the host is lowered by a preexisting infectious disease and
a new parasite sets up an infection, this is termed secondary infection.
Focal infection (focal sepsis)

Due to infection or sepsis at a localised site such as appendix or tonsils,
generalised effects are produced.
Cross-infection
When a patient is already suffering from a disease, a new infection is set up
from another host or another external source.
Nosocomial infection
Cross-infections occurring in hospitals.
Iatrogenic infections
These are physician induced infections resulting from investigative,
therapeutic or other procedures.
Endogenous infections
If the source of infection is from within the host’s body, then it is termed as
endogenous infection.
Exogenous infections
If the source of infection is from outside the host’s body, then it is termed as
exogenous infection.
Atypical infections
It is characterised by an absence of characteristic clinical manifestation of the
particular infectious disease.
Latent infection
Following infection some parasites may remain in the tissues in a latent or
hidden form, proliferating and producing clinical disease when the host
resistance is lowered.
Carrier
A person who harbours the pathogenic microorganisms without suffering any
ill-effects from it.
Healthy carriers
A healthy carrier is one who harbours a pathogen but has never suffered from
any disease due to the pathogen.
Convalescent carrier
A convalescent carrier is one who has recovered from the disease and
continues to harbour the pathogen in his/her body.
Contact carrier
These are persons who acquire the pathogen from the patients.
Paradoxical carrier
These are patients who acquire the pathogens from another carrier.
Vector
A living entity (animal, insect or plant) that transmits the aetiological agent.
Vehicle
A nonliving entity that is contaminated with an aetiologic agent and as such is
the mode of transmission for that agent.
Mode of transmission
Means by which aetiological agents are brought in contact with the human
host (e.g. infected blood, contaminated water, insect-bite).
Direct contact
Spread of infection through contaminated food or intravenous solutions.
Indirect contact
Spread of infection from a patient to patient through the hands of health care
workers (MRSA, rotavirus).
Droplet contact
Spread of infection by inhalation of droplets (>5 µm diameter) that cannot
travel more than 3 feet (pertussis).
Air-borne contact
Spread of infection by inhalation of droplets (≤5 µm in diameter) that can
travel large distances on air currents (tuberculosis).
Vector-borne contact
Diseases that spread by vector such as mosquitoes (malaria) or rats (rat bite
fever).
1. Aseptic precautions in the operating room (Fig. 12.13)
a. The operating room must have a negative bacterial culture, hence it

should be fumigated.
b. A strong disinfectant should be used to clean the floor.
c. Impervious packed paper, aluminium foil or clear plastic wraps may be
used to cover surfaces that can be contaminated by blood or saliva and
are difficult or impossible to disinfect. The coverings should be
removed, discarded and then replaced with clean material between
patients.
d. Light handles, switches, table tops, etc. are liable to accumulate
infective material. Surfaces should be cleaned and dried with a solution
of 70% isopropyl alcohol that helps in preventing infection. Blood, pus
stains should be removed and disposable clothes should be used.
e. Hypochlorite solution containing 1% chlorine or 2% glutaraldehyde is
used as disinfectant in cases of metallic surfaces. The solution left for
minimum of 3 min in drying will help to prevent spread of infection.
f. Clear plastic disposable sleeves may be used to cover tubes and hoses.
g. Good ventilation will help in maintaining clean atmosphere.
2. High Speed Evacuation

High speed evacuation tips not only take up excess saliva and water, but they
also remove excess droplets and aerosolised pathogens that spray from high
speed handpiece. They are available in disposable and autoclavable forms.
3. Handling and disposal of sharp instruments (Fig. 12.14,12.15)

Sharp instruments like scalpel blades should be handled carefully. Recapping
of a needle increase the risk of unintentional needle stick injury. Needles
should not be recapped and should be bent or broken before disposing. When
multiple injections are required, it is more prudent to place the unsheathed
needle into a sterile field between injections rather than recapping the needle.
Disposable syringes and needles, scalpel blades and other sharp items must be
placed into puncture-resistant containers located as close as practically
possible to the area in which they are used.
FIGURE 12.14 Sharps containers.
4. Barrier technique
Use of gloves
Gloves are used during both examination and treatment, wherein contact with
skin, mucosa or body fluid is encountered. Changing gloves between patients
or when they are torn or punctured is mandatory.
Gowns
The use of gowns, aprons or lab coats is required when splashes of the skin or
clothing with body fluids are likely to occur. They should be made of or lined
with fluid proof material and should protect all areas of exposed skin of the
operator and the patient.
Masks and head caps

The procedure of drying the teeth with air during an examination aerosolises a
higher concentration of bacteria than cough. There is a possibility of bacteria
loaded aerosols caused by air rotor and ultrasonography scalers colonising the
nasal flora. A well-fitting mask which has efficient filtering capacity not only
prevents aerosols from coming in contact with the operator’s face but also
protects the patient from the droplets falling from the mouth and nose of the
operator. But a mask that is worn for a prolonged period of time can act as a
nidus of potentially pathogenic bacteria rather than as a barrier to the
transmission of nasal, oral and skin organisms.
Protective eyewear
Human eyes are particularly susceptible to infection and injury because of
poor vascularity and decrease in immune capacities. Glasses or a face shield
should be worn while working on a patient to prevent trauma to the eye tissue
from flying droplets or aerosols containing infectious microbe-laden debris.
However, these can become a source of infection and cross-contamination if
used continuously for different patients without disinfection. Two per cent
glutaraldehyde is used as a disinfectant.
Face shields
Should be used when splattering of fluids is expected. (Fig. 12.15)
FIGURE 12.15 Face mask.
Sterilisation in dentistry
Dental instruments can be classified as:
1. Critical
2. Semicritical
3. Noncritical
Critical
instruments include items that are used for invasive procedures and come into
direct contact with soft tissue or bone. Sterilisation is the preferred choice for
all critical instruments. (e.g. forceps, surgical burs, chisels).
Semicritical
instruments include items that are not intended to penetrate but may come
into contact with oral tissues. If they cannot be sterilised, high level
disinfection is recommended.
Noncritical
instruments include those items which do not come into contact with oral and
body fluids. These items do not require sterilisation or high level disinfection,
e.g. JCs, cavity liners, restorative materials.
Sterilisation of dental equipment
1. Routine sterilisation of handpieces is essential. For those ultrasonic

scalers, handpieces and air syringes that cannot be sterilised, proper
scrubbing with detergent and water and drying followed by wiping
with a suitable chemical disinfectant which remains in contact with the
instruments for the specified period of time is essential. Then, rinse in
water to remove the chemical residue. Plastic disposable sleeves may
be used to cover tubes.
2. Check valves should be used in dental units to prevent water retraction
of potentially infective materials. Water cooled handpieces should be
run for 20–30 s between patients and for a few minutes at the start and
end of each day.
3. While performing surgery, sterile saline should be used as a
coolant/irrigant.
4. Use handpieces with a built-in suck back feature, which prevents any
residual water from going into the next patient’s mouth.
Some handpieces can be sterilised by dry heat. The handpieces should be

carefully cleaned and lubricated with special heat-resistant oils. Other
handpieces, which have sealed bearings or which have been pressure
lubricated with appropriate oils can be autoclaved. The instructions given by
respective manufacturers regarding the cleaning, lubrication and sterilisation
are of importance and should be followed.
Prevention of biofilms
Dental water lines provide an environment favourable for rapid proliferation
of biofilms. Planktonic organisms which are suspended in the bulk fluid
quickly colonise the chemically inert water lines. Motile bacteria are attracted
towards low molecular weight organic matter and settle on them. Organic
conditioning films quickly form on the water bearing surface and serve as
substrate for bacterial attachment. After contact with the substrate, the cells
express genes associated with adhesion and begin the formation of biofilm.
‘Biofilm is defined as a microbially derived sessile community characterised by

cells that are irreversibly attached to a substrate or to each other, are
embedded in matrix of extracellular polymeric substances that they have
produced and exhibit an altered phenotype with respect to growth rate and
gene transcription’.
Low flow rates, periods of stagnation and low shear stress associated with
laminar flow regimes characteristic of water in narrow bore tubing seems to
favour the formation of biofilm in dental water lines. A typical dental unit
water system is of 10 and 0.5 mm diameter tubing. The volume of fluid
contained in this tubing rarely exceeds 60 mL. For a fixed volume of a fluid,
the surface area in a cylinder (the water tubing) increases dramatically as the
diameter increases. Therefore, the surface available for the growth of dental
films in the unit is large compared with the surface area in a larger diameter
line such as a water main supply. Water used in dental treatment must,
therefore, run a lengthy gauntlet of biofilm colonised surfaces, collecting
detached clumps of biofilms and microbial by-products on its way to the
unsuspecting patient.
Frequently isolated waterline organisms and their potential for
pathogenicity in humans are depicted in Table 12.2.
Table 12.2
Waterline organisms and potential for pathogenicity in humans

Organism Potential pathogenicity
Pseudomonas aeruginosa Wound infection
Septicaemia
Pneumonia
Other Pseudomonas species and burkholderia Wound infection
Septicaemia
Pneumonia
Legionella pneumophila Pneumonia
Wound infection
Pontiac fever
Aquatic mycobacteria Wound infection
Pneumonia
Moraxella species Conjunctivitis
Endocarditis
Flavobacterium (Chryseobacterium) Endocarditis
Pathogenic amoebae Conjunctivitis
Gastroenteritis
Meningitis
Cladosporium (fungus) Granulomatous pneumonitis
Oral flora Transmission of periodontal pathogens
The Centres for Disease Control and Prevention in ‘Recommended Infection

Control Practices for Dentistry, 1993’ urged dentists to:
• Install and maintain antiretraction valves on the dental units.

• Flush units at the beginning of the day and between patients.
• Use of sterile solutions for procedures involving cutting of the bone.
• Use of good quality water that would contain fewer than 200 CFU/mL
of heterophobic, mesophilic water bacteria in unfiltered output.
Most investigators have attempted to improve water quality by flushing the

lines with fresh water and introducing antimicrobial chemical. A number of
commercially available agents or devices are now available that control or
eliminate biofilms in dental equipment.
Sterilisation procedures
Presoaking
Placing the instrument in a presoaking solution (phenolic compounds)
prevents drying of debris, helps to dissolve or soften organic debris and
sometimes helps in microbial killing.
Cleaning
It facilitates sterilisation. Cleaning can be done either by hand scrubbing or
with the use of ultrasonic devices.
Corrosion control and lubrication

Instruments must be dried prior to sterilisation to decrease chances of
corrosion. The nonstainless steel instruments should be coated with a rust
inhibitor.
Packaging
The instruments can be packed individually or in small groups and distributed
on sterile or disposable disinfected trays for use at chair side. For wrapping,
thin paper bags should be avoided as they will permit sharp and pointed
instruments like sickle scalers to protrude and may cause injury during
handling. See through polyfilm bags or pouches facilitate instrument
identification.
Sterilisation
Autoclaving is the most accepted method of sterilisation of surgical
instruments as it eliminates bacteria, viruses, fungi and spores. It works on the
principle of steam under pressure of 15 lb at 121°C for 20 min or 30 lb at 134°C
for 3 min. It has excellent penetration, facilitating exposure of all instrument
surfaces to the steam. It has a relatively short cycle time and can sterilise
water-based liquids. Dry heat ovens or the unsaturated chemical vapour
sterilisers are the other means of sterilisation. Ultraviolet light may kill
microorganisms that are directly exposed to the light; however, the light may
not reach all the surface of an instrument. A temperature of 160–170°C
maintained for 1 h is capable of sterilisation. This method is acceptable for
cloth goods and paper items.
Handling sterile instruments

Post sterilisation procedures involve drying, cooling, storage and distribution.
As far as possible the sterile packages or trays should not be handled, till
required for use, to reduce recontamination.
Storage
Sterile packs and trays should be kept in dry, low dust, low traffic areas away
from sinks and sewer of water pipes, at least a few inches above the floor.
Distribution
Sterilised packs containing functional sets or individual items can be placed on
sterile, disposable trays for use at chair side. The instruments which are
disinfected in a liquid germicide should be handled aseptically with sterile
tongs, kept on sterile trays and then covered. Placing unwrapped or wrapped
instruments in drawers for direct use at chair side is not recommended.
Protective measures
Vaccination against hepatitis B is highly effective, safe and stable for oral
surgeons and dental staff. These injections do not give lifelong immunity and
booster dose after 5 years is recommended.
a. Prevention of needle stick injuries

b. Disposal of waste
A. Needle stick injury

Needle stick injuries are wounds caused by needles that accidentally puncture
the skin. Needle stick injuries are a hazard for people who work with
hypodermic syringes and other needle equipment. These injuries can occur at
any time: during use, disassembling or disposal. Needle stick injuries transmit
infectious diseases, especially blood-borne viruses. In recent years, concern
about AIDS, hepatitis B and hepatitis C has prompted research to find out the
causes of these injuries and develop measures to prevent them. Despite
published guidelines and training programmes, needle stick injuries remain an
ongoing problem.
Accidental punctures by contaminated needles can inject hazardous fluids
into the body through the skin. There is potential for injection of hazardous
drugs, but injection of infectious fluids, especially blood, is by far the greatest
concern. Even small amounts of infectious fluid can spread certain diseases
effectively. Accidental injection of blood-borne viruses is the major hazard of
needle stick injuries, especially the viruses that cause AIDS (HIV), hepatitis B
and hepatitis C. The risk of infection after exposure to infected blood varies by
blood-borne pathogen. The risk of transmission after exposure to HIV-infected
blood is about 0.3%, whereas it is estimated to be around 100 times greater for
hepatitis B virus (30%), and as high as 10% for hepatitis C virus.
Nursing and laboratory staff usually experience 30% to 50% of all injuries
during clinical procedures.
Causes
Equipment design
Safer innovative devices using protected needle devices or needle-free systems
with self-sealing ports would alleviate many of these injuries. Syringes with
safety features reduce needle stick injuries.
Recapping
Recapping can account for 25% to 30% of all needle stick injuries. Often, it is
the single most common cause.
It is extremely dangerous to hold a needle in one hand and attempt to cover
it with a small cap held in the other hand. Injuries occur in three different
ways:
Improper disposal
Virtually all needle stick injuries are from needles that have either been lost in
the workplace or thrown into regular garbage. Janitors and garbage handlers
can also experience needle stick injuries or cuts from ‘sharps’ when handling
trash that contains needles or scalpels.
Prevention
Preventing needle stick injuries is the most effective way to protect workers
from the infectious diseases that needle stick accidents transmit. A
comprehensive needle stick injury prevention programme would include:
• Employee training
• Safe recapping procedures
• Effective disposal systems
• Improved equipment design
Employee training
To reduce needle stick injuries, an effective programme must include
employee training. Specifically, the training programmes should address:
• Risk of injury
• Potential hazards
• Recommended precautions for use and disposal of needles
• Procedures for reporting injuries
• The importance of hepatitis B vaccination where appropriate
Single-handed scooping
Recapping can be safe when people lay the cap on a flat surface and scoop it
onto the tip of a syringe held in one hand. They must keep the free hand away
from the sheath and well behind the exposed needle.
Disposal
Workers should place needles in wide mouth, puncture-proof containers.
Place disposal containers specifically where needles are used to make safe
disposal possible without recapping. Replace the containers before they are
completely filled. Make sure that they are sealed, collected and disposed off in
accordance with local regulations for biomedical waste.
Management of needle stick injury
• Stop all operative procedures

• Identify and examine the wound
• Immediately wash but do not scrub the injury
• Encourage bleeding
• Blood specimen of both the patient and the health care worker should
be taken for testing.
Management of needle stick injury with known infection
Hepatitis B
Source: HBsAg Negative

• No further action necessary
Source
HBsAg Positive or Unknown
Exposed person already received a full course of hepatitis B vaccine
• If hepatitis B antibody (anti-HBs) level is known to be > 100 IU/mL and

a booster dose has been given 5 years after the primary course, no
further action is needed (long-term immunity can be assumed). If it is
more than 2 year since the primary course was given, but the 5-year
dose has not been given, it should be given now.
• If the post primary vaccination course anti-HBs level is unknown
or < 100 IU/mL, take a 10 mL clotted blood sample for the level to be
measured.
▪ Level >100 IU/mL: No treatment
▪ Level < 100 IU/mL: Give vaccine booster.
Exposed person not vaccinated
• Start course of hepatitis B vaccine.

• Hepatitis B immunoglobulin (HBIG) will also be required. It is given
intramuscularly at a different site to the vaccine if the exposure is
considerable. Seek advice from medical microbiologists. HBIG should
be given as soon as possible after exposure and certainly within 48 h. It
is of no value if given later than one week after exposure.
Exposed person vaccinated but not completed full course
• Take 10 mL clotted blood and measure antibody level.

• Level >100 IU/mL: No further action necessary but vaccine course
should be completed at recommended intervals.
• Level < 100 IU/mL: Give further dose and complete vaccine course.
Seek advice from medical microbiologists regarding intervals. HBIG
will also be required if exposure is considerable.
Hepatitis C
There is no specific prophylaxis or vaccination available against hepatitis C.
There is, therefore, no immediate action that needs to be taken following
exposure to a possible hepatitis C source.
Exposed health care workers should be managed as follows:
Known hepatitis C infected source
• Obtain baseline serum for storage from health care worker

• Obtain clotted blood sample (serum) for hepatitis C virus RNA testing
at 6 and 12 weeks
• Obtain serum for HCV antibody (anti-HCV) at 12 and 24 weeks.
Source known to be uninfected with hepatitis C following testing at time

of incident

• Obtain follow-up serum if symptoms or signs of liver disease develop.
Hepatitis C status of source unknown

• A risk assessment should be performed of the likelihood that the
source is hepatitis C positive (assessed by clinician in charge of patient
or occupational health or consultant microbiologist)
High risk—Manage as known infected source

Low risk—Obtain serum for anti-HCV testing at 24 weeks.
Health care workers found to have acquired hepatitis C infection following

occupational exposure should be referred immediately for specialist
assessment. Early treatment of acute hepatitis C infection may prevent chronic
hepatitis C infection.
Human immunodeficiency virus (HIV)
• This procedure applies to all possible exposures, whether they involve

staff, patients or members of the public.
• If there is a risk of HIV exposure, individuals must be dealt with
urgently to obtain prophylaxis as soon as possible and preferably
within 1 h.
• If the source is in a high risk group or exposure is considerable, the
source patient should be tested for HIV antibody. This requires
informed consent to be given. These tests are not performed out of
hours for this indication. The decision whether or not to start
prophylactic treatment must not be based solely on the results of an
HIV antibody test and any prophylaxis should be given within an
hour of exposure.
• For any exposure incident when the source patient is known it is
recommended that hepatitis B, C and HIV tests are carried out as a
routine from that patient. For high risk sources or exposures, these
tests should be arranged as quickly as possible.
• A blood sample must be taken from the injured or exposed person and
sent to the microbiology laboratory to be stored. This will be used for
future testing if necessary.
• The risk of seroconversion following a single percutaneous exposure to
HIV is only 0.3%; and following mucous membrane and skin
exposure, 0.1% and < 0.1% respectively.
Three types of exposure pose a risk
• Percutaneous exposure, e.g. needle stick

• Exposure of broken skin
• Mucous membrane exposure
The risk of transmission is increased with
• Hollow bore needles

• Needles/sharps that are visibly blood stained
• Needles that have been in an artery or vein
• A high viral load in the source, e.g. patient with AIDS/terminally ill.
Postexposure prophylaxis (PEP)
• Postexposure prophylaxis should be considered whenever there has

been exposure to material known to be or strongly suspected to be,
infected with HIV.
• High risk body fluids are: blood, amniotic fluid, vaginal secretions,
semen, breast milk, CSF, peritoneal fluid, pericardial fluid, synovial
fluid, unfixed tissues and organs and saliva in association with dental
surgery.
• Postexposure prophylaxis should not be offered following contact
through any route with urine, vomitus, saliva and faeces unless they
are visibly blood stained.
The following should be recommended:
• Zidovudine 300 mg and lamivudine 150 mg BD

• Nelfinavir 1.25 g BD.
Management of needle stick injuries and accidents involving exposure to
blood and body fluids is depicted (Fig. 12.14).
FIGURE 12.13 Examples of universal symbols for blood and body

fluid protection: (A) wash hands, (B) wear gloves when likely to
touch body, mucous membranes or nonintact skin, (C) wear plastic
apron when clothing is likely to be soiled, (D) wear mask/eye
protection when likely to be splashed and (E) place intact
needle/syringe units and sharp in designated disposable container.
Refer to Chapter 6 Management of Medically Compromised.
B. Disposal of waste
Proper disposal of hospital waste is of paramount importance because of its
infectious and hazardous characteristics (Tables 12.3–12.4).
Table 12.3
Colour coding and type of container for disposal of biomedical
wastes
Notes: 1. Colour coding of waste categories with multiple treatment options as defined
in Schedule I, shall be selected depending on the treatment option chosen, which shall
be as specified in Schedule I. 2. Waste collection bags for waste types needing
incineration shall not be made of chlorinated plastics. 3. Category 3 if disinfected locally
need not be in containers/bags.
Table 12.4
Categories of biomedical waste in India

Option Waste category Treatment and disposal
Category Human anatomical waste Incinerationa/deep burial
No. 1 (Human tissues, organs, body parts)
Category Animal waste Incinerationa/deep burial
No. 2 (Animal tissues, organs, body parts carcasses,
bleeding parts, fluids, veterinary hospitals
colleges, discharge from hospital, animal
house)
Category Microbiology and biotechnology waste Local
No. 3 (Waste from laboratory cultures, stocks or autoclaving/microwaving/incinerationa
specimens of microorganisms, live or
attenuated vaccines, human and animal cell
culture used in research and infectious
agents from research and industrial
laboratories, waste from production of
biological, toxins, dishes and devices and
for transfer of cultures)
Category Waste sharps Disinfection (chemical
No. 4 (Needles, syringes, scalpels, blades, glass, etc. treatmentb/autoclaving/microwaving
that may cause puncture and cuts. This and mutilation shredding)
includes both used and unused sharps)
Category Discarded medicines and cytotoxic drugs Incinerationb destruction and drugs
No. 5 (Wastes comprising of outdated, disposal in secured landfills
contaminated and discarded medicines)
Category Solid waste Incinerationb autoclaving/microwaving
No. 6 (Items contaminated with blood and fluids
including cotton, dressings, soiled plaster
casts, lines, beddings, other material
contaminated with blood)
Category Solid waste Disinfection by chemical treatmentc
No. 7 (Wastes generated from disposable items autoclaving/microwaving and
other than the waste sharps such as tubings, mutilation/shreddingd
catheters, intravenous sets etc.)
Category Liquid waste Disinfection by chemical treatmentc
No. 8 (Waste generated from laboratory and and discharge into drains
washing, cleaning, house-keeping and
disinfecting activities)
Category Incineration ash Disposal in municipal landfill
No. 9 (Ash from incineration of any biomedical
waste)
Category Chemicals used in production of biological, Chemical treatmentc and discharge
No. 10 chemicals used in disinfection, as insecticides, into drains for liquids and secured
etc landfill for solids
a
Deep burial shall be an option available only in towns with population less than
5 lakhs and in rural areas.
b
There will be no chemical pretreatment before incineration. Chlorinated plastics shall
not be incinerated.
c
Chemical treatment using least 1% hypochlorine solution or any equipment chemical
reagent. It must be ensured that chemical treatment ensures disinfection.
d
Mutilation/Shredding must be such so as to prevent unauthorised reuse.
WHO classified waste in the following manners:
• General nonhazardous
• Sharps
• Chemical
• Infectious
Sharps
Objects such as needles, syringes, lancets (sharps) and other sharp objects used
for medical purposes should be placed in medical sharps container or a heavy
plastic or metal container. The sharps container should be puncture-proof with
a tight-fitting lid.
Infectious waste
Infectious wastes are collected in metallic containers, decontaminated and then
disposed. The metallic container is autoclaved for reuse.
CHAPTER 13
Incisions and Flaps
Incision
Principles of Wound Incision
Intraoral incisions
Intraoral Flap design
Classification of intraoral surgical flaps
• Sulcular full thickness flaps (full mucoperiosteal flap)
• Mucogingival flaps (limited mucoperiosteal flap)
• Intraoral locoregional flaps
Flap reflection
Flap retraction
Extraoral incisions
Extraoral flap designs in Oral Surgery
Skin grafts
Incision
Incision refers to a fine cut produced surgically by a sharp instrument that
creates an opening into an organ or space in the body. Incisions are used to
gain surgical access to deeper tissues with minimal damage to the surrounding
vital structures. A sound anatomical knowledge is thus essential in planning
incisions.
A ‘pen grasp’ is used to hold the scalpel in one hand, while the other hand is
used to firmly hold and stabilise the skin or mucosa. Incision should be made
in a single firm continuous stroke of uniform depth to the full thickness. Multiple
interrupted strokes can cause tearing of the tissues and hence excessive scar
formation.
Principles of wound incision

1. The surgical site has to be maintained in a sterile and aseptic technique.
2. The length and direction of incision:
a. to permit sufficient operating space and optimum exposure
b. the direction of wound heal naturally is from side-to-side,
not end-to-end
c. the arrangement of tissue fibres in the area to be dissected
varies with tissue type
d. the best cosmetic results when incision is made in the
direction of the tissue fibres
3. The incision should be placed along the Relaxed Skin Tension Lines
(Langer’s line)
a. these are the skin lines that are oriented perpendicular to
the direction of the underlying muscle fibres
b. it is determined by examination of patient’s natural skin
creases at rest
4. Fusiform excision
a. performed with longitudinal axis running parallel to the
Langer’s lines
b. the length should be 4 times with the width of the defect to
produce an accurate approximation of skin edges without
dog ear formation
c. Dog ears refers to the areas of redundant skin and
subcutaneous tissue resulting from a wound margin being
longer on one side than the other it can be corrected by
i. incremental oblique placement of sutures
ii. fusiform excision of the dog ear which lengthens
the scar considerably
5. Basic surgical skills of wound incision
a. marking of important landmarks
b. application of a gentle traction to the skin to avoid wrinkles
c. the operator should not direct the incision in an outward
direction
d. a single firm continuous stroke through the subcutaneous
fat should be used with cross hatches with ink or marking
pen for accurate wound closure
e. cuts in different planes should be avoided

1. All surgical instruments used for cutting or incising should be sharp
and of appropriate size.
2. While incising the tissues firm, continuous strokes should be used.
3. Avoid cutting the vital structures like nerve, vessels, etc.
4. Instruments should be perpendicular to the epithelial tissue. This angle
creates sharp wound edges that heal with minimal scar tissue
formation.
5. Long incisions not only give better access and ease in tissue separation,
they also heal faster.
6. Avoid horizontal and severely angled vertical incisions: Horizontal and
severely angled incisions sever more collagen fibres and gingival blood
vessels as the blood vessels and collagen fibres which attach to the
periosteum in the gingiva course parallel to the long axis of the teeth.
The flap shrinks excessively during surgery due to contraction of the
cut collagen fibres. As a result, extensive tension is placed on the soft
tissues leading to tearing of sutures followed by subsequent scar
formation.
7. Avoid incisions over bony eminences: Radicular eminences, like the canine
often fenestrates through the cortical bone or covered with very thin
bone with a poor blood supply. Soft tissue fenestrations may result
from these bony defects if incisions are made over them. Vertical
incisions must be made parallel to the long axis of the teeth and always
made over solid interdental bone.
8. Incisions should be placed and flaps repositioned over solid bone: Incision
must never be placed over areas of periodontal loss or periradicular
lesions. In the absence of good bone support to the repositioned edges
of the mucoperiosteal flap, in adequate blood supply results which in
turn leads to necrosis and sloughing of the soft tissue.
9. Avoid incisions across major muscle attachments: Difficult repositioning of
the flap and healing by secondary intention resulting in scar tissue
formation if incisions are made across major muscle attachments. This
is avoided by including the muscle attachment within the flap.
10. Tissue retractor must rest on solid bone: The extension of the vertical
incision must be sufficient to allow the tissue retractor to sit on bone
thereby leaving the site of surgery well exposed. Inadequately
extended vertical incision will produce a possibility of traumatizing
the mucosal tissue at the base from the retractor which in turn affects
the blood supply of the tissue.
11. Provide adequate visual and operative access with minimal soft tissue trauma:
Horizontal incision for mucoperiosteal flaps usually extend lateral to
one or two teeth which is to be treated. This is helpful in providing
adequate access, minimal tension and soft tissue stretching.
12. Never split the involved interdental papilla: Vertical incision must intersect
the horizontal incision and terminate in the intrasulcular area at the
mesial or distal line angle of the tooth. A vertical incision or
intersection of the horizontal incision should never split the involved
interdental papilla. It can either be included or excluded in a flap
design.
13. Involve the entire mucoperiosteum: The entire mucoperiosteum (marginal,
interdental and attached gingiva, alveolar mucosa and periosteum)
must be included in the flap. Less surgical trauma and better surgical
haemostasis can be achieved with full thickness flaps due to the
maintenance of the supraperiosteal blood vessels which supply these
tissues.
14. The apex of the flap should never be wider than the base. Exception
when a major artery is present in the base. Sides of the flap should be
parallel to each other, or convergent from the base (Fig. 13.1).
15. The length of the flap must not exceed twice the width of the base.
16. An axial blood supply must be included in the base of the flap.
17. The base of the flap should not be stretched or twisted excessively
since this will compromise the supplying vessels.
FIGURE 13.1 Flap design—base wider than apex.

Intraoral incisions
Intraoral incisions and transoral incisions are made to gain access
predominantly to the dentoalveolar structures as in endodontic surgery, ridge
augmentation, dental implants, sinus lift, extraction of the impacted teeth etc.
In addition they play an important role in surgical access to various sites like
zygomaticomaxillary buttress, lateral pyriform aperture, mandibular angle
body, symphysis in case of fracture fixation and bone graft harvest.
Though, intraoral wounds heal uneventfully with minimal scar and
complications, the choice of the flap design is important for good surgical
access and less complications.
Flap design
Flap design selection varies with each surgical procedure and various other
factors to dictate the selection on an individual case basis. The factors to be
considered are: (1) anatomy, (2) access needed, (3) types of restorations at
surgical site, (4) width of attached gingiva, (5) bone thickness and (6) muscle
attachment.
Classification of intraoral surgical flaps

There are two major categories of flap designs depending on the location of
the horizontal component of the incision. Further, the flap designs are
classified based on geometric terms (triangular, rectangular and trapezoidal)
for easy identification.
1. Sulcular full thickness flaps (full mucoperiosteal flap)

The sulcular full thickness flap design involves an intrasulcular
horizontal incision along with reflection of the marginal and interdental
gingival tissue as part of the flap (Fig. 13.2A−C).
a. Triangular (one vertical releasing incision).
b. Rectangular (two vertical releasing incisions).
c. Trapezoidal (broad-based rectangular).
d. Horizontal (no vertical releasing incision).
2. Mucogingival flaps (limited mucoperiosteal flap)
The mucogingival flap design has a submarginal horizontal or
horizontally oriented incision and the marginal or interdental papilla is
not included in the flap.
a. Submarginal curved (semilunar).
b. Submarginal scalloped rectangular (Luebke− Ochsenbein).
3. Locoregional flaps
Some local flaps can be used for smaller defects in maxillofacial region as
tongue flap for oral submucous fibrosis and palatal flaps for oroantral
fistulae.
FIGURE 13.2 (A) Full thickness mucoperiosteal flap rose exposing

mandibular symphysis for graft harvest. (B) Cross-sectional view
shows flap design with marginal gingiva left intact. (C) Illustration
showing full thickness mucoperiosteal flap.
1. Sulcular full thickness flaps (full mucoperiosteal flap)

(a). Triangular flap (Fig. 13.3A–C)
Triangular flap is created by a horizontal, intrasulcular incision and a vertical
releasing incision. The primary advantage of this flap design is that it allows
good wound healing, resulting from minimal disruption of the vascularity to
the flap tissue and need of minimal sutures for flap reapproximation. The
main disadvantage is the limited surgical access due to the single vertical
releasing incision. Exposure of the root apices of long teeth is difficult owing to
the limited surgical access.
FIGURE 13.3 (A) Triangular flap. (B) Triangular flap exposing
periapical lesion. (C) Illustration of triangular flap.
Distal relaxing incision provides an additional access in a reflected-

triangular flap. A relaxing incision is a short vertical incision placed in the
marginal and attached gingiva. It is located to the extent of the horizontal
incision opposite to the vertical releasing incision. This also relieves the flap
retraction tension while achieving adequate surgical access.
It is recommended for posterior teeth as it provides favourable surgical
access and excellent wound healing. Due to the anatomic structures
contraindicating other flap designs, only the triangular flap with mesial
vertical incision is recommended for mandibular posterior teeth.
(b). Rectangular flap

Rectangular flap is formed by an intrasulcular, horizontal incision and two
vertical releasing incisions. The main advantage of this flap is the increase in
surgical access to the root apex. It is especially useful for mandibular anterior
teeth, multiple teeth and teeth with long roots like maxillary canines. For
posterior teeth this flap design is not recommended due to the distal vertical
incision that causes suturing problems due to extremely limited space in that
area. The main disadvantages of the rectangular flap are:
1. Difficult reapproximation of the flap margins and wound closure.

2. Difficult postsurgical stabilisation as only the sutures hold the flap
tissues in position.
3. Greater chance for postsurgical flap dislodgment.
(c). Trapezoidal flap (Fig. 13.4A–C)

Trapezoidal flap is similar to the rectangular flap except that the two vertical
releasing incisions intersect the horizontal, intrasulcular incision are at an
obtuse angle. A broad-based flap with the vestibular portion wider than the
sulcular portion is obtained by the angled vertical releasing incisions. This flap
is desirable based on the assumption of providing a better blood supply to the
flapped tissues.
FIGURE 13.4 (A−B) Trapezoidal flap. (C) Illustration of full

thickness mucoperiosteal flap.
However, blood vessels and collagen fibres in the mucoperiosteal flap are
oriented in a vertical direction and the angled vertical releasing incisions may
damage the vital structures. This results in more bleeding, disruption of the
vascular supply to the unflapped tissues and flapped tissues shrinkage. Hence,
it is contraindicated in periradicular surgery.
(d). Envelope flap (Horizontal flap) (Fig. 13.5A–C)

Envelope flap is also known as horizontal flap and is made by a horizontal,
intrasulcular incision with no vertical releasing incision. Due to the limited
surgical access this flap has limited use in periradicular surgery. Its application
is limited to repair of cervical defects, root perforations, resorption, caries etc.
FIGURE 13.5 (A) Crevicular incision. (B) Envelope flap. (C)
Illustration showing envelope flap.
2. Mucogingival flaps (limited mucoperiosteal flap)

(a). Semilunar flap (Fig. 13.6)
This is a horizontal incision with a dip towards the incisal aspect in the centre
of the flap, resembling a half-moon. It is not generally recommended for
periradicular surgery because of inadequate visual and operative access but
may be utilized for incision and drainage procedure. More often this flap
design leaves a noticeable scar.
FIGURE 13.6 Semilunar incision exposing periapical lesion.
(b). Submarginal scalloped rectangular (Luebke−Ochsenbein)

The flap design calls for a scalloped incision in the middle of the attached
gingiva. The angle of the incision in relation to the cortical plate is 45 degree
because this angle provides the widest cut surface, allowing for better
adaptation once the flap is repositioned. The purpose of the scalloped
horizontal incision is to provide a guide for the correct repositioning of the
elevated flap for suturing. Therefore, it is important to scallop the incision,
precisely tracing the gingival margin. Thus, attached gingiva around the
crown margin will remain intact.
Mesial or mesiodistal vertical releasing incisions permit adequate access to
the surgical site without violating the integrity of the attached gingiva around
the tooth or crown. The vertical incision of the mucogingival flap should be
parallel.
The junction where the horizontal scalloped incision in the attached gingiva
meets the vertical incision should be rounded to promote smoother and faster
healing. When the intersection of these two incisions is made at a sharp 90
degree angle, it heals very slowly and leaves a small, hard, knobby scar. This
design is most suitable for crowned teeth, where there is an aesthetic concern
for open crown margins as a result of the surgery.
The major advantages are:
i. The marginal or interdental gingiva are not involved

ii. It does not expose the crestal bone.
Disadvantages are excessive bleeding, possibility of flap shrinkage, delayed

healing and scar formation—all because of vertically oriented blood vessels
and collagen fibres.
3. Intraoral locoregional flaps

(a). Tongue flap (Fig. 13.7A−B)
Tongue is a highly vascular organ where anterior based, posterior based or
lateral flaps can be raised based on the proximity of flap to the defect. Tongue
flaps are commonly used in anterior palatal fistula and oral submucous
fibrosis.
FIGURE 13.7 (A) Lateral tongue flap for the correction of oral
submucous fibrosis. (B) Tongue flap that is posteriorly based.
(b). Palatal flap (Fig. 13.8A–C)

Palatal flaps are axial flaps based on the greater palatine artery useful in
closure of small palatal defects, oroantral fistulae. They may be used as
pedicled finger flaps or island flap.
FIGURE 13.8 (A) A large oroantral fistula. (B) Palatal flap based on
greater palatine artery for closure of fistula. (C) Illustration of
palatal pedicled flap based on greater palatine artery for oroantral
fistula closure.
Flap reflection
Flap reflection is the process of separating the soft tissues (gingiva, mucosa
and periosteum) from the surface of the alveolar bone. This process must
begin in the vertical incision a few millimetres apical to the junction of the
horizontal and vertical incisions. The periosteum and its superficial tissues
from the cortical plate are elevated gently with the help of periosteal elevator.
The marginal and interdental gingiva is separated from the underlying bone
and the opposing incisional wound edge by directing the elevator coronally
without applying a dissectional force.
This approach is referred to as undermining elevation, and it allows all the
reflective forces to be directed to the periosteum and the bone. After reflection
of the attached gingival tissues, elevation is continued more apically lifting the
alveolar mucosa along with periosteum until adequate surgical access is
obtained. On complete flap reflection, small tissue tags, cortical retained
periosteal tissues can be noted which should not be damaged or removed as
they play an important role in reattaching the flap.
Flap retraction
Flap retraction is the process of holding in position the reflected soft tissues.
Proper flap retraction depends on: (1) adequate flap extension and proper
mucoperiosteal reflection, (2) selection of the appropriate size and shape of the
retractor and (3) position of the retractor—must act as a passive mechanical
barrier resting on solid bone. Improper retraction will result in soft tissue
trauma and an extended surgical time. This may delay the wound healing.
Frequent saline irrigation of the periosteal surface prevents dehydration.
Extraoral incisions
Extraoral incisions are head and neck incisions which are away from the oral
cavity (Fig. 13.9). Extraoral incisions are made taking into consideration few
factors as healing potential, hidden scar, vital structures function etc.
• Relaxed skin tension lines—incisions are made predominantly along the

relaxed skin tension lines not crossing facial subunits. This helps in
good healing, less scar formation and thus avoiding unaesthetic scars.
• Vital structures—the incisions are made such that the vital structures
the nerve, vessels are not breached. Example: submandibular incision
is made two-finger width inferior to the mandibular lower border
which avoids damage to the marginal mandibular branch of the facial
nerve.
• The incisions are made such that the final scar lies in unexposed
regions of head and neck. Example: bicoronal incision (Fig. 13.10).
• Incisions are made such that scar contracture should not create
deformity. Example: ectropion following a subciliary incision.
• Incisions are best made close to the target site of surgery—though,
sometimes the incisions are made distant from the surgical site for
functional and aesthetic reasons. Example: Gillies approach for
zygoma elevation.
• The length of the incisions—depends on the amount of exposure. Longer
incision heals at the same rate as shorter incision.
Some of the commonly used extraoral incisions for accessing the
maxillofacial region include
• Bicoronal incision (Fig. 13.10A−B)—Frontal bone fracture
• Preauricular incision (Fig. 13.11)—Alkayat−Bramley for TMJ approach
• Submandibular incision (Fig. 13.12A−B)—Mandibular angle fracture
fixation
• Lateral eyebrow incision (Fig. 13.13)
• Transconjunctival incision (Fig. 13.14)
• Subciliary incision (Fig. 13.15)
• Infraorbital incision (Fig. 13.9)
• Weber−Ferguson incision (Fig. 13.16A−B)—Maxillectomy
FIGURE 13.9 Markings for extraoral incision. 1. Preauricular

incision; 2. lateral eyebrow incision; 3. upper blepharoplasty
incision; 4. subciliary incision; 5. infraorbital incision; 6.
retromandibular incision; 7. submandibular incision.
FIGURE 13.10 (A) Marking for bicoronal incision made posterior to
the hairline. (B) Raising a bicoronal flap along subgaleal plane.
FIGURE 13.11 Marking for preauricular incision to approach TMJ.

FIGURE 13.12 (A) Submandibular incision to expose mandibular
lesion. (B) Delivery of resected mandible via submandibular
approach.
FIGURE 13.13 Lateral eyebrow incision exposing zygoma fracture.

FIGURE 13.14 Transconjunctival approach to orbital floor
reconstruction with titanium mesh.
FIGURE 13.15 Subciliary incision exposing infraorbital rim that is
reconstructed with graft.
FIGURE 13.16 (A) Weber−Ferguson incision marking. (B) Weber

−Ferguson incision exposing entire maxilla in case of radical total
maxillectomy for carcinoma of maxilla.
Extraoral flap designs in oral surgery

When the wound or defect cannot be closed primarily. Flaps are raised to close
the defect. Flaps are tissues that are transferred with a blood supply; it can
consist of any type of tissue and most commonly flaps are used for skin and
mucosa.
Classification of flaps
Based on blood supply
a) Random flap
b) Axial flap
c) Island flap, e.g. submental flap
d) Free tissue flap (Fig. 30.12 A−B, refer Chapter 30)
Based on location of the flap
a) Local—Tissue adjacent to the defect

b) Regional—Refer to those flaps recruited from different areas of the
same part of the body. (Fig. 13.17)
c) Distant flaps—Are harvested from different parts of the body. E.g.:
pectoralis major myocutaneous flap (Fig. 30.15 and 30.16; Refer to
Chapter 30: Management of Head and Neck Tumours)
FIGURE 13.17 Forehead flap is taken for the correction of the
defect on the right ala of the nose.
Based on the configuration
• Examples of these flaps include bilobed, rhomboid v−y plasty

(Fig. 30.14) and Z-plasty
Based on the method of transfer from donor site
a) Advancement flaps (Fig. 13.18)

b) Rotation flaps (Fig. 13.19)
c) Transposition flap
d) Interpolated flaps
FIGURE 13.18 Hairy nevus excision done and a local advancement
flap has been taken for closure of the defect.
FIGURE 13.19 (A−C) Nasolabial flap has been taken as a

rotational flap for the closure of the defect on the right buccal
mucosa.
Based on the composition
• Cutaneous
• Fasciocutaneous
• Myocutaneous
• Skin graft + Myocutaneous
• Osteomyocutaneous (e.g. Free fibula graft)
• Tendocutaneous
• Sensory
Classification of grafts for defects

a) Thin Split thickness Skin Graft
b) Thick Split thickness Skin Graft
c) Full thickness Skin Graft
d) Composite Skin Grafts
e) Nerve Grafts
f) Tendon Grafts
Skin grafts (Fig. 13.20−13.22)

FIGURE 13.20 Level at which the split thickness skin graft and full
thickness skin graft are prepared.
FIGURE 13.21 Harvesting of a Split thickness Skin graft using a
hand held Humby’s knife from the right thigh.
FIGURE 13.22 (A) Full thickness skin graft harvested from the right
groin crease the donor site was closed primarily (B) the Recipient
site is shown—second stage of ear reconstruction for microtia.
Split thickness Skin Graft are usually taken with skin knives or powered
dermatomes. The most commonly used sites are the thighs and buttocks. The
Split thickness graft is then meshed to improve the ‘take’ of the graft by
allowing the exudate to escape.
Types:
• Thin: 0.2−0.3 mm
• Thick: 0.45−0.75 mm
Full thickness (Wolfe) Skin Graft is prepared from the donor site by cutting the
skin without the underlying fat. The commonly used sites are the groin crease
and neck where if the defect is small can allow primary closure of the donor
site.
CHAPTER 14
Suturing Materials and

Techniques
Ideal requirements for suture materials

Biological response of tissues to suture materials
Size of the suture materials
Classification
Absorbable suture
Nonabsorbable suture
• Monofilament
• Multifilament
Natural absorbable suture materials
Catgut
Synthetic absorbable materials
Polyglycolic acid (Dexon)
Polyglactin 910 (Vicryl)
Polydioxanone (PDS)
Polytrimethylene carbonate (Maxon)
Nonabsorbable suture materials
Natural nonabsorbable suture materials
Silk
Linen
Synthetic nonabsorbable suture materials
Nylon
Polypropylene (Prolene, Surgilene)
Braided polyesters (Mersilene, Dacron)
Polybutester
Needles
Straight needles
Curved needles
• Eyed needles
• Eyeless (swaged) needles
Suture methods
Simple interrupted suture
Simple continuous suture
Locking continuous suture
Mattress suture
Vertical mattress suture
Horizontal mattress suture
Subcuticular suture
Figure of eight suture
Knot
Principles of knot
Types of knots
Removal of sutures
Staples
Wound closure tapes
The purpose of a suture is to hold tissues in apposition until the wound has
healed sufficiently to be self-supportive.
The art of suturing wounds is by no means a recent endeavour. Unique
methods of closing wounds have existed in many ancient cultures. Galen (75
AD) was the first to experiment with catgut. In 1869, Lord Joseph Lister
developed the concept of both impregnating chromic acid in catgut and
sterilising suture materials. Halstead proclaimed the advantages of silk over
catgut in the early part of 20th century and, as a result, silk soon became the
most common suture material in surgical practice. Today a wide array of
suture materials and needles are available and it is essential to be aware of the
basic properties in conjunction with proper suturing techniques to maximise
the outcome of any oral surgical procedure.
Sutures function primarily to maintain wound closure and to promote
wound healing during the time when the wound is most vulnerable. The
wound healing process can be affected by the amount of suture material used,
suture type, the suturing technique and amount of tension in the suture.
Ideal requirements for suture materials

• Should have high tensile strength to hold the wound margins
appropriately till the healing is complete.
• Should not be allergic or cause any tissue inflammation.
• Should have least capillarity to avoid retaining the inflammatory
transudate at the wound.
• Should have good knot stability.
• Should be easily sterilised.
• Should be visible in the surgical field.
• Should be affordable.
Biological response of tissues to suture materials

A cellular response occurs whenever a foreign object is implanted in a living
tissue. This response is generally very mild with most surgical sutures though
marked if complicated by infection or trauma. If uncomplicated, the acute
response usually changes in about 3 days and the original population of
neutrophils is replaced by predominantly monocytes, plasma cells and
lymphocytes.
Size of the suture materials

The suture materials are available in various sizes depending upon its tensile
strength. The standard for identifying varying tensile strengths of a given
suture material is determined by the number of zeros. The smaller the cross-
sectional diameter, the more zeros the suture has. Sizes start with zero and the
diameter decreases with increasing number (1-0, 2-0 ... 10-0). Thus, 4-0 nylon
has a greater diameter than 6-0 nylon and therefore a greater tensile strength.
Classification
Sutures can be conveniently classified into three groups (Table 14.1):
• Natural and synthetic
• Absorbable and non-absorbable
• Monofilament and multifilament.
Table 14.1
Suturing materials: monofilament and multifilament

Suture material Absorbable Non-absorbable
Monofilament Surgical gut (plain and chromic) Polyamide
Collagen (plain and chromic) Polypropylene
Monocryl Stainless steel
Polydioxanone II (PDFII) Polyester
Polyglactin 910
Multifilament Polyglycolic acid Surgical silk
Polyglactin 910 Surgical linen
Polyglactin 910-Rapid Cotton
Polyamide braided
Polyester braided
Stainless steel
Absorbable suture
These are suture materials that are digested or hydrolysed by the enzymes
present in the body or by other mechanism. Thus they require no removal
from the surgical site. The actual dissolution time of the suture material
depends on: material type, tissue blood supply, tissue structure and degree of
fluid accumulation on suture material.
• Natural
• Synthetic
Non-absorbable suture
These materials cannot be metabolised by the body’s natural mechanism,
therefore they should be removed by the surgeon at the end of healing or not
removed and left in place in repair of vascular/neural structures.
• Natural
• Metallic
• Synthetic
I. Monofilament
This consists of single strand of suture material.
Advantages
• Monofilament sutures are more smooth and strong.

• They do not allow any bacteria to survive.
Disadvantages
• Monofilament sutures cannot be handled well like multifilament

sutures.
• Monofilament sutures have to be handled properly and delicately
without any damage to the strand during surgical procedures to avoid
any breakage postoperatively.
II. Multifilament
This consists of several filaments twisted or braided together, can be coated to
allow smooth movement into tissues (Fig. 14.1).
FIGURE 14.1 Suture materials: (A) monofilament, (B) braided and
(C) catgut.
Multifilament sutures are generally easier to handle and to tie than

monofilament sutures, but they can harbour bacteria and are not suitable in
the presence of contamination and infection. This transfer of microbes from the
oral cavity through the multiple filaments into deeper tissue is called as
“Wicking effect”.

Natural absorbable suture materials
Catgut (Fig. 14.2)
Types:
• Plain gut
• Chromic gut
This natural product, also called surgical gut is made of collagen harvested
from submucosal layer of the small intestine of sheep and the serosal layer of
cattle small intestine (cattle intima). Although used for centuries, it is
gradually fading from use because gut suture material has poor tensile
strength, poor in vivo knot stability and high tissue reactivity. However, gut
that is soaked in chromic acid salts will usually have a delayed absorption
time and a reduction in tissue reactivity compared with untreated catgut. Gut
usually retains its strength for 2–3 weeks. Fast absorbing gut is a newer form
of catgut not treated with chromic salts. This can also be used as a
percutaneous suture in split-thickness skin grafts or in children where it is
difficult to remove sutures. One can usually find a synthetic material
preferable to catgut. This is because the newer synthetic materials have
substantially decreased tissue reactions and have more predictable absorption.
Catgut undergoes resorption by proteolysis (proteolytic enzymes).
FIGURE 14.2 Chromic catgut.
Synthetic absorbable materials

Polyglycolic acid (dexon)
This polymer of glycolic acid, introduced in 1970, was the first synthetic
absorbable suture material to become available. It was renowned for its
excellent tensile strength and knot stability. In addition it has delayed
absorption and diminished tissue reactivity compared to catgut. The
absorption of polyglycolic acid is by hydrolysis when compared to the
proteolytic absorption of catgut.
Polyglactin 910 (vicryl) (Fig. 14.3)

Vicryl, introduced in 1974, was the next synthetic material to be marketed.
This suture is a co-polymer of lactide and glycolide, polyglactin 910,
manufactured with a coating of polyglactin 370 and calcium stearate. This
lubricant coating provides vicryl its excellent handling and smooth tie down
properties. Vicryl is degraded by hydrolysis like all synthetic polyesters and
thus causes minimal tissue reaction. Vicryl is braided and comes in either a
clear undyed or violet-dyed form.
FIGURE 14.3 Polyglactic acid (vicryl).
Polydioxanone (PDS) (Fig. 14.4)

Polydioxanone is a polymer made from paradioxanone and was marketed as
having prolonged tensile strength in vivo compared with Vicryl or Dexon.
Therefore, PDS can prove useful in situations where extended wound tensile
strength is required. Polydioxanone is hydrolysed more slowly than other
synthetic absorbables. Complete absorption occurs about 180 days after
implantation, but its foreign body reactions were found to be minimal. A
disadvantage of using PDS is that it is more difficult to use than the braided
synthetics because of intrinsic stiffness. Polydioxanone II is a newer product
that has decreased stiffness and smoother handling characteristics than PDS
while keeping the original tensile strength qualities.
FIGURE 14.4 Polydioxanone (PDS).
Polytrimethylene carbonate (maxon)

This synthetic monofilament is the newest absorbable material prepared from
polyglyconate, a co-polymer of glycolic acid and trimethylene carbonate. It
was developed to combine the excellent tensile strength knot stability of PDS
with improved handling properties. Maxon provides wound support over an
extended period of time. Maxon is much more supple and manageable than
PDS, with 60% less rigidity and minimal memory. Although the cost of Maxon
is more than Vicryl or Dexon, its improved strength and handling
characteristics make it the absorbable suture material of choice.
Non-absorbable suture materials

Non-absorbable sutures are generally defined as filamentous material that are
resistant to the degradation mechanisms of living mammalian tissue.
However, the term non-absorbable is relative because many of these sutures
are eventually degraded.
Natural non-absorbable suture materials

Silk (Fig. 14.5)
Silk is created from natural protein filaments spun by the silkworm larva as it
builds a cocoon. Modern silk is braided, soft and perhaps the easiest suture
material to handle and tie. Unfortunately, it has the lowest tensile strength of
any material tested. It elicits more inflammatory reaction than any other suture
except catgut. Silk also has a high capillary quality due to its braiding and
should be avoided in areas prone to infection (i.e. distal extremities). In
cutaneous surgery, it can be used around the eyelids and lips where it lies flat,
causes minimal irritation and has a low potential for infection.
FIGURE 14.5 Silk.
Linen
Linen is a cellulose material made from flax. It is twisted to form a fibre to
make a suture. Tissue reaction is similar to silk and the material has good knot
stability. It gains 10% tensile strength when wet and it is fairly unique in this
respect. It is very extensively used for tying pedicles and as ligatures. It has
excellent knotting properties.
Synthetic non-absorbable suture materials

Nylon (Fig. 14.6)
This suture, introduced in 1940, is a synthetic polyamide polymer fibre and
was the first synthetic suture material. Nylon is the most widely used non-
absorbable suture in cutaneous surgery as a monofilament (Ethilon,
Dermalon). It is popular because of its high tensile strength, excellent elastic
properties, minimal tissue reactivity and low cost. The main disadvantage to
using nylon is its prominent memory which subsequently leads to an
increased number of knot throws (three to four) to hold a given stitch in place.
Ethilon can be soaked in alcohol to decrease its memory and increase its
pliability. Multi-filamentous braided nylon suture (Nurolon, Surgilon) are
seldom used in cutaneous surgery because of a slightly higher infection rate
and an increased cost. Nevertheless, the braiding makes them more pliable
and easier to handle.
FIGURE 14.6 Nylon.
Although nylon is classified as a non-absorbable suture, it still encounters

partial degradation through hydrolysis at a very slow rate. Thus nylon would
be more appropriately classified as slowly absorbable suture rather than as a
non-absorbable suture. A study comparing clear monofilament nylon and
polyglycolic acid in buried sutures demonstrated less clinical inflammatory
response with nylon.
Polypropylene (prolene, surgilene) (Fig. 14.7)

Polypropylene is a plastic suture formed by the polymerisation of propylene
by means of a catalyst. Prolene is an extremely inert suture whose tissue
reactivity and tensile strength are comparable to that of nylon. It has a very
smooth surface with low adherence to tissue which is ideal for a subcuticular
intra-dermal suture because it tends to slide out smoothly at the time of suture
removal. Its extreme smoothness does compromise knot security and extra
throws are required to compensate for this drawback. Prolene is especially
noted for its plasticity. When swelling occurs, this suture will stretch to
accommodate the wound, thus there will be little cutting through the tissue.
When wound swelling recedes, the suture will remain loose.
FIGURE 14.7 Polypropylene (Prolene).
Braided polyesters (mersilene, dacron)

Polyester fibres are polymers that are formed as nylon by condensation
polymerisation. Braided polyesters were manufactured to provide the same
high tensile strength and low tissue reactivity as the mono filaments, but with
improved qualities in handling and knot security. Polyester sutures are either
coated or uncoated. Mersilene and Dacron are uncoated braided polyesters
that have a rough surface that produces drag when pulled through tissues and
when knots are set. In order to ameliorate this problem, coated polyesters such
as Ethibond were developed. They are not commonly used due to relatively
higher costs and the coating’s susceptibility to ‘cracking’ after knots are tied.
Polybutester
Polybutester is the newest of the non-absorbable sutures and is a thermoplastic
co-polymer composed of butylene terephthalate and polytetramethylene ether
glycol. It is a monofilamentous suture that was designed to be stronger, less
stiff and possess lower coefficient of friction than either nylon or
polypropylene. A unique feature of polybutester is its elasticity and flexibility.
This suture has the capacity to stretch 50% of its length at loads of only 25% of
its knot breaking level. This elasticity at low loads has the clinical advantage of
elongation of the suture when wound oedema occurs and maintenance of
tension when the oedema recedes. This characteristic reduces the potential for
suture marks and suture cut-through. Being monofilamentous, it induces little
inflammatory reaction when implanted in skin. The cost of polybutester is
approximately equivalent to that of polypropylene.
A comparison of all suture materials is elaborated in Table 14.2.
Table 14.2
Comparison of suture materials
Needles
Needles are made of either stainless steel or carbon steel. There are basically
two shapes of needles (Fig. 14.8A−B).
i. Straight
ii. Curved
FIGURE 14.8 (A) Surgical needles. (B) Parts of a surgical needle.
Straight needles
Types
Round bodied—Circular or oblong in cross-section and gradually tapers to a
point.
Taper cut—Triangular in cross-section and are sharp enough to finely pass
through keratinised mucosa.
Uses
• For closure of thoracic, iliac or abdominal region.

• In maxillofacial surgery, the needle is used for the passage of circum-
mandibular or circum zygomatic wires.
Curved needles
Curved needle is usually used for skin and mucous membrane surgery. The
curvatures come in various types such as 1/4, 3/8, 1/2 and 5/8 (Fig. 14.9).
FIGURE 14.9 Types of curved needle.
Types (Fig. 14.10)
1. Round bodied
2. Taper cut
3. Conventional cutting
4. Reverse cutting
FIGURE 14.10 Types of curved needle.
Conventional cutting—has one of the three cutting edges on the internal

surface of the needle.
Reverse cutting—the internal surface is flat. It is the most popularly used
needle.
Uses
• Tapered needles are used for closing muscle or fascia.

• Cutting needle is used for keratinised mucosa, skin or subcuticular
layers where the tissue is difficult to penetrate.
Another type of classification

Another type of classification that is commonly used (Fig. 14.11).
FIGURE 14.11 Eyed and eyeless (swaged) needles.

1. Eyed needles
These needles can be reused. The suture material is tied in the eye of the
needle and passed through the tissue. Since the eye is larger than the diameter
of the suture material, the needle causes tissue trauma. Split-eyed needle used
for easy threading and release of suture is also available.
2. Eyeless (swaged) needles

In this type of needle, the suture material is inserted into the needle hollow
during manufacturing and the metal is compressed to seal around the suture
material. These needles cannot be reused. Eyeless needles are ideal for use in
surgery as they cause minimal tissue trauma. Different shapes and types of
eyeless needles are available and are required for various surgical procedures.
Advantages of eyeless needles
1. They are also called atraumatic needles since they cause minimal
trauma to the tissue during suturing (single strand of thread
throughout the surgical tissues causing minimal tissue disruption
compared to the double strands of the eyed needle).
2. No need of prior sterilisation, since it is supplied as a pre-sterilised
pack.
3. Disposable after single use, hence hygienic and no issues of loss of
sharpness.
4. Sharp tip helps in precise and efficient completion of suturing.
5. Less time consuming when compared to eyed needle, no need of
sterilising and threading the needle.
6. No issue of accidental unthreading of the needle during surgery.
• The needle should be grasped with the help of needle holders at
approximately 3/4th of its distance from the tip of the needle.
• The needle should never be held at the suture end as it is the weakest
point of the needle and grasping at this point results in either bending
or breakage of the needle.
• The needle should pierce the tissue perpendicular to its surface, as
piercing the tissue obliquely may result in a tear.
• The curved needles should be passed through the tissues following the
curvature of the needle to prevent tearing of the tissues.
• The suture should be placed equidistant (2–3 mm) from the incision
line. The depth of penetration should also be equal on both sides of the
line.
• The needle should be passed from mobile tissue to the fixed tissue.
• When one side of the tissue is thinner than the other side, then the
needle should pass from the thinner to the thicker side.
• Similarly, when one side is deeper and the other side is superficial, the
needle should pass through the deeper to the superficial side.
• The distance from the incision point to the needle penetration should
be less than the depth to which the needle penetrates into the tissues in
order to cause eversion of wound margin when the suture is tied.
• The suture should not be tied so tightly that it results in blanching of
the tissues. The suture should just approximate the wound margins.
• The knot should not be placed over the wound margins.
• Each suture should be placed 3–4 mm apart. The spacing between the
sutures depends upon the type of tissues which are approximated.
When sutures are placed upon areas of underlying muscular activity
they should be close to each other.
• When length of tissue on one side of wound is longer than the other,
suturing it would result in dog ear formation. In order to eliminate
this, the excessive tissue should be undermined and an incision at
approximately 30 degree to the original incision is directed at the
undermined tissue. The extra tissue is pulled over the incision, the
appropriate amount is excised and the wound is closed (Fig. 14.12).
FIGURE 14.12 Suturing method to eliminate dog-ear formation.
The choice of suture material, needle and type of suturing depends on:
a. Location of the wound

b. Thickness of the wound edges
c. Tension exerted on the wound
d. Approximation of wound edges
e. Any additional requirements such as haemostasis, cosmetic needs, etc.
Suture methods
Refer Table 14.3 for different suturing methods and indications.
Table 14.3
Suturing methods and indications
S. Suturing Indication
no. method
1. Simple Most commonly used
interrupted No specific indication
2. Simple • Long wounds with minimal wound tension and good wound
continuous approximation
• To secure split or full thickness grafts
• Areas of cosmetic importance as less scarring occurs
3. Locking Areas of moderate wound tension with good vascularisation but requiring
continuous additional haemostasis, e.g. scalp, post auricular, alveoloplasty
4. Vertical Areas that require wound eversion and to reduce wound tension eliminate
mattress dead space
5. Horizontal Provide strength and wound eversion and hence used in wounds under high
mattress tension
6. Subcuticular • Areas in which wound tension is minimal and dead space has already been
eliminated
• Cosmetic area
7. Figure of 8 Closure of extraction sites and other intraoral sites that require papillary
adaptation
Simple interrupted suture (Fig. 14.13)

Simple interrupted suture is the most commonly used suture method. The
sutures are placed independently. The distance between each suture and the
incision line can be varied according to the necessity and convenience. This
suture provides great strength.
FIGURE 14.13 Simple interrupted suture.
Advantages
• Selective adjustments of wound edges can be made.

• Failure of one suture does not necessarily prejudice the others.
Disadvantages
• Can lead to suture marks (rail road track scars on the cutaneous
surfaces) after postoperative oedema has occurred.
• Since there are increased numbers of knots they tend to reduce the
strength of the thread by up to 50%.
Simple continuous suture (Fig. 14.14)

The running continuous suture provides rapid secure closure with an even
distribution of tension along the length of the wound, preventing excess
tightness in any one area. This technique also provides additional wound
eversion, accomplished by everting the wound edges with fingers or an
instrument as the needle enters and exits the skin surface. It provides more
water-tight closure as required by intraoral bone grafting. It should not be
used in areas where there is already existing tension.
FIGURE 14.14 Simple continuous suture.
Indication
Well approximated wounds with minimal tension that have been initially
created by well placed buried sutures.
Advantages
• The advantage of this method is that it is quick and has fewer knots.
• If the tissues swell in one area, the remaining suture can provide a
degree of slack that will help relieve the pressure.
Disadvantages
It is not possible to free a few sutures at a time in continuous suture. Even
when one suture breaks, the whole closure is affected.
Locking continuous suture (Fig. 14.15)

This is similar to the continuous suture, but with an added advantage that a
degree of locking is provided by withdrawing the sutures through its own
loop. Due to the locking mechanism, the tissues align themselves
perpendicular to the incision. Secondly, it prevents the continuous tightening
of the suture as the wound closure progresses.
FIGURE 14.15 Locking continuous suture.
Mattress suture
Mattress sutures are commonly used in the region of abdomen or hip and not
head and neck. Hence, it is useful in closing the wound of iliac and rib bone
graft. It provides more tissue eversion than the simple interrupted sutures.
Mattress sutures are of two types:
• Horizontal mattress
• Vertical mattress
1. Vertical mattress suture (Fig. 14.16)

Vertical mattress sutures are similar to simple sutures, but an additional bite
through the wound edge is used to ensure edge eversion. This suture is placed
by first taking a large bite of the tissue from the wound edge and crossing
through the tissue to an equal distance on opposite side of the wound. The
needle is then reversed and returned with a very small bite at the
epidermal/dermal edge in order to closely approximate the wound edge.
FIGURE 14.16 Vertical mattress suture.
Advantages
• Advantages include decreasing the dead space and providing

increased strength across a wound.
• It does not interfere with healing as the suture runs parallel to the
blood supply.
Disadvantages
• The disadvantages are that fine wound edge approximation is difficult.

• Prominent suture marks can form if the sutures are not taken out
earlier than in other suturing techniques.
2. Horizontal mattress suture (Fig. 14.17)

In this technique, eversion and the continuity provide a very versatile closure.
Hence, it is often used for intraoral bone grafting. The needle is passed from
one edge of the incision to the other and again from the latter to the first edge.
The procedure is continued till the entire length of the incision and a knot is
then tied.
FIGURE 14.17 Horizontal mattress suture.
Disadvantages
Blood supply to the flap edge may be diminished and can cause necrosis and
dehiscence if not used properly.
Subcuticular suture (Fig. 14.18A−B)

This procedure was popularised by Halstead in 1893, who explained that the
procedure may be used with no knots by having the ends exit a short distance
from the wound and taping them to the skin.
FIGURE 14.18 Subcuticular suture.
In this procedure, the needle penetrates skin ahead of incision and exits
within the wound. Needle is then inserted on opposite side of the incision in a
continuous fashion. At the end of incision, the suture is brought out at a
distance from the wound. By pulling both ends of the suture, incision is closed
and the suture ends are taped to skin.
Advantages
The subcuticular suture can be left in place more than 1 week in areas of
wound tension or underneath a cast with minimal problems of suture marks
and skin irritation.
Disadvantages
Disadvantages of the subcuticular closure are that it takes time to perform and
does not evert wound edges. It can still be an ideal suturing technique in
certain locations of the body where minimising suture marks can be
appreciated.
Figure of eight suture (Fig. 14.19)

It is used for the closure of the extraction sites. This suture provides a good
adaptation of the gingival papilla along the adjacent teeth.
FIGURE 14.19 Figure of eight suture.
Knot
A knot is an intertwining of threads for the purpose of joining them. Suture
security is the ability of the knot and material to maintain tissue
approximation during the healing process. Failure is generally the result of
untying owing to knot slippage or breakage. Since the knot strength is always
less than the tensile strength of the material, when force is applied, the site of
disruption is always the knot. This is because shear forces produced in the
knot lead to breakage. Knot slippage is determined by the nature of the
material, suture diameter and type of knot. Monofilament and coated sutures
(Teflon, silicon) have a low coefficient of friction and a high degree of slippage
whereas braided sutures such as uncoated Dacron and catgut have greater
knot security because of their coefficient of friction.
A Sutured knot has three components (Fig. 14.20A−B)

a. The loop created by the knot.
b. The knot itself, which is composed of a number of tight ‘throws’, each
throw represents a weave of the two strands.
c. The ears, which are the cut ends of the suture.
FIGURE 14.20 (A) Various knot components prior to completion.

(B) Completed knot anatomy.
Principles of knot
1. Knot must be tight and firm to avoid slippage.
2. Knots should not lie over the incision line to avoid wicking of bacteria.
3. Avoid crushing or crimping of suture materials by not using
haemostats or needle holders on them except on the free end for tying.
4. Do not tie the suture too tightly because tissue necrosis may occur.
5. At the end of knot placement there should be no tissue blanching.
6. During knot placement, the thread ends must be kept taut with
adequate traction to avoid loosening the first loop.
7. Coated and monofilament sutures require additional throws for knot
security and to prevent slippage.
Types of knots
I. Square knot, half hitch knot or single knot
II. Granny knot
III. Reef knot
IV. Triple throw knot
V. Surgeon’s knot
1. Square knot or half hitch knot or single knot (Fig. 14.21): Single loop
formed by a clockwise or counter clockwise throw of one thread over
the other.
2. Granny knot (Fig. 14.22): A single loop formed by two throws, both in
same direction (clockwise or counter clockwise). It has more holding
power than a square knot.
3. Reef knot (rif = fold, knot used to gather a ship’s sail to reef in a strong
wind) (Fig. 14.23): Loop formed by two throws first clockwise and
secondly counter clockwise or vice-versa.
4. Triple throw knot: As the name says, 3 throws; first two similar to reef
knot as a clockwise and counter clockwise throw followed by a third
throw similar to the second. This is more reliable and standard method
in surgery.
5. The surgeon’s knot is a square knot with an extra throw (two clockwise
followed by one anticlockwise).
FIGURE 14.21 Square knot.

FIGURE 14.22 Granny’s knot.
FIGURE 14.23 Reef knot.

Removal of sutures
Sutures should be removed atraumatically and cleanly as possible. Principles
of suture removal are as follows:
1. The area should be swabbed with hydrogen peroxide for removal of

encrusted necrotic debris, blood and serum from the sutures.
2. A sharp suture cutting scissor should be used to cut the loops of
individual or continuous sutures. It is often helpful to use a No. 23
explorer to help lift the sutures if they are within the sulcus or in close
opposition to the tissue. This will avoid tissue damage and
unnecessary pain.
3. During removal, the cut end of the knot is held gently and the suture is
removed towards the incision line. This is to prevent the tension across
the wound.
Staples
The principle of using staples in surgery is similar to paper stapling device
(Fig. 14.24A–D).
FIGURE 14.24 (A) Stapler-easy to grip cartridge for delivering

staples. (B) Staple pin. (C) Staples used for the closure of
bicoronal flap. (D) Specially designed extractor for staple removal.
Even though not regularly used in oral and maxillofacial region, staples are
often very effective for closing wounds. They are made of stainless steel and
combine the highest tensile strength of any suture material in use today with
low incidence of tissue reaction and infectious complications. For these
reasons, it is common to use staples to close wounds that are under a great
deal of tension, e.g. scalp closure in bicoronal flap. In these instances, staples
provide excellent wound edge eversion without strangulation of the tissue and
result in minimal crosshatch scarring. Staples can also be applied much faster
than the sutures, which is an advantage in closing long linear wounds. Staples
come in two sizes: regular and wide. They are dispensed from light weight,
easy to grip cartridge. Specially designed extractors are used for staple
removal although this can be accomplished by haemostat.
Wound closure tapes

Modern cutaneous tapes have an important role in wound closure and have
certain advantages that sutures and staples cannot provide (Fig. 14.25). The
benefits of using tapes to hold wound edges together is that the skin surface is
not penetrated with a needle and iatrogenic trauma is thus minimised. In
addition, they maintain the integrity of the epidermis, resulting in less tension
to the wound and are more resistant to infection than sutured wounds.
However, they cannot maintain adequate deep tissue approximation or skin
edge eversion when used alone, therefore they are commonly used in
conjunction with sutures or staples.
FIGURE 14.25 Wound closure tapes used at the incision sites.
CHAPTER 15
Haemorrhage and Shock
Haemorrhage
Classification
Causes of haemorrhage
Clinical features of acute blood loss
Haemostasis
Mechanism of haemostasis
Methods of achieving haemostasis
Mechanical methods
• Pressure
• Haemostat
• Sutures and ligation
Chemical methods
• Adrenaline
• Thrombin
• Surgicel
• Surgicel fibrillar
• Oxycel
• Gelatine sponge or gelfoam or surgifoam
• Microfibrillar collagen (Avitene)
• Fibrin glue
• Styptics and astringents
• Alginic acid
• Natural collagen sponge
• Fibrin sponge
• Bone wax
• Ostene (a new water-soluble bone haemostatic
agent)
Thermal agents
• Eletrocautery/surgical diathermy
• Cryosurgery
• Lasers
Shock
Classification
Pathogenesis
Endogenous compensatory mechanisms
• Microcirculation
• Neuroendocrine mechanism
• Renal mechanism
Management of hypovolaemic shock
Haemorrhage
Haemorrhage is the escape of blood from the cardiovascular system to the surface of the
body or into the body tissues or cavities.
Classification
Haemorrhage can be classified in several ways for ease of identification and
treatment.
I. Based on the source of blood loss
• Arterial haemorrhage
• Venous haemorrhage
• Capillary haemorrhage
The vessel from which the bleed is occurring can be identified by the colour,
pulsation, vigour of flow and the presence of a spurt. Table 15.1 describes the
method of identification of the vessel of the bleed.
Table 15.1
Diagnosis of source of bleeding (or) blood loss
II. Based on the time of occurrence
• Primary haemorrhage
• Secondary haemorrhage
• Reactionary haemorrhage
1. Primary haemorrhage
Primary haemorrhage is the bleeding that occurs at the time of injury or
surgery.
2. Secondary haemorrhage
• Secondary haemorrhage is also recurrence of bleeding, it occurs weeks

after injury or even later than that.
• Infection is the cause for reopening of the bleeder vessel in most cases.
• It is typically seen in patients with retained root tips or foreign
materials in extracted socket.
3. Reactionary (intermediate) haemorrhage
• Reactionary haemorrhage is recurrence of the bleeding within 24 h of

the injury or surgery.
• It is caused by dislodgement of the clot following rise of blood
pressure after the injury.
• Restlessness in the post-injury or postoperative period can also lead to
either dislodging of the clot or slipping of the ligature.
• Coughing and vomiting increases the venous pressure, especially in
the neck veins and this is often the cause for bleeding from extraction
site or thyroidectomy wounds in the immediate postoperative period.
• This may also occur after the vasoconstrictive effect of the local
anaesthetic wears off. Adrenaline or epinephrine causes
vasoconstriction by its action on the alpha receptors of the smooth
muscles in the peripheral arterioles. However, after the alpha effect
has worn off, it produces a rebound vasodilatation by its action on β2
receptors. This rebound beta effect can occur when a concentration of
1:50,000 or 1:100,000 of epinephrine used. This can occur even hours
after the patient has been discharged from the hospital after the
surgical procedure.
III. Based on visualisation of the haemorrhage
• External haemorrhage
• Internal haemorrhage
External haemorrhage
Bleeding onto the exterior as in skin laceration or bleeding through an orifice
as epistaxis or otorrhoea bleeding.
Internal haemorrhage
• Internal or concealed haemorrhage occurs in injuries to abdominal

viscera.
• It is typically seen in rupture of the spleen.
• The diagnosis has to be made from history and clinical signs of blood
loss like pallor, rising pulse rate and falling BP.
IV. Based on clinical signs of haemorrhage
• Petechial haemorrhage
• Ecchymosis
• Haematoma
Causes of haemorrhage
• Trauma
• Infections
• Local irritants
• Congenital malformations
• Surgical (intraoperative/postoperative)
• Haemorrhage due to abnormalities in clotting factors
1. Clotting factor deficiencies
i. Hereditary—haemophilia A, haemophilia B
thrombocytopaenia.
ii. Anticoagulant, antiplatelet or fibrinolytic
therapy—warfarin, coumarin, heparin,
enoxaparin, aspirin, clopidogrel, argatroban,
alteplase, tirofiban, dipyridamole, eptifibatide,
fondaparinux.
iii. Liver disease (Factor II, VII, IX, X deficiencies).
2. Dysfunction of clotting—multiple myeloma
• Haemorrhage due to abnormalities in platelets
a. Deficiencies
▪ Idiopathic thrombocytopaenia purpura
▪ Secondary thrombocytopaenia purpura
▪ Leukaemia
b. Thrombocytosis
c. Dysfunction—thrombocytopaenia
• Haemorrhage due to systemic disease
a. Viral infection
b. Scurvy
c. Allergy
Clinical features of acute blood loss

1. Increasing pallor
2. Increasing pulse rate
3. Restlessness
4. Air hunger (deep respiration)
5. Cold clammy skin
6. Thirst
7. Tinnitus
8. Blindness
9. Blood pressure—it must be remembered that falling of BP is not a sign
of acute blood loss. A normal or slightly raised BP can be recorded.
Collapse and death can occur suddenly.
10. Urinary output—can be reduced in case of acute blood loss.
11. Haemoglobin level—not immediately changed but may fall after some
hours.
The bleeding tendency of any patient can be assessed by means of
haematological investigations. These lists of tests are termed the ‘coagulation
profile.’ Patients with liver disease, a previous history of haemorrhage, under
an anticoagulant therapy, a familial history of blood dyscrasias may be
advised to be subjected to an investigation prior to any oral surgical
procedure. The coagulation profile includes:
• Clotting time (CT)

• Bleeding time (BT)
• Prothrombin time (PT) and international normalised ratio (INR)
• Activated partial thromboplastin time (APTT)
• Factors assay.
Refer to Chapter 4 Diagnostic Aid—Haematological, Biochemical and

Microbial Investigations for detailed description and interpretation of these
tests.
Haemostasis
The mechanism of cessation of extravasation of blood.
Mechanism of haemostasis
Coagulation is a process during which, the injured blood vessel wall
components trigger a series of reactions to counteract and reduce the
extravasation of blood by transforming the cells and the components of blood
into an insoluble gel (clot or thrombus) to plug and seal the injury site
(Flowchart 15.1).
FLOWCHART 15.1 Summary of reactions involved in haemostasis.
When there is a tissue injury leading to extravasation of blood, the body

aims to stem the bleed by initiating steps as depicted in Fig. 15.1.
1. Vasoconstriction
2. Primary haemostasis by platelet plug formation
3. Secondary haemostasis by initiation of coagulation cascade
4. Tertiary haemostasis by consolidation of the fibrin clot.
FIGURE 15.1 Illustration of stages in haemostasis.

1. Vasoconstriction
The damaged blood vessel helps to limit blood loss by slowing down the flow
by narrowing the lumen. This is controlled by
Local control factors: Vasoconstrictors such as thromboxane A2, serotonin,
fibrinopeptide B are released at the site of the injury.
Systemic control factors: Epinephrine from the adrenal glands stimulates
general vasoconstriction.
2. Primary haemostasis by platelet plug formation

A physical barrier that plugs the tear in the wall of the blood vessel is the
immediate goal of haemostasis and this is accomplished by the platelets.
Platelet adhesion: Damage to blood vessels causes exposure of collagen fibres
to which platelets adhere to form a one-cell-thick carpet. Integrins, von
Willebrand factor promote the adherence of platelets to the endothelial cells of
the blood vessels.
Platelet activation or secretion: On activation platelets release local factors,
such as adenosine diphosphate (ADP), thromboxane that causes more platelets
to aggregate.
Platelet aggregation: A platelet plug is formed by self-association of the
platelets.
Platelet aggregation can be inhibited naturally by the absence of calcium,
presence of prostacyclins or by administrations of drugs like aspirin. The
platelet plug thus formed is still weak and therefore a bleed should not be
‘wiped’ but ‘dabbed’ using the capillary action of a dry towel.
3. Secondary haemostasis or the coagulation cascade

Tissue injury or injury to blood vessels prompts platelets to aggregate at the
site of injury. These platelets release factors that begin secondary haemostasis
(coagulation cascade) wherein the weak, soluble platelet aggregate matures to
form the insoluble ‘clot’. This cascade is mediated by a number of factors
(Table 15.2). When the injury causes the blood to come in contact with the
collagen in the walls of the traumatised blood vessels, the intrinsic pathway or
contact activation pathway is initiated which involves the sequential activation
of factor XII (Hageman factor), factor XI (plasma thromboplastin antecedent),
factor IX (Christmas factor) and factor VIII (antihaemophilic haemoglobin).
Tissue injury or vascular wall injury launches the extrinsic factor which is
triggered by the release of tissue thromboplastin (factor III) from the damaged
vascular or tissue cells. The extrinsic pathway is stimulated when the factor III
meets factor VII (stable factor). Both pathways activate coagulation factor X
(Stuart–Prower factor) which leads to the conversion of pro-thrombin (factor
II) to thrombin (activated factor IIa). Thrombin then stimulates the formation
of fibrin (factor Ia) from fibrinogen (factor I) Flowchart 15.2. Fibrin in
combination with fibrin stabilising factor (Factor XIII), forms a stable fibrin clot
at the site of injury. This also initiates a thrombus resolving cascade where the
fibrinolytic agents, such as plasmin form fibrin degrading products
Flowchart 15.3. Any excess amounts of clotting factors which are formed are
inactivated by fibrin inhibitors, such as antiplasmin, antithrombin III and
protein C, limits clot formation.
Table 15.2
Factors of the coagulation cascade
Factor Other name Pathway

Factor I Fibrinogen Both
Factor II Prothrombin Both
Factor III Tissue factor, tissue thromboplastin Extrinsic
Factor IV Calcium Both
Factor V Proaccelerin, labile factor, accelerator (Ac) globulin Both
Factor VI Accelerin
(Va)
Factor VII Proconvertin, serum prothrombin conversion accelerator (SPCA) Extrinsic
Factor VIII Antihaemophilic factor A, platelet cofactor 1, anti-haemophilic globulin Intrinsic
(AHG)
Factor IX Christmas factor, platelet thromboplastin component (PTC), Intrinsic
antihaemophilic factor B
Factor X Prothrombinase, Stuart−Prower factor Both
Factor XI Plasma thromboplastin antecedent (PTA) Intrinsic
Factor XII Hageman factor, contact factor, glass factor Intrinsic
Factor XIII Fibrin-stabilising factor (FSF), Protransglutaminase, fibrinoligase, Both
fibrinase
FLOWCHART 15.2 Pathway of coagulation.
FLOWCHART 15.3 Activation of plasmin.
Clot formation or coagulation can be inhibited in states of

hypercoagulability using drugs like warfarin, heparin, coumadin, etc.
4. Tertiary haemostasis consolidation of fibrin clot

Tertiary haemostasis comprises of:
1. Maturation of the clot

2. Cross linking of fibrin monomers within the clot
3. Controlled activation of the fibrinolytic system.
This phase of haemostasis determines the lifespan of the clot. When the
initial clot is formed, the clot undergoes shrinkage as the platelets attached to
the fibrin strands contract. The clot becomes a tightly sealed patch (Fig. 15.2).
This process of reinforcement is called clot retraction.
FIGURE 15.2 Fibrin mesh.
Clot dissolution can be inhibited by drugs like tranexamic acid,

desmopressin, epsilon amino caproic acid, etc.
Methods of achieving haemostasis

1. Mechanical methods
• Pressure
• Haemostat
• Sutures and ligation
2. Chemical methods
• Adrenaline
• Thrombin
• Surgicel
• Surgicel fibrillar
• Oxycel
• Gelatine sponge: Gelfoam/Surgifoam
• Microfibrillar collagen (Avitene)
• Fibrous glue
• Styptics and astringents
• Alginic acid
• Natural collagen sponge
• Fibrin sponge
• Bone wax
• Ostene: A new water-soluble bone haemostatic agent
3. Thermal agents
• Eletrocautery/Surgical diathermy
▪ Monopolar diathermy
▪ Bipolar diathermy
• Cryosurgery
• Lasers
1. Mechanical methods
Pressure
Firm pressure should be applied over the bleeding site using either fingers or
gauze for at least 5 min. This would control most haemorrhages by
counteracting the hydrostatic pressure of the bleeding vessel.
Haemostat
Application of haemostat at the bleeding points helps in direct occlusion of the
bleeding vessel.
Sutures and ligation

Severed blood vessels may be tied with ligatures. A ligature replaces the
haemostat as a permanent method of effective haemostasis. For large pulsatile
artery, a transfixation suture to prevent slipping is indicated. Non-resorbable
sutures such as silk and polyethylene are used as they evoke less tissue
reaction.
2. Chemical methods
Adrenaline
Topical application of adrenaline brings about vasoconstriction of bleeding
capillaries (Fig. 15.3). Adrenaline is available in ampoule, which is applied
with the help of gauze. The concentration of 1 in 10,000 is used for haemostasis
over the oozing site.
FIGURE 15.3 Adrenaline.
Thrombin
Thrombin helps in converting fibrinogen into fibrous clot and acts as
haemostat.
Surgicel
Surgicel was introduced in 1940 as an oxidised cellulose polymer obtained by
dissolving pure alpha-cellulose in an alkaline solution (Fig. 15.4).
• It acts by forming acid products from partial dissolution that
coagulates the plasma proteins to form a black or brown sticky
gelatinous clot.
• The applied surgicel resorbs from the site in 4 to 8 weeks.
• However, the disadvantage is that the surgicel clot is not formed by
normal physiological mechanism.
FIGURE 15.4 (A) Surgicel. (B) Surgicel in use for craniofacial

surgery.
Surgicel fibrillar
• This is modified surgicel or oxidised regenerated cellulose in layers

that can be adapted to irregular surfaces and inaccessible areas.
• Complete resorption occurs in 2 weeks.
Oxycel
• Oxycel is an oxidised cellulose polymer product.

• This absorbable haemostatic material is manufactured by controlled
oxidation of cellulose using nitrous dioxide.
• The cellulosic acid (cytotoxic acid) present in oxycel has affinity for
haemoglobin which leads to the formation of artificial clot.
• It should be applied on the dry surface as the acid formed during the
wetting process inactivates the thrombin.
• The platelets plug into its meshwork like surface and helps in clot
formation.
• In addition, the pressure of the mass itself enhances the coagulation.
• It has bacteriostatic property because of its relatively low pH.
• At this pH few bacterial proteins are deactivated and denatured,
making the bacteria more sensitive for antibiotics.
• It favourably attaches to bone in extraction socket with satisfactory
haemostasis.
• It is available in gauze form or pellet form.
• Oxycel is composed of hollow ‘twisted tubule’ fibres in comparison to
the irregular solid fibres of surgicel.
Gelatine sponge or gelfoam or surgifoam
• Gelfoam is manufactured from purified pork skin gelatine (Fig. 15.5A

−B).
• This is a nonantigenic and completely absorbable material.
• It has the capacity to absorb 45 times its weight in blood.
• It resorbs completely in 4 to 6 weeks.
FIGURE 15.5 (A) Gelfoam. (B) Comparison of Surgicel and

Gelfoam.
Microfibrillar collagen (Avitene)
• Collagen derived from bovine skin causes contact activation in

addition to direct platelet aggregation.
• In spite of its advantage of causing minimal swelling it tends to reduce
platelet count in normal individuals and ineffective in
thrombocytopaenia.
• Its absorption time is 3 months.
Fibrin glue
• It is a biological adhesive which contains thrombin, fibrinogen, factor

VII, aprotinin.
Styptics and astringents
• Precipitates protein and arrests bleeding.

• Commonly used styptics and astringents are Monsel’s solution
containing ferric subsulphate and tannic acid.
• Thrombin and gelatine sponge are now widely used.
Alginic acid
• This is available in powder form in special 5-mg packages.

• It is placed over the bleeding sites, a protective film is formed over the
bleeding site, this film com presses the capillaries and stabilises the
blood clot in place.
Natural collagen sponge
• This is a white sponge material, non-antigenic and fully absorbable. It

stimulates the platelet aggregation thereby enhancing haemostasis.
• It activates coagulation factors XI and XIII.
• It is preferred in patients who are susceptible for haemorrhage after
dental surgical procedures.
Fibrin sponge
• The fibrin sponge is non-antigenic and is obtained from bovine

material.
• It is chemically treated to avoid allergic reactions.
• It is applied on the bleeding site especially in post-extraction socket.
• It stimulates coagulation thereby forming a normal clot; it also acts as a
temporary plug over the small injured blood vessels.
• The fibrin sponge is fully absorbed by the tissues within 4–6 weeks.
Bone wax
• Bone wax is a sterilised, non-absorbable mix of waxes.

• Bone wax consists of seven parts by weight of wax (white bees wax,
paraffin wax and an isopropyl ester of palmitic acid), two parts of
olive oil and one part of phenol.
• It is white and available as a solid rectangular plate weighing 2.5 g.
• It is indicated in cases of bleeding from the bone or from chipped
edges of bone.
• The bone wax is softened with the fingers to a desirable consistency
and then applied over the bleeding site.
• Its haemostatic mechanism is through mechanical obstruction of the
osseous cavity containing the bleeding vessels.
• Frequent use may lead to the formation of wax granuloma (foreign
body).
Ostene (a new water-soluble bone haemostatic agent)
• Earlier, the formulations containing naturally obtained bees wax were

used as bone wax which interfered with the normal healing process
and caused inflammatory reactions.
• Ostene is a new bone haemostatic agent, made of water-soluble
alkylene oxide copolymers.
• Ostene showed no incidence of adverse response in the cortical defect
site, medullary cavity or the surrounding tissue.
• With the use of the conventional bone wax, foreign body response
including fibrous tissue infiltration by macrophages, giant cells and
lymphocytes at the sites of the bone defects are not uncommon.
• Further bone wax also displaced the bone marrow and interfered with
bone ingrowth into the defects.
• Ostene, a water-soluble bone haemostatic agent has shown no adverse
tissue response or the interference with bone healing as seen with the
use of bone wax.
3. Thermal agents
Surgical cutting instruments have been modified using thermal agents in order
to achieve haemostasis during surgery. Delivery of heat or cold during the
cutting can be done by electric current (electrocautery), laser beam (like
argon), liquid nitrogen (cryosurgery), radio frequency energy etc. These
thermal agents coagulate and seal the blood vessels as they cut achieving
haemostasis and a bloodless field during surgery. These instruments are also
useful in the surgery of vascular lesions like haemangiomas that can
potentially cause life threatening intraoperative bleeding.
Electrocautery/surgical diathermy
Electrocautery is a surgical technique that depends on thermal effect of electric
current. In electrocautery/surgical diathermy, a high frequency current is
applied to a specific area of the body for the purpose of removal of unwanted
tissue, coagulation, or to create a surgical incision. The frequency of current
used in surgical diathermy units are in the range of 1–3 MHz. Electrocautery is
cleaner, safer and more efficient than many of the alternatives. The instrument
used to perform this procedure is also known as an electrocautery.
Properties of surgical diathermy

Diathermy uses high-frequency electrical current to produce coagulation.
It can also be used to cut as well as cauterise tissue. Electrical frequency
used by diathermy is in the range of 300 kHz to 3 MHz.
In this procedure, the electro conductivity of the human body is used and
the patient’s body forms part of the electrical circuit, the electric current used
usually has no effect on muscles.
Types of diathermy
• Monopolar
• Bipolar
Monopolar diathermy
Monopolar diathermy consists of (Fig. 15.6):
i. High-frequency AC generator (over 20,000 Hz)

ii. Regulator
iii. Foot control
iv. Active electrode
v. Indifferent electrode
FIGURE 15.6 (A) Diathermy equipment. (B) Diathermy indifferent

electrode. (C) Monopolar diathermy tips (active electrode). (D)
Bipolar diathermy tip.
High frequency AC generator—generates alternating current at a very high
frequency.
Regulator—controls the current generated by the AC.
Foot control—the passage of current is controlled by the foot control.
Active electrode—it is the tip of the instrument.
Indifferent electrode—it is a flat electrical plate which is placed on the patient.
When the foot control is pressed, the current passes between the instrument
tip (active electrode) and indifferent electrode. As the surface area of the
instrument tip is less than that of the indifferent electrode (the electrical plate),
high current density is produced around the active electrode which results in
localised heating around the tip of the instrument and minimal heating is
produced at the indifferent electrode.
Bipolar diathermy
Bipolar diathermy consists of:
i. Low power AC generator

ii. Foot control
iii. Two electrodes combined in an instrument (e.g. forceps).
When the foot control is pressed, a low power AC is generated and passes
through the two tips of the same instrument. When the tips are brought
together, a circuit is created producing a localised current. As the current
produced is of small power, the instrument is used only for coagulation and
not for cutting.
Advantages
Diathermy reduces the risk of spark ignition of the anaesthetic gases. The
effect produced by the diathermy depends upon the current intensity and
waveform used. By changing the intensity of the current, various functions are
possible.
Coagulation—small bleeding vessels and capillaries can be coagulated with
the help of this instrument.
Cutting—soft tissues with diffuse capillary network can be incised using
diathermy.
Fulguration—destruction of tissue using an electric current is known as
fulguration. Small growths like papilloma, leukoplakia, etc. can be removed
using diathermy.
Risk and caution
• Can interfere with pacemaker function.

• Arcing can occur when the tip contacts other metal instruments or
implants.
• Superficial burns can occur in spirit-based skin preparation.
• Diathermy burns can occur under indifferent electrode if plate is
improperly applied.
• The indifferent electrode should not be placed near bony ridges.
• The operator should use rubber footwear so as to avoid accidental
burn.
• Should not be used near isolated vascular pedicles or nerves.
Cryosurgery
Cryosurgery is the process of rapidly freezing tissue by exposing it to intensely
low temperatures. Usually a probe containing liquid nitrogen is used. While it
is not an ideal coagulating method, cryosurgery does minimise the extent of
blood loss in extensive ablative surgeries.
Effects of rapid freezing
• Increased concentration of intracellular solutes

• Reduction in intracellular water
• Cell shrinkage
• Cell membrane damage
• Formation of intracellular ice crystals
• Formation of extracellular ice crystals
Technique of application
1. Spray technique
2. Probe technique
3. Forceps technique
General clinical uses
• Solar keratoses
• Seborrhoeic keratoses
• Viral warts
• Skin tags
• Xanthelasmas
• Lentigenous macules
• Actinic cheilitis
• Erosive lichen planus
There are also reports of successful treatment of basal cell carcinoma of skin,
tongue carcinoma and other aggressive jaw lesions.
Cryosurgery is not useful in controlling active bleeding. Since the properties
of lasers were more beneficial and user friendly, laser has replaced cryo-
surgery in many surgical applications.
Apparatus
The apparatus consists of a container in which the pressurised refrigerant
media (gases) are stored as liquid gases. The refrigerant media generally used
are liquid nitrogen at a temperature of –196°C. Other refrigerants are carbon
dioxide, nitrous oxide and freon which may reach a temperature of –20° to –
90°C. A probe is connected to the container through a tube. This probe is
applied on the region of the abnormal tissue. The time required for destruction
of the tissue by the probe depends upon the temperature reached, size of the
lesion and type of the tissue. Freezing and thawing are done alternatively as
many times as necessary for the lesion. This process destroys the tissues.
Disadvantages
1. Delayed bleeding
2. Paraesthesia
3. Neuropathy
4. Nitrogen gas insufflation (nitrogen gas bubbles in skin)
5. Alopecia
6. Cartilage necrosis
Lasers
Laser helps in coagulating small blood vessels. Refer to Chapter 50 Recent
Advances for further reading.
Shock
Shock is a clinical condition characterised by inadequate tissue perfusion and hence
cellular hypoxia.
Classification
Shock can be classified based on the aetiology as:
1. Hypovolaemic shock
2. Vasogenic shock
a. Anaphylactic shock
b. Hypoadrenal shock
c. Systemic inflammatory response syndrome (SIRS)
d. Traumatic shock
3. Cardiogenic shock
4. Septic shock
5. Neurogenic shock
Pathogenesis
Obstruction in the cycle of oxygen delivery to the cell due to failure or
malfunction in any system results in cellular hypoxia leading to vicious cycles
that result in shock. The basic pathology in all forms of shock is impairment of
microcirculation and deranged cell metabolism.
Hypovolaemic shock is explained in detail in this chapter.
The chain of reactions that lead to hypovolaemic shock:
Endogenous compensatory mechanisms
Mild to moderate hypovolaemia is usually compensated by endogenous
mechanisms. They aim to restore circulating blood volume and adequate
blood pressure for vital organ perfusion. The physiological response to
hypovolaemia and the clinical symptoms of the same are explained in
Table 15.3. When there is severe hypovolaemia, these endogenous mechanisms
fail leading to a state called hypovolaemic shock that leads to multi-organ
failure (as depicted in the chain reaction above).
Table 15.3
Classification of response to hypovolaemia

Class Blood loss Physiological response to hypovolaemia
Class I Up to 15% (750 mL) BP Normally compensated by body
Pulse rate
Respiratory rate
Tissue perfusion
Mild tachycardia
Class 15%–30%— (800–1500 • Tachycardia
II mL) • Tachypnoea
• ↑ Diastolic BP
[← Peripheral vascular constriction ← catecholamines ←

hypovolaemia]
• ↑ Pulse pressure
• ↑ Capillary refill time
• Skin—cold and moist
Class 30%–40%— (1500–2000 • Detrimental to survival of vital organs
III mL) • Classic signs of inadequate tissue perfusion
▪ Marked tachycardia (120–140 beats/min)
▪ Tachypnoea
▪ ↓ Systolic BP
▪ Marked vasoconstriction
▪ Diaphoresis
▪ Anxiety
▪ Restlessness
▪ ↓ Urinary output
Class >40% Immediate life threatening situation
IV 1. Marked tachycardia
2. ↓ Systolic BP <60 mmHg
3. Very narrow pulse pressure
4. Marked diaphoresis
5. Obtunded mental state
6. No urinary output
1. Microcirculation
Peripheral vasoconstriction occurs during hypovolaemia leading to redirection
of major volume of blood to the essential organs. This maintains the critical
blood pressure for tissue perfusion in the vital organs like kidney, brain and
heart at the expense of gastrointestinal tract and skin. This mechanism fails
when systolic blood pressure drops to the critical level of less than 60 mmHg.
2. Neuroendocrine mechanism
Hypovolaemia and hypotension induced hypoxia detected by chemoreceptors
and baroreceptors induce an autonomic response. This is characterised by
decreased vagal activity and decreased adrenergic activity resulting in
compensatory tachycardia and thus increased cardiac output. In addition,
epinephrine and ACTH induced cortisol secretion increases glycogenolysis,
gluconeogenesis with decreased peripheral glucose uptake.
3. Renal mechanism
The kidney helps to maintain circulatory blood volume by renal shut down or
acute renal failure, a complication of hypovolaemic shock. This mechanism
aims to conserve body electrolytes and water.
Management of hypovolaemic shock

1. Monitoring of vitals: Pulse, blood pressure (both arterial and venous).
2. Assessment of state of shock by haemodynamic parameters such as
cardiac output, oxygen saturation, etc.
3. Attempt to restore circulating blood volume immediately through
intravenous fluid administration Flowchart 15.4.
4. Identify the cause of blood loss and treat the cause.
FLOWCHART 15.4 Management of hypovolaemic shock.
CHAPTER 16
Wound Care
Surgical drains
Indications
Principles
Types of drains
Gauze drains
Simple rubber drains
• Corrugated rubber drain
Suction drains
• Hemovac
• Jackson-Pratt drain system
Complications
The most common cause for operative infection and pain is debris that left
behind within the wound. Wound debridement or ‘toilet of wounds’ is thus an
important step in avoiding postoperative complications.
Debridement includes the removal of any pathological tissues such as tooth
follicle, sinus tract, food debris, remnants of tooth, bone and any other particle
that may hinder the normal healing process.
Surgical drains
Surgical drains are used for evacuation of pus, pooled blood, serum from
wound, other fluids (e.g. lymph) from the body cavities. It may also be used to
eliminate potential dead space. Drains are usually made of inert material such
as latex, polyvinyl chloride (PVC), silastic and polyurethane polymers, which
induce minimal tissue reaction.
Indications
• Clean wounds with potential of inadequate haemostasis (e.g. exposed
medullary bone)
• Contaminated or infected wounds
• Following incision of an abscess
• To obliterate postsurgical dead space that may fill with blood, serum
(haematoma, seroma) and get subsequently infected
• Treatment of osteomyelitis of mandible (drainage and irrigation)
• Drainage of maxillary antrum through nasal antrostomy
• To maintain graft in close relation to the recipient bed.
Principles
• Insert the drain into the most dependent part of the cavity
• In cases of infections as abscess and/or osteomyelitis noncollapsible
drain that facilitate irrigation shall be chosen
• Drain should preferably exit the wound through a separate stab
incision away from the necrotic unhealthy tissue
• Fix it with a suture or any other device to prevent the drain from
getting dislodged into or away from the wound
• Check regularly for the patency of the drains
• Drain removal: When the discharge ceases drain can be removed at
48 h or earlier if drainage becomes minimal
• Drains are also used in clean wound, when there is significant
potential for dead space formation with resultant haematoma or
seroma.
Types of drains
There are three classes of drains commonly used in oral and maxillofacial
surgery:
1. Gauze drains (open passive drains)

2. Simple rubber drains (open passive drains)
3. Suction drains (closed active drains)
1. Gauze drains (Fig. 16.1)

• Nonmedicated or medicated (Iodoform)
• Promote clotting of blood and plasma
• Act as plug rather than drains
• Gauze drains are rarely used nowadays except for few indications as
marsupialised cavity
FIGURE 16.1 Gauze drain for maxillary sinus exiting through nasal
antrostomy.
2. Simple rubber drains (Fig. 16.2)

Simple rubber drains include:
• Red rubber catheter

• Rubber dam material
• Latex Penrose drain
• Corrugated rubber drain, etc
FIGURE 16.2 (A) Simple drain—perforated and nonperforated. (B)
Simple drain placed for draining Ludwig’s angina.
Corrugated rubber drain

Rubber sheet with corrugations on the surface. One end is inserted into the
dead space containing the fluid and the other end projects out through the
incision line. Antiseptic solutions can be instilled through these drains in deep
wounds.
Functions
• Evacuates pooled blood, infected materials thus eliminating dead

space
• Maintain patency of wound
• Provide a channel for movement of pus/blood by pressure or gravity
Advantages
Adaptable, soft, inexpensive.
Disadvantages
• Do not prevent clotting

• Do not facilitate irrigation
• Do not allow suction to be applied to wound
• Require a bulky external dressing to absorb the drainage that
potentiates infection.
3. Suction drains (Fig. 16.3)

Suction drains act by eliminating pooled blood, serum from the wound cavity
as well as dead space, thus drawing separated tissue surfaces together. It
consists of polyethylene tubing (perforated/nonperforated) attached to a
closed suction system (sterile container).
FIGURE 16.3 (A) Suction drain (Hemovac). (B) Vacuum drain in
place after TMJ surgery.
Example: Hemovac, Jackson–Pratt drain system (J–P system).
Hemovac
Hemovac consists of a perforated polyethylene tube with a radiopaque
marker. This is a closed suction system, where the tube is attached to the
compressible vacuum-generating device. The evacuated material is collected
and maintained in a closed sterile container.
Advantages
• Avoids bulky absorptive dressing that holds contaminants against the

wound.
• The amount of drainage can be assessed easily.
• As the drainage is collected in sterile container it can be used for
culture and sensitivity.
Disadvantages
• The rigid polyethylene tubing can irritate tissues.

• Lumen often becomes clogged by adjacent connective tissues muscles
or necrotic debris.
• Cannot facilitate irrigation.
• Presence of drain increases risk of infection.
• Risk of damage to adjacent vital structures from suction.
Jackson–Pratt drain system

This type of drain system was introduced by Frederick E. Jackson and Richard
A. Pratt, III in 1971. In maxillofacial facial surgery, this drain is commonly
used after neck dissections, temporal bone resections and sialadenectomies.
This system also plays a major role in the drainage and irrigation of facial
abscess, osteomyelitis of mandible, elimination of dead space and prevention
of haematoma formation. The J–P drain system consists of flat and round
perforated drain made of high tensile strength silicone rubber, suction
reservoir, extension tubing, T tubes, etc.
Advantages
• Soft nature of silicone rubber resists intraluminal clotting

• Does not cause erosion of adjacent vessels or compress nerves
• It can also be used as an irrigating drain in case of abscess or
osteomyelitis
• Reliable aerobic culture can be obtained
• No need of separate puncture wound, as the flat shaped drain can be
brought out through the same incision line.
Disadvantage
Bulkier than simple rubber or Hemovac drain.
Complications
• Drains can stimulate a foreign body reaction in the adjacent tissues.
• Rigid drain can damage vital structures as vessels, glands, etc. Soft
drains such as Penrose drains, J–P system avoids this complication.
• Round drain creates an area of dead space around its site of securing to
tissues that collects fluid, organisms and impedes healing. Flat drains
such as J–P system avoids this complication.
• Potentiation of infection by drain itself.
• Blockage of drain.
• Drain can slip into or out of the surgical site.
SECTION VI
Minor Oral Surgery
Chapter 17: Exodontia

Chapter 18: Impaction
Chapter 19: Endodontic Surgery
Chapter 20: Preprosthetic Surgery
Chapter 21: Dental Implantology
CHAPTER 17
Exodontia

Absolute contraindications
Relative contraindications
Surgical Plan
Anaesthesia
Local anaesthesia for extraction
General anaesthesia for extraction
Intra-alveolar extraction
Position of the patient
Position of the operator during extraction
Mechanical principles in tooth extraction
Armamentarium
Order of extraction
Postoperative instructions
Extraction of deciduous teeth
Open method (transalveolar extraction)
Indications
Complications occurring during the surgical procedure
Complications occurring after the surgical procedure
Soft tissue injury
Extraction of the wrong teeth
Fracture of the teeth during extraction
Fracture of tooth root
Fracture of the alveolus
Fracture of tuberosity
Displacement of the tooth into the maxillary sinus
Creation of oroantral fistula
Fracture of mandible
Breakage of instruments
Luxation of adjacent tooth
Injury to inferior alveolar nerve
Injury to lingual nerve
Swallowing of teeth
Aspiration of teeth
Dislocation of condyle
Complications occurring after the surgical procedure
Presence of bony spicule
Haemorrhage
Dry socket
Infection
Ideal tooth extraction is
The painless removal of the whole tooth, or root, with minimal trauma to
the investing tissues, so that the wound heals uneventfully & no post-
operative prosthetic problem is created.
(Geoffray L Howe)
Exodontia or extraction is a minor oral surgical procedure performed for the

therapeutic removal of teeth from the oral cavity, using proven techniques and
specialised instruments, causing minimal trauma to the attaching apparatus
and least injury to the surrounding tissues, in a pattern conducive to
uneventful healing in order to achieve best possible prosthetic rehabilitation.
Intra-alveolar (closed) extraction of teeth is the wrenched removal of an
erupted tooth by expansion of the bony alveolar socket alone, using principles
of lever, wedge and wheel.
Transalveloar (open) extraction is a minor surgical procedure performed
for the therapeutic removal of impacted, unerupted teeth that includes access
through a surgical flap for visualisation and appropriate bone removal to
create a path for delivery and facilitate extraction.

• Deeply carious tooth with pulpal pathology: Either acute or chronic
pulpitis where a successful endodontic therapy is not possible or
patient unwilling.
• Teeth with apical pathology: A tooth with apical pathology should be
extracted if it fails to respond to conservative treatment. Such teeth are
extracted before they involve the adjacent teeth.
• Periodontitis: Periodontally compromised teeth, which are not
salvageable by periodontal therapy and teeth with guarded prognosis.
• Malpositioned and overerupted teeth: Should be extracted if they
disturb the occlusal harmony.
• Impacted: If the impacted tooth is found to be responsible for facial
pain, periodontal disturbance of the adjacent tooth, TMJ problems or
bony pathology like cyst.
• Retained deciduous teeth: If the primary tooth is retained beyond its
chronological age of shedding, it should be extracted to prevent the
malocclusion of the permanent dentition.
• Tooth in the line of fracture: Teeth which are in the line of fracture
should be extracted if
▪ There is a potential source of infection (dental caries, fractured
teeth).
▪ Their retention interferes with the reduction of the fractured
segments.
• Teeth with fractured root: Teeth with a vertical fracture extending into
the root of the tooth cannot be treated conservatively.
• Orthodontic purpose: For the purpose of the orthodontic treatment
certain permanent molars or premolars are extracted (therapeutic
extraction). Serial extraction is also one of the entities wherein
judicious extraction of certain deciduous teeth is done to provide
enough space for the proper eruption of the permanent teeth.
• Prosthetic purpose: Extraction of one or two teeth is justified if it aids
in better design or stability of the prosthesis.
• Before radiation therapy (teeth in line of fire): Patients who have to
undergo radiation therapy for malignant tumour should undergo
extraction of those teeth, which have poor prognosis and are prone to
get infected. This is done to prevent the incidence of
osteoradionecrosis.
• Prophylactic extraction: This procedure is done after a thorough
medical examination in patients with a persistent low-grade fever or
with certain forms of arthritis and iritis. It is also done as a pre-surgical
prophylaxis for patients who have a higher risk of bacterial
endocarditis or rheumatic fever. It may require the removal of all non-
vital teeth as well as those of questionable vitality in an effort to
eradicate all foci and potential foci of infection. Richards in 1932 showed
bacteremia in patients after infected tooth extraction, Okell & Elliott
(1935) showed in a study that Streptococcus viridans was present in the
blood stream in 75% of the 40 patients after extraction. The use of local
anesthetic solution due to the presence of a vasoconstrictor, has shown
a decrease in the rate of spread of infection.
• Root fragments: Fragments of root should be removed as soon as they
are found. However, small pieces of roots may be left as such in the
socket as long as it does not cause any problem. But with advancing
age, it is always risky to leave the fragments, hence should be
removed. In edentulous patients, fractured segments present under
the mucosa constantly get irritated from the overlying denture
resulting in chronic ulcers, which may sometimes undergo neoplastic
changes. The root fragment may themselves undergo cystic or other
pathological changes.

All contraindications whether local or systemic can be relative or absolute
depending upon the general condition of the patient. Whenever the
contraindication is absolute, extreme care must be taken before the extraction
to avoid any risk to the patients.
Systemic conditions falling under this include:
• Uncontrolled diabetes
• Leukemia
• Renal failure
• Cirrhosis of liver
• Cardiac failure
Diabetes
If extraction is carried out in an uncontrolled diabetic patient, he/she would be
more prone to develop infection in the extraction wound extending into the
surrounding tissues. This is due to the deposition of cholesterol in the
peripheral circulation (thinning of arterioles) and secondly, the chemotactic
mechanism, which helps in wound healing, is impaired in diabetic patients.
Diabetic patients undergoing minor surgical procedures may precipitate
into diabetic ketoacidosis due to stress. The stress response leads to a chain of
metabolic and neurohormonal changes, which creates a mechanism for coping
up with stress. The hyperglycaemia induced due to stress is attributed to the
hypersecretion of counter regulatory hormones such as catecholamines,
glucagons, cortisol and growth hormones that antagonise the effect of insulin
by increasing glucose production. This results in a surge in the circulating
glucose from glycogenolysis and impaired use of glucose (hyperglycaemia
impairs glucose use and residual insulin secretion).
Hypertension (Table 17.1)

Hypertension can be of mainly two types:
• Primary—unknown cause (essential hypertension)

• Secondary—which occurs secondary to any other systemic disease
Table 17.1
Guidelines for extraction considering blood pressure in adults
Blood ASA Dental therapy considerations

pressure classification
(mmHg)
<140 and I • Observe routine dental management
<90 • Recheck in 6 months
140–159 II • Recheck blood pressure before dental treatment for three
and/or consecutive appointments; if all measurements exceed these
90–94 guidelines, medical consultation is recommended
• Observe routine dental management
• Implement stress reduction protocol as indicated
160–199 III • Recheck blood pressure in 5 min
and/or • If still elevated, perform medical consultation before beginning
95–114 dental therapy
• Observe routine dental therapy
• Implement stress reduction protocol
>200 IV • Recheck blood pressure in 5 min
and/or • If elevated, do not perform dental therapy, routine or emergency,
>115 until elevated blood pressure is corrected
• Refer to hospital if immediate dental therapy indicated
Extraction can be carried out in mild or moderate hypertension, i.e. when

the systolic pressure is less than 200 mmHg and the diastolic pressure less
than 110 mmHg. Extraction is contraindicated when the blood pressure
exceeds the aforementioned values.
Cardiac disease
The cardiac conditions that most frequently complicate exodontia are
myocardial infarction, angina pectoris and cardiac decompensation. The
surgeon has to follow a few preventive measures such as:
• Obtaining a detailed history preoperatively

• Always obtain the treating physician’s consent
• In the indicated pathologies, administer antibiotics to avoid bacterial
endocarditis due to S. viridans that invades the bloodstream, following
an extraction
• Stress reduction protocol should be followed
Patients on steroid therapy

Patients on steroids may have suppression in the output of
adrenocorticotrophin hormone from the pituitary gland. Even patients for
whom the steroid therapy had ceased years ago show insufficient adrenal
secretion to withstand the stress of an extraction. A physician’s opinion should
be sought and steroids should be prescribed a day or two before and after the
extraction. A detailed history of the systemic complications should be obtained
preoperatively to avoid any adrenal crisis due to stress.
Pregnancy
Special consideration before an extraction in pregnant patient.
• A detailed history about the patient ruling out other related systemic
complications.
• If any other complication is foreseen, an expert opinion from a
gynaecologist should be obtained.
• If the procedures are elective, then the treatment should be scheduled
during the second trimester, which is considered as the optimum time.
• Patient should be positioned comfortably in supine position or left
lateral if feasible.
• Local anaesthetics such as lignocaine, bupivacaine and codeine are
believed least likely to harm a foetus.
• Emergencies because of pain, infection or other acute problems can be
accomplished under general anaesthesia, bearing the safety norms. If
general anaesthesia (GA) is necessary, combination of an intravenous
short-acting barbiturate (pentothal), muscle relaxant (succinylcholine)
and nitrous oxide is the method of choice.
• Drugs to be avoided in pregnant patient are as follows:
▪ Aspirin and other nonsteroidal antiinflammatory drugs
(NSAIDs)
▪ Carbamazepine
▪ Chloral hydrate (if chronically used)
▪ Chlordiazepoxide
▪ Corticosteroids
▪ Diazepam and other benzodiazepines
▪ Diphenhydramine hydrochloride (if chronically used)
▪ Morphine
▪ Pentazocine hydrochloride
▪ Phenobarbital
▪ Promethazine hydrochloride
▪ Propoxyphene
▪ Tetracycline
▪ Metronidazole
Blood dyscrasias
• Anaemia, haemorrhagic diseases such as haemophilia and leukaemia

are blood dyscrasias that present many problems during extraction.
• Profuse bleeding complications should be dealt with careful
evaluation. A preoperative laboratory investigation confirming the
integrity of coagulation cascade avoids complications.
• An expert opinion from a haematologist can be acquired to avoid
complications during recovery of the patient. Refer to Chapter 6
Management of Medically Compromised.
Patients on anticoagulant therapy

Patients on anticoagulant therapy who are to undergo oral surgical procedure
may face prolonged postoperative haemorrhage and/or fatal thromboembolic
accidents or within 6 months of myocardial infarction. Preoperative
assessment of the blood clotting and profile including BT, CT, PT, INR is
mandatory. Refer to Chapter 6 Management of Medically Compromised.
Toxic goitre
Extraction can precipitate a thyroid crisis in known hypertensive patient. The
symptoms manifested by a patient with thyroid crisis are altered
consciousness, restlessness (which is uncontrollable even with heavy
sedation), cyanosis and delirium with an extremely rapid, thready pulse and
high temperature. Under these conditions no surgical procedures should be
performed and the patient requires medical attention.
Jaundice/Hepatitis
The postoperative complication of this condition is haemorrhage. If extraction
is imperative, prophylactic doses of vitamin K should be administered before
operation. Care is taken in use of local anaesthesia (LA) and drugs that
metabolise in the liver in order to avoid workload on the liver.
Renal disorders
Nephrotic patients pose a challenge during exodontia, as extraction of
chronically infected teeth often provokes an acute nephritis. Nephrotic
patients should always undergo dental procedures after due consent from the
concerned physician.
Patient on renal dialysis and heparination can undergo extraction, following
certain protocols. Refer to Chapter 6 Management of Medically Compromised.
Medically compromised patients

Treatment for this group of patients is the most challenging and risky task,
and hence preoperative evaluation of these patients’ general condition is must.
Any associated systemic condition can interfere with the dental treatment.
Iatrogenic effects due to drug interaction should be avoided.
Extraction of teeth in recently irradiated patients

This group of patients needs special attention as the blood supply to the jaws
is reduced due to radiation therapy. Osteoradionecrosis is the condition of the
jaws, which occurs as a result of trauma added with infection, and hence it is
advisable to avoid extraction in these conditions.

A tooth can be atraumatically and successfully extracted out of the socket
depending upon the technique used, morphology of the tooth, its position in
the dental arch and condition of the surrounding bone.
Before the removal of the tooth, preoperative radiographs are taken for
assessment of the tooth to be removed.
The preoperative assessment should cover the following points:
• Morphology of the crown

▪ Normal
▪ Macroform/microform
▪ Abnormal/deformed
• Morphology of the roots (dilacerated, fused, impacted, ankylosed,
hypercementosed or divergent roots)
• The density of the bone surrounding the tooth
• The relationship of the tooth to adjacent teeth and other important
anatomical structures as inferior alveolar canal
• Presence of any pathology of the tooth or the bone surrounding it
• Condition indicating dental or dentoalveolar deformities such as
osteitis deformans, hypercementosis, cleidocranial dysostosis—hooked
root, therapeutic irradiation, osteopetrosis, etc.
Indications
1. Previous difficulty with extractions and attempted extractions

2. Close approximation with important anatomical structures
3. Abnormal root pattern—third molars, misplaced canine
4. Tooth having periodontal problem and some sclerosis—
hypercementosis
5. Trauma to tooth—fracture of tooth, roots and alveolar bone
6. Isolated and unopposed maxillary molars
7. Partially erupted, unerupted tooth and retained roots
8. Delayed erupting or having abnormal crown
Surgical Plan
Based on complete evaluation of the patient the surgeon must decide whether
the treatment should be undertaken in the hospital or in the dental office. Also
to be considered are the types of anaesthesia—local or general, the number
and frequency of visits. Supportive measures such as preoperative sedations,
antibiotics, dietary supplements and other drugs must be considered based on
the surgical plan and patient’s general physical condition. Surgical
consideration as needed for bone removal, soft tissue removal, sectioning of
tooth, etc. are assessed preoperatively.
Anaesthesia
Most of the minor surgical procedures can be performed under local
anaesthesia successfully; however, in certain situations, general anaesthesia
may be necessary, e.g. when the patient is allergic to local anaesthetic,
uncooperative patient. Choice is determined by a group of factors such as type
or extent of the operation, patient’s preference (physical or mental condition),
age of the patient, condition of the operative site (presence of infection) and
place of operation (dental setup/hospital setup).
Local anaesthesia for extraction

For the extraction of erupted and the impacted ones, local anaesthesia is the
safest available method. But there are certain restrictions of local anaesthesia
such as:
• Some conscious patients cannot tolerate lengthy surgical procedures

carried out under local anaesthesia.
• Children under the age of 8 years cannot differentiate between the
sensation of pain and pressure and hence they presume pressure as
pain and become uncooperative. Even an older individual who is
nervous can have the same problem.
• If there is an area of acute infection, it is not advisable to inject the local
anaesthetic solution in that area for risk of spreading infection and
failure of anaesthetic effect due to acidic environment.
General anaesthesia for extraction

For shorter procedures lasting less than 10 min, intravenous injection followed
by inhalation anaesthesia is suitable but if the procedure is beyond this time,
an endotracheal intubation should be used.

Teeth can be extracted in two ways:
• Closed or intra-alveolar. In this technique, the tooth is extracted in a

simple manner using forceps.
• Open or transalveolar. In this technique, amucoperiosteal flap is elevated
and the tooth is extracted surgically.
Intra-alveolar extraction
Position of the patient
The best possible position is one that is comfortable for both the patient and
the surgeon. This position should allow the surgeon to keep his/her arm close
to his/her body, which lends stability and support and also allows to keep
his/her wrist straight enough to deliver maximum controlled force to the
patient’s tooth through the forceps. The force should be delivered with the
arm and shoulder but not with the hand.
Position of the patient’s head, neck and trunk (Fig. 17.1)

The chair is adjusted in such a way that the head, neck and trunk are in one
line, this will nullify any strain caused by stretching it backward or pushing it
forward.
FIG. 17.1 Position of patient–head, neck and trunk in one line.
Angulation of the chair

When the mouth is open, the chair is angulated in such a way that the
operative field is in the most visible and accessible position. The chair should
be angulated in such a way that the occlusal surface of the mandibular teeth
are parallel or at 10 degree to the floor, when the operator is working on the
mandibular teeth and standing in front of the patient.
When the operator is standing behind the patient, the angle of the occlusal
plane of the mandibular teeth is increased until the tooth or teeth can be
grasped without placing the dentist or his/her arm and hand in an awkward
position.
When working on the maxilla, the chair should be angulated so that the
occlusal plane of the maxillary teeth is between an angle of 45 and 60 degree to
the floor.
Height of the chair

Procedures on the mandible (Fig. 17.2): The occlusal plane of the mandibular
teeth should be at or slightly below the level of surgeon’s elbow.
FIG. 17.2 Position of the operator during extraction of fourth
quadrant teeth. Note the surgeon’s elbow above the mandibular
occlusal plane. ( Scan to play Exodontia–extraction of 48)
Procedures on the maxilla (Fig. 17.3): The occlusal plane of the maxillary teeth
should be above the level of the surgeon’s elbow towards his/her shoulders.
FIG. 17.3 Position of the operator during extraction of maxillary

teeth–note the surgeon’s elbow below the maxillary occlusal plane.
( Scan to play Exodontia–extraction of 28)
Position of the operator during extraction

The surgeon should position him-/herself in such a way that he/she can apply
the forces necessary for extraction without any stress to his/her own back or
shoulders. The dentist should stand as erect as possible with his/her weight
equally distributed on each foot.
For the extraction of maxillary teeth (Figs. 17.4–17.6)
The surgeon should stand on the right side and in front of the patient with the
bent elbow for posterior and straight for anterior teeth and should apply the
forceps onto the tooth while the other hand holds the alveolus with the finger
and thumb on either side of the involved tooth.
FIG. 17.4 Extraction of maxillary teeth. Position of the surgeon in

front of the patient. Note the surgeon’s elbow below the maxillary
occlusal plane.
FIG. 17.5 Extraction of maxillary anterior teeth—dominant (right)
hand holds the forceps while nondominant (left) hand supports the
alveolus. ( Scan to play Exodontia–extraction of 23)
FIG. 17.6 Extraction of maxillary right posterior teeth. Dominant

hand holds the forceps while nondominant hand supports the
alveolus.
For the extraction of mandibular teeth (Figs. 17.7–17.9)

The surgeon should stand on the right side of the patient for both the
quadrants. For the extraction of the left lower side, the operator should stand
in front of the patient; and for the right lower side, the operator should stand
behind the patient. Apart from supporting the alveolus on each side by the
thumb and forefinger, the left hand should also support the mandible.
FIG. 17.7 Dominant hand holding the forceps nondominant hand

retracts cheek, tongue in addition to supporting the mandible.
FIG. 17.8 Extraction of right mandibular posterior teeth. Forceps
beaks engage the buccal and lingual furcation. Nondominant hand,
thumb and forefinger retract and support the alveolus while the
palm and remaining fingers support the mandible.
FIG. 17.9 Extraction of mandibular anterior teeth. Forceps beaks

applied to the CEJ. Nondominant hand thumb and forefinger
retracts and support the alveolus.
Access and visual field
Good access and clear visual field is important for successful removal of the
teeth.
Use of controlled force

The forces applied to remove teeth should be always kept under control.
Elevators help in widening the periodontal ligament space thus loosening the
teeth before its removal. Forceps help in the removal of the teeth by applying
rotatory forces and buccal and lingual movements.
Unimpeded path of removal

Whenever there is any resistance to the removal, sectioning of the teeth
(odontectomy) should be considered. Malposed, impacted and deeply carious
teeth do not have a clear path of removal and therefore must be sectioned
before removal.
Expansion of bony socket

Expansion of bony socket is specially considered for forceps extraction. When
force is applied, bony socket expands resulting in slow separation of
periodontal ligament from bone.
Mechanical principles in tooth extraction

Once adaptation and securing the grip of the instrument over the tooth is
done, the forces to be applied should be in a predetermined direction, which
depends on certain mechanical principles. A clear understanding of these
principles is very necessary to carry out an extraction successfully.
The following mechanical principles are used in extracting a tooth:
• Lever principle of first order

• Wedge principle
• Wheel and axle
Lever principle
The lever principle has three basic components: fulcrum, effort and load. In a
lever of first class, the position of fulcrum is between the effort and the load. In
this principle to gain a mechanical advantage, the effort arm on one side of the
fulcrum should be longer than the load arm on the other side of the fulcrum.
The force is transmitted at the long effort arm and a mechanical advantage is
gained at the short load arm (Fig. 17.10).
FIG. 17.10 Lever principle. x-long arm; y-short arm; E = Effort

(handle, hand), R = Resistance (tooth), F = Fulcrum (alveolar
crestal bone).
Application
Forceps (Fig. 17.11)

When used alone, this principle is not of much advantage in forceps. However,
if used in combination with wheel and axle, it proves useful. The hinge of the
forceps acts as a fulcrum while the two arms represent each component of the
lever. The length of the handle in relation to the blade represents the
mechanical advantage. To gain a mechanical advantage, the grip should be
farther from the fulcrum and the blade should be shorter.
FIG. 17.11 Lever principle in forceps. Hinge = fulcrum,
beaks = short arm, handles = long arm, teeth = resistance,
hand = effort.
Elevators (Fig. 17.12)

This principle is used in elevators wherein the handle of the elevator
represents the effort and the working end, which engages the tooth represents
the load.
FIG. 17.12 Lever principle in elevators. Tooth and working

tip = load, handle = effort, external oblique ridge (buccal
bone) = fulcrum.
Wedge principle
The wedge consists of two movable inclined planes with a base on one end
and a blade on the other end, which overcomes a large resistance at right
angles to the applied force. The effort is applied to the base of the plane and
the resistance has its effect on the slant side (Fig. 17.13).
FIG. 17.13 Wedge principle. E = Effort, R = Resistance,

F = Fulcrum, Mechanical advantage of wedge is 2.5.
Application (Figs. 17.14 and 17.15)

Wedge principle can be used as a sole principle in extracting a tooth. However,
it is more frequently used in conjunction with lever principle. According to
this principle a wedge can be used to split, expand or displace the portion of
the substance that receives it.
FIG. 17.14 Wedge principle in elevators—insertion of straight
elevator between the tooth and the alveolar bone expanding the
PDL space.
FIG. 17.15 Wedge principle in forceps—beaks of forceps inserted

between the mucoperiosteum and tooth, further into PDL space
causing slow alveolar bone expansion.
Elevators
Elevators can also be used based on this principle, for example, when luxating
a tooth from its socket, a straight elevator is applied between the tooth and the
bone to separate the attachment of the periodontal ligament from the bone as
described previously.
Extraction forceps
The forceps is applied using this principle. For carrying out extraction, the tip
of the forceps is inserted in between the mucoperiosteum and surface of the
tooth. When the beaks are inserted further, the mucoperiosteum gets
displaced, the bony sockets are expanded which results in slow separation of
the periodontal ligament from the bone.
Wheel and axle

Wheel and axle is a simple machine being a modified form of lever. The effort
is applied to the circumference of wheel which turns the axle so as to raise the
weight. Greater the diameter of the wheel, more is the mechanical advantage
(MA) (Fig. 17.16).
FIG. 17.16 Wheel and axle. x-radius of wheel; y-radius of the axle,
E = effort, R = resistance, mechanical advantage of crossbar is
4.6.
Application
Applied to elevators (Fig. 17.17A–D)

Crossbar elevators are used for removing the mandibular roots based on this
principle. The working point of this elevator is engaged deep into the space
between the tooth root and the bone and the handle (compared to the wheel) is
rotated. The root is removed from its socket by moving about a circumference
of the circle (compared to the axle), which the roots would have made if they
continued on around.
FIG. 17.17 (A) Illustration of wheel and axle in a car. (B) Wheel and
axle principle in elevators. Position 1—the working point of
crossbar engages the space between the tooth and bone at the
furcation. Note the hand in pronation. (C) Position 2—the working
tip and handle rotates around its axis (axle) with handle acting as
wheel. Note supination of the hand. (D) Demonstration in skull
model application of elevator tip into the buccal furcation.
Extraction forceps (Figs. 17.18 and 17.19)

To remove a tooth, the beaks of the forceps are applied firmly on either side of
the tooth and force is applied in the form of an arc. According to the principle
of wheel and axle, when the force is applied on the handle of the forceps it
results in a bodily rotation of the tooth in the socket, which is ultimately
delivered out.
FIG. 17.18 Application of wheel and axle principle for forceps.
FIG. 17.19 Wheel and axle principle. Note the position of the hand
away from the axle for the mechanical advantage.
To gain a mechanical advantage, always hold the forceps handle (compared

to the wheel) as farther away as possible to increase the effort arm (compared
to the axle). While using the forceps applying this principle, the periodontal
attachment gets ruptured due to the bodily rotation of the tooth. This principle
can be used separately or in conjunction with wedge or lever principle in
removing the teeth.
Armamentarium
The armamentarium for extraction of erupted teeth is wide with variety of
elevators and forceps.
Elevators (Figs. 17.20–17.22)

Elevators are used primarily as levers. A lever is a mechanism for transmitting
a modest force with the mechanical advantage of a long lever arm and a short
effector arm. When correctly used, they are very safe and efficient but when
misapplied they may cause damage to the tissues, bones and other structures.
Parts of an elevator
An elevator has the following parts:
• Handle—this part is used for holding the instrument

• Shank—this part connects the handle with the blade
• Blade—this part of the instrument engages the crown or the root to be
removed
Indications for the use of elevators
• To reflect mucoperiosteum
• Elevators can be used to widen the periodontal ligament space before
applying the forceps for extraction (wedge/lever principle)
• To luxate and remove the tooth from its socket which cannot be engaged
with forceps
• To remove a fractured or carious tooth or roots which might fracture
when engaged with beaks
• To remove interradicular bone
• To remove a fractured root when the fracture line is below the cervical
margin of alveolar bone
Classification of elevators
According to the form:
• Straight
• Angular
• Crossbar
Commonly used elevators are:
• Periosteal elevators
• Crossbar elevators
• Apexo elevators
1. Periosteal elevators
Periosteal elevators are used particularly for the reflection of the
mucoperiosteum from the underlying bone before extracting the teeth
(Fig. 17.23).
2. Apexo elevators (Figs. 17.24–17.26)
Apexo elevators are used for removal of fractured root, impacted maxillary
third molars and impacted cuspids. They are available in various numbers.
• No. 301 straight Apexo elevators are used for the removal of fractured
roots (at the gingival line) of maxillary central and lateral incisors,
bicuspids and cuspids. These elevators are applied on the mesial and
distal sides of the root by using wedge principle to expand the socket.
Finally, when the socket has expanded sufficiently, rotary motion is
applied to remove the root from the socket.
• No. 73 and 74 elevators are used for removing the impacted maxillary
third molars.
• No. 4 (302) and 5 (303) Apexo elevators are used when the mandibular
root has fractured below the gingival line. In these elevators, the blade is
at 90-degree angle to the handle. These are used in a similar manner as
that of the straight Apexo elevators. The No. 4 elevators can be applied on
the mesial aspect of the left lower fractured roots, as well as on the distal
aspect of the fractured root in the right lower side. Similarly, the No. 5
Apexo elevators can be used on the distal side of the fractured roots in the
left lower side, as well as on the mesial side of the fractured roots in the
right lower side. After applying these forceps on the respective sides of
the fractured root, apical and rotary pressure is applied to gain a depth of
2–3 mm in between the fractured tooth root and the bone to expand the
socket. If this depth is not obtained, a purchase point can be drilled before
inserting the elevator. Alternatively, this pressure is applied on the mesial
and distal side of the root until it luxates out of the socket.
Crossbar elevators
Crossbar elevators are used particularly for removal of mandibular molar
roots and impacted mandibular third molars. It is also known as Winter’s
crossbar elevator. It is available in various numbers such as 11L and 11R, 14L
and 14R, 1L and 1R.
They work on the principle of wheel and axle and can extract with extreme
forces.
No. 11L and 11R. No. 11L crossbar elevator is used for removing right lower
third molar wherein the thick buccal plate acts as fulcrum. The elevator is
inserted from the buccal aspect of the right lower third molar to engage
between the bifurcation of the molar and the elevator is rotated to lift the
tooth out of the socket.
Similarly, No. 11R is used for removing the left lower third molar. These
elevators can also be used to remove the vertically impacted third molars and
roots of horizontally impacted third molars.
No. 14L and 14R. No. 14L elevator (also No.11L) is used to remove the
mesial roots of the right lower molars and distal roots of lower left molars by
engaging the elevator in the adjacent socket wherein the intervening septum
is thin.
No. 14 R elevator (also No.14R) is used in a similar manner to remove the
distal roots of right lower molars and mesial roots of left lower third molars.
No. 1L and 1R. No. 1L and 1R elevators are used to extract vertically
impacted third molars and also for luxating the maxillary and mandibular
teeth before removing them. The elevator is wedged in between the teeth and
anteroposterior force is applied to loosen them, which are then removed with
forceps.
Precautions to be followed in using elevators
• We should never use the adjacent tooth as a fulcrum as this will damage
or even luxate the adjacent tooth.
• We should always use finger guard to protect the patient tissue as
slipping of the instrument tip into the soft tissue might cause tissue
damage.
• The forces applied through the instrument should be under control;
failing to do so would cause fracture of the maxilla, mandible or the
alveolar process. So a control of the instrument with index finger on the
shank is mandatory (Fig. 17.27).
• The instrument tip should deliver the force in the correct direction to
avoid the accidental forcing of the tooth into maxillary antrum.
FIG. 17.20 Application of periosteal elevator in a prying motion—
Lever principle.
FIG. 17.21 (A) Parts of an elevator. (B) Cryer’s paired—right

(R)and left (L). (C) Cross bar paired—mesial (M)and distal (D). (D–
E) Various types of elevators.
FIG. 17.22 Application of periosteal elevator (prying motion).
FIG. 17.23 Periosteal elevator.

FIG. 17.24 (A) No. 301 straight Apexo elevators. (B) No. 73 and
No. 74 Apexo elevators. (C) No. 302 Apexo elevators and No. 303
Apexo elevators.
FIG. 17.25 (A–E) Removal of root using No. 301 Apexo elevators.
FIG. 17.26 Removal of root tip using No. 302 Apexo elevator.
FIG. 17.27 (A) Crossbar–palm grasp with the index finger placed
over the shank for delivery of controlled force. (B) Application of
elevator demonstrated in a skull model. (C) Application of Cryer’s
elevator in extraction of maxillary third molar.
Forceps
Forceps or elevators are the main instruments used in the extraction of teeth.
Forceps help in dilatation of the alveolar socket, luxation of the tooth and its
removal.
Parts of the forceps
• Pair of handles
• Pair of beaks
• A hinge
The upper jaw forceps have beaks, which are parallel to the long axis of the
handle; the beaks of the lower jaw forceps are at right angle to the long axis of
the handles (Fig. 17.28A–K).
FIG. 17.28 (A) Parts of a forceps. (B) Forceps for extraction of
mandibular anterior teeth and roots. Note approximation of beaks
in root forceps whereas beaks do not meet in the other. (C)
Forceps for extraction of mandibular molars. Two types based on
axis of working end in relation to handle. (D) Application of forceps
for extracting mandibular molar. (E) Buccal and lingual beaks of
mandibular molar forceps designed to engage the furcation
between the mesial and distal roots. (F) Forceps for extraction of
maxillary molars, right and left. (G) Forceps for extraction of
maxillary anterior teeth. (H) Right maxillary molar forceps—buccal
beak is pointed to engage the furcation between MB and DB roots;
palatal beak is rounded to engage the single palatal root. (I)
Special armamentarium for extraction of maxillary teeth. (J)
Maxillary bayonet forceps with angled beaks facilitating extraction
of last molar. Implication of the name is from bayonet gun. (K)
Maxillary cow horn forceps, mandibular cow horn forceps,
implication of the name cow horn.
Principles of use (Fig. 17.29A–F)
The forceps is applied with an apical pressure by inserting the beaks on the
buccal/labial and lingual/palatal aspect of the tooth, in between the bone and
the surface of the tooth so that the beaks rest on the root/roots of the tooth. The
beaks of the forceps should be parallel to the long axis of the tooth. This results
in a minimum apical movement of the tooth and expansion of the socket.
FIG. 17.29 Method of usage of forceps for extraction of teeth. (A)

Before extraction. (B) Apical pressure applied with forceps. (C)
Application of lingual pressure. (D) Application of buccal pressure.
(E) Rotational force applied. (F) Tractional force applied and tooth
removed by the buccal aspect.
Force application
When buccal force is applied, it results in the expansion of the buccal plate.
This movement causes the pressure to be concentrated on the crest of the
alveolar ridge on the buccal aspect and also causes lingual apical pressure.
Then lingual force is applied with a similar concept as aforementioned but in a
lingual direction.
The buccal and lingual forces are applied in combination for the removal of
most of the teeth. As in the maxilla, the palatal bone is thicker when compared
to the buccal bone, the teeth are removed via strong buccal force and less
vigorous palatal force (if stronger palatal force is applied the palatal root tip
may fracture which is hard to retrieve). In the mandible also, the buccal bone
is thinner than the lingual bone particularly in the anterior teeth. Therefore,
the anteriors and the premolars are removed via strong buccal force and less
vigorous lingual force. However, in the molar region, the buccal plate of bone
is thicker; hence, strong lingual force should be applied and the tooth is
removed through the buccal force.
Then rotational pressure is applied on the tooth, which causes expansion of
the socket and rotation of the tooth around its fulcrum, which usually lies near
the apical tip of the tooth root. If the roots of the tooth are very long or if they
are curved or multiplied, then root fracture is more likely when using
rotational force. Conical single rooted are circular in cross-section with
cylindrical root, e.g. maxillary central incisor and mandibular premolars.
Rules to be observed in the application of forceps (Figs. 17.30–17.32)
1. The correct forceps for the particular tooth to be extracted must be

selected.
2. Grasp the forceps at the far end of the handles so that they are almost
covered by the palm of the hand. Do not grasp the forceps near the
beaks.
3. The long axis of the forceps beaks must be parallel to the long axis of
the tooth.
4. Forceps beaks must be grasped firmly on sound root structure and not
on the enamel of the tooth crown.
5. Make certain that the beaks of the forceps do not impinge on adjacent
teeth during the luxation.
FIG. 17.30 Forceps should be grasped at the far end of the handle
away from the beaks for maximal mechanical advantage.
FIG. 17.31 Long axis of forceps beak must be parallel to that of the
tooth without impinging adjacent teeth.
FIG. 17.32 Forceps beak should grasp firmly on sound root

structure (CEJ).
Forces applied for different teeth
Basic forces exerted in extraction of maxillary teeth in normal position in

the arch
As already mentioned, the first pressure applied for the extraction of all
maxillary teeth is apical force. The beaks of the forceps should engage the neck
of the tooth, resting on cementum. Then apply pressure as follows:
Tooth Steps in the procedure Forceps and elevators used

Central Labial pressure, then lingual pressure, then Maxillary universal forceps
incisors labial pressure with mesial rotation.
Lateral Labial pressure, then lingual pressure, then Maxillary universal forceps
incisors labial pressure with mesial rotation.
Cuspids Labial pressure, then lingual pressure, then Maxillary universal forceps
labial pressure with mesial rotation.
First Buccal pressure, lingual pressure and Maxillary universal forceps or no.
bicuspids removal in the buccal direction. 150 forceps
Second Buccal pressure, lingual pressure and removal Maxillary universal forceps or no.
bicuspids in the lingual or buccal direction. 150 forceps
First and Buccal pressure, slight palatal pressure and Maxillary right or left molar
Second distal rotation. forceps for the respective side
Molars
Third molar Maxillary right or left third
molar forceps
Cryer’s paired—right (R) and
left (L)
Basic forces exerted in extraction of mandibular teeth in normal position

in the arch
Similar to the maxillary teeth, the first force is the apical force so that the beaks
of the forceps rest on the cementum. Then apply pressure as follows:
Tooth Steps in the procedure Forceps and elevators used

Central, lateral Labial pressure, lingual pressure; slight Vertical hinge mandibular
incisors and mesial to distal force and removal in the forceps (mandibular anterior
cuspids labial direction. forceps)
First and second Buccal pressure, with slight mesio-distal Vertical hinge mandibular
bicuspids rotation. forceps (mandibular anterior
forceps)
First and second Buccal pressure, lingual pressure and Mandibular molar forceps
molars removal in the buccal direction. (vertical or horizontal hinge
forceps)
Mandibular cow horn
forceps
Third molar Buccal pressure and removal in the buccal or Mandibular right or left
lingual direction. third molar forceps
(Straight elevator)
Straight Bein elevator
(Coupland’s elevator)
Order of extraction
Extraction of the teeth in the maxillary arch should be performed before
mandibular arch as the upper arch gets anaesthetised earlier than the lower
arch. Moreover, extraction of upper arch prior to the lower arch prevents any
inadvertent fall of enamel or amalgam debris into the extraction socket in the
lower arch. This rule can be applied in all cases except for the removal of
impacted teeth.
• Extraction of the most posterior tooth in the dental arch is done first;
this causes haemorrhage to collect in the posterior region so that the
vision to the surgical field is not affected in the anterior region.
• If complete extraction has to be done in a patient with full complete set
of teeth or in whom it is difficult to extract, first molar and canine are
extracted after their adjacent teeth are removed. This results in a better
purchase on the tooth and also has the advantage of earlier plate
expansion resulting from adjacent extractions. These two teeth are
encased in the so-called bony pillar of the face.
• Following the above rules, the order of extraction in an arch of a jaw is:
▪ Third molar
▪ Second molar
▪ Second premolar
▪ First molar
▪ First premolar
▪ Lateral incisor
▪ Canine
▪ Central incisor
In a clinical practice, it is judicious to instruct the patient orally and in a
written form concerning exactly what to do in the next few days. These
instructions normally include:
• Bleeding: The patient must bite firmly on gauze placed over the wound
for 30–45 min. In case bleeding continues, another gauze is placed over
the wound for a further hour.
• Edema: After the procedure, the extra oral placement of cold
compresses (ice pack wrapped in a towel) over the surgical area is
recommended every 15–20 min at a time, and repeated every half
hour, for at least 4–6 h.
• Oral hygiene: The patient should be advised to brush and floss, but
should be advised to avoid the area of surgery. Rinsing the mouth is
not allowed for the first 24 h. After this, the mouth may be rinsed with
salt water, 3–5 times a day for 3–4 days.
• Antibiotics and analgesics: Antibiotics are mandatory for patients who
undergo any invasive procedure. Many study show evidence that
antibiotics administered preoperatively or postoperatively reduce the
risk of infection, pain and dry socket after tooth extraction. Analgesics
advised (e.g. NSAIDS and opioids but not salicylates, aspirin) should
be consumed, as long as the pain persists.
• Diet: The patient’s diet on the day of the surgical procedure must
consist of cold, liquid foods (pudding, yogurt, milk, cold soup, orange
juice, etc.).
• Removal of sutures: Intraoral sutures are usually removed in a week.
Extraction of deciduous teeth

Extraction of deciduous teeth differs slightly from the normal extraction
method used for the permanent teeth. Unlike the permanent teeth, dental
radiographs are essential before the extraction of any tooth.
Indications for extraction of primary teeth
• Gross dental caries involving the pulp that cannot or does not deem
salvage
• Retained deciduous teeth which interfere with the normal eruption of
their permanent successor
• Primary tooth with periapical pathology
• Primary tooth with root fracture
• Serial extraction
Serial extraction
Serial extraction is a form of interceptive orthodontic treatment, which aims to
relieve crowding at an early stage so that the permanent teeth can erupt into
good alignment, thus reducing or avoiding the need for later orthodontic
therapy.
• Chronologically, crowding may become manifested at 7 years of age

on eruption of the incisors, at 10–12 years on eruption of the canines,
premolars or during the adolescence in the form of late labial segment
imbrications.
Indications
• The patient should be between 8 and 9 years of age with crowding of

incisors.
• The fundamental arch relationship should be normal (Angle class I)
showing harmony between skeletal and muscular system.
• Arch length deficiency as compared to tooth material is the most
important indication for serial extraction.
This is indicated by:
▪ Absence of physiological spacing
▪ Unilateral or bilateral premature loss of deciduous canines
with midline shift
▪ Malpositioned or impacted lateral incisor that erupt palatally
out of the arch
▪ Markedly irregular or crowded upper or lower anteriors
▪ Localised gingival recession in the lower anterior region is a
diagnostic feature of arch length deficiency
▪ Ectopic eruption of teeth
▪ Mesial migration of buccal segment
▪ Abnormal eruption pattern and sequence
▪ Lower anterior flaring
▪ Ankylosis of one or more teeth
• There should be normal or reduced overbite and all the teeth should be
seen on radiograph and in good position to erupt.
• There should be a large arch perimeter deficiency of 10 mm or more.
Contraindications
Serial extraction is contraindicated in a number of conditions:
• Class II and III malocclusion with skeletal abnormalities

• Spaced dentition
• Anodontia/oligodontia
• Open bite and deep bite
• Class I malocclusion with minimal spaced efficiency
• Unerupted malformed teeth, e.g. dilaceration
• Extensive caries or heavily filled first permanent molars
• Mild disproportion between arch length and tooth material that can be
treated by proximal striping
Methods
Different procedures have been described by different authors such as;
• Dewel’s method (1978); 8½ years [CD4]

• Tweed’s method (1966); 8 years [DC4]
• Nance’s method (1940); DC4
Dewel’s method–CD4
Proposed a 3 serial extraction procedure
• Removal of deciduous canines to create space for the alignment of the

incisors (between 8 and 9 years)
• A year after, the removal of deciduous first molars to aid quick
eruption of the first premolars
• This is followed by the extraction of first premolars to permit the
permanent canines to erupt in their place
• In some cases, a modified Dewel’s technique is followed wherein the
first premolars are enucleated at the time of extraction of the first
deciduous molars
• This is necessary in the mandibular arch where the canines often erupt
before the first premolars.
Tweed’s method–DC4
• This method involves the extraction of the first deciduous molars

around 8-years of age.
• This is followed by the extraction of first premolars and the deciduous
canines simultaneously.
Nance method–DC4
Nance method is similar to DC4 Tweed’s method.
Extraction technique
Young children have very elastic bone, which expands rapidly when pressure
is applied. The permanent successor of deciduous teeth usually lies below
them and may be closely related to the roots of the deciduous teeth; therefore
extreme care must be taken while extracting the deciduous teeth. During
extraction, if the root is broken it can be left as such because, though not
always, it will get naturally resorbed. Secondly, inadvertent removal of the
root may jeopardise the permanent tooth bud lying below it.
The forceps used for extraction are comparatively smaller than those used
for extraction of the permanent teeth. For extracting mandibular and maxillary
anteriors, labial pressure with mesial rotation is applied and removed to the
labial side. For removing the maxillary and mandibular molars, buccal
pressure is applied followed by lingual pressure and is removed to the lingual
side. The forces required to remove the tooth are very less and the forceps
need not be inserted too deep along the root. The elevators can be used for the
removal of deciduous roots. In case of molars they should be applied distally
for the removal of distal root and mesially for the removal of mesial roots.
If by accident the unerupted or partially erupted permanent tooth is
removed during extraction, it should be carefully replaced into the crypt or
socket and the wound closed. The patients should be instructed not to disturb
that area. The use of curettes should be avoided to remove the granulation
tissue after the extraction of the primary tooth.
Extraction of submerged deciduous teeth

When a deciduous molar undergoes ankylosis of the roots during replacement
resorption, the alveolarbone envelopes this deciduous teeth which seems to
have partially or fully submerged. These teeth are usually identified during
regular radiography. Occasionally they might be a source of infection leading
to sinus formation.
The roots of the submerged tooth are often very slim and have a very thin
periodontal membrane covering or are in direct contact with the bone. It is
extremely important to ensure that all the roots are removed during extraction.
Removal of submerged deciduous teeth is similar to removal of impacted
teeth.
Open method (transalveolar extraction)

Transalveolar extraction refers to surgical removal of a tooth or root that
involves bone removal.
Indications
• Any tooth or root which cannot be removed using elevators or forceps

• Unerupted teeth, impacted teeth
• Tooth with extensively curved or dilacerated roots
• Endodontically treated teeth or grossly carious teeth
• Hypercementosed or ankylosed teeth
• Retained root fragments.
The principles and surgical procedures of transalveolar extraction (open

method) are explained in detail in Chapter 18 on Impaction.
1. Complications occurring during the surgical
procedure
• Soft tissue injury
• Extraction of the wrong teeth
• Fracture of the teeth during extraction
• Fracture of tooth root during extraction
• Fracture of the alveolus
• Fracture of tuberosity
• Displacement of the tooth in to the maxillary sinus
• Creation of oroantral fistula
• Fracture of mandible
• Breakage of instrument
• Luxation of adjacent tooth
• Injury to inferior alveolar nerve
• Injury to lingual nerve
• Swallowing of teeth
• Aspiration of teeth
• Dislocation of condyle
2. Complications occurring after the surgical

procedure
• Presence of bony spicule
• Haemorrhage
• Dry socket
• Infection
Soft tissue injury (Figs. 17.33–17.35)
Types and causes
Abrasion
These injuries are caused by careless use of rotary instruments.
FIG. 17.33 Soft tissue injury—abrasion of corners of mouth from
retraction.
FIG. 17.34 Soft tissue injury—thermal injury from heated rotary

instruments.
FIG. 17.35 Soft tissue injury—oedema and mucosal injury.
Thermal injuries
Caused when instruments taken out from autoclave or hot air oven are used
immediately intraorally.
Mucosal tears
These are caused due to injudicious use of instruments, improper elevation of
flap or the exercise of excessive force.
Prevention
• Take extreme care during the handling of the rotary or other hand
instruments.
• Cool the instruments properly before using to prevent thermal injuries.
Mucosal tears can be prevented by proper designing and elevation of
the flap, by proper handling of the flap and by gentle and effective
manipulation of the elevators.
• Properly retract the cheek and lips during dental procedures thus
avoiding trauma from instruments.
Management
• If the tear or abrasion is large, suturing should be done for closure.

• Scars produced due to thermal injuries can be managed by the
application of petroleum jelly or topical antiseptic/analgesic.
Extraction of the wrong teeth

Management
• Inform the patient.

• Replace the tooth inside the socket as soon as possible and splint it.
• If immediate replacement is not possible, place the tooth in a proper
medium like saliva (the tooth can be held in the buccal vestibule), milk
or water.
• This is followed by treatment and follow up as for traumatic avulsion
and reimplantation.
Fracture of the teeth during extraction
Causes
• Application of the wrong forceps

• Improper application of the forceps
• Improper application of force
• Extensively carious teeth
• Root canal treated teeth
• Endodontically treated teeth
• Curved or hypercementosed root
• Ankylosed root.
Prevention
• Proper radiographic assessment of the shape and degree of carious

involvement of the teeth and root and the condition of the
surrounding bone.
• Proper forceps technique, i.e. proper selection of instrument, proper
application of the forceps and proper application of the force.
• Using transalveolar removal technique whenever intraalveolar
extraction is not feasible.
Management
• When the fracture involves the crown of the tooth appropriate

restoration should be placed.
• Incase of root fracture remove the tooth or root fragment completely
whenever possible.
• In case of close proximity of a small root fragments (less than 5 mm) to
the sinus or inferior alveolar nerve, leave the root as it is unless it is
infected.
Fracture of tooth root
Fracture of the tooth root is a common complication encountered during
extraction. There are many factors responsible for root fracture.
Causes
• Improper technique
• Application of incorrect instrument and force
• Ankylosed teeth or hypercementosed teeth
• Condensing osteitis
• Excessively curved roots
• Endodontically treated teeth
• Teeth with gross filling
• Extensively carious teeth
• Uncooperative patient
Consequences of retained roots

Retained roots may act as a source of infection. They might be a chronic source
of irritation giving rise to neuralgic pain. When large retained roots are lying
in the submucosa just beneath the denture, the overlying mucosa constantly
gets inflamed and may interfere with the proper functioning of the denture.
Methods for retrieval of fractured root

Using appropriate elevators, roots fractured at various levels can be removed.
Forceps with slender beaks can be used to remove certain roots. Reamers
can also be used to retrieve roots. The technique is shown in Fig. 17.36A–D. If
the aforementioned methods fail, transalveolar removal should be attempted.
FIG. 17.36 Removal of fractured root using reamer. (A) Fractured
palatal root in relation to 26. (B) Reamer used to engage the root.
(C) Fractured root removed with reamer. (D) Figure showing the
extracted tooth and its fractured root.
Fracture of the alveolus
Causes
• Improper application of the instruments

• Application of excessive force
• Lack of support to the alveolus during extraction
• Brittle alveolar bone
• Ankylosed teeth
Prevention
• Proper radiographic assessment of the tooth and the surrounding

alveolar structure.
• Proper application of the forceps and elevators.
• Avoid exertion of excessive force.
• Support the alveolus properly during extraction.
Management
• When the bone fragment is completely detached from the periosteum
it is advisable to remove it along with the teeth and suture the flap
back.
• When the bone is attached to the periosteum, it can be replaced back
and the flap closed.
Causes
• In cases where the antrum extends into the tuberosity, the extraction of
third molar can result in fracture of the tuberosity.
• Exertion of excessive force and improper force application.
• Fusion of the roots of second molar with the unerupted third molar
(concrescence)
• Divergent roots of the third molar or hypercementosed third molar.
Prevention
• Take radiographs before extraction to assess the condition of the third

molar and surrounding structures.
• Avoid the exertion of inadvertent force.
• Support the alveolus during extraction.
Management
• If the fractured segment is small, a mucoperiosteal flap is elevated and

the tuberosity is removed along with the tooth, followed by wound
closure.
• If the fractured segment is large and the mucoperiosteum is attached to
the bone, it should be replaced and splinted.
• Prescribe antibiotics, analgesics and nasal drops if the fracture involves
the antrum.
• Removal of the tooth should be done after the healing of fractured site.
Displacement of the tooth into the maxillary sinus
Causes
• The roots of the upper back teeth are always in close approximation to
the maxillary sinus. Sometimes the antral cavities may be large and
may dip in between the apices of the posterior teeth.
• With advancing age the degree of pneumatisation of the maxillary
sinus increases and the antral walls become very thin. Eventually the
roots of the posterior teeth are covered only by thin lamellae of bone,
which fracture easily and result in the disappearance of the root tip
during its removal.
• Sometimes the shape of the tooth may be such that it slips into the
maxillary antrum (like the popping of an orange seed) once the extraction
forceps are applied.
• When there is an isolated maxillary molar, the bone surrounding it
becomes dense and cortical. The sinus dips into the surrounding
edentulous area and thus the tooth becomes prone to fracture and
displacement into the sinus.
Prevention
• Application of appropriate force, which effectively removes the teeth

without any fracture of bone or teeth.
• Avoid injudicious instrumentation to remove a broken root tip.
• Proper radiographs should be taken before the extraction to assess the
proximity of the root tip to the sinus.
• Support the jaw and the alveolus adequately before extraction.
Management
• Confirm the presence and location of the tooth or root tip in the sinus-
using radiograph.
• Once the location is confirmed, keep a nozzle connected to a powerful
suction device at the entrance of the fistula to recover the root.
• Pack along piece of roller gauze into the sinus through the opening and
remove it with a jerk, the root tip or the tooth might sometimes be
removed along with the gauze.
• If none of the aforementioned procedures solves the problem then
Caldwell-Luc operation is carried out.
Creation of oroantral fistula (Fig. 17.37)
Causes
• Close proximity of the posterior teeth to the sinus predisposes to an

oroantral fistula during the extraction of these teeth.
• Injudicious instrumentation to remove a broken root tip.
• All the conditions, which apply to the cause of displacement of the
teeth into the maxillary sinus.
FIG. 17.37 Oroantral fistula in right maxillary molar region.
Prevention
Same as that for displacement of the teeth into the maxillary sinus.
Management
• As far as possible leave the clot as it is and do not disturb it.

• Prescribe antibiotics, analgesics, nasal drops and nasal decongestants
to control any infection.
• For large defects surgical closure is done. Refer to Chapter 32 Maxillary
Sinus and its Implications.
Fracture of mandible
Causes
• Atrophic mandible as in old age

• Existence of any bony pathology
• Excessive/inadvertent force application
• In case of removal of vertically impacted third molar
Prevention
• Proper preoperative assessment of the type of impaction and the

density of the bone before extraction
• Proper support of the jaw during extraction
• Application of adequate force
Management
• Inform and reassure the patient

• ORIF of the fracture accordingly. Refer to Chapter 44 Mandibular
Fractures.
Breakage of instruments (Fig. 17.38)
Causes
• Application of excessive force

• Defect in manufacturing
• Old and worn out instruments
FIG. 17.38 (A) Broken instrument—radiograph showing broken tip
of straight elevator in mandibular left third molar region. (B) Clinical
intraoperative picture showing removal of foreign body. (C) Clinical
intraoperative picture showing removal of foreign body.
Prevention
• Proper selection of the instrument

• Proper handling and usage
Management
• Remove the burs or elevator tips with a haemostat if it is visible.

• If impacted deeply, surgical removal of the instrument is advised
unless contraindicated as in close proximity to vital structures.
Luxation of adjacent tooth
Causes
• Improper instrumentation
• No support to the adjacent structures during extraction
Prevention
• Proper technique and careful handling of the instruments

• Support the adjacent teeth adequately before extraction
Management
• Reposition the tooth inside the socket and splint it

• The tooth should be treated endodontically after 1 week.
Injury to inferior alveolar nerve

Injury to the inferior alveolar nerve may result in paraesthesia or anaesthesia
of the nerve’s dermatome tongue, lip or chin.
Causes
• During the removal of an impacted mandibular third molar, which is

in close proximity to the inferior alveolar nerve.
• Careless manipulation of the instruments resulting in nerve damage.
Prevention
• Proper radiographic assessment of the proximity of the impacted third

molar to the inferior alveolar nerve before its removal.
• Careful manipulation of the instruments.
Management
Nonsurgical management
Delaying surgical repair of injured inferior alveolar nerve is recommended
because most patients are known to recover spontaneously to some degree.
Surgical management
• Decompression if impingement of nerve is present

• Microneurovascular surgery. Refer to Chapter 34 Orofacial Neuropathy
Injury to lingual nerve
Causes
• The nerve may be damaged during the removal of the third molar
when the lingual cortex fractures.
• There is a risk of damage during the elevation of the lingual
mucoperiosteum.
Prevention
Proper technique and careful manipulation of the instruments.
Management
• Reassure the patient, and review regularly.

• If there are no symptoms of recovery or Tinel sign, attempt nerve
repair. Refer to Chapter 34 Orofacial Neuropathy.
Swallowing of teeth
Causes
• Careless handling of the instruments

Management
• Check for breathing difficulty.

• Check for dislodgement of teeth in pyriform fossa by
radiograph/indirect laryngoscopy.
• Confirm the presence of teeth in the GIT.
• Prescribe laxatives.
• Confirm the expulsion of the tooth using serial radiographs.
Aspiration of teeth
• Perform Heimlich manoeuvre and try to retrieve the tooth.

• If unsuccessful, check for breathing.
• Secure emergency airway by cricothyrotomy or tracheostomy Refer to
Chapter 7 Medical Emergencies and their Management, Chapter 10 General
Anaesthesia for details.
Dislocation of condyle
Causes
• Causes. Refer to Chapter 40 Internal Derangements and Condylar

Dislocation
• Exertion of excessive force
• Failure to support the mandible adequately during extraction
• Number of previous episodes of dislocation
Prevention
• Proper exertion of adequate force

• Support the mandible during extraction
Management
• Take a radiograph of the area.

• If the condyle is dislocated into the middle cranial fossa, refer to an
oral surgeon.
• Manual reduction of anterior displacement of the condyle requires
downward pressure on the retro-molar region and simultaneous
upward pressure on the chin.
• Long-standing dislocation may require prolonged traction on the
mandibular ramus under general anaesthesia or open reduction.
• Management of fracture dislocation is either conservative, which aims
at the restoration of a normal dental occlusion and intermaxillary
fixation accepting the displaced position of the condyle or operative
and surgically repositioning of the displaced condyle and internal
fixation of the condylar fracture.
• Recurrent dislocation may also be treated conservatively with a Barrel
bandage, by injection of sclerosant solutions into the pericapsular area
to produce tightening of the capsule or by a variety of operative
procedures, which include capsular plication and laminectomy.
• Reduction of simple condylar dislocation can often be accomplished
with simple analgesia alone or in combination with infiltration of a
local anaesthetic agent into the periarticular tissues. Oral or
intravenous sedation may be necessary. General anaesthesia may be
required if the previous methods fail.
• Operative correction of recurrent dislocation requires general
anaesthesia and several days of in-patient stay.
Complications occurring after the surgical

procedure
Presence of bony spicule
Cause
Improper and careless technique of extraction.
Prevention
Checking the socket for any sharp edges before closure.
Management
Filing or removal of the bony spicule.
Haemorrhage
Bleeding is a common sequela of oral surgery. Refer to Chapter 15 Haemostasis
in Oral Surgery for details. This may be seen in patients.
• With systemic cause

• Without any systemic cause
There are three type of postoperative bleeding:
• Primary—Occurs continuously after the surgery

• Reactionary—Haemorrhage restarts after a period of about 3 h
• Secondary—Occurs after a few days
Causes
In patients without any systemic cause

Primary
• Local infection
• Tear of any major blood vessel
• Punctured wound
Reactionary
• Disturbance of the clot due to activities like chewing hard substances,

gargling, consuming alcohol and taking warm food
• Reactionary vasodilation of the blood vessels which had contracted
during administration of the vasoconstrictors along with the local
anaesthesia
Secondary
• Blood clot may be infected by certain bacteria like streptococci which

may dissolve the clot and result in bleeding.
• Acute ulcerative necrotising bleeding.
In patients with a systemic cause
Hereditary
• Haemophilia
Acquired
• Hypertension
• Anticoagulant therapy
• Vitamin K deficiency
• Thrombocytopaenia
• Liver disorders
Prevention
• A proper medical history of the patient should be taken to detect any

systemic disorders.
• The necessary investigations, i.e. prothrombin time (PT), partial
thromboplastin time (PTT), bleeding time, clotting time, test for
detection of clotting factors, etc. should be performed in suspected
cases.
• In such cases, the extraction should be carried out taking due
precautions.
• Avoid unnecessary incision or flap elevation or any other trauma to the
tissues.
• In haemophilic patients, the lacking clotting factor should be
administered before the extraction.
Management
• As soon as continuous bleeding is detected, apply digital pressure

continuously for 2–3 min. If the bleeding stops, close the wound by
using sutures which helps to stabilise the clot.
• If the bleeding continues, it may be coming from the bony socket. Pack
the bony socket with Gelfoam, fibrin foam, surgical or bone wax.
• If the bleeding continues despite these measures, identify the bleeding
point and cauterise it with diathermy. The associated blood vessel may
be ligated.
• A sample of blood may be sent fortesting to find out any systemic
involvement. Appropriate treatment for the cause can then be given.
Dry socket
The first time that this term ‘dry socket’ appeared in the literature was in 1896,
used by Crawford. Dry socket is a postoperative complication that occurs after
a dental extraction. It has been defined as a ‘postoperative pain in and around the
dental alveolus, which increases in severity at some moment between the first and
third day after a dental extraction, accompanied by partial or total disintegration of the
intra-alveolar clot, causing foul smell’.
Many terms have been used as synonyms of dry socket that includes painful
dry socket, necrotic alveolar socket, alveolagia, delayed extraction, localised
osteomyelitis, fibrinolytic osteitis, alveolar osteitis, osteomyelitis postextraction
syndrome, fibrinolytic alveolitis and localised alveolar osteitis.
Aetiology
The following factors are considered as possible aetiology in the development
of dry socket:
• Difficult or traumatic extraction. A bigger trauma would produce a

delay in the alveolar healing and it could provoke a thrombosis of the
underlying vessels as well as lesser resistance to infection in the
alveolar bone.
• Use of oral contraceptives. Oestrogens and other drugs activate the
fibrinolytic system in an indirect way (increasing the factors II, VII,
VIII, X and the plasminogen), contributing to premature destruction of
the clot and the development of dry socket.
• Hormonal changes. The changing levels of endogenous oestrogens
during the menstrual cycle would also influence.
• Tobacco. The mechanism through which tobacco interferes in alveolar
healing is the incorporation of pollutants in the wound or the suction
effect on the clot in formation.
• Inadequate intraoperatory irrigation. Inadequate irrigation of the
alveolus can also play a role in the formation of dry socket. Use of an
anaesthetic solution with vasoconstrictor or an intraligamentous
technique of anaesthetic in which the anaesthetic is deposited very
near to the alveolus, mainly if the anaesthetic is colder than the
corporal temperature increases the incidence of dry socket in these
patients.
• Advanced age of patients, immunocompromised state, extraction site
in the mandible, excessive or exaggerated irrigation of the socket can
all contribute to the formation of dry socket.
Clinical features
• Pain typically appears on the second or third day after the extraction
and it usually lasts either with or without treatment about 10 or
15 days.
• Pain is localised to the extraction socket, which will be sensitive to
even gentle probing.
• Although, suppuration is not evidenced, a sharp pain persists that
increases with suction or mastication and lasts several days.
• Halitosis is invariably present. The condition probably arises as a result
of complex interaction between surgical trauma, local bacterial
infection and various systemic factors.
• It is common for the pain to radiate to the ear and the ipsilateral side of
the head. There is usually absence of a normal healthy postextraction
blood clot in the socket, which may be empty or contain fragments of
disintegrating blood clot.
• Radiological studies do not show important alterations and in
advanced phases rarefaction areas can be detected.
Aetiopathogenesis
After tooth extraction, an orderly sequence of events causes normal tissue
healing. The alveolar socket fills with blood that undergoes coagulation and
contraction. Angioblastic ingrowth occurs into the clot, while epithelium
covers the clot. Fibroplasia into the clot then ensues, with cellular elimination
of fibrin and blood debris. A variable amount of osteoid is then produced by
induced mesenchymal cells. Woven bone is formed, followed by osteoblastic
and osteoclastic activity that ends in mature bone, often with some loss of total
bone volume.
This sequence of normal healing does not always occur. In some instances,
early clot formation in the socket is followed by premature clot necrosis or
loss, accompanied by pain and a fetor oris. The classic triad of early extraction
socket clot loss/necrosis, pain and fetor oris has been termed dry socket or
alveolitis sicca dolorosa. Intense pain in the extraction site may radiate and
may be accompanied by low-grade fever and ipsilateral lymphadenopathy.
Histologically, this syndrome shows an intense focal osteomyelitis, with
healing in 1–4 weeks by sequestration or resorption of the necrotic socket wall
bone and delayed secondary intention.
Theories of dry socket:
• Birn’s fibrinolytic theory

• Bacterial theory
According to Birn’s fibrinolytic theory, after the extraction of a tooth an

inflammatory process begins that could affect the formation and retention of
the clot. Laboratory and clinical studies have shown an increase of fibrinolytic
activity in the pathogenesis of dry socket. The fibrin would disintegrate due to
the effect of kinase liberated in the inflammation process or due to direct or
indirect activation of the plasminogen, which affects the stability of the clot
and facilitates the development of dry socket.
Plasminogen is a single-chain glycoprotein, which is synthesised in liver and
released into the circulation. Plasminogen is then activated by proteolytic
cleavage into the active form, plasmin, which in turn acts proteolytically on
fibrinogen and fibrin, causing clot dissolution and forming a number of fibrin
degradation products. Active plasmin is quickly inactivated in the general
circulation by antiplasmins. Therefore, plasmin activity against fibrin is
thought to be almost completely limited to that caused by plasminogen
previously absorbed into a fibrin clot. The absorbed plasminogen is cleaved
into plasmin by one or more plasminogen activator substances.
Bacterial theory, comes endorsed by the existence of a high count of bacteria
around the extraction site in patients who suffered from alveolar osteitis as
compared to those who did not suffer from it. Anaerobic microorganisms are
generally found and the alveolar pain is due to the effect of the bacterial toxins
on the nerve endings in the alveolus. Dry socket is also more frequent in
patients with poor oral hygiene or in previously existing pericoronitis or
concomitant periodontal illness.
Actinomyces viscosus and Streptococcus mutans have been related to dry
socket, because it has been demonstrated that they retard the alveolar
postextraction healing in an animal model. Additionally, a fibrinolytic activity
has been observed, which increases with Treponema denticola, a
periodontopathogenic microorganism. This infection never appears in
children, before colonisation of the mouth by Treponema denticola.
Preventive measures
• A comprehensive history with identification of risk factors should be

taken.
• Preoperative oral hygiene measures to reduce plaque levels to a
minimum should be instituted.
• Where the clinical history and/or radiographic examination suggest a
particularly difficult extraction, consideration should be given to an
elective transalveolar approach.
• All extractions should be completed with the minimum amount of
trauma, the maximum amount of care and as rapidly as possible
depending upon the experience of the operator.
• Avoid extracting lower third molars in the presence of active infection
or ulcerative gingivitis.
• Appropriate antibiotic prophylaxis should be administered, for
difficult lower third molar bony impactions, for immunocompromised
patients and for patients with a history of previous pericoronitis or
ulcerative gingivitis.
• Patients, who smoke, should be advised to cease smoking
preoperatively and for at least 2 weeks postoperatively while the
socket heals.
• Wherever possible, in female patients using oral contraceptives,
extractions should be performed during days 23 through 28 of the
tablet cycle, when fibrinolytic system is suppressed.
• Patients should be advised to avoid vigorous mouth rinsing for the
first 24 h postextraction and to use gentle tooth brushing and mouth
rinses for 7 days postextraction.
Management
• Patients should be radiographed to exclude the possibility of retained

fragments of tooth or foreign body.
• The affected socket should be gently irrigated with 0.12% warmed
chlorhexidine and all debris dislodged and aspirated. In extremely
painful cases, local anaesthesia may be required and in this instance
regional nerve blocks should be employed wherever possible.
• Intra-alveolar pastes consisting of zinc oxide eugenol paste, anaesthetic
and an antibiotic (metronidazole) can be placed. They act principally
by increasing the drug concentration locally, diminishing their
secondary effects, avoiding the entrance of remains of food to the
alveolus and protecting the exposed bone from local irritation in
addition to the use of eugenol as obtundant. Place a strip of paste
soaked surgical gauze loosely in the socket. Do not exert pressure on
the socket when placing the strip.
• The complications secondary to the placement of dressings in the
treatment of an established dry socket are ignored, although some
local complications have been described after the placement of these
dressings.
• Despite the logical supposition that topical steroid use may decrease
the intense local inflammation and hence decrease postextraction clot
breakdown, the literature does not support the use of topical steroid
antiinflammatory medications in extraction sites. However, the topical
application of an emulsion of oxytetracycline and hydrocortisone has
been shown to significantly decrease alveolar osteitis after impacted
mandibular third molar removal. Unfortunately, contribution of the
antibiotic cannot be separated from that of the steroid in these studies.
• Earlier investigations into the fibrinolytic nature of alveolar osteitis
indicated that the topical use of parahydroxybenzoic acid (PHBA) in
extraction wounds significantly decreased the incidence of mandibular
third molar dry socket in a dose-dependent fashion. However,
antibacterial nature of PHBA may have contributed to these findings.
• Appropriate analgesics as the nonsteroidal antiinflammatory drugs are
useful in managing pain.
• When it is considered that socket dressings are no longer required the
patient can be instructed in home socket irrigation techniques using
0.12% chlorhexidine.
• Patients should be kept under review until they are pain free and
socket healing is ensured.
Infection
The state or condition in which the body (or part of the body) is invaded by an
infectious agent (e.g. a bacteria, fungus or virus), which multiplies and
produces an injurious effect.
Causes
• Contaminated needle
• Contaminated local anaesthetic solution
• Needle passing through an already infected site
• Inadequate aseptic preparation
Prevention
• Antibiotic prophylaxis has been shown to decrease the risk of infection

in certain types of surgery
• Use disposable needles
• Avoid repeated use of the same needle
• Aseptic preparation of the surgical site
Management
• Empirical therapy should be primarily directed against Staphylococcus

(common bacterium in the oral cavity).
• Deep-seated infections require broad-spectrum antibiotics and
investigation for possible surgical intervention (incision and drainage).
CHAPTER 18
Impaction
Theories of impaction
Theories of mandibular impaction
Aetiology of impaction
Local causes
Systemic causes
Pericoronitis
Causes
Symptoms
Treatment
Indications for removal
Contraindications for removal
Classification
Based on the nature of the overlying tissue
Winter’s classification
Pell and Gregory’s classification
Clinical evaluation
General examination
Local examination
Factors complicating the removal of mandibular third
molar
Radiological assessment
Types of radiographs used
Interpretation of the radiograph
Surgical removal of impacted third molar
Anaesthesia
Mucoperiosteal flap
Elevation of the flap
Removal of bone with bur
Removal of bone with chisel
Removal of the tooth
Debridement of wound and wound closure
Other techniques in third molar removal
Lingual split technique (Kelsey Fry technique)
Classification of impacted maxillary third molars
Classification based on anatomic position
Sequelae of impaction and indications for removal
Assessment of maxillary third molar
Radiographic examination
Factors complicating the removal of impacted maxillary third
molar
Armamentarium
Surgical procedure
Incision and flap
Elevation and bone removal
Wound toilet and closure
Complications
Impacted cuspids
Aetiology
Positions of impacted cuspids
Localising impacted maxillary cuspids
Clinical clues
Radiographic localising
Classification of impacted maxillary canines
Classification based on position in the dental arch
Field and Ackerman classification (1935)
Treatment
Factors determining treatment
Treatment options
Techniques
Surgical technique
Removal of impacted cuspids in class I position
Removal of impacted cuspid in class ii position
Removal of impacted cuspids in class iii position
Impacted tooth: A tooth which is completely or partially unerupted, is

positioned against another tooth, bone or soft tissue so that its further eruption
is unlikely and described according to its anatomic position (Fig. 18.1).
Unerupted tooth: A tooth not having perforated the oral mucosa (includes both
teeth with and without apex closure). Unerupted teeth may or may not be
impacted (Fig. 18.2).
Partially erupted: When the tooth has failed to erupt into a normal functional
position but has crossed the bone barrier and has not reached the occlusal line.
The terms unerupted and partially erupted are commonly applied to normally
developing as well as impacted teeth, the two states being separated by the
event of clinical emergence. It is important that impaction is clearly
distinguished from normal development.
Ankylosed tooth: When the cementum of the tooth is fused to the alveolar bone
and there is no periodontal ligament in between, a tooth is considered to be
ankylosed (Fig. 18.3).
Malposed tooth: A tooth, unerupted or erupted, that is in an abnormal position
in the maxilla or mandible. An impacted tooth may be malposed or unerupted.
However, the reverse does not apply (Fig. 18.4).
Ectopic/displaced teeth: A tooth is ectopic if malpositioned due to congenital
factors or displaced by the presence of pathology (Fig. 18.5).
FIGURE 18.1 (A) Impacted partially erupted tooth 48. (B) Impacted
tooth (48).
FIGURE 18.2 (A) Clinically unerupted and impacted tooth (38). (B)
Unerupted and impacted tooth 38 and 48.
FIGURE 18.3 Ankylosed tooth (37) with obliteration of periodontal
ligament space and is malposed in position.
FIGURE 18.4 Malposed tooth in abnormal position (37).
FIGURE 18.5 Multiple impacted teeth displaced due to odontogenic

keratocyst evident as multilocular radiolucencies.
While diseased erupted teeth can be removed by simple intra-alveolar

extraction using forceps, some teeth require surgical transalveolar extraction
techniques. These teeth are usually impacted, unerupted, partially erupted,
submerged, fractured below the cementoenamel junction (CEJ),
endodontically treated, ankylosed teeth, etc. These teeth may require bone
removal and a different set of armamentarium for removal. Since they require
bone removal, these treatments are minor surgical procedures requiring
aseptic environment and patient preparation.
Frequency of impacted teeth occurs in the following
order
1. Mandibular third molars
2. Maxillary third molars
3. Maxillary cuspids
4. Mandibular bicuspids
5. Mandibular cuspids
6. Maxillary bicuspids
7. Maxillary central incisors
8. Maxillary lateral incisors
Theories of impaction
(By Durbeck) Many theories have been proposed owing to high incidence of
mandibular third molar impaction. One of the most popular theories is
insufficient development of the retromolar space. Few other theories are
described below:
Theories of mandibular impaction
• Orthodontic theory (small jaw-decreased space):

Jaws develop in downward and forward direction, while as the teeth
move in a forward direction; the presence of dense bone decreases the
movement of teeth in a forward direction. Growth of the jaw and
movement of teeth occurs in forward direction, anything that interferes
with such moment will cause an impaction (small jaw-decreased space).
A dense bone decreases the movement of the teeth in forward direction.
Causes for the increased density of bone are (1) acute infection, (2) local
inflammation of PDL, (3) malocclusion, (4) trauma, (5) early loss of
primary teeth and arrested growth of the jaw, leading to insufficient
space available for normal eruption. This condition is without doubt the
cause of impaction.
• Nodine’s Phylogenic theory (Nodine 1943) [More-functional
masticatory force—better the development of the jaw]:
Nature tries to eliminate the disused organs. This causes elimination of
the unused teeth which causes congenital absence of third molars. It is
also known that in about 10% of the Caucasian race, third molars are
lacking, as the mandible and maxilla decreased in size leaving
insufficient room for third molars i.e., used makes the organ develop
better, disuse causes slow regression of the organ. Due to changing
nutritional habits, our civilisation have practically eliminated needs for
large powerful jaws, thus, over centuries the mandible and maxilla
decreased in size leaving insufficient room for third molars.
• Mendelian theory:
Heredity is the most common cause. An individual may inherit small jaws
from one parent and a complement of large teeth from the other, i.e.
hereditary transmission of small jaws and large teeth from parents to
children. This may be an important etiological factor in the occurrence
of impaction, i.e. small mandible with impaction of second and third
molars.
• Pathological theory:
Osteosclerosis in the third molar area, caused by the early disease of
adjacent molars, cause chronic infections affecting an individual and
may bring the condensation of osseous tissue further preventing the
growth and development of the jaws.
• Endocrinal theory:
Increase or decrease in the growth hormone secretion may affect the size
of the jaws. An imbalance of endocrine activity leads to the lack of
growth of the jaws, this lack provides a cause for impaction.
• Nature and nurture theory:
Described by A. J. MacGregor explains that impaction can occur due to a
mismatch in size and shape of teeth and jaws. This can be due to
a. Primate evolution owing to the increase in brain size with
the sacrifice of the jaw size without reduction in the teeth
size.
b. Change of diet of the modern civilisation due to under used
teeth
c. Loss of use of weapons by the civilisation as cooking
decreases tough and abrasive food
With all these changes it is important to note that the dentition
has not reduced in size as it should have in attrition. Attrition
causes increased muscle activity that stimulates jaw growth
but instead there has been an increase in impaction. This is
due to the absence of constant chewing due to high-calorie
cooked food.
Aetiology of impaction
Berger lists the following local and systemic causes of impaction.
Local causes
• Irregularity in the position and pressure of the adjacent tooth.

• Density of the overlying or surrounding bone.
• Localised chronic inflammation with resultant increase in density of
the overlying mucous membrane.
• Lack of space due to underdeveloped jaws. Arch length and tooth size
discrepancy.
• Obstructions: It can be a soft or hard tissue obstruction caused by
retained deciduous teeth, thick fibrous alveolar mucosa or chronically
inflamed mucosa, dense bone with inflammatory changes due to
odontome, cyst or odontogenic tumour that prevents eruption at the
chronological age.
• Dilaceration: Abnormal path of eruption of the tooth due to traumatic
forces during the eruption period.
• Over retained deciduous teeth.
• Ectopic position of tooth bud.
Systemic causes
General causes
A. Prenatal causes: Heredity

B. Postnatal causes: All those conditions that may interfere with the
development of the child, such as:
1. Rickets
2. Anaemia
3. Congenital syphilis
4. Tuberculosis
5. Endocrine dysfunctions
6. Malnutrition
C. Rare conditions:
1. Cleidocranial dysostosis
2. Oxycephaly
3. Progeria
4. Osteopetrosis
5. Cleft palate
Pericoronitis
Pericoronitis refers to inflammation of soft tissues around and covering the
partially or completely erupted third molar.
Causes
• Bacterial growth beneath the soft tissue flap covering the partially or
completely erupted third molar.
• Trauma caused to the soft tissue flap overlying the mandibular third
molar by the cusps of the opposing maxillary third molar. This is
mainly due to supraerupted maxillary third molars opposing an
unerupted or partially erupted mandibular third molar. This
inflammation along with the bacterial invasion causes pericoronitis.
Symptoms
• The overlying soft tissues show the four cardinal signs of inflammation
namely pain, redness, swelling and warmth.
• Trismus is seen due to involvement of the temporalis, medial
pterygoid, pterygomandibular raphe, which is contained in the soft
tissues overlying the partially or completely erupted third molar.
• Chills, fever, malaise and halitosis are present.
• Regional lymph nodes may be enlarged, tender and indurated.
Treatment
When the condition is due to supraeruption of the maxillary third molar, it
should be extracted. The patient should be explained significance of the
removal of the maxillary third molar. Due to the over-eruption, normal contact
between the maxillary second and third molar is lost which facilitates food
impaction, bacterial growth and loss of interseptal bone and subsequent loss of
the second and third molar. Hence, the removal should be considered.
The pericoronitis can be treated in the following manner:
• Conservative method
• Surgical removal of the overlying flap
• Surgical removal of the tooth
Conservative method
Irrigation with warm saline should be done beneath the flap. A 10cc syringe
with a 20 gauge needle which can be bent slightly to gain a better access can be
used.
Alternatively, 1cc iodine solution can also be used to irrigate beneath the
flap. The usually used irrigating solution consists of:
• Phenol 5%, 6cc

• Tincture of aconite, 12cc
• Tincture of iodine, 18cc
• Glycerine, 24cc
Patient should be instructed to irrigate the area every hour and appropriate
antibiotics should be prescribed. Irrigation is carried out until the acute
symptoms subside and after this the tooth is extracted. If the tooth can erupt in
a normal position and help in the functioning, the overlying flap should be
removed.
Surgical removal of the overlying flap
Operculectomy
Operculum is the dense fibrous flap which covers about 50% of the occlusal
surface of a completely or partially erupted mandibular third molar. The
removal of this flap is known as operculectomy. It is not easy to remove this
flap as the tissues are freely movable and slides away beneath the usual
scalpel or scissors.
This flap can be best removed with the help of electrosurgical scalpel or
radiosurgical loop.
Electrosurgical scalpel
The advantages of using electrosurgical scalpel are:
• There is no necessity to apply pressure to cut the tissues as with a

usual scalpel and, the tissues can be cut accurately as there is no lateral
or sliding movement of the flap.
• Due to coagulation of the small capillaries, bleeding in the site is
reduced and visibility is increased.
Radiosurgical loop
However, the most efficient method for removing this dense fibrous
mucoperiosteal tissue is to use a radiosurgical loop. The radiosurgical loop is
placed beneath the flap as far posteriorly as possible. Now the current is
applied and the loop moved superiorly resulting in the cutting of the bulk of
the tissue. Once the flap is removed, the tissue distal to the tooth is excised to
remove the distal crypt. This helps in the proper eruption of the tooth if it is
properly positioned.

• Infections: Removal of any symptomatic impacted tooth should be
considered with food impaction causing halitosis, especially where
there have been one or more episodes of infection such as pericoronitis
(75%–80% of patients with impacted third molar develop
pericoronitis), cellulitis, abscess formation; or untreatable
pulpal/periapical pathology (Fig. 18.6A–C).
• Unrestorable caries: Removal should be considered when there is
caries in the impacted tooth or when there is caries in the adjacent
second molar tooth which cannot be satisfactorily treated without
removal of the third molar (Fig. 18.7).
• Periodontal diseases: When there is periodontal disease between the
third and second molar, early removal of the impacted third molar will
result in repair of the injured periodontium and is therefore beneficial.
Untreated impacted teeth are particularly prone to cause bone loss
distal to the adjacent teeth due to pressure effect.
• Dentigerous cyst formation: Other related pathologies which expand
the bone and results in pathological fracture (Fig. 18.8).
• External resorption of the second molar: Caused by the pressure of the
third molar on 2nd molar (Fig. 18.9).
• Buccoverted impacted molars: May cause cheek bite, frictional
keratosis or traumatic fibroma mandating extraction (Fig. 18.10).
• Third molar removal may occasionally be indicated for orthodontic
reasons.
• Removal of the third molar may be indicated prior to orthognathic
surgery, e.g. when a sagittal split osteotomy is planned, removal of the
third molar diminishes the risk of surgical complications with regard
to that of osteotomy.
• Prophylactic removal in presence of specific medical and surgical
conditions.
• Fracture of the mandible in the third molar region or when a tooth is
involved in tumour resection.
• Atypical pain from an unerupted third molar is the most unusual
situation and it is essential to avoid any confusion with
temporomandibular joint (TMJ) or muscle dysfunction before
considering removal.
• Impacted teeth in edentulous ridge that causes ulcerations in the
mucosa under a denture.
• Third molar removal may be considered for autogenous
transplantation to a first molar socket.
FIGURE 18.6 (A) Pericoronitis in relation to 48. (B) Food impaction
in relation to impacted partially erupted 38. (C) OPG showing
grossly decayed left lower second and third molar with periapical
radiolucency.
FIGURE 18.7 Dental caries in 37 (unrestorable) with horizontal
impacted 38.
FIGURE 18.8 Displaced tooth (37) from pathologic dentigerous
cyst.
FIGURE 18.9 External resorption of 46 from impacted 47 and 48.
FIGURE 18.10 Buccally placed 48 causing ulceration from cheek
bite.
Contraindications for removal

• Impacted teeth which are likely to erupt successfully and have a
functional role in the dentition should not be removed.
• Partially impacted teeth which can be used as an abutment in the
construction of fixed partial denture.
• Medical history contraindicates surgical procedure.
• Deeply impacted third molars in patients with no history of any bony
pathology to avoid damage to the vital structures.
• Third molars should not be removed in patients where the risk of
surgical complications is judged to be unacceptably high or where
fracture of an atrophic mandible may occur.
Classification
Systematic and meticulous classification of the position of the impacted teeth
helps in assessing the best possible path of removal of the impacted teeth and
also in determining the amount of difficulty which would be encountered
during removal.
i. Based on the nature of the overlying tissue

ii. Winter’s classification
iii. Pell and Gregory’s classification
I. Based on the nature of the overlying tissue

Based on the nature of overlying tissue, impacted mandibular third molar can
be classified into:
i. Soft tissue impaction

ii. Hard tissue impaction
Soft tissue impaction

The presence of dense fibrous tissues overlying the teeth sometimes prevents
its normal eruption. This is frequently seen in cases of permanent central
incisors, in which early loss of primary teeth with subsequent masticatory
trauma to the ridge results in fibrosis.
Hard tissue impaction

When the teeth fail to erupt due to obstruction caused by the overlying bone, it
is known as hard tissue impaction. Here the impacted tooth is completely
encased in bone so that, when the soft tissue flap is reflected, the tooth is not
visible. Extensive amount of bone must be removed and the tooth may require
sectioning before removal (odontectomy).
II. Winter’s classification

It is based on the inclination of the impacted third molar tooth to the long axis
of the second molar.
Mesioangular: Long axis of 3rd molar bisects the long axis 2nd molar at or
above occlusal plane (Fig. 18.11).
FIGURE 18.11 Mesioangular 38—(A) long axis of 38 bisects the

long axis 37 above the occlusal plane. (B) Interradicular bone width
between 37 and 38 is more than interradicular bone width between
36 and 37.
Distoangular: Long axis of 3rd molar away from long axis of 2nd molar
(Fig. 18.12) at the level of occlusal plane (Fig. 18.13).
FIGURE 18.12 Distoangular—(A) long axis of 48 is away from long

axis of 47 at the level of occlusal plane. (B) The interradicular bone
between 47 and 48 is almost obliterated and less than that
between 46 and 47.
FIGURE 18.13 Winter’s classification: (A) Horizontal, (B)

Mesioangular impacted 38, (C) Vertical, (D) Distoangular impaction
of 38.
Horizontal: Long axis of 3rd molar bisect long axis of 2nd molar at right
angle (Fig. 18.14).
FIGURE 18.14 Horizontal—long axis of 38 bisects long axis of 37
at right angle.
Vertical: The long axis of the impacted tooth runs parallel to the long axis of
the second molar (Fig. 18.15). Buccal or lingual: In combination to the above
described impaction, the tooth can also be buccally or lingually impacted (Figs.
18.16–18.18).
FIGURE 18.15 (A) Vertical—the long axis of the impacted 48 runs

parallel to the long axis of the 47. (B) Vertical—interradicular bone
width between 47 and 48 equal to interradicular bone width
between 46 and 47.
FIGURE 18.16 Buccoverted 48.
FIGURE 18.17 (A) Mesioangular impacted 38 in OPG. (B) CBCT

showing linguoversion of mesioangular impacted 38. (C) 3D CBCT
showing linguoversion of mesioangular impacted 38.
FIGURE 18.18 (A) Class I—measuring the distance between distal
surface of 47 and anterior border of ramus. (B) The distance
between distal surface of 47 and anterior border of ramus
measured as 9.7 mm. (C) Class I 48—the mesiodistal width of 48
equal to the earlier measurement of 9.7 mm.
Transverse: Tooth completely impacted in the buccolingual direction.

This is the most commonly used classification since it classifies the teeth
according to inclination and each inclination has some definite path of
withdrawal of the teeth. The classification also assesses the difficulty of
removal to some measure. For example, mesioangular impactions are very
easy to remove and distoangular impactions are the most difficult ones to
remove.
III. Pell and Gregory’s classification
(A). Based on their relationship with the anterior border of the

mandible
Class I: The anteroposterior diameter of the tooth is equal to the space
between the anterior border of ramus of the mandible and distal surface of the
second molar tooth (Fig. 18.18).
Class II: A small amount of bone covers the distal surface of the tooth and
the space is inadequate for eruption of the tooth, i.e. mesiodistal diameter of
the tooth is greater than the space available (Fig. 18.19).
FIGURE 18.19 (A) Class II—measuring the distance between distal

surface of 37 and anterior border of ramus. (B) The distance
between distal surface of 37 and anterior border of ramus
measured as 5.9 mm. (C) Class II 38—the mesiodistal width of 38
is measured 8.8 mm more than the earlier measurement of
5.9 mm.
Class III: Tooth is located completely within the ramus of the mandible–
least accessible (Fig. 18.20).
FIGURE 18.20 Class III—38 located completely within mandibular

ramus.
(B). Based upon the amount of bone covering the impacted tooth and
relation to occlusal plane
Position A: Occlusal plane of the impacted tooth is nearly in the same level as
the occlusal level of the adjacent second molar tooth (Fig. 18.21).
FIGURE 18.21 Position-A—occlusal plane of 48 is at same level as
occlusal level of 47.
Position B: Occlusal plane of the impacted tooth is in the midway between

the cervical line and the occlusal plane of the adjacent second molar tooth
(Fig. 18.22).
FIGURE 18.22 Position-B—occlusal plane of the impacted 38 is in
the midway between the cervical line and the occlusal plane of 37.
Position C: Occlusal plane of the impacted tooth below the level of cervical
line of the second molar tooth (Fig. 18.23). This can be applied for the
maxillary teeth also.
FIGURE 18.23 Position-C—occlusal plane of the impacted 48 is
below the level of cervical line of 47.
(C). Based on long axis of the impacted tooth

It is similar to the one as proposed in the Winter’s classification (described
Fig. 18.13).
Clinical evaluation
Initial assessment should include a full medical and dental history, extraoral
and intraoral clinical examination. Positive findings from this examination
should determine whether removal is indicated and should include
radiological assessment.
General examination
The general examination should be done in a similar manner as for any other
surgical procedure. The presence of any systemic disorders or diseases should
be detected and precautions should be taken accordingly before surgery.
Patients should also be assessed for undergoing certain therapies like
irradiation therapy and organ transplantation.
• Age and general fitness are important. Increasing age adds to the
difficulty of the removal.
• The presence of facial swellings and enlarged, tender lymph nodes
indicates presence of active infection and treatment should be deferred
till it is treated.
Local examination
• The eruption status of the impacted tooth: The amount of visibility of

the third molar crown is assessed. Completely or partially visible teeth
are less difficult to extract than completely impacted teeth.
• Occlusal relationship: The occlusal relationship of the maxillary third
molars to the mandibular third molars should be assessed.
• The presence of local infection like pericoronitis: The inflammation of
the soft tissues covering the crown of the erupting tooth, increases
vascularity making the procedure difficult.
• Periodontal status: The presence of pocket around the impacted third
molar or the second molar tooth should be assessed.
• Caries in or resorption of, the third molar and the adjacent tooth: Due
to lack of space, there may be food impaction in the area distal or
mesial to the impacted tooth leading to dental caries. This factor
may/may not facilitate extraction.
• Resorption of the second molars: Due to lack of space the impacted
third molar might impinge on the second molar root resulting in
resorption. Following removal of the impacted third molar, the second
molar should be assessed for endodontic or periodontic intervention
depending upon the degree of resorption and pulpal involvement.
• External oblique ridge: The external oblique ridge buccal to the third
molar is palpated to identify its position. If it is low vertical and
posterior to the tooth, it indicates the presence of thin bone buccal to
third molar. If it is high and forward it indicates a thick cortex of ridge
is present buccal to third molar which makes extraction difficult.
• Internal oblique ridge: The internal oblique ridge lingual to the third
molar is palpated to identify its position. If it is posterior to third
molar it indicates thin bone lingually. If it is anteriorly placed the
lingual cortex in relation to the third molar is anticipated to be
nonyielding.
• Upper third molar: Position of upper third molar and its relation to
lower third molar is checked. The indentations of the upper third
molar on the mandibular pericoronal flap indicate extraction of upper
third molar also.
• Soft tissue assessment: Thickness of the buccal soft tissue indicates the
retractability of the cheek. Difficulty in retraction is encountered in
well built patients and also in submucous fibrosis.
• Regional lymph nodes: Swelling and tenderness of the regional lymph
nodes may be indicative of infection of the third molar.
• Temporomandibular joint function: Preoperative assessment of the
TMJ function is done to:
1. Amount of mouth opening: To gauge the degree of
difficulty in surgery
2. Preexisting TMJ pathology: To avoid prolonged mouth
opening and excessive forces on the joint thereby
preventing worsening of the condition.
Factors complicating the removal of mandibular third molar
• Preexisting joint problem: Preexisting joint problem creates a risk of

dislocation or derangement during procedure. Restriction in joint
motion causes reduced mouth opening and difficulty in surgical
procedure.
• Position of the impacted third molar: Deeper the impacted tooth is
buried inside the hard tissues, the more difficult it is to remove it.
• Thickness of the oblique ridge: The presence of a thick oblique ridge
poses difficulty in buccal traction of the impacted tooth during
removal.
• Surrounding bone: Dense surrounding bony socket resists the easy
removal of the tooth. In young age, the bone is expandable and as age
advances, the bone becomes sclerosed and brittle.
Radiological assessment
The purpose of a careful radiological evaluation is to complement the clinical
examination by providing additional information about the third molar, the
related teeth and anatomical features and the surrounding bone. This is
necessary in order to make a sound decision about the proposed surgical
procedure, the most appropriate location for this to take place and to highlight
aspects of management which may require specific mention to the patient.
Types of radiographs used
• Intraoral periapical (IOPA) radiograph

• Bitewing radiograph
• Lateral oblique radiograph
• Orthopantomograph (OPG)
• CBCT (in indicated cases)
Intraoral periapical radiograph (Fig. 18.24)
An IOPA radiograph is the simple and most suitable radiograph for the
assessment of the lower molar. An ideal IOPA radiograph should show whole
of II and III molar, bone surrounding III molar and inferior dental canal.
FIGURE 18.24 (A) An ideal IOPA radiograph showing whole of 46,

47 and 48, bone surrounding 48 and IAC. (B1) OPG showing
impacted tooth and its relation to IAC, (B2) Extracted impacted
tooth.
The film should be placed such that
• Mesial edge should lie no further forward than mesial surface of 1st
molar for vertical, mesioangular, distoangular impactions.
• Central ray should pass parallel to occlusal surface of 2nd molar and
pass through the distal cusps of 2nd molar at right angle’s to the film.
If the central ray is correctly angled
• Lingual and buccal cusps of 2nd molar are superimposed on one

another in the same vertical and horizontal plane, giving rise to
enamel cap appearance.
• Contact point between 1st and 2nd molar should be clearly defined as
a check on the free state of contact point between 2nd and 3rd molar.
Disadvantages
• Gagging of the patient

• Deflection of the film by the soft tissues lying in the floor of the mouth
• The deeply impacted tooth may not be visible in the radiograph
• It cannot completely reveal the buccal-lingual version of the impacted
tooth
• Two-dimensional image of three-dimensional structure.
Frank’s technique of localising mandibular canal

Frank suggested that a modification of the ‘tube-shift’ method can be used to
determine whether the mandibular canal is medial to, lateral to or below an
impacted mandibular third molar. This technique was first described by
Richards. The principle involved is the same as that of the ‘Clark shift’ to
localise a maxillary impacted cuspid.
• By placing two films in identical positions in the mouth, when taking a

lower impacted third molar radiograph and changing the position of
the X-ray tube, we can determine whether the canal lies lingually or
buccally to the impaction; or in the same plane as the tooth.
• An IOPA radiograph of the third molar is taken by conventional
method with the X-rays directed perpendicular to the tooth with no
vertical or horizontal angulations.
• A second IOPA radiograph is taken by directing the X-rays 25degree
below the plane of occlusion. This will make a distant object move
downward in relation to an object in the foreground; if mandibular
canal lies lingual to impaction, it will move downward in relation to
the roots of the third molar.
• If the canal on the buccal side of roots will appear to move upward on
the roots.
• If the canal remains in the same position, it is directly below the roots or
passes between the roots or is in a groove in the root substance
apically, lingually or buccally.
• The ‘Rule of SLOB’ (same side lingual and opposite side buccal) is
applicable here as it is to ‘tube-shift’ technique.
Bitewing radiograph
• In Class I–II impacted mandibular 3rd molars the actual relationship of
the 2nd and 3rd molars is made by correctly angled bitewing film.
• Central ray is directed through the crown of the 2nd molar at right
angle to the film with 0 degree vertical angulations.
Occlusal radiograph
Occlusal radiograph for mandibular 3rd molar assessment is done by placing
the film over the occlusal surface of lower molar and positioned till the distal
edge of the film is in contact with the anterior border of ramus. It helps in
viewing the buccal or lingual version of the impacted tooth.
• Should be taken for all difficult teeth and particularly when tooth is
completely unerupted.
• Provides an alternative view to the periapical film of the roots of
horizontal teeth especially in the presence of third root.
• Essential for buccolingually placed teeth to identify the position of
crown and shape of the roots.
• Shows the thickness of lingual alveolar plate, in buccally placed molar.
Lateral oblique view

Is useful in assessing:
• Deeply buried teeth

• Grossly misplaced teeth
• Impacted teeth involved in secondary pathology
Disadvantages
• Distance between film and tooth is greater thereby leading to reduced

definition.
• Angulation of central ray is such that the relationship between 2nd and
3rd molars is not accurately shown.
• Because of inevitable distortion, it is of limited value in the diagnosis.
Orthopantomogram
Indications
a. In patient with exaggerated gag reflex where IOPA radiograph may not
be possible.
b. Tooth cannot be projected onto the IOPA film because of its position.
c. There is pathologic lesion larger than that of the film such as cysts,
tumours and fracture.
d. The third molar is in close relationship to lower border of mandible.
Advantages
• Viewing both the upper and lower jaw in one radiograph (Fig. 18.25).
• Detailed description of the anatomy of the hard tissues surrounding
the impacted tooth.
• Position of the too thin relation to the canal.
• Details of the bone surrounding the tooth.
FIGURE 18.25 An OPG showing impacted teeth of both jaws in

single film.
CBCT
Cone beam CT (Fig. 18.26) is indicated in:
• Completely impacted teeth in abnormal position.

• Relationship of the impacted tooth to the canal is questionable using
other radiographs.
• Ectopic presentations.
• Multiple impacted teeth.
• Associated with pathologies like dentigerous cyst, odontoma, etc.
FIGURE 18.26 (A) CBCT axial coronal and sagittal sections
showing the multiple impacted teeth. (B1) CBCT reconstructed 3D
image. (B2) Extracted multiple and supernumerary teeth. (C)
Demonstration of nerve root relationship traced in CBCT. Note the
extracted tooth root demonstrating grooving of root by canal. (D)
Reconstructed panoramic view using CBCT.
Assessment of access
Easy access to the impacted teeth is determined by the inclination of the
radiopaque line caused by the external oblique ridge (Fig. 18.27).
• When the radiopaque line is more horizontal, access is easy, when it is

more vertical, access is poor.
• If the radiopaque line is situated behind the impacted tooth, the access
is good, if it is situated in front of the tooth, the access is poor.
FIGURE 18.27 (A) External oblique ridge evident as radiopaque

line crossing 3rd molar horizontally down indicating excellent
access. (B) External oblique ridge evident as radiopaque line
crossing 3rd molar vertically down indicating poor access.
Assessment of position and depth
• The orientation of the impacted mandibular third molars may be

mesioangular, distoangular, vertical or horizontal.
• When a vertical impaction is present the anteroposterior width of the
interdental septum between the second and third molars is similar to
that of the septum between the first and second molars. Whereas,
when distoangular impaction is present the interdental septum
between the second and third molars is narrower than between the
first and second molars.
• They may be present at varied depth inside the mandibular jaw bone.
Ectopic positions (in the coronoid or condylar process), though rare,
do exist.
WAR lines
Position and depth of the impacted mandibular third molar can be determined
by means of George Winter’s WAR lines. George Winter described three
imaginary lines drawn on the standard radiograph with different colours such
as white, amber and red.
White line
White line is drawn along the occlusal surfaces of the erupted mandibular
molars and extended over the third molar region posteriorly. The axial
inclination of the impacted tooth can be seen apparently (Fig. 18.28).
• The occlusal surface of the vertically impacted third molar is parallel to

the white line.
• The occlusal surface of the third molar with distoangular impaction
meets the white line in front of the third molar.
• The occlusal surface of the third molar with mesioangular impaction
meets the white line behind the third molar.
• The occlusal surface of horizontally impacted third molar meets the
white line in a perpendicular direction.
• Indicates
▪ The depth of the tooth within the mandible.
▪ Relationship of occlusal surface of impacted tooth with the
erupted molars.
FIGURE 18.28 White (W) line—along the occlusal surfaces of
erupted mandibular molars.
Amber line
Amber line is drawn from the surface of the bone on the distal aspect of the
third molar to the crest of the interdental septum between the first and second
mandibular molars. This line represents the margin of the alveolar bone
covering the third molar (Fig. 18.29).
FIGURE 18.29 Amber (A) line.
Red line
Red line is an imaginary line drawn perpendicular from the amber line to an
imaginary point of application of the elevator. Usually this point is the CEJ on
the mesial surface of the impacted tooth (exception is the distoangular
impaction where the point of application of the elevator is on the CEJ on the
distal aspect). The length of the red line indicates depth of the impacted tooth
(Table 18.1). With each increase in length of the red line by 1 mm, the impacted
tooth becomes three times more difficult to remove (Fig. 18.30).
Table 18.1
WAR line and its implications

WAR Line extension Significance
line
W- Drawn along the occlusal surfaces of the Indicates the depth of the tooth within
White erupted mandibular molars and extends the mandible Relationship of occlusal
line posteriorly over the third molar region surface of impacted tooth with the
erupted molars
A- Drawn from surface of the bone distal to the Indicates the height of the margin of
Amber third molar to the crest of the interdental the alveolar bone enclosing the tooth
line septum between the first and second molars Indicates the amount of vertical
bone that requires removal for the
extraction of the third molar
R-Red It is the perpendicular line drawn from the Longer the red line, more difficult
line amber line to the imaginary point of the extraction
application for the elevator (all types-mesial, <5 mm—less difficult
distoangular-distal) For every 1 mm increase after 5 mm
difficulty increases by 3 times
>5 mm—Advised under GA
≥9 mm—very difficult, denuding of
distal root of second molar may
mandate the removal of second
molar also
FIGURE 18.30 Red (R) line.
Assessment of the roots of the impacted tooth

Position and root pattern of the impacted as well as the adjacent tooth may
create difficulty while removing the impacted tooth. These are also the factors
which determine the point of application and line of withdrawal. The eruption
status of the impacted tooth should be assessed because the status of
formation of root determines the time of removal.
Length of the root
• The ideal time to remove the impacted teeth is when the root is two-
third formed. In this stage, the roots will be blunt and removal is very
easy (Fig. 18.31).
• When the root is one-third formed, as the tooth tends to roll in its crypt
like ball in a socket, which prevents easy elevation (Fig. 18.32).
• If the tooth is not removed during the formative stage and the entire
length of the root develops, the possibility increases for abnormal root
morphology and for fracture of the root tips during extraction
(Fig. 18.33).
FIGURE 18.31 Ideal time of extraction—two-third root formation.
FIGURE 18.32 (A) A crown only formed with no root development.

(B) One-third root formation.
FIGURE 18.33 Complete root formation with severe dilacerated

root and acute curvature at risk of fracture.
Fusion of root
• The roots may be fused into a single, conical root or as separate distinct
roots (Figs. 18.34, 18.35).
• The fused, conical roots are easier to remove than widely separated
roots.
FIGURE 18.34 Fused conical root.
FIGURE 18.35 Impacted third molar with distinct separate roots.
Curvature of the root

The curvature of the tooth roots also plays a role in the difficulty of extraction
(Fig. 18.36).
• Severely curved or dilacerated roots are more difficult to remove than

straight or slightly curved roots. The apex area of the radiograph
should be carefully assessed for the presence of small, abnormal and
sharply hooked roots that would fracture during removal.
• Convergent roots are comparatively easier to remove than the
divergent roots.
FIGURE 18.36 (A) Unfavourable dilacerated tooth. (B) Abnormal
root dilaceration difficult to remove. (C) Dilacerated roots.
Width of the root

The total width of the roots in the mesiodistal direction should be compared
with the width of the tooth at the cervical line. If the tooth root width is greater
or has hypercementosis, the extraction will be more difficult. More bone must
be removed or the tooth must be sectioned before extraction (Fig. 18.37).
FIGURE 18.37 Mesiodistal root width greater than cervical width
indicative of difficulty in removal.
Root of the second molar

If the second molar roots are smaller in relation to the impacted tooth or are
fused and conical, care must be taken not to luxate the second molar during
the elevation. Similarly, absence of first molar leaves the second molar
unsupported. During elevation inadvertent luxation or dislodgement of
second molar should be avoided.
Assessment of bone texture

Texture of the bone varies between individuals, with age and site within the
same individual. In younger age group, the bone is cancellous and elastic
whereas it becomes dense and sclerosed as the age advances. The nature of the
bone is the factor which decides the choice of bur or chisel used to remove
bone. If the bone is less dense as in younger individuals, it is easier to cut with
bur than the chisel. While removing a maxillary third molar, a buccal
approach is preferred to the palatal approach since it is surrounded by spongy,
egg-shell thin cortical bone on the buccal and distal aspect whereas, more bone
is present on the palatal aspect (Fig. 18.38).
FIGURE 18.38 Cancellous and elastic bone—ease of extraction.
Assessment of relationship with inferior alveolar nerve

Sometimes the inferior alveolar canal can be seen crossing the roots of the
mandibular third molar. When it is very obvious in the radiograph, the patient
should be informed about the possible postoperative impairment of sensation
over the area supplied by the inferior alveolar nerve.
Changes related to the tooth root
Normally, a tooth will be of uniform radiopacity throughout. When there is
any darkening or decrease in the radiopacity of the tooth it indicates that the
density of the tooth structure and cortical lining of the inferior alveolar canal is
decreased in that area, due to the grooving of the tooth by the canal and its
contents. When the canal crosses only the apex of the tooth, apical notching or
bifid root apex may be seen.
Changes related to the canal
• The inferior alveolar canalis represented by two radiopaque lines and

disruption or interruption in continuity of these lines indicates that a
deep grooving of the tooth root by the canal is present.
• When there is a break in continuity of only the upper radiopaque line,
an apical notch is present which indicates that only the tooth apex is
grooved by the canal.
• The complete perforation of the tooth root by the canal is extremely
rare and when this occurs both the radiopaque lines of the canal are
lost in the area of perforation and the canal actually seems to be
converging towards the tooth root. This is due to displacement of the
roof and floor of the canal towards each other when it perforates the
tooth root.
• The canal may sometimes appear to be diverting when it perforates the
tooth root completely. This is due to eruption of the tooth which drags
the contents of the canal along with it.
Seven radiological signs had been suggested by Howe and Poyton

(1960)
The relationship between the mandibular third molar tooth and the inferior
alveolar canal is indicated by the seven radiological signs. Four of these signs
are related to the root of the tooth and the other three are changes in the
appearance of the inferior alveolar canal.
Darkening of the root
• The density of the root is not altered by the overlapping of the tooth
and inferior alveolar canal.
• Impingement of the canal on the tooth root results in the loss of density
of the root, resulting in darkening of the root (Fig. 18.39).
FIGURE 18.39 Darkening of the roots-loss of density of the root.
Extracted 48 showing grooving of the root apex by canal.
Deflected root
• Deflected roots or root shooked around the canal are seen.

• There will be abrupt deviation of the root, when the root reaches the
inferior alveolar canal.
• Deflection of the root either to buccal or lingual side or to both sides, so
that the roots may completely surround the canal.
• It may also be deflected to the mesial or distal aspect (Fig. 18.40).
FIGURE 18.40 Deflected root-roots deflected buccally and lingually

surrounding the canal.
Narrowing of the root
• Narrowing of the root on crossing the canal implies that the greatest
diameter of the root has been involved by the canal.
• It may also be associated with deep grooving or perforation of the root.
Dark and bifid root
• Dark and bifid root appears when the inferior alveolar canal crosses
the apex.
• It is identified by the double periodontal membrane shadow of the
bifid apex.
Interruption of the white line(s) (Fig. 18.41)
• Radiologically the inferior alveolar canal appears as the two

radiopaque lines (the ‘roof’ and ‘floor’ of the inferior alveolar canal).
• Disappearance of this white line (either one or both) immediately
before it reaches the tooth structure is considered to be interrupted.
• The interruption of the white line(s) indicates deep grooving of the
root.
• Narrowing of the inferior alveolar canal indicates the perforation of the
root.
• The interruption of the white line is considered to be a ‘danger sign’
indicating the true relationship between tooth root and canal.
FIGURE 18.41 Interruption of the white line.
Diversion of the inferior alveolar canal
• The canal changes its direction when it crosses the mandibular third
molar and is considered to be diverted.
• There will be upward displacement of the canal along with its
contents, during the eruption of the third molar.
Narrowing of the inferior alveolar canal
• Narrowing of the inferior alveolar canal is appreciated when the canal

crosses the root of the mandibular third molar.
• Diameter of the canal is reduced.
• Narrowing of the canal may be due to
▪ Downward displacement of the upper border of the canal.
▪ Displacement of the upper and lower borders towards each
other resulting in hourglass appearance.
• The hourglass shape may indicate partial or complete encirclement
(Fig. 18.42).
FIGURE 18.42 Narrowing of the inferior alveolar canal.
Assessment of difficulty of removal

Wharfe’s assessment (Fig 18.43)
Scoring details for Wharf’s assessment are depicted in Table 18.2.
Table 18.2
Scoring details for Wharfe’s assessment

1. Winter’s classification Horizontal 2
Mesioangular 1
Vertical 0
Distoangular 2
2. Height of the mandible 1–30 mm 0
31–34 mm 1
35–39 mm 2
3. Angulation of II molar 1–59 degree 0
60–69 degree 1
70–79 degree 2
80–89 degree
90 degree + 3
4
4. Root shape and development
a) Less than 1/3rd complete 2
b) 1/3rd to 2/3rd complete 1
c) More than 2/3rd complete: Complex 3
Favourable curvature 2
Unfavourable curvature 1
5. Follicles Normal 0
Possibly enlarged −1
Enlarged −2
Impaction relieved −3
6. Path of exit Space available 0
Distal cusp covered 1
Mesial cusp also covered 2
Both covered
Total 3
33
FIGURE 18.43 Wharfe.
Crown of the impacted tooth

Teeth with large bulbous crown and prominent cusps are difficult to remove
when compared to small conical crowns and flat cusps. In cases of tooth
impaction wherein the withdrawal of the third molar is obstructed by the
presence of the second molar, the cusps of the third molar may impinge on the
second molar and cause root resorption of the second molar. In such cases, the
impacted tooth will have to be sectioned for removal (Fig. 18.44).
FIGURE 18.44 Large bulbous crown with prominent cusps—difficult
to remove.
Pederson’s scale
Pederson proposed a modification of the Pell–Gregory scale that included a 3rd
factor, the angulation of the molar (mesioangular, horizontal, vertical or
distoangular) Table 18.2. The Pederson scale is designed for evaluation in OPG.
Table 18.3
Pederson’s scale
Classification Value
Spatial relationship
Mesioangular 1
Horizontal transverse 2
Vertical 3
Distoangular 4
Depth
Level A: High occlusal level 1
Level B: Medium occlusal level 2
Level C: Deep occlusal level 3
Ramus relationship space available
Class 1: Sufficient space 1
Class 2: Reduced space 2
Class 3: No space 3
Difficulty index
Very difficult 7–10
Moderately difficult 5–6
Slightly difficult 3–4
Surgical removal of impacted third molar

Procedure for surgical removal of the tooth (Fig. 18.45) varies depending upon
the following factors:
• The type and degree of impaction (local or general anaesthesia).

• Amount of soft tissue exposure to aid removal of bone (type of flap).
• Amount and technique of bone removal (chisel or bur).
• Odentectomy—need to divide the tooth prior to delivery.
Anaesthesia
Mostly the procedure is performed under local anaesthesia which is obtained
by nerve block of the inferior alveolar nerve, lingual nerve and long buccal
nerve.
General anaesthesia is indicated when the impacted tooth is situated deep in
the jaw bone (when the red line is more than 5 mm) and when more than two
impacted molars have to be removed at a time.
Inicision
Most commonly used are:
• Wards
• Modified Wards (for horizontal lower 3rd molar impaction)
Mucoperiosteal flap
Ideal requirements of the flap
• It should provide adequate exposure of the operative site.

• The base of the flap should be wide so that the soft tissues get adequate
blood supply after wound closure.
• To avoid soft tissue trauma during surgical procedures, the flap should
expose the entire site of operation.
• The flap should not be extended too far distobuccally in which case it
might injure the buccal vessels, cause postoperative trismus (due to
the trauma to the temporalis muscle) or herniation of the buccal pad of
fat into the operating field.
• The incision should be designed so that the flap can be primarily
closed over solid bone.
• The incision should not damage any of the vital anatomic structures
(Fig. 18.45).
• The following are the different types of the incisions employed
(Fig. 18.46):
▪ Envelope flap
▪ L-shaped flap
▪ Bayonet flap
▪ Triangular flap
FIGURE 18.45 Clinical demonstration of surgical removal of
mesioangular impacted 48.
FIGURE 18.46 Different types of flaps for surgical removal of third
molar. (A) Envelope flap, (B) L-shaped flap, (C) Bayonet flap with
Wards incision, (D) Trapezoidal flap.
Envelope flap
The flap extends from the mesial papilla of the mandibular first molar and
passes around the neck of the teeth to the distobuccal line angle of the second
molar.
Now the incision line extends posteriorly and laterally up to the anterior
border of the mandible. Care should be taken not to damage the lingual nerve.
The advantage of this flap is that the wound heals quickly.
L-shaped flap
This flap suits only the buccal approach since it is difficult to raise a lingual
flap from this approach. The posterior limb of the incision extends from a
point just lateral to the ascending ramus of the mandible into the sulcus. It
passes distolateral to periodontium by avoiding or including it depending
upon the proximity of the third molar with the second molar. The junction
between the limbs may be curved and the incision made in one sweep or it
may be angled.
Triangular flap
Triangular flap is indicated in cases where the impacted tooth is deeply
embedded in the bone and requires extensive bone removal. The flap design is
discussed in detail in the Chapter 19 on Endodontic Surgery.
Bayonet flap
This incision has three parts: distal or posterior, intermediate or gingival and
an anterior part. The posterior part of the incision goes round the gingival
margin of the second and even the first molar, before turning into the sulcus. It
joins the gingival margin of the second molar anywhere from the lingual to the
buccal side.
The intermediate part of the incision can be carried forward to a variable
extent. It extends entirely around the buccal margin of the second molar to end
in the papilla in between the first and second molars. The anterior part of the
incision is angled from the gingiva margin in a forward and downward
direction towards the sulcus. The disadvantage of this flap is that the
overextension of the incision into the sulcus may cause brisk oozing of blood
from the venous plexus. It can be avoided by making the anterior part of the
incision more oblique in direction.
Elevation of the flap

To allow an adequate exposure of the bone and the tooth a full thickness
mucoperiosteal flap should be elevated. Periosteal elevator can be used to
elevate this flap. After the elevation of the buccal flap, the lingual soft tissue
must be reflected. This is accomplished by means of a periosteal elevator
which is inserted under the periosteum and passed in a distolingual direction
to reach the lingual border of the mandible. Now the flap is elevated very
carefully, avoiding any damage to the lingual and mylohyoid nerve.
Once the flap has been raised adequately appropriate retractors (Bowdler-
Henry, Austin, etc.) are used to retract the flap.
Bone removal
The amber line determines the amount of bone covering the impacted tooth
which has to be removed for applying the elevator to remove the tooth. The
red line determines the depth of the ‘point of application’ of the elevator.
When the entire crown lies above and in front of the amber line, there is no
necessity to remove the bone. In other cases, bone can be removed with the
help of chisel or burs.
Removal of bone with bur

Moore–Gillbe collar technique
The bur is used to create a gutter around the neck of the impacted tooth. On
the buccal and the distal aspect, the bone must be removed to expose the entire
crown till the CEJ. When the bone is removed around the distolingual region,
care must be taken by the operator to avoid any damage to the lingual flap and
lingual nerve. When point of application of the elevator is on the mesial side,
adequate bone must be removed so that the elevator stands up at an angle of
45 degree to the mandible without any support. The area should be irrigated
constantly with saline during the drilling procedure to avoid bone necrosis.
The tooth should not be removed unless enough space exists where the tooth
can be displaced. When the tooth has been removed using appropriate
elevator, sharp bony edges should be removed and smoothened.
Removal of bone with chisel

Buccal bone may also be carved away by chiselling. When using chisel for
removing the bone in the mandibular third molar region, the mandible should
be adequately supported.
Mandibular Grains
The bone trajectories of the mandible must be borne in mind before using the
chisel. This method depends upon the mandible having grains similar to
wood. The grains are related to the direction of the fibres which in turn are
related to haversian systems and the blood supply. In the third molar region,
the bone trajectories run parallel to the oblique ridge. The use of chisel parallel
to the grains may cause the cut to extend towards the first molar the ramus
distally and cause a fracture. To prevent this phenomenon, mesial and distal
vertical stop cuts are made initially before using the chisel on the buccal
aspect.
To make this procedure effective, the mallet is used with a loose, free-
swinging wrist motion that gives maximum speed to head of the mallet
without introducing the weight of the arm or body into the blow. To plane
bone with a chisel, the bevel has to be turned towards the bone. To penetrate
the bone, turn the bevel away from the bone. The disadvantage of this
technique is that it cannot be used for older patients.
Bone is removed bucally, distally and superiorly. A vertical step cut is made
down to the level of the lower part of the third molar crown. This cut is placed
as near as possible to the second molar without causing damage.
The chisel is now rotated so that the bevel is downwards and the bone is
pared off buccally. This is usually done in two or three passes, which may
extend to the distolingual surface. If a definite angle is formed in the
horizontal plane at the junction of body of the mandible and coronoid process
and the tooth itself is in lingual obliquity, a lingual buttress may be seen. This
can be detached with a vertical blow from the chisel taking care that the split
runs parallel with body of the mandible rather than the ascending ramus.
There is no need to remove this piece of bone unless it is very loose. Indeed its
dissection may damage the lingual or mylohyoid nerves. At some stage, the
crown will be sufficiently cleared to allow the insertion of an elevator to push
the tooth upwards.
Removal of the tooth

The removal of bone should establish sufficient space between the height of
the contour of the impacted tooth and the bone to permit the application of an
elevator. Similarly, sufficient bone should be removed distal to the impacted
tooth to make a space into which the impacted tooth can be displaced while
removal (Figs. 18.47, 18.48).
FIGURE 18.47 (A) Radiographic assessment indicating need for

odontectomy. (B) Demonstration of odontectomy along the long
axis of the tooth. (C) Demonstration of odontectomy by crown root
section just beneath the CEJ.
FIGURE 18.48 Crown root sectioning of a mesioangular impacted

tooth.
The straight elevator should be applied on the mesial CEJ of the impacted
tooth and sufficient force should be applied so that the tooth rotates in an arc
whose midpoint is located at the apex of the distal root and is delivered out of
the socket. In some situations sectioning of the tooth in multiple segments
should be considered before removal, due to the difficulty which is predicted
to be encountered in the path of removal of the tooth. The direction of the
tooth sectioning primarily depends upon the angulation of the impacted tooth.
Care must be taken not to injure the lingual nerve while sectioning the tooth.
Advantages of odontectomy
Pell and Gregory stated the following advantages of splitting technique:
• Amount of bone to be removed is reduced.

• The time of operation is reduced.
• The field of operation is small and therefore damage to adjacent teeth
and bone is reduced.
• Risk of jaw fracture is reduced.
• Risk of damage to the inferior alveolar nerve is reduced.
Disadvantages of odontectomy
• In elderly patients, splitting of the tooth is difficult due to the sclerosis

of the tooth structure.
• Sometimes due to the presence of shallow grooves on the tooth
structure, splitting is difficult.
• Vertically impacted tooth with bulbous crown and prominent cusps
are usually impacted below the distal convexity of the second molars.
Vertical splitting of the third molar is indicated here which permits the
removal of the distal root and portion of the crown attached to it. Then
the mesial root and crown attached to it can be rotated along an arc,
the centre of which lies in the tip of the mesial root to be delivered out.
• In case of mesioangular impaction with bulbous crown, mesial portion
of the crown which is impacted beneath distal convexity of the second
molar can be split at the cementoenamel margin by means of bur or
osteotome. The crown can now be moved distally into the space
created earlier and removed. The roots are then elevated into the space
occupied by the crown and removed.
• If the roots are unfavourably curved, the roots can also be divided at
the bifurcation and then removed separately.
Debridement of wound and wound closure

The wound should be debrided to eliminate particulate bone chips and debris
which might have accumulated during the surgery. Periapical curette can be
used to debride the socket mechanically. The sharp margins of the bone
should be smoothened using a bone file. Following this, careful irrigation with
sterile saline should be carried out thoroughly under the reflected tissue flaps.
The wound should now be closed with sutures. The initial suture is placed
on the distal aspect of the second molar. Additional sutures are placed in the
anterior and posterior limbs of the incision. Sometimes the wound may be left
to heal by granulation tissue formation wherein no sutures are placed, but it is
packed with gauze soaked with Whitehead’s varnish.
Other techniques in third molar removal
Lateral trephination technique

This procedure was first described by Bowdler-Henry to remove any partially
formed and unerupted third molar in the age group of 9–16 years. The
advantage of this technique is that the bone healing is excellent without any
loss of alveolar bone around the second molar.
Technique
• Local anaesthesia is preferred over general anaesthesia unless the

procedure has to be performed bilaterally.
• Once the anaesthesia is secured, the external oblique ridge is palpated
and an S-shaped incision is made.
• The incision line starts from the retromolar fossa and extends across
the external oblique ridge curving down along the reflection of the
mucous membrane above the vestibule and ends anterior to the first
permanent molar.
• A full thickness mucoperiosteal flap is elevated and retracted using a
Bowdler-Henry retractor.
• Using a round bur, the buccal cortical plate over the third molar crypt
is trephined till it covers the entire anteroposterior length of the crypt.
Following this, a vertical cut is made on the external plate at its
anterior margin.
• At the posterior end of the crypt, a second cut is made through the
outer plate at an angle of 45 degree from the trephine holes.
• Now the buccal plate is fractured to expose the third molar crypt using
a chisel vertically over the trephine holes. The fractured buccal plate
can be removed using a curved haemostat.
• Using an elevator, the impacted tooth is delivered out of the crypt.
• Care should be taken not to leave any follicular remnants and also not
to injure inferior alveolar canal while debriding the follicular sac.
• The bony margins are smoothened, the wound irrigated and closed.
Lingual split technique (Kelsey Fry technique)

This method was introduced by Sir William Kelsey Fry. It takes advantage of
the thinness of the lingual cortical plate, avoids and preserves plate and hence
preserves the buccal plate and external oblique ridge.
Procedure
• The incision is made on the 3rd molar region exposing the tooth
surrounding bone. A mucoperiosteal flap is elevated on the buccal side
to expose the bone enclosing the impacted tooth. A vertical stop cut is
made in the anterior end of the impacted tooth using a chisel.
• The chisel is placed horizontally with the bevel facing downwards just
below the vertical stop cut and a horizontal cut is made extending
backwards.
• A point of application for an elevator is made with a chisel by excising
the triangular piece of bone bounded anteriorly by the lower end of
the stop cut and above by the anterior end of the horizontal cut.
• The distolingual bone is now fractured inward by using chisel. The
chisel is held at an angle of 45 degree to the bone surface and pointing
in the direction of second premolar on the contralateral side. The
cutting edge of the chisel is kept parallel to the external oblique ridge
and a few light taps are given with the mallet that separates the lingual
plate from the alveolar bone and hinges it inward on the soft tissue
attached to it. At this point care must be taken that the cutting edge of
the chisel is not held parallel to the internal oblique ridge as this may
lead to the extension of the lingual split to the coronoid process.
• The ‘peninsula’ of bone which then remains distal to the tooth and
between the buccal and lingual cuts is excised.
• A sharp, pointed, fine-bladed straight elevator is then applied to the
mesial surface of the tooth and minimum of force is used to displace
the tooth upward and backward out of its socket.
• As the tooth moves backward, the fractured lingual plate is displaced
from its path of withdrawal, thus facilitating delivery of the tooth.
After the tooth has been removed from its socket, the lingual plate is
grasped in fine haemostats and the soft tissues are freed from it by
blunt dissection.
• The fractured lingual plate is then lifted from the wound, thus
completing the saucerisation of the bony cavity.
• The bone edges are smoothened with bone files; the wound is irrigated
with saline and closed with sutures.
Advantages
• It is a quick technique
• Helps in removal of lingually impacted third molar without much of
buccal bone removal
• This technique helps in reduction of the size of the residual blood clot
by means of saucerisation of the socket.
It is mostly indicated in children in whom the bone is very elastic. General

anaesthesia is preferred.
Complications (Fig. 18.49)
• Swelling
• Trismus
• Bleeding
• Neurologic
▪ Lingual nerve damage—paraesthesia of tongue
▪ Inferior alveolar nerve damage—paraesthesia lower lip
• Fractured lingual plate
• Loss of tooth into submandibular and sublingual space
• Mandibular fracture
• Second molar
▪ Hypersensitivity
▪ Distal periodontal pocket
▪ Gingival recession
FIGURE 18.49 Lingual plate fracture in ankylosed 3rd molar

Classification of impacted maxillary third molars
The classification of impacted maxillary teeth is similar to mandibular teeth
but variations do exist. The following are the classifications which are
commonly used.
Classification based on anatomic position
I. Relative depth of the impacted maxillary third molar in bone (Pell

and Gregory)
Class A: The lowest portion of the crown of the impacted maxillary third molar
is on a line with the occlusal plane of the second molar (Fig. 18.50).
FIGURE 18.50 Class A impacted 18.
Class B: The lowest portion of the crown of the impacted maxillary third
molar is between the occlusal plane of the second molar and the cervical line
(Fig. 18.51).
FIGURE 18.51 Class B impacted 18.
Class C: The lowest portion of the crown of the impacted maxillary third
molar is at or above the cervical line of the second molar (Fig. 18.52).
FIGURE 18.52 Class C impacted 18.
II. The position of the long axis of the impacted maxillary third molar
in relation to the long axis of the second molar
1. Vertical (Fig. 18.53)

2. Horizontal (Fig. 18.54)
These may also occur
▪ Mesioangular (Fig. 18.55)
▪ Distoangular (Fig. 18.56)
▪ Inverted
▪ Buccoangular
▪ Linguoangular
FIGURE 18.53 Vertical impacted 18.
FIGURE 18.54 Horizontal impacted 18.
FIGURE 18.55 Mesioangular impacted 28—long axes of second
and third molars meeting occlusally.
FIGURE 18.56 Distoangular impacted 28.
III. Relationship of the impacted maxillary third molar to the maxillary

sinus (Fig. 18.57)
1. Sinus approximation (SA): No bone or a thin partition of bone between
the impacted maxillary third molar and the maxillary sinus is known
as ‘maxillary sinus approximation’ (Fig. 18.58).
2. No sinus approximation (NSA): 2 mm or more of bone between the
impacted maxillary third molar and the maxillary sinus is known as ‘no
maxillary sinus approximation’ (Fig. 18.59).
FIGURE 18.57 18 showing sinus approximation and 28 showing no

sinus approximation
FIGURE 18.58 Sinus approximation (SA).
FIGURE 18.59 No sinus approximation (NSA).
Sequelae of impaction and indications for removal

Pain
May be due to pericoronitis, dental caries exposure or closer of adjacent
surface of maxillary 2nd molar. Pericoronitis, is rare in the upper jaw and
seldom gives rise to those extensive infection as seen in lower 3rd molar.
Over-eruption of the upper 3rd molar

This may occur after the lower 3rd molar has been removed, leading to
impinging of retromolar soft tissue resulting in ulceration.
An unopposed maxillary 3rd molar also tends to act as a food trap and
become carious.
Upper wisdom teeth erupting towards cheek (Fig. 18.60)

This will lead to inflammation and oedema of the mucosal tissue of the cheek.
FIGURE 18.60 Buccoverted 28 impinging on buccal mucosa
causing ulceration.
It may also impinge on coronoid process and cause a bite of convenience

causing jaw deviation.
Exacerbation of pericoronitis of lower third molar

Due to upper third molar impingement on the overlying gum pad.
Before construction of full upper denture

It is necessary to extract an upper unerupted third molar tooth, before
construction of full upper denture, which will fit over that area. However,
asymptomatic maxillary 3rd molar which are completely embedded in bone
need not be removed unless the patient is to be fitted with a full upper
denture.
Assessment of maxillary third molar

This must establish
1. The state of eruption

2. Any buccolingual displacement
3. Tooth impaction against 2nd molar
4. Size of the mouth and mouth opening
5. Space around the 3rd molar—when mouth open/closed
I. Intraoral periapical film ideally should show the 2nd molar and whole of
3rd molar.
II. Lateral oblique and OPG indicated when the 3rd molar is high in the
maxilla or when the patient will not tolerate an IOPA radiograph.
(a). Position of tooth
i. Vertical: It will erupt normally unless it is lying apical to the 2nd molar.
ii. Distovertical: When the tooth erupts, it may traumatise the mucosa
overlying the ascending ramus as it is directed distally.
iii. Mesioangular: It becomes impacted against the distal aspect of the
maxillary 2nd molar.
iv. Partially erupted: May become carious or cause pocketing around the
2nd molar and consideration should be given to prognosis of latter
before and after surgery.
(b). Morphology of the tooth

Morphology of upper third molars is very variable, particularly in the number
of roots. These are often multiple and fine. Divergent fine roots present a
problem in extraction because they may fracture during surgical removal.
Factors complicating the removal of impacted

maxillary third molar
1. Maxillary sinus approximation
2. Presence of maxillary 3rd molar within or immediately above the roots
of 2nd molar
3. Fusion of maxillary 3rd molar with roots of maxillary 2nd molar
4. Abnormal root curvature and hypercementosis
5. Proximity to the zygomatic process of maxilla
6. Extreme bone density—in elderly patients
7. Follicular space filled with bone—in elderly patients
8. Difficult to access the site due to small orbicularis oris muscle
9. Inability to open the mouth widely.
Armamentarium
The armamentarium required for the surgical removal of impacted maxillary
3rd molar are similar to those used for mandibular 3rd molar.
The main modifications are in the categories of elevators and forceps:
1. Upper molar forceps

2. Miller or Potts elevator
3. Curved scalpel blade (No. 12)—facilitates making of incision on the
tuberosity
Surgical procedure
Incision and flap
Incision is made starting beyond the tuberosity in the hamular notch with a
No. 12 blade. The mucous membrane overlying the tuberosity is incised from
the distal most portion of the tuberosity forward (anteriorly) until the
midpoint of distal surface of the upper 2nd molar.
The incision is continued buccally around the neck of 2nd molar to the
interproximal space of 1st molar and then towards the mucobuccal fold at 45
degree angle. This last incision is made with no. 15 BP blade. The
mucoperiosteal flap is raised with Howarth periosteal elevator and is retracted
by a broad periosteal elevator. The palatal portion of mucoperiosteum over the
tuberosity is loosened and held by sutures thus providing adequate access to
remove the overlying bone (Fig. 18.61).
FIGURE 18.61 (A) Envelope flap for exposing impacted

supernumerary and 28. (B) Triangular mucoperiosteal flap was
raised to expose the impacted tooth in 18. (C) Impacted 18
extracted using mesial point of elevation.
Elevation and bone removal

The overlying bone is usually not dense and can be readily removed with
chisel or rongeurs to expose the crown. Bone surrounding the height of
contours should be removed providing sufficient space between the height of
contour of the impacted tooth and the bone to permit an elevator. Appropriate
elevator is inserted above the height of contour and using the buccal plate as a
fulcrum, the tooth is elevated buccally and distally from the alveolus. Extreme
care is taken to avoid driving the tooth inadvertently into the maxillary sinus
or pterygomaxillary space.
Wound toilet and closure

Debridement of the socket and smoothing of bone margins is carried out
before the wound is closed. Sutures are placed to hold the wound edges
securely together.
Complications
Intraoperative complications
They are:
1. Fracture of tuberosity
2. Dislodgement of tooth into maxillary antrum
3. Dislodgement of tooth into soft tissues
4. Damage to adjacent 2nd molar
This is the most common complication occurring during third molar surgery.
This problem does not occur in completely unerupted third molars as the
tooth itself constitutes most of the tuberosity. Fracture of tuberosity is more
likely to occur when forceps are used in the extraction of tooth.
If the fractured tuberosity has periosteal attachment indicative of
vascularity, then the wound is closed primarily.
Dislodgement into maxillary sinus

This occurs most commonly when the tooth is partially erupted with a conical
root and extraction is attempted with an extraction forceps. It may also occur
when the elevator is incorrectly applied. If entire tooth is dislodged into the
antrum, removal is done through ‘Caldwell Luc approach’.
Dislodgement into the soft tissue

Usually this occurs when an inadequate flap is raised. The tooth should be
localised by radiographs followed by early surgical removal to avoid infection.
Damage to adjacent molar

This occurs due to uncontrolled use of burs or chisel.
Accidental subluxation of the second molar occurs during elevation of the
third molar, if the 2nd molar has conical root or is unsupported mesially by 1st
molar.
II. Postoperative complications
1. Infection
2. Dry socket
3. Oroantral fistula
Impacted cuspids
The most common impacted tooth after mandibular third molars is maxillary
canine. Since these impactions are asymptomatic, they are incidentally found
on radiographic examinations. However, impaction of mandibular canines is
less common. Unerupted canines occur 20 times more frequently in the
maxilla than in the mandible. They are almost always rotated from 60 to 90
degree on their longitudinal axis.
Aetiology
The factors that have been suggested for the failure of eruption of maxillary
cuspids as described by Dewel are:
1. Hard palatal bone offers more resistance to eruption than alveolar bone
on the ridge.
2. Thick mucoperiosteal soft tissue covering the anterior part of hard palate is
dense and resistant than other soft tissues of the oral cavity.
3. Eruption of teeth depends to some extent on an associated increase in
apical development. This aid to eruption is minimised in maxillary
cuspid as root formation completes at the time of eruption.
4. Greater the distance a tooth must travel from its point of development,
greater the possibility of deflection and resultant impaction. This is
true for maxillary cuspid.
5. During development the crown of the permanent cuspid lies
immediately lingual to the apex of primary cuspid root. Any
pathological change in primary cuspid thereby easily causes deviation
in the position and direction of growth of permanent cuspid tooth bud.
6. Delayed resorption of primary cuspid root can affect eruption of
permanent cuspid.
7. The canines are the last of permanent tooth to erupt hence they are
vulnerable for a long period of time to any unfavourable
environmental influences.
8. The cuspids erupt between teeth already in occlusion and are usually
competing for space.
9. Primary cuspid has a lesser mesiodistal diameter than that of the
permanent cuspids thus providing less space.
Positions of impacted cuspids

• In maxilla, the malposed cuspids are found three times as frequently
on the palatal side of the arch than on the labial side.
• They are almost always rotated upon the longitudinal axis and are
usually in an oblique position.
• In mandible, the cuspids are rarely found in a horizontal position or on
the lingual side of the dental ridge, being located most often on the
lateral surface of mandible.
Localising impacted maxillary cuspids

Clinical clues
1. Presence of distinct bulge in the palate or on the buccal aspect of the

maxilla.
2. If canine is labially impacted, there will be a deflection of the lateral
incisor (apical portion of root lingually and the crown labially).
Radiographic localising
The position of the upper canine is assessed from radiographs which are taken
in two planes to give three-dimensional impressions of the tooth and
associated structures. They are:
1. Intraoral periapical films

2. Vertex occlusal film
These are supplemented with
i. Oblique occlusal films

ii. Anterior occlusal films
iii. True lateral films
iv. Tangential views films
v. CBCT
Intraoral periapical film

More than one IOPA may be necessary to cover the whole length of the tooth
adequately and to show the vertical and anteroposterior relationship to
adjacent teeth, antrum and nose. Parallax method of Clarks (1909) or tube shift
technique is useful in identifying the buccopalatal position of the tooth.
Radiographic localisation
Principle of Parallax by Charles A. Clark:
By changing the angulation of the X-ray beam, an apparent displacement of
the object to be localised was seen, when the reference object is considered as
the tooth closest to the object to be localised, the image of the object that is
farther (palatally or lingually placed object) from the X-ray tube moves in the
same direction as the tube, whereas the image of the object closer to the X-ray
tube (buccally placed object) moves in the opposite direction. This technique
was introduced by Clark. He used a horizontal shift of the tube; Richards
introduced the concept of a vertical shift (Figs. 18.62, 18.63).
FIGURE 18.62 This image illustrates the first step of Clark’s tube
shift technique for the localisation of the canine in a buccolingual
plane. A bucally impacted 13 and palatally impacted 23 have been
illustrated. The corresponding radiographs A1 and B1 shows
similar position of the canines due to the central X-ray
perpendicular through the objects. Radiographs A1 and B1 do not
localise the tooth’s position.
FIGURE 18.63 This image illustrates the second step of Clark’s
tube shift technique for the localisation of the canine in a
buccolingual plane. The X-ray tube has been shifted distally in both
cases to differentiate the position of the canine in the subsequent
radiograph. Radiograph B2 shows a shift of the canine towards the
premolars (distal-shift) which is the same side of the X-ray tube
(Same side—Lingual or Palatal). Radiograph A2 shows a shift of
the canine towards the incisors (mesial-shift) which is opposite to
the position of the X-ray tube (Opposite side—Buccal)
Keur introduced another technique: where the occlusal radiograph and the
combination of panoramic and occlusal radiographs were used to localise the
object.
Vertex occlusal film

This shows the buccopalatal relationship of canine to the roots of adjacent
teeth.
Supplementary films
• True lateral film shows the vertical height of acanine and its
relationship to the nose and antrum.
• Tangential view will show a canine erupting buccal to incisor teeth.
• Oblique and anterior occlusal film shows the whole of the canine
where it cannot be seen on periapical films. These films should only be
used to examine the morphology of the canines. CBCT (Fig. 18.64)—
CBCT is a low radiation CT scan useful in localising canine position
preoperatively.
FIGURE 18.64 (A) CBCT localising a palatal placed canine. (B)

CBCT localising a palatal placed canine—class I semivertical.
Classification of impacted maxillary canines

Classification based on position in the dental arch
Class I Impacted cuspids in palate
1. Horizontal
2. Vertical
3. Semivertical
Class II Impacted cuspids on buccal surface
1. Horizontal
2. Vertical
3. Semivertical
Class III Impacted cuspids located both in the palatal process and labial
maxillary bone (e.g. crown on the palate and the root passes through between
the roots of adjacent teeth in the alveolar process and ends in the labial or
buccal surface of maxilla).
Class IV Impacted cuspids located in the alveolar process usually vertically
between the incisor and bicuspid.
Class V Impacted cuspid located in an edentulous maxilla.
Field and Ackerman classification (1935)

Maxillary canines
a. Labial position (Fig. 18.65):

1. Crown in intimate relationship with incisors
2. Crown well above the apices of incisors
b. Palatal position (Fig. 18.66):
1. Crown near the surface, in close relationship to roots of
incisors
2. Crown deeply embedded in close relationship to apices of
incisors
c. Intermediate position
1. Crown between lateral incisors and 1st premolar roots
2. Crown above these teeth with crown labially placed and
root palatally placed or vice versa
d. Unusual positions
1. In nasal or antral wall
2. In infraorbital region
FIGURE 18.65 (A–C) Buccal impacted maxillary canine.
FIGURE 18.66 (A–C) Bilateral impacted maxillary canines with

dilacerated root.
Mandibular canines
a. Labial position:
1. Vertical (Fig. 18.67)
2. Oblique
3. Horizontal
b. Unusual positions
1. At inferior border
2. In mental protuberance (Fig. 18.68)
3. Migrated to the opposite side along with the original nerve
supply
FIGURE 18.67 Bilateral mandibular impacted canine in vertical
labial position.
FIGURE 18.68 Bilateral mandibular impacted canines in unusual

position of mental protuberance.
Treatment
Factors determining treatment
a. Age of the patient

b. Stage of tooth development
c. Position of impacted tooth
d. Evidence of root resorption of adjacent permanent teeth.
Treatment options
i. No treatment
ii. Surgical removal of unerupted canine
iii. Surgical exposure of the crown with or without orthodontic treatment
iv. Surgical repositioning
v. Surgical transplantation
1. No treatment (to leave the tooth in situ)

The patient may not be willing to undergo any type of treatment if there is no
occlusal disharmony and in case there is a persistent deciduous canine. But the
patient must be educated regarding the possible complication of leaving
behind the impacted canine in situ.
2. Surgical removal
Indications
1. Impacted canine is located very far from the occlusal plane

2. No other methods are possible to retain the tooth
3. The patient is not willing to undergo orthodontic treatment for longer
duration
4. Leaving behind may result in resorption of adjacent dental structures
5. Pathological changes in the crypt like infection, cyst formation, etc
6. The required space does not exist for the canine tooth in functional
position
7. Because of unfavourable anatomy of the tooth, other methods, like
repositioning is not likely to be successful.
The prognosis of the retained deciduous canine must be assessed and the
patient must be informed regarding further treatment.
Contraindications
1. When the cuspid can be brought into normal position surgically or

orthodontically.
2. Medically compromised patients, presenting with impacted cuspids.
Techniques
Operative plan:
a. Study radiographs
b. Classify impaction
c. Plan the type of soft tissue flap
d. Decide whether sectioning of tooth is needed.
Factors complicating the surgical removal
1. Proximity to the adjacent teeth

2. Proximity to the antral and nasal cavities
3. Formation of oroantral fistula leading to acute sinusitis.
Surgical technique
Removal of impacted cuspids in class I position (Figs. 18.69,
18.70)
Soft tissue flap
1. No. 12 BP blade is used to incise the tissues around the neck of the teeth
beginning on the lingual side of the maxillary central incisor and
extending to distal of 2nd bicuspid.
2. The flap is raised as a mucoperiosteal flap from the hard palate by
means of periosteal elevator until the bone is exposed.
FIGURE 18.69 (A–H) Maxillary bilateral palatal impacted canines
removed by surgical transpalatal approach.
FIGURE 18.70 Mandible canines—unusually impacted in mental

protuberance removed surgically.
Bone removal
• After reflecting the flap, it can be retracted by help of a flat bladed

instrument such as Austin retractor or Howarth periosteal elevator.
• Alternatively, the flap can be retracted by the help of tie sutures, tied
around the necks of opposite side teeth.
• Bone is removed circumferentially 3 mm around the crown of the
impacted tooth being careful not to damage the roots of adjacent teeth.
• Enlarge the size of the opening with burs so that the complete crown
may be seen.
Elevation of tooth
• An appropriate elevator is placed on one side of the crown and with

the palatal bone as the fulcrum; the impacted tooth is lifted from its
crypt in the palate. Extreme care should be taken to prevent injury to
the adjacent teeth.
• If this does not remove the impacted tooth, enlarge the opening and
repeat the procedure, using two elevators in the same way.
• If the tooth is still not luxated, the tooth requires crown root sectioning
and extraction.
Wound irrigation and closure
• All the debris, spicules are removed and bony margins trimmed.
• Tooth follicle is removed if present and the flap is sutured back into
position.
• The flap is compressed onto the palatal bone with a gauze palatal
packing placed for 4 h. Alternatively a compound stent or clear acrylic
plate (prepared preoperatively) may be used to prevent haematoma
collection and to maintain sustained pressure.
Removal of impacted cuspid in class II position

Labially placed impacted canine—can be exposed by using
1. Trapezoidal flap—two vertical limbs

2. Semilunar flap—no vertical limb
3. Triangular flap—only one vertical limb
After the mucoperiosteal flap is raised; bone is removed by using a chisel or

bur to expose the crown. Using the labial cortical plate as a fulcrum, the
elevator is inserted into the space between the bone and the tooth, to luxate the
tooth. If the bone overlying the root is too thick and unyielding, the tooth is
divided to remove the crown and root separately. Wound is debrided and
closed primarily.
Removal of impacted cuspids in class III position

(A). Crown in the palatal bone and root on buccal side
A semicircular flap is raised to expose the root apex. Circumferential bone
removal is done exposing the root. Root is sectioned and delivered labially.
Palatal flap is outlined and mucoperiosteal flap reflected and the bone
overlying the crown is removed to expose the periphery completely. A blunt
instrument is placed in contact with the root end of the crown through the
buccal crypt and tapped with a mallet, driving the crown out of its crypt
palatally. The flap is replaced and the wound closed primarily.
(B). Maxillary cuspid lying in the line of arch—along alveolar crest

When an impacted maxillary cuspid occurs in an edentulous jaw and lies in
the line of arch along the alveolar crest, every effort must be made to retain as
much bone as possible since they provide part of hard tissue of denture
bearing area.
Osteoplastic flap
A trapezoidal flap, slightly longer than the total width of the canine, is
designed in relation to the impacted canine. The bone is osteotomised along
the incision line using chisel and mallet. A buccal osteomucoperiosteal flap is
raised exposing the canine. The impacted canine is removed in toto or in
sections accordingly with minimal bone loss. After tooth removal the
osteomucoperiosteal flap is replaced and primary closure performed.
CHAPTER 19
Endodontic Surgery
Indications for endodontic surgery

Surgical drainage
Incision and drainage
• Incision
• Drain placement
Cortical trephination
Periradicular surgery
• Premedication
• Anaesthesia and haemostasis
• Soft tissue management
• Hard tissue management
Osteotomy
Periradicular curettage
Root-end resection
Root-end retropreparation
Corrective surgery
• Perforation repair
• Periodontal repair
• Root resection/hemisection
• Bicuspidisation
Replacement surgery (extraction/replantation)
Intentional replantation
Implant surgery
Endodontic implants
• Indications
• Technique
• Advantages
• Disadvantages
Root-form osseointegrated implants
Endodontic microsurgery
Advantages of surgical operating microscope
Traditional endodontic surgery versus microsurgery
Endodontic surgery encompasses surgical procedures performed to remove

the causative agents of periradicular pathosis and to restore the periodontium
to a state of biologic and functional health.
Indications for endodontic surgery

Refer (Table 19.1).
Table 19.1
Endodontic surgery: indications
1. Need for surgical drainage

2. Failed nonsurgical endodontic treatment
a. Irretrievable root canal filling material
b. Irretrievable intraradicular post
3. Calcific metamorphosis of pulp space
4. Procedural errors
a. Instrument fragmentation
b. Nonnegotiable ledging
c. Root dilacerations
d. Symptomatic overfilling
5. Anatomic variations
a. Root perforation
b. Apical root fenestration
6. Biopsy
a. Formation of periapical granuloma or cyst
b. Draining sinus tract
c. Nonresponsive to root canal treatment
7. Conservative procedures
a. Root resorptive defects
b. Root caries
c. Root resection
d. Hemisection
e. Bicuspidisation
f. Teeth with ceramic crowns
8. Replacement
a. Replacement surgery
i. Intentional replantation (extraction/replantation)
ii. Posttraumatic
b. Implant surgery
i. Endodontic
ii. Osseointegrated
Contraindications
However, following are the contraindications for endodontic surgery:
1. Poor periodontal health of the tooth with grade III mobility (bone loss).
2. Poor patient’s medical status—systemic diseases like leukaemia,
uncontrolled diabetes, anaemia, thyrotoxicosis, etc.
3. Local anatomical factors like nasal floor, maxillary sinus, mandibular
canal and its neurovascular bundle and mental foramen.
4. Traumatic occlusion which can’t be corrected.
5. Short root length.

Classification of endodontic surgery is depicted in Table 19.2.
Table 19.2
Endodontic surgery: classification
I. Surgical drainage
1. Incision and drainage (I & D)
2. Cortical trephination (fistulative surgery)
II. Periradicular surgery
1. Curettage
2. Biopsy
3. Root-end resection
4. Root-end preparation and filling
III. Corrective surgery
1. Perforation repair
i. Mechanical (iatrogenic)
ii. Resorptive (internal and external)
2. Root resection
3. Hemisection
4. Bicuspidisation
IV. Replacement surgery (extraction/replantation)
V. Implant surgery
1. Endodontic Implants
2. Root-form osseointegrated implants
I. Surgical drainage
Surgical drainage is indicated when purulent and/or haemorrhagic exudate
forms within the soft tissue or the alveolar bone forming a periradicular
abscess. A significant reduction of pain and a decrease in the length of
morbidity will follow the release of pressure and evacuation of the by-
products of inflammation and infection. Surgical drainage may be
accomplished by: (1) incision and drainage (I & D) of the soft tissue and (2)
trephination of the alveolar cortical plate (3) Apical trephination through the
apical foramen.
1. Incision and drainage

Fluctuant soft tissue swelling occurs when periradicular inflammatory exudate
exits through the medullary bone and cortical plate. Once perforating the
cortical plate, the exudates spread into surrounding soft tissues. When this
occurs, an incision should be made through the focal point of the localised
swelling to relieve pressure, eliminate exudates and toxins and stimulate
healing.
Learning the correct timing for incision and drainage takes experience.
Caution should always be exercised with hard, indurated swellings, especially
when accompanied by a fever. Such an infection can extend into fascial planes
and anatomic spaces and become life threatening. Unfortunately, incision into
a diffuse or indurated swelling before its localisation is often unsuccessful. In
this situation, it has been suggested that the patient be placed on appropriate
systemic antibiotic therapy and instructed to use hot salt water ‘mouth holds’
(¼–½ tsp of salt in a 10–12 oz glass of hot water) in the swollen area to assist in
localisation of the swelling to a more fluctuant state. The clinical situation
should be monitored every 24 h. As soon as the swelling has localised and a
fluctuant area has developed, surgical drainage should be performed.
Local anaesthesia
Whenever possible, nerve block injection is the preferable method for
obtaining local anaesthesia. However, when block injections are impractical,
anaesthesia will be limited to local infiltration. When local infiltration is used,
oral mucosa in the area to be injected should be dried and a topical anaesthetic
placed. Local anaesthetic should be deposited peripheral to the swollen
mucoperiosteal tissues. Injections directly into the swollen tissue should be
avoided because it is painful, may cause spread of infection and does not
produce effective anaesthesia. Patients should be warned that, as a result of
the effects of inflammation and infection, local anaesthesia may not eliminate
all discomfort associated with this procedure. This discomfort, however, is
usually minimal and transient in nature.
Incision
On administration of the appropriate block and/or infiltration anaesthesia,
surgical area should be isolated with sterile gauze sponges. Incision should be
horizontal and placed at dependent base of the fluctuant area. This will allow
the greatest release (flow) of exudates (Fig. 19.1A, B). The exudates should be
aspirated and a sample collected for bacteriologic culture. Probing with a
curette or haemostat into the incisional wound to release exudates entrapped
in tissue compartments will facilitate a more effective result.
FIGURE 19.1 (A, B) Incision placed at the dependent base of the

abscess.
Drain placement
The use of drains following an incision and drainage procedure is
controversial. Patients with localised or diffuse intraoral swellings, even if
mild extraoral swelling is present, do not usually require drains following
incision and drainage procedure. When sufficient drainage has occurred,
epithelial closure of the incisional wound will follow. Insertion of a drain is
only indicated when initial drainage is limited and in cases presenting with
moderate to severe cellulitis and other positive signs of an aggressive infective
process. The drain may be made of either iodoform gauze or rubber dam
material cut in an ‘H’ or ‘Christmas tree’ shape. It may be sutured in place for
added retention and should be removed after 2–3 days.
2. Cortical trephination
Cortical trephination is a procedure involving perforation of the cortical plate
to accomplish release of pressure from accumulation of exudates within the
alveolar bone. This is a limited use procedure for pain control with potential
negative complications. Patients who present with moderate to severe pain but
with no intraoral or extraoral swelling may require drainage of periradicular
exudates to alleviate the acute symptoms. Treatment of choice for these
patients is apical trephination, drainage through the root canal system. Apical
trephination involves penetration of the apical foramen with a small
endodontic file and enlarging the apical opening to the size of No 20k or No
25k file to allow drainage from the periradicular lesion into the canal space.
The decision to perform apical or cortical trephination is based primarily on
clinical judgement regarding urgency of obtaining drainage and also on the
feasibility of removing intra-radicular post and root canal obturation material.
Cortical trephination involves making an incision through mucoperiosteal
tissues and perforating the cortical plate with a rotary instrument (Fig. 19.2).
Good quality diagnostic radiographs and careful clinical examination will aid
in determining the appropriate trephination site. The site most often
recommended is at or near the root apex. Cortical trephination should always
be initiated from a buccal approach, never from the lingual or palatal
approach. A No 6 or No 8 round bur in a high-speed handpiece is used to
penetrate the cortical plate. A reamer or K type file is then passed through the
cancellous bone into the vicinity of the periradicular tissues. It is not necessary
to pass the instrument directly to the root apex to achieve effective results. The
clinician must exercise good judgement to avoid anatomic structures such as
the maxillary sinus, neurovascular contents of the mandibular canal and
mental foramen as well as the tooth itself.
FIGURE 19.2 Perforation of cortical plate.
II. Periradicular surgery

As endodontic surgery encompasses all the surgical procedures that are not
strictly limited to apical procedures, the use of term ‘periradicular’ is more
rational as opposed to periapical.
Periradicular surgical procedures regardless of their indication share a
number of concepts and principles:
• Need for profound local anaesthesia and haemostasis

• Management of soft tissues
• Management of hard tissues
• Surgical access, both visual and operative
• Access to root structure
• Periradicular curettage
• Root-end resection
• Root-end preparation
• Root-end filling
• Soft tissue repositioning and suturing
• Postsurgical care
All of these concepts and principles may not be used in any given surgery.
However, strict adherence to and application of these principles will greatly
influence the success of the surgical treatment.
Premedication
The following drugs are used in endodontic practices and are recommended
before and after endodontic surgery.
• Antiinflammatory analgesics. It is recommended that the patient (average

weight of 150 lbs) take ibuprofen (400 mg) just before surgery to
minimise the postsurgical inflammatory response. To minimise
bleeding problems during surgery, the dose should not be taken
sooner. With this regimen most patients will not require narcotic pain
medication.
• Tranquillisers. If a patient is very anxious about the surgery, sublingual
triazolam or 10 mg diazepam taken 15–30 min before the surgery
provides relief.
• Antibiotics. As stated previously, medically compromised patients (e.g.
with advanced diabetes, heart valve disease) must be premedicated in
accordance with the most recent AHA recommendations.
• Antibacterial rinses. To reduce oral microflora, the patient should be
instructed to use a 0.12% chlorhexidine gluconate mouth rinse the
night before surgery, the morning of surgery and 1 h before surgery.
Rinsing after the surgery for 1 week reduces microorganisms in the
oral cavity and promotes better healing.
Anaesthesia and haemostasis

The injection of a local anaesthetic agent that contains a vasoconstrictor has
two equally important objectives: (1) to obtain profound and prolonged
anaesthesia and (2) to provide good haemostasis during the surgical
procedure.
Selection of anaesthetic agent

The selection of an appropriate anaesthetic agent should always be based on
the medical status of the patient and the desired duration of anaesthesia.
Important differences between two major groups of local anaesthetic agents,
the esters and amides lie in their manner of metabolism and the potential for
allergic reactions. Esters have a much higher allergic potential than do amides.
Lidocaine, an amide type is the preferred local anaesthetic agent for
periradicular surgery because of its capability to produce a profound and
prolonged local anaesthesia with a lower potential for allergic reaction.
Haemostasis
Haemostasis in periradicular surgery can be considered in three phases: (1)
presurgical, (2) surgical and (3) postsurgical.
1. Presurgical haemostasis
The choice of vasoconstrictor in the local anaesthetic will have an effect on
both duration of anaesthesia and quality of haemorrhage control at the
surgical site. Vasopressor agents used in dentistry are direct-acting,
sympathomimetic (adrenergic) amines that exert their action by stimulating
special receptors (alpha- and beta-adrenergic receptors) on the smooth muscle
cells in microcirculation of various tissues. These agents include epinephrine
(adrenalin), levonordefrin and levarterenol (noradrenaline).
The action of a vasopressor drug on the microvasculature depends on: (1)
predominant receptor type and (2) receptor selectivity of vasopressor drug.
Alpha-receptors predominate in oral mucosa and gingival tissues, whereas
beta-receptors predominate in skeletal muscle. Epinephrine receptor
selectivity is approximately equal for alpha- and beta-receptors. Stimulation of
the alpha-adrenergic receptors will result in contraction of the smooth muscle
cells in the microvasculature with a subsequent reduction of blood flow
through the vascular bed. Stimulation of beta-adrenergic receptors will result
in relaxation of the smooth muscle cells in the microvasulature with a
subsequent increased blood flow. Epinephrine is the most effective and most
widely used vasoconstrictor agent in dental anaesthetics.
Injection sites and techniques

In addition to the choice of anaesthetic and vasopressor agents, sites and
technique of injection are important factors as well. Nerve block anaesthesia
involves injection in close proximity to a main nerve trunk that is usually
located some distance from the surgical site. Thus, the vasopressor agent in the
anaesthetic preparation used in nerve block anaesthesia will not significantly
affect the blood flow at the surgical site.
Haemostasis cannot be achieved by injecting into distant sites. Only small
vessels of microvasculature are affected by the injected vasopressor; larger
vascular channels are not. Therefore, additional injections must be
administered in the soft tissues in the immediate area of the surgery. This is
accomplished by local infiltration using a higher concentration (1:50,000
epinephrine) of vasopressor in the anaesthetic solution. It is important to note
that whatever technique is used to obtain anaesthesia, infiltration in the surgical
site is always required to obtain haemostasis.
Infiltration sites of injection for periradicular surgery are always multiple
and involve deposition of anaesthetic throughout the entire surgical field in
the alveolar mucosa just superficial to the periosteum at the level of the root
apices. Following block anaesthesia, using a 30 gauge needle with the bevel
towards bone, a small amount of solution (0.25–0.50 mL) should be slowly
deposited. The needle tip is then moved peripherally (mesially and distally)
and similar small amounts are slowly injected in adjacent areas.
Rate of injection in the target sites directly affects the degree of haemostasis.
Recommended injection rate is 1 mL/min, with a maximum safe rate of
2 mL/min. Rapid injection produces localised pooling of solutions in the
injected tissues, resulting in delayed and limited diffusion into adjacent
tissues. This results in minimal surface contact with microvascular bed and
less than optimal haemostasis.
2. Surgical haemostasis
Local haemostasis can be achieved by pressure technique of pressing cotton
pellets or gauze in the bony crypt for a few minutes. However, if bleeding
persists, topical haemostats are considered. Topical haemostats are classified
based on their mode of action: Table 19.3.
Table 19.3
Haemostatic agents
A. Mechanical agents
Bone wax
B. Chemical agents
Epinephrine saturated cotton pellets
Other vasoconstrictors
Ferric sulphate solution
C. Biologic agents
Thrombin USP
D. Absorbable haemostatic agents
i. Intrinsic action
Gelfoam
Absorbable collagen
Microfibrillar collagen haemostats
ii. Extrinsic action
Surgicel
iii. Mechanical action
Calcium sulphate
3. Postsurgical haemostasis
After the flap is sutured, haemostasis is achieved by an ice-cold wet sterilised
gauze placed over the sutures to stabilise the flap and control oozing of the
blood from the surgical sites. The gauze should be placed into the mucobuccal
fold for about 1 h and an ice pack should be applied to the cheek 10 min on, 5
min off, for 1–2 h.
Soft tissue management

Soft tissue management consists of flap design, incision, elevation, retraction,
repositioning and suturing. Soft tissue management is important to gain
adequate access to the surgical site and to ensure good postsurgical healing.
These goals can be achieved by selecting a proper flap design, making a
precise incision, elevating and retracting the flap with minimum trauma to the
tissue, repositioning and suturing the flap precisely into its position (refer to
Chapter 13 Incisions and Flaps).
Hard tissue management

Hard tissue management of periradicular surgery involves four stages: (1)
osteotomy, (2) curettage and biopsy, (3) root-end resection and (4) root-end
retropreparation.
Osteotomy
Osteotomy is the removal of the facial cortical plate to expose the root-end and
must be approached with a visualised 3D mental image to ensure that it is
made exactly over the apices (Fig. 19.3A, B). Periapical radiographs imaged
perpendicular to the roots from two different horizontal angles are done to
ascertain the length and curvature of the roots, position of the apices in
relation to the crown and number of roots. Additionally, proximity of each
apex to apices of adjacent teeth, mental foramen, inferior alveolar nerve and
antrum can be ascertained.
FIGURE 19.3 (A, B) Removal of cortical bone to expose the full
extent of lesion.
Clinician should superimpose the virtual image gained from the

radiographs and clinical examination onto the cortical plate to precisely locate
the root-end. The exact location of the apex can be determined by two
methods:
1. Using the tooth length measurement obtained from a well-angled

radiograph, a small surgical defect is created on the surface. A small
amount of radiopaque material like gutta percha is placed and a direct
radiograph exposed. The radiopaque material provides guidance for
the position of the root apex.
2. Locate the body of the root coronal to the apex where bony covering is
thinner. Then working in an apical direction, bone covering the root is
slowly removed with light brush strokes until root apex is identified.
The root surface can be distinguished from the surrounding osseous
tissue, by the following factors: (1) root structure generally has a
yellowish colour, (2) roots do not bleed when probed, (3) root texture is
smooth and hard as opposed to the granular, porous nature of bone
and (4) the periodontal ligament that can be stained by methylene blue
dye that surrounds the rooot.
Generation of heat
is of major importance during osseous tissue removal by bur as heating bone
tissue above 60°C results in interruption of blood flow and tissue necrosis. The
heat production can be minimised by the use of:
1. Liquid coolant during bone removal. The coolant functions by: (1)
dissipating the heat generated and (2) keeping the cutting flutes of the
instruments free of debris.
2. Light brush strokes with short, intermittent cutting.
Visual and operative accesses

are the factors that determine the osteotomy size. Failure to achieve sufficient
visual and operative access results in increased time required for the surgical
procedure, increasing the stress level of the surgeon and trauma to adjacent
tissues.
Periradicular curettage (Fig. 19.4)

Periradicular curettage involves removal of the periradicular inflammatory
tissue and is best accomplished by using sharp surgical bone curettes and
angled periodontal curettes. Administering a local anaesthetic solution
containing a vasoconstrictor into the soft tissue mass will reduce the
possibility of discomfort to the patient during the debridement process and
will also serve as haemostatic at the surgical site.
FIGURE 19.4 (A–C) Image showing well defined unilocular

radiolucency involving 21, 22, 23. (D, E) Cyst enucleation, (F)
Excised specimen.
Entire tissue mass is removed by inserting the bone curette, between the soft
tissue mass and the lateral wall of the bony crypt with the concave surface of the
curette facing the bone (Fig. 19.5A). Pressure is applied against the bone as the
curette is inserted (Fig. 19.5B). As the periphery of the lesion is freed the
concave portion of the curette is turned towards the soft tissue and used in a
scraping manner to free the lesion from the deep walls of the bony crypt
(Fig. 19.5C). Then, the tissue is placed in buffered formalin and sent for
histopathologic examination.
FIGURE 19.5 (A) Placement of curette with concave surface facing

bone. (B) Pressure applied against bone. (C) Schematic
representation of tissue freed by turning concave surface towards
the tissue.
Root-end resection
Periradicular curettage only eliminates the effect (periapical lesion) of the
leakage but not the cause/origin of the lesion. Hence, periradicular curettage
without root-end resection and root-end filling should never be considered as
a terminal treatment in periradicular surgery unless associated with
concurrent orthograde root canal treatment.
Factors determining amount of root resection

They can be classified as:
1. Biologic factors:
Persistent symptoms and continued presence of a periradicular lesion
2. Technical factors:
a. Intraradicular posts
b. Crowned teeth without posts
c. Irretrievable root canal filling materials
d. Procedural accidents
Three important factors are to be considered before performing a root-end

resection:
1. Instrumentation
2. Extent of root-end resection
3. Angle of root-end resection
1. Instrumentation: The choice of bur type and the use of either a low- or
high-speed handpiece for root-end resection are considered. A smooth,
flat, resected root surface is preferred clinically and may promote
tissue healing. Plain fissure burs, both high- and low-speed, produce
the smoothest resected root surface. The plain fissure bur and a low-
speed handpiece results in the least gutta percha distortion.
2. Extent of root-end resection: The amount of root to be resected is depends
on various factors that have to be evaluated on an individual case by
case basis. The factors are:
a. Visual and operative access to the surgical site (Fig. 19.6)
b. Anatomy of the root
c. Incidence of lateral canals and apical ramifications at the
root-end—3 mm root-end resection significantly eliminates
the major anatomic entities
d. Number of canals and their position in the root.
e. Need to place a retrofilling material surrounded by solid
dentine
f. Presence and location of procedural error
g. Presence and extent of periodontal defects
h. Level of remaining crestal bone
3. Angle of root-end resection: The root-end resection must be done
perpendicular (90 degree) to the long axis of the root whenever
possible (Fig. 19.7). In situations where a perpendicular bevel may not
be possible as in the mesiolingual root of the mandibular first molar, a
10 degree bevel may be used. Two major reasons that prevent the use
of acute bevel angle (<90 degree) for root resections are: (1) acute bevel
angle results in an uneven or incomplete resection of the apex with the
buccal aspect resected completely leaving the lingual part partially or
not resected at all and (2) bevelling results in opening of dentinal
tubules on the resected root surface that may communicate with the
root canal space and result in apical leakage even after retrofilling
(Fig. 19.8A, B).
FIGURE 19.6 Resection of buccal root to gain access to the lingual
root (access for palatal root is about 0–10 degrees).
FIGURE 19.7 Resected root surface should be flat and smooth.
FIGURE 19.8 (A) Numerous dentinal tubules opened on bevelled
root resection. (B) Less number of dentinal tubules open on a root
resected flatly.
Root-end retropreparation
The purpose of a retropreparation in periradicular surgery is to create a cavity
to receive a root-end filling. The preparation for and the placement of root-end
filling is recommended whenever root resection has been performed as the
resection is found to disturb the gutta percha seal. An ideal retropreparation
must be a class I preparation at least 3 mm into root dentine with walls parallel
to the anatomic outline of the pulp space. Thorough knowledge about the root
canal morphology is of utmost importance in retropreparation. An isthmus or
anastomosis is a narrow connection that is frequently present between root
canals of the same root. Isthmus can be either complete or incomplete and
usually they contain pulp tissue. Thus, isthmus is a significant factor in
determining the design and placement of the root-end preparation.
Five requirements have been identified for retropreparation; they are:
1. Apical 3 mm of the root canal must be freshly cleaned and shaped

2. Preparation must be parallel to the anatomic outline of the pulp space
3. Adequate retention form must be created
4. All isthmus tissue must be removed
5. Remaining dentine walls should not be weakened.
Traditional retropreparation technique involves use of either miniature

contra-angle or straight handpiece with a small round or inverted cone bur
and is dependent on the physical access available around root apex. These
preparations are often placed obliquely into the root, resulting in a risk of
perforation and/or weakening of the dentine walls (Fig. 19.9A, B).
FIGURE 19.9 (A) Obliquely placed retropreparation with
conventional handpiece. (B) Perforation and weakening of dentinal
walls.
Ultrasonic retropreparation technique solves the major inadequacies of the

traditional bur preparation (Fig. 19.10). Ultrasonic microtips are very narrow
in diameter (i.e. about one-tenth the size of a conventional microhead
handpiece). Specially designed tips produce smooth cutting with relatively
little chatter when the tips are activated against the dentinal walls of the apical
preparation. A light touch with a brush type motion with irrigation should be
used for maximum cutting efficiency.
FIGURE 19.10 Ideal retropreparation achieved with ultrasonic.
Advantages of ultrasonic preparation are:
• Better access, especially in difficult-to-reach areas (e.g. a lingual apex)

• More thorough debridement of tissue debris
• Conservative preparations tracing the long axis at a precise depth of
3 mm
• Precise isthmus preparations with parallel canal walls for better
retention of filling materials
Retrofilling material (Box 19.1)

The purpose of placing a retrograde filling is to provide a tight, biocompatible
apical seal, which prevents the leakage of potential irritants from the root
canal into the periradicular tissues (Figs. 19.11, 19.12). Box 19.2 summarises the
ideal properties for a retrofilling material. Numerous materials beginning from
silver amalgam, zinc oxide-eugenol to a more recent mineral trioxide
aggregate (MTA) have been used as a retrofilling material. Box 19.3
enumerates the retrofilling materials used from time immemorial to the
present day. So far, no material appears to be anideal root-end filling material.
Materials that most closely meet the requirements are: (1) intermediate
restorative material (IRM), (2) super EBA and (3) MTA. IRM and super EBA
are modified zinc oxide-eugenol cement whereas MTA principally consists of
compounds containing calcium and phosphorus ions. MTA is hydrophilic
with excellent biocompatibility and has a superior sealing ability of all the
available retrofilling materials. The unique advantage is the regeneration of
new cementum over MTA. However, difficult manipulation and long setting
time are the greatest disadvantages of MTA (Fig 19.13).
Box 19.1 Instruments for apical placement of fillings
• Reverse fill carriers—two, one large and one small

• Reverse fill pluggers—two, one large and one small
• Amalgam squeeze clothes (used if amalgam is being employed as reverse
filling material)
• Stellate plastic instrument
• Miniature reverse fill mirrors
• Miniature head aspirator tips—to fit on surgical aspirator, but much
smaller than normal size; may be fabricated by cutting and bevelling tip
from a 16-gauge needle and using an adapter on the usual aspirator tip
holder
• Ultrasonic holder and appropriate tips
FIGURE 19.11 Placement of retrofilling material using carrier.
FIGURE 19.12 Condensation of material.
Box 19.2 Ideal properties for retrofilling materials

Ideal retrograde filling materials
• Should be well tolerated by periapical tissues

• Should adhere (i.e. ideally bond) to the tooth structure
• Should be dimensionally stable
• Should be resistant to dissolution
• Should promote cementogenesis
• Should be bactericidal or bacteriostatic
• Should be noncorrosive
• Should be electrochemically inactive
• Should not stain tooth or periradicular tissue
• Should be readily available and easy to handle
• Should allow adequate working time, then set quickly
• Should be radiopaque
Box 19.3 Retrograde filling materials
• Amalgam
• Gutta percha
• Gold foil
• Titanium screws
• Glass ionomers
• Ketac silver
• Zinc oxide-eugenol
• Cavit
• Composite resins
• Polycarboxylate cement
• PolyHEMA
• Bone cements
• IRM
• Super EBA
• Mineral trioxide aggregate (MTA)
FIGURE 19.13 (A–E) Root end retropreparation with retrofilling.
Soft tissue repositioning and suturing

After completion of the root-end filling, a radiograph is taken to evaluate the
placement of the root-end filling and to check for the presence of any root
fragments or excess root-end filling material. The surface of the flap between
the mucoperiosteum and the alveolar bone is thoroughly examined to remove
any debris or foreign material that may be present. Then the elevated
mucoperiosteal tissue should be gently replaced to its original position with
the incision lines approximated as closely as possible. A surgical gauze,
slightly moistened with sterile saline is applied gently with firm pressure to
the flap tissue for 2–3 min before suturing. Tissue compression, both before
and after suturing enhances clotting and also approximates the wound edges.
Suturing approximates the incised tissues and stabilises the mucoperiosteal
flap until reattachment occurs. The major problem in oral tissues is the
constant bathing of the suture material and suture tract with saliva containing
a high concentration of microbes that may gain entrance to underlying tissues.
Currently, removal of the sutures is recommended within 48 h. The
interrupted suturing technique provides far better flap adaptation than the
continuous technique and is the most commonly used for endodontic surgery.
Sutures should not stretch or close an incision too tightly as the former results
in a flap tear and the later compromises circulation and increase the chance for
the sutures to tear loose on swelling.
Postsurgical care
Most likely surgical sequelae include:
1. Pain
2. Bleeding and swelling
3. Ecchymosis
4. Infection
5. Transient paraesthesia
Important components of postsurgical care include

(1) genuine expression of concern and reassurance to the patients regarding
both their physical and emotional experience and (2) good patient
communication—postsurgical instructions conveyed both verbally and in
written manner.
1. Do not do any difficult activity for the rest of the day. Be careful and do
not bump the face where the surgery was done. Should not drink any
alcohol or use any tobacco (smoke or chew) for next 3 days.
2. It is important to have a good diet and drink plenty of liquids for the
first few days of the surgery.
3. Do not lift up the lip or pull back the cheek to look at where surgery
was done. This may pull the stitches loose and cause bleeding.
4. A little bleeding from the surgical site is normal. This should only last
for a few hours. There may be little swelling and bruising of the face.
This should only last for a few days.
5. Place an ice bag (cold) on face where surgery was done. Leave it on for
20 min and take it off for 20 min. Do this for 6–8 h.
6. After 8 h, the ice bag should not be used. The day after surgery, put a
soft, wet hot towel on the face where the surgery was done. Do this as
often as possible for the next 2–3 days.
7. Discomfort after the surgery should not be bad, but the area will be
sore. Use the pain medication recommended.
8. Rinse the mouth with 1 tablespoon of chlorhexidine mouthwash 2 times
a day, once in the morning and once at night for 5 days.
9. It is important to remove the stitches after 2 days.
Corrective surgery
Corrective surgery is categorised as surgery involving the correction of defects
in the body of the root other than the apex. Corrective surgical procedures
may be necessary as a result of procedural accidents, resorption, root caries,
root fracture and periodontal disease. Corrective surgery may involve
periradicular surgery, root resection—removal of an entire root from a
multirooted tooth leaving the clinical crown intact (Fig. 19.14), hemisection—
the separation of a multirooted tooth and the removal of a root and the
associated portion of the clinical crown (Fig. 19.15) or intentional replantation.
Reparative defects of the root and associated procedures are classified as
follows:
a. Mechanical
b. Resorptive and root caries
2. Periodontal repair
a. Guided tissue regeneration
b. Root resection/hemisection
c. Bicuspidisation
FIGURE 19.14 Root resection.

FIGURE 19.15 Hemisection.
a. Mechanical
Perforations are procedural accidents that can occur during root canal or
postspace preparation. High potential areas for perforations are pulp chamber,
floor of molars, distal aspect of the mesial root of mandibular molars and
mesiobuccal root of maxillary molars. Corrective surgery should be reserved
for those teeth when internal repair is not a treatment option or when internal
repair has failed.
Midroot perforations, such as those resulting from postspace preparations
should be immediately sealed internally, if possible or calcium hydroxide
should be placed as an intracanal dressing and sealed at the subsequent
appointment. If the perforation is excessively large or long standing, a full
mucoperiosteal flap should be reflected, the perforation site identified and the
repair made with an appropriate repair material. If the perforation is located in
the apical third of the root, a root-end resection, extending to the point of the
perforation and a root-end filling should be considered as a more effective and
efficient way of handling this clinical situation.
b. Resorption (external or internal) and root caries
Repair of a defect on the root surface depends to a large extent on whether
there is communication between the resorptive defect and the oral cavity
and/or the pulp space. When communication between the resorptive defect
and the oral cavity exists, corrective surgery is usually indicated.
In case of a resorptive defect that opens into the gingival sulcus, the
approach depends to a great extent on the location and extent of the defect. It
is approachable from the buccal or facial side, a full mucoperiosteal flap
should be raised and extent of the defect visualised. If the resorptive defect has
not extended into the pulp space, it is restored with a suitable material. If the
defect extends into the pulp space, a temporary internal matrix (large gutta
percha point) is placed in the root canal and the resorptive defect repaired.
After that the flap is repositioned and stabilised with sutures and the
endodontic treatment can be completed at the same or subsequent
appointment.
2. Periodontal repair
a. Guided tissue (bone) regeneration

Before the advent of guided tissue bone generation and demineralised freeze
dried bone allografts, extensive periodontal defects required extraction or root
amputation. The quality and quantity of the alveolar bone regenerated with
GTR is found to be superior than without the GTR and an allograft.
b. Root resection/hemisection
This refers to the removal of one or more roots of a multirooted tooth while
other roots are retained. It is a logical way to eliminate a weak diseased root to
allow the stronger roots to survive which, if retained together, would
collectively fail.
Advantages
1. Salvaging and retaining two-third or even one-half of a tooth might add

sufficient support to maintain arch integrity.
2. Also, as root amputations almost always involve molar teeth and
frequently the most posterior abutment or an aid to the posterior
abutment, retaining even half a tooth could avoid the need for a
removable prosthesis and enable the patient to use fixed prosthesis or a
splint.
Indications
1. Existence of periodontal bone loss to the extent that periodontal
therapy and patient maintenance do not sufficiently improve the
condition.
2. Destruction of a root through resorptive process, caries or mechanical
perforations.
3. Surgically inoperable roots that are calcified, contain separated
instruments or grossly curved.
4. The fracture of one root that does not involve the other.
5. Conditions that indicate the surgery will be technically feasible to
perform and the prognosis is reasonable.
Contraindications
1. Lack of necessary osseous support for the remaining root or roots.

2. Fused roots or roots in unfavourable proximity to each other.
3. Remaining root or roots endodontically inoperable.
4. Lack of patient motivation to properly perform home care procedures.
General rules for root amputation

Root amputations are usually performed for reasons in one of two general
categories: either a severe periodontal defect is present or an endodontic or
restorative problem is involved. Once it is determined that an indication for
amputation is present, a careful evaluation must be made of the tooth segment
that is to remain before any surgical procedures are performed.
Importance of root anatomy

Length, width and contour of the root are important factors in determining
where the resective cut is made and the strength of the remaining tooth
structure. Hence, a thorough knowledge of root anatomy is mandatory before
any root amputation procedure is attempted.
Endodontic therapy prior to root amputation

Whenever possible, canal fillings should be placed in the roots to be retained
prior to the amputation. This may be accomplished either at a preceding
appointment or at the same appointment but before the surgery.
Although, the root to be amputated requires no canal filling to seal the apex,
placement of a filling often facilitates the surgical procedure in aiding the
location of the root.
Root amputation on periodontally involved teeth

When amputation is performed for a root with a severe periodontal lesion,
there is no need to raise a flap. If either the vertical cut or the crown-
precontouring technique is utilised, the objective is still to separate the root to
be amputated from the rest of the tooth at the furcation. Placing a straight
elevator into the furcation and giving it a slight rotatory movement determines
that the separation has been obtained. If separation is complete, the root being
amputated will move in one direction while the portion of the tooth that is to
remain will move in the opposite direction. If the entire tooth moves in one
direction, further preparation of the furcation must be performed.
After separation is verified, the root should not be delivered until the crown
of the segment that is to remain has been reshaped. Any sharp edges that
might cut the tongue or cheek are trimmed with the tapered diamond stone
burs. The occlusal height is reduced to prevent strong occlusal contact during
mastication of tough or chewy foods and a modified preparation for the
restoration to be placed may be performed. All this is done with the root to be
amputated still in place to prevent amalgam, gold or temporary fillings,
calculus, tooth or other debris from being pushed into the socket.
The patient is instructed to rinse vigorously with mouthwash and any
remaining debris in the area is removed by suction and evacuation. The angled
elevators are used to loosen the root and may be sufficient to perform the
complete root extraction. If a greater grasp on the root is required, suitable
forceps are used.
Root amputation on teeth with normal periodontal support

In cases where there is relatively normal bone, a flap will be required to
deliver the amputated root. Once the flap is raised, the bone around the root to
be amputated is removed using a tapered fissure carbide bur with the airotor
and waterspray. Bone is similarly removed in the furcation area to allow direct
visualisation of the position where the root joins the rest of the tooth. Using
the vertical root technique, which will be described for each molar tooth, the
operator separates the root to be amputated from the remainder of the tooth at
the furcation. A straight elevator is used in the furcation to see whether
interdental bone has been removed to deliver the root. If the root does not
appear to be loosen in its socket, further removal of bone may be needed. For
maxillary molars, both buccal and lingual bone may require reduction.
There should be no hesitancy to remove alveolar bone closely surrounding a
root to be amputated as it makes the procedure much easier and this bone
would be resorbed after the amputation anyway. For mesiobuccal roots of a
maxillary first molar which frequently have a distal curvature near the apex, it
is often wise to remove all the buccal bone to the apex prior to using any
elevation. As with periodontally involved teeth, crown of the remaining
segment is trimmed prior to the amputation. The flap is sutured in place after
root removal.
Cautions to observe before amputation procedure
The techniques involved in root amputation are not complex, particularly
when a severe periodontal defect is present. In many cases, surgical procedure
is well within the technical ability of most general practitioners. The greatest
number of failures must be attributed to the inability of the dentist to restore
altered tooth form correctly or, in the absence of sufficient supporting
structures, to retain the remaining portion of the tooth. Therefore, before any
indications for root amputation are considered, it must be ascertained that
these two more important considerations can be satisfied:
Sufficient support available for the segment to be retained

When the indication for root amputation is a hopeless periodontal defect on
one root, periodontal evaluation of the segment that is to be retained is done.
Furcation involvements that require amputation do not always limit
themselves to the surface of one root but often destroy the bony septum of the
adjacent root as well. When one root is amputated, the neighbouring retained
roots may still have an irrepairable periodontal condition. This condition is
found in mandibular molars with severe furcation involvement. Regardless of
which root is amputated, the retained root may still have a severe periodontal
lesion or insufficient bony support on the surface that had been adjacent to the
furcation. This is particularly likely when the roots have little spread and thus
minimal bone between them.
Proper restoration of retained segment

Another indication for root amputations is severe tooth destruction, often due
to furcation caries. In these cases, the retained segment must be restorable or
else the entire procedure will fail. After root amputation some type of post or
coronal root stabilisation must be used, followed by a core that covers the
entire root face. In most instances, remaining segment is not restored as a
single unit, but rather splinted directly or by use of a pontic to one or more
adjacent teeth.
If this regimen of post, core, crown and probably splint is not practical or
possible, the root amputation should not be performed. In certain cases, the
prognosis after amputation may be questionable and the dentist is reluctant to
place a complex prosthesis until the outcome is more certain. With this in
mind, a temporary prosthesis may be fabricated but should be replaced by
more desirable restorative method when success is gained.
Instrumentation for root amputation
• The instruments needed specifically for root amputation are as follows:

• Surgical length or long shank fissure burs—sizes 700, 701, 557 and 558
—used to separate roots and remove overlying bone.
• Long tapered fissure diamond stones—used to smoothen retained
tooth segment.
• Elevators—straight (wide and narrowtip); set of Potts or other angle
elevators; apical elevators.
• Forceps—upper and lower universal forceps and root tip forceps, plus
any other favourite forceps used for single-rooted teeth.
• If a flap is to be raised during amputation procedure all the
instruments needed for periapical surgery will be required in addition
to instruments needed for root amputation procedure.
Methods of root resection
Vertical cut method

This is used for hemisection wherein the pathologic root and its associated
portion of the crown is also removed. The vertical cut method utilises a long
shank, tapered fissure carbide bur to section through the entire crown and root
to the furca in gaining separation. Water is not needed while making this
preparation on solid tooth structure, particularly on maxillary teeth where the
spray would collect on the mouth mirror and interfere with vision. However,
irrigation followed by suction and evacuation is needed periodically to
remove the tooth and temporary filling debris that tends to collect within the
preparation and in the furcation area where bone should not be overheated.
It must always be remembered that both bifurcations and trifurcations are
some distance from the occlusal surface of the tooth. Therefore, a deep
preparation is required before an elevator is used to see if separation is gained.
If the elevator is used prematurely, a large section of crown may be snapped
off, which may make subsequent restoration more complex or the root may
fracture at an undesirable angle. If doubt exists as to the depth of the cut, a
radiograph can be taken for verification of the position.
Advantages of vertical cut method
• Direct visualisation of the bur penetration ensures that the preparation

will be in the correct position.
• Removal of that portion of the crown that is over the root prevents
undesirable postoperative occlusal forces.
• Position of each cut, based on the anatomy of the furcation, allows the
root to cleave along desirable angles.
• Allows excellent visualisation of the furcation after amputation for any
needed trimming or smoothening with long shank, tapered fissure
diamond stones.
With a vertical preparation, crown over the amputated root is removed and
any occlusal stresses are dissipated along the long axes of the remaining roots.
The restorative dentist is cognizant of the need for modified occlusal shape in
a new crown and there are no areas for collection of debris. The indication of
root amputation may have been furcation involvement and it is much easier
for both the dentist and the patient to gain access for cleaning the new
furcation area without a bulky portion of the crown impeding the way.
Presurgical crown-contouring method

This technique is extremely useful in treating maxillary molars with
periodontal defects. Occlusal reduction should be considered before
proceeding with crown-contouring (Fig. 19.16A). The presurgical crown-
contouring method involves trimming the portion of the crown over the root
to be amputated to gain separation (Fig. 19.16B). In this technique, it is
important that the root to be amputated has a canal filling prior to the surgery
because the gutta percha or amalgam provides an important landmark.
FIGURE 19.16 (A, B) Trimming the crown of the involved tooth.
A tapered fissure bur is used to trim back the crown over the root to be
amputated, with the depth of the preparation being approximately at the
cementoenamel junction. After some crown reduction has been accomplished,
surface of the root will start to come into view to aid in further preparation.
The position of the canal filling marks the centre of the root. As soon as the
furcation is visualised, separation and extraction may be accomplished by the
methods previously described.
Horizontal preparation
This preparation utilises a horizontal/oblique cut to amputate the involved
root at the point where it joins the crown without the crown being altered in
the preparation. This technique is termed root amputation and is not the
preferred method of choice in most cases because cutting the tooth in this
manner leaves a deep trough between the crown and the alveolar mucosa,
which acts as an obvious nidus for food and debris. Also, because crown has
not changed in configuration, any occlusal pressures over the amputated root
will tend to put severe stress from an undesirable direction on the remaining
roots.
Anatomical considerations for root amputation procedures
Maxillary first molar

Each of the molar tooth possesses a specific reason why root amputation
procedures may fail, even assuming that the indications and treatment are
correct. In the maxillary first molar, amputation of the distobuccal root has, by
far, the most favourable outlook. Distobuccal roots occupy much less area in
the furcation then do the other two roots. The natural curvatures of the
mesiobuccal and palatal roots will give resistance to all directions of stress
without the distobuccal root. For this reason, the tooth need not be splinted to
adjacent teeth—a fact not true in any other molar amputation and finally, the
procedure is the easiest to perform among maxillary molar amputation
procedures. Long-term prognosis for distobuccal root amputation in the
maxillary first molar is very favourable.
Mesiobuccal and palatal amputations do not show success as distobuccal
removals. Both of these roots are quite large with retentive curvatures. Errors
in surgery occur with palatal root amputations because the operators often
think that the root is larger than it truly is. Conversely, surgical errors occur
with mesiobuccal root amputations because the operator often thinks that the
root is smaller than it truly is. If either of these roots is removed, splinting to
one or more adjacent teeth is mandatory. The restoration, when either root is
removed, is very complex because of the shape of the remaining root in the
furcation.
Amputation of the mesiobuccal root

The greatest problem in amputation of mesiobuccal root of the maxillary first
molar is failure to recognise the considerable buccolingual width involved.
The operator is fooled into thinking that the root is very slender, as indicated
in the routine radiograph and so the root is cut much too far buccally, leaving
a spicule in the tri-furcation. If the amputation were performed for periodontal
reasons, this remaining root spicule would perpetuate the retention of debris
in the furcation and negate the effectiveness of treatment.
Vertical cut method is used to separate the lines of the furcation. It is usually
a relatively simple matter to make a buccal cut because the buccal groove
correctly marks the position of the underlying furca. This cut is carried a few
millimetres towards the centre of the tooth. Next, initial mesial cut is made at a
position approximately two-third the distance from the buccal surface of the
crown to the lingual surface. This usually conforms to the position where
lingual extension of mesioocclusal cavity preparation terminates. Again, the
cut is carried a few millimetres towards the centre of the tooth. These two cuts
are joined with deep penetration of the fissure bur and should conform to the
furcation position.
As suggested in the rules for amputation, a straight elevator verifies the
separation. A snapping sound may occur when the elevator is used and the
operator may fear that the root has cracked in an undesirable position. On the
contrary, cleavage generally will occur right through the furcation to separate
any portions that were not cut by the fissure bur. The remaining segment is
trimmed and the root amputated.
If the presurgical crown-contouring method is used, entire coronal portion is
trimmed back over the root until the furca is visualised.
Amputation of the mesiobuccal root, in both the maxillary first and second
molars, is strongly discouraged because of the difficult shape to work with, the
presence of the depression in the furcation area, the need for splinting to an
adjacent tooth and the frequent errors in removal of this root.
Amputation of the distobuccal root

The buccal cut is placed in the same position as for amputating the
mesiobuccal root. The distal cut is placed half the distance between the buccal
and palatal surfaces of the tooth and then both cuts are connected with deep
penetration of the bur along the lines of the schematic drawing. Once
separation is verified and the remaining crown contoured, the root is removed.
The amputation of the distobuccal root unquestionably is the best tolerated
of all amputation procedures from a longevity standpoint. The retained palatal
and mesiobuccal roots are large and retentive and offer excellent support for
the altered tooth. From a mesial view, the palatal root curves first to the
lingual and then to the buccal, whereas the mesiobuccal root from the buccal
view curves first to the mesial and then to the distal. Thus all directions of
torquing are resisted.
Because of the strength of the remaining roots, it is not mandatory for the
tooth so treated to be splinted to an adjacent abutment. In other cases of root
amputation on a maxillary molar, mesiobuccal or palatal or any two roots,
splinting to an adjacent tooth must be accomplished.
Amputation of a palatal root

Amputation of a palatal root is often a complicated procedure, even if a severe
periodontal condition is present. In addition, restoring two buccal roots is a
difficult problem. Therefore, two buccal roots should be retained only when
no other solution is available.
Unless the periodontal condition is so severe that a pocket reaches the apex
of the palatal root, a flap should be raised for the amputation procedure.
Otherwise the root’s considerable length, width and curvature often make it
difficult to remove.
Mesial and distal cuts only are used to gain separation from the buccal roots.
Care should be exercised in use of the elevator to verify the separation because
the thinner buccal roots may become loosened. A tapered fissure carbide used
to remove bone mesial and distal to the palatal root before any delivery is
attempted.
Amputation of both buccal roots

If both buccal roots are to be amputated, mesial, distal and buccal cuts are
made as described earlier. The roots are delivered separately. It is unwise
merely to make the mesial and distal cuts and then attempt to remove the
buccal roots in one section. The apical curvatures of these two roots often are
towards each other and any bone remaining between them may cause
considerable problems.
Amputation of palatal and distobuccal roots

Because of considerable bulk of the mesiobuccal root, it is possible to retain it
alone in certain cases and amputate both distobuccal and palatal roots. This
should be done only in cases where there are no other molar abutments
available and where there are sufficient anterior abutments to support and
stabilise the mesiobuccal root.
Maxillary second molars

Maxillary second molars have furcations at higher levels, roots closer together
and more differences in size and shape then do first molars. The mesial roots
are larger, with deeper depressions and hence are more retentive than the
distal root. If the mesial root can be saved, it aids in tooth support. However,
mesial root is more difficult to treat endodontically, so periapical failures are
common. The root is difficult to restore, particularly when a post and core is
placed. The distal root is easier to treat endodontically and to restore, but it is
not as retentive. Root amputation for maxillary second molars should be
avoided at an even higher level than those for the first molar. There are a
number of reasons for this:
1. There are several variants in anatomy of this tooth, even though the
most common condition is, similar to the adjacent maxillary first molar,
with three separate roots. However, even in this condition, root fusions
of any combination (palatal to either buccal or two buccals to each
other) may be present and are very difficult to diagnose prior to
initiating the procedure. Attempting to amputate a fused root is
frustrating and very difficult.
2. Another variation, which occurs approximately 10% of the time,
involves this tooth having only two roots, with the buccal root
containing a single (most common) or two canals. Performing
endodontic treatment prior to root amputation is very helpful in
visualising these conditions because the canal fillings make the roots
easier to identify on radiographs.
If only one buccal root is present, difficulties encountered by surgical and

prosthetic treatment contraindicate root amputation. Fortunately conditions
requiring amputation with this root configuration occur rarely.
When three separate roots are present, mesiobuccal root is very wide
buccolingually with a higher than previously anticipated percentage of two
canals, just as is in the first molar. Therefore, if the tooth is treated
endodontically just to have an amputation of another root, with a high
percentage of two canals are located, chance of endodontic failure will be high.
When mesiobuccal root is root to be amputated, problems with the
buccolingual width and position of the tooth being so far posterior make the
surgical procedure quite difficult, even with a large periodontal defect and a
flap. As in the first molar, amputation of the mesiobuccal root in the second
molar requires splinting.
Amputation of the distobuccal root is complicated by its posterior position,
but has the advantage of usually not having a tooth behind it. With a large
periodontal defect, crown-contouring method works very well. Usually
amputation of the distobuccal root will not require restoration with splinting
to an adjacent tooth.
Amputation of the two buccal roots to keep a strong palatal root,
particularly when the buccal roots are severely involved periodontally, is not
complicated surgically. However, restoring this root must involve splinting to
an adjacent root. If the first molar is present and not seriously involved
periodontally, it would be better to extract the entire second molar rather than
keep only a palatal root. Therefore, this procedure requires a restorable third
molar to be adjacent. Root amputation of the palatal root alone to keep the two
buccals is very rarely attempted.
Amputation of mesiobuccal root

The buccolingual width of mesiobuccal root is still quite wide compared to
mesiodistal width, even though it is not as wide as the root of the first molar.
The amputation procedure is similar; however, a slight variation is that the
mesial cut is placed slightly closer to the contact point between the first and
second molars.
Amputation of distobuccal root
Amputation of distobuccal root of the maxillary second molar is very similar
to that performed on the first molar. However, because the distal root may be
slightly wider, distal cut is placed slightly more to the lingual aspect.
Amputation of both buccal roots

As in the maxillary first molar, both roots of the second molar may require
amputation. However, because of the smaller size of the palatal root compared
with that of the first molar, such a procedure should be attempted only when
adjacent support is available for splinting. Use of palatal root alone as a distal
abutment is hazardous otherwise. For the amputation, as in the first molar,
mesial, buccal and distal vertical cuts are made and each of the buccal roots is
removed separately.
Amputation of adjacent roots of maxillary molars

A common site for a severe periodontal lesion is between the maxillary first
and second molars. Surgical treatment for such a condition will often involve
amputation of distobuccal root of the maxillary first molar. Loss of that root
leaves the mesiobuccal and palatal roots, which are generally excellent
retentive roots for the first molar.
However, amputating the adjacent roots of these teeth, i.e. distobuccal root
of the first molar and the mesiobuccal root of the second molar is not advised.
They have stated that the teeth are complicated to restore, the shapes
developed are difficult for the patient to maintain in health and the patient
might have speech difficulties.
Amputation of distobuccal root of both first and second molars

This procedure is possible and does not lead to severely weakened teeth, as
would amputation of the mesiobuccal root of both molars.
Mandibular molars
With mandibular second molars, again there are many more variants than for
first molars, the furcation is farther from the gingival line and the root apices
are usually closer—all complications or outright contraindications to
successful amputations. Root amputation procedures on mandibular molars
are usually referred to as hemisections. Because of the two roots present, one-
half of the crown and one root are removed. In addition, another procedure
referred to as bicuspidisation may be performed on mandibular molars, in
which a separation is made between the roots but neither is removed (Figs.
19.17, 19.18).
FIGURE 19.17 Vertical cut extended into the furcation.
FIGURE 19.18 Separation of the weakened root from the tooth.
Amputation of the mesial root

Vertical cut method is excellent for amputation of either root of a mandibular
molar. Because there are no clues on the crown as to the position of the furca,
use of a silver point placed in the bifurcation will greatly aid in the placement
of the vertical cut. Since many molars have amputations because of the
existence of furcation invasion, it is often simple to make a gentle curve in a
size 40 silver point and insert it through the furca from the lingual to the
buccal aspect.
Even in cases where no furcation damage is present, it is wise to remove
bone in that area so the silver point can be inserted as a guide. If the cuts are
not made in the correct position, too much tooth structure may be removed,
making the restorative situation difficult or the furcation problem may remain.
It is then a simple procedure to cut through the crown with a long shank,
tapered fissure carbide bur in the airotor to the position indicated by the silver
point. The complete separation gained is determined when the point may be
removed occlusally through the preparation. Placing a straight elevator into
the vertical cut and rotating slightly may test separation further. The two roots
will move in opposite directions if separation is complete.
Radiographic verification should be mage prior to cutting the crown into
two. The fissure bur is used to cut deeply into the crown in the position that is
assumed to be correct, but the cut is carried only approximately three-fourth of
the distance towards the furcation. At this point, a radiograph is taken with
the film placed at a perfectly perpendicular position to the cut. The radiograph
should verify if the cut were extended, it would go directly between the two
roots. If the extension of the cut would go into a portion of the root, proper
alteration in direction must be made, carried deeper but not into the furcation
and reradiographed to ensure the correctness of direction.
As with the Maxillary molars, distal portion of the tooth is trimmed. Lower
universal forceps are used to extract the mesial root, by using buccolingual
rocking action. If the root is not delivered easily in a periodontally involved
case, a flap should be raised and buccal bone removed until the root becomes
loose. If a flap has already been raised and the root remains tight, it may be
necessary to remove buccal and lingual bone almost to the apex. In many cases
the bone that fills the depression on the mesial and distal surfaces of the root is
sufficient to provide retention.
After root extraction furcation area is trimmed with the tapered fissure
diamond stone to ensure that no spicules are present to cause further
periodontal irritation. Sutures may be needed to close the wound.
Amputation of distal root

The procedure is almost identical to that used for amputation of the mesial
root. The silver point is inserted and the vertical cut made into the bifurcation
to gain separation. The distal root is usually easier to deliver because it has a
more consistent conical shape.
The mesial root of the mandibular first molar is generally wider and more
retentive than the distal root. Many dentists do not realise this and think of the
distal as the larger root. Because of its size and the deep mesial and distal
concavities that it contains, mesial root is able to stand strongly in a splinted
situation, either with the second molar or with the bicuspids anterior to it.
Retaining distal root of first molar with mesial root of second molar
Mesial root of the mandibular first molar has considerably more area available
for periodontal ligament attachment than does the distal root. When a
furcation defect is present that affects both roots equally, it is far better to
amputate the weaker distal root and retain the mesial root.
However, in some cases periodontal condition is so bad for the mesial root
that its retention is precluded. If the second molar is very weak or missing, this
distal root can act as a posterior abutment with proper restoration. If the
second molar is strong, it probably would be best to extract such a first molar,
rather than use this short, straight root as an abutment. In some cases, second
molar is also involved periodontally. If a furcation defect is present,
amputating distal root of the second molar may create a favourable situation.
Resulting combination of distal root of the first molar and mesial root of the
second molar splinted together and attached anteriorly to replace the removed
mesial root of the first molar offers one of the most retentive conditions
available following root amputation. The result is another molar; only this
time the mesial root of the new molar is really a distal root. The new mesial
root curves to the distal and then to the mesial and new distal root curves first
to the mesial and then to the distal. Because most mandibular first molars and
virtually all second molars have roots that curve towards each other, the
resultant molar created here has roots curving away from each other,
producing a retentive combination superior to either of the original molars.
Much more bone is present between the two roots of the new molar than were
present between the roots of the old molars.
If a flap has been raised, same postoperative instructions should be given. If
the root has been amputated for periodontal reasons without a flap,
postoperative discomfort is usually minimal and instructions should be the
same as those given for a simple extraction. In the latter case, postoperative
bleeding, common for periodontally involved teeth, may cause alarm to the
patient. Therefore, instructions should include a statement that hot liquids
must be avoided for the first day after surgery.
Vital root amputation

It is most desirable to amputate a periodontally involved root after the canals
of the roots that are to remain have been sealed. In most cases, careful
diagnosis and periodontal evaluation make it possible to ascertain in advance
when a root will require amputation. However, in certain cases it becomes
extremely difficult to determine whether a root amputation will be necessary
or which root will require such a procedure prior to the retraction of tissue
during periodontal surgery. Most often these situations occur in maxillary
molars, in which trifurcations are more difficult to probe in radiograph than
bifurcations.
If a question arises as to which root of a maxillary molar will be amputated
during periodontal surgery, it is a simple matter to have all three roots filled in
advance and to make the choice with the area surgically exposed. However, it
is not unusual for a serious defect to develop between the maxillary first and
second molar that requires amputation of either the distal root of the first
molar or the mesial root of the second molar. The final decision might require
waiting until the time of surgical exposure for an unimpeded view of the area
for best evaluation. To put the patient through treatment time and expense of
root canal fillings to surgery seems incorrect.
In such instances, it is better to perform the amputation immediately with
the vital pulp than to halt surgery and endodontic emergency treatment is
performed at the surgical appointment. Objectives of this emergency treatment
would be to remove the part of the pulp that might initiate a painful condition
and to seal off the portion of the tooth through which microorganisms might
enter. Later, the patient may be rescheduled for completion of the endodontic
therapy.
Problems of vital root amputation

Certain problems do occur if no pulpal treatment is performed at the time of
the surgery. The exposed pulp may become inflamed and an acute pulpitis
transpires, causing pain in addition to the postoperative discomfort that
normally follows periodontal surgery. If a chronic pulpitis is present, as it
might be in a periodontally involved tooth, further trauma to the injured pulp
might cause a severe exacerbation. Because of the close relationship between
the pulp and the periodontal structures, the inflamed pulp might adversely
affect healing of the periodontal condition. Also, it might be more difficult to
perform the endodontic therapy with a severe contamination of the pulp
caused by the amputation. To avoid these problems, it is suggested that
endodontic emergency treatment be performed when a root is amputated from
a periodontally involved but untreated tooth.
Bicuspidisation
Bisection or bicuspidisation refers to a division of the crown that leaves the
two halves and their respective roots. Through bicuspidisation a single molar
tooth can be converted into two bicuspids. Indications for the procedure are
severe bone destruction in the bifurcation but excellent support on the
nonfurcation sides of each root or severe destruction of tooth structure in the
furcation area. If both roots are to be retained, there should be a considerable
spread between them for restorative procedures to be successful. If a greater
spread is needed and there is room on the distal aspect, orthodontic
movement may be employed to spring the distal root distally and give a more
desirable interfurcal area that allows for efficient patient home care. If the
spread is minimal, it is best to amputate the less strong root and restore
accordingly.
The procedure involves making the vertical cut after endodontic therapy.
The crowns and furcation areas are trimmed with the diamond stone. The
restoration will include two separate post and core crowns with a
superstructure that allows for adequate hygiene in the area.
Replacement surgery (extraction/replantation)
Intentional replantation
Grossman defined intentional replantation as the act of deliberately removing
a tooth and—after examination, diagnosis, endodontic manipulation and
repair, returning the tooth to its original socket.
Indications
1. Inadequate interocclusal space to perform nonsurgical endodontic

treatment caused by the patient’s limited range of motion of TMJ and
associated muscles.
2. Nonsurgical treatment and retreatment are not feasible because of canal
obstructions.
3. Surgical approach for periradicular surgery is not practical because of
limiting anatomic factors.
4. Nonsurgical and surgical treatments have failed and symptoms or
pathoses persist.
5. Visual access is inadequate to perform root-end resection and root-end
filling.
6. Root defects exist in areas that are not accessible through a
periradicular surgical approach without excessive alveolar bone loss.
7. To thoroughly examine the root or roots on all surfaces to identify or
rule out the presence of a root defect.
Contraindications
• Poor periodontal condition

• Furcation involvement
• Widely divergent or curved roots
• Medically compromised patients
Prognostic factors
Three factors that determine the outcome of replantation are:
1. Keeping the extraoral time as short as possible.

2. Maintaining the periodontal ligament cells on the root surface moist
with saline or Hanks balanced salt solution.
3. Minimising the damage to the cementum and periodontal ligament
cells by gentle elevation and extraction of the tooth.
Procedure
1. Following incision of the periodontal fibres, the tooth is slowly and
gently elevated.
2. Appropriate forceps are applied and without injury to the buccal,
lingual plates and to the interradicular bone the tooth is extracted
atraumatically.
3. Following the extraction, immediately cover the tooth with gauze
saturated with normal saline, leaving only the apex exposed.
4. The gauze should be frequently saturated during the procedure to keep
the roots wet.
5. Resect the apical 3–5 mm with a new, sharp fissure bur under copious
irrigation. This will provide an apical space for pooling of fluids in the
postoperative phase.
6. Using a small round bur prepare a cavity 3 mm deep into the apical
foramina.
7. Seal the root-end cavity with retrofilling material.
8. Curette the apical region of the socket to remove granulation tissue and
the recently accumulated blood. Irrigate thoroughly with 0.9% saline.
Gently reinsert the tooth, pushing it back slowly into the socket so that
pooled blood will escape from the socket.
9. Stabilise with wire or with composite if the tooth is mobile. If fixation is
required it should be removed after 7 days.
10. Reduce occlusal surface of the opposing maxillary tooth to minimise
occlusal trauma. The patient should be advised not to chew on the
tooth for up to 2 weeks.
Implant surgery
Two types of endosteal implants fall under the purview of endodontics: (1)
endodontic implants and (2) osseointegrated implants (endosseous implants).
Endodontic implants
Endodontic implant is defined as ‘utilising an existing tooth by placing a metal
post down into one of the root canals of the tooth and extending into the bone’.
It is a rigid structure which extends through the root canal into the periapical
osseous tissue, to lengthen the existing root anchorage and to provide stability
to the tooth.
Indications
1. It is indicated in teeth with severe periodontal disturbance and

extensive bone loss.
2. Teeth that have lost a good portion of alveolar support can be stabilised
and maintained by the use of endodontic endosseous implants.
3. Endodontic implant is also used as an aid to pulpoperiodontal therapy.
Technique
A perfectly round preparation must be reamed through the root apex and into
the alveolar bone. Failure to do so will result in leakage around the implant-
dentine interface and eventual failure of the implant. Another critical area is
structural weakening of the walls of the root as a result of dentine removal in
an attempt to create a round apical orifice. This structural weakness may result
in root fracture either at the time of implant placement or as a result of
functional stresses on the tooth. It is also important that the periodontal
condition that has led to the periradicular bone loss be stabilised before
endodontic implant placement. If not, the case will fail as a result of continued
progression of the periodontal disease.
Advantages
1. These implants are not exposed to the oral environment.

2. The area of bone prepared for the implant will not be extensive.
3. The angulations of the implant can easily be established through the
root canal.
4. They act as stabilisers when the loss of periodontal support is more.
5. Increases the crown-root ratio.
6. They provide better anchorage and stability to mobile teeth.
7. It helps to stabilise the overdenture abutment.
Disadvantages
1. Root fracture.
2. Technique-sensitive procedure.
Root-form osseointegrated implants

Osseointegration is defined as ‘the direct structural and functional connection
between ordered, living bone and the surface of a load-carrying implant’.
Biochemicals as well as bacterial factors have long been recognised to play a
substantial role in osseointegration maintenance. Of the recent advancements
in implant surgery, the most applicable to the practice of endodontics is
immediate implant placement. Implant placement immediately following
tooth extraction offers several advantages over the conventional protocol:
a. Incorporation of two procedures into one appointment

b. Expediency of total treatment time
c. Minimisation of osseous collapse as well as resorption, maintenance of
soft tissue architecture
Osseointegrated implants (endosseous implants): discussed further in

Chapter 21 Dental Implantology.
Endodontic microsurgery
Microsurgery is limited to a surgical procedure on exceptionally small and
complex structures with the aid of an operating microscope. Microscope
allows the surgeon to assess pathologic changes more precisely and to remove
pathologic lesions with a far greater precision, thus minimising tissue damage
during the surgery. Precision is a key element in endodontic microsurgery
because of the restricted access to the surgical field. The triad of
magnification, illumination and microinstruments provides the greater
accuracy required (Fig. 19.19).
Advantages of surgical operating microscope
1. Visualising the surgical field

2. Evaluating the surgical technique
3. Reducing the number of radiographs needed
4. Expanding patient education through video use
5. Providing reports to referring dentists and insurance companies
6. Creating documentation for legal purposes
Traditional endodontic surgery versus microsurgery

Procedure Traditional surgery Microsurgery
1. Identification of the apex Sometimes difficult Precise
2. Osteotomy Large (>10 mm) Small (<5 mm)
3. Root surface inspection Imprecise Precise
4. Bevel angle Large (45 degree) Small (<10 degree)
5. Isthmus identification Nearly impossible Customary
6. Retropreparation Approximate Precise
7. Root-end filling Imprecise Precise
FIGURE 19.19 Endodontic microsurgery
CHAPTER 20
Preprosthetic Surgery
Ideal edentulous ridge

Residual ridge resorption (RRR)
Pathophysiology
Atrophic maxilla and mandible
Goals of preprosthetic surgery
Patient evaluation
Treatment planning
Alveolar ridge preservation
• Extraction techniques
• Preservation of uninfected root stumps
Alveolar ridge augmentation
Mandibular augmentation procedures
• Superior border augmentation
• Inferior border augmentation
• Visor osteotomy
• Interposition bone grafting (modified visor
osteotomy)
• Maxillary augmentation procedure
• Onlay grafting
• Sinus lift
• Maxillary and mandibular augmentation
• Alveolar ridge distraction
• Augmentation in combination with orthognathic
surgery
Alveolar ridge correction
• Alveoloplasty
Primary alveoloplasty
Secondary alveoplasty
• Tori removal
Maxillary torus or torus palatinus
Mandibular tori or torus mandibularis
Mylohyoid ridge reduction
Genial tubercles reduction
Maxillary tuberosity reduction
Tuberoplasty
Orthognathic surgery
Frenectomy
Labial frenectomy
Lingual frenectomy
Vestibuloplasty or ridge extension procedures
Labiobuccal vestibuloplasty of maxilla
• Mucosal advancement vestibuloplasty
• Maxillary pocket inlay vestibuloplasty
• Grafting vestibuloplasty
Mandibular vestibuloplasty techniques
• Labial approach
Kazanjian’s technique
Godwin’s technique
Lipswitch vestibuloplasty
Clark’s technique
Lingual vestibuloplasty
Trauner’s technique
Caldwell’s technique
Combination of buccal and lingual vestibuloplasty
Obwegeser’s technique
Redundant tissue excision
Alveolar flabby ridge (hypermobile soft tissues on the
alveolar ridge)
Denture granuloma
Epulis fissuratum (inflammatory fibrous hyperplasia,
denture fibrosis)
Reactive inflammatory hyperplasia of the palate
Mental nerve transposition
Repositioning of inferior alveolar nerve (IAN)
IAN lateralisation (IANL)
IAN transposition (IANT)
Preprosthetic surgery is concerned with the surgical modification of the

alveolar process and its surrounding structures to enable the fabrication of a
well-fitting, comfortable and aesthetic dental prosthesis. When the natural
dentition is lost from periodontal disease, trauma, pathologies as cyst, tumour
or extraction, the alveolus and the surrounding soft tissue undergoes variable
changes. Some of these changes may be unfavourable for the ridge to undergo
dental rehabilitation. There may be:
• Bone loss with irregularities

• Prominences
• Undercuts
• Superficial location of mental nerve and foramen with associated soft
tissue changes
• Scarring and changes in insertion of the perioral muscles
• Reduced vestibular depth
• Flabby hypertrophic ridge
These unfavourable changes mandate correction before attempting for a

dental rehabilitation. In addition certain preexisting conditions as maxillary
and mandibular tori, prominent maxillary tuberosity pose problems in dental
rehabilitation with prosthesis.
Ideal edentulous ridge

Goodsell had recommended the following criteria for a healthy and ideal
edentulous ridge for dental rehabilitation:
• Adequate bony support for the dentures—the bony ridge should have
adequate width and height and U-shape for a denture to be retentive
and efficient.
• The bone should be covered with adequate soft tissue—the covering
oral mucosa should have adequate uniform thickness.
• The ridge should not have any undercut or sharp ridges.
• No bony or soft tissue protuberances should be present.
• It should have adequate buccal and lingual sulci depth.
• It should not have any scar bands that prevents normal seating of the
denture.
• No muscle fibres or frena should dislodge the prosthesis.
• Relation of maxillary and mandibular ridge should be satisfactory in
all the planes.
• No soft tissue hypertrophies or redundancies should be present on the
ridge or the sulci.
Residual ridge resorption (RRR)

The term used for the diminishing quantity and quality of the residual ridge
after removal of teeth (Fig. 20.1). Rate of the resorption depends upon the
general health status of the patient, the shape, size and density of the residual
alveolar ridge and the amount of masticatory forces exerted by the patient
with or without denture.
FIGURE 20.1 Residual ridge resorption.
Pathophysiology
• Secondary maxillary/mandibular bone loss is an insidious regressive

remodelling of alveolar and even basal bone that is a sequela of tooth
loss. This secondary process is referred to as edentulous bone loss.
• The secondary bone loss is related to its characteristic anatomy,
metabolic state, jaw function and prior use of any prosthesis.
• Bone requires stimulation referred to as ‘the minimum essential strain’
to maintain its normal strength, dimension and function.
• Both insufficient strain and excessive loads can lead to regressive
remodelling of bone.
• Edentulous ridge undergoes classically extreme ridge resorption in
long-term edentulism with no rehabilitation; similarly ridge
underneath poorly fitting improper denture shows the extreme bone
loss.
• Anatomic factor—Dolicocephalic faces have greater vertical ridge
dimensions than brachycephalic faces.
• Metabolic factors—Nutritional and endocrine disorders affecting bone
as osteoporosis, osteomalacia, hyperparathyroidism, Cushing
disorder, have significant influence on bone remodelling and
resorption. They also affect osseous reconstructive surgery.
Mercier’s classification of residual ridge resorption (1995)
I Minor ridge modelling

II Sharp atrophic mandible alveolus
III Basal bone only
IV Basal bone resorption
Cawood and Howell classification of Residual ridge resorption
• Class I—Dentate (Fig. 20.2)

• Class II—Immediate postextraction (Fig. 20.3)
• Sub: no defect, buccal wall defect/multiwall defect or deficiency
• Class III—Convex ridge form, with adequate height and width of alveolar
process (Fig. 20.4)
• Class IV—Knife-edge form with adequate height but inadequate width of
alveolar process (Fig. 20.5)
• Class V—Flat-ridge form with loss of alveolar process (Fig. 20.6)
• Class VI—Loss of basal bone that may be extensive but follows no
predictable pattern
Sub: marginal resection defect or continuity defect (Fig. 20.7)
FIGURE 20.2 Class I dentate.
FIGURE 20.3 Class II immediate postextraction.

FIGURE 20.4 Class III convex ridge form with adequate alveolar
height and width.
FIGURE 20.5 Class IV knife-edge form with adequate height but

inadequate width of alveolar process.
FIGURE 20.6 Class V flat ridge form with loss of alveolar process.
FIGURE 20.7 Class VI completely edentulous atrophic mandible

showing severe RRR with loss of alveolar and basal bone.
Atrophic maxilla and mandible (Fig. 20.8)
• Due to certain pathological diseases like ectodermal dysplasia,

osteomalacia and osteoporosis, the residual alveolar ridge might
resorb.
• Nutritional deficiency also leads to ridge resorption.
• Prolonged usage of denture may exert compression in certain stress
bearing area of the edentulous ridge resulting in resorption.
• Extraction of mandibular or maxillary teeth in groups or singly at
different periods of life may lead to differential resorption of the ridge
resulting in a ‘roller-coaster’ type or ‘hills and valleys’ type of ridge.
• Improper alveoloplasty techniques carried out at the time of extraction
predisposes to increased ridge resorption.
• Chronic periodontal diseases result in vertical or horizontal loss of
alveolar bone which becomes evident after extraction.
• Presence of sharp buccal plate after extraction, presence of bony
exostoses and maxillary or mandibular tori also cause irregularity of
the alveolar ridge.
• Disuse of the alveolar ridge is also one of the common causes of
atrophy of the ridge.
FIGURE 20.8 (A–C) Completely dentulous mandible with normal

position of mental foramen 10–12 mm from alveolar crest. (D, E)
Completely edentulous mandible after recent loss of teeth
(extracted) with unchanged position of mental foramen and no
evident ridge resorption. (F) Completely edentulous mandible with
loss of teeth in different time periods. Left posterior zone of disuse
atrophy from long-term absence of stimulation. (G) Atrophic left
alveolar ridge with superior positioned mental foramen after no
dental rehabilitation for many years. (H) Right posterior edentulous
irregular ridge after recent loss of teeth from extraction. (I)
Completely edentulous mandible with severe resorption and
superiorly positioned mental foramina requiring mental nerve
repositioning. (J) Mandibular resorption pattern evident by
posterior and lingual version of alveolar ridge. (K) Mandibular ridge
resorption more on buccal and posterior direction while maxillary
resorption creates a buccal and anterior shift of ridge resulting in
Class III. (L) Atrophic mandible with knife edge meagre alveolar
bone with residual basal bone only.
Goals of preprosthetic surgery

• To provide adequate height, length, breadth, width and shape of
residual tissue with which the ridge can support and retain the
denture and withstand masticatory stress.
• To help in proper speech and deglutition.
• Satisfy the aesthetic concerns of the patient.
• Remove all the hard and soft tissue protuberances and undercuts.
• Provide adequate vestibular depth.
• Provide appropriate frenal attachment.
• Achieve proper jaw relationship in anteroposterior, transverse and
vertical dimension.
• Relocate the mental nerve and establish correct vestibular depth.
• Reduce the pain and discomfort produced by the denture pressure on
a narrow alveolar ridge and unsupported (by soft tissue) alveolus due
to the presence of superficial mental nerve or an impacted or buried
tooth or root which was asymptomatic prior to denture placement.
• Insert endosseous implant.
Indications
Specific indications for preprosthetic surgery include:
1. Complete or partial edentulism secondary to early tooth loss (as in

anodontia, ectodermal dysplasia)
2. Naturally occurring reduction of the residual bony ridge
• Jaw atrophy (Class II–VI)
• Mucosal atrophy
• Interarch changes (vertical, anterior/posterior, transverse)
• Reduction of denture bearing area
• Muscle hypotonia
• Facial changes
3. Pain (not remedial by conventional prosthetic measures) due to:
• Mucositis (a burning discomfort of the mucous membrane)
• Neuropathy (alteration of sensation of the lips varying from
objective/subjective paraesthesia to anaesthesia or pain arising
from traumatised nerve trunks)
• Local recurrent ulceration of unsupported crestal soft tissues
and thin atrophic mucosa
• Temporomandibular joint pain
• Dental roots or unerupted teeth
4. Dysfunction (not remediable by conventional prosthetic means) of:
• Mastication
• Speech
• Deglutition
5. Disproportionate growth of the jaws or facial skeleton producing
mechanically impossible conditions for mastication and denture
retention. This skeletal deformity may be:
• Class II or relative mandibular retrusion/maxillary protrusion
• Class III or relative mandibular protrusion/maxillary retrusion
6. Craniofacial deformity which results from abnormal growth patterns of
the skull base and facial skeleton.
7. Oligodontia, anodontia: a naturally occurring failure of tooth
development.
8. Enhanced gag reflex: patients have an excessive sensitivity of the soft
palate which if contacted produces ‘retching’.
Contraindications
1. General contraindications to surgery—medically compromised state.
2. Generalised bone disorders as osteoporosis, hyperparathyroidism, etc.
3. Patient on bisphosphonate therapy—at risk of osteochemonecrosis
(BRONJ).
4. Patient with history of head and neck irradiation recently.
Patient evaluation
A thorough patient evaluation is very essential before beginning any surgery
to receive prosthesis. A complete history should be taken and physical
examination should be carried out:
• Chief complaint of the patient.

• The patient’s aesthetic and functional goals must be assessed and
clinician should determine if these needs can be met with.
• The patient’s psychological adaptability helps in determining the
efficient use of dentures by them.
• Evaluation of previous experience with the prosthesis further helps in
assessing the patient’s ability to adapt to the prosthetic treatment.
• General health status, any medications being taken and risk values
should be evaluated.
Intraoral soft tissues examination
• Quantity and quality of the overlying tissues should be determined.

The mucosa ideally should be firm and keratinised and not flabby.
• The vestibule should be manually palpated to assess for adequate
depth for self cleansability, any inflammation, ulceration or growth.
• Muscle attachment and frenal attachment with the alveolar crest
should be assessed as these are often responsible for loss of peripheral
seal of denture during mastication and speech.
• Lingual vestibular depth and attachment of mylohyoid muscle on the
lingual aspect of the mandible should be evaluated as this
accompanied with the movement of the tongue are responsible for the
displacement of lower denture.
• Soft tissues and bony pathologies if present should be investigated.
• A thorough examination of the palatal vault and soft palate for lesions,
papillary hyperplasia or abnormalities interfering with denture
placement.
Intraoral bony structures examination
• All the areas of the maxilla and the mandible should be inspected,
palpated and radiographically examined and models should be
assessed.
• The bony ridge of the maxilla and the mandible should be evaluated
for the presence of gross irregularities like exostoses, undercuts,
prominences, tori, sharp mylohyoid ridges, etc.
• Attachment of the frena and the muscles in alveolar crest should be
evaluated.
• The ridge should have proper contour, height, width and shape.
• The interarch relationship of the maxilla and the mandible in all three
planes is to be determined. The interarch distance especially in the
region of maxillary tuberosity should be assessed for any vertical
excess of the tuberosity.
• The interarch resistance is assessed. In case of deficiency from
supraerupted opposing tooth onto ridge, it is planned for coronoplasty
or extraction.
Radiological evaluation (Fig. 20.9)

• Plain radiographs: Intraoral and orthopantomograph (OPG), lateral
cephalogram for routine assessment
• CBCT scan: For assessment of pathologies, impactions
• Radiologic assessment is a useful preoperative assessment aid in:
▪ Detecting any embedded root apices and impacted teeth
▪ Presence of cyst and tumour
▪ The position of the mental foramen in relation to ridge crest to
assess risk of compression under denture as well as in
planning implant placement
▪ The density of the maxillary and mandibular bone to evaluate
risk of resorption, suitability for implant placement
▪ Position of inferior alveolar canal for implant placement
▪ Height and width of alveolar ridge to plan implant placement
or need for augmentation
▪ Relation of maxillary sinus to alveolar crest to assess adequate
height of alveolar bone, pneumatisation of alveolar ridge,
need for sinus lift, sinus disease if any impacted tooth in
sinus, etc.
FIGURE 20.9 (A) Completely edentulous atrophic mandible with
severe RRR mental foramen 4 mm from alveolar crest requiring
mental nerve repositioning and bone graft augmentation. (B) CBCT
coronal section showing pneumatisation of left maxillary ridge even
though the alveolar height and width are preserved. (C) CBCT
alveolar ridge pneumatisation requiring sinus lift. (D) CBCT used to
assess maxillary alveolar ridge and relation to sinus before implant
placement. (E) CBCT used to measure alveolar ridge height width
and relation to inferior alveolar canal (IAC) before implant
placement. (F) CBCT used to trace IAC course before planning
implant placement in mandible.
Treatment planning
• A thorough evaluation should be followed with an appropriate
treatment plan.
• The type of surgery, type of anaesthesia and the expected
postoperative sequelae should be explained to the patient before
surgery. Whenever possible, informed consent should be obtained
prior to the surgery.
• If there is any benign growth or cyst, they should be treated first. Small
benign pathological entities can be removed at the time of tooth
extraction.
• When planned for total extraction a dental diagnostic cast aids in
treatment plan.
• When extraction of the teeth is planned in stages, extraction of teeth in
one area should be accomplished first and ridge preparation done
later. This allows the patient to retain at least some dentition for a
longer time. Whenever possible, a few occluding teeth should be left
until last visit, so that the patient does not bite against a healing ridge.
• Alveoloplasty should be deferred until all the teeth have been
extracted to permit healing of sockets and filling of any periodontal
defects with bone and allow some spontaneous resorption of
prominent or undercut areas which give best chance for maintaining
the greatest amount of bone.

Alveolar ridge preservation
Most of the measures which are undertaken to prevent or reduce the
prosthetic difficulties are related to extraction of teeth. Conservative extraction
techniques using periosteotomes to maintain alveolar continuity, orthodontic
guided tooth or root extraction, immediate grafting of extraction sites, relief of
undercuts using bone grafts or hydroxyapatite (HA) augmentation and guided
tissue regeneration are some of the current techniques in ridge preservation.
Proper radiographs should be taken prior to extraction of any teeth to detect
the presence of any abnormality related to the teeth and predict the difficulty
in removing the teeth. In edentulous ridge, the radiographs help in viewing
any retained root apices, embedded teeth or other bony pathologies.
A. Extraction techniques (Fig. 20.10)

• Meticulous extraction technique with appropriate extraction forceps
can avoid most of the difficulties of prosthetic rehabilitation.
• Avoid improper soft tissue handling, extreme forces in extraction that
causes buccal bone fracture, injudicious bone removal for root
retrieval.
• When multiple teeth are extracted in a quadrant, primary alveoloplasty
is required.
• In case of multiple teeth extraction in maxillary anterior, canine
extraction is done prior to premolars to prevent alveolar bone fracture.
When premolars and lateral incisor are extracted before canine
extraction, the long root of canine fractures the thin buccal cortex
along with portions of alveolar bone of adjacent sockets.
• After extraction, the socket should be compressed with the thumb and
forefinger to reposition the expanded socket.
• Any sharp bony spicule or other debris like loose bone, calculus should
be removed prior to suturing (Intraseptal alveoloplasty) (Fig. 20.22).
• When the tooth root is fractured, it should be removed with minimum
manipulation (like dividing the roots or removing via apicectomy
window) preserving the crestal bone, so that adequate bony support is
present for the denture construction.
• Wherever possible, anosteoplastic flap (i.e. the bone is mobilised with
attached mucoperiosteum) should be raised during removal of buried
teeth, root apices or cyst.
• If the radiograph shows a fractured tooth root with normal
surrounding periodontal ligament and vital pulp, it can be left as such,
as they do not pose any danger but when it is related to granuloma or
cyst or otherwise, it should be removed.
• Periodontally involved teeth should be extracted early to prevent
excessive bone loss.
• Ankylosed tooth, hypercementosis or long dilacerated root are
extracted by transalveolar method with judicious bone removal since
buccal cortex fracture occurs with intra-alveolar extraction.
FIGURE 20.10 Edentulous mandible with impacted tooth.
B. Preservation of uninfected root stumps

In edentulous ridge, if uninfected root stumps are present without any
periodontal disease or periapical pathology, it may be retained to maintain the
alveolar ridge height and width. These roots if firmly placed in the ridge can
also be used to support denture with precision attachments as ball retained
dentures.
Alveolar ridge augmentation

The augmentation of the bone is achieved by building up the atrophied jaw
bone using autogenous bone, allogenic bone or alloplastic material
(Table 20.1).
Table 20.1
Mandibular and maxillary augmentation procedures

1. Superior border augmentation
a. Bone graft
b. Bone graft and rhBMP-2/PRP
c. Alloplastic graft
d. Alveolar transport distraction osteogenesis (DO)
2. Inferior border augmentation
a. Bone grafts
b. Cartilage graft
3. Interpositional or sandwich bone grafting
a. Bone graft
b. Cartilage graft
c. Hydroxyapatite blocks
4. Visor osteotomy
5. Onlay grafting
Maxillary augmentation procedures
1. Onlay bone grafting
2. Onlay grafting of alloplastic material
3. Interpositional or sandwich graft
4. Sinus lift procedures
5. Bone graft and rhBMP-2
6. Alveolar transport DO
Criteria for ridge augmentation (Fig. 20.11)
• Gross atrophy of the jaws with the risk of mandibular fracture.

• Atrophy of the jaws with knife-edge ridge causing prosthetic
difficulties.
• Insufficient alveolar dimension for implant placement.
FIGURE 20.11 (A) Knife-edge alveolar ridge indicated for ridge
augmentation before prosthetic rehabilitation. (B) CBCT showing
severe atrophic mandible with knife-edge ridge, insufficient
alveolus for implant placement. (C, D) Partial anodontia with
resorbed maxilla and mandible indicated for augmentation.
Goals of ridge augmentation
• Restoration of the optimum ridge height and width, vestibular depth,

ridge form and optimum denture bearing area.
• To increase retention and stability of the denture.
• To attain a proper interarch relationship.
• To protect and prevent injury to anatomic vital structures such as the
neurovascular bundle, maxillary sinus, mental nerve.

Mandibular augmentation is a procedure used to improve the height, strength
and contour of an extremely deficient mandible before placement of a denture
or an implant. Autogenous bone or allogeneic bone or alloplastic material can
all be used for this purpose as a source of bone graft material. Recently the use
of rhBMP-2 and alveolar distraction osteogenesis has gained immense
popularity. The following are different techniques for mandibular
augmentation (Table 20.1).
1. Superior border augmentation

Superior border augmentation was described by Davis in the year 1970. This
procedure is indicated when mental foramen is situated in the superior border.
In this procedure, autogenous bone graft is used. The rib graft with or without
addition of rhBMP-2 in absorbable collagen sponge (ACS) can be fixed to the
superior border of the mandible (Fig. 20.12).
Two segments of the rib about 15 cm long are obtained. The rib is contoured
by vertical scoring in the inner surface. The second rib is cut into small pieces
to later pack against the solid rib. Fixation is done by means of transosseous
wiring, circumferential wiring or miniplate or microplates.
FIGURE 20.12 Superior border augmentation for atrophic knife-

edge maxillary ridge using rib graft and rhBMP-2.
Disadvantages of this procedure include
• Morbidity of the donorsite

• Secondary surgical site
• Necessity of the patient to withdraw denture till the surgical wound
heals for a period of 6–8 months.
• Postoperative resorption of the graft is common. This has been
overcome well by concurrent use of rhBMP-2.
2. Inferior border augmentation (Fig. 20.13)

This technique was first described by Sanders and Cox in the year 1986 for
reconstruction of a resected mandible. This procedure is indicated to prevent
and manage fractures of an atrophic mandible.
FIGURE 20.13 Inferior border augmentation with rib graft.
Indications
• Augmentation of severely atrophic edentulous mandible.

• Prevention of pathological fracture of atrophic edentulous mandible.
• Management of malunion or nonunion of edentulous mandible.
Procedure
A submandibular incision is made from angle to angle region and
subplatysmal dissection is done to the inferior border of the mandible. An
incision through periosteum is made from the angle of mandible of one side to
the other. Two ribs obtained are abutted against the lingual and buccal aspect
of the inferior border. The graft material is fixed to the mandible by means of
circum mandibular wiring. The flap is closed primarily.
Advantages
• Does not obliterate the vestibule

• Interim denture can be worn immediately
• No change in vertical dimension
• Graft is not subjected to direct masticatory force
Disadvantages
• It will not correct the abnormalities of denture bearing areas

• It will not protect a highly placed mental nerve
• Donor site morbidity
• Resorption of the graft
• Presence of scar
3. Visor osteotomy (Fig. 20.14)

This technique was first described by Harle to overcome the resorption of free
onlay bone graft. This technique is designed wherein the muscle insertion to
the mandible and nutrient supply are maintained.
• The mandible is divided buccolingually by a vertical osteotomy from

external oblique ridge of one side of the mandible to the other side.
• The osteotomised lingual segment is pushed superiorly and fixed with
the buccal segment using stainless steel wire in the lower border of the
lingual segment and upper border of the buccal segment.
FIGURE 20.14 Visor osteotomy.
4. Interposition bone grafting (modified visor osteotomy) (Fig. 20.15)

This procedure is also known as sandwich grafting and is similar to visor
osteotomy. Here the vertical osteotomy cut is made only in the posterior
region to divide the segments buccolingually. A horizontal osteotomy is
performed in the anterior mandible to divide the anterior segment superiorly
and inferiorly and bone grafting (usually cancellous bone from iliac crest) is
done into the osteotomised gap and the two osteotomised segments are fixed
with wires.
FIGURE 20.15 Interpositional bone grafting.
Advantages
• The rate of resorption is less when compared to onlay grafts.

• Incidence of nerve paraesthesia is less when compared to visor
osteotomy.
Maxillary augmentation procedure
1. Onlay grafting (Fig. 20.16)

Onlay grafting of the edentulous maxilla or mandible is done when there is
adequate bone height but inadequate bone width.
FIGURE 20.16 Maxillary bone grafting. (A) Atrophic edentulous

maxillary ridge. (B) Bone graft taken from the mandible (C) graft
placed in maxilla.
Procedure
Autogenous bone graft
• Bone grafting of the maxilla using autogenous bone from the mandible
or costochondral rib graft (described by Terry et al) is performed to
increase the height and width of the maxillary alveolar process. To
facilitate good closure and to achieve good undermining of tissues, a
high vestibular incision is made and mucoperiosteal flap is reflected to
expose the alveolar ridge. The rib graft is harvested and placed over
the alveolar defect. The wound is closed with sutures.
• Hydroxyapatite crystals—grafting can also be done using allograft like
hydroxyapatite as described by Obwegeser, wherein a vertical incision
is made in the midline and mucosa is tunnelled on both sides of the
midline. Hydroxyapatite crystals are mixed either with blood or saline
and injected through this incision.
2. Sinus lift (Fig. 20.17)

Due to excessive pneumatisation of the maxillary antrum and atrophy of the
maxillary ridge, floor of the sinus almost comes to lie very close to the
maxillary alveolar crest. Maxillary sinus lift procedure is carried out to lift the
floor of the sinus lining by placing a graft in between the maxillary sinus lining
and the floor of the maxillary antrum in the posterior aspect.
FIGURE 20.17 Sinus lift procedure.
The various materials used for this surgical procedure are:
• Iliac crest cancellous graft

• Rib graft
• Hydroxyapatite
Technique
In 1977, Tatum was the first to perform the sinus lift operation. He introduced
a crestal approach to the sinus membrane which was later on, changed in 1986
to a modified Caldwel-Luc lateral window approach.
• An incision is made on the alveolar crest extending from canine to the

tuberosity region with two vertical releasing incision placed.
• Full thickness flap is elevated and horizontal bony cut is made
inferiorly 2–4 mm above the floor of the sinus.
• A vertical bony cut is made perpendicular to the horizontal cut in the
anterior region parallel to the lateral nasal wall. Another vertical cut is
made posteriorly perpendicular to the inferior horizontal cut in the
region of the maxillary buttress. Two vertical cuts are joined superiorly
by an interrupted osteotomy cut to create a hinged bony window. The
bone is feathered till grey colour of the maxillary sinus is seen.
• A surgical curette is placed between the bone and the antral lining in
the inferior osteotomy cut and the bone is gently peeled from inside of
the lining of the sinus.
• The graft is now inserted between the lining and the floor of the sinus.
• The flap with its intact periosteum is approximated over the graft and
closed with interrupted sutures.
• Instead of bone graft rhBMP-2 can also be used by the same technique.
Maxillary and mandibular augmentation
Alveolar ridge distraction

Refer to Chapter 36 Distraction Osteogenesis for further reading (Figs.
20.18–20.20).
FIGURE 20.18 (A) Horizontal alveolar distraction osteogenesis. (B)
Vertical alveolar distraction osteogenesis.
FIGURE 20.19 (A, B) Technique for intraoral vertical distraction
osteogenesis of the alveolar ridge.
FIGURE 20.20 Vertical distraction osteogenesis.
Alveolar ridge distraction refers to alveolar reconstruction by means of bone

transport technique whereby the transport segment would be moved using a
special device called distractor.
Alveolar ridge augmentation can be divided into two categories:
▪ Vertical augmentation, in which the transport alveolar segment is

translated vertically and the height of the alveolar ridge is increased.
▪ In horizontal augmentation, the transport alveolar segment is
translated horizontally, thereby increasing the alveolar ridge width.
Indications
• Partial defects of the vertical alveolar ridge

• Partial defects of horizontal alveolar ridge
• Alveolar insufficiency with sufficient basal bone (segmental)
Contraindications
• Cases of inadequate bone volume, especially in severe atrophic
mandible with only basal bone with danger of fractures
• Osteoporosis
• Systemic or osseous disorders
Advantages
• No visible scars
• No bone harvesting required
• Dental implants can be placed 3 months after surgery
• Shortening of the entire treatment time
• Precise positioning of the device
• Transport of vital alveolar bone, safe blood supply
• Less resorption
• No infection problems
• No periodontal problem
• Early vascularisation of new bone
• Teeth vitality remain intact
Disadvantages
• Temporary nerve disturbance is possible.

• A second intervention for removal of the distractor under local
anaesthesia is mandatory.
Augmentation in combination with orthognathic surgery

Orthognathic surgery is used in combination with augmentation techniques
for reconstruction of edentulous mandible or maxilla. Surgeries normally used
are anterior maxillary osteotomy and Le Fort I osteotomy with interpositional
bone grafting.
Alveolar ridge correction

1. Alveoloplasty (Fig. 20.21)
A well-contoured smooth ridge is essential for proper construction of denture.
While contouring the ridge, it is highly essential to remember that greater the
excision of bone, greater will be the resultant resorption. Therefore, the
procedure of contouring should be limited to the excision of irregular sharp
ridges and unfavourable undercuts which are unsuitable for the denture
construction.
FIGURE 20.21 Alveoloplasty performed during extraction.
Goals of alveoloplasty
• To provide optimal ridge contour quickly.

• The alveolar ridges should be left as broad as possible for maximum
distribution of the masticatory load.
• The ridge need not be perfectly smooth but sharp irregularities should
be removed and the edges should be rounded.
• The mucosa covering the ridge should have uniform thickness, density
and compressibility for even transmission of the masticatory forces to
the underlying bone.
• In younger patients, less amount of bone should be removed as the
process of resorption extends for longer number of years than the
older patients.
a. Primary alveoloplasty
Primary alveoloplasty is the term used to describe the trimming and removal
of the labiobuccal alveolar bone along with some interdental and
interradicular bone and is carried out at the time of extraction of teeth.
Indications
• Patients with prominent and dense alveolar bone undergoing

extraction.
• Done as a procedure prior to the construction of an immediate denture.
Technique
When alveolar bone remodelling surgery is done at the time of extraction of
teeth, the technique is named primary alveoloplasty.
• The crevicular incision is placed along free gingival margin and a full
thickness mucoperiosteal envelope flap or a triangular flap is elevated
which extends up to one tooth distance on either side of the sockets.
• A sharp cutting rongeurs forceps is held with one beak beneath the
bony rim of the socket and the other on the crest of the ridge.
• Small pieces of required amount of bone are removed and bone file is
used to smoothen the bone.
• The mucous membrane is then held with sutures over the
interradicular bony septa.
• If any excess flap is present, it is trimmed away and the edges are
approximated.
• In case of immediate denture, the previously prepared template is
fitted on and noted for the presence of any pressure points indicated
by the blanching of the mucosa under the transparent acrylic template.
If such pressure points are present, they should be trimmed again.
Dean’s intraseptal primary alveoloplasty (Fig. 20.22)

This procedure helps in eliminating anterior maxillary undercuts and reducing
the large anterior maxilla by removing the interseptal bone between the teeth.
The procedure involves preparation of six anterior teeth and sometimes the
premolars are included. The advantage of this technique is that since it retains
much of the compact labial cortical bone, it reduces resorption of the bone
postoperatively. According to Dean, the most posterior teeth should be
removed first to preserve the integrity of labial cortical plate and avoid any
disturbance to its blood supply. Dean’s intraseptal alveoloplasty is based on
the following biological principles:
• The prominence of the labial and buccal alveolar margin is reduced to

facilitate the reception of dentures
• The muscle attachments are undisturbed
• The periosteum remains intact
• The cortical plate is preserved as a viable onlay bone graft with an
intact blood supply
• Because the cortical bone is spared, postoperative resorption is
minimised
FIGURE 20.22 Dean’s intraseptal alveoloplasty. (A) Before
extraction. (B) Alveolar sockets after extraction of anterior teeth.
(C&D) Interseptal bone removed. (E) Buccal bone plates fractured
using finger pressure (F) Wound closure.
Indications
• To decrease gross maxillary overjet

• Adequate bone height
• Multiple extractions
Technique
• Incision is made along the gingival margin with epithelial attachment

(crevicular incision) and interdental papilla attached to the respective
teeth.
• An envelope flap is raised as conservatively as possible.
• Now the teeth are extracted starting from the canine to the incisors.
• After extraction of the teeth, the interradicular bony septa should be
removed with a rongeur forceps or rotatory drill introduced into the
socket to separate the labial and palatal cortical plate.
• A V-shaped excision of the bone is done in the labial cortical plate
distal and posterior to the canine eminence as close to the alveolus as
possible.
• Thus three sides of the labial cortex become free and the labial cortex
becomes a freely movable osteoperiosteal graft attached to only the
mucoperiosteum from which it receives its blood supply.
• Now finger pressure is applied to the labial cortical plate which is
collapsed towards the socket. Sutures are placed to stabilise the
tissues.
b. Secondary alveoplasty (Fig. 20.23)
• When bone corrective surgery is done on the edentulous ridge for

irregularity after the initiation of extraction socket healing, it is termed
as secondary alveoplasty. A sharp knife-edge like edentulous ridge
causes great denture irritation. They are usually found in the anterior
part of the mandible. Localised tenderness over such ridge on
palpation or on wearing denture is common. The ridge may also show
an irregular pattern known as feather edged ridge.
• Incision should be made on the crest of the alveolar ridge.
• Usually an envelope flap would suffice, but releasing incision can be
made on the labial or buccal side to provide a broad base to the flap.
• Bony contouring is accomplished with bone files, rongeurs or burs.
• The ridge is made free of sharp irregularities and is not aimed at
perfectly smooth ridge requiring excessive bone removal. Digital
palpation can be used to determine the uniformity of the ridge.
• Once satisfying results are obtained, the region is irrigated copiously
with saline to remove debris, small avascular bone pieces at risk of
necrosis and the flaps closed.
FIGURE 20.23 Alveoloplasty performed on edentulous ridge.
2. Tori removal
Tori are small developmental anomalies that occur in constant sites on the jaw
bones.
a. Maxillary torus or torus palatinus (Fig. 20.24)

A torus palatinus is an exostosis found along the suture line of the hard palate.
Not all the tori require to be removed as all of them do not cause prosthetic
difficulty. Sometimes the bony exostoses may be present on the buccal
buttressing bone.
FIGURE 20.24 Removal of maxillary tori. (A) Placement of incision.

(B) Elevation of flap. (C) Depth cut made with bur.
Indications for removal for maxillary tori
• Smooth maxillary torus can be ignored but when it is extensively

irregular, large and extends beyond the junction of the hard and soft
palate and interferes with the postdam seal of the denture, it should be
removed.
• Sometimes the torus may be subjected to constant trauma during
mastication.
• When it interferes with normal speech.
• When the patient fears of malignancy.
Technique
• Before surgical excision of the tori an impression should be made and

the models prepared.
• The tori should be removed in this model and an acrylic stent made.
• AY-incision for small tori and a double Y-incision for the large tori is
made. A full thickness mucoperiosteal flap is elevated carefully to
expose the tori entirely.
• The tori is divided by transverse and anteroposterior bur cuts to a
depth of 1–2 mm above the level of horizontal palatal shelf in order to
prevent any fracture of the palate and perforation into the nasal cavity.
• These cut sections are removed with the help of a chisel and mallet.
• The surface should be finely smoothened using large bone files or
vulcanite bur. The torus can also be removed with the help of rotary
burs alone without the use of chisels, but this may cause accidental
perforation into the nasal cavity or trauma to the soft tissues.
• This area should be copiously irrigated and the mucoperiosteal flap is
trimmed accordingly and sutured back.
• The acrylic stent which was initially constructed must now be inserted.
• This stent supports the flap and prevents any haematoma formation
and covers the wound. The stent can be used as long as the wound
healing is completed.
Complications
The risk of creation of oronasal fistula is more owing to the thin palatal shelf.
b. Mandibular tori or torus mandibularis (Fig. 20.25)

It is an exostoses located on the lingual aspect of the mandible in the region of
the premolar above the mylohyoid line. They may be unilateral or bilateral.
FIGURE 20.25 (A) Clinical image showing removal of bilateral

mandibular tori. (B) Mandibular tori removal. Mucoperiosteal flap
elevated to expose the tori followed by depth cuts using bur.
• It is removed if lower denture is to be constructed.

• It should be removed if there is chronic irritation.
• Very rarely, it is removed when the patient fears of malignancy.
• Inferior alveolar nerve and lingual nerve block are given along with
local infiltration anaesthesia on the tori.
• Once anaesthetised, an incision is made on the crest of the alveolar
ridge for sufficient length to expose the entire tori.
• In case of edentulous patients, incision can be placed on the lingual
gingival sulcus.
• Soft tissues are elevated using a periosteal elevator to expose the tori.
• Using a chisel, bur or rongeur, tori is removed and the rough bony
surface is smoothened using a bone file.
• Excess soft issue is trimmed, wound irrigated and sutured back.
FIGURE 20.26 (A) Mandibular tori in a dentulous arch. (B) CBCT

showing torus mandibularis on the lingual aspect of the mandible.
(C) Surgical excision of mandibular tori—demonstration. (D) Tori
excised. (E) Excised tori—specimen.
Precaution
• To prevent formation of sublingual haematoma, while removing

bilateral mandibular tori, the flap should be kept intact in the midline.
• A piece of gauze is placed below the torus to be removed to prevent
the loss of excised bone into the soft tissues since displacement of bone
chips may lead to sublingual space infection.
3. Mylohyoid ridge reduction (Fig. 20.27)

Mandibular lingual shelf area contains mylohyoid ridge and houses the third
molar tooth. This area is used extensively by the prosthodontists to extend the
lingual flanges of the mandibular denture to gain stability and retention.
FIGURE 20.27 Posterior mandibular ridge resorption with

prominent mylohyoid ridge and higher muscle attachment.
This shelf, along with the mylohyoid muscle insertion, becomes more
prominent and superficial in due course of time due to atrophy of the
mandible. A sharp lingual shelf interferes with the denture construction and
insertion and the mylohyoid muscle attachment here dislodges the denture.
Therefore, this shelf needs to be reduced and the mylohyoid muscle
attachment should be released.
Technique
• A linear incision is made on the crest of the ridge, on the posterior

aspect of the mandible, laterally and superiorly on the external oblique
ridge.
• A full thickness mucoperiosteal flap is elevated to expose the lingual
shelf area and the mylohyoid muscle.
• Care should be taken to avoid any injury to the lingual nerve in this
area.
• The mylohyoid muscle is released by sharply incising the muscle
attachment at bony origin.
• A chisel is then placed parallel to the ramus and in accordance with the
direction of the bone grain of the mandible and the shelf is split off.
• The bone is trimmed and smoothened with the help of bur and bone
files. The wound is closed with sutures after irrigation with saline.
• Immediate replacement of the denture helps in repositioning the
muscle attachments inferiorly; however, downward repositioning can
be best established with the help of a rubber catheter placed in the
floor of the mouth and securing it with sutures passed through the
skin with an awl. The catheter is retained in position for a period of
5 days.
4. Genial tubercles reduction (Fig. 20.28)

Genial tubercles are the bony projections located on the lingual aspect of the
mandible, two on either side of the midline which gives attachment to the
genial muscles. The two genial tubercles located superiorly are more
prominent than the inferior due to the gross resorption of the mandibular
ridge. This may elevate the ridge lingually giving a shelf-like appearance and
making the anterior lingual seal impossible. This is also a frequent site of
ulceration when a lower denture is used.
FIGURE 20.28 Resection of genial tubercles. (A) Superior position
of the genial tubercle interference in the lingual seal of denture. (B)
The tubercle exposed, genioglossus muscle is secured. (C) Genial
tubercles resected.
Technique
• An incision is placed in the midline in an anteroposterior direction and

the tubercles are exposed by blunt dissection.
• The muscle is secured using catgut before separating the tubercle.
• Using bur, chisel or rongeurs, the tubercle is removed and the rough
bony margins are smoothened using file.
• The wound is closed using suture.
5. Maxillary tuberosity reduction (Fig. 20.29)

Enlarged maxillary tuberosity may be either fibrous or bony in nature.
Unilateral hypertrophic maxillary tuberosity is favourable for construction of
denture if sufficient space exists between the tuberosity and the ascending
ramus of the mandible for the denture flange to fit in without any difficulty
during opening and closing of mouth. However, bilateral hypertrophic
tuberosity needs reduction.
FIGURE 20.29 (A) Elliptical incision made on the crest of the
alveolar ridge. (B) Reflection of the buccal flap to expose the bony
tuberosity. (C & D) Excision of the submucosal fibrous tissue for
reduction.
Causes of enlarged tuberosity
• Prolonged retention of maxillary third molar with loss of mandibular

third molar resulting in supraeruption of the maxillary molar along
with alveolar hyperplasia.
• Enlargement of the maxillary antrum with the pneumatisation of the
tuberosity region.
• Gingival fibromatosis.
Technique
Crestal approach
• An interarch space of at least 1 cm should exist between maxillary and

mandibular arches in the posterior region for proper construction of
denture. A radiograph of the tuberosity region would help in detecting
if the enlargement is a fibrous or bony one.
• Usually this is a combined procedure which requires removal of both
soft and hard tissue.
• A wedge-shaped or elliptical incision is made on the crest of the
alveolar ridge to the depth of the bone. This piece of the tissue is then
removed.
• The buccal and palatal margins of the flap are then thinned by
removing the submucosal tissues beneath these flaps.
• A rongeurs or a large oval bur is used to remove the bony undercut.
• The area is then smoothened with the help of bone files and irrigated
with saline.
• Before closure, undermined buccal and palatal flaps may need to be
trimmed for proper approximation. The wound is closed primarily.
Lateral approach
When tuberosity is very narrow and overlying keratinised mucosa requires to
be preserved for vestibuloplasty in this region, a lateral rather than a crestal
approach is adapted for reducing the tuberosity.
• An incision is made on the lateral side of the maxillary ridge inferior

enough to pass below the malar buttress.
• Two relaxing incisions are made on either side of the crestal incision
anteriorly and posteriorly and the flap is retracted and submucosal
excision of the fibrotic tissue is done.
• The sulcus is extended superiorly from the lateral incision to deepen
the sulcus. The palatally based flap is now advanced to cover the bone
and line the newly created sulcus and it is sutured here to the new
periosteum.
• A maxillary denture splint is used to stabilise the tissue in the new
position.
6. Tuberoplasty (Fig. 20.30)

The tuberosity, hamular notch region helps in retention of denture and also
aids in peripheral seal of the maxillary denture. This procedure is undertaken
to increase the depth between the hamular notch and the distal aspect of the
maxilla. In this technique, to deepen the hamular notch the pterygoid plate
and the hamulus are repositioned in the posterior direction.
FIGURE 20.30 Maxillary tuberoplasty.
The residual ridge resorption pattern of maxilla and mandible is very variable.
Commonly maxilla resorbs in a posterosuperior direction while mandible
resorbs in anteroinferior direction. This results in Class III anterior ridge
relation very often requiring jaw correction (Figs. 20.31, 20.32). Similarly
variable resorption pattern of either jaw in posterior can also mandate
segmental jaw surgery for favourable occlusion.
1. Mandibular osteotomy procedures

2. Maxillary osteotomy procedures (Fig. 20.33A–G)
3. Combination procedures
4. Segmental jaw surgeries (Figs. 20.34, 20.35)
FIGURE 20.31 Class III relation of maxillary edentulous ridge
against mandibular teeth requiring corrective orthognathic surgery.
FIGURE 20.32 CBCT showing Class III skeletal relation of

completely edentulous maxilla and mandible.
FIGURE 20.33 (A) Anterior maxillary edentulism post trauma.

Skeletal Class III relation. (B) Post traumatic deformity with no
dental support for upper lip. (C) Le Fort I maxillary osteotomy and
advancement. (D) Dental implant placement in anterior maxilla. (E)
rhBMP-2 in ACS placement for ridge augmentation. (F) Primary
closure. Note advancement of maxilla with favourable occlusion.
(G) Prosthetic rehabilitation with incisors in Class I relationship.
FIGURE 20.34 (A) Partially edentulous resorbed maxilla with

reduced interarch space. Note altered mandibular occlusal plane
superiorly to right. (B) Exposure of the edentulous maxillary
alveolus. (C) Mandibular segmental subapical osteotomy—planned
cuts with excess bone removal on left to correct occlusal cant. (D)
Osteotomy performed with oscillating saw. (E) Implant placement
in maxilla with primary onlay bone grafting with bone harvested
from mandible. (F) Primary closure showing adequate interarch
space with mandibular occlusal plane modified.
FIGURE 20.35 (A) Implant placement in mandibular anterior

edentulous region. (B) Subapical osteotomy—segmental surgery
to achieve Class I incisor relation, primary bone grafting done in
relation to the implant.

Classification of soft tissue procedures
• Soft tissue recontouring

• Soft tissue reductions
• Soft tissue excision
• Soft tissue repositioning
• Soft tissue grafting
1. Frenectomy
A frenum is a fold of tissue or muscle connecting the lips, cheek or tongue to
the jawbone (Figs. 20.36, 20.37). A frenectomy is removal of one of these folds
of tissues. Patients receiving dentures may need a frenectomy if the position of
a frenum interferes with the proper fit of the denture thereby frequently
ulcerating and reducing the stability of the denture (Fig. 20.38A, B).
FIGURE 20.36 (A) High frenal attachment in maxilla requiring labial

frenectomy. (B) Lower labial high frenal attachment requiring
frenectomy.
FIGURE 20.37 (A–D) Clinical pictures of labial frenectomy.
FIGURE 20.38 Lingual frenectomy.
Procedures performed on the labial frenum and lingual frenum are termed
as labial frenectomy and lingual frenectomy, respectively.
Technique
1. Simple excision
2. Z-Plasty
3. Localised vestibuloplasty with secondary epithelialisation
4. Laser assisted frenectomy
Labial frenectomy
• Local infiltration anaesthesia is used to anaesthetise the labial frenum

at its origin and insertion.
• Once anaesthetised, upperlip is everted so that the frenum is kept taut.
• Using two haemostats, the fibres of the frenum are locked (the first
haemostat is placed parallel to the labial surface of the alveolar ridge
and in contact with the mucosa covering the labial surface of the
mucobuccal fold and the second haemostat is placed parallel to the lip
and perpendicular to the first haemostat).
• The haemostats are kept in such a way that their tips touch each other
so that the entire fibrous tissue of the frenum which has to be removed
lies within the haemostat.
• Using a No.11BP blade the frenum is excised by cutting the outer
surface of both the haemostats so that the excised tissue comes out
separately along with the haemostats.
• Now the lateral margins of the wound are undermined and the wound
is sutured without tension.
Lingual frenectomy (Figs. 20.38, 20.39)

This procedure is performed when there is ankyloglossia (tongue-tie) or when
there is high lingual frenal attachment. This attachment binds the tongue to
the lingual surface of the alveolar ridge. Lingual frenectomy is performed in
these patients even when prosthesis is not required as it interferes with the
normal speech. Once the teeth are lost, it disturbs the stability of the denture
each and every time when the tongue is moved.
FIGURE 20.39 Lingual frenectomy—lingual frenal attachment to

alveolar ridge.
Technique
• A 3–0 silk suture is passed through the midline of the tongue around
2 cm from the tip (traction suture).
• This is done to hold the tongue up so that the frenum becomes taut.
• Using a sharp scissors, a cut is made 1–2 cm midway between the tip of
the tongue and the lingual surface of the mandible.
• The cut is made in such a way that the blades of the scissors are
parallel to the floor of the mouth.
• Care should be taken not to injure the submandibular duct, papilla and
the blood vessels in the floor of the mouth.
• In certain cases genioglossus muscle should also be dissected in
addition to the lingual frenum.
• The wound margins are undermined, approximated and closed
without tension.
2. Vestibuloplasty or ridge extension procedures

Vestibuloplasty is a surgical procedure wherein oral vestibule is deepened by
changing the soft tissue attachments. Vestibuloplasty can be done either on the
labial or the lingual side.
Goals of the surgery
• To increase the size of denture bearing area

• To increase the height of the residual alveolar ridge
Labiobuccal vestibuloplasty of maxilla

Different techniques for labial vestibuloplasty are:
i. Mucosal advancement vestibuloplasty (submucosal vestibuloplasty)

ii. Pocket inlay vestibuloplasty
iii. Grafting vestibuloplasty
i. Mucosal advancement vestibuloplasty

This procedure is also known as submucosal vestibuloplasty wherein the
mucous membrane of the vestibule is undermined and advanced to line both
sides of the extended vestibule. The prerequisite for this kind of procedure is
that there should be presence of adequate amount of bone and healthy
mucosa. Different types of mucosal advancement vestibuloplasty are:
i. Closed submucous vestibuloplasty (Obwegeser)

ii. Open view submucous vestibuloplasty
Closed submucous vestibuloplasty (Fig. 20.40)
This procedure is indicated where there is enough bone and healthy tissues
but with muscle attached closer to the alveolar crest.
FIGURE 20.40 Closed submucosal vestibuloplasty of the maxilla.

(A) Incision made. (B) Blunt dissection done. (C) Stent placed to
maintain the depth of the vestibule.
Objectives
• To extend the vestibule for providing additional ridge height.

• To prevent relapse by excising or transferring sub-mucous tissue and
the muscles to a position farther from the crestal ridge.
Technique
• A vertical incision is made in the midline of the vestibule extending till

the mucogingival junction.
• Blunt dissection is carried out separating mucosa from the submucosa
to create a submucosal tunnel.
• The tunnel is extended till the zygomatic buttress on either side.
• Next supraperiosteal dissection is carried, freeing the underlying
muscles and connective tissue from the periosteum.
• The vertical incision is closed and as tent is placed for 10–14 days after
adapting the mucosa to the deepened vestibule.
Open view submucous vestibuloplasty (Obwegeser)

Wallenius advocated an open method to overcome the relapse of the closed
vestibuloplasty. A horizontal incision is made in the mucogingival junction. A
thin mucosal flap is elevated by submucosal dissection followed by
supraperiosteal dissection to the desired extent, excising muscle and
subcutaneous tissues. Stay sutures are used to fix the flap to the periosteum
deep in vestibule. The free flap is returned to its original position and sutured.
ii. Maxillary pocket inlay vestibuloplasty
This procedure is used for extension of ridge in the atrophic maxilla. Here
pockets are created on either side of the pyriform aperture and denture flanges
are extended into these pockets for stability. Preoperatively patient’s denture
is modified with extended labial flanges.
Technique
• Incision is made along the vestibule from one zygomatic buttress to the
other.
• Supraperiosteal dissection is carried out and two pockets are created
on either side of the pyriform aperture extending up to the level of
levator anguli oris.
• In midline, the dissection is performed up to the pyriform aperture.
• Care should be taken not to cause any injury to the nasal cavity.
• Impression of the pouch is made with impression compound before
placing the graft.
• Now, labial flanges of the prefabricated denture are lined with gutta
percha and is covered with split thickness graft (the raw surface facing
pyriform aperture) and inserted into these pouches.
• The denture is fixed in this position with circumzygomatic wires and
wound margins sutured to the graft. The wires remain in place for a
week.
• New dentures are constructed after a period of 6 weeks.
• In order to prevent contracture of the pouches, the denture must be
worn for a period of one year throughout day and night.
Advantages
• Better retention of the dentures.

• Helps to restore deficiency in the region of nasolabial fold with
improved contour.
iii. Grafting vestibuloplasty (Fig. 20.41)
Indications
• When the available bone is in adequate to compensate for relapse of

the vestibuloplasty.
• When a bone graft has been previously placed in the surgical site.
• When a large surgical defect is present.
FIGURE 20.41 Kazanjian’s method of vestibuloplasty.
Grafts used
• Skin graft
• Mucosal graft (palatal and buccal mucosa)
• Xenograft
• Amnion
Advantages
• There lapse caused by contracture of the wound margin is reduced.

• Due to early covering of the surgical defect patient discomfort is
reduced.
• Healing is faster.
Disadvantage
Depending on the type of the graft a second wound would be present at the
donor site.
Obwegeser’s skin graft technique (1959)

The difference is that here the raw surface of the ridge with its periosteal
attachment is covered with a split thickness skin graft in order to maintain the
depth of the vestibule at the desired level. Mucosal grafts can also be used for
this purpose.
In all the ridge extension procedures, a new prosthesis is made after
4–5 weeks. The flange of the new denture should be of sufficient length to
maintain the new depth of the sulcus. The denture flange should not irritate
the periosteal surface. In spite of all the efforts to increase the vestibular depth,
50% relapse can take place. Therefore, overcorrection is done to compensate
this relapse. When the residual bony ridge is too small to perform
overcorrection, a free epithelial graft should be considered to cover the
wound.
Mandibular vestibuloplasty techniques
Mandibular vestibuloplasty is performed to deepen the labial/buccal or lingual
sulcus. It also involves muscle repositioning.
Labial approach
An incision is made deep in the sulcus and supraperiosteal dissection is
carried out till the predetermined depth. The raw surface heals by secondary
epithelialisation. The drawback of this surgery is that in process of healing the
sulcus tends to obliterate due to scar contracture. In order to prevent scar
contracture, techniques have been designed to reposition or ‘switch’ mucosa to
cover the raw defect of the deepened vestibule. They are:
• Kazanjian’s technique
• Godwin’s technique
• Lipswitch technique
• Clark’s technique
Kazanjian’s technique (1935) (Fig. 20.41)
• An incision is made in the mucosa of the lip and a large flap of labial
and vestibular mucosa is retracted.
• The mentalis muscle is detached from the periosteum to required
depth and the vestibule is deepened via supraperiosteal dissection.
• A flap of the mucosa is turned downwards from the attachment of the
alveolar ridge and is placed directly against the periosteum to which it
is sutured.
• A rubber catheter stent can be placed in the deepened sulcus and
secured with percutaneous sutures. This catheter helps to hold the flap
in its new position and maintain the depth of the vestibule. It is
removed after 7 days.
• The labial donor site is coated with tincture of benzoin compound and
the surface heals by granulation and secondary epithelialisation.
Contracture of the wound margins takes place.
Godwin’s technique (1947)

It is similar to the Kazanjian’s method in which a flap of labial mucosa is
raised, but the vestibule is deepened by subperiosteal stripping instead of
supraperiosteal dissection.
• The periosteum and the connective tissue attached to it are pushed

downwards and the flap of labial and vestibular mucosa is placed
against the bone and sutured to the connective tissue beyond the
deepened vestibule with the help of resorbable sutures.
• Now, a rubber catheter is placed in the deepened sulcus and secured
by means of percutaneous sutures. The catheter is left in place for
11 days.
• Mean while raw tissue on the labial side is packed with zinc oxide-
eugenol dressing, which heals by secondary epithelialisation and scar
contracture.
The greatest disadvantage of Kazanjian’s and Godwin’s technique is that the

scar contracture which takes place on the labial side leads to reduction in the
vestibular depth.
Lipswitch vestibuloplasty
It was described by Kethley and Gamble. In this procedure, mucosal flap
containing labial and vestibular mucosa is raised in a similar way as in
Kazanjian’s and in Godwin’s technique which has its free margin in the lip and
the base attached to the crest of the alveolar ridge. However, here the
periosteum is incised high in alveolar ridge below the crest and it is reflected
from the bone. This flap consisting of periosteum, connective tissue and
muscle is turned outwardly and sutured to the margins of the raw labial
surface. Now the mucosal flap is turned downwards against the bare bone and
sutured to the periosteum deep in the vestibule.
Clark’s technique (1953) (Fig. 20.42)

Clark’s technique is the reverse technique of the Kazanjian’s technique. It is
based on the following principles:
• Raw surface on connective tissue contracts, whereas when covered

with epithelium will have minimum contracture.
• Raw surface on bone does not undergo contracture.
• For repositioning and fixation, epithelial flap must be undermined
adequately.
• Soft tissues which are repositioned tend to return to their normal
position, therefore over correction is necessary.
FIGURE 20.42 Clark’s method of vestibuloplasty.
The flap is pedicled off from the lip, the raw surface on the bone is left
exposed.
• An incision is made slightly labial to the crest of the alveolar ridge.

• The dissection is carried out supraperiosteally till the desired depth of
the sulcus.
• The lip mucosa is undermined up to the vermilion border so that free
edge of the mucosal flap is secured to the periosteum deep in the
sulcus.
• The raw surface on the bone heals by granulation tissue formation and
epithelialisation without contracture. Initially the depth of the sulcus is
maintained for a long time.
Drawback of the technique is that relapse is common since the attachment of

the lip musculature to the alveolar bone shifts towards the alveolar crest,
obliterating the sulcus.
Lingual vestibuloplasty
Lingual vestibuloplasty is used in patients with extensively resorbed
mandible. Mylohyoid and genioglossus muscles attached to the lingual aspect
of the mandible interfere with the stability of the prosthesis and try to dislodge
them. In these patients, extension of the lingual sulcus (or lowering of the floor
of the mouth) can help in increasing the denture retention and stability by
increasing the surface area.
Following methods are adapted for lingual vestibuloplasty:
• Trauner’s technique
• Caldwell’s technique
Trauner’s technique (1952)

• An incision is made in the floor of the mouth extending from the third
molar of one side to the third molar of the other side.
• The mucosa is reflected lingually and supraperiosteal dissection is
carried out, once mylohyoid muscle is exposed a haemostat is passed
through this muscle in the canine region and the muscle fibres incised
on the haemostat to avoid any injury to the periosteum and the lingual
nerve.
• Now the mucosa and the mylohyoid muscle are secured with
percutaneous sutures to the lower border of the mandible.
• On the lingual side of the mandible, a split thickness skin graft can be
used on a stent to cover the raw periosteal surface.
Caldwell’s technique (1955)
• An incision is made in the crest of the posterior mandibular ridge

extending from one molar to the other molar region.
• Subperiosteal dissection is carried out and a full thickness
mucoperiosteal flap is elevated and reflected medially. The mylohyoid
muscle is detached and mylohyoid ridge is removed or reduced.
• The subperiosteal stripping is carried out till the desired depth and
sometimes even to the inferior border of the mandible. A rubber
catheter is placed in the bottom of the lingual sulcus and secured with
percutaneous suture. It is left in place for 7–10 days.
Combination of buccal and lingual vestibuloplasty (Fig. 20.43)
Obwegeser’s technique (1963)
• The lingual sulcusis first deepened as described by Trauner.

• Genioglossal fibres are detached leaving the medial and inferior fibres
to maintain muscular control of the tongue.
• The mylohyoid muscle attachment is detached next.
• Now the labiobuccal vestibule is deepened as described by Obwegeser
for skin graft vestibuloplasty.
• The edges of the buccal and the lingual flaps along with mylohyoid are
sutured to each other below the inferior border of the mandible with
the help of awl. Entire alveolar ridge is now covered with skin graft.
• A previously prepared stent is lined with a split thickness skin graft
and is ligated to the mandible with circumferential sutures. The stent
is removed after 7–10 days.
FIGURE 20.43 Obwegeser’s technique—grafting vestibuloplasty.
3. Redundant tissue excision

A. Alveolar flabby ridge (hypermobile soft tissues on the
alveolar ridge) (Fig. 20.44)
As a result of resorption of the residual alveolar bone or ill-fitting dentures or
both, excessive hypermobile tissue can be seen on the residual alveolar ridge.
This is most commonly seen in maxillary anterior region most commonly as a
part of Kelly’s combination syndrome.
FIGURE 20.44 Removal of hypermobile tissue from the maxillary
alveolar ridge.
Kelly’s combination syndrome

In 1972, Kelly collectively called the sequential destructive changes in the hard
and soft tissues of the oral cavity seen in patients requiring singular
restoration of a completely edentulous arch opposing a natural dentition as
combination syndrome.
The characteristic features that occur when an edentulous maxilla is
opposed by natural mandibular anterior teeth, are:
• Loss of bone from the anterior portion of the maxillary ridge

• Overgrowth of the tuberosity
• Papillary hyperplasia of the hard palatal mucosa
• Extrusion of mandibular anterior teeth and
• Loss of alveolar bone and ridge height beneath the removable partial
denture bases, also called anterior hyper function syndrome
As these soft tissues are compressible, stability of the denture is jeopardised

(the denture will have a rocking movement) which in turn increases the
possibility of bone resorption. Occasionally, overlying soft tissue may get
ulcerated due to trauma which further affects the stability of the denture. If left
untreated, these unsupported alveolar tissues may increase in size and even
prolapse towards the palatal direction.
Technique
• Two parallel incisions are made on the lingual and buccal aspect of the
tissue to be excised.
• Using periosteal elevator excess soft tissues are removed from the
underlying bone.
• Tunnelling of mucoperiosteum is done and the ends are approximated
and sutured.
B. Denture granuloma (Table 20.2)

Denture granuloma is a sequela of wearing an ill-fitting denture. An ill-fitting
denture and its flanges compress the adjacent soft tissues causing formation of
ulcers and granulation tissues. These granulation tissues organise into fibrous
tissues and the lesion becomes permanent.
• Early lesions can be treated by discontinuation of the denture

following which the lesion shrinks and disappears. New dentures
should then be reconstructed.
• Late lesions are mostly accompanied by resorption of the underlying
bone, so care must be exercised not to remove the unwanted lesion
and to preserve the little sulcus that remains after excision, thereby not
affecting the stability and retention of the future prosthesis. This is
achieved by removing the granulation tissue with a combination of
blunt and sharp dissections leaving the underlying periosteum and
muscle intact. Care should be taken not to injure the mental nerve
while performing the procedure on the mandible.
Table 20.2
Howe’s classification of denture granuloma
Situation of the lesion Treatment

Class Lesions entirely situated upon the Heals well with minimum scarring
I mucoperiosteum
Class Lesions entirely attached to the mucous The wound should not be closed under
II membrane of the cheek, lip or floor of the tension; heals by primary intention
mouth
Class Lesions whose attachments saddle and Needs epithelial covering
III obliterate the reflection of mucous membrane
C. Epulis fissuratum (inflammatory fibrous hyperplasia, denture

fibrosis)
Epulis fissuratum is a generalised hyperplastic enlargement of the mucosa and
fibrous tissue in the vestibular and alveolar area which often results from
chronic denture irritation. The condition is usually inflamed and affects the
stability and comfort of the denture (Fig. 20.45).
FIGURE 20.45 Epulis fissuratum in maxillary anterior region in

relation to denture.
Before undertaking the surgical procedure, the patient is asked to

discontinue the denture for a period of 2 weeks in order to reduce the
inflammation caused due to the denture.
• If the lesion is small, base of the growth is held with the help of Allis
forceps and excised completely taking care not to violate the
periosteum and retaining as much attached mucosa as possible
(Fig. 20.46A, B).
• Sometimes, sharp submucosal dissection is done to form a flap
followed by sharp submucosal excision of the growth. The flap is then
sutured back to the periosteum in order to maintain the vestibular
depth.
• When severely scarred tissues are present, excision or submucosal
dissection of the growth leads to extensive contracture relapse and loss
of vestibular depth. Therefore, in these cases the epulis is first excised
followed by supraperiosteal placement of free mucosal palatal graft to
extend the depth of the vestibule.
• Denture splints can be used to protect the graft site.
FIGURE 20.46 (A) Epulis fissuratum in left maxillary posterior
region in relation to sharp edge of complete denture (inset). (B)
Surgical excision of the growth at the base of the lesion.
D. Reactive inflammatory hyperplasia of the palate (Fig. 20.47)

Reactive inflammatory hyperplasia of the palate is characterised by the
presence of red nodules or papillary growth on the palatal mucosa. It is a
sequela of chronic use of ill-fitting maxillary complete or partial denture.
Sometimes construction of a denture on a preexisting papillomatosis also leads
to the situation (Fig. 20.48).
• Initial treatments involve discontinuation of the denture or reduce its

use.
• If candidiasis is present, it should be treated first with appropriate
antifungal agents and the denture should be relined.
• Small masses can be removed with the help of curette by scraping on
the surface of the palate until the corium is reached.
• Mucoabrasion can be done with slow-moving, non-gouging bur at a
slow speed accompanied with copious irrigation.
• Electrocautery and loop electrodes can also be used for complete
excision. The loop is used slowly in a paintbrush fashion, but may
require several procedures for complete removal. The proper depth of
excision is till the submucosa. Care should be taken not to penetrate
the periosteum as this might result in sloughing of the palate resulting
in delayed healing.
• Once the growths are excised, a relined denture or a prefabricated
acrylic stent with soft reline must be used to prevent haemostasis and
for wound protection.
• Usually healing by epithelialisation is complete within 3–5 weeks.
FIGURE 20.47 Removal of papillary hyperplasia.

FIGURE 20.48 Inferior alveolar nerve repositioning.
4. Mental nerve transposition

Gross resorption of the alveolar bone may lead to mental foramen becoming
superficial until it comes to the crest of the ridge. When this occurs mental
nerve may be subjected to pressure from dental flange which causes a dull
burning sensation or sudden sharp severe pain. The pain can be elicited
during mastication or by applying digital pressure. In some cases, pain can be
eliminated by simply relieving the denture in that area provided the denture
has enough support for the remaining denture wearing area. Preoperative
radiograph is taken to assess the level of mental foramen.
Technique
• The nerve is approached via along incision made in the crest of the
alveolar ridge.
• If the mental foramen is located on the crest of the ridge, the incision
should curve lingually to avoid the foramen.
• Mucoperiosteal flap is reflected and the mental foramen and the
neurovascular bundle are located. The nerve should be retracted
carefully and held with hook.
• A vertical groove is drilled below the mental foramen on the buccal
cortex with a dental drill.
• The nerve is now repositioned in the inferiorly created cortical groove.
• The nerve can be secured to the new position with the help of
absorbable haemostatic gauze such as the surgicel and the
mucoperiosteal flap is sutured back.
• Postoperative anaesthesia may persist if there happen to be any
damage caused to the nerve during surgery.
Repositioning of inferior alveolar nerve

(IAN) (Fig. 20.48)
Dental implants are often placed in the posterior mandible, but in many cases,
the bone has so severely atrophied that sufficiently long fixtures cannot be
placed without encroaching on the inferior alveolar nerve (IAN).
IAN lateralisation and IAN transpositions are surgical procedures that
reposition the IAN for the purpose of implant placement without bone
augmentation.
In 1987, Jenson and Nock carried out IANT for the placement of dental
implants in posterior mandibular regions.
IAN lateralisation (IANL)

IANL is defined as the lateral reflection of the IAN without incisive nerve
traction (preservation of the incisive nerve and lateralisation of inferior
alveolar neurovascular bundle posterior to the mental foramen).
IAN transposition (IANT)

In IANT, a corticotomy is done around the mental foramen and the incisive
nerve is transacted (incisive neurovascular bundle is sacrificed), to allow
transposition of both the mental foramen and the IAN such that the mental
foramen is repositioned more posteriorly.
Advantages
• Prevents injury to the IAN and vessels during implant placement in

edentulous posterior atrophic mandible
• Eliminates the need for bone grafts
• Greater implant stability
• Indicated during orthognathic surgeries, such as lower border shaving
and total mandibular subapical osteotomy
CHAPTER 21
Dental Implantology
Evolution of dental implant materials

Types of implants
Endosteal implants
Early subperiosteal implant
Early transosteal implants
Features of successful implants
Biological considerations for implant-tissue integration
Soft tissue-implant surface interface
Bone-implant interface
Fibro-osseous integration
Osseointegration
Implant surface treatment
Classification of implants
Based on the implant-tissue interface
Based on design and location
Based on function
Based on implant materials
Based on implant design
Classification of the bone
Lekholm and Zarb classification
Cawood and Howell classification
Endosteal implants
Root form implants
Classification of root form endosteal implants
Cylinder-type implant
Screw-type implant
Blade form implants
One-stage and two-stage implant surgeries
Assessment of bone for implant placement
Bony criteria for implant placement
Bone height
Bone width
Bone length
Bone angulation
Patient evaluation
Patient selection
Components of implant
Implant body regions
Crest module
Body of the implant
Surgical procedure
Anaesthesia
Incision design—anterior mandible
Implant placement
Implants for completely edentulous patients
Types
Ball and socket removable overdenture
Bar-retained removable overdenture
Cement-retained fixed bridge
Screw-retained fixed bridge
All-on-four concept
Loading concept
Criteria for immediate loading
Implant failure
Early failure
Late failure
Removal of mobile implant
Removal of fractured implant
Counter-torque ratchet technique (CTRT)
Piezo tips
High-speed burs
Trephine burs
Peri-implantitis
Causes of peri-implantitis
Clinical diagnosis
Typical signs and symptoms of peri-implantitis
Contributing factors
Treatment of peri-implantitis
Comparison of normal teeth and implants
Gingiva and peri-implant soft tissues
Junctional epithelium
Biological width
Periodontal ligament and osseointegration
Peri-implantitis and periodontitis
Zygomaticus implants
Classification
Indications and contraindications
Disadvantages
Technique
Surgical access
Osteotomy preparation
Implant insertion
Postoperative care
Complications
Dental implants are surgically fixed substitutes for roots of missing teeth.
Embedded in the jaw bone, they act as anchors for a replacement tooth or teeth
crown or a full set of dentition. Dental implantology is the study of the art and
science concerned with surgical insertion and restoration of materials and
devices restoring the partially or totally edentulous patient to function.
In general, it is divided into:
• Implants used to restore completely edentulous arch.

• Implants used to restore the partially edentulous arch (Fig. 21.1).
FIGURE 21.1 (A–D) Restoration of partially edentulous space with
implants.
Procedure of replacing single missing tooth with dental implants has high
success rates, does not compromise the adjacent natural dentition, yields high
patient satisfaction and is documented in a variety of locations in the dental
arch.
Evolution of dental implant materials

The first implants made from nonautologous materials date back to 1819 by
Maggiolo who placed a single-stage gold implant without a crown to heal
passively in a fresh extraction site. Crown was added after healing. However,
this procedure was followed by intense pain and gingival inflammation. Metal
implant devices like gold, platinum, silver, lead, iridium, tantalum, stainless
steel, etc. were developed in the early 20th century. Surgical cobalt-chromium-
molybdenum alloy was introduced in oral implantology in 1938 by Strock. As
an implant material, vitallium superceded titanium, which is more body
compatible.
Today implants are made predominantly of titanium (pure titanium or a Ti-
Al-V alloy). Several procedures are available to increase surface area, i.e. to
increase the contact surface to the bone and thus achieve better bone
integration (osseointegration): TPS (titanium plasma spray) coating,
sandblasting, surface, etching, laser structuring or HA (hydroxyapatite)
coating.
Dental implant:
(According to Glossary of Prosthodontic Term (GPT), 9th edition)
Dental implant\den’tl implant:
1. A prosthetic device made of alloplastic material(s) implanted into the

oral tissues beneath the mucosal and/or periosteal layer and on or
within the bone to provide retention and support for a fixed or
removable dental prosthesis; a substance that is placed into and/or on
the jaw bone to support a fixed or removable dental prosthesis;
2. The portion of an implant that provides support for the dental implant
abutment(s) through adaptation on (eposteal), within (endosteal), or
through (transosteal) the bone.
Although dental implants may be classified by their silhouette or

geometrical form (i.e. fin, screw, cylinder, blade, basket, root form, etc.)
generally dental implants are classified based on their anchorage component
as it relates to the bone that provides support and stability. Thus, there are
three basic types of dental implants: eposteal dental implants, endosteal dental
implants and transosteal dental implants. Some dental implants possess both
eposteal and endosteal components (by design or subsequent anchorage
change); the decision as to what anchorage system provides the most support
at initial placement determines which category is used to best describe the
dental implant. The dental implant(s) provide bony support via the dental
implant attachment while the dental implant abutment(s) connect the dental
implant to the fiden or removable dental prosthesis;
syn, ENDOSTEAL DENTAL IMPLANT, EPOSTEAL DENTAL IMPLANT,
TRANSOSTEAL DENTAL IMPLANT; comp, MUCOSAL INSERT
Types of implants (Fig. 21.2)

Endosteal implants
An endosteal implant is an alloplastic material surgically inserted into a

residual bony ridge primarily as a prosthodontic foundation.
—Carl E. Misch
FIGURE 21.2 Types of implants. (A) Subperiosteal. (B)
Transosteal. (C) Endosteal—root form. (D) Endosteal—blade form.
Endosteal (in the bone) implant is the most commonly used type of implant
which is placed directly into the bone, like natural tooth roots and can be used
for many purposes. These types include root form (screws and cylinders) or
blade form surgically placed into the jaw bone. Each implant holds one or
more prosthetic teeth. This type of implant is generally used as an alternative
for patients with bridges or removable dentures. Since this implant is placed
into the bone, sufficient bone width should be available. This type of implant
is discussed in detail later in this chapter.
Early subperiosteal implant

To overcome the problem of insufficient bone width to place an endosteal
implant, subperiosteal implant can be placed on and around bone. A
subperiosteal implant is a framework specially fabricated to fit on top of
supporting areas in the mandible or maxilla under mucoperiosteum with
perimucosal extensions for support and attachment of prosthesis.
Early transosteal implants

Transosteal implants were inserted through an extra-oral incision below the
chin with a series of projections that penetrate the mandible from its inferior
border and were connected by a bone plate that rests on the inferior border of
the mandible. Several of the projections completely transverse the mandible to
enter the oral cavity and anchor the lower denture.
Transosteal implants could only be used in the anterior mandible due to the
complex nature of the surgical approach this implant modality has not enjoyed
widespread popularity. Its primary indication was in the very atrophic
mandible where root form implants might further compromise the strength of
the jaw.
Implants
Indication
Patient with edentulous space who do not accept removable prosthesis
Patient with lack of neuromuscular control
Patient with high gag reflex
Replacement of a single tooth
In condition where use of other modalities of replacement has deleterious
effect on tissues
Very long edentulous span
Low tissue tolerance
To resolve psychological problems associated with edentulism
In situations, where implant achieves superior results in terms of functions
and aesthetics
1. Patient with poorly controlled diabetes

2. Patient with blood dyscrasias, ischaemic heart disease, cerebral palsy or
immunocompromised patients
3. Patient on bisphosphonates or other antiangiogenic drugs
4. Jaw bone radiation less than 1 year before implant placement
5. Acute psychotic disorders
6. Acute bone resorption
7. Poor patient acceptance/cooperation
8. Underlying bone atrophy due to abnormal stress
9. Metabolic disorders
10. Musculoskeletal disorders
11. Focal and systemic disorders
12. Oral submucous fibrosis with limited mouth opening
13. Drug or alcohol dependence
14. Patient who lack manual dexterity
15. Renal osteodystrophy
16. Pregnancy
17. Regional malignancy
Relative contraindication
1. Patients with uncontrolled diabetes mellitus

2. Significant history of smoking
3. Cardiac patients with stable condition
4. Patient on antidepressant or anticoagulant
5. Habits like bruxism or tongue thrusting
6. Endocrine disorders
7. Trismus
8. Chronic maxillary sinusitis (for maxillary implant which may require
sinus lift procedures-direct or indirect)
9. Erosive diseases
10. Hyposalivation
Features of successful implants
1. Implant should be immobile or with mobility less than 1 mm when

tested clinically.
2. Vertical bone loss should be less than 0.2 mm annually following the
implant’s first year of service.
3. Infections, paraesthesia, neuropathies or violation of anatomical
structures like mandibular canal, nasal passage or maxillary sinus
should be absent.
4. Success rate should be 85% after 5 years and 80% after 10 years.
Biological considerations for implant-tissue

integration
Soft tissue-implant surface interface
The dental sulcus epithelium is more permeable to fluids, cells and
immunoglobulins. The junctional epithelium is a very specialised structure
characteristic to dental apparatus. At the junctional epithelium-tooth interface,
basement lamina is seen with ultramicroscopic hemidesmosomes. Such a
unique feature has only made it possible for biomaterials like tooth to
penetrate the epithelium without breaking its integrity.
A similar tissue-implant interface is required for a healthy implant to
function in the oral cavity. In practice, an oracin positive layer has been found
at the implant-tissue interface. The collagen fibres at this junctional region are
seen at right angles to the implant surface. The tight cuff of the fibrous
connective tissue which runs parallel to the implant surface supports the
epithelial seal and forms an effective barrier to peri-implant pocket formation
and bone loss.
Bone-implant interface
The recent success of dental implants relates directly to the discovery of
methods to maximise the amount of bone-implant contact.
Theories on bone to implant interface

There are two basic theories regarding the bone-implant interface:
1. Fibro-osseous integration (Linkow 1970, James 1975, and Weiss 1986)

2. Osseointegration (supported by Branemark, Zarb, and Albrektsson
1985)
1. Fibro-osseous integration
Weiss’s theory of fibro-osseous integration

Weiss stated that the presence of collagen fibres at the interface between the
implant and bone is a peri-implant membrane with an osteogenic effect. He
believed that the collagen fibres invest the implant, originating at the
trabeculae of cancellous bone on one side, weaving around the implant, and
reinserting into a trabeculae on the other side. He suggested the early loading
of an implant.
However, the collagen fibres around the implant are oriented differently
from fibres in the periodontal ligament of natural teeth. The implant fibres are
usually irregular and parallel to the implant body rather than perpendicular
like periodontal ligament fibres. (Fig. 21.3 A,B).
FIGURE 21.3 (A) Comparison of attachment of normal teeth and
the implant. 1. Natural tooth crown. 2. Artificial tooth crown. 3. Gum
tissue. 4. Implant abutment. 5. Gum tissue. 6. Screw type implant.
7. Bone. 8. Fibres holding tooth to bone (periodontal ligament). 9.
Bone attaches directly to implant—osseointegration (B)
Histopathological image showing osseointegration.
Fibro-integration is seen with implant systems that may have a good initial
success rate but whose success rates drop off rapidly in the long-term.
2. Osseointegration (Fig. 21.4)

(According to Glossary of Prosthodontic Term (GPT), 9th edition) (1) The
apparent direct attachment or connection of osseous tissue to an inert,
alloplastic material without intervening fibrous connective tissue; (2) the
process and resultant apparent direct connection of an exogenous material’s
surface and the host bone tissues, without intervening fibrous connective
tissue present; (3) the interface between alloplastic materials and bone.
FIGURE 21.4 Fibrointegration and osseointegration.
The discovery of osseointegration has undoubtedly been one of the most

significant scientific breakthroughs in dentistry over the past 10–20 years. With
osseointegration, a clinical reality, the root form implant became
implantology’s most dominant design. Osseointegration, as first defined by
Branemark, denotes at least some direct contact of living bone with the surface
of an implant, at the light microscopic level of magnification.
Branemark’s Theory of osseointegration

In 1985, Branemark, Zarb, and Albrektsson defined Osseointegration as the
direct structural and functional connection between ordered, living bone and
the surface of a load–carrying implant. Brånemark proposed that implants
integrate such that the bone is laid very close to the implant without any
intervening connective tissue. The titanium oxide permanently fuses with the
bone, as Brånemark showed in 1950s.
Rigid fixation is denoted by the absence of mobility with 1–5 N force applied
in vertical or horizontal direction. There are four main factors necessary to
achieve a successful osseointegrated bone-to-implant interface. These factors
include:
a. Biocompatible material
b. Implant precisely adapted to prepared bony site
c. Atraumatic surgery to minimise soft tissue damage
d. Immobile, undisturbed healing phase
a. Biocompatible material
The suitability for dental implant stems from the material’s biocompatibility.
Direct contact between titanium and bone has been proven over time to
withstand the forces of occlusion without loss of stability. A result of this
direct contact has been the phenomenon of osseointegration.
This is the reaction of the adjacent bone to the implant and is determined by
morphology, chemical composition, load and the characteristics of the implant
surface. The qualities of implant material that contribute to successful
osseointegration have been determined by various researchers: (1) choice of
raw material, (2) macrostructure, (3) microstructure and (4) surface cleaning.
Choice of raw material (titanium)

Titanium is a plentiful material with many applications in dentistry and
orthopaedics. The rates of successful integration of titanium in the body are
high inspite of the fact that the biological mechanism is not perfectly
understood. Titanium is very reactive and under normal conditions,
spontaneously forms a layer of titanium oxide that isolates the material and
protects it from further chemical reaction. It is this inert state that prevents the
surrounding tissues from causing it to release ions that can react with organic
molecules.
Titanium excels in its strength to weight ratio and as such requires a small
amount of material to achieve the rigidity necessary for implants. Its
mechanical qualities are almost identical to those of stainless steel.
Pure titanium is a metal with high density, ductility, malleability and impact
resistance. There are different types of pure titanium and titanium alloys used
in the production of dental implants. Titanium is graded, for the most part, by
its percentage of oxygen which influences the material’s strength.
Macrostructure
The geometry of the implant influences its initial stability at the time of
placement. The threads of the implant (in screw-type implants) act to increase
the surface area and to distribute the axial forces of occlusion.
Microstructure
Many studies have emphasised the importance of surface texture. The object of
texture is to increase the surface area of the implant and thus the area of bone-
implant contact. Research has shown that rougher the surface, faster the
osseointegration.
An examination of the forces that must be employed to detach an integrated
implant has determined that the torque required for removal is up to 30%
higher in implants where the surface has been roughened.
Roughness on a scale of even 1 nm influences the electric field in the area of
the implant. Increasing the van der Waals forces encourages the biomolecular
bonds between particles. However, it also facilitates the growth of bacteria.
The solution has been used to keep the neck of the implant polished to reduce
plaque retention where the implant is exposed to the oral cavity.
The current methods of creating a roughened surface are based upon
sandblasting particles of aluminium or titanium oxide or acid etching the
surface. Most manufacturers employ a combination of these methods.
With a scanning electron microscope (SEM), it is possible to see the pits of
1.5 µm that are created as a result of the sprayed particles and those even
smaller that are due to the action of etching with acid.
b. Implant precisely adapted to prepared bony site

Cylindrical preparations are most predictably made in an accurate shape.
Precision instrumentation and a technically sound surgical procedure will
minimise the distance between the implant and bone.
c. Atraumatic surgery to minimise soft tissue damage

Atraumatic surgery is required to allow minimal mechanical and thermal
injury to occur. If the gap between the implant and the bone can be minimised
and surgery is atraumatic, embryonic bone will rapidly be laid down between
the implant and the bone, which will then mature into the lamellar load-
bearing bone.
d. Immobile undisturbed healing phase
i. It has been shown that fibrous connective tissue encapsulation will

occur when an implant is loaded too soon after insertion, while a direct
bone-implant interface forms when the implant is left undisturbed in
the bone for a sufficient period of time.
ii. The first month after fixture insertion is the critical period for initial
healing. When loads are applied to the implants during the initial
healing period, primary fixation may be destroyed. Relative motion of
an implant prevents the embryonic bone from being replaced by the
mature lamellar bone.
iii. Once the initial stability of the implant has been achieved, it needs to
be maintained throughout the healing phase. Should the patient desire
to continue wearing the removable prosthesis during the healing
period, it is important that a soft liner be placed in the removable
denture to further decrease load transfer to the implant.
iv. The bone in the mandible is generally denser than the bone in the
maxilla. Since the maxilla is primarily a cancellous bone,
osseointegration requires a longer healing period. When placing
maxillary implants, it is crucial to obtain the primary stabilisation for
successful osseointegration.
v. The achievement of successful osseointegration is first assessed at the
second surgery. Once the abutment is attached to the implant body, the
surgeon should carefully check for any signs of clinically detectable
mobility. An immobile implant at this stage indicates successful
osseointegration. Detectable mobility at this stage indicates that fibrous
connective tissue has encapsulated the implant.
vi. If mobility is detected, the implant should be removed at that time.
The failed site is allowed to heal and another implant can be placed at a
later time. Once a successful osseointegration bone-to-implant interface
has been achieved, masticatory function at least equal to that of natural
dentition is generally possible.
Implant surface treatment
Concerning the surface of the implants
1. Sand-blasted implant surface is particularly effective in a good quality,

dense bone (D1–D2), where a high congruence between the implant
and the bone bed is guaranteed.
2. Hydroxyapatite plasma-sprayed implants are supplied in the shape of
screw or cylindrical implants. The apatite bioactive coating helps attach
the implant in the bone bed, ensuring high primary stability of
implants, also in bones of lower quality (D3–D4) and increasing the
tolerance to the congruence achieved during a surgical operation. It is
recommended for use in bones of low density, cancellous bone or an
augmentation, even though the bed may not be quite congruent. The
cylindrical shape of some implants enables easy insertion and a high
primary stability, also in distal parts which are difficult to access.
Implants with chemically treated surface are the first implants combining
the advantages of a self-drilling implant shape with a bioactive surface. This
helps to reduce the healing period and a high primary stability of the implant
is ensured. A bioactive surface enabling a direct bond with the bone tissue
ensures the balanced distribution of mechanical strain on the bone bed.
Classification of implants
Implants have been classified based on the following criteria:
I. Based on the implant-tissue interface
a. Direct bone-implant interface, e.g. endosseous implants

(osseointegration)
b. Indirect interface, e.g. blade and subperiosteal implants
Note: Formerly, attempts were made to reproduce the biological tooth

attachment, but such fibrous attachment has given way for the concept of
osseointegration.
II. Based on design and location
a. Submucous
b. Supraperiosteal
c. Subperiosteal
d. Endosseous
e. Transosseous
f. Endodontic
III. Based on function
a. Retentive implants
b. Supportive implants
Retentive type has the sole purpose of providing additional retention for
the prosthesis, e.g. mucosal inserts and magnetic implants. The entire
functional load is transmitted through the mucous membrane.
Supportive type provides support to the prosthesis. At the same time,
mucous membrane and teeth are relieved from any functional load. They may
be intraosseous or extraosseous (subperiosteal).
IV. Based on implant materials
a. Metallic implants
b. Polymer implants
c. Ceramic implants
d. Vitreous carbon implants
V. Based on implant design
a. Branemark implant—Threaded screw

b. Core-vent implant—Open basket with vents combined with threads
c. IMZ implant—Rough plasma sprayed implant surface
d. Stryker implant—Fluted design
VI. Based on loading protocol
a. Conventional loading/delayed loading/2 stage loading

b. One stage protocol:
- Immediate loading
- Early loading
Classification of the bone

I. Lekholm and Zarb classification
Lekholm and Zarb classified the jaws according to the bone quality and
quantity (Fig. 21.5). The jaw bone shape is classified on a five-degree scale (A–
E) and the jaw bone quality on a four-degree scale (1–4).
A. Bone shape
A. Most of the alveolar ridge present
B. Moderate residual ridge resorption
C. Some basal bone resorption has taken place
D. Initial resorption of the basal bone
E. Extreme resorption of the basal bone
B. Bone quality
1. Indicates almost homogeneous compact bone
2. A thick layer of cortical bone surrounds a cord of dense
trabecular bone
3. A thin layer of cortical bone surrounds a cord of dense
trabecular bone
4. A thin layer of cortical bone surrounds a cord of trabecular
bone of low density
FIGURE 21.5 Lekholm and Zarb classification.
The jaw shape is determined prior to surgery at the clinical and radiological
examination
II. Cawood and Howell classification (Fig. 21.6)
A. Classification of anterior mandible (anterior to mental foramen)

B. Classification of posterior mandible (posterior to mental foramen)
C. Classification of anterior maxilla
D. Classification of posterior maxilla
FIGURE 21.6 Cawood and Howell classification. (A) Anterior
mandible. (B) Posterior mandible. (C) Anterior maxilla. (D)
Posterior maxilla.
The different types indicate:

I. Dentate
II. Immediate postextraction
III. Convex ridge form
IV. Knife edge ridge form
V. Flat ridge form
VI. Loss of basal bone that may be extensive but follows no predictable
pattern
III. Misch classification
D1—Dense cortical bone

D2—Dense thick cortex and coarse trabeculae
D3—Porous thin cortex and fine trabeculae
D4—Fine trabeculae
Endosteal implants
A two-stage threaded titanium root form implant was first represented in
North America by Branemark in 1978. Endosteal implants are placed directly
into the jaw bone. The bone area must be sufficient to support the implant in
height, width and length.
Endosteal implants can be of root form or blade form. The type of implant
selected is based on the amount of bone, quality of the bone and patient’s
expectations of how the final restoration will look, feel and function.
Subsequent to Branemark, many other root forms have been introduced.
Some are traditional screws (ITI—plasma sprayed), others have platforms
rather than threads (Stryker). The IMZ implant is a press-fit stress broken
titanium plasma. It is surgically placed within alveolar and basal bone; it is
further subdivided into root form and blade form implants.
The minimal vertical dimension of bone for endosteal implant placement is
8 mm. It is important to leave at least 2 mm of bone between the apical end of
the implant and the inferior alveolar canal. Bone width is also an important
consideration for successful osseointegration.
Implants should have a minimum of 1 mm of bone on the buccal and lingual
aspects of the dental implant. Therefore, for a 4 mm diameter implant, 6 mm of
available bone width is necessary.
Root form implants
• Root form implants mimic the basic shape of the natural root.
• Available in variety of lengths, widths and designs including cylinders
(also known as press-fit) and screws (also referred to as threaded) or a
combination of the two.
• May be used in any area of the mouth.
• May replace one or more teeth.
• Root forms are further divided based on design into:
a. Cylinder root form implants (press-fit type)—depend on a
coating to provide microscopic retention and/or bonding to
the bone and are usually pushed or trapped into a prepared
bone site.
b. Screw root forms (threaded type)—threaded into a bone
site and have macroscopic retentive elements for initial
bone fixation.
The choice of whether to use a threaded implant or a press-fit is dependent

on the quality of the bone that will support the implant and what will be
placed upon the implant when it is healed.
Classification of root form endosteal implants (Fig. 21.7)

The 1988 National Institutes of Health consensus statement on dental implants
and the American Academy of Implant Dentistry recognise the term ‘root
form’.
FIGURE 21.7 Types of root form implants. (A) Titanium screw. (B)
HA (Hydroxyapatite) screw. (C) HA cylinder. (D) Titanium plasma
spray cylinder. (E) Combined form.
Combination root forms have macroscopic features of both the cylinder and
screw root forms. The screw or combination root form designs may also
benefit from microscopic retention to bone by the additional of coatings. Root
forms have also been described by their means of insertion, healing, surgical
requirements, surface characteristics and interface.
I. Their macroscopic body design can be:

II. Their surface can be:
III. They are available as:
IV. Three basic screw-threaded geometrics exist:
Cylinder-type implant
Most cylinder implants are essentially smooth-sided and bullet-shaped
implants and require a bioactive or increased surface area coating for retention
in the bone. If these same materials were placed on a threaded design, the
surface area of the bone contact would be more than 30% higher compared
with the smooth cylinder design (Table 21.1).
Table 21.1
Comparative features of screw type and cylindrical type implants

Screw type (threaded) Cylinder-type (press-fit)
Turned into the site within the bone following A press-fit implant has smooth walls and is
preparation of the site tapped into the site
30%–500% greater surface area than the Less surface area; lesser contact area
cylindrical type; greater bone contact
Requires greater force for placement A cylinder-type implant may be pressed into the
bone by hand in all bone types
Screw-type implant
• A solid screw implant body design with a blunt apex offers significant
advantages to the practitioners with limited experience or limited
availability of different implant systems.
• The most common thread outer diameter is 3.75 mm, a 0.4 mm depth
of thread, with a crest module approximately 2 mm in height and
crestal diameter of 4.1 mm. Various lengths range from 7 to 20 mm;
lengths from 10 to 16 mm are the most widely used.
• A solid screw permits the preparation and placement of the implant in
dense cortical bone as well as in fine trabecular bone. The surgery may
be easily modified to accommodate both extremes of bone density.
• The solid screw permits the implant to be removed at the time of
surgery if placement is not ideal.
• A solid implant may perforate the inferior border of the mandible,
nares or maxillary sinus without inherent complication if the apex is
smooth or blunted.
• The solids crew may be plasma spray-coated with titanium or
hydroxyapatite to marginally increase the functional surface area,
microlock the bone and/or take advantage of biochemical properties
related to the surface coating (e.g. bone bonding or bone growth
factors).
• The functional surface area of threaded implant is greater than a
cylinder implant by a minimum of 30% and may exceed 500%,
depending on the thread geometry. This increase in functional implant
surface area decreases the stress imposed on the bone-implant
interface and is also dependent on thread geometry.
Blade form implants

Blades are wedge-shaped or rectangular in cross-section. They are generally
2.5 mm in width, 8–15 mm in depth and 15–30 mm in length. These implants
are flat rectangles of metal with one or two metal prongs on one side. A blade
implant is placed in the jaw so that the prongs stick out into the mouth where
they will support crown or bridges.
One-stage and two-stage implant surgeries

Endosteal implants can be used singly or in multiples.
They are also categorised as: (1) one-stage and (2) two-stage. One-stage
endosteal implants are placed into the bone and project immediately through
the mucosa into the oral cavity. Two-stage implants are first placed into the
bone to the level of the cortical plate. The oral mucosa is then sutured over the
implant and left for a prescribed healing period. The healing period is
dependent upon the quality of the bone but usually lasts at least 3 months and
can be up to 6–9 months. At a second surgery, the mucosa is reflected from the
superior surface of the implant and an extension collar or abutment is placed
on the implant, which projects into the oral cavity.
Assessment of bone for implant placement

Characteristic bone volume changes after tooth loss were evaluated in the
mandible by Atwood. Atwood’s description for the mandible was presented
by Fallschussel in 1986. These six categories range from fully resorbed to
moderately wide and high, narrow and high, short and high, wide and
reduced in height and severely atrophic.
• As a general guideline 1.5 mm of surgical error is maintained between

the implant and any adjacent landmark. This is especially critical when
opposing landmark is the mandibular nerve.
• However, experience has demonstrated implant may proceed without
complication through the cortical plate of the maxillary sinus or
inferior border of the mandible or next to the cribriform plate of a
natural tooth.
• Yet, if the implant should become mobile or affected by peri-implant
disease, the adjacent landmark may be adversely involved.
• Similarly, if the sinus becomes infected or the adjacent tooth suffers
from periodontal disease, the implant may be affected.
Bony criteria for implant placement
• Bone height
• Bone width
• Bone length
• Bone angulation
• Crown/Implant ratio
Bone height
The height of available bone is measured from the crest of the edentulous
ridge to the opposing landmark, such as maxillary sinus or mandibular canal
in the posterior regions. Anterior regions are limited by maxillary nares or
inferior border of the mandible. Maxillary canine eminence region offers
greater height of available bone than the maxillary anterior or posterior
regions.
FIGURE 21.8 Position of implant in relation to inferior alveolar

nerve (minimum of 2 mm height between apex of the implant and
the inferior alveolar canal).
A panoramic radiograph is still the most common method used for this
purpose. The minimum bone height for predictable long-term endosteal
implant survival approaches 10 mm. Failure rates reported in the literature are
consistently higher for shorter implants, independently from the manufacturer
design, surface characteristic and type of application. There should be a
minimum of 2 mm height between apex of the implant and the inferior
alveolar canal (Fig. 21.8). In maxilla, excessive pneumatisation of the maxillary
antrum and atrophy of the maxillary ridge, floor of the sinus almost comes to
lie very close to the maxillary alveolar crest. Maxillary sinus lift procedure is
carried out to lift the floor of the sinus lining by placing a graft in between the
maxillary sinus lining and the floor of the maxillary antrum in the posterior
aspect (Fig. 21.9 A–D).
FIGURE 21.9 Sinus lift procedure. (A, B) Intraoral view showing

infracturing of the bony window and lifting of the left maxillary
sinus. (C) Preoperative OPG showing reduced bone height in
relation to 26, 27 and 28. (D) Postoperative OPG showing
adequate bone fill favourable for implant placement. ( Scan to
play Direct Sinus Augmentation technique)
Bone width
The width of available bone is measured between the facial and lingual plates
at the crest of the potential implant site. Crest of the edentulous ridge is
supported by a wider base. Once adequate height is available for implants,
primary criterion affecting long-term survival of endosteal implants is the
width of available bone. Root form implants of 4.0 mm crestal diameter
usually require more than 5.0 mm of bone width to ensure sufficient bone
thickness and blood supply around the implant for predictable survival. These
dimensions provide more than 0.5 mm bone on each side of the implant at the
crest. Because bone usually widens apically, this minimum dimension rapidly
increases. In case of bony defects local regional bone graft, bone shavings near
the implant area and corticocancellous graft can be used (Figs. 21.10–21.13).
FIGURE 21.10 (A–E) Bone shavings for small bony defects in

relation to the implant.
FIGURE 21.11 (A) Odontome in the anterior maxillary region in
relation to 21. (B, C) Exposure and removal of the odontome.
(D) Bony defect in the excised area. (E) Excised mass. (F) Bone
graft taken from external oblique ridge region.(G–I) Filling of the
bony defect using the graft. (J) Graft retained using screw. (K, L)
Bone fill in the defect area after a period of 3 months. (M, N)
Implant fixation in the grafted area. (O) Preoperative OPG showing
odontome in the 21 region. (P) Postoperative OPG showing
odontome removed and graft retained with screw. (Q) Implant in
relation to 21.
FIGURE 21.12 (A) Implant placement in 13 region. (B) Buccal wall
defect in relation to implant. (C) Cortical graft from the right
zygomaticomaxillary buttress region using rongeur (locoregional
site of harvesting). (D) Cortical graft obtained from the
zygomaticomaxillary buttress region. (E–I) Use of bone mill for the
ease of adaption of the graft in the defect area. (J) Cortical bone fill
of the defect. (K) Abutment placement after 3 months. (L) Dental
rehabilitation.
FIGURE 21.13 (A–J) Simultaneous implant placement and ridge
augmentation using mandibular symphysis bone graft. (K)
Preoperative radiograph. (L) Postoperative radiograph.
Bone length
Mesiodistal length of available bone in an edentulous area is often limited by
adjacent teeth or implants. The length of available bone necessary for
endosteal implant survival depends on the width of bone. For bone of more
than 5 mm width, a minimum mesiodistal length of 7 mm is usually sufficient
for each implant. A width of bone less than 5 mm requires a 3.2 mm implant
with compromise such as less surface area and greater crestal concentration of
stress. In the narrower ridge, it is often indicated to place two or more
implants of smaller diameter when possible.
Bone angulation
Bone angulation is the fourth determinant for available bone. Ideally, it is
aligned with the forces of occlusion and is parallel to the long axis of the
prosthodontic restoration. The incisal and occlusal surfaces of the teeth follow
curve of Wilson and curve of Spee. This results in roots of the maxillary teeth
being angled towards a common point approximately 4 inches away. The first
premolar cusp tip is usually vertical to its root apex. The mandibular roots
flare, so the anatomic crowns are more lingually inclined in the posterior
regions and labially inclined in the anterior area, compared to the underlying
roots.
Patient evaluation
Prior to the placement of implants the patient should be assessed: (1) medical
and dental history, (2) clinical examination and (3) radiographic examination.
A thorough medical and dental history is taken to rule out any systemic or
dentofacial disease which is contraindicated for implant placement. Periapical
and panoramic radiographs provide adequate information with reference to
the volume and quality of bone and the location of anatomical limiting factors.
Abnormal jaws relation, atrophic ridge, inadequate and shallow vestibule,
abnormal tongue position are some of the structural diseases of the oral cavity
which interfere with denture retention. Emotionally intolerant, perfection
seeking patients may not be willing to wear the dentures. All these factors
Radiographic evaluation
Periapical radiograph
Advantages
• It helps to identify the interradicular space, prognosis of adjacent teeth,

location of critical structures
• Useful in case of single tooth implant
Disadvantage
• Limited value in determining bone quantity and density
Cephalometric evaluation
• To identify anterior alveolus and the relationship of lingual plate to the

patient’s skeletal anatomy
• To access the loss of vertical dimension, interarch relation and crown
to implant relation
OPG
• To identify vertical bone height and general dental status

• Gross anatomy and rule out pathology of jaw
• To monitor prosthetic outcome
CT
• To analyse bone height, width, density and distance from vital

structures
• To also guide the position and orientation of implants
• Acrylic template with barium sulphate film helps to precisely identify
position and orientation of proposed implant
CBCT (Fig. 21.14)
• To trace mandibular canal, maxillary sinus

• To analyse bone quality and measurements of available bone
FIGURE 21.14 (A, B) CBCT images showing the measurement of
bone height and width for implant placement.
Advantage
• Mainly reduced radiation exposure with sectional images can be

obtained
• Reduced cost when compared to CT
• Accurate determination of number and size of implant
Patient selection
1. The clinician should ensure that the provision of implants will provide
better prosthodontic service.
2. General health condition and dental status should be evaluated.
3. Availability of sufficient bone should be verified to accommodate the
implant. Ridge should be at least 5 mm in width to accommodate any
type of implant with a marginal safety of 1 mm on either side; 10 mm
in vertical height (in maxilla from alveolar crest to the sinus floor and,
in mandible, from the alveolar crest to the mandibular canal).
4. In mandibular region, bony contour below the mylohyoid line must be
evaluated. If extensive undercuts are present, the implant might
perforate the lingual cortex.
5. Study models are necessary to evaluate the occlusion and determine the
correct positioning of implants.
6. Radiographic evaluation should be done to aid in the diagnosis.
Implant treatment protocol

Components of implant
A generic language for endosteal implants has been developed by Misch and
Misch (Figs. 21.15, 21.16). Endosteal implants presented in this text have
segmented portions placed in different phases.
FIGURE 21.15 Implant design.
FIGURE 21.16 (A, B) Implant kit with drills of various sizes. (C)
Implant driver. (D) Torque wrench with implant driver. (E)
Handpiece. (F) Handpiece with external and internal irrigators.
Implant body regions

The components of the implant body may be separated into:
• Crest module
• Body
• Apex
Crest module
Crest module of an implant is that portion designed to retain the prosthetic
component in a two-piece system. It also represents the transition zone from
the implant body design to the transosteal region of the implant at the crest of
the ridge. It may also be designed to exit the soft tissue in some implant
systems. The abutment connection area often has a platform on which the
abutment is set, the platform offers physical resistance to axial occlusal loads.
The crest module is often smoother to impair plaque retention if crestal bone
loss occurs.
Body of the implant

Body of the root form implant is either screw type or cylindrical. There are
many other variations which would be discussed later.
Other components of a dental implant system
• Cover screw
• Transepithelial portion (permucosal extension, healing abutment)
• Abutment
• Superstructure
• Transfer coping
• Prosthetic coping
• Analogue
Cover screw (Fig. 21.17)

It is placed in the first stage surgery and is used to cover the implant to
prevent bone, soft tissue or debris from invading the abutment connection
area during healing.
FIGURE 21.17 (A) Cover screws. (B) Healing abutments.
Healing abutment
It is attached to the implant in the second stage surgery after removing the
cover screw. This portion extends from the implant above the soft tissues and
results in the development of a perimucosal seal around the implant.
Abutment (Fig. 21.18)

The abutment is the portion of the implant that supports and/or retains a
prosthesis or implant superstructure. Three main categories of implant
abutment are described according to the method by which the prosthesis or
superstructure is retained to the abutment: (1) an abutment for screw retention
uses a screw to retain the prosthesis or superstructure, (2) an abutment for
cement retention uses dental cement to retain the prosthesis or superstructure
and (3) an abutment for attachment uses an attachment device to retain a
removable prosthesis.
FIGURE 21.18 Implant abutments.
Many manufacturers classify the prosthesis as fixed whenever cement

retains the prosthesis, fixed/removable when screws retain a fixed prosthesis,
and removable when the restoration is removed by the patient. An abutment
for screw retention uses a hygienic cover screw placed over the abutment to
prevent debris and calculus from invading the internally threaded portion of
the abutment during prosthesis fabrication between prosthetic appointments.
Superstructure (Fig. 21.19)

A superstructure is defined as a metal framework that fits the implant
abutment and either provides retaining of an overdenture with attachments or
provides the framework for a fixed prosthesis.
FIGURE 21.19 Implant suprastructure.
Transfer coping (Fig. 21.20)

An impression is necessary to transfer the position and design of the implant
or abutment to a master cast for prosthesis fabrication. A transfer coping is
used in traditional prosthetics to position a die in an impression. A transfer
coping is used to position an analogue in an impression material requiring
elastic properties.
FIGURE 21.20 Transfer copings.
Indirect transfer coping is screwed into the abutment or implant. The

indirect transfer coping remains in place when the set impression is removed
from the mouth. Indirect transfer coping is parallel-sided or slightly tapered to
allow ease in removal of the impression and often has flat sides or smooth
undercuts to facilitate reorientation in the impression after it is removed. A
direct transfer coping usually consists of a hollow transfer component and
often a square and long central screw to secure it to the abutment or implant
body. After the impression material is set, direct transfer coping takes
advantages of impression materials having rigid properties and eliminates the
error of permanent deformation because it remains within the impression until
the master model is poured and separated.
Prosthetic coping
A prosthetic coping is a thin covering, usually designed to fit the implant
abutment for screw retention and serve as connection between the abutment
and the prosthesis for superstructure. A prefabricated coping usually is a
metal component machined precisely to fit the abutment. A castable coping
usually is a plastic pattern cast in the same prosthesis or supra-structure,
secured to the implant body or abutment with a prosthetic screw.
Analogue (Fig. 21.21)

An analogue is fabrication of the master cast to replicate the retentive portion
of the implant body or abutment. After the master impression is obtained, the
corresponding analogue is attached to the transfer coping and assembly is
poured in stone to fabricate the master cast.
FIGURE 21.21 Implant analogue.
Implant stent
Surgical template is defined as a guide used to assist in proper surgical
placement and angulations of dental implants. The main objective of the
surgical template is to direct the implant drilling system into the bone and
provide accurate placement of the implant according to the surgical treatment
plan (Fig. 21.22).
FIGURE 21.22 Implant stent.
Computer-aided design/computer-
assisted manufacturing (Cad/CAM)-based surgical
guide
Computer-aided design/computer-assisted manufacturing (CAD/CAM)
technology uses data from CT scan to plan implant rehabilitation. CT images
are converted into data that are recognised by a CT imaging and planning
software. This software then transfers this presurgical plan to the surgery site
using stereo-lithographic drill guides. The surgical templates fabricated by this
technology are preprogrammed with individual depth, angulations,
mesiodistal and labiolingual positioning of the implant.
Advantages
1. Precise placement of implants

2. Conservation of anatomic structures
3. Three-dimensional technology allows precise evaluation of anatomic
points such as the size of the maxillary sinus in the upper jaw and
location of the alveolar nerve in the lower jaw
4. Precise analysis of osseous topography
5. Provides information about size, direction, and bone location for
accurate positioning of implants
6. High observed accuracy of 0.1 mm
7. Reduced surgical exposure time
8. Less invasive, flapless surgery, and, therefore, less chance of swelling
9. Less postoperative strain on dentist and patient
10. Transparency of material which allows seeing through the model
11. To summarise stereolithography fabrication process
12. A CT scan procedure is performed with a radiographic template
fabricated using radio-opaque marker in place
Disadvantages
1. Lack of visibility and tactile control during the surgical procedure

2. Insufficient mouth opening jeopardises surgical procedure
3. A risk of damage to vital anatomical structures
Surgical procedure
Anaesthesia
Most endosseous implant operations can be performed using local anaesthesia
with or without conscious sedation. A careful review of the patient’s medical
history may reveal medical problems that limit the amount of local anaesthesia
or epinephrine that can be administered or that the patient’s condition must be
monitored by a clinician trained in anaesthesia, such as an anaesthesiologist or
an oral and maxillofacial surgeon.
Routine inferior alveolar nerve blocks and maxillary infiltration anaesthesia
provide satisfactory local anaesthesia for the implant patient. Local
anaesthesia infiltrated directly into the planned incision line reduces bleeding
and simultaneously performs a hydropic dissection. This eases the
subperiosteal dissection during development of a full thickness muco-
periosteal flap.
The specific local anaesthetic is chosen by operator preference. Lidocaine 1%
or 2% (Xylocaine) with 1:100,000 or 1:20,000 epinephrine or a similar
anaesthetic is most commonly used. Longer-acting anaesthetics can also be
used if the clinician and patient desire anaesthesia time for 6–8 h.
Intravenous conscious sedation is useful for the anxious patient or for the
patient who is undergoing a lengthy procedure. One disadvantage with
sedation is the lack of the patient’s ability to close the mouth gently during the
procedure. Often, when placing implants, the surgeons ask the patient to close
the mouth gently to confirm the implant angulation using paralleling pins.
This shows the expected retaining screw emergence.
Conscious sedation may be replaced by general anaesthesia in patients with
extreme dental phobia, requiring bone graft harvesting from multiple intra-
oral or extraoral sites.
Principles of flap design
1. Clear incision to avoid the need for retracting and elevation is done
using periosteal elevator
2. Clear visibility of the operating site using long incision
3. Removal of minimal amount of periosteum to retain the maximum
vascular supply
4. Papilla should be elevated in total instead of bisecting
5. Tension relieving incision is placed obliquely to avoid stretching or
tearing
6. Allow for proper identification of important anatomical landmarks
7. Identification of the contours of the adjacent teeth, as well as the
concavities or protrusions on the surface of the bone, is essential and
will facilitate implant placement
8. All wounds should have clean edges, which will facilitate closure and
optimise healing by primary intention
9. Permitting the raising of a full mucoperiosteal flap ensures that it has a
good vascular supply
10. Flap blood perfusion must be maintained up to the point at which the
ratio of length to the width of the parallel pedicle flap equals 2:1
11. The tissue flap must be kept moist at all times to help avoid shrinkage
and dehydration of the tissue
12. It is imperative to provide for closure away from the submerged fixture
installation or augmentation site
13. Minimal tension during reapproximation and after suturing is
important to avoid impairment of the circulation at the wound
margins
14. Tissue trauma, such as stretching, tearing, or distortion, should be
avoided through appropriate and careful reflection and manipulation
of tissue flap
15. Avoid oblique relieving incisions over prominent root surfaces because
recession may result if there is an underlying bony dehiscence
16. In cases of reduced quantity of keratinised tissue, it is beneficial to
position the crestal incision toward the palatal aspect, the area where
more keratinised tissue as it extends onto the palatal mucosa
17. Avoid any local or external pressure on the wound during the healing
period
Incision design—anterior mandible

The two most popular incisions for placement of implants into the anterior
mandible are: (1) crestal and (2) vestibular.
Crestal incision
The crestal incision is useful when mandible has sufficient height, the mentalis
and lip musculature insert below the alveolar crest. For the patient with an
adequate (at least 4 mm) band of attached gingiva, the incision provides
excellent access to both the labial and lingual regions for visualisation during
implant placement. A full thickness mucoperiosteal flap is raised. The
reflection should be sufficient to visualise the area of operation.
Vestibular incision
• For a patient without an adequate band of attached gingival tissue or

for a patient whose mentalis muscle inserts close to the crest, a
vestibular incision is recommended.
• High muscle attachment with the mobile tissue against the labial
portion of the implant’s abutment requires simultaneous
vestibuloplasty or presurgical soft tissue grafting.
• The incision is made in the lip mucosa and a lingual based, mucosa-
only flap is developed superficial to the mentalis musculature. Once
the crest of the mandible is reached, a periosteal incision is made and
the periosteum is reflected labially, exposing the labial cortical bone.
• The implant sites are prepared following manufacturer’s
recommendations.
• After implant placement, the mucosa flap is sutured to the depth of the
vestibule with the periosteum reflected labially, ‘switching’ their
positions. This lip-switch procedure provides nonmobile tissue labial
to the implant.
• The partially denuded lip tissue is allowed to heal secondarily. In
atrophic mandible (less than 10 mm in vertical height), one must be
careful to avoid stripping the mentalis muscle from the symphysis. In
general, 10 mm of mentalis muscle should be left attached to the
mandible to avoid chin laxity, otherwise known as a witch’s chin.
Phase I (Fig. 21.23A–G)
• Local anaesthesia is administered.

• An incision is made, slightly buccal on the mandible or palatal to the
maxillary crest.
• A full thickness flap is raised with a periosteal elevator.
• After adequate exposure and retraction, remove any irregularity with a
rongeur or round bur.
• Transfer the prepared surgical template to mouth for implant placement
direction.
• Preparation should involve sterile water irrigation when drilling the bone.
• High-speed motor should not exceed 1000 rpm and low-speed motor
should not exceed 40–50 rpm.
• The osteotomy site is enlarged at the alveolar crest with a guide drill then
the osteotomy site is then gradually enlarged with sequence drills.
• If multiple implants are being placed, special parallel pins should be
inserted into the implant sites to aid in placement and to maintain
parallelism.
• If the implant is to be placed in dense mandibular bone, osteotomy site is
tapped or prethreaded with a thread former but at low-speed to create
threads in the walls of the osteotomy site.
• Avoid any contamination of the implant before its insertion into the
prepared site.
• The carrier is removed and the implant is seated in its final position.
• The operative site is then thoroughly irrigated and all sharp bony edges
smoothened.
FIGURE 21.23 Two-stage surgical procedure for implant
placement: (A–G stage I) (H–O stage II). (A) Incision made. (B)
After contouring the bone osteotomy is carried out with the help of
a template. (C) Osteotomy completed. (D) Implants placed with the
help of fixture mounts. (E) Fixture mounts removed after placing
implants. (F) Placement of the cover screws. (G) Closure. (H) After
a period of 3–4 months, the cover screw is exposed and removed.
(I) After healing transfer coping is fixed. (J) Impression made and
implant analogue fixed. (K) Cast poured. (L) Abutment fixed. (M)
Abutment manipulated for the construction of suprastructure. (N)
Abutment transferred into the oral cavity and final contouring. (O)
Luting of the FPD to the implant abutment.
Flap versus flapless design (Fig. 21.24)

Traditionally, access for implant placement has been by a flap approach.
Studies have demonstrated that flap reflection often results in bone resorption
around the natural teeth. Postsurgical tissue loss from flap reflection has also
been reported.
FIGURE 21.24 (A) Punch approach. (B) Half punch approach. (C)
Mid crestal. (D) Palatal/lingual crestal. (E) Mesial papilla
preservation. (F) Distal papilla preservation. (G) Double papilla
preservation.
Implant placement
Implant surgery should be performed in a sterile environment to avoid
contaminating the implant fixture as contamination of the implant surface can
result in a lack of osseointegration. Once the implant is firmly placed and
seated, cover screws are then placed into the implant body. The surgical site is
irrigated, the mucosal flap sutured and closed with 3–0 black silk. Sutures are
removed after 7–10 days. Following implant surgery, the patients are given
antibiotics and analgesics. (Figs. 21.25, 21.26)
FIGURE 21.25 (A–J) Sequential steps showing rehabilitation of
edentulous space with implants.
FIGURE 21.26 (A–L) Sequential steps showing removal of 12–22
and replacement with implant.
Phase II (Fig. 21.23H–O)

After 3 or 4 months, the abutment analogue is now attached into the transfer
coping and cast poured. A superstructure or the prosthetic restoration is
constructed on the implant or abutment and delivered to the patient. Fixation
of the prosthesis to abutment may be either by screw or luting.
Implants for completely edentulous patients

Types of implants for edentulous patients:
• Ball and socket removable overdenture
• Bar-retained removable overdenture
• Screw-retained fixed bridge
• Cement-retained fixed bridge
Types
a. Ball and socket removable overdenture (Fig. 21.27)
• May require 2–4 implants depending on the amount and quality of

bone present.
• This may be the simplest way to replace an ill-fitting denture.
• This type of overdenture is better suited for the lower jaw instead of
the upper jaw.
• The implants have ‘ball-type’ inserts screwed or cemented into the
denture. These inserts will then fit into ‘O-ring’ type of recipient sites
in the underside of the denture.
FIGURE 21.27 Ball and socket type for edentulous ridge.
b. Bar-retained removable overdenture (Fig. 21.28)
• May require 2–6 implants depending on the amount and quality of

bone, as well as for which jaw (upper or lower) the overdenture is
being planned.
• The bar-retained overdenture is frequently used in the upper jaw if the
patient has had a severe gagging problem with a conventional full
upper denture.
• When patients have had severe bone resorption from previously
wearing a lower denture, a new denture or a ball and socket supported
implant overdenture which rests on the gums may compress the
underlying mental nerve which lies in close approximation with this
severely resorbed residual alveolar ridge. Bar-retained overdenture is
recommended in resorbed ridge where the mental foramen lies at the
level of alveolar crest.
FIGURE 21.28 (A, B) Bar type edentulous implant.
c. Cement-retained fixed bridge (Fig. 21.29)
• Usually 4–10 implants may be needed. Four implants would not be

adequate in most situations. Ten implants or in some cases even more
may be used when amount of bone only allows for very short
implants.
• It is more aesthetic since individual crowns are placed over the
implants.
FIGURE 21.29 (A–C) Prosthesis retained by luting cement. (D–F)

Screw-retained prosthesis.
The patient’s ability to clean around the crowns and implants is important
when considering implant retained full mouth prosthesis.
d. Screw-retained fixed bridge (Fig. 21.29)
• May need 4–6 implants depending on the amount and quality of the
bone present.
• The teeth are built upon a metal base through which screws are
inserted and, in turn, secure the teeth into the implants.
• The metal base does not come into contact with the gums and sits, like
a ‘platform’ above the gums. This ‘high water line’ may be
inconvenient for some cases, especially for upper teeth replacements.
All-on-four concept (Figs. 21.30, 21.31)

All-on-four technique enables a full arch of teeth to be replaced with just four
dental implants. This technique eliminates the traditional need of 6–8 implants
for conventional full arch implant treatment. All-on-four implants are actually
similar to the normal screw-like implants but the implants are positioned at a
specific angle in the jaw bone. The two central implants are placed at the
conventional angle of 90 degree to the alveolar ridge, while the two lateral
implants posteriorly are placed at a 45 degree angle. All implants are placed
anterior to mental foramen. This means that more bone is utilised in the
stabilisation and support of the implant allowing for a whole set of teeth to be
replaced rather than fewer teeth.
FIGURE 21.30 Surgical guide for proper implant placement.

FIGURE 21.31 (A, B) Implant placement based on all-on-four
concept with fixed denture.
Advantages
• Only four implants are required instead of 6–10

• The need for expensive bone grafting and sinus lift in most cases can
be avoided
• Cheaper than traditional full arch fixed bridge techniques
• Aids the prevention of further bone loss in the jaw
• Requires minimal recovery time
Loading concept
• Early occlusal loading refers to functional loading between 2 weeks
and 3 months of implant placement.
• Nonfunctional immediate restoration refers to implant prostheses
placed within 2 weeks of implant placement with no direct functional
occlusal loading.
• Nonfunctional early restoration refers to implant prostheses delivered
between 2 weeks and 3 months from implant placement.
• Delayed occlusal loading refers to the restoration of an implant more
than 3 months after placement.
Immediate loading can be described as a technique in which the implant

supported restoration is placed into functional occlusal loading within 48 h of
implant insertion.
Criteria for immediate loading
1. Surgery-related factors (single most important variable for success of

immediately loaded implants)
2. Host-related factors
3. Implant-related factors
4. Occlusion-related factors
Surgical factors
• Torque
• Implant placement technique
Torque during implant placement is a good predictor of implant stability.

Studies have reported that implants placed with an insertion torque greater
than 30–35 N cm resulted in higher success rates for immediate loading.
Proper implant placement technique includes copious irrigation both
internally and externally to maintain temperatures less than 47°C for
prevention of necrosis of the surrounding bone.
Host factors
• Tobacco use
• Oral hygiene
• Medications
• Systemic diseases such as human immunodeficiency virus
(HIV)/acquired immunodeficiency syndrome (AIDS)
• Diabetes mellitus
• Osteoporosis
• Teeth associated with a history of trauma, infection or periodontal
disease with active inflammatory response may not be candidates for
immediate implant placement or immediate loading.
Implant-related factors
• Screw design type

• Implant length and diameter
• Surface texture-roughened implant surface shows improved success
rates
Occlusal factors
• Maximal interocclusal contacts without lateral contacts is

recommended.
• Parafunctional habits or compromised occlusion should not receive
immediate loading options.
Implant failure
Implant failure can have a multifactorial aetiology.
Early failure
• Heating of the bone during osteotomy preparation

• Osteotomy inappropriate for the implant site
• Implant contamination during surgery
• Poor bone quality
• Lack of primary stability
• Macromotion caused by overload or parafunction
Late failure
• Peri-implantitis
• Poor oral hygiene
• Poor implant design
• Occlusal trauma
• Implant fracture
• Implant overload
Even when implants are nonmobile, indications for their removal may exist,
such as fracture, malposition, infection, pain and advanced peri-implantitis.
In cases of advanced peri-implantitis or implant fracture, removal of the
affected implant is usually necessary.
Removal of mobile implant

This occurs due to complete loss of bone-to-implant contact. A mobile implant
may easily be removed by rotating it counter-clockwise using a driver,
counter-torque ratchet or forceps. Rotating with minimum luxation allows
reduced trauma and damage to the surrounding bone and soft tissue.
Removal of fractured implant

These may be partially or fully osseointegrated (Fig. 21.32).
FIGURE 21.32 (A–F) Sequential steps showing removal of

fractured implant abutment.
Techniques of implant removal
• Counter-torque ratchets
• Piezo tips
• High-speed burs
• Elevators
• Forceps
• Trephine burs
Counter-torque ratchet technique (CTRT)

This is the least invasive technique for removing an implant without
damaging surrounding structures.
This should be used if the implant is able to be engaged and reverse-torqued
until mobile. Care must be taken with narrow-diameter implants that are less
than 4 mm in dense cortical bone to avoid implant fracture.
Piezo tips
Piezo tips allow for better intraoperative control than high-speed burs during
bone-cutting because they prevent damage to the surrounding soft tissue.
It is less efficient for deep cuts into bone and when the cutting speed is
decreased the tip’s temperature rises.
High-speed burs
The use of high-speed burs under copious irrigation is an efficient method to
remove a failed implant.
Air from the high-speed handpiece can be forced into a surgical wound or a
laceration in the mouth causing an air embolism.
When using high-speed burs, the residual apical part of the implant should
be carefully approached in order to prevent damage to anatomical structures
such as the sinus floor, inferior alveolar nerve and mental foramen.
Trephine burs (Fig. 21.33)

The smallest effective size trephine should be selected to avoid collateral
damage to the neighbouring bone, teeth and/or implants. The internal
diameter of the trephine needs to be slightly larger than the implant to avoid
engaging the implant body. This technique is one of the most invasive options
for implant removal.
FIGURE 21.33 (A–J) Sequential steps showing removal of
fractured implant using trephine and forceps, followed by
replacement with another implant.
Osteomyelitis may occur as a complication after using trephine bur,

particularly if bone is overheated. Trephine burs are only indicated when
absolutely necessary and the retrieval procedure should be carefully planned
and performed under copious irrigation with cooled saline.
The coronal half of bone around the implant should be removed to loosen
the implant, at which point elevators, forceps and torque drivers may be used.
Combination technique
If the integrated implant cannot be removed with less invasive methods, the
piezo tips or drill are used to remove sufficient supporting bone around the
coronal parts of the implant. The counter-torque ratchet or forceps are then
employed to remove the implant to reduce damage to the surrounding bone.
If there is no movement, a bur or trephine can be used to cut through the
surrounding cortical bone and into the trabecular bone. The reverse-torque
technique is then attempted again. The goal is to preserve the remaining bone
as much as possible. Alternating between the counter-torque ratchet and the
elevator and occasionally drilling with the bur or trephine can then be used in
combination to remove the implant.
Surgical complication of implant therapy
Implant complication
Intraoperative complications
Wrong angulation:
Implant angulations is yet another determinant for implant success. Proper
angulation should be determined according to the future prosthesis with the
consideration of bucco-lingual, apico-coronal and mesiodistal positions.
Surgical guides and proper treatment planning can alleviate angulation
problems.
Improper implant location
Adjacent teeth should be at least 1.5 mm from the implant body and more
than 3–4 mm between adjacent implants to prevent horizontal bone loss as
well as to preserve aesthetics.
Nerve injury
Sinus or nasal floor perforation
Intraoperative bleeding due to perforation of inferior alveolar vessels in
mandible
Risk sites in the posterior mandible include the sublingual fossa and lingual
cortex. The posterior superior alveolar and infraorbital arteries are located
approximately 19 mm above the maxillary alveolar ridge, and the anastomoses
of these arteries can pose a risk during sinus lift procedures by lateral window
preparation.
Cortical plate perforation

Sinus membrane complications
Postoperative complication
• Postoperative infection
• Peri-implantitis
• Cover screw exposure (healing period)
• Bleeding
• Swelling
• Transient pain or paraesthesia
• Neuralgia
• Fracture
• Implant mobility
• Recession
Anatomy-related complications
Nerve injury:
Possible causes of nerve injury include poor flap design, traumatic flap
reflection, accidental intra-neural injection, traction on the mental nerve in an
elevated flap, penetration of the osteotomy preparation and compression of
the implant body into the canal.
Bleeding:
Potential causes include incision of arteries in soft tissue, osteotomy
preparation and lateral wall sinus lift procedures.
Cortical plate perforation:
When preparing osteotomy sites or placing implants in areas with minimal
labial plate thickness, or if the implant is placed too buccally, a fenestration or
dehiscence implant defect is a common finding. A fenestration leaves intact bone
coronally with the exposed threads at the apical portion of the crest, whereas a
dehiscence defect has the coronal portion of the implant exposed (Fig. 21.34).
FIGURE 21.34 (A) Fenestration. (B) Dehiscence.
Sinus membrane complications:

Sinus complications often occurred when the membrane is perforated at the
time of surgery. Perforations were more common in areas with minimal
amount (<5 mm) of residual alveolar bone.
Devitalisation of adjacent teeth:
Dilacerated roots and excessive tilting in the mesiodistal direction that
invade the implant space often prevent ideal placement. If a drill and/or
implant fixture invades the PDL space, hard tooth structure and/or vital pulp
of the adjacent teeth, this will lead to endodontic lesions.
Procedure related complications

Mechanical complications
Lack of primary stability
Mandibular fracture
Ingestion and aspiration
Peri-implantitis
Peri-implantitis is an implant-related condition which is increasingly being
noticed in the clinical setting, contributing to a significant proportion of
implant failures (Figs. 21.35, 21.36).
FIGURE 21.35 Normal implant—soft tissue anatomy and peri-
implantitis.
FIGURE 21.36 (A,B) Peri-implantitis—loss of attachment to the
surrounding bone.
Implant failure due to peri-implantitis, however, is a multifactorial disease

process most likely attributed to the interaction of certain host factors, e.g.
microbiology, genetic susceptibility and host modifying factors.
A peri-implant disease is a descriptive term used to describe a nonspecific
inflammatory reaction in the host tissues. ‘Peri-implantitis’ should be
distinguished from ‘peri-implant mucositis’ in that the former is defined as,
‘an inflammatory reaction with loss of supporting bone in the tissues
surrounding a functioning implant’, while the latter involves a reversible
inflammation localised to the soft tissues only. Peri-implantitis may display
some or all the following symptoms: bleeding on probing, increased probing
pocket depth, mobility, suppuration and pain.
Bacterial infection is most often described in relation to biofilms (defined as
one or more communities of microorganisms embedded in a glycocalyx of
aqueous solutes attached to a solid surface). The solid, often roughened,
implant surface provides an environment which is susceptible to the tenacious
adherence of a biofilm.
The mucosal attachment at the implant neck has striking similarities with
the dentogingival junction. Such similarities are both morphological and
functional and allow the establishment of the local protective host response
which represents a key factor for long-term success of osseointegrated
implants. Several evidences suggest that bacterial aggression may result in
disturbances of this local equilibrium and lead to apical migration of the
mucosal attachment of the implant.
Causes of peri-implantitis
• Several experimental studies suggest that plaque accumulation can

cause progressive bone loss around implant.
• It has also been stated that overloading the dental implant may result
in loss of marginal bone.
Clinical diagnosis
The well-advanced peri-implantitis lesion may be clearly identifiable via
evidence of radiographic bone loss, mobility and clinical signs of infection. It is
the early lesion that poses the greatest challenge to the clinician and is
undoubtedly of greatest value in order to avoid further bone resorption and
subsequent loss of the implant. Diagnosis of peri-implantitis relies on crude
parameters commonly used for the diagnosis of periodontal diseases.
Typical signs and symptoms of peri-implantitis
• Evidence of vertical destruction of the crestal bone, often ‘saucer-

shaped’
• Formation of a peri-implant pocket (>4 mm)
• Bleeding or suppuration after gentle probing
• Tissue redness and swelling
• Mobility (insensitive in detecting early implant failure)
Contributing factors
• Roughened implant surfaces would provide a greater surface area for

bacterial invasion and that once this surface becomes exposed to the
oral environment, control of infection is difficult.
• Dental plaque and the associated microorganisms.
• Smoking is an established risk factor for chronic periodontitis and
undoubtedly contributes to an increased risk of implant loss.
• The periodontal status of the remaining dentition has recently received
more attention, due to the suggestion that putative periodontal
pathogens originate from the adjacent natural teeth.
• Lack of keratinised gingiva around implants may increase the
susceptibility to plaque-induced peri-implantitis.
Treatment of peri-implantitis
• The disturbance and/or removal of the bacterial biofilm in the peri-

implant pocket by using special scalers.
• ‘Decontamination’ and conditioning of the surface of the implant with
local drug delivery system.
• Correction via reduction or elimination of sites that cannot be
adequately maintained by oral hygiene measures.
• Establishment of an effective plaque control regime.
• Reosseointegration.
Comparison of normal teeth and implants

(Fig. 21.37)
1. Gingiva and peri-implant soft tissues
In the healthy adult, gingival margin is located on the enamel. A complex
group of gingival connective tissue fibres that form well defined bundles of
interdental fibres, dentogingival fibres, are inserted into the root
cementoenamel junction and they depend on the presence of natural teeth.
FIGURE 21.37 (A, B) Comparison of junctional epithelium in natural
teeth and implant. AB, Alveolar bone crest; C, Cementum; CT,
Connective tissue; D, Dentine; F, Fibroblast; GE, Gingival
epithelium; IP, Implant; IT, Intermediate prothesis; IJE, Implant
junctional epithelium; JE, Junctional epithelium; M, Marrow space;
P, Periodontal ligament; V, Rich vascular supply. Note the cross-
hatch pattern of CT in natural teeth when compared to the parallel
arrangement to the surface of the intermediate prosthesis.
In case of implants, a transmucosal element protrudes through the overlying

mucosa which adapts around the implant. The collagen fibres within the peri-
implant mucosa run parallel to the abutment with no insertion in the abutment
surface, whereas in periodontitis they run perpendicular to the roots. The
papilla around the single implant may be supported by collagen fibres
attached to the adjacent natural tooth. But in case of implants without any
neighbouring natural teeth, formation of soft tissue papilla is less predictable.
2. Junctional epithelium
In natural healthy teeth, the junctional epithelium is attached to the enamel by
hemidesmosomal contacts and a basal lamina like structure formed by the
epithelial cells. Normal junctional epithelium can be regenerated from the
adjacent oral mucosa following excision/damage. It is therefore well-equipped
to deal with problems of any breach in the integrity of the junctional
epithelium both around natural teeth and implants.
3. Biological width
It is the zone of attached connective tissue that separates the underlying
alveolar bone from the apical termination of the junctional epithelium. The
length of the junctional epithelium is about 1.5 mm and the connective tissue
zone is about 2 mm wide. This may vary in various implant systems.
Periodontal probing of natural teeth forms an important part of any dental
examination. The probe penetrates the junctional epithelium to some degree
while examining and this penetration increases in the presence of
inflammation. It stops usually about 2 mm from the bone.
In implants, probing depth is generally deeper than around the natural
teeth. Hence, clinicians are advised to rely on radiographic assessment of bone
level rather than probing.
4. Periodontal ligament and osseointegration

Periodontal ligament is a complex structure of 0.1–0.2 mm width, which
provides support to the natural teeth. The Sharpey’s fibres are embedded in
the root cementum and alveolar bone. Blood supply and connective tissue
ground substance provide the other key elements of the supporting
mechanism. It has a delicate proprioceptive mechanism by which even minute
changes in the masticatory load on the tooth can be detected. Forces
transmitted through the periodontal apparatus can lead to remodelling and
tooth movement as seen in orthodontic movement of teeth.
On the contrary, precise nature of osseointegration at the molecular level is
not yet defined. At the low power microscopic level, bone is very closely
adapted to the implant. However, at a higher magnification, a small gap can
be identified, occupied by the intervening collagen rich zone near the bone
and an absolute phenomenon. It only represents the proportion of the total
implant surface that is in contact with bone. It is similar to ankylosis where
absence of mobility and the absence of intervening fibrous tissue is the
indication of successful osseointegration.
Peri-implantitis and periodontitis

The microorganisms responsible for both the conditions seem to be the same.
The destruction of the supporting tissues of teeth and implants has many
similarities.
Peri-implantitis affects the entire circumference of the implant resulting in a
‘gutter’ like bone loss filled with inflammatory tissue. But, teeth affected by
periodontitis have irregular loss of supporting tissues, confining to proximal
surfaces leading to infrabony defects. In both the clinical entities, the
destructive inflammatory lesions have stages in which the disease process is
rapid, called ‘Burst phenomenon’. It is followed by periods of relative
dormancy.
The zygomaticus system, developed as part of the Brånemark system, allows
reconstruction of a severely resorbed maxilla without the need for bone
grafting. This approach is especially recommended for cases in which the
maxillary sinuses extend anteriorly up to the bicuspid area. These implants
were introduced in 1998 by Professor Per-Ingvar Brånemark and his team at
the Institute of Applied Biotechnology from the University of Gothenburg.
This graft-less technique, also called the ‘zygoma technique’ uses the
cheekbone (zygoma bone) to anchor the longer zygomatic implants.
The implant is a titanium endosteal implant. These are self-tapping screw-
shaped implants in commercially pure titanium with a well-defined machined
surface. They are available in eight different lengths ranging from 30 to
52.5 mm and their diameter tapers from 4 mm superiorly to 5 mm at the
fixture level. They present a unique 45 degree angulated head to compensate
for the angulation between the zygoma and the maxilla. The path of the
zygoma implant lies along the crest of the zygomaticomaxillary buttress
(ZMB), and its external hex fixture head emerges in the second premolar–first
molar area.
Classification
Aparicio C in 2011 proposed a classification for zygomatic implant patients
based on the zygoma anatomy guided approach (ZAGA). The morphology of
the lateral sinus wall, residual alveolar crest and the zygomatic buttress was
taken into major concern. The five basic anatomical groups were named as
ZAGA 0, ZAGA 1, ZAGA 2, ZAGA 3 and ZAGA 4 (Fig. 21.38).
FIGURE 21.38 ZAGA classification. ( Scan to play Zygoma
implants)
Type Characteristics
ZAGA • Anterior maxillary wall is very flat.
0 • Implant head is located on the alveolar crest.
• Implant body has an intrasinus path.
ZAGA • Anterior maxillary wall is slightly concave.
• Drill has performed the osteotomy slightly through the wall.
• Implant body has an intrasinus path.
ZAGA • Anterior maxillary wall is concave.
• Drill has performed the osteotomy through the wall.
• Implant body has an extrasinus path.
ZAGA • Anterior maxillary wall is very concave.
• Drill has performed the osteotomy following a trajectory that goes from the palatal to
the buccal alveolar bone.
• Implant body leaves the concave part of the anterior sinus wall to penetrate into the
zygomatic bone so that the middle part of the implant body is not touching the most
concave part of wall.
ZAGA • Maxilla and the alveolar bone show extreme vertical and horizontal atrophy.
4 • Implant head is located buccally of the alveolar crest (there is no or minimal osteotomy
at this level).
• Drill has arrived at the apical zygomatic entrance following a path outside the sinus
wall and most of the implant body has an extrasinus/extramaxillary path.
Indications and contraindications
Advantages
1. Avoids use of grafts in atrophic maxilla.

2. No additional donor site morbidity.
3. Zygomatic implants placed with 2–4 traditional premaxillary implants
can be either immediately loaded, or, more traditionally, a final fixed
prosthesis can be placed after a 6 months healing period.
4. Good anchorage from tough zygomatic bone which enhances stability
of prosthesis.
5. Zygomatic implants do not necessarily require hospitalisation, which is
usually needed for autogenous bone harvesting from the iliac crest.
6. The total treatment time is routinely 6 months or less for zygomatic
implants compared with grafting with subsequent implant placement.
7. Less number of patient visits.
8. Fewer implants are required to support a prosthesis compared with
traditional bone grafting and implant placement.
9. The overall laboratory fees are equal to or slightly less than those for
traditional implants.
Disadvantages
1. Difficulty in implant placement and the palatal emergence profile.

2. Because the platform of the zygomatic implant might be palatal to the
crest, the perception is that the patient will feel excess bulk and have
problems with the prosthesis.
3. Placement of the zygomatic implant is limited by the anatomy of the
zygoma.
4. The surgical access to the zygoma and orbital rim requires a surgeon
who has experience with surgery in this area.
5. Although the palatal emergence of the implant does add to the
difficulty of maintaining oral hygiene, minimal long-term phonetic
sequelae from the prosthesis design have been reported.
6. Technique sensitive.
7. Not cost effective.

Surgical access
• The patient may have either general anesthesia or deep sedation for
this surgery.
• Incision is made slightly palatal to the crest, and a full thickness
reflection is performed.
• Be aware of the anatomical landmarks to prevent unnecessary injuries
and complications.
• Dissect to the level of the infraorbital foramen which assists with
anatomic orientation of the implant.
• Then place a retractor in the frontozygomatic notch (incisura) to
facilitate visualisation of the apical point of the implant.
• Using a round bur, make a window of approximately 10 mm × 5 mm
on the lateral wall of maxilla to expose the sinus membrane.
• Lift the sinus membrane from the bone and allow it to retract into the
sinus. This elevation should allow direct visualisation of the inner
aspect of the zygoma.
FIGURE 21.39 Sequential steps showing placement of zygomatic
implnat.
• Identify the implant trajectory and starting point for drilling using
depth gauge from the zygomaticus instrument set, which is aligned
over the planned path of the zygomaticus implant to give the surgeon
direct visualisation of the location for the sinus window.
• Aim for the middle of the retractor during the drilling sequence.
• Using a long round bur make an entrance mark into the maxilla from
the palatal aspect of the ridge, traverse the sinus, and score the inner
aspect of the zygoma which will create a purchase point for the next
drill (maximum speed ≤ 2000 rpm).
• Continue with 2.9 mm pilot drill, until it penetrates the outer cortical
layer of the zygomatic bone at the frontozygomatic notch (incisura)
followed by a transition 2.9-mm twist drill which has a guide to enter
the hole in the palate and zygoma, and opens up the hole to the final
size in the zygoma.
• Now determine the implant length using the staright depth indicator.
• Widen the osteotomy with pilot drill 3.5 mm through the previously
made osteotomy.
• Again continue the osteotomy with the twist drill 3.5 mm to finalise the
osteotomy.
Implant insertion
• Verify the depth of the prepared osteotomy using the angled depth
indicator to ensure the selected implant length.
• Irrigate the sinus before inserting the implant.
• Insert the implant in the prepared bone site with 20 Ncm setting on the
drilling unit. The setting may be increased to 50 Ncm to facilitate
implant insertion.
• As the insertion torque reached 40–50 Ncm, use the Z handle to tighten
the implant manually until the implant apex engages in the zygomatic
bone.
• Now place the screw driver into the screw head of the implant mount
and verify the correct position of the implant platform (the shaft of the
screw driver must be perpendicular to the crest of the ridge).
• Irrigate the apical implant portion thoroughly.
• Remove the implant mount and place the cover screw using the cover
screw driver.
• Place the remaining implants.
• Close the flap and wait for sufficient healing (for 6 months) or reline
the existing denture and immediately load the denture.
Postoperative care
• Appropriate antibiotics and analgesics to be prescribed for a week.
• Soft diet.
• Maintain oral hygiene.
Complications
• Postoperative sinusitis
• Oroantral fistula formation
• Periorbital and subconjunctival haematoma
• Facial oedema
• Lip lacerations
• Pain
• Temporary paraesthesia
• Epistaxis
• Gingival inflammation
• Orbital penetration/injury
• Difficulty in speech articulation and hygiene
SECTION VII
Space Infections
Chapter 22: Head and Neck Space Infections, Part -I

Chapter 23: Head and Neck Space Infections, Part -II
Chapter 24: Head and Neck Space Infections, Part -III
Chapter 25: Osteomyelitis, Osteoradionecrosis and
Osteochemonecrosis
CHAPTER 22
Head and Neck Space

Infections, Part -I
Physiology of the infection and inflammatory response

Aetiology of odontogenic infections
Microbiology of odontogenic infections
Stages of infection
Periapical abscess
Dentoalveolar abscess
Cellulitis
Mechanism of spread of infection
Routes of spread
Direct spread
Indirect spread
Odontogenic infection
Infection that originates from the dental pulp, periodontium and jawbones or
in tissues that closely surround it.
Periapical infection/abscess
Dental infection that spreads across the pulp to the area extending beyond the
apex of the tooth and is localised at that site. When the localised periapical
infection undergoes an acute exacerbation with pus formation within the bony
confines, it becomes periapical abscess.
When a periapical abscess extends beyond the confines of the dentoalveolar
bone into the vestibular space (space between oral vestibular mucosa and
buccinator mucosa), it becomes a classic dentoalveolar abscess. It remains as a
thick-walled cavity containing pus.
Cellulitis
When a periapical infection fails to localise as abscess, it results in cellulitis
where infection rapidly spreads through fascial tissue planes diffusely.
Depending on the virulence of the organism and host resistance, these
bacterial infections have a potential to spread beyond the bony confines of the
tooth and jawbones into the surrounding soft tissues, by hydrostatic pressure,
following the path of least resistance, into loose areolar connective tissue of the
fascia that surrounds the muscles. This type of tissue is easily destroyed by the
hyaluronidases and collagenases produced by the bacteria, thus opening
potential spaces surrounding the muscles.
Most of these infections can be managed by early extraction of the offending
tooth, incision and drainage.
Introduction of antibiotics has a profound influence on the treatment of
odontogenic infections. Significance of this type of infection lies in that when
untreated or improperly treated, it can cause life-threatening complications by
spreading to distant vital structures, e.g. intracranial, retropharyngeal,
pulmonary or pleural infections. The complications arising from odontogenic
infections can have systemic manifestations that may, in turn, have a serious
effect on the patient’s general health status to the point of becoming life-
threatening.
Thus, such innocuous periapical infections have a potential to develop into
life-threatening deep fascial infections. Though incidence, severity, morbidity
and mortality of odontogenic infections have declined after the advent of
antibiotics, basic knowledge of management of such infections is necessary to
prevent morbidity.
Physiology of the infection and inflammatory

response
Any infection arouses a cell-mediated or humoral immune response from the
host. If the host is not immunocompromised, a sequelae of inflammatory
changes take place as follows (sequelae of pulpal pathology):
• Vasodilatation of the arterioles—causing hyperaemia
• Extravasation of plasma rich in plasma proteins, antibodies and
nutrients into the surrounding tissues
• Collection of leucocytes
• Leucotoxin, increases permeability allowing polymorphs into the area
• Exudate forms fibrin, walling off the region
• Macrophages—phagocytosis of bacteria, dead cells
Aetiology of odontogenic infections

Dental caries
Dentoalveolar abscess usually develops by extension of dental caries lesion
causing the spread of bacteria to the pulp via the dentinal tubules. When the
decay reaches the dental pulp, it will lead to pulpitis. Infection from here may
spread to supporting bone resulting in periapical abscess, which in turn may
spread subperiosteally. The pulp responds to infection either by rapid acute
inflammation involving the whole pulp which quickly becomes necrosed or by
development of a chronic localised abscess with most of the pulp remaining
viable.
• Traumatic root fracture or pathological exposure due to tooth wear.

• Traumatic pulpal exposure due to dental treatment.
• Through periodontal membrane and accessory root canal.
• Rarely by anachoresis, i.e. seeding of the organisms directly into the
pulp via pulpal blood supply during bacteraemia.
• Periapical abscess may occur in seemingly intact but devitalised teeth
(trauma, cracks or decay under fillings).
• Periapical and periodontal abscess may result from chronic gingivitis
and periodontitis.
Pericoronitis
Partially impacted third molars with a gingival flap serves as a nidus of food
accumulation and infection, very often leading to space infection.
Microbiology of odontogenic infections

Of all the infections resulting from microorganisms contained in the oral flora,
the leading ones are related to dental pathology (odontogenic infections).
Almost all are polybacterial, caused by five different species, on average and
by mixed aerobic–anaerobic flora, especially Gram-positive aerobic, anaerobic
cocci and Gram-negative anaerobic bacilli in more than 95% of cases.
Approximately, 5% of odontogenic infections are caused by aerobic bacteria,
35% are due to anaerobic bacteria and the remaining 60% are jointly caused by
aerobes and anaerobes (Table 22.1).
Table 22.1
Bacterial causes of odontogenic infection

Microorganism
Aerobic
Gram-positive cocci
Streptococcus sp.
Streptococcus (group D) sp.
Staphylococcus sp.
Eikenella sp.
Gram-negative cocci (Neisseria sp.)
Gram-positive bacilli (Corynebacterium sp.)
Gram-negative bacilli (Haemophilus sp.)
Miscellaneous
Anaerobic
Gram-positive cocci
Streptococcus sp.
Peptococcus sp.
Peptostreptococcus sp.
Gram-negative cocci (Veillonella sp.)
Gram-positive bacilli
Eubacterium sp.
Lactobacillus sp.
Actinomyces sp.
Clostridia sp.
Gram-negative bacilli
Prevotella sp., Porphyromonas sp.
Bacteroides sp.
Fusobacterium sp.
Miscellaneous
Of the aerobic bacteria involved in odontogenic infections, streptococci

represent roughly 90% and staphylococci 5%. Neisseria sp., Corynebacterium sp.
and Haemophilus sp. are encountered only infrequently. There is a greater
abundance of anaerobic bacterial species (Table 22.1). Gram-positive cocci
represent one-third of the total, and Gram-negative bacilli are isolated in
approximately half of the infections. Prevotella, Porphyromonas and Bacteroides
sp. contribute 75%, and Fusobacterium sp. the remaining 25%. The infections
caused by these microorganisms follow a well-defined pattern of evolution.
Following inoculation in deep tissue, there is a proliferation of aerobic
bacteria, such as the more invasive and virulent Streptococcus sp., which leads
to a decrease in the tissue oxidation–reduction potential, thereby creating the
ideal conditions for anaerobic bacteria to proliferate; these anaerobic bacteria
will predominate or may be the only ones encountered in suppurative and
chronic phases of the infectious process.
Factors affecting spread of orofacial infections are depicted in Table 22.2.
Table 22.2
Factors affecting spread of orofacial infection
I. Systemic factors
a. Microbial factors
• Level of virulence of the causative organism
• Number of organisms introduced into the host
b. Host factors
• General state of health
• Integrity of surface defences
• Capacity of inflammatory and immune response
• Level of immunity
• Impact of medical intervention
c. Combination of both factors
II. Local factors
a. Alveolar bone and periosteum Natural defence

b. Neighbouring soft tissues, muscles
Stages of infection
Odontogenic infections generally pass through three stages before they
undergo resolution:
1. During 1–3 days—the swelling is soft, mildly tender and doughy in

consistency.
2. Between 5 and 7 days—the centre begins to soften and the underlying
abscess undermines the skin or mucosa making it compressible. The
underlying pus may be seen through the epithelial layers making it
fluctuant.
3. Finally, there is a resolution of the abscess that may be spontaneous or
after surgical drainage. During the resolution phase the involved
region is firm on palpation due to the process of necrotic tissues and
bacterial debris removed by the macrophages and alternating repair
mechanism.
Periapical abscess
• An abscess is a thick-walled cavity containing pus.

• Periapical abscess refers to an abscess of odontogenic origin that occurs
mainly in relation to root apices. It may be confined to the alveolar
bone, perforate through the bone reaching the surface or invade the
soft tissues subperiosteally or supraperiosteally. Abscess formation
may be well circumscribed or may be associated with regional
cellulitis.
• Staphylococcus is associated with abscess formation that produces
coagulase (coagulase-positive staphylococci) in contrast to association
of Streptococci in cellulitis.
• Differences between periapical and periodontal abscesses are depicted
in Table 22.3.
Table 22.3
Differences between periapical and periodontal abscesses

Features Periapical abscess Periodontal abscess
Site Usually over the apex of tooth Usually over gingival third of alveolar process
Aetiology Necrosis of pulp Periodontal pockets
Tooth mobility Only in late stages In early stages
Age Young and middle age Middle to older age
The infection that has extended beyond the alveolar bone and comes into the
adjacent soft tissues as a localised form is known as dentoalveolar abscess.
Cellulitis
Cellulitis is defined as ‘diffuse, nonsuppurative inflammatory reaction of the
fascial tissue planes (submucosal or subcutaneous) or loose connective tissues
usually as a result of bacterial odontogenic infections’.
Clinical findings
Cellulitis of head and neck involves the face and orbit commonly. Cellulitis of
clinical importance involving bilateral submandibular, sublingual and
submental spaces is called Ludwig’s angina.
Cellulitis presents with classical clinical findings of diagnostic values:
• Acute onset (short duration of within 3 days).

• Fever and malaise.
• Swelling of the involved tissues causing facial asymmetry.
• Skin over the swelling appears erythematous, shiny and nonpinchable.
It may show secondary changes as discolouration.
• Swelling is painful and tender with firm board like consistency and
induration.
• Regional lymphadenopathy is common.
• Ludwig’s angina—presents classically as swelling of lower face
extending to the neck. Involvement of the floor of the mouth causes
raising of the tongue, extension to the neck (laryngoedema) may cause
airway obstruction—hyperventilation, increased respiratory rate, use
of accessory muscles of respiration (sternocleidomastoid), which may
further spread to mediastinum (mediastinitis). (Refer to Chapter 24
Head and Neck Space Infections.)
• Cellulitis may involve the orbital tissues resulting in orbital cellulitis.
• Orbital cellulitis. Periorbital and orbital cellulitis may result from
maxillary infection. It is an uncommon sequelae, usually seen in
immunocompromised patients.
Classification of orbital cellulitis

Chandler et al. classification of orbital cellulitis includes five groups.
Group I: Inflammatory oedema (preseptal cellulitis, periorbital cellulitis)
(Figs. 22.1 and 22.2)
• Swelling of the eyelids with mild orbital oedema.

• Upper eyelid (usually medial part) is involved in the initial stages.
• More advanced stage includes ‘chemosis’ (swelling of the conjuctiva).
FIG. 22.1 Preoperative view of the patient with preseptal cellulitis

(canine space infection).
FIG. 22.2 Postoperative view.
Group II: Orbital cellulitis
• Infiltration of the orbit, leading to oedema, congestion, proptosis,

motor and visual impairment.
Group III: Subperiosteal abscess
• Accumulation of purulent foci within subperiosteal space leads to

nonaxial displacement and tenderness.
• Displacement of the globe is nonaxial and reflects the site of the
abscess.
Group IV: Orbital abscess
• Progression of intraorbital cellulitis or spread from subperiosteal space

leads to intracoronal or extracoronal loculations.
• Severe ophthalmoplegia, orbital cellulitis, visual loss and marked
proptosis produced by localised necrosis and abscess formation within
central orbital fat.
Group V: Cavernous sinus thrombosis
• Proptosis and fixation of the globe, usually with visual loss and
development of similar signs in the opposite orbit frequently
associated with signs of meningitis.
Differences between cellulitis and abscess are depicted in Table 22.4.
Table 22.4
Differences between cellulitis and abscess

Features Cellulitis Abscess
Duration 3–7 days More than 5 days
Size Large Small
Localisation Diffuse Circumscribed
Palpation Hard and tender Fluctuant
Skin Thickened, board hard Undermined and shiny
Temperature Warm Moderately warm
Loss of function Severe Moderately severe
Tissue fluid Serosanguinous Pus
Bacteria Mixed Anaerobic
Degree of seriousness Very severe Moderate to severe
Mechanism of spread of infection

Oral infection may originate in the pulp of the tooth and extend via the root
canals into the periapical tissues and may become dispersed through the
medullary bone. It may also originate in the periodontal tissues and spread to
the adjacent bones. The infection may become localised or extend diffusely. In
the bone, it might perforate the cortical plate and discharge pus via a sinus on
the outer skin surface or might remain confined within the bone.
The type and virulence of the microorganisms involved and the
immunological condition of the patient influence the degree of spread of
infection. Some organisms remain localised whereas other organisms tend to
spread rapidly through the tissues along the lines of least resistance into the
tissue spaces (Flowchart 22.1). To a greater degree muscle attachments
determine the route taken by the infection.
FLOWCHART 22.1 Aetiopathogenesis.
Routes of spread
Direct spread (Flowcharts 22.2–22.4)
1. Spread into the superficial soft tissues may:

• Localise as a soft tissue abscess.
• Extend through the overlying oral mucosa or skin, producing
a ‘sinus’ connecting the main abscess cavity to the exterior.
• Extend through the soft tissue to produce cellulitis.
2. Spread may occur into the adjacent fascial spaces, following the path of
least resistance resulting in space infection, which can further lead to
life-threatening septicaemia. Such spread is dependent on the
anatomical relation of the original abscess to the adjacent muscle
attachment and fascial planes. Infection via fascial planes often spreads
rapidly and for some distance from the original abscess site.
Occasionally, it may cause severe respiratory distress as a result of
occlusion of the airway by oedema. (Refer to Chapter 24 Head and Neck
Space Infections.)
Sequelae: Odontogenic infection → Space infections → Septicaemia.
3. Infection may extend into deeper medullary spaces of alveolar bone
producing a osteomyelitis. (Refer to Chapter 25 Osteomyelitis,
Osteoradione crosis and Osteochemonecrosis.)
FLOWCHART 22.2 Spread of infection in maxillary teeth.

FLOWCHART 22.3 Spread of infection in mandibular teeth.
FLOWCHART 22.4 Routes of spread of infection.
Indirect spread (Flowchart 22.4)

1. Lymphatic routes to regional nodes in the head and neck region
(submental, submandibular, deep cervical, parotid and occipital).
Usually involved nodes are tender, swollen and rarely may suppurate
requiring drainage.
2. Haematogenous routes to other organs such as brain is possible
through deep facial vein and pterygoid venous plexus that
communicate intracranially with cavernous venous sinuses.
CHAPTER 23
Head and Neck Space

Infections, Part -II
History taking
Laboratory investigation
Radiological investigation
Clinical features of odontogenic infections
Principles of management of odontogenic infections
Treatment of the causes
Excision of sinus
Antibiotic therapy
Supportive therapy
Evaluation of a patient with odontogenic infection follows the same basic

principles of diagnosis as with any oral disease. The steps include:
1. Thorough history taking

2. Clinical examination (general and regional)
3. Investigations—laboratory and radiological
4. Diagnosis and treatment planning.
It is, however, important in case of odontogenic infections to have an
immediate quick assessment of the patient’s vital signs and general condition
prior to a complete evaluation. This should include:
• Examination of patency of airway and breathing

• Examination for toxicity
• Examination for any CNS changes.
This would help in planning for any emergency medical or surgical

intervention (e.g. tracheostomy) if needed.
History taking
In case of odontogenic infections, this should mainly include:
• Onset, duration and course of present condition

• Any associated symptoms such as fever, chills, etc.
• History of extraction or any other trauma to the site
• Previous history of similar infection and treatment administered
• History of any radiotherapy administered
• History of recurrent infections.
This would include general and regional (extraoral and intraoral)
examinations.
General examination
• Measurement of vital signs

• Examination of thorax, abdomen, heart and extremities
• Review of all systems
• Generalised lymph node examination.
• Skin changes—swelling, redness, ulcers, etc.

• Bony enlargements
• Lymph node swellings
• Presence of any sinus openings, fistula, etc.
• Restrictions in mouth opening—trismus
• Ophthalmic examination.
Swelling (consistency, fixity), discharge, dental caries, deviation of tissues
(tongue, uvula).
Other than the usual laboratory investigations, it is imperative to do a bacterial
culture and an antibiotic sensitivity test. This will help in directly eliminating
the source of infection.
Radiological investigation
Conventional radiographic methods may be used to determine the underlying
cause (carious/impacted teeth, foreign body).
Computed tomography (CT) and magnetic resonance imaging (MRI) are
especially useful in special infections as they clearly show the extent of soft
tissue damage. Moreover, with the advent of 3D CT and other advances in
imaging the extent can be studied in all planes. Other than their diagnostic and
prognostic uses, these imaging methods can also be used as treatment aids,
e.g. in CT-guided percutaneous drainage.
Clinical features of odontogenic infections

Clinical features may include a nonvital tooth with or without a carious lesion,
a large restoration, evidence of trauma, swelling, pain, redness, trismus, local
lymph node enlargement, sinus formation, rise in temperature and malaise.
The latter two symptoms are direct consequence of increased levels of
systemic inflammatory cytokines such as interleukins and tumour necrosis
factors in response to bacterial products such as lipopolysaccharides (i.e.
endotoxins). The cardinal signs of inflammation are present. If they are absent,
then it is an indication that the infection is spreading to the deeper tissues.
Rubor or redness
Present when infection is close to the tissue surface; markedly seen in light
complexioned patients. It is due to vasodilatation.
Tumour or swelling
Due to accumulation of fluid exudate or pus.
Calor or heat
It is the result of inflow of warm blood from the deeper tissues, increased
velocity of blood flow and increased rate of metabolism.
Dolour or pain
It is due to the pressure on sensory nerve endings caused by distention of
tissues by oedema or spreading of infection, liberated or activated factors such
as kinins, histamine, metabolites or bradykinin-like substances on nerve
endings.
Loss of function
Reflected as difficulty in chewing, swallowing and respiratory embarrassment.
Also associated with the reflex inhibition of muscle movements associated
with pain.
Pyrexia
Elevation of temperature is one of the significant signs of infection (normal
oral temperature 97.7 to 99.5°F).
Lymphadenopathy
In acute infections, lymph nodes are enlarged, soft and tender. In chronic
infections, nodes are less firm, often nontender. Suppuration of the nodes
occurs when infecting organism overwhelms the local defence mechanism in
the node and produces excessive cellular reaction and collection of pus.
Presence of halitosis
Due to intraoral pus discharge.
Algorithm for management of odontogenic infections
• Assess disease severity and systemic state.

• Emergency surgical or medical intervention as needed.
• Evaluate patient.
• Decide on setting of care (outpatient or admission).
• Pus/discharge—swab for culture and sensitivity test.
• Start antibiotics empirically and then change as per sensitivity test.
• Treat surgically with adjunctive medical support.
• Rehabilitate.
• Evaluate the patient frequently.
Principles of management of odontogenic infections

Treatment of the causes
Most infections have a distinct cause and only surgical treatment will prevent
worsening and recurrence, though antibiotics play a supportive role. In early
cases, surgical treatment may be as simple as root canal treatment of the
suspected tooth, or alternatively simple tooth extraction followed by oral
antibiotics. However, in advanced infection resulting in space infection and
septicaemia, management strategies shift to medical management. Surgically,
most cases can be approached transorally. Removal of the cause (usually
tooth) is followed by incision and drainage of the infection. Early diagnosis,
prompt empirical antibiotic treatment together with early removal of the cause
can prevent most complications and result in early recovery. Therefore,
management of acute odontogenic infections involves both surgical and
supportive therapies. Depending upon the stage of infection, treatment will
vary from tooth extraction to evacuation of pus as in cases of abscess in
extraoral space infections.
• Incision and drainage (I&D) is the foremost surgical method in treating

space infection.
Objectives
• Create an escape route for the necrotic tissues, pus and microbes from
the tissue space.
• Removal of dead tissue, pus, toxins and infective material that facilitate
better immune defence mechanism.
• Effectively reduce the surface area of infected tissue and thus
minimising the dosage of antibiotic required.
• Blunt dissection into the tissue spaces breaks the pus locules and
fibrous barrier, thus facilitating reach of the antibiotics into the
infective site.
• Drainage is used for culture and sensitivity (C&S) based on which
empirical antibiotic therapy may be continued or changed (Fig. 23.1).
FIGURE 23.1 Incision and drainage of a submandibular space
infection.
Indications
• Space infections (primary) that has localised pus collection with a

clinically evident point of fluctuance. Example: buccal space infection
with point of fluctuance on face.
• Space infections (secondary) that has pus collection with no clinical
sign of fluctuance but requires immediate drainage to prevent
progression. Example: masseteric space infection—only clinical sign is
trismus.
• Nonsuppurative space infection such as Ludwig’s angina, where I&D
serves as a method of decompression of the tissue planes, but could be
lifesaving.
Principles
In all cases, the following principles must be observed:
1. Follow the shortest and most direct route to the accumulation of

exudate or pus, but always preserving the integrity of anatomical
structures.
2. Performing incisions with aesthetic criteria in areas of minimal impact
as on the face. Example: buccal space infections can be drained
intraorally or extra-orally by placing incisions in nonaesthetic zone
along lower border of mandible.
3. Place the incisions in areas of healthy mucosa or skin, avoiding areas
with fluctuation and atrophic alterations.
4. Perform strictly cutaneous or mucosal incisions (with a No. 11 blade).
5. The incision is penetrated using haemostat or sinus forceps in closed
position, advanced into the pus locules, by blunt dissection in open
position of the sinus forceps. The haemostat is withdrawn in the same
position in open state to avoid damage to anatomical structures such as
nerves, vessels (Hilton’s method of drainage).
6. Choice of appropriate drainage material is according to the site of
infection. Avoid using gauze as a drainage material, since secretions
would be retained and coagulate, thereby creating a tamponade that
would cause the infection to persist.
The principles, methods and techniques of drainage are dealt in detail in

Chapter 16 Wound Care.
Excision of sinus
In most of the cases, the abscess escapes the tissue spaces spontaneously,
through a sinus if left without any treatment for sufficient period of time. Pus
discharge through the skin in a location unfavourable for drainage follows and
the resulting scar is always puckered, thickened and depressed. Further, the
sinus will become chronic unless the original source of infection is removed,
and it is subjected to exacerbations and remissions with attempts at healing
during the quiescent phase. To treat this sinus, an elliptical incision is made
around its external orifice so that on closure the scar lies in Langer’s line
without puckering. This is done with a scissors, using which the sinus tract is
followed to its source which is usually found on the bony surface of the jaws.
Then a deep soluble suture is inserted to eliminate the dead space and the skin
wounds are closed with careful eversion of the edges.
Antibiotic therapy
Odontogenic infections are caused by a highly predictable group of bacteria,
so choice of the initial antibiotic is empirical. More than 90% of odontogenic
infections are caused by aerobic and anaerobic streptococci, peptostreptococci,
prevotella, fusobacterium and bacteroides.
As the first-choice therapy
• Synthetic penicillin and cephalosporin

• Amoxicillin/clavulanic acid 2 g 1 h prior to starting the surgical
intervention, followed by 2 g every 12 h for 5–7 days. This is the most
appropriate option, since it offers greater coverage than penicillin
against oral streptococci and beta lactamase. Alternatively, third or
fourth generation cephalosporins are active against Gram-positive and
Gram-negative anaerobic bacteria and have bone penetrating
properties.
Other alternative regimens
• Clindamycin 300 mg every 6 h (per os), for 5–7 days.

In all cases, treatment must be initiated approximately 1 h prior to
performing surgery.
• Culture sensitivity test should be routinely performed, using drains,
pus cells; this is of clinical significance in:
▪ When the patient fails to respond to empirical antibiotic
therapy and after treatment of the causes within 48 h.
▪ When the infection is disseminated to other fascial spaces
despite initial treatment.
▪ In an immunosuppressed patient or if he/she has a prior
history of bacterial endocarditis and does not respond to the
initial antibiotic.
Supportive therapy
Apart from antibiotic therapy, patients with facial cellulitis may require
complementary measures, particularly in severe cases with considerable
systemic involvement or in life-threatening situations. Analgesics,
nonsteroidal antiinflammatory drugs (NSAIDs) and nutritional support are
mandatory. Patients with infection and fever present a considerable loss of
body fluids—250 mL for every degree (centigrade) temperature rise.
Ambulatory patients must drink 8–10 glasses of water or any other liquid.
Intravenous fluids can be given to those patients who are hospitalised to
improve hydration. The daily calorie requirement also increases by up to 13%
for each degree (centigrade) above normal body temperature. Thermal agents
should be used to aid the body defences and not in a futile attempt to regulate
localisation. Heat produces vasodilatation and increased circulation, more
rapid removal of tissue breakdown products and greater influx of defensive
cells and antibodies. A crucial aspect to be considered in these patients is the
potential risk of onset of respiratory impairment, requiring airway monitoring,
perhaps even on an emergency basis, by means of endotracheal intubation,
cricothyrotomy or tracheotomy.
CHAPTER 24
Head and Neck Space

Infections, Part -III
Potential spaces
Topazian classification
Classification based on clinical significance
Classification according to involvement of spaces
Based on mode of involvement
Grodinsky and Holyoke classification
Suprasternal space (of burns)
Contents
• Boundaries of canine space
• Contents
• Teeth involved
• Surgical management
Buccal space
• Boundaries of buccal space
• Contents
• Teeth involved
Infratemporal space
• Boundary
• Contents
• Neighbouring spaces
• Involvement
• Spaces related to lower jaw
Submental space
• Boundary
• Contents
• Involvement
• Neighbouring space
Surgical management
Submandibular space
• Boundary
• Contents
• Involvement
• Spread
Sublingual space
• Boundary
• Contents
Secondary fascial spaces
• Temporal space
• Boundaries
• Contents
• Differential diagnosis
• Management
Submasseteric space
• Boundary
• Contents
• Boundary
• Contents
• Boundary
• Contents
• Boundary
• Contents
• Complications
Life threatening complication of orofacial infections
Ludwig’s angina
• Aetiology
• Odontogenic
• Pseudo-Ludwig’s angina/Pseudo-Ludwig’s phenomena
• Microbiology
• General examination
• Regional examination
• Potential complications
• Diagnosis
• Treatment
• Distant spread
Carotid space infection
Cerebral abscess
Meningitis
Cavernous sinus thrombosis
Mediastinitis
• Diagnosis
• Potential complications
• Medical management
• Surgical intervention
Necrotising fasciitis of the head and neck
• Causative organism
• Management
The head and neck region has structures separated from each other through
specific natural connective tissue barriers called fascia. (Fascia means fibrous
connective tissue which binds together various structures of the body). These fascial
layers can be anatomically divided into superficial and deep. The fascial
spaces are potential spaces formed by the various fascial layer’s division and
unions at different levels. They are separated by pus, blood, drain or surgical
instruments during surgery (Flowchart 24.1).
FLOWCHART 24.1 Spread of maxillary and mandibular dental
infection into fascial spaces.
Potential spaces
Soft tissue infections of head and neck are commonly encountered in routine
practice of oral and maxillofacial surgery, In case of infection the classic signs
and symptoms—pain, swelling, surface erythema, lymphadenopathy, and
systemically-fever, malaise, toxic appearance, and an elevated white blood cell
count is present.
Shapiro defined fascial spaces as potential spaces between the layer of
fascia. These spaces are normally filled with loose connective tissues and
various structures like veins, arteries, glands, lymph nodes, etc. Space is a
misnomer. There are no voids in the tissues in actual reality.
Purulent exudate accumulates in these potential tissue spaces, which are not
actual spaces till purulent exudate is formed. This exudate (pus) destroys the
loose connective tissue and separates the anatomical boundaries of the
compartment. Some of these potential spaces are compartments which
contains structures like submandibular salivary gland, lymph nodes or buccal
pad of fat. Normally these structures are surrounded by deep connective
tissue (Fig 24.1, Flowchart 24.2).
FIGURE 24.1 Pathways of dental infections.
FLOWCHART 24.2 Sequelae of dental caries.

Topazian classification
Flowchart 24.3
FLOWCHART 24.3 Topazian classfication (based on clinical

significance).
Classification based on clinical significance

(Table 24.1)
Table 24.1
Spaces based on clinical significance

Primary maxillary spaces Canine (infraorbital)
Buccal
Infratemporal
Primary mandibular spaces Submental
Submandibular
Sublingual
Buccal
Secondary fascial spaces Masseteric
Pterygomandibular
Superficial and deep temporal
Lateral pharyngeal
Retropharyngeal
Prevertebral
Classification according to involvement of spaces

(Fig. 24.2)
Based on mode of involvement
Direct involvement: Primary spaces
1. Maxillary spaces
2. Mandibular spaces
FIGURE 24.2 Anatomical spaces of head and neck.
Indirect involvement: Secondary spaces

Grodinsky and Holyoke classification
This classification is based upon the data of dissected materials spread of
injected masses and infections observed clinically. Grodinsky and Holyoke
designated these spaces by numerals (spaces of anterior triangle) and
numerals followed by letter ‘A’ (spaces of posterior triangle) as follows:
Space 1 Superficial fascial compartment

Space 2 Potential space between the superficial layer of deep fascia and
the deep layer of the sternothyroid–thyrohyoid sheath.
Space 2A Space between the superficial layer of deep fascia and the sheath
of the posterior belly of the omohyoid muscle.
Spaces 3 and 3A Visceral compartment and space within carotid sheath,
respectively.
Space 4 Space between two laminae of prevertebral fascia.
Space 4A The potential space between the superficial layers of deep fascia
and the scalenus fascia.
Space 5 This is a potential space between prevertebral fascia and vertebral
bodies limited laterally up to transverse processes of vertebrae.
Space 5A This lies in the posterior triangle deep to scalenus fascia. This
space, posterior to the scalenus fascia, lies between the deep muscles of
the back of the neck.
The number, position, shape and curvature of roots and their apices
determine the common site of localisation of abscess (Table 24.2).
Table 24.2
Localisation of dental abscess

Teeth Common site
Mandibular incisors Labial/Lingual
Mandibular canines Labial
Mandibular premolars Buccal
Mandibular molars Buccal
Maxillary incisors Labial
Maxillary canines Labial
Maxillary first premolars Labial and palatal
Maxillary second premolars Buccal
Mandibular molars Buccal and palatal
Fascia are sheets of dense connective tissue which separates structures that pass
over each others during movements and pathway for neurovascular structures.
According to Hollinshead:
I. Superficial fascia
II. Deep cervical fascia
A. Anterior layer
1. Investing fascia
2. Parotidomasseteric fascia
3. Temporal fascia
B. Middle layer
1. Sternohyoid–omohyoid division
2. Sternothyroid–thyrohyoid division
3. Visceral division
a. Buccopharyngeal
b. Pretrachael
c. Retropharyngeal
C. Posterior layer
1. Alar division
2. Prevertebral division
Suprasternal space (of Burns)

The suprasternal space (of Burns) is a space of the inferior neck. Superficial
fascia splits below the level of the hyoid bone to form two spaces:
1. It forms the lower part of the root of the posterior triangle, the fascia
splits into two layers, both of which are attached to the clavicle.
2. It forms the lower part of the roof of the anterior triangle and the fascia
splits in form the suprasternal space or the space of the ‘burns’. The
layers pass down to get attached one to the anterior, the other to the
posterior border of the manubrium sterni.
Contents
• Sternal head of sternocleidomastoid muscle

• Anterior Jugular vein anastomoses
• Lymph nodes
• Interclavicular ligament

Canine space
Boundaries of canine space (Fig. 24.3)
Superficial and superior—Quadratus labii superioris
Inferior—Orbicularis oris
Deep—Levator anguli oris, anterior surface of maxilla
Medial—Levator labii superioris alaeque nasi
Lateral—Zygomaticus major
FIGURE 24.3 Boundaries of canine space.
Contents
• Angular artery and vein

• Infraorbital nerve
Quadratus labii superioris originates from above the infraorbital foramen

and overlaps the levator anguli oris muscle, which originates below the
infraorbital foramen.
When root of the canine is long and origin of the levator anguli oris is low,
infection from canine travels the medial border of the levator anguli oris into
the canine space (the region between the anterior surface of the maxilla and
overlying levator muscles of upper lip). If the swelling is untreated, pus points
out below the medial corner of the eye by emerging in between quadrates labii
superioris and levator labii superioris alaeque nasi.
Teeth involved
Maxillary canine, 1st premolar infection and sometimes mesiobuccal root of
first molars
Clinical features (Fig. 24.4 A, B)
• Periapical abscess of canine usually present as labial sulcus swelling

and less commonly as palatal swelling
• Swelling of the cheek and upper lip (vestibular abscess)
• Obliteration of the nasolabial fold (pus accumulation in the nasolabial
fold)
• Oedema of the lower eyelid.
• Marked periorbital oedema forcing the eyelid to close.
• Marked tenderness and redness in the facial tissue.
FIGURE 24.4 (A) Preoperative view—left canine space infection.

(B) Postoperative view—resolution following extraction of infected
canine.
Surgical management
The incision is made intraorally high in the maxillary labial vestibule. Insert a
small haemostat through the levator anguli oris into the abscess cavity, place a
rubber drain and suture into the lower margin of the vestibular incision.
Buccal space
Boundaries of buccal space
Superior—Zygomatic arch
Inferior—Inferior border of mandible
Anterior—Posterior border of the zygomatic bone above and depressor
angulioris below
Posterior—Anterior border of the masseter muscle
Medial—Buccinator muscle and its fascia
Lateral—Skin and subcutaneous tissue.
FIGURE 24.5 Spread of infection to buccal space.
Contents (Figs. 24.5–24.7)
• Space filled with buccal pad of fat (adipose tissues)

• Parotid duct
• Anterior and transverse facial artery and vein.
Teeth involved
Maxillary and mandibular premolars and molars.
Infections from maxillary premolars and molars usually perforate the buccal
aspect of the alveolar process. Relationship of the root apices to the attachment
of the buccinator muscle is the factor that determines whether localisation is
intraoral or extraoral or deep into buccal space. If perforation is below the
buccinators attachment in maxilla, swelling will be located in the oral vestibule
whereas in the reverse situation the infection extends laterally to the
buccinator muscle forming a buccal space abscess.
The buccal space contains the buccal pad of fat and is therefore continuous
posteromedially around the fat with the pterygoid space through the interval
between the buccinator and anterior border of the coronoid process.
Infections from mandibular molars and pericoronitis of the third molar can
also produce a buccal space infection. Buccal space infection will also extend
into the infratemporal surface by coursing along the masticatory fat pad.
Clinical features
There is an obvious and dome-shaped swelling on the anterior aspect of the
cheek beginning at the lower border of the mandible, extending upwards to
the level of zygomatic arch.
Surgical management
Two stab incisions for drainage of buccal space abscess are made extraorally
through the skin and subcutaneous tissue with No. 11 scalpel blade, below the
lower border of the mandible for a dependent drainage. A curved haemostat is
inserted through the anterior incision into the abscess cavity; exited through
the posterior incision; the beaks are opened and a strip of rubber drain is
grasped; the haemostat is then withdrawn carrying the drain through the
tissues. The ends are tied with suture to prevent dislodgement. This incision
also hides the scar in the shadow of the mandible. In case of buccal space
abscess, intraoral incision is not preferred because it is difficult to maintain a
patent opening for drainage since the buccinator muscle tends to contract
especially when a vertical incision is made. If an intraoral incision is preferred,
horizontal incision should be placed just above the depth of the vestibules.
This not only prevents damage to the parotid duct, but also provides
dependent drainage.
FIGURE 24.6 (A) Preoperative view showing right buccal space

infection. (B) Through and through drain placement. (C) Drainage
in most dependent region of swelling.
FIGURE 24.7 (A) Buccal space infection—lateral to buccinator. (B)

Buccal space infection—plane of spread lateral to buccinator
muscle.
Infratemporal space
Also called as ‘retrozygomatic space’ as it is partly situated behind the
zygomatic bone.
Boundary
Superior—Skull base-sphenoid crest
Inferior—Lateral pterygoid muscle
Medial—Lateral pterygoid plate
Lateral—Temporalis muscle and tendon
Anterior—Maxillary tuberosity
Posterior—Mandibular condyle
Contents
• Internal maxillary artery (second part)

• Pterygoid venous plexus
• Mandibular division of trigeminal nerve
• Medial and lateral pterygoid muscles
Neighbouring spaces
• Buccal space
• Superficial temporal space
• Inferior petrosal sinus space
Involvement
Infratemporal fossa may also become secondarily infected from infections of
the submasseteric, parotid and lateral pharyngeal spaces.
Clinical features
The swelling is characterised by severe trismus and pain. If the swelling is
present over the tuberosity area then extraorally the swelling can be seen over
temporomandibular joint and zygomatic arch. From here it extends to the
cheek and if left untreated, may involve the whole side of the face and optic
neuritis might also occur. Occasionally, the swelling may also extend into the
neck. The presence of pterygoid plexus of veins makes the infection of the
infratemporal space dangerous. Emissary veins connect the pterygoid plexus
with the cavernous sinus. Therefore, infections from here can spread to the
cavernous sinus and present with symptoms like headache, irritability,
photophobia, vomiting and drowsiness.
Surgical management
Infratemporal space can be reached either intraorally or extraorally.
Internal approach (Kruger) consists of an incision made in the buccolabial
fold lateral to the maxillary third molar. A curved haemostat is introduced
carefully behind the tuberosity of the maxilla and directed medially and
superiorly within the cavity. A drain is then inserted.
According to Laskin, a vertical incision is made medial to the upper extent
of the anterior border of ramus of the mandible. A haemostat is introduced
and passed superiorly into the infratemporal region and a drain is introduced.
In the presence of severe trismus, intraoral approach may not be possible.
In such cases, external approach consists of a horizontal incision made just
above the zygomatic arch (at the junction of frontal and temporal process of
the zygoma). A curved haemostat is introduced and directed in an inferior and
medial direction into the infratemporal space followed by the insertion of a
drain. The main disadvantage of this procedure is that it cannot produce a
dependent drainage.
Spaces related to lower jaw
Submental space
Boundary (Fig. 24.8)
Superior—Mylohyoid muscle
Inferior—Skin and subcutaneous tissue, platysma and deep cervical fascia
Medial—Single midline space with no medial wall
Lateral—Anterior belly of digastric (bilateral)
Anterior—Mandible
Posterior—Hyoid bone
FIGURE 24.8 Boundaries of submental space.

FIGURE 24.9 Submental space infection.
Contents
• This space has no vital structures

• Lymph nodes and anterior jugular veins
Involvement (Fig. 24.9)

Infection from lower incisors, lower lip, chin, tip of the tongue and anterior
part of floor of the mouth can spread to the submental lymph nodes and
subsequently cause infection of the submental space.
Neighbouring space
Submandibular space
Clinical features
Swelling in the midline, in the region of the chin and the region just beneath it.
Surgical management
The incision for drainage is made bilaterally through the skin, subcutaneous
tissue and platysma muscle at the most inferior aspect of the swelling. Rubber
drain is inserted through one incision, exited through the other and secured
with the help of sutures and dressing applied.
Submandibular space
Boundary (Fig. 24.10A)
Lateral—Skin, superficial fascia, investing fascia, platysma
Medial—Mylohyoid, hyoglossus, superior constrictor, styloglossus
muscles
Superior—Inferior and medial surface of the mandible and attachment of
mylohyoid muscle
Inferior—Anterior and posterior belly of digastrics muscle
FIGURE 24.10 (A) Boundaries of submandibular space. (B, C)

Infection of submandibular space.
Contents (Fig. 24.10B)
• Submandibular salivary gland and lymph nodes

• Facial artery
• Lingual nerve
• Lymph nodes
Submandibular space is enclosed by the investing layer of deep cervical

fascia and lies lateral to the sub-mental space.
Involvement (Fig. 24.10C)

Infection from the mandibular molars, most commonly second and third
molars, penetrates the thin lingual plate to pass directly into the
submandibular space (inferior to the attachment of mylohyoid muscle).
Infection from submental and sublingual spaces can pass backwards via
lymphatics.
Infection from the submandibular salivary gland may pass via lymphatics to
the submandibular lymph node
Infection from the middle third of the tongue, posterior part of the floor of
the mouth, maxillary teeth, cheek, maxillary sinus and palate
Neighbouring spaces
• Sublingual space
• Submental space
• Lateral, pharyngeal space
• Buccal space
Clinical features (Figs. 24.11A, 24.12)

Swelling is seen over the lower border of the mandible at the point where the
facial artery crosses it. Mouth opening is restricted. Swelling is seen beginning
at the lower border of the mandible and extending till the level of hyoid bone
in a shape of inverted cone.
FIGURE 24.11 (A) Left submandibular space infection. (B) Incision
and drainage established.
FIGURE 24.12 (A) Ludwig’s angina—I&D and tracheostomy done.
Note the devascularised skin overlying the swelling indicative of
necrotic tissue underneath. (B) Submandibular space infection—
inferior to mylohyoid muscle.
Difficulty in swallowing and moderate trismus seen
Spread
There are no anatomical barriers between the bilateral submandibular and
submental spaces hence the infection can easily spread across the midline and
involve the submandibular space on the contralateral side.
The submandibular space communicates with the sublingual space around
the posterior border of mylohyoid muscle
Submandibular space infection may extend backwards to involve the
parapharyngeal spaces.
Surgical management
Two stab incisions are made at the inferior aspect of the swelling in the
shadow of the mandible. The dissection is carried out through one of the
incisions with the curved haemostat in the abscess cavity. Blunt dissection
avoids the risk of injuring the facial artery, anterior facial vein and facial nerve.
The haemostat is passed through one incision and out through the other. A
thin rubber drain is passed through the stab incisions with the help of the
haemostat. The ends of the drain are sutured to prevent dislodgement.
FIGURE 24.13 (A) Boundaries of sublingual space. (B) Infection of
sublingual space.
FIGURE 24.14 Sublingual space.
Sublingual space
Boundary (Figs. 24.13, 24.14)
Superior—Mucosa of the floor of the mouth

Inferior—Superior surface of mylohyoid muscle
Medial—Midline raphae
Lateral—Medial surface of mandible
Contents
• Deep part of submandibular gland, sublingual gland and their

draining ducts (Wharton’s duct and ducts of Rivinus)
• Lingual nerve
Infections, which take a route on the lingual aspect of the mandible at a

point above the origin of the mylohyoid muscle and below the mucosa of floor
of the mouth, end up in sublingual space. These infections usually arise from
mandibular premolars or molars or from any direct trauma to the region.
Neighbouring spaces
• Submandibular space
• Lateral pharyngeal space
Clinical features
Swelling is seen on the anterior part of floor of the mouth, interferes with
swallowing and has severe tenderness.
Difficulty in speaking.
Floor of the mouth is raised and the tongue may be pushed superiorly
causing airway obstruction.
Source: Chronic Decayed mandibular anterior teeth, infected ranula,
infected lymph node with purulent discharge—lymphadenitis or an extension
of infections of the submandibular space.
Surgical management
Surgical approaches to the submental space for incision and drainage
Drainage of the abscess is obtained through
1. Extra oral approach—an external transverse skin incision between the

hyoid bone and the inferior border of the mandible.
2. Intra oral approach—Drainage can be obtained transorally by incising
the mucosa in the anterior part of the floor of the mouth, the incision
should be placed parallel to the submandibular duct. Blunt dissection
is indicated so as to not injure the lingual nerve or the submandibular
ducts.
When the submandibular space is affected, simultaneously both spaces
can be reached via a submandibular approach (extraoral).
Secondary fascial spaces (Fig. 24.15)
Temporal space
Temporal space has two compartments: superficial and deep.
FIGURE 24.15 Masticatory space.

Boundaries (Fig. 24.16)
Superficial compartment
Laterally—Temporal fascia
FIGURE 24.16 Boundaries of superficial and deep temporal

spaces.
Medially—Lateral surface of the temporalis muscle
Deep compartment
Laterally—Medial surface of the temporalis muscle
Medially—Temporal bone
Contents
Superficial temporal vessels, auriculotemporal nerve and temporal fat pad.
Clinical features
Patient complains of severe pain and trismus. Swelling is more obvious in the
superficial temporal space infection and will be restricted by the outline of the
temporal fascia superiorly and laterally and by the zygomatic arch inferiorly.
In case of associated buccal space infection, swelling has a characteristic
dumbbell shape due to absence of swelling over the zygomatic arch. A deep
temporal space infection produces less swelling and there will also be pain
and trismus.
Surgical management
Intraoral incision for drainage of the temporal abscess is same as that of
infratemporal space. The haemostat is passed superiorly along the lateral
aspect of the coronoid process to enter the superficial compartment. If
haemostat is passed superiorly along the medial aspect of the coronoid
process, it will enter the deep temporal compartment. In case of severe
trismus, an extraoral approach can be used to gain access into the temporal
space. This incision is also same as that used for extraoral incision of
infratemporal space. At first, the haemostat is passed medially to enter the
superficial space and later on blunt dissection is done through the temporalis
muscle to enter into the deep temporal space. Intraoral approach is preferred
over extraoral since intraoral approach provides more dependent drainage
over the entire area whereas the extraoral approach does not enter the inferior
aspect of the temporal space. Moreover, intraoral approach prevents the fibres
of the temporalis muscle from contracting against the drain and affecting the
flow of pus from the deep temporal space.

Parotid space is enclosed by the superficial layer of the deep cervical fascia
surrounding the parotid gland.
Extension of odontogenic infections into the parotid space is difficult since
the fascial covering is firmly attached to the gland. Parotid space can be
invaded by infections from the pterygomandibular, submasseteric or lateral
pharyngeal spaces.
Clinical features
Swelling extends from the zygomatic arch to the lower border of the mandible
anteriorly and from the anterior border of the mandible to retromandibular
region posteriorly.
Swelling everts the lobule of the ear and presents with severe pain especially
while eating. Intraorally pus may be milked from the parotid duct. Trismus is
not a sign of this space infection.
Differential diagnosis
Submasseteric space infection

Trismus will be present.
Management
The pus within the parotid space is present in different loculations, which
necessitates for a wide area of approach. Large incision is made in the
retromandibular area from lower aspect of lobule of the ear to angle of the
mandible. Blunt dissection with a haemostat is done avoiding injury to the
branches of the facial nerve. Multiple drains are used for drainage of the pus.
A curved incision at the angle of the mandible can also be made; blunt
dissection is done with a haemostat and a drain is placed.
Submasseteric space
Boundary (Figs. 24.17, 24.18)
Anterior—Buccal space, parotidomasseteric fascia

Posterior—Parotid gland and its fascia
Superior—Zygomatic arch
Inferior—Inferior border of mandible
Superficial or medial—Ascending ramus
Deep or lateral—Masseter muscle
FIGURE 24.17 Submasseteric space.
FIGURE 24.18 Illustration showing submasseteric space.
Contents
Masseteric artery and vein.
Especially pericoronitis of vertical or distoangular mandibular third molars
leads to submasseteric space abscess. Presence of buccinator muscle
attachment and position of the mandibular third molar in relation to it
determine the backward extension of pericoronal pus. This space
communicates freely with temporal space superiorly.
Neighbouring spaces
• Buccal space
• Pterygomandibular space
• Superficial temporal space
• Parotid space
• Infratemporal space
Clinical features (Figs. 24.19, 24.20)

Extraorally, the swelling is seen mainly over the angle of the mandible. It is
restricted to the masseter muscle as the forward spread is confined by the
tendon of temporalis, which is inserted into the anterior border of the ramus.
The lower border of the ramus controls inferior spread. Sometimes the
posterior mandibular sulcus may be obliterated. The infection is characterised
by severe trismus and throbbing pain. Chronic submasseteric space infection
can be punctuated by recurrent exacerbation, which can be controlled through
drainage and antibiotics but without a complete resolution. The masseter
muscle is more responsible for blood supply of ramus of the mandible than the
body, which is mainly supplied by mandibular artery. Because of this,
ischaemia results in that part of the bone denuded of periosteum by the
abscess, which leads to osteomyelitis with sequestrum formation. Extent of
bone destruction depends upon the area of bone in contact with the pus. Often
submasseteric infection leads to subperiosteal new bone deposition beneath
the periosteum, an important clue to the diagnosis.
FIGURE 24.19 (A) Submasseteric space infection. (B)

Postoperative view.
FIGURE 24.20 Illustration showing left submasseteric space
infection in relation to infected 38.
Surgical management
A vertical incision is made intraorally along the external oblique line of the
mandible. A haemostat is inserted through this incision and passed posteriorly
along the lateral aspect of the ramus beneath the masseter muscle and the
beaks are opened for free escape of the pus. A rubber drain is inserted and
sutured to the incision margin. Extraoral approach involves a small incision
beneath the angle of the mandible and blunt dissection is done with the help of
the haemostat. A rubber catheter is inserted in the wound for drainage.
Peritonsillar abscess
However, there is no trismus or dental involvement in this condition. (Refer
page 547)
Anterior—Buccal space
Posterior—Parotid gland with lateral pharyngeal space
Superior—Lateral pterygoid muscle Inferior—Inferior border of mandible
Superficial or medial—Lateral surface of medial pterygoid muscle
Deep or lateral—Medial surface of ascending ramus of mandible
FIGURE 24.21 Boundaries of pterygomandibular space.
Contents
Mandibular division of trigeminal nerve, inferior alveolar artery and vein
Infection can spread to pterygomandibular space from mandibular third
molar region especially from pericoronitis involving the third molar. Infection
can also be caused by contaminated needle and maxillary third molar.
Infection can also spread into the parapharyngeal space by extending medial
to the medial pterygoid space.
Neighbouring spaces
• Buccal space
• Lateral pharyngeal space
• Submasseteric space
• Deep temporal space
• Parotid space
• Peritonsillar space
Clinical features
Extraorally, the swelling is not very obvious. Intraorally, there is visible
swelling of the soft palate on the same side, swelling of the anterior tonsillar
pillar and deviation of the uvula to the opposite side. The patient has severe
trismus and dysphagia. Therefore in cases of pterygomandibular space
infection, we have to carefully examine intraorally using anaesthetic spray to
arrive at a proper diagnosis.
Surgical management
Because of the severe trismus either general anaesthesia is used or the
mandibular nerve is blocked extraorally with local anaesthetic. The incision for
drainage is made between medial aspect of the ramus of mandible and the
pterygomandibular raphe, and the abscess cavity is opened by blunt dissection
using a haemostat. Rubber drain is placed and sutured to one of the margins
of the incision to prevent dislodgement. This would help in sufficient
drainage.

Anterior—Superior and middle pharyngeal constrictor

Posterior—Carotid sheath, stylohyoid, styloglossus and stylopharyngeus
Superior—Skull base
Inferior—Hyoid bone
Superficial or medial—Superior pharyngeal constrictors and
retropharyngeal space
Deep or lateral—Medial pterygoid muscle and capsule of parotid gland
FIGURE 24.22 Lateral pharyngeal space.
Contents
Carotid artery, internal jugular vein, vagus nerve, and cervical sympathetic
chain
Lateral pharyngeal space may be infected from abscess extending
backwards from the mandibular third molar area or more commonly, one
passing laterally from the tonsillar abscess. Infection can also spread
backwards from a sublingual, submandibular and pterygomandibular space
infection.
Neighbouring spaces
• Pterygomandibular
• Submandibular
• Peritonsillar
• Sublingual
• Retropharyngeal
Clinical features
Severe pain on the affected side of throat and dysphagia are present. The
tonsil, tonsillar pillar and uvula are seen to be displaced to the medial side.
The four cardinal signs of lateral pharyngeal abscess are trismus, induration
and swelling of angle of the jaw, fever and pharyngeal bulging. Rotation of the
neck away from the side of the swelling causes severe pain from tension on the
ipsilateral sternocleidomastoid muscle. Complications of lateral pharyngeal
abscess include septic jugular thrombophlebitis and carotid artery erosion.
Inequality of the pupils due to involvement of cervical sympathetic and
bleeding from nose, mouth or ear can be a warning of such a disastrous sequel.
These infections have a potential to spread upwards causing cavernous sinus
thrombosis, meningitis and brain abscess. They can also spread into the
retropharyngeal space.
Surgical management
There are multiple approaches to the lateral pharyngeal space: intraoral,
extraoral and a combination of both.
Intraoral incision can be either transpharyngeal or lateral. The
transpharyngeal approach is made through the tonsillar fossa, but this
approach is not recommended since adequate drainage is very difficult to
obtain.
Intraoral approach is more easily performed in making an incision between
the ramus and medial pterygoid and dissecting bluntly with a haemostat
medial and posterior to the medial pterygoid muscle into the parapharyngeal
space. All peroral incisions are contraindicated when there has been prior
haemorrhage no matter how minimal. Extraoral submandibular incision is the
safest approach and should be used if there is any involvement of posterior
compartments. In extraoral approach, an incision is made anterior and inferior
to angle of the mandible and blunt dissection with haemostat is carried
superficially and medially along the medial pterygoid muscle into the
pharyngeal space. In the combined intraoral and extraoral approach, the
lateral mucosal incision is made and a large curved haemostat is passed lateral
to the superior constrictor and medial to the medial pterygoid muscle. A blunt
dissection is carried out posteroinferiorly below the angle of the mandible. The
tip of the instrument is palpated extraorally anterior to the
sternocleidomastoid and a cutaneous incision is made over the tip. This
technique offers direct access into the lateral pharyngeal space and aids in
correct placement of the external incision in a swollen face. A drain is inserted
and sutured to the wound margin to allow drainage.
Anterior—Superior and middle constrictors

Posterior—Alar fascia
Superior—Skull base
Inferior—Fusion of alar and prevertebral fascia at T4
Superficial or medial—Common space, no wall
Deep or lateral—Carotid sheath and lateral pharyngeal space
FIGURE 24.23 Retropharyngeal space.
Contents
Lymph node, no major structures.
Clinical features
Clinical symptoms include pain, fever, stiffness of the neck, dyspnoea,
drooling and dysphagia. Bulging of the posterior pharyngeal wall is often
more prominent on one side because of adherence of the median raphe of the
prevertebral fascia, but this is difficult to appreciate. Retropharyngeal abscess
should be considered the most dangerous deep neck space abscess, because
complications include supraglottic oedema with airway obstruction, aspiration
pneumonia due to rupture of the abscess and acute mediastinitis. It represents
the main avenue for spread of infections into the mediastinum. Mediastinitis is
the most feared complication that may result in empyema or pericardial
effusion. If the infection perforates the alar layer posteriorly, it enters the
danger space (between alar and prevertebral layers), which extends down the
entire mediastinum to the level of diaphragm. This condition is characterised
by dyspnoea and chest pain.
Surgical management
In most of the cases, the retropharyngeal space abscess will result from an
extension of lateral pharyngeal space infection and therefore will not be
drained independently.
In conditions where independent drainage is necessary, an intraoral
approach is made. A vertical incision is made on the pharyngeal wall lateral to
the midline. Using a haemostat, abscess cavity is opened by blunt dissection
while the patient is in Trendelenburg position to avoid aspiration of the pus.
In case of concern about the rupture of the abscess, extraoral approach is
used for drainage. An incision is made along the anterior border of the
sternocleido-mastoid inferior to hyoid bone and the muscle and carotid sheath
retracted laterally. Dissection between the carotid sheath and the inferior
constrictor helps in the drainage of retropharyngeal space.
Danger space: It is the potential space between the alar and prevertebral
division of the deep layer of the deep cervical fascia.
Why is it danger?
The danger space at its inferior border it is continuous with the posterior
mediastinum containing vena cava, arch of aorta, thoracic duct, tracha and
oesophagus. Erosion of the major blood vessels, lower airways and upper
digestive tract leads to death of the patient.

Peritonsillar abscess or quinsy is a deep neck infection that is usually
secondary to contiguous spread from the local sites or as a complication of
acute tonsillitis that is rarely life threatening in itself. It can spread to involve
the lateral pharyngeal space. The peritonsillar space is a potential space of
loose areolar tissue that surrounds the tonsil and is bounded laterally by
superior constrictors.
Clinical features
The infection is characterised by swelling of the tonsils, uvular displacement,
trismus and muffled voice. The infection generally starts in the intratonsillar
fossa, which is situated between the upper pole and body of the tonsil and
eventually extends around the tonsil. Quinsy is usually unilateral but can
rarely occur bilaterally. Most abscesses occur in younger patients who present
with fever, sore throat and dysphagia.
Complications
Spontaneous rupture and aspiration, contiguous spread to pterygomaxillary
space.
Surgical management
If the patient is not seen until the pus is formed or if the antibiotic therapy
fails, the abscess must be drained. But since peritonsillar abscess often tends to
recur, tonsillectomy should be performed 6–8 weeks after formation of the
abscess.
Life threatening complication of orofacial

infections
Related to lower jaw:
• Ludwig’s angina
• Mediastinitis
• Involvement of carotid sheath
Related to upper jaw:
• Intracranial complications like cavernous sinus thrombosis, brain

abscess, dural meningitis and osteomyelitis of skull
• Retrobulbar cellulitis leading to blindness
Ludwig’s angina
Ludwig’s angina is a form of a firm, acute, toxic and severe diffuse
cellulitis/induration that spreads rapidly, bilaterally affecting the
submandibular, sublingual and submental spaces. It was first described by
Wilhelm Friedreich Von Ludwig in 1836. The term ‘Ludwig’s angina’ was
coined by Camerer in 1837, who presented the classic case of Ludwig’s angina
which was described in 1836 by Wilhelm Ludwig.
Classic Ludwig angina—Definite bilateral involvement of all the three spaces i.e.,
submandibular, sublingual and submental spaces.
The word ‘angina’ derived from Latin word ‘angere’ meaning suffocation or
choking sensation; and the word ‘Ludwig’ from the person who first described
it. Ludwig presented the classical features of the disease and successfully
treated the same for Franklin NN.
The condition has established for its unique identity among general medical
personnel with three ‘F’
It was to be feared
It rarely become fluctutant
And it was often fatal
Other names:
• Marbus strangulatorius: chocking effect of the disease

• Angina maligna
• Garrotillo: Spanish version for Hangman’s noose
Aetiology
Ludwig’s angina is a disease primarily of dental origin although various
causes can also be related.
Odontogenic
1. Odontogenic infection
Dental aetiology has been reported as the causative factor in 90% of cases,
either as primary dental infection or as postextraction phenomena.
It is generally of dental origin, following infection of the second and third
mandibular molars (70%–80%). The roots of these teeth often spread
below the crest of the mylohyoid muscle, leading to periapical infection
that reaches the submandibular space and from here, bilaterally to the
contralateral submandibular, submental and sublingual spaces.
Acute dentoalveolar abscess (commonly from mandibular 2nd
and 3rd molar)
Acute periodontal abscess
Acute pericoronal abscess (in relation to erupting 3rd molar)
Infection from these causes may spread to submandibular spaces, buccal
space, sublingual space, pterygomandibular space. Mostly originate in
association with mandibular second and third molars due to its
anatomical relationship of the teeth and the involved spaces. The buccal
bone around the teeth is thicker than the lingual bone.
2. Traumatic injuries of orofacial region
• Compound/comminuted mandibular fractures
• Oral soft tissue lacerations
• Puncture wounds of floor of the mouth
• Osteomyelitis secondary to compound mandibular fractures
3. Submandibular and sublingual sialadenitis
4. Secondary infections of oral malignancies
5. Pharyngeal infection or tonsillitis.
6. Iatrogenic: Use of contaminated needle for giving local anaesthesia
7. Cervical lymphoid tissues
8. Miscellaneous: Foreign bodies such as fish bone
Pseudo-Ludwig’s angina/pseudo-Ludwig’s phenomena

This term is applied to cases of nondental origin.
Microbiology
• As Ludwig’s anginais commonly of dental origin, streptococci, or

mixed oral flora are the most commonly reported organisms.
• Presence of staphylococci, E. coli, Pseudomonas and anaerobes including
Bacteroides, Pepto streptococcus, Prevotella species, fusospirochetes have
also been isolated.
• The role of anaerobes as primary or synergistic organisms should not
be omitted in culture.
Clinical features
General examination
General constitutional symptoms: Patient looks toxic, very ill, dehydrated,
chills and malaise.
Marked pyrexia
Difficulty in swallowing (dysphagia)
Impaired speech and hoarseness of voice
Regional examination
Extraoral examination:
• Bilateral suprahyoid swelling is observed, with a hard, cardboard-like

consistency.
• Swelling is firm/hard brawny involving bilateral submandibular and
submental regions which soon extend down the anterior part of the
neck of the clavicles, swelling present with ill-defined borders. It is
nonpitting, not-fluctuating and tender on palpation.
• Airway obstruction and cyanosis may occur due to progressive
hypoxia
• Difficulty in swallowing and breathing, chills, fever, increased salivation,
restricted tongue movements and inability to close the mouth are the most
salient presenting clinical features of the illness.
• Early presentation has no suppuration but occurs late in the course of
disease. Further, this phenomenon appears very rapidly and does not
respect any anatomic barrier.
Mouth remains open due to the oedema of sublingual tissues and there is a
resultant raised tongue with restricted movements.
• Shallow breathing with accessory muscles of respiration being used

and respiratory rate may be raised
• Severe muscle spasm leading to trismus with restricted mouth opening
and also jaw movement.
• Fatal death may occur in untreated case of ludwig’s angina within 10–
24 h due to asphyxia.
Intraoral examination:
• Swelling develops rapidly and involves sublingual spaces causing

elevation of tooth against the palate.
• Increased salivation, stiffness of tongue, difficulty in swallowing with
hot potato speech is noted.
• Drooling of saliva due to reduced control of muscles and jaw posture.
• Backward spread of infection leading to oedema of the glottis, which
leads to obstruction of airway.
• Development of Stridor being the alarming sign for fatal extension
necessitating emergency intervention to keep airway patent.
Potential complications
It is a potentially serious infection that can lead to septicaemia, upper
respiratory airway obstruction and provoke oedema of the epiglottis.
On the other hand, it can also spread to the submassetric, pterygopalatine
spaces, parapharyngeal and paratonsillar spaces and from there it can proceed
to the mediastinum, producing thoracic empyema.
Aspiration pneumonia and vascular erosion have been cited as possible
complications. The most common cause of mortality is acute obstruction of the
airways.
Rarely the infection may spread below and reach close to carotid sheath,
pterygopalatine fossa, leading to cavernous sinus thrombosis with subsequent
meningitis
If untreated ludwig’s angina can be fatal within 12–24 h due to asphyxia.
Diagnosis
Diagnosis is made on the basis of clinical findings, although CT studies can
help to determine the extent of the infection, especially when there is abscess
formation.
Treatment
Ludwig’s angina should be considered as the life-threatening emergency.
Treatment must be vigorous and initiated early with administration of
antibiotics as for any odontogenic infections and prophylactic incision and
drainage of the spaces involved, without waiting for fluctuation to appear. The
airway must also be controlled, often requiring tracheostomy.
Surgical management (Fig. 24.24 A–J)

Surgical management is necessary in case of rise of tissue tension and as a
provision for drainage. In a classic case of Ludwig’s angina, little amount of
pus is evacuated. Bilateral drainage of submandibular spaces along with the
drainage of sublingual and submental spaces is the recommended therapy. It
is preferable to drain sublingual and submental spaces separately to avoid
perforation of the mylohyoid muscle.
FIGURE 24.24 (A) Preoperative view showing raised tongue
position, trismus and facial distress. (B) Swelling of bilateral
submandibular, submental, left masseteric, infratemporal and
temporal spaces. Skin appears erythematous and shiny. (C)
Orthopan tomogram showing grossly decayed left mandibular
second and third molars. (D) Blunt dissection done into both
submandibular and submental spaces breaking the pus locules.
(E) Active pus discharge. (F) Removal of the source of infection—
extracted mandibular left second and third molars. (G) Through
and through drain placement connecting both submandibular and
the submental spaces. (H) Stab incision made for drainage of left
temporal space. (I) Irrigation using two-way drain. (J) Postoperative
view after 1 week.
Distant spread
Distant spread can occur by means of the bloodstream, essentially via internal
jugular vein in the same direction as the blood flow. Cardiac colonisation can
result, leading to bacterial endocarditis, although the disease may be seeded
practically in any organ. It can also follow a retrograde pathway towards
cavernous sinus of the skull, establishing thrombophlebitis at some point in
the facial venous system. Aseptic thrombus is formed, replete with
microorganisms, which can then spread to distant areas, causing the much
feared neurological complications, such as thrombosis of the cavernous sinus,
encephalic abscesses and meningitis.
Carotid space infection (Fig. 24.25)

Carotid space infection produces a tender swelling in the lateral aspect of the
neck under the sternocleidomastoid muscle. Patients will experience pain on
palpation while rotating the head laterally. Usually there will be torticollis
towards the unaffected side.
FIGURE 24.25 Carotid space.
An incision is made along the middle third of the anterior border of the
sternocleidomastoid muscle. Through a vertical incision, carotid sheath is
exposed carefully after retracting the muscle posteriorly. Internal jugular vein
should be ligated to prevent infection if it is thrombosed.
Lincoln’s highway: It is a potential space within the carotid sheath, which

extends from jugular foramen and carotid canal to the mediastinum.
Cerebral abscess
Cerebral abscess may be the consequence of cavernous sinus
thrombophlebitis, but can also be due to septic metastasis and bacteraemia
accompanying odontogenic infections. Organisms on reaching the brain
produce inflammation, localised oedema and septic thrombosis.
Brain abscesses have been associated with oral manipulations such as dental
extractions, dental and periodontal surgery and injection of local anaesthetics
or dental prophylaxis, which suggests that the mechanism responsible for
producing septicaemia is not as critical as the host response. There has been an
increase in the incidence of brain abscesses in immunocompromised patients,
in both transplant recipients as well as in AIDS patients. Brain abscesses are
rare, with a prevalence of 1 per 1, 00, 000 inhabitants and a mortality rate of
0%–24%.
Cerebral abscesses consist of localised suppurative areas inside the cerebral
parenchyma, preferentially located in the temporal lobe, followed by the
cerebellum. They can occur following brain trauma, after surgery or they may
be secondary to septic infection located anywhere in the body that can
disseminate by means of direct spread or via the bloodstream, as seen in
odontogenic infections.
The agents that are isolated from samples of brain abscess contents depend
on the source of infection; when the cause is dental, Streptococcus viridans,
Bacteroides, Actinobacillus actinomycetemcomitans have all been isolated.
Clinical signs necessarily depend on location of the infection site in the brain,
but common symptoms result from elevated intracranial pressure, with
intense headache, nausea and projectile vomiting. Cerebral irritation may
present as convulsions, asphyxia, changes in character and behaviour, when
the frontal lobe is involved. The patient may also present temporal-spatial
disorientation, etc. Diagnosis is confirmed by means of a CT scan and
papillary stasis evident with ophthalmoscope. Other signs and symptoms are
hemiplegia, papilloedema, hemisensory deficit and abducent nerve palsy.
Management
The main line of management is antibiotics, antiinflammatory drugs, steroids
and mannitol to reduce cerebral oedema as well as surgical drainage.
Meningitis
Meningitis is the most commonly occurring neurological complication, albeit it
is rare. It may develop from metastatic spread or it may be due to nearby
thrombophlebitis.
Clinical features
Clinically, it debuts with intense headache, mental confusion, irritability,
stupor, high fever with chills, vomiting and stiff neck (Brudzinski’s sign).
Convulsions may occur.
Kernigs sign: Flexing the patient’s hip 90 degree then extending the patient’s
knee causes pain
Brudzinski’s sign: Flexing the patient neck causes flexion of the patient’s hip
and knees.
Diagnosis:
It is based on cerebrospinal fluid analysis cloudy or purulent opalescent
fluid obtained on spinal tap. Upon examination of the CSF,
polymorphonuclear leucocytes as well as elevated protein levels and
decreased glucose levels are detected.
Management
Neurological complications require hospital care. Initiating treatment with
chloramphenicol 4 g/day IV because of its broad-spectrum activity, associated
with penicillin G at a dose of 24 million units/day IV, while the microorganism
is being identified through culture and sensitivity, and its sensitivity profile is
being determined. The maintenance of hydroelectrolytic balance is also
recommended in addition to controlling cerebral oedema and preventing
collapse and shock.

When a thrombus is formed at some point in the facial venous system, it can
undergo retrograde spread towards the cavernous sinus, giving rise to
thrombosis. It has been estimated that 7% of all cases of thrombosis of the
cavernous sinus are of dental origin. The infection begins with unilateral
involvement, but can develop bilaterally through the intercavernous sinuses.
Route:
1. Danger area of face (external route): Infection from the face and lip is
carried by facial and angular veins and nasofrontal veins (danger area
of face) to the superior ophthalmic veins which enters through superior
orbital fissure to the cavernous sinus
2. Pterygoid plexus of veins (internal route): Infection from dental origin
enters the pterygoid plexus from posterior maxillary region from here
through inferior orbital fissure into the terminal part of the inferior
ophthalmic vein and then through the superior orbital fissure into the
cavernus sinus
3. Emissary vein: Pterygoid plexus is connected to cavernous sinus
through emissary vein.
External route (facial route) is a very rapid short fulminating course because
of large open system of veins leading directly to cacernous sinus. Infection
from one side will involve the opposite side through circular veins.
Clinical features
The first symptoms to appear are eye pain, sensitivity of the eyeball to
pressure and signs of severe toxic infection, high fever, chills, tachycardia and
sweating. Pulsatile exopthalmos is seen where the carotid pulse is transmitted
through retrobulbar oedema. Subsequently, venous obstruction produces
palpebral oedema, ptosis, tearing of the eye, chemosis and retinal bleeding.
When the process progresses further, cranial nerves are also affected,
producing ophthalmoplegia and palpebral ptosis; corneal reflexes are
decreased or absent and mydriasis results. The involvement of cranial nerves
III, IV, VI and the carotid sympathetic plexus also occur. The organisms that
have been identified as causal agents are Streptococcus, Staphylococcus and
Gram-negative bacteria.
Late complications like thrombophlebitis are seen in untreated cases.
Advanced stage presents with toxemia, meningitis, stiffness of neck with
positive Kernigs and Brudzinski’s sign and Biot’s respiration,
Eagleton criteria Diagnostic criteria were suggested by Eagleton prior to the
introduction of modern investigative procedures and comprise of:
1. A known site of infection or septicaemia.

2. Early destructive signs (such as full retinal veins, proptosis,
exophthalmos, collateral venous circulation).
3. Oculomotor pareses and trigeminal nerve involvement.
4. Neighbourhood abscesses from the thrombophlebitis situated in the
orbit, nasopharynx, occiput or neck.
5. Symptoms of complication such as headache, papilloedema and
meningeal signs.
Treatment
Early diagnosis is necessary for prompt treatment and favourable prognosis.
Treatment involves therapy with antibiotics and steroids.
Heparinisation—to prevent the extension of thrombosis. Heparin 20,000
units in 1.5 L of 5% dextrose or Dicumarol 200 mg may be given orally for first
day and 100 mg daily.
Mannitol—to reduce oedema
Surgical drainage
Mediastinitis
Odontogenic infections and Ludwig’s angina are uncommon, but when they
occur, they are life threatening due to airway obstruction or mediastinitis. The
spaces that are mainly involved are lateral pharyngeal space and the
retropharyngeal space. In the neck, the muscles and aponeurosis are oriented
in the vertical plane, creating a space that joins the posterior part of the mouth
with the mediastinum, in a chimney-like manner. This is where the major
structures, the carotid artery, vagus nerve and internal jugular vein covered by
perivascular fascia pass through. When this area becomes infected, it can lead
to mediastinitis, also known as descending necrotising mediastinitis. It is an
uncommon and serious complication. The rapid spread of cellulitis tends to be
due to both aerobic, as well as anaerobic bacteria, in a synergistic fashion.
Clinical features
The clinical signs are classically presented by these abscesses in the
parapharyngeal and retropharyngeal spaces include dysphagia, dyspnoea,
stiff neck and oesophageal regurgitation. Swelling appears on the side of the
neck underneath the sternocleidomastoid muscle. It is painful on palpation
and, on a functional level, causes stiff neck. When infection reaches the
mediastinum, the patient experiences retrosternal pain, severe dyspnoea and
nonproductive cough. It may also present as oedema and crepitation in the
upper thorax. The patient’s general health status deteriorates with fever and
chills.
Diagnosis
The anteroposterior chest X-ray reveals broadening of the mediastinal space
and presence of air at this level. Lateral X-ray of the neck reveals displacement
of posterior wall of the pharynx together with the presence of free gas.
Mortality rate associated with this form of mediastinitis is high, often due to
difficulty in making an early diagnosis, since dysphagia, dyspnoea, swelling of
the neck and crepitation are all late signs of the condition.
Potential complications
Mediastinitis can course with severe complications such as septicaemia,
abscess formation, pleural effusion, empyema, compression of the local blood
vessels, pericarditis and death. When there is vascular involvement there will
be septicaemia, with abrupt rise in temperature, chills, sweats and shock.
Medical management
In these patients, intravenous administration of antibiotics at maximum doses
and support measures that can only be given in intensive care units (ICU) are
mandatory. The association of penicillin G and metronidazole or
chloramphenicol against the anaerobes is often considered shock therapy;
when the Gram-negative microorganisms are also involved, gentamicin or
tobramycin is added.
Surgical intervention
Surgical intervention is aimed at incision and drainage. A transcervical
approach has been recommended, performing a wide incision in the area of
the anterior edge of the sternocleidomastoid muscle and reaching all the way
to the mediastinum by means of blunt, finger dissection through the
pretracheal space. This procedure reduces the risk of injuring vascular
structures. After abundant irrigation of the affected spaces, continuous suction
drains are placed. During the postoperative period, the patient must be placed
in the Trendelenburg position to facilitate drainage of the mediastinum.
Necrotising fasciitis of the head and neck

(Fig. 24.26)
Necrotising fasciitis of the head and neck is a multimicrobial, uncommon soft
tissue infection that spreads very quickly. It is characterised by formation of
large necrotic lesions and gas formation, located in the subcutaneous tissue
and in the superficial fascia. As the disease progresses, muscle and skin
involvement develops, giving rise to myonecrosis and spots in the area, as a
consequence of the feeder vessels that pass through the infected fasciae.
FIGURE 24.26 Necrotising fasciitis of face.
If the necrotising fasciitis does not receive surgical care, generalised toxicity
occurs with multisystem organ failure. Necrotising fasciitis is a rare, but
potentially fatal disease that occurs predominantly in the limbs and abdominal
wall following trauma or surgery and less commonly in the head and neck.
Dental infections comprise the most frequent cause in the head and neck
although it can also be due to pharyngeal infections. Immunosuppressed
states of peripheral vascular disease and diabetes mellitus have also been
reported to be predisposing factors, although the illness has also been detected
in healthy patients.
Causative organism
Aerobic microorganisms, particularly Group A-haemolytic Streptococcus and
Staphylococcus, were initially considered to be the causal agents in necrotising
fasciitis. It was later demonstrated that the strict anaerobes played a very
important role, representing a mixed or synergistic infection. Microorganisms
of the Bacteroides genus, Proteus, coliforms and Peptostreptococcus have been
isolated, as have been Enterobacter and Pseudomonas. The fulminating nature of
the necrotic process is the result of a symbiotic relationship between both
types of bacteria, with alteration of the oxygen reduction potential and a
microenvironment that fosters the growth of anaerobic bacteria. Bacterial
enzymes and cell wall components play an essential role in local tissue
destruction, dissemination of the infection and systemic toxicity.
Clinical features
• The initial clinical signs and symptoms are non-specific, soft tissue
involvement which then progresses, producing gangrene of the
subcutaneous cell tissue and muscular aponeurosis.
• There may be intense pain at the onset of the disease, whereas during
the course of illness, paraesthesia or even anaesthesia may develop in
the affected area as a result of nerve involvement.
• As the necrotising fasciitis evolves, the skin is affected; it turns purple
or dark with poorly defined edges.
• Vesicles later appear with a foul-smelling, purulent exudate.
• Cutaneous necrosis is detected on the fourth or fifth day. Over the
time, necrotic tissue begins to separate with suppuration
(approximately on the eighth day).
• If the necrotising process continues to spread, it involves the
neighbouring tissues and provokes local or systemic complications,
such as neck organ involvement, pneumonia, pulmonary abscess,
vascular erosion, venous thrombosis and cranial neuropathies.
• The associated manifestations as fever, crepitation and other features
of sepsis may be present.
• Computerised axial tomography and magnetic resonance imaging are
the most useful imaging studies for early diagnosis of necrotising
fasciitis, detecting gas in the soft tissues and deep spaces of the neck.
Management
In these patients, the disease must be recognised very quickly. This is a
difficult task due to the nonspecific nature of the clinical presentation. It is not
hard to confuse necrotising fasciitis with cellulites of dental origin, erysipelas
and with gangrenous necrosis due to Clostridium.
Treatment is based on antibiotic therapy, dental treatment of affected teeth
and surgical drainage of the lesion. Initially, broad-spectrum antibiotics are
administered intravenously and are aimed at eliminating the causative
microorganisms of the odontogenic infections. These antibiotics can be
subsequently modified, once the culture results and antibiogram are obtained.
Immediate surgical treatment is obligatory, with incisions and drainage, in
addition to vigorous debridement of the fasciae, subcutaneous tissue, muscles
and necrotic skin, requiring general anaesthesia in most cases. It is important
that the airway be maintained open, since they may be compromised as a
result of the oedema and necrosis produced by the necrotising fasciitis.
Intubation is difficult in these patients and tracheostomy is often needed.
Infections might pass anteromedially across the genial muscles into
sublingual space on the other side. Infections can also spread to submental and
submandibular spaces and lead to Ludwig’s angina. Sublingual space also
communicates with the parapharyngeal space at the posterior border of the
mylohyoid muscle lateral to hyoid bone.
Surgical management
An intraoral incision is placed at the base of the alveolar process in the lingual
sulcus. Care should be taken not to injure the sublingual gland, lingual nerve
and submandibular duct. To evacuate the pus a haemostat is inserted in the
anterior and posterior direction and beneath the sublingual gland. A rubber
drain is placed and sutured to avoid displacement. When infection crosses the
midline there will be a bilateral swelling of the sublingual space, in which case
a bilateral incision is made to drain the pus.
CHAPTER 25
Osteomyelitis,
Osteoradionecrosis and
Osteochemonecrosis
Osteomyelitis
Aetiology
Pathogenesis
Classification
Acute suppurative osteomyelitis
Chronic suppurative osteomyelitis
Infantile osteomyelitis
Diffuse sclerosing osteomyelitis
Focal sclerosing osteomyelitis
Garre’s chronic nonsuppurative sclerosing osteitis
Management of osteomyelitis
Medical management
Surgical (supportive) management
Sequestrectomy
Saucerisation
Decortication
Resection
Osteoradionecrosis
Risk factors
Pathogenesis
Marx’s theory: 3 ‘H’ concept—hypocellularity, hypoxia
and hypovascularity
Clinical findings
Treatment
Osteochemonecrosis
Mechanism of bisphosphonates
Stages of BRONJ
Risk factors
Prevention modalities of BRONJ
Treatment strategies
Treatment of medication-related osteonecrosis of the jaw
Osteomyelitis
Osteomyelitis is primarily an inflammation of the medullary portion of the
bone. The process rarely is confined to the endosteum and usually affects the
cortical bone and the periosteum also. Therefore, osteomyelitis may be
considered as an inflammatory condition of the bone that begins as an
infection of the medullary cavity, rapidly involves the Haversian system and
quickly extends to the periosteum of the area. When infection becomes
established in the calcified portion of the bone, the pus in the medullary cavity
and subperiosteal compartment compromises or obstructs the blood supply.
Following ischaemia, the infected bone becomes necrotic.
Aetiology
Odontogenic infections:
1. In the jaws, contiguous spread of odontogenic infections that originate

from pulpal or periapical tissues is the primary cause of infection.
2. Trauma, especially untreated compound fractures, is the second
common cause.
3. Infection from periostitis after gingival ulcerations, lymph nodes,
infected furuncles or lacerations and haematogenous origin may also
cause, although, they are less common in jaw osteomyelitis.
Low incidence of osteomyelitis of the jaws is remarkable considering high
frequency and severity of odontogenic infections. This low incidence is a result
of host resistance capable of overcoming the virulence of the microorganism.
The virulence of the microorganisms overpowers when there is a reduction in
the host defence mechanism or jaw vascularity. Therefore they are important
in the onset and severity of osteomyelitis.
Systemic and local conditions that alter the host’s resistance influence the
course of the disease include:
• Diabetes mellitus, autoimmune disorders, agranulocytosis, anaemia

especially sickle cell, leukaemia, AIDS, syphilis, malnutrition,
chemotherapy for cancer, steroid drug use.
• Alcohol and tobacco abuse are frequently associated with
osteomyelitis.
• Conditions that alter vascularity of bone predispose patients to
develop osteomyelitis. These include: radiation, osteoporosis,
osteopetrosis, Paget’s disease, fibrous dysplasia, bone malignancy and
bone necrosis caused by mercury, bismuth and arsenic.
Pathogenesis
• Extensive blood supply of the maxilla makes it less prone to
osteomyelitis when compared to the mandible. The thin cortical plates
and the porosity of the medullary portion preclude infections from
becoming confined in the bone and facilitate spread of oedema and
purulent discharge into adjacent tissues.
• The mandible, in this aspect, resembles long bones with a medullary
cavity, dense cortical plates and well-defined periosteum.
• The cortical bone is enveloped by periosteum which consists of an
outer fibrous layer and an inner layer of osteogenic cells.
• Compromise of blood supply is a critical factor in the establishment of
osteomyelitis. Primary blood supply to the mandible is from the
inferior alveolar artery, while periosteal supply is from a secondary
source.
• Acute inflammation that causes hyperaemia increased capillary
permeability and infiltration of granulocytes is the trigger that leads to
osteomyelitis. When proteolytic enzymes are released along with the
destruction by bacteria, vascular thrombosis will ensue, causing tissue
necrosis. If this pus is not walled off by the host, confining it in an
abscess, or if the pus does not escape to surrounding soft tissues from
the medullary bone, then the process of osteomyelitis is initiated.
• Necrotic tissue, dead bacteria within white blood cells (pus)
accumulate, increasing the intramedullary pressure resulting in
vascular collapse, venous stasis and ischaemia.
• Pus travels through the Haversian system and the nutrient canals and
accumulates beneath the periosteum which gets elevated from the
cortex and further decreases the blood supply. When inferior alveolar
neurovascular bundle is compressed, thrombosis and ischaemia
accelerates. This results in osteomyelitis-induced inferior alveolar nerve
dysfunction.
• If the pus continues to accumulate then periosteum is penetrated
developing mucosal and cutaneous abscesses with fistulae. The
periosteum in children is less bound to the cortical bone thus allowing
for more extensive elevation.
• With good host defence mechanism, the chronic inflammation
regresses and granulation tissue forms. Necrotic bone becomes
separated from the viable bone (sequestra).
• Small sections of bone may become completely lysed while larger ones
may become isolated by a bed of granulation tissue encased in a
sheath of new bone (involucrum).
• Sequestra may be revascularised, remain quiescent, resorb, or become
chronically infected requiring surgical removal for complete resolution
of the infection. When involucrum is penetrated by channels, called
cloacae, pus escapes to the epithelial surface creating fistulae (Fig. 25.1).
FIGURE 25.1 Pathogenesis of mandibular osteomyelitis.
Classification
Osteomyelitis can be classified according to duration, presence of suppuration
and cause.
Suppurative osteomyelitis
• Acute suppurative
• Chronic suppurative
▪ Primary (no acute phase preceding)
▪ Secondary (follows acute phase)
• Infantile
Nonsuppurative osteomyelitis
• Diffuse sclerosing
• Focal sclerosing
▪ Proliferative periostitis (Garre’s periostitis ossificans)
• Osteoradionecrosis
Other special and less common forms are: syphilitic, tuberculous, brucellar,
fungal, viral, chemical, Escherichia coli and Salmonella osteomyelitis.
Acute suppurative osteomyelitis

Acute suppurative osteomyelitis is a serious sequela of a periapical infection
that results in a diffuse spread of the infection throughout the medullary
spaces with subsequent necrosis of a variable amount of bone. History may
reveal any one of the following: recent extraction, infection, debilitating
disease.
Clinical features
• Deep intense jaw pain

• Abscess
• High intermittent fever
• Paraesthesia of the lip (classic symptom)
• No fistulae
• Diffuse swelling
• Loosening of teeth
• Pus discharge
• Trismus
Radiographic features
On initial examination, often no radiographic findings or localised periapical
radiolucency are seen. Radiographic changes occur between 10 and 20 days. A
well-defined trabeculation of medullary bone is lost giving an irregular patchy
moth-eaten appearance. If inadequately treated, progression to subacute or
chronic form may occur depending on the host immune defences.
Chronic suppurative osteomyelitis

Chronic suppurative osteomyelitis may develop after acute phase of the
disease has subsided (secondary), or it may arise from a dental infection
without a preceding acute stage (primary). History of previous episode of
acute suppurative osteomyelitis or odontogenic infection may be seen
(Fig. 25.2).
FIGURE 25.2 (A) Suppurative osteomyelitis. (B) OPG showing
bone destruction in the molar area with diffuse sclerotic bone.
(C1) OPG showing diffuse bone destruction in the molar region
and sequestrum in the premolar region. (C2) CT of the same
person showing destruction of bone in the region of premolar and
molar.
Clinical features
Clinical features of chronic suppurative osteomyelitis are similar to that of
acute osteomyelitis in a milder form. Acute exacerbations of the chronic stage
may occur periodically. Paraesthesia of the lip may be seen, though not
classically seen in chronic suppurative osteomyelitis.
Irregular radiolucent areas superimposed on more sclerotic and
nontrabeculated zones (Fig. 25.2B, C).
Infantile osteomyelitis
Although an uncommon disease for the jaws, it merits special attention since it
involves risks with ocular, intracranial spread and subsequent facial
deformities. Infantile osteomyelitis is believed to occur by haematogenous
route or from perinatal trauma that occurs few weeks after birth and usually
involves the maxilla.
Clinical features
• Facial cellulitis centred about the orbit

• Inner and outer canthal swelling
• Palpebral oedema
• Closure of the eye and proptosis
• Purulent discharge from the nose and medial canthus
Generalised symptoms include fever, irritability, malaise, anorexia,

dehydration and even convulsions and vomiting. Intraoral buccal or palatal
fistulae may be occasionally present.
Investigations
Radiographic change is noted early, CT scans may be used to investigate
extension of orbital abscess, possible dural extension or involvement of the
sinus. Leucocytosis is usually present and the usual offending microorganism
is Staphylococcus aureus.
Diffuse sclerosing osteomyelitis

Diffuse sclerosing osteomyelitis is a chronic condition and represents a
proliferative reaction of the bone to a low-grade infection. The portal of entry
for the infection is diffuse periodontal disease.
Clinical features
Diffuse sclerosing osteomyelitis occurs at any age. Often the disease shows no
clinical sign of its presence. In some cases, the first symptom may be a fistula
on the mucosal surface. The patient may complain of vague pain and a bad
taste.
Radiographic findings
Extensive radiopaque lesion, at times bilateral. Mimicks Paget’s disease of the
bone in having a cotton wool appearance.
Focal sclerosing osteomyelitis

Focal sclerosing osteomyelitis is another chronic condition which occurs in
cases of extremely high tissue resistance or in cases of low-grade medullary
infection which causes endosteal or periosteal reactions.
Clinical features
Most common in younger individuals in the mandibular first molar region
with mild pain and decreased sensitivity in the tooth related to the radiopacity
with no specific clinical findings.
The IOPA radiograph demonstrates pathognomonic well circumscribed
radiopaque mass of sclerotic bone surrounding and extending below the apex
of one or both roots. The border of the lesion may be smooth and distinct or
may appear to blend into the surrounding bone.
Garre’s chronic nonsuppurative sclerosing osteitis

In 1983, Garre described a distinctive type of chronic osteomyelitis as a ‘focal
gross thickening of the periosteum’ of the long bones with peripheral reactive
bone formation resulting from mild irritation or infection. It is essentially a
periosteal osteosclerosis.
Clinical features
It occurs commonly in children and young adults. Mandible is affected more
commonly than maxilla. The patient usually presents with a complaint of
toothache or pain in the jaw and bony hard swelling in the outer surface of the
jaw.
An IOPA radiograph often reveals a carious tooth opposite the hard bony
mass. This mass of bone is smooth, may calcify and itself show a thin but
definite cortical layer.
• Plain radiography of the mandible depicts area of local decalcification

or sclerosis.
• CT scanning or MRI allows early diagnosis and extent of the disease.
Single photon emission computed tomography (SPECT) imaging is
gaining importance in the recent times.
Management of osteomyelitis
The principle treatment goal in the management of the osteomyelitis is the
complete eradication of the causative microorganism (Table 25.1). Treatment
protocol for the management of osteomyelitis includes the eradication of the
foci, meticulous debridement and removal of dead bone and application of
antibiotic therapy by culture sensitivity. The supportive measures include the
surgical managements like sequestrectomy, decortications, resection and
reconstruction and hyperbaric oxygen therapy. The treatment strategies vary
depending on the type of the osteomyelitis. In case of acute osteomyelitis, the
antibiotic therapy is the mainstay of treatment when compared to surgical
treatment (minor debridement may be needed in some cases). In contrast, the
chronic osteomyelitis requires surgical intervention in the management of
necrotic bone and dead space.
Table 25.1
Basic principles of management of osteomyelitis

Basic principles of management of osteomyelitis
Primary treatment measures

• Bacterial culture and antibiotic sensitivity
• Empirical antibiotic started immediately. Change if needed following results of culture
sensitivity
• Analgesics
• Drainage
• Debridement
• Eliminate source of infection
Supportive measures
• Sequesterectomy
• Decortication if needed
• Hyperbaric oxygen therapy (especially for osteoradionecrosis)
• Resection and reconstruction
The primary treatment measure is the antibiotic therapy. The IV antibiotic

treatment should be started once the culture specimen is obtained. The
antimicrobial therapy should be adjusted based on the culture and sensitivity
report. The antibiotic regimen should be continued if there is improvement in
clinical signs (decrease in pain, swelling, erythema and fever). If there is no
improvement in clinical signs the surgical intervention is required. Surgical
treatment is indicated in cases of joint involvement, the presence of abscess in
the bone or subperiosteally and in case of lack of improvement after 48 h of IV
antibiotic therapy. Hence, the surgical treatment is not indicated in acute cases
if it is responsive to antibiotics. The subacute and chronic cases are indicated
for surgical management due to chronic bone changes.
Medical management
The major pathophysiology involved in the development of osteomyelitis is
the compromised local vascularity due to thrombosis. Disrupted blood supply
to the bone causes development of necrosis. Improving the vascularity and the
elimination of the thrombosis should be accomplished for the complete cure.
The most frequent microorganisms associated with osteomyelitis are the
Streptococcus viridans, Peptostreptococcus, Eikenella corodens, Fusobacterium sp.
and Actinomyces sp. The first line of management should be the prompt
diagnosis of the type of osteomyelitis by both clinical history and radiological
examination. The treatment is based on the type of osteomyelitis.
In acute osteomyelitis without abscess formation, antibiotics are the primary
mode of treatment. In case of acute osteomyelitis associated with subperiosteal
or bone abscess, surgical debridement should be considered. Chronic
osteomyelitis with periosteal bone involvement and abscess formation can be
effectively treated by surgical management only supported by antibiotics.
Factors affecting medical management

Specimen should be obtained for gram staining, aerobic and anaerobic culture
and also for antibiotic sensitivity testing. Antibiotic therapy is usually started
empirically with the IV broad spectrum antibiotic before the culture specimen
is obtained. The choice of the antibiotic therapy depends on the type of
infecting organism, duration of infection; susceptibility of the organism,
amount of tissue destruction present, patient’s age and systemic conditions.
Once the organism is identified and its susceptibility ascertained antibiotic
therapy can be modified. Details regarding the culture sensitivity tests can be
read in Chapter 4 Diagnostic Aid—Haematological, Biochemical and
Microbiological Investigations.
Recovery of the patient’s clinical condition is the most important factor in
determining the shift of the IV antibiotics to the oral antibiotics. The positive
finding which denotes good response to antibiotic treatment are absence of
fever, improvement in symptoms like malaise, tenderness, anorexia, night
pain and reduction in CRP.
Slow clinical response indicates virulent or resistant organisms. In such
cases the IV antibiotic should be continued instead of shifting to the oral
therapy.
If there is no clinical response within 48 h of medical management, the
possibility of the presence of bone abscess should be suspected. Reevaluation
by additional CT or MRI and surgical management should be considered.
Surgical (supportive) management

The primary indication of surgical management is the presence of abscess
within the bone (chronic). Lack of response to high dose parenteral antibiotic
therapy is another important indication for the surgical management (acute).
The reason for antibiotic therapy failure should be carefully analysed before
proceeding to the surgical treatment. Reexamination of the culture sensitivity,
antibiotic dose and identification of any other possible reason like bone or soft
tissue abscess should be undertaken. If no possible reason can be correlated,
CT or MRI should be preformed to locate the possible abscess. Appropriate
surgical management should be considered.
The following surgical procedures should be considered for the
management of osteomyelitis
• Sequesterectomy
• Saucerisation
• Decortication
• Resection
Sequestrectomy (Fig. 25.3)

The process by which necrotic bone is separated from the living bone is called
Sequestration and the dead bone thus formed is called sequestrum. The
resorption of living bone around the dead bone results in the formation of the
sequestrum. When both endosteal and periosteal blood supply are
compromised extensive sequestrum formation results. This is more common
in Staphylococcal infections since they produce more potent necrotising toxin
than Streptococci, which are more likely to cause resorption. The bone is often
radiopaque since dead bone including sequestra attracts calcium. Periosteal
bone is usually deposited and an involucrum (new bone) may form to
strengthen the jaw.
FIGURE 25.3 (A, B) Sequestrectomy.
Procedure
Using the preoperative radiograph, which shows the exact location of the
sequestrum, the site of incision is decided. The approach may be either
intraoral or extraoral. To expose entire sequestrum, intraoral incision is made
over the alveolar ridge, but in many instances, entry can be gained by excising
the fistulous tract. Following this, soft tissue is detached from the bone by
blunt dissection and the sequestrum is lifted and removed. In case of partial
attachment of the sequestrum to the bone beneath, it is separated by using an
air drill or sharp osteotome. Rongeurs are used to remove any remaining
necrotic bone. If the sequestrum is encased by involucrum, a window must be
cut to allow it to be taken out.
This is also done using an air drill or a sharp curette. The border of the
necrotic bone is identified by the initiation of bleeding during drilling. The
excision of bone should be made at least 1.5 cm in front of or behind the area
of the radiographic bone necrosis.
The cavity is thus exposed and almost always contains granulation tissues.
This should not be disturbed. The defect should be packed with iodoform
gauze, moistened with compound tincture of benzoin and the wound should
be irrigated daily until complete healing by granulation occurs.
Saucerisation (Fig. 25.4)
When saucerisation is performed in combination with sequestrectomy, the
incision is made longer than usual to expose the entire infected portion of the
bone and extended through the periosteum. Whenever possible the sinus tract
should be included. The periosteum is stripped off the part of the cortex,
which is to be removed. The walls of the bone overhanging the cavity resulting
from the removal of the sequestrum are chipped off with the use of rongeurs
or sharp osteotomes. This exposes extension of the disease. The additional
sequestra and granulation tissue present should be cleaned out and more of
the cortex should be removed if necessary to saucerise the cavity completely so
that the overlying tissue can be pressed into it to eliminate the dead space. The
bone is made smooth with the help of bone files or round burs. The wound is
packed tightly with gauze covered with antibiotic ointment and the flap is
loosely sutured over it. The packing is removed after 3–7 days and replaced
several times until the exposed raw surface of the bone is epithelialised. There
is minimal or no risk of fracture of jaws with this type of procedure. In case
complete primary suture is not feasible, because the infected bone cannot be
removed completely or because there is active suppuration, the wound may be
packed open loosely with gauze and closed later. This procedure is done
mainly in the mandible. Saucerisation of the maxilla is rarely required.
FIGURE 25.4 Saucerisation.
Decortication (Fig. 25.5)

First introduced in 1917 by Mowlem, decortication involves removal of the
chronically infected cortex; usually the buccal and the inferior border are
removed 1–2 cm beyond the affected area. It can be used as initial treatment of
primary or secondary chronic osteomyelitis or more commonly when initial
conservative treatment has failed.
FIGURE 25.5 Decortication.
Procedure
1. Full thickness mucoperiosteal flap is reflected buccally and extended to

the inferior border.
2. Involved teeth are removed.
3. The buccal cortex and inferior borders are removed until bleeding bone
is encountered.
4. Primary closure is achieved and pressure dressing is applied to provide
better support of the bone bed with its related vascular soft tissue.
Drain or antibiotics are used in-situ.
In case of excessive debridement, adequate stabilisation and reconstruction

to support the remaining bone is necessary.
Complications
1. Undue bleeding which may occur in the bone.

2. Injury to the mandibular nerve resulting in anaesthesia of the lip.
3. Fracture of the weakened bone.
Postoperative treatment
Antibiotic treatment should be continued for 10 days to 2 weeks
postoperatively or longer if signs of infection persist. Intravenous infusion of
distilled water with 5%–10% glucose is required to counteract dehydration.
Diet should be rich in protein and vitamins and complete bed rest is essential.
Resection
Indications for resection

Excision of a part of the mandible is seldom necessary. Most patients with
osteomyelitis can be cured by antibiotic treatment combined with
sequestrectomy and saucerisation. However, if the patient has constant
recurrences for many years or months and is suffering from disability and
pain, the disease may have to be treated by resection. After resection is done
continuity of the mandible can be restored with the help of bone grafts or
other reconstruction techniques.
Procedure
The patient is properly prepared to increase his/her general resistance to
infection at an optimal level. Antibiotic therapy is started 24 h before
operation. IMF is done, reconstruction plate contoured and screws drilled
before resection in order to maintain preoperative occlusion.
Mandibular resection can either be partial or total. Partial resection involves
preservation of the condylar and coronoid processes. Condylar and coronoid
processes may be preserved by sectioning the ramus horizontally with an
osteotome. Segment of mandible thus excised is easily lifted from its soft tissue
bed.
Total disarticulation of the mandible involves complete stripping of the
coronoid and condylar processes.
Therefore, insertions of the lateral and medial pterygoid, temporalis and
masseter should be detached with a periosteal elevator taking care to always
keep it in contact with the underlying bone to avoid damage to internal
maxillary artery and vein and pterygoid plexus of veins. After all the muscle
and ligamentous attachments are free from the mandible, it may be removed
by grasping it with a large bone-holding forceps and literally rolling it out of
the glenoid fossa. The wound is closed in layers to eliminate the dead space
and if any infection is present or haematoma formation is suspected, a rubber
drain may be placed. To reduce the postoperative scar contracture temporary
condyle prosthesis or an intraoral splint is used. However, usage of such
appliances is discouraged as these may cause the mucosal closure to take place
under tension leading to dehiscence of the wound. When anterior part of the
jaw is to be removed, insertion of geniohyoid and genioglossus muscles have
to be stripped which results in the falling back of the tongue and interference
with breathing. A silk suture placed through the anterior aspect of the tongue
in such cases pulls the tongue forward and prevents any difficulty with
breathing. If airway is very much compromised, prophylactic tracheotomy
Osteoradionecrosis
Osteonecrosis is a term derived from the Greek words osteon = bone,
nekros = dead, osis = condition, Meaning the destruction and death of bone tissue,
such as from ischaemia, infection, malignant neoplastic disease or trauma.
In the maxillofacial bones, osteonecrosis is commonest and of significance
because of two main sources—
• Radiation, i.e. osteoradionecrosis

• Bisphosphonate-related osteonecrosis of the jaw (BRONJ), i.e.
osteochemonecrosis.
Osteoradionecrosis (ORN) or postradiationosteo-necrosis (PRON) (Figs.

25.6, 25.7)
It was first described by Regaud 1920.
FIGURE 25.6 (A) OPG showing osteoradionecrosis of the right jaw.

(B) Osteoradionecrosis of the left mandible in an 80-year-old man.
(B1) CT showing destruction of left mandible, (B2) 3D CT showing
destruction of buccal cortical bone. (C) Hemisection of the
mandible of the corresponding side is carried out as a result of
osteoradionecrosis.
FIGURE 25.7 Postradiation exposed necrotic bone in right

mandible.
Osteoradionecrosis is an exposure of nonviable, nonhealing, nonseptic

lesion in the irradiated bone, which fails to heal without intervention.
It is the radiation induced wound healing defect.
Definition:
Exposed irradiated bone that has failed to heal over a period of 3 months in
absence of local tumours (Harris, 1992). It may be chronic or progressive.
In years past, the radiation therapist used ortho-voltage therapy and there
was a high incidence of ORN. However, the modern radiation therapists use
megavoltage, which is felt to be less harmful to the bone and soft tissues.
Aetiology:
Doses above 50 Gy usually are required to cause this irreversible damage.
Dental extraction and denture trauma after radiation therapy.
Types of osteoradionecrosis
1. Spontaneous ORN (39%)—degradative function exceeds new bone

production.
2. Trauma induced ORN (61%)—reparative capacity of bone is
insufficient to overcome an insult.
Bone injury can occur through direct trauma:
1. Tooth extraction [84%],

2. Related cancer surgery or biopsy [12%],
3. Denture irritation [1%] or
4. By exposure of the oral cavity to the environment secondary to
overlying soft tissue necrosis.
Risk factors
The risk of developing ORN depends on:
1. Primary site
2. T stage of the malignancy
3. Proximity of the tumour to bone—bone is 1.8 times as dense as soft
tissue and thereby absorbs a proportionately larger dose of incident
radiation than does soft tissue.
4. Dentition—dentate patients have 2.6-fold higher risk
5. Type of treatment (external beam RT, brachytherapy, surgery and
chemotherapy)
6. Time of radiation dose delivery: Radiotherapy results in continuous
damage to the tissues at both cellular and humoral level. If the
stipulated dose is given in a rapid phase, the recovery of remaining
normal viable cells is prevented and thus causing more loss of normal
cells than anticipated. There are different schemes of fractionated
delivery of irradiation which are aimed at reducing the complications
of radiotherapy.
7. Radiotherapy dose: Patients who receive a total of 80 Gy have 2.9-fold
higher risk of developing osteomyelitis.
8. Mode of delivery, location and volume of irradiated tissue: The
conventional external beam irradiation causes more complications due
to exposure of the lesion as a whole. Especially, in areas of less blood
supply such as the posterior part or surgically manipulated parts are at
risk of osteoradionecrosis. This is overcome by more localised delivery
such as the brachytherapy. In brachytherapy, the delivery of radiation
is localised, thus limiting the radiation damage to adjacent tissues.
9. Status of oral hygiene—inadequate oral hygiene:
The cell damaged during irradiation is not compensated by the cell
multiplication over the time, resulting in mucositis and xerostomia.
This is accelerated further with poor oral hygiene, ill fit-ting tissue-
borne prosthesis leading to odontogenic and periodontal infections
which in turn leads to osteoradionecrosis.
10. Surgery: The chances of developing osteoradionecrosis increases with
jaw surgery after radiotherapy. This is due to the reduction in blood
supply to the tissues. The potential risk of osteoradionecrosis in jaw
surgery prior to radiotherapy has also been suggested. This may be
due to reduction in periosteal blood supply in a marginal mandibular
resection, unstable fixation of the mandibular split osteotomy leading
to malunion or nonunion and inadequate tissue coverage of the bone
after resection of a tumour.
External radiotherapy has shown more detrimental effects than

brachytherapy. The risk of developing osteoradionecrosis is decreased if
hyperfractionation techniques and intensity-modulated radiotherapy (IMRT)
are used. The prevalence of osteoradionecrosis was 20.1 and 6.6% in
conventional fractionation and hyperfractionation groups, respectively. In
studies using IMRT, researchers found that PRON developed in up to 0.01% of
patients.
Risk factors for developing ORN include old age, poor nutritional status of
the patient and prolonged tobacco or alcohol abuse.
Pathogenesis
ORN was first described by Marx in 1983 as hypovascularity, hypocellularity
and local tissue hypoxia.
Marx’s theory: 3 ‘H’ concept— hypocellularity, hypoxia and

hypovascularity
• Following radiotherapy, hyperemia, inflammation and endarteritis

occur in the mandible, periosteum and the related soft tissues. This
eventually results in thrombosis, cellular death, progressive
hypovascularity and fibrosis.
• The irradiated block becomes less cellular and lacks fibroblasts,
osteoblasts and undifferentiated osteocompetent cells.
• The irradiated tissues become hypovascular, hypocellular and hypoxic.
This is mainly due to the damage of DNA, RNA and other cellular
units by the free radicals released from water molecules.
• The free radicals such as hydrogen ions, hydroxyl ions react with the
nucleotide or amino acid sequences resulting in cell death, or total
reversible repair or repairs with some impaired function.
• Mandible is more prone for ORN (it occurs in 5%–15% of cases) than
maxilla. This is because the mandible is supplied mainly by the
inferior alveolar artery whereas the maxilla is supplied by the anterior,
middle and posterior superior alveolar arteries and collateral blood
vessels.
Marx proposed three types of osteoradionecrosis
Type I
ORN that is seen soon after radiotherapy due to devascularisation resulting
from combined side effect of surgery and radiation.
Type II
ORN that occurs many years after radiotherapy following a known traumatic
episode. These results from vascular endarteritis of nutrient vessels of the jaw
bone combined with poor wound healing of surrounding soft tissues.
Type III
ORN occurring between 6 months and 3 years post radiotherapy with no
specific preceding traumatic episode.
Clinical findings
Mandible is commonly affected than maxilla due to microanatomy and less
vasculature.
Posterior mandible is commonly affected than anterior portion because of
radiation treatment for tumours in this region.
The patient complains mainly of pain, bad breath and food lodgement in the
affected area. On examination the bone is exposed and the associated soft
tissues are ulcerated and necrosed. Additional findings such as intraoral or
extraoral fistula, mandibular discontinuity, or evidence of secondary local or
systemic infection may also be present.
Loss of mucosal covering and exposed bone are hallmark of
osteoradionecrosis.
Why mandible at an increased risk?

Generally a bone—with more tenuous blood supply and more
mechanically stress—more susceptible to the development of
osteoradionecrosis.
The craniofacial skeleton receives its blood supply in three distinct
manners:
Vessels that enter the bone via direct muscular attachments, periosteal
perforators, and intramedullary vessels
In a study by Bras et al., radiation induced obliteration of the inferior

alveolar artery was consistently found in osteoradionecrosis of mandible and
was felt to be a dominant factor in the onset of the disease.
Treatment
The treatment of osteoradionecrosis of the mandible is aimed at:
1. Removal of the necrotic bone.

2. Enhancement of vascularity of the remaining radiation damaged
tissues.
Marx protocol
• Stage I—A total of 30 hyperbaric oxygen exposures at 2.4 atmospheres

absolute pressure (ATA) for 90 min in a multiplace chamber or 2.0
ATA for 120 min in a monoplace chamber is needed. The wound is
examined for signs of improvement such as mucosal cover, resorption
of nonviable bone, or a decrease in the size of the exposure. Patients
with improvement are labelled stage I responders and additional dives
up to 60 is given until full mucosal covering is achieved. The stage I
nonresponders are treated by stage II protocol.
• Stage II—Undergo a transoral debridement/sequestrectomy which
attempts at primary mucosal closure. With postoperative healing, an
additional 10 sessions of hyperbaric oxygen exposure is given. If there
is wound dehiscence with bone exposure, stage III protocol is adhered.
Patients excluded from entering stage I because of fistula formation,
fracture, or inferior border of the mandible osteolysis undergo initial
hyperbaric oxygen therapy consisting of 30 dives.
• Stage III—Undergo mandibular resection of the necrotic segment until
the bone margins yield viable bone, i.e. till bleeding is encountered. In
those with orocutaneous fistula, the involved skin and fistulous tract
are excised followed by closure.
• Stabilisation of the segments of the mandible is done with an external
fixator or maxillomandibular fixation and the patient undergoes
additional hyperbaric oxygen therapy postoperatively.
• Stage III R: Marx proposes that the reconstructive surgery should be
done 10 weeks after resection thus enabling the graft to be placed, into
a sufficiently vascular and cellular bed with intact mucosa. Before
reconstruction, an additional 20 dives were planned with 10 dives
postoperatively. Mostly, autogenous particulate bone and marrow
within a custom-made stainless steel metal crib or autogenous
particulate bone and marrow within a freeze-dried allogenic bone
framework is used for reconstruction of mandible in such patients.
Management:
Initial treatment—control of infection if present.
Gentle irrigation of the soft tissue margins—removes debris and reduces
inflammation.
Supportive treatment with fluids and a liquid or semi liquid diet high in
proteins and vitamins.
Pain may be controlled with
• Narcotic analgesics
• Bupivacaine
• Alcohol nerve blocks
• Nerve avulsion
• Rhizotomy
Hyperbaric oxygen therapy

Pentoxifylline
Clodronate
Antioxidant (Vitamin E)
Hyperbaric oxygen (HBO) therapy (Fig. 25.8)

Hyperbaric oxygen therapy for radiation-damaged tissue was introduced in
1973 by Greenwood, Gilchrist and Mainous.
Since there is a decrease in vascularity and cellularity of both hard and soft
tissues following irradiation of the bone, the hypoxic compromised tissues
when challenged by a traumatic episode fail to heal. Delayed fibroblastic
activity in neocollagen formation results in chronic nonhealing wound. These
wounds commonly get infected secondarily. The goal of treating ORN is to
overcome hypoxia and increase vascularity of tissues. In order to increase
tissue oxygenation, the patient is subjected to increased oxygen concentration
and pressure. HBO therapy consists of 100% oxygen administered at more
than one absolute atmospheric pressure. This 100% oxygen is a means of
increasing the oxygen dissolved in plasma and tissues that in turn induces
angiogenesis in the compromised tissues.
Methods of delivery
Hyperbaric oxygen therapy is administered in a chamber called the
hyperbaric chamber which may be monoplace (single patient) or multiplace
(multiple patients). Each session ranges from 90 to 120 min where patient
breathes 100% oxygen at 2 to 2.4 ATA. Each session is termed a dive. A total
of 20–30 dives spanning 5 days a week is planned preoperatively.
Mechanism of action
The timeframe post HBO session when there exists an elevation of the oxygen
within hypoxic tissues has shown:
• To enhance the recruitment and function of leukocytes.

• Induces fibroblast growth, increased collagen formation.
• HBO stimulates angiogenesis in the healing tissue.
• Inhibits aerobic and anaerobic bacteria.
• To inhibit bacterial toxin formation.
• Hyperbaric oxygen increases the amount of oxygen in tissue fluids by a
10-fold factor. Oxygen can be delivered to the depths of a tissue where
vascularity is poor or compromised.
Contraindication:
1. Untreated pneumothorax—(Absolute contraindication)

2. Pregnancy
3. Emphysema
4. Upper respiratory tract infection
5. Uncontrollable fever
6. Optic neuritis
7. Ear problems
FIGURE 25.8 Hyperbaric oxygen chamber.

Pentoxifylline and vitamin E
Pentoxifylline lowers blood viscosity, increases tissue oxygen level, reduces
fibroblast proliferation and increases collagenase activity; it is used to treat
intermittent claudication.
Vitamin E is an antioxidant. These drugs have been used to treat advanced
cases of ORN, with promising results. These drugs are believed to promote
healing,
Recent guidelines
Prevention of osteoradionecrosis
• Every patient should have a dental assessment prior to radiotherapy

for the best outcome following cancer treatment.
• Extraction of all teeth before radiotherapy has been recommended
• Removal of all teeth of poor prognosis, generally considered less than 5
years, is recommended
• Extractions are planned with the view to avoiding extractions in the
future.
• Removal of all mandibular molars in fields over 60 Gray, unless the
patient has excellent oral hygiene
Preventive regime
• If the mouth becomes too sore during radiotherapy a soft brush may be
necessary for a time, supplemented with chlorhexidine mouth wash,
which may be diluted with equal volume of water if too sore on the
mucosa.
• In addition a fluoride regime, either high fluoride toothpaste fluoride
gel in splints for 10 min each day or alcohol free fluoride mouth rinse.
• Saliva substitutes should be pH neutral.
• Dentures should be regularly checked for pressure areas and adjusted
but it may be preferable to avoid dentures.
Extractions after radiotherapy

Although undesirable, it may become necessary to extract teeth from the
irradiated jaw.
Patients should be informed of the risk and be observant for early signs of
ORN.
Recommendations:
• 0.2% chlorhexidine mouthwash prior to extractions

• Amoxicillin 3 g orally 1 h pre extraction (or if allergic 600 mg
clindamycin)
• Postoperative amoxicillin 250 mg tds or metronidazole 200 mg tds for
3–5 days
• Minimal trauma, simple extraction of mobile teeth
• Primary closure for firm teeth, by a minimal periosteal flap and
alveolectomy
• An experienced operator
• Possibly preoperative hyperbaric oxygen for mandibular molars in
areas of high radiation
• Review after 5 days, weekly review until healing is complete
Osteochemonecrosis
Bisphosphonate related osteonecrosis of the jaw (BRONJ) is a condition where
necrosis of the jaw bone occurs subsequent to dental infection or therapy in a
patient being treated with bisphosphonates.
The American Association of Oral and Maxillofacial Surgeons (AAOMS)

define BRONJ (q.v.) as ‘exposure of portions of the jawbone in patients who
have been exposed to bisphosphonates that has persisted for more than
8 weeks with no history of radiation therapy to the jaws’.
The three diagnostic criteria of BRONJ are:

1. Currently on bisphosphonate therapy or a history of bisphosphonate
therapy.
2. Exposed, necrotic jaw bone nonhealing for more than 8 weeks.
3. No history of radiation therapy to the head and neck.
Bisphosphonates—common uses
• Prevention and treatment of osteoporosis in postmenopausal women

• Increase bone mass in men with osteoporosis
• Treatment of glucocorticoid-induced osteoporosis
• Treatment of Paget’s disease of bone
• Hypercalcaemia of malignancy
• Bone metastases of solid tumours—breast and prostate carcinoma;
other solid tumours
• Osteolytic lesions of multiple myeloma
Classification:
Oral Etidronate
Clodronate
Pamidronate
Ibandronate
Risedronate
Intravenous Pamidronate
Ibandronate
Zolendronate
Mechanism of bisphosphonates
Bisphosphonate inhibits osteoclastic activity. Because osteoblastic activity is
coupled tightly to osteoclastic activity, this in turn, suppresses the bone
turnover. Bisphosphonates are administered in conditions such as
osteoporosis (where the osteoclastic activity is elevated) and cancer affecting
the bone, in particular multiple myeloma and metastatic tumours (for
example, metastatic breast, prostate and lung cancers). It is also used in a
variety of less common conditions such as Paget’s disease of bone and
osteogenesis imperfecta of childhood.
Side effects:
Impaired osteoclast function
Bone becomes too dense—choking capillary network
Avascular bone necrosis
Osteochemonecrosis (BRONJ)
Stages of BRONJ
Stage 1
Exposed bone with absence of pain and infection.
Stage 2
Pain may be associated with suppuration or infection and intraoral sinus track
formation.
Stage 3
Extraoral fistula, exposed necrotic bone extending beyond the region of the
alveolar bone, pathological fracture, osteolysis extending to the inferior border
or oroantral communication.
Various staging systems are advocated. Recently, Mawardi has reported the
occurrence of BRONJ even in the absence of exposed bone (stage 0).
Risk factors
I. Drug-related factors
A. Bisphosphonate used: Amino bisphosphonates as zoledronate is more

potent than non-aminobisphosphosphonates, pamidronate which in
turn is more potent than oral bisphosphonates; the IV route of
administration results in a greater drug exposure than the oral route.
B. Duration of therapy: Longer duration shows increased risk.
II. Local risk factors include
A. Dentoalveolar surgery
1. Extractions
2. Dental implant placement
3. Periapical surgery
4. Periodontal surgery involving osseous injury
B. Local anatomy
1. Mandible
a. Lingual tori
b. Mylohyoid ridge
2. Maxilla
a. Palatal tori
According to American Association of Oral and Maxillofacial Surgeons
(q.v.) ‘it has been observed that lesions are found more commonly in the mandible
than the maxilla (2:1 ratio) and more commonly in areas with thin mucosa overlying
bony prominences such as tori, bony exostoses and the mylohyoid ridge’.
C. Concomitant oral disease

Periodontal and dental abscesses.
III. Demographic and systemic factors
A. Age: Risk increases with aging especially with IV bisphosphonates

B. Race: Caucasian
C. Cancer: Risk is highest for multiple myeloma followed by breast cancer
when treated with IV bisphosphonates.
D. Osteopaenia/osteoporosis
The following factors are thought to be risk factors for BRONJ:
1. Corticosteroid therapy
2. Diabetes
3. Smoking
4. Alcohol use
5. Poor oral hygiene
6. Chemotherapeutic drugs
Prevention modalities of BRONJ

The following are the prevention modalities of BRONJ for patients treated
with bisphosphonates:
• A detailed full mouth examination should be done prior to treating the

patient with an IV bisphosphonates.
• Extraction of teeth, restoration of optimal periodontal health and
needed invasive procedures should be performed before starting the
therapy.
• The studies conducted by two task force members of the AAOMS with
approximately 50 patients concluded that the risk of developing
BRONJ associated with oral bisphosphonates increases only when the
duration of therapy exceeds 3 years.
• However, comorbidities, such as chronic cortico-steroid use increase
the risk.
• Dental surgery can be done in these patients after cessation of oral
bisphosphonates 3 months before and 3 months after the dental
surgery, provided the systemic conditions are stable.
Treatment strategies
A. Patients about to initiate intravenous bisphosphonate treatment

The treatment objective for this group of patients is to minimise the risk of
developing BRONJ.
• Although a small percentage of patients receiving bisphosphonates

may develop osteonecrosis of the jaw spontaneously, majority of
affected patients develop this complication following dentoalveolar
surgery. Therefore if systemic conditions permit, initiation of
bisphosphonate therapy should be delayed until dental health is
optimised. This decision must be made in conjunction with the
treating physician and dentist and other specialists involved in the
care of the patient.
• Nonrestorable teeth and those with a poor prognosis should be
extracted. Other necessary elective and preventive dentoalveolar
surgery should also be completed at this time.
• Based on experience with osteoradionecrosis, it appears advisable that
bisphosphonate therapy should be delayed, if systemic conditions
permit, until the extraction site has mucosalised (14–21 days) or until
there is adequate osseous healing.
• Dental prophylaxis, caries control and conservative restorative
dentistry are critical in maintaining functionally sound teeth.
Preventive, noninvasive care must be continued indefinitely.
• Patients with full or partial dentures should be examined for areas of
mucosal trauma, especially along the lingual flange region.
• It is critical that patients be emphasised about the importance of dental
hygiene and regular dental evaluations and specifically instructed to
report any pain, swelling or exposed bone.
• Medical oncologists should evaluate and manage patients scheduled to
receive IV bisphosphonates similar to those patients scheduled to
initiate radiation therapy to the head and neck. The osteoradionecrosis
prevention protocols are guidelines that need to be adhered to for
bisphosphonate therapy also.
B. Asymptomatic patients receiving intravenous bisphosphonates
• Maintaining good oral hygiene and dental care is of paramount

importance in preventing dental disease that may require
dentoalveolar surgery.
• Procedures that involve direct osseous injury should be avoided.
• Nonrestorable teeth may be treated by removal of the crown and
endodontic treatment of the remaining roots.
• Placement of dental implants should be avoided in the oncologic
patients exposed to the more potent intravenous bisphosphonate
medications (zole-dronic acid and pamidronate) on a frequent dosing
schedule (4–12 times per year).
C. Asymptomatic patients receiving oral bisphosphonate therapy
• Patients receiving oral bisphosphonates are also at risk for developing

BRONJ, but to a much lesser degree than those treated with
intravenous bisphosphonates.
• BRONJ can develop spontaneously or after minor trauma. In general,
these patients seem to have less severe manifestations of necrosis and
respond more readily to stage specific treatment regimens.
• Elective dentoalveolar surgery does not appear to be contraindicated in
this group. It is recommended that patients be adequately informed of
the risk of compromised bone healing.
• The risk of BRONJ may be associated with increased duration of
treatment with oral bisphosphonates, i.e. over, 3 years, based on
experience with 50 such patients by two Task Force members. For
individuals who have taken an oral bisphosphonate for less than 3
years and have no clinical risk factors, no alteration or delay in the
planned surgery is necessary. This includes any and all surgeries
common to oral and maxillofacial and periodontal surgeries.
• It is suggested that if dental implants are to be placed, informed
consent should be provided related to possible future implant failure
and possible osteonecrosis of the jaws if the patient continues to take
an oral bisphosphonate. Such patients should be placed on a regular
recall schedule. It is also advisable to either alternate dosing of the
bisphosphonate, provide a drug holiday or switch to an alternative
therapy.
Drug holiday
For those patients who have taken an oral bisphosphonate for less than 3
years and have also taken corticosteroids concomitantly, the prescribing
provider should be contacted to consider discontinuation of the oral
bisphosphonate (drug holiday) for at least 3 months prior to oral surgery, if
systemic conditions permit.
The bisphosphonate should not be restarted until osseous healing has
occurred. These strategies are based on the hypothesis that concomitant
treatment with corticosteroids may increase the risk of developing BRONJ
and that a ‘drug holiday’ may mitigate this risk.
MRONJ (Medication-related osteonecrosis of the jaw)

In 2014, the American Association of Oral and Maxillofacial Surgeons
(AAOMSs) suggested to change the nomenclature from bisphosphonate-
related osteonecrosis of the jaw (BRONJ) to MRONJ to accommodate the
growing number of osteonecrosis cases involving the maxilla and mandible
associated with other antiresorptive (denosumab) and antiangiogenic
therapies.
MRONJ drugs:
1. Antiresorptive
a. Bisphosphonates (BPs)
– Aminobisphosphonates
– Non-aminobisphosphonates
b. Receptor activator of nuclear factor kappa-B ligand [RANK-
L] inhibitors
– Denosumab
2. Antiangiogenic
Bevacizumab
Tyrosine kinase inhibitor (Sunitinib, Sorafenib)
mTOR inhibitor (Sirolimus)
The risk of developing MRONJ associated with oral BPs is very low, and it
increases when the duration of therapy exceeded 4 years.
Treatment of medication-related
osteonecrosis of the jaw
Multidisciplinary team approach
Stage 0
A medical treatment (antiseptic, analgesic, antibiotic, and antiphlogistic
therapy) and management of local risk factors are indicated.
Low-level laser therapy is a possible choice for treatment of osteonecrosis by
helping reparative process, improving osteoblastic index, and stimulating
lymphatic and blood capillaries growth.
A careful follow-up for the evolution to a greater stage is necessary.
Stage 1
If exposed and necrotic bone or fistulae are present, they are rinsed with
antiseptic fluids and covered with an adhesive paste, 3 times a day. In the
absence of healing tendency, after 8 weeks, it is possible for a surgical
debridement approach.
Stage 2
After 2 weeks of medical therapy to reduce inflammatory symptoms, a
surgical debridement is indicated. It should be more conservative as possible
but extended as large as necessary to a complete removal of affected bone.
Antibiotic and antiphlogistic treatments are administered.
Follow-up examinations are necessary.
Stage 3
Marginal or segmental osteotomies are recommended for severe cases.
Invasive surgery is indicated only if it could improve patient’s quality of
life.
In other cases or if patient rejects surgery, a conservative approach to control
symptoms and to prevent the osteonecrosis progression is administered Refer
Table 25.2 for MRONJ staging & treatment strategies.
Table 25.2
Staging and treatment strategies

MRONJ staginga Treatment strategies‡
At risk category No apparent necrotic bone in patient who have been • No treatment
treated with either oral or IV bisphosphonates indicated
• Patient education
Stage 0 No clinical evidence of necrotic bone, but nonspecific clinical • Systemic
findings, radiographic changes and symptoms management,
including the use of
pain medication and
antibiotics
Stage 1 Exposed and necrotic bone, or fistulae that probes to bone, in • Antibacterial mouth
patients who are asymptomatic and have no evidence of infection rinse
• Clinical follow-up on
a quarterly basis
• Patient education and
review of indications
for continued
bisphosphonate
therapy
Stage 2 Exposed and necrotic bone, or fistula that probes to bone, • Symptomatic
associated with infection as evidenced by pain and erythema in the treatment with oral
region of the exposed bone with or without purulent drainage antibiotics
• Oral antibacterial
mouth rinse
• Pain control
• Debridement to
relieve soft tissue
irritation and
infection control
Stage 3 Exposed and necrotic bone or a fistula that probes to bone in • Antibacterial mouth
patients with pain, infection and one or more of the following; exposed rinse
and necrotic bone extending beyond the region of alveolar bone, (i.e. • Antibiotic therapy
inferior border and ramus in the mandible, maxillary sinus and zygoma and pain control
in the maxilla) resulting in pathologic fracture, extraoral fistula, oral • Surgical
antral/oral nasal communication, or osteolysis extending to the inferior debridement/resection
border of the mandible of sinus floor for longer term
palliation of infection
and pain
a
Exposed or probable bone in the maxillofacial region without resolution for greater
than 8 weeks in patients treated with an antiresorptive and/or an antiangiogenic agent
who have not received radiation therapy to the jaws.
‡
Regardless of the disease stage, mobile segments of bony sequestrum should be
removed without exposing uninvolved bone. The extraction of symptomatic teeth within
exposed, necrotic bone should be considered since it is unlikely that the extraction will
exacerbate the established necrotic process.
SECTION VIII
Maxillofacial Pathologies
Chapter 26: Cysts of the Oral Cavity

Chapter 27: Odontogenic Tumours
Chapter 28: Nonodontogenic Tumours
Chapter 29: Oral Cancer
Chapter 30: Management of Head and Neck Tumours
Chapter 31: Salivary Gland Pathologies
Chapter 32: Maxillary Sinus and its Implications
Chapter 33: Orofacial Cleft
Chapter 34: Orofacial Neuropathy
CHAPTER 26
Cysts of the Oral Cavity
Classification
Odontogenic and nonodontogenic cyst derivatives
Development of cyst
• Cyst initiation and formation
• Cyst enlargement
• Mural growth theory
• Osmotic theory
• Bone resorption theory
Cyst regression
Diagnosis of cysts
Clinical findings
• Contrast studies
Aspiration
Biopsy
Management
Objectives of treating cyst
Considerations before selection of treatment
Principles of treatment selection
Marsupialisation (cystotomy)
• Indications of marsupialisation
• Procedure
• Advantages of marsupialisation
• Disadvantages of marsupialisation
• Modifications
• Procedure
Enucleation (cystectomy)
• Indications
• Advantages of enucleation
• Disadvantages of enucleation
• Procedure
Partsch II—Enucleation with primary closure
Enucleation with open packing
Enucleation and Curettage
Enucleation and Peripheral ostectomy
Enucleation and chemical cauterisation
Enucleation and cryotherapy
Complications of untreated cysts
Odontogenic keratocyst (OKC)
Dentigerous cyst (follicular cyst)
KRAMER (1974):
’Cyst is defined as a pathological cavity having fluid, semifluid or gaseous
contents and which is not created by the accumulation of pus’. Most cysts, but
not all, are lined by epithelium.
TRUE CYSTS: Cyst which is lined by epithelium, e.g. dentigerous cyst,
radicular cyst etc.
PSEUDOCYSTS: Cyst which is not lined by epithelium, e.g. Solitary bone
cyst, Aneurysmal bone cyst, traumatic bone cyst
Cysts can occur within the bone or soft tissues. They are of different types and
may be asymptomatic or associated with swelling and pain. Cysts are
generally slow growing, expansible lesions.
Classification
Several systems have been devised for classifying cysts and tumours of the
jaws. Some of these classification systems are based on clinical, radiographic or
morphologic parameters. Other systems categorise lesions totally on their
aetiology. The WHO classification divides cysts according to aetiology.
A distinction is drawn between the autonomous developments of the
majority of cyst varieties and the inflammatory pathogenesis of the most
common radicular cyst.
Flowchart 26.1
FLOWCHART 26.1 Shear’s classification.
*According to the WHO classification of 2005, the keratocystic odontogenic

tumour and calcifying epithelial odontogenic tumour have been moved back
into the cyst category as odontogenic keratocyst (OKC) and calcifying
odontogenic cyst (COC) due to insufficient evidence of tumerogenesis.
Reference—Update from the 4th Edition of the World Health Organization
Classification of Head and Neck Tumours: Odontogenic and Maxillofacial Bone
Tumors. Head and Neck Pathol. 28 February 2017.
Odontogenic and nonodontogenic cyst

derivatives
The epithelium associated with each of the odontogenic cyst is derived from
one of the following sources:
Flowchart 26.2
FLOWCHART 26.2 Epithelial remnants.

Development of cyst (Fig. 26.1)
There are three phases of cyst development:
• Cyst initiation—bacterial invasion and inflammation of periapical

tissues leads to formation of periapical granuloma.
• Cyst formation—proliferation of epithelial lining, death of central cells
and formation of a small cavity.
• Cyst enlargement—initiation is different for each group of cyst whereas
the enlargement process is most likely similar for all epithelium lined
cysts, with some variations.
FIGURE 26.1 Odontogenic and nonodontogenic cysts. (A)

1. Gingival 2. Eruption 3. Lateral periodontal 4. Residual
5. Periapical (radicular) 6. Dentigerous 7. OKC. (B) 1. Nasolabial
cyst 2. Nasoalveolar cyst 3. Globulomaxillary cyst 4. Nasopalatine
cyst 5. Cyst of palatine papilla 6. Median palatal cyst.
1. Cyst initiation and formation
• Initiation of cyst formation is mostly from odontogenic epithelium.

However, the stimulus which initiates this process is not known.
• Proliferation of epithelial lining low-grade infection of nonvital pulp
stimulates the cell rests of Malassez in the periapical periodontal
membrane to proliferate and form arcades at the periphery of the
periapical granuloma (chronic periapical lesion as a result of nonvital
pulp); they eventually form a confluent layer sealing off the apical
foramen and the contained granulation tissues and cell infiltrate
liquefies.
• The cells proliferate in layers from the surface of the adjacent vascular
connective tissues. This connective tissue becomes organised as the
cyst capsule.
• The number of epithelial layers is determined by the period of viability
of each cell as it is separated from the basement membrane by the
dividing basal layer and the rate at which maturation and
desquamation occurs.
2. Cyst enlargement
Once cyst formation has been initiated, it continues to grow and enlarge.
Malcolm Harris (1975) summarised various theories of cyst expansion.
Various researchers have further modified the theories later on as follows:
A. Mural growth theory

B. Osmotic theory
C. Bone resorption theory
A. Mural growth theory

Cyst expansion by this theory is explained by two proportions.
1. Peripheral cell division:

Cyst enlarges at the peripheries because of active division of epithelial
cells lining the cyst in response to any irritating stimulus. Contents of
the cyst will support the cystic lining and it can cause rapid resorption
of surrounding bone to accommodate the enlarging cyst.
2. Accumulation of cellular contents:
Kramer (1974) proposed to explain the enlargement of OKC’s. He explained
that as mural squamous are shed off the lining epithelium they accumulate
there by increasing the cyst volume. The sites of expansion and growth are
represented by finger like projections which are zones of active cell division or
proliferation.
The finger like projections is formed by OKC as they have poor bone resorbing
properties. Hence, they proliferate along the cancellous bone which is less
dense than the cortical bone. This explains why keratocyst very rarely cause
expansion or resorption of the cortical plates.
Kubota et al (2002) showed in his study that interleukin (IL)-1α stimulates
enzymatic degradation of extracellular matrices of the bone around the cyst
causing expansion of OKC.
Oka et al. (2005) studied the effects of positive intracystic fluid pressure in
OKCs. He proposed that the positive pressure plays a crucial role in OKC
growth via stimulating the expression of IL-1 in epithelial cells.
B. Osmotic theory
Accumulation of fluid within the cyst wall causes the expansion of the cyst
wall. James and Tratman proposed the osmotic theory or dialysis to explain
the hydrostatic enlargement of cyst. The mean osmolality of cystic fluid is 10
millimoles higher than the serum, this gradient causes the accumulation of all
the shed degenerated cells from the cyst lining. In addition, the inadequate
lymphatic drainage further favours the accumulation of the fluid from the
capsular capillaries thereby aiding the cyst enlargement.
C. Bone resorption theory

Harris et al. proposed that the cystic capsule contains very potent bone
resorbing factors like Prostaglandin PGE2, PGE3 and leukotrines. [Keratocyst
found to secrete very less amount of bone resorbing factors per unit surface
area compared to other cysts. This explains the burrowing nature or
intramedullary growth of the keratocyst]. Increased internal pressure also
causes bone resorption and enlargement of cyst cavity. The expansion causes
egg shell crackling on palpation due to microcracks on the thinned out cortical
bone. Complete resoption and perforation of cortical bone occurs on further
expansion.
Following mechanisms are involved in the cyst enlargement:
• Increase in the volume of contents

• Hyperosmosis
• Resorption of surrounding bone when the cyst develops within bone
• Increase in cyst surface area.
Increase in the volume of contents
• In mucous secreting cysts, the accumulation of mucous explains the

increase in volume.
• The cyst consists of prostaglandin E2 (PGE2) and leukotrienes.
• Inflammatory cells which are seen in the capsule also release cofactors.
• Lymphocytes release lymphokine, osteoclast activating factor (OAF)
and monocytes release interleukin I, which stimulates the fibroblasts to
release prostaglandins.
• This cyst enlargement is determined by the continous stimulation of
epithelial proliferation.
Osmotic theory of enlargement: Main (1970), Harris and Toller (1975)
• Increased osmolarity of cyst fluid may play a role in the enlargement.

• Osmotic difference between the serum and cystic fluids is related to
the proteins present within the cystic fluid such as large molecules of
globulins, albumin, fibrinogen and fibrin degradation products, which
are responsible for the increase in osmotic pressure of a cyst which, in
turn, results in cyst expansion (Figs. 26.2, 26.3).
FIGURE 26.2 Pathogenesis of cyst formation.
FIGURE 26.3 (A) Supernumerary teeth in relation to maxillary left

lateral incisor area associated with the periapical cyst. (B) Note the
cystic expansion of the palatal area.
Increase in cyst surface area
• Mural growth in the form of epithelial proliferation is one of the

essential process by which the surface area of sac increases basically by
peripheral cell division or by accumulation of cellular contents.
• A multicentric pattern of cyst growth brought about by the
proliferation of local groups of epithelial cells as in the keratocysts,
result in cystic expansion.
• Collagenase activity as in primordial and radicular cysts by way of
increased collagenolysis.
• Unremitting growth of certain epithelial linings due to high mitotic
values as in keratocysts.
Cyst regression
Any process that leads to the involution of cyst epithelium, e.g. extraction of
tooth or reduction of intracystic pressure as with marsupialisation, may cause
connective tissue capsule to regress and the cavity to be filled by bone or scar
tissue.
Diagnosis of cysts
Clinical findings
• Nonvital tooth (Fig. 26.2)—radicular or periapical cysts are associated

with nonvital tooth or root stumps.
• Expansion of the jaw (Figs. 26.3A, 26.4A)—the expansion of the cyst
stimulates the periosteum to form a new layer of bone, resulting in the
jaw enlargement, obliterating the buccal vestibule intraorally and
extraorally may present as a facial deformity (Fig. 26.5A–E). As the
cyst expands, the bone covering the centre of the convexity of the cyst
becomes thin and is indented with pressure. Later on, the fragile outer
shell of the bone cracks and this produces a sensation of ‘egg shell
cracking’ on palpation.
• Percussion of the teeth overlying the solitary bone cyst produces a dull or
hollow sound in contrast with the high-pitched note produced by
percussing normal teeth. Teeth adjoining an odontogenic keratocyst,
fissural cyst, lateral periodontal cyst, solitary bone cyst and
nonodontogenic cyst are vital, whereas those associated with
periapical cyst are nonvital.
• Neurapraxia of the mandibular neurovascular bundle may be caused
due to acute infection of cysts in the mandible resulting in pressure
from pus accumulation in the sac.
• A sinus tract may be detected in some cases where the cyst had
discharged intraorally or extraorally.
• If the infected cyst is present inside the maxillary antrum, sinusitis may
be caused.
• Solitary bone cyst usually occurs in the mandible whereas periodontal
cyst can occur anywhere in the alveolar process. Dentigerous cysts are
usually associated with impacted canines (Fig. 26.6A, B), premolars
and molars. Nonodontogenic cysts like nasopalatine cysts usually occur
in the upper jaw whereas Stafne’s bone cyst exclusively occurs beneath
the mandibular canal. Odontogenic keratocysts are often associated
with lower third molar region.
• Expansion of the cyst causes loosening of the teeth.
• Missing teeth in the dental arch may be due to the presence of
odontogenic keratocyst.
• In edentulous patients, a change in the fitting of denture may occur due to
the presence of swelling.
FIGURE 26.4 (A) Cystic expansion causing facial deformity

extraorally. (B) OPG showing ill defined multilocular radiolucency
with sclerotic margin occupying right mandibular body.
FIGURE 26.5 (A, B) Obliteration of the right lower buccal vestibule
from jaw expansion. (C) Exposure of the cystic lesion transorally.
(D) Enucleated cyst. (E) Packing of the enucleated cystic cavity.
FIGURE 26.6 (A, B) Dentigerous cyst associated with impacted 13

—enucleation.
• A typical odontogenic cyst appears radiolucent with a well-defined

radiopaque margin though there are variations to the standard
pattern.
• Periapical and occlusal views give essential information as far as small
cysts are concerned (Fig. 26.7). For large cysts, extraoral radiographs
like lateral oblique and PA view of the mandible, Waters’ view for the
maxilla supplement the intraoral radiograph.
• Occlusal radiographs are especially used for viewing the degree of
palatal bone destruction in the cysts of the maxilla.
• Lateral oblique view gives valuable findings of the cyst present in the
lower border of the mandible whereas posteroanterior view provides
comprehensive images of the cysts present in the symphysis, body and
the ramus of the mandible.
• Waters’ view is used to view cysts present in the maxillary sinus.
• Orthopantomograms (Fig. 26.8) help in viewing the entire jaw.
FIGURE 26.7 Intraoral periapical radiograph showing well-defined
radiolucency in relation to 41 and 42.
FIGURE 26.8 OPG showing well-defined unilocular radiolucency
with sclerotic margin in the right mandibular premolar region.
Contrast studies
To find out the exact size and relation of the cysts whose extent is doubtful,
water-soluble contrast solutions can be injected into them after removing the
cystic fluid. The injection should be carried out cautiously to avoid painful
excess pressure in the cystic cavity. Similarly, aspiration of the cystic cavity
should also be done in a manner to avoid any negative pressure inside the
cavity. The radiopaque dye is filled and essential radiographs are taken after
which the contrast medium is removed by aspiration.
Aspiration (Figs. 26.9, 26.10)

Aspiration indicates nature of the cystic lesion and also helps in differentiating
the maxillary cyst and maxillary sinus. It is done under local anaesthesia with
the help of a wide bore needle. The aspirated fluid is studied to find out the
nature of the lesion. Aspiration of air indicates that the needle has entered the
antrum. If there are no contents on aspiration, it indicates a tumour
(Table 26.1).
FIGURE 26.9 (A, B) Frank pus aspirated from an infected cystic
lesion of right mandible.
FIGURE 26.10 Blood tinged straw-coloured fluid aspirated from the

radicular cyst.
Table 26.1
Cyst aspirates and their specific features
Biopsy
Biopsy is the gold standard for determining the type of cysts and to
differentiate them from neoplasms.
Management
Objectives of treating cyst
1. Complete elimination of the pathologic lesion

2. Cause minimal destruction and damage to the surrounding soft and
hard tissues
3. Restore normal function
Considerations before selection of treatment

Related teeth
• All the teeth related to the cyst and displaced by the cyst must be
tested for preoperative pulp vitality.
• The cyst sac must be separated carefully from the thin bone lamina
surrounding the apices of vital teeth.
• Most of the teeth continue to give vitality responses immediately after
removal of the cyst, some regain considerable sensitivity after a period
of months but a few remain insensitive permanently.
• There is a clinical impression that function stimulates more rapid bone
generation and it may be reasonable to retain teeth, even on a
temporary basis, to provide this stimulus to the alveolar and basal
bone.
• In case of a keratocyst, eradication of the lesion is much more
important than preservation of related teeth and the teeth are not
preserved at the expense of incomplete removal of the cyst
(Fig. 26.11A–D).
FIGURE 26.11 (A) OPG showing multilocular radiolucency in left

mandibular ramus diagnosed as OKC. (B) Segmental resection
done as a curative surgery for OKC. (C, D) Resected mandibular
specimen showing bicortical expansion.
Fracture and risk of fracture (Fig. 26.12A–C)

Continuous and progressive enlargement of a cyst may eventually lead to a
pathological fracture. This is indicated by a slight click, a brief increase in pain
or the sudden onset of mental nerve paraesthesia in case of mandible. There is
considerable potential for regenerative bone growth after the release of
intracystic pressure. In case of fracture or risk of pathologic fracture (residual
basal bone after treatment is less than 1 cm), reinforcement with bone graft
and reconstruction plate is mandatory.
FIGURE 26.12 (A–C) Multilocular cystic lesion in the mandible

involving the lower border—at risk of pathologic fracture.
Inferior alveolar nerve involvement (Fig. 26.13)

Separation of cyst wall from the inferior alveolar neurovascular bundle can be
accomplished with temporary or no interruption of nerve function.
FIGURE 26.13 Lytic cystic lesion of right mandible ramus involving

the inferior alveolar nerve—the patient clinically had paraesthesia
of right lower lip.
Principles of treatment selection

There are certain principles, which need to be considered with respect to the
treatment of the cyst:
1. The lining should be removed or rearranged in order to eliminate it

from the jaw.
2. The tooth germ, the unerupted or partially erupted teeth should be
conserved as far as possible and should be allowed to erupt.
3. Preservation of the adjacent vital structures like neurovascular bundle,
nasal or antral lining mucosa, etc.
• In 1892, Partsch explained a procedure known as Partsch I
operation. This treatment was put forward previously as a
definitive treatment for cysts, and consisted of Decompression
where the overlying epithelium, bone and the deroofing of the
cyst was done primarily followed by Marsupialisation which
was achieved by suturing of the cyst lining to the oral
epithelium and then packed with sterile medicated gauze to
keep the cyst cavity open. The rationale at that time was that
it decompresses the cyst and stops growth of the cyst and
helps in new bone formation.
With the advent of antibiotics and the routine use of endotracheal

intubation, the management of dental cysts changed. In1910, Partsch
suggested enucleation and primary closure of cysts of small size. This is
known as the Partsch II procedure, Enucleation or Cystectomy. It became the
most accepted treatment, because with adequate antibiotic cover and sterile
technique it was associated with a more rapid and predictable final result.
References:
1. Partsch C. U¨ berkiefercysten. Deutsche Monatsschrift Fur

Zahnheilkunde 1892;10:271–304.
2. Partsch C. Zurbehandlung der kieferzysten. Deutsche Monatsschrift Fur
Zahnheilkunde 1910;28:252–60.
Flowchart 26.3
FLOWCHART 26.3 Treatment of cyst.
Marsupialisation (cystotomy) (Figs. 26.14–26.16)

It the earliest treatment used and was first described by Partsch in 1892. In this
process a window of 1 cm is made into the cyst and lining is sutured to oral
mucosa process to convert the cyst into pouch so that cyst is decompressed
and it exposes the cystic lining into oral environment. Mandibular cyst
marsupialised into oral cavity and maxillary cyst marsupialised into maxillary
sinus and nasal cavity. Cavity is then regularly packed open with iodoform
gauze coated with tincture benzoin till endeosseous healing.
FIGURE 26.14 Marsupialization of a maxillary cyst. (A) Buccal cyst
encroaching on the maxillary sinus wall. A buccal mucoperiosteal
flap raised, bone and cystic lining removed to sufficient size and
the cyst contents removed. (B) Marsupialization of a mandibular
cyst, the mucoperiosteal flap was raised; exposure of the cyst
cavity and packed with iodoform gauze coated with tincture of
benzoin.
FIGURE 26.15 Marsupialisation of sublingual dermoid cyst.
(A) Sublingual dermoid (B) Fluid aspirated (C) Contents removed.
(D) Lining sutured to the adjacent mucosa.
FIGURE 26.16 (A) OPG showing well-defined radiolucency

involving right mandibular body. (B) Transoral approach of the cyst.
(C) Decamping of the cyst roof. (D) Cystic cavity maintained as
open cavity by suturing the cyst lining to the oral mucosa.
(E) Healing granulating cystic cavity markedly reduced in size after
2 weeks.
This procedure might fail if the opening is allowed to close before the cavity
is completely obliterated. This can be avoided by making the ostium as large
as the diameter of the cyst. In case of large cystic cavity, the cyst cavity must be
packed and it should be removed after every meal for cleaning the cavity.
Indications of marsupialisation
• It is indicated in young children as this procedure preserves the tooth

germ associated with the cyst and helps in normal eruption of the
teeth. Similarly, in adolescents it helps in the eruption of the
unerupted tooth associated with the cyst, which would have been
damaged if enucleation was done.
• In case of large cysts where enucleation would result in pathologic
fracture, marsupialisation is used to preserve the bony integrity.
In cases when the cyst is in close proximity with vital structures whose
integrity has to be preserved in order to prevent the formation of oronasal or
oroantral fistula or when injury to adjacent neurovascular structures or
damage to a vital tooth has to be avoided. (Fig. 26.14 A, B)
When apices of many adjacent erupted teeth are involved within a large
cyst, marsupialisation is done to maintain the vitality of these teeth.
Procedure
Marsupialisation can be performed either under general or local anaesthesia.
The cystic contents are aspirated in the beginning.
Elevation of flap
Usually an H-shaped incision is made on the cyst, the lining turned outwards
and sutured to the mucosa. Small area of lining epithelium may be dissected
and sent for biopsy at this stage.
Alternatively, a circular, elliptical or oval incision can also be used wherever
essential.
Hydrostatic dissection
The mucoperiosteal flap can be easily elevated when it rests on bone.
However, in cases where the bone has been completely resorbed, the
mucoperiosteum lies in direct contact with the cyst. Here, the cyst can be easily
removed by the use of hydrostatic dissection. A cartridge syringe with a fine
needle is inserted through the mucoperiosteum and bone is contacted from the
lesion and injection at this point begins to raise the mucoperiosteum from the
underlying bone and cyst wall.
Removal of bone
Bone removal is done either by the use of a rotary bur or rongeurs depending
upon its thickness. Removal of the bone should be done to the maximum
diameter of the cyst whenever possible.
The remaining of the cyst lining is exposed to the mouth with raw edges at
its circumference. Sometimes this lining may be left to granulate and
epithelialise, but most often it is sutured to the mucoperiosteum at its
periphery.
Packing of the cavity

After suturing the lining epithelium to the adjacent mucoperiosteum, the
cavity is packed with suitably medicated ribbon gauze (e.g. Whitehead’s
varnish) and sutured.
Approximately 10 days after operation, the pack is removed. In case of large
cysts, sedation or analgesia should be administered for changing the first
dressing. The cavity is repacked. When the wound has completely healed, it is
usually possible to take an alginate impression for the construction of an
acrylic plug.
Indications for using plug
• In case of a small bony opening compared to the large size of the cyst
cavity. This kind of bony opening is made because of anatomic
consideration or to preserve adjacent teeth or other important
structures.
• In case of opening surrounded by loose connective tissue (sulcus
mucosa) where in scar contracture reduces the size of the opening to
one-fourth of its original size. Therefore, the opening here should be
maintained with the use of a plug.
The slow process of bone regeneration now begins and the patient is seen at
monthly intervals for progressive reduction in the depth of the plug, but the
diameter at the opening must be fully maintained. Bone replacement takes
place faster in the body and angle of mandible than in the maxilla. However,
in all large cysts the patient is usually under surveillance for 18–20 months
before he/she is able to discard the plug. Although there is often extensive
bone regeneration, the alveolar contour usually has a degree of depression and
distortion.
Features of a plug
• The plug should be retentive and maintain the patency of the cavity.
It should not irritate the mucosa.
• The plug should never reach till depth of the cavity, as this would
interfere with the bone regeneration and filling process.
• The plug can be attached to the dentures in case of edentulous patients.
• Intermittently, the plug should be vented to avoid pressure build up
within the cavity.
• The plug should be designed such that it is not swallowed or inhaled
by the patient.
Advantages of marsupialisation
It is a relatively simple procedure and poses no risk to the adjacent vital
structures. It does not create an oronasal or oroantral fistula. It consumes less
time and there is less blood loss.
Disadvantages of marsupialisation
• Pathological lining of the cyst cavity, if left behind might pose a cause
for development of neoplastic changes in the future.
• Healing can be delayed in cases of large cyst in older patients and cyst
perforating the palatal mucosa.
• It has to be regularly irrigated to prevent infection.
• Prolonged healing time.
• Regular cleansing of the cavity is needed failing which may lead to
infection.
• Inconvenience for patients.
• Formation of tissue pockets that may lodge food material.
Modifications
1. Waldron’s procedure—Marsupialisation followed by enucleation

Decompression of a cyst involves any technique that relieves the pressure
within the cyst that causes it to grow. Decompression may be performed by
making a small opening in the cyst and keeping it open with a drain. The cyst
is kept open initially by a medicated gauze pack and subsequently by an
acrylic plug. Bone regeneration occurs and the cavity reduces in size.
Decompression is not a definitive treatment, but allows a second stage of
enucleation to be undertaken on a much smaller lesion which otherwise would
have been impossible.
2. Marsupialisation by opening into the maxillary sinus or nose (Figs.

26.17, 26.18)
This procedure can be applicable in case of an extensive cyst of the maxilla that
occupies a large portion of the antrum.
FIGURE 26.17 Marsupialisation by opening into the nose. (A)

Freeing of the collapsed cyst from its mucosal attachments. (B)
The antral lining that is fused with the cyst is sacrificed and excised
along with the cyst to assure complete removal. (C) Intranasal
antrostomy to allow drainage from the maxillary sinus and also to
bring out the end of the packed medicated gauze.
FIGURE 26.18 (A–C) Cyst in the maxillary region involving the

sinus. Note the artery forceps introduced through inferior meatus
evident in maxillary sinus (nasal antrostomy).
Procedure
• The entire cystic lining is removed unless there is concern about

damage to adjacent vital structures. This would also aid the cavity
walls to be covered by normal respiratory mucosa rather than a
squamous epithelium.
• The cystic lining is removed in one piece to ensure that the removal is
complete, because incomplete removal would lead to the formation of
residual cyst from the remaining tissue.
• The entire partition between the cyst and antrum should be removed
to provide continuity between the cavities.
• Now, a small intranasal antrostomy is established and packing of the
combined cyst–sinus cavity with any one of the following is done:
▪ Iodoform gauze coated with tincture benzoin
▪ Antral balloon
▪ Foley catheter with balloon
▪ Sterile polyethylene tube
• A curved haemostatis passed via the nostrils into the antrostomy made
in inferior meatus to pull the end of the drain outwards and it is
secured by means of suture or tape.
• Careful closure of the wound without tension must be ensured.
Enucleation (cystectomy)
Enucleation involves complete removal of the cyst lining and its contents.
Intraoral approach is usually the method of choice for enucleation although
rarely an extraoral approach through the submandibular skin may be
indicated. To gain maximum advantage of the method, it is usually completed
by primary closure, although on occasion it can be combined with open
packing.
Indications
• Small cysts
• Small or large cysts not endangering vital structures or risk of
pathologic fracture
• Cysts as odontogenic keratocysts that have a high recurrence rate
Advantages of enucleation
• Entire cystic lining is removed making the entire pathologic tissue

available for microscopic study.
• Rapid healing occurs as the wound is closed primarily.
Disadvantages of enucleation
• In young people, tooth germ or unerupted teeth involved with the cyst
are extracted or removed with the lining of the cyst.
• Pathological jaw fractures can occur in case of enucleation of a large
cyst.
• The procedure endangers the adjacent vital structures.
Direct observation of wound healing as in case of marsupialisation is not
possible.
Procedure
Partsch II—Enucleation with primary closure (Figs. 26.19–26.22)
Intraoral approach
Incision and elevation of the flap
• The usual principles of flap design are applicable here too but with
certain modifications depending upon the individual cyst and its
location.
• When the teeth are involved, the incision should be placed around the
teeth regardless of whether they should be retained or extracted. This
incision would provide complete access and help in easy repair.
Secondly, it permits satisfactory closure of the defect if unexpected
extraction of a tooth or teeth becomes necessary during the operation.
• When the teeth are affected periodontally or when artificial crown is
present, it is wise to avoid the necks of the gingival crevice and place
the incision away from the necks of the teeth.
• For ease of repair in edentulous areas of the jaw, an incision is placed
along the crest.
• The ascending or descending limbs of the incision diverge towards the
buccal sulcus and are placed well away from the swelling. This
permits the final suture line to be on sound supporting bone.
FIGURE 26.19 Enucleation with Primary Closure. (A) Access to the

cyst has been indicated in red, for deroofing of the cyst and
exposure of the cystic lining. (B) Cyst enucleated along with
extraction of the tooth if indicated and mucoperiosteal flap
repositioned and sutured.
FIGURE 26.20 Enucleation and Peripheral Ostectomy.

Histologically the cyst was diagnosed as Odontogenickeratocyst.
(A, B) 3D CT and Axial CT views showing the same. (C) Transoral
exposure of the cyst. (D, E) Cyst Enucleated and reduction of
peripheral bone with powered hand piece. (F) Primary closure
achieved.
FIGURE 26.21 (A) Intraoral periapical radiograph showing a well-
defined radiolucency between 12 and 13. Histologically the cyst
was diagnosed as calcifying epithelial odontogenic cyst. (B) OPG
showing the same. (C) Transoral exposure of the cyst. (D, E) Cyst
enucleation. (F) Enucleated cystic lining. (G) Postenucleation bony
cavity.
FIGURE 26.22 Enucleation of periapical cyst. (A) Preoperative
swelling due to periapical cyst. (B) Mucoperiosteal flap elevated
and the bone overlying the cyst removed. (C, D) Cyst removed
from the bony cavity using spoon type curette. (E) Wound closure.
Bone removal
• The thin overlying bone should be preserved. In some large lesions

after the peripheral elevation of the mucoperiosteal flap, the bone can
be penetrated and elevated as an osteomucoperiosteal flap.
• Where this valuable overlying bone cannot be saved, mucoperiosteum
is elevated and overlying bone is removed with an acrylic bur, gouges
or rongeurs, sufficient to create good access for the enucleation of the
sac.
Enucleation of the cyst

The cyst should be removed entirely without tearing or puncturing. When
separating the cyst lining from inferior alveolar neurovascular bundle, antral
floor and apices of teeth, good care should be taken. Dissection using blunt
instruments is preferred. In places where the lining of the cyst is adherent to
the cavity, a piece of rolled gauze is held with a haemostat and inserted
between the cavity and the cystic lining. Otherwise the cyst can be aspirated so
that the sac shrinks, access and visibility increases. After thorough irrigation,
inspection of the cavity and its margins are done, followed by closure with
sutures).
Enucleation with open packing (Fig. 26.23)

This technique is preferred in cases of infected large cyst wherein primary
closure of the cyst might lead to breakdown of the wound and interfere with
healing.
FIGURE 26.23 (A) Well-defined large unicystic radiolucency in right

mandibular third molar region with previous history of extraction.
(B, C) Enucleation. (D) Packing of the cystic cavity with iodine
gauze. (E1) Preoperative OPG. (E2) Postoperative OPG showing
spontaneous bone fill reducing the cavity size.
Mucoperiosteal flap is raised and the cyst enucleated as described above,

but instead of primary closure, the flap is turned into the bone cavity. It is
fixed with a half-inch medicated gauze pack for 10 days. A change of pack is
followed by the construction of an acrylic plug as used in marsupialisation.
In case of extremely large defects where pathological fractures are
suspected, bone graft can be used to obliterate the cavity. Autogenous bone
grafts are the preferred method.
Enucleation and curettage

It denotes scrapping of the cyst cavity with in exact thickness of surrounding
bone by hand instruments. Recurrence rate is highest with this method (9%–
62%). Adjuncts such as Carnoy’s solution or cryotherapy may be used along with
it.
Enucleation and peripheral ostectomy
It involves enucleation of the cyst along with an inexact thickness of
surrounding bone by powered rotary instruments. Methylene blue dye can be
used to mark the bone (Fig. 26.20).
Enucleation and chemical cauterisation

After enucleation Carnoy’s solution is applied into the cavity. Carnoy’s
solution was first used as a medicament in surgery by Cutler and Zollinger in
1933. It is a powerful fixative, haemostatic and a cauterising agent which
penetrates cancellous spaces in the bone and devitalises and fixes the left out
epithelial remnant cells. Its average depth of bone penetration of this solution
is to a depth of 1.54 mm, nerve penetration to 0.15 mm, and mucosa to a depth
of 0.51 mm after 5 min of application.
Composition:
• 1 gm of ferric chloride
• 1 mL of glacial acetic acid
• 3 mL chloroform
• 6 mL of absolute alcohol
Mechanism of action of Carnoys solution:

Carnoy’s solution is a fixative agent where absolute alcohol hardens the
tissue by shrinking it, glacial acetic acid swells tissue and prevents
overhardening, chloroform increases the speed of fixation and ferric chloride
acts as a dehydrating agent.
Precautions:
Among all the ingredients of Carnoy’s solution, chloroform is considered to
be very hazardous and should be used in a well ventilated hood by wearing
masks.
Side effect:
• Neurotoxic—Nerve should be protected using bone wax

• Necrosis of maxillary sinus
• Better to use fresh solution
Enucleation and cryotherapy

Liquid nitrogen has the ability to devitalise bone in situ and leave osseous in
organic framework untouched. It acts by direct damage from intracellular and
extracellular ice crystal formation leading to cell death. Also it creates osmotic
and electrolytes disturbance in cell. After enucleation, cystic cavity is sprayed
with liquid nitrogen twice for 1 min, with 5 min thaw between freezes.
Advantages:
• Bony matrix is left in place to act as scaffold for new osteogenesis.
• Bone grafts can be placed immediately to promote healing and
decreasing risk of pathological fracture.
• Act as haemostasis agent and reduce scarring.
Resection
Resection is to either do a marginal resection (surgical removal of a lesion
intact and a small area of uninvolved bone, maintaining the continuity of the
bone) or a segmental resection (surgical removal of a segment of the mandible
without maintaining the continuity of the bone) in the mandible whereas in
maxilla the resections are classified as partial maxillectomy (alveolectomy) or
subtotal or total maxillectomies. Resections have the lowest recurrence rate
(0%) but the highest morbidity rate because reconstructive measures are
necessary to restore jaw function and aesthetics.
Complications of untreated cysts

Cysts that are not treated have potential complications which include the
following:
1. The cystic content being a rich source of bacterial nutrition could lead
to secondary infection. This could spread into tissue spaces causing
cellulitis or osteomyelitis (Fig. 26.24).
2. On expansion, the cyst can cause damage to the surrounding tissues
and vital structures. Fast growing cysts exert a pressure on the
surrounding bone leading to resorption. Further it could cause
‘pressure effects’ on nerves and vessels that may cause symptoms of
paraesthesia, neuropraxia or decreased blood flow.
3. The cystic lining may act as precursors to odontogenic tumours or
primary intraosseous carcinoma. Untreated dentigerous cysts have
been reported to give rise to ameloblastomas and primary intraosseous
carcinoma.
4. Resorption of surrounding bone may lead to thinning down of the bone
that predisposes the jaw bones to pathologic fractures (especially
odontogenic keratocysts) or may cause oroantral fistula.
5. Loss of vitality of teeth.
6. Gross facial deformation.
FIGURE 26.24 (A) A clinical picture of osteomyelitis of the
mandible as a complication of an untreated right cystic lesion. (B)
Segmental resection showing the perforated lytic lesion.
Odontogenic keratocyst (OKC)

First described by Philipsen in 1956, the odontogenic keratocyst (OKC) is a
dilemmatic odontogenic developmental cyst of oral and maxillofacial region
which has gained very special attention since last 2 decades. It is a rare and
benign locally aggressive developmental cyst.
Many prior attempts have been made to classify these cysts from 1887 to
finally WHO 2017. Previously classified under developmental odontogenic
cyst of jaw by WHO in 1971 and 1992. Redesignation of the OKC as the KCOT
by the World Health Organization (WHO) was based on the well-known
aggressive behaviour and the high recurrence rate, its histology and new
information regarding its genetics as per 2005 classification.
The most controversial decision in the 2017 classification was to move
keratocystic odontogenic tumour back into the cyst category as OKC because
the evidence supporting that hypothesis of neoplasia is considered
insufficient. And also the term Primordial cysts have been dropped and are no
longer used synonymously for OKC.
(Reference—Update from the 4th Edition of the World Health Organization
Classification of Head and Neck Tumours: Odontogenic and Maxillofacial Bone
Tumors. Head and Neck Pathol. 28 February 2017).
Evolution of OKC from cyst to tumour to cyst again based on WHO classifications
Dental cyst (John Hunter, 1774)

Dermoid Cyst ( Mikulicz, 1876)
Primordial cyst (Robinson, 1945)
Keratocystoma (Shear)
Odontogenic keratocyst (Philisen, 1956 and Pindborg and Hansen, 1963)
Benign neoplasm (Toller, 1967)
Odontogenic keratocyst (WHO, 1971)
True benign cystic epithelial neoplasm (Ahlfors, 1984)
Keratocystic odontogenic tumor (Benign neoplasm) (WHO, 2005)
Pathogenesis and clinical presentation:
• Origin: Most OKCs (60%) arise from dental lamina rests or from the
basal cells of oral epithelium and are thus primordial origin OKCs and
the remaining 40% arise from the reduced enamel epithelium of the
dental follicle and are thus dentigerous-origin OKCs.
• Age and gender: It occurs at all ages with peak incidence in 2nd and
3rd decades of life, with male:female ratio of 1.6:1.
• Site:
▪ Location wise it is occurs most frequently in mandible than in
maxilla.
▪ It occurs mostly as intraosseous lesion though peripheral
counterpart also has been reported in buccal gingiva at canine
region of the mandible.
▪ In mandible it occurs usually in angle—ascending ramus
region (69%–83%) and often the mandibular cyst crosses the
midline.
▪ Maxillary cyst may involve sinus and nasal floor, premaxilla
and maxillary third molar region. OKC may also arise from
TMJ.
▪ Multiple OKCs is the feature of Nevoid Basal Cell Carcinoma
(Gorlin syndrome) (Box. 26.1).
• Signs and Symptoms:
▪ Mostly asymptomatic, swelling appears late as the cyst
initially extends in the medullary cavity along the path of
least resistance, rather than expanding the cortex (early
stage).
▪ Pain, swelling with discharge and paraesthesia of the lower lip
and teeth (late stage)
▪ Displacement of teeth during expansion
▪ Maxillary lesions get infected and are detected earlier than the
mandibular lesions due to their close proximity to antrum
▪ Enlarging maxillary lesion produce displacement and
destruction of floor of orbit and proptosis of eye
▪ The expansion of the cyst is very minimal in the initial stage
and it is due to the classical characteristic of the cyst to grow
in anteroposterior direction in the medullary space of the
bone.
▪ Buccal expansion more common than the palatal or lingual
expansion.
▪ Percussion of teeth produce dull hollow sound
▪ Perforation of bony cortex seen during enlargement
▪ Associated with missing tooth (not always)
▪ Displacement of inferior alveolar canal in an abnormal
position (large lesions)
• Syndromes associated with multiple OKC are Nevoid Basal cell
carcinoma syndrome (NBCCS), Gorlingoltz syndrome, Marfans
syndrome, Ehlers danlos syndrome, Noonans syndrome, Orofacial
digital syndrome, Simpson–Golabi–Behmel syndrome (Bakaeen et al.,
2004; Gonzalez-Alva et al., 2008).
• Radiological features:
▪ OKC presents as well defined unilocular or multilocular (25%–
40%) radiolucent lesion with smooth margin (corticated
margin in secondarily infected cases) and has several
radiological variants.
▪ Associated with teeth either in pericorornal, interradicular or
periapical or in association with missing teeth.
▪ Most commonly involve molar ramus area.
▪ Multilocular cystic lesion may appear as one large cyst with
few smaller daughter cyst.
▪ Borders: Smooth or scalloped suggesting unequal growth
activity.
▪ Buccal expansion with resorption of the lower cortical plate
sometimes with perforation of bone.
▪ Resorption of adjacent tooth root Fig. 26.25
Box 26.1 Nevoid Basal Cell Carcinoma Syndrome

Features
Features of Gorlin’s Syndrome
Cutaneous
▪ Basal cell epitheliomas

▪ Milia
▪ Palmar pits
▪ Plantar pits
▪ Epidermal cysts of skin
▪ Subcutaneous calcifications
▪ Cleft lip or palate
▪ Polydactyly
Skeletal
• Odontogenic keratocysts
• Bifid ribs
• Scoliosis
• Mandibular prognathism
• Increased calvarial diameter
• Well-developed supraorbital rims
• Spina bifida of cervical or thoracic spine
• Hyperpneumatisation of paranasal sinuses
• Short fourth metacarpals
• Marfanoid build
Ocular
• Glaucoma
• Cataracts
• Coloboma of the iris
• Hypertelorism
• Strabismus
• Nystagmus
Neurologic
• Calcified falx cerebri

• Mental retardation
• Cerebral tumours
• Agenesis of corpus callosum
• Calcified tentorium cerebelli
Sexual
• Undescended testes
• Ovarian tumours
• Hypogonadism
FIGURE 26.25 Radiographic variants of OKC.
Radiological types of keratocyst (Main 1970)
• Replacement type: Cyst which forms in the place of normal teeth.

• Envelopmental type: Cyst which embraces an adjacent unerupted tooth.
• Extraneous type: Cyst which occur in asending ramus away from the teeth.
• Collateral type: Cyst which occurs adjacent to the root of teeth which are indistinguishable
radiologically from lateral periodontal cyst.
• Histological features:
WHO (Phillipen 2005) – OKC

• Regular parakeratinised stratified squamous epithelium without rete ridges
• Epithelium is 5–8 cell layers thick
• Well defined epithelial basal layer with columnar or cuboidal epithelium cells frequently
containing basophilic nuclei in palisaded fashion described as ‘picket fence or tombstone
appearance’
• Parakeratotic layers with corrugated surfaces
• Loss of characteristic cellular and architectural feature in the presence of inflammatory
infiltrates
• Cystic wall composed of fibrous connective tissue which is thin and usually uninflamed.
• Mitotic figures frequently present in the suprabasal layers
• Others findings are satellite cysts, daughter cysts solid epithelial proliferation, odontogenic
rests basal layer budding may be seen. Fibrous connective tissue wall may get mineralised
and may include cholesterol crystals and Rushton bodies.
• Recurrences:
It has a high rate of recurrence of about 25%–60%. The mean time of

recurrence for males was found to be 4 years and for females it came out to be
7 years.
Causes and factors responsible for recurrence of OKC
• Incomplete removal of cystic lining

• Thin and friable nature of epithelial lining,
• Higher level of cell proliferative activity in the epithelium.
• Budding in the basal layer of the epithelium
• Bony perforation.
• Adherence to adjacent soft tissue.
• Supraepithelial and subepithelial split of the epithelial lining.
• Parakeratinisation of the surface layer
• Remnants of dental lamina epithelium not associated with original OKC and development
of new OKC in the adjacent area.
• Growth of new OKC from satellite cyst/daughter cyst/remnants/cell rests.
• Molecular changes and genetics:

▪ Dysregualtion (Mutation) of PTCH (patched) tumour
suppressor gene involved in both NBCCS and sporadic OKC
occur on chromosome 9q22.3-q31.
▪ Loss of heterozygosity in loci which is related to DNA
imbalance, revealing deletion of tumour suppressor genes.
▪ Cell proliferation markers, such as p53, Ki67, and PCNA, as
well as certain cytokeratins and suppression of apoptosis-
related markers, such as bcl-2 and Bax were also identified.
Pathogenesis of OKC:
Hedgehog signalling pathway and PTCH mutation explain the pathogenesis of
OKC. PTCH (patched) and SMO (smoothed) forms a receptor complex in cell
membrane which has a suppressor effect on growth signal transduction. If
PTCH is mutated this inhibitory effect is lost and proliferative and stimulating
effects of SMO dominates the inhibition. SHH (sonic hedgehog ligand) binding
to PTCH also releases this inhibition and facilitates the growth signal
(Fig. 26.26A, B).
FIGURE 26.26 (A) PTCH (patched)-SMO (smoothed) receptor
complex in the cell membrane- suppressor effect on growth signal
transduction. SMO inactivation by PTCH (B) PTCH mutation or
SHH binding causes the loss of inhibitory effect and proliferative
and stimulating effect of SMO outweighs the inhibition.
• Malignant transformation:
Rarely, OKCs may undergo malignant transformation into Primary

Intraosseous Squamous Cell Carcinoma (PIOSCC). Patients persisting with
unresolved disease after treatment should be investigated for malignant
transformation. Detailed histopathological examination of OKC specimens is
recommended to detect small foci of SCC which may be present in the
epithelium.
• Aspiration:
▪ OKC aspirate contains characteristic odorless thick, creamy,
dirty white, viscoid suspension of keratin resembling pus
(shimmering keratin crystals)
▪ Total protein less than 4 g/100 mL
▪ Other contents: Cholesterol crystals, hyaluronic acid, keratin,
rushton bodies, heaparin and chondroitin sulphate
▪ Histologically: Myxoma, Ameloblastoma, Central giant cell
granuloma, Odontogenic cysts.
▪ Radiographically: Dentigerous cyst (40%), Residual cysts,
radicular cyst, lateral periodontal cysts (25%), primordial cyst
(25%), globulomaxillary cyst (10%), unicystic ameloblastoma,
A-V malformation, fibroosseous lesion at initial stages.
Treatment modalities for OKC:
• A thorough evaluation is required before coming to a particular

treatment plan as the very nature of OKC is high rate of recurrence.
• Treatment of OKC depends on patient age, size and location of cyst,
soft tissue involvement and histological variant of lesion.
• Treatments are usually classified as: (refer to page no. for the
procedures)
i. Conservative like enucleation
ii. Enucleation with curettage
iii. Enucleation with peripheral ostectomy
iv. Enucleation with Carnoy’ solution with or without
peripheral ostectomy
v. Enucleation and cryotherapy
vi. Marsupialisation (decompression)
vii. Marsupialisation with cystectomy: (Waldron’s method)
viii. Resection
• Although enucleation helps to provide complete specimen for
histopathologic examination, but it shows recurrence rates as high as
30%–60% and 0% with resections (Figs. 26.27, 26.28).
FIGURE 26.27 Marginal/En bloc resection of OKC in right

mandibular body. (A, B) 3D CT scan and OPG showing the extent
of the lesion. (C, D) Marginal mandibulectomy and the specimen.
(E) Reconstruction of the bony defect with Rib graft. (F) Closure of
the wound.
FIGURE 26.28 Segmental resection of OKC in left mandibular
ramus—condyle unit. (A, B) 3D CT scan and OPG showing the
extent of the lesion. (C) Segmental resection done and the
specimen. (D, E) Rib graft shaped in the form of mandibular ramus
and body and reconstruction of the bony defect. (F) Closure of the
wound.
Advanced and future treatment modalities

Due to the recent advances and thus determination of molecular basis of this
entity, a new novel methodology concentrating on molecular aspects has been
devised. The SHH pathway can be blocked at different levels, and SHH
inhibitors could serve as attractive antitumour agents. According to some
studies, cyclopamine, a plant-based steroidal alkaloid, blocks activation of
SHh pathway caused by oncogenic mutation. Other studies also show
antagonists of SHh signalling factors could effectively.
Management by Bramley (1971, 1974):

1. Single small cystic lesion with regular spherical outline—enucleation from intraoral
approach
2. Larger or less accessible lesions with regular spherical outline—enucleated from an
extraoral approach
3. Unilocular lesions with scalloped or loculated periphery and small multilocular lesions
—Marginal resection (maintaining the continuity of posterior and inferior borders as in
the ascending ramus, angle, and body of mandible
4. Large multilocular lesion with or without cortical perforation—resection and primary or
secondary reconstruction
Dentigerous cyst (follicular cyst)
• Developmental odontogenic cyst that originates by separation of

dental follicle from around the crown of an unerupted tooth and is
attached to tooth at the cementoenamel junction.
• This is the most common type of developmental odontogenic cyst,
making about 20% of all epithelium lined cyst of the jaws.
• Usually seen in teenagers/young adults, although can occur over a
wide age range.
• Develops from accumulation of fluid (including glycosaminoglycans)
between reduced enamel epithelium of dental follicle and crown of
unerupted tooth.
• Vast majority are developmental odontogenic cysts but may have
inflammatory pathogenesis.
• Inflammation progressing from root apex of carious or necrotic
deciduous tooth brings about development of dentigerous cyst around
underlying, unerupted permanent tooth.
• Impossible to histologically distinguish inflamed developmental
odontogenic dentigerous cyst from those induced by inflammation.
Site
• By definition, a dentigerous cyst occurs in association with an

unerupted tooth
• Most commonly around permanent mandibular third molars (wisdom
teeth)
• Somewhat less common around permanent maxillary third molars,
maxillary cuspids, mandibular second premolars, but any tooth may
be involved.
• Rarely involves supernumerary teeth and odontomas.
• Distinctly rare to occur around unerupted primary teeth.
Pathophysiology
• In normal tooth development, tooth enamel is produced by the enamel

organ, an ectodermally derived specialised epithelium.
• After enamel formation is complete, the enamel organ epithelium
atrophies.
• This reduced enamel epithelium eventually merges with the overlying
mucosal epithelium to form the initial gingival crevicular epithelium
of the newly erupted tooth.
Dentigerous cysts form when fluid accumulates between the reduced
enamel epithelium and the crown of the unerupted tooth.
Clinical features: Age and gender predilection: 2nd and 3rd decades of life
between 1 and 30 years of age and slight male predilection and prevalence
being higher for whites.
Always associated with unerupted or impacted tooth. Common sites—Most
often they involve unerupted mandibular third molars, maxillary canines,
maxillary third molars and mandibular second premolars. These cysts may
also be found enclosing a complex, compound odontomas or involving a
supernumerary tooth.
May be small/asymptomatic, identified on routine radiographs taken for
unrelated reasons or for imaging to investigate delayed tooth eruption
Only extensive lesions result in facial asymmetry, extreme displacement of
teeth, severe resorption and pain.
Dentigerous cyst involving an unerupted 3rd molar results in:
• Expansion of the cortical plate.

• Displacement of the 3rd molar towards the lower border of the
mandible.
• Compression against the inferior alveolar nerve.
• Hollowing out of the entire ramus upto the coronoid process.
Dentigerous cyst involving an unerupted maxillary cuspid results in:
• Anterior maxillary expansion.

• No pain unless secondarily infected.
• Most commonly a well-defined, unilocular radiolucency on X-ray

• Often has sclerotic rim
• Can cause resorption of adjacent teeth
• Three different radiographic relationships between involved tooth and
cyst described:
• Central variety:
Most common radiographic relationship
▪ It develops around and surrounds the entire crown of tooth,
thus tooth appears to be erupting into the cyst (Fig. 26.29A)
• Lateral variety:
▪ It develops at lateral tooth root and only partially surrounds
crown (see Clinical images, Fig. 26.29B)
• Circumferential:
▪ It develops around crown and extends down the root(s), thus
roots also appear within the cyst
• Bilateral dentigerous cysts are uncommon.
• Radiolucent area should be at least 3–4 mm to delineate an enlarged
follicle (Fig. 26.29C)
FIGURE 26.29 Radiographic variants of dentigerous cysts. (A)

Central (B) Lateral (C) Circumferential.
Histologic features
• The histopathologic features of dentigerous cysts vary, depending on

whether the cyst is inflamed or not inflamed
• In the noninflammed type, thin flattened epithelial lining which is 2–4
cell layer thick with connective tissue wall is seen
• In the inflamed dentigerous cyst, the epithelial lining may show
varying amounts of hyperplasia with the development of rete ridges
and more definite squamous features
Aspiratory content/ treatment:
• Aspiration yields thin, watery, yellow straw-coloured fluid

• The usual treatment for a dentigerous cyst is careful enucleation of the
cyst together with removal of the unerupted tooth
• This permits decompression of the cyst, with a resulting reduction in
the size of the bone defect. The cyst can then be excised after some
time with a less extensive surgical procedure
• Unicystic ameloblastoma
• OKC
Bilateral buccal bifurcation cysts

• Enlarged dental follicles
• Multiple hyperplastic calcifying follicles
• Mucolipidosis Type III, or pseudo-Hurler polydystrophy
• Maroteaux-Lamy syndrome, also known as mucopolysaccharidosis
type VI
• Amelogenesis imperfecta
• Tuberous sclerosis, or cleidocranial dysplasia
Treatment:
• Varies based on age, maturity, anatomic position and relative

importance of tooth involved, size of cyst, presence of additional
neoplasms; also patient preference, including cosmetic and functional
considerations
• Enucleation of entire cyst with extraction of the associated tooth is
most common approach
• Marsupialisation
• Removal of the cyst sparing the permanent tooth
• Requires close follow-up to monitor for recurrence
Prognostic factors
• Excellent prognosis, almost never recurs with complete enucleation,
however follow-up radiographic studies recommended
• Recurrence may indicate incomplete excision or possibly incorrect
original diagnosis
• Tooth-sparing marsupialisation procedures may have higher risk of
cyst recurrence/persistence
• Rarely, second neoplasms can arise from dentigerous cysts, most
commonly:
▪ Ameloblastoma
▪ Squamous cell carcinoma
▪ Intraosseous mucoepidermoid carcinoma
• Localised areas of ‘bud like’ proliferations of cystic epithelial cells may
be seen in few areas, which are known as ‘Mural proliferations’ and
they indicate the development of Ameloblastomas which also prove
the development of ameloblastoma from lining of dentigerous cyst.
Cysts: Classification
CHAPTER 27
Odontogenic Tumours
Benign tumours
Tumours of odontogenic epithelium without odontogenic
ectomesenchyme
Ameloblastoma
• Pathogenesis
• Clinical classification
• Radiographic features
• Prognosis
Calcifying epithelial odontogenic tumour (pindborg
tumour)
• Pathogenesis
• Histopathological features
Treatment
Squamous odontogenic tumour
• Pathogenesis
• Clinical and radiographic features
• Treatment
Adenomatoid odontogenic tumour
• Treatment
Tumours of odontogenic epithelium with odontogenic
ectomesenchyme with or without dental hard tissue
Ameloblastic fibroma
• Pathogenesis
• Treatment
Ameloblastic fibro-odontoma
• Pathogenesis
• Treatment
Ameloblastic odontoma (odontoameloblastoma)
• Treatment
Odontomas
• Complex odontoma
• Compound odontoma
Mesenchyme and/or odontogenic ectomesenchyme with or
without included odontogenic epithelium
Odontogenic fibroma
• Central odontogenic fibroma
• Peripheral odontogenic fibroma
Odontogenic myxoma
• Pathogenesis
• Treatment
Cementomas
• Benign cementoblastoma
Malignant tumours
Malignant ameloblastoma
Ameloblastic carcinoma
Intraalveolar carcinoma
• Pathogenesis
• Treatment
Odontogenic sarcoma
• Treatment and prognosis
Ameloblastic fibrosarcoma
According to Sir Rupert Willis, a tumour or neoplasm is defined as ‘an

abnormal mass of tissue, the growth of which is uncontrolled and
uncoordinated with that of the normal tissue and persists in the same
excessive manner even after the cessation of the stimulus that evoked the
change’.
The term ‘odontogenic’ signifies all the primordial tissues—epithelium,
mesenchyme and ectomesenchyme of the tooth-forming apparatus. Any
aberrance or abnormal proliferation of such tissue at any stage of
differentiation gives rise to an odontogenic tumour. The oral tissues retain
some remanence of these embryonic tissues, postnatally. These tissues have
inherent potential for replication and growth, the stimulus for which has been
controversial. These dormant cells and tissues that give rise to the odontogenic
tumour histologically resembles the native embryonic tissue of origin and is
unique to the jawbones.
The possible source of the cells that give rise to their odontogenic tumours
are:
• Cell rests of Serres

• Cell rests of Malassez
• Oral epithelium
• Ectomesenchyme/mesenchyme
The jaw tumours that arise from tissues other than the tooth-forming tissues
are referred to as nonodontogenic and is not exclusive to the jawbone. As with
all tumours they are classified as benign and malignant according to their
biologic behaviour (Table 27.1).
Table 27.1
Classification of odontogenic tumours
Benign tumours
1. Odontogenic epithelium with mature, fibrous stroma; odontogenic ectomesenchyme not
present
i. Ameloblastomas
• Solid/multicystic
• Extraosseous/peripheral
• Desmoplastic
• Unicystic
ii. Squamous odontogenic tumour (SOT)
iii. Calcifying epithelial odontogenic tumour (CEOT)
iv. Adenomatoid odontogenic tumour (AOT)
v. Keratinising cystic odontogenic tumour (KCOT)
2. Odontogenic epithelium with odontogenic ectomesenchyme with or without dental hard
tissue formation
i. Ameloblastic fibroma
ii. Ameloblastic fibrodentinoma
iii. Ameloblastic fibro-odontoma
iv. Complex odontoma
v. Compound odontoma
vi. Odontoameloblastoma
vii. Calcifying cystic odontogenic tumour
viii. Dentinogenic ghost cell tumour
3. Mesenchyme and/or odontogenic ectomesenchyme with or without odontogenic
epithelium
i. Odontogenic fibroma (epithelium poor and epithelium rich types)
ii. Odontogenic myxoma or fibromyxoma
iii. Cementoblastoma
Malignant tumours
1. Metastasising, malignant ameloblastoma
2. Ameloblastic carcinoma
i. Primary
ii. Secondary (dedifferentiated), intraosseous
iii. Secondary (dedifferentiated), extraosseous
3. Primary intraosseous squamous cell carcinoma (PIOSCC)
i. PIOSCC solid type
ii. PIOSCC derived from odontogenic cysts
iii. PIOSCC derived from keratocystic odontogenic tumour (KCOT)
4. Clear cell odontogenic carcinoma
5. Ghost cell odontogenic carcinoma
6. Ameloblastic fibrosarcoma
7. Ameloblastic fibrodentino and fibroodontosarcoma
Classification was approved at the Editorial and Consensus Conference held in

Lyon, France (WHO/IARC) in July 2003 in conjunction with the preparation of the
new WHO Blue Book volume Pathology and Genetics of Tumours of the Head and
Neck.
Benign tumours
Odontogenic tumours are uncommon lesions that are derived from the
specialised dental tissues. The odontogenic tumours are mostly central
tumours although occasional extraosseous tumours are found.
Tumours of odontogenic epithelium without

odontogenic ectomesenchyme
Ameloblastoma
In 1885, Malassez coined the term ‘adamantinoma’. In 1934, Churchill replaced
the term ‘adamantinoma’ which implies formation of hard tissue with the now
accepted term ameloblastoma. Ameloblastoma has been defined by Robinson
as ‘usually unicentric, nonfunctional, intermittent in growth, anatomically
benign and clinically persistent’.
It is a low-grade, malignant, basaloid tumour with a variable range of
histopathologic patterns, clinical forms and behaviour.
Pathogenesis
Ameloblastoma is believed to be derived from
• Epithelial rests of Malassez (remnants of the sheath of Hertwig

contained in the periodontal ligament of the erupted teeth).
• Epithelium of odontogenic cysts—17% are associated with impacted
teeth and dentigerous cysts.
• Disturbance of developing enamel organ—may result from trauma or
chemical insult in utero.
• Basal cells of surface epithelium—thought to result from invagination
of the basal cell of epithelium into the developing jawbone.
• Heterotopic epithelium—epithelium from other areas of the body (e.g.
pituitary gland) that migrates to the jaw.
Clinical features
• Average age of occurrence of ameloblastoma is between 20 and

40 years.
• 80% occurs in the mandible, with 75% of these in the molar and ramus
region and 20% in the maxilla.
• Often associated with an impacted mandibular third molar.
• Ameloblastomas usually start to grow in the cancellous bone of the
mandible and may attain a substantial size before the outer contour of
the bone is appreciably altered. Later both lingual and buccal aspects
of the mandible expand.
• They can reach an enormous size without either invading or ulcerating
the overlying epithelium.
• Pain or sensory nerve damage occur only if infection supervenes.
• Trauma due to extraction, removal of cyst, etc. is thought to be
associated with the incidence of ameloblastoma.
• Radiograph shows resorption of the associated teeth.
Clinical classification
• Unicystic ameloblastoma
• Conventional or multicystic or solid ameloblastoma
• Peripheral (extraosseous) ameloblastoma
• Malignant ameloblastoma
• Pituitary ameloblastoma (craniopharyngioma or Rathke’s pouch
tumour)
Conventional or solid ameloblastoma (Fig. 27.1A–I)

The classic picture is a multilocular appearance where numerous, well-defined
cystic spaces of varying diameter are seen. When radiolucencies are small,
lesion is described as having a honeycomb or soap bubble configuration.
Ameloblastoma grows within the medullary cavity, causing scalloping of the
inner cortex by pressure erosion. The erosion may be so severe that only a thin
shell of the original cortex remains at the periphery of the lesion. Lesions in
dentulous regions cause root resorption and tooth displacement.
FIGURE 27.1 (A) Swelling in left mandible obliterating vestibular
sulcus. (B) OPG showing multilocular radiolucency with soap
bubble appearance in left mandible body (33–38) with involvement
of inferior cortex. Note resorption of teeth. (C–E) 3D CT scan
showing the lesion with areas of perforation. (F) Intraoperative view
exposing the lesion. (G–I) Segmental resection using oscillating
saw.
Histopathological features
Histologically, most ameloblastomas fall within two major morphologic
configurations—follicular and plexiform types. The plexiform type consists of
interlacing strands of narrow or wide odontogenic epithelial trabeculae. The
follicular type consists of small to large odontogenic epithelial nests (the
follicles) and variously shaped and sized ameloblastomatous islands.
Major histologic features

Subtypes of ameloblastoma are:
1. Follicular type (most common type): Central mass of polyhedral cells

surrounded by a layer of cuboid or columnar cells.
2. Plexiform type: Tumour epithelium arranged in irregular masses. Each
mass is bounded by a layer of columnar cells.
3. Acanthomatous type: Compression of stellate reticulum into a
squamoid mass with squamous metaplasia and keratinisation in the
centre of the tumour island. This usually occurs in follicular type.
4. Basal cell type: Assume a basal cell appearance throughout the lesion.
It is the least common type.
5. Granular cell type: Granular transformation of the epithelial cells. The
cells are large and may be cuboidal, columnar or rounded. The
cytoplasm is filled with acidophilic granules.
6. Desmoplastic type: This contains cords and strands of
ameloblastomatous islands in a densely collagenised stroma.
Unicystic ameloblastoma
It is defined as a single cystic cavity that shows ameloblastomatous
differentiation in the lining. Unicystic ameloblastoma deserves separate
consideration based on its clinical, radiographic and pathologic features and
its response to treatment. Whether the unicystic ameloblastoma originates de
novo as a neoplasm or it is the result of neoplastic transformation of cyst
epithelium is not yet known (Fig. 27.2A–C).
FIGURE 27.2 (A) CT scan reveals bone loss in the retromolar

region associated with the unerupted 37. Note the buccal and mild
lingual cortical erosion. (B) Intraoperative view showing excision of
the lesion. (C) Excised specimen with the unerupted 37.
Clinical and radiographic features

Unicystic ameloblastomas are most often seen in young patients with 50%
diagnosed in the second decade of life. More than 90% of unicystic
ameloblastomas are seen in posterior mandible. This lesion typically
surrounds the crown of an unerupted mandibular third molar and resembles
dentigerous cyst.
Histopathology (Ackermann’s classification)

Three histopathologic variants, namely, luminal, intraluminal/plexiform and
mural types of unicystic ameloblastoma have been recognised.
• The luminal types consist of a fibrous connective tissue wall, totally or

partially lined by ameloblastomatous epithelium.
• The intraluminal type consists of one or more nodules of
ameloblastoma projecting from the cystic lining into the lumen of the
cyst.
• In the mural type the fibrous wall is infiltrated by typical follicular or
plexiform ameloblastoma. This is the only variant with high
recurrence rate.
Peripheral (extraosseous) ameloblastoma
• Soft tissue counterpart of the central intraosseous ameloblastoma.

• Occurs in alveolar mucosa with no direct involvement of the
underlying bone.
• Slight predilection for the mandible than maxilla.
• Average age: 40–60 years.
• Slow growing and cause little or no bone erosion.
• Microscopically similar to the multicystic variant.
Pituitary ameloblastoma craniopharyngioma/Rathke’s pouch tumour
• Neoplasm of the CNS that grows in a pseudoencapsulated mass in the

suprasellar or intrasellar area with tendency to grow into the frontal,
temporal lobe or encroaching brain stem.
• Most common tumour of childhood and adolescents with an average
age of 3–23 years.
• It consists of 25% of all CNS tumours regardless of age.
• Derived from cell rests of the craniopharyngeal duct formed by
Rathke’s pouch (oral ectoderm).
• Histologically similar to oral ameloblastoma but also contains irregular
calcified masses as well as occasional foci of metaplastic bone or
cartilage, ghost cells and sometimes tooth materials.
Surgical management
• Ameloblastomas are generally slow growing but locally invasive

tumours and have a high recurrence rate after treatment.
• Lesions of the mandible are often aggressive and subsequently
perforate the cortical bone.
• Tumour normally extends beyond radiographic margins in cancellous
bone but not at the cortical margin.
• Curettage of ameloblastomas, which was favoured in the past, is now
not advocated because of the high recurrence rate associated with it.
Residual tumour cell will likely be left at the tumour-bone margin
following curettage.
• Ameloblastomas are best treated by resection of the lesion with a
marginal clearance of 1.5–2 cm of normal bone to prevent recurrence.
• The lesion may be resected as block resection with or without
continuity defect based on the integrity of inferior cortex.
• Radiologically a minimum of 1 cm residual mandible inferior cortex is
required postoperatively to prevent pathologic fracture.
• Inferior alveolar nerve should be sacrificed if it lies within the lesion.
• The main risk with mandibular ameloblastomas is extension into the
soft tissues when it becomes difficult to define the tumour margins
and vital structures may be endangered.
• Maxillary ameloblastomas are particularly dangerous, partly because
the bones are considerably thinner than those of the mandible and
present less effective barriers to spread. Therefore, radical excision is
essential, preferably maxillectomy.
• Peripheral ameloblastomas are treated by excision, as usually there is
no alveolar bone involvement. If prior biopsy indicates involvement of
bone, block resection with continuity defect is the choice of treatment.
• Unicystic ameloblastoma have good prognosis with less recurrence
rate following curettage. But mural unicystic ameloblastoma has high
recurrence rate and is always treated similar to solid or multicystic
ameloblastoma.
Prognosis
Ameloblastoma is a persistent, locally invasive lesion and has a high
recurrence rate. Recurrence rates of 10%–20% have been reported after
enucleation and curettage of unicystic ameloblastoma. A recurrence rate of
15% is reported after marginal resection of conventional ameloblastomas.
Calcifying epithelial odontogenic tumour (pindborg tumour)

This rare neoplasm was first described as a separate entity by Pindborg (1956).
Pathogenesis
The tumour is thought to arise from the epithelial elements of the enamel
organ. The specific site of origin is controversial. It is either from stratum
intermedium or reduced enamel epithelium.
Clinical features
• The tumour occurs at any age with equal sex distribution.
• Occurs mainly in the premolar and molar regions.
• Affects the mandible twice as frequently as the maxilla.
• It presents usually as an expansile, painless, slow growing swelling.
• Most commonly associated with impacted or embedded teeth.
• Has a variable radiographic appearance.

• May appear as a unilocular radiolucent area, mimicking an
odontogenic cyst.
• As it progresses, it tends to become multilocular or honeycomb as a
result of destruction of bone and deposition of calcium.
• Most characteristic feature is diffuse radiopacities within the lesion.
These are frequently present uniformly throughout the lesion giving a
driven-snow appearance.
• A distinct picture of trabecular and sheets of large squamoid shaped

epithelial cells with prominent intercellular bridges are found.
• Binuclear and even trinuclear cells may be present.
• The connective tissue is inconspicuous between the islands and sheets
of epithelium. Prominent or scattered calcifications in concentric
crenate like shapes (Liesegang rings) may occur in the amyloid areas
which account for the radiopacities.
Treatment
• Surgical treatment of this tumour should be case specific and based on

anatomic location, size and perforation of the bone.
• Marginal or segmental resection is the treatment of choice because of
the recurrence rate following curettage and enucleation. Immediate or
delayed reconstruction can be performed.
• The tumour recurs after inadequate treatment.
Squamous odontogenic tumour

Squamous odontogenic tumour is a rare benign odontogenic neoplasm that
was first described in 1975 and is now recognised as a distinct entity.
Pathogenesis
These tumours arise from rests of dental lamina or may be from epithelial rests
of Malassez.
• Squamous odontogenic tumours have been seen in patients at an

average age of 38 years with no site predilection for either jaw.
• A triangular radiolucent defect lateral to the root or roots of the teeth is
seen radiographically.
Microscopically, squamous odontogenic tumour is distinctive and consists of
varying shaped islands of bland appearing squamous epithelium in a mature
fibrous connective tissue stroma.
Treatment
• Conservative local excision appears to be effective for patients with

squamous odontogenic tumour.
• Maxillary squamous odontogenic tumours may be somewhat more
aggressive than the mandibular lesions with a greater tendency to
invade adjacent structures because of the nature of the maxillary bone.
Adenomatoid odontogenic tumour

Adenomatoid odontogenic tumours are benign lesions formerly known as
adenomatoid ameloblastoma; their behaviour is different from that of
ameloblastomas and they have no glandular component.
The tumour is thought to arise from epithelium of the dental lamina
complex or its remnants, though it is considered as a hamartoma by many.
Clinical features
• Occurs as a slow growing painless swelling usually in the anterior

maxilla.
• Occurs in persons between 10 and 21 years of age.
• Females are more commonly affected.
• Most of the lesions occur anterior to the canine tooth and are
frequently associated with impacted or unerupted teeth.
• Appears as a well-defined radiolucency with margins showing definite
sclerosis.
• May enclose a part of the root usually on the lateral aspect.
The most characteristic features are nodules or whorls of spindle shaped or
cuboidal epithelial cells. It is well encapsulated. Calcified materials, large
eosinophilic masses, usually PAS positive are seen in the tissues.
Treatment
The tumour is encapsulated and the marrow space around the lesions is free of
tumour, so the lesions may be removed by simple curettage or enucleation.
Tumours of odontogenic epithelium with

odontogenic ectomesenchyme with or without
dental hard tissue
Ameloblastic fibroma
Ameloblastic fibroma is a benign mixed odontogenic tumour histologically
similar to ameloblastomas.
Pathogenesis
Arises from odontogenic epithelial and mesenchymal cells of the enamel organ
and dental papilla.
Clinical features
• Slow growing asymptomatic lesion causing eventual expansion of the

jaw.
• Typically found in the first 2 decades.
• Males and females are equally affected.
• Most of the lesions appear in the mandible, with majority occurring in
the posterior region.
Appears as a multilocular radiolucency with sclerotic margins. It ranges from
1 to 8 cm in diameter.
This tumour has a dense fibrous capsule enclosing epithelial and connective
tissue components. The epithelium consists of ameloblast like or cuboidal cells.
The connective tissue collagen production resembles that of the immature
dental papilla.
Treatment
Conservative excision is the treatment of choice. Resection including 0.5–1 cm
of clinically sound bone is advocated. Recurrence in these cases depends upon
the completeness of excision.
Ameloblastic fibro-odontoma
This benign tumour consists of an ameloblastic fibroma combined with an
odontoma. It was defined as a neoplasm having the general features of an
ameloblastic fibroma while containing dentine and enamel. It is a more
common and less aggressive lesion.
Pathogenesis
Ameloblastic fibro-odontoma arises from an abnormal proliferation of
odontogenic epithelium of a permanent tooth germ. Proliferating epithelium
as well as calcified tooth tissues are seen in this tumour. The epithelial cells
differentiate into functional ameloblasts before enamel matrix production.
Clinical features
• It is a slow growing, expansile lesion with little tendency to infiltrate

bone.
• Patient presents with swelling, mild pain, altered occlusion and
delayed eruption of teeth.
• Occurs in younger patients—mean age being 8 years.
• No sex predilection.
• Appears with the same frequency in the maxilla and mandible, most
likely in the molar–premolar area.
It lacks typical ameloblastoma epithelium and has an abundant stroma of
immature dental papilla like mesenchyme.
Appears as a well circumscribed radiolucent area with opaque odontomatous
tissue.
Treatment
Conservative excision with a margin of sound bone is the treatment of choice.
Ameloblastic odontoma (odontoameloblastoma)

Ameloblastic odontoma is classified as a rare neoplasm characterised by the
presence of enamel, dentine and odontogenic epithelium resembling that of an
ameloblastoma, both in structure and behaviour. It is a tumour in which
odontogenic cells give rise to both an ameloblastoma and a composite
odontoma. It is more aggressive than the ameloblastic fibro-odontoma.
Clinical features
• Occurs in any age group, particularly during childhood.

• The mandible is more frequently involved than the maxilla.
• The site of predilection is the molar–premolar region.
• Patient gives a history of slow expansion of the jaw, dull pain and
disturbance of occlusion.
Appears as a well defined unilocular or multilocular radiolucent area
containing numerous dense opacities either as solid masses or small particles.
These opacities may or may not resemble miniature teeth. The lesion causes
destruction of bone by infiltration.
The tumour shows a variety of cells and tissues, which include ameloblasts,
enamel, dentine, stellate reticulum like tissue, dental papilla and cementum.
The characteristic feature is the presence of cells resembling typical
ameloblastoma.
Treatment
Surgical management is same as that of ameloblastomas, because of its
resemblance of behaviour to it, namely, progressive infiltration and local
destruction of surrounding tissues.
Odontomas
• Odontomas are hamartomas and one of the most common odontogenic

tumour.
• They are the end products of anomalous completion or incompletion of
tooth formation by odontogenic epithelium and ectomesenchyme.
• They tend to form during the period of odontogenesis approximately
up to 20 years.
• They contain all the four dental tissues—enamel, dentine, pulp and
cementum.
• They are slow growing and asymptomatic, occurring particularly in
the incisor–canine region and third molar region.
• They are revealed on routine radiographic examination or while
examining the reason for cause of persistence of a deciduous tooth or
as a cause of obstruction to the eruption of permanent tooth.
• Odontomas have been divided into two types radiologically and
histologically: (1) complex odontoma and (2) compound odontoma.
Complex odontoma
Complex odontoma consists of an irregular calcified mass of hard and soft
dental tissues, displaying a disorderly and haphazard arrangement of calcified
dental structures.
Structural differentiation is poor, having little resemblance to the normal
form of tooth. Frequently, it forms a cauliflower-like mass of hard dental
tissues which is surrounded by a fibrous follicle.
Pathogenesis
Complex odontomas develop from the dental lamina or enamel organ in place
of a normal tooth. Any injury in the area of tooth formation is also thought to
induce odontomas.
Clinical features
• Odontomas form hard masses that are usually asymptomatic.

• It is less common than the compound odontoma.
• Mandible is most frequently affected.
• Commonly seen in the second and third molar regions.
• Occurs in second and third decades of life.
Complex odontoma appears as a irregular dense radiopaque mass,
surrounded by a thin radiolucent area, overlying a displaced unerupted tooth
(Fig. 27.3A, B).
FIGURE 27.3 Odontoma. (A) OPG showing a large radiopaque
mass in the right maxillary sinus. (B) Coronal CT showing a large
mass in the right maxillary sinus which is surrounded by fibrous
capsule with destroyed lateral sinus wall and its resorption.
Arrangement of dental tissues, enamel, enamel matrix, dentine, pulp tissue
and cementum is disordered, but has a radial pattern frequently. These tissues
are frequently surrounded by a thin connective tissue capsule.
Treatment
• Odontomas have limited growth potentials and are biologically inert.

• Treatment is by enucleation or curettage if the odontoma is a potential
source of obstruction to erupting teeth or if it is a possible focus of
infection.
• Large complex odontomas should be cut in segments for removal in
order to conserve normal bone and prevent jaw fracture.
Compound odontoma (Fig. 27.4A–H)

Compound odontoma consists of calcified tooth like structures or miniature
teeth.
FIGURE 27.4 Compound odontoma. (A) Clinically missing 21,
replaced by an irregular hard swelling. (B) OPG showing multiple
small tooth-like structures in the region of 21, 22. (C) CBCT (Cone
beam CT) showing the multiple odontomes. (D, E) Intraoperative
view of removal of the compound odontomas from anterior maxilla
and excised specimen. (F) Left mandibular retromolar region
exposed for graft harvesting. (G) Primary reconstruction of the
alveolar defect with the harvested graft (stabilised with stainless
steel screw). (H) After 6 months, OPG revealing dental
rehabilitation with implant.
Pathogenesis
Compound odontoma may be produced by repeated divisions of a tooth germ
or by multiple budding off from the dental lamina with formation of many
tooth germs. They begin as soft lesions within the bone over the period of
tooth formation.
Clinical features
• It is a slow growing, noninfiltrative lesion.

• Occurs most commonly in the maxilla, especially in the anterior jaw
(incisor–canine region).
• Seen in the second and third decades of life.
• Failure of eruption of permanent teeth is seen due to interference from
the compound odontoma.
Compound odontoma is seen as a packet of malformed or dwarfed teeth or
tooth like forms surrounded by a thin radiolucent zone.
Histologically, the lesion is composed of anatomically distinct, small, well
formed or numerous dwarfed teeth with enamel, dentine, pulp and cementum
surrounded by a connective tissue capsule which represents the follicle.
Treatment
• Surgical removal by enucleation is the treatment of choice, as

compound odontoma can predispose to cystic change and cause
considerable bone destruction.
• The odontomas can be approached through intraoral mucosal incision
and removal of adequate overlying bone to expose the lesion.
• When fully calcified, the odontomas do not recur. Recurrence is more
common after inadequate removal of the early soft stage of the lesion.
Removal of the entire soft tissue portion is recommended to prevent
recurrence.
Mesenchyme and/or odontogenic ectomesenchyme

with or without included odontogenic epithelium
Odontogenic fibroma
Odontogenic fibroma is classified as a benign, relatively rare connective tissue
tumour that contains a variable amount of inactive odontogenic epithelium.
Odontogenic origin of this tumour is confirmed by its formation only in the
jaws and by the presence of epithelial rests occasionally. The lesion is found
both intraosseously—central odontogenic fibroma and extraosseously on the
gingiva known as peripheral odontogenic fibroma.
Central odontogenic fibroma
Pathogenesis
It is thought to be derived from the mesenchymal portion of the tooth germ,
either from the dental follicle, papilla or periodontal ligament.
Clinical features
• Wide range of age distribution with a mean of 23–37 years.

• Females are more frequently affected.
• Has a predilection for occurrence in the maxilla, anterior to the first
molar.
• Most tumours are related to the roots of the teeth.
• Appears as an asymptomatic, progressive enlargement of the jaw.
• Remains unrecognised until a swelling becomes apparent or on routine
radiographic examination.
• Displacement of adjacent teeth and mobility of teeth may become
apparent.
• Appears as a sharply defined radiolucency in a tooth bearing area.

• Small lesions are unilocular while large ones tend to show
multiloculation.
• May cause root resorption and root divergence.
• Most of these lesions are associated with unerupted or displaced teeth.
• Occasionally a patchy radiopacity is seen, which gives the lesion a
ground-glass appearance.
• They are separated into a simple type (Gardner, 1980) which resembles
a dental follicle (WHO) and a complex type, which contains more
abundant epithelium and foci of dentinoid or cementum like material.
• The simple type consists of delicate fibrous tissue in ground substance.
Rests of odontogenic epithelium are lacking.
• The complex type consists of cellular fibrous connective tissue and
spindle shaped fibroblasts which are often arranged in interlacing
bundles having a whorled arrangement.
• Inactive odontogenic epithelium is dispersed as islands or strands in
the connective tissue stroma.
• The odontogenic fibroma is more cellular and has a greater abundance
of collagen when compared to odontogenic myxoma.
Treatment
• Odontogenic fibromas separates out from the bone easily and thus can
be treated by enucleation and curettage.
• Recurrence is not common with these lesions.
Peripheral odontogenic fibroma

Clinically this tumour is mistaken for a fibrous epulis. It can only be
differentiated histologically by the presence of odontogenic epithelial rests.
Clinical features
• The lesion appears as a pink, firm, sessile or pedunculated mass on the

attached gingiva, particularly of the anterior teeth.
• Found more frequently in the mandible.
• No specific sex predilection.
• Occurs from first to eighth decade.
• The lesions measure around 1–3 cm and are found anterior to the
second premolar.
Calcifications are seen more commonly in these lesions than the central
lesions.
The tumour consists of cellular and collagenous fibrous tissue and small
discrete strands or rests of epithelial content. Calcifications may be present.
Treatment
Excision is the preferred treatment for extraosseous odontogenic fibroma.
Odontogenic myxoma (Fig. 27.5A, B)

Odontogenic myxoma is an odontogenic tumour, based on the evidence that it
is distributed in the jaws and facial skeleton. It is a benign, nonencapsulated,
slow growing, infiltrative tumour of mesenchymal tissue.
FIGURE 27.5 (A) Odontogenic myxoma in a 40-year-old female
showing expansion of buccal and lingual cortical plate.
(B) Corresponding CT image showing expanded buccal and lingual
cortical bone.
Pathogenesis
It is thought to arise from the primitive mesenchyme (of dental papilla) of the
tooth germ.
Clinical features
• Has a wide age range, but occurs mostly in the second and third
decades of life.
• Females are frequently affected at a mean age of 28–30 years.
• Both jaws are affected with a slight preponderance in the mandible.
• Usually unilateral, but may extend beyond the midline.
• It appears as an asymptomatic, slow growing fusiform swelling of the
jaw with the overlying mucosa uninvolved.
• The myxoma starts as a central mass and tends to spread slowly
through the marrow spaces; followed by expansion of bone.
• Appears as a unilocular or multilocular radiolucency with well defined

or moth eaten margins.
• The most common appearance is as a radiolucent area with scalloped
margins and trabeculations giving a honeycomb or soap bubble
appearance.
• May cause displacement of teeth in involved dental areas.
The mesenchymal cells are spindle shaped or angular with long, fine
protoplasmic processes in a loose mucoid intercellular material. The tumour
margins are ill-defined and peripheral bone is progressively invaded and
resorbed.
Treatment
• Myxomas are benign but can infiltrate widely.

• Enucleation and curettage are restricted to unilocular lesions of 1–2 cm
in diameter.
• Teeth within the limit of the lesion should also be removed.
• Chemical cauterisation of the tumour bed may be of value.
• Enucleation or curettage of large lesions is associated with high
recurrence.
• Large lesions should be treated by wide excision or enbloc resection
including a perimeter margin of tumour free bone, followed by
reconstruction.
• Radical treatment should be considered for recurrent cases.
Cementomas
Cementoma is the term given to a group of lesions of the jaws producing
cementum like calcifications.
These tumours contain either acellular or cellular cementum.
Benign cementoblastoma
Benign cementoblastoma is considered as the only true neoplasm of cemental
origin. Benign cementoblastoma is a benign neoplasm of connective tissue that
forms a mass of cementum like tissue fused to the root of a tooth. It is defined
by the WHO as a neoplasm characterised by the formation of sheets of
cementum like tissue, which may contain a very large number of reversal lines
and may be unmineralised at the periphery of the mass or in the more active
growth areas.
Pathogenesis
Though exact pathogenesis of cementoblastoma is not known, connective
tissue of the periodontal ligament and dental follicle are thought to give rise to
the lesion.
Clinical features
• Clinically it is characterised as a painless bony expansion of the jaw.

• It is slow growing, but eventually produces a large lesion that may
expand and resorb the lateral and medial cortical bone.
• Occurs in the age range of 15–30 years, but most commonly seen in the
second decade.
• Mandible is more commonly affected with a predilection for the molar
and premolar regions.
• Often detected during routine examination.
• The lesion usually appears as a solitary, well defined radiopacity with

a peripheral radiolucent rim attached to the root of a tooth.
• Centre of the lesion appears mottled and at the periphery, radiating
trabeculae of calcified tissue may be seen.
• Root resorption is common.
• Central part of the lesion consists of a cementum like tissue containing

reversal lines and has a pagetoid appearance.
• The trabeculae radiating from the centre of the tumour have prominent
cementoblasts.
• At the periphery, there is a broad zone of unmineralised tissue and the
mass has a fibrous capsule.
Treatment
Extraction of the related tooth and complete enucleation of the mass have been
suggested. Recurrence is highly unlikely.
Malignant tumours
Malignant ameloblastoma
• Malignant ameloblastoma are the lesions that have metastasised yet
retain classic ameloblastoma like microscopic appearance.
• Very aggressive with poor prognosis.
• Very few cases are reported and varied treatment modalities are
followed.
Ameloblastic carcinoma
• The metastasis of ameloblastoma that undergoes malignant

transformation of the epithelial component into a well differentiated
carcinoma is called ameloblastic carcinoma.
• In these cases, primary ameloblastoma of the jaw bone remains
unchanged.
• Causes swelling of the jaw and also pain.
• Grows rapidly than conventional ameloblastoma.
• Mandible is most frequently involved.
• Root resorption, perforation of the buccal and lingual plate of the jaw.
• Radiographic features shows an ill-defined area of radiolucency, with
focal radiopacities within the radiolucency.
Intraalveolar carcinoma
Clinical features
• Very uncommon disease.

• Men are affected more frequently than women.
• Can occur at any age.
• Mandible is affected two times more commonly than maxilla.
• Presence of swelling of the jaws with pain and mobility of the teeth in
the involved area.
Pathogenesis
Intra-alveolar carcinoma develops due to malignant transformation of the
epithelial lining of odontogenic or nonodontogenic ameloblastomas.
Not characteristic.
It has alveolar or plexiform pattern with the peripheral cells of the tumour
masses showing palisading appearance which resembles odontogenic
epithelium.
Treatment
Surgical resection is preferred over radiotherapy. Distant metastasis of the
tumour occurs frequently and hence prognosis is poor.
Odontogenic sarcoma
Clinical features
• It is a malignant counterpart of odontogenic fibroma.

• It is a very rare tumour.
• It is an aggressive and destructive lesion which produces a fleshy and
bulky growth.
• At times pain may be present.
Malignant cells exhibit a considerable mitotic activity and resemble immature
fibroblasts. They appear as elongated cells containing ovoid nuclei with
varying degree of pleomorphism.
Treatment and prognosis

This condition is treated by radical surgery and resection of the affected jaw.
The prognosis is poor.
Ameloblastic fibrosarcoma
Clinical features
• It is a malignant counterpart of ameloblastic fibroma.

• It is an extremely rare condition.
• Most common in young adults.
• No sex predilection.
• Mandible is affected more commonly than maxilla.
• Tumour mass grows rapidly and causes destruction of the jaw bone
and loosening of teeth.
• Generally the condition is not painful.
• Very rarely, ulceration and bleeding of the overlying mucosa can be
seen.
• Appear as large multilocular radiolucencies.

• Extensive areas of bone destruction with irregular and indistinct
margins from expansion or thinning of cortical bone are seen.
• Mostly shows malignant transformation of a benign ameloblastic

fibroma.
• Malignant mesenchymal cells show increased cellularity with the
fibroblasts being bizarre and pleomorphic with hyperchromatic nuclei.

The condition is treated by radical resection. Recurrence is common; hence,
prognosis is poor.
CHAPTER 28
Nonodontogenic
Tumours
Osteoma
Gardner’s syndrome
• Treatment
Osteoid osteoma
Cemento-ossifying fibroma
• Histopathologic features
• Treatment
Fibrous dysplasia
• Pathogenesis
Monostotic fibrous dysplasia
Polyostotic fibrous dysplasia
• Treatment
Cherubism
• Grading of variable clinical presentations of cherubism
• Treatment
Central giant cell granuloma
• Clinical and radiographic features
Giant cell tumour
Paget’s disease of bone (osteitis deformans)
• Diagnosis
Nonodontogenic tumours as the name suggests are tumours that arise from
tissues other than the tooth or tooth-forming tissues. They can occur in the
jaw, with or without the involvement of other bones of the skeleton. These
tumours can be the oral manifestations of a generalised disorder like
polyostotic fibrous dysplasia, Paget’s disease, Brown tumour.
Nonodontogenic tumours of the jaws comprise of tumours which are solely
made up of bone or cartilage and fibrosseous lesions which may contain bone,
fibrous tissue, osteoid, cartilage and cementum.
Osseous tumours are slow growing, cause bony expansion and facial
deformity. A few of the most common nonodontogenic tumours are
elaborated in this chapter.
Osteoma
Osteomas are benign odontogenic tumours that consist of mature, compact,
cancellous bone and are found most frequently in the mandible (Fig. 28.1A–E).
They are characterised by proliferation of either compact or cancellous bone
usually in an endosteal or periosteal location.
FIGURE 28.1 Osteoma. (A) Bony hard swelling in left mandible. (B)
CBCT (cone beam CT) showing an osseous tumour (osteoma) in
relation to mandible left canine/premolar region. (C–E)
Intraoperative picture showing resection of the osteoma and the
excised specimen.
Compact osteomas are slow growing and consist of dense lamellae of bone
arranged like layers of onion with occasional blood vessels. No haversian
system is seen. Cancellous osteomas consist of trabeculae of bone with marrow
spaces in between and are surrounded by a lamellated cortex.
Osteomas are most commonly seen in young adults and anywhere between
2nd and 5th decades. These occur both in males and females.
Clinical features
• Osteomas are classified into two types: (1) central (endosteal) osteomas
and (2) peripheral (periosteal) osteomas.
• Osteomas that arise on the surface of bone from the periosteum or
from the bone itself are called peripheral osteomas.
• They contain either cancellous or compact bone.
• They occur anywhere on the maxilla (hard palate and maxillary sinus)
and the mandible (angle more common).
• They present as slow growing, asymptomatic, bony hard masses
causing asymmetry of the affected bone when they enlarge to
sufficient proportions.
• Lesion in the maxillary sinus may cause sinusitis, headache and
ophthalmic symptoms depending on the site of the lesion.
• Endosteal osteomas are those that develop from inner surface of the
cortex of bone or centrally within the medullary bone.
• They are discovered during routine radiographic examination, as they
are small and asymptomatic.
• They may cause localised expansion of the jaw, if enlarged.
Gardner’s syndrome
Gardner’s syndrome is an important marker of internal malignancy. Multiple
peripheral osteomas of the jaws or sino-orbital region should give rise to
suspicion of possibility of Gardner’s syndrome. It is inherited as an autosomal
dominant trait.
The syndrome comprises:
1. Adenomatous polyps of the large intestine with a high malignant

potential
2. Multiple osteomas of the jaws, skull or long bones
3. Multiple desmoid tumours
4. Epidermal and trichilemmal cysts of skin
5. Compound odontomas
6. Impacted supernumerary and permanent teeth
Endosteal lesion appears as well-circumscribed radiopaque mass surrounded
by a radiolucent line. Periosteal form manifests as a sclerotic mass.
Histopathologic features
• The tumour is composed of either relatively dense mature, lamellar,

compact bone with sparse marrow tissues or lamellar trabeculae of
cancellous bone with abundant marrow tissue between the trabeculae.
• Osteons and haversian canals are seen in the compact type.
Treatment
• Conservative excision is the appropriate treatment.

• Small, asymptomatic, nonprogressive deep lesions need not be
removed and can be observed periodically.
• Osteomas causing functional and aesthetic problems are removed
surgically. Endosteal osteomas are usually approached intraorally and
enucleated.
• Periosteal osteomas require surgical excision as they cause swelling
and facial symmetry.
• Osteomas attached to the lingual surface of the mandibular alveolar
process, buccal surface of the alveolar portion of the mandible and
coronoid process can be approached intraorally.
• Osteomas present on the inferior border, angle and external surface of
the ramus of the mandible can be approached via extraoral incision.
• Maxillary sinus osteomas are removed through a Caldwell-Luc
approach. Once the osteoma is exposed, it is removed by means of
burs and osteotomes.
Osteoid osteoma
• It is a rare benign osseous tumour.
• The mandible is affected twice as frequently as the maxilla.
• It is seen in age group less than 30 years.
• Classical presenting symptom is pain, which is characteristically worse
at night.
• Local soft tissue swelling is present.
• Radiographically it appears as a small radiolucency surrounded by
densely sclerotic bone. It is more frequently cortical than medullary in
site. The lesion is usually less than 1 cm in size.
• On histological examination, a nidus consisting of osteoid and woven
bone, which is in trabeculae of irregular length and width and rimmed
by osteo-blasts is seen.
• Treatment is by excision or curettage.
Fibro-osseous lesions are a group of lesions of mesen-chymal tissue origin. It
has been classified by Waldron (Table 28.1).
Table 28.1
Waldron’s classification of fibro-osseous lesions
I. Fibrous dysplasia
• Polyostotic
• Monostotic
II. Reactive (dysplastic) lesions in the tooth bearing area presumably of the periodontal
ligament origin
• Periapical cemento-osseous dysplasia
• Focal cemento-osseous dysplasia
• Florid cemento-osseous dysplasia
III. Fibro-osseous neoplasms
• Cemento-ossifying fibroma
• Ossifying fibroma
• Cementifying fibroma
Cemento-ossifying fibroma
Ossifying fibroma is considered as a benign fibro-osseous neoplasm arising
from undifferentiated cells of the periodontal ligament tissue. It consists of
bone, cementum and fibrous tissue in varying proportion. Cementifying and
ossifying fibromas are now considered as the same and are categorised
together as cemento-ossifying fibroma.
Clinical features
• It is a slow-growing, painless expansile lesion that replaces normal

bone as it enlarges.
• The first presenting symptom of the patient is facial asymmetry.
• Commonly appears between 20 and 40 years of age.
• Females are more frequently affected than males in a ratio of 5:1.
• Occurs more commonly in the mandibular premolar or molar region.
• It is confined to the periapical region of the jaws in contrast to the more
diffuse distribution of fibrous dysplasia.
• Juvenile presentation of this lesion are extremely aggressive and may
involve both the jaws (Fig. 28.2A–J).
FIGURE 28.2 A rare juvenile aggressive cemento-ossifying fibroma
of both jaws. (A) Swelling of midface and lower face in a 1½ year
old boy. (B, C) CT scan showing a variable multilocular expansile
mass in maxilla and mandible. (D) Preoperative intraoral view
showing obliteration of the vestibular sulcus and prominent bony
hard swellings in maxilla and mandible. (E) Resection of the mass
on right and left side of the maxilla. (F) Transoral exposure of the
mandibular lesion. (G) Biopsied specimen of maxilla for
histopathologic examination. (H, I) Resected mandibular specimen.
(J) Digital X-ray image of the resected mandible.
• It is well circumscribed and radiolucent with a sharply defined border
between the lesion and adjacent normal bone.
• The appearance is variable.
• The radiolucent stage progresses to a radiopaque stage as the matrix is
mineralised.
• A fully mature lesion appears as radiopaque mass surrounded by a
thin radiolucent rim.
• The lesions have well-defined capsules. They consist of numerous

stellate or spindle-shaped fibroblasts.
• Collagen fibres are arranged in whorled or stori-form pattern.
• Trabeculae of woven bone with osteoblastic rimming and also lamellar
bone are seen.
• Spherical cementicle-like calcifications are also found.
• Focal presence of osteoblasts along the surface of bone deposits
distinguishes a cemento-ossifying fibroma from a fibrous dysplasia.
• Spicules of bone which can be recognised radio-graphically as well as
microscopically are of diagnostic importance.
Treatment
Cemento-ossifying fibromas have a definable capsule and can be readily
enucleated by intraoral approach. Large lesions which distort the jaws require
local resection and bone grafting if necessary. Prognosis is good.
Fibrous dysplasia
Fibrous dysplasia is a condition characterised by replacement of normal bone
by an excessive proliferation of fibrous connective tissue intermixed with
irregular bony trabeculae. There is arrest of bone development in woven bone
stage with failure to mature to lamellar bone. It is a congenital dysplastic
disease of bone that may occur in a single bone or multiple bones.
It was first described by Von Recklinghausen in 1891. In 1937, Albright
described a syndrome of poly-ostotic fibrous dysplasia. Lichtenstein in 1938
delineated the clinical spectrum and pathological anatomy, which he named
fibrous dysplasia. It is a benign but, at times, destructive disease.
Pathogenesis
• Exact aetiology of this condition is not known. Lichtenstein and Jaffe

indicated an aberrant activity in the bone-forming mesenchymal
tissues as the cause.
• Presence of an activating mutation in the gene that codes for Gs alpha
membrane associated protein in patients with fibrous dysplasia may
result in altered proliferation and differentiation of osteoblastic cells.
• It is also thought to develop as a result of postzygotic mutation in the
GNAS I (guanine nucleotide-binding protein, alpha-stimulating
activity polypeptide I) gene.
• Fibrous dysplasia presents as a painless, slow enlargement of the
involved bone. Normal appearance of a bone is altered, causing
expansion in various directions, presents as facial asymmetry or
pathological fracture of an extremity. The lesions are recognised in
early childhood, grow slowly and stabilise in early adult life. There is a
tendency for the disease to arrest with skeletal maturation or by
puberty. But this is unpredictable and may not happen by puberty.
• Two forms of fibrous dysplasia have been described:
▪ Monostotic—where one bone is involved.
▪ Polyostotic—where several bones are involved along with
cutaneous and endocrine abnormalities.
Monostotic fibrous dysplasia

It is more common than the polyostotic form and accounts for 80% of cases
(Fig. 28.3A–F).
• It is characterised by focal but poorly circumscribed fibro-osseous

replacement of an area of bone. The jaws, particularly the maxilla, is
the most frequently affected site.
• Frontal bone is the other bone in the craniofacial skeleton that is
commonly involved.
• Other frequently involved bones include ribs, femur, long bones and
skull.
FIGURE 28.3 Monostotic fibrous dysplasia. (A, B) Expansile bony
hard swelling in left maxilla causing facial deformity in a 14-year-
old boy. (C–E) CT showing expansile mass in left maxilla,
encroaching maxillary sinus almost obliterating the sinus. Note the
ground glass appearance of the mass. (F) Intraoperative view
showing the mass during paring down procedure.
Clinical features
• Onset of the disease usually occurs during the 1st or 2nd decade of life.
• The lesion forms a diffuse painless, smooth rounded swelling.
• It is usually but not always unilateral.
• As the lesion grows and expands facial asymmetry develops.
• Buccal cortical plate expansion is common.
• Displacement of teeth can cause malocclusion.
• Interference with normal eruption of teeth may occur.
• Normal occlusion is often seen, as normal teeth erupt.
• While the disease develops in the maxilla, outer surface of the alveolar
process is extremely enlarged.
• Maxillary lesions frequently involve adjacent bones such as zygoma,
sphenoid, maxillary sinus and floor of orbit. In the mandible, the
mandibular body area is most frequently affected.
• Typical appearance is a homogeneous radiopacity with numerous

trabeculae of woven bone giving a ground glass or orange peel
appearance.
• An important feature is that the lesion merges imperceptibly with
surrounding normal bone without a circumscribed border.
• The lesion may also present as a radiolucent area with patchy irregular
opacities.
• Consists of areas of loose cellular fibrous tissue interwoven with

irregular trabeculae and newly formed bone.
• The trabeculae are discrete, slender and accurate or branched. Some
are slender and C-shaped called ‘Chinese characters’ trabeculae.
• Osteoblasts are scattered throughout the substance of the trabeculae.
• Lamellar bone formation is not seen in the classic microscopic picture
of fibrous dysplasia.
Polyostotic fibrous dysplasia
• Polyostotic fibrous dysplasia is more uncommon (Fig. 28.4A–D).

• Several or many bones may be involved. Females are more often
affected in a ratio of 3:1. When seen with cutaneous pigmentation
(café-au-lait macules), the disease is termed Jaffe-Lichtenstein
syndrome.
• McCune-Albright syndrome comprises polyostotic fibrous dysplasia,
skin pigmentation and endocrine abnormalities. Precocious sexual
development and onset of puberty in females is the common
endocrine disorder.
• Polyostotic fibrous dysplasia is more frequent in childhood. Involves
head and neck region in 50% of cases.
• A jaw lesion may be the most conspicuous feature. Skin pigmentation
consists of brown macules 1 cm or more with an irregular outline.
• Risk of sarcomatous change is greater in polyostotic disease and
typically develops in early adult life.
FIGURE 28.4 Polyostotic fibrous dysplasia. (A, B) Expansile bony
hard swelling involving maxilla and mandible causing
displacement, tipping of teeth and facial deformity. (C, D) 3D CT
showing osseous expansion of maxilla and mandible.
Treatment
• Radiotherapy is contraindicated because of its potential for malignant

transformation as it may lead to postradiation bone sarcoma.
• Small lesions may only require biopsy for confirmation and periodic
follow-up.
• Lesions that cause functional disability or cosmetic deformity are
treated by osseous recontouring.
• Surgical intervention is generally done following active growth stage
and during the period of stabilisation of the disease process.
• Entire disease cannot be eradicated by surgery, it is only a sculpting
manoeuvre to improve the patient’s appearance and provide a better
functional masticatory apparatus.
• Complete excision of the lesion is not possible because of the diffuse
nature of the lesion and poorly defined borders.
• In many cases, disease tends to stabilise and essentially stops enlarging
when skeletal maturation is reached. Adolescents have the potential
for continued progression of the dysplastic process after surgery, so
treatment is delayed as long as possible.
• Lesions involving anterior wall of the maxilla and the zygoma can be
approached intraorally. Extension of the lesion into the nasal or
posterior maxillary areas require an extraoral approach through a
Weber-Ferguson facial flap. Lesions of the mandible connected to the
alveolar ridges or inner aspect of mandible are approached intraorally,
whereas lesions in the posterior mandible are best accessed through a
submandibular incision.
• Periodic follow-up is necessary because of the possibility of
spontaneous malignant transformation.
Cherubism
Cherubism is a rare developmental jaw condition that is generally inherited as
an autosomal dominant trait with high penetrance but variable expressivity.
Clinical features
• Onset is typically between the ages of 6 months and 7 years.

• Severely affected cases are manifested before 1 year of age, whereas
mild forms are not evident until 10–12 years of age.
• Most cases are identified between the age of 2 and 7 years.
• Males are more commonly affected than females.
• The lesion presents as a painless, slow expansion of affected areas of
the jaw.
• Mandible, particularly the region of the angle is frequently involved.
• Maxilla is less commonly affected, though its involvement is usually
associated with widespread mandibular diseases.
• Involvement of the anterior maxillary segment produces the most
characteristic deformity.
• Expansion of the anterior maxilla causes stretching of the skin and
retraction of the lower lid exposing the sclera. As a result, the patient’s
eyes appear to be turned upwards.
• Inverted ‘V’ shape of the palate is due to maxillary expansion.
• Premature exfoliation of primary teeth and absence or displacement of
permanent teeth.
• Regional lymphadenopathy is seen as a result of reactive hyperplasia
and fibrosis.
Grading of variable clinical presentations of cherubism

• Grade I: Bilateral involvement of ascending rami of mandible.
• Grade II: Bilateral maxillary tuberosity involvement along with
ascending rami of the mandible.
• Grade III: Extensive involvement of anterior and posterior regions of
the maxilla and mandible.
• Grade IV: Extensive involvement of anterior and posterior region of
the maxilla and mandible along with involvement of coronoid and
condylar process.
• Produces well-defined multilocular radiolucencies of the affected

portions of the jaws (Fig. 28.5).
• Expansion and thinning of cortical bone.
• Displaced or malformed teeth evident within the radiolucency.
FIGURE 28.5 Coronal CT of a 6-year-old child with cherubism

showing bilateral jaw expansion.
Characterised by the presence of cellular and vascular fibrous tissue
containing many multinucleated giant cells.
Treatment
• Surgical intervention consisting of curettage or debulking of lesion

with recontouring is the treatment of choice.
• Observation of patients till postpubertal stage to assess regression of
the lesion and final deformity present may be treated.
• Extensive lesions interfering with function may be treated surgically.
• Repeated procedures may be necessary to provide the desired result.
Central giant cell granuloma

Giant cell granuloma is considered widely to be a nonneoplastic lesion.
Although formerly designated as ‘giant cell reparative granuloma,’ there is
little evidence that the lesion represents a reparative response.

Giant cell granuloma may be encountered in patients ranging from 2 to
80 years of age, although more than 60% of all cases occur before the age of 30.
A majority of giant cell granulomas are noted in females and approximately
70% arise in the mandible. Lesions are more common in the anterior portions
of the jaws and mandibular lesions frequently cross the midline.
1. Nonaggressive lesions make up most cases, exhibit few or no

symptoms, demonstrate slow growth and do not show cortical
perforation or root resorption of teeth involved in the lesion.
2. Aggressive lesions are characterised by pain, rapid growth, cortical
perforation and root resorption. They show a marked tendency to
recur after treatment, compared with the nonaggressive types.
Radiographically, central giant cell lesions appear as radiolucent defects,
which may be unilocular or multilocular with well-demarcated margins.
• Presence of few to many irregularly distributed multinucleated giant

cells in a background of ovoid to spindle-shaped mesenchymal cells.
• There is evidence that these giant cells represent osteoclasts, although
others suggest the cells may be aligned more closely with
macrophages.
Central giant cell lesions of the jaws are usually treated by thorough curettage.
Excision of aggressive lesion is required. In patients with aggressive tumours,
three alternatives to surgery are: (1) intralesional corticosteriods, (2) exogenous
calcitonin (3) interferon alpha-2 are being investigated. In spite of the reported
recurrence rate, long-term prognosis of giant cell granulomas is good and
metastasis does not develop.
Giant cell tumour

The question of whether true giant cell tumours, which most often occur in the
epiphyses of long tubular bones, occurence in the jaws has been argued for
many years and is still unresolved (Fig. 28.6). Although most central giant cell
lesions can be distinguished histopathologically from the long bone tumours, a
number of jaw lesions are undistinguishable microscopically from the typical
giant cell tumour of long bones. In spite of histopathologic similarity, these
jaw lesions appear to have a biologically different behaviour from long bone
lesions, which have higher recurrence rates after curettage and show
malignant change in up to 10% of cases. Metastasis from a mandibular
tumour, however, has been reported. It has been suggested that giant cell
granulomas of the jaws and giant cell tumours of the extragnathic skeleton are
not distinct and separate entities; rather, they represent a continuum of single
disease process modified by the age of the patients, location of the lesions and
possibly other factors that are not yet understood.
FIGURE 28.6 Axial CT of a 22-year-old male with giant cell
granuloma showing expansion of the jaw.
Paget’s disease of bone (osteitis deformans)

Paget’s disease of bone is a disease characterised by abnormal and anarchic
resorption and deposition of bone, resulting in distortion and weakening of
the affected bones (Fig. 28.7A–J). Causes of Paget’s disease are unknown, but
inflammatory, genetic and endocrine factors may be contributing agents.
FIGURE 28.7 Paget’s disease of craniofacial bone. (A, B) Facial

deformity with ‘Leonine facies’ after juvenile onset of Paget’s
disease of craniofacial bones—note frontal bossing, depressed
nasal bridge and telecanthus. (C–F) CT scan showing cortical
expansion with irregular bone deposition of mandible, maxilla,
zygoma, occiput, temporal, parietal, frontal, sphenoid, ethmoid and
cervical bones. (G–J) 3D CT scan showing the deformed
craniofacial bones.
Clinical features
• The disease principally affects older people and is rarely encountered
in patients below 40 years of age.
• Men are affected more often than women.
• Lumbar vertebrae, pelvis, skull and femur are the most commonly
affected bones.
• Affected bones become thickened, enlarged and weakened.
• Paget’s disease affecting the skull generally leads to a progressive
increase in the circumference of the head.
• Maxillary disease, which is far more common than mandibular
involvement, results in enlargement of the middle third of the face.
• In extreme cases, alteration results in a lion-like facial deformity
(leontiasis ossea).
• Nasal obstruction, enlarged turbinates, obliterated sinuses and
deviated septum may develop secondary to maxillary involvement.
• Alveolar ridges tend to remain symmetric but become grossly
enlarged.
• If the patient is dentulous, enlargement causes spacing of the teeth.
• Radiographically, early stage of Paget’s disease reveals a decreased

radiodensity of the bone and alteration of the trabecular pattern.
• Particularly in the skull, large circumscribed areas of radiolucency may
be present (osteoporosis circumscripta).
• During osteoblastic phase of the disease, patchy areas of sclerotic bone
are formed, which tend to become confluent. Patchy sclerotic areas are
often described as having a ‘cotton wool’ appearance.
• Histopathology shows an apparent uncontrolled alternating resorption

and formation of bone.
• In the active resorptive stages, numerous osteoclasts surround bone
trabeculae and show evidence of resorptive activity.
• A characteristic microscopic feature is the presence of basophilic
reversal lines in the bone.
• These lines indicate the junction between alternating resorptive and
formative phase of the bone and result in a ‘jigsaw puzzle’ or ‘mosaic’
appearance of the bone.
Diagnosis
Patients with Paget’s disease show high elevations in serum alkaline
phosphatase levels and normal blood calcium and phosphorus levels along
with elevated urinary hydroxyproline levels. Newer and more sensitive
markers of bone resorption as N-telopeptides and pyridinoline cross-link
assays are available.
• Although Paget’s disease is chronic and slowly progressive, it is

seldom the cause of death.
• Patients with limited involvement and no symptoms, often require no
treatment.
• Use of parathyroid hormone antagonists, such as calcitonin and
biphosphonates can reduce bone turnover and improve biochemical
abnormalities.
• In many instances, acceptable control has been obtained with the
newer biphosphonates, such as etidronate, pamidronate, alendronate,
tiludronate or risedronate. In mild cases, a single infusion of a
biphosphonate is often associated with year long remissions.
• Development of a malignant bone tumour, usually an osteosarcoma is
a recognised complication of Paget’s disease.
CHAPTER 29
Oral Cancer

Aetiopathogenesis
• Aetiology
• Exophytic lesions
• Ulcerative lesions
• Histologic features
• Modes of spread
Histologic variants of squamous cell carcinoma
Basaloid squamous cell carcinoma
Verrucous carcinoma or Ackerman tumour
• Prognosis
• Management
Basal (rodent ulcer)
Ewing’s sarcoma (endothelial myeloma, round cell sarcoma)
Multiple myeloma (plasma cell myeloma, plasmacytoma)
• Oral manifestations
• Laboratory features
Tumours of the head and neck comprise an important group of neoplasia, the
incidence of which is increasing in many parts of the world. More than 95% of
the carcinomas of the oral cavity are of squamous cell type, in nature. They
constitute a major health problem in developing countries, representing a
leading cause of death. According to World Health Organization (WHO),
carcinoma of oral cavity in males in developing countries is the sixth most
common cancer after lung, prostrate, colorectal, stomach and bladder cancer,
while in females, it is the tenth most common cancer. Since, the oral cavity is
more accessible to complete examination; early detection of precancerous and
cancerous lesions is possible but either due to ignorance or inaccessibility of
medical care, the disease gets detected in the later stages.
Tumour progression in epithelia has been classified as normal, hyperplastic
(nondysplastic), dysplastic, carcinoma in situ and invasive carcinoma. The
majority of the initial alterations of precancerous and cancerous oral lesions
are not readily recognisable, on clinical or histopathological examination.
Tobacco and alcohol are the two most important known risk factors for the
development of oral cancer. Cofactors in oral squamous cell carcinoma (OSCC)
include dietary factors, immunodeficiency and viral infections from human
papilloma virus (HPV)-16/18. The higher incidence of carcinoma of the head–
neck in relation to other malignancies in India, may be due to use of tobacco in
various forms, consumption of alcohol, low socioeconomic condition related to
poor hygiene, poor diet and rampant viral infections.

Oral cancer is commonly associated with regional metastasis to neck nodes,
which has been graded according to the site of involvement according to the
Memorial Sloan-Kettering classification (Fig. 29.1; Table 29.1).
FIGURE 29.1 Memorial Sloan-Kettering Cancer Center

classification of cervical lymph nodes.
Table 29.1
Memorial Sloan-Kettering Cancer Center classification of cervical lymph nodes

(Fig. 29.1)
Levels Region Landmarks
IA Submental triangle Triangle bounded by anterior belly of the digastric and the
mylohyoid
IB Submandibular Triangle bounded by the anterior and posterior belly of the
triangle digastric and body of mandible
II Upper Nodes around the middle third of IJV
jugular/jugulodigastric
nodes
IIA Anterior to the spinal Digastric muscle superiorly and the hyoid bone or the carotid
accessory nerve bifurcation inferiorly
IIB Posterior to the spinal Digastric muscle superiorly and the hyoid bone or the carotid
accessory nerve bifurcation inferiorly
III Middle jugular Carotid bifurcation superiorly to the cricothyroid notch
nodes/juguloomohyoid inferiorly
IV Lower jugular nodes Omohyoid muscle superiorly to the clavicle inferiorly
V Posterior triangle Along the lower half of the spinal accessory nerve and the
transverse cervical artery. Also includes supraclavicular nodes
VI Anterior triangle Hyoid bone superiorly to the suprasternal notch inferiorly
IJV, Internal jugular vein.
Oral cancer has been conventionally graded and staged according to the
TNM classification by American Joint Committee on Carcinoma (AJCC) for
ease of communication and prognosis prediction (Tables 29.2 and 29.3).
Table 29.2
TNM classification by AJCC
T—Primary tumour
TNM FIGO
TX Primary tumour cannot be assessed
T0 No evidence of primary tumour
Tis Carcinoma in situ
T1 Tumour 2 cm or less in greatest dimension
T2 Tumour more than 2 cm but not more than 4 cm in greatest dimension
T3 Tumour more than 4 cm in greatest dimension
T4a (lip) Tumour invades through cortical bone, inferior alveolar nerve, floor of mouth or
skin (chin or nose)
T4a (oral Tumour invades through cortical bone, into deep/extrinsic muscle of tongue
cavity) (genioglossus, hyoglossus, palatoglossus and styloglossus), maxillary sinus or skin
of face
T4b (lip Tumour invades masticator space, pterygoid plates or skull base, or encases
and internal carotid artery
oral
cavity)
N—Regional lymph nodes
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest dimension

N2a Metastasis in a single ipsilateral lymph node, more than 3 cm but not more than
6 cm in greatest dimension
N2b Metastasis in multiple ipsilateral lymph nodes, not more than 6 cm in greatest
dimension
N2c Metastasis in bilateral or contralateral lymph nodes, not more than 6 cm in greatest
dimension
N3 Metastasis in a lymph node more than 6 cm in greatest dimension
M—Distant metastasis
MX Distant metastasis cannot be assessed
M1 No distant metastasis
M2 Distant metastasis
Table 29.3
Stage grouping
Aetiopathogenesis
Tobacco and alcohol
Chewing of tobacco with betel quid, smoking and heavy alcohol consumption
are the main risk factors.
Betel quid and areca nut

Betel quid chewing produces reactive oxygen species (ROS) which are
detrimental to oral mucosa and can be directly involved in tumour initiation
process by inducing mutation, or by making the mucosa susceptible to betel
quid ingredients and environmental toxicants.
Alcohol
Alcohol may act as a solvent and enhance the penetration of carcinogens into
target tissues. Acetaldehyde, which is an alcohol metabolite, has been
identified recently as a tumour promoter.
Viruses
Viruses that are known to cause cancer such as HPV (cervical
cancer), Hepatitis B (liver cancer), and EBV (a type of lymphoma), are all
DNA viruses. HPV has been found to be associated with several types of
human cancer, inclusive of cervical, vulvar, vaginal, penile, anal, and head-
and-neck cancers.
HPV-16/18 is detected in condylomas, focal epithelial hyperplasia,
squamous cell papilloma and malignant oral lesions.
Diet
Fruits and vegetables (high in vitamins A and C) are described as protective in
oral neoplasia, whereas meat and red chilli are thought to be risk factors.
Family history of head and neck squamous cell carcinoma (HNSCC)

The ability to repair DNA damaged by tobacco carcinogens, such as
benzo[a]pyrenediol epoxide is defective in some patients with head and neck
cancer. These patients show an increased susceptibility to chromosome
damage by mutagens.
Immune deficiency
A defective immune response, as seen in a human immunodeficiency virus
(HIV)-infected individual, may predispose to cancer. The most common oral
malignancy in HIV-infected patients is Kaposi sarcoma and the human herpes
virus type 8 (HHV-8) has been implicated as the aetiological agent.
Lymphoma, mostly non-Hodgkin B cell lymphoma in HIV-infected
individuals, or other immunosuppressed states, is commonly associated with
Epstein-Barr virus (EBV) and may occur in the head and neck region.
Squamous cell carcinoma of the lip is more common in transplant recipients
receiving immunosuppressive therapy, but HIV infection does not predispose
to intraoral squamous cell carcinoma.
HPV in oral cancer
The association of HPV with oral cavity and oropharyngeal cancer was
first reported by Loning et al. and de Villiers et al. in 1985. HPV types
detected were classified into
(i) nononcogenic (low-risk, such as HPV6, 11, 26)

(ii) oncogenic (high-risk, such as HPV16, 18, 31)
(Figs. 29.2–29.4)
FIGURE 29.2 Hallmark of cancer.
FIGURE 29.3 Recent hallmarks.
FIGURE 29.4 Field cancerisation.

(p53, pRb–Tumor suppressor gene)
Field cancerisation:
The term ‘field cancerisation’ was proposed by Slaughter et al. Field
cancerisation (also termed field change, field change cancerisation, field
carcinogenesis, cancer field effect or premalignant field defect) is a biological
process in which large areas of cells at a tissue surface or within an organ are
affected by a carcinogenic alteration(s).
The term field cancerisation has been utilised to explain the followings: (1)
Oral cancer developing in multifocal areas of a precancerous change; (2)
abnormal tissues surrounding the tumour; (3) oral cancer often consisting of
multiple independent lesions that may coalesce; (4) the persistence of
abnormal tissue even after surgery may explain secondary primary tumour
and recurrences.
Sunlight
Broad spectrum UV radiation is a known carcinogen.

According to the WHO histological publication of oral and oropharyngeal
tumours, oral squamous cell carcinoma is described as a tumour consisting of
irregular nests, columns or strands of malignant epithelial cells, infiltrating
subepithelially. The tumour cells may resemble any or all of the layers of
stratified squamous epithelium (Figs. 29.5 and 29.6).
FIGURE 29.5 Squamous cell carcinoma—exophytic growth.
FIGURE 29.6 Squamous cell carcinoma—ulceroproliferative lesion.
Aetiology
• Unknown.
• Use of alcohol and tobacco.
• Irritation from poorly fitting dentures.
• Environmental exposure to paint fumes, plastic by-products, wood
dust, asbestos and gas line fumes.
• EBV and HPV infection.
Differential diagnosis of squamous cell carcinoma of oral cavity is depicted in
Table 29.4.
Table 29.4
Differential diagnosis of squamous cell carcinoma of oral cavity

Benign lesions Malignant lesions
Lichen planus Melanoma
Pyogenic granuloma Lymphoma
Tuberculous ulcers Sarcoma
Benign papilloma Minor salivary gland malignancies
Keratoacanthoma Metastatic tumour
Follicular lymphoid hyperplasia
Necrotising sialometaplasia
Granular cell tumour
Squamous cell carcinoma is most often characterised as exophytic or ulcerative

or a combination of both.
Exophytic lesions
• Less common, slower growing and less infiltrative.

• They can become deeply infiltrative and invasive in advanced cases.
Ulcerative lesions
• More common.
• They appear as red or greyish ulcers with heaped up edges that bleed
easily.
• Deeply infiltrative.
Predilection for area where saliva tends to pool, e.g. floor of mouth and
neighbouring sites (side of the tongue).
Clinical features
Early lesions
• Asymptomatic
• White or red patches
• Small exophytic growth
• Small indolent ulcer
Intermediate lesions
• Persistent ulceration
• Induration
• Fixation to underlying structures
• Lymph node enlargement (Fig. 29.7)
FIGURE 29.7 (A, B) A 32-year-old female with squamous cell
carcinoma of the left side of the mandible. Stage IV or end stage
disease involving skin and mandibular space causing restriction in
mouth opening.
Advanced lesions
• Haemorrhage or necrosis of exophytic mass

• Destructive crater-like ulcer with raised or rolled edges
• Pain, paraesthesia
• Bone destruction, invasion, fracture
• Mobility of teeth
Histologic features
Graded from low to high by degree of keratinisation, nuclear pleomorphism
and frequency of mitoses.
Low-grade tumours
• More extensive keratinisation, infrequent mitoses and little nuclear

pleomorphism.
• Maintain orientation from basal to keratinised layers.
High-grade tumours
Little keratin, increased mitosis and extreme nuclear pleomorphism.
Well differentiated
• Presence of keratin pearls, masses of prickle cells within connective

tissue surrounded by basal cell with central keratinisation.
• Basement membrane is absent.
Moderately differentiated
• Keratin pearls are sparse or absent

• Prickle cells are more pleomorphic
• A typical mitotic figures
Poorly differentiated (anaplastic)
• No keratin
• Extreme pleomorphism and hyperchromatism
• Cells cannot be recognised as keratinocytes
Modes of spread
Local infiltration
Spreads in centrifugal manner in soft tissue, but altered when bone is
encountered.
Various modes of spread in bone
• Via periosteal or subperiosteal layer, particularly on lingual alveolar

aspect of mandible.
• Through periodontal membrane when teeth are present.
• Diffuse spread within marrow cavity.
• Perineural spread, especially along inferioralveolar nerve, most often
proximally, in direction of pterygoid fossa and skull base and then
towards trigeminal ganglion.
• It also spreads via lymphatics and blood stream.
Histologic variants of squamous cell

carcinoma
• Basaloid squamous cell carcinoma—aggressive variant
• Verrucous squamous cell carcinoma
Basaloid squamous cell carcinoma

• Characterised by basaloid cells that are arranged in nests or cords with
pseudoglandular spaces and a high mitotic rate
• Worse prognosis
• Develop distant metastasis more frequently
Verrucous carcinoma or Ackerman tumour

• Low-grade variant
• Found in elderly (>60 years) who chew tobacco or consume snuff
• Characterised by their whitish, warty, bulky, cauliflower-like growth
with a broad base.
• Grossly, described as ‘pebbly, mammillated’ in appearance or piled up
in rugal folds with deep cleft-like spaces between them.
• Predilection for buccal mucosa.
Histologic features
• Thickened epithelium, prominent surface keratin, down growth of

club-shaped fingers of hyperplastic epithelium that push rather than
infiltrate deeply towards an intact basement membrane.
• Prominent inflammatory reaction in the underlying connective tissue.
Verrucous hyperplasia, chronic hyperplastic candidiasis,
pseudoepitheliomatous hyperplasia.
Prognosis
Characterised by an extension of lesion into underlying connective tissue,
deep to adjacent normal epithelium. It has more favourable prognosis.
Management
Surgical resection.
Basal (Rodent ulcer)

• It affects facial skin.
• More common in older age group.
• Slow-growing tumour which infiltrates locally; pattern of spread
laterally rather than deep.
• It does not metastasize.
Histologic features
• Clumps of cells lying in a connective tissue stroma.

• Peripheral palisading: Clumps contain basophilic cells which resemble
immature cells of basal cells of epidermis with a peripheral layer of
columnar cells packed together surrounded by a basement membrane.
• Morphoeic pattern: Small groups of tumour cells sparsely scattered in
more than usually abundant stroma. At the margins, thin strands of
tumour cells infiltrate surrounding tissues.
• Sclerosing: If fibrosis is marked.
• In case of infiltrative lesions, the morphemic and sclerosing patterns
are seen (Fig. 29.8).
FIGURE 29.8 Basal cell carcinoma.
Clinical features
• Early stage presents as a nodule giving a pearly appearance, which is

also the diagnostic feature.
• In larger lesions pearly appearance is not apparent immediately and
the diagnostic feature is the presence of telangiectatic vessels.
• Pearling is made more obvious by stretching the skin to blanch it. The
translucent pearl then becomes readily recognised.
Gorlin–Goltz syndrome is characterised by:
• Multiple basal cell carcinomas after puberty, mainly on exposed sites,

can also occur on unexposed sites.
• Multiple keratocysts in jaws.
• Growth abnormality of facial skeleton.
• Anomalies of ribs.
• Calcification of falx cerebri.
• Frontal and temporoparietal bossing, hypertelorism and mandibular
prognathism.
Ewing’s sarcoma (endothelial myeloma,

round cell sarcoma)
Ewing’s sarcoma is an uncommon malignant neoplasm, which occurs as a
primary destructive lesion of bone that most commonly involves the pelvis
and lower extremities.
Origin of the cells might be derived from marrow endothelium or from
undifferentiated cells of the reticuloendothelial system.
Clinical features
• This neoplastic disease occurs predominantly in children and young

adults, rarely in older patients.
• An episode of trauma often precedes development of the tumour.
• Pain is of intermittent nature and swelling of the involved bone is often
the first clinical sign and symptom of Ewing’s sarcoma.
• Bones most commonly affected are long bones of the extremities,
although the skull, clavicle, ribs, shoulder and pelvic girdles may be
involved, as well as the maxilla and mandible.
• When there is involvement of the jaws, there is facial neuralgia and lip
paraesthesia.
• Appearance of the jaw swelling is often relatively rapid and the
intraoral mass may become ulcerated.
• Patient might present with low-grade fever and an elevated white
blood cell count due to presence of infection (Fig. 29.9).
FIGURE 29.9 (A) Panaromic radiograph of a 26-year-old female
with Ewing’s sarcoma showing bone formation. (B) CT image
showing bone formation both buccally and lingually.
• The lesion is destructive in nature and produces an irregular diffuse

radiolucency within the bone.
• A common characteristic radiographic feature is the formation of
layers of new subperiosteal bone producing the so-called ‘onion skin’
appearance on the film. This thickened cortex is usually infiltrated by
the tumour.
• Osteophyte formation may also be visible in the radiograph and in
such cases may be similar to the ‘sunray’ appearance of osteosarcoma.
Histologic features
• Ewing’s sarcoma is an extremely cellular neoplasm composed of solid

sheets or masses of small round cells with very little stroma, large
round or ovoid nuclei.
• Mitotic figures are common. Many tiny vascular channels may also be
present.
• Necrosis is also a common microscopic feature.
• Tumour cells of Ewing’s sarcoma contain histochemically
demonstrable intracytoplasmic glycogen.
• It has been common for metastatic foci to appear in other bones and
organs, such as lungs and lymph nodes, within a matter of few weeks
or months.
• Integrated therapies are surgery, multiagent chemotherapy and
radiotherapy.

Osteosarcoma is a malignancy of mesenchymal cells that have the ability to
produce osteoid or immature bone. Osteosarcoma is the most common
primary neoplasm originating within bone. Osteosarcomas of the jaws are
uncommon and account for 6%–8% of all osteosarcomas.
Clinical features
• These tumours have been seen in patients ranging from young

children to the elderly, but these occur most often in the third and
fourth decades of life.
• Maxilla and mandible are involved in about equal frequency.
• Mandibular tumours arise more frequently in the posterior body.
These are more common in the horizontal ramus rather than the
ascending ramus.
• Swelling and pain are the most common symptoms.
• Loosening of teeth, paraesthesia in the area supplied by the mental
nerve and nasal obstruction especially in the cases of maxillary
tumours may be seen.
• Some patients report symptoms for relatively long periods before
diagnosis, which indicates that some osteosarcomas of the jaws grow
rather slowly.
• Metastasis to lungs develops early.
• Radiographic findings vary from dense sclerosis to a mixed sclerotic

and radiolucent lesion to an entirely radiolucent process.
• The classic ‘sunburst’ or ‘sunray’ appearance caused by osteophytic
bone production on the surface of the lesion is noted frequently.
• An important early radiographic change in patients with osteosarcoma
consists of a symmetric widening of the periodontal ligament space.
• Presence of widening of inferior dental canal, widening of periodontal
ligament and sunray effect is pathognomonic of osteosarcoma.
Essential microscopic criterion is direct formation of osteoid by malignant
mesenchymal cells. The tumour cells may vary from relatively uniform round
or spindle-shaped cells to highly pleomorphic cells with bizarre nuclear and
cytoplasmic shapes. The amount of matrix materials produced in the tumour
may vary considerably.

Osteosarcoma of the jaws is rapidly invasive. Early radical excision is the first
requirement. This may be combined with pre or postoperative radiotherapy
and adjuvant chemotherapy. Recurrence of tumour in excised margin is the
major problem.
Multiple myeloma (plasma cell myeloma,

plasmacytoma)
• Multiple myeloma is a neoplasm of bone. It originates from cells of the
bone marrow.
• These cells resemble plasma cells, which are common constituents of
an inflammatory infiltrate.
• The neoplasm is thought to be of multicentric origin; lesions arising in
numerous areas at approximately the same time, but each independent
of the other lesions.
Clinical features
• Multiple myeloma occurs mostly in adults, although it may occur in

much younger persons with a predilection for men than women.
• Patients usually present with pain as an early feature of the disease
and because of the destruction of bone, pathological fracture is fairly
common.
• Swelling over the areas of bone involvement may be detected.
• Destruction of haematopoietic bone marrow can result in anaemia,
fatigue, thrombocytopaenia with purpura, epistaxis, infection and
fever due to leucopaenia.
• Renal disease results from hypocalcaemia and the overwhelming
amounts of light-chain proteins in the blood.
Oral manifestations
• Signs and symptoms of jaw involvement include pain, swelling,

expansion of the jaw, numbness
• Abnormal healing after extractions, mandibular fracture and mobility
of teeth.
• In addition, extraosseous lesions occur, which may resemble gingival
enlargements or epulis.
• Extension of the disease to the lymph node, skin and viscera are also
encountered.
• Radiographic examination usually reveals numerous sharply punched-

out areas in numerous bones of active haematopoiesis like vertebrae,
ribs, skull, jaws and ends of long bones. These lesions may vary in size
from a few millimetres to a centimetre or more in bone reaction.
• Diffuse destructive lesions of bone may also occur.
Laboratory features
• Certain laboratory findings help in establishing the diagnosis of

multiple myeloma. Many patients exhibit a hyperglobulinaemia
resulting in a reversal of the serum albumin–globulin ratio, and an
increase in total serum protein to a level of 8–16 g%.
• In addition, presence of Bence Jones protein that coagulates when the
urine is heated to 40–60°C, disappears when the urine is boiled and
reappears if cooled.
• Anaemia is also a common finding in multiple myeloma.
Histologic features
• Usually the lesion is composed of sheets of closely packed cells

resembling plasma cells. These are round or ovoid cells with
eccentrically placed nuclei exhibiting chromatin clumping in a
‘cartwheel’ or ‘checkerboard’ pattern.
• Two nuclei within a single cell membrane are seen rarely. A
perinuclear halo may be present.
• Russell bodies are common.
• Plasma cell neoplasms demonstrate monoclonal light chains within the
cytoplasm of plasma cells.
• Chemotherapy is presently the treatment of choice for multiple

myeloma using alkylating agents such as melphalan or
cyclophosphamide, in combination with prednisone. Another common
regimen is vincristine, doxorubicin and dexamethasone.
• Localised radiotherapy can be given for palliation of painful bone
lesions.
• Bone marrow transplant has been used for patients who do not
respond to chemotherapy.
• Chemotherapy is associated with a variety of side effects, most notably
bone marrow depression.
• Radiation therapy is also used, often in combination with
chemotherapy.
CHAPTER 30
Management of Head
and Neck Tumours
Surgical management
Types of neck dissection
Surgical management of jaw tumours
Curettage
Mandibular en-bloc resection
Mandibular segmental resection
Mandible reconstruction
Maxillectomy
• Maxillectomy via Weber-Ferguson approach
Radiotherapy
Fractionation
Multiple ports
Effects of radiation
• Skin and mucous membrane
• On the salivary glands
• On taste buds
• On teeth
• On bone
• Mandibular dysfunction
Radiosensitisers
Radioprotectors
Radiation mitigator
Chemotherapy
Chemotherapy approaches
Chemoprevention
Intralesional chemotherapy
Topical chemotherapy
Surgical management
Surgical management remains the primary modality of management of oral
cancer. The principle of treating oral cancer is eradication of the disease.
Cancer of the head and neck is the region, which is highly vascular with rich
lymphatic drainage; this facilitates early metastasis to regional lymph nodes.
Surgical management of metastatic neck nodes includes neck dissection
(Table 30.1 and Figs. 30.1 and 30.2).
Table 30.1
Surgical management (Fig. 30.3)
Neck dissection Level of nodes cleared

Commando operation Hemimandibulectomy, hemiglossectomy, Level I to VI,
SCM, SAN, IJV
Radical neck dissection (RND) Level II to VI, SCM, SAN, IJV
Modified radical neck dissection Level II to V, SCM, IJV
(MRND) I
Modified radical neck dissection Level II to V, IJV
(MRND) II
Modified radical neck dissection Level II to V
(MRND) III
Supraomohyoid neck dissection Level I to III
(SOHND)
Posterolateral neck dissection Levels II, III, IV and V and retroauricular suboccipital
(PLND) nodes
Lateral ND Levels II, III, IV
Anterior compartment ND Only group VI
IJV, Internal jugular vein; SAN, spinal accessory nerve; SCM, sternocleidomastoid.
FIGURE 30.1 A Flowchart depicting the management of positive or
negative neck nodes.
FIGURE 30.2 Clinical Stages according to ‘T’ and ‘N’ status.

Types of neck dissection
• Classical radical neck dissection (Crile’s neck dissection)
The classic procedure involves en bloc removal of the cervical lymphatics,
internal jugular vein, spinal accessory nerve, submandibular gland,
sternocleidomastoid muscle and the primary tumour. This usually
cause disadvantages such as shoulder drop due to loss of accessory
nerve supplying the trapezius muscle, neck deformity, facial swelling,
numbness, neuromas and may also cause severe postirradiation
complications such as carotid rupture (Fig. 30.4A).
• Modified radical neck dissection (MRND) (Fig. 30.4B)
This type of neck dissection involves preserving undoubtful
nonlymphatic structures in the neck, while removing all nodal groups
(IV). Preserving the spinal accessory nerve is done at Erb’s point,
where the nerve exits the posterior SCM and the greater auricular
nerve arises from under it (Fig. 30.3).
▪ Type I MRND preserves only the spinal accessory nerve.
▪ Type II preserves the accessory nerve and the internal jugular
vein.
▪ Type III preserves these structures as well as the
sternocleidomastoid muscle.
▪ MRND III is also called the functional neck dissection. MRND
should be performed when there is an evidence of nodal
disease or there is a risk of probable nodal metastasis and
surgery is being performed for the primary cancer.
Advantages include improved shoulder function, lower morbidity and
mortality for bilateral neck dissections, protection for the carotid
artery, staging for prognosis and/or use of adjuvant therapy, less
cosmetic deformity and less facial oedema. Disadvantages include
possibility of leaving positive nodes behind, or cutting into positive
nodes and seeding cancer.
• Selective neck dissection
Selective neck dissection (SND) is a modification of the RND in which
one or more lymph node groups are preserved. The SND is divided
into subtypes:
▪ the supraomohyoid neck dissection, (SOHND) (Fig. 30.4 A-C)
▪ the posterolateral neck dissection,
▪ the lateral neck dissection, and
▪ the anterior compartment neck dissection.
FIGURE 30.3 Important structures of the neck.
FIGURE 30.4 (A) Radical neck dissection. (B) Modified radical

neck dissection: one or more of the nonlymphatic structures are
preserved. (C) Supraomohyoid neck dissection.
Surgical management of jaw tumours

Curettage
Curettage involves the use of hand instruments like curettes to remove benign
and malignant lesions like osteoblastoma and ameloblastoma.
• Vital structures may need to be sacrificed in cases of aggressive lesions.

• Care should be taken not to leave behind any remnants of the
pathologic tissue as to prevent recurrence.
• A margin of normal bone may also be removed by curettage to ensure
the whole tumour is removed (some tumours extend by infiltration
beyond the clinical or radiographic tumour–bone interface).
• Once the lesion is curetted out, sharp bony margins are smoothened
with a bur or rongeur.
• Small bony defects can be closed primarily.
• Large defects are allowed to heal by secondary intention. The wound is
packed with a strip of gauze coated with tincture benzoin or topical
antibiotic. One end of the gauze exits through a separate stab incision
for retired letter. The wound is sutured with resorbable or
nonresorbable sutures. The pack is removed once granulation tissue
forms.
Mandibular en-bloc resection (Fig. 30.1A–C)
• In this procedure, the tumour is removed along with a rim of

uninvolved bone, while maintaining the continuity of the jaw.
• This is the treatment of choice for small aggressive lesions with high
recurrence rate.
• Post-resection, a minimum of 1 cm height of normal bone must be
present to avoid pathologic fracture.
Mandibular segmental resection (Fig. 30.5A–C)

In this technique, continuity of the inferior border is not maintained.
Depending on the extent of involvement, the condyle and coronoid may or
may not be included. Extraoral approach, though the inferior border of the
mandible is exposed, masseter and medial pterygoid muscles are reflected off
from the ramus of the mandible. Similarly, temporalis muscle is reflected off
the coronoid process and the mylohyoid muscle from the lingual surface of the
mandible.
• A bone cut is made anterior to the lesion extending till the inferior
border of the mandible, using either a Gigli saw or bur.
• Once the cut is made, the segment is rotated laterally, on entering the
mandibular foramen, the inferior alveolar bundle is identified and
ligated.
• The condyle is then freed from the lateral pterygoid muscle and the
mandible disarticulated.
• Haemostasis is achieved and closure accomplished by approximating
the buccal and the lingual mucoperiosteal flaps.
• Similarly, the lip and submandibular incisions are approximated and
closed in layers.
• A drain may be placed to avoid collection of fluid in the dead space.
• Pressure dressing is applied.
FIGURE 30.5B Ameloblastoma of anterior mandible segmental
resection. (A) Transoral exposure of the lesion. Note the
subperiosteal dissection in the anterior mandible in the regions of
buccal perforation. (B) Resection of the lesion with minimal
elevation of lingual periosteum in relation to the proposed transport
disc. (C) Resected specimen.
FIGURE 30.5A A- Mandibular En-block resection.
Mandible reconstruction
The reconstruction of the resulting defect may be treated primarily or
secondarily depending on the diagnosis of the lesion. Defect from aggressive
lesions with high recurrence rate are reconstructed secondarily. Mandible
reconstruction ranges from simple reconstruction plate, free bone grafts,
microvascular vascularised graft to distraction osteogenesis or use of rhBMP-2
with free grafts (Figs. 30.6–30.10).
FIGURE 30.6 Reconstruction ladder.
FIGURE 30.7 Least favoured form of reconstruction—
reconstruction plate. (A) Preoperative view of the patient showing a
mild lower facial asymmetry. (B) Marking for right submandibular
incision. (C) Exposure of the lesion via submandibular approach.
(D) Preplating. (E) Resection of the lesion. (F) Resected specimen.
(G) Placement and fixation of the reconstruction plate according to
the planned position of the template. (H) Primary closure of the
surgical wound. (I) OPG showing fractured reconstruction plate.
FIGURE 30.8 OPG showing mandible, reconstruction using
microvascular fibula graft transfer followed by dental rehabilitation.
FIGURE 30.9 Transport distraction osteogenesis. (A–B) Note the
skin over the swelling is inflamed and adherent to the underlying
bone lesion. (C) Resected specimen. (D) Plate guided univector
unidirectional straight mandibular distractor. (E) Fixation of the
mesh footplates and completion of planned osteotomy. (F–H)
Sequential OPG showing the movement of transport disc with daily
activation.
FIGURE 30.10 Juvenile cemento-ossifying fibroma of mandible
reconstructed with nonvascularised rib grafts with rBMP-2 and
titanium reconstruction plate. (A) Preoperative view showing
elevated and distorted right alar base and nostril. Note the
displacement of teeth in cortical expansion with foci of internal
radiopaque masses. Note the peripheral osteocondensation zone
with displacement of teeth. (B–C) Preoperative CT. (D) Transoral
exposure of the mandibular lesion. (E) Segmental resection of the
mandible from angle to angle. (F) Harvested rib grafts. (G)
Adaptation and fixation of the rib grafts to the reconstruction plate.
(H) rhBMP-2 supplementation to the surgical site through
absorbable collagen sponge (ACS). (I) Two-week postoperative
view showing restoration of facial contour. (J) Postoperative CT
after 6 months showing reestablishment of mandibular continuity
with dense homogenous mandible.
FIGURE 30.11 Maxillectomy via Weber–Ferguson approach. (A)
Odontogenic tumour in the right palatal region. (B) Limited
maxillectomy of right maxilla. (C) Resected maxilla.
FIGURE 30.12 (A–B) A case of verrucous carcinoma.

FIGURE 30.13 (A) Squamous cell carcinoma of the right lateral
border of tongue. (B) Incision marking for performing a wide
excision of the primary tumour. (C) Subplatysmal dissection
exposing right anterior and posterior triangles. (D) After dissection
the lower border of the sternocleidomastoid (SCM), the internal
jugular vein (IJV) is identified and ligated. (E) Neck dissection—IJV
ligation and clearance of level I–V lymph nodes. (F) Ligation of the
branches of the external carotid artery. (G) Dissection continued in
the posterior aspect of the anterior triangle of the neck to remove
the fibrofatty tissue along with the radical neck dissection
specimen. (H) Dissection performed to identify the posterior belly
of the digastric muscle. (I) Ligation of the upper part of the IJV. (J)
After completion of the radical neck dissection prior to excising the
radical neck dissection specimen, viewing the clearance of the
level IV, III, II and I lymph nodes along with the SCM, IJV and
fibrofatty tissue. (K) Excised tumour of tongue. (L) Cleared lymph
nodes of lymphatic chain.
FIGURE 30.14 (A) Defect. (B) Forehead flap. (C) Division of the
flap. (D–E) Postoperative view.
FIGURE 30.15 (A–B) Regional free flap from the frontal region to
cover the defect on the nose.
FIGURE 30.16 Closure of palatal defect using temporalis
myofascial flap. (A) Palatal defect. (B) Raising temporalis
myofascial flap. (C) Tunnelling the flap to palatal region. (D)
Muscle flap sutured to palatal defect.
FIGURE 30.17 (A) Basal cell carcinoma. (B) Regional flap rotated
to cover the defect of excision.
FIGURE 30.18 (A–B) Bakamjian flap used to cover the defect of
excision.
FIGURE 30.19 Pectoralis major myocutaneous flap. (A) Carcinoma
—buccal mucosa. (B) Excision incision. (C) Tumour tissue
removed with nodes. (D) Hemimandibulectomy. (E) Incision
marked for pectoralis major myocutaneous flap. (F) Flap raised.
(G) Flap tunnelled to buccal defect site. (H) Closure of oral region.
(I) Closure of donor site. (J) Complete closure of the defect.
FIGURE 30.20 (A) Erythromatous candidiasis on the dorsum of the
tongue. (B) Candidiasis seen on the palate. (C)
Pseudomembranous candidiasis.
Maxillectomy (Fig. 30.11A–C)

In case of tumours involving the maxilla, a partial or total maxillectomy is
done depending on the extent of involvement of the tumour (Fig. 30.12A–B).
Maxillectomy via Weber–Ferguson approach
• An incision is made to split the lip along the philtrum up to and

around the alar base, continuing along the lateral surface of the nose
up to the medial canthus of the eye. The incision can also be extended
beneath the lower eyelid up to the lateral canthal region.
• The lip incision is made from the skin to the mucous membrane,
continuing intraorally to the buccal sulcus incision extending
posteriorly to the tuberosity.
• The soft tissue incision is carried down till the bone of the lateral wall
of maxilla.
• A subperiosteal flap is elevated extending superiorly till the
infraorbital rim, thus exploring the lateral surface of the maxilla and
the zygoma.
• Depending on the planned level of osteotomy like limited (alveolar),
subtotal or total maxillectomy, the osteotomy cuts are made buccally.
• The cut is the next ended into the hard palate, which is sectioned along
the floor of the nose.
• The pterygoid plates are then separated using a curved osteotome to
separate the maxilla.
• The sectioned maxilla is then removed and haemostasis achieved.
• A skin graft can be used to cover the raw wound.
• The defect is packed with a tincture benzoin gauze and maintained
with a maxillary splint or obturator.
• The skin incisions are closed in layers.
• Some of the surgical salvage and reconstructive procedures as partial
glossectomy, pectoralis major myocutaneous (PMMC) flap, forehead
flap, etc. can be used (Figs. 30.13–30.19).
Radiotherapy
Tumour cells in stages of active growth are more susceptible to ionising
radiation than adult tissues. The faster the cells are multiplying or the more
undifferentiated the tumour cells, the more likely that radiation will be
effective.
Radiation prevents the cells from multiplying by interfering with their
nuclear materials. Normal host cells are also affected by radiation and must be
protected as much as possible during treatment.
The principal methods employed are:
• X-ray therapy
▪ Superficial X-ray therapy 45–100 kV
▪ Kilovoltage X-ray therapy 300 kV
• Electron therapy
• Surface applicator (radium mould)
• Interstitial implantation—radium or equivalent source
Most commonly radiation is delivered externally by the use of large X-ray

generators. The normal amount of tolerable radiation for a person should not
be exceeded and adjacent uninvolved areas are spared by the use of protective
shielding.
The patient’s host tissues are protected from radiation by two mechanisms
of delivery: (1) fractionation and (2) multiple ports.
Fractionation
Fractionation of the delivery of radiation means that instead of giving the
maximal amount of radiation a person can withstand at one time, smaller
increments of radiation (fraction) are given over several weeks, which gives a
time period for the normal tissues to recover between doses. The tumour cells,
however, are less liable to recover between doses.
Multiple ports
The second method employs multiple ports for radiation exposure. Instead of
delivering the entire dosage through one beam (port), multiple beams are
used. All beams are focused on the tumour but from different angles. Thus, the
tumour is exposed to the entire dosage of radiation. In this method, normal
tissue exposure is reduced more as compared to fractionation method.
Radiation therapy is generally delivered on a 5-day-a-week basis in any of
the several delivery schemes. The general therapeutic dose for head and neck
cancer falls between 60 and 72 Gy, most commonly delivered on a once-a-day
schedule. Fractionated regimens that deliver the radiation on a twice-a-day
basis have shown greater efficacy in tumour elimination and even
hyperfractionated plans have been designed. The intensity of side effects, most
notably mucositis, with the later approaches, however, has all but disallowed
their use.
Effects of radiation (Table 30.2)

I. Skin and mucous membrane
• Usual treatment schedule 200 rad/day for 6–7 weeks.

• Skin reaction prominent in 2–4 weeks; peak in 5–6 weeks; resolving by
6–8 weeks.
Table 30.2
Short-term and long-term effects of various treatment modalities
Treatment modalities Short-term effects Long-term effects

Surgery Difficulty swallowing and Tissue and bone loss
speaking Functional problems
Anaesthesia Cosmetic concerns
Paraesthesia Difficulty swallowing and
speaking
Radiation Mucositis Xerostomia
Altered taste Increased risk of periodontal
Increased risk of infections disease and caries
(e.g. Candita albicans) Postradiation osteonecrosis
Trismus Telangiectasia
Chemotherapy and Nausea and vomiting Bane marrow suppression,
targeted therapy leading to enamel erosion increasing the risk of infection
Mucositis Neuropathy
Skin rash Loss of appetite
Increased bleeding Possible renal, pulmonary and
ototoxicity
Surgery and Mucositis Tissue and bone loss
chemoradiation Stomatitis Increased risk of periodotal
Xerostomia disease and caries
Altered taste Bone marrow suppression,
Pain increasing the risk of infection
a. Mucositis
• Prominent in 1–2 weeks, peak in 4–5 weeks.

• Clears shortly after or at completion of therapy.
• Occurs when rate of epithelial growth and repair is exceeded by effects
of radiation, resulting in epithelial thinning, erosion and ulceration.
• First sign: Whitish appearance of mucosa due to hyperkeratinisation
and intraepithelial oedema or red appearance due to hyperaemia.
• Pseudomembrane formation most likely represents ulceration with
fibrinous exudates with oral debris and microbial components.
• Nonkeratinised mucosa is involved first.
• Late changes in mucosa: Endarteritis and vascular changes with
hypovascularity and hyalinisation of collagen.
• Metallic dental restorations and appliances produce secondary
radiation when present in the path of radiation beam.
• Oral defences are compromised:
▪ Decreased mucosal cell turnover, increased permeability and
loss of mucosal barrier, changes in saliva secretion, reduced
levels of antimicrobial factors in saliva, loss of protective
mucus and diluting effects.
▪ Impairment of mobility of oral structures leads to decreased
cleansing of local irritants and food products.
▪ Changes in oral flora are seen particularly with Streptococcus
mutans, lactobacilli, Candida and gram-negative bacilli.
▪ Both skin and mucous membrane are tissues with a basal
germinal cell compartment producing cells that differentiate
to form the fixed, postmitotic functional cells, which are
eventually lost. Both respond to radiation by an increase in
mitotic activity of germinal cell compartments.
Management of mucositis
Palliation of mucositis is through topical anaesthetic and coating agents.
1. Diluting agents: For hydrating and diluting by rinsing. For example,

saline bicarbonate rinses, frequent rinses with water, dilute H2O2
rinses.
2. Coating agents: Kaolin/pectin (kaopectate), aluminium chloride,
aluminium hydroxide, magnesium hydroxide, hydroxypropyl
cellulose, sucralfate (cytoprotective agent which forms a barrier and
may stimulate release of prostaglandins).
3. Lip lubrication: Water-based lubricants (KY Jelly), lanolin.
4. Topical anaesthetics: Dyclonine HCl, xylocaine HCl, benzocaine HCl,
diphenhydramine HCl.
5. Analgesic agents: Benzydamine HCl is a nonsteroidal agent. It has
analgesic, anti-inflammatory and mildly anaesthetic properties. It may
stabilise cell membranes, inhibit degranulation of granulocytes and
alter synthesis of prostaglandins.
6. β-Carotene: This reduces the severity of mucositis during chemotherapy
and radiotherapy.
b. Candidiasis (Fig. 30.20A–C)
II. On the salivary glands
Xerostomia
• Results from direct effect on major salivary glands.

• Parotid and submandibular glands produce 55%–80% of total salivary
flow.
• Salivary glands are affected when upper limit of field is at chin to
mastoid.
• Doses more than a total dose of 3000 Gy poses a risk if all major glands
are in the field of radiation.
• Irreversible effects occur with a total dose of 6000 Gy for 5 weeks.
• Decrease in the rate of salivary flow occurs in the first week of
treatment due to atrophy and necrosis of acinar cells, changes in the
vascular connective tissues and altered neurologic function.
• Serous acini are affected earlier. This results in thick and viscous
secretions.
• Changes in composition of saliva results due to decrease in secretory
IgA and buffering capacity and acidity. This affects microbial flora and
remineralising potential of teeth (Fig. 30.21).
FIGURE 30.21 Xerostomia. Note the dry gingival mucosa and

cervical caries.
Management
1. Stimulation of remaining salivary gland function

• Use of sialogogues, which stimulate salivary secretion.
• Pilocarpine is a parasympathomimetic agent, which has a
major effect on muscarinic–cholinergic receptors of acinar
cells. Recommended dose is up to 15 mg/day.
• Anetholetrithione: It increases the number of cell surface
reception on acinar cells. Synergetic effect is attained with the
use of both pilocarpine and anetholetrithione.
• Bethanechol and bromhexine: These stimulate
parasympathetic nervous system and thus help in increasing
the secretion of saliva.
2. Radiobiologic approach to protect salivary glands from radiation
• WR-2721: In rodents, the salivary glands are known to
selectively concentrate this radioprotective agent. It provides
protection against both acute and chronic changes.
• Isoproterenol
▪ It induces DNA synthesis and proliferation in
salivary gland.
▪ Single injection results in high proportion of cells
induced to undergo one cycle of proliferation.
▪ Ideally, cell proliferation is stimulated during
intervals between radiation treatments.
• Prophylactic use of pilocarpine (5 mg q.i.d.) stimulates salivary
glands during radiotherapy. Patients who begin radiotherapy
with higher initial flow rate retain more residual flow.
3. Palliation of xerostomia
• Mouth wetting agents or saliva substitutes can be used.
• Frequent sipping of water and moist diet may be helpful.
• Carboxymethyl cellulose is also useful.
III. On taste buds
• It may occur as a primary effect of radiation or secondary to

xerostomia.
• Doses less than 2000 rad decrease taste activity.
• Complete subjective loss is seen at 3000 rad, which recovers 60–
120 days after the completion of the treatment.
IV. On teeth
Caries
• Patients with more than 105 S.mutans and 104 Lactobacillus are
considered to be at high-risk for caries development.
• Usually, caries is associated with xerostomia. This radiation caries
affects the gingival third and incisal cusp tips of teeth.
Aetiology of caries
• Lack of production of saliva results in the loss of remineralising

potential
• Loss of buffering capacity of salvia
• Increased acidity of saliva
• Change in bacterial flora of saliva
Management
• Oral hygiene maintenance

• Manage xerostomia
• Use of fluorides to harden tooth structures
• Topical fluorides and chlorhexidine rinses to reduce levels of S. mutans
Stunted development of tooth
• Results due to defective mineralisation

• Stunted root growth is seen in children
Management
• Extract the teeth with doubtful prognosis 7–10 days before

radiotherapy or within 7–10 days after commencement of
radiotherapy with antibiotic coverage.
• Avoid surgical extractions wherever possible.
V. On bone
Refer to Chapter 25 Osteomyelitis, Osteoradionecrosis and Osteochemonecrosis.
VI. Mandibular dysfunction
• It occurs due to fibrosis of muscles

• Mandibular discontinuity
Treatment
• Physiotherapy
• Occlusal stabilisation appliances
• Mandibular stretching exercises
• Trigger point injection
• Analgesics
• Tricyclic medication
Radiosensitisers
Radiosensitisers are compounds that sensitise the tumour cells to radiation
during radiotherapy (Box 30.1).
Box 30.1 Radiosensitisers
• Hyperbaric oxygen
• Carbogen
• Nicotinamide
• Metronidazole and its analogs (misonidzole, etanidazole, nimorazole)
• Hypoxic cell cytotoxic agents (Mitomycin-C, Tirapazamine)
• Membrane active agents (procaine, lidocaine, chlorpromazine)
• Radiosensitising nucleosides (5-Fluorouracil, Fluorodeoxyuridine,
Bromodeoxyuridine, Iododeoxyuridine, Hydroxyurea, Gemcitabine,
Fludarabine)
• Texaphyrins (motexafi gadolinium)
• Suppressors of sulphhydryl groups (N-Ethylmalemide, Diamide and
Diethyl maleate)
• Hyperthermia
• Novel radiosensitisers (paclitaxel, docetaxel, irinotecan)
Radioprotectors
Radioprotectors are chemical compounds that protect the nontumour (normal)
cells from radiation during radiotherapy (Box 30.2).
Box 30.2 Radioprotectors

Amifostine
Nitroxides (tempol)
Other antioxidants (glutathione; lipoic acid; vitamins A, C and E;
superoxide dismutase)
Cysteine and cysteamine
Melatonin
Novel radioprotectors (tetracyclines and fluoroquinolones)
Radiation mitigator
Radiation-induced late normal tissue toxicity includes ongoing mitotic cell
death and perpetually active cytokine cascades that can lead to vascular
damage, tissue hypoxia and excessive extracellular matrix deposition.
Radiation mitigators aim to interrupt these cascades or intervene to prevent
the perpetuation of damage and thus reduce the expression of toxicity
(Box 30.3).
Box 30.3 Radiation mitigator
Palifermin
Halofuginone
TGF-β
Keratinocyte growth factor
ACE inhibitors (Captopril, Enalapril, Ramipril)
COX-2 inhibitors/NSAIDS (Celecoxib, Aspirin, Ibuprofen)
Chemotherapy
Chemicals that act by interfering with rapidly growing tumour cells are used
for treating many types of malignancies.
As with radiation, chemicals are not very selective but affect normal cells to
some extent. Most of these agents are given intravenously, but recently intra-
arterial injections have been given. Because the agents are delivered
systemically, they adversely affect different body systems; most notable is the
haematopoietic system, which is considerably affected because of its rapid rate
of cellular turnover. Thus, patients who are undergoing chemotherapy are in a
delicate balance between effectiveness in killing the tumour cells and anaemia,
neutropaenia and thrombocytopaenia. Infections and bleeding are therefore
common complications in these patients.
To reduce the toxicity of a single agent given in large quantities, multiple-
agent therapy is the preferred method. Many patients are given 3–5 agents at
the same time. Each may work at a different point in the life cycle of the
tumour cell, thus increasing effectiveness with less toxicity to the host. Intra-
arterial therapy is reserved for T3 and T4 lesions because of the difficulties in
performing and maintaining catheterisation, excessive local tissue toxicity and
difficulties in repeated therapy. The drugs are introduced through branches of
the external carotidartery, including even the superficial temporal branch in
retrograde fashion. Vincristine, bleomycin and methotrexate in various
combinations have been used, but more recent protocols include platinum
compounds most commonly in combination with 5-fluorouracil (5-FU). In
cases of sarcoma, most regimens are combinations of vincristine, actinomycin
D, cyclophosphamide and doxorubicin (adriamycin). Chemotherapy finds its
main role as a support for radiation and/or surgical care. It is most effective for
lesions confined strictly to the soft tissues.
Chemotherapy approaches
Chemotherapeutic agents are used in several therapeutic regimens and
approaches, including combination therapy, induction chemotherapy,
concomitant chemotherapy, adjuvant chemotherapy, palliative chemotherapy
and chemoprevention. These approaches are described in relation to head and
neck squamous cell carcinomas, which are the primary focus of head and neck
oncology.
Chemoprevention
• Chemoprevention includes strategies to prevent or reverse
carcinogenesis before an invasive cancer develops or to prevent a
second primary cancer in patients who have had a previous cancer
cured. Clearly, the most effective preventive strategy for upper
aerodigestive tract cancer is the cessation of smoking.
• Retinoids: Molecular biology has provided new information on how
retinoids regulate gene expression and has led to the development of
synthetic retinoids, which may be less toxic and more effective in the
prevention of cancer.
• The use of chemopreventives should be limited to controlled clinical
trials.
Intralesional chemotherapy
Intralesional injection of vinblastine, vincristine or interferon has been shown
to be effective in the local control of epidemic Kaposi’s sarcoma and can be
used in combination with systemic chemotherapy or radiotherapy. If
necessary, lesions are reinjected at 3–6 week intervals.
In one study, 40% of Kaposi’s sarcoma lesions (n = 35) required only one
injection for control, 31% required two injections and 29% required three
injections. No lesions required more than three injections for initial control;
some lesions recurred later and required additional injections.
Topical chemotherapy
Actinic keratosis lesions have been effectively treated with the application of
5% fluorouracil cream.
Fluorouracil cream is applied twice daily until the area exhibits a significant
inflammatory reaction and ulceration (usually 3–4 weeks). Similar topical
application of fluorouracil in selected cases of multiple superficial basal cell
carcinomas, as may be seen in basal cell naevus syndrome, has been effective.
Topical therapy, however, is not effective for invasive lesions and results
needless delay in definitive therapy. Surgical excision is still the treatment of
choice for most cases of basal cell carcinoma.
CHAPTER 31
Salivary Gland
Pathologies
Development of salivary glands

Structure of salivary glands
Surgical anatomy
Parotid gland
Submandibular gland
Sublingual gland
Regulation of salivary secretion
Composition of saliva
Functions of saliva
Diagnosis of salivary gland diseases
Salivary gland investigations
• Salivary gland imaging
• CT and MRI
• CT sialography
• Magnetic resonance imaging (MRI)
Ultrasonography
Use of saliva as a diagnostic fluid
BIOPSY
Developmental diseases
Obstructive disorders
Sialolithiasis (salivary calculi; salivary stones)
Mucocele (mucous extravasation phenomenon, mucous
escape reaction)
Ranula
Infections and systemic diseases
Sialadenitis
Mumps
Sialadenosis
Idiopathic diseases
Autoimmune diseases
Benign lymphoepithelial lesion
Sjögren’s syndrome
Neoplasms of salivary glands
Benign tumours of salivary glands
• Pleomorphic adenoma
• Warthin’s tumour (papillary cyst adenoma
lymphomatosum)
Malignant tumours of the salivary gland
• Mucoepidermoid carcinoma (MEC)
• Adenoid cystic carcinoma (ACC)/Cylindroma
There are three major paired salivary glands, namely, the parotid,
submandibular and sublingual glands. Besides these, there are a multitude of
minor salivary glands, situated in the oral cavity but also found in the
pharynx, larynx and the sinuses (Fig. 31.1). The minor salivary glands are
about 600–1000 in number and mostly located at the junction of hard and soft
palate.
FIGURE 31.1 Diagrammatic representation of the location of the
major salivary glands.
About 1500 mL of saliva is secreted per day. The pH of saliva from resting
glands is slightly less than 7 but during active secretion, it rises to 8. The saliva
produced by these glands functions as lubricant for speech, helps in
swallowing and mastication, has antibacterial and immunological properties
and acts as an immune mediator.
Development of salivary glands

• Development of glandular tissue involves the interaction of oral
epithelium and underlying mesenchyme. These interactions are
known as proximate tissue interactions or secondary induction. These
interactions regulate initiation and growth of glandular tissue and
cytodifferentiation.
• As epithelial bud forms during development, the bud close to
stomodeum differentiate into main excretory duct and most distal
portions differentiate into secretory end pieces.
• Origin of epithelial bud is ectodermal in parotid and minor salivary
glands and endodermal in submandibular and sublingual glands.
• Parotid gland originates near the corner of stomodeum by 6th week of
intrauterine life.
• Submandibular gland originates from floor of mouth at the end of 6th
week of intrauterine life.
• Sublingual glands arise lateral to the submandibular glands at about
8th week of intrauterine life.
• Minor salivary glands develop in specific areas of the oral cavity by
12th week of intrauterine life.
Structure of salivary glands (Fig. 31.2)

• Compound tubuloacinar glands
• Merocrine in secretion
• Arranged as grapes on vine; the stem correspond to the ductal system
and grapes represent the acini.
• The basic secretory unit of the salivary gland consists of:
▪ Acinar cells
▪ Myoepithelial cells
▪ Ductal system
• The acini are of three types—serous, mucus and mixed
• Myoepithelial cells—surround the acinar and duct cells and are
contractile in function. Ducts are intercalated, striated and excretory.
Basal cells of the intercalated duct and excretory duct cells are capable
of giving rise to fully differentiated ductal epithelial cells and it is this
significant feature that gives rise to the bicellular theory of
tumourigenesis, which states that all tumours either arise from
intercalated duct stem cells (pleomorphic adenoma, Warthin tumour,
oncocytoma, acinic cell carcinoma, and adenoid cystic carcinoma) or
excretory duct stem cells (squamous cell carcinoma and
mucoepidermoid carcinoma).
• There is a capsule, which supports and surrounds the ducts and acini.
• Connective tissue extends into the gland as a septum and divides the
gland into lobes and acts as a conduit for nerves, vessels and
lymphatics. It also contains inflammatory cells, namely, plasma cells,
fibroblasts, macrophages, lymphocytes and IgA.
FIGURE 31.2 Microstructure of Salivary Glands.
Surgical anatomy
Parotid gland
Parotid gland is the largest of the salivary glands and is a predominantly
serous gland. In adults, it occupies a position from the zygomatic arch
downward about 6 cm to just below the angle of the mandible and from just in
front of the ear extending forward 3 or 4 cm on the surface of the masseter
muscle. It is inverted pyramidal in shape with the apex towards the angle of
the mandible and the base at the external acoustic meatus.
The capsule of the parotid gland is extensive and is derived from the
investing layer of deep cervical fascia (Table 31.1; Fig. 31.3A).
Table 31.1
Relations of parotid gland

Borders Structures
Anterior Masseter m.
Ramus of mandible
Anteromedial Medial pterygoid m.
Stylomandibular fascia
Medial Styloid process superomedially
Transverse process of the atlas inferomedially
Posteromedial Stylohyoid m.
Posterior belly of the digastric m.
Posterior Mastoid process of the temporal bone
Sternocleidomastoid m.
Lateral Investing layer of deep cervical fascia helping form the capsule
Superior External acoustic meatus
Condylar head of the mandible articulating in the glenoid fossa
Inferior Angular tract of Eisler between the angle of the mandible and the
sternocleidomastoid m.
FIGURE 31.3 (A) Anatomy of parotid glands, (B) Faciovenous

plane of Patey
Structures within the gland
• Arteries—external carotid artery, posterior auricular, superficial

temporal and maxillary artery
• Veins—retromandibular vein forms from superficial temporal and
maxillary vein
• Nerves—facial nerve
• Parotid duct (Stensen’s duct)—parotid duct extends from anterolateral
surface on the masseter muscle parallel to zygomatic branch 1.5 cm
below it. It is 35–50 mm in length and 3 mm in diameter
• At the anterior border, it bends and pierces the buccal fat of pad and
buccinator muscle and opens into the oral cavity opposite the crown of
maxillary 2nd molar
• Faciovenous plane of Patey (Fig. 31.3B)
Blood supply
External carotid artery supplies the parotid gland. The venous drainage from
the gland is to posterior facial vein and then to internal jugular vein through
the common facial vein.
Nerve supply
The auriculotemporal nerve carries secretomotor fibres to the parotid gland
and frequently anastomoses with the temporal branch of the facial nerve.
Lymphatic system
The parotid gland contains two layers of lymph nodes: superficial and deep.
These two lymph nodes ultimately drain into the superior deep cervical nodes.
Applied anatomy of the parotid gland
• The parotid gland swelling tends to be very painful owing to the

unyielding tense lateral (outer) fascial capsule. The gland swelling is
usually evident externally in late stage of disease due to the medial
loose capsule.
• The facial nerve is closely related to the parotid gland, which should be
considered during the surgeries involving the gland.
Submandibular gland
Submandibular gland is the second largest of the salivary gland weighing 10–
15 g (Fig. 31.4 A, B). It contains both serous and mucous secreting glandular
elements. This gland lies in the submandibular triangle or digastric triangle. It
is J-shaped. The largest portion of the gland lies below the mylohyoid muscle.
It extends as far anteriorly to the anterior belly of digastric and posterior to the
stylomandibular ligament which keeps it separate from the parotid gland.
FIGURE 31.4 Anatomy of Submandibular gland.
At the posterior border of the mylohyoid muscle, a process of the gland

curves upwards around the muscle and extends medially towards the
genioglossus muscle to lie in lateral sublingual space. It is divided into
superficial and deep parts by mylohyoid muscle (Table 31.2).
Table 31.2
Relations of submandibular gland

Borders Structures
Anterior Sublingual gland
Posterior Posterior belly of digastric, Stylohyoid and Parotid gland
Medial Hyoglossus and styloglossus
Lateral Mylohyoid muscle and Superficial part of the gland
Superior Lingual nerve and Submandibular ganglion
Inferior Hypoglossal nerve
Submandibular duct (Wharton’s duct)

Submandibular duct emerges at anterior end of deep part. It is 5 cm long and
runs forward between the mylohyoid and hyoglossus muscle and then onto
the genioglossus muscle opening on floor of mouth on the summit of lingual
papilla at the side of frenulum of tongue.
Nerve supply
The parasympathetic nerve supply is via the chorda tympani nerve, which
carries preganglionic fibres to the submandibular ganglia. Postganglionic
fibres originate in this ganglion and pass to the gland. The sympathetic nerve
fibres are carried along the lingual artery to the gland.
Lymphatic drainage
The lymphatic drainage is into the submaxillary nodes and then to the jugular
chain.
Applied anatomy
The tortuous course of the submandibular duct leads to stagnation of saliva
and thus leads to the formation of salivary stone.
Sublingual gland
Sublingual gland is the smallest of the salivary gland and usually weighs 2 g.
It is mucous in nature. It is almond-shaped and lies in the sublingual
depression on the inner surface of the mandible, near the symphysis under the
mucosa of the floor of the mouth. It is located above the mylohyoid line of the
mandible and rests on the mylohyoid muscle. There is no discrete capsule for
the sublingual gland. There are around 20 small sublingual ducts known as
ducts of Rivinus opening into floor of mouth. Main duct known as Bartholin’s
duct opens into submandibular duct.
Nerve supply
The nerves of the glands are the parasympathetic secretory nerves from the
chorda tympani nerve, the sympathetic nerves are from the plexus on the
facial artery and the sensory nerves are from the lingual nerve.
Lymphatic drainage
Lymphatic drainage is to the submental and submandibular lymph node
groups.
Minor salivary glands

Minor salivary glands have been estimated to number between 600 and 1000.
They are small, independent, predominately mucous glands except Von
Ebner’s glands, which is a serous gland. Though these glands are found in
almost every part of the oral cavity, they are predominant in posterior palate.
This is of significance, due to the high occurrence of malignant tumours in the
posterior palate.
Applied anatomy
Since minor salivary glands are superficially located they are more prone to
traumatic lesions such as mucoceles.
Regulation of salivary secretion

• Secretion of fluid and electrolytes are regulated by alpha receptors and
muscarinic action through Ca2+ mediated pathway.
• Secretion of proteins is regulated through the action of beta receptors
via cyclic AMP pathway.
Saliva is a complex fluid comprising many organic and inorganic substances
(Table 31.3).
Table 31.3
Parotid Submandibular
Organic
Proteins 250 mg/dL 150 mg/dL
Urea 3 mmol/L 7 mmol/L
Uric acid 15 mg/dL 2 mg/dL
Lysozymes 2.3 mg/dL 1.5 mg/dL
IgA 4 mg/dL 2 mg/dL
Amylase 1 IU/L 0.025 IU/L
Inorganic
Sodium 23 mEq/L 21 mEq/L
Potassium 20 mEq/L 17 mEq/L
Chloride 23 mEq/L 20 mEq/L
Bicarbonate 20 mEq/L 18 mEq/L
Calcium 2 mEq/L 3.6 mEq/L
Phosphate 6 mEq/L 4.5 mEq/L
Inorganic components of saliva
• Calcium and phosphate: Concentrations are important both in relation to

acid dissolution of tooth enamel and precipitation of dental calculus.
• Hydrogen carbonate: Hydrogen carbonate is an important buffer.
• Fluoride: Fluoride concentrations in saliva are low and very similar to
those in plasma and extracellular fluids. However, the increase in the
fluoride intake will transiently increase plasma level fluoride thus
increasing salivary fluoride level.
• Thiocyanate: Thiocyanate is a component of an antibacterial system in
saliva.
• Sodium, potassium and chloride: Sodium, potassium and chloride vary at
different flow rates.
• Lead, cadmium, copper: Saliva may reflect systemic concentrations of
some ions.
• Iodine: Iodine is stored by the salivary glands and secreted into saliva.
Organic components of saliva
• Mucins: Glycoproteins with more than 40%carbohydrate in the

molecule are termed as mucins. They act as lubricants on the epithelial
surfaces throughout the digestive tract.
• Proline-rich proteins: Both parotid and submandibular saliva contain
glycoproteins rich in proline. Their role in lubrication is probably
small.
• Digestive proteins: Amylase is the main digestive enzyme in saliva, but
its action is limited by the amount of time the food stays in the mouth
and it is inactivated by gastric acid. Parotid lipase is important only
when pancreatic lipase secretion is reduced.
• Proteins with antimicrobial properties: Sialoperoxidase, lysozyme,
lactoferrin and IgA have antibacterial property, the histatins have
antifungal property.
• Proteins binding calcium: Statherin and the acidic proline-rich proteins
bind calcium and reduce calculus formation. The proline-rich proteins
constitute the major protein fraction of parotid saliva.
• Blood group substances: ABO blood group substances in saliva have
been identified in criminal cases involving bite marks.
• Sugars: A number of small sugars are found in saliva; concentrations of
salivary glucose follow those of plasma glucose level but are lower.
• Lipids: Steroid hormones are found in saliva in proportion to their free
concentration in plasma.
• Amino acids, ammonia, urea, sialin: A number of nitrogen-containing
compounds in saliva are converted to ammonia by plaque bacteria.
Functions of saliva
Composition of saliva endows it with several mechanical protective functions,
some physical biochemical and antibacterial or antiviral properties.
• The layer of mucus protects the underlying oral mucosa from local
irritants preventing (mucosa) desiccation.
• The glycoproteins in saliva have some of the lubricating properties of
polysaccharides and help the tongue, oral mucosa and teeth to
function smoothly in speaking and swallowing.
• Mineral content of the saliva aid in posteruption maturation of the
teeth.
• Calcium and phosphate help to prevent teeth dissolution in plaque.
The lubricating activity reduces wear.
• The bicarbonate and phosphate exert antibacterial activity within
plaque by their buffering ability.
• The secretory IgA present in the saliva appears to be able to
agglutinate bacteria and make them more readily phagocytised.
• Salivary lysozymes found in secretions of all major glands acts as a
muramidase by hydrolysing glycopeptides containing muramic acid
in bacterial cell wall.
• Lactoferrin, an iron binding protein, present in saliva may be able to
inhibit bacterial growth by denying them iron.
• Lactoperoxidase with hydrogen peroxidase and the thiocyanate ion
can inhibit Lactobacillus and carcinogenic Streptococci.
Diagnosis of salivary gland diseases

Parotid gland
• Normal parotid gland is not evident clinically unless enlarged.
• Parotid swelling classically causes ear lobule elevation (superficial
lobe), lateral pharyngeal or retromandibular angle swelling (deep
lobe).
• Parotid gland can be palpated in the preauricular, inferior auricular
and postauricular regions.
• Palpate the gland and nodes bilaterally.
• Gently dry the opening of Stensen’s duct with gauze, milk the gland by
external compression to observe salivary flow.
Submandibular gland
• The submandibular gland is checked by bimanual palpation, by placing

a finger of one hand in the submandibular region and another
intraorally in the floor of the mouth.
• The submandibular nodes are palpated by tipping the patient’s head
slightly down and forward to relax the tissues. ‘Cup’ the mandible
with thumb and fingers and palpate bilaterally. Draw tissue against
the lateral border of the mandible. Use bidigital and circular
compressions.
• The gland is palpable by bimanual palpation (intraoral–extraoral)
whereas the node is not evident by this manoeuvre (palpable only
extraorally).
Salivary gland investigations
Salivary gland imaging

Imaging techniques help to diagnose and differentiate the salivary gland
diseases from other diseases. Imaging plays an important role in the diagnosis
of many salivary gland diseases and disorders. The various imaging
techniques include:
• Plain radiography
• Sialography
• Computed tomography (CT)
• Ultrasonography (USG)
• Magnetic resonance imaging (MRI)
• Radioisotope scanning
Plain-film radiography
Plain radiographs have been used widely to visualise calcification within the
salivary glands. They have been used to demonstrate bony changes adjacent to
those structures and to show distant effects of salivary disease such as
metastases but has been effectively replaced by advanced imaging modalities.
It has the potential to identify unrelated pathoses in the area of the salivary
glands that may be mistakenly identified as salivary gland disease, such as
resorptive or osteoblastic changes in adjacent bone causing periauricular
swelling mimicking a parotid tumour.
Panoramic and conventional postero-anterior (PA) skull radiographs may
demonstrate bony lesions, thus eliminating salivary pathosis from the
differential diagnosis.
A plain film radiograph may demonstrate a deep antegonial notch,
overdeveloped mandibular angle, and exostosis on the outer surface of the
angle in cases of masseter hypertrophy.
Intraoral radiography
• Periapical radiograph
Extraoral radiography
• Panoramic projection
• Lateral projection
• PA skull projection (with puffed cheek)
Calcification within the glands
• Calculi present in Wharton’s duct are best demonstrated by the use of

the intraoral occlusal films, those situated in the submandibular gland
by occlusal or extraoral films.
• Calculi in the parotid duct canals can be demonstrated on an extraoral
film that is placed at a right angle to the surface of the face, with the
direction of the tube parallel to the cheek, the exposure is made when
the cheek is blown outwardly or laterally by the patient (puffed cheek
view). This provides less superimposition of the osseous structures.
Other projection used for parotid gland is the frontal view.
• Intraoral views are most easily achieved using a dental radiography
set. The value of intraoral views in identifying stones in the
submandibular and parotid ducts is well known. The periapical film is
placed between the teeth and the cheek and is an extremely sensitive
method of demonstrating radiopaque calculi in the parotid duct.
Disadvantages
• Limited soft tissue in formation
• Low sensitivity for involvement of adjacent bony structures
• Exposure to radiation doses
Sialography
It is a specialised procedure for radiographic demonstration of major salivary
glands by introducing radiopaque contrast medium into the ductal system is
termed as sialography (Figs. 31.5–31.15).
FIGURE 31.5 Normal sialographic view of submandibular gland.

FIGURE 31.6 Normal sialographic view of parotid gland.
FIGURE 31.7 Dilation of the ductal orifice.
FIGURE 31.8 Cannulation at the ductal orifice.

FIGURE 31.9 Sialograph showing tree in winter appearance.
FIGURE 31.10 Sialograph showing submandibular stricture.
FIGURE 31.11 Sialograph of parotid gland demonstrating

narrowing and strictures of Stensen’s duct.
FIGURE 31.12 Sialograph showing cherry blossom appearance in

Sjogren’s syndrome.
FIGURE 31.13 Schematic demonstration of sialograms. (A)
Sialolithiasis (B) Sjögren’s disease (C) Sialoadenitis (D) Neoplasm.
FIGURE 31.14 Sialography performed in submandibular gland
showing normal sialograph.
FIGURE 31.15 Sialography showing salivary fistula as a
complication after retromandibular approach to condylar fracture.
The various contrast agents and sialographic appearances have been

enumerated in Tables 31.4–31.6.
Table 31.4
Contrast agents used for sialography

Aqueous based solutions Oil based solutions
Contrasts agents Contrasts agents
1. Ionic aqueous solutions Diatrizoate • Iodised oil, e.g. Lipiodol (iodised poppy seed oil)
(Urografin) Metrizoate (Triosil)
2. Nonionic aqueous solutions lohexol
(Omnipaque)
Advantages Advantages
• Easily introduced because of low • Densely radiopaque, and thus good contrast
viscosity
• Easily and rapidly removed from the
gland
• Easily absorbed and excreted if
extravasated
Disadvantages Disadvantages
• Less radiopaque, and thus less • High viscosity, thus slow excretion. High pressure is
contrast needed to introduce the contrast agent
• Low viscosity and thus fast excretion • Risk of calculi dislodgement into the main duct
• Foreign body reaction from remnants of contrast
materials
Table 31.5
Sialographic appearances
Normal ductal architecture ‘Branched leafless tree’ appearance
Normal ductal structure in Tree in winter appearance
parotid gland
Normal ductal structure in Bush in winter appearance
submandibular gland
Nonopaque sialolith Voids
Sialadenitis Sialectasis appearance—appearance of focal collection of contrast
medium within the gland
Sialodochitis Sausage link appearance
Sjogren’s syndrome Snowstorm appearance of punctate sialectasis or cherry blossom
appearance or branchless fruit laden tree appearance
Intraglandular neoplasm Ball in hand appearance
Table 31.6
Pathological conditions and sialographic appearance

Normal sialographic appearance Pathological conditions and sialographic
appearance
Parotid gland
• Main duct diameter (1–2 mm wide) and
filled completely and uniformly
• The duct structure within the gland
branches regularly and tapers gradually
towards the periphery of the gland, the so-
called tree in winter appearance
Submandibular gland Calculi
• Main duct diameter (3–4 mm wide) and • Filling defect(s) in the main duct
filled completely and uniformly • Ductal dilatation proximal to the calculus
• Branching duct structure tapering • The emptying phase usually shows contrast
gradually towards the periphery—the so- medium retained behind the stone
called bush in winter appearance Sialodochitis
• Dilatation
• Stricture of the main duct, sausage link
appearance with calculi
Sialadenitis
• Dots or blobs of contrast medium within the
gland, an appearance known as sialectasis, ‘This
is due to inflammation of the glandular tissue
and saccular acinar dilatation’
Sjogren’s syndrome
• Widespread dots or blobs of contrast medium
within the gland, an appearance called punctate
sialectasis or snowstorm
Indications
To determine the following:
• Presence and/or position of calculi or other ductal obstruction.

• Extent of ductal and glandular destruction secondary to an
obstruction.
• Extent of glandular breakdown.
Contraindications
• Allergy to the contrast agent (especially iodine).

• Acute infection/inflammation (discharge of pus from the duct
opening).
• Radiographs showing calculus close to the duct opening—risk of
dislodgement into the gland.
Different sialographic techniques
• Simple injection technique

• Continuous infusion pressure-monitored technique
Phases of the procedure

The sialographic procedure is divided into three phases:
• Preoperative phase
• Filling phase
• Emptying phase
Step 1: Preoperative phase

This involves taking preoperative (scout) radiographs, to assess the following:
• Position and/or presence of any radiopaque obstruction.
• Position of shadows of normal anatomical structures that may overlie
the gland, such as the hyoid bone.
Step 2: Filling phase
• A lacrimal or periodontal probe is used to dilate the sphincter at the

ductal orifice before the passage of a cannula which is a blunt needle
or catheter connected by extension tubing to a syringe containing
contrast agent.
• Contrast solution is then slowly infused until the patient feels
discomfort (usually between 0.2 and 1.5 mL, depending on the gland
being studied). These iodine containing agents render the ductal
system radiopaque.
• The filling phase can be monitored by fluoroscopy or with static films.
The radiographs are taken, ideally at least two different views at right
angles to one another.
Step 3: Emptying phase

The gland is allowed to empty for 5 min without stimulation.
The use of lemon juice at this stage to aid excretion of the contrast medium
is often advocated.
CT and MRI
Magnetic resonance imaging (MRI) has become the diagnostic tool of choice in
assessing most masses in the head, while computed tomography (CT) is still
the most useful imaging modality in the neck. The advantage of MRI over CT
is in its superior soft tissue resolution, while CT retains the advantage in
defining cortical bone. MRI, however, is much more sensitive in the soft tissue
component of bone, i.e. the marrow space. Therefore, MRI provides the best
definition of tumour margins and better localises the extent of regional spread,
particularly along nerves.
Uses of CT scanning
• CT is remarkably sensitive to the presence of calcification and may

demonstrate intraductal or intraglandular calculi, which have escaped
detection on good quality plain radiographs.
• CT scanning helps to define the cystic wall better and thus helps to
differentiate between the fluid containing masses like cyst, abscess, etc.
• The unexpected involvement of adjacent bony structures in a
malignant or inflammatory process is sometimes revealed by CT,
which is excellent in demonstrating periosteal reaction and early
cortical destruction.
Disadvantages of CT scan for salivary gland imaging
• Parenchymal disease is not well displayed by CT.

• In almost all cases, the appearances given by the autoimmune diseases,
sialadenitis and sialosis are similar, showing enlarged glands with
increased attenuation. Fatty change may also be apparent as areas of
lower attenuation.
• CT cannot image the facial nerve and its ability to identify lesions as
being in the superficial or deep lobes relies on indirect markers.
• Masses within the salivary glands are usually well shown, although
the limited soft tissue contrast inherent to this technique may require
administration of intravenous contrast medium to render some lesions
apparent.
CT sialography
Tumours would be better delineated from the surrounding parenchyma if the
parenchyma were opacified with intraductal contrast media. Although
majority of salivary tumours are distinguishable by conventional CT, a
minority has defied detection, even when intravenous contrast has been
administered. CT sialography has also been used to predict the tumour as
being superficial or deep to the plane of the facial nerve, the rationale being
that the course of the parotid duct and the facial nerve lie in similar planes.
Intravenous contrast media are used in the CT of salivary glands for two
reasons:
• To obtain information about the nature and extent of a tumour

• To help delineate blood vessels from lymphadenopathy
Advantages
• Wide field of view

• Very sensitive for soft tissue calcification and bone involvement
• Usually good soft tissue discrimination
• Not operator dependent
Disadvantages
• Difficult to scan in planes other than axial plane

• May require intravenous contrast for best results
• Radiation dose received is high
Magnetic resonance imaging (MRI)

Magnetic resonance imaging relies on the electromagnetic properties of
protons and particularly in relation to the energy released when such particles
decay from high to a relatively low energy state within an externally applied
magnetic field. MRI differs markedly from CT in its apparent sensitivity to
calcification. Heavily calcified tissue such as cortical bone or calculi produces
no significant signal on MRI and is thus distinguished as a ‘signal void’. This
means that neither calculi nor dystrophic calcification within a tumour are
visible.
Uses
• Sjogren’s disease
• Neoplasms: Tumour delineation is assisted in many cases by
gadolinium administration. The edge of a lesion may be better
evaluated following contrast and the internal structure of tumours can
be seen in the images. Unsuspected infiltration of a malignant process
beyond the confines of the gland may be seen after gadolinium
administration.
• In Vascular lesions magnetic resonance angiography (MRA) are used
in demonstrating the intraglandular and extraglandular blood vessels
in case of any lesions involving or related to the gland. Additionally,
the extent of vascular malformations in the region of the salivary
glands can be well appreciated.
Advantages
• Non-ionising radiation
• Excellent soft tissue (including bone marrow) discrimination
• Ability to reconstruct images in any scan plane
• Not operator dependent
Disadvantages
• Not widely available

• Poor cortical bone detail
• Long scanning time
• Restricted field of view in some circumstances
• Not tolerated by all patients
Ultrasonography (Fig. 31.16)
Ultrasonography imaging relies upon the transmission of high-frequency
sound, which is attenuated as it passes through tissue, at a rate dependent
upon the acoustic properties of that tissue and upon the frequency of the
incoming waveform.
FIGURE 31.16 Ultrasonograph showing the presence of calculus in

the Wharton’s duct.
Uses
• Presence of solid or cystic masses can be detected

• Calculi of the salivary glands can be detected
• Can detect masses present within the gland and outside the gland
• It helps to differentiate between intraparotid neoplasms from a
superficially located lesion extrinsic to the gland
Radioisotope scanning or scintigraphy

The functional basis is a gamma ray-emitting radionuclide, which is directed
to a particular area of interest through ingestion, inhalation or intravenous
injection. The emitted radiation is detected by a gamma camera consisting of a
scintillation crystal and photomultipliers (hence the term scintigraphy)—
following computer processing, the activity is displayed in either static or
dynamic modes. The radioisotope commonly used is Technetium-99m (99mTc).
The principal limitation of the radioisotope scan is resolution. Tumour less
than 1 cm in diameter cannot be evaluated.
Uses
• It is particularly used in the diagnosis of obstructive sialadenitis. They

help to differentiate between acute obstructive and nonobstructive
sialadenitis
• Helps in the detection of certain tumours
Advantage
Pathophysiological information is good for assessment of metastatic spread.
Disadvantages
• Poor anatomical discrimination

• Risk of allergic reaction/anaphylaxis from the radioisotope
Interventional radiology
Interventional radiological techniques are used for minimally invasive
procedures with imaging control.
Guided biopsy techniques

Guided biopsy is used widely in many areas of the body, primarily as a
method of obtaining material for histological or microbiological examination
that would otherwise only be available by open operation.
• CT-guided techniques enable a two-dimensional image using skin

markers as a guide, from which the entry point, angulation and depth
of insertion of the biopsy device may be electronically planned.
• Ultrasonically guided biopsy is particularly suited to relatively
superficial regions and not only gives a real-time image of the process,
but also has the ability to image the needle tip as it is guided into the
target lesion.
Dilatation of duct strictures

The high viscosity of the oil-based sialographic contrast media has encouraged
attempts to dilate minor duct strictures by hydrostatic pressure transmitted
via these agents. High pressure angioplasty balloon catheters may be used for
dilating stenosed ducts. Such balloons are advanced through the duct system
in their deflated state and are inflated once accurately positioned across the
stricture. A minimal papillotomy may be required for initial passage. The
balloons are accurately sized for maximal working dimension and can
therefore be used with negligible risk of duct rupture (Table 31.7).
Table 31.7
Imaging modalities and their uses
R/O, Rule out.
Use of saliva as a diagnostic fluid
1. Changes in salivary composition and flow rate in salivary gland

disease.
▪ Sialadenitis: Sodium and chloride secretion increased

▪ Sjogren’s syndrome: Increased sodium and chloride concentration and
decreased phosphate concentration. IgA is increased. Rate of salivary
flow is reduced. In addition, there are changes in the relative
concentrations of some minor salivary proteins
▪ Cirrhosis of liver: Calcium, potassium, protein and amylase
concentrations are increased. Rate of flow of saliva is also increased
▪ Xerostomia: Flow rate decreased
▪ Sialorrhoea: Flow rate increased
2. The relationship of saliva flow rate and composition to oral disease

▪ There is no association between salivary ionic composition with dental
caries or periodontal disease.
▪ Salivary IgA concentration is higher in subjects with more dental caries.
3. Salivary changes in systemic disease
▪ Generalised immunological reactions as seen in transplant rejection,

which may affect major salivary glands, reducing the rate of secretion
and raising sodium and chloride concentrations.
▪ Cystic fibrosis causes decreased secretion from submandibular,
sublingual and minor salivary glands with marked increase in salivary
calcium from these glands.
▪ Aldosterone increases reabsorption of sodium in the striated ducts,
reducing the salivary sodium concentrations and may increase
potassium levels. The sodium–potassium ratio in saliva can therefore
indicate normal, excess or deficient aldosterone secretion.
▪ Calcium and phosphate concentrations in saliva are thought to be
raised in hyperparathyroidism.
Biopsy
• Biopsy of salivary glands is mainly used to aid in the diagnosis of

Sjogren’s syndrome, sarcoidosis and benign lymphoepithelial lesion.
• The most promoted biopsy technique is the extraoral incisional parotid
biopsy. It is uncommon for facial nerve damage, salivary fistula,
excessive bleeding or difficulty in identifying the parotid gland to
occur.
• Submandibular gland biopsy is also done through an extraoral
approach; mostly an excisional biopsy.
• Fine-needle aspiration biopsy (FNAB) is widely recognised as a practical
and useful technique in the diagnosis of masses of the head and neck.
It has a high accuracy rate in the diagnosis of lesions of the salivary
glands. It is also a valuable adjunct to physical examination of patients
with masses in the salivary glands. A palpable enlargement or tumour
may be accessible to FNAB for cytology.
• Fine-needle aspiration cytology (FNAC) results in accurate diagnosis in
90%–100% of mixed tumours and Warthin’s tumour, the most
common salivary gland tumour.

Salivary gland diseases are classified as depicted in Table 31.8; Box 31.1.
Table 31.8
Infectious and noninfectious salivary gland diseases

Infectious Noninfectious
• Virus—Mumps, coxsackie A, parainfluenza and cytomegalovirus Sjogren’s
• Bacterial—Staphylococcus aureus, streptococcus pyogens, streptococcus syndrome
viridans, pneumococcus, actinomycetes, etc. Sarcoidosis
• Surgical mumps Radiation
• Medication causing xerostomia therapy
Allergens
Box 31.1 Classification of salivary gland diseases.

Developmental disorders
• Aberrancy
• Aplasia and Hypoplasia
• Hyperplasia
• Atresia
• Accessory ducts
• Diverticuli
• Congenital fistula
Functional disorders
• Sialorrhoea
• Xerostomia
• Sialolithiasis
• Mucous plug
• Stricture and stenosis
• Foreign bodies
• Extra-ductal causes
Cyst
• Mucocele (Mucous extravasation/mucous retention cyst

• Ranula
Infectious and systemic diseases
• Bacterial sialadenitis
Tuberculosis
Cat scratch disease
• Viral sialadenitis
AIDS-associated adenitis
Cytomegalovirus
Mumps
• Radiation sialadenitis
• Electrolyte sialadenitis
• Chronic sclerosing sialadenitis (Kuttner tumour)
• Immune sialadenitis
• Miscellaneous
Sarcoidosis
Cystic fibrosis
Sialadenosis
• Hormonal sialadenosis
• Neurohumoral sialadenosis
• Dysenzymatic sialadenosis
• Malnutritional sialadenosis
• Mucoviscidosis
• Drug induced sialadenosis
Idiopathic diseases
• Necrotising sialometaplasia
• Angiolymphoid hyperplasia with eosinophilla and kimura disease
• Cheilitis glandularis
Autoimmune diseases
• Uveoparotid fever
• Benign lymphoepithelial lesion/Mikulicz’s disease
• Sjogren’s syndrome
• Recurrent non-specific parotitis
Miscellaneous
• Allergic sialadenitis
Developmental diseases
Developmental
• Aplasia/Hypoplasia
• Agenesis
• Atresia of duct and congenital strictures
• Aberrancy
• Accessory ducts and lobes
• Haemangiomas
• Polycystic disease of parotid glands
• Heterotrophic salivary glands
• Adenomatoid hyperplasia of mucous glands
• Oncocytosis
• Mucous extravasation phenomenon mucocele

• Mucous retention phenomenon ranula
• Sialolithiasis
Strictures
Infectious and systemic diseases
• Bacterial sialadenitis
Tuberculosis
Cat scratch disease
Syphillis
Recurrent subacute chronic sialadenitis of childhood
• Viral sialadenitis
AIDS-associated sialadenitis
Cytomegalovirus
Mumps
• Radiation sialadenitis
• Electrolyte sialadenitis
• Chronic sclerosing sialadenitis (Kuttner tumour)
Sialadenitis
Benign
• Warthin’s tumour
Sialorrhoea
Sialorrhoea or excessive salivation, is an uncommon condition and has
various causes.
Causes
• Aphthous ulcers or ill-fitting dentures.

• Individuals with gastroesophageal reflux disease (GERD) have
episodic hypersecretion of saliva, or ‘water brash’, as a protective
buffering system to neutralise stomach acid.
• It is a well-known clinical feature of rabies and heavy-metal poisoning.
• Medications used to treat dementia such as antipsychotic agents and
cholinergic agonists in Alzheimer’s type and myasthenia gravis.
• Neurological diseases such as cerebral palsy, Parkinson’s disease, or
amyotrophic lateral sclerosis (ALS) result in drooling due to poor
neuromuscular control.
• Mentally challenged patients and patients who have undergone
surgical resection of the mandible.
Clinical features
• Excessive saliva production produces drooling and choking, causing

social embarrassment.
• In children with mental retardation or cerebral palsy, the uncontrolled
salivary flow may lead to macerated sores around the mouth, chin,
and neck that can become secondarily infected.
• Constant soiling of bed linens and clothes can pose a significant
problem for the parents and caretakers of these patients.
• An interesting type of supersalivation of unknown aetiology has been
termed Idiopathic paroxysmal sialorrhoea is a condition where an
individual experiences short episodes of excessive salivation lasting
from 2 to 5 min and are associated with a prodrome of nausea or
epigastric pain.
• Some causes of sialorrhoea are transitory or mild, and no treatment is

needed.
• For GERD patients, medical management for their reflux can be
beneficial.
• Anticholinergic medications decrease saliva production but also
produce unacceptable side effects.
• Transdermal scopolamine has been tried with some success, but it
should not be used in children younger than age 10. Intraglandular
botulinum toxin injection has shown to be successful in reducing
salivary secretions, with duration of action that varies from 6 weeks to
6 months.
• Several surgical techniques have also been used successfully to control
severe drooling in individuals with poor neuromuscular control such
as:
▪ Relocation of the submandibular ducts (the ducts are
repositioned posteriorly to the tonsillar fossa, thereby
redirecting salivary flow and minimising drooling).
▪ Relocation of the parotid ducts.
▪ Submandibular gland excision plus parotid duct ligation.
▪ Ligation of the parotid and submandibular ducts.
▪ Bilateral tympanic neurectomy with sectioning of the chorda
tympani.
Xerostomia
Xerostomia refers to dry mouth and it is frequent, but not always, associated
with salivary gland hypofunction.
Causes
Box 31.2
Box 31.2 Causes of Xerostomia.
Local factors
Decreased mastication
Smoking
Mouth breathing
Developmental origin
Salivary gland aplasia
Iatrogenic origin
Medications
Radiation therapy to the head and neck
Chemotherapy
Water metabolite loss
Impaired fluid intake

Haemorrhage
Vomiting/diarrhoea
Systemic diseases
Sjogren syndrome
Diabetes mellitus
Diabetes insipidus
Sarcoidosis
Human immunodeficiency virus (HIV) infection
Hepatitis C infection
Graft versus host disease (GVHD)
Psychogenic disorders
Clinical features
• Reduction in salivary secretions, and the residual saliva appears either

foamy or thick and ‘ropey’.
• Patient complains of difficulty in mastication and swallowing.
• Dental caries seen especially at the cervical region and tooth roots.
• Mucosa appears dry.
• Often the tongue appears to be fissured along with atrophy of the
filiform papillae.
• The clinician may encounter examining gloves sticking to the mucosal
surfaces.
• Due to the reduction in the salivary flow, the cleansing and
antimicrobial activities are compromised resulting in oral candidiasis.
• Maintenance of good oral hygiene and use of oral hygiene products

that contain lactoperoxidase, lysozyme, and lactoferrin is advised.
• Artificial saliva is available and aids in the patient comfort, as may
continuous sips of water throughout the day.
• Sugarless candy can be used to stimulate salivary flow.
• Discontinuation or dose modification can be done if the dryness is
secondary to the patient’s medication.
• Systemic pilocarpine a parasympathomimetic agonist can be used as a
sialagogue at doses of 5–10 mg, 3–4 times daily, it can be an effective
promoter of salivary secretion.
• Frequent dental visits are recommended due to the increased
susceptibility to dental caries.
• Fluoride applications can be used to help prevent decay, and
chlorhexidine mouth rinses minimise plaque build-up.
Sialolithiasis (salivary calculi; salivary stones)

Sialolithiasis is the formation of salivary calculi/stone (Sialolith) in the salivary
gland or duct resulting in the mechanical obstruction of the salivary flow.
Sialolith
Sialoliths are calcified structures that develop within the ductal system of a
major or minor salivary gland. They usually formed around the central nidus
with layers of the inorganic material. It forms initially as the organic nidus
which gradually increases in size progressively by deposition of layers of
inorganic and organic substances. The rate of formation is about 1 mm/year.
They are yellowish white in colour, single or multiple, round, ovoid or
elongated, measuring about 1–10 mm.
Composition:
• Inorganic salts of calcium and phosphate like hydroxyapatite,

octacalcium phosphate.
• Organic nidus like desquamated epithelial cells, bacteria, bacterial
decomposition, glycoprotein, mucopolysaccharides, etc.
• Foreign bodies like tooth brush bristles, finger nails, wood splinters,
hair, blade of grass, fish bones.
Sialolithiasis is both a cause and a consequence of chronic recurring

sialadenitis and it is frequently a cause of acute suppurative sialadenitis
(Fig. 31.17).
FIGURE 31.17 Occlusal radiograph of the mandible showing a

radiopaque mass in the floor of the mouth on the right side
denoting a submandibular gland calculus.
Aetiology
The exact cause of sialolith formation is not known but three prerequisites
stand out as primary etiologic factors:
i. A neurohumoral condition, leading to salivary stagnation

ii. A nidus or matrix for stone formation
iii. A metabolic mechanism favouring precipitation of salivary salts into
the matrix in the presence of coexisting inflammation
Risk factors:
• Dehydration—increase in viscosity and concentration of saliva
• Anorexia/Fasting—decreases the demand for the saliva
• Drugs and medications—antihistamines, antipsychotics,
antidepressants, antihypertensives, anticholinergics, diuretics, etc.
• Irradiation/Radiotherapy
• Tobacco smoking
• Sjogren’s syndrome
• Hypercalcemia
• Gout (uric acid accumulation)
Increased incidence for formation of sialoliths in the submandibular gland is

due to the following factors:
• The pH of saliva from submandibular gland is about 6.8–7.1 (alkaline),

as opposed to the more acidic product of parotid gland (6.3–7.4).
• In addition, submandibular gland contains a greater concentration of
calcium and phosphate salts, in the form of apatites mainly.
• The relative alkalinity, in conjunction with alteration in the salivary
calcium–phosphorus ratio, causes the salivary apatite to exceed its
solubility product, resulting in precipitation of these salts.
• The mucous content of the submandibular gland and its secretions
may become more viscous than those of the parotid gland.
• The duct of the submandibular gland is longer, tortuous and situated
at a lower level than its orifice (nondependent) leading to increased
salivary stagnation in the duct, which can lead to increased calculus
formation.
Clinical features
• Sialolithiasis occurs in men twice as often as in women. There is a peak

incidence between 30 and 50 years of age and submandibular gland is
the most common site of involvement accounting to 80%.
Signs and symptoms

Clinical presentation of sialolithiasis varies. On occasion, there may be a total
absence of subjective symptoms, in such cases the sialoliths are identified by
accidentally during radiographic examination. In other cases,
• Meal time syndrome:

Patients complain of moderate to severe pain associated with swelling
during and after eating the food (especially the production of saliva is
at peak). The swelling may be diffuse and sometimes resembles
cellulitis. Gradual reduction of pain and swelling is noted during the
rest period. History of recurrent swelling is seen when the flow is
stimulated and is continued till there is complete obstruction. Pain is
mainly due to increased pressure in the duct due to obstruction.
• Occasionally patients report spontaneous extrusion of small calculi
from the ducts.
• The most common finding on examination is point tenderness in the
region of the hilum or, near Wharton’s duct of the submandibular
gland.
• Fever occurs due to secondary infection associated with tenseness,
tenderness, trismus, decreased or absent salivary flow.
• A gelatinous, cloudy, mucopurulent material is seen in basically clear
and adequate saliva. This mucopurulent material is derived from the
inflammatory ductal changes caused by calculus blockage and salivary
stagnation.
• If treatment is not instituted early, pronounced exacerbations are seen,
characterised by an acute suppurative process with attendant systemic
manifestations. Pus may exude from the duct orifice.
• The mucosa around the duct is inflamed, particularly in the floor of the
mouth where swelling, redness and tenderness are present along the
course of Wharton’s duct.
• The glands are enlarged, tender and tense. Palpation of the gland and
the duct causes pain and a flow of pus.
Diagnosis
Diagnosis is mainly done by careful bimanual palpation and digital
manipulation. Palpation in the floor of the mouth along the duct may reveal
the presence of stone if it is present in the duct. Inability to milk saliva from
duct orifice confirms the presence of calculi/obstruction in the path of salivary
flow.
Radiograph
Occlusal radiograph, lateral view, lateral oblique mandibular view, AP views
(intraoral and extraoral)
Sialography plays an important role in identifying the location of calculus.
USG is an inexpensive and noninvasive method, used to detect stones more
than 2 mm.
CT—to detect the gland enlargement especially in chronic cases.
Scintigraphy and MRI
Complications
• Acute and chronic suppurative sialadenitis due to bacterial infection of
the gland
• Sialoangiectasis (dilatation of salivary duct) due to salivary stasis by
sialolith, stricture, chronic infection
• Mucocele—due to salivary retention phenomenon
• Atrophy of gland due to complete obstruction of the duct
Treatment
• Conservative treatment with local heat, massage and sialogogues.

• Enhanced use of sialogogues, sour food intake, salivary gland massage,
hyperhydration for facilitating spontaneous removal of stone
• If the stones are located within the duct intraoral approach is indicated
(Fig. 31.18).
• If the stone is present within the gland and if there are irreversible
ductal and glandular changes within the gland, removal of involved
gland through an extraoral approach is indicated.
• In the acute phase, standard care includes antibiotic, analgesic and
good oral hygiene.
• Surgical intervention for drainage of pus is sometimes necessary. Once
the acute stage subsides, definitive surgical treatment can be
instituted.
FIGURE 31.18 (A) Submandibular salivary gland calculus present

at the entrance of the duct. (B) Calculus removed.
Sialodochoplasty
• Sialodochoplasty refers to salivary duct repair by widening the orifice

and shortening of the salivary duct.
• It is usually performed during sialolithotomy to prevent re-stenosis or
re-narrowing of the ductal system.
• The duct may simply be stitched open, or may require a stent to be left
in place for 7–10 days in order to heal properly (Fig. 31.19).
FIGURE 31.19 Sialodochoplasty procedure. (A) Cannulation of the

ductal orifice. (B) Incision of the oral mucosa and the
submandibular duct epithelium. (C) The duct epithelium is now
sutured to the oral mucosa and the cannula left within the duct for
7–10 days to keep the duct patent.
Removal of parotid gland calculi

Parotid gland duct is the location of 6%–10% of salivary calculi. The calculi
may be located at four basic sites:
• Impacted at the papilla

• In the submucous part of the duct
• In the extraglandular part of the duct external to buccinators muscle
• In the intraglandular part of the duct
The technique of removal depends on the site of location of calculi.
1. Papilla and submucous part of the duct

▪ Calculi in this region can be released by slitting of the papilla.
▪ Using a sharp scissors, a short cut is made in the anterior
portion of the way into the duct, from the orifice.
▪ If the calculus is not dislodged, as soon as the scissors
removed, gentle pressure of the gland will force a quantity of
saliva along the duct, washing out the calculus.
2. Extraglandular part of duct external to buccinator muscle
Calculi in this part of the duct can be removed through an incision in the
intraoral aspect of the check
▪ A traction suture is then placed just anterior to the papilla. A Y-
incision is made through the mucosa around the papilla with
the tail of the Y directed forwards.
▪ Blunt dissection is carried out to separate the mucosa and
submucosa from the buccinator muscle.
▪ The tip of the triangle containing the papilla and duct is freed
from the undersurface.
▪ The upper and lower flaps are mobilised and stay sutures are
placed to hold the flaps out of the way.
▪ Dissection is then carried out laterally into the cheek and
posterior to the point where Stensen’s duct pierces the
buccinator muscle and turns posteriorly. A suture is then
looped around the duct and is retracted medially into the
mouth.
▪ Once the site of calculus is located, an incision is made parallel
to the long axis of the duct and the stone is removed.
▪ The tissues around the duct are closed with absorbable sutures
leaving the incision in duct open.
3. Intraglandular portion of the duct
If the calculus is located posterior to the accessory portion of parotid
gland, it is generally in the intraglandular course of the parotid duct.
These calculi can be removed by an extraoral approach similar to the
one used for a parotidectomy (Fig. 31.20, 31.21).
FIGURE 31.20 Relationship of the facial nerve to the parotid gland.
Removal of submandibular gland calculi

The most frequent location of submandibular gland calculi is extraglandular.
They can be present in the anterior or posterior portions of submandibular
duct and also in the intraglandular portion of the duct.
1. Anterior portion of submandibular duct

▪ Anterior calculi are those that lie anterior to the mandibular
second molars. A suture is then passed into the floor of the
mouth around the duct, posterior to the stone to prevent its
posterior dislodgement.
▪ A suture is placed across the duct anterior and posterior to the
site of calculus.
▪ Traction on these two sutures will steady the tissue in the
surgical site by making it taut.
▪ An incision is now made along the line of the duct (along a line
that bisects the angle between the root of the tongue and the
sublingual plica) and over the stone.
▪ The duct is about 3–4 mm in diameter, pale greyish in colour
and identified by the network of fine capillaries that course its
surface.
▪ Once the duct is identified, it is mobilised and a suture is
passed under it so that it may be pulled anteriorly. The
calculus is identified; and a longitudinal incision is placed
over the duct and the sialolith released.
The incision in the duct is not sutured to prevent stricture formation. The
patient is encouraged to drink fluids and use lemon drops to encourage
salivary flow and maintain patency of the duct (Fig. 31.22).
2. Posterior portion of submandibular duct
▪ A lacrimal probe can be inserted into the ductal orifice and
through the anterior portion of the duct tracing the duct.
▪ An incision is then made in the mucosa opposite the premolar
teeth. The duct is traced posteriorly, identifying lingual nerve
as it crosses where it is retracted and protected.
▪ Pressure is placed against the lower pole of the gland to raise
the upper pole superiorly (since the submandibular duct
emerges from the upper and anterior part of the upper pole of
the submandibular gland) into the surgical field. The duct is
then incised parallel to the long axis of the duct and the
calculus removed.
▪ The mucosal tissues closed with interrupted sutures leaving
the incised duct open.
3. Intraglandular portion of submandibular duct
FIGURE 31.21 (A–C) Parotidectomy. (A) Gland is identified. (B,C)

Removal of parotid gland.
FIGURE 31.22 (A, B) A bulge on the right side of the floor of the
mouth indicating the presence of submandibular gland calculus.
(C) Occlusal radiograph of the same person showing an oblong
radiopacity of the calculus in the right side of the mandible. (D)
Excised calculus.
FIGURE 31.23 Removal of submandibular gland. (A) Incision

placed. (B) Submandibular gland exposed. (C) Gland excised. (D)
Wound sutured.
Presence of calculus in the intraglandular portion of the duct affecting the

functioning of the gland or infection is an indication for removal of the gland.
If the stone is small and the gland is asymptomatic and sialographically
normal, it can be left in place and observed for any change in position or
function of parenchyma of the gland. If it is symptomatic with abnormal
glandular structure, sialadenectomy is done (Fig. 31.23).
Cysts
Mucocele (mucous extravasation phenomenon, mucous escape
reaction)
Mucocele results from rupture of a salivary gland duct and subsequent
spillage of mucin into the surrounding soft tissues. This spillage is due to local
trauma in many cases. Mucoceles are not true cysts because they lack an
epithelial lining.
Clinical features
• Mucocele typically appears as dome-shaped mucosal swellings

ranging from one to several centimetres in size.
• They are most common in children and young adults. The spilled
mucin below the mucosal surface often imparts a bluish translucent
hue to the swelling; however deeper mucoceles may be normal in
colour.
• The lesion characteristically fluctuant, but some long-standing
mucoceles are firm on palpation (Fig. 31.24).
FIGURE 31.24 Picture showing mucocele in the region of the left

cheek.
Lower lip is the most common site for the mucoceles, accounting for more
than 60% of all the cases.
Mucoceles usually are found lateral to the midline. Less common sites
include the buccal mucosa, anterior, ventral surface of tongue and are known
as ranula when occurring in the floor of mouth.
On microscopic examination, mucocele shows an area of spilled mucin
surrounded by granulation tissue response.

Some mucoceles are short-lived lesions that rupture and heal by themselves.
Many lesions, however, are chronic in nature and local surgical excisions are
necessary.
To minimise the risk of recurrence, when the area is excised, adjacent minor
salivary glands should be removed as it may be the source of the lesion. The
excised tissue should be submitted for microscopic examination to confirm the
diagnosis and rule out the possibility of a salivary gland tumour. The
prognosis is excellent, although occasional mucoceles will recur; prompting re-
excision, especially if the other surrounding minor glands are not removed
(Fig. 31.25).
Ranula
‘Ranula’ is a term used for retention cysts of salivary gland origin occurring in
the floor of the mouth. The name is derived from the Latin word rana, which
means frog, because of the resemblance of the bulging cyst wall to a frog’s
translucent underbelly.
Formation of ranula occurs by two mechanisms:
1. Partial obstruction of the distal end of the duct with dilation resulting is
an epithelial lined cyst (mucous retention cyst)
2. Disruption of the duct with formation of a connective tissue line space
(mucous extravasation or pseudocyst). The source of the cystic fluid is
believed to be the sublingual glands in the most common form of
ranula.
Clinical features
Two varieties of cysts are seen (simple ranula and plunging ranula) that have
different clinical behaviour, appearance and they require different methods of
treatment.
• Simple ranulas are true retention cysts.

• An unusual clinical variant, the plunging or cervical ranula is a cyst
that occurs beyond the mucous membranes of the oral cavity into the
floor of the mouth, through a hiatus of the mylohyoid muscle and into
the fascial planes of the neck. This occurs when the spilled mucin
dissects through the mylohyoid muscle and produces swelling within
the neck.
• Ranula appears as a blue, dome-shaped translucent fluctuant swelling
in the floor of the mouth.
• They are usually painless and unilateral with increasing size.
• They can cause deviation of the tongue.
• They can cross the midline submucosally, at times.
• They may rupture spontaneously with extrusion of a thick, translucent
fluid into the mouth. The wall then rapidly heals and the cyst
subsequently reforms (Fig. 31.26).
FIGURE 31.25 (A, B) Surgical removal of a mucocele.

FIGURE 31.26 Simple ranula.
Treatment
Ranulas do not regress spontaneously and require definitive surgical therapy.
Marsupialisation is the treatment of choice.
It involves excision of the superior wall of the lesion and suturing of the
inner wall to the mucosa of the floor of the mouth. If recurrence is seen,
excision in continuity with the alkaline sublingual gland of origin is done
(Fig. 31.27).
FIGURE 31.27 Total excision of Ranula. (A) Excision of the entire
mucus-filled capsule and the sublingual gland of origin. (B) Noted
here are the preserved branches of the lingual nerve posterior to
the ranula (single arrow) and the submandibular duct (double
arrows).
Infections and systemic diseases

Sialadenitis
Sialadenitis is the inflammation of the salivary glands that can arise from
various infectious and noninfectious causes.
Causes
• The most common viral infection is mumps, although a number of

other viruses also can affect the salivary glands, including coxsackie A,
parainfluenza and cytomegalovirus (in neonates).
• Most bacterial infections arise as a result of ductal obstruction or
decreased salivary flow, allowing retrograde spread of bacteria
throughout the ductal system. Blockage of the duct can be caused by
sialolithiasis, congenital strictures or compression by an adjacent
tumour. Decreased flow can result from dehydration, debilitation or
medications that inhibit secretions.
• One of the most common causes of sialadenitis is recent surgery after
which an acute parotitis (surgical mumps) may arise.
• Medications that produce xerostomia as a side effect also can
predispose patients to such an infection.
• Most cases of acute bacterial sialadenitis are due to Staphylococcus
aureus, but they also may arise from Streptococci or other organisms.
• Noninfectious causes of salivary inflammation include Sjogren’s
syndrome, sarcoidosis, radiation therapy and numerous allergens.
Acute bacterial sialadenitis
Clinical features
• Acute bacterial sialadenitis is most common in the parotid gland and is

bilateral in 10%–25% of cases.
• The affected gland is swollen and painful and the overlying skin may
be erythematous in colour. An associated low grade fever may be
present along with trismus. A purulent discharge is often observed
from the duct orifice when the gland is massaged.
• Recurrent or persistent ductal obstruction most commonly caused by
sialoliths can lead to a chronic sialadenitis. Periodic swelling and pain
occur within the affected gland, usually developing at meal time when
salivary flow is stimulated. Sialography often demonstrates sialectasis
(ductal dilatation) proximal to the area of obstruction.
• Subacute necrotising sialadenitis is a form of salivary inflammation
that occurs most commonly in young adults. The lesion usually
involves the minor salivary glands of palate, presenting as a painful
nodule that is covered by intact, erythematous mucosa. Unlike
necrotising sialometaplasia, the lesion does not ulcerate.
In patients with acute sialadenitis, accumulation of neutrophils is observed
with the ductal system and acini. Chronic sialadenitis is characterised by
scattered or patchy infiltration of the salivary parenchyma by lymphocytes
and plasma cells.

Initial treatment of acute sialadenitis includes
• Appropriate antibiotic therapy

• Rehydration of the patient to stimulate salivary flow
• Surgical drainage may be needed if there is abscess formation
Although this regimen is usually sufficient, high mortality rate has been
reported in debilitated patients because of the spread of the infection and
sepsis.
Surgical management of chronic sialadenitis depends on the severity and
duration of the condition. Early cases that develop secondary to ductal
blockage may respond to removal of the sialoliths or other obstruction.
If sialectasia is present, dilated ducts can lead to stasis of secretions and
predispose the gland to further sialolith formation. Surgical removal of the
affected gland may be necessary, in case of extensive inflammatory destruction
of the salivary tissue.
Subacute necrotising sialadenitis is a self-limiting condition that usually
resolves within 2 weeks of diagnosis without treatment.
Mumps
Mumps sialadenitis is the most common of all salivary gland diseases. It is a
nonsuppurative, acute sialadenitis of viral origin. It is a contagious,
generalised disease that presents as a painful enlargement of the salivary
glands.
• The virus mumps causes an acute febrile illness with a prodromal

period of 2–3 weeks.
• Mumps primarily infects young adults and children, classically 6–
8 years of age. Mumps virus has an incubation period of 2–3 weeks
and is transmitted by direct contact or in droplets of saliva.
• The onset is sudden with fever, headache and painful swelling of the
parotids. Usually one gland is infected first and then the other, in 70%
of cases there is bilateral involvement.
• Painful swelling occurs rapidly, reaches a maximum size within 1–
3 days.
• Trismus may be present, with some difficulty in chewing.
• Stensen’s duct orifice is swollen and erythematous, but there is no
purulent material in the saliva. The symptoms subside in 3–7 days.
• Orchitis (testicular swelling).
• Oophoritis (Inflammation of ovary).
• Rash.
• Chipmunk cheeks.
Diagnosis
Diagnosis is usually made on a clinical basis during epidemics. Serum
antibodies to the mumps S and V antigens with a titre of greater than 1:192
indicate recent infection. The viruses usually affect the epithelium, although
the first changes on histologic study are perivascular oedema and white blood
cell infiltrates. A diffuse infiltration of the glandular parenchyma by
mononuclear cells with acinar degeneration is observed.
Complications
The most important complication of mumps includes parotid gland sialectasia
with recurrent chronic and even acute suppuration. Complications of mumps
result from generalised viraemia and include pancreatitis (diabetes secondary
to pancreatic fibrosis) orchitis (sterility secondary to gonadal involvement),
oophoritis, myocarditis, aseptic meningitis, nephritis, sensory neural hearing
loss (frequently unilateral).
The condition resolves spontaneously in 5–10 days. Symptomatic relief of
pain and fever is necessary and prevention of dehydration is essential.
Sialadenosis
Sialadenosis is an unusual noninflammatory, non-neoplastic disorder
characterised by salivary gland enlargement, particularly involving the
parotid glands.
Clinical features
Sialadenosis usually appears as a slowly growing swelling of the parotid
glands, which may or may not be painful. The condition is usually bilateral,
but it also can be unilateral. In some patients, submandibular glands can be
involved. Decreased salivary secretion may occur. Sialography demonstrates a
‘leafless tree’ pattern, which is thought to be caused by compression of the finer
ducts by hypertrophic acinar cells.
Conditions associated with sialadenosis
A. Endocrine
▪ Diabetes mellitus
▪ Diabetes insipidus
▪ Acromegaly
▪ Hypothyroidism
▪ Pregnancy
B. Nutritional
▪ General malnutrition
▪ Alcoholism
▪ Anorexia nervosa
▪ Bulimia
C. Neurogenic medications
▪ Antihypertensive drugs
▪ Psychotropic drugs
▪ Sympathomimetic drugs used for treating asthma
Microscopic examination reveals hypertrophy of the acinar cells, sometimes 2–
3 times greater than normal size.

Clinical management of sialadenosis is often unsatisfactory because it is
closely related to the control of the underlying cause. Pilocarpine recently has
been reported to the beneficial in the treatment of bulimic patients with
sialadenosis.
Idiopathic diseases
Necrotising sialometaplasia is an uncommon, locally destructive inflammatory
condition of the salivary glands. Although the cause is uncertain, most authors
believe it is the result of ischaemia of the salivary tissue that leads to local
infarction. The importance of this lesion rests in the fact that it mimicks a
malignant process, both clinically and histopathologically.
A number of potential predisposing factors have been suggested, including
the following:
• Traumatic injuries
• Intraoral injections
• Ill-fitting dentures
• Upper respiratory infections
• Adjacent tumours
• Previous tumours
It has been suggested that these factors may play a role in compromising the
blood supply to the involved glands, resulting in ischaemic necrosis. However,
many cases occur without any known predisposing factors.
Clinical features
• Necrotising sialometaplasia most frequently develops in the palatal

minor salivary glands.
• Hard palate is affected more often than the soft palate. About two-
thirds of palatal cases are unilateral, with the rest being bilateral or
midline in location.
• Necrotising sialometaplasia also has been reported in other minor
salivary gland sites and occasionally, in the parotid gland.
• The submandibular and sublingual glands are rarely affected.
• Although it can occur at almost any age, necrotising sialometaplasia is
most common in adults; the mean age of onset is 46 years. Males are
affected nearly twice as often as females.
• The condition appears initially as a non-ulcerated swelling often
associated with pain or paraesthesia with crater-like ulcer that can
range from less than 1 cm to more than 5 cm in diameter appearing
within 2–3 weeks.
• Microscopic appearance of necrotising sialometaplasia is characterised

by acinar necrosis in early lesions, followed by associated squamous
metaplasia of the salivary ducts.
• Although, mucous acinar cells are necrotic, the overall lobular
architecture of the involved glands is still maintained. There may be
liberation of mucin, with an associated inflammatory response.
• The squamous metaplasia of the salivary ducts can be striking and
produce a pattern that is easily misdiagnosed as squamous cell
carcinoma.
Treatment
The lesion is self-limiting in most instances and heals uneventfully.
Autoimmune diseases
Benign lymphoepithelial lesion
In the late 1800s, Johann von Mikulicz-Radecki described a patient with an
unusual bilateral painless swelling of the lacrimal glands and all the salivary
glands. Histopathologic examination of the involved glands showed an
intense lymphocytic infiltrate, with features that are today recognised
microscopically as the benign lymphoepithelial lesion. The clinical
presentation came to be known as Mikulicz disease.
Clinical features
Most benign lymphoepithelial lesions develop as a component of Sjogren’s
syndrome. Those not associated with Sjogren’s syndrome are usually
unilateral, although occasional bilateral examples are seen. Benign
lymphoepithelial lesion most often develops in adults, with a mean age of
50 years.
Microscopic examination of the benign lymphoepithelial lesions shows a
heavy lymphocytic infiltrate associated with destruction of the salivary acini
with epimyoepithelial islands.
Sjögren’s syndrome
Sjogren’s syndrome is a chronic, systemic autoimmune disorder that
principally involves the salivary and lacrimal glands, resulting in xerostomia
and xerophthalmia.
Two forms of the disease are recognised:
1. Primary Sjogren’s syndrome (Sicca syndrome alone; no other

autoimmune disorder is present)
2. Secondary Sjogren’s syndrome (the patient manifests Sicca syndrome in
addition to another associated autoimmune disease).
The cause of Sjogren’s syndrome is unknown.

Although it is not a hereditary disease, there is evidence of a genetic
influence. It has also been suggested that viruses, such as Epstein-Barr virus
(EBV) or Human. T cell lymphotrophic virus may play a pathogenetic role in
Sjogren’s syndrome, but evidence for this is still speculative.
Patient with Sjögren syndrome have an increased risk for lymphoma, higher
than the normal population. These tumours may arise initially within the
salivary glands or within lymph nodes. With advent of modern molecular
pathology techniques, early detection is possible.
B-cell monoclonality (e.g. in situ hybridisation, polymerase chain reaction
(PCR). Many salivary gland infiltrates formerly thought to represent benign
lymphoepithelial lesions are now being diagnosed as lymphomas.
These tumours are predominantly low grade non-Hodgkin’s B cell
lymphomas of the mucosa-associated lymphoid tissue (MALT lymphomas).
Clinical features
• Predominantly women above 40 years of age are affected. However, it

may occur in men and young adults.
• Parotid gland is more frequently involved.
• Typical features of the disease are the dryness of the mouth and eyes,
(xerostomia & xerophthalmia) which often results in painful and
burning sensation.
• Apart from this, various secretory glands of nose, larynx, pharynx and
vagina are involved with this dryness.
Laboratory findings
• In patients with Sjogren’s syndrome, the erythrocyte sedimentation
rate (ESR) is high and serum immunoglobulin levels, especially
diagnostic; their presence can be helpful to the diagnosis.
• A positive rheumatoid factor (RF) is found in 75% of cases, regardless
of whether the patient has rheumatoid arthritis. Antinuclear
antibodies (ANA) may also be positive in most patients. Two
particular nuclear autoantibodies: anti–SS A (anti-Ro) and anti–SS B
(anti-La), frequently are found, especially in patients with primary
Sjogren’s syndrome (Box 31.3).
• Immunoflorescence: Speckled pattern due to anti-Ro & anti-La
Box 31.3 Criteria for Sjogren’s syndrome.
1. Ocular symptoms (at least one of the following)

• Use of a tear substitute more than 3 times daily
• Persistent, troublesome dry eyes for longer than 3 months
• Recurrent sensation of sand or gravel in the eye
2. Ocular signs (at least one of the following)
• Positive Rose-Bengal stain
• Positive Schirmer test
3. Oral symptoms (at least one of the following)
• Feeling of dry mouth every day for at least 3 months
• Need to drink liquids in order to swallow dry food
• Recurrent feeling of swollen salivary glands as an adult
4. Oral signs (at least one of the following)
• Parotid sialography
• Salivary gland scintigraphy
• Unstimulated whole saliva (Less than 1.5 mL/15 min)
5. Histopathology: Focal lymphocytic sialadenitis of major or minor
salivary gland
6. Laboratory abnormalities (at least one of the following)
• ANA (Anti-nuclear antibody)
• IgM rheumatoid factor (anti-IgG Fc)
• Anti-ss-A or anti-ss-B
Basic microscopic finding in Sjogren’s syndrome is a lymphocytic infiltration
of the salivary glands, with destruction of the acinar units. If the major glands
are enlarged, microscopic examination usually shows progression to a
lymphoepithelial lesion.
Treatment of the patient with Sjogren’s syndrome is mostly supportive.
• The dry eyes are best managed by periodic use of artificial tears with a
slowly dissolving methylcellulose preparation, such as Lacrisert
(Merck) or Restasis (Allergan), on a daily basis.
• In addition, attempts can be made to conserve the tear film through the
use of sealed glasses to prevent evaporation.
• The eyes also often require topical antibiotics such as sulphacetamide or
ophthalmologic gentamycin.
• Sealing the lacrimal punctum pack in the inner margin of the eyelids
also can be helpful by blocking of the normal drainage of any lacrimal
secretions into the nose.
• Artificial saliva is available for the treatment of xerostomia: sugarless
candy or gum can help to keep the mouth moist.
• Symptoms often can be relieved by the use of oral hygiene products
that contain lactoperoxidase, lysozyme and lactoferrin. Sialagogues
such as pilocarpine and cevimeline can be useful to stimulate salivary
flow if enough functional salivary tissue still remains.
• Because of the increased risk of dental caries, daily fluoride
applications may be indicated in dentulous patients.
• Antifungal therapy often is needed to treat secondary candidiasis.

Box 31.4
Box 31.4 WHO histologic classification of tumours of

the salivary glands, 2005.
Benign epithelial tumours
Pleomorphic adenoma
Myoepithelioma
Basal cell adenoma
Warthin’s tumour
Oncocytoma
Canalicular adenoma
Sebaceous adenoma
Lymphadenoma
Sebaceous
Nonsebaceous
Ductal papillomas
Inverted ductal
Papilloma
Intraductal papilloma
Sialadenoma
Papilliterum
Cystadenoma
Malignant epithelial tumours
Acinic cell carcinoma

Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Polymorphous low-grade adenocarcinoma
Epithelial-myoepithellial carcinoma
Clear cell carcinoma, not otherwise specified
Basal cell adenocarcinoma
Sebaceous lymphadenocarcinoma
Cystadenocarcinoma
LGCCC
Mucinous adenocarcinoma
Oncocytic carcinoma
Salivary duct carcinoma
Carcinoma ex pleomorphic adenoma
Carcinosarcoma
Metastasising pleomorphic adenoma
Small cell carcinoma
Large cell carcinoma
Lymphoepithelial carcinoma
Sialoblastoma
Soft tissue tumours
Haemangioma
Haematolymphoid tumours
Haematolymphoid tumours
Hodgkin’s lymphoma
Diffuse large B-cell
Lymphoma
Extranodal marginal zone-B cell lymphoma
Secondary tumours
Abbreviation: LGCCC, Low-grade cribriform cystadenocarcinomas.
Aetiology
Viruses
• Epstein-Barr virus
• Polyoma virus
• Cytomegalo virus
• Human papilloma virus type 16 and 18
Radiation
• Substantial evidence exists for the relation of radiation exposure and

development of salivary gland tumours.
• Studies have shown relative risk for benign and malignant salivary
gland tumours increased in the Japanese population after atomic bomb
explosion in Hiroshima and Nagasaki, two cities of Japan.
• Therapeutic radiation doses in the head and neck region increase the
risk of development of salivary gland tumours. A dose of 140 rad of
dose is enough to increase the risk.
• Diagnostic dental radiograph could also play a role in tumour
initiation.
Occupations
• Asbestos mining
• Shoe manufacturing
• Manufacturing of rubber products
• Wood working
• Automobile industry
Hormones
• Endogenous hormones may play role in salivary gland tumours

• One study showed that 80% of normal salivary gland samples positive
for oestrogen receptors
• Same study also found that increased levels of these oestrogen
receptors in salivary gland tumours
The staging of the salivary gland tumours is different from that of the other
head and neck tumours (Box 31.5).
Box 31.5 TNM classification (AJCC).

Primary tumour (T)
• TX—Primary tumour cannot be assessed

• T0—No evidence of primary tumour
• T1—Tumour 2 cm or less in greatest dimension without
extraparenchymal extension
• T2—Tumour more than 2 cm but not more than 4 cm in greatest
dimension without extraparenchymal extension
• T3—Tumour having extraparenchymal extension without seventh nerve
involvement and/or more than 4 cm but not more than 6 cm in greatest
dimension TNM classification (AJCC)
• T4a—Tumour invades skin, ear canal, mandible and/or facial nerve
• T4b—Tumour invades skull base and/or, pterygoid plates and/or encases
carotid artery
Regional lymph nodes (N)
• NX—Regional lymph nodes cannot be assessed N0—No regional lymph

node metastasis
• N1—Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest
dimension
• N2—Metastasis in a single ipsilateral lymph node, more than 3 cm but not
more than 6 cm in greatest dimension or in bilateral or contralateral
lymph nodes, none more than 6 cm in greatest dimension
• N2a—Metastasis in a single ipsilateral lymph node, more than 3 cm but
not more than 6 cm in greatest dimension
• N2b—Metastasis in multiple ipsilateral lymph nodes, not more than 6 cm
in greatest dimension
• N2c—Metastasis in bilateral or contralateral lymph nodes, not more than
6 cm in greatest dimension
• N3—Metastasis in a lymph node more than 6 cm in greatest dimension
Distant metastases (M)
• MX—Distant metastasis cannot be assessed

• M0—No distant metastasis
• M1—Distant metastasis
AJCC stage grouping
• Stage I—T1 N0 M0
• Stage II—T2 N0 M0
• Stage III— T3 N0 M0, T1, 2, 3 N1 M0
• Stage IVA—T1,2,3 N2 M0
T4a N1,2 M0
• Stage IVB—T4b Any N M0
Any T N3 M0
• Stage IVC—Any T Any N M1
AJCC—American Joint Committee on Cancer
Treatment
The treatment options for salivary gland tumours ranges from transoral minor
salivary gland tumour excision surgery to total excision of the major salivary
glands based on the type and severity of the disease and the involvement of
the adjacent structures as follows.
• Transoral minor salivary gland tumour surgery

▪ Soft tissue palatal excision
▪ Soft tissue excision of salivary gland tumours in the oral
mucosa
▪ Palatectomy
• Maxillectomies
▪ Hemi maxillectomy
▪ Total maxillectomy
• Parotid gland surgeries
▪ FNAC for diagnostic cytology
▪ Incisional parotid biopsy
▪ Superficial parotidectomy
▪ Total parotidectomy with nerve preservation
▪ Total parotidectomy with nerve transection and nerve grafting
▪ Excision of the deep lobe of the parotid gland (Table 31.9).
Table 31.9
Surgical procedures for the salivary gland tumours

No. Procedure Indications
01. Soft tissue palatal excision Benign and low grade malignant tumours of the palatal
mucosa
E.g.—Pleomorphic adenoma and low-grade
mucoepidermoid carcinoma.
02. Soft tissue excision of Benign tumours and mucous retention phenomena
salivary gland tumours in E.g.—Pleomorphic adenomas, canalicular adenomas.
the oral mucosa
03. Palatectomy Low grade and intermediate grade malignant tumours
E.g.—Polymorphous low-grade adenocarcinoma.
04. Maxillectomy Malignant tumours of the palatal mucosa
E.g.—
1. Intermediate and high grade mucoepidermoid carcinoma
2. Adenoid cystic carcinoma
3. Squamous cell carcinoma
05. Fine needle aspiration for • Solitary parotid gland masses.
diagnostic cytology • To assess the effect of treatment.
• To obtain tissue for special studies.
06. Incisional parotid biopsy To confirm or rule out autoimmune or systemic diseases of the
salivary gland tissues.
07. Superficial parotidectomy • Benign tumours in the superficial lobe and some low grade
malignant tumours.
• Also indicated in cases of Sjogren syndrome, HIV parotitis,
symptomatic sialosis, parotid injuries, refractory sialocele or
salivary cutaneous fistulae.
08. Total parotidectomy with Benign and low-grade malignant tumours that encroach upon
nerve preservation or extend into the deep lobe.
09. Total parotidectomy with Malignant tumours of the superficial lobe that require
nerve transection and aggressive resection and diffuse benign tumours of both lobes.
nerve grafting
10. Excision of the deep lobe Benign and low-grade malignant tumours located and limited
of the parotid gland to the deep lobe of the parotid gland.
Benign tumours of salivary glands
Pleomorphic adenoma
Pleomorphic adenomas occur predominantly in parotid gland, followed by
submandibular glands and minor salivary gland. They are rarely seen in the
sublingual gland. It can occur at any age, but the peak incidence is in the
fourth and fifth decades of life. There is a slight female preponderance.
Clinical features
• Pleomorphic adenoma is the prototypical benign tumour but yet a true

neoplasm, i.e. it will continue to grow or regrow If not completely
removed, but it is incapable of metastasis.
• Pleomorphic adenomas of the parotid gland have no distinctive
features, but are painless, firm mass in the superficial lobe of the
parotid gland and a painless, firm mass in the posterior palatal
mucosa.
• They do not cause facial palsy and, if neglected, can reach an enormous
size.
• 80% of all pleomorphic adenomas in the parotid gland develop in the
superficial lobe, which constitutes 80% of the parotid gland.
• Curtain sign: Tumour can’t be moved above zygomatic arch.
• Raised ear lobule
• Dumb-bell tumour of parotid (deep lobe of parotid is affected)
• Deep lobe swelling passes through patey’s tunnel
• Pleomorphic adenomas arising in the deep lobe go usually unnoticed
for years, until it reaches a size that creates symptoms like dysphagia
or gagging.
• Intraorally, palate is the most common site of occurrence although it
can occur in buccal mucosa, lips or tongue. They present as slow
growing swelling with intact surface.
• Benign: Warthin’s tumour, basal cell adenoma.

• Malignant: Mucoepidermoid, adenoid cystic, and acinic cell
carcinomas.
• Nonsalivary gland neoplasms: Haemangiomas, lymphangiomas,
lipomas, and lymphomas within parotid lymph nodes.
Microscopy
Histopathology is characterised by the presence of capsule and epithelial cells
arranged as sheets and duct like areas. These duct like areas contain
eosinophilic material and surrounded by myoepithelial cells giving a ‘swarm
of bee’ appearance. There is also evidence of myxoid areas, chondroid areas
and rarely osteoid areas (Table 31.10).
Table 31.10
Salivary gland neoplasms

Benign salivary gland tumours Malignant salivary gland tumours
• Slow growing • Sometimes fast growing
• Soft or rubbery consistency • Sometimes hard consistency
• 85% of parotid tumours are benign • 45% of minor gland tumours are malignant
• Do not ulcerate • May ulcerate and invade bone
• No associated nerve signs • May cause cranial nerve palsies
Plasmacytoid cells are also seen. Depending on the amount of histological

morphology of pleomorphic adenomas can be classified as: predominantly
myxoid, with areas of cellularity, cellular areas with myxoid areas and
predominantly cellular types respectively.
Myoepithelial tumours are rare and can be regarded as a variant of
pleomorphic adenoma. The myoepithelial cells predominate but some
elements of a pleomorphic adenoma are present.

Pleomorphic adenomas, although capable of malignant change, are benign,
but expand and grow in localised areas of proliferation to form irregular
nodular masses. These tumours have good prognosis with superficial or total
parotidectomy or sialoadenectomy as required (Box 31.6; Figs. 31.28–31.30).
Pleomorphic adenoma is radio-resistant.
Box 31.6 Anatomic landmarks for facial nerve

identification during parotidectomy.
• Tragal pointer
• Tympanomastoid suture line
• Digastric muscle attachment to digastric groove
• Retrograde dissection from distal nerve branch
• Nerve within the temporal bone
FIGURE 31.28 Superficial parotidectomy procedure. (A) Note the
tumour in the superficial lobe at the tail of the parotid gland and the
vital structures within the gland. (B, C) Blunt Dissection starts at
the inferior pole of the gland and proceeds upwards separating the
main trunk of the facial nerve from the superficial lobe. (D) All the
facial nerve branches identified and successively dissected and the
superficial lobe of the gland removed in a single block.
FIGURE 31.29 Total parotidectomy procedure. (A) Tumour present

in the deep lobe also. Initial procedure starts with superficial
parotidectomy followed by deep lobe parotidectomy. (B) Complete
parotid gland is removed preserving the facial nerve and its
branches.
FIGURE 31.30 (A, B) Pleomorphic adenoma of the left parotid
gland.
Management problems include the following:
• The risk of damage to the facial nerve is great, particularly when

removing irregularly shaped tumours.
• Biopsy of parotid glands tumours is not feasible because of their ability
to seed in the line of incision to produce multiple recurrences.
• The capsule is often in complete and its integrity cannot be assumed if
there is an unwise attempt at enucleation.
• Mucinous tumours can readily burst to produce multiple seedlings if
enucleation is attempted.
• Removal of recurrences, which are typically multifocal, becomes more
difficult with each attempt and the end result can be innumerable
nodules of tumour, spreading along the neck far beyond the original
site. Markers to predict recurrence are MUC1/DF3
• Treatment of recurrences increases the risk of having to resect the facial
nerve.
• The chances of malignant change are greater in recurrences, with
increase in subsequent recurrence and may be increased further if
radiotherapy is used.
Warthin’s tumour (papillary cyst adenoma lymphomatosum)

Papillary cystadenoma lymphomatosum is a benign hamartomatous or
reactive proliferation of salivary gland ductal cells and lymphoid elements
commonly referred to as a Warthin’s tumour.
Pathophysiology
A Warthin tumour is believed to arise from the incorporation of salivary gland
cells into lymph nodes during their development; these later become reactive
and induce a proliferation of both salivary and lymph node elements.
Clinical features
• Warthin’s tumours are common tumours of the parotid glands
exclusively in the superficial lobe and periparotid lymph nodes. They
are painless and firm to doughy masses.
• It is said to occur most frequently in the ‘tail’ of the parotid gland, which
is the most inferior and posterior portion of the gland below the ear
and the angle of the mandible.
• They occur as synchronous and metachronous tumours which mean
that they appear bilaterally and two or more tumours occur
simultaneously at the same time or years later in the same or opposite
gland or may even recur as a new tumour in residual elements of a
treated gland.
• They can occur even in the minor salivary glands of the oral cavity.
• It affects in the proportion of male/female ratio of 10:1 within the age
ranges of 50–70 years.
• Warthin’s tumours usually cause soft painless swellings, but
sometimes there can be pain or rapid expansion, probably as a result
of the partly cystic nature of most of them. Occasionally, the tumour is
bilateral or multifocal in a single gland.
Etiopathogenesis
• Smoking (irritates ductal epithelium)

• Autoimmune
• Heterotrophic lymphoid tissue
• Delayed hypersensitivity reactions
• Viral aetiology, namely Epstein-Barr virus
• Benign: Pleomorphic adenoma, basal cell adenoma.

• Malignant: Mucoepidermoid, adenoid cystic, and acinic cell
carcinomas.
• Other lymph node-related diseases within the parotid gland:
Lymphoma, HIV-related parotitis, and tuberculosis-related
lymphadenitis (particularly in HIV infected patients).
Microscopy
There is presence of papillary projections into cystic cavity lined by double
layer of cells, which are columnar or cuboidal and rarely polygonal in shape.
Oncocytes are also frequently encountered. There is evidence of dense
lymphoid infiltrate.
Investigation
Tumour presents as ‘hot spots’ with technetium-99-pertechnetate, other
neoplasms show either normal uptake or ‘cold nodule’.
• Warthin tumour must be excised with a superficial parotidectomy

which aids in both, a diagnostic biopsy as well as the definitive
treatment for this tumour and the cut specimens often reveal the
characteristic finding of a soft, sponge-like, multicystic lesion
containing thin, brown fluid.
• Prognosis is good and has rare incidence of recurrences, unless
incomplete excision and multicentricity becomes a concern.
Oncocytoma
Oncocytoma is a rare benign tumour that almost exclusively affects the
parotids, particularly in the elderly. It consists of large, eosinophilic cells with
small compact nuclei and is typically arranged in solid cords. There is presence
of characteristic granules that represent altered mitochondria and are visible
with phosphotungstic acid haematoxylin (PTAH) stain.
Other adenomas
• Canalicular adenomas particularly affect the upper lip and consist of

small darkly staining cells in a tubular or trabecular pattern, but
sometimes resembling an adenoid cystic carcinoma.
• Basal cell adenomas are of different types, namely, solid, membranous,
etc. and are mostly encountered in the major salivary glands especially
the parotid glands.
• Ductal papillomas may also be rarely encountered.
Adenomas other than pleomorphic adenoma respond to enucleation or

simple excision.
Malignant tumours of the salivary gland

Carcinomas of the salivary glands are uncommon. They comprise less than 1%
of all cancers of the head and neck. The most common malignant major
salivary gland tumours are the parotid followed by submandibular and
sublingual glands. Malignant minor salivary gland tumours are mostly
localised in the soft palate, followed by the paranasal sinuses/nasal cavity and
the tongue.
Mucoepidermoid carcinoma (MEC)
Mucoepidermoid carcinoma is most common malignant tumour of salivary
gland. It is the second most common tumour of salivary glands in children and
the most common tumour of parotid glands. It contains mucous cells,
intermediate cells and epidermoid cells.
Variants
• Sclerosing MEC
• Intraosseous MEC
Clinical features
• Shows wide age predilection from 2nd to 7th decades

• Most common malignant tumour in children
• Shows slight female predilection (3:2)
• Some tumours are associated with previous history of radiation
therapy
• It can occur in both major and minor glands, being predominant in
major glands
• Features for major glands
▪ Most common in parotid gland (50%)
▪ Appears as an asymptomatic swelling with duration of less
than 1 year
▪ Pain, trismus, discharge from ear, dysphagia. Facial palsy
develop in high grade tumours.
• Features for minor glands
▪ Common in palate (20%)
▪ Other sites—lower lip, floor of mouth, tongue and retromolar
area
▪ Appear as a symptomatic swellings which are sometimes
fluctuant and have blue or red colour appearance that can be
mistaken for mucocele
• Lesion with ulceration has aggressive clinical course
Gross findings
• Appear relatively well circumscribed

• Appear as partially encapsulated
• Difficult to determine the accurate border
• Cut surface shows cystic spaces and contain mucoid material
• Focal haemorrhage sometimes present if biopsy or FNAC has been
performed
Microscopy
• Characterised by the presence of a variety of cells and growth patterns

• The tumour’s biologic behaviour of extremely low grade to highly
aggressive nature depends primarily on the histology.
• Based on this histologic grading, the treatment decisions are made.
• These cells form the basis for recognition and grading
• These cells include:
▪ Mucous cells
▪ Epidermoid cells
▪ Intermediate cells
▪ Clear cells
• Squamous cell carcinoma
• Retention cysts
• Adenosquamous carcinoma
• Treatment depends on:

▪ Location
▪ Histological grade
▪ Clinical stage
• Early stage tumours of parotid gland are treated by subtotal
parotidectomy with preservation of facial nerve
• Submandibular gland tumours are treated by total sialadenectomy
• For low grade tumours modest marginal clearance of 5 mm may be
needed but for high grade tumours wider excision is required
• If the underlying bone is destructed that should be excised
• Regional node dissection (RND) is indicated for patient with evidence
of metastasis
• Postoperative radiotherapy is needed for some aggressive lesions
Prognosis depends on grade and stage
• Low grade—good prognosis (cystic)

• Intermediate grade
• High grade—poor prognosis—(perineural invasion)
• Submandibular gland involvement—poor prognosis
• Minor glands—good prognosis
• Recurrence rate—25%
Intraosseous mucoepidermoid carcinoma (MEC)
• Rarely salivary gland tumours arise centrally with the jaws

• Most common is intraosseous MEC
• Other rare tumours include:
▪ Adenoidcystic carcinoma(ACC)
▪ Benign and malignant mixed tumours
▪ Adenocarcinoma
▪ Acinar cell adenocarcinoma (ACAC)
▪ Monomorphic adenoma
Pathogenesis
Entrapped ectopic salivary gland tissue may be responsible for intraosseous
salivary gland (IOSG) tumours.
In maxillary tumours—sinus lining may be the source.
Clinical features
• Common in middle age

• Shows light female predilection
• More in mandible than maxilla
• Most frequent presenting symptom is cortical swelling
• Radiograph reveals—unilocular or multilocular radiolucency
• Some associated with unerupted teeth—misdiagnosed clinically as an
odontogenic cyst
Histopathology
• Same as soft tissue MEC

• Most are low grade in nature
Treatment
Surgery is the first line of treatment. Prognosis is fairly good and there are
cases reported with local recurrence and metastasis.
Adenoid cystic carcinoma (ACC)/Cylindroma (Fig. 31.31 A–O)

Adenoid cystic carcinoma is a clinically and pathologically well-defined entity
and occurs primarily in the major salivary glands (submandibular gland) and
relatively frequent in the oral accessory salivary glands, particularly the palate.
FIGURE 31.31 (A–O) Adenoid cystic carcinoma (ACC) of the right

maxilla involving the orbit—Total right maxillectomy with orbital
exenteration.
Clinical features
• Occur in older individual

• Show equal sex predilection
• Slow growing tumour
• Pain and tenderness occur during tumour growth
• Fixation to skin and surrounding structures develop in later stages
• Perineural and perivascular spread
• Cause paralysis of facial nerve
• In minor salivary glands, it presents as a swelling or mass
• Symptoms of facial pain and swelling characterise the ACC of
maxillary antrum
• Radiograph is necessary for assessing the extent of osseous destruction
• In major salivary gland—mostly occur in parotid and submandibular
gland, rarely in sublingual gland
• In minor salivary gland—palate is most common followed by tongue,
cheek, upper lip, floor of mouth, oropharynx and lower lip, orbit
• The characteristic feature of ACC is perineural invasion, which
accounts for high incidence of recurrence despite aggressive therapy
Gross findings
• Present as a fairly well defined mass within the substance of involved

gland
• Oncut section—tumour lacks encapsulation, but can be demarcated
from surrounding salivary gland tissue
Microscopic findings
• Adenoid cystic carcinoma has variety of microscopic patterns

• The cells that form various patterns and are uniform in size, shape and
staining qualities are called isomorphic cells
• Various microscopic patterns:
▪ Cribriform
▪ Tubular
▪ Solid
Investigations
1. FNAC
▪ Aspiration biopsy consist of round or ovoid basophilic cells
arranged in branching structures
▪ Amorphous, hyaline globoid structures with tumour cells is
the characteristic feature of ACC
2. Immunohistochemistry It reveals the presence of two cell population:(1)
ductal cells and (2) myoepithelial cells
• Polymorphous low grade adenocarcinoma (Fig. 31.32A–C)

• Salivary duct carcinoma
FIGURE 31.32 (A–C) Polymorphous low grade adenocarcinoma of

palate—Surgical excision.
• Surgical excision is the treatment of choice

• As it is very much prone to local recurrence and eventual distant
metastasis, adjunct radiotherapy will improve patient survival
• Regional lymph node metastasis is uncommon
• Prognosis is poor because of local recurrence and distant metastasis
• Solid pattern has worst prognosis
• Tumours arising in maxillary sinus and submandibular gland has poor
prognosis
• Perineural invasion has little effect on prognosis
• Metastatic spread most commonly occurs to lungs and bones
• Lesions in the palate and maxillary sinus may invade upward to the
brain
Frey syndrome
(Auriculotemporal syndrome, Baillarger syndrome, Dupuy syndrome,
Gustatory sweating syndrome)
Frey syndrome is characterised by unilateral flushing and sweating of the
facial skin innervated by the auriculotemporal nerve (neck, parotid region, and
frontotemporal scalp), which occurs in response to gustatory or olfactory
stimuli. [Gustatory sweating]
Aetiology:
• In infants, trauma to the auriculotemporal nerve during forceps-
assisted delivery
• Congenital aberration of the auriculotemporal nerve fibres, between
the parasympathetic and sympathetic pathways
• Parotid surgery, especially after excision of the superficial lobe or
drainage of a parotid abscess.
• TMJ surgery
• Rare causes like mandibular condylar fracture, blunt trauma, herpes
zoster, associated CNS disorders such as syringomyelia, epilepsy, and
meningioma of the cerebellopontine angle tumour.
Pathophysiology:
Auriculotemporal nerve is a sensory branch of the posterior division of the
mandibular division of the trigeminal nerve. It receives the postganglionic
parasympathetic secretomotor fibres from the otic ganglion, for parotid
glands. Damage to these autonomic fibres causes misdirection of regenerating
parasympathetic fibres to join with the sympathetic fibres of the great
auricular nerve, (7th nerve) which supplies sweat glands and blood vessels,
during the process of healing. Because of this, any gustatory stimulus
produces erythema and sweating instead of salivation (Fig. 31.33).
FIGURE 31.33 Pathophysiology of Frey’s syndrome.
Diagnosis:
Suspicious area is painted with iodine and allowed to dry and then dusted
with corn starch or potato flour. Sweating is then encouraged via sialogogue
(lemon). If positive, the reaction causes change of colour from yellow to black.
Treatment:
Topical:
• Antiperspirant—for mild symptoms

• 20% aluminium chloride for a period of 1–2 months
• Anticholinergic—Topical glycopyrrolate
Intradermal:
Intradermal injection of Botulinum Toxin A. Response may last for a period
of 6 months. If the treatment is unsuccessful, then surgery is considered.
Radiation:
Radiation of 50 Gy indicated for symptomatic patients
Surgery:
• Auriculotemporal nerve resection

• Tympanic neurectomy
CHAPTER 32
Maxillary Sinus and its

Implications
Groups of sinuses
Functions of the sinuses
Defence system in the sinuses
Maxillary sinus
• Development
• Anatomy
• Drainage of the sinus
• Lining of the epithelium
• Size of the sinus
• Arterial supply
• Venous drainage
• Nerve supply
• Lymphatic drainage
• Applied anatomy
• Radiologic assessment
• Classification of diseases affecting maxillary sinus
Maxillary sinusitis
Classification
Diagnostic criteria for rhinosinusitis
• Major
• Minor
Acute maxillary sinusitis
• Pathophysiology
• Signs and symptoms
• Investigations
• Management
Chronic maxillary sinusitis
• Causes
• Pathophysiology
• Clinical findings
• Investigations
• Diagnosis
• Management
Complications of untreated maxillary sinusitis
• Periorbital cellulitis
• Cavernous sinus thrombosis
Oroantral fistula
Aetiology
Clinical features of acute oroantral fistula
Investigations to confirm the presence of fistula
Management of acute oroantral fistula
• Surgical procedures for closure of oroantral fistula
• Postoperative care
• Complications
Chronic oroantral fistula
• Management
Caldwell-Luc procedure
Indications
Instruments
Surgical procedure
Traumatic disease
Haematoma in maxillary sinus
• Treatment
Iatrogenic disease
Teeth displaced into sinus
• Aetiology
• Diagnosis
• Management
Antral rhinoliths
• Treatment
Advances in the management of maxillary sinus disease
Functional endoscopic sinus surgery (FESS)
Conventional sinus surgery versus functional
endoscopic sinus surgery
Preoperative assessment
Indications
Procedure
Postoperative complications
Paranasal air sinuses are air-filled, mucosa-lined cavities which develop in

facial and cranial bones and the spaces communicate with the nasal airway.
The complex anatomy of the paranasal sinuses as well as their many functions
makes the sinuses an interesting and rewarding topic of study.
Groups of sinuses
There are four groups of sinuses (Fig. 32.1):
FIGURE 32.1 Paranasal air sinuses.

Functions of the sinuses
1. Reduction of skull weight (pneumatisation of sinus)
2. Humidification and warming of inspired air
3. Absorption of shock to the face or skull and secretion of mucus to assist
with air filtration and mechanical rigidity
4. Pressure damping
5. Areas for the production of mucus to moisten the nasal chambers and
inspired air
6. Vocal resonance and diminution of auditory feedback
7. Give some assistance in olfactory function by evenly distributing
inspired air in the olfactory region
8. Increasing the olfactory area
9. Heat insulation for intracranial structures
The four paranasal sinuses develop as outpouchings of the nasal mucosa.

They remain connected to the nasal cavity via narrow ostia with a lumen
diameter of 1–3 mm. The sinuses are lined with ciliated mucoperiosteum,
which is thinner and less richly supplied with blood vessels and glands than
the mucosa of the nasal cavity. Cilia sweep mucus towards the ostia. The ostia
of the frontal, maxillary and anterior ethmoid sinuses open into the
ostiomeatal complex, which lies in the middle meatus lateral to the middle
turbinate. The posterior ethmoid and sphenoid sinuses open into the superior
meatus and sphenoethmoid recess. The ostiomeatal complex is important
because the frontal, ethmoidal and maxillary sinuses drain through this area
(Fig. 32.2).
FIGURE 32.2 Lateral wall of the nose showing opening of the
maxillary sinus.
Defence system in the sinuses

Healthy sinuses are sterile and contain no bacteria. The nasal passage, on the
other hand, normally contains many bacteria that enter the nostrils.
Maintaining sinus health depends on a cycle that involves a number of
important factors and processes:
• The sinuses are lined with a membrane that secretes mucus, which
drains down into the nasal passage through a small channel in each
sinus. The mucous membranes must be intact and free of injury.
• The mucous must be fluid in order to flow freely while being sticky
enough to absorb pollutants and entrap bacteria.
• The mucus must also contain sufficient amount of bacteria-fighting
substances, including immune factors called antibodies.
• Small, hair-like projections called cilia must move in unison to propel
mucous outward, expelling bacteria and other particles.
• The sinus passages must be open to allow mucous drainage and the
circulation of air through the nasal passage.
• Sinuses frequently become infected due to obstruction of normal
drainage and negative pressure in a sinus can cause headache.
Neoplasms, which arise in the sinuses, can be occult for quite a long
time, so that they are usually very advanced at the time of diagnosis.
Maxillary sinus
Maxillary sinus (sinus maxillaris or antrum of Highmore), the largest of the
paranasal sinuses is a pyramidal cavity in the body of the maxilla. In 1651,
Highmore described maxillary sinus, but its existence was known before his
description. The possible relation between dental pathology and the spread of
infection to the maxillary antrum was later on described by John Hunter.
Development
Maxillary sinus is the first of the sinuses to develop. The maxillary sinus
appears as a shallow groove on the medial surface of the bone at about the 4th
month of foetal life, but does not reach its full size until after the second
dentition. At birth, it measures about 7 mm in the dorsoventral direction and
at 20 months it is about 20 mm. The expansion of the sinus normally stops
around eruption of the permanent teeth. Sometimes it may pneumatise further
after removal of one or more of the maxillary posteriors which extends into the
residual alveolar process.
Anatomy
• Maxillary sinus is the largest of the paranasal sinuses, pyramidal in

shape and located within the body of the maxillary bone.
• Its apex, directed laterally, is formed by the zygomatic process.
• Its base directed medially is formed by the lateral wall of the nose.
• The alveolar process of the maxilla forms the floor.
• Many projections are seen on the floor of the antrum corresponding to
the roots of the first and second molar teeth. Its nasal wall or base
presents a large, irregular aperture, communicating with the nasal
cavity. In the articulated skull, this aperture is much reduced in size by
the following bones: uncinate process of the ethmoid above, ethmoidal
process of the inferior nasal concha below, vertical part of the palatine
process behind and a small part of the lacrimal bone above and in
front.
• The sinus communicates with the middle meatus of the nose, generally
by two small apertures between the above mentioned bones. In the
fresh state, usually only one small opening exists, near the upper part
of the cavity; the other is closed by mucous membrane.
• On the posterior wall are the alveolar canals, transmitting the posterior
superior alveolar vessels and nerves to the molar teeth.
• The infraorbital canal usually projects into the cavity as a well marked
ridge extending from the roof to the anterior wall; additional ridges
are sometimes seen in the posterior wall of the cavity and are caused
by the alveolar canals. The size of the cavity varies in different skulls
and even on the two sides of the same skull.
Drainage of the Sinus (Figs. 32.3, 32.4)

In the anterosuperior part of its base is an opening through which it
communicates with the lower part of the hiatus semilunaris; a second orifice is
frequently seen in or immediately behind the hiatus.
FIGURE 32.3 Lateral wall of the nose showing position of exit of

maxillary sinus and relationship to the ducts of adjacent air
sinuses.
FIGURE 32.4 Schematic diagram showing opening of the maxillary
sinuses into middle meatus. Note the ostium is in the upper third of
the sinus cavity.
Hiatus semilunaris is bounded inferiorly by sharp concave margin of

uncinate process of the ethmoid bone and leads into a curved channel, the
infundibulum, bounded above by bulla ethmoidalis and below by lateral
surface of uncinate process of the ethmoid.
Anterior ethmoidal cells open into the front part of the infundibulum and
this, in slightly more than 50% of subjects, is directly continuous with the
frontonasal duct or passage leading from the frontal air sinus. But when
anterior end of the uncinate process fuses with front part of the bulla, this
continuity is interrupted and frontonasal duct then opens directly into anterior
end of the middle meatus. Below the bulla ethmoidalis and partly hidden by
the inferior end of the uncinate process, is the ostium maxillare or opening
from the maxillary sinus. In a frontal section, this opening is seen to be placed
near the roof of the sinus. An accessory opening from the sinus is frequently
present below the posterior end of the middle nasal concha.
Lining of the epithelium

The maxillary sinus is lined by pseudostratified ciliated columnar epithelium.
In acute inflammation, increase in neutrophils is found whereas in chronic
conditions increase in lymphocytes and plasma cells are found. In case of
prolonged chronicity, cilia might be lost and the lining cells show dysplastic
changes.
Size of the sinus

The size of the sinus varies in different skulls and even on the two sides of the
same skull. The adult capacity varies from 9.5 to 20 cc, average about 14.75 cc.
• Vertical height opposite the first molar tooth 3.75 cm

• Transverse breadth 2.5 cm
• Anteroposterior depth 3 cm
Arterial supply
Facial, infraorbital and greater palatine arteries
Venous drainage
Facial and pterygoid plexus of veins.
Nerve supply
Infraorbital, anterior, middle and posterior superior alveolar nerves—all
branches of V2 (maxillary division of trigeminal nerve).
Lymphatic drainage
Submandibular nodes and upper deep cervical lymph nodes
Applied anatomy
Dental infection and root anatomy:
The most common teeth whose roots are in close approximation to the
maxillary sinus are second maxillary molar followed by first and third molars,
second premolar, first premolar, and canine.
Maxillary sinus in adult:
In adults, the distance between apical ends of maxillary posterior tooth with
the floor of the sinus is approximately 1–1.2 cm but in some individuals this
gap may be still lesser. In some cases, floor of the sinus lies in between the
roots of the adjacent teeth or adjacent roots of the same tooth, which causes
elevation of floor of the sinus.
Maxillary sinus in child:
Completion of pneumatisation occurs about 15 years of age, hence the
chances of creating an oroantral fistula in a patient below the age of 15 years
are comparatively lesser than in an adult.
Oroantral fistula and maxillary sinus:
Large sinuses may cause risk of fracture of sinus wall when force applied
during extraction of maxillary posteriors resulting in oroantral fistula
Presence of an unerupted tooth in the maxillary tuberosity is a potential line
of weakness.
Periapical infection and maxillary sinus:
Periapical infection of tooth which is in relation with maxillary antrum
might cause an oroantral fistula. Acute or chronic periapical infection may
secondarily involve the maxillary sinus. The pus may discharge into the sinus
increasing the fluid level, and the extraction of such tooth might result in
oroantral fistula (Fig. 32.5).
FIGURE 32.5 Relation maxillary sinus to the maxillary posterior

teeth.
Antral puncture:
• Antral puncture (intranasal antrostomy) can be carried out by

puncturing into the sinus cavity through the middle meatus in
children and the inferior meatus in adults creating a point of
dependent drainage.
• In case of acute sinusitis, pus is formed inside the antrum which in
turn increases the intra-antral pressure because of occlusion of the
lining mucosa by inflammation. This pressure, in turn, compresses the
nerves within the antral lining.
Tumours in maxillary sinus:
Since walls of the maxillary sinus are thin any tumours which develop here
may erode these walls and present as a swelling on the cheek, palate or buccal
mucosa.
Tumours of maxillary sinus involving the anterior and infratemporal walls
on enlargement causes swellings of cheek as these are thin.
Tumours penetrating the floor of sinus presents as swelling in the palate or
buccal sulcus. Loosening of teeth around the side of destruction of tumour is
seen.
Tumour involving the posterior wall causes paraesthesia of the gingiva or
teeth in maxillary molar area due to destruction of posterior superior alveolar
nerves.
Tumours involving the roof of sinus cause paraesthesia of infraorbital nerve.
Orbital involvement causes alteration of pupillary level, diplopia, strabismus,
proptosis.
Tumours involving the medial wall (nasal side) cause the obstruction of
nostrils and may protrude through the nostrils.
Ohngren’s line is an imaginary line extending from medial canthus of the eye
to the angle of the mandible, which divides the maxillary antrum into the
infrastructure (anteroinferior) and suprastructure (posterosuperior) and is
significant in determining the stage of antral tumours. In general, tumours
below this line have a better prognosis than tumours above it.
Canine fossa:
Since wall of the sinus is very thin in the area of canine fossa, it can be used
for diagnostic aspiration; site for Caldwell-Luc procedure.
Mucous lining of maxillary sinus:
Sinus is lined by pseudostratified columnar ciliated epithelium which might
regenerate once the infection is treated. But in cases where the lining is
stripped, nasal mucosa extends through the ostium.
Fractures in middle third of face
Fractures of middle third of the face might cause fracture of the sinus walls
since these are very thin. Lefort I, II, III show disturbance in the wall of the
maxillary sinus. Zygomatic butress may be pushed into the maxillary sinus
during fracture of zygomatic bone.
Developmental anomalies:
• Crouzon syndrome: Early synostosis (fusion) of sutures produces

hypoplasia of the maxilla and maxillary sinus together with the high
arched palate.
• Treacher Collins syndrome: Associated with grossly and symmetrically
underdeveloped maxillary sinus and malar bones.
• Binders syndrome: Associated with midfacial hypoplasia with smaller
maxillary length and maxillary sinus hypoplasia.
Clinical examination:
• Extraoral examination:
Pain and tenderness, swelling over the prominence of
cheek bones
• Intraoral examination:
Pain and tenderness, swelling if present may be seen in
the canine fossa and zygomatic buttress.
• Transillumination test:
Affected sinus shows reduced transmission of light due to accumulation of

fluid, debris, pus and thickening of the sinus mucosa.
Radiologic assessment (Fig. 32.6)

The radiologic assessment of maxillary sinus is usually done along with all
other paranasal sinuses.
FIGURE 32.6 (A) Intraoral periapical radiograph showing the

posterior teeth in connection with maxillary sinus. (B) OPG (C)
Submentovertex view (D). Water’s view (occipitomental view) for
evaluation of sinus pathology (E) Axial CT section showing nasal
polyp in left maxillary sinus. (F) CT section showing mixed density
of left maxillary sinus from haematoma with air entrapment
following zygoma fracture.
Standard radiographs
Intraoral radiographs: Occlusal, lateral occlusal and periapical views
Extraoral radiographs: Waters’ view (occipitomental view), Caldwell’s
view, Lateral view, and submentovertex or base view. OPG, PA view
Others: CT, MRI
Intraoral views:
Intraoral views helps in locating and retrieving the foreign bodies like teeth,
root tips, osseous fragments and also for planning. Helps to differentiate the
root apices which are intra-antral but extramucosal
Extraoral view:
• The lateral view shows the bony perimeter of the frontal, maxillary and
sphenoid sinuses.
• Caldwell’s view shows the bony perimeter of the frontal sinus. Helpful
in cases of pansinusitis
• Waters’ view shows the outline of the maxillary sinuses, some of
anterior ethmoid air cells and the orbital floors.
• The submentovertex view evaluates the sphenoid sinus and the anterior
and posterior walls of the frontal sinuses.
• The superimposition of fine bony structures on standard radiography
precludes the accurate evaluation of the anatomy of the ostiomeatal
channels.
CT scan
• It optimally displays bone, soft tissue and the air facilitates accurate
depiction of anatomy and extent of disease in and around the
paranasal sinuses.
• CT scan clearly shows the fine bony anatomy of the ostiomeatal
channels.
• Coronal plane optimally shows the ostiomeatal unit, the relationship of
the brain and ethmoid roof and the relationship of the orbits to the
paranasal sinuses (Fig. 32.7).
• Sagittal reconstructions can be obtained for a morphologic orientation.
Various distances and angles can be measured to aid in the passage of
instruments during surgery. The frontal recess is best visualised on the
sagittal images.
FIGURE 32.7 Coronal view maxillary sinus showing ostium,
maxillary sinus opening through the middle meatus.
MRI
• MRI has proved most helpful in the evaluation of regional and

intracranial complications of inflammatory sinus disease and their
surgical management, in the detection and staging of neoplastic
processes and an improved display of anatomic relationships between
the intraorbital and extraorbital compartments.
• MRI is helpful in diagnosing fungal concretions, mucoceles and
cephaloceles.
Classification of diseases affecting maxillary sinus

Diseases affecting maxillary sinus are classified as depicted in Table 32.1.
Table 32.1
Diseases affecting maxillary sinus: classification
1. Maxillary sinusitis
a. Odontogenic
b. Inflammatory
• Acute
• Subacute
• Chronic
a. Acute
b. Chronic
3. Traumatic
a. Haematoma in the sinus
4. Iatrogenic
a. Tooth or root displaced into the sinus
5. Tumour–carcinoma of maxillary sinus
6. Antral rhinoliths
Odontogenic sinusitis
Intimate anatomical relation of the upper teeth to the maxillary sinus promotes
the development of periapical or periodontal odontogenic infection into
maxillary sinusitis.
Aetiology:
1. Infections (periapical abscess, common cold, upper respiratory

infection)
2. Trauma (fracture of antral floor and walls)
3. Allergy
4. Neoplasm or cyst of odontogenic origin
6. Displaced tooth or root
The most common cause of maxillary sinus by oral infection is due to

periapical abscess, as the roots of molars (first and second molars) are in close
proximity to the sinus.
Clinical features:
Sinonasal symptoms includes:
Unilateral nasal obstruction, rhinorrhoea, and/or foul odour and taste.
Headaches, unilateral anterior maxillary tenderness and postnasal drip. Mild
swelling in the cheek is seen.
Dental symptoms includes:
Severe throbbing pain due to collection of pus in the apical region within the
bone. Unpleasant smell or taste in mouth. Mobility of teeth (depending on the
periodontal involvement)
Diagnosis:
The accurate diagnosis of odontogenic maxillary sinusitis is particularly
important, because its pathophysiology, microbiology and treatment differ
from those of other forms of maxillary sinusitis. Radiologic imaging can
provide useful adjunct information in the diagnosis of sinusitis and
particularly whether an odontogenic source may be responsible for the
infection.
Management:
Elimination of the source of the infection (e.g. removal of an external dental
root from the sinus cavity, extraction, or root canal therapy of causative tooth)
is necessary to prevent recurrence of the sinusitis.
Adequate care must be taken during extraction to avoid oroantral fistula.
Antibiotic prophylaxis and nasal decongestant should be used.
Maxillary sinusitis
Classification
Maxillary sinusitis is classified according to the duration of its course into: (1)
acute, (2) subacute and (3) chronic maxillary sinusitis.
• Acute maxillary sinusitis (AMS) has a sudden onset and duration of

4 weeks or less. Disease symptoms resolve completely with
appropriate treatment and long-term therapy is not required.
• Subacute maxillary sinusitis has duration of 4–12 weeks. It is not a
distinct disease entity, but it may require therapy differing from that
employed in patients with either acute or chronic maxillary sinusitis.
• Recurrent subacute maxillary sinusitis occurs at least 4 times per year
with each episode lasting 7–10 days. The symptoms of recurrent
subacute maxillary sinusitis are the same as those of AMS and they are
completely absent in between episodes.
• Chronic maxillary sinusitis has duration of at least 12 weeks. Either a
sudden worsening of baseline chronic maxillary sinusitis symptoms or
appearance of new symptoms characterises acute exacerbation of
chronic maxillary sinusitis. Chronic and subacute maxillary sinusitis
may require surgical consultation and management, but AMS can
usually be managed by physicians in an ambulatory care setting.
Diagnostic criteria for rhinosinusitis

In 1997, the Rhinosinusitis Task Force of the American Academy of Otolaryngology–
Head and Neck Surgery developed a now well-accepted classification of
rhinosinusitis that relies on two major criteria that help to identify whether or
not a patient has rhinosinusitis primarily on the basis of symptoms.
Signs and symptoms
Major
• Facial pain/pressure
• Facial congestion/fullness
• Nasal obstruction/blockage
• Nasal discharge/purulence, discoloured posterior drainage
• Hyposmia/anosmia
• Purulence on nasal examination
• Fever (acute rhinosinusitis only)
Minor
• Headache
• Fever (non-acute rhinosinusitis)
• Halitosis
• Fatigue
• Dental pain
• Cough
• Ear pain/pressure/fullness
• Acute bacterial rhinosinusitis has been defined as sudden in onset and
with duration of less than 4 weeks (self-limited viral infection and
bacterial infections).
• Invasive fungal rhinosinusitis—patients with acute rhinosinusitis where
the inciting pathogen is neither viral nor bacterial. They have acute
invasive fungal rhinosinusitis (IFRS), which is almost always confined to
patients with altered host defences.
• Chronic rhinosinusitis is a group of disorders characterised by
inflammation of the mucosa of the nose and paranasal sinuses of at
least 12 consecutive weeks duration.
Acute maxillary sinusitis

Acute maxillary sinusitis (AMS) may be clinically defined as an inflammatory
response involving mucous membranes of the nasal cavity and paranasal
sinuses. Most cases of AMS involve inflammation of more than one of the
paranasal sinuses, most commonly maxillary and ethmoid sinuses. When all
the paranasal sinuses are either acutely or chronically infected, the condition is
called pansinusitis, which may be either unilateral or bilateral.
Pathophysiology
Maxillary sinusitis is a disease of multifactorial aetiology. Factors that
contribute to AMS include: (1) host factors and (2) environmental factors. The
ostia are the most important foci for development of disease. Inflammatory
changes of the ostiomeatal complex result in decreased mucociliary clearance,
retention of secretions and decreased sinus ventilation. Swelling of the mucosa
impedes drainage and creates an environment predisposed to the
development of infection. A wide range of different conditions may increase a
patient’s risk for AMS.
Host factors
• Genetic factors
• Congenital conditions
• Allergy and immunity
• Anatomic abnormalities
• Systemic disease
• Neuromechanisms
• Neoplasms
Environmental factors
• Infectious agents
• Trauma
• Noxious chemicals
• Medications
• Surgery
Aetiology
Conditions that predispose patients to the development of maxillary sinusitis.
• Infection (viral, bacterial, fungal)

• Allergy
• Oroantral communication
• Anatomic abnormality of the ostiomeatal complex
• Nasal anatomic variations (septal deviation, concha bullosum, Haller
cells)
• Cystic fibrosis
• Immune deficiency (common variable, IgA, IgG subclass, specific
antibody)
• Acquired immunodeficiency syndrome (AIDS)
• Dental infection
• Wegener’s granulomatosis
• Swimming/diving
• Topical nasal medications
• Cocaine abuse
• Injury
Microbiology
Bacteria
The bacteria most often isolated from patients with acute sinusitis are
Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis.
However, Staphylococcus aureus, other streptococci and anaerobes may also be
isolated from patients with bacterial AMS.
Viruses
These cause vast majority of cases of AMS. Viruses that have been cultured
from the sinus cavity include rhinovirus, influenza virus A and B, corona
virus, respiratory syncytial virus, adenovirus, enterovirus and parainfluenza
virus.
Fungi
These may colonise paranasal sinuses and can cause subacute or chronic
maxillary sinusitis. This is generally rare in immunocompetent individuals,
but sinus infections in patients with diabetes and impaired immunity have
been associated with Aspergillus and mucormycosis. Other causes of fungal
sinus infection include phaeohyphomycosis, Pseudallescheria and
hyalohyphomycosis.
Signs and symptoms
Extraoral
• Headache
• Facial pain/pressure/swelling
• Mild fever, chills
• Nasal obstruction/blockage
• Nasal or postnasal discharge/purulence (by history or physical
examination)
• Fatigue
• Hyposmia/anosmia
• Cough
• Ear pain
Intraoral
• Halitosis
• Presence of fistula
• Discharge of pus from fistula into the mouth
• Teeth in the area of the sinus may be painful and mobile
Investigations
Transillumination
This is a method of examination performed in a darkened room. A light is
placed in the mouth. It transilluminates normal sinus but fails to do so in
presence of pus, polyps or thickening of antral membrane due to acute or
chronic infection.
Rhinoscopy
Anterior rhinoscopy reveals pus draining downwards with oedema and
erythema of mucosa.
Waters’ view
• Waters’ view is the screening tool for all paranasal sinuses.

• It gives a clue regarding involvement of other sinuses.
• The level of fluid and any deviation of the septum that is obstructing
the ostium can be detected.
• Other foreign bodies can also be detected.
Management
Symptomatic therapy
• Primary aim of symptomatic or supportive therapy for patients with

AMS is to facilitate drainage of the sinuses and nasal passages.
• Patients should be hydrated, analgesics (such as nonsteroidal anti-
inflammatory drugs—NSAIDs and topical anti-inflammatory
preparations) and decongestant should be administered to relieve pain
and malaise associated with AMS.
• Oral and topical decongestants (adrenergic receptor agonists) are often
used in patients with AMS because they are thought to widen ostial
patency and reduce turbinate swelling.
• Use of topical corticosteroids to reduce inflammation may be beneficial
in AMS in patients with chronic rhinitis or recurrent infections. These
drugs have the potential to decrease local sinus ostial inflammation,
oedema and obstruction.
NSAIDS: Paracetamol, aspirin, ibuprofen

Antimicrobial therapy
The goals of antimicrobial treatment in patients with bacterial maxillary
sinusitis are to restore the sinuses to health, reduce the risk for rare severe
complications of infection (e.g. meningitis, brain abscess) and prevent
development of chronic disease.
Once the decision to administer antimicrobial therapy has been made, there
are a number of factors that must be weighed in selection of a specific therapy.
These include potency, efficacy, dosing schedule, local patterns of pathogen
resistance, knowledge of patient’s allergies, and probability of patient’s
compliance with the required treatment regimen.
Erythromycin: 250–500 mg 4/day for 5 days
Amoxicillin 250–500 mg 3/day for 5 days
Decongestant
These drugs reduce excess vascularity of the lateral nasal wall thereby
improving the opening of the ostium reducing the nasal congestion.
Nasal drops or sprays: Ephedrine sulphate 0.5%–1% in normal saline, 6
hourly
Xylometazoline hydrochloride 0.1%: shrinks the mucosa and eliminate the
mucosal discharge
Mucolytic agents
• They reduce the viscosity of the mucus and increase drainage by the
ciliary complex.
• Ordinary steam inhalation, camphor, menthol, tincture benzoin, etc.
are used.
• Inhalations of these mucolytic agents, in steaming water 4 and 5 times
a day followed by nasal decongestants help in relieving the
discomfort.
Chronic maxillary sinusitis

Chronic maxillary sinusitis refers to inflammation of the sinus membrane for
duration of at least 12 weeks. Either a sudden worsening of baseline chronic
maxillary sinusitis symptoms or appearance of new symptoms characterises
acute exacerbation of chronic maxillary sinusitis. Prominent symptoms during
acute exacerbation present as pain and tenderness in the area of antrum and
unilateral foul discharge through posterior nares.
Causes
• Allergy
• Chronic rhinitis
• Chronic infection in the frontal or ethmoidal sinuses
• Chronic maxillary sinusitis of odontogenic origin: Constant dental
infection–Infections of the maxillary sinus from an infected tooth or
after the extraction of a tooth with perforation of the antrum occur
frequently
• Causative organisms: Staphylococci, streptococci and Gram-positive
organisms may be found
• Periapical abscess gaining access into the maxillary sinus due to close
proximity of the involved tooth with the floor of the sinus
• Infections of neoplasm or cysts of odontogenic origin
• Fracture of the maxillary floor
• Displaced tooth into the maxillary sinus
Pathophysiology
Chronic inflammation may cause hyperplasia or atrophy of the lining
epithelium. Multiple polyp formation or degeneration of epithelium, where
the cilia are lost can be seen. The ostium may be blocked completely due to
oedema thus affecting drainage of the sinus.
Clinical findings
• The predominant symptom is severe pain of constant and localised

character. This pain may be referred to the cheek and frontal region
above the eye.
• If it affects the eye ball, the ethmoidal sinuses may be involved. In most
cases, adjacent teeth become extremely sore.
• Discharge into the nose may at first be profuse, but soon it assumes a
mucopurulent form, dripping into the nasopharynx from where it is
expectorated or swallowed.
• If the head is bent forward, it may run out of the nostril.
• In maxillary sinusitis that originates from diseased teeth, the secretion
has a foul, saprophytic odour.
• General toxaemia accompanies the disease, with chills, sweats, a rise in
temperature, often nausea and dizziness.
• Breathing may be obstructed or impaired on the side involved by the
antral infection.
Investigations
• Radiographic view: Waters’ view.
• The sinus reveals radiopacity on the affected side due to the presence
of fluid.
• Thickening of lining membrane.
• In case of presence of tooth or root, the characteristic outline is seen
within the sinus.
Diagnosis
• Anterior rhinoscopy shows nasal congestion and mucopurulent

material in middle meatus.
• History of: (1) repeated attacks of acute mucopurulent rhinitis, (2)
long-standing nasal or postnasal discharge.
• Inspection of oropharynx may reveal pharyngeal exudates.
• Prolapse of polypoidal mass into the mouth forming a lump may be
seen.
• Transillumination—negative.
• Presence of chronic oroantral fistula may be an associated finding.
Management
Goals of management
General goals for treatment of the patient with odontogenic sinusitis that is
bacterial are:
• To control infection
• Diminish tissue oedema
• Reverse sinusostial obstruction so that the mucopus can drain
Medical and surgical management
• Appropriate antibiotic therapy.

• Nasal drops or inhalations of decongestants.
1. If the chronic sinusitis is caused by chronic periapical
infection, then the affected tooth must be extracted and the
socket surgically closed completely as there is a risk of
oroantral fistula formation.
2. In case, the cause is a foreign body, such as tooth or root in
the sinus, it is necessary to retrieve these foreign bodies
prior to considering any other form of treatment.
3. The presence of a chronic pyogenic sinusitis subsequent to
an oroantral fistula requires surgical closure of fistula. The
polyps found at operation should also be removed.
a. The antrum should be irrigated with warm
saline or Betadine daily.
b. Once the antral washouts appear to be clear, the
fistula should be repaired surgically.
4. In cases, where there is no oroantral fistula present, but
there is chronic maxillary sinusitis nonresponsive to other
conservative regime, then a surgical drainage should be
considered.
Surgical drainage:
The thin medial wall of the antrum is punctured by introducing the sharp
trocar and cannula along the floor of the nasal cavity inferior to inferior
turbinate. The trocar is withdrawn and the pus is drained under pressure
through suction tip. Warm saline irrigation should be done till symptoms
resolves.
Complications of untreated maxillary sinusitis

Due to the proximity of paranasal sinus to the eyes and brain, complications of
sinusitis can be divided into two broad categories: orbital and intracranial.
These infections usually originate from ethmoid sinus and extend into the
orbit and associated soft tissues through any of the following mechanisms:
• Direct extension to the orbital wall

• Retrograde spread through veins between the sinuses and the orbit
It is very rare for the infection to spread through lymphatics because they
are absent in the orbit. If not effectively treated the following serious
complications may occur rarely:
• Cellulitis
• Abscess
• Meningitis
• Cavernous sinus thrombosis
• Osteomyelitis
• Oroantral fistula
Periorbital cellulitis
This is also known as preseptal cellulitis, which is oedema and inflammation
of the skin and muscle anterior to the orbital septum. This results due to
impairment of venous drainage from these tissues. There are no visual
symptoms.
Depending on the size of the abscess, associated mass effect and degree of
inflammation, ocular muscles and visual acuity are variably affected. This
process may subsequently result in an abscess of the orbital tissues if allowed
to progress.

This occurs as a sequelae of direct extension or retrograde thrombophlebitis of
ethmoid or sphenoid sinuses.
Clinical features
• Proptosis
• Chemosis
• Restriction of extraocular mobility
• Visual loss
• Signs of meningitis
• Intracranial complications occur less frequently than orbital
complications
Oroantral fistula
Oroantral fistula is a pathological communication between oral cavity and
maxillary sinus. Immediate oroantral fistulae usually do not have any
epithelial lining but chronic oroantral fistulae are epithelialised.
Aetiology
Extraction of teeth
• The sinus attains its maximum size by the age of 15; therefore,
perforation is more common in adults than in children.
• Sometimes, the roots of the posterior teeth are in close proximity with
the sinus floor. There might be only a thin lamina of bone or
sometimes only the antral mucosa may be present in between the root
apices and the maxillary antrum. This is due to greater degree of
pneumatisation of the maxillary sinus. In such cases, chances of
creation of oroantral fistula are greater during extraction of teeth
(Fig. 32.8).
• Oroantral fistula may be created in an attempt to remove the fractured
root from the socket.
• The shape of the tooth might be such that when extraction forceps are
applied, the tooth slips into the antrum like the popping of the ‘orange
seed’ held between the fingers.
• Periapical lesions of teeth: The periapical lesions which are in close
proximity with the sinus floor and necrotic lesion of the maxilla such
as noma may erode the sinus floor.
• Multiple and extensive fractures of the facial region.
• Osteomyelitis of the maxilla.
• Malignancy involving the maxillary sinus
• Removal of a large cyst or resection of large tumour involving maxilla.
FIGURE 32.8 Schematic diagram showing distobuccal root in close

proximity to maxillary sinus. (A) Decayed tooth. (B) Broken root
after extraction.
Extraction
• The most common reason of oroantral fistula is the iatrogenic, which

occurs while extracting the maxillary tooth. Roots of premolar, molar
and canine are close to the floor of sinus making them more
vulnerable.
• During teeth removal, if the root or the tooth is forced into the sinus,
oroantral fistula may form.
• Chronic periapical condition where there is loss of lamina dura the
apex of the tooth is in direct contact with the sinus lining. The lesion
destroys the sinus floor, creating oroantral fistula.
• Commonly the first maxillary molar tooth’s palatal root which breaks
during extraction might create an oroantral communication.
• During extraction, if a conical maxillary molar tooth slips into the
maxillary antrum, especially along the tuberosity fracture, an oroantral
perforation will form.
• Use of contaminated or diseased maxillary implant dentures forms the
fistula.
• Surgical removal of impacted teeth (maxillary third molar,
supernumerary), submerged, hypercementosis, geminated, diverged
root teeth carries the risk of inadvertent breech in continuity of
antrum.
• Apicoectomy of root which is adjoining with the sinus lining will
create OAF.
• Attempt to retrieve retained apices in posterior teeth by ‘blind
instrumentation’ might result in displacement of root into the
maxillary sinus through perforation.
• Implant dentures can cause considerable destruction of the antral floor
creating OAF.
Surgeries
• When the incision line during Caldwell-Luc procedure does not heal,
oroantral fistula may develop.
• Careless use of instruments during maxillary sinusitis surgery may
perforate the sinus mucosa and floor.
• Maxillary sinus surgery performed for removing a large abscess or
cystic lesion may lead to fistula formation.
• Marsupialisation (surgical conversion of a closed cavity into an open
pocket) performed on defective alveolar antral wall may also result in
the fistula.
• Orbital floor fracture treated by antral pack support by Caldwell-Luc
incision. Usually the end of the pack is sutured to the buccal vestibule,
and the pack is removed through the buccal vestibule creating the
orifice. If the orifice fails to heal it might lead to OAF.
• Partial maxillectomy (malignancy or antral neoplasm) involves the
removal of alveolus, part of palate and antral walls creating OAF.
Extensive facial trauma
• Extensive mid-facial trauma, particularly, because of sharp objects or

missiles inserted into the sinus via mouth will lead to oroantral fistula.
Even gunshot injuries/penetrating type of injuries affecting the sinus
walls creates huge defect resulting in OAF.
Neoplasms
• Malignant granuloma and other malignant disorders of the maxillary

sinus may erode the oral cavity.
• The tumours may penetrate the lateral wall of the sinus.
• Tumours of the upper jaw may reach into the sinus, forming the
fistula.
Syphilis:
Gummatous lesion of palate results in extensive OAF due to destruction of
bone. Secondary and tertiary form of syphilis involving nose may create OAF.
Osteomyelitis:
Osteomyelitis is commonly seen in mandible, but rarely the maxillary
osteomyelitis might occur in some systemic conditions like diabetes,
leukaemia, uraemia and irradiation.
Clinical features of acute oroantral fistula
• Fluid regurgitation and escape of air through the nose from the mouth.
• Unilateral epistaxis. This is due to escape of blood from the sinus into
the nose through the ostium.
• Enhanced column of air which causes a change in the vocal resonance
and consequently change in the voice.
• Severe pain in the involved region.
Investigations to confirm the presence of fistula
• Probing: A simple probe can be used to detect the presence of fistula.

However, injudicious use can create a fistula in healing tissue.
• Nose blowing test: A cotton wisp is kept near the fistulous opening and
the patient is asked to blow the nose with closed nostrils and open
mouth. In the presence of oroantral communication air will pass
through the defect and will displace the cotton wisp, whereas any
blood present will be seen to bubble.
• Mouth mirror test: The patient is made to perform valsalva manoeuvre,
with a mouth mirror placed facing the oral opening of fistula. If the
mirror gets fogged, it indicates presence of oroantral communication.
• Suction test: A suction nozzle when placed over the fistula will create a
sound similar to that produced by an empty bottle when it is blown.
This sound cannot be heard when the sinus is chronically infected.
• When the patient is asked to hold fluid within the mouth, fluid can be
seen escaping through the nose. Betadine can be mixed with the fluid
to differentiate between nasal secretion and rinsing fluid.
Management of acute oroantral fistula

The blood clot formed at the opening should be preserved to promote healing
and closure of the opening.
Surgical procedures for closure of oroantral fistula

If circumstances permit, bony defect should be covered with a mucoperiosteal
flap. All these flaps should follow the basic requirements of an ideal flap.
Types of flap which can be employed for the closure of oroantral fistula are
depicted in Table 32.2.
Table 32.2
Closure of oroantral fistula: types of flap
1. Buccal flap
a. Von Rehrmann flap
b. Moczair flap (sliding buccal flap)
2. Palatal flap
a. Ashley’s flap
b. Kruger’s modification of Ashley’s flap
3. Combination of buccal and palatal flaps
a. Bridge flap
4. Buccal pad of fat
5. Tongue flap
a. Posteriorly placed dorsal tongue flap
b. Laterally placed tongue flap
6. Turnover flap or hinge flap
7. Nasolabial flap
8. Gold foil
9. Polyglycolic acid mesh or Vicryl mesh
Immediate closure
The simplest method is primary closure of the socket by mucoperiosteal flaps,
obtained by reducing the height of the bony socket. The flaps are
approximated and are loosely sutured over the defect. This requires minimum
time, surgical skill and facilities and can be done in all cases at risk of oroantral
fistula (Figs. 32.9, 32.10).
FIGURE 32.9 (A–C) Immediate closure.

FIGURE 32.10 Immediate closure of large sinus opening in the
tuberosity region after extraction.
Buccal flap (Von Rehrmann flap) (Fig. 32.11):
• The fistulous tract is excised by placing an incision 2–3 mm around the

orifice. The entire epithelium of the fistula along with any nasal polyp
(as in chronic fistula) should be removed.
• Incisions are made on either side of the orifice and extended into the
buccal sulcus. Buccal vestibular height may be affected through this
procedure.
• Moczair flap: A modification of this flap where the buccal flap is raised
anterior to the defect, buccal of healthy teeth, following which the flap
is slided into the defect horizontally (buccal sliding flap).
• Whenever conditions permit, it is better to use an undercut buccal flap
lined with periosteum.
• A broad-based buccal flap is raised by means of subperiosteal
dissection, which is carried out well above the reflection of the mucous
membrane. A horizontal cut is then made through the periosteum
alone above the reflection and inherent elasticity of the mucous
membrane then permits the mucosa to be advanced and sutured to the
palatal mucoperiosteum without tension. It is convenient to incise the
periosteum with a No. 12 scalpel blade.
• Bleeding should be completely controlled to prevent any haematoma
formation inside the sinus.
• Horizontal mattress sutures should be employed for this purpose and
left in situ for 2 weeks.
• This is an excellent method of repair which, however, requires more
operating time and surgical skill and is often accompanied by some
postoperative haematoma formation and loss of depth in the buccal
sulcus.
FIGURE 32.11 (A–C) Closure of oroantral fistula using buccal flap.
Palatal flap (Ashley’s flap) (Fig. 32.12)

It is not always possible to cover oroantral communications situated high up in
the sulcus with a buccal flap, even when the soft tissues lying either behind or
in front of the defect are utilised. In such cases, it is often better to use a palatal
mucoperiosteal flap based upon its blood supply.
• The fistulous tract is excised as previously mentioned.

• The outline of the palatal flap should be marked and incised.
• The palatal flap should be elevated carefully preserving the greater
palatine artery. It is then rotated and approximated with the buccal
margin.
• Kruger’s modification: A back cut at the posterior end of the flap for ease
of rotation and avoid kinking.
• Palatal flaps tend to shrink when elevated from the bone and their
thickness and consistency make them more difficult to reposition than
buccal flaps.
• The bare bony base of the resultant palatal defect may be covered by a
pack, composed of Whitehead’s varnish on ribbon gauze, held in
position by means of mattress sutures inserted into the margins of the
attached mucoperiosteum.
FIGURE 32.12 (A–C) Illustrations showing closure of oroantral
fistula using palatal flap. (D–G) Intraoperative view showing the
closure of oroantral fistula using palatal flap. ( Scan to play
Oroantral fistula closure by Palatal Flap)
Whitehead’s Varnish:
• Benzoin 10 parts 44 g
• Storax 7.5 parts 33 g
• Balsam of tolu 5 parts 22 g
• Iodoform 10 parts 44 g
• Solvent—ether to 1 floz or 100 parts
Advantages
• The rich blood supply of the palatal flap provides satisfactory healing.
• Buccal vestibular height is unaffected. Hence, prosthetic rehabilitation
is unimpaired.
Combination method
In combination method, both buccal and palatal flaps are used to cover the
defect.
• Usually used when re-repair is required.

• The thick covering gives more strength and reduces shrinkage.
Pedicled buccal pad of fat

This procedure can be employed when all other methods had failed to yield
proper result.
• A circular incision is placed around the fistula and the epithelial lining
is removed.
• Two diverging vertical incisions are placed, one on mesial aspect and
one on the distal aspect of the fistula.
• Now the trapezoid-shaped buccal flap is elevated from the alveolar
bone to the depth of the vestibular sulcus.
• Buccal pad of fat can be exposed by a vertical incision of 1 cm long on
the posterior aspect of the zygomatic buttress region.
• Following this, the buccal pad of fat should be advanced along the
bony defect to be sutured in the margin of the palatal tissue without
any tension.
• Finally, buccal flap can be sutured over the pedicled buccal pad of fat
which derives its blood supply from the superficial temporal and facial
arteries.
Bridge flap (Figs. 32.13, 32.14)
• Commonly employed in edentulous maxilla.

• After excising the lining epithelium covering the fistulous tract,
incisions are placed transversely across the line of the arch.
• On the palatal aspect, length of the bridge is limited by the presence of
palatine artery.
• Buccally, flap can be elevated sufficiently and lifted over the fistula
without tension.
• The bridge must be wider than the bony defect.
• The bridge is shifted to cover the fistula and the raw area is allowed to
epithelialise.
FIGURE 32.13 (A–C) Pedunculated bridge flap is used to close the
oroantral fistula in an edentulous maxilla.
FIGURE 32.14 Bridge flap in partially edentulous maxilla. (A) CT
showing Infected right maxillary sinus in relation to the edentulous
region. Note the complete obliteration of the sinus by the infection.
(B) Oroantral fistula in relation to the right maxillary edentulous
region. (C) Excision of the fistulous tract. (D) Raising of the buccal
flap. (E) Removal of the thin necrotic bone. (F, G) Raising of the
palatal flap based on greater palatine artery. (H, I) Nasal
antrostomy. (J) Sinus cavity packed with betadine gauze. (K)
Primary closure of the communication. Note the raw area in the
palate which will heal by secondary epithelialisation. (L)
Postoperative view at the end of 2 weeks. (M) Postoperative view
at the end of 4 weeks showing complete secondary healing.
Postoperative care
1. The patient should be instructed to avoid blowing his/her nose.

2. Antibiotics and analgesics Antibiotics are used to eliminate any
infection and prevent any further infection of the sinus. Culture and
sensitivity test can be done to determine the appropriate antibiotic.
Analgesics are used to control postoperative pain.
3. Nasal drops and inhalations Ostium of the maxillary antrum is
situated high up on the wall of the sinus and decongestant nasal drops
and inhalations (e.g. ephedrine, benzoin) should be prescribed for use
by the patient whenever it is essential to ensure the patency of this
natural opening. This is necessary in the presence of maxillary sinusitis
and during the postoperative period after repair of an oroantral
communication.
Nasal drops should be instituted whenever a freshly created oroantral
opening has been repaired and should be continued until healing is
complete.
4. Mechanical support for the flap Whichever method is utilised to cover
the bony defect, additional support for the flap should be provided by
covering the area with either an acrylic extension to a denture or a
shellac base plate. The cover may be either ligated to adjacent teeth if
any are present or sutured to the soft tissue overlying edentulous
regions.
5. Nasal antrostomy It is performed by introducing a nasal rasp through
the nostril below the inferior turbinate bone. It enters the sinus when
force is applied. By moving the rasp back and forth, an oblong aperture
can be created for drainage of the cavity. Alternatively, nasoantral bone
may be removed with an osteotome and the nasal mucosa cut on three
sides, leaving it attached only at the floor of the nose so that it can be
folded into the antral cavity.
• Along strip of plain or iodoform tape saturated with
petrolatum (a uterine pack may be employed) is inserted. End
of the tape is pulled through the created stoma and hence the
nostril. Since it is to be taken out through the nose, it should
be carefully folded into the antral cavity to facilitate removal.
• Finally, the mucoperiosteal flap is replaced and primary
closure done.
Complications
The flap might breakdown, either due to poor blood supply owing to
improper design or by excessive suture tension. Condition of the antrum
should be reviewed carefully, especially if the antrum was not drained by
means of a nasoantral perforation. A new closure may be attempted after the
infection in the sinus has been cleared up.
Chronic oroantral fistula

A persistent acute oroantral communication may lead to a chronic oroantral
fistula. Any oroantral fistula present for more than a period of 15 days is known
as chronic oroantral fistula. Due to persistence of the communication, the sinus
gets infected by the oral microorganisms. Hence, goal of the treatment should
be eradication of the infection and closure of the fistula.
Clinical features
• Continuous unilateral foul smelling nasal discharge.

• Unpleasant taste may result due to discharge of postnasal drip down
the pharynx from the posterior nares.
• Systemic complication includes pyrexia, malaise, headache and
anosmia.
• Healing of fistulous tract will be delayed by projection of the polyp
from the antrum into the oral cavity.
Management
• The first aim of treatment is to eliminate any coexisting antral

infection. Oroantral reflux can be prevented by insertion of a well-
fitting acrylic base plate, which covers the defect without entering it.
• The antrum is washed out with warm normal saline, usually via the
fistula, twice weekly until a clean return is obtained. Decongestant
nasal drops and inhalations are prescribed for use by the patient and
antibiotic therapy is sometimes required.
• When treatment of this nature is employed most oroantral fistulae
shrink in size and may even heal spontaneously, especially if there is
any epithelium lining the track is removed either by cauterising the
track with a silver nitrate solution or trichloroacetic acid or by
freshening the edges of the fistulous track with a barbed broach.
• Antral lining is sometimes said to prolapse through any defect in the
bony wall of the maxillary air sinus. It has been proved that these soft
tissue projections are usually polypoid in nature. In vast majority of
instances careful examination will reveal presence of an oroantral
fistula and a chronically infected antrum. It is imperative that such
lesions should be biopsied and sent for histologic examination at the
earliest opportunity.
Caldwell-Luc procedure
George Caldwell (1893) and Henri Luc (1897) described a new method of
entering into the maxillary sinus where two separate openings are made, one
in the canine fossa to gain access to the antrum and other in the nasoantral
wall for drainage. Therefore, this procedure has been known as Caldwell-Luc
procedure.
Two radical antrum operations have been devised; one is Caldwell-Luc and
the other is Denker operation. In Denker operation, perforation in the canine
fossa is extended medially to include the piriform aperture and join the
window cut under the inferior turbinate bone. Caldwell-Luc operation is
preferred, since Denker operation frequently interferes with innervation of the
teeth.
Indications
The Caldwell-Luc procedure is used for:
• Removal of teeth and fragments of roots or impacted teeth in the antrum.

• Treatment of chronic maxillary sinusitis with polyps and cystic
degeneration of the mucosa.
• Excision of cysts and benign tumours of the maxillary sinus.
• For management of haematoma or haemorrhage in the maxillary sinus.
• To treat fractures involving floor of the orbit or anterior maxillary sinus
wall (transantral repair).
Instruments
Instruments especially needed for sinus surgery are:
• Retractors
• Nasal speculum
• Periosteal elevator
• Gouge
• Nasal trocar
• Kerrison or backbiting forceps
• Rongeurs
• Antral rasp
• Antrum curettes
Surgical procedure
(Figs. 32.15 and 32.16)
• Incision generally extends from apex of the canine down to near the
gingival margin and posteriorly to the second molar. In edentulous cases,
it is carried to and along the alveolar ridge.
• The incision should be larger than the window to be cut in the bone.
• The mucoperiosteum is then detached and retracted till the infraorbital
ridge taking care to preserve integrity of the infraorbital nerve.
• A small gouge is used to perforate centre of the canine fossa. This hole is
enlarged by means of rongeurs or backbiting (Kerrison) forceps until it is
large enough to allow introduction of at least the index fingers. The finger
is used to palpate the lining of the sinus.
• Blood and pus contained in the sinus are removed by means of the
aspirator. Bleeding may be arrested by inserting small sponges saturated
with adrenaline.
• The antrum is inspected using small light such as a nasopharyngoscope to
illuminate the antral walls. It facilitates inspection of the contents of the
sinus and helps to determine the state of the membrane lining it. This
method helps to find out foreign bodies, such as cotton or strips of gauze,
etc. pushed in through a tooth socket.
• If the entire antral membrane is thickened, hyperplastic or altered by
cystic degeneration and filled with polyps, all the diseased tissue should
be removed.
• Granulomatous tissue may be found on the floor of the sinus if an
abscessed tooth has been the cause of the infection or if a perforation had
been made while extracting a tooth tissue. A curette may be useful for
removing the inflammatory granulation.
• The socket should be allowed to fill with a healthy blood clot and finally
gingival margins may be approximated by a suture.
FIGURE 32.15 Caldwell-Luc operation.

FIGURE 32.16 (A–C) Removal of a third molar through Caldwell-
Luc procedure.
Traumatic disease
Haematoma in maxillary sinus (Fig. 32.17)
A fracture involving infraorbital artery or posterior superior alveolar vessels
injury frequently results in a haematoma formation in the maxillary sinus.
Usually haemorrhage stops spontaneously.
FIGURE 32.17 (A) CT section showing chronic sinusitis. Note the

thickened hyperdense sinus lining with central hypodensity of air.
(B) Haematoma in left maxillary sinus due to trauma. Note the air-
fluid demarcation.
Usually the blood, which accumulates in the maxillary sinus, is eliminated

by the activity of the ciliated epithelium of the antral membrane promoting
normal drainage through the ostium. If the haematoma is not removed,
infection might occur.
Radiologically this is evident by air-fluid demarcation in the CT scan, in
contrast to chronic sinusitis where the sinus lining appears as thickened hyper-
dense mass with central hypodensity of air.
Treatment
• Nasal decongestants.
• Uncontrolled bleeding into sinus with epistaxis may require surgical
haemostasis: Surgery consists of a Caldwell-Luc procedure by which
the bleeding vessel in the sinus is located. Oxidified cellulose is
applied and held in place by an iodoform pack, which is allowed to
protrude from the nostril. It may be withdrawn gradually or
completely.
Iatrogenic disease
Teeth displaced into sinus
Foreign body, which usually is displaced into the maxillary sinus is a tooth or
a fragment of a tooth root.
Aetiology
1. Absence of intervening bone in between the tooth root and antrum.

2. Aggressive instrumentation to retrieve fractured maxillary molar root.
3. Solitary maxillary molar around which the bone is dense and cortical,
extraction of which may lead to fracture of the alveolus.
4. The tooth may displace into the maxillary antrum during extraction just
like an orange seed if there is no intervening bone and the instrument
slips of the tooth.
Diagnosis
The root fragments do not always penetrate the membrane of the antrum.
Frequently they can be found between the membrane and the bony wall.
Sometimes a radiograph shows the root in the sinus when it actually is outside
between the bone and the mucoperiosteum. Apart from intraoral periapical
radiograph (IOPA), upper occlusal PNS (posterior nasal spine) view can also
be used.
Management
1. Powerful suction is kept at the entrance of the fistula and the root
recovered.
2. If the tooth is lying loose in the antrum, it can be removed by packing
roller gauze and withdrawing in a jerky motion.
3. Surgical approach (Caldwell-Luc operation). Saline is continuously
irrigated into the sinus through the window created by the Caldwell-
Luc procedure.
Formation of whirlpool inside the sinus is observed, which can displace the
root from its position and then it can be retrieved.
Antral rhinoliths
There are two types of rhinoliths:
i. Rhinoliths around an endogenous nucleus such as red blood cells or pus

cells.
ii. Rhinoliths formed around exogenous material such as roots of teeth or
any other foreign body. Salts required for formation of the rhinoliths
are from lacrimal secretions. Sometimes they are covered with
granulation tissue. They vary in colour from black to brown and lighter
shades. Diagnosis through radiograph may be difficult. Differentiation
from osteoma or odontoma must be made.
Treatment
Antral rhinoliths can be removed by buccal antrostomy and if infection is
present, by Caldwell-Luc procedure. Antibiotic therapy is indicated to prevent
or treat infection if present. The mass to be removed may be so large (giant
rhinoliths), in that case it must be crushed before removal.
Advances in the management of maxillary

sinus disease
Functional endoscopic sinus surgery (FESS)
Rhinology and sinus surgery have undergone a tremendous expansion since
the discourses of Messerklinger and Wigand in the late 1970s. Imaging
advances, increased understanding of the anatomy and pathophysiology of
chronic sinusitis and image guided surgery have allowed surgeons to perform
more complex procedures with increased safety. Functional endoscopic sinus
surgery (FESS) is a minimally invasive technique used to restore sinus
ventilation and one of the primary approach used today for the surgical
treatment of recurrent acute or chronic infective sinusitis. It is called functional
because it aims to return the working of the sinus to normal. This procedure is
usually reserved for use in patients in whom medical treatment has failed.
The goal of FESS is to return the mucociliary drainage of the sinuses to
normal function. The paranasal sinuses are maintained in a healthy state by
ventilation through the individual ostia and by a mucociliary transport
mechanism that keeps a continuous protective layer of mucus flowing out of
the sinuses.
Conventional sinus surgery versus functional endoscopic

sinus surgery
Functional endoscopic sinus surgery (FESS) differs from conventional surgical
approach in which:
It stresses a careful diagnostic work-up to identify the underlying cause.
• Surgery is less extensive.

• Less removal of normal tissues.
• Surgery can frequently be performed on an outpatient basis without
the necessity for nasal packing.
• Better visualisation is obtained during surgery by the use of
endoscopes.
• Reduced scar tissue formation and nerve damage to the teeth.
Preoperative assessment
Cornerstone of accurate diagnosis and treatment is thorough history and a
complete physical examination, including nasal endoscopy. Before considering
surgery, evaluation should clearly indicate that chronic sinusitis is responsible
for the patient’s symptoms.
Indications
Endoscopic sinus surgery is most commonly performed for inflammatory and
infectious sinus diseases. Most common indications for endoscopic sinus
surgery are:
• Chronic sinusitis refractory to medical treatment

• Recurrent sinusitis
• Nasal polyposis
• Antrochoanal polyps
• Sinus mucoceles
• Excision of selected tumours
• Cerebrospinal fluid (CSF) leak closure
• Orbital decompression (e.g. Graves’ ophthalmopathy)
• Optic nerve decompression
• Dacryocystorhinostomy (DCR)
• Choanalatresia repair
• Foreign body removal
• Epistaxis control
Contraindications
• Orbital abscess
• Frontal osteomyelitis with Pott’s puffy tumour.
• Previously failed endoscopic procedures associated with CSF
rhinorrhoea and frontal sinus disease.
• Nasal and sinus malignancies.
Procedure
• After suitable vaso constriction using cocaine or ephedrine, middle

turbinate is identified. This is the most important landmark for the
procedure.
• Uncinectomy: FESS may begin with uncinectomy either by direct
visualisation of the uncinate process or by medialisation of the middle
turbinate. On the lateral wall of the nose at the level of the anterior end
of the middle turbinate lies the uncinate process Uncinectomy is
performed at the most anterior portion of the uncinate process in order
to avoid incising the nasolacrimal duct and grasped using Blakeseley
forceps and then removed. Complete uncinectomy is important
otherwise it will lead to failure of the surgery which is the most
common cause.
• Maxillary antrostomy: Now the maxillary sinus ostium can be easily
identified and visualised following uncinectomy. It is usually at the
level of the inferior edge of the middle turbinate. A sharp cutting
instrument is used circumferentially to enlarge the maxillary ostium to
a diameter of 1 cm so that it allows adequate outflow. Care should be
taken to avoid penetrating into the lamina papyracea.
• Anterior ethmoidectomy: Next, the ethmoid bulla should be identified
and opened. A J-shaped curette may be used to open the bulla at its
interior and medial aspect. Then the Anterior ethmoid air cells are
opened, allowing better ventilation but leaving the bone covered with
mucosa. This minimal surgery will often be sufficient to greatly
improve the function of the ostiomeatal complex and therefore
provide better ventilation of the maxillary, ethmoidal and frontal
sinuses.
• If the sinus disease is limited to the anterior ethmoid cells and the
maxillary sinus, the procedure may end with simple anterior
ethmoidectomy and maxillary antrostomy and if radiographic
interpretation shows disease spread to the posterior ethmoidal and
sphenoidal cells, then dissection should further continue with
posterior ethmoido-frontosphenoidectomy.
• Once the procedure is complete and haemostasis is achieved, an
antibiotic gauze pack is placed into the nostril.
Postoperative care
• Nose should be kept free from build-up of crusts as much as possible.

• In patients with gross inflammation or polyps, a short course of
systemic steroids combined with antibiotics will hasten postoperative
recovery.
• Nasal packing is removed prior to discharge of the patient.
• The patient is to be discharged with nasal spray and antibiotics, as well
as instructions for a follow-up visit in 1 week.
• If a spacer was placed in the middle meatus, it should be removed or
suctioned away on the first postoperative visit.
• Bleeding
• Synechiae formation
• Orbital injury
• Diplopia
• Orbital haematoma
• Blindness
• CSF leak
• Direct brain injury
• Nasolacrimal duct injury/epiphora
• Orbital haematoma/postoperative proptosis requires immediate
removal of nasal packing, urgent ophthalmologic consultation and
emergency lateral canthotomy.
Extended uses of FESS
• Endoscopic dacryocystorhinostomy
• Endoscopic orbital decompression
CHAPTER 33
Orofacial Cleft
Prevalence
Evolution of theories of cleft embryo pathogenesis
Normal and abnormal morphogenesis of the lip and primary
palate
Normal and abnormal morphogenesis of the secondary palate
Classifications of oral and facial clefts
Tessier’s classification of orofacial clefts
Genes
Inheritability
Associated anomalies
Syndromic clefts
Unilateral cleft lip
Nose
Lip
Bilateral cleft lip
Nose
Lip
Cleft palate
Hard palate
Soft palate
Problems faced by cleft children and their management
Management of patients with cleft lip and palate
Sequence of procedures
Primary correction
Feeding plate
Presurgical orthopaedics
Nasoalveolar moulding
• Unilateral cleft lip
• Bilateral cleft lip
Lip adhesion
Lip repair
Evolution of lip repair
Unilateral cleft lip repair
Tennison triangular flap
• Advantages
• Disadvantages
Millard rotation advancement repair
• Advantages
• Disadvantages
Delaire technique of muscular reconstruction (functional
repair)
Noordhoff technique
Primary unilateral cleft nose repair
Bilateral cleft lip repair
Techniques
Primary bilateral cleft nose repair
Palate repair
History
Timing of repair
Procedures
Von Langenbeck operation
Wardill–Kilner–Veau Operation
Closure of palatal fistulae
Symptoms
Timing of closure
Procedure
Velopharyngeal incompetence
Normal VP function and the defect
Treatment
• Prosthetic management of VPI
• Surgical management of velopharyngeal
incompetence (pharyngoplasty)
Speech therapy
Gingivoperiosteoplasty
Primary bone grafting
Secondary alveolar bone grafting
Goals of secondary alveolar bone grafting
Bone grafting
Procedure
Primary bone grafting, premaxillary setback
Alveolar distraction osteogenesis
Orthodontic treatment
Aims of orthodontic treatment for children with clefts
Distraction osteogenesis
Distraction osteogenesis in cleft maxillary hypoplasia
Rhinoplasty
Nose revision
Nose tip
Nasal septum
Lip scar revision
Abbe flap
Prosthesis for cleft patients
Types of prosthesis
Head gears
Pharyngeal obturators
Fixed and removable partial dentures
Dental implants
Congenital deformities
The abnormalities in the appearance or function that occur due to unusual
occurrence(s) in the embryological development sequence during the
intrauterine period.
Cleft lip
A congenital deformity that presents as an abnormal lack of continuity of the
lip musculature, lip skin and the mucous membrane. The unusual breach can
extend from the base of the nose to the free margin of the lip. The deformity
may range from a simple notch at the free margin to a complete disjointed lip
that also results in a nasal deformity. This most commonly occurs in the upper
lip (Fig. 33.1A–B).
FIGURE 33.1 (A) Incomplete cleft lip. (B) Complete cleft lip.
Microform cleft
A mild abnormality of the (upper) lip that may or may not be due to an
aberrance or discontinuity in the lip musculature. It may manifest as a ridge-
shaped philtral column (Fig. 33.2).
FIGURE 33.2 Microform cleft lip.

Cleft palate
An abnormal discontinuity in the palatal musculature, mucous membrane
with or without involvement of the hard palate, that may extend from the
uvula to the alveolus (Fig. 33.3).
FIGURE 33.3 Cleft palate.
Simonart’s band
In some complete clefts, the nasal floor on the cleft side is sometimes bridged
by skin giving an appearance of an intact nasal sil. This band of skin is termed
Simonart’s band (Fig. 33.4).
FIGURE 33.4 (A–B) Simonart’s band.

Submucous cleft
A cleft or discontinuity that is present only in the palatal musculature without
any breach of mucous membrane.
A condition in which the velopharyngeal closure (required for intelligible
speech) that is produced by posterior and superior movement of the soft
palate by the contraction of the levator veli superioris and the medial and
anterior movement of the pharyngeal walls by the contraction of the superior
pharyngeal constrictor is impaired resulting in nasal twang in speech. This
condition is often found in patients with cleft palate.
Palatal fistula
A breach in continuity of the palate that results in an abnormal communication
between the nasal cavity and the oral cavity. It can also be of traumatic or
oncogenic origin (Fig. 33.5).
FIGURE 33.5 Palatal fistula.
Oronasal fistula
An abnormal breach in continuity on the floor of the nose that forms a
communication between the anterior nasal airway and the buccal sulcus.
Alveolar cleft
An abnormal breach in continuity of the alveolar bone of the maxilla occurring
most commonly in the region between the lateral incisor and canine that may
manifest as a simple notching of the alveolus to a complete discontinuity
resulting in a fistulous tract between the nasal floor and the mouth (Fig. 33.6).
FIGURE 33.6 Alveolar cleft with oronasal fistula.
Prevalence
Cleft lip is the most common congenital deformities of the face. WHO report of
the International Collaborative Research on Craniofacial Anomalies (2001)
states that a child is born with a cleft somewhere in the world approximately
every 2½ min. The available data that were included in the systematic review
of literature and major international registries published in 2012 indicate an
average prevalence of approximately 1 in 700 live births. The ethnic and
geographical variation ranges from 3.4 to 22.9 per 10,000 births.
The studies that were conducted abroad were collected from registries. In
India, a population study conducted in 2001 at Andhra Pradesh which
calculated the incidence of clefts in each district by registering the total
number of live births in each district and dividing it by the number of children
who had clefts and were below 1 year in the same district at Andhra Pradesh
shows an incidence of 1.09 in 1000 live births which is significantly less than
the Caucasian and Filipino population studies and significantly higher than in
African population.
Evolution of theories of cleft embryo

pathogenesis
1. His’ theory: The classical doctrine of Wilhelm His (1874) concerning the
formation of the face stated that the ‘mid-portion is occupied by the
oral cavity which is remarkably wide and angular; the lateral borders
are formed by two maxillary processes. Above the mouth, the large
expanse of the frontal process is found. Two clefts originate from the
mouth on each side and end as blind pits. The first of these is the nasal
cleft, which runs up into the frontal process to form the olfactory pit.
The second cleft lies between the frontal process and the maxillary
processes and ends up at the lens placode to become the nasooptic
furrow. The nasooptic furrow remains open for some time, but
eventually closes to form the nasolacrimal duct’.
2. Based on His’ theory, Arey (1947) hypothesised cleft lip as failure of
fusion of the median nasal and maxillary processes, supported by Patten
(1961) who stated, ‘it is quite obvious that such a (cleft) lip is located at
the line where, during the second month of development, the maxillary
process should have fused with the naso-medial process’.
3. Mesodermal reinforcement of branchial membranes—conceptual
sequence (Stark theory).
a. Oral dimple pushes ectoderm into the stomadeum.
b. Endoderm of the primitive gut lines the other side near the
diverticulum.
c. Upper lip exists as bilamellar branchial membrane: both
laminae consisting of ectoderm (epithelial wall of
Hochstetter and Veau).
d. Branchial membranes represent transient structures which
are reinforced and filled out by mesoderm in the period of
organogenesis (first trimester).
e. The mesoderm will form bone, cartilage, muscle, nerve,
blood vessels and lymphatics.
f. The mesoderm migrates around both sides of the head as
well as over it.
g. Failure of mesodermal delivery from the migratory route
over the head results in forebrain maldevelopment or
arhinencephaly (Fig. 33.7), in which at least the olfactory
lobes are deficient and there will be associated medial cleft
of the lip.
h. Mesodermal deficiency of the malar region: Treacher
Collins syndrome
i. Deficiency in the first branchial arch: Macrostomia,
hemignathia, preauricular tags, etc.
j. Mesodermal reinforcement of branchial membranes is
necessary. When sufficient deposit of mesoderm is made,
the bilamellar membrane splits apart. When reinforcement
fails totally, ectoderm rupture is complete. Partial
reinforcement results in partial rupture.
4. Neuromeric theory (Michael Carstens): The human embryo has its own
neuroanatomical map for embryogenesis. The embryonic central
nervous system develops in discrete segmental craniocaudal units of
neural crest cells called neuromeres.
• Lip closure involves mesenchymal ‘flow’ from the lateral lip
elements towards the prolabium. For this to occur, the
epithelium covering the lateral lip element, the skin bridge
(nasal floor) and prolabium must undergo a genetically
induced breakdown.
• Foetal epithelial and mesenchymal tissues interaction is
regulated by the expression of:
▪ Signalling molecules: members of transforming
growth factor beta (TGFβ), fibroblast growth factor
(FGF), sonic hedgehog (Shh), Wnt and tumour
necrosis factor (TNF).
▪ Transcription factors: Msx1, Pax9, Osr2, Runx2,
Twist-1, etc.
• There are three forms of protein (called Sonic hedgehog
[SHH], Indian hedgehog and Desert hedgehog) coming from
three different genes playing an important role in craniofacial
development.
• The function of SHH is to maintain epithelial stability.
• In order for the mesodermal facial processes to fuse as they
come into proximity to each other, there must be epithelial
breakdown at their leading edges. Interaction between the
SHH present in the soft tissues and bone morphogenic protein
type 4 (BMP4) produced by the underlying bone is the key to
the relationship between bone and soft tissue clefts.
• The absence or deficiency of an appropriate BMP4 signal will
lead to restricted expression of SHH, abnormal persistence of
epithelium and failure of mesenchymal fusion.
• If a bony cleft is present, a local reduction in BMP4 will lead to
persistent epithelialisation of the facial processes an inability
to fuse.
FIGURE 33.7 Hemiarhinia with cleft palate.

Normal and abnormal morphogenesis of the lip
and primary palate
Central face development begins with the appearance of nasal placodes as
local ectodermal thickening on either side of the inferior aspect of the
frontonasal process.
The neural crest-derived mesenchyme soon condenses and proliferates at
the border of the placode. The lateral and medial rims expand outwards to
form a pit or a groove. The nasal pit becomes deeper as the lateral and the
medial processes grow and it is further bounded on its floor by maxillary
process of first branchial arch.
Definitive formation of primary palate begins at the bottom of the nasal pit
with the meeting of medial surface of the lateral process and lateral surface of
the medial process. The apposed epithelia form an epithelial seam that is
almost immediately obliterated by autolysis and replaced by mesenchyme.
About the same time, medial processes converge with each other and form an
epithelial seam, which is also autolysed and replaced by mesenchyme.
Continued expansion of the mesenchymal cell population helps to give rise to
the eventual smooth contour of the upper face.
• By day 24, one can clearly identify the frontonasal process which is
bounded on each side by a pair of first arch-derived maxillary process.
• By day 28, the nasal placode is evident.
• By day 33, the nasal pit is deep and prominently bounded by the medial
and lateral processes.
• The maxillary processes grow rapidly and soon approach each other at
the medial process. The primary palate forms at the bottom of the nasal
pit with the meeting of the medial surface of the maxillary process and
lateral surface of the medial process.
• By days 40–48, fusion of lateral processes occur more superiorly and
anteriorly with the medial process. At the same time, the medial processes
merge with each other to form the intermaxillary segment. This segment
gives rise to the philtrum and the premaxilla, an area of the palate
bounded by two lines from the incisive foramen to the alveolar bone
between the lateral incisor and canine on each side. The lateral parts of
the upper lip, the maxilla and the secondary palate are formed from the
maxillary processes.
• By the 14th week of development, the facial contour of the newborn is
virtually complete.
Pathogenic mechanisms that are associated with abnormal primary palate

formation (cleft lip) in humans are currently mere speculation. From the above
description, it should be obvious that the critical aspects of development are
the convergence of facial processes, appearance in the right place, achieving
the correct shape and size and having no obstruction to fusion.
There is some evidence that the lateral process is deficient in human
embryos with cleft lip with or without palate (CL ± P). There are, of course,
many other possibilities and it is likely that in humans the pathogenesis of
CL ± P is quite heterogeneous.
Normal and abnormal morphogenesis of the

secondary palate
Human palate is derived from two projections from the paired maxillary
processes of the first branchial arches, termed ‘palatal shelves’. Initially these
shelves are in a vertical position on each side of the developing tongue, but as
the mandible grows, the tongue moves downwards and the shelves become
more horizontal and grow towards each other. By the 8th week of
development, the shelves have grown sufficiently large to approximate each
other and begun to fuse anteriorly. Fusion is completed posteriorly by the 17th
week of embryonic life.
These shelves also fuse with the primary palate and the nasal septum, which
develops as a downgrowth from the merged medial processes. During fusion
of all these structures, the apposed epithelia form an epithelial seam that soon
breaks down and allows complete fusion and mesenchymal continuity.
Many extracellular and cell surface molecules are thought to be involved in
palatal development, some of which are sure to be critical to such cell–cell
interactions as adhesion, organisation and communication. One possible
molecule is histocompatibility cell surface antigens.
Experiments in mice regarding these antigens (called H-2) have shown
patterns characteristic of progressive stages of embryonic palate development.
Shelves in the vertical position have showed a diffuse fluorescent staining for
H-2 in the mesenchyme. Upon palatal shelf elevation with epithelial fusion
and subsequent breakdown, the fluorescent staining for H-2 is localised
beneath the nasal epithelium only. Certainly, other important molecules are
involved in palatal development.
This example illustrates that without a molecular understanding of palate
formation, we do not have the complete understanding of the process. Much
work remains to be done. As with the development of the primary palate,
secondary palate formation is complex and there are numerous potential
possibilities for developmental failure:
• A structural abnormality within the shelves would prevent their

movement to the horizontal position.
• The shelves could be normal but too narrow and thus unable to meet
each other in the midline.
• A reduction in shelf force would bring about a delay in their
movement to the horizontalisation, causing an opportunity to be
missed for fusing at the appropriate developmental time.
• Anything that interferes with the displacement of the tongue from
between the shelves at the right time would delay or prevent that
shelves from becoming horizontal.
• Disproportionate growth of the head could make it wider than normal,
so that the shelves would fail to reach each other.
• The epithelia of the shelves could fail to fuse for various cellular and
molecular reasons. The pathogenesis of human palatal clefting is, like
that of the lip, certain to be heterogeneous.
Finally, it should be noted that cleft palate which is frequently associated

with cleft lip is thought to be a secondary malformation that results from
mechanical obstruction by the tongue. The lip defect results in a large
premaxilla in the region of the primary palate, which appears to stop the
tongue from moving forward and downward. Instead, it remains arched
between the shelves and obstructs their horizontal movements and subsequent
fusion.
The cleft lip results from failure of the medial nasal and maxillary processes to
fuse between the 4th and the 6th week of foetal development. Clefting of the
palate results when the left and right palatal processes fail to elevate and fuse
in the midline between the 8th and the 12th week of foetal development.
It is generally accepted that the majority of clefts are a product of both a
genetic susceptibility and an environmental insult to the developing foetus.
Classifications of oral and facial clefts

Name and Classification Scoring
year
Davis and Group I: Prealveolar cleft
Ritchie Group II: Postalveolar cleft
(1922) Group III: Alveolar cleft
Veau (1931) Group 1: Cleft of soft palate only
Group 2: Cleft of the hard and soft palate extending no further than the
incisive foramen, thus involving the secondary palate alone
Group 3: Complete unilateral cleft, extending from uvula to the incisive
foramen, thus the uvula to the incisive foramen in the midline, then
deviating to one side and usually extending through the alveolus at the
position of the future lateral incisor tooth
Group 4: Complete bilateral cleft, resembling Group 3 with two clefts
extending from the incisive foramen through the alveolus
Kernahan A. Incomplete cleft of the secondary palate
and Stark B. Complete cleft of the secondary palate (extending as far as the incisive
(1958) foramen)
C. Incomplete cleft of the primary and secondary palate
D. Unilateral complete cleft of the primary and secondary palate
E. Bilateral complete cleft of the primary and secondary palate
Primary palate: Prolabium, premaxilla and anterior septum
Secondary palate: Incisive foramen to uvula
Harkins’ 1. Cleft of primary palate
and a. Cleft lip
associates i. Unilateral: Right, left (Extent: one-third, two-thirds, complete)
(1962) ii. Bilateral: Right, left (Extent: one-third, two-thirds, complete)
iii. Median (Extent: one-third, two-third, complete)
iv. Prolabium: Small, medium, large
v. Congenital scar: Right, left, median (one-third, two-thirds,
complete)
b. Cleft of alveolar process
i. Unilateral: Right, left (Extent: one-third, two-thirds, complete)
ii. Bilateral: Right, left (Extent: one-third, two-thirds, complete)
iii. Median (Extent: one-third, two-thirds, complete)
iv. Submucous: Right, left, median
v. Absent incisor tooth
2. Cleft of palate
a. Soft palate
i. Posteroanterior: One-third, two-thirds, complete
ii. Width: Maximum (mm)
iii. Palatal shortness: None, slight, moderate, marked
iv. Submucous cleft (Extent: one-third, two-thirds, complete)
b. Hard palate
i. Posteroanterior (Extent: one-third, two-thirds, complete)
ii. Width: Maximum (mm)
iii. Vomer attachment: Right, left, absent
iv. Submucous cleft (Extent: one-third, two-thirds, complete)
3. Mandibular process clefts
a. Lip extent: One-third, two-thirds, complete
b. Mandible (Extent: one-third, two-thirds, complete) Lip pits:
Congenital lip sinuses
4. Naso-ocular: Extending from the narial region towards the medial
canthus
5. Oro-ocular: Extending from angle of the mouth towards the palpebral
fissure
6. Oro-aural: Extending from the angle of the mouth towards the tragus
of ear
Pfeiffer Incomplete cleft was stippled and complete cleft was striped using the
(1966) schematic diagram.
Kernahan The striped Y classification: The involved area is filled in by pen and
(1971) provides graphic demonstration of the site and extent of cleft
involvement. The arms of the Y represent the primary palate (the lip,
alveolar process to the incisive foramen) and the stem of the Y
represents the secondary palate, posterior to the incisive foramen.
Stippling the appropriate segments is employed to show the extent of
gross clefts; and the horizontal lines, possible submucous Simonart’s
bands.
1. Right lip
2. Right alveolus
3. Right alveolar process to the incisive foramen
4. Left lip
5. Left alveolus
6. Left alveolar process to the incisive foramen
7. Hard palate
8. Hard palate
9. Soft palate
Elsahy, 1973 Triangle 1: Triangle 5: Left
Modification Right nostril nostril floor
of Kernahan floor Square 6: Left lip
Square 2: Square 7: Left
Right lip alveolus
while Square 8: Hard
Square 3: palate on the
Right left side
alveolus anterior to
Square 4: incisive
Hard palate foramen
anterior to
the incisive
foramen on
the right
side
Squares 9 and 10: Hard palate

Square 11: Soft palate
Circle 12: Posterior pharyngeal wall (to show VPI)
Circle 13: Premaxilla (to show protrusion of the premaxilla)
Spina (1974) Group 1: Preincisive foramen clefts (clefts lying anterior to the incisive
foramen)
Clefts of the lip with or without an alveolar cleft
a. Unilateral
i. Right and left (total when they reach the alveolar arcade or partial)
b. Bilateral
i. Total
ii. Partial (on one or both sides)
c. Median
i. Total
ii. Partial
Group 2: Transincisive foramen clefts (clefts of the lip, alveolus and
palate)
a. Unilateral (right/left)
b. Bilateral
Group 3: Postincisive foramen clefts
a. Total
b. Partial
Group 4: Rare facial clefts

Millard Nasal floor was included in Kernahan’s striped Y for further clarity. He
(1977) added inverted triangles atop the upright triangular segments 1 and 5
to stand for the right and left aspects of the nasal arch, respectively. In
his symbolic representation, horizontal lines in these nose segments, of
density proportionate to the degree on nasal deformity, can be used to
mark it. Horizontal lines can also be employed to show submucosal
clefts. Stripling depicts overt clefts
Schwartz This system is Comparative table showing three ways of listing all 63 possibilities
(RPL— based on the of clefting
Right- Kernahan Y Description of Anatomic components (Kernahan) RPL
Palate-Left and classifies the type of cleft system
System), clefts using anatomic
1992 three digits components
(one for the L LIP 4 1
left side of the L LIP + L ALV 45 2
Y, another for L LIP + L ALV + 456 3
the right side L PRMX
and a third for SUBMUC 9 10
the base of the L LIP + SUBMUC 49 11
Y). Each digit L LIP + L ALV + 459 12
may assume a SUBMUC
value between L LIP + L ALV + 4569 13
1 and 3,
PRMX +
reflecting the
SUBMUC
number of
affected S PAL + 89 20
components SUBMUC
in each limb
of the Y. They L LIP + S PAL + 489 21
listed 63 SUBMUC
possibilities of L LIP + L ALV + 4589 22
clefting and S PAL +
scored them SUBMUC
based on L LIP + L ALV + 45689 23
Kernahan’s L PRMX + S PAL
system + SUBMUC
H PAL + S PAL + 789 30
SUBMUC
L LIP + H PAL + 4789 31
S PAL +
SUBMUC
L LIP + L ALV + 45789 32
H PAL + S PAL +
SUBMUC
L LIP + L ALV + 456789 33
L PRMX + H
PAL + S PAL +
SUBMIC
R LIP 1 100
R LIP + LIP 14 101
R LIP + L LIP + 145 102
ALV
R LIP + L LIP + L 1456 103
ALV + L PRMX
R LIP + SUBMUC 19 110
R LIP + L LIP + 149 111
SUBMUC
R LIP + LIP + L 1459 112
ALV + SUBMUC
R LIP + L LIP + L 14569 113
ALV + L PRMX +
SUBMUC
R LIP + S PAL + 189 120
SUBMUC
R LIP + L LIP + S 1489 121
PAL + SUBMUC
R LIP + L LIP + L 14589 122
ALV + S PAL +
SUBMUC
R LIP + L LIP + L 145689 123
ALV + L PRMX +
S PAL +
SUBMUC
R LIP + H PAL + 1789 130

S PAL +
SUBMUC
R LIP + L LIP + H 14789 131
PAL + S PAL +
SUBMUC
R LIP + L LIP + L 145789 132

ALV + H PAL + S
PAL + SUBMUC
R LIP + L LIP + L 1456789 133
ALV + L PRMX +
H PAL + S PAL +
SUBMUC
R LIP + R ALV 12 200
R LIP + R ALV + 124 201
L LIP
R LIP + R ALV + 1245 202
L LIP + L ALV
R LIP + R ALV + 12456 203
L LIP + L ALV +
L PRMX
R LIP + R ALV + 129 210
SUBMUC
R LIP + R ALV + 1249 211
L LIP SUBMUC
R LIP + R ALV + 12459 212
L LIP + L ALV +
SUBMUC
R LIP + R ALV + 124569 213
L LIP + L ALV +
L PRMX +
SUBMUC
R LIP + R ALV + 1289 220
S PAL +
SUBMUC
R LIP + R ALV + 12489 221
L LIP + S PAL +
SUBMUC
R LIP + R ALV + 124589 222
L LIP + L ALV +
S PAL +
SUBMUC
R LIP + R ALV + 1245689 223
L LIP + L ALV +
L PRMX + S PAL
+ SUBMUC
R LIP + R ALV + 12789 230

H PAL + S PAL +
SUBMUC
R LIP + R ALV + 124789 231
L LIP + H PAL +
S PAL +
SUBMUC
R LIP + R ALV + 1245789 232
L LIP + L ALV +
H PAL + S PAL +
SUBMUC
R LIP + R ALV + 12456789 233

L LIP + L ALV +
L PRMX + H
PAL + S PAL +
SUBMUC
R LIP + R ALV + 123 300
R PRMX
R LIP + R ALV + 1234 301
R PRMX + L LIP
R LIP + R ALV + 12345 302
R PRMX + L LIP
+ L ALV
R LIP + R ALV + 123456 303
R PRMX + L LIP
+ L ALV + PRMX
R LIP + R ALV + 1239 310
R PRMX +
SUBMUC
R LIP + R ALV + 12349 311
R PRMX + L LIP
+ SUBMUC
R LIP + R ALV + 123459 312
R PRMX + L LIP
+ L ALV +
SUBMUC
R LIP + R ALV + 1234569 313
R PRMX + L LIP
+ L ALV + L
PRMX +
SUBMUX
R LIP + R ALV + 12389 320
R PRMX + S PAL
+ SUBMUC
R LIP + R ALV + 123489 321
R PRMX + L LIP
+ S PAL +
SUBMUC
R LIP + R ALV + 1234589 322

R PRMX + L LIP
+ L ALV + S PAL
+ SUBMUC
R LIP + R ALV + 12345689 323
R PRMX + L LIP
+ ALV + L +
PRMX + S PAL +
SUBMUC
R LIP + R ALV + 123789 330
R PRMX + H
PAL + S PAL +
SUBMUC
R LIP + R ALV + 1234789 331
R PRMX + L LIP
+ H PAL + S PAL
+ SUBMUC
R LIP + R ALV + 12345789 332
R PRMX + L LIP
+ L ALV + H PAL
+ S PAL +
SUBMUC
R LIP + R ALV + 123456789 333
R PRMX + L LIP
+ L ALV + L
PRMX + H PAL +
S PAL +
SUBMUC
SUBMUC
ALV, Alveolus; PRMX, premaxilla; H PAL, hard palate; S PAL, soft
palate; SUBMUC, submucous palate.
Friedman #1, 6: Nostril #5, 10:

(1991) arch Preincisive
(including trigone
ala) 0 = no
#2, 7: Nasal involvement
floor 1 = partial cleft
(including 2 = complete cleft
sill) X = not rated
0 = no
involvement
1 = cleft
microform
2 = mild
deformity
3 = moderate
deformity
4 = severe
deformity
X = not rated
#14, 15: #11: Hard palate

Prolabium 0 = no
0 = no involvement
protrusion 1 = posterior 1/3
1 = mild cleft
protrusion 2 = posterior 2/3
(≤45°) cleft
2 = moderate 3 = complete cleft
protrusion X = not rated
(>45°, <90°)
3 = severe
protrusion
(≥90°)
X = not rated
#3, 8: Upper #12: Soft palate

lip or velum
0 = no 0 = no
involvement involvement
1 = cleft 1 = cleft
microform microform of
(a, b)1 uvula (a, b, c)4
2 = 1/3 cleft lip 2 = submucous
3 = 2/3 cleft lip cleft of velum
4 = complete (a, b)5
cleft lip 3 = posterior 1/3
X = not rated of velum
4 = posterior 2/3
of velum
5 = complete cleft
of velum
of velum
X = not rated
#4, 9: #13:
Alveolus Velopharyngeal
0 = no valve function
involvement 0 = no
1 = cleft impairment
microform 1 = mild
(a, b)2 impairment
2 = partial 2 = moderate
cleft impairment
3 = complete 3 = severe
cleft (a, b)3 impairment
X = not rated X = not rated
NOTES:
1. Record as:
1a = subcutaneous cleft
1b = notch in the vermilion border
2. Record as:
1a = submucous cleft
1b = notch
3. Record as:
3a = absence of maxillary arch collapse
3b = presence of maxillary arch collapse
4. Record as:
1a = hypoplasia of musculus uvulae
1b = septate uvulae
1c = bifid uvulae
5. Record as:
2a = overt
2b = occult
Mortier and Mortier et al. developed a dual
Martinot scale, which included two
(1997) indicators: one corresponding to
the severity of the cleft (ISS or
initial severity score) and another
related to the surgical result (PRS
or postoperative results score).
This indicator considered seven
features to describe the patient.
A comparison of the ISS and PRS
allows for more objective
judgment of the surgical result.
However, it has been applied
only to unilateral incomplete
clefts of the primary palate
Ortiz– A mathematical expression was
Posadas developed to characterise clefts
et al. (2001) of the primary palate, including
the magnitude of palatal
segment separation and the
added complexity of bilateral
added complexity of bilateral
clefts, yielding a numerical score
that reflects overall complexity of
the cleft. Clefts of the secondary
palate are also considered in a
separate score
Percy UCL nose
Rossell– Mild: Only horizontal
Perry (2009) displacement of the nose on the
cleft side
Moderate: Horizontal and
vertical displacement of the
nose
Severe: Horizontal, vertical and
posterior displacement of the
nose
BCL nose
Mild: Columellar length is 2/3 to
1/3 of nasal height
Moderate: Columellar length is
up to 1/3 of nasal height
Sever: There is no visual
evidence of the columella
UC lip
Mild: Cupid’s bow rotation less
than 30°
Moderate: Cupid’s bow rotation
between 30° and 60°
Severe: Cupid’s bow rotation
greater than 60°
BC lip
Mild: Prolabium height if 2/3 of
lateral lip segment heights
Moderate: Prolabium is between
2/3 and 1/3 of lateral lip
segment height
Severe: Prolabium height is less
than 1/3 of lateral lip segment
height
Primary palate
Mild: Difference is less than
5 mm
Moderate: Difference between 5
and 10 mm
Severe: Difference greater than
10 mm
Secondary palate
If X is cleft width measured at
hard palate posterior border
level Y is sum of breadths of
palatal segment diameter
measured at the same lever as
X, A ratio is computed: X/Y
Mild: Ratio less than 0.2
Moderate: Ratio between 0.2 and
Moderate: Ratio between 0.2 and
0.4
Severe: Ratio greater than 0.4
Tessier’s classification of orofacial clefts

The breach in continuity that occurs at birth at any other part of the face other
than the lip is termed orofacial clefts. These are also called Tessier’s clefts since
Paul Tessier was one of the first to classify them and his classification is still
used by many (Fig. 33.8).
FIGURE 33.8 Tessier’s craniofacial clefts.
Tessier 0–14. The midline cleft is a median craniofacial dysrhaphia. The cleft
involves median encephalocele, the ethmoid (duplication of the crista galli),
the nose (duplication/pneumatisation of the septum and columella), maxilla
and lip. Absence of prolabium of lip and premaxilla. Absence of columella
giving impression of arhinencephaly. Hypertelorism or hypotelorism may be
present due to the absence of premaxilla (Fig. 33.9).
FIGURE 33.9 Tessier 0, 14.
Tessier 1–13. It is paramedian craniofacial cleft. It separates the dome of the

alar cartilage and occasionally presents in the lip as in cleft lip. In the forehead
region, No. 13 is the cranial equivalent of the facial cleft 1. It affects the frontal
bone, the olfactory groove of the cribriform plate. Then it passes between the
nasal bones and the frontal bones of the maxilla causing teleorbitism
(hypertelorism). Inferiorly it reaches the alveolar bones (Fig. 33.10).
FIGURE 33.10 Tessier 1,13.
Tessier 2–12. Identical to preceding cleft, but more lateral, but not paranasal.
On the soft tissue, it affects the ala of the nose, between the summit and the
base of the ala of the nose the alar cartilage, on the lip. On the skeleton, it
traverses the lateral mass of the ethmoid (hyperteleorbitism); it does not have
a precise location on the forehead. The glabella is flattened and the frontal
sinus is enlarged. No. 12 cleft is the cranial equivalent of No. 2 cleft. Nasal
hemiatrophy, the supernumerary nostrils and the proboscis lateralise are
probably different degrees and forms the same paracentral defect.
Tessier 12. It is located medial to the medial canthus. The frontal process of
the maxilla is flat (telecanthus). The cleft crosses the lateral mass of the
ethmoidal and frontal bone, which is also flat. The frontal sinus is enlarged.
On the soft tissue there is a coloboma of the root of the eyebrow (Figs. 33.11
and 33.12).
FIGURE 33.11 Tessier 2,12.
FIGURE 33.12 Tessier 2 arhinia—obliteration of the right piriform

aperture.
Tessier 3–11. Medial orbitomaxillary cleft (oculonasal or Moran I cleft). This

cleft passes obliquely across the lacrimal groove. The frontal process of the
maxilla and the medial wall of the maxillary sinus are affected. The cleft
traverses across the lacrimal segment of the lower eyelid and passes around
the alar base in the nasolabial fold region and traverses the lip and alveolar
ridge like a cleft lip. Tessier 11 corresponds to Tessier 3. Tessier 11.
Superomedial orbital cleft. In this cleft coloboma of the medial third of the
upper eyelid that extends into the eyebrow is seen. Skeletal malformations of
this cleft are not seen (Fig. 33.13).
FIGURE 33.13 Tessier 3—bilateral cleft across nasolacrimal

groove (oculonasal cleft).
Tessier 4–10. Median orbitomaxillary cleft (oculofacial I or Moran II). It

passes almost vertically through the lacrimal segment of the inferior eyelid,
the infraorbital rim and floor of the orbit (medial to the infraorbital nerve); it
passes through the maxillary sinus in the cheek (causing an extrophy of the
sinus) and continues on the lip between the philtral crest and commissure. On
the alveolar bone, it occupies the usual position of the maxillopalatine clefts.
On the skull the no. 10 cleft corresponds to the facial cleft no. 4. Tessier 10.
Central superior orbital cleft. It is located at the medial third of the
supraorbital rim, lateral to the supraorbital nerve and extends across the roof
of the orbit and the frontal bone (encephalocele). Coloboma of the medial third
of the upper eyelid is present and it continues to join the scalp hair line (Figs.
33.14 and 33.15).
FIGURE 33.14 Tessier 4—median orbitomaxillary cleft.

FIGURE 33.15 Right-side Tessier 4, left-side Tessier 7.
Tessier 5. Lateral orbitomaxillary cleft (oculofacial II or Moran III). It

traverses the lower eyelid in its medial three on the cheek; it appears as a
groove and extends to the lip near the labial commissure. On the skeleton, it
traverses the infraorbital rim, the floor of the maxilla lateral to the infraorbital
foramen and the maxillary sinus and finally passes through the alveolar bone
in the premolar region (Fig. 33.16).
FIGURE 33.16 Tessier 5.
Tessier 6, 7 and 8. When found together, they form the Treacher Collins-
Franceschetti syndrome (Fig. 33.17).
FIGURE 33.17 Tessier 6, 7 and 8 Treacher Collins syndrome with

cleft of malar bones and mandibular hypoplasia. Zygomatic arch
and lateral orbital walls are absent.
Tessier 6. Intermaxillozygomatic cleft. It is located between the maxilla and

malar bone and opens into the inferior orbital fissure, it does not involve the
alveolar bone but the posterior portion of the maxilla is short. The palate is
high-vaulted and there is a relative choanal atresia. The coloboma of the lower
eyelid is located between the medial and lateral thirds. On the cheek there is a
vertical groove which is directed towards the labial commissure or the angle of
the mandible. This cleft usually belongs to the Treacher Collins-Franceschetti
syndrome.
Tessier 7. Temporozygomatic cleft. The zygomatic arch is absent or atrophic,
the ascending ramus of the mandible is short, the condyle and the coronoid are
often absent. The absence of the coronoid is associated with the absence of the
temporal muscle. The height of the maxilla is reduced and the alveolar wall is
hypoplastic. Incomplete clefts have been found either in the molar region or
between the maxillary tuberosity and the pterygoid. The soft tissue anomalies
include microtia and atrophy or absence of the temporal muscle. This cleft
corresponds to Treacher Collins-Franceschetti syndrome and also to hemifacial
microsomia (Otomandibular syndrome) (Fig. 33.18).
FIGURE 33.18 Tessier 7—lateral facial cleft with hypoplasia of the

mandible and zygomatic bone.
Tessier 8. Frontozygomatic cleft. It is common to Treacher Collins-

Franceschetti and Goldenhar syndromes. The bony defects predominate in the
Treacher Collins-Franceschetti, whereas the soft tissue malformations are more
marked in the Goldenhar syndrome. In Treacher Collins-Franceschetti, there is
the absence of the malar bone, lateral border of the orbit, which is formed by
the greater wing of the sphenoid and it extends both anteriorly and medially.
In the Goldenhar syndrome, the skeleton is more or less normal but there is a
dermatocele or a true cleft of the lateral canthus is seen (Fig. 33.19).
FIGURE 33.19 Tessier 8—true cleft of the lateral canthus with
dermatocele (Goldenhar syndrome).
Tessier 9. Superolateral orbital cleft. It traverses the lateral third of the upper
eyelid and the superolateral angle of the orbit. It is the cranial equivalent of
facial cleft no. 5 (Fig. 33.20).
FIGURE 33.20 Tessier 9—superolateral orbital cleft.

The aetiology of both cleft lip with or without cleft palate (CLP) and isolated
cleft palate (CP) is thought to be multifactorial, with both genetic and
environmental factors playing an important role.
Clefts of the lip and palate may also be found in association with other
congenital anomalies like cardiac anomalies, clubbing, spina bifida, mental
retardation, meningocoele, etc. and may occur as part of a syndrome.
However, such syndromic cases constitute only 3% of the cleft population. In
most cases, cleft lip or cleft palate occurs as a singular deformity without any
associated anomalies.
A ‘nonsyndromic’ cleft is so termed when the affected individual has no
other systemic or physical problems or any evidence of delay in motor or
cognitive development.
Nonsyndromic cleft is thought to be a complex or multifactorial trait and is
not attributable to any single gene. It is an effect of both environmental and
genetic factors.
Cleft palate as an isolated finding is both genetically and embryologically
distinct from cleft lip with or without cleft palate. Cleft palate in isolation
rarely occurs in members of the same family. This suggests that the major
causative genes for nonsyndromic cleft lip differ from those resulting in
isolated cleft palate, although these defects may share one or two susceptibility
genes of smaller effect. Both types of clefts are formed due to genetic
aberrations and are inheritable.
Genes
Four categories of genes for which there are results suggestive of a genetic
susceptibility to OCs are as follows (Table 33.1):
1. Genes expressed in a particular area of the embryo or in a particular

period of the palatine arch development, such as the transforming
growth factors alpha and beta (TGF alpha, TGF beta 2, TGF beta 3).
2. Genes having biological activities linked to the OC’s pathogenesis
without direct involvement, e.g. the retinoic acid receptor (RAR), the
methylene tetrahydrofolate reductase receptor (MTHFR) and the folic
acid receptor (FOLR1).
3. Genes or locus identified in experimental animals as the homeotic
genes MSX-1 and MSX-2.
4. Genes involved in the interaction with the xenobiotics metabolism as
those in P-450 cytochrome system.
Table 33.1
Genes associated with orofacial clefting

Candidate Gene Name of gene Type of
gene map cleft
locus associated
TGF-a 2p13 Transforming growth factor alpha CL/Cp,
CPO
TGF-p 19q13.1– Transforming growth factor beta CL/CP
q13.3
MSX-1 4p16.1 Homeobox gene (HOX7) CL/CP
RAR-a 17q12 Retinoic acid receptor alpha CL/CP
DLX-2 2q32 Distal-less homeobox 2 CPO
BCL-3 19q13.1 B-cell leukaemia/lymphoma 3 CL/CP
2q32 Unknown gene but different than DLX2: possible candidate CPO
gene include FN1, IHH, IGFBP2 and IGFBP5
4q25– Unknown gene CL/CP
q31.1
6q23 Unknown gene CL/CP
17p11.1– Unknown gene that may increase cleft palate susceptibility or CPO
p11.2 work synergistically to increase susceptibility in Van der
Woude syndrome that maps to 1q32–q41
CL/CP, Cleft lip with or without cleft palate; CPO, cleft palate only.
Though genetic susceptibility is primary cause, certain environmental factors
predispose expression of the gene, making it multifactorial. Several
environmental factors have been implicated in the OC aetiology. The folic acid
supplementation before and during conception has been found effective in the
prevention of neural tube defects. Folic acid deficiency may be responsible for
various malformations through a common mechanism that interferes with the
embryonic development, depending on the maternal or embryo genotype.
Advanced maternal age and consanguinity have also been investigated as
possible causes for phenotypic expression of the genotype.
Teratogenic agents that have been implicated with the potential to cause
clefts are as follows:
1. Smoking
2. Alcohol intake (ethyl alcohol)
3. Drugs such as phenytoin, diphenyl hydantoin, methotrexate,
aminopterin, retinoids and sodium valproate
4. Pesticides such as dioxin
5. Hyperthermia during pregnancy
Inheritability
If the first child has a cleft, the chance of the second child also being affected
with cleft lip or palate is around 30–40 times the risk in the general population.
Monozygotic twins (identical and therefore sharing the same genes) are far
more likely to be concordant for CL/P (where either both are affected or both
unaffected), the concordance rate being 25%–40%, than dizygotic twins, who
share only half of their genes in common; the concordance rate in them being
3%–6%.
Associated anomalies
Although CL/P occurs most frequently as an isolated anomaly, it may be
associated with other congenital defects. Association with cardiovascular
system accounts for 24% of cases and association with malformations of the
upper or lower limbs or the vertebral column accounts for 33%. Cases with
associated malformations are more likely to have combined cleft lip and palate
or cleft palate only, rather than a cleft lip alone. Around 15% of all associated
malformations are multiple and include cases that may be divided into
recognised syndromes, chromosomal anomalies (e.g. trisomy 13, 18 and 21)
and teratogens.
Syndromic clefts
A few patients with clefts do not fall into the ‘multifactorial inheritance’
category and these individuals usually make up approximately 3% of a clinical
cleft population. Most of these group of patients have identifiable syndromes.
There are over 400 syndromes associated with cleft lip or palate, which may be
due to single gene disorder and therefore follow a Mendelian inheritance.
Some of the common syndromes associated with CL/P are depicted in next
column.
Syndromes associated with cleft lip and palate
1. Chromosomal
a. Trisomy 13
b. Trisomy 18
c. Velocardiofacial syndrome (22qll deletion)
2. Non-Mendelian
a. Pierre Robin sequence
b. Goldenhar syndrome (Fig. 33.21)
3. Mendelian disorders
a. Ectrodactyly-ectoderm 11
b. Dysplasia-clefting syndrome (AD)
c. Gorlin syndrome (AD)
d. Oto-palato-digital syndrome (XL)
e. Oral-facial-digital syndrome (XL) (Fig. 33.22)
f. Smith-Lemli-Opitz syndrome (AR)
g. Stickler syndrome (AD)
h. Treacher Collins syndrome (AD) (Fig. 33.23)
i. Van der Woude syndrome (AD) (Fig. 33.24)
4. Unknown
a. De Lange syndrome
b. Kabuki syndrome
5. Teratogenic
a. Foetal alcohol syndrome
b. Foetal phenytoin syndrome
c. Foetal valproate syndrome
AD, Autosomal dominant; AR, autosomal recessive; XL, X-linked inheritance.
FIGURE 33.21 Goldenhar syndrome: with bilateral cleft lip,

macrostomia, strabismus, coloboma and ear deformity.
FIGURE 33.22 Polydactyly occurring with cleft.
FIGURE 33.23 Treacher Collins syndrome: inheritable condition

with absence of zygomatic arch, micrognathism, cleft palate, low
set ears.
FIGURE 33.24 (A–B) Van der Woude syndrome: congenital lip pits.
The abnormality is minimal in incomplete clefts and maximum in wide
complete clefts. There is a characteristic skeleton deformity in all clefts. This is
due to the abnormal growth of the skeleton in pre- and postnatal period which
accentuates the original deformity due to embryological failure (Fig. 33.25A–
B).
FIGURE 33.25 (A) Incomplete UCLP. (B) Complete UCLP.
Nose
The premaxilla is externally rotated, the lateral segment is retroposed and nose
is rotated towards the normal side. The columella is deviated to the opposite
side; the columella on cleft side being short. The nasal floor is completely cleft
and the nostril is transversely placed on the cleft side. The septum is deflected
to the opposite side, the caudal end being dislocated from the vomerine
groove and is seen in the opposite nostril.
Lip
The muscles comprising the orbicularis oris of the lips are unable to balance
each other, as mesenchyme from which they develop fail to penetrate between
layers of the maxillary processes. The orbicularis oris in its development from
lateral to medial side fails to meet the fellow on the opposite side and turns
upwards at the cleft to insert partially into its margin with some fibres
extending up towards the anterior nasal spine and base of columella medially
and the alar base laterally. The labial vessels also pass upwards in the margins
of the cleft.
Bilateral cleft lip

In complete cases, central frontonasal segment is not attached to the maxilla
and so there is marked forward projection of the premaxilla (Fig. 33.26A–B).
The abnormal forward projection of the premaxilla is due to a marked forward
position of the alveolar bone and the hypoplastic maxilla on both sides.
FIGURE 33.26 Bilateral clefts. (A) Incomplete bilateral cleft. (B)
Complete bilateral cleft.
Nose
The nasal deformity is symmetrical when the cleft is symmetrical on both
sides. The septum is straight, the columella is absent, there is no columella-
labial angle and the base of the ala is flared. There is no nostril floor. The nasal
lip is flat with wide separation of the medial crura.
Lip
In the bilateral cleft lip, mesenchyme does not penetrate the processes from
either side. As no muscle develops from the medial nasal process, there is
neither muscle behind the prolabial skin, nor does it have any hair follicles.
The abnormal insertion of the orbicularis oris pulls the medial and lateral
crura of the alar cartilage outwards from the cleft and makes it fall down like a
visor across the opening of the nasal passage.
Cleft palate
When the muscles of the cleft palate are unable to attach to each other across
the midline of the cleft, they become reoriented towards a fixed point and
stream towards the half of the posterior nasal spine of their side of the cleft.
There is convergence of the fibres of levator veli palatini, palatopharyngeus
and uvular muscles to form a compact bundle which is inserted into the
postnasal spine, edge of cleft and posterior edge of hard palate.
The tensor veli palatini and levator veli palatini are thinner and hypoplastic
in cleft palate. In clefts of hard palate, there is deficiency of mucosa and bone,
whereas in cleft of soft palate there is deficiency of mucosa and hypoplasia of
muscles which are abnormally inserted.
Hard palate
In unilateral cleft, the vomer is joined to the palatal shelf on the noncleft side,
along its medial edge. The palatal shelf on the cleft side is smaller in width and
length than noncleft side.
Soft palate (Fig. 33.27A–C)

The abnormal velar musculature in cleft was first described by Veau (1931).
The tensor having passed around the hook of hamulus, forms a thick fibrous
triangular insertion into the lateral part of, posterior edge of the hard palate.
This is very different to the normal, thinner, expanded and presumably more
elastic palatalal poneurosis. The levator, palatopharyngeus and palatoglossus,
unable to meet in the midline, pass more anteriorly to be inserted into the
margins of the cleft, the oral and nasal mucosa, the abnormal palatal
aponeurosis and into the back of the hard palate. Near the midline, the levator
and palatopharyngeus fuse to form what Veau called the ‘cleft muscle’.
FIGURE 33.27 (A–B) Normal anatomy of the palate. (C) Abnormal

anatomy of palate.
Problems faced by cleft children and their
management
A child born with cleft lip with or without palate would experience the
following problems in addition to abnormal appearance. The cleft
rehabilitation protocol addresses the same without causing any damage to
their potential to grow normally. The protocol aims to provide these children a
normal quality of life as possible.
1. Feeding problems
2. Associated systemic anomalies
3. Speech
4. Ear infections
5. Malocclusion and maxillary growth retardation
6. Scarring
Feeding problems and regurgitation

In order to suckle milk, the baby needs to create an airtight seal around the
nipple with the lips and exert negative pressure to express the milk. Cleft
children are unable to exert adequate pressure due to the loss of muscle
continuity in the lip and the communication between mouth and nose if there
is a cleft in the palate. Despite these problems, many children learn to suckle.
However, if there is an associated cleft palate, care needs to be taken to
prevent regurgitation of fluids causing respiratory problems. These children
need to be burped more often and the feeding posture should be more upright
to prevent regurgitation. Feeding plate or palatal obturators are of use if
delivered a few days after birth.
In case the children are unable to suckle at the breast, a feeding consultant
can train the parents to tape the cleft lip together in order to provide lip seal
and thereby provide more suction pressure. If all fails, the children have to be
trained on the bottle. The nipple hole can be enlarged to enable the child to
extract more milk with less pressure. Special feeding bottles have been
designed for cleft children to provide nutrition till the baby’s weight is
adequate for performing the cleft lip repair surgery. Few children may need a
feeding tube if aspiration is not preventable and prove to be life threatening.
The suckling problem will be solved once the lip repair (3 months) is done.
Regurgitation will minimise after primary palatal repair (9 months). The
children can be weaned normally.
Associated deformities
In children with associated deformities of the vital organs like the heart (velo-
cardio-facial syndrome) or airway (Pierre Robin’s), it will require urgent
attention to alleviate the imminent threat to life and future complications.
Children with severe airway problems (obstructive sleep apnoea) due to
micrognathia may need mandibular/maxillary expansion prior to the primary
lip/palate surgery.
Speech
Even after palatal repair, speech may be affected. This may be attributed to
several factors: velopharyngeal incompetence (VPI) causing hypernasality,
oronasal fistula (ONF) causing a nasal twang, malocclusion or lip
incompetence causing problems in pronunciation, hearing disability causing
impaired speech learning, learning disability, etc. VPI and ONF can be
corrected surgically. Physical obstructions can be cleared surgically or
orthodontically. Cleft children should be under the care of a speech therapist
till the improper speech patterns are rectified.
Ear infection
Cleft children are susceptible to ear infection. The malposition of the
eustachian tube results in more frequent middle ear infection. Some children
may require myringotomy to prevent hearing loss.
Malocclusion
It may occur due to missing lateral incisor, impacted canine, failure of maxilla
to grow or due to maxillary arch collapse. A combination of orthodontics,
orthognathic surgery and distraction are warranted to correct the maxillary
hypoplasia that develops after palatal repair. Missing teeth can be replaced
using implant supported prosthesis.
Maxillary growth retardation

Decreased maxillary growth in cleft children is the most common problem
encountered in the cleft children which accentuates as the child grows. Both
anteroposterior and transverse growth of the maxilla is restricted in children
with cleft palate necessitating procedures to bring the dental arch into Class I
alignment.
They often present with:
1. Severe Class III skeletal malocclusion.

2. With or without collapse and posterior crossbite.
This maxillary growth discrepancy is attributed to the following reasons:
1. Early surgical manipulation of the periosteum of the hard palate or the

vomer.
2. Intrinsic deficiency of growth of the cleft maxilla.
3. The inter-arch discrepancy that exists at birth.
4. Discontinuity between the maxillary growth centre and the cleft
maxillary segment.
Management of maxillary hypoplasia:
1. Early presurgical orthopaedic alveolar moulding to bring the alveolar

arches to a favourable position before primary repair.
2. Early premaxillary set back to correct extremely prognathic premaxilla.
3. Pre- and postsurgical orthodontics to bring the teeth in favourable
alignments.
4. Palatal expansion.
5. Orthognathic surgery.
6. Distraction osteogenesis.
Cosmetic defect
Lip defect, nasal deformity (deviated nose in case of UCLP; flat and broad
nose in case of BCLP), maxillary hypoplasia and collapse, missing lateral
incisor/canine. The lip is primarily repaired in early childhood. If the scar is
not aesthetic, it can be revised again after puberty. The nasal defect is repaired
primarily during the primary lip surgery and the secondary finite revision
surgery is performed after the skeletal hypoplasia is corrected.
Management of patients with cleft lip and

palate
Sequence of procedures
1. Primary
a. Feeding plate/presurgical alveolar moulding
b. Primary lip and nose repair
c. Primary palatal repair
2. Secondary
a. Secondary alveolar bone grafting
b. Pharyngoplasty
c. Orthodontic treatment
d. Orthognathic procedures/distraction osteogenesis
e. Rhinoplasty and scar revision of the lip
Primary correction
Before primary corrective surgeries are attempted, the surgeons attempt to
prepare the child for best postoperative results.
Feeding plate
Once the infant born with anomalies is stabilised and overcomes the obstacles
to thrive, the first and foremost problem encountered is that of feeding. While
suckling is a natural instinct, inability to create and hold negative pressure in
the mouth due to the lip and palate cleft may need to be addressed. Since the
cleft of the palate can only be repaired by the 10th month, regurgitation of the
fluids into the nose while feeding is very common. The parent and the infant
would find it much more comfortable if there is a physical barrier between the
nasal cavity and the nose. An acrylic palatal plate that serves as an obturator is
of much use in such cases. It may also be used as an orthopaedic appliance to
mould the alveolar fragments together (Fig. 33.28). However, infant
acceptance of the palatal plate often depends on how soon the plate is
delivered. The sooner the plate is delivered, the easier the baby accepts the
same. Usually plates delivered before 48 h from birth are best accepted by
infants.
FIGURE 33.28 Feeding plate or Hotz plate assists in feeding the

child without nasal regurgitation can be used as an orthopaedic
appliance for moulding the cleft segments to a more favourable,
symmetric position before performing lip repair.
A monthly check up of the feeding plate is essential to accommodate growth

of the palate.
The postoperative success of a cleft lip surgery is in making the child look and
function as ‘normal’ as possible. The success of surgery depends on the degree
of preoperative deformity. Larger the width of the cleft, more displaced the
nose, worser the deformity and consequently the postoperative result. Most
cleft centres prefer to operate on the child only by the third month. The time
from birth to the primary lip surgery can be used for orthopaedically
manipulating the alveolar fragments supporting the lip and the nasal
cartilages to a more favourable position to promote tension-free closure and
improve the postoperative result as much as possible. These techniques vary
greatly from simple removable intraoral appliances using passive forces to
fixed appliances requiring surgical placement and the concomitant use of
active force to rearrange the skeletal segments.
The various techniques used for achieving the same are as follows:
1. The feeding plate modified as an ‘intra-alveolar moulding plate’: The

feeding palatal obturator with additional thickness of acrylic anterior
to the alveolar ridge that is protruding and space posterior to the arch
to allow the pressure while suckling to mould the arches to a more
normal position
2. Strapping of the lips or the premaxilla using rubber bands: Pressure
across the lips may contribute to some moulding (Fig. 33.29A–B)
3. Head gear like appliances
4. Nasoalveolar moulding appliances
5. Lip adhesion
FIGURE 33.29 (A) Strapping of bilateral cleft lip using rubber bands
to orthopaedically manipulate the prognathic premaxilla to a more
favourable position before lip surgery. (B) Strapping also assists in
decreasing the width of the cleft and in bringing the lip segments
closer to each other.
Nasoalveolar moulding
Levels of hyaluronic acid which is a component of the proteoglycan
intercellular matrix was found to be high in infants’ blood and this may
contribute to the elasticity of the nasal cartilages in the neonatal period.
Presurgical nasoalveolar moulding is the technique by which the alveolus and
the nasal cartilages are moulded to a more favourable position.

The unilateral cleft lip nose is asymmetric at the alar base (due to collapse of
cleft side alveolar segment) with a tilted columella and a flattened, concave
and depressed lateral crus. The aim of presurgical nasoalveolar moulding is to
align and bring the alveolar cleft segments as close together as possible for
achieving correction of the nasal cartilage and soft tissue deformity. This is
accomplished by adding a nasal stent to the labial vestibular flange of a
conventional intraoral moulding plate. The nasal stent and alveolar moulding
plate are adjusted over a period of 3 months to achieve nasal and alveolar
symmetry, nasal tip projection and contact of the cleft alveolus just before
primary lip, nasal and alveolar surgical repair. The nasoalveolar orthopaedic
appliance is retained in position with surgical tapes and elastics applied to the
cheeks and cleft lip segments. The presurgical reduction in osseous and soft
tissue cleft deformity is supposed to reduce the magnitude of the surgical
challenge, ensuing in improved surgical outcomes.
Since orthopaedic appliances have a potential to harbour bacteria
(lactobacillus, Streptococcus mutans), these nasoalveolar moulding devices are
used in the edentulous alveolar ridge and removed at lip repair, long before
the eruption of primary teeth.
Bilateral cleft lip

The bilateral cleft lip nasal deformity presents with the short or absent
columella and the excessively wide prolabium. In the method of nasoalveolar
moulding and columella elongation, the posterior lateral alveolar ridges are
moulded to an appropriate width to accept the premaxilla between them. The
premaxilla is then retracted by using the moulding plate in conjunction with
external tape and elastics. Bilateral nasal stents are extended into the nostril
aperture from the vestibular flange of the intraoral moulding plate. A band of
soft acrylic presses against the nasolabial fold. The combined effect of pushing
the nasal tip forward and pressing back on the nasolabial fold results in
gradual tissue expansion and lengthening of the columella. The domes of the
lower lateral nasal cartilages are also brought together in the midline and the
intranasal lining is expanded simultaneously.
Lip adhesion
Partial suturing of the cleft lip segments in order to manipulate the fragments
nearer to each other is called lip adhesion.
This may be the first repair to be employed for the very difficult and wide
cleft. Most commonly used in wide bilateral clefts in which the premaxilla is
protrusive and inadequate tissue is available for primary repair. The lip
adhesion is performed and after few months of remodelling of the maxilla
secondary to lip tension, primary repair can be completed. This procedure has
also been used to approximate lip and alveolar segments in wide unilateral
cleft.
Lip repair
There are several excellent methods for correcting the cleft of the lip. However,
the technique chosen, the type of cleft, the amount of tissue available, scarring
tendency of the patient and surgical skills of the surgeon determine treatment
outcome. The ‘rule of 10s’ to determine timing of cleft lip repair should denote
weight of at least 10 pounds, haemoglobin of 10% and an age of at least
10 weeks. However, literature reports of choice of timing of cleft lip repair
range from several days of age to 6 months.
Most of the surgeons prefer to undertake the surgery only when the child is
older, usually between 3 and 6 months. With reduced risk of anaesthesia, they
feel that they can spend more time and get a better result when the lip and
nose are more developed.
Evolution of lip repair

Surgical approximation of the cleft lip segments has been tried for many
centuries. The first successful repair of lip can be traced back to China as early
as AD 390. In early years, edges of the cleft were excised and approximated in
a straight-line with figure-of-eight sutures fastened around the pin inserted to
hold the cleft fragments together. The early techniques used were only a
straight-line closure, resulting in scarring which made the repaired lip look
shorter. The muscle position was ignored. But it was only from 16th century
onwards that cleft lip repair for a cosmetic purpose was widely practiced.
Since then several attempts have been made to overcome this cosmetic
deformity and different techniques have been used. Rose (1833) used curved
incisions with concavities apposed and Thompson (1912) used straight
incisions running obliquely across the lip to gain length (Fig. 33.30). With time
the technique evolved in an aim to achieve good muscular action and least
scarring. The aims of cleft closure now are to obtain good muscle alignment,
an acceptable scar and an evenly balanced lip.
FIGURE 33.30 Rose and Thompson procedure.
Unilateral cleft lip repair

The most popular techniques on which the rest of the modifications are based
on are as follows:
1. Tennison triangular flap repair

2. Millard rotation advancement repair
Tennison triangular flap (Fig. 33.31)
• Tennison in 1952 used the height of the normal side of the lip for
estimating the repaired side. A wire was used, bent into a Z shape. The
two sides were marked with this to give a method of measurement
that is simple, preserves the Cupid’s bow and gives a zigzag scar,
which helps to hide the scar and remove the telltale straight closure.
• In this operation, a cut to correct upward tilt of Cupid’s bow is made
on the lower one-third of the lip. The gap is filled with a triangle of
skin, muscle and mucosal flap from the lower end of lateral lip
element giving it a nice fullness in the lower one-third of lip.
• Other modifications of triangular flap were practiced by Mirault
(1844), Blair (1926), Brown (1945), Randall (1959) and Cronin (1957).
FIGURE 33.31 Tennison’s triangular flap procedure.
Advantages
• Relative ease with which Cupid’s bow is brought from its angulated,
upright position to a horizontal level.
• The added tissue on medial side gives a natural protrusion in this area.
• Lengthening of the vertical height of cleft side lip is achieved.
Disadvantages
• Philtral column is not restored

• Does not address the nasal deformity as well as Millard repair does
• Muscular elements reattachment is not attended to
• May produce a lip that is too long
• Z-shaped scar on cleft side
Millard rotation advancement repair (Fig. 33.32)
• In this repair, the tilted Cupid’s bow is rotated down following a

curved incision extending under the columella, i.e. the medial side of
the lip is rotated down by a medial incision carried up under the
columella. This allows rotation of the misplaced Cupid’s bow and
philtral dimple into a normal position. The high rotation gap created is
filled with a triangular flap comprising skin, muscle and mucosa from
upper part of lateral side of cleft.
• The resultant scar is hidden under the nose or follows the natural line
of the philtrum.
FIGURE 33.32 (A–C) Millard’s rotation advancement repair. (
Scan to play Unilateral Cleft lip correction surgery)
Advantages
• It is a technique that allows variation as the surgeon progresses with

the operation.
• The resultant scar follows natural lines in the lower half of the lip and
provides a scar that is simple to revise.
• Preserves Cupid’s bow and philtral dimple.
• Preserves pleasing outward pointing of the lower portion of the lip.
• Method is a highly flexible one, which permits constant modification.
• The lip is tightest in its upper part, where it should be and has more
fullness in its lower portions, where these features are desirable.
Disadvantages
• Difficult to get adequate rotation and optimal lateral flap in wide cleft
lip.
• In order to obtain a suitable flap, it may be necessary to take off too
much of lateral vermilion, thereby causing noticeable asymmetry of
Cupid’s bow.
Long-term follow-up of the techniques have proven that geometric

alignment of the lip segments alone is not sufficient. In order to achieve
functional repair, muscle alignment repair is very important to achieve an
aesthetic as well as a functional lip. The results of a repaired cleft lip which
may look excellent is not constant, until the muscles within it are properly
aligned. Therefore, it is important to get good muscle union. If this is achieved,
the alignment of the lip will be satisfactory both aesthetically and functionally
and the skin scar will not be unsightly.
Delaire technique of muscular reconstruction (functional repair)

Though the rotation advancement technique was widely used due to its
excellent results, it often resulted in smaller nostrils due to lack of muscular
approximation. Delaire proposed an enhancement to the rotation
advancement technique of performing a wide dissection of the lateral lip and
nasal elements with approximation of the muscles of the lip and the nose. This
technique has gained popularity and is widely used with individual
modification added by surgeons.
• Muscular reconstruction involves separating the superficial nasolabial

musculature including lip levators from the deeper orbicularis muscle
and their concomitant anatomical repositioning.
• Dissection of the nasolabial muscle group under the cleft lip is done
from the lateral cleft lip incision.
• The alar incision should be thus limited in the area of the cleft alar
base.
• Suturing the deep plane (nasal muscle complex) medially towards the
septum will raise the nostril floor and pull the nasal web towards the
midline and obstruct the nostril (Talmant, 1993).
• The inferior head of the constrictor nasi muscle can be found just
below the nostril web and dissected free.
• It can then be sutured inferomedially to the premaxilla in the area of
the lateral incisor tooth to avoid this problem. This is the correct
anatomical position of the myrtiformis muscle.
• Additionally, the transverse nasalis must be dissected out between the
upper and lower cartilages on the cleft side to allow elevation of the
cleft side alar cartilage.
• A superior plane is then created by suturing the deep, superior part of
the lateral orbicularis oris muscle to the fibrous tissue at the base of the
septum in front of the anterior nasal spine. These crossing sutures that
are created help correct the vertical distension of this region of the lip.
• The remainder of the orbicurlaris oris muscle is then to be joined by
suturing to its opposing member. The resultant muscular junction
should be just lateral to the midline to mimic a philtral ridge and the
muscles can also be overlapped to assist in this procedure
(Fig. 33.33A–D).
FIGURE 33.33 (A–D) Delaire technique—separating the superficial
nasolabial musculature including lip levators from the deeper
orbicularis muscle and their concomitant anatomical repositioning.
Noordhoff technique
The Noordhoff’s modification of Millard rotation advancement cheiloplasty
technique of lip repair is focused on simultaneous primary nasal repair along
with lip repair.
The salient points of this technique are as follows:
1. Usage of the inferior turbinate flap for lining the nasal base (piriform
area).
2. Dissection of the orbicularis ori, from skin to minimise horizontal scar
at the foot of the ala.
3. Avoiding the back cut incision to lengthen the cleft side philtrum.
Using a triangular skin flap superior to the white skin roll for rotation.
4. Cleft side vermilion red line and white skin roll sutured parallel to the
noncleft side red line and white roll.
5. Avoiding periosteal stripping or dissection over the maxilla to prevent
growth retardation.
6. Repositioning the cleft nasal cartilages, using the alar transfixion
sutures for recreating the alar groove and fixation.
7. Prevention of scar contracture by complete wound closure.
8. Inserting a silicone nasal former postsurgically for splinting the delicate
cartilages.
Primary unilateral cleft nose repair

Even though the nose is deformed correction was deferred till adolescence to
prevent any growth disturbance due to stripping of the perichondrium.
However, a few surgeons have advocated concurrent, early nose repair
(Delaire, 1975, 1978; McComb, 1975, 1985, 1990, 1996; Salyer, 1986, 1987;
LaRossa, 1993; Noordhoff, 1995; Thompson, 1995). The technique had been
criticised for the development of secondary scar contracture and stenosis
(Berkeley, 1959; Tan and Pigott, 1993). However, with increased
understanding of cleft anatomy and development, less invasive and more
effective techniques are now employed for primary nose repair along with the
lip.
• McComb specifically made no incisions in the nasal lining to avoid the

previously reported problems with nasal stenosis (Fig. 33.34).
▪ The first surgical step is to widely undermine the nasal skin
from the nostril rim to nasion.
▪ Access is gained from the lip incisions.
▪ Sutures over bolsters are passed from intranasal up towards
the nasion, thus lifting the cleft lower lateral cartilage (LLC).
▪ Drooping of the nostril rim has not reoccurred and in some
cases the vestibular oblique ridge has been corrected.
• Thompson (1995) has modified the original LeMesurier technique with
the addition of a primary nasal correction through intranasal incisions.
▪ Dissection between the upper lateral cartilages (ULC) and
lower lateral cartilage (LLC) accomplished.
▪ Long-term intranasal splinting is necessary with this
technique, probably to avoid the previously reported
problems of nasal stenos is with these types of multiple or
complex intranasal incisions.
• Bardach (1995) concentrated on the nasal floor, important for nostril
symmetry and alar base elevation, but ignores the rest of the cleft nasal
deformity; thus, results are less than with other techniques.
FIGURE 33.34 Primary rhinoplasty—dissection of the
malpositioned alar cartilage with anatomical repositioning of the
nasal septum.
Type of Advantage Disadvantage

repair
Millard Allows adjustments at the time of Difficult to master, especially in wide clefts; has
(1976) surgery, places the scar in an difficulty in obtaining adequate lip length; and
anatomically correct position and has a tendency towards vertical scar contracture
reinforces the nostril sill and a constricted nostril on the cleft side
Tennison Lengthens the shortened lip of Horizontal scars
and cleft side Muscle repair not stressed
Randall Preserves cupid bow
triangular
flap
Nakajima Triangular flap is placed in upper Muscle and nose not repaired
(1993) lip or nostril sill where it is
camouflaged
Delaire Muscular reconstruction through
lateral cleft lip incision
Noordhoff A lateral buccal flap and
(1995) turbinate flaps are created.
These provide mucosal lining
and decrease scarring,
allowing the depressed cleft
alar base to be advanced
without latter relapse
• Salyer (1986) used bolster sutures and stents to assist in the correction.
• Turdek et al. (1997) advocated primary septal cartilage repositioning
to decrease nostril asymmetry.
Bilateral cleft lip repair

The problem in treating bilateral clefts of the lip and palate is the forward
projection of the prolabium and premaxilla on the vomer at the tip of the nose.
The degree of projection varies greatly in both anteroposterior and lateral
deviations.
When position of the premaxilla is normal or protrusion is moderate, the lip
can be repaired over it with little tension. Excessive protrusion is a
complicating factor to the planned repair of lip. Attempts to repair over a
conspicuously protruding premaxilla may result either in actual dehiscence of
the wound or spreading of the scar because of excessive tension. In these cases,
early orthopaedics and elastic pressure over the prolabium are to be
considered before primary lip repair. Presurgical orthopaedics to improve
position of the prolabium is advocated. Sometimes in cases of late lip repair
where premaxilla has grown to disproportionate levels and cannot be
managed orthopaedically, sectioning of the premaxilla needs to be done. This
is done posterior to the premaxillary—vomerine epiphyseal line to minimise
the possibility of maxillary growth retardation.
Techniques
A satisfactory bilateral cleft lip repair must restore the orbicularis muscle
circumorally if the upper lip is to function properly. Also, needed is an
adequately deep upper buccal sulcus, which separates the lip from adhesion to
the premaxilla, again allowing for normal function and growth and
development of the muscles. A few techniques of bilateral lip repair are as
follows:
1. Straight-line closure (Veau III operation).

2. Adaptation of Tennison unilateral cleft lip repair (Fig. 33.35A).
3. Millard repair of complete and incomplete bilateral clefts (Fig. 33.35B).
4. Black’s technique (Fig. 33.36A–L), Skoog techniques, Manchester
method, Barsky (Veau II), Primary Abbe Flap.
FIGURE 33.35 (A) Tennison and Randall bilateral lip repair
technique. (B) Millard two-stage method of lip repair and elongation
of the columella. (i) A shaped philtrum is outlined with a turn-down
flap of prolabial vermilion; the lateral prolabial tissues become the
forked flaps. Circum-alar marks design the alar base flaps; lateral
lip marks show the turn-down of vermilion flaps carrying the white
roll of the mucocutaneous junction. (ii) The lateral mucosa and
muscle are sutured together behind the prolabium, which has been
elevated temporarily. (iii) The lip has been approximated, a slight
excess of the vermilion flaps creating a tubercle. The fork flaps are
sutured end-on to the alar base flaps, their raw surfaces being
approximated to form a mound in the floor of the nose for future
columellar lengthening. The banked forked flaps are then dissected
out and moved to the columella in the preschool stage to achieve
columellar lengthening.
FIGURE 33.36 Black’s technique. (A) Outline of incisions. (B) Infra-
nasal view shows flaps remaining attached as posterior hinges
turn-down flaps and flaps remaining attached to the premaxilla.
Incisions continue directly posteriorly from the lateral advancement
flaps and from the lateral base of the triangular flaps along the cleft
margins, in preparation for the repair of the nostril floors. The
prolabium (PL) is elevated with attached vermilion as the superiorly
based flap. An acute vermilion—cutaneous angle is relieved by an
incision underneath. PM, premaxilla. (C) The flaps are sutured
together in the midline of the premaxilla. The flaps are ready to be
approximated. The muscles have been liberated from their
abnormal superior insertion and rotated to better orientation to
meet each other and restore orbicularis continuity. (D) Muscles
repaired. At this stage the prolabial flap may be dropped; the flaps
may be rotated into place; and the skin may be repaired. (E)
Complete skin repair. (F) Postoperative appearance. (G) Bilateral
cleft lip. (H) The philtral flap is elevated (including subdermal soft
tissue) off the premaxilla up to the anterior nasal spine. (I)
Curvilinear incisions are drawn at the juncture of the alar bases
and lateral labial elements. Nostril rim incisions are marked and
extended along the inside edge of the upper columella. The lateral
labial elements are disjoined from the alar bases. These basilar
flaps are freed from the piriform attachments by incision along the
inferior cutaneous–mucosal (inter-cartilaginous) junction. The
mucosal incisions on the underside of the lateral elements are
extended distally, on the anterior side of the gingivolabial sulcus, to
the premolar region. With a double-hook on the muscle layer, the
lateral labial elements are widely dissected off the maxilla in the
supraperiosteal plane. (J) Nasal floor reconstructed. (K) Lip and
sulcus reconstruction done. (L) The percutaneous sutures are
removed and the nostrils are cleaned 5–6 days postoperatively.
Intrauterine cleft lip repair

has also been proposed and some animal studies have proved successful.
Wound healing has been after intrauterine repair of surgically created lip
defects in animal models (Hallock, 1985; Sullivan, 1989; Longaker, 1991; Estes
et al., 1992; Oberg et al., 1995). Since collagen does not accumulate, wound
healing resembles regeneration leading to more normal looking lips.
However, nasal deformity correction has not been recorded. Benefits of foetal
surgery for cleft lip at this time do not outweigh the risks.
Primary bilateral cleft nose repair

Bilateral cleft children often present with a broad nose, with a very shortened
columella, blunt nasal tip and loss of nasal projection. This is due to the
position of the alar cartilages that are often splayed, rotated caudally, subluxed
from their normal anatomic position (Broadbent and Woolf, 1984; Mulliken,
1985, 1992; McComb, 1986). A prognathic or microform premaxilla and the
absence of muscle tone in the prolabium may compound the nasal deformity.
Primary nose correction has often been deferred due to the tiny size of the
cartilages of the nose and the almost absent columella. However, some
surgeons believe that delayed nasal reconstruction makes the cartilages rigid
as they mature, making corrections difficult and increasing the rate of relapse
(Mulliken, 1995).
• A number of techniques were devised for delayed ‘columellar

lengthening’, involving transfer of tissue from the broad prolabium or
shifting tissue from the nasal floor (Cronin and Upton, 1978).
• Broadbent and Woolf (1984) described a case of primary medial
advancement of the alars combined with excision of skin from the
broad tip.
• The Cronin and the forked flap were unaesthetic and hence not
preferred due to the excessive scarring that occurs at the columella.
• McComb (1975), the pioneer of primary columellar elongation,
struggled for 15 years while using the forked flap for columellar
lengthening. He was discontented with the abnormal nostril shape,
broad tip, overly long columella and web of scars at the foot of the
columella (McComb, 1986).
• McComb (1990) presented a new method of using a cutaneous incision
to approximate and suspend the flattened, splayed alar cartilages,
while narrowing the nasal tip by cutaneous V-Y-plasty for primary
nasal repair. He published a 4-year follow-up of his experience after
assessing the results (McComb, 1994).
• Mulliken (1987) described a technique for repositioning the alar domes
and reorganising the nasal soft tissues (Mulliken, 1992). He
demonstrated by anthropometry that nasal tip protrusion and
columellar length can be compared to that of noncleft children by the
time they are 5 years of age (Mulliken, 1995).
• In 1991 Trott and Mohan, by dissecting the anterior surface of the
middle crura and correcting the displaced alar cartilages through open
rhinoplasty, improved the nasal tip by lifting the prolabium and
columella (Fig. 33.37).
• Continuity of both the deep and superficial fibres of orbicularis oris
muscle is important for lip movement and symmetrical facial
expression. The unapposed pull of levator labii superioris alaque nasi
muscle makes the nostrils flare and elevate when these children smile.
This can be prevented by securing the alar bases to the underlying
orbicularis muscle to mimic the action of depressor labii inferioris
alaque nasi muscle (Mulliken, 1995).
• Before embarking on primary rhinoplasty, growth changes must also
be considered (Farkas et al., 1992, 1993). Columellar protrusion and
nasal projection, which is often retarded in the cleft children, can be
reconstructed slightly larger to match the retardation that is deemed to
occur later. Features such as interalar distance, prolabial length and
width, and total upper labial height that are likely to grow more than
that of the noncleft nose should be reconstructed smaller-than-normal
(Mulliken, 1995, 1997).
• Kohout et al. (1998) recorded the change in nasolabial angle, from
infancy to adolescence. They found that the nasolabial angle decreased
with age, changing from obtuse angle to almost 90° in most children
with repaired bilateral cleft. Columellar and upper lip inclination to
the vertical also increased. This was attributed to enhancement in lip
support and growth of the untouched septum and lateral cartilages.
• Primary nasal surgery is therefore done based on the necessity of the
situation, viewing the existing structural deformity, the growth
potential and the muscular action.
FIGURE 33.37 Primary rhinoplasty (BCLP). (A) Bilateral cleft lip.

(B) Using a semi-open approach through bilateral rim incisions, the
anterior surface of the slumped and splayed lower lateral cartilages
is exposed by scissor-dissection. This dissection continues
superiorly over the upper lateral cartilages and across the dorsal
septal junction. (C) The genua are apposed. (D) The lateral crura
are elevated and secured to the ipsilateral upper lateral cartilage.
(E) Postoperative appearance of the child after 8 years.
Palate repair
The hard palate is supported by bony shelves with mucosal coverings, while
the soft palate consists of muscle with mucosal covering. Early repair of the
cleft of the hard and soft palate is undertaken with two main objectives: to
make the process of eating and drinking easier by preventing the regurgitation
of the food through the nose and to correct and improve the speech by the
time the child starts to speak. The most significant goal in surgical
reconstruction of the palate is providing a normal anatomical environment for
the development of normal speech.
History
• In 1764, Le Monnier, a French dentist, attempted the first palate

closure.
• The first detailed description of the closure of a cleft soft palate was
given by Carl Von Graefe in 1816.
• In 1826, Johann Dieffenbach was the first surgeon to close a cleft in the
hard palate.
• Historically, the father of modern-day palatoplasty is Bernhard Von
Langenbeck, was the first to elevate bipedicled mucoperiosteal flaps
with lateral relaxing incisions.
• In the early 20th century, the significance of having a repaired palate
long enough to close off the velopharyngeal port was recognised by
Billroth.
• A variety of pushback procedures were developed in an attempt to
lengthen the palate.
Timing of repair
Timing of the surgical repair of lip and palate has been controversial among
cleft surgeons. In 1921, Sir Harold Gillies wrote, ‘Close the lip early and repair
the palate prior to speech’.
Most cleft surgeons do believe that the palate should be closed prior to the
time that the child begins to speak. The main area of controversy surrounds
the timing of hard palate repair because it is believed that early repair results
in scar tissue formation and limitation of maxillary growth. Early soft palate
repair preceding hard palate closure is recommended by some. But most
surgeons close the hard and soft palate as early as 6–9 months of age and
almost always before 18 months of age. The protocol for timing of repair
differs from centre to centre and the surgeon’s preference. The single most
important factor in achieving good speech results is the reconstruction of the
muscular levator mechanism, regardless of the technique or sequence used.
Procedures
Anatomic basis for cleft palate repair is that in cleft condition muscles of the
palate are hyoplastic and have abnormal insertions on the posterior edge of
hard palate and along the margins of hard palate cleft. This abnormal insertion
contributes to the overall shortness of the palate and, due to the fact that the
levator sling cannot be created, may result in inability of the palate to reach the
posterior pharyngeal wall and achieve velopharyngeal competence. Thus,
unless these muscles are carefully detached from their abnormal insertions,
rotated medially and realigned in the midline to recreate the levator sling,
correct muscle function is impossible. The different techniques followed are as
follows:
I. Von Langenbeck operation (Fig. 33.38A–D)

II. V–Y pushback palatoplasty (Kilner–Wardill) (Fig. 33.39A–H)
III. Furlow double opposing Z-plasty (Fig. 33.40A–D)
IV. Anterior vomer flap (Veau) (Fig. 33.41A–G)
V. Intravelar veloplasty
FIGURE 33.38 Von Langenbeck operation. (A) The incisions. (B)

The mucosa of the hard palate is elevated between the bone and
the periosteum. The major palatal vessels are identified and
stretched out of the canals. (C) The nasal mucosa is closed and
the muscles sutured side to side. After being detached from their
insertion. (D) The oral closure.
FIGURE 33.39 The Wardill–Kilner technique of primary cleft palate

repair. (A) Intraoperative view. (B) A V-Y lengthening results in a
lengthened palate with an exposed area of bone at the sides that is
gradually granulates and epithelises. The levator muscles are
detached, reoriented and sutured either end-to-end or in an
overlapped position. (C) Closure of nasal layer and muscle
approximation. (D) Postoperative view. (E) Wide cleft palate. (F)
Palatal flaps raised nasal layers approximated. (G) Oral layer
closed (double layered closure), raw areas packed with tincture
benzoin. (H) Postoperative view after 10 years of follow-up. (
Scan to play Palatoplasty - Cleft palate surgery)
FIGURE 33.40 The Furlow double Z plasty technique of primary

cleft palate repair. The levator muscles included in the posteriorly
based flap of the oral mucosal Z plasty and the levator from the
other side is included in the posteriorly based nasal mucosal flap.
The Z plasty in the nasal mucosa is the reverse of the one in the
oral mucosa. (A) The incision marking. (B) The anterior palate
closed with vomer flap. (C) The nasal mucosal closure. Note that
the levator muscle has been reoriented in the transverse direction.
(D) Suturing completed. By achieving lengthening within the soft
palate, large mucoperiosteal flaps from the hard palate are
avoided. In addition, the orientation of the levator muscles is
improved and they are closed in an overlapped position.
FIGURE 33.41 Vomer flap. (A) Elevation of the vomer flap. (B) The
vomer flap is sutured in an overlapping fashion to the opposite oral
mucosal flap. (C) Completed two-layer closure. Upper inset—oral
view. Lower inset—coronal view. (D) Elevation of the
mucoperiosteal flap from the vomer. (E) Suturing of the vomer flap
to the nasal layer. (F) Closure of the oral layer. (G) Postoperative
image.
Von Langenbeck operation

It is an established procedure that includes the elevation of large
mucoperiosteal flaps from the hard palate. It is a side-to-side approximation of
the cleft margins of both the hard and soft palate, with detachment of the
levator muscles from their bony insertions and use of long relaxing incisions
laterally to close the hard palate without tension. It does not include a
lengthening manoeuvre (Fig. 33.38A–D).
Wardill–Kilner–Veau Operation
To increase the anteroposterior length of the palate at the time of primary
palatoplasty, various mucoperiosteal flap manoeuvres in the hard palate have
been recommended. A V–Y lengthening operation is done in the tissues of the
mucoperiosteum of the hard palate. The rigid mucoperiosteum probably
maintains the length that is achieved, although a similar amount of
lengthening must be obtained in the nasal mucosa of the soft palate. This V–Y
pushback palatoplasty includes lateral relaxing incision and bilateral island
flaps based on the posterior palatine arteries (Fig. 33.39A–H).
Secondary surgery is mandatory in some cases because certain cosmetic and
functional defects cannot be assessed fully or managed before the cessation of
growth. Also, secondary surgery can overcome the shortcomings of the
primary surgery. For example, adult nose shape develops in the teens. When
the inherited shape is superimposed on an unpredictable amount of
underdevelopment of the underlying maxillary bone, due to the cleft and also
due to the corrective surgery, it may be seen that final correction must await
the stabilisation of these factors. It must also wait corrective movements on the
underlying bone and teeth which may be undertaken by the orthodontist in
the early teens and major surgery on the maxilla which may be undertaken in
the late teens. It has been considered that operation on certain tissue earlier
may impair its growth potential by damaging its blood supply or restricting its
growth by scar tissue.
Closure of palatal fistulae

Palatal fistulae must be considered functional complications related to the type
of primary repair. The fistula may be present in front of, through or behind the
alveolus or in the main hard palate.
Symptoms
• Increased nasalance in speech with articulatory difficulty.

• Regurgitation of fluids to the nose.
• Halitosis.
• Increased incidence of ear and paranasal sinus infections.
Timing of closure
When it comes to the timing of the procedure, closure of a fistula may be done
at any age and probably the sooner the better, provided that it is causing
symptoms and suitable tissues are available.
Procedure
The simplest method of closure is with the palate tissue adjacent to the fistula.
This can be made to provide a lining for the nose from one side of the fistula,
the tissue ‘flap’ being hinged on the scar at the cleft margin. The oral layer is
made by sliding a flap of mucosa sideways across the hole (Fig. 33.42A–D). In
cases of large, persistent palatal fistula, a tongue flap (Fig. 33.43A–F) or a
temporalis flap is used. Palatal obturators have also been used in cases where
the blood supply of the palate is compromised beyond capacity for repair.
FIGURE 33.42 (A) Palatal fistula. (B) Raising a mucoperiosteal flap

from the hard palate. (C) Closure of oral layer in V-Y fashion. (D)
Packing the exposed palatal bone area with gauze soaked with a
haemostat.
FIGURE 33.43 (A) Large persistent palatal fistula. (B) Marking for
anteriorly based pedicled tongue flap. (C) Pedicled tongue flap
used for closure of palatal fistula. (D) Division of pedicle. (E)
Primary closure. (F) Postoperative appearance of tongue flap used
for palatal fistula correction.
Velopharyngeal incompetence (VPI) is the term used when the patient is
diagnosed as being unable to raise the velum to meet the posterior pharyngeal
wall to seal the nasal airway during speech. In the early 20th century, Bilroth
recognised the significance of having a repaired palate long enough to close off
the velopharyngeal port instead of merely closing the palatal defect to achieve
good speech. The most common cause of VPI are as follows:
• Cleft of the secondary palate
• Scarred palate preventing muscular action of the palatal elevators
• Short palate
• Presence of a palatal fistula or fistulae
• Submucous cleft palate
• Neuromuscular abnormalities (congenital or acquired)
• Adenoidectomy
• Congenital VPI of unknown aetiology
Normal VP function and the defect

Velopharyngeal closure is a sphincteric valving operation essential to normal
speech, whistling, blowing, swallowing and sucking. Velopharyngeal (VP)
mechanism for speech requires the upward and backward movement of the
soft palate (valving), simultaneous with medial movement of the lateral and
sometimes posterior aspects of the pharyngeal walls (sphincteric) (Fig. 33.44A–
B). This activity creates a seal that effectively separates the nasal and oral
cavities and facilitates the supraglottal pressure, oral air flow and resonance
necessary for adequate speech. This movement of the soft palate and the
posterior wall of the pharynx can be assessed using lateral cephalogram
(Fig. 33.45). The main muscles of velopharyngeal closure are the levator veli
palatini, uvulus muscle and palatopharyngeus with lesser contribution from
superior fibres of the superior constrictor. In velopharyngeal dysfunction of
any cause, air resonates in the nose and nasopharynx. This is called hypernasal
resonance, as opposed to reduced or hyponasal resonance which is heard
during common cold or where adenoidal hyperplasia reduces the
nasopharyngeal space. Frequently air can be heard hissing, bubbling or
snorting from the nose (nasal escape, turbulence or emission).
FIGURE 33.44 (A) Velopharyngeal incompetence. Movement and

elevation of palate limited by scarring. (B) Elevation of the posterior
wall of the pharynx, the Passavant’s ridge while the patient
attempts to speak. The soft palate being short, is unable to close
the velopharyngeal port resulting in VPI.
FIGURE 33.45 Lateral cephalometric X-ray of a bilateral cleft child
at rest and during phonation. Note the inability of the velum to raise
to close the velopharyngeal port resulting in VPI.
Patients may also grimace by using their nasal or facial musculature in an

attempt to prevent air escaping down the nose.
Treatment
Following primary cleft palate surgery, secondary techniques for the
correction of VPI include palatal lengthening procedures, pharyngeal flaps,
augmentation of posterior pharyngeal wall with soft tissue or implants,
sphincteric reconstruction and prosthetic obturators.
The age of the patient, aetiology of VPI (congenital vs acquired), length of
time that VPI has been present and general intellectual capabilities of the
patient can all influence the choice of treatment and likelihood of success.
Surgical treatment should form part of a strict protocol and the following
options are recommended.
Prosthetic management of VPI

The palatal lift procedure using speech bulb is used in young children to
overcome VPI so that speech may develop. Pharyngeal speech aid is also used
in adults to compensate soft tissue. The speech bulb is designed to elevate the
soft palate when temporary treatment of VPI is required. Treatment can be
started at the age of 4–5 years. Active speech therapy is started at this age.
Speech bulb is advisable before any surgical intervention for VPI. The speech
bulb aids in proper articulation of the speech and reduces hypernasality. If this
fails, surgery should be considered.
Surgical management of velopharyngeal incompetence

(pharyngoplasty)
Velopharyngeal incompetence is usually corrected surgically. The aim of the
operation is to close the velopharyngeal aperture but leaving a sufficient
resting gap to permit nasal resonance to occur normally on the sounds ‘m’, ‘n’
and ‘ng’, to allow comfortable nasal breathing while eating and sleeping and
normal drainage of the nasal cavity. Surgical correction of velopharyngeal
incompetence is not a new concept. In the 16th century, Pierre France (1561)
indicated an awareness of connection between cleft palate and poor speech.
During the 19th century, surgical procedures were developed that are still
being used in modified forms.
Closure of palatal fistula

Palatal fistulae must be considered the functional complication related to the
type of primary repair. Fistulae that are symptomatic or likely to become so
should be closed. Unfortunately, for some patients for whom palate re-repair
is not appropriate, particularly those whose VPI is not due to a cleft and those
with severe tissue deficiency. For those patients, whose palatal function cannot
be adequately improved, a number of operations have been devised which
alter the shape of the nasopharynx to reduce its size and make the closure
easier. These operations are collectively called pharyngoplasties.
Revision of palatoplasty and velar lengthening

Inadequate movement of entire soft palate but normal movement of the
pharyngeal musculature implies in complete, limited or complete absence of
restoration of muscle continuity at the time of primary surgery. Revision of
palatoplasty must be the procedure of choice. This approach has the additional
benefit of lengthening the palatal soft tissues.
Pharyngeal surgery
Despite the evidence that revision palatoplasty might be more appropriate in
the first instance, pharyngeal surgery with or without palatal lengthening
remains a popular first-line method of managing velopharyngeal in
competence. Two surgical techniques are followed depending on the
abnormality found: posterior or lateral pharyngeal wall surgery.
Posterior (flap) pharyngoplasty

Posterior pharyngeal flap surgery is well established, with a long history back
to 19th century. These procedures may be superiorly or inferiorly based. The
superiorly based flap is more popular, with its base at the level of the tubercle
of the atlas and its insertion into the soft palate at predetermined points.
Lateral (sphincter) pharyngoplasty

The concept of surgical creation of a dynamic sphincter pharyngoplasty to
provide velopharyngeal closure rather than a pharyngeal flap to control the
size of pharyngeal orifice was first introduced by Hynes in 1950 (Fig. 33.46,
33.47A–D). The sphincter is formed from the posterior tonsillar pillars, which
are raised, including the palatopharyngeus, rotated and sutured end to end.
This procedure is designed to reduce the size of the lateral ports and tighten
the central area.
FIGURE 33.46 (A–D) Hynes pharyngoplasty—clinical pictures.

FIGURE 33.47 (A–D) Illustration of Hynes pharyngoplasty.
Speech therapy
If the cleft palate repair had not significantly contributed to the improvement
of speech, then a secondary surgery in the form of pharyngoplasty would be
required which could improve articulation of speech. But it is the speech
therapy which can directly improve articulation and communication skills.
If significant velopharyngeal insufficiency persists following primary repair
of the palate, there may be nothing a speech therapist could do to improve the
articulation to any significant extent. If on the other hand, there is
velopharyngeal sufficiency for speech, no gross collapse of the alveolar arch
and disturbance to maxillofacial growth is minimised, it is much easier for the
speech therapist to effect speech changes.

1. Gingivoperiosteoplasty
2. Primary bone grafting
3. Secondary alveolar bone grafting
4. Alveolar distraction
Gingivoperiosteoplasty
Stripping of periosteum from the bone is avoided till bone growth is complete
for fear of losing growing potential. However, a few surgeons practice a form
of early alveolar cleft repair by suturing the periosteum of the cleft alveolar
ridges together.
Primary bone grafting

The maxilla with cleft has a bony deficiency at the canine-lateral incisor region.
This may be accompanied by a hypoplastic or absent lateral incisor. Lack of
bone at the anterior maxilla results in:
1. Lack of bone for permanent canine eruption or orthodontic treatment.

2. Unequal distribution of the growth impetus of the premaxillary
vomerine suture which leads to:
a. Premaxillary protrubance and lateral segments collapse in
bimaxillary cleft.
b. Collapse of minor segment (cleft side maxillary alveolus)
and unequal anteroposterior position of minor and major
segments (noncleft side maxillary alveolus) in unilateral
cleft.
c. Midfacial growth retrusion.
d. Poor arch forms.
e. Inadequate alveolar bone.
In order to prevent these sequel, the bone deficiency can be filled with bone
or bone substitutes. This concept of treatment is called alveolar bone grafting.
This aims to eliminate oronasal fistulae, create bone support for tooth
eruption, restructure the hypoplastic piriform aperture and provide nasal base
elevation.
Depending upon the timing of this surgery, this treatment has been termed
primary, early secondary or secondary alveolar bone grafting.
1. Primary bone grafting is performed in children younger than 2 years of

age.
2. Early secondary bone grafting is performed between 2 and 5 years of
age.
3. Secondary bone grafting is performed greater than 5 years of age.
Early stripping of periosteum from the maxilla, especially the premaxillary-
vomerine suture, could result in maxillary growth retardation. Hence, the
timing of alveolar bone grafting (ABG) depends on the individual needs of the
cleft child and the protocol followed by the cleft surgeon. The protocol of cleft
repair differs from surgeon to surgeon and the timing of the bone grafting is
still a controversy.
Primary bone grafting is advocated by less number of surgeons. The aim of
primary bone grafting is to achieve early stabilisation of the maxillary arches
and to obliterate alveolar oronasal fistula (nasal fluid escape and improved
oral hygiene).
Since the iliac crest is still cartilaginous in children below 5 years, the rib is
the source of bone for the treatment. Currently, with the availability of rhBMP-
2, a second (donor) site morbidity resulting from graft harvesting can be
avoided. In bilateral clefts, with protrusion, a premaxillary setback is
concurrently performed.
Secondary alveolar bone grafting

Bone grafting of the alveolus has become an essential part in the contemporary
surgical management of many orofacial cleft deformities. Any patient born
with a complete cleft should be considered for alveolar grafting. Secondary
alveolar bone grafting in the mixed dentition, before the eruption of
permanent canine, is now established as the treatment for residual alveolar
defect in cleft lip and palate patients. An important issue in alveolar cleft
management is the timing of bone graft placement. Primary bone grafting is
done in patients younger than 2 years of age, whereas secondary bone grafting
is done generally between the age of 7 and 11 years. With few exceptions
primary or very early bone grafting has been abandoned because of the risk of
maxillary growth disturbance.
Goals of secondary alveolar bone grafting
• Stabilisation of maxillary arch

• Closure of vestibular and palatal oronasal fistulae
• Provision of bone of sufficient quantity and appropriate quality to allow
not only eruption of the permanent lateral incisor and canine teeth but
also maintenance of adequate bone about the root of the permanent
central incisor adjacent to the cleft
• Provision of support for the soft tissue nasal base and reconstruction of
the hypoplastic piriform aperture
• Provision of suitable bony architecture of the premaxilla and anterior face
of the maxilla on the cleft side to support accurate nasolabial muscle
reconstruction
• Provision of adequate bone stock for ultimate placement of
osseointegrated implant
• To provide better periodontal support for teeth bordering the cleft
Bone grafting
Most bone grafting techniques utilise cancellous bone to promote the
formation of new bone. Autogenous cancellous bone has been shown to be an
active osteogenic substance that can produce rapid healing in osseous defects.
In cancellous bone grafts, viable cells are transplanted and early
revascularisation is noted within 1 week and full revascularisation within
3 weeks under ideal conditions.
For successful bone grafting of alveolar defects, certain conditions must be
satisfied. A watertight repair of the palatal cleft and the nasal lining and a
secure closure of the soft tissue across the anterior alveolus are essential.
Atraumatic surgical technique, avoidance of heat generation during the
harvesting of the graft and storage of bone particles in a saline soaked sponge
to avoid desiccation are important in maintaining cell viability before
transplantation.
Procedure
In older patients, iliac bone has been most frequently used since it is a rich
source of purely cancellous bone. In children under the age of 9–10 years, one
cannot expect to find large amounts of cancellous iliac bone, since apophysis
of the iliac crest is still largely cartilaginous. The cancellous bone is harvested
through a short incision over the iliac crest. A trap-door of cortical bone is
raised, hinged on the inner edge of the crest. By means of a small gouge and
sharp spoon, thin slivers of cancellous bone are removed, leaving the inner
and outer cortical plates intact. The cortical lid is replaced and held in position
by absorbable sutures (Fig. 33.48A–F).
FIGURE 33.48 Harvesting the iliac cancellous bone graft. (A) Skin
incision placed 1 cm posterior to the anterior superior iliac spine
along the iliac tubercle. (B) Layerwise dissection done followed by
the periosteal incision. Subperiosteal dissection done exposing the
anterior iliac crest. (C–D) Anterior posterior and medial osteotomy
done raising a laterally based osteoplastic flap exposing the
cancellous marrow. (E) Cancellous bone marrow harvested using a
bone scoop. (F) Harvested iliac cancellous bone graft.
The cleft area is widely exposed through incisions along the edges of the
cleft, midway between the palate and the nasal floor. Superiorly based flaps
are developed for nasal lining and inferiorly based flaps are reflected caudally
for closure of the palate. All soft tissues within the cleft are completely
removed. The nasal layer suturing is completed and then the palatal
mucoperiosteal flaps are brought together with everting mattress sutures.
This leaves a well-defined pear-shaped cavity. The cancellous bone is now
packed into the alveolar defect, with a layer of bone chips also placed
subperiosteally on the front of the hypoplastic maxilla and under the alar base
and nostril sill. The bone grafts are then covered by suturing together the
lateral and medial flaps and across the ridge of bone grafts to the palatal
mucoperiosteum (Fig. 33.49A–D).
FIGURE 33.49 Secondary alveolar bone grafting for alveolar cleft

repair using cancellous iliac bone graft. (A) Oronasal fistula distal
to the central incisor and medial to canine. (B) Oronasal fistula
leading to the alveolar cleft. (C) Mucoperiosteal flap raised to
expose the alveolar cleft. (D) Dissection of the anterior maxilla and
the cleft is carried out and, when required, incisions can be made
on the palatal surface to facilitate closure of the anterior palatal
cleft. After dissection and closure of the nasal lining, the bone graft
is packed into the deficient area. An undercutting of the superiorly
based flap from the surface of the upper lip is performed to allow
tension-free closure over the bone graft.
In recent times, we have been able to substitute the bone with rhBMP-2
soaked in absorbable collagen sponge (ACS) (Fig. 33.50A–D). Details regarding
the same are explained in Chapter 50 Recent Advances.
FIGURE 33.50 Secondary alveolar bone grafting for alveolar cleft
repair using rhBMP-2. (A) Oronasal fistula. (B) Alveolar cleft
exposed for the placement of the graft. (C–D) Recombinant bone
morphogenetic protein (rhBMP-2) graft bound to absorbable
collagen sponge (ACS) placed in the alveolar cleft and the buccal
layer closed.
Primary bone grafting, premaxillary setback

Most of the reports on primary bone grafting described the use of autogenous
rib, which has a high ratio of cortical to cancellous bone. In cleft patients, most
grafting procedures have been performed with cortical or corticocancellous
bone from rib, tibia or iliac crest (Fig. 33.51A–J).
FIGURE 33.51 (A–D) CT of a bilateral cleft child with prognathic
premaxilla. (E) Prognathic premaxilla. (F) Sliding osteotomy of the
vomer done posterior to the premaxillary—vomerine epiphyseal
line in order to setback the prognathic premaxilla. (G–H) Premaxilla
stabilised using interdental wires and alveolar cleft repaired by
secondary alveolar bone grafting using rhBMP-2 bound to ACS. (I–
J) Postoperative CT showing good bone formation with
stabilisation of premaxilla.
Alveolar distraction osteogenesis

Alveolar distraction is a relatively novel method for creating new
intramembranous bone and soft tissue based on the biological principle of
tension and stress and it is used to create bone and soft tissue similar to those
adjacent to the surgical site. This method corrects both hard and soft tissue
defects creating an adequate volume of bone, into which implants might be
placed and histogenesis process creates normal perialveolar architecture
(Fig. 33.52A–I).
FIGURE 33.52 Alveolar cleft closure by distraction. (A) Alveolar

cleft with oronasal fistula. (B) Alveolar transport distractor. (C–D)
Osteotomy of the alveolus to create a dentoalveolar transport
segment for closing the alveolar cleft. (E–F) Fixing the modified
distractor device to the transport segment and the distal bone
segment. (G) A sleeve is placed on the distractor to prevent
damage to the lip. (H) After completion of transport distraction,
docking and device removal. (I) After prosthetic rehabilitation.
Orthodontic treatment
• The aim of orthodontic treatment is to provide an dentition that is in
proper alignment and function. The anterior maxillary dentition
should be symmetrical around the facial midline. This arrangement
facilitates and improves the quality of the orthognathic surgery.
• Orthodontic treatment takes place at three different stages depending
upon the severity of the cleft. The stages are: (i) functional
orthognathic treatment in infants; (ii) anterior crossbite correction in
mixed dentition; and (iii) orthodontic treatment of the permanent teeth
during adolescence before treatment of the orthognathic deformity.
• Early orthodontic treatment involves orthopaedic movement of the
alveolar or dentoalveolar arches before the primary surgeries. The
purpose of this treatment is to align the lateral dentoalveolar arches
and to reposition the premaxilla in case of bilateral cleft lip. Palatal
plate and headgears are used for this purpose (Fig. 33.53A–B).
• Orthodontic treatment during mixed dentition period is most often
neglected. Minor crossbites occur quite often and deciduous lateral
incisor may be absent or hypoplastic. This tooth should be maintained
as an extraction may widen the existing cleft and thus make the
treatment procedure difficult.
• A removable appliance with Adams clasp for retention and Z-spring or
anterior expansion screw to move the incisors may be used. Functional
appliance such as bite plane or Frankel’s appliance may also be
chosen.
• Expansion of the arches is better performed before bone grafting since
expansion of the palatal arches can open up palatal fistulae.
• Secondary alveolar bone grafting facilitates canine eruption and it
should be performed before final orthodontic alignment (Fig. 33.54A–
B).
• The main orthodontic treatment should be carried out before the
treatment for the orthognathic problem. Minor orthodontic tooth
movement such as crossbite may be required before the treatment.
• Maxillary expansion is required in case of small dentoalveolar segment
with minor crossbite. The maxilla may be expanded by means of quad
helix or fixed palatal arch or by means of a removable appliance with a
midline screw.
FIGURE 33.53 (A–B) Head gear with maxillary expansion
appliance.
FIGURE 33.54 (A) OPG of a unilateral cleft child showing right

alveolar cleft, retained deciduous right maxillary lateral incisor with
impacted right maxillary permanent canine and microform right
maxillary lateral incisor. (B) After grafting the alveolar cleft with
rhBMP-2, orthodontic treatment done. Note the eruption of the
lateral incisor through the graft and achievement of arch form (all
permanent teeth except the impacted maxillary canine).
Aims of orthodontic treatment for children with clefts
• To achieve an optimal occlusion and dentofacial aesthetics within the

constraints imposed by the underlying skeletal pattern.
• To keep the duration of treatment to a minimum period.
• To accomplish as much as possible during periods of active treatment.
Many children who have undergone the repair of a cleft lip and palate develop
an increasing deformity of the facial structures as they grow, particularly as
they pass through adolescence. This is particularly due to underdevelopment
of the maxilla and relatively greater growth of the mandible which leads to a
concave facial profile and disproportion between the height of the middle and
lower thirds of the face (Fig. 33.55) These deformities can be corrected through
orthognathic surgery. Usually this involves a maxillary osteotomy at Le Fort I
level less often osteotomy at a higher level may be needed, combined with
mandibular or genial osteotomies (Fig. 33.56).
FIGURE 33.55 (A–B) Skeletal class III occlusion in a patient with

unilateral cleft lip due to maxillary hypoplasia. Orthodontic
treatment done to align teeth prior to orthognathic surgery for
correction of the skeletal deformity. (C) Lateral cephalogram
showing maxillary hypoplasia, dish face deformity, class III
occlusion. (D) Lateral profile showing protrusive, pendulous lower
lip with sunken upper face. (E) Unilateral cleft lip facies with
maxillary hypoplasia and nasal deformity.
FIGURE 33.56 Le Fort I advancement for the correction of cleft

maxillary hypoplasia. (A) Exposure of the maxilla by vestibular
incision. (B) Le Fort I osteotomy. (C) The osteotomised maxilla
advanced and fixed using titanium advancement plates and
screws. (D) Preoperative profile—before maxillary advancement
surgery. (E) Postoperative profile—after maxillary advancement
surgery. (F) Preoperative facial appearance —before maxillary
advancement surgery. (G) Postoperative facial appearance—after
maxillary advancement surgery.
Maxillary hypoplasia can give rise to increasing psychosocial problems,

difficulties in mastication, pain and speech abnormalities, all of which would
make early surgical correction desirable. Unfortunately, extensive surgery to
the maxilla at an early age may cause damage to unerupted teeth, contribute to
retardation of future maxillary growth or create an ideal occlusion which is
later disrupted by disproportionate maxillary and mandibular growth. For
these reasons, orthognathic surgery is usually delayed until facial growth is
complete.
Distraction osteogenesis
Distraction osteogenesis is a technique of bone lengthening by gradual
movement and subsequent remodelling. The idea behind this concept is the
law of tension-stress, stating that gradual traction on the living tissues creates
stresses that stimulate and maintain the regeneration and active growth of
certain tissue structures.
Concept of applying distraction osteogenesis to the treatment of craniofacial
deformities was not conceived until 1972, when Snyder used a Swanson
external fixator to lengthen a canine mandible. In this experiment, he
surgically shortened one side of the mandible by removing a 1.5 cm segment
and allowed the bone to heal. This created a large crossbite that was surgically
corrected 10 weeks later by attaching an external fixator, performing an
osteotomy and slowly expanding the device until the crossbite was
normalised. Refer to Chapter 36 Distraction Osteogenesis.
Distraction osteogenesis in cleft maxillary hypoplasia

Experience with the midface advancement techniques in the past few years
indicates that distraction osteogenesis is a viable treatment option for
lengthening of the hypoplastic midface. It could be recommended as a first
alternative in the deficiencies of the midface for an ideal three-dimensional
hard and soft tissue reconstruction, with excellent outcome.
Distraction osteogenesis is an easy, predictable, reliable technique that
allows soft and hard tissue reconstruction without the need of bone and soft
tissue grafting. It is a well-accepted modality for a predictable correction of
osseous deficiencies with vascular bone in patients with cleft deformity and
provides a safe and effective method of bone lengthening (Figs. 33.57 and
33.58).
FIGURE 33.57 Le Fort I advancement by maxillary distraction using
rigid external device. (A–B) Preoperative view—before maxillary
advancement by distraction. (C) Lateral cephalogram showing
severe maxillary hypoplasia. (D) Exposure of maxilla by crevicular
incision. (E) Le Fort I osteotomy and downfracture. (F) Rigid
external distractor (RED) halo fixed to the cranium. (G) RED in
distraction phase—note improvement of profile. (H) RED fixed to
the dental arch to distract the downfractured maxilla. (I)
Postdistraction occlusion—overcorrection achieved to compensate
for relapse. (J–L) Postdistraction occlusion, postoperative facial
appearance after maxillary distraction (after 1 year follow-up).
FIGURE 33.58 Internal maxillary distraction. (A–E) Unilateral cleft
lip and palate facies: maxillary hypoplasia, concave facial profile,
skeletal class III malocclusion, collapsed maxillary arch.
Postalveolar bone grafting, planned for presurgical orthodontics
and internal maxillary distraction. (F–I) Presurgical orthodontics
initiated before distraction. (J) Exposure of the maxilla through a
vestibular approach. (K) Le Fort I osteotomy performed and the
internal maxillary distraction device fixed to the anterior surface of
the zygoma. (L) The internal distractor fixed to the osteotomised
maxilla (left). (M) The internal distractor fixed to the osteotomised
maxilla (right). (N) The activating arm exposed intraorally in the
buccal sulcus. (O–P) Facial appearance at the end of distraction.
(Q) Intraoperative view at the removal of distractor device after
complete consolidation. (R–S) Comparison of lateral cephalogram
showing change in skeletal relation from class III to class I. (T)
Postdistraction occlusion showing achievement of class I incisor
relationship. (U–V) Postdistraction orthodontics continued for
dental arch alignment. (W) Postdistraction facial appearance. (X)
Postdistraction facial profile.
Rhinoplasty
Nose revision
The nasal deformity is enormously important. It almost invariably becomes
worse with age. This deformity is very complex in its three-dimensional
components and is widely considered to be difficult or impossible to correct
perfectly.
Nose tip
Secondary corrections of the nose include balancing operations of the tip. It
can be observed quite often that cleft side will not project so far forward and
the nostril-rim will hang down. When viewed from below, the cleft side nostril
apex will be too far back and the cleft side alar base will either be too far back,
too high or too low. Surgeons use a group of procedures to correct these. Very
often, all the tissues required for the reconstruction are present and simply
need to be rearranged or adjusted but rarely a shortage of bone, cartilage, skin
or mucosal lining may be present. In such cases, bone may be taken from the
hip bone or a rib; cartilage from the nasal septum or from the concha of the ear
through a little cut at the back; skin can be taken from the back of the ear and
mucosa from the lining on one side of the nasal septum or inside of the cheek
(Fig. 33.59A–R).
FIGURE 33.59 Secondary rhinoplasty for the correction of
unilateral cleft lip nose defect. (A–B) Predistraction facial
appearance— showing maxillary hypoplasia. (C–D) Facial
appearance after maxillary advancement by distraction and
orthodontic alignment. (E) Worm’s eye view of the nose showing:
depressed, hypoplastic ala on the cleft side with septal deviation.
(F) Costal cartilages harvested for nasal reconstruction. (G) Open
rhinoplasty—nasal cartilages exposed through a transcolumellar
incision. (H–I) Augmentation of the dorsum with a costal cartilage.
(J–K) Augmentation of the columella and the right hypoplastic ala
using a costal cartilage graft. (L) Redrapping the skin followed by
primary closure. (M–N) Postoperative appearance showing
augmented columella, aesthetic nasolabial angle and symmetric
alae. (O–R) Postoperative appearance showing straight profile with
aesthetic nasolabial angle, symmetric alar base and alar cartilages,
reconstructed nasal sill and acceptable nasal projection.
Nasal septum
The operation depends on the fact that septal cartilage is always convex. It is
therefore scored on its concave side, which makes the concavity flatten. The
nasal cavities are then packed to hold the cartilage straight while it heals. But
the cartilage and soft tissues have a ‘memory’ and may try to drift back to their
original position. Therefore, a perfect alignment is hard to achieve in all cases.
The nasal correction is done after orthodontic and orthognathic correction of
the maxilla and mandible (Fig. 33.60A–M).
FIGURE 33.60 (A–C) Preoperative view showing hypoplastic
maxilla in skeletal class III with depressed cleft left ala and
concave profile. Note the reverse overjet and class III incisor
relation. (D–E) Le Fort I osteotomy and maxillary advancement
fixed using titanium miniplate. (F) Occlusion at the end of surgery
and postsurgical orthodontics showing class I incisor relation and
missing 22. (G–H) Missing 22 replaced with implant supported
prosthesis. (I) Open rhinoplasty via transcolumellar incision and
infracartilaginous incisions exposing the deviated nasal septum.
(J–K) Caudal septal resection, dorsal and alar augmentation with
costal cartilage grafts. (L–M) Postoperative appearance showing
change in facial and nasal profile to straight profile and aesthetic
nasal projection.
Lip scar revision

Though rarely but abnormalities do occur after cleft lip repair, the most
common being asymmetry of the Cupid’s bow. Many techniques are followed
for the correction of these deformities like V–Y advancement flap,
Kapetansky’s pendulum flaps, Abbe flap, etc.
Abbe flap
Due to lack of tissue and short appearance of the upper lip, normal lower lip
may look protuberant. In the cleft patients, upper lip usually lies on the bony
maxilla which lacks the proper amount of forward projection. In some
patients, in addition, the original lip repair may not have produced a normal
Cupid’s bow. In such cases, a very satisfactory solution may be achieved by
transferring a wedge of the full thickness flap from the lower lip to the upper
lip. This flap is sutured to the upper lip and forms a bridge of tissue which
divides the mouth opening into two. This remains in place for 10–14 days
while the tissue picks up a new blood supply, after which the bridge is divided
and both top and bottom lip scars completed (Figs. 33.61–33.63).
FIGURE 33.61 (A–B) Abbe flap.
FIGURE 33.62 (A–B) Abbe flap and rhinoplasty.
FIGURE 33.63 Lip revision using Abbe flap and rhinoplasty. (A–C)
Secondary cleft deformity—short hypoplastic mid upper lip,
underprojected nose with short columella. (D) Open rhinoplasty via
transcolumellar incision. (E) Columellar strut and tip graft in place
followed by interdomal suture to define columella and tip defining
points. (F) Marking for Abbe flap. (G) Abbe flap used to reconstruct
the mid upper lip. (H–J) Abbe flap in place during the period of
vascularisation prior to division. (K–M) Postoperative view after
division of the Abbe flap showing aesthetic upper lip and nasal
projection.
Prosthesis for cleft patients
The usual prosthetic treatment is replacement of a tooth or teeth in the line of
the cleft. If the anterior segment in a complete bilateral cleft has not been
surgically stabilised, fixed prosthetics should be considered.
Unrepaired clefts are usually restored using a combination of fixed and
removable appliance.
Types of prosthesis
Intraoral prosthesis includes artificial replacements that reconstruct the
missing parts of the oral cavity.
• Implant prostheses are nonliving substitutes that are placed within the
patients’ tissues to support or reconstruct an anatomic part.
• Treatment appliance: Used in the course of patient’s treatment for
shaping or applying force to tissues. These are not called prostheses,
because they do not actually duplicate an anatomic part.
Infant feeding prosthesis (palatal plate). The purpose of this prosthesis is

to provide a normal contour to the defective alveolar process and palate. Thus,
tongue can flatten and press the nipple into the palate during normal suckling
movements, e.g. palatal plate.
Head gears
They are used during the growth period to intercept or correct the
malocclusion as well as to distalise the maxillary dentition or maxilla itself.
They derive anchorage from the cervical or cranial regions.
Pharyngeal obturators
This is a device that prevents air from escaping into the nasal cavity by sealing
of the posterior pharyngeal wall during speech, for example, speech bulb. It is
composed of three components: (i) maxillary appliance, (ii) a palatal extension
and (iii) a nasopharyngeal section.
The maxillary appliance acts as a source of retention and resists the
dislodging forces of the nasopharyngeal section. The palatal extension is the
connection between the maxillay appliance and the nasopharyngeal section. It
is usually constructed as a loop so that the nasopharyngeal section will not
rotate on it. The nasopharyngeal section of the obturator acts to separate the
oral and nasal cavity.
Fixed and removable partial dentures

The fixed partial denture is used to replace and restore the missing teeth by
using the support of adjacent teeth. Removable prosthesis is usually a
modified partial denture, which restores the teeth and associated alveolar and
supporting structures to achieve an aesthetic and functional result.
Dental implants
For cleft palate patients, restoration of the single missing tooth to provide an
abutment for small bridges appears to be the primary indication for implants
in these patients (Fig. 33.60F–H). Considering the increasing number of dental
implants used in the general population, this treatment modality will
undoubtedly play a role in prosthodontic consideration of the treatment of the
cleft patients.
CHAPTER 34
Orofacial Neuropathy

• Parts of the neuron
• Epineurium
• Nerve fibres
• Types of nerve fibres
• Fascicles
• Neuromas
Traumatic nerve injuries
• Neurapraxia
• Axonotmesis
• Neurotmesis
Classification of nerve injuries
Inflammation
• Neuritis
Facial nerve pathology
Anatomy of facial nerve
Facial palsy
• Aetiology of facial palsy
Bell’s palsy
• Aetiology
• Clinical features of bell’s palsy
• Clinical evaluation
• Diagnosis
• Topognostic testing
• Electrophysiologic tests
• Imaging studies
• Prognosis
• Management
Neuralgia
Trigeminal neuralgia
• Anatomy
• Aetiology
• Aetiological theories
• Pathophysiology
• Diagnosis
• Classification
• Diagnostic test
• Management
• Postoperative care
Anaesthesia dolorosa
Geniculate neuralgia
Sphenopalatine neuralgia (Sluder’s neuralgia)
Paratrigeminal neuralgia of Raeder
Neuron is an excitable cell, which consists of nerve cell body and all its
processes that is specialised for reception of stimuli and conduction of the
nerve impulses. They vary in size and shape but each possesses a cell body
from whose surface projects one or more processes called neurites. The neurites
are further classified into axons and dendrites.
Allodynia Pain caused to a stimuli, which usually does not provoke pain.
Analgesia Absence of pain to stimuli, which normally causes pain.
Causalgia Chronic progressive disease causing persistent burning pain.
Following nerve injury, allodynia and hyperpathia may occur; initially
there is vasomotor and pseudomotor dysfunction which later progresses
to atropic changes.
Dysaesthesia Anabnoxious, abnormal sensation, may be spontaneous or
evoked.
Hyperaesthesia Elevated response to stimuli, this excludes response of special
senses.
Hyperalgesia An exaggerated response to normally painful stimuli.
Hyperpathia A symptom associated with some neurological disorder
characterised by elevated response to stimuli mainly when the stimuli is of
high threshold and repetitive in nature.
Neuralgia Pain in the areas specific to the nerve supply.
Neuritis Inflammation of the nerve or nerves.
Neuropathy Any changes in a nerve that creates a pathologic or functional
dysfunction.
Nociception Pain perception resulting from stimulation of nociceptors.
Nociceptor A sensory receptor that responds to any damaging stimuli or
normal stimuli, which may become damaging if it is prolonged.
Pain threshold The lowest stimuli potential at which the pain is perceived by
the individual.
Pain tolerance level The highest stimuli potential that the subject can tolerate.
Parts of the neuron (Figs. 34.1 and 34.2)
Nerve cell body

It is a mass of cytoplasm in which nucleus is embedded. It is bounded
externally by a plasma membrane.
FIGURE 34.1 (A–C) Nerve anatomy.

FIGURE 34.2 Multipolar neuron.
Dendrites
The nerve cell has 5–7 processes called dendrites that extend outward from the
cell body and arborise extensively.
Axon
A neuron has a long fibrous axon that originates from the axon hillock of the
cell body.
Axon hillock
Thickened area of the cell body.
Initial segment
The first portion of the axon.
Synaptic knobs
The axon is divided into terminal branches, each ending in a number of
synaptic knobs. They contain synaptic vesicles or granules, which contain
synaptic transmitters, which are secreted by the nerves and stored.
Myelinated neurons
Outside the CNS, the axon is myelinated, i.e. the axon acquires a sheath of
myelin, a protein–lipid complex made up of many layers of the cell membrane
of Schwann cells.
Nodes of Ranvier
The myelin sheath envelops the axon except at the endings and nodes of
Ranvier. They are periodic 1 mm constrictions and that are about 1 mm apart.
Epineurium
The epineurium is the outermost covering of a peripheral nerve. The
epineurium is made of areolar connective tissue and has numerous blood
vessels, which supply the peripheral nerve. Though, highly dense collateral
supply is provided to the nerve, disruption in blood supply may occur causing
many kinds of nerve injuries.
Nerve fibres
Nerve fibres occupy 25%–75% of the cross-section of a nerve. The composition
of nerve fibre in a nerve varies on its type and location. They may be
myelinated or unmyelinated. The myelinated nerve fibres are thicker (2–
25 mm) than the unmyelinated fibres (0.2–3 mm).
Types of nerve fibres
Fascicles
Clusters of nerve fibres, which form bundles, are called fascicles. The fascicle is
covered by perineurium. From the surgical aspect, the perineurium is the
smallest structure in peripheral nerve where the sutures are placed. Fascicular
diameter ranges from 0.04 to 3 mm. Fascicles are organised as a single fascicle
or in bands as they course along the nerve. The fascicles are embedded in
epineural connective tissue and epifascicular interfascicular epineurium.
Peripheral nerves are classified as monofascicular, oligofascicular and
polyfascicular. Monofascicular nerves such as the terminal branches of digital
nerves which have one main fascicle with many small nerve fibres. They are
generally either pure sensory or pure motor in function. Oligofascicular nerves
have less number of fascicles, they may be pure or mixed with both sensory
and motor function. Example: Ulnar nerve at the elbow. Polyfascicular nerves
consist of a number of minute fascicles. Example: Radial nerve in the upper arm.
Physiology of nerve injury

Following a trauma to the axon, many biochemical and histological changes
occur in the cell body proximal and distal to the site of the injury. The extent of
damage to nerve depends on the distance from the injury to the cell body
(proximal injuries usually more severe than distal injuries), the type of injury
(crush injuries more severe than clean transections), the age of the patient
(older individuals sustain more severe injury than younger patients),
nutritional and metabolic status of the patient.
Physiology of nerve healing

The Schwann cells surround both myelinated (one Schwann cell per nerve
fibre) and unmyelinated (one Schwann cell per several nerve fibres) nerves,
and they play a major role in nerve survival and regeneration following injury.
The myelin sheath does not survive a nerve injury but the Schwann cells do,
and they provide a supportive role in the production of neurotropic factors
(such as nerve growth factor) that enhance neural recovery. Nerve healing
involves both degeneration and regeneration. The nerve cell body responds
with an increased metabolic phase with a heightened production of RNA
(protein synthesis) and breakdown of Nissl’s substance for export from the cell
body with the accumulation of particulate cellular debris. Within days, axonal
sprouts begin to bud and extend from the proximal nerve stump in the area of
injury. Each axon may have as many as 50 collateral sprouts from the proximal
nerve stump with random orientation toward the distal nerve stump. A high
level of activity of Schwann cells occurs which begin to form new myelin
‘conduits’ in anticipation of the arrival of the new axonal sprouts. Nerve
growth factors produced influence the direction of sprouting and guide the
new axons into the newly formed myelin sheath conduits, known as the bands
of Büngner. In the event spontaneous neural regeneration will occur. If one or
more of the reparative processes fail to occur at the appropriate time and
location, there may formation of a neuroma and lack of spontaneous
neurosensory recovery. This failure may be due to a variety of reasons
including advanced local tissue scarring, insufficient neurotrophic and
neurotropic factor production, or malaligned nerve stumps separated beyond
the critical size defect to allow spontaneous reconnection (Fig. 34.3).
FIGURE 34.3 (A–E) Neural wound healing mechanisms.
Neuromas
A neuroma is caused due to local injury to peripheral nerves, which presents
as a painful, submucosal bump. Most neuromas are surgically excised.
Neuroma is not classified as a tumour; it is only a series of changes taking
place after a local injury to the peripheral nerve. They are the consequences of
disrupting a peripheral nerve during surgery or trauma. After recovery, the
regenerated nerve fibres arrange themselves in a disorganised manner, as they
are unable to penetrate into the severed nerve sheath. This results in the
formation of a painful disorganised mass in the area of injury.
Nerve regeneration is stimulated by Schwann cells and trophic factors as
nerve growth factors. There is exaggerated expression of these trophic factors
in neuroma formation.
Histological features of traumatic neuromas include presence of clusters of
small peripheral nerve fibres, this feature differentiates it from the
neurilemmoma and neurofibroma.
Treatment
Traumatic neuroma is surgically excised. Recurrence is rare and there is no
risk of malignant transformation.
Types of neuromas
Neuromas are classified by gross morphology into the following types:
• Amputation (stump) neuroma,

• Neuroma-in-continuity (central or fusiform neuroma), and
• Lateral neuromas that are either lateral exophytic neuromas or lateral
adhesive neuromas (Fig. 34.4).
FIGURE 34.4 Types of neuromas.

Disorders of nerve are classified as depicted in Table 34.1.
Table 34.1
Classification of disorders of nerve
1. Traumatic injuries
a. Neurapraxia
b. Axonotmesis
c. Neurotmesis
d. Traumatic neuroma
2. Inflammation
a. Neuritis
3. Neuralgias
a. Trigeminal nerve neuralgia
b. Bell’s palsy
c. Glossopharyngeal neuralgia
d. Sphenopalatine neuralgia
4. Specific types of injuries
a. Injection injuries
b. Irradiation
c. Compression neuropathies
5. Tumours
a. Benign and malignant
Traumatic nerve injuries

In 1943, Seddon subdivided nerve injuries into three main types depending
upon the continuity of the nerve (Figs. 34.5–34.6). The three types are:
neurapraxia, axonotmesis and neurotmesis.
Neurapraxia
In this case, there is a break in impulse transmission down the nerve fibre and
recovery takes place without Wallerian degeneration.
Anterograde (Wallerian) ascending degeneration of axons

When an axon of the central nervous system is severed, its distal (ascending)
segment, being separated from its cell body, quickly degenerates and
disappears and its investing myelin sheath undergoes a slower breakdown
into simpler lipids that are eventually catabolised. This process is called
anterograde or Wallerian degeneration.
Causes
• Concussion or shock like trauma to the nerve

• Compression from blunt trauma
FIGURE 34.5 (A–C) Traumatic nerve injuries—Seddon
classification. (A) Neuropraxia, (B) Axonotmesis, (C) Neurotmesis.
FIGURE 34.6 Response of the nerve fibre to different types of

injuries.
Loss of function
• Reversible within hours to months of the injury

• Average recovery time is about 6–8 weeks
Axonotmesis
Axonotmesis refers to greater severity of nerve injury than neurapraxia where
there is loss of continuity of the axon and the myelin sheath though the
connective tissue framework of the nerve (the encapsulating tissue, the
epineurium and perineurium) are preserved.
Clinical features
• Wallerian degeneration
• Loss in motor and sensory function of the nerves
• Retrograde proximal degeneration of the axon
Regeneration
Proximal lesion may grow distally as fast as 2–3 mm/day and distal lesion as
slowly as 1.5 mm/day.
Neurotmesis
Neurotmesis is the most severe lesion with complete loss of continuity of axon
inclusive of the connective tissue capsule, thereby creating the risk of no
recovery.
Cause
• Severe contusion
• Stretch
• Lacerations
Structures involved
The axon with encapsulating connective tissue loses their continuity. The
extreme degree of neurotmesis is transection. This results in a complete loss of
motor, sensory and autonomic functions. The cut end of axons if are wide
apart, a reparative tendency in the form of axonal regeneration causes a
neuroma to form in the proximal stump.
Classification of nerve injuries (Fig. 34.7)

FIGURE 34.7 Sunderland’s classification.
Inflammation
Neuritis
‘Neuritis’ is the term applied to describe inflammation of a peripheral nerve,
mostly associated with degenerative changes in nervous tissue.
Multiple neuritis or polyneuritis is a disease, which symmetrically affects
most of the peripheral nerves simultaneously.
Types
• Localised
• Multiple/polyneuritis
Aetiology
1. Localised
a. Exposure to cold
b. Following trauma to a nerve
c. Stretching of a nerve
d. Nerve may share extension of neighbouring inflammation
e. Vascular lesions, e.g. occlusion of a blood vessel or
haemorrhage into the nervous tissue
2. Generalised
Infection—due to invasion of microorganisms.
• Toxic—metallic or chemical poisoning, alcoholic
• Metabolic—vitamin deficiencies, pernicious anaemia
• General disorders—gout, rheumatism, tubercle, carcinoma
• Autoimmune diseases in which the body’s natural defences
attack the peripheral nerves, e.g. systemic lupus
erythematosus (SLE), idiopathic peripheral neuropathy (In
case of autoimmune diseases, the peripheral nerves are
damaged by the auto antibodies.)
• Diabetes mellitus
• Toxaemia of pregnancy
Signs and symptoms
• In localised neuritis, the patient complains of pain of boring character

along the course and distribution of the nerve.
• On examination, the involved region is slightly erythematous and
sensitive to pressure; oedema and painful muscular movement along
the affected nerve.
• Numbness, loss of tactile function is noted as the disease progresses,
finally resulting in muscular atrophy.
• Degeneration occurs in the nerve or nerve sheath.
• Mild cases such as exposure to cold or injury may recover in a few
days.
• While severe cases such as those damaged by the pressure of an
unreduced fracture may last for months.
Facial nerve pathology

Facial nerve injury leads to facial palsy or Bell’s palsy. Bell’s palsy is an
idiopathic paresis or paralysis of the facial nerve of sudden onset. The name
was coined after Sir Charles Bell who demonstrated the separation of the
sensory and motor innervations of the face.
The facial nerve has three functions: (i) maintaining the muscular tone,
without which the facial tissues droop, (ii) facial muscular activity such as
closing the eyes or labial movement, (iii) emotional expression.
Acute facial nerve paralysis is not an uncommon clinical term to a surgeon.
To provide a correct diagnosis and management of patients with acute facial
nerve paralysis needs, a vivid understanding of the anatomy and function of
the facial nerve is essential.
Anatomy of facial nerve (Figs. 34.8–34.9)

The facial nerve consists of a motor and a sensory part, the later being
frequently described under the name of the nervus intermedius (pars
intermedii of Wrisberg).
FIGURE 34.8 Course of the facial nerve.
Branches of facial nerve transmit a combination of sensory, motor and

parasympathetic fibres.
Courses:
• Intracranial course
• Extracranial course
Intracranial course of facial nerve

The nerve arises from the lateral part of the lower border of the pons and
begins as two roots: a large motor root and a small sensory root (the part of
the facial nerve that arises from the sensory root is sometimes known as the
intermediate nerve).
Along with the eight cranial nerve, the two roots enter the internal acoustic
meatus.
In the meatus, the motor root lies over a groove in the eighth nerve and the
sensory branches passes between them. The roots leave the internal acoustic
meatus, and enter into the facial canal, which is a ‘Z’ shaped structure. Within
the facial canal, the two roots fuse to form the facial nerve and then the nerve
forms the geniculate ganglion (a ganglion is a collection of nerve cell bodies)
at the anteroposterior part of promontory.
Later they give rise to the greater petrosal nerve (parasympathetic fibres to
glands), the nerve to stapedius (motor fibres to stapedius muscle), and the
chorda tympani (special sensory fibres to the anterior 2/3 tongue).
FIGURE 34.9 Schematic diagram of the course and branches of
facial nerve.
Extracranial course
The facial nerve exits the skull through the stylomastoid foramen, and passes
near the lateral border of the styloid process.
The first extracranial branch to arise is the posterior auricular nerve. It
provides motor innervation to the some of the muscles around the ear.
Immediately distal to this, motor branches nerve to digastric to the posterior
belly of the digastric muscle and nerve to stylohyoid to the stylohyoid
muscle.
The main trunk of the nerve, now termed the motor root of the facial nerve,
continues anteriorly and inferiorly into the parotid gland within the parotid
gland, the nerve terminates by diving into five branches: temporal branch,
zygomatic branch, buccal branch, marginal mandibular branch, cervical
branch (Table 34.2).
Table 34.2
Facial nerve: branches
1. In the facial canal (Fig. 34.10)

a. Nerve to stapedius
b. Chorda tympani
c. Greater petrosal nerve
2. At the stylomastoid foramen
a. Posterior auricular
b. Posterior belly of digastric
c. Stylohyoid
3. On the face—terminal branches within the parotid gland (Fig. 34.11)
a. Temporal
b. Zygomatic
c. Buccal
d. Marginal mandibular
e. Cervical
4. Communicating branches—communicate with the sensory nerve distributed in its
origin
Motor Functions (Figs. 34.10 and 34.11)
• Nerve to stapedius—supply the stapedius muscle in the middle ear.

• Posterior auricular nerve—intrinsic and extrinsic muscles of the outer
ear. It also supplies the occipital part of the occipitofrontalis muscle.
• Nerve to the posterior belly of the digastric muscle—innervates the
posterior belly of the digastric muscle.
• Nerve to the stylohyoid muscle—innervates the stylohyoid muscle.
FIGURE 34.10 Parasympathetic efferents of facial nerve.
FIGURE 34.11 Somatic motor branches of facial nerve.
Temporal branches It passes over the zygomatic arch to the temporal region
and supplies the auricularis anterior and superior, the frontalis, the orbicularis
oculi and the corrugators supercilii.
Zygomatic branches Courses over the zygomatic, supplies the orbicularis
oculi.
Buccal branches They are larger than other branches; it divides mainly into
deep and superficial branch. Superficial branches run over the muscles of the
face and supply them. The deep branches run beneath the zygomaticus. It
supplies the zygomaticus, the quadratus labii superioris, the buccinator and
the orbicularis oris.
Mandibular branch It runs down the platysma and supplies the platysma
and the muscles of the lower lip and chin.
Cervical branch It pierce from the apex of parotid and courses downward in
the neck and supply the platysma.
Special sensory functions
The chorda tympani branch of the facial nerve is responsible for innervating
the anterior 2/3 of the tongue with the special sense of taste.
Parasympathetic functions
Greater petrosal nerve combine with deep petrosal nerve to form the nerve of
the pterygoid canal, which then passes through the pterygoid canal to enter
the pterygopalatine fossa, and synapses with the pterygopalatine ganglion.
Branches from this ganglion then go on to provide parasympathetic
innervation to the mucous glands of the oral cavity, nose and pharynx, and the
lacrimal gland.
Chorda Tympani combine with the lingual nerve (a branch of the
trigeminal nerve) in the infratemporal fossa and form the submandibular
ganglion. Branches from this ganglion travel to the submandibular and
sublingual salivary glands.
Facial palsy
Aetiology of facial palsy
1. Trauma
Trauma is a common cause of facial nerve paralysis. Facial nerve injuries
related to soft tissue laceration or avulsion makes up the majority of
extracranial facial nerve injuries. The immediate, standardised assessment of
soft tissue injuries provides the clinician with the most appropriate
documentation of the injury to facilitate initiation of the appropriate surgical
intervention.
Among the temporal bone fractures, 80% of them are longitudinal fractures.
The fracture line is along the longitudinal axis of the temporal bone causing an
external auditory canal disruption temporomandibular (TM) rupture and
possible ossicular damage or haemotympanum. Facial nerve injury occurs in
10%–20% of these fractures with the injury most common in the perigeniculate
region.
Temporal bone injury due to gunshots results in facial paralysis in 50% of
cases. This is because of the direct or indirect injury sustained by the nerve; it
may be due to the force of a bullet or the fragmented bone itself.
The facial nerve can also be injured during middle ear and mastoid surgery.
2. Herpes zoster oticus (Ramsay Hunt syndrome)

Herpes zoster oticus (Ramsay Hunt syndrome) is a disease of the facial nerve,
which is caused by the reactivation of the inert varicella zoster virus in the
geniculate ganglia, occurs mainly when the cell-mediated immunity is
depressed.
Patient usually presents with pain in the ear, followed by lower motor
neuron paralysis. Vesiculation in the external ear, loss of tears due to
involvement of the greater superficial petrosal nerve and loss of ipsilateral
taste are characteristic features. There may also be unilateral perceptive
deafness, tinnitus and vertigo due to involvement of the eighth nerve.
Initial symptoms are similar to Bell’s palsy, but pain is more severe.
Characteristic herpetic eruptions occur over the palate, concha, external
auditory canal. Other features include severe otalgia, facial paralysis and facial
numbness. Patient may have sensorineural hearing loss (SNHL). When the
vestibulocochlear nerve is involved, patient complains of vertigo, tinnitus and
vomiting.
Treatment includes steroids, valacyclovir 1 g per oral t.i.d. and proper eye
care.
3. Otitis media
Otitis media is the most common feature preceding facial nerve palsy. Chronic
otitis media may cause facial palsy; this may be due to prolonged
inflammation, osteitis compressing the facial nerve or secondary to
cholesteatoma.
Good eye care, irrespective of the line of management is essential. Periodic
application of natural tear eye drops protection of eyes from dust by wearing
safety goggles.
4. Tumours
When the facial palsy evolves slowly over more than 3 weeks, facial twitching,
features of adjacent cranial nerve deficits, recurrent ipsilateral involvement,
associated adenopathy or a palpable neck or parotid mass may occur.
5. Melkersson–Rosenthal syndrome
Melkersson–Rosenthal syndrome is a rare disease characterised by a typical
triad recurrent orofacial oedema, recurrent facial palsy and lingua plicata
(fissured tongue). The persistent or recurrent non-pitting facial oedema in
these patients cannot be explained by infection, malignancy or connective
tissue disorder. Facial paralysis and lingua plicata occur in half of the patients.
6. Congenital facial paralysis

Newborn facial paralysis is a rare disorder of the newborn (0.23% of live
births). The major cause is birth trauma. History of difficult delivery, facial
oedema, injury along the extracranial course of the nerve and
haemotympanum are elicited.
Mobius syndrome is a rare neurological disorder characterised by absence of
facial expression, lack of lateral movement of the eyes and may have limb
abnormalities, the facial symptoms are mainly due to underdeveloped
abducent and facial nerve.
A rare cause of isolated newborn facial paralysis is dysgenesis of the
intratemporal facial nerve.
7. Other causes
Sarcoidosis
One variant of sarcoidosis, Heerford’s disease is characterised by uveitis, mild
fever, non-suppurative parotitis and cranial nerve paralysis. Facial nerve is the
most commonly involved cranial nerve and paralysis usually starts abruptly
days to months after the parotitis.
Lyme disease
Lyme disease is an infectious disease caused by the tick-borne bacteria Borrelia
burgdorferi. Facial paralysis (unilateral or bilateral) and deafness are the
characteristic features of the disease. The facial paralysis usually recovers to
normal.
Marcus Gunn or jaw-winking syndrome

This rare condition may be congenital or posttraumatic. This is characterised
by ptosis or palpebral movement (winking) stimulated by mandible
movement as chewing.
Bell’s palsy
It is defined as the idiopathic paresis or paralysis of the facial nerve of sudden
onset (unilateral lower motor neuron paralysis of sudden onset, not related to
any other disease elsewhere in the body).
Sex: Women (mostly in the pregnant women in the third trimester of
pregnancy)
Age: Middle aged
Recurrence: Most commonly in diabetic
Side: Unilateral very rarely bilateral. Positive family history is also reported
Bell’s palsy is mainly idiopathic. However, an association of Bell’s palsy
with herpes simplex virus infection has been noted. This is suggested by the
presence of HSV antibodies in these patients when compared to that of
normal.
Diagnosis: A symptom-based approach in internal medicine
A patient with Bell’s palsy will typically present with acute onset, painless
facial weakness (lower motor neurone distribution) with a normal ear, nose
and throat (ENT) examination.
Bell’s palsy
• Painless
• Acute
• Lower motor neurone (distribution of facial weakness)
• Systemically well
• Your examination is otherwise normal
Aetiology
1. Cold hypothesis: Exposure to extreme cold.

2. Rheumatic hypothesis: Rheumatic swelling might press the nerve
against the wall of the fallopian canal.
3. Ischaemic hypothesis: Vasospasm due to cold, anoxia, CO2 excess,
injury, toxic drugs, allergy, hormonal influence, vasomotor instability.
4. Immunological hypothesis: Cell mediated autoimmune response to
Guillain Barre syndrome causes Bells palsy.
5. Viral hypothesis: The possible viral aetiological agents includes
adenoviruses, mumps and the herpesvirus family (Herpes simplex
virus 1, Herpes simplex virus 2 and Varicella zoster virus).
Clinical features of Bell’s palsy

Before testing the function of the nerve, one should compare the facial
expression and movement between the two sides of the face (Fig. 34.12A–B).
• Impaired blinking—inability to blink or close the eyes, tearing and dry

eyes.
• Sagging cheek—facial droop and difficulty making making facial
expressions, like smiling
• Flattening of the nasolabial crease (characteristic features of facial
palsy)
• Papillitis of the fungiform papillae of the affected side, speech may be
slurred
• Increased lacrimal secretions as the eye is partially opened
• Diminished taste sensation in anterior half of the tongue
• Exaggerated sound in the affected side (hyperacusis) due to the
paralysis of stapedius muscle, but also occurs independently
FIGURE 34.12 (A–B) Bell’s palsy.
Symptoms of Bell’s palsy can be summarised as:
• Altered lacrimal secretion

• Altered salivary secretion
• Impairment of taste perception (anterior two-thirds of tongue)
• Hyperacusis (sounds heard abnormally loudly) on affected side
• Weakness of all the facial muscles
• Drainage of tears from affected side is impaired as eyelids cease to oppose
to eyeball, which also stimulates excessive eye watering
• Cornea is vulnerable due to impaired eye closures
• Weakness around mouth impairs speaking (slurred), eating (food collects
down between gum and cheek) and drinking (may dribble)
Clinical evaluation
• A detailed and careful history is essential for the patient with facial
nerve paralysis.
• The on set of symptoms, duration, rate of progression, chronology of
events and associated features such as blurring of vision, hearing
impairment, ear pain or any drainage from ears.
• History of prior episodes, family history, medical history (diabetes,
pregnancy, autoimmune disorders, cancer), history of trauma and
surgical history (otologic, rhytidectomy, parotidectomy) are noted.
• Head and neck examination, detailed examination of the ears, eye
(papilloedema), precise palpation of parotid glands, auscultation of
neck for abnormal sounds such as carotid bruits and complete
neurological examination is necessary.
Diagnosis
Following basic functions are examined:
1. Raising the eyebrows to test frontalis corrugator activity.

2. Tightly closing the eyes for orbicularis oculi sphincter function.
3. Asking the patient to grin or smile, to examine the retractor muscles
acting on the angles of the mouth.
4. Taste may also be tested.
5. Patient is asked to blow out the air, hold air in mouth and whistle.
Bell’s palsy usually develops over hours to days. The peak involvement
usually happens within several days (Table 34.3 and Table 34.4).
Table 34.3
Difference between upper motor neuron (UMN) and lower motor neuron (LMN) type of
cranial nerve (CN) VII palsy
UMN LMN type

Upper face is unaffected, only lower half of the face is affected, Both upper and lower half of the
i.e. eyes can be closed, forehead can be wrinkled but there will face is affected
be inability to show the teeth due to weakness of lip and
buccinators
Emotional movements not affected in unilateral cases. In case Emotional movements are lost
of bilateral lesions, the whole lower half of the face is
paralysed; hence, affecting emotional movements
Bell’s phenomenon*—absent Bell’s phenomenon*—present
No atrophy of facial musculature Fasciculation/atrophy on the
affected side
Taste sensation retained Taste sensation may be lost
Corneal reflex not affected Corneal reflex absent
Hemiplegia—associated with ipsilateral hemiplegia or Hemiplegia—may be an isolated
hemiparesis or monoplegia phenomenon, in case associated
with hemiplegia, it is always
crossed
Plantar response—extensor on the paralysed side of the face Plantar response—flexor on the
paralysed side of the face, may
be extensor on the opposite side
Examples: cardiovascular accident, CNS neoplasm, multiple Examples: Bell’s palsy, Lyme’s
sclerosis disease
*
Bell’s phenomenon—upward and inward rotation of the eyeball when the patient tries
to close his/her affected eyes.
Lower motor neuron damage occasionally arises following head injuries.
Mild pain behind the ear is common at onset, as is a subjective sensation of
‘numbness’ of the affected side.
Table 34.4
Degree of voluntary movement in facial paralysis

Grade Degree Description
I Normal Normal facial movements; no synkinesis
II Slight Mild deformity, mild synkinesis, good forehead function, slight asymmetry
III Moderate Obvious facial weakness, frontalis activity present, good eye closure,
asymmetry, Bell’s phenomenon present
IV Moderately Obvious weakness, increasing synkinesis no forehead motion
V Severe Very obvious facial paralysis, cannot close eye
VI Total Complete facial paralysis
Bell’s palsy progresses in hours to days, usually reaches peak after several
days. Most patient complain of mild pain may be due to altered sensation in
the affected region. The grade is determined as per house classification system,
depending on the extent of voluntary movement. Supranuclear (central)
lesions cause the contralateral voluntary lower facial paralysis (Fig. 34.13A–B).
The frontalis muscle is unaffected due to its bilateral innervation. In central
lesions, emotional response such as facial expressions on laughing or crying
may be retained. Bell’s phenomenon is the characteristic feature of upward
and outward movement of the eyeball when the patient attempts to close the
eyelids, this sign occurs in peripheral lesion.
All patients with facial paralysis should undergo formal audiological testing
for reflexes and tympanometry.
Any patient presenting with facial paralysis should undergo formal
audiological testing, including pure tone, air and bone conduction, speech
discrimination, reflexes and tympanometry. If asymmetry is found on the
audiogram, an auditory brainstem response (ABR) and/or MRI should be
obtained.
FIGURE 34.13 (A–B) Upper motor neuron lesion (UMNL) sparing
the upper half of the face. (C–D) Lower motor neuron lesion
(LMNL) affecting the entire half of face on the affected side. (Bell’s
Palsy).
Topognostic testing
This includes tests to determine the level of lesion indicated by loss of function
in branches distal to injury.
Test Nerve tested Function assessed

Schirmer test for lacrimation (GSPN) Greater superficial petrosal nerve Rate of lacrimation
Stapedial reflex test Stapedial branch Hyperacousis
Taste testing Chorda tympani nerve Loss of taste
Salivary flow rates and pH Chorda tympani Salivary flow rate
Electrophysiologic tests
These tests are of significance in patients with complete paralysis for
determining prognosis for return of facial function and when decompression
surgery is considered.
Imaging studies
• Facial bone CT scan or plain radiographs: Potential causes like petrous

bone fractures or bony metastasis can be detected.
• CT brain: In stroke, multiple sclerosis or acquired immunodeficiency
syndrome (AIDS); CNS involvement is considered.
• MRI: Neoplasm of the temporal bone, brain, parotid gland or other
structure.
MRI images the course of the facial nerve through the temporal bone as
well as extracranial course in face and glands.
Prognosis
Prognosis for Bell’s palsy is generally good; with 85%–90% of the patients fully
recover within 1 month. Other 15% show no signs of recovery for 3–6 months
due to complete degeneration. Complications are higher in those where the
recovery is slow. The degree of paralysis determines the prognosis of the
patient. Incomplete paralysis have good prognosis than the complete
paralysis.
Management
Treatment of Bell’s palsy is variable, ranging from observation to surgical
decompression.
Medical management
Eye care
Irrespective of the treatment, good eye care is essential to prevent corneal
degeneration and erosion. Periodic application of natural tear drops during
daytime and lacrilube ointment before sleeping is done. Gentle massage over
the eyelids while sleeping and use of moisture chamber are helpful. Patient is
advised to cover the eyes with protective goggles when going outside. Oral
prednisone in a divided dosage of 1 mg/kg/day may be prescribed to minimise
degeneration, to relieve pain and helps in early recovery.
Surgical decompression
It is hypothesised that the facial nerve may undergo pathological compression
injury due to oedema at the fallopian canal (facial canal). Surgical
decompression may decrease oedema and allows axoplasmic flow. This
procedure is usually carried out through the middle fossa approach. It is
preferred within 2 weeks that is before the irreversible damage to nerve fibres.
It is not done in an only hearing ear.
Surgical management
Surgical management is divided into two major sections:
• Primary management describes common clinical practice with respect
to acute extracranial facial nerve injuries. Direct facial nerve repair,
nerve grafts and nerve sharing or transposition are included.
• Delayed or secondary interventions aimed at facial reanimation or
aesthetic improvements are described in the second section. The
second section details both static suspension procedures and dynamic
neuromuscular transfers used to provide facial reanimation.
Timing for open nerve injury repair
• Immediate primary repair—can be done when a microsurgical

expertise is available.
• Delayed primary repair—if conditions are unfavourable, repair is
done within 1 week after nerve injury.
• Early secondary repair—after appearance of granulation tissue in the
wound.
Primary management
Neurorrhaphy
Indications
Direct neurorrhaphy is especially indicated when sharp precise lacerations of
the facial nerve have occurred. Example: razor blade, knife or glass injury.
Technique (Fig. 34.14A–C)

Direct repair of the facial nerve should be accomplished by a skilled
microsurgeon under optimal conditions.
Partial parotidectomy is often required to gain adequate exposure for nerve
anastomosis. Bipolar cautery is used where necessary within close proximity
to the nerve. A bloodless field is required to achieve appropriate visualisation
of the nerve ends. The proximal nerve must be identified by visual inspection.
Orientation and depth are key features used to identify the nerve.
Identification of the nerve

High levels of magnification and trimming of the nerve allow characterisation
of the structure at the proximal end. These procedures and electrical
stimulation can be used within 3 days of transection for confirmation of the
nature of the distal segment.
FIGURE 34.14 (A–C) Neurorrhaphy.
Suturing of the nerve

The identified segments must be minimally dissected to preserve blood supply
to the remaining nerve segments.
The nerve ends are carefully and completely trimmed. Direct simple
perineural sutures are used to achieve approximation. Careful coaptation is
necessary to prevent scar tissue ingrowth during the time of axonal
regeneration. Nylon or prolene sutures (10-0) are typically used. A surgeon’s
knot and two additional square throws are adequate. The ideal anastomosis
uses a minimal number and volume of suture to limit the inflammatory
response to these materials. A taper-cut needle has the advantage of being
easy to pass while causing minimal trauma to the nerve. Generally, needles in
the range of 50–75 µm are most applicable.
Guided nerve regeneration

Placement of a conduit to guide axonal sprouting and regeneration across a
nerve gap from proximal to distal portions of a nerve. This technique is
successful only in short nerve gaps (<3 cm) when used in peripheral trigeminal
nerve repairs. An alloplastic nerve conduit (polyglycolic acid or
polytetrafluoroethylene) has been used with limited success in TN5 injuries,
but only in minimal nerve gaps (Fig. 34.15) (Table 34.5).
FIGURE 34.15 Guided tissue regeneration.
Table 34.5
Materials for entubulation (conduit) repair
Autogenous materials
a. Collagen
b. Muscle
c. Fascia
d. Vein
Alloplastic materials
a. Polyglycolic acid
b. Polyester
c. PTFE
d. ePTFE
e. Silicone, polymeric silicone
Allogeneic materials
a. Cadaveric nerve allograft
ePTFE, Expanded polvtetrafluoroethylene; PTFE, polytetrafluoroethylene.

Graft neurorrhaphy
Indications
The procedure of nerve grafting is identical to that of direct nerve repair, with
the exception of requiring an additional anastomosis for each nerve branch
treated.
Autogenous nerve grafts remain the standard when all other treatments are
compared. Tubulisation with alloplastic materials remains a procedure most
applicable and appropriate to the experimental microsurgical laboratory.
Generally, nerve grafting is required following avulsive type injuries.
Common donor sites
• Greater auricular nerve—used when total length of nerve graft

required is small.
• Sural nerve—used following extensive injuries or resections of
multiple facial nerve branches.
• Antebrachial cutaneous nerve (recently)—structure in the proximal
forearm involves many branches that are often suitable to the
replacement of multiple branches of the facial nerve.
Reproducible result of nerve graft reconstruction of facial nerve defects can

be best appreciated by comparing the procedure to immediate grafting of the
facial nerve in radical parotidectomy.
Great auricular nerve (Fig. 34.16)

Great auricular nerve is easily identified in relation to the external jugular vein
(posterior and parallel).
Surface marking
A useful additional external reference is produced by dropping a
perpendicular line at the midpoint of a line drawn from the mastoid to the
angle of the mandible. A cervical skin crease is used to camouflage the donor
site incision.
Technique
The degree of elevation of skin platysma flaps along the superficial plane of
the superficial layer of the deep cervical fascia depends on the length of nerve
required. In general, a maximum useful nerve length is 6–8 cm. The nerve is
isolated posterior to the jugular vein and dissected to its entrance into the
parotid. Branching of the nerve can prove useful in the nerve defect site and
this should be used to its full advantage. Proximal dissection of the nerve is
typically limited by the passage of the nerve deep to the posterior border of
the sternocleidomastoid muscle.
FIGURE 34.16 Greater auricular nerve.
Sural nerve (Fig. 34.17)

Sural nerve is the branch of tibial nerve in the middle of the popliteal fossa. It
supplies skin on the lower half of the back of the leg and whole of the lateral
border of the foot up to the tip of the little toe. The greatest advantage of using
sural nerve in facial nerve grafting is its abundant length. As much as 40 cm of
nerve is available for harvest, the diameter of the nerve is approximate to that
of most of the cranial nerves. The most ideal use is in the case of multiple facial
nerve defects in the separate branches of facial nerve or in extracranial defects
involving the facial nerve trunk only.
Indication
Cases in which the defect originates at the trunk and extends to multiple
branches are most well suited to reconstruction with either the greater
auricular nerve or antebrachial cutaneous nerve. A branching pattern of the
sural nerve can be harvested from its extreme distal course, but this requires
incision and dissection across the ankle joint.
Technique
The sural nerve segment that is typically harvested is the distal portion of the
lower leg after the point at which it becomes superficial to the muscular fascia
overlying the gastrocnemius. In this position, it is easily identified adjacent
(medial) to the lesser saphenous vein posterior to the lateral malleolus. Serial
small horizontal incisions or a single longitudinal incision is used. Particular
attention should be given to the management of the proximal nerve stump.
This should be placed into a pocket within adjacent muscle and secured by
suture.
Complication
Neuroma formation on a superficially located nerve stump can be a source of
considerable patient discomfort.
FIGURE 34.17 Sural nerve.
Medial antebrachial cutaneous nerve

Medial antebrachial cutaneous nerve can be harvested from the upper
extremity with minimal morbidity. It originates from the medial cord of the
brachial plexus in the majority of cases (78%). The nerve is relatively easy to
identify secondary to its location adjacent to the basilic vein. Near the
antecubital fossa the nerve typically divides into the anterior and posterior
branches.
Indications
The anterior branch is most useful for facial nerve reconstruction because it
has multiple branches suitable to the replacement of the facial nerve.
Technique
Harvest of the medial antebrachial cutaneous nerve is accomplished by
making a cutaneous incision parallel to the plane formed by the fascial plane
separating the biceps and triceps muscles. The depths of incision and
dissection must remain within the subcutaneous plane. The nerve is easily
found along the course of the basilic vein. It is appropriate to dissect the nerve
distally to the point of numerous branches to identify a pattern and size most
consistent with the demands of the facial nerve defect.
Cross-facial nerve grafting (Fig. 34.18)

The use of the normal facial nerve on the uninjured side has obvious useful
clinical indications. In such cases, patient re-education to achieve nerve
stimulation is not required. The principle is really quite simple. A branch of
the normal facial nerve is sacrificed (a buccal branch being the most
appropriate) and a sural nerve graft passed through a subcutaneous tunnel to
allow either neurorrhaphy or to serve as a nerve conduit to use in conjunction
with or without a microvascular neuromuscular transfer at the opposite side.
Nerve transposition
Two situations exist wherein nerve transposition can prove exceptionally
useful:
• The first such condition is when there has been isolated segmental
injury to a crucial (mandibular or zygomatic) branch of the facial
nerve. In such cases, transposition of a less critical segment of the facial
nerve (frontal, cervical) can be accomplished and direct anastomosis
can be completed to the distal portion of the injured nerve.
• The second of these conditions is that in which extreme proximal facial
nerve is injured. The hypoglossal nerve can be transposed and sutured
to the trunk of the distal facial nerve. In these cases, major drawback is
mass movement of the face, but the outcome compares favourably
with that of microvascular neuromuscular transfer and cross-facial
nerve grafting.
Secondary management of facial nerve injuries

Late reconstruction of facial nerve injuries is sometimes required. In such
cases, the surgeon must weigh carefully the benefit of each modality of
treatment in order to select the most appropriate reconstruction for each
individual patient. Static procedures have particular merit in their simplicity
and single surgical intervention. Complex neuromuscular reconstructions
require multiple procedures and a long interval of healing prior to extensive
re-education and rehabilitation. It is critical to ensure that the anticipated
outcome of each procedure is clearly understood.
FIGURE 34.18 Cross-facial anastomosis.
Surgical technique I: temporalis lengthening with fascia lata (Figs.

34.19–34.20)
A 2 cm wide strip is prepared behind the level of the helix insertion on the
paralysed side. The incision lines are made in the temporal region and brought
backwards, forwards and downwards in the preauricular region extending
inferiorly as far as the level of the tragus.
Skin and subcutaneous tissue are elevated to reveal the temporoparietal
fascia and the zygomatic arch. The portion of the arch measuring about 18 mm
lying above the temporalis muscle is excised with bone drills and left pedicled
to the masseter. This procedure allows free movement of the muscle during
excursions.
The temporalis muscle is then traced inferiorly up to its attachment in the
coronoid. To release its attachment, an intraoral coronoidotomy is planned. An
incision is made on the external oblique ridge, intraorally and the ascending
ramus is exposed. The coronoid with its tendinous attachment is identified
and osteotomy of the coronoid is done just below the insertion of temporalis.
The bulk of the temporalis is elevated extraorally taking care not to damage
the maxillary artery or mandibular nerve.
To harvest the required fascia lata graft, an ‘S’-shaped incision is made over
the lateral aspect of the thigh. This curved incision prevents undue scar
contraction and muscle hernia. The broad sheet of fascia lata over the costus
lateralis muscle measuring about 6 × 12 cm is stripped away.
FIGURE 34.19 (A–B) Temporalis lengthening using fascia lata for

facial palsy.
FIGURE 34.20 (A–H) Facial reanimation with temporalis

lengthened with fascia lata: (A) Preoperative photograph. (B)
Harvesting fascia lata from the lateral aspect of the thigh. (C)
Harvested fascia lata. (D) Intraoral coronoidectomy to release
temporalis from its insertion. (E) Fascia lata sutured to the
temporalis. (F) Fascia lata divided into three strips; central strip
wound around the modiolus. (G) Upper and lower strips of the
fascia lata tunnelled to the upper and lower lip. (H) Postoperative
photograph.
Advantage of using fascia lata is primarily based on the fact that it does not
require a lot of blood supply for its survival. The fascia is then carefully
stitched to the ends of the temporalis in an overlay fashion with 2-0 ethilon
and secured tightly.
A vertical incision is made at the site of the new nasolabial groove, more
medial than the original, keeping in mind the lateral drift, which proceeds due
to loss of muscle tone. A tunnel is created subdermally between the nasolabial
and preauricular incisions. The ends of the fascia with the attached muscle are
passed through the tunnel and brought out at the nasolabial incision. At this
juncture, the broad sheet is divided into a narrow upper and a lower strip
leaving the middle strip broader.
The upper strip is then again tunnelled subdermally to a smaller vertical
incision, lateral to the contralateral philtral column of the upper lip. Similarly,
the lower narrow strip is tunnelled into the lower lip and affixed to the dermis
at the point lateral to the midline of the unaffected side, the broad middle
sheet is then passed around the partially atrophied orbicularis oris muscle,
which thereby acts as a sling at the angle of the mouth. All these transfers are
made as tight as possible.
Surgical technique II: temporalis lengthening without fascia lata

(Fig. 34.21A–E)
• The incision is made at the temporal region, just within the hairline
about a pinna’s length above the ear. It is then taken in a curve
backwards and downwards well behind the main branches of the
temporal vessels to the upper most skin attachment of the pinna. The
incision is then made anterior to the tragus and then moved
endaurally. At this point, the incision is made across the notch
between the helix and the tragus and passed posterolateral to the
tragus, in the anterior wall of the external auditory meatus where it
can be cosmetically concealed. The incision line is then traversed
inferiorly within the external auditory meatus, adjacent and parallel to
the tragus till its inferior border and finally out again to the skin crease
in front of the lobe of the ear.
• Using blunt and sharp dissection, superficial fascia and preauricular
fascia are lifted as parts of the skin flap. At the level of the tragus, the
skin is dissected off the cartilage of the tragus and its continuation of
the cartilage of the external auditory canal.
• An incision is made on the superficial temporal fascia parallel to the
zygomatic arch continuing inferiorly between the two layers of the
temporalis fascia.
• Subperiosteal dissection on the zygomatic arch is done by sweeping
movements of the elevator connecting both zygomatic and external
orbital rim dissections.
• The exposed zygomatic arch is sectioned and shifted inferiorly,
attached to the masseter muscle.
• Intraoral coroidotomy is done.
• Temporalis aponeurosis is incised 1 cm be low the temporal crest to
leave a strip of tissue for the final suturing of the muscle.
• The entire muscle is dissected off the squamous temporal bone by an
elevator.
• A 4 cm incision is made in the nasolabial crease excising skin in
elderly. A subcutaneous tunnel is made in the fat plane connecting
nasolabial crease to temporal region.
• The coronoid process with the temporalis tendon is guided into the
tunnel.
• The coronoid process is dissected off the muscle and removed.
• The temporalis tendon, spread 3–4 cm wide, sutured to the perioral
muscles.
• The temporalis muscle body is then stretched and sutured to the
aponeurotic strip on the anterior portion of the crest. The traction of
the muscle before its fixation, creates an overcorrection of the
paralysed side. The zygomatic arch is refixed.
• Contralateral myectomies are almost always necessary for better
symmetry done by intraoral approach.
Static suspension (Fig. 34.22A–E)

The utilisation of static procedures following facial nerve injury is the oldest of
the accepted methods of secondary management of facial nerve injuries. Static
suspension of the face can achieve acceptable reconstruction of the nasolabial
fold and labial commissure that hides the deformity, except during facial
animation.
Autogenous tissue is preferred for facial suspension. Most commonly, the
fascia lata is used. The fascia is harvested as a wide strip that can then be
adapted to provide a number of sites of inset for the suspension.
The flaccid facial musculature can also be suspended to the zygoma using
sutures.
The superior portion of a face-lift incision is used with subcutaneous
dissection accomplished to the sites of planned inset. Separate incisions at the
insertion sites are required to secure the fascia to the dermis. Permanent
sutures are used to secure the fascia at these distal sites first. Appropriate
tension is then placed on the graft and it is sutured to the superficial
musculoaponeurotic system (SMAS) or temporal fascia. It is generally
preferable to apply tension in such a manner as to place the nasolabial fold,
oral commissure and lips in a position approximating the midpoint of a smile.
Allowances must be made for the relaxation that occurs as a result of
gravitational effects and skin creep. Patients must be aware of this prior to
surgery because the immediate postoperative appearance can resemble that of
a snarl.
Previous methods that attempted to use temporalis muscle and fascia were
reported to result in animation of the face. The true outcome of such cases was
generally equal to that of static suspension because preservation of the
neurovascular supply to the muscle and achieving appropriate relaxed tension
were extremely difficult.
Neuromuscular transfer (Fig. 34.23A–B)

The gracilis muscle has been popularised for dynamic facial reanimation.
Other muscles used for this purpose include serratus anterior and pectoralis
minor. This is primarily of historical note because of the current popularity of
the gracilis transfer. A significant decrease in the muscle bulk can be achieved
by selective harvest of that portion of the muscle innervated by the anterior
branch of the obturator nerve. Intraoperative identification of this portion of
the muscle is easily accomplished by selective use of a nerve stimulator. This
procedure often follows an initial cross-face facial nerve graft procedure by a
number of months. The muscle is inset in a manner much the same as that of
static suspension.
FIGURE 34.22 (A–C) Static suspension. (D) Preoperative
photograph. (E) Postoperative photograph.
FIGURE 34.23 (A–B) Facial reanimation with neuromuscular

transfer using gracilis muscle.
Correction must be made for the contraction of the muscle following

transection in the process of the transfer. This is commonly accomplished by
marking the muscle with vascular staples at predetermined lengths prior to
transection. The muscle is then stretched to the original dimension at the time
of inset. Microvascular anastomosis is typically accomplished using the facial
artery and vein as recipient vessels.
In most cases, neural anastomosis is accomplished to a cross-face facial
nerve graft. Many critical variables in the surgical technique have a significant
effect on the overall outcome. Experience with this procedure is therefore
necessary to achieve an acceptable result. Indications for this procedure are
rare. It is recommended that patients requiring this procedure can be managed
at a selected few referral centres experienced in its execution.
Neuralgia
A simple definition of neuralgia can be ‘pain which follows the paths of
specific nerves’.
Trigeminal neuralgia
Trigeminal neuralgia (TN), also called tic douloureux, is the most common of
the cranial neuralgias and chiefly affects individuals older than 50 years of age.
Other names: Tri facial neuralgia, Fothergill’s disease, Tic douloureux

Tic—a sudden, spasmodic, painless, involuntary muscular contraction,
especially involving the facial muscles
Douloureux—painful
International Association for the Study of Pain (IASP) defined trigeminal
neuralgia as ‘sudden usually unilateral severe brief stabbing recurrent pain in the
distribution of one or more branches of the Vth cranial nerve’.
International Headache Society (IHS) the trigeminal neuralgia may be
defined as ‘painful unilateral affliction of the face characterized by brief electric shock
like pain limited to the distribution of one or more divisions of trigeminal nerve’.
Anatomy
It is the largest cranial nerve. Its sensory part supplies to the face, greater part
of scalp, teeth, oral and nasal cavities (Fig. 34.24A–C). Its motor part supplies
the muscles of mastication.
It divides into three branches: ophthalmic, maxillary and mandibular
(Flowchart 34.1).
FLOWCHART 34.1 Branches of trigeminal nerve. ASAN, anterior
superior alveolar nerve; MSAN, middle superior alveolar nerve; PP,
pterygopalatine; PSAN, posterior superior alveolar nerve.
Course
The trigeminal nerve is continuous with the ventral surface of the pons, by a
small motor root and a large sensory root. The fibres of the sensory root arise
from the cells of the trigeminal (semilunar or gasserian) ganglion. This
ganglion occupies a recess (Meckel’s cave) in the dura mater. The ganglion is
crescent shaped. The other nuclei are: sensory nucleus, motor nucleus and
spinal nucleus. The branches of the unipolar cells of the ganglion are divided
into peripheral and central branches. The peripheral branches are grouped to
form the ophthalmic and maxillary nerves and the sensory part of the
mandibular nerve. The central branches constitute the sensory root, which
leaves the ganglion backwards and medially to enter the pons.
Ophthalmic nerve
Superior and smallest division of trigeminal nerve, wholly sensory, gives
branches to the eyeball, lacrimal gland, conjunctiva, part of the mucous
membrane of nasal cavity, skin of the nose, eyelids, forehead and scalp. Arises
from the anteromedial part of the trigeminal ganglion and passes forwards in
the cavernous sinus close to its lateral wall and below the oculomotor and
trochlear nerves. Just before entering the superior orbital fissure, it divides into
three branches, i.e. lacrimal, frontal and nasociliary.
Maxillary nerve
The maxillary nerve is a true sensory nerve. It originates in the middle of the
trigeminal ganglion and passes horizontally forward along the lateral wall of
the cavernous sinus.
• It exits the skull through the foramen rotundum into the

pterygopalatine fossa.
• It exits the pterygopalatine fossa to enter the orbit through the inferior
orbital fissure.
• Within the orbit it continues as infraorbital nerve occupying the
infraorbital groove and canal.
• It exits the orbit through the infraorbital foramen as labial, palpebral
and nasal branches.
FIGURE 34.24 (A–C) Branches of trigeminal nerve and distribution
of sensory fibres to each division.
Mandibular nerve
• Largest division of the trigeminal nerve.

• Consists of a large sensory and a small motor root.
• The nerve passes through the foramen ovale to enter the infratemporal
fossa.
• The two roots unite just below the foramen forming a single main
trunk, which lies between the tensor velipalatini medially and lateral
pterygoid laterally.
• The main trunk then divides into a small anterior and a large posterior
trunk providing branches to the tongue, mandible, all muscles of
mastication, etc. (Fig. 34.25).
Applied anatomy
• The ophthalmic division supplies the skin and conjunctiva of the upper
eyelid, the lacrimal gland, themesial part of the skin of the nose, the
forehead and the scalp as far as the vertex. Lesions of the ophthalmic
division result in loss of corneal reflex and cutaneous sensation in its
dermatome. Trophic changes in the cornea (neuropathic keratitis) may
occur.
• The maxillary division supplies the cheek, temple, lower eyelid (skin
and conjunctiva), the side of the nose, the upper lip, the upper teeth,
nasal mucosa, the upper part of the pharynx, hard palate, part of the
soft palate, the tonsils. Lesions of the maxillary divisions lead to loss of
sensation in its dermatome with loss of the palatal reflex.
• The third or mandibular division supplies the lower part of the face,
the lower lip, the ear, the tongue and the lower teeth. It also supplies
parasympathetic fibres to the salivary glands. The mandibular division
is joined by the motor root and this innervates the muscles of
mastication. The motor root originates from a small nucleus, medial to
the main sensory nucleus and partly also from nerve cells scattered
around the cerebral aqueduct.
Lesions of this division lead to diminished salivary and lacrimal
secretions and trophic ulcers of the mouth, nose and cornea. Taste is
spared though loss of general sensation in anterior two-thirds of the
tongue occurs. Weakness of the muscles of mastication is often a
prominent feature.
FIGURE 34.25 Innervation of the muscles of mastication.
Aetiology
Trigeminal neuralgia (TN) is classified based on the aetiology: idiopathic and
secondary. Secondary TN is due to secondary lesions, which are as follows.
Tumours
• Acoustic neurinoma
• Chondroma at the level of the clivus
• Pontine glioma
• Epidermoid cyst
• Metastases
• Lymphoma
Vascular defects
• Pontine infarct
• Arteriovenous malformation in the vicinity
• Persistence of a primitive trigeminal artery
• Pulsatile compression by the adjacent superior cerebellar artery (more
rarely, anteroinferior artery)
Inflammatory
• Multiple sclerosis (MS)

• Sarcoidosis
• Lyme disease neuropathy
Aetiology
Vascular causes (intracranial vascular compressions)
Vascular compression is the most common cause of TN. Distortion of the root
entry zone of the trigeminal nerve at the pons by an arterial loop (superior
cerebellar artery) or by venous compression by arteriovenous malformation.
Dental cause
Maxillary and mandibular divisions are affected.
Infections/Viral aetiology
Various granulomatous and nongranulomatous infections.
Postherpetic neuralgia because of previous history of varicella infection and
the presence of viral lesions in the ganglion can be a aetiological factor.
Multiple sclerosis
Presence of sclerotic plaque at the root entry zone of trigeminal nerve (mostly
young patient with bilateral involvement).
Petrous ridge compression
Compression of the nerve at the dural foramen or over the petrous tip can
cause TN.
Posttraumatic neuralgia
Traumatic neuroma resulting from trauma may lead to neuralgic pain.
Intracranial tumours
Impingement of meningiomas of cerebello pontine angle and meckels cave,
AV malformations, aneurysms and vascular compressions can cause TN.
Aetiological theories
1. Diseases-related theory:
Vascular diseases, multiple sclerosis, diabetes mellitus, rheumatism and
others.
2. Direct trauma to the nerve:
Peripheral part of TNS:
a. Allergic hypothesis due to odontogenic inflammatory diseases,
otolaryngological pathology, getting cold and others.
b. Compression syndrome hypothesis due to the narrowing of the
osseous canals, trauma.
Central part of TNS:
c. Neurovascular compression hypothesis at the root entry zone
due to arteriovenous malformation, vestibular schwannoma,
meningiomas, epidermoid cysts, tuberculomas, various other
cysts and tumours, aneurysm, vessels aggregation and
occlusion due to arachnoiditis and others.
3. Polyaetiologic origin:
All possible aetiological factors that can affect TNS and evoke
demyelination and dystrophy.
Pathophysiology
Mechanism of pain production remains controversial. Trigeminal neuralgia is
typical of neuropathic pain where the mechanism of pain is altered. The small
and large nerve fibres are altered such that they can be easily triggered by
minimal stimuli such as a vibration.
Demyelination of these nerve fibres causes uncontrolled firing of small
unmyelinated trigeminal nerve fibres. Lack of inhibitory inputs from large
myelinated nerve fibres cause prolonged excitation of the smaller trigeminal
fibres to the stimuli. Involvement of the central nervous system is also
suggested due to the delay between stimulation.
Pathogenesis of idiopathic TN is unclear. Studies have suggested that the
compression of the artery or vein over the ganglia or nerve causes ectopic
impulses resulting in pain. Most commonly, superior cerebellar artery is the
compressing artery. Compression causes demyelination of the trigeminal roots
at these sites. Reactivation of the herpes simplex virus (HSV) has also been
suggested, but may not be the sole causative factor.
Clinical features
• Trigeminal neuralgia is a chronic condition though symptoms may not

be present for few months.
• It typically manifest as a sudden unilateral, intermittent, paraoxysmal,
sharp, shooting, lancinating, shock like pain.
• The pain is lightning like, sudden in onset, lasts over few seconds, the
numerous episodes of this typical pain; the patient may describe it as a
continuous pain.
• The pain is so severe that it prevents eating or drinking. The nerves
affected are usually stereotyped for a particular patient and lie within
the sensory distribution of the trigeminal nerve.
• The attack is precipitated by touching the superficial trigger points.
• Refractory period between each episodes is very short, may be 1 or
2 min.
• After the episode, a bothersome sensation is present over the region.
• Mandibular or the maxillary divisions is commonly involved,
ophthalmic division is the least affected.
• Pain is always unilateral and does not shift sides, though bilateral cases
have been described.
• Trigger points:
▪ V1—supraorbital ridge of the affected side
▪ V2—skin of the upper lip, ala nasi or cheek or on the upper
gums
▪ V3—lower lip, teeth or gums of the lower jaw, rarely tongue
• The various stimuli precipitating the episode:
▪ Touching
▪ Applying heat or cold to the cheek
▪ Gum chewing
▪ Yawning
▪ Talking
▪ Wind blowing on the face
▪ Gustatory stimuli and vibration
• Stimuli vary with patients and are consistent for each patient.
• Attack do not occur during sleep is one of the characteristic of the
disorder (Flowchart 34.2).
FLOWCHART 34.2 Important clinical features of trigeminal

neuralgia.
Diagnosis
The diagnosis of TN is purely clinical. Haematological investigations at
regular intervals are important in patient on drug therapy. Radiologic
investigations are important. Secondary TN (e.g. multiple sclerosis, cysts,
vascular pathologies, etc.) can be rule out with help of MRI. Sensory testing is
not done routinely, but quantitative sensory testing (QST) and evoked
potentials may play an important role in differentiating between symptomatic
and idiopathic TN.
Sweet’s diagnostic criteria
1. It is paroxysmal.
2. It may be provoked by light touch to the face.
3. It is confined to trigeminal distribution.
4. It is unilateral.
5. The clinical sensory examination is normal.
Classification (Table 34.6)
1. Classical
2. Symptomatic
Table 34.6
Diagnostic criteria proposed by IHS (International Headache Society)

Classic Symptomatic
A. Paroxysmal attacks of pain lasting from a A. Paroxysmal attacks of pain lasting
fraction of a second to 2 min, affecting one or more from a fraction of a second to 2 min,
divisions of the trigeminal nerve, and fulfilling with or without persistence of aching
criteria B and C between paroxysms
B. Pain has at least one of the following B. Pain has at least one of the following
characteristics: characteristics:
• Intense, sharp, superficial or stabbing • Intense, sharp, superficial or stabbing
• Precipitated from trigger zones or by trigger • Precipitated from trigger zones or by
factors trigger factors
C. Attacks are stereotyped in the individual patient C. Attacks are stereotyped in the individual
patient
D. There is no clinically evident neurologic deficit D. A causative lesion, other than vascular
compression, has been demonstrated by
special investigations and/or posterior fossa
exploration
E. Not attributed to another disorder
Diagnostic test
Diagnostic injection of local anaesthetic agent into the patients trigger zone
should temporarily eliminate all pain.
Positive: Sensitive trigger zones in the peripheral areas are blocked and the
patient will be completely relieved of pain even for prolonged duration.
Procedure (Table 34.7)
Table 34.7
Differential diagnosis of Trigeminal neuralgia
Diagnosis Important features

Dental infection or Well localised to tooth; local swelling and erythema; appropriate
cracked tooth findings on dental examination
Temporomandibular Often bilateral and may radiate around ear and to neck and temples; jaw
joint pain opening may be limited and can produce an audible click
Persistent idiopathic Often bilateral and may extend out of trigeminal territory; pain often
facial pain (previously continuous, mild to moderate in severity and aching or throbbing in
‘atypical facial pain’) character
Migraine Often preceded by aura; severe unilateral headache often associated
with nausea, photophobia, phonophobia and neck stiffness
Temporal arteritis Common in elderly people; temporal pain should be constant and often
associated with jaw claudication, fever and weight loss; temporal
arteries may be firm, tender and non-pulsatile on examination
Imaging
• Imaging studies are indicated to differentiate idiopathic TN from

secondary TN.
• MRI is preferred to CT due to its better resolution of the posterior
fossa.
• MRI can identify MS plaques and pontine gliomas.
• Magnetic resonance angiography (MRA) can locate a vascular
compression.
• Advanced techniques enables to view enlarged sections of the pontine
area that can manifest a neurovascular conflict (e.g. posteroinferior
cerebellar artery compresses the trigeminal root). Though the vascular
abnormalities are noted by conventional angiogram, its relation with
underlying trigeminal nerve cannot be appreciated.
Other tests
• Clinical neurological testing with a blink reflex study, bilateral delay in

response to the stimulation on the affected side reveal a lesion in the
trigeminal nerve whereas a normal blink reflex is seen in idiopathic
TN.
• Selectively blocking the nerve ending with local anaesthetic infiltration
(2% Xylocaine; 1:80000 concentration) is valuable in the determination
of the affected periphery (Flowchart 34.3).
FLOWCHART 34.3 Local anesthetic diagnostic test.
Management
Management can be categorised as:
1. Medical care: Palliative treatment and drugs

2. If not responding to the medical care, surgical management is considered
3. Peripheral procedures
4. Ganglion procedures
5. Open operation
6. Central procedures
Medical care
Management of a patient with TN includes pharmacological therapy,
percutaneous procedures, surgery and radiation therapy. Usually the first line
of treatment is pharmacological therapy. Initially the patient responds well,
but prolonged drug therapy may become ineffective. Some patients are
refractory to any type of treatment. Treatment is custom made for each patient
depending on the patient’s age, general condition. Removal of the primary
cause is necessary in case of secondary TN.
• Carbamazepine (Tegretol, Carbatrol). It remains the standard drug of

choice for TN.
• Phenytoin (Dilantin) is not as effective as carbamazapine, but
sometimes a patient may respond to it and not to carbamazepine. The
dose varies with patients.
• Baclofen has been used successfully in the literature.
• Clonazepam (Klonopin) is moderately effective but is not used due to
its adverse effects (e.g. sedation) and dependence.
• Amitriptyline (Elavil), Gabapentin (Neurontin), Lamotrigine (Lamictal)
are other drugs which are useful in the treatment of TN.
Medical management of TN
Surgical management
• Peripheral surgery
• Ganglion procedures
• Open operations
Peripheral surgery
This surgery is done very close to the area where the trigger area is located:
cryotherapy, alcohol block, laser and neurectomy (Fig. 34.26A–B). These give
short-term pain relief and cause few complications. Many patients, however,
need to continue the medication. They are now rarely used and are only
suitable when other procedures are not possible.
FIGURE 34.21 (A–E) Facial reanimation with temporalis

lengthened without fascia lata (Labbe’s technique): (A)
Preoperative photograph. (B) Temporalis muscle harvested from
the temporal fossa. (C) Once coronoidectomy is done, the
temporalis is tunnelled to the extraoral incision at the nasolabial
crease and sutured to the paralysed zygomatic major muscle. (D)
Temporalis repositioned and is sutured back to the temporal fascia
in the temporal fossa. (E) Postoperative photograph.
Ganglion procedures
These procedures advocate percutaneous approaches to the trigeminal
ganglion via the foramen ovale. Alcohol was the neurolytic agent most
commonly used. But nowadays three main techniques remain in common use:
(i) thermocoagulation, (ii) glycerol injection and (iii) balloon compression.
FIGURE 34.26 (A–B) Neurectomy.
Needle placement
The technique of needle placement is common to all of these. Although the
pioneering operations were done free hand, image intensification or hardcopy
radiographs are almost universally employed now for visualisation of the
position of the foramen and then for confirmation of the depth of penetration
and the position of any contrast medium used.
Approaches
Anterior approach is more commonly used. The patient lies on a radiolucent
table with the neck well extended. The foramen ovale is best visualised with
the X-ray tube placed for a submentovertex projection.
The entry point for the needle is about 15 mm lateral to the angle of the
mouth. It is best to infiltrate the skin and cheek with local anaesthetic even if
the procedure is done under general anaesthesia, as the needle is less likely to
penetrate the buccal mucosa if the cheek is swollen. The needle is initially
directed slightly laterally for the same reason and then towards the foramen.
The position of this is determined from surface markings: it lies in the base of the
skull at the intersection of a sagittal plane through the inner canthus of the
ipsilateral eye and a coronal plane through the zygoma 2.5 cm anterior to the
tragus. The lateral pterygoid is usually just medial to the line.
Engagement of the needle in the foramen is best confirmed by biplanar
radiology, but some clinical signs may be apparent. If insufficient local
anaesthetic is used in local anaesthesia cases, penetration of the mandibular
nerve will be extremely painful. Even careful local anaesthetic administration
at this point does not usually make the remainder of the procedure painless. In
general anaesthesia cases, fibrillation of the ipsilateral masseter may be
apparent as the nerve is entered.
Radiofrequency thermocoagulation
The needle used here has an insulated shaft and a bore sufficient for the
passage of a radiofrequency electrode. It is reusable and therefore must be
kept well sharpened. An indifferent electrode is usually a simple hypodermic
needle inserted obliquely into the skin of the forehead. Once the
radiofrequency needle is in the foramen ovale, it is advanced into the
trigeminal ganglion. When it is correctly placed, CSF should emerge on
removal of the stylet as the ganglion contains CSF. The electrode is inserted
just beyond the tip of the needle and low amplitude current is applied using a
lesion generator.
The patient, who by this stage must be awake and co-operative, is asked to
indicate where on the face the stimulation is felt. A picture of a face held in
front of the patient is useful here. The position of the electrode is adjusted
sequentially until stimulation is felt in the normal distribution of the patient’s
trigeminal neuralgia.
When the patient and surgeon are quite happy that this is the case, a short-
acting intravenous anaesthetic is given and the radiofrequency lesion made.
Glycerol injection
This procedure may be done entirely under local anaesthesia—indeed it is
very difficult without the co-operation of the patient as the position on the
operating table has to be changed and the head kept still and flexed for
sometime afterwards. A 16 G spinal needle is used and is inserted through the
foramen ovale into the ganglion until CSF is obtained on withdrawal of the
stylet. The patient is made to sit up, supported with the head fixed. A
modified dental chair is useful. In this position, an injected fluid with a higher
specific gravity than CSF will lie within the ganglion or in Meckel’s cave or
outline the inside of the ganglion, the latter being preferable.
Adjustment of the needle will be required if the contrast is extradural or if it
diffuses rapidly away from the cave. The contrast is evacuated and replaced
with 0.5–0.75 mL of pure glycerol. The patient is transferred back to the ward
with the head to be maintained in the same position for at least 2 h.
Balloon compression
This is technically the easiest of the three procedures but once again requires
general anaesthesia. A 4 FG Fogarty catheter is used, the balloon being primed
with X-ray contrast medium from a 1 mL syringe. A 12 gauge spinal needle is
required. In this case, it is advanced only just into the foramen ovale and the
balloon catheter passed through it. This should be discernible on image
intensification. If the needle is passed too far, the balloon will pass
intracranially rather than into the ganglion and if not far enough it will be
extradural or will not pass. When inflated, the balloon should take on the
shape of Meckel’s cave and should appear pear-shaped. No more than 0.75 mL
of contrast should be injected and prior to full inflation the needle should be
withdrawn slightly to prevent the balloon bursting on it. If the balloon takes
on a regular oval shape, it is not within the cave and should be repositioned.
The balloon should remain inflated for 1 min.
Hazards
Hazards common to all percutaneous procedures relate to haemorrhage
caused by inappropriate placement of the needle, usually in the foramen
lacerum and thus the basal carotid artery or by the needle transgressing a
vessel in its appropriate trajectory.
Extracranial bleeding may cause facial swelling or bruising but is not
serious. Intracranial bleeding is rare but may cause all the symptoms and
complications of subarachnoid haemorrhage. Progressive and gentle
manipulation of the needle, particularly once the foramen ovale is entered,
with frequent radiologic checks, helps to reduce the incidence of untoward
events. Infective complications are so rare that few surgeons use antibiotic
prophylaxis.
Radiosurgery
Stereotactically focused radiotherapy—provided either by an adapted linear
accelerator or by the so-called ‘Gamma Knife’—has increasingly found a place
in the treatment of vascular lesions and tumours.
The mechanism of action here is clear. When directed at the root entry zone
of the trigeminal nerve, however, radiosurgery has also proved effective in
reducing or abolishing the symptoms of trigeminal neuralgia. It is not yet clear
for how long this effect will last or what is its rationale, although like many of
the procedures above it presumably causes focal damage to the root and
interrupts the ‘short circuits’ generating neuralgia.
Open operations
Microvascular decompression
This has virtually replaced all other open procedures and in many centres is
the first-line treatment in patients whose pain is refractory and who are able to
tolerate surgery.
Technique
The patient is placed in the lateral position and a 5–6 cm retromastoid incision
is made on the affected side. A small craniotomy or craniectomy is made up to
the confluence of the transverse and sigmoid venous sinuses. This represents
the junction of the tentorium and the petrous temporal bone. An opening is
made in the dura up to this junction and cerebellum is retracted gently while
CSF is aspirated. Under the microscope, the right-angled corner between
tentorium and petrous is identified and followed medially. The petrosal vein is
encountered next and may be safely divided. Just medial to this, the trigeminal
nerve root will come into view.
The root is examined closely and arachnoid adhesions divided. In most
cases, a compressing vessel will be seen medial to the nerve at the root entry
zone—the area where its rootlets enter the pons. This is usually a branch of the
superior cerebellar artery. Any artery encountered in this region must be
treated with the utmost respect as most are end vessels and obstruction or
division results in a stroke. The offending vessel is carefully dissected away
from the nerve, upon which a groove is often then seen where it has been
compressed.
If it is possible to displace the vessel permanently—if for instance, it is a
loop and may be displaced lateral to the nerve—this is done, but more
commonly the vessel is merely dissected off the nerve and then separated
permanently from it by the interposition of an inert material such as Teflon
wool. It is important to avoid kinking the artery as this may obstruct or
compromise blood flow. Before this is done, a thorough search of the length of
the nerve must be carried out to ensure that there are no other compressive
vessels. If no artery is found but a vein is compressing the nerve, this should
be treated similarly although the chances of cure of symptoms are less good.
After meticulous haemostasis, retraction is withdrawn and the craniotomy
closes. The patient is closely observed overnight and may usually be
discharged within 3–5 days.
Trigeminal root section

This is rarely used nowadays, although it enjoyed popularity as the standard
operation for trigeminal neuralgia from its introduction in the early 1900s by
Frazier until the 1950s.
This operation was originally performed via a subtemporal, extradural
route, exposing the ganglion and dividing the sensory root—sparing the motor
root—as close to the brainstem as possible. Although this inevitably caused
facial numbness, often involving the ophthalmic division of the nerve and
rendering the patient liable to keratitis, particularly when the greater
superficial petrosal nerve was damaged, it was nevertheless extremely
successful at relieving neuralgia. In 1932, Walter Dandy published data
recommending an approach to the root in the posterior fossa, dividing it only
partially and affording pain relief with considerable preservation of sensation.
More importantly, he later suggested that pain might be caused by
compression of the root at its entry zone by an aberrant artery—the basis of
trigeminal neuralgia as it is understood today.
In cases refractory to percutaneous techniques or microvascular
decompression, partial root section is still occasionally used. It is important to
be sure of the diagnosis of trigeminal neuralgia, however, when considering
this move, as other types of facial pain may be made worse or will at best not
respond. It is most frequently performed when a re-exploration for recurrent
neuralgia reveals no vascular compression.
Potential hazards of posterior fossa surgery include cranial nerve damage
(5th, 7th or 8th) from excessive retraction or manipulation; vascular damage,
particularly to perforating vessels; and postoperative haemorrhage causing
cerebellar or brainstem compression. These are extremely rare in experienced
hands.
Central procedures
Surgical lesions of the brainstem or sensory tracts have an uncertain place at
present in the treatment of facial pain and probably no place in trigeminal
neuralgia. Tractotomy and dorsal root entry zone (DREZ) lesions have been
performed for desperate patients and in careful hands have produced some
good results, but potential complications are many and pain relief
unpredictable. Electrical stimulation of central target areas rather than
destruction is currently being evaluated and has had some success in
otherwise intractable facial pain.
Postoperative care
All surgical procedures carry a risk of sensory loss. While this may be
inconvenient when affecting the second or third trigeminal divisions,
anaesthesia of the first division and thus of the cornea is potentially highly
dangerous as unrecognised scarring can lead to blindness.
All patients should therefore have an eye shield applied until they are co-
operative enough for corneal sensation to be tested. If sensation is absent and
fails to return, special glasses with side panels should be worn and the patient
instructed about appropriate eye care.
Routine clinical observations are sufficient for patients following
percutaneous procedures and they can usually be allowed home the same or
the following day. Open procedures carry more serious risks. Observation in
an intensive care or high dependency unit is recommended as the
development of a posterior fossa haematoma, while exceedingly rare, is a life-
threatening emergency. The patient will often have headache or will be dizzy
or nauseated for a day or two and will not usually be discharged until the
third or fourth postoperative day.
If pain is abolished by the procedure, medication may be withdrawn
immediately although some patients prefer a gradual withdrawal.
Anaesthesia dolorosa
This is a condition in which a localised area usually in the face has severe pain
and numbness occurs mainly after an injury to the trigeminal nerve. The pain
is continuous, burning, gnawing or pricking type. The commonest cause is
traumatic injury to the trigeminal nerve during surgery. The pain is usually
refractory to medications. Surgical interventions including focused injury to
the brain stem (tractotomy of the nucleus caudalis), deep brain stimulation
and premotor cortex stimulation have shown poor prognosis.
Geniculate neuralgia
This rare condition is characterised by severe pain in and around the ears. The
pain is pricky, flickering or shooting type. Sometimes, it may be associated
with trigeminal or glossopharyngeal neuralgia. Women are more affected than
men usually in the 2nd or 3rd decades. Cold, noise, swallowing or touch may
trigger an episode. Other related symptoms include increased salivation, bitter
taste, tinnitus and vertigo.
Aetiology
• Geniculate neuralgia (GN) is mainly caused by the compression of

somatic sensory branch of facial nerve and sometimes V, VIII, X
nerves.
• In sufferers of GN, signals sent along the nerve are altered and
interpreted by the geniculate ganglion.
• Occasionally, GN may be followed by herpes zoster oticus (Ramsey-
Hunt syndrome), where cold sores occur on the ear drum or ear.
• Facial paresis (weakness), tinnitus, vertigo and deafness may be
present.
Sphenopalatine neuralgia (Sluder’s neuralgia)
• A neuropathic disorder consisting of neuralgic, motor, sensory and

gustatory involvement of the sphenopalatine ganglion more common
in women (2:1) than men.
• The features are unilateral headache behind the eyes with pain in the
upper jaw or soft palate, with occasional aching in the back of the
nose, the teeth, the temple, the occiput or the neck.
• The pain is associated with nasal and/or sinus congestion, swelling or
redness of nasal mucous membranes, tearing and redness of the face.
• Sphenopalatine neuralgia has similar features of cluster headache. In
case of Sluder’s neuralgia, the duration of pain is longer and is
associated with inflammation of the mucosa.
• Ganglion blocks provide intermediate pain relief, either by intranasal
or direct technique. Removal of the primary cause of Sluder’s
neuralgia, if evident, is required.
Paratrigeminal neuralgia of Raeder
• Paratrigeminal neuralgia of Raeder is a syndrome characterised by

unilateral, intense throbbing pain in the face along the region of the
ophthalmic division of the trigeminal nerve associated with eye and
skin changes (oculosympathetic palsy). Other findings include
drooping of the eyelid and contraction of the pupil (miosis). The
symptoms are more pronounced in the morning. In case of chorda
tympani (branch of VII cranial nerve) involvement, patient complains
of altered taste sensation (dysguesia).
• Group I: Patients with symptomatic paratrigeminal neuralgia usually
have multiple parasellar cranial nerve defects, including tumours and
lesions. A neuropathic quality of pain is present.
• Group II: The migrainous form with oculosympathetic palsy is of
unknown cause, but may be associated with upper respiratory
infection, pneumonia, otitis media, chronic sinusitis and dental
abscess.
SECTION IX
Dentofacial Deformities
Chapter 35: Orthognathic Surgery

Chapter 36: Distraction Osteogenesis
CHAPTER 35
Orthognathic Surgery
Classification
Maxillary deformities
• Maxillary prognathism
• Maxillary retrognathism or hypoplasia
• Transverse maxillary deficiency
Mandibular deformities
• Mandibular prognathism
• Mandibular retrognathism
Combined deformities
• Skeletal anterior open bite
• Skeletal deep bite
Patient evaluation
• Patient history
• Radiographic and imaging analysis
• Dental model analysis
Presurgical orthodontics
• Advantages
• Presurgical aids in orthodontics
Postsurgical orthodontics
• Goals
Model surgery
• Purpose
• Indications
• Advantages
• Disadvantages
Surgical splints
• Advantages
• Construction of splints
Treatment of dentofacial deformities goals
• Growth modification
• Orthodontic camouflage
Maxillary osteotomy procedures
Single tooth osteotomy
Anterior segmental maxillary osteotomy
• Indications
• Technique
• Posterior segmental maxillary osteotomy
• Indications
• Surgical technique
• Variations of posterior segmental maxillary
osteotomy
Le Fort I osteotomy
• Indications
• Surgical technique
• Modifications
Le Fort II osteotomy
Le Fort III osteotomy
Mandibular osteotomy procedures
Ramus osteotomy
• Extraoral vertical ramus osteotomy
• Intraoral vertical ramus osteotomy
• Bilateral sagittal split osteotomy
Mandibular body osteotomy
• Anterior body osteotomy
• Posterior body osteotomy
• Mid-symphysis osteotomy
Segmental subapical mandibular surgeries
• Anterior subapical mandibular osteotomy
• Posterior subapical mandibular osteotomy
• Total subapical mandibular osteotomy
Genioplasty
• Horizontal osteotomy with anteroposterior
reduction
• Double sliding horizontal osteotomy
• Vertical reduction genioplasty
• Tenon technique
• Vertical augmentation
• Alloplastic augmentation
Dentofacial deformities and common surgical
approaches
Various features of a human face put together in different proportions give a

diverse variety. Dentofacial deformity refers to any deviation from the normal
and accepted facial proportions and dental relationships bring about
unpleasant facial appearance, mental depression and decreased level of
confidence for the patient. Dentofacial deformities affect approximately 20% of
the population.
Patients with dentofacial deformities may demonstrate varying degrees of
functional and aesthetic compromise.
Such malformation may be isolated to one jaw or may involve multiple
craniofacial structures. They may be expressed to varying degrees in the
horizontal, vertical and transverse facial planes. Dentoalveolar abnormalities
may deceive the observer as a skeletal abnormality. Thus differentiating
dentoalveolar deformity from skeletal abnormality becomes a diagnostic
challenge, before planning an orthognathic surgery.
Envelope of discrepancy (Profit) It shows how much of change can be
produced by various treatment modalities in three planes of space. (i.e.
anteroposterior, vertical and transverse planes)
The word ‘orthognathic’ comes from the Greek word ‘ortho’ meaning to
straighten and ‘gnathia’ meaning jaw. Orthognathic surgery thus means to
straighten a jaw. Orthognathic surgery is defined as ‘the art and science of
diagnosis, treatment planning and execution of treatment to correct
musculoskeletal, dentoosseous and soft tissue deformities of the jaws and
associated structures’.
Many patients with severe dentofacial deformities (Table 35.1) can benefit
from corrective orthognathic treatment. With the advent of distraction
osteogenesis, orthognathic surgery has become a secondary option for
hypoplasia/deficiency. But orthognathic surgery remains the prime surgical
treatment in managing skeletal excess efficiently. Osteotomy refers to simple
bone cut whereas osteotomy means the removal of a portion of the bone. The
fundamental biology behind orthognathic surgery is that the maxillary and
mandibular bones are intentionally sectioned and repositioned at the desired
sites to correct the dentofacial deformities (Fig. 35.1A, B).
Table 35.1
Classification of dentofacial deformities
Skeletal Description Underlying skeletal problem

deformity
Angle Class II Short mandible in anterior–posterior plane 1. Maxillary hyperplasia in
anterior–posterior plane
Angle Class III Long mandible in anterior–posterior 1. Maxillary hypoplasia in
plane/short maxilla in anterior–posterior anterior–posterior plane or
plane 2. Mandibular hyperplasia in
anterior–posterior plane or
3. Combination
Vertical Long maxilla in vertical 1. Maxillary hyperplasia in vertical
maxillary
excess (VME)
Bimaxillary Proclined anterior bimaxillary alveolus 1. Bimaxillary dentoalveolar
protrusion hyperplasia in anterior–posterior
plane
Open bite Nonoccluding anterior teeth 1. Reverse curve of Spee or
2. Posterior vertical maxillary
excess
3. Short mandibular ramus or
4. Combination
Facial Deviated jaw/chin 1. Unilateral condylar hyperplasia
asymmetry or
2. Unilateral mandibular
hyperplasia or
3. Chin deviation
FIGURE 35.1 Envelope of discrepancy.
Indications for orthognathic surgery:
• Very severe dentoalveolar problems that cannot be corrected by

orthodontics alone.
• Severe class II, class III and transverse skeletal discrepancies.
• Vertical discrepancies: Long face and short face.
• Congenital craniofacial syndromes.
• Facial asymmetry.
Classification (Table 35.1)

Timing of surgery
As a general rule early jaw surgery has an inhibitory effect on further growth,
hence surgery should be delayed in patients who have excessive growth
problems and can be considered earlier for patient with growth deficiencies
but not before adolescent growth spurts (Box 35.1).
Box 35.1 Timing of surgery
Nature of Recommended time of orthognathic treatment

problem
After growth completion.
• Maxillary
excess
• Maxillary Maxillary advancement may be delayed till adolescent growth spurt.
deficiency
Treated best when growth is completed, assessed by hand-wrist radiograph

• Mandibular or serial cephalometric tracing.
excess
Girls: 14–16 years, Boys: approximately 18 years.

• Mandibular
deficiency
Early surgical intervention recommended only when abnormal growth

• Asymmetry worsens the existing situation.
Early surgery not recommended.

• Long face
Similar to mandibular deficiency problem.

• Short face
Maxillary deformities (Figs. 35.2–35.4)

I. Maxillary prognathism
• Short hypotonic lip with poor lip seal

• Increased lower facial height
• Patient has a convex profile
• Most of the patients have abnormal muscle activity, e.g. abnormal
buccinators activity results in a constricted, narrow upper arch leading
to posterior crossbite.
• The mentalis muscle may be hyperactive giving a prominent chin
button
• Increased overjet, overbite and curve of Spee
• The molar relation may be Angle class II malocclusion
FIGURE 35.2 (A) Preoperative view showing short upper lip and
maxillary excess. (B) Postoperative view.
FIGURE 35.3 (A, A’) Maxillary anteroposterior excess. (B, B’)

Maxillary anteroposterior deficiency (cleft). (C, C’) Vertical
maxillary excess.
II. Maxillary retrognathism or hypoplasia
• Sagging upper lip giving an old look

• Deficient paranasal prominence
• Concave facial profile
• Angles class I or class III malocclusion
• Incisors in edge to edge or with reverse overjet
• If associated with zygoma hypoplasia, zygoma prominence will be
diminished with scleral show
III. Transverse maxillary deficiency
• Most common skeletal deformity associated with maxillary vertical

and anteroposterior hypoplasia
• Unilateral or bilateral posterior crossbite
• Crowded, rotated and palatally or buccally displaced teeth
• Narrow and tapering maxillary arch form—hourglass shaped high,
narrow palatal arch.
Mandibular deformities (Figs. 35.5–35.7)

I. Mandibular prognathism
• Increased lower facial height with prominent chin

• Oblique mandibular plane
• The patient usually has a concave profile
• The molar relation may be class III
• Posterior crossbites are common due to narrow and short upper arch
but broad lower arch
FIGURE 35.4 (A, A’) Vertical maxillary deficiency. (B, B’)

Combination of anterior–posterior and transverse maxillary
deficiency. (C, C’) Transverse maxillary deficiency.
FIGURE 35.5 (A, A’) Mandibular anteroposterior excess. (B, B’)
Mandibular anteroposterior deficiency. (C, C’) Hemimandibular
elongation.
FIGURE 35.6 (A, B) Genial deficiency—Microgenia. (C–E) Genial

excess.
FIGURE 35.7 (A, A’) Genial asymmetry. (B, B’) Open bite. (C, C’)
Deep bite.
II. Mandibular retrognathism
• Reduced lower facial height

• Posteriorly positioned chin
• Convex profile
• May be associated with obstructive sleep apnoea
• Angles class II malocclusion
Combined deformities (Fig. 35.8)

I. Skeletal anterior open bite
• The patient often has a long and narrow face

• Lower facial height is increased
• Short upper lip with excessive show of maxillary incisors
• A steep mandibular plane angle
• Cephalometric examination shows:
▪ A downward and forward rotation of the mandible
▪ In some patients, an upward tipping of the maxillary skeletal
base can be observed
▪ Another common feature is a posterior vertical maxillary
increase
FIGURE 35.8 (A–C) Combined maxillary and mandibular deformity.
II. Skeletal deep bite

Skeletal deep bites are usually of genetic origin. Forward and upward rotation
of the mandible with or without downward and forward inclination of the
maxilla results in this skeletal deep bite.
• Reduced anterior facial height

• Horizontal growth pattern of the face
• A reduced interocclusal clearance (freeway space)
• A cephalometric examination reveals that most of the horizontal
cephalometric planes such as mandibular plane, Frankfort horizontal
(FH) plane, sellanasion (SN) plane, etc. are parallel to each other.

The overall patient management entirely depends upon the thorough
evaluation and diagnosis of the deformity. Any failure on the side of the
clinician to recognise the major functional and aesthetic problems might have
undesirable and complicated outcomes.
Diagnosis and treatment planning for any orthognathic case is established
through proper interaction and communication of both orthodontist and
maxillofacial surgeon (Table 35.2; Flowchart 35.1).
Table 35.2
Typical presentation of maxillofacial deformities
FLOWCHART 35.1 Diagnosis and Treatment planning
Patient evaluation
Includes thorough evaluation and diagnosis for overall patient management.
The sequence in evaluating a patient for orthognathic surgery should follow
the below four main areas:
I. Patient concerns or chief complaints

II. Clinical evaluation
III. Radiographic and imaging analysis
IV. Dental model analysis
I. Patient concerns
Most of the patient’s get satisfied with the treatment outcome based on their
initial perceptions and their concerns prior to surgery failing which will affect
the psychological health of the patient. Every patient’s chief concerns should
include the following questionnaire which helps in developing a preliminary
problem list and helps identify patients with unrealistic expectations:
• What are your concerns or problems?

• Have you had previous treatment and what was the outcome?
• Why do you want the treatment?
• What are your expectations from the treatment?
II. Clinical evaluation

Clinical evaluation for orthognathic surgery includes:
• Patient history
• Clinical photographs
• Patient preparation for dentofacial evaluation
• Dentofacial evaluation
Patient history
A thorough medical history, dental history, physical examination and
laboratory investigation should be done to rule out or identify patients with
airway problems, connective tissue or autoimmune diseases, bleeding
disorders or other pathologic conditions that may preclude or modify surgery.
Clinical photographs
• Essential for documentation and can be used for photometric analysis.

• Also to obtain soft tissue landmarks for angular and linear
measurements.
Patient preparation for dentofacial examination

Before proceeding with the patient’s facial evaluation it is important to seat the
patient in the following position:
• Sitting upright in a straight-backed chair.

• The pupillary plane should be parallel to the floor.
• Natural head position: It is the most important factor in which the
patient’s head is positioned in a way that the clinical Frankfort
horizontal plane (defined as the line from the tragus of the ear to the
bony infraorbital rim) is parallel to the floor. Most standardised
measurements throughout the treatment are obtained in this position
only.
• Centric relation—Usually the patient is asked to position the tongue at
the most posterior aspect of the palate while gently closing the teeth
together.
• Lips should be relaxed as it allows in evaluating the vertical facial
height, tooth to lip measurements, lip incompetences and coincidences
of the dental midlines.
Dentofacial evaluation (Fig. 35.9)

The goals of dentofacial examination are to evaluate and document the
following problems:
• Extraoral examination (macro- and miniaesthetics)

• Intraoal examination (microaesthetics) and
• Functional examination
FIGURE 35.9 Facial aesthetics.
Macroaesthetics
The facial features for macroaesthetic examination are evaluated from the
frontal and lateral profile views as listed in the Flowchart 35.2.
FLOWCHART 35.2 Macroaesthetics.
Miniaesthetics (Fig. 35.18)

The miniaesthetic examination includes the following features:
1. Vertical characteristics of the smile

• Lip-tooth-gingival relationships
• Gingival display on smile
• Philtrum height
• Clinical crown height
• Maxillary incisors inclination
2. Transverse characteristics of the smile (Fig. 35.19)
• Arch form
• Buccal corridor
• Cant of the transverse occlusal plane
• Lower lip, chin, throat angle: It is the angle between a line drawn
from the lower lip to the soft tissue pogonion and a line
drawn tangentially to the soft tissue contour below the body
of the mandible. The normal angulation is 110 degree ± 8
degree. A large angle indicates recessive chin while low
angulation suggests an excessive chin.
Microaesthetics
• Occlusal relationship
• Anterior deep bite or open bite
• Anterior overjet and any crossbite
• Health of the dentition
• Tooth size discrepancies
• Curve of Wilson
• Curve of Spee
• Dental crowding or spacing
• Missing and carious teeth
• Periodontal evaluation
• Transverse, vertical and anteroposterior discrepancies
• Anatomical, functional tongue abnormalities
• Attrition
Oral examination helps to find out functional and aesthetic deformities of

the dentofacial structures.
Any temporomandibular joint (TMJ) dysfunction or pathosis should be
detected prior to surgery. Any nasal trauma, nasal airway obstruction,
allergies, sinus problems, predominant mouth breathing, etc. are evaluated.
III. Radiographic and imaging analysis

Cephalometric analysis can be an aid in the diagnosis of skeletal and dental
problems and as a tool for simulating surgery and orthodontics. A number of
cephalometric analyses are commonly used for orthodontic case analysis.
These analyses are primarily designed to harmonise the malpositioned teeth
with the existing skeletal pattern.
For the purpose of cephalometric analysis, following landmarks of planes on
the lateral skull radiograph are essential (Figs. 35.20, 35.21).
FIGURE 35.20 Important landmarks on a lateral skull radiograph
for cephalometric analysis.
FIGURE 35.21 Important planes on a lateral skull radiograph for
cephalometric analysis.
Cephalometric hard and soft tissue landmarks (Tables 35.3, 35.4)
Cranial base
The base line for comparison of most of the data in this cephalometric analysis
is a constructed plane called horizontal plane (HP). It is constructed by
drawing a line 7 degree from the line SN. It is a substitute to Frankfort plane.
Most of the measurements are made from projections either parallel or
perpendicular to horizontal plane. The length of the cranial base is measured
from Ar to N and parallel to HP.
Table 35.3
Hard tissue landmarks on Cephalograph

SELLA (S) The centre of the pituitary fossa
NASION (N) The most anterior point of the nasofrontal suture in the midsagittal
plane
ARTICULARE (Ar) The intersection of the basisphenoid and the posterior border of the
condyle mandibularis
PTERYGOMAXILLARY The most posterior point on the anterior contour of the maxillary
FISSURE (PTM) tuberosity
SUBSPINALE (A) The deepest point in the midsagittal plane between the anterior nasal
spine and prosthion, usually around the level of and anterior to the
apex of the maxillary central incisors
POGONION (Pg) The most anterior point in the midsaggital plane of the contour of the
chin
SUPRAMENTALE (B) The deepest point in the midsagittal plane between infradentale and
Pg. usually anterior to and slightly below the apices of the mandibular
incisors
ANTERIOR NASAL The most anterior point of the nasal floor; the tip of the premaxilla in
SPINE (ANS) the midsagittal plane
MENTON (Me) The lowest point on the contour of the mandibular symphysis
GNATHION (Gn) The midpoint between Pg and Me, located by bisecting the facial line
N-Pg and the mandibular plane (lower border)
POSTERIOR NASAL The most posterior point on the contour of the palate
SPINE (PNS)
MANDIBULAR PLANE A plane constructed from Me to the angle of the mandible (Go)
(MP)
NASAL FLOOR (NF) A plane constructed from PNS to ANS
GONION (Go) Located by bisecting the posterior ramal plane and the mandibular
plane angle
Table 35.4
Soft tissue landmarks on Cephalograph

GLABELLA (G) The most prominent point in the midsagittal plane of the forehead
COLUMELLA The most anterior point on the columella of the nose
POINT (Cm)
SUBNASALE The point at which the nasal septum merges with the upper cutaneous lip in
(Sn) the midsagittal plane
LABRALE A point indicating the mucocutaneous border of the upper lip
SUPERIUS (Ls)
STOMION The lower most point of the vermilion of the upper lip
INFERIUS
(Stms)
STOMION A point indicating the superior border of the lower lip
INFERIUS (Stm)
LABRALE A point indicating the mucocutaneous border of the lower lip
INFERIUS (Li)
MENTOLABIAL The point of greatest concavity in the midline between the lower lip and the
SULCUS (Si) chin (Pg)
SOFT TISSUE The most anterior point of soft tissue chin
POGONION
(Pg’)
SOFT TISSUE The constructed point between soft tissue pogonion and the soft tissue
GNATHION menton; can be located at the intersection of the subnasale to soft tissue
(Gn’) pogonion line and the line from C to Me
SOFT TISSUE The lowest point on the contour of the soft tissue chin; found by dropping a
MENTON (Me’) perpendicular from horizontal plane through menton
CERVICAL The inner most point between the submental area and the neck located at the
POINT (C) intersection of lines drawn tangent to the neck and submental areas
Horizontal skeletal profile analysis (Fig. 35.22A, B)
Horizontal skeletal profile analyses are made parallel to HP. These are very
important because most surgical corrections are primarily made in the
anteroposterior direction.
FIGURE 35.12 Transverse proportions. (A) Intercanthal distance
—35 ± 3 mm. (B) Interpupillary distance – 65 ± 3 mm. (C) The
palpebral fissure width should be equal to the intercanthal
distance.
Degree of skeletal convexity
The angle of facial convexity is measured by the angle formed by the line NA
and the line from A to Pog. The N-A-Pog angle gives an indication of the
overall facial convexity, but does not specify the diagnosis that whether the
maxilla or the mandible is at fault.
A positive angle of convexity denotes convex face and a negative angle
denotes concave face. A clockwise angle is positive (+), a counter clockwise
angle is negative (–).
A line perpendicular from HP is dropped through N. Horizontal position of
A is measured from this perpendicular line. This measurement describes the
apical base of the maxilla in relation to N and enables to determine if the
anterior part of the maxilla is protrusive or retrusive. Similarly, position of
point B from this perpendicular line describes the horizontal position of the
apical base of the mandible in relation to N. When inferior anatomical
landmark is measured in relation to the superior structure, the positive sign (+)
denotes anterior and the negative sign (–) denotes posterior.
Thus, these measurements are useful in the planning of treatment of
maxillary or mandibular advancement or reduction.
N-Pog is measured in the same manner as NA and NB and indicates the
prominence of the chin. These measurements determine if there is horizontal
genial hyperplasia or hypoplasia and useful in the planning of treatment as
augmentation and reduction genioplasty, anterior mandibular horizontal
advancement or reduction and total mandibular horizontal advancement or
reduction.
Vertical skeletal profile analysis (Fig. 35.23)

Vertical skeletal discrepancy may reflect anterior, posterior or complex
dysplasia of the face. Therefore, vertical skeletal cephalometric measurements
are divided into anterior and posterior components.
• Anterior component: The anterior component is subdivided into

measurements of: (1) the middle third facial height (distance from N to
ANS) that is measured perpendicular to HP and (2) the lower third
facial height which is a measurement from ANS to Gn and is
measured perpendicular to HP.
• Posterior component: Posterior maxillary height is the length of a
perpendicular line dropped from HP intersecting the PNS. The
divergence of the mandible posteriorly is shown by the mandibular
plane angle (MP-HP), which is the angle formed between Go, Gn and
HP. This angle helps in relating the posterior facial divergence with
respect to the anterior facial height.
FIGURE 35.16 (A) The normal nasolabial angle is 90 to 105
degree. (B) The normal nasal projection angle with a line tangent
to the dorsum of the nose and the angle created by the line
perpendicular to Frankfort horizontal should be 36 degree for
males and 34 degree for females.
Vertical skeletal measurements help in the diagnosis of anterior, posterior

and total maxillary hyperplasia or hypoplasia and also clockwise or counter
clockwise rotation of the maxilla and mandible.
Surgical correction of these problems includes total maxillary vertical
advancement or reduction, anterior maxillary vertical augmentation or
reduction, posterior maxillary vertical augmentation or reduction,
combination of anterior and posterior maxillary vertical augmentation or
reduction and mandibular ramus rotation and ramus height reduction.
Normal cephalometric values (Table 35.5)

Tracing for cephalometric studies (Fig. 35.24): The tracing should be made
under suitable conditions—a darkened room, a well-illuminated viewing
screen blanked off with card to leave a window just large enough for the
radiograph, a good quality tracing sheet fixed to the radiograph with clear
adhesive tape and a hard pencil are required. Radiograph should be oriented
with the Frankfort plane (or HP plane) parallel to the bottom edge of the
screen, because a number of landmark definitions depend on head orientation.
Table 35.5
Normal cephalometric values
Interpretation of tracing: By comparison of angular measurement with

normal values, one can interpret the results of analysis to give a diagnosis of
the patient’s presenting skeletal pattern. Comparison of the findings from the
original and the final cephalometric radiographs will allow us to assess the
outcome of treatment.
Apart from cephalometric studies, CT scanning and MRI are also used
extensively.
IV. Dental model analysis (Fig. 35.25A, B)

Proper model analysis improves understanding and development of the
presurgical orthodontic goal. There are 10 basic dental model evaluations that
should be made:
1. Arch length: The arch length measurement should correlate with the
width of the teeth and availability of alveolar bone. These
measurements give an idea whether the tooth needs to be extracted or
not.
2. Tooth size analysis: It refers to the correlation of the mesiodistal width of
the upper teeth to that of the lower teeth. This is primarily seen in the
anterior six maxillary and mandibular teeth.
Bolton’s analysis: Total width of six upper anterior teeth = 1.3 × total
width of lower six anterior teeth. Average is 77.5 ± 3.5. This analysis
helps in determining disproportion in size between maxillary and
mandibular teeth.
3. Tooth position in context of orthognathic analysis: This refers primarily to
the angulation of the maxillary and mandibular incisors relative to the
basal bone. This analysis determines whether extractions are necessary,
whether spaces need to be created and what kind of mechanics should
be used for teeth correction.
4. Arch width analysis: This refers to the evaluation of the intra-arch
width between the maxilla and mandible. This is best analysed by
holding the models in the occlusal position that is to be achieved with
the orthodontic and surgical corrections and then access the transverse
relationship. Arch width analysis is helpful in determining presurgical
orthodontic mechanics as well as selecting appropriate surgical
procedures.
5. Curve of occlusion: This has a significant influence on whether it can be
corrected orthodontically whether extractions will be necessary or
whether surgical intervention is indicated to level the occlusal plane.
6. Cuspid-molar position: This dictates the occlusal functions. It is preferable
to have class I cuspid-molar relation.
7. Overbite and overjet relationship.
8. Tooth arch symmetry: There might be significant asymmetry within each
arch such as cuspid on one side may be more anteriorly placed than the
cuspid on other side. Correction may require special orthodontic
mechanics, unilateral extraction or additional surgical procedures.
9. Buccal tooth tipping (comparison of right and left symmetry within each
other): This evaluates the position of the occlusal surfaces of the
maxillary posterior teeth, in a medial-lateral direction. If maxillary
posterior teeth are tipped buccally, it may be difficult to achieve a
proper occlusal relationship.
10. Missing, broken down or crowned teeth: This may influence treatment
designs. If a tooth is nonrestorable and requires extraction in a
potential osteotomy location, the extraction space may need to be
closed orthodontically or the space maintained.
FIGURE 35.17 Chin projection.
(A) A line perpendicular to the clinical Frankfort horizontal (CFH)
plane through subnasale should be 3 ± 3 mm anterior to the chin.
(B) A line tangent to the globe should fall on the infraorbital soft
tissues ± 2 mm.
Presurgical orthodontics
The orthodontist is responsible for moving the teeth to a more desirable
position over the basal bone in preparation for surgical repositioning in all the
three planes—anteroposterior, vertical and transverse. It facilitates the
planned skeletal and facial correction (Flowchart 35.3).
FLOWCHART 35.3 Orthodontic tooth movement for the surgical
patient
The basic presurgical orthodontic goals are:
• Position the long axis of the maxillary central incisors so that the final
position would be approximately 22 degree to the NA line, with the
labial face of the incisors 4 mm anterior to that line
• Position the mandibular central incisors so that final position will be
approximately 20 degree to the NB line, with the labial face of the
incisors 4 mm anterior to that line.
• Aligning: Align and position the teeth over the basal bone.
• Levelling: Avoid excessive intrusion or extrusion of the teeth
(Flowchart 35.4).
• Decompensate teeth: Also called as ‘Reverse orthodontics’ and it is one of
the major goals in presurgical orthodontics. Establish the
anteroposterior position of incisors and usually worsens the
malocclusion to fully reveals the skeletal discrepancies
(Flowchart 35.5).
• Adjust the tooth size discrepancies: Done by recontouring the
interproximal contact areas or by closing or opening the spaces
between the maxillary or mandibular anterior teeth.
• Correct the rotated teeth.
• Avoid class II and class III mechanics (unless required for dental
decompensation).
• Avoid orthodontic movements that can be performed more predictably
with surgery.
• Arch compatibility: It is the last step done in which the transverse arch
width discrepancies are corrected with stable and predictable
orthodontic movements through orthodontic camouflage or surgery
(Flowchart 35.6).
FLOWCHART 35.4 Positioning teeth in the vertical dimension

FLOWCHART 35.5 Positioning incisors in the anteroposterior (AP)
dimension
FLOWCHART 35.6 Positioning teeth in the tansverse dimension
Advantages
• Relapse tendencies are controlled

• Total treatment time is reduced
• Results in proper intraoperative interdigitation
• Allows quick and easy postsurgical orthodontic correction
• Allows effective surgical correction
• Improves results in terms of stability and occlusion
Presurgical aids in orthodontics

While performing orthognathic surgery, if any surgical procedure is
considered to help the treatment, it is known as surgical aid to orthodontics.
Following are some of the common surgical aids to orthodontic treatment:
1. Serial extraction
2. Therapeutic extraction
3. Removal or surgical exposure of unerupted teeth
4. Extraction of submerged deciduous molars, removal of odontomes
5. Correction of diastema
6. Corticotomy
Postsurgical orthodontics
Four to six weeks after the surgery, when the surgeon confirms the satisfactory
healing, the stabilising arch-wires are replaced by light arch wires and
occlusion is allowed to settle.
Goals
• Closure of residual spaces

• Root paralleling at the extraction sites
• Maximum interdigitation
• Finer tooth alignment
• Retention of the reoriented oral musculature to prevent relapse
• Aggressive postsurgical orthodontics if the occlusion is not perfect
initially postsurgery, the surgeon and/or orthodontist must
aggressively apply the appropriate elastic mechanics.
• Ideal overbite and overjet
• To stabilise the results obtained through the surgery
• Changing arch wires.
• Final positioning of the teeth usually takes 3–12 months or sometimes
longer depending on the orthodontic requirements.
• Orthodontic retainers to provide transverse support to the width of the
maxillary and mandibular dental arches and maintain the dental
alignment.
Model surgery
Model surgery is the dental cast version of cephalometric prediction of
surgical results. When the teeth are highly irregular or when the maxillary and
mandibular arch forms are incompatible, model surgery is impossible without
simulating the presurgical orthodontic treatment. In this case, a diagnostic
setup is done first and then the setup models are moved as they might be at
surgery.
In its simplest form, model surgery requires nothing more than articulating
the pretreatment casts by hand in a possible postsurgical position. Mandibular
advancement can be simulated, for instance, by sliding the lower cast forward
relative to the upper cast. It is easier to study the possible tooth relationship if
the casts are mounted temporarily on arbitrary articulators so that they are
held in the desired position. The better the occlusion without any tooth
movement, it is easier to articulate the casts by hand and vice versa.
Purpose
• To determine the magnitude and direction of skeletal movements

• To determine the size and shape of the osteotomies especially
interdentally
• To provide a splint for surgical correction
• To provide a comparative reference to the occlusal result actually
achieved as noted on release of intermaxillary fixation
Indications
Model surgery is used in double jaw surgery, as well as single jaw surgery
where unoperated jaw will act as a template.
Advantages
• The simulation of the patient’s facial structure functionally and

spatially in three dimensions.
• The surgeon can correlate the relevant information and arrive at the
surgical prediction in three dimensions.
• Model surgery gives an accurate 1:1 replica of the patient’s dentition
allowing an increased accuracy in prediction when compared to the
10% discrepancy seen in cephalometric distortion.
• Model platform and block is capable of accurately measuring
articulator mounted models in three planes of space, which allows the
surgeon to carry out accurate model surgery movements on a full-
sized anatomic articulator.
Disadvantages
• Condyles are never perfectly symmetrical; therefore, the model

surgery performed on the mounted casts give slightly inaccurate
readings.
• There can be errors related to the actual model orientation itself.
• There can be measurement errors related to instruments and
perspective.
Surgical splints
Surgical splints are also known as occlusal wafer splints. They are utilised in
the operating room to position the teeth and add to stabilisation. They are
used during the surgery as well as postsurgically.
Advantages
1. Provide a clearly visualised goal for the surgeon at the operating table
2. Aids in positioning bone fragments correctly to aid healing
3. Possible to put teeth in a planned position at surgery, even if they do
not interdigitate perfectly without a splint
4. Surgical splints are utilised in the following procedures:
• Maxillary surgery
• Mandibular ramus surgery
• Segmental jaw surgery
• Dual jaw surgery
Construction of splints
The splint is made on the casts as they have been related by model surgery.
After they have been checked by the surgeon and orthodontist, the following
steps are undertaken:
1. Stabilise cast with plaster or stone, so that no shift occurs as splint is

fabricated.
2. Articulator is opened to allow for enough thickness of splint material.
3. Self-curing acrylic is formed into the desired U-shaped configuration.
Care is taken to avoid rolling the acrylic excessively, as this causes
cracks and bubbles.
4. Lay the U-shaped roll of uncured acrylic on the lower occlusal surface.
The casts are then closed onto it. At this point, the casts must be firmly
secured to the articulator. If the casts shift, splint dictates wrong
position at surgery.
5. While the acrylic is still soft, scissors/scalpel is used to trim the excess
on the labial aspect. Ensure that it does not tear away while carrying
out this procedure.
6. After the acrylic has cured, a semitrimmed splint with occlusal
indentations is obtained.
7. Trim away excessive bulk labially and lingually with burs. Buccal
aspect of splint must be contoured to avoid interference with
orthodontic appliances and to allow visual determination of proper
seating during surgery. The acrylic should be relieved on lingual
aspect of anterior teeth and distal aspect of buccal segment cusp tip to
allow a smooth arc of closure.
8. Trim occlusal surfaces so that only shallow occlusal indentations
remain.
9. Finally, place bur holes along labial and buccal surface for attaching
splint to the archwires.
10. Routine finishing and polishing must be carried out for patient’s
comfort and maintenance of oral hygiene.
Treatment of dentofacial deformities goals

• To reposition bone and dentoalveolar segments into normal
relationship
• To provide best functional aesthetic results along with stability
Mild deformities can be corrected using orthodontic tooth movement. For

severe skeletal deformities, there are three options: (1) growth modification,
(2) orthodontic camouflage and (3) orthognathic surgery.
Growth modification
Growth modification can be achieved in children, in whom the growth
potential is still present, through: (1) orthopaedic appliances like head gear,
chin cup and (2) myofunctional appliances.
Orthodontic camouflage
When the skeletal deformity is very mild and any further change is not
expected, orthodontic camouflage should be considered. Establishing normal
overjet and overbite can compensate a few discrepancies, e.g. in case of mild
skeletal class II malocclusion, the maxillary teeth can be retracted and the
mandibular teeth slightly proclined to camouflage the skeletal deformity.
Camouflage should not be done at the expense of undesirable facial aesthetics
though there might be some compensation of the same. The utmost
significance in orthodontic camouflage is given to the ultimate facial aesthetics
and occlusional stability.
The fundamental goal of orthognathic surgery is to reposition basal bone and
the dentoalveolar segments into normal relationship and to provide best
functional aesthetic results along with stability (Table 35.6) Box 35.2.
Table 35.6
Goals for orthognathic surgery

Basic therapeutic goals Examples
Functions Normal mastication, speech, ocular function, respiratory function
Aesthetics Establishment of facial harmony and balance
Stability Prevention of short- and long-term relapse
Minimising of treatment time Provision of efficient and effective treatment
Box 35.2 Maxillary surgeries
1. Segmental osteotomy of the maxilla

a. Single tooth osteotomy
b. Corticotomy
c. Surgically assisted rapid maxillary expansion (SARME)
d. Anterior segmental maxillary osteotomy
• Wassmund technique
• Wunderer technique
• Epker’s anterior maxillary osteotomy
• Cupar’s technique
e. Posterior subapical osteotomy of maxilla
• Kufner
• Schuchardt
• Perko and Bell
2. Total maxillary osteotomy
a. Lefort I
b. Lefort II
c. Lefort III
Guidelines for performing osteotomy
• Bell in 1975 proved that the blood supply to the osteotomised segment
will be maintained adequately, if at least one soft tissue pedicle is
preserved intact. Therefore, the design of the soft tissue incision
should be such that it follows Bell’s principle.
• The neurovascular bundle should be preserved during the osteotomy
cut.
• The cut should be done under constant irrigation in order to avoid
necrosis of the tissues due to excessive heat produced by the
micromotor.
• The cut for subapical surgery should be a minimum of 4–5 mm away
from the root apex and for that matter any osteotomy cut should not
jeopardise the integrity of the periodontal ligament of any tooth.
• The osteotomised portions should be well approximated without any
bony or soft tissue interference.
Maxillary osteotomy procedures

From 1969 to 1975, Bell carried out extensive research studies on Rhesus
monkeys and performed many maxillary osteotomies which lead to its
popularity. He experimented and studied revascularisation and bone healing
of the various osteotomy procedures. He proved that if at least one soft tissue
pedicle is preserved intact, blood supply to the osteotomised segments can be
maintained. This was the biological basis for many maxillary osteotomies.
Single tooth osteotomy (Fig. 35.26A–C)

Single tooth osteotomy is used for correction of tooth malposition, dental
ankylosis, or closure of a diastema. Because soft tissue pedicle to the
dentoalveolar segment is relatively small, some surgeons have been reluctant
to use this technique for fear of compromising vascular supply and causing
ischaemic necrosis of the involved segment. Benefits of this surgical technique
are a reduction in treatment time and a lower incidence of dental relapse when
compared with conventional orthodontic therapy. Drawbacks of the procedure
include injury to the adjacent teeth, periodontal compromise of the treated
tooth or adjacent tooth and devitalisation of teeth. These factors lead to pulpal
necrosis, colour change, root resorption and possibly the need for endodontic
therapy.
FIGURE 35.15 Facial profile analysis.
Surgically assisted rapid maxillary expansion (SARME)

(Fig. 35.27)
Rapid maxillary expansion is a technique used in treating transverse
maxillomandibular discrepancy. It was first described in 1860 by Angell and
later reintroduced by Haas in 1961. The SARME procedure is a combination of
distraction osteogenesis and controlled soft tissue expansion. SARME is
successful in children prior to sutural closure. It is best performed before the
transverse maxillary growth ceases and the maxillofacial sutures closure
which is at skeletal age 14–15 years in females and 15–16 years in males. The
expansion is achieved usually by using jackscrew appliances mostly the Hass
and Hyrax appliances.
Indications
• Transverse maxillary deficiency >5 mm discrepancy and with

unilateral or bilateral posterior skeletal crossbite that may result from
one of the following maxillomandibular combinations.
i. Narrow maxilla and normal mandible,
ii. Normal maxilla and wide mandible or
iii. Narrow maxilla and wide mandible.
• Failed orthodontic expansion.
• Large amount of expansion or preference to avoid potential increased
risk of segmental osteotomies.
• Presence of significant buccal gingival recession in the canine bicuspid
region of the maxilla or very thin and delicate gingival tissues.
• Nasal stenosis.
Technique
• Also called a subtotal Lefort I maxillary osteotomy.

• The mandibular dentition should be decompensated before surgery to
allow assessment of the amount of transverse expansion necessary and
to prevent postexpansion relapse.
• The appliance must be placed preoperatively and the appliance key
must be present in the operating suite to allow intraoperative
activation.
• A horizontal incision is made in the maxillary vestibule from the 2nd
molar region of one side to the same area on the opposite side.
• Bilateral maxillary osteotomy from the pyriform rim to the
pterygomaxillary fissure.
• Release of the nasal septum to prevent septal deviation during
expansion.
• Midline palatal osteotomy extending interdentally between the
maxillary incisors and from the anterior nasal spine to the posterior
nasal spine.
• Osteotomy of the lateral nasal wall anteriorly of about 1.5 mm.
• Bilateral release of the pterygoid plates.
• Activation of the appliance with a total widening of 1–1.5 mm with
evaluation for symmetric expansion and the surgeon should check that
the both maxillae are adequately mobile.
• Soft tissue closure including alar base cinch and V-Y closure to control
the soft tissues of the nasal base and upper lip.
Following the surgery the maxilla should remain stationary for at least
5 days before initiating the expansion at a rate of 0.5 mm/day. Expansion
greater than this, may cause gingival recession on the mesial side of the central
incisors.
Complications
Intraoperative complications are similar to those that occur in Lefort I
osteotomy like:
• Intraoperative haemorrhage
• Pain and discomfort due to tightness at the nasal root—glabellar area
and posterior orbit.
• Devitalisation of the teeth
• Gingival recession on the mesial side of the central incisors.
Anterior segmental maxillary osteotomy (Fig. 35.28)

Segmental maxillary surgery was performed for many years before total
maxillary osteotomy became popular. In 1921, Cohn Stock performed the first
maxillary segmental osteotomy. He performed a wedge-shaped osteotomy
through transverse palatal incisions; followed by a greenstick fracture of the
anterior maxillary segment that was retracted, but the segment relapsed in
4 weeks duration. Later, this procedure was modified with variations in
incision designs depending on the desired osseous movements.
FIGURE 35.10 Vertical proportions (Frontal and Profile views).

(A) Upper facial 3rd—From the hairline to the glabella. (B) Middle
facial 3rd—Glabella to subnasale. (C) Lower facial 3rd—Subnasale
to soft tissue menton. All the facial 3rd proportions should be in
1:1:1 ratio.
FIGURE 35.11 Rule of Five. The face is divided sagittally into five
equal parts from helix to helix of the outer ears. A line from the
inner canthus should be coincident with the alar base of the nose.
A vertical line from the outer canthus of the eyes should be
coincident with the gonial angles of the mandible. The outer two-
fifth of the face is measured from the lateral canthus to the lateral
helix, which represents the width of the ears.
FIGURE 35.13 Transverse symmetry. The nasal, maxillary,
mandibular and chin midlines are assessed in relation to the Mid
Sagittal plane (MSP). Left to right facial symmetry is assessed.
FIGURE 35.18 Incisor display. Normal upper tooth to lip
relationship should expose 2.5 ± 1.5 mm of incisal edge with the
lips in repose.
FIGURE 35.19 Transverse occlusal plane. It should be parallel to
the interpupillary plane and any changes usually indicate
infraorbital hypoplasia, orbital dystopia or exophthalmos.
FIGURE 35.22 (A) Horizontal skeletal angle of convexity. (B)
Horizontal skeletal profile.
FIGURE 35.23 Vertical skeletal and dental measurements.
Indications
• To correct the protrusion of the maxillary teeth with normal incisor

axial inclination to the alveolar bone
• To correct the anterior open bite provided vertical maxillary excess is
not present
• Correction of premaxilla in a vertical plane as required in anterior deep
bite or open bite
• When orthodontic therapy cannot be accomplished for the retraction of
the maxillary teeth as in pathological resorption or dental ankylosis
• To improve facial appearance in prognathic maxilla with competent
lips and adequate lip length
Technique
Wassmund technique (Fig. 35.29A–C)
• In 1935, Wassmund described a technique for maxillary osteotomy,

which was used widely and is used to this day with slight
modification.
• A vertical incision is made between the canine and premolar extending
to the nasal floor and muco-periosteum is reflected posteriorly and
superiorly. While reaching the apical region of the canine, reflection is
carried out to the inferolateral border of the nasal pyriform aperture.
The mucoperiosteum of the pyriform aperture is reflected using a free
elevator.
• If planned, first premolar is extracted at this stage. A midline sagittal
incision on the palate gives better visibility and access to the palatal
midline for performing the palatal osteotomy. The palatal mucosa is
reflected by tunnelling past midline and care is taken not to injure the
anterior palatine vessels.
• The bony cut is made on the buccal aspect of the alveolus using bur or
reciprocating saw. The cut is taken vertically upwards and turned
medially to the pyriform aperture so that 3–5 mm of intact bone
remains above the apex of the canine tooth.
• Next step is transpalatal osteotomy of the palatal bone from the
alveolus of one side to that of the other side. Care should be taken not
to injure the palatal soft tissues. Towards the midline, palatal bone is
hard to cut due to difficult access and increased thickness of the bone.
This region can be cut through a midpalatine incision in the
anteroposterior direction.
• Now, the maxillary segment has to be separated from the nasal
septum. Sometimes this can be done through finger pressure. Usually
a vertical incision is placed over the anterior nasal spine. Reflection of
mucoperiosteum is done from the nasal spine and cartilaginous nasal
septum. The septum is separated from the anterior maxillary segment
using a nasal osteotome.
• At this stage, dentoalveolar segment can be split in the midline, if
required. This is done by tunnelling and using a straight fissure bur
and an osteotome. This is useful in cases of closure of diastema and
minor adjustments in apposition of the canine.
• The folds on the soft tissue are checked to ascertain that there is no
hindrance to proper blood flow. Soft tissue is closed using 3-0 catgut.
FIGURE 35.14 Upper lip length. Measured from the subnasale to

stomion superius. Normal value for males 22 ± 2 mm and for
females 20 ± 2 mm and upper lip should be one-third the length of
the lower facial third.
FIGURE 35.24 Lateral cephalogram showing cephalometric tracing
done for Burstone’s analysis.
FIGURE 35.25 (A, B) Dental model analysis.
FIGURE 35.26 Single tooth osteotomy for repositioning superiorly

positioned central incisor. (A) Incision. (B) Osteotomy cut.
(C) Repositioning.
FIGURE 35.27 Surgically assisted rapid maxillary expansion

(SARME) (A) Frontal view of the completed surgically assisted
maxillary expansion. (B) Palatal view of the Hass expansion device
in place with the vectors of expansion demonstrated.
FIGURE 35.28 Anterior maxillary osteotomy.
FIGURE 35.29 Wassmund technique. (A) Buccal bone cut. (B)

Exposure of the palate. (C) Separation of the nasal septum.
Wunderer technique (Fig. 35.30A–C)

This technique (1963) is suitable especially when second premolar is to be
extracted. The labial approach is same as that of the Wassmund procedure.
The palatal surgery is started once the buccal part of the surgery is completed.
FIGURE 35.30 Wunderer technique for repositioning anterior
segment. (A) Buccal bone cut. (B) Transpalatal incision made; flap
elevated and palatal cut made. (C) Maxillary segment separated.
In Wunderer technique, a transverse palatal cut anterior to the planned

osteotomy site is made. Then the soft tissue is raised posteriorly a little behind
the planned osteotomy site. The osteotomy is now performed. In the midline,
bone is little harder but access to the palate is very good and the cut can be
done as far posteriorly as the second molar. Anterior segment can be
mobilised and separated from the nasal septum, once the bony cuts are
completed. It is then positioned and fixed using prefabricated occlusal splint
and soft tissue closure is done.
It is similar to Wassmund technique except for palatal exposure by
transverse palatal incision with margins away from osteotomy site.
Epker’s anterior maxillary osteotomy

In this technique, either the first or the second premolars are to be extracted. A
transverse incision is made in depth of the sulcus from behind the planned
osteotomy site to the opposite side. Subperiosteal dissection is done only
superiorly. The pyriform aperture is exposed and nasal mucoperiosteum is
dissected on the lateral wall and floor. The cartilaginous nasal septum is
elevated from the vomerian groove in the anterior nasal crest of the maxilla.
The dissection is carried out for about 15 mm posteriorly. Subapical
osteotomy is done leaving 3–5 mm of healthy bone above the teeth apices. The
vertical osteotomy is done after tunnelling the mucoperiosteum at the
interdental region; all bone cuts including those of palate are done from
labiobuccal side. When this alveolar osteotomy is done, care should be taken
not to injure the palatal tissues. For this, a finger should be kept in the palatal
area, which helps to feel the bur perforating the bone. After completion of the
subapical and alveolar osteotomy, a midline osteotomy is done if necessary,
like in cases of midline diastema and in cases where the intercuspid distance
has to be increased. About 15 mm of anterior portion of nasal crest of the
maxilla is removed for better visualisation in the transpalatal osteotomy.
With a straight osteotome transpalatal osteotomy is completed and the
anterior maxilla is down fractured. The palatal mucoperiosteum is carefully
separated from the palate posterior to the osteotomy site. With a large round
bur the required ostectomy is done. The osteotomy sites are inspected for any
bony protuberances and intermaxillary fixation is done using arch-wire on
previously applied orthodontic gadgets. Intermaxillary fixation is required for
a period of 1–2 weeks only.
Cupar’s anterior maxillary osteotomy (Fig. 35.31 A–E)

It is a minor version of total maxillary osteotomy down fracture technique. A
buccal vestibular incision is created, allowing direct access to the anterior
lateral maxillary walls, pyriform aperture, nasal floor and septum. Sequence of
osteotomies is operator dependent, but general procedure involves completion
of the vertical buccal and horizontal osteotomies.
The nasal mucosa is elevated from the superior surface of the maxilla. Nasal
septum is first released from the maxillary crest. Horizontal osteotomy is
performed followed by vertical osteotomy, which is performed bilaterally
between the teeth. Through this vertical cut, transpalatal osteotomy is
completed with either a reciprocating saw or an osteotome. A finger is placed
on the palatal mucosa to palpate the osteotome in an attempt to protect the
palatal tissue from injury by the osteotome.
The transpalatal osteotomy is now completed under direct visualisation
from above, allowing excellent access to the nasal crest of the maxilla and mid-
palatal bone for osseous recontouring.
Occlusal stent stabilisation, osseous wiring, skeletal fixation, rigid internal
fixation or a combination of these methods completes fixation of the anterior
maxillary osteotomy (AMO).
Advantages
• Direct access to the nasal structures to allow for manipulation of the

cartilaginous septum, thus preventing any deformities due to buckling
• Preservation of blood supply through an excellent palatal pedicle
• Ability to remove bone from the palate under direct visualisation after
the anterior maxilla has been down fractured
• Excellent access to the superior maxilla for reduction of vertical
maxillary excess or bone grafting
• Easy placement of rigid internal fixation
Posterior segmental maxillary osteotomy

Posterior maxillary osteotomy (PMO) was originally described in 1959 by
Schuchardt as a two-stage procedure for the correction of open bite
deformities. Indications cited for PMO today are more extensive.
FIGURE 35.31 (A–E) Cupar’s anterior maxillary osteotomy.
Indications
• Posterior maxillary alveolar hyperplasia

• Total maxillary hyperplasia (when combined with AMO)
• Spacing in the dentition that can be closed by anterior repositioning of
the posterior segment
• Transverse excess or deficiency
• Posterior open bite
• Correction of posterior crossbite
Surgical technique
• Posterior maxillary osteotomy is most commonly performed as a

single-stage procedure through a buccal vestibular incision extending
from the canine region to that of the second molar below the
zygomatic buttress.
• Alternatively, vertical incisions in the region of the anterior and
posterior osteotomies can be created and combined with a parasagittal
palatal incision.
• If indicated, dental extraction is carefully performed to preserve
alveolar bone.
• The palatal osteotomy is generally performed transantrally through the
buccal horizontal osteotomy.
• A palatal incision is generally not required unless medial movement of
the maxillary segment greater than a few millimetres is planned or the
mobilised segment will not be able to be positioned appropriately. In
this case, a parasagittal incision can be created away from the area of
the planned osteotomy. Reflection of the palatal flap to remove bone
under direct visualisation must be done with caution in order to
preserve the palatal vasculature.
• Horizontal buccal osteotomy is completed at least 5 mm above the
apices of the teeth using either rotary instrumentation or a
reciprocating saw from the location of the anterior vertical osteotomy
to the maxillary tuberosity. An appropriate amount of bone is
removed when performing the osteotomy to allow for superior
repositioning of the posterior maxillary segment.
• Vertical osteotomy can then be performed through an extraction site or
space created orthodontically using a fine fissure bur or spatula
osteotome. Care must be taken to preserve at least 1 mm of bone
support along the root surfaces of the adjacent teeth in order to
prevent a periodontal defect.
• Palatal osteotomy is usually performed with a curved osteotome
placed through the horizontal osteotomy site, with the operator’s
finger on the palatal tissues to ensure complete osseous sectioning
while minimising palatal perforation.
• Posterior vertical osteotomy can be performed through a third molar
extraction site or by pterygomaxillary separation. With the latter
technique, a subperiosteal tunnel is created posteriorly to localise the
pterygomaxillary junction in a manner similar to that used during the
total maxillary osteotomy.
• The disjunction is then completed using a curved osteotome oriented
in an anterior, inferior and medial direction. Posterior dentoalveolar
segment is down fractured with finger pressure and previously
inaccessible regions, such as the medial and posterior extents of the
osseous segment, are recontoured if indicated.
• Posterior segment is positioned into the acrylic splint derived from
model surgery and the mandible is rotated into position to ensure that
there are no occlusal interferences.
• In most circumstances, miniplate fixation is adequate, although
skeletal fixation, direct osseous wiring or the surgical stent alone can
be used, provided there is adequate bone contact and sufficient
number of teeth for stability.
• Bone grafts are indicated if there are large gaps at the osteotomy site.
• If rigid fixation is not used, surgical stent should be maintained for 3–
6 months or replaced by a retentive orthodontic appliance to prevent
relapse of the segments.
Variations of posterior segmental maxillary osteotomy

1. In 1970, Kufner made only a horizontal incision above the apices of the
involved teeth, gaining access to the palatal aspect.
2. Perko in 1972 and later Bell in 1975 made a hockey stick incision along
the midline of the palate as far forwards as the incisive papilla and
then carried it out laterally anterior to the proposed osteotomy site.
Le Fort I osteotomy (Figs. 35.32, 35.33)

In 1972, Martin Wassmund introduced a surgical procedure for moving the
entire maxilla. This operation, which has been since called Le Fort I osteotomy
or total maxillary osteotomy, was first used to correct open bite. The maxilla
was not completely sectioned from its bony attachments initially but as time
elapsed and with increase in clinical experience, evolution of sound surgical
and biological principles, surgeons became more aggressive and complete
mobilisation of the maxilla and adequate fixation was accomplished.
FIGURE 35.32 Le Fort I osteotomy. (A) Osteotomy cut. (B)

Osteotomy cut completed on both sides. (C) Nasoseptal osteotome
used to separate the nasal septum from maxilla. (D) Separation of
maxilla from pterygoid plate. (E) Completely separated maxilla.
FIGURE 35.33 (A–F) Intraoperative pictures showing Le Fort I
osteotomy.
Le Fort I osteotomy has become the workhorse of orthognathic surgical

procedures. It can be used to correct a variety of maxillofacial problems.
Indications
• Vertical maxillary excess

• Vertical maxillary deficiency
• Anterior- posterior maxillary deficiency (maxillary hypoplasia)
• Facial asymmetry
Surgical technique
The procedure is performed under general anaesthesia, preferably
hypotensive anaesthesia. Lidocaine 2% with 1:100,000 epinephrine is
infiltrated into the mucosal tissues of the upper lip. A horizontal incision is
made in the maxillary vestibule from the 2nd molar region of one side to the
same area on the opposite side. A mucoperiosteal flap is raised to expose the
anterior nasal floor, pyriform aperture, lateral walls of the maxilla, zygomatic
crests and pterygomaxillary junction. A nasoseptalosteotome is used to
separate the nasal septum from the maxilla. The bone is sectioned 4–5 mm
above the apices of teeth extending from the lateral part of the pyriform rim
posteriorly across the canine fossa and through the zygomatic maxillary crest.
The anterior, posterior and inferior parts of the lateral nasal wall can be
sectioned transantrally under direct vision. Posterior aspect of the lateral
maxilla and the posterolateral antral wall is cut by malleting a spatula
osteotome posteriorly until contact is made with the dense perpendicular plate
of the palatine bone. Final step then involves pterygomaxillary disjunction by
using a sharp curved osteotome medially and anteriorly into the
pterygomaxillary suture to separate the maxillary tuberosity from the
pterygoid plates. The maxilla is down fractured by inferior pressure against
the anterior portion of maxilla and forward pressure against the tuberosity.
This can be facilitated by use of Tessier’s mobilisers or disimpaction forceps.
The maxilla is then wired into occlusion by using a splint with intermaxillary
fixation. Stabilisation of the maxilla is then achieved by interosseous wires or
miniplate fixation done at the nasal and zygomaticomaxillary buttresses of the
proximal and distal segments. These two sites have buttress bone to
symphysis fixation.
When large osseous gaps are created at the ostectomy sites, bone grafts are
laid across them for added stability and rapid union. Lateral walls of the
maxilla and the zygomatic buttress are two critical areas. Autogenous
corticocancellous bone harvested from the iliac is most commonly used.
Modifications
Many technical modifications of the Le Fort I osteotomy are feasible to
facilitate anteroposterior, vertical or horizontal movements of the anterior and
posterior portions of the maxilla. The level of the osteotomy cut can also be
varied according to individual patient needs (Figs. 35.34–35.36).
FIGURE 35.34 Le Fort I osteotomy. (A) Fixation after superior

repositioning. (B) Fixation after maxillary advancement.
FIGURE 35.35 Le Fort I osteotomy. (A, B) Preoperative and
postoperative views.
FIGURE 35.36 Segmenting of the maxilla. (A) Two paramedian

osteotomies and one transverse osteotomty lines. (B) Maxilla
segmented into 4 pieces.
Segmenting the maxilla

Transverse discrepancies between the dental arches, vertical steps in the
maxillary occlusal plane and space remaining in the maxillary arch are
indications to segment the maxilla. When segmenting the maxilla, two
paramedian osteotomies and one transverse osteotomty are used. Once
mobilisation is accomplished, the palatal soft tissues pedicled to the island of
bone may be relaxed to permit expansion and/other maneuvers.
Two-piece Le Fort I osteotomy
In case of extreme vertical and anteroposterior excess, a classical Le Fort I in
combination with anterior maxillary osteotomy may be required (Fig. 35.37A–
D).
FIGURE 35.37 (A–D) Le Fort I with anterior maxillary osteotomy.
In cases of transverse horizontal maxillary deficiency, maxillary expansion

can be achieved by segmenting the maxilla after a conventional Le Fort I
osteotomy. With the maxilla in the down fractured position, the midpalatal
bone or parasagittal palatal bone can be osteotomised through appropriate
interdental space transpalatally. First, the thick part of the anterior maxilla is
sectioned with a fissure bur, then the palatal cuts are completed. The bone is
then completely sectioned by the use of an osteotome. Anterior maxilla may be
divided by malleting an osteotome between the central incisors and then
directed posteriorly as it transects the deeper portion of the mid-palatal suture
and splits the interseptal bone. This step is done in case of midline diastema
(Fig. 35.38A–D). The maxilla is then divided into two segments and can be
moved laterally to correct the horizontal deficiency.
The most common indication for this technique is the need to move the
maxilla laterally by more than 8 mm in noncleft cases and the need to
simultaneously repair an oronasal fistula, graft alveolar clefts and expand the
palate in cleft palate patients.
Quadrangular Le Fort I osteotomy (Fig. 35.38A–D)

First described by Obwegeser as a Le Fort I osteotomy in which the osteotomy
was placed as high as possible, from the tuberosity area around the whole
maxilla, staying just beneath the infraorbital foramen.
FIGURE 35.38 (A–D) Le Fort I with midline osteotomy.
This modification of Le Fort I osteotomy is indicated in patients with

maxillary zygomatic horizontal deficiency, class III skeletal malocclusion and
normal nasal projection. Coexisting vertical maxillary excess or deficiency or
maxillary transverse deficiency can be treated with quadrangular Le Fort I
osteotomy.
Surgical procedure: The incision is same as that for a conventional Le Fort I
osteotomy. The maxillary exposure is done superiorly to visualise the
infraorbital nerve and infraorbital rim, the lacrimal fossa medially and lateral
orbital rim laterally. Anterior body of the zygoma is also exposed to varying
degrees, depending on the necessity. Septal cartilage is detached from the
maxillary crest anteriorly and the vomer is detached from the palatal midline
posteriorly with a fine chisel. The bone cuts are then made starting from the
pyriform rim at the level of the infraorbital nerve and extending laterally just
inferior to the infraorbital foramen to the zygoma body. At this point the cut
makes a right angle and proceeds inferiorly through the buttress and lateral
antral wall to the pterygopalatine fissure. Posterior osteotomy cut is completed
just anterior to the pterygoid plate with a fine chisel. The same line of
osteotomy cut is performed on the other side and all bone cuts are checked for
completeness. The maxilla is then down fractured with finger pressure on the
anterior maxilla and forward pressure on the tuberosity region. The mobilised
maxilla is then secured to the mandible with a prefabricated splint and
intermaxillary wires.
Le Fort II osteotomy (Fig. 35.39A–G)

Severe paranasal hypoplasia extending to the infraorbital rims necessitates a
Le Fort II osteotomy as described by Henderson and Jackson (1973), but it
should be understood that this is not a common occurrence.
FIGURE 35.39 Le Fort II osteotomy. (A, B) Osteotomy cut. (C)
Separation of the maxilla from the pterygoid plate and mobilisation.
(D, E) Preoperative and postoperative profile views. (F, G)
Preoperative and postoperative occlusion.
Exposure is gained through a bicoronal incision or bilateral paranasal

incisions. The former is a more extensive procedure, possibly entailing medial
canthal disruption; the latter results in potentially visible external scar.
Intraoral access was also described for Le Fort II osteotomy.
The medial orbital floor, infraorbital rim, medial orbital wall and lacrimal
sac are exposed in a subperiosteal plane. Medial canthal tendons are left
undisturbed. An osteotomy is made with a side-cutting bur down the medial
orbital wall behind the lacrimal groove. It is extended medially to the
infraorbital nerve area through the orbital floor, over the anterior maxilla and
caudally as far as possible. Aufricht retractor is inserted from one paranasal
incision to the other to retract the dorsal nasal skin and the osteotomies are
connected at the nasal dorsum using a reciprocating saw. Any unconnected
areas are cut with a fine osteotome; exposure for the osteotomies is improved
with the bicoronal approach. Through a posterior buccal sulcus incision,
osteotomy cuts are located and are extended across the maxillary tuberosities
to the pterygomaxillary fissures. Maxillary tuberosities are separated from the
pterygoid plates with a curved osteotome. To complete the osteotomy, a
curved osteotome is placed in the transverse cut across the nasofrontal
junction and is driven posteriorly and inferiorly to separate the vomer from
the anterior skull base. Mobilisation of the maxilla is achieved as in the Le Fort
I procedure.
Management of the fistula, bone grafting of the cleft, fixation and
postoperative management differs little from the Le Fort I osteotomy. The
infraorbital rim defects are accurately bone grafted through the paranasal
incisions. Anterior osteotomy sites are filled with inlay and onlay bone grafts
using the buccal sulcus approach. Split cranial bone grafts are readily available
when a coronal approach is used (Jackson, Pellett and Smith, 1983). Wire or
multiple screws and miniplates placed from the frontal bone to the nasal
skeleton provide secure fixation of the central maxilla to the skull. If nasal
height is lacking a split cranial bone graft can be placed beneath the dorsal
nasal skin and secured with two screws or wire to provide a cantilever type of
dorsal graft.
Le Fort III osteotomy (Fig. 35.40A–J)

Gillies and Harrison (1950–1951) reported the first high maxillary (a modified
Le Fort III) osteotomy in a patient with craniofacial dysostosis. Through
external incisions they performed transverse osteotomies that separated the
nasal bones from the frontal bones. Osteotomy of the orbital floor was placed
immediately within the infraorbital margin and extended across the floor of
the orbit to the medial orbital wall anterior to the lacrimal groove. Osteotomies
were also performed through frontal processes of the maxilla to diminish the
width of the nose. Temporal process of the zygoma was divided on each side.
An osteotome was then introduced into the pterygomaxillary junction.
Anterior to the greater palatine foramen, an incision was made transversely
across the mucoperiosteum of the hard palate, extending laterally and
posterior to the alveolar ridge. The hard palate was divided and the line of
osteotomy was rejoined at the pterygomaxillary junction. In this way, spatial
relationships of the soft palate were undisturbed. The operation was
completed by severing the septum with a pair of large scissors introduced
through the osteotomy line at the root of the nose. Intermaxillary fixation was
established.
FIGURE 35.40 Le Fort III osteotomy. (A–D) Mobilisation and bone
graft. Scan to play Crouzon syndrome correction with Le Fort III
midfacial advancement) (E, F) Le Fort III osteotomy intraoperative
view. (G–J) Preoperative and postoperative view.
Mandibular osteotomy procedures

An abnormal occlusion with class III molar relation with reverse incisal overjet
is most commonly due to excessive growth of mandible. In these cases, mostly
an obvious facial deformity will be evident. Facial features associated with
mandibular excess include prominence of the lower third of the face,
particularly in the area of the lower lip and chin in anteroposterior and vertical
dimension.
Mandibular excess was one of the first dentofacial deformities recognised as
being best treated by a combination of orthodontics and surgery. Although,
surgical techniques for the correction of mandibular excess were reported as
early as the late 1800s, widespread use of currently accepted technique began
in the middle of this century.
Initially techniques for the treatment of mandibular prognathism dealt with
the deformity by removing sections of bone in the body of the mandible,
which allowed the anterior segment to be moved posteriorly. Subsequently,
osteotomy techniques performed in ramus of the mandible were popularised
by Caldwell and Letterman. In this technique, lateral aspect of the ramus is
exposed through a submandibular incision, the ramus is sectioned in a vertical
fashion, entire body and anterior ramus of section of the mandible are moved
posteriorly, which places the teeth in proper occlusion. Proximal segment of
the ramus overlaps the anterior segment and the jaw is stabilised during the
healing phase with bone plates or screws or immobilised using intermaxillary
fixation (Box 35.3).
Box 35.3 Mandibular surgeries
1. Ramus osteotomy
a. Extraoral vertical ramus osteotomy (EVRO)
b. Intraoral vertical ramus osteotomy (IVRO)
c. Bilateral sagittal split osteotomy (BSSO)
2. Body osteotomy of mandible
3. Subapical body osteotomy
a. Anterior subapical osteotomy
b. Posterior subapical osteotomy
c. Total subapical osteotomy
4. Genioplasty
a. Horizontal osteotomy with anteroposterior reduction
b. Double sliding horizontal osteotomy
c. Vertical reduction genioplasty
d. Tenon technique
e. Alloplastic augmentation
Ramus osteotomy
Anteroposterior movement of the mandible is achieved by ramus osteotomy.
In 1954, Caldwell and Letterman described a vertical subsigmoid osteotomy
(or ramus) through an extraoral approach. In 1957, Obwegeser H and Trauner
R put forward the sagittal split osteotomy of the ramus, which was versatile in
technique. Gonial arc is found to have a superior movement. This is due to the
forces of the pterygomassetric sling. Gonial Arc is found to have a superior
movement this is due to the forces of the ptrygomassetric sling.
Various procedures of ramus osteotomy are: (1) extraoral vertical ramus
osteotomy, (2) intraoral vertical ramus osteotomy and (3) sagittal split
osteotomy.
Extraoral vertical ramus osteotomy (Fig. 35.41)
• A submandibular skin incision is placed about 1.5 cm below the angle

of the mandible. Incision is extended down to the platysma which is
then divided. Marginal mandibular nerve lies below the platysma
running parallel to and often below the lower border of the mandible
crossing the facial vessels superficially as it passes upwards. After
identification and protection of marginal mandibular nerve, dissection
is carried out and the periosteum is reflected superiorly to the level of
sigmoid notch on the lateral aspect of the ramus.
• Lateral aspect of the ramus is inspected for the small bulge to identify
the position of mandibular foramen. This small bulge was first
described by Caldwell and Lettermann in 1984. Later, this landmark
gained surgical significance with Alling, Behrman (Behrman’s BMP),
Hall et al, Levine and Topazian (antilingual prominence). This
landmark is present in only some individuals and is highly variable in
relation to mandibular foramen (Tanas Study, 1979). The osteotomy
cut is performed posterior to the mandibular foramen to avoid any
injury to the mandibular nerve. A vertical bony cut is made from
sigmoid notch to the lower border near the angle of the mandible. The
proximal segment is separated from rest of the mandible and is
detached from the medial pterygoid muscles. This proximal segment is
placed laterally on the distal segment of the mandible. Decortication of
the distal segment is carried out on the medial aspect of the overlap
area and the proximal segment is decorticated on the lateral aspect.
The proximal segment overlaps the distal fragment on the outer aspect
with intraosseous wiring or bone plates. There can be variations of this
basic osteotomy procedure.
• The osteotomy site may be left to become a pseudo-joint or stabilised
by transosseous wire or miniplate or bicortical screws.
• Wound closure is done in layers. The skin may be closed by
monofilament 6-0 or smaller sutures. A pressure dressing is applied
for the first 24–48 h. Sutures are removed after 5 days and the wound
supported by steristrips for a period of another 1 week.
FIGURE 35.41 Extraoral vertical ramus osteotomy.
Subsigmoid oblique subcondylar osteotomy

This was first advocated by Robinson and Hinds in 1955. The cut is extended
from the sigmoid notch to the posterior border. After subsigmoid vertical cut,
the condylar segment is overlapped on the ramus of the distal (tooth bearing)
segment. It is stabilised by transosseous wiring. Depending on the amount of
posterior replacement, sectioning of the coronoid process is determined. These
procedures can also be used for advancement of mandible along with the use
of bone grafts fitted between the distal and proximal segments.
Advantages
• Adequate access
• Adequate control of bony fragments
• Good surface contact between the bony fragments
• Minimal relapse tendency
• Gonial angle contour can be changed
• No loss of teeth or arch size
Disadvantages
• Scar formation due to extraoral incision. If the patient has keloid
tendency, then this approach is contraindicated
• Potential damage to the mandibular branch of facial nerve
• Bleeding may occur due to injury to the retromandibular vein or
masseteric artery where it crosses laterally through the sigmoid notch
• Applicable only for mandibular setback and not advancement
Intraoral vertical ramus osteotomy (Fig. 35.42)
• Introduced by Caldwell and Letterman in 1954.

• The incision is similar to that of sagittal split osteotomy where anterior
border of the ramus is exposed. Lateral border is exposed by
subperiosteal dissection. The pterygoid-masseter sling at the inferior
and posterior border is stripped.
• If fixation is planned, medial aspect of the ramus above the lingula is
dissected subperiosteally to the posterior border. The width need only
be enough to pass the wires.
• Osteotomy in this case extends from the sigmoid notch to the inferior
border, behind the entry of the mandibular nerve into the mandible.
An appropriate mandibular posterior border retractor as Bauer or
channel retractor is used to engage posterior border and retract soft
tissue laterally.
• An oscillating saw at 30 degree angulation is used to do the vertical cut
and care should be taken to orient the cut such as to prevent injury to
the soft tissues. After osteotomy is completed, condylar segment is
overlapped laterally over the mandible. To facilitate tension-free
placement of the condylar segment, the medial pterygoid attached to
the medial aspect may be stripped in anterior region of the segment.
• The proximal segment must always overlap the distal laterally. In cases
of medial overlap, the pharyngeal air space may be narrowed
postoperatively. If this occurs immediately reshift the patient to the
operating table for correcting the position of proximal segment.
FIGURE 35.42 Intraoral vertical ramus osteotomy.
Advantages
• No external scar
• No risk of injury to the marginal mandibular nerve
Disadvantages
• Difficulty in visualisation of and access to the area

• Applicable only for mandibular setback
Bilateral sagittal split osteotomy (Figs. 35.43, 35.44)

Bilateral sagittal split osteotomy can be used to correct both mandibular
prognathism as well as retrognathism. It is the most versatile mandibular
osteotomy.
FIGURE 35.43 (A–J) Bilateral sagittal split osteotomy (BSSO).
FIGURE 35.44 BSSO with genioplasty. (A–C) Preoperative view
showing mandibular anteroposterior excess and increased anterior
lower facial height and occlusion. (D, E) Intraoperative view
showing BSSO with reduction genioplasty. (F–H) Postoperative
view and occlusion.
The bilateral sagittal split osteotomy (BSSO) as introduced by Obwegeser

and Trauner in 1957 has undergone many modifications over the years.
Technique
• An incision is placed over the anterior aspect of the ramus, running

down the mid-ramus over the external oblique ridge till the first molar
tooth region. The incision then curves down to the buccal vestibule.
• Retracting the tissues buccally, before the placement of incision,
prevents exposure of the buccal pad of fat which is an unwanted
interference during surgery.
• Mucoperiosteal flap elevation is done above the lateral aspect of the
mandible at the molar region until the inferior border.
• Medial periosteal elevation is done very carefully. Level of lingula and
mandibular foramen is ascertained as it is usually in the deepest
concavity of the anterior border of the ramus. The dissection should be
above the mandibular foramen and, using an elevator, lingula is
exposed subperiosteally.
• Osteotomy is done by cutting the cortical bone above the lingula. The
cut extends just posterior the mandibular foramen. Cut is taken
anteriorly to anterior border of the ramus of the mandible and is then
continued along external oblique ridge to the second molar region
over the lateral cortical plate. A vertical cut is made in this region; the
depth of the cut should be kept minimal here; just enough to reach the
cancellous bone. This cut should include the inferior border to control
the splitting. After cortical cut is completed, a small spatula osteotome
is malleted to the site from the medial cut to vertical cut. Osteotome
should be directed laterally to prevent injury to the neurovascular
bundle. During the process of splitting, neurovascular bundle is
visualised and care should be taken to maintain it to the distal
fragment.
• This procedure is repeated on the opposite side.
• Sagittal split osteotomy can be used for both advancement and
backward positioning of the mandible.
• In cases of mandibular advancement, medial pterygoid muscle is
separated from the inferior border of the distal segment with
periosteal elevator. When the mandible is set back the medial
pterygoid and masseter may have to be stripped to prevent the
displacement of the condylar segment posteriorly. When condylar
segment overlaps the medial tooth bearing segment, overlapping part
is excised and condylar segment is allowed to be on the cancellous part
without any tension, taking care that the proximal segment with
condyle is in its anatomic position in the glenoid fossa. This is the most
important step during fixation to prevent condylar sag.
• Rigid internal fixation using plates and screws or lag screws is the best
way of fixation.
• Other methods are lower border wiring, upper border wiring and
circum-ramus body wiring.
Wound closure
Wounds are well irrigated with saline and haemostasis achieved followed by
3-0 chromic catgut or vicryl.
Postoperative sequelae
• Oedema may be expected, which resolves in 2 weeks.

• Diminished sensation of lips may be experienced by some patients,
mainly due to injury to the inferior alveolar nerve. More than two-
third of the patients experience some sensory deficit even after 1 year.
But most of the patients are satisfied with the overall result and adjust
to the sensory deficit.
Complications
• Injury to the neurovascular bundle

• Malpositioning of the condylar segment (proximal)
• Bad split, multiple undesirable splits
• Excessive bleeding.
Injury to inferior alveolar neurovascular bundle

Continuity of neurovascular bundle should be maintained throughout the
process. If mistakenly the nerve is transected, the cut ends should be
microanastomosed.
Malpositioning of condylar segment

Care should be taken while wiring the segment. Improper transosseous wiring
can pull or push the condylar segment to an untoward position. When the
maxillomandibular fixation (MMF) is released, an open bite is the most
common presentation requiring surgical recorrection.
Bad splits
Wrong splits may occur at the lingual cortical plate. Poor split may occur at
the condylar segment. This poor split is usually due to the removal of the last
molar at the time of surgery. Therefore, it is advisable to remove the third
molar 6 months before the surgery. The main reason for poor split is the use of
wrong fulcrum on the lateral segment.
Excessive bleeding
Bleeding can occur from the inferior neurovascular bundle, facial vessels,
medullary bed and rarely from retromandibular vein. Except for the facial
vessels, bleeding can be controlled by local measures. But in case of facial
vessels, they have to be identified and ligated. Using channelled retractor with
the cup to hold the inferior border prevents injury to the facial vessels to a
great extent.
Advantages
• Greater flexibility in repositioning the distal tooth bearing segment

• Better cancellous bone contact which enhances healing
• No external scar and injury to the marginal mandibular nerve
• Minimum alteration in the position of condyles and the muscles of
mastication.
Disadvantage
Chances of injury to the inferior alveolar nerve are greater.
Modifications
• Trauner and Obwegeser (1957) made a horizontal cut just above the
mandibular foramen on the mesial side of ramus. The vertical cut was
taken down the anterior border of ramus of the mandible. An oblique
cut was made through the lateral cortex towards angle of the jaw. It is
a good technique for mandibular setback but had poor bone contact
with mandibular advancement. Aseptic necrosis of angle due to
extensive stripping of the pterygomasseteric sling may occur.
• Dalpont (1961) modified the sagittal split by advancing the oblique cut
towards the molar region and making the vertical cut through the
lateral cortex. The main problem with setbacks was interference
between the retropositioned distal fragment and the mastoid process
where occasional pressure on the facial nerve may occur as well.
• Hunsuck (1968) shortened the cut through the medial cortex of the
ramus by taking it only as far as the mandibular foramen, which
prevented occasional shattering of the ramus in mandibular setbacks.
• Bell and Schendel (1977) and Epker (1978) made an anterior vertical cut,
through which whole of the lower border was sectioned through and
through using a bur. The split is kept more laterally by directing fine
osteotomes down the inner surface of the lateral cortex to produce
easier splitting and greater protection for the inferior dental nerve.
Blood supply to the ramus is preserved as the need to strip the
pterygomasseteric sling is eliminated.
Mandibular body osteotomy

Blair (1907) was the first person to describe body osteotomy of the mandible. It
can be performed between adjacent teeth, through preexisting edentulous
space or through the extraction sites.
There are three types of body osteotomies. They are: (1) anterior body
osteotomy, (2) posterior body osteotomy and (3) mid-symphysis osteotomy.
Anterior body osteotomy (Fig. 35.45A–C)

Anterior body osteotomy is a common term used for the osteotomies
performed anterior to the mental foramen.
FIGURE 35.45 (A–C) Anterior body osteotomy.
Procedure
Small vestibular incisions are made bilaterally leaving attached gingiva intact
in the first or second premolar regions. Superiorly, mucoperiosteal tunnelling
is carried out till the alveolar crest and inferiorly till the inferior border of the
tooth to be extracted. Mental nerve and its branches should be taken care of to
avoid injury. Lingually, a periosteal elevator is inserted through the extraction
site subperiosteally to protect the lingual soft tissue during osteotomy cuts.
Vertical osteotomy cut is started in the socket at the alveolar margin, involving
both buccal and lingual cortices, going towards the inferior border. Entire
extraction socket should be utilised and cuts are made parallel to each other or
slightly convergent from buccal to lingual for better approximation.
To prevent periodontal defects, care should be taken not to remove
excessive crestal bone. Same procedure is repeated on the opposite side. If
some bony interference is present, immediately occlusal splint is tried and
osteotomy cuts are modified. Once accurate fit of the occlusal splint is
achieved, fragments are stabilised at the superior margin by passing figure-of-
eight wires around the necks of the canine and premolar and inferiorly by
using miniplate fixation or intraosseous wiring. Wound is closed in a single
layer. Modified step osteotomy is preferred over straight vertical osteotomy, to
avoid damage to the mental nerve and to have better bony contact.
Posterior body osteotomy (Fig. 35.46 A–C)

Thoma (1943) described the Y-shaped and trapezoid ostectomy of the posterior
body of the mandible to correct open bites. Posterior body osteotomy is a term
used for the osteotomies performed posterior to the mental foramen. Here the
preservation of neurovascular bundle is of utmost importance. It is not
commonly used nowadays.
FIGURE 35.46 (A–C) Posterior body osteotomy.
Procedure
• Make two vestibular incisions, one tooth anterior and one tooth distal
to the osteotomy site. The distal incision can be extended posteriorly
up to the external oblique ridge for more relaxation.
• The cut is started superior to the neurovascular bundle and finished
through both the cortices.
• At the level of the neurovascular bundle small window is made by
removal of only external cortex and thus exposing the neurovascular
bundle.
• The nerve hook is inserted to pull the bundle towards buccal side and
lingual osteotomy cut is completed.
• Then neurovascular bundle is retracted gently upward, so that the
inferior border cut can be completed through and through.
• Same procedure is repeated on the other side and the fragments
approximated in such a way that the neurovascular bundle is not
damaged.
• The occlusal splint is fitted properly and the osteotomised segments
fixed with either intraosseous wiring or bone plating at the inferior
border.
Mid-symphysis osteotomy
Mid-symphysis osteotomy can be used to widen or narrow the anterior arch
width. If it is combined with posterior or anterior body osteotomy, then
complete vestibular incision can be planned.
Procedure
An incision is placed posterior to the mental foramen. A mucoperiosteal flap is
elevated from the cervical region of the anterior teeth. The mucoperiosteum on
the lingual side is tunnelled with the periosteal elevator. Osteotomy is done
using a reciprocating saw or a fissure bur. In case of narrowing of the
mandible, a space must be created in the midline by orthodontic means or
extraction of a tooth. Two vertical osteotomy cuts are given. In case of
expansion, bone grafting is advised to fill the gap. Care is taken to place the
osteotomy cuts without damaging the roots of the teeth.
Segmental subapical mandibular surgeries

Segmental subapical mandibular surgeries can be used to reposition the
anterior, posterior or entire mandibular dentoalveolar segment.
Anterior subapical mandibular osteotomy

Hullihen (1949) was the first person to perform an anterior subapical
osteotomy to correct an anterior open bite. Hofer (1942) & Kole (1959)
popularised the subapical technique for mandibular horizontal deficiency and
excess.
Indications
• To advance or retrude the lower anterior segment

• To close anterior open bite
Procedure
• An incision in the lower lip approximately 15 mm from the vestibule.

Incision extends from first bicuspid of one side to first biscuspid of the
opposite side. Anterior mandible is degloved to the inferior border.
• Dissection proceeds posteriorly along the inferior border until the
mental neuromuscular bundle is visualised.
• Osteotomy can be accomplished with rotatory instruments or with
appropriate microsaws. After the vertical cut is completed, a
horizontal cut is made connecting the vertical cuts 5 mm below the
apices of the anterior mandibular teeth. Remainder of the osteotomy is
completed using a thin osteotome or a spatula chisel.
• Modified osteotomy—a midline osteotomy may be incorporated in case
of midline diastema (Fig. 35.47 A–C).
• Extended osteotomy—sometimes the osteotomy may be extended into
existing edentulous spaces if feasible (Fig. 35.48A–C).
• Cut segment can now be mobilised with gentle pressure at the
osteotomy site to the desired position.
• Closure is done in a layered fashion. 4-0 resorbable chromic sutures are
placed submucosally, followed by vertical mattress sutures to close the
mucosal layer. Then, external pressure is applied for 5–7 days to
prevent oedema and haematoma formation.
Kole’s modification: kole modified by excising a horizontal wedge of
bone from symphysis and inferior border of mandible to shorten facial
height.
FIGURE 35.47 Anterior subapical with midline osteotomy. (A–C)

Anterior with midline split, mandibular subapical osteotomy.
FIGURE 35.48 Extended anterior subapical osteotomy. (A–C)

Anterior mandibular extended subapical osteotomy utilising the
edentulous space.
Posterior subapical mandibular osteotomy (Fig. 35.49A, B)

This technique is used rarely, as it is technically difficult and there is a high
risk of injury to the inferior alveolar neurovascular bundle. But with the
proper acquired skill, it can be used successfully.
FIGURE 35.49 (A, B) Posterior subapical mandibular osteotomy for

superior repositioning.
Procedure
• A horizontal vestibular incision is made and muco-periosteal flap

reflected slightly upward and downward till the inferior border of the
mandible.
• Here the anterior vertical cut is taken in the area of extracted or
missing first premolar or first molar and second vertical cut is placed
behind the last existing molar. The horizontal cut is taken below the
apices of the teeth, protecting the neurovascular bundle.
• Both the vertical cuts are carried out from the alveolar crest till above
the level of neurovascular bundle.
• The portion of the buccal cortex that overlies the nerve bundle is
removed. This window should extend several millimetres posterior to
the distal vertical cut. The window is made in such a way that the cut
extends only in the buccal cortex and the bone is removed with
osteotome and saved.
• After identification and protection of the nerve bundle, lingual cortex
is osteotomised.
• Both vertical cuts are also completed till the horizontal cut level and
entire segment is mobilised with the osteotome in the desired position.
• The segment can be stabilised by fixing the occlusal splint and by
placing a circum mandibular wire over the splint. The outer cortical
bony plate, which was saved, should be fitted prior to suturing.
Total subapical mandibular osteotomy (Fig. 35.50A–D)
This technique is again not performed routinely, as it is technically difficult
and there is a high risk of damage to the neurovascular bundle.
FIGURE 35.50 (A–D) Subtotal mandibular osteotomy.
Indications
• To reposition the entire mandibular dentoalveolar segment either

anteriorly, posteriorly or superiorly
• For lengthening of lower third of the face
Procedure
• Circumvestibular incision is made from the retro-molar area of one

side of the mandible to the opposite side; care should be taken to
identify the mental neurovascular bundle which is skeletonised with
blunt dissection to avoid damage.
• The buccal cortical bone above and below the neurovascular canal is
cut with a fissure bur, and then removed with an osteotome. Vertical
reference marks are made anteriorly and posteriorly on the buccal
cortical bone before making the horizontal cut. Reciprocating and
oscillating saws are most commonly used.
• After exposing the neurovascular bundle through lateral cortical
osteotomy, horizontal osteotomy can be completed safely by
positioning it between the apices of the teeth and inferior alveolar
neurovascular bundle.
• Design of the osteotomy varies depending on the desired movement of
the dentoalveolar segment.
• When advancement is required oblique osteotomy is performed in the
retromolar region in order to increase contact surface area between the
osteotomised bone segments. In advancement cases, care should be
taken not to overstretch the nerve. It can tolerate 3–6 mm of stretching.
When dentoalveolar component is to be posteriorly repositioned, bone
is removed via a vertical osteotomy in the third molar region.
• Segmentalisation of the alveolus is completed by performing the
vertical osteotomy through an extraction site or between adjacent teeth
using a sagittal saw or fine osteotome.
Genioplasty (Fig. 35.51A–C)

Genioplasty is the surgical technique used to alter the size, morphology,
position and projection of the bony chin with concomitant changes in the
surrounding soft tissues. Otherwise known as mentoplasty, chin surgery is
commonly combined with other orthognathic procedures. About 15% of all
dentofacial deformities primarily involve the chin. Genioplasty can be used as
a single procedure or it can be used as an adjunctive procedure along with
other major osteotomies of the jaw bone.
FIGURE 35.51 (A–C) Genioplasty.
In 1942, Hofer was the first to describe osteotomy of the anterior lower
border of the mandible via an extraoral submental incision. Later, in 1957,
Trauner and Obwegeser described intraoral approach or labial sulcular
incision, to the osteotomy of the anterior mandibular lower border.
Deformities of the chin should be considered in all three planes—AP,
vertical and transverse, as the morphology of the symphysis region is highly
variable in different individuals, even with the same basic types of dentofacial
deformities (Box 35.4).
Box 35.4 Different techniques of genioplasty
• Horizontal osteotomy with advancement
• Horizontal osteotomy with anteroposterior reduction
• Tenon technique
• Double sliding horizontal osteotomy
• Vertical reduction genioplasty
• Vertical augmentation genioplasty
• Alloplastic augmentation
Horizontal osteotomy with advancement
• A bidirectional incision is placed just above the depth of the vestibule

and extended bilaterally till the canine region approximately. Once
mucosa has been incised, it is undermined, where upon the mentalis
muscle is divided on a bevel inferiorly towards the bone. Reflection of
the periosteum from the anterior mandible can be accomplished.
• Periosteum should be left intact on the inferior border and a minimum
of 5–10 mm of periosteum should be maintained in the midpoint of the
anterior mandible so that soft tissue support and blood supply are
maintained.
• To facilitate repositioning following any asymmetric or symmetric
movements with anterior, posterior or vertical changes, midline and
paramid line orientation lines should be inscribed in the bone with a
small bur.
• It is important to inscribe the proposed line of osteotomy at a level
approximately 5 mm below the canine root as well as 10–15 mm above
the inferior border. The orientation of the osteotomy should extend
proximally 4–5 mm below the lowest mental foramen.
• More parallel the osteotomy with the occlusal and mandibular plane,
more pure is the anteroposterior movement. In case of vertical
shortening, osteotomy angle should become more acute compared
with mandibular plane. The osteotomy can be completed with the
reciprocating oscillating saw.
• Upon completion of osteotomy, different techniques can be utilised to
stabilise and reposition the inferior fragment including unicortical or
bicortical wires, bone plates, prebent chin plates or lag screws. While
using transosseous wiring, degree of advancement available can be
limited to the overall symphyseal thickness and this must be
determined before deciding on the method of stabilisation.
Horizontal osteotomy with anteroposterior reduction

The surgical procedure is same as that for advancement, but proximal tips of
the mobilised fragments should be reduced to ensure a smooth transition
along the inferior border and avoid palpable ‘wings’. The surgeon must also
consider the potential changes in the anterior vertical height when planning
the orientation of the osteotomy.
Double sliding horizontal osteotomy

Sometimes the chin is so deficient that the double sliding horizontal osteotomy
must be used. Surgical technique involves creation of the stepped intermediate
wafer of bone between the inferior fragment and mandible, which is also
advanced to provide bony contact between the upper and lower fragments.
Vertical reduction genioplasty (Figs. 35.52–35.54)

Vertical height changes can be effected during advancement or setback by
altering the angle of the osteotomy. Magnitude of this change is proportional
to the amount and direction of the horizontal movement. Approximately, 3–
5 mm of vertical change can be obtained. If in case a greater shortening of the
chin is required, with or without anteroposterior movement, a wedge
reduction is indicated and this can be accomplished using the tenon technique.
It is often easier to remove the wedge from the superior tables fragment but
intraoperative care is important to avoid sectioning tooth roots and still
leaving an adequate inferior fragment.
FIGURE 35.52 Vertical reduction genioplasty. (A–D) Anterior
mandibular subapical osteotomy with reduction genioplasty.
FIGURE 35.53 (A) Preoperative frontal view showing incisal
exposure at rest, short upper lip, hyperactive mentalis muscle and
increased lower facial height. (B) Postoperative view showing
improved facial appearance.
FIGURE 35.54 (A) Preoperative profile view showing increased
lower facial height, everted lower lip from hyperactive mentalis
muscle. (B) Postoperative view showing altered facial proportion,
aesthetic nasolabial angle and mentolabial sulcus. Note the
improved chin prominence from autorotation of mandible.
Tenon technique
In 1974, Michelet and associates described this technique. Here, symmetry is
ensured by the tenon and the visual inspections of the proximal extensions.
Only a single lag screw is required for stabilisation. But amount of
advancement is limited by the overall thickness of the anterior mandible.
Surgical procedure is almost the same as that described previously. A U-
shaped monocortical osteotomy is created centrally on the symphysis. Lateral
extension should be below the mental nerves, which connect to the superior
aspects of the tenoncorticotomy. Full thickness osteotomies are completed on
the lateral extensions and only through the lingual cortex on the superior of
the tenon. Resulting full thickness bone behind the tenon facilitates the
mortising of the tenon and lag screw fixation. When posterior movement is
desired, the ‘U’ is inverted and osteotomy is completed with mortising of the
tenon, which is now on the inferior fragment, into the mandible.
Vertical augmentation
Vertical augmentation is indicated when lower facial height is to be increased.
In such cases, the deficit is especially in the mandibular alveolus or in the
symphysis. Vertical augmentation is accomplished by interpositional grafting
or alloplastic implant placement between the osteotomised segments
following osteotomy of the mandible. Autogenous bone and hydroxyapatite
are the most commonly used materials.
Alloplastic augmentation
Alloplasts are used for anteroposterior, vertical or more importantly lateral
augmentation. The products of osseous genioplasty include possibility of
asymmetric advancement and inadvertent narrowing of the anterior mandible
with large advancements. Use of alloplast with lateral extensions can eliminate
this problem. There are various techniques used for insertion of an alloplast.
Placement through the submental floor can be combined with open lipectomy
or liposuction. Intraoral surgical approaches include a vestibular incision or a
midline vertical incision with a tunnelling technique. Implants can be used to
lengthen the anterior mandibular dimension by extending below the anterior
mandibular border as well as to augment the parasymphyseal region to a
greater extent than the single piece osseous genioplasty. Implants should be
stabilised with transosseous wires or position screws to ensure immobility.
Chin implants are usually placed in a subperiosteal pocket that requires no
fixation except for the surrounding soft tissue pressure which holds them in
place.
Soft tissue closure

It is essential that the mentalis muscle is approximated accurately. Incision
should be closed in two to three layers and a pressure dressing is applied to
minimise haematoma formation.
FIGURE 35.55 (A, B) Hemifacial microsomia.

FIGURE 35.56 (A, B) Facial asymmetry due to facial clefting.
FIGURE 35.57 (A, B) Hemimandibular hyperplasia.

FIGURE 35.58 (A–C) Parry Romberg syndrome.
FIGURE 35.59 (A, B) Post condylar fracture maxillomandibular

facial asymmetry—Note the occlusal cant. (C, D) Mandibular
asymmetry—Note no occlusal cant present.
FIGURE 35.60 Radiographic methods for assessing facial
asymmetry. (A) Orthopantomograph (B) PA cephalogram (C) 3D
CT reconstruction.
Complications
• Prolonged neurosensory changes attributable to direct nerve injury or

traction neurapraxia
• Excessive resorption of bone or avascular necrosis of the mobilised
segment can occur. This can be avoided by maintaining a broad
vascularised soft tissue pedicle
• Haemorrhage and airway compromise are rare complications
• Chin ptosis results from inferior redraping of soft tissues of the chin.
Signs include flattening of labiomental fold, excessive lower tooth
display and lip incompetence. Usual cause is total stripping of
mentalis muscle and improper reattachment
• Bone resorption under alloplasts can take place
• Devitalisation of teeth may result from compromise of pulpal blood
flow. Therefore, it is recommended that osteotomies be carried out
5 mm below the longest tooth root
Facial asymmetry (Figs. 35.55–35.59)

Facial asymmetry is a variation in the configuration of one side of the face
from the other when viewed in relation to a projected mid sagittal plane. It
comprises of a heterogeneous group of craniofacial disorders characterised by
significant alterations in dental relationships as well as facial form that are
readily apparent even to the untrained individual and these present significant
psychosocial issues for patients and families. Some severe malocclusions are
beyond the scope of orthodontic therapy alone, and some orthognathic
deformities are beyond single-jaw surgery. Although a one-jaw osteotomy
might improve function and aesthetics, bimaxillary, two-jaw, or double-jaw,
surgery is often indicated for larger-magnitude anteroposterior (AP)
discrepancies, most open bite deformities, and most cases of skeletal
asymmetries (Box 35.5).
Box 35.5 Etiology of facial asymmetry
1. Congenital
• Haemifacial microsomia
• Cleft lip and cleft palate
• Craniosynostosis: Plagiocephaly
• Congenital haemifacial hyperplasia
2. Developmental
a. Primary growth deformities
• Parry Romberg syndrome
• Haemimandibular hyperplasia
• TMJ ankylosis
b. Secondary growth deformities
• Sternocleidomastoid torticollis
• Duchenne’s muscular dystrophy and cerebral palsy
3. Acquired
• Condylar trauma
• Juvenile idiopathic arthritis
• Degenerative joint disease
Clinical patient assessment

The usual comprehensive methods of patient evaluation includes the chief
complaint, and with additional information gained from the history of the
present illness, the answers to pertinent questions regarding a history of facial
trauma, arthritis involving other joints, and genetic or congenital
malformations may be identified. A physical examination of the head and
neck region in the patient with a facial asymmetry should include:
• Diagnostic records:
I. Photographs
II. Radiographic records
III. Dental casts
IV. Growth assessment
• Location of asymmetry:
Visual inspection of the entire face including facial subunits for symmetry
in the vertical and horizontal planes.
• Tissues involved:
Palpation of the face to differentiate between soft and hard tissue defects.
• Dimensions involved:
I. Comparison of dental and facial midlines with each other
and with the central facial axis.
II. Inspection for gonial angle asymmetry or differences in the
degree of antegonial notching.
III. Analysis of the relationship between the upper lip and the
maxillary central incisors.
IV. Inspection for malocclusion, occlusal cants, excessive
inclination of anterior teeth, dental crowding, open bite
occlusal relationships, the maximal interincisal opening,
and the presence of mandibular deviation upon opening.
V. Comprehensive examination of TMJ functions including
protrusion and lateral excursion movements.
• Timing of presentation:
Early childhood onset or adult onset of the facial asymmetry.
Radiographic assessment (Fig. 35.60)

Radiographic assessment of facial asymmetry can be done using various
options available such as:
• Panoramic radiograph
• Posteroanterior cephalometric radiograph
• Lateral cephalometric radiograph
• 3D CT
• Stereolithographic models
• Bone scans
Grummon’s frontal cephalometric analysis
Frontal posteroanterior (PA) cephalometric analyses have been used for
several decades. Several analyses were developed primarily for surgical use
but many of these analyses provide information but have their own
limitations.
Grummon’s PA ceph analysis was developed to provide clinically relevant
information about specific locations and amounts of facial asymmetry. This
information can be correlated with lateral cephalometric data to complete a
three-dimensional facial assessment.
Anatomical landmarks (Fig. 35.61)
FIGURE 35.61 PA cephalogram anatomical landmarks and

abbreviations used. A1, Upper central incisor edge; Ag, Antegonial
notch; ANS, Anterior nasal spine; B1, Lower incisor edge; Cg,
Crista Galli; Co, Condylion (most superior aspect of the condyle);
Fr, Foramen Rotundum; J, Jugal process; Me, Menton; MSR, Mid
sagittal reference line at crista galli; NC, Nasal cavity at the widest
point; Z, Frontozygomatic suture (medial aspect); ZA, Zygomatic
arch.
Analysis technique
A midsagittal reference line (MSR)

MSR is a key reference line normally runs vertically from Cg through ANS to
the chin area (Me). Construction of MSR varies from patient to patient and if
the location of Cg is in question, an alternative method is to draw a line from
the midpoint of the Z plane through ANS (or) it can be drawn as a line from
the midpoint of the Z plane through the midpoint of an Fr-Fr line.
Horizontal planes (Fig. 35.62)

Four planes are drawn to show the degree of parallelism and symmetry of the
facial structures.
I. Zygomatic frontal sutures (Z-Z1),

II. The centres of the zygomatic arches (ZA–ZA1),
III. The medial aspects of the jugal processes (J–J1).
IV. Another plane is drawn at menton (Me) parallel to the Z plane.
FIGURE 35.62 Horizontal planes. Z–Z1, ZA–ZA1, J–J1, Plane

drawn at menton paralled to Z plane.
Mandibular morphology (Fig. 35.63)
Left and right triangles are formed from the heads of the condyles (Co), the
antegonial notches (Ag), and menton. These are split by the ANS-Me line and
compared. Linear values, angles, and anatomy can be measured.
FIGURE 35.63 Mandibular morphology. Co–Ag–Me: Co1–Ag1–Me.
Volumetric comparison (Fig. 35.64)

Two ‘volumes’ (polygons) are calculated from the area defined by each Co–
Ag–Me and the intersection with a perpendicular from Co to MSR.
FIGURE 35.64 Volumetric comparison. Co–Ag–Me and the
intersection with a perpendicular from Co to MSR.
Maxillomandibular comparison of asymmetry (Fig. 35.65)

Perpendiculars are drawn to MSR from J and Ag, and connecting lines from
Cg to J and Ag. This produces two pairs of triangles, each pair bisected by
MSR. If perfect symmetry is present, the four triangles become two, J-Cg-
J1and Ag-Cg-Ag1. This is a quick and easy method to assess symmetries in
both jaws.
FIGURE 35.65 Maxillomandibular comparison of asymmetry. J-Cg-
J1 and Ag-Cg-Ag1.
Linear asymmetries (Fig. 35.66)

The vertical offset as well as the linear distance is measured from MSR to Co,
NC, J, Ag and Me. Asymmetry is compared by the differences between them
on either side of the face.
FIGURE 35.66 Linear asymmetries. MSR to Co, NC, J, Ag, and
Me.
Maxillomandibular relation
Distances are measured from the buccal cusps of the upper first molars (on the
occlusal plane) along the J perpendiculars. The Ag plane, MSR, and the ANS-
Me plane are also drawn to depict the dental compensations for any skeletal
asymmetries in the horizontal or vertical planes.
Surgical treatment
In general, treatment planning of facial asymmetry is similar to that of
orthognathic surgery, except that, depending upon the specific skeletal
abnormality, more emphasis is placed on the frontal, as opposed to the profile,
view during the examination. Despite the available radiologic studies, the
clinical examination is the most important diagnostic tool in cases of facial
asymmetry and it should be remembered that body posture, mannerisms, and
the presence of facial hair and various hairstyles may mask a facial asymmetry
and may direct the treatment plan in an erroneous direction.
Dentofacial deformities and common surgical approaches

Dentofacial deformities and common surgical approaches are depicted in
Tables 35.5 and 35.7.
Table 35.7
Dentofacial deformities and surgical approaches
Dentofacial deformities Surgical approaches

Class II division 1 malocclusion with normal overbite— • Modified sagittal ramus
characterised by maxillary excess and mandibular deficiency osteotomies
• Augmentation genioplasty
Class I division 1 deformity with deep bite—characterised by • Modified sagittal ramus
maxillary excess and mandibular deficiency with excessive osteotomies
overlapping of the maxillary teeth over the mandibular teeth
Class II division 2 deformity—maxillary excess with • Modified sagittal ramus
mandibular deficiency with the presence of lingually inclined osteotomies
upper central incisors and labially tipped upper lateral incisors
overlapping the central incisors
Vertical maxillary excess without open bite • Le Fort-superior
repositioning of the maxilla
Class II deformity with open bite • Segmental total subapical
superior maxillary
repositioning
• Surgical control of nasal and
upper lip aesthetics
Mandibular prognathism • Class III sagittal ramus
osteotomies
Maxillary deficiency • Maxillary advancement with
simultaneous maxillary
expansion and autogenous
bone grafting
Class III deformity with open bite • Superior repositioning of the
maxilla with mandibular
setback and possible
genioplasty
Midface dentofacial deformity • Modified Le Fort III
osteotomy
Bimaxillary protrusion with or without open bite • Posterosuperior maxillary
repositioning with
mandibular setback and bony
augmentation genioplasty
Class I vertical maxillary excess with or without open bite • Superior repositioning of
maxilla with possible
genioplasty
Transverse maxillary deficiency • Bilateral combined
orthodontic surgical
expansion of total maxilla
Asymmetric class II dentofacial deformity • Modified or reverse sagittal
ramus osteotomies with
optional genioplasty
Asymmetric class III dentofacial deformity • Asymmetric mandibular
setback with optional
genioplasty
Complications in orthognathic surgery
• Complications due to osteotomy procedure. (Table 35.8)

• Complications based on time frames. (Fig. 35.67)
Table 35.8
Complications
Maxillary osteotomies Mandibular osteotomies Genioplasty
• Haemorrhage • Nerve injury • Nerve injury
• Dental trauma • Poor osteotomy splitting • Dental trauma
• Poor down fracture • Poor segment alignment • Mobilisation
• Mobilisation • Bleeding • Stabilisation
• Soft tissue injury • Impacted wisdom teeth • Mandible fracture
• Positioning problems • Condylar positioning • Unaesthetic soft tissue changes
• Stabilisation • Dental trauma • Bleeding
• Unaesthetic soft tissue changes • Stabilisation
• Nerve injury • Mobilisation
• Airway compromises
FIGURE 35.67 Complications based on time frame.

CHAPTER 36
Distraction Osteogenesis
Biology of distraction osteogenesis

History of development of craniofacial distraction
• Advantages
• Disadvantages
• Indications
• Contraindications
Distractor device
Devices
Imaging of callus and its radiographic stages
Distraction osteogenesis means stimulating spontaneous, new bone

production between vascular bone surfaces, moved apart by gradual
separation (distraction). Most commonly, the bone is fractured by a
corticotomy and then fractured fragments are separated from each other using
a special device (distractor) at a rate of 1 mm/day, following 5 days latency.
Corticotomy is osteotomy of the bone cortex, preserving the local
vascularity of both periosteum and medullary canal.
Latency period is the time of immobilisation following a corticotomy when
the initial fracture healing response bridges the fractured bone surfaces, prior
to initiating distraction.
Rate of distraction is the number of millimetres per day at which the bone
surfaces are distracted apart. (The usual rate is 1 mm/day.)
Rhythm of distraction is the number and amount of increments in which
the ‘rate of distraction’ is achieved. (The bone can be distracted at a rhythm of
0.25 mm 4 times a day to achieve the rate of 1 mm/day, i.e. 4 × 0.25 mm = 1
mm.)
Transformation osteogenesis is the change of nonosseous interpositions (e.g.
fibrocartilage in nonunions, synovial cavities in pseudoarthrosis or muscle/fat
in delayed unions) into normal bone by combined compression and distraction
forces, sometimes supplemented by a corticotomy.
Bone transportation is the regeneration of segmental bone defects by
combined distraction and transformation osteogenesis.
Healing index is the number of months taken for treatment (from operation
to complete consolidation), for each centimetre of new bone length.
Oral surgeons come across clinical situations in which bone growth or

augmentation is required as part of treatment, for example loss of bone tissue
due to tumour resection or avulsive trauma, resorption of the edentulous
alveolar arches beyond capacity for prosthetic rehabilitation, hypoplasia of the
maxilla or mandible hampering occlusion and appearance. In such situations
where bone augmentation or growth is required, the simplest option is to use a
bone graft. Named according to the (donor) site of origin, a graft can be
autogenous (harvested from one’s own body), allogenous (harvested from the
same species), alloplastic (synthesised), etc. When compared with all forms of
grafts, the autogenous grafts provide the best results with least rejection rates.
However, harvesting autogenous bone graft from the patient’s body requires a
second site of surgery and is always associated with some morbidity at the
donor site. Added to the morbidity of harvesting a large graft and its
questionable survival, soft tissue tension due to acute stretching over the
augmented bone has also posed problems during graft procedures, limiting
their applications. A technique which can avoid these problems but provide
native bone augmentation was developed by orthopaedic surgeons for long
bones which were later adapted for use in the maxillofacial skeletal defects.
This technique was termed ‘distraction osteogenesis’.
Biology of distraction osteogenesis

‘Distraction osteogenesis’ is the technique wherein the bones surrounding the
deficient site are manipulated to spontaneously regenerate the required
volume of native bone by stretching its healing capacity. It is a well-known
fact that bone has a capacity to fuse with heal with the surrounding soft tissue
has a capacity to remodel according to the shape of the bone. This ‘osteogenic’
capacity of the bone to fuse when the fractured fragments are approximated is
due to a sequence of events that occur during fracture healing. Spontaneous
regeneration of bone is also witnessed after removal of osteolytic lesions from
the bone. However, there is a critical limit that exists and usually
immobilisation is recommended for proper healing to occur. In distraction
osteogenesis, the capacity of the bone to spontaneously regenerate and fuse is
subjected to tensile mechanical stresses. Thus, during distraction, the
mechanical stress applied on the healing bone callus initiates changes within
the tissues that trigger growth factors which in turn signals differentiation of
the cells into bone forming cells resulting in new bone formation.
History of development of craniofacial

distraction
The discovery of this technique is first attributed to Codivilla (1905).
However, Ilizarov is named the ‘Father of Distraction’ since he laid down the
biologic principle for regenerating hard and soft tissue which was further
developed as ‘a law of tension stress effect’. He popularised the technique in
orthopaedic surgery in the 1970s.
The ability of the bone to remodel according to the forces applied on it has
been used by dentists even in the 18th century. Reports of usage of both
traction and compression forces have been recorded. In 1728 Fauchard has
described the usage of a custom-made palatal plate for the expansion of
collapsed maxillary arch for the correction of crowding. These forces only
resulted in dental movement and not actual bone growth. Wescott in 1859 used
a telescopic bar fixed between two clasps for correcting crossbite in a 15-year-
old girl. This appliance effectively widened the palate. However, the author
reported that the treatment was time-consuming.
The basic concept of achieving bone growth by applying traction force to
fractured fragments was developed by orthopaedic surgeons. Hippocrates, more
than 2000 years ago, has described the treatment of broken bones by physical
manipulation.
Many others have tried a hand at this technique way back, even in the 14th
century.
In the 14th century, Guy de Chauliac applied traction force on displaced
fracture segments using pulleys and ropes.
Malgaigne (1847) introduced hook fixation to transmit the forces directly to
the bone introducing the concept of external skeletal fixation.
His device consisted of a halo frame with hooks. The hooks could be moved
and controlled by rotating a screw.
Codivilla in 1905 introduced bone lengthening by osteotomy of the femur
and proposed that bone and its surrounding soft tissues could be lengthened
by gradual distraction of the osteotomised fragments. He applied intermittent
pulls to the osteotomised femur while the limb was in a plaster cast. However,
because of high complication rate, the method did not catch on.
As mentioned earlier, distraction osteogenesis owes its origin to the Siberian
orthopaedic surgeon, GA Ilizarov. While his clinical insights and experimental
biology are the foundation of the modern-day clinical science that is known
today as distraction osteogenesis, several others have experimented on the
concept.
In the 1950s, Ilizarov applied his new concept for the treatment of fractures,
bone deformities and defects of the bone. He designed a circular external
fixation device, which is still used and is named after him. The circular
fixation device could immobilise and apply traction or tensile force on the
bone segments it is attached to by means of screws. Using the same, he proved
that on applying gradual tensile forces to fractured bone fragments, new bone
can be regenerated and length of the bone was increased.
He developed a theory for his treatment concept that he named ‘The Laws of
Tension Stress’. He developed a protocol for the treatment and applied the
same for lengthening limbs shortened by trauma or a congenital defect. His
clinical experiences led him to lay down the biological principles of distraction
—namely ‘The Ilizarov Effects’ describing the effect of tension stress on
regeneration of tissues. Usage of distraction on long bones was thus initiated
and developed successfully by Ilizarov and the concept soon became popular
and the effect of the same on load bearing, joint morphology, blood supply
and muscle growth was studied and published.
The application of distraction osteogenesis to the membranous facial bones
needed several adaptations including reduction in the size of the devices. In
1972, Snyder used an external fixation device of the mandible to lengthen a
canine mandible. He first removed 1.5 cm of bone from the canine mandible
and allowed it to fuse in order to surgically shorten it. This resulted in a
significant crossbite. Ten weeks later, he used the external fixation device to
expand the mandible by distraction osteogenesis. He osteotomised the
mandible and then moved the segments apart until the crossbite was
corrected. This was the first report of attempt at the application of distraction
osteogenesis to the craniofacial skeleton.
This leads to the development of customised miniature distraction devices
to fit the craniofacial skeleton later.
History at a glance
14th Guy de Chauliac applied continuous traction for fracture reduction

century
1847 Malgaigne described the concept of external fixation
1905 Codivilla proposed that bone and its surrounding soft tissue could be lengthened by
gradual distraction
1921 Putti designed unilateral device for femoral lengthening
1926 Wassmund initially described a technique like distraction osteogenesis for the
correction of malocclusion
1927 Wassmund advanced hypoplastic maxilla
1927 Rosenthal (coined the term distraction osteogenesis) tried distraction osteogenesis in
the craniofacial skeletal level
1927 Abbott described lengthening of tibia
1939–45 Treatment of congenital anomalies using distraction osteogenesis
(World
War II)
1948 Allan incorporated a screw device that more accurately controlled the rate of
distraction
1954 Ilizarov examined biology of limb lengthening. Established principles to maximise
the osteogenic outcome and cause ideal soft tissue response
After 1972 Snyder et al.—animal studies—and Karp et al., McCarthy et al.—clinical
investigations (after long gap since 1954 practiced)—proved normal osseous
formation in the elongated area
1977 Michielli and Miotti performed unilateral mandibular osteotomy to create an anterior
crossbite
1984 Kutsevliak and Sukachev experimental 1.2 cm lengthening of a normal canine
mandible using the Ilizarov’s principles
1989 First clinical mandibular distraction performed and reports were published in 1992–
94
In 1976, Michieli and Miotti repeated Snyder’s experiment using an internal

device. The New York University (Karp et al.) performed a histologic analysis
of the ossification of the canine mandible after distraction osteogenesis and
based on the laboratory results, distraction osteogenesis was attempted in
human mandibles. This series was published in 1992 and 1994. Joseph
McCarthy was the first surgeon to publish a report on the successful
application of the Ilizarov’s principles of tension stress to lengthen a mandible
by distraction osteogenesis. Later this technique was used for the correction of
micrognathia in haemifacial microsomia, Nager’s syndrome, etc. Since then
the concept has been applied to the bones of the craniofacial skeleton for the
correction of deficiencies.
Advantages
1. Avoids second site of surgery for bone harvest

2. Avoids graft rejection, incompatibility, foreign body reaction, etc.
3. Augments native bone
4. Soft tissue around the bone is also regenerated
5. There has been evidence of even nerve growth at the distracted site
6. Can be used to lengthen as well as increase the breadth
7. Even grafted bone can be distracted
8. Does not hamper bone growth when performed in growing children
9. Relapse rate is much less compared to conventional bone graft and
orthognathic surgery due to simultaneous soft tissue histogenesis
Disadvantages
1. The patient needs to tolerate the device. Patient compliance is necessary

till the consolidation is completed
2. Duration of the treatment is longer
3. May require at least two surgeries; however, biodegradable ones are
being developed to eliminate the need to remove the distractor after
consolidation of the callus
4. Device failures are common
5. Technique sensitive
6. Requires meticulous treatment planning
7. Expense of procuring a device
8. External devices can cause scarring
9. Infection
10. Improper consolidation or failure to consolidate may worsen the
condition
Indications
1. Reconstruction of posttraumatic/post-resection segmental defects

2. Reconstruction of resorbed alveolar bone
3. Mandibular hypoplasia as in haemifacial hypoplasia, Pierre Robin’s
syndrome, Treacher Collins’, etc.
4. Maxillary hypoplasia especially cleft maxillary hypoplasia, Crouzon
syndrome, Pfeiffer syndrome, etc.
5. Expansion of constricted palate
6. Widening narrow mandibular arch
7. Sutural expansion in craniosynostosis
8. Rapid canine retraction
9. In TMJ ankylosis: for reconstruction of neo-condyle and for correction
of mandibular hypoplasia
10. Closure of cleft alveolus
11. Correction of velopharyngeal insufficiency (VPI) by palatal distraction
Contraindications
1. Generalised bone disorders as osteoporosis, osteogenesis imperfecta,

osteopetrosis, etc.
2. Poor patient compliance: Uncooperative patients or patients unwilling
for daily activation as mental retardation, inability to complete the
treatment procedure and need for regular incremental distraction
3. History of poor fracture healing (fibrous dysplasia,
hyperparathyroidism)
4. Aggressive jaw tumour: Primary resection should be followed by 1 year
disease-free interval
5. Preexisting TMJ disorders: Chances of improvement as well as
worsening of problem
6. Not willing for multiple surgeries and long duration treatment strategy
of distraction osteogenesis (DO).
Since distraction involves the stretching of the fibrous union that is formed
after a fracture, it involves five main stages.
1. Osteotomy
Where the bone to be manipulated is osteotomised as atraumatically as
possible.
2. Latency period
During the latency period, the device is not activated and is used for
immobilisation of the osteotomised segments. This period extends from the
time of osteotomy to the beginning of active distraction. This allows time for
the primary healing cascade to initiate and fibrous union to be formed
between the osteotomy surfaces. Primary bone callus is formed. Distraction
protocol according to Ilizarov defines 5–7 days latency. Literature reports of
latency range from 0 to 14 days. If the duration of latency is too short, it may
result in improper callus formation and lead to failure of consolidation. If the
latency period is long, it will result in ossification of the callus and failure of
the distraction treatment due to calcification.
3. Distraction period
The period during which the two osteotomised segments are moved apart,
usually at the rate of 1 mm/day till the desired length, is achieved. In this
phase, the traction force that is delivered to the bone segments through the
distractor induces new cell formation and the distraction gap. The frequency
of distraction and the rate of distraction are crucial factors during this phase.
4. Consolidation period
It is the time taken for bone filling (calcification) to occur between the
distracted and osteotomised segments. The distractor device is held in place
till the bone matures completely. The distractor is removed at the end of this
stage after radiographic evidence of establishment of osseous continuity. The
time taken for the callus to calcify and mature varies according to the volume
of callus generated. It usually ranges between 4 and 12 weeks with a mean of
about 8 weeks. In an attempt to enhance and accelerate the consolidation,
several ‘osteo-inductors’ have been incorporated into the callus. Reports of use
of BMP-2, PRP, growth hormones, chitosan, osteoblast-like cells derived from
mesenchymal cells, etc. have been recorded. The maxillary bones require
longer time for consolidation than the mandible.
5. Remodelling phase
The period of bone remodelling after the removal of distractor is called
remodelling phase. It starts with full functional muscle load followed by
continuous shrinkage and remodelling.
Distraction can be classified in different ways.
Depending on site, number of osteotomies, type of bone lengthening,
vectors, anchoring of the device, placement of the distractor, placement of the
activation arm, the distraction can be classified as follows:
I. According to site where it is used
a. Mandibular
• Condyle
• Condyle/ramus
• Body
• Symphysis
b. Maxillary
c. Alveolar
• Extraosseous
▪ Vertical
▪ Horizontal
▪ Combined
• Intraosseous
▪ Implant distraction
▪ Internal replacement device
d. Palatal
• Transverse
• Posterior
e. Craniofacial
II. According to the vectors

The distractor appliance is designed to move the bone segments away from
each other. Unlike long bones, the facial bones are curved and therefore it is
not always enough to just move the bone segments apart from each other in a
straight line in order to achieve the desired reconstruction. Therefore, the
distractors of the maxillofacial region are designed, not just to move the host
bone fragments apart but also to change the direction of the movement in
order to achieve a curvilinear path. The capacity of the distractor to change
direction is named as the ‘vector’ of the distractor.
a. Univector: The distractor has the capacity to move the host bone
segments in just one direction
b. Bivector: The distractor has the capacity to move the host bone
segments in two directions
c. Multivector: The distractor has the capacity to move the host bone
segments in multiple directions
III. According to the placement of the distractor
a. Intraoral
b. Extraoral
IV. According to the anchorage
a. Toothborne—fixed to the teeth by bands

b. Boneborne—fixed to the bone using plates and screws
V. According to the number of sites of neo-osseogenesis and bone

fragments involved (Fig. 36.1A–C)
a. Monofocal
b. Bifocal
c. Trifocal
d. Tetrafocal
Monofocal: The surgical fracture creates a ‘distraction gap’ for unilateral

traction of the separated bone segments. In this, one fragment is considered
fixed and the other mobile.
Bifocal: Reconstruction of a segmental defect by sectioning a bone segment
along the proximal end of the defect and then transporting it across the defect
to the distal end of the defect. The segment of bone that is moved across the
defect is called the ‘transport disc’. Reconstruction by bifocal transport
distraction is frequently used in segmental mandibular resections.
Trifocal: In cases where larger segment needs to be reconstructed, especially
one that crosses the midline, two segments of bone (transport discs) are
sectioned from both ends of the continuity defect and moved towards each
other till they meet and they are fused together after they meet. This expedites
reconstruction of large bone defects using transport distraction since the time
taken for a single disc to travel the entire distance is halved. This also
overcomes the problem of premature consolidation in long distractions. In a
similar way, multiple transport discs can be used for creating the mandibular
archform. Since distraction can create only linear bone, in order to create a
curved mandibular bone, multiple transport discs can be created, each
angulated from each other at a small degree, to produce multiple straight lines
that can on the whole resemble an arch.
FIGURE 36.1 (A) Monofocal distraction. (B) Bifocal distraction. (C)

Trifocal distraction.
VI. According to the age for which it is designed
a. Paediatric
b. Adult
VII. Depending on site where tensional stress was induced (applicable for
bone with epiphysis)
a. Callotasis: Distraction of fracture callus

b. Physeal distraction: Distraction of the bone growth plate. These are of
two types.
i. Distraction epiphysiolysis: Rapid bone segment separation
resulting in fracture of epiphysis.
ii. Chondrodiastasis: Slower rate of distraction allowing
stretching of the growth plate without fracture.
Distractor device
Distractor is the device that is used to push the two osteotomised segments of
bone apart from each other in order to stimulate bone formation between the
segments by stretching the fibrous connective tissue that forms between the
segments after 5 days of latency. The distractor must also hold the segments
rigidly in place till the bone consolidation is complete.
Distractors are usually made of titanium to increase tissue compatibility, but
stainless steel ones are also available and they are cheaper.
Parts
Although distractors are designed as per requirement, every distractor must
have the following parts.
1. Foot plates/fixation plates (Fig. 36.2)

The device is anchored rigidly to the osteotomised segments using these
plates. Usually these plates are fixed to the fragments to be separated using
screws. In some cases, wires may also be used. These fixation devices could
vary as per the distractor used. In external distractors, the fixation could be
achieved using pins or wires. In toothborne distractors, the distractor could be
fixed using bands to the teeth. In transpalatal distractors, the anchorage is
through jagged surfaces and not through screws.
FIGURE 36.2 Fixation plates.
2. The distraction screw (Fig. 36.3)

This part usually consists of a screw, encased in a sleeve, (to prevent tissue
catching) that, when rotated, can move the two foot plates apart.
Clockwise movement: Moves the plates apart.

Anticlockwise movement: Moves the plates together.
FIGURE 36.3 Distraction screw.
3. Activation arm (Fig. 36.4)

The activation arm is the part of the distractor that is placed externally for
activation. It can be placed inside the mouth (intraoral) by piercing the mucosa
or the face (extraoral) by piercing the skin. This activation arm when rotated
will rotate the distraction screw in a calibrated manner to move the
osteotomised segments apart. Usually one full turn is calibrated to bring about
a movement (distraction) of 0.5 mm. This may vary according to distractors.
The activation arm could be flexible or rigid depending upon the ease of the
surgeon. The activation arm in some distractors is made detachable so that it
can be removed after the completion of the distraction phase, at the
commencement of the consolidation phase.
FIGURE 36.4 Activation arm.
4. Activation screw driver (Fig. 36.5)

The activation screw driver should fit the activation arm precisely. The device
when turned will rotate the activation arm to deliver the desired distraction.
Motorised distractors have also been developed to provide calibrated,
continuous, uniform microtraction eliminating the need for daily incremental
rotation using screw drivers.
FIGURE 36.5 Activation screw driver.
5. Stabilisation arm (Fig. 36.6)

In a few situations, especially in long distractions, another component may be
required to stabilise and guide the distractor in its vector. For example in
plate-guided transport distractors, an additional arm guides the distraction
fragment around the reconstruction plate.
FIGURE 36.6 Stabilisation arm.
6. Vector manipulating knobs (Fig. 36.7)

One of the main complications in the application of DO technique to the facial
skeleton is that due to the complex shape of the bones involved, the vector
needs to be predetermined. In some cases, it may not be practically feasible to
place the distractor at a desired angulation to the osteotomy. There may also
be a need to manipulate the callus to obtain the desired shape. In such cases,
an additional component that can change the orientation of the distraction
vector is required. Advanced distractors may have this incorporated in the
design.
FIGURE 36.7 Vector manipulating knobs (rigid external multivector

maxillary distractor).
Devices
The different types of distractor are illustrated in Figs. 36.8–36.15.
FIGURE 36.8 Rigid external distractor (RED).
FIGURE 36.9 Two pairs of maxillary internal distractors (left and

right) with flexible activation arms that can be easily placed in the
maxillary buccal sulcus.
FIGURE 36.10 Mandibular internal univector distractor with rigid

and flexible activation arms.
FIGURE 36.11 Mandibular external pin retained multivector
distractor.
FIGURE 36.12 Craniofacial internal distractor.
FIGURE 36.13 Plate-guided mandibular transport distractor.

FIGURE 36.14 Maxillary alveolar transport distractor/vertical
alveolar distractor.
FIGURE 36.15 Symphyseal transverse mandibular

distractor/vertical alveolar distractor.
Rate and rhythm of distraction

Determination of ideal rate of distraction depends on many factors.
• The maximum rate that can induce bone growth without fracturing the
callus.
• The maximum rate that can ensure nerve and soft tissue regeneration.
• Although the influence of the rate and rhythm of distraction to
regenerate bone formation has been methodically studied, there has
not been a consensus on the exact rate of distraction.
• Ilizarov suggests that a distraction rate of 1 mm a day in four
increments of 0.25 mm each offers better results.
• Although the majority of the authors agree with the distraction rate of
1 mm/day, Chin and Toth used a distraction rate of up to 3 mm/day
and Ramchiel et al. established a rate of 2 mm/day. Concerning the
frequency of activation, twice daily increments of 0.5 mm each seems
to be the most accepted conduct.
• Meyer et al. advocate variable rate set on a case-by-case basis
considering the many individual variables involved.
• Excellent bone regeneration and a favourable soft tissue response have
been reported with a rate of distraction of 1 mm/day performed at a
highly fractionated, continuous rhythm.
• Bone tissue can effectively withstand both tensile and compressive
loads, with a tensile strength of 12,000 psi and a compressive strength
of 15,000 psi. However, muscles and nerves cannot take that amount of
tensile pressure.
• A slower rate of distraction provides better muscle accommodation to
bone lengthening.
• Abnormalities have been detected in muscles lengthened with a rate
higher than 0.7 mm/day. Rapid rates of distraction were associated
with gross changes including disorganisation of muscle structure,
necrosis and significant accumulation of connective tissue in the
interstitium.
• Normal muscle regeneration was evident only with a rate of
0.4 mm/day. Although muscle adaptation requires a slower rate of
distraction than the bone, premature consolidation of the bone
regeneration may occur at a rate below 0.5 mm.
• To balance bone and soft tissue regeneration, an empirically founded
optimal distraction rate of 0.75–1 mm/day is currently practiced
worldwide.

Effect of distraction on muscles
A daily rate of 0.75 mm performed in one increment can potentially cause
atrophy and necrosis, thickening of endomysium and perimysium,
proliferation of fibroblasts and sclerosis (Fig. 36.16). Dividing the same daily
distraction rate into four equal increments resulted in enhanced preservation
of muscle tissue. Automated distraction with 720 increments/day would
provide the best results. A fractionated rhythm of distraction minimises
distraction-induced injury to skeletal muscles and promotes more effective
myogenesis. An increased frequency of distraction induces higher DNA
synthesis, thereby providing better muscle growth and regeneration during
lengthening.
FIGURE 36.16 Microscopic zones visible during the activation

phase. C, Central zone—unorganised mesenchyme-like cells with
neo-angiogenesis; PC, para central zone—onion-like configuration
of mesenchyme-like cells with collagen formation; PD, proximal
distal zone—new woven bone trabeculae aligned with osteoblasts;
v, Area of neo-angiogenesis; mf, Mineralisation front—
preosteoblasts maturing into osteoblasts.
Biomechanical and biologic factors that determine success of the

distraction
1. Minimally invasive corticotomy with preservation of osteogenic tissues,

periosteal and endosteal blood supply
2. Adequate duration of latency
3. Proper fixation of the bone fragments allowing movement in desired
vector only
4. Precise angulation of osteotomy and device to achieve calculated vector
of distraction
5. Optimal rate, rhythm and length of distraction
6. Sufficient time for consolidation and remodelling in a stress free
environment without functional loading
Fracture healing and distraction osteogenesis

Fracture healing is a tissue repair sequence that is initiated when there is an
injury to the skeletal structure. This sequence attempts to reestablish the
continuity and function of the bone, when there is a breach in continuity.
Distraction osteogenesis is an enhancement of the fracture healing sequence
wherein the response of this healing sequence to further mechanical assault in
the form of a strain is used for the benefit of the patient. Both are intrinsic,
biological response of the body in response to injury. They are initiated,
controlled and mediated by local and systemic molecular mechanisms that can
induce, inhibit and modulate fibroblasts, chondroblasts, osteoblasts,
endothelial cells and other cells that are involved in bone formation
(Table 36.1). The chemical modulators that are responsible for the healing
cascade are as follows:
1. Cytokines that are involved in inflammation

2. Transforming growth factor beta superfamily
3. Mediators involved in angiogenesis
Table 36.1
Biologic process related to the stage of fracture repair
Stage of fracture repair Biological processes

Inflammation Haematoma
Inflammation
Recruitment of mesenchymal stem cells
Cartilage formation and periosteal response Chondrogenesis and endochondral ossification
begins
Cell proliferation in intramembranous
ossification
Vascular ingrowth
Neo-angiogenesis
Cartilage resorption and primary bone Phase of most active osteogenesis
formation Bone cell recruitment and woven bone
formation
Chondrocyte apoptosis and matrix proteolysis
Osteoclast recruitment and cartilage resorption
Neo-angiogenesis
Secondary bone formation and remodelling Bone remodelling coupled with osteoblast
activity
Establishment of marrow
Distraction osteogenesis treatment sequence comprises following three

stages (Table 36.2):
1. Latency phase
2. Distraction phase
3. Consolidation phase
Table 36.2
Stages of distraction osteogenesis and their biologic processes

Stage of Biological processes
distraction
osteogenesis
Latency Haematoma
Inflammation
Recruitment of mesenchymal stem cells
Periosteal callus and cartilage formation

Active distraction The callus is stretched
Cartilage resorption and endochondral bone formation
Formation of a central fibrous interzone comprised of fibroblast cells and
collagen fibres aligned parallel to the vector of elongation
Neo-angiogenesis between collagen fibre bundles
Osteoblast recruitment and arrangement along the new vessels, followed
by intramembranous ossification and bone column formation
Consolidation Bone columns interconnect
Osteoclast recruitment Remodelling
These stages have been studied in long bone; however, in maxillofacial

region both fracture healing and distraction osteogenesis occur by
membranous ossification.
1. The latency initiates fracture healing cascade. Primary inflammatory

response has been initiated and at the end of the phase fibrous union
must be established but ossification should not have initiated.
2. Bone regeneration in distraction occurs by mechanotransduction when
the callus is subjected to tensile force in the distraction phase. When
healing callus is subjected to longitudinal, mechanical strain, the
proliferative and biosynthetic functions of the osseous and
surrounding soft tissue are stimulated through integrin-dependent
signal transduction. This results in the formation of a central fibrous
zone of chondrocytes, fibroblasts, oval cells (morphological
intermediate between fibroblasts and chondrocytes) named the fibrous
interzone. Osteoblasts at the interzone differentiate and deposit osteoid
along collagen bundles formed by the fibroblasts. The mineralisation
proceeds parallel to the orientation of the collagen fibres resulting in
the formation of the ‘zone of microcolumn formation’. The cell rich
zone between the fibrous interzone and microcolumn formation is the
‘primary matrix’ or ‘mineralisation front’ (Fig. 36.16).
3. After the planned amount of distraction is done, consolidation phase
begins. During this phase the osteoid formed in the distraction phase
undergoes mineralisation into mature bone and later remodelling.
Consolidation phase is usually 2–3 times the length of distraction
period. Molecular signalling proteins regulate the translation of
induced strain to bone regeneration. The tensile strain across the
distracted fragments induces bone regeneration through molecular
signalling proteins.
Consolidation of the callus after distraction occurs by three types.
1. Fibrous to chondroid bone formation: Transchondroid ossification by

chondrocyte like cells
2. Early stages of ossification: Endochondral ossification
3. Later stages of ossification: Intramembranous bone formation
(predominant mechanism of ossification)
Differences between fracture healing and distraction

The TGF β family of morphogens and angiogenic factors in addition to the
inflammatory mediators are the prime mediators in inducing fracture healing
and distraction osteogenesis (DO). The timing and level of expression of these
mediators mark the difference. In the absence of angiogenesis, fracture bone
healing totally fails whereas distraction heals by cartilage formation. Other
primary differences are listed in Table 36.3.
Table 36.3
Differences between fracture healing and distraction osteogenesis

Duration Fracture healing Distraction osteogenesis
7 days Endochondral bone Membranous bone formation
formation
7–14 days Cartilaginous tissue Initial vascularisation by the endosteal vessels
resorbs and undergoes followed by neo-angiogenesis driven by active
apoptosis distraction
Primary neo- Angiogenesis is directly proportional to rate of
angiogenesis within distraction
the periosteum
Less vascularisation
than DO
17–20 days Fracture callus calcifies The central zone exhibits large quantities of
with primary bone unmineralised osteoid
formation Medullary space of the regenerate is most
External callus is more vascular
vascular than internal BMP-2 and 4: Bone formation
callus
BMP-2: Expressed in
the inflammatory
phase
BMP-4: Endochondral
and primary bone
formation
VEGF Higher Lower
Angiopoietins Angiopoietin—2 is higher Angiopoietin—1 is higher
Imaging of callus and its radiographic
stages
Continuity of the fibrous callus is important for the success of the distraction
treatment (Figs. 36.17 and 36.18, Table 36.3). However, the distraction site can
only be visualised after complete consolidation in routine radiographs. Earliest
evidence of new bone formation can be assessed only using ultrasonography.
Ultrasonography is the only noninvasive means of visualising the distraction
callus before the consolidation. The new bone appears as longitudinally
arranged echogenic foci within the distraction site which progressively
increases in number and size and coalesce into a single echodense focus of
bone.
FIGURE 36.17 Radiographic observation of the distraction callus

reveals the following stages in callus maturation.
FIGURE 36.18 Ultrasonographic imaging of distraction callus
before consolidation.
Diagrammatic representation of radiographic stages of consolidation

Type Diagram Radiographic characteristics
0 Distraction gap is radiolucent with no evidence of
any mineralisation
1A Bony spicules visible at the proximal and distal

margins of the distraction gap, near the host bone
1B Distinct scattered spicules of mineralisation
visible as radiopaque flecks in the distraction gap
2A Evidence of larger island of mineralisation

adjacent to the host bone lesser in width than the
host bone
2B Mineralisation zones visible where the width of

one mineralisation zone is lesser than the host
bone while the other is almost as wide as host
bone
2C Mineralisation zone adjacent to both host bones is

of width equal to the host bone but there is a zone
of radiolucency in the centre
3A Continuous mineralisation zone across the

gap unequal to the width of the host bone
margins
A continuous zone of radiopacity showing
mineralisation across the distraction gap less
in width than the host bone
3B Continuous zone of mineralisation across the

distraction gap with width equal to that of host
bone but with some defects in the middle
3C Uniform, continuous mineralisation across the

entire distraction chamber, equal to the width of
the host bone
4A Uniform, mineralisation zone across the

distraction chamber equal to the width of the host
bone margins with one border of regeneration
showing corticalisation
4B Uniform mineralised bone with cortication of

both borders bridging the distraction gap
The following are cases treated by distraction osteogenesis (Cases 1–9). Each
case and the distractor used are unique.
Case 1: Toothborne palatal distraction

Indication: Constricted maxilla
Device: Transpalatal toothborne custom-made distractor
Vector: Univector
Osteotomy: Midpalatal
(A) Constricted maxillary arch. Expansion device placed after

midpalatal osteotomy. (B) Expanded arch showing correction of
crossbite.
Case 2: Symphyseal distraction for mandibular

widening (Hanhart syndrome)
Indication: Severe mandibular arch constriction due to Hanhart

syndrome
Device: Symphyseal distractor
Osteotomy: Symphyseal
(A) Patient with Hanhart syndrome, with very narrow mandible. (B)
Symphyseal osteotomy done. (C) Symphyseal distractor in situ. (D)
Widening of the mandible performed as much as condylar rotation
would permit. (E) Cessation of distraction. Callus regenerated on
completion of distraction. (F) Postoperative profile improved.
Case 3: Mandibular univector intraoral distractor for

the correction of mandibular hypoplasia in haemifacial
microsomia
Indication: Facial asymmetry due to mandibular hypoplasia

Device: Mandibular distractor
Vector: Univector
Osteotomy: Ramus
(A) Preoperative asymmetric facial profile with deviated chin, lip
cant and flattening of the right lower face. (B) Postoperative facial
profile with correction of facial asymmetry, deviated chin, lip cant
and flattening of the right lower face. (C) OPG showing hypoplasia
of the left ramus: hemifacial microsomia type 1 with distractor
placed parallel to the ramus and the osteotomy cut perpendicular
to the distractor. (D) Completion of distraction—consolidation in
progress. Mandibular facial height is symmetric.
Case 4: Bilateral mandibular external multivector
device used for the correction of mandibular
hypoplasia in Treacher Collins syndrome
Indication: Severe mandibular asymmetry, retrognathia with open bite

Device: 3DX mandibular external distractor
Vector: Multivector
Osteotomy: Angle of the mandible
(A) Preoperative profile: A boy with Treacher Collins syndrome with

severe mandibular hypoplasia causing severe respiratory problems
and sleep apnoea. (B) Preoperative facial appearance lip
incompetence with inability to place tongue within the mouth. (C) 3
DX—external mandibular multivector distractor in situ with
osteotomy at the angle of the mandible. (D) Postoperative profile
showing mandibular lengthening. (E) Postoperative facial
appearance showing lip competence and placement of tongue
within the mouth, correction of open bite.
Case 5: Bilateral mandibular intraoral horizontal ramus

distractor used for the correction of micrognathia in
Pierre Robin syndrome
Indication: Micrognathia
Device: Intraoral horizontal ramus distractor
Vector: Univector
(A) Preoperative profile: A boy with Pierre Robin’s syndrome with

micrognathia causing severe respiratory problems and sleep
apnea. Preoperative facial appearance lip incompetence with
inability to place tongue within the mouth. (B) Postoperative view
showing mandibular lengthening (C-D) Bilateral intraoral horizontal
ramus mandibular univector distractor in situ with osteotomy at the
ramus of the mandible. (E) Postoperative OPG.
Case 6: Maxillary univector distraction for the
correction of cleft maxillary hypoplasia
Indication: Severe maxillary hypoplasia that cannot be treated by

orthognathic maxillary advancement alone
Device: Maxillary internal distractor
Osteotomy: Le Fort I
(A) Class 3 malocclusion in a cleft child due to maxillary

hypoplasia. (B) Concave facial profile. (C) Le Fort I osteotomy
done and intraoral maxillary distractor with flexible activation arms
placed on the maxilla with the stable arm fixed rigidly to the
buttress of the zygoma. (D) Preoperative cephalogram and
postoperative cephalogram. (E) Activation of the distractor using
the activator. (F) Postoperative class 1 occlusion achieved. Note
the flexible activation arm can be seen in the buccal sulcus. (G)
Postoperative corrected profile.
Case 7: Maxillary multivector rigid external distraction

(RED) for the correction of cleft maxillary hypoplasia
Indication: Severe maxillary hypoplasia
Device: Rigid external maxillary distractor
Vector: Multivector
Osteotomy: Le Fort I
(A) Cleft maxillary hypoplasia causing concave profile. (B) Class III
malocclusion with open bite. (C) Lateral cephalogram showing
maxillary hypoplasia and open bite. (D) Le Fort I osteotomy done
and RED fixed and maxilla distracted anteriorly and downwards.
(E) Postoperative cephalogram class I occlusion with over
correction achieved. (F) Postoperative facial profile. (G) The use of
multivectoral rigid external distractor for a Le fort III advancement
has been illustrated in the diagram.
Case 8: Vertical alveolar distraction of anterior

mandible for implant placement
Indication: Alveolar ridge augmentation

Device: Vertical alveolar distractor
Vector: Univector
Osteotomy: Osteotomy of the dentoalveolar segment of the anterior
mandible
(A&B) Preoperative intraoral and OPG showing the residual

alveolar ridge. (C) Placement of vertical alveolar distractor in the
mandible for ridge augmentation. (D) Postconsolidation OPG
showing the amount of bone formed. (E) Mandibular alveolar
distractor.
Case 9: Multifocal transport distraction for

reconstruction of mandible after resection of
ameloblastoma
Indication: Loss of mandibular continuity after resection of

ameloblastoma
Device: Herford plate-guided mandibular transport distractor
Vector: Univector
Osteotomy: Two transport discs created from the remaining mandibular
ramus. One of the transport discs was fixed to the mandibular
reconstruction plate and sectioned again to create a new transport disc
in order to achieve the mandibular ‘U’ form
OPG of the mandible before excision of the tumour
After removal of the tumour and fixation of the reconstruction plate,

two distractors were fixed bilaterally and two segments transported
medially 1 mm per day
The left-side fragment was fixed to the reconstruction plate and the
same transport segment fragmented for the next stage distraction
OPG of the mandible after completion of the distraction

After removal of the distractors and fixing the fragments to the
reconstruction plate
CT after device removal
Case 10: Craniofacial distraction
Indication: Midfacial hypoplasia due to Pfeiffer syndrome

Device: Craniofacial internal distractor
Vector: Univector
Osteotomy: Le Fort III
(A) Child with Pfeiffer syndrome. (B–D) Lateral orbital rim exposed
through a bicoronal approach and the craniofacial distractor fixed
with plate on the cranium and the movable plate on the lateral
orbital rim after Le Fort III osteotomy. The activator placed
transcutaneously on the cranium.
Case 11: Craniofacial distraction
Indication: Midfacial hypoplasia due to Crouzon’s syndrome

Device: Kawamoto Craniofacial internal distractor
Vector: Univector
Osteotomy: Le Fort III
(A, B) Teen with Crouzon’s syndrome showing class III skeletal
relationship. (C) Lateral orbital rim exposed through a bicoronal
approach and the craniofacial distractor fixed with fixed plate on
the cranium and the movable plate on the lateral orbital rim after Le
Fort III osteotomy. The activator placed transcutaneously on the
cranium. (D–E) Facial profile and skeletal relationship after
completion of distraction. Scan to play Le Fort III advancement
with internal distractors for Crouzon Syndrome)
SECTION X
TMJ
Chapter 37: Anatomy of TMJ

Chapter 38: TMJ Disorders
Chapter 39: TMJ Ankylosis
Chapter 40: Internal Derangements and Condylar Dislocation
CHAPTER 37
Anatomy of TMJ
Embryology
Joint anatomy
Structural anatomy
Articular surface
Glenoid fossa
Articular eminence
Condyle
Capsule
Synovial membrane
Ligament supporting and limiting the joint
Accessory ligaments
• Stylomandibular ligament
• Sphenomandibular ligament
Meniscus
Vascular supply and innervations
Functional anatomy
Surgical anatomy
The temporomandibular joint (TMJ) is a complex craniomandibular

articulation that involves two separate synovial joints (right and left) that
function in unison. TMJ is a diarthrodial, compound and ginglymoarthrodial
synovial joint (ginglymus—hinge or rotation, arthrodial—sliding or
translation) composed of two articulating surfaces as
i. Temporal surface (mandibular fossa or glenoid fossa—temporal bone)
(Fig. 37.1)
ii. Condylar surface (mandibular condyle) (Fig. 37.2)
FIGURE 37.1 Glenoid fossa (inferior view). The condyle at rest is

seated in the glenoid fossa in close relation with the capsule and
the disc. Note that the adult condyle narrows down to the neck—
safety mechanism in trauma, preventing the fracture of the thin
glenoid fossa.
FIGURE 37.2 Components of TMJ. Lateral sectional view.
Embryology
• The TMJ begins development in the 10th week of gestation
• Two mesenchymal condensations develop each for the temporal bone
(glenoid fossa) and the condylar components
• The intervening mesenchyme also shows a condensation of cells that
differentiate into the intervening disc (meniscus)
• The temporal and condylar mesenchymal cells differentiate into
osteoblast to lay membranous bone
• The centre of the condylar component develops into white
fibrocartilage that facilitates subchondral bone formation
(endochondral mechanism), thus contributing for condylar growth till
adulthood
• The meniscus develops into a highly cellular vascular disc that
continues anteriorly into the lateral pterygoid muscle and posteriorly
as discomalleolar ligament (Pintos ligament)
Joint anatomy
The joint anatomy can be described based on three aspects as
• Structural anatomy
• Functional anatomy
• Surgical anatomy
Structural anatomy
The TMJ is a synovial joint with a joint capsule lined by synovial membrane
lubricated and nourished by synovial fluid (Figs. 37.3 and 37.4). But unlike
other synovial joints, the articulating surface is not covered by hyaline
cartilage but by white fibrocartilage, leading to the controversy of terming the
joint as weight-bearing or non-weight-bearing joint. The joint with its two
bony surfaces is separated by the articular disc called as meniscus.
FIGURE 37.3 Lateral view showing capsule and ligaments.

FIGURE 37.4 Medial view.
Articular surface
The articular surfaces of the joint are temporal component and condylar
component. The temporal bone surface consists of the articular eminence
(convex) and the glenoid fossa (concave). The articular surface of the
mandibular component includes the mandibular condyle.
Glenoid fossa
The glenoid fossa otherwise also known as mandibular fossa is the concave
depression on the petrous part of the temporal bone at its inferior surface. It is
bounded posteriorly by petrotympanic fissure and anteriorly by articular
eminence. The fossa has medial and lateral rims. The lateral rim proceeds into
the zygomatic tubercle anteriorly and into the postglenoid tubercle posteriorly.
The medial rim is lateral to the spine of the sphenoid bone and the foramen
spinosum along with its middle meningeal artery. A thin fibrous layer covers
the fossa.
The chorda tympani nerve appears at the medial end of the petrotympanic
fissure close to the spine of sphenoid. The roof of the fossa is thin and
separates the brain from the joint cavity; therefore, during surgical
manipulation, extreme precaution should be taken to prevent perforation of
the roof of the glenoid fossa.
Articular eminence
The articular eminence is present anterior to the glenoid fossa consisting of a
descending slope, a transverse ridge (its a medial extension of the zygomatic
tubercle) and an ascending slope. The eminence is covered by dense, compact,
fibrous connective tissue that consists primarily of collagen with a few fine
elastic fibres. The fibrous covering is thickest at the descending slope of the
eminence. Underlying the fibrous tissue covering is the chondroid bone.
Unlike the glenoid fossa, the articular eminence is subjected to loading during
function.
Condyle
• The adult condyle is elliptical in shape, the long axis being angled
backwards at 15–33 degree to the frontal plane. The long axis of each
condyle is approximately at right angles to the body of mandible.
• Condyle has a medial tubercle and a lateral tubercle. The tubercles
provide attachments to the medial and lateral collateral ligaments.
• A thick layer of fibroelastic tissue which contains fibroblasts and
chondrocytes covers the condyle’s articular surface.
• The fibrous layer covering the posterior aspect of the adult condyle is
very thin and applied directly to the underlying bone. But over the
convexity, it becomes thicker with an intervening layer of
fibrocartilage. The presence of cartilage facilitates the condyle to adapt
to excess loading by becoming hyperplastic. In the aging condyle, only
remnants of the cartilage remain and it becomes calcified.
• The condylar head is eliptical in shape converges medially the
horizontal axis when extended intersects at 145 to 160 degrees at the
foramen magnum. This degree signifies the presence of condylar
disease (Fig. 37.5).
FIGURE 37.5 Intersection at foramen magnum.
Capsule (Fig. 37.6)

The joint is enclosed by a fibroelastic highly vascular connective tissue capsule
that encircles the joint creating a closed joint cavity. Above the disc the capsule
is a loose envelope, whereas below it is taut.
• Superiorly, the capsule is attached laterally to articular eminences,

lateral rim of glenoid fossa, posterior glenoid tubercle, posteriorly to
squamotympanic fissure, medially to medial rim of glenoid fossa,
spine of sphenoid, sphenomandibular ligament, articular eminence
• Inferiorly, the capsule encircles the neck of condyle
• Laterally, the capsule thickens to form the lateral TMJ ligament
FIGURE 37.6 Joint capsule.
Synovial membrane
The inner surface of the TMJ capsule and the nonarticulating surfaces of
articular disc are lined with synovial membrane. Various synovial villous
projections are present in the anterior, posterior, medial and lateral recesses of
the joint cavities.
There are two sources for the synovial fluid: one is from plasma by dialysis
and the other is by secretion from type A and B synoviocytes. Its volume is
assessed by Toller in 1961 using contrast radiography studies, and he
estimated that the upper compartment can accommodate volume of about
1.2 mL of fluid without undue pressure, whereas the lower compartment had
a capacity for about 0.9 mL.
The fluid exists under negative intra-articular pressure. The surface tension
of the synovial fluid helps in spread of the fluid over the articular surfaces as a
capillary film, thus helping lubrication of the joint during movement of the
condyle. It contains glycoprotein known as lubricin which helps in lubrication
and reduces the friction between the articular surfaces of synovial joints.
Ligament supporting and limiting the joint (Fig. 37.3 & 37.4)
The joint ligaments include extracapsular lateral TMJ ligament and accessory
ligaments.
Extracapsular ligaments include the lateral temporomandibular ligament
that is related to the capsule laterally which is attached to the articular tubercle
above and lateral, posterior border of condylar neck below. The fibres are
directed obliquely posteroinferiorly. On the contrary, the medial condyle has
thin weak horizontal band. The lateral ligament supports the mandibular
condyle and limits external lateral movement.
Ligaments of TMJ
• Functional ligaments (major)

- Collateral ligaments
- Capsular ligament
• Accessory ligaments (minor)
- Sphenomandibular ligament
- Stylomandibular ligament
• Other ligaments
- Otomandibular ligament
- Discomalleolar ligament
Pinto ligament
Tanaka ligament
- Mallelomandibular ligament
Accessory ligaments
This includes the stylomandibular and sphenomandibular ligaments.
Stylomandibular ligament
The stylomandibular ligament is a specialised band of the deep cervical fascia
extending from apex of styloid process to the posterior surface and angle of
mandibular ramus. This accessory ligament of the joint limits extreme of
anterior movement of the condyle in relation to fossa.
Sphenomandibular ligament
This flat thin band which is extending from spine of sphenoid to the lingula of
mandible is considered as remnant of Meckel’s cartilage. This ligament acts
similar to the stylomandibular ligament.
Meniscus (Fig. 37.7)

The disc or the meniscus which is present between the condyle and the
temporal bone is semilunar, avascular, noninnervated, fibrocartilaginous
structure.
FIGURE 37.7 Attachment of the capsule and the meniscus. 1.
Condyle. 2. Disc. 3. Capsule.
It acts as a shock absorber and provides protection to the bony components

of the joint. Sagittal section of the disc reveals an anterior fibrous band
(anterior disc ligament), thin intermediate zone and posterior fibrous band
(posterior disc ligament). The anterior fibrous band has a superior stratum
which inserts itself on the ascending slope of the articular eminence and an
inferior stratum which inserts inferiorly at the condyle’s anterior aspect.
The anterior fibrous band of meniscus, the capsule and the condyle fix with
the superior head of tendons of lateral pterygoid muscle.
In addition to the blood vessels, parotid tissue is usually found between the
posterior capsule and the postglenoid tubercle. The parotid gland extends
from this location medially until it reaches the lateral wall of the pharynx.
Enlargement of the parotid, therefore, could impinge on the posterior capsule
of the TMJ and cause pain during closure of the mouth or during chewing
movements.
The posterior fibrous band (posterior ligament) of the meniscus is a

bilaminar structure. The superior lamella of the posterior fibrous band
(ligament) is attached to the posterior margin of the glenoid fossa at the
squamotympanic fissure. The inferior lamella of the posterior fibrous band
(ligament) attaches with the condyle in the posterior aspect. The area between
the lamellae is filled with highly vascular and innervated loose areolar
fibrofatty tissue.
Medially and laterally, the meniscus is firmly attached to the periosteum of
the condyles’s medial and lateral poles through the medial and lateral
collateral ligaments. The most medial portion of the disc is connected
posteriorly to a ligament referred to as the discomalleolar or Pinto’s ligament.
The attachments of the disc to the condyle are of significance since the shape
of the joint compartment changes during translatory movements according to
position of the condyle.
There are four capsular sulci (recess) situated at the posterior and anterior
ends of the upper and lower joint compartments.
Superior stratum of the posterior bilaminar zone limits the posterosuperior
recess and the superior stratum of the anterior ligament limits the
anterosuperior recess. The inferior stratum of the anterior bilaminar zone
limits the boundary of anteroinferior recess and the inferior stratum of the
posterior bilaminar zone limits the boundary of posteroinferior recess.
Muscles that are closely related to the joint (Table 37.1) and influence joint
movements include lateral pterygoid, temporalis and masseter muscles.
Among the three muscles, the lateral pterygoid is explained here.
Table 37.1
Muscles closely related to the temporomandibular joint (Fig. 37.11)
The lateral pterygoid muscle consists of two heads, upper and lower. The
lower head of the lateral pterygoid muscle arises from the outer surface of the
lateral pterygoid plate and the pyramidal process of the palatine bone and the
adjacent portion of the maxillary tuberosity. The superior head originates from
the upper third of the lateral pterygoid plate and the infratemporal surface of
the greater wing of the sphenoid lateral to the foramen ovale. The fibres from
the two heads get closer and almost unite before their insertion sites. The
medial half of the condylar fovea receives most of the fibres of both heads of
the lateral pterygoid muscles. The upper head inserts some of its fibres
(∼15%) into the medial portion of the anterior band of the disc.
Spasm of the inferior head of the lateral pterygoid could lead to medial disc
displacement. Also, such an anatomic relationship may be important during
normal medial rotation of the condyle-disc complex during chewing (Figs.
37.8–37.10).
FIGURE 37.8 Muscles of mastication (lateral view).

FIGURE 37.9 Muscles of mastication (posterior view).
FIGURE 37.10 Temporomandibular joint articulation. (A) In closed

position. (B) In open position.
Depression of mandible Elevation of mandible

• Lateral pterygoid • Temporalis
• Digastric • Masseter
• Geniohyoid • Medial
• Mylohyoid • Pterygoids
Protrusion of mandible Retraction of mandible
• Lateral pterygoids • Posterior fibres of temporalis
• Medial pterygoids
Vascular supply and innervations

The TMJ is primarily supplied by the maxillary artery and superficial temporal
artery. The branches of maxillary artery that supplies the joint are the deep
auricular artery, anterior tympanic artery and ascending pharyngeal artery.
These vessels converge into the canal of joint creating a vascular return
supplying the joint and the disc.
FIGURE 37.11 Action of muscles closely related to the TMJ—

elevators, depressors, protrusors and depressors of mandible.
The venous drainage of the joint is through superficial temporal vein,

maxillary plexus and posterior venous plexus.
The joint is innervated by auriculotemporal, maxillary and temporal nerve.
Hilton’s law states that nerves which supply a joint also innervate the
muscle that moves it. This is well demonstrated by the TMJ which is supplied
principally by the auriculotemporal and also by the branches of masseteric and
posterior deep temporal nerves.
Functional anatomy
Functionally, the joint has two components and four articulating surfaces.
Two components
1. Meniscotemporal (upper)
2. Meniscomandibular (lower)
Four articulating surfaces
1. Articulating facets of temporal bone

2. Articulating facets of condyle
3. Superior surface of disc
4. Inferior surface of disc
The mandible may be depressed, elevated, protruded or retracted. These

mandibular movements are possible as a result of the synchronous and
alternating movement of the condyle-meniscus unit in both TMJ. The TMJ
exhibits rotational (hinge) movement in the lower compartment and sliding
(translational) in the upper compartment.
• When the mouth is opened, the condyles rotate around a common

horizontal axis resulting in the first 10 mm of mouth opening. This
initial movement occurs exclusively in the lower joint cavity by pure
hinge or rotation. At the same time, the disc slides forwards and
downwards on the temporal bones.
• With further mouth opening (beyond 10 mm), the condyle further
rotates and then translates or glides forwards and downwards in
contact with the lower surface of the articular disc. This movement
results from the attachments of each disc to the medial and lateral
poles of the head of the mandible and also from the contraction of the
lateral pterygoid.
• The forward sliding of a disc stops when the fibroelastic tissue of the
disc is stretched to its limit. The condylar hinging and gliding
forwards occurs until it articulates with the most anterior part of disc
and the mouth is opened fully.
• When the mouth is closed, the movements are reversed. Initially, each
condylar head glides backwards and then hinges on the disc which is
held forwards by the lateral pterygoid muscle. The muscle relaxes
gradually allowing the articular disc to glide backwards and upwards
on the temporal bone.
• In the rotatory movements of grinding or chewing, the head of one
side with its disc glides forwards, rotating around a vertical axis which
passes immediately behind the head as the contralateral head
translates forward. These alternating movements swing the mandible
from side to side. The medial and lateral pterygoid muscle of each side
acts alternately to facilitate this action.
Surgical anatomy
Anatomical relations
Relations
Anteriorly Mandibular notch, lateral pterygoid, masseteric artery and vein
Posteriorly Parotid gland, superficial temporal vessels, auriculotemporal nerve
Laterally Skin and fascia, parotid gland, temporal branches of facial nerve
Medially Tympanic plate, spine of sphenoid, auriculotemporal and chorda tympani nerve,
middle meningeal artery, maxillary artery
Superiorly Middle cranial fossa, middle meningeal vessels
Inferiorly Maxillary artery and vein
• The main trunk of the facial nerve exits the skull through the
stylomastoid foramen (Fig. 37.12A–C).The suture line, which lies
between the tympanic and mastoid portions of the mastoid bone, is a
reliable anatomic landmark because the main trunk of the facial nerve
lies 6–8 mm inferior and anterior to the tympanomastoid suture.
Approximately 1.3 cm of the facial nerve is visible until it divides into
temporofacial and cervicofacial branches.
• Al Kayat and Bramley (1979) have observed that the distance from the
lowest point of the external bony auditory canal to the bifurcation was
about to be 1.5–2.8 cm and distance from the postglenoid tubercle to
the bifurcation was around 2.4–3.5 cm.
• The most variable measurement was the point at which the upper
trunk crosses the zygomatic arch which ranged from 0.8 to 3.5 cm
anterior to the most anterior portion of the bony external auditory
canal.
• The temporal branch of the seventh nerve (facial nerve) emerges from
the parotid gland and crosses the zygoma under the temporoparietal
fascia to innervate the frontalis muscle.
• The auriculotemporal nerve provides most of the innervation to the
capsule of the TMJ itself. The anterior portion of the joint also receives
innervation from the masseteric nerve and the posterior deep temporal
nerve. The articular cartilage on the surface of the condyle, glenoid
fossa and the avascular meniscus itself has no innervations (Fig. 37.13).
FIGURE 37.12 (A) Surgical landmarks for identifying the main trunk
of facial nerve and the temporal–facial division during TMJ
dissection. (B) Variability of the point where the upper trunk of the
facial nerve crosses the zygomatic trunk deep to the
temporoparietal fascia can be appreciated. The nerve crosses the
point from 0.8 to 3.5 cm anterior to the bony auditory canal. Hence,
the plane of dissection must be deep to the temporoparietal fascia
as the tissues will be retracted anteriorly to gain access to the TMJ
capsule. (C) The incision is extended inferiorly till the soft tissue
attachment of the ear lobule and also the superior arm of the
incision can be extended into the temporal hairline at a 45 degree
angle if greater anterior retraction of the surgical flap is necessary.
FIGURE 37.13 Auriculotemporal nerve emerging from the
mandibular division of the trigeminal nerve coursing behind the
condylar neck, innervates the majority of the capsule and meniscal
attachment tissues.
Surgical approaches to TMJ (Fig. 37.14)

The classic surgical approaches to the TMJ are as follows:
• Preauricular approach
Modified preauricular incisions (Thoma’s, Blair’s, Dingman’s, Alkayat and
Bramley’s, Popowich and Crane’s modification of Alkayat and Bramley’s)
• Endaural approach (Lemport’s)
• Postauricular approach
• Submandibular approach (Risdon’s)
• Retromandibular/postramal approach (Hind’s)
• Rhytidectomy approach
• Coronal approach
• Intraoral
• Capsular incisions
FIGURE 37.14 Approaches to the TMJ.
Ideally, the selected approach should accomplish the following:
• Maximise the area of exposure for the specific procedure

• Prevent injury to the branches of the facial nerve
• Avoid damage to the major blood vessels (e.g. internal maxillary
artery, retromandibular vein)
• Avoid damage to the parotid gland
• Cosmetic wound closure by utilising the natural skin creases
Preauricular approach
• Gold standard approach for TMJ and often used by oral and
maxillofacial surgeons.
▪ The preauricular incisions used today are essentially
modifications of the Blair curvilinear or inverted-L incision.
• Layers of dissection (Fig. 37.15)
▪ The incision is approximately 3–4 cm in length and is outlined
at the preauricular skin crease in front of the tragus.
▪ Initial incision is sharply through the skin and subcutaneous
tissue including the SMAS layer until the glistening
temporalis fascia is visualised.
▪ Blunt dissection should be done above and below the
zygomatic arch along the external auditory meatus to the
same depth.
▪ The flap should be reflected anteroinferiorly.
▪ Make an oblique incision through the superficial layer of the
temporalis fascia and continue the dissection below the arch
just superficial to the capsule of the temporomandibular joint.
▪ Incision through the joint capsule opens into the upper joint
space and an additional incision of the lateral collateral
ligament of the TMJ disk, enters the inferior joint space.
▪ Once the TMJ has been repaired, a layerwise closure is needed
(Figs. 37.16 and 37.17).
FIGURE 37.15 Layers of dissection.
FIGURE 37.16 Preauricular approach. (A) Skin incision in the
preauricular crease. (B) Blunt dissection done anteroinferiorly and
oblique incision made on the superficial layer of temporalis fascia.
(C) Blunt dissection of the temporalis fascia exposing the joint
capsule. (D) Incision of the joint capsule and the lateral discal
ligament exposing the upper and lower joint space. (E, F)
Layerwise closure.
FIGURE 37.17 Modifications of preauricular approach. (A) Blair’s

inverted hockey stick, (B) Thoma’s, (C) Dingman’s and (D) Alkayat
and Bramley’s.
Endaural approach
It is a cosmetic modification of the preauricular approach. Here skin incision is
incorporated over the prominence of the tragus itself (Fig. 37.18).
FIGURE 37.18 (A–C) Endaural approach.
Postauricular approach
In the postauricular approach, the incision is made posterior to the ear and
involves the sectioning of the external auditory meatus. Excellent
posterolateral joint space and condylar exposure are afforded with this
technique (Fig. 37.19).
FIGURE 37.19 Postauricular approach. (A) Incision is placed 3–

5 mm parallel and posterior to the postauricular flexure. (B, C)
External auditory canal is sectioned and flap retracted anteriorly.
Submandibular (Risdon’s) approach (Fig. 37.20)

Indicated for approaching the ramus and the neck of the condyle.
• Incision must be parallel and placed within the skin tension line 1.5–
2 cm below the mandibular inferior border.
• Layers of dissection:
▪ Skin.
▪ Subcutaneous tissue.
▪ Sharp division of platysma muscle exposing the superficial
layer of deep cervical fascia which forms the capsule around
the submandibular gland.
▪ The most important step is dissection through the superficial
layer of deep cervical fascia, as the facial artery and vein and
the marginal mandibular nerve traverse this layer.
▪ Facial artery and vein need to be ligated if the area of interest
is anterior to the masseteric notch.
▪ Division of the pterygomasseteric sling.
▪ Submasseteric dissection until the entire area of interest has
been exposed.
▪ Repair followed by a layerwise closure needs to be achieved.
FIGURE 37.20 (A, B) Submandibular approach.
Retromandibular (Hind’s) approach
• Indicated for surgeries involving the area on or near the condylar neck,
condylar head, or ramus of mandible itself.
• When compared with submandibular incision, the distance from the
skin incision to the area of interest is minimised in this approach.
• Layers of dissection is same as submandibular approach except the
location of the incision which is placed vertically behind the posterior
border of the ramus.
Rhytidectomy approach (Fig. 37.21)
• Also known as facelift approach.

• It is a variant of the retromandibular approach.
• The main advantage of the rhytidectomy approach is the minimally
visible facial scar.
• The disadvantage is the additional time required for closure of
incision.
• It is a combination of preauricular, retromandibular and postauricular.
• Incision is made in front of the ear extending up into the hairline above
and curves around the bottom of the ear below and then behind it,
usually ending near the hairline on the back of the neck.
FIGURE 37.21 Rhytidectomy approach.
Coronal approach (Figs. 37.22)
• Hemicoronal or bicoronal approaches are used in very complicated

cases and extensive surgeries in the upper and midface regions.
• Advantageous as the scar is hidden within the hairline.
FIGURE 37.22 Bicoronal approach. (A) Incision and reflection of
flap (B) Periosteal flap elevated (C) Access to frontal, midfacial and
zygomatic temporal region shown.
Capsular Incisions (Figs. 37.23)
• Incision on the capsular ligament to approach the TMJ space is used for
surgical management of Internal derangement.
FIGURE 37.23 Capsular incisions. (A) Horizontal incision over the

lateral rim of the glenoid fossa. (B) Horizontal incision below the
lateral rim of the glenoid fossa. (C) Horizontal incisions above and
below the disc. (D, E) L-shaped incisions. (F) T-shaped incisions.
(G) Cross-hair incisions. (H) Open sky incisions. (I) Vertical
incisions. The lateral pole of the condyle and lateral aspect of the
remodelled posterior attachment (broken lines) are illustrated.
CHAPTER 38
TMJ Disorders

Structural (disorders arising within the joint)
Developmental
Acquired
Functional
Temporomandibular joint disorders classification
Inspection
• Dental examination
• Occlusal evaluation
• Range of mandibular movement
Palpation
• Neurological tests
Auscultation
Electromyographic investigation
Drugs
Occlusal splints
Intermaxillary fixation
Local anaesthesia
Structural and developmental disorders of the condyle
• Condylar hyperplasia
• Hemimandibular elongation
• Hemimandibular hyperplasia
• Hemifacial hypertrophy
• Condylar hypoplasia and aplasia
Acquired disorders
• Traumatic arthritis
• TMJ Osteoarthritis
• Rheumatoid arthritis (RA)
• Psoriatic arthritis
• Condylar fracture
• Dislocation
• TMJ ankylosis
• Tumours
• Ankylosing spondylitis (Marie–Strumpell disease)
Myofascial pain dysfunction syndrome (MPDS)
History
Pathophysiology and Mechanisms
Symptoms
Signs
Diagnosis
Radiography
Treatment
Surgical management
Temporomandibular joint (TMJ) disorders refer to the group of disorders of

the TMJ as a result of primary or secondary degenerative changes within the
joint or muscle hyperfunction or parafunction (Tables 38.1 and 38.2).
Table 38.1
Bell classification of TMD
Table 38.2
Categories of clinical TMD conditions according to the RDC-TMD
I: Muscular diagnoses
A: Myofascial pain
B: Myofacial pain with limited opening
II: Disk displacement
A: Disk displacement with reduction
B: Disk displacement without reduction and with limited opening
III: Arthralgia, osteoarthritis and osteoarthrosis
A: Arthralgia
B: Temporomandibular joint (TMJ) osteoarthritis
C: Temporomandibular joint (TMJ) osteoarthrosis

I. Structural (disorders arising within the joint)
1. Developmental
i. Condylar hyperplasia
ii. Hemimandibular elongation
iii. Hemimandibular hyperplasia
iv. Condylar hypoplasia and aplasia
2. Acquired
i. Traumatic arthritis
ii. Suppurative arthritis
iii. Osteoarthritis
iv. Rheumatoid arthritis (RA)
v. Psoriatic arthritis
vi. Infection from contagious disease that spreads from other tissue like TB,
syphilis
vii. Metabolic disorders like gout
viii. Condylar fracture
ix. Dislocation: acute, chronic, recurrent (habitual)
x. Posttraumatic—ankylosis
xi. Internal derangement
xii. Tumours
• Benign: Para/juxta-articular chondroma
• Malignant: Para/juxta-articular chondrosarcoma, osteosarcoma
(Codman’s tumour)
Metastatic condylar tumours, synovial osteochondromatosis
xiii. Synovial fistula and synovial cyst of TMJ
xiv. Ankylosing spondylitis (Marie–Strumpell disease)
II. Functional
1. Disorders arising from structures outside the joints

2. Myofascial pain dysfunction syndrome (MPDS)
Temporomandibular joint disorders

classification
• Intra-articular origin or intrinsic disorder
• Extra-articular origin or extrinsic disorder
Intrinsic Disorder
1. Trauma
• Dislocation, subluxation
• Haemarthrosis
• Intracapsular fracture, extracapsular fracture
2. Internal disc displacement

• Anterior disc displacement with reduction
• Anterior disc displacement without reduction
3. Arthritis
• Osteoarthritis
• Rheumatoid arthritis
• Juvenile rheumatoid arthritis
• Infectious arthritis
4. Developmental defects
• Condylar agenesis or aplasia—unilateral/bilateral

• Bifid condyle
• Condylar hypoplasia
• Condylar hyperplasia
5. Ankylosis
6. Neoplasm
• Benign tumours (Osteoma, osteochondroma, chondroma)

• Malignant tumours (Osteosarcoma, chondrosarcoma, fibrosarcoma,
synovial sarcoma)
Extrinsic disorder
1. Masticatory muscle disorder
• Protective muscle splinting

• Masticatory muscle inflammation
• Masticatory muscle spasm
2. Problems that result from extrinsic trauma
• Traumatic arthritis
• Fracture
• Internal disc derangement
• Tendonitis
• Contracture of elevator muscle
History
• History of onset, duration, frequency and dental treatment are
important to assess the acute or chronic nature of the disease.
• Factors like pain, click or dysfunction are to be considered while
eliciting the history.
• History of trauma and history of dental treatment can usually pinpoint
the aetiology of the disease.
A physical examination should include inspection, palpation and auscultation
to ascertain that an abnormality (pain, click) or dysfunction is present which,
in turn, helps the clinician for better diagnosis.
Inspection
Interincisal distance on mouth opening, facial asymmetry and deviation of
mouth on opening or closing, preauricular swelling, occlusal cant,
malocclusion, occlusal derangements, improper dental restoration or
prosthesis, attrition of teeth decreasing the vertical dimension should be noted
(Fig. 38.1).
FIGURE 38.1 (A) Normal ramus condylar unit. (B) Condylar
agenesis—child (first arch syndrome). (C) Hemimandibular aplasia.
(D–E) Hemimandibular hypoplasia. (F) Hemifacial atrophy (Parry
Romberg’s syndrome). (G) Hemifacial atrophy. (H) Treacher
Collins syndrome in child. (I) Treacher Collins syndrome in adult.
Dental examination
There must be evaluation for evidence of bruxism such as attrition of teeth,
cheek or lip ridges caused by trapping of the mucosa during clenching habits.
Any premature occlusal contacts and high points in the restoration should be
checked for degenerative condition of TMJ.
Occlusal evaluation
Occlusion class should be recorded according to Angle’s classification (Class I,
Class II and Class III). Examining the dentition and occlusion provide very
useful information about the occlusal relationship, freeway space, overjet and
overbite, prosthesis, the evidence for bruxism or other oral habits and their
possible effects on dentition (attrition and wear facets), periodontium or other
oral structures. Recording the number of missing teeth, particularly loss of
posterior occlusal contact is important as this situation may predispose the
TMJ to degenerative joint diseases especially in presence of bruxism. Any
premature tooth contacts should be detected.
Range of mandibular movement

The distance between the incisal edges of the upper and lower teeth is
measured together with the overjet and overbite, thus the total range of
opening is known. The lateral excursions and any accompanying pain should
be noted. The normal maximal interincisal distance ranges from 35 to 50 mm.
The lateral deviation of mandible in certain conditions is a significant sign.
Abnormal protrusive movements are important and frequent, translation of
the condyles is the initial movement/sign.
• Lateral motion should be 7–10 mm to both the right and left.

• Normal protrusive range is 7–10 mm.
The lateral aspect of the TMJ should also be palpated while the jaw is closed
and opened. The presence of subluxation or recurrent dislocation of one or
both condyles can be determined by abnormal palpation during movement.
If the range of motion is limited, attempt should be made to determine
whether limitation is due to:
• Contracture of one or more of the muscles associated with jaw closure

• Nonreducing anterior displacement of articular disc (closed lock)
• Coronoid process interference
• Haematoma or infection
• Some other conditions such as fibrous ankylosis or scleroderma
Palpation
Tenderness on palpation suggests the presence of fracture, synovitis or
capsulitis of the joint. The jaw is palpated for evidence of enlargement (muscle,
mandible) and any unusual features such as movement of disc (hypermobility)
felt during activity. The overlying skin is checked for temperature and
consistency in case of any inflammatory condition.
Muscle tenderness
Facial muscles are palpated for tenderness. Masseter is palpated with finger
and thumb. Temporalis may be examined while the patient is clenching the
teeth and at the same time, attempting to move the jaws sideways.
Lateral pterygoid can be palpated with a finger pushed into the retromolar
area of the maxilla. This type of examination is indicated in case of muscle
related disorders (myospasm, myalgia, myofascial pain dysfunction
syndrome).
Neurological tests
The trigeminal nerve supplies sensation to the superficial and deep structures
of the head and face and motor function to the muscles of mastication. Sensory
nerve activity is assessed by applying pressure, cotton wool and pin-pricks to
the distribution areas of the trigeminal nerve. This test helps the clinician in
diagnosing the myofascial pain.
Auscultation
Noise is assessed by stethoscope and classified as either click (closed click or
opened click) or crepitus (Fig. 38.2) though it may be difficult to determine
whether a noise is from one joint or both.
FIGURE 38.2 Auscultation.
After the advent of MRI and computed tomography (CT) scans, conventional
radiographic procedures hold little importance but when cost factors are
inhibitory, such radiographs may help in diagnosis. Radiography of TMJ is
considered difficult because of the superimposition of the surrounding
structures that occurs in conventional angulations.
In suspected TMJ disorders involving articulating surfaces that include the
hard tissues, CT scan is the best diagnostic modality. In the TMJ disorders
including the disc, MRI and arthrography are excellent diagnostic tools.
Laboratory investigations are indicated in case of TMJ disorders where
primary diseases are diagnosed by biochemical and serological tests, e.g. gout,
infectious arthritis/suppurative arthritis (TB, syphilis), rheumatoid arthritis.
Electromyographic investigation
The use of electronic instruments or devices helps in monitoring the activity of
disordered TMJ, e.g. surface electromyography (EMG), thermography,
sonography and mandibular kinesiology (jaw tracking).
Drugs
Drugs such as antiinflammatory agents, tranquilisers, muscle relaxants and
antidepressants can be used as diagnostic aid in case of MPDS where
diagnosis of the root cause is very difficult.
Occlusal splints
They can also be used as a test to diagnose MPDS. In dentulous patients, splint
may be placed over the abraded teeth to check out the aetiology. In case of full
denture wearers, occlusal splint may be used to establish/detect whether over
closure is contributing to an osteoarthrosis (osteoarthritis).
Intermaxillary fixation
When there is severe pain of uncertain origin, intermaxillary fixation (IMF)
may be applied. This is diagnostic, as it relieves pain if the source is the TMJ
(condylar fracture) or masticatory muscle (prevents overstretching of muscles).
Local anaesthesia
When pain is suspected as arising from an area of muscle, injection of small
amount of local anaesthetic into the respective muscles is advised to establish
the diagnosis.
For example, injection in the masseter muscle may be indicated to detect
myospasm of masseter; thus this test should be correlated with clinical
findings, signs and symptoms.
Structural and developmental disorders of

the condyle (Flowchart 38.1)
Condylar hyperplasia
Condylar hyperplasia (CH) is a condition of mandibular condyles creating
overgrowth of the mandible, first described by Robert Adams. Bilateral active
condylar hyperplasia causes progressive prognathism. Unilateral condylar
hyperplasia can cause progressive facial asymmetry and articular disc
dislocations (Fig. 38.3A–D).
FLOWCHART 38.1 Growth problems involving TMJ.
FIGURE 38.3 Hemimandibular elongation. (A) Increased vertical

growth on the right side. (B) Contralateral crossbite. (C) Deviation
of the mouth on opening towards the normal side. (D) CT image
showing condylar hyperplasia.
Obwegeser and Makek (1986) differentiated hyperplasia of the condyle into

three categories: (i) Type I—hemimandibular elongation (HME), (ii) Type II—
hemimandibular hyperplasia (HMH) and (iii) Type III—combination of types I
and II.
Hemimandibular hyperplasia—enlargement of the condyle, condylar neck,
ramus, body, with tilting of the occlusal plane.
Hemimandibular enlargement—condylar neck enlargement, variable
displacement of the ramus without tilting of the occlusal plane (Table 38.3).
Table 38.3
Obwegeser’s classification of condylar hyperplasia

Types Clinical findings Histological findings
Type I • Chin deviation towards contralateral • Excessive growth in the
(hemimandibular side horizontal vector
elongation) • Midline shift to contralateral side • Condyle often unaffected
• Lingual deviation of contralateral • Elongated mandibular ramus
mandibular molars • Misshapen and slender
• Possible posterior crossbite condylar neck
Type II • Sloping rima oris with minimal chin • Excessive growth in the
(hemimandibular deviation vertical vector
hyperplasia) • Supraeruption of maxillary molars on • Enlarged and often irregularly
affected side shaped condylar head
• Possible open bite • Neck of condyle can be
• No midline shift thickened and/or elongated
Type III (combination • Chin deviation towards contralateral • Excessive growth in vertical
of Type I and II) side with a sloping rima oris and horizontal vectors
• Midline shift • Enlarged condylar head, neck
• Possible open bite and/or cross bite and ramus
• Irregularly shaped condylar
head, neck and/or ramus
Two distinct patterns of overgrowth are observed
1. The condyle itself may become enlarged, associated with lengthening of

the ramus. It may lead to an open bite on the affected side if the
process proceeds fast and the maxillary teeth and alveolar process do
not compensate with overdevelopment. Asymmetry of the mandible is
seen. The deviation of the chin is generally less marked.
2. The other pattern of overgrowth is characterised by a condyle of
normal size and shape with excessive growth at cartilage-bone
interface which results in an elongated condylar neck, a marked shift of
the mandibular midline to the contralateral side and crossbite. This
may or may not result in increased vertical growth in addition to the
excessive horizontal growth component.
Radiograph
Standard multiview cephalometric films, CT and MRI allow for measurement
of asymmetry. Longitudinal studies provide information on growth changes
and velocity. To assess the occurrence of active growth, bone scans are
routinely used.
Treatment
• Condylectomy to ensure removal of the growing cartilage.

• More conservative condylar shave (condyloplasty) can also be
performed in certain cases.
• Correction of facial asymmetry by orthognathic procedures or
orthomorphic surgery.
Hemimandibular elongation (Fig. 38.4)
Clinical features
1. Horizontal displacement of the mandible and chin towards the

unaffected side.
2. Mild mandibular protrusion.
3. Lip line slopes down towards the affected side.
4. Lateral crossbite on the unaffected side.
5. The occlusal plane sometimes slopes upwards to affected side. This,
together with the lip line, reflects secondary over eruption of the
maxillary teeth on the affected side to maintain a functional dental
occlusion.
6. In severe cases, a lateral open bite is occasionally seen on the affected
side.
7. The displacement of the midline is greater at the anatomical mid-chin
than at the incisor midline, so that there appears to be an apical drift of
the incisors towards the unaffected side.
FIGURE 38.4 3D CT showing hemimandibular elongation. (A–B)
Hemimandibular elongation on the right side. (C) Left side normal.
Age group
Generally during early adolescence.
Nature of the deformity

It generally worsens throughout the period of mandibular growth and ceases
when the growth stops (second decade).
Radiologic appearance
The anomaly is best demonstrated in posteroanterior view, while
orthopantomograph demonstrates the length and any gross enlargement of
the neck of condyle. Scintigraphy during the period of active growth
demonstrates hyperactivity in the condyle of the affected side, reflecting the
increased metabolic activity of the affected condyle.
Treatment
In cases of hemimandibular elongation, condylar surgery is not necessary. It is
advisable to wait till the cessation of mandibular growth before embarking on
surgery. Tomoscintigraphy when available would obviously be advantageous
in doubtful cases.
• In the fully developed condition, following any presurgical

orthodontics, spatial correction is required.
• In the simpler cases where there is no cant of the occlusal plane, a
bilateral mandibular ramus osteotomy is usually sufficient to achieve a
reasonable result. In addition, a genioplasty is sometimes necessary to
achieve symmetry of the chin.
• In patients with occlusal cant, the maxillary occlusion plane can be
corrected using a Le Fort I osteotomy in addition to the mandibular
surgery.
Hemimandibular hyperplasia
Hemimandibular hyperplasia always presents with the same general
appearance as hemimandibular elongation (Figs. 38.5–38.7). This varies in the
degree of development, depending on the age at which abnormal growth
commences, the degree of abnormal growth and its duration.
FIGURE 38.5 Hemimandibular hyperplasia. (A) Hemimandibular

hyperplasia on the left side–Note the bowing of the inferior border
of the mandible on the left side. (B) Occlusal cant on the left side.
(C) Midline shift noticed in the lower anterior towards the left side.
Age group
• 5–8 years of age.

• Abnormal mandibular growth usually ceases at or shortly after the
cessation of general growth, but occasionally it continues for a few
years.
Clinical features
1. The condition is characterised by a three-dimensional enlargement of one

side of the mandible.
2. There will be an enlargement of the condyle, condylar neck, ascending ramus
and the body.
3. The abnormal growth terminates precisely at the symphysis, giving rise
to a sharp demarcation at that site (Figs. 38.6 and 38.7).
4. Inferior border lies at a lower level on the affected side and shows a
marked convexity or bowing when viewed laterally.
5. There is minimal or no displacement of the chin, although morphology
of the soft tissues may appear slightly distorted towards the normal
side and the lip line slopes downwards to the affected side.
6. There is no shift of the incisor midline and there is often a lateral open
bite on the affected side Fig. 38.6.
7. Downward cant of the maxillary plane due to overeruption of the teeth
on the affected side for compensation Fig. 38.5.
8. Pain in the region of the affected TMJ is common. Hemimandibular
hyperplasia is a more aggressive condition than hemimandibular
elongation, progressing more rapidly and resulting in considerably
more anatomical distortion.
FIGURE 38.6 (A) Case of hemimandibular hyperplasia. Note the

facial asymmetry. (B) Facial asymmetry as a result of hyperplasia
on the left side. (C) Right side normal and note the inferior border
lies at a lower level (bowing) on the affected side. (D) Left side
hyperplasia of the mandible.
FIGURE 38.7 3D CT showing combinations of hemimandibular

hyperplasia and elongation. (A) Hemimandibular hyperplasia and
elongation on the right side. (B) Left side normal. (C) Right side
hyperplasia and elongation of the mandible. (D) Base of the skull—
notice the hyperplasia and elongation of the mandible on the right
side.
Diagnosis
Radiographically, the whole mandible on the affected side is enlarged and the
inferior dental canal is displaced towards the lower border.
• Orthopantomograph (OPG) demonstrates a pathognomonic

appearance. The ascending ramus is elongated, mainly due to an
irregular and deforming enlargement of the condyle and elongation
and thickening of the condylar neck; the angle is characteristically
rounded off, with the lower border bowed downwards to a position
lower than the contralateral side.
• As in cases of hemimandibular elongation, tomoscintigraphy is carried
out during the period of active growth demonstrates hyperactivity in
the condyle of the affected side.
• Scintigraphic assessment is done to determine the active and inactive
sites of the mandible this helps the surgeon to decide the treatment
procedure.
Management
In hemimandibular hyperplasia, some form of condylar surgery
(condylotomy, condyloplasty) during the growth period will arrest or retard
growth, thus limiting the amount of secondary anatomical distortion. There is
now fairly general agreement that some form of condylar surgery should be
performed for the active condition as soon as the diagnosis has been made.
The treatment protocols are:
1. High condylectomy to arrest the condylar growth

2. Articular disc repositioning
3. Concomitant orthognathic surgery
• Maxillary Le Fort I osteotomy
• Intraoral vertical ramus osteotomy
• Mandibular contouring
If at the time of diagnosis, the maxilla is also affected then two jaw surgeries
may be necessary. The orthodontic treatment should precede and follow the
surgical treatment for the end-stage corrections. The secondary canting of the
maxillary plane can be corrected by means of a Le Fort I osteotomy. Bowing of
the lower border of the mandible is resected intraorally. Care must be taken to
determine the exact position of the mandibular canal prior to operation; it can
then be accurately marked out and the neurovascular bundle dissected prior to
completion of the horizontal osteotomy. A compensatory sliding genioplasty
will sometimes be necessary in addition to other mandibular surgical
procedures.
Hemifacial hypertrophy
• It is also known as facial gigantism a very rare congenital condition.

• Asymmetrical growth or development of the body or any part of the
skull.
• The condition results due to the localized overgrowth of a single tissue
or all of the tissues.
Diagnostic criteria
1. Unilateral enlargement of the viscerocranium.

2. Enlargement of all the tissues.
Clinical features
• Evident at birth and become accentuated with age, especially at

puberty.
• Unilateral enlargement of cerebral hemisphere and mental retardation.
• Lips, tongue, palate, maxilla and dentition are all enlarged.
• Associated with various neoplasm such as adrenocortical carcinoma,
adrenal neuroblastoma, hepatoblastoma, adrenal adenoma and
undifferentiated sarcoma of the lung.
• Reduced life span.
• It is distinctive due to involvement of all the tissues in that region.
• It is the only condition where the teeth are enlarged (Fig. 38.8).
FIGURE 38.8 Hemifacial hypertrophy. (A–B) Showing unilateral

enlargement of the face.
Condylar hypoplasia and aplasia

Condylar hypoplasia is characterised by facial deformity expressed on the
affected side by a short mandibular ramus. This may occur unilaterally or
bilaterally (Fig. 38.9).
FIGURE 38.9 Condylar hypoplasia (craniofacial microsomia

syndrome). (A) Condylar hypoplasia seen on the left side. (B)
Occlusal cant. (C) Deviation of mouth on opening towards affected
side.
Unilateral condylar hypoplasia (Figs. 38.10–38.11)
• Shortening of mandibular vertical height occurs on the affected side.

• Midline shift towards the same side.
• Shifting of the chin towards the shorter side of the face.
• Deviation of the mandible on mouth opening.
• Occlusal cant.
FIGURE 38.10 Unilateral mandibular hypoplasia (craniofacial

microsomia syndrome).
FIGURE 38.11 Unilateral condylar hypoplasia. (A) Left condylar
hypoplasia, deviation of chin and occlusal canting seen. (B)
Normal right side of the mandible. (C) Hypoplastic condyle with
reduced mandibular vertical height on the left side.
This condition may occur from birth (congenital) due to pharyngeal first or
second arch malformation or it may result from trauma, infection or
irradiation during the growth period. Some of the common syndromes with
hemimandibular hypoplasia as a component are:
• Goldenhar–Gorlin syndrome
• First and second branchial arch syndrome
• Craniofacial microsomia
• Dyke–Davidoff–Masson syndrome
• Femoral-facial syndrome
Bilateral condylar hypoplasia (Fig. 38.12)

When mandibular shortening occurs on both sides, it results in micrognathia
or small mandible. Bird-like face, retruded chin with a small mandibular arch
characterises this condition. When this occurs congenitally, it causes
respiratory distress due to obstruction of the pharyngeal airway by falling
back of the tongue.
FIGURE 38.12 Bilateral mandibular hypoplasia (Treacher Collins
syndrome).
Bilateral condylar hypoplasia is seen in:
• Pierre Robin syndrome

• Treacher Collins syndrome
• Nager’s syndrome
• Townes–Brocks syndrome
• Branchio-oto-renal syndrome
• Branchio-oculo-facial syndromes
• Stickler’s syndrome
In certain special deformities such as craniofacial microsomia, thalidomide

embryopathy, Treacher Collins syndrome, there may be major deficiencies of
the condyle ranging from hypoplasia to aplasia. In Nager–de Reynier
syndrome, the condyle may be aplastic or dysplastic. Robin sequence (RS)
occurs in isolation (nonsyndromic) or in association with other anomalies
(syndromic). The difference in mandibular length was significant. It is known
that disc displacement is one of the factors inducing condylar marrow signal
abnormalities.
Treatment
Severe mandibulofacial dysostosis (Treacher Collins syndrome) should be
treated earlier in the growing period itself in order to avoid secondary
deformities because the mandibular ramus is lengthened as the secondary
dentition is erupting.
This can be achieved either by:
• Growth centre transplantation

• Graft
• Distraction osteogenesis
• Orthognathic surgery and orthodontics
i. Growth centre transplantation (Fig. 38.13): Ideally, successful

rehabilitation of individuals with condylar abnormalities should result
in a structurally and functionally satisfactory TMJ. In addition, when
dealing with severe condylar dysplasia in young growing individuals,
treatment objectives should be directed at establishing a region where
adaptive growth can occur. Insertion of a cartilaginous graft, typically
an autograft, in the osteotomy site is the most common method used to
accomplish the desired result. Costochondral rib grafts (costochondral
junction of the 5th, 6th or 7th rib) are most suitable for this purpose as
they can be transplanted as growth centre replacements to achieve
mandibular growth.
ii. Graft: Sunken cheeks can be augmented using autogenous fat grafts
(lipoinjection) or allogenous materials as fillers.
iii. Distraction osteogenesis: Distraction osteogenesis is a powerful
technique for creating new bone for lengthening of the mandible
without the need for bone grafting and associated donor site
morbidity. Slow lengthening of the osseous segments results in soft
tissue histogenesis, a combination of gradual stretching of the soft
tissues and cellular proliferation.
An increased number of myocytes, along with adaptations in sarcomere
length, have been reported in muscle in response to distraction
osteogenesis, this process is termed as Distraction Histiogenesis. These
favourable adaptive changes maintain the soft tissue attachments to the
bone and hence there is a greater blood supply to the distraction site in
mandible than with conventional osteotomies. They also allow greater
mandibular lengthening, with minimal or no relapse.
New multidirectional buried intraoral distraction devices have overcome
some of the obstacles of earlier external distraction devices and produce
good vector control, occlusion and aesthetic results. The occlusal
outcomes are aided by concomitant orthodontic therapy.
iv. Orthognathic surgery and orthodontics: A combination of maxillary
and mandibular osteotomies can be performed to correct the skeletal
deformity caused by the condylar hypoplasia after cessation of growth.
Bilateral sagittal split osteotomy (BSSO) is the workhorse osteotomy of
traditional mandibular advancement surgery for correction of
micrognathia.
FIGURE 38.13 (A) Unilateral condylar hypoplasia. (B) Deformed

mandibular ramus and condyle. (C) Costochondral graft. (D)
Placement of costochondral graft in the ostectomy site. (E) Two
years after costochondral growth centre transplantation.
Advancements greater than 10 mm require a long sagittal split, which can be

technically difficult to achieve. Unilateral facial asymmetry can be corrected by
using a combination of maxillary and mandibular osteotomies and camouflage
procedures. Le Fort I osteotomy with derotation to correct the occlusal cant;
followed by vertical subsigmoid osteotomy and mandibular contouring often
yields good symmetry and aesthetic results.
Acquired disorders
Traumatic arthritis
Any traumatic incident involving the TMJ may lead to acute arthritis, site of
the inflammation being the capsule. Chronic trauma to the joint due to trauma
from occlusion is also responsible for osteoarthrosis. Traumatic arthritis
characterised by tenderness of the affected joint and restricted movement,
which cause the mandible to deviate to the affected side on opening. There
may be oedema around the joint and restriction of mouth opening due to pain
presenting as classic trismus. Trismus is defined as a prolonged, spasm of the jaw
muscles by which normal opening of the mouth is restricted.
Other than traumatic arthritis a variety of other causes for trismus are
present as depicted in Table 38.4.
Table 38.4
Causes of trismus
A. Congenital
• Trismus pseudocamptodactyly syndrome
• Arthrogryposis multiplex congenita
• Craniocarpotarsal dysplasia
• Hemifacial microsomia
• Fibrodysplasia ossificans progressiva
• Birth injury
B. Traumatic (acute)
• Fractures of mandible, zygomatic or temporal bones
• Haematomas in the joint or muscle of mastication
• Local anaesthetic injection injury
• Paradoxical muscle spasm following head injury
• Anterior dislocated meniscus
• Postsurgical (e.g. third molar removal, TMJ surgery)
C. Neoplastic (benign)
• Mesenchymal tumours of the TMJ and surrounding structures (e.g. osteochondroma)
• Enlargement of the coronoid process of the mandible
Neoplastic (malignant)
• Chondrosarcoma
• Osteosarcoma
• Tumours of the oropharynx (Trotter’s syndrome)
• Metastatic disease of the mandible and infratemporal fossa
D. Neuromuscular disorder
Parkinson’s disease
E. Reactive (acute)
• Septic arthritis
• Tetanus
• Osteomyelitis of the mandible and temporal bone
• Abscesses of the submasseteric, lateral pharyngeal, pterygomandibular, submandibular
and temporal spaces
• Tonsillitis and peritonsillar abscess
• Parotid abscess
• Mumps
• Cancrum oris
Reactive (chronic)
• TMJ ankylosis (fibrous and bony)
• Systemic sclerosis
• Submucous fibrosis
• Radiation therapy
• Myofascial pain dysfunction syndrome (MPDS)
• Ankylosing spondylitis
• Myositis ossificans traumatica
F. Psychogenic
• Hysterical trismus
• Hyperventilation syndrome
G. Drug induced
• Extrapyramidal reaction (facial dyskinesia)
• Strychnine poisoning
Treatment of the trismus is usually treating the cause followed by

physiotherapy. Long-term trismus may require surgical removal of the
coronoid processes and the temporalis muscle attachment, followed by
physiotherapy.
TMJ Osteoarthritis
Osteoarthritis is a chronic noninflammatory and degenerative disease affecting
the articular cartilage of joints. It is the most common skeletal disease of
human body affecting the TMJ.
Pathology
Earliest degenerative changes are seen in articular cartilage, as proteoglycans
are lost at the surface. Chondrocytes are stimulated and DNA synthesis
increases. Growth of surrounding bone is stimulated, resulting in osteophyte
formation. Subchondral pseudocysts become evident as synovial fluid passes
through the cartilage and cortical bone to fill the marrow cavities.
Clinical features
• Usually 5th decade—slow onset of disease with mild symptoms.

• Usually one TMJ is involved (but may be bilateral), symptoms are
usually unilateral.
• Women are more likely to be afflicted with TMJ involvement.
• Pain in the joint and muscles of mastication, causing limitation of
mandibular motion.
• Joint noises, especially crepitus.
• Osteophyte formation and marginal bone thickening leads to palpable
masses over preauricular region.
Investigations
• Plain films and CT scans can reveal flattening of the condylar head,
cyst formation of subchondral bone, joint narrowing, osteophyte
formation and subchondral sclerosis.
• MRI, arthrographs can reveal disc perforations and dislocations.
Treatment
• Initial intervention should limit excessive and recurrent trauma.

• Moderate exercise and physical therapy should be started to
strengthen the musculature supporting the joints.
• NSAIDs to reduce pain.
• In severe case, thermal therapy can be obtained with ultrasonography
and infrared heat.
• Orthopaedic procedures (debriding loose bodies, osteotomy and
prosthetic replacement) should be reserved for patients with
retractable pain.
Rheumatoid arthritis (RA)

Rheumatoid arthritis (RA) is an autoimmune disease predominantly affecting
diarthrodial joints. It can affect the joint at any age. Juvenile rheumatoid
arthritis (Still’s disease) may be of varying severity.
Aetiology
• Genetic susceptibility
• Autoimmune response
• Increased HLA-DR4 antigen, correlated with increased levels of
rheumatoid factor
Pathophysiology
Synovial membrane proliferation and outgrowth causes erosion of articular
cartilage and subchondral bone. After microvascular injury, synovial cells
proliferate, swell and are infiltrated by mononuclear cells and T lymphocytes.
The production of inflammatory mediators, which is stimulated by the RA
cells, result in the production of proteinases and prostaglandin. Collagenases
are responsible for typical erosions seen over the joint surface.
Clinical features
• Intermittent pain, swelling and progressive limitation of joint motion.

• Characteristically, the joints of the hands and feet are first affected.
• Preauricular joint pain on chewing and moving.
• Advanced disease leads to decreased range of motion and stiffness.
• Decreased bite force, muscle tenderness.
• Clicking, crepitus and tenderness of the joint on palpation.
• Limitation of motion occurs as the bone is destroyed and joint space is
filled with scar tissue leading to fibrous ankylosis.
• Progressive class II occlusion develops resulting in retrognathia/bird-
face deformity and apertognathia may result when the disease occurs
in young children.
Radiograph
Early pathology is not revealed as RA starts in soft tissues. Erosion, subcondral
cyst, osteophyte formation, marginal proliferation and abnormal flattening of
the condyle head, loss of joint space, are seen as the process continues. Anterior
and posterior condylar erosion results in Sharpened pencil appearance. MRI
reveals TMJ disc destruction, displacement and joint effusions. Advanced RA
reveals shortening of the posterior ramus, premature posterior occlusal
contacts and antegonial notching.
Treatment
Conservative methods
Drug therapy
• Antiinflammatory drugs (salicylates, NSAIDs, corticosteroids), soft

diet, avoiding extreme jaw movements.
• If NSAIDs are ineffective, disease modifying antirheumatic drugs such
as hydroxychloroquine, gold, penicillamine or the cytotoxic agents like
methotrexate or cyclophosphamide are considered.
• Drug of choice for juvenile rheumatoid arthritis (JRA) patients is
methotrexate.
• Intra-articular steroids are contraindicated in the acute phase.
• Surgery is reserved for intractable pain and for correction of
complications including ankylosis and micrognathia.
Surgical methods
• High condylectomy is the procedure of choice for intractable pain
• Arthroplasty for total joint reconstruction using alloplasts
• Synovectomy
Psoriatic arthritis
Psoriatic arthritis resembles the rheumatoid type, but it is associated with
psoriasis, a dermatologic disease. Skin exacerbations and remission of joint
disturbances coincident with the skin lesions differentiate the disease from
rheumatoid arthritis. The serological tests for rheumatic fever are negative.
There is a high incidence in women.
Aetiology
• Genetic component
• Presence of HLA-B27 antigen
Clinical features
• TMJ involvement is described as episodic, sudden and usually

unilateral
• Limitation of mandibular movements
• Morning stiffness, crepitus, eventual loss of interincisal opening
• In advanced disease, ankylosis can occur
Diagnosis
Diagnosis is suggested by presence of arthritis in a patient with psoriatic skin
or nail lesions.
• Asymmetric joint involvement

• Negative testing for RF
• Absence of rheumatoid nodules
• Hyperuricaemia in 20% cases
Radiographs
Temporomandibular joint involvement in early psoriatic arthritis is evident on
radiographs as erosions, flattening of condylar head, osteoporosis and joint
space narrowing.
Laboratory findings
• Hypoproliferative anaemia
• Elevated ESR
Treatment
• Systemic treatment should be undertaken

• Reduce loading on the joint
• In severe cases, immunosuppressive agents such as methotrexate have
been used
Condylar fracture
A fracture dislocation of the condylar head can result in a mechanical
obstruction and limit jaw function. Fractures of the zygomaticomaxillary
complex can cause limited jaw function by a direct impingement of the
complex on the coronoid process of the mandible. Refer to Chapter 44
Fractures of the Mandibule for details regarding condylar fractures.
Dislocation
Refer to Chapter 40 Internal Derangements and Condylar Dislocation.
TMJ ankylosis
Temporomandibular joint ankylosis is usually the result of trauma. More
common in the younger patients, following an intracapsular mandibular
fracture. Refer to Chapter 39 TMJ Ankylosis.
Tumours
Any tumour in the area of the TMJ and/or muscles of mastication can
significantly cause jaw hypomobility. Both benign and malignant lesions affect
the condyles and synovial components of the joint.
Ankylosing spondylitis (Marie–Strumpell disease)

This is a chronic inflammatory disease involving the articulations of spine and
adjacent soft tissues. It has a high sex ratio of male:female sufferers (8:1).
Clinical features
• Symptoms are due to imperfect head posture caused by the vertebral

lesions.
• The most common complaints are of pain, stiffness, decreased range of
motion and eventually ankylosis.
• Extra-articular manifestations such as iritis, uveitis and cardiac
symptoms are common in patients with TMJ involvement.
Radiograph
Radiographic findings include erosion of the condyle and fossa, osteophyte
formation and subchondral sclerosis. As disease progresses, severe narrowing
of the joint space becomes evident.
Treatment
The load must be reduced across the joint by the use of acrylic splints. The
drug with proven efficacy is sulphasalazine. Surgical intervention should be
limited to those patients with severe crippling disease.
I. Functional disorders
Temporomandibular joint pain/dysfunction syndrome named by Schwartz has
a plethora of synonyms as facial arthromyalgia, MPDS, temporomandibular
joint dysarthrosis, mandibular pain dysfunction syndrome and
temporomandibular joint arthrosis. It is the only situation in which no organic
lesion has been detected clinically.
MFP (Myofacial pain) is the most common muscle pain disorder. It is an
acute to chronic condition that includes the presence of regional pain
associated with tender areas called trigger points (TrPs), which are expressed
in taut bands of skeletal muscles, tendons or ligaments (Figs. 38.14–38.15).
FIGURE 38.14 (A & B) Trigger point complex & its outcome.

FIGURE 38.15 Trigger points and associated pattern of referred
pain. (A) Trigger point—the anterior temporalis. Pain occurs as
temple, frontal and retroorbital headaches and pain in the maxillary
anterior teeth. (B) Trigger point—the deep masseter trigger point.
Pain occurs as preauricular pain, ear aches and pain in the
maxillary posterior teeth. (C) Trigger point—the middle masseter
trigger point. Pain occurs as temple, frontal and retroorbital
headaches and as pain in the maxillary anterior teeth (All the
muscles in A, B and C zones are also activated by clenching,
bruxism and other oral parafunctional habits.). (D) Trigger point
—the splenius capitus trigger point in the posterior cervical area.
Pain occurs as posterior cervical pain, vertex headache and frontal
headache (These muscles are also activated by clenching and
forward head pressure.).
History
• Costen (1934)—occlusal aetiology in TMJ pain. (Bite raising era).
• Schwartz (1956)—coined the term ‘TMJ pain dysfunction syndrome’
and reported that the spasm of masticatory and perimasticatory
musculature leading towards the symptoms.
• Laskin in 1969 implicated pshychophysiological theory for MPDS. He
suggested that mechanical factors (malocclusion) along with the
physchophysiological stress motivated oral habits leads to muscle
fatigue and painful spasm. To stress the role played by the muscles,
Laskin suggested that the term ‘Myofascia pain dysfunction syndrome’ as
more accurate to describe.
Aetiology of MPDS:
• Tooth muscle theory

• Prosthetic problems
• Malocclusion
• Psychophysiology theory
• Steep angulation of articular eminence
Pathophysiology and Mechanisms (Flowchart 38.2)
Mechanisms
Because there are no specific anatomic changes in the myogenous pain, there
are no conclusive mechanisms identified in nontrauma cases. Therefore, there
are several processes that may explain the development and persistence of
masticatory myogenous pain.
1. Repetitive strain hypothesis (Flowchart 38.3)

2. Neurophysiologic hypothesis
Tonic muscular hyperactivity may be a normal protective adaptation to
pain instead of its cause. Phasic modulation of excitatory and inhibitory
interneurons supplied by high threshold sensory afferents may be involved.
3. Central hypothesis
Convergence of multiple afferent inputs from the muscle and other
visceral and somatic structures in the lamina I or V of the dorsal horn
on the way to the cortex can result in perception of local and referred
pain.
4. Central biasing mechanism
Multiple peripheral and central factors may inhibit or facilitate central
input through modulatory influence of the brainstem. This may explain
the diverse factors that can either exacerbate or alleviate the pain such
as stress, repetitive strain, poor posture, relaxation, medications,
temperature change, massage, local anaesthetic injections and electrical
stimulation.
FLOWCHART 38.2 Pathophysiology of myofacial pain.
FLOWCHART 38.3 Repetitive strain hypothesis.
Pathological changes
TMJ
No organic changes can be detected clinically. In early lesions, there is a loss of
usual smooth surface zone and development of an uneven surface. In later
stages, there is total loss of the entire amorphous layer and the superficial
collagen masses consist only of small diameter fibrils. Disorganisation of the
articular surface occurs in case of more severe and prolonged disorder.
Muscles
• Pathological changes in muscles are indefinite.

• Raised intramuscular pressure attributing to oedema.
• Increased blood flow.
• Degranulating mast cells seen in histological examination of painful
muscles.
• No evidence of increased level of creatine kinase.
Laskin’s Cardinal symptoms of MPDS:

1. Pain or discomfort anywhere about the head or neck.
2. Limitation of motion of the jaw.
3. Joint noises—grating, clicking, snapping.
4. Tenderness to palpation of the muscles of mastication (Fig. 38.14).
Symptoms (Table 38.5)
1. Pain. This can be localised to the joint or referred to the head, neck or
shoulders. Dull aches are more common.
2. Limitation of mandibular movement. Range of mouth opening is
limited, which may be either constant or intermittent, occurring only at
the start or end of the day.
3. Muscle hyperactivity. The incidence of upper and lower tooth contact
during sleep is greater in dysfunction patients who are not aware of
their bruxism.
4. Abnormal muscle activities. Unilateral chewing that may have been
acquired after a dental ailment, such as pericoronitis or because of a
grossly deficient dentition.
5. Clicking. Clicking is common and usually bilateral. It can occur at any
point of jaw movement and there may be multiple clicks. Recent
studies indicate that clicking may be due to intra-articular thickening.
It frequently occurs without pain.
6. Locking. It is an interruption of movement associated with clicking.
Locking of the jaw may occur at regular times of the day, the most
common being on awakening.
7. Emotional factors. Emotional problems are concerned with situations
of uncertainty, which involves secretion of catecholamines.
Table 38.5
Associated symptoms in myofascial pain dysfunction syndrome
(MPDS)
Trigger points: Trigger points are sources of constant deep pain, which
produces referred pain, in a predictable area/pattern depending upon the
region involved. Palpation of trigger points gives rise to ‘Jump sign’
(Fig. 38.15)
Trigger Zone: A circumscribed region near a nerve, often in the head and
neck region which, when stimulated, may elicit marked neuralgia
accompanied by lightning pain.
Tender points: Circumscribed regions in muscle, which on palpation
produce intense pain in the same region, of palpation. No referred pain is
present.
Signs
1. Joint tenderness. Tenderness of the joint when palpated either in the

preauricular region or from within the external auditory meatus.
2. Muscle tenderness. Tenderness of the masticatory muscles may be
noted, especially the masseter, anterior part of temporalis and lateral
pterygoid.
3. Abnormalities of mandibular movement. Lateral deviations are
diagnostically helpful. Grossly deficient occlusion may account for
some abnormal movements.
Diagnosis
A provisional diagnosis of a pain/dysfunction syndrome is made when no
clinically detectable organic lesion can be found to account for the patient’s
symptoms and signs.
• Therapeutic anaesthetic block

• Tigger point injections
Radiography
• When degenerative disease is not suspected, standard lateral

transcranial views help to reveal that no unsuspected pathological
feature is present.
• When degenerative disease is suspected, then a special view such as
the transpharyngeal might be needed to supplement the standard films.
• Tomography offers an improvement since the position of the focal plane
is reproducible. But this applies only to fixed areas such as glenoid
fossa.
• The function of the joints can be assessed by arthrography (injection of
radiopaque fluids) or by studying images during movement. It is not a
method of routine use, skill is needed to produce and interpret
arthrographs.
• MRI
Treatment
Conservative management
1. Placebo
Placebo effect for treatment of pain/dysfunction syndrome is by using splints
and mock adjustment of the occlusion.
2. Reassurance
The quality of doctor/patient relationship is very important for the success of
treatment as it may help to reduce the emotional problem of the patient and
they must be reassured that there is no serious disease. In a few cases,
reassurance alone may be sufficient. Patient’s occupation must be considered,
as it may be necessary to advice sick leave.
3. Occlusal correction
Patient should perform bilateral mastication. Any dental pain, substandard
restoration, missing teeth should be treated. Habits can be corrected by
exercises.
4. Soft diet
To reduce loading forces on joint and reduce muscle activity.
5. Splints
A splint inactivates facial muscles, decompresses intracapsular tissue,
establishes balanced occlusal plane, repositions the jaw, stabilises the disc and
restores vertical dimension.
Rationale for the use of splint therapy in the treatment of myofascial pain.
• Allows free mandibular movement

• Decreased muscular activity
• Provides stable dental occlusion
• Aids in cognitive awareness of bruxism
Types of splints
• Stabilisation splint
• Mandibular repositioning splint
• Pivot splint
• Soft splint
• Bite plane splint
Stabilisation splint
The most commonly used splint in the treatment of myofascial pain is stabilisation
splint. It is a full-coverage maxillary or mandibular splint incorporating even
posterior contact at the point of maximum closure. The splint usually has
anterior disocclusion in protrusive as well as canine guidance or group
function in lateral excursions.
Resilient splint (soft splint) (Fig. 38.16)

Usually this is a full-coverage ‘mouth guard’ that can be used with good
immediate results in patients suffering from myofascial pain. They are soft
vinyl plastic occlusal splints made by vacuum-cupping techniques. Their chief
application is for patient’s daytime clenching habits. The advantage of a
resilient splint is that it can be fabricated in the dental office and is less
expensive.
FIGURE 38.16 Soft splint.

Bite plane splint
Bite plane splint, also known as the Hawley’s bite plane, which has been used to
reduce muscle activity and treat patients with myofascial pain.
• Anterior bite splints: Indicated in case of nocturnal bruxism. It

consists of an upper acrylic plate without occlusal cover. Relief from
symptoms occurs within a few days of its use. It should be worn for at
least 3 weeks.
• Full occlusal splints: Failure of anterior bite splints should be followed
by the full-coverage occlusal splints fabrication. These are made of
acrylic. Its occlusal surface should be planar, such that it offers three-
point articulation in any excursion of the mandible.
6. Drugs
• NSAIDs are helpful in reducing pain and inflammation.

• Antiinflammatory action of corticosteroids is greater than NSAIDs. Can
be given intra-articular or orally.
• Anxiolytics to reduce anxiety, as anxiety and muscle tension appear to
be related, e.g. diazepam 5–10 mg.
• Muscle relaxants. Methocarbamol, chlorzoxazone are effective.
• Antidepressants Tricyclic antidepressant, monoamino oxidase (MAO)
inhibitors. They are helpful because of the close relation between pain
and depression.
7. Intermaxillary fixation
When pain is severe, application of intermaxillary fixation relieves symptoms
by inducing absolute rest.
8. Thermal agents
They help in decreasing pain; increasing muscle relaxation and increasing the
range of motions.
a. Superficial moist/dry heat: Superficial heat produces a therapeutic effect

by elevating pain threshold, altering nerve conduction velocity and
decreasing muscle tension. Muscle relaxation may also result from
analgesic effects of heating.
b. Ultrasonography-deep: They help to increase the elasticity of soft tissues.
It has an antiinflammatory effect.
c. Phonophoresis: Delivery of topically applied medicines using USG.
For TMJ inflammation, pulsed ultrasonography is applied at a frequency of
3 MHz and low intensity of 0.5–0.8 w/cm2 per 5–8 min. Exercise combined
with ultrasonography reported a higher percentage of pain relief.
9. Cold
Cold can be used to control inflammation by application of ice packs, ice cubes
or ice-soaked towels to the TMJ. Cold elevates the pain threshold by
decreasing nerve conduction velocity.
10. Iontophoresis
It is a battery-powered system used to deliver water-soluble ionising drugs
through the skin. Common drugs used are dexamethasone sodium phosphate,
methyl prednisolone and lidocaine hydrochloride.
11. TENS
Transcutaneous electric nerve stimulation (TENS). TENS provides symptomatic
pain relief. TENS employs a small, portable, battery-operated unit. Frequency,
pulse width and amplitude of an alternating current that is to be administered
to the patient by electrodes are adjustable.
It works on the basis of the ‘gate control theory’ of Melzack and Wall. TENS
has been designed to enhance the healing process by reducing the effect of
inflammation.
12. Home exercise programme for hypomobility

Patients with limited mouth opening with associated inflammation should be
instructed to open and close the mouth with the tongue against the palate.
This should be performed numerous times throughout the day. This helps in
increasing the range of joint movement and to increase muscle relaxation.
13. Pressure-point techniques
• Extraoral, intraoral massage or pressure-point techniques may be

offered to the muscles of mastication.
• Therapeutic exercises can be given to muscles of mastication by having
the patient place one fist under the chin to resist mouth opening.
14. Muscle injection

It is given to inactivate the trigger point, reduce muscle pain and enhance
muscle relaxation. Trigger point injection reduces muscle pain and
contracture. It is useful when thermal agents and stretching exercises have
failed to alleviate muscle dysfunction. 0.5 cc of local anaesthesia (without
epinephrine) is injected into each site. The muscle is then passively or actively
stretched.
15. Intra-articular injection
• Intra-articular injection of steroids has a place in some cases with acute

pain and inflammation in relation to the joint.
• If the conservative measures have failed, surgery should be
contemplated for the treatment of pain/dysfunction syndrome.
• When joint dysfunction has continued without relief over a period of
years, structural damage begins to take place. Surgical procedures are
directed towards relief of joint pain due to overloading.
Laskin & Block (1986) suggested phase I-IV for management of MPDS
(Fig. 38.17).
FIGURE 38.17 Phases of therapy for MPDS by Laskin and Block

(1986).
Surgical management
When all the conservative measures fail and in some cases of irreducible,
medially displaced meniscus, surgery is the last resort.
Various surgical procedures are:
1. Arthrocentesis and lavage (refer Chapter 50, page no. 1160)

2. Arthroscopy
3. Disc repositioning
4. Disc removal
5. Disc removal and
• Autologous graft disc replacement
• Alloplastic disc replacement
6. Condylotomy
7. Condylectomy
CHAPTER 39
TMJ Ankylosis
Aetiology
Trauma
Infection and inflammation of the TMJ
• Primary inflammation of the joint
• Secondary inflammation
Arthritis
• Ankylosing spondylitis
• Psoriatic arthritis
Kazanjian classification (1938)

Miller et al (1975)
Sawhney classification
• Type I ankylosis
• Type II ankylosis
• Type III ankylosis
• Type IV ankylosis
• Reankylosis
Joram Raveh, Thierry Vuillemin Classification
Ninth Shanghai Classification
Unilateral TMJ ankylosis
• Extraoral findings
• Intraoral findings
Bilateral TMJ ankylosis
• Extraoral findings
• Intraoral findings
Management
• Kaban protocol for the management of TMJ ankylosis

in children
Condylectomy
Gap arthroplasty
Interposition arthroplasty
• Costochondral grafts in the treatment of TMJ ankylosis
• Autogenous fat
• Auricular cartilage
• Temporalis muscle flap
Complication of TMJ ankylosis surgery
Postoperative physiotherapy
Management of secondary deformity
False ankylosis
Temporomandibular joint ankylosis (TMJ) is a unique condition of the joint

that restricts the joint mobility progressively, thus limiting all jaw functions.
The condition is a form of ectopic calcification that, when it occurs during
childhood, may lead to significant facial deformity due to restriction in
mandibular growth and development. Considering ankylosis as a
phenomenon, the onset of infection and inflammation of the TMJ may be
avoided, but once the process starts, it cannot be stopped. The
aetiopathogenesis of this condition has been hypothesised and has not been
concluded with enough proof.
Aetiology
I. Trauma
• Trauma to the joint in childhood has been the foremost and
commonest accepted aetiology of TMJ ankylosis (Fig. 39.1;
Flowchart 39.1).
• Factors such as the presence or absence of mobility during the healing
phase, a normal disc acts as a physical hindrance to the transarticular
bony fusion and patient’s age at the time of injury are key variables
determining outcome.
FIGURE 39.1 Difference in trauma to condyle in children and

adults. (A) In the child, trauma to the condyle results in an
intracapsular fracture and haemarthrosis with highly osteogenic
tissues, the fibroosseous mass may result in ankylosis. (B) In the
adult, trauma transmitted through the long axis of the mandible
results in a fracture dislocation of the condyle with a resultant
empty fossa.
FLOWCHART 39.1 Process of ankylosis following trauma.
II. Infection and inflammation of the TMJ

Primary inflammation of the joint. That may either be of infective origin or
autoimmune in nature. The most common infections of the TMJ that may
result in ankylosis are tuberculosis Staphylococcus aureus, Neisseria gonorrhoeae
and Haemophilus influenzae.
Secondary inflammation. Due to a nearly local process (e.g. mastoiditis and
otitis media), it has been implicated as a cause of TMJ ankylosis.
III. Arthritis
A. Rheumatoid arthritis
Rheumatoid arthritis is a chronic inflammatory systemic disorder principally
affecting the synovial joints; TMJ is also affected. Severe limited motion occurs
as the bone is destroyed and the joint space is filled with scar tissue leading to
fibrous ankylosis.
B. Ankylosing spondylitis
Ankylosing spondylitis (Marie–Strumpell disease, rheumatoid spondylitis) is a
chronic progressive inflammatory disease primarily involving the articulations
of the spine and adjacent soft tissues. The sacroiliac joint is always involved,
with fewer cases affecting peripheral joints such as the hip, shoulder and TMJ
leading to ankylosis.
C. Psoriatic arthritis
Psoriatic arthritis is characterised by the triad of (1) psoriasis, (2) erosive
polyarthritis and (3) negative result of a serologic test for rheumatoid factor.
Psoriatic arthritis has been considered predisposing to ankylosis.

The transformation of the haematoma into osteogenic nidus is the widely
accepted theory in the pathophysiology of TMJ bony ankylosis, but this theory
could not answer the exact mechanism of TMJ ankylosis. The right and left
joints are dependent on each other; the degree of ankylosis on one side affects
the opposite side. Various animal studies and hypotheses have been proposed
to understand the pathogenesis of TMJ ankylosis.
• The development of traumatic TMJ bony ankylosis may be the course

of bone healing of two injured articular surfaces under the interference
of opening movement, which is similar to the hypertrophic nonunion
in long bones.
• Markey et al. experimented on young monkeys to create TMJ
ankylosis. They attempted a surgical intracapsular fracture and
intramaxillary fixation to restrict the jaw movements. They concluded
that the condylar fracture followed by long-term fixation did not
induce ankylosis, the jaw movements resumed to normal after the
correction of the fracture.
• Hohl et al. subjected the condylar fracture in monkeys with various
modalities such as mechanical damage, chemical damage and bone
grafting and bacterial infection. They concluded that the mechanical
damage coupled with bone grafting significantly induced TMJ
ankylosis.
• Using sheep model, Miyamoto et al. and Matsuura et al. concluded
that when the mandibular movement is restricted, the chance of TMJ
ankylosis increased.
• Miyamoto et al. stated that the joints where the intra-articular bone
transplant was placed showed development of ankylosis faster than
the normal subject. He implied the importance of the biomechanics of
normal joint function.
• According to Bjornland and Haanaes, the chances of TMJ ankylosis
increased greatly in the absence of the disc. Miyamoto et al.
demonstrated that the disc guards the TMJ from the occurrence of
intracapsular fibrous ankylosis.
• Soung Min Kim studied the fractured condylar neck portion. The
sections from the sample were subjected to histological and
immunohistochemical staining. He observed a widespread chondroid
hyperplasia with rich hyaline cartilage strongly positive for BMP-4 but
sparse for BMP-2 associated with hyperplasia of the synovial
membrane. He elucidated that the callus formed at the site of fracture
forms the hyperplastic chondroid tissue and its further growth is
continuously backed by the surrounding synovial tissue leading to
TMJ ankylosis.
Location
• Intra-articular
• Extra-articular
Types of tissues involved
• Bony
• Fibrous
• Fibroosseous
Extent of fusion
• Complete
• Incomplete
1. Kazanjian classification (1938)

He pioneered the TMJ ankylosis classification. Accordingly, TMJ ankylosis
was subdivided into
• Extra-articular ankylosis
• Intra-articular ankylosis
▪ Extra-articular or false ankylosis is due to the pathological
changes in the structures surrounding the TMJ causing
limitations in mouth opening. Radiographic and laminogram
findings illustrate normal-appearing TMJ and joint spaces.
▪ Intra-articular or true ankylosis is caused by the fibrous or
bony adhesions between the articular surfaces of the
mandibular condyle and glenoid fossa. The diagnosis of true
ankylosis in a patient with limited mouth opening is arrived
by evidence of condylar deformation, loss of joint spaces and
abnormal bone formation in and around the TMJ in the
radiograph.
2. Miller et al (1975)
• False ankylosis:
▪ Myogenic
▪ Neurogenic
▪ Psychogenic
▪ Bone impingement
▪ Fibrous adhesion
• Tumours
3. Sawhney classification (Figs. 39.2–39.6)
• True (intra-articular) and false (extra-articular)

• True ankylosis as type I, II, III and IV.
FIGURE 39.2 Type I ankylosis.
FIGURE 39.3 Type II ankylosis.
FIGURE 39.4 Type III ankylosis.
FIGURE 39.5 Type IV ankylosis.
FIGURE 39.6 (A) Type I ankylosis. Condylar head is flattened or

deformed in close approximation to the upper joint space. Dense
fibrous adhesion is present within. (B) Type II ankylosis. Bony
fusion of the condylar head in the outer aspect of the articular
surface either anteriorly or posteriorly and limited to a small area.
(C) Type III ankylosis. A bony block bridging the mandibular ramus
and zygomatic arch. The atrophic condylar head is displaced and
is either free or fused to the medial aspect of the superior portion of
the ramus. (D) Type IV ankylosis. A wider bony block bridges the
mandibular ramus and zygomatic arch, extending and obliterating
the upper joint space and completely replacing the architecture of
the joint.
Type I ankylosis
Where the condyle is medially angulated and associated with a deformed
articular fossa together with a mild-to-moderate amount of new bone
formation.
Type II ankylosis
Where there is no recognisable condyle or fossa but instead a large mass of
new bone extending from the ramus to the base of the skull.
Type III ankylosis

Usually results from a medially displaced fracture dislocation with bone
bridging the mandibular ramus to the zygomatic arch.
Type IV ankylosis
Found when the joint architecture is replaced completely by bone with fusion
of the condyle, sigmoid notch and coronoid process to the zygomatic arch and
glenoid fossa.
While this classification is useful in categorising primary ankylosis as per
radiographic evidence, it cannot be applied in cases with reankylosis where
the ankylotic mass has very little resemblance to normal joint anatomy after
the previous gap arthroplasty. We have modified this classification further to
denote reankylosis cases in order to facilitate treatment planning.
Reankylosis was classified accordingly into six categories to facilitate
treatment planning.
Reankylosis
Type 1
Fibrous ankylosis, reduction in joint space with clear demarcation of the
borders of the temporal and condylar components.
Type 2
Bony ankylosis between the condylar region and temporal bone, without
involving the coronoid process or the sigmoid notch.
Type 3a
Ankylosis between condyle and temporal bone with hyperplasia of the
coronoid process without ankylosis.
Type 3b
Ankylosis involving the coronoid and the condylar region without obliteration
of the sigmoid notch.
Type 4
Complete bony union of the condyle and coronoid process to the temporal
component, in which sigmoid notch could not be delineated.
Type 5
Ankylosis involving the zygomatic arch.
4. Joram Raveh, Thierry Vuillemin classification
Class Ankylotic bony tissue limited to the condylar process and articulate fossa
1
Class The bone mass extends out of the fossa involving the medial aspect of the skull base up to
2 the carotid–jugular vessels
Class Extension and penetration into the middle cranial fossa
3
Class Combination of class 2 and class 3
4
5. Ninth Shanghai classification
Type is fibrous ankylosis without bony fusion of the joint

A1
Type is ankylosis with bony fusion on the lateral side of the joint, while the residual condyle
A2 fragment is bigger than 0.5 of the condylar head in the medial side
Type is similar to A2, but the residual condylar fragment is smaller than 0.5 of the condylar
A3 head
Type is ankylosis with complete bony fusion of the joint
A4
The clinical presentation of TMJ ankylosis is dependent on the age of onset,
duration of the disease process before approaching the surgeon and the type of
ankylosis. The classical findings described below are of true bony ankylosis in
patients afflicted of the disease early in childhood. TMJ ankylosis that occurs
after cessation of condylar growth (adult onset) presents only with restricted
mouth opening with no other facial deformities.
Unilateral TMJ ankylosis (Figs. 39.7–39.10)

Extraoral findings
1. Gross facial asymmetry.

2. Convex profile.
3. Ipsilateral side shows roundening of lower face with prominent
antegonial notch and ill-defined gonium.
4. Chin shifted to ipsilateral side of the midline.
5. The contralateral normal side shows a flattened elongated appearance.
6. The ramal height and lower facial height on ipsilateral side are shorter
or lesser than contralateral side.
7. Restricted mouth opening.
8. On opening the mouth, mandible deviates to the affected side.
9. On palpating preauricular region, the joint movements will be less or
not palpable on the affected side.
FIGURE 39.7 Preoperative view showing flattened left side face
with deviation of chin to right side.
FIGURE 39.8 Preoperative profile view showing retruded chin.
FIGURE 39.9 Preoperative coronal CT section showing obliteration
of right joint space. Note the mushrooming deformity and increased
mediolateral width of right condylar head.
FIGURE 39.10 Preoperative 3D CT showing right TMJ ankylosis.
Intraoral findings
1. Decreased maximal interincisal distance.

2. Occlusal cant.
3. Dental caries and periodontal disease from poor oral hygiene,
inaccessibility for maintaining good oral hygiene.
4. Mandible deviates to affected side on opening mouth.
5. Multiple teeth—impacted or submerged.
Bilateral TMJ ankylosis

Extraoral findings
1. Gross facial deformity—Andy Gump appearance or bird face

deformity. ‘Vogelgesicht’ (Andy Gump was the a cartoon character
from the early 20th century in an extremely popular comic strip, The
Gumps Andy was chinless with an oversized moustache, prominent
nose and bald head with his mouth appearing as a small hole in his
neck) (Figs. 39.11–39.14).
2. Highly convex profile.
3. Retrognathism and micrognathia.
4. Reduced thyromental angle and hyomental distance.
5. Reduced lower facial height but anterior facial height usually greater
than posterior facial height
6. Double chin.
7. Bilateral reduced mandible height with steep mandibular plane angle.
8. Restricted mouth opening.
9. Bilateral preauricular palpation reveals no joint movements in true
bony ankylosis.
FIGURE 39.11 (A & B) Image showing retruded chin with reduced

lower facial height.
FIGURE 39.12 Image showing Andy Gump cartoon character.
FIGURE 39.13 Preoperative CT scan showing retrognathia with
shortened ramal height bilaterally.
FIGURE 39.14 CT lateral view showing severe retrognathia with
shortened ramal height.
Intraoral findings
1. Reduced or nil maximal interincisal mouth opening.

2. Dental caries or periodontal disease from poor oral hygiene due to
inaccessibility.
3. Multiple teeth—impacted or submerged.
4. The presence of occlusal cant depending on variation in onset of
ankylosis bilaterally.
5. In fibrous ankylosis minimal jaw movement may be seen usually with
no deviation.
Diagnosis
• History of infection or trauma (birth trauma/falls/previous infection of

the ear)
• Clinical examination (reduced interincisal opening/diminished/no TMJ
movements/scar on the chin due to trauma)
• Radiological findings
Clinical examination is the prime method of diagnosing ankylosis, though
radiological investigation helps in
1. Differentiating fibrous ankylosis from bony ankylosis.

2. Degree of involvement of joint.
3. Extra-articular ankylosis if any (involvement of zygoma, coronoid
process).
4. Medial extent of the ankylotic mass.
a. Mediolateral width of the ankylotic mass.
b. Relation of the mass to the vital structures medially such as
mandibular nerve, internal carotid artery (Joram Raveh
classification).
5. Preoperative surgical planning for resection and reconstruction.
6. Preoperative planning for associated secondary, deformity correction as
distraction osteogenesis, orthognathic surgery, orthomorphic surgery,
etc.
The suggested radiologic films are OPG for initial screening, though CT scan
with 3D reconstruction is more useful in assessing the extent of ankylosis and
presurgical planning.
Management
The management strategy for TMJ ankylosis is dependent on the stage of
ankylosis, the associated deformity and age of presentation (Flowchart 39.2).
FLOWCHART 39.2 Our protocol for management of ankylosis.
Definitive management of TMJ ankylosis is total removal of the ankylotic

mass. The ectopic bone mass is resected. The treatment concept is similar to
creating a nonunion between the osteotomised bone ends.
• Condylectomy
• Gap arthroplasty: Create a gap with minimum space of 1 cm
• Interpositioning a material: Soft tissue-temporalis myofascial
flap/perichondrium (costochondral graft—CCG) is the desired
interposing materials.
• Active mobilisation of the joint
The well-known and widely followed protocol for managing TMJ ankylosis
is the one proposed by Kaban.
Kaban protocol for the management of TMJ ankylosis in children
1. Aggressive excision of fibrous and/or bony mass.

2. Coronoidectomy on affected side.
3. Coronoidectomy on opposite side if steps 1 and 2 do not result in
maximal interincisal opening (MIO) of 35 mm or to point of dislocation
of opposite side.
4. Lining of joint with temporalis fascia or the native disc, if it can be
salvaged.
5. Reconstruction of ramus condyle unit (RCU) with either DO or CCG and
rigid fixation.
6. Early mobilisation of jaw; if DO used to reconstruct ramus condyle unit
(RCU), mobilise day of surgery; if CCG used, early mobilisation with
minimal intermaxillary fixation (not 10 days).
7. Aggressive physiotherapy.
Aims and objectives of surgery
1. Release of ankylosed mass and creation of a gap to mobilise the joint.

2. Creation of a functional joint.
3. To reconstruct the joint and restore the vertical height of the ramus.
4. To prevent recurrence.
5. To restore normal facial growth pattern.
6. To improve aesthetics and rehabilitate the patient (cosmetic surgery may
be carried out at a later date or at second phase).
Condylectomy
It is indicated in:
1. Severe arthrosis.
2. Various types of arthritis.
3. Malunited condylar fractures with limitation of motion and pain
during mastication.
4. Condylectomy can also be performed in cases of fibrous ankylosis
where the articular space has not been completely eliminated.
Condylectomy is carried via preauricular incision making horizontal cut at

the level of condylar neck preserving the vital structures on the medial side of
condylar neck. Resection of part of condyle should be done on ramus side
below and upper fibrous attachment side above. Smoothening of the resected
bone is done and the wound closed in layers (Fig. 39.15).
FIGURE 39.15 Condylectomy.
Disadvantages
• Loss of vertical height of the ramus.
• In case of bilateral condylectomy, it may create an anterior open bite.
• In unilateral cases, there may be deviation of the jaw on opening.
Gap arthroplasty
Ankylosis is a synarthrosis and hence the first attempt at ankylosis release
consists of simple bone division to separate the ramus from the cranial base
and creating a pseudoarthrosis (Fig. 39.16). However, the high osteogenic
potential of the bone margins promotes reunion between the osteotomised
segments, in an attempt to reduce the union between the bone margins.
• The width of bone removal is crucial and there are different opinions
regarding the amount of bone removal. Several authors recommend a
minimum gap of 1 cm, to prevent reankylosis.
• Because of the high recurrence rate of ankylosis following simple bone
division, the osteoarthrectomy, or the gap arthroplasty, was conceived
in an effort to reduce recurrence rates by increasing the distance
between the osteotomised bone ends of the ramus and cranial base.
Judicial amount of tissues should be removed; unnecessary removal of
functional muscles restricts the mobility of the mandible, a shortened
ramus resulting in open bite and a possible pit defect in the back of the
jaw.
• The commonest causes of reankylosis are inadequate resection of
ankylotic mass, failure to interpose a soft tissue material, failure to
identify ipsilateral and contralateral coronoid hypertrophy and
inadequate physiotherapy.
• Even when the gap is enlarged, the masticatory muscles further exert a
pull on the mandible, drawing it closer to the cranial surface, bridging
the gap between the raw surfaces, hence it is necessary to introduce an
inert material as ‘interpositional material’ between the two raw bone
surfaces in close proximity to each other and in an environment
conducive to fibrosis and callus formation, to prevent the fusion of the
margins to maintain the pseudoarthrosis.
FIGURE 39.16 (A) Illustration showing gap arthroplasty. (B)
Preoperative CT showing TMJ ankylosis. (C & D) Intraoperative
view showing gap arthroplasty with Excised specimen.
Interposition arthroplasty
Gap arthroplasty with various interpositional materials is the widely followed
corrective surgery for TMJ ankylosis.
Hence, interposition arthroplasty was the choice of treatment. The selection
and preference of interposition material had been a controversial subject over
the decade.
Common interpositional grafts used in TMJ ankylosis

(Flowchart 39.3)
Autogenous
• Muscle (temporalis, pterygomasseteric sling).

• Fascia (temporalis, fascia lata, dura).
• Skin (dermis, full thickness).
• Cartilage: Auricular, costal, iliac crestal cartilage.
• Sternoclavicular, metatarsal bone grafts.
• Fat (groin, buccal).
• Combined (muscle and fascia with or without periosteum).
FLOWCHART 39.3 Materials used for interpositional arthroplasty.
Allogenic (cryopreserved, freeze dried or lyophilised)
• Cartilage: Costal (costal cartilage)

• Dura
Alloplastic
• Metallic (titanium, gold and tantalum)

• Silastic
• Acrylic
Xenograft (bovine)
• Collagen
• Cartilage
Autogenous interpositioning material

Autogenous interpositioning materials are the most commonly used.
Costochondral grafts in the treatment of TMJ ankylosis
The costochondral graft had been used for reconstruction of TMJ over the
years. Gillies in 1920 used the costochondral grafts in temporomandibular joint
reconstruction. The advantages of costochondral grafts are the biological
compatibility, simple work technique, accessibility, functional adaptability,
versatility and minimum additional morbidity for the patient.
This graft is similar in its structural and physical properties of that of
mandibular condyle. The concept of transplanting growth centre is with the
hope of the graft growing in correspondence to contralateral TMJ, thus
preventing facial asymmetry and avoiding abnormal occlusion.
Kaban has stated the advantages of costochondral grafts (CCG) as follows:
1. As an autogenous material, eliminating the possibility of a foreign body

reaction.
2. A cartilaginous articulating surface.
3. The possibility of permanent bony union and biologic remodelling in
response to function.
4. Growth potential.
5. Minimal donor site morbidity.
Complications associated with the usage of this graft are donor site
morbidity, such as pneumothorax, pleuritic pain and the unpredictability of
fate of the graft.
The costochondral junction known as the rib growth-steering centre
generally is expected to develop in length equal to the normal side of the
mandible. However, the graft tends to grow unpredictably resulting in various
growth anomalies in the graft (Flowchart 39.4).
FLOWCHART 39.4 Fate of CCG.
1. Overgrowth in length
This complication occurs when the transplantation is done during the growth
spurt.
2. Overgrowth in mass
Overgrowth in mass of the cartilage part of the costochondral graft has also
been observed.
3. Undergrowth of graft
The graft sometimes tends to grow at a rate lesser than contralateral normal
condyle.
4. Reankylosis
The rate of reankylosis after costochondral rib grafting is most common in
adult patients, especially individuals with multiple previous operations
because this patient population is prone to heterotopic bone formation.
Autogenous fat
In 1914, Murphy reported the usage of autogenous fat for interpositioning
after lysis of TMJ ankylosis and Rattan V (2006) has published reports
favouring the use of fat grafts in the TM joint after release of ankylosis.
Dimitroulis postulated that the fat grafts are normally fragile, is less compliant
when placed alone, when it is harvested and placed in situ along with the
dermis, it is more stable and easily handled in the operative site such as in gap
arthroplasty. When dermis fat graft is harvested from groin, the graft is
convoluted on itself with the dermis surfaces brought together. The
subcutaneous fat is cut precisely to fill the gap, the dead space after gap
arthroplasty. The advantages of dermis fat grafts were reduced rate of
reankylosis and infection, minimal donor site morbidity, easy sculpting of
graft according to requirement and the hidden scar.
Fate of the CCG (Flowchart 39.4)
Author Reasons
Peltomak and The growth potential of the costochondral grafts is dependent on the height
Hakkinens of the cartilaginous portion.
(based on a From various studies on human costochondral junction, it has been
series of rat suggested that the interval between the bone–cartilage junction to the
experiments) germinative zone should be approximately 0.4–0.5 cm depending on:
• Function of the mandible
• Inherent growth capacity
• Hormonal factors
Kaban and In order to retard the chance of bony reankylosis, 3–4 mm of cartilage on the
Perrott graft is adequate, provided a centre of growth is present in the graft. It also
causes remodelling of the ramus condyle unit. Placement of a graft cartilage
longer than needed results in overgrowth of the grafted sites with mental
deviation
Tideman and The incidence of costochondral junction and overgrowth of the graft following
Doddridge reconstruction surgery may be lessened by the use of smaller cartilage cap
Peltoma The trigger factor for growth is accelerated by the presence of excessive
cartilaginous part in the graft and may be responsive to intrinsic or local factor
Auricular cartilage
The graft is biologically inert, with sufficient bulkiness, will remain viable and
can partially compensate for partial loss of the condyle. Its concavo-convex
shape can fit the anatomy of the fossa. The graft seemed resistant to pressure
and its smooth surface is supposed to allow sliding movement.
The auricular cartilage has the advantage of being harvested in the same
surgical field, reported to be viable and its contour was adaptable to the
articular fossa after gap arthroplasty. The authors have also reported difficulty
in stabilisation, excessive elasticity and thinness, with susceptibility to
perforation or fracture of the graft. Moreover, the ear cannot yield enough
cartilage to cover type IV ankylosis defects without losing its dimensional
stability. Therefore, donor site deformity cannot be ruled out.
Temporalis muscle flap

The temporalis muscle flap is the commonest interpositional material used in
the treatment of ankylosis. The advantages of the temporalis muscle flap are
its ease of elevation, reliable blood supply, proximity to the maxillofacial
structures and camouflage of the incision within the hairline. It is a workhorse
and has been extensively used for craniofacial reconstruction of the orbit,
palate, buccal tissue and even for facial reanimation (Fig. 39.17).
FIGURE 39.17 (A) Preauriculotemporal incision extending from the
preauricular skin fold slightly superoposterior to the helix. (B)
Temporalis composite pedicle flap dimension extends towards the
posterior temporal region. (C) Elevation of the flap. The flap edges
are coaptated with multiple 4–0 Vicryl suture to prevent separation
and shredding. (D) The muscle flap is turned into the glenoid fossa.
(E) The flap is secured in place with multiple sutures through
residual medial distal tissues and transosteal tissues and
transosteal suture through the lateral rim of the zygomatic arch.
The periosteal surface lines the glenoid fossa and the fascia
surface faces the condylar surface.
The proximity of the temporalis to the operative site, its attachment to the
coronoid process and it receives blood from the internal maxillary artery
which passes through deeper layer of the muscle enables it to be turn around
without any implication to its vitality. In addition, the fan-shaped muscle itself
and the deep temporal fascia over it provide a protective covering.
Pogrel and Kaban in 1990

The flap which may be of only fascia or both fascia and muscle is
circumvolved lower to the zygomatic arch and into the synovial space. The
zygomatic arch may be slightly thinned off to reduce the heftiness.
Balaji SM in 2003 reported favourable results using modified temporalis
muscle anchorage in craniomandibular reankylosis, which was followed up
for 6 years (Figs. 39.18–39.22). In this method, the muscle flap was placed
between the bony stumps and the distal border of the muscle was sutured to
the submandibular tissue.
FIGURE 39.18 Temporalis myofascial flap raised.

FIGURE 39.19 Temporalis flap prepared for interposition and
anchorage.
FIGURE 39.20 Proposed mechanism of Frey syndrome.
FIGURE 39.21 Temporalis flap interpositioning.
FIGURE 39.22 Submandibular anchorage of temporalis flap.
The modified temporalis myofascial flap was believed to provide smooth

movement of the condyle and its function is closer to that of the original disc
than in the conventional TMF flap. Furthermore, the temporalis muscle
wrapped in the fascia is somewhat elastic, so it is suitable as a cushion in the
joint. Wrapping the muscle with the fascia also increased bulk of the flap.
Hence the elasticity and increased bulk of the flap can aid in the prevention of
postoperative open bite, which is caused by shortening of the ramus after
removal of the ankylotic mass.
Osteotomy of the zygomatic arch or tunnelling of the temporalis under the
zygomatic arch is done to prevent compression of the flap. The usage of the
temporalis flap had been proved with excellent surgical results in the
management of the most difficult TMJ ankylosis cases and in patients having
undergone multiple operations.
Advantages
1. Muscle grafts are viable when pedicled on their own blood supply; the
temporalis is shown to have rich blood supply from three arteries and
when procuring the muscle flaps inferiorly based on deep temporal
arteries, the graft was proven to be viable.
2. The proximity of the muscle to the temporomandibular joint eases the
surgical procedure.
3. The adequate dimensions of the muscle provide a robust graft of
adequate thickness when combined with its fascia.
4. The fan-shaped nature permits a wide arc of rotation.
5. There is possibility of stabilising the graft when secured with sutures to
the pericapsular tissues or the adjacent structures of the joint.
6. Though temporal hollowing was noticed in some cases, no other donor
site morbidity was associated nor complications were encountered.
Complication of TMJ ankylosis surgery
Intraoperative
• Haemorrhage (damage of any superficial temporal vessels, transverse

facial artery, inferior alveolar vessels and internal maxillary artery,
pterygoid plexus of veins, etc.)
• Damage to the external acoustic meatus
• Damage to the parotid gland (salivary gland fistula)
• Damage to the auriculotemporal nerve (Frey syndrome)
• Damage to the zygomatic and temporal branch of facial nerve
• Damage to the teeth
Postoperative
• Infection
• Open bite
• Reankylosis (recurrence)
Frey syndrome
• Facial neuropraxia
• Venous thrombosis
• Otitis externa and otalgia
• Facial scarring
Auriculotemporal syndrome, Baillarger syndrome, Dupuy syndrome,
Gustatory sweating syndrome.
Frey syndrome is characterised by unilateral flushing and sweating of the
facial skin innervated by the auriculotemporal nerve (neck, parotid region and
frontotemporal scalp), which occurs in response to gustatory or olfactory
stimuli. [Gustatory sweating] (Fig. 39.20).
Aetiology
• In infants, trauma to the auriculotemporal nerve during forceps-

assisted delivery
• Congenital aberration of the auriculotemporal nerve fibres, between
the parasympathetic and sympathetic pathways
• Parotid surgery, especially after excision of the superficial lobe or
drainage of a parotid abscess.
• TMJ surgery
• Rare causes like mandibular condylar fracture, blunt trauma, herpes
zoster, associated CNS disorders such as syringomyelia, epilepsy and
meningioma of the cerebellopontine angle tumour.
Pathophysiology
Auriculotemporal nerve is a sensory branch of the posterior division of the
mandibular division of the trigeminal nerve. It receives the postganglionic
parasympathetic secretomotor fibres from the otic ganglion, for parotid
glands. Damage to these autonomic fibres causes misdirection of regenerating
parasympathetic fibres to join with the sympathetic fibres of the great
auricular nerve (7th nerve), which supplies sweat glands and blood vessels,
during the process of healing. Because of this, any gustatory stimulus
produces erythema and sweating instead of salivation.
Diagnosis
Suspicious area is painted with iodine and allowed to dry and then dusted
with corn starch or potato flour. Sweating is then encouraged via sialogogue
(lemon). If positive, the reaction causes change of colour from yellow to black.
Treatment
Topical
• Antiperspirant—for mild symptoms

• 20% aluminium chloride for a period of 1–2 months
• Anticholinergic—topical glycopyrolate
Intradermal
Intradermal injection of Botulinum Toxin A. Response may last for a period of
6 months. If the treatment is unsuccessful, then surgery is considered.
Radiation
Radiation of 50 Gy indicated for symptomatic patients.
Surgery
• Auriculotemporal nerve resection

• Tympanic neurectomy
Reankylosis
Cause
• Insufficient gap between the resected fragments

• Fracture of the reconstructed costochondral graft
• Loosening of costochondral graft due to inadequate/improper fixation
to the ramus
• Inadequate coverage of glenoid fossa in interpositional arthroplasty
• Inadequate postoperative physiotherapy
• Naturally higher osteogenic potential with high rate of periosteal
osteogenesis causes recurrence in children
Postoperative physiotherapy
Kaban et al. suggest that the success of the meticulous surgical reconstruction
is dependent on good physiotherapy and patient acceptance. And hence early
physiotherapy is important in disrupting adhesions and subsequent soft tissue
contractions.
Alloplastic
Silicone
As in the case of alloplastic condylar prosthesis, chronic inflammatory giant
cells, reactions with lymphadenopathy, tendency to slip from its implanted
site with proclivity to fragmentation and reankylosis have been reported
following the usage of silicone as an interpositional material.
Acrylic
Borcbakan (1968) pioneered the acrylic condyle for surgical management of
TMJ ankylosis. The usage of acrylic is a simple and safe procedure. But
displacement, extrusion and risk of reankylosis did not support this material
as a favourable material in interposition after gap arthroplasty.
Alloplastic TMJ prosthesis

Total knee and hip joint replacements have been successfully performed in
orthopaedic surgery. Surgical correction of TMJ ankylosis involves excision
and total reconstruction with alloplastic or autogenous materials.
The main advantage of the usage of alloplastic prosthesis over autogenous
grafts is that it obviates the necessity for the second surgical site. Hence, donor
site morbidity is not a problem.
Alloplasts are fabricated as an exact replica of the anatomic structure which
will restore the form and function of the structure when placed in situ. They
are adapted to their related bony surfaces than that of autogenous grafts.
Active jaw movements can be done by the patient in a day or two after
surgery. But the history of prosthetic TMJ replacements is distraught with
severe failures and patient rejections, withdrawals and much litigation. The
potential side effects of the alloplasts are infection, postoperative pain, loss of
joint mobility due to development of adhesions, resorption or erosion of
glenoid fossa, foreign body or allergic reaction to implant components and
displacement of implant.
The success of managing TMJ ankylosis depends on achieving mandibular
movements that are nearly normal and unrestricted mouth opening; however,
a deviation to the affected side usually remains from lack of lateral pterygoid
function. Rarely does this function return. Except for the unpredictable
growth-related disturbances, the costochondral grafting technique provides an
excellent ‘adaptive centre’ based on the functional matrix theory.
Management of secondary deformity

The secondary deformity of face results commonly from long-standing TMJ
ankylosis of paediatric onset. The deformity has both cosmetic and functional
effects. The cosmetic effects are borne by both mandible and maxillae. The
resulting occlusal cant, restricted mandible growth and secondary maxillary
undergrowth require both jaw surgeries. Simultaneous maxillomandibular
distraction or conventional orthognathic surgery is indicated. In case of functional
effect on the posterior pharyngeal airspace, TMJ ankylosis may be associated
with obstructive sleep apnoea, thus demanding management of both
conditions.
False ankylosis
False ankylosis is restriction of mandibular movement due to extra-articular
afflictions. Miller et al. (1975) classified false ankylosis into six groups:
1. Myogenic causes include fibrosis within muscles possibly due to an
organisation of an intramuscular haematoma.
2. Neurogenic group includes central nervous system lesions or
cerebrovascular accidents, which produce an inhibition of masticatory
muscle activity.
3. Psychogenic group refers to hysterical trismus.
4. Bone impingement will be caused by extra-articular malformations
such as exostosis of the coronoid process, zygomatic fracture
impinging on the mandibular movements.
5. Fibrous scar tissue can form in any soft tissue, which has been subjected
to trauma. Typical examples are those in the skin following thermal
damage or radiation therapy.
6. False ankylosis due to tumours depends on their site and nature.
False ankylosis:
1. Muscular trismus—pericoronitis, infection adjoining the muscles of

mastication involving submasseteric, pterygomandibular, infra-
temporal or submandibular spaces.
2. Muscular fibrosis—muscular fibrosis from any long-standing
dysfunction like arthritis and myositis.
3. Myositis ossificans—progressive ossification of muscles after injury and
haematoma formation especially of the masseter muscle results in
inability to open the mouth.
4. Tetany—hypocalcaemia causes the spasms of muscles producing
difficulty in opening of the mouth.
5. Tetanus—acute infectious disease caused by Clostridium tetani is
represented by an early symptom of lock-jaw because of persistent tonic
spasm of the muscles.
6. Neurogenic causes—neurogenic causes like epilepsy, brain tumour and
embolic haemorrhage in medulla oblongata causes hypomobility of the
jaw.
7. Trismus hystericus—disease of psychogenic origin.
8. Drug induced spasms—drug-induced spasms like in strychnine
poisoning
9. Mechanical blockade—mechanical blockade by osteoma or elongation of
the coronoid process of the mandible there by reducing its movement
under the zygomatic arch.
10. Fracture of the zygomatic arch—fracture of the zygomatic arch with
inward buckling.
11. Fracture of the mandible—trauma causing fracture of the mandible
leads to reflex spasm of the muscles and hence trismus.
12. Scars and burns of the face—scars and burns of the face also restrict the
movements of the jaw. Postirradiation fibrosis leads to hypomobility of
the mandible.
13. Cleft palate operations—produce fibrosis of the pterygomandibular
raphe and, consequently, limitation of mouth opening.
14. Submucous fibrosis—submucous fibrosis results in tense fibrous bands
in the cheeks which stretch from mandible to maxilla limiting movement
of the mandible, tongue and soft palate.
Treatment of false ankylosis

Use of mechanical aids from simple acrylic screw wedge to more complicated
exercises is beneficial.
CHAPTER 40
Internal Derangements
and Condylar
Dislocation

Clinical and diagnostic features of internal derangement
Aetiology
Trauma
• Macrotrauma
• Microtrauma
Pathogenesis of internal derangement
Condylar dislocation
Pathogenesis
Causes of dislocation
Extrinsic causes
• Trauma
• Occlusal factors
• Connective tissue disorders
• Psychogenic
• Drugs
Clinical features
Management
Internal derangement is defined as a disturbance in the normal anatomical

relationship between the disc and the condyle that interferes with smooth
movement of joint and cause momentary catching, clicking, popping, locking.
This condition was first described by Hey and Davies (1814) as a localised
mechanical fault interfering with smooth action of a joint.

When the mouth is opened, the mandibular heads rotate around a common
horizontal axis in combination with a gliding forward and downward
movement in contact with the lower surface of the articular discs.
Simultaneously, the discs move both forward and downward on the
temporal bones. This results from the attachments of each disc to the lateral
and medial poles of the condyles and from the contraction of the lateral
pterygoid. The forward gliding of the disc ceases when the posterior
attachment to the temporal bone has been stretched to its limits.
Thereafter, further hinging and anterior gliding movement of each condyles
continues until they articulate with the most anterior part of the disc and the
mouth is open fully (Fig. 40.1)
FIGURE 40.1 Temporomandibular joint articulation (i) in closed

position, (ii) in open position.
While closing the mouth, the movements are reversed. In the first phase,
each mandibular head glides backwards and then hinges on its disc, which is
held forward by the lateral pterygoid. Finally, this relaxes to allow the disc to
glide backwards and upwards on the temporal bone.
Etiopathogenesis
TMJ disc derangements can be classified into four clinical settings:
• Disc incoordination,
• Disc displacement with reduction,
• Disc displacement without reduction and
• Anchored-disc phenomenon.
Disc incoordination
Disc incoordination represents the earliest indication of an increase in the
frictional properties of the joint. The patients often describe the need to
perform a special maneuver to achieve a normal opening of the mouth, or they
may complain of an annoying terminal jolting sensation associated with
mandibular closing. Usually there is no pain, but when present, it is typically
not chronic and appears to be related to the instability of the condyle-disc
relationship (Fig. 40.2A,B).
Disc displacement with reduction

Disc displacement with reduction is a condition in which the articular disc has
usually moved in an anteromedial position following the shape of the condyle
and anterior slope of the glenoid fossa as well as the influence of the lateral
pterygoid muscle. Posterior, medial and lateral displacements can also occur.
Reduction refers to the ability of the condyle to negotiate around the disc, with
the ability of the disc to assume a normal position in relation to the condyle
and glenoid fossa. Normally in these patients, mouth opening is accompanied
by a clicking or popping sound that is produced as the condyle passes over the
posterior portion of the disc and it returns to a normal position. Clicks are
typically reciprocal, occurring both during mouth opening and during mouth
closing and patients do not have pain.
Disc displacement without reduction

In disc displacement without reduction (closed lock), mouth opening becomes
limited as the mandibular condyle fails to pass over the posterior band of the
articular disc. In symptomatic patients, the overloading and stretching of the
highly innervated retrodiscal tissue elicits pain at the affected joint.
Mandibular deviation to the affected side can be observed in unilateral cases.
Anchored disc phenomenon

The anchored disc phenomenon, or acute disc displacement without
reduction, is characterized by a sudden, severe and persistent limited mouth
opening that is considerably more decreased than disc displacement without
reduction (10 - 30mm).
Wilkes Classification for Internal Derangement of the TMJ
Stage Characteristics Imaging

I. Early Painless clicking Slight forward disc
No restricted Normal osseous contours
motion
II. Occasional Slight forward disk
Early/Intermediate painful clicking Early disk deformity
Intermittent Normal osseous contours
locking
Headaches
III. Intermediate Frequent pain Anterior disk displacement
Joint tenderness Moderate to marked disk thickening
Headaches, Normal osseous contours
Locking
Restricted motion
Painful chewing
IV. Chronic pain, Anterior disk displacement
Intermediate/Late headache Marked disk thickening
Restricted motion Abnormal hone contours
V. Late Variable pain, Joint Anterior disk displacement with disk perforation
crepitus and gross deformity
Degenerative osseous changes
In this condition the disc is not anatomically displaced and a suction-cup

effect occurs, where the disc becomes adherent to the articular eminence due
to a vacuum effect in the joint space, and the presence of increased joint
viscosity.
Clinical and diagnostic features of internal

derangement
• History of severe pain on yawning
• History of direct trauma to the joint years earlier
• Clicking sound in the joint during mouth opening and closure. (The
clicking sound was earlier considered characteristic of internal
derangement with reducing disc, though now not significant)
• Joint tenderness, especially with function
• Deviation to affected side: This characteristically occurs in disc
displacement with or without reduction
• Disc displacement with reduction: After the initial 10 mm of mouth
opening (rotation or hinge) jaw deviates to affected side (Tables 40.1,
40.2)
• Disc displacement without reduction: Jaw deviation starts from the
initiation of mouth opening and progresses till end of mouth opening
• Trismus: Present only in disc displacement without reduction
• Elimination of pain following local anaesthesia of the affected joint
Table 40.1
Staging of internal derangement—Wilkes

Stage I Early reducing disc displacement
Stage II Late reducing disc displacement
Stage III Nonreducing disc displacement—acute/subacute
Stage IV Nonreducing disc displacement—chronic
Stage V Nonreducing disc displacement with osteoarthrosis
Table 40.2
Comparison of disc displacement and MPDS
A condition called myofascial pain dysfunction syndrome is a clinical entity

closely related to internal derangement. These two conditions are difficult to
differentiate but with varied treatment strategy.
Aetiology
Trauma
Trauma to the TMJ can be macrotrauma or microtrauma according to
magnitude of the traumatic force.
Macrotrauma
Macrotrauma can be direct or indirect.
Direct trauma
• Trauma to mandible in open mouth position

• Can also be iatrogenic
▪ Intubation procedures
▪ Third molar extractions
▪ Long dental appointments
▪ Overextension of jaw as yawning
Indirect trauma
Cervical flexion-extension injury
Microtrauma
• Bruxism or clenching
• Malocclusion—traumatic
Pathogenesis of internal derangement

• Internal derangement is a progressive anterior and medial subluxation
of meniscus from its normal position at rest (Fig. 40.2).
• Previous trauma may lead to stretching of lower lamina of bilaminar
zone, allowing posterior band to sublux forward in relation to
condylar head in centric relation. The first abnormality seen is a click
on opening.
• The open click represents the posterior band relocating posteriorly
over the condyle from its subluxed position.
• Pain at this stage represents the meniscus beginning to lose its
insertion into lateral pole.
• Following further trauma (acute or chronic), the meniscus subluxes
progressively forwards and medially, so that it cannot regain its
position over condylar head on wide opening.
• Inflammation associated with damage to meniscal attachments and
joint surface by incorrect positioning of meniscus leads to formation of
exudates and eventual adhesions and fibrosis. This fibrosis maintains
meniscus in subluxed position and the joint becomes locked.
FIGURE 40.2 (A) Representation of reciprocal clicking, secondary

to anterior displacement with reduction. (B) The closed-lock
position, secondary to anterior displacement without reduction.

This is a condition characterised by no organic disease of the joint but
characterised by clinical findings similar to internal derangement. (Refer
Chapter 38 TMJ Disorders).
Condylar dislocation (Condylar dislocation,

Subluxation, Hypermobility of TMJ)
Dislocation of the TMJ occurs when the mandibular condyle is displaced
anteriorly beyond the articular eminence and its inability to descend back to
its normal position. In 1832, Sir Astley Cooper proposed principles for
diagnosis and treatment of dislocation and introduced the terms complete
dislocation and imperfect dislocation (subluxation).
Dislocation is classified as follows:
1. Based on Position
– Anterior
– Posterior
– Medial
– Lateral
– Superior
2. Based on symmetry
– Unilateral
– Bilateral
3. Based on number of occurrences
– Recurrent
– Non-recurrent
4. Based on aetiology
– Traumatic
– Nontraumatic (spontaneous)
5. Based on time of presentation
– Acute
– Chronic
• Subluxation is defined as a displacement of condyle out of the glenoid

fossa and anterosuperior to the articular eminence, which can be
reduced by the patient (self-reduced). It may be unilateral or bilateral.
• True dislocation is one in which the patient cannot reduce it by himself
and requires expert assistance for reduction.
• Habitual or recurrent dislocation refers to frequent and repeated episodes
of recurrent dislocation that can be manipulated back into position
(Fig. 40.3). Also referred as Subluxation or hypermobility.
• Dislocation can be unilateral or bilateral.
FIGURE 40.3 Dislocation of the mandible.
Subluxation—incomplete dislocation
Luxation—dislocation
Recurrent dislocation—repeated dislocation with no strong psychological
components
Pathogenesis
The stability of any joint depends on three factors:
1. The integrity of ligaments associated with the joint: Laxity of the

temporomandibular ligament and joint capsule predisposes the joint to
dislocation. Looseness of the capsule and ligaments can result from
inadequate healing from injury and from long standing degenerative
joint disease.
2. Dyssynchronous muscle function: Abnormalities of neuromuscular
mechanisms which control the muscles of mastication may be
associated with dislocation. The condyle protractors fail to relax as the
condyle reaches its most anteroinferior position in relation to the
articular eminence on opening and the elevators simultaneously
contract to dislocate the mandible into the infratemporal fossa. Spasm
of the lateral pterygoid and other muscles of mastication when the
condyle reaches the crest of articular eminence on its return to glenoid
fossa causes dislocation.
3. Bony architecture of the joint surfaces: Myrhaug observed that a deep
overbite was frequently associated with a deep glenoid fossa and a
steep articular eminence, which may be conducive to dislocation.
The disc-condyle relationship also plays a role in TMJ dislocation,

principally in patients with anterior disc dislocation with reduction. It occurs
as a result of the condyle snapping over the posterior surface of the disc at or
near the apex of the articular eminence and then translating over the anterior
edge of disc beyond the eminence. The disc comes to rest between the
eminence and posterosuperior surface of the condyle, causing a mechanical
block and preventing the return of the condyle to the glenoid fossa.
• Laxity of ligaments
• Capsule and ligament injury
• Nonsynchronised muscle function
• Morphologic condition of condyle and eminence
Causes of dislocation
• Intrinsic causes
• Extrinsic causes
Intrinsic causes
Joint overextension predisposing to dislocation may be caused by wide jaw
opening as in yawning, vomiting, singing/laughing loudly, blowing wind
instruments, and seizure disorder. It is associated with spasm of lateral
pterygoid and other muscles of mastication resulting in locking of condylar
head into abnormal anterior position in the infratemporal fossa causing
inability to close the mouth.
Extrinsic causes
Extrinsic trauma may also result in dislocation with injury to capsule and
ligaments.
Trauma
• Injudicious use of gag during intubation for general anaesthesia (GA)

• Dental extraction
• Flexion-extension injury to the mandible
• Endoscopy
Occlusal factors
• Excessive tooth abrasion

• Severe malocclusion
• Loss of dentition (leading to overclosure and loss of vertical
dimension)
Connective tissue disorders
• Hypermobility syndrome
• Ehlers-Danlos syndrome
• Marfan syndrome
Psychogenic
• Habitual dislocation
Drugs
• Antipsychiatric drugs
• Phenothiazines—may produce extrapyramidal effects resulting in
spasm
Miscellaneous causes
• Internal derangement
• Dyssynchronous muscle function
• Contralateral intra-articular obstruction
• Loss of vertical dimensions
Clinical features
• Inability to close the mouth
• Preauricular depression evident on the skin
• Excessive salivation
• Tense, spasmatic muscles of mastication
• Severe pain of the TMJ
• Condyle palpable anterior to articular eminence
These are the features common to acute/chronic dislocation and

unilateral/bilateral cases.
Unilateral dislocation
• Mouth is open and the mandible deviated to the opposite side.

• Deviation produces lateral cross and open bite.
• Teeth cannot be closed into occlusion.
• Difficulty in mastication and swallowing.
• Affected condyle is impalpable.
• Drooling of saliva with speech difficulty.
Bilateral dislocation
• Pain
• Difficulty in speech and excessive salivation.
• Drooling of saliva due to difficulty in swallowing.
• Mouth opens in protruded position.
• Restricted range of mandibular movements.
• Bilateral preauricular hollow.
• Gagging of occlusion (molar teeth)
• Anterior open bite
Diagnosis
• Clinical history and examination
• Radiological examination
▪ OPG
▪ TMJ views
▪ Plain and contrast CT
▪ 3D CT
▪ MRI
Management
Management can be nonsurgical and surgical.
Conservative management should be done before employing aggressive
therapies, It is necessary to reduce tension, anxiety or muscle spasm by
reassuring the patient and prescription of sedatives or tranquilizers.
Nonsurgical management
Acute dislocation
Acute dislocation requires immediate treatment. Manual reduction can be
done with or without the use of local anaesthesia immediately or within 72 h.
Beyond that duration reduction may be done under sedation/LA or general
anaesthesia.
Dingman and Natwig: recommended use of local anaesthesia based on the
theory that dislocation is maintained by muscle spasm secondary to painful
stimuli arising from the capsule. On injection of ligno-caine into the glenoid
fossa or the muscles of mastication, sensory reflex mechanism of the joint is
blocked and the muscle spasm is overcome respectively.
Reduction-Nilaton technique: (Fig. 40.4) The patient is made to sit upright in
a chair with the clinician standing in front, sometimes behind based on
convenience. The thumbs of the clinician are covered with gauze or a
protective covering and positioned over the lower molar teeth bilaterally. The
index fingers are placed under the inferior border of the mandible. The
posterior aspect of the mandible is depressed inferiorly to depress the condyle,
while the chin is elevated anteriorly and the entire mandible is pushed backwards with
the palm. The mandible is moved downward backwards and then upwards, thus
manipulating the condyle back into position (Fig. 40.5). After reduction, the
mandible should be immobilised using Barton’s bandage for several days to
allow for capsular repair, muscle rest, and prevention of recurrence.
FIGURE 40.4 (A) Nilaton’s technique of reduction padding of the
operator’s finger (thumb) before reduction (using gauze). (B)
Anterior bilateral dislocated condyle with inability to occlude. (C)
Padded thumbs placed over the occlusal surface of the mandibular
molars (Step 1). (D) Padded thumb placed over the external
oblique ridge buccal to the mandibular molars to avoid injury.
(E&F) Other fingers of the hand grasp the mandible supporting the
lower border, the palm of the hand placed against the chin.
Reduction including downward, backwards and upwards motion of
the dislocated mandible. (G) Barton’s bandage.
FIGURE 40.5 Hippocratic method or the Bimanual mandibular
manipulation in a downward-posterior direction to disengage the
condyle from its open locked position posterior to the articular
eminence.
Other methods of reduction include wrist pivot reduction or by use of

interdental bite blocks.
• In cases of bilateral dislocation, the reduction can occur simultaneously

or one at a time.
• Can also be done under GA with the help of muscle relaxants.
• Use of sedatives and tranquillisers prior to manipulation also helps in
facilitating reduction.
• IMF for 10–14 days after reduction is recommended to allow
inflammation and oedema to subside and prevent redislocation.
Chronic/long standing dislocation

Encountered mainly in elderly persons. Long standing/chronic dislocation
over time develops fibrous adhesions between the disc, condyle and articular
eminence. Jaw muscles and ligaments also undergo fibrous change, preventing
nonsurgical reduction.
• Manual reduction assisted by use of GA and a muscle relaxant is

helpful.
• If this fails, then an open reduction should be considered.
• A hole is drilled and a traction wire is passed through the inferior
border of the ramus or a hook placed in the sigmoid notch (Finck’s
technique) to aid in distracting the condyle inferiorly and repositioning
the condyle into the fossa.
• Older techniques include use of Astley Cooper’s basculation and
Stromeyer’s forceps.
• Condylotomy can also be done either by a blind (Gigli saw) or open
approach.
• Bilateral ramus osteotomy can be done to restore the occlusion, leaving
the condyles in dislocated position.
Chronic recurrent dislocation
• IMF for a prolonged period of 4–6 weeks, but relapse occurs.

• The laxity of the capsule and the ligaments can be corrected by chemical
capsulorrhaphy by using 0.5% sodium tetradecyl sulphate. This causes
pericapsular fibrosis, limiting excursion of condylar head.
• Surgical correction is the ideal treatment for these cases.
Surgical management
Surgical procedures can be divided into 5 categories by MILLER & MURPHY
1976:
I. CAPSULE TIGHTENING PROCEDURE:

a. Capsulorrhaphy: Shortening capsule
b. Vertical incision and overlapping of capsule
c. Turning downward & suturing a strip of temporal fascia
II. CREATION OF NEW MUSCLE BALANCE:
a. Shortening & scaring of muscles
III. DIRECT RESTRAIN OF CONDYLE:
a. Temporalis fascia sutured to capsule
b. Sling of fascia lata threaded through hole in zygomatic arch
and hole in condyle and tightened
IV. REMOVAL OF MECHANICAL OBSTRUCTION:
a. Meniscectomy
b. Condylectomy
c. Eminectomy by Myrhang (1951)
V. CREATING MECHNAICAL OBSTRUCTION
a. LINDERMAN: Osteotomy turning down the articular
eminence
b. MAYER: Placement of graft from zygoma to emnence
c. DAUTRY: Osteotomy of zygomatic arch and down fracture
d. FINDLEY: Inserting a L-shaped pin in zygoma process:
I. Capsule tightening procedure
1. Use of sclerosing agent: Injection of sclerosing agent into the capsular

space of the TMJ. The aim is to cause fibrosis with resultant tightening
of the capsule, which could prevent or limit exaggerated condylar
movement.
• Alcohol, tincture of iodine, 5% sodium psylliate, sodium
morrhuate, 3% sodium tetradecyl sulphate and autologous
blood have been used.
• Associated with side effects like pain, muscle tenderness,
temporary nerve paresis and excessive salivation.
• IMF may be used as an adjuvant treatment to aid in the
development of mature fibrosis within the joint.
2. Strengthening of the ligaments by surgically exposing the temporalis
fascia and suturing a flap of fascia onto the capsular ligament.
3. Capsular plication: This involves exposure of the capsule, followed by an
incision vertically through the body of the ligaments. The incision
margins are then overlapped and sutured. This technique violates the
joint cavity. To overcome this, several sutures are placed along the
inferior aspect of the capsule, to tighten the capsular ligaments
(Fig. 40.6).
4. Ligamentorrhaphy: This technique involves anchoring the lateral
ligaments of the capsule to the periosteum of the zygomatic arch,
followed by IMF for a week.
5. Capsulorrhaphy: Surgical shortening of capsule.
FIGURE 40.6 Capsular plication. The exposed lateral capsule is
incised. (A) T shaped incision on the capsule. (B) Inverted
L shaped incion.
II. Creation of new muscle balance
1. Active physiotherapy to strengthen the suprahyoid muscles thereby

counterbalancing the action of the lateral pterygoid muscle.
2. Injection of 500 mouse units of type A Botulinum toxin 1 cm anterior to
the condyle in a slightly open mouth position, so as to inject into the
lateral pterygoid (around 100 mouse units every 2–4 months to achieve
long-term effects). The aim is to weaken the lateral pterygoid muscle
sufficiently to prevent dislocation. Contraindicated in patients with
impaired neuromuscular function.
3. Lateral pterygoid myotomy: First described by Boman. In this technique,
the attachment of the muscle to condylar neck and anterior aspect of
disc is exposed and divided, followed by IMF for 7–10 days. The
disadvantage is loss of translator movement in the joint (Fig. 40.7).
4. Closed condylotomy: (Tansen and Lamber) to affect the lateral pterygoid
muscle indirectly. A Gigli saw is used intraorally to bisect the condylar
neck thus eliminating the effect of spasticity of lateral pterygoid.
However, there is a potential for bleeding from the internal maxillary
artery.
5. Shortening of all muscles by severing & scar formation
FIGURE 40.7 (A) Lateral pterygoid myotomy. (B) Silastic band is
applied to prevent reattachment.
III. Direct restrain of condyle
1. Georgiade advocated ligation of the coronoid process to the zygomatic

arch anterior to the articular tubercle.
• Two holes are drilled; one into the condylar neck and the
other into the zygomatic arch.
• A Dacron mesh suture is passed through the 2 holes and
tightened, thereby restraining the condyle.
2. Scarification of the temporalis tendon at its area of insertion: An intraoral
incision is made in the posterior regions along the external oblique
ridge. The tendinous fibres are dissected off from the ascending ramus
and sutured to the reflected periosteum and oral mucosa. The incision
is then sutured. This creates a horizontal scar which may tighten the
tendon and limit the range of motion.
This procedure is technique sensitive and associated with the risk of buccal
nerve hypoaesthesia.
IV. Removal of bony obstruction
1. Meniscectomy
2. Condylectomy: Reidel in 1883 performed the first condylectomy for
treatment of dislocation. Later Henny and Baldridge (1957) advocated
this procedure. It is an intracapsular procedure and involves removal
of the entire articular surface of the condyle, above the attachment of
the lateral pterygoid. The resulting pseudoarthrosis may limit the
range of mandibular motion. Use of chewing gum in early
postoperative period is recommended. Modification of this involves
condylectomy along with lateral pterygoid myotomy (Fig. 40.8).
Occlusion will return to normal after 4 weeks of surgery; if not,
selective grinding is done to eliminate premature contact.
3. Eminectomy: First introduced by Myrhaug (1951).
FIGURE 40.8 High condylar shave with; (A) Sagittal saw. (B) Bone
file.
This involves reduction of height of eminence to allow free forward and

backwards movements of the condyle. It is important to remove the most
medial part of the eminence. It does not interfere with internal structure of the
joint. Success rate is 100% (Fig. 40.9).
FIGURE 40.9 Eminectomy.
Complications: Pneumatisation of eminence and dural tear during its

removal
• Recurrent subluxation
• Formation of postoperative osteophytes
• Crepitus and pain
V. Creating mechanical obstruction
a. Glenotemporal osteotomy: Glenotemporal osteotomy of the TMJ

(Norman) with interpositional bone grafts is to augment the height of
the articular eminence for TMJ subluxation.
b. Dautry (1967): This involves down fracture of zygomatic arch just
anterior to the eminence (Fig. 40.10).
FIGURE 40.10 (A, B) Dautry’s procedure involving down-fracture of
the zygomatic arch.
Procedure: A preauricular approach is used to access the zygomatic arch.

Subperiosteal dissection is done over the arch.
An oblique cut is made through arch, running in a downward and forward
direction, to divide the lower border just anterior to eminence. Using
controlled pressure, the arch is first sprung laterally and then downwards to
fit into a groove on under surface of eminence. A greenstick fracture should
occur at the zygomatic temporal suture, thus giving the segment some
rebound elasticity to provide stability in its altered position.
It is preferred in younger individuals (<40) to reduce the likelihood of
sutural fracture because of increasing brittleness with age.
Advantages:
• Does not violate joint space

• Allows immediate normal anterior movement with little limitation in
maximal opening
Disadvantages:
• Risk of fracture of distal segment

• Resorption of distal segment
c. Mayer (1933) inserted bone grafts over eminence to increase the height,
thus blocking the movement of the condyle. A large piece of zygomatic
process is laid anterior to eminence and maintained by a groove in the
underlying temporal bone.
d. Iliac or calvarial bone grafts may be used to augment the eminence.
The capsule can be displaced posteriorly to create a space for graft
placement. Bone resorption is higher with iliac grafts.
e. Alloplastic graft: Use of vitallium mesh implants, miniplates and
silastic blocks to increase the height of the eminence.
f. Findlay advocated the use of ‘L’-shaped pins anchored to the zygomatic
process of temporal bone anterior to the condyle (Fig. 40.11).
g. Distraction osteogenesis Currently eminence augmentation using
distraction osteogenesis is under study.
FIGURE 40.11 The use of a L- shaped plate on the zygomatic arch

that acts as a mechanical hindrance to the condyle while opening
the mouth.
SECTION XI
Maxillofacial Trauma
Chapter 41: Emergency Management and Preliminary Examination of a

Trauma Patient
Chapter 42: Basic Principles of Management of Maxillofacial Trauma
Chapter 43: Dentoalveolar Fracture
Chapter 44: Fractures of the Mandible
Chapter 45: Maxillary Fractures
Chapter 46: Orbitozygomatic Complex
Chapter 47: Naso-Orbito-Ethmoid Fracture
Chapter 48: Frontal Bone Fractures
CHAPTER 41
Emergency Management
and Preliminary
Examination of a Trauma
Patient
Aetiology of maxillofacial injuries

Extrinsic causes
Intrinsic causes (pathologic fractures)
Basic principles in management of patients with maxillofacial
injuries – initial assessment
Primary survey
• A—Airway with cervical spine control and
• B—Breathing and ventilation
• C—Circulation with haemorrhage control
• D—Disability determined by a brief Neurological
examination
E—Exposure and complete examination of the patient
Examination of the oral cavity
• Soft tissue examination
• Neurological examination
• Skeletal examination
• Dental examination
• Soft tissue examination
• Neurological examination
• Skeletal examination
Imaging of maxillofacial injuries
Maxillofacial evaluation—summary
Maxillofacial injuries are relatively common form of trauma in everyday life,

so it is essential for us to know the primary care and definitive management
these injuries. The maxillofacial injuries can be simple or complex with
missing tissues. Early treatment and rehabilitation these injuries helps to
restore the form and function.
Severe trauma can lead to death. Death from trauma has a trimodal
distribution and follows the following patterns. The first peak of injury is
within seconds or minutes of the incident happening due to the injuries to the
brain, brain stem, high spinal cord, heart and great vessels. The survival
possibility is very remote.
The second peak occurs few minutes to hours after the incident. The critical
time from injury to the definitive surgical treatment is called the ‘golden hour’
of trauma. Deaths in this group can be preventable if proper remedies are
delivered for the conditions such as sub- and extradural haematomas or
haemopneumothorax. This golden hour can be enhanced by the level of
prehospital first aid and paramedical personnel aid at the site of an accident to
the trauma victim.
Aetiology of maxillofacial injuries

Road traffic accident is considered to be the primary cause of maxillofacial
trauma. The other causes are:
• Assaults
• Falls
• Sport injuries
• Gun shot and war injuries
• Work-related causes like industrial mishaps
• Miscellaneous causes
Maxillofacial fractures can be classified into: (i) extrinsic causes and (ii)
intrinsic causes.
Extrinsic causes
1. Direct violence (fracture at the site of impact).

2. Indirect violence (fracture caused due to transmission of impact, i.e.
countercoup fractures).
3. Due to excessive muscular contracture (e.g. fracture of coronoid due to
sudden reflex contracture in the temporalis muscle).
Intrinsic causes (pathologic fractures)

These are fractures that occur due to intrinsic weakness of the bone and not
due to force of impact. Pathologic fractures occur because of underlying bony
or systemic diseases.
Pathologic fractures are the fractures secondary to the bony or systemic
disease. Pathological fractures are caused by a slight rise in otherwise normal
forces such as bending, torsional, compressive or shearing forces. Most of the
times, the weight of the patient is enough to cause the fracture, especially in
the mandible, it may be chewing force resulting in a spontaneous fracture
without an apparent trauma. The bony pathology which are capable of
causing pathologic fracture are neoplasia, large bone cysts, osteoporotic bone,
osteoradionecrosis causes secondary to nutritional deficiencies,
hyperparathyroidism, localised chronic bone infection (chronic osteomyelitis),
osteoporotic bone due to disuse following prolonged external fixation or
removal of a rigid internal device.
Basic principles in management of patients with

maxillofacial injuries – initial assessment
The examination of patient with maxillofacial injuries takes place in three
stages:
1. Immediate assessment and treatment of life-threatening condition

2. General clinical examination of the patient
3. Local examination of maxillofacial and neck region
The two principles in the management of the severely injured patient are:
1. Prompt evaluation and management of life-threatening emergencies

2. To save life and to restore function
Patients with maxillofacial injuries may have sustained other bodily injury,
which may constitute an actual threat to life or be of higher priority than facial
trauma. It is therefore always necessary to make a rapid assessment of a newly
injured patient and institute any emergency resuscitation before proceeding
with a more detailed examination.
Maxillofacial injury, albeit rarely, threatens the patient’s airway and
constitutes the highest priority in the treatment schedule.
Trauma management consists of a rapid primary survey to identify
potential life-threatening conditions, the resuscitation of vital functions if
possible, followed by a more detailed secondary assessment and finally
initiation of definitive care.
Primary survey
During the rapid primary survey, life-threatening conditions are recognised
and treated without delay. They can be summarised by the ABCs.
A—Airway with cervical spine control

B—Breathing and ventilation
C—Circulation with haemorrhage control
D—Disability, neurological status
E—Exposure; complete examination of the patient
Maxillofacial injuries compromise the airway due to the following reasons:
1. Obstruction of nasal and oral airways by blood clot, saliva, bone, teeth
and part of dentures.
2. Inhalation of any of the above.
3. Obstruction of the nasopharynx and oropharynx by backward
displacement of tongue and its attachments as in symphyseal fractures
of the mandible.
4. Occlusion of the oronasopharynx by downward and backward
displacement of the fractured maxilla.
5. Soft tissue oedema of the face.
A—Airway with cervical spine control and B—Breathing and

ventilation
• The primary aim of airway management is to achieve maximum

oxygenation of the tissues. If the airway is compromised, attempts are
made to get a patent airway which includes a chin lift or jaw thrusting
manoeuvre and the removal of any foreign debris, either manually or
by the use of a portable suction machine. (Refer to Chapter 7 Medical
Emergencies and Their Management).
• It is very important to recognise the risk of cervical spine injury and to
prevent any movement of the cervical spine while attempting to
achieve a patent airway. Therefore, the patient’s head and neck should
not be hyperextended or hyperflexed to establish or maintain an
airway. It is better to assume a cervical spine injury in any patient especially
with a blunt injury above the clavicle unless proven otherwise. Cervical
injury can be excluded by appropriate radiographs. Until then a hard
cervical collar should be worn and supported by a sandbag and a tape.
• If airway obstruction is due to displaced and impacted fractured
maxilla, restoration of its normal position can be carried out by digital
disimpaction of the maxilla. This is done by placing the index and
middle fingers in the posterior choanae and drawing the maxilla
upward and forwards, with maintaining countertraction on the
forehead to ensure that cervical spine is not displaced.
• It is very important to recognise obvious respiratory distress signs as:
anxiety, tachypnoea more than 25/min, stridor, intercostal retraction,
using accessory muscles of respiration, hoarseness of voice, pallor,
tachycardia, an increase in blood pressure, signs of hypoxia,
hypercapnia, confusion, agitation, unconsciousness and cyanosis.
• If the patient is unconscious or has shown signs of altered
consciousness and is unable to maintain his/her airway above
measures, a definitive airway is indicated. This usually requires
endotracheal intubation but if this is not possible (e.g. in gunshot
injuries or missile injuries) then a surgical airway (tracheostomy) may
be required.
Airway management can be summarised as:
• Recognise the airway obstruction

• Positioning of the patient in a semiprone with head slightly lowered
posture
• Clear the nose and oral cavity by suctioning
• Give nasopharyngeal/oropharyngeal tube
• Tongue should be pulled out and jaw thrusting should be done
• Endotracheal intubation if the patient is unconscious
• Cricothyrotomy
• Tracheostomy
• Oxygen administration/artificial ventilation
C—Circulation with haemorrhage control

The initial step in managing haemorrhage is to minimise the blood loss by
controlling any obvious bleeding and minimise or prevent shock. Tachycardia
is the earliest measurable clinical sign because in the early stages the
circulatory response to blood loss is progressive vasoconstriction of the
cutaneous visceral and muscle circulation to preserve the blood flow to the
kidneys, heart and brain. At cellular level, cells compensate by shifting to
anaerobic metabolism, which contribute to the development of metabolic
acidosis. Correction of this state requires adequate oxygenation, ventilation
and appropriate fluid resuscitation.
Haemorrhage is best controlled by direct pressure on the bleeding point
applied via dressings and bandages or manual pressure. It is inappropriate to
explore wounds and tourniquet is contraindicated for the majority of wounds.
Intravenous access will be essential with large bore intravenous catheters (16
gauge or larger) inserted into a suitable peripheral vein in the antecubital fossa
or other accessible sites.
When the bleeding has been controlled, the lost fluid must also be replaced.
Ideally, the patient should be given whole blood that has been properly typed
and cross-matched. During initial fluid management, vital signs are assessed
while monitoring the blood pressure, pulse, urinary output and central venous
pressure. Majority of the fractures of facial skeleton are closed injuries and in
spite of the extensive nature of the skeletal damage, severe haemorrhage is
unusual. When there are extensive soft tissue lacerations, particularly missile
injury or assaults, these require urgent attention as local blood loss can be
considered.
Epistaxis (nasal bleeding) of some degree is an inevitable consequence of
injury to the central middle third of the face. It usually stops spontaneously or
is easily controlled by packing the nose through anterior nares using the
ribbon gauze soaked in saline or adrenaline 1:1000 strength but only problem
with adrenaline is the rebound haemorrhage. Profuse haemorrhage into the
nasopharynx from terminal branches of maxillary artery in association with Le
Fort I, II or III fractures. This may be life-threatening both from the point of
view of actual blood loss and obstruction of the airway. A postnasal pack is
needed in such extreme situation.
D—Disability determined by a brief Neurological examination

After the establishment of the airway and stabilisation of the cardiovascular
system, neurological examination is done to evaluate the level of
consciousness. Those patients who arrive in an unconscious state or, more
importantly, those patients who arrive alert and then become unconscious
should receive a rapid neurological assessment. To assess the patient’s level of
consciousness, the AVPU mnemonic can be used.
A: Alert
V: Responds to vocal stimuli
P: Responds only to painful stimuli
U: Unresponsive
In the unconscious patient, differential diagnosis has to be established

regarding the cause of unconsciousness.
A very rapid ‘mini-neurological’ examination, which can establish the
patient’s level of consciousness, pupil size reaction to light and the presence or
absence of any lateralising signs, can be of significant help in the subsequent
management.
Assessment of conscious level—Glasgow Coma Scale

This is an essential component of the neurological examination. Terms such as
‘stuporose’, ‘semiconscious’ and ‘obtunded’ are ill-defined and a clear
description of the patient’s level of arousal and response to stimuli is more
helpful. Systematic assessment of the unconscious patient by the application of
the Glasgow Coma Scale provides a grading of coma by using a numerical
scale, which allows serial comparison and may provide prognostic
information. GCS is described by Teasdale and Jennett in 1974. This scale relates
clinical observations under the three headings of motor response, verbal
response and eye opening and allows any changes over a period of time to be
rapidly appreciated (Table 41.1).
Table 41.1
Assessment of conscious level

Glasgow Coma Scale Score
Eye opening (E)
Spontaneous 4
To speech 3
To pain 2
Nil 1
Motor response (M)
Obeys 6
Localises 5
Withdraws 4
Abnormal flexion 3
Extensor response 2
Nil 1
Verbal response (V)
Oriented 5
Confused conversation 4
Inappropriate words 3
Incomprehensible sounds 2
Nil 1
Coma score = E + M + V
Minimum 3
Maximum 15
Paediatric Glasgow Coma Scale Eye opening (E) and motor response (M) same as
adults
Best verbal response (V) is rated as below:
Age appropriate verbalisation 5
Cries but consolable, irritable, uncooperative, aware of environment 4
Irritable, persists cries, inconsistently consolable 3
Inconsolable crying, unaware of the environment 2
None 1
Determining the level of consciousness is extremely important. The patient

is next asked to move the extremities and sharp objects are used to test the
level of sensory function.
Cervical spine fracture can be identified using six cardinal signs of cervical
cord injury:
• Flaccid extremities
• Diaphragmatic breathing
• Ability to flex the forearms but not extend
• Facial grimace in response above but not below the clavicles
• Hypotension with evidence of haemorrhage
• Priapism
E—Exposure and complete examination of the patient

The clinician should know the cause of trauma, which will alert him/her
regarding the type of injury. For example, trauma caused due to sharp objects
may result in penetrating injuries to nerves and vessels. A blunt trauma most
likely results in fracture of the facial skeleton.
Quick and helpful information can be obtained from the patient or his/her
attender. A mnemonic that is helpful in the immediate assessment of the
patient is AMPLE.
A: Allergies
M: Medications the patients may be taking
P: Past illness
L: Last meal
E: Events preceding the injury
It is necessary to enquire about the patient’s last meal for two reasons:
1. Alcoholic drink—causes altered sensorium, thus GCS is not applicable

2. Decreases the gut mobility and tendency to vomit from trauma
contraindicates general anaesthesia
Therefore, nasogastric suction and techniques to prevent vomiting and
aspiration during intubation and anaesthesia must be employed in the
traumatised patient. Extreme caution must be exerted during the insertion of
nasogastric tube in patients with Le Fort II and III injuries as the tube may
penetrate the anterior cranial fossa if it is passed injudiously. A deterioration
in patient’s alertness usually indicates increasing intracranial pressure (ICP) in
which an epidural haematoma requires immediate surgical intervention.
The oral examination should follow the order:
• Soft tissues
• Nerves
• Skeleton
• Dentition
The maxillofacial examination should proceed in the following order:
• Soft tissues
• Nerves
• Skeleton
Examination of the oral cavity

Examination of the oral cavity should be started only after the establishment of
the airway and stabilisation of the cardiovascular system.
Soft tissue examination

Evaluation as well as treatment are performed from inside out and bottom up.
The oral and pharyngeal soft tissues should be evaluated for lacerations or
penetrating injuries. The tongue is often lacerated. If excessive bleeding is
present, it should be controlled immediately and the soft tissue injuries must
be explored for tooth fragments and foreign bodies. The orifices of Stensen’s
and Wharton’s ducts must be evaluated for patency and salivary flow.
Soft tissue swelling or ecchymosis should be identified as they frequently
reflect an underlying bone injury. Sublingual haematoma is the most common
sign indicative of mandibular fracture.
Vertical lacerations in the alveolar gingiva are frequently associated with
underlying mandibular, maxillary or alveolar arch fractures. An anterior–
posterior laceration of the hard palate is usually associated with paramedian
fractures of the palate.
Neurological examination
The nerves commonly injured as a result of oral and perioral trauma are:
1. Inferior alveolar nerve: This nerve is frequently injured as a result of
mandibular fractures. May result in lip anaesthesia on affected side,
which may be permanent.
2. Lingual nerve: This nerve is less commonly injured. Injury to lingual
nerve results in anaesthesia or paraesthesia of the anterior two-third of
the tongue. In addition, since the chorda tympani fibres are carried by
the lingual nerve, injury to this structure also results in alteration in
taste.
Skeletal examination
• Skeletal examination is commenced with mandible. Laceration of the

chin indicates associated subcondylar fractures resulting from blunt
injuries. The evaluation of the mandible is done by both intraoral and
extraoral observation and palpation. Palpation of the oral and facial
soft tissues may disclose pain, crepitation and induration, which are all
significant clinical findings.
• Pain, swelling and induration may indicate infection associated with
the mandibular fracture especially those which are at least 48 h old.
Because mandibular fractures that involve the dentition are always
compound fracture and frequently become infected.
• Inability to open the mouth more than 35 mm or deviation of 6 mm to
right or left indicates either the presence of a mechanical problem or
trismus secondary to mandibular fracture or pre-existing
temporomandibular joint (TMJ) disorder.
• Pain in and around the preauricular or masseteric area indicates injury
to the condyle or the mandibular angle and deviation of the mandible
on opening the mouth indicates the presence of condylar fracture.
• Bilateral subcondylar fracture is characterised by limited mouth
opening, an anterior open bite and preauricular pain. In case of
edentulous patients or in patients who have lost their posterior teeth,
the fracture is just indicated by a decrease in the posterior interarch
width. Bleeding of the external auditory canal in a child also indicates
condylar fracture and these fractures may lead to ankylosis and
restricted growth in untreated cases.
• By evaluating the patient’s occlusion and by firm bimanual palpation,
fractures involving mandibular body, symphysis and angle can be
detected. Crepitation, mobility and step abnormalities in the patient’s
occlusion are pathognomic of mandibular fracture.
• Palatal ecchymosis indicates associated palatal fracture.
Dental examination
Quantity, quality and occlusal relationship are evaluated, which are of
considerable assistance in establishing the diagnosis and also in treatment
planning. The dentition must be evaluated for:
• Fractures, either horizontal or vertical.

• Mobility, either due to root fracture or periodontal problem.
• Bleeding from the gingival crevice either due to trauma or periodontal
disease.
• Missing teeth. If teeth are missing, chest and abdominal radiographs
must be reviewed. Although displaced teeth are usually swallowed,
the main stem bronchi and the lungs should be carefully evaluated.
Soft tissue examination

A thorough inspection and careful examination is a very important part of the
evaluation of maxillofacial injuries. The clinician should look for any bleeding
from lacerations or penetration of any foreign body and ensure that the
penetration has not affected any vital structures. Laceration in hair bearing
areas should be exposed by shaving the hair adjacent to the injuries; however,
eyebrows should not be shaved. The clinician should never neglect a small
laceration indicating a penetrating wound of upper or lower eyelid and should
assume that such injury is associated with a globe injury until proved
otherwise. Penetrating wound of soft palate may extend into middle cranial
fossa and transverse penetrating injury in the neck region must be assumed to
injure major vessels and requires arteriogram for evaluation.
The surgeon should look for orbital or periorbital injuries, which manifest as
subconjunctival haemorrhage. Similarly, TMJ injuries or middle cranial fossa
injuries manifest as bleeding from external auditory canal.
Basilar skull fractures may result in cerebrospinal fluid (CSF) otorrhoea. A
perforation and bulging of tympanic membrane (haematotympanum) usually indicates
basilar skull fracture. Importance should also be given to evaluation of the nose,
particularly the nasal septum, for the presence of septal haematoma. A nasal
examination may also reveal CSF rhinorrhoea, which is indicative of fracture
involving base of the skull and the escape of CSF through ethmoid, the
sphenoid or frontal sinus and more commonly through cribriform plate area of
ethmoid.
Tissue discolouration should be noted. Ecchymosis behind the ear is known
as Battle’s sign, which is indicative of basilar skull fracture involving middle
cranial fossa. Bilateral periorbital ecchymosis (raccoon eyes) is commonly seen
as a result of fracture of the base of the anterior cranial fossa. A cracking sound
in the subcutaneous tissue usually indicates the presence of air within the
tissues. A soft tissue radiograph confirms this finding.
Subcutaneous emphysema is not uncommon in upper airway injuries,
particularly those involving the walls of the maxillary sinus, frontal sinus,
orbital roof and medial wall fracture.
Neurological examination
The following nerves are examined prior to the injection of local anaesthesia
and induction of general anaesthesia:
Facial nerve
Functions of this nerve can easily be evaluated in a conscious patient by asking
the person to use the muscles of facial expression. If the patient is unconscious,
nerve stimulators can be used. But this evaluation should be completed and
noted prior to the injection of local anaesthetic or the induction of general
anaesthesia.
Infraorbital nerve
In case of fractures of zygomaticomaxillary complex, Le Fort II fractures,
orbital rim fractures and orbital blowout that involve the inferior orbital
fissure infraorbital nerve maybe damaged.
Olfactory nerve
Injury to this nerve results from fracture of the midface that involves the
cribriform plate of ethmoid. Anosmia resulting from damage to the olfactory
nerve is usually permanent.
Oculomotor nerve
Presence of dilated pupil indicates oculomotor nerve damage, which usually
results from intracranial nerve compression due to increasing intracranial
pressure. The clinician must also remember that anisocoria (unequal size of the
pupil) can be a normal finding; however, serious intracranial injuries and
increasing ICP must be excluded before one can assume that a dilated pupil is
a normal finding in a trauma patient.
Abducent nerve
Injury to the abducent nerve results in lateral rectus muscle dysfunction on
lateral gaze. It is most commonly seen in a patient who has suffered
deceleration type of injuries. Abducent nerve palsies are common because of
the long, bony intracranial course.
Optic nerve
Injury to this nerve results from fractures surrounding the optic foramen,
which may result from the compression of bone. Early identification of the
injury and decompression of the optic nerve in cases involving optic foramen
injuries may salvage the patient’s vision. In the unconscious patient, optic and
occulomotor nerve function can be evaluated by using the consensual light
reflex.
Skeletal examination
• Zygoma and maxilla are assessed. Bleeding spots in the maxillary

buccal fold and class III open bite malocclusion indicate a maxillary
fracture. Occlusal derangement occurs due to the force of the injury,
which drives the maxilla posteriorly and inferiorly.
• Bimanual palpation of the maxilla involves placing of one hand on the
forehead, which stabilises the head and the other hand manipulating
the maxilla to check its mobility. Movement of the maxilla within the
soft tissue indicates maxillary fracture.
• Palpation over the nasofrontal suture helps in diagnosing fracture in
this area, which is indicative of Le Fort II (pyramidal) or Le Fort III
(craniofacial dysjunction) maxillary fracture. Le Fort I (horizontal or
Guerin) fracture is diagnosed by manipulating the buccal fold with the
help of thumb and index finger.
• Lack of mobility of maxilla does not rule out a maxillary fracture, since
it could be impacted.
• Infraorbital rim is palpated for the presence of step deformity, which
may indicate either an isolated fracture of zygoma or a Le Fort II level
injury. The area of the frontozygomatic suture is now palpated.
• Considerable displacement of the lateral orbital bone may result in
displacement of the lateral canthal ligament in turn resulting in
diplopia. Lateral orbital rim fracture can occur either in isolation or in
association with the fractures involving the zygoma. Therefore, it is
always safer to evaluate the visual acuity and extraocular movements.
Examination of the zygomatic complex is done by palpation of the
zygomatic arch and buttress. Any injury to the zygomaticofacial or
zygomaticotemporal nerve in this region would result in anaesthesia
or paraesthesia of the soft tissues in case of arch fracture. Intraoral
palpation of the zygomatic buttress may disclose a step deformity,
which is a common finding in fractures of the zygoma. Frequently
referred to as ‘trimalar fractures’ are in fact ‘quadrimalar’ with fracture
present at the frontal suture, infraorbital rim, arch and buttress.
• The nose is evaluated for haemorrhage, CSF rhinorrhoea and septal
haematoma. CSF is usually associated with bleeding. However,
presence of CSF in the blood can be detected with the help of a simple
test in which a drop of fluid is placed on handkerchief and the classic ‘bull’s
eye sign or ring test’ develops. It is also identified by the tramline
pattern.
• The naso-orbital-ethmoid (NOE) complex is evaluated. The nose is
examined for any deviation or saddle deformities. Measurement of the
intercanthal distance beyond 32 mm indicates the presence of
traumatic telecanthus. Combination of obtuse medial canthal angle,
increased intercanthal distance and flattened nasal bridge is indicative
of fracture of NOE complex. Severe injuries of the NOE complex might
be an indication of fractures involving the frontal bone and the
associated sinus.
• The lower border of the mandible is palpated for any step deformity or
crepitus. Bimanual palpation of the mandible is done to elicit the
fracture site. Any step or derangement in the occlusion is also an
indication of mandibular fracture.
Imaging of maxillofacial injuries

Plain radiographs are ‘gold standard’ in maxillofacial trauma. Management of
maxillofacial injury is rarely an emergency and definitive management can be
deferred until radiographs of diagnostic quality can be obtained and a
treatment plan can be formulated.
Radiographs which are ideal in mandibular series are:
1. Panoramic radiograph (orthopantomograph [OPG])

2. Posteroanterior view of mandible (PA mandible)
3. Townes’ view of mandibular condyle
4. Cephalometric radiograph
Orthopantomograph provides an excellent two-dimensional view of

mandible. To assess fracture displacement adequately in all three-planes PA
mandible and Townes’ views are necessary.
When OPG unit is not available or when the patient’s physical condition
does not allow then posteroanterior and Townes’ views can be supplemented
with lateral and submentovertex radiographs.
For evaluation of maxillary fractures Waters’ sinus view (paranasal sinus
[PNS] view) is needed. PNS view with submentovertex view provides
valuable information regarding the maxillary, zygomatic, nasal and periorbital
regions. These views can be supplemented with OPG, nasal bone radiographs
and CT of orbital floors in cases of blow-out type injuries.
Computed tomography scanning in the coronal and axial planes provides
the extent of maxillofacial injuries.
3D reconstruction of CT scans can also be of assistance particularly in
fractures involving severe frontal bone and NOE injuries. However, magnetic
resonance imaging (MRI) is of little benefit in the assessment of traumatised
patients. Arteriography is indicated in patients with severe bleeding that is
difficult to control and in patients with penetrating injuries that involve major
vessels.
Maxillofacial evaluation—summary
• Patients with facial fractures usually have multiple trauma in the whole
body, still isolated facial injuries are common.
• The patient with facial fractures especially when unconscious is always
suspected to have cervical vertebrae and managed accordingly.
• Midfacial injuries may be associated with respiratory problems or loss of
consciousness; this warrants emergency airway stabilisation.
• In case of suspected midface fractures, transnasal intubation is not
preferred. Transoral intubation or cricothyrotomy is the treatment of
choice.
• In case of fracture of cervical vertebrae, transoral intubation is
contraindicated as it necessitates extension of neck, in such cases
cricothyrotomy or tracheostomy is done.
• Epistaxis is often present in traumatic facial injuries, uncontrolled
epistaxis leads to hypovolaemic shock or obstruction to air flow. This
needs prompt attention and intervention. The principle of management
remains the same though more caution is required while instrumenting
the nose in case of suspected skull base fracture.
After the ABCs (control of airway, breathing and circulation), the history is
taken and physical examination is performed. Identification and management
of the intracranial injury or CSF leak, or ophthalmologic injury is the main
concern. Because any delay in the management of these condition results in
irreversible damage.
• Visual acuity should be done and it is an important ophthalmologic

examination that may indicate any undetected injury to the eye.
• Traumatic optic neuropathy, open globe injuries, any signs of retinal
injury such as monocular diplopia are emergencies and need immediate
ophthalmic consultation.
• When CSF rhinorrhoea is not pronounced, the patient is questioned about
salty taste of saliva or postnasal drip. Tramline appearance is not
appreciated during active epistaxis.
• CSF leak is usually found in frontal sinus, cribriform plate or fovea
ethmoidalis fractures. Following ophthalmologic examination, face, ears,
nose, mouth and mandible should be examined systematically.
CHAPTER 42
Basic Principles of
Management of
Maxillofacial Trauma
Anatomic consideration
Principles of fracture repair
Fracture reduction
Closed reduction
• Closed manipulation
External reduction devices
Intraoral or extraoral traction
Open reduction
Fixation
Indirect fixation (closed fixation)
• Intermaxillary fixation or maxillomandibular
fixation (IMF or MMF)
▪ Direct interdental wiring
▪ Risdon’s wiring
▪ Interdental eyelet wiring (Ivy loop
method)
▪ Continuous or multiple loop wiring
▪ Arch bars
▪ Cap splints
▪ Intermaxillary fixation screws
• Suspension wires
▪ Lateral (Adam)
▪ Central (frontal suspension)
▪ Circum zygomatic suspension
▪ Zygomatic buttress suspension
▪ Infraorbital
▪ Pyriform aperture
▪ Peralveolar suspension
• External pin fixation
▪ Bone clamps
▪ Kirschner wires
▪ Haloframes
▪ Plaster of Paris head cap
▪ Box frame
Direct fixation (internal fixation)
• Semirigid fixation
▪ Transosseous wiring
▪ Noncompression miniplate osteosynthesis
• Rigid fixation
▪ DCP
▪ EDCP
▪ Lag screws
▪ Reconstruction plate
▪ THORP
▪ Locking plate
Fracture healing
Primary bone healing
Gap healing
Contact healing
Secondary bone healing
Initial reaction
Cartilaginous callus (soft callus) formation
Hard callus (bony callus) formation
Remodelling
Complications
Infection
Ankylosis
Nerve injury
Plate fracture
CSF leak
Epiphora
Globe injuries
Diplopia
Nonunion
Malunion
Delayed union
Soft tissue injury and management
Contusions
Abrasions
Lacerations
Avulsion
Penetrating wounds
Restoring form and function is the ultimate goal of facial fracture repair.
Hippocrates described bandaging of fractures as a means of stabilisation. His
bandages immobilised the fractured segment and allowed healing. In 1960,
Luhr developed and used the compression plate. In the 1970s, Michelet and
Champy developed the method of using small, bendable noncompression
plates along the support structure of the mandible as a semirigid means of
fixation. This revolutionised the application of miniplate for widespread
maxillofacial fractures.
Anatomic consideration
The craniofacial skeleton is made up of 22 bones. These bones surround
different cavities that form the skull such as orbital cavity, nasal cavity, oral
cavity, maxillary sinuses, etc. In the craniofacial skeleton, thin bony walls are
connected by thicker bony portions.
These thick bony portions are referred to as ‘buttresses’ and are a key factor
in the reconstruction of panfacial fractures. They were described by Sicher and
Tandler (1928), Merville (1974) and later expanded by Gruss and Mackinnon
(1986). These buttresses maintain the various dimensions of the face such as
height, width, anteroposterior projection, etc. They are also the lines along
which the masticatory forces and other dynamic forces are distributed. The
reduction and fixation of panfacial fractures is done at the various buttresses
to maintain the architecture of the facial skeleton.
There are two main divisions of buttresses:
1. Horizontal buttresses (anterior posterior buttresses)
a. Frontal buttress—consists of supraorbital rims and glabellar region.

b. Zygomatic buttress—consists of zygomatic arch, body and infraorbital
rim.
c. Maxillary buttress—consists of basal bone of maxillary arch.
d. Mandibular buttress—consists of basal bone of mandibular arch.
2. Vertical buttresses
a. Nasomaxillary/medial buttress consists of frontal process of the maxilla

and maxillary process of frontal bone.
b. Zygomaticomaxillary/lateral buttress consists of zygomatic process of
frontal and maxillary bones, lateral orbital rims and lateral part of
zygomatic body.
c. Pterygomaxillary/posterior buttress consists of pterygoid plates of the
sphenoid bone and maxillary tuberosities.
d. The condyle and posterior ramus may also be considered as a vertical
buttress.

There are two main theories in the management of panfacial fractures:
1. Bottom up and inside out

This sequence involves reduction of all the fractures keeping the mandible as
base. Mandibular fracture is first reduced and the rest of the fractures are
reduced sequentially from down upwards and at each level the fixation is
done from the innermost bone proceeding outward (Table 42.1), e.g. a nasal
bone fracture is reduced first and a zygomatic fracture is reduced next.
Table 42.1
Comparison of bottom up and top down
Bottom up and inside out Top down and outside in

1. Tracheostomy 1. Tracheostomy
2. Repair of palatal fracture 2. Repair of frontal sinus fracture
3. Maxillomandibular fixation 3. Repair of zygomaticomaxillary complex
fractures
4. Repair of condylar fractures (including arches) 4. Repair of naso-orbito-ethmoidal fractures
5. Repair of mandibular fractures (angle, 5. Repair of Le Fort fractures (including
symphysis, ramus) midpalatal split)
6. Repair of zygomaticomaxillary complex fractures 6. Maxillomandibular fixation
(including arches)
7. Repair of frontal sinus fracture 7. Repair of condylar fractures
8. Repair of naso-orbito-ethmoidal bone fracture 8. Repair of mandibular fractures
(symphysis, body, ramus)
9. Repair of maxilla
2. Top down and outside in

In this sequence the calvarium is used as a base. The fixation of other bones is
done from the topmost proceeding downward, e.g. a frontal bone fracture is
first addressed before a maxillary fracture. The mandibular fracture is reduced
last and at each level the fixation is done from the most lateral bone inwards,
e.g. a mandibular angle fracture reduction precedes the reduction of a body or
symphysis fracture.
Principles of fracture repair

This includes:
1. Reduction
2. Fixation
3. Immobilisation
4. Early return of function
I. Fracture reduction
There are basically two techniques of fracture reduction:
1. Closed technique
2. Open technique
Closed reduction
Closed reduction refers to reduction of the fracture segments to their previous
anatomic and functional position by manipulation without direct visualisation
of the fracture. Closed reduction is often followed by closed fixation. Healing
of the bone occurs by secondary intention with callus formation.
Closed manipulation
The dentulous fracture segments especially of mandible can be reduced by
closed manipulation unless extremely displaced from muscular forces. These
segments guided by the occlusion of teeth can be reduced and fixed by closed
method.
External reduction devices (Fig. 42.1A–C)

When the fractured segments do not override much, manipulation using
instruments can be employed to bring the segments to occlusion. For example:
• Rowe’s disimpaction forceps can be used to disimpact the fractured

maxilla and bring it to occlusion.
• Midpalatal split maxillae are reduced by Hayton William forceps.
• Walsham forceps can be used to manipulate certain nasal fractures.
• Asch forceps for septal fracture reduction.
FIGURE 42.1 (A) Fracture reduction using Rowe’s maxillary

disimpaction forceps. (B) Septal fracture reduction with Asch
forceps. (C) Walsham forceps for nasal bone fracture reduction.
Intraoral or extraoral traction

They are employed in cases where reduction has been delayed or in cases
where muscular forces prevent effective manipulation. Intraoral traction
involves fixation of prefabricated arch bars to the maxillary and mandibular
arches and traction of the segments to normal occlusion using elastics.
Extraoral traction, on the other hand, involves anchorage from the intact skull
for traction. The process of traction is extremely slow and the patient is
encouraged to open and close the mouth to facilitate the elastic traction.
When satisfactory occlusion is achieved, elastics are removed and
intermaxillary fixation is done using wires.
Open reduction
Open reduction is the surgical intervention for reduction of the fractured
segments. After introduction of antibiotics, possibility of surgical opening of
facial bone fractures increased significantly. This is especially important with
respect to the facial skeleton, where an exact reduction results in an optimal
functional and aesthetic result. Healing takes place by primary intention
where no callus formation occurs during healing. Usually it is followed by
direct fixation of the fracture fragments with internal fixators.
II. Fixation
The second principle of fracture management is fixation of the reduced
fracture fragments in the desired position. The fractured fragments can be
fixed by direct and indirect methods.
Indirect fixation (closed fixation)
A. Intermaxillary fixation or maxillomandibular fixation (IMF OR

MMF)
It refers to immobilisation of the maxilla and mandible in maximal
intercuspation position with the aid of wiring in a closed position. It is done by
means of wires, arch bars and splints.
Indirect fixation (Closed Reduction)
A. Intermaxillary fixation or maxillomandibular fixation (IMF or MMF).

B. Craniomaxillary or craniomandibular suspension
C. External fixation.
D. Bone Clamps
E. Kirshner wires
F. Haloframes
G. Plaster of Paris head cap
H. Box frame
Advantages
• Relative simplicity
• Low cost
• Less time consuming
• Noninvasive nature of treatment
• Not much of skill or operator dexterity required
• Bridging of small bony defects possible as healing occurs by callus
formation
Disadvantages
• Poor oral hygiene

• Attainment of absolute stability is not possible
• Cannot be done in noncooperative patients
• Atrophy of muscles and loss of biting force
• Temporomandibular joint may be affected
Indications
• Minimally displaced fracture

• Unilateral condylar fracture
• When the patient cannot afford for a more sophisticated method of
treatment: cost factor
• When the patient cannot undergo lengthy procedure involving general
anaesthesia
Contraindications
• Severe asthma, respiratory disorders

• Chronic obstructive lung disease
• Gastrointestinal disorders
• Psychiatric or neurological problems
• Mentally retarded patients
• Seizures
This procedure is performed by the fact that when the teeth of a fractured
jaw are fixed in the correct occlusion, the bone fragments supporting them, in
most cases, will also be satisfactorily reduced. This may not be possible in
cases where the teeth are not of a suitable number, shape and quality. Hence,
wiring is indicated in patients who have adequate number of good shaped
teeth. Wire is stretched to about 10% before using. The wires should not be
stretched beyond their limit as they might become work hardened.
1. Direct dental wiring
a. Direct interdental wiring (Gilmer wiring)

This technique provides a simple and rapid method of immobilisation of the
jaws.

A prestretched 0.35 mm diameter soft stainless steel wire of 15 cm in length is
taken and the middle portion of the wire is twisted around a tooth. The free
ends are twisted together to form a plaited tail around 3 cm in length. Similarly
other teeth are also attached with wires and twisted. Intermaxillary fixation is
effected after reduction of the fracture and twisting the separated tails together
in the upper and lower jaws. To avoid any trauma to the soft tissues the cut
ends are bent away from the tissues or may be covered by wax or gutta-
percha. This technique should only be considered as a first aid method for
achieving temporary immobilisation of fractured fragments.
FIGURE 42.2 (A–C) Direct interdental wiring.
Advantages
• Simple
• Rapid method
Disadvantages
• Wire tends to break

• Broken wires cannot be replaced unless all other wires are removed
To overcome these disadvantages, interdental eyelet wiring is used.

b. Risdon’s wiring (Fig. 42.6A–C)
A 26-gauge 25 cm long wire is twisted around the necks of the second molar
teeth on each side and both the ends are twisted together for their entire
length. The twisted wires from both the ends are brought together in the
midline and final twisting is done here after adapting this wire to the necks of
the teeth on the buccal side. This forms the base wire. Additional interdental
wires are used to secure the base wire to the distal surface from the buccal side
and below the base wire and it is turned around the tooth on the lingual side
and brought back again on the buccal side through the mesial aspect of the
tooth above the base wire. The two ends are twisted together and tucked
inside the nearest interdental space.
c. Button wiring
Leonard in 1977 used titanium buttons.
2. Interdental eyelet wiring (Ivy loop method)
Preparation of eyelet wires (Fig. 42.3 A–F)

A prestretched 0.35 mm stainless steel wire of 3 m length is taken. Now the
wire is again divided into several segments of 15 cm each. Eyelet wires are
made by twisting the middle of each length of wire around the shaft of a rod
of 3 mm diameter. Two and a half twists suffice and ends of the eyelet wire
are cut off obliquely to equalise their length and to produce a sharp point,
which will readily pass through the interdental space (Fig. 42.4).
• The eyelets are drawn into the interdental spaces and twisted tight.
While pushing and twisting these wires on the lingual or palatal
aspect, one must be careful as the eyelet tends to get displaced and
become loose. Therefore, these wires should be pushed down on the
lingual or palatal aspect with appropriate instruments.
• The wires seen on the palatal or lingual side should be turned and bent
like ‘W’ by splitting the two ends of the wire. Each end of the ‘W’ is
inserted into the mesial and distal of the adjacent teeth. The distal wire
is passed into the eyelet and twisted with the mesial end. The
procedure can be done under local or general anaesthesia depending
upon the severity of fracture, status of the patient, etc.
• Approximately 5 wires should be placed on the upper jaw and 5 wires
in the lower. The fracture is reduced by passing the wires through the
eyelets from upper to the lower jaw.
• The position of the eyelet wires should be such that a cross-bracing effect
is achieved when the tie wires are threaded through them. The cross-
bracing prevents some kind of mobility of the mandible which might
be present if the eyelets were placed immediately above each other.
• Before twisting the tie wires, teeth which require extraction should be
removed and the throat pack should be removed (if done under
general anaesthesia).
• The tightening of the tie wires should begin from molar area of one
side and then on the other side working to reach the incisor area. This
is done so because if the wires are tightened on one side first, a
crossbite might be produced and if the anterior wires are tightened
first, a posterior crossbite might be produced
• The wires should be tied loose first. The final tightening is done only
after establishing the occlusion properly. The sharp ends of the
tightened wires should be tucked in such a manner that it does not
cause any ulceration.
• Eyelets are used by clove hitch method when there are edentulous
spaces around the tooth.
FIGURE 42.3 (A–F) Interdental eyelet wiring.

FIGURE 42.4 Maxillomandibular fixation using Ivy eyelets for angle
fracture.
3. Continuous or multiple loop wiring (Fig. 42.5 A–F)

Stout described this technique of wiring in which blocks of teeth in either jaw
is wired and elastic traction is used to reduce the fracture. A modified
technique was also described by Obwegeser.
FIGURE 42.5 (A–F) Continuous or multiple loop wiring.
FIGURE 42.6 (A–C) Risdon’s wiring.
Technique
A 26-gauge 30 cm long stainless steel wire is laid along the buccal surface of
the teeth starting from the midline going back along the posterior surface of
the existing last tooth in the arch below its contact point and then emerges
through its anterior interdental space. Now the wire is passed around the
buccal wire and through the same interdental space. At this stage, a pliable
rod of approximately 3 mm diameter and 5 cm length is passed through this
wire loop and is laid along the buccal surface. The wire on the lingual or
palatal side is then passed through the interdental spaces of the remaining
teeth and around the rod and the buccal wire in a sequential manner so that
entire quadrant is enclosed. Finally, the ends of the wire lie on the buccal side
which are pulled together tight and twisted. The twisted end is cut short and
pressed into the interdental space.
This wiring is completed on all the four quadrants. The rod is now
withdrawn with a rotatory pull. The loops are tightened and bent towards the
sulcus if elastic traction is to be used as shown in Fig. 42.5 (F) and are bent
towards the occlusal surface of the tooth if tie wires are to be used as shown in
Fig. 42.5 (E).
4. Arch bars
Two types of arch bars are available:
i. Prefabricated (Fig. 42.7).

a. Jelenko
b. German silver
c. Erich
ii. Custom made—prepared individually for a specific patient.
a. Acylic
b. Cast silver
c. Schuchardt acrylic arch bar
d. Stanhope’s modification of Schuchardt’s
e. Directly bonded arch bar
FIGURE 42.7 Erich arch bar.
Indications for use
1. When the remaining teeth are insufficient to allow efficient eyelet

wiring.
2. When the distribution of the teeth in the arch is such that efficient
intermaxillary fixation is not possible.
3. In cases of simple dentoalveolar fractures or where multiple tooth-
bearing fragments in either jaw requires reduction into an arch form
before intermaxillary fixation is applied.
4. As an integral part of internal skeletal suspension in the treatment of
fractures involving the middle third of the facial skeleton.
5. In cases where external skeletal fixation is planned, an anterior
projection bar is attached to an individually made arch bar.
6. Where laboratory and technical facilities are inadequate or nonexistent.
Operative technique
• The fracture is first reduced and the teeth in the main fragments of the
fracture are tied to a metal bar which is adapted to the dental arch.
Various types of arch bar available are Erich type, German silver and
Jelenko type.
• It is wise to place the wires for securing the arch bar around the teeth
away from the fracture in order to prevent subluxation of the teeth
involved in the fracture line. To be retentive, the wires holding the bar
must lie below the contact points and, if possible, around the necks of
the teeth.
• The arch bars have hooks or other provisions for maintenance of
intermaxillary fixation. Small notches created on the bar with the help
of a file prevent the wires from slipping. The hooks in the upper jaw
face in an upward direction whereas the hooks in the lower jaw face
downward direction.
• The arch bar is adapted to the buccal surface of the lower and upper
jaws by bending first at the buccal surface of the last teeth on one side
and passing across the midline to the opposite side.
• Now the arch bar is secured to each tooth using a 0.35 mm soft
stainless steel wire. Each wire passes over the bar mesially, around the
tooth and under the bar distally. The ends of the wire are twisted on
the buccal side.
• Once the fragments have been tightly secured to the arch bar, it is
difficult to correct any errors in a vertical displacement of the
occlusion. It is advisable, therefore, not to tighten any ligatures until
all have been inserted and any vertical displacement has been
corrected by articulating the jaws.
• Intermaxillary fixation is achieved by passing tie wires around the
lower arch bar and inserting them either through hook, around the
upper arch bar. A more rigid fixation can be achieved by threading the
tie wire through the wire loop, which will secure the arch bar to the
teeth. The tie wires are first pulled, tightened and then cut so that the
end can be bent over the bar into an interdental space where it will not
cause soft tissue damage (Fig. 42.8).
FIGURE 42.8 Maxillomandibular fixation using arch bars to
preserve dental occlusion.
5. Cap splints
For many years, cap splints were used as a significant means of immobilisation.
The possible indications for their use in the present days are confined to the
following:
• For prolonged fixation on the mandibular teeth in a patient with

fracture of the tooth-bearing segment of the mandible and bilateral
displaced fractures of the condylar neck.
• In a case, where a portion of the mandible is missing with considerable
soft tissue loss. Here the cap splint helps in maintaining the correct
relationship of remaining tooth-bearing segments till the
reconstruction is completed.
• In patients with severe periodontal disease in which case temporary
retention is essential for proper fracture healing. Here the cap splint
helps to splint the loose teeth together and facilitates the application of
the intermaxillary fixation.
• Cap splints are also used for extraoral fixation in case of complicated
midfacial fractures which particularly involves mandible.
Procedure for construction of cap splint

• Certain modifications have to be done during the impression making
of fractured jaw considering the restricted mouth opening presence of
blood and excessive secretion of saliva. Impression trays can be cut
according to the area of preference. Impression of each fragment can
be made separately using segmental trays.
• The mouth should be thoroughly cleaned before making impression.
Soft alginate can be used for the purpose of impression making.
• After manufacturing, cap splints are placed with appropriate cement.
• The splints are manufactured either with a cast silver alloy or acrylic or
with small hooks and cleats to which elastic bands are attached and
reduction is done by intermaxillary elastic traction. However, in cases
of prolonged operative treatment, operative reduction should be
preferred.
• When segmental splints are made, after reduction the splints should be
assembled using locking bars which provide continuity of the splint
round the whole mandibular arch. The locking bars are soldered to
individual plates which in turn can be screwed to the corresponding
plates on the splint segments.
Disadvantage
• Time consuming.
6. Gunning splint
Refer to Chapter 44 Mandibular Fractures.
7. Bonded modified orthodontic brackets

Orthodontic brackets can be bonded onto teeth and intermaxillary fixation
applied with the help of elastic bands. This type of intermaxillary fixation can
be used for fractures with minimum displacement. The orthodontic brackets
have to be modified by attaching small hooks on them for application of the
elastic bands.
8. Intermaxillary fixation screws

Arch bars and wires have a chance of accidental skin puncture causing risk of
HIV/hepatitis transmission.
Karlis first described the use of cortical bone screw fixation for treating
mandible.
Advantages
1. Ease of application.
2. Decreased operating time—decreased overall cost.
3. Decrease risk of disease transmission.
Armamentarium
• 24 g wire
• IMF screws
• Screwdriver
Disadvantages
1. Lacks tension band effect.

2. May interfere with internal fixation plates, so recommended for only
minimally displaced fracture.
1. Local anaesthesia medial to canine (upper and lower).

2. Self-tapping IMF screw 8–14 mm length is inserted in transmucosal
fashion/mucosa incised with No. 15 blade.
3. Care taken to avoid iatrogenic injury to mental nerve branches.
4. 24 g wires used for MMF.
FIGURE 42.9 (A) IMF screws. Note the head is double headed with
a hole for gaining entry of wire. (B) Wire passed through the hole in
the IMF screw head. (C) MMF done using IMF screws.
B. Craniomaxillary or craniomandibular fixation and other

wiring techniques
Internal wire suspension was first described by Adams in 1943. Here the lower
jaw is connected by soft stainless steel wires of 0.5 mm diameter to areas of
facial skeleton above the fracture line; thus, sandwiching the fractured portion
between mandible and the unfractured portion of the facial skeleton. The
advantage of this method of fixation is that they require only minimum
armamentarium.
Suspension wiring techniques

Techniques Use
Frontal Le Fort III/II (stable mandible)
Lateral (Thoma/Adam) Le Fort II/III (unstable mandible)
Central/Glabella (Kufner)
Circum zygomatic (Cupero) Le Fort II/I
Zygomatic buttress Le Fort I
Infraorbital Le Fort I
Lateral pyriform/pyriform apertures Le Fort I
Anterior nasal spine
Except circum zygomatic, all other suspensions require exposure of

suspension point.
Tightening of suspension is done after occlusion is established and MMF
applied for 6 weeks.
1. Lateral (Adam)
The zygomatic process of the frontal bone is exposed through an incision
made in the lateral third of the eyebrow just above the frontozygomatic suture.
A hole is drilled 5 mm above the frontozygomatic suture in the posterior direction
towards the infratemporal region. Stainless steel wire of 0.5 mm diameter is
passed through this hole. Using an awl the wire is passed beneath the
zygomatic arch to enter into the buccal sulcus intraorally where it is secured to
the arch bar (Figs. 42.10–42.12, 42.14, A).
FIGURE 42.10 (A) Technique for suspension from frontal bone

(lateral): (A) suspension wire introduced through a lateral eyebrow
incision using an awl, (B) wires passed through the bur holes near
the frontozygomatic suture and passed beneath the zygomatic
bone and (C) wires secured appropriately to the arch bar.
FIGURE 42.11 (A) Preoperative clinical photograph. (B–C) 3D CT

scans showing fracture lines. (D) Frontal suspension (lateral) pull
out wire.
FIGURE 42.12 (A–E) Adam suspension for Le Fort II fracture.
2. Central (frontal suspension)

This technique was introduced by Kufner but is of little significance.
3. Circum zygomatic suspension

The zygomatic arch is used as the stable bone for suspension. The wire is
passed as a sling around the arch using a bone awl.
The free ends are exited through buccal vestibule opposing first molar and
fastened to maxillary and/or mandibular arch bars.
An awl is introduced extraorally at the junction of zygomatic and temporal
bone medial to the zygomatic arch in a downward and forward direction so as
to enter the buccal sulcus intraorally in the region of second molar. A 0.5 mm
diameter stainless steel wire is attached to the tip of the awl and the
instrument is withdrawn to lie just above the zygomatic arch without
emerging out from the skin. Now the instrument is passed on the lateral aspect
of the zygomatic arch in the same direction as previously mentioned. The free
ends of the wire are secured to the arch bar (Fig. 42.13A–C).
FIGURE 42.13 (A–C) Circum zygomatic mandibular suspension

technique.
4. Zygomatic buttress suspension

A 3 cm incision is made in the region of premolar and molar in the depth of
the vestibular sulcus. Blunt dissection is done to expose the inferior border of
the zygomatic buttress. Using a bur, a hole is drilled on the zygomatic buttress
and a 0.5 mm diameter stainless steel wire is passed through it. The two ends of
the wire are then attached to suitable loops of the arch bar (Fig. 42.15 B).
5. Infraorbital
Here, a 3 cm vestibular incision is made in the region of canine and dissected
subperiosteally to expose the inferior orbital margin lateral to the infraorbital
foramen. Using a bur, a hole is drilled in an upward and posterior direction; a
0.5 mm stain less steel wire passed through the hole, withdrawn into the
mouth and appropriately attached to the loops of the arch bar.
Care is exercised not to injure the orbital globe while drilling or introducing
the wire (Fig 42.14 B).
FIGURE 42.14 (A and B): A: Adam’s Lateral suspension wiring. B.
Suspension through infraorbital rim.
6. Pyriform aperture
A 2 cm transverse incision is made in the upper labial sulcus above the lateral
incisor tooth and the pyriform aperture of the nose is exposed by elevating the
periosteum. The nasal mucosa is elevated and protected using a periosteal
elevator. A hole is drilled 1 cm away from the free margin of the pyriform
aperture from medial to lateral side. A 0.5 mm diameter stainless steel wire is
passed through this hole; the two ends are withdrawn and attached to a
suitable loop of the intermaxillary fixation (Fig. 42.15).
FIGURE 42.15 (A and B): A: Suspension through rim of the
pyriform aperture. B: Zygomatic buttress suspension.
7. Peralveolar suspension
A gunning type of splint is used and the position of holes on the palatal aspect
of the splint is marked on the underlying palatal mucosa. Peralveolar awl is
passed through the alveolus in the buccal sulcus, piercing the palate at the
marked position. Using an awl, a 0.5 mm diameter soft stainless steel wire is
passed through this hole on the palatal surface and withdrawn through the
buccal sulcus. The two ends of the wire are twisted over the gunning type
splint and turned over. The same procedure is repeated on the opposite side.
Disadvantages
1. Incomplete fixation of fracture fragments.

2. Insufficient visualisation of fracture by closed reduction.
3. Compression against cranial base to wedge fracture segments.
4. Lack of compensation of dislocating forces directed posteriorly →
cannot ensure facial projection.
5. Tooth-borne appliances offer only direct control on occlusal level of
fracture.
6. It does not anatomically reconstruct buttress of midface.
7. Three-dimensional stability not obtained.
8. Patient discomfort.
Complications
Commonly midface shortening and widening with retrusion of paranasal
areas occur.
8. Circumferential wiring
This method of wiring is done through open reduction and is useful for
treating fractures at the angle of the mandible and few oblique fractures in the
body of the mandible.
Procedure
The wiring can be done by passing a 0.45 mm diameter stainless steel wire
circumferentially around the mandible. The technique is similar to that of the
wiring for gunning splint. In yet another variation for the fixation of the
oblique angle fractures of the mandible, a wire is passed through the upper
border of the proximal segment, after removal of the third molar and then
around the lower border of the distal part of the mandible.
C. External pin fixation

Either craniomandibular or craniomaxillary fixation can be established
through any one of the following methods:
i. Craniomandibular fixation. Mandible is fixed by means of rods and

universal joints to the cranial vault and the fractured middle third is
sandwiched in between.
ii. Craniomaxillary fixation. After establishing the occlusion, upper jaw is
attached by means of rods and universal joints to the cranial vault.
These methods are especially useful where the fractures can be
reduced so that they remain impacted and there is only a minimum
displacement.
External pin fixation techniques have played an important role in the

management of fractures of the face and extremities (Fig. 42.16). Advances in
bone plating systems and other technical developments have substantially
reduced the indications for external devices. External fixation devices such as
Hoffman pins and the Morris biphase apparatus are useful for certain cases.
FIGURE 42.16 External pin fixation.
Indications
• Severe traumatic loss of bone.

• Severely atrophic mandibles that prevent the use of plates.
• Fractures complicated by osteomyelitis.
• Infected and nonunited fractures.
• Edentulous mandibular fractures previously treated by closed
reduction.
External pin fixations are increasingly managed by open rigid fixation

techniques. Avulsive gunshot wounds to the jaw once initially stabilised with
external pins are now considered for internal fixation with reconstructive
plating devices. External pin fixation for maxillofacial applications has become
synonymous with the term ‘the Joe-Hall-Morris appliance’.
Procedure
• External pin fixation consists of insertion of titanium or stainless steel

pin approximately 3 cm in length on each fragment of the fracture.
• These pins diverge by each other and are connected by a rod through
universal pin joints. These rods also have attachments to the lower cap
splints. This pin fixation is not rigid and often supplemented by
intermaxillary fixation.
• Pin fixation is most commonly used in immobilisation of central
middle third fractures. A skin incision is placed at the junction of
medial two-third and the lateral one-third of the eyebrow, 1 cm above
the supraorbital arch.
• A bur hole is drilled here towards the centre of the eyeball until the
hard cortical plate is reached. A ‘wood screw’ pattern pin is inserted here
until it is firm, the depth of insertion should not be more than 5 mm.
The same procedure is repeated on the opposite side.
D. Bone clamps
This system of external fixation for mandibular fractures is used very rarely.
Here the fragmented segments are secured by clamps attached to the lower
border of the mandible and from these clamps the pins project, which are
connected by external rods as in case of external pin fixation. This system best
known as Brenthurst splint was used in the past to overcome the disadvantages
of the stainless steel external pin fixation.
E. Krishner wires (Fig. 42.17)

These are rarely used for temporary fixation of the fractured mandible. The
fracture segments are held together in position. After reduction the wire is
drilled through the cortex on one side of the fracture via an extraoral approach
and passed through the medullary cavity of the undamaged bone on either
side of the fracture. More recently, K-wires are also used for comminuted
fractures of the body of the mandible. A horseshoe-shaped K-wire is adapted to
the buccal aspect of the mandibular arch and the ends are inserted into two
holes drilled into anterior border of the mandible. The fractured segments are
ligated to this semirigid frame.
FIGURE 42.17 Fixation with K-wire.
F. Haloframes (Fig. 42.18)

In 1943, Grafort described the first metal haloframe. It is mainly indicated for
fractures of the supraorbital ridges which require a higher point of fixation in
the cranium. It consists of a circular frame which encircles the head and is
attached to the skull by means of four pins. Two of these pins are positioned
anteriorly on the temporal crest and two pins posteriorly above and behind
the mastoid process to engage the temporal bone. The screw pins engage only
the outer table of the skull. The halo is linked to the anterior projection bar of
the silver cap splint or gunning type splints either on the maxilla or mandible
by standard stainless steel rods and universal joints. It has the disadvantage
that it projects backwards from the head and prevents the patient from lying
down comfortably on the back of the head.
FIGURE 42.18 Diagrammatic representation of fixation with
haloframe.
A modification of this haloframe has been made to overcome this problem.

The modified haloframe encircles only three-fourth of the skull and leaves the
occiput free.
G. Plaster of paris head cap

Use of plaster of Paris as a head cap is being replaced by the recent techniques.
This is useful in cases where there is extensive fracture of the cranial vault that
cannot be managed by haloframes or pins. The construction of the head cap
should be accurately fitting and comfortable since ill-fitting or uncomfortable
head cap may not serve the purpose. To construct a head cap, plaster of Paris
bandage is immersed in water. The first bandage is wound tightly around the
head above the supraorbital ridges. The second bandage is applied higher up
in the forehead surrounding the occiput. Now, retention framework is
attached to it by means of a third bandage.
This method is used for patients with middle third fracture who have also
sustained fractures of the cranial vault such that the haloframe cannot be
applied. In patients who cannot resort to general anaesthesia due to trauma to
the chest or other reasons, a plaster of Paris head cap can be applied linked to
the cap splints.
Alternately plaster of Paris head-chin cap can also be applied wherein the
fractured maxilla is suspended in between the skull and the mandible.
H. Box frame
The box frame is a rigid form of craniomandibular fixation. Two supraorbital
pins are inserted and two pins are inserted into the mandible slightly above
the lower border in the canine region. These four pins are connected by rods
and universal joints. It does not require to be fixed to the occluding dentition
by means of an anterior connecting bar (Fig. 42.19).
FIGURE 42.19 Diagrammatic representation of fixation with box

frame.
Direct fixation (internal fixation)
Internal or direct fixation of the fracture segments refers to the surgical
method of fixation of the fracture segments by direct visualisation using
hardware like stainless steel wires or plate and screws by load bearing or load
sharing osteosynthesis depending on the extent or severity of the fracture.
• Semirigid fixation (usually require supportive MMF)

i. Transosseous wiring
ii. Noncompression miniplates
• Rigid fixation without IMF is primarily achieved through bone plates.
There are basically three main systems of fixation of mandibular
fractures:
i. Compression plates
ii. Lag screws
iii. Reconstruction plate
Semirigid fixation
Semirigid fixation refers to the fixation of fracture fragments with wire or
noncompression miniplate that provide some degrees of rigidity though not
sufficient enough for the jawbones to start withstanding masticatory forces. It
usually requires a short duration of supportive MMF for immobilisation.
A. Transosseous wiring (Fig. 42.20A–B)

Transosseous wiring refers to direct wiring across the fracture line. It is cheap,
easy to use and biologically well tolerated by the patients. It is a kind of
semirigid fixation. Most of the time it is associated with IMF if occlusal
discrepancies exist. It is an effective method of fixation and immobilisation of
the mandible and the angle.
FIGURE 42.20 (A) Technique for transosseous wiring. (B) Types of
transosseous wiring for fixation of fracture of the angle of the
mandible with minimum displacement.
In the midfacial fractures, wiring is commonly done at sites like:
• Frontonasal sutures
• Zygomaticofrontal sutures
• Orbital rim
• Zygomaticomaxillary sutures
• Zygomatic bone
• Alveolar bone
Minimum specialised equipment is required for this method of fixation.
Technique
• Two holes are drilled with a small round bur on either side at an
adequate distance from the fracture line and soft stainless steel wire of
0.45 mm diameter is passed through the holes across the fracture. This
is to provide stability and to prevent the wire from cutting out as it is
twisted and tightened.
• This procedure is effected following disimpaction and reduction of the
maxilla.
• Accurate reduction of the fractured segments is done by twisting the
wires tightly and the twisted wire is tucked into the nearest hole. The
reduction of the fractured segments should be done independently
with the teeth in occlusion.
• Wires are applied on the upper border or the lower border depending
upon the type of fracture. Transosseous wiring can be done either
through intraoral or extraoral approach. The transosseous wiring at
the upper border of the mandible either through intraoral or extraoral
incision is preferred for the fractures of the angle of the mandible with
minimum displacement or for the edentulous area of the body
fracture. It is sufficient for the upper border wire to pass through the
outer cortical plate alone as the fixation is always combined with IMF.
• Extraoral incision at the inferior border is preferred for the grossly
displaced fracture of the angle of the mandible; fracture of the
edentulous mandible, malunited fractures and in cases of nonunion of
fracture.
• Fractures of the symphysis region can be approached via an intraoral
incision. Fractures of this region have a tendency to gape at the inferior
border due to the presence of mylohyoid muscle. Transosseous wires
placed at this region are helpful in controlling the fracture segments
even when the wire is passed only through the outer cortex.
• Similarly, in case of multiple fractures of the symphysis, multiple
transosseous wiring of the major fragments are done through an
intraoral approach.
• Usually a single lower border wire is not sufficient to stabilise the
fractured segments especially when the fracture line is oblique. The
segments tend to override. In such cases, a figure-of-eight wiring along
with the conventional wiring is done.
• An alternate method is where the wires are reinforced by passing
stainless steel tubing passed through them. The tubing rests on the
outer cortex of the mandible in a groove created artificially.
• In an extremely oblique vertical fracture of the mandibular body, two
wires can be used to secure the fracture segments and provide rigid
fixation by passing the two wires through both the outer and the inner
cortical plates and twisting them at the lower border.
Disadvantages of transosseous wiring
• It does not provide three-dimensional stability.

• Micromovement at the fracture site results in delayed healing.
B. Noncompression miniplate osteosynthesis
Champy lines and his coworkers argued that compression plates were
unnecessary because there is a natural line of compression existing along the
lower border of the mandible. On the basis of this, they suggested that
fractures of the angle of the mandible can be secured with single plate as near
to the upper border as feasible. In case of fracture of the parasymphysis region,
two plates are ideally advised one juxta-alveolar and one at the lower border.
This is to overcome the torsional forces of rotation at the symphysis. This can
be used virtually in all types of mandibular fractures.
Champy et al. modified the technique proposed by Michelet and described
the scientific basis for miniplate application in the treatment of mandibular
fracture. They determined ‘the ideal line of osteosynthesis’ (well known as
Champy’s line of osteosynthesis) where miniplate fixation is most stable.
Champy’s line of osteosynthesis (Fig. 42.21)

Mandible is a blunt V-shaped tubular bone. It consists of dense outer and
inner cortical plate with cancellous bone in between. Similarly, cortical bone
along the external oblique ridge and the inferior region of the chin is thick and
dense. The dense bone provides an excellent anchorage for osteosynthesis
screws. However, fixation of the screws in the region of the alveolar process is
difficult due to presence of roots of the teeth. Masticatory forces produce
tensional forces in the alveolar region or at the upper border and compression
forces at the lower border. This explains the cause of distraction of fracture
segments in the upper border and compression in the lower border.
FIGURE 42.21 Champy’s line of osteosynthesis.
According to Champy, the transitional zone in between the areas of tension

and compression is the line of zero force running along the inferior alveolar
nerve. Plates are placed along this line.
Champy calculated the forces applied to these plates under physiological
strains and produced the most desirable shape of minimum thickness and
reasonable malleability to neutralise the harmful tension forces that causes
displacement of the fracture segments.
Miniplates
Originally Champy made these plates using stainless steel, but currently
titanium plates are also available (Fig. 42.22A–C).
FIGURE 42.22 (A) 2 mm stainless steel miniplates of varied

patterns and shapes. (B) Titanium miniplates: top row—2 mm
plates, bottom row—1.5 mm plates. (C) Comparison of 2 and
1.3 mm titanium X-miniplates.
These plates are known as noncompression miniplates. Miniplates are

available with self-tapping monocortical screws. These screws which are
approximately 7 mm long and 1.5 mm in diameter are applied to the outer
cortical plate after reduction. These plates are available in various sizes and
shapes. These plates and screws provide three-dimensional stability and
placement of these plates with the provision for two screws on either side of
the fracture resists the anteroposterior and rotary movement of the fractured
segment.
Areas of plate application
• Champy recommended single noncompression miniplate on the

superior border of the mandibular angle fractures on the external
oblique ridge (Fig. 42.23A–B).
• For fractures posterior to the mental foramen, a single plate is placed
below the dental roots and above the inferior alveolar nerve.
• For fractures anterior to mental foramen, two plates are necessary to
neutralise the torsional forces: one is placed in the subapical region
and the other along the lower border of the mandible (Fig. 42.24).
FIGURE 42.23 (A) Titanium miniplate in external oblique ridge. (B)

Miniplate along external oblique ridge.
FIGURE 42.24 Two miniplates in symphysis to overcome torsional
forces.
Procedure
Three possible approaches may be used for the insertion of the plates:
extraoral, intraoral or combined. However, an intraoral approach is preferred
over the other two. Once the intraoral incision is made, the periosteum is
elevated as far as required. Using a scalpel divide the muscle attachment, as
these can be very adherent to the bone. Following this reduction of the fracture
ends is done.
Once the reduction of the fractured fragment is achieved, plates are inserted
and fixed with four monocortical screws, placed in such a way as to include
two on each side of the fracture line. The screws should have a minimum
length of 5 mm, but in case of thicker cortical layer a longer screw (8 mm at
angle) must be employed (Fig. 42.25).
FIGURE 42.25 Screws of variable sizes. Top row—1.5 mm
thickness and length of 4, 6, 8 and 10 mm. Bottom row—2 mm
thickness and length of 4, 6, 8, 10 and 12 mm.
Principles in application of plates for fixation of mandible fractures
• Temporary intraoperative stabilisation of the fragments can be

achieved with transosseous wires or miniplates.
• Loose screws must be replaced with an emergency screw; if the
emergency screw also slips, it must be removed and that plate hole left
empty or a longer plate can be applied.
• Plates are slightly overbent to close the lingual aspect of the fracture.
• Minor bone recontouring of irregularities on the buccal cortex may
facilitate better plate adaptation.
• Poor plate adaptation causes fracture displacement during placement
and tightening of the screws.
• Screw holes are prepared under irrigation using a drill guide to
facilitate proper preparation of the bone.
• Proper plate positioning minimises the chance of impaling the
mandibular canal with a drill or a screw.
Rigid fixation
Rigid fixation refers to the direct method of fracture fixation where the
hardware or implant used for fixation provides sufficient rigidity for the
jawbone to withstand masticatory stresses. Usually rigid fixation avoids the
need for immobilisation by MMF or other means. This technique does not
allow micromotion of fracture segments during normal function.
Rigid fixation includes:
• Compression osteosynthesis
a. DCP
b. EDCP
c. Lag screw
• Fixation osteosynthesis
a. Locking plate
b. Reconstruction plate
c. THORP
A Swiss study group called Arbeitsgemeinschaft für Osteosynthesefragen

(AO) was developed by Maurice E Müller, Robert Schneider, Hans
Willenegger and Martin Allgöwer to conduct research in bone healing, with
particular reference to the influence of the mechanical environment of the
fracture upon its healing pattern. They devised the AO compression
osteosynthesis.
Goals of the AO/ASIF technique for rigid fixation
1. Anatomic reduction of bone fragments.

2. Functionally stable fixation of the fragments.
3. Preserving the blood supply to the fragments by atraumatic surgical
procedures.
4. Early, active and pain free mobilisation.
Healing by primary intention can be achieved only by anatomic

approximation of the fractured fragments.
1. Anatomic reduction of bone fragments

It implies that occlusal and basal reductions are of equal importance. In closed
reduction, the aim is to achieve only occlusal reduction and not the basal
reduction. In order to achieve open or rigid fixation is required. This in turn
results in complete anatomic approximation which can be possible only when
occlusal reduction is done preoperatively. Occlusal reduction should be done
prior to screw fixation as the technique of rigid fixation does not allow any
correction after fixation.
2. Functionally stable fixation of the fragments
Stable fixation of the fragments is highly essential in order to avoid
interfragmentary gap, which in turn reduces motion-induced osteolysis.
Stability mentioned here refers to absolute stability, i.e. absence of relative
motion between the plates and the bone and also between the bone ends. This
is achieved by prestressing/preloading of the screw. The relative motion can be
prevented by anchoring free end plate with the single screw that is inserted
under tension. Other screws should be placed under minimal tension, which
finally results in direct bony union of fracture.
3. Preserving the blood supply (vascularity)

Preserving the blood supply to the bone fragments and soft tissue by using an
atraumatic surgical technique is an essential preventive measure against poor
healing and infection. Normally fracture producing trauma disrupts local
blood flow to the mandible, hence the procedure, in turn, should be
atraumatic.
4. Early, active and pain free mobilisation

Immediate, pain free, oral opening is so critically important which makes open
reduction ahead of conventional IMF. Benefits are prevention of tracheostomy
in severe maxillofacial injuries, normal food intake and ability to speak and
interact socially.
A. Compression plates
The compression plates are placed on AO/ASIF principles. These plates,
however, skilfully adapted to the mandible, the upper border and the lingual
cortices open up during the final tightening of the screws, resulting in
malocclusion (Fig. 42.26A–B).
FIGURE 42.26 (A–B) Opening up of the upper border of the

mandibular fracture when fixed with compression plates in the
lower border.
In order to overcome all these pitfalls, these plates included two pear-
shaped holes at the extreme ends of the plate. These holes had the widest
diameter near the fracture lines. The compression plate is placed in such a way
that the two holes lie on either side of the fracture line. The screw is inserted in
the narrowest part of the bone such that after tightening its head comes to rest
in the wider diameter of the bone. Since the upper border opens up during the
application of compression, a tension band should be applied at the level of
alveolus before tightening the screws (Figs. 42.27 and 42.28).
FIGURE 42.27 (A–B) Fixation with compression plates with pear-

shaped holes at the end
FIGURE 42.28 Compression plate.

Absolute stability is the goal of compression osteosynthesis.
a. Dynamic compression plates (DCPs)

These are the fixation plates designed to produce compression between the
bone fragments on activation.
Compression produced by DCP is 300 kPa/cm2 (600 N). This compression is
less than the compressive strength of bone, thereby produces no bone necrosis.
Indication
Nonoblique fracture with good bony apposition after reduction.
Contraindications
1. Severely oblique fracture

2. Comminuted fracture
3. Fracture with bone loss
Properties of plate
1. The plate has inclined plane in the hole proximal to the fracture. As the
screw is tightened it moves down the inclined plane, thereby
translating the bone fragments towards the fracture site.
2. The highest portion of inclined plane lies on the outer aspect of hole.
3. Compression screw: The screw placed in the height of inclined plane that
moves towards fracture site on tightening.
4. Static/passive screw: The other hole where screws placed in the lowest
point in hole creates no compression on tightening.
5. Minimum of two screws in each side of fracture, with the outer holes
acting as passive screw.
6. Unfavourable fracture requires longer plate with more holes.
The use of more screws increases the stability of plate and decreases the
risk of screw loosening.
7. Order of fixation
• 1 and 2 proximal to the fracture on either side (compression
screws), 3 and 4 the hole next to the compression screws on
either side (passive screws). 5 and more distal to the passive
screws
8. Plate bending: Overbend about 1–2 mm is done intentionally to prevent
lingual cortical widening when placed on the buccal cortex.
9. Bicortical screws (self-tapping screws) are used.
10. Fixations protocol
• Place screw 1—do not tighten
• Place screw 2—tighten fully
• Now tighten screw 1 completely creating interface
compression.
• Place 3, 4, 5—passive screw
Disadvantages
1. Require precise adaptation of plate to bone, else on tightening it alters

reduction thereby creating malocclusion.
2. If used on oblique fracture, the fragments slide over one another
creating malocclusion.
3. Maladapted plate in anterior mandible creates widening of mandible.
5. In fracture with good reduction and no bone loss, compression plate
tightening causes stripping of screws, splintering of bone adjacent to
fracture.
6. Ideally compression plates should be placed on tension zone, i.e.
superior border of mandible. Due to anatomic reasons (presence of
teeth), the plate is placed in inferior border. This mandates the
placement of arch bar or transosseous wiring or miniplate (angle) in
the tension zone superiorly.
b. Eccentric dynamic compression plate (EDCP)

It is based on the principle of compression osteosynthesis. It differs from DCP
in its application in situations where tension band application is not possible
as:
• Presence of impacted third molar with angle fracture.

• Edentulous mandible fracture.
• Avulsion of bone from fracture site.
Plate design
The outer holes have inclined planes oblique in relation to long axis of plate
whereas the inner holes are devoid of any plane inclination.
Mechanism
1. The fracture is reduced and the plate is adapted to the inferior border.
2. The two inner screws are placed first creating compression at the inferior
border of the fracture site.
3. Holes are drilled in eccentric position in outer holes of the plate. The
screws are placed and tightened.
4. This allows the bony fragments to rotate around the axis of inner
screws producing compression at the superior border.
5. This form of compression produces the greatest advantage of even
distribution of forces along the length of fracture.
Advantage
Even distribution of forces along length of fracture.
Disadvantages
• Technique sensitive
• Results are not found to be superior to other fixation methods
Lag screws
Compression of the fractured fragments can be accomplished by means of lag
screws. This technique was applied for the treatment of oblique fractures in
long bones. Few oblique mandibular fractures can also be treated through this
method.
Principle
A screw that glides through the cortex of one fragment and engages the cortex
of the opposite fragment with its threads, draws the fragments together and
compresses them when tightened. Gliding holes and thread hole must be
coaxial.
Applications (Fig. 42.29A–B)
• When a cortex screw is used the gliding hole should match the outer
diameter of the thread, while the thread hole matches the diameter of
the shank. The screws are packed in a position, which bisects the angle
formed by the lines perpendicular to the fracture line and to the long
axis of the bone.
• In case of mandible, lag screw is used for oblique surface fractures.
Here lag screw can be placed across the fracture surface without
causing any damage to the nerves and vessels. A lag screw can
produce functional stability only when the fracture surfaces are large
enough to accommodate two or three lag screws.
• Lag screws can also be used as a supplementary to plate fixation. In
case of increased obliquity of the fracture surfaces, the lag screw
neutralises the shearing force by transferring some of the primary
tension to shearing force and thus prevents displacement of the
fracture fragments.
• Lag screw can also be used for refixation of temporary mandibular
osteotomy.
• Single lag screw can be used for the internal fixation of mandibular
angle fracture. Here the fracture segments are reduced following
which the gliding and thread holes are made using percutaneous drill
guide and the screw is introduced through the same route.
FIGURE 42.29 (A) Principle of fixation with lag screw. Note the
gliding hole and the thread hole. (B) Fixation of mandibular fracture
with lag screws.
B. Fixation osteosynthesis
This includes:
1. Reconstruction plates
2. THORP
3. Locking plates
Indications
• Oblique fracture
• Comminuted fracture
• Loss of bone fragments in fracture
• Questionable postoperative compliance
• Nonatrophic edentulous fracture
Reconstruction plate
Reconstruction plates are thick, rigid plates primarily used in reconstruction of
mandible following resection. They are also used in mandible fracture
involving multiple segments. In contrast to semirigid fixations (miniplate), the
bone fragments adapt to the reconstruction plate providing the rigid fixation
of the fragments (Fig. 42.30).
FIGURE 42.30 Reconstruction plate.
THORP (titanium hollow screw osseointegrated reconstruction plate)

This was developed by Raveh as a modified reconstruction plate. In the
THORP system, the plate has a thickness of 3.0 mm, with a 4.0-mm screw
diameter. Special locking screws are inserted into each screw head to perform
the locking principle between the bone-anchored screw and the corresponding
plate hole.
Aim
• To provide stability to fractured bone fragments without applying

pressure to underlying bone.
• This prevents focal ischaemia, bone necrosis, screw loosening and plate
mobility, thereby reducing the risk of infection and malunion.
THORP consists of reconstruction plate and anchor screws.
Mechanism
Anchor screws osseointegra te with bone
↓
↑ Stability over time
↓ Friction with the hole in plate
↓
↑ Stability to plate and fracture segments
↓ Bone resorption
Disadvantage
The screws and plate osseointegrate with bone making removal difficult.
Locking plate
Locking plates have a 2.5-mm thickness and screws of either 2.4- or 3.0-mm
diameter, which lock with their thread at the screw head into the inner thread of
the plate hole. This feature of locking plate makes the plate screw unit, act as a
single fixation unit, thereby reducing plate screw mobility. This reduces the
chances of infection and nonunion. In the locking plates, a bending screw is
temporarily inserted in the area, where a screw insertion is intended, so that
during the bending process the inner thread of the plate hole is not deformed.
The disadvantages of THORP have been replaced by locking plate
(Fig. 42.31A–C).
FIGURE 42.31 (A) Locking plate. (B) Locking plate showing
serration designed for locking of the screw to plate. (C)
Comparison of screw head between conventional and locking
screws.
Fracture healing
Fracture results in a well-defined progression of tissue responses that are
designed to remove tissue debris, to reestablish vascular supply and to
produce a new skeletal matrix. The timing and the specific histology of the
process that occur to accomplish healing are dependent on the location of the
injured bone as well as on local and systemic factors. Bone healing can be by
primary or secondary intention. Spontaneous bone healing without surgical
intervention and healing that occurs after semirigid fixation process occurs by
secondary intention. Healing by primary intention occurs only when following
conditions are met: excellent anatomic reduction, minimal or no mobility and good
vascular supply at the fracture site. Primary healing process occurs after rigid
fixation process.
Primary bone healing

Primary bone healing occurs when enough rigidity and anatomic reduction
exists. It also takes place in cancellous bone without rigid stabilisation if no
gross mobility is present. Osteogenic cells and capillaries proliferate in the
medullary bone on both sides of fracture, forming new bone along the fracture
site. The healing that occurs in cortical bone fractures in which rigid fixation
been accomplished occurs in two different ways:
i. Gap healing
ii. Contact healing
Gap healing
Even with rigid fixation by means of a device that produces a stable
relationship between the fracture ends under the deforming forces produced
by muscle pull and function, a perfect anatomic reduction rarely exists. When
small gaps occur between bone segments, within a few days after fracture, gap
healing begins at these points. Blood vessels from periosteum, endosteum or
haversian canals invade the gaps, bridging mesenchymal osteoblastic
precursors. Bone is deposited directly on the surfaces of fracture fragments
without resorption and without intermediate cartilage formation.
• Gap <0.3 mm—lamellar bone forms directly.

• Gap between 0.3 to 1 mm—woven bone forms first followed by
lamellar bone.
Formation of lamellar bone occurs over a period of 6 weeks. Lamellar

bundles are oriented at right angles to the longitudinal axis of remaining bone.
Over several months, remodelling then leads to a change in the direction of
bundles to reorient them along the long axis of repaired bone.
Contact healing
In areas in which contact is achieved, the interfragmentary gap is essentially
zero. Since vascular and cellular ingrowth cannot proceed as it does in fracture
in which a gap exists, a special process of bone formation occurs.
Osteonal remodelling: Contact healing occurs through formation of a bone
metabolising unit (BMU), a bone remodelling unit (BRU) or a bone repair unit
(BRU) which is all synonyms for the newly forming (or regenerating) osteon.
Advancing group of osteoclasts followed by vessels and cells differentiate
into osteoblasts and form new bone.
Cutter cones: Osteoclasts begin to cut away cores on either side of the
fracture, progressing towards the fracture site, through necrotising bone and
into opposing bone ends proceeding at a rate of 50–80 mm/day. The resulting
bone provides a pathway for vessel ingrowth and osteoblastic proliferation
with formation of new bone.
Osteon forms at a rate of 1–2 mm/day.
Complete reconstruction of cortex takes place within 6 months. Gap healing
begins almost immediately in areas where a space of up to 1 mm exists
between fracture ends. Gaps are filled by appositional bone formation;
remodelling then restores the architecture.
In areas of contact healing, consolidation is achieved through haversian
remodelling alone. Osteoclasts produce pathways between fracture fragments,
which are then bridged by newly formed regenerating osteons.
Secondary bone healing

Secondary bone healing refers to spontaneous healing without surgical
intervention and after semirigid fixation.
The following phases can be described in the secondary bone healing
process: (i) initial stage, (ii) cartilaginous callus, (iii) bony callus and (iv)
remodelling.
During the initial stage, haematoma formation occurs, concurrent with
inflammatory response, which brings new vascularity and mesenchymal cells
that differentiate to form a fibrocartilaginous callus. This fibrocartilaginous
callus then ossifies to form the bony callus, which subsequently undergoes
remodelling and functional adaptation in much the same way as the
preinjured bone.
Initial reaction
Disruption of blood vessels and subsequent decrease in blood supply,
accompanied by generation of heat leads to hypoxia and cellular death at the
fracture site. This produces necrosis of the bone ends to a variable distance.
This aseptic necrosis leads to inflammation and oedema. Release of numerous
vasoactive angiogenic pyrogens, produces vasodilation within a few hours of
injury. Haemorrhage from dilated, damaged vessels of endosteum, periosteum
and haversian systems leads to haematoma formation. This clot is invaded by a
variety of blood-borne elements. In addition to granulation tissue within the
haematoma, fragments of bone and muscle may be found. The small nonvital
muscle undergoes autolysis within 5–10 days, while pedicled vascularised
muscle undergoes fibrosis. Small bone fragments may undergo surface
deposition of bone by migrating periosteal cells, while devitalised marrow
undergoes fatty degeneration.
Initiation of cellular proliferation occurs within 8–12 h; DNA synthesis and
proliferation by cells of cambium layer begins. These cells are pluripotent in
nature which gives rise to osteoblasts, fibroblasts and cells with chondrogenic
potential. This process initially involves the periosteum of entire injured bone,
but decreases over a few days to the area of fracture only. As these cells
proliferate, capillary ingrowth begins and the fibroblasts formed during the
proliferative stage migrate into wound and begins to lay collagen.
Granulation tissue is a combination of collagen and rich capillary network.
In this stage, a low tension as well as low pH is noted in granulation tissue;
these conditions trigger a response within the haematoma towards formation
of hyaline cartilage. Any movement between bone fragments, when not
immobilised causes continued compression and tension at the site of fracture
and directs cells towards the formation of cartilage.
Cartilaginous callus (soft callus) formation

Callus formation begins externally as well as internally. Externally, nodules of
cartilage are separated by fibrous septa; blood vessels within these septa
increase rapidly.
First, further calcification of cartilage takes place, with trapping of
chondroblasts and conversion to chondrocytes. Second, osteoblasts increase in
number and osteoclasts become apparent for the first time.
At the same time, internal callus between bone ends also forms. This area has
a better blood supply; therefore, less necrosis takes place. No intermediate
fibrocartilage is formed instead of osteoblasts from the endosteum form as
internal bony callus directly.
When the bone begins to heal after fracture, a callus forms around the
fracture site to stabilise the involved area, increasing the strength and stiffness
of bones (against bending and torsion) during the healing period.
Hard callus (bony callus) formation

Cartilaginous callus undergoes calcification into woven bone. The spaces
within the cartilaginous callus allow for further vascular ingrowth which leads
to increase in oxygen tension and transportation of nutrients to the site which are
conducive to formation of osteoblasts. The osteoblasts deposit osteoid on the
spicules of calcified cartilage and the osteoid then undergoes a calcification
process, forming bone. The process begins peripherally.
Initially, the bone that is formed is randomly arranged (woven bone). It then
undergoes organisation and changes to lamellar bone during the final stage of
healing.
Remodelling
Woven bone undergoes remodelling into lamellar bone. This slow process
progresses in accordance with Wolff’s law which states that, ‘Change in
functional state of bone causes structural or architectural changes in tissue through
bioelectric field production’.
As osteoclasts participate in remodelling by resorption of bone, factors are
released that help drive and direct the remodelling process. One of the factors
is bone morphogenetic protein (BMP), a collagenous-resistant glycoprotein
which acts as a mitogen and transforming growth factor. BMP induces
differentiation of mesenchymal cells towards bone formation.
Factors affecting bone healing

The regulation of bone repair is a complex process that requires interplay
between hormones, systemic and local growth factors. The proliferative
response of osteoprogenitor cells in the periosteum, endosteum and marrow as
well as the production of the cartilaginous–fibrocartilaginous matrices and
fibro-osseous callus, can be conceptualised as the results of cell–cell
interactions and cell–matrix interaction (Tables 42.2 and 42.3).
Table 42.2
Growth factors found in the fracture callus
BMP, Bone morphogenetic protein; TGF-beta, transforming growth factor-beta.
Table 42.3
Polypeptide growth factors involved in bone healing

I. Vascular ingrowth Plasma fibronectin
• Anchors cells in the ground substance
• Required for collagen formation
Endothelial cell-derived growth factor
• Mitogen
II. Callus formation Platelet-derived growth factor
• Mitogenic: Fibroblasts, bone cells
• Activates monocytes
• Promotes bone resorption
Epidermal cell growth factor
• Mitogen: Cartilage, bone
• Inhibits type I bone collagen synthesis
Fibroblast growth factor
• Mitogen: Fibroblasts, chondrocytes
Insulin-like growth factor
• Chondrocyte proliferation
• Chondrocyte proteoglycan synthesis
• Nerve growth factor
• Mitogen
III. Bone • Epidermal growth factor
formation/remodelling phase
Promotes bone resorption
Fibroblast growth factor
Promotes bone resorption in high doses
• Insulin
Synergistic effect with bone growth factors
• Interleukins (monocytes products)

• IL-1:
• Fibroblast proliferation
• Collagenase production
• Prostaglandin production
• IL-2:
• T-cell growth factor
• Stimulation of bone resorption by osteoclastic activation factor
(OAF) production
Complications
Infection
• In some studies, particularly those without antibiotics, infection may
occur in more than 50% of patients.
• Systemic factors include alcoholism, immunocompromised patients
and lack of antibiotic coverage.
• Local factors include poor reduction and fixation, fractured teeth in the
line of fracture and comminuted fractures.
• When infection is present it must be managed with debridement of
sequestra, drainage and antibiotic therapy. Apply rigid internal
fixation with or without intermaxillary fixation across the fracture site.
If a gap is present between the bone ends, a bone graft may be
necessary.
General cause of infection
• Haematogenous spread of infection leading to osteomyelitis

• Ischaemia caused by reduced blood supply
– Atropic edentulous mandible
– After radiotherapy
• Persistent movement of fracture fragments—because of inadequate
reduction and fixation.
In closed reduction if proper dental occlusion is not
achieved.
• Interposition of soft tissues between fragments
• Metabolic and systemic factors
– Osteoporosis, osteomalacia
– Paget’s disease
– Primary and secondary hyperparathyroidism
– Chronic renal diseases
– Long-term steroid therapy
– Chronic-iron, vitamin-deficiency
• Preexisting local condition
– Cysts
– Unerupted teeth
– Primary or secondary neoplasm
– Irradiated bone
Ankylosis
• Ankylosis is a rare complication of mandibular condyle fractures.

• It is most likely to occur in children and is associated with
intracapsular fractures and immobilisation of the mandible.
• It is believed to occur secondary to intra-articular haemorrhage,
leading to abnormal fibrosis and ultimately ankylosis.
• Ankylosis may result in disturbed growth and underdevelopment of
the affected side in children.
Nerve injury
• The inferior alveolar nerve and its branches are the most commonly
injured nerves. The prominent sign of inferior alveolar nerve deficit is
numbness or other sensory changes in the lower lip and chin.
• In degloving injuries there could be avulsion of the mental nerve at
mental foramen (Fig. 42.32).
• Damage to the marginal mandibular branch of the facial nerve is rare.
More commonly, nerve damage caused by trauma in the region of the
condyle, ramus and angle of the mandible and by lacerations along its
course is seen.
• Most of the sensory and motor functions of these nerves improve and
return to normal with time.
FIGURE 42.32 Avulsive injury of mental nerve at mental foramen.
Plate fracture
The plates might be fractured. The cause is the so-called metallic fatigue, a
situation that usually occurs when the plate supports an excessive and
prolonged mechanical load, almost always due to the absence of underlying
bone, e.g. reconstruction plates with bone defect bridging.
If the plate has also been excessively manipulated during the moulding
process, this phenomenon may occur.
CSF leak
Although not common, CSF leaks that were not noted preoperatively have
been reported after the treatment of midface fractures, most commonly
nasoethmoid, Le Fort II and Le Fort III fractures. Fractures through the
cribriform or fovea ethmoidalis are the most common causes. Frontal sinus
fractures which can occur in conjunction with midface fractures are another
common source. CSF leaks predispose to meningitis and cases of meningitis
secondary to posttraumatic CSF leaks have been reported years later.
Epiphora
Injuries to the lacrimal system either at the time of injury or iatrogenic,
secondary to open reduction and internal fixation, can result in epiphora.
Posttraumatic ectropion, again from injury or secondary to lower lid surgical
approaches can also lead to epiphora. Lacrimal injuries usually require (DCR)
dacryocystorhinostomy and ectropion requires a lid tightening procedure.
Globe injuries
The more common of these would include injury to the cornea (e.g. secondary
to injury during transconjunctival approach) or penetrating injuries from
scalpels, wires or drill bits. Ophthalmologic consultation is mandatory in these
injuries and any complaint of eye pain or feeling of foreign body in the eye
after surgery must be evaluated.
Diplopia
During the reduction of midface fractures, an already fractured orbital floor
can be mobilised inadvertently and cause herniation or entrapment of the
inferior rectus muscle.
Orbital floor exploration and reconstruction should be performed after other
related fractures are repaired to prevent the postoperative diplopia.
Nonunion
Nonunion means that the fracture is neither united nor will unite on its own.
• Nonunion indicates a lack of bony healing between the segments that

persist indefinitely without evidence of bone healing unless surgical
treatment is undertaken to repair the fracture.
• Nonunion is characterised by pain and abnormal mobility following
treatment.
• Radiographs demonstrate no evidence of healing and in later stages
show rounding off and sclerosis of the bone ends, a condition referred
to as eburnation.
• Nonunion includes the condition of fibrous union referred to
previously when there is a degree of stability.
Nonunion may occur in a number of circumstances some of which are

preventable:
i. Infection of the fracture site. The underlying teeth in the line of fractures
should be considered for possible extraction as they may be a nidus for
infection.
ii. Inadequate reduction and immobilisation.
iii. Unsatisfactory apposition of bone ends with interposition of soft
tissue.
iv. Excessive stripping of periosteum especially in comminuted and
edentulous fractures.
The remaining causes of nonunion may be impossible or very difficult to

overcome and are as follows:
1. The ultra-thin edentulous mandible in elderly debilitated patient

complicated by decreased vascularity and systemic factors.
2. Loss of bone and soft tissue as a result of severe trauma, e.g. missile
injury.
3. Inadequate blood supply to fractured site, e.g. after radiotherapy.
4. The presence of bone pathology, e.g. malignant neoplasm.
5. General diseases, e.g. osteoporosis, severe nutritional deficiency,
disorder of calcium metabolism. Table 42.4 indicates the aetiology of
nonunion.
Table 42.4
Aetiology of nonunion
1. Bone necrosis on either side of the fractured site

• Due to infection or ischaemia
• Infection may be local or systemic
2. Local causes of infection at fracture site
• Nonvital tooth in the line of fracture
• Preexisting acute infection like gingivitis, pericoronitis, periodontitis
• Compound fractures which get contaminated by saliva or exposed to external
environment
• Foreign bodies like tooth fragment, root tips, denture fragments or other external objects
• Contamination of bone pins, wires or screws
Malunion
• Malunion is defined as malalignment of the healed bony segments.

Not all malunions are clinically significant.
• More likely than nonunion.
• When a dentate portion is involved in the malunion, a malocclusion
can result.
• These malocclusions may be treated with orthodontics or osteotomies
after complete bony union.
• It may also result in facial asymmetry, enophthalmos, ocular dystopia,
etc.
• Secondary repair is much more difficult to carry out. The only method
of prevention is meticulous technique.
Delayed union
Delayed union and nonunion occur in approximately 3% of fractures. The
term ‘delayed union’ is difficult to define precisely as factors like the site and
patient’s age are considered. It must be assumed that the healing process has
been disturbed. This is as a result of local factors such as osteoporosis or
nutritional deficiencies.
Management
No active intervention is necessary in the short term. A fracture in which
fibrous union has occurred will frequently progress to slow bony
consolidation during the ensuring 12 months after injury. Fibrous union may
be an acceptable result in an elderly edentulous patient. However, in a
younger dentate, individual prosthetic replacement of missing teeth is
impractical if any mobility at a fracture site remains and at some point
nonunion has to be accepted and treated.
Soft tissue injury and management

Soft tissue injuries of the face not only create physical damage, but can also
carry with them a strong psychologic component. Often devastating
appearance of these injuries requires the clinician to approach treatment in a
systematic fashion, to allow for exacting repair. As with any injury, the first
step should be to treat emergency conditions and stabilise the patient.
Mentally, one needs to define and classify the wounds, while formulating a
treatment plan and surgical approach. In general terms, a wound is defined as
any disruption of the normal anatomic relationships of tissues as a result of
injury. More specifically, soft tissue injuries of the face are categorised into the
following types:
1. Contusions
2. Abrasions
3. Lacerations
a. Simple laceration
b. Stellate laceration
c. Flap-like laceration
4. Avulsion
5. Puncture wound
Contusions
Contusions typically follow blunt trauma, which results in oedema and
haematoma formation in the subcutaneous tissues. The overlying skin and
mucosa are left intact. The haematoma usually resolves without treatment
unless it is infected or very large in size.
Management
When associated with lacerations the margins of the contused tissue should be
excised. Usually the margin is undermined at the subcutaneous level for
closing the layer without any tension. If contusion and laceration involves vital
structure, treatment should be delayed till the contusion resolves.
Hypopigmentation or hyperpigmentation of the area of the injury can be
sometimes noted.
Abrasions
Abrasions, on the other hand, are the result of a deflecting-type of trauma and
result in the loss of the epithelial and papillary layers of the skin. Subsequent
defect leaves a raw, bleeding, exposed reticular layer. This kind of injury is
very painful due to the exposed nerve endings.
Management
The dirt and other small particles should be cleaned from the wound by
washing with a soap solution under local anaesthesia. It should be irrigated
sufficiently with saline; then covered with a layer of antibiotic and finally
dressed with gauze. When the wound is very deep, significant scarring from
granulation tissue results.
Excessive sunlight exposure of the abraded skin wound results in
permanent hyperpigmentation.
Lacerations
Lacerations may be produced by either blunt or sharp trauma and can be
further subdivided based on their pattern and depth of penetration.
Lacerations might have contused, ragged or stellate margins or may involve
avulsion of tissues. They may be associated with injury of the underlying
vessels, nerves and bones. These types of wounds are usually highly
contaminated with dirt, small particles of glass, bony splinters, etc.
Management
Simple lacerations
are usually clean and therefore require minimum debridement (Fig. 42.33A–
D). Contaminated lacerations should be thoroughly cleaned, foreign particles
removed and the wound closed.
FIGURE 42.33 (A) Columella rupture as clean laceration. (B)

Primary closure. (C) Clean wound. (D) Primary closure with
minimal debridement suffice.
Stellate lacerations
In ragged lacerations, ragged edges should be trimmed with scalpel to
facilitate closure (Fig. 42.34).
FIGURE 42.34 Stellate laceration in lower lip showing ragged
edges.
Flap-like lacerations
require significant undermining of soft tissues. Minimal debridement of
involved tissue should be employed and the wound margin trimmed for
closure. Pressure dressings of such lacerations help in minimising the dead
space and thus limiting haematoma under the tissues.
Degloving laceration
Typically occurs from high energy shearing forces, wherein the entire jawbone
is exposed (Fig. 42.35).
FIGURE 42.35 Degloving of mandible with lip laceration.
Avulsion
An avulsion injury refers to the complete loss of tissue, leaving a break or gap
in skin continuity. Careful examination of avulsed injury may reveal that the
tissue margins have been retracted or rolled under the wound margin.
Management
When there is small amount of loss of tissue, the wound margins may be
undermined and closed without tension.
If there is significant loss of tissue, a skin graft or local flaps may be used to
close the raw wound surface.
Penetrating wounds
Puncture wounds are injuries caused by direct penetration of an object
through the skin barrier.
Management
Wound should be thoroughly debrided and closed in layers.
Supportive therapy
1. Pain control
Avoid giving powerful analgesic which depresses the level of consciousness
and respiration.
Avoid morphine which depresses the cough reflex and leads to aspiration
especially in head injury patients. It also leads to constriction of pupil and
masks the early signs of head injury. If sedation is required then diazepam 5 or
10 mg dose till desired or Pentazocine 15–30 mg can be used. It is always best
to use NSAIDs to control the pain.
2. Tetanus prophylaxis
Tetanus toxoid is given for prophylaxis against Clostridium tetani. American
College of Surgeons committee on trauma recommendation on tetanus care is
summarised as follows:
Previously immunised individuals
a. Fully immunised individuals if last dose of toxoid was given within

10 years, administer 0.5 mL absorbed toxoid for tetanus prone wounds.
If more than 5 years has elapsed since the last dose, this booster may be
omitted if excessive toxoid injections have previously been given.
b. Partially immunised individuals and last dose was received more than
10 years ago, 0.5 mL absorbed toxoid is administered for both tetanus
prone and nontetanus prone wounds.
Individuals not adequately immunised

When the patient has received only one or no previous injections of toxoid or
the immunisation history is unknown.
a. Nontetanus prone wounds. Administer 0.5 mL of absorbed toxoid.

b. Tetanus prone wounds
• Administer 0.5 mL absorbed toxoid
• Administer 250 units antitetaum serum (ATS)/tetanus
immunoglobulin (TIG)
Administer medications using different syringes and sites for each different
injection.
Control of infection
Since most of the maxillofacial injuries are compound it acts as a potential
source of infection.
Antibiotics are usually given for fractures which are exposed to saliva or
external environment. A combination of a penicillin and metronidazole is one
of the suitable choices. The use of prophylactic antibiotics in CSF leakage is
controversial and opinion of neurosurgeon should be sought.
• Surgical dressing: An antibiotic dressing prevents further contamination

of wound. Pressure dressing in large wounds helps in the prevention
of formation of dead space and haematoma.
• Drains: Drains help in drainage of pus or other exudates in deep
wounds. It is usually placed in between the sutures. It is removed after
48 h. If drain is active after 48 h a new drain should be replaced.
CHAPTER 43
Dentoalveolar Fracture
Aetiology and risk factors

Classification
WHO classification
Andreasen/WHO classification
Clinical findings
• Soft tissue lacerations
• Damage to teeth
• Alveolar fractures
Management
Avulsed tooth
Extraoral storage media
Reimplantation and splinting
• Preparation of the root
• Splinting of teeth
Dentoalveolar injuries are defined as those in which avulsion, subluxation or fracture

of the teeth occurs in association with a fracture of the alveolus. This type of injury
may occur alone or in conjunction with some other type of mandibular fracture.
The dental and the dentoalveolar segments of the oral cavity, especially the
anterior portion, are a common site of trauma in all age groups.
Aetiology and risk factors

• Dental and jaw development: Children at higher risk from
uncoordinated movement, contact sports
• Force of the injury: Amount, direction and location of maximal force
▪ Low velocity impact: Dentoalveolar fracture
▪ High velocity impact: Dental fracture
▪ Indirect injury: Blow to chin
• Anatomy of the jawbones: Prognathic maxilla and mandible are higher
risk of trauma (Fig. 43.1A–B)
• Position of the teeth within the jawbone: Proclined incisors at greater
risk (Fig. 43.2A–D)
• Primary or permanent dentition
• Periodontal health of the teeth: Periodontally poor teeth at risk of
avulsion at low force (Fig. 43.3)
• Poor laryngoscopy technique
• Extreme biting force during seizure, comatose patients, drug abuse,
familial dysautonomia
• Jaw position during trauma: Occluded or open mouth posture
• Malocclusion
▪ Teeth out of occlusion (open bite)
▪ Teeth forced into occlusion (crossbite, scissor bite)
• Types of object
▪ Sharp object: Clean crown fracture
▪ Blunt object: Root fracture, luxation
FIGURE 43.1 (A–B) Prognathic maxilla at high risk of trauma. Note

the nonvital and fractured anterior teeth.
FIGURE 43.2 (A–D) Proclined incisors with increased overjet at
greater risk for trauma.
FIGURE 43.3 Proclined periodontally compromised anterior teeth—
at risk of avulsion from low force impact.
Classification
FIGURE 43.4 A Class I. Simple fracture of the crown of 11

involving enamel. Note nonvital 21 (Class IV).
FIGURE 43.5 Class II extensive crown fracture involving dentine
but no pulp exposure.
FIGURE 43.6 Class III extensive crown fracture involving dentine

with pulp exposure in 12. Note avulsed 41 (Class V).
FIGURE 43.7 Class IV traumatised tooth with loss of crown
structure that has become nonvital in 11.
FIGURE 43.8 Class V tooth lost due to trauma 21. Note Ellis Class
I fracture in 11.
FIGURE 43.9 Class VI fracture of tooth with no loss of tooth
structure.
FIGURE 43.10 Class VII displacement of tooth without crown or
root fracture.
FIGURE 43.11 Class VIII fracture of crown en masse.

FIGURE 43.12 Class IX fracture of deciduous teeth.
Ellis and Davey’s classification (1960)

Class I Fracture of the crown confined to the enamel only
(Fig. 43.4)
Class II Fracture of the crown involving the enamel and substantial portion of dentine
(Fig. 43.5) but without pulpal exposure
Class III Fracture of the crown involving the enamel and substantial portion of dentine
(Fig. 43.6) along with pulpal exposure
Class IV Fractured tooth becomes nonvital (crown structure may or may not be lost)
(Fig. 43.7)
Class V Tooth lost due to trauma
(Fig. 43.8)
Class VI Fracture of root of the tooth (crown structure may or may not be lost)
(Fig. 43.9)
Class VII Traumatised tooth is displaced without fracture of crown or root
(Fig. 43.10)
Class VIII Fracture of crown en masse
(Fig. 43.11)
Class IX Fracture of deciduous teeth
(Fig. 43.12)
Many systems have been developed to classify various injuries to the teeth
and supporting structures resulting from trauma.
The present classification was based on International Classification of Dental
and Stomatological Diseases presented by WHO. This was later modified by
Andreasen, which applies to the effects of trauma to hard dental tissues and
pulp, periodontal tissue, supporting bone, gingival and oral mucosa, based on
anatomy, prognosis and treatment.
WHO classification
WHO gave following classification in 1978 with code numbers corresponding
to International Classification of Diseases.
• 873.60—Fracture of enamel only

• 873.61—Fracture of enamel and dentine without pulp exposure
• 873.62—Fracture of crown involving the pulp
• 873.63—Fracture of root
• 873.64—Fracture of both crown and root
• 873.66—Displacement of tooth within the socket (luxation)
• 873.67—Movement along the long axis of the tooth (intrusive or
extrusive)
• 873.68—Loss of tooth (avulsion)
• 873.69—Other injuries such as soft tissue lacerations
This classification was modified by Andreasen as follows:
• 873.64—Uncomplicated fracture of both crown and root but no pulpal

involvement
• 873.64—Complicated fracture of the crown and root without pulpal
involvement
• 873.66—Concussion
• 873.66—Subluxation
• 873.66—Lateral luxation
Andreasen/WHO classification
Injuries to hard dental tissues and pulp (Fig. 43.13A–G)
• Condition of pulp should be noted at the time of injury and at various

times following traumatic incidence.
• Radiographic examination should be done in the area of suspected
injury.
FIGURE 43.13 (A) Crown infraction. (B–C) Uncomplicated crown
fracture. (D) Complicated crown fracture. (E) Uncomplicated
crown-root fracture. (F) Complicated crown-root fracture. (G) Root
fracture.
Infraction/fracture of enamel
• Microcracks or incomplete fracture lines within the enamel with no loss

of crown structure.
• Craze lines running parallel with direction of enamel rods and ending
at dentinoenamel junction. It can occur alone or can be a sign of
concomitant attachment injury where force taken up by attachment
injury leaves enough force to crack the enamel.
Uncomplicated crown fracture

An uncomplicated crown fracture is a fracture limited either to enamel only or
to the enamel and dentine without pulpal involvement.
Complicated crown fracture

A complicated crown fracture is fracture of both enamel and dentine with
pulpal involvement.
Uncomplicated crown-root fracture

An uncomplicated crown-root fracture involves enamel, dentine and
cementum with no involvement of the pulp.
Complicated crown-root fracture
A complicated crown-root fracture is a fracture involving enamel, dentine and
cementum with pulpal involvement.
Root fracture
A root fracture involving dentine, cementum and the pulp.
Injuries to the periodontal tissues (Figs. 43.14 and 43.15)
FIGURE 43.14 (A–B) Extrusive luxation. (C) Intrusion in a child. (D)

Intrusion 12, avulsion 11.
FIGURE 43.15 (A) Concussion. (B) Subluxation. (C) Intrusive
luxation. (D) Extrusive luxation. (E–F) Lateral luxation. (G)
Retained root-crown fracture. (H) Exarticulation.
Concussion
A concussion is an injury to the tooth-supporting structures with no mobility
or loss of tooth, but with pain on percussion.
Subluxation (loosening)
Subluxation is an injury to the tooth-supporting structures wherein there is
increased mobility of the tooth but no loss of tooth.
Intrusive luxation (central dislocation)

Intrusive luxation is movement of tooth into the alveolar bone with alveolar
socket fracture. The treatment is controversial as one school of thought is to
surgically reposition the intruded tooth and the other advising initial splinting
followed by orthodontic extrusion of the affected tooth.
Extrusive luxation (peripheral dislocation partial avulsion)

An extrusive luxation is partial or incomplete dislocation of the tooth out of
the alveolar socket.
Lateral luxation
Lateral luxation is movement of the tooth in any direction except along the
vertical axis, occurring along with alveolar socket fracture or comminution.
Retained root fracture

A retained root fracture is a fracture with retention of the root segment but
loss of the crown segment.
Exarticulation (complete avulsion)

An exarticulation occurs when the entire tooth is displaced out of the alveolar
socket.
Injuries to the supporting bone (Fig. 43.16A–G)
FIGURE 43.16 (A) Comminution of the alveolar socket. (B–C)

Fracture of the alveolar socket wall. (D–E) Fracture of the alveolar
process. (F–G) Fracture of the mandible and maxilla.
Comminution of the tooth socket

Crushing and comminution of the alveolar socket can occur together with
intrusive and lateral luxation.
Alveolar socket wall fracture

A fracture of the alveolar socket is confined to the buccal/labial or
lingual/palatal wall of the socket.
Fracture of the alveolar process
A fracture of the alveolar process may or may not include the tooth socket.
Fractures of the mandible or maxilla

A fracture involving the base of the mandible or maxilla and often the alveolar
process, but the alveolar socket may or may not be involved.
Injuries to the gingiva or oral mucosa
Laceration of gingiva or oral mucosa

Trauma by a sharp object causing a shallow or deep tear wound in the oral
mucosa (Fig. 43.17).
FIGURE 43.17 Gingival tear and step deformity in association with

dentoalveolar fracture.
Contusion of gingiva or mucosa

Trauma by the impact of a blunt object causing a bruise resulting in
submucosal haemorrhage without a break in the mucosa.
Abrasion of gingiva or oral mucosa

A superficial injury as a result of grazing or scraping of the mucosa, causing a
raw, bleeding surface, constitutes an abrasion of the gingival or oral mucosa.
Clinical findings
1. Soft tissue lacerations
• Inspection may reveal a full thickness wound of the lower lip or a

ragged laceration on its inner aspect caused by impingement against
the lower anterior teeth (Fig. 43.18A–B).
• There is usually substantial bruising of the lips and there may be
portions of tooth or foreign bodies embedded in the soft tissues
(Fig. 43.19A–F).
• Lacerations of the gingiva and deformity of the alveolus may be seen
(Fig. 43.20).
• In the mandibular anterior region ‘degloving’ injury may occur due to
impact of the chin on some resilient surface.
FIGURE 43.18 (A) Mandibular dentoalveolar fracture with avulsion

of teeth. Trauma to the lower lip indicated by ragged laceration. (B)
Laceration of upper lip during trauma to 12.
FIGURE 43.19 (A) Traumatised region, healing lip injury. (B)
Intraoral periapical radiograph of lip showing radiopaque foreign
body inside lip tissue. (C) Wound explored and foreign body
extracted. (D–E) Foreign body is fractured tooth fragment of 11.
Corresponding in shape to the fracture edges. (F) Healed wound
after 1 week.
FIGURE 43.20 Lacerations of the gingiva and deformity of the

alveolus.
A horizontal tear occurs in the buccal sulcus at the junction of the attached
and free gingiva. Paraesthesia or anaesthesia of lower lip may result from chin
or lip laceration.
2. Damage to teeth
• Missing, mobile, extruded or intruded teeth.

• Fracture of the crown of individual teeth.
• Any missing fragments of crown or missing fillings should be noted as
these may be embedded within the soft tissues or more rarely
swallowed or inhaled.
• Exposure or near exposure of the pulp chamber. This requires
immediate treatment.
• Fractures of the roots of teeth or excessively mobile teeth.
• Derangement of occlusion.
• Vertical split or a horizontal fracture just below the gingival margin
resulting from indirect trauma against the opposing dentition or
violent impact by a small hard object such as missile.
• Multiple fractured but firm teeth indicating that the jaws were
clenched during trauma.
• Electrical or thermal vitality tests at this stage of injury are unreliable
and are of little use in determining the eventual prognosis for the pulp.
3. Alveolar fractures (Figs. 43.21 and 43.22)

Fractures of the alveolus may be present with or without associated injury to
the teeth and jaw.
FIGURE 43.21 Alveolar fracture involving right maxillary dental
segment.
FIGURE 43.22 (A–B) Multiple teeth avulsion with dentoalveolar

fracture of mandibular anterior teeth segment.
Very commonly the alveolar fracture is associated with the mandibular

fracture making clinical diagnosis difficult.
• Crepitations on palpation and inability to close the jaw from premature

contact of teeth are findings common for alveolar fracture and jaw
fracture.
• Blood tinged saliva is a common finding of alveolar fracture from
gingival tear.
• Posterior open bite may occur with fractures of the anterior alveolar
process.
• A complete alveolar fragment may be displaced into the soft tissues of
the floor of the mouth and occasionally can be completely covered by
mucosa.
Intraoral periapical radiographs and orthopantomographs are useful aids in
diagnosis.
Management
Avulsed tooth (Fig. 43.23A–J)
Tooth avulsion occurs when the periodontal ligament attachment is torn and
the tooth is ‘expelled’ from the socket. This results in pulp necrosis and leaves
viable periodontal ligament cells on most of the root surface. The most
commonly involved teeth in both dentitions are the maxillary central incisors.
This usually occurs between 7 and 10 years of age, when the permanent
incisors are erupting. According to Andreasen, the loosely structured
periodontal ligaments and resilient alveolar bone surrounding erupting teeth
provide minimal resistance.
FIGURE 43.23 (A–J) Treatment of avulsion of maxillary and
mandibular anterior teeth following trauma.
Avulsion of the tooth always results in necrosis of the pulp. The necrotic
pulp tissue is highly susceptible to bacterial infections. If revascularisation
does not occur or if not treated endodontically, the pulp space will inevitably
get infected. If the tooth is excessively dried before it is replanted into the
socket, the damaged periodontal ligament cells will cause a severe
inflammatory reaction over the surface of the root resulting in resorption.
The goal of reimplanting teeth after traumatic avulsion is to retain a viable
pulp and periodontal ligament tissue that assist reattachment and avoid root
resorption. The success of reimplantation is inversely proportional to the
length of time the tooth is out of the socket. In addition, the type of
extraalveolar storage once the tooth has been avulsed is a significant factor
determining tooth survival. Reimplanting the tooth within 15–20 min of
avulsion prevents the loss of normal periodontal ligament cells and has a
favourable long-term prognosis.
• Emergency treatment at the accident site.
• Replant the avulsed tooth back into its socket if possible or put in an
appropriate storage medium.
• As mentioned, injury to the periodontal ligament attachment that
occurred during the trauma is unavoidable but excessive drying,
which damages morphology and functioning of the periodontal
ligament cells, should be prevented. It is best to replant the tooth
within 15–20 min of avulsion.
Extraoral storage media
• Milk is considered the best medium because of its availability, pH

compatibility to vital cells, freedom from bacteria and its ability to
preserve the vital periodontal ligament cells for up to 3 h post
avulsion.
• Saline (1 teaspoon of salt added to 8 ounces of water).
• Saliva soaked towel.
• The buccal vestibule or under the tongue, unless there is a risk of
aspiration or swallowing, or in a container.
• Water is the least favoured storage medium because the hypotonic
environment leads to rapid cell breakdown and increased
inflammation after replantation. Storage in tap water has been
documented to have adverse effects of periodontal healing and is not
recommended for cleaning or transportation of avulsed teeth.
• Transport containers with specialised cell culture media like Viaspon
and Hanks’ balanced salt solution (HBSS) are found to be highly
effective in preserving the viability of tissues of the periodontal
ligaments for a long duration. The benefit of such a system is the inner
suspension netting and removable basket that allows gentle cleaning
without crushing the periodontal ligament.
Reimplantation and splinting

Andreasen proposed that the following conditions be considered before
reimplanting a permanent tooth:
1. The avulsed tooth should not have advanced periodontal disease.

2. The alveolar socket must be reasonably intact to provide a seat for the
avulsed tooth.
3. There should be no orthodontic considerations such as overcrowding of
the teeth.
4. The extraalveolar period should be considered, if the tooth is
reimplanted within 30 min of avulsion, there is a good chance of
successful reimplantation. For extraalveolar periods greater than 2 h,
complications associated with marked root resorption increase
significantly.
5. The stage of root development should be assessed. In teeth with
incomplete root formation, survival of the pulp tissue is possible if
reimplanted within 2 h of avulsion.
Preparation of the root

Preparation of the root depends on stage of tooth maturity (open versus closed
apex) and the dry time (duration of time after avulsion and before placement
in a storage medium). A dry time of up to 60 min is considered optimal after
which periodontal ligament cells are less likely to survive.
Extraoral dry time less than 60 min
Closed apex
The root should be rinsed with water or saline to get rid of debris and
replanted as gently as possible.
Open apex
Gently rinse off debris, soak in doxycycline for 5 min or cover with
minocycline followed by reimplantation.
Extraoral dry time more than 60 min
Closed apex
Place in acid for 5 min to remove the periodontal ligament, soak in fluoride and
replant. If dry time is more than 60 min and preserving the periodontal
ligament need not be considered, then endodontic treatment must be
performed extraorally. By removing all remaining periodontal ligament,
chances of inflammatory response on replantation is minimised. The tooth
should then be kept in 2% stannous fluoride for 5 min and replanted.
Open apex
This is controversial but is often treated as closed apex by extraoral root canal
treatment followed by reimplantation.
Preparation of the socket

The socket should not be disturbed before replantation. Any obstacle or blood
clot, if any, is gently aspirated with no aggressive manipulation of the socket.
Splinting of teeth
• During healing, a splinting technique done for an adequate duration of
time that allows physiologic movement of the tooth decreases the
incidence of ankylosis.
• Semirigid (physiologic) fixation for 1–2 weeks is recommended.
• The splint should accommodate physiologic movement, should have
no memory (so the tooth is not moved during healing) and should not
impinge on the gingiva.
When the tooth is not optimally positioned, bite should be adjusted to avoid
traumatic occlusion. The involved tooth should be splinted with a semirigid
acid-etch resin splint of 7–10 days. Recent studies have indicated that rigid
splinting of reimplanted teeth increases the extent of root resorption. A minimum of
1 week is sufficient to create enough periodontal support for maintaining the
tooth in position. Therefore, splinting is required for 1–2 weeks. The only
exception is when tooth avulsion has occurred along with alveolar fractures,
for which 4–8 weeks is the suggested time of splinting.
Dentoalveolar fractures
Dentoalveolar fracture requires early reduction and stabilisation or
immobilisation by splinting to adjacent stable teeth. The wiring techniques are
simple and rapid immobilisation of the alveolar segments utilising the teeth
for support is possible:
1. Direct interdental wiring

2. Continuous or multiple loop wiring
3. Arch bars—Stabilisation with arch bars give the best form of
immobilisation, though sometimes a simple resin composite splint may
also help.
CHAPTER 44
Fractures of the
Mandible
Applied surgical anatomy of mandible

Classification of mandibular fracture
Factors affecting displacement of the fracture
Clinical findings
Management
Condylar fractures
Aetiology
Mechanism of injury
Clinical features of unilateral condylar fractures
Clinical features of bilateral condylar fractures
Investigations
Management
• Principles of treatment of condylar fracture
• Treatment protocol for different types of condylar
fracture
• Technique
Complications
• Ankylosis of the temporomandibular joint
• Interference with growth
Management of fractures of edentulous jaw
Open versus closed treatment
Intraoral versus extraoral approach
Subperiosteal versus supraperiosteal exposure
Type of internal fixation hardware
Simultaneous bone grafting
Mandibular fractures occur twice as often as midfacial fractures; however,

force required to fracture the mandible is almost 4–5 times as the maxilla.
Applied surgical anatomy of mandible

• Mandible is a long tubular bone bent into a blunt V-shape. The
strength of the mandible lies in the dense cortical plates. The cortical
bone is thicker anteriorly and at the lower border of the mandible,
whereas posteriorly the lower border is relatively thin. The central
portion consists of cancellous bone (Fig. 44.1).
• Mandible may be compared to an archery bow which is strongest
anteriorly in the midline with progressively less strength towards the
condyles where fracture is more prone to occur.
• The shape of the mandible varies considerably with age and growth,
whereas the tooth plays a major role in determining the mandibular
height (Fig. 44.2).
• Alveolar process has a lingual and buccal plate of thin compact bone.
Shape of the alveolar process is dependent on the presence or absence
of teeth. After the extraction of the teeth, the alveolar process
undergoes resorption continuously and therefore becomes atrophic.
• The mandible is unique in its function in the following respect. Any
movement of the mandible results in movement of both the condyles
with respect to the skull base. Though condyles are the articular
surface of the mandible anatomically, occlusal surface of the
mandibular teeth subserves this role functionally.
• Bones usually fracture at the site of tensile strength, as resistance to
compressive force is greater in them. In 1961, Huelke showed that
forces applied to symphysis menti, mandibular body or mental
foramen lead to strains at the condylar neck and also along the lingual
plates in the opposite molar region. The mandible is a strong bone, the
energy required to fracture it ranging from 44.6 to 74.4 kg/m.
• Trajectories of force (mandible): A line of stress extends from one
condyle to the other passing along the symphysis. These lines of
orientations of the bony trabeculae correspond to the pathway of
maximal pressure and tension. The major advantages of these
trajectories are that it dissipates the forces from body of mandible to
condyle thus preventing middle cranial fossa injury (Fig. 44.3).
• Sometimes an impact which might fail to cause a fracture may result in
capsulitis. Capsulitis refers to an effusion of the inflammatory
synovial fluid into the joint cavity or bleeding into the cavity resulting
in haemarthrosis.
• When this occurs in young children, it results in ankylosis of the TMJ
and hinders the normal growth potential of the condyle. Occasionally
condylar head may be driven backwards which tears the external
auditory meatus and causes bleeding from the external ear.
• Periosteum of the mandible does not significantly influence the site of
mandibular fracture or its displacement. However, it is of significance
in the treatment of edentulous fractures.
• Muscles attached to the mandible considerably influence the
displacement of the fractured segments.
• Fractures of mandible between mental foramen and mandibular
foramen pose a risk to the inferior alveolar neurovascular bundle. The
mental nerve runs with the inferior alveolar artery and injury to the
canal produces numbness of the ipsilateral lip and chin.
• Blood supply of the mandible is via the inferior alveolar artery that
runs in the inferior alveolar canal. Additionally, blood supply from
surrounding periosteum plays a very important role in healing,
especially in the elderly and in injuries that include the canal.
• In severely atrophic mandible, there is greater dependency on the
periosteal blood supply; therefore, minimal stripping of the
periosteum to be done in case of open reduction.
FIGURE 44.1 Anatomy of the mandible.
FIGURE 44.2 Variable mandibular morphology with age.
FIGURE 44.3 Trajectories on mandible.
For ease of understanding and learning, this chapter has been presented in
three parts, namely, mandible fractures (symphysis, parasymphysis, body
angle, ramus), condylar and edentulous fractures (Box 44.1).
Box 44.1 Area of weakness

Mandible as a single bone has many areas of weakness where the fracture is
more likely to occur. These vulnerable areas become the frequent site of
fracture than other areas.
• Junction of the alveolar bone and mandibular basal bone—

dentoalveolar fractures tend to occur independently or with other
fractures.
• Symphysis—fusion of two bony halves of mandible occur in the
symphysis at the age of 12 months, making them more vulnerable.
• Parasymphysis—presence of incisive fossa and mental foramen creates
the natural susceptibility for fracture to occur lateral to mental
prominences.
• Angle—junction of thicker mandibular body and comparatively thinner
ramus of mandible naturally creates a line of weakness in angle.
• Condyle—slender condyle neck makes more vulnerable for fracture.
Direct trauma to chin may cause the condylar neck fracture as protective
mechanism avoiding middle cranial fossa injury.
• Teeth—edentulous mandibles are more vulnerable than the dentulous
mandible (due to loss of teeth and resorption of alveolar bone). Presence
of long rooted canine and impacted molars make them vulnerable for
fracture.
Classification of mandibular fracture (Box

44.2 and Box 44.3)
Box 44.2
I. Dingman and Natvig anatomic classification (Fig. 44.4A–H)
a. Midline: Fractures between central incisors

b. Symphysis: Fractures occurring within the area of the midlife of the
mandible
c. Parasymphysis: Bounded by vertical lines distal to the canine teeth
d. Body: From distal symphysis to a line coinciding with the alveolar
border of the masseter muscle usually including the third molar
(between canine region and the angle)
e. Angle: Triangular region bounded by the anterior border of the masseter
muscle to the posterosuperior attachment of the masseter muscle
(usually distal to the third molar)
f. Ramus: Bounded by the superior aspect of the angle to two lines forming
an apex at the sigmoid notch
g. Condylar process: Area of the condylar process superior to the ramus
region
h. Coronoid process: Includes coronoid process of the mandible superior
to the ramus region
i. Dentoalveolar process: The region that would normally contain teeth
II. Kazanjian and Converse classification

Kazanjian and Converse classified mandibular fractures by the presence or
absence of serviceable teeth in relation to the line of fracture. This may be
helpful in determining treatment.
Class I: Teeth are present on both sides of the fracture line

Class II: Teeth are present only on one side of the fracture line
Class III: Patient is edentulous
III. Kruger and Schilli classification
1. Relation to external environment

a. Simple or closed
b. Compound or open
2. Types of fracture
a. Incomplete
b. Greenstick
c. Complete
d. Comminuted
3. Dentition of jaw with reference to use of splints
a. Sufficiently dentulous jaw
b. Edentulous or insufficiently dentulous jaw
c. Primary and mixed dentition
4. Localisation
a. Fractures of symphysis between canines
b. Fractures of canine region
c. Fractures of body of mandible between canine and angle of
mandible
d. Fracture of angle of mandible in third molar region
e. Fractures of mandibular ramus between angle of mandible and
sigmoid notch
f. Fractures of coronoid process
g. Fractures of condylar process
IV. Spiessel classified mandibular fracture based on
1. Number of fragments (F)

2. Location of fracture (L)
3. Status of the occlusion (O)
4. Soft tissue involvement (S)
5. Associated fracture (parallel fracture of the facial skeleton) (A)
Classification of fractures by number of fragments and presence of a bone

defect (F0–F4)
• F0: Incomplete fracture

• F1: Single fracture•F2: Multiple fracture
• F3: Comminuted fracture
• F4: Fracture with a bone defect (fracture with bone loss)
Classification of fractures by site (L1–L8)
• L1: Precanine
• L2: Canine
• L3: Postcanine
• L4: Angle
• L5: Supra-angle
• L6: Condylar process
• L7: Coronoid process
• L8: Alveolar process
Classification of fractures by Occlusal displacement (O0–O2)
• O0: No malocclusion
• O1: Malocclusion
• O2: Nonexistent occlusion (edentulous mandible)
Classification of fractures by soft tissue involvement (S0–S4)
• S0: Closed
• S1: Open intraorally
• S2: Open extraorally
• S3: Open intra- and extraorally
• S4: Soft tissue defect
Associated fractures (A0–A6)
• A0: None
• A1: Fractures or loss of tooth
• A2: Nasal bone
• A3: Zygoma
• A4: Le Fort-I
• A5: Le Fort-II
• A6: Le Fort-III
Biomechanics of mandibular fracture

The mandible is involved in 70% of patients with facial fractures. In general,
incidences of fractures of the mandibular body, condyle and angle are
relatively similar, while fractures of the ramus and coronoid process are rare.
The condyle and angle represent the commonest site of fracture in the
mandible.
Box 44.3 Types of fracture

Simple fractures
• Linear fracture which are not in communication with the exterior—Rowe

and Killey.
• Fracture in which the overlying integument is intact—Kruger.
Compound fracture
A fracture in which an external wound involving the skin, mucosa or
periodontal membrane communicates with the break in the bone.
Complex Fracture
A fracture in which there is considerable injury to the adjacent soft tissue or
adjacent parts: may be simple or compound.
Comminuted fracture
A fracture in which bone is splintered or crushed.
Greenstick fracture
A fracture in which one cortex of the bone is broken, the other cortex being
bent (seen in children).
Pathological
Fracture due to existing pathology:
1. Generalised skeletal deformity

2. Localised skeletal deformity
Impacted fracture
A fracture in which one segment is firmly driven into another.
Indirect fracture
A fracture at a point distant from the site of injury.
Atrophic fracture
A spontaneous fracture resulting from atrophy of the bone, as in edentulous
mandible.
FIGURE 44.4 (A) Symphysis fracture. (B) Fracture parasymphysis.
(C) Fracture of body of the mandible. (D) Angle fracture. (E)
Ramus fracture. (F) Condylar fracture. (G) Coronoid fracture. (H)
Mandibular dentoalveolar fracture.
Ramus and coronoid process

Fractures involving ramus result in minimum displacement, as a result of
being splinted by the presence of masseter muscle on the lateral aspect and
medial pterygoid on the medial aspect. Similarly fracture of the coronoid also
results in minimal displacement as it is splinted by the tendons of the
temporalis muscle. Sometimes injuries which cause rupture of the insertion of
these tendons might displace the coronoid fragment upwards towards the
infratemporal fossa.
Angle
Fractures of this region involve the junction of the posterior end of the alveolar
process and the body of the mandible with the ramus, from where the fracture
line extends downwards.
Angle fractures are caused due to impact over the same side of the mandible
between the canine and second molar region or from violence to chin point on
the opposite side. Fractures at the angle of the mandible are influenced by
medial pterygoid and masseter.
Among these the force of contraction exerted by the medial pterygoid is
more and results in the upwards, forwards and inwards displacement of the
posterior fragment.
Symphysis and parasymphysis region

In the midline fracture of the symphysis, mylohyoid and geniohyoid muscles
act as stabilising forces and there is no displacement. However, when the
fracture line is oblique it results in overriding of the fragments under the
influence of geniohyoid and mylohyoid muscles.
A bilateral parasymphysis fracture readily displaces the fractured segment
posteriorly under the influence of genioglossus and geniohyoid muscles. This
fracture may be associated with loss of tongue control and obstruction of the
airway due to falling back of the tongue.
Canine region is more prone to fracture because of the long root of the
canine which makes the bone weaker and also this is the region of maximum
curvature in the dental arch.
Comminuted fractures (Fig. 44.5)

When the comminuted fracture involves ramus or angle of the mandible
where strong muscle attachments are present, the displacement is minimal
due to sandwiching of the fragments between the muscles.
FIGURE 44.5 Comminuted mandibular fracture.
Factors affecting displacement of the fracture (Fig. 44.6)
• Muscular pull on the fractured segment

• Force of the impact
• Site and direction of the fracture line
• Presence of teeth in the fracture segments
• Favourable or unfavourable fractures (Box 44.4)
FIGURE 44.6 Bilateral mandible body fracture—multiple fractures
displaced anteriorly from digastric muscle pull.
Box 44.4 Favourable/unfavourable fractures (Fig. 44.7-

44.11)
An important classification of mandibular angle and body fractures relates to
the direction of the fracture line and the effect of muscle action on the fracture
fragments. Angle fractures may be classified as:
1. Favourable
a. Vertically favourable
b. Horizontally favourable
2. Unfavourable fractures
a. Vertically unfavourable
b. Horizontally unfavourable
In general, vertical fractures have resistance to medial pull and horizontal

fractures have resistance to upward pull.
Favourable fractures
When the muscle pull resists the displacement of fractured fragments, then
the fracture line is considered favourable.
Unfavourable fractures
When the muscle pull distracts the fractured fragments away from each other,
resulting in displacement is called as unfavourable fractures.
Horizontally favourable
When the fracture line passes from the alveolar margin, downward and
forward, then upward displacement of posterior segment is prevented by
physical obstruction caused by body of mandible.
Horizontally unfavourable
If the fracture line passes downward and backward, then the upward
displacement of the posterior segment is unopposed which is referred as
‘horizontally unfavourable’. Sometimes the upward displacement can be
prevented by the presence of a tooth on the posterior segment which comes
into contact with maxillary tooth.
The masseter, temporalis and medial pterygoid cause upward
displacement.
Medial pterygoid causes upward and medial displacement of the proximal
segment.
Horizontal fractures are best seen in lateral oblique and OPG.
Vertically favourable
In this type of fracture, the fracture line passes from the outer or buccal plate
obliquely backward and lingually, which will tend to resist the muscle pull in
medial direction.
Vertically unfavourable
In this type of fracture, the fracture line runs from the inner lingual plate
obliquely backwards and buccally, resulting in medial displacement.
Vertical fractures are best seen in occlusal radiograph (for viewing
buccolingual direction).
Muscles responsible—medial pterygoid and lateral pterygoid cause medial
displacement of proximal segment.
FIGURE 44.7 Muscles—direction of action on mandible.
FIGURE 44.8 (A–B) Horizontally favourable and horizontally
unfavourable. (C–D) Vertically favourable and vertically
unfavourable.
FIGURE 44.9 Muscle attachment to the mandible (angle and

parasymphysis fracture).
FIGURE 44.10 Parasymphysis favourable and unfavourable

fracture (Vertically).
Clinical findings
• Indirect signs: Swelling, ecchymosis, erythaema, abrasion and

lacerations may present as indirect signs of injury or impact.
Laceration or contusion in chin may indicate a symphyseal injury
causing symphysis fracture with or without bilateral condyle fracture
(Figs. 44.12–44.14).
• Facial deformity: There may be obvious deformity in the bony contour
of the mandible and if considerable displacement has occurred, the
patient is unable to approximate the anterior teeth together and the
mouth remains in open posture (open bite).
• Inability to occlude teeth (Fig. 44.15): Except angle, ramus and condyle,
all mandibular fractures are compound into the mouth and blood-
stained saliva is frequently observed dribbling from the corners of the
mouth.
• Palpation should begin bilaterally in the condylar region and then
continue downwards and along the lower border of the mandible.
Bone tenderness is almost pathognomonic of a fracture, even an
undisplaced fracture. Displaced fracture present as palpable step
deformity in lower border and crepitus from movement of fracture
ends.
FIGURE 44.11 (A) Unfavourable fracture. (B) Favourable fracture—
undisplaced angle fracture—sandwiched between medial pterygoid
and masseter muscles (Horizontally).
FIGURE 44.12 (A–D) Indirect sign of fracture—swelling and
laceration in preauricular region seen in ramus fracture.
FIGURE 44.13 (A) Indirect sign of symphysis fracture—chin
laceration. (B) Indirect sign of symphysis fracture sutured wound in
chin region. (C) Indirect sign of symphysis fracture—sutured
wound in chin. (D) Indirect sign of fracture—sutured lacerations.
FIGURE 44.14 Facial deformity from mandible fracture with

displacement.
FIGURE 44.15 Inability to occlude teeth—bilateral condylar
fracture.
• Buccal or lingual sulci are examined for ecchymosis or clots

(Fig. 44.16).
• On the lingual side, mucosa of the floor of the mouth overlies the
periosteum of the mandible, which, if breached following a fracture,
will invariably be the cause of any leakage of blood into the lingual
submucosa causing sublingual haematoma (Coleman’s sign). Small
linear haematomas, particularly in the third molar region, are reliable
indicators of adjacent fracture.
• Step defects in the occlusion or alveolus are noted along with any
obvious lacerations of the overlying mucosa and gingival tear
(Fig. 44.17).
• Change of occlusion is one of the significant sign which suggests a
mandibular fracture. Change of occlusion might be caused due to a
fractured tooth, fractured alveolar process, fractured mandible or due
to trauma to the TMJ.
• Mobility between the fracture segments can be elicited by palpation.
• Any pain, tenderness or limitation of movement during full range of
mandibular movements is indicative of fracture (Box 44.5)
FIGURE 44.16 Buccal sulcular ecchymosis in a case of mandibular

angle fracture.
FIGURE 44.17 Step deformity in occlusion (A) Parasymphysis
fracture, (B) Symphysis fracture.
Box 44.5 Clinical features of fracture at various sites of

mandible
Fracture of the angle
• Swelling at the angle externally and there may be obvious deformity.

• Laceration of skin or mucosa. Step deformity behind the last molar tooth
may be visible which is more apparent if no teeth are present in the molar
region.
• Undisplaced fractures are usually revealed by the presence of a small
haematoma adjacent to the angle on either the lingual or buccal side, or
both.
• Anaesthesia or paraesthesia of the lower lip may be present on the side of
the fracture.
• Inability to close the jaw causing premature dental contact.
• Occlusion is often deranged. Movements of the mandible are painful and
range of movements is reduced.
• Trismus to some degree is usually present.
• Anterior open bite is seen in bilateral angle fracture.
• Ipsilateral open bite is seen in unilateral angle fracture.
• Retrognathic occlusion and flattened appearance of the lateral aspect of
the face.
• Movement or crepitus at the fracture site can be felt.
Fracture of body
• The physical signs and symptoms like swelling and bone tenderness
similar to that as seen in fracture of angle of mandible.
• Even slight displacement of the fracture causes derangement of the
occlusion.
• Premature contact occurs on the distal fragment because of the displacing
action of the muscles attached to the ramus.
• Fractures between adjacent teeth tend to cause gingival tears.
• When there is gross displacement, inferior dental artery may be torn and
this can give rise to severe intraoral haemorrhage.
• Sublingual haematoma or ecchymosis in floor of mouth—COLEMAN
SIGN.
• Flattened appearance of lateral aspect of face.
• Inability to open or close the jaw.
• Crepitation on palpation.
• IAN paraesthesia: Fractures of the body of mandible are often associated
with injury to the inferior dental nerve in which case there will be
paraesthesia or anaesthesia on one or both sides of the lower lip.
• Molar teeth in particular may be split longitudinally in the fracture line
and cause considerable discomfort.
Fractures of parasymphysis and symphysis
• These fractures are commonly associated with fractures of one or both the
condyles.
• This fracture may be missed if occlusion is undisturbed locally.
• The presence of bone tenderness and a small lingual haematoma may be
the only physical signs.
• Sublingual haematoma or ecchymosis in floor of mouth—COLEMAN
SIGN.
• Posterior open bite or unilateral open bite is seen in parasymphysis
fracture. Posterior crossbite can result from midline symphysis fractures.
• Crepitation on palpation is noted in symphyseal fracture.
• Inability to close the jaw causing premature dental contact.
• A retruded chin can be caused by bilateral parasymphyseal fracture.
• Fracture line is often oblique which allows overriding of the fragments
with lingual inversion of the occlusion on each side.
• These fractures are associated with severe concussion and may contribute
to loss of tongue control and obstruction of the airway.
Fracture of ramus
• They are uncommon.
• Flattened appearance of the lateral aspect of face.
• Inability to open or close the jaw.
• Swelling and ecchymosis usually noted both extraorally and intraorally.
• Tenderness over the ramus and movements produce pain over the same
area.
• Severe trismus.
Fracture of coronoid process
• The fracture can be caused by direct trauma to the ramus but is rarely in
isolation. It is usually considered to result from reflex contracture of the
powerful anterior fibres of the temporalis muscle.
• This fracture is difficult to diagnose clinically.
• Tenderness over anterior part of the ramus.
• Painful limitation of movement, especially during protrusion of the
mandible may be found.
Following are types of radiologic studies that are helpful in the diagnosis of
mandibular fractures:
• Periapical view
• Occlusal view
• Panoramic radiograph (Fig. 44.18A–F)
• Lateral oblique radiograph
• Posteroanterior radiograph
• Reverse Townes’ view
• TMJ including tomograms
• Computed tomography (CT) scan
FIGURE 44.18 (A) OPG showing loss of continuity at symphysis—
symphysis fracture. (B) OPG showing radiolucent fracture line
extending from medial of right canine to midline inferiorly—
symphysis fracture and right subcondylar fracture. (C) Right
parasymphysis—symphysis fracture associated with impacted
canine.(D) Left mandible body showing loss of continuity with gross
displacement. (E) Isolated right angle fracture with tooth in line of
fracture widening the mesial socket. (F) OPG showing loss of
continuity in left canine (distal) and right angle with tooth in line of
fracture.
Periapical dental films
The most detailed view and can be used for nondisplaced linear fractures of
the body as well as alveolar process and dental trauma.
Mandibular occlusal view

This view demonstrates the discrepancies in the medial and lateral position of
body fractures and also shows anteroposterior displacement in the symphysis.
Panoramic radiograph
The single most informative radiological study used in diagnosing mandibular
fractures is the panoramic radiograph, showing the entire mandible, including
condyles. Combination of a posteroanterior view and a pantomogram obviates
the need for further radiographs and significantly reduces the overall radiation
dose to the patient (Fig. 44.18).
Advantages
• Simplicity of the technique

• Ability to visualise the entire mandible in one radiograph
• Good detail
Disadvantages
• The technique requires the patient to be upright, which may make it

impractical in the severely traumatised patient.
• It is difficult to appreciate buccolingual bone displacement or medial
condylar displacement.
• Fine detail is lacking in the TMJ area, the symphysis region and the
dental and alveolar process region.
• Panoramic radiographic equipment is not present in all hospital
radiology facilities.
• Inpatient with fracture of symphysis, chin-rest position is very difficult
which, in turn, results in distorted view (out of focal trough).
Lateral oblique view

This view helps in the diagnosis of fracture in ramus, angle and posterior
body.
Double fracture line

When the outer and inner compact plates tend to fracture independently, the
fracture line from the outer plate after crossing the tooth root and periodontal
ligament reaches the lingual plate at the oblique angle in a different level than
the buccal plate creating the double fracture line on lateral oblique view.
Posteroanterior view
This view demonstrates any medial or lateral displacement of fractures of the
ramus, angle, condyle, body and symphysis. Midline or symphyseal fractures
can be well visualised.
CBCT/CT scan (Fig. 44.19)

CT scan with 3D reconstruction reveals undisplaced as well as degree of
displacement, thus helping in treatment planning. Fractures not evident in
OPG are also diagnosed through CT scan.
FIGURE 44.19 CBCT showing mandible right ramus fracture not

evident in OPG (above).
Management
The management of mandible fracture is similar to any other fracture; the
factors of special consideration are as follows:
1. Restoration of mandibular form and projection.
2. Occlusion-based on the wear facets present the pre-existed occlusion is
determined and restored.
3. Stable fixation for early use of jaw to withstand masticatory forces.
4. Restoring the normal TMJ movements and function.
5. In case of displaced fracture compressing inferior alveolar nerve,
fracture reduction and fixation should relieve nerve compression.
Reduction of fracture
Reduction of fracture means the restoration of a functional alignment of the
bone fragments. In mandible reduction must be anatomically precise where
teeth are present. The presence of teeth provides an accurate guide.
There are two types of reduction:
1. Closed reduction is done by manual manipulation of the teeth or gradual

reduction by elastic traction done, e.g. simple and undisplaced
fractures can be reduced by closed method.
2. Open reduction is done by direct vision, i.e. by exploration of fracture
(e.g. widely displaced, multiple fractures are reduced by open
method).
Closed reduction
Indications
Favourable fractures: Closed reduction reduces the risk of morbidity.

Grossly comminuted fractures: Excellent blood supply of the face would
facilitate the small fragments of the bones to coalesce and heal, whereas
open reduction would jeopardise the vascular supply of the fragments.
Fractures of the severely atrophic edentulous mandible: Open reduction
would require the stripping of the periosteum which is the major source
of blood supply to the edentulous mandible. Therefore, closed
reduction should be the treatment of choice.
Lack of soft tissue overlying the fracture site: Bone plates, screws, wires
would interfere with the bone union by further disrupting the soft
tissue covering.
Fractures in children involving the developing dentition: Open reduction
might pose a risk to the developing tooth bud.
Infected fractures: Infected fracture may create life-threatening surgical
risk and delayed healing, hence closed reduction is indicated.
Condylar fractures: Mostly treated by closed reduction when there is
minimal disturbance in occlusion and in cases of nondisplaced fracture.
Open reduction (Figs. 44.20–44.22)
Indications
• Unfavourable fractures at the symphysis or body or angle of the

mandible.
• Displaced bilateral condylar fractures.
• Delayed treatment of displaced fracture fragments.
• Malunited mandibular fractures.
• Mandibular fracture opposing an edentulous maxilla.
• Edentulous mandibular fracture with severe displacement.
• When closed reduction is contraindicated for medically compromised
patients (e.g. severe seizure disorders, psychiatric or neurologic
problems).
• Complex facial fractures: Such fractures can be reconstructed best after
open reduction and fixation of the mandibular segments to provide a
stable base for restoration.
• Other fractures: Consider open reduction with primary bone grafting in
fractures of a severely atrophic edentulous mandible with severe
displacement of the fracture segments or a nonunion after closed
reduction of a severely atrophic edentulous mandible fracture.
FIGURE 44.20 Open reduction and internal fixation with two

miniplates along Champy’s lines of osteosynthesis for displaced
symphysis fracture.
FIGURE 44.21 Open reduction and internal fixation of
parasymphyseal fracture.
FIGURE 44.22 Open reduction and internal fixation of body fracture

according to Champy’s lines of osteosynthesis.
Surgical approaches for the management of mandibular fractures

(Fig. 44.23)
Selection of type of surgical approaches depends on various criteria like level
of fracture, existing laceration, other associated fractures, surgical exposure,
cosmetic concern and type of fixation. Adequate exposure is necessary for
proper reduction and fixation of fracture.
FIGURE 44.23 Approaches to mandible. 1. Preauricular approach.
2. Transparotid approach. 3. Retromandibular approach. 4.
Submandibular approach. 5. Postauricular approach.
Through existing laceration

In some fractures, the access to the fracture fragment is done through already
existing lacerations following the Langer’s line or relaxed skin tension lines
(RSTL) (Fig. 44.24).
FIGURE 44.24 Mandible approached using the existing laceration.

Intraoral vestibular approach
The intraoral approach is the simple and commonly used approach for
fracture of symphysis, body and parasymphysis. Incision is made through the
mucosa in the vestibule approximately 5 mm away from the attached gingiva
(in the mucogingival junction). Care should be taken regarding the mental
nerve, when the incision is extended posterior to the canine. So when
vestibular approach is used for mandibular body fractures, the incision should
be placed superior to the mental nerve (Fig. 44.25).
FIGURE 44.25 Intraoral approach to symphysis.
Posterior vestibular approach

This type of approach is preferred for fracture of body, angle and ramus of
mandible. Skeletonisation (freeing of mental nerve) should be done for better
retraction of soft tissues. The nerve to be taken care of in posterior vestibular
approach is the sensory buccal nerve which crosses the upper anterior rim of
the ascending mandibular ramus in the region of the coronoid notch which is
at risk of transsection which on injury causes numbness in the buccal mucosal
region. Therefore, to protect the nerve, the posterior dissection is to be
extended bluntly as soon as the lower coronoid notch is reached (Fig. 44.26).
Submental approach
This approach is mainly used to treat anterior mandibular body and
symphysis fractures. These fractures are usually approached and treated by
the intraoral approach, but based on the difficulty or severity of the fracture, or
the presence of a laceration in that region, can mandate the use of an extraoral
approach via the submental route (Fig. 44.27).
FIGURE 44.26 Intraoral approach to the angle.
FIGURE 44.27 Submental approach.

Submandibular approach
Submandibular extraoral approach is mainly indicated for fractures which are
not suitable by intraoral approach; also it allows satisfactory manipulation of
fragments, good control of lingual cortex.
This approach is mostly used in cases of communited fractures and atrophic
mandible. Incision is placed 2–3 cm below the inferior border of the mandible.
Care should be taken for marginal mandibular nerve, facial artery and vein
which are encountered during this approach. The length of the incision
depends on the extent of fracture line and the type of internal fixation
technique (refer Chapter 37).
Retromandibular approaches
This approach is mainly used for condylar head and neck or ramus as it
exposes the entire ramus from behind the posterior border. Main structures in
this approach are the retromandibular vein and the facial nerve (refer
Chapter 37).
Preauricular approach
Preauricular approach is mainly used for mandibular condylar head and neck
fractures (refer Chapter 37).
Fixation (Figs. 44.28–44.31)

Rigid or semirigid fixation can be achieved either by direct or indirect
techniques. Refer to Chapter 42 Basic Principles in the Management of
Maxillofacial Trauma.
FIGURE 44.28 Transosseous wiring by Hayton-Williams technique
for open reduction and fixation of angle fracture.
FIGURE 44.29 Open reduction internal fixation (ORIF) of mandible

angle fracture. OPG shows two radiolucent lines. Intraoperative
observation of a single fracture line indicates its oblique course
from buccal to lingual cortex.
FIGURE 44.30 ORIF of combination fractures (right body and left
angle).
Immobilisation of fracture
Following accurate reduction of the fragments, the fracture site must be
immobilised to allow bone healing to occur.
The period of intermaxillary fixation depends upon the type, location,
number and severity of the mandibular fracture, patient’s general health
condition, age and method employed for reduction and stabilisation: the
recommended immobilisation period for mandibular fractures correlates with
the bony callus stage of secondary bone healing.
• The average recommended immobilisation period for mandibular

fractures is 6 weeks.
• Treatment of edentulous mandibular fractures with closed reduction
techniques requires a longer period of IMF when compared with
dentate patients.
• Age-related bony changes, including thinner mandible and a
decreased cancellous volume contribute to the increased
immobilisation period required for bony union.
The following is simple guide to the time of immobilisation of fractures

involving the tooth-bearing area (Killey and Kay). Young adult with fracture of
the angle receiving early treatment in which tooth is removed from the
fracture line—3 weeks. If:
a. Tooth retained in fracture line, add 1 week

b. Fracture at the symphysis, add 1 week
c. Age 40 years and above, add 1 week
d. Children and adolescents, subtract 1 week
Applying this guide it follows that a fracture of symphysis in a 40-year-old

patient where the tooth in the fracture line is retained requires 6 weeks of
immobilisation (i.e. basic 3 weeks + 1 week for less favourable site + 1 week
allowed for age + 1 week for tooth retained in the line of fracture) (Box 44.6)
Box 44.6
Management of teeth in line of fracture
Teeth in the line of fracture are potential source of infection and may interfere
with healing of the fracture in the following manner:
• The pulp might become necrotic as a result of trauma to the teeth which
acts as a source of infection
• The involvement of the teeth makes the fracture compound into the mouth
with exposure of periodontal ligament
• The teeth may have some preexisting periapical lesion
According to Killey and Kay, indications for removal of a tooth from

fracture line are illustrated below.
Teeth which need to be retained in the fracture line (Fig. 44.31)
• Tooth which is intact but present in the line of fracture and shows no
evidence of mobility or inflammation can be retained with antibiotic
coverage.
• A second molar in the posterior segment of the fracture should be
retained to prevent superior displacement of the posterior fracture
segment during intermaxillary fixation.
• Attempt to save the cuspids, which are the cornerstone of occlusion.
FIGURE 44.31 (A–F) Open reduction and internal fixation (ORIF)
for mandible angle fracture using the buttressing bone of external
oblique ridge. Note tooth in line of fracture is retained.
Condylar fractures
Condylar injuries deserve special consideration from the rest of the mandible
because of its anatomical differences and healing potential. Condyle is a link in
the direct continuity of the mandible from glenoid fossa to the ramus of
mandible. Condylar fractures are very common representing around 25%–35%
of all mandibular fractures.
There are basically three types of injuries seen in temporomandibular joint.
Contusion
It involves soft tissue injuries such as that to ligaments, muscles, synovium
and may cause formation of inflammatory exudates or haemarthrosis. A tear
in the meniscus may result in osteoarthritic changes.
Dislocation
Usually this occurs in the anterior direction. However, occasionally this can be
in the posterior, central or rarely lateral direction.
Fracture
This can occur either inside the capsule or outside the capsule in the
subcondylar region.
Aetiology
• Injury caused by a moving object as in case of direct injury, violence,

sports, etc.
• Injury caused when an individual falls or hits a surface while in
motion as in case of parade ground fracture fall due to syncope
without making any effort to protect the face.
Mechanism of injury
Trauma causing condylar injury (Lindahl, 1977)
1. Kinetic energy imparted by a moving objectthrough the tissues of a static

individual, e.g.
• Trauma sustained from a fist, during sporting activities.
• Some industrial accidents.
2. Kinetic energy derived from the movement of the individual and expended
upon a static object, e.g.
• Parade ground fracture—fall of the victim without any
attempt to protect the face with the hands owing to the
sudden loss of consciousness in syncope.
• Fall during an epileptic attack.
3. Kinetic energy which is a summation of forces derived from a
combination of (1) and (2) generally produces a more severe type of
injury, e.g.
• Road traffic accident
Classification of condylar fracture

Unilateral and bilateral fractures
Intracapsular (high condylar) fracture and extracapsular (low condylar)
fractures
Intracapsular: Fractures involving articular surfaces or fractures running
through the condylar neck just below the articular surface.
Extracapsular: Fractures not involving the articular surfaces but running
from the deepest concavity of the sigmoid notch to posterior direction.
Wassmund’s classification
In 1934, Wassmund described five types of condylar fractures.
Type I is defined as a fracture of the neck of the condyle with relatively

slight displacement of the head. The angle between the head and the
axis of the ramus varies from 10 to 45 degree. He states that these
fractures tend to reduce spontaneously.
Type II fractures produce an angle from 45 to 90 degree, resulting in
tearing of the medial portion of the joint capsule.
Type III fragments are not in contact and the head is displaced medially
and forward owing to traction of the lateral pterygoid muscle. The
fragments are generally confined within the area of the glenoid fossa.
When the capsule is torn and the head is outside the capsule, he
recommended an open reduction for this type of fracture.
Type IV fractures of the condylar head articulate on or in a forward
position with regard to the articular eminence.
Type V group consists of vertical or oblique fractures through the head of
the condyle and Wassmund suggested a bone graft to reconstitute the
condylar head when considerable displacement of the fragments has
occurred.
MacLennan system: MacLennan, in 1952, proposed a system based on the

relationship of the proximal and distal fracture segments to each other. It is
composed of four divisions:
• Nondisplaced: No displacement of fragments.

• Fracture deviation: This type consists of a simple angulation of the
fracture segments without overlap or separation. This includes the
greenstick fracture commonly seen in children.
• Fracture displacement: This group of fractures is characterised by overlap
of the proximal and distal fracture segments. The overlap may be
anterior, posterior, lateral or medial. Medial displacement is seen most
commonly because of the anteromedial pull of the lateral pterygoid
muscle.
• Fracture dislocation: The condylar head is completely outside the glenoid
fossa and, therefore, outside the capsule.
Lindahl classification (1977)

Lindahl classification system was based on a very well-conceived and well-
designed prospective investigation of 123 patients with 138 mandibular
condyle fractures. It requires radiograph in two planes at right angles to each
other.
A. Fracture level
Condylar head fracture/intracapsular: By definition, a condylar head fracture
is within the capsule and is therefore termed as intracapsular.
• Vertical (anteroposterior sagittal split) (Fig. 44.32)

• Compression (expansion—mushroom shaped) (Fig. 44.33)
• Comminuted
Condylar neck: The radiographic constriction representing the condylar

neck corresponds anatomically to region of inferior attachment of joint
capsule (Fig. 44.34).
Subcondylar: Region below the neck extending down to the most inferior
part on the sigmoid notch anteriorly, while its posterior limits are situated
more inferiorly corresponding to the point of maximum curvature of natural
concavity of posterior border of the mandible in that region (Fig. 44.35).
B. Relationship of condylar fragment to mandible
• Undisplaced (Fig. 44.36)

• Deviated—simple angulation of condylar process in relation to mandibular
fragment without overlap (Fig. 44.37)
• Displaced with medial overlap of the condylar fragment (Fig. 44.38)
• Displaced with lateral overlap of the condylar fragment (Fig. 44.39)
• Anteroposterior overlap (infrequent)
• Without contact between fragments (Fig. 44.40)
C. Relationship of condylar head to fossa
• No displacement: Joint space appears normal

• Displacement: Joint space is increased, but condyle is related to the glenoid
fossa. Lindahl subdivided this into slight displacement and moderate
displacement, but quantification is difficult (Fig. 44.41).
• Dislocation: Condylar fragment is completely out of the fossa (usually
anteromedial)
D. Injury to meniscus
It may be torn, ruptured or herniated in forward, backward direction.
FIGURE 44.32 Bilateral condylar head fracture—anteroposterior
sagittal split.
FIGURE 44.33 Condylar head fracture from compression injury—
mushroom-shaped expansion.
FIGURE 44.34 Condylar neck fracture.
FIGURE 44.35 Subcondylar fracture.
FIGURE 44.36 Undisplaced condylar neck fracture.

FIGURE 44.37 (A–B) Deviated condylar fragment at an angulation
to the mandibular fragment without overlap.
FIGURE 44.38 (A–C) Displaced condylar fracture with medial
overlap of condylar segment.
FIGURE 44.39 Displaced condylar fracture—lateral overlap of the

condylar segment.
FIGURE 44.40 Condylar fracture with no contact between the

fragments.
FIGURE 44.41 Displaced condylar fragment with increased joint
space—condyle still related to the glenoid fossa.
Clinical features of unilateral condylar fractures (Fig. 44.42A–D)
• Swelling and tenderness over the affected preauricular area.

• Haemorrhage from ear on that side results from laceration of the
anterior wall of the external auditory meatus. It is important to
distinguish bleeding originating in the external auditory canal from
the middle ear haemorrhage. The latter signifies a fracture of the
petrous temporal bone.
• Ecchymosis of the skin just below the mastoid process on the same side.
This particular physical sign also occurs with fractures of the base of
the skull when it is known as ‘Battle’s sign’.
• If the condylar head is dislocated medially, a characteristic hollow over
the region of the condylar head may occur.
• On opening the mouth, mandible deviates towards the side of the
fracture.
• Occlusion: Unilateral posterior crossbite or contralateral open bite
(gagging of the occlusion on the ipsilateral molar teeth) and
retrognathic occlusion may also be associated. Displacement of the
condyle from the fossa or overriding of the fractured condylar neck
shortens the ramus on that side producing the malocclusion.
• Painful limitation of protrusion and lateral excursion to the opposite
side.
• Palpation (preauricular or intra-aural) reveals reduced or no palpable
condylar movement on ipsilateral side in comparison to contralateral.
• Cerebrospinal fluid (CSF) otorrhoea involving condylar fracture in
association with middle cranial fossa.
FIGURE 44.42 (A) Swelling in right preauricular region with
restricted mouth opening in right condylar fracture. (B) Swelling
over left preauricular area in relation to subcondylar fracture. (C)
Left condylar fracture causing premature occlusion on left with
open bite on right side. (D) Deviation of mandible towards left in left
condylar fracture. Note swelling on right angle in association with
right angle fracture.
Clinical features of bilateral condylar fractures
• The signs and symptoms for unilateral fracture may be present on both
sides.
• Swelling over both fracture sites.
• Overall mandibular movement is usually more restricted than in
unilateral fracture.
• If there is displacement of the condyles from the glenoid fossa or
overriding of the fractured bone ends, an anterior open bite is classically
present (Figs. 44.43 and 44.44).
• Pain and limitation of opening and restricted protrusion and lateral
excursions.
• The appearance of an elongated face may be the result of bilateral
subcondylar fracture.
• Bilateral condylar fractures are frequently associated with fracture of
the symphysis or parasymphysis.
FIGURE 44.43 Anterior open bite from bilateral condyle fracture.
FIGURE 44.44 Bilateral condylar fracture causing premature

gagging of posterior occlusion and anterior open bite.
Investigations
Recent advances in the field of imaging technology have enabled in the
assistance of accurate diagnosis and localisation of condylar injuries.
1. Conventional radiography
Orthopantomogram (OPG)
(Fig. 44.45) and lateral oblique view of mandible—the overall relationship of
proximal and distal fragments in the anteroposterior plane.
FIGURE 44.45 OPG showing bilateral condylar neck fracture with

displacement.
PA mandible
Good representation of the proximal and distal fragments in a mediolateral
plane.
Reverse Townes’
view is ideal for showing medial displacement of condyle and condylar neck
fractures.
Transcranial lateral
views of the TMJ are helpful in detecting condylar fractures and anterior
displacement of the condylar head.
2. Computed tomography
Helpful in defining the relationship of the condylar proximal fragment to the
glenoid fossa and also in delineating the pattern of high intracapsular
fractures. Tomography consists of CT scans and MRI.
CT scans demonstrate the changes in the relationship of condyle to
mandibular fossa more precisely than the conventional radiographs
(Fig. 44.46A–D).
FIGURE 44.46 (A) 3D CT scan showing medially displaced right
condylar fracture fragment with loss of continuity in the left
mandibular body region. (B) Axial section at the level of mandibular
ramus showing anteromedially displaced right condylar segment.
(C) Axial section at the level of mandibular condyle showing
absence of condylar head in the right glenoid fossa indicating
displacement of the fractured fragment. (D) Coronal section at the
level of mandibular ramus showing anteromedially displaced right
condylar segment.
3. MRI
Magnetic resonance imaging (MRI) is used in the diagnosis of internal
derangement of the temporomandibular joint and muscular injuries.
Coronal scanning allows a full assessment of medial displacement of the
disc.
Management
Principles of treatment of condylar fracture

Condylar fracture depends upon the patient’s age, and can be treated either
conservatively or surgically by open reduction.
There are three main treatments advocated for condylar process fractures:
1. Conservative: This involves immobilisation by intermaxillary fixation.

The time duration for this treatment may range from 7 to 10 days as in
case of unilateral fracture to 4 weeks or more as in bilateral fracture.
2. Functional: The principle is that the risk of ankylosis can be prevented
by active movement.
3. Surgical: A variety of surgical approaches have been advocated using
bone plates to provide fixation of the fragments reestablishing a
functional joint.
Treatment protocol for different types of condylar fracture
• In the youngest age group (0–2 years)—the highly vascularised and

highly osteogenic condylar environment necessitates the
encouragement of active jaw function, which is helped by analgesics as
a means of combating joint ankylosis.
• In the 3–12 years age group—jaw function is encouraged to promote
growth by virtue of the high regenerative and remodelling potential
which is inherent in this age group. The treatment is completely
functional for both unilateral and bilateral condylar fractures. IMF
may be required for a period of 7–10 days in case of extreme pain.
In significant fracture displacement of the condylar process with extensive
soft tissue injury, a myofunctional interocclusal appliances may be used
to help offset subsequent scarring, contracture and collapse of
mandibular ramus height. Ultimately the purpose of the myofunctional
appliances is to promote normal mandibular growth in the face of
adverse traumatic events and disrupted hard and soft tissue anatomy.
• In the 13–18 years age group—they have decreased remodelling
capacity compared to young age groups and may occasionally result
in abnormally shaped condylar heads or shortened ramus heights that
may lead to persistent malocclusion. Apart from the possibility of
intermaxillary fixation for 2–3 weeks, consideration may also be given
to surgery in rare situations of persistent gross occlusal disruptions or
severely restricted jaw functions.
• Adults:
▪ Unilateral intracapsular fractures in adults
This kind of fracture does not cause much of a deformity.
Therefore, conservative treatment is considered appropriate
and IMF for a period of 2–3 weeks in case of malocclusion.
▪ Bilateral intracapsular fractures in adults
An intermaxillary fixation for a period of 3–4 weeks is
recommended as the amount of displacement of both the
condyles may be different. Physiotherapy after IMF prevents
any restriction of mouth opening.
▪ Unilateral extracapsular fractures in adults
A low condylar neck fracture is treated by open reduction
technique in case of severe malocclusion caused by the
fracture or dislocation. No effective treatment is undertaken,
if the fractured segments are not displaced and there is no
disturbance to the occlusion.
▪ Bilateral extracapsular fracture in adults
Usually this fracture results in instability and gross
displacement of the mandible. IMF is not reliable for the
proper reduction of the fractured site though it may establish
occlusion. Open reduction of at least one side to establish the
normal height is recommended and then the treatment
protocol is same that for unilateral extracapsular fracture.
When bilateral extracapsular fracture is associated with other
gross midfacial fracture, open reduction of the both the sides
Technique
Closed technique (conservative treatment) (Figs. 44.47–44.49)
Indications
• Condylar fracture with minimum displacement and minimal occlusal

disturbance and in cases of slight deviation of the mandible on
opening the mouth.
• Children or young adults.
• Intracapsular fracture.
FIGURE 44.47 Maxillomandibular fixation (MMF) for conservative
management of condylar fracture.
FIGURE 44.48 Anterior and right lateral open bite in left mandibular
condyle fracture.
FIGURE 44.49 Postoperative occlusion after conservative
management with maxillomandibular fixation
When closed reduction is performed, following adaptations take place in

order to facilitate the masticatory function, by restoring the articulation: (i)
neuromuscular adaptations, (ii) skeletal adaptations and (iii) dental adaptations.
Neuromuscular adaptations
The only mechanism whereby the mandible can be positioned into a normal
occlusal relationship early after injury is by complex neuromuscular
adaptations in the muscles of mastication. However, neuromuscular
adaptations can be considered early, short-term adaptations that assist in
positioning the mandible until a new skeletal articulation has been
reestablished.
Skeletal adaptations
A slowly developing adaptation that occurs within the masticatory system
after condylar process fracture is the development of a new
temporomandibular articulation.
This adaptation begins immediately after injury and continues for many
months afterward. The extent of condylar regeneration has been shown to be
extremely variable with age.
Open reduction of the condylar process eliminates the need for extensive
remodelling; closed treatments also affect the extent to which a new condylar
process will regenerate. It has been shown that physiotherapy provides a more
favourable environment for condylar regeneration than immobilisation of the
jaw.
Dental adaptations
Adaptations that occur along with the skeletal adaptations just described are
within the dentoalveolus. With closed treatment of condylar fractures,
extrusion of the incisors and intrusion of the molars has been demonstrated.
Conservative treatment applies to all kinds of unilateral or bilateral fractures
other than those with gross displacement. Primary goal of conservative and
functional treatment is to facilitate active jaw movements as early as possible
and as long as the patient can bring his/her teeth into occlusion.
Open reduction and internal fixation (Fig. 44.50A–L)

The objective of surgical treatment is achieved by exposure of the condylar
fragment, reduction to the normal relationship and fixation in that position.
There are certain indications for open reduction of condylar fractures.
FIGURE 44.50 (A) Preoperative view showing anterior open bite.
(B) Preoperative CT showing bilateral condylar neck fractured and
displaced medially. (C) Preoperative CT scan coronal view
showing bilateral condylar neck fractured and displaced medially.
(D) Marking for modified preauricular incision—left side. (E)
Dissection of preauricular tissue exposing the zygomatic arch and
fractured condyle distal segment. (F) Condylar fragment retrieved
through pull technique. (G) Miniplate adapted and fixed to the distal
segment of mandible. (H) Fracture reduced and fixation done—left
side. (I) Condylar fracture—ORIF in right side (similar to left side).
(J) Primary closure of the surgical site. (K) Postoperative view—
anterior open bite corrected and occlusion achieved. (L)
Postoperative OPG. ( Scan to play Open reduction and internal
fixation of condyle fracture)
Fractures with a deviation of 10–45 degree or a shortening of the ascending
ramus ≥2 mm should be treated with ORIF, irrespective of level of the fracture.
General justifications for open treatment include anatomical reduction,
occlusal stability, rapid function, maintenance of vertical support, avoidance of
facial asymmetry, lower postoperative incidence of temporomandibular joint
disorders and no maxillomandibular fixation (MMF).
Surgical approaches
• Preauricular approach
▪ Alkayat–Bramley
▪ Endaural
▪ Rowe’s extension
▪ Obwegeser’s modification
▪ Hockey stick
• Retromandibular approach
• Submandibular approach
• Intraoral approach
• Bicoronal (bilateral condylar fracture along with frontal bone fracture)
(Box 44.7)
Box 44.7 Zide and Kent’s absolute and relative

indications
Absolute indications
1. Fracture dislocation of the condyle into the middle cranial fossa.

2. Inability to achieve occlusion by closed reduction due to the interlocking
of the fractured condylar segments.
3. Lateral fracture dislocation of the condyle.
4. Compound fractures of the condyle like that due to gun shot wounds or
invasion by other foreign objects.
5. If a foreign object is suspected to be present in the site of fracture,
surgery is deferred for a period of 1–2 weeks for the resolution of the
oedema and haemarthrosis.
Relative indications
1. Unilateral or bilateral condylar fractures wherein IMF is not

recommended due to systemic problems like severe respiratory
disorder, psychiatric problems, refractory behaviour, mental
retardation or any other neurological problem.
2. Bilateral condylar fractures in case of edentulous patients where
splinting is not recommended for reasons like atrophic residual alveolar
ridge.
3. Bilateral condylar fractures with comminuted midface fractures. Here
condylar fracture has to be fixed before the treatment of the other
complicated fractures.
4. Bilateral condylar fractures in patients with orthognathic problems such
as retrognathia or prognathia, open bite with periodontal problems are
lack of posterior support and mandible requiring reconstruction.
Methods of immobilisation of condyle
• Transosseous wiring
• Kirschner wire
• Intramedullary screw
• Bone pins
• Bone plating
Transosseous wiring
This is used for low subcondylar fractures. The condyle is approached through
the submandibular incision and the holes are drilled in the fragmented
segments and wire is passed across the major segment. A pull through wire is
used for passing the wire through a hole drilled in the minor fragment.
Preauricular incision is preferred for a high condylar fractures. Here the
fragments are drilled obliquely from the external surface to the fracture
surface in order to decrease the risk of injuring maxillary artery and other
blood vessels and to facilitate the insertion of wire.
In case of dislocation of the condyle due to fracture, transosseous wiring
should be assisted with other methods of fixation to counteract the pull of the
lateral pterygoid.
Kirschner wire
Kirschner wire is inserted into the condylar fractured segment after drilling a
passage through it. The remaining part of the wire is placed on the lateral
aspect of the ramus of the mandible in a groove which is drilled vertically.
Kirschner wire is now secured with transosseous wires.
Intramedullary screws
Petzel (1982) described the use of an intramedullary screw transfixing the distal
and proximal fragments through a submandibular approach. Kitayama (1989)
described the use of a similar type of screw via an intraoral approach. Both
techniques require specialised instrumentation and considerable expertise.
With the introduction of more accurate methods of direct fixation, there is a
decline in the indication for the use of this method of immobilisation.
Bone pins
Two pins are inserted on either side of the fracture site and connected by a
condylar head and universal joints. This technique is no longer in use and if at
all practiced is very rare.
Bone plating (Fig. 44.51)

The usage of bone plates had revolutionised the trend towards the surgical
approach of condylar fractures.
FIGURE 44.51 Different types of plates used for internal fixation of

condylar fracture.
Bone plates provide both rigidity and stabilisation with an added advantage
of easy application. Bone plates can be applied through intraoral or extraoral
techniques.
Complications
1. Ankylosis of the temporomandibular joint (Fig. 44.52)

Ankylosis refers to abnormal immobility and consolidation of the TMJ leading
to significant or complete limitation of the mouth opening. According to
Laskin, the factors predisposing to ankylosis are as follows:
FIGURE 44.52 Left TMJ ankylosis in an 18-month-old child with

history of trauma at the age of 8 months.
a. Age of the patient

The predisposition is greater in younger patients (below 10 years) than the
older individuals.
b. Site and type of fracture

Intracapsular fractures are associated with high risk of ankylosis. According to
Laskin, the close contact between the glenoid fossa and the condylar stump is
the factor which results in the development of ankylosis in a condylar fracture.
This is most likely to occur in intracapsular fractures than with extracapsular
fracture.
c. Prolonged immobilisation
According to some authors, prolonged immobilisation may be a contributory
cause for ankylosis.
d. Damage to meniscus
The meniscus acts as a barrier between the condylar head and the glenoid
fossa.
Therefore, bony union does not occur in a condylar fracture wherein the
meniscus is intact. This suggests the cause of ankylosis when the condylar
fracture results in the destruction of the meniscus.
Little doubt exists that the subject of the condylar fracture and their
management will continue to spark controversy in the oral and maxillofacial
surgery community. Many new ideas, as well as older ones, require further
investigation and clinical research to continually advance our understanding
of this complex and relevant area.
2. Interference with growth

Disturbance of growth is seen in small proportion of children in whom the
fracture involves condylar cartilage and the articular surface. In addition,
fibrous or bony ankylosis of TMJ may be seen in some cases. This decreases
the normal functional movements of the jaw which further inhibits growth. So,
the effect of damage to this area will cause failure of development of condylar
process as well as retarded growth of the mandible on the affected side.

Edentulous mandibles present a particular challenge to the facial surgeon
(Fig. 44.53). The thin bone and poor blood supply make treatment of these
fractures particularly difficult.
• Nonunion is the most feared complication when treating these

fractures.
• In edentulous patients, occlusion is not a consideration and fracture
union is the major objective.
• The difficulty in treating these fractures is the lack of thick bone to
place screws in and the lack of teeth for IMF.
• The advantage of the edentulous status of the mandible is that
fractures rarely compound into mouth due to the absence of teeth.
Therefore, the chances of infection are negligent whenever closed
technique is adopted as a method of fracture reduction. Second,
absence of teeth implies that the fragments need not be reduced to
accurate occlusion. The inaccuracy in the reduction can be
compensated by using dentures.
• The issue of blood supply to the edentulous mandible during open
procedures is of great concern due to age-related occlusion of the
inferior alveolar artery partially correlated with the loss of teeth and
the subperiosteal plexus being the major blood supply to the
mandible.
FIGURE 44.53 OPG showing fracture in the edentulous region of

partially edentulous mandible.
FIGURE 44.54 Edentulous mandible fracture—bucket handle
displacement.
Fracture of the edentulous mandible causes extreme downward and

backward displacement of the mandible causing a ‘bucket-handle appearance’.
This appearance is due to any one or a combination of the following factors:
• An edentulous mandible is always resistant to fracture since there is a

high degree of resorption in the alveolar region (Fig. 44.54).
• It is very common to see a bilateral body fracture of an edentulous
mandible.
• Attachment of the mylohyoid muscle is at a higher level when
compared to normal dentate mandible.
• The digastric and mylohyoid cause a download backward movement
of the fractured segment, this reduces pharygeal airway space leading
to respiratory distress.
Management of fractures of edentulous jaw

The problem with edentulous fracture fixation is the absence of occlusion for
reference and stability. Therefore several techniques have been used by
surgeons for achieving a stable mandible for form and function.
Techniques for treatment that were in use include the following:
1. Closed reduction with splint fixation

2. Open reduction (intraoral or extraoral) with transosseous,
circumferential wire ligation and transfixation Kirschner wires
3. Percutaneous intramedullary pinning
4. Intraoral open reduction with bone graft and maxillomandibular
fixation
5. External splint fixation appliance
6. Extraoral open reduction and fixation with malleable mesh
7. Extraoral open reduction and fixation with bone plating
Closed reduction with splint fixation
• Gunning splints used as means of closed reduction for the edentulous

mandible are more accurately described as gunning type splints. In
1866 Gunning originally made vulcanite splints for fractured dentate
mandible.
• Gunning splints are modified dentures which have bite blocks in the
place of teeth and a provision of space in the incisor region for feeding.
These splints can be used either in the upper or lower edentulous jaws.
• In case of completely edentulous patients, immobilisation is carried out
by attaching the upper splint to the maxilla by peralveolar wires and the
lower splint to the mandibular body by circumferential wires.
• The upper and the lower splints are connected with wires or elastic
bands for intermaxillary fixation.
• A slightly overclosed relation of the gunning splint helps in effective
reduction. To minimise the entry of food particles under the fitting
surface, the splint edges should overextend around the sulcus.
Construction
• The impression of the mandible is taken and the splints are constructed
on models obtained from these impressions. However, when the
mandible is badly fractured, it is difficult to obtain an adequate
impression. Sometimes it is possible to make use of the patient’s
existing dentures if they are available. However, models constructed
from the fitting surface of dentures are usually inaccurate and under
extended.
• Using acrylic resin, the splints are constructed and the fitting surface is
lined with black gutta percha. In a slightly overclosed relationship, the
occluding surfaces can be made to fit together satisfactorily.
• Alternatively a trough can be cut in the occlusal surface of one splint
and filled with gutta percha. The opposing occlusal surface is then
shaped to fit into the trough and a satisfactory fit obtained at operation
by softening the gutta percha and pressing the two splints together.
• Intermaxillary fixation is done by applying hooks into each.
• Modification of the patient’s dentures can also be used as splint if these
have been preserved. During operation it is necessary to adapt the
splint to the alveolus of each jaw after reduction.
Peralveolar wiring of upper splint

An awl is used along with a 0.45 mm soft stainless steel wire to fix the upper
splint to the alveolus. This is done by passing the wire through the alveolus
high up in the canine area on each side and then through an appropriately
positioned hole in the palatal portion of the splint. The free ends are together
twisted over the splint, cut short and bent in less than one of the hooks or
cleats.
Circumferential wiring for lower splint

By means of circumferential wires, the lower splint is attached to the reduced
mandible. For this purpose, a curved awl is pushed through the skin beneath
the mandible and directed into the mouth on the lingual side of the bone. A
0.45 mm soft stainless steel wire is passed through the tip of the awl and the
instrument is withdrawn until the lower border of the mandible without
coming out of the skin.
Now the wire is taken along the lower border of the mandible onto the
buccal surface of the mandible and pushed into the oral cavity and the wire
detached from the awl. To avoid any ‘sawing’ of the soft tissues, the wire should
be applied as close to the bone as possible. The splints are provided with hooks or
cleats on their buccal surface. Once these splints have been attached to each
jaw, they are connected by elastic bands or wire loops utilising these hooks or
cleats to establish intermaxillary fixation.
When the patient’s own denture is available at the time of fracture, it can be
used as a splint. At the end of the treatment, during the removal of the per
alveolar or circumferential wiring, it is recommended to prescribe antibiotic
coverage to prevent any infection caused due to the passage of the wire.
Disadvantages
• Food stagnation between the poorly fitting surface of the splint and the
mucosa results in a foul smell within 4–6 weeks.
• Candida-induced stomatitis is usual finding owing to lack of oral
hygiene.
• Splints are considered inefficient as a method of immobilisation,
particularly when the mandible is very thin.
Open reduction and internal fixation

Now with the advent of many animal and human studies, open reduction and
internal fixation have gained significant importance. The five criteria of surgical
importance for success of edentulous mandible fracture management are as
follows:
• Open versus closed treatment

• Intraoral versus extraoral approach
• Subperiosteal versus supraperiosteal dissection
• Type of internal fixation hardware: miniplates versus more rigid plates
and locking versus nonlocking systems
• Simultaneous bone grafting versus no grafting
Open versus closed treatment
Open reduction and fixation
Advantages
• Direct visualisation of the fragments

• Perfect reduction (because the bone ends are so small, advocates of
open treatment believe that closed treatment cannot truly reduce these
bone fragments, resulting in a high rate of nonunion)
• Excellent stability of the segments
• Early return to normal function
Disadvantages
• The meagre blood supply of the atrophic mandible is further
compromised with periosteal stripping.
• The poor health of elderly patient may contraindicate open reduction
and fixation.
Intraoral versus extraoral approach
Intraoral approach
Advantages
• Lack of an external scar

• No risk of injuring the branches of the facial nerve
• A simple 1-layer closure
Disadvantages
• Presence of the inferior alveolar nerve at the level of the alveolar crest,
which can be easily injured during incision and dissection
• Possibility of contamination of the fracture
• Increasing the risk of infection
• Any bone graft required would be performed through a contaminated
area
Extraoral approach
Extraoral open reduction and fixation with bone plating

Bone plates are used for direct osteosynthesis of the edentulous mandible for
the displaced fractures and the fractures of the angle. Bone plates, particularly
noncompression miniplates, are used for the fixation of the thin edentulous
mandible. They are relatively easier to apply in an edentulous mandible and
patient feels more comfortable during the period of healing. Extensive
elevation of the periosteum is required for the application of the bone plates,
which seriously compromises the blood supply of the fracture site, therefore it
is suggested that the bone plates should be applied with intervening attached
periosteum.
Extraoral open reduction and fixation with malleable mesh

Orthopaedic metallic mesh and plating devices have been appropriately used
in the reduction and immobilisation of facial fractures and in some
orthognathic surgeries. Stainless steel and titanium have been used in the
manufacturing of mesh.
Advantages of the mesh over the orthopaedic plates in the management of
fractures are as follows:
• The titanium mesh implants give different options for the placements
of the screws which may be inserted into the bone at any number of
sites at the mesh–bone interface.
• Open mesh enables the surgeons to have direct vision of the fracture
site for proper alignment of the fragments and the various sizes of the
mesh allows the fracture sites to be properly engaged, reduced and
fixed.
• Firm stabilisation provided by the mesh prevents any form of relapse
occurring due to the muscle traction.
Advantages
• Facilitates applying devices to manipulate the fracture fragments and

maintain them in their proper position against the pull of retractors
and associated muscles.
• Allows fracture reduction and temporary fixation readily.
• Application of internal fixation devices is also facilitated.
• Allows treatment of a fracture with less periosteal stripping of the
mandible.
Disadvantages
• Leaves an undesirable scar

• Possibility of injuring branches of the facial nerve and associated
anatomic structures
Subperiosteal versus supraperiosteal exposure

Performing a supraperiosteal dissection removes those soft tissue attachments
through which the blood supply flows into the periosteum. Therefore the
concept of avoiding disruption of periosteal blood supply to mandible is now
obsolete. Conventional subperiosteal dissection for open reduction and
fixation has become standard approach.
Type of internal fixation hardware

The initial treatment strategies were directed towards minimal hardware of
miniplates that commonly fractured under stress. Locking plate/screw systems
have become available over the past 10 years. These systems had potential
advantages in treating fractures of the atrophic mandible as the plate does not
have to be perfectly adapted to the underlying bone. Recently the 2.0 mm bone
plates has been widely used in atrophic mandibular fractures as the plate is
thinner, easier to bend and adapt, there is less likelihood that it will become
palpable or exposed through the soft tissues. The lower height of the plate also
decreases the risk of interference with denture wear.
Simultaneous bone grafting

This was used for ultrathin edentulous mandible and was first introduced by
Obwegeser in the year 1973. Autogenous rib graft was the preferred graft. A
5 cm length of rib graft is obtained and is split into two pieces and placed on
either side of the fracture site and they are stabilised using circumferential
wires or reconstruction or miniplate hardwares.
The potential advantage of using bone grafts during surgery to treat
edentulous fractures is that the graft is likely to aid in fracture union or
healing. When two adjacent bone fragments have become devitalised, then a
cancellous autograft may be necessary to promote revascularisation. If no bone
graft is placed, then healing may not occur in the atrophic mandible. This is
especially important where the patient wishes to have the plate removed later
to resume use of dentures.
CHAPTER 45
Maxillary Fractures
Applied anatomy of the maxilla

Classification of fractures of maxilla
Le Fort fractures
Le Fort I (low level or Guerin fractures/floating maxilla)
Le Fort II fractures (pyramidal fractures)
Le Fort III fractures (suprazygomatic fracture or
craniofacial dysjunction)
Investigations
Management of Le Fort fractures
• Problems associated with treatment of middle third

fracture
• Surgical approaches for open reduction and
fixation
Reduction, fixation and immobilisation
• Classification of methods of maxillary fracture
fixation
• Le Fort I fracture
• Le Fort II fracture
• Le Fort III fracture
• Palatal fracture management
Late consequences of fractures of middle third of facial
skeleton
Fractures of the midface are predominantly seen in the younger generation.
Motor vehicle accidents remain the most common cause of midfacial fracture,
followed by blunt injury due to assault. Midfacial fracture results in distortion
of the patient’s contour and the involvement of the masticatory system, ocular
system, olfactory apparatus and nasal airway.
The maxillae form a significant part of the midfacial skeleton giving a facial
midface prominence.
Applied anatomy of the Maxilla (Figs. 45.1–45.3)

Maxilla forms the largest part of middle third of the face and contributes to the
formation of the orbit, nasal cavities and hard palate. The body of each maxilla
is hollowed or pneumatised by the presence of maxillary sinus. The maxillae
have four processes: frontal, zygomatic, alveolar and palatine. The maxillae
are designed to absorb the masticatory forces. The midface acts as a
‘matchbox’ located below and ahead of the brain. When the midface
experiences force due to a blow or fall, it can easily crumble due to the bones
being fragile. These fragile bones are surrounded by thicker bones of the facial
buttress system responsible for strength and stability (Fig. 45.1).
FIGURE 45.1 Pictorial depiction of strength of the bones of skull

and face.
FIGURE 45.2 The bony pillars of the face.
FIGURE 45.3 Skeletal buttresses of the face. (A) Horizontal

buttresses. (B) Vertical buttresses. (C) Angulation of the frontal
bone and sphenoid to the occlusal plane.
The midface skeleton consists of cancellous segments enclosed within a thin

layer of compact bone and reinforced by a tough frame of ‘buttresses’
(structural pillars). Forces that are applied to the face are absorbed and
transmitted by the buttress system. These buttresses are of two types, vertical
and horizontal buttresses. Masticatory forces are transmitted to the skull base
primarily through the vertical buttresses, which are joined and additionally
supported by the horizontal buttresses. The buttress help to determine the
areas of fracture and stabilisation.
The midface is anchored to the cranium through this framework:
• Vertical buttresses: Nasomaxillary sutures, zygomaticomaxillary sutures

and pterygomaxillary junction.
• Horizontal buttresses: Frontal bar, orbital rims, zygomatic processes of
temporal bone, maxillary alveolus and palate and serrated edges of
greater wing of the sphenoid.
There is more tendency of fracture in areas of stress concentration and areas

of weakness. Based on these factors, Le Fort in 1901 described the classical
patterns of facial fractures, occurring through the junctions of horizontal and
vertical buttresses, at suture lines and thinner segments of bone. The fractures
of the midface are not always classical as mentioned by Le Fort, because of the
complex nature of force causing fracture. Fractures may be isolated or
combinations. They may be unilateral or bilateral Le Fort fracture.
Classification of fractures of maxilla

All these fractures may be unilateral or bilateral or be associated with fractures
of the zygomatic complex (Table 45.1). There may be midline separation of the
maxilla or the fracture may extend into the frontal or temporal bone.
Table 45.1
Fractures of midface: classification
1. In 1901, Rene Le Fort, based on his experimental work with cadavers, classified
maxillary fractures according to the level of injury as:
a. Le Fort I
b. Le Fort II
c. Le Fort III
2. Marciani modification (1993)
a. Le Fort I: Low maxillary fracture
b. Le Fort Ia: Low maxillary fracture/multiple segments
c. Le Fort II: Pyramidal fractures
d. Le Fort IIa: Pyramidal and nasal fractures
e. Le Fort IIb: Pyramidal and NOE fractures
f. Le Fort III: Craniofacial dysjunction
g. Le Fort IIIa: Craniofacial dysjunction and nasal fractures
h. Le Fort IIIb: Craniofacial dysjunction and NOE fractures
i. Le Fort IV: Le Fort II or III fractures and cranial base fractures
j. Le Fort IVa: Le Fort II or III fractures and cranial base fractures + supraorbital rim
fractures
k. Le Fort IVb: Le Fort II or III fractures and cranial base fractures + anterior cranial base
l. Le Fort IVc: Le Fort II or III fractures and cranial base fractures + anterior cranial fossa
and orbital wall fractures
3. Hendrickson classification of palate fracture (1998)
a. Type I: Alveolar
- Ia: Anterior alveolar (incisor)
- Ib: Posterior alveolar (premolar molar)
b. Type II: Sagittal
c. Type III: Parasagittal
d. Type IV: Para alveolar
e. Type V: Complex
f. Type VI: Transverse
4. According to Rowe and Williams (1985)
a. Fractures not involving the occlusion
- Central region
i. Fractures of the nasal bones and/or nasal septum
• Lateral nasal injuries
• Anterior nasal injuries
ii. Fractures of the frontal process of the maxilla
iii. Fractures of type (a) and (b) which extend into the ethmoid bone (nasoethmoid)
iv. Fractures of type (a), (b) and (c) which extend into the frontal bone
- Lateral region: Fractures involving the zygomatic bone, arch and maxilla (zygomatic
complex) excluding the dentoalveolar component
b. Fractures involving the occlusion
- Dentoalveolar
- Subzygomatic
i. Le Fort I (low level or Guerin)
ii. Le Fort II (pyramidal)
- Suprazygomatic
i. Le Fort III (high level or craniofacial dysjunction)
LE Fort fractures (Fig. 45.4)

The classic description of the Le Fort fractures has been principally based on
the work of Rene Le Fort (1901), who classified the fractures by his
experiments. Low velocity forces were used to produce fracture patterns, which
are now known as Le Fort I, II, III and IV (Marciani). However, there exists
combination of fracture patterns with extension into the nasoethmoid and
orbital regions. It is to be remembered that maxilla is a paired bone as right
and left. So, a combination of Le Fort fractures is more common than the classic
description as by Rene Le Fort, for example right Le Fort II and left Le Fort I
fracture maxillae or different fracture lines on the same maxilla as right
maxillary combined Le Fort I and II fracture patterns (Fig. 45.5A–B). Clinical
diagnosis is more classically determined by meticulous examination through
radiograph and CT scan helps in treatment planning.
FIGURE 45.4 Le Fort fracture lines.
FIGURE 45.5 (A) Right Le Fort II and left Le Fort I. (B) Right Le
Fort II and left Le Fort III.
Le Fort I (low level or guerin fractures/floating maxilla)

This is a horizontal fracture above the level of the nasal floor including the
dental component.
Fracture line (Fig. 45.6): The fracture line extends backwards along the
maxilla from the pyriform fossa.
• Laterally—lateral margin of the anterior nasal aperture—lateral wall of

maxillary sinus below the zygomatic buttress—the lower one-third of
the pterygoid laminae and associated palatine bone.
• Medially—lower third of the nasal septum—lateral margin of the
anterior nasal aperture (the lateral wall of the nose) proceeding
posteriorly to join the lateral fracture behind the tuberosity.
FIGURE 45.6 Le Fort I fracture line.
Force
This type of fracture results from application of horizontal force just above the
apices of the maxillary teeth. A Le Fort I fracture, which often escapes
diagnosis is the one, which results due to transmission of blow from the
opposite jaw, which is often impacted.
Signs and symptoms
• Swelling of the upper lip and cheeks (Fig. 45.7).

• Ecchymosis present in the maxillary buccal sulcus from shearing of
soft tissue or periosteal tear (Fig. 45.8).
• Nasal block: Mucosal tear in maxillary/ethmoid sinus may induce
bleeding causing a nasal block forcing the patient to undergo oral
breathing (Fig. 45.9).
• Eye or ocular signs are usually absent.
• Guerin sign: Ecchymosis in the palate in the area of greater palatine
foramen bilaterally is a classic finding of Le Fort I fracture though not
seen in all cases.
• Occlusion: Undisplaced incomplete LeFort I fractures usually cause no
occlusal disturbance. But complete Le Fort I fractures classically show
varying degrees of anterior open bite. This is from backward and
downward distraction of posterior maxilla resulting from inferior
traction of the medial pterygoid muscle towards the mobile maxillary
fragment. This posterior gagging of occlusion is a potential threat to
airway (Fig. 45.10).
• Teeth fracture: Due to impaction of the mandibular teeth against the
maxillary counterpart, damage to the cusp of individual maxillary
teeth may be seen (Fig. 45.11).
• Palatal fracture: Commonly midpalatal split is associated with Le Fort
I evident as linear mucosal tear in midpalate. The associated palatal
fracture could be any of the Hendrickson classification (Fig. 45.12)
patterns with or without oronasal communication depending on the
amount of separation between the fragments from the effect of
bilateral medial pterygoid. With Le Fort I, the teeth and maxilla will
move, but the nose and upper face will stay fixed.
• Cracked-pot sound: Percussion of the maxillary teeth results in
distinctive ‘cracked-pot sound’, similar to the sound produced when a
cracked China pot is tapped with a spoon.
• Floating maxilla: Mobility of the dentulous segment of the maxilla.
• Palpation reveals tenderness and step deformity along the pyriform
aperture, buccal sulcus and tuberosity regions.
FIGURE 45.7 Swelling of upper lip and cheek in association with
Le Fort I fracture.
FIGURE 45.8 Buccal ecchymosis of Le Fort I fracture of maxilla.
FIGURE 45.9 Nasal block from haemorrhage due to nasal mucosal
tear in Le Fort fracture.
FIGURE 45.10 Mild derangement in occlusion associated with Le

Fort I fracture.
FIGURE 45.11 Teeth fracture and posterior open bite on right side
following Le Fort I maxillary fracture.
FIGURE 45.12 Parasagittal palatal fracture associated with Le Fort
I fracture.
Maxillary fractures are distinguished into Le Fort I, II and III based on the
classical mobility (Fig. 45.13, Table 45.2).
• Step 1: Left palm is placed over the forehead, with the thumb over right
lateral orbital rim (frontozygomatic junction), index finger over left
frontozygomatic junction or alternatively the frontonasal junction can also
be assessed simultaneously.
• Step 2: The maxilla is grasped firmly at the anterior portion of alveolus
and not the teeth. The maxilla is checked for mobility with concurrent
mobility in bilateral frontozygomatic junction.
• Step 3: Frontonasal junction at the root of nose is grasped with left thumb
and index finger while palm stabilises the cranium at forehead.
• Step 4: Repeat step 2 checking for dental segment maxilla mobility with
concurrent mobility in frontonasal junction.
• Step 5: Place two fingers as of left hand one on each infraorbital rim, all
the time palm stabilises the cranium at forehead.
• Step 6: Repeat step 2 and check for concurrent mobility felt at both
infraorbital rims.
FIGURE 45.13 Clinical examination of maxillary fractures: (A–B)
Step 1. (C–D) Step 2. (E) Step 3 and 4. (F) Step 5.
Table 45.2
Comparison of site of mobility evident in different fracture levels
Le Fort II Fractures (Pyramidal Fractures)

Le Fort II fracture is a pyramid-shaped fracture, when involving both maxillae.
Fracture line
This fracture runs (Fig. 45.14) anteriorly—thin middle area of the nasal bones or
frontonasal junction crossing the frontal processes of the maxillae, into the
medial wall of each orbit, crosses the lacrimal bone behind the lacrimal sac—
turns forward to cross the infraorbital margin—slightly medial to or through
the infraorbital foramen—extends downwards and backwards across the
lateral wall of the antrum—below the zygomaticomaxillary suture—middle
one-third of the pterygoid laminae horizontally.
FIGURE 45.14 Le Fort II fracture line.
Posteromedially—separation of the block from the base of the skull is

completed via the nasal septum and may involve the floor of the anterior
cranial fossa.
Force
Le Fort II fracture is a result of force applied near the level of the nasal bones.
Signs and symptoms
• Swelling: Gross oedema of the middle third of the face gives an

appearance of ‘moon facies’’ to the patient (Fig. 45.15).
• Subcutaneous emphysema is sometimes evident by crepitus felt on
palpation. This is due to direct communication between the sinus
cavities and the soft tissues of the face.
• Telecanthus: Commonly the swelling over the nasal bridge may give
illusion of telecanthus (pseudotelecanthus) and true telecanthus when
associated with naso-orbito-ethmoid fracture.
• Epistaxis, epiphora are common especially in displaced fracture of
maxilla involving or impinging the lacrimal sac or nasolacrimal duct
(Fig. 45.15).
• Bilateral circumorbital or periorbital oedema, ecchymosis giving an
appearance of ‘raccoon eyes’ is seen in both Le Fort II and Le Fort III
fractures (Fig. 45.16).
• Subconjunctival haemorrhage develops rapidly and is restricted to
medial aspect of eyeball though not always. The differentiating factor
is the subconjunctival haemorrhage of Le Fort II maxillary fracture,
which has its posterior limit demarcated laterally; whereas this
demarcation is lost in Le Fort III zygomaticomaxillary complex
fractures.
• Chemosis or oedema of conjunctiva is a common finding.
• CSF rhinorrhoea may be present but not always as in Le Fort III
fractures.
• Enophthalmos, limitation in ocular mobility from muscle entrapment
and diplopia are possible findings as the fracture line involves the
medial wall and medial floor of orbit.
• Anaesthesia or paraesthesia of the cheek as a result of injury to the
infraorbital nerve due to the fracture of the inferior orbital rim.
• Step deformity at the infraorbital rims or nasofrontal junction is
noticed. Zygoma and arch are intact, no loss of malar prominence
unless associated with zygomaticomaxillary complex fractures.
• Ecchymosis or haematoma is seen in the buccal sulcus opposite to the
maxillary first and second molar teeth as a result of fracture at the
zygomatic buttress or in palate in association with greater palatine
arterial damage (Fig. 45.17).
• Sometimes massive nasal or pharyngeal haemorrhage occurs causing
upper airway obstruction. Nasal packing or other means of surgical
intervention is done immediately.
• Midline or paramedian split of the palate is common with Le Fort II
seen as mucosal tear with oronasal communication (Fig. 45.18).
• Retropositioning of the whole maxilla and gagging of the occlusion are
seen creating anterior open bite. Class III malocclusion may be seen in
anterior force impacting the maxilla creating a dish face deformity.
Lengthening of face occurs due to separation of middle third from the
skull base (Fig. 45.19).
• When maxillary alveolus is grasped anteriorly, the midfacial skeleton
moves as a pyramid and the movement can be detected at the
infraorbital margin and the nasal bridge.
• Palpation of vestibule reveals tenderness with step deformity at
zygomaticomaxillary buttress regions.
FIGURE 45.15 Moon facies from gross oedema and subcutaneous
emphysema of middle third of face with pseudo telecanthus and
epistaxis.
FIGURE 45.16 Characteristic raccoon eyes of Le Fort II and III—

periorbital oedema and ecchymosis.
FIGURE 45.17 Palatal ecchymosis in Le Fort II maxillary fracture

(Guerin sign).
FIGURE 45.18 Midpalatal split in association with Le Fort II
fracture.
FIGURE 45.19 Class III jaw position and anterior open bite
following Le Fort II and NOE fractures.
Le fort III fractures (suprazygomatic fracture or craniofacial

dysjunction)
Le Fort III fractures are usually a component of panfacial fractures resulting
from high velocity trauma.
They rarely occur in isolation and are usually accompanied by skull base
fractures and complex Le Fort I, II and III fractures.
Fracture line extends from
• Anteriorly: The fronto nasal suture—transversely backwards, parallel

with base of the skull, to full depth of the ethmoid bone including the
cribriform plate.
• Posteromedially: Within the orbit—the fracture passes below the optic
foramen into the posterior limit of the inferior orbital fissure. From the
base of the inferior orbital fissure, the fracture line extends in two
directions:
i. Backwards across the maxillary fissure to fracture the roots
of the pterygoid laminae
ii. Laterally across the lateral wall of the orbit separating the
zygomatic bone from the frontal bone
• Posterolaterally: From the orbit—inferior orbital fissure—lateral wall
of orbit into the frontozygomatic suture. In addition, fracture of the
zygomatic arch is an integral part of Le Fort III completing the
separation of facial bones from cranium. In this way, the entire middle
third of the facial skeleton becomes detached from the cranial base
(Fig. 45.20).
• Force: The force causing the fracture is at the level of the orbit. The
force is mainly through the lateral orbit, which is contrary to that of Le
Fort II.
FIGURE 45.20 Le Fort III fracture lines depicted in a CT.
Signs and symptoms

All the clinical findings of Le Fort II will be present. In addition,
• Characteristic raccoon eyes, ‘dish face’ deformity (concave profile) with

lengthening of the face (Fig. 45.21).
• ‘Hooding of eyes’ may be seen due to separation of the frontozygomatic
suture causing loss of support to the suspensory ligament of
Lockwood and all attachments to Whitnall tubercle (Fig. 45.22).
• Enophthalmos, hypoglobus, diplopia with altered canthal position
(slant).
• Subconjunctival haemorrhage involving entire eye with no posterior
limit seen.
• Saddle nose deformity commonly with associated naso-orbito-ethmoid
fracture.
• CSF rhinorrhoea. Refer to Chapter 48 Frontal Bone Fractures (Fig. 45.23).
• CSF otorrhoea in associated skull base fractures.
• Loss of lateral facial projection from zygomatic arch fractures.
• Decreased mouth opening from zygoma impinging coronoid process
and severe posterior gagging of teeth from midface inferior distraction
from muscle (medial/lateral pterygoid, masseter) pull.
• Occlusion—deranged with severe anterior open bite, class III
malocclusion, commonly associated with teeth or dentoalveolar
fractures. When lateral displacement has taken place tilting of the
occlusal plane and gagging of one side is seen.
• Posterior nasal bleed or pharyngeal bleed from nasopharyngeal tear
commonly requiring intervention to arrest bleeding.
• Mobility of entire midfacial skeleton as a single unit maxillary mobility
with simultaneous mobility felt at both frontozygomatic regions and
nasal bridge.
• Tenderness and step deformity will be palpable at bilateral lateral
orbital rims, zygomatic arch deformity and nasal bridge (Table 45.3).
FIGURE 45.21 Typical dish face appearance with retruded maxilla
—Le Fort II maxillary fracture
FIGURE 45.22 Hooding of eyes, left eye enophthalmos,
hypoglobus and altered canthal position with restricted mouth
opening.
FIGURE 45.23 CSF rhinorrhoea in Le Fort III fracture.
Table 45.3
Significant clinical features of Le fort I, II, III fractures

Le Fort I Le Fort II Le Fort III
Swelling in upper lip Oedema of midface: Moon Dish face deformity of face
and cheek facies Raccoon eyes, Hooding of
Ecchymosis of Subcutaneous emphysema eye
maxillary buccal sulcus Telecanthus/pseudotelecanthus Enophthalmos,
Nasal block Epistaxis/epiphora hypoglobus, diplopia
Guerin sign Bilateral circumorbital oedema: Subconjunctival
Teeth fracture Raccoons eye haemorrhage
Palatal fracture Subconjunctival haemorrhage Saddle nose deformity
Cracked pot sound Chemosis/oedema of CSF rhinorrhoea/CSF
Floating maxilla conjunctiva otorrhea
CSF rhinorrhea Craniofacial dysjunction
Enophthalmos Posterior gagging of
Anesthesia/paraesthesia of occlusion, anterior open
cheek bite
Step deformity of infraorbital Posterior nasal bleed
rim Mobility of entire midfacial
Gagging of occlusion with skeleton
anterior open bite Decreased mouth opening
Midline or paramedian split of
the palate
Airway obstruction
Investigations
Plain films of the facial skeleton can be helpful in diagnosis, but a CT scan will
invariably be ordered if there is any significant midface fracture.
I. Radiographic examination
Routine examination of the face includes the Waters’ view (PA view with
cephalic angulation), a Caldwell view (PA view), a lateral view and
occasionally a submentovertex view. Various views in the frontal projection to
confirm that the skeletal structures of the middle and posterior cranial fossa
are projected away from the facial skeleton are needed, in at least one
radiographic view. In other terms, if one of the views does not provide details
of a particular facial bone, it may be visible in another projection. Waters’
projection gives a detailed evaluation of the facial skeleton.
McGrigor and Campbell (1950) described a system for examining the
occipito-mental film by following four lines, which cover most of the sites of
injury. By following these lines when examining the OM film it reduces the
chances of failing to detect the fracture (Fig. 45.24).
1. First line across the zygomaticofrontal sutures, the superior margin of

the orbit and the frontal sinus
2. Second line across the zygomatic arch, zygomatic body, inferior orbital
margin and nasal bone
3. Third line across the condyles, coronoid process and the maxillary
sinus
4. Fourth line across the mandibular ramus, occlusal plane
5. Fifth line (Trapnell’s line) across the inferior border of the mandible
from angle to angle
FIGURE 45.24 McGrigor and Campbell lines (1–4), Trapnell’s line
(5).
Indirect signs of fracture

There are three radiological abnormalities, which are seen due to fracture but
which also occur in other condition. These features with the history of trauma
in a patient should increase the suspicion for fracture.
• Soft tissue swelling

• Opacification of maxillary sinus (Le Fort I, II, III and zygomatic
feature)
• Soft tissue emphysema (very rare but useful sign in case of fracture
involving nasal cavity and paranasal sinus)
(emphysema—present as multiple small radiolucencies or overall increase in

radiolucency of the soft tissues)
II. Computed tomography (CT) (Fig. 45.25A–B)

Conventional radiographic examination is uncertain and sometimes
misleading. CT scan of the face provides a vivid evaluation of facial pathology
than the conventional radiography. Axial and either direct (depending on the
patient’s condition) or reconstructed coronal images. 3D reconstruction of the
CT scan aids in diagnosis and treatment planning.
FIGURE 45.25 (A) CT Scan coronal section and 3D reconstruction

showing loss of continuity in anterolateral wall of sinus, lateral wall
of nasal cavity with paramedian palatal split. (B) Right Le Fort I and
II combination fracture, right nasal bone fracture and left high Le
Fort I fracture with midpalatal split along with mandibular
symphysis fracture. Note: pterygoid plate fracture.
Management of Le Fort fractures
General principles
The aims of the treatment are as follows:
1. Restoration and preservation of functions of the vital structures mainly

by establishing normal skeletal architecture.
2. Re-establishing dental occlusion, ocular position, ocular mobility and
orbital volume is the primary concern of the surgeon. The two areas of
reference for reconstruction are cranium and dental occlusion.
3. The facial bones suspend from the skull base, which is an integral part
of cranium. IMF/MMF is done to restore the dental occlusion; it is done
prior to the surgery to protect the masticatory function. MMF/IMF may
be performed before or during the fracture repair, it may be removed
immediately after the surgery or left in place postoperatively
(Fig. 45.26).
FIGURE 45.26 Maxillomandibular fixation to preserve dental

occlusion.
Timing of the surgery
The timing of surgery is controversial, some support immediate repair in a
stable patient. Preferably, the fracture repair can be delayed 7–14 days
allowing oedema to subside providing manipulation of bones and soft tissues.
But delaying surgery beyond two weeks is not encouraged due to risk of
fibrosis and healing process taking place at the fractured site. Further, late
repair is difficult to operate because of the contraction of the soft tissue
envelope. The results of such surgeries are not satisfactory. But, when the
patient is haemodynamically unstable or has an increased intracranial
pressure (ICP), the time of surgery is deferred.
Problems associated with treatment of middle third fracture
1. Airway maintenance
The reduction of fractures of the middle third requires general anaesthesia,
which can be administered through nasal intubation (Le Fort I), submental or
tracheostomy (Le Fort II and III). Oral intubation can be indicated when there
is extensive soft tissue injury to the nose and in emergency securing of airway.
2. Complexity of fractures
Le Fort fractures often do not present as a fracture of single block of bone
though it tends to fracture at the predicted lines of weakness. These fractures
often present as a complex of Le Fort I, II and III types of fractures, resulting in
injury, which is extremely complicated.
Though occlusion is the general guide for reduction, establishment of
occlusion merely corrects the relative position of the maxilla and the mandible.
Restoration of facial form requires the provision of some internal support
within the maxillary antrum and nasal passages.
3. Fixation
Fixation requires an immobile point for support. As the lower jaw is movable,
it is not possible to fix the fractured maxilla to the mandible to stabilise the
middle third of the facial skeleton. To avoid this, following accurate reduction
using mandible as a guide, the middle third must be immobilised by attaching
it to a fixed point. The stable point is the bone superior to the fracture. The
stable bone is used to suspend the fracture segment (e.g. Circum zygomatic
suspension for Le Fort I—where the zygoma is used as a stable bone) or
fixation (e.g. zygomaticomaxillary and piriform buttress bone is used as points
of fixation in Le Fort I).
Surgical approaches for open reduction and fixation

Various surgical approaches are available for management of maxillary
fracture through open reduction and fixation. The chosen approach depends
on the planned site of fixation; sometimes a preexisting facial wound may be
feasible.
Bicoronal and hemicoronal (Fig. 45.27)

Surgical approach of choice for Le Fort III and sometimes Le Fort II (for
frontonasal fracture fixation). The technique provides complete degloving of
the entire frontal area including the lateral orbital wall and rim, nasofrontal
area and the zygomatic arches. Subgaleal plane remains the plane of dissection
until the supraorbital rims after which a subperiosteal plane dissection
continued down over the nasal area.
FIGURE 45.27 Bicoronal and hemicoronal incision.
Midfacial degloving (Fig. 45.28)
Indication
Le Fort I, II, III combined fractures. This technique was popularised by
Maniglia. The technique involves a wide labiovestibular incision in
combination with release of soft tissue envelope around the piriform margin
and nasal skeleton. This approach allows access to the anterior surface of
maxillae, infraorbital rims, body of zygoma and the entire nasal skeleton. This
technique, in combination with bicoronal approach, favours exposing the
whole facial skeleton.
FIGURE 45.28 Midfacial degloving.
Transconjunctival/subciliary (Fig. 45.29)
Indication
Le Fort II, III.
FIGURE 45.29 Transconjunctival and subciliary incision.
Transconjunctival and subciliary approaches are widely used for reduction

and fixation of the infraorbital rim. In addition, it facilitates the orbital floor
reconstruction in orbital blowout fractures. Though the subciliary approach
has less risk to the cornea and a relatively quick technique it has high risk of
ectropion and visible scar. Transconjunctival approach is scarless, does not
create ectropion and provides approach to the infraorbital rim alone.
However, when combined with lateral canthotomy, it can be used to approach
the frontozygomatic suture too. This approach is therefore advantageous since
it avoids a second approach.
Transantral
Indication
Orbital floor fracture in Le Fort II, III. The antral surface of the orbital floor, the
lateral nasal wall and the inner aspects of the zygoma and the zygomatic
buttress can be visualised through the anterior maxillary wall. If this wall is
broken due to the trauma, access to the orbitozygomatic complex can be
gained through the same. As this approach can be used for stabilising the
orbital blowout fracture by packing the maxillary antrum, the defect can be
surgically created too. The packing can bring out through the defect or
through the nasoantral window. Rigid fixation of the orbital floor can also be
performed with endoscopic assistance.
Nasoantral window
The technique requires creation of a nasoantral window under the inferior
turbinate to allow introduction of instruments into the maxillary sinus. The
instrument is advanced until its blunt tip is against the hollow of the interior
surface of the zygoma. By applying manual pressure over the zygoma while
maintaining pressure on the inner surface of the zygoma with the instrument,
the zygoma can be fairly easily manipulated bimanually. Palpation of the
fracture lines and/or the malar eminence is used to evaluate the reduction.
Internal fixation can then be carried out, if needed.
Other localised approaches
Lateral brow approach (Fig. 45.30)
FIGURE 45.30 Lateral brow approach.
For lateral orbital rim fracture in Le Fort III direct fixation, Le Fort II and I
indirect (Adam) suspension.
Transoral approach
For access to the anterolateral walls of maxilla in Le Fort I and II fracture
reduction and direct fixation as well as in indirect suspension.
Reduction, fixation and immobilisation
The reduction, fixation and immobilisation of all three Le Fort fractures are
dealt here. Refer to Chapter 42 for the details of the Basic Principles of
Management of Maxillofacial Trauma.
Classification of methods of maxillary fracture fixation (Table 45.4)
Craniomandibular fixation
Mandible is fixed by means of rods and universal joints to the cranial vault
and the fractured middle third is sandwiched in between.
Table 45.4
Methods of maxillary fracture fixation
1. Internal fixation
a. Direct osteosynthesis (preferred method of treatment)
- Miniplates and screws
- Transosseous wiring
b. Suspension wires (ancillary method of treatment)
- Frontal–central or laterally placed
- Circum zygomatic
- Infraorbital
- Pyriform aperture
- Peralveolar
2. External fixation (less frequently used method of treatment)
a. Craniomandibular
- Halo frame
- Box frame
- Plaster of Paris
b. Craniomaxillary
- Pin fixation
- Halo frame
- Plaster of Paris
Craniomaxillary fixation
After establishing the occlusion, upper jaw is attached by means of rods and
universal joints to the cranial vault. These methods are especially useful where
the fractures can be reduced so that they remain impacted and there is only a
minimum displacement.
Le Fort I fracture
Isolated Le Fort I fractures of maxilla differ in the degree of mobility. The
fractured block is reduced to occlusion.
Reduction (Fig. 45.31A–D)

• Finger manipulation is sufficient to reduce fractures, which are loosely
mobile. However, reduction of impacted fractures is quite difficult and
requires instruments such as Rowe’s disimpaction and Hayton
Williams forceps.
• One pair of Rowe’s disimpaction forceps is used. The unpadded blade is
passed into the nostril and padded blade into the mouth and the palate
is grasped tightly in between. The operator now stands behind the
patient, grasps the two forceps and manipulates to disimpact the
maxilla and bring it to place. A rocking motion with constant anterior
traction frees the impacted segment.
• Sometimes it may not be possible to disimpact a firmly impacted
maxilla using the disimpaction forceps alone; in such cases the fracture
line should be exposed through an incision in the buccal sulcus and
mobilised using an osteotome before using the disimpaction forceps.
• Disimpaction and reduction of the maxillae are rendered more difficult
in the presence of a split in the palate. In such cases, Hayton-Williams
forceps can be used to apply the traction from the buccal aspect of the
alveolar process and medial compression is exerted until the two
halves of the upper jaw are approximated.
FIGURE 45.31 (A) Le Fort I fracture with occlusal derangement. (B)

Midpalatal split. (C) Fracture reduction using Rowe’s maxillary
disimpaction forceps. (D) Maxillary dentulous fragment mobilised
by downward and anterior traction.
Fixation (Fig. 45.32A–B)
Fixation may be by direct or indirect means. Direct fixation involves transoral
exposure of the fracture line and miniplate or transosseous wire fixation at the
buttress bone (lateral piriform rim and zygomaticomaxillary buttress). Indirect
fixation involves suspension and MMF for 4–6 weeks of immobilisation.
FIGURE 45.32 (A) Fracture exposure by transoral approach. (B)

Fracture fixation with miniplate and dental occlusion stabilised by
MMF.
• Undisplaced Le Fort I with minimal occlusal discrepancy—simple MMF

for 4 weeks or direct fixation with no MMF.
• Displaced mobile Le Fort I with anterior open bite—direct fixation or
indirect suspension with MMF.
• Comminuted fractures not amenable to plate or wire fixation are treated
with MMF and suspension.
• In an edentulous patient, the same line of management is followed but if
intraosseous fixation is not feasible, a custom acrylic occlusal splint or
patient’s own denture is used to determine the vertical dimension, which
is less important in such patients. After rigid fixation, the MMF can be
removed at the end of the procedure.
Le Fort II fracture
Reduction
Disimpaction is carried out in a similar manner as in Le Fort I fracture using
Rowe’s disimpaction forceps. During disimpaction extreme care should be taken
because this fracture usually involves base of the skull, which might be further
disrupted if manipulated indiscriminately.
Whenever this fracture is present along with Le Fort I type, disimpaction of
the tooth-bearing portion can be done with the help of Rowe’s disimpaction
forceps, but it might be difficult to mobilise the remaining fragment.
However, mobilisation of this fragment can be carried out by grasping the
nasal septum with Asch’s or Walsham’s forceps and simultaneously exerting
forward finger pressure from behind the soft palate.
Fixation
Fixation may be by direct or indirect means. Direct involves miniplate or
transosseous wire fixation at the ZM buttress, infraorbital rim and frontonasal
junction including nasal bones. Indirect involves suspension and MMF for 4–
6 weeks of immobilisation (Fig. 45.33A–B).
FIGURE 45.33 (A) Le Fort II fracture fixation with miniplate at ZM

buttress. (B) Fixation of the fracture segment using miniplate at
infraorbital rim.
• Undisplaced Le Fort II with minimal occlusal discrepancy—circum

zygomatic suspension with MMF for 4 weeks or direct fixation at
zygomaticomaxillary buttress alone may suffice.
• Displaced mobile Le Fort II with anterior open bite—direct fixation or
indirect suspension (Adams) with MMF (Fig. 45.34A–H).
• Comminuted fractures not amenable to plate or wire fixation are treated
with MMF and suspension.
• The associated complications such as CSF rhinorrhoea, lacrimal
obstruction require appropriate management. Refer to Chapter 48 Frontal
Bone Fractures.
FIGURE 45.34 (A) Bilateral Le Fort II fracture—resolved periorbital
oedema and ecchymosis. (B) Deranged occlusion—anterior open
bite. (C) CT scan showing bilateral combined Le Fort I and II
fracture. (D) Fracture reduction—mobilisation of maxilla. (E)
Maxillary fracture dental segment repositioned in class I occlusion.
(F) Right Adams’ suspension wire placed using bone awl through
lateral brow approach. (G) Left Adams’ suspension wire placed
using bone awl through lateral brow approach. (H) Indirect
suspension and craniomandibular fixation.
Le Fort III fracture

Le Fort III fractures usually occur in association with other fractures of the
facial skeleton such as nasoethmoidal, zygomatic, orbital and Le Fort type I.
The reduction of these structures should be done in the same order as
previously mentioned. When Le Fort III fractures occur in isolation the
displacement caused is minimal and reduction is established by exposing the
frontozygomatic suture. The management includes semi rigid fixation at
frontozygomatic, frontonasal, orbital floor reconstruction, zygomaticomaxillary
buttresses, zygomatic arch and maintaining occlusion. The associated
complications such as CSF rhinorrhoea, lacrimal obstruction require
appropriate management. Refer to Chapter 48 Frontal Bone Fractures.
Palatal fracture management

• Large segment, sagittally oriented palatal fractures could be stabilised
with rigid internal fixation (Box 45.1).
• Complete rigid fixation of the palate consists of fixation across the hard
palate (oral aspect) and at four sites in the maxilla (bilateral pyriform
buttresses and zygomaticomaxillary buttress).
• Comminuted palatal fractures are managed by palatal splinting and
intermaxillary fixation.
• Hendrickson type II, III and IV palatal fractures can be managed by
rigid fixation.
Box 45.1 Palatal fracture

The types of palatal fracture patterns were studied and classified based on CT
scans: The six palatal fracture types are as follows:
i. Anterior and posterolateral alveolar

ii. Sagittal
iii. Parasagittal
iv. Paraalveolar
v. Complex
vi. Transverse
Late consequences of fractures of middle third of facial

skeleton
• Inadequately reduced fractures may result in ‘facial’ deformity

(Fig. 45.35).
• Obstruction of the nasolacrimal duct due to Le Fort II fractures results
in epiphora, dacryocystitis (an infected mucocele).
• Late enophthalmos develops as a consequence of expansion of the
orbital volume (Figs. 45.36–45.37).
• Failure of recovery of oculomotor nerve and abducens nerve result in
strabismus, ptosis and diplopia.
• Paraesthesia in the distribution of the ophthalmic and maxillary
branches of the trigeminal nerve.
• Fractures involving cribriform plate of ethmoid may result in anosmia.
• Nonunion might occur in cases of extensively comminuted fractures.
• Malocclusion and soft tissue entrapment (Fig. 45.38A–D).
• Palatal fistula (oronasal communications) (Fig. 45.39A–F).
FIGURE 45.35 Posttraumatic facial deformity from untreated right
Le Fort II, zygomaticoorbital complex fracture
FIGURE 45.36 Late enophthalmos in right eye with infraorbital
depression following untreated Le Fort II fracture.
FIGURE 45.37 Axial sections showing enophthalmos of the right

eye due to trauma.
FIGURE 45.38 (A) Right posterior open bite following untreated Le
Fort II fracture. (B) Refracturing of right maxilla dentulous segment
and occlusion achieved closing the open bite. (C) Fixation of the
osteotomised fragments using titanium miniplates. (D) Le Fort II
fracture—nonunion and soft tissue entrapment.
FIGURE 45.39 (A) Midpalatal split with palatal mucosal tear
associated with right Le Fort II and left Le Fort I fracture. (B) CT
showing right Le Fort II and left Le Fort I fracture associated with
midpalatal bony split. (C) Secondary palatal fistula from untreated
midpalatal split. (D) Creation of the nasal layer using the
perifistulous palatal mucosa. (E) Nasal layer formed by suturing the
everted perifistulous palatal oral mucosa. (F) Palatal layer
approximated by Langenbeck technique as classically used in cleft
palate repair.
CHAPTER 46
Orbitozygomatic
Complex
Anatomy
Orbital fractures
Orbital blow-out fracture
Blow-in fractures
Fracture displacement
Clinical finding
• Circumorbital oedema and ecchymosis
• Subconjunctival haemorrhage
• Flattening of the malar prominence
• Flattening over the zygomatic arch
• Pain
• Epistaxis
• Trismus
• Abnormal nerve sensibility
• Alteration of globe level
• Displacement of palpebral fissure
• Crepitation from air emphysema
• Ecchymosis of the maxillary buccal sulcus
• Enophthalmos
• Diplopia
Timing of repair
Immediate repair
Repair within 2 weeks
• Indications for open reduction
Surgical approach
• Extraoral approach
• Intraoral approach
Fracture reduction
Indirect reduction or closed reduction
Gillies temporal fossa approach
Transverse buccal sulcus incision (Keen’s or
Balasubramaniam approach)
Surgical approaches to the orbit
Fixation technique
One-point fixation
Two-point fixation
Three-point fixation
Four-point fixation
• Indications for orbital exploration
• Factors influencing choice of biomaterial
• Postoperative complications
The zygomatic bone occupies a prominent position in the facial skeleton. It

also contributes to the major portion of the lateral wall and floor of the orbit.
Direct trauma to the region of zygoma is more common. Zygomatic fractures are
the second most common facial fractures after nasal bone fractures. Often, fractures
of the orbit occurs as an isolated blow-out fracture or as a part of facial
fractures usually, the zygoma. Thus, the term, zygomatic complex fracture,
was coined as the zygomatic bone is intimately associated with maxilla, frontal
and temporal bones (all contributing to the orbital framework). Restoration of
the zygomatico-orbital complex is essential to maintain shape and function of
the orbit.
Anatomy
The zygomatic bone forms the major buttress of facial skeleton (Figs.
46.1–46.5). It is a thick and strong bone that is quadrilateral in shape. The
zygoma plays a major role in facial contour. The zygomatic bone has four
processes: the temporal, orbital, maxillary and frontal bone. The bony orbit
consists of a base, an apex and four walls. The base of the orbit, which opens
into the face, has four borders. Frontal bone forms the superior margin.
Inferior margin is formed by maxilla and zygomatic bone. Medial margin is
formed by frontal bone, lacrimal bone and maxilla. Zygomatic and frontal
bones form the lateral margin. The apex contains the optic canal through
which bony orbit communicates with the middle cranial fossa. The floor and
the lateral wall of the orbit have contribution from the orbital plate of the
zygomatic bone.
FIGURE 46.1 Anatomy of orbital bones (bones—maxilla, frontal,

zygomatic, ethmoid, lacrimal, sphenoid, palatine; Mnemonic: Many
Friendly Zebras Enjoy Lazy Summer Picnics).
FIGURES 46.2–46.5 Topographic anatomy of zygoma and its
relation to other bones.
Orbit is the bony socket, which are bilateral and symmetrical cavities in the
skull. The orbital contents comprise the eyes, the eyelids; extraocular muscles;
cranial nerves II, III, IV, V and VI; ciliary ganglion and short ciliary nerves;
blood vessels; the lacrimal gland within its sac and nasolacrimal duct,
ligaments such as medial and lateral palpebral ligaments, check ligaments and
suspensory ligament. The boundaries of orbit are formed by seven bones
(frontal, ethmoid, lacrimal, maxilla, palatine, sphenoid, zygomatic bones) of
which the ethmoid, lacrimal and palatine bones are the weaker bones.
• Roof (superior wall)—formed by the frontal bone and the lesser wing
of the sphenoid
• Floor (inferior wall)—formed by the maxilla, palatine and zygomatic
bones
• Medial wall—formed by the ethmoid, maxilla, lacrimal and sphenoid
bones
• Lateral wall—formed by the zygomatic bone and greater wing of the
sphenoid
• Apex—located at the opening of the optic canal, the optic foramen
• Base—opens out into the face bounded by the eyelids
Surgical spaces of the orbit:
• Subperiosteal space
• Peripheral space
• Central space
• Tenon’s space

• Because the zygoma is a thick bone, it is rare to have an isolated
fracture of the zygoma. Most commonly, the fracture extends through
adjacent bones, which are often thinner. In 1990, Manson and
cowokers proposed a method of classification based on the pattern of
segmentation and displacement.
• Low-energy zygoma fractures: They result in minimal or no
displacement. These types of fractures often are seen at the
zygomaticofrontal suture, and the inherent stability usually
obviates the need for reduction.
• Middle-energy zygoma fractures result in fracture of all
buttresses, mild-to-moderate displacement and comminution
of bone.
• High-energy zygoma fractures: The zygomatic fractures are
associated with panfacial fractures often extending through
the glenoid fossa resulting in skull base fractures.

• The zygomatic arch is the most prominent bone on lateral aspect of
head along with the external ear. Commonly when there is a blow or
trauma impending to the face, as a reflex the face turns away to protect
the eyes. This very often results in isolated zygomatic arch fracture.
• Zygomatic arch fractures tend to occur in two or three places along the
arch of the zygoma. A fracture may occur at each end of the arch as
well as in the middle, resulting in a V-shaped fracture or a W-shaped
deformity. This can impinge on the underlying temporalis muscle,
resulting in trismus and cosmetic deformity (Fig. 46.21).
FIGURE 46.21 (A) V type zygomatic arch fracture. (B) Clinical
deformity. Note: the flattening of the malar prominence.
A zygomaticomaxillary fracture results from a direct blow to the cheek. The

fractures occur at the articulation of the zygoma with the frontal bone and the
zygomatic arch. These fractures are orbital fractures because the internal orbit
can be disrupted by the displacement of the zygomatic body. The maxillary
component of this fracture may include the anterolateral wall of the maxillary
antrum.
Zygomaticomaxillary fractures are often associated with severe facial
oedema, so the true extent of the injury may be obscured. As with other
fractures involving the orbit, diplopia may be reported by the patient.
Depression of the inferior orbital rim or paraesthesia in the distribution of the
infraorbital nerve suggests extension into the orbit or maxilla.
Orbital fractures
Orbital blow-out fracture (Fig. 46.6)
This is an entity that needs to be addressed in association with
zygomaticoorbital fractures. There are two theories, which explain the
mechanism of orbital blow-out fractures (Fig. 46.8).
• Hydraulic theory states that when an object of diameter greater than

the orbital rim strikes the incompressible eyeball it thrusts posteriorly
raising the intraorbital pressure. The raised intraorbital pressure
causes the floor of the orbit to fracture in its weakest part. The broken
bony part along with soft tissues of the floor of the orbit will herniate
into the maxillary sinus (Fig. 46.6).
• Buckling theory states that when there is blunt trauma to the face, a
pressure wave is transmitted posteriorly and bony orbit is compressed
anteroposteriorly. This causes the weakest bony orbit to buckle and
crackle. Herniation and incarceration of the inferior oblique muscle
into maxillary antrum leads to diplopia on upward gaze (Fig. 46.7).
FIGURE 46.6 Hydraulic theory. The classical nature of impact in
the causation of a blow-out fracture of the orbit.
FIGURE 46.7 Buckling theory. A more pointed direct impact

particular on the inferior orbital rim can also cause a blow-out
fracture of the floor of the orbit.
FIGURE 46.8 Mechanism of orbital blow-out fracture.
Most orbital blow-out fractures occur in the medial and inferior orbital
walls. The medial orbital wall has a thickness of only about 0.2–0.4 mm but is
strengthened by the bony structure of the ethmoidal sinus. Therefore, a greater
force is needed to fracture the medial wall and floor than would be required to
fracture the floor only.
Blow-in fractures
A blow-in fracture is an inwardly displaced fracture of the orbital rim or wall
resulting in decreased orbital volume.
This is not very common fracture. It was first described by Dingman and
Natvig in the year 1964. The most common clinical findings found in these
types of fractures are:
• Proptosis—because of decreased orbital volume together with

restricted ocular mobility and diplopia
• Globe rupture
• Superior orbital fissure syndrome
• Orbital nerve injury
If the fractured segment is not too much displaced, usually it does not
require any treatment. But fractures of the lateral orbital wall, irrespective of
the direction of displacement are treated surgically.
Fracture displacement
• The complexity of the zygomatic complex fracture mainly depends on
the degree and direction of displacement of fractured segment
(Fig. 46.9A–D). In isolated arch fractures medial and downward
displacement of the fractured fragment is more common reflecting the
direction of blow. Such fragments impinge on the coronoid process
and interfere with movements of the mandible. Sometimes when the
zygomatic arch fracture is associated with coronoid fracture; it deems
definitive reduction to prevent the high risk of extra-articular
ankylosis.
• Medially displaced isolated arch fractures and rotation of the zygoma
around the vertical axis are stable after simple reduction. The vertical
axis passes through the frontozygomatic suture and the first molar
tooth. Around the vertical axis, the fractured fragment will be
displaced medially or laterally, i.e. inward or outward.
• Inferiorly displaced isolated arch fractures, rotation of the zygoma
around the horizontal axis, en bloc dislocations and comminuted
fractures are unstable after simple reduction. The horizontal axis
passes through the infraorbital foramen and the zygomatic arch. These
fractures are separated at the frontozygomatic suture. So, there will be
upward or downward displacement of the fractured fragment.
• Downward displacement with separation at the frontozygomatic
suture will lead to detachment of lateral attachment of suspensory
ligament of Lockwood of eye altering the visual axis. Inward and
posterior displacement of fractured fragment does not produce this
effect. But they also interfere with eye movement because of
attachment of orbital adnexa with orbital floor.
• Role of muscle pull in zygomatic arch fractures is very crucial. The
muscle pull exerted by masseter over zygomatic bone and arch
fractures is opposed by temporalis fascia.
FIGURE 46.9 (A) Vertical axis of rotation—medial displacement.
(B) Vertical axis of rotation—lateral displacement. (C) Horizontal
axis of rotation—superior and outward. (D) Horizontal axis of
rotation—inferior and inward.
Classification of zygomatic fracture

Knight and Northwood classification (1961) of zygomatic fracture on the
basis of occipitomental view:
1. No significant displacement
2. Fracture of zygomatic arch only
3. Unrotational body fracture
4. Medial rotational body fracture
5. Lateral rotational body fracture
6. Complete rotational body fracture
Rowe and Killey classification (1968)
Type I: No Significant displacement

Type II: Fractures of the zygomatic arch
Type III: Rotation around the vertical axis
a. Inward displacement of orbital rim
b. Outward displacement of orbital rim
Type IV: Rotation around the longitudinal axis
a. Medial displacement of the frontal process of zygomatic bone
b. Lateral displacement of the frontal process of zygomatic bone
Type V: Displacement of the complex bloc
a. Medial
b. Inferior
c. Lateral (rare)
Type VI: Displacement of the orbitoantral partition
a. Inferiorly
b. Superiorly (rare)
Type VII: Displacement of orbital rim segments
Type VIII: Complex comminuted fractures
Rowe and Williams classification

Vertical axis: It is an imaginary line running through the frontozygomatic
suture and the first molar tooth.
Any displacement of the fracture in this axis becomes stable after reduction.
Horizontal axis: It is a line running through the infraorbital foramen and
zygomatic arch. When displacement occurs in this axis, it results in separation
of frontozygomatic suture and the reduction of these fractures is unstable.
1. Fractures stable after elevation

a. Arch only (medially displaced) (Fig. 46.10)
b. Rotation around the vertical axis
i. Medially (Fig. 46.11)
ii. Laterally
2. Fractures unstable after elevation
a. Arch only (inferiorly displaced) (Fig. 46.12)
b. Rotation around the horizontal axis
i. Medially (Fig. 46.13)
ii. Laterally (Fig. 46.14)
c. Dislocation en bloc
i. Inferiorly (Fig. 46.15)
ii. Medially (Fig. 46.16)
iii. Posterolaterally (Fig. 46.17)
d. Comminuted fractures (Fig. 46.18)
Manson et al classification:
Based on amount of energy dissipated and findings in CT Scan Manson et al
classified zygomatic fractures in 1990
1. High energy fractures

2. Moderate energy fractures
3. Low energy fractures
Zingg et al classification:
Type A—incomplete zygomatic fracture with fractures involving only one
zygomatic pillar:
a. Type A1: the zygomatic arch fracture

b. Type A2: lateral orbital wall
c. Type A3: infraorbital rim fracture
Type B: Complete, monofragment zygomatic fractures with fracture and

displacement along all four articulations. (tetrapod fracture)
Type C: Multifragment fractures involving fragmentation of the zygomatic
body
Larsen and Thomsen classification
1. Group A: Stable fracture—showing minimum or no displacement,

requires no treatment.
2. Group B: Unstable fracture—great displacement and disruption of
frontozygomatic suture and comminuted fractures, requires reduction
and fixation.
3. Group C: Stable fractures—types of zygomatic fracture, which require
reduction but no fixation.
Fractures of zygomatic arch not involving the orbit
1. Minimum or no displacement (Fig. 46.19)

2. Comminuted fractures (Fig. 46.20)
3. V-type in fracture (Fig. 46.21)
4. W-type fracture
Henderson’s classification (1973)
1. Undisplaced fracture, any site

2. Zygomatic arch fracture only
3. Tripod fracture with undistracted frontozygomatic suture
4. Tripod fracture with distracted frontozygomatic suture
5. Pure blow-out fracture of the orbit
6. Fracture of the orbital rim only
7. Comminuted fracture or other than above
FIGURE 46.10 Isolated medially displaced left zygomatic arch
fracture.
FIGURE 46.11 Zygoma fracture medially displaced around the

vertical axis.
FIGURE 46.12 Inferiorly displaced arch fracture.
FIGURE 46.13 Zygoma fracture with medial rotation around the

horizontal axis.
FIGURE 46.14 Lateral rotation around the horizontal axis.
FIGURE 46.15 Inferiorly displaced en bloc zygoma fracture.

FIGURE 46.16 Medially displaced en bloc zygoma fracture.
FIGURE 46.17 Laterally displaced en bloc zygoma fracture.

FIGURE 46.18 Comminuted fracture.
FIGURE 46.19 Undisplaced zygomatic arch fracture.
FIGURE 46.20 Comminuted arch fracture.
Clinical finding
1. Circumorbital oedema and ecchymosis (Fig. 46.22)
2. Periorbital bleeding
occurs following fracture of the orbital rim. It may be localised to the inferior
lid and infraorbital area or may be generalised around the entire orbital area.
FIGURE 46.22 (A) Circum orbital oedema. (B) Periorbital
ecchymosis.
Soll in 1977 defined the following types of orbital haemorrhages.
• Haemorrhage anterior to the orbital septum causing eye lid

ecchymosis
• Subperiosteal haematoma
• Haemorrhage posterior to the orbital septum including
subconjunctival haemorrhage
• Haemorrhage with in the muscle cone.
3. Subconjunctival haemorrhage
Subconjunctival haemorrhage (Fig. 46.23A–B) (limited to the lateral third of
the eye) is seen as a result of tear in the periosteum of the orbital rim.
However, its absence does not exclude orbital rim fracture. It appears
characteristically bright red due to absorption of atmospheric oxygen across
the transparent bulbar conjunctiva.
FIGURE 46.23 (A) Subconjunctival haemorrhage (SCH) and lateral

orbital haematoma. (B) SCH associated with zygomatic fracture
characteristically exhibiting the posterior limit.
4. Flattening of the malar prominence
The body of zygoma provides a characteristic prominence to the face
bilaterally called the malar prominence. This prominence is lost resulting in
flatness in medially displaced zygoma fractures. Flattening of the cheek can be
assessed by viewing the patient from above standing behind comparing the
two sides of the face. The clinician should firmly depress the fingers into the
oedematous soft tissues by palpating along the infraorbital areas. The full
effect of the flattening of the cheek can be apparent only after the oedema has
settled.
5. Flattening over the zygomatic arch

Direct injury to the lateral aspect of the face commonly fractures the prominent
zygomatic arch. Low force causes buckling of the arch where as heavy force
causes transmission of force to the body of zygoma resulting in zygoma
fracture. Clinically, arch fractures present as a dimple or depression over the
lateral face (Fig. 46.24 A–B).
FIGURE 46.24 (A) Flattening of the malar prominence from

medially displaced zygoma fracture. (B) Depression over the
zygomatic arch indicative of medially displaced arch fracture.
6. Pain
Unless the fractured segment is mobile, normally the patient will not complain
of severe pain. But tenderness may be present.
7. Epistaxis
As the maxillary sinus drains into the nose through the middle meatus,
unilateral haemorrhage from the nose is possible whenever there is
haemorrhage into the sinus as a result of disruption of the sinus mucosa.
8. Trismus
Trismus occurs as a result of downward displacement of zygoma impinging
on the coronoid process. It is most commonly seen in isolated fracture of the
zygomatic arch. If the mouth was closed during the time of injury, the patient
may not be able to open the mouth (Fig. 46.25A) or be able to carry out lateral
movement and protrusion of the mandible. If the patient sustains injury in
mouth open position, the zygoma may impinge on coronoid process in
mandibular depressed state causing inability to close the mouth (Fig. 46.25B).
FIGURE 46.25 (A) Trismus from depressed zygoma fracture

impinging on coronoid process. Note: the decrease in space
between the coronoid process and the arch on the left in
comparison to right. (B) Infero-medially displaced zygoma
impinging on coronoid process in edentulous depressed mandible
causing inability to close mouth.
9. Abnormal nerve sensibility

Anaesthesia or paraesthesia of the infraorbital nerve as a result of neuropraxia
or neurotmesis is more common in displaced fractures than in undisplaced
fractures. Anaesthesia of the temple and cheek may be present as a result of
injury to the zygomaticotemporal and zygomaticofacial branches. They may
also exhibit anaesthesia of one side of the upper lip and upper teeth due to
injury to infraorbital nerve on that side. The period of anaesthesia depends
upon the degree of nerve injury. Recovery usually occurs between 6–9 months.
10. Alteration of globe level (Fig. 46.26)

This depends on the level at which fracture of the lateral orbital rim occurs. If
the fracture is above the Whitnall’s tubercle (it is the point of insertion on the
lateral wall of orbit just below the frontozygomatic suture for the attachment
of suspensory ligament of Lockwood, which supports the globe), the bone is
displaced downwards and also hooding of the upper eyelids. This alteration in
globe level may also cause diplopia.
FIGURE 46.26 Hypoglobus of the left eye from orbitozygomatic

fracture.
11. Displacement of palpebral fissure (Fig. 46.27)
Since the lateral canthal ligament is attached to the Whitnall’s tubercle in the
orbital rim, displacement of the zygoma displaces the palpebral fissure along
with it producing an antimongoloid slant.
FIGURE 46.27 Lateral canthal dystopia from inferiorly displaced

Whitnall’s tubercle.
12. Crepitation from air emphysema (Fig. 46.28)

Tearing of the lining mucosa as a result of fracture through the sinus wall may
cause air to escape into the facial soft tissues if pressure within the sinus is
greater than that within the tissues, which causes crepitation on palpation.
FIGURE 46.28 Soft tissue emphysema arising from
zygomaticomaxillary complex fracture seen clinically and in CT.
13. Ecchymosis of the maxillary buccal sulcus

Ecchymosis of the maxillary buccal sulcus in the area of the zygomatic buttress
is an important sign in fracture of the maxillary bone or zygomatic arch.
14. Enophthalmos (Fig. 46.29)

Enophthalmos is posterior and inferior displacement of eyeball within the
orbit. This is caused either by increase in the volume of the orbit due to
fracture of its walls or escape of orbital fat or both. This occurs most commonly
as a result of lateral or inferior displacement of zygoma and/or disruption of
inferior, medial or lateral orbital walls. It presents as sunken eye appearance,
supratarsal hooding and lid retraction. An exophthalmometer (e.g. Hertel) can be
used to assess globe projection where a difference of 2 mm or more is
significant. Very commonly enophthalmos is associated with restriction in
eyeball movement (elevator) from inferior rectus and inferior oblique muscle
entrapment (Fig. 46.30A–B).
FIGURE 46.30 (A) Exophthalmometer. (B) Measuring the sagittal
globe position
FIGURE 46.29 (A) Enophthalmos of the right eye from orbital blow-
out in a laterally displaced zygoma fracture with lid retraction and
supratarsal hooding. (B) Enophthalmos and restriction in eyeball
elevation in the right eye.
15. Diplopia
Diplopia is a very serious complication of the zygomatic fracture where the
patient experiences blurred double vision.
Types of diplopia
1. Temporary or permanent
2. Monocular or binocular
Temporary or permanent
Temporary diplopia
This results from haematoma or oedema of the extraocular muscles and lasts
only for 5–7 days.
Permanent diplopia
This results from paralysis or muscle entrapment within the fractured
segments. This is a more serious cause of diplopia, which if left uncorrected
can lead to permanent diplopia.
Monocular or binocular
Monocular diplopia
Monocular diplopia is double vision through one eye, with the other eye closed.
It requires immediate expert opinion. This indicates a serious cause such as
detached lens or some other traumatic injury of the globe.
Binocular diplopia
This occurs as a result of zygomatic fractures. In case of binocular diplopia,
when looking through both the eyes simultaneously, double vision is
experienced by the patient.
Causes
• Haematoma or oedema around the extraocular muscles interfering with

their actions.
• Disruption in the attachment of inferior rectus or inferior oblique muscle
causes displacement of muscle attachment.
• Orbital floor fracture, which leads to herniation of the periorbital fat into
the maxillary sinus.
• Neuromuscular injury resulting in paralysis of the muscle.
• Fibrous tissue formation and adhesions between the globe and orbital
floor.
Test for diplopia (Box 46.1)
1. Finger gaze
A finger is held in front of the patient at a distance of an arm’s length and
moved inall directions as the patient’s eyes follow the finger. Patient is asked
to report any double vision. Diplopia should be tested in all the nine directions
of gaze.
Box 46.1 Tests for diplopia
1. Finger gaze
2. Traction test (forced duction test)
3. Lees screen (Hess Diplopia chart)
4. Diplopia chart
5. Field of binocular single vision (BSV)
2. Forced duction test (Traction test) (Fig. 46.31)

Diplopia caused due to oedema or haematoma of the extraocular muscles
usually resolves in 5–7 days, but diplopia as a result of failure to rotate the eyes
superiorly indicates paralysis (neurological) or entrapment (mechanical) of the
muscle within the fractured segments. To differentiate between these two
causes of diplopia, forced duction test is carried out under topical anaesthetic.
FIGURE 46.31 Forced duction test performed intra operatively to

analyse the function of the rectus muscles.
With the tissue holding forceps hold the tendon of the inferior rectus muscle
and rotate the eyeball superiorly with other movements. A failure to rotate the
eyes superiorly indicates paralysis or entrapment of the muscle within the
fractured segment.
The forced duction test is also done as an intra operative procedure under
G.A, for patients subjected to the test pre operatively. In this the efficiency of
the performed corrective procedure can be analysed. The direction of the traction
should be performed outward and towards the direction of the movement of the affected
muscle. If the globe is pushed inward during the test false positive result may
be obtained.
3. Hess diplopia chart (Lees screen)

Hess chart is used to measure the degree of diplopia. The test helps in identifying
the nonfunctioning extraocular muscle. When done on every alternate day, the
progress of diplopia can be monitored. In this test, dissimilar images are
projected for each eye at 1 m distance with the patient wearing green or red
goggles. A red test object is held against a screen and the patient tries to
indicate the position of the object by touching it with a green tipped wand. The
result of the patient’s effort is charted when the head is held still and they
move their eyes from the primary position to the horizontal right and left
extremes of movements. This is repeated when looking above, to the right
above and left above. The equivalent lower positions are also charted.
4. Diplopia chart
This can be a simple useful tool for diagnosis of diplopia especially in the
absence of a Hess chart. A vertical bar of light is viewed through red and
green goggles at a fixed distance from the eye. The bar light is moved into each
direction of gaze and the patient describes the image separation and
appearance.
5. Field of binocular single vision (BSV)

The field of BSV is a test used to describe the area of BSV, and hence diplopia.
The patient is seated at the perimeter, with the chin central to fixation. The
target is moved outwards until the patient recognises diplopia and the point is
marked. The target is then moved further until one image disappears,
normally due to occlusion by facial contours and this point is marked. The
inner ring describes the area of BSV; the outer ring describes the limits of the
binocular field of fixation.
Complication
There are two important syndromes associated with zygomaticoorbital
fractures: superior orbital fissure syndrome and orbital apex syndrome.
Superior orbital fissure syndrome

This syndrome occurs in fractures extending to posterior third of the orbit. It is
a combination of ophthalmoplegia (due to paralysis of cranial nerves III, IV &
VI), ptosis, proptosis, subconjunctival haemorrhage, loss of corneal and
accommodation reflexes and decreased sensation in the forehead.
Orbital apex syndrome

This syndrome occurs when the fracture line extends to optic canal damaging
the optic nerve. There is blindness in addition to the features of the superior
orbital fissure syndrome. Both the syndromes can be managed by giving high
dose steroids. In nonresponding cases surgical decompression is done.
Oculocardiac reflex syndrome (Fig. 46.32)
The oculocardiac reflex also known as Aschner phenomenon is a triad of
bradycardia, nausea, and syncope. It is caused by incarceration of orbital soft
tissue in an orbital trapdoor fracture. It is an indication for urgent repair.
Fracture reduction and release of the muscle and/or connective tissue should
be done to avoid life-threatening cardiac arrhythmias and it also avoids ischaemic
necrosis of the muscle that may lead to fibrosis and permanent restrictive
strabismus (Flowchart 46.1).
FLOWCHART 46.1 Oculocardiac reflex.
FIGURE 46.32 Oculocardiac reflex pathway.

Timing of repair
Immediate repair
• Diplopia with CT evidence of an entrapped muscle or periorbital tissue
associated with nonresolving oculocardiac reflex.
• Entrapment that causes an oculocardiac reflex with resultant
bradycardia and cardiovascular instability.
• Heart block, nausea, vomiting or syncope are the associated features.
• History of periocular trauma, little ecchymosis or oedema, marked
extraocular motility, restriction of vertical eye movements.
• Orbital floor fracture with entrapped muscle or perimuscular soft
tissue especially white-eyed blowout fracture in children.
• Early enophthalmos/hypoglobus causing facial asymmetry.
• White-eyed orbital blow-out fractures—white-eyed blow-out fractures are
more common in children. In children, the flexible bone tends to bend
rather than break causing acute incarceration of herniated tissue in a
trap-door effect due to the greater elasticity of bone in younger
children. The orbital tissue is entrapped between the bony fragments
impairing the blood supply. So, these fractures are known as white-
eyed blow-out fractures. Patients may experience acute nausea,
vomiting and headache; persistent activation of the oculocardiac reflex
can occur.
Repair within 2 weeks

• For symptomatic diplopia with positive forced duction test
• Indication of an entrapped muscle or perimuscular soft tissue on CT
examination
• Minimal clinical improvement over time
• Large floor fracture causing latent enophthalmos or significant
hypoglobus
• Progressive infraorbital hypoesthesia
Indications for open reduction
• Severely displaced fractures

• More than two fracture fragments and need for fixation
• Needs orbital reconstruction
• Cosmetic reasons
• Functional disabilities
• Nerve, vessel or muscle compression

A variety of methods, ranging from conservative treatment to surgical
treatment by closed reduction of the fracture or open reduction with fixation,
can be successfully used to treat ZMC fractures.
Conservative Treatment
Conservative treatment is indicated if there is minimal or no displacement of
the fractured bones, or in those cases involving medically compromised
patients or more elderly for whom invasive surgical procedures and a general
anaesthesia are contraindicated.
Surgical approach
The surgical plan for reduction and fixation determines the sites requiring
exposure of fracture.
Extraoral approach
• Lateral (supraorbital) eye brow approach—Dingman approach

(Fig. 46.33)
• Upper eyelid approach
• Gillies temporal approach (indirect reduction)—indicated in cases
which are stable after reduction and require no fixation (Fig. 46.34)
• Infraorbital approach (Fig. 46.35)
• Bicoronal/Hemicoronal approach (Fig. 46.36) theoretically, this is the
best approach for open reduction and internal fixation. The zygoma
fracture reduction is complete if the sphenozygomatic suture is
reduced. This suture can be visualised only by this approach.
Moreover, this approach is ideal in zygomatic complex fractures
involving the frontal bone, orbital roof reconstruction, arch fracture
requiring fixation and laterally displaced zygoma fracture requiring 3-
or 4-point fixation.
• Subtarsal approach (Fig. 46.37)
• Subciliary/infraciliary approach (Fig. 46.38)
• Transconjunctival approach or inferior fornix approach (Fig. 46.39)—
Preseptal approach
—Retroseptal approach
• Percutaneous approach (Fig. 46.40)—Stacey bone hook and Carroll-
Girard screw
FIGURE 46.33 Dingman approach—lateral eyebrow incision and
exposure of the fracture segment.
FIGURE 46.34 Gillies temporal approach.

FIGURE 46.35 Infraorbital approach for zygoma fracture reduction
and fixation.
FIGURE 46.36 Bicoronal approach for zygoma complex fracture
reduction and fixation.
FIGURE 46.37 (A) Subtarsal approach for zygoma fracture

reduction fixation and orbital floor reconstruction. (B) Dotted line
indicates subtarsal incision (skin–muscle flap).
FIGURE 46.38 Subciliary approach for zygoma fracture reduction

and fixation.
FIGURE 46.39 Transconjunctival or inferior fornix approach.
FIGURE 46.40 (A) Zygoma fracture reduction using Carroll–Girard

screw. (B) Zygoma fracture reduction using Stacey bone hook.
Intraoral approach
• Transoral (maxillary vestibular) approach: Keen or Balasubramanium

approach—useful approach for reducing isolated arch fractures
(Fig. 46.41)
• Endoscopic transantral approach
FIGURE 46.41 Buccal sulcus approach (Keen’s approach).
Infraorbital rim, orbital floor, inferior portions of medial and lateral walls all
can be exposed via lower eyelid incisions effectively. In case of zygomatic
complex fractures involving frontal bone, coronal approach is ideal, though an
additional incision for orbital floor is required.
Fracture reduction
The basic principle of fracture management is fracture reduction, fixation and
immobilisation. The only bone fracture in head and neck, which is treated by
indirect (closed) reduction and no fixation is zygoma fracture (indicated).
Indirect reduction or closed reduction

As it is not practical to achieve digital reduction of all the fractures, indirect
reduction is carried out which involves disimpaction and reduction of the
fracture by direct application of an instrument to the deeper aspect of the
zygomatic bone through an indirect approach remote from the fracture line.
1. Gillies temporal fossa approach (Fig. 46.42)

This approach was introduced by Gillies in 1927 for the reduction of the
zygomatic complex fractures, which are stable. The rationale for this approach
is that the temporal fascia is attached to the superior aspect of the zygomatic
arch and outer aspect of the zygomatic bone whereas the temporalis muscle
passes beneath the zygomatic arch to get attached to the anteromedial surface
of the coronoid process. Beneath the fascia and above the temporalis muscle,
there is a potential space where an instrument can be passed which could engage
the temporal surface of the impacted zygomatic bone. From here the fractured
zygomatic bone or the arch can be elevated.
FIGURE 46.42 (A) Gillies temporal approach for indirect reduction
of zygoma fracture using Bristow’s elevator. (B) Gillies temporal
approach for indirect reduction of zygoma fracture demonstrated in
skull using Rowe’s zygoma elevator.
Procedure
An incision of about 2.5 cm length is made between the two branches of the
superficial temporal artery at an angle of 45° to the upper limit of the
attachment of the external ear. Dissection is carried out till the temporal fascia.
A Bristow’s elevator is passed down through this incision beneath the
zygomatic bone, which is then gradually reduced to its position. The incision
is then closed in layers. Rowe pattern zygomatic elevator can also used in this
approach for the reduction of the zygomatic fracture. This instrument has a
blade and oval handle similar to the Bristow’s pattern, but also incorporates a
lifting handle, which is attached by a strong hinge with a positive stop near the
origin of the other handle. The external or lifting handle is designed so that its
extremity is the same length as the tip of the internal or elevating blade and
thus the extent of the insertion may be assessed accurately at all times unlike
Bristow’s elevator. Bristow’s elevator has a disadvantage of using the temporal
bone as fulcrum causing risk of fracturing the temporal bone during the
procedure. This was overcome by the design in Rowe’ zygoma elevator.
2. Transverse buccal sulcus incision (Keen’s or

Balasubramaniam approach) (Fig. 46.43, 46.41)
A bone hook can be passed from a transverse incision made in the region of
buccal sulcus and the fractured segment can be reduced. An incision 1 cm in
length is made in the buccal sulcus behind the zygomatic buttress. A bone
hook or rowe’s zygomatic elevator is passed behind, supraperiosteally, to
contact the deep part of the zygomatic bone; here an upward, outward and
forward pressure is exerted. The advantage of this method is that less amount
of force is required for reduction.
FIGURE 46.43 Transoral maxillary vestibular approach (Keen’s or

Balasubramaniam approach).
Surgical approaches to the orbit (Fig. 46.44)

• Transconjunctival (inferior fornix transconjunctival using a retroseptal
or preseptal route) (Fig. 46.39)
• Transcaruncular (medial transconjunctival)
• Transconjunctival with lateral skin extension (lateral
canthotomy/swinging eyelid)
• Combination of inferior (A) and medial (B) transconjunctival
• C-shaped incision [i.e. Combination of inferior (A) and medial
transconjunctival (B) plus lateral skin extension (C)]
FIGURE 46.44 Approaches to the orbit. (A) Lateral eyebrow

incision. (B) Upper blepharoplasty incision. (C) Lateral canthotomy
incision. (D) Transcaruncular incision. (E) Lynch incision. (F) Upper
lid skin crease incision. (G) Transconjunctival incision. (H) Medial
transcaruncular extension. (I) Transconjunctival incision with lateral
skin extension.
Fixation technique
Direct fixation through open reduction: Plate and screw technique.
Internal orbital reconstruction: Transantral approach/endoscopic.
One-point fixation
Indication: Undisplaced fracture at frontozygomatic suture, simple
noncomminuted zygomatic complex fracture (Fig. 46.45).
FIGURE 46.45 One-point fixation at frontozygomatic suture.
Approach: The frontozygomatic suture approached through supraorbital

eyebrow approach is a satisfactory location for fixation. The maxillary
vestibular approach is sufficient to expose the zygomaticomaxillary buttress.
One-point fixation with a miniplate following the cardinal bends stabilises the
fracture efficiently. One-point fixation in the zygomaticomaxillary buttress
region can avoid unsightly scars and give high satisfaction with surgical
outcome in selected patients with zygoma fractures.
Two-point fixation
Indication: Displaced fracture unstable after reduction (Fig. 46.46).
FIGURE 46.46 Two-point fixation at frontozygomatic suture and

infraorbital rim.
Fracture at frontozygomatic suture, infraorbital rim and buttress.

Approach: Exposure of frontozygomatic suture through lower eyelid incision
(infraorbital rim) or the maxillary vestibular incision (zygomaticomaxillary
buttress). A 2-point fixation using a low profile plate at frontozygomatic
suture and a strong plate at zygomaticomaxillary buttress or at the infraorbital
rim will suffice.
Three-point fixation
Indication: Grossly displaced zygoma fracture (Fig. 46.47).
FIGURE 46.47 Three-point fixation.
Fixation is done at frontozygomatic suture, zygomaticomaxillary buttress

and the infraorbital rim. Good reduction of these three sites mostly reduces the
arch fracture, which is not fixed (avoiding the coronal incision/preauricular).
Four-point fixation
This is controversial as to the order of fixation (Fig. 46.48). The four-point
technique is unique from the three-point technique in that the surgeon
visualises the zygomatic arch. The order of placement of the plates will be
dependent on the least damaged landmarks. The zygomatic arch is an
excellent reference to restore proper anteroposterior projection of the midface.
FIGURE 46.48 Four-point fixation for zygoma fracture.
In addition to fracture fixation, some additional procedures as lateral

canthal ligament resuspension (canthopexy) may be required (Fig. 46.49).
FIGURE 46.49 Lateral canthal ligament resuspension.

Zygomatic arch fractures may be reduced effectively by closed reduction. A J-
shaped, curved hook elevator is inserted just below the zygomatic arch
anterior to the articulating eminence through a preauricular transcutaneous
stab incision. After positioning the tip of the hook directly under the
dislocated bone fragments, reduction is achieved by well controlled lateral
traction (Fig. 46.40).
There is no need for rigid internal fixation, because the temporalis and
masseter muscles and fascia, along with the adjacent soft tissues, splint the
arch sufficiently to stabilise the fragments. No functional loads should be
exerted that will result in displacement.

Indications for orbital exploration (Fig. 46.50)
Orbital exploration is indicated in the following situations:
• Severe comminution
• Displacement of orbital rim
• Orbital floor displacement with orbital contents into the maxillary
sinus
• Orbital floor defect greater than 2 cm
• Combination of inferior and medial wall fractures
• Suspected involvement of orbital apex
• Positive forced duction test
FIGURE 46.50 Orbital blow-out fracture in association with zygoma
complex fracture.
Orbital floor reconstruction should be done secondary to restoring the outer

framework. There is an array of biomaterials available for floor reconstruction
(Table 46.1) (Figs. 46.51 and 46.52).
Table 46.1
Biomaterials in orbital floor reconstruction

Autogenous Allogenic materials (allografts, xenografts) Alloplastic materials
materials
Types Contain no living cells but possess Types
• Autogenous osteoinductive and/or osteoconductive • Nonresorbable alloplasts
bone (Fig. 46.51) properties. Provides a structural • Metallic mesh
• Cranium framework for growth of host tissues (Fig. 46.52)
• Anterior wall of Types • High-density porous
maxillary sinus • Lyophilised fascia polyethylene
• Mandible • Homologous bone • Hydroxyapatite
• Rib • Homologous cartilage • Silicones and
• Iliac • Xenografts (rarely used) polytetrafluoroethylene
• Autogenous • (Teflon)
cartilage • Resorbable alloplasts
• Conchal • Polylactide
• Septal • Polyglactin
• Costal • Vicryl mesh
• Polydioxanone plates
(PDS)
• Gelatin film
Advantages Advantages Advantages
• Relative • Do not require a second operative site • Elimination of donor site
resistance to • Less operative time morbidity
infection • Decreased operative time
• Incorporation by • Multitude of sizes and
the host into new shapes available
bone
• Lack of host
response against
the graft
Disadvantages Disadvantages Disadvantages
• Second operative • Antigenicity of the material • Foreign bodies reactions
site • Transmission of infectious disease • Host reaction to the
• Patient material
morbidity
• Increased
operative time to
harvest
• Limited quantity
• Variable
amounts of
resorption
FIGURE 46.51 Autogenous bone graft (split rib graft) for orbital
floor reconstruction.
FIGURE 46.52 Nonresorbable alloplastic titanium mesh for orbital

floor reconstruction.
Factors influencing choice of biomaterial
• Defect size
• Multiple walls involvement
• Adaptation to internal contours
• Restoration of proper volume
• Presence of adjacent sinus cavity
• Prevention of displacement
• Adhesions/restriction of ocular mobility
• Early versus late repair
• Risk of further trauma
• Retrobulbar haemorrhage:
Though rare, is a serious complication of all the fractures involving orbit.

The vision should be closely monitored and any change like development of
pain, dilatation of pupil, proptosis, ophthalmoplegia and decreased visual
acuity should alert the surgeon to the retrobulbar haemorrhage. Surgical
decompression should be done through a conjunctival incision or endoscopy
along with medications like mannitol, acetazolamide and steroids to decrease
the intraocular pressure.
Clinical Features:
• Severe aching pain

• Progressive loss of vision
• Proptosis
• Increased intraocular pressure
• Marked subconjunctival haemorrhage
• Gross eyelid swelling
• As vision is lost pupil become fixed and dilated
Management of retrobulbar haemorrhage:
*
Normal Intraocular pressure (IOP) of human eye is 12 to 22 mm Hg
• Malar asymmetry
• Visual disturbances
• Loss of vision—vision loss caused by injuries directly to the globe, the
optic nerve, or the visual pathway and retrobulbar haematoma
• Rapid recognition of ophthalmic injury is important in case of
zygomaticoorbital fracture for several reasons
• Persistent diplopia
• Orbital dystopia
• Enophthalmos
• Sensory deficits involving the infraorbital nerve
• Compromised ocular function
• Persistent oculocardiac reflex
CHAPTER 47
Naso-Orbito-Ethmoid
Fracture

Bony structures of the region
Nasal bone and septum
Lacrimal apparatus
Medial canthus
Anterior tendon
Posterior tendon
Nasal bone fracture
Types
Clinical findings
Management
Reduction
• Closed reduction
• Open reduction
Methods of immobilisation
• Intranasal splinting
• Extranasal splinting
Naso-orbito-ethmoidal complex fracture
Clinical findings
Radiologic examination
Principle of management
• Early case
• Late case-secondary deformity
Sequence of management
Fracture reduction and fixation
• Canthopexy
Lacrimal system management
Epicanthus fold management
• Abduction: Rotation of the eyeball away from the midline.

• Adduction: Rotation of the eyeball towards the midline.
• Ocular dystopia: Change in the position and the axis of the eyeball.
• Orbital dystopia: Change in position of the bony orbits.
• Ectropion: The outward turning (eversion) of the lower eyelid
resulting in exposure of the palpebral conjunctiva.
• Enophthalmos: Displacement of the eyeball posteriorly and inferiorly
within the orbit resulting in a sunken eye appearance.
• Entropion: Inward turning (inversion) of the lower eyelid.
• Epiphora: Tearing of the eye due to inability of the lacrimal fluid
(tears) to drain through the nasolacrimal duct into the nasal cavity.
• Exophthalmos: Anterior positioning of the eyeball from the orbital
socket resulting in bulging eye appearance.
• Lagophthalmos: Inability of the upper eyelid to follow the eyeball
movement resulting in no or incomplete closure of the palpebral
fissure.
• Strabismus (squint): Lack of coordination between the extraocular
muscles of the right and left eyes resulting in lack of synchronised,
symmetric movement of the eye.

The naso-orbito-ethmoid region (NOE) is the central region at the junction of
upper and middle third of the facial skeleton. Post-traumatic reconstruction of
this region is challenging due to its multidimensional anatomy, that is
contributed by various bones and associated soft tissue structures such as the
lacrimal apparatus, medial canthus, eyeball, etc. The key structure in these
fractures is the ‘central fragment’ of bone to which the medial canthal tendon
attaches. It is essential to identify and anatomically reduce this fragment to
prevent postoperative telecanthus. Hence, it is imperative to have thorough
knowledge of the skeletal buttresses of the face as follows (Fig. 47.1):
• Horizontal buttresses:
▪ Frontal bar
▪ Orbital rims
▪ Alveolar process
▪ Inferior border of mandible
• Vertical buttresses:
▪ Nasomaxillary
▪ Zygomaticomaxillary
▪ Pterygomaxillary
FIGURE 47.1 Skeletal buttresses of the face. (A) Horizontal

buttresses. (B) Vertical buttresses.
Bony structures of the region

The bones contributing for the structural framework of this region are
(Fig. 47.2):
• Nasal bone
• Frontal process of maxillae
• Medial orbital wall
• Ethmoid
• Frontal bone
• The floor of the anterior cranial base
FIGURE 47.2 Anatomy of nasoorbital region.
The frontonasal buttresses can effectively resist the energy transmitted from
a direct anterior blow as against a lateral blow. As the thick nasal bridge
collapses, the forces are dissipated into the ethmoidal air cells acting as an
airbag or the natural ‘crumple zone’ minimising incidences of direct cerebral
injury.
Nasal bone and septum

• Nose is a confluence of rigid bones, the roof of which is the paired
nasal bones and flexible cartilaginous struts (Fig. 47.3).
• The septum in the midline of the nose is made up of the perpendicular
plate of ethmoid posterosuperiorly, cartilaginous septum
anteroinferiorly and the vomer posteroinferiorly.
• Laterally, the nasal bone articulates with the frontal process of the
maxilla, posterior to the frontal process of the maxilla is the lacrimal
bone.
• The thicker part of the nasal bone interdigitates with the nasal process
of the frontal bone and the inferior, thinner part of the nasal bone is
attached to the upper lateral cartilage and overlap the cephalic borders
of the upper lateral cartilages by 7–11 mm.
• The nasal bone comprising the superior half are rectangular bones that
articulate with each other in the midline, in the shape of a tent with the
septum (perpendicular plate of the ethmoid posteriorly and the septal
cartilage anteriorly) as the prop.
• The area where the septum, the perpendicular plate of the ethmoid,
upper lateral cartilages and the nasal bones meet is referred to as the
key-stone area. The dorsum is supported by the perpendicular plate of
ethmoid and the septal cartilage in this area.
FIGURE 47.3 Anatomy of nasal bone and septum.
Lacrimal apparatus
a. Puncta: The punctum is a small orifice located at medial end of upper
and lower eyelids, in an elevation called the lacrimal papillae, faces
posteriorly so as to evert medially. Obstruction or narrowing (stenosis)
of the puncta causes epiphora (excessive tearing).
b. Canaliculi and ampulla: Vertical canaliculi is 2 mm long and the
horizontal canaliculi is 8 mm long, both join at a right angle called the
ampulla.
c. Nasolacrimal sac and duct: This common canaliculi open in
nasolacrimal sac, which is guarded by valve of Rosenmuller. The
nasolacrimal sac opens into the nasolacrimal duct, which is 6–21 mm in
length and opens into inferior nasal meatus. The valve of Hasner guards
the opening of the duct.
FIGURE 47.4 (A) Anatomy of the lacrimal drainage system. (B)
Image showing muscles on the medial wall of the eye.
Medial canthus
The medial canthal complex of the eyelids is attached to the medial bony orbit
and the muscles are arranged in a special manner (Figs. 47.4–47.5). The medial
canthal tendon originates at the medial border of the upper and lower tarsal
plates. Medially, the tendon inserts into the anterior lacrimal crest and nasal
bone. Posteriorly the ligament continues as the lacrimal fascia, towards the
posterior lacrimal crest. Its inferior border is free, while its superior border
continues into the medial orbital periosteum.
FIGURE 47.5 Image showing medial canthal ligament and its
attachments.
Anterior tendon
The anterior horizontal tendon is the strongest component and is attached
most firmly at the anterior lacrimal crest. The vertical component of the
anterior tendon is less firmly secured to the medial orbital rim, several
millimeters above the insertion of the horizontal tendon, whereas the posterior
lacrimal crest attachments are the weakest. The resultant vector of these
attachments suggests that resuspension of the entire complex following
disruption should be posterior and superior to the anterior lacrimal crest. The
periosteum on all sides of the tripartite medial canthal complex is very thin, so
fixation of the medial canthal tendon must be more secure, that is into bone.
Posterior tendon
The posterior element of the medial canthal tendon is formed by the deeper
thin fibres of the preseptal and pretarsal muscle, referred to as the Horner’s
muscle, Duverney’s muscle, tensor tarsi and pars lacrimalis. These fibres angle
posteriorly at the medial end of each tarsal plate superior to the upper ampulla
and inferior to the lower ampulla (the vertical short portion of each
canaliculus, not after punctum). They have a common interlacing insertion
into the lacrimal bone a top and behind the posterior lacrimal crest.
For ease of learning, fractures of the NOE region has been dealt separately
as isolated nasal bone fracture and NOE complex fractures.
FLOWCHART 47.1 Pathophysiology of NOE fractures.
Nasal bone fracture

It is the most common fracture of the facial bones due to its prominent
location, though it may go unnoticed. Nasal bones are the commonest of the
facial bone fracture due to its eminent front position on the face. They are not
life threatening, but subsequently lead to aesthetic and functional deformities.
Children are more protected from nasal fractures due to the more
cartilaginous portion of the nose than the adults (Table 47.1 and Fig. 47.6A).
Types
• The extent of fracture to the nasal bones depends on the direction of
the force applied (anterior or lateral).
▪ Anterior direction: Force from the front of the face (bridge of the
nose) may result in severe flattening of the nasal bones and
septum. Broadening of the nasal bones with flaring of the
nasal width occurs leading to flattened depressed nose
(Fig. 47.6B). Untreated anterior injuries will leave a flattened
nose with thickened bridge, which becomes worse if lacrimal
bones and orbital laminae of the ethmoid bones are involved.
▪ Lateral direction: While lateral forces cause only fracture and
sinking of the ipsilateral nasal bone and may be potent
enough to cause contralateral nasal bone (Fig. 47.6C). Septal
fractures are commonly found in lateral injuries where the
nasal pyramid is deviated by at least one-half the nasal width
resulting in creation of an asymmetric nasal pyramid with
deviation. Nasal fractures from lateral trauma typically are
less severe in nature and have a better prognosis than those
from frontal force injuries.
If the lateral types of injuries left untreated, it will result in
deviation of the nose to one side, with probably a blockage of
both nares.
• Paediatric nasal trauma:
▪ Septal haematomas are more commonly seen in paediatric nasal
trauma. Untreated haematoma may lead to infection, septal
destruction and long-term nasal deformity and airway
obstruction (Fig. 47.7A–B).
▪ Avoidance of over aggressive treatment of paediatric nasal
fractures is important to prevent damage to the nasal septal
growth centres responsible for midface development.
Table 47.1
Rohrich classification of nasal bone fracture
Type 1: Simple unilateral fracture

Type 2: Simple bilateral fracture
Type 3: Comminuted fracture (Fig. 47.8)
Type 4: Nasal bone fracture associated with septal injury
Type 5: Naso-orbito-ethmoid fracture
FIGURE 47.6 (A) Isolated right nasal bone fracture with mild lateral
displacement. (B) Nasal fractures resulting from lateral impact. X
moderate force and Y severe force. (C) Nasal fractures resulting
from anterior impact. X moderate force and Y severe force.
FIGURE 47.7 (A) Untreated septal haematoma resulting in
deformed septum and nasal obstruction. (B) Asymmetric nasal
pyramidal deviation of septum.
FIGURE 47.8 Comminuted undisplaced isolated nasal bone

fracture.
Physical examination and history plays an important role in diagnosis. The
high incidence of old unrecognised fractures from insignificant trauma
precludes the use of CT/X-ray for confirming nasal bone fractures.
Clinical findings
• Pain and swelling of nasal region.
• Flattening or other deformation of the shape of nose (Fig. 47.9).
• Epistaxis or bleeding from the nose.
• CSF leaks if there is comminuted fracture of the cribriform plate of the
ethmoid. Sometimes the CSF may pass backwards down the throat
and the patient might complain of salty taste.
• Airway blockage due to bleeding, fluid discharge or tissue swelling
leading to nasal vestibular stenosis.
• Crepitus—the crackling heard and the sensation felt when broken
bones are moved over each other. This could also be due to tissue
emphysema from air entry from nasal cavity into the soft tissues
overlying nasal bone.
• Nasal septum may be deviated to one side in lateral type of injuries,
while saddle type depression of the bridge is seen in anterior
fracturing force (Fig. 47.10A–B).
• A step-deformity may be palpated.
• Nasal fractures are frequently accompanied by lid oedema, bilateral
circumorbital ecchymosis more marked on the affected sides, chemosis
and subconjunctival haemorrhage if they involve the orbital complex.
• Involvement of deeper bony component of medial orbital wall will
result in displacement of medial canthal ligament. Bowerman (1985)
concluded that the intercanthal measurement more than 35 mm is an
indicator for medial canthal displacement. The displacement may be
unilateral or bilateral.
FIGURE 47.9 Secondary deformity from untreated nasal fracture.

FIGURE 47.10 (A) Septal deviation. (B) Right nasal bone fractured
and displaced medially causing septal deviation and asymmetric
piriform aperture.
Management
Reduction
Reduction of nasal fracture can be done either by open technique or closed
technique. In most of the cases closed reduction is performed successfully. The
best time for reduction is earliest after injury. Sometimes it is useful to allow
the oedema to subside before attempting reduction. But delay in reduction
causes difficulty in the approximation of the nasal fragments due to fibrosis
and malunion making the fractured fragments less mobile.
Closed reduction
Indications for closed reduction
• Unilateral or bilateral fracture of the nasal bones

• Fracture of the nasal septal complex that is minimally deviated
Technique
• Reduction can be done either under local anaesthesia or general

anaesthesia using Walsham’s and Asch’s septal forceps (Figs. 47.11 and
47.12).
• The unpadded blade of the Walsham’s forceps is passed through the
nostril while the padded blade remains externally. The fractured nasal
bone and frontal process of the maxilla are secured between the two
blades.
• The reduction is done by applying force in the opposite direction of the
fracturing force, usually anterolateral direction.
• Rarely laterally displaced segments require external direct pressure.
• For the reduction of septal fractures, Asch forceps may be introduced
with one blade in each nostril engaging the septum on either side
reducing the fractured segment. Sometimes the cartilaginous septum
may be dislocated from its anatomic position in central groove in
maxilla (tongue in groove position). The septal cartilage can be
grasped and repositioned into its groove.
• The lacrimal bones and the medial wall of the orbit on each side are
compressed using digital pressure to reestablish the narrow bridge of
the nose.
FIGURE 47.11 (A–B) Septal fracture reduction with Asch forceps.
FIGURE 47.12 (A–B) Nasal bone fracture reduction with Walsham

forceps.
Open reduction
The septum remains as an impediment to the reduction of nasal pyramid.
When the septal fragments are interdigitated with one another, the septum
cannot be reduced properly resulting in a deviated bony pyramid. Such cases
are an indication to open approach.
Similar to NOE, surgical approaches to nasal bone fracture are used. For
cosmetic reason bicoronal flap is most desirable. The fracture fragments are
reduced and fixed with miniplates or microplates.
Packing and postoperative care are the same as described for closed
reduction. In cases involving the disruption of medial canthal ligaments of the
eye canthopexy is done in addition.
Indications for open reduction
• Extensive fractures
• Deviation of the nasal pyramid greater than one half width of the nasal
bridge
• Open septal fracture
• Persistent deformity after closed reduction
Contraindications
Undisplaced nasal fracture causing no cosmetic deformity; no management.
In case of severe nasoethmoid complex fractures, it is advisable for open
reduction. Sometimes, reduction of an uncomplicated simple fracture in
panfacial trauma may trigger or aggravate cerebrospinal leak.
Complications
Early
• Epistaxis is common with nasal fractures and may recur with the
reduction.
• Haematoma is always a concern and must be evacuated.
• CSF rhinorrhoea is uncommon but may occur when fractures extend to
include the cribriform plate.
• Haematoma always poses an early attention and treatment. CSF
rhinorrhoea is rare but is anticipated when fractures extend to include
the cribriform plate.
Late
• Nasal obstruction
• Secondary nasal deformity (Fig. 47.13)
• Saddle nose deformity (Fig. 47.14)
• Synechia (adhesion) (Fig. 47.15)
• Septal perforation
FIGURE 47.13 Secondary deformity due to nasal fracture.

FIGURE 47.14 Saddle nose deformity.
FIGURE 47.15 Synechia.
Methods of immobilisation
Splinting may be required for immobilisation, though some simple fractures
require no splinting.
Intranasal splinting
• Ribbon gauze
• Silicone splint (Fig. 47.16A–B)
FIGURE 47.16 (A) Silicone sheet for intranasal splint. (B) Silicone
splint in place after septoplasty to support septum.
Use of ribbon gauze is the most standard method of providing intranasal

support once the fracture is reduced. Ribbon gauze of 12–15 cm length is taken
and inserted into the nose in layers beginning from above downwards.
Over packing the nose causes displacement of the reduced fractured
segments; care need to be taken not to overpack the nose.
Internal packing or splints is not mandatory in all cases. During nasal
fracture reduction, the intranasal silastic splints may be sutured in situ only
when the septum is reduced. The intranasal pack supports the septum as well
as prevents adhesion of the septum and the lateral wall.
Disadvantages
• Inadequate anteroposterior support

• Difficulty in breathing through the nose
• Potential source of infection
Extranasal splinting
• Plaster of Paris (POP) (Fig. 47.17)

• Lead splints
FIGURE 47.17 Extranasal splint with Plaster of Paris.
The most commonly employed extranasal splint is the POP splint. This
consists of eight layers of POP bandage, which is cut so as to produce a strip of
plaster across the bridge on either side of the nose along with frontal
extension. This bandage should be applied when the POP is still wet and
moulded to the shape of the nose. The splint should not extend onto the soft
part of the nose. The nasal splint is held in position by surgical tape externally.
It should remain in position for 1 week. Considering the mobility of the
segments and the amount of bleeding, antibiotic-impregnated gauze packing
can be kept in each nostril for 1–5 days.
When POP splint cannot provide support and stability, lead plates can be
used on either side of the nose for splinting. These lead plates consist of two
holes and are fitted on each side of the nose with the help of tantalum or
stainless steel sutures, which are passed into the holes and beneath the nasal
bones. This splint is left in place for a period of 3 weeks.
Naso-orbito-ethmoidal complex fracture

Three distinct patterns have been described, based on velocity and point of
impact. They may occur as an isolated injury or in association with other major
facial fractures (Table 47.2 and Flowchart 47.1).
FIGURE 47.18 Markowitz and Manson classification of nasal-

orbital-ethmoid (NOE) fractures. (A) Type I. (B) Type II. (C) Type
III.
Table 47.2
Markowitz and Manson classification (Fig. 47.18)
Type I Nasal-orbital-ethmoid fractures (Fig. 47.19)

• Simplest form of nasal-orbital-ethmoid fracture.
• Involves only one portion of the medial orbital rim with its attached medial canthal tendon.
• Unilateral or bilateral form.
• In case of bilateral complete type I fracture, there is usually medial canthal tendon
displacement and hence stabilisation of the osseous monoblock suffices.
Type II Nasal-orbital-ethmoid fractures (Fig. 47.20)
• A bilateral or unilateral form.
• May involve large segments or comminuted.
• The canthus remains attached to a large central segment.
• Fixation of the fracture segments suffices usually with no specific resuspension of ligament.
Type III Nasal-orbital-ethmoid fractures (Fig. 47.21)
• Comminution involving the central fragment of bone where the medial canthal tendon
attaches.
• The canthus is rarely avulsed completely, though the fragments of bone are so small that
reconstruction is not possible.
• Transnasal wiring or other forms of resuspension of the canthus is required.
• The bony framework if beyond fixation is reconstructed secondarily.
FIGURE 47.19 Type I NOE fracture.
FIGURE 47.20 Type II NOE fracture in association with

zygomaticoorbital fracture.
FIGURE 47.21 Type III comminuted NOE fracture bony fragments
beyond fixation.
Clinical findings
• Periorbital and nasal oedema, ecchymosis and emphysema (Fig. 47.22).

• Depressed nasal dorsum from telescoping of nasal dorsum into
ethmoid region (Fig. 47.23).
• Widening of the nasal base.
• Obtuse frontonasal angle giving a pig snout appearance of the nose.
• Commonly associated with septal fracture evident as shifted nasal
midline (Fig. 47.24).
• Subconjunctival haemorrhage is usually restricted to the medial aspect
of eyeball (Fig. 47.25).
• Saddle nose deformity.
• Shortened palpebral fissure (Fig. 47.26).
• Shallow nasoorbital valley.
• CSF rhinorrhoea—In severe impact, the forces could extend fracture to
skull base causing dural tear from displaced fracture segments.
• Anti mongoloid slant
• Blindness or diminished visual acuity (Fig. 47.27): This occurs in severe
posteriorly displaced NOE fracture compressing optic nerve. This can
be detected by bedside swinging flashlight test (unconscious) and finger
counting or Snellen chart in conscious patient.
• Epicanthal fold—Posttraumatic epicanthal fold is usually associated
with telecanthus. Along with canthopexy, this fold requires correction
for cosmesis (Figs. 47.28 and 47.29).
• Epiphora—Persistent tearing of eyes usually occurs due to obstruction
of lacrimal apparatus at various levels. Blockage of the lacrimal
excretory apparatus that is the canaliculi, the lacrimal sac or the
nasolacrimal duct may occur due to compression of the displaced bone
fragments or may be severed by such fragments. Very rarely CSF may
leak into the orbit or conjunctiva (orbitorrhoea) clinically presenting as
epiphora.
• Traumatic Telecanthus or Pseudohyperteleorism (Figs. 47.30 and 47.32).
FIGURE 47.22 Periorbital oedema, ecchymosis, nasal deformity,

depressed nasal bridge.
FIGURE 47.23 Depressed nasal dorsum from telescoping of nasal
dorsum into ethmoid region.
FIGURE 47.24 Septal fracture in association with nasal bone

fracture.
FIGURE 47.25 Right eye shows subconjunctival haemorrhage
(SCH) restricted to lateral aspect. Left eye shows SCH on medial
and lateral aspect showing conjoined NOE fracture.
FIGURE 47.26 Telecanthus, almond-shaped eye, epiphora,

shallow nasoorbital valley, obliterated canthal bay and shortened
palpebral fissure.
FIGURE 47.27 Posttraumatic globe rupture causing blindness in
left eye.
FIGURE 47.28 Posttraumatic deformity—left eye orbital dystopia,
hypoglobus, enophthalmos with supratarsal hooding. Depressed
nasal bridge and reduced nasal projection.
FIGURE 47.29 Left eye showing obliteration of the caruncle and

epicanthal fold.
FIGURE 47.30 Telecanthus—illustrated in a case of naso-orbito-
ethmoid fracture.
FIGURE 47.31 Enophthalmos, hypoglobus, orbital and ocular

dystopia, telecanthus.
This is a classical finding in naso-orbito-ethmoid fracture due to disruption

or displacement of medial canthal ligament. Telecanthus refers to increased
intercanthal distance with normal interpupillary distance. Normal intercanthal
distance is 30–35 mm. Usually intercanthal distance is equal to the distance
between inner and outer canthi (width of the eye). Among the deformities
from NOE fracture, the telecanthus is most difficult to treat (Table 47.3). The
diagnostic tests for telecanthus is summarised in Table 47.4.
Table 47.3
Clinical features of NOE fractures

Nasal Ocular Others
• Pain • Periorbital oedema or • CSF rhinorrhoea
• Nasal deformity ecchymosis • Dural tear
• Nasal oedema • Step-offs at orbital rims • Paraesthesias of supraorbital or
• Laceration • Subconjunctival supratrochlear nerves
• Epistaxis haemorrhage • Midface retrution
• Crepitus • Diplopia • Sinusitis
• Tenderness • Enophthalmos or • Meningitis
• Flattened nasal exophthalmos
bridge • Infraorbital nerve
• Elevated nasal tip paraesthesia
• Septal deviation • Injury to ethmoidal
• Septal haematoma vessels
• • Blindness
Hyposmia/anosmia
FIGURE 47.32 Interpupillary and intercanthal distances.
Radiologic examination
Occipitomental view (10 and 45 degree) is helpful as initial screening tool. CT
scan examination is extremely useful in assessing the degree of fracture and
the displacement.
Principle of management
1. Early case
• The early cases of isolated NOE fracture and combined maxilla, NOE
fracture requires assessment for functional and cosmetic defect. The
functional aspect is dealt with ocular injuries, orbital fracture
reduction and need for reconstruction, integrity and patency of
lacrimal apparatus or recannulation. The cosmetic aspect is dealt with
correction of telecanthus, canthal dystopia and epicanthal fold.
• Type I and II require fracture fixation with mini-plates or microplates.
• Type III fracture is comminuted that cannot be reduced and fixed by
ORIF. The soft tissue deformity is corrected. Immediate bone grafting
may be required if there is gross comminution of key bone buttresses
or the orbital walls (Table 47.4).
• Primary repair of canthal ligament by resuspension.
• Epicanthal fold may require surgical correction.
Table 47.4
Diagnostic criteria for telecanthus
• Intercanthal distance >35 mm is indicative of canthal spread.

• Palpebral fissure is narrowed and almond shaped.
• Medial angle of the eye is blunted with obliteration of the caruncle.
• On palpation of the canthal ligament diminished tension is noticed.
• Eyelids become lax and the epicanthal folds become more prominent. The flattening of the
nasoorbital valley is the earliest indication.
• Eyelid traction test/bowstring test (Fig. 47.33)
▪ The eyelid traction test is used to determine the detachment of medial canthal ligament.
▪ The medial canthal ligament will be taut and will withstand like a subcutaneous
bowstring when the lower eyelid is laterally retracted. If the medial canthal tendon is
disrupted no bowstring will be seen or palpated.
• Furness test
▪ This test is performed by grasping the skin overlying the medial canthus with the small
tissue forceps. A lack of creasing or underlying resistance by the underlying bone is
indicative of underlying fracture. The bimanual examination requires placing an
instrument (e.g. a Kelly clamp) high into the nose, with its tip directly beneath the medial
canthal tendon. Gentle lifting with the contralateral finger palpates the canthal tendons
and allows an assessment of the instability of the tendon attachment and the necessity for
open reduction.
FIGURE 47.33 Eyelid traction test (bowstring test).
2. Late case-secondary deformity

The late cases of NOE fracture classically present as upper midface deformity
with saddle nose deformity, widened and depressed nasal bridge and
traumatic telecanthus. The primary management is aimed at cosmetic
camouflage.
Sequence of management
1. Reconstruction of the cranial base, frontal bandeau and outer orbital

frame, frontonasal buttress and orbital rim
2. The nasal dorsum should be reconstructed and nasal projection
restored, ideally by plating the bone fragments or by using grafts that
can be cantilevered from the glabella with miniplates
3. Medial canthal ligament—canthopexy
4. Lacrimal system
5. Epicanthal fold
6. Nasal plaster
Fracture reduction and fixation

The fracture is reduced and fixed following the basic principles of open
reduction and internal fixation.
Refer to Chapter 42 Basic Principles of Management of Maxillofacial Trauma.
Canthopexy
Transnasal wiring (Figs. 47.34 and 47.35)

In this technique soft stainless steel wire is threaded through the stump of the
medial canthal ligament and tightened over a toggle wire or a stable insertion
point on the contralateral side using a Kelsey fry awl or mustarde’s
canthopexy awl. The medial canthal ligament of the affected side is then
suspended to the contralateral nasal bone or contralateral medial canthal
ligament.
FIGURE 47.34 Transnasal wiring.
FIGURE 47.35 Transnasal wiring—using Ogilvie needle.
Disadvantages of the conventional technique
• An anterior migration of the medial canthus

• Deformation of the canthal bay
• Epiphora due to blocking of the nasolacrimal duct orifice
• Inadequate reduction of the telecanthus
• Unnecessary involvement of the normal, unaffected medial orbital wall
of the contralateral side
To overcome these disadvantages cantilevered Y plates are used to

reposition the displaced medial canthal ligament.
Modified cantilevered Y plates (Fig. 47.36A–D)

The drawback with the conventional technique is that anterior migration of the
canthus was found invariably in all the cases. The medial canthal ligament
(MCL) has a tripartite attachment which has anterior, posterior and superior limbs
attached to the lacrimal crest. The resultant vector of this attachment is
towards the upper end of the posterior lacrimal crest. Therefore, MCL requires
to be attached more posteriorly to prevent anterior migration of the canthus
after attachment. To solve this purpose a Y-shaped miniplate is fixed on the
lateral aspect of the nose, whose long arm is directed posteriorly into the orbit
and the MCL is suspended to the long arm of the plate using 3–0 silk sutures
or stainless steel wires.
FIGURE 47.36 (A–C) Modified Y plate canthopexy. (D)
Postoperative CT showing modified cantilevered Y plate
canthopexy.
Advantages of the cantilevered Y plates
• Involves only the deformed side.

• In comminuted fracture, acts as pseudolacrimal crest.
• The use of a miniplate resolves the need for an intact posterior lacrimal
crest.
• Indeed the suspended long arm of the miniplate not only acts as a
pseudoposterior lacrimal crest but also provides the surgeon with a
range of attachment point for the medial canthal tendon.
• Provides a more anatomic, posteromedial attachment of the medial
canthal ligament.
• The depth of attachment point to the miniplate allows the surgeon
more freedom in achieving symmetry of lid contour.
• Can also be used bilaterally.
• Safe and simple method.
• Attachment is adjustable.
• Can be used in acute NOE fractures along with other grafts and
fixations.
Lacrimal system management

The lacrimal system is often affected in NOE fracture though undetected. The
soft tissue lacerations, if present, should be carefully sutured with
recannulation of the duct using fine bore polyethylene or silicone tube or
dacryocystorhinostomy (Fig. 47.37A–E).
FIGURE 47.37 (A–E) Dacrocystorhinostomy procedure using
silicone tube.
Epicanthus fold management (Fig. 47.38A–C)

Epicanthal fold occurs with telecanthus in naso-orbito-ethmoid fracture.
FIGURE 47.38 (A) Outline of incision made along the fold. (B)
Switching the Z-flaps, the upper and lower flaps are transposed.
(C) Z-plasty completed.
The following are the techniques that ‘redistribute’ the skin of the epicanthal
fold for correcting the epicanthal fold.
• Z-plasty
• Y-V plasty
• Modified V-Y plasty
• V-W plasty (Flowers/Roveda method of correction of epicanthal folds)
• Quadrilateral jumping-man flap technique of Mustarde.
FLOWCHART 47.2 Complications of naso-orbito-ethmoid fractures.

CHAPTER 48
Frontal Bone Fractures
Surgical anatomy
• Mucosal lining
• Sinus drainage
• Frontonasal duct
Applied anatomy
Current surgical options in the management
Surgical approaches
Factors determining the treatment plan
Surgical exploration and fracture reduction with or without
fixation
Indications
Technique
Obliteration of sinus cavity
Indications
Materials used for obliteration of sinus cavity
• Autogenous grafts
• Alloplastic alternatives
Technique
Cranialisation
Indications
Technique
Early complications
Early major complications
• CSF leak
• Meningitis
• Pneumocephalus
Early minor complications
Late complications
Mucocele
Brain abscess
Osteomyelitis
Contour defect
CSF fistula
Surgical anatomy
The frontal bone is a single bone of the cranium and the skull base which is of
membranous origin. It has a large squamous portion and an orbital portion.
The squamous portion forms the anterior limit and floor of the anterior cranial
fossa (Figs. 48.1–48.4). It is responsible for the frontal prominence (bossing),
glabella and the superciliary arches of the forehead defining the upper facial
contour. The orbital portion contributes to the roof of the orbits bilaterally. It
has an outer table and an inner table with diploë in the middle. The anterior
portion of the squamous frontal bone houses the frontal sinus (Figs. 48.5–48.7).
The frontal sinus is often considered an extension of anterior ethmoidal air
sinus into the frontal bone. Though frontal sinus appears apparently as a
single sinus, it usually has a septum dividing the sinus unequally as right and
left. This septum often has a leftward deviation. Frontal sinus is of variable
sizes and it may also be absent (agenesis). The posterior wall of the sinus is the
only limiting structure between the sinus and the cranial cavity and its
contents making it significant. The frontal bone is a prominent bone of the
craniofacial skeletal framework that commonly takes up the forces in trauma
safeguarding vital structures.
FIGURE 48.1 Frontal view.
FIGURE 48.2 Right lateral view.
FIGURE 48.3 Left lateral view.
FIGURE 48.4 Oblique view.
FIGURE 48.5 CT axial section showing the frontal sinus enclosed
by anterior and posterior walls of frontal bone.
FIGURE 48.6 CT sagittal section showing the frontal sinus
enclosed by anterior and posterior walls of frontal bone.
FIGURE 48.7 CT coronal section showing frontal sinus and its
relation to nasal cavity. Note: the bony septum dividing the sinus
into left and right chambers.
Mucosal lining
• The sinus is lined by mucoperiosteal lining with mucous secreting

glands. The mucosal lining of the frontal sinus is a characteristic
mucoperiosteal blanket lining the frontal sinus, frontonasal duct and
ethmoidal air cells.
• The lining mucosa has its venous drainage through venules passing
the foramina of Breschet in the posterior wall of the sinus providing
an intracranial communication to dural venous sinuses. The lining
mucosa invaginates the foramina and has the potential of forming
mucocele, if incompletely removed during obliteration or
cranialisation procedures.
Sinus drainage (Fig. 48.8A–B)

The frontal sinus eventually drains into the middle meatus either directly by a
frontonasal duct or indirectly through the frontal recess or ethmoidal
infundibulum. The frontonasal duct is a variable duct absent in 85% of the
population. It may range from few millimetres to 2 cm. If an identifiable duct
is present, it opens into the posteromedial floor of the sinus.
FIGURE 48.8 Frontal sinus and frontal recess and their anatomy.
Frontonasal duct
The frontonasal duct has a foramen located in the posteromedial floor of the
sinus. Its course is highly variable, running caudally from a few millimetres to
up to 2 cm. A true identifiable duct may be absent in up to 85% of frontal
sinuses, wherein the frontal sinus drains indirectly through ethmoid air cells to
the middle meatus.
Applied anatomy
• Frontal sinus being air-filled, deformable cavity acts as a mechanical
barrier to protect brain and eyes from trauma.
• The sinus is lined by respiratory epithelium that secretes mucus and
drains into the frontonasal ostium and duct.
• Interference with the drainage mechanism of the sinus or disease in the
lining mucosa predisposes to sinusitis or mucocoele. Mucocoele can
act as an expanding tumour that can erode the bone, thereby creating a
mass effect on the brain or producing a cosmetic deformity.
• Frontal sinus infection has a risk of spread to adjacent eyes and brain.
• Persistent cerebrospinal fluid (CSF) rhinorrhoea in combined posterior
table fracture with a dural tear creates a nasofrontal communication
that poses risk of spread of infection leading to life-threatening
meningitis, brain abscess, etc.

The frontal bone being more prominent and broader than the surrounding,
weaker facial bones guards the brain from direct injury. The anterior sinus
wall can withstand between 350 and 1000 kg of force before fracturing. This is
higher than what other facial bones can endure. On encountering a force that
is higher than the tolerance of the frontal bone, it fractures. Force received by
the frontal bone can propagate and cause concomitant fracture of the weaker
bones of the orbit and nasoethmoid complex also. Forces that are capable of
fracturing the outer (anterior) table of the frontal bone may also fracture the
inner (posterior) table and the floor of the anterior cranial fossa, especially the
fovea ethmoidalis and the cribriform plate. Comminuted fractures of the outer
and inner tables of the frontal bone may also be associated with dural tears
leading to CSF rhinorrhoea.

The anatomical components that determine the fracture classification:
• The anterior table

• The posterior table
• The frontonasal duct
• Injury to the dura
• Presence of CSF leak
• Open cerebral trauma
Type 1: Simple, isolated fracture of the outer table (anterior wall) without
comminution, or concomitant naso-orbito-ethmoid or orbital rim
fractures (Fig. 48.9A–B).
Type 2: Comminuted fracture of the outer table with involvement of naso-
orbito-ethmoid complex and/or orbital rim (Fig. 48.10A–D).
Type 3: Combined outer and inner table (posterior wall) fractures where
fracture of the inner table is undisplaced without any dural injury
(Fig. 48.11).
Type 4: Combined inner and outer table fractures with dural tear and
consequent CSF leak (Fig. 48.12).
Type 5: Combined outer and inner table fractures with dural tear, CSF
leak, loss of soft and hard tissue and severe disruption of the anterior
cranial fossa (Fig. 48.13).
FIGURE 48.9 (A–B) Type 1 frontal bone fracture with minimal

displacement.
FIGURE 48.10 (A) Type 2 frontal bone fracture involving the orbital
rim. (B) Frontal bone fracture involving medial orbital wall. (C)
Outer table fractured and displaced. (D) Intraoperative view.
FIGURE 48.11 Type 3 anterior and posterior wall fracture with
minimal displacement of posterior wall.
FIGURE 48.12 Type 4 comminuted anterior and posterior wall
fracture with dural injury.
FIGURE 48.13 Type 5 comminuted anterior and posterior wall
fracture with loss of tissue.

Inspection
• Frontal oedema (Fig. 48.14)

• Periorbital oedema (Fig. 48.15) and ecchymosis (Fig. 48.16)
• Soft tissue emphysema in the frontal, nasal, periorbital, ethmoid
regions
• Forehead laceration (Fig. 48.17)
• Depression in the forehead that is visible and palpable (Fig. 48.18A–C)
• Flattening of the forehead (Fig. 48.19)
• CSF rhinorrhoea escape of CSF through nose evident as clear,
translucent fluid. Examination of nasal discharge is done to
differentiate CSF from nasal mucous secretion or blood.
FIGURE 48.14 Frontal oedema and ecchymosis.
FIGURE 48.15 Periorbital oedema associated with frontal and NOE
fracture. Note: clear fluid from right nostril possibly CSF
rhinorrhoea.
FIGURE 48.16 Periorbital ecchymosis in relation to frontal and skull
base fracture. Note the sutured laceration in forehead and CSF
otorrhoea.
FIGURE 48.17 Forehead laceration.
FIGURE 48.18 (A) Visible depression in glabellar region. (B–C)

Secondary deformity following frontal bone fracture—frontal
depression.
FIGURE 48.19 Flattened forehead.
CSF rhinorrhoea
CSF fluid
CSF is a clear body fluid that is found in the subarachnoid space which is the
space between arachnoid mater and pia mater. It cushions and buffers the
cortex. Whenever any disruption in dural tear occurs along with a skull base
fracture, there is a high risk of CSF leak. An important determining factor of
CSF leak is the resultant pressure gradient.
Formation
The CSF production occurs at the choroid plexus in the ventricles of the brain
at a rate of 20 mL/h approximating 500 mL daily and circulates the entire
central nervous system within the subarachnoid space. Cerebrospinal fluid is
a colourless, clear, fluid and typically devoid of cells and consists of water,
electrolytes, glucose, amino acids and various proteins.
Comparison of plasma and CSF composition

Composition Plasma CSF
Na+ (mM) 155 151
K+ (mM) 4.6 3.0
Mg2+ (mM) 0.7 1.0
Ca2+ (mM) 2.9 1.4
Cl− (mM) 121 133
(mM) 26.2 25.8
Glucose (mM) 6.3 4.2

Amino acids (mM) 2.3 0.8
Protein (mg/100 h−1) 6500 25
▪ Lower than plasma value, ▪ higher than plasma value.

CSF rhinorrhoea refers to leaking of CSF through the nose presenting as frank,
clear or blood stained nasal discharge. When patient is in supine position, CSF
rhinorrhoea manifests as postnasal drip giving a salty taste.
Causes
In the adult patients, it is helpful to broadly classify CSF leaks into two
categories:
• Spontaneous CSF leaks.

• CSF leak occurs as a result of an osseous defect at the skull base coupled
with a disruption of the dura mater and arachnoid mater with a resultant
pressure gradient.
Examples:
• Traumatic
• Surgery (iatrogenic)
• Tumours
Bedside tests
Halo test
A drop of the bloody discharge from the nose is placed on a white cloth
surface. If it contains CSF, this will diffuse in a radial pattern along with
blood. CSF will migrate farther than the blood, forming a ‘halo’ effect
(Fig. 48.20).
FIGURE 48.20 Halo test positive for CSF.
Tramline sign
In case of mixed CSF rhinorrhoea and epistaxis, a typical tramline effect is
produced where the CSF (transparent) alternates with the dried blood
producing a tramline pattern. This pattern is created by the continuous flow
of CSF as it washes away the centre, while the peripheral blood coagulates. In
reclined position, this finding may be absent due to escape of CSF into the
posterior pharynx.
Starch test
This test is to differentiate between CSF and nasal secretions. Nasal secretion
will dry and stiffen the linen while CSF does not. This may indicate the need
for further investigations to confirm.
Diagnostic testing
Strategies for diagnostic testing for CSF rhinorrhoea may be divided into two
groups:
1. Identification of a substance that can serve as a chemical marker of CSF.

2. Administration of agents that can document the presence of
communication between the intradural space and extradural space.
Chemical markers
Sensitive and specific marker of CSF. Colour change indicates presence

Glucose—Glucose of CSF mixed with nasal secretions
oxidase test strips
β2-transferrin Reliable marker of CSF
Beta-trace protein (β- Second most common protein found in CSF after albumin. Detection of
TP) (β-TP has 100% sensitivity and specificity
Imaging studies
A. CT scan
1. High-resolution CT is the best diagnostic imaging aid to identify a CSF

leak and confirm the site of abnormality.
2. CT scan helps to identify the causative skull base defect, the origin,
extent and degree of damage.
B. MRI
1. MRI is never the first line of imaging modality for CSF leak.
2. As it cannot delineate the hard tissue bony defect as efficient as CT, it is
indicated when a tumour or mass is suspected as the cause of CSF leak.
C. CT cisternography
CT cisternography is an imaging modality that includes the administration of
intrathecal administration of radiopaque contrast (metrizamide) followed by
CT scanning.
It aids in identifying the precise location of a CSF leak in patients with active
clear nasal drainage. The disadvantage of CT cisternography is that patients
with intermittent CSF leaks may show false negative studies.
D. Nuclear medicine studies
1. Radionucleotide tracers used for cerebrospinal fluid are

a. Intrathecal fluorescein
b. Radioactive iodine (I-131)-labelled serum albumin (RISA)
c. Technetium Tc 99m-labelled serum albumin
d. Diethylene triamine pentaacetic acid (DTPA)
e. Radioactive indium (In-111)-labelled DTPA
2. Nuclear isotopes are injected into the spinal canal. When these isotopes
circulate around the brain, they may leak into the nose or sinuses and
collect on cotton pads inserted into the nose. After a number of hours,
these pads are removed and analysed for the presence of these nuclear
isotopes.
3. This study is safe, but it cannot precisely identify the location of the leak.
The isotope is also absorbed into the circulatory system and can leak
into the nose and sinus via the normal blood stream, thus giving false
positive results.
Management
Conservative treatment
• Subarachnoid drainage through a lumbar catheter

• Strict bed rest—2 weeks
• Head elevation
• Advising patient to avoid coughing, sneezing, nose blowing and straining
• Stool softeners
• Prophylactic antibiotics (possible)
Surgical management
Transcranial techniques
Fascia lata grafts, muscle plugs and pedicled galeal flaps may be used. A
tissue sealant, such as fibrin glue, may be used to hold the grafts in position.
The well-recognised and potential morbidities of these techniques include
brain compression, haematoma, seizures and anosmia. Despite direct access to
the skull base defect, failure rates are quite high. For these reasons,
extracranial techniques are now preferred in most circumstances.
Extracranial techniques
Endoscopic management has emerged as the primary technique for the
surgical management of skull base defects causing CSF rhinorrhoea.
Palpation
• Bony step in the supraorbital ridge or glabella.

• Paraesthesia/anaesthesia in the supraorbital and supratrochlear nerve
dermatome.
• Crepitation from soft tissue emphysema or fracture segments.
Neurological and ophthalmic examination
• Test for any associated neurological deficit and visual acuity.

• A fundoscopic as well as ocular motility test must be done to rule out
injury to the optic nerve and other orbital contents.
Plain skull radiographs
The plain films are of limited use nowadays after the advent of CT and MRI.
True lateral view

Anterior and posterior walls.
Waters’ view
Periphery of frontal sinus (Fig. 48.21).
FIGURE 48.21 Waters’ view showing frontal bone fracture.
Submentovertex view
Posterior wall.
CT scan
In patients with evidence of brain injury with change in consciousness or
mental agility. A noncontrast CT of brain to evaluate intracranial bleed,
pneumocephalus and other brain injuries.
CT scan can be used to detect
• Frontal bone fractures

• Displacement of the fracture fragments
• Associated intracranial injuries
▪ Intracranial haemorrhage
▪ Haematoma—extradural haematoma, subdural haematoma,
intracerebral haematoma
▪ Pneumocephalus (Fig. 48.22)
▪ Foreign body
▪ Cerebral injury—contusion, laceration
• Fracture involving optic foramina, orbital apex and sella region (in
patients with evidence of decrease in visual acuity or loss of colour
vision)
• Involvement of the frontal sinus
▪ Anterior wall fracture
▪ Posterior wall fracture and displacement (which determines
the treatment plan)
▪ Haemosinus
▪ Mucocele
▪ Pyocoele
▪ Foreign body
▪ Sequestrum
▪ Brain herniation from dural tear
FIGURE 48.22 Pneumocephalus associated with type V frontal
bone fracture.
Radiological examinations specific for CSF rhinorrhoea

High-resolution CT cisternogram and/or nasal endoscopy after the
administration of intrathecal fluorescein.
CSF scintigraphy
Scintigraphy is done with radioactive tracers like 99m Tc—human serum
albumin, iodine 131 human serum albumin injected into the lumbar
subarachnoid space through lumbar puncture followed by a CT scan. CSF
leaks are evident as hotspots or areas of increased uptake.
CT cisternography
In case of persistent CSF leak from fistulae CT scanning in fine cuts (2 mm),
using agents like 99m Tc or metrizamide can be used to identify the position of
the fistula.
3D CT (Fig. 48.23A–D)
• To visualise the amount of deformity

• To plan reconstruction
• To fabricate stereolithography model.
FIGURE 48.23 (A) 3D CT showing displaced fracture involving
frontal bone. (B–D) Reconstructed 3D CT showing comminuted
fracture of the frontal bone associated with midface and
mandibular lingual Cortez fracture.
MRI
can be used to supplement CT scan, since mucocoele and brain are isodense in
CT.

Current surgical options in the management
• Exploration and fracture reduction without further intervention on the
sinus
• Frontal sinus obliteration
• Frontal sinus cranialisation
Surgical approaches
• Access through the preexisting laceration if feasible (Fig. 48.24).
• Intranasal endoscopic approach (Fig. 48.25).
• Bicoronal approach (Fig. 48.26A–B).
• Other approaches (Figs. 48.27 and 48.28)
▪ Lynch (Sewall) incision
▪ Butterfly or brow incision
▪ Open sky
▪ Gullwing (eyeglass or spectacle incision)
FIGURE 48.24 Approach through preexisting laceration in

forehead.
FIGURE 48.25 Intranasal endoscopic approach to the frontal sinus.
FIGURE 48.26 (A) Marking for bicoronal incision. (B) Bicoronal

incision and degloving exposing the fracture. A, Anterior; P,
Posterior.
FIGURE 48.27 Lynch (Sewall) incision.
FIGURE 48.28 Illustration of approaches to the frontal sinus.
Factors determining the treatment plan (Flowcharts

48.1 and 48.2)
1. Anterior wall fracture
a. Isolated or combined with posterior wall
b. Comminuted with or without displacement
c. Degree of cosmetic deformity
2. Posterior wall fracture
a. Amount of displacement
b. Dural tear
c. Pneumocoele
d. Associated intracranial injury
3. Frontonasal duct involvement
a. Partial or complete obstruction predisposing to mucocoele
formation
b. CSF rhinorrhoea
FLOWCHART 48.1 Management of nondisplaced frontal sinus

fracture.
FLOWCHART 48.2 Management of displaced frontal sinus fracture.

1. Surgical exploration and fracture reduction with
or without fixation
Indications
• Anterior (outer) table fracture with cosmetic deformity

• No evidence of frontonasal duct injury
• CSF rhinorrhoea
• Intact sinus lining
Technique
In patients with displaced anterior table fractures, without frontonasal duct
obstruction and minimal or no posterior table disruption, preservation of sinus
function is indicated. Sinus function is maintained by simply repairing the
anterior table by stabilising the bony fragments with low-profile titanium
plates and screws or biodegradable fixation. Biodegradable plates and screws
are ideally used in frontal sinus fractures and provide a safe alternative
(Fig. 48.29A–E).
FIGURE 48.29 (A) Preoperative view showing depressed forehead.
(B) Bicoronal incision and degloving of the skull to expose the
frontal bone area. (C) Elevation of the fractured anterior table
fragment. (D) Rigid fixation of the fragment using miniplate and
screws. (E) Wound closure using metal staples. Immediate
postoperative appearance showing forehead contour restoration.
2. Obliteration of sinus cavity

Indications
• Patients with displaced anterior tables—unstable after reduction

• Patients with frontonasal duct obstruction
• Persistent CSF rhinorrhoea and fistula
Materials used for obliteration of sinus cavity
Autogenous grafts
• Bone
• Muscle
• Fat
• Fascia
• Pericranial flap
• Adipose stem cells (ASC) with growth factors with or without β-
tricalcium phosphate (β-TCP)
Alloplastic alternatives
• Hydroxyapatite
• Methyl methacrylate
• Bioactive glass
Technique (Fig. 48.30A–G)

Obliteration of the sinus cavity is a procedure wherein the sinus lining is
carefully removed, followed by filling up of the cavity with the appropriate
chosen material.
• Through a bicoronal approach, fracture site is approached.

• The fractured anterior wall is removed exposing the sinus cavity.
• The sinus lining is removed from all walls taking care to remove the
lateral, posterior, inferior, orbital and ethmoid aspects.
• Frontonasal canal is totally blocked by forcibly impacting a wedge or
plug of cancellous bone or the chosen material above the invaginated
nasal mucosa.
• The entire sinus cavity is filled, followed by fixation of the anterior
wall fragments.
• In case of comminuted fractures, reconstruction is performed with
bone grafts.
FIGURE 48.30 (A) Preoperative view of the patient with draining
pyocele in left frontal sinus region. Coronal CT section showing
mucopyocele occupying the frontal sinus. (B) Obliteration of the
frontal sinus using fat and fixation of the anterior table with
miniplate. (C) Postoperative view of the patient after 3 months. (D)
CT coronal section showing right frontal sinus fracture. (E)
Illustration showing obliteration of the right frontal sinus using fat
graft. (F) CT sagittal section showing frontal sinus fracture. (G)
Illustration showing obliteration of the frontal sinus with fat graft.
Cranialisation
In most frontal sinus fractures there exists a communication between the
frontal air sinus and intracranial spaces. Integration of the intracranial space
with the fractured frontal sinus by removing the sinus lining, posterior sinus
wall and obliteration of the sinus cavity using the cranial contents is called
cranialisation (Fig. 48.31).
FIGURE 48.31 Cranialisation procedure. (A) Image showing
fracture of inner and outer table of frontal sinus. (B) Cranialisation
procedure where the frontal sinus has been obliterated completely.
Indications
• Severely displaced and comminuted frontal sinus fractures with

significant posterior table involvement and dural lacerations.
• Persistent CSF leak and/or brain injury.
• Pyocoele of the frontal sinus with extensive destruction of the posterior
wall.
• A large osteoma of the posterior frontal sinus wall.
• By transfrontal approach, an osteoplastic flap is raised following which

the entire posterior wall is removed or resected (secondary), thus
allowing the cranial contents to herniate anteriorly into the frontal
sinus region.
• The frontal sinus mucosa is completely removed from all walls and
recesses.
• Careful invagination of the nasal mucosa into the frontonasal canal is
done following which the canal is wedged with plugs of cancellous
bone or other material to achieve a hermetic seal. The floor is
reinforced using vascularised galeal frontalis or pericranial flap. This
isolates cranium from the nasal cavity.
FIGURE 48.32 (A) Preoperative view: frontal depression and
preexisting sutured laceration. (B) Frontal bone fracture with
communition of inner table and associated pneumocephalus. (C)
Frontal sinus exposed through an osteoplastic (outer table) flap.
(D) Harvested tensor fascia lata for plugging the frontonasal duct
creating hermetic seal. (E) Osteoplastic flap with anterior table
repositioned and fixed with miniplate, frontalis muscle used for
wound closure. (F) Wound closed in layers.

Frontal bone fractures involving the anterior and posterior tables and frontal
sinus may cause complications related to the sinus, intracranial, orbital or
nasal structures.
Early complications Late complications

1. Major early complications 1. Mucocoele or a mucopycoele
a. CSF leak 2. Brain abscess
b. Meningitis 3. Osteomyelitis
c. Pneumocephalus 4. Contour defect
2. Minor early complications
a. Forehead pain
b. Transient anaesthesia of the forehead
c. Transient diplopia
d. Wound infections
Early complications
The following complications may occur within the first few weeks of surgical
intervention:
1. Early major complications
a. CSF leak
CSF leak is the most frequent and significant major complication.
Signs and symptoms of CSF leak

Rhinorrhoea—Clear translucent fluid leaking through the nose usually with
salty taste.
• It does not mix with blood

▪ Tramline sign
▪ Halo test
▪ Starch test
• Headache
• Change in mental state
• Pseudoepiphora
• Delayed leaks may present in a variety of other unusual ways
Examination of a CSF leak
• Presence of glucose
• Absence of eosinophil
• β2-transferrin analysis is performed for definite confirmation
Treatment
• Most leaks are obviously seen after injury and cease shortly after
definitive treatment of the craniofacial injury which comprises fixation
of the fractures or formal dural repair.
• Persistent CSF leaks beyond 3 weeks should be repaired by adequate
stabilisation of associated fractures.
• Occasionally, however, CSF leaks are delayed in onset, sometimes by
many months or even years should be treated surgically.
Management of CSF leak in the postoperative period
• Bed rest
• Prophylactic antibiotic
• Lumbar drainage
b. Meningitis
The most feared early complication is meningitis. Meningitis may or may not
be associated with a CSF leak. Early diagnosis is necessary to reduce the
morbidity and potential mortality from meningitis.
Signs of meningism (meningeal irritation)
• Photophobia
• Headache
• Neck stiffness or rigidity
• Positive Kernig’s sign
Management
Any signs of fever, nuchal rigidity or altered sensorium indicates meningitis.
The immediate management includes a lumbar puncture and medical
management with empirical antibiotics with good CSF penetrance. Further the
draining CSF may be cultured for the microbial colonies and the sensitive drug
identified.
Lumbar puncture
Indications
• Diagnosis of bacterial meningitis requiring intrathecal antibiotics is the

only indication for lumbar puncture following acute head injury.
• Chronic CSF leak leading to increased production of CSF should be
drained following closure of the fistula or defect.
Contraindications
Signs of meningeal irritation may be present after injury, usually due to
subarachnoid haemorrhage.
These findings alone are not an indication for lumbar puncture.
Complication
Transtentorial herniation, uncal herniation, or the development of a mid-brain
pressure coning with consequence of brainstem compression.
Lumbar puncture may be performed only if absolutely necessary and even
then only when the possibility of raised ICP (intracranial pressure) has been
excluded by clinical and CT examination.
c. Pneumocephalus
Pneumocephalus refers to gas within the cranial cavity, which may be present
in any of the intracranial compartments though frontal, subdural or
intracerebral locations are most common.
Mechanisms
There are two mechanisms of posttraumatic pneumocephalus:
Inverted bottle mechanism

As CSF escapes from the cranium, air enters into the negative pressure area
created by the CSF exit. This is similar to air replacing fluid when it is poured
from an inverted bottle.
Ball-valve mechanism
Post trauma, a cough or a sneeze may force air into the cranial cavity by
pressure through the traumatic opening. This air then cannot exit because the
meninges or brain tamponades the leak (Fig. 48.33).
FIGURE 48.33 Pneumocephalus.
Clinical findings
Pathognomonic finding
‘Bruit-hydroaerique’ or ‘cranial succession splash’. This is a splashing sound heard
by patient on postural change which may also be heard on auscultation of the
head.
Nonspecific symptoms
• Headache
• Nausea
• Vomiting
• Vertigo
Tension pneumocephalus
Pneumocephalus acting as a mass lesion compressing the brain producing
headache, psychosis and meningeal signs.
Radiological findings
Pneumocephalus is evident in CT as hypodense region (density of air)
occupying cerebral space.
Treatment
Definitive treatment includes repair of the underlying dural tear and fistula.
In tension pneumocephalus, decompression can be done as an emergency
procedure using burr holes before definitive treatment.
2. Early minor complications
a. Forehead pain
b. Transient anaesthesia of the forehead
c. Transient diplopia
d. Wound infections (self-limited) resolves within 2–3 weeks
Late complications
Late complications are uncommon but with significant consequences.
• Mucocele
• Brain abscess
• Frontal bone osteomyelitis
• Frontal contour defect
• CSF fistula
1. Mucocele
Obstruction of the frontonasal duct is a significant predisposing factor in the
development of complications such as mucocele. Mucocele cause bone erosion
and are capable of involving the sinuses, orbit and cranium. They develop as
early as a few months or as late as several years after the initial operation.
Complete removal of the mucocele is the goal of management. Endoscopic
marsupialisation of mucocele (limited success rates) may also be done.
2. Brain abscess
Spread of infection along the periarteriolar spaces of Virchow, the arterial
supply of the brain parenchyma results in brain abscess, which is rare and
potentially fatal.
Symptoms
• Loss of appetite
• Fatigue
• Lethargy
• Subtle changes in personality
Treatment includes intravenous antibiotics, which can cross the blood brain
barrier and has high CSF penetrance.
3. Osteomyelitis
It is a rare complication. Frontal bone osteomyelitis was called Pott’s puffy
tumour in the preantibiotic era. Management is done by complete removal of
the frontal bone, treatment with antibiotics and subsequent reconstruction at a
later stage.
4. Contour defect
Lack of rigid fixation and subsequent frontal bone loss results in frontal
contour defect. Introduction of miniplate and microplate fixation and the use
of primary bone grafts have resulted in the eradication of frontal contour
defect.
5. CSF fistula
CSF fistula may form as a part of skull base injury and persist with no clinical
signs. Any transient increase in intracranial pressure can result in CSF
rhinorrhoea as a late complication. CSF fistula requires diagnosis through CT
cisternography followed by surgical closure.
SECTION XII
Miscellaneous
Chapter 49: Medicolegal Considerations in Dentistry

Chapter 50: Recent Advances
CHAPTER 49
Medicolegal
Considerations in
Dentistry
Law
Crime and penal code
Malpractice
Rashness and negligence
• Elements of a negligence claim
Consent–contract between doctor and patient
• Informed consent
• When a patient threatens to sue
• Patient abandonment
Criminal liability of doctors in death during medical procedures
Law
The function of law is primarily to maintain order in social relationship and
protect the legitimate interest of members of a given society. This is achieved
by laying down a variety of norms for social behaviour through the legislative
process, ensuring its observance in social harmony through the administrative
process and adjudicating disputes in enforcement through the judicial process.
The law and its enforcement system have become complicated and diversified
with the advancement of civilization, consistent with the felt needs of the
society, thus have emerged major branches of the legal system such as criminal
law, commercial law, labour law, administrative law, consumer protection, etc.
Tooth injury is considered as a grievous injury and is punishable under law
according to the Indian Penal Code (IPC).
Crime and penal code

The word crime in its broad sense may be explained as an act of commission or
omission that is baneful to the society in general.
Human beings are morally autonomous, with the basic faculty to
understand reality and distinguish right from wrong, able to contribute to the
developing social norms, to understand and internalise them, competent to
decide how to act and capable of realising that decision. This concept dictates
the boundaries of penal law and influences the principles of criminal
responsibility.
The substantive criminal law of our country is found in the Indian Penal
Code, as well as in other local and special laws. With regard to the condition of
criminal responsibility, the Indian Penal Code is the sole authority. Medical
negligence is predominantly a civil matter.
The moral and ethical responsibilities associated with the practice of
dentistry are well recognised, but the legal obligations between the dentist and
the patient are often less well understood. In recent years, the number of
malpractice claims against dentists has been increasing swiftly.
Malpractice
Malpractice is defined as negligent actions of professionals while performing their
professional duties.
Although medical treatment is generally perceived as being beneficial, in
some circumstances the administration of treatment can make a health care
practitioner liable to criminal action. Medical malpractice may give rise to two
common law actions in tort. The first, that of trespass to the person or battery,
is of limited significance. The second, that of negligence, forms the basis of
most malpractice claims. Battery is the unlawful application of force to another
person without his consent and if done intentionally or recklessly, as opposed
to negligently is a crime as well as tort at common law.
Rashness and negligence

Criminal rashness is undertaking a dangerous or risky act with the knowledge
that it is risky and that it may cause injury, but without the intention of
causing injury. The criminality lies in running the risk of doing such an act
with recklessness or indifference to the consequences. There is a distinction
between a negligent act and a rash act.
A negligent act is not doing something that a reasonable man would have
done or doing something that a prudent man would not do in the given
circumstances. Rashness is a positive act committed by the accused and
negligence is the wilful inaction on the part of the accused so as to drive him
within the mischief of negligence. It is the criminal rashness and negligence,
which endangers human life or the personal safety of others that renders an
act of offence under the penal code.
Such an act is considered as an offence if:
i. The act is the cause of the hurt.

ii. The act is done with criminal rashness or negligence and is of such a
degree as to endanger human life or personal safety of others.
This applies only if the grievous hurt caused is the direct result of the rash
or negligent act, not a remote result of the act.
Elements of a negligence claim

Negligence is defined as a conduct that falls below the standard established by law for
the protection of others against unreasonable risk of harm.
In order to establish a valid negligence claim, following elements must exist:
• A duty of care was owed by the dentist to the patient.

• Dentist violated the applicable standard of care.
• Patient suffered a compensable loss or injury.
• Such an injury was caused in fact and proximately by the substandard
care.
Duty of care means that the patient had accepted for treatment and therefore
the dentist is obliged to provide a certain standard of accepted care to the
patient. Duty does not prevent the dentist from refusing to prescribe treatment
or to perform a procedure which the dentist does not believe is indicated, but
the physician cannot refuse to provide care once the relationship is
established.
A violation to provide an applicable standard of care must be demonstrated.
Standard of care generally means that degree of care and skill, which is
expected of a reasonably competent practitioner in the same class to which he
belongs, acting in the same or similar circumstances.
It has to be proven that the patient had suffered loss or injury due to failure
of the dentist to provide the applicable standard of care.
Consent–contract between doctor and patient
The object of consent in a medical treatment or a surgical procedure involving
interference of human body is that every human being has a right vested with
him to determine what should be and should not be done with his body. Any
encroachment upon this right invites liability on the invader.
Responsibility of a doctor towards his patients begins the moment he agrees
to examine the case. A doctor–patient relationship pertains to a legally binding
contract wherein nowadays it has become obligatory as well as mandatory, to
obtain a specific consent before the commencement of a treatment.
The Indian Contract Act defines consent: ‘Two or more persons are said to
consent when they agree upon the same thing in the same sense’.
Informed consent
Consent may be written or implied. A patient approaching a medical
practitioner for treatment impliedly gives his consent for medical procedures
undertaken by the said doctor. Such a hypothetical consent when judged
subjectively may expose the doctor to the danger of being accused by the
patient, who by using the benefit of hindsight, would deny the fact of giving
consent, even when full disclosure of methodology of treatment, risk involved
in it and even side effects if any, had been clearly made aware before hand.
Therefore, to avoid accusations of this sort, it is always advisable to obtain a
specifically written consent (i.e. an express consent) from the patient, which
thereafter makes the contract unchallengeable on the grounds of ‘lack of
consent’. Express consent may compulsorily be obtained even in diagnostic
procedures such as radiology, CT scan, etc. A legally valid consent is that
obtained from the patient/his parent/guardian/attendant, as the situation
warrants and not from a stranger to the scenario.
The goal of the informed consent is to provide patients with as much
information as possible on any specific problems that the patient may have
their relationship to overall health and methods of managing them.
Informed consent actually consists of three phases:
• Discussion
• Written consent
• Documentation in the patient’s chart
1. Discussion
• Nature of the disease, injury or deformity

• Purpose, goals of treatment and consequences of not treating
• The proposed treatment
• Limitation of the treatment
• Anticipated or common side effects
• Possible complications of treatment and its frequency
• Type of anaesthesia to be used
• Treatment alternatives
• Uncertainties about final outcome, including a statement that the
treatment has no absolute guarantees or warranties
2. Written consent
Once the discussion regarding the treatment is over, the dentist should get a
written informed consent signed by the patient or the parent or legal guardian
in case of children. This written consent includes all the discussions carried out
between the doctor and the patient, described in easily understandable terms.
Consents should be written in a language well understood by the patient. The
consent form should not contain technical or medical terminologies. Consent
must be obtained at a time when the patient is mentally capable of giving it.
Medical liability theory involves the concept of lack of consent to a
procedure enabling a patient to recover damages, even if the medical
procedure was successful. In a lawsuit for negligence, the patient needs only to
prove that the treatment was in some way harmful and that was not disclosed
by the doctor.
The written consent
1. Should be legible
2. Contains only those terms and abbreviations, which are
comprehensible to similar licensees
3. Contains adequate identification of the patient
4. Indicates the date of all provided professional services
5. Contains pertinent and significant information concerning the patient’s
condition
6. Reflects what examinations, vital signs and tests were obtained,
performed or ordered, findings and results of each
7. Indicates the initial diagnosis and the patient’s initial reason for seeking
the licensee’s service
8. Indicates the medications prescribed, dispensed or administered and
strength of each
9. Reflects the treatment performed or recommended
10. Documents the patient’s progress during the course of treatment
provided by the licensee
3. Documentation in the patient’s chart

The final phase of the informed consent procedure is to document in the
patient’s chart that an informed consent was obtained. The first documented
information that is reviewed by the patient’s attorney (in case if the patient
sues the doctor) is this documented record. The document should include a
note stating that the discussion took place. The written consent form should be
included in the chart.
The following is the information that should be included in the chart:
1. Chief complaint
2. Clinical findings
3. Dental history
4. Medical history
5. Current medication
6. Drug allergies
7. Radiographic findings and interpretations
8. Recommended treatment
9. Informed consent
10. Therapy actually instituted
11. Suggested follow up
Other information often overlooked that should also be included in every

chart are as follows:
1. Any medical prescriptions given to the patient

2. Date and time of appointments
3. Missed appointments
4. Any laboratory tests done and the results obtained
5. Postoperative instructions and care given
6. Discharge of the patient (with or without consent of the doctor)
Advantages of the informed consent

Apart from fulfilling the legal obligations, the informed consent has the
following advantages:
• A patient who understands the nature of the problem well and has
practical and sensible expectations is less likely to sue.
• A documented informed consent prevents any claim based on
misunderstanding or unrealistic expectations of the treatment by the
patient.
Situations where informed consent is not taken

There are three special situations in which an informed consent may deviate
from these guidelines:
• On the specific request of the patient, all the aspects of treatment and
complications are not informed but this must be documented in the
chart.
• Sometimes it is not appropriate to provide all the information to the
patient.
• In case of an emergency or if the patient is unconscious, a doctor can
lawfully operate on or give other treatment to the patient who is
incapable of consenting to his doing so, provided that the operation or
treatment is necessary to save life of the person or to save him from
permanent disability or from unnecessary pain and sufferings.
Complications
Although the dentist takes extreme care and precision regarding the diagnosis,
treatment planning and surgical technique, sometimes the final result is not
satisfactory and desirable. In such cases, the dentist should make it a point to
discuss the case frankly.
When a patient threatens to sue

Certain precautions have to be considered whenever a patient or his attorney
threatens to sue the dentist against any malpractice.
• All such threats should be reported at once to the malpractice

insurance carrier.
• As far as possible, the dentist must not admit accountability or error.
This is because admission or other information disclosed during
discussions may ultimately be used against the dentist during lawsuit.
• As a final point, it is very important that no alterations are made in the
patient’s dental record. Records must be handled carefully and should
not be misplaced or destroyed.
Patient abandonment
Certain situation might arise wherein the dentist may be unable to complete a
treatment plan scheduled for the patient.
Such problems include:
• Failure of the patient to return for the necessary appointments

• Failure of the patient to follow explicit instructions
• A total breakdown of communication and loss of rapport between the
dentist and the patient
To avoid being accused of patient abandonment, the dentist should follow

certain steps before discontinuing.
1. A letter is sent to the patient, indicating the intention of the dentist to

withdraw from the case and the unwillingness to provide further
treatment.
a. The letter should be sent by certified mail and it should be
made sure that it has been received by the patient
b. The letter should be followed with a copy by regular mail
c. Unless it is required by the state law, the dentist need not
state a reason. Never offer incompatibility as justification
2. The patient’s condition must be stable and not emergent. Care must be
provided during the time frame (15–30 days) given to the patient to
find a new provider.
Criminal liability of doctors in death during medical

procedures
A doctor is not criminally liable for his patient’s death, unless his negligence or
incompetence passes beyond a mere matter of compensation and shows such a
disregard for the life and safety as to amount to an offence against the state.
Section 304-A deals with cases where a rash and negligent act results in the
death of a person. Section 304-A reads ‘Whoever causes death of a person by
doing any rash or negligent act not amounting to culpable homicide shall be
punished with imprisonment of either description for a term which may
extend to 2 years or with fine or with both’. This section was added by an
amendment of the Indian Penal Code in 1870. Mere carelessness is not
sufficient, but the act should result in the death of a person.
In order to impose a criminal liability on a doctor, it is necessary that the
death should have been the direct result of a rash or negligent act of the
accused and that act should be the proximate cause of the death.
An employer cannot be held guilty under the criminal law, where death or
hurt, (simple or grievous) has been caused by the rashness and negligence of
his servant or employee. Hence, a doctor cannot be held liable under criminal
law for any rash or negligent act done by his employee.
CHAPTER 50
Recent Advances
Bone substitutes
Healing of bone graft
Alloplastic implants
Ideal properties of an alloplastic material
Advantages
Types of alloplastic materials
• Dimethylsiloxane (silicone)
• Polytetrafluoroethylene
• Polyethylene (Medpor)
• Polyester
• Acrylics
• Calcium phosphate ceramics
Osteoactive agents
Transforming growth factor-β
Platelet-derived growth factor
Platelet-rich plasma
Bioactive polypeptides
Recombinant bone morphogenetic proteins
Stem cells
TMJ Arthrocentesis
TMJ Prosthesis
Properties of laser
Laser production
Laser physics
Classification of lasers
Laser tissue interaction
Indications in oral surgery
Application of laser in oral surgery
Physics forceps
Zygomaticus Implants
Principle
Technique
Precautions
Stereolithography
Endoscopy
Robotic surgery
Advantages
Disadvantages
Bone substitutes
The bone healing is a complex and multifactorial process and takes longer
time compared with soft-tissue healing. There are numerous steps involved in
this healing process which can be influenced to redirect the growth according
to the necessity. This allows many bone grafting technologies that have been
used to regenerate bone, creating, perhaps, an array of options. Bone
substitute materials can be classified based on the combination of their source
of origin and mineral content. The source can be subclassified further by
species and by where the bone graft is taken (Table 50.1).
Table 50.1
Types of bone substitutes

Types of bone substitutes
Autograft • Taken from host
• Gold standard in bone grafting
• Only graft source with osteogenic potential
Allograft • Graft taken from a genetically similar donor
• Cadaveric graft
Xenograft • Graft taken from a genetically dissimilar donor
• Most commonly bovine or porcine source
Alloplasts or synthetic grafts • Graft not taken from a living donor
• There is no cellular or protein products in this graft
Autogenous bone grafts from local or distant site of the same individual or
allogenic bone graft from another individual are the most famous and reliable
grafts. The use of allogenic grafts was associated with immunogenic problems.
They were initially treated by freezing technique, followed by other methods
such as freeze drying, deproteinating and demineralising techniques were
developed to deal with immunogenicity. Although widely used in various
clinical situations, the limitations of the grafts like harvest-site morbidity and
limited availability have encouraged the development of new materials
(alloplast). Alloplasts have been developed to replace bone and to overcome
the disadvantages of other types of bone replacement. These are demineralised
bone matrix formulations and synthetic ceramic materials. The device of these
materials has laid open the door to fascinating possibilities. Their ability to
augment and replace the craniofacial skeleton is used in the facial and plastic
reconstructive surgery. The process of bone healing must be considered for the
better understanding of the bone regeneration.
Healing of bone graft

Bone healing is a unique process similar to that of the embryonic bone
formation. The healing of the bone graft depends upon the recipient site blood
supply, oxygen tension and stability of bone segments. Healing of the bone
graft may be by primary bone healing or by secondary bone healing
(intermediate cartilaginous phase).
Primary bone healing of bone implies direct contact or a gap of less than
1 mm between bone fragments. This healing process occurs by osteoclasts
working in groups to create a cutting cone. Following this cutting cone of
osteoclasts are osteoblasts secreting osteoid for future mineralisation
(Fig. 50.1).
FIGURE 50.1 Primary bone healing. (I) Osteoclastic cutting cone
crossing the fracture gap. (II and III) Bone reconstitution by the
trailing osteoblasts.
Secondary bone healing occurs through the formation of a callus within

which osteoid is produced and mineralisation occurs. This type of bone
healing can be divided into the following three major phases (Fig. 50.2).
1. Inflammatory phase (haematoma formation)

2. Reparative phase (soft and hard callus formation)
3. Remodelling phase
FIGURE 50.2 Secondary bone healing.
These principles of primary and secondary bone healing can be applied to

bone graft healing. The type of graft material used, block versus particulate,
dictates which healing process occurs.
Creeping substitution: It is a process by which the cortical bone graft healing
occurs, and it is similar to that of primary bone healing. Once the
nonvascularised graft material is transferred to the defect, osteoclasts create
voids in the graft material that are filled with osteoid from osteoblasts. This
osteoid then becomes mineralised, undergoes remodelling and maturation.
Ideally, the grafted bone would be completely resorbed, and new bone would
be formed. The grafted bone remains as necrotic centres mixed with the newly
formed bone.
Bone apposition: It is a process of bone healing that occurs in particulated
cortical or cancellous bone grafts. This apposition of bone is followed by
resorption of the graft material. Ideally, there is complete resorption of the
graft material, which is replaced by mature bone. Because cancellous grafts do
not have to first undergo resorption before apposition, they revascularise
faster than cortical block grafts. There is a much higher percentage of newly
formed bone and greater resorption of the graft material when particulate
grafts are used.
Reconstruction of craniomaxillofacial region may be achieved with bone
grafting or endosseous implant. The basic difference among the bone grafts
and the implants must be appreciated to understand the complex healing
process of both. By definition, the bone grafting procedure refers to as the
surgical removal of the living tissue, along with or without its blood supply,
from the harvested donor site to the host bed. The implant refers to the
surgical placement of the nonviable biocompatible material. Autogenous bone
grafts have cells with bone forming ability, platelets and fibrin. The survival of
osteoblasts in the endosteum and haematopoietic cells may be around 5 days
after transplantation, owing to their capability to absorb nutrients from the
adjacent tissues (Flowchart 50.1). Initial regeneration begins within hours of
placement of grafts. After revascularisation of the graft, the bone forming units
are formed from the circulating stem cells which are attracted to the wound
followed by remodelling process which is the end phase of bone healing.
FLOWCHART 50.1 Healing of the bone graft.
Alloplastic implants
The advent of the alloplastic implant has reduced many complications which
arise as a result of autograft and allografts. The alloplastic materials offer
many advantages like no risk of immunologic reactions and graft rejection,
reduced disease threat, simplification of operative procedure and an
unrestricted supply of implant material. The selection of proper alloplastic
implant material must be done with utmost care because each implant type
and material has unique properties. Cautious surgical techniques are essential
in reducing the risk of infection and extrusion.
The major aesthetic areas of the facial skeleton like malar, midface area, nose
and chin offer the structural configuration to the face. Based on the aesthetic
necessity of the individual, the implantation procedures are carried out to
achieve symmetry and balance.
Various alloplastic materials have been used in the earlier days for soft and
bony augmentation which includes ivory, acrylics and precious metal remains
(gold cleft palate implants and ivory nasal inlays, etc.).
Better knowledge about the host tissue and implant interface response has
led to the improvement of bioactive implants. Proper surgical procedure
influences both the short- and long-term outcome in the facial skeletal
augmentation.
The success of an alloplastic implant material depends upon the following:
• Relation between the implant and the host.

• The host reaction.
• Location of the implant.
• Technique used by the operator.
• Function of the implant.
• The implant material.
Ideal properties of an alloplastic material

Before the selection of the implant for the skeletal or soft-tissue augmentation,
the surgeon should consider the qualities of the selected implant for the safety
and durability of the placed implant.
• The material should be biocompatible with any type of tissues in the

human body.
• The material should be readily available either in blocks or precarved
forms.
• Sterilisation should be possible when necessary.
• It should have better adaptability and flexibility to allow better
adaptation between the host tissue–implant interface.
• The material should have the natural feel when placed in the tissue.
• It should have stability when placed and resistant to migration from its
position.
• It should be porous enough to allow the tissue ingrowths.
• It should not have shape memory which may cause implant mobility,
extrusion from its site or resorption.
• It should be readily retrievable if necessary.
• It should be easy to shape and secure.
• It should be reliable and safe.
• It should be osteoconductive and allow ingrowth of calcified tissue.
• It should have appreciable colour match to the skin tissue when used
in scanty tissue areas.
• It should allow additional augmentation if necessary.
Advantages
• Availability of material and simplification of operative procedure.

• No need for tissue harvest.
• Decreased duration of an anaesthesia required.
• Extensive range of compositions of synthetic material provides various
combinations of strength, elasticity and durability to choose.
Types of alloplastic materials

The following are the different types of alloplastic materials used in the field of
oral surgery.
Dimethylsiloxane (silicone)
Dimethylsiloxane (silicone) is a rubber implant material with or without
polymer fabric. It has been used for various surgical applications. It is
available both as a preformed template and can be customised using room
temperature vulcanising silicone. This implant material has ‘memory’
characteristics and requires adaptation in the ‘relaxed’ state according to the
bone contour.
Advantages
• It can be easily modified intraoperatively using scalpel or scissors.

• Easy fixation to the underlying tissues using a screw or suture.
• Sterilisation is possible either by autoclave or by radiation with no
damage to the material.
• Inert and does not cause surrounding tissue reaction.
Disadvantages
• Active bending of the material may cause extrusion or resorption of the

bone.
• Formation of a thin fibrous capsule only and there will be no ingrowth
of the tissue.
Uses
Frontal, orbital, zygomatic, nasal, paranasal, nasal dorsum, chin, maxillary,
malar, ear, parasymphyseal and mandibular deficiencies augmentation.
Polytetrafluoroethylene
• Polytetrafluoroethylene (PTFE) was initially promoted as Proplast. The

material was banned due to its disintegration and foreign body
response in temporomandibular joint (TMJ) reconstruction for
replacement of glenoid fossa.
• Gore and associates marketed the material as Gore-Tex which is
considered as a polymer (microporous) of PTFE. It is then used for the
augmentation of various soft-tissue and skeletal defects.
• It can be obtained in the range of 1-, 2- and 4-mm sheets permitting
modifications in shape and positioned beneath the soft tissues.
• It has noninterconnected surface holes with 10–30 mm pore sizes
which is favourable for tissue ingrowth, allowing fibrous tissue
capsulation in a minimal level.
Advantages
• Gore-Tex causes very less foreign body response, forming a fibrous

encapsulation.
• Micropores allow some soft-tissue ingrowths which offer some
stability.
• It should be removed easily if necessary.
Uses
Augmentation in areas of the face like lips and nasolabial folds as a subdermal
implantation.
Polyethylene (Medpor)
Polyethylene is a porous substance with increased tensile strength and sizes of
the pores are in the range of 125–250 mm. This material can be shaped or
customised to adapt in a required tissue space. The foreign body reaction is
minimal and it results in the formation of thin fibrous encapsulation. This
fibrous capsule helps in the reduction of contraction. Carving and shaping is
difficult and it is not actually osteoconductive, despite it permits ingrowth of
soft tissue and vascular supply through its porosity.
Uses
It has various uses and is being used in the augmentation of midface, chin and
mandibular region.
Polyester
Biodegradable polyesters are polymers that are degraded in the body at
physiologic pH from weeks to months. They are used for chin and nasal
augmentation.
Acrylics
• Polymethyl methacrylate (PMMA)

• Hard-tissue replacement (HTR)
• Bioplant HTR
PMMA resin is the material used as bone cement for joint prosthesis in
orthopaedic surgery. The mixture of a monomer liquid and a polymer powder
results in the formation of a rigid, almost translucent plastic by exothermic
reaction. Preoperatively models are prepared and implants are fabricated
using this model, for using in operating theatre after sterilisation, thus
avoiding the surrounding tissues damage due to exothermic reaction during
mixing. Impregnation of antibiotics to the mixture aids to avoid bacterial
inoculation and related complications. Incorporation of the metal mesh
provides additional strength and helps in reducing the risk of fracture.
Uses
Predominantly used in oral and cranial reconstruction procedures for full-
thickness skull defects.
Disadvantages
• Unbearable odour and it releases teratogenic fumes. Cool irrigation

must be applied to compensate the high temperature during reaction.
• Cannot be placed in opportunistic microorganisms residing areas
because they have a higher affinity for this surface (e.g. oral cavity,
paranasal sinuses, etc.).
HTR is obtained by the combination of polyhydroxyethylmethacrylate and

PMMA.
HTR contains interconnecting pores and a coating of calcium hydroxide,
thus giving negative charge for the material. It is hydrophilic and a very
strong material. It was initially used for dental work in the earlier days, and is
currently available as a preformed implant material which can be customised
using CT scan illustrating patient’s defect.
Uses
• Augmentation and filling of very large defects in the cranium and
other regions.
• Effective in preserving ridge height and width after tooth extraction,
hence extensively used for ridge augmentation.
Bioplant HTR is a synthetic bone alloplast of a calcified copolymer

(polyhydroxyethylmethacrylate and PMMA) and calcium hydroxide.
Calcium phosphate ceramics
• Hydroxyapatite and other calcium materials are well known for their
interaction with each other and their ability to incorporate into living
bone tissue (Figs. 50.3–50.8). Both porous and dense ceramic forms are
used as implants.
• They are fragile and easily breakable, although they are nonresorbable.
They have excellent biocompatibility as well as they can bond to bone
by natural cementing process.
• They are osteoconductive and permit for tissue infiltration with lack of
a fibrous encapsulation. However, it does not have the osteoinductive
property.
• Nonceramic forms are also available in the powder form that can be
mixed during operation to fill any defects in the bone.
FIGURE 50.3 (A) Preoperative image showing bone deficiency in

relation to 11 (B) Extraction of 11.
FIGURE 50.4 Filling the extracted socket with Bio-Oss.
FIGURE 50.5 Note the complete filling of the extracted socket with
Bio-Oss .
FIGURE 50.6 Approximation of flap before closure.
FIGURE 50.7 Wound closed.

FIGURE 50.8 Schematic overview of BMP expression during
different stages of fracture healing. The indicated days are
dependent on the bone and fracture type.
Uses
Limited to mandibular ridge augmentation and as interposition grafts in facial
osteotomies.
Disadvantage
Due to the lack of strength and likely to fracture, it cannot be used in stress-
bearing areas.
Osteoactive agents
An osteoactive agent is defined as the material with potential to stimulate
bone deposition. The osteoinduction phenomenon was first described by Urist
and his coworkers. The bone matrix has found to stimulate the bone formation
when implanted within the muscle of many animal species. The specific
extract from the bone was identified as the protein was named as bone
morphogenetic protein (BMP). They are differentiated as osteoinducers,
osteopromotors or bioactive peptides.
Transforming growth factor-β

Transforming growth factor beta (TGF-β) group proteins are grouped under
osteopromotors, which have the ability for bone healing. The BMP family is
found to include TGF-β. All stages of bone healing are found to involve TGF-
β.
• In the primary inflammatory phase, platelets release TGF-β resulting in

the proliferation of mesenchymal cell.
• It acts as a chemotactic factor for cells causing bone formation,
stimulates angiogenesis and limits the activity of the osteoclast cells in
the revascularisation phase.
• At the commencement of osteogenesis phase, the TGF-β increases
osteoblast mitoses. The regulation of osteoblast function results in the
increase of bone matrix synthesis. TGF-β inhibits type II collagen;
however, it promotes the type I collagen.
• During the process of remodelling, they help in bone cell turnover.
• At high concentrations, TGF-β suppresses osteoblastic proliferation
and differentiation (biphasic effect).
TGF-β is considered to be more efficient when compared with BMP in those

conditions where there is a necessity for bone healing instead of bone
induction. The combination of BMP and TGF-β is found to improve the
osteoinduction property to an alloplastic implant and also makes it
osteopromotive too. The carrier media for TGF-β is still under progress unlike
BMP.
Platelet-derived growth factor

Platelet-derived growth factors (PDGFs) are angiogenic in nature, help in the
proliferation as well as chemotaxis for connective tissue cells including
deposition of matrix which is essential for healing of bone.
Insulin-like growth factors (IGFs) have the ability to amplify bone cell
mitosis and bone matrix deposition. Both PDGF and IGF have the ability to
work together and produce the synergistic effect during the repair phases of
bone healing. PGDF–IGF-saturated devices are used in cases of defects
associated with dental implants for increased bone healing.
TGF-β and PDGF are the important growth factors of the platelets.
Degranulation of the platelets results in the release of those factors which are
essential for the initiation of healing of graft.
Platelet-rich plasma
Platelet-rich plasma (PRP) is coagulated platelet prepared from the person’s
own blood by centrifugation process, followed by sequestering and
concentrating the platelets, the PGDF and TGF-β for clinical use.
Principle
Thrombin generation and fibrin formation are promoted by the adherence and
aggregation of platelet at the site of vascular injury.
• Platelets release growth factors (PDGF, TGF-β), cytokines (PF4,

CD40L), chemokines and active metabolites responsible for neo-
angiogenesis, tissue repair and regeneration.
• Concentrating platelets in a fibrin clot or glue generates a higher dose
of these healing proteins where it is applied.
• Cell membrane receptors of cancellous bone grafts have the ability to
respond to those growth factors as evidenced by monoclonal antibody
assessment.
Mechanism of action
• Platelets release various growth factors like PDGF, vascular endothelial

growth factor, transforming growth factors β1 and β2 (TGF-β1 and
β2), basic fibroblast growth factor and platelet-activating factor-4
which play a major role in wound healing.
• These growth factors are responsible for the following early wound
healing process.
▪ Increase in cell mitosis.
▪ Increase in production of collagen.
▪ Attracting other cells to the injury site.
▪ Vascular ingrowth initiation.
▪ Cell differentiation initiation.
• PDGF stimulates healing of connective tissue and helps in the
activation of bone regeneration by initiating angiogenesis and
stimulating macrophages.
• TGF-β acts as a growth factor aid in the repair and regeneration of
connective tissue as well as differentiation. It also acts as an effective
inhibitor of osteoclast cells formation, resorption of bone and
favouring formation of bone.
• Both PDGF and TGF-β facilitate the following:
▪ Repair of connective tissue and regeneration of bone.
▪ Trigger adjacent cells like preosteoblasts for mitosis (increase
in numbers).
▪ Induce preosteoblasts differentiation into mature osteoblasts,
thus helping in the initiation of remodelling of bone.
▪ Tissue healing.
▪ Bone mineralisation.
Marx et al. reported their evidence of nearly 3 times higher radiographic

maturation rate and increased histomorphometric bone density in grafts with
PRP in comparison to grafts without PRP (Flowchart 50.2).
FLOWCHART 50.2 Preparation of PRP gel.
Uses
• PRP has extensively used to support tissue healing.
• PRP is clinically used to promote healing of bone and tissue.
• Used in maxillofacial reconstruction and periodontal regenerative
therapy.
• Extraction socket healing: Use of PRP in extraction sockets aids in
reducing postoperative pain and inflammation, though no systematic
acceleration of osseous healing at the postextraction site could be
demonstrated. Moreover, lower rate of alveolar osteitis, less pain and
denser radiographic bone healing were found when PRP was placed
into third molar extraction sockets.
• Dental implants: PRP may be used to promote osseointegration and
bone regeneration during the placement of dental implants.
• Bone graft enhancer: When PRP is used along with particulate bone
grafting materials, PRP acts as a biologic adhesive which holds
together the particles, making the graft material manipulation much
easier. PRP may be used as an additive to nonvascularised bone grafts
in alveolar cleft, critical size bony defects and mandibular continuity
defects.
Bioactive polypeptides
The bioactive polypeptides may act as osteoinducers or osteoenhancers. P-15
and OSA-117MV are the two short amino acid chain peptides that have
demonstrated the bone activity. P-15 polypeptide has a conformational
arrangement known as the ‘beta bend’, which promotes bone induction and
growth when used in some in vitro studies. The octenyl succinic anhydride
(OSA) molecule is smaller than P-15 and was used in the treatment of
osteoporosis where OSAs effect is concentrated in areas of high stress. Studies
have started to explore the local effects of this peptide, and initial reports
suggest that it may enhance the osteoinductive effect of demineralised bone
matrix.
Recombinant bone morphogenetic proteins

BMPs are naturally occurring anabolic proteins in the body found in various
tissues like bone, cartilage, musculature and connective tissue.
BMP family
• BMPs are subfamily of TGF-β superfamily.

• The TGF-β superfamily is composed of more than 40 members, such as
TGF-βs, nodal, activin and BMPs.
• There are 20 different proteins have been named BMPs in human, but
all members do not have the capacity to induce bone (osteogenic
potential).
• BMP-1 is a metalloprotease and does not possess osteogenic properties.
• BMP-2 and 4 compose of one osteogenic group.
• BMP-3 and 13 function as BMP antagonists.
• BMP-5, 6, 7, 8, 9 and 10 form another osteogenic group.
BMP in bone
• BMPs are produced by osteoprogenitor cells, namely osteoblasts,

chondrocytes and platelets.
• After release, they are temporarily stored in extracellular matrix.
• Regulatory effect of BMPs depends upon target cell type, its
differentiation stage, local concentration of BMP, as well as the
interactions with other proteins.
• BMPs induce chondrogenesis, osteogenesis, angiogenesis and
extracellular matrix.
Recombinant bone morphogenetic proteins (rhBMP)

These are osteoinductive protein additives derived through recombinant
tissue engineering technology. These consist of the osteoinductive component
of several tissue engineering products that can induce de novo bone
formation in the site these are implanted.
Osteoinductive properties of BMP

Implantation of rhBMP results in a complex series of cellular events:
1. Mesenchymal cell infiltration

2. Cartilage formation (in endochondral ossification)
3. Vascularisation
4. Bone formation
5. Bone remodelling along with population by haematopoietic bone
marrow elements (Table 50.2).
Table 50.2
Overview of BMP characteristics
The BMPs are different from other osteoinductive products by their
mechanism of action at the cellular level. The BMPs are differentiation factors,
causing mesenchymal cells to differentiate into bone and cartilage-forming
mature cells.
BMPs can replace the use of autogenous bone graft with an off-the-shelf
material containing the BMP and an inert carrier system (Fig. 50.9).
FIGURE 50.9 (A) Preoperative clinical photograph of the patient

with unilateral alveolar cleft. (B) CT scan showing the alveolar cleft.
(C) BMP in a commercially available package. (D) BMP powder
and the absorbable collagen sponge prior to mixing. (E) Surgical
exposure of the alveolar cleft. (F) Packing of the alveolar cleft with
BMP. (G) Postoperative clinical photograph. (H) Postoperative 3D
CT scan showing closure. (I) Regenerated new bone visible during
implant placement.
History
• In 1965, Marshall Urist demonstrated the potential of demineralised

bone to form bone which could be extracted from its organic
component using chaotropic agents. These proteins were responsible
for its osteogenic capacity.
• In 1979, Urist coined the term BMPs.
• Hari Reddi et al. succeeded in the preparation of a special solvent of
dissociative extractants for extracting BMPs. They were the first to
identify, isolate and purify the signals of BMP.
• John Wozney and colleagues at Genetics Institute enabled the cloning
of BMPs creating rhBMP which paved the way for its mass
production.
Advantages
• As differentiation factors, they induce the formation of their own bone

in host (patient) when used.
• Bone is formed by BMP, which functions and remodels in a way
appropriate for the anatomic site and biomechanical environment in
which it is placed.
• More conducive to normal growth, tooth eruption, mechanical
manipulation and osseointegration than other forms of grafts.
Need for a carrier or scaffold

BMPs can be rapidly eliminated by the body if it is not bound to a carrier. The
ideal carrier must bind BMP till all the differentiation processes are complete
and resorb in time to provide space for the developing bone to form. The
currently used carrier is absorbable collagen sponge.
Clinical application in oral surgery
• rhBMP-2 and rhBMP-7 are two of the molecules in clinical use, are
produced by biotechnology process using recombinant DNA
technology which offers unlimited supply and substantial control over
purity and reproducible activity
• Cleft alveolar bone grafting (FDA approved) (Fig. 50.9A–I)
• Sinus lift (FDA approved)
• Alveolar ridge augmentations
• Postresection reconstruction after ensuring tumour-free condition
• Enhancing mineralisation in distraction callus
• Treatment of fracture malunions
• Critical size cystic bony defects
Complications
Exaggerated inflammatory response

The early postoperative course shows an extreme inflammatory reaction
sometimes endangering life as in neck swelling following use in mandible.
Preoperative elective tracheostomy may become mandatory.
Ectopic bone formation

Ectopic bone formation is a potential side effect when used in spine surgery,
though not reported in use in maxillofacial region.
Nonresponders
In some patients, the body may not respond to the rhBMP-2 showing no
desired osseous regenerative effects.
Stem cells
The developed tissue engineering technology has brought the possibilities,
where the hybrids of biomaterials seeded with osteocompetent cells can be
used as an implant. These ‘hybrid grafts’ were porous matrix, on which bone
marrow cells could grow.
Using bone marrow as the source of cells is logical as bone marrow contains
stem cells which have the ability to differentiate various cell lines, including
the bone producing osteocompetent cells. Seeding of bone marrow cells into
porous matrix enhances the osteogenic potential of the matrix as a hybrid.
Another advantage of the tissue culturing technique is that bone marrow cells
can be further expand in numbers. These bone marrow-derived cells are
responsive to the influence of dexamethasone and 1,25-
dihydroxycholecalciferol and they can be influenced to differentiate in the
direction of bone cells. Human bone marrow cells have the ability to adhere to
the porous coral matrices and matrices made of hydroxyapatite. The
combination of coral scaffold and in vitro-expanded marrow stromal cells has
been used as tissue-engineered artificial bone graft (hybrid grafts), which has
been used to treat a large segmental long bone defects in the murine model
with morphogenesis leading to complete recorticalisation and medullary canal
formation. The bone cells can be harvested using special devices, e.g. suction
trap, and could be used for the same individual at a later date by
cryopreservation.
The aim of internal fixation for skeletal fractures and osteotomies is to achieve
undisturbed proper fracture healing. Although plates and screws are used for
fixation, their need is only temporary, until the fracture union has occurred.
Titanium plates and screws are the gold standard for fixation of various
craniofacial surgeries and their use in maxillofacial trauma surgery is well
documented (Fig. 50.10).
FIGURE 50.10 Bioresorbable plate. Scan to play

Craniosynostosis correction with Resorbable plates and screws)
Disadvantages inherent to rigid fixation system using plates
• Growth disturbances
• Migration of fixed plate
• Need for second surgery for its removal
• Reduced compatibility with advanced imaging aids
• Long-term palpability
• Thermal sensitivity
• Malunion of the site
• Difficult in controlling the postoperative occlusion
Consequences of not removing the plate
• Palpable or prominent hardware

• Loosening of fixed plates and screws
• Pain and infection
• Wound dehiscence in the surgical site
• Thermal sensitivity
• Plate migration
In addition, there are studies which proved rigid internal fixation adversely
affect skeletal growth and development in growing children, which led to the
development of biodegradable hardware that is strong, biocompatible,
adaptable and provides enough stability to allow fracture healing and then
resorbs quickly without a foreign body reaction.
Bioresorbable polymer science has evolved during the last 10 years and
there has been a significant improvement in the mechanical properties of
degradable plates and screws. Presently, these plates provide optimal strength
and degradation time.
History of absorbable implants

The possibility of using biodegradable devices in bone surgery has been
studied extensively for more than 50 years. The first clinical trials of the use of
such materials in fracture surgery took place more than 40 years ago, with
disappointing results. As the stability of the devices was not adequate, the
osteosynthesis did not result in rigid, function-stable fixation.
Various researches around 1970s have resulted in major improvements.
Implant fabrication was accomplished by melt moulding and extrusion of the
polymer into pins and rods. In the late 1970s and early 1980s, more complex
designs like screws and small plates became possible.
Advances in polymer chemistry and material processing methods have
improved the quality of biodegradable materials to the extent that its clinical
use has become safe. Stability has been achieved and maintained for a
sufficiently long time to allow normal bone healing to occur.
Chemical composition of absorbable implants

Alpha compounds such as polyglycolic acid (PGA), polylactic acid and
polyesters polyparadioxanon are organic macromolecular compounds which
can be degraded and absorbed by the human body. They also have the
chemical and physical properties which are necessary for internal fixation
devices.
Mechanism of action
Bioresorbable plate is converted into CO2 and H2O via bulk hydrolysis by the
body and metabolised by the liver with the theoretical advantage of gradual
degradation in order to reduce the risk of local inflammation and osteolysis.
The foreign body reactions seen usually with the more rapidly degrading
polymers such as PGA are not typically seen with these materials.
Features of this system
• Tensile and flexural strength are comparable to titanium plating

system.
• Easy to adapt with aid of heat pack in the surgical site.
• Wide selection of implant sizes and shapes are available.
• Convenient hex-drive break-away delivery system which simplifies
screw placement.
• No growth restriction and implant migration for paediatric craniofacial
reconstruction.
• It is resorbed completely so no need for a second surgery.
• No late-stage inflammatory reaction.
Advantages of resorbable plates
• Small and compact

• Biocompatible
• Adaptable to the surgical site
• Posses adequate stability to achieve bony union
• Subsequently resorbs in a timely fashion
Titanium versus biodegradable plates

The biodegradable material is softer and weaker than titanium plates and it
requires tapping to place the screws. In titanium plates, firm pressure and
‘tight’ screw placement are favourable, but in case of biodegradable screws it
needs only be ‘finger tight’ and care must be taken when placing them into
thin bone. Excessive torque should not be applied to avoid the breakage of the
screw head. The resorbable plates and screws are not radiographically
apparent, hence postoperatively the radiolucent screw holes can be identified.
These screw holes also serve as a measure of degradation time in which once
the hole is no longer visible in the radiograph it can be assumed that it has
been resorbed.
The use of biodegradable materials in paediatric craniofacial surgery has
been favourable and this has made the use of these materials in orthognathic
and maxillofacial trauma surgery. Although resorbable plates and screws are
biomechanically inferior to titanium, they appear to offer equivalent results
when compared with similar metal fixation devices in an animal model. Two
major differences are that it needs heating device to provide malleability and
we need to tap bone before screw placement. The mandible and forehead have
relatively flat and gently curved surfaces, which do not require enough
bending, whereas in the zygoma and orbit, more complex shaping of the
plates may be needed. The major concern is the performance of these materials
when exposed to the functional demands of the maxillofacial skeleton.
Uses of biodegradable plates
• Fixation of fractures involving the tooth-bearing area of the mandible

(as in children with unerupted permanent teeth).
• Bone-anchored method of maxillomadibular fixation.
• Very low load-bearing fracture of the midface region.
• Fixation of paediatric craniofacial osteotomy.
• The use of resorbable plates and screws for fixation of paediatric facial
fractures is well tolerated and effective. It helps in realignment and
stable positioning of rapidly healing fracture segments while
eliminating the need for the removal by second surgery.
Selection of patient for the use of resorbable plates (Fig. 50.11)

The paediatric facial trauma patient invokes several different considerations
that are not present in the adult. First, the paediatric population has the huge
advantage of an accelerated healing in a very short time with very few
complication which is aided by the well-vascularised tissues of the face.
Second, through the assistance of growth and an inherent ability to adapt,
recovery of damaged orofacial tissues and function is much better than in the
adult.
FIGURE 50.11 Fixation with bioresorbable plate.
Although they have various advantages, certain differences do exist in the

paediatric facial trauma patient that must be considered. These include an
appreciation of the unique characteristics and anatomy of the developing
immature face, the different facial injury patterns that occur in the paediatric
patient and the potential growth implications from traumatised facial
structures that make long-term follow-up of these patients important.
TMJ arthrocentesis
Arthrocentesis is a safe and rapid procedure used to treat a multitude of
disorders affecting the TMJ first described by Nitzan and colleagues in 1991 to
treat acute closed lock jaw. It is the least invasive of the surgical techniques.
Treatment is generally indicated when other nonsurgical and pharmacologic
methods have failed. Patients who fail conservative measures are candidates
for arthrocentesis. Patients with TMJ internal derangements without reduction
who do not respond to nonsurgical management benefit from arthrocentesis
and/or arthroscopic lysis and lavage.
Indications
• Acute and chronic limitation of opening because of anteriorly

displaced disk without reduction.
• Chronic pain with good range of motion and anterior disk
displacement with reduction.
• Degenerative osteoarthritis.
• TMJ open lock where the condyle is entrapped anterior to a lagging
disk.
• Possible sources of pain that include impingement, compression and
inflammatory changes in the retrodiscal tissues.
• Inflammatory changes in the synovial membrane with joint effusion
and capsulitis.
Contraindications
• Patients who have not undergone appropriate

conservative/nonsurgical and pharmacologic treatment.
• Bony or fibrous ankylosis.
• Have extracapsular sources of pain.
• Pathology involving bony degeneration, osteophytes and bone
spicules.
• Disk perforation.
Mechanism of arthrocentesis
The concept is based on the observation that simple lysis and lavage of the
upper joint space via arthroscopy removes the inflammatory mediators as well
as alters the intra-articular pressure through the addition of more fluid and is
highly successful in reestablishing normal range of mouth opening in patients
with symptomatic TMJ disease.
FIGURE 50.12 (A–B) TMJ arthrocentesis landmarks for insertion of

needles.
1. The procedure is usually performed with intravenous conscious
sedation and local anaesthesia but can be performed with local
anaesthesia also.
2. Technique involves the insertion of two 18-gauge needles into the
superior joint space of the TMJ.
3. The patient is seated inclined at a 45-degree angle with the head turned
to the opposite side to provide an easy approach to the affected joint.
4. After preparation of the preauricular area, the external auditory meatus
is blocked with cotton and a local anaesthetic is infiltrated.
5. The Holmlund–Hellsing line is drawn with marker between the lateral
canthus and the apex of tragus (canthotragal line).
6. A marking point is made at about the midportion of the external tragus.
From this point, approximately 10 mm anterior and 2 mm inferior to
the line, the maximum concavity of the fossa is located and the
posterior needle is inserted at this point at a 45-degree angle from
posterior to anterior and from inferior to superior.
7. Then the upper joint space is distended with approximately 2 mL of
Ringer solution.
8. Confirmation of placement of the posterior needle into the upper joint
space is made by observing the mandible’s movement during injection
or by backflow into the syringe when pressure is released.
9. A second point corresponding to the height of the articular eminence is
marked at 20 mm anterior to the midtragal point and 10 mm below the
cantho-tragal plane. This can function as a landmark for the placement
of the second portal for the outflow of irrigant.
10. Slight adjustment of the needles may need to be made if the outflow is
sluggish.
11. The upper joint space is then irrigated with 100–300 mL of Ringer
solution.
12. The outflow is intermittently occluded during the irrigation to distend
the joint space.
13. After completion of the irrigation, medication (steroid or hyaluronic
acid) may be placed in the upper joint space.
14. Once the procedure is completed, the mandible is moved through
opening, excursive and protrusive movements.
15. The range of motion and presence of any mechanical interference to
movement are noted.
16. After the procedure the patient is given a mild analgesic and instructed
to perform range-of-motion exercises. This is continued for about a
week.
Complications
• Temporary facial nerve weakness or paralysis.

• Preauricular swelling from either extravasation of fluid.
• Haematoma.
• Occlusal changes from distention of the upper joint space.
These complications are temporary and generally resolve within 24 h.
TMJ prosthesis
Alloplastic TMJ prosthesis represents a safe and predictable way to restore
TMJ-acquired defects. The history of total joint fossa/condyle alloplast used for
reconstruction of the TMJ is primarily checked because of significant
complications associated with prosthesis containing Proplast-Teflon, as it has a
tendency to fragment under prolonged cyclical loading, this resulted in a
locally destructive foreign body giant cell reaction (Fig. 50.13; Tables 50.3 and
50.4).
FIGURE 50.13 TMJ prosthesis.
Table 50.3
Indications and contraindications of TMJ Prosthesis
Indications Contraindications
• Congenital and developmental disorders (condylar agenesis, • Growing patients
condylar hyperplasia) • Uncontrolled systemic
• Neoplasia disease
• Severe degenerative disease • Psychiatric instability
• Severe inflammatory disease • Active infection
• Posttraumatic deformities • Allergy to prosthetic
• Ankylosis components
• Previous failed autogenous reconstructions • Uncontrolled
• Previous failed alloplastic reconstructions parafunction
Table 50.4
Advantages and disadvantages
Advantages Disadvantages
• Decreased operating time • Cost
• Immediate function/no need for postoperative • Possible need for replacement
MMF • No growth potential
• No donor site • Plain film imaging of contralateral often
• Patient-specific devices available difficult
• Simultaneous correction of malocclusions • Possible displacement
possible • Possible fixation failure
• Wear
These alloplastic TMJ prostheses are available as stock and custom-made

prostheses, and in North America, three companies produce total joint
prosthesis. TMJ concepts (Ventura, CA) produce a patient-specific device only,
whereas Biomet Microfixation (Warsaw, IN) and TMJ Medical Inc (Salt Lake
City, UT) produce both stock and patient-specific devices. Both the fossa and
condyle of the TMJ Medical device are constructed of surgical grade cobalt–
chromium–molybdenum alloy. The fossa component of the Biomet
Microfixation device is made of ultra-high-molecular-weight polyethylene
(UHMWPE), whereas the ramus–condyle unit is constructed of cobalt–
chromium alloy with the under surface of the ramus portion, which lies
adjacent to bone, being titanium plasma sprayed. The fossa portion of the TMJ
concept device has an articulating surface of UHMWPE attached to a
commercially pure titanium body, which lies against the cranial base and
zygomatic arch. The mandibular component of this device is made from
medical grade titanium, except for the condylar head, which is made of cobalt–
chromium–molybdenum alloy (Table 50.5).
Table 50.5
Comparison between stock and custom-made total TMJ prosthesis

Stock prosthesis Custom-made
prosthesis
• Make fit • Made to fit
• Lower cost • Higher cost
• Shorter treatment time frames • Longer
• Removal of bone treatment time
• More difficult to obtain primary stability frames
• Potential micromovement • No or minimal
• Placement versatility removal of bone
• Potential for longer surgical time • Easier to obtain
• Limited use for large or difficult anatomic defects primary
• It has a fossa component of three sizes (small, medium, large) made stability
completely of ultrahigh molecular weight polyethylene; three different • No
lengths—45, 50 and 55 mm; and two different widths—standard and micromovement
narrow • Less placement
versatility
• Potential for
less surgical
time
• Excellent for
large or difficult
anatomic
defects
Technique
Stock prosthesis
1. The standard surgical technique with this type of prosthesis requires

periauricular and submandibular or retromandibular approaches.
Alternatively, a ‘facelift approach’ can be used.
2. Once exposure of the TMJ and mandibular ramus is achieved, a
condylar osteotomy is done if necessary.
3. Approximately between 2 and 2.5 mm of space are required between
the articular surface and the residual mandible to be able to fit the
prosthetic parts.
4. A large-barreled burr or a reciprocating rasp is then used to flatten the
articular eminence to adapt the fossa component.
5. After properly sizing it, the fossa component is implanted before fitting
and placement of the mandibular ramus component is performed.
6. If indicated, fat grafts can be implanted around the condylar head.
7. At this point MMF is released. (Depending on the case and surgeon
preference, MMF is done either at the beginning or during the
procedure.)
8. Occlusion should be checked and layer wise closure to be done.
9. A strict sterility protocol is recommended to avoid the potential risk of
postoperative infection.
Custom-made prosthesis
1. The process for construction of this type of device starts with a thin-cut
maxillofacial CT scan that is used for the construction of a
stereolithographic model.
2. This model is then studied to determine if any osteotomies are to be
made to achieve the necessary clearance for the placement of the
prosthetic parts.
3. The surgeon approves the prosthetic design after a wax-up is done in
the stereolithographic model.
4. The fossa component has a titanium mesh backing with an ultrahigh
molecular weight polyethylene articulating surface.
5. The mandibular component has a body made of machined alloyed
titanium with a condylar head of chrome–cobalt–molybdenum alloy.
6. Similar to the surgical technique for the stock prosthesis, MMF is done
at the beginning of the procedure or intraoperatively, depending on
the case and surgeon’s preference.
7. Periauricular and submandibular or retromandibular approaches are
also used to access the TMJ and the mandibular ramus.
8. Modifications to these approaches are sometimes required, depending
on the size of the acquired defect.
9. Once these areas are exposed, the necessary planned osteotomies are
performed. The fossa component is placed and secured first, followed
by the mandibular component.
10. If indicated, fat grafts can be implanted around the condylar head.
11. At this point MMF is released and occlusion is checked. In bilateral
cases both joints are accessed and prepared before the placement of the
prosthesis, as will facilitate their placement.
12. Sterility is paramount in avoiding contamination and potential
infection of the prosthesis.
Complications
Complications with these types of reconstruction include
• hardware failure,
• infection, and
• heterotopic bone formation.

‘Laser’ is an acronym for light amplification by stimulated emission of
radiation. Lasers are intense, focused, parallel beams of electromagnetic
energy of selective monochromatic wavelengths.
History
• In 1958, Schawlow and Townes proposed the principles of lasers as

dissection tools.
• In 1960, Maiman created the first operational laser which was a ruby
laser which emitted brilliant red beam of light.
• This was followed by the development of argon, carbon dioxide,
Nd:YAG lasers which are the most widely used in oral surgery.
• The continuous wave CO2 laser was developed in 1965 by Polanyi and
associates.
• In 1990, the FDA approved the use of 3.0-W Nd:YAG laser in dentistry.
Properties of laser
• Laser light is monochromatic because it generates a beam of single

wavelength, which is invisible if its wavelength is outside the visible
part of the spectrum.
• Each wave of light is coherent or identical in physical shape and size.
This means the amplitude and the frequency of all the waves of
photons are identical.
Laser production
• Light (electromagnetic wave) and its energy packets are called

photons.
• Photon on interaction with the stable atomic system will rise to a
higher energised state. This is called absorption.
• Now, this energised atomic state can emit a photon and decay to a
more stable atomic state. This is called spontaneous emission.
• However, if a photon interacts with an atomic system that is already in
an excited state, the decay of that system occurs, this results in the
release of two photons: the original photon and the photon emitted by
decay of the system.
• The emitted two photons are of equal wavelength and they are
coordinated in time and space. This process is called stimulated
emission and is the underlying principle of laser physics.
• The emitted wavelength is directly dependent on the specific lasing
medium.
• The laser optical resonating chamber consists of two mirrors. One is
totally reflective, adding to the stimulated emission by reflection of the
radiation, and the other is partially transmissive which allows for
escape of a specific wavelength of energy.
• The emitted radiant energy is extremely intense and is also
unidirectional or collimated (there is little divergence of the radiant
energy beam). The beam is monochromatic (the wavelength of the
photons is the same) and coherent (all waves being exactly in phase
with each other in both time and space).
• If the laser beam is then passed through a lens, the emitted radiant
energy can be focused to a very small beam diameter or spot size.
There is little or no radiant energy is wasted; this very small intense
beam of energy capable of cutting, coagulating or vaporising tissue
exists.
• The radiant energy of a laser must be absorbed by the target tissue and
converted to heat. Laser energies of different wavelengths have
specific absorptive characteristics in tissue.
• The target tissue should be exposed to the laser energy for the briefest
time which would produce desired thermal effect. Different types of
lasers (e.g. Argon, CO2, etc.) emit radiant energy of different
wavelengths, hence they can be used only on specific types of tissue
(Fig. 50.14; Box 50.1).
FIGURE 50.14 Laser chamber.
Box 50.1 Classification of Lasers

Classification of lasers
1. Based on ionising property

• Ionising laser: e.g. Xenon (308 nm), Excimer (193–351 nm)—
Halide gases. Due to its DNA mutagenic property, they are not
used in oral surgery.
• Nonionising lasers: e.g. Argon, CO2. All lasers used in oral
surgery belong to this group.
2. Based on visibility
a. Visible spectrum: Argon (blue green), Ruby (red)
b. Invisible spectrum: Nd:YAG (near-infrared)
3. Based on state of laser medium
a. Solid: e.g. Ruby, Nd:YAG
b. Liquid: Dye lasers
c. Gas: e.g. CO2, Argon
4. Based on delivery system
a. Noncontact or free beam laser system with angled mirrors to
direct the beam at 90 or 120 degree, e.g. CO2
b. Contact laser—Nd:YAG
c. Both contact and noncontact—Hol:YAG
5. Based on exposure time
Exposure time is ‘the amount of time the operator keeps the laser light
directed at the tissues’.
a. Continuous wave—no fluctuation of the beam with time,
uniform flow of radiation.
b. Pulsed wave—delivers photons in the form of single pulses or
trains of pulses (rate = pulses/s).
c. Super pulsed—reaches higher peak powers per pulse decreasing
lateral tissue damage.
d. Ultra pulsed—increased pulse speed for precise tissue removal
with less lateral tissue damage.
e. Flash scanned—continuous wave in circular patterns using
movable mirrors reducing the contact period and thus
reducing lateral tissue damage.
f. Q switch or quality switching—all energy is concentrated to
single intense pulses (bursts) of short duration, approximately
25 ns.
6. Based on tissue interaction
a. Soft tissue: e.g. Diode laser.
b. Hard tissue: e.g. Excimer and erbium lasers are strongly
absorbed by dental hard tissue.
7. Based on medium of laser
a. CO2
b. Ruby
c. Argon
d. Er:YAG
e. Nd:YAG
f. Hol:YAG
g. KTP (modified version of Nd:YAG)
h. Copper vapour
i. Excimer
j. HeNe (Helium–Neon)
k. Alexandrite
Laser physics
• Laser light is produced by a chain reaction of atoms.

• For laser production, a source of energy and a laser medium are
required.
• The source of energy could be electrical, chemical or another light
source.
• The laser medium can be in solid, liquid or gaseous state.
• The lasers are named based on the laser medium used. Example: CO2,
Argon, Ruby.
• Both the medium and the energy source are contained within the laser
tube. The energy source excites the medium, thereby the atoms are
charged to an excited state. The energised atoms interact with each
other and return to the ground state emitting photons of identical
wavelength (monochromatic).
• The photons oscillate at the same wavelength, unidirectional and in
parallel fashion (collimation).
• As the photons continue to travel within the laser chamber, they excite
more atoms producing more photons. This process is called as
amplification of the laser beam.
• When the laser chamber is opened, the laser beam can be delivered as
monochromatic, collimated beam. This property of coherence allows
the laser to be focused to a precise point in a delivery system.
• The laser could be delivered through
▪ Fibre optic cable
▪ Articulated arm
▪ Hollow wave guide
• Tissue delivery can be done through contact or noncontact mechanism
(free beam).
Laser tissue interaction
• Each laser has a particular wavelength.

• When laser is directed at a tissue, tissue components called
chromospheres determine the tissue’s inherent absorption capacity for
a particular wavelength.
• Each type of laser emits a different wavelength which is specific for
target tissue, whether it is soft (mucosa) or hard (hydroxyapatite),
absorbs those wavelengths differently. The laser’s efficiency depends
on the tissue’s ability to absorb or reflect the generated wavelength.
• The CO2 laser is unique among soft-tissue lasers as its wavelength is
absorbed by water rather than tissue pigments. Because mucosa is
75%–90% water, it absorbs the CO2 wavelength easily.
• Haemoglobin has affinity for green and blue light of Argon laser.
• Four types of tissue reactions occur with laser (Fig. 50.15):
▪ Reflection
▪ Scattering
▪ Transmission
▪ Absorption
• Absorption and scattering are the most important of the tissue
reactions.
• The amount of absorption determines the amount of selective tissue
destruction, whereas the amount of scattering determines the
peripheral tissue damage.
• The temperature effects of laser on the tissue vary depending on the
amount of temperature increase created by the laser energy.
FIGURE 50.15 Laser—tissue reactions.

Nonthermal reactions
The quantum energy of the laser photons is utilised to excite certain specific
molecules called sensitisers. For example, dye molecules which predominantly
accumulate in tumorous tissues will be excited on absorption of laser light.
After transfer of internal energy, this excitation energy will be transmitted to
oxygen molecules resulting in the formation of singlet radicals of oxygen
which are a cell toxin causing a purely phototoxic effect.
Thermal reactions
Medical lasers are used for cutting and coagulation. During coagulation the
tissue passes through various stages of thermal damage until vaporisation
occurs at several 100°C.
The factors determining thermal reactions are as follows:
1. Wavelength-dependent penetration depth of the laser light.

2. Thermal diffusion inside the tissues.
3. Exposure time of the laser light, its pulse length and consequently its
power density (Table 50.6).
Table 50.6
Changes of the optical, thermal and mechanical properties of tissues during laser
irradiation
• 37–60°C: Thermal reactions

Tissue 1. During continuous irradiation (0.25 s) of 30 J/cm2, tissues are easily
retraction coagulated.
• >60°C: Protein 2. On reducing the interaction time to 0.001 s the heat which produced cannot
denaturation be diffused into the tissue, resulting in local overheating and the tissue
and vapourises at temperatures >300°C.
coagulation 3. On reducing the exposure time to several hundred microseconds can result
• 90–100°C: in insufficient time to vapourise the tissue and it will ablate explosively into
Carbonisation fragments.
and charring 4. If time is further reduced to nanoseconds (10−9 s), optical breakdown will
• >100°C: Tissue occur within the laser, focus plasma will be created which will expand and
ablation produce a cavitation bubble which collapses subsequently.
Ablative effect of laser light

The ablation of soft and hard tissues depends on the high absorption of laser
light in the tissue in order to reach the ablation threshold with the initial
fraction of the pulse energy alone. Shorter the pulse, the lower is the ablation
threshold. The ablation process and the occurrence of tissue fragmentation
start after 2 µs and continue for free-running lasers with a pulse length of up
to 500 µs, until the pulse energy drops below the ablation threshold. The
necrotic zone is wider than the theoretical penetration depth of the light as the
remaining energy has the ability to penetrate tissue and even propagate by
thermal diffusion.
CO2 lasers
• Developed in 1964.
• Rays of the CO2 laser with a wavelength of 10.6 µm are absorbed in
water-based tissues, resulting in the vaporisation of intra- and
extracellular fluid and the disintegration of cells.
• The CO2 laser can be used in different modes, ranging from continuous
wave to pulsed modes in the range of microseconds emitted with a
defined frequency. Example:
a. Excision of benign oral lesions such as papillomas,
fibromas, haemangiomas, mucoceles, gingival overgrowth,
mucosal frenulas, aphthous ulcers, tongue ties
(ankyloglossia), premalignant lesions such as oral
leukoplakias and erythroleukoplakias
b. Preprosthetic surgery
c. Periodontal surgery
d. Guided tissue regeneration
e. Oral cancer resections
• Some studies have supported the use of the CO2 laser for the surgical
treatment of oral malignancies in the early stages (e.g. T1N0 and T2N0
carcinomas) or even more advanced stages of verrucous carcinoma.
• Although its wavelength can be absorbed by hydroxyapatite, the CO2
primarily is a soft-tissue laser.
Advantages
• Instant disinfection
• Nearly bloodless surgery
• Favourable wound healing
• Minimal scarring
• Decreased postoperative pain
In animal models, shorter pulse duration has resulted in a less extensive

damage zone and earlier wound healing. Histopathologically, different
thermal damage zones have been described with different laser modes. It has
been speculated that delayed wound healing may be due to the extent of the
lateral thermal damage zone.
Nd:YAG lasers
• Used in dentistry since 1990.

• These lasers are absorbed by pigmented tissue; the darker the tissue,
the more readily this wavelength is absorbed.
Uses
• Soft-tissue surgery in prosthetics, periodontics, cosmetic, paediatric

and orthodontic procedures.
• The FDA has also approved this wavelength for removing first-degree
enamel caries. Although the Nd:YAG can remove pigmented surface
carious lesions, its ability to cut hard tissue does not approach that of
the erbium series of lasers.
Semiconductor diode lasers
• Diode lasers were first introduced in dentistry in 1995.

• Absorbed easily by pigmented tissue, diode lasers are also the smallest
and most light weight dental lasers available, comparable in size to an
ultrasonic scaler unit.
Uses
• Diode lasers are also approved by the FDA for soft-tissue procedures
and for bleaching (Fig. 50.16). Bactericidal effect of diode lasers has
been used in connection with infected root canals and periodontal
pockets.
FIGURE 50.16 Bleaching done with lasers.
Erbium lasers (ER:YAG and ER, CR:YSGG)
• The erbium series of dental lasers consists of two wavelengths with

similar but not identical properties, the Er:YAG (erbium:yttrium-
aluminium-garnet) wavelength (2940 nm) and the Er, Cr:YSGG
(erbium-chromium:yttrium-scallium-gallium-garnet) wavelength
(2790 nm).
• The two lasers also differ in terms of their ability to absorb water and
hydroxyapatite. Er:YAGs ability to absorb hydroxyapatite is higher
than Er, Cr:YSGG; therefore, the laser drilling with Er:YAG resulted in
greater mass removal of dentine and a smaller increase in pulpal
temperature compared with the Er, Cr:YSGG.
• The Er:YAG dental laser was first approved for caries removal and
cavity preparation in 1997.
• These wavelengths have a high affinity for hydroxyapatite in tooth
structure and osseous structure and the highest water-absorption rate
available for any dental wavelength.
Uses
• During class V gingival lesion or root caries, these wavelengths can be

used to contour the soft tissue or to perform a gingivectomy that will
expose the decay and remove the carious lesion without using
infiltration or block analgesia.
• Erbium wavelengths cannot coagulate and cauterise bleeding tissue as
well as the CO2 and Nd:YAG soft-tissue wavelengths. Therefore, they
are not indicated for soft-tissue procedures except in procedure that
does not require sealing off capillaries, e.g. when preparing a bed for a
soft-tissue graft.
• These wavelengths are mainly used for hard-tissue procedures as to
remove dental caries without the need for analgesia.
• Er:YAG is considered superior to other wavelengths when performing
procedures like the removal of lipopolysaccharides from root surfaces
without charring, melting or carbonising the root surfaces.
Indications in oral surgery
1. Incision
a. Biopsies (incisional/excisional)
b. Abscess (incision and drainage)
2. Preprosthetic procedures
a. Frenectomy
b. Frenotomy
c. Crown lengthening
d. Gingivectomy/gingivoplasty
e. Vestibuloplasty
3. Aphthous ulcer treatment
4. Haemostasis
5. Operculectomy
6. Implant recovery
7. Pulpotomy
8. Removal of filling material like gutta-percha or resin
9. Sulcular debridement
Application of laser in oral surgery
Since lasers were first introduced to surgery in 1970, the FDA has approved
the use of seven different wavelengths for use in dentistry (Table 50.7). These
wavelengths can be used for different procedures in oral surgery.
Table 50.7
FDA-approved wavelengths
Wavelength in nanometres (nm) Absorption
Nd:YAG 1064 Pigment
Diode 810–830 Pigment
Diode 980 Pigment
Er, Cr:YSGG 2790 Water
Er:YAG 2940 Water
CO2 10,600 Water
Er:YAG 810–830 Water
The FDA-approved soft- and hard-tissue applications are presented in

Tables 50.8 and 50.9.
Table 50.8
FDA-approved soft-tissue procedures
• Abscess incision and drainage

• Aphthous ulcer treatment
• Biopsies (incisional/excisional)
• Crown lengthening (soft tissue only)
• Haemostatic assistance
• Fibroma removal
• Frenectomy
• Frenotomy
• Gingival excision/incision
• Gingivectomy/gingivoplasty
• Operculectomy
• Oral papillectomy
• Tissue retraction for impression
• Vestibuloplasty
• Exposure of unerupted or partially erupted teeth
• Implant recovery
• Lesion (tumour) removal
• Leukoplakia
• Pulpotomy
• Pulpotomy as an adjunct to root canal therapy

• Removal of filling material, like gutta-percha or resin, as an adjunct treatment during root
canal retreatment
• Sulcular debridement (removal of diseased or inflamed soft tissue in the periodontal
pocket) to improve clinical indices, including gingival index, gingival bleeding index, probe
depth, attachment level and tooth mobility
Table 50.9
FDA-approved hard-tissue procedure
• Removal of caries
• Cavity preparation
• Etching of enamel
• Enameloplasty, excavation of pits and fissures for placement of sealants
• Cutting, shaving, contouring and resection of oral osseous tissue
• Apicoectomy
• Endodontics
Skin/dermatologic
• Laser resurfacing
• Laser blepharoplasty
• Laser treatment of tattoos, pigmentation disorders and various other
vascular disorders, such as port-wine stains, facial telangiectasia and
so on.
• Hair reduction by laser
• Non-ablative laser rejuvenation of wrinkles
Caries removal
Currently, there are two laser machines available for caries removal. Cavity
removal can be accomplished with two currently available laser machines.
Both lasers have the ability to remove decay tooth caries within a tooth and
prepare the surrounding enamel cavity for bonded fillings. The major
advantage over traditional methods is that the need for anaesthesia is greatly
reduced or eliminated over the traditional methods. Laser energy dramatically
reduces the bacterial level found in dental tooth caries decay and has been
demonstrated to enhance the tooth’s ability to ‘heal’ in situations where case of
‘deep cavities’ had existed. However, there were several limitations in caries
removal using laser like inability to adequately remove amalgam fillings,
onlays and metal crowns.
Curing and tooth whitening

Lasers have become important in curing or hardening the bonding materials.
Curing the filling and bonding material is less time-consuming. Teeth
whitening can be done using special solutions which are applied over the
tooth surface in the dental office and activated by laser energy. Even colour
changes of several shades are possible in a very short time. Dramatic changes
can be seen in even the most difficult cases when laser treatment is combined
with at-home tray-based whitening systems.
Dentinal hypersensitivity
The prevalence of treatment-resistant dentinal hypersensitivity has diminished
considerably with the advent of desensitising agents. On the other hand, the
placement of fillings using composites and inlays has brought a new reason
for the very same. Gershman has proved that dentinal hypersensitivity can be
successfully treated with laser therapy. Mild pulpitis requires higher doses
when compared to common dentinal hypersensitivity and repeated
treatments. Frequently sensitivity due to abrasion can be treated in a single
application.
Herpes simplex
Oral herpes (HSV1) is a common condition to be seen in the dental office. As
with any HSV1 treatment, a treatment in the early prodromal stage is most
successful. Immediate results can be seen, like complete reduction in the pain
level, and the blisters will disappear within a few days. Unlike Acyclovir, there
are no side effects. It has also been proved that the laser therapy can even be
used in the latent period between the attacks to reduce recurrence rate.
The therapeutic lasers provide beneficial response in the treatment of pain,
inflammation, oedema and wound healing.
Mucositis
Mucositis is the major side effect in patients undergoing radiotherapy and/or
chemoradiotherapy. Nutrition is troublesome and therapy regimen may have
to be suboptimal for this reason. Although laser therapy is used to treat
mucositis, using laser therapy before radiotherapy/chemotherapy will reduce
the mucosal irritation.
Pain
Laser therapy can reduce or eliminate pain of various origins. Irradiating the
operated area postoperatively before anaesthesia wears off will substantially
eliminate the postoperative discomfort after surgery.
Paraesthesia
Paraesthesia may occur after some oral surgical procedures, especially in the
mandibular region. Laser therapy has been used to eliminate or reduce such
complications.
TMJ
The treatment should be concentrated in the joint areas in case of arthritic
cases, whereas in myogenic cases the muscular insertions and trigger points
should be concentrated. Conventional treatment should also be used in
addition to laser therapy to improve the treatment outcome.
Tinnitus/vertigo
Patients with Mienere’s disease (tinnitus/vertigo) have tension in the
masticatory, neck and trapezius muscles. Relaxation of the tension in these
muscles and occlusal stabilisation procedures (occlusal adjustment, bite splint)
will minimise or eliminate the symptoms of tinnitus and vertigo in these
patients. Laser therapy has been proved to be a successful tool to promote
muscular relaxation and pain relief in these patients.
Zoster
Herpes zoster in the course of trigeminal nerve should be treated in its early
phase. Some zoster attack may be followed by a condition called postherpetic
neuralgia that persists for years or even life-lasting. Laser therapy is an
economical, noninvasive treatment method without any side effects.
Other uses
It can also be used in periodontal or gum procedures as recontouring or
reshaping gums, removing extra or diseased gum tissue due to the use of
certain medications or periodontal disease, removing the bacteria in
periodontal pockets to promote healing, tumour ablation, reducing the blood
loss by sealing small blood vessels, for sealing lymph vessels to reduce
swelling and the spread of tumour cells, to treat some skin conditions,
including warts, moles, tattoos, birthmarks, scars and wrinkles.
Advantages
• Increased bone healing

• Reduced risk of infection
• Less need for anaesthesia or injections
• Less bleeding
• Less noise than the traditional dental drill
• Less postoperative pain
• Better results
• Ability to do more than one procedure in a single appointment
Precaution
The only physical risk in laser therapy is the damage to the eyes, especially
when using an invisible and collimated (parallel) beam. Care should be taken
by using suitable protective goggles by the patient for extraoral therapy in the
face. As all the therapeutic lasers are well above the ionising spectrum level,
there is no risk of cancerous changes.
Side effects
• Temporary increase of pain in chronic conditions: There could be a

temporary acute exacerbation in chronic conditions causing pain.
• Tiredness after the treatment: This could be due to pain relief where the
pain previously has prevented a normal relaxation pattern.
• Redness and a feeling of warmness in the irradiated area as a result of
increased microcirculation.
Physics forceps
Dr. Richard Golden developed the physics forceps in 2004. They aid in the
instrumentation for the extraction of teeth (Fig. 50.17).
FIGURE 50.17 (A) Upper anterior forceps. (B) Upper right posterior
forceps. (C) Upper left posterior forceps. (D) Lower universal
forceps. (E) Upper third molar forceps. (F) Lower third molar
forceps.
Technique
Popularly referred as ‘beak and bumper’ technique. The ‘beak’ is placed on the
palatal or lingual root of the tooth into the gingival sulcus, whereas the
‘bumper’ is positioned on the buccal or facial aspect at the mucogingival
junction. After engaging the forceps only wrist movement until resistance is
felt. It is based on the first-class lever principle, thereby delivering a
mechanical advantage. Constant steady pressure is applied parallel to the long
axis of the tooth with the wrist only using the bumper as a pivot or fulcrum
(Fig. 50.18; Flowchart 50.3).
FIGURE 50.18 Step 1: Reflection of mucoperiosteal flap. Step 2:

Engage the beak into the gingival sulcus. Step 3: Application of
force.
FLOWCHART 50.3 Mechanism of tooth extraction by physics

forceps.
Uses
• Extractions of grossly decayed teeth

• Orthodontic extraction
• In cases of intentional tooth replantation
• For immediate implants
Advantage
• Preserves the socket and alveolar bone

• Minimal trauma to surrounding soft tissues
• Reduces the duration of procedure
• Atraumatic extractions
• Eliminates complications like root tip fractures
• Simple to use
• Not very technique sensitive
Disadvantage
• Expensive
• Cannot be used in special conditions like severe crowding
• Potential for being misused
• Damage to buccal plate
The Zygomaticus System, developed as part of the Brånemark System, allows
reconstruction of a severely resorbed maxilla without the need for bone
grafting. This approach is especially recommended for cases in which the
maxillary sinuses extend anteriorly up to the bicuspid area. These implants
were introduced in 1998 by Professor Per-Ingvar Brånemark and his team at
the Institute of Applied Biotechnology from the University of Gothenburg.
This graft-less technique, also called the ‘zygoma technique’, uses the
cheekbone (zygoma bone) to anchor the longer zygomatic implants.
The implant is a titanium endosteal implant which is self-tapping screw-
shaped implants with a well-defined machined surface. They are available in
eight different lengths ranging from 30 to 52.5 mm and their diameter tapers
from 4 mm superiorly to 5 mm at the fixture level. They present a unique 45-
degree angulated head to compensate for the angulation between the zygoma
and the maxilla. The path of the zygoma implant lies along the crest of the
zygomaticomaxillary buttress, and its external hex fixture head emerges in the
second premolar–first molar area.
Classification
Aparicio C. in 2011 proposed a classification for zygomatic implant patients
based on the zygoma anatomy-guided approach (ZAGA). The morphology of
the lateral sinus wall, residual alveolar crest and the zygomatic buttress was
taken into major concern. The five basic anatomical groups were named as
ZAGA 0, ZAGA 1, ZAGA 2, ZAGA 3 and ZAGA 4 (Fig. 50.19; Table 50.10).
FIGURE 50.19 ZAGA classification.
Table 50.10
ZAGA classification
Type Characteristics
ZAGA • Anterior maxillary wall is very flat.
• Implant body has an intra-sinus path.
ZAGA • Anterior maxillary wall is slightly concave.
• Drill has performed the osteotomy slightly through the wall.
• Implant body has an intra-sinus path.
ZAGA • Anterior maxillary wall is concave.
• Drill has performed the osteotomy through the wall.
• Implant body has an extra-sinus path.
ZAGA • Anterior maxillary wall is very concave.
• Drill has performed the osteotomy following a trajectory that goes from the palatal to
the buccal alveolar bone.
• Implant body leaves the concave part of the anterior sinus wall to penetrate into the
zygomatic bone so that the middle part of the implant body is not touching the most
concave part of wall.
ZAGA • Maxilla and the alveolar bone show extreme vertical and horizontal atrophy.
4 • Implant head is located buccally of the alveolar crest (there is no or minimal osteotomy
at this level).
• Drill has arrived at the apical zygomatic entrance following a path outside the sinus
wall and most of the implant body has an extra-sinus/extra-maxillary path.
Indications and contraindications (Box 50.2)
Advantages
1. Avoids use of grafts in atrophic maxilla.

2. No additional donor-site morbidity.
3. Zygomatic implants placed with two to four traditional premaxillary
implants which can be either immediately loaded or, more
traditionally, after a 6-month healing period.
4. Good anchorage from tough zygomatic bone which enhances stability
of prosthesis.
5. These implants do not necessarily require hospitalisation, in contrast to
autogenous bone harvesting from the iliac crest.
6. The total treatment time is routinely about 6 months or even less for
zygomatic implants when compared with transitional bone grafting
and implant placement.
7. Less number of patient visits.
8. Less number of implants are required to support a prosthesis compared
with traditional bone grafting with subsequent implant placement.
9. The overall laboratory fees are equal to or slightly less than those for
traditional implants.
Box 50.2 Indications and contraindications for

Zygomatic implants is patients with maxillary atrophy
Indications and contraindications for zygomatic implants is
patients with maxillary atrophy
Indications
• Atrophic patient who insists on continuous wear of the denture

• Moderate to advanced posterior maxillary alveolar atrophy
Relative indication
• Maxillofacial defects resulting from tumour or trauma
Contraindications
• Acute sinusitis
• Inability to adequately open the mouth
• Medically compromised patients
• Acute trismus
• Presence of mandibular dentition (may interfere with surgical access)

• Uncontrolled chronic sinus disease
• Unilateral defects
Disadvantages
1. Difficulty in placement of implant and the palatal emergence profile.

2. As the zygomatic implant platform is palatal to the crest, the patient
will feel excess bulk and may have problems with the prosthesis.
3. Zygomatic implant placement is limited by the anatomy of the zygoma.
4. Surgical access to the zygoma and orbital rim need a surgeon who has
surgical experience in these area.
5. Difficulty in maintaining the oral hygiene due to palatal emergence of
the implant, along with this minimal long-term phonetic sequelae from
the prosthesis design have also been reported.
7. Not cost-effective.
Technique
Surgical access
• The patient may have either general anaesthesia or deep sedation for
this surgery.
• Incision is made slightly palatal to the crest, and a full-thickness
reflection is performed.
• Be aware of the anatomical landmarks to prevent unnecessary injuries
and complications.
• Dissect to the level of the infraorbital foramen which assists with
anatomic orientation of the implant.
• Then place a retractor in the frontozygomatic notch (incisura) to
facilitate visualisation of the apical point of the implant.
• Using a round bur, make a window of approximately 10 mm × 5 mm
on the lateral wall of maxilla to expose the sinus membrane.
• Lift the sinus membrane from the bone and allow it to retract into the
sinus. This elevation should allow direct visualisation of the inner
aspect of the zygoma.
• Identify the implant trajectory and starting point for drilling using
depth gauge from the zygomaticus instrument set, which is aligned
over the planned path of the zygomaticus implant to give the surgeon
direct visualisation of the location for the sinus window.
• Aim for the middle of the retractor during the drilling sequence.
• Using a long round bur make an entrance mark into the maxilla from
the palatal aspect of the ridge, traverse the sinus and score the inner
aspect of the zygoma which will create a purchase point for the next
drill (maximum speed ≤2000 rpm).
• Continue with 2.9 mm pilot drill, until it penetrates the outer cortical
layer of the zygomatic bone at the frontozygomatic notch (incisura)
followed by a transition 2.9-mm twist drill which has a guide to enter
the hole in the palate and zygoma, and opens up the hole to the final
size in the zygoma.
• Now determine the implant length using the straight depth indicator.
• Widen the osteotomy with pilot drill 3.5 mm through the previously
made osteotomy.
• Again continue the osteotomy with the twist drill 3.5 mm to finalise the
osteotomy.
Implant insertion (Fig. 50.20)
• Verify the depth of the prepared osteotomy using the angled depth
indicator to ensure the selected implant length.
• Irrigate the sinus before inserting the implant.
• Insert the implant in the prepared bone site with 20 N cm setting on
the drilling unit. The setting may be increased to 50 N cm to facilitate
implant insertion.
• As the insertion torque reached 40–50 N cm, use the Z handle to
tighten the implant manually until the implant apex engages in the
zygomatic bone.
• Now place the screwdriver into the screw head of the implant mount
and verify the correct position of the implant platform (the shaft of the
screwdriver must be perpendicular to the crest of the ridge).
• Irrigate the apical implant portion thoroughly.
• Remove the implant mount and place the cover screw using the cover
screw driver.
• Place the remaining implants.
• Close the flap and wait for sufficient healing (for 6 months) or reline
the existing denture and immediately load the denture.
FIGURE 50.20 Zygomaticus implant placement procedure.
Postoperative care
• Appropriate antibiotics and analgesics to be prescribed for a week.

• Soft diet.
• Maintain oral hygiene.
Complications
• Postoperative sinusitis
• Oroantral fistula formation
• Periorbital and subconjunctival haematoma
• Facial oedema
• Pain
• Temporary paraesthesia
• Epistaxis
• Gingival inflammation
• Orbital penetration/injury
• Difficulty in speech articulation and hygiene
Ultrasonography has been used for decades for cutting tissues. Ultrasonic
cutting of soft tissues is commercially available which has been used in
various disciplines and environments. Ultrasonic cutting of bone is possible,
and alveolar bones that have been cut ultrasonically will heal uneventfully.
Piezoelectric surgery is developed as a new osteotomic and osteoplastic,
innovative technique which uses piezoelectric ultrasonic vibrations. It can be
used for precise and safe osteotomy procedures due to its characteristic
micrometric and selective cut in contrast to the traditional hard- and soft-
tissue management methods using rotating instruments.
History
Tomaso Vercellotti, in 1988, invented the piezosurgery instrument to
overcome the limits of traditional instruments in oral bone surgery.
Piezosurgery instrument uses a modulated ultrasonic frequency which
permits highly precise and safe cutting of hard tissue. It can be adjusted to
target only the mineralised tissues, by adjusting the microvibrations (60–
200 mm/s), which spares the nerves, vessels and soft tissue.
Although ultrasonic osteotomies were first described by Horton et al. more
than 20 years ago, this approach was not used for many years. It was only
around 2000, Vercellotti et al. renewed this approach for nerve and soft tissue
protecting surgery.
It is a promising novel and alternative method when compared with the
conventional hard- and soft-tissue management using rotary instruments. It
has three major characteristics: (1) a micrometric (microvibrations) cut of 60–
200 µ/s, (2) a selective cut which cuts only hard tissues but not soft tissues and
(3) the air–water cavitation effect of the ultrasonic device gives a relative
blood-free surgical field.
It was first used for preprosthetic surgery, alveolar crest expansion and
sinus grafting procedures. It is used for multipiece maxillary osteotomies and
to overcome many of the complications of this delicate surgery on hard and
soft tissues.
Need for piezoelectric surgery

Bone is a hard tissue and many cutting or drilling osteotomes are very crude
tools. In specific, rotating instruments are potentially injurious to the bone and
the soft tissues, due to the production of excessively high temperatures during
osseous drilling, which can induce marginal osteonecrosis and reduces bony
regeneration. It is widely and strongly recommended to use a careful surgical
technique, and frictional heating should be reduced using saline irrigation.
Safe and precise osteotomies without any osteonecrotic damage can be
achieved using piezoelectric surgery which produces micrometric and
selective cut. The major advantage is that this device works only on
mineralised tissues and spares soft tissues and their blood supply.
Principle
Piezoelectric effect produces microvibrations. Certain ceramics and crystals
deform when deformation of certain ceramics and crystals occurs when an
electric current is passed across them resulting in oscillation of the ultrasonic
frequency.
Technique
The equipment consists of piezoelectric hand-piece and foot switch which are
connected to the main unit through which power is supplied and there are
holders for hand-piece and irrigation fluids. The hand-piece is supplied with
several autoclavable tool tips called inserts, which are coated either with
titanium or with diamonds in various grades. The microvibrations that are
created in the piezoelectric hand-piece cause the inserts to move between 60
and 210 µm, providing the hand-piece with power exceeding 5 W.
Cooling can be achieved using the peristaltic pump with a jet of solution
which discharges from the insert, and the flow can be adjusted around 0–
60 mL/min which helps in removing the debris from the cutting area.
According to the planned task the power and frequency modulation setting of
the device can be selected on a control panel with a digital display and a
keypad. The unit uses a frequency of 25–29 kHz, which is adjustable. This
adjustability prevents the insert from impacting the bone and overheating can
be avoided while maintaining optimum cutting capacity.
The instrument was originally designed for augmentation surgeries in
implant operations, like sinus lift and ridge expansion. Bone cutting procedure
in maxillofacial surgeries in the boosted mode will be the efficient setting with
maximum irrigation. The hand-piece should be firmly guided over the bone
without excessive force. While cutting, irrigation should be maintained
properly to avoid heating of the bone. Short pause may be advisable after
prolonged cutting as the hand-piece will become warm and it is necessary to
cool down before next use (Fig. 50.21).
FIGURE 50.21 Piezoelectric unit.
Advantages
• The major advantage is the bone specific cutting sparing the vital
neurovascular bundles and soft tissue. In addition, it provides better
visualisation of the surgical field, ensures its great safety.
• Useful during neurosurgical procedures when there are anatomic
difficulties because of poor intraoperative visibility or the presence of
delicate anatomic structures.
• Reduced bleeding tendency due to selective and thermally harmless
nature of the piezosurgery instrument.
• Can be used in both local or general anaesthesia operations.
• Exact, clean and smooth cut geometries during surgery due to its
precise nature of the instruments.
• Excellent wound healing postoperatively, with no nerve and soft-tissue
injuries have been hardly reported.
• It can be used even for minor operations. As it is highly selective and
accurate in targeting hard tissue, it can be used for more complex oral
surgery cases, as well as to other interdisciplinary problems.
Precautions
• Excessive mechanical force from the instrument tip may injure or

perforate the soft-tissue structures, like mucous membrane of the
maxillary sinus or a cyst follicle.
• After a prolonged period of application, pronounced increase in
temperature is noted in the area of the hand-piece. Therefore, it
remains to be clarified whether a transmitted thermal alteration of
hard- and soft-tissue structures can be caused by intraoral
piezosurgery.
• The possible side effects such as thrombogenesis or impaired bony
blood circulation need to be examined before the use of piezosurgery.
In case of poorly vascularised mandible, the thrombosis of its
intraosseous vessels may lead to obvious clinical problems.
Stereolithography (Fig. 50.22)
FIGURE 50.22 Stereolithographic model.
It is a form of technology using 3D printing for creating models, prototypes,

patterns and production of parts in layers using photopolymerisation.
Photopolymerisation is a process which causes linkage of chains of molecules
in the presence of light, thereby forming polymers. These polymers form a
body of a 3D solid. Chuck Hull in 1984 coined the term ’Stereolithography’.
Technique
Functions by focusing an ultraviolet (UV) laser on a photopolymer resin vat.
The computer aids in manufacturing or computer aided design software
(CAM/CAD) is utilised for the UV laser to draw a preprogrammed design or
shape the photopolymer resin vat. As photopolymers are sensitive to
ultraviolet light, the resin is solidified photochemically and a single layer of
the desired 3D object is formed. 3D object is completed by repeating this
process for each layer of the design.
The thickness varies from typically 0.05 to 0.15 mm for a single layer of the
design. Modelling for medical purpose involves use of CT or MRI.
Materials
Models are available in acrylic, polyurethane.
Uses
• To create accurate 3D models

• To create prototypes for products
• In medical modelling
• Complete replacement of TMJ
• In diagnosis of congenital craniofacial deformities
• Preoperative planning
• Designing implant
• Manufacture of implant
• Orofacial prosthesis
• For patient education and motivation
Advantages
• Capable of producing any design

• High accuracy
• Quick
• Visualisation as a model
• Prefabrication of custom acrylic resin cranial implants
Disadvantages
• Expensive
• Accuracy influenced by multiple factors
• Brittle if made of acrylic
Endoscopy (Fig. 50.23)

FIGURE 50.23 Endoscope.
With the advancement in technology, minimally invasive surgeries are

possible with endoscopes.
Endoscope was first used by Takagi in 1918. The surgeon gets a clear view
of the structures in and around the surgical field through a monitor.
Parts
Endoscope has the following parts:
• A rigid or flexible tube

• A light delivery system
• A lens system
• Videoscopes
• A pathway for the entry of medical instruments or manipulators
• Suction
Uses
• Diagnosis
• Trauma surgery (e.g. condylar fracture)
• Orthognathic surgery
• Sialoendoscopy for sialolith removal (‘basket approach’ is used)
• Retrieval of foreign bodies
• Removal of implants displaced from their location (e.g. into the
maxillary sinus)
• Biopsy
• Fibre optic intubation in difficult or narrow airway
• Cauterise a bleeding vessel
• Surgeries of the maxillary sinus (FESS)
Advantages
• Minimally invasive
• Less chance of damage to vital structures
• Minimal scarring
• Accurate visualisation
• Better access than other approaches
• Faster healing
• Reduced hospital stay
Disadvantages
• Expensive
• Needs technical skill and expertise
• Time consuming in the early stages
Robotic surgery
Head and neck region is complex with many vital vessels and muscles criss-
crossing each other. Surgical manipulation in this area requires adequate
knowledge, skill and dexterity. Hence the constant endeavour of maxillofacial
surgeons was to develop a minimally invasive surgery (MIS) that can be well
tolerated. It should provide rapid recovery with lower pain, better cosmetic
results as well as minimal use of postoperative drugs. Robotic-assisted
precision surgeries offer this type of MIS in several surgical specialties. With
better options of automation and optics, the dexterity of the machines has
drastically improved over the time. This new modality has been demonstrated
as safe, cost-effective, reliable as well as better in terms of outcome as
compared with time-tested conventional modalities.
Conventional surgical approach requires large surgical incisions and
dissection often including airways that culminate in major tissue
inflammation, functional compromise and significant postoperative morbidity
at least for considerable period of time. The MIS employs latest video imaging
as well as endoscopic technology and instrumentation to overcome certain
limitations the head and neck surgeon often faces:
• A limited range and restricted handling of instrumentation.
• Training often limited to ‘line of sight’ and surgeon comfortable with
tissue in sight.
• Increased deviation in normal anatomy.
• Compromised 3D preoperative imaging.
The robotic surgery unit is about 25 years old. The first units were marketed
in 1985 and the latest transoral robotic surgery unit has been marketed since
2009. The unit has a vision cart, surgical cart and surgeon’s console. The
surgical cart has multiple (usually 4) robotic arms that can be operated from a
console through wireless remote, including one camera and others having
precision surgical instruments. The vision cart has video-assisted visualisation
with computer and optic enhancement, which is made up of light sources,
insufflators and image control hardware. The surgeon’s console has provision
for two images, one for each eye creating a 3D image to improve depth
perception and accuracy. Attached provisions are hand manipulators, pedals
for controlling optics, instrument arm, focus adjustments and so on.
Advantages
The advantages of robotic-assisted head and neck surgery are as follows:
• Enhanced visualisation: The high power camera and in-built optic

system ensures amplified visual picture ensuring perception of high-
quality images in real clinical situation.
• Elimination of physiologic tremors and scale motion: The unit
eliminates hand tremors, fulcrum effect of instruments especially
when insertion of endoscopes is involved. The torque, force and scale
motion are greatly reduced leading to better surgery, lower iatrogenic
injury ensuring safer surgery.
• Multiarticulated instruments: Simultaneous, coordinated handling of
multiple instruments such as drill, suction and electrocautery units in
controlled environment.
• Fatigue reduction: The unit instils a confidence, reduces time of
surgery owing to clear field, precision and accurate manipulation. All
of these lead to reduced surgical time as well as fatigue reduction to
the surgical team.
• Restore proper hand–eye coordination: High-resolution camera and
accurate robotic handling ensures proper hand–eye coordination.
• Telesurgery: The modality ensures distance remote surgery as
surgeons console can be kept away and the remaining unit can be
connected through high-speed Internet.
Disadvantages
The disadvantages of the system include the following:
• Absence of tactile sensation: In course of surgery, it is mandatory for

the feel of a resistance, a bone and so on to guide the surgery. Robotic
system lacks this aspect as the procedure is not performed by hand.
• Equipment size and weight: The system is large and heavy, hence
mobility of instruments and careful handling is essential.
• Cost of the device is enormous, so is the maintenance. Therefore, the
cost of the surgery increases.
• New technology and training periods are issues that need to be taken
care of.
Index
A
Abbe flap, 759, 780
ABC's mnemonic, 975
Abducent nerve, 979
Abscess, 10
submasseteric, lateral pharyngeal, pterygomandibular, submandibular and
temporal spaces, 934
Absorbable
implants, 1160
suture, 318
Abutment, 433, 491, 494
ACC, See Adenoid cystic carcinoma (ACC)
Accessory ligaments, 910
minor, 910
ACE inhibitors, 60
Acetaminophen (paracetamol), 69, 163
Acetylcholine theory, 178
Acetyl salicylic acid (aspirin), 162
Ackermann's classification, 619
Ackerman tumour, 647
Actinomyces viscosus, 376
Actinomycin D, 669
Actinomycosis, 11, 28
Activated partial thromboplastin time (APTT), 63
Activation screw driver, 883
Acute bacterial sialadenitis, 694
Acute dislocation, 965
Acute maxillary sinusitis (AMS), 715, 716
Acute mucopurulent rhinitis, 718
Acute myocardial infarction, 133, 144
Acute suppurative osteomyelitis, 557
Adamantinoma, 618
Addison disease, 15, 145
Adduction, 1108
Adenocarcinoma, 706
Adenoid cystic carcinoma (ACC), 673, 704
Adenomas, 703
Adenomatoid hyperplasia, 684
Adenomatoid odontogenic tumour, 622
Adrenal crisis, 133, 139, 145
Adrenaline, 141, 170, 182, 222, 237
Adrenal insufficiency, 109, 139
Adson tissue holding forceps, 257
Agenesis, 1126
of corpus callosum, 598
Agglutination test, 77
Aggressive lesions, 638
AIDS, 11, 28, See also Human immunodeficiency virus (HIV)
Airway, 128
maintenance, 250
management, 255
Alanine aminotransferase (ALT), 67, 68–70
Alar retractor, 250, 263
Albert stain, 71
Albumin, 67, 68
Alcohol, 212, 291, 642, 816
nerve blocks, 567, 816
Alcuronium, 240
Aldehyde, 292
Alendronate, 640
Alginic acid, 338
Alkaline phosphatase (ALP), 66–68
Alkayat-Bramley approach, 1053
Alkayat, Crane's modification, 915
Allergic hypothesis, 812
Allergic stomatitis, 24
Allis forceps, 257
Allodynia, 790
Allogenous grafts, 657, 878, 932
All on four concept, 505
Alloplastic
disc replacement, 941
graft, 452, 969
implants, 1151
material, types, 1152
Allopurinol, 60, 68
Alveolagia, 375
Alveolar cleft, 732, 736, 771
Alveolar distraction, 776
osteogenesis, 776
Alveolar osteitis, 375
Alveolar ridge
augmentation, 452
distraction, 456
preservation, 449
Alveolar socket wall fracture, 1017
Alveoloplasty, 457
Ameloblastic
carcinoma, 628
fibroma, 618, 623
fibro-odontoma, 623
fibrosarcoma, 629
odontoma (odontoameloblastoma), 623
Ameloblastoma, 10, 27, 618, 623, 624
Amifostine, 668
Amino acid decarboxylase test, 71
Aminobisphosphonates, 572
Aminoglycosides, 69, 74
Amitriptyline, 816
Ammonium carbonate, 174
Amnesia, 219
Amoxicillin, 152, 717
Ampicillin, 153, 158
Amputation, 792
AMS, See Acute maxillary sinusitis (AMS)
Amylase, 676
Amyl nitrite, 174
Anaemia, 15, 28, 650
Anaesthesia dolorosa, 819
Anaesthetic gases, 221
Analgesia, 220, 374, 590, 790
Analgesics, 105, 109, 141, 161, 219
Analogue, 496
Anaphylaxis, 140–141, 683
Anaplasia, 82
Andreasen classification, 1014, 1019, 1021
Aneurysmal bone cyst, 613
Aneurysms, 10, 11
Angina maligna, 547
Angina pectoris, 103, 136
Angiography, 32, 47, 53
Angular cheilitis, 117, 122
Angular tract of Eisler, 673
Ankylosed tooth, 380, 381
Ankylosing spondylitis, 922, 934
Ankylosis, 922
Anophthalmia, 17
Anosmia, 716, 717
Anotia, 15, 18
Antacid, 219, 220
Anterior disc displacement
with reduction, 922
without reduction, 922
Anterior dislocated meniscus, 934
Anterior ethmoidectomy, 729
Anterior middle superior alveolar nerve block, 188
Anterior segmental maxillary osteotomy, 843, 845
Wassmund technique, 846
Wunderer technique, 847
Anterior subapical mandibular osteotomy, 863, 864
Kole's modification, 863
Anterior superior alveolar nerve, 189
block, 189
Anterior vomer flap (Veau), 763
Antiangiogenic therapies, 572
Antiautonomic premedication, 219, 220
Antibiotics, 148
prophylaxis, 221
Anticholinesterases, 242
Anticonvulsant drugs, 222
Antidepressants, 940
Antiemetic, 219, 220
Antifibrinolytics, 112
Antifungal agents, 159
Antihistamine, 109, 114, 115, 124, 141, 148
Anti-inflammatory drugs, 165
Antimicrobial, 148
Antinuclear antibodies, 696
Antioedematous substances, 168
Antioxidant (Vitamin E), 567
Antiperspirant, 707
Antiplatelet drugs, 124, 333
Antiretroviral therapeutic agents, 120
Antiseptic, 284, 291
Anti-SS A, 696
Anti-SS B, 696
Antiviral agents, 160
Antral rasp, 726
Antral rhinoliths, 715, 728
Antrochoanal polyps, 729
Antrum curettes, 726
Antrum of Highmore, 711
Anxiolysis, 219
Apexo elevators, 359, 360
Aphthous ulcer, 23–24, 28, 122
Aplasia-unilateral/bilateral, 922
Aponeurosis, 751
Apoptosis, 82
APTT, See Activated partial thromboplastin time (APTT)
Arch bars, 987, 1022
Arch length, 838
Arch width analysis, 838
Arhinencephaly, 741
Arhinia, 744
Aromatic ammonia, 124
spirits of, 174
Arthritis, 922, 933
Arthrocentesis, and lavage, 941
Arthrography, 32, 54
Arthrogryposis multiplex congenita, 934
Arthroscopic biopsy, 93
Arthroscopy, 941
biopsy, 93
Articular cartilage, 911, 914
Articular eminence, 963, 964
Asch forceps, 272, 983
Aschner phenomenon, 1096
Asepsis, 255, 284
Ashley's flap, 721, 722
6 A's of premedication, 219
Aspartate aminotransferase (AST), 67, 68
Aspergillus, 717
Aspiration, 27, 141, 584
biopsy, 33, 85, 90
risk of, 1021
of teeth, 373
Aspirator, 726
Aspirin, 162, 668, 717
Assays for anti-HIV test, 118
AST, See Aspartate aminotransferase (AST)
Asthma, 107, 136
Astley Cooper's basculation, 965
Astringents, 336
Ataxia telangiectasia, 15
Atracurium, 240
Atropine, 110, 124, 125, 170
Attenuation, 681
Atypical infection, 296
Atypical pain, 384
Augmentin, 122, 153
Auriculotemporal nerve, 673
resection, 707
Auriculotemporal syndrome, 707
Austin retractor, 250, 261, 401, 418
Autoclave tape, 289
Autogenous fat, 932, 954
Autoimmune diseases, 696
Autologous graft disc replacement, 941
Autolysis, 734
Auxiliary techniques, 184
Avitene, 336, 337
AV malformations, 27, 585
Avulsed tooth, 1019
Avulsion, 1007, 1020
treatment of, 1020
Awls, 273
long, 273
short, 274
Axial flap, 313
Axle, 357
Axonal regeneration, 794
Axon hillock, 790
Axonotmesis, 793, 794
B
Babcock forceps, 258
Bacillus stearothermophilus, 289
Bacitracin, 148, 160
Backbiting forceps, 726
Backhaus towel clip, 255
Baclofen, 816
Bacterial theory, 375, 376
Bacteroides, 521, 548
Baillarger syndrome, 707
Bakamjian flap, 664
Ball and socket removable overdenture, 499
Ball in hand appearance, 679
Balloon compression, 816, 818
Balloons analysis, 683
Balsam of Peru, 173
Balsam of tolu, 722
Barbed broach, 726
Barbiturates, 60, 68, 69, 99, 108, 136
Bard-Parker blades (BP), 256
Bartholin's duct, 675
Barton's bandage, 965
Basal (rodent ulcer), 648
Basal cell carcinoma, 340, 598, 648, 664, 703
Basal cell epitheliomas, 598, 619
Basaloid squamous cell carcinoma, 647
Basaloid tumour, 618
Basic life support (BLS), 125, 126
Basilar flaps, 761
Basophils, 58, 61, 62
reversal lines, 639
stippling, 59
Bat ears, 15
Bauer's retractor, 263
Bayonet flap, 404, 405
Bayonet forceps, 364
B-cell monoclonality, 696
BCL-3, 748
Beckhaus towel clips, 250
Beckwith-Wiedemann syndrome, 23
Behchet syndrome, 27
Bell's palsy, 167, 793, 796, 799, 800
Bence Jones protein, 650
Benign
cementoblastoma, 628
lymphoepithelial lesion, 696
para/juxta-articular chondroma, 922
tumours, 618, 699
chondroma, 922
osteochondroma, 922
osteoma, 922
Benzocaine HCl, 666
Benzodiazepine, 171, 219, 222, 234
Benzoin, 722, 724
Benzydamine HCl, 666
Beriberi, 69
Berkefeld filter, 290
Berylliosis, 11
Beta propiolactone, 293
Bethanechol, 667
Bevacizumab, 572
Bicoronal approach, 919, 1098
Bicoronal incision, 312, 313, 854
Bicuspidisation, 432, 440
Bifid condyle, 922
Bifid ribs, 598
Biguanides, 293
Bilateral cleft lip, 750
Bilateral neck dissections, 654
Bilateral sagittal split osteotomy (BSSO), 858, 859, 933
Bilirubin, 67
Bimanual palpation, 676
Bimaxillary dentoalveolar hyperplasia in anterior- posterior plane, 824
Bimaxillary protrusion, 824, 875
Binders syndrome, 713
Binocular diplopia, 1094
Binocular single vision, 1094
Bioactive polypeptides, 1157
Biocompatible material, 481, 1151
Biological width, 512
Biopsy, 82, 684
guidance, 683
Bioresorbable plates, 1159
TMJ arthrocentesis, 1161
TMJ prosthesis, 1163
Biosafety mask, 293
Biot's respiration, 552
Biphosphonates, 640
Biplanar radiology, 817
Bipolar cautery, 281
Bipolar diathermy, 339
Bird face deformity, 948
Bird-like face, 932
Birn's fibrinolytic theory, 375
Birth injury, 934
Bisecting cone technique, 34
Bisphosphonates (BPs), 569, 570, 572
Bite plane splint, 940
Bitewing radiograph, 33, 391
Bivector, 882
Bjork flap, 131, 132
Black's technique, 759, 761
Blades, 250, 256
form implant, 487
handles, 250, 256
Blair curvilinear, 915
Bleeding disorders, 113
Bleeding time (BT), 58, 63, 333, 352
Bleomycin, 669
Blindness, 730
Block resection, 621
Blood urea nitrogen, 67, 69
Blow in fracture, 1084
BLS, See Basic life support (BLS)
Blue bloaters, 107
Blunt trauma, 793, 976
Blurring of vision, 800
BMP-2, 881
Bohn nodules, 10, 606
Bolton's analysis, 838
Bone
cell turnover, 1155
clamps, 993
density scanning, 32, 54
file, 268
gouge, 268
grafting, 452, 454, 455, 467, 513, 771
marrow
biopsy, 86
depression, 651
suppression, 666
pins, 1055
plating, 1055
resorption theory, 578
scan, 32, 52
scintigraphy, 52
scoop, 269
substitutes, 1150
transportation, 878
wax, 338, 425, 594
Bone graft healing, 772, 1150
bone apposition, 1150
creeping substitution, 1150
demineralising, 1150
deproteinating, 1150
freeze drying, 1150
Bone matrix deposition, 1156
Bone mineralisation, 1156
Bone morphogenetic proteins, 1157
Bone regeneration, 1157
Bone substitutes, types, 1150
alloplasts/synthetic grafts, 1150
autograft, 1150
xenograft, 1150
Bony pillar of face, 366
Borrelia burgdorferi, 799
Botryoid variant, 605
Bottom up and inside out theory, 982
Botulinum, 686
toxin A, 707
Bowie-Dick test, 289
Box frame, 984, 994
Brachycephaly, 15
Brachytherapy, 565
Brain abscess, 1140
Brain mask, 254
Brain mask airway (BMA), 254
Brain stem, 819
Bramley's, Crane's modification, 915
Branched leafless tree appearance, 679
Branchial arch syndrome, first/second, 932
Branchial cleft cyst, 615
Branchio-oculo-facial syndromes, 932
Branchio-oto-renal syndrome, 931, 932
Branchless fruit laden tree, 679
Branemark's theory of osseointegration, 481
Breathing, 126, 132, 975
Brenthurst splint, 993
Bridge flap, 724, 725
Brin's fibrinolytic theory, 376
Bromhexine, 667
Bromodeoxyuridine, 668
Bronchodilator, 107, 124, 144
BRONJ criteria, 570
Brown's test, 289
Brown tumour, 67
Brudzinski's sign, 551
Brush biopsy, 33, 89
BSSO, See Bilateral sagittal split osteotomy (BSSO)
Buccal antrostomy, 728
Buccal bifurcation cyst, 612
Buccal nerve block, 204
Buccal pad of fat, 723
Buccal space, 527, 528, 536, 544, 548
Buccal vestibule, 1021
Buccinator muscle, 689
Buckling theory, 1084
Bulimic patients, 695
Bull's eye appearance, 28
BUN, 69
Bupivacaine, 180
Burs, 271
Burst phenomenon, 513
Bush in winter appearance, 679, 680
Butyl cyanoacrylate spray, 173
Bypass grafts, 103
C
Café-au-lait macules, 636
Cafe au lait spots, 15
Calcified falx cerebri, 598
Calcifying epithelial odontogenic tumour, 578, 618, 621
Calcifying odontogenic cyst (COC), 578, 607
Calcitonin, 640
Calcium displacement theory, 178
Calcium phosphate ceramics, 1154
Calcium sulphate, 425
Calculi, 677, 678, 680, 688, 689, 690
Caldwell-Luc incision, 720
Caldwell-Luc procedure, 371, 413, 472, 614, 633, 713, 726, 728
Callotasis, 883
Callus formation, 983, 1003
Calor, 526
Calvarial diameter, increased, 598
Canalicular adenomas, 703
Canaliculi, 1109, 1110
Cancrum oris, 934
Candida, 666
skin test, 78
Candidiasis, 30, 73, 89, 117, 121, 160, 475
Canine space, 14, 523, 535
Canthopexy, 1103, 1115, 1117, 1121, 1122
modified Y plate, 1122
transnasal wiring, 1121, 1122
Capillary fragility test, 63, 64
Cap splints, 988
Capsular
incisions, 915
ligament, 910
plication, 967
Capsule, 910
Capsulitis, 1025
Capsulorrhaphy, 967
Captopril, 668
Carbamazepine, 816
Carbatrol, 816
Carbenicillin, 153
Carbogen, 668
Carboxymethyl cellulose, 667
Carcinomatous ulcer, 23, 24
Cardboard-like consistency, 548
Cardiac arrest, 128, 133, 140, 144, 145
Cardiac arrhythmias, 1096
Cardiac emergencies, 133
Cardiopulmonary resuscitation (CPR), 125, 126
Caries, 666, 667
Carisoprodol, 172
Carnoy's solution, 594
β-Carotene, 666
Carotid artery, 654
Carotid bifurcation, 643
Carotid body tumour, 25
Carotid space infection, 549
Cartwheel, 650
Catalase test, 71
Catgut suture material, 319
Cat's paw retractor, 250, 261
Cauliflower-like mass, 624
Causalgia, 790
Cavernous lymphatic spaces, 615
Cavernous sinus thrombosis, 523, 719
Cawood and Howell classification, 444, 485
residual ridge resorption, 444
CBCT, See Cone beam CT (CBCT)
CCD (charged coupled device), 44
CCG, See Costochondral graft (CCG)
CD4 T cell counts, 119
Ceftabiprole, 174
Celecoxib, 668
Cell rests of Malassez, 578, 605, 618
Cell rests of Serres, 618
Cellulitis, 24, 120, 151, 154, 383, 423, 522
Cementifying fibroma, 633
Cementoma, 627
Cemento-ossifying fibroma, 633
Cement-retained fixed bridge, 499, 504
Central giant cell granuloma, 638
Central giant cell lesions, 638
Centrally acting analgesics, 163
Centrally acting muscle relaxant, 240
Central odontogenic fibroma, 626
Central or fusiform neuroma, 792
Central (endosteal) osteomas, 632
Cephaloceles, 714
Cephalometric
analysis, 835
Cephalosporins, 60, 73, 114, 153
Cephalosporins-ceftaroline, 174
Ceramic implants, 484
Cerebellar artery, 812
Cerebral abscess, 549
Cerebrospinal fluid (CSF), 729, 817, 818, 978
leak, 729, 730, 980, 1005
rhinorrhoea, 17, 978–980, 1069, 1070
scintigraphy, 1132
Cervical cord injury, 976
Cervical ranula, 692
Cervical spine fracture, 976
Cervical spine X-ray, 218
Cevimeline, 697
Champy's line of osteosynthesis, 996
Channel retractor, 250, 262
Cheatle forceps container, 250
Cheatle sterilizer forceps, 250
Checkerboard pattern, 650
Cheek retractor, 250
Cheilitis, 17
Cheiloplasty, 757
Chemical capsulorrhaphy, 965
Chemical cauterisation, 627
Chemical markers, 1131
Chemiclaving, 289
Chemiluminescence, 33, 93
Chemoprevention, 669
Chemosis, 522
Chemotactic factor, 1155
Chemotherapy, 650, 668–669
Cherry blossom, 679
Cherubism, 637, 638
Chest compression, 126
Chest X-ray, 217
Chick-Martin test, 293
Chin asymmetry, 831
Chin deviation, 824
Chinese characters trabeculae, 636
Chin implants, 869
Chin lift manoeuvre, 128
Chin ptosis, 869
Chin to throat angle, 831
Chin vertically long, retruded, 829
Chisel, 266
Chitosan, 881
Chlorhexidine, 686
Chlorpromazine, 668
Chlorzoxazone, 172
Chocking effect, 547
Choking capillary network, 567
Cholesterol crystals, 585, 600
Cholinergics, 69
Chondrodiastasis, 883
Chondroid, 700
Chondroitin sulphate, 600
Chondroma, 26, 812, 922
Chondrosarcoma, 922, 934
Chorda tympani, 797, 820
nerve, 675, 909, 913
Christmas disease, 66, 112
Chronic dislocation, 964, 965
Chronic maxillary sinusitis, 715, 718
Chronic obstructive pulmonary disease, 107
Chronic oroantral fistula, 724
Chronic sinusitis, 729
Chronic suppurative osteomyelitis, 558
Chryseobacterium, 299
Cicatricial pemphigoid, 30
Cieszynski's rule of isometry, 34
Ciliary ganglion, 1096
Ciliated epithelium, 727
Ciprofloxacin, 148, 151
Circle system, 224
Circulation, 975
Circumferential wiring, 992
Circumorbital oedema, 15, 17
Circumzygomatic technique, 470, 992
Cladosporium, 299
Clark shift, 391
Clark's technique, 471
tube shift technique, 414
Classification
ankylosis, 945
bone, 442
condylar fracture, 1045
cystic, 578, 607
diseases of maxillary sinus, 715
disorders of nerve, 793
distraction, 881
impacted maxillary canines, 415
impacted maxillary third molars, 408
impaction, 385
implants, 479
intraoral surgical flap, 307
laser, 1166
mandibular fracture, 1025
maxillary fractures, 1063
maxillary sinusitis, 715
neoplastic, 607
odontogenic tumours, 618
odontome associated type, 607
oral and facial clefts, 736
orbital cellulitis, 522
salivary gland diseases, 684, 685
shock, 341
simple, 607
suture material, 318, 319
TMJ disorders, 922
zygomatic fracture, 1085
Class III skeletal malocclusion, 752
Clavulanic acid, 153, 528
Clear cells, 605
CLED (cysteine lactose electrolyte deficient), 72
Cleft lip, 10, 263, 598, 732, 733, 734, 749, 750
blind pits, 733
first branchial arch, 734
His' theory, 733
neuromeric theory (Michael Carstens), 734
prolabium, 734
signalling molecules, 734
sonic hedgehog (Shh), 734
Stark theory, 733
transforming growth factor beta (TGFb), 734
tumour necrosis factor (TNF), 734
Cleft muscle, 751
Cleft palate, 10, 598, 732, 734, 736, 747, 751
raspatory, 250
Cleft rehabilitation, 752
Clicking, 939
sound, 961
Clindamycin, 60, 106–108, 122, 155
Clinical stages according to ‘T’ and ‘N’ status, 655
Cloacae, 557
Clodronate, 567
Clonazepam, 816
Closed condylotomy, 968
Closed lock, 924
Closed submucous vestibuloplasty, 469
Clostridium perfringens, 71
Closure of fistula, 719
Clotrimazole, 159
Clotting factors, 63, 66
Clotting time (CT), 63, 64
Clover leaf skull, 15
Co-agglutination test, 76
Coagulation, 334, 335
cascade, 334, 335
factors, 65
profile, 32, 58, 63–66
screening, 218
COC, See Calcifying odontogenic cyst (COC)
Codeine, 165
Codman's tumour, 922
CO2 lasers, 1167
Cold, 791
hypothesis, 799
nodule, 702
spot, 52
Collagen, types, 1155
Collagen (plain and chromic), 318
Collagenous-resistant glycoprotein, 1003
Collateral ligaments, 910
Coloboma, 15, 598, 742, 749
Columella, 741
absence of, 741
lengthening, 760
Commando operation, 654
Comminuted fractures, 993, 1004, 1029, 1039
Comminution
alveolar socket, 1017
tooth socket, 1017
Common peroneal nerve, 805
Compensable loss/injury, 1144
Complementary metal oxide semiconductor (CMOS) sensor, 44
Complement fixation (CF) test, 77, 79
Complete blood count, 32
Complete cleft lip, 732
Complex odontoma, 624
Complications
bone healing, 1004
hyperparathyroidism, 1004
osteoporosis, 1004
Paget's disease, 1004
drains, 346
extraction, 368
tracheal intubation, 231
Compliment fixation test, 77
Composite odontoma, 623
Composite skin grafts, 315
Compound odontoma, 603, 625
Compression
osteosynthesis, 997, 998
plates, 998
syndrome hypothesis, 812
Computed tomography (CT), 32, 44, 52, 526, 667, 677, 679, 681, 683
Concave facial profile, 825, 829
Concussion, 1016
Conduction block, 795
Condylar agenesis, 922
Condylar aplasia, 922
Condylar dislocation, 373, 374, 936, 963
anterior, based on position, 963
Condylar erosion, 935
Condylar fractures, 922, 978, 982, 1028, 1045, 1046, 1048, 1050–1052
aetiology, 1045
classification, 1045
Lindahl classification, 1046
bilateral condylar, 1046
deviated condylar fragment, 1047
displaced condylar fracture, 1047
fracture level, 1046
subcondylar fracture, 1047
undisplaced condylar neck fracture, 1047
MacLennan system, 1045
Wassmund's classification, 1045
clinical features of
bilateral condylar fractures, 1050
unilateral condylar fractures, 1048–1050
complications, 1055
ankylosis of the temporomandibular joint, 1055
investigations, 1050
reverse Townes, 1050
transcranial lateral, 1050
management, 1051
closed technique, 1052
open reduction and internal fixation, 1053
parade ground fracture, 1045
Zide and Kent's absolute and relative indications, 1055
Condylar hyperplasia, 52, 824, 922, 926
Condylar hypoplasia, 922, 930
Condylectomy, 941, 951
Condyloplasty, 930
Condylotomy, 929, 930, 941, 965, 968
Cone beam CT (CBCT), 32, 48, 49
Congenital coagulation defects, 110
Congenital deformities, 732
Congenital epulis, 25
Congenital scar, 737
Congenital strictures, 693
Congenital syphilis, 382
Congestive heart failure, 104
Conjunctivitis, 27
Conscious sedation, 243
Consent-contract between doctor and patient, 1145
informed consent, 1145
Conservative enucleation, 605
Conservative excision, 623
Contact carrier, 296
Contact healing, 1002
bone metabolising unit, 1002
cutter cones, 1002
Haversian remodeling, 1002
osteonal remodeling, 1002
Contraceptives, 60, 63, 65, 68, 69
Contrast, 818
agents used for sialography, 679
medium, 584
radiography, 55
studies, 584
Contusion, 794, 1007
Convalescent carrier, 296
Conventional
cutting, 323
fractionation, 565
multicystic/solid ameloblastoma, 619
Convex profile, 825
COPD, See Chronic obstructive pulmonary disease
Copper malleable retractor, 250
Core needle biopsy-Trucut biopsy, 86
Corneal reflex, 800
Coronal approach, 915
Corrugated rubber drain, 344
Corrugators supercilii, 798
Cortical block grafts, 1150
Cortical bone screw fixation, 989
Cortical trephination, 423
Corticosteroid, 124, 139, 140, 165
Corticotomy, 841, 843, 878
Corynebacterium, 521
Corynebacterium diphtheriae, 71, 72
Costochondral graft (CCG), 933
fate of, 954
Costochondral junction, 953
Cotton wool appearance, 559, 639
Counter-torque ratchet technique (CTRT), 506
Cover screw, 494
Cow horn forceps, 364
Coxiella burnetii, 287
Coxsackie A, 693
CPR, See Cardiopulmonary resuscitation (CPR)
Cracked pot sound, 1065, 1070
Cracked tooth, 815
Cranialisation, 1126, 1137
Cranial nerve (CN) VII palsy, 801
Craniocarpotarsal dysplasia, 934
Craniofacial distraction, 881, 886
Craniofacial internal distractor, 903
Craniofacial microsomia, 931, 932
Craniomandibular fixation, 992, 1074
Craniomaxillary fixation, 1074
Craniopharyngioma, 619
Craniosynostosis, 262
Crater-like ulcer, 646
Craze lines, 1015
C-reactive protein, 106
Creatinine clearance, 67
Crenate like shapes (Liesegang rings), 622
Crepitations on palpation, 1019
Crestal approach, 463
Crestal incision, 498
Crest module, 494
Cricothyroid notch, 643
Crile's neck dissection, 654
Crime and penal code, 1144
Crossbar, 358
elevators, 359
Cross-facial anastomosis, 806
Cross facial nerve grafting, 805
Cross infection, 296
Crouzon's syndrome, 17, 713, 903
Crown infraction, 1015
Crusts, 729
Cryosurgery, 340
Cryotherapy, 594, 597, 816
CSF rhinorrhoea, 1130
bedside tests, 1130
chemical markers, 1131
CSF fluid, 1130
halo test, 1130
imaging studies, 1131
management, 1131
starch test, 1130
tramline effect, 1130
CT, See also Computed tomography (CT)
CT cisternography, 1131, 1132
CT sialography, 681
Culture and sensitivity test, 32, 724
Culture media, 72
Cupar's anterior maxillary osteotomy, 847
Cupid's bow, 755
Cupped ears, 15
Curettage, 422, 594, 655
Curtain sign, 700
Curved needle, 323
Curve of occlusion, 839
Curve of Spee, 825, 834
Curve of Wilson, 833
Cushing disorder, 444
Cushing's syndrome, 98
Cutaneous wart, 26
Cyclic AMP pathway, 675
Cyclic neutropaenia, 27
Cyclobenzaprine, 172
Cyclophosphamide, 650, 669, 935
Cylinder type implant, 486
Cylindroma, 704
Cyst, 578, 691
aspirates, 585
daughter, 599
dentigerous, 27
dermoid/epidermoid, 25, 585, 615
development of, 578
enlargement, 578
eruption, 605
extravasation, 612
fissural, 585, 608
follicular, 602
formation, 578
glandular odontogenic, 606
globulomaxillary, 608
haemorrhagic, 612
idiopathic, 612
infected, 585
initiation, 578
median mandibular, 610
median palatal (palatine), 609
mucous extravasation, 614
nasopalatine duct, 609
nonodontogenic fissural, 608
paradental, 612
regression, 581
sebaceous, 26
Stafne's bone, 27
static bone, 613
tract, 615
true, 578
Cystectomy, 587, 592
Cystic
degeneration, 726
hygroma, 25, 615
Cytodifferentiation, 672
Cytokines, 581, 888
Cytological biopsy, 32
Cytology, 88
Cytomegalovirus, 78, 119, 693, 697
Cytopathology, 82
D
Dacron, 321, 322, 328
Dacryocystorhinostomy (DCR), 729
Dalfopristin-quinupristin, 174
Danger area of face, 551
Danger space, 547
Daptomycin, 174
Dark ground microscopy, 70
Davis and Richie classification, 736
DC4 Tweed's method, 367
Dean's intraseptal primary alveoloplasty, 458
Decompression, 587
Decortication, 559, 560, 561
Deep bite, 828
Deep brain stimulation, 819
Degeneration, 793, 795
Degenerative joint disease, 934
Degree of keratinisation, 646
Degree of skeletal convexity, 836
Degree of voluntary movement in facial paralysis, 801
Dehiscence, 510
Delaire technique, 757, 758
Delayed extraction, 375
Delayed union, 878, 1006
Demyelination, 813
Denker operation, 726
Denosumab, 572
Dense fibrous capsule, 623
Dense sclerosis, 649
Dental implant, 478–516
Dental infection, 815
Dental model analysis, 838
arch length, 838
arch width analysis, 838
Bolton's analysis, 838
orthognathic analysis, 838
overbite and overjet relationship, 839
tooth arch symmetry, 839
tooth size analysis, 838
Denta scan, 32
Dentigerous cyst, 27, 585
Dentist act, 4
Dentoalveolar abscess, 520, 522, 548
Dentoalveolar fracture, 1011
Andreasen/WHO classification, 1014
Ellis and Davey's classification, 1013
WHO classification, 1014
management, 1019
avulsed tooth, 1019
extraoral storage media, 1020
splinting of teeth, 1021
Dentoalveolar injuries, 1012
Dentofacial deformities, 824, 874
Angle Class II, 824
Angle Class III, 824
Denture, 724
fibrosis, 474–475
granuloma, 474
Deoxycholate citrate agar, 72
Depolarising muscle relaxants, 241
Depolarizing block, 240
Derangement of occlusion, 1019
Dercum's disease, 25
Dermal hypersensitivity, 78
Dermatocele, 746
Desmoplasia, 82
Desmopressin, 111–113, 115, 335
Desmopressin (deamino-8-D arginine vasopressin) (DDAVP), 108
Developmental defects, 922
Deviated jaw/chin, 824
Devitalisation of teeth, 845
Dewel's method, 367
Dexamethasone, 651
Diabetes, 11, 12, 23, 61, 69, 73, 99, 108
Diabetes mellitus, 99
Diabetic ketoacidosis, 69, 100, 145, 351
Diagnosis, and treatment planning, 829
model surgery, 842
Diagnostic criteria proposed by IHS (International Headache Society), 814
Diagnostic fluid, 683
Diagnostic injection, 814
Diathermy, 103, 251, 281, 338
Diatrizoate, 679
Diazepam, 103, 108, 109, 114, 124, 125, 136
Diethyl ether, 238
Difficult intubation, 216, 228, 230
Diffuse sclerosing osteomyelitis, 559
Digastric, 643, 797
groove, 700
muscle, 797
nerve, 797
Digital imaging, 44
Dilaceration, 382
Dilantin, 816
Dilute H2O2 rinses, 666
Diluting agents, 666
Dingman and Natvig classification, 1025
Dingman, designed mouth gag, 275, 965
Dingman's modified preauricular incisions, 915
Diphenhydramine, 124, 169
HCl, 666
Diplopia, 206, 208, 713, 730, 816, 1094
binocular, 1094
chart, 1094
monocular, 1094
test for, 1094
binocular single vision, 1094, 1095
diplopia chart, 1094
finger gaze, 1094
Lees screen, 1094
traction test, 1094
Direct brain injury, 730
Direct dental wiring, 985
Gilmer wiring, 985
Risdon's wiring, 985
Direct fixation (internal fixation), 994
compression plates, 994
lag screws, 994
noncompression miniplates, 994, 995
reconstruction plate, 994
semirigid fixation, 994
transosseous wiring, 994, 995
Direct immunofluorescence, 77, 91, 92
Direct interdental wiring, 985, 1022
Disarticulation, 563
Disc (hypermobility), 924
Disc diffusion susceptibility test, 74
Discomalleolar ligament, 908, 910
Disc repositioning, 941
Diseases affecting maxillary sinus
classification, 715
Disinfectant, 284, 291, 293
Dislocation, 922
acute/chronic/recurrent (habitual), 922
of condyle, 373
Disorders arising, structures outside joints, 922
Disposal of wastes, 302
Dissecting forceps, 250, 256
Distant metastasis, 629
Distraction
epiphysiolysis, 883
histiogenesis, 932
osteogenesis, 456, 457, 657, 659, 753, 780
period, 881, 889
phase, 888
screw, 883, 884
Distractor device, 776, 782, 883
DLX-2, 748
DNA gene probes, 75
Dog ear formation, 306
Dolorosa, 819
Dolour, 527
Dome-shaped, 691, 692
appearance of pseudocysts, 614
Dorsal root entry zone (DREZ) lesions, 819
Doxorubicin, 651, 669
Doxycycline, 151
Drain placement, 423
Dressings, 173
Driven-snow appearance, 622
Drug holiday, 572
Dry heat, 285
Dry mouth, 697
Dry socket, 375
aetiopathogenesis for, 375, 523
Dual degree qualification, 6
Dual-energy X-ray absorptiometry (DEXA) scan, 32, 54
Ductal papillomas, 703
Ducts of Rivinus, 540, 675
Duct strictures, 683
Duke's method, 64
Dumb-bell tumour of parotid, 700
Dupuy syndrome, 707
Duty of care, 1145
Dwarfed teeth, 625
Dyclonine HCl, 666
Dyke-Davidoff-Masson syndrome, 931, 932
Dynamic
compression plates, 998
bicortical screws, 999
compression screw, 999
plate bending, 999
static/passive screw, 999
imaging, 52
Dysaesthesia, 790
Dysphagia, 703
Dysplasia, 82
Dysrhythmia, 102
Dystrophy, 813
E
Eagleton criteria, 552
Ear infection, 752
Early failure, 506
Early loading, 484
Early subperiosteal implant, 480
Early transosteal implants, 480
Ecchymosis, 10, 29, 978, 1034, 1036, 1048
Echocardiogram (ECG), 106, 213, 216
Ectomesenchyme/mesenchyme, 618
Ectopic bone formation, 1159
Ectopic/displaced teeth, 380
Ectopic tooth, 380
Ectropion, 1108
Edentulous mandibles, 1041, 1056
fracture-bucket handle displacement, 1057
Egg shell crackling, 580, 582
Ehlers-Danlos syndrome, 964
E7 inactivates the retinoblastoma protein pRb, 644
Electrical or thermal vitality tests, 1019
Electrical stimulation, 819
Electric shock, 808
Electrocautery, 281, 338, 339
Electromyography (EMG), 925
Electron microscopy, 70
Electron therapy, 657
Electrophysiologic tests, 801
Electrosurgical scalpel, 383
Elevator, 357, 359
muscle, contracture of, 922
ELISA (Enzyme-linked immunosorbent assay), 76, 77, 118
Emergency
drugs, 124
equipment, 124
management, 125
Eminectomy, 967, 968
Emissary vein, 552
EMLA cream, 221
Emphysema, 568, 978, 1067
Emptying phase, 679
Enalapril, 668
Enamel organ, 623
En-block resection, 656
Encapsulated gland, 703
Encephalocele, 15
Endaural approach, 915, 917
Endocarditis prophylaxis, 156, 158
Endochondral mechanism, 908
Endocrinal theory, 382
Endodontic, 484
implants, 441
microsurgery, 442
Endogenous
compensatory mechanism, 341
infection, 296
nucleus, 728
Endoscopy, 728, 1178
biopsy, 93
cauterise, 1179
dacryocystorhinostomy, 730
fibre optic intubation, 1179
foreign bodies, 1179
orbital decompression, 730
sialoendoscopy, 1179
Endosseous implants, 484, 1150
Endosteal
dental implant, 479
implant, 441, 479
osteomas, 633
Endothelial myeloma, 648
Endotracheal tube, 250
Enophthalmos, 15, 1093, 1096, 1106, 1108
Entropion, 1108
Entubulation (conduit) repair, materials for, 804
Enucleation, 427, 587, 592, 703
Envelope flap, 309, 310, 404
Envelope of discrepancy, 824
Enzyme-linked immunosorbent assay (ELISA), 77, 118
Enzyme profile, 71
Eosinophilic masses, 622
Eosinophils, 58, 61, 62, 702
Ephedrine, 724
Ephedrine sulphate, 717
Epicanthus fold management, 1124
Epidermolysis bullosa, 30
Epilepsy, 137
Epimyoepithelial islands, 696
Epinephrine, 103–105, 107, 110, 124, 141
Epineurium, 790
Epiphora, 1005, 1067, 1070, 1076, 1108, 1109
lid tightening procedure, 1005
posttraumatic ectropion, 1005
Epistaxis, 17, 111, 113, 332, 727, 729, 976
Epithelial remnants, 579
Epithelial rests of Malassez, 622
Epithelial seam, 734
Epker's anterior maxillary osteotomy, 843
Eposteal dental implant, 479
E6, promote degradation of p53, 644
Epstein- Barr virus (EBV), 122, 642, 644, 696
Epstein's pearl, 10, 606
Epulis, 650
fissuratum, 474–475
Erbium lasers, 1166, 1169
Erb's point, 655
Erosion, 935
Erythema, 717
multiforme, 28
Erythrocyte sedimentation rate (ESR), 32, 58, 61–63
Erythromycin, 717
Etanidazole, 668
Ether, 165, 173, 174, 238, 723
Ethinamate, 172
Ethmoidal air cells, 1126
Ethmoido-frontosphenoidectomy, 729
Etidronate, 640
Eustachian tube, 752
Evolution of theories of cleft embryo pathogenesis, 733
Ewing's sarcoma, 648
Exanthemas, 78
Exarticulation, 1016, 1017
Excision, 638
biopsy, 33, 84, 85, 87, 89, 90
Exfoliative cytology, 32, 89
Exodontia, 350–377
Exogenous
calcitonin, 638
infection, 296
material, 728
Exophthalmos, 15, 17, 110, 552
Exophytic, 644
mass, 646
Exostosis, 460
Extended osteotomy, 863
External
carotid artery, 673
haemorrhage, 332
pin fixation, 992, 993
External pin fixation, 992
craniomandibular fixation, 992
craniomaxillary fixation, 992
External reduction devices, 983
Asch forceps, 983
Hayton William forceps, 983
Rowe's disimpaction forceps, 983
Walsham forceps, 983
Extra-articular origin, 922
Extracapsular fracture, 922
Extraction forceps, 357
Extraction of teeth, techniques, 354
closed/intra-alveolar, 354
open/transalveolar, 354
Extranasal splinting, 1116
Extraoral
incision, 312
storage media, 1020
traction, 984
vertical ramus osteotomy, 857
Extraosseous, 607
lesions, 650
odontogenic fibroma, 627
Extrapyramidal reaction (facial dyskinesia), 934
Extrinsic disorder, 922
Extrusive luxation, 1015, 1016
Eyed needles, 324
Eyeless (swaged) needles, 324
Eyelet wiring, 985
Eyes intercanthal distance, 831
F
Face-lift incision, 807
Face masks, 225, 250, 253
Facial aesthetics, 831
analysis, 831
Facial arthromyalgia, 936
Facial asymmetry, 824, 869
Facial canal, 797
Facial clefting, 870
Facial divergence, 831
anterior, 831
posterior, 831
Facial gigantism, 930
Facial nerve, 681, 700, 703
anatomy of, 796
branches, 797
course of, 796
paralysis, 208, 798
pathology, 796
Facial numbness, 818
Facial palsy, 15, 699, 798
Facial paresis, 819
Facial profile, 15, 831
Facial reanimation, 803, 806
Facial twitching, 799
Facial weakness, 799
Faciovenous plane of Patey, 674
Fallopian canal, 802
False ankylosis, 958
Fascia, 532
Fascicles, 791
Fasciculation, 801
Father of distraction, 878
Fatty change, 681
Favourable fractures, 1029, 1030, 1039
Feeding plate, 753
Femoral-facial syndrome, 931, 932
Fenestration, 510
Fentanyl, 151, 220, 232, 244
Ferguson mouth gag, 275
Ferric sulphate solution, 425
FESS, See Functional endoscopic sinus surgery (FESS)
Fibre optic cable, 1166
Fibrillation, 817
Fibrin foam, 374
Fibrin glue, 338
Fibrinolytic alveolitis, 375
Fibrinolytic osteitis, 375
Fibrin sponge, 338
Fibrodysplasia ossificans progressiva, 934
Fibro-osseous integration, 481
Fibro-osseous lesions, 633
Fibro-osseous neoplasms, 633
Fibrosarcoma, 922
Fibrous ankylosis/scleroderma, 924
Fibrous capsule, 607, 628
Fibrous dysplasia, 10, 633, 635
Fibrous encapsulation, 1155
Fibrous epulis, 626
Fidaxomicin, 174
Field and Ackerman classification, 415
Field block, 184
Field cancerisation, 644
Field of radiation, 666
Figure of eight suture, 328
Filling phase, 679
Filtration, 289
Finck's technique, 965
Fine-needle aspiration biopsy (FNAB), 90
Fine-needle aspiration cytology (FNAC), 33, 84–86, 90, 684, 699, 703, 706
Finger gaze test, 1094
First branchial arch syndrome, 931
Fischer 1-2-3 technique, 199
Fissure, 10
Fistula, 10, 717
Fistulous tract, 732
Fixation, 847–849, 851
osteosynthesis, 997, 1001
Fixation osteosynthesis, 1001
locking plates, 1001
reconstruction plates, 1001
Thorp (titanium hollow screw osseointegrated reconstruction plate), 1001
Fixation plates, 883
Flap composition, based on, 315
Flap design, 306
Flap location, 314
Flap reflection, 311
Flaps configuration, 314
Flash pasteurisation method, 287
Flavobacterium, 299
Flexible fibreoptic endoscope, 252
Flexometallic (spiral embedded) tube, 254
Floating maxilla, 1064
Flocculation test, 77
Floor of mouth, 615
Florid cemento-osseous dysplasia, 633
Fluconazole, 121, 160
Fluorescence microscopy, 70, 92
Fluoride, 676, 686
Fluorodeoxyuridine, 668
Fluoroquinolones, 156
5-Fluorouracil, 668, 669
FNAB, See Fine-needle aspiration biopsy (FNAB)
FNAC, See Fine-needle aspiration cytology (FNAC)
Foam cells, 585
Focal cemento-osseous dysplasia, 633
Focal infection, 296
Focal nodular thickenings, 605
Focal sclerosing osteomyelitis, 559
Foci of infection, 350
Focused injury, 819
Fogarty catheter, 818
Foley's catheter, 278
Folic acid, 748
Follicular type features, 619
Foot control, 339
Foot plates, 883
Foramen caecum, 615
Foramen lacerum, 818
Foramina of Breschet, 1126
Forceps, 250, 251, 255–259, 265, 267, 269
Fordyce granules, 30
Forehead flap, 657
Foreign bodies, 687, 727
aspiration, 141
removal, 729
Formaldehyde, 292, 293
Four-point fixation, 1103
Fovea ethmoidalis, 980
Fractionation, 661
Fracture, 922
alveolar process, 1017
alveolus, 370, 1019
angle, 1036
body, 1036
coronoid, 974
process, 1026, 1036
crown en masse, 1013
deciduous teeth, 1013
displacement, 980, 997, 1045
healing, 878, 880, 888, 889, 1002
mandible, zygomatic or temporal bones, 934
ramus, 1036
symphysis, 1036
tuberosity, 370
Fracture reduction, 983
Fractures of mandible, 1023
approaches to mandible, 1041
biomechanics of, 1026
Champy's lines of osteosynthesis, 1040
classification of, 1025
Dingman and Natvig anatomic classification, 1025
clinical features of, 1036
clinical findings, 1031
Coleman sign, 1036
extraoral examination, 1031
facial deformity from, 1034
favourable/unfavourable fractures, 1030
fracture line, 1044
horizontally favourable and horizontally unfavourable, 1031
indirect sign of fracture-swelling and laceration, 1033
parasymphysis favourable and unfavourable fracture, 1031
ramus fracture, 1039
surgical approaches for management, 1041
intraoral approach to
angle, 1042
symphysis, 1042
intraoral vestibular approach, 1041
Langer's line or relaxed skin tension lines (RSTL), 1041
open reduction internal fixation (ORIF), 1043, 1044
posterior vestibular approach, 1041
preauricular approach, 1042
retromandibular approaches, 1042
submandibular approach, 1042
submental approach, 1042
types of fracture, 1029
atrophic, 1029
comminuted, 1029
complex, 1029
compound, 1029
greenstick, 1029
impacted, 1029
indirect, 1029
pathological, 1029
simple, 1029
types of reduction, 1039
closed, 1039
open, 1039
unfavourable fracture, 1032
Frankfort horizontal (FH) plane, 829
Frankfort mandibular plane angle, 829
Frankfort plane, 835
Frank technique, 391
Free tissue flap, 313
Frenectomy, 465
Frey syndrome, 707
Frictional hyperkeratosis, 30
Friedman classification, 740
Frontal bone, 1126–1140
Frontal bone fractures
applied anatomy, 1127
cerebrospinal fluid (CSF) rhinorrhoea, 1127
mucocoele, 1127
complications, 1137
CSF leak, 1138
brain abscess, 1140
CSF fistula, 1140
frontal bone osteomyelitis, 1140
frontal contour defect, 1140
mucocele, 1140
lumbar puncture, 1139
ICP (intracranial pressure), 1139
meningitis, 1138
signs of, 1139
pneumocephalus, 1139
Ball-valve mechanism, 1139
inverted bottle mechanism, 1139
cranialisation, 1137
indications, 1137
technique, 1137
management, 1132
frontal sinus cranialisation, 1132
frontal sinus obliteration, 1132
surgical approaches, 1132
Frontal recess, 1127
Frontal sinus, 1127
Frontal sinus fractures
displaced, management of, 1135
Frontal sinus injury
biomechanics of, 1127
CT scan
Frontal suspension, 989
Frontal view analysis, 831
Frontonasal duct, 1127
Frontonasal process, 735
Frontozygomatic cleft, 746
Frozen section, 33, 93
biopsy, 33
Fulguration, 340
Full occlusal splint, 940
Full thickness (Wolfe) skin graft, 315, 316
Functional endoscopic sinus surgery (FESS), 728
Functional ligaments, 910
Functional orthognathic treatment, 777
Functional problems, 666
Functional repair, 757
Functions of saliva, 676
Fungal concretions, 714
Fungal infection, 121
Furlow double opposing Z plasty, 763
Furlow double Z plasty, 766
Fuse, 797
Fusobacterium, 151, 152, 155, 521
G
Gabapentin, 816
Gadolinium, 682
Gamma camera, 51
Gamma glutamyl transferase (GGT), 67–70
Gamma knife, 818
Ganglion procedure, 815, 816
Gap arthroplasty, 951
Gap healing, 1002
Haversian canals, 1002
lamellar bundles, 1002
Gardner's mallet, 267
Gardner's syndrome, 633
Garre's osteomyelitis, 557
Garre's periostitis ossificans, 557
Gas, 293
Gastroesophageal reflux disease, 684
Gate control theory, 941
Gauze drain, 344
Gelatin liquefaction test, 71
Gelfoam, 337, 374
absorbable collagen, 425
General anaesthesia (GA), 212–243
for extraction, 354
Generalised viraemia, 695
Genetic aberrations, 747
Genial asymmetry, 828
Genial deficiency, 827
Genial excess, 827
Genial tubercle reduction, 451
Geniculate ganglion, 797
Geniculate neuralgia (GN), 819
Geniohyoid muscles, 615, 1029
Genioplasty, 860, 866–868
based on time frame, 876
complications, 875
different techniques of, 866–869
vertical reduction, 867
GGT, See Gamma glutamyl transferase (GGT)
Giant cell reparative granuloma, 638
Giant cell tumour, 639
Giant rhinoliths, 728
Gigli saw, 270, 965
Gillie's approach, 312, 1100
Gillie's needle holder, 260
Gillie's temporal fossa approach, 1100
Gingival cyst, 585
adult, 605
newborn, 606
Gingival fibromatosis, 22
Gingivoperiosteoplasty, 771
Ginglymoarthrodial synovial joint, 908
Glabella, 742
Glasgow coma scale, 976
Glass bead steriliser, 291
Glenoid fossa, 563, 673, 908, 909
Glenotemporal osteotomy, 968
Globe injuries, 1005
transconjunctival approach, 1005
Glossopharyngeal neuralgia, 793, 819
Glutaraldehyde, 285, 292, 297, 298
Glutathione, 668
Glycerine, 383
Glycerol, 817
injection, 816, 817
Glyceryl trinitrate, 104
Glycogen-rich clear cells, 605
Glycoproteins, 676
GN, See Geniculate neuralgia (GN)
GNAS I (guanine nucleotide-binding protein, alpha-stimulating activity
polypeptide I) gene, 635
Gnathion, 39, 836
Godwin's technique, 471
Goggles, 802
Goldenhar-Gorlin syndrome, 932
Goldenhar syndrome, 17, 746
Golden hour of trauma, 974
Goldman fox, 256
Goldman index, 218
Gonorrhoea, 27
Gorlin-Goltz syndrome, 648
Gorlin's syndrome, 598, 749
Gouge, 726
Gow-Gates techniques, 200
Gracilis muscle, 808, 809
flap, 809
Grafting vestibuloplasty, 470
Graft neurorrhaphy, 803
Gram-negative bacilli, 666
Grand mal, 144
Granny knot, 328
Granular cell type, 619
Greater auricular nerve, 707, 804
Greater palatine nerve, 183
block, 186, 191
Greater petrosal nerve, 797
Griseofulvin, 148
Grodinsky and Holyoke classification, 534–535
Ground glass, 636
appearance, 626
Growth, 10
centre transplantation, 932
completion, 825
modification, 843
Grummon's frontal cephalometric analysis, 873
frontal posteroanterior (PA), 873
Gs alpha membrane associated protein, 635
Guedel airway, 253
Guedel blade, 250
Guided biopsy technique, 683
Guided nerve regeneration, 803
Guided tissue regeneration, 432, 804
Gummatous ulcer, 24
Gumps, 948
Gunning splint, 988
Gustatory stimuli, 707, 813
Gustatory sweating syndrome, 707
H
Habitual dislocation, 964
Haemagglutination inhibition (HI) test, 79
Haemangioma, 10, 13–17, 22, 23, 25, 26–28
Haemarthrosis, 110, 922
Haematocrit, 60
Haematological
diseases, 110
investigations, 58
profile, 333
Haematoma, 11, 25, 111–113, 143, 207, 727
in joint/muscle of mastication, 934
in maxillary sinus, 727
Hemifacial microsomia, 869, 880, 934
Hemimandibular
elongation, 827, 922
hyperplasia, 870, 922
Haemoglobin (Hb), 58
Haemophilia, 10–11, 65
haemophilia A, 110
haemophilia B, 112
Haemophilus, 106, 153, 521
Haemophilus influenzae, 716
Haemorrhage, 17, 143, 207, 209, 222, 332
disorders, 133
Haemostasis, 333–336, 424, 729
Haemostat, 258, 336
Haemostatic agents, 425
Hairy naevus, 16
Hairy tongue, 30
Halitosis, 375, 527, 716, 717, 764
Haloframes, 993
Halofuginone, 668
Halogens, 293
Halo test, 1130, 1138
Halothane, 99, 102, 107, 114, 236
Halstead approach, 197
Hamartoma, 622
Hamulus, 751
Hand foot and mouth disease, 30
Hand scrub technique, 294
Hangman's noose, 547
Hanhart syndrome, 894
Hanks' balanced salt solution (HBSS), 441
Hard palate, 460, 606, 609, 632, 657, 695, 751
Hard tissue
handling instrument, 266
landmarks on cephalograph, 836
Hawley's bite plane, 940
Hayton-William forceps, 251, 271, 983, 1074
Hazards, 818
HBO therapy, 568
HBSS, See Hanks' balanced salt solution (HBSS)
3 ‘H’ concept, 565
Head and neck squamous cell carcinoma (HNSCC), 642
Head gears, 754, 777, 785
Healed nerve, 794
Healing
abutment, 494
of bone graft, 1150
index, 878
lip injury, 1018
ulcer, 24
Healthy carrier, 296
Heamangioma, 585
Hearing impairment, 800
Heat, 285
Hedgehog signalling pathway, 600
Heinz-Ehrlich bodies, 59
Heister mouth gag, 275
Hemifacial atrophy, 13–14
Hemifacial microsomia, 11
Hemimandibular elongation, 927
Hemimandibular hyperplasia, 871, 928
Hemi maxillectomy, 699
Hemiplegia, 801
Hemirhinia, 15
Hemostatic forceps, 258
Hemovac, 345
drain, 280
Henderson's classification, zygomatic arch fractures, 1088
Hendrickson classification, palatal fracture, 1068
HEPA-filter, 293
Hepatitis A, 78
Hepatitis B, 78, 120, 301, 642
Hepatitis C, 78, 301
Hepatitis D, 78
Hepatitis test, 32
Hereditary benign intra-epithelial dyskeratosis, 30
Hermetic seal, 1137
Herpangina, 30
Herpes simplex virus (HSV), 29, 799, 813
antibodies, 799
Herpes zoster oticus, 798
Herpetic ulcer, 24
Herpetiformis dermatitis, 30
Hess diplopia test, 1094
Hess test, 64, 115
Heterotopic epithelium, 619
Hexachlorophene detergents, 294
HHV-8, 644
Hiatus of the mylohyoid muscle, 692
Hiatus semilunaris, 711
High-grade tumours, 647
Highly convex profile, 948
High-speed burs, 507
High-vaulted, 742
Hills and Valleys ridge, 445
Hilton's law, 913
Hilton's method of drainage, 528
Hilton's operation, 265
Histatins, 676
Histocompatibility, 735
HNSCC, See Head and neck squamous cell carcinoma (HNSCC)
Hodgkin's lymphoma, 25, 698
Hollowing out, 603
Hollow wave guide, 1166
Home exercise programme, 941
Honey bear enema, 102
Honeycomb or soap bubble configuration, 619, 627
Hook of hamulus, 751
Horizontal buttresses, 982, 1062
frontal, 982
maxillary, 982
zygomatic, 982, 991
Horizontal flap, 309
Horizontal fracture, 1019
Horizontally favourable fracture, 1030
Horizontally unfavourable fracture, 1030
Horizontal mattress suture, 326
Horizontal plane, 835
Horizontal skeletal angle of convexity, 837
Horizontal skeletal profile, 837
analysis, 835, 935
Horizontal tear, 1018
Hot air oven, 286
Hot spots, 52, 702
Hotz plate, 753
Hounsfield number, 47
Hourglass, 398, 825
Howarth periosteal elevator, 266
Howell-Jolly bodies, 59
H-shaped incision, 588
HSV, See Herpes simplex virus (HSV)
Human immunodeficiency virus (HIV), 77, 116, 118, 300
HIV-1 culture, 118–119
HIV tests, 32, 642
HIV wasting syndrome, 117
Human papilloma virus, 122, 642
type 16 and 18, 697
Humby's knife, 316
Humoral immunity, 79
Hyalinisation, 666
Hyaluronic acid, 600, 754
Hyaluronidase, 168
Hydrating agent, 124
Hydraulic theory, 1083
Hydrocortisone, 166, 169
Hydrogen carbonate, 675
Hydrostatic dissection, 588
Hydroxychloroquine, 935
Hydroxypropyl cellulose, 666
Hynes pharyngoplasty, 770
Hyoid bone, 615, 643
Hyomental distance, 948
Hyperacusis, 800
Hyperaesthesia, 790
Hyperalgesia, 790
Hyperbaric oxygen, 559, 668
Hyperdense sinus lining, 727
Hyperfractionation, 565
Hyperglobulinaemia, 650
Hyperglycaemia, 100, 133, 145, 351
Hypernasality, 752
Hyperparathyroidism, 444
Hyperpathia, 790
Hyperpneumatisation, 598
Hyperpolarization, 178
Hypertelorism, 15, 598, 741
Hypertension, 98, 351
Hyperthyroidism, 11, 15, 109–110, 182
Hypertrophic acinar cells, 695
Hyperventilation, 135
syndrome, 934
Hypnotics, 170
Hypocalcaemia, 650
Hypoglobus, 1096
Hypoglycaemia, 100, 133, 138–139, 145
Hyposmia, 716, 717
Hypotelorism, 741
Hypothalamic-pituitary-adrenal (HPA) axis, 109
Hypovascularity, 666
Hypovolaemic shock, 341, 342
Hypoxia, 60, 102, 107, 108, 137, 230, 231
Hysterical trismus, 934
I
IAN lateralisation (IANL), 476
IAN transposition (IANT), 476
Iatrogenic, 296, 715, 727
Ibuprofen, 151, 162, 164, 668, 717
ICP, See Intracranial pressure (ICP)
Ideal edentulous ridge, 444
Idiopathic paroxysmal sialorrhoea, 685
Idiopathic thrombocytopenia, 113
IgA, 676
Iliac crest, 772
Image/CT-guided biopsy, 84, 86
Imaging studies, 554, 801, 814, 1131
IMF, See Intermaxillary fixation (IMF)
Immediate loading, 484, 506
Immobile implant, 483
Immobilization, 988
Immune electron microscopy (IEM), 77
Immunochromatography, 77
Immunodiffusion, 79
Immunofluorescence (IF) test, 79
Immunological hypothesis, 799
Immunologic diagnostics, 76
Impacted tooth, 350, 380
Impaired blinking, 800
Implant, 484, 487, 494, 506, 782, 1175
IMRT, See Intensity-modulated radiotherapy (IMRT)
Incineration, 285, 303
Incision
biopsy, 33, 83
and drainage, 422, 527, 610
parotid biopsy, 699
Incisive foramen, 736
Incoming waveform, 682
Incomplete cleft lip, 732
Indications
marsupialisation, 588
tracheal intubation, 228
Indifferent electrode, 339
Indirect Coombs test, 77
Indirect fixation, 984, 993, 994
Indirect immunofluorescence, 77, 91
Induction, of anaesthesia, 231
Infant feeding prosthesis, 785
Infantile osteomyelitis, 558
Infected ranula, 541
Infection, 795
arthritis, 922
control, 44, 116, 121, 296, 573
diseases, 116
endocarditis, 105
mononucleosis, 78
Inferior alveolar nerve block, 197
Inferior border augmentation, 453
Inferior rectus muscle, 1005
entrapment, 1005
herniation, 1005
Inflammatory fibrous hyperplasia, 474–475
Influenza virus A and B, 716
Informed consent, 1145
phases, 1145
discussion, 1145
documentation, patient's chart, 1146
written consent, 1145
Infraction/fracture of enamel, 1015
Infradentale, 836
Infraorbital, 186, 194, 312, 1097
Infratemporal space, 537
Inhalation anaesthesia, 354
Initial reaction, 1003
aseptic necrosis, 1003
haematoma, 1003
Initial segment, 790
Injuries to gingiva or oral mucosa, 1017
Injuries to periodontal tissues, 1015
concussion, 1015
subluxation, 1015
Injuries to supporting bone, 1017
Inorganic filters, 290
Inorganic salts, 687
In situ hybridisation, 696
Instruments, 250, 271
Insulin-like growth factors, 1156
Intensity-modulated radiotherapy (IMRT), 565
Intercalated, striated and excretory ducts, 672
Intercellular bridges, 622
Interdental eyelet wiring (Ivy loop method), 986
cross-bracing, 986
Interferon alpha-2, 638
Interlacing bundles, 626
Intermaxillary fixation (IMF), 925, 965, 967
screws, 989
Intermaxillary segment, 735
Intermaxillozygomatic cleft, 742
Internal acoustic meatus, 797
Internal disc
derangement, 919, 922
displacement, 922
Internal haemorrhage, 332
Internal jugular vein (IJV), 643
Interocclusal clearance (freeway space), 829
Interposition arthroplasty, 952
Interstitial implantation-radium source, 661
Intra-alveolar carcinoma, 628
Intra-alveolar clot, 375
Intra-alveolar extraction, 354
Intra-alveolar (closed) extraction, 350
Intra-articular injection, 941
Intra-articular origin/intrinsic disorder, 922
Intracapsular fracture, 922
Intracranial course, of facial nerve, 797
Intracranial pressure (ICP), 977
Intracranial vascular compressions, 812
Intraductal contrast media, 681
Intraglandular, 690
neoplasm, 679
Intralesional
chemotherapy, 669
corticosteriods, 638
Intraluminal type, 621
Intramedullary screw, 1055
Intranasal antrostomy, 712
Intranasal splinting, 1115
Intraocular pressure (IOP), 1105
Intraoral incision, 307
Intraoral periapical radiograph (IOPA), 33
Intraoral traction, 984
Intraoral vertical ramus osteotomy, 858
Intraosseous, 607
injection, 184
Intraosseous mucoepidermoid carcinoma (MEC), 604, 704
Intraosseous salivary gland (IOSG) tumours, 704
Intrapulpal injection, 177, 178, 184
Intraseptal injection, 184
Intravelar veloplasty, 663, 763
Intravenous anaesthetic (induction) agents, 231
Intrinsic disorder, 922
Intrusion, 1016
Intrusive luxation, 1016
Intubation, 211
Inverted-L incision, 915
Inverted pear, 608
Involucrum, 557
Iodine, 676, 707
based aqueous solutions, 48
based oil solutions, 48, 679
Iodoform, 588, 723
pack, 727
tape, 724
Ionizing radiation, 262
Iontophoresis, 801, 940
IOP, See Intraocular pressure (IOP)
Ischaemia, 556, 799, 1096
Island flaps, 313, 764
Islands of bland, 622
Isoechoic image, 55
Isoflurane, 217, 237
Isomorphic cells, 704
Isoproterenol, 584, 667
Isotopes, 48
Ivy method, 63
J
Jackson-Pratt drain system, 345, 346
Jaffe-Lichtenstein syndrome, 636
Janeway lesions, 106
Jaw thrust manoeuvre, 128
Jensen Middleton Rongeur, 268
Jigsaw puzzle, 639
Joe-Hall-Morris appliance, 992
Joint noises, 938
Joram Raveh classification, 950
Jug-handle view, 42
Jugulodigastric lymph nodes, 20
Junctional epithelium, 512
Juvenile cemento-ossifying fibroma, 660
Juvenile rheumatoid arthritis, 922, 935
K
Kanamycin, 160
Kaolin, 666
Kapetansky's pendulum flaps, 780
Kaposi's sarcoma, 28, 84, 117, 119, 122, 644
Karyorrhexis, 82
Kawamoto distractor, 903
Kazanjian and Converse classification, 945, 1026
Kazanjian's technique, 471
KCOT, See Keratinising cystic odontogenic tumour (KCOT)
Keen's approach, 1100
Kelly's combination syndrome, 473
Kelsey Fry technique, 407–408
Keplerian optical system, 280
Keratin, 600, 606
Keratinising cystic odontogenic tumour (KCOT), 597, 618
Keratitis, 818
Keratoacanthoma, 29
Keratocystic odontogenic tumour, 578, 598
Kernahan and Stark classification, 736
Kernahan classification, 737
Kernahan's striped Y, 738
Kernig's sign, 551
Kerrison forceps, 726
Ketamine, 107, 220, 234
Ketoconazole, 73, 121, 160
Kidney function tests, 32
Kilovoltage X-ray therapy 300 kV, 657
Kirschner wires, 993
Kleeblattschadel anomaly, 15
Klonopin, 816
Knight and Northwood classification, 1085
Knot, 327
granny, 328
half hitch, 328
reef, 328
single, 328
square, 328
surgeon's, 328
triple throw, 328
Kocher's forceps, 250, 258
Koplik spots, 29
Kruger and Schilli classification, 1026
Kufner technique, 849
Kussmaul breathing, 100
L
Labbe's technique, 808
Labial frenectomy, 465
Labiobuccal vestibuloplasty, 468
Laceration, 794, 1007, 1008
flap-like, 1007
gingiva, 1018
simple, 1007
stellate, 1007
Lacrimal apparatus, 1009
Lacrimal system management, 1123
Lacrimation, 801
Lacrisert, 697
Lactate dehydrogenase (LDH), 67, 68
Lactobacillus, 666, 667
Lactoferrin, 676, 686
Lactoperoxidase, 676, 686
Lactose dehydrogenase, 67, 68
Lagophthalmos, 1108
Lag screws, 861
Lamina papyracea, 729
Lamotrigine, 816
Lanes forceps, 258
Langenbeck's retractor, 250, 260
Langerhan's histiocytes, 92
Langer's line, 306, 528
Lanolin, 666
Large multilocular lesion, 602
Larsen and Thomsen classification, 1088
Laryngeal mask airway (LMA), 128, 226, 227, 228, 230, 250, 254
Laryngoscope, 229, 250–252
fibreoptic, 250
rigid, 250
Laser, 340, 816, 1165, 1167
Lasers based on medium, 1166
alexandrite, 1166
argon, 1166
CO2, 1166
copper vapour, 1166
Er:YAG, 1166
excimer, 1166
HeNe (helium-neon), 1166
Hol:YAG, 1166
KTP (modified version of Nd:YAG), 1166
Nd:YAG, 1165, 1166
ruby, 1166
Lasers indications, in oral surgery, 1169
aphthous ulcer treatment, 1169
crown lengthening, 1169
frenectomy, 1169
frenotomy, 1169
gingivectomy/gingivoplasty, 1169
haemostasis, 1169
implant recovery, 1169
operculectomy, 1169
vestibuloplasty, 1169
Lasers in oral surgery, classification, 1166
contact laser, 1166
continuous wave, 1166
diode laser, 1166
dye lasers, 1166
erbium lasers, 1166
flash scanned, 1166
invisible spectrum, 1166
ionising laser, 1166
noncontact laser, 1166
nonionising lasers, 1166
pulsed wave, 1166
super pulsed, 1166
ultra pulsed, 1166
visible spectrum, 1166
Lasers in oral surgery, properties, 1165
coherent, 1165
monochromatic, 1165
Laser tissue interaction, 1167
absorption, 1167
nonthermal reactions, 1167
reflection, 1167
scattering, 1167
transmission, 1167
Late failure, 506
Latency period, 878
Latency phase, 888
Latent infection, 296
Lateral
approach, 463
based on position, 963
cephalogram, 32, 38, 39
eyebrow incision, 312
luxation, 1015, 1016
ND, 654
periodontal cyst, 605
pharyngeal space, 524, 545
processes, 735
pterygoid, 812, 817, 908
myotomy, 968
trephination technique, 407
window preparation, 509
Lateral orbitomaxillary cleft, 742
oculofacial II or Moran III, 742
Lateral (sphincter) pharyngoplasty, 770
Latex agglutination test, 76
Layers of onion, 632
Lead, cadmium, copper, 676
Lead splints, 1116
Leafless tree pattern, 695
Lees screen, 1094
Le Fort fractures, 271, 982, 1063, 1071
Le Fort I, 777, 779, 1064, 1074
Le Fort II fracture, 1066, 1076
Le Fort III fracture, 1069, 1070, 1076
Le Fort III osteotomy, 855, 856
Le Fort II osteotomy, 854
Le Fort I osteotomy, 457, 779, 781, 849, 851
indications, 849
modifications, 851
segmenting maxilla, 851
surgical technique, 849
Legionella pneumophila, 299
Lekholm and Zarb classification, 484
LeMesurier technique, 758
Lemon drops, 690
Lemport's endaural approach, 915
Leontiasis ossea, 639
Leprosy, 28
Leukoedema, 30
Leukotrienes, 581
Levator sling, 763
Levator veli palatini, 751, 766
Lever, first order principle, 356, 1172
Levine sign, 137
Lichen planus, 30
Lidocaine, 668
Ligamentorrhaphy, 967
Light brush strokes, 426
Lindahl classification, 1046
Linear gingival erythema, 122
Linen, 320
Linezolid, 174
Lingual nerve, 185, 196, 197
block, 204
Lingual split technique, 407–408
Lingual vestibuloplasty, 472
Lingua plicata, 799
Lip adhesion, 754, 755
Lipase, 676
Lip defect, 753
Lip form, 831
mentolabial sulcus, 831
projection, 831
size, 831
Lip incompetence, 829
Lipiodol, 679
Lip lubrication, 666
Lipoma, 25, 26
Lips, 831
competency, 831
lower lip length, 831
pits, 19
repair, 755, 764
closure of palatal fistulae, 764
velopharyngeal incompetence, 766
scar revision, 780
Abbe flap, 780
upper lip length, 831
Lipswitch technique, 471
Lipswitch vestibuloplasty, 471
Liquid coolant, 426
Liquid media, 70
Liquid nitrogen, 597
Liquid nutrient broth, 72
Lister's sinus forceps, 265
Liver disorders, 11
Liver function test, 32, 67, 217
LMA, See Laryngeal mask airway (LMA)
Loading concept, 505
Local anaesthesia (LA), 178–210
diagnostic test, 815
for extraction, 353
injection injury, 934
toxicity, 141
Local excision, 622
Local infiltration, 184, 185
Localised alveolar osteitis, 375
Localised osteomyelitis, 375
Localised radiotherapy, 651
Locking, 939
continuous suture, 326
plate, 1002
Locoregional flap, 307
Lohexol, 679
Long buccal nerve block, 196
Long face, 825
Long mandible in anterior-posterior plane, 824
Long maxilla in vertical, 824
Lorazepam, 172, 219
Loss of appetite, 666
Lowenstein-Jensen medium, 72
Lower eyelid, 742
Lower facial height decreased, 829
Lower jugular nodes, 643
Lower lip, chin, throat angle, 833
Lower lip everted, 829
Lower lip thin, 829
Lower motor neuron (LMN), 801
paralysis, 798
Lower third broad, 829
Low-grade tumours, 647
L-shaped flap, 404, 405
L-shaped pins, 969
Ludwig's angina, 522, 524, 527, 547
Luminal types, 621
Lupus erythematosus, 28
Lyme disease, 799
neuropathy, 812
Lymphadenitis, 541
Lymphadenopathy, 19, 116, 119, 375, 524
Lymphangioma, 23, 615
Lymphatic drainage, 675
Lymph nodes in neck, 19, 20
Lymphocytes, 61, 62
Lymphogranuloma venereum, 20
Lymphokine, 581
Lymphomas, 11, 19
Lysozyme, 676, 686
M
MacConkey agar, 72
MacLennan classification, 893
Macroaesthetics, 831
Miniaesthetics, 831
Macroglossia, 23
Macrolides, 154
Macrostomia, 17, 19
Macule, 10
Magnesium hydroxide, 666
Magnetic resonance angiography (MRA), 682, 814
Magnetic resonance imaging (MRI), 32, 47, 48, 50, 52, 677, 679, 682, 683, 965
Malar bones, 746
Malar rash, 28
Malignant
ameloblastoma, 619, 628
melanoma, 22
para/juxta-articular chondrosarcoma, osteosarcoma, 922
pleomorphic adenoma, 27
transformation, 644
tumours, 618, 628, 922
salivary gland, 703
Mallampati criteria, 216
Mallelomandibular ligament, 910
Mallet, 267
Malposed tooth, 380
Malpractice, 1144
MALT lymphomas, 696
Malunion, 1006
Management
by Bramley, 602
positive/negative neck nodes, 654
Mandible (mandibular)
anatomy, 1024
anteroposterior deficiency, 827
anteroposterior excess, 827
applied surgical anatomy of, 1024
area of weakness, 1025
body, 32, 862
branch, 798
deficiency, 825
deformities, 828
dental midline to symphysis, 831
dentoalveolar fracture with avulsion of teeth, 1018
en-bloc resection, 656
excess, 825
fossa, 909
fracture, 977, 978, 980, 982, 993, 1025
grains, 405
hyperplasia in AP plane, 824
and infratemporal fossa, metastatic disease of, 934
kinesiology (jaw tracking), 925
morphology, 873
ANS-Me line, 873
antegonial notches, 873
condyles, 873
morphology with age, 1024
nerve, 205, 806, 809
osteotomies, 857–876
pain dysfunction syndrome, 936
prognathism, 598, 648, 828
ramus, 32
reconstruction, 657, 659
repositioning splint, 940
retrognathism, 828
segmental resection, 656
surgeries, 844
and temporal bone, osteomyelitis of, 934
Marbus strangulatorius, 547
Marcus Gunn or jaw-winking syndrome, 799
Marfan syndrome, 964
Marginal
clearance, 621
mandibular branch, 797
resection, 597
Marie-Strumpell disease, 922, 936, 944
Markowitz and Manson classification, 1117
Maroteaux-Lamy syndrome, 604
Marsupialisation (cystotomy), 587, 588, 692
Marx protocol, 567
Marx theory, 565
Mass detection, 683
Masseter, 812, 911
Masticatory muscle
disorder, 922
inflammation, 922
spasm, 922
Matrix materials, 650
Mattress suture, 326
Maxillary
anteroposterior deficiency, 826
anteroposterior excess, 826
antrostomy, 729
antrum, 712
augmentation, 454
deficiency, 825
deformities, 825
dental midline to MSP, 831
division of trigeminal nerve, 712
fractures, See Maxillary fractures
growth retardation, 752
hyperplasia
in anterior-posterior plane, 824
in vertical, 824
hypoplasia, 752, 780, 824
in anterior-posterior plane, 824
nerve, 810
block, 193, 194
pocket inlay vestibuloplasty, 469–470
processes, 735
prognathism, 825
3rd molars impaction, 408
retrognathism/hypoplasia, 825
sinus, 633, 711
sinusitis, 715
surgeries, 843
tuberosity reduction, 463
vertical, 825
Maxillary fractures
applied anatomy of the maxilla, 1062
classification, 1063
classification of methods of fixation, 1074
Guerin fractures/floating maxilla, 1064
indirect signs of fracture, 1071
investigations, 1070
late consequences of fractures of middle third of facial skeleton, 1076–1079
late enophthalmos, 1078
midpalatal split, 1079
posttraumatic facial deformity, 1077
Le Fort, 1063–1064, 1066, 1068
management of Le Fort, 1071
methods of maxillary fracture fixation, 1074
palatal fracture, 1077
bicoronal and hemicoronal, 1072
lateral brow, 1073
transoral, 1074
midfacial degloving, 1072, 1073
transconjunctival/subciliary, 1072, 1073
Maxillary osteotomies, 844–855, 875–876
Maxillectomy, 621, 657, 699
Maxillofacial evaluation, 980
hypovolaemic shock, 980
midfacial injuries, 980
Townes' view, 980
transnasal intubation, 980
Maxillofacial trauma, 974
extradural haematomas, 974
golden hour, 974
osteoporotic bone, 974
osteoradionecrosis, 974
Maxillomandibular asymmetry, 831
Maxon, 320
McCune-Albright syndrome, 636
MCH (Mean corpuscular haemoglobin), 58
MCHC (Mean corpuscular haemoglobin concentration), 58
MCV (Mean corpuscular volume), 58
Meal time syndrome, 687
Measles, 29
Mechanical devices, 265
haemostatic clips, 265
stapling devices, 265
Mechanical principles, in tooth extraction, 356
Mechanical support for flap, 724
Mechanical ventilation, 224
Mechanism of action of Carnoy's solution, 594
Mechanoreceptor, 791
Mechanotransduction, 889
Meckel's cartilage, 910
Meckel's cave, 817, 818
Medial and lateral processes, 735
Medial antebrachial cutaneous nerve, 805
Medial, based on position, 963
Medial canthus, 1109
Medial orbitomaxillary cleft, 742
Medial pterygoid, 198, 207, 382, 544, 563
Median orbitomaxillary cleft, 742, 745
oculofacial I or Moran II, 742
Mediastinitis, 522, 552
Medical management, of TN, 816
Melanoma, 15, 22, 24, 29, 85
Melkersson-Rosenthal syndrome, 799
Melphalan, 650
Membrane expansion theory, 178
Membrane filters, 290
Mendelian theory, 381
Meningitis, 551, 717, 1138
Meniscectomy, 968
Meniscus, 909, 910
Mentalis muscle, 825
Mentalis strain with lip closure, 829
Mental nerve, 185, 203, 204, 476, 586
Mental retardation, 598
Menton, 832, 836
Meprobamate, 172
Mercier's classification, 444
Merocrine, 672
Mesenchymal tumours, of TMJ, 934
Mesenchyme, 734
Metabolic disorders like gout, 922
Metallic implants, 484
Metallic suture material, 319
Metastatic condylar tumours, 922
Metastatic foci, 649
Methocarbamol, 172
Methods, serial extraction, 366
Methotrexate, 669, 935
Methyldopa, 69
Methylene blue dye, 594
Methyl test, 71
Metrizoate, 679
Metronidazole, 69, 108, 115, 120, 155, 668
Microaesthetics, 831
Microcracks, 1015
Microfibrillar collagen, 337, 425
Microform cleft lip, 732
Microgenia, 827
Microlux, 33
Microlux DL, 87
Microsaws, 271
Microsurgery, 442
Microtia, 15
Microvascular anastomosis, 808
Microvascular decompression, 818
Microvascular reconstruction (vascularised bone graft), 657
Midazolam, 124, 125, 136, 171, 219, 234
Middle jugular nodes, 643
Middle superior alveolar nerve, 183
block, 188
Midface fracture, 980, 1005
Midfacial degloving, 1072, 1073
Midfacial hypoplasia, 903
Midsagittal reference line (MSR), 873
Fr-Fr line, 873
Z plane, 873
Midsymphysis osteotomy, 863
Mikulicz disease, 696
Milk, 1020
Milk saliva, 688
Millard classification, 738
Millard rotation advancement repair, 755–756
Millard two-stage method, 760
Mineral trioxide aggregate (MTA), 430
Miniaesthetics, 833
Miniplates, 855
Minnesota retractor, 250
Minor salivary glands, 606, 672
Miosis, 820
Misch classification, 485
Misonidzole, 668
Missile injury, 976
Mitomycin-C, 668
Mitosis, 647
Mivacurium, 241
Mobile implant, 506
Mobius syndrome, 799
Model surgery, 842
Modes of spread, 647
Modified cantilevered Y plates, 1122
Modified radical neck dissection (MRND) I-III, 654
Modified visor osteotomy, 454
Moist heat, 286
Molecular diagnostics, 75
Monoamino oxidase (MAO) inhibitors, 940
Monocular diplopia, 980, 1094
Monocytes, 58, 61, 62
Monofilament suture material, 319
Monofocal, 882
Monopolar diathermy, 339
Monostotic, 633, 635
fibrous dysplasia, 635
Moon facies, 1067
Moon's probe, 250
Moore-Gillbe collar technique, 402, 405
Moran I cleft, 742
Moraxella species, 299
Morphine, 164
Morphoeic pattern, 648
Mosaic appearance, 639
Moth eaten margins, 627
Motor root, 797
Motor to muscle spindle, 791
Motrigine, 816
Mouth gag, 275
Mouth prop, 276, 277
MPDS, See Myofascial pain dysfunction syndrome (MPDS)
MS, See Multiple sclerosis (MS)
MSX-1, 748
MTA, See Mineral trioxide aggregate (MTA)
MUC1/DF3, 700
Mucicarminophilic material, 606
Mucin, 676, 691, 692
Mucinous tumours, 700
Mucocele, 585, 614, 684, 688, 691, 692, 714
Mucociliary drainage, 728
Mucoepidermoid carcinoma (MEC), 698–699
intraosseous, 703
sclerosing, 703
Mucogingival flap, 307, 309
Mucolipidosis type III, 604
Mucolytic agents, 717
Mucoperiosteal flap, 309, 404
full, 307
Mucopyocele, 1136
Mucormycosis, 717
Mucosal advancement vestibuloplasty, 468
Mucosal cell turnover, 666
Mucosal insert, 479
Mucosal lining, 759, 780, 1126
Mucositis, 448, 510, 663, 1171
Mucous acinar cells, 696
Mucous extravasation, 614
Mucous retention cyst, 614, 692
Multiagent chemotherapy, 649
Multifactorial inheritance, 748
Multifilament suture material, 319
Multinucleated giant cells, 638
Multiple fracture, 1019
Multiple independent lesions, 644
Multiple myeloma, 569, 650
Multiple polyp, 718
Multiple ports, 661–662
Multiple sclerosis (MS), 812
Multiple teeth avulsion, 1019
Multipolar neuron, 791
Mumps, 694, 695, 934
skin test, 78
Mural growth theory, 578
Mural proliferations, 604
Mural type, 621
Mural unicystic ameloblastoma, 621
Muscarinic action, 675
Muscle relaxation, 172, 239
Muscular fibrosis, 958
Muscular trismus, 958
Mycobacterium tuberculosis, 287
Myelinated neurons, 790
Myelin injury, 795
Mylohyoid, 185, 462, 615, 643, 674
Myocardial infarction, 104, 137
Myoepithelial cells, 672
Myofascial pain dysfunction syndrome (MPDS), 922, 934, 936, 938
Myositis ossificans traumatica, 934
N
Naevus, 30
Nager's syndrome, 880, 932
Nakajima technique, 759
Naloxone, 124, 244
Nance method-DC4, 367
Naproxen, 163
Narcotic antagonist, 124
Nasal
anatomy, 831
antrostomy, 724
bone, 855, 980
fracture, See Nasal fracture
decongestants, 727
deformity, 732, 753
floor reconstructed, 761
hemiatrophy, 742
muscle complex, 757
obstruction, 717
pit, 734
placode, 735
polyposis, 729
rasp, 724
septum, 978, 1076
sil, 732
speculum, 250, 264, 726
spray, 730
stenosis, 757
tip to mid-sagittal plane, 831
trocar, 726
twang, 732, 752
web, 757
Nasal bone fracture, 982, 983, 1111
clinical findings, 1111
crepitus, 1111
CSF leaks, 1111
comminuted undisplaced isolated, 1113
isolated right, 1112
management, 1111
closed reduction, 1113–1115
methods of immobilisation, 1115–116
extranasal splinting, 1116
intranasal splinting, 1115
lead splints, 1116
POP splint, 1116
ribbon gauze, 1115
silicone splint, 1115
open reduction, 1115
complications, 1115
indications for, 1115
saddle nose deformity, 1115
secondary deformity, 1115
synechia, 1115
reduction, 1111–1113, 1111–1115
radiographic features, 1111
Rohrich classification, 1111
secondary deformity, 1113
types, 1111
anterior direction, 1111
lateral direction, 1111
unilateral or bilateral fracture, 1113
untreated septal haematoma, 1113
Nasion, 757, 836
Nasoalveolar moulding, 754
appliances, 754
Nasoantral perforation, 724
Nasoantral window, 1073
Nasolabial angle, 763, 784, 829, 831
Nasolabial cyst (Kledstadt's cyst), 608
Nasolacrimal duct injury/epiphora, 730
Nasolacrimal groove, 745
Nasolacrimal sac, 1109
Naso-orbito-ethmoidal complex fracture, 1116
bedside swinging flashlight test, 1117
CSF rhinorrhoea, 1117
epicanthus fold management, 1124
epiphora, 1117
hypoglobus, 1120
lacrimal system management, 1123
fine bore polyethylene, 1123
silicone tube, 1123
Markowitz and Manson classification, 1117
orbitorrhoea, 1117
pathophysiology, 1117
canthopexy, 1121
cosmetic camouflage, 1119
pig snout appearance, 1116
pseudohyperteleorism, 1117, 1119–1120
subconjunctival haemorrhage, 1119
telecanthus, 1121
Naso-orbito-ethmoid fracture, 982, 1107
anatomy of region, 1108
bony structures of region, 1108
lacrimal apparatus, 1109
medial canthus, 1109
anterior tendon, 1110
posterior tendon, 1110
nasal bone and septum, 1109
Naso-orbito-ethmoid region, anatomy of, 1108
Duverney's muscle, 1110
Horner's muscle, 1110
pars lacrimalis, 1110
tensor tarsi, 1110
tripartite medial canthal complex, 1110
valve of Hasner, 1110
vomer, 1109
Nasopalatine nerve block, 192
Nasopharyngeal airway, 128, 225, 253
Nasoseptal osteotome, 850
Natural collagen sponge, 338
Natural head position, 830
Natural penicillin, 152
Natural suture material, 319
Nature and nurture theory, 382
Natwig, 965
Nausea, 1096
NBCCS and sporadic OKC on chromosome, 600
Neck dissection, 654
Necrotic alveolar socket, 375
Necrotising fasciitis, 553
Necrotising sialometaplasia, 646, 695
Necrotizing stomatitis, 122
Necrotizing ulcerative
gingivitis, 122
periodontitis, 122
Needle biopsy, 84, 85, 90
Needle breakage, 141, 206
Needle cricothyrotomy, 128, 130
Needle holder, 250, 259
Needle placement, 816
Needle stick injury, 300
Negligence, 1144
Negligent act, 1144
Neisseria stain, 71, 521
Neomycin, 160
Neoplasm, 680, 922
Neoplastic (benign/malignant), 934
Neostigmine, 242
Nerve
anatomy, 791
avulsion, 567
block, 184
cell body, 790
conduction, 178
to digastric, 797
fibres, 790
types of, 791
grafts, 315
identification, 803
injury to, 790, 791, 803, 875
stapedius, 797
stylohyoid, 797
transposition, 805
Neural anastomosis, 808
Neuralgia, 790, 808, 819
Neural wound healing mechanisms, 792
Neurapraxia, 582, 793
Neurectomy, 816, 817
Neurites, 790
Neuritis, 790, 793, 795
Neuroectodermal tumour, 10
Neurofibroma, 16, 25
Neurological examination, trauma patients, 976
Neurologic disorder, 115
Neurologic examination, 925
Neuroma, 792, 794
exophytic, 793
lateral adhesive, 793
types of, 793
Neuroma-in-continuity, 792
Neuromeric theory, 734
Neuromuscular blocking drugs, 239
Neuromuscular disorder, 934
Neuromuscular transfer, 803, 808, 809
Neuron, 790, 791
Neuropathic keratitis, 811
Neuropathy, 666, 790
Neurorrhaphy, 803
Neurotmesis, 793, 794
Neurovascular compression hypothesis, 812
Neurovascular conflict, 814
Neutralisation (Nt) test, 79
Neutrophils, 58
Nevoid basal cell carcinoma syndrome features, 598
Newer beta lactum antibiotics, 174
Newer fluorquinolones (trovafloxacin), 174
Newer macrolides, 174
Nicotinamide, 668
Nidus, 633
Nikolsky sign, 30
Nilaton technique, 965
Nimorazole, 668
Ninth Shangai classification, 947
Nitrate reduction test, 71
Nitroglycerine, 103, 124
Nitrous oxide, 107, 110, 115, 236
Nitroxides (tempol), 668
Nociception, 790
Nociceptor, 790
Nodes, 643
Nodes of Ranvier, 790
Nodine's phylogenic theory, 381
Nodule, 10
Noma, 28
Nonabsorbable suture material, 318
Nonaggressive lesions, 638
Non-aminobisphosphonates, 572
Noncompression miniplates, 994
Non-depolarising muscle relaxants, 237, 240
Nonionising radiation, 290
Nonnucleotide reverse transcriptase inhibitors (NNRTIs), 120
Nonobstructive sialadenitis, 682
Nonoccluding anterior teeth, 824
Nonodontogenic tumours, 632–640
Nononcogenic, 644
Nonopaque sialolith, 679
Nonsteroidal agent, 666
Nonsteroidal anti-inflammatory drugs (NSAIDs), 161
Nonsyndromic cleft, 747
Nonthermal reactions, 1167
Non-toothed forceps, 250, 257
Nontraumatic (spontaneous), based on aetiology, 963
Nonunion, 878
Non-vascularised bone graft, 657
Nonvital tooth, 581
Noordhoff technique, 731, 757
Normal ductal architecture, 679
Normal ductal structure in, 679
Normal neuromuscular transmission, 239
Nose-chin position, 41
Nose septum, 780
Nose tip, 780
Nosocomial infection, 296
Nuclear medicine, 51
Nuclear pleomorphism, 647
Nucleic acid probe test, 75
Nucleotide reverse transcriptase inhibitors (NRTIs), 120
Numbness, 795, 798, 800
Nursing mother, 151
Nylon, 320, 803
Nystagmus, 598
Nystatin, 151, 159
O
Oblique lateral view, 32, 43
Obliteration of sinus cavity, 1136
Obstructive disorder, 686
Obwegeser's coronoid retractor, 261
Obwegeser's technique (1963), 470, 472
chin retractor, 250
long (Obwegeser), 250
ramus retractor, 250
short, 250
Occipitomental view, 40
Occlusal cant, 870
Occlusal projections, 34–35
Occlusal view radiograph, 32, 34
Occlusal wafer splints, 842
Ochsner's artery forceps, 258
Octenyl succinic anhydride (OSA), 1157
Ocular dystopia, 1006, 1108
Oculocardiac reflex, 1096
pathway, 1096
syndrome, 1096
Oculomotor nerve, 979
Oculomotor pareses, 552
Oculonasal cleft, 742, 745
Oculosympathetic palsy, 820
Odontectomy, 402, 406
Odontogenic ectomesenchyme, 623
Odontogenic fibroma, 626
Odontogenic ghost cell carcinomas, 607
Odontogenic infection, 520–523
Odontogenic keratocyst (OKC), 27, 578
multiple, 598
Odontogenic myxoma, 626, 627
Odontogenic sarcoma, 629
Odontoma, 624, 728
Oedema, 209, 717
Ogilvie needle, 1122
Ohngren's line, 713
OKC, See Odontogenic keratocyst (OKC)
Olfactory nerve, 979
Oligonucleotide probes, 75
Omohyoid muscle, 643
Oncocytoma, 673, 698, 702
Oncocytosis, 684
Oncogene, 82, 644
Oncoprotein, 82
One-point fixation, 1100
One-stage implant, 487
ONF, See Oronasal fistula (ONF)
Onion skin appearance, 649
Onlay grafting, 454
Oophoritis, 694, 695
Open apex, 1021
Open bite, 824, 828
Open method, 368
Open operation, 815
Open view submucous vestibuloplasty (Obwegeser), 469
Operating microscope, 281
Operculectomy, 383
Ophthalmic nerve, 810
Ophthalmoplegia, 523
Opioid, 163–165
Optic nerve, 979
Oral candidiasis, 686
Oral CDx, 87, 89
Oral cleft (OC), aetiology of, 747
Oral epithelium, 618
Oral flora, 299
Oral intubation, technique of, 229
Oral/nasal pharyngeal airway, 250
Orange peel appearance, 636
Orbital abscess, 729
Orbital apex syndrome, 1095
Orbital blow-out fracture, 1096, 1104
Orbital bones
anatomy of, 1082
surgical spaces of orbit, 1083
Orbital cellulitis, 522
Orbital decompression, 729
Orbital dystopia, 1105, 1108
Orbital floor exploration, 1006
Orbital floor reconstruction, 1103
biomaterials in, 1104
allogenic, 1104
alloplastic, 1104
autogenous, 1104
positive forced duction test, 1104
postoperative complications, 1105
retrobulbar haemorrhage, 1105
management, 1105
Orbital fractures, 1083
blow-in fracture, 1084
blow-out fracture, 1083
buckling theory, 1084
hydraulic theory, 1083
C-shaped incision, 1100
transcaruncular, 1100
transconjunctival, 1100
Orbital injury, 730
Orbit floor reconstruction, 1073
Orbitozygomatic complex, 1081, 1082–1105
Orchitis, 694, 695
Order of extraction, 366
Organic filters, 290
Organic nidus, 687
Oroantral fistula, 597, 715, 719
closure of oroantral fistula, types of flap, 721
buccal flap, 721
Moczair flap, 721
Von Rehrmann flap, 721
buccal pad of fat, 721
bridge flap, 721
gold foil, 721
nasolabial flap, 721
palatal flap, 721
Ashley's flap, 721
Kruger's modification, 721
tongue flap, 721
turnover flap/hinge flap, 721
extraction, 720
fluid regurgitation, 721
mouth mirror test, 721
nasal drops and inhalations, 724
nose blowing test, 721
orange seed, 719
probing, 721
suction test, 721
unilateral epistaxis, 721
Oroantral reflux, 724
Oronasal fistula (ONF), 17, 732, 752
Oropharyngeal airway, 128, 225, 253
Oropharynx, 21
tumours of, 934
Orthodontic camouflage, 841, 843
Orthodontic theory (small jaw-decreased space), 380
Orthodontic treatment, 777
Orthognathic analysis, 838
Orthognathic surgery, 753, 777, 824–825, 874
Orthokeratinised epithelium, 585
Orthomorphic surgery, 950
Orthopantomogram (OPG), 32, 37
Orthostatic hypotension, 134
Osler's nodes, 106
Osler-Weber-Rendu syndrome, 15
Osmolality, 67
Osmotic theory, 578
Osseointegration, 442
Osseous recontouring, 637
Ossifying fibroma, 633
Ostene, 338
Osteoactive agents, 1155
bioactive polypeptides, 1157
platelet-derived growth factor, 1152, 1156
platelet-rich plasma, 1156
stem cells, 1159
transforming growth factor, 1152, 1155
Osteoarthritis, 922, 934
Osteoblast mitoses, 1155
Osteochemonecrosis, 174, 448, 569
Osteochondroma, 934
Osteoclast cells, 1155
Osteoclastic cutting cone, 1151
Osteogenesis, 1155
Osteoid osteoma, 633
Osteo-inductors, 881
Osteoma, 632, 728
Osteomalacia, 444
Osteomyelitis, 507, 520, 524, 543, 720
induced inferior alveolar nerve dysfunction, 556
postextraction syndrome, 375
Osteopenia, 54
Osteopetrosis, 382
Osteophyte, 935
formation, 649
Osteoporosis, 54, 444, 1157
circumscripta, 639
Osteoradionecrosis, 563
Osteosarcoma (osteogenic sarcoma), 640, 649, 922, 934
Osteotome, 267
Osteotomy, 261–263, 384, 426
cut, 844
Ostia, 710
Ostiomeatal channels, 713
Ostiomeatal complex, 710, 729
Ostiomeatal unit, 714
Ostium, 711, 718, 724
Otalgia, 798
Otitis media, 799
Otomandibular ligament, 910
Otomandibular syndrome, 746
Ovalocytes, 59
Overbite, 825
Overjet, 825
Oxcarbazepine, 816
Oxidase test, 71
Oxidified cellulose, 727
Oxycel, 337
Oxycephaly, 15, 382
Oxygen, 174, 221
P
Packaging, 299
Paclitaxel, 668
Paget's disease, 10, 556, 570, 639
bone (osteitis deformans), 639
Pain, 666, 791
threshold, 790
tolerance level, 790
Palatal cysts of newborn, 606
Palatal expansion, 753
Palatal fistula, 732, 764, 768
Palatal flap, 307, 311, 419
Palatal fracture management, 1076
Palatal shelves, 735
Palatectomy, 699
Palate repair, 763
timing of repair, 763
von Langenbeck operation, 763
Wardill-Kilner-Veau operation, 764
Palatopharyngeus, 766
Palifermin, 668
Palliation, of xerostomia, 667
Palpation, 1131
Pamidronate, 640
Pancreatitis, 695
Pancuronium, 107, 240
Panfacial fractures, 982
Panoramic film, 33
p24 antigen, 118
Papillary hyperplasia, 29
Papilloedema, 800
Papilloma, 26
Papule, 10
Paracetamol, 163, 717
Paradoxical carrier, 296
Paradoxical muscle spasm, 934
Paraesthesia, 206, 208, 558, 597, 1131
Parainfluenza, 693
Parakeratotic cells, 615
Parallel cone technique, 34
Paranasal sinuses, 710
ethmoid, 710
frontal (paired), 710
maxillary (paired), 710
sphenoid (single), 710
Parapharyngeal tumour, 25
Parasympathetic reflexes, 220
Paratrigeminal neuralgia of Raeder, 820
Parkinson's disease, 934
Parotid abscess, 934
Parotid duct, 681
Parotidectomy, 690, 700, 701
Parotid fistula, 11
Parotid glands, 673, 674
Parotidomasseteric fascia, 542
Parotid sialography, 697
Parotid space infection, 542
Parotitis, 693
Parry Romberg syndrome, 870
Partial glossectomy, 657
Partially erupted tooth, 380
Partial maxillectomy, 597
Partial thromboplastin time (PTT), 65
PAS positive features, 622
Passive haemagglutination, 79
Pasteurisation, 287
Pathological theory, 382
Pathologic fracture, 656
Patients with cleft lip and palate
sequence of procedures, 751
PA view skull, 38
PCR (Polymerase chain reaction), 75–76
PCV (Packed cell volume), 59
Pearling, 648
Peau d'orange, 26
Pebbly, mammillated, 647
Pectoralis major myocutaneous (PMMC) flap, 314, 657, 665
Pectoralis minor, 808
Pederson's scale, 399
Pedicled buccal pad of fat, 723
Pedunculated bridge flap, 724
Pell and Gregory's classification, 385, 386
Pell-Gregory scale, 399
Pemphigus, 24, 30
Pen grasp, 306
Penicillamine, 935
Penicillin, 109, 120, 152
Penrose drains, 346
Pentazocine, 165
Pentobarbital sodium, 171
Pentoxifylline, 567
Peptone medium, 72
Peralveolar awl, 991
Peralveolar wiring, 1058
Percutaneous approach, 1098
Perforation repair, 432
Periapical cemento-osseous dysplasia, 633
Periapical cyst, 27, 611
Periapical infection, 520
Perichondrium, 757
Pericoronitis, 376, 382, 384, 411, 521, 542
Peri-implantitis, 510
Perineural invasion, 82
Perineural spread, 704
Periodontal
cyst, 585
ligament cells, 1020
repair, 433
Periodontitis, 513
Periorbital cellulitis, 719
Periosteal
elevators, 250, 259, 266, 359, 726
osteomas, 633
reaction, 681
Peripheral
acting muscle relaxant, 239
ameloblastoma, 621
blood smear, 58
dislocation partial avulsion, 1015
(extraosseous) ameloblastoma, 619, 621
giant cell granuloma, 29
neoplastic calcifying odontogenic cysts, 607
nerve stimulation, 242
odontogenic fibroma, 626
ostectomy, 594
osteomas, 632
palisading, 648
periosteal osteomas, 632
procedures, 815
surgery, 816
Periradicular
curettage, 426
surgery, 424
Peritonsillar abscess, 934
Perivascular spread, 704
Permanent diplopia, 1094
Petechiae, 10, 29
Pethidine, 165
Petrolatum, 724
Petrotympanic fissure, 909
Pfeiffer classification, 737
Pfeiffer syndrome, 902
Pharyngeal
exudates, 718
obturators, 785
tonsils, 21
walls, 732
Pharyngoplasty, 768, 770
Phase
cyst formation, 611
enlargement, 611
initiation, 611
Phenobarbital, 171
Phenol 5%, 6cc, 383
Phenol coefficient, 293, 294
Phenytoin, 816
Philtral dimple, 756
Philtral flap, 761
Philtral ridge, 757
pH of saliva, 687
Phonophoresis, 940
Phosphorus levels, 639
Phosphotungstic acid haematoxylin (PTAH) stain, 702
Photometric analysis, 830
Physeal distraction, 883
Physics forceps, 1172
Picket fence or tombstone, 600
Pierre Robin syndrome, 752, 880, 932
Piezoelectric surgery history, 1176
Piezo tips, 507
Pilocarpine, 667, 686, 695, 697
Pinchter type towel clip, 250
Pindborg tumour, 578, 618, 621
Pink puffers, 107
Pintos ligament, 908, 910
Piped medical gas and vacuum (PMGV) system, 221
Pituitary ameloblastoma, 619, 621
Pivot splint, 940
Pixel, 47
Plagiocephaly, 15, 16
Plantar response, 801
Plaque, 10
Plasma cells, 694
Plasmacytoid cells, 700
Plasmacytoma, 650
Plasminogen, 376
Plaster of Paris head cap, 993
Platelet count, 60
Platelet derived growth factor, 1004
Platelet disorders, 113
Platelet-rich plasma (PRP), 115, 452, 881
Plates-titanium, 274
Pleomorphic adenoma, 699
Plexiform type, 619
Plunging Ranula, 692
Pneumatisation, 741
of sinus, 710
Pneumocephalus, 1139
Pneumocystis carinii pneumonia (PCP), 117
Pneumonia, 299
pontiac fever, 299
Pocket inlay vestibuloplasty, 469
Pogonion, 833, 836
Poikilocytes, 59
Poliglecaprone 25 suture, 322
Polybutester, 321
Polycythaemia, 59, 60
Polydactyly, 749
Polydioxanone II (PDFII), 318
Polydioxanon suture material, 320
Polyester, 318, 1153
Polyethylene, 1104, 1123
Polyethylene tubing, 345
Polyglactin 910, 318
Polyglycolic acid, 318, 803
Polymerase chain reaction, 75, 696
Polymer implants, 484
Polymyxin B, 160
Polyoma virus, 697
Polyostotic, 633, 635
fibrous dysplasia, 636
Polypropylene suture, 322
Polyps, 717
Polytetrafluoroethylene, 803, 1104, 1153
Pons, 797, 809
Pontine infarct, 812
Poor lip seal, 825
Porphyromonas, 521
Positron emission tomography (PET), 32, 52
Postalveolar cleft, 736
Postanaesthetic intraoral lesions, 209
Postauricular approach, 915
Posterior auricular nerve, 797, 798
Posterior body osteotomy, 862
Posterior crossbite, 752, 825
Posterior nasal spine (PNS) view, 728
Posterior (flap) pharyngoplasty, 770
Posterior segmental maxillary osteotomy, 848, 849
Posterior subapical mandibular osteotomy, 864
Posterior superior alveolar nerve, 183
block, 186
Posterior to spinal accessory nerve, 643
Posterior triangle, 643
Posterior vertical maxillary excess, 824
Posterolateral neck dissection (PLND), 654
Post exposure prophylaxis, 302
Postganglionic nerve fibre, 791
Postincisive foramen clefts, 738
Postoperative bleeding, 374
primary, 374
reactionary, 374
secondary, 374
Postpubertal stage, 638
Postoperative proptosis, 730
Postradiation osteonecrosis, 666
Postsurgical (third molar removal, TMJ surgery), 934
Post surgical care, 431
Postsurgical haemostasis, 426
Postsurgical orthodontics, 753, 841
Posttraumatic ankylosis, 922
Postural hypotension, 133, 134
Potential spaces, 532
Pott's puffy tumour, 729
Power drill instrument, 270
Powerful suction, 728
p53, pRb-Tumour suppressor gene, 644
Prealveolar cleft, 736
Preanaesthetic evaluation, 212
Preauricular incisions, 312, 915
Preauricular sinus, 15
Prednisolone, 124, 165, 651, 802
Pregnancy, 115, 149, 150
tumour, 10
Preincisive foramen clefts, 738
Premature exfoliation, 638
Premaxilla, 736, 761
Premedication, 424
Premotor cortex stimulation, 819
Preoperative phase, 679
Presoaking, 299
Pressure, 336, 791
effects, 597
point technique, 641
Presurgical draping and asepsis, 250
Presurgical haemostasis, 425
Presurgical orthodontics, 782, 839, 840
alveolar moulding, 752
Pretragal incision, 809
Primary alveoloplasty, 457
Primary bone grafting, 771
premaxillary setback, 773
Primary bone healing, 1002, 1151
Primary closure, 611
Primary haemorrhage, 332
Primary haemostasis, 334
Primary infection, 296
Primary intraosseous squamous cell carcinoma (PIOSCC), 600
Primary palate, 734
Primary rhinoplasty, 762
Primordial cysts, 598
Principles and guidelines, of flap design, 306
Principles of
forceps, 356
knot, 328
mechanical ventilation, 224
suturing, 324
tooth removal, 356
Procaine, 180, 668
Proclined anterior bimaxillary alveolus, 824
Profile analysis, 833, 835
Progeria, 382
Prolabium, 736, 741, 761
Prolene, 321
sutures, 803
Proline, 676
Promethazine hydrochloride, 172
Promontory, 797
Prophylaxis, 148, 155, 156
Propofol, 233, 238
Propoxyphene, 165
Proprioception, 791
Proptosis, 15, 522, 713
Prostaglandin E2, 581
Prosthesis, for cleft patients, 782
dental implants, 785
dentures, 785
head gears, 785
pharyngeal obturators, 785
Prosthetic coping, 494
Prosthetic surgery, 444–476
Prosthion, 836
Protease inhibitors, 120
Protective measures, 300
Protective muscle splinting, 922
Proteolytic enzymes, 556
Prothrombin time (PT), 58, 63, 65, 67
PRP gel, preparation of, 1156
Prying motion, 360
Pseudoarthrosis, 951
Pseudocholinesterase deficiency, 242
Pseudoglandular spaces, 647
Pseudo-Hurler polydystrophy, 604
Pseudomembranous candidiasis, 121, 667
Pseudomembranous colitis, 155
Pseudomonas aeruginosa, 299
Psoriasis, 15
Psoriatic arthritis, 922, 935, 936, 945
PTCH mutation, on chromosome, 600
Pterygoid chisel, 266
Pterygoid plexus of veins, 551
Pterygomandibular space, 524, 544
Pterygomaxillary point, 836, 851, 855, 982
Ptosis, 14, 552
PTT, See Partial thromboplastin time (PTT)
Puffed cheek view, 677
Pulmonary function test, 217
Punch biopsy, 83, 84
Punched-out areas, 650
Puncta, 1109
Punctate sialectasis/snowstorm, 680
Pupillary plane, 830
Purulent discharge, 694
Pus, 688, 717
Pustule, 10
Pyogenic granuloma, 22, 28
Pyostomatitis vegetans, 29
Pyrexia, 527
Pyridinoline cross-link assays, 640
Pyriform, 845, 991
Q
Quadrangular Le Fort I osteotomy, 853
Quantitative sensory testing (QST), 813
Quinsy, 547
R
RA, See Rheumatoid arthritis (RA)
Raccoon eyes, 978, 1067, 1068
Radiation, 290, 651, 663, 668, 934
Radical excision, 621
Radical neck dissection (RND), 654
Radicular cyst, 611
Radiofrequency thermocoagulation, 817
Radiographic assessment of facial asymmetry, 872
Radiographic film size, 33
Radioisotopes, 51, 677, 682
Radiological signs, 397
Radiological types of keratocyst, 599
Radionucleotide imaging, 32
Radionuclide imaging, 683
Radiopharmaceuticals, 51
Radioprotectors, 668
Radiosensitisers, 668
Radiosurgery, 818
Radiosurgical loop, 383
Radiotherapy, 649, 657, 700
RAE tracheal tube, 254
Raised or rolled edges, 646
Ramipril, 668
Ramsey-Hunt syndrome, 798, 819
Ramus osteotomy, 857
Random flap, 313
Ranula, 585, 614, 692
RAR-a gene, 748
Rare facial clefts, 738
Rashness and negligence, 1144
Rate and rhythm of distraction, 885
Rate of distraction, 878, 881
Rathke's pouch tumour, 619, 621
Raynaud phenomenon, 28
RBC count, 60
Reactionary haemorrhage, 332
Reactive (acute/chronic), cause of trismus, 934
Reactive hyperplasia, 638
Reactive oxygen species (ROS), 642
Reankylosis, 947, 953
Recombinant bone morphogenetic protein (rhBMP), 657, 1157
rhBMP-2, 452, 657, 773, 774
Reconstruction ladder, 657
Reconstruction plate, 657, 884, 901
Recontouring, 638
Rectangular flap, 309
Recurrent
dislocation, 374, 963, 965
herpes simplex virus, 122
sinusitis, 729
subacute maxillary sinusitis, 715
Red blood cell indices, 60
Red line, 394
Reduced enamel epithelium, 605, 621
Reduced thyromental angle, 948
Reducibility, 26
Reduction-Nilaton technique, 965
Redundant tissue excision, 473
Reef knot, 328
Reflex activity, 232
Regional flap, 664
free, 663
Regulator, 339
Reimplanted teeth, 1021
Reiter syndrome, 27
Relaxed skin tension lines, 306
Relocation of ducts, 686
Remodelling, 1003
phase, 881
Removal of sutures, 329
Renal disorders, 108
Renal function tests, 69
Re-narrowing, 688
Replacement therapy, 111, 112
Replantation, 440
Resection, 561, 563
Residual ridge resorption (RRR), 444–448
Resorbable plate fixation, 1160, 1161
Respiratory epithelium, 614
Respiratory stimulants, 124
Restasis, 697
Re-stenosis, 688
Restricted mouth opening, 948
Restrictive strabismus, 1096
Rests of Serres, 605
Retained root-crown fracture, 1016
Retained root fracture, 1015
Retentive implants, 484
Retinal injury, 980
Retinoids, 669
Retractors, 250, 260, 726
with light source, 250, 264
Retrofilling material, 429
Retrograde dissection, 700
Retrograde filling, 427, 428, 430
Retromandibular approach, 915
Retromandibular vein, 673
Retropharyngeal space, 546
Retruded chin, 829
Revascularisation of graft, 1151, 1155
Reversal lines, 628
Reverse curve of Spee, 824
Reverse cutting, 323
Reverse Townes' view, 32, 42
Rheumatic hypothesis, 799
Rheumatoid arthritis (RA), 696, 922, 934–935
Rheumatoid factor, 696
Rheumatoid spondylitis, 944
Rhinitis, 717
Rhinoplasty, 753, 780
Rhinoscopy, 717, 718
Rhinosinusitis, 715, 716
Rhinovirus, 716
Rhizotomy, 567
Rhythm of distraction, 878
Rhytidectomy approach, 915
Ribbon gauze, 590, 722, 976, 1115, 1116
Ribosomal RNA, 75
Rideal-Walker test, 293
Ridge extension procedures, 466
Ridge-shaped philtral column, 732
Rigid fixation, 849
Rigid splinting, 1021
Ring forceps, 258
Risdon's wiring, 985
Risedronate, 640
Ristocetin cofactor assay, 113
Robertson cooked meat medium, 72
Robin sequence (RS), 932
Robotic surgery, 1179, 1180
Rodent ulcer, 24
Roller gauze, 728
Rongeur forceps, 267, 590, 726
Root amputation, 433
Root form implants, 442, 486
Root fracture, 1015
Root resection/hemisection, 432, 433
Root resulting in resorption, 1019
Rose and Thompson procedure, 755
Rose-Bengal stain, 697
Rotary and power drill instrument, 270
Rotary bur, 590
Rotator, 356
Roth spots, 106
Rouleaux formation, 59
Rowe and William classification, 1085
Rowe's, 271, 272, 983, 1053
Rubella, 78
Rubor, 526
Rule of SLOB, 391
Rumpel-Leede test, 64
Rushton bodies, 600, 611
Russell bodies, 650
Ryles' tube, 278, 279
S
Safety levels of LA, 182
Salbutamol, 124, 136
Saline, 1021
bicarbonate rinses, 666
Saliva, 683, 686, 801, 1021
glands, 672–704
imaging, 677
scintigraphy, 697
Salyer technique, 757, 759
S and V antigens, 694
Sarcoidosis, 20, 799, 812
Sarcomatous change, 636
Saucerisation, 561
Sausage link appearance, 679, 680
Sawhney classification, 946
Scaffold, 597
Scalpel, 250, 256
Scaphocephaly, 15, 16
Scarification of temporalis tendon, 968
Scar revision, 753
Schirmer test, 697, 801
Schistocytes, 59
Schwartz classification, 739
Scintigraphy, 32, 688
Scissors, 250, 256
Sclerosis, 622, 648
Sclerotic rim, 606
Scoliosis, 598
Scope of surgeon, 4
Scopolamine, 686
Scout radiographs, 679
Screw-retained fixed bridge, 499, 505
Screw type implant, 486
Secondary alveolar bone grafting, 772
Secondary alveoloplasty, 451
Secondary bone healing, 1003, 1150, 1151
inflammatory phase, 1150
reparative phase, 1150
Secondary haemorrhage, 332
Secondary haemostasis, 334
Secondary induction, 672
Secondary infection, 296
Secondary palate, 736
Secondary reconstruction, 602
Secondary rhinoplasty, 784
Second branchial arch syndrome, 931
Secretory acini, 614
Sedatives, 170, 171
Seddon classification, 794, 795
Segmental demyelination, 794
Segmental resection, 597, 602
Segmental subapical mandibular surgeries, 863
Seitz filter, 290
Seizures, 115, 137
Seldin, 266
retractor, 250
Selective neck dissection (SND), 654
Sella, 836
Sella nasion (SN) plane, 829
Semiconductor diode laser, 1169
Semilunar flap, 309
Semilunar/gasserian ganglion, 809
Semirigid (physiologic) fixation, 994, 1021
Semisynthetic penicillin, 152
Sensors, 44
Sensory root, 797
Sentinel lymph node biopsy, 93
Septic arthritis, 934
Septum, 741
Sequestra, 557
Sequestrectomy, 561
Serial extraction, 366
Serous, mucus and mixed, type of acini, 672
Serratiopeptidase, 169
Serratus anterior, 808
Serum albumin-globulin ratio, 650
Serum alkaline phosphatase, 639
Serum creatinine, 67, 69, 100
Serum uric acid, 67
Severe resorption, 603
Sevoflurane, 237
Sharpened pencil appearance radiograph, 935
Shave biopsy, 85
Shears classification, 579
Sheath of Hertwig, 618
Shellac base plate, 724
Shimmering gold or straw-coloured fluid, 611
Shimmering keratin crystals, 600
Shock, 340
Short circuits, 818
Shortened columella, 759
Short face, 825
Short hypotonic lip, 825
Short mandible in anterior-posterior plane, 824
Short mandibular ramus, 824
Short maxilla in anterior-posterior plane, 824
Short upper lip, 828
Sialadenitis, 91, 679, 680, 683, 692
Sialadenosis, 695
conditions associated with, 695
Sialagogue, 686
Sialectasis, 680, 694
Sialin, 676
Sialoadenectomy, 700
Sialoadenitis, 680
Sialoangiectasis, 688
Sialodochitis, 679, 680
Sialodochoplasty, 688, 689
Sialogogues, 688, 707
Sialograms, 680
Sialography, 32, 677, 680, 681, 683, 694
Sialolithiasis, 11, 680, 686, 687, 693
Sialoperoxidase, 676
Sialorrhoea, 683, 684
Sicca syndrome, 696
Sickle cells, 59
Sickle screen test, 218
Sigmoid notch retractor, 250
Signal void, 682
Silent chest, 144
Silicone, 957, 1104
splint, 1115, 1116
Silicosis, 11
Silk, 320
Silver amalgam, 430
Simonart's band, 732
Simple continuous suture, 325
Simple curettage, 622
Simple interrupted suture, 325
Simple ranula, 692
Simple rubber drain, 344
Single photon emission computed tomography (SPECT), 32, 52, 53
Single tooth osteotomy, 844
Sinonasal symptoms, 715
Sinus approximation (SA), 410
Sinus bradycardia, 1096
Sinus cavity, obliteration of, 1136
Sinus drainage, 1127
Sinus lift, 455
Sinus mucoceles, 729
Sinus ventilation, 728
Sjögren's disease, 680
Sjogren's syndrome, 52, 679, 683, 686, 696
criteria for, 697
primary, 696
secondary, 696
Skeletal anterior open bite, 828
Skeletal class III occlusion, 778
Skeletal deep bite, 829
Skeletal examination, trauma patients, 977
crepitation, 978, 980
flattened nasal bridge, 979
mandible, bimanual palpation, 980
step abnormalities, 978, 980
traumatic telecanthus, 979
trimalar fractures, 979
Skeletal hypoplasia, 753
Skeletal muscle relaxant, 239
Skin appendages, 615
Skin hook, 250, 262
Skin rash, 666
Skin tags, 15
Skoog technique, 759
Skull form, 15
Slide agglutination test, 76
Sluder's neuralgia, 793
Smith's bone spreader, 269
Smith spreader, 269
SMO (smoothed) forms, 600
Smooth contour, 735
S. mutans, 667
Snowstorm appearance, 679, 680
Soda lime, 224
Sodium, potassium and chloride, 676
Sodium psylliate, 967
Sodium tetradecyl sulphate, 965
Sodium thiopentone, 233
Soft palate, 672, 751
Soft splint, 940
Soft tissue analysis, 977
Soft tissue examination, 978
basilar skull fracture, 978
bilateral periorbital ecchymosis, 978
cerebrospinal fluid (CSF) otorrhoea, 978
Soft tissue excision, 699
Soft tissue handling instruments, 250
Soft tissue injury, 368, 1006
Soft tissue lacerations, 1017
Soft tissue palatal excision, 699
Solar cheilitis, 30
Solitary bone cyst, 582, 585
Sonic hedgehog ligand (SHH), 600
pathway, 602
Sonography, 925
Space of burns, 534–535
Spacer, 730
Special diagnostic stains, 33
Specific receptor hypothesis, 178
SPECT, 52
Speech therapy, 752, 770
Sphenomandibular ligament, 910
Sphenopalatine nerve, 183
Sphenopalatine neuralgia, 793, 819
Spiessel classification, 1026
Spina bifida, 598
Spine of sphenoid, 909
Spreader, 269
Spreading ulcer, 24
Squamous cell carcinoma, 24, 28, 600
Squamous odontogenic tumour, 622
Squamous papilloma, 29
Square knot, 328
Squint, 1108
‘S’- shaped incision, 806
Stabbing recurrent pain, 808
Stabilisation arm, 884
Stabilisation splint, 940
Stab incision, 550
Stable angina, 103, 136
Stafne's bone cyst, 27, 582, 585, 613
Stage, 644
of distraction, 881
and grading of oral cancer, 642
Standard of care, 1145
Stapedial reflex test, 801
Stapedius, 797
muscle, 800
Staphylococci, 718
Staphylococcus aureus, 71, 694, 716
Staples, 329
Starch test, 1130, 1138
Statherin, 676
Static bone cavity, 613
Static procedures, 805
Static suspension, 807, 809
Status asthmaticus, 133
Status epilepticus, 133, 137, 138, 144
Steam sterilisers, 287
Steep mandibular plane angle, 828, 948
Stem cells, 657, 1159
Stensen's duct, 673, 689
Sterilisation, 285
Steriolithography, 1177
amplifier, 1177
ceramic rings, 1177
photopolymerisation, 1177
Steroid, 165
therapy, 351
Stickler's syndrome, 931, 932
Still's disease, 935
Stimulants, 174
Stomatitis, 666
Stomatocytes, 59
Storax, 722
Strabismus, 15, 17, 598, 713, 1078, 1108
Straight-line closure, 755
Straight needle, 323
Strapping, 754
Stratum intermedium, 621
Streptococci, 694, 716, 718
Streptococcus mutans, 376, 666, 754
Streptococcus pneumoniae, 716
Streptokinase, 168–169
Stress reduction protocol, 98, 102
Stricture, 680
Striped Y classification, 737
Stromeyer's forceps, 965
Structural abnormality, 735
Strychnine poisoning, 934
Sturge-Weber syndrome, 15
Stylet, 817
Stylohyoid muscle, 798
Stylohyoid nerve, 797
Stylomandibular ligaments, 910
Stylomastoid foramen, 797
Styptics, 336
Subacute maxillary sinusitis, 715
Subacute necrotising sialadenitis, 694
Subciliary approach, 1073
Subciliary incision, 312
Subcuticular suture, 327
Sublingual dermoid, 23
Sublingual gland, 614, 692
Sublingual haematoma, 977
Sublingual space, 540
Subluxation, 922, 962, 963, 968, 1016
Submandibular approach (Risdon's), 915
Submandibular gland, 674
Submandibular incision, 312, 313, 454, 615
Submandibular nodes, 712
Submandibular space, 524, 527, 538
Submandibular triangle, 643
Submarginal scalloped rectangular flap, 307
Submasseteric space, 542
Submental flap, 313
Submental space, 538
Submental/submandibular lymph node, 675
Submental triangle, 643
Submentovertex view, of radiological examination, 32, 41, 713
Submucous, 484
cleft, 732
fibrosis, 22, 934, 958
Subperiosteal, 484
Subsigmoid oblique subcondylar osteotomy, 858
Subtarsal approach, 1098
Subtotal Le Fort I maxillary osteotomy, 845
Subtotal or total maxillectomies, 597
Subtotal parotidectomy, 703
Succinylcholine, 241
Suckle, 752
Sucralfate, 666
Suction drain, 345
Sugarless candy, 686
Sulcular full thickness flaps, 307, 308
Sulphacetamide, 697
Sunburst, 650
Sunderland classification, 795
Sunray appearance, 649
Sunray effect, 650
Superficial and deep ranula, 614
Superficial erosion of bone, 606
Superficial parotidectomy, 699, 701
Superficial shave biopsy, 85
Superficial temporal and facial arteries, 723
Superficial X-ray therapy 45-100 kV, 657
Superior, based on position, 963
Superior border augmentation, 452
Superior orbital fissure syndrome, 1084
Supernumerary nostrils, 742
Superolateral orbital cleft, 746
Superomedial orbital cleft, 742
Supportive implants, 484
Supportive therapy, 528
Suppurative arthritis, 922
Supraclavicular nodes, 643
Supraglottic airway, 128, 226–228
Supramentale, 836
Supraomohyoid neck dissection (SOHND), 654
Supraorbital approach, 1097
Supraorbital nerve, 742
Supraorbital rim, 742
Supraperiosteal, 484
Supra vital stains, 33
Sural nerve, 804, 805
Surface applicator (radium mould), 657
Surface charge theory, 178
Surgeon's knot, 328
Surgical anatomy, 673
Surgical/bone wax, 374
Surgical cement, 173
Surgical ciliated cyst, 614
Surgical cricothyrotomy, 128, 130
Surgical curettes, 269
Surgical decompression, 802
Surgical drain, 279, 344, 422, 719
closed drain, 280
corrugated rubber drain, 280
disadvantages, 280
Hemovac drain, 280
open drain, 279
tube drains, 280
Surgical emphysema, 143
Surgical gut (plain and chromic), 318
Surgical haemostasis, 425, 727
Surgical linen, 318
Surgical loupes, 280
Surgical operating microscope, 442
Surgical resection, 648
Surgical splints, 842
Surgical suction apparatus, 278
Surgicel, 336
Surgicel fibrillar, 336
Suspension wires, 989
Suture, 318
and ligation, 336
material, 318
monofilament, 318
multifilament, 318
synthetic material, 320–321
methods, 325
of nerve, 803
Suxamethonium chloride, 241
S. viridans, 351
Swab holder, 255
Swallowing of teeth, 373
Swarm of bee, 700
Sweet's diagnostic criteria, 813
Swelling, 10, 25–26
Sympathetic reflexes, 220
Symphysis fracture, 1027
Synaptic knobs, 790
Syncope, 125, 133, 1096
Syndromes associated with cleft lip and palate, 749
Synechiae formation, 730
Synkinesis, 795
Synovial
cyst, 922
fistula, 922
membrane, 910
osteochon dromatosis, 922
sarcoma, 922
Syphilis, 23, 27
infection from contagious disease, 922
Systemic lupus erythematosus (SLE), 795
Systemic sclerosis, 934
T
Tachycardia, 975
‘Tail’ of the parotid gland, 702
Tanaka ligament, 910
Target cells, abnormal RBC, 59
Taste testing, 801
T cell lymphotrophic virus, 696
Technetium-99m, 52, 682
Teeth displaced into sinus, 727
Teeth in line of fire, 350
Tegretol, 816
Telangiectasia, 10, 15, 666
Telecanthus, 742, 979, 1067, 1121
diagnostic criteria, 1121
N-Telopeptides, 640
Temazepam, 219
Temporal branches, 797, 798
of facial nerve, 673
Temporalis, 805–809
lengthening, 805, 806
with fascia lata, 805
without fascia lata, 807
muscle flap, 954
myofascial flap, 664
Temporal space, 541
Temporary diplopia, 1094
Temporomandibular joint (TMJ), 922
ankylosis, 15, 871
fibrous/bony, 934
arthrosis, 936
disorders, 922–941
classification, 922
dysarthrosis, 936
dysfunction, 835
pain dysfunction syndrome, 936
Temporozygomatic cleft, 742
Tender points, 939
Tendon grafts, 315
Tendonitis, 922
Tennison and Randall bilateral lip repair technique, 760
Tennison triangular flap, 755
Tenon technique, 868
Tensor veli palatini, 751
Tentorium, 818
Teratogenic agents, 748
Tertiary haemostasis, 335
Tessier, 741–747
arhinia, 744
superolateral orbital cleft, 747
Tetanus, 934, 958, 1009
Tetanus prophylaxis, 1009
Tetany-hypocalcaemia, 958
Tetracycline, 151, 155
Tetrafocal distraction, 882
Texaphyrins, 668
Thayer–Martin medium, 72
Theories of dry socket, 375
Thermal agents, 338, 940
Thermal pain, 791
Thermal reactions, 1167
Thermocoagulation, 816
Thermocouple, 289
Thermography, 925
Thick split thickness skin graft, 315
Thierry Vuillemin classification, 947
Thin split thickness skin graft, 315
Thiocyanate, 676
Thiosulphate citrate bile salts sucrose (TCBS), 72
Thompson's modified nasal correction through intranasal incisions, 758
Three ‘F’ mnemonic, 547
Three-point fixation, technique, 1103
Threshold potential, 178
Thrombin, 336, 425
Thrombocytopaenia, 60, 113
Thrombocytosis, 60
Thrombophlebitis, 552
Thyroglossal cyst, 25
duct, 615
Thyroid crisis, 110
Thyroid storm, 110
Thyromental distance, 216
Thyrotoxicosis, 109
Tibial nerve, 805
Tic douloureux, 808
Tigecyclin, 174
Tiludronate, 640
Timing
of closure, 766
for open nerve injury repair, 803
of repair, 763
of surgery, 825
Tincture benzoin, 173, 588, 656, 718
Tincture of aconite, 383
Tincture of iodine, 383
Tinel sign, 373
Tinnitus, 819
Tirapazamine, 668
Tissue and bone loss, 666
Tissue biopsy, 33
Tissue engineering, 657
Tissue forceps, 250, 257
Allis forceps, 250
Babcock's forceps, 250
Haemostat (artery forceps), 250
Kocher's forceps, 250
Lane's forceps, 250
Titanium hollow screw osseointegrated reconstruction plate (THORP), 1001
Titanium plates, 996, 1134
TMJ, See Temporomandibular joint (TMJ)
TN5 injuries, 803
TNM classification (AJCC), 642, 643, 698
oral cancer, 643–644
Tobacco, 642
Toluidine blue, 87
Tomography, 44
Tongue and cheek retractor, 260
Tongue depressor, 250, 264
Tongue flap, 307, 769
Tonsillitis, 20
abscess, 934
Toothed forceps, 250, 257
Tooth root, 727
Tooth size analysis, 838
Topazian classification, 533
Top down and outside in theory, 982
Topical chemotherapy, 669
Topical local anaesthesia, 186, 666
Topiramide, 816
Torus mandibularis, 460, 461
Torus palatinus, 460
Total disarticulation, 563
Total maxillectomy, 699
Total parotidectomy, 699
Total sialadenectomy, 703
Total subapical mandibular osteotomy, 865
Tourniquet test, 115
Towel clip, 255
Tower skull, 15
Townes-Brocks syndrome, 931, 932
Tracheal intubation, 228
equipment for, 228
Tracheal window, 132
Tracheostomy, 130, 131, 996
tube, 228, 229, 250, 255
Traction test, 1094
Tractotomy, 819
Tragal pointer, 700
Trajectories of force (mandible), 1024, 1025
Tramline test, 1130, 1138
Tranexamic acid, 111, 112, 115
Transalveolar extraction, 368
Transantral repair, 726
Transconjunctival approach, 1098
Transconjunctival incision, 313
Transcutaneous electric nerve stimulation (TENS), 940
Transdermal glyceryl trinitrate (GTN), 221
Transfer coping, 494, 496
Transfer method, of flaps, 314
advancement flaps, 314
interpolated flaps, 314
rotation flaps, 314
transposition flap, 314
Transformation osteogenesis, 878
Transforming growth factor, 1155
TGF, 668, 748
Transillumination, 717, 718
positive, 615
Transincisive foramen clefts, 738
Translucency, 26
Translucent blue, 614
Transoral exposure, 656
Transosseous, 484
wiring, 858, 995
Transosteal dental implant, 479
Transport distraction osteogenesis, 657
Transverse maxillary deficiency, 825, 826
Transverse skeletal discrepancies, 824
Transverse symmetry, 831
Trapezoidal flap, 309, 420
Trapezoid-shaped buccal flap, 723
Trauma, 715, 922, 1018
Traumatic (acute), 934
Traumatic arthritis, 922, 933
Traumatic, based on aetiology, 963
Traumatic bone, 27
cyst, 612, 613
Traumatic neuroma, 792, 793, 812
Traumatic optic neuropathy, 980
Traumatised region, 1018
Traumatised tooth, 1013
Trauner's technique, 472
Treacher Collins-Franceschetti syndrome, 713, 734, 742, 746
Tree in winter appearance, 678, 679, 680
Trephine burs, 507
Treponema denticola, 376
Triamcinolone acetonide emollient paste, 173
Triangular defect, 622
Triangular flap, 308, 404, 405
Tricyclic antidepressant, 940
Trigeminal nerve, 183, 809
Trigeminal neuralgia, 793, 808
clinical features, 814
Trigeminal root section, 818
Trigger factors, 814
Trigger points, 813, 936, 939
Trigonocephaly, 15, 16
Tripelennamine hydrochloride, 169
Triple throw knot, 328
Trismus, 207, 539, 542, 694, 703, 933, 961
hystericus, 958
pseudocamptodactyly syndrome, 934
Trocar, 277, 719
Trotter's syndrome, 934
Trucut biopsy, 86
True dislocation, 963
Tuberculosis, 11, 23, 116
infection from contagious disease, 922
test, 32
tuberculous ulcer, 23, 24
Tuberoplasty, 464
Tube-shift method, 391
Tubocurarine, 240
Tumours, 526, 563, 578, 922
tumour-bone interface, 655
tumour-carcinoma of maxillary sinus, 715
Turdek method of primary septal cartilage repositioning, 759
Turricephaly, 15–16
Tweed's method-DC4, 367
Two piece Le Fort I osteotomy, 852
Two-point fixation, 1102
Two-stage implant, 487
Two-thirds of dorsal surface swelling of tongue, 610
Tympanic neurectomy, 686, 707
Tympanomastoid suture line, 700
Tyrosine kinase inhibitor, 572
U
Ulcer, 10, 23–24, 644
Ultra-pasteurisation method, 287
Ultrasonic and sonic vibration, 291
Ultrasonography, 32, 56, 677, 682, 683
Uncinate process of ethmoid, 711
Uncinectomy, 729
Uncomplicated crown-root fracture, 1015
Undescended testes, 598
Unerupted tooth, 353, 380
Unfavourable fractures, 1030
Unicameral bone cyst, 612
Unicystic ameloblastoma, 604, 619
Unilateral, symmetry, dislocation, 963
Unilateral cleft lip, 749, 754
repair, 755
Unilateral condylar hyperplasia, 824
Unilateral mandibular hyperplasia, 824
Unilocular lesions, 602
Unipolar cautery, 281
Universal precautions, 121, 297
Unmyelinated fibres, 790
Unstable angina, 103, 136
Untreated maxillary sinusitis, complications of, 719
Upper deep cervical lymph nodes, 712
Upper lip length, 831
Upper motor neuron (UMN), 801
Urea, 676
Urease production test, 71
Urethritis, 27
Uric acid, 67
Urinary hydroxyproline levels, 640
UV radiation, 644
Uvula, 21, 732
Uvulus muscle, 766
V
Vacuum, 221
Vacuum-assisted biopsy, 86
Vagolytics, 124
Valacyclovir, 799
Valving, 766
Vancomycin, 148, 156
Varicella zoster virus, 29, 122, 800
Vascular ingrowth initiation, 1156
Vascular stents, 104
Vasoconstrictors, 181, 182
Vasodilators, 181
Vasovagal syncope, 133
Vazirani-Akinosi's closed-mouth mandibular block, 201–203
Veau classification, 751
Veau III operation, 759
Vector, 296
manipulating knobs, 884
Vecuronium, 241
Velar lengthening, 768
Velo-cardio-facial syndrome, 752
Velopharyngeal closure, 766
Velopharyngeal competence, 763
Velopharyngeal incompetence (VPI), 732, 752, 766, 767, 769
Velopharyngeal (VP) mechanism, 766
VELscope, 87
Vermilion flaps, 760
Verrucous, 10
carcinoma, 25, 647, 661
squamous cell carcinoma, 647
Vertical buttresses, 982
nasomaxillary/medial buttress, 982
pterygomaxillary/posterior buttress, 982
zygomaticomaxillary/lateral buttress, 982
Vertically favourable fracture, 1030
Vertically unfavourable fracture, 1030
Vertical mattress suture, 326
Vertical maxillary deficiency, 826
Vertical maxillary excess (VME), 824, 826
Vertical skeletal profile analysis, 837
anterior component, 837
Vertical split, 1019
Vertigo, 819
Vesicle, 10
Vesiculation, 798
Vestibular incision, 498
Vestibuloplasty, 466
Viaspon, 1021
Vicryl suture material, 319
Vincristine, 651, 669
Viral hypothesis, 799
Viral infection, 122
Visor osteotomy, 454
Visual acuity, 980
Visual impairment, 522
Visualisation, 728
Vital root amputation, 439
Vitamin K, 65
Vitamin A, 668
Vitamin C, 668
Vitamin E, 668
Vitiligo, 15
Vitreous carbon implants, 484
Vizilite plus, for selection of biopsy, 87
Vizilite stain, 33
Voids, sialographic appearances, 679
Volkmann's canal, 557
Volkmann's scoop, 269
Volumetric comparison, 873
Vomer, 737, 752
Vomer flap, 767
Von Ebner's glands, 675
Von Langenbeck operation, 763
Von Rehrmann flap, 721
von Willebrand disease, 65, 113
Voxel, tissue attenuation, 47
VPI, See Velopharyngeal incompetence (VPI)
V-Y advancement flap, 780
V-Y-plasty, 760
V-Y pushback palatoplasty, 763
Kilner-Wardill, 763
W
Waldron's classification, 633
Waldron's procedure, 591
Wallerian, 793
degeneration, 793, 794, 795
Walsham's and Asch's septal forceps, 1113
Walsham's forceps, 272, 1076, 1113
Wardill-Kilner technique, 765
Wardill-Kilner-Veau operation, 764
WAR lines, 392
Warthin's tumour (papillary cyst adenoma lymphomatosum), 700
Wash leather slough, 24
Wassmund classification, 1045
Wassmund technique, 846
Water brash, 684
Waters' view, 32, 584, 713, 717
Watertight repair, 772
Weber-Ferguson approach, 657, 661
facial flap, 637
incision, 313, 314
Web of scars, 760
Wedge biopsy, 83, 84
Wedge principle, 357
Wegener's granulomatosis, 28, 716
Weider's retractor, 250
Weiss's theory of fibro-osseous integration, 481
Well circumscribed, 703
Well-defined radiolucency, 622
Well-developed supraorbital rims, 598
Westergren method, 62, 357
Western blot, 77, 118
Wharfe's assessment, 399
Wharton's duct, 540, 675
Wheel and axle principle, 357, 358
White blood cell count, 61
White-eyed orbital blow-out fractures, 1096
Whitehead's varnish, 173, 590
White line, 392
White sponge naevus, 30
Wicking effect, 319
Wide bore needle, 584
Wilkes staging of internal derangement, 962
Wilson and Blair medium, 72
Wilson score, 216
Winter's classification, 385
Wintrobe method, 62
Wire cutter, 274
Wire pusher, 274
Wire twister, 274
Wood screw, 993
World Health Organization (WHO)
classification of odontogenic tumours, 618
classification of wastes, 302
classify cysts, 597
histologic classification of tumours of salivary glands, 2005, 698
osteoporosis classification, 54
Wound
tapes, 330
Written consent, 1145
Wrong teeth, extraction of, 369
WR-2721 radioprotective agent, 667
Wunderer technique, 847
X
Xenograft, 470, 952
Xerophthalmia, 696
Xerostomia, 666, 683, 685, 686, 696
causes of, 686
X-ray therapy, 657
Xylocaine, 173, 666
Xylometazoline hydrochloride, 717
Y
Y-incision, 689
Y plates, 1121, 1122
Z
ZAGA (zygoma anatomy-guided approach) classification, 1173
Zide and Kents, absolute and relative indications for fracture, 1055
Ziehl-Neelsen stain, 71
Zinc oxide eugenol, 430
Z-spring, 777
Zygomatic arch fractures, 1083
classification of, 1085
fractures not involving orbit, 1088–1089
Henderson's, 1088
Knight and Northwood, 1085
Larsen and Thomsen, 1088
Rowe and Killey, 1085
Rowe and Williams, 1085
horizontal axis, 1086
vertical axis, 1085
clinical finding, 1089
circumorbital oedema and ecchymosis, 1089
crepitation from air emphysema, 1092
degree of nerve injury, 1092
displacement of palpebral fissure, 1092
enophthalmos, 1093
epistaxis, 1090
flattening, 1090, 1091
globe level, 1092
periorbital bleeding, 1089
subconjunctival haemorrhage, 1090
trismus, 1090, 1091
types of orbital haemorrhages, 1089
fixation technique, 1100
four-point fixation, 1104
one-point fixation, 1100
plate and screw technique, 1100
three-point fixation, 1103
two-point fixation, 1102
fracture displacement, 1084
horizontal axis of rotation, 1085
vertical axis of rotation, 1085
fracture reduction, 1100
Balasubramaniam approach, 1100
Bristow's elevator, 1100
closed reduction, 1103
Gillies temporal fossa approach, 1100–1101
Rowe' zygoma elevator, 1100
principles of treatment, 1097
bicoronal approach, 1098
bicoronal/hemicoronal approach, 1098
Carroll-Girard screw, 1099
Dingman approach, 1097
extraoral approach, 1097
Gillies temporal, 1097
inferior fornix approach, 1099
infraorbital approach, 1097
intraoral approach, 1098
invasive surgical procedures, 1097
Keen's approach, 1099
Stacey bone hook, 1099
subciliary approach, 1098
subtarsal approach, 1098
transconjunctival approach, 1099
Zygomatic arch projection, 42
Zygomatic bone, 995
Zygomatic branch, 798
Zygomatic buttress, 991
Zygomatic elevators, 272
Zygomatico-orbital fractures, mechanism of, 1083
high-energy zygoma, 1083
low-energy zygoma, 1083
middle-energy zygoma, 1083
Zygomatic tubercle, 909
Zygomaticus, 798
implants, 1173
external hex fixture head, 1173

Textbook of Oral Surgery - Balaji 3rd Edition

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Textbook of Oral Surgery - Balaji 3rd Edition

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Textbook of Oral

S.M. Balaji MDS, PhD, DSc (Hans)

Preface to the Third Edition

Preface to the First Edition

Section I: Definition and Scope of Oral Surgery

Chapter 1: Definition and Scope of Oral Surgery

Dentistry (ADA Definition)

What a graduate should know

Chapter 2: History Taking and Clinical Examination

Magnetic resonance imaging

Chapter 4: Diagnostic Aid—Haematological, Biochemical and Microbiological

Chapter 5: Histopathological Investigation

Section III: Medical Management in Oral Surgery

Chapter 6: Management of Medically Compromised

Congestive heart failure

Chronic obstructive pulmonary disease

Congenital coagulation defects

Chapter 7: Medical Emergencies and their Management

Chapter 8: Therapeutics in Oral Surgery

Sedatives and hypnotics

Dressings to protect wounds and relieve pain

Stimulants for circulatory failure, syncope and collapse

Section IV: Anaesthesia in Oral Surgery

Chapter 9: Local Anaesthesia

Electrophysiology of nerve conduction (Fig. 9.1)

Basic injection techniques

Intraoral techniques (Fig. 9.7)

Intraoral techniques (Fig. 9.37)

Complication of local anaesthesia

Chapter 10: General Anaesthesia

Delivery of anaesthetic gases and vapours

Managing the airway

Maintenance of anaesthesia: inhalational (volatile) agents and intravenous

Muscle relaxation during anaesthesia: neuromuscular blocking drugs and

Section V: Principles of Practising Oral Surgery

Chapter 11: Armamentarium

Presurgical asepsis and draping

Soft tissue handling armamentarium

Instruments used for reflecting the mucoperiosteal flap

Instruments used for management of fractures

Chapter 12: Sterilisation and Disinfection

Operating room decorum

Chapter 13: Incisions and Flaps

Principles of wound incision

Principles and guidelines for flap designs

Extraoral flap designs in oral surgery

Skin grafts (Fig. 13.20−13.22)

Chapter 14: Suturing Materials and Techniques

Absorbable suture materials

Non-absorbable suture materials

Wound closure tapes

Chapter 15: Haemorrhage and Shock

Chapter 16: Wound Care

Section VI: Minor Oral Surgery

Chapter 17: Exodontia

Indications for extraction

Contraindications for extraction

Assessment of teeth for extraction

Techniques of extraction of teeth

Principles of tooth removal

Chapter 18: Impaction

Maxillary third molars

Chapter 19: Endodontic Surgery

Classification of endodontic surgery