ENDODONTICS

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ENDODONTICS
Fourth edition

Kishor Gulabivala BDS, MSc, FDS RCS (Edin), PhD, FHEA

Professor and Head of Endodontology, Honorary Consultant in Restorative Dentistry
Head of Department of Restorative Dentistry, UCL Eastman Dental Institute, London, UK

Yuan-Ling Ng BDS, MSc, MRD RCS (Eng), PhD, FHEA

Senior Clinical Lecturer in Endodontology, Director of Masters Programmes in
Endodontology, UCL Eastman Dental Institute, London, UK

Edinburgh  London  New York  Oxford  Philadelphia  St Louis  Sydney  Toronto  2014
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© 1995 Times Mirror International Publishers Limited

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 Foreword
Fifty years ago, when we were young dental students, the treatment of
dental, pulpal and periapical disease was taught in a disciplined fashion
according to the principles of G.V. Black and Louis Grossman. Our uni-
versity teachers were greatly influenced by these pioneers of dental learn-
ing and consequently, we were introduced to treatment modalities in stages
following the natural history of the disease process. This was done in a
very practical and mechanical way. We were brought to graduation on a
diet of hollow tubes, apical seals, culturing techniques, and potent topical
drug therapy. Endodontics was presented as an adjunct to the restorative
aspects of dental care, and at that time, it was delivered as a small part of
the overall interests of Departments of Conservative and Operative Den-
tistry. The reasons for this are probably historical. Conservative techniques
were used to deal with the destructive outcomes of dental caries, tooth
surface loss, and trauma. This loss of coronal integrity of teeth allowed
the invasion of micro-organisms. Endodontics involved the treatment of
ensuing infections. It was natural to consider endodontics as a component
of Conservative Dentistry.
Postgraduate study at the Eastman Dental Institute improved our under-
standing and refined our performance in the delivery of restorative care.
We realised that there was an essential need to base our clinical work on
the cornerstones of Endodontics, Periodontics and a reliable working
knowledge of Occlusion. Endodontology, the science that underpins endo-
dontics, took on a primary role in our appreciation of dental diseases. We
found the clinical discipline most satisfying and, when correctly applied,
we were able to achieve predictable clinical outcomes. During this period
of our development, we benefited greatly from the tutelage of the late Fred
Harty, who not only encouraged us to learn more about endodontology but
also supported our efforts to disseminate our knowledge as widely as pos-
sible, all at a time when endodontics was not defined as a speciality in the
UK, and the British Endodontic Society was in its infancy.
Endodontics has now come of age and has become an important aspect
of patient care. The biological basis for the subject is understood and
research into the pathological processes and clinical outcomes of treatment
have led to clearly established evidence based therapies. It is pleasing to
see the rise in numbers of specialists in this area of clinical activity. The
establishment of dedicated departments and professorial positions to
progress the subject and to maintain essential standards is also applauded.
Kish and Paula are to be congratulated for their hard work in producing
this 4th Edition of Endodontics. They have presented a well re-organised
and richly illustrated text that unifies modern evidence-based thinking. It
will be of value to all students, practitioners and specialists, who possess
an enthusiastic interest in endodontics. It is with great pride that we
commend this work to readers.
Chris Stock
Dick Walker

The first edition of this book (1988), “A Colour Atlas of Endodontics”,
was published under the editorship of Jack Messing and Chris Stock and
consisted of 21 short, practical chapters. A wonderfully illustrated book,
it met the needs of the time. Endodontics was still in the early stages of
gaining recognition as a specialized discipline in the UK. A realization was
dawning that experts with deep knowledge and advanced skills could make
a unique contribution to patients’ needs. The book focused on techniques
and “how to” questions, with lots of useful practical tips. The final, single
page chapter on “The Way Ahead”, alluded to the lack of evidence-base
in endodontics, the rise in demand for complex treatment and the need for
general dental practitioners to improve their skills, despite the develop-
ment of specialisms. This proved a prophetic vision.
The second edition (1995), “Color Atlas and Text of Endodontics”, was
led by Chris Stock with three newly enlisted editors (Kishor Gulabivala,
Dick Walker and Jane Goodman). The book retained its practical and
technique-oriented approach through its 17 chapters, but started with a
more robust scientific, biological and clinical rationale, reflecting the
growing maturity of the discipline in the UK. The approach met the chang-
ing needs of the general dental practitioner, who faced more challenging
cases as informed patients sought and demanded higher levels of service.
The editors embraced the pictorial story-board concept to convey the
message to its readership in a simple, coherent style.
The third edition (2004), “Endodontics” (editors: Stock, Walker, Gula-
bivala), retained its richly illustrated essence and was more emphatically
founded in scientific and clinical rationale. The maturity of the book
reflected the evolving needs of the general dental practitioner, who was
seeking to acquire greater sophistication about endodontics. The discipline
had finally gained recognition as a specialty in the UK in 1998. In parallel,
the commercial sector recognized the potential in the growth of endodontic
service provision and fueled their research and development wings to
innovate and supply a burgeoning number of instruments and materials.
Along with the technical revolution came the need for clinical experts who
could explain and disseminate the proliferating plethora of new techniques
utilizing the emerging products. It was therefore, challenging to describe
all the techniques in a book, there were simply too many. Instead, the
editors appreciated the need to distil the principles, allowing dentists to
learn the core essence, which they could apply to any technique. The
editors had been privileged enough to ride the crest of the wave of these
exciting developments in endodontics, as they nurtured masters and spe-
cialty training programmes, as well as having ran specialist endodontic
clinics in hospital and practice settings.
This fourth edition (2014), retains one of the previous editors (K Gula-
bivala), Chris Stock and Dick Walker having taken a well-earned retire-
ment from their illustrious careers, and includes a new co-editor, Yuan-Ling
(Paula) Ng. The latter, a long-serving clinician and teacher, has been
instrumental in helping to advance the clinical evidence-base for endodon-
tics through research, as well as being the programme director for the
endodontic masters programmes at the Eastman Dental Institute. This
latest book will continue the tradition established in previous editions. It
Preface
updates and enhances its evidence-based and rationalized clinical approach,
whilst upholding the richly illustrated perspective, to serve the visually-
dependent learning framework of many aspiring endodontists. The book
is significantly re-organized into four sections: section 1, establishing the
scientific and clinical rationale; section 2, prepares the reader for the pre-
requisites of treatment; section 3, describes the core treatment details; and
section 4, discusses the interfaces between disciplines, as the growth of
specialisms has altered the dynamics between clinicians who have devel-
oped higher skills and knowledge in defined areas. The approach also
demanded the incorporation of new material and chapters to ensure a
comprehensive coverage of subject matter.
The endodontic service needs of the UK population is currently deemed
to be best met by three levels of expertise: the general dental practitioner
serving the core needs; the dental practitioner with enhanced endodontic
skills to manage the moderately complex cases; and finally, the specialist
tier serving the needs of patients with more complex problems. It is hoped
that this book will serve practitioners at different levels of service delivery:
(1) inspire the advanced undergraduate dental student about to enter prac-
tice; (2) help the general dental practitioner to consolidate their knowledge
and skills after graduation; (3) form the basis of advancement for the
practitioner with enhanced skills; and (4) lay the preliminary foundation
for the aspiring specialist. Whilst the evolution of this book is described
in the context of the UK healthcare system, various streams of evidence
(endodontic journals, epidemiological data, international conferences and
global perspectives of health sciences) suggest that the same process of
evolution is endemic across the globe, making the text relevant wherever
endodontic practice prevails.
The editors recognize that book-learning alone cannot enhance technical
and clinical skills, however practical the information. Theory must be
assimilated into working knowledge through vigilant and reflective prac-
tice. Rare individuals are able to make this transition independently but
most require various levels of hands-on instruction, coaching and mentor-
ing. Advanced endodontic skills are developed through parallel and inte-
grated cognitive, visual, technical and clinical effort and discipline. The
refinement of personal discipline, conscientious attitude and detailed atten-
tion necessary for successful endodontics, happily create the right attributes
for life-long personal development and fulfillment. This philosophy was
also embodied by Aristotle who is quoted to have said:
Excellence is an art won by training and habituation.
We do not act rightly because we have virtue or
excellence, rather we have those because we acted
rightly. We are what we repeatedly do. Excellence
then is not an act but a habit.
We hope that this book will be only the beginning of the reader’s journey
of development in this fascinating field.
Kishor Gulabivala
Yuan-Ling (Paula) Ng
 Acknowledgements

The editorship and authorship of this book has changed over the last three In addition, the following have contributed various images in the past:
editions, during which time the concept and content of the book has evolved
through constant feedback and various contributions. The presented version Professor Ramachandran Nair, Mr JF Roberts, Mr FJ Hill, Late
in this edition is significantly updated but still carries the vestiges of previ- Professor GB Winter, Professor Paul Speight, Dr John Bennett, Mrs
ous authors and editors’ contributions. The editors would like to acknowl- P Barber, Dr Nicky Mordan, Mr J Morgan, Dr Elisabeth Saunders,
edge and thank the following for their previous contributions: Professor Michael Tagger, Professor Paul Dummer, Late Professor
Thomas Pitt Ford, Professor Callam Youngson, Dr Margaret Byers,
Dr Christopher JR Stock Dr Melody Chen, Professor Ivor Kramer, Late Dr Jakob Valderhaug,
Professor Richard T Walker Dr Lars Laurell, Miss Noushin Attari, Miss Angela Christie, Dr Michael
Dr Jane Goodman RN Collins, Dr Peter Endo, Dr David Dickey, Dr Ben Johnson, Dr Paul
Dr Jackie E Browne King, Dr Koos Marais, Dr Joe Omar, Dr Paul O’Neilly, Dr Alistair
Dr Ian Cross Spiers, Dr Peng Hui Tan, Dr J Woodson.
Dr Carol Mason
Dr Shahrzad Rahbaran The editors gratefully acknowledge the effort of various Masters level
Dr John D Regan postgraduate students whose research projects have contributed images to
Professor Paul R Wesselink this book. They are:

Ms Monika Sharma, Mr Shailesh Rojekar, Ms Naomi Richardson,

Ms Chrisa Oikonomou, Ms Athena Iacovidou, Ms Glynis Evans, Mr Aws
Alani, Ms Maysoon Haji, Mr Rahul Arora, Mr Benjamin Long, Mr Sui
Fei Leung, Mr Ian Alexander, Mr TH Aung, Mr Paul Brennan.

The editors would also like to thank J van der Meer for providing
images, Jeffrey Chan for his photographic expertise, Dr William Cheung
& Associates, Robert Ng’s surgery for the use of his practice and equip-
ment as an example, and Rahul Goria for use of his surgery as an example.
Prof Ian Eames for the use of images on irrigation from Computational
Fluid Dynamics.

Ian Alexander BDS, MSc
Senior Clinical Teaching Fellow
Coordinator of Diploma in Endodontic Practice
UCL Eastman Dental Institute, London, UK
Proof-reading of chapters 8 & 9
Ulpee Darbar BDS, MSc, FDS RCS
Consultant in Restorative Dentistry & Clinical Director
Department of Periodontology
UCLH Trust, London, UK
Provided intellectual content for chapter 12
Rachel Leeson BDS, FDS RCS, PhD, FHEA
Senior Clinical Lecturer in Oral Surgery
Director of Masters Programme in Oral Surgery
UCL Eastman Dental Institute, London, UK
Provided main intellectual content for chapters 16 and 17
Alyn Morgan BChD, MSc
Senior Clinical Teaching Fellow
Coordinator of Diploma in Endodontic Practice
UCL Eastman Dental Institute, London, UK
Proof-reading of chapters 8 & 9
Alexander Mustard BDS, MFDS RCS, MSc
Teacher in Endodontology
UCL Eastman Dental Institute, London, UK
Provided main intellectual content for chapter 15; proof-reading of
chapters 4 & 10
Contributors
Farhad B. Naini BDS, MSc, PhD, FDS RCS, M Orth RCS, FDS
Orth RCS, GCAP, FHEA
Consultant Orthodontist Kingston & St George’s Hospitals, London;
Honorary Senior Lecturer Craniofacial Anatomy, Biology &
Development St George’s Medical School, University of London,
London, UK
Provided intellectual content for chapter 13
Murray Saunders BDS, MGDS RCS, MSc
Honorary Lecturer in Endodontology/Specialist in Endodontics
Coordinator of Short Course Modules
UCLH Trust, London, UK
Proof-reading of chapters 6 & 9
Morgana Eli Vianna BDS, MSc, PhD, FHEA
Clinical Lecturer in Endodontology
Coordinator of Masters Programmes in Endodontology
UCL Eastman Dental Institute, London, UK
Provided figures 3.5, 3.27, 3.28, 3.48; tables 3.3 & 3.5; and
proof-reading of chapter 3
Wicher Joerd van der Meer BDS
Teacher, University Hospital of Groningen;
Staff Member, Centre for Special Care Dentistry, Assen;
Honorary Research Associate
UCL Eastman Dental Institute, London, UK
Provided intellectual content for section on CBCT for chapter 4;
generated and provided 3D images in figures 1.40, 2.9, 3.1, 3.5,
3.8, 3.11, 4.64, 4.65, 4.66, 4.67, 8.55; tables 4.12, 4.13; proof-
reading of chapter 15
 Introduction to endodontology and endodontics

DEFINITION OF ENDODONTOLOGY AND ENDODONTICS

The Consensus Report of the European Society of Endodontology (2006)

defines this discipline thus:
“Endodontology is concerned with the study of the form, function and
health of, injuries to and diseases of the dental pulp and periradicular
region, their prevention and treatment; the principal disease being apical
periodontitis, caused by infection. The aetiology and diagnosis of dental
pain and diseases are integral parts of endodontic practice. The scope of
the special area of dental practice known as endodontics is defined by the
educational requirements for the training of a dentist, as described by the
European Society of Endodontology in the undergraduate curriculum
guidelines for Endodontology (European Society of Endodontology 2001;
De Moor et al. 2013).
Endodontic treatment encompasses procedures that are designed to
maintain the health of all or part of the dental pulp. When the dental pulp
is diseased or injured, treatment is aimed at preserving normal periradicu-
lar tissues. When apical periodontitis has occurred, treatment is aimed at Fig. 1.1  Pulpal and Periapical disease
restoring the periradicular tissues to health: this is usually carried out by
root canal treatment, occasionally in combination with surgical endodon-
In summary therefore, a breach in the integrity of the tooth (first line of
tics. The scope of endodontics includes, but is not limited to, the differen-
defence) exposes dentine, which simultaneously stimulates the pulp to
tial diagnosis and treatment of oro-facial pain of pulpal and periradicular
produce local exudative inflammation (second line of defence) and odon-
origin; prevention of pulp disease and vital pulp therapy; pulp extirpation
toblasts to proliferate secondary dentine (third line of defence) and peritu-
and root canal treatment; root canal treatment in cases of apical periodon-
bular dentine (fourth line of defence). Death of the pulp tissue leaves only
titis; (root canal) retreatment in case of post-treatment apical periodontitis;
the final and fifth defensive barrier, the periradicular inflammatory lesion
surgical endodontics; bleaching of endodontically treated teeth; treatment
to prevent invasion of the body by bacteria (Fig. 1.1).
procedures related to coronal restoration by means of a core and/or a post
The dental pulp may also succumb through acute traumatic injury to the
involving the root canal space and/or endodontically related measures in
neurovascular bundle supplying the tooth; where in case of sterile necrosis,
connection with crown-lengthening and forced eruption procedures and
infection may be delayed for up to six years or longer unless there is a
treatment of traumatized teeth.
breach in the tooth structure allowing bacteria to invade. A rational
As part of dentistry’s main goal to maintain a healthy, natural dentition
approach to management of these inflammatory diseases requires an
for the public, the aim of endodontic treatment is to preserve functional
understanding of the normal structure and function of teeth with their sur-
teeth without prejudice to the patient’s health. Every dental practitioner is
rounding tissues. A clear understanding of the aetio-pathogenesis of pulpal
expected to be able to recognize and treat effectively pulpal and periapical
and periapical diseases leads to insight about the principles of their man-
injuries and diseases that are commonplace and within the skills acquired
agement. Treatment approaches therefore consist of control of bacterial
by graduates of dental schools in Europe (European Society of Endodon-
infection of dentine surfaces, prevention of their recontamination and
tology 2001; De Moor et al. 2013). The cases that are beyond an individual
adaptation and apposition of filling materials to create an environment
dental practitioner’s means concerning diagnostic and/or technical alterna-
within which the body is able to effect healing. Treatment aimed at pre-
tives should be referred to a colleague who has completed specialty train-
serving a functional pulp by facilitating resolution of pulp inflammation
ing in Endodontology (European Society of Endodontology 1998) or to a
is called vital pulp therapy. Treatment aimed at preserving a functional
colleague who has acquired the necessary expertise elsewhere”.
tooth by facilitating resolution of periapical inflammation is called root
canal treatment. Root canal treatment may also be used to prevent apical
BRIEF INTRODUCTION TO PULPAL/PERIAPICAL DISEASE periodontitis, when the pulpal inflammation is judged to be beyond resolu-
tion; or the tooth is judged to need elective devitalisation for restorative
Pulp disease consists of inflammation of connective tissue (the pulp) which reasons. Treatment aimed at recovering some element of pulp functionality
in common with inflammatory responses in other parts of the body can be after effecting management of periradicular inflammation associated with
caused by any type of injury (mechanical, physical, chemical, thermal or immature teeth in young patients is called regenerative pulp therapy.
electrical). Such transient injury is usually followed by good pulpal recov-
ery within 3-4 weeks. Persistent, progressive and permanently damaging
inflammation may be caused by unremitting injury of the pulp through any REFERENCES
means, however, the most common clinical cause is oral bacteria. As yet Quality guidelines for endodontic treatment: consensus report of the European Society
undefined pathogens interact with the pulp directly or via the medium of of Endodontology. International Endodontic Journal 39, 921–930, December 2006.
European Society of Endodontology, 2001. Undergraduate curriculum guidelines for
dentine and lead to its ultimate demise. Death and necrosis of the pulp endodontology. Int Endod J 34 (8), 574–580.
tissue leaves an unprotected central cavity within the tooth, allowing bac- De Moor, R., Hülsmann, M., Kirkevang, L.L., Tanalp, J., Whitworth, J., 2013.
teria to invade, colonise, contaminate and infect the root canal space, Undergraduate Curriculum Guidelines for Endodontology. Int Endod J [Oct 4.
doi:10.1111/iej.12186].
eventually leading to periradicular inflammation which manifests clini- Guidelines for specialty training in Endodontology. International Endodontic Journal 31,
cally as a radiographic radiolucency, with or without symptoms. 67–72, January 1998.
 1
Section 1 Rationale for disease management
Tooth organogenesis, morphology and physiology
  K Gulabivala, Y-L Ng
TOOTH DEVELOPMENT
Many readers approach human embryology with a view to satisfying aca-
demic test requirements and may even believe such academic knowledge
to be far removed from clinical practice. Yet this book begins with this
fascinating subject, not merely to lay an academic foundation for the
knowledge of endodontics but because contemporary practice recognizes
that these biological processes hold the key to future therapeutic strategies.
Regenerative treatment approaches depend upon insight from develop-
mental processes to engineer the growth of new tissues to replace those
that are diseased or damaged. The ultimate may even be to grow whole
replacement teeth on demand, in situ or for implantation. Among the clini-
cians involved should be endodontists in whose field of knowledge and
practice these procedures should lie. Any clinician involved in delivering
procedures that even border on regenerative techniques should have a basic
understanding of tooth development and its associated structures.
The “intelligence” or “activating force” that directs the precise coordi-
nation of multiple cell line activity, growth, migration, induction, fusion
and disintegration with such control and symphonic grace, still eludes us.
In our current state of knowledge, we are left merely to describe the
observable and timed changes gleaned through various biological studies.
Experimental studies also give us some insight about the genomic and
proteomic involvement in the process, even though the picture is far from
complete. Yet there is already sufficient intuitive knowledge to enable the
culture of tooth tissues and whole teeth in the laboratory, albeit in a neo-
phytic way (Fig. 1.1).
EARLY DEVELOPMENT OF TEETH
The primitive mouth cavity is evident as a slit-like space lined by ectoderm
in the 3–4-week-old human embryo. It is located under the surface of the
brain capsule and above the pericardial sac where the heart forms. The
mouth cavity is still separated from the primitive pharynx by the oropha-
ryngeal membrane. The mandibular processes grow ventrally on each side
of the head to meet gradually in the midline, where they form the lower
border of the mouth opening. The maxillary processes arise from the upper
surfaces of the origin of the mandibular process and likewise grow towards
the midline, to form the upper border of the mouth below the brain capsule
(Fig. 1.2). The maxillary and mandibular processes are essentially exten-
sions of mesenchyme tissue covered by ectoderm. The ectoderm is a layer
of low columnar epithelial cells, resting on a basal lamina which separates
them from the mesenchymal tissue, which originates from the neural crest
cell line. In some regions, such as the tooth-bearing part, the epithelium
has a more superficial part, which consists of 2–3 layers of flattened cells.
At this stage, the maxillary and mandibular processes do not show separate
lip or gum regions; the development of the lips, cheeks and gum regions
is closely associated with the development of the dental lamina, from
which teeth arise.
PRIMARY EPITHELIAL BAND, VESTIBULAR BAND AND
DENTAL LAMINA
The first indication of formation of tooth development structures becomes
evident at 6 weeks of embryonic life when the oral epithelium in the lateral
© 2014 Elsevier Ltd. All rights reserved.
regions of the maxillary and mandibular processes proliferate and then
spread towards the midline where they become continuous into horseshoe-
shaped bands. These bands are not evident on the surface but project into
the underlying mesenchyme and are called the primary epithelial bands.
During the seventh week of embryonic life, the primary epithelial band
divides on its deep surface into two processes; the outer, thicker one
becomes the vestibular lamina (responsible for the later separation of lips/
cheeks from gums) and the inner, smaller one becomes the dental lamina
(which later gives rise to the teeth) (Fig. 1.3). As the dental lamina grows
in length, it penetrates deeper into the mesenchyme; at the front of the
mouth in a lingual direction, to form a shelf-like projection and at the back
of the mouth remaining more vertical (Fig. 1.4). It is not known whether
this results from active invagination of the lamina or upward proliferation
of the mesenchyme.
ENAMEL ORGANS
A short while after formation, the dental lamina thickens into small rounded
swellings, involving the whole thickness from free edge to the base of
attachment to the oral epithelium. These are the enamel organs of the
deciduous teeth with four in each quadrant (2 incisors, canine and first
deciduous molar) (see Fig. 1.4). The dental lamina continues to grow
backwards, giving rise to further enamel organs for the second deciduous
molar (10-week embryo), and the permanent molars (first permanent molar
at 16-week embryo; second and third permanent molars after birth). At 10
weeks of embryonic life, the enamel organs and dental lamina conform to
a catenary curve. As the tooth germs grow, the spacing between them is
reduced. There is at this early stage no indication of the successional per-
manent teeth, which develop later by budding off from the lingual aspects
of each deciduous enamel organ.
DENTAL PAPILLA
The mesenchymal tissue surrounding the developing enamel organ
responds by proliferation to form a dense mass of cellular tissue. This gives
rise to the dental papilla (primitive pulp) and the follicular sac for each
tooth bud. The enamel organ in the “bud” stage appears as a simple, spheri-
cal to ovoid, epithelial condensation that is poorly morpho- and histo-
differentiated. The epithelial component is separated from the adjacent
mesenchyme by a basement membrane. The combination of enamel organ,
dental papilla and follicular sac are collectively known as the tooth germ
(Fig. 1.5). The enamel organ becomes concave on its papillary surface and
begins to grow at the rims so as to encircle the dental papilla, which, at
this stage, is partly capped by the enamel organ (hence “cap” stage) (Fig.
1.6) and progressively embraces a greater volume of it, to be called the
“bell” stage (Fig. 1.7). At the cap stage, the centre of the concavity devel-
ops a projection of epithelium called the enamel knot (Fig. 1.6), which
soon disappears by programmed cell death (apoptosis) and seems to con-
tribute cells to the enamel cord. The enamel knot represents an important
regulatory signalling centre during tooth development by producing bone
morphogenetic proteins (BMP-2, BMP-7), fibroblast growth factor (FGF–
p21 cyclin-dependent kinase inhibitor), sonic hedgehog (Shh), WNT and
transcription factors. These signals regulate growth and development of
the epithelial folds that correspond to the cusp pattern of the mature tooth.
 Tooth organogenesis, morphology and physiology  3

Fig. 1.1  Something to

Buccal lamina
chew on (courtesy of
Takashi Tsuji, Tokyo
University of Science)

Enamel niche

Enamel organ

Fig. 1.4  The primary enamel organ

Vestibular band

Tongue

Medial nasal process

Lateral nasal process Eye placode

Maxillary process

Mandibular process

Enamel niche
Cardiac sac

Fig. 1.2  Maxillary and mandibular processes in the head of human embryo
(approx. 5 weeks)

Mesenchyme
Tongue Mesenchyme Dental papilla Enamel organ Bone

Fig. 1.5  The tooth germ

involved in the process, by which the cap stage is transformed into the bell
stage or that it is a focus for the origin of stellate reticulum cells.

VESTIBULE FORMATION
Concurrent with the enamel organ development, the vestibular band
growth continues apace. At around the time of the cap stage, a vertical
cleft becomes established in the vestibular band, separating the formative
lips and cheeks from the formative gums (Fig. 1.8). As for the dental
lamina, the vestibular band development progresses backwards.

Vestibular band
Dental lamina
Fig. 1.3  The dental lamina
The primary enamel knot also determines the position of the secondary
enamel knots corresponding to the site of the future cusps. The enamel
cord is a strand of cells seen at the early bell stage of development. When
present, it overlies the incisal margin of a tooth or the apex of the first
cusp to develop. It has been suggested that the enamel cord may be
CHANGES TO AND FURTHER DEVELOPMENT OF
DENTAL LAMINA FOR PERMANENT MOLARS
As the enamel organ is reaching the cap stage, so the dental lamina length-
ens and divides into buccal and lingual parts, though the function of this
is unknown. By the time the enamel and dentine formation begins during
early bell stage, the dental lamina connecting the tooth germs to the oral
epithelium starts to degenerate leaving a network of strands and clumps
of epithelial cells. At the same time, the dental lamina continues to grow
 4  Tooth organogenesis, morphology and physiology

Enamel organ

Tongue
Dental lamina

Enamel

Vestibular band
Dentine
Dental papilla

Mylohyoid muscle

Bone

Fig. 1.8  The formative lips and cheeks separated from the formative gums at
the advanced “bell” stage

Dental papilla Enamel knot

backwards to give rise to the permanent molars but, by this stage, is sepa-
Fig. 1.6  The enamel organ at “cap” stage
rated from the oral epithelium.

DEVELOPMENT OF SUCCESSIONAL
PERMANENT TEETH
The enamel organs for the successional teeth arise so differently from the
permanent molars that it raises the question of whether the permanent
molars should actually be regarded as part of the deciduous series. During
Enamel septum External enamel epithelium the fourth month of fetal development, an epithelial process appears on
the lingual aspect of each enamel organ; this becomes the lamina for the
successional teeth (Fig. 1.9), giving rise to tooth germs in like manner to
the deciduous teeth.

DIFFERENTIATION OF ENAMEL ORGANS

Although the cells of the enamel organ originate from the same source,
those at the outer layer appear different in that they are low columnar and
continuous with the basal layer of the oral epithelium. The deeper cells
are rounder and more closely packed. As the enamel organ enters the cap
stage, the outer cells become taller. From this stage, the cells on the outer
aspect become differentiated into the “external enamel epithelium” on the
outer convex aspect, and the “inner enamel epithelium” on the inner
concave aspect. The two layers meet at the rim of the enamel organ known
as the cervical loop, which remains an active site of cellular proliferation
until the entire tooth is mapped out (Fig. 1.10). It is the epithelial part of
the adult stem cell niche.
During the cap stage, the cells within the enamel organ become sepa-
rated from one another, maintaining contact only at the desmosomal
attachments, giving rise to a star-like appearance which gives their new
name of stellate reticulum. This delicate and loosely formed tissue gains
in volume during the bell stage; the spaces between the cells are occupied
by extracellular material with significant quantities of glycosaminogly-
cans. The function of this tissue appears to be nutritive, particularly before
calcification begins and also supportive (physically) during calcification.
Also at the bell stage, a further distinct layer of cells becomes evident
between the internal enamel epithelium and the stellate reticulum. It is
Stellate reticulum Dental papilla Internal enamel
epithelium called the stratum intermedium and is 2–3 cells thick. The formation of
dentine and enamel begins very soon after this stage is reached; the enamel
Fig. 1.7  The enamel organ at “bell” stage originating from the internal enamel epithelium, which gives rise to the
 Tooth organogenesis, morphology and physiology  5

ameloblasts. As the mineralizing matrices of enamel and dentine are laid

Epithelial nest
down, the shape of the crown becomes fixed.
Dental lamina

Enamel
DIFFERENTIATION OF DENTAL PAPILLA, DENTAL
FOLLICLE AND SHEATH OF HERTWIG
Dentine
Permanent successor
During the above differentiation of the enamel organ, there are concurrent,
although subtle changes in the dental papilla. The loosely packed cells of
the papilla, which are derived from the neural crest (ectomesenchyme)
become infiltrated by delicate fibres, capillaries and nerve fibres during the
bell stage in preparation for the formative task ahead. The innervation
remains simple until birth, after which there is a conspicuous increase in
this system.
As the enamel organ envelops the dental papilla, a mesenchymal cellular
condensation appears around the outer aspect of the external enamel epi-
thelium, which is continuous around the dental papilla beyond the rim of
the enamel organ. This is the primordium of the dental follicle or sac. The
follicle becomes innervated as soon as it appears during the cap stage. The
role of the dental follicle is to provide nutrition and blood supply for
the enamel organ, maintain relationship to the oral mucosa, control the
form and size of the bony cavity, in which the developing tooth germ lies
and, finally, to give rise to the periodontal membrane when the tooth is
erupted. It also contributes to differentiation of cementoblasts and the
formation of cementum.
Once the enamel organ has mapped out the entire form of the clinical
crown, further growth at the cervical loop is geared towards development
of the root. From this point onwards, the internal and external enamel
epithelia are not separated by the stratum intermedium and stellate reticu-
lum but grow as a two-layered epithelial wall, which is now called the
sheath of Hertwig. The sheath of Hertwig maps out the shape of the root(s)
(see Fig. 1.10). It is disposed in a simple tube for a single root, and in a
Dental papillae Bone
more complex form for multiple roots. This is achieved by the inward
Fig. 1.9  The enamel organ for the successional tooth growth of horizontally directed processes of epithelium.

DIFFERENTIATION AND FUNCTION OF

THE TOOTH GERM
As mentioned earlier, the precise nature of the reciprocal inductive influ-
ences is still being elucidated. It was originally thought that the ectodermal
components controlled the induction in the mesenchyme but there is
Stellate reticulum mutual inductive facilitation. The role of innervation in controlling events
is still to be determined.
Enamel The fully differentiated enamel organ is depicted in Figure 1.10, and
Dentine consists of: (1) the external enamel epithelium; (2) the stellate reticulum;
(3) the stratum intermedium; (4) the internal enamel epithelium. At the
Pulp growing rim of the enamel organ, the internal and external epithelia are
Internal enamel continuous but separated from the mesenchyme by the basal lamina. This
epithelium also separates the tooth germ from the vascular tissue of the follicle.
External enamel
The calcified tissues of the teeth, enamel, dentine and cementum all
epithelium develop between the internal enamel epithelium (including its root-ward
continuation in Hertwig’s sheath) and the dental papilla. The basal lamina
separating the internal enamel epithelium and dental papilla represents the
enamel–dentine junction, separating the ectodermal derivative, enamel,
from the mesenchymal derivative, dentine. Following the epithelial–
mesenchymal interactions at the future enamel–dentine junction, the amel-
Epithelial sheath ogenesis and dentinogenesis occur almost simultaneously. The odontoblasts
of Hertwig of the developing dental pulp initiate dentine matrix formation prior to the
Bone
beginning of amelogenesis. They produce collagen that is formed into
bundles pointing towards the cells of the internal enamel epithelium which
are, at this stage, known as pre-ameloblasts. Enamel is laid down between
Fig. 1.10  The enamel organ at “late bell” stage the epithelial surface of the basal lamina and the outwardly retreating
 6  Tooth organogenesis, morphology and physiology
Dental
Dental lamina Ectoderm Placode Bud Cap
Mesenchyme
Bell Late bell
Enamel
Dentine
Pulp
Bone
Fig. 1.11  Schematic model of the molecular regulation of tooth development.
Signal molecules (BMP: bone morphogenic proteins; FGF: fibroblast growth
factors; Shh: sonic hedgehog; TNF: tumour necrosis factor) mediate the
interaction between epithelial (green) and mesenchymal tissues (blue) and
regulate the expression of genes in the responding tissues (shown in boxes).
Signalling centres (red) appear in the epithelium reiteratively and secrete
locally many different signals that regulate morphogenesis and tooth shape.
(Adapted with permission from Thesleff I (2003) Epithelial-mesenchymal
signalling regulating tooth morphogenesis. J Cell Sci 116(9),1647-8)
ameloblasts; the thickness of the enamel being determined by the extent
of migration of the ameloblasts. Dentine is laid down between the mesen-
chymal surface of the basal lamina and the inwardly migrating dentine-
forming cells, the odontoblasts, which originate from the dental papilla.
The thickness of the dentine is determined by the distance migrated by the
odontoblasts. The continual formation of dentine leads to progressive
reduction in the size of the pulp cavities and root canals of the teeth.
Cementum is laid down on the surface of the dentine that is not covered
by enamel after the Hertwig’s sheath starts to break up.
MOLECULAR REGULATION OF TOOTH DEVELOPMENT
Tooth development is a very complex process involving many growth
factors and transcription factors that help ensure an ordered and controlled
development of individual tooth germs, as well as the entire dentition.
Epithelial–mesenchymal interactions require signalling between the two
major components of the tooth germ. Bioactive molecular signals (i.e.
transcription factors, growth factors, cytokines) are produced in a specific
spatial and temporal sequence, such that the cascade of events results in a
tooth with the appropriate tissues and shape. A model of the molecular
regulation of tooth development from initiation to crown morphogenesis
(Thesleff, 2003) is given in Figure 1.11.
ANATOMICAL ANOMALIES
Tooth characteristics such as size, shape, number and structure are geneti-
cally determined as evident from the above section. The most stable teeth
in the human dentition, showing minimum genetic variation are the
canines, central incisors and first molars. The most variable teeth are the
maxillary lateral incisors, the second premolars and the second and third
molars. Malformed teeth may display bizarre pulp-space configurations.
Most commonly this occurs in invagination, evagination, talon cusps,
dilacerations and gemination (Fig. 1.12). Table 1.1 below gives a
classification of the malformations and a brief summary of the presenting
features, which may or may not affect endodontic management. Given the
variation in degree of severity, each case must be judged on its own merits
as far as management is concerned.
TOOTH MORPHOLOGY
Failure to understand the root form and root canal anatomy of the teeth
that we treat is rather like setting out on a long journey without a road
map. The technical execution of endodontic procedures demands a thor-
ough understanding and knowledge of tooth and root canal system mor-
phology. If performance of the procedural elements of endodontic treatment
were likened to sport or crafts, then knowledge of the tooth anatomy would
be akin to knowledge of the sports playground, court or pitch, or the craft
medium.
Endodontic treatment involves controlled manipulation of dentine,
forming the bulk of the tooth, in order to shape or sculpt, scrub or clean,
fill and seal in a controlled way. It is the terrain of the endodontic “sport-
sperson” or the medium of the endodontic craftsman.
Insight about tooth and root canal morphology should, therefore form
the foundation of endodontic management and requires dedicated study.
An understanding of the pulp–space anatomy of teeth is a prerequisite
to the delivery of high-quality root-canal treatment. Many of the problems
attributable to failure in endodontic treatment relate to an inadequate
understanding of the three-dimensional nature of the pulp space. In treat-
ment, it is important to develop a visual picture of the likely location and
number of root canals in a particular tooth. It may be necessary to take
more than one preoperative radiographic view to gain as much information
as possible about the nature of the pulp space before proceeding with the
therapy.
TOOTH AND ROOT SHAPES
VARIATION BY TOOTH TYPE
Every dentist is familiar with the characteristics of tooth shape and should
be able to identify each tooth type if confronted with extracted teeth, by
type and quadrant. Anterior teeth are genetically evolved to help incise
food; they have incisal edges and single roots to guide excursive mandibu-
lar movements. Posterior teeth are evolved to crush and grind food; they
have cusps and multiple roots to support biting loads. The incisive edges
of the anterior teeth are in line with the buccal cusps of the posterior teeth.
The lingual cusps of the posterior teeth decrease in size towards the front
and are represented in the anterior teeth by the cingulum (Fig. 1.20). The
canines form the junction or buttress between the anterior and posterior
teeth, often taking the majority of the lateral guiding forces, reflected in
their longer and bulkier roots.
VARIATION BY RACE
The development of the dental tissues is genetically driven. The growth
and migration of the internal and external enamel epithelium in defining
the crown and root forms of teeth is particularly heritable. Familial and
racial traits affect the three-dimensional spatial configuration of the tooth
and pulp space. As roots continue development after eruption and when
under functional load, root form may be influenced by functional factors.
Most human populations are of very mixed origins, although some com-
munities have remained isolated. Genetic and functional influences have
led to the development of characteristic traits in certain populations (Table
1.3). The Australian aborigines and the Eskimos have the largest teeth,
while the Bushmen of South Africa and the Lapps have the smallest teeth.
 Tooth organogenesis, morphology and physiology  7

A B C

D
E
F

Fig. 1.12  Pulp-space configurations in teeth with developmental anomalies: (a–c) Tooth invagination, (d) tooth evagination, (e,f) Talon cusp, (g) dilaceration (h,i)
gemination

Table 1.1  Presenting features of tooth malformations

Condition Features Effect on endodontic management

DISTURBANCES OF EPITHELIAL–MESENCHYMAL INTERACTIONS AFFECTING THE SIZE OF TEETH
Microdontia Small teeth affecting maxillary lateral incisor or wisdom teeth; unless part As for small teeth
of general disorder, such as hypopituitarism
Macrodontia Uncommonly affects single teeth; may affect all teeth in pituitary gigantism As for large teeth
DISTURBANCES OF EPITHELIAL–MESENCHYMAL INTERACTIONS AFFECTING THE SHAPE OF TEETH
Gemination (Fig. 1.12h,i) Represents an aborted attempt at division of a single tooth bud into two Once access resolved, root could be manageable
by an invagination. Presents as a tooth with two (partial or complete)
crowns and a single root
Fusion (Fig. 1.13) Represents a fusion of two tooth buds; the extent of fusion is dependent Management complicated by unusual morphology
on the stage at which it happens. Varies from a single large tooth to a
large tooth with separated crowns or roots with confluent dentine
Concrescence Represents the fusion of two teeth by cementum only Should not affect management except in isolation
Dilaceration A sharp bend or curvature in the root induced by trauma or bony As for any tooth with root curvature; problem will be
interference during root formation diagnosis
Talon cusp (Fig. 1.14) Anomalous talon-like projection of enamel and dentine from lingual Endodontic management may be required if talon needs to
surface of maxillary or mandibular incisors; it contains a pulp horn be trimmed to accommodate occlusion or prevent other
problems. Root morphology should be normal
8  Tooth organogenesis, morphology and physiology

Table 1.1  Continued

Condition Features Effect on endodontic management

DISTURBANCES
DISTURBANCESOF
OFEPITHELIAL–MESENCHYMAL
EPITHELIAL–MESENCHYMALINTERACTIONS
INTERACTIONSAFFECTING
AFFECTINGTHE
THESHAPE OFTEETH
SIZE OF TEETH
Tooth invagination (Dens Apical proliferation of a portion of the internal enamel epithelium of the Endodontic management often required and complicates
in dente) enamel organ into the dental papilla or from retarded growth of part of management; severity case dependent
the tooth germ. Severity is variable. Invagination may or may not
communicate with the pulp. Oehlers provided a classification (Table 1.2).
Not an uncommon condition. Often affects anterior teeth, as well as
posterior teeth
Tooth evagination Caused by an evagination of the crown surface during tooth formation. Causes early pulp necrosis as the evagination breaks off or is
(Fig. 1.15) Typically affects mandibular premolar occlusal surfaces in Chinese ground down; elective modified pulpotomy is indicated.
populations Once pulp becomes necrotic, endodontic management
normal, except that the root may be incompletely formed
Taurodontism Term used to describe anomaly in which the body of the tooth is enlarged No treatment is necessary but endodontic management akin
at the expense of the root. Subclassified into hypotaurodont, to a large tooth with short roots. Difficulty in locating and
mesotaurodont, hypertaurodont. Anthropological interest. May affect instrumenting canals
one or more molars
Supernumerary roots Developmental condition resulting in additional root(s). May affect any Complicates location and negotiation of the canals, which
tooth but particularly mandibular premolars and canines may have unpredictable configuration
Odontome (Fig. 1.16) May comprise many small, discrete, simple, tooth-like structures (compound None
odontome) or a calcified mass with no resemblance to rudimentary teeth
(complex odontomes)
DISTURBANCES OF EPITHELIAL–MESENCHYMAL INTERACTIONS AFFECTING THE NUMBER OF TEETH
Anodontia Complete absence of teeth None
Hypodontia Absence of some teeth None
Hyperdontia Increased number of teeth either by appearance of supernumerary or None
supplemental tooth/teeth
DISTURBANCES IN STRUCTURE OF TEETH
Amelogensis imperfecta Group of hereditary structural anomalies of enamel. Entirely an ectodermal In severe cases, pulp chambers can be sclerosed complicating
problem with normal mesodermal components. May affect organic endodontic management. Less severe cases may not pose
matrix (hypoplasia), mineralization (hypocalcification) or maturation a problem
(hypomaturation). Loss or damage to enamel affects the pulp–dentine
complex and can result in endodontic problems
Enamel hypoplasia A range of genetic defects may cause defective formation of enamel matrix Management affected as above; variable
causing hypoplasia. Teeth may appear in a variety of ways. Depending on
the severity may affect dentine loss and hence the pulp–dentine complex.
Enamel hypoplasia may also be caused by environmental influences, such as
fevers, systemic or local infections, nutritional deficiencies,
hypocalcaemia, fluoride intake, birth injuries, trauma
Hypophosphataemia Familial disorder due to an inborn error of metabolism. Enamel is Management not affected but outcomes can be
hypoplastic, the pulp chambers are large. Apparently intact teeth are unpredictable
prone to becoming necrotic and infected
Hypophosphatasia Hereditary disorder in which alkaline phosphatase deficiency causes rachitic Management not affected but outcomes unpredictable
like bone changes. Teeth may become loose due to an inadequate
cementum, by which token, the pulps may also become involved
Dentinogenesis Also called hereditary opalescent dentine or odontogenesis imperfecta. The Severely affects endodontic management, which is near
imperfecta mesodermal components of the tooth are affected during formation. The impossible because of challenge in locating the canal
deficient dentine is unable to support the enamel, which fractures and it system and in manipulating the dentine
causes the teeth to be discoloured. Dentine is rapidly worn and the pulps
become rapidly obliterated. Periapical pathoses is not common
Dentinal dysplasia Rare hereditary condition affecting dentine formation. The enamel is No treatment possible
unaffected and teeth appear and erupt normally. The roots are short and
the pulp chambers obliterated; periapical pathoses is common. Teeth
exfoliate early
Regional odontodysplasia Condition of unknown aetiology affecting one or several teeth; often No management is possible
anterior teeth. The teeth exhibit delayed or failed eruption; their shape
is markedly altered, often with defective mineralization. Radiographic
appearance is characteristic with a marked reduction in radiodensity
giving the teeth a ghost-like appearance
Shell teeth Dentinal disturbance of formation in which the enamel is normal. The No management is possible
dentine is extremely thin and pulp chambers are enormous. The roots are
extremely short. Radiographically, the teeth appear as shells
Enamel & dentine aplasia A condition in which both the enamel and dentine are atypical and fail to No management is possible
lay down secondary dentine in response to pulpal stimulation or
attrition, resulting in pulp exposure. Differs from amelogenesis and
dentinogenesis imperfecta and no other structures are affected. There is
complete aplasia of enamel and dysplasia of dentine. Pulp chambers are
extremely large, cementum is normal and teeth are pigmented
Dentine hypocalcification Normal dentine is calcified by mineralization in globular deposition, Unknown but it is likely that canal debridement would be
interspersed by interglobular uncalcified matrix. The dentine is softer affected
 Tooth organogenesis, morphology and physiology  9
Fig. 1.13  Fusion Fig. 1.14  Radiograph of malformed maxillary
canine (Talon cusp)
Table 1.2  Types of invagination
Type l The enamel-lined invagination is of the minor form and
confined within the crown; it does not extend beyond
the level of the external amelo–cemental junction
Type 2 (Fig. 1.17) The enamel-lined invagination invades the root but
remains confined within it as a blind sac. It may,
however, communicate with the pulp. The invagination
does not breach the periodontal ligament and may or
may not be grossly dilated; in the former case, there is
often a corresponding dilation of the root or crown
Type 3a (Fig. 1.18) The lined invagination penetrates through the root and
opens apically or laterally at a foramen, sometimes
referred to as a “second or pseudo foramen”, in the
root. There is usually no communication with the pulp,
which lies compressed within the wall around the
invagination process. The invagination may appear to be
completely lined by enamel but, more often, a portion
of it is lined by cementum. As in Type 2, there may or
may not be a dilatation of the tooth
Type 3b (Fig. 1.19) As in Type 3a but it communicates with the periodontal
ligament at the apical foramen without communicating
with the pulp
The Lapps have long and well-developed roots. In Bantu races of Africa,
the mandibular molars increase in size posteriorly. Characteristics such as
size, shape and fissure patterns are also genetically determined.
The study of root and canal anatomy has endodontic and anthropo-
logical significance. Familiarity with variations in tooth anatomy and
Fig. 1.15  Tooth evagination
Fig. 1.16  (a) Multiple compound odontomes removed
from the (b) apical region of the maxillary first molar
characteristic features in various racial groups can aid location and
negotiation of canals, as well as their subsequent management. There is
variation in shape and number of roots and canals among the different
races. These variations appear to be genetically determined and may be
important in tracing the racial origins of populations. One example of
such variation is the mandibular first molar with three roots. This variant
has a frequency of less than 5% in Caucasoid people (British, Dutch,
German, Finnish and other European), African (Bushmen, Bantu, Senega-
lese), Eurasian and Indian populations, whereas in those with Mongoloid
traits, such as the Chinese, Eskimos and Native Americans, it occurs with
a frequency of up to 40%. Another variation is the C-shaped root and canal
configuration”. Seldom found in Caucasoid people, they have a relatively
high prevalence in mandibular second molars of Chinese and Lebanese
populations.
Caucasoid people’s maxillary first and second molars have similar
root and canal morphology. The majority have two buccal and one palatal
root emerging from a common short root trunk. Anomalous variations,
such as fused roots are seen occasionally in first molars but more fre-
quently in second molars. Another less frequently reported variation
limited to second molars is the double palatal root/canal. In the three-
rooted molars, the majority of palatal and distobuccal roots possess the
Vertucci type I canal system (simple, single canal). The complexity of
the mesiobuccal roots of first and second maxillary molars was noted by
Hess & Zurcher (1925) but only became the focus of more detailed and
repeated investigations after the study of Weine et al. (1969). The canal
anatomy of maxillary molars of other racial groups is less frequently
investigated.
 10  Tooth organogenesis, morphology and physiology

Fig. 1.17  Dens invagination Type 2 Fig. 1.18  Dens invagination Type 3a Fig. 1.19  Dens invagination Type 3b Fig. 1.20  Occlusal view of maxillary
teeth

Fig. 1.21  Partial

Table 1.3  Characteristic traits in various races
obliteration of the pulp
Mongoloid
space
(Eskimos, American
Characteristic Indians, Chinese) Negroid Caucasoid
Shovel-shaped incisor Common Uncommon Uncommon
Carabelli’s cusp on 1st Uncommon Uncommon Quite common
molar
Enamel pearls Common Uncommon Uncommon
Mandibular 3rd molars Commonly missing Rarely missing Can be missing
Mandibular 2nd molar Common Common Uncommon
with 5 cusps
Supernumerary teeth - Common -

The external form and size of the tooth is clearly fixed at formation but
the internal surface continues to change throughout life, even after root
Table 1.4  Eruption times of adult teeth
maturity, as secondary dentine is laid down continuously and maybe
supplemented by tertiary dentine in response to caries, tooth surface
Year Tooth loss and occlusal wear. With the passage of time, the pulp volume
6–7 16/26/36/46 31/41 therefore decreases (Fig. 1.21). This process can occur at different rates in
7–8 11/21 32/42 different teeth.
8–9 12/22 In premolar and molar teeth, laying down of dentine at the roof of the
9–10 13/23 33/43 pulp chamber is less than that at the floor of the pulp chamber. In addition
10–11 14/24 34/44 to this decrease in the height of the pulp chamber, there is also a decrease
11–12 15/25 35/45 in the mesiodistal width of the pulp chamber; however, canals do not
12–13 17/27 37/47 become completely occluded or sclerosed. Even though the coronal portion
17–22 18/28 38/48 of the canal system may become obliterated, the apical portion usually
remains patent. Such canals can be difficult to locate and treat when the
remaining pulp becomes infected (Fig. 1.22).

PULP SPACE AND ITS MORPHOLOGIC PATTERNS

VARIATION BY TIME
An understanding of the processes that lead to a fully formed tooth helps
in differentiating the various patterns or configurations that occur in the
anatomy of roots and pulps. Calcification times, eruption and apical root
closure dates provide important information in this regard. If eruption
dates can be remembered (Table 1.4), as a general rule, the calcification
of the tooth crown is complete 3 years before eruption and root end closure
3 years after eruption.
CLASSIFICATIONS OF PULP SYSTEMS
In describing the internal anatomy of teeth, it is probably more appropriate
to refer to the morphology of the pulp space, which is alternatively known
as the root canal system. The pulp space is that part of the pulp–dentine
complex which, in a healthy tooth, is occupied by the pulpal tissue, that
is, the space within the hard tissue of teeth in which, in health, the pulp
resides. Due to the structure of the pulp–dentine complex, this also includes
 Tooth organogenesis, morphology and physiology  11

Type I Type II Type III Type IV

Fig. 1.22  Radiograph of sclerosed Fig. 1.23  Cleared Fig. 1.24  Weine’s classification of canal morphology
root canal in maxillary lateral incisor mandibular molar

Type I (1) Type II (2-1) Type III (1-2-1) Type IV (2) Type V (1-2) Type VI (2-1-2) Type VII (1-2-1-2) Type VIII (3)

Fig. 1.25  Vertucci’s classification of canal morphology

over 20% of the dentine in the form of tubules. In disease, the space
Type (2-1-2-1) Type (3-1) Type (3-2) Type (2-3) Type (3-4)
becomes the province of microorganisms.
The pulp space is complex and bears little resemblance to the stylized
diagrams that are often used to explain the traditional terms used in
describing the anatomy of the pulp. It has to be appreciated that the out-
lines, shapes, and positions of pulp chambers, root canals and pulpal–
periradicular foramina are highly variable. Canals may branch, divide,
rejoin and present forms that are considerably more involved than many
textbooks of anatomy depict for simplicity; yet these simple forms serve
to convey the essential canal structure found in teeth. The complex nature
of the pulp space is typified by the appearance of an extracted molar ren-
dered transparent (Fig. 1.23).
Despite this complexity, it is useful to describe the patterns of root canal
Fig. 1.26  Gulabivala’s additional canal morphological groups
system found in human teeth. Few have tried because of the degree of
variation evident. Weine et al. (1969) used a four-group classification to
describe the canal systems in the MB roots of maxillary molars (Fig. 1.24),
which was believed could be applied universally. Zillich & Dowson (1973)
CHARACTERISTICS OF THE PULP SPACE
used an eight-group classification, which does not appear to have found A number of generalized observations can be made on the characteristics
favour. Vertucci (1984) produced a more complex and extensive classifica- of the pulp space that have a significant bearing on the practice of
tion (Fig. 1.25) to which Gulabivala et al. (2001, 2002) added a number endodontics.
of further groups (Fig. 1.26). These have been more frequently adopted In cross-section, root canals tend to take on the shapes of the roots.
for application in other studies. Where roots are wide in a buccolingual direction, the pulp space tends to
 12  Tooth organogenesis, morphology and physiology

A B

Fig. 1.27  Sectioned roots of a Fig. 1.28  Proximal canal complexity in (a) an incisor, (b) a molar Fig. 1.29  Buccal and approximal
mandibular molar views of a central incisor

Fig. 1.30  Cleared maxillary molar Fig. 1.31  Cleared maxillary premolar Fig. 1.32  Buccal radiograph of Fig. 1.33  Approximal radiograph of
mandibular first premolar the mandibular first premolar

take on similar proportions to the outline of the root or there may be more
than one root canal (Fig. 1.27).
Roots and root canal systems display simple forms in the mesiodistal Table 1.5  Roots of teeth with two canals (%)
dimension, giving a simple radiographic projection; however, this masks
great complexity and curvatures in the buccolingual dimension (Fig. 1.28), Tooth Maxillary Mandibular
which is not revealed by conventional radiography. Roots and canals are Incisor Rare 41
rarely straight even when they appear so in a normal clinical radiographic Canine Rare 14
projection (Fig.1.29). Cleared specimens further reinforce the complex First premolar 84 (62 with 2 roots) 30
anatomy (Figs 1.30, 1.31). As a result, the volume of the pulp space is Second premolar 40 11
much greater than the normal buccal view might suggest. First molar 71 (MB root) 87 (M root)
Single roots do not necessarily have single root canals. Even when 38 (D root)
clinically there appears to be a single opening into a root canal, separation Second molar 3 roots/3 canals 2 roots/3 canals
can lead to two distinct canals (Figs 1.32, 1.33). Table 1.5 shows the fre- Root fusion common Root fusion common
quency of two canals in various tooth types. Typically, maxillary anterior
 Tooth organogenesis, morphology and physiology  13
Fig. 1.34  Pulpal fin in central incisor Fig. 1.35  Approximal
radiograph of maxillary
canine with pulpal
cervical bulge
Fig. 1.38  Cleared mandibular Fig. 1.39  Cleared maxillary premolar
second molar
teeth possess the type 1 canal system (single central canal following
the shape of the root), while the mandibular anterior teeth may possess
type 1 or other configurations (types 2, 3, 4 – see Weine classification) as
the frequency of two canals is between 40 and 50%. Maxillary first and
mandibular second premolars tend to have a type 1 canal system, while
the maxillary second and mandibular first premolars can possess more
complex systems. The mesiobuccal roots of maxillary molars and the
mesial roots of mandibular molars tend to possess complex canal systems
(types 2–4 etc), while the palatal and distobuccal roots of maxillary molars
tend to possess the type 1 canal. The distal root of mandibular molars
may frequently have either a type 1 or type 2 canal system. Characteristics
in the form of fins (Fig. 1.34) exist in oval roots with two canals, while
cervical bulges (Fig. 1.35) may occur on the palatal aspect of maxillary
canine teeth.
Generally, the diameters of root canals decrease towards the apex of the
root where they tend to be narrowest, 0–1.5 mm from the foramina. The
term used to describe the narrowest point is the apical constriction, which
may be oval, round or irregular. From this point, the canal widens into the
foramen, which may open onto the root surface anywhere between 0 and
0–3mm B
C
D
F
Fig. 1.36  Relationship between root tip, apical Fig. 1.37  Cleared
foramen, and apical constriction: A = root apex; mandibular first
B = apical constriction; C = root canal; premolar
D = cementum; E = dentine; F = apical foramen
A B
C D
Fig. 1.40  Classification of apical constrictions: (a) traditional single
constriction; (b) tapering constriction; (c) parallel constriction; (d)
multiconstricted (Reproduced from Dummer et al. 1984)
3 mm from the root apex (Fig. 1.36). There may of course be more than
one apical foramen (Figs 1.37–1.39). Dummer et al. (1984) described four
types of constriction in anterior and premolar teeth (Fig. 1.40).
Lateral, secondary and accessory canals
Lateral communications arise when the pulp is supplied by collateral vas-
culature anywhere along the length of the root and vary in size from a few
microns in width to the size of a main canal. Such lateral communications
have been demonstrated in histological sections (Fig. 1.41), cleared teeth
(Fig. 1.42) and clinical radiographs (Fig. 1.43). The blood vessels passing
through these canals (Fig. 1.44) allow interchange of inflammatory break-
down products between the pulp and the periodontal tissues, which may
influence the outcome of endodontic treatment and periodontal health.
De Deus (1975) defined lateral canals as extending from the main canal
in the middle third of the root (body) to the periodontal ligament; the
 14  Tooth organogenesis, morphology and physiology

Table 1.6  Average lengths of teeth (mm)

Tooth Maxillary Mandibular

Central incisor 22.5 20.7
Lateral incisor 22.0 21.1
Canine 26.5 25.6
First premolar 20.6 21.6
Second premolar 21.5 22.3
First molar 20.8 21.0
Second molar 20.0 19.8

Table 1.7  Diameters (mm) of apical foramen by tooth and root type

Tooth/root type Diameter of apical foramen (mm)

Fig. 1.41  Lateral canal evident on histological Fig. 1.42  Cleared
Maxillary incisors 0.289 ± 0.121
section mandibular second
Mandibular incisors 0.263 ± 0.190
molar with lateral
canal Maxillary premolars 0.210 ± 0.171
Mandibular premolars 0.368 ± 0.184
Maxillary molars
Fig. 1.43  Radiograph
Palatal root 0.298 ± 0.062
of lateral canal in
obturated maxillary Mesial root 0.235 ± 0.101
premolar Distal root 0.232 ± 0.066
Mandibular molars
Mesial root 0.258 ± 0.343
Distal root 0.392 ± 0.078

Data extracted from Morfis et al., 1994

Table 1.8  Mean volume and standard deviation (SD) of dental pulp cavities

Maxillary Mandibular
Tooth type Mean volume (mm3) SD Mean volume (mm3) SD
Central incisor 12.4 3.3 6.1 2.5
Lateral incisor 11.4 4.6 7.1 2.1
Canine 14.7 4.8 14.2 5.4
Fig. 1.44  Minor blood First premolar 18.2 5.1 14.9 5.7
vessels entering lateral Second premolar 16.5 4.2 14.9 6.3
canals (courtesy of Prof. First molar 68.2 21.4 52.5 8.5
I Kramer) Second molar 44.3 29.7 32.9 8.4
Third molar 22.6 3.3 31.1 11.2

Source: Fanibunda, 1986

depth of insertion of working instruments (Table 1.6). This information

secondary canals as similar extensions in the apical region of the root; and
an accessory canal as branching off from the secondary canal to the peri-
odontal ligament. In examining 1140 cleared teeth, he found that 27%
showed these ramifications, the majority of which were located in the
apical region; the premolars and molars showed the greatest variety of
ramifications but they are not exclusive to such teeth (see Fig. 1.28).
combined with the average diameters (Table 1.7) show the canals to be
capillary-tube-like. The mean volumes of the pulp spaces for each tooth
type are given in Table 1.8, which depicts surprisingly large overall
volumes. However, the information currently available may not be wholly
applicable to teeth in patients of non-Caucasoid origin. Practitioners who
regularly treat Negroid or Mongoloid populations are aware that these
values do not coincide with their clinical experiences.
TOOTH, ROOT AND CANAL MORPHOLOGY BY
TOOTH TYPE

DIMENSIONS OF THE PULP SPACE MAXILLARY INCISORS

It is useful to appreciate the dimensions of the pulp space to understand The root is bulky for the central incisor and slender for the lateral incisor,
the physico-dynamic fluid exchange problems inherent in root canal treat- with a triangular, circular or oval cross-section that becomes rounder as it
ment. The average lengths of teeth would also help determine the likely approaches the apex. The canal is type 1, tapering in shape, with an
 Tooth organogenesis, morphology and physiology  15
Fig. 1.45  Buccal radiograph of Fig. 1.46  Radiograph of lateral
central incisor and proximal incisor with two roots
radiograph of central incisor with
lateral canal
Fig. 1.49  Radiograph of malformed Fig. 1.50  Radiograph of extracted mandibular
maxillary lateral incisor incisors
irregular triangular (base facing labially) or oval cross-section cervically,
which also gradually becomes round towards the apex. Generally, there is
very little apical curvature in central incisors and, where it is present, it is
either distal or labial. It is extremely rare for these teeth to have more than
one root or root canal. It has been suggested that up to 60% of central
incisors have accessory canals (Fig. 1.45).
The lateral incisors are smaller, following the same pattern but the apex
is often curved, generally in a distopalatal direction. Extra roots and second
canals are more likely to be found in lateral incisors (Fig. 1.46), as are
developmental grooves and invaginations (Figs 1.47–1.49).
MANDIBULAR INCISORS
These teeth have a single root which is narrow mesiodistally and wide
labiolingually. Over 40% of these teeth have two canals, which usually
join in the apical third (Fig. 1.50). The highest recorded figure for two
Fig. 1.47  Radiograph of lateral Fig. 1.48  Congenital grooving in a
incisor with an invagination maxillary lateral incisor
Fig. 1.51  Approximal groove Fig. 1.52  Specimen
on mandibular incisor root maxillary canine
separate apical foramina is 5.5%. The canal configuration maybe type 1,
2 or 3, in that order of frequency. When two canals are present, the labial
is straighter, with the division in the cervical third.
In teeth with a single root canal, the canal is normally straight but may
curve to the distal (and less often to the labial) side. The grooving found
on the mesial and distal surfaces of the roots of these teeth (Fig. 1.51)
makes them susceptible to perforation if over-instrumented.
MAXILLARY AND MANDIBULAR CANINES
These teeth tend to be the longest of all. The root is wide and irregularly
tapered labiopalatally and regularly tapered mesiodistally. The canal is
type 1 and has an oval shape cervically and begins to become round in
cross-section in the apical third, where there may be a distal curve. The
canal often has a bulge on the palatal aspect in the coronal third (Figs 1.52,
1.53). It can very rarely present with two roots (Fig. 1.54).
 16  Tooth organogenesis, morphology and physiology

Fig. 1.53  Specimen Fig. 1.54  Maxillary Fig. 1.55  Radiograph of extracted mandibular Fig. 1.56  Mandibular Fig. 1.57  Radiograph
maxillary canine cleared canine with 2 roots canines canine with two roots of mandibular canine
with two roots

Fig. 1.58  Radiograph of extracted maxillary first Fig. 1.59  Cleared Mongoloid Fig. 1.60  Radiograph of extracted maxillary
premolars maxillary first premolar second premolars

The mandibular canine resembles the maxillary canine, although its
dimensions are smaller (Fig. 1.55); it is the longest mandibular tooth. The
root is narrow mesiodistally but wide labiolingually; it rarely has two
roots. The canal configuration is type 1, 2, or 3 with up to 20% having
two root canals (Figs 1.56 1.57). The type 1 variant follows the cross-
sectional shape of the root, while the others have a rounder cross-section
after the division.
MAXILLARY PREMOLARS
molar configuration, although the buccal canal sometimes starts as a single
canal in the pulp chamber.
The maxillary second premolar tends to be single-rooted with a single
canal (85%), which is wide in a buccolingual direction (Fig. 1.60). The
canal configurations are type 1, 2, 3, or 4 in that order, although the last
variety may be more common than thought. Where there are two canals
they tend to converge apically. The remainder (15%) has two roots, each
with a single type 1 canal configuration. The cervical canal configuration
is variable as in the first premolar, from oval to figure eight.

The maxillary first premolar has variable morphology but is generally

considered to have two roots and two canals (Fig. 1.58). The frequency of
two roots is more than 55% in Caucasoids and less than 20% in Mongol-
oids. The roots maybe completely separate or arise as twin projections
from a common mid-trunk. Irrespective of race and number of roots, these
teeth tend to have two canals (Fig. 1.59) with canal configurations of type
3, 2 and 1, in that order. The cross-section of the canal in the cervical third
may be oval or a figure of eight shape. As another variant, 2–6% of these
teeth have been reported to have three roots and three canals, following a
MANDIBULAR PREMOLARS
The mandibular first premolar has a bulkier crown compared to the cuspid,
yet its root is more slender and shorter. The root (and the canal) has an
oval cross-section with the narrower dimension oriented mesiodistally. The
majority of these teeth have a single canal with a type 1 configuration.
However, a variably quoted proportion (15–30%) presents with a division
of the canal in the apical half or third into buccal and lingual branches
(Fig. 1.61), the latter of which is more difficult to find. The canal
 Tooth organogenesis, morphology and physiology  17

Fig. 1.61  Radiograph of mandibular first premolar Fig. 1.62  Extracted specimen Fig. 1.63  Cleared root of Fig. 1.64  Radiograph of extracted
with two roots of mandibular first premolar mandibular first premolar mandibular second premolar

Fig. 1.65  Right Fig. 1.66  Maxillary first molar with Fig. 1.67  Four canal orifices in Fig. 1.68  Groove in the floor of a
maxillary first molar two mesiobuccal canals maxillary first molar maxillary first molar

configurations are type 1, 2 or 4 (Figs 1.62, 1.63). Three canals appear in
less that 2% of the teeth. The existence of C-shaped canals has also been
reported in these teeth.
The mandibular second premolars tend to be single-rooted with a single
centred type 1 canal, which is wide in a buccolingual direction (Fig. 1.64).
Two canals occur in 25% of cases, when the floor of the pulp chamber
extends well below the cervical level with canal configurations of type 2,
3 or 4 in that order. About 1% may have three canals with two buccal and
one lingual.
MAXILLARY FIRST MOLARS
The maxillary first molars are three rooted, two buccal and one palatal.
The mesiobuccal root is broad in the buccopalatal plane and narrow in
the mesiodistal plane, similar to a maxillary premolar root configuration.
The root generally exits the crown mesially and can abruptly curve
distally. The distobuccal root is the smallest and can vary in cross-section
from round to oval with the narrow dimension oriented mesiodistally;
it can curve mesially in the apical third. The palatal root is the bulkiest,
oval, with the widest dimension oriented mesiodistally, and generally
curves buccally in the apical third. The mesiobuccal root often curves
distopalatally in the apical third of the root (Fig. 1.65). The tooth usually
has four root canals, the additional canal being located in the mesiobuccal
root (Fig. 1.66).
The pulp chamber floor has a quadrilateral shape, although it is some-
times described as triangular. All the orifices of the canals lie mesial to the
oblique ridge, allowing it to be maintained intact during access prepara-
tion. The orifice of the palatal canal is the most prominent and lies beneath
the mesiopalatal cusp. The orifice of the mesiobuccal canal is located
beneath the mesiobuccal cusp. The minor mesiobuccal (or mesiolingual or
MB2) and distobuccal canals are located by their relation to the main
mesiobuccal canal; the distobuccal canal is not related to the distobuccal
cusp. The distobuccal canal lies 2–3 mm to the distal and slightly to the
palatal aspect of the mesiobuccal canal. The mesiolingual canal (MB2) lies
on a line joining the major canal and the palatal canal orifice, 1.82 mm to
the lingual on average (Fig. 1.67). As both the canals lie on the buccopala-
tal plane, they are often superimposed on the preoperative radiograph. The
presence of a groove on the floor of the pulp chamber may be an indication
of the likelihood of a second mesiobuccal canal orifice (Fig. 1.68), which
may be only fully exposed after the removal of dentine in the area (Fig.
1.69). The mesiobuccal root can have canal configurations of type 1, 2, or
 18  Tooth organogenesis, morphology and physiology

Fig. 1.69  Mesiobuccal canals Fig. 1.70  Buccal Fig. 1.71  Maxillary Fig. 1.72  Maxillary Fig. 1.73  Maxillary
evident following removal of the curvature of a palatal first molar with an second molar with second molar cleared
groove root of a maxillary first extra root buccal root fusion
molar

Fig. 1.74  Extracted Fig. 1.75  Cleared two-rooted Fig. 1.76  (a) Three-rooted mandibular molar (b) five-rooted mandibular molar
mandibular first molar mandibular first molar

MANDIBULAR FIRST MOLARS

3; in addition to following the curvature of the root, the main mesiobuccal
canal may also curve buccopalatally.
The distobuccal root has a single type 1 canal as does the palatal but
the latter can rarely have two canals as well. The distobuccal canal is the
shortest of the three canals and leaves the pulp chamber in a distal direc-
tion but may curve mesially in the apical half of the root. The palatal canal
is the largest and longest of the canals and tends to curve buccally in the
apical 4–5 mm (Fig. 1.70). This curvature is not apparent on the radio-
graph. The variable anatomy of the tooth extends to extra roots and canals
(Fig. 1.71).
MAXILLARY SECOND MOLARS
The maxillary second molar is a smaller replica of the first molar with
similar root and canal morphology. The roots are less divergent and root
fusion (between the two buccal roots giving one buccal and one palatal
root) is possible (Figs 1.72, 1.73), which might give rise to a reduction in
the number of canals. The buccal canal orifices tend to be closer together.
Teeth with three roots and four canals are prevalent, though the mesiolin-
gual canal is more difficult to find. The canal configuration in the mesiobuc-
cal root may be type 2 or 3.
Mandibular first molars usually have two roots (Fig. 1.74), one mesial and
one distal. The mesial root exits the crown in a mesial direction and then
gradually curves distally in the apical third. The distal root is narrower
buccolingually but equal in mesiodistal width compared to the mesial root.
The distal root often curves mesially. In a Mongoloid variation (which may
occur in over 40% of such teeth), a supernumerary distolingual root is
present (Fig. 1.75), which is smaller and curved. A rare five-rooted man-
dibular molar is shown in Fig. 1.76.
The pulp chamber floor is trapezoidal rather than triangular. The orifices
of both mesial and distal canals lie in the mesial two-thirds of the crown,
hence the access cavity is located in this part of the crown.
The two-rooted molar usually has a canal configuration of three canals;
two canals in the mesial root and one in the distal root (Fig. 1.77). The
canal configuration in the mesial root is type 3 in 55–85% according to
different reports and type 2 in the remainder. The mesiobuccal canal is the
most difficult canal to treat because of its tortuous path. It leaves the pulp
chamber in a mesial direction, which alters to a distal direction in the
middle of the root. From the proximal perspective, the mesiobuccal canal
curves to the buccal first and then lingually. The coronal part of the mesio-
lingual canal is straighter and then curves buccally in the middle third.
 Tooth organogenesis, morphology and physiology  19

Fig. 1.77  Mandibular first molar Fig. 1.78  Radiograph of mandibular first molar Fig. 1.79  Cleared mandibular
with three canals with four canals first molar with five canals

Fig. 1.80  Clinical radiograph of mandibular Fig. 1.81  Mandibular Fig. 1.82  Clinical radiograph of mandibular Fig. 1.83  Buccal
second molar second molar with second molar radiograph of
fused roots extracted second molar

The single distal canal (type 1) is usually larger and more oval in cross-
section (sometimes kidney shaped) and has a tendency to emerge on the
distal side of the root surface short of the anatomical apex. More than 25%
of the distal roots have two canals, half of which have separate apical
foramina (type 2 or 3 configurations) (Fig. 1.78). The frequency of second
distal canals appears to be higher in Mongoloid teeth, and specimens with
five canals have been observed (Fig. 1.79). When a second distolingual
canal is present, it tends to curve towards the buccal. There have been case
reports of five and six canals and the presence of a third mesial canal.

MANDIBULAR SECOND MOLARS Fig. 1.84  Approximal Fig. 1.85  Lingual view Fig. 1.86  Cleared
radiograph of the of extracted specimen specimen
This tooth can have many morphological variants, although in general, the
extracted second molar
most common type has the same pattern as the mandibular first molar. In
Caucasoid mandibular second molars, the mesial root has two (occasion-
ally one) canals and the distal root usually has only one canal (type 1 teeth with C-shaped roots do not always have C-shaped openings. Those
configuration) (Fig. 1.80). The prevalence of canal configuration is differ- with C-shaped orifices do not always have continuous C-shaped canals.
ent in the mesial root compared to the first mandibular molar; in this case,
type 2 is more common than type 3. The roots tend to be closer together
and may fuse (Fig. 1.81). Rarely, only one canal is present when both roots
MAXILLARY AND MANDIBULAR THIRD MOLARS
are fused (Figs 1.82–1.86). In Mongoloid teeth, the fusion of roots is The root form and canal anatomy of maxillary third molars is highly vari-
common and where roots are incompletely separated interconnections are able. It may possess three roots (Fig. 1.88) but more often fusion occurs
likely, giving rise to the C-shaped canal (Fig. 1.87). It would seem that and only one or two canals are evident (Fig. 1.89).
 20  Tooth organogenesis, morphology and physiology

A B A B

Fig. 1.87  C-shaped canal in Fig. 1.88  (a) Maxillary third molar (b) Fig. 1.89  (a) Maxillary third molar (b)
mandibular second molar maxillary third molar cleared maxillary third molar cleared

A B A B

Fig. 1.90  (a) Extracted mandibular third molar Fig. 1.91  (a) Extracted mandibular third molar
(b) cleared mandibular third molar (b) cleared mandibular third molar

The roots and root canals of the mandibular third molars tend to be short
Fig. 1.92  Radiograph of mandibular
and poorly developed (Fig. 1.90). The anatomy tends to vary and where
incisors with root canal division
there is root fusion the canals also fuse (Fig. 1.91).

Fig. 1.93  Radiograph

CLINICAL INTERPRETATION AND MENTAL IMAGING of mandibular molar
with an extra distal root
Management of the clinical problems generated by pulpal and periapical
conditions requires unique surgical management skills, particularly where
the clinician has to negotiate the labyrinths of directly invisible space
inside teeth. The treatment calls for a highly developed tactile skill to feel
or “see” through the finger tips. This may seem far-fetched, however, even
normal vision requires cognitive recognition of visual signals, without
which nothing is seen. Clinicians will have encountered the problem
of looking but not seeing. The point is that “seeing” is more to do with
cognitive patterns and pictures than sense information. Both tactile and
visual sense information may be converted to mental images. To this
extent, it is important to cultivate the ability mentally to visualize in three and tooth projections. In the absence of three-dimensional imaging tech-
dimensions. niques, dentists have managed to perfect this skill to a high art.
Management of endodontic problems can be enhanced by integration of It is possible to glean information with regard to the pulp-space configu-
information from several sources: rations of teeth by using a degree of clinical intuition. Clues may be gained
from radiographs by developing a sense of the three-dimensional charac-
• knowledge of tooth morphology teristics of teeth when viewing normal projections. Root canals that disap-
• tactile information from scouting canal systems clinically pear radiographically are an indication of canal division (Fig. 1.92). It is
• interpretation of clinical and radiographic clues. always wise to trace the periodontal ligament space. This is a most useful
The first point is self-evident. The second must be acquired by informed exercise when searching for extra roots (Fig. 1.93). Thickening of the
coaching and practice in a skills laboratory, using extracted teeth. The last space in periradicular areas other than the apical region may indicate the
is an integrated skill that is developed from insight about tooth morphology presence of lateral and accessory canals (Figs 1.94, 1.95).
 Tooth organogenesis, morphology and physiology  21

C
A

A
B

Fig. 1.94  Periradicular radiolucencies Fig. 1.95  Obturated incisor with

in a maxillary incisor apical and lateral canals
Fig. 1.97  Low-power view of Fig. 1.98  High-power view
pulp–dentine complex: A = cell-free of pulp–dentine complex:  
A B C zone A = mineralized dentine;
B = predentine; C = odontoblasts

Buccal lamina

Enamel niche
Enamel organ

Fig. 1.99  Developing tooth germ at the “bell stage”

Fig. 1.96  Ground section of crown of tooth: A = enamel; B = dentine;
C = pulp

Knob-like appearance of roots may indicate curvatures and the unusual

presence of vertical lines suggests gross concavities of the root surface.
Further information can be obtained from tactile perception and the angu- A
lation of instruments within root canals.

ANATOMY AND PHYSIOLOGY OF

THE PULP–DENTINE COMPLEX
THE DENTAL PULP
The dental pulp is a minute piece (approximately 25 mm3) of connective
tissue akin to any other in the body and consists of cells, nerve fibres and
blood vessels embedded in a gel-like ground substance. Its unique char-
acteristic is that it is surrounded by a layer of specialized cells called
odontoblasts, which secrete and encase the connective tissue in a rigid hard
tissue shell called dentine (Fig. 1.96). Also uniquely, the odontoblast cell
bodies do not become embedded in the mineralized matrix but remain at
its inner boundary, while a cellular process extends into and traverses the
dentine shell from each odontoblast. The odontoblastic processes therefore
penetrate and give “vitality” to the dentine. The dentine and pulp are
consequently referred to as the pulp–dentine complex (Figs 1.97, 1.98).
The initial three-dimensional spatial distribution of the odontoblasts
arranged on a basement membrane, the size and shape of which is
B
Fig. 1.100  Predentine (A): B = odontoblast layer
presumably a polygenic autosomal trait, maps out the final morphological
form of each tooth in the dental arch (Fig. 1.99). The relative contribution
of genetic and epigenetic factors is unknown.
As dentine matrix is progressively laid down during tooth development,
the odontoblastic process simultaneously grows longer and the cell body
recedes centrally. The dentine matrix progressively becomes mineralized
in the wake of the prelaid organic matrix, causing a hard, calcified tissue
to form. The advancing front of dentine matrix remains unmineralized and
is called predentine (Figs 1.98, 1.100). The organic matrix containing
 22  Tooth organogenesis, morphology and physiology

Fig. 1.101  Fig. 1.103  Sclerosis of

Calcospherites dentine (A) caused by
caries

Fig. 1.104  Deep

abfraction lesion
exposes and involves
Fig. 1.102  Ground
many more tubules in a
section of tooth at  
sclerotic (A) response
the cemento–enamel
junction

collagenous (collagen type I, type I trimer, type V) and non-collagenous

(proteoglycans, glycosaminoglycans, γ-caboxyglutamate-containing pro-
teins and phosphoproteins) secretory products is exocytosed into the pre-
dentine, while some components, such as phosphoproteins and osteocalcin,
are released at the mineralizing front. The mineralizing front has an irregu-
larly advancing boundary, which is sometimes shaped into domes called
calcospherites (Fig. 1.101). The net effect is that as each of the millions Fig. 1.105  Primary (A) and irregular
secondary (B) dentine
of odontoblasts lay down dentine matrix and withdraw towards the centre
of the dental pulp, a hard but resilient shell of dentine is created. This is,
permeated by millions of tubules each containing a cellular process, pos-
sessing an approximately radial distribution from the dental pulp. Dentine
is protected by a covering of the relatively more brittle layer of enamel in
the crown and a less brittle and thinner layer of cementum in the root (Fig.
1.102). In about 10% of teeth, these protective covering layers do not meet,
leaving a gap of uncovered dentine at the neck of the tooth. In the crown,
the dentinal tubules follow a gentle S-shaped curve (Fig. 1.102), with the B
consequence that dentinal injury to the surface covering enamel affects the
pulp at a more apical level (Fig. 1.103). A deeper cavity would also trau-
matize more tubules and cause greater damage (Fig. 1.104).
The idea that odontoblast processes extend through the full length of A
the dentinal tubules through the life of the tooth is controversial. One belief
is that some processes may recede by terminal decay, while others extend
the full distance. The remainder of the tubule is filled with a unique
protein-rich, dentinal fluid, which is a transudate that is normally under
positive pressure. Fluid exchange may take place either from the pulp Immediately adjacent to the odontoblastic layer is a zone of connective
outwards or in the reverse direction. tissue, which is relatively free of cells, called the “cell-free zone” (see
The odontoblasts form a single layer of cells but, because of the differ- Fig. 1.97). It tends to disappear during periods of cellular activity in a
ences in the level of their nuclei, an illusion of a multilayered structure is young pulp or in older pulps where reparative dentine is being formed
created in histological section (see Fig. 1.100). Odontoblasts are incapable (Fig. 1.105).
of further division once fully mature and, if damaged, may be replaced The remainder of the pulp consists of ground substances which are
from undifferentiated mesenchymal cells present in the pulp. embedded cells, that include fibroblasts and inflammatory cells, collagen
 Tooth organogenesis, morphology and physiology  23

Fig. 1.108  Change in direction of

A A secondary dentinal tubules: A = pulp;
B = secondary dentine; C = change in
direction of tubules; D = primary
dentine

Fig. 1.106  Pulp tissue elements: A = ground substance D

Fig. 1.107  High-power

view of lateral
communication
between dentinal Fig. 1.109  Active
tubules deposition of irregular
secondary dentine:  
A = globular dentine
at mineralizing front;  
A B = widened predentine
B

fibres and a complex network of blood vessels and nerve fibres (Fig.
1.106). The ground substance contains the fibroblasts responsible for pro-
ducing the proteins and carbohydrates that form the viscous substance of
the matrix. The ground substance accommodates humoral and immune
cellular infiltrates produced during inflammatory responses. Lymphatic
vessels help to clear away exuded fluid and macromolecules and return
the tissue to status quo.
Biological or chronological ageing may reduce the cellular and neurov-
ascular elements and thereby reduce the ability of the aged pulp to respond B
to injury. The pulp tissue has a rich neurovascular supply that reaches it
via arterioles and nerve bundles through the apical foramina and lesser
accessory supplies via lateral canals in the root. These allow an exchange
of tissue fluid between the periodontal and pulpal tissues, otherwise the
cementum is impervious to macromolecules (a feature that makes survival A
of the tooth by root canal treatment feasible).
The structure of the mineralized dentine is depicted in (see Fig. 1.102).
There may be up to 65 000 tubules per square millimetre at the pulpal end
and 15 000 tubules per square millimetre at the dentine–enamel junction.
Fig. 1.110  Irregular deposition of secondary dentine (A) due to caries (B)
The diameter of the tubules is about 3 µm near the pulp and less than 1 µm
peripherally. The dentinal tubules account for 45% of the surface area near
the pulp and 1% of the total surface area near the dentine–enamel junction. on of dentinogenesis at the termination of tooth formation. Irregular sec-
The dentinal tubules, which are interconnected by lateral tubules (Fig. ondary dentine, as the name implies, is laid down unevenly at a rate of
1.107) make up 20–30% of the volume of dentine. Primary dentine formed about 3 µm per day, in response to noxious external stimuli, such as dental
during the development of the tooth is laid down at a rate of 4 µm per day. caries, attrition, and abrasion (Figs 1.105, 1.109, 1.110). It is laid down by
Secondary dentine is laid down by the same odontoblasts that formed the newly differentiated odontoblast-like cells replacing those damaged by the
teeth but after they are fully developed. It is laid down at the much slower noxious stimuli; therefore, the tubules and processes are not continuous
rate of about 0.8 µm per day and is formed evenly over the entire pulpal with primary and secondary dentine.
surface; it is also known as physiological or regular secondary dentine. It The name peritubular dentine is given to the tissue laid down by the
may be distinguished from primary dentine by the slight and sudden odontoblast process within the tubules. It is 40% more mineralized than
change in the direction of the tubules (Fig. 1.108). This change in direction intertubular dentine (mineralized tissue between tubules) and lacks a fibril-
and rate is thought to be due to the switching off and then switching back lar matrix (Fig. 1.111). The formation of peritubular dentine is thought to
 24  Tooth organogenesis, morphology and physiology

B
C

A B

Fig. 1.111  Cross-section of dentinal tubules: Fig. 1.112  SEM images showing (a) mineralized tubules contrasted with (b) demineralized tubules
A = peritubular dentine; B = interbutular dentine;
C = odontoblast process

Fig. 1.113  Translucency of root Fig. 1.114  Vascular

caused by sclerosis of dentine Venular architecture (courtesy of
network Prof. I Kramer)

Supply
Supply arteriole
capillary
network

Terminal
capillary
network

be a normal age change and may be accelerated by stimuli, such as caries,

attrition and abrasion. Occlusion of the dentinal tubules by this process
and by mineral crystals (Fig. 1.112) is called sclerosis and gives aged roots
their characteristic translucency (Fig. 1.113).

THE VASCULAR SUPPLY
The arrangement of the vascular system in the pulp is uniquely developed
and organized to help overcome the problems of its non-compliant encap-
sulation within the rigid dentine shell. The structure of the vascular archi-
tecture alters and adapts according to metabolic needs as the tooth develops.
It may be visualized as consisting of: (1) the main supply arterioles; (2)
the supply capillary network; (3) the terminal capillary network; (4) the
venular network (Fig. 1.114).
The main supply arterioles, usually 5–8 in number are branches of the
dental arteries that enter through the apical foramina, pass centrally through
the pulp and arborize. Some branches of these vessels run along the root
canal wall as they advance towards the coronal pulp giving off lateral
branches, which terminate in a supply network of capillaries (Figs 1.115–
1.118). It consists of ascending and descending branches, which are ori-
ented perpendicular to the dentine surface. They supply and drain the
terminal capillary network, which reach the odontoblastic layer where they
divide extensively to form a plexus below (Fig. 1.119) and within (Fig.
1.120) it. This is oriented parallel to the dentine surface in the crown, is
400–500 µm wide and diminishes in width towards the root. The venous
return is collected by a network of capillaries that unite to form venules,
which primarily course down the peripheral part of the pulp and drain into
the main venules (2–3) in the central portion of the pulp (Fig. 1.121). Some
minor vessels may enter through lateral canals but these cannot provide
sufficient collateral circulation (Fig. 1.122).
 Tooth organogenesis, morphology and physiology  25

A B

Fig. 1.115  A transverse section through the root pulp (P) of a human
mandibular premolar. The rectangular demarcated area in (a) is magnified in
(b). Note the numerous nerve fibre bundles (NB), some of which are closely
associated with blood vessels (BV) to form neurovascular bundles (inset in b). Fig. 1.118  Relationship of arterioles Fig. 1.119  Capillary plexus adjacent
OB = Odontoblasts. Magnifications: (a) ×55, (b) ×130, inset ×225. and capillaries in the pulp to dentine to the dentine (courtesy of Prof.  
(Reproduced with permission from Nair PNR, Schroeder HE (1995) Number (A) (courtesy of Prof. I Kramer) I Kramer)
and size spectra of non-myelinated axons of human premolars. Anat Embryol
192, 35-41)
Fig. 1.120  Capillary
(A) from the
subodontoblastic plexus

Fig. 1.121  Venules (arrowed)

coursing through centre of pulp

Fig. 1.116  Network Fig. 1.117  High-power view of network of

of blood vessels in the blood vessels in the pulp (courtesy of Prof.  
pulp (courtesy of Prof. I Kramer)
I Kramer)

FUNCTIONAL ASPECTS OF THE BLOOD SUPPLY

The microcirculation serves the nutritional, metabolic and homeostatic
needs of the tissues and receives a high luxury perfusion compared to other
oral tissues. As in most tissues, only a fraction of the capillaries are per-
fused under normal conditions. The pulp was originally thought to be a
fragile tissue, susceptible to rapid death as a result of even minor inflam-
mation, by virtue of its encasement in a rigid dentine shell, which it was prevented. Tissue pressure changes are localized by the shunting away of
thought could lead to strangulation of the apical supply vessels. Elegant blood and fluid from the inflamed area, as well as by the “barrier” effect
experiments demonstrated that apical strangulation of blood vessels was of the ground matrix. The shunting of fluid volume is effected via arterio-
not inevitable because the spread of inflammation could be contained (Fig. venous and venous–venous shunts. The arteriovenous pressure difference
1.123). A unique feature in the arrangement of vascular flow is that a in the pulp is low (20–40 mmHg). The presence of lymphatic vessels (Fig.
build-up of unsustainable pressure in the non-compliant dentine shell is 1.124), disputed until recently, facilitates the return of larger molecules
 26  Tooth organogenesis, morphology and physiology

Fig. 1.122  Minor blood vessels entering lateral Fig. 1.123  Localized inflammation Fig. 1.124  Lymphatic vessel in feline dental pulp
canals (courtesy of Prof. I Kramer) of the pulp (arrowed) (from Bishop & Malhotra, 1990)

and blood cells back to the circulation. The mean velocities of vascular
fluid are approximately 1.5 mm/s in the primary feeding arterioles, decreas-
ing to 1 mm/s in secondary arterioles, 0.5 mm/s in terminal arterioles, and
0.2 mm/s in the capillary bed. It then increases to 0.4 mm/s and then
0.6 mm/s in the collecting and final venules, respectively. One feeding
arteriole may supply 100 capillaries.
The vasomotor tone controlling the flow of blood is moderated by sym-
pathetic nerve fibres and chemical and humoral mediators, which may be
both vasodilators and vasoconstrictors. In contrast to most tissues, reactive
hypoxaemia and functional hyperaemia are not observed in the pulp.
Occlusion of the external carotid arteries produces reactive hyperaemia in
oral tissues but not in the pulp. The response of the pulp under vascular
stress is therefore to shut down, in marked contrast to other tissues.

THE NERVE SUPPLY

The dental pulp is richly innervated with both sensory (large diameter,
myelinated A fibres and small diameter, non-myelinated C fibres, the
majority of the latter group) and autonomic nerve fibres (serving the vas-
cular supply) (Figs 1.125, 1.126). The nerve bundles enter the pulp through
the apical foramen together with the blood vessels (see Fig. 1.115). As the
nerve bundles pass through the pulp coronally, they divide into smaller
branches until, ultimately, single axons form a dense network near the
pulp–dentine border called the plexus of Raschkow (Fig. 1.127). The most
extensive innervation is concentrated in the pulp horns. Furthermore, indi-
vidual axons may branch into many terminal filaments, which in turn, may
enter the dentinal tubules (Fig. 1.128). One axon may innervate up to a
100 dentinal tubules. These usually only penetrate the tubules up to 100
or 200 µm. Some of the tubules may contain several nerve fibres. The true
contribution to the functions of the pulp by the nerve supply is probably
more complicated then originally thought, considering the diversity of the
neuropeptides they produce. Apart from their sensory function they play
an important part in neurogenic inflammation (Fig. 1.129).
FUNCTIONAL ASPECTS OF THE NERVE SUPPLY
The autonomic nerve supply consists of sympathetic fibres that control the
microcirculation. The sensory innervation consists of at least two, and
possibly three different types of fibres. The faster conducting myelinated
Fig. 1.125  A transmission electron micrographic reconstruction of an axon
bundle containing both myelinated (AN) and non-myelinated (CN) axons. Note
the absence of a perineureum around the nerve fibre bundle. The demarcated
area is magnified in Figure 1.130. FI = fibroblasts, SC = Schwann cells.
Magnification: ×5360. (Reproduced with permission from Nair PNR, Schroeder
HE (1995) Number and size spectra of non-myelinated axons of human
premolars. Anat Embryol 192, 35-41)
Aδ fibres are thought to be responsible for the sharp, localized cutaneous
type of dentinal pain. The slower conducting, unmyelinated C fibre is
thought to give rise to the duller throbbing less localized pain. Drilling,
probing, air-drying, heating and cooling dentine stimulate the Aδ fibres.
Application of hyperosmotic fluids to the exposed dentine surface may
also stimulate the Aδ fibres. This sensitivity of dentine is explained by the
“hydrodynamic theory” (Fig. 1.130). The common feature of the above
stimuli is that they all cause a rapid movement of fluid in the dentinal
tubules. This causes a mechanical distortion of the tissue in the pulp–
dentine border resulting in the stimulation of the Aδ fibres. Dentine
 Tooth organogenesis, morphology and physiology  27
Fig. 1.126  A magnified view of the demarcated area in Figure 1.129 showing
detail of non-myelinated axons, variation in size of the non-myelinated axons.
(AN = myelinated axons, SC = Schwan cells). Magnification: ×9110.
(Reproduced with permission from Nair PNR, Schroeder HE (1995) Number
and size spectra of non-myelinated axons of human premolars. Anat Embryol
192, 35-41)
Fig. 1.127  Plexus of
Raschkow
Fig. 1.128  Nerve axon in dentinal tubule (arrowed)
sensitivity may, therefore be increased by opening up the dentinal tubules
by acid etching; conversely, blockage of the tubules, such as by potassium
oxalate crystals prevents fluid flow and leads to desensitization of dentine.
Blockage of the dentinal tubules by sclerosis over time would also lead to
desensitization.
During electric pulp testing, the Aδ fibres are stimulated first because
they have a lower stimulation threshold. Increase in stimulus intensity is
conveyed by an increase in the frequency of firing and by the recruitment
of more Aδ fibres; if the stimulus becomes noxious, C fibres may also
be stimulated giving rise to a strong unpleasant sensation. The relative
unreliability of electric pulp testing of young teeth with immature roots
may be explained by the scarcity of Aδ fibres in their pulps at this stage
of development.
The C fibres may be activated by thermal, mechanical or chemical
stimuli reaching the deeper parts of the pulp. Dentinal stimulation does
Fig. 1.129  Immunocytochemical section showing CGRP-IR nerve fibres
branching extensively in the coronal pulp and entering into dentine for up to
0.1 mm but avoiding reparative dentine (RD). (Reproduced with permission
from Byers MR, Taylor PE, Khayat BG et al (1990) Effects of injury and
inflammation on pulpal and periapical nerves. J Endod 16, 78-84)
Fig. 1.130 
Hydrodynamic theory: A = nerve plexus; B = odontoblast; C = dentine; D = Aδ
nerve fibre; E = odontoblast process; F = dentinal tubule; G = fluid movement
stimulates Aδ nerve fibre
not activate the C fibres unless some element of damage occurs to the pulp
tissue, such as raising the pulp temperature to about 44°C. Similarly,
extreme cold temperatures reaching the pulp may stimulate the C fibres.
The C fibres are thought to play an important role in the development
of the dull and poorly localized symptoms associated with pulp
inflammation.
The third type of nerve called the Aβ fibre is myelinated and has the
fastest conduction velocity. They are thought to respond to non-noxious
mechanical stimulation of the intact crown and may be important in the
regulation of mastication and loading of teeth. They do, however, also
 28  Tooth organogenesis, morphology and physiology

B Fig. 1.133  Cementocytes in cellular cementum

(arrowed)

Fig. 1.132  Ground section showing the relationship

Fig. 1.131  Periodontal ligament supporting teeth between cementum, radicular dentine and enamel:
in alveolar bone (arrowed) A = enamel; B = dentine; C = cementum

respond to stimulation of dentine. In addition to the different nerve fibres

and the types of their stimulation, their threshold of stimulation may also
vary, as may that of the patients’ perception and tolerance of pain. This
results in a wide range of pain descriptors and makes diagnosis of condi-
tions of the pulp unreliable on the basis of the symptoms alone.
The normal pulp contains few inflammatory cells, the exception being
some dendritic antigen-presenting cells and T lymphocytes, which are
probably recirculating rather than resident. At early stages of pulp infec-
tion, there is a non-specific inflammatory response dominated by poly­
morphonuclear leucocytes and macrophages. A specific antibacterial
immune response follows and consists of lymphocytes, macrophages and
plasma cells.
THE PERIRADICULAR TISSUES
These consist of cementum, periodontal ligament and alveolar bone
(Fig. 1.131).
CEMENTUM
Cementum covers the radicular dentine (Fig. 1.132). It abuts the enamel
in 70%, overlaps it in 20% and is separated from it by a gap in about 10%
of the teeth, which may help explain cervical sensitivity in young teeth
without abrasion as the gingiva matures. The cementum is principally an
inorganic tissue which is more impervious than dentine. It is because of
this property of cementum that root-canal treatment is at all possible. It
consists of three types of cemental tissue: (1) cellular; (2) acellular; and
(3) intermediate.
Cellular cementum contains cementocytes (Fig. 1.133) that communi-
cate with each other via canaliculi and also with dentine. It is usually found
in the apical and furcation regions of the tooth. Sharpey’s fibres may be
found embedded in cellular cementum (Fig. 1.134).
A B
Fig. 1.134  Sharpey’s fibres in cementum (arrowed):
A = unmineralize tissue; B = mineralized tissue
Acellular cementum (Fig. 1.135) forms the innermost layer and is devoid
of cells. It covers almost the whole root surface in a thin hyaline layer,
which has incremental lines running parallel to the root surface. It contains
closely packed periodontal fibres (Sharpey’s fibres) that are mineralized.
Intermediate cementum is found in the region of the cemento–dentinal
junction, which has the characteristics of both cementum and dentine. Near
the enamel it may have characteristics of aprismatic enamel.
Functions
Functions of cementum include attachment, tooth wear compensation
and repair.
Cementum provides the attachment for the periodontal ligament fibres,
which suspend the tooth from the alveolar bone. It is laid down through
life in compensation for loss of occlusal tooth substance and plays a
most important physiological role in the repair of resorbed cementum
and dentine. The breakdown in this normal mechanism may result in
external root resorption, which may manifest clinically if extensive enough.
Cementum formation around the apical foramina is thought to be a
desirable end-result of successful healing following root-canal treatment
(Fig. 1.136).
 Tooth organogenesis, morphology and physiology  29

B
A
A

B
A

B
C
C
C

Fig. 1.135  Cementum; dentine, periodontal Fig. 1.136  Healing of periapex with cementum Fig. 1.137  Gingival, transeptal and alveolar crest
ligament and alveolar bone: A = periodontal formation (arrowed); A = periodontal ligament; fibres – longitudinal view: A = gingival fibres;
ligament; B = acellular cementum; C = dentine; D B = root canal; C = alveolar bone (courtesy of Prof. B = transeptal fibres; C = alveolar crest fibres
= alveolar bone T Pitt Ford)

Fig. 1.138  Oblique

fibres – longitudinal
view A A

Fig. 1.139  Oblique fibres – transverse view: A = polyhedric spaces containing

blood vessels; B = ligament fibres

A B

PERIODONTAL LIGAMENT
Periodontal ligament is a dense fibrous connective tissue which supports
and attaches the tooth to its alveolar socket (see Fig. 1.131). Its principal
component is collagen, which is embedded in a gel-like matrix. The fibres
are arranged in specific groups with individual functions. These include
gingival, trans-septal, alveolar crest (Fig. 1.137), horizontal, oblique (Figs
1.138, 1.139) and apical fibres. Another important component is the oxyta-
lan fibre. Functional adaptation may take place in the broad zone known C
as the intermediate plexus (Fig. 1.140). The main cells are fibroblasts and
occasional defence cells. The root sheath of Hertwig, which helps in the B
formation of the root, does not involute completely after completion of
root formation but degenerates into what resembles a perforated bag of Fig. 1.140  Intermediate plexus: A = dentine; B = intermediate plexus;
epithelial cells (Fig. 1.141), called the rests of Malassez (Fig. 1.142). The C = alveolar bone
 30  Tooth organogenesis, morphology and physiology
Fig. 1.141  “Perforated bag” appearance of epithelial Malassez cells
Fig. 1.143  Vascular communications Fig. 1.144  Normal periodontal
at the root apex ligament
perforations are quite large and the intercommunicating strands of epithe-
lial tissue may not all be seen in a given histological section. These cells
can proliferate when stimulated by inflammation to form a cyst. They also
produce cytokines and participate in the apical defence response.
Blood supply
Blood supply to the periodontal ligament originates from the inferior
dental artery. Arterioles enter the ligament near the apex of the root from
the lateral aspects of the alveolar socket and branch into capillaries within
the ligament in a polyhedric pattern along the long axis of the root (see
Fig. 1.139). The collagen fibres run through the polyhedral spaces. The
blood vessels are located closer to the bone than to the cementum. Com-
munications between the vasculature of the pulp and periodontal ligament
may be evident, especially near the root apex and furcation (Fig. 1.143).
Venules drain to the apex or through apertures in the bony wall of the
socket and into the marrow spaces.
Fig. 1.142  Rest of Malassez
Fig. 1.145  The tooth in Figure 1.148 Fig. 1.146  Disused periodontal
following crown placement. Premature ligament. Note the lack of proper
occlusal contact caused overloading orientation of fibres in a narrow
and widening of periodontal ligament ligament
Nerve supply
Nerve bundles enter the periodontal ligament through numerous foramina
in the alveolar bone. They branch and end in small rounded bodies near
the cementum. The nerves carry pain, touch and pressure sensations and
form an important part of the feedback mechanism of the masticatory
apparatus.
Functions
The ligament has a proprioceptive function and acts as a viscoelastic
cushion by virtue of its fibres and hydraulic fluid systems (blood vessels
and their communications with vessel reservoirs in the bone marrow and
the interstitial fluid of the ligament). The ligament has great adaptive
capacity. It responds to functional overloading by widening to relieve the
load on the tooth (Figs 1.144–1.147). The radiographs in Figures 1.144
and 1.145 show the same tooth before and after placement of a crown with
a premature occlusal contact: in Figure 1.145, the periodontal ligament
 Tooth organogenesis, morphology and physiology  31

Fig. 1.147  Overloaded periodontal Fig. 1.148  Alveolar bone Fig. 1.149  Trabeculae in spongy bone
ligament with oblique fibre
orientation and resorption of bone

space is noticeably wider. Figure 1.146 shows a histological view of a Fig. 1.150  Osteoclasts
disused tooth with a lack of proper orientation of fibres in a narrow liga- (arrowed) in Howship’s
ment. Figure 1.147 shows the periodontal ligament of a tooth under normal lacunae
heavy occlusal load, with evidence of adjacent bone resorption causing the
ligament to widen; this widening should be distinguished from that which
occurs in response to pathological irritation. The periodontal ligament also
plays an important part in the eruption of teeth and healing, for example
following surgery or trauma. Vascular channels between the pulp and peri-
odontium form pathways for transmission of both inflammation and micro-
organisms between the tissues.

ALVEOLAR BONE
Fig. 1.151  Relationship
Alveolar bone is that part of the maxilla and mandible which supports the between alveolar bone
teeth by forming the “other” attachment for fibres of the periodontal liga- and cemento–enamel
ment (Fig. 1.148). It consists of two plates of cortical bone separated by A junction in health:  
spongy bone (Fig. 1.149). In some areas, the alveolar bone is thin with no A = cemento–enamel
spongy bone (Fig. 1.148). The alveolar bone and the cortical plates are junction; B = alveolar
thickest in the mandible. The spaces between the trabeculae of the spongy bone
B
bone are filled with marrow, which consists of haematopoietic tissue in
early life and of fatty tissue later (Fig. 1.149). The shape and structure of
the trabeculae reflect the stress-bearing requirements of the particular site.
The surfaces of the inorganic parts of the bone are lined by osteoblasts,
which are responsible for bone formation: those which become incorpo-
rated within the mineral tissue are called osteocytes and maintain contact the cemento–enamel junction (Fig. 1.151) but, in periodontal disease, it
with each other via canaliculi; osteoclasts are responsible for bone resorp- may lie much more towards the apex of the root.
tion and may be seen in the Howship’s lacunae (Fig. 1.150). Cortical bone
adjacent to the ligament gives the radiographic appearance of a dense
white line next to the dark line of the ligament (see Figs 1.144, 1.145). REFERENCES AND FURTHER READING
Bone is a dynamic tissue, continually forming and resorbing in response Bishop, M.A., Malhotra, M.P., 1990. An investigation of lymphatic vessels in the feline
to functional requirements. In addition to such local response to needs, dental pulp. Am J Anat 187, 247–253.
bone metabolism is under hormonal control. It is easily resorbed under the De Deus, Q.D., 1975. Frequency, location, and direction of the lateral, secondary, and
accessory canals. J Endod 1 (11), 361–366.
influence of inflammatory mediators at either the periapex or the marginal Dummer, P.M., McGinn, J.H., Rees, D.G., 1984. The position and topography of the
attachment. In health, the crest of the alveolus lies about 2 mm apical to apical canal constriction and apical foramen. Int Endod J 17 (4), 192–198.
 32  Tooth organogenesis, morphology and physiology
Fanibunda, K.B., 1986. A method for measuring the volume of human dental pulp
cavities. Int Endod J 19, 194–197.
Gulabivala, K., Aung, T.H., Alavi, A., et al., 2001. Root and canal anatomy of Burmese
mandibular molars. Int Endod J 34 (5), 359–370.
Gulabivala, K., Opasanon, A., Ng, Y.-L., et al., 2002. Root and canal anatomy of Thai
maxillary molars. Int Endod J 35, 56–62.
Hess, W., Zurcher, E., 1925. The anatomy of the root canals of the teeth of the
permanent and decidous dentitions. William Wood & Co., New York.
Morfis, A., Sylaras, S.N., Georgopoulou, M., et al., 1994. Study of the apices of human
permanent teeth with the use of scanning electron microscope. Oral Surg Oral Med
Oral Pathol 77 (2), 172–176.
Oehlers, F.A.C., 1957. Dens invaginatus (dilated composite odontome): I. Variations of
the invagination process and associated anterior crown forms. Oral Surg Oral Med
Oral Pathol 10 (11), 1204–1218.
Thesleff, I., 2003. Epithelial-mesenchymal signalling regulating tooth morphogenesis.
J Cell Sci 116 (9), 1647–1648.
Vertucci, F.J., 1984. Root canal anatomy of the human permanent teeth. Oral Surg Oral
Med Oral Pathol 58, 589–599.
Weine, F.S., Healey, H.J., Gerstein, H., et al., 1969. Canal configuration in the
mesiobuccal root of the maxillary first molar and its endodontic significance. Oral
Surg Oral Med Oral Pathol 28, 419–425.
Zillich, R., Dowson, J., 1973. Root canal morphology of mandibular first and second
premolars. Oral Surg Oral Med Oral Pathol 36, 738–744.

Biological and clinical rationale for vital pulp therapy
The aim of this chapter is to outline the biological basis for prevention and
management of pulp disease. A rational approach to the treatment of
disease requires an understanding of the pathological process, which in
turn, demands knowledge of the normal anatomy and physiology of the
involved tissues (see Chapter 1). Given the low-compliance encapsulation
of the pulp and its apparent fragility as a tissue, it was once believed that
relatively minor events could precipitate pulp necrosis and infection. Yet,
the pulp shows remarkable resilience and ability to repair and survive an
aggressive oral environment and generally unsympathetic dental interven-
tions. Clearly the pulp–dentine complex is adapted for such survival and
this chapter explores the interplay between host mechanisms and restora-
tive factors that determine the direction of the outcome.
FUNCTIONS OF THE PULP
The functions of the pulp are stated to be formative (dentine) and defensive
(through the pulp–dentine complex, inflammatory and immune responses).
Once the tooth is fully formed, the pulp mainly serves a defensive function.
The pulp is not a vestigial organ, as indicated by the definite change in the
rate at which dentine is deposited once tooth formation is complete. Hypo-
thetically, if secondary dentine deposition continued at the rate of primary
dentine formation, the almost complete obliteration of the pulp would
result in a tooth with very different mechanical properties. By inference,
the raison d’être of the pulp and dentine must be to provide a tooth with
the resilient characteristics necessary for withstanding masticatory load.
Note that the tooth is considered the hardest structure in the body and
referred to as a non-compliant environment from a fluid dynamics perspec-
tive. Yet, from a mechanical perspective, dentine can flex at a microstrain
level, detectable by sensitive strain gauges. This microscopic deformation
of the tooth under occlusal load must, by the principle of homeostatic
mechanisms, be detectable by proprioceptors in the pulp; however, direct
evidence for the existence of proprioceptors in the pulp is absent. The
presence of Aβ fibres, which serve a proprioceptive function, offers an
attractive, if partial, explanation for the apparently greater susceptibility
of pulpless teeth to fracture.
Defence reactions are essential for the survival of the pulp. The most
obvious and widely described defence reactions include: the initial inflam-
matory response in the pulp; blockage of the involved dentinal tubules by
large molecular substances in the transudate; the sclerosis of the dentinal
tubules by mineral deposition and formation of peritubular dentine; and,
finally, the laying down of secondary and tertiary dentine (Fig. 2.1).
The pulp–dentine complex has been thought of as a sensory organ that
warns against developing disease (e.g. caries or other forms of surface
tooth tissue loss) by eliciting pain. In this role, the warning system is not
effective given the proportion of teeth whose pulps become irreversibly
inflamed apparently without prior pain. The recently exposed dentine may
become sensitive over a few days but, thereafter, as the pulp recovers, the
sensitivity too would subside.
The first line of sensory defence involves stimulation of the low-
threshold cutaneous-type Aδ nerve fibres, responsible for the sensation of
the characteristic sharp, lancinating dentinal pain elicited by stimulating
dentine by probing, air blast, hyperosmotic fluids, extreme temperatures
or occlusal loading (in the cracked tooth syndrome). Inflammation in the
© 2014 Elsevier Ltd. All rights reserved.
2
Section 1 Rationale for disease management
K Gulabivala, Y-L Ng  
vicinity of the exposed tubules reduces their threshold and leads to hyper-
algesia or hypersensitivity. In addition, it also allows stimulation of the
higher threshold C fibres that are responsible for the deep-seated, less
localized, duller, throbbing pain associated with pulpitis. Stimulation of
proprioceptive Aβ nerve fibres may forewarn the owner of impending
overloading of the tooth.
In addition to sensory defences, the inflammatory response of the pulp
contributes to recruitment of the full array of non-specific and specific
immunological responses (see Chapter 3). This system protects the pulpal
soft tissue against external molecular or microbial assault. An extremely
important function of the pulp–dentine complex, which often works simul-
taneously with inflammation, is secondary (reactionary) or tertiary (repara-
tive) dentine formation (Fig. 2.2) together with dentinal tubule sclerosis
(calcification) (Fig. 2.3) to block off further ingress of noxious factors. It
is likely that severe inflammation may interfere with the dentinal response
by disturbing the odontoblastic function.
Reparative processes within the pulp–dentine complex mimic develop-
mental processes. During tooth formation, molecular signals (growth
factors) between epithelial and mesenchymal cells control the induction
of odontoblast differentiation. The growth factors have a profound effect
on various cellular activities and are found throughout the body. A subclass
of these molecules, called the transforming growth factor-beta (TGF-β)
family, is responsible for signalling odontoblast differentiation. The dif-
ferentiated odontoblasts synthesize and secrete the TGF-βs together with
other growth factors and sequester them into the dentine matrix, which
then becomes calcified. The subsequent dissolution of the dentine matrix
as a result of caries, tooth surface loss or restorative procedures releases
these molecules again to exert their influence on healing. TGF-β molecules
released by mild dentine–pulp injury diffuse along a concentration gradi-
ent down the dentinal tubules, against the outward flow of dentinal fluid,
and stimulate viable odontoblasts to lay down reactionary dentine. Injury
that is severe enough to damage odontoblasts irreversibly requires their
replacement from the pulpal mesenchymal cell pool. This is a lengthier
and more complex process requiring the migration and differentiation of
new cells followed by secretion of a new matrix. The resulting dentine is,
therefore less well organized and known as reparative dentine (see Fig.
2.1). An important factor that may interfere with the reparative process is
a continuing microbial challenge as a result of coronal leakage, as well as
the toxicity of any restorative material, which would both intensify the
inflammatory process (Fig. 2.4).
CAUSES OF PULP INJURY
The pulp may be injured in a variety of direct and indirect ways. These
are summarized in Table 2.1 (Figs 2.5–2.7). The pulp may be injured
either by interference with its blood supply or by damage to, or through,
the pulp–dentine complex. Direct interference with the blood supply
may occur in acute (impact) or chronic (occlusal) traumatic injuries.
Injuries through the pulp–dentine complex may occur by: (1) induction
of cracks or fractures in the tooth structure (through acute or chronic
traumatic injuries); (2) exposure of dentine through natural (attrition,
abfraction), dietary (attrition, erosion), parafunctional (attrition, abrasion),
habitual (attrition, abrasion), pathological (caries, resorption) or iatrogenic
 34  Biological and clinical rationale for vital pulp therapy
Fig. 2.1  Primary (A) and irregular Fig. 2.2  Secondary dentine
secondary (B) dentine deposition caused by caries and its
treatment
Fig. 2.5  Effect of attrition on dentine Fig. 2.6  Effect of caries on the pulp: A = inflamed
pulp tissue
(operative or cosmetic) processes; or (3) direct exposure and damage to
the pulp.
Exposure of dentine through any of the mentioned processes would
induce direct physical injury to odontoblastic processes and the cell body.
The disruption would cause the tight junctions between odontoblasts to
separate and be pushed away centrally into the pulp; this would allow
pathways of fluid flow from the pulp to open up. Equally, the pulp would
then be open to stimulation by microbial factors by diffusion, albeit against
the tide of outward flowing dentinal fluid. The degree of such exposure to
flowing or diffusing substances would be dependent on the surface area of
exposure, permeability of the dentinal tubules and depth of dentine damage.
The permeability of dentinal tubules is affected by several factors, includ-
ing involvement in the carious process, physiological response, pathologi-
cal response, exposure to acidic oral environment, calcification, and
coverage by restorative materials. The rate of damage to the dentine,
whether carious or non-carious, may also influence the ability of the pulp
to defend itself. The dentine reputedly has a strong buffering capacity
against the inflow of bacterial substances by binding them to the walls of
the tubules.
The physiopathological mechanisms in place, namely, inflammation,
outflow of dentinal fluid, temporary blockage of tubules by protein mol-
ecules, followed later by mineralization (dentinal sclerosis) and formation
of reactionary dentine help to close off the avenues of direct pulp exposure,
in time. If such closure were not possible because of a precompromised
pulp unable to generate the reparative response, then the unrelenting inflow
Fig. 2.3  Sclerosed dentinal tubules Fig. 2.4  Bacteria in dentinal tubules
(arrowed) (low-power view)
Fig. 2.7  Effect of cavity preparation on the pulp
of microbial stimulants would eventually lead to chronic inflammation and
pulpal demise. The mechanism for such progression may begin with an
accumulation of polymorphonuclear leucocytes (PMNs) at the boundary
of the pulp–dentine complex with migration of these phagocytic cells into
the dentinal tubules. Observation of this phenomenon was originally mis-
interpreted as “aspiration of odontoblasts”. This would be followed by
migration of macrophages, particularly if an irritating or allergenic mate-
rial had been deployed.
These would then be followed by the specific response, including T and
B lymphocytes. The chances of pulp necrosis may be enhanced when the
accumulation of PMNs is profuse.
Protection of the pulp–dentine complex is, therefore dependent on cov-
erage of the exposed dentine using restorative materials. Such coverage
may simply aim to provide a protective layer or simultaneously replace
the missing tissue, restoring form, function, aesthetics and speech. The
complexity and invasiveness of the restorative procedures may in turn also
induce further damage to the pulp, but this is seen as a necessary calculated
risk in order to afford the final protection, just as it is in any elective
surgery. It is, however, important to appreciate the damaging effect of
restorative procedures. A key initial problem is the manner by which the
material is attached to the tooth structure; whether this involves mechani-
cal or chemical retention, each has its advantages and disadvantages.
The relative importance of the different factors causing pulp injury,
when restorative procedures are employed, has been debated at length and
the emphasis has changed from one set of factors to another. In the 1950s
 Biological and clinical rationale for vital pulp therapy  35

Fig. 2.8  Migration of

Table 2.1  Pulp injury
PMNs into the tubules
Relation to treatment Damaging agent Studies
as a result of injury

Preoperative factors Cervical exposed Ten Cate 1994

dentine (genetically
determined)
Tooth surface loss Lundy & Stanley 1969
(acquired) erosion Tronstad & Langeland 1971
Attrition Meister et al. 1980
Abrasion Rosenberg 1981
Abfraction Stanley et al. 1983
Caries Brannstrom & Lind 1965
Reeves & Stanley 1966
Massler 1967
Langeland 1987
Trauma Andreasen & Andreasen 1994
Tooth subluxation or
avulsion
Tooth fracture
Enamel
Dentine pulp exposure
Periodontal disease Seltzer et al. 1963
Mazur et al. 1964
Rubach & Mitchell 1965
Bender & Seltzer 1972
Langeland et al. 1974
Czarnecki & Schilder 1979
Dongari & Lambrianidis 1988
Intraoperative factors Tooth preparation Marsland & Shovelton 1957
Intracoronal Shovelton & Marsland 1958
Extracoronal Langeland 1959
Iatrogenic pulp Hartnett & Smith 1961
exposure
Morrant & Kramer 1963 Fig. 2.9  Direct injury to odontoblasts
Hamilton & Kramer 1967
Marsland & Shovelton 1970
Morrant 1977
provided that microbial leakage at the interface between restorative mate-
Turner et al. 1989
rial and dentine was controlled. Even exposed pulps dressed with such
Ohshima 1990 materials healed over time, provided that persistent injury, due to microbial
Other restorative Langeland & Langeland 1965 microleakage was eliminated, which in these studies, was often achieved
procedures with a barrier of zinc oxide/eugenol cement. There is evidence, however,
Local anaesthesia Suzuki et al. 1973 that resin particles propelled into the pulp may induce a foreign body
Pin placement Cotton & Siegel 1978 response. They may also interfere with the immune defence of the pulp
Cavity cleaning Spangberg et al. 1982 and weaken its potential to defend against bacterial challenge.
Impression taking Kim et al. 1984 Current understanding of the complex interplay between size of cavity,
Temporization Plamondon et al. 1990
remaining dentine thickness (see Figs 2.6, 2.7), restorative material, micro-
Electrosurgery Nixon et al. 1993
bial leakage and pulp inflammation, remains hazy, but a large part may be
Orthodontics Odor et al. 1994
attributed to the presence of bacteria in the cavity (Qvist et al., 1989). The
Restorative materials Cox 1987
Dentine liners Cox et al. 1987
degree of injury to the pulp and its ability to survive is dictated in large
Temporary materials Qvist 1993
part by the amount of remaining dentine, viable odontoblasts, and integrity
Permanent materials Jontell et al. 1995 of the neuroinflammatory and immune responses. It is important to pre-
Katsuno et al. 1995 serve as much dentine as possible as it provides a natural buffer to further
Gwinnett & Tay 1998 injury. Cutting deeper cavities or crown preparations increases the number
Smith et al. 2002
of dentinal tubules involved, reduces the survival of odontoblasts and
Postoperative factors Microbial microleakage Brannstrom & Nyborg 1971
Any preoperative factor Vojinovic et al. 1973
increases the degree of pulp inflammation and migration of PMNs into the
Bergenholtz et al. 1982
tubules (Fig. 2.8). The injury to the pulp is probably due to a combination
Browne & Tobias 1986 of direct injury to odontoblasts (Fig. 2.9) and the pulp by dehydration, heat
Mejare et al. 1987 generation (Fig. 2.10), and microbial and chemical factors reaching the
pulp (Fig. 2.11). Heat generation may be influenced by bur type (diamond
or tungsten, large or small), rotation speed (type of hand-piece), duration
and 1960s, the effect of restorative procedures and toxic restorative materi- and nature of bur contact (intermittent or continuous, high or low interfa-
als (silicate and zinc phosphate restorative materials) was uppermost in cial pressure, bur stalling), cutting technique (slot versus surface removal),
the minds of researchers. Controlled animal and human histological studies vibration and adequacy of coolant spray. Although it is difficult to quantify
at the end of the 1960s and early 1970s revealed that pulp injury caused the threshold of dentine thickness critical to pulp survival, less than
by restorative procedures and “toxic” restorative materials was reversible 0.25 mm results in severe inflammation. Additionally, teeth with cavities
 36  Biological and clinical rationale for vital pulp therapy
A B
Fig. 2.10  Incandescence caused by Fig. 2.11  Bacteria (a) lining the surface of cut dentine (high-power view), (b) in dentinal
dry cutting of dentine tubules
A B
Fig. 2.12  Microleakage under (a) well-filled and (b) poorly-filled restorations
contaminated by microbial leakage have even more severe pulp
inflammation.
Restorations fail and are associated with postoperative complications,
most frequently as a result of the effects of microbial microleakage (Fig.
2.12). The postoperative complications include:
• dentine hypersensitivity
• marginal staining
• restoration corrosion or degradation
• secondary caries
• pulp inflammation and death.
Microbial leakage is enhanced in larger cavities where there is a greater
marginal interface exposed to the oral environment. There is also a greater
potential for tooth deformation under load, causing increased strain at the
marginal junction and making breakdown in the marginal integrity between
restoration and cavity, more likely. The choice of restorative material also
influences the degree of microbial leakage. Zinc oxide/eugenol is the most
effective material for preventing microbial leakage, although resin-
modified glass ionomer cements may also be useful in this regard. Enamel-
bonded or dentine-bonded composites, counterintuitively do not always
perform well in preventing microbial leakage; a distinction should be made
between bonding and a “microbial seal”. Bonded restorations are rarely
sealed along their entire boundary at placement because of factors, such
as material properties, manipulation variables and setting-related dimen-
sional changes. Furthermore, in function, the restoration may lose bonding
integrity due to mechanical, chemical and thermal stresses and strains, all
of which could facilitate nano- or microleakage.
Fig. 2.13  Localized pulp
inflammation
Factors, such as restorative material, cavity dimensions and design,
acid-etching and microbial leakage all influence the degree of pulp inflam-
mation. A complex interplay between these variables leads to damage of
the pulp. The emphasis on microbial leakage in no way reduces the poten-
tial role of restorative procedures and materials in the demise of the pulp.
In clinical practice, teeth undergoing treatment may have a history of
previous treatment and, therefore, pulp inflammation, which may go undi-
agnosed if asymptomatic. It is, therefore, entirely possible that restorative
intervention, however minimal, superimposed upon pre-existing pulp
inflammation or fibrosis may be sufficient to tip the balance and cause its
apparent “sudden” death, necrosis, infection and symptoms.
Open dentinal tubules may provide a persistent pathway for bacteria and
their products leading to persistent chronic inflammation of the pulp and
ultimately to its demise. Open dentinal tubules associated with a healthy
pulp do, however, offer some resistance to bacterial invasion compared to
those in a non-vital pulp. The period of time it may take for the pulp to
die has not been defined but, depending on the initial condition, nature of
the continuing stimulus, and the pulp response, it may sometimes take
many months, if not years. In contrast, the clinical impression can be that
the transition from pulpitis to apical periodontitis may take place over a
matter of days. In such cases, it is likely that asymptomatic pulpitis was
incumbent for an indeterminate period beforehand.
SEVERE INFLAMMATORY AND DEGENERATIVE CHANGES
IN THE PULP
SPREAD OF PULPAL INFLAMMATION
If a localized zone of dentinal tubules remains patent following odontob-
last injury, only the associated portion of the pulp will be inflamed (Fig.
2.13). The process of inflammation spread from this localized site to the
 Biological and clinical rationale for vital pulp therapy  37
Fig. 2.14  Severe inflammation
affecting most of the pulp
A B
rest of the pulp is not fully understood. It is presumably related to the
ability of the pulp to close off dentinal tubules by the action of replacement
odontoblasts from undifferentiated mesenchymal cells. If this fails to wall
off the source of inflammation, then it would become persistent and
chronic. It can be envisaged that the greater the number of adjacent den-
tinal tubules involved and the greater the degree of odontoblast injury, the
larger the volume of pulp tissue affected by inflammation. The localized
response may or may not progress to more severe inflammation depending
on stemming of the provoking factors. Progression of the inflammation
may produce a range of histological pictures, including areas of chronic
inflammation coexisting with microabscesses, gross PMN accumulation
and partial necrosis (Fig. 2.14). Unfortunately, all these histological pic-
tures of pulp disease have a poor correlation with clinical signs and symp-
toms; in 50% of cases, the pulp remains asymptomatic. This makes clinical
diagnosis of the state of the pulp extremely difficult as the tissues are
hidden from direct view and examination. Adding to the complexity of
this diverse picture is the finding that, in some cases (usually young
patients), even in the presence of vital healthy pulp tissue in the roots
(Fig. 2.15a), there may be radiographic evidence of periapical change
(Fig. 2.15b) associated with coronal pulp inflammation. A reasonably clear
distinction between different states of the pulp can only be made between
vital (albeit inflamed) and completely necrotic pulps using currently avail-
able pulp tests.
Under the specific condition of traumatic impact injuries, sudden sever-
ance of the blood supply can result in total necrosis of the pulp without
any intervening infection, inflammation or subsequent radiographic peri-
apical change. Such change would then only become evident in the event
A B
Fig. 2.15  (a) Pulp chamber containing vital pulp tissue; (b) radiograph of the
same tooth, showing periapical area around palatal root before opening into
the pulp
Fig. 2.16  (a) Longitudinal section of tooth, showing a large round
stone in the pulp chamber; (b) calcified stone in the pulp chamber
of subsequent infection of the necrotic pulp. Such pulps have been shown
to remain uninfected for up to 6 years.
DYSTROPHIC PULP CALCIFICATION
A common finding in the pulp in all age groups is the presence of dys-
trophic calcification or pulp stones. These are more common in teeth with
diseased pulps but may also be found in unerupted teeth. The precise
stimulus for calcification is unknown but may be presumed to be mediated
via the mechanisms stimulated by growth factors and leading to odon-
togenesis from mesenchymal cells. A recent theory suggests a role for
nanobacteria or particles but this remains far from widely accepted so far.
There are two types of calcifications; those which are smooth and rounded
are formed by concentric laminations and found commonly in the coronal
pulp (Fig. 2.16a), whereas the irregular calcifications without laminations
are found more commonly in the radicular pulp (Fig. 2.17a). These may
sometimes take the shape of rods or leafs. The laminated stones grow in
size by the addition of collagen fibrils to their surface (Fig. 2.16b), whereas
the irregular type of pulp stones form by calcification of pre-existing col-
lagen fibre bundles (Fig. 2.17b). Some regard the calcifications as a dys-
trophic change, but these calcifications are not always found in association
with degenerative changes. The main clinical significance of pulp calcifi-
cation lies in the technical difficulty it can cause during root-canal treat-
ment. Sometimes the calcification may be extensive enough to almost
obliterate the pulp space (Fig. 2.18). These changes may make the location
and negotiation of canals difficult. Furthermore, dislodged stones may be
pushed apically to cause a blockage. Irregular calcification in the canal
 38  Biological and clinical rationale for vital pulp therapy
A B
Fig. 2.17  (a) Longitudinal section of tooth: note irregular calcification in the
root canal; (b) irregular calcifications in the radicular pulp
A B
Fig. 2.18  (a,b) Examples of almost complete obliteration of pulp space by
calcification
also has the potential to harbour bacteria and make their elimination more
difficult.
PRINCIPLES OF PULP DISEASE PREVENTION
AND TREATMENT
It may be concluded from the foregoing that the fundamental principle of
pulp disease prevention is prevention of exposure of dentine, minimal
removal of this precious tissue and prevention of access of the underlying
pulp tissue to direct or indirect injury. More particularly, persistent micro-
bial assault is to be avoided. Approaches to prevent caries are well known,
including prevention of occlusal caries by using fissure sealants, fluoride
delivered through various means, control of the frequency of intake and
residence of refined carbohydrates in the mouth and plaque control. These
approaches have had qualified success because of issues of patient
compliance.
Despite such efforts and even if they were completely effective, it is
evident that physiological and pathological conditions, as well as unpre-
dictable life events, would not allow prevention of exposure of dentine for
very long. The increasingly longer life spans conferred by protected
western lifestyles, along with the inevitable wear and tear of teeth, are
likely sooner or later to lead to exposed dentine and an increase in the
prevalence and incidence of pulpal and periapical disease. Teeth, it seems,
are not designed to meet the demands of parafunction precipitated by
stressful modern lifestyles, nor are they designed to withstand the onslaught
of acidic foods, drinks and regurgitation precipitated by poor feeding
habits and other gastrointestinal problems. It is true that ancient man also
suffered from attrition albeit more due to function than parafunction,
however, by all accounts theirs was a shorter life span. Tooth surface
loss has become an endemic problem in modern society (prevalence
was 15% in 2009) but it is also coupled with much longer life spans.
This will therefore create a challenge for the dental profession in the
future (The UK Information Centre For Health And Social Care. Adult
Dental Health Survey 2009; http://www.hscic.gov.uk/pubs/dentalsurveyfull
report09 Accessed June 2013).
Coverage of exposed dentine with restorative materials, as a principle
of treatment, either with or without bonding, has failed because no material
seems capable of establishing and maintaining a permanent bond for the
life of the tooth. It is fortunate that the innate healing mechanisms of the
pulp–dentine complex have evolved to prevail over most of the compro-
mising conditions, under which teeth are placed during their life spans.
Instead, the principle of prevention and treatment will, in the future,
need to focus on finding effective ways to control microbial colonization
of tooth surfaces and ingress to the pulp. This will need to be coupled with
an understanding of the natural innate defence mechanisms inherent in the
pulp better to harness them to manage incipient disease. This also means
the discovery of better and more effective ways to detect pulpal disease at
an early stage. Tooth integrity must be preserved through conservative
management of any dental disease. By the same token, the epidemic of
contemporary cosmetic dentistry must be resisted or else more conserva-
tive means found to meet the demand for preconceived and standardized
aesthetic dental form.
Developments in conservative management of caries have taken us
away from the rigid adoption of Black’s principles of cavity preparation,
which having served the populations well for their time, have been suc-
ceeded by new cavity design principles. These are predicated upon a better
understanding of the natural history of caries, its biology, tooth biomechan-
ics and properties of dental materials. Two main approaches have been
tried; the first involves an adaptation of fissure sealing for caries treatment
(as opposed to prevention); and the second, the so-called “Atraumatic
Restorative Technique”. The aim of placing sealants over caries therapeuti-
cally is to arrest active non-cavitated lesions. Previous studies found that
caries beneath the sealant did not progress as long as the sealant was intact.
The number and viability of microorganisms in infected dentine were also
found to reduce significantly when there was no communication with the
oral environment. Atraumatic restorative treatment has been actively pro-
moted by the World Health Organization as a viable approach to meet the
need for treatment of dental caries in underserved populations that mainly
receive extractions when seeking dental care. Atraumatic restorative treat-
ment uses manual excavation of dental caries without the need for anaes-
thesia and the use of expensive equipment and restores the cavity with
glass ionomer cement that bonds to the tooth structure and releases fluoride
to stimulate remineralization.
RATIONALE FOR VITAL PULP THERAPY
When prevention and conservative management have failed to protect
teeth and the dentine surface begins to encroach on the pulp, means need
to be found to protect or regenerate the pulp–dentine complex. Procedures
designed to preserve or regenerate the pulp–dentine complex of compro-
mised teeth have been labelled, indirect pulp capping, direct pulp capping
and pulpotomy. To this traditional list may be added the new category of
“regenerative pulp therapy” and perhaps even regenerative tooth replace-
ment in the future. The rationale behind and consequences of these proce-
dures should be properly understood before they are used.
A potentially compromised pulp may present itself in a variety of ways.
The pulp may be breached or nearly breached because of caries, tooth
 Biological and clinical rationale for vital pulp therapy  39
Fig. 2.19  Necrotic/inflamed pulp
below pulp exposure
surface loss, acute traumatic injury or cavity preparation. In each case, the
operator has to estimate the pre-existing state of the pulp, the extent of
pulp injury and the degree of microbial contamination. In the case of an
acute or chronic (tooth surface loss) traumatic injury, the hard tissue wound
is clearly seen and its history will reveal the extent of damage at the
surface. The nature of the acute injury will give an indication of the prob-
able damage to the pulp and its chances of success. When dealing with a
deep carious lesion, the picture is less clear as the extent of the carious
lesion in its proximity to the pulp will not be obvious. Its acute or chronic
nature will provide some insight into the degree of pulp injury as judged
by loss of odontoblasts and inflammation. Estimation of the degree of
damage is made by a number of clinical assessments. The first assessment
is to judge the histological state of the pulp. This judgement is made on
the history of pain, examination findings, pulp tests and radiographs. The
poor correlation between the histopathology of the pulp and clinical signs
and symptoms leaves the operator with an educated guess. Despite this, it
has often been stated that teeth exhibiting no history of pain or signs of
periapical disease and a positive response to pulp tests stand a good chance
of success following vital pulpal therapy. Conversely, teeth exhibiting
severe throbbing, spontaneous pain, made worse by hot stimuli and keeping
the patient awake may not fare well using this approach. The second
assessment is to estimate the proximity of the carious lesion to the pulp
and, lastly, to guess the extent to which the superficial pulp may be necrotic
and contaminated by bacteria (Fig. 2.19).
The aim of the treatment is to remove as much of the infected hard or
soft tissue as possible and to restore the tooth with a bacteria-tight restora-
tion in order to preserve the health of the residual pulp tissue, leaving it
inflammation-free.
The differences between the procedures labelled indirect pulp capping,
direct pulp capping and pulpotomy reside mainly in the depth and extent
of injury to the pulp and, consequently, the burden of recovery. Each more
radical procedure confers greater damage on the residual pulp calling upon
higher tissue regeneration demands for recovery. In the case of the indirect
pulp cap, by definition, the dentine should be intact, even if it is thin. There
may be damage to the odontoblasts but the potential for recovery of the
pulp–dentine complex should be the highest. In the case of the vital pulp
therapies, the essential dentine barrier is missing, so the emphasis is on an
adequately healthy, albeit inflamed pulp, to regenerate the dentine barrier
through stimulation and differentiation of pulp stem cells to secrete and
mineralize a new functional tertiary dentine layer. In successful cases, the
newly formed pulp–dentine complex may be almost indistinguishable
from the remaining dentine (Fig. 2.20). If the pulp is too inflamed or
fibrotic, there may be insufficient capacity to regenerate, in which attempts
Fig. 2.20  A pulpotomized tooth with
almost normal looking odontoblastic
layer and relatively uninflamed pulp.
Note the inclusions in the dentine
coronal to the pulpotomy
at repair may create a calcific barrier but may not possess the structural
integrity or full defensive ability of a normal pulp–dentine complex. Such
deficient barriers may eventually succumb to the effects of microbial colo-
nization, whereas a fully functional pulp–dentine complex would eventu-
ally lead to an inflammation-free pulp. Judging the outcome (regeneration/
repair/non-healing) is somewhat subjective, with opinions varying about
the amount of time given from 6 weeks to 6 months.
REGENERATIVE PULP THERAPY
This is a relatively newly tried approach with a limited evidence-base. It
is supported only by case reports/series, many of which have involved
mandibular premolars devitalized by occlusal wear or breach of a dens
evaginatus, leaving the root incompletely formed. The cases involved have
periapical lesions and sometimes even suppuration. The proposed manage-
ment consists of conventional access under rubber dam isolation, flushing
of the root canal using a dilute sodium hypochlorite solution, followed by
dressing with a mixture of antibiotic (ciprofloxacin, metronidazole, mino-
cycline) or calcium hydroxide paste within the coronal half to three-
quarters of the canal. The latter helps to control the infection without
damaging any mesenchymal stem cells in the periapical tissues containing
the residue of the formative dental papilla. Once the infection is controlled,
the paste is removed and the canal debrided. Bleeding is then induced by
over-instrumentation of the periapical tissues or the residual dental papilla,
to encourage the influx of stem/mesenchymal cells. The tooth is then
dressed with mineral trioxide aggregate (MTA) over the blood clot and
permanently restored. Follow up of such cases has demonstrated resolution
of the periapical lesion, thickening of the root walls internally, as well as
continued root growth with evidence of continued deposition of hard tissue
within the root. However, the outcome of continued root development is
not as predictable as increased thickening of the canal walls. Crown dis-
coloration produced by the minocycline is an undesirable outcome. Histol-
ogy on dog teeth undergoing this procedure suggests that, in some cases,
the new tissue is dentine-like and, in other cases, it is cementum-like with
the invasion of bone and periodontal ligament into the root canal. The latter
are not pulp parenchymal tissues, suggesting that the outcome is not
always tissue regeneration but wound repair.
ASSESSMENT OF SUCCESS OF VITAL PULP
THERAPY PROCEDURES
All cases of vital pulp therapy should be followed up to determine outcome.
An initial assessment at between 6 and 12 weeks is recommended,
 40  Biological and clinical rationale for vital pulp therapy
Fig. 2.21  Calcific bridge
formation
A B
Fig. 2.22  (a,b) Root formation continues after successful pulpotomy
followed by 6- and 12-monthly reviews. At each review, a history of
symptoms is obtained and an examination carried out to assess tenderness
to palpation of adjacent soft tissues, tenderness to pressure and percussion
of the tooth, signs of radiographic pulpal and periapical changes and
responses to pulp tests. However, pulp tests may not be as fruitful in pul-
potomized teeth. In the case of pulp capping and pulpotomy, additional
tests include checking the presence and integrity of the calcific barrier
(Fig. 2.21) radiographically and by removal of the dressing and direct
probing. Although an initial examination at 6 weeks has been suggested,
this can be modified by the radiographic assessment. If there is no evidence
of a complete bridge formation, the treatment is considered to be a failure
and conventional root canal treatment must be considered. In addition, in
the case of incompletely formed roots, there should be radiographic evi-
dence of progressing root formation (Fig. 2.22). Once root formation is
complete, some believe that it is desirable to carry out root-canal treatment
in order to avoid the complications of continued calcification of the root-
canal system, which may render the procedure more difficult at a later
stage (Fig. 2.23). This is not, however, a universally accepted axiom and
many consider that the residual pulp would be healthy (see Fig. 2.20) and
should only be removed if restorative requirements for restorative reten-
tion dictate so.
PROBABILITY OF SUCCESS OF VITAL PULP
THERAPY PROCEDURES
CONSERVATIVE MANAGEMENT OF CARIES
Fissure sealing of occlusal caries
The approach of sealing occlusal caries appears to be at least partially
successful; a recent study (Bakhshandeh et al., 2011) reporting that 7.4%
A B
Fig. 2.23  (a) Complete root formation following pulpotomy; (b) elective
devitalization following completion of root formation
of sealants for occlusal caries were partially or totally lost and 7.5% of
those sealants retained had caries progression underneath.
Atraumatic restorative therapy (ART)
According to a recent meta-analysis (de Amorim et al., 2011), the pooled
survival rates of single-surface ART restorations using high-viscosity glass
ionomer in permanent teeth were 85% (95% CI: 77%, 91%) and 80% (95%
CI: 76%, 83%) over the first 3 and 5 years, respectively. The pooled one-
year survival rate for multiple-surface restorations was 80% (95% CI:
76%, 83%).
Indirect pulp capping (one-step versus
step-wise excavation)
A clinical trial (Bjorndal et al., 2010) including only adult permanent teeth
reported pulpal exposure to be a complication during the final excavation
in 18% of cases, and 74% of carious teeth undergoing a step-wise excava-
tion procedure remained vital and free of periapical disease at one year
postoperatively. The age of patients, presence of preoperative pain and
pulpal exposure during excavation were significant prognostic factors.
Direct pulp capping
A systematic review (Aguilar & Linsuwanont, 2011), including 10 studies
published between 1971 and 2010, reported the pooled success rates of
direct pulp capping using calcium hydroxide or MTA as the capping mate-
rial in permanent teeth with cariously exposed pulps to be as follows: 88%
at 6 months to 1 year, 95% at 1–2 years, 88% at 2–3 years, and 73% at 3
years or more, postoperatively. MTA was found to be superior to calcium
hydroxide and teeth with immature apices were associated with signifi-
cantly more successful outcomes.
Pulpotomy
A systematic review (Aguilar & Linsuwanont, 2011) reported that partial
(six studies) or full (seven studies) pulpotomies using calcium hydroxide
or MTA in permanent teeth with carious pulpal exposure achieved a more
predictable outcome than direct pulp capping, and sustained high pooled
success rates: 98–99%; 93–99%, respectively. The outcome was not influ-
enced by the capping material or the maturity of the root apex.
 Biological and clinical rationale for vital pulp therapy  41
FACTORS AFFECTING OUTCOME OF VITAL
PULP THERAPY
The most important factors affecting the outcome of vital pulp therapy are:
the maturity of the root apex, pre-existing health of the pulp; adequate
removal of infected hard or soft tissues; careful operative technique to
avoid damage to residual pulp tissues; and elimination of microbial leakage
around the final restoration. It can be difficult to gauge the health of the
residual pulp as it is a matter of subjective assessment and relies on experi-
ence in pulp diagnosis. The degree of pulp bleeding upon exposure is a
more reliable tool to judge the status of the pulp than the preoperative
clinical signs and symptoms. Continued bleeding after 10 minutes, even
after rinsing with sodium hypochlorite solution, may suggest that the
residual pulp was still heavily inflamed and a complete pulpectomy may
be a more effective treatment modality. Removal of infected tissue is a
matter of subjective experience but may be aided by various dyes. The
final factor is reliant upon the correct choice of restorative material and its
adequate manipulation to prevent leakage.
Factors, such as age and health of the patient, size and nature (carious
or traumatic) of pulp exposure, and its duration of exposure to the oral
environment (up to 48 hours) do not in themselves compromise outcomes
of vital pulp therapy.
FUTURE APPROACHES TO PULP REGENERATION AND
VITAL PULP THERAPY
Innovation should by definition recognize the flaws and potential in current
approaches. It is evident that high success rates can be achieved in vital
pulp therapy but that predictability is uncertain because of flaws in the
manner in which the main predictors can be judged clinically. The main
predictors are: (1) the preoperative health of the pulp; (2) elimination of
source of inflammation; (3) treatment to provide the optimal conditions
for healing and tissue regeneration; (4) exclusion of future microbial mic-
roleakage. Innovation should therefore focus on ways to enhance predict-
ability and operator performance in each of these areas. That is, it is
necessary to have better methods for judging the health of the remaining
pulp, that infection can be eliminated or controlled predictably, that a more
biologically based and predictable means of ensuring healing and regen-
eration is found, and that bacterial microleakage can be more predictably
excluded.
It has been suggested that extension of adhesive dentistry to pulp
capping may be one innovation but, while short-term studies show reason-
able early tissue responses, this approach does not actually deal with the
main areas for improvement cited above. Given the extensive clinical data
currently available for the conventional approaches, described above, it is
premature to abandon these procedures in favour of such new methods
that, as yet, have little evidence to support them.
Another putative innovation is the use of MTA (Fig. 2.24) as a pulp
capping agent given its biocompatibility with pulpal and periapical tissues.
While the evidence for pulpal healing of healthy pulp tissue is good, this
approach again fails to address the key innovation parameters. It may
perhaps facilitate better healing but this seems fortuitous rather than by
design.
A promising approach to engineering more effective healing and regen-
eration would be to adopt biomimetic approaches that recruit natural
growth factors and stem cells to stimulate regeneration and healing
with the use of scaffolds as necessary. These approaches may be used to
regenerate both the pulp and the pulp–dentine complex. Potential regenera-
tive endodontic techniques, which have been investigated include: root
canal regeneration via blood clotting; postnatal stem cell therapy; pulp
Fig. 2.24  Mineral trioxide aggregate
(MTA)
implantation; scaffold implantation; injectable scaffold delivery; three-
dimensional cell printing; and gene delivery.
The ultimate would be the in vitro growth of teeth and their implantation
into the mouth to order, however, this seems decades away.
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Biological and clinical rationale for root-canal treatment and
management of its failure
Uncontrolled pulp disease (inflammation) spreads from the pulp chamber
and main canals via the intercommunicating lateral canals and apical
foramina to the periradicular tissues (Fig. 3.1); channels which normally
serve to feed the pulp tissue with their neurovascular supply. While this
apparently simple event of the inflammatory border passing the threshold
of the tooth boundary may not seem that important, clinically, it is associ-
ated with a reduction in the success of root-canal treatment by 10–20%. It
may well be that the critical boundary is that of the associated microbial
front. Root-canal treatment is a therapeutic procedure used to prevent apical
periodontitis when pulpal disease is considered too advanced to manage
by vital pulp therapy but apical periodontitis is not yet established. Root-
canal treatment is also a therapeutic procedure used to cure apical periodon-
titis when pulpal disease has advanced to its sequela, apical periodontitis.
The details of the treatment procedure are covered in Chapter 8, suffice
it to say that it is a technically demanding protocol requiring a mastery
and integration of tactile, spatial and cognitive senses. In a busy general
practice, therefore, the performance of this feat holds sway over biological
considerations in the dentist’s mind. The prevalence of apical periodontitis
and the need for such treatment, worldwide, has underpinned the com-
mercial development of instruments, materials and techniques to make
root-canal treatment more efficient and putatively effective. However, the
outcome data on periapical healing demonstrate that such technical and
technological advances have not been matched by improvements in success
(Fig. 3.2). As pointed out by others in the field of endodontology in the
past, true advances cannot ignore biological considerations, either in the
design of treatment strategy or its execution in practice.
A three-dimensional conceptualization of the dynamic interplay between
infection, inflammation and healthy tissue may help to improve visualiza-
tion of how treatment procedures might influence biological events and
thus aid periapical disease control. An understanding of the process of
spread of infection and inflammation, their establishment in the periradicu-
lar tissues and treatment must begin with knowledge of the normal struc-
ture and physiology of the involved tissues.
AETIOPATHOGENESIS OF PERIAPICAL DISEASE
AETIOLOGICAL FACTORS IMPLICATED
Initial uncertainty about the bacterial origin of periapical disease gave room
for other theories to become established, including stagnant tissue fluid
and necrotic pulp tissue. The former theory was conclusively disproved
by Goldman and Pearson (1965). Histological studies have also shown
growth of connective tissue and cementum-like hard tissue on root-canal
walls after a 7-month exposure of apical tissues to necrotic pulp tissue.
Bacteria
The credit for demonstrating a definitive causal association between bacte-
rial infection and periapical lesion development is extended to Kakehashi
et al. (1965), who compared the pulpal and periapical reactions to experi-
mental pulp exposure in germ-free and conventional rats. The teeth in the
former case exhibited healing, while the latter showed pulp necrosis and
periapical lesion development. The causal relationship between root-canal
infection and periapical disease was further consolidated when Sundqvist
(1976) recovered no cultivable bacteria from traumatized, intact teeth with
© 2014 Elsevier Ltd. All rights reserved.
Section 1 Rationale for disease management
K Gulabivala, Y-L Ng
3  
an absence of periapical disease, while showing 18 out of 19 teeth associ-
ated with periapical disease to yield positive cultures.
Bacterial products
Bacterial products, such as sialic acid, M protein, various enzymes, cell-
capsule and cell-wall constituents, and particularly lipopolysaccharide
(LPS), have all been implicated in initiation of periapical disease. A posi-
tive correlation between the presence of LPS and periapical lesions and/
or symptoms has been confirmed in many studies.
Although bacteria have been the most common microorganisms consid-
ered in root-canal infections, other domains of extracellular (Eucharya and
Archaea) or intracellular (Viruses) life have also been associated with
periapical disease.
Fungi
The presence of fungi in root canals has been reported in numerous studies
(Table 3.1) and has been considered to be a potential cause of endodontic
failure in root-filled teeth but definitive evidence is lacking. Various fungi
(Candida, Aspergillus, Penicillium, Fusarium, Aureobasidium, Exophiala,
Eurotium, Cladosporium) have been isolated from root canals.
Archaea
Archaea, the third domain of life, which are found in a wide variety of
environments, and in close association with eukaryotes including metazoa,
have been implicated in human health and disease via syntrophic and
antagonistic interactions with bacteria. Members of the genus Methanogens
are the only archaea detected in the human body in primary and secondary
root-canal infections by amplification of the mcrA gene. The low diversity
of archaea in root canals, with only two phenotypes identified (Methano-
brevibacter oralis, “phylotype 3” mcrA gene) may imply a limited role.
HOST FACTORS IMPLICATED
Periapical disease is the result of interaction between bacteria (or their
products) and the host defences. Both the non-specific and specific branches
of host defences are recruited to defend against the threat of invasion of
the body by bacteria. The periapical lesion is, therefore, the retreat of the
bone tissue away from the source of infection, creating space for the body’s
defensive elements to migrate into the immediate vicinity of the infection
to counter it (Fig. 3.3).
Knowledge of the composition of periapical lesions is based on histopa-
thology of samples of long-standing lesions of unknown activity and often
undefined clinical status. Nevertheless, the full range of immune mecha-
nisms has been implicated in the development of the periapical lesion (Figs
3.4, 3.5).
The clinical course of the periapical lesion varies giving many presenta-
tions that have been classified into: acute apical periodontitis; chronic apical
periodontitis; acute periapical abscess or suppuration (without sinus tract);
chronic periapical abscess or suppuration (with sinus tract); and radicular
cysts. The relative contribution of the normal inflammatory and immune
responses varies in these clinical variants. The essential nature of the lesion
(except in the incipient lesion) is chronic inflammatory (or granulomatous)
tissue, meaning that the two principal elements, inflammation and attempts
at healing are coexistent. Depending on the state of the lesion there may be
 44  Biological and clinical rationale for root-canal treatment and management of its failure

a variable degree of tissue destruction, with the consequent concentration of

A B
Fig. 3.1  (a,b) Spread of inflammation from the pulp chamber and main
canals via the intercommunicating lateral canals and apical foramina to the
periradicular tissues
polymorphonuclear leucocytes (PMNs) and macrophages in the vicinity of
the apical foramina. The importance of the diagnostic category may lie in
the role it may play in prognosticating on the outcome of treatment.
Chronic inflammation implies persistence of the irritant stimulus (bac-
teria and their products), in this case because of the protective sanctuary
of the root-canal system, which the host defences can access only to a
limited degree (Fig. 3.6). Therefore, in addition to the ubiquitous PMNs
and macrophages, a small population of eosinophils and mast cells, various
proportions of the immune (lymphocyte and plasma) cells are also evident.
Epithelial cells may be present in variable proportions (up to 50%) as
arcades of proliferating cells that may help to form a barrier across the

Buchbinder (1941)
Castagnola & Orlay (1952)
Grahnen & Hansen (1961)
Engstrom & Lundberg (1965)
Harty et al. (1970)
Heling & Tamshe (1970)
Cvek (1972)
Werts (1975)
Adenubi & Rule (1976)
Heling & Shapira (1978)
Jokinen et al. (1978)
Kerekes (1978)
Kerekes (1978)
Barbakow et al. (1980)
Cvek et al. (1982)
Boggia (1983)
Klevant & Eggink (1983)
Pekruhn (1986)
Bystrom et al. (1987)
Halse & Molven (1987)
Safavi et al. (1987)
Akerblom & Hasselgren (1988)
Sjogren et al. (1990)
Murphy et al. (1991)
Cvek (1992)
Ried et al. (1992)
Peak (1994)
Friedman et al. (1995)
Calisken & Sen (1996)
Peretz et al. (1997)
Sjogren et al. (1997)
Lilly et al. (1998)
Ricucci et al. (2000)
Weiger et al. (2000)
Chugal et al. (2001)
Peak et al. (2001)
Benenati & Khajotia (2002)
Cheung (2002)
Hoskinson et al. (2002)
Peters & Wesselink (2002)
Chugal et al. (2003)
Huumonen et al. (2003)
Field et al. (2004)
Khedmat (2004)
Chu et al. (2005)
Moshonov et al. (2005)
Aqrabawi (2006)
Doyle et al. (2006)
Gesi et al. (2006)
Conner et al. (2007)
Molander et al. (2007)
Sari & Duruturk (2007)
Chevigny et al. (2008)
Cotton et al. (2008)
Penesis et al. (2008)
Siqueira et al. (2008)
Witherspoon et al. (2008)
Hsiao et al. (2009)
Tervit et al. (2009)
Liang et al. (2011)
Ng et al. (2011)
Ricucci et al. (2011)
Liang et al. (2012)

Combined

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1

Probability of success - stress

Fig. 3.2  Forest plot showing pooled and individual studies (1941–2012) probability of periapical healing following primary root canal treatment based on strict
criteria
 Biological and clinical rationale for root-canal treatment and management of its failure  45

Table 3.1  Literature relating to isolation of yeasts from root canals

Prevalence of yeasts Yeast species

Author Year No. of samples (teeth) Previous RCT Study method/culture media in root canal recovered
Slack 1953 514 Root canal dressing Nutrient broth 5.8% Not speciated
Robertson’s broth
MacDonald et al. 1957 46 No Connaught penicillinase 2.2% Not speciated
Dextrose broth
Difco thioglycollate broth
Leavitt et al. 1958 154 No Trypticase soy broth 10% Not speciated
76 No Dextrose broth 5% Not speciated
Hobson 1959 98 No Nutrient broth 0.6% Not speciated
Robertson’s broth
Jackson & Halder 1963 214 No Sabouraud’s broth 26% Candida albicans
Glucose broth
214 Yes Sabouraud’s broth 33.6% C. albicans
Glucose broth
Wilson & Hall 1968 263 No Robertson’s meat broth 1.9% Not speciated
Sabouraud’s liquid medium
263 Poly-antibiotic paste Robertson’s meat broth 6.8% Not speciated
Sabouraud’s liquid medium
Goldman & Pearson 1969 563 No Trypticase soy broth 0.5% Not speciated
Blood agar (BA)
Kessler 1972 6 No BA 16% Not speciated
Slack 1975 560 No Nutrient broth 5.2% Not speciated
Robertson’s broth
Matusow 1981 1 case report Yes Schaedler broth agar – C. albicans
Thioglycolate broth
Kinirons 1983 1 case report No Histological examination – Candida species
Tronstad et al. 1987 40 Yes Brucella BA 10% C. albicans
Damm et al. 1988 2 case reports No Histological examination – Candida species
Nair et al. 1990a 9 Yes Transmission microscopy 22% Not speciated
Najzar-Fleger et al. 1992 292 No Sabouraud agar 55% Candida species
Sen et al. 1995 10 No Scanning electron microscopy 40% Not speciated
Lomcali et al. 1996 8 No Scanning electron microscopy 25% Not speciated
Waltimo et al. 1997 967 Yes A range of media 4.9% C. albicans
C. glabrata
C. guillermondii
C. incospicia
Sundqvist et al. 1998 54 Yes Brucella BA 3.7% C. albicans
Molander et al. 1998 120 Yes Brucella BA, semi-liquid 4.2% C. albicans
medium (HCMG-Sula)
Baumgartner 2000 24 No Molecular technique 21% C. albicans

(From Egan et al., 2002)

apical foramina, as part of sinus tracts (Fig. 3.7a) or as the lining of devel-
oping cysts (Fig. 3.7b). Other tissue elements found in the periapical lesion
include endothelial cells and fibroblasts, both being found where there are
attempts at healing.
The three-dimensional distribution of these cellular elements is thought
by some to fall into zones (Fig. 3.8), based on an animal model of bone
infection, but others refute this concept, believing the cellular distribu-
tion to be too random for discrete zonal partition. Perhaps both views are
correct, with zonal organization more evident in the pure chronic lesion
and zonal disorganization brought about by repeated acute exacerbations.
Earlier studies concentrated on the proportions of different cell types in
the periapical lesions to gain insight into the types of reactions prevalent
but there is a limit to the inferences that can be drawn. Later studies
focused on the phenotypic evaluation of cell surface markers (CD recep-
tors) using monoclonal antibodies to define the relative proportion of cell
subsets giving insight into their activity and roles in the progression of the
lesion. The periapical lesion is T lymphocyte dominated, although B lym-
phocytes are also present. The relative proportions of T and B lymphocytes
may be dependent on the nature of the lesion; the T/B cell ratio is reported
to be significantly higher in lesions containing radicular cysts than
granulomas and apical scar lesions. T lymphocytes are the predominant
lymphocytes in periapical granulomas, while B lymphocytes and plasma
cells may occur with greater frequency in “advanced” periapical lesions.
T cells may also be more numerous in refractory periapical granulomas,
while B cells may be relatively more numerous in periapical cysts.
Plasma cells have been demonstrated to be actively producing antibod-
ies in peripical lesions. Members of the tumour necrosis factor family of
receptors and ligands, receptor activator nuclear factor kappa B (NF-κB
or RANK), ligand (RANKL) and osteoprotegerin (OPG), which are
involved in bone metabolism, are found in increased levels when T and B
lymphocytes and macrophages infiltrate chronic periapical lesions. The
relative ratio of RANKL/OPG may be a key determinant of RANKL-
mediated bone resorption (see Fig. 3.5).
The neural and immune systems also interact in controlling the non-
specific and specific defensive responses and it is also possible that micro-
organisms participate in this regulatory function. The ultimate goal is to
decipher the mechanisms involved so that a model can be constructed
describing the entire sequence of interactions between the cellular (micro-
bial and host) and neural components leading to the progressive develop-
ment of the stable (in size) yet dynamic (in activity) periapical lesion. This
 Fig. 3.3  Gross structure Monocytes
of a periapical lesion. PMNs Blood vessel
Note zonal distribution Macrophages
of cellular types
PMNs
PMN
Macrophage
Infected root canal
IL-1

IL-11

IL-8 IL-12 IL-6 IL-10

TNF-α

IFN-γ Th1 Th2 TReg

GM-CSF IL-13
Bone
IL-4
Apical
peridodontitis
IL-2

B cells Plasma cells

Antibodies

Osteoclast Stimulate bone resorption: Chemotactic factor to other cells

IL-1, IL-6, IL-10, IL-11,
IL-13, TNF-α, GM-CSF
Inhibit bone resorption:
IL-4, IFN - γ
Secreted by the cells
Stimulate other cells
Inhibit other cells
Stimulate cell differentiation

Polymorphonuclear leukocytes: PMN

Helper lymphocytes: Th1, Th2
Regulatory lymphocytes: TReg
Interleukins: IL-1, IL-2, IL-4, IL-6, IL-8, IL-10, IL-11, and IL-13
Granulocyte/macrophage colony stimulating factor: GM-CSF
Interferon: IFN – γ
Tumour necrosis factor: TNF-α

Fig. 3.5  Schematic diagram depicting dynamics of periapical lesion (courtesy

of Morgana Vianna)

Initial presentation of the antigen may cause a non-specific

response followed by a specific response if necessary. There
may be interaction between the two types. If the body is
presensitized, specific reaction begins immediately.

non-specific response specific response

immediate reaction of dilatation

of blood vessels leads to: cellular immunity humoural immunity
formation of tissue exudate
(fluid dilutes and pre-existing
acute T lymphocytes B lymphocytes
antibodies neutralize antigens)
inflammation
formation of cellular exudate helper T cells antigen
controlled by (polymorphonuclear leucocytes
chemical and macrophages engulf dead
mediators tissue and foreign matter) killer T cells activator T cells plasma cells

kinins, histamine, complement system C1–C9, plasmins

hageman factor, prostaglandins, leucotrienes suppressor
T cells
lymphokines antibodies
(neutralize foreign matter IgG, IgA, IgM,
and mediate inflammation) IgD, IgE.
(neutralize antigens)
persistence of antigens leads to
interaction between specific and over-reaction of these defences causes tissue damage and
non-specific responses and healing is known as hypersensivity. The reactions are classified
to bring about chronic inflammation into four types according to the components involved:
chronic
(characterized by dense cellular
inflammation type 1 — immediate or anaphylactic reaction - IgE + mast cell
infiltrate — mainly lymphocytes,
type 2 — cytotoxic reaction - IgM, IgG + cell surfaces
plasma cells, monocytes, epithelioid
type 3 — immune complex reaction - IgM, IgG = antigen complex
cells, giant cells, polymorphonuclear
type 4 — delayed hypersensitivity reaction - T cells + antigen
leucocytes and fibroblasts)

Fig. 3.4  Simplified and schematic chart of defence/immune reactions

 Biological and clinical rationale for root-canal treatment and management of its failure  47
D D
Bacteria
requires synthesis of information from human and animal studies at both
cellular and molecular levels. The mechanisms coordinating all these ele-
ments have not yet been fully elucidated, although it is known that some
of them function as cascades.
The molecular components implicated include: cytokines (including inter-
leukins, tumour necrosis factors and colony-stimulating factors); interferons;
arachidonic acid and metabolites; matrix metalloproteinases; adhesion mole-
cules; kinins; complement system; fibrinolytic peptides; vasoactive amines;
lysosomal enzymes; prostaglandins; leukotrienes; and neuropeptides.
The neuropeptides implicated in this process are calcitonin gene-related
peptide (CGRP), substance P, vasoactive intestinal polypeptides, dopamine
hydrolase, and neuropeptide Y. The most interesting among these is the
Fig. 3.6  Bacteria at the apical foramen of
a tooth affected with apical periodontitis
(D = dentine). The canal ramifications on
the right and left, clogged with bacteria,
are magnified in the circular insets. Note
the strategic location of the bacterial
clusters at the apical foramina. The
bacterial mass appears to be held back  
by a distinct wall of neutrophilic
granulocytes. Obviously, any surgical and/
or microbial sampling procedures of the
periapical tissue would contaminate the
sample with the intraradicular flora:
magnification: ×65, insets ×340 (courtesy
of Dr PNR Nair)
Bacteria
possible role of CGRP, which has been implicated both in the response to
pulp and periapical injury (Fig. 3.9).
Viruses
The role of viruses in the pathogenesis of periapical disease has been
investigated with a focus on their effect on symptoms, suppuration and
epithelial and cystic proliferation. As intracellular residents in host cells,
their presence may modify the host response. The viruses investigated and
found include the Herpes simplex (HSV-1/2), varicella zoster (VZV),
Epstein-Barr (EBV), human cytomegalo- (HCMV), human herpes-6
(HHV-6), human herpes-7 (HHV-7), and human herpes-8 (HHV-8) and the
human papilloma (HPV) viruses.
 48  Biological and clinical rationale for root-canal treatment and management of its failure

Fig. 3.7  (a) Epithelium- Fig. 3.9 

lined sinus tract   Immunocytochemical
(Valderhaug, 1974).   section showing
(b) proliferation of calcitonin gene-related
epithelial tissue adjacent peptide (CGRP) nerve
to the apical foramen fibres in pulp horns and
also extending to the
apical (A) part of the
root canal: En = enamel
(Byers et al., 1990)

information. A polymicrobial infection stimulates the host response, the

relevance of its composition and pathogenicity are discussed later.
The pathogenesis of periapical lesions has been studied in a variety of
animal models by artificial induction. The models include rats, rabbits,
dogs, ferrets, cats, and monkeys (Fig. 3.10a–c). The findings are inter-
preted with caution because the microbiota and host responses may be
different from the human condition.
As the root-canal infection develops and matures, it progresses apically
in the root canal until certain, as yet undefined, elements, either bacterial
B products or bacteria themselves, are in a position to stimulate the periapical
tissues via the apical foramina (Fig. 3.10c,d). In a host previously
unexposed to the bacteria, the initial response is non-specific acute inflam-
mation. This comprises first a fluid exudate induced by altered vascular
permeability, which is mediated by several biochemical cascade systems
consisting of preformed plasma proteins acting in parallel to initiate, prop-
Zone of stimulation
agate and control the inflammatory response (see Fig. 3.4). These include:
(1) the complement system, which creates a cascade of chemical reactions
Zone of irritation that promotes opsonization, chemotaxis, and agglutination; it produces the
membrane attack complex; (2) the kinin system, which generates proteins
Zone of contamination (e.g. bradyknin) capable of sustaining vasodilation and other physical
inflammatory effects; (3) the coagulation system or clotting cascade,
Zone of infection which forms a protective protein mesh over the sites of injury; and (4) the
fibrinolysis system, which acts in opposition to the coagulation system,
to counterbalance clotting and generate several other inflammatory
mediators. Subproducts of these cascades may be responsible for further
Fig. 3.8  Zones of FISH activation of the responses, enhancing the inflammatory process. In
addition, products of metabolism such as arachidonic acid, also contribute
to the production of proinflammatory mediators (leukotrienes and
A SYNTHESIZED MODEL OF PATHOGENESIS AND prostaglandins).
NATURAL HISTORY OF PERIAPICAL DISEASE This is followed in rapid succession by a cellular exudate, consisting
principally of PMNs, macrophages, dendritic cells and natural killer (NK)
The precise and complete picture of pathological mechanisms involved in cells, which also release cell inflammatory mediators to augment the
the genesis of the periradicular lesion is unclear, so a “synthesized” model inflammatory process (see Fig. 3.5). The PMNs are attracted to the site
of the possible sequence of events is proposed here from the available by a number of bacteria-derived chemoattractants, such as the peptide
 Biological and clinical rationale for root-canal treatment and management of its failure  49

B C

Fig. 3.10  (a) Monkey’s oral cavity used in experiments by Valderhaug (1974); (b) monkey model of apical
D periodontitis (Valderhaug, 1974); (c) apical progression of root canal infection and establishment of apical
granuloma (Valderhaug, 1974); (d) localization of apical infection by a well-defined granuloma

F-Met-Leu-Phe that constitutes the amino terminus of many bacterial
proteins, and other pathogen-associated molecular patterns (PAMPs)
including components of lipopolysaccharides, mannose and teichoic acids.
In a previously exposed host, these activate the innate immune response
by interaction with different receptors known as pattern recognition recep-
tors (PRR). The PRR, such as the family of Toll-like receptors (TLRs), are
present mainly on macrophages, neutrophils, and dendritic cells (DCs).
Other receptors present on phagocytes with an important role in the
immune response are those for complement, cytokines, interleukins, and
immunoglobulins.
Phagocytosis of accessible bacteria and their products begins with adhe-
sion of the phagocyte surface receptors to bacteria or immune-coated cells;
they are internalized in phagosomes and digested by respiratory bursts and
generation of reactive oxygen species (ROS).
The initial exudate will also bring with it any circulating specific anti-
bodies that may be present. The PMN migration would also then be further
stimulated by activation of complements C3b and C5a via antigen–
antibody-complex formation. The overall effect of pre-existing immunity
is better confinement of the bacteria to their source (apical foramina),
requiring only a sparse cellular infiltrate to deal with them and a fibro-
encapsulation of the rich granulation tissue (see Fig. 3.10d). In contrast,
lack of pre-existing immunity results in poorer bacterial confinement as
well as that of the cellular infiltrate, which is more diffuse and spread into
the trabecular system. These histological pictures translate into radio-
graphic views of well circumscribed, smaller, and better-demarcated peri-
apical radiolucencies compared to more diffuse and extensive lesions,
respectively. The acute response may be accompanied by the usual clinical
signs of pain and tenderness on percussion of the tooth, which may feel
elevated in the socket, but it may also be too transient and minimal to be
noticed. So far, little bone resorption is likely to have taken place and little
obvious radiographic change would be discernible (Fig. 3.11a).
Since the bacteria and their products are not removed, because of their
seclusion in the root-canal system, a delayed immune response is mounted
and the specific immune response commences. These responses are medi-
ated by direct stimulation of the host cells by the bacteria and their prod-
ucts, as well as cascade triggers from subsequent responses. Unlike the
innate response, the adaptive or acquired immune response depends on
activation of the lymphocyte; it involves specificity with a wide spectrum
of diverse recognition patterns, memory, self-restraint, and tolerance to
components of the organism itself. Although the main cells involved in
acquired immune response are lymphocytes, antigen-presenting cells
(APCs) play a key role in their activation, presenting antigens associated
with molecules of the major histocompatibility complex (MHC) to T
lymphocytes.
 50  Biological and clinical rationale for root-canal treatment and management of its failure
A B
Fig. 3.11  (a) Incipient acute inflammation; (b) established chronic
inflammation
Depending upon the nature of the stimulus and host susceptibility, a
whole range of effects may be manifested, including Types 1–4 hypersen-
sitivity reactions (see Fig. 3.4). The magnitude of the response varies from
individual to individual, depending upon both the stimulus and the host
characteristics. In some cases, the host response may be exaggerated
causing greater damage than the bacterial assault. Other host-dependent
factors, which are genetically determined, may also play a part in modulat-
ing the response but these are so far poorly studied for periapical disease.
Deficiency in function and quantity of polymorphonuclear leucocytes
may result in susceptibility to severe infection and development of larger
periapical lesions in both animals and humans. Conversely, systemic
administration of a biological response modifier to increase PMN produc-
tion reduced periapical bone destruction by 40%. In diabetic patients who
have impaired PMN function, the findings have been contradictory. On the
one hand, such patients had a disproportionately high percentage of clini-
cally severe pulpal infections but, on the other hand, the expected higher
prevalence of periapical lesions did not materialize. Furthermore, in an
animal study, the size of lesions induced in non-obese diabetic rats and
controls were not significantly different.
The effect of specific acquired immunity on periapical destruction has
only been investigated in animal models. Genetically engineered rats with
profound defects in both humoral and cellular immunity were less likely
to localize infection to the root-canal system and developed gross orofacial
abscesses and septic shock. This is consistent with the finding that non-
immunized animals have an inflammatory infiltrate resembling early
osteomyelitis extending into the trabecular system of the bone More
recently, genetic factors (low-producer of interleukin 6 [IL-6], intermedi-
ate- and high-producer of IL-1β, low-producer of tumour necrosis factor-α
[TNFα]) have been implicated in the development of symptomatic dental
abscesses.
The clinical progression of the lesion may take one of several paths,
including: acute apical abscess formation, an intensely painful event until
bone resorption relieves some of the tissue pressure; chronic suppuration
with sinus tract formation; or conversion to a chronic, stable but dynamic
state (see Fig. 3.11b).
Bacteria entering the periapical tissues would normally be removed
rapidly by PMNs and macrophages; the latter release leukotrienes and
prostaglandins. The former class of these molecules attracts more macro-
phages to the site and the latter contribute to bone resorption, creating
space for invasion by more immune cells. The activated macrophages also
continue to produce a variety of other mediators of inflammation, includ-
ing IL-1, TNF-α, chemotactic factors such as IL-8, IL-10, IL-12, and
interferon gamma (IFN-γ). These cytokines intensify the local vascular
response, osteoclastic bone resorption, and can provoke a general alert by
endocrine stimulation of fever and output of acute phase proteins and other
serum factors. The IL-1 and TNF-α act in concert with IL-6 to upregulate
the production of haemopoietic colony stimulating factors that are able to
mobilize more PMNs and pro-macrophages from bone marrow. Death of
bacteria, PMNs and macrophages in this encounter can result in suppura-
tion, which may follow an acute or a chronic course (Fig. 3.12). In the
latter case, cytokines and lipopolysaccharides from bacterial breakdown
products may stimulate the epithelial cells in the rests of Malassez to
proliferate and line a tissue path for pus to escape to a body surface
(usually intraoral). Roughly half of all induced periapical lesions (in a
monkey study) developed sinus tracts (see Fig. 3.7a). The relative preva-
lence of various clinical presentations in the unchecked disease process
(natural history), that is the numbers that convert to acute or chronic
abscesses (with or without sinus tracts) or become chronic asymptomatic
granulomas, is unknown. It is likely that the majority follow an asympto-
matic chronic progression.
The most rapid phase of lesion expansion takes place between the 7th
and 15th days (according to one animal study), followed by a slower
expansion in the following 30 days, when the lesion will become apparent
by radiography. From 15 days onwards, the lymphocytes predominate in
the cellular infiltrate (50–60%), followed by PMNs (25–40%), then
macrophage–monocytes, plasma cells and blasts. The lymphocytes are
mobilized by the proinflammatory IL-1 and TNF-α. The T-helper (TH)
cells predominate in the active phase of the lesion expansion, whereas the
T-suppressor (TS) cells predominate in the more chronic lesions. The rela-
tive balance of these two cell types, therefore appears to be involved in
modulation of lesion growth. In molecular terms, the TH-mediated mecha-
nisms involve production of γ-interferon, which activates macrophages to
produce bone-resorptive mediators IL-1β, IL-1α, IL-4, IL-5, and IL-6,
which stimulate antibody production and ultimately form immune com-
plexes. Sixty per cent of the total bone-resorbing activity of interleukins
is attributed to IL-1β, while the rest is due to IL-1α, TNF-α and lympho-
toxin (LT). Arachidonic acid and its metabolites also participate in bone-
resorbing activity as do numerous other mediators, but the precise
synchronization of events is far from clear. The macrophages may also be
stimulated to produce the same factors by phagocytosis of bacteria and
activation by LPS, while the TH cells may also participate in direct bacte-
rial killing and produce LT.
An interesting phenomenon in chronic inflammatory periapical lesions
is the observation that PMNs are chemoattracted to the apical foramina,
where they congregate to form an almost continuous “barrier” to the egress
of bacteria. In other cases, this barrier is formed by proliferation of epi-
thelial cells by mechanisms already mentioned (Fig. 3.13).
The chronic lesions may undergo acute exacerbations as a result of
changes in the balance between the bacteria and host responses or due to
the proliferation of specific bacteria. Such acute phases, accompanied by
invasion of the periapical lesion by viable bacteria (many of which will
die there) (see Fig. 3.12) may also result in increase in the size of the
periapical lesion.
The change in the relative balance between the bacteria (and their prod-
ucts) and the host defences causes variations not only in the histological
but also the clinical picture, although there is no strict correlation between
the histological and clinical pictures. The range of conditions may be clas-
sified as follows.
ACUTE PERIAPICAL INFLAMMATION
This is an uncommon presentation, but once clinically encountered is
instantly recognizable and never forgotten. It arises when the transition
from pulpal to periapical infection and inflammation occurs more rapidly
than allowed by the process of periapical bone resorption. The result is an
accumulation of PMNs and oedema due to the vascular response in the
apical periodontal ligament, giving rise to severe pain. The tooth may
feel raised in the socket, accompanied by acute tenderness to touch. At
this early stage, there may not be any obvious periapical tenderness to
 Biological and clinical rationale for root-canal treatment and management of its failure  51

Fig. 3.12  A massive periapical plaque

associated with an acute lesion. Note the
mixed nature of the flora. Numerous
dividing cocci (DC, middle inset), rods
(lower inset), filamentous bacteria and
spirochaetes (S, upper inset) can be seen.
Rods often reveal a Gram-negative cell
wall (double arrowhead), some of them
showing a third outer layer (OL). The
circular areas 1, 2 and 3 are magnified  
in the middle, upper and lower insets,
respectively: D = dentine; C = cementum;
NG = neutrophils. Original magnification
×2680; upper inset ×19 200; middle
inset ×11 200; lower inset ×36 400 (from
Nair, 1987)

palpation but it soon becomes apparent (Fig. 3.14a). There would be no
demonstrable radiographic periapical change (Fig. 3.14b). Subsidence of
the pain is accompanied by the appearance of a periapical area and the
transition of the inflammation to a chronic state.
CHRONIC PERIAPICAL INFLAMMATION
The histological picture of this entity is as described in detail above. It is
clinically asymptomatic and presents as a radiographic periapical radiolu-
cency (Fig. 3.15). The asymptomatic radiographic image masks a quiet
dynamism and an array of histological variations in cell composition
(described above) and epithelial proliferation with or without cystic
change.
EPITHELIAL PROLIFERATION AND CYSTS
The epithelial rests of Malassez may be stimulated to proliferate by
inflammatory mediators. The pattern of proliferation is variable, with
the formation of strands, arcades or rings of epithelial clusters at the
junction of the uninflamed connective tissue and granulation tissue
 52  Biological and clinical rationale for root-canal treatment and management of its failure

Fig. 3.13  The endodontic flora in the

apical third of a periapically affected
human root. The flora appears to be
blocked by a wall of neutrophils (NG in b)
or an epithelial plug (EP in c). Note the
dense aggregates of bacteria sticking to
the dentine wall (AB in b) and similar
ones (SB in b) along with loose
connections of bacteria (insert in c)
remaining suspended in the root canal
among neutrophils. A cluster of an
apparently monobacterial colony is
magnified in e. Electron micrographs
show bacterial condensation on the
surface of the dentine wall, forming thin
(d) or thick (f) layered bacterial plaques.
The rectangular demarcated portion in  
(a) and the circular one in (c) are
magnified in (b) and the inset in (c),
respectively: GR = granuloma,
D = dentine. Original magnification:
(a) ×50; (b) ×400; (c) ×40 (inset ×400);
(d) ×2440; (e) ×3015; (f) ×3215 (from
Nair 1987)

A B C

F E D

(see Fig. 3.7b). Proliferation may also occur within the body of the granu-
loma, where it presumably helps to plug the apical foramina and limit
egress of bacteria and their toxins (see Fig. 3.13). In some instances, these
epithelial plugs bulge out into the periapical lesion, forming a sac con-
nected to the root and continuous with the root canal, termed a “Bay
or apical pocket cyst” (Fig. 3.16a,b). In these cases, microorganisms from
the root canal have direct access to the “cyst” cavity and may invade it
(Fig. 3.16c).
A true cyst has been defined as a separate pathological, epithelium-lined
cavity usually containing fluid or semi-solid material. It does not com-
municate with the root canal or any other opening (see Fig. 3.16a,d) and
develops in periapical lesions. It was once believed that large circum-
scribed radiolucent lesions with a sclerotic border were likely to be cysts
but such a correlation has not been proven. However, lesions of the size
shown in Figure 3.16e are likely to show cystic change. The bay cyst
should by inference heal by elimination of the bacterial contamination of
the root canal. Successful treatment of the true cyst may require surgery
if conventional root-canal treatment fails to resolve it. This supposition
remains to be proven.
The exact aetiology and mechanisms of cyst formation are not clear.
The epithelium may surround an abscess or granuloma, cutting off the
tissues within from their nutrient source and causing their degeneration.
The molecular mechanisms that stimulate proliferation of epithelial cells
considered crucial in generating the cyst have not yet been elucidated.
Several endogenous regulatory mediators (cytokines, prostaglandins,
interleukins, keratinocyte growth factor, epidermal growth factor) contrib-
ute to cell proliferation. In an established periapical cyst, the basal cells
of the lining epithelium retain the potential as unipotent stem cells capable
of cell division on inflammatory stimulation. The cyst can persist and grow
in size; proliferation markers (e.g. ki67) in the lining epithelium and Notch
signalling (which also regulates embryonic development, adult tissue
homoeostasis, stem/progenitor cell maintenance, differentiation, and pro-
liferation) are involved in the activation of epithelial cells in periapical
cyst walls.
 Biological and clinical rationale for root-canal treatment and management of its failure  53

An alternative theory for genesis of cysts is that dividing epithelial cells
grow until the central cells are starved of their nutrient source, causing
their degeneration.
The method of cyst enlargement is also speculative. Theories involve
selective absorption of fluids and an active biochemical interaction between
the cyst wall and adjacent tissues. Whatever the final explanation, it is
clear that cysts tend to grow and may be considered an independent patho-
logical entity within another pathological entity, the granuloma (see Fig.
3.16d). The relative proportions of granulomatous and cyst tissue may
vary. Although the reported prevalence of cysts among apical periodontitis
lesions varies from 6% to 55%, meticulous serial sectioning and strict
histopathological criteria show the actual prevalence of the cysts to be well
below 20%. As such, it could be argued that while the granulomatous
lesion may be treatable by removal of the aetiological agents from the
canal, the cyst, having become independently established, may continue
to flourish until specifically inhibited or disrupted.
CHRONIC SUPPURATIVE PERIAPICAL INFLAMMATION
In some cases, the conflict between the bacteria and the defence cells,
which are primarily the PMNs, results in the death of many bacteria and
host cells without either side gaining the upper hand. The accumulation of
dead cells and the consequent release of lysosomal enzymes results in the
formation of pus. This is usually conveyed to the nearest body surface by
the formation of a sinus tract, which over time, becomes lined by epithe-
lium (see Fig. 3.7a). Clinically, there may be a draining sinus tract, which
may sometimes be raised to form a “gumboil” (Fig. 3.17a) or rarely may
drain extra-orally to the skin (Fig. 3.18). The patient may complain of bad
taste in the mouth but rarely pain; there may sometimes be some mild
discomfort especially on palpation adjacent to the involved tooth. The
radiographic picture (Fig. 3.17b) would be similar to the previous category,
however, the sinus tract presents the opportunity for placing a gutta-percha
point in it, to trace its source if there is any doubt (Fig. 3.17a).
ACUTE PERIAPICAL ABSCESS/CELLULITIS
This entity may arise from any of the other categories described so far.
When it arises directly from acute periapical inflammation without any
other transition, it is an exquisitely painful condition. The pain usually
subsides as soon as a periapical lesion forms and pressure is relieved.
Opening access to such a tooth is difficult and is aided by applying
pressure to the tooth with a finger while drilling, as vibration from the

A B

Fig. 3.14  (a) Tenderness to palpation over maxillary left lateral incisor and canine; Fig. 3.15  Radiographic appearance of chronic
(b) definite evidence of radiographic periapical change is lacking periradicular inflammation

Fig. 3.16  (a) Bay and true cysts: A = true cyst; B = bay cyst; C = granuloma;
D = epithelium; E = alveolar bone; F = dentine; G = root canal; H = cementum;
I = periodontal ligament. (b) Histological section showing a bay cyst (A):
A
B = granuloma;

A
B

B
 54  Biological and clinical rationale for root-canal treatment and management of its failure
D D C B A
hand-piece causes the discomfort. The abscess is caused by an influx of
large numbers of bacteria into the periapical area that overwhelm the
defences (see Fig. 3.12). This causes a rapid influx of large numbers
of PMNs. The rapid death of large numbers of cells and the release of
lysosomal enzymes causes an accumulation of pus called an “abscess”.
The highly acidic environment causes the further death of surrounding
tissues and may lead to further exacerbation. Classically, it consists of a
Fig. 3.16  Continued (c) Bacteria in a
radicular cyst. Note the distinct epithelial
lining (EP) of the cyst lumen (LU) and a
cluster of neutrophils (NG) showing
phagocytosed bacteria. The upper inset in
(a) shows an overview of the well-
encapsulated cyst (CY). The electron
micrographs in (b) and (c) show the
several types of membrane-delimited
phagosomes (P1 to P6) containing
bacteria. Note the close adherence of
bacteria and the phagosome membrane
in P1 and P2, although a clear space is
visible between them in P3. An electron-
dense coating of varying thickness may
be distinguished on the bacterial surface
in P4 and P5. Note the bacterium in P6 is
devoid of such a coating but the
phagosome contains several membrane-
delimited granule-like structures: D =
dentine; NU = nucleus. Original
magnification (a) ×100: (left inset ×10,
right inset ×850); (b) ×12 800 (upper inset
×8900, lower inset ×17 500); (c) (lower
inset ×8900, upper inset ×17 500) (from
Nair 1987). (d) Histological section of true
cyst (D). A = root apex; B = root canal; C
= granuloma. (e) Large periradicular cyst
associated with mandibular incisors
pathological cavity filled with pus and lined by a pyogenic membrane,
which consists of granulation tissue. Clinically, there would be various
degrees of swelling and pain (Fig. 3.19a,b) and the tooth would feel ele-
vated in the socket. If severe, and accompanied by an allergic response,
there is a large exudative component leading to a build-up of fluid pressure
(Fig. 3.19c). The position of the swelling depends on the tissue planes
(themselves determined by muscle and fascia attachments) through which
 Biological and clinical rationale for root-canal treatment and management of its failure  55
A B
A B
pus spreads and accumulates (Fig. 3.19e–g). The lymphatic system is
frequently involved in dental infections and gives an indication of the
pattern of spread. Lymphadenitis, which comprises an enlargement and
tenderness of the lymph nodes (Fig. 3.19d) may be present, as well as
lymphangitis, characterized by an inflammation of the lymphatic vessels.
The viable bacteria, cellulitis and pus may spread through the lymphatic
system and along tissue planes formed by mucles and fascia, causing a
spreading cellulitis with pyrexia, and the patient to feel unwell. The tissue
space compartments where pus and exudate gather are described in detail
in Chapter 10. Spreading cellulitis, typical of streptococcal microorgan-
isms, manifests as a diffuse firm swelling and can lead to life-threatening
conditions. If a maxillary tooth is involved, cavernous sinus thrombosis
may develop where infection of the tissues of the face may spread intrac-
ranially via the interconnecting venous system, probably via the facial vein
to the cavernous sinus. If a mandibular tooth is involved, Ludwig’s angina
may be a risk. Prior to the antibiotic era, the mortality for Ludwig’s angina
exceeded 50%, since the antibiotic era, and along with improved imaging
and surgical techniques, mortality for the condition currently averages at
8%. Patients with Ludwig’s angina (Fig. 3.19h,i) become seriously ill, with
marked pyrexia, and swallowing, speaking and breathing difficulties. If
the glottis becomes involved the patient may die within 12–24 hours. The
condition should be identified early and the patient referred urgently for
medical attention (see details in Chapter 10).
PERIAPICAL OSTEOMYELITIS
This is a very rare but serious progression of a periapical infection. Chronic
osteomyelitis of the jaws is usually due to mixed anaerobic infection.
The local infection spreads in a diffuse manner through the medullary
spaces causing the necrosis of bone or, more specifically, the cells that
line the mineralized bone (osteoblasts and osteoclasts) and fill the medul-
lary spaces (haematopoietic or fatty cells). The spread may be limited
or extensive. PMNs fill the medullary spaces and destroy osteoblasts
lining the bony trabeculae, allowing the process of bone resorption to
Fig. 3.17  (a) Chronic suppurative periradicular
inflammation (gutta-percha point in sinus);  
(b) radiograph of the same tooth
Fig. 3.18  Sinus tract draining extra-orally from (a) a
mandibular incisor and (b) a mandibular canine
commence leading to the formation of bony sequesters. The patient’s
temperature is elevated, lymph nodes are swollen and pain is severe.
The teeth may be loosened but there may not be obvious swelling in the
early stages. Untreated, the acute osteomyelitis can progress to a chronic
stage, which is less symptomatic but just as serious and merits prompt
treatment.
PERIAPICAL OSTEOSCLEROSIS OR
CONDENSING OSTEITIS
Information is scarce on this relatively common presentation. It is thought
to be a low-grade response of the body to mild irritation. A subdued
response is caused by the buffering effect of intervening healthy tissue,
for example, when the coronal part of a pulp is necrotic and infected while
the apical portion is still vital. The intervening pulp tissue reduces the
potency of the infection and its molecular products and, therefore, their
direct impact on the periapical tissues. The effectively lowered dose stimu-
lates bone deposition as opposed to resorption causing increased bone
density with mild chronic inflammation in the marrow spaces. Clinically,
the lesion is asymptomatic and presents as various grades of radiopacity
surrounding a severely widened periodontal ligament space (Fig. 3.20). In
rare instances, the inflammation is sufficient to cause apical root resorption
at the same time (Fig. 3.21). The condition should not be confused with
other radiopaque lesions, such as caused by benign tumours or dysplastic
changes; 60% of radiopaque lesions are of periapical origin.
NATURE OF THE PERIAPICAL LESION ASSOCIATED
WITH TREATED TEETH
Much of the research on human periapical tissue has been conducted on
undefined samples, that is, it is not known whether the sample was associ-
ated with treated or untreated teeth. Many investigators have assumed that
the responses would be the same. Only a few studies have focused on
 56  Biological and clinical rationale for root-canal treatment and management of its failure

Maxillary anterior

Labial exit
Palatal exit
A Maxillary posterior

B Buccal exit Maxillary sinus exit

Mandibular

Lingual, above mylohyoid Buccal, above masseter

Lingual, below mylohyoid Buccal, below masseter

E

Fig. 3.19  (a) Right facial and infraorbital swelling associated with maxillary canine; (b) intraoral view of swelling in (a); (c) spreading submandibular swelling;
(d) localized submandibular swelling (arrowed); (e–g) line diagrams showing the pathways of spread of infection; (h,i) treatment of Ludwig’s angina
 Biological and clinical rationale for root-canal treatment and management of its failure  57

Localized infection Spreading cellulitis

Palate

Oral cavity

Masseter

Normal tongue Swollen tongue

Tongue muscles

Mylohyoid muscle Sublingual space

Mandible Geniohyoid muscle

Mylohyoid nerve and artery
Submandibular gland
Platysma
Digastric muscle

Dermal tissues

F Swollen mandibular tissues

Parotid gland

Mandible

Medial pterygoid
muscle Masseter

Pathways of
infection spread
Buccal space
and buccal I
H
pad of fat

Fig. 3.19  Continued

specified tissue samples, either from treated teeth or untreated teeth. A
quantitative comparison of lymphocytes and their subsets in periapical
lesions harvested from treated or untreated teeth has shown differences in
the inflammatory infiltrate and relative proportions of T, B and TH cells.
The short-term (7–14 days) response of apical tissues to different root-
canal treatment procedures may result in atypical lesions with total cellular
destruction in the centre and PMNs aggregated at the periphery, possibly
as a result of sodium hypochlorite extrusion.
Periapical lesions persistent over a longer term may represent persistent
chronic inflammation as a result of residual intraradicular infection (Fig.
3.22), established extraradicular infection (Figs 3.23, 3.24), a foreign body
response (Fig. 3.25) or a radicular cyst (Fig. 3.26).
 58  Biological and clinical rationale for root-canal treatment and management of its failure

A B

Fig. 3.20  Periradicular condensing Fig. 3.21  (a) Apical resorption associated with condensing osteitis;
osteitis associated with 35 (b) access cavity into the same tooth shows vital but inflamed pulp tissue

Fig. 3.22  Axial sections through the

surgically removed apical portion of the
root with a therapy-resistant periapical
lesion (GR). Note the cluster of bacteria
visible in the root canal (BA). Parts (b–e)
show serial semi-thin sections taken at
varying distances from the section plane of
(a) to reveal the emerging (b) and gradually
widening (c–e) profiles of an accessory root
canal (AC). Note that the accessory canal  
is clogged with bacteria (BA). Original
magnification: (a) ×52; (b–e) ×62 (from Nair
et al., 1990)

B C

A D E
 Biological and clinical rationale for root-canal treatment and management of its failure  59
A B
ASSOCIATION BETWEEN ROOT-CANAL MICROBIOTA
AND PERIAPICAL LESION DEVELOPMENT
A range of periapical responses to the root-canal microbiota has been
described above, raising the question of whether the variations are funda-
mentally due to differences in host response or types of microbiota. It is
a clinically attractive proposition to be able to segregate different types of
microbiota that not only have different pathogenicity but also different
susceptibilities to treatment and, therefore, merit specific treatment
protocols.
The fundamental reason for accurate identification of bacteria from root
canals is to disclose those bacteria or combinations that may play key
roles in the progress of the disease or its acute exacerbation and especially
Fig. 3.23  Actinomyces in the body of a
human periapical granuloma. The colony
(AC in a) is magnified in (b). The
rectangular area demarcated in (b) is
magnified in (c). Note the starburst
appearance of the colony with needle-like
peripheral filaments surrounded by few
layers of neutrophilic granulocytes (NG),
some of which contain phagocytosed
bacteria. A dividing peripheral filament
(FI) is magnified in the inset. Note the
typical Gram-positive wall (CW):  
D = dentine. Original magnification:
(a) ×60; (b) ×430; (c) ×1680; inset ×6700
(from Nair & Schroeder 1984)
those that may be resistant to conventional therapy or are implicated in
treatment failure.
The counter-view is that it would be difficult to segregate the effect of
individual species in non-specific polymicrobial infections; the problem
of attribution being further confounded by subspecies variation, which
could also account for different pathogenicity.
Animal investigations found changes in the root-canal microbiota to be
associated with development of the periapical lesion. During the critical
period of periapical lesion expansion (between days 7 and 15), the bacte-
rial load did not increase but the proportion of strict anaerobes and the
proportion of Gram-negative bacteria doubled. The mean number of cul-
tivable species (≈3.5) per tooth remained the same during lesion develop-
ment but the overall diversity increased on day 15. Therefore, the critical
period of lesion expansion correlated with the root-canal microbiota
 60  Biological and clinical rationale for root-canal treatment and management of its failure
B C D
becoming more anaerobic and Gram-negative without increase in total cell
numbers.
In classical studies in a monkey model, uninfected teeth did not develop
periapical lesions while most of the infected teeth developed periapical
lesions. They found that the proportion of facultative anaerobic species
decreased and strict anaerobic species increased during the experimental
period. The ratio of obligate anaerobic to facultative anaerobic bacteria
increased from 1.7 (7 days) to 3.9 (90 days) to 6.5 (180 days) and finally
to >11.3 (1060 days). The major site of infection was the main canal fol-
lowed by dentine and then the apical part of the canal. The apical micro-
biota is the most likely to influence changes in the periapical tissues by
virtue of its proximity.
Fig. 3.24  Fungus in the root canal and
apical foramen of a root-filled (RF in a
and d) tooth with a therapy-resistant
periapical lesion (GR in a and d). The
rectangular demarcated area in (a) is
magnified in (d). Note the two clusters  
of microorganisms located between the
dentinal wall (D) and the root filling
(arrows in d). Those microbial clusters are
stepwise magnified in (c) and (d). The
circular demarcated area in (b) is further
magnified in the lower inset in (d). The
upper inset is an electron microscopic
view of the orgnisms. They are about
3–4 µm in diameter and reveal distinct
cell wall (CW), nuclei (N) and budding
forms (BU). Original magnifications:  
(a) ×33; (b) ×330; (c) ×132; (d) ×59; lower
inset × 530; upper inset × 3400 (from
Nair et al., 1990a)
To account for the possible contribution of unsampled or uncultivated
bacteria in the pathogenesis of lesions, eleven isolated strains (including
eight strains from one tooth, representing its total cultivable infection)
were inoculated in freshly necrotized monkey teeth, in various combina-
tions, but always in equal proportions. After 6 months, the “eight-strain
collection” (Prevotella oralis [formerly Bacteroides oralis], Fusobacte-
rium necrophorum, Fusobacterium nucleatum, Streptococcus milleri,
Enterococcus faecalis [formerly Streptococcus faecalis], Peptostreptococ-
cus anaerobius, Actinomyces bovis and Propionibacterium acnes) was
recovered from all teeth but in the same proportions in which it had been
recovered from the original tooth. This strongly suggested that selective
pressures were at play in the root-canal system to reproduce the “same
 Biological and clinical rationale for root-canal treatment and management of its failure  61
A B
C D
infection”. Other combinations did not survive as effectively, while some
species were not recovered at all, suggesting that the cultured isolates were
the main core of the functional microbiome.
Periapical destruction was consistently associated with the mixed infec-
tions but not with the single-strain infections, where some periapical
inflammation was evident depending upon the extent and type of bacteria
surviving. Of the single strains inoculated, only Enterococcus faecalis
survived in every case. Prevotella oralis (formerly Bacteroides oralis),
which dominated all mixed infections, did not survive as a monoinfection.
Inoculation of Staphylococcus aureus, Streptococcus sanguis, Pseu-
domonas aeruginosa and Bacteroides fragilis as monocultures in root
canals could also elicit periapical responses.
Fig. 3.25  Apical periodontitis (AP)
characterized by foreign body giant  
cell reaction to gutta-percha cones
contaminated with talc (a). The same  
field when viewed in polarized lights (b).
Note the birefringent bodies distributed
throughout the lesion (b). The apical
foramen is magnified in (c) and the
rectangular demarcated area in (c) is
further enlarged in (d). Note the
birefringence (BB) emerging from slit-like
inclusion bodies in multinucleated giant
cells. Magnifications: (a, b) ×25; (c) ×66;
(d) ×300 (from Nair, 1998)
In summary, periapical disease is caused by a polymicrobial infection
of the root-canal system with a direct relationship between the size of
periapical lesion and diversity of infection.
Despite several species being implicated by association with sympto-
matic apical periodontitis (Table 3.2), a cause–effect relationship remains
elusive. Black-pigmented Gram-negative anaerobic rods (Black-pigmented
Bacteria; BPB), especially Prevotella melaninogenica (formerly Bacter-
oides melaninogenicus), as well as Parvimonas micra (formerly Pepto-
streptococcus micro) were originally implicated in purulent infections. The
presence of black-pigmented Gram-negative anaerobic rods does not,
however, consistently result in acute abscesses. Other species have also
become associated with the presence of symptoms, including Actinomyces
 62  Biological and clinical rationale for root-canal treatment and management of its failure

Fig. 3.26  (a) Longitudinal radiographs of a periapically affected left central incisor of a 37-year-old woman over a period of 4 years and 9 months of clinical
management. Note the large eccentrically located apical radiolucency observed before (a) and immediately after (b) root filling. The lesion did not show any
reduction in size in control radiographs taken 14, 28, 40 and 44 months (c–f) after endodontics. Apical surgery was performed (g) and the periapical area shows
distinct bone healing (h,i) within 1 year of surgery (from Nair et al., 1993). (b) Axial section through the apical biopsy removed from the radiolucent area visible
in (a) & (g). The large lesion is encapsulated with a narrow rim of dense capsular connective tissue (CT) and contains a distinct lumen lined with stratified
squamous epithelium (EP). Note the vast number of cholesterol clefts (CS) concentrated in the connective tissue at the distocervical aspect of the lesion. The
luminal centre contains pale staining necrotic tissue (NT) and the rest of the lumen is filled with dark staining erythrocytes, among which cholesterol spaces can
be seen. The large rectangular demarcated area is further magnified in (d) (from Nair et al., 1993). (c) Section of a true apical radicular cyst. (d) Presence of vast
numbers of cholesterol clefts (CS) in the lesion. The cholesterol spaces are surrounded by multinucleated giant cells (GC), of which a selected one is magnified in
the inset. Note the large number of nuclei (NU). Original magnification ×98 (inset ×322) (from Nair et al., 1993)

species, Finegoldia magna (formerly Peptostreptococcus magnus), non-
pigmented Prevotella and Porphyromonas species, Peptococcus species,
Eubacterium species, Propionibacterium species, spirochaetes; and Fuso-
bacterium species (Table 3.2). Given the ecological basis for infections, it
is likely that the cause of symptomatic exacerbation is complex and related
to the number of bacterial cells, strain variants, nature of interaction
between species/strains, and other as yet unknown microbial factors. Since
the outcome is also dependent upon interaction between the microbiota
and the host, compromising factors such as viruses could conceivably play
a part, as may other immune burdens. Although the true basis for acute
exacerbation of periapical lesions is still unclear, molecular studies com-
paring acute and chronic infections have suggested that some strains are
associated with acute cases more than chronic cases. More recently, pyro-
sequencing, which allows massive parallel sequencing, has suggested the
existence of specific consortia related to location in root canals, disease
severity and clinical presentation. The most abundant phyla in acute infec-
tions were Fusobacteria with predominance of the genera Fusobacterium
and Parvimonas.
NATURE OF THE ROOT-CANAL MICROBIOTA
The picture of the root-canal infection has continued to evolve as new
research methods have revealed more of the “hidden jigsaw puzzle”. The
polymicrobial nature of the root-canal infection may be defined by its
diversity; which in turn is made up of species richness (number of unique
taxa within a niche) and species evenness (the relative abundance of each
taxon within the niche). Few studies have determined the true diversity of
the root-canal environment; the majority of studies were based on root-
canal sampling, microbial isolation, their identification by biochemical
expression or gene sequencing (Fig. 3.27).
 Biological and clinical rationale for root-canal treatment and management of its failure  63

C D

Fig. 3.26  Continued

Table 3.2  Symptomatic primary apical periodontitis and its association with specific taxa

Year of Type of Year of Type of

Study publication study Species involved Study publication study Species involved
Sundqvist 1976 Culture Bacteroides spp. Brauner & Conrads 1995 Culture Streptococcus spp.
Sundqvist et al. 1979 Culture Bacteroides melaninogenicus Gomes et al. 1996 Peptococcus spp.
Peptostreptococcus micros Eubacterium spp.
Griffe et al. 1980 Culture Actinomyces spp. Porphyromonas spp.
Yoshida et al. 1987 Culture Finegoldia magna (former Propionibacterium spp.
Peptostreptococcus magnus) Fusobacterium spp.
1
Prevotella and Porphyromonas Wasfy et al. 1992 Culture Streptococcus spp.
spp. Baungartner et al. 1999 Culture No associations were reported
Fukshima et al. 1990 Culture Peptostreptococcus spp. Jung et al. 2000 Culture No associations were reported
Peptococcus spp. Siqueira et al. 2001 PCR No associations were reported
Eubacterium spp. Siqueira et al. 2002 PCR No associations were reported
Hashioka et al. 1992 Culture Prevotella and Porphyromonas Jacinto et al. 2003 Culture Prevotella spp.
spp.
Peptostreptococcus spp.
Peptostreptococcus spp.
Foschi et al. 2005 PCR Treponema denticola
Peptococcus spp.
Montagner et al. 2010 PCR Treponema denticola
Eubacterium spp.
Treponema socranskii
Gomes et al. 1994 Culture Prevotella and Porphyromonas
spp. Treponema medium
Peptostreptococcus spp. Treponema amylovorum

1
Former Bacteroides spp.
 64  Biological and clinical rationale for root-canal treatment and management of its failure

A B C D E F

G H I J

Biochemical Identification Molecular Identification by DNA /RNA technology

1 TATTGGGCGT AAAGCGAGCG CAGGCGGTTC TTAAGTCTGA TGTGAAAGCC

51 CCCGGCTCAA CCGGGGAGGG TCATTGGAAA CTGGGAGACT TGAGTGCAGA
101 AGAGGAGAGT GGAATTTCCA TGTGTAGCGG TGAAATGCGT AGATATATGG
151 AGGAACACCA GTGGGCGAAG GCGGCTCTCT GGTCTGTAAC TGACGCTGAG
201 GCTCGAAAGC GTGGGGAGCA AACAGGATTA GATACCCTGG TAGTCCACGC
251 CGTAAACGAT GAGTGCTAAA GTGTTGGAGG GTTTCCGCCC TTCAGTGCTG
301 CAGCAAACGC ATTAAGCACT CCGCCTGGGG AGTACGACCG CAAGGTTGAA
351 ACTCAAAGGA ATTGACGGGG GCCCGCACAA GCGGTGGAGC ATGTGGTTTA
Gram staining 401 ATTCGAAGCA ACGCGAAGAA CCTTACCAGG TCTTGACATC CTTTGACCAC
+ 451 TCTAGAGATA GAGCTTTCCC TTCGGGGACA AAGTGACAGG TGGTGCATGG
Catalase tests 501 TTGTCGTCAG CTCGTGTCGT GAGATGTTGG GTTAAGTCCC GCAACGAGCG
551 CAACCCTTAT TGTTAGTTGC CATCATTTAG TTGGGCACTC TAGCGAGACT

K L M N

Fig. 3.27  Schematic diagram showing sampling, culture, isolation and identification. (a) Selection of a suitable case; (b) access cavity after rubber dam isolation
and decontamination of the working field; (c) microbial sampling using sterile paper points at full length of the root canal; (d) placement of the paper points in
a transport medium. In a microbiology laboratory; (e) 10-fold serial dilutions are performed; (f) aliquots of the serial dilutions are plated on blood agar plates;  
(g) plates are incubated for 24–48 h under aerobic and 7–21 days under anaerobic conditions (Anaerobic work station; Don Whitley Scientific Ltd, West
Yorkshire, UK); (h) example of a plate with microbial growth originated from a primary root canal infection (dilution 1 : 10); (i) colonies are isolated according  
to their morphological characteristics on agar plates; (j) subdivided into two and plated on two blood agar plates and incubated under aerobic and anaerobic
conditions; (k,l) the pure colonies are stained and observed under microscopy. A catalase test is also performed. (m) According to these preliminary tests,
biochemical tests are selected for microbial identification (example of a biochemical identification kit for anaerobic bacteria: Rapid ID 32 A from bioMérieux,
Craponne, France); (n) the clinical isolates can also be submitted to molecular identification techniques by DNA/RNA techniques and comparison to a collection
of sequences from several sources (i.e. Genebank). (courtesy of Morgana Vianna)

Different approaches to sampling and novel sequencing approaches
(pyrosequencing of DNA) may extend the list of taxa further. So far, the
main contribution seems to be in the refinement of the taxonomic assign-
ments at different levels (phyla, classes, orders, families, and genera)
rather than identification at species or strain level.
SPECIES RICHNESS OR QUALITATIVE ANALYSIS
OF MICROBIOTA (Table 3.3)
Studies before the 1960s, lacking the advantage of advanced anaerobic
culture techniques, found mainly aerobic and facultative organisms with
some strict anaerobes (streptococci, lactobacilli, Gram-negative cocci, and
a range of anaerobic bacteria). As strict anaerobic culture techniques
improved, many more strains and species were isolated and identified,
although identification often lagged behind isolation. Most of these species
originated from the oral cavity and some from other parts of the body or
the general environment. The unique milieu of the root-canal system only
allows the survival of select bacterial species, giving rise to different pro-
portional composition of the microbiota compared to oral and periodontal
niches. Molecular techniques, such as polymerase chain reaction (PCR)
and its derivatives, for detection and identification of bacteria brought the
next major advance in resolution of the picture of microbial diversity
implicated in root-canal infections. This was mainly because detection was
not reliant on being able to culture bacteria; yet unculturable bacteria are
 Biological and clinical rationale for root-canal treatment and management of its failure  65

Table 3.3  Representative taxa in untreated root canal infections associated with apical periodontitis (courtesy of Morgana Vianna)

Firmicutes Actinobacteria Fusobacteria

Enterococcus faecalis Acidaminococcus spp. Leptotrichia spp.
Acidaminobacter spp. Actinomyces meyeri Fusobacterium necrophorum
Anaerococcus Actinomyces naeslundii Fusobacterium nucleatum
Bacillus flexus Actinomyces odontolyticus Fusobacterium varium
Bacillus megaterium Actinomyces radicidentis Spirochaetes
Bacillus pumilus Actinomyces viscosus Treponema spp.
Clostridium spp. Arthrobacter Synergistetes
Enterococcus faecium Arthrobacter Synergistetes spp.
Enterococcus hirae Bifidobacterium spp
Eubacterium brachy Brachybacterium spp.
Eubacterium nodatum Corynebacterium diphtheriae
Eubacterium spp. Dietzia maris
Finegoldia magna Eggerthella lenta
Gemella haemolysins Micrococcus luteus
Gemella morbillorum Micrococcus lylae
Lactobacillus casei Propionibacterium acnes
Lactobacillus fermentum Propionibacterium propionicum
Lactobacillus gasseri Rothia mucilaginosa
Lactobacillus rhamnosus Rothia spp.
Leuconostoc spp. Slackia exigua
Megamonas spp. Proteobacteria
Mitsuokella spp. Acinetobacter lwoffii
Mogibacterium Actinobacillus spp.
Pediococcus acidilactici Campylobacter curvus
Peptococcus spp. Campylobacter rectus
Peptoniphilus Campylobacter sputorum
Peptostreptococcus anaerobius Citrobacter spp.
Ruminococcus spp. Eikenella corrodens
Selenomonas sputigena Enterobacter spp.
Staphylococcus aureus Escherichia spp.
Staphylococcus epidermidis Haemophilus influezae
Staphylococcus hominis Kingella spp.
Staphylococcus warneri Klebsiella pneumoniae
Streptococcus anginosus Neisseria spp.
Streptococcus constellatus Pasteurella spp.
Streptococcus gordonii Proteus spp.
Streptococcus infantis Pseudomonas aeruginosa
Streptococcus minor Bacteroidetes/Chlorobi group Bacterial cell structure
Streptococcus mitis Porphyromonas asaccharolytica and oxygen tolerance

Streptococcus mutans Porphyromonas endodontalis Gram-positive aerobic cocci

Streptococcus oralis Porphyromonas gingivalis Gram-positive aerobic rod
Streptococcus pyogenes Prevotella buccae Gram-negative aerobic cocci
Streptococcus salivarius Prevotella intermedia Gram-negative aerobic rod
Streptococcus sanguinis Prevotella loeschei Gram-positive facultative cocci
Streptococcus sobrinus Prevotella melaninogenica Gram-positive facultative rod
Streptococcus suis Prevotella oralis Gram-negative facultative rod
Stretococcus intermedius Prevotella oris Gram-positive facultative cocci
Veillonella dispar Fibrobacteres/Acidobacteria Gram-positive anaerobic rod
Veillonella parvula Fibrobacter spp. Gram-negative anaerobic rod

estimated to comprise between 50% and 90% of the environmental micro-

biota and somewhat less of the oral microbiota. Advances in molecular
culture techniques, such as real-time quantitative PCR, and now pyrose-
quencing have added further to the resolution of the picture of the infected
root canals. They have shown the presence of the three domains of life,
Eubacteria (“true bacteria”), Eucarya (fungi), and Archaea (Methanogens)
(Fig. 3.28). This is placed into context by the general tree of life (Fig.
3.29). The most represented phyla were Proteobacteria (43%), Firmicutes
(25%), Fusobacteria (15%), Bacteroidetes (9%), and Actinobacteria (5%)
(Table 3.3).
SPECIES EVENNESS OR QUANTITATIVE ANALYSIS
OF MICROBIOTA (Table 3.4)
The representatives of the bacterial taxa listed in Table 3.3 are not all
present in every infected tooth. The mean total number of cultivable bac-
teria in infected teeth is estimated to range from 101 to 108 CFUs/mL with
a mean of 105 CFUs per root-canal sample. The relative proportions vary
from study to study and from tooth to tooth and this is consistent with that
in other infections. The number of cultivable genera per tooth ranges from
0 to 16 with mean range between 6 and 9.2. The range of number of
66  Biological and clinical rationale for root-canal treatment and management of its failure

Fig. 3.28  (a) General molecular tree of life (ToL) based on rRNA sequence
Bacteria comparisons. The diagram compiles the results of many rRNA sequence

acteria
comparisons. Only a few of the known lines of descent are shown.

ria
Firmicu
(Reproduced from Pace NR (2009) Mapping the tree of life: progress and

acte
Chlorobi
Ve Th

Acidob
rru ria t prospects. Microbiology and Molecular Biology Reviews 73(4), 565–76.  

nob
erm
Ge co cte plas
WS
tes
mm mi
oto Copyright © 2009, American Society for Microbiology. All Rights Reserved).  

Acti
a
cro ob oro ia

7
atim
6
an chl acter
ga

TM
on bia y (b) The hierarchy of biological classification’s eight major taxonomic ranks.  
e
ad C b dria
ete teo Mitochon (c) Phylogentic tree built of enviromental sequencing data as representative
Bac
tero s Pro
idet 1 phyla found in infected root canals as reported by Özok et al. (2012)
es OP1
Chlorofl
exi BRC1

s
ll ate

Fungi
ge

ls
fla

ima
a no

An
C ho lga
e
Origin dA
Re
ts
Plan
s
Stramenopile
Crenarchaeota Alveolates
Acan
tham
Archaea oeba
e
Eug
Euryarchaeota leno Vertebrates
zoa
He

Urochordates
ter
olo

Angiosperms Gymnosperms
BOL
Tric

bo

rRNA sequence change

se
Diplomo

BAQ1
omo

a
nad

Unresolved branching order

nads

Eucarya
s

A Slime molds
Arthropods
Echinoderms

Life Firmicutes Ascobolus

Proteobacteria Nematode Molluscs

Domain Amoeba
Spirochaetes
Sponges
Kingdom Chlamydiae
OD1 Neurospora
Phylum OD11 Ferns
Coelenterates Heliozansus
OP3
Class Yeasts
TG1
Green algae
Order Fusobacteria
Ciliates
Deinococcus-Thermus
Family Synergistes Brown algae Diatoms
Actinobacteria
Genus
BRC1 Dinoflagellatos
Acidobacteria
Red algae
Nitrospira
Thermomicrobia Mitochondria
Plantomycetes Chloroplasts
Verrucomicrobia Purple bacteria
WS3 Archaebacteria
Species
Bacteroidetes
Tenecutes Cyanobacteria
Cyanobacteria
TM7
OP9 Gram positive bacteria
Synergistes Myxobacteria
B C
Fig. 3.29  General tree of life
 Biological and clinical rationale for root-canal treatment and management of its failure  67

Table 3.4  Quantification of bacterial load by culture and real-time CULTURE STUDIES
quantitative PCR (qPCR)
Morphological studies do not give the identity of bacteria and so require
Year of supplementation by cultivation or in situ hybridization studies. In common
Study publication Type of study with the morphological studies, these also focus on the coronal–apical
Kantz and Henry 1974 Culture 107 bacteria/mL of sample distribution of bacteria in root canals and the penetration of bacteria into
Zavistocki et al. 1980 Culture 107.7 bacteria/gm of sample dentine. The earliest studies on infection distribution were interested to
Byström et al. 1987 Culture 101–107 bacteria/mL determine the existence of infection in periapical tissues because of the
Ando and Hoshino 1990 Culture 103 bacteria/gm of sample controversy caused by the focal infection theory. The chronic periapical
Sato et al. 1993 Culture 101–106 bacteria/mL lesion can remain sterile even when the root canal is infected. The fact that
Brauner and Conrads 1995 Culture 105 bacteria/sample
the majority of periapical lesions heal upon tooth extraction suggests that
Dougherty et al. 1993 Culture 101–106 bacteria/mL
only rarely do infections properly become established extraradicularly.
Vianna et al. 2006 Real-time PCR 4.6×104–6.7×107 gene copy
numbers/mL Cultivation of bacteria from apical (5 mm) samples similar to those
Blome et al. 2008 Real-time PCR 2.6×105–2.6×107 bacterial described by Nair (1987) in his light and electron microscopy study
counts (described below) showed the presence of Actinomyces, Lactobacillus,
Saito et al. 2009 Real-time PCR 2.8×105–2.09×109 cells/ black-pigmented Bacteroides, Peptostreptococcus, non-pigmented Bacter-
samples
oides, Veillonella species, Enterococcus faecalis, Fusobacterium nuclea-
tum and Streptococcus mutans. The majority (68%) were strict anaerobes.
The microbiotia invading the deep layers (0.5–2.0 mm) of dentine in
cultivable species per tooth is currently estimated at 1–12 with mean root canals of carious teeth is mostly (80%) composed of strict anaerobes.
ranges from 2.0 to 5.7 per tooth. According to culture quantification, the The predominant bacteria are Gram-positive rods (68%) and Gram-positive
total concentration of aerobes and anaerobes is nearly equal. In contrast, cocci (27%). Lactobacillus (30%), Streptococcus (13%) and Propionibac-
teeth undergoing root-canal treatment have a residual microbiota with a terium species (9%) are dominant. A similar study of teeth with undefined
cell concentration of between 101 and 103 CFUs per sample. There is a coronal status but evaluating the full thickness of dentine found a more
general trend towards later studies showing higher numbers of species per diverse microbiota consisting of a mix of Gram-positive and Gram-
tooth but this is not universally true. The numbers probably reflect better negative types including Prevotella, Porphyromonas, Fusobacte­rium,
cultivation and identification techniques. Peptostreptococcus, Actinomyces, Streptococcus, Propionibacterium,
Studies using culture-independent techniques reveal the overall diver- Lactobacillus and Bifidobacterium species. The presence of Gram-negative
sity of root-canal infections to be much higher than findings using culture- bacteria in the inner layers of root canal dentine has been confirmed by
dependent techniques. The mean total number of gene amplicons by the finding of lipopolysaccharide in dentine up to 300 µm in depth.
real-time PCR (qPCR) in infected teeth is estimated to range from 104 to Cementum from apical portions of roots harvested during apical surgery
109 gene copy numbers per root-canal sample. The discrepancy with CFU may show the presence Prevotella, Fusobacterium, Peptostreptococcus,
counts may be explained by the fact that each bacterium may have multiple Eubacterium and Campylobacter species. This observation can be recon-
copies of a gene. Pyrosequencing reveals the mean number of species/ ciled with previous studies if the teeth are associated with sinus tracts.
phylotypes in apical root samples to range from 13 to 130. Some researchers have investigated the penetration of bacteria and their
products into cementum from the periodontal surface but the positive find-
DISTRIBUTION AND PHYSIOLOGICAL STATUS ings remain controversial. The reason is that they imply that such bacteria
OF INTRARADICULAR MICROBIOTA could coexist with vital, perhaps healthy pulps and others have shown that
vital pulps resist invasion by bacteria.
Insight about the distribution and physiological status must be synthesized
from different study sources as a single research method is not available
to lend comprehensive evidence.
MICROSCOPY STUDIES
It is intuitively evident that bacteria gain access to the root-canal system Several microscopy surveys (light, dark-field, fluorescent, confocal, TEM
by a number of routes. The commonest is through the crown by means of and SEM) of teeth have shown the pattern of bacterial invasion and associ-
a carious exposure, through open dentinal tubules in the crown or root, ated pulp necrosis. A “synthesized view” is presented below based on the
through lateral canals either before devitalization via blood vessels com- observations from these studies.
municating with the periodontium or after exposure to the oral environ- Bacterial invasion usually begins in the coronal part of the tooth and
ment due to periodontal disease. Cracks in the tooth (enamel and/or root and is concentrated there (Fig. 3.30). The distribution from here into
dentine) also allow root-canal infection. Another less common route is by the canal system is associated with two factors: the presence or absence
anachoresis; a term used to denote infection of a chronically inflamed area of pulp chamber exposure; and the presence or absence of a periapical
by a blood-borne infection or a bacteraemia. For this condition to be ful- lesion. As a rule, bacteria are evident lining the canal wall in biofilms,
filled, the pulp must be intact but chronically inflamed, it is unlikely that which are discontinuous (covering 30–50% of the surface area) and vari-
a necrotic canal would be infected in this way. The point of entry of the able in thickness (Fig. 3.31), with thinner and less coverage in teeth with
bacteria is likely to dictate the nature and distribution of the subsequent intact pulp chambers. The biofims may also extend along other surfaces,
infection within the tooth. such as necrosing pulp tissue (Fig. 3.32) and degenerating vascular chan-
Studies on the nature of microbiota in root canals far outnumber those nels. Bacteria appear in smaller numbers in the root canals as the apical
seeking to reveal the distribution of bacteria. Our collective knowledge is terminus is reached in teeth with intact pulp chambers (Fig. 3.31) but
based on light, dark-field, fluorescent, confocal and electron microscopic where the pulp chambers are cariously exposed, the canals are more evenly
(scanning electron microscopy [SEM], transmission electron microscopy coated with a bacterial plaque. Even then, the plaque is not continuous
[TEM]) studies, cultivation studies and analysis of distribution of bacterial over the entire surface (Fig. 3.33). In teeth without periapical lesions, vital
toxins. pulp tissue may be present apically and, if so, the intensity of the infection
 68  Biological and clinical rationale for root-canal treatment and management of its failure
Root canal space
Root dentine
Bacterial biofilm
Fig. 3.30  Bacterial distribution in the coronal part of the tooth and root
Fig. 3.31  Sparse and discontinuous canal wall coverage with biofilm (red
staining) of a tooth with intact pulp chamber and apical periodontitis. Bacterial
distribution (in red) as revealed by in situ hybridisation using universal (EUB) and
streptococcal (Strep) rRNA probes. Attempts 1 & 2 are separately stained sections
tapers off towards it (Fig. 3.34). In teeth with periapical lesions, the infec-
tion follows one of several courses: in some, the colonization is concen-
trated in the coronal and middle portions of the root; in others, the
colonization is concentrated in the coronal and apical portions (Fig. 3.35);
in yet others, the distribution is concentrated in the middle and apical por-
tions. This might suggest a variation in nutritional sources in the canal
systems. The patterns confirm the diversity perspective that each infection
is unique.
Microscopy studies can only reveal bacterial morphotypes, so the
description is limited (Fig. 3.36). A significantly greater percentage of
coccoid and rod forms are noted in the coronal rather than the apical parts
of canals, whereas the distribution of motile rods does not differ. In con-
trast, the percentage of filaments and spirochaetes are slightly higher in
the apical than the coronal parts of the canal (Fig. 3.37). A significant cor-
relation is noted between the size of the apical radiolucency and the per-
centage of spirochaetes present. Occasionally, yeasts or fungi may also be
evident, sometimes in the process of budding (Fig. 3.38).
TEM observation of the apical portions (5 mm) of cariously exposed
teeth confirms that the bulk of the microbiota exists as a loose collection
of a variety of morphologically distinct forms consisting of cocci, rods and
filamentous forms (see Fig. 3.13). Nair’s first description (1987) was that
the bacteria appeared suspended in an apparently moist canal lumen, with
less frequent, dense aggregates observed sticking to the dentinal wall of
the root canal or existing free among vast numbers of PMNs in the canal
lumen. In acute cases, the PMNs can penetrate in vast numbers to line the
biofilm on the canal wall and even extend to the coronal part of the canal
(Richardson et al., 2009) (Fig. 3.39a,b). At higher magnification, these
PMNs can be seen to be actively phagocytosing the intracanal bacteria
(Fig. 3.39c).
The dense aggregates were described as clusters of morphologically
uniform cells. The interbacterial spaces were described as filled with an
amorphous extracellular matrix. Independent of these tooth-adhering
monobacterial aggregates, the dentinal wall was described as covered by
single or multilayered bacterial condensations containing various morpho-
types. The filamentous forms were often adherent perpendicular to the
canal wall with coccoid forms arranged in strings in the same direction.
Cocci occasionally attach to the filaments to give a corncob appearance
(Fig. 3.40). Nair modified his interpretation later (personal communica-
tion) that the majority of the bacteria were probably in biofilm form.
Deposits resembling bacterial plaque are also evident in the apical 2 mm
of the root canal. Epithelial cells or a wall of PMNs often plugs the apical
canal terminus. In acute cases, there may be a massive apical biofilm filling
the entire circumference of the canal (Fig. 3.41). In those cases where the
microbial front extends into the periapical lesion, there may be extensive
tissue necrosis and acute PMN response. In the latter instance, the chronic
granulomatous tissue immediately around the tooth apex may be lysed and
occupied by an apparently young apical plaque. SEM or LM views reveal
scalloped root resorption (Fig. 3.42) with multilayered bacterial plaque
embedded in an extracellular matrix. Such extraradicular extension of
bacteria (Fig. 3.43) is, however, rare; one microscopy study showing a
prevalence of about 6%.
Bacterial penetration into dentine is only evident in the presence of pulp
necrosis. Tubule colonization has been shown to be facilitated by the
adherence of specific bacteria to the Type 1 collagen present in dentinal
tubules (Fig. 3.44). The predentine is easily and commonly infected but
the calcified dentine less so. Bacterial penetration into dentine around the
root canal is confined to the close proximity of the root canal (Fig. 3.45),
where nutrients are available and bacteria are able to grow and multiply
(Fig. 3.46). In some teeth, bacteria may be evident penetrating up to a third
or a half of the depth of dentinal tubules where they end in a vital periodon-
tal membrane. Only in cases where the tubules end in necrotic periodontal
tissue are the bacteria observed along the entire length of the dentinal
tubules (Fig. 3.47). Dentine tubule infection is less evident in the apical
part because of the sparcity of tubules but may be deeper, particularly in
cariously exposed teeth. Cementum is rarely infected except in the pres-
ence of extraradicular infection.
IN SITU HYBRIDIZATION MICROSCOPY STUDIES
Culture of root-canal samples allows isolation of bacteria and their iden-
tification by biochemical or genetic means but, by definition, the site
context is lost as is the relationship with the canal, its contents and other
species. Despite all efforts, culture may also bias the relative proportions
of bacteria found. Microscopy retains relational context of the bacterial
cells with the site but fails to provide identification more sophisticated than
cell morphology. In situ hybridization (Fig. 3.48) provides a means of
combining the advantages of both techniques. Bacterial cells can be identi-
fied in situ by means of specific probes, which target cell structure or
 Biological and clinical rationale for root-canal treatment and management of its failure  69
components. Examples of in situ hybridization labelling of bacteria in
root-canal sections include gold labelling of bacterial cell surface antigens
(Fig. 3.49), gold labelling of 16SrRNA probes (Fig. 3.50), fluorescent in
situ hybridization (FISH) of universal bacterial 16S rRNA probes (Fig.
3.51), FISH of spirochaetes (Fig. 3.52), FISH of streptococci (see Fig.
3.35). The technique is able to help depict the distribution of bacteria over
the canal surface, as well as the distribution of specific species such as
streptococci. The streptococci specific biofilm was always a smaller per-
centage of the overall biofilm coverage; the percentage of streptococci
generally decreased as exposure to the external oral environment reduced.
The level of Streptococus infection in exposed teeth with periapical patho-
sis was less than that of samples with exposure but no perapical
Fig. 3.32  Bacterial biofilm extending along
necrosing pulp tissue. Bacteria (yellow arrow)
within necrotic tissue (black arrow) (×40 top and
×100 bottom)
pathogenesis. This suggests that the Streptococci are initial colonizers and
that perhaps with biofilm maturity they are outnumbered by other species.
The technique should enable the dissection of the local niche ecology in
combination with insight about bacterial physiology. Figure 3.52 shows a
typical ecological picture with different morphotypes clustering in pat-
terned format around some part of the dying pulp, from which one species
is deriving nutrient directly, while other morphotypes appear to be arranged
around the primary species (interpretation by Prof Bill Costerton).
In summary, the overall picture of the intraradicular microbiota is a
crude one of a variable distribution of bacteria within the root-canal system
and dentine. The state at any given time may represent the stage of infec-
tion with bacteria extending up to and sometimes beyond the apical canal
 70  Biological and clinical rationale for root-canal treatment and management of its failure
Fig. 3.33  Canals evenly coated with a discontinuous bacterial plaque in a
tooth with exposed pulp and apical periodontitis. Bacterial distribution (in red)
as revealed by in situ hybridisation using universal (EUB) and streptococcal
(Strep) rRNA probes. Attempts 1 & 2 are separately stained sections
Fig. 3.34  Vital pulp tissue present in the infected canal of a tooth without
periapical lesion. Bacterial distribution (in red) as revealed by in situ
hybridisation using universal (EUB) and streptococcal (Strep) rRNA probes.
Attempts 1 & 2 are separately stained sections
terminus. The depth of penetration into dentine is also variable but gener-
ally appears to be confined within the area close to the root canal and is
probably dominated by Gram-positive bacteria, mostly streptococci. In
rare instances in chronic lesions, the bacteria may proliferate beyond the
apical foramen and into the periapical lesion. Mainly anaerobic bacteria
have been demonstrated in the periapical tissues, perhaps associated with
foreign or dead (cellular or dentinal) material, to which the defence cells
have no or limited access. The bacteria may also be found embedded in
an extracellular plaque-like matrix covering the external surface of the
root. The bacteria in this plaque have been observed to be mainly cocci
and rods but fibrillar forms may be present too. The main species impli-
cated in periapical tissue invasion include Actinomyces species and Pro-
pionibacterium propionicum. Many others from the root-canal microbiota
have also been implicated but their true presence in the periapical tissues
A C
B D
Fig. 3.35  Bacterial colonization concentrated in the coronal and apical
portions of root canal. Bacterial distribution (in red) as revealed by in situ
hybridisation using universal (EUB) and streptococcal (Strep) rRNA probes.
Attempts 1 & 2 are separately stained sections
Fig. 3.36  Different bacterial morphotypes in biofilm seen under TEM
remains controversial because of the difficulties of obtaining an uncon-
taminated sample. In the majority of chronic periapical lesions, no bacteria
may be found, although bacterial invasion of the periapical tissues is a
common event in acute exacerbation where, for unknown reasons, the
root-canal bacteria overwhelm the local periapical defences.
IMPORTANCE OF MICROBIAL ECOLOGY
AND BIOFILM PHYSIOLOGY IN THE TREATMENT
OF ROOT-CANAL INFECTION
MICROBIAL ECOLOGY
Periapical lesion development is dependent upon the nature of the mixed
infection, the succession of bacterial species within it and its ultimate
 Biological and clinical rationale for root-canal treatment and management of its failure  71

Fig. 3.37  Greater Fig. 3.38  Budding

percentage of filaments yeasts present in
and spirochaetes in the infected root canal
apical than the coronal
parts of the canal

Dentine

Bacterial
biofilm
Dentine
Bacterial
biofilm
PMNs PMN
layer

B
A C

Fig. 3.39  PMNs (a = light microscopy, b = SEM) lining the biofilm on the canal wall and (c) actively phagocytosing the intracanal bacteria

Fig. 3.40  Cocci attached to the filaments giving a Fig. 3.41  Massive apical biofilm filling the entire Fig. 3.42  Apical root resorption with multilayered
corncob appearance circumference of the canal of a tooth associated bacterial plaque embedded in an extracellular
with acute apical periodontitis matrix
 72  Biological and clinical rationale for root-canal treatment and management of its failure

Root

Extraradicular Granulation tissue

biofilm

Dentine Cementum

Fig. 3.43  Extraradicular extension of bacteria Fig. 3.44  Bacterial cells attached to collagen fibres
in dentinal tubules

A B C D

Fig. 3.45  (a) Adequate root filling demonstrated on radiograph; (b) periapical surgery and root resection of the tooth shown in (a) (arrowed) shows stained root
dentine; (c) resected root showing stained/infected dentine (2.82); (d) histological view of the root end shown in (c), showing infected dentinal tubules (S)

Fig. 3.46  Bacteria in
tubule with evidence of
cell division
survival. It is influenced by, as yet, undiscovered ecological factors in the
root-canal system. Studies, have therefore, focused on the nature of bacte-
rial interactions with their environment.
Interactions between microorganisms and their biotic (living) and
abiotic (non-living) surroundings are important in enabling their survival.
The restricted nature of the root-canal microbiota suggests selective pres-
sures. A study of associations between bacteria in root-canal systems by
isolating all cultivable bacteria from a large number of root canals associ-
ated with periapical disease and calculating the likelihood of pairs of
bacteria occurring together has confirmed:

• positive associations between some species: Fusobacterium

nucleatum and Parvimonas micra (formerly Peptostreptococcus
 Biological and clinical rationale for root-canal treatment and management of its failure  73

Fig. 3.47  Presence of bacterial clusters in

the root dentine, slightly coronal to the
periapical area shown in Figure 3.12.
Note part of the apical plaque is visible
peripheral to the cementum (CE) and
clusters of bacteria (BA) existing in
apparently disintegrating dentinal tubules.
Original magnification ×5300; inset
×12 800 (from Nair, 1987)

Sample fixation, resin

embedding & sectioning

Hybridization

Probe
Fluorescent dye
Ribosomes

Target (16SrRNA)
Fluorescently labelled
oligonucleotides (probes) Washing & Drying

Visualization with CLSM

Fig. 3.48  Schematic digram showing in situ hybridization procedures for bacterial identification (courtesy of Athena Iacovidou & Morgana Vianna)

micros); Porphyromonas endodontalis, Selenomonas sputigena and
Wolinella recta; Prevotella intermedia and Parvimonas micra;
Peptostreptococcus anaerobius and Eubacterium species
• negative associations between other species: Propionibacterium
propionicum, Capnocytophaga ochracea and Veillonella
parvula.
The positive and negative associations are thought to be due to nutri-
tional interactions (Fig. 3.53), local physiological conditions (Eh, pH),
bacteriocins and bacterial coaggregation or physical attraction and binding.
Microbial interactions within communities enable them to evolve,
depending on the local environmental variations, thus supragingival and
subgingival plaque only a few millimetres apart develop vastly differently
 74  Biological and clinical rationale for root-canal treatment and management of its failure

Dentine

Biofilm

Canal lumen

Fig. 3.49  Gold labelling of Prevotella cell surface Fig. 3.50  Gold labelling of Fusbacterium Fig. 3.51  Fluorescent in situ hybridization (FISH) of
antigens 16SrRNA using rRNA probes universal bacterial 16S rRNA probes

Fusobacterium
Capnocyto-
eubacterium Strepto-
phaga
prevotella coccus Veillonella
Eikenella
peptostrepto- actinomyces
corrodens
coccus

NH4 lactate
Necrotic
tissue succinate CO2
formate menadione

haemin H2
acetate

Spirochaetes Porphyromonas endodontalis Campylobacter Eubacterium

Porphyromonas gingivalis wolinella alactolyticum
Prevotella intermedius Bacteroides gracitis
PMN

Fig. 3.53  Nutritional interactions between some common root canal pathogens

ends when a relatively stable assembly of populations, called a climax

Fig. 3.52  FISH labelling of spirochaetes, showing a classical ecological scenario
depending on their salivary and serum nutritional sources, respectively. A
similar model is proposed for the root-canal microbiota: coronal leakage
may allow salivary ingress and facultative organisms to grow in the coronal
part of the canal, whereas serum from the apical part of the canal may
favour the growth of proteolytic bacteria at the root apex. Evidence for
this may be the patterns of bacterial growth in root canals described earlier.
The root-canal environment has a unique natural history in terms of a
nutritional source in the human body, though it has not been characterized
adequately in its necrotic, infected state from an ecological point of view.
It begins with a very rich supply of vital tissue during the stages of pulpal
inflammation but once it becomes necrotized, the nutritional supply is
rapidly exhausted as the environment is secluded by the dentine shell. The
key fluid nutritional sources such as saliva, serum, blood, inflammatory
exudate may become limited. Where even minimal nutritional streams are
available in the form of saliva leakage coronally and inflammatory exudate
apically, bacterial communities may become established. As the initial
habitat is altered by the primary colonizers, secondary invaders join and
may replace them. According to classical ecological theory, succession
community, is achieved. This concept has been difficult to apply to micro-
bial communities in the general environment as random disturbances
prevent the community from ever reaching equilibrium, although this
may well be achieved in the secluded root-canal environment in chronic
cases. In the later stages of an enclosed root-canal infection, therefore the
bacteria presumably enter some sort of a starvation or dormant phase,
although this aspect has not specifically been investigated in root-canal
sites. If dormancy does play a significant part, then it may help contribute
to the chronic nature of periapical disease. The overall ecological picture
is one of a complex polymicrobial community that may function as one
in response to its environment and presumably to treatment as well.
In contrast to restricted microbiota in enclosed root-canal systems with
minimal diversity, it is also possible to encounter teeth with wide microbial
diversity with evidence of suppuration. In such teeth, it is possible to see
the presence of PMNs in the canal system, lining the bacterial biofilm (see
Fig. 3.39a,b) and, indeed, attempting to phagocytose the cells (see Fig.
3.39c). The extravascular life span of such cells is only 2–3 days, therefore
impying a very dynamic and nutritionally rich environment in stark con-
trast to the above view.
The interdependence of different bacterial species and with their envi-
ronment must be the key to the success of root-canal treatment. The
 Biological and clinical rationale for root-canal treatment and management of its failure  75

treatment procedures (mechanical and chemical) essentially interfere with Growth and reproduction rates, as well as metabolic rates, may vary
the environment, killing some bacteria and, by a domino effect, indirectly within a biofilm depending upon its composition and activity. Local varia-
killing other species by altering the nutritional, physiological and toxic tions in such aspects can result in concentration and electrostatic gradients.
balance. The surviving bacteria are usually those physiologically “hardy” As cells reproduce, the colonies change shape and develop into stacks, the
enough to resist changes in the environment induced by the treatment and size and extent of which are controlled; water channels between the stacks
capable of living independently of other species in the unique nutrition- serve as a primitive circulatory system to transmit messaging molecules.
depleted conditions. That is, the organisms are “hardy” because of their Some cells develop slow metabolism and take on the role of persisters,
capacity to adapt. This means that a poor first attempt at root-canal treat- others may become detached from the biofilm and may become transiently
ment may result in a more recalcitrant infection to eradicate at the next planktonic to achieve dissemination. In this way, a highly specialized and
attempt. It is, therefore biologically most sensible to launch the most cooperative community develops, akin to a multicellular organism, capable
comprehensive effort at eradicating the infection at the first attempt. of sensing its environment and responding to changes within it.
The size, shape and composition of the colonies are variable and depend-
BIOFILM AND PLANKTONIC PHYSIOLOGY ent on the physiological activity of the community. They are partly dictated
by the relative proportion of extracellular matrix (ECM), the composition
Aggregations of microorganisms in communities at surface interfaces, of which is generally described as polysaccharide but varies according to
exhibiting well-defined structures, organization and cooperation, division the nutrition available, as well as its function. The ECM is a store-house
of labour, succession and specialized survival strategies have become
known as biofilms. Bacterial cells can live a nomadic existence, drifting
for finding nutrition and suitable environments for growth, reproduction Plasma
membrane Cell wall
and survival (Fig. 3.54); this is known as a planktonic existence. The same
Ribosomes Capsule
species may also live a sedentary existence by locating a suitable environ-
Plasmid
ment, in which nutrition is plentiful and safety is assured for growth,
Pilli
reproduction and survival; such an existence is known as a biofilm exist-
ence (Fig. 3.55). The latter existence is difficult to find, particularly for
single species, but may be engineered by cooperation between multiple
species with collective properties enabling a more effective and efficient
utilization of available resources. Such cooperation leads to the formation
of the most primitive, yet in its own way a sophisticated community. As
in any community, such cooperation requires communication, which
occurs in the form of chemical messaging, known as quorum sensing. The
messaging molecules are released into the environment by multiple cells,
if a sufficient amount of the messaging molecule is produced, a critical
threshold is exceeded to trigger a variety of changes and events. This
Bacterial flagellum
includes the switching on and off of key genes to facilitate growth, repro-
duction, secretion of and control of the nature of the extracellular matrix, Cytoplasm
expression of virulence genes, etc. The same species may be planktonic Nucleoid material (circular DNA)
or biofilm producing; simply as a function of the genes expressed despite
the relatively simple genomes they possess. Fig. 3.54  Schematic diagram of a planktonic bacterium

Stage 1 Stage 2 Stage 3 Stage 4 Stage 5

Stage 1 - Initial attachment:

Stage 2 - Irreversible attachment:
Stage 3 - Maturation I:
Stage 4 - Maturation II:
Stage 5 - Dispersion:

Dentine

Tubules

Fig. 3.55  Schematic diagram of the classical five stages of biofilm formation
 76  Biological and clinical rationale for root-canal treatment and management of its failure
or “junk-yard” for excreted molecules, including DNA, which forms an
important element of it. The relative proportion of cell to ECM varies
according to physiological activity and nutritional availability and can
range between 30% and 70%.
The first reliable, in situ, observation of the root-canal microbiota that
revealed both attached biofilms and planktonic bacteria suspended in fluid,
came from Nair as late as 1987. Since then other evidence has emerged.
It is not known whether the “suspended” bacteria were in fact suspended
in fluid or matrix-embedded. If suspended, it was not clear if they had
simply been shed from the root-canal surface or were growing independ-
ently. The relative distribution of biofilm and planktonic phenotypes in the
root-canal system is not yet known but these may dictate the properties of
the infection, in particular those that allow biofilm persistence after treat-
ment. The concept of the root-canal microbiota as a biofilm is a relatively
recent one in the endodontic literature, although it was described in the
second edition of this book in 1994.
Root-canal infection then is essentially a bacterial biofilm coating the
dentine surface, including the tubules to variable depths and extending to
the apical foramina and sometimes beyond. The biofilm is usually patchy
and discontinuous (see Figs 3.31–3.35); different populations of bacteria
may communicate with each other through fluid films or fluid columns by
the medium of molecular messengers. Individual cells within this coopera-
tive may respond to their immediate surroundings and neighbours by
switching on or off relevant genes for survival. Nutrition depletion may
slow their metabolism and allow some to enter a dormant state. This may
also make them uncultivable if sampled. The bacterial population may,
therefore be diverse in terms of species and phenotypes (both biofilm and
planktonic). This inter-reliance of the bacterial species is both therapeuti-
cally useful, as well as potentially problematic.
The relative mount and composition of ECM in biofilms within
root-canal systems are currently unknown. It is, however, important to
determine this property because it would play a major role in biofilm
eradication.
Given the complexity of the root-canal anatomy, it is highly unlikely
that bacterial killing agents would reach all aspects of the root-canal
system and biofilm in adequate concentration. Reliance is placed on using
adequate concentrations of antibacterial agents so that sufficient dosage is
achieved along a diffusion gradient to effect killing or an ecological shift.
It is probably because of the inter-reliance and inter-dependence among
bacteria that the more fastidious species are killed in a chain sequence akin
to a domino effect because of deprivation of their nutrients and stimulants
(such as quorum sensing) from their neighbouring partner species. Root-
canal treatment, therefore probably works by a combination of direct and
indirect killing effects. The importance of indirect killing is probably
underestimated in modern endodontics and is why knowledge of biofilm
physiology may be therapeutically advantageous.
Conversely, biofilm existence also confers a range of defensive survival
strategies. If a sufficiently effective attempt is not made to eradicate the
biofilm, then its innate tendency would be to detect the changes and adapt
to launch events to facilitate survival. Recognition that root-canal infection
is an “intelligent”, multicellular-organism-like biofilm, is important in
devising strategies for treatment because bacteria in biofilms are more
resistant to killing. This is because:
• the exopolysaccharide in which the bacteria are embedded may
restrict diffusion of the antibacterial agents to the cells
• different layers of cells may similarly act as barriers to diffusion
• slower-growing bacterial cells, persister cells, metabolically
inactive cells or dormant cells are more resistant to killing
• cells may exhibit specific resistance mechanisms
• biofilm phenotypes may be inherently more resistant.
Effective treatment techniques should recognize these problems and be
sufficiently efficacious at the first attempt (visit) to prevent the infection
from becoming dominated by the surviving, more resistant strains.
PREVENTION AND TREATMENT OF PERIAPICAL DISEASE
BIOLOGICAL AND CLINICAL PERSPECTIVE
ON A TECHNICALLY DRIVEN
CHEMOMECHANICAL PROCEDURE
Based on the fact that periapical lesions develop as a result of the interac-
tion between bacteria (and their products) and the host defences, it is clear
that their prevention or resolution depends upon preventing or terminating
this interaction.
Prevention of apical periodontitits applies to the clinical situation where
it is judged that the pulp is irreversibly inflamed to the point that vital pulp
therapy would not resolve the problem and requires pulpectomy. By defini-
tion, apical periodontitis has not yet become established implying an
absence of bacterial colonization of the apical root-canal anatomy and the
probable presence of vital, healthy pulp tissue. The purpose of the chemo-
mechanical treatment then would be to extirpate the pulp and prevent
infection becoming established as the natural defence system of the pulp
is sacrificed. The implication is that the procedure demands asepsis as
a prime requirement. The technical aspects of the protocol may not be
so important and are focused principally on removal of the pulp tissue
(Fig. 3.56). This is validated by the fact that the success rates (judged
by conventional radiography) are high (90–99%) regardless of protocol
(Fig. 3.57a).
Once the periapical lesion has become established, variation in the
technical delivery of the chemomechanical protocol makes a greater
impact (see Fig. 3.57b). Overall, the challenge is a different one because
the purpose now is not merely to prevent infection but to remove the bacte-
rial biofilm and effect a switching-off of the host response. The challenge
seems to be greater still if the periapical lesion is larger as it is associated
with a more diverse infection. A number of approaches have been used to
achieve this general aim.
The healing process after root-canal treatment has not been deeply
researched but can be conceptualized using “Fish’s zones” (see Fig. 3.8)
in a chronic inflammatory lesion. The removal of bacteria and their prod-
ucts should result in the reduction, if not (ideally) elimination of the zones
of infection and contamination. This allows the macrophages in the zone
of irritation to invade the areas previously occupied by the zones of infec-
tion and contamination in order to remove dead cells and debris. This
process also makes way for the osteoblasts and fibroblasts, together with
new in-growing blood vessels and nerve fibres from the outermost and
active zone of stimulation to proliferate into the zone of irritation. In this
way, gradual healing takes place from the boundary of the lesion inwards
until a normal periodontal ligament is established. Provided that the
pluripotential cells in the periodontal tissues, in particular, have not been
irreversibly damaged, ideal healing would eventually result in regeneration
and the formation of cementum over the apical terminus, isolating the
root-canal system completely from the periapex (Fig. 3.58) but this is not
an inevitable end result. Incomplete removal of the infection would reduce
but not eliminate the inflammatory area and, in fact, this is generally the
case (Fig. 3.59). This implies that residual infection in the apical anatomy
is the norm following completion of root-canal treatment and that an
ongoing interaction beyond the end of treatment, between the residual
infection, root filling material and host defences plays a definitive role in
determining the final outcome. This explains several clinical observations
about periapical healing outcomes. It explains why, despite variations and
changes in the technical aspects of the chemomechanical protocol, the
 Biological and clinical rationale for root-canal treatment and management of its failure  77

Fig. 3.56  Extirpation of vital pulp tissue

Isthmus Dentine
Pulp tissue tags
in the isthmus and surface Pulp
on canal walls tissue

Rarely observed
odontoblastic
processes
being pulled out
of their tubules
Residual pulp
tissue apically

Virtually intact
Residual pulp tissue
extirpated pulp tissue
partially torn apically

Adenubi & Rule (1976)

Heling & Shapira (1978)
Jokinen et al. (1978)
Halse & Molven (1987)
Safavi et al. (1987)
Akerblom & Hasselgren (1988)
Sjogren et al. (1990)
Peak (1994)
Peretz et al. (1997)
Lilly et al. (1998)
Cheung (2002)
Hoskinson et al. (2002)
Chugal et al. (2003)
Chu et al. (2005)
Moshonov et al. (2005)
Aqrabawi (2006)
Doyle et al. (2006)
Gesi et al. (2006)
Conner et al. (2007)
Chevigny et al. (2008)
Liang et al. (2011)
Ng et al. (2011)
Ricucci et al. (2011)
Liang et al. (2012)

Combined

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1

A Probability of success for primary root canal treatment on teeth with vital pulp

Fig. 3.57  Forest plots showing (a) pooled and individual studies’ (1976–2012) probability of periapical healing following primary root-canal treatment in vital
teeth based on strict criteria;
 78  Biological and clinical rationale for root-canal treatment and management of its failure

Auerbach (1938)
Buchbinder (1941)
Castagnola & Orlay (1952)
Heling & Tamshe (1970)
Cvek (1972)
Werts (1975)
Adenubi & Rule (1976)
Heling & Shapira (1978)
Jokinen et al. (1978)
Barbakow et al. (1980)
Cvek et al. (1982)
Boggia (1983)
Pekruhn (1986)
Bystrom et al. (1987)
Halse & Molven (1987)
Safavi et al. (1987)
Akerblom & Hasselgren (1988)
Sjogren et al. (1990)
Murphy et al. (1991)
Friedman et al. (1995)
Calisken & Sen (1996)
Peretz et al. (1997)
Sjogren et al. (1997)
Lilly et al. (1998)
Weiger et al. (2000)
Cheung (2001)
Hoskinson et al. (2002)
Peters & Wesselink (2002)
Chugal et al. (2003)
Huumonen et al. (2003)
Khedmat (2004)
Chu et al. (2005)
Aqrabawi (2006)
Doyle et al. (2006)
Conner et al. (2007)
Molander et al. (2007)
Sari & Duruturk (2007)
Chevigny et al. (2008)
Cotton et al. (2008)
Penesis et al. (2008)
Siqueira et al. (2008)
Hsiao et al. (2009)
Mente et al. (2009)
Tervit et al. (2009)
Ng et al. (2011)
Ricucci et al. (2011)
Liang et al. (2012)

Combined

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1

B Probability of success of primary root canal treatment of teeth with non-vital pulp and periapical

Fig. 3.57  Continued (b) pooled and individual studies’ (1938–2012) probability of periapical healing following primary root canal treatment in non-vital teeth
with periapical radiolucency based on strict criteria

Fig. 3.58  Low-power view of healing
by cementum formation when
Sealapex is used. (Black particles are
residual Sealapex and root filling
material) (courtesy of Prof. M Tagger)
success rates of root-canal treatment have not improved over the last
century (Fig. 3.60). It explains why the success rates are so sensitive to
the apical length of root-canal debridement (Fig. 3.61). It further explains
why the periapical lesion can take so long to heal after termination of the
treatment procedure (Fig. 3.62).

TECHNICAL ASPECTS OF THE

CHEMOMECHANICAL PROCEDURE
Periapical disease is managed by root-canal treatment, which may be
defined as a series of steps (mechanical and chemical), the efficacy of each
sequential step dependent on that of the previous step. It consists of the
following sequential steps performed under aseptic conditions:

• access to the pulp chamber through the crown of the tooth (coronal
access)
• location of all canal orifi in the pulp chamber floor
 Biological and clinical rationale for root-canal treatment and management of its failure  79
14/16 (88%) root apices
contained evidence of
residual bacteria/bacterial
biofilm
Fig. 3.59  Residual bacterial biofilm present in the apical portion of root canals following root-canal treatment (Nair et al., 2005)
• obtaining access to all apical canal termini by sensitive negotiation
of the canals
• determining the length of the instrument path to the canal
termini
• maintaining access to all canal termini while also maintaining the
canals centred in the root as they are progressively shaped to a
regular taper (radicular access) to facilitate delivery of the
antibacterial irrigant and ultimately the root filling material to the
entire root-canal system
• chemical treatment of the entire root-canal system surface
and space to facilitate removal of the bacterial biofilm and
residual pulp tissue (a process dominated by control of fluid
dynamics)
• continued chemical treatment to control residual bacterial biofilm
between visits (the coronal access is sealed and the tooth left for a
period of at least a week)
• re-entry to the root-canal system at the next visit to assess
response to debridement (signs, symptoms, intraradicular
Nair PN, Henry S, Cano V et al (2005)
Microbial status of apical root canal
system of human mandibular first molars
with primary apical periodontitis after
‘one-visit’ endodontic treatment.
Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 99, 231–52
observation, culture test/bacterial presence test outcome) and
facilitate decision on need for further debridement or obturation
• in the presence of continued signs and symptoms or positive
culture test/bacterial presence test, the root-canal system is
reassessed to evaluate whether some part of the anatomy has been
missed; the chemomechanical step is repeated
• in the absence of signs and symptoms and a negative culture
test/bacterial presence test, the root-canal system is filled to the
canal termini (obturation).
The stages prior to root filling are usually sufficient to achieve periapical
healing (Fig. 3.63). The purpose of root filling is said to be to fill the root-
canal system with an inert material (usually gutta-percha and a sealer) to
seal off the periapical tissues from the canal system and, in turn, from the
oral environment. It also helps incarcerate residual infection in the root-
canal system. The permanent access cavity restoration or the permanent
tooth restoration provides the definitive coronal seal preventing reinfection
of the root-canal system.
 80  Biological and clinical rationale for root-canal treatment and management of its failure

Buchbinder (1941) Grahnen & Hansen (1961)

Castagnola & Orlay (1952) Engstrom & Lundberg (1965)

Combined Combined

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1
Probability of success - strict (studies published before 1960) Probability of success - strict (studies published in the 1960s)

Harty et al. (1970) Barbakow et al. (1980)

Heling & Tamshe (1970) Cvek et al. (1982)
Cvek (1972) Boggia (1983)
Werts (1975) Klevant & Eggink (1983)
Adenubi & Rule (1976) Pekruhn (1986)
Heling & Shapira (1978) Bystrom et al. (1987)
Jokinen et al. (1978) Halse & Molven (1987)
Kerekes (1978) Safaviet al. (1987)
Kerekes (1978) Akerblom & Hasselgren (1988)

Combined Combined

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1
Probability of success - strict (studies published in the 1970s) Probability of success - strict (studies published in the 1980s)

Ricucci et al. (2000)

Weiger et al. (2000)
Chugal et al. (2001)
Peak et al. (2001)
Benenati & Khajotia (2002)
Sjogren et al. (1990) Cheung (2002)
Murphy et al. (1991) Hoskinson et al. (2002)
Peters & Wesselink (2002)
Ried et al. (1992) Chugal et al. (2003)
Field et al. (2004)
Cvek (1992) Chu et al. (2005)
Moshonov et al. (2005)
Peak (1994) Aqrabawi (2006)
Calisken & Sen (1996) Conner et al. (2007)
Molander et al. (2007)
Peretz et al. (1997) Sari & Duruturk (2007)
Chevigny et al. (2008)
Sjogren et al. (1997) Cotton et al. (2008)
Penesis et al. (2008)
Lilly et al. (1998) Witherspoon et al. (2008)
Ng et al. (2011)
Combined Combined

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1
Probability of success - strict (studies published in the 1990s) Probability of success - strict (studies published in the 2000s)

Fig. 3.60  Forest plots showing pooled and individual studies’ probability of periapical healing following primary root-canal treatment based on strict criteria by
decades of publication

The culture test during root-canal treatment has fallen out of favour in
contemporary practice for a variety of reasons. The issue, though, remains
controversial and there are some who still practise it. The outcome meas-
ures at the end of root-canal treatment are absence of clinical signs and
symptoms of persistent periapical disease and, curiously in the mind of
the practitioner, the radiographic appearance of the root filling (its shape
and homogeneity). The definitive outcome measure (in conjunction with
absence of signs and symptoms), however, is periapical healing, since the
treatment is aimed at resolution of the periapical disease (Fig. 3.64).
Although the majority of periapical lesions heal within one year, healing
can take anything up to 4 years or longer (see Fig. 3.62) as measured by
sequential conventional radiographs, which follow the diminution in the
size of the periapical radiolucency until normal architecture is restored.
The use of cone-beam computed tomography (CBCT), which may be more
sensitive to detection of periapical healing, may give healing rates and
durations that are longer but would not alter the factors affecting treatment
outcome.
EFFECT OF CHEMOMECHANICAL AND OBTURATION
PROCEDURES ON BIOLOGICAL EVENTS
Numerous studies have evaluated the effect of different stages of root-
canal treatment on the intraradicular bacterial flora, both qualitatively and
quantitatively. Some studies merely report positive culture tests whereas
others have identified and quantified intraradicular bacteria before and
after various stages of treatment.
 Biological and clinical rationale for root-canal treatment and management of its failure  81
Harty el al. (1970)
Heling & Tamshe (1970)
Adenubi & Rule (1976)
Heling & Shapira (1978)
Jokinen et al. (1978)
Kerekes (1978)
Kerekes (1978)
Heling & Kischinovsky (1979)
Barbakow et al. (1980)
Klevant & Eggink (1983)
Halse & Molven (1987)
Peak (1994)
Hoskinson et al. (2002)
Aqrabawi (2006)
Doyle et al. (2006)
Liang et al. (2011)
Ng et al. (2011)
Ricucci et al. (2011)
Combined
0 0.1
Harty el al. (1970)
Heling & Tamshe (1970)
Adenubi & Rule (1976)
Heling & Shapira (1978)
Jokinen et al. (1978)
Kerekes (1978)
Kerekes (1978)
Heling & Kischinovsky (1979)
Barbakow et al. (1980)
Klevant & Eggink (1983)
Halse & Molven (1987)
Peak (1994)
Hoskinson et al. (2002)
Aqrabawi (2006)
Doyle et al. (2006)
Liang et al. (2011)
Ng et al. (2011)
Ricucci et al. (2011)
Combined
0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9
Root fillings extending more than 2 mm from the radiographic apex
Harty el al. (1970)
Heling & Tamshe (1970)
Adenubi & Rule (1976)
Heling & Shapira (1978)
Jokinen et al. (1978)
Kerekes (1978)
Kerekes (1978)
Heling & Kischinovsky (1979)
Barbakow et al. (1980)
Boggia (1983)
Klevant & Eggink (1983)
Halse & Molven (1987)
Sjogren et al. (1990)
Cvek (1992)
Peak (1994)
Hoskinson et al. (2002)
Aqrabawi (2006)
Doyle et al. (2006)
Liang et al. (2011)
Ng et al. (2011)
Ricucci et al. (2011)
Combined
0 0.1
Root fillings extending beyond the radiographic apex
Fig. 3.61  Forest plots showing pooled and individual studies’ probability of
periapical healing following primary root-canal treatment based on strict
criteria by apical extent of root fillings
0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9
Root fillings within 2 mm from radiographic apex
0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9
The effect of the steps up to and including the “mechanical preparation”
of the canal(s) on the microbiota has been tested using only water or saline
as the irrigant. Taken collectively, the studies show that negative cultures
were achieved on average in 25% of the cases (range 4.6–53%). When
sodium hypochlorite (concentration range 0.5–5.0%) irrigation supple-
mented the steps up to “mechanical preparation”, the frequency of negative
cultures immediately after debridement increased to an average of 75%
(range 25–98%).
Most studies report culture reversals during the interappointment period
when active antibacterial dressing is not used in the root-canal system
between appointments. The reversals are due to regrowth of residual bac-
teria or recontamination by bacterial leakage around the access cavity
dressing.
Classical and well-controlled studies (Sundqvist’s group) evaluated the
effect of various root-canal treatment procedures on the microbiota both
qualitatively and quantitatively. They tested the effect of mechanical prep-
aration, saline or sodium hypochlorite irrigation (0.5%, 5.0%, 5.0% with
1 EDTA), the addition of ultrasonic activation to the irrigation and calcium
hydroxide dressing; each addition to the chemical canal preparation
improved the antibacterial effect, reducing residual bacteria further. They
found the antibacterial action to reduce the number of bacteria from an
initial range of 102–108 cells to 102–103 fewer cells after initial debride-
ment, further reducing down to no recoverable cells (from the prepared
part of the root-canal system) after interappointment dressing with calcium
hydroxide. It was notable that the infection was more difficult to control
when the diversity of the initial infection was greater, i.e. there were more
species in greater abundance. Calcium hydroxide dressing is also effective
after mechanical preparation and irrigation with water. The efficacy of
dressing with calcium hydroxide has recently become controversial
because of emerging studies showing limited efficacy.
The collective antibacterial action during root-canal treatment has
not been shown to cause persistence of any particular species. Specific
bacteria, therefore, were not implicated in persistent infections during
primary (first attempt) root-canal treatment. In contrast, data from
secondary (second attempt) root-canal treatment showed that certain
species were more prevalent after biomechanical procedures than others
1 suggesting that they may be more resistant to treatment protocols, contrary
to the previous view. The persistent species were Enterococcus faecalis,
Streptococcus species, Staphylococcus species, Lactobacillus species, Pro-
pionibacterium species, Actinomyces species, yeasts, other Gram-positive
bacteria.
Even though most longitudinal studies of the root-canal microbiota do
not definitively show resistance of particular species, other studies suggest
that Gram-positive bacteria are found with an unexpectedly high frequency
in post-treatment cultures. In further monkey-model experiments from
Moller’s group, facultative bacteria were found to be more resistant to
chemomechanical treatment than anaerobic species from a 4-strain infec-
tion (Streptococcus milleri, Peptostreptococcus anaerobius, Prevotella
oralis, Fusobacterium nucleatum). In addition, the survival rate of a
5-strain infection including Enterococcus faecalis was higher.
The role of the root filling appears to be a subsidiary one in helping to
control residual infection, since absence of a root filling makes no apparent
difference to the healing (see Fig. 3.63). Obturation of infected but already
prepared canals resulted in some degree of effect in controlling the remain-
ing infection, presumably by incarcerating it.
1
EFFECT OF PERSISTENT BACTERIA ON ROOT-CANAL
TREATMENT OUTCOME
A preobturation negative culture result can increase treatment success by
an average of 12% (range 0–26%). A mixture of many factors led to the
 82  Biological and clinical rationale for root-canal treatment and management of its failure

Adenubi & Rule (1976)

Adenubi & Rule (1976)
Heling & Shapira (1978)

Benenati & Khajotia (2002)

Chu et al. (2005)

Sari & Duruturk (2007) Sari & Duruturk (2007)

Siqueira et al. (2008)

Combined Combined

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1
6 months 36 months

Engstrom & Lundberg (1965)

Grahnen & Hansen (1961)
Adenubi & Rule (1976)
Pekruhn (1986) Engstrom & Lundberg (1965)
Murphy et al. (1991) Adenubi & Rule (1976)
Trope et al. (1999)
Cvek et al. (1982)
Huumonen et al. (2003)
Doyle et al. (2006) Cvek (1992)

Sari & Duruturk (2007) Chugal et al. (2003)

Penesis et al. (2008) Sari & Duruturk (2007)
Siqueira et al. (2008)

Combined Combined

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1
12 months 48 months

Harty el al. (1970) Werts (1975)

Adenubi & Rule (1976)
Adenubi & Rule (1976)
Heling & Shapira (1978)
Klevant & Eggink (1983)
Ried et al. (1992)
Molander et al. (2007) Peak (1994)
Sari & Duruturk (2007) Sjogren et al. (1997)
Cotton et al. (2008) Benenati & Khajotia (2002)
Siqueira et al. (2008) Peters & Wesselink (2002)
Aqrabawi (2006)
Liang et al. (2011)
Chevigny et al. (2008)
Liang et al. (2012)
Ricucci et al. (2011)

Combined Combined

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1
24 months 29+ months

Fig. 3.62  Forest plots showing pooled and individual studies’ probability of periapical healing following primary root-canal treatment in non-vital teeth with
periapical radiolucency based on strict criteria by duration following treatment completion

A B A B

Fig. 3.63  (a,b) Periapical healing by cleaning Fig. 3.64  (a,b) Delayed healing caused by extruded filling material from the
alone distobuccal canal of a maxillary second molar (arrowed)
 Biological and clinical rationale for root-canal treatment and management of its failure  83
gradual abandoning of the culture test in clinical practice. One criticism
was that numerous factors could potentially account for treatment outcome
but were not all considered in these studies. One large study (Seltzer et al.,
1963) in particular contributed to the demise of the culture test but even
their study showed a 10% difference in success in favour of the negative
culture test when periapical disease was present. The outcome is even
worse when a positive culture test result combines with the presence of a
periapical lesion.
The bacteria in preobturation cultures include Enterococcus, Streptococ-
cus, Staphylococcus, Lactobacillus, Veillonella, Pseudomonas, Fusobac-
terium species and yeasts. Some studies have found no relationship
between individual species and treatment failure but others have. While
the overall failure rate for cases with positive cultures was 31%, that for
teeth with Enterococcus species was 55% and for teeth with Streptococcus
species was 90% (Frostell, 1963); in another study, good quality root-canal
treatment on 54 teeth with asymptomatic periapical disease gave an overall
success rate of 74%, but teeth with Enterococcus faecalis had a success
rate of 66% (Sundqvist et al., 1998). These associations cannot be regarded
as cause–effect and a relationship should also be sought between numbers
of bacteria and treatment outcome. The success rate for teeth with no
bacteria was 80% while that for teeth with bacteria in the canal before
obturation was 33%.
A more recent monkey-model study (Fabricius et al., 2006) used the
same 4- or 5-strain infection model to test the effect of debridement
and obturation procedures on outcome. When bacteria remained after
chemomechanical debridement, 79% of the root canals were associated
with non-healed periapical lesions, compared with 28% when no
bacteria were found to remain. Combinations of several residual bacterial
species were more frequently related to non-healed lesions than were
single strains. When no bacteria remained at the end of chemomechanical
debridement, healing occurred independently of the quality of the
root filling. In contrast, when bacteria remained, there was a greater
correlation with non-healing in poor-quality root fillings than in techni-
cally well-performed fillings. In root canals where bacteria were found
after removal of the root filling, 97% had not healed, compared with
18% for those root canals with no bacteria detected upon removal
of root filling. The study emphasizes the importance of reducing bacteria
below detection limits before permanent root filling in order to achieve
optimal healing conditions for the periapical tissues. It also reinforces the
view that obturation does indeed play a role when there is residual
infection.
Regardless of the technique for obtaining a culture, the use of a
negative culture test results to inform progress of treatment has a
positive impact on treatment outcome. The association of specific species
with treatment failure is not well established but the identity of the small
group of species isolated from positive cultures is relatively constant and
may hold answers to treatment resistance and failure. It is, however,
important to account for the other factors that influence root-canal treat-
ment outcome.
FACTORS AFFECTING OUTCOME
OF ROOT-CANAL TREATMENT
Clinical judgement of the outcome of treatment is based on the absence
of signs of infection and inflammation, such as pain, tenderness to percus-
sion of the tooth, tenderness to palpation of the related soft tissues, absence
of swelling and sinus and radiographic demonstration of healing of the
periapical lesion (if sufficient time has lapsed), with a completely normal
periodontal ligament space.
Absence of signs and symptoms of periapical disease but a persistence
of a periapical radiographic radiolucency may indicate either healing by
Fig. 3.65  Fibrous
healing (histological
view)
repair with fibrosis (Fig. 3.65) or persistent chronic inflammation. Only
time and acute exacerbation will identify the latter, whereas the former
should remain asymptomatic.
A systematic review and meta-analysis of the factors affecting root-
canal treatment outcome revealed the following: the mean success rate is
83% when a vital pulpectomy is carried out as there is no established
infection; this reduces to 72% when the root-canal treatment procedure is
aimed at eradicating an established infection associated with a periapical
lesion.
The factors having a major impact on root-canal treatment outcome
were:
• presence and size of periapical lesion
• apical extent of root-canal treatment in relation to radiographic
apex
• outcome of culture test
• quality of root-canal treatment judged by radiographic appearance
of root filling
• quality of the final coronal restoration.
The factors having minimal effect on root-canal treatment outcome
were:
• age of patient
• gender of patient
• general health of patient
• treatment technique (preparation, irrigation and obturation material
and technique) other than length control.
The improvements in techniques of mechanical and chemical canal
preparation have not resulted in increases in success rates over the last
century (see Fig. 3.60).
It is notable that all the factors having a strong influence on
treatment outcome are associated in some way with root-canal infection.
Further improvements in root-canal treatment outcomes may, therefore
be obtained by understanding the nature of the root-canal infection (espe-
cially apical) and the manner in which the microbiota is altered by
treatment.
CAUSES OF ROOT-CANAL TREATMENT FAILURE
When guideline standard root-canal treatment is performed, the failure rate
is 10–20%. When the treatment is technically substandard, as described
for a high proportion of root-canal treatments performed in general prac-
tice across the world (Fig. 3.66), the success rates are lower.
The causes of root-canal treatment failure may be summarized as
follows:
Microbial (persistent periapical inflammation)
• intraradicular (persistent or new infection)
• extraradicular (pre-existing or precipitated by treatment)
 84  Biological and clinical rationale for root-canal treatment and management of its failure

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Fig. 3.66  Prevalence of root-treated teeth associated with periapical radiolucency

Non-microbial (persistent periapical inflammation/pathosis or new
inflammation/pathosis)
• true cyst
• foreign body reaction to: cholesterol crystals, extruded dentine
chips, extruded calcium hydroxide, extruded sealer, extruded
gutta-percha filling material, extruded amalgam, or extruded
cellulose components from paper points, cotton wool, or pulses
INTRARADICULAR MICROBIOTA ASSOCIATED WITH
FAILED ROOT-CANAL TREATMENT
Microbial species recovered from root-treated teeth with persistent periapi-
cal disease are presented in Table 3.5, which shows a different spectrum
compared to that in untreated teeth. The microbiota is dominated by Gram-
positive bacteria (Fig. 3.67), many of which are coccoid facultative anaer-
obes. The retrieval of bacterial samples from obturated root-canal systems
is compromised by the need to remove root-filling material first, which
may kill the bacteria present. The most frequently identified species are
Enterococcus faecalis, Propionibacterium species, Streptococcus species,
Lactobacillus species, Peptostreptococcus species, and yeasts.
The species recovered from root-treated teeth reside in accessory canals
(see Fig. 3.22), in dentinal tubules (see Fig. 3.47) or in the main canal
alongside the root filling (see Fig. 3.24). They are a subset of those found
in untreated teeth though the diversity and quantity is reduced. Unlike
untreated teeth, treated teeth appear to contain few mixed cultures, often
only three, two or one cultivable species are found with a mean of only
1.7 species per tooth. Teeth with poor root fillings have the highest bacte-
rial counts (103–105) with a maximum of 3–6 cultivable species per canal
and a diversity that resembles that of untreated teeth, perhaps reflecting
poor treatment technique. Enterococcus faecalis is the commonest species
and, when it is present in small numbers in the primary infection, it is
easily eliminated, but if it infects in large numbers it is difficult to
eradicate.
Although specific bacterial species have not been implicated as being
resistant to treatment in longitudinal studies, the presence of specific
groups of bacteria in root-treated teeth suggests that other than being
survivors from the pre-existing infection they may be contaminants intro-
duced during treatment. This may be due to:
• inadequate tooth isolation
• poor asepsis
• leakage of the access dressing
• access cavity being left open for drainage.
EXTRARADICULAR MICROBIOTA ASSOCIATED WITH
FAILED ROOT-CANAL TREATMENT
Obtaining a sample from the periapical tissues without contamination is
notoriously difficult. Approaches include either sampling through the root
 Biological and clinical rationale for root-canal treatment and management of its failure  85

Table 3.5  Representative taxa in treated teeth with persistent apical periodontitis (courtesy of Morgana Vianna)

Firmicutes Actinobacteria Fusobacteria

Acidaminococcus Actinomyces naeslundii Fusobacterium spp.
Bacillus megaterium Actinomyces odontolyticus Leptotrichia spp.
Enterococcus faecalis Actinomyces radicidentis
Enterococcus faecium Actinomyces viscosus
Eubacterium lentum Brachybacterium spp.
Eubacterium limosum Corynebacterium diphtheriae
Eubacterium spp. Dietzia maris
Finegoldia magna Micrococcus luteus
Gemella morbillorum Propionibacterium spp.
Lactobacillus casei Propionibacterium acnes
Lactobacillus fermentum Propionibacterium propionicum
Lactobacillus gasseri Proteobacteria
Lactobacillus rhamnosus Campylobacter sputorum
Leuconostoc spp. Citrobacter spp.
Bacterial cell structure
Parvimonas micra Eikenella corrodens
and oxygen tolerance
Peptococcus spp. Escherichia spp.
Peptoniphilus Klebsiella pneumoniae Gram-positive aerobic cocci
Peptostreptococcus spp. Neisseria spp. Gram-positive aerobic rod
Staphylococcus aureus Proteus spp. Gram-negative aerobic cocci
Staphylococcus epidermidis Pseudomonas aeruginosa Gram-negative aerobic rod
Streptococcus anginosus Bacteroidetes/Chlorobi group Gram-positive facultative cocci
Streptococcus gordonii Porphyromonas spp. Gram-positive facultative rod
Streptococcus mutans Porphyromonas endodontalis Gram-negative facultative rod
Streptococcus mutans Prevotella spp. Gram-positive facultative cocci
Streptococcus pyogenes Prevotella intermedia Gram-positive anaerobic rod
Streptococcus sanguinis Prevotella melaninogenica Gram-negative anaerobic rod
Veillonella spp. Selenomonas sputigena Gram-negative anaerobic cocci

canal or directly through the soft tissues, either method being susceptible
to contamination. Many studies that have obtained periapical tissue have
taken scrapings, which may include microorganisms from the apical part
of the root canal.
The bacterial front may extend beyond the apical foramen and into the
periapical lesion. It is possible that establishment of infection in this site
may lead to its change to adapt to the new site. Such a periapical infection
may then seed new infection into the root-canal system and become a
source of treatment resistance. This has been a topical area of research
interest and controversy. The problem of its study is compounded by the
assertion that extraction of teeth causes pumping motion that may move
the bacterial front and artificially alter the morphological relationships
existing in vivo. Therefore, not only can periapical tissues be contaminated
from the root canal but the root canal may be contaminated from the peri-
apical tissues. Such movement of bacteria due to bulk flow of fluid caused
by pressure changes could indeed occur but is less likely when the coronal
part of the tooth is intact.
Periapical abscesses associated with untreated teeth appear to be domi-
nated by Streptococcus, Peptostreptococcus and Bacteroides species, a
finding consistent with the presence of these groups in root canals of teeth
associated with symptoms. The profile of bacteria found in periapical
tissues in cases of “extraradicular infection” is somewhat different (Table
3.6). In addition to the above groups they include Actinomyces, Propioni-
bacterium, Fusobacterium, Prevotella and Staphylococcus species; these
groups overlap considerably with those observed in teeth with symptoms.
Some regard the two main groups of bacteria involved in extraradicular
infections to be confined to Actinomyces (see Fig. 3.23) and Propionibac-
terium species.
A. israelii is a repeated culprit in therapy-resistant cases and is by far
the most common species involved in actinomycosis. A. israelii is the most
prevalent Actinomyces species isolated from human abscesses; however,
Actinomyces gerencseriae (formerly A. israelii serotype II) is also preva-
lent, found in 56% and 25% of human abscesses, respectively. Using
checkerboard DNA–DNA hybridization analysis of root-canal samples
from teeth diagnosed with periapical abscesses, A. israelii and A. gerenc-
seriae have been reported in 14.8% and 7.4% of samples, respectively;
however, the role of A. gerencseriae in persistent infection after root filling
is unknown. Recently, a new Actinomyces species, Actinomyces radiciden-
tis, was found to be involved in post-treatment disease. Using PCR-based
detection, it has been shown to be present in untreated root-canal infections
and root-filled teeth with chronic apical periodontitis, although its preva-
lence in both types of infection was low.
CYSTS AND THEIR MANAGEMENT
The cyst is an independent pathological entity within a granuloma (see
Figs 3.16d, 3.26c). The granulomatous component of the lesion may
respond to removal of the aetiological agents from the canal but the cyst
component may survive (see Figs 3.26a,b). Cholesterol needles, which
leave the so-called cholesterol clefts in histological views (see Figs
3.26b,d) may be associated with a foreign-body type response. Successful
treatment of the cyst may require its enucleation, decompression by punc-
ture or induction of acute inflammation in the vicinity. Enucleation has
been reliably tested without significant recurrence but the effectiveness of
the decompression method is less well documented. Healing can vary from
 86  Biological and clinical rationale for root-canal treatment and management of its failure

Fig. 3.67  Transmission electron

microscopic view of the bacterial mass
(BA, upper inset) illustrated in Figure
3.22a. Morphologically, the bacterial
population appears to be composed only
of Gram-positive, filamentous organisms
(arrowhead). Note the distinct Gram-
positive wall in the lower inset. The upper
inset is a magnification of the bacterial
cluster (BA) in Figure 3.22a. Original
magnification: ×3400; upper inset ×132;
lower inset ×21 300 (from Nair et al.,
1990)

being rapid to slow and unpredictable, and the approach allows no proper
opportunity for biopsy. However, it is a valuable means of reducing the
cyst’s size before surgical enucleation. The last method, of inducing acute
inflammation in the cyst’s vicinity, requires instrumentation through the
apical foramen as advocated by Bhaskar (1972). This rather unpredictable
procedure has not gained wide support. Despite the overall lack of clarity
about the pathogenesis and approaches to treatment of cysts, the therapeu-
tic regimen for all periapical lesions associated with compromised pulps
is clear. In view of the inability to differentiate diagnostically a granuloma
from a cyst clinically and the high rate of success of conventional
non-surgical root-canal treatment, this approach is the preferred method
of first treatment of all periapical lesions associated with necrotic and
infected pulps. If upon follow up, a technically adequate root-canal treat-
ment does not lead to resolution, then a surgical approach should be
considered.
FOREIGN BODY RESPONSE AND ITS MANAGEMENT
In a small proportion of cases following treatment, and sometimes preced-
ing it (if the tooth has been left on open drainage), foreign material may
 Biological and clinical rationale for root-canal treatment and management of its failure  87

Table 3.6  Bacteria associated with extraradicular infections

Study Sample size (n) Type of study Dominant species

Open lesions (sinus tracts)
With or without sinus tract
(mixed cases)
Closed lesions (no sinus tracts)
Happonen et al. (1986) 16 Culture Actinomyces, Propionibacterium
Haapasalo et al. (1987) 1 Culture Propionibacterium, Fusobacterium
Tronstad et al. (1987) 5 Culture Mixed
Tronstad et al. (1990) 1 Culture Mixed
Weiger et al. (1995) 12 Culture Streptococci, Prevotella
Vigil et al. (1997) 13 Culture Clostridium, Fusobacterium
Gatti et al. (2000) 7 (36) Culture Actinomyces, Streptococci, Bacteroides
Signoretti et al. (2011) 1 Cuture Actinomyces naeslundii, Actinomyces meyeri,
Propionibacterium propionicum, Clostridium
botullinum, Parvimonas micra, Bacteroides ureolyticus
Noguchi et al. (2005) 27 Cloning of mixed 16S Porphyromonas gingivalis, Tannerella forsythia, and
rRNA gene products Fusobacteriuim nucleatum among others
Happonen et al. (1985) 7 Culture Actinomyces, Propionibacterium
Nishimura (1986) 1 Culture Actinomyces
Tronstad et al. (1987) 3 Culture Mixed
Sjogren et al. (1988) 1 Culture Propionibacterium
Barnett et al. (1990) 1 Culture Actinomyces, Bacteroides
Vigil et al. (1997) 15 Culture Propionibacterium, Staphylococci, Streptococci
Abou-Rass & Bogen (1998) 13 Culture Actinomyces, Streptococci, Propionibacterium
Bogen & Slots (1999) 20 Culture Bacteroides
Sunde et al. (2000a) 30 Culture Mixed
Sunde et al. (2000b) 34 Culture Streptococci, Bacteroides, Fusobacterium, Actinobacillus

Fig. 3.68  Needle used by a patient in trying to Fig. 3.69  Cellulose extruded into periapical tissue Fig. 3.70  Pulse granuloma
keep the canal clean

find its way into the canal and is then displaced into the periapical tissues, Fig. 3.71  Delayed
either by the patient in trying to keep the canal clean (Fig. 3.68) or by the healing associated with
dentist. Examples of foreign matter found in periapical tissues include extruded amalgam
needles and wires (Fig. 3.68), cotton wool or paper points (Fig. 3.69),
pulses causing a pulse granuloma (Fig. 3.70), dentine chips, root-filling
materials, including sealer (see Fig. 3.64), amalgam (Fig. 3.71), gutta-
percha (Fig. 3.72) and other materials, such as talc on the gutta-percha
(see Fig. 3.25) and calcium hydroxide (Fig. 3.73).
If the material is causing persistent pathoses or symptoms, it should be
surgically removed. The biopsy would reveal a picture of a frustrated
attempt by multinucleated giant cells derived from macrophages to engulf
and phagocytose the foreign material. Small amounts of extruded material
are normally removed by the body without problem (Fig. 3.74).
 88  Biological and clinical rationale for root-canal treatment and management of its failure

A B C A B

Fig. 3.72  (a–c) Delayed healing associated with extruded gutta-percha Fig. 3.73  (a,b) Delayed healing associated with extruded
calcium hydroxide

B A

Fig. 3.74  (a,b) Extruded sealer resorbed by the host Fig. 3.75  (a) Radiographic and (b) histologic images showing fibrous tissue repair
following surgical endodontic treatment in the maxillary left lateral incisor associated with
a preoperative large periapical radiolucency

FIBROUS HEALING
The outcome of healing of tissues damaged by inflammation and necrosis
as might be caused by a periapical lesion, is either repair or regeneration.
In the majority of cases, the final outcome would be regeneration. However,
it is possible that root-canal treatment may lead to healing by fibrous tissue
repair, particularly in the case of large lesions that damage both cortical
plates (Figs 3.65, 3.75).
INITIAL MISDIAGNOSIS
This is of course not a true cause of failure of root-canal treatment but is
a failure to manage the original problem correctly. At secondary referral
centres, this is not an uncommon presentation. Common causes of misdi-
agnosis of pulpal/periapical disease include temporomandibular joint
(TMJ) dysfunction, sinusitis, other non-odontogenic causes of pain, peri-
odontal disease, lateral periodontal cysts, normal anatomy presenting as a
radiolucency (mental foramen, incisive foramen, maxillary sinus, etc).
MANAGEMENT OF FAILED PREVIOUS TREATMENT
AND OUTCOME OF ROOT-CANAL RETREATMENT
When root-canal treatment fails to resolve periapical disease, it is often
considered appropriate to retreat the tooth using conventional approaches,
especially when the previous treatment is technically deficient (Fig. 3.76a).
This requires removal of the previous root-filling material and any other
material placed for restorative reasons. Correction of any iatrogenic pro-
cedural errors may also be required, if possible. All material must be
removed in its entirety to ensure delivery of antibacterial agents to all
 Biological and clinical rationale for root-canal treatment and management of its failure  89
A
B C
Grahen & Hansson (1961)
Bergenholtz et al. (1979a&b)
Molven & Halse (1988)
Sjogren et al. (1990)
Friedman et al. (1995)
Sundqvist et al. (1998)
Hoskinson et al. (2002)
Farzaneh et al. (2004)
Gorni & Gagliani (2004)
Caliskan (2005)
0 0.1 0.2 0.3 0.4 0.5 0.6
Probability of success for retreatment on teeth with apical periodontitis
Fig. 3.77  Forest plot showing pooled and individual studies’ probability of
periapical healing following root-canal retreatment on teeth with apical
periodontitis based on strict criteria
surfaces of the root-canal dentine (Fig. 3.76b&c). The success rates of
retreatment are generally perceived to be lower compared to primary treat-
ment because of:
• obstructed access to the apical infection and/or
• a potentially more resistant bacterial flora.
The outcomes from a range of studies shows that the mean weighted
success rate is 66% (Fig. 3.77), about 6% lower than in the case of primary
treatment on teeth with apical periodontitis. The factors affecting outcomes
of root canal retreatment are otherwise identical to those affecting primary
root canal treatment; a separate and further consideration is therefore not
given here.
PERIAPICAL SURGERY AND RETROGRADE SEAL
In a proportion of cases, the conventional chemomechanical approach
alone does not resolve the problem either because it may not allow access
to the infection or the cause is non-microbial. In the case of microbial
causes of failure, the infection site may be in the apical canal anatomy (see
Fig. 3.22), in the apical dentinal tubules (see Fig. 3.45a–d) or extraradicu-
lar (see Fig. 3.23). In these instances, a surgical approach to the periapex
may be required in addition to the conventional approach (see Fig. 3.45b).
Extraradicular infection cannot be diagnosed before primary treatment. It
is rather a differential diagnosis arrived at by initial conventional treatment
of the intraradicular infection. The healing process in such cases may
follow a more complicated pathway. Initially, there may be attempts at
healing if the primary intraradicular source of infection is also a major
component of the lesion, so there may be a reduction in the size of the
periapical lesion. The persistent extraradicular infection would, however,
frustrate attempts at complete healing. If the extraradicular infection is the
major source of the problem, there may be no change after treatment.
The surgical procedure consisting of the incisional and dissectional
wounds concluding with the apical resection of the root (see Fig. 3.45c)
Fig. 3.76  (a) Tooth with technically
deficient root canal treatment;  
(b,c) having undergone root canal
retreatment
would then inflict additional trauma to the site and change the picture
altogether. The procedure would hopefully remove the causative factors
leaving a complicated wound to heal by a process that is different from
the one in response to conventional root-canal treatment. The healing
essentially involves epithelial and connective tissue resolution processes
that are interdependent. The first step is the formation of an epithelial seal,
which matures with the nutrient support from the developing underlying
connective tissue. Reattachment of the mucoperiosteal flap may be com-
promised by the presence of periodontal disease. Further connective tissue
healing consists of removal and organization of the clot into periosteum,
alveolar bone, cementum and periodontal ligament. The apical root resec-
tion creates a surface of exposed dentine with a root-canal outline, which
0.7 0.8 0.9 1 is large and filled with a material of variable toxicity. The exposed dentinal
surface may become covered with cementum (see Fig. 3.58) if the tubules
are not infected but none forms over the root canal over which fibrous
tissue develops. If a retrograde filling material, such as mineral trioxide
aggregate (MTA) is used, its osteogenic potential may allow better cover-
age of the root-end by regeneration of tissues as opposed to repair.
FACTORS AFFECTING THE OUTCOME
OF SURGICAL RETREATMENT
Meta-analysis of prospective data on the outcome of surgical endodontic
treatments on teeth with periapical radiolucency performed by a modern
technique (using magnification, root-end resection with minimal or no
bevel, retrograde cavity preparation with ultrasonic tips, and modern ret-
rograde root-canal filling) revealed complete healing in 30–93% of cases
with a pooled success rate of 92% (95% CI 86%, 95%). Another meta-
analysis reported the pooled success rate of treatment using a microsurgi-
cal (94%; 95% CI 89%, 98%) was more favourable than traditional
root-end surgery (59%; 95% CI 55%, 63%). However, the studies included
in the latter meta-analysis differed in design, case selection, duration after
treatment when outcome was assessed, and preoperative non-surgical
treatment. The difference between the microsurgery and traditional
approaches may, therefore have been exaggerated.
The factors having a major impact on surgical retreatment outcome
were:
• presence and size of periapical lesion
• loss of cortical plate
• quality of the pre-existing root-canal filling judged
radiographically
• placement of root-end filling
• quality of the coronal restoration.
The factors having minimal effect on surgical retreatment outcome
were:
• age of patient
• gender of patient
• general health of patient
• tooth type
• preoperative signs and symptoms.
 90  Biological and clinical rationale for root-canal treatment and management of its failure
A B
ALTERNATIVE APPROACHES
TO ROOT-CANAL TREATMENT
It is unfortunate that even in these times of evidence-based practice, some
alternative practices persist. The philosophy adopted by some operators
has been that the root-canal system anatomy is so complex that adequate
biomechanical debridement is impossible and time-consuming. Conse-
quently, they advocate the use of chemical agents to fix the organic pulp
tissue together with any bacteria with a reduced emphasis on asepsis and
mechanical preparation. A variety of materials (e.g. N2), all containing
formaldehyde as the fixative agent, has been used. When used together
with some degree of mechanical preparation, and the material is confined
within the root-canal system, the technique may, in some instances, provide
successful results. However, there is no scientific body of evidence to
substantiate this practice as a predictable procedure. Furthermore, it has
been demonstrated that the fixed pulpal tissue is antigenically altered and
can stimulate an immune response on its own, whereas unfixed necrotic
tissue cannot.
When such material is inadvertently extruded (Fig. 3.78a), there are
serious consequences. The toxicity of the material can cause necrosis and
can alter nerve function. The clinical manifestations of these include
severe pain and paraesthesia, especially when the material is extruded into
the inferior dental canal (Fig. 3.78b). Of course, the same sequelae are
likely if other materials are extruded into the nerve canal, but most of these
resolve spontaneously over time, whereas this is less likely with the
formaldehyde-containing materials.
REFERENCES AND FURTHER READING
Abou-Rass, M., Bogen, G., 1998. Microorganisms in closed periapical lesions. Int
Endod J 31 (1), 39–47.
Alavi, A.M., Gulabivala, K., Speight, P.M., 1998. Quantitative analysis of lymphocytes
and their subsets in periapical lesions. Int Endod J 31, 233–241.
Ando, A., Hoshino, E., 1990. Predominant obligate anaerobes invading the deep layers
of root canal dentine. Int Endod J 23, 20–27.
Barnett, F., Stevens, R., Tronstad, L., 1990. Demonstration of Bacteroides intermedius in
periapical tissue using indirect immunofluorescence microscopy. Endod Dent
Traumatol 6 (4), 153–156.
Baumgartner, J.C., Falker, W.A. Jr., 1991. Bacteria, in the apical 5 mm of infected root
canals. J Endod 17, 380–383.
Baumgartner, J.C., Watkins, B.J., Bae, K.S., et al., 1999. Association of black-pigmented
bacteria with endodontic infections. J Endod 25 (6), 413–415.
Baumgartner, J.C., Watts, C.M., Xia, T., 2000. Occurrence of Candida albicans in
infections of endodontic origin. J Endod 26 (12), 695–698.
Bergenholtz, C., 1974. Microorganisms from necrotic pulp of traumatized teeth. Odontol
Rev 25, 347–358.
Bergenholtz, G., Lekholm, U., Liljenberg, B., et al., 1983. Morphometric analysis of
chronic inflammatory periapical lesions in root-filled teeth. Oral Surg Oral Med Oral
Pathol 55, 295–301.
Berkovitz, B.K.B., Holland, G.R., Moxham, B.J., 2009. Oral anatomy, histology and
embryology. Mosby.
Bhaskar, S.N., 1972. Non-surgical resolution of radicular cysts. Oral Surg 34, 458–476.
Fig. 3.78  (a) Extrusion of filling material into the inferior dental
canal; (b) zones of anaesthesia (inner) and paraesthesia (outer)
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Section 2  Preparation for delivery of endodontic treatment
Diagnosis of endodontic problems
THE NATURE OF ENDODONTIC DIAGNOSIS
Diagnosis is the art of systematic use of verified or unverified information
to derive the identity or cause of a problem; it involves objective and intui-
tive processes. The clinician will often call upon objective processes but
also (sometimes unknowingly) relies heavily on intuitive processes. Intui-
tion is an inner faculty not well defined by scientific disciplines but is well
recognized in other areas of knowledge. The best example of its power is
given by the ability of the patient to intuit a cause without any scientific
grounding in the problem. Such a process alone is not sufficient for a clini-
cian but supplements objective, learnt processes. Diagnosis has been
defined in a variety of ways (Table 4.1). It is one of the more intellectually
stimulating parts of clinical practice, which brings out the detective zeal
in the clinician.
The process of diagnosis is a complex one, involving several diverse
aspects. The identification of a disease is based on knowledge of its pathol-
ogy, natural history and its presenting features (Table 4.2).
The presentation of any disease is subject to normal variation, which
may be depicted by its Gaussian distribution, classically described as a
bell curve (Fig. 4.1).
The variations are a function of genetically expressed biological differ-
ences between patients and the anatomical conjunction within which the
disease manifests. Dentists are normally taught the “central tendency”, that
is, the commonest presentation; it being too difficult and complicated to
teach each of the variations that may present in reality. A practical clinical
interpretation to augment this theoretical knowledge is, therefore neces-
sary and is acquired through supervised clinical practice, where a teacher
shows the links between clinical manifestations and the embedded theo-
retical picture of histopathology and physiology. Subsequent independent
practice upon graduation requires vigilant tracking of the outcome of all
diagnostic decisions; that is, did their judgement solve the patient’s
problem. The problem of coincidental resolutions can only be overcome
through dedicated, conscientious, active, repeat experience, which allows
a definitive pattern of outcomes to be consolidated. The dentist, thus
through a process of mind application and intuition learns to recognize
when their decision was correct and when the favourable outcome may
simply have been a coincidence. It stands to reason that a peripatetic
dentist who does not work for long in any one place is unlikely to develop
such integration and consolidation of diagnostic insight (see Table 4.2).
Through the gathering of such experience, the use of basic pathological
principles, together with the aid of intuitive processes, the dentist is able
to develop the ability to recognize the “outliers” that present at the extremes
of the Gaussian distribution. To reach such a status requires considerable
active experience.
In the interests of efficiency, experienced dentists may learn to apply a
heuristic approach, whereby they reduce the identification of a problem to
certain key or pathognomonic features (Table 4.3). This can work if applied
with due diligence and caution but is a trap for misdiagnosis if applied
without a proper foundation.
Clinical diagnosis is predicated upon the systematic gathering of
information, first through a dialogue with the patient to determine their
perspective on the problem, and second through a process of observation.
© 2014 Elsevier Ltd. All rights reserved.
4
K Gulabivala, Y-L Ng  
The ability/skill to gather accurate information through interview and
interrogation is an art mastered through experience. Although received
wisdom suggests that patients should be allowed to convey their problems
in their own way and words, experienced diagnosticians will firmly iterate
that histories are taken not given.
Information gathering continues with the examination, which is a com-
bination of direct observation to detect signs of variations from the normal,
manipulation of various afflicted parts with the aim of determining texture,
shape, mobility, response and, finally, stimulation to elicit the reported
symptoms. Each of these must be performed with clear insight of the
outcome sought and potential confounders inherent in the process.
The gathered information is integrated into an overall picture, which
requires the ability/skill to extrapolate and interpret presenting features
based on knowledge of the disease process and its possible unusual pres-
entations. This process is actually nothing more than pattern recognition,
which has become a science and discipline in its own right.
The implication of this is that the process of assimilation of information
and pattern comparison may begin early in the diagnostic pathway, the
clinician need not wait for all the information to be gathered before
forming an opinion of the likely outcome. This may be viewed as biased
thinking in some quarters but is in actual fact merely recognition of how
our brain functions. Active but cautious adoption of the principle enables
the history to be garnered efficiently and effectively by virtue of the fact
that the clinician will be able to intuit those aspects that require confirma-
tion and those aspects that require rejection. That is, it allows the clinician
to take rather than be given the history. Similarly, the process of examina-
tion is directed towards confirmation of that which is expected (positive
or negative), according to the preliminary diagnosis. Lack of confirmation
should signal that the problem may either be an outlier, or that a different
conclusion may hold true. Some clinicians may argue that such an approach
may lead to the missing of vital signs. This is not actually so, particularly
if the clinician is conscientious in their search. The mind must, by defini-
tion, be open to all possibilities at the same time. The ability to “see” is
critical; this is not merely related to good eyesight and conditions for
vision but, more importantly, to the existence of the relevant “recognition
information” in the “mind’s eye”. That is, the mind must first be prepared
thoroughly to “see” by visualization of assimilated theoretical knowledge,
which is tempered and integrated through active (with mind switched on)
clinical experience.
THE NATURE OF ENDODONTIC PROBLEMS
The clinician will be examining the patient for a relatively small variety
of disorders in an endodontic assessment, yet the process seems complex
and confounds many dentists. The prime reason for this is that there is
considerable overlap in the presenting descriptions of various conditions
and it remains for the discerning clinician to tease out subtle discriminating
differences. In many cases, the patient seeks treatment because of overt
signs and symptoms, some of which have an obvious diagnosis, but many
conditions are silent (sign and symptom-free) and discovered only by
chance on routine examination. Common disorders, which may be revealed
during an endodontic assessment are given in Table 4.4.
 94  Diagnosis of endodontic problems

interaction between dentist and patient, which by definition, must therefore

PATIENT ASSESSMENT
At the first appointment, the dentist must assess and characterize the
patient, their dental problem and treatment need before actually embarking
on any treatment, since numerous factors affect management and treat­
ment choice. This process of assessment requires an “intimate and open”
Table 4.1  Definitions of diagnosis
The identification of a disease from its signs and symptoms
The analysis of the cause of a problem
The art of using scientific knowledge to identify disease processes and to
distinguish one disease from another
The art and science of detecting deviations from health and the cause and
nature thereof
The process of identifying a condition by comparing the presenting features
with all (or other) pathological processes that may produce similar signs and
symptoms
Table 4.2  Prior conditions for accurate diagnosis
Knowledge of the disease process and principal presenting features
Prior knowledge tempered by prior experience of its presenting features
The ability/skill to gather information through interview, interrogation and
examination
The ability/skill to extrapolate and interpret presenting features based on
knowledge of disease process and possible unusual presentations – pattern
recognition
Table 4.3  Processes in diagnosis
The identification of a disease based on prior experience and knowledge of its
presenting features
The heuristic approach to reducing the identification of a problem to certain
key or pathognomic features
The recognition of an entity despite its unusual presentation
be mutually consented.
INFORMED CONSENT AND RECORD-KEEPING
The principle of informed consent is that the clinician informs the patient
about the procedures (history, examination, special tests) and their risks;
the patient of a sound and capable mind weighs the risks and gives permis-
sion for the procedure to be undertaken. This permission should ideally be
recorded on a signed consent form. The patient may withdraw consent at
any time, when the dentist must stop, otherwise they could be in breach
of the common law of assault.
Accurate, clear records must be kept of all presenting, diagnostic and
treatment information. What is written on a patient’s record card and in
reports to specialists or referrers will be used as evidence in any legal
disputes.
THE NATURE OF PRESENTING COMPLAINTS
The nature of primary presenting complaints from endodontic patients is
diverse and can embrace pain, discomfort, aesthetics, infection, and func-
tion. These are also sometimes confused with, or superimposed by, various
anxieties (Table 4.5).
The clinician’s task is to identify and propose relevant and appropriate
solutions for the patient’s problems. The complicating aspect in this task
is that the search for a single direct cause–effect relationship between a
presenting feature and cause (Table 4.6) is confounded by the many
sources of the presenting complaint (Table 4.7). The clinician must there-
fore appreciate the potential decision-tree and be ready to filter the received
information through their diagnostic sieve to derive the single or as may
be the case, multiple superimposed causes.
The intelligence gathering involves three sources of information, the
history, examination and special tests.
Table 4.5  Patients’ presenting complaints and anxieties

Primary (actual)
Pain (spontaneous or stimulated by eating or drinking)
Cannot eat/drink (cannot bite, take hot or cold)
Table 4.4  Simplified classification of endodontic conditions
Swelling/infection
Discoloured tooth
Dentinal pain
Broken tooth/filling
State of the pulp
Tooth/gum does not feel right/feels different
State of periradicular tissues
Bad odour/taste
Tooth cracks/fractures
Iatrogenic problems Secondary (fear of)
Resorption Anxiety about
Anatomical anomalies Disease and its effects
Non-endodontic conditions Treatment
Mimicking pain Cost/loss of earnings
Mimicking periapical disease Appearance

Fig. 4.1  Distributions for normal and disease states

without (a) or with (b) overlapping presentations

No
Disease disease
No
Disease disease

A B
 Diagnosis of endodontic problems  95

HISTORY TAKING
Wilfred Trotter on listening
the power of attention, of giving one’s whole mind to the
patient without interposition of anything of one’s self.
Although a patient attends the dentist to identify and resolve their
problem, they will often have a preconception about the origin of the
problem, which may result in them limiting the scope of information
they may be prepared to share with the clinician. There may be a need to
break the preconception first so as to enable the patient to be more open
and free with the sharing of their experience and insight. The importance
of the detail for obtaining a resolution for the patient should not be
underestimated.
Another curious problem in free information sharing is the patient with
an “intellectual ego”, who becomes very defensive when asked a basic
question, such as “can you describe the pain?” They may respond with,
“Well, it is just a toothache”; suggesting that they somehow feel it beneath
themselves to share such basic insight with the expert whose responsibility
they believe it is to identify and resolve their problem. The real problem
often is that they find it difficult to articulate their experience and feel
diminished by not being able to do so. They may be pacified to learn that
toothache comes in many forms and it can indeed be very difficult to
describe for most people but that attempting to do so would help to identify
their problem. Such grudging compliance may sometimes also hide other
issues, to which the dentist should be alert.
To capture the patient’s attention and confidence requires many things,
including a confident approach by the dentist, which in turn, demands
sound knowledge and experience. The patient should be allowed to relate
the details of their problem in their own words (as iterated by Wilfred
Trotter) but the process should be managed to make it ordered, systematic
and free of digression. If necessary, the clinician should be prepared gently
but firmly to redirect the patient’s thoughts and memory if the information
presented is incomplete.
The purpose is to get the patient to relate their experience as accurately
as possible. The difficulty in achieving this in endodontic patients is poten-
tially multilayered. The patient’s experience of their problem may have
affected their state of mind due to anxiety, loss of sleep, loss of appetite
and a general feeling of malaise. In addition, the patient may not have the
vocabulary to describe their experience or the memory to recall it. While
the dentist is trained to receive information in a particular order and has a
set vocabulary for what may be experienced by the patient, they may not
have personal experience of the problem. Conversely, the patient is not
trained to describe their experience, especially using the “set” vocabulary
and order, in which the dentist is trained to receive it. Information exchange
would be significantly enhanced by dentists acquiring personal experience
of the full range of problems that they have to deal with (but this may
prove impractical or unethical!). The challenge is therefore one of inade-
quacy of information exchange.
Listen carefully to the patient’s explanation of their condition and use
the patient’s own words to record it. Obtain a detailed description of any
pain: its nature or character (sharp, dull, aching, throbbing, radiating);
continuous or intermittent; initiating, exacerbating or relieving factors;
duration; frequency; association with time of day, events, cycles (e.g.
menstrual), habits, eating, drinking, physical or mental activity, etc, should
all be noted; the effectiveness of analgesics should be recorded.

MEDICAL HISTORY
Table 4.6  Sources of the presenting complaints
Tooth structure problems
A medical history is taken to find out whether the patient has any health
Tooth structure problems Sources of inflammation
problem or is taking medication that could affect the treatment. The most
Caries State of the pulp convenient way of recording such information is to use a checklist that is
Tooth surface loss State of periapical tissues
kept in the patient’s file, such as that shown in Table 4.8.
Dental resorption Periodontal disease
There is no medical condition that specifically and definitively contrain-
Tooth cracks/fractures
Tooth/root perforation Non-endodontic conditions dicates endodontic treatment, however, if there is any doubt, it is best to
Anatomical anomalies Mimicking periapical disease
consult the patient’s medical supervisor. Conditions such as diabetes mel-
litus, bleeding disorders, anticoagulant therapy, blood-borne viruses,
Sources of pain immunosuppression or epilepsy may affect treatment. The incidence of
Dentinal pain infective endocarditis in patients with cardiac abnormalities is increased
Pulpal pain with diabetes mellitus, immunosuppression, alcohol dependence, haemo-
Periradicular pain dialysis and intravenous drug abuse. In the UK, guidelines published by
Non-odontogenic pain
the National Institute of Clinical Excellence do not recommend the pre-
scription of antibiotic prophylaxis for infective endocarditis.

Table 4.7  Cross-tabulation of Endodontic conditions with possible presenting complaints

Diagnosis Pain H/C Pain TTP Pain Drink Can’t bite Swelling Discoloured tooth Bad taste Bad odour
Dentinal √ X √ √ X √ X X
Pulpal √ √ √ X X √ X X
CTS √ √ √ √ X X X X
Periapical √ √ √ √ √ √ √ √
Vertical root fracture √ √ √ √ √ √ √ √
Resorption √ X √ X √X √ √ √
Periodontal √ √ √ √ √ X √ √

CTS: crack tooth syndrome; H/C: hot/cold; TTP: tender to percussion

 96  Diagnosis of endodontic problems

Table 4.8  Checklist for recording patient information

No Yes Details
Have you had rheumatic fever or a heart murmur?
Have you had heart trouble or high blood pressure?
Do you have antibiotic cover for dental treatment?
Do you tend to bleed excessively or bruise easily?
Do you suffer from asthma, TB, bronchitis or any other chest conditions?
Do you suffer from renal (kidney) disease?
Have you had liver disease (jaundice or hepatitis)?
Do you suffer from epilepsy?
Do you have any allergies to medicines or latex?
Are you pregnant?
Have you ever had depression or mental illness?
Are you currently taking any medicine?
Are you currently receiving treatment from you General Practitioner or any other specialist?
Have you ever been admitted to hospital?
Do you smoke? If so how many and how long?
Do you drink alcohol? If so how many units per week?
Do you have any other illness we should know about?

Fig. 4.2  Consultation Fig. 4.3  Any facial

swelling should be
noted

Fig. 4.4  Facial swelling

A is best seen from above
the patient

The initial consultation is most effectively carried out beside a desk with
both patient and clinician seated; patients find this less stressful than
immediately being asked to sit in a dental chair (Fig. 4.2).

DENTAL HISTORY CLINICAL EXAMINATION

The patient’s attitudes to dental treatment must be assessed during the first
appointment to determine the patient’s likely compliance. It is appropriate
to assess the patient’s previous record of dental care and their compliance
with it. Their experience (positive or negative) and economic status may
determine their current attitude to treatment. Previous negative experi-
ences may also have created a nervous or anxious predisposition that may
compromise or alter compliance. Their perception of endodontic treatment
and ability to withstand long or short sessions is crucial to judge from the
outset. Patients may prefer a particular time of day for personal or medical
reasons.
SOCIAL HISTORY
Habits such as smoking and alcohol use should be characterized for their
effect on the patient’s well-being and healing potential.
Extraoral
Extraoral examination is carried out for facial swelling, asymmetry, ten-
derness of muscles of mastication and the temporomandibular joints, nerve
responses (Table 4.9) and the presence of enlarged lymph nodes. Facial
swelling is best viewed from above the patient (Figs 4.3, 4.4).
Ease of oral access
An assessment should be made of the ease of access, particularly to the
posterior part of the mouth. As a general guide, if a patient’s mouth will
not open wide enough to allow two fingers to pass between the incisors,
root-canal treatment of the molars may be compromised (Fig. 4.5). Some
patients, with small mouths, particularly the elderly, find it difficult to keep
their mouth sufficiently wide open for long periods, using a mouth prop,
which they may relax upon during treatment, does help (Fig. 4.6).
 Diagnosis of endodontic problems  97

Table 4.9  Examination of cranial nerve injury

I Olfactory Ask the patient to smell and identify something familiar (e.g. vinegar)
II Optic Observe for visual reflexes by shining a pen torch into one eye and check for pupil constriction
III Occulomotor Ask patient to follow your finger with their eyes and ask if they experience double vision during upward or inward eye movement.
Observe for ptosis (drooping of the eyelid), and mydriasis (pupil dilation)
IV Trochlear Ask patient to follow your finger with their eyes and ask if they experience double vision during downward eye movement
V Trigeminal Sensory branch: Lightly touch the face with a piece of cotton wool and then a blunt probe on the forehead, cheek and jawline. Lightly
touch the cornea with cotton wool and observe for corneal reflex
Motor supply: Ask patient to clench their teeth and observe and palpate the bulk of the masseter and temporalis muscles; ask patient
to open their mouth against resistance; gently tap the patient’s chin and observe for jaw jerk reflex
VI Abducent Ask patient to follow your finger with their eyes and ask if they experience double vision during lateral eye movement. Observe for
the affected eye turning inward
VII Facial Ask patient to raise their eyebrows, close their eyes against resistance and puff out their cheeks and show their teeth
VIII Vestibulocochlear Test for hearing loss by clicking your fingers next to the mastoid process
IX Glossopharyngeal Test for gag reflex by touching the soft palate
X Vagus Ask the patient to say “aah” and observe the movement and any deviation of the uvula
XI Spinal accessory Ask patient to shrug their shoulders and turn their head against resistance
XII Hypoglossal Ask patient to stick their tongue out and observe for any signs of wasting, fasciculations or deviation of the tongue

Fig. 4.5  Access Fig. 4.7  Poor oral

assessed with two hygiene
fingers

Fig. 4.6  Mouth props Fig. 4.8  Periodontal

condition

Intraoral
The purpose of the oral examination is multifold. The first remit is direct
visual detection of any variation from normal. The direct visual examina- Fig. 4.9  Loose bridge
tion is facilitated by drying the tissues, use of good illumination, transil- abutment with caries
beneath
lumination and magnification. This is secondarily followed by tactile
manipulation of the affected part to decipher any further variations
from normal. Finally, direct stimulation (by air, fluids, touch, pressure,
percussion or electrical current) of affected parts may be used to reproduce
or elicit the complaint or symptoms. Local anaesthesia may also be used
to aid further location of pain by selectively abolishing sensation.
The intraoral soft tissues, oral hygiene (Fig. 4.7), general periodontal
condition (Fig. 4.8), presence of caries (Fig. 4.9), missing or unopposed
teeth (Fig. 4.10), quality and quantity of dental treatment (Fig. 4.11), tooth
surface loss and faceting (Fig. 4.12) should all be assessed.
 98  Diagnosis of endodontic problems

Fig. 4.10  Missing and unopposed Fig. 4.13  Soft tissue examination
teeth

Fig. 4.11  General

dental state
Fig. 4.14  Two-
dimensional face
diagram for mapping
areas of altered
sensation

Fig. 4.12  Tooth surface

loss and faceting

BACK FRONT

Fig. 4.15  Example of BPE score grid and criteria for coding
1 0 3
2 2 4*

Code Criteria

0 No pockets >3.5 mm, no calculus/overhangs, no bleeding after probing (black band completely visible)

1 No pockets >3.5 mm, no calculus/overhangs, but bleeding after probing (black band completely visible)

2 No pockets >3.5 mm, but supra- or subgingival calculus/overhangs (black band completely visible)

3 Probing depth 3.5–5.5 mm (black band partially visible, indicating pocket of 4–5 mm)

4 Probing depth >5.5 mm (black band entirely within the pocket, indicating pocket of 6 mm or more)

* Furcation involvement

Both the number and the * should be recorded if a furcation is detected - e.g. the score for a sextant could be 3*
(e.g. indicating probing depth 3.5–5.5 mm PLUS furcation involvement in the sextant).

SOFT TISSUE EXAMINATION
The soft tissues, consisting of the cheek mucosa, tongue, floor of mouth,
palate, sulcular fold, and those overlying the alveolus should all be
assessed, after wiping with gauze, by direct visual observation for signs
of inflammation, sinus tract openings, induration, swellings, fibroepithelial
growth, ulcers or discoloration (Fig. 4.13).
The purpose of tactile stimulation is to determine whether the tissues
are allodynic, hyperalgesic, tender or normal. A light touch may be applied,
such as with a cotton bud to see if pain is elicited, indicating neuropathic
changes. An increasing degree of force is applied by finger palpation to
determine the presence of tenderness, which the patient is asked to confirm.
The areas of altered sensation should be mapped on a diagram in the
records (Fig. 4.14).
Hard and soft swellings should also be recorded on diagrams for extent,
site, size, texture, consistency (bony, firm, fibrous, soft), mobility, fixity
and fluctuance. Soft swellings should be palpated with two fingers to detect
fluctuance. One finger is placed at either end of the swelling and pressure
applied; if the swelling is fluctuant, movement of the fluid beneath the oral
mucosa will be felt.
PERIODONTAL EXAMINATION
A general periodontal examination should be performed to characterize the
periodontal status as part of the overall treatment plan, resulting in a basic
periodontal examination (BPE) score (Fig. 4.15). The purpose is to deter-
mine and segregate any problems arising from marginal periodontal prob-
lems. More specifically, it is essential to exclude local, deep, isolated

Fig. 4.16  Mobility Fig. 4.17  Use of fibreoptic light
showing tooth fracture
A B
Fig. 4.19  (a) Burlew disc; (b) wood stick; (c) tooth slooth
Table 4.10  Miller classification (tooth mobility)
Class I Tooth can be moved less than 1 mm in the buccolingual or
mesiodistal direction
Class II Tooth can be moved 1 mm or more in the buccolingual or
mesiodistal direction
No mobility in the occlusoapical direction (vertical mobility)
Class III Tooth can be moved 1 mm or more in the buccolingual or
mesiodistal direction
Mobility in the occlusoapical direction is also present
probing defects, signalling tooth anomalies, fractures, or sinuses (see
Chapter 12).
A part of this assessment includes a determination of any periodontal
overloading, manifesting in tooth mobility, fremitus or tooth drifting.
Mobility of a tooth is assessed by placing a finger on one side and pressing
with an instrument or another finger from the other (Fig. 4.16). The amount
of movement is judged in relation to an adjacent tooth. Mobility may be
graded as slight (grade 1), which is considered normal, moderate (grade
2), or extensive (grade 3) in a lateral or mesiodistal direction, combined
with vertical displacement in the alveolus (Table 4.10).
TOOTH EXAMINATION
Direct visual examination of teeth, following drying and under good direct
illumination, should consist of a general assessment of the dentition, start-
ing with the teeth present, their restorative status judged in terms of caries,
restorations (their quality and extent), tooth surface loss (attrition, erosion,
abrasion, abfraction), cracks, fractures and infractions. The number and
Diagnosis of endodontic problems  99
Fig. 4.18  Mandibular molar with
distal fracture
C
distribution of the asymptomatic teeth should be characterized in a general
summary.
The specific endodontically involved teeth will require a more detailed
assessment as may adjacent teeth, which might act as controls and poten-
tial future abutments. Apart from the assessments mentioned above, the
teeth will need to be manipulated in a variety of ways.
Transmission of a powerful light through teeth will show interproximal
caries and (of particular interest in endodontics) cracks, infractions and
fractures. Extraneous light is reduced; the fibreoptic light placed next to
the neck of the tooth and moved along its surface. The light will not pass
across the fracture line due to reflection, so the part of the tooth nearest to
the light is bright and that beyond the fracture remains dark: Figure 4.17
shows this effect. Figure 4.18 shows a mandibular first molar with a
coronal restoration removed – a fracture line is visible in the distal wall.
Pressure or force may be applied to teeth to elicit different types of
information about the periodontium and the tooth. Pressure may be applied
to teeth in different directions so that they act as instruments of palpation
of the periodontal ligament. Just as palpation of the soft tissues is gradu-
ated, so pressure application to teeth is graduated by slowly increasing it.
Such manipulation may help locate the presence of localized inflammation
in the periodontal ligament.
At the extremes of the pressure stroke, the tooth may begin to deform
allowing any cracks to open. This, in a vital tooth, is detected as a sharp
dentinal pain, which may be felt on pressure application or release. In a
non-vital tooth, a periodontal sensation, rather than a dentinal sensation is
evident. Since cracks may be localized to individual cusps, this examina-
tion is enhanced by the use of a hard or viscous substance (such as a
Burlew disc, rolled rubber dam, wooden stick, an inlay seater or tooth
slooth®), which facilitate isolation of increased pressure to individual
cusps (Fig. 4.19).
 100  Diagnosis of endodontic problems
Using an impact force rather than graduated pressure, allows a different
sort of assessment as the tooth moves differently in the viscoelastic peri-
odontal ligament. Gentle tapping with a finger (both vertically and later-
ally) and then with an instrument will locate a tender tooth but it is a
harsher test and usually gives a slightly different result to a pressure test
(Fig. 4.20). If ankylosis of a tooth is suspected, tapping with an instrument
handle in the long axis of the tooth will confirm the diagnosis: an anky-
losed tooth has a distinctive high-pitched ring.
PULP TESTING
Recently, the alternative term “sensibility testing” has come into common
dental parlance. The authors feel the use of this term is incorrect. The test
stimulates Aδ nerve fibres, which are the same nerves that respond to
dentinal stimulation, albeit via the dentinal tubules and the hydrodynamic
mechanism. The term “sensitivity” testing would, therefore seem more
appropriate, although the term sensibility has the advantage of distinguish-
ing between stimulation of Aδ nerve fibres directly versus indirectly via
the hydrodynamic mechanism. Although the terms, sensitivity and sensi-
bility are cited interchangeably in the English dictionary, the former term
is better used to depict physical response and the latter term emotional
response.
As the pulp is not open for direct inspection of its status, an indirect
method is required. As yet, there is no means for imaging the pulp tissues
to achieve this insight. Current methods, therefore merely serve to stimu-
late the pulp in the hope of eliciting a neural (Aδ fibre) response, which
serves as a surrogate measure for determining that the nerve function
viability stands for pulp viability. This does not though mean that the pulp
is inflammation-free. The outcome sought is therefore either “positive
response” or “negative response”. Some research methods assess the
Fig. 4.20  Percussion test
C (c) patient controls the pulp
B
A
D
E
presence or absence of a viable blood supply (laser Doppler, pulse oxime-
try) but these instruments have not yet been developed for routine clinical
use. Contemporary pulp testing can quantify neither disease nor health,
and should not be used to judge the degree of pulpal disease. Pulp tests
are best used to determine the existence of pulp necrosis and all are prone
to false positives and negatives. Each type of pulp test works through a
slightly different mode of stimulation and, therefore, it is prudent to use
all of them to triangulate a consensus.
Electric pulp tester
The electric pulp tester (EPT) delivers a graduated increase in electric
current (alternating or direct) to excite a response from the Aδ nerve fibres
within the viable pulp. Most modern pulp testers are monopolar, meaning
there is only one probe.
An example of a pulp tester, the Analytic Technology Endo Analyser,
is shown (Fig. 4.21a). This instrument has a dual function acting as both
a pulp tester and an electronic apex locator (EAL). When used as a pulp
tester, a pulsating stimulus is produced starting at a low value, which
increases automatically. The pulse amplitude of the stimulus begins at 15
volts and rises to a maximum of 350 volts.
Pulp testing technique
The test and control teeth should be dried and isolated with cotton wool
or rubber dam (see Fig. 4.21b), the latter applied as small strips placed
between the teeth. Contacts may also be isolated by inserting acetate strips
between teeth. A conducting medium must be used – the one most readily
available is toothpaste. The pulp tester is applied to the middle third of the
tooth, avoiding contact with the soft tissues, and any restorations. A lip
electrode is placed over the patient’s lip. If the pulp is vital the patient
describes feeling a sensation which is variously described as tingling,
vibration, pain, shock. Before testing the tooth in question, it is important
to educate and acclimatize the patient to the sensation first on a control
tooth. The patient is instructed that they should only respond to a sensation
that matches the one elicited from the control tooth (assuming the pulp in
this tooth is normal). Asking the patient to respond to any sensation will
yield a false positive because if the potential difference is high enough, a
sensation could be elicited from the periodontal ligament or adjacent teeth.
A more user-friendly method is to ask the patient to hold the lip electrode.
The plastic cable is held in one hand and the metal electrode between the
forefinger and thumb of the other hand as shown in Figure 4.21c. This
method allows the patient to have control by releasing their finger grip on
the metal electrode when they feel the defined (not any) sensation; thus
reducing the element of an anxiety-driven response. Electric pulp testers
Fig. 4.21  (a) Unit has a dual
function both as a pulp
tester and an apex locator;
(b) pulp tester applied to
buccal surface of tooth
isolated with strips of rubber
dam (toothpaste used as  
a conducting medium);  
tester; (d) special tip for  
pulp testing beneath crowns;
(e) pulp testing beneath
crown

Fig. 4.22  Application of hot Fig. 4.23  Running a rubber wheel on
gutta-percha stick on tooth surface the tooth
A B
Fig. 4.25  (a) Ethyl chloride is sprayed onto a cotton bud; (b) cold cotton bud applied to mid third of
buccal surface of tooth
should be used with caution on patients who have a cardiac pacemaker;
although modern pacemakers are shielded from electrical interference.
Pulp testing of crowned teeth is possible provided a small area of
dentine or enamel is available for electrical contact without touching the
gingival tissue. A special tip for the Analytic Technology pulp tester (see
Fig. 4.21d) is being used on the patient shown in Figure 4.21e. Electric
pulp testing cannot discriminate partial pulp necrosis as may happen in the
different roots of a molar tooth.
Thermal pulp testing
Thermal pulp testing involves either applying or removing heat from a
tooth. A variety of methods is available to deliver the heat.
Heat
Dry heat
This can be delivered with a commercially available, electrically-heated
element, or else crudely, commonly available dental surgery materials may
be deployed. The end of a stick of gutta-percha or composition (3 mm) is
gently heated in a flame, tested on the gloved hand for warmth and lack
of adherence and applied to the suspect tooth. The tooth surface should be
lightly coated with petroleum jelly to prevent the composition/gutta-percha
from sticking (Fig. 4.22); local anaesthetic should be kept to hand in case
of a sharp reaction. Another crude method which has been suggested but
is not recommended here, is to generate heat by running a rubber wheel
on the tooth using a standard hand-piece (Fig. 4.23).
Hot water
Patients reporting pain due to hot food or drink do not always respond to
the above tests. The stimulation requires that the heated medium penetrates
particular parts of the mouth and reaches the involved tooth in the same
way. This situation can only be replicated using the appropriate medium,
normally hot water. Hot water should be sipped and held in the mouth,
first over the mandibular quadrant on the affected side and then over the
maxillary quadrant if this does not elicit a response. If this fails, an
Diagnosis of endodontic problems  101
Fig. 4.24  Flooding the isolated tooth
site with hot water
Fig. 4.26  Ice stick prepared by filling
the discarded plastic protective cover
for hypodermic needles with water
and freezing them
Table 4.11  Temperature of different refrigerants
Refrigerants Temperature (°C)
Ethyl chloride −26
Hygenic® Endo-Ice −50
ROEKO® Endo-Frost −50
Carbon dioxide −78.5
alternative method is to use rubber dam to isolate each tooth in turn and
then flood the site with hot water (Fig. 4.24), the temperature of which
must simulate the hot beverage eliciting the patient’s pain. If a response
is obtained, the suspect tooth is anaesthetized and the heat test repeated.
Cold
Several methods can be used to deliver this test; the difference between
them lies in how the reduced temperature is achieved and, therefore, what
the temperature is (Table 4.11). The simplest and most common test is a
blast of air from the triple syringe. Another common method is to soak a
cotton bud with a volatile refrigerant, such as ethyl chloride, Endo-Ice
(811-97-2 1,1,1,2 Tetraflouroethane > 90%) or Endo-Frost (mixture of
butane [30–50%], propane [30–50%] and isobutane [10–20%]); the evapo-
ration causes frosting, which is then applied to the tooth (Fig. 4.25). An
alternative method is to prepare ice sticks by filling the discarded plastic
protective covers for hypodermic needles with water and freezing them
(Fig. 4.26). To make them ready for use, one end is removed by warming
it slightly in the hand (Fig. 4.27). Carbon dioxide probes (Fig. 4.28) offer
an intense reproducible response, and do not affect the adjacent teeth (which
an air blast or ice stick may do) but require a carbon dioxide canister.
LOCATION OF SOURCE OF PAIN
Pulpal and some forms of non-odontogenic pain can be notoriously dif-
ficult to localize. A useful way to determine the location of pulpal pain in
 102  Diagnosis of endodontic problems
A B
Fig. 4.27  Ice stick applied to tooth Fig. 4.28  (a) Apparatus required for carbon dioxide pulp testing; (b) carbon dioxide stick
Fig. 4.29  The bevel of
the needle should point
away from the tooth
a quadrant of teeth with several possible candidates is to block individually
their nerve supply to see if the pain is abolished. The problem is that such
precise localization of anaesthesia is difficult and the technique relies on
precise delivery of the local anaesthetic agent. The pain is first provoked
and then an infiltration injection of local anaesthetic may be used to iden-
tify the tooth. An intra-ligamental injection localizes the effect of the
analgesic better, although the proximal teeth may still be affected. Note
that the bevel of the needle in Figure 4.29 points away from the tooth to
allow easier penetration into the periodontal ligament. For mandibular
posterior teeth, nerve blocking may begin with infiltration, proceed to
mental block and then inferior dental nerve block.
Cutting a test cavity
As a last resort, a test cavity may be cut in a tooth which is believed to be
pulpless. In the authors’ experience, this test is not reliable because a posi-
tive response may be obtained from a tooth with a necrotic pulp due to
vibration effects.
Further tooth evaluation
On occasion, it may be necessary to carry out a preliminary procedure
before the final treatment plan can be made. For example:
• crowns and bridge retainers should be assessed for cementation
failure; the retainer should be firmly depressed apically and then
pulled axially, repeatedly to elicit bubbles at the margin as a sign
of decementation
• remove a restoration to examine the floor of the cavity for
a fracture
• control temporomandibular joint (TMJ) and muscle pain
• remove a post to assess feasibility of orthograde root-canal
retreatment
• open a pulp chamber to assess feasibility of locating a sclerosed
root canal.
OCCLUSAL EXAMINATION
Part of the role of tooth examination is to establish tooth mobility,
tenderness on pressure or percussion, as well as structural damage from
parafunction. As these may all be influenced by occlusal contacts, it is
appropriate to establish whether the pattern of static and dynamic occlusal
contact relationships may have contributed to these findings or would
contribute to the planning and management of the restoration of the
involved tooth.
This is done by recording the static occlusal relationship in maximal
intercuspal position, the retruded contact position and the slide between
the two. The excursive guiding contact surfaces should be noted (in pro-
trusive and left and right lateral excursions). Most importantly, the pres-
ence of any non-working or working side interferences, as well as fremitus
on the involved teeth should be noted as these may be the cause of mobility
or tenderness.
This is also a convenient time to note occlusal space requirements for
any restoration and whether there has been loss of occlusal space due to
caries or loss of restoration or tooth attrition.
IMAGING TECHNIQUES
Imaging technologies have been developed in medicine to aid non-invasive
visualization of the hidden tissues under investigation. The perfect tool is
not yet in existence. Any departure in their ability to detect disease or
health is measured by their sensitivity or specificity, respectively. The
perfect imaging tool would have 100% sensitivity and specificity; that is,
it would detect disease or health without fail. Commonly used imaging
techniques in medicine include, radiography, its computerized variant
(computed tomography), which allows three-dimensional rendering,

magnetic resonance imaging and ultrasound imaging. In dentistry, the
imaging techniques are confined to conventional radiography and cone-
beam computed tomography (CBCT).
CONVENTIONAL RADIOGRAPHIC ASSESSMENT
This is of the utmost importance. Preoperative periapical radiographs
should be taken using the paralleling technique (Fig. 4.30). If a patent sinus
is present preoperatively, a radiograph may be taken with a size 30 gutta-
percha point in place. The point should be inserted into the sinus and gently
teased by rolling the tip back and forth between the fingers until resistance
or discomfort is encountered (Fig. 4.31).
If endodontic treatment is being considered, the following should be
assessed on radiographs: shape, curvature and number of roots; presence
and morphology of root canals; size of pulp chamber; type and size of
coronal restoration; presence of periradicular disease; periodontal bone
loss, internal or external resorption; and root fracture. If the tooth has been
treated previously, it should be possible to assess the type of root-filling
material used and the presence of any procedural errors, such as perfora-
tion, untreated canals or a fractured instrument. The radiograph will often
Fig. 4.30  Radiograph
taken with parallel
technique
A B
Fig. 4.31  (a) Gutta-percha in sinus; (b) depth of insertion of gutta-percha; (c) gutta-percha point placed in sinus visible on radiograph
Fig. 4.32  Maxillary first
molar with furcal bone
loss, inflammatory
resorption, and possible
perforation into
furcation with gutta-
percha. Tooth to be
extracted
Diagnosis of endodontic problems  103
indicate to the operator the cause of the problem and the probable ease of
treatment. In Figure 4.32, the radiograph shows a maxillary first molar
with horizontal and furcation bone loss, possible inflammatory resorption
of the distobuccal root and a gutta-percha point passing into the furcation.
The tooth should be extracted. Figure 4.33 shows two maxillary premolars,
the first of which has a periapical radiolucency and an inadequate paste
root filling, the second showing gross caries in the coronal portion of the
root canal. The first premolar was root filled (Fig. 4.34) and the second
extracted and replaced with bridgework.
Accurate dental radiographs are an essential requirement for the prac-
tice of endodontics. High-quality periapical radiographs improve initial
diagnosis and assist greatly in success of treatment. Operators should
endeavour to achieve high technical standards in order to ensure accuracy
and minimize the number of film exposures needed to complete a clinical
procedure. It is important to have a clear understanding of the materials,
equipment, techniques and safety standards governing this discipline.
The reader is referred to a specialist book on radiography for such
knowledge.
Conventional films versus digital image recording
The fastest films available, consistent with satisfactory diagnostic results,
should be used. F-speed film is replacing E-speed film as the fastest avail-
able, saving a further 20–25% on exposure compared with E-speed film
when processed optimally. Size 0 films (34×22 mm) are suitable for chil-
dren and for anterior teeth, size 2 films (40×30 mm) for posterior teeth
and adults.
Digital radiology (DR) offers many potential advantages in dental and
endodontic practice. The detectors for DR exist in two forms: solid-state
detectors (sensors) and photostimulable phosphor plates. DR sensors use
miniature TV camera charge-coupled devices (CCD) or complementary
metal oxide semiconductor (CMOS) chips that are sensitive to light in
combination with a scintillator layer that converts X-rays to light. The
CCD/CMOS sensor is connected to a computer to display the image on a
C
Fig. 4.33  Inadequate
root filling in first
premolar and gross
caries in second
premolar
 104  Diagnosis of endodontic problems
Fig. 4.34  First premolar root treated. Second Fig. 4.35  RVG imaging system
premolar due for extraction
monitor. Direct conversion DR detectors have also been described in other
fields of medical imaging and may play a more important role in the future.
The first digital imaging system was radiovisiography (RVG; Trophy
Radiologie, Vincennes, France). It eliminated the time spent processing
X-ray films and possessed a zoom function, which allowed the magnifica-
tion of selected areas to try to improve diagnostic performance (Fig. 4.35).
Digital image quality has improved with the further development of these
intraoral sensors and is now comparable with that of E-speed film (Fig.
4.36). The advantage of DR sensors for endodontic treatment is the imme-
diate availability of the image. The disadvantages are the high cost and
thickness of the sensor.
Phosphorescent screens or photostimulable phosphor plates (PPP) are
sensitive to X-rays and generate a latent image that is scanned with a
laser scanner and converted to a digital image. The image can be erased
from the phosphor plate by exposing the sensor to intense white light,
thus making the sensor reusable. The advantage of PPP is that they have
roughly the same dimensions compared to conventional radiographs and
that the sensor plates are relatively inexpensive.
Due to the development of wireless technology such as “bluetooth” for
other applications, the first wireless CMOS sensors have already been
introduced, such as the Schick CDR® wireless system (Fig. 4.37). Even
though these sensors have a tiny battery pack as power supply, they have
about the same dimensions as the corded equivalents but are more
expensive.
The advantages of digital imaging are the instant availability; secure
storage and archiving of the digital data. The images can be accessed from
different computers in a network, as well as transmitted as necessary.
Comparing the different technologies
The traditional film can be regarded as the gold standard. It does, however,
come with certain disadvantages related to storage and processing: The
film package needs to be unpacked in a dark or safelight environment;
the chemicals used for processing (developer and fixer) are a burden to
the environment; the development procedure is sensitive to temperature,
development time and concentration of the chemicals. The film, once
developed, needs inspection with the aid of a magnifying glass. All the
radiographs need to be stored and archived physically. All these issues are
solved when employing digital radiography. Even though PPP need to be
scanned after exposure, this can be regarded as an automatic process
that almost eliminates human error. When comparing the different
Fig. 4.36  Schick intraoral sensors
technologies, there are a number of factors to consider. The spatial resolu-
tion can be used to characterize the image sharpness and is expressed
in line pairs per millimetre. In a study that compared conventional film
(F speed film), PPP and DR sensors, the highest spatial resolution was
found for the conventional film even though a few DR sensors were able
to match this resolution. In the same study, the highest contrast resolution
was achieved by most of the DR sensors. The widest range of exposure
and the highest dosages permitting a diagnostic image were obtained with
PPP systems and a few DR sensors. This contradicts the common belief
that digital radiography will always lead to dose reduction. Longer expo-
sure times may cause blooming artifacts with most DR sensors (Fig. 4.38)
but will leave the radiographic contrast of PPP largely unchanged. This
implies that the clinician should make sure that the lowest possible expo-
sure time for the DR system is chosen.
As the computer hardware seems to double its performance every
two years (Moore’s Law), concomitant improvement in the number
of pixels per DR sensor area, the signal to noise ratio and reduction in
amount of radiation required to generate an image would be expected in
the future.
Film holders
Film holders are devices designed to hold the film in a stable position
within the patient’s mouth, avoiding the need to hold the film by hand.
Many incorporate beam-aiming devices to prevent “cone cutting” and
some also include a device for rectangular collimation (Fig. 4.39). Their
use improves the diagnostic quality of the image and allows the position
of the film and beam to be reproduced during subsequent recall
assessment.
Film holder systems include:
• modified Spencer-Wells forceps
• Rinn XCP system including anterior and posterior film holders
(Fig. 4.40)
• Masel precision film holders (Fig. 4.41)
• RinnEndoray film holder – a holder designed for taking paralleling
technique radiographs in the presence of endodontic hand
instruments (Fig. 4.42). The film holder incorporates a “basket”,
which fits over the crown of the tooth and endodontic instruments,
and on to which the patient bites lightly. The X-ray beam may be
aligned with the handle and centred through a centring ring.
 Diagnosis of endodontic problems  105

Fig. 4.38  Blooming

artifacts due to long
exposure times

Fig. 4.39  Circular

beam-aiming device
with recesses for
rectangular collimator
A

Fig. 4.40  Rinn XCP film

holders

Fig. 4.41  Masel

precision film holder

Fig. 4.37  (a–c) Digital images

 106  Diagnosis of endodontic problems
Fig. 4.42  Rinn Endoray film holder with basket Fig. 4.43  Film/sensor holder and
beam-aiming device in use
Radiation safety and regulations
The Ionizing Radiations Regulations 1999 and the Ionizing Radiation
(Medical Exposure) Regulations 2000 (IRMER) lay down requirements
for the safe use of radiation in the workplace and for the protection
of patients, staff and the general public. It is the responsibility of all
staff to be familiar with legislation relevant to them. The dangers of
excessive radiation are minimal, provided simple precautions are observed.
Four categories of personnel are identified under the IRMER 2000
regulations:
1 the referrer who requests the radiograph
2 the practitioner whose responsibility is to decide if the radiograph
can be justified
3 the operator who carries out any aspect of the exposure procedure
4 the employer (legal person) who takes responsibility for the
radiation installation and staff working within it.
In dental practice, the dental surgeon may fulfill several or all of these
roles. The most important decision any practitioner should make is whether
the use of X-rays is clinically necessary. Safety considerations of radio-
logical techniques fall into three areas:
1 the patient
2 the operator
3 the equipment.
Patients
To justify any radiograph, the risk to the patient from an X-ray exposure
must be outweighed by the benefit of the diagnostic information given by
the radiograph. The risk must be minimized by reducing the dose as far
as possible. Techniques should be used which avoid exposures passing
towards the patient’s body and gonads. Paralleling technique for periapical
radiographs is preferred for this reason. Lead aprons are no longer recom-
mended for routine dental radiography since the use of such techniques
with modern, high kilovolt equipment, rectangular collimation and fast
films produce less scatter towards the body and are more effective at reduc-
ing dose.
Exposures need to be set to the minimum exposure time possible.
Patients should not hold the film packet in position with their fingers; film
holders or forceps should be used (Fig. 4.43) and no one other than the
patient should be within the controlled area during the exposure. The
controlled area is an exclusion zone around the X-ray tube head when it
Fig. 4.44  Thermoluminescent
dosimeter
is in operation. It extends for a distance of 2 m around the tube head and
patient (for tubes operating at up to and including 70 kV) and for a distance
along the primary beam until it is attenuated by a radiopaque wall or shield
of suitable thickness.
Operators and other staff
All staff involved in dental radiography should understand the dangers of
radiation and be conversant with the precautions necessary for proper
handling of equipment and patients. Every practice should appoint a Radi-
ation Protection Supervisor (RPS) from within the dental staff to oversee
day-to-day radiation safety, and a Radiation Protection Advisor (RPA) – a
qualified medical physicist – to advise the practice on radiation protection
measures and to carry out equipment checks. Local rules relating to radia-
tion protection in the practice should be conveniently displayed. Only
people adequately trained for their role should take part in dental radiog-
raphy and no one under 16 years should be allowed to work with ionizing
radiation.
Several units are used for measuring radiation:
1 The exposure is a measure of the energy of the X-ray beam
emitted by the X-ray tube. It measures ionization per unit mass of
air and is expressed in units of coulombs per kilogram (C kg−1)
2 Radiation absorbed dose (D) is the amount of energy absorbed
from the X-ray beam per unit mass of tissue. It gives the absorbed
energy in joules/kg and is expressed in Grays (Gy) and milliGrays
(mGy)
3 The effective dose (E) is a measure that considers the relative harm
of the radiation emitted and the relative sensitivity of the tissues
exposed. This then allows doses from different investigations of
different parts of the body to be compared, by converting all doses
to an equivalent whole body dose. It is expressed in Sieverts (Sv)
and milliSieverts (mSv)
Staff exposure to radiation should be closely monitored, using
film badges or thermoluminescent dosimeters (Fig. 4.44) if an
individual’s workload exceeds 150 radiographs per week or if an
X-ray tube is relocated. Radiation dosage is reduced if the
following precautions are observed:
▸ the operator must stand outside the controlled area
▸ the operator should never hold the film, tube housing or patient
during the exposure
▸ when not in use the X-ray machine should be disconnected from
the mains to prevent inadvertent exposure
 Diagnosis of endodontic problems  107

Fig. 4.45  Simple Fig. 4.47  Paralleling

magnifying viewer technique for maxillary
central incisors

Fig. 4.48  Digital image of maxillary

central incisors using paralleling
Fig. 4.46  Mount for
technique
radiographs

▸ an exposure warning display should light up outside a door,

during exposure, if the door may be opened directly into the
controlled area during radiography Fig. 4.49  Parallel image

▸ in the case of an accidental overexposure, the incident should be of maxillary posterior

teeth
reported to the Health & Safety Executive and records kept for
50 years.

Viewing and storage equipment

Viewers
The greatest amount of diagnostic information is gained when a radiograph
is viewed under magnification on a clean viewing box and masked to
exclude extraneous light. A simple viewer that magnifies the image and
cuts out glare is illustrated in Figure 4.45.

Mounts
Radiographs should be named, dated and filed systematically. They may
be stored in the patient’s clinical records but should ideally be mounted to
protect the film during examination, storage or referral. It is usual to place
radiographs in labelled pouches or to laminate them between two sheets
of acetate (Fig. 4.46), either by stapling the sheets together using adhesive
transparent “sticky-back plastic” or by using a heat-sealing laminating
machine.
Radiographic techniques
Paralleling periapical projections
The ideal imaging geometry for a radiograph would place the object and
film close together, with their long axes parallel. The X-ray beam would
then be directed at 90° to the long axes of these two structures. It is rarely
possible to achieve this ideal positioning in the mouth, except in the lower
molar area, but it is usually possible to align the tooth parallel with the
film with a small separating distance. A separation of object and film
creates magnification of the object, but this is overcome in the paralleling
technique by the use of a longer focal spot to object distance (ffd), creating
a more parallel beam.
A film holder with a beam-aiming device is necessary to support the
film upright in the mouth and to ensure accurate alignment of the colli-
mated beam. Figure 4.47 shows a paralleling periapical radiograph of the
central incisors being taken using a Rinn film/sensor holder and localizing
ring. The resultant digital radiographic image is also shown (Fig. 4.48).
The advantages of paralleling technique are:
• greater geometric accuracy (e.g. Fig. 4.49)
• reproducibility
• fewer retakes (films held securely and technique less prone to
errors)
 108  Diagnosis of endodontic problems
Fig. 4.50  Parallel image of maxillary molar roots Fig. 4.51  Use of forceps to position intraoral film
(see Fig. 4.55 for bisecting angle view)
Fig. 4.53  Bisecting angle periapical projection of Fig. 4.54  Image produced by
maxillary central incisors misplaced film in bisecting angle
technique
• lower radiation dose (beam not directed towards the body trunk,
finger not holding film and, therefore, not irradiated, use of high
kilovolt modern machines)
• superior images of maxillary molar roots (zygomatic buttress
projected above the molar apices (Fig. 4.50)
• superior image of bone margins
• superior images of interproximal regions (the positioning is closer
to that of bitewings, therefore interproximal caries may be
assessed).
Inevitably, this technique has some limitations, being more difficult to
achieve ideal positioning in patients with shallow palates, with a pro-
nounced gag reflex or with rubber dam in place. Alternatives involve the
use of forceps (Fig. 4.51).
Bisecting angle periapical projections
In this technique, the film is placed against the tooth and the angle between
the long axis of tooth and film is visualized and bisected. The X-ray beam
is centred on the apex of the tooth, transecting the bisecting line at 90°
(Fig. 4.52). In the lower molar region, the film and tooth may be almost
parallel but, in the upper anterior regions, a considerable angle may result
between the tooth and the film causing a pronounced angulation of the
beam downwards towards the body (Fig. 4.53).
The bisecting angle technique may be performed without film/sensor
holders (although the patient must then hold the film with forceps), is quick
Fig. 4.52  Principle of the bisecting
angle periapical projection
Fig. 4.55  Superimposition of the zygomatic arch
in bisecting angle technique (see Fig. 4.50 for
parallel view)
and easy to use with rubber dam in place and is relatively comfortable for
all patients, even those with small mouths. It is, however, difficult to avoid
distortion and an accurate image can never be guaranteed. Other faults
such as displaced or bent films and “cone cutting” are more likely than
with film/sensor holders (Fig. 4.54). Anatomical structures such as the
zygomatic arch are frequently superimposed over the apices of the upper
posterior teeth and the relationship between roots, other anatomical struc-
tures and alveolar bone may be distorted (Fig. 4.55). It is also difficult to
reproduce a periapical view for review and recall purposes.
Parallax techniques
Horizontal and vertical parallax techniques are most useful in endodontics
in the diagnostic and treatment phases. The principle works on the basis
that a set of objects distributed in three-dimensional space, although having
fixed and unique relative relationships, will appear to have altered relative
relationships depending on the viewing perspective. As an analogy, when
driving along a highway through countryside, trees closer to the highway
“move” in the opposite direction of travel, while those in the distance
appear to “move” in the same direction of travel. Applied to X-ray images,
if two images are obtained from two different horizontal angles, the appar-
ent shift in position of an object (relative to a reference object) in the
opposite direction to the X-ray tube signifies that it is closer to the tube
(i.e. on the buccal aspect), while an object exhibiting an apparent shift in
position in the same direction, will be further away from the tube (i.e. on
 Diagnosis of endodontic problems  109

Fig. 4.56  Horizontal parallax used to Fig. 4.57  Horizontal parallax used to Fig. 4.58  Horizontal parallax used to Fig. 4.59  Horizontal parallax used to
identify perforated post and post identify perforated post and post identify perforated post and post identify perforated post and post
preparation preparation preparation preparation

Fig. 4.62  Vertical

parallax used to
improve imaging of
palatal root of maxillary
molar

Fig. 4.63  Vertical

parallax used to
improve imaging of
Fig. 4.60  Horizontal parallax used to Fig. 4.61  Horizontal parallax used to
palatal root of maxillary
identify perforated post and post identify perforated post and post
molar
preparation preparation

the lingual aspect). This principle is enshrined in the SLOB rule, which
stands for “Same Lingual, Opposite Buccal”. Horizontal parallax can be
used to indicate the position of intradental structures in relation to the
external surface of the tooth. This is very useful in the identification of
location of perforations (Figs 4.56–4.61). Both horizontal and vertical
parallax can be used to good effect selectively to image individual roots
of a multirooted tooth (Figs 4.62, 4.63).

computer will reformat the data-slices of the patient to obtain three-

CONE-BEAM COMPUTED TOMOGRAPHY (CBCT)
The two-dimensional radiograph has many limitations when considering
the diagnostic possibilities. This is mainly because the surrounding
anatomy is superimposed, generating “noise” in the region of interest. This
problem can be overcome by a computed tomographic scan of the region.
In traditional CT, a gantry containing a rotating X-ray tubehead projects a
narrow collimated fan-shaped beam onto an array of detectors. The patient
is slowly advanced through the circular aperture in the centre of the gantry
while the tubehead and reciprocal detectors rotate around the patient. The
dimensional and multiplanar images. The high cost and high effective dose
are the most important factors leading to a slow uptake of CT scans in
endodontics until the development of the cone-beam CT (CBCT), which
is an alternative 3D X-radiation imaging technique. In a CBCT machine
(Fig. 4.64), an X-ray source projects a cone-shaped beam, hence the name
cone-beam CT, onto a flat image receptor. The receptor can be an image
intensifier in combination with a digital camera system or it can be a digital
detector. The combination of the (usually) pulsed X-ray source and the
reciprocal detector results in up to 600 images in one rotation of 180° or
 110  Diagnosis of endodontic problems
Fig. 4.64  The principle of the CBCT is a cone- Fig. 4.65  The CBCT dataset is reconstructed to images that can be viewed in different planes: axial,
shaped beam projecting X-ray source and a sagittal and coronal (courtesy of Dr WJ van der Meer)
reciprocal image receptor that rotates once around
the head of the patient (courtesy of Dr WJ van der
Meer)
Fig. 4.66  The CBCT machines are available for scanning lying down, standing up or sitting down
(courtesy of Dr WJ van der Meer)
360°. The computer reconstructs these images to a 3D volume (Fig. 4.65).
Algorithms for this reconstruction have been available since the 1980s,
but the computer power of commercially available computers at that
time was insufficient for these kinds of calculations. At present, the recon-
struction of up to 600 exposures to the corresponding images in three
orthogonal planes (axial, sagittal and coronal) only takes a couple of
minutes. The CBCT machines are available for scanning patients lying
down, as in traditional CT scanners but also for scanning patients sitting
down or standing up (Fig. 4.66). The machines also differ in the size of
the field of view (FOV) and the options for adjusting this FOV (Fig. 4.67).
As a rule of thumb, it can be stated that the larger the FOV (and thus the
sensor), the higher the price of the machine. For endodontic diagnostic
purposes, a small FOV equivalent to the size of several teeth, is usually
sufficient.
The effective dose for a patient is determined by the X-ray source
(continuous or pulsed), the kilovoltage and amperage used, the amount of
filtering, the FOV and the resolution needed for the dataset (Table 4.12).
Higher resolution images will require more images and, therefore, a longer
exposure time. The disadvantage of higher resolution exposures is not only
the higher effective dose for the patient but also the extended rotation time.
A longer scanning time will increase the chances of motion artefacts due
Fig. 4.67  For endodontic purposes a small FOV
is usually required. Even though many CBCT
machines are able to reduce their FOV in a vertical
direction (B), a machine that is also able to reduce
the FOV in a horizontal direction (C) will greatly
reduce the effective dose for the patient. These
machines are best suited for endodontic
diagnostics (courtesy of Dr WJ van der Meer)
to movements of the patient during the scan. Ideally, a scan should be
acquired with a high resolution, a short scan time with a low effective dose
for the patient. As some of these factors impose conflicting requirements,
a balance needs to be found between the parameters. For endodontic diag-
nosis, a small FOV should suffice, reducing the effective dose and the
anatomical area to be examined. The importance of this lies in the fact that
the clinician is responsible for the dataset, including anatomy outside the
oral cavity. This implies the need to ensure correct reporting from a quali-
fied radiologist on such radiographic data.
When comparing the CBCT datasets with traditional 2D radiographs,
the CBCT datasets reveal 38% more periapical lesions than traditional
radiographs. When comparing measurements made on traditional radio-
graphs and CBCT datasets the latter seem to be more accurate and the
errors seem to be small and clinically insignificant.
The UK Health Protection Agency’s Radiation Protection Division
(2009) and the Joint Position Statement of the American Association
 Diagnosis of endodontic problems  111

Table 4.12  Dental cone-beam CT machines

Model Field of view (mm) Voxel size (mm) Scan time (s) Reconstruction time kV Effective dose (microSv)
Ewoo (Vatech)Pax Uni3D 50 × 50 0.2 8 18 s 50–90 25–60
(2 models) 80 × 50 mm 17.5–20 25 s
Ewoo (Vatech)PaX Duo3D 50 × 50 to 120 × 85 0.12–0.2 15–24 32–59 s 50–90 25–60
Ewoo (Vatech) PaX Reve3DS 50 × 50 to 150 × 150 0.12–0.25 15–24 27–105 s 50–90 25–-60
Ewoo (Vatech) PaX Zenith3D 50 × 50 to 240 × 190 0.08–0.3 15–24 10–221 s 50–120 25–60
Ewoo (Vatech) Master3DS 160 × 70 0.2–0.25 15–24 9–51 s 50–90 25–60
240 × 190
Ewoo (Vatech )PicassoTrio 120 × 70 0.2 15–24 25 s 50–90 25–60
Gendex/KaVo/Icat 130 × 170 0.12–0.40 5, 8, 9 of 25 120 s 96–120 68
Illuma 140 × 180 0.09–0.40 20–40 2–4 min 120 58–300
Kodak 9000 3D 50 × 37 0.076–0.200 13.9 <2 min 60–90 Not available
Kodak 9500 90 × 150 0.200 2 min 60–90 Not available
184 × 206
Morita 3D Accuitomo170 40 × 40 0.080,0.125 5.4–30.8 1–4 min 60–90 22 (40 × 40);
170 × 120 0.160, 51 (60 × 60)
0.250
Morita Veraview epocs3De 40 × 40 0.125 9.4 4 min 60–90 30 (40 × 40)
40 × 80
Morita Veraview epocs3D 40 × 40 0.125 9.4 4 min 60–-90 30 (40 × 40)
40 × 80
Newtom 5G 60 × 60 to 18 × 16 0.075– 0.3 18–36 Less than 1 min 110 Not available yet
Newtom VG 150 × 110 0.3 18 Less than 1 min 95 50–100
Newtom VGi 120 × 75 to 150 × 150cm 0.15–0.30 18 Less than 1 min 110 50–100
PlanmecaProMax3D 80 × 80 to 40 × 50 0.160 × 0.160 × 0.160– 18 30–150 s 84 50–80
0.320 × 0.320 × 0.320 µm
Planmeca Proma x3DMAX 50 × 55 to 220 × 170 0.100 × 0.100 × 0.100– 18–30 30–150 s 96 50–80
0.400 × 0.400 × 0.400
Planmeca Promax3DS 50 × 50 to 50 × 80 0.100 × 100 × 100– 18 30–150 s 84 50–80
0.200 ×0.200 × 0.200
Scanora 3D 60 × 60 to- 0.133 3–6wer-kelijke 1–2in 60–85 29–38
130 × 145 0.35 best ra-ting)
Sirona Galileos Comfort 150 (spherical diameter) 0.15–0.30 14/2–6 2.5–4.5 min 85 70*
Sirona Galileos Compact 150 × 120 (ellipsoid) 0.15–0.30 14/2–6 4.5 min 85 45*

cases of contradictory or non-specific signs and symptoms, the assessment

Table 4.13  Effective patient dose (µSv) of intraoral radiograph, dental
of root resorption and, possibly, the diagnosis of dentoalveolar trauma.
panoramic tomograph and CBCT

Effective patient dose (µSv) QUALITY ASSURANCE

Dental intraoral radiograph 10–20 Good quality radiographs are required for accurate diagnosis. If high
Dental panoramic tomograph 246
standards of image quality are to be maintained and radiation dose to
CBCT with small field of view (6″) 487–6527
the patient minimized, a quality assurance programme for radiography is
CBCT with large field of view (12″) 687–10737
essential and is mandatory under UK legislation. Such a programme is
composed of:

• written procedures for the acquisition and processing of

of Endodontists and the American Academy of Oral and Maxillofacial
Radiology (2011) made the following recommendations for the use of
CBCT in dentistry:
• CBCT should not be used when other lower dose forms of
radiographs can provide adequate diagnostic information
(Table 4.13)
• use of CBCT must be properly justified
the
• for endodontics, limited volume is preferred over large volume
CBCT.
CBCT is an indispensable diagnostic tool for endodontics, but should
be limited to those cases where traditional radiographs provide insufficient
information. The endodontic indications for using CBCT are preparation
of endodontic surgery, diagnosis and treatment planning of teeth with
unusual anatomy, anatomic superimposition unresolved with 2D imaging,
radiographs
• system of quality-control measures which are carried out at
a
regular, predetermined intervals
• systems for the monitoring and audit of image quality in order to
identify errors and enable their correction.
This requirement is applicable to both conventional and digital radiog-
raphy. An important aspect of quality assurance is the identification of film
faults – these must be recognized and understood in order to correct the
error. The reader is referred to a specialist textbook for details.
INTERPRETATION OF RADIOGRAPHS
The interpretation of radiographs should be approached in a logical fashion
in order to avoid mistaking an artefact or area of normal anatomy for
an abnormality. The operator should be familiar with the radiographic
 112  Diagnosis of endodontic problems

Fig. 4.69  Appearance

of large maxillary
Enamel Metallic
restoration antrum
Dentine 'Burnout'

Pulp Root
chamber canal
Cancellous
Lamina bone
dura
Periodontal
Periradicular ligament
radiolucency space

Fig. 4.68  Radiographic appearance of posterior teeth Nasal fossa

Nasal septum
Anterior nasal spine
appearances of normal anatomical structures before attempting to identify Incisive foramen
abnormalities. Periodontal ligament space
Root canal
NORMAL RADIOGRAPHIC LANDMARKS Lamina dura
Median suture
Enamel, dentine and cementum
Enamel is the most radiopaque structure in the mouth. Dentine is darker Outline of the nose
and has a uniform density. Cementum cannot be distinguished from
Anterior restorations
dentine. Radiographic “burn out” occurs in the cervical region, between
the cement–enamel junction and the alveolar crest, and may be confused
with root caries or secondary caries beneath a mesial or distal box
(Fig. 4.68).
Fig. 4.70  Radiographic appearance of anterior maxillary region
Cancellous bone
The trabeculae have a coarser pattern in the mandible than in the maxilla, Fig. 4.71  False
widening of the PDL
where they are slightly denser, finer and more lace-like.
space in mandibular
Periodontal ligament second molar –
evidence of presence of
This appears as a narrow, even radiolucent line around the root surface. It periradicular lesion on
is also referred to as the periodontal ligament (PDL) space. Genuine wid- distal root of the first
ening of this space is indicative of apical pathosis. This feature is critical molar
in assessing the presence of disease related to an infected pulp.

Lamina dura
This is the name given to the white line forming the lining of the tooth
socket seen on radiographs and represents the margin of the socket. This
feature is less critical than the PDL space in determining the presence of
apical pathosis.

Pulp space COMMON ERRORS IN INTERPRETATION

The pulp chamber and larger root canals are usually readily visible on the
radiograph, but finer canals are more difficult to see. Root canals that
appear to be completely sclerosed rarely are. Stones are common in the
pulp and present as a problem only when they obliterate root canals.
Maxillary antrum
This may extend from the premolar region in the maxilla to the tuberosity.
The floor of the antrum may be closely associated with the roots of the
premolar and molar teeth and may dip between the roots (Fig. 4.69). The
floor of the antrum appears as a white cortical line and should be carefully
traced to check continuity when possible periapical change is suspected.
The anterior maxillary region
Figure 4.70 identifies common landmarks in this region.
False widening of the periodontal ligament space
The dark appearance of the periodontal ligament space may become more
pronounced when an air space (such as the maxillary antrum) or other
radiolucency is superimposed on it, giving the erroneous impression of
widening of this space (Fig. 4.71). Similarly, the white line of the lamina
dura may appear less opaque when an air space or other radiolucency is
superimposed on it (Fig. 4.72) making it less visible and increasing the
impression of breakdown of normal anatomical features at the apex. Thus,
apical pathosis may be suggested when a radiolucent area is superimposed
over a normal apex.
The maxillary antrum
The margin of the maxillary antrum may appear loculated and take on the
appearance of a cyst (Fig. 4.73).
 Diagnosis of endodontic problems  113

Fig. 4.72  Superimposed incisive Fig. 4.73  Large maxillary antrum, which may be Fig. 4.74  Maxillary lateral incisor
canal cyst giving impression of loss confused with a cyst with a periradicular lesion – maxillary
of lamina dura around the apex of a central incisor with superimposed
maxillary incisor incisive canal

Fig. 4.75  Inferior dental canal, which may be Fig. 4.76  Radiographic appearance of a mental Fig. 4.77  Inferior dental canal and
confused with periradicular lesion foramen mental foramen, which might be
confused with periradicular lesion

Incisive foramen
This circular or oval radiolucent shadow of the incisive foramen may be
superimposed over the apex of a central incisor and be mistaken for a
periapical lesion (Fig. 4.74).
Inferior dental canal
The mandibular or inferior dental canal runs from the mandibular foramen
on the medial aspect of the ascending ramus of the mandible to the mental
foramen in the premolar region. It is seen as a radiolucent band that may
be close to or coincident with the roots of the lower molar and premolar
teeth. Here it may be mistaken for a lesion (Fig. 4.75).
Mental foramen
The mental foramen is situated below and distal to the apex of the man-
dibular first premolar (Fig. 4.76). Occasionally, the angulation of a periapi-
cal radiograph may result in superimposition of the structure on the apex
of one of the premolars. The foramen may then be confused with a per-
iradicular lesion (Fig. 4.77).
 114  Diagnosis of endodontic problems
LESIONS INVOLVING THE PERIODONTAL
LIGAMENT SPACE
Periradicular lesions
These are the most common apical radiolucencies. Long-standing lesions
and those from a chronic inflammatory process are usually well defined
(Fig. 4.78) and may even develop a radiopaque margin of reactive bone
(Fig. 4.79). Early lesions are identified by thickening of the periodontal
ligament space (Fig. 4.80) – these can progress to discrete areas of radi-
olucency (Fig. 4.81) and may, at a later stage, become larger and more
diffuse in appearance (Fig. 4.82).
Lateral periradicular lesions
Widening of the periodontal ligament space and formation of radiolucen-
cies unrelated to the apex (Fig. 4.83) are associated with infection within
the lateral canals. These canals may become visible only after canal obtura-
tion (Fig. 4.84).
FRACTURED ROOT LESIONS
Radiolucencies associated with the pathosis around cracked roots are often
widespread along the involved root (Fig. 4.85). The ability to determine
the presence of a crack will depend upon the plane of the fracture in
Fig. 4.78  Maxillary lateral incisor Fig. 4.79  Mandibular molar with periradicular
with well-defined periradicular lesion lesion with radiopaque margin
Fig. 4.81  Discrete periapical radiolucency Fig. 4.82  Mandibular molar with large diffuse
periradicular radiolucency
relation to the main X-ray beam (Fig. 4.86). If the beam does not pass
through the fracture, it may well remain undetected.
PERFORATION LESIONS
Perforations (Fig. 4.87a) can lead to rapid bone loss, the diffuse appearance
of the radiolucency reflecting the more acute inflammatory process initi-
ated. The presence of a post-retained restoration in a tooth with a large
diffuse lesion involving more than just the apical region should arouse
suspicion of a perforation or fracture (Fig. 4.87b).
SCLEROSING OSTEITIS
This appears as a zone of peripheral radiopacity (Fig. 4.88) and is indica-
tive of a long-standing, low-grade apical infection, which gives rise to a
circumscribed proliferation of the periapical bone. It is usually related to
a pulp that is in the process of degeneration. The condition is often
symptomless.
LESIONS NOT OF INTRAPULPAL ORIGIN
It is important to be able to distinguish lesions of endodontic origin from
those arising from other disease processes.
Periodontal lesions
Periodontal lesions within bone can give rise to radiographic changes,
which can be confused with periradicular areas (Fig. 4.89). The teeth
involved usually remain vital despite the bone loss.
Fig. 4.80  Periodontally involved maxillary molar
with widening of the periodontal ligament space
of the mesiobuccal root
Fig. 4.83  Central incisor with lateral
periradicular radiolucency

Fig. 4.84  Central incisor with
obturated lateral canal
Fig. 4.87  (a) Maxillary second premolar with
root perforation; (b) extracted perforated second
premolar
Fig. 4.85  Diffuse radiolucency
related to fractured maxillary incisor
B
Fig. 4.89  Periodontal
lesion associated with
mandibular molar
Diagnosis of endodontic problems  115
Fig. 4.86  Maxillary central incisor
with horizontal root fracture
Fig. 4.88  Sclerosing osteitis related to the mesial
root of a mandibular first molar
Idiopathic osteosclerosis
Areas of dense bone may frequently be encountered within the trabecular
spaces and may represent a developmental anomaly or, occasionally, a
compensatory response to abnormal stress. The radiographic appearance
may closely resemble that of sclerosing osteitis. However, the tooth reacts
normally to vitality testing (Fig. 4.90).
Fibro-cemento-osseous dysplasia
Fibro-cemento-osseous lesions present in their early stages as radiolucent
areas, commonly in relation to the apices of the mandibular incisors known
here as periapical fibro-cemento-osseous dysplasia (Fig. 4.91). These
lesions mature over a 5- to 10-year period with gradual infill of dense
cemento-osseous material to create radiopacities. The teeth remain vital
and endodontic treatment is not required.
 116  Diagnosis of endodontic problems
Fig. 4.90  Dense bony trabecular Fig. 4.91  Fibro-cemento-osseous-dysplasia related
pattern around the roots of vital to a mandibular molar
teeth
Other local and systemic pathosis
Many inflammatory, cystic and neoplastic lesions may arise in the jaws
which are not of endodontic origin (Fig. 4.92). These are capable of
destroying or remodelling neighbouring bone and of displacing or resorb-
ing teeth. In many cases, the teeth remain vital if the lesion originates
outside the periodontium. The clinician should always be alert to the pos-
sibility of non-dental causes of bone destruction.
The origin of such lesions may be divided into:
• infections (localized and spreading)
• trauma
• cysts (odontogenic and non-odontogenic)
• tumours (benign and malignant)
• giant cell lesions
• fibro-cemento-osseous lesions
• metabolic and endocrine lesions
• idiopathic lesions.
DIAGNOSTIC CATEGORIES
Once the patient has been assessed, the information from the history, clini-
cal examination and tests is integrated into an overall decision about the
nature of the problem. The main diagnostic categories with their classical
presentation features are described below. It is important to bear in mind
that these descriptions represent the central and commonly presenting
findings; the actual presentation may vary.
NORMAL PULP
This will be asymptomatic and give only a mild, transitory response to
stimulation with thermal or electrical tests. Percussion and palpation do
not cause pain. Radiographs show a definite pulp chamber and canal which
will be smaller and narrower in the older patient. The width of the peri-
odontal ligament is normal, with no evidence of resorption.
Dentinal pain may be experienced when the dentine is exposed to the
oral cavity, with thermal changes or exposure to sweet food or drink. The
pulp is not normally affected.
CONCUSSED PULP
The pulp may be concussed following trauma to the tooth and may not
respond to thermal or electrical stimulation for a period of weeks or
Fig. 4.92  Extensive radiolucency produced by a
lesion of non-endodontic origin
months. The tooth should be checked at regular intervals until the pulp
tests return to normal; root-canal treatment should only be considered in
conjunction with a second sign of pulp necrosis and infection, namely,
periapical change.
REVERSIBLE PULPITIS
Hot or cold stimuli will cause a quick sharp pain, which may linger for
seconds after the stimulus is removed as a dull aching sensation. The pain
does not radiate and the tooth is otherwise symptomless. The radiograph
shows no periapical radiolucency.
IRREVERSIBLE PULPITIS
The pain encountered in this condition may vary – from none to spontane-
ous intermittent paroxysms or continuous pain; it has an aching, throbbing
quality and may radiate from the maxilla to the mandible or vice versa.
Pain commonly occurs at night, when it may be worse than during the day
because lying down increases the intrapulpal pressure; the pain will typi-
cally disturb sleep. The throbbing is due to a hyperalgesic or allodynic
neural response, which is intermittently stimulated by the rise and fall in
vascular and tissue pressure, synchronous with the heart beat. In the early
stages, the patient is unable to locate the affected tooth but, as pulpal
inflammation spreads and toxins pass out through the apical foramen, the
tooth may become painful to touch. Involvement of Aβ nerve fibres may
also begin to localize the pain. Application of heat or cold will generally
start the pain, which gradually increases in intensity and severity, then
slowly dies away and may last for a few minutes up to several hours. Pain
will typically be worse with hot than cold stimuli, in fact, as the pulpitis
becomes advanced, cold stimuli may begin to relieve the pain. Radio-
graphs will show changes associated with the root apex when the pulpitis
is advanced enough to make the transition to incipient apical periodontitis;
occasionally apical rarefaction will occur at an earlier stage during pulpitis,
particularly in younger patients. Figure 4.93 shows a mandibular first
molar with coronal caries. The patient was experiencing episodes of pain
particularly at night and the tooth was tender. There is a widened periodon-
tal ligament space around both the mesial and distal roots. There is a halo
of condensing osteitis around the distal root.
PULPAL NECROSIS
Necrosis may occur following irreversible pulpitis or as a result of trauma
disrupting the blood supply to the pulp. Thermal and electrical pulp testing
 Diagnosis of endodontic problems  117

Fig. 4.93  Irreversible pulpitis of mandibular first Fig. 4.94  Mandibular second molar with well- Fig. 4.95  Posterior abutment to a bridge with
molar showing a widened periodontal ligament defined periradicular area early radiographic changes
space around both apices

Fig. 4.98  Pulp extirpated and canals

prepared

Fig. 4.96  Bridge removed showing Fig. 4.97  Carious exposure with
gross caries hyperaemic pulp

will produce no response although, in a posterior tooth, the pulp tissue in

more than one of the canals may be vital, which makes tests inconclusive.
In most cases, a radiograph will show periapical changes. In Figure 4.94
a periapical radiolucent area is evident around the apical portion of the
root of the distal molar. When pulpal disease has spread to the periradicular
tissue, the tooth frequently responds to palpation and percussion.

ACUTE PERIAPICAL INFLAMMATION

Acute inflammation of the periodontal ligament may be due to an exten-
sion of pulpal disease, trauma, a high restoration or endodontic treatment
that has inadvertently been extended beyond the apical foramen. If the
inflammation is caused by trauma, the pulp may remain vital. The tooth is
very tender to touch. Radiographic change will be minimal, but may show A B
slight widening of the periodontal ligament. Figure 4.95 shows the poste-
rior abutment tooth to a bridge, which had become decemented and carious Fig. 4.99  (a) Patient with swelling and pyrexia; (b) patient one week later
(Fig. 4.96); the pulp was still vital (Fig. 4.97). The pulp was extirpated
and root canals prepared (Fig. 4.98).
inflammation. A chronic lesion may flare up into an acute apical abscess
ACUTE APICAL ABSCESS – in such cases, there will be periapical rarefaction.

An acute apical abscess implies the presence of purulent exudate around

the apex. The tooth is extremely tender to touch and palpation of the
overlying gingiva painful. Swelling develops in the later stages and the
tooth becomes mobile. Pain usually abates when the swelling appears. In
severe cases, the patient is febrile. The patient in Figure 4.99a has swelling
and pyrexia, which has disappeared a week later following treatment (Fig.
4.99b). Radiographically, the appearance is similar to acute periapical
CHRONIC APICAL PERIODONTITIS
This is a long-standing asymptomatic inflammation around the root apex.
From time to time, the patient may become aware of the tooth. Radiolu-
cency is apparent, although this varies from a widened periodontal liga-
ment to a large area (Fig. 4.100). There may be evidence of a sinus tract
in the suppurative variant. The pulp will be non-vital.
 118  Diagnosis of endodontic problems
A B
Fig. 4.101  (a,b) The maxillary first molar with a crack was
associated with severe pain on biting, which was
subsequently resolved and replaced by apical and periodontal
ligament pain
Fig. 4.100  Lateral incisor with large
periapical radiolucency
RESORPTION
Internal
Internal resorption occurs as a result of chronic pulpitis. The tooth is
usually symptomless. Diagnosis is made by the appearance of a smooth
widening of the pulp on the radiograph. Root-canal treatment should be
carried out without delay.
External
External resorption may present in several forms. It is important to identify
the type of resorption so that appropriate treatment may be given. The
main difficulty is in differentiating between internal and external resorp-
tion. Radiographs are invaluable in the diagnosis (see Chapter 11).
CRACKED OR FRACTURED TEETH
The obvious cause of cracked or fractured teeth is trauma but both restored
and unrestored teeth with no history of trauma may fracture due to chronic
fatigue failure due to parafunction. The incidence of tooth fracture is
highest in the second mandibular molar, usually in the sagittal plane.
Fractures can be difficult to diagnose and, because both the pulp and the
periodontium may be affected, the range of symptoms is wide.
Fractured crown with vital pulp (cracked tooth syndrome)
This condition can present in a range of different ways, hence the designa-
tion of the term “syndrome”. It is commonly associated with a non-
localized or localized pain associated with eating, often but not always,
hard foods. There may be a history of trauma due to biting on a hard food
or object but more often the patient cannot remember any traumatic inci-
dent. The severity of the symptoms usually depends on the extent of the
crack and degree of pulp involvement. At the early stages, there will be
dentinal pain with cold and hot stimuli, as well as with sweet and sour
liquids. The character of the pain on biting will be similar to the dentinal
pain. The crack is almost always extremely difficult to locate or identify
as it will not yet be stained. A classical pathognomonic sign is pain on
Fig. 4.102  Root fracture affecting
the mesiobuccal root of the maxillary
right first molar
biting or release from biting on a hard or viscoelastic material. As the crack
propagates and involves the pulp to a greater extent, the pain on stimula-
tion and biting will linger as a dull aching sensation as pulpitis sets in.
Establishment of irreversible pulpitis will then become superimposed upon
a severe pain on biting, the tooth will be easily localized. At a later stage
still, the pulpal pain will abate to be replaced by apical and periodontal
ligament pain. The pain on cold and hot stimuli will have disappeared and
the pain on biting will now have a dull character in contrast to the sharp
dentinal character at the outset. The pulp will stop responding to sensitivity
tests at this stage and by now the crack may be visible due to staining
(Fig. 4.101).
Fractured crown with non-vital pulp
This may be asymptomatic or may cause mild intermittent pain of a dull
nature on chewing.
Fractured crown and root with a non-vital pulp
The fracture is usually long-standing and is easier to locate than in the
case of vital pulp for two reasons: (1) the fracture line will have become
stained and will show up with fibreoptic light; and (2) the pain will be due
mainly to stimulation of the periodontal ligament as the fractured parts
move during mastication. The pain may be due to localized inflammation
of the periodontal ligament, which may become allodynic; this means that
it may respond to hot or cold fluids percolating into the crack but the
character of the pain is different from the dentinal-like pain in the case of
a tooth with a vital pulp.
Fractured root with a vital or non-vital pulp
The patient will complain of a nondescript pain on biting; the fracture may
not be obvious radiographically. In vital teeth, the cause of the fracture is
parafunction; it is not uncommon in Chinese populations. In non-vital
teeth, the fracture may start from the apex of the root and be associated
with a root-filling procedure, probably due to excessive use of force during
treatment (Fig. 4.102).
PERIODONTAL PAIN
Although it is traditionally regarded that marginal periodontal diseases are
due to chronic inflammation and are pain-free, patients can and do present
with mild, vague dull aching sensations from teeth with periodontal
disease, which abates with good oral hygiene and reduction in inflamma-
tion. The presentation is very characteristic and is often described as

feeling like an itch or irritation around the tooth, which is relieved by
pressure.
Acute periodontal conditions can also cause more severe and character-
istic pains but, as these have become less common, they are more easily
midiagnosed.
NON-ODONTOGENIC PAIN
The dentist’s role is to be familiar with and identify causes of dental pain
but they must be familiar with and vigilant in detecting pain that is not
of dental origin. Patients will often display tell-tale signs of uncharac­
teristic presentations. The problem is as prevalent as 12% of patients
referred to a tertiary referral centre and so is dealt with in greater detail in
Chapter 16.
Diagnosis of endodontic problems  119
FURTHER READING
American Association of Endodontists; American Academy of Oral and Maxillofacial
Radiology, 2011. Use of cone-beam computed tomography in endodontics Joint
Position Statement of the American Association of Endodontists and the American
Academy of Oral and Maxillofacial Radiology. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 111 (2), 234–237.
Dummer, P.M., Hicks, R., Huws, D., 1980. Clinical signs and symptoms in pulp disease.
Int Endod J 13 (1), 27–35.
Holroyd, J.R., Gulson, A.D., 2009. The radiation protection implicationsof the use of
cone beam computed tomography (CBCT) in dentistry – what you need to know.
Health Protection Agency, Centre for Radiation, Chemical and Environmental
Hazards, Radiation Protection Division, Didcot.
Seltzer, S., Bender, I.B., Ziontz, M., 1963. The dynamics of pulp inflammation:
correlations between diagnostic data and actual histologic findings in the pulp. Oral
Surg Oral Med Oral Pathol 16, 846–871, 969–977.
Whaites, E., 2007. Essentials of dental radiography and radiology, 4th ed. Churchill
Livingstone.
 5
Section 2  Preparation for delivery of endodontic treatment
Treatment planning
  K Gulabivala, Y-L Ng
OVERALL HEALTH AND ORAL CARE OF PATIENTS AND
THE ROLE OF ENDODONTICS WITHIN IT
Dentistry may be viewed as a speciality of medicine, yet it is itself a
diverse and broad discipline. Dentists are trained to recognize the majority
of commonly presenting oral problems and to manage them appropriately
through a process of selecting the right course of treatment for each patient.
Many dental or oral problems may be managed in different ways depend-
ing on the judgement about the presence, progression and morbidity of the
disease, the options available for management and the needs of the patient.
The dentist will have been trained, by necessity, to recognize only the
commonly presenting tendencies in each disease. Further personal experi-
ence and development may lead to recognition of rarer presentations as
well. The typical pattern of clinical behaviour in the primary care (practice)
setting is that recognition of a problem will lead to the triggering of a set
treatment protocol. Such treatment patterns, based on clinical rationale but
also shaped and influenced by business and management needs may lead
to the passive application of heuristic principles to select treatment. On
the whole, this approach probably works when preceded by active learning
through assessment of personal outcomes over a lengthy period. However,
the recognition and management of the full spectrum of complex oral and
dental problems requires an approach based on deeper understanding of
the problem and a higher level of engagement of cognitive, technical and
clinical skills, acquired through specific advanced training. The breadth of
complex restorative problems has increased in modern populations because
of better general health and longer survival of people and their teeth.
Surviving teeth are more ravaged by repair of disease and wear and tear.
The restorative challenges posed coupled with the desire of people to
retain functional and aesthetic dentitions into later life have driven the
development of the restorative subspecialities of endodontics, periodontics
and prosthodontics into ever more complex scenarios. The opportunities
of specialization have allowed clinicians to develop their skills and
knowledge in a restricted area of practice to a much higher level, but
usually to the exclusion of other generalist skills. Conscientious general
dental practitioners in many countries are, therefore, faced with the pros-
pect of making a judgement about their own knowledge and skill limitation
in the context of what a colleague with specialist status may achieve. Ideo-
logical, philosophical, financial, medico-legal and indemnity frameworks
have, therefore guided the development of a referral culture for specific
items of care. This does, however, mean that the onus of ensuring the
coordinated and appropriate delivery of whole mouth and patient care rests
with the referring general dental practitioner, in conjunction with other
specialists and the medical practitioner where necessary. Honest and criti-
cal recognition of personal limitation is a key aspect of any governance
structure that enables either further appropriate personal development or
referral.
Conversely, the knowledge and skills of endodontics must be deployed
judiciously to ensure that the patient receives appropriate care, meaning
that the specialist must also understand the broader context within which
their expertise is exercised. In simple terms, this means that the dentist
should be well versed in all aspects of dentistry, understanding the role of
each aspect in overall patient management, as well as being aware of
potential overlaps and interactions between the subdisciplines. In the
context of a healthcare profession, the “endodontist” must, therefore be a
human being first, dentist second and endodontist last (Fig. 5.1).
© 2014 Elsevier Ltd. All rights reserved.
The general dental practitioner with a special interest in endodontics
will have the advantage that they will grasp both the broader aspects of
the patients’ needs, as well as be able to deliver a higher level of care in
endodontics, albeit perhaps not at a specialist level. The foregoing also
means that a dentist uncomfortable with the practice of dentistry and
seeking escape into a limited area of practice because it is their area of
greatest comfort will seldom make the rounded clinician that a good endo-
dontist should be.
The underlying rule in the appropriate utilization and coordination
of the proliferating specialisms is effective and professional communica-
tion between the healthcare workers. Such communication should be
recorded in writing and formalized in letters. Since these become impor-
tant legal records, their composition demands appropriate care and
professionalism.
TREATMENT OPTION SELECTION AND
TREATMENT PLANNING
Treatment planning, as the term implies, is the planning of the manage-
ment of a patient’s dental and oral problems in a systematic and ordered
way that assumes a complete knowledge of the patient’s needs, the precise
nature of the problems and the prognoses of possible management options
under consideration. In the case of simple dental problems, the dentist may
be able to identify the problem efficiently, characterize it together with the
patient’s needs and select the correct management option expeditiously. In
the case of complex dental problems, it may be rare for both patient and
dentist to develop such complete pictures of the problems and outcomes
of restorative options as early as the first consultation. The dentist must
gauge the problems correctly, as well as the patient’s attitude, motivation
and compliance. The phase of assessment (establishment of a more com-
plete picture of the problem(s) and patient compliance), therefore, often
overlaps with the phases of decision making, planning and delivery of
treatment (Fig. 5.2).
Anticipation of a particular treatment outcome does not increase cer-
tainty of its achievement but careful planning with attention to detail may.
The term “provisional treatment plan” is used to describe the interim plan
containing overlapping phases of diagnosis and treatment, when further
information is sought to garner a clearer picture to determine a firmer
action plan. A “definitive treatment plan” emerges as the information
becomes more complete and the wishes of the patient and dentist crystal-
lize into a more concrete, mutually acceptable proposal. This implies an
ongoing process of information exchange and informed consent whereby
the full extent of risks and benefits are shared and acted upon.
Even under the best set of circumstances, the most complete and defini-
tive picture of the problems may not be reached because of deficiencies
in diagnostic certainty and prognostic data on treatment outcomes. Despite
this, dedicated, active practice, with continuous proactive personal devel-
opment may propel a dentist to the state of mastery of their field relative
to contemporary knowledge. Variations inherent in dentists’ philosophy,
knowledge, experience, skills and judgement can give rise to differences
in treatment planning between clinicians. Conscientious dentists, there-
fore, strive for improvement throughout their professional lives in what
has now become formally recognized as continuing professional develop-
ment (CPD). Active engagement in CPD is mandatory in some countries
but not all. Unfortunately, some dental practitioners take the receipt of

Decision
making
Endodontist
Assessment
Dentist Planning
Human being
Fig. 5.1  Hierarchical importance of knowledge Fig. 5.2  Interrelationship between assessment and
context decision making, planning and delivery of
treatment
their practising licence as the end of formal professional development.
Their frame of reference extends no further than the teachings at under-
graduate level. Decision-making for them is a matter of following the
simple heuristic decision-tree delivered as expedient undergraduate teach-
ing. Their knowledge is therefore written in black and white, is clear and
simple and may still serve the needs of those patients falling into the
“central tendency” of disease presentation. It may not, however, serve
those presenting with problems lying on the fringes of the normal distribu-
tion of the particular disease. The intellect and skills of such practitioners
may consequently be stunted from flowering into their full potential.
The true scale of difficulty in treatment planning is only truly appreci-
ated by those conscious and conscientious enough to endeavour to improve
the service delivered to their patients. It is exemplified by the realization
of the conscientiously developing dentist that the more they begin to
understand the more they realize the extent of their knowledge limitation.
A central pillar of clinical governance is the responsibility on each dentist
to engage in ongoing personal development.
The aim of this chapter is to highlight the factors important in planning
the endodontic management of pulpal and periradicular diseases and how
to prioritize them in the context of the patient’s overall dental and oral
needs. Treatment planning encompasses the phases of:
● defining the problem
● dialogue with the patient (mutual interrogation and negotiation
between patient and dentist) that leads to selection of the best
course of action
● delivery of the planned treatment in an effective and efficient
sequence.
THE IDEAL TREATMENT-PLANNING SCENARIO
The textbook depiction of treatment planning commences at the first
encounter with the patient, when a full assessment is made of the patient’s
overall dental and oral problems. In this diagnostic phase, a detailed sys-
tematic appraisal is made in the classical manner described in Chapter 4.
The end point of this is a series of conclusions about the general health of
the patient and their current oral and dental problems; these will be juxta-
posed with the patient’s own perception of their problem(s) and desires
for correction of the same. The dentist’s insight will include the state of
the patient’s dentition, periodontium, the teeth (presence of caries or tooth
surface loss and their pulpal and periapical status), any restorations
and soft tissues. A number of different solutions will be possible for man-
agement of each of the patient’s problems but the specific treatment options
Treatment planning  121
Delivery
of
Treatment
Fig. 5.3  Orthopantomogram (OPG) of difficult
problems
Box 5.1  Treatment plan
Scenario – a patient presents in pain with a poorly maintained mouth,
several carious and periapical lesions and gingival inflammation. Following
history and examination, the treatment plan is as follows but beyond pain
management is conditional on compliance. It includes:
1. Diet investigation
2. Scale and polish and oral hygiene instruction
3. Management of carious lesions and preventive measures
4. Extraction of unrestorable teeth
5. Root canal treatment of teeth with apical periodontitis
6. Root canal retreatment of root-filled teeth with apical periodontitis
7. Periapical surgery if required
8. Provision of crowns
9. Replacement of missing teeth with fix or removable prostheses
selected will be dictated by the particular effects of interaction of these
problems on the patient’s desires, which may include their well-being,
aesthetic demands, and functional requirements (eating, speaking, social-
izing). Factors such as technical feasibility, cost and time involved, den-
tist’s preferences based on their skills and knowledge, and the patient’s
age, means, wishes and compliance in oral care may all play a part in
determining the final outcome. In the ideal scenario, each option should
be evaluated in an objective way taking the above factors into account,
weighing the effectiveness and projected long-term prognosis (based on
outcome data) with compliance, cost and time commitment. As the number
of dental problems to be addressed increases (Fig. 5.3), so does the interac-
tion between options for individual problems. This may have the overall
effect of either complicating management or simplifying it because more
radical solutions (such as extraction) become more appropriate. In any
case, the options will be discussed with the patient and, after appropriate
dialogue, negotiation and clarification, a mutually agreed choice of treat-
ment or “treatment plan” will emerge (Box 5.1).
In essence, the process consists of assessing and accounting for the
relevant problems at the level of the patient (their personal perspective on
health and social well-being), then at the level of oral function (eating,
speaking and aesthetics), and then at the level of the tooth (specific tooth-
related problems). The dentist must understand clearly (defining the
problem) what the patient expects at the first level. The dentist and patient
will need to have a clear and open discussion (dialogue and negotiation)
about concordance between the desired and the possible, at the second
level. The dentist must use their skills and knowledge to deliver the inte-
grated treatment that will meet the patient’s expectations at the tooth level.
 122  Treatment planning

Fig. 5.4  Example of

Box 5.2 Plan of treatment endodontic problem
managed in isolation
The “plan of treatment” to deliver the “treatment plan” will consist of
checks to gauge compliance and success in pain management. It may
progress as follows:
1. Treatment of acute problems including incision and drainage, first stage
root canal treatment, extractions
2. Immediate denture if necessary, oral hygiene instruction, diet instruction
and fluoride mouthwash
3. Stabilize carious lesions in conjunction with scale and polish and
reinforcement of oral hygiene instruction
4. Gauge compliance in home-care and gingival health with further oral
hygiene instruction as necessary
5. Provide definitive plastic restorations for carious teeth in order of priority
dependent on presence of sensitivity and integrity of temporary restorations
6. Complete root canal treatments on predictably restorable teeth
7. Carry out periapical surgery, if necessary
8. Review prognosis of treated teeth, design definitive removable or fixed
prosthesis and decide on teeth requiring cast restorations (compliance
should be absolute at this stage)
9. Provide crowns
10. Provide definitive prostheses

A plan is then made of the sequence in which treatment will be executed,

called the “plan of treatment” (Box 5.2). This may be defined as a strategic
list or maybe detailed by visit. Once the treatment is completed, the patient
will be recruited to a recall system to evaluate and maintain the work. At
these recall reviews, note will be taken of any changes and dealt with Fig. 5.5  Example of
according to a preplanned scheme for dealing with failure. Planning for endodontic problems
failure should be considered as part of the overall long-term treatment that have complex
restorative implications
plan.

THE REALITY OF PRACTICE, INFORMED CONSENT AND

MEDICAL RECORDS

In general dental practice, where a patient has often been under long-term
care by a particular practice or dentist, the majority of interactions with
the patient are part of continuing care. A plan of management will have
been established at the first encounter at some point in the past and, in the
simplest cases, requires no more than a review (recall) to evaluate a change
in overall status and provide motivation for maintenance. Under these Fig. 5.6  (a)
Symptomless 25 has
circumstances, the sudden precipitation of a pulpal or periapical problem
been reviewed for some
may be managed in isolation as long as there are no complex restorative time and now has a
implications (Fig. 5.4). Where there are such complex restorative implica- sinus; (b) the same 25
tions, the lack of insight or desire (on the part of the dentist) to tackle them has been retreated and
may influence outcome of the endodontic problem (Fig. 5.5). It is therefore is now under review to
important that a rational analysis of the situation is performed conscien- assess healing before
tiously and difficult restorative decisions taken promptly as necessary, making a decision
about restorative
rather than procrastinating to another time when the situation is likely to
options
be worse. Recognition of personal limitations in knowledge and skills, or
seeking appropriate referral, is the key to finding a solution. A
It is not uncommon and perfectly valid for patients on long-term recall,
to have the supervising dentist place individual teeth on probation to
review their status at a subsequent time because of uncertainty about a
diagnosis or the progression of a lesion (Fig. 5.6a). A number of potential
problems, not causing current difficulties will, therefore have been identi-
fied but a mutually agreed decision made between patient and dentist to
leave the tooth/teeth alone and periodically review them. Such a plan of
action is not uncommon both in unrestored mouths and in those that are
heavily restored and on the borderland of catastrophic transition to a dif-
ferent, perhaps partially edentulous state. The latter situation describes the
not uncommon condition of an ageing or restoratively ravaged dentition, B
where one further change could precipitate a radical review of the overall

dental strategy for the patient, with major implications of time and cost.
Small changes to the situation may be managed by minimal intervention
and a “patchwork” approach but this also demands a more vigilant rather
than complacent review strategy. The situation, however, must be clearly
recognized and understood by both the patient and dentist using the
so-called informed consent approach. The tooth in Figure 5.6a has been
retreated (Fig. 5.6b) and placed on continuing review until a mutually
agreed decision can be reached with regards to which of the previously
discussed restorative options to pursue.
It is not unheard of that, under some circumstances, with the passage of
time, the mutually agreed plan may be forgotten or fades from memory,
particularly where detailed medical or dental records are not maintained.
Under these circumstances, the precipitation of a pulpal or periapical
problem and even worse multiple problems that occur in rapid succession
may cause the need for a radical review of the options. The sudden accu-
mulation of such unfavourable events may prompt the patient to seek a
second opinion. The nature of this next encounter, in all likelihood with
somebody with a different philosophical perspective, may raise different
opinions about the previous management. The precise nature of the previ-
ous mutually agreed treatment plan might not be fully appreciated in the
absence of accurate and detailed records. The vagaries and subtleties that
lead to differences in management approach may cause patient dissatisfac-
tion, which sometimes (and in contemporary society increasingly fre-
quently) leads to legal action. It is therefore considered best practice to
keep detailed records of initial findings, option appraisals, discussions,
rationale for decisions and informed consent for treatment.
FACTORS INFLUENCING TREATMENT PLANNING
Treatment planning may be categorized into a very broad spectrum of
complexity from simple isolated problems to those multiple problems
requiring complicated multidisciplinary management. At its most complex,
treatment planning is a challenging, complicated and rewarding decision-
making process for both the clinician and patient that involves a two-way
dialogue (interrogation and negotiation), leading preferably to short-,
medium-, and long-term goals for the management of the patient’s denti-
tion. Difficulties are often caused by the contradictory desires, require-
ments and perceptions of both dentist and patient. The ways in which these
may be resolved are numerous, even forming the basis for practice-
marketing strategies. The factors influencing the decision-making process
are many and can be classified into general patient factors, professional
background and philosophy of the dentist, general oral and dental condi-
tion, and local factors related to the problem tooth (teeth). Factors that may
confound the process include differences in perception and expectations
between the dentist and patient. The dentist must be aware of the potential
for such problems and be prepared to take appropriate action to circumvent
them.
This hypothetical yet familiar illustration of operator and patient per-
spectives, which many will identify with, illustrates some sources of prob-
lematic communication. Clear and effective communication is the key to
arriving at a mutually satisfactory treatment plan.
The vagaries of decision making are further defined and explored by
examining different case scenarios based on a relatively simple problem.
ILLUSTRATION OF FACTORS AFFECTING TREATMENT
DECISION MAKING USING MAXILLARY INCISORS AS
AN EXAMPLE
The options available to treat endodontic problems include dentine and
pulp protection, vital pulp therapy, root canal treatment, root canal retreat-
ment or periradicular surgery (including root-end management, root repair,
Treatment planning  123
Table 5.1  Weighing of prognosis and relative cost of endodontic and
restorative options (based on average figures)
Relative
Treatment option cost Prognosis (% survival/years)
Root canal treatment 1.0 Difficult to determine as
dependent on individual
Conventional retreatment 2.3
prognostic factors
and new post retained
restoration
Each case has to be weighed
Surgical endodontics 1.5 independently
Extraction/leave unrestored 0.2
Extraction/denture 1.4
Extraction/bridge 3.8
Extraction/implant 4.3
NB: the relative cost may change depending on contemporary and local trends.
root resection or extraction). The last option also requires a consideration
of the alternative restorative options. Apart from feasibility, the cost and
long-term priorities of the patient have to be weighed.
A cost–benefit analysis should be performed to aid the decision-making
process as illustrated in Table 5.1. The outcome of such an analysis,
though, is likely to be different depending upon the exact details of the
situation. A recent health economic study using a Markov model evaluat-
ing the cost-effectiveness of clinical intervention over the life-time of an
adult patient revealed that root-canal treatment is highly cost-effective as
a first line intervention for a maxillary central incisor. Orthograde retreat-
ment is also cost-effective, if a root-canal treatment subsequently fails, but
surgical retreatment is not. Implants may have a role as a third line inter-
vention if root canal retreatment fails.
As an example, consider the various presentations of an endodontic
problem associated with a maxillary central incisor in an otherwise intact
dental arch.
SCENARIO 1
Consider the not uncommon scenario of the pulp in a maxillary incisor of
an otherwise intact dentition becoming compromised by a severe traumatic
injury in a young, mature adult (Fig. 5.7a). The options of vital pulp
therapy or root-canal treatment may be considered. The choice will centre
on the prognosis of each treatment (based on biological factors) and the
long-term benefit to the patient. If the tooth is not restoratively compro-
mised and the root is mature, the high prevalence of pulp necrosis in such
cases may lean the decision towards root-canal treatment and the appropri-
ate restoration as having a high chance of success (Fig. 5.7b,c). Other
restorative factors may not come into the equation at this stage but will be
discussed with the patient.
SCENARIO 2
If, under the same circumstances, the patient was younger with an incom-
pletely formed root, the decision may now lean towards the more con-
servative vital pulp therapy (Fig. 5.8a) in order to aid completion of root
formation and improve the long-term restorative prognosis (Fig. 5.8b). In
the event that the traumatic injury in such circumstances is accompanied
by severe coronal tooth fracture, the restorative prognosis may be further
jeopardized (Fig. 5.9). Consideration of early replacement may have to be
tempered by the psychological need to avoid loss of the tooth, as well as
to delay permanent replacement during the growth phase of the individual,
especially if an implant-retained crown is a possible alternative. The com-
promised tooth may, therefore, be retained as a suitable space maintainer
until a more definitive solution can be executed.
 124  Treatment planning
A C
Fig. 5.7  (a) Traumatized maxillary incisor; (b) maxillary incisor following endodontic treatment. (c) maxillary incisor restored
A
B B
Fig. 5.8  (a) Traumatized maxillary incisor with an open apex, receiving pulp
therapy; (b) traumatized maxillary incisor root filled following root closure
SCENARIO 3
Consider an identical scenario but where a traumatized, intact, mature,
maxillary central incisor has been left untreated for years as the pulp
slowly succumbs and the patient seeks attention either because of an acute
infection or the discoloration caused by secondary dentine formation and/
or pulp necrosis (Fig. 5.10a). On radiographic examination, it is found that
the canal is sclerosed (Fig. 5.10b) and only evident in the apical third of
the root associated with a periapical lesion. Now other considerations
come into play, including the potential for successful outcome by conven-
tional or surgical means, as well as the desire for correcting the discolora-
tion. In the matter of the former problem, it has to be established whether
the operator is confident of locating the canal using a conventional coronal
approach (Fig. 5.10c), which would improve the chances of success (Fig.
5.10d). If not, injudicious dentine removal may result in compromised
restorability of the tooth. A surgical approach may stand a better chance of
finding the canal but may not help eradicate the major part of the infection
in the root-canal system, compromising the chances of successful healing
(Fig. 5.11). In addition, the absence of access to the pulp chamber also
compromises the chances of internal bleaching of the tooth to help correct
A
Fig. 5.9  (a) Maxillary central incisors with root-canal treatment to control
apical periodontitis and inflammatory resorption following traumatic injury;
(b) same teeth affected by replacement resorption, were subsequently
replaced with implant-retained crowns
the discoloration. In this scenario, there is an increasing number of uncer-
tainties as outcomes are less predictable. The decision-making now has to
be aided by weighing the relative chances of success of the different endo-
dontic options and, finally, also the restorative/aesthetic outcome.
SCENARIO 4
Consider that the same scenario presents many years later but this time
without having caused the patient any symptoms, the sole concern being
tooth discoloration. The intact tooth will in all probability give negative
pulp test responses and may or may not be associated with a periapical
radiolucency. In the case of a periapical radiolucency, the decision is
easier, as it would be reasonable to recommend root-canal treatment,
bleaching (Fig. 5.12) and, if necessary, a porcelain veneer to mask residual
discoloration caused by increased thickness of sclerosed dentine. The
morbidity of treatment, that is, the potential of an acute flare-up, should
also be considered since about 10–15% of teeth associated with asympto-
matic periapical radiolucencies, without sinus tracts, become acute on
 Treatment planning  125

Fig. 5.10  (a) Discoloration of tooth following trauma; (b) radiographic evidence of
D pulp calcification and dentine sclerosis; (c) example of sclerosed canal in maxillary
incisor; (d) canal successfully negotiated and obturated

Fig. 5.11  (a) Sclerosed canal in central

incisor managed by apicectomy and
root-end filling; (b) the treatment failed
and required a further procedure when
retrograde root canal treatment was
performed; (c) final retrograde root filling

B
A C

commencement of root-canal treatment. The decision is even more diffi-
cult in the absence of a periapical radiolucency because of the potential to
infect a necrotic pulp and precipitate further problems. If the pulp chamber
and canal space is obliterated, locating and accessing the canal for root-
canal treatment may be problematic. External bleaching may be considered
as the sole treatment.
SCENARIO 5
Consider another variation on the above scenario, where the tooth has
already been root treated and restored with a post-crown. The patient now
presents years later with a periapical lesion (Fig. 5.13a). This confronts
the dentist with additional endodontic and restorative dimensions that must
be considered. The endodontic question to address is the reason for
treatment failure. The causes of failure include persistent intraradicular
infection, new intraradicular infection, extraradicular infection, cyst,
foreign body reaction, healing by scar tissue and radicular fracture. It is
virtually impossible to predict which of these factors may be the prime
causative factor in the absence of other clinical clues. The presence of
acute infection may narrow down the options. The presence of an unin-
strumented apical canal space may suggest persistent infection whereas, a
recently decemented and recemented post crown may suggest a newly
established infection or root fracture. If intraradicular infection is impli-
cated, then conventional retreatment may be the treatment of choice. In
this case, the restorability of the tooth, the retrievability of the post-core
and root filling should be weighed up, as should the potential for root
fracture during post removal. The natural consequence of this will also be
the need for revising the root-canal treatment and placing a new post
 126  Treatment planning
Fig. 5.12  (a) Central
incisor requiring
endodontic treatment
and bleaching; (b)
bleached central incisor
A sodes of swellings and pus discharge associated with the gums above these
B It was now clear that conventional root canal retreatment plus surgery
A B
Fig. 5.13  (a) Post-crowned incisor with periapical lesion; (b) retrograde
apical treatment of post-crowned incisor
crown. The chances of success using this approach should be weighed
against a surgical option where the existing crown is preserved (assuming
good pre-existing margins, contours and aesthetics) and retrograde apical
treatment considered (Fig. 5.13b). This has the advantage of correcting
causes of failure other than intraradicular infection. It must be remembered
that if a conventional approach is selected and the cause of the problem
turns out to be extraradicular infection or a cyst, surgical correction may
still be required in addition. Under these circumstances, the decision-
making process is therefore more complicated. If it is found that the root
length is short or that the restorative management is compromised by the
existing canal shape, size and length, extraction and prosthetic replacement
should also be considered.
Under these circumstances, further assessments have to be made for
alternative replacements. The options include leaving alone, a denture,
bridge or implant. A number of factors now need to be considered, includ-
ing the size and shape of the vault of the palate (for a denture), the restora-
tive status of the adjacent teeth, including their size for the purposes of
adhesive bonding, the quality and quantity of bone in the site at present
as a possible indicator of bone after extraction for an implant and, finally,
the occlusal relationship with opposing teeth. The prognoses of each of
these options, as well as their cost, should be considered.
SCENARIO 6
Consider a further variation on the above scenario where two central inci-
sors had received crowns to engineer aesthetic correction of a severe class
2 division 1 malocclusion. The patient was happy with the result but, over
time, suffered some gingival recession and the beginning of repeated epi-
teeth. The maxillary right central incisor had been root treated and restored
with a post-crown, while the left central incisor just had a ceramic crown.
The two teeth are now associated with a very large periapical lesion (Fig.
5.14a). Despite the aesthetic compromise, the patient’s priority was pre-
serving the teeth. The quality of the root-canal treatment in both was
suspect. Given the restorative uncertainty, the previous operator had
decided on a surgical approach and felt decompression of the lesion may
be useful given the size of the lesion. Having tried this for some months,
it was apparent that the approach was not going to work and referred the
patient for further care.
would be required. Treatment commenced first with the left incisor without
the post (see Fig. 5.14b); after conventional debridement, there was mar-
ginal resolution of symptoms but persistent swellings continued. It was
decided to remove the crown and post from the right central incisor, which
proved extremely challenging because the core and post were almost at
right angles, revealing the extent of aesthetic correction, which the patient
had forgotten. Both teeth were opened and debrided with continuous drain-
age of a straw-coloured fluid from the right central incisor (see Fig. 5.14c).
It was noticed, however, that irrigation in one tooth resulted in outflow
from the other tooth and vice versa (see Fig. 5.14d). The two teeth were
clearly connected by a common cystic lesion, a diagnosis obvious in con-
trast to the previous scenario. After repeat debridement, there was no
abatement in the exudate and through and through surgery would be
inevitable.
A new indirect customized post-core was constructed of gold alloy in
readiness for a single visit obturation and surgery. The teeth were opened
and debrided, the exudate, although reduced, was still ongoing from the
right incisor. The left incisor was therefore obturated (see Fig. 5.14e).
Surgical access was obtained to the periradicular area of both incisors, the
lesion curetted and the crypt temporarily filled with gauze to control bleed-
ing. The right central incisor was root filled using a through and through
technique and the new post-core was cemented (see Fig. 5.14f). The peri-
apical aspects were then cleaned and the root filling burnished in retro-
grade fashion (see Fig. 5.14g). Postoperative healing was uneventful and
there have been no further episodes of swellings; healing is progressing
favourably. This case illustrates that multiple factors need to be accounted
for and some bravery is required in pursuing treatment goals, based on
first principles tempered with experience. Implant therapy may be selected
by some but, with the extent of bone loss, that was not a realistic option
to begin with, even with socket preservation. It was necessary to achieve
periapical healing with regeneration of bone to give the patient a future
chance with implants. In the final analysis, the patient was free of signs
and symptoms of disease and had new aesthetic crowns.
SCENARIO 7
The superimposition of a medical condition, such as diabetes or a history
of IV bisphosphonate treatment may sway the balance of the decision
depending upon the predictability of the outcome. The type of endodontic
 Treatment planning  127

C
B D

Fig. 5.14  (a) Two maxillary incisors

associated with a very large periapical
lesion; (b) root canal retreatment
commenced on the left incisor without
the post; (c) straw-coloured fluid  
exudes from the right central incisor;  
(d) irrigation in one tooth results in
outflow from the other tooth and vice
versa; (e) the left incisor root filled;  
(f) the right central incisor obturated
using a through and through technique
with a new post-core cemented; (g)
periapical aspects of the two incisors
cleaned and the root fillings burnished
in retrograde fashion

E G

Fig. 5.15  Multirooted

maxillary premolar
treatment planned for a particular patient should take into account the
patient’s general health and dental state.

SUMMARY OF FACTORS AFFECTING

TREATMENT PLANNING
The above illustration shows how the balance of the decision may be
swayed by the interaction of a number of variables, including the age,
endodontic and restorative status of the tooth and that of adjacent teeth,
the overall and specific periodontal condition of involved teeth, the overall
and specific occlusal relationship of involved teeth, the expectations and Fig. 5.16  Mandibular
means of the patient, and the prognoses and cost of the different treatment molar with iatrogenic
options. problems
Similar considerations apply to posterior multirooted teeth. However,
the root canal anatomy and its influence on management prospects have
also to be considered (Fig. 5.15). The situation becomes further compli-
cated in teeth that have been previously treated and may have iatrogenic
problems, such as broken instruments (Fig. 5.16) and canal transportation
(Fig. 5.17).
The complexity of interacting factors increases further when more
than one tooth is involved, whether they are adjacent or separated by
 128  Treatment planning
Fig. 5.17  Radiograph of root-treated molar with Fig. 5.18  Patient requiring extensive treatment
evidence of canal transportation
Fig. 5.19  Very carious, periodontally involved Fig. 5.20  Provisional sedative restoration in a
mandibular molar molar
other teeth or in different arches. Where multiple teeth are involved, each
should be independently evaluated initially and then the interacting aspects
considered. It will often be intuitively obvious when the simple solution
should take precedence over extravagantly complicated efforts to preserve
teeth at all costs.
Once the treatment options have been selected, the next phase involves
the planning of the sequence of delivery of the treatment. In the case of
single teeth, this is straightforward because it is purely tooth-related, but
becomes increasingly complicated with involvement of multiple teeth, of
which some may be symptomatic and others may require temporization.
THE SEQUENCE OF TREATMENT DELIVERY
Figure 5.18 shows the case of a patient with multiple restorative and
endodontic problems.
There are three stages in the planning process. These are:
● planned initial treatment
● planned definitive treatment
● planned review.
PLANNED INITIAL TREATMENT
Immediate relief of symptoms
The immediate relief of pain is a valuable service and should precede
other forms of treatment. The provision of emergency endodontic care for
Fig. 5.21  Endodontic treatment
commenced in painful fractured
molar
patients in pain of pulpal or periradicular origin need not be anxiety-
ridden or time-consuming, and can assist in building the reputation of a
practitioner.
The treatment required for the immediate relief of pain may be obvious
− for example a very carious, periodontally involved, unrestorable tooth
may be extracted (Fig. 5.19).
Where a tooth has recurrent caries, treatment of the provoked pain may
only require the removal of caries, placement of an indirect pulp cap with
calcium hydroxide, and the placement of a provisional sedative restoration
(Fig. 5.20).
Where the appropriate treatment is not quite so obvious, as in some
cases of post-restorative pain, interim relief may be achieved by correction
of occlusal interferences and inadequate or excessive approximal contacts,
to allow the stressed pulp to recover from the restorative episode.
Cracked teeth with symptoms of irreversible pulpitis may require endo-
dontic treatment for the relief of symptoms before making a definitive
decision about the restorative future of the tooth. For example, endodontic
treatment may be commenced in a painful tooth with a suspected fracture
before undertaking further investigations to establish the true prognosis
(Fig. 5.21).
Teeth with established intraradicular infection may present with severe
pain and/or localized or diffuse swelling (Fig. 5.22a). Treatment in these
situations is based on the need for the establishment of drainage (Fig.
5.22b), thorough disinfection of the tooth and, where necessary, the pre-
scription of analgesics and antibiotics. The use of antibiotics alone in the
relief of acute symptoms is inappropriate.

Fig. 5.22  (a) Swelling
of the palate related   incisor
to endodontic
intraradicular infection;
(b) drainage established
in a mandibular canine
B
Fig. 5.23  Endodontic
stabilization of maxillary
first premolar
Stabilization
Stabilization involves halting the progress of primary dental disease in the
dentition. Caries, periodontal disease and cracks in teeth fall into this
category.
When disease is at an advanced stage and threatens the survival of a
tooth or teeth, its progression may be controlled without the delivery of
full effective, definitive treatment. The most easily understood example of
this is the dressing of carious teeth to arrest caries progression and protect
the pulp. The primary phase in periodontal therapy may involve oral-
hygiene instruction and debridement. Teeth with cracks may have ortho-
dontic bands placed around them to prevent propagation of the cracks.
The same principle may be applied to pulpally involved teeth. Endo-
dontic treatment may be instituted and the canals in the teeth provisionally
dressed to control the development of periradicular disease without com-
pleting the definitive therapy (Fig. 5.23).
Endodontically speaking, the teeth are placed “ ‘on hold” while other
aspects of the patient’s total care are being managed.
Prevention
A patient’s understanding and beliefs about dental disease and its treatment
may affect their motivation, attitude to attendance and compliance with
treatment. Initial planned treatment should always incorporate an element
of behavioural conditioning to address the patient’s beliefs and attitudes.
Treatment planning  129
Fig. 5.24  Endodontically unsound
This approach is crucial for the long-term prevention of dental caries and
periodontal disease.
Effective planning should always incorporate prevention. In addition to
the identification of the aetiology of the dental disease present, patient
education becomes the basis of any preventative regimen. This may
include dietary advice, home oral-health measures, and the use of fluoride
supplements.
PLANNED DEFINITIVE TREATMENT
Definitive treatment options may involve pulp or dentine protection, pulp
therapy, root-canal treatment, root-canal retreatment, surgical treatment,
review or extraction. Where the loss of teeth becomes a factor then replace-
ment options should be considered. These involve the construction of
fixed and removable prostheses or the provision of implants. The choice
of treatment may be influenced by specific factors. Decisions made in both
simple and more complex treatment plans should follow the knowledge
gained from research and evidence-based practice.
General restorative considerations
The general state of a patient’s dentition is an indicator of dental disease
experience. The age, condition, maintenance of restorations and the pres-
ence of recurrent disease are all factors that may influence the decision
making.
Not all teeth with pulpal and periradicular disease are candidates for
endodontic treatment and, on occasions, the retention of a pulpally com-
promised tooth should be questioned if it unnecessarily complicates the
restorative plan. One such example is an endodontically compromised
remaining incisor, where the restorative option is a removable prosthesis
(Fig. 5.24). Conversely, teeth with perfectly normal pulps may be judged
to require endodontic treatment for restorative reasons, as in the case of
the restorative realignment of teeth or overdenture construction (Fig. 5.25).
Endodontic treatment of teeth with low-grade symptoms or potentially
compromised pulps may also be considered when there is the likelihood
of them receiving extensive restorations or they are required as abutments
for fixed prostheses (Fig. 5.26). The difficulty and expense of treating teeth
with large cast or ceramometal restorations should be borne in mind.
Strategic importance of teeth
Before deciding whether to retain or extract a tooth, the importance of a
particular tooth in the dental arch should be considered. Clearly, unop-
posed and functionless teeth (Fig. 5.27) are strategically less important
than single standing teeth, which often prevent the need for a free-end
saddle denture (Fig. 5.28).
 130  Treatment planning

A A

Fig. 5.27  Unopposed molar

B
B
Fig. 5.26  (a) Molar requiring restoration with
Fig. 5.25  (a) Elective root canal treatment for
questionable vitality; (b) molar endodontics
mandibular canine; (b) overdenture in place
completed prior to restoration
Fig. 5.28  Tooth defending the need for a free-end
saddle

Fig. 5.29  Root-filled

tooth with loss of
periodontal support

Periodontal support
Active periodontal disease is a contraindication for embarking on root-
canal treatment unless symptoms demand otherwise in a tooth with pre-
dictable periodontal prognosis. Conversely, loss of periodontal attachment
on its own is not a contraindication for endodontic treatment. Provided a
tooth has, or can be made to have, a healthy albeit reduced periodontal
apparatus, endodontic treatment may be carried out (Fig. 5.29). History of
periodontal disease may complicate root-canal treatment due to dystrophic
calcification (see Chapter 12).

Implants
The apparent success of single-tooth implants has prompted extravagant
claims in some quarters to the effect that the treatment modality may spell
B
the end of endodontics. This has proved to be unfounded as originally
predicted. Implants are just one of several tooth replacement options and Fig. 5.30  (a) Clinical image of implant-retained
nothing more. They have good fixture survival rates but suffer from pros- crowns; (b) radiograph of single tooth implants
thodontic complications rather more frequently (Fig. 5.30). Most patients
will wish to retain their own natural teeth and extraction must be a con-
sidered decision based on exhaustion of all possibilities to save them

within a reasonable time and cost frame. A cost–benefit analysis of the
options showed retention of the tooth to be a better option (Moiseiwitsch
& Caplan, 2001), but this will be a changing comparison as the cost of the
treatment changes.
Restorability of teeth
Following endodontic treatment, it should be possible to restore a tooth to
function and health. Particular attention needs to be given to the support
that can be provided for a coronal restoration and the position of finishing
margins, which should preferably be maintained supragingival. Restorabil-
ity should be assessed at the outset (discussed further in Chapter 13). If
the prospects of providing a predictable restoration seem remote, extrac-
tion should be considered (Fig. 5.31).
Good treatment strategies should also take into account possible failure.
By planning for failure, operators and patients are placed in a much better
position to cope with outcomes that are not as originally hoped for. Through
informed consent, compromised teeth may be maintained for up to 10
years with plastic restorations (Fig. 5.32).
C
A
A B
A
B C
Fig. 5.32  Compromised tooth (a) Fig. 5.33  (a–c) Access to the tooth is affected by limited mouth opening and the nature of occlusal
maintained up to 10 years with an plane; attempts to access the 46 are affected by the hand-piece pivoting on the incisors
amalgam restoration (b)
Treatment planning  131
Access to the tooth and root-canal system
Access to the tooth is a prime consideration and may be affected by mouth
opening, as well as the nature of the occlusal plane (Fig. 5.33). At least
two fingers width opening is required at the incisors as a general rule.
Patients with a history of radiotherapy or submucous fibrosis may have
restricted access (Figs 5.34, 5.35). Access may also be compromised in
maxillary molars with distobuccal orientation; opening the mouth leads to
translation of the coronoid process forwards over the occlusal surface of
the tooth compromising access.
Together with mouth opening, the ability to maintain the mouth open
for a reasonable period of time should also be considered. Some patients
with temporomandibular joint (TMJ) or masticatory muscle problems
may find this difficult. The use of mouth props may be considered (see
Chapter 4).
Some patients cannot tolerate rubber dam; given the importance of
airway protection, it may need to be considered whether root-canal treat-
ment should be considered without rubber dam. It should rarely be neces-
sary to do so.
Fig. 5.31  (a–c) Extraction should be
considered for this case if the prospects of
providing a predictable restoration seem
remote
132  Treatment planning

Fig. 5.34  Restricted Fig. 5.36  Overzealous access in

access as a result of mandibular incisor leads to
limited mouth opening unnecessary loss of dentine
due to radiotherapy

Together with mouth opening, the demands of access cavity preparation

A for straightline access in posterior teeth may need to be carefully consid-
ered when using motor-driven nickel–titanium instruments. Access and
root-canal preparation can influence the amount of remaining coronal tooth
substance. Good access facilitates root-canal treatment but injudicious
access may make the restoration of the tooth more difficult or compromise
tooth survival (Fig. 5.36).

Tooth anatomy and orientation

It is well to judge the tooth anatomy from the outset; consider the
tooth anomalies discussed in Chapter 1. The orientation of teeth may
also compromise access and complicate delivery of root-canal treatment
B (Figs 5.37, 5.38).

Canal anatomy
Bizarre root forms and root-canal anatomy, congenital grooves and dilac-
erations may all present difficulties if root canal treatment is attempted
(Fig. 5.39). These unusual forms may affect the outcome of treatment.
Teeth with complex root canal systems demand additional forethought and
planning to anticipate difficulties. Different strategies may be used to
prepare canals or to deliver the irrigants and obturating materials.

Sclerosed canals
Root canals that are not visible radiographically may be difficult to locate
and negotiate if root canal treatment is necessary (Fig. 5.40). However, in
many cases they are possible to locate and treat (Figs 5.41, 5.42). It is
impossible to prejudge the ability to locate the canal until an attempt has
C
been made to locate it. Location demands knowledge of anatomy more
than magnification; in single-rooted teeth the goal is to drill dead centre,
Fig. 5.35  (a–d) The so the skill is in maintaining hand-piece orientation; experience allows
tooth in Figure 5.34 location without deviation. Teeth with a history of trauma experience
was accessed from the progressive narrowing of the pulp space. Such teeth should be reviewed
buccal surface radiographically and, if there is evidence of sclerotic change, endodontic
treatment should not be contemplated until there are radiographic per-
iradicular indications of necrotic change occurring within the canal.

Single or multiple visit treatment

It is becoming popular for specialists to favour the completion of root-
D
canal treatment in one visit. Currently accepted criteria for the completion
of root-canal treatment include lack of symptoms and a prepared pulp

Fig. 5.37  Access compromised by lingual
orientation of 46 tooth
Fig. 5.39  (a) Mandibular premolar
requiring treatment; (b) irregular root
form of the premolar;   B
B (c) complex canal anatomy of the
premolar
space free of microorganisms. When considering whether to complete
treatment in one visit or more it is worth thinking about the possible advan-
tages and disadvantages of both the single and multiple visit approach.
Where root-canal treatment is being performed on a vital tooth, the bac-
terial content of the tooth is minimal and a single-visit approach is favoured,
thus reducing the possibility of bacterial entry into the tooth through
coronal leakage of the provisional restoration. The single visit also allows
for immediate and intimate knowledge of the canal anatomy of the tooth
and all important reference points. Patients also favour single visits because
there is less time spent in the dental office with less anxiety and local
Treatment planning  133
Amalgam restoration
Distolingually
deviated
access
preparation
Pulp chamber
Prepared and filled canals outline
Fig. 5.38  Access initially malaligned almost leading to perforation (Fig. 5.37)
A
Fig. 5.40  (a,b) Sclerosed pulp chamber and canals in multirooted teeth
anaesthetic. Patients with medical histories that require the administration
of antibiotics for treatment also benefit from receiving care in a single visit.
When dealing with a long-standing infection in a tooth with a large
periapical radiolucency, swelling or with a sinus tract, it may be wise to
consider the disinfection of the tooth over more than one visit. This
approach allows greater time and the use of a medicament to supplement
the chair-side irrigation and disinfection procedures. Retreatment cases
lend themselves to a multivisit approach because of the time required to
remove restorations and root fillings, and the presence of resistant bacterial
strains.
 134  Treatment planning
C
B
A
A Fig. 5.42  (a) Sclerosed root canal in mandibular premolar; (b) drilling to locate canals; (c) canal in
mandibular premolar located and treated albeit initially deviated
A B
Previous root-canal treatment
The decision to retreat a previously root-filled tooth (Fig. 5.43) should be
based on clear criteria; retreatment may be initiated because of clear signs
of previous treatment failure (symptoms, sinus tracts, persistent or devel-
oping radiolucencies) or to improve the technical quality of the root-canal
treatment (as judged radiographically) prior to a new permanent
Fig. 5.41  (a) Sclerosed root canal in
maxillary incisor; (b) drilling to locate
canals; (c) canal in maxillary incisor located
and treated, albeit slightly deviated initially
Fig. 5.43  (a) Maxillary molar requiring retreatment
because of evidence of treatment failure; (b) maxillary
molar following retreatment
restoration (Fig. 5.44). In any case, the dentist must first decide whether
any iatrogenic problems evident are surmountable to regain access to the
apical anatomy. Consideration should be given to remaining tooth struc-
ture, the thickness of roots, the width of previous canal preparation, pres-
ence of canal transportation, presence of perforations, evidence of missed
root-canal anatomy, the presence and type of separated instruments, and
their location in relation to canal curvatures (Fig. 5.45). Although it is

A
Fig. 5.44  Maxillary molar requiring treatment Fig. 5.45  (a) Mandibular molar with silver points requiring technical revision; (b) mandibular molar
revision prior to restoration following retreatment
A B
never clear what features may be correctable before entering the root-canal
system, an attempt should be made to predict the outcome based on experi-
ence. The practitioner should always assess their ability to improve on the
existing situation. If this ability is in doubt, referral to a colleague special-
izing in this area should be considered.
The management of symptom-free periradicular radiolucencies in previ-
ously root-treated teeth seems to give rise to considerable management
variation. The inclination of a dentist to propose endodontic retreatment
is variable. There does not appear to be a definite retreatment criterion for
stable symptomless periradicular radiolucencies. The judgement may be
decided by an estimation of future problems based on restorative needs.
The replacement of coronal restorations in endodontically treated teeth
can occasionally give rise to symptoms, but why this should be so is not
fully understood. It has been suggested that coronal leakage, altered occlu-
sal loading, the effects of post-space preparation and restoration cementa-
tion hydrostatic pressures may account for the problems. Previously
root-treated teeth requiring new restorations should be examined with care
and, if the adequacy of the sealing of the pulp space is in doubt, retreat-
ment should be considered.
Where post-retained restorations exist in teeth requiring endodontic
treatment, a choice has to be made regarding the approach to treatment.
Conventional retreatment is likely to damage the restoration, and post
removal might precipitate a root fracture; but it gives a better opportunity
to clean the canal system and eliminate coronal leakage as a possible cause
Treatment planning  135
B
Fig. 5.46  (a) Lateral incisor fails to
respond to conventional root canal
treatment; (b) surgery performed to
eradicate possible extraradicular infection;
(c) resolution of the periradicular lesion
for failure. It does not, however, allow treatment of extraradicular infection
or other biological and causes. Conversely, a retrograde surgical approach
addresses the extraradicular infection or biological cause, and preserves
existing restoration, but fails to address any coronal leakage and does not
enable thorough canal system cleaning (Fig. 5.46).
In cases involving retreatment of teeth with large periapical radiolucen-
cies, the use of decompression (Fig. 5.47) to reduce the lesion size and
biopsy techniques to establish a clear diagnosis, should be considered.
DECISION-MAKING PROCESS FOR ROOT CANAL
RETREATMENT, SURGERY OR EXTRACTION
When failure of the previous root-canal treatment is confirmed and retreat-
ment is indicated, the general and local factors (Box 5.3) affecting the
prognosis and feasibility of non-surgical versus surgical retreatment should
be assessed carefully. The patient should be informed about the prognosis
of the tooth and the available treatment alternatives and participate in the
choice of treatment. The operator should make a decision about the point
at which the case should be better managed surgically, the tooth should be
better extracted and replaced with a prosthesis or the patient referred to a
specialist based on complexity index (Fig. 5.48), the set-up in the dental
practice, his/her/their experience and capability, as well as the patient’s
inclination and medical condition.
 136  Treatment planning
B C
D placement of flanged cannula; (e) Radiographic
E evidence of decompression
Box 5.3 Factors affecting prognosis and feasibility of non-surgical versus
surgical retreatment
Patient’s general factors
• Awareness and expectation
• Time and financial commitment
• Medical condition
• Access (two fingers opening) (see Fig. 5.34)
Major anatomical structures in proximity of the root end
Maxillary sinus
Greater palatine vessels
Inferior alveolar and mental nerves
Local tooth factors
• Type and condition of coronal restoration
• Type and condition of post
• Type of root filling material
• Presence of blockage due to packed dentine debris or sclerosed canals
• Presence of ledges
• Presence and location of fractured instruments
• Presence and location of perforations
ANATOMICAL CONSIDERATIONS FOR
SURGICAL RETREATMENT
It is essential for all surgeons to have an intimate knowledge of the tissues
they will be operating on. In endodontic surgery, the tissues are collec-
tively known as the periodontium (Figs 5.49, 5.50). The tissues of the
periodontal apparatus include dentine, cementum, bone, periodontal liga-
ment and alveolar mucosa. Understanding the strengths and weaknesses
of each of these tissues will allow the operator to manipulate the tissues
to ensure the greatest chance of complete healing. The clinical appearance
of these tissues in health (Figs 5.51, 5.52) should be appreciated.
A complete examination of the surgical site allows the surgeon to
become familiar with the local anatomical features, as well as the broader
aspects of the orofacial anatomical structures (Figs 5.53, 5.54). Some
major anatomical structures of interest include the maxillary sinus, the
greater palatine vessels and the inferior alveolar and mental nerves (Fig.
5.55). In addition, local structures such as the root anatomy and the rela-
tionship of the tooth to the periodontal apparatus and adjacent teeth must
Fig. 5.47  (a) Large periapical lesion in mandible;
(b) lesion situated between left mandibular lateral
incisor and canine; (c) penetration of lesion; (d)
be considered. The design of the flap will be determined, in the main, by
these anatomical considerations and by the demands of surgical access.
In addition, a thorough understanding of the radicular anatomy will
enable the operator to anticipate the presence of isthmi, anastamoses, and
other anatomical complexities that could harbour bacteria or their prod-
ucts. This in turn will facilitate the design of the root-end preparation.
SYSTEMIC CONSIDERATION FOR
SURGICAL RETREATMENT
As in all areas of dentistry, the necessity for collection and analysis of all
relevant medical information prior to treatment is obvious. The basis for
this has been established elsewhere in this book. However, a number of
issues requiring emphasis will now be discussed briefly.
A review of the main systems will provide a framework for establishing
the health status of the patient. A written medical questionnaire completed
by the patient prior to treatment is essential. However, studies have indi-
cated that the most effective means of gathering medical history details
are for the practitioner to interview the patient directly. A combined
approach will undoubtedly provide the most accurate assessment overall.
As demographic studies indicate, the population of the western world
is an ageing one. Edentulousness is no longer accepted as an integral part
of growing old. Consequently, an increasing number of medically-
compromised patients will be presenting for both surgical and non-surgical
endodontic treatments. Generally, few special considerations need to be
taken for surgical patients that do not apply equally to non-surgical patients.
The main areas where exceptions occur are related to haemostasis during
and subsequent to the surgical procedure.
Root fractures
Fractures that communicate with the oral environment provide a route for
infection. Vertically fractured teeth (Figs 5.56, 5.57) have a worse prog-
nosis than those with horizontal fractures (Fig. 5.58), which are also easier
to detect radiographically, unless they are high up coronally. It is likely
that a proportion of such teeth do not survive because the dentist is pes-
simistic about the prognosis based on intuition and experience; Figures
5.59 and 5.60 illustrate what a patient’s optimism can achieve; these hori-
zontally root fractured teeth survived 30 years and 20 years, respectively
 Treatment planning  137

Assessment for root canal retreatment

Consider patient’s awareness, medical condition, time and financial commitment

Not ready for re-

Ready for re-treatment
treatment

Cause of failure
Vertical root fracture Adequate
Symptomatic Asymptomatic RCT and
Perforation at cervical level
antibacterial
Inadequate RCT medication used

Resection of the Adequate access (2 fingers opening)

Extraction Follow up
fractured root or Yes No
extraction
History of decementation or Consider referring to
presence of leakage/caries in coronal cast restoration specialist
No Yes

Retained by post Remove cast restoration for

retreatment
Yes No

Quality of post Leave cast restoration for

retreatment
Good Inadequate

Root end in close proximity to vital

structure i.e. nerve, maxillary sinus
No Yes Assess degree of difficulties (scale of 10) based on the cause of canal obstruction
1 2 3 4 5 6 7 8
Consider surgical Consider extraction GP GP with Ledge Short/poorly Fractured Packed Sclerosis Fractured Long/well Fractured
retreatment or non-surgical re- core fitting post instrument or dentine and instrument or fitting post instrument or
treatment silver point debris missing silver point silver point
protruding canal(s) within straight around a
into pulp part of canal curve
chamber

Fig. 5.48  Hypothetical decision-making algorithm for root canal retreatment that may vary with dentist’s ability

Alveolar mucosa

Mucogingival junction
Alveolar bone
Attached gingiva
Periodontal ligament
Free gingiva Palatal mucosa
Cementum
Gingival sulcus Gingival fibres
Pulp
Dentine
Bone
Enamel
Epitheluim Submucosa Periosteum

Fig. 5.49  Diagrammatic section of periodontium Fig. 5.50  Diagrammatic section through mucoperiosteum
 138  Treatment planning
Fig. 5.51  Clinical picture of healthy
oral tissues: AG = attached gingivae;
MGJ = mucogingival junction; OM =
alveolar mucosa
Fig. 5.54  Frenae – position and level of
attachment
Fig. 5.57  Vertical fracture in an
anterior tooth
Fig. 5.53  Maxillary tori
Fig. 5.52  Stippled appearance of
attached gingivae
Fig. 5.55  Mental nerve location
Fig. 5.56  Vertical fracture of a
maxillary molar (arrowed)
Fig. 5.59  (a) Incisor with
longstanding (30 yrs)
horizontal fracture; (b)
radiograph of the tooth in
(a) indicating survival
Fig. 5.58  Horizontal fracture of a B despite an absence of
maxillary incisor interventive treatment
 Treatment planning  139

because the patient did not allow extraction. On the other hand, the dentist
could be accused of being unjustifiably optimistic in the illustrated case
of an attempted splinting of the horizontally root fractured tooth with a
dowel (Fig. 5.61). Horizontal root fractures may also occur in premolars
(Fig. 5.62) and molars (Fig. 5.63), usually through traumatic episodes.
Crown-root fractures passing through the attachment apparatus and
involving alveolar bone require careful assessment to establish accurately
the endodontic and restorative needs of the remaining tooth substance.
Posterior teeth with fractures involving the floor of the pulp chamber have
poor long-term prospects.
Root resorption
The loss of tooth structure due to resorption may lead to fracture (Fig.
5.64). The prognosis for teeth affected by internal resorption is better
because of a more limited communication with the periodontium. The
process may be arrested by pulp removal and, provided the remaining
tooth substance is strong enough, the tooth can be retained (Fig. 5.65).
Treatment of resorption arising on the external surface of the root is less
predictable (Fig. 5.66). External inflammatory resorption associated with
root-canal infection is treatable and responds to root-canal treatment. The

Fig. 5.63  Horizontal root fractured

molar (arrowed)

Fig. 5.61  Splinted horizontal root

Fig. 5.62  Horizontal root fractured
fractured tooth
Fig. 5.60  Horizontal root fractured premolar (arrowed)
tooth survived 20 years

Fig. 5.65  (a) Radiographic evidence of internal resorption in a mandibular

molar; (b) root canal treatment will arrest the resorption

Fig. 5.66  Molar with

both internal and
external resorption

Fig. 5.64  (a) Mandibular premolar with internal

resorption; (b) same tooth fractured through
resorption
 140  Treatment planning

treatment of other types of external resorption is unpredictable. Defects
can be repaired surgically (Fig. 5.67) and also made supragingival. There
is, however, a tendency for this type of external resorption to continue.
Cone-beam computed tomography (CBCT) may be used to assess the
three-dimensional distribution of the tooth structure loss before deciding
on management (Fig. 5.68).
PLANNED REVIEW
Factors that may lead to secondary failure of a previously successful
root canal treatment include recurrent caries and coronal leakage (Fig.
5.72), caries extending into the root canal (Fig. 5.73) or furcation, root
fracture (Fig. 5.74) or perforation (Fig. 5.75).
In conclusion, all dental treatment should be undertaken applying the
principle of continuous review. Endodontic treatment provides definite
indications for scheduling review appointments and should be looked upon
as an integral part of treatment planning.

Reassessment and re-evaluation of the status of dental health of patients Fig. 5.68  (a,b) CBCT
is an integral part of the planning process. It involves examining the patient aids assessment of the
again; often taking elements of the history again, re-establishing a diag- 3D distribution of tooth
nosis, and formulating a new treatment plan for whatever new or residual structure loss
problems are encountered.
Clinical and radiographic follow up, at regular intervals for an indefinite
period, are essential for the assessment of endodontic treatment. Observa-
tion periods of at least 4 years are desirable (Fig. 5.69). Endodontic treat-
ment should be assessed annually.
Indications of success are absence of pain, swelling, sinus tract, other
symptoms, no loss of function, and radiographic evidence of a normal
periodontal ligament space around the root.
The outcome of treatment is considered uncertain if a radiographically A
evident radiolucency has remained the same size or diminished in size
without complete regeneration (Fig. 5.70).
Treatment is considered to have failed if a previously normal periapex
now exhibits a radiographic radiolucency or a pre-existing radiolucency
has increased in size (Fig. 5.71), or there is conflicting evidence with
respect to symptoms and radiographic evaluation. For example, a tooth
may have persistent low-grade symptoms and yet appear healthy clinically
and radiographically. It has been found that such symptoms are consistent
with a healing lesion and will resolve spontaneously within one year. In
some cases, such mild discomfort persists, particularly when palpating
over the root apex. This may be because bone remodelling during healing
results in the root apex being palpable through the mucosa. This is simply
a mechanical problem rather than a biological one and does not require
treatment, merely reassurance.

Fig. 5.67  (a) External B

root resorption at
surgery; (b) surgical
repair of the resorptive Fig. 5.69  (a)
defect with glass Periradicular lesion
ionomer cement related to bridge
abutment; (b) healing
following root canal
treatment (one year
later)

B B
 Treatment planning  141

B
A
Fig. 5.70  (a) Postoperative radiograph of lesion;
(b) lesion remains static Fig. 5.71  (a) Pre-existing lesion; (b) lesion increasing in size

Fig. 5.72  Caries leading Fig. 5.73  Caries in a

to failure of restoration root canal

Fig. 5.74  Root fracture Fig. 5.75  Root

induced during root perforation revealed in
filling post-obturation
radiograph

REFERENCES AND FURTHER READING Pennington, M.W., Vernazza, C.R., Shackley, P., et al., 2009. Evaluation of the
cost-effectiveness of root canal treatment using conventional approaches versus
Kvist, T., Heden, G., Reit, C., 2004. Endodontic retreatment strategies used by general replacement with an implant. Int Endod J 42 (10), 874–883.
dental practitioners. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 97 (4),
502–507.
Moisiewitsch, J.R.D., Caplan, D., 2001. A cost–benefit comparison between single tooth
implant and endodontics. J Endod 27, 235.
 6
Section 2  Preparation for delivery of endodontic treatment
Pre-endodontic management
  K Gulabivala, Y-L Ng

Endodontics can be one of the most satisfying aspects of dental practice,
provided it is performed in a well-managed working environment. Consid-
eration should be given to specific organizational requirements, which
affect the operator, the staff, the patient and, ultimately, the tooth to be
treated. The practice of endodontics has become very gadget-oriented and
may demand a vast array of small instruments and equipment, depending
upon the operator’s preferences, as well as large adjunctive equipment,
such as the operation microscope and X-ray machine. Nurses may grow
to abhor endodontic cases if they are not fully engaged or involved in the
management of the patient. Nurses may also find preparation for an endo-
dontic case laborious in comparison to other procedures. The growth of
specialized equipment and materials for various disciplines has enor-
mously complicated the management of ergonomic practice. Endodontic
procedures also rate highly on the list of medico-legal challenges posed to
defence organizations. It is well to consider, systematically and thoroughly,
the clinical operatory, nurse support, operator and medico-legal aspects,
patient and finally, the tooth.
THE CLINICAL AREA
cervical trays without hand-piece and 3-in-1 cord fittings will also allow
instruments to be approximated to the tooth being treated.
Customized carts have been favoured among endodontists since they
provide easy and ergonomic access to a range of hand-pieces, including
air-rotors, slow speed motors, reducing speed/controlled torque hand-
pieces, ultrasonic or sonic instruments, irrigation devices and obturation
devices (Fig. 6.3). Some believe that the development of cordless devices
may obviate the need for cart or mobile systems. However, given the pace
of change in equipment and material available demands flexibility and it
seems the best way to achieve this is not to have fixed worktops but
mobile, multilayered systems providing an increased area within easy
reach (Fig. 6.4). The mobile systems may be stored away in a separate
area where they can be replenished and be ready for use in any surgery.
The trend may be toward having separate mobile units for different
Fig. 6.1  Example of a
sub-optimally designed
operatory

The clinical area, office or “operatory”, benefits from having a fresh,

bright, warm and welcoming atmosphere. The design, layout and décor
help contribute a great deal to enhance its image and comfort for the
patient. An environment designed and constructed to allow staff to work
efficiently, with comfort and ease, will decrease stress, encourage smooth,
relaxed working days, and increase job satisfaction. The operatory should
be designed in an uncluttered fashion to facilitate unhindered movement
to and from the working area. The image (Fig. 6.1) shows a sub-optimally
designed operatory with poor space and access.

EQUIPMENT LOCATION, STORAGE AND DELIVERY

The organization of endodontic equipment requires careful thought and
should be planned to satisfy the needs of the operator’s working methods
and nursing support. Dental equipment companies are increasingly aware
of the rapidly changing needs and will help facilitate redesign to meet
modern requirements. Thought should be given to the frequency and
sequence of use of equipment and materials on a procedure basis, followed
by the ergonomic manner in which the procedure could be delivered. This
will have implications for how the equipment is laid out within easy reach
and where the responsibility lies for smooth delivery in sequential fashion.
Engineers have even given thought to the design of a computer controlled
dispensing machine that delivers the correct endodontic tool in timely and Fig. 6.2  Mobile cabinet
ordered fashion.
In traditional surgeries, cabinetry and cupboards in an L- or U-shaped
configuration should be placed within the working area of both operator
and assistant. Work can often be simplified by considering the most useful
positions to place the more commonly used instruments. The key element
here is the basic space within which this is fitted. Figure 6.1 shows an
operatory that could potentially be effective but is severely compromised
by lack of sufficient space.
The distance traversed by hand instruments during operative procedures
should be minimized; the use of a mobile cabinet or cervical tray (Fig.
6.2) may help achieve this. A mobile cabinet provides flexibility with a
worktop area and drawers, which may be sited close to the patient. Simple

© 2014 Elsevier Ltd. All rights reserved.


Fig. 6.3  (a) Well-designed operatory; (b) with customized endodontic cart
(courtesy of R Goria)
speciality or procedure work. Such a system should also be complemented
by an effective restocking system that prioritizes the most frequently used
items. Finally, the system should be adaptable enough to allow immediate
and easy integration of new equipment and materials, which appear on the
market annually, without disrupting the previous system.
Thought should be given to rapid turnaround between patients, so that
disinfection can be facilitated and the new set-up delivered by exchange
of a mobile unit. Flow and space should be streamlined so that used equip-
ment is directly transferred for washing and disinfection.
WORK SURFACE ORGANIZATION
The work surfaces of dental units and cupboards are readily contaminated
by aerosol from the use of hand-pieces, triple syringe sprays and ultrasonic
instruments, and therefore, selected surfaces should be easy to maintain
clean. The junction between the work surface and the wall should cove to
aid cleaning. Any joints on the work surface should be sealed to prevent
accumulation of contaminated matter and allow cleaning.
Between clinical sessions, all work surfaces, including those that are
apparently uncontaminated, should be cleaned with a detergent or a micro-
bicidal disinfectant.
Pre-endodontic management  143
Fig. 6.4  (a,b) A well-
designed surgery using
built-in cabinetry with
multilayered system for
storage of specialized
equipment (courtesy of
RPY Ng)
B
Contamination zones
Work surfaces should be defined as zones of high or low contamination.
Surfaces liable to become contaminated with body fluids or infected
matter should be identified and designated high contamination zones.
These areas benefit from impervious disposable coverings that can be
changed and the surface beneath cleaned between patients. All disposable
and sterilizable instruments and trays fall within this area (Fig. 6.5).
Low contamination zones include all other areas that, during normal
clinical procedures, are not expected to become coated with infected mate-
rial. In these areas, procedures should be adopted to limit the number of
surfaces touched each time a patient is treated. The operator should be
 144  Pre-endodontic management
Fig. 6.5  Work surface in high contamination zone covered with sterilized
impervious disposable coverings (green)
Fig. 6.6  Bacterial
growth on agar plates
from hand prints of a
right-handed clinician
(a) before and (b) after
hand washing using
Hibiscrub hand cleanser
A water lines (Fig. 6.8).
B ● rotary instruments, friction grip burs, conventional burs, safe-ended
aware that their hands are generally contaminated and hand-washing tech-
niques have gained a high priority in helping to eliminate serious infection
spread in hospitals. Figure 6.6 shows bacterial growth on agar plates from
hand prints before and after hand washing using Hibiscrub hand cleanser.
Water supplies
All waterlines and airlines should be fitted with antiretraction valves to
help prevent contamination of the lines. Water retraction valves may aspi-
rate infected material back into the tubing. Hand-pieces with water sprays
should be allowed to discharge water into the sink for 20–30 seconds after
each patient. Overnight microbial accumulation can be reduced if the
hand-piece is run for two minutes at the beginning of each day. Many units
now have a bottled water system, disinfectants advised by the manufac-
turer may be run through the system at the end of each day to reduce the
Fig. 6.7  Dental unit waterline
decontaminant – Alpron solution
(Quality Water Specialists Ltd,
Yorkshire) containing citric acid,
sodium-p-toluolsulphonechloramide
<0.2%, EDTA and sodium
tosylchloramide
A B
Fig. 6.8  Bacterial growth on agar plate from dental unit line water
(a) before and (b) after treatment with Alpron solution
microbial load and prevent the build-up of biofilm. Specific agents, such
as Alpron (Fig. 6.7) are now available to eradicate biofilms in dental unit
INSTRUMENTATION AND STORAGE
A very wide range of instruments designed specifically for endodontic
treatment is available. Some of these instruments have been used for many
years; others are new and, in some cases, highly technical. The instruments
described in this book are readily available and commonly used, while a
range of customized instruments named by their inventors or modifiers are
also available.
Generally used instruments and materials include:
● basic instruments packs
burs, Gates–Glidden burs
● hand instruments, barbed broaches, files, other root-canal
instruments
● rubber dam and accessories
● power-assisted instruments, nickel–titanium rotaries, ultrasonic
● measuring devices, electronic, rulers, gauges, stops
● instrument and post-retrieval kits
● irrigating syringes and needles
● paper points
● gutta-percha points both ISO and larger non-ISO tapers
● instruments for lateral and vertical compaction of gutta-percha
● instruments for thermomechanical compaction of gutta-percha
● equipment for thermoplastic injection of gutta-percha
● equipment for solid core gutta-percha techniques.
Consideration must be given to storing, cleaning and sterilizing all these
items.

The basic instrument pack
A presterilized basic pack (Fig. 6.9) is required for all routine root canal
procedures. The pack contains:
● front surface mirror
● two endodontic locking tweezers
● canal probe
● Briault probe
● long-shanked excavator
● endodontic pluggers
● gutta-percha gauge
● flat plastic
● metal ruler
● mixing spatula
● Mitchell’s trimmer.
Use of the front surface mirror overcomes the problems associated with
double images, which are produced when the reflecting surface is beneath
a layer of glass. The endodontic locking tweezers allow small items to be
gripped safely and transferred between assistant and operator (Fig. 6.10).
They are particularly useful when handling gutta-percha points, paper
points and cotton-wool pledgets. The tips of the beaks should be blunt and
grooved. A Mitchell’s trimmer may be used to remove cement and either
temporary or permanent crowns. The canal probe or DG 16 should be
long, fine, sharp and strong. It is used to feel the floor of the pulp chamber
when locating canal orifices. A Briault probe is used to feel for overhangs
when removing the roof of the pulp chamber and to check the internal
margins of any restorations. Two other probes, although not included in
the basic kit, are useful in periodontal assessment: the explorer EXD3CH
(Fig. 6.11) (used to examine restorations, such as bridges), furcation probe
with markings (for measuring the extent of periodontal furcation involve-
ment in posterior teeth); and a pocket measuring probe with a fine shank,
blunt end, and millimetre markings (as illustrated in Chapter 11). Long-
shanked excavators (Fig. 6.12) come in a range of designs to allow access
Fig. 6.9  Presterilized
basic instrument pack
Fig. 6.10  Endo-locking
tweezers
Fig. 6.11  Explorer
EXD3CH
Pre-endodontic management  145
to the pulp chamber. These are used for scooping out the remains of the
pulp and excess gutta-percha; also for flicking away pulp stones. The flat
plastic assists in placement of inter-appointment provisional restorations.
The ruler is used to measure and set instrument lengths. The nurse can
provide initial measurement but the operator may wish to use a finger-ring
held ruler for checking or fine adjustments.
Operation microscope
There are many brands of Dental Operating Microscopes available on the
market. They vary by the optical system; a continuous zoom versus series
of steps of magnification (3.4×, 5.1×, 8.5×, 13.6×, 21.3×); fixed versus
inclinable binoculars; halogen, Xenon or LED illumination; and manual
versus foot pedal for hands-free operation. Installation of video camera
and monitor or assistant scope could facilitate four-handed endodontic
practice. The former set-up would allow the dental assistant to carry out
other tasks and for documentation purposes. The type of microscope and
installation (ceiling mounts, wall mounts, floor-stands, custom-mounts)
may be limited by the size of the dental surgery and the quality of the
ceiling and walls. An optimal mounting arrangement would facilitate easy
access and positioning, as well as make best use of the available surgery
space (Fig. 6.13).
X-ray machine
All medical devices, including X-ray machines, purchased for use in
countries within the European Union should have acquired CE (stands for
Communauté Européenne, i.e. European Community) marking according
to the Medical Devices Regulations 2002. The wiring must comply with
BS 7671: 2008, 17th edition. Each newly installed X-ray machine must
receive a Critical Examination (IRR99 reg 31) by the installer confirming
the correct function of safety systems, leakage exposure rates and in-beam
dose. An acceptance test must be performed prior to clinical use and,
thereafter, routine tests at suitable intervals.
Current dental X-ray machines are normally microprocessor-controlled
digital devices with touch contact keyboards to set the exposure time and
area to be exposed. The tube voltage of most current machines is 70 kV
and must comply with a suitable British or international standard for con-
struction. Most current machines are suitable to be used with conventional
and digital radiographic techniques.
Fig. 6.12  Long-shanked
excavator
Fig. 6.13  Wall mounted
microscope (courtesy of
RPY Ng)
 146  Pre-endodontic management

Fig. 6.14  A cordless hand-held Fig. 6.15  Computer

dental X-ray machine monitor connecting to a
digital system (courtesy
of RPY Ng)

Dental X-ray machines come in a variety of configurations including

mobile units or wall, floor column or dental unit mounted machines.
Recently, a number of cordless hand-held dental X-ray machines with
high-frequency, 60 kV DC X-ray generator have become available (Fig.
6.14). The advantages of these hand-held units include flexibility in posi-
tioning, spacing saving and economy as a single device can serve multiple
surgeries. However, the X-ray tube, X-ray control circuitry, and high
voltage generator (transformer) contained in a single, lead shielded housing
may increase the risk of operator exposure to radiation as a result of tube
leakage and radiation back scatter. The back scatter can be reduced by a
properly deployed lead acrylic disc surrounding the exposure aperture
cylinder to absorb and limit this unnecessary dose. A theoretical increase
in patient dose from these units could result from repeated exposure
required due to operator/patient movement.
Operation of the dental X-ray machine should comply with current
legislations governed by: B

● The Ionising Radiations Regulations 1999 (IRR99), which aims to

keep occupational exposure to dentist, dental nurses and others
from ionizing radiations as low as reasonably practicable (ALARP)
and
● The Ionising Radiations (Medical Exposures) Regulations 2000
(IR(ME)R) which aims to minimize patient exposure during
medical procedures. A Fig. 6.16  (a) Ultrasonic handpiece
and (b) tips
A dental practice must draft Written Procedures for the use of dental
X-ray equipment including:
● Identifying patients – to link each patient with their medical X-ray viewer
history, test results and any treatment specified by the practitioner
● Identifying those authorized to use dental X-ray equipment as Radiographic viewers or computer monitor connecting to a digital system
Practitioner, Referrer or Operator should also be sited within easy reach. They may be placed on a nearby
● A procedure to enquire about a female patient’s pregnancy status work surface, or on a mounted, adjustable arm (Fig. 6.15).
● A Quality Assurance programme
● Patient dose assessment NON-SURGICAL RETREATMENT DEVICES
● Diagnostic reference levels
It is important to use some form of magnification during non-surgical
● Procedures for documenting the evaluation of each radiograph
retreatment – if you can see it, you can probably do it, for example remov-
along with all pertinent details
ing a trough of dentine around a post or fractured instrument requires good
● Written protocols for operating each X-ray unit.
magnification, good lighting, and a steady hand. Longer appointments are
Each employer is responsible for ensuring that all Practitioners, Refer- required for retreatment cases, in particular for removal of foreign material
rers and Operators are suitably trained. Normally, a practice should from root canals. Ultrasonic units and tips (Fig. 6.16) are very useful
appoint a Radiation Protection Supervisor. Persons responsible for expos- equipment for cutting a trough around embedded metallic material. There
ing X rays should be suitably trained, a record of current training should is equipment specifically designed for removal of coronal cast restorations
be recorded and regular refresher training scheduled and audited by the (Fig. 6.17), posts (Fig. 6.18), fractured instruments (Figs 6.19, 6.20) and
employer. for repair of strip perforation.
 Pre-endodontic management  147

A
B

Fig. 6.17  (a) Instruments for crown or bridge

D
removal; (b) Wamkey® for removal of crown

C E

Fig. 6.19  (a) Steiglitz and (b) endodontic fine-beaked forceps, (c) instrument removal
system (IRS), (d) Cancellier tubes and cyanoacrylate glue, (e) ultradent tubes as an
alternative to Cancellier tubes

A B

Fig. 6.20  Masserann kit

Fig. 6.18  (a) Ivory miniature post puller; (b) Eggler post puller; (c) Ruddle
post-removal system; (d) Gonon post-removal system
 148  Pre-endodontic management

SURGICAL ARMAMENTARIUM 4 periodontal curettes

4 root-end filling carrier and plugger (Fig. 6.27)
A complete armamentarium should be available for surgical endodontic 4 tissue forceps
procedures to include those items required for all surgical procedures 4 needle holder (Fig. 6.28a)
including: 4 suture scissors (Fig. 6.28b)
● sterile towels ● endodontic instruments for canal preparation and obturation may
● gauze swabs and ribbon also be required.
● bowl for saline irrigant
● irrigating syringe or irrigation tubing CLEANING AND STERILIZATION
● aspiration equipment
● local analgesic equipment All instruments contaminated with oral and other body fluids should be
● rear-venting surgical hand-piece (Fig. 6.21a) cleaned and sterilized after use. There are three stages to the sterilization
● Lindeman bone-cutting (Fig. 6.21b) and tapered diamond burs process: presterilization cleaning; sterilization; and storage. The surgery
● ultrasonic unit and root-end preparation tips (Fig. 6.22) should be designed to facilitate a dirty-to-clean workflow to prevent recon-
● needles and suitable suture material tamination of decontaminated instruments. An example layout (Fig. 6.29)
● an endodontic surgical tray (Fig. 6.23), which should include: for essential quality requirements for setting up a decontamination area is
4 front-surface mirror and small microsurgical mirrors given by the Health Technical Memorandum 01-05: Decontamination in
4 hooked, curved and angled probes primary care dental practices. Dentists should note the manufacturers’
4 college tweezers instructions and ensure these are followed. There is a progressive move
4 a range of surgical scalpels (Fig. 6.24) towards using instruments once only. Many nickel–titanium rotary instru-
4 periosteal elevators (Fig. 6.25) ments have a sign on the packet showing a number 2 with a diagonal line
4 periosteal retractors (Fig. 6.26) running through it, which means for one use only (Fig. 6.30). It should be
4 bone curettes noted that a new packet of files should be sterilized before use unless

A B

Fig. 6.21  (a) A high-speed surgical hand-piece

with rear-venting exhaust in order to avoid
development of surgical emphysema; (b) a
Lindeman bone-cutting bur Fig. 6.22  Dentsply Tulsa Dental ProUltra™ tips Fig. 6.23  Surgical tray

Fig. 6.24  Scalpel blades Fig. 6.25  Elevators


A
Fig. 6.26  Retractors
Fig. 6.27  (a) Micro-Apical Placement (MAP) System (Dentsply-Maillefer, Ballaigues, Switzerland); (b) Messing gun;
(c) Dovgan carrier; (d) MTA block and Lee’s carver; (e) retrograde pluggers
it arrives in a presterilized pack; this trend is also increasing but the
sizes that are presterilized are limited. Many dental instruments are now
available for one use only and are presented in presterilized packs. It is
important to note that the Department of Health, UK (Health Technical
Memorandum 01-05: Decontamination in primary care dental practices
Pre-endodontic management  149
Fig. 6.28  (a) Needle holder; (b) suture scissors
2009) recommends endodontic files and reamers should only be reused on
the same patient on condition that the instruments are marketed as reusable
and the dental practice’s registered manager is satisfied that the tracing and
audit procedures used are such as to exclude error in identifying the
instrument(s) and associating them with the correct patient.
 150  Pre-endodontic management

Ventilalation input Ventilalation

extraction or input
Wash-hand Wash-hand
basin (optional) basin

Clean zone Dirty zone

Out
Out In

(optional, dependent
upon space and layout)
Ultrasonic cleaner
(optional)
Rinsing Washing
Inspection and Inspect and where sink sink
Instrument flow storage Sterilizer applicaple, pack Deliver
Airflow

Notes
1. The use of an ultrasonic cleaner is optional. Where such a cleaner is not provided, handling difficulties will be reduced by siting the washing sink
near to the rinsing sink or by combining both sinks through the installation of a double-bowl sink assembly.

2. Practices may increase the number of sterilizers if capacity and service continuity dictates.

Fig. 6.29  Example layout of essential quality requirements (from Health Technical Memorandum 01-05)

Fig. 6.30  Symbol Fig. 6.31  Washer-

indicating single use disinfector
only

PRESTERILIZATION CLEANING
Used instruments may be heavily contaminated with body matter which
harbours and protects microorganisms. The instruments should be cleaned
thoroughly before being sterilized. Whenever possible, cleaning should be
undertaken using an automated and validated washer-disinfector (Fig.
6.31) in preference to manual cleaning, as a washer-disinfector includes a
disinfection stage that renders instruments safe for handling and inspec-
tion. Manual cleaning should be considered only where the manufacturer
specifies that the device is not compatible with automated processes
(including ultrasonic cleaning) or when the washer-disinfector is temporar-
ily unavailable. Exceptionally, where local experience indicates that pre-
washing may be helpful (for example in the removal of tenacious dental
materials), such action may be appropriate before automated cleaning.
Manual cleaning should be performed using a long-handled brush with
soft plastic bristles, warm water (45°C or lower, a higher temperature will
coagulate protein and inhibit removal) and a detergent specifically formu-
lated for manual cleaning of instruments. Chlorhexidine handscrub,
washing-up liquid, cleaning creams or soap should not be used as these
agents, in particular chlorhexidine, make proteins adhere to steel. Gross
debris is removed from small files by stabbing them into sponges impreg-
nated with detergent. The person cleaning instruments should always wear
protective gloves to avoid inoculation with debris. Ultrasonic baths may
be used to enhance removal of gross debris. A detergent should be used in
the bath, not a disinfectant. Washer-disinfectors are the most reliable way
of presterilization cleaning but must not be used as a substitute for steri-
lization (Health Technical Memorandum 01-05: Decontamination in
primary care dental practices, Department of Health, UK 2009).
STERILIZATION
Pressure steam (autoclave) sterilization is the preferred method for the
sterilization of most instruments used in the clinical setting. It is effective
and has a reasonably short cycle (3 min at 134°C). The effectiveness of
autoclaving wrapped instruments in sterilizing chambers that are not evac-
uated has been called into question and steam-sterilizers with a vacuum
phase are generally recommended. However, this type of sterilization has
the disadvantage of causing corrosion and dulling of sharp instruments and
is unsuitable for sterilizing cotton wool and paper products.
Checking successful sterilization
Successful sterilization depends upon the consistent reproducibility of
sterilization conditions. Autoclaves should therefore be validated before
 Pre-endodontic management  151

use and their performance monitored routinely. Correct operation of the
autoclave must be checked every day that the autoclave is used. This can
be achieved by recording the readings given as printouts or readings on
the instrument panels. The readings should be compared with the recom-
mended values.
STORAGE
The most convenient storage systems for endodontic instruments involve
the use of trays, and boxes. Many autoclavable metal containers for endo-
dontic files are available but the move towards single use for presterilized
root canal files would suggest these metal boxes are obsolete.
File holders and stands
There are several file holders on the market; they carry enough instruments
for one treatment or part of the treatment (Fig. 6.32). This simple stand
for files closes flat to prevent the instruments falling out in the
autoclave.
Files may be placed in a foam insert held in a file stand or by an Endor-
ing (Fig. 6.33). This finger-held device allows the operator or nurse to have
both hands free. A ruler lies in front and small cups may be placed at the
side, for example EDTA paste. The foam insert has been specially devel-
oped so that files placed in it may be sterilized in an autoclave. The foam
inserts are one use only and provide a convenient way of disposing of the
instruments into a sharps container after use. Using the insert in this way
reduces the chance of a needle stick injury.
INFECTION CONTROL
Each practice must have an infection-control policy. This describes the
practice policy for all aspects of infection control and provides a useful
guide to the training necessary for each member of staff. Clinical staff
should be vaccinated against the common illnesses shown in the list below.
The immune status of staff must be checked for rubella and hepatitis B.
All dental staff should have an appropriate hepatitis B immunization
record, which is recorded and updated. At the time of writing no dentist
in the UK who was HIV seropositive was legally entitled to practice clini-
cal dentistry, however, from 2013, the Department of Health in England
announced that dentists with HIV can practice providing they can prove
that they are taking antiretroviral drugs and are being monitored. (Dentists
who are hepatitis B positive can continue to practice normally.)
Recommended vaccinations for dental staff:
● diphtheria
● hepatitis B
● pertussis
● poliomyelitis
● rubella
● tetanus
● tuberculosis.
Fig. 6.34  Rack for
endodontic syringes

Pastes and medicaments

A wide variety of pastes and medicaments are available for endodontic
treatment, many of them housed in syringes. A suitable rack for these is
shown in Figure 6.34. Sleeves are available for cross-infection control.
After each use the sleeve and tip are discarded. Figure 6.35 shows calcium
hydroxide being placed into the canal system with a capillary tip.

Fig. 6.32  File holder

Fig. 6.33  Endoring

(SybronEndo, Orange, Fig. 6.35  Calcium
CA, USA) hydroxide syringe in use
 152  Pre-endodontic management
During the history taking, patients might disclose that they are HIV or
HBV carriers. HBV carriers and patients with HIV who are otherwise well
may be treated routinely in dental practice, but patients with HIV who are
in ill health or who have oral manifestations of the disease should be
referred for expert advice. Confidentiality should always be preserved and
the obligation to provide care realized. Refusal to treat these patients is
illogical – undiagnosed carriers of infectious disease pass undetected
through practices every day. Operators who are HBV- or HIV-positive
should seek appropriate advice.
Dental interest in Creutzfeld–Jakob disease (CJD) and prion-related
conditions centres on the risk of their transmission from human to human
during dental treatment. There is no known case of this happening.
However, those patients suspected of being infected require special
infection-control procedures. “Prions”, the infectious agents that cause
CJD and related conditions, are much more difficult to destroy than con-
ventional microorganisms. Suspected cases should be referred to hospital
for dental treatment. In the UK, the government banned the reuse of root-
canal instruments because of the risks involved.
All staff should understand the modes of transmission of infections,
sterilization and infection-control requirements, the proper use of protec-
tive clothing and equipment, the remedial actions to be taken in the event
of accidents, the importance of general hygiene and of keeping immuniza-
tions up to date.
Inoculation injuries are the most common route for transmission of
blood-borne viral and other infections in dentistry. Great care should be
taken when handling all sharps and specially designated bins should be
used in their disposal. Needle-protection devices are available and should
be used for re-sheathing. Each practice should have a policy to record and
manage inoculation injuries promptly and appropriately.
THE DENTAL NURSE
The dental nurse should be well trained and hold a relevant qualification.
In a specialized field such as endodontics, advanced in-house training is
also necessary to ensure that the nurse fully understands the various tech-
niques employed and how they can support and facilitate the delivery
of care. Emergency and resuscitation training requirements should also
be met.
Fig. 6.36  Rubber dam, eye protection and Fig. 6.37  Nurse seated slightly higher than
waterproof bib operator
ANTICIPATION
One of the greatest assets a dental nurse can possess is the ability to antici-
pate the needs of patient and operator. The nurse should be aware of the
aspects of care that optimize a patient’s comfort, safety and protection.
Dental nurses should be encouraged not to adjust the patient’s chair until
the medical history has been established – and certainly not before explain-
ing what is about to happen – because sudden chair movements may
frighten patients unnecessarily. Particular attention should be paid to the
angulation of the chair and the head position. It is wise to ask the patient
if they are comfortable.
The patient must wear spectacles, to protect their eyes, and a disposable
waterproof bib (Fig. 6.36). These items protect against splashes, dropped
instruments and spillage of sodium hypochlorite.
With the patient supine, the assistant should sit slightly higher than the
operator to allow adequate visibility (Fig. 6.37). Adjustment of the light
is the nurse’s responsibility.
If patients spend long periods lying supine, the chair should be returned
to the upright position slowly on completion of treatment, and the patient
asked to sit for a moment or two before leaving the chair – this will prevent
problems arising from postural hypotension.
In order to provide effective operator support, the nurse must anticipate
the actions of the operator. Clinical procedures should be understood and
learned thoroughly and a rationalized work sequence developed between
the operator and nurse. Use of arranged spoken and unspoken signals
improves the efficiency and flow of working movements (Fig. 6.38).
CLOSE SUPPORT
The specific operations involved in endodontics are generally delicate and
require a high level of concentration on the part of the operator. Control
of the operating field is one of the main aims of close support. The operator
and nurse control visibility and illumination, soft tissues, moisture and
saliva, instruments, water coolants and contaminants.
In endodontics, the greatest aid in achieving this degree of control is a
dental (rubber) dam. Isolation using a dental dam can greatly improve
efficiency by gaining time normally lost by patients rinsing, dentists con-
tinually changing wet cotton rolls and assistants struggling with saliva
ejectors. According to the European Society of Endodontology guidelines
Fig. 6.38  Example of hand signal indicating
transfer of file
 Pre-endodontic management  153

Fig. 6.40  Close support aspiration Fig. 6.41  Surgical tip used for the aspiration of
sodium hypochlorite

Fig. 6.39  Rubber dam placement

Fig. 6.43  Transferring new paper point to the

operator

Fig. 6.44  Measuring working length

Fig. 6.42  Exchange of paper points

(2006), root-canal treatment procedures should be carried out only when Fig. 6.45  Instrument
the tooth is isolated by rubber dam to prevent salivary and bacterial con- transfer to foam insert
tamination, prevent inhalation and ingestion of instruments and prevent
irrigating solutions escaping into the oral cavity.

INSTRUMENT TRANSFER
This should be smooth, safe, and unobtrusive and require a minimum
amount of movement on the part of the operator. Transfer of instruments
should take place in the so-called transfer zone, which lies over the
patient’s neck at chin level. Instrument exchange becomes important
during the preparation and obturation phases of root-canal treatment, when
the system of parallel transfer can be employed to advantage as it allows
the alternate exchange of instruments to be accomplished speedily.
A dental nurse can be of considerable help during rubber dam placement the nurse who spears the instrument into the sponge. This simple move-
(Fig. 6.39), instrument transfer, canal irrigation, and suction procedures. ment reduces the chance of needle stick injury.
Figure 6.40 shows the nurse holding the aspirator tip close to the tooth
without hindering the operator’s access. Similarly, a small surgical tip is THE OPERATOR AND MEDICO-LEGAL CONSIDERATIONS
placed close to the tooth (Fig. 6.41) so that sodium hypochlorite may be
removed efficiently without obstructing the operator’s view. Paper points A letter from a solicitor alleging that a patient has been treated negligently
and gutta-percha points are exchanged between operator and nurse effi- has a dramatic and lasting impact on any dental practitioner however
ciently using endo-locking tweezers with the parallel technique. Figure experienced or well qualified. Unfortunately, these letters are arriving with
6.42 shows the nurse removing a paper point and placing a new paper ever-increasing frequency, in line with the increasing frequency of claims
point in the operator’s hand (Fig. 6.43). Notice that the instruments lie against health professionals. This section is designed to help the dental
parallel to each other during transfer. practitioner, particularly when carrying out endodontic treatment, to reduce
The nurse should also be able to judge the length of hand instruments the risk of receiving such letters.
required and set working lengths precisely when instructed (Fig. 6.44). A Although the section has been written from the English law perspective,
quick and efficient method of transferring an instrument after use to the it should be emphasized that some of the recommendations given may
nurse is shown in Figure 6.45, the operator holds the instrument towards differ in other jurisdictions. While the law may differ slightly between
 154  Pre-endodontic management
countries, there is no doubt that, provided a dentist carries out endodontic
treatment to the best of his/her ability, explains the treatment to the patient,
keeps careful records, and maintains good communication at all times, the
chances of litigation will be greatly reduced.
According to the insurers and indemnity organizations during recent
years, endodontic treatment is a common source of claims for compensa-
tion, and of allegations of professional misconduct to dental regulatory
bodies.
The main type of complaints received by defence bodies include:
● poor communication
● unsatisfactory treatment
● failure to make an appropriate diagnosis
● incorrect or unnecessary treatment
● fee dispute
● post-treatment complication.
NEGLIGENCE
A dentist assumes a duty of care under common law when a patient is
accepted for treatment. If the dentist is negligent and infringes that duty
of care, with the result that the patient suffers avoidable harm, the patient
is entitled to be compensated for the loss and damage sustained. To succeed
in an action for negligence, the patient must prove, on the balance of prob-
abilities, that the dentist owed them a duty of care, breached that duty by
some act or omission, and that, as a direct consequence of the breach of
duty, some loss or damage followed.
To prove the practitioner acted negligently, the patient must prove he/
she departed from what is considered to be standard practice by a respon-
sible dental body. If the dentist has acted in accordance with an accepted
view on endodontics then it is unlikely that he/she will be found negligent.
However, one of the problems in dentistry, and in particular in endodon-
tics, is that there may be more than one responsible body and each may
hold a different view. It is the responsibility of the dentist to keep up-to-
date with advances in endodontics and to be aware that the view they are
following is current.
DENTAL AND MEDICAL RECORDS
A dentist must always obtain a medical history from a patient before com-
mencing treatment and check the history for any changes at subsequent
visits. Full contemporaneous records are also a prerequisite for responding
constructively to a complaint, or successfully defending a disciplinary
action or negligence claim. If, for example, a patient alleges that the treat-
ment was unnecessary or inappropriate, the patient records, including
X-rays, will almost invariably prove essential to refute such an allegation
by confirming the investigations leading to the decision to undertake
endodontic treatment. Likewise, radiographs may be essential to refute
allegations of unsatisfactory treatment.
The use of apex locators is now well established in endodontics, but
pre- and post-treatment radiographs are still necessary to demonstrate both
the tooth and supporting tissues and the quality of the final root canal
treatment. The European Society of Endodontology guidelines (2006)
suggest that, even if an apex locator is used, the working length should be
verified by a dental radiograph during the procedure.
In the absence of such adequate clinical records to corroborate the den-
tist’s account of events, the courts may be more likely to accept the
patient’s evidence than that of the dentist. This is because the court may
well consider the patient’s recollection of a single event or a limited
number of consultations to be more reliable than that of the dentist, who
may have cared for many hundreds or thousands of patients during the
interval since the treatment in question.
Digital radiographs are acceptable dento-legally, but care should be
taken to ensure that the software system prevents tampering with the
images. Similarly, computer-held records are acceptable dento-legally,
provided the software incorporates suitable safeguards to protect the integ-
rity of the data. Digital data should be backed up to prevent loss in the
case of damage or theft of computer equipment.
Clinical records should include the following:
● patient’s complaints and symptoms
● relevant medical, dental, and social histories
● clinical signs and examination findings
● special tests, such as pulp tests, radiographs, and radiographic
findings
● diagnosis and treatment plan
● local analgesia type and amount given
● working-length measurement(s)
● instrumentation and preparation
● type of root-filling materials used
● number of radiographs taken
● temporary restorations
● any complications or mishaps.
CONSENT
Dentists must obtain valid consent from their patients prior to treatment.
It is very common nowadays for a dissatisfied patient or their advisor to
criticize a dentist not only in the performance of the endodontic treatment
itself, but also in having failed to obtain valid consent.
The need to obtain consent is an ethical/professional duty, as well as a
legal duty. The General Dental Council’s guidance to dentists Maintaining
Standards states:
A dentist must explain to the patient the treatment proposed, the risks
involved and alternative treatments and ensure that appropriate consent
is obtained.
If a general anaesthetic or sedation is to be given, all procedures must
be explained to the patient. The onus is on the dentist to ensure that all
necessary information and explanations have been given either
personally or by the anaesthetist/sedationist. In this situation written
consent must be obtained.
The three principles of consent are:
● giving the patient adequate information
● competency/capacity of the patient (i.e. his/her understanding of
the information supplied)
● non-coercion of the patient into giving the consent (i.e. the consent
must be given freely).
To satisfy the first principle, the dentist must ensure that the patient has
adequate information and fully understands the intended treatment:
● the purpose
● the procedures involved
● how the procedures will be carried out
● the feasible options such as osseo-integrated implants, given their
long-term success rates, where this is a viable and reasonable
choice – equally, if extraction alone, or in combination with some
other form of prosthesis, is a reasonable option the patient should
be informed, so they can make a balanced judgment
● the significant risks and
● the prognosis.
 Pre-endodontic management  155

The provision of adequate information in relation to the risks that must REFERRAL FOR TREATMENT
be highlighted to a patient has seen a shift in recent years in many jurisdic-
tions throughout the world. The previously held (and still held in certain The responsibility for obtaining consent to endodontic treatment rests with
jurisdictions) “professional standard” was that the patient should be fore- all treating dentists. If the patient is being referred to an endodontic spe-
warned of all substantial risks as deemed appropriate by responsible and cialist, some responsibility for the consent process remains with the refer-
relevant bodies of professionals. In many countries, including the USA ring dentist.
and Australia, this has moved towards a “patient standard”, by which The requirements of the dentist depend on the reason for the referral. If
practitioners should forewarn of all risks that might influence the patient’s the patient is referred for an opinion only, the referring dentist needs to
choice not to consent to a specific procedure. Accordingly, if one is in ensure that the patient understands the reasons for the referral. If the patient
doubt as to whether to warn about a potential complication or risk, it would is referred for treatment, the referring dentist should explore other treat-
be sensible to err on the side of caution and so inform the patient. Further- ment options with the patient and explain the endodontic treatment prior
more, the giving of such warnings should be noted in the records. to referral.
If the treatment proposed is complex, and arguably all endodontic treat- It is the duty of the referring dentist to provide the endodontist with
ment is complex, or if several treatment options are available, the discus- information concerning the history of the tooth, investigations and inter-
sions with the patient should be clearly documented in the records. Indeed, ventions carried out, as well as general information about the medical,
the General Dental Council requires a written treatment plan and fee esti- dental and social histories of the patient. Relevant radiographs should be
mate for all expensive and/or extensive treatments. The advice is to issue made available to the endodontist.
a patient with the treatment plan in duplicate and ask the patient to sign Likewise, the endodontist should communicate with the referring
and return one copy, confirming agreement to the treatment and fees. The dentist, if appropriate following initial assessment, and always upon com-
signed copy of the plan should be retained in the records but always be pletion of treatment. Details of the findings, diagnosis and treatment
aware that the signed plan will only be one piece of documentary evidence together with a final radiograph, type of temporization, recommendations
that may help to prove that consent was obtained. It should not be used as for final restoration and any follow up should be sent to the referring
a substitute for a two-way dialogue with the patient and notes of such dentist.
discussions in the records.
Note that written consent is required by the General Dental Council for THE PATIENT
any treatment under any form of sedation or general anaesthesia.
EDUCATION AND INFORMATION
TREATMENT COMPLICATIONS All treatment should be fully explained to the patient before any is carried
out. Patients who understand the treatment that they are about to undergo
Separating an endodontic instrument during treatment and leaving a
will be less anxious, easier to handle and more appreciative. Information
portion of the instrument in situ, or creating a perforation may not be
may be made available in the waiting room – patients are most receptive
negligent. However, with few exceptions, it is negligent not to recognize
in the few minutes before their appointment – in the form of leaflets pro-
the complication, to omit to inform the patient, and not to make arrange-
duced by the practice or commercially available (Fig. 6.46). In the clinical
ments for remedial treatment/review. Patients are entitled to a prompt,
area, the dentist may use models (Fig. 6.47), which make the procedures
honest explanation of any mishap or complication. Arrangements should
easier to explain: a patient will understand the radiographs better if he or
be made to remedy the situation, in so far as is possible, and any referring
she is given a basic knowledge of anatomy. Digital radiography, which
dentist or other dentist involved in the patient’s treatment, should be
shows an enlarged image of the patient’s tooth on a monitor, is helpful in
informed. Patients are entitled to receive, and should be offered referral
providing an explanation of the treatment.
for, a second opinion or specialist opinion/treatment where appropriate.
All actions in relation to a mishap or complication should be recorded in
the clinical notes.
Fig. 6.46  Patient information
PROTECTION OF THE PATIENT
If a dentist should fail to protect the oropharynx from ingestion of foreign
bodies, such as inhalation or swallowing of an endodontic instrument, it
is likely that any resultant claim will be indefensible. It is the dentist’s
duty to protect the patient from such harm/injury. The patient’s profes-
sional advisors may well plead that the “action speaks for itself” – res ipsa
loquitur – and the burden of proof will shift from the patient to the dentist.
Accordingly, the dentist will have to prove that he was not negligent and
that he used all adequate precautions to prevent the damage. This may
prove difficult because all responsible endodontic opinion advocates the
use of a dental rubber dam as the only adequate and effective measure to
prevent ingestion of endodontic instruments. Therefore, if small instru-
ments are swallowed or inhaled, the precautions taken were inadequate
and the dentist may be successfully sued with all the attendant stress and
publicity that this would entail.
Similarly, it is recommended that all patients undergoing treatment
should wear protective spectacles, and that their clothing should be pro-
tected from spillages.
 156  Pre-endodontic management
Fig. 6.47  Education
models
Most (if not all) patients attending the dental practice for the first time
will be nervous. A calm, pleasant manner, showing that you are concerned
about the patient’s welfare, will make treatment easier for both patient and
operator.
ANAESTHESIA AND ANALGESIA
Pain control is a most important aspect of endodontic procedures: the
patient’s confidence will be gained if they undergo a painless procedure.
Analgesia removes pain sensation without loss of tactile sense. Anaesthe-
sia results in complete loss of all sensation, and may be induced locally
or generally (when the patient will lose consciousness). In dentistry, anal-
gesia is usually all that is required because we wish merely to remove pain;
occasionally, with an injection, we may achieve anaesthesia, but this is
surplus to requirements. Local anaesthesia is more accurately described as
local analgesia. In dentistry, local analgesic agents are usually combined
in a single carpule with vasopressors. The function of the vasopressor is
to provide local haemostasis and to delay the absorption of the analgesic
agent. This, in turn, prolongs the duration of action of the analgesic.
Adrenaline (epinephrine) is the most effective, potent and frequently used
vasopressor. In healthy patients, the influence of the adrenaline (epine-
phrine) injected with the local anaesthetic tends to be minor in most
patients provided the injection is administered slowly and avoids a direct
intravascular bolus of adrenaline. This is true of all concentrations of
adrenaline (epinephrine) available in combination with local analgesic.
Absolute contraindications to the use of adrenaline (epinephrine) include
cases where the patient has uncontrolled hyperthyroidism. Administration
of exogenous adrenaline (epinephrine) could provoke a “thyroid storm” or
“crisis”. Other conditions that require special consideration prior to admin-
istration of vasopressor agents include unstable angina, cardiac arrhyth-
mias, history of myocardial infarction, hypertension and uncontrolled
diabetes. Although not absolutely contraindicated, caution should also be
exercised in patients on tricyclic antidepressants.
Before treatment begins, the type of analgesia or anaesthesia must be
chosen. Guidelines for this decision are given below.
Routine root-canal treatment
Regional or infiltration local analgesia is all that is necessary.
Acute hyperaemic pulp
Regional or infiltration analgesia is usually adopted, followed by addi-
tional local analgesic (see Chapter 10).
Fig. 6.48  Good haemostasis permits clear
inspection of the root and surrounding tissues
Surgical retreatment
In surgical endodontic procedures, good haemostasis is an absolute require-
ment especially during root-end preparation and root-end filling and in
corrective procedures. Good haemostasis allows for clear inspection of the
resected root surface and facilitates placement of a root filling by providing
a blood-free environment (Fig. 6.48).
Vasopressors such as adrenaline (epinephrine) in a local anaesthesia
carpule exert their influence on blood flow by stimulating α1-adrenergic
receptors found on the smooth muscle cells of the microcirculation in the
alveolar submucosa. It is important to avoid injection into skeletal muscle,
as the predominant receptor type here is β2-adrenergic, stimulation of
which results in vasodilation. This would cause an increase in local blood
flow, more rapid removal of the analgesic agent with concomitant loss of
profound analgesia, and a loss of haemostasis control.
Problems arising during and after surgery are frequently encountered
with patients with bleeding disorders. It is therefore imperative that
any patient with a history of bleeding disorder or those taking anticoagu-
lant medications should be referred to their medical practitioners for
further assessment and adjustment of their medications. If necessary, a
number of haematological tests can be used to assess the patient’s
status, and these are readily available in many centres in most communi-
ties. These screening tests include platelet count and function tests, acti-
vated partial thromboplastin time (APTT) and international normalized
ratio (INR) formerly known as the prothrombin time (PT). The INR
allows for the interpretation of PT with respect to variations among
laboratories.
Anxious patient
Gag reflex
In mild cases, once the rubber dam is applied treatment may be carried
out routinely with local analgesia as the patient has an effective barrier
and is unaware of instruments or fingers in his or her mouth. In the more
severe cases, intravenous sedation or relative analgesia will control the
reflex.
Relative analgesia
This is a safe, easy technique using varying quantities of a mixture of
nitrous oxide (N2O) and oxygen (O2) administered via a nasal mask.
However, difficulties may arise in that the nosepiece may hinder the opera-
tor in root treatment and endodontic surgery in the maxillary incisal region.
Other disadvantages include the set-up costs and the possible hazards of
air “pollution” within the surgery environment.

Oral sedation
A suitable benzodiazepine may be prescribed for the night before
and/or one hour preoperatively. Many drugs are available for this purpose
and the operator is advised to consult the relevant literature for correct
dosage, contraindications, precautions and other important data. In
common with oral, nasal, and intravenous sedation, consent for the proce-
dure and pre- and postoperative instructions must be in writing and be
obtained before the sedative is taken. For all types of sedation, the operator
must be chaperoned, and a responsible adult must accompany all patients
home.
Nasal sedation
Concentrated forms of midazolam are being produced, which can be
sprayed into the nasal cavity resulting in a rapid onset (about 10 minutes)
of action. This technique is especially suited for patients with physical or
learning difficulties, and for children.
Intravenous sedation
Intravenous sedation may be used for any endodontic procedure. It has a
quicker recovery time and is considered safer than general anaesthesia,
making it more suitable for the ambulatory patient. In the UK, there is no
place for general anaesthesia except in the hospital setting. Indeed, only
“conscious sedation” is permitted, a state in which the patient is calm,
relaxed, and in verbal contact with the operator. In other parts of the world,
notably the USA, “deep sedation” is also utilized but requires substantial
skill and experience on the part of the sedationist.
Intravenous sedation is ideally administered by an anaesthetist or dedi-
cated sedationist. The technique involves using various drugs, most com-
monly the benzodiazepines, such as diazepam and midazolam. Analgesics
are occasionally given in addition to a benzodiazepine to produce a finer
quality of sedation and to raise the pain threshold; this is particularly useful
for those who find local anaesthetic injections disproportionately painful,
and in patients in whom inferior dental blocks do not “take” very well.
Patients with medical conditions such as Parkinson’s disease or epilepsy,
as well as those with strong gag reflexes, can be controlled well with this
technique. Anti-sialogogues, such as atropine may be added to the sedation
to produce a dry field.
Careful titration of these drugs by an appropriately trained and skilled
sedationist allows long and/or difficult procedures to be carried out with
relative ease, particularly for anxious patients, most of whom welcome the
side effect of profound amnesia!
MEDICATION
Following treatment, the patient should be advised to take a suitable anal-
gesic for any postoperative pain. There is some evidence to show that
taking a non-steroidal anti-inflammatory drug one hour before treatment
can reduce postoperative pain.
Patients who are already on medication must be advised of any change
during the endodontic treatment. The patient’s medical advisor should be
contacted if it is thought necessary to alter the dosage or to stop a drug
that has been prescribed (e.g. warfarin or steroid therapy).
PATIENTS REQUIRING ANTIBIOTIC COVER
The advice on patients at risk from infective endocarditis (Table 6.1)
has changed following recommendations from the National Institute for
Clinical Excellence (NICE). Some patients (those who have already suf-
fered an attack of infective endocarditis or require a general anaesthetic
and are either allergic to penicillin or have already had more than one
Pre-endodontic management  157
Table 6.1  Patients at risk from infective endocarditis
History of infective endocarditis Rheumatic heart disease
Ventricular septal defect Degenerative valve disease
Patent ductus arteriosus Persistent heart murmur
Coarctation of the aorta Atrial septal defect repaired with a patch
Prosthetic heart valve
course of penicillin in the previous month) are at special risk and may
benefit from referral to hospital for endodontic treatment.
All patients at risk should be encouraged to maintain a high degree of
oral health to reduce the severity of possible bacteraemias. Patients who
require endodontic surgery should be advised to take a chlorhexidine
mouthwash starting 24 hours before surgery and continuing for 4–5 days
afterwards. However, allergic reaction to chlorhexidine is a possibility.
PATIENTS WITH HIV/HBV
Every patient must be considered a possible source of infection from
herpes simplex 1 and 2, HBV and HIV. The operator should always wear
barrier protection: gloves; mask; and protective spectacles during treat-
ment, and gloves should be changed after each patient. The risks of trans-
mission of HBV during dental treatment are well known, but HIV is less
easily transmitted. By providing a physical barrier between the operating
site and the patient’s saliva, a rubber dam reduces the contaminated aerosol
effect and, therefore, the risk of infection. All health workers should
receive regular vaccination against hepatitis B. HIV-positive patients in
good health may be treated in general dental practice but, if they show
evidence of ill health or oral manifestations of disease, then they should
be referred to special units for advice or treatment.
THE TOOTH
REMOVAL OF CALCULUS AND PLAQUE FROM TEETH
Prior to careful examination of the involved tooth and its isolation, it is
important to remove any calculus and debris. This will facilitate examina-
tion, as well as prevent impaction of debris and calculus into the periodon-
tium during rubber dam application. It may also be convenient at this point
to floss through the contacts where rubber dam is to be applied to ensure
freedom of contact. It is sometimes necessary to trim overhanging amal-
gams or to remove them prior to satisfactory isolation.
REMOVAL OF CARIES/RESTORATIONS
Any carious, leaking or suspect restorations must be removed. The
amalgam restoration illustrated (Fig. 6.49) is obviously surrounded by
secondary caries and should be removed (Fig. 6.50). Both radiographic
and clinical signs of caries should prompt entire removal of the restoration
prior to consideration for endodontic treatment.
When a bridge abutment or crown requires root-canal treatment, they
should always be checked to see if they have been decemented by hooking
a Briault or American Pattern probe under the pontic, near the retainer,
and applying pressure to remove them: bubbles around the retainer margins
of bridges and, in extreme cases, a slight sucking noise indicate decemen-
tation. Even solitary crowns may sometimes be sufficiently devoid of
luting cement without actually coming off and it is worth applying control-
led axial force with a pair of towel clips to ensure absence of looseness.
 158  Pre-endodontic management

Fig. 6.49  Carious Fig. 6.50  (a) Amalgam removed;

maxillary premolar (b) caries removed and access gained

Fig. 6.51  Decemented

distal abutment of
posterior bridge

A C
B

Fig. 6.52  (a–c) Staining of cotton wool caused by leakage around residual restorative material

In the case illustrated (Fig. 6.51), the bridge must be removed. More subtle
signs of leakage should be sought, including marginal discoloration of the
tooth or staining of the restoration, both from the external aspect, as well
as from within the access cavity when it is judged that the existing restora-
tion is sound enough to keep and work through. Even at the second visit
of root-canal treatment, the cotton wool placed in the access cavity partly
(to prevent the temporary restoration from blocking the canals) should be
examined for signs of staining (second function) caused by possible
leakage around residual restorative material (Fig. 6.52). This in itself is a B
good reason for using a cotton wool barrier, it is not placed for preventing
leakage as some believe and on this basis criticize its use.
A Fig. 6.53  (a,b) A tooth that is not
predictably restorable
ASSESSMENT OF RESTORABILITY OF TEETH
Large plastic restorations (amalgams and composites) and crown or bridge
retainers make it difficult to assess the long-term restorative prognosis of
teeth without their removal. Such restorations should usually be removed
PROVISIONAL RESTORATION OF
and an assessment made of the residual tooth tissue in the context of a
BROKEN-DOWN TEETH
future predictable restoration so as to avoid the embarrassing situation The most important reason for placing provisional restorations in/on
of satisfactorily root treating an unrestorable tooth (Fig. 6.53). It is broken-down teeth is to protect and retain the occlusal and proximal space
difficult to give clear guidelines for restorability but an attempt is made in that will be occupied by any future restoration. A common problem is that
Chapter 14. neglect of such space preservation allows occlusal and/or mesial tooth
 Pre-endodontic management  159

Fig. 6.56  Cemented copper band

Fig. 6.54  Floor of pulp chamber in a severely
broken-down tooth
Fig. 6.55  Clamp retained with etched composite

drifting with consequent loss of space rendering the tooth unrestorable Fig. 6.57  Cutting a copper band
without complicated orthodontic intervention.
Broken-down teeth should be restored to meet space protection criteria,
as well as to allow the placement of a rubber dam. More definitive restora-
tion of the tooth before root treatment is unnecessary, time-consuming,
and may jeopardize the final restoration. The best possible view of the
floor of the pulp chamber is seen in severely broken-down teeth (Fig. 6.54),
although such rampant access cavity preparation is not recommended!
It is usually possible to place a clamp on a broken-down tooth but, on
rare occasions, some build up or a crown lengthening procedure is required Fig. 6.58  Trimming a copper band
to remove excess gingival tissue and expose the margins of the tooth. using a stone
If a clamp cannot be placed because of significant loss of tooth sub-
stance, the tooth may be built up with a restorative material, such as a
light-cured composite to allow clamp placement and temporary filling
(Fig. 6.55). Another option is to fit and cement a copper band or steel
orthodontic band around the tooth with glass ionomer cement. The band
must fit accurately otherwise the attachment apparatus will be damaged
and at subsequent visits confuse the judgement of progress of treatment,
the tooth under treatment and its neighbour is poor, consideration should
as the patient may report the tooth to be tender on pressure. Where pos-
be given to its replacement with one that has a better contact relationship
sible, the band must be left clear of the gingival margin. The case illus-
in order to protect the periodontal tissues. This is especially important in
trated (Fig. 6.56), shows a first mandibular molar with a fracture line in
periodontally susceptible patients.
both the distal and buccal walls of the crown. A copper band was selected,
Periodontal probing defects around teeth scheduled for endodontic treat-
cut (Fig. 6.57) and trimmed with a stone to fit (Fig. 6.58), cotton wool
ment should be measured in detail using continuous point charting (as
placed in the pulp chamber with softened stick gutta-percha over the top,
shown in Chapter 12) and recorded; in molars, exposed furca should also
and the band cemented.
be properly characterized. These provide a baseline for assessment of the
Where the tooth tissue loss is great enough to prevent easy placement
effect of endodontic treatment.
of a rubber dam clamp, the predictable restorability of the tooth must be
questioned. Alternative options should be carefully considered before pro-
gressing further. ISOLATION USING RUBBER DAM AND
OTHER DEVICES
PERIODONTAL TISSUE MANAGEMENT Rubber dam isolation is the single most useful procedure for making den-
tistry and in particular endodontics easier. It has many advantages, which
There are several reasons why the periodontal tissues should receive atten-
can be listed as follows:
tion before root-canal treatment, including removal of excess tissue to
allow the placement of a rubber dam. The periodontal health around the ● Safety: Rubber dam undoubtedly provides the best protection for
tooth margin is examined, any inflammation pointed out to the patient and the oropharynx and should be used during root canal treatment
oral hygiene instruction given. Inflammation-free gingival tissues make (Fig. 6.59). They further protect the soft tissues of the mouth and
for easier and cleaner tooth isolation. Furthermore, any discomfort caused lips from the potentially caustic effects of any root canal irrigants
by local gingival inflammation will be eradicated before commencing or medicaments.
root-canal treatment and enable confusion-free evaluation of the tooth as ● Prevention of cross-infection: Rubber dam acts as a barrier and
treatment progresses. If a surgical procedure is planned, gingival tissues prevents aerosol formation from the mouth when air-driven or
free of inflammation provide the best tissue texture for surgical manipula- ultrasonically activated instruments are used in the mouth. Not
tion and provide a predictable outcome in replacement of the tissues. only is the risk of cross-infection from such aerosol eliminated but
Root-canal treatment of molar teeth will be often followed by a permanent the patient is also protected from the surgical environment. Perhaps
restoration, often a crown whose accurate margin placement is reliant upon most importantly, the barrier prevents salivary microorganisms
good gingival health. When the proximal contact between a restoration in from entering the root canal environment.
 160  Pre-endodontic management

Fig. 6.61  Rubber dam forceps

Fig. 6.59  Rubber dam protecting a patient’s Fig. 6.60  Rubber dam punch
oropharynx

● Comfort: Contrary to popular belief, rubber dam confers a Fig. 6.62  Rubber dam
comfortable working environment for the patient, dentist and nurse. and plastic frame
It is very rare that a patient may find a rubber dam to be
uncomfortable. The reasons are usually feelings of claustrophobia,
breathing difficulties, activation of gagging reflex or latex allergy.
Each of these may be appropriately addressed and it is rare that a
patient cannot be convinced of the benefits of a rubber dam. In
fact, once used to it, most will demand its use for treatment. Latex
allergies appear to be on the increase and non-latex rubber dam is
available as an alternative.
● Controlled operating field simplifies procedures: Rubber dam
provides retraction of the lips and facial tissues and also helps keep
the tongue out of the field, although the extent of retraction is
determined by the manner in which the rubber dam is framed. A
number of options are available and discussed later. It also Fig. 6.63  Clamps from
improves visual and manual access and provides a clean and left to right – 14, 13a,
controlled operating field. It reduces the need for the patient to W8a, 1
rinse, although they should still be able to swallow and
communicate reasonably well. All of this contributes to an
improvement in overall efficiency of treatment.

RUBBER DAM KITS

Rubber dam is manufactured in different coloured squares of two sizes:
130 and 150 mm. The larger square is the most convenient for endodon-
tics. A variety of thicknesses are available; heavy (0.25 mm) or extra heavy
(0.3 mm) are the least likely to tear. The rubber dam has one shiny and
one mat surface, these are important in the context of the orientation used
during application (explained later).
The punch (Fig. 6.60) may be used to make several different-sized holes
in the dam but only one medium-sized hole is usually necessary. If several
teeth need to be isolated a rubber stamp can be used to locate the holes
precisely. The stamp becomes unnecessary when rubber dam is used rou- largely on personal preference, though the main criterion for selection is
tinely and for single tooth isolation only. that the jaws provide a four-point contact for best stability. Root-canal
Forceps (Fig. 6.61) allow clamps to be placed and removed from teeth. treatment requires only a small number of clamps that will be used rou-
The beaks should be deep enough to allow the clamp to be fitted around tinely. The four clamps shown in Figure 6.63 are sufficient to cover most
the gingival margin in a small mouth. situations.
Frames (Fig. 6.62) should be wide enough to provide good access with
good retaining spikes for the dam. Retracting frames that provide better
cheek retraction using a band that passes around the neck are also avail-
APPLYING THE DAM
able, although rarely used nowadays. Root-canal treatment usually requires isolation of a single tooth. Two
Clamps are manufactured in a wide variety of shapes and sizes to suit commonly used methods for placing the dam are described. The first of
different teeth and situations. The choice of which one to select depends these is to fit the clamp so that all four jaws are in contact with the tooth

Fig. 6.64  All four jaws should be in
contact with the tooth
Fig. 6.65  Jaws in contact with tooth
– viewed from above
Fig. 6.68  Dam fitted to anterior teeth without
clamps
Fig. 6.67  Clamp and dam carried to the tooth
together
(Figs 6.64, 6.65). Having ensured that the clamp is stable on the tooth, a
single hole is punched in the dam if the clamp is wingless and, if winged,
a larger hole is made (by punching a second hole beside the first one or
selecting a larger punch), the dam is then stretched over the clamp bow
and the tooth (Fig. 6.66). The second method is to insert the wings of the
clamp into a hole punched in the dam, then carry the dam and clamp to
the mouth and place them over the tooth (Fig. 6.67); the dam is then
slipped off the wings so that it lies around the neck of the tooth.
In both these situations, the rubber dam may not have sufficient oppor-
tunity to slip through the contact points to a stable position at the gingival
margin around the entire circumference of the tooth. As a consequence,
the dam may allow some seepage of saliva around its margins. This may
be conveniently stemmed with a commercially available gasket, such as
Oral Seal. This is a paste that is applied to the margin of the dam in small
quantities. It absorbs moisture and stems the passage of saliva.
A less commonly used method of rubber dam application but one that
gives a better seal is that used in operative dentistry when several teeth
are isolated together. In this method, the clamp(s) is/are preselected as
described. The rubber dam is prepared by punching holes designed to
match the size and distribution of the teeth so that the sheet is positioned
centrally over the operative site, to cover the mouth completely without
unequal tension on any side when the frame is applied. The rubber dam is
applied by stretching the rubber at selected holes to thin it down. The edges
are then “knifed” into contact between the teeth. This ensures that the
rubber dam lies at about the same level around the circumference of the
tooth. The dam is inverted, after drying the teeth with a triple syringe, by
employing a flat plastic to insert the edge of the dam into the gingival
Pre-endodontic management  161
Fig. 6.66  Rubber is stretched over
clamp bow and tooth
Fig. 6.69  Split-dam technique
Fig. 6.70  The lower (dependent) edge of the
rubber dam is folded up to create a pouch to
capture fluid overspill from handpiece water-
coolant and irrigation when suction fails to  
control it.
crevice. When the mat surface faces away from the patient’s face, the
inverted dam surface facing the tooth is also mat and this facilitates the
stability of the dam as it is held in position by friction. Although applica-
tion in this way is a little more time-consuming, it is worth the time spent
because of the moisture-free isolation it provides. The rubber dam clamps
are then applied to hold the sheet in place.
In the anterior part of the mouth, the dam may be fitted without clamps
(Fig. 6.68) using rubber or wooden wedges. In those cases where the tooth
is severely broken down, there are two options either use the split-dam
method (Fig. 6.69) or build a retaining wall on the tooth being treated (see
Fig. 6.55).
The rubber dam frame may be applied to the front of the dam or to the
back depending on preference. When applied to the front, an additional tip
is to create little pockets at the bottom corners to collect waste irrigant
from the tooth and to prevent it from spilling onto the patient (Fig. 6.70).
This is particularly useful for single operators working without continuous
nursing support.
 162  Pre-endodontic management
OTHER DEVICES
Many other devices are used to protect the oropharynx but none of them
are as effective as rubber dam.
REFERENCES AND FURTHER READING
Abbott, P.V., 2004. Assessing restored teeth with pulp and periapical diseases for the
presence of cracks, caries and marginal breakdown. Aust Dent J 49 (1), 33–39.
Bolam v Friern Barnet Hospital Management Committee, 1957. 1 WLR 582.
Department of Health, 1990. Principle recommendations of the report of an expert
working party on general anaesthesia, sedation, and resuscitation in dentistry. HMSO,
London.
Department of Health, 2001. Guidance notes for dental practitioners on the safe use of
x-ray equipment. National Radiological Protection Board 2001: Information Services,
Chilton, Didcot, Oxon OX11 0RQ [information@nrpb.org.uk].
Department of Health, 2009. Health Technical Memorandum 01-05: Decontamination in
primary care dental practices. DH, London.
General Dental Council, 1997. Maintaining Standards – Guidance to Dentists on
Professional and Personal Conduct [and subsequent amendments]. GDC, London.
Nelson, C.A., Hossain, S.G.M., Al-Okaily, A., et al., 2012. A novel vending machine for
supply of root canal tools during surgery. J Med Engin Technol 36, 102–116.

The aim of this chapter is to outline the technical and clinical elements of
prevention and management of pulp disease. The rationale was established
in Chapter 2. The general principles of disease management covered previ-
ously apply equally well to the primary and secondary dentitions as will
be evident from Chapter 1. However, primary teeth bring special chal-
lenges of management and are covered here first before describing the
management of secondary permanent teeth.
MANAGEMENT OF THE PRIMARY DENTITION
Retention of the primary dentition until the time of natural exfoliation is
important for several reasons. Primary teeth have important roles in mas-
tication, appearance, speech development and space maintenance for the
permanent successors. Therefore, there are clear psychological advantages
of conserving rather than extracting such teeth.
Endodontic treatment of primary teeth differs from that of permanent
teeth for three main reasons – tooth morphology, physiology and pathol-
ogy. Techniques and medicaments used in primary teeth differ due to these
factors and because of the processes of physiological root resorption and
exfoliation.
MORPHOLOGY OF PRIMARY TEETH
The enamel and dentine of primary teeth are thinner and the pulp chamber,
with its extended horns, larger in proportion than in permanent teeth (Fig.
7.1). Caries progresses relatively more rapidly to the pulp in the primary
dentition.
Primary molars have irregularly shaped ribbon-like root canals with
lateral branches. The floor of the pulp chamber is thin and there are numer-
ous accessory canals in the interradicular area. The permeability of the
dentine in this region often leads to interradicular rather than periapical
bone loss associated with infected primary molars (Fig. 7.2).
The roots of the primary teeth are in close relationship to the developing
permanent successor and will undergo physiological resorption during
the process of exfoliation (Fig. 7.3). Materials used within the root canal
system must, therefore, also be resorbable. Their close proximity means
that trauma to, or infection of, primary teeth may affect the developing
successor. Possible sequelae include enamel defects, arrested development
or cyst formation.
PULP DISEASE IN PRIMARY TEETH
Inflammatory pulpal changes in response to caries occur more rapidly in
primary teeth compared to permanent teeth, soon becoming irreversible.
Symptoms from such pathological changes in primary teeth may not
become severe until the later stages of necrosis and abscess formation
(Fig. 7.4).
Diagnosis of pulp disease in young children is complicated by their
inability to articulate the problem, which is difficult enough for an adult
(see Chapter 4); furthermore, they may respond unpredictably to subjective
clinical tests. Techniques used in the management of pulp disease in per-
manent teeth cannot, therefore, be reliably used in the primary dentition.
Methods of objectively measuring inflammatory changes in the pulps of
primary teeth by molecular (e.g., prostaglandin) assays are under assess-
ment but not yet ready for implementation.
© 2014 Elsevier Ltd. All rights reserved.
7
Section 3 Delivery of endodontic treatment
Vital pulp therapy
Y-L Ng, K Gulabivala  
TECHNIQUES OF PULP THERAPY
INDIRECT PULP CAPPING
Carious lesions should usually be fully excavated before teeth are restored.
A clinical dilemma may be presented by the finding of deep caries in an
asymptomatic tooth exhibiting no clinical or radiographic evidence of pulp
disease in a child whose cooperation or attention span would preclude
progress to pulpotomy. Indirect pulp capping may be used in such instances.
Its success relies on the observation that the advancing carious front is
almost free of cariogenic bacteria. Provided that the overlying infected
dentine is removed, a small amount of softened dentine may be left in the
deepest part of the cavity and covered with a thin layer of setting calcium
hydroxide and then zinc oxide eugenol or reinforced glass ionomer cement.
The tooth should then be definitively restored to achieve an optimal
coronal seal with an adhesive or preformed metal restoration. The tooth
may then be reviewed clinically and radiographically to ensure that pro-
gression of pulp disease does not lead to periapical involvement. This
avoids a second operative visit, which is an obvious advantage for
children.
DIRECT PULP CAPPING
This technique is generally contraindicated for the primary dentition.
Pathological changes progress rapidly within the pulps of primary teeth
and their healing ability is limited. Pulpal inflammation usually persists
and progresses to internal root resorption and then necrosis, particularly
when calcium hydroxide is used to dress the exposed pulp (Fig. 7.5). Use
of the technique may be justified in exceptional circumstances, such as to
manage a small traumatic exposure in otherwise sound dentine during
cavity preparation. Haemorrhage from the exposure should be minimal
and easily controlled by gentle application of a cotton pledget soaked in
sterile water/saline. Further haemorrhage would indicate more severe
pulpal inflammation and pulpotomy would be the treatment of choice. If
the bleeding is easily arrested, calcium hydroxide or mineral trioxide
aggregate (MTA) (Table 7.1) may be used to dress the wound, followed
by tooth restoration.
Biodentine™, which is a new biocompatible and bioactive calcium sili-
cate based material (see Table 7.1), has been advocated for use as a dentine
“replacement”, as well as a direct pulp capping agent. It has been shown
to have the potential to induce transforming growth factor β1 (TGF-β1)
release from human pulp cells and early dental pulp mineralization but
further laboratory and long-term clinical outcome studies are required.
VITAL PULPOTOMY
This technique involves removal of the inflamed coronal pulp tissue, while
maintaining the residual vital radicular pulp tissue. Formocresol, which
had been the medicament of choice for fixation of such pulps in primary
teeth, is being gradually replaced by new materials, due to the concerns
about its safety in humans. The newly adopted materials include
Ledermix® for management of anaesthetic failure in hyperalgesic pulps,
ferric sulphate for haemostasis, and mineral trioxide aggregate as the
pulpotomy agent.
The indications for pulpotomy in a restorable tooth include absence
of the following: spontaneous or persistent pain, abscess or sinus,
 164  Vital pulp therapy

Fig. 7.1  Comparison of adult and primary molars Fig. 7.2  Caries and intraradicular bone loss in Fig. 7.3  Resorption of primary molar roots
(arrowed) primary molars

Fig. 7.4  Abscess associated with Fig. 7.5  Internal root resorption Fig. 7.6  Caries removal
primary molar

Fig. 7.7  Sectioned

Table 7.1  The constituents of MTA™ and Biodentine™
MTA™
Tricalcium
Dicalcium silicate
Tricalcium aluminate
Tetracalcium aluminoferrite
Calcium sulphate
Bismuth oxide
primary molar
Biodentine™
POWDER
Tricalcium silicate (C3S) (main core material)
Dicalcium silicate (C2S) (second core material)
Calcium carbonate and oxide (filler)
Iron oxide (shade)
Zirconium oxide (radiopacifier)
LIQUID
Calcium chloride (accelerator)
Hydrosoluble polymer (water reducing agent)

interradicular bone loss, or internal resorption. It may also be used to avoid

extraction, such as in the area of a haemangioma or child with a bleeding
disorder.
The contraindications for pulpotomy are the converse of indications,
plus permanent teeth being close to eruption and those who are medically
immunocompromised or at risk of endocarditis.
Procedure: quick reference guide
1 Adequate local analgesia and isolation, preferably with a rubber dam,
are essential. All peripheral caries should be removed prior to
entering the pulp chamber. The pulp chamber is then entered via the
exposure (Figs 7.6, 7.7).
2 The entire roof of the pulp chamber is removed to leave no
overhangs so that removal of the pulp tissue is not compromised. It is
important at this stage that the bur is not taken any deeper into the
cavity, since this would endanger the thin floor of the pulp chamber
(Figs 7.8, 7.9).
3 The coronal pulp is removed using a large sharp excavator or round
bur. The chamber is irrigated with saline and moist cotton wool
pledgets are applied to control haemorrhage and identify the pulp
stumps (Figs 7.10, 7.11).
4 If haemostasis is not readily achieved, 15.5% ferric sulphate solution
is applied to the pulp stumps with a microbrush for 15 seconds
 Vital pulp therapy  165

Fig. 7.8  Prior to access preparation Fig. 7.9  After removal of roof of pulp chamber Fig. 7.10  Removal of pulp chamber contents

Fig. 7.11  Pulp stumps remaining Fig. 7.12  Removal of cotton wool Fig. 7.13  Pulp stumps appear dark brown

followed by thorough rinsing and soaking up of excess moisture with Fig. 7.14  Zinc oxide
a slightly moist cotton pledget. Diluted (0.5%) sodium hypochlorite restoration
solution may also be applied to achieve haemostasis; persistent
haemorrage at this stage indicates residual pulp inflammation and
pulpectomy or extraction should be followed.
5 On removal of the cotton wool, the radicular pulp stumps should
appear bright or dark red without haemorrhage (Figs 7.12, 7.13).
6 Once haemorrhage has been arrested, MTA mixed with sterile water
to a “wet sand” consistency is then applied over the radicular pulp
and the tooth definitively restored with glass ionomer cement and a
stainless-steel crown (Figs 7.14, 7.15).

Fig. 7.15  Stainless-steel

DEVELOPMENT OF ALTERNATIVE APPROACHES crown
TO VITAL PULPOTOMY IN PRIMARY TEETH
Bone morphogenic proteins
With the techniques of molecular biology, progress has been made in the
purification of factors with bone inductive properties. The generic term for
this family of proteins is bone morphogenic proteins or BMPs. If BMPs
induce dentine, as well as bone, a true biological pulp capping and pul-
potomy agent will be available.
 166  Vital pulp therapy
Fig. 7.16  Stainless-steel crowns Fig. 7.17  Stainless-steel crown being fitted
Fig. 7.18  Resin crown formers in place Fig. 7.19  Resin crowns
Other methods
Pulpotomy techniques have been developed using electrosurgery, argon
laser and CO2 laser. However, results have been conflicting when com-
pared to the success of the formocresol pulpotomy. Further research is
required into these newer methods.
RESTORATION OF ENDODONTICALLY TREATED
PRIMARY TEETH
Endodontically treated primary teeth are weakened by the destruction of
tooth tissue during preparation. It is important that the definitive restora-
tion has the necessary strength to support the tooth structure and provides
an adequate seal following the endodontic treatment. For these reasons,
the most suitable restorations are stainless-steel crowns for posterior teeth
and composite-resin strip crowns for anterior teeth (Figs 7.16–7.19). The
reader is referred to other texts for details of the techniques.
FOLLOW UP AND COMPLICATIONS
When a primary tooth has been endodontically treated, it must be regularly
reviewed clinically and radiographically. The primary tooth may develop
signs and symptoms of acute or chronic infection. These may manifest as
swelling, sinus formation, tenderness to percussion, or mobility. Radio-
graphically, pathological root resorption must be distinguished from physi-
ological root resorption. Areas of bone loss may appear on follow up or
fail to heal following pulpectomy. Cyst formation may occur or there may
be arrested development of the permanent tooth. An infected primary tooth
may give rise to a hypoplastic permanent tooth, sometimes known as a
“Turner tooth” (Fig. 7.20).
In the majority of cases, when treatment fails, extraction is the preferred
option, rather than subjecting the underlying successor to greater risk.
Fig. 7.20  Turner hypoplasia
MANAGEMENT OF THE SECONDARY OR
PERMANENT DENTITION
OPTIMAL MANAGEMENT OF CARIES
Prevention of caries is principally non-operative, involving plaque control,
fluoride and diet modification. The role of operative dentistry is to repair
uncleansable cavities, which could be considered to be part of plaque
control. It is important to assess the current caries activity and caries risk
status when designing the management programme. An occurrence of two
or more new carious lesions per year is considered a high rate of lesion
activity and progression.
The possible risk factors include:
• medical conditions or medications causing low salivary flow and
dry mouth
• parents and/or siblings with active caries
• frequent sugar-containing snacks or drinks
• poor oral hygiene (indicated by plaque deposits or gingivitis)
• erupting molars
• deep pits and fissures and
• existing unsatisfactory restorations requiring replacement.
PRINCIPLES OF RESTORATION OF CAVITIES
A functional pulp–dentine complex requires responsive and vital odonto-
blasts that are able to lay down protective secondary or tertiary dentine.
Their conservation is enhanced by an absence of pulp inflammation and
protection of the dentine with a covering layer. Sublinings of calcium
hydroxide, zinc polycarboxylate or zinc oxide/eugenol cements (in decreas-
ing order of influence) have proved effective. Composite resins and resin-
modified glass ionomer cements can be effective but can be more technique

sensitive and, therefore, need greater care in placement. Deep cavities,
therefore, should preferably be lined with calcium hydroxide and overlaid
with zinc oxide/eugenol. This may limit the opportunity to use composite
resin in posterior teeth, which is ironic considering the irrational restric-
tions imposed on use of amalgam in some countries. While mercury has
toxic properties, there is little evidence of its toxic effect on the health of
patients or dentists when used in amalgam using modern dispensing,
mixing and placement methods. Care should equally be directed when
removing amalgams for replacement by tooth-coloured restorations.
Resin-modified glass ionomers should be sublined with calcium hydroxide
and their direct contact with dentine in deep cavities avoided.
Reactionary dentine response is important in increasing the dentine
thickness postoperatively and is positively related to the size of the cavity,
remaining dentine thickness, acid etching and microbial leakage. The
greatest reactionary dentine response is seen in cavities with remaining
dentine thickness between 0.25 and 0.5 mm and especially in the presence
of microbial leakage. It may be that this depth is optimal for the stimula-
tion effects of solubilized growth factors released during restorative pro-
cedures and able to reach the pulp. However, when dentine thickness is
reduced further, the damage to odontoblasts also increases, thereby result-
ing in a reduced reactionary dentine response. Restorative material plays
a minor role in stimulating reactionary dentine but, for obvious reasons,
its effect is enhanced by reduced dentine thickness (especially below
0.5 mm). Calcium hydroxide dressing produces the maximum response
and zinc polycarboxylate cement no response; this effect is probably medi-
ated via the stimulation of odontoblasts.
The approaches to prevention of microbial leakage may be divided
into two:
1 those seeking to reduce the gap between the restoration and the
tooth (including attempts at adhesion)
2 those using the antibacterial properties of materials to inhibit
microbial leakage.
Predictable reduction of the restoration/cavity gap is dependent upon
the properties of the material and its optimal manipulation, taking into
account the resilience of teeth and the interfacial interaction between
A B
E
D
Vital pulp therapy  167
restorative material and tooth tissue. For successful adhesive restoration
of teeth, the restoration must deform in phase with the tooth under all
loading conditions. Unfortunately, so far no material is able to meet these
demands for long periods, consequently, all adhesively retained materials
fail at some point in time after placement and allow microbial leakage.
While much emphasis has been placed on reduction or elimination of
the gap at the tooth/restoration interface to reduce microleakage, little, if
any, emphasis has been placed on the reduction of microbial leakage,
specifically. The closest approach is the use of zinc oxide/eugenol as a
base under amalgam restorations, though the effect of this material if
placed directly against the pulp must be considered. Eugenol is strongly
antibacterial and has neurotoxic and anodyne properties but is toxic to pulp
tissue, and therefore, must be lined by calcium hydroxide. Unfortunately,
the material cannot be used in conjunction with composite (aesthetic)
restorative materials because of its potential to interfere with their setting
reaction. Another option is to use a resin-modified glass ionomer as a
sublining but over a layer of calcium hydroxide. The durability of the
antibacterial effect of zinc oxide/eugenol has been questioned, however, it
need only last as long as the pulp–dentine complex takes to lay down a
defence (dentinal sclerosis and secondary dentine formation) against
further ingress of bacteria and their products. It could be argued that the
same applies to adhesive techniques. The crucial point is that the principle
of this approach assumes that the defence of the pulp–dentine complex is
fool-proof and not compromised by pre-existing inflammation, the depth
of cavity or the restorative material. The potential inability to block off all
dentinal tubules is the weak link in the ability of the pulp to survive, and
therefore, perpetuate its life to resist further onslaughts.
SMEAR LAYER AND ITS MANAGEMENT
Dentine or, more specifically, hydroxyappatite has the natural characteris-
tic that when it is cut or ground with metal, a deformed smear layer is
generated; in dentine this consists of organic and inorganic matter (Fig.
7.21a). Although the smear layer prevents good adaptation of restorative
material in the cavity, it may be best to retain it to protect the pulp from
the effects of microbial leakage. A reasonable compromise is to remove
C
Fig. 7.21  (a) Smear layer produced by cavity
preparation (SEM view); (b) partial removal of smear
layer using 3% hydrogen peroxide (SEM view);  
(c) removal of smear layer by EDTA (SEM view);  
(d) removal of smear layer by phosphoric acid to
reveal dentinal tubule openings (SEM view); (e) SEM
view of hybridized layer with resin overlying and
penetrating the dentinal tubules
 168  Vital pulp therapy

the smear layer partially so that the surface layer is removed leaving the
dentinal plugs intact (Fig. 7.21b). Use of 3% hydrogen peroxide may be
sufficient for this purpose in most instances. Newer generations of dentine
adhesives dictate what happens to the smear layer. In some cases, it is
retained and reinforced, in others, it is partially removed and, in others, it
is removed completely using acids, such as ethylenediamine tetra-acetic
acid (EDTA) (Fig. 7.21c) or phosphoric acid (Fig. 7.21d). It is intended
that the resin enters the surface layer of dentine to form what has become
known as the hybridized layer (Fig. 7.21e).
PRACTICAL APPROACHES TO MANAGEMENT OF
CARIES AND RESTORATION OF TEETH
dentine has been reached, a bur may be used to complete the preparation
as the advancing carious front is irregular. If considered necessary, the
surface of dentine may be scrubbed with 3% hydrogen peroxide to remove
only the superficial layer of the smear layer; the smear in the dentinal plugs
would remain intact. A sublining of setting calcium hydroxide should be
placed to facilitate repair and kill any residual bacteria in the dentine, as
Fissure sealant
Fluid-filled
Early enamel
caries tubules

The initial enamel white spot lesion (Fig. 7.22) only requires non-operative Translucent
treatment and preventive management. If caries has progressed into the dentine
dentine with demineralized dentine evident on radiographs or extending
through half of the thickness of dentine (Fig. 7.23), operative intervention
with a minimally invasive approach is required to prevent and avoid pulp
exposure. Pulp
The most conservative operative treatments include sealing of the
carious lesion or atraumatic restorative treatment (ART). Sealing of carious Fig. 7.24  Schematic diagram of sealing of carious lesion
lesions involves rubber dam isolation of the tooth, etching of the affected
tooth surface with 38% phosphoric acid, rinsing with water spray, air-
drying, and application of resin sealant (Fig. 7.24). ART involves removal
of soft carious dentine using hand instruments and filling the cavity with
an adhesive restorative material (Fig. 7.25).
Caries
Conventional management of carious lesions involves excavation of
carious dentine, placement of a layer of base material and restoration of
the cavity with amalgam or adhesive restorative material.
In treating a carious lesion (see Fig. 7.23), the following principles
should give optimal results: a conservative cavity should be cut to access
and remove softened, carious dentine (Fig. 7.26a), ensuring that all periph-
eral caries is removed (Fig. 7.26b). This may be achieved with a diamond Excavation of caries Removal of undermined enamel
bur in an air-rotor to breach the enamel. Subsequent removal of the carious
dentine may be facilitated by an appropriate sized stainless steel round bur
in a slow hand-piece and water spray. Very carious dentine tends to smear
and will clog the bur. Use of a sharp excavator may be efficient. Once hard

Fig. 7.22  Sclerosis of

dentine (A) caused by
A caries

Fissure caries Caries removal

Fig. 7.23  Established carious lesion

with cavitation

Placement of glass ionomer cement Simple restoration carving to

with simple occlusal form remove marginal excess

Fig. 7.25  Schematic diagram of ART of carious lesion


A B
D E
Fig. 7.26  (a) Removal of carious dentine in Figure 7.23; (b) completed preparation; (c) sublining with calcium
hydroxide; (d) lining with zinc oxide/eugenol; (e) placement of amalgam
well as to reharden it (Fig. 7.26c); a subsequent lining of zinc oxide/
eugenol should then be placed to prevent the effect of microbial leakage
on the pulp (Fig. 7.26d). Finally, a well-adapted amalgam restoration
should be placed to ensure an absence of marginal leakage (Fig. 7.26e).
TREATMENT OF THE DEEP CAVITY AND
“COMPROMISED” PULP
As long as the pulp–dentine complex remains physiologically intact and
functional, the pulp is likely to maintain its ability to recover after restora-
tive procedures. The pulp, therefore, becomes compromised when the
pulp–dentine complex is damaged beyond functional repair or is anatomi-
cally breached with severe damage to the underlying pulp tissue. The
treatment of the pulp compromised by exposure or near exposure, due to
deep caries or trauma may either involve attempts at its preservation by
vital pulp therapy or elective sacrifice by pulpectomy and root-canal treat-
ment. The choice of approach is based on the operator’s perception of the
chance of success and long-term prognosis given by the options. This
decision is also likely to be significantly influenced by the overall treatment-
planning considerations. A single tooth in an otherwise intact arch, to be
restored with a plastic restorative material provides opportunity for con-
venient review and correction and lends itself to a conservative approach.
A tooth scheduled for a cast restoration, on the other hand, provides more
limited scope for convenient correction and root-canal treatment is often
considered more pragmatic.
In a case where there are no overriding restorative considerations, the
choice between preservation of the pulp or its extirpation is guided by the
clinician’s preconceptions about vital pulp therapy derived from their
teachers and early clinical experience. In this respect, two schools of
thought have arisen: one believes in the viability of the pulp and its pres-
ervation and the other in its inherent susceptibility to long-term failure.
Members of the latter school of thought argue that the success rates of
primary root-canal treatment on teeth with vital pulps are higher (95%).
They further state that irregular calcification and internal resorption in the
canal treated by vital pulp therapy might render root-canal treatment more
difficult at a later stage. They would further claim that the potential for
pulp death and infection could reduce the chances of success of delayed
root canal treatment to 85%. The only circumstance in which they would
Vital pulp therapy  169
C
Fig. 7.27  Incompletely formed root
advocate vital pulp therapy is in the treatment of a tooth with an incom-
pletely formed or immature root (Fig. 7.27).
Proponents of vital pulp therapy, on the other hand, would offer success
rates of 85–90% for these procedures if the cases are properly selected and
executed and they would counter the evidence for pulp calcification and
significant internal resorption. In addition, in its strong favour, a tooth
with a preserved vital pulp may be considered to be less susceptible to
fracture.
Procedures designed to preserve the pulp have been labelled, indirect
pulp capping, direct pulp capping and pulpotomy. To this traditional list
may be added the new category of “regenerative pulp therapy” in the
future. The rationale for these was covered in Chapter 2.
A potentially compromised pulp may present in various ways: including
with a frank breach in the pulp, or nearly breached. The cause may be
caries, tooth surface loss, acute traumatic injury or cavity preparation,
regardless of which, the operator must estimate the pre-existing state of
the pulp, the extent of pulp injury and the degree of microbial contamina-
tion. The aim of the treatment is to remove as much of the infected hard
or soft tissue as possible and to restore the tooth with a bacteria-tight
restoration to preserve the health of the residual pulp tissue.
Indirect pulp capping
This clinical procedure (Fig. 7.28) has drawn some controversy in recent
years. The technique is used when excavation of all the carious dentine
from the pulpal surface might risk a traumatic breach in the pulp through
the thin but sound dentine overlying the pulp (Fig. 7.28a). When such an
eventuality is predicted clinically, some of the carious dentine over the
pulp (not peripherally) is left (Fig. 7.28b) and dressed with calcium
hydroxide to kill residual bacteria and to encourage remineralization and
dentine repair (Fig. 7.28c). This is followed by the application of a layer
of zinc oxide/eugenol to prevent microbial leakage (Fig. 7.28d). The tooth
is then restored with a permanent material that excludes microbial leakage
so that the lesion does not become reactivated (Fig. 7.28e). If an adhesive
composite material is to be used, then resin-reinforced glass ionomer
cement may be more suitable. Neither zinc oxide/eugenol nor resin-
reinforced glass ionomers should be applied directly to deep dentine
because of their potential to cause odontoblast and pulp injury. After this,
if there are no clinical symptoms and the tooth shows signs of continuing
 170  Vital pulp therapy
B
A C
D E
Fig. 7.28  Indirect pulp capping: (a) initial caries lesion; (b) caries removal; (c) calcium hydroxide dressing; (d) zinc
oxide/eugenol sub-lining; (e) final amalgam seal
vitality, two alternatives have been suggested. One is to restore the tooth
permanently. The second is to remove the dressing after an arbitrary period
of 3 months to excavate the residual carious dentine in the hope that sec-
ondary or reactionary dentine formation in the intervening period would
prevent exposure. This latter approach is not supported by the rate of
secondary dentine formation. At 3 µm per day, only 0.27 mm of dentine
would be formed in 3 months, perhaps an inadequate thickness to prevent
a traumatic exposure.
A practical problem with this technique is that it is difficult to gauge the
residual depth of the carious lesion. An unacceptable thickness of carious
dentine may be left behind together with necrotic pulp tissue adjacent to
the lesion (Fig. 7.29). It has been suggested that the accepted guideline
that dentine softening and staining precede bacterial invasion may not be
completely valid and that bacterial invasion of hard dentine is a distinct
possibility. Indirect pulp capping is therefore an unpredictable procedure.
Success relies on the correct diagnosis of the pulp condition and leaving
only a small amount of carious dentine, covered by an antibacterial lining
material.
Another partial caries excavation procedure is the stepwise (two-stage)
excavation procedure (Fig. 7.30), which is very similar to indirect pulp
capping. The main difference between the two procedures is that indirect
pulp capping involves almost complete removal of the affected dentine,
leaving a thin layer of demineralized dentine and re-entry is not attempted.
In stepwise excavation, the first excavation is aimed at changing the caries
environment only. It includes complete excavation of the peripheral dem-
ineralized dentine, but only minimal removal of the superficial necrotic
and demineralized dentine on the pulpal floor/wall for retention of a tem-
porary restoration. Further excavation close to the pulp should be avoided.
This will leave a soft, wet, discoloured dentine, which is then lined with
a calcium hydroxide base material and the cavity is temporarily sealed
with glass ionomer cement. After 8–12 weeks, the cavity is re-entered and
the second/final excavation is undertaken to remove the soft dentine,
leaving only central yellowish or greyish hard dentine (equal to the hard-
ness of sound dentine, as judged by gentle probing). The pulpal floor/wall
of the cavity should be protected with a calcium hydroxide base before
permanent restoration of the cavity.
Fig. 7.29  Necrosis of pulp, due to
microleakage
Direct pulp capping
Successful treatment of pulp exposures is guided by the same prerequisites
of healthy pulp – low bacterial contamination and absence of subsequent
microbial leakage. When excavation of deep caries leads to a traumatic
exposure of the pulp, relatively minor bacterial contamination of the pulp
tissue is assumed. Pulps left exposed to salivary contamination for several
hours following traumatic injury may still be successfully pulp-capped.
Minor contamination of the exposure by saliva during the operative pro-
cedures is unlikely to affect the outcome. The most important factor in the
successful outcome is a healthy pulp (minimally inflamed and capable of
replacing lost odontoblasts). The pulp is likely to be healthier in younger
teeth and, although it has been demonstrated that the success rates may be
higher in such teeth, age is not always a good prognostic indicator.
Direct pulp capping (Fig. 7.31) involves good isolation of the tooth to
control the field, preferably by rubber dam. The cavity should be caries
free and the pulp wound should ideally be fresh and gently exuding blood
or serum (Fig. 7.31c). This is followed by gentle washing of the exposed
pulp surface with sterile water or saline to remove any contaminants,
debris and dentine chips. The surface may be decontaminated by washing
with a 0.5% solution of sodium hypochlorite. This will help to achieve
haemostasis but, if bleeding persists, haemostasis is achieved using wet
cotton pellets with most of the moisture removed, dry pellets may cause
continued bleeding on removal. Continued profuse bleeding for over
approximately five minutes (Fig. 7.32) is a sign of severe pulp inflamma-
tion and a more radical approach to treatment should be considered. Once
bleeding has stopped the surface of the wound is dressed with a setting or
non-setting calcium hydroxide material (see Fig. 7.31d). It is important
that this is placed over vital tissue and not a blood clot. Traditionally, this
is then covered with a zinc oxide/eugenol base to eliminate microbial
leakage to the exposure (see Fig. 7.31e). If a composite restorative material
is to be used, a resin-modified glass ionomer may be considered as an
alternative base over the calcium hydroxide. The permanent, well-adapted
restorative material is then placed (see Fig. 7.31f). In the last decade,
mineral trioxide aggregate, a bioactive material has become a frequently
used pulp capping material because of its biocompatibility and hard tissue
conductive and inductive properties.
 Vital pulp therapy  171

Fig. 7.30  Schematic diagram showing the stepwise

Presenting caries lesion Caries excavation and cavity Calcium hydroxide dressing over
preparation leaving deep pulp covered by zinc oxide-eugenol
excavation procedure
caries over the pulp and then glass ionomer cement

Development of tertiary dentine Further excavation of caries New calcium hydroxide dressing over
over the pulpal surface pulp covered by zinc oxide-eugenol
and then definitive restoration

A B C

D E F

Fig. 7.31  Direct pulp capping: (a) initial caries lesion; (b) cavity preparation; (c) caries-free cavity with pulp Fig. 7.32  Profuse bleeding from
exposure (arrowed); (d) exposure dressed with calcium hydroxide; (e) zinc oxide/eugenol sub-lining; (f) final hyperaemic pulp
amalgam seal

There does not appear to be a relationship between the size of the
exposure and the success rate, even though it was firmly believed at one
time that the larger the exposure the poorer the prognosis. It may be
expected that carious exposures would have a lower success rate but
studies indicate that in the absence of previous pulpal symptoms, success
rates may be similar to those of traumatic exposures. The key elements of
successful outcome are good pre-existing potential for replacement of
odontoblasts and a good reparative dentine response in conjunction with
an absence of microbial leakage that could compromise healing by causing
inflammation.
Pulpotomy
This is the term applied to the removal of coronal pulp tissue when the
exposed pulp (Fig. 7.33a) is believed to be too severely contaminated by
bacteria or inflamed to give a satisfactory prognosis.
 172  Vital pulp therapy
A B
D E
Fig. 7.33  (a) Pulp exposure, due to traumatic fracture; (b) removal of superficial necrotic pulp; (c) irrigating the pulpal
wound; (d) haemostasis; (e,f) application of calcium hydroxide; (g) zinc oxide/eugenol dressing
The extent of pulp tissue removal is not strictly defined. In the case of
fractured teeth with exposed pulps, the pulp surface may exhibit one of
two reactions:
• proliferation of the epithelium covered pulp (pulp polyp) where the
inflammation is limited to a depth of 2 mm, or
• superficial necrosis with inflammation of the pulp penetrating
several millimetres from the exposure site.
The principles of therapy are identical to direct pulp capping except
that the exposure is larger and the calcium hydroxide is applied deeper
into the root. The aim of the procedure is to remove superficial necrotic
pulp tissue to reach healthy tissue. Success of the procedure is therefore
reliant upon the removal of necrotic and inflamed tissue. It is believed
that this is best and most atraumatically achieved with an abrasive diamond
bur used at high speed with adequate water cooling in an intermittent
light stroking approach to minimize implantation of dentine chips into
the exposure (Fig. 7.33b). All debris must be removed to achieve a clean
wound (Fig. 7.33c). After haemostasis is achieved as described above
(Fig. 7.33d), calcium hydroxide is gently applied without pressure (Fig.
7.33e,f) and is covered with a layer of zinc oxide/eugenol mixed to a thin
C
F
consistency (Fig. 7.33g). Some operators advocate cutting a step in the
cavity to support a plastic or Teflon disc on which is placed the zinc
oxide/eugenol dressing. As before, an alternative is a sub-base of resin-
reinforced glass ionomer cement if a composite material is to be used.
As for direct pulp capping, MTA has become the material of choice for
pulpotomy in the last decade. If MTA is used, a moist cotton pledget is
placed over the material to facilitate its setting. The cavity is then tem-
porarily sealed and then re-accessed in the next appointment to check the
setting of the MTA before placement of a permanent restoration. Discol-
ouration associated with the use of MTA is a major side effect for teeth
in the aesthetic zone.
Regenerative pulp therapy
This is a relatively newly tried approach with a limited evidence-base.
It is supported only by case reports/series and should not be used as a
routine procedure without properly consenting the patient with all risks
and potential benefits. The latest literature should be consulted for an
up-to-date procedural guideline. The principles were covered in Chapter
2. Figure 7.34 shows schematic drawing of regenerative pulp therapy
procedures. The procedure has been accepted by the ADA.
 Vital pulp therapy  173

FURTHER READING
Tooth exhibits continued root
Following debridement and formation with increase in length Bjørndal, L., 2008. Indirect pulp therapy and stepwise excavation. J Endod 34 (Suppl. 7),
S29–S33.
antibiotic paste dressing, and wall thickness
Duggal, M.S., Curzon, M.E.J., Fayle, S.A., et al., 1995. Restorative techniques in
Apical papilla associated blood clot is induced in root
paediatric dentistry. Martin Dunitz, London.
with immature tooth with canal by apical over- Duggal, M.S., Gautam, S.K., Nichol, R., et al., 2003. Paediatric dentistry in the new
necrotic pulp instrumentation millennium: 4. Cost-effective restorative techniques for primary molars. Dent Update
30, 410–415.
New pulp Fejerskov, O., Kidd, E., 2008. Dental caries: the disease and its clinical management,
tissue 2nd ed. Blackwell Munksguard Ltd, Oxford.
Fuks, A.B., 2008. Vital pulp therapy with new materials for primary teeth: new
Blood directions and treatment perspectives. J Endod 34 (Suppl. 7), S18–S24.
clot Nadin, G., Goel, B.R., Yeung, C.A., et al., 2003. Pulp treatment for extensive decay in
primary teeth. Cochrane Database Syst Rev (1), CD003220.
Rodd, H.D., Waterhouse, P.J., Fuks, A.B., et al., 2006. British Society of Paediatric
MTA Dentistry. Pulp therapy for primary molars. Int J Paediatr Dent 16 (Suppl. 1), 15–23.

Coronal
seal

Fig. 7.34  Schematic drawing of regenerative pulp therapy procedures

 8
Section 3 Delivery of endodontic treatment
Non-surgical root-canal treatment
  K Gulabivala, Y-L Ng
PRINCIPLES OF ROOT-CANAL SYSTEM MANAGEMENT
The treatment of choice for management of periapical disease is the elimi-
nation of microorganisms and their products from the root-canal system.
Microorganisms may be found in suspension in the root-canal system in
the apical part but they mostly colonize canal walls and dentinal tubules
to a variable degree up to the apical foramina. A microbial biofilm with a
variable thickness and properties coats the dentinal wall (Fig. 8.1); where
the pulp chamber is exposed, the coverage is continuous but, in teeth with
intact pulp chamber walls, the coverage is patchy. Bacteria penetrating the
dentinal tubules may be considered to be extensions of the main canal
biofilm resulting in a three-dimensional form that may resemble a “hairy
worm”! In addition to the biofilm, there is also a variable penetration into
the tubules of bacterial products and toxins, such as lipopolysaccharide.
The complex three-dimensional form of root-canal systems adds to the
difficulty of the task of decontaminating its surface.
It is in fact impossible to sterilize the root-canal system with available
equipment, materials and techniques. It is therefore fortunate that sterility
is not a precondition to successful outcome of root-canal treatment. Root-
canal treatment procedures work because the reduction in microbial and
microbial product content of canal systems together effect a collective
diminution in their pathogenicity, which promotes periradicular healing.
The part played by altered pathogenicity in periapical healing is demon-
strated by the presented case, in which despite lack of direct access to the
apical part of the root-canal system, almost complete periapical healing
was brought about (Fig. 8.2). The precise mechanisms leading to complete
biofilm eradication are not fully understood, but it is clear that both the
mechanical and chemical components of canal preparation play a role.
Root-canal system management may, therefore be thought of in
terms of:
• Mechanical intraradicular preparation
• Chemical intraradicular preparation
1 intra-appointment medication
2 interappointment medication
• Root-canal system obturation.
PRINCIPLES OF MECHANICAL
INTRARADICULAR PREPARATION
The purpose of the mechanical aspect of intraradicular preparation is to
create access to the root-canal system. The aim of this extension of the
coronal access cavity or to name it by its function, the radicular access
cavity (conventionally known as canal preparation) is to obtain and main-
tain “patency” to the apical part of the root-canal anatomy (Fig. 8.3). The
shape of the radicular access cavity is a general tapering form that may
have a circular (Fig. 8.4a) or slightly eccentric cross-sectional (Fig. 8.4b)
configuration. The final form depends on the initial shape of the root-canal
system and the form imposed by the mechanical preparation, which is
dictated by the instruments and the manner in which they are manipulated.
The mechanical preparation typically involves using metal instruments of
graded sizes to:
• negotiate instruments of sufficient size to the apical terminus of
the root-canal system without losing patency
© 2014 Elsevier Ltd. All rights reserved.
• shape the radicular access to a predefined taper, sufficient to allow
antibacterial agents and root-filling materials to be delivered to the
full extent (all surfaces) of the root-canal system in a controlled
way.
The precise shape and size is therefore determined by the requirements
for irrigant delivery and root-filling placement.
These goals should be achieved by controlled removal of intraradicular
dentine such that the original shape and curvature of the main root canal(s)
are retained (Fig. 8.5). This together with a relatively conservative final
preparation size helps to ensure that the root is neither excessively weak-
ened nor perforated. In narrow uncomplicated canal systems, the mechani-
cal preparation alone may be sufficient to effect almost complete removal
of the microbial biofilm (Fig. 8.6). However, this is a rare achievement
even in anterior, single-rooted teeth (Fig. 8.7). The truth is that there is
always a variable proportion (30–50%) of residual non-instrumented
surface in the root-canal system (Figs 8.3, 8.8, 8.9). This finding suggests
that it is not necessary to file or plane all surfaces of the root-canal system
for a successful outcome; therefore, the adjunctive chemical preparation
must play the important role of reaching all surfaces.
PRINCIPLES OF CHEMICAL INTRARADICULAR
PREPARATION AND INTRA-APPOINTMENT
ROOT CANAL IRRIGATION
In order for the chemical agent to reach all surfaces of the root-canal
system, a sufficient path must exist and the flow of the fluid irrigant must
be facilitated. This requires that obstructions in the path have to be cleared.
Prior to mechanical preparation, the root-canal system may have pulp
tissue in various states of disintegration, dystrophic pulp calcification or
pulp stones, and bacterial biofilm coating walls and disintegrating tissue
(see Fig. 8.1). The process of mechanical preparation would disrupt and
displace such contents as the canal was being enlarged by dentine removal.
The dentine chips generated from the shaping process would add another
element to the canal content. This heterogeneous mass of organic and
inorganic tissue needs to be flushed out of the canal system.
Pure flushing action is restricted by the viscously-dominated environ-
ment of the root-canal system, so a key element of irrigation is fluid
dynamics. Strategies for delivering, mixing and replacing the irrigant must
be effective. In addition, pure flushing action is only effective for loose
debris; most of the contents are likely to be attached or adherent, and must,
therefore be loosened by agitation or chemical solvent action. Therefore,
the act of flushing must be prolonged, repetitive and occur in parallel or
in alternation with mechanical preparation.
Once the mechanical shaping is completed, a final effort can be made
to reach all instrumented and, particularly, uninstrumented surfaces to
allow chemical “scrubbing” of the entire root-canal wall to remove biofilm
from the uninstrumented surface and any contaminated smear layer from
the instrumented surface.
The process of bacterial biofilm disruption by antibacterial fluids and
dressings is complicated by two problems:
1 the challenge of delivering the irrigant to the narrow and distant
apical anatomy, as well as all the ramifications diverging off along
the length of the root-canal system (Fig. 8.10)
 Non-surgical root-canal treatment  175

A B

Fig. 8.2  (a,b) Periradicular healing despite inability to negotiate full length of
canals

Fig. 8.3  (a,b) Canal

preparation (orange
channels) as a radicular
access to the root canal
system (green) in (b)

Fig. 8.1  (a) A microbial biofilm covering the canal wall; (b) CLSM images
(×40) of biofilm stained with Pisum sativum lectin, showing the distribution
of extracellular polysaccharide matrix from cross-sectional and surface
perspectives

A B

Fig. 8.4  Longitudinal and transverse sections showing

prepared canal
the canal (a) before and (b) after preparation

A = prepared canal shape B

 176  Non-surgical root-canal treatment

E
F

A D
B

Fig. 8.5  (a–f) Controlled removal of intraradicular dentine with original shape and curvature of main root canal(s) retained (courtesy of Imran Azam)

Fig. 8.6  (a,b) Narrow uncomplicated canal system (courtesy

of Krupti Denhard)

A B

A B C

Fig. 8.7  (a) Irregular wide-root canal in maxillary canine; (b) wide, “blunderbuss” canal in an incompletely formed root; (c) sectioned teeth showing variable
canal system shape
 Non-surgical root-canal treatment  177

A B C

A = before preparation
B = after mechanical preparation
C = after chemomechanical preparation
A B C

Fig. 8.8  These diagrams are reproduced from the cleared tooth Fig. 8.9  (a–c) Cleared teeth showing root filling material penetrating into non-
shown in Figure 8.3; (a) before preparation; (b) after mechanical instrumented anatomy
preparation; (c) after chemomechanical preparation

A B C D

undebrided
mechanically debrided
B chemically debrided
A

Fig. 8.10  Ramifications Fig. 8.11  (a,b) Effect of narrow and widely tapered preparations on complex canal anatomy:
diverging off along the length (A) before preparation; (B) after narrow-taper preparation; (C) after wide-taper preparation;
of the root canal system (D) after mechanical preparation and use of irrigant with ability to dissolve debris and destroy
(courtesy of Michael Jones) bacteria

2 the challenge of delivering irrigant to the depths of the

multilayered, three-dimensional microbial biofilm with its
polysaccharide matrix protection (see Fig. 8.1).
Therefore, this implies that the final stage of irrigation consists of deliv-
ering the irrigant to all parts of the root-canal system, while allowing
sufficient time for chemical penetration and dissolution. Wider and larger
radicular access cavities may allow better delivery of chemical agents to
the uninstrumented surface, especially the all important and highly complex
apical anatomy. However, a balance has to be struck between the desire
to improve delivery of chemical agents through larger preparations and
that to maintain the strength of the tooth, which requires maintenance of
the bulk of dentine (Fig. 8.11). A B
The first problem may be overcome by enlarging and shaping the radicu-
Fig. 8.12  (a,b) Preparation to facilitate needle Fig. 8.13  Deep
lar access sufficiently to allow the irrigant to be delivered to the apical
placement penetration of irrigant
anatomy using an appropriately sized, narrow-gauge “endodontic” needle needle in wide
(Fig. 8.12) or some form of agitation. The inference is that in naturally unprepared canal
wide, straight canals, minimal mechanical preparation should be required
(Fig. 8.13).
The second problem may be overcome by using a high enough concen-
tration or alternatively sufficient volume of irrigant through continuous
replenishment to give long-lasting chemical potency. The combined action
 178  Non-surgical root-canal treatment
A B
of mechanical and chemical cleaning is more efficient than either method
alone, and allows a more conservative canal preparation as reliance
on dentine removal for decontamination (a forlorn hope) is reduced.
This is the so-called “chemomechanical” method of root-canal system
preparation.
Canal preparation in teeth requiring pulpectomy, that is, vital pulp
removal, has similar but not identical aims. The concern in such teeth is
to remove not microorganisms but pulp tissue which may, in due course,
become necrotic and possibly infected (Fig. 8.14). In the case shown, the
uninstrumented apical portion of the distal canal has resulted in the devel-
opment of incipient periapical disease. It is therefore useful if the selected
irrigant both dissolves organic tissue and destroys microorganisms.
To summarize, irrigation may be thought of as serving several functions;
each of these functions dominates one of three distinct phases of irrigation
during preparation:
Phase 1 – during canal negotiation and apical enlargement – the
main requirements are to lubricate the smooth penetration of the
instruments in the tight channels to the apical terminus and flush out
generated debris
Phase 2 – during mechanical shaping to a final taper – the
requirement is mainly to flush out generated debris and to dissolve
attached and adherent organic fragments and to facilitate their
flushing out
Phase 3 – after mechanical shaping is complete – the main
requirement is to deliver the chemically active irrigant to all canal
surfaces through active or dynamic irrigation.
PRINCIPLES OF CHEMICAL INTRARADICULAR
PREPARATION AND INTERAPPOINTMENT
INTRACANAL MEDICATION
The main rationale for using such intracanal medication between appoint-
ments is to help complete the aim of root-canal system preparation, that
is, to degrade residual microbial biofilm and organic tissue and to kill
remaining bacteria that have escaped primary debridement. The medica-
ment should, therefore, also prevent bacterial recolonization of the root-
canal system, from either those bacteria left behind after preparation or
new invaders through lateral communications or the coronal access. In
addition, it would be useful if the medicament possessed a range of other
properties that would suppress pain and facilitate apical healing. A root-
canal medicament should therefore ideally:
1 Be able to kill all root canal bacteria with a long-lasting
antibacterial effect
2 Not be inactivated by the presence of organic material
3 Be able to help degrade residual organic material, including pulp
tissue or microbial biofilm
4 Not be irritating to periapical tissues or have systemic toxicity
Fig. 8.14  (a,b) Development of periradicular area
around distal root following vital extirpation
Fig. 8.15  (a,b) Root
treated tooth with only an
apical “seal”
A B
5 Be able to induce regeneration of periapical tissues
6 Not affect the physical properties of the temporary access cavity
restoration or be able to diffuse through the temporary seal
7 Be easily placed and removed
8 Be radiopaque
9 Have anodyne properties
10 Not stain or weaken the tooth.
PRINCIPLES OF ROOT-CANAL SYSTEM OBTURATION
Following debridement and medication of the root-canal system, it would
be logical to prevent migration of microorganisms from the oral cavity or
root-canal system to the periradicular tissues. The purpose of obturation
of the root-canal system and placement of an adequate coronal restoration
is to prevent such recontamination by establishing a continuous barrier to
the passage of microorganisms and their products.
In the past, the main emphasis was placed on establishing an apical
“seal” (Fig. 8.15). However, in recent years, the importance of the coronal
seal has been appreciated more fully. The purpose is therefore to “seal”
the entire root-canal system, including the coronal entry. Cases have been
reported which demonstrate that it is possible to achieve resolution of
periradicular lesions following root-canal preparation and coronal seal
alone or even spontaneous resolution of a lesion following caries removal
and placement of a coronal restoration (Fig. 8.16)! Therefore, obturation
of the root-canal system should begin with the root-canal filling and
finish with an integrated, well-designed and executed coronal restoration
(Fig. 8.17).
The aims and objectives of obturation therefore are:
• to establish a barrier to the passage of microorganisms from the
oral cavity or root-canal system to the periradicular tissues
• to “entomb” or “incarcerate” and isolate any microorganisms that
may survive the shaping and cleaning process
 Non-surgical root-canal treatment  179

Fig. 8.16  (a,b) Fig. 8.17  Postoperative

Spontaneous resolution of radiograph of non-
a lesion following caries surgical root canal
removal and placement of treatment on lower
a coronal restoration in a molar tooth with
tooth with a necrotic pulp well-designed and
integrated coronal
restoration

A B

Fig. 8.18  Removing Fig. 8.19  Removing

the roof of the pulp the roof of the pulp
chamber chamber

Incorrect Correct Incorrect Correct

Fig. 8.20  (a) Mandibular first molar with

incomplete removal of pulp chamber roof;
(b) roof of pulp chamber being removed
by ultrasonic tip; (c) roof of pulp chamber
removed

A
C
B

• to prevent leakage into the canal system of potential nutrients that
would support microbial growth
• reduce the risk of bacterial movement or fluid percolation into
to
the canal system space from the gingival sulcus or periodontal
pockets.
The concept of a “hermetic” or “airtight” seal in endodontics is errone-
ous since all restorative materials leak to some extent on a nano- or micro-
scale. The precise level of the seal required has not been defined. It suffices
to say that all efforts should be made to hinder the invasion of microorgan-
isms. This may simply be a function of the surface preventing colonization
rather than the quality of marginal adaptation affecting a “seal”.
This chapter describes the objectives of root-canal system preparation
and obturation and reviews the advantages and disadvantages of the
various practical approaches. In order to achieve satisfactory canal prepa-
ration, the entry point to the root-canal system should be suitably prepared
and shaped first.
CORONAL ACCESS CAVITIES
PRINCIPLES OF CUTTING A CORONAL ACCESS CAVITY
These are to:
1 Remove the roof of the pulp chamber so as to provide good visual
and tactile access to the entrances of the main root
canals (Figs 8.18, 8.19). It is a common fault to leave remnants of
the pulp chamber roof together with some pulp remnants (Fig.
8.20)
2 Provide straightline access to the first curve in the root canal (Fig.
8.21). The walls of the coronal access cavity should not deflect an
instrument placed into a canal
3 Avoid damage to the floor of the pulp chamber, so as to avoid
perforation of the pulp chamber floor and make it easier to locate
the canal entrances (Fig. 8.22). The natural shape of
 180  Non-surgical root-canal treatment

Fig. 8.21  Straightline access Fig. 8.22  Avoid

damaging the floor of
the pulp chamber
Fig. 8.24  Lack of resistance form Fig. 8.25  Access burs
leads to intracoronal displacement of
temporary filling

A B
A
Fig. 8.23  (a) Conserve tooth substance; (b) access cavity too large

the floor funnels and tends to guide an instrument into the

canal orifice
4 Conserve as much tooth substance as possible to prevent
weakening and fracture of the remaining tooth consistent with the
above aims (Fig. 8.23)
5 Provide coronal and apical resistance form so that the temporary
access cavity seal remains intact until the final restoration is placed
(Fig. 8.24).
B

CUTTING THE CORONAL ACCESS CAVITY
Initial penetration into dentine is made with a tungsten-carbide, domed-
fissure, cross-cut bur aimed towards the largest part of the pulp chamber.
When penetration to dentine is through a porcelain crown or enamel, a
round diamond bur is used to cut through these brittle materials first before
changing to a tungsten-carbide bur to cut through the metal or dentine
beneath (Fig. 8.25). Once the roof of the pulp chamber has been pene-
trated, a safe-ended, tapered, diamond bur, or similar-shaped tungsten-
carbide bur, is used to reduce the risk of damaging the pulpal floor while
the roof is removed. The depth of penetration can be judged by holding
the hand-piece containing the bur against the parallel view preoperative
radiograph, or using the measuring tool available on digital radiographic,
systems (Fig. 8.26). Older teeth have smaller pulp chambers and, therefore
require a smaller access cavity. Additionally, the floor may have calcified
pulp tissue attached and care must be taken to remove it (Fig. 8.27).
Fig. 8.26  Judging access cavity Fig. 8.27  (a) Calcified tissue and
depth pulp remnants; (b) pulp chamber
thoroughly cleaned and canals
prepared
Younger, immature teeth have large pulp chambers and probably should
not have their entire roof removed to avoid unnecessary weakening of the
tooth (Fig. 8.28). Thought must be given to the type of permanent restora-
tion that will be used afterwards as this will alter the shape and approach
to cutting the coronal access cavity. For example, in the case of an onlay,
the walls of the access may be reduced before the canal-root treatment is
carried out or, in the case of an anterior tooth which is to be crowned and
is lingually inclined, consider access from the labial aspect (Fig. 8.29).
Radiographs (Fig. 8.30) show that straightline access can be just as effec-
tive from the buccal aspect as from the lingual.
 Non-surgical root-canal treatment  181

OUTLINE SHAPE and shape of the cavity is dictated by the size and shape of the pulp
chamber and will therefore, tend to be smaller in older patients.
The outline shape of coronal access cavities is dictated by the shape of the In anterior teeth, straightline access into the canals of incisors and
pulp chambers which, in turn, follow that of the tooth in cross- or longi- canines requires that the cavity must be cut high up on the tooth near the
tudinal section (Fig. 8.31). The standard shapes of coronal access cavities incisal edge. This type of access cavity will leave the cingulum intact,
for different tooth types are given in Figures 8.32–8.39. The actual size which provides the maximum retention for a full crown later. At the same
time, it is important not to breach the labial enamel and dentine, as doing
Fig. 8.28  Incomplete removal of pulp so, may predispose the tooth to develop cracks in the enamel in the future.
chamber roof in an immature tooth
The shape of the pulp chamber and, therefore, the coronal access cavity,
still allowing straight-line access to
the canals
of the maxillary first molar is rhomboid due to a widening over the palatal
canal orifice. The second and third molars show a mesiodistal flattening
of the pulp chamber, which also lies nearer the mesial aspect of the tooth.
The access to the mandibular first molar is also rhomboid in shape
because the distal canal is either broad buccolingually or because there are
two separate canals. The second and third molar access cavity is more
triangular as there is usually only one distal canal.

LOCATION OF THE CANAL TERMINUS AND

DETERMINATION OF CANAL AND WORKING LENGTH

POINT OF TERMINATION OF CANAL PREPARATION

It is impossible to determine the apical extent of contamination of a root-
canal system clinically; it is best to assume contamination up to the apical

A B A B

Fig. 8.29  (a,b) Buccal access in mandibular anterior tooth Fig. 8.30  (a) Buccal view of mandibular anterior teeth; (b) Approximal view of
mandibular anterior teeth

Fig. 8.31  (a) Cross-sections of teeth showing

relationship between pulp and external occlusal surface;  
(b) longitudinal section of teeth showing the relationship
between pulp and external surface

A B
 182  Non-surgical root-canal treatment

A
A B

B C B

Fig. 8.32  (a,b) Maxillary incisor Fig. 8.33  (a,b) Mandibular incisor; (c) mandibular incisor viewed Fig. 8.34  (a,b) Maxillary canine
from the incisal edge

A B A B A B

Fig. 8.35  (a,b) Mandibular canine Fig. 8.36  (a,b) Maxillary premolar Fig. 8.37  (a,b) Mandibular premolar

A B A B

Fig. 8.38  (a,b) Maxillary first molar Fig. 8.39  (a,b) Mandibular molar
 Non-surgical root-canal treatment  183

Radiographic film Tooth with file

X-Ray tube

A B C

Fig. 8.40  (a–c) Apical deltas filled with thermoplasticised gutta-percha

(AlphaSeal)

foramina in all cases with necrotic pulps and to clean the canal system to
this/these point(s). It is safest to clean to the apical termination of root
canals even in cases where the tooth is vital but failure to do so will not
jeopardize success in such cases. However, it is crucial to ensure that Projected image from
instrumentation and treatment materials do not extend beyond the root- distal curvature
canal system as this may reduce the prospects of a successful outcome.
Distal root curvature
Projected image from
CLINICAL LOCATION OF THE ROOT-CANAL SYSTEM buccal curvature Buccal root curvature
TERMINUS/TERMINI
Root-canal systems have been classified in different ways, including by Fig. 8.41  Line diagram showing radiographic views of file in a root that
the number of termini they exhibit (see Chapter 1). Locating the apical curves distally or buccally
termini of the root-canal system exactly is an art rather than a precise
science. Several methods are used to triangulate the terminal point(s) of
the root-canal system, they include:

• radiography
• electronic apex locators
• tactile sense
• paper point.
Each of the methods is analysed independently first and then a way of
combining them offered.

Radiographic method
The first problem is that the root-canal system often ends in an apical delta
so that there is not just one but several apical foramina. The diagnostic
endodontic file will pass into only one of these (Fig. 8.40).
The second problem is that the radiographic view with a file in the canal
provides a two-dimensional picture of a three-dimensional root-end, in
A B
which the file may be disposed in any plane within a 360° circumference
(Fig. 8.41). Unless a single root-canal system exit is disposed at exactly Fig. 8.42  (a) Preoperative parallel view radiograph; (b) periapical radiograph
right angles to the X-ray beam and film, the radiographic technique can with diagnostic files
never estimate the position of the apical terminus accurately.
The traditional protocol for canal length determination using radio-
graphic technique alone is as follows. An estimate of the approximate
length of the tooth is made from a preoperative parallel radiograph (Fig.
8.42). A file is placed in the root canal about 1 mm short of this estimated Fig. 8.43  Angled
length, ensuring that a coronal reference point is selected that is reproduc- periapical radiograph
with diagnostic files
ible, stable and durable. The file should be large enough to be visible on
the radiograph (e.g. size 10 but size 08 may also suffice). It is best not to
commence apical instrumentation before understanding the location of the
canal terminus, as irreversible damage is easily incurred at the early stages.
A parallel radiograph is then taken (Fig. 8.42b). In teeth with multiple
canals, diagnostic files should be placed in all canals and a single view
taken to minimize exposure to radiation (Fig. 8.43). Canals may exit on
the root surface at a variable distance and position from the root tip and it
is impossible to judge the three-dimensional distribution of apical foramina
satisfactorily from radiographs (Fig. 8.44). This pair of images shows three
 184  Non-surgical root-canal treatment
A B
A B
A Fig. 8.46  Relationship
between root tip, apical
0–3mm B which case the distance between the file tip and a point 1 mm short of
foramen, and apical
constriction: A = root apex;
C B = apical constriction;
D C = root canal;
F
D = cementum;
E = dentine; F = apical
E foramen
roots, with files that appear flush with the radiographic root tip but which
are actually extended past the apical foramina. Figure 8.45 shows a case
taken from a clinical study, in which a cemented file that is apparently
flush with the root tip is actually extended well beyond the apical foramen.
An average distance of 1 mm short of the radiographic apex is widely
accepted as a reasonable estimate of the terminal position of the canal, but
this may be inaccurate by up to 3 mm (Fig. 8.46).
Once a parallel view periapical radiograph of the tooth with diagnostic
file(s) in the canal has been obtained, working length is calculated taking
account of image distortion by comparing the actual and radiographic
distance between the tip of the file and the reference point indicated by
the rubber stop.
1 In most cases, the tip of the file will be short of the radiographic
apex. This is often accepted as the length of the canal if the
distance is within 1 mm (as in the lateral incisor: Fig. 8.47a). If the
discrepancy is greater than 1 mm, then the distance between the
file tip and the radiographic apex should be measured and 1 mm
subtracted from this measurement (as in the central incisor:
Fig. 8.47a). This residual discrepancy is added to the length of the
diagnostic file to give the estimated length of the canal (Fig 8.47b,c).
Fig. 8.44  (a,b) Discrepancies between radiographic
images of files and reality in relation to the root apex
Fig. 8.45  (a,b) Discrepancy between radiographic
images and reality (taken from a clinical study)
2 In some cases, the file may be longer than the radiographic apex, in
the radiographic apex should be measured (Fig. 8.48). Subtracting
this figure from the length of the diagnostic file will give the length
of the canal.
Electronic apex-locator method
The reliability of contemporary electronic apex locators (EALs) has
increased to a point where many clinicians rely almost exclusively on them
although they do not give 100% reliability. The European Society of
Endodontology guidelines state that having used the apex locator, a con-
firmatory radiograph should be taken.
Electronic apex locators (Fig. 8.49) in theory enable the location of the
true position of the apical terminus, utilizing the fact that root canals, in
common with other tubes with one end immersed in an electrolyte solu-
tion, exhibit certain electrical characteristics that are relatively constant.
The parameter of importance is the abrupt change in impedance of the
root canal as the terminus is approached and bypassed. The impedance in
question is measured between a point along the length of the root canal
and the oral mucosa (Fig. 8.50). Introduction of electrolytes into the root
canal causes the impedance to drop and the gradient of impedance along
the canal to decrease. The impedance value at the apical foramen, that is,
between the periodontal ligament and the oral mucosa, measured via the
root canal is a relative constant. This value is used to calibrate commercial
EALs, but the impedance characteristics of the canal coronal to the apical
foramen are not factored in. EALs should therefore always be used to
achieve the “zero” reading for greatest accuracy and not any point short
of this.
EALs work by applying an alternating current between two electrodes,
one of which is attached to the file and the other via a clip to the lip or
cheek mucosa (Fig. 8.51a,b). The frequency of this current, which also
influences impedance, is usually fixed in a given make of instrument but
 Non-surgical root-canal treatment  185

1mm
4mm

B C

A Fig. 8.47  (a) Diagram reproduced from Figure 8.42b. Correct length in 12 accepted. Short length in 11 is
corrected; (b,c) adjusted diagnostic files and final root fillings

1mm
1mm

Fig. 8.49  RootZX apex locator (J Morita)

60
Mean resistance (k ohms)

40
A A
30

Fig. 8.48  (a) Overextended file; (b) diagram reproduced from (a) shows corrected 20

length 10

0
0 1 2 3 4 5 6
Distance from apex (mm)

Dry canal Water Neosono/Evident Rs (n = 18)

Fig. 8.50  Electrical impedance of root canals at different distances

from the apical foramen with water-filled and dry canals. Also shown
is the average calibration of a typical apex locator
 186  Non-surgical root-canal treatment
A B
D
E
Fig. 8.51  (a,b) Connection of electrodes to file and cheek; (c–e) apex indication in different apex locators; (f) file placed to length indicated at “zero” by apex
locator
Fig. 8.52  Elements
Diagnostic Unit
(SybronEndo)
differs between makes. As the file is passed down the canal, the EAL
measures the impedance and compares the value with its calibrated stand-
ard. A countdown scale indicates a “zero” or “apex” reading when the
calibrated value is matched (Fig. 8.51c–e). All currently available conven-
tional EALs use this principle but display the information differently. The
current generation of EALs has overcome the problem with electrolytes
in root canals by measuring the impedance at multiple current frequencies.
The Root ZX (J Morita, Kyoto, Japan) (see Fig. 8.49) compares the ratio
of impedance at two frequencies to derive the apical position. The Apex
Finder AFA (Discontinued) claimed to derive the information from five
different frequencies. The Elements Diagnostic Unit (SybronEndo) (Fig.
8.52) claims to be a fourth generation apex locator measuring resistance
C
Fig. 8.53  Raypex® 5
(VWD)
and capacitance separately rather than the resultant impedance; it then
putatively searches for comparative values in a lookup matrix generated
from in-vivo studies. The Raypex® 5 (VDW) (Fig. 8.53), which also uses
multiple frequencies, claims to be a fifth generation apex locator with
greater accuracy.
The accuracy of different models of EALs has been tested clinically and
shows slightly variable results for the same EALs in different studies and
for different EALs in the same study. These differences may be attributed
to many factors, including conditions of use and calibration of the instru-
ment. Each instrument requires practice in use to become familiar with its
idiosyncrasies before it can be used with confidence. EALs are reliable but
should not be relied upon in all circumstances. If there is any doubt about

A B
Fig. 8.55  Patterns of apical constriction: (a) classic, (b) tapered, (c) parallel and (d) multiple (adapted from Dummer et al (1984) – images courtesy of WJ van der
Meer)
the reading, a radiograph must be taken. Potential problems in use include
short-circuiting if the file touches a metal restoration, if the canal contains
excessive moisture, or if the size of the file is too small. Clinicians should,
having used the EAL to obtain a “zero” length reading, take a check radio-
graph (see Fig. 8.51f). The greatest advantage of the EAL, is that having
obtained and confirmed this base-line reading, the working length and
patency may be monitored continuously throughout canal preparation with
each file placed to length or just short. This confers tremendous confidence
to the clinician during the procedure.
Tactile method
Some clinicians claim that it is possible to gauge the apical constriction
of the root-canal system by tactile sense. There are several problems with
this claim. First, not all teeth possess an apical constriction due to the
presence of apical resorption caused by apical periodontitis (Fig. 8.54).
Second, the ability to gauge the apical constriction relies on the pre-
existence of a natural canal taper that has a minimal constriction only at
the termination of the canal; Dummer et al (1984) observed four distinct
patterns of apical constriction (Fig. 8.55). Third, the tactile detection of
the apical constriction relies upon the selection of a file size that will first
bind only at the apical constriction. Given that the size and anatomy of
the apical constriction varies considerably, this method is reliant upon
several preconditions, as well as the fortuitous selection of the correct
instrument size. Taking these factors collectively, it is highly unlikely that
tactile sense alone can be used to gauge the position of the apical terminus,
although it has been shown that the chances are improved by a step-down
preparation approach.
Paper-point method
Another recommended method is the use of a sequence of paper points
that show the position of the apical foramen by virtue of the junction of
tide-mark of the blood-wetted and dry tip of the paper point. Although this
Non-surgical root-canal treatment  187
Fig. 8.54  (a) Apical root resorption: histological view; (b) apical root
resorption: SEM view
C D
can aid apical foramen location in some cases, it is unreliable by itself
because of seepage of exudate or blood into the canal and by capillary
action along the paper point.
Combined method for determining position
of canal terminus
None of the methods described so far are infallible. The recommended
approach to location of the terminus of the root-canal system is first to use
an EAL to obtain the “zero” reading. The diagnostic file should not fit too
loosely in the canal otherwise a less accurate reading will be obtained. The
length of the file at this reading is recorded from a stable reference point
on the crown. The file(s) is replaced to the same length and a radiograph
taken using a parallel view radiograph. The file should appear to be within
the confines of the root apex, although sometimes, the radiograph shows
the file to be extruded, while the EAL indicates a consistent reading; this
may be because the root thins out sufficiently for it to be invisible at the
apex. In any case, if the file appears to be longer, the EAL reading should
be rechecked for consistency. A final judgement should be made about the
true position of the canal terminus by triangulation of the lengths from the
different sources, as well as tactile sense and paper points.
DETERMINATION OF WORKING LENGTH
The working length is the length to which each instrument is used in the
root canal. It is not necessarily the same length as that of the canal from
the reference point to the canal terminus. Some instruments may be used
to the full length of the canal, while others may be used at various prede-
termined lengths short (step-back) or long (patency) of it.
Once the length of the canal has been determined, it is necessary to
decide whether the series of root-canal instruments will be set to that
length or short of it. Many factors dictate the length to which instruments
will be used in the canal. The goal of the negotiation phase of canal prepa-
ration is to enlarge the canal to at least size 30 (ISO) just short of the canal
 188  Non-surgical root-canal treatment
terminus. That is, to preserve the original size of the apical foramen as far
as possible. If the canal is to be prepared to a wide non-ISO taper (0.06
plus), then it is considered that preparation to size 20 or 25 may be suf-
ficient. The optimal size of the apical preparation is size 30. If the operator
is very meticulous, the length to which the canal is prepared can be con-
trolled to within 0.25 mm and the files may be set to 0.25 mm short of the
canal length. If, on the other hand, the operator has poorer control it may
be prudent to set the instruments up to 1 mm short of the canal length. The
former is always preferable and good endodontists will strive for such
accuracy. In addition, the following factors may further affect the decision
to modify the length to which the canal is instrumented:
1 When apical root resorption is evident, the canal terminus may be
“blunderbuss” shaped and, therefore, allow extrusion of endodontic
materials (see Fig. 8.54). One school of thought suggests that
instrumentation should be shorter. Another suggests that the
resorption is caused by microbial infection in the site and so
requires vigorous apical preparation up to the full length
2 When the root tip is very narrow there may be a risk of root
perforation if the root is prepared to a significant diameter to the
full length (Fig. 8.56)
A B C
Fig. 8.56  (a–c) Risk of root perforation in case of very narrow root tip
(courtesy of Reem Sairafi)
A B C A
Fig. 8.57  (a,b) Sudden apical curve in root canal; (c) risk of apical perforation in narrow
root tips
3 When in addition to the narrow roots they also exhibit a sudden
apical curve (Fig. 8.57), small flexible files may be used to the full
length but larger files (above size 25) should be used to shorter
lengths.
Different files may therefore be used to different (working) lengths. All
of this, of course, presumes that the operator has exceptionally good
control of the instruments, is conscious of the attention to detail necessary
in measuring the files (up to 0.25 mm) and of problems, such as “rubber
stop slippage” and parallax in judging the position of the file in relation
to the coronal reference point. Lack of adherence to these basic principles
is a common fault exhibited by inexperienced operators.
Displacement of the (rubber) stops on the files, which designate length,
is a problem that must be prevented by selecting tightly fitting stops. Some
stops are more susceptible to displacement than others (Fig. 8.58). Loss
of the reference point is another important cause of error. It may occur
either because of lack of care in properly recording it in the medical notes
or because the original reference has been lost due to breakage of tooth or
restoration. In either case, the length must be re-established before pro-
ceeding further. Once again, having used an EAL at the outset makes
redetermination of the length is easier.
MAINTAINING CANAL INSTRUMENTATION
TO ITS TERMINUS
In addition to operator-induced errors in maintaining canal length, opera-
tors should also be aware that the length of the curved canal will inevitably
change as it is prepared. This is because as the canal is prepared, its
increased width allows the rigid metal instruments to take a straighter and
shorter path to the apical terminus (Fig. 8.59). In addition, if patency is
lost, the canal will appear shortened while, if patency is maintained and
the reference point is constant, the file will be extruded past the terminus.
If the coronal part of the canal is prepared before the definitive measure-
ment of the canal length, then the change in canal length during preparation
is minimized. Given the ease of use of EALs, it is best to maintain constant
vigilance over changes in length during canal preparation by frequent
monitoring of length with the apex locator.
B
Fig. 8.58  (a,b) Different types of stops

Fig. 8.59  Change in length of canal
as it is prepared: A = file before
instrumentation; B = file after
instrumentation
A
Fig. 8.61  (a,b) Simple tubular canals encompassed by tapered canal preparation:
A = before preparation; B = after mechanical preparation; C = after chemical
irrigation with sodium hypochlorite
RELATIONSHIP BETWEEN THE RADICULAR ACCESS,
ITS DIMENSIONS AND ROOT-CANAL ANATOMY
Historically, the mechanical preparation of root-canal treatment had been
considered the most important aspect of bacterial debridement. There has
been a paradigm shift in the way that mechanical preparation is now
viewed; it can now be regarded as no more than an extension of the coronal
access cavity into the root, that is, it is a radicular access cavity. This is
principally because of the relative proportion of the canal wall surface that
remains uninstrumented; up to half of the surface must be cleaned by
means other than instrument planing.
It has traditionally been held that canals should be prepared by control-
led dentine removal so as to produce a regular taper with the minimum
diameter at the apical constriction or canal terminus and the maximum
diameter at the coronal end; at the same time, maintaining the original
shape of the canal as far as possible to preserve the strength and integrity
of the root. Its original shape, therefore, also dictates the overall shape of
the prepared canal.
The apical diameter or degree of taper, to which the canal should be
prepared has been a subject of much debate. The choice is usually based
on personal preference and individual clinical experience rather than on
sound scientific rationale. Widely tapered canals may allow better irrigant
penetration, better debridement and probably better obturation if using the
cold lateral compaction or warm vertical compaction techniques, but these
benefits are achieved at the expense of root strength and possibly long-term
survival of the tooth. Advocates of narrowly prepared canals argue that
a taper that allows irrigant penetration using narrow needles is sufficient
for debridement and that obturation of such canals can be satisfacto­
rily achieved with thermoplasticized gutta-percha techniques. Narrowly
tapered preparations, if they allow adequate cleaning and obturation, are
Non-surgical root-canal treatment  189
Fig. 8.60  Narrowly
tapered preparation
A B C
undebrided
mechanically debrided
B chemically debrided
more desirable as they do not compromise root strength (Fig. 8.60). Based
on the irrigation requirements of the root-canal system, teeth may be
divided into simple or complex canal systems.
SIMPLE CANAL SYSTEMS (TYPES A, B AND C)
In simple canal systems with narrow circular cross-sections (Type a),
preparation to a regularly tapered radicular access cavity may entirely
encompass the original canal system (Figs 8.61–8.63). In such cases,
cleaning may be achieved almost wholly by mechanical preparation with
little reliance on the irrigant.
In contrast, in simple canal systems with wide non-circular but regular
cross-sections (Type b – such as canines, some premolars, distal and
palatal roots of molars, teeth with C-shaped canals), preparation to a regu-
larly tapered radicular access cavity may not allow complete debridement
solely by mechanical preparation (see Figs 8.7, 8.64–8.66). C-shaped
canals could be treated as broad distal canals in lower molars that may
result in two separate or overlapping tapers (Figs 8.67, 8.68a,b) prepared
to allow sufficient access for irrigation. Alternatively, if filing is used then
a continuous coronal shape may be created (Fig. 8.68c,d). Access for
irrigation is excellent in such teeth and, therefore, only minimal filing of
the canal walls is usually required. In simple canal systems with narrow
circular cross-sections but minor fins and ramifications extending off them
(Type c), mechanical preparation would remove most microbes and organic
tissue except from the uninstrumented accessory anatomy (Fig. 8.69).
Examples of such anatomy may be drawn from all tooth types (Fig. 8.70),
showing root-filled teeth, in which the main canals have been prepared to
a taper and filled but the accessory anatomy may remain undebrided if a
proper irrigation regimen is not used.
 190  Non-surgical root-canal treatment

Fig. 8.62  Regularly COMPLEX CANAL SYSTEMS

tapered radicular access
cavity preparation In teeth with more complex, irregular canal systems, the prepared radicular
encompassing the access cavity remains encompassed or surrounded by the original irregular
original canal system canal system to a greater or lesser degree and may only be partly discern-
(courtesy of Krupti ible or not at all. Examples may be drawn from mesial roots of mandibular
Denhard)
or maxillary molars, mandibular incisors and some premolars, usually only
when viewed proximally though. Figure 8.71 shows an example where the
prepared radicular access cavities would be partially discernible. Figure
8.72 shows an example where two of the original canals would be com-
pletely contained by the prepared radicular access, whereas the final canal
would include the prepared radicular access cavity within its pre-existing
bounteous space. Figures 8.3a, 8.8, 8.73 show examples in which the
original anatomy would subsume the radicular access cavity.
Examples of root-filled teeth in this category, rendered transparent,
show the variable relationship between the instrumented radicular access
cavity and the uninstrumented portion of the root-canal system (Fig. 8.74).
Figure 8.74e,f show an example of a case in which the radicular access
cavity is barely visible as the original canal anatomy encompasses the
prepared shape.
Fig. 8.65  (a,b) Incomplete
debridement solely by
mechanical preparation
(courtesy of Ian Alexander)

A B
A B

Fig. 8.63  (a,b) Regularly tapered radicular access cavity preparation almost
encompassing the original canal system; Type A system

Fig. 8.64  Sectioned roots of a

mandibular molar showing Type A
system in mesial root and Type B
system in the distal root

A B

Fig. 8.66  (a,b) Incomplete debridement solely by mechanical preparation in

Type B system (courtesy of Maysoon Haji)
Fig. 8.67  (a) C-shaped canal in mandibular second
molar with diagnostic instruments in place; (b)
C-shaped canal obturated to reveal two overlapping
tapers (courtesy of Dr Yea-Huey Melody Chen)

A B
 Non-surgical root-canal treatment  191

C
A B

Fig. 8.68  (a) C-shaped root; (b) C-shaped canal in mandibular second molar; (c) C-shaped canal in
mandibular second molar with diagnostic instruments in place; (d) C-shaped canal obturated to reveal
continuous single canal (courtesy of Dr Yea-Huey Melody Chen)

Fig. 8.69  (a,b) Simple main canals with complex

intercommunications. Example of Type C system: A = before
A preparation; B = after mechanical preparation, C = after A
chemomechanical preparation

Fig. 8.71  (a,b) Simple main canals with complex

intercommunications: A = before preparation; B = after
mechanical preparation; C = after chemomechanical
A B C preparation

Fig. 8.70  (a–c) Root-filled canals showing instrumented and uninstrumented canal
walls (Example of Type C system)
 192  Non-surgical root-canal treatment

A B
A B
Fig. 8.72  (a,b) Effect of mechanical and chemical cleaning on complex irregular
canal systems: A = before preparation; B = after mechanical preparation; C = after
mechanical preparation and sodium hypochlorite irrigation

C D

A B

Fig. 8.73  Effect of mechanical and chemical cleaning on complex irregular canal systems:
A = before preparation; B = after mechanical preparation; C = after mechanical
preparation and sodium hypochlorite irrigation

MECHANICAL PREPARATION OF THE TAPERED

RADICULAR ACCESS CAVITY E F

Fig. 8.74  (a,b) Root-filled canals showing instrumented and

The tapered radicular access cavity may be prepared either with hand
instruments, rotary automated instruments or a combination of the two. In
contemporary practice, it is common to use a hybrid approach. It is an
attractive proposition to prepare the tapered access using automated instru-
mentation. While root canal instrumentation has seen tremendous advances,
hand instruments have certainly not become redundant, particularly for
negotiation. The advances in rotary automated instrumentation now enable
much easier shaping of root canals although the instruments must be used
with great care in acutely curved or multicurved canals to avoid breakage.
MECHANICAL PREPARATION OF THE RADICULAR
ACCESS BY HAND INSTRUMENTATION
Mechanical preparation of the radicular access requires the controlled
removal of dentine by manipulation of root canal instruments. Acquisition
of such skills requires dedicated practice under the guidance of an effective
coach.
The cultured touch developed by a skilled operator should be able to
discriminate through constant and vigilant practice, the following:
uninstrumented canal walls; (c,d) filling of ramifications
between canals with thermoplasticised gutta-percha; (e,f)
root-filled teeth in which the tapered canal preparation is
encompassed by the original canal shape
• the ability to gauge the diameters and curvatures in a root-canal
system by tactile exploration and to form the information into a
three-dimensional mental image
• the ability further to modify and refine the three-dimensional
mental image using clues from radiographs and knowledge about
common anatomical traits in various tooth types
• the tactile awareness to discern the “feel” of dentine, dentine chip
plug, soft tissue plug, root filling material or other foreign object
• the ability to cut dentine in a controlled way using either a filing
(push–pull) or a rotary (clockwise and counter-clockwise) motion
that maintains the original canal curvatures.
 Non-surgical root-canal treatment  193

Fig. 8.75  Kerr K-reamer No. 25 Fig. 8.76  Kerr K-Flex file No. 25 Fig. 8.77  Micro Mega Hedstroem No. 25

These two basic motions of the hand-instrument that remove dentine,

work in essentially different ways.

Rotary motion
In rotary motion, the instrument cuts best when the cutting edge is oriented
almost parallel to the long axis of the instrument, such as in the reamer
(Fig. 8.75). The progressive decrease in the pitch of the flutes by making
the twists in the metal shank tighter renders the cutting edges at a greater
angle to the long axis and closer to the perpendicular of the long axis, as
in a file (Fig. 8.76). This means that the latter instrument is suitable for
both rotary use, as well as push–pull filing. The closer the cutting edges
are to being perpendicular to the long axis of the instrument, the better
suited it is to use for filing or push–pull action (Fig. 8.77). In addition to
the orientation of the cutting flutes, the manner in which the edges engage
dentine and cut it is different in the two motions.
In rotary motion, cutting is reliant upon engaging opposing walls of the
canal dentine by screwing and apical feeding. The file engages dentine
much in the same way as a screw may engage wood (Fig. 8.78). The
threads or cutting edges wind into the dentine. No lateral forces are
involved, only torque. The operator has only to gauge the torque required
to engage the dentine. The amount of dentine engaged depends on the
relative mismatch in the diameter of the instrument and that of the canal
Fig. 8.78  Threaded screw Fig. 8.79  Deformed hand instrument
and the degree to which it is screwed into the canal. Therefore, the amount entering a piece of wood
of dentine engaged is a function of the degree of apical feed of the instru-
ment. In a perfectly circular canal whose taper is almost matched with that
of the instrument, apical feed and lateral engagement of the dentine may
be almost proportional. However, in reality, canals are irregular, with the
files only contacting intermittently at selected opposing points. There is,
therefore, a mismatch between rotational motion, apical feed and apical
advancement. Many technique manuals erroneously give instructions on
the degree of clockwise or anticlockwise rotation without any mention of
the degree of apical feed or torque that should be used. As a consequence,
rigid pursuit of such instructions may lead to procedural errors, particularly
where the file tip is unconstrained. The operator must balance the degree
of apical feed with the degree of torque required and this insight can only
be acquired by vigilant practice. To understand how the instrument cuts
dentine in rotary motion, imagine a screw being rotated clockwise into a A
matching hole in a piece of wood (Fig. 8.78). As it screws in, it engages
the substrate. Rotation in the anticlockwise direction will allow it to
unscrew back out of the wood along a path identical to the screwing-in
motion. If, however, apical force is applied while the screw is rotated
anticlockwise, instead of backing the screw out, the wood engaging the
threads is fractured. This is the principle of the balanced force technique.
Its correct practice requires an understanding and a “feel” for the torque
forces that the instrument and dentine can tolerate. In unpractised hands,
there is a potential for overstressing the metal instrument with its conse-
quent deformation (Fig. 8.79) or fracture (Fig. 8.80). Alternatively, by the
laws of physics, an equal and opposite force is imposed on the dentine, Fig. 8.80  (a) Fractured K-Flex tip;
which may also fracture if its breaking threshold is exceeded, which can B (b) instrument fracture due to torsional
easily occur when there is thin apical dentine. However, the common fatigue
 194  Non-surgical root-canal treatment
A B
Fig. 8.81  Ledging and excessive dentine removal Fig. 8.82  (a,b) Thread cut into dentine
(arrowed) by screwing instruments into root
canal
outcome is that dentine is removed in an uncontrolled fashion resulting in
procedural errors (Fig. 8.81). Another problem is that in circular, narrow
canals, the entire circumference of the instrument may be engaged and
with progressive apical feeding result in a considerable length and, there-
fore, surface area of the instrument becoming engaged with dentine simul-
taneously. As this happens, a progressively greater force is required to feed
the instrument in further, imposing greater and greater force on both the
instrument and dentine; the ultimate result is what is known as “taper
lock”. Screwing instruments into the root canal in this fashion will impose
enormous stresses both on the instrument and the root; it may also result
in a thread being cut into the dentine (Figs 8.82, 8.83).
The surest way of reducing the amount of force applied in torque is to
limit the degree of apical feed and, therefore, the amount of dentine
engaged. The file is only fed in until slight resistance is met, then the file
is turned anticlockwise with or without apical force. Rapid cycling clock-
wise and anticlockwise without heavy torque in a stem-winding or watch-
winding motion enables the gentle negotiation and enlargement of the
canal without risk of procedural errors. This works best in canals where
the instrument does not bind simultaneously around its entire circumfer-
ence; conversely, in narrow, tight canals, this technique can be demanding
on finger-strength and endurance. It is the sort of instrument manipulation
that causes finger calluses; it is interesting though that the formation of
calluses, far from reducing sensitivity to touch increases sensitivity. As in
all rotary techniques, the flutes of the instruments should always be cleaned
frequently to facilitate adequate cutting.
Push–pull filing
In contrast, in push–pull filing, the entire circumference of the instrument
can rarely be engaged for more than one stroke. In this method of cutting,
the sharp edges are ideally oriented perpendicular to the direction of file
movement. Other than in the situation where the file is rotated into engag-
ing the dentine and then pulled (also a valid approach to cutting), push–pull
filing requires the application of a lateral or interfacial force to enable the
file to engage dentine. This is akin to using a wood-file on a piece of wood.
A wood-file held lightly against the wood will remove few wood shavings.
Pressing on the wood-file harder will allow it to engage the wood surface
more effectively and remove more wood shavings. In the same way, an
endodontic file is more effective when it is rigid enough to engage dentine
when lateral interfacial force is applied. In contrast to a wood-file, the
lateral force on a root-canal instrument cannot be applied directly to the
file but is exerted on the handle in the hope that this will be transmitted
along the length of the file. As the instrument is tapered towards its tip,
A B
Fig. 8.83  (a,b) Thread cut into dentine (arrowed) by
screwing instruments into root canal
the lateral force will be greatest at the handle and progressively reduce
towards the tip. A file that is too flexible will simply tend to bend away
from the dentine surface on application of a lateral force. The advantage
of the reducing lateral force apically is that a natural taper will be created.
This poses an interesting dilemma when a curved canal has to be instru-
mented; on the one hand, flexible instruments are required to negotiate the
canal without producing procedural errors but, on the other hand, some
rigidity is required to control application of lateral force. Very flexible
instruments, such as those made from nickel–titanium are not effective for
filing techniques, yet are better for a rotational approach. It is therefore
more effective, when using a push–pull filing technique to control the
actions of the apical portion of the file by preshaping the coronal part of
the canal first. This enables the tactile sensation of preparing the apical
part to be discerned without coronal hindrance. In order to control dentine
removal along the entire length of the instrument, the interfacial force must
be controlled over its entire length. Other strategies to overcome this
problem are discussed below.
Design of hand instruments
A skilled operator must understand and know the tools(s) he/she uses. The
manner of manipulation has to be based on the cutting properties of
the instrument. The mode of manufacture, orientation and sharpness of
the cutting edges, as well as the response to use and to sterilization on the
cutting properties, should be aspects the operator should be familiar with.
The root-canal instruments available may be manufactured from metal
wires of different alloys (stainless steel, carbon steel, titanium, nickel–
titanium), cross-sectional shapes and diameters. These alloys have differ-
ent physical and chemical properties: carbon steel is the most brittle, rigid
and susceptible to corrosion; stainless steel is more resilient; titanium is
more flexible; and nickel–titanium is the most flexible. The cross-sectional
shapes of instruments may be square (K-file – Fig. 8.84), triangular
(K-reamer – Fig. 8.85), rhomboid (K-Flex-file – Fig. 8.86), circular (Hed-
stroem file – Fig. 8.87) or S-shaped (Unifile).
These shapes have a bearing on the physical properties of the instru-
ments. The cutting edges may be generated by twisting the metal shaft
along its long axis or by machining it. When twisted, the square blank
produces the most rigid instrument; the triangular shape is more flexible
and the rhomboid more flexible still. When machined, the depth of cut
used to produce the flutes dictates the flexibility and strength of the instru-
ment. The helical angle thus produced, influences the optimal mode of use
(rotational or push–pull). Machined instruments generally tend to be more
susceptible to fracture, unless they have been specifically heat-treated.
 Non-surgical root-canal treatment  195

Fig. 8.84  Kerr K-file No. 25 Fig. 8.85  Kerr K-reamer No. 25 Fig. 8.86  Kerr K-Flex file No. 25

D16 D0

D16 D3 TIP
75º
D0

3mm
16mm

D16 16mm D0

Fig. 8.87  Kerr Hedstroem No. 25 Fig. 8.88  Dimensional formula for files and Fig. 8.89  Dimensional formula of an H-type
reamers: D = diameter instrument (ANSI specification No. 58:  
D = diameter)

Twisted instruments Fig. 8.90  Bayer

Hedstroem No. 25
These instruments are designed to meet the requirements of the American
National Standards Institute (ANSI) for endodontic K-type files and
reamers, which lay down the dimensional formulae for size, taper, length
of cutting blade and tip angle (Fig. 8.88). A number of companies manu-
facture stainless steel instruments to these specifications and include the
K-file (Kerr), K-reamer (Kerr), K-Flex file (Kerr), TripleFlex (Kerr), Flex-
ofile (Maillefer) and Zipperer Flexicut (Anteos). At present, “Twisted file”
(SybronEndo) is the only nickel–titanium instrument system generated by
twisting the NiTi wire with R-phase heat treatment.
Fig. 8.91  McSpadden
engine-driven nickel–
Machined instruments titanium file No. 25
A number of conventional and new generations of instruments are
machined. Only the H-type instrument is governed by the ANSI specifica-
tion (No. 58) (Fig. 8.89). Several companies manufacture H-files, all of
which have different designs and properties despite the specification. The
H-file is manufactured from a blank of circular cross-section. The flutes
are produced by machining a single helix into the metal stock, producing
a series of intersecting cones, which increase in size from tip to handle
(Fig. 8.90). The depth of flute or the residual bulk of metal in the central
portion of the file determines the strength and flexibility of the instrument. thermomechanical processing procedure, they cannot be twisted, given
The blades thus formed are virtually at right angles to the dentine surface their structural memory (Fig. 8.91).
and so the most efficient cutting motion is a pulling stroke; no dentine will
be removed by the push stroke. Rotating the instrument with the tip of the
instrument engaged in dentine is a common cause of its fracture.
MECHANICAL PREPARATION OF THE RADICULAR
Other examples of machined instruments include Light Speed (Sybro-
ACCESS BY AUTOMATED DEVICES
nEndo) and Sonic shaper (Micro-mega). Most of the nickel–titanium Most operators are attracted by the idea of using an automated instrument
instruments are also machined. This is because without the proprietary that will make root-canal preparation easier and quicker. Many automated
 196  Non-surgical root-canal treatment

Fig. 8.92  Early design

Table 8.1  Nickel–titanium rotary instruments – advantages and
for nickel–titanium
disadvantages
rotaries
Advantages Disadvantages
• A gradual evenly tapered radicular • Attempting to negotiate narrow
access is produced in the root-canal curved (especially double curved)
system that facilitates its canals, without preparing a pilot
Radial land
obturation channel with hand instruments will
cause instrument fracture
Flute Broad radial land
• Fewer instruments are required to • Fracture may occur unexpectedly
achieve the desired shape without any sign of permanent
deformation
Fig. 8.93  Radial land
• It takes less time to shape the • More expensive than stainless steel
radicular access into the root-canal • Becomes dull quicker than stainless on the Quantec
system steel instrument
• Using the instruments in a • Shape memory makes it more difficult
hand-piece allows better vision to access root canals in posterior teeth
particularly with the small headed and to negotiate acute and double
hand-pieces now available curves

devices have been introduced onto the market through the years, with
reciprocal, vertical, and random movement and both sonic and ultrasonic
oscillation. Nickel–titanium rotaries (non-ISO taper), since their introduc-
tion in 1995, have taken an increasing share of the market. There are many
advantages to these instruments and many improvements have been made
since their early advent; universal acceptance though is still prohibited by
their expense. The reason for choosing nickel–titanium is that it is five Fig. 8.94  The
times more flexible and more resistant to fracture when compared to stain- alternating cutting edge
less steel. in a RaCe instrument
The final radiograph of a root filling in a nickel–titanium rotary prepara-
tion looks smooth and shows a gradual even taper; this may, in part, be
due to the action of the rotating instrument packing debris into the crevices
and accessory anatomy. The importance of removing microorganisms and
debris is paramount, so a system that uses both a reciprocating and oscil-
lating movement may be more appropriate. Such a movement may
be able to clean the asymmetric shapes found in root canals more
effectively.
Table 8.1 shows the advantages and disadvantages of rotary over hand
instrumentation.

Nickel–titanium rotary instruments

There are many different nickel–titanium rotary instruments available on
the market. The first generation had many design faults, but better designs
are gradually appearing. All of these instruments are prone to fracture and
most are technique-sensitive. Conventional nickel–titanium rotaries
require a light touch, with a slow in and out pecking movement within the
canal and must be run at the recommended speed. Protaper (Dentsply-
Maillefer) shaping files, which have a cross-section similar to that of
reamers, are used like a brush laterally and selectively to cut dentine on
the outstroke.
The majority of the nickel–titanium rotary instruments are machined
by computer-controlled grinders from a round blank, which allows com-
plicated designs to be manufactured. The original concept was to produce
a screw-type design similar to a wood screw but with radial lands (Fig.
8.92). The most recent Reciproc® (VDW), Wave One™ (Dentsply) instru-
ments are used in reciprocating movement.
Radial lands
In the first generation of instruments, the radial lands were spaced equally
apart so that when the instrument rotated it tended to be pulled into the
root canal. The result was that the apical portion of the instrument bound
in the root canal and increased the chance of fracture. Breaking up the
screw design by varying the distances between the radial lands reduced
the screw-in effect and helped to prevent breakage. The wide radial land,
although providing more metal and therefore strength behind the cutting
edge, also increased the area of metal in contact with the wall of the canal.
To reduce friction against the wall, the radial land may be relieved (Fig.
8.93). A more recent approach has been to reduce the width of the radial
land to just a cutting edge, which further reduces the frictional resistance
against the wall of the canal. Several manufacturers have produced a tri-
angular cross-section; one of them adding an alternating cutting edge
(RaCe; Fig. 8.94). A coke bottle effect has also been devised where the
diameter of the instrument varies in a waveform up the shank to reduce
resistance with the wall.
Flutes
The flute is the cut-away portion of the shank in between the radial lands.
Debris removed from the canal or cut from the wall collects within the
flutes. If the flutes become tightly packed with debris while the instrument
is rotating there is an increased chance of fracture. The design of the shape
of the flute is important. A gradual increase in the depth of the flutes from
the tip of the instrument up the shank means that, when the instrument is
rotating, the debris will be forced into the larger flute spaces. Debris is
therefore removed from the root canal.
 Non-surgical root-canal treatment  197

A B

Fig. 8.95  Non-end-cutting or safety tip Fig. 8.96  (a) Profile GT – side view; (b) this instrument has been based on the original ProFile so it
shows wide radial lands

A A
A

B B B

Fig. 8.97  (a) The Quantec – side view; (b) the
Quantec has two radial lands, which are relieved
to reduce friction against the root canal wall
Fig. 8.98  (a) The K3 – side view; (b) the K3 shows
three radial lands in cross-section, two of which
are relieved. The flutes increase in depth towards
the top of the shank, the shallower flutes near the
tip impart additional strength to the instrument.
The radial lands are spaced at varying distances
apart reducing the pull-in effect
Fig. 8.99  (a) The Hero – side view; (b) Hero 642
– the numbers relate to the tapers. The coronal
and middle portion of the canal is prepared to 06
and 04 taper respectively and the apical portion to
02. Note narrow radial lands

Safety tip
The majority of nickel–titanium instruments have been designed so that
they do not cut at the tip (Fig. 8.95). It is obvious that if the tip had an
aggressive cutting action the instrument would tend to cut into the wall of
the root canal when a curve was reached.
Figures 8.96–8.101 show both side views and cross-sections of Profile,
Quantec, K3, Hero, Pro Taper, RaCe, nickel–titanium rotary instruments.
The latest instruments WaveOne (Fig. 8.102), Reciproc (Fig. 8.103), and
Twisted file (Fig. 8.104) are also shown.
Initially, the disadvantage of automated instruments is the loss of tactile
sense but with time and practice this can be acquired to an extent. It has
been demonstrated that experience results in fewer instrument fractures
and better-shaped canals. The tactile skills required are different from
those required for hand instruments. Which automated device is “best” is
a matter of personal preference.
Unconventional instrument design
A novel instrument design has been marketed recently, called the self-
adjusting file (Fig. 8.105). It is machined from nickel–titanium and resem-
bles a mesh formed into a cylinder. The single instrument is compressible
and may be inserted into any canal shape with a minimal size equivalent
to ISO size 20; this means the canal must be prepared to a minimum glide
path of this size first. Its advantage is that when it is activated with a vibra-
tory push–pull action, it conforms to the shape of the canal and enlarges
 198  Non-surgical root-canal treatment

A A

Fig. 8.102  (a,b) Wave one

B B

Fig. 8.100  (a) Pro Taper – side view; (b) the Pro
Taper is similar to the Hero in cross-section. It has
a variable taper along the shank. The cutting
action is fairly aggressive
Fig. 8.101  (a) The RaCe – side view; (b) RaCe
stands for reamer with alternating cutting edge.
The alternating cutting edge reduces the tendency
for the instrument to be pulled into the canal. The
instrument cuts aggressively and may make a
clicking sound when being used Fig. 8.103  Reciproc

The majority were devised to overcome the problem of uneven prefer-

Fig. 8.104  Twisted file Fig. 8.105  Self-adjusting file
it evenly, retaining the original shape of the canal. It is particularly advan-
tageous for C-shaped and oval canals. Negotiation and enlargement of
complex, narrow canals are more problematic with a higher rate of lattice
strut fracture. The system has an integrated irrigation device.
PREPARATION OF THE RADICULAR ACCESS
IN CURVED CANALS
The achievement of a controlled, regularly tapered, radicular access prepa-
ration in curved canals is the ultimate challenge in endodontics. Many
ingenious strategies have been devised to enable the attainment of this goal
using rigid metal instruments.
ential contact during push–pull filing. The advent of the rotational mode
of instrument manipulation and the flexibility of non-ISO-taper nickel–
titanium instruments have revolutionized the approach to negotiation and
shaping of curved canals, respectively. Hand-instrumentation skills are
still a requisite feature of root-canal treatment because negotiation and
shaping of acutely and double-curved canals is not predictably possible
using conventional nickel–titanium instruments due to risk of fracture. The
attainment and retention of such tactile skills demands the continual use
of stainless steel instruments in practice. Automated instrumentation may
facilitate easier shaping of canals but initial negotiation and enlargement
is better achieved with stainless steel instruments. It is therefore necessary
to be aware of how to maintain canal curvatures using both modes of
instrument manipulation. Although, in theory, rotational manipulation of
instruments should enable more effective maintenance of canal curvatures,
the authors have witnessed that those with established filing habits may
find it difficult to adapt to rotary skills. Conversely, those with established
habits in rotational manipulation may find it difficult initially to adapt to
a filing technique. Clearly, a different set of tactile skills is required. The
tactile skills required for manipulation of nickel–titanium instruments are
different still but easily acquired if stainless steel instrument skills are
already established.
Maintaining curvature with a push–pull filing mode of
instrument manipulation
As already described, the only situation in which uniform dentine removal
can be guaranteed during filing is when the file engages tightly around its
entire circumference (Fig. 8.106a). However, immediately after the first
 Non-surgical root-canal treatment  199

A B C

Fig. 8.106  (a) File fitting tightly in the canal; (b) circumferential filing: anticurvature filing: 3× on B, Fig. 8.107  Ledging
M, L; 1× furca; (c) file fitting loosely in the canal with preferential points of contact

A B

Fig. 8.108  Zipping Fig. 8.109  (a,b) Transportation of the apical foramen

stroke and thereafter with each subsequent stroke, the file becomes pro-
gressively looser and a lateral force has to be applied to the file in numer-
ous different directions (traversing 360°) as the file is moved
circumferentially around the canal, while conducting a push–pull motion
(Fig. 8.106b). Once the file is loose in a curved canal, however, its natural
tendency to straighten up will only allow preferential contact at certain
points along its length (Fig. 8.106c). These points are predictably at the
outer aspect of the major curve apical to the curve, on the inner aspect of
the curve at the height of the curve and either at the inner curve or outer
curve coronal to the curve, depending upon the direction in which the
lateral force is applied. The contacts result in procedural errors, such as
ledging (Fig. 8.107), zipping (Fig. 8.108), transportation of apical foramen
(Fig. 8.109), and perforation (Fig. 8.110). Strategies to avoid such uneven
preferential contacts involve ways of reducing them.
There are two elements to such uncontrolled forces and dentine removal:
1 the tendency of the file to straighten to its normal shape
2 the tendency of the file to cut along its entire length and
surface area.
These problems may be overcome by:
• reducing the restoring force with which straight files lean against
the curved canal
• reducing or controlling the length and surface area of the file that
is actively engaged in cutting at any given time.
Reducing the restoring force
This can be achieved in a number of ways:
1 Precurving the file – the restoring force may be reduced by
achieving a closer match in the curvature of the instrument with
that of the canal. Assuming that an accurate match is obtained, this
match is true only in one position (Fig. 8.111). The greater the
amplitude of the filing stroke the greater the mismatch at the
extremes of the filing stroke. Therefore, the amplitude must also
be reduced. Files may be precurved by using a cotton wool roll or
using commercial devices (Fig. 8.112). The curve perpendicular to
the X-ray beam is estimated from the radiograph and any curve in
 200  Non-surgical root-canal treatment

A B

Fig. 8.110  (a,b) Perforation Fig. 8.111  Precurved file matches

canal curvature in only one position

B C

B A

Fig. 8.112  (a,b) Commercially available devices for Fig. 8.113  (a) Use of small file as explorer; (b,c) curvature (in two planes) of file removed from the
precurving files mesiobuccal canal in (a)

the planes parallel to the X-ray beam must be estimated by tactile Fig. 8.114  Files are
sense and the curvature on initial explorer files (Fig. 8.113). Files precurved at different
that are to be used at different lengths in the canal relative to the levels depending on the
curvature should be appropriately precurved (Fig. 8.114) depth of insertion into
the canal
2 Use of flexible files – the restoring force in more flexible files is
naturally lower. Some makes of instrument are more flexible by
virtue of their cross-sectional shape (Fig. 8.115) or material of
construction, such as nickel–titanium
3 Greater use of smaller files – smaller instruments (size 20 and
below) are more flexible and so their use until larger instruments
are able to negotiate without force may reduce adverse dentine
removal (Fig. 8.116)
4 Use of intermediate sized files – The transition from one file to the
next can also be made easier by the use of half sizes, e.g. sizes 12,
17, 22, 27 and 32 (Fig. 8.117). This reduces the force required to
negotiate the files apically and also the probability of procedural
errors.
 Non-surgical root-canal treatment  201

A Fig. 8.117  “Golden medium” intermediate files

(12, 17, 22, 27, 32, 37)

B B A B

Fig. 8.115  (a) Maillefer “Golden Medium” No. 27; Fig. 8.116  (a,b) Loss of length caused by forcing Fig. 8.118  (a,b) Preflaring allows more direct
(b) Girofile No. 25 large instruments into canals too early apical access

A B C

Fig. 8.119  (a) Severe strip perforation; (b) furcal view of mesial root of extracted tooth; (c) cross-section of a mesial root. Ideal removal of dentine during
preparation (shaded area): B = buccal; M = mesial; L = lingual

Reducing or controlling the length or area of file actively
engaged in cutting
This can be achieved in a number of ways:
1 Modified canal preparation techniques – preparing the coronal
part of the canal first in a corono-apical or crown-down approach
removes coronal binding and allows more controlled preparation
of the apical part of the canal with the apical part of the file
(Fig. 8.118)
2 Modified manipulation of instruments – the manner in which the
instruments are manipulated can allow a restricted part of the canal
or instrument to be engaged, increasing the control over dentine
removal
• Anticurvature filing – denotes filing preferentially away from
the inner curve or furcal aspect of the root canal, the site of
potential perforation (Fig. 8.119). This method, which involves
filing the buccal, mesial and lingual walls of the root canal
with more strokes than the furcal wall by a ratio of 3 : 1, is
effective (see Fig. 8.106b). However, simply following the
prescription without regard for tactile feedback, flexibility of
the file and controlled manipulation of the file will render it
ineffective. The technique does not work with files that are
too flexible and a degree of straightening may be inevitable
(Fig. 8.120)
• Modified use of files – files may be used in such a way that
their area of contact is reduced. For example, in the crown-
down-pressureless technique, only the tips of the instruments
are used for cutting. The file is placed in the canal until it binds
(Fig. 8.121) and is then rotated twice without apical pressure to
remove dentine at this binding point.
 202  Non-surgical root-canal treatment
Fig. 8.120  Mild straightening Fig. 8.121  Modified use of files:
despite anticurvature filing A = circular movement of file;
B = only the tip of the
instrument engages and cuts
dentine
3 Modified instruments – the idea of only using the apical part of
instruments has been extended by the development of instruments
that have cutting edges only in their apical part, such as Light
Speed (Fig. 8.122). These instruments are particularly useful for
gauging the apical size of the canal.
Maintaining curvature with a rotational mode of hand
instrument manipulation
The mechanics of rotational action of hand instruments were described
before. The approach is inherently conducive to maintenance of canal
curvatures. However, this cannot be taken for granted. It is possible for
some operators to lose control and straighten curved canals even with this
technique (Fig. 8.123). Furthermore, operators often have to practise the
method to achieve satisfactory canal widening. When minimal instrumen-
tation is performed, the tendency is to produce narrowly tapered radicular
access cavities (Fig. 8.124). However, some operators are able to produce
widely tapered radicular access cavities using supposedly identical proto-
cols (Fig. 8.125). The difference lies in the degree of instrument manipula-
tion and the amount of apical feed and force used. Unlike the filing
technique, the numbers of variables that require control are limited and
interrelated. They are:
• degree of apical feed of the instrument (synonymous with and
proportional to the degree of rotation when visualized as feeding a
screw into a hole, i.e. a well-fitting match between canal and
instrument)
• frequency of clockwise and anticlockwise rotation (without or with
apical pressure on anticlockwise rotation – file may rotate out, stay
at the same level or be advanced further apically)
• degree of apical pressure accompanying the anticlockwise torque
affects the degree of dentine cutting
• degree of rotational torque (in both clockwise and anticlockwise
rotation) affects the depth of dentine cut.
Fig. 8.122  Light Speed instrument
tip
Fig. 8.123  Loss of
canal curvature in
mesiobuccal root of
maxillary molar using a Fig. 8.124  Mesiobuccal canal with narrowly
rotational technique tapered radicular access using rotational
manipulation
Fig. 8.125  Example of
widely tapered radicular
access using rotational
manipulation
A combination of aggressive apical feed and rotational torque, espe-
cially with larger rigid instruments can lead to loss of curvature in the
radicular access.
The degree of canal widening is controlled by the size of the instrument
used, as well as the degree of manipulation (rotational cycling). Excessive
cycling may lead to uncontrolled dentine removal.
A combination of any of the above strategies may be used to prepare
radicular access cavities that maintain the original curvature of the root
canals (Figs 8.126, 8.127).
Maintenance of double curves
Root-canal systems often contain main canals (continuous pathways traced
by root-canal instruments from canal orifice to terminus) that exhibit two
or more curvatures. These double curves may both be in the same plane
or different planes. Most of the time, the second curves are not radiographi-
cally visible because they occur within the plane of the X-ray beam. The
operator tends to act on the curve visible from the radiograph but is likely
to be ignorant of the other plane. A discerning operator may detect the

A B C
A
A
B B
Fig. 8.127  (a,b) Radiographs of treated cases Fig. 8.128  (a,b) Straightening coronal curve in the
where the natural canal contour has been distal root
maintained
additional curve as an unaccounted resistance to file manipulation. There-
fore, when the filing technique is used, the undetected curve may be
straightened and, if the root dentine is thin, it may result in a strip perfora-
tion in the furcation. The use of a gentle rotational technique is more likely
to retain the curve.
Sometimes the double canal curvatures will be evident in the same
radiographic plane. These are difficult to maintain using a filing technique
alone. Either the coronal (Fig. 8.128) or apical curve (Fig. 8.129) may be
straightened. The preparation of such curves with automated nickel–
titanium rotary instruments is only possible if the curves are gentle and
the canal already wide (Fig. 8.130). Otherwise, there will either be damage
to dentine or the file will fracture (Fig. 8.131). When more severe curves
in two planes are present, only hand instrumentation with a rotational
Non-surgical root-canal treatment  203
Fig. 8.126  (a–c) Original curvature of root canals
maintained
A
B
Fig. 8.129  (a,b) Straightening apical curve on the
mesial root
technique will achieve the desired result (Figs 8.132, 8.133). The size of
the taper may have to be limited, placing greater reliance on the chemical
preparation.
Preparing a regularly tapered radicular access and
gauging it
The ability to prepare a well and regularly tapered radicular access is based
on two factors:
1 knowing when to stop using a given instrument. Under-use of an
instrument may leave the taper too narrow and over-use, too wide
2 knowing how to gauge the canal taper (or “feel” the diameter at
specified lengths using the tips of equivalent sized instruments.
 204  Non-surgical root-canal treatment
A B
Fig. 8.130  Curvature in opposite Fig. 8.131  (a–c) Damage to dentine and file separation during preparation
directions in the same plane of canal with double curvature without appropriate glide path
A B
Fig. 8.132  (a) Diagnostic radiograph of severe curves in two planes; (b) successful
treatment of the severe multiple curves
Gauging the canal taper is the most underrated aspect of learning to
prepare canal systems to a consistent and predictable shape. Unlike the
taper of a crown preparation, that of the canal is not visible until the canal
is filled and radiographed, which is too late for any modification. The taper
can, however, be felt using a series of diameter-graded instruments.
Gauging a radicular access cavity, therefore, means placing accurately
measured instruments into the prepared canal to the precisely judged
coronal reference points and feeling their tightness (or looseness) at their
appropriate lengths. In order to prepare a regular taper, it is essential that
each instrument, at its respective length (whether 1 mm or 0.5 mm step-
back), exhibits precisely the same degree of tightness or looseness.
The design of the Light Speed instrument lends itself very well to canal
gauging because only its tip can bind to the canal wall.
The advent of non-ISO taper nickel–titanium instruments with a prede-
termined taper has meant that a single instrument, that is, the one used to
finish the entire radicular preparation, can be used to gauge the canal taper.
However, if the same instrument is overused, particularly with a brushing
motion, the same problem of loss of taper control may arise even with
these instruments.
RECOMMENDED APPROACH TO PREPARING THE
RADICULAR ACCESS
There is an almost infinite number of techniques to prepare the radicular
access cavity. Various strategies have been devised to help dentists prepare
root canals. The techniques have been divided into two groups:
1 apical–coronal techniques (e.g. standardized, step-back techniques)
(Fig. 8.134)
C
Fig. 8.133  Successful treatment of the maxillary
right second premolar with severe multiple curves
2 coronal–apical techniques (e.g. step-down, double flared, crown-
down-pressure-less techniques) (Fig. 8.135).
These simply describe the direction in which canals are progressively
enlarged; either starting coronally and then progressively enlarging towards
the apex (coronal–apical); or, starting at the apex and progressively enlarg-
ing the entire canal with the emphasis on segmentally stepping back from
the apex to the coronal part (apical–coronal). Normally, the mechanical
preparation of the radicular access is divided into four phases:
1 Preparation of coronal flare to the beginning of the first canal
curve or to two-thirds the estimated length of the canal if there is
an absence of a curve
2 Determination of canal length to apical terminus by negotiation
of small instruments (ISO size 08, 10) to full length with precise
length establishment as previously described
3 Negotiation and enlargement of the canal to the accurately
confirmed length using hand instruments in a rotational mode of
manipulation, preferably a gentle stem-winding technique to at
least ISO size 30
4 Final shaping to achieve a regular taper.
Coronal preflaring
The benefits of coronal preflaring are:
• it allows early debridement of the coronal part of the canal that
contains the bulk of organic and microbial debris, reducing the risk
of carrying this material to the apical end and its extrusion through
the apical foramina

Coronal access
and preflare
Working length
determination
Apical enlargement
Final flare
Fig. 8.134  Apical– Fig. 8.135  Coronal–apical preparation techniques
coronal preparation
techniques
• early coronal widening enables better and deeper penetration of
irrigant earlier in the preparation, reducing the risk of blockage of
apical foramina with dentine “mud” (viscous mix of dentine debris
and dissolving pulp tissue)
• preparation of the coronal portion of the canal tends to remove
interferences, smoothens access and shortens the effective canal
length; determination of canal length after such enlargement
reduces the problem of changing canal length as it is prepared
• allows better tactile discernment and control over apical
it
instrumentation.
The coronal preflaring can be achieved in any one of a number of ways
according to personal preference. The traditionally taught approach is by
filing the coronal part of the canal using either Hedstroem or K-type files;
and then refining the shape with Gates–Glidden drills as in the step-down
technique (Fig. 8.136). It is important to maintain patency beyond the point
of instrumentation with a small instrument.
The instrumentation may also be performed in a step-down approach
using rotational manipulation to achieve a similar result, as in the double-
flare technique (Fig. 8.137).
Alternatively, the coronal part of the canal may be opened and flared
with nickel–titanium orifice openers or rotary instruments (Fig. 8.138).
This is an efficient and effective means of achieving this goal.
Negotiation to the full length of canal and
length verification
Having preflared the canal, its full length is accurately determined as previ-
ously described.
Non-surgical root-canal treatment  205
Pulp Initial pulpal surface
Working length
determination
Canal enlargement after
apical negotiation
Canal enlargement after final flaring
Negotiation to the full length of canal and
its apical enlargement
The apical part of the canal should now be negotiated with a series of hand
instruments of progressively increasing size up to ISO size 20–30, to the
full length without deviating from the canal curvature. Again a number of
approaches are available but the safest way is to use a gentle stem-winding
technique that does not remove excessive amounts of dentine. The instru-
ments may be used in a corono-apical (Fig. 8.139 ) or apico-coronal (Fig.
8.140) sequence according to preference. Alternatively, nickel–titanium
rotary instruments may be used for negotiation of full length of canals
(Fig. 8.141). However, caution should be exercised if canals are narrow
or severely curved because instrument fracture through rotational torque
or cyclic fatigue is a significant risk without creating a glide path. Newer
02 taper rotary nickel–titanium instruments are available for creation of
such a glide path.
Where the canal system is relatively wide at the outset and does not
require negotiation as such, the apical part of the canal should be gauged
to determine its size after length determination. The process of shaping
may then be commenced directly, bypassing the negotiation step.
Final shaping of the radicular access
This may be achieved by using hand instruments to gauge the canal taper
in a stepback filing approach (Fig. 8.142) or a stepback rotational motion
approach (Fig. 8.143). Alternatively, the instruments may be used in step-
down fashion.
A preferred current approach is to use nickel–titanium rotary instru-
ments for final shaping of the radicular access to the required final taper,
which rarely needs to be greater than 0.06 (Fig. 8.144).
 206  Non-surgical root-canal treatment
A B
D E
CHEMICAL TREATMENT OF ROOT-CANAL SYSTEMS
AND ROOT-CANAL IRRIGATION
This aspect of root-canal system preparation, although described sepa-
rately for convenience, is performed simultaneously with the mechanical
preparation and does in fact also precede and succeed it (Fig. 8.145).
The function of irrigants may be summarized as follows:
• lubrication of the instruments
• flushing out of root canal debris
• chemical degradation of residual pulp tissue
• chemical degradation of the smear layer on the instrumented surface
• chemical degradation of the microbial biofilm both on the
instrumented and, more importantly, on the uninstrumented surface
• antibacterial action against the root canal microbiota.
Lubrication: This relies on the irrigant having properties that enable it to
be interposed as a thin layer between instrument and canal wall, facilitating
Fig. 8.136  Coronal preflaring – progressive
enlargement at same length using a
push-pull filing motion and refined by
planing motion of rotating Gates–Gidden
drills. (a) File with size 10 to 16–18 mm  
or beginning of the curve; (b) file using
Hedstroem size 15 to same length:  
F = filing; (c) Hedstroem file size 20
to 16–18 mm: F = filing motion;
(d) Hedstroem file size 25 to 16–18 mm:  
F = filing motion; (e) refine coronal flare
with Gates–Glidden drill sizes 1–3 used in
a planing motion: A = Gates–Glidden 3;
B = Gates–Glidden 2; C = Gates–Glidden
1; R = rotational motion
C
friction-free movement. Lubricants also come in the form of gels and include
EDTA-containing pastes, such as RCPrep and File-eze. Other agents, such
as Glyoxide or Glyde contain carbamide peroxide (an oxidizing agent).
Flushing action: A reasonably low viscosity of the irrigant should facili-
tate flow and flushing of the root-canal space. However, the viscously
dominated environment of the root-canal space due to its small volume
renders the fluid relatively static. Therefore, this demands various strate-
gies to help mix and agitate the solution in the root-canal system.
Degradation of pulp tissue: The best solution for degrading pulp tissue
is sodium hypochlorite (Fig. 8.146). These figures show degradation of an
extirpated pulp over 10 minutes when the tissue is fully exposed in a large
volume container, where access to unreacted sodium hypochlorite is unim-
peded. In stark contrast, such access within the root-canal system would
be exceptionally restricted. It is therefore necessary actively to ensure that
unreacted solution reaches the tissue in all parts of the root-canal system.
This is done via the radicular access, both during and after its preparation.
Diffusion of unreacted molecules, however, demands very frequent
 Non-surgical root-canal treatment  207

A B C D

Fig. 8.137  Coronal preflaring – using rotational instrument manipulation in a progressive step down approach. (a) Introduce small file (No. 10) to full WL to
establish patency: WF = without filing; (b) instrument to size 35 at about 14 mm: R = rotational motion; (c) instrument with file 30 to 1 mm deeper than size 35;
(d) instrument with size 25 to 1 mm deeper than size 30

Fig. 8.138  (a) Coronal flaring achieved

using nickel–titanium orifice shapers
using a pecking motion; each narrower
instrument advancing further than the
last; (b) coronal flaring achieved using
increased taper nickel–titanium rotary
instrument; note the desired
straightening of the outer curve

A B

replenishment of the solution in the radicular access. Higher concentration
solutions (5%) may enable better diffusion along a gradient but its use
must be balanced against the problem of over-weakening the dentine by
depleting its collagen content. Concentrations up to 3% are sufficient for
antibacterial effect and tissue-degradation effect in most cases. Higher
concentrations may be used intermittently in the case of non-responding
infections or where canal patency is compromised by compacted apical
debris. Sodium hypochlorite is a caustic solution and has the potential to
corrode equipment (Fig. 8.147), bleach clothes and cause a severe reaction
if extruded through the apical foramen. A good rubber dam seal must be
ensured (Fig. 8.148). It is also prudent to check prior to treatment whether
the patient is allergic to household bleach.
Degradation of the smear layer: Some operators consider this to be a
very important aspect of root-canal treatment because the smear layer is
thought to harbour bacteria and prevent sufficient adaptation of the root-
filling material. There is, however, no definite proof that the smear layer
reduces success rates. Weak organic acids, such as ethylenediaminetetra-
acetic acid (EDTA) 17% may help remove the smear layer if irrigation
with it reaches and reacts with the layer (Fig. 8.149).
Degradation of the microbial biofilm: The microbial biofilm contains an
aggregate of microbes and extracellular polysaccharide matrix (ECPM),
which are both highly adherent to the canal wall. The multiple bacterial
cell layers covered by the additional thickness of ECPM, which may
exceed the bacterial cell volume, renders biofilm removal a difficult task.
Removal is certainly facilitated by organic tissue solvents, such as sodium
hypochlorite and chelating agents, such as EDTA. The EDTA helps by
chelating and sequestering heavy metal ions, which normally act as bridges
to bond bacteria together in the biofilm. EDTA is routinely used in micro-
biology laboratories to wash bacterial cells free of the extracellular polysac-
charide and to separate them. EDTA is likely to play an important role in
degrading the biofilm on the uninstrumented walls of the root-canal system;
this is therefore a more significant function than smear layer removal.
 208  Non-surgical root-canal treatment

R
R R
R

D
C
B
A

Fig. 8.139  Negotiation of full length of canal: using step-down rotational instrumentation (a) size 40, (b) size 35, (c)
size 30, (d) size 25, (e) size 20 at full WL. Apical enlargement may be continued to desired size by adopting another
“wave” of instrumentation starting with a larger sized instrument

Antibacterial action against the root canal microbiota: Perhaps the most
significant action of the irrigant must be its ability to kill all elements of
the root canal microbiota. A number of different antibacterial agents have
been used, which exhibit a range of actions against the various bacteria
(Table 8.2).
The temptation to use multiple agents should be avoided because at best
they may potentiate each other (although the literature does not currently
support this suggestion) or at worst they may neutralize each other. An
example of the latter is the precipitate formed by mixing chlorhexidine
with sodium hypochlorite. The latter combination has been shown to
reduce the success rates of root-canal treatment.
MECHANICS OF ROOT-CANAL IRRIGANT DELIVERY
AND ITS ACTIONS
The purpose of the radicular access cavity is to facilitate delivery of the
fluid irrigants that will help to debride chemically the uninstrumented
surfaces free of the microbial biofilm and other debris. In order that access
to the entire root-canal system is maintained during the radicular access
preparation, the dentine filings, chips and pulp debris generated or dis-
placed must be flushed out of the system. During the initial negotiation
of the canal system, depending on the relative fit or mismatch between
instrument and canal walls, debris occupying or attached to the canal
system wall may be compressed, compacted, pushed and smeared into the
accessory anatomy. As instrumentation proceeds apically through a pro-
gressively narrower channel, the potential for such displacement and com-
paction increases and some of the debris may be ousted through the apical
foramina. It is preferable that such compaction and displacement is avoided
and that the debris is flushed out through the coronal access.
Initial preflaring of the canal allows the coronal-most debris to be
washed out and creates a reservoir for easier delivery of the irrigant to the
apical parts of the root-canal system. In conjunction with this, the selection
of a good delivery system and good wetting characteristics of the irrigant
are also crucial.

F F
F
B C
Fig. 8.140  (a) File with size 10 to WL; (b) file with size 15 at WL; (c) file with size 20 at WL; (d) file with size 25 at WL
0.08/20 0.06/20 0.04/20
Fig. 8.141  The use of nickel–titanium rotary graduated tapers
The irrigant solution has been traditionally delivered using a hypoder-
mic needle and syringe (Fig. 8.150), particularly with the intention of
injecting it into the apical part of the root-canal system. Even assuming
an absence of any obstructing debris, injection of irrigant into the coronal
part of the canal does not lead to its penetration to the apical part unless
the needle is jammed into the canal (Fig. 8.151). This is because, under
normal circumstances, the fluid dynamics in a root canal result in a
so-called “stagnation plane”, beyond which the fluid does not penetrate
(Fig. 8.152). The position of the stagnation plane is influenced by the
needle design (Fig. 8.153). The stagnation plane is furthest away from the
needle tip in the flat open-ended needle design, followed by the bevel-
ended and then the side-cut needle designs, with the side-vented needle
Non-surgical root-canal treatment  209
F
D
F
F
A B
Fig. 8.142  (a) Stepping back by 1 mm from WL at size 30; (b) stepping back
by 2 mm from WL at size 35;
faring worst of all in this property. A smaller diameter needle (Fig. 8.154)
and higher extrusion force (higher Reynolds numbers) may displace the
stagnation plane apically by a small margin only (Fig. 8.155). This means
that the only way to move the stagnation plane further apically is to posi-
tion the needle tip further apically by using a smaller needle or enlarging
the preparation further; although the latter is not ideal (see Fig. 8.12). A
narrow-gauge needle (27 or even better 30) is recommended for deeper
needle and, therefore, irrigant penetration (Fig. 8.154). Use of the narrower
needle may reduce the rate of injection and make control difficult because
of the force required to extrude it. Some space is required adjacent to the
needle to prevent extrusion through the apical foramen (Fig. 8.151). There
is clearly an anatomical limit to how close to the canal terminus even the
 210  Non-surgical root-canal treatment

R
F R
F

C D E F

Fig. 8.142  Continued  (c) stepping back by 3 mm from WL at size 40; (d) stepping back by 4 mm from WL at size 45; (e) stepping back by 5 mm from WL at size
50; (f) refining coronal flare with Gates–Glidden if necessary

R
R
R
R

A B C D

Fig. 8.143  (a) Size 25 at full WL; (b) size 30; (c) size 35; (d) size 40;

smallest needle may be placed, yet apical delivery of irrigant is most
important. A strategy for ensuring that irrigant replacement does occur
apically is called “recapitulation”. This is illustrated in Figure 8.156 . This
is the single most important aspect of root canal preparation. As the canal
is sequentially instrumented, each series of strokes and increment in instru-
ment size leads to the generation of more and more dentine debris, which
will be loosely suspended in the irrigant fluid in the canal system (Fig.
8.156a). Since the stagnation plane prevents the fluid from reaching the
apical zone, the fluid in the stagnant zone becomes increasingly saturated
with debris. In the presence of sodium hypochlorite the organic material
may begin to dissolve, thereby increasing the viscosity of the apical solu-
tion. The dentine debris suspended in an increasingly sticky and viscous
solution, therefore begins to form what is recognized clinically as “dentine
mud”. The increasingly dense dentine mud may reach such a state of vis-
cosity that it could be mechanically propelled apically by the piston effect
of the sequentially larger instruments used during canal preparation,
thereby blocking the apical canal foramina. The irrigant fluid in the zone
beyond the stagnation plane must, therefore, be replaced frequently. This
is achieved by using a small file, such as 08 or 10, inserted to the
full working length to agitate the solution in a push–pull motion. This
action mixes the fresh coronal solution with the saturated apical solution
beyond the stagnation plane, thereby diluting it (Fig. 8.156d). This process
of dilution in the zone apical to the stagnation plane is called
recapitulation.
Given that the apical anatomy may contain several apical exits in a delta,
it is important that the entrance to it is not blocked. It is therefore
 Non-surgical root-canal treatment  211

R R

A B C

E F

Fig. 8.143  Continued  (e) size 45; (f) size 50

Fig. 8.146  Dissolution of extirpated pulp tissue

placed in a dish of 3% sodium hypochlorite over
D
0.5 (b), 5 (c) and 10 (d) minutes

Fig. 8.147  Corrosion of

Endosonic hand-piece
with sodium
hypochlorite

0.04/25 0.06/25 0.08/25

Fig. 8.144  The use of rotary nickel–titanium instruments to achieve final

shaping

Canal preparation time line

Canal negotiation Canal enlargement Canal shaping Completed enlargement

Table 8.2  Efficacy of commonly used irrigants in bacterial killing and

biofilm disruption
Phase 1 Lubrication
Sodium
Action/agent hypochlorite Iodine Chlorhexidine EDTA
Phase 2 Flushing
Bacterial killing +++++ +++++ +++ +
Dissolution +++++ + − −
Phase 3 Biofilm penetration +++++ ++++ ++ ++
Canal irrigation time line Biofilm break-up +++++ − − ++++

Fig. 8.145  Irrigants and their functions; phase 3 consists of dynamic irrigation + = degree of activity; − = no activity
 212  Non-surgical root-canal treatment

A B

Fig. 8.148  Well-sealed rubber dam Fig. 8.149  (a) Smear layer formed by instrumentation; (b) smear layer removed

A B

A = tip of B = apical extent

A hypodermic needle B of irrigant flow

Fig. 8.150  Hypodermic needle and syringe Fig. 8.151  Needle binding encourages extrusion Fig. 8.152  (a,b) Hypodermic needle in cleared
of irrigant canine tooth showing apical extent of needle
(A) and irrigant deposition (B)

A
B

Fig. 8.153  (a) Needle designs; (b) position of the stagnation plane for different type of needles Fig. 8.154  Different gauges of needle are
available in all types

considered prudent to pass a small file (size 08) just beyond the apical
foramen to ensure its patency. This is called patency filing. It also allows
the periapical status of infection and inflammation to be gauged by allow-
ing apically pressurized pus or exudate to be vented into the canal, where
it may be detected. Blocking apical foramina at the first appointment in
this manner is equivalent to a single visit obturation, even though the root
filling may not have yet been placed. Both recapitulation (within canal
terminus) and patency (beyond canal terminus) filing should be performed
frequently.
Avoidance of apical blockage is academic, if the simpler task of avoid-
ing compaction of tissue, biofilm and debris in the main canal cannot be
achieved. Negotiating the main canals requires sensitive instrument
passage combined with gentle agitation to facilitate carriage of the irrigant/
lubricant apically. Any loosened debris should either be flushed away or
allowed to dissolve. Patience is required in this early and critical stage,
when the potential for blockage and damage is greatest. Delivery of boli
of irrigant should be frequent with agitation, mixing and carriage of the
irrigant apically each time until the apical terminus is reached with a small
file (06 or 08) as tracked by an EAL.
DYNAMIC IRRIGATION AFTER MECHANICAL
PREPARATION OF THE CANAL SYSTEM IS COMPLETE
Once the radicular access preparation is complete, the chemical agents
may be delivered with a syringe and needle into the apical part of the
radicular access; its further penetration to the accessory and peripheral
anatomy may occur either by diffusion along a concentration gradient
(inefficient) or bulk flow driven by agitation (efficient). Clearly, the latter
method is preferable but would have to be actively facilitated as mere
needle delivery is insufficient.
 Non-surgical root-canal treatment  213

ReN = 100 ReN = 200 Fig. 8.155  Displacement

of the stagnation plane
apically by using smaller
needle and higher
extrusion force
1 Gutta-percha cone
pumped in and out
2 of canal

Position of 3
stagnation
plane 4

5 Direction of fluid flow

in canal system due
6 Position of to pumping motion
stagnation
7 plane
x/D

Dynamic
Mean/median
irrigation

Vol 3.3 0.0 7.6 29.6 22.4 0.01 5.5 0.0 10.7 2.0 8.1±10.2/4.4

Static
Mean/median
irrigation

Vol 0.0 1.0 0.0 0.0 1.4 0.0 0.0 0.0 0.8 0.0 0.3±0.5/0.0
B
Fig. 8.157  (a) Diagram displays fluid flow resulting from manual agitation; (b)
irrigant extrusion (bleached zone in pink agar) following gutta-percha cone
agitation of irrigant in the embedded roots
A B

As the irrigant is delivered, its contact with debris and organic material
B will rapidly deplete its oxidizing power, constant replenishment by fresh
irrigant is therefore essential. A major initial challenge is that the reactive
irrigant will have become spent by the time it reaches the peripheral site.
Frequent intermittent replenishment with fresh irrigant and its mixing is
required but is time-consuming; therefore adequate time should be allowed
for the irrigant to be replaced and to act, even if the radicular access
preparation may have been completed quickly.
The strategies for delivering, agitating, and mixing the irrigant into the
complex anatomy from the prepared radicular access have increased multi-
fold in recent years as this need became better understood. The approaches
may be classified into:

• Manual agitation: using hand-files propelled in a push–pull motion;

C D
Fig. 8.156  (a) Canal containing dentine-saturated irrigant; (b) fresh irrigant
replaces coronal saturated irrigant (arrowed): A = needle tip; (c) deeper needle
placement allows deeper replacement of irrigant (arrowed): A = needle tip; (d)
recapitulation to mix apical dentine-saturated irrigant with coronal fresh
irrigant: B = small file
a gutta-percha cone used in a push–pull motion (Fig. 8.157a)
• Sonic agitation: using SonicAir® activated file; EndoActivator®;
Vibringe® (vibrating needle attached to a syringe) (Fig. 8.158)
• Ultrasonic agitation: using Irrisafe file; ProUltra syringe (vibrating
needle); ultrasonically activated normal file (Fig. 8.159)
• Pressure/vacuum agitation: EndoVac; RinsEndo; NIT system
(Fig. 8.160).
 214  Non-surgical root-canal treatment
Sonic Air
Endo Activator
Vibringe
Fig. 8.158  Sonic agitation devices
Fig. 8.160  Pressure/vacuum agitation devices
The simplest method is to reciprocate a gutta-percha cone to agitate the
irrigant (see Fig. 8.157a). With this method, there is an increased risk of
irrigant extrusion through the apical foramina (see Fig. 8.157b). The
optimal method for maximizing wall shear stress and reducing apical
extrusion is to use a gutta-percha cone that fits well apically but is slightly
loose coronally.
Activation of irrigant with sonic or ultrasonic devices involves the agita-
tion of either a syringe-delivered bolus of fluid in the canal or by simul-
taneous delivery (via a custom-reservoir) and agitation. The sonic devices
available for irrigant agitation include the Sonic Air Endo Handpiece
(Micromega 1500, Besancon, France), which is driven by air pressure to
produce vibration frequencies of 1500–3000 Hz and which also drives
stainless steel files to aid simultaneous canal preparation. The EndoActiva-
tor® system (Advanced Endodontics, Santa Barbara, CA, USA) is electri-
cally driven and works at the much lower frequencies of 33, 100, and
167 Hz. It was designed to use polymer tips of various sizes (ISO size 15,
Irrisafe file
UItrasonic file
ProUItra
Fig. 8.159  Ultrasonic agitation devices
Fig. 8.161  (a–c) Acoustic microstreaming
around an ultrasonically activated file
25, 35) and tapers (0.02, 0.04) for agitation of the irrigant to avoid the
potential risks of instrument separation associated with metal files, ledge
formation and canal transportation. Preliminary data on debris and smear
layer removal were promising. Vibringe consists of a sonically activated
device attached to a syringe, which is said to create agitation as the irrigant
is delivered.
Much higher frequencies of vibration of the working tip (in the ultra-
sonic range, 20–40 kHz) are achieved with either magnetostrictive or
piezoelectric devices. Magnetostrictive transducers produce an elliptical
motion at the working tip, while piezoelectric transducers produce longi-
tudinal or transverse linear motions. In either case, the oscillations are
damped by contact of the file with the canal wall, also reducing the acous-
tic microstreaming (Fig. 8.161). Acoustic microstreaming is enhanced by
higher power output and greater flexibility of the file, therefore a small
size is better. To maximize acoustic microstreaming, it is best to use the
ultrasonically energized file without contacting the canal walls; this is

Fig. 8.162  EndoVac®
irrigation system
achieved by precurving the instrument and using it after canal preparation
is complete. That is, the so-called but mislabelled “passive ultrasonic
irrigation”, meaning unconstrained oscillation.
EndoVac® is a simple but ingenious device, which delivers the irrigant
into the coronal chamber but sucks the irrigant down into the canal through
an attachment that passes to the apical end of the radicular preparation
(Fig. 8.162). There are two sizes of attachments, the smaller of the two is
liable to blockage if the instructions are not followed. So far, the research
has proved positive. Another device, the NIT®, also uses simultaneous
delivery and suction but this time through a single needle allowing separate
flows in the inner and outer casings.
RinsEndo is an automated device operated by attachment to a hand-
piece coupling. It uses alternating positive and negative pressure changes
to drive irrigant into the root-canal system. It is moderately effective.
Apart from agitation, the exchange of irrigant relies on diffusion along
a concentration gradient from the main radicular access where the bolus
is deposited towards the peripheral anatomical aspects. The efficacy of this
also demands a higher delivered concentration, which could damage the
dentine in the radicular preparation. If the antibacterial agents reach the
bacteria in subinhibitory doses, there is a chance of inducing resistance to
them. This has been demonstrated not only for antibiotics but also for the
antiseptic agents mentioned above.
In the majority of cases, these efforts are sufficient to eradicate the
bacterial flora from the coronal aspects of the canal and also mostly from
the middle aspects of the root-canal system. However, the challenge lies
in complete eradication from the apical part, where the bacterial biofilm
usually remains virtually intact in the apical anatomy. It is therefore useful
to use additional antibacterial measures that continue to work in the inter-
appointment period. Over-vigorous efforts to debride the apical anatomy
could result in irrigant extrusion.
PHOTOACTIVATED DISINFECTION
Photoactivated disinfection (PAD) has been used to aid decontamination
of the canal system. A photosensitive agent, such as toluidine blue O
(Sigma Ltd, Poole, UK) is used to tag the bacteria selectively and trigger
the release of bactericidal radicals when stimulated by a light of an
Non-surgical root-canal treatment  215
Fig. 8.163 
Photoactivated
disinfection
appropriate wavelength (Fig. 8.163). The conceptual problem with this
may be that first, the fluid photosensitive agent must be delivered to the
vicinity of the target, and secondly, that the light must reach the tagged
bacteria at an adequate intensity to stimulate the chemical reaction.
Although studies report a definite antibacterial effect, consistent with other
chemical approaches, a 100% kill is not achieved and neither does it prove
to be as effective as sodium hypochlorite. The approach is therefore sug-
gested as an adjunct until conventional chemomechanical preparation is
complete.
INTERAPPOINTMENT INTRACANAL MEDICATION
Since the beginning of the practice of root-canal treatment, a variety
of chemically active materials have been placed into the root-canal
space either temporarily (antiseptics and antibiotics) or permanently
(formaldehyde-containing materials) for various reasons. Many of these
practices were not based on properly evidenced rationale. In modern endo-
dontics, the placement of specific chemicals during the interappointment
period between visits of a multivisit procedure forms part of the chemical
preparation of the root-canal system prior to obturation.
No single root-canal medicament has proved capable of meeting all of
the requirements listed previously and it is therefore not surprising that a
vast range of different agents have been tried. Many agents have been tried
empirically or based on laboratory tests only. There is little clinical research
on the efficacy of most of these, and use of particular materials tends to
be propagated on the basis of personal preference. The vast array of materi-
als may be divided for analysis into groups of like chemical structures and
mode of function.
PHENOL-BASED AGENTS
These, which were once the most commonly used agents, include phenol,
parachlorophenol, camphorated parachlorophenol, camphorated mon-
oparachlorophenol, metacresyl acetate, cresol, creosote, eugenol and
thymol. Gradually over the years more dilute solutions were adopted and
have now largely fallen out of favour. Their antibacterial effect is not long
lasting and they are able to diffuse through the temporary filling material
and cause an unpleasant taste in the mouth while some even soften the
filling material.
Phenol and camphorated monochlorophenol (CMCP)
Pure phenol was not widely used because of its toxicity but its chemical
modification monochlorophenol was adopted because of its lower toxicity
and improved bactericidal effect. A solution of CMCP was made by dis-
solving monochlorophenol crystals in camphor. This agent is also largely
out of favour, although still available as Cresophene (Fig. 8.164a) and
presumably used. It is a clear, slightly yellow solution containing 0.10 g
of dexamethasone base, 5 g of thymol, 30 g of parachlorophenol and
64.90 g of camphor per 100 g. It is also available as CMCP (Fig. 8.164b),
containing 35% parachlorophenol and 65% camphor.
 216  Non-surgical root-canal treatment

A B

Fig. 8.164  (a) Cresophene; (b) CMCP Fig. 8.165  Metacresyl acetate

Metacresyl acetate or cresatin

This has been favoured by some clinicians because it was thought to have
low irritation potential and anodyne action but the latter is unproven. These
materials are now largely out of favour because of their limited antibacte-
rial effect (in both range and duration), toxicity and absence of other posi-
tive features. It is however still available (Fig. 8.165) and recommended
for pulpotomy and infected canals with vital tissue.

ALDEHYDES
These materials (formaldehyde-containing preparations, formocresol, glu-
teraldehyde) have mainly been used in paedodontics. They have no role
in the treatment of permanent teeth. Formaldehyde-containing materials
have been used for their antimicrobial and fixative properties but they are
very toxic to the periradicular tissues and, furthermore, fixed tissue is
potentially antigenic. Gluteraldehyde also has the potential to cause hyper-
sensitivity reactions.

HALIDES
These include sodium hypochlorite, iodine-potassium-iodide, and a com-
bination of calcium hydroxide and iodoform preparations (Vitapex®,
Metapex®, Forendo®).
Sodium hypochlorite fulfils the most important criteria of antibacterial
effect and tissue dissolution, but its efficacy as a medicament is limited
because chemical reaction depletes its effect rapidly. In addition, since the
canal would need to be flooded, there may be an interaction with the
temporary filling material.
Iodine-potassium iodide has low toxicity and good antibacterial effect
in vitro. It is easily made by mixing 4 g of potassium iodide with 2 g of
iodine and 94 mL of water. The canal needs to be flooded but its long-term
effectiveness is not known. It has probably not gained favour because of
its potential for allergic responses and tooth staining.
Iodoform and calcium hydroxide preparations (Vitapex®, Diapex®
Metapex®, Forendo®, CalPlus®; Fig. 8.166) are recently introduced
medicaments with little information from controlled clinical studies. They
appear to combine the best effects of iodoform and calcium hydroxide but
their support is currently mainly anecdotal.
ANTIBIOTICS
Multiantibiotic pastes were originally introduced by GB Winter and D
Rule of the Paedodontic Department at the Eastman, London in the 1960s.
The rationale was to achieve antibacterial effect without damaging the
Fig. 8.166  Iodoform and calcium hydroxide preparations
crucial dental papilla in immature teeth requiring root-canal treatment.
Topical application of antibiotics (such as bacitracin, neomycin, poly-
myxin, chloramphenicol, tyrothricin and nystatin) in the root canal
remained popular with some clinicians, though with only one study from
Grossman supporting the outcomes. The substances are not toxic to the
periapical tissues, do not stain teeth and are active in the presence of
organic material. Since no single antibiotic is active against all the bacteria
found in the root canal system, a combination of antibiotics with different
ranges of activity is used, usually in the form of a paste.
Objections raised to the use of antibiotic pastes include the possibility
of developing resistant strains, possible sensitization of the patient and
development of an allergic response. Although all of these are possibilities,
and a few cases of allergic response have been recorded, there is no over-
whelming evidence against their use. However, their efficacy has not been
thoroughly tested in properly controlled clinical studies. Where they have
been tested (clindamycin and penicillin), the results have been reasonably
favourable but not comparable to calcium hydroxide.

Fig. 8.167  Ledermix®
The interest in antibiotics was renewed following the rise in their topical
use in localized periodontal pockets. A number of commonly used sys-
temic antibiotics were tried in combination, including metronidazole, cip-
rofloxacin and minocycline. The interest was further raised when they
were adopted for root-canal dressing in cases of pulp revascularization or
regeneration.
STEROIDS
Steroids (prednisolone, triamcinalone, hydrocortisone, dexamethasone)
have been used in root canals mainly for pain relief and anti-inflammatory
action; there is some clinical evidence of their anodyne action. These
materials have no other beneficial quality and, therefore, they may be
mixed with other antibacterial agents, such as calcium hydroxide or anti-
biotics. The commercially available paste popularly used in this manner
is Ledermix® (Fig. 8.167), which also contains the antibiotic tetracycline.
It has been suggested that Ledermix® can stain teeth when exposed to
light, so an alternative product (Odontopaste®), has used 5% clindamycin
hydrochloride and 1% triamcinolone acetonide instead to prevent tooth
staining. It also contains 0.5% calcium hydroxide with a caution that it
should not be mixed in a 50 : 50 ratio with calcium hydroxide because it
would destroy the steroid; this is a practice recommended by some for
Ledermix®. However, mixing these materials reduces the release of indi-
vidual components rather than providing synergism. The disadvantage of
the use of these substances is the depressive effect they have on the host
defence mechanisms, including inflammation. Their use may also bring
the risk of a bacteraemia.
CALCIUM HYDROXIDE
This material had gained wide popularity and acceptance as an intracanal
medicament as it is effective against most root-canal bacteria and, addi-
tionally, has the ability to degrade residual organic tissue, making it more
susceptible to dissolution by sodium hypochlorite at a subsequent appoint-
ment. The duration of the antibacterial effect is dependent upon the con-
centration and volume of the material but it has lasting effect because of
its low solubility. A saturated solution effectively provides a store of unre-
acted ions ready to go into solution as the dissolved ions are removed. The
material is quite irritating if extruded and can cause localized necrosis that
is self-limiting. Extrusion may be accompanied by severe pain lasting
Non-surgical root-canal treatment  217
A B
Fig. 8.168  (a,b) Closure of wide apices – apexification
A B C
Fig. 8.169  (a–c) Apexogenesis
12–24 hours. It is for this reason that some clinicians prefer to mix it with
a steroid paste. This ability to cause localized necrosis may help to form
a hard calcific barrier at the junction with the periapical tissues. It is there-
fore a useful intracanal medicament for closure of immature apices (Fig.
8.168), apexogenesis (Fig. 8.169), intracanal perforation repairs (Fig.
8.170) and horizontal root fractures (Fig. 8.171) before obturation. These
latter actions may also be facilitated by the property of calcium hydroxide
to solubilize the dentine matrix, releasing sequestered growth factors.
Calcium hydroxide is also readily available, inexpensive, simple to
place and relatively simple to remove from the root-canal system. It does
not stain the tooth or affect the temporary restoration. Another benefit
attributed to calcium hydroxide is its ability to dry weeping canals. The
reason for this is unclear but it is probably related to the antibacterial effect
of the material and possibly the inactivation of toxins. Calcium hydroxide
has been recommended for treatment of external inflammatory and internal
resorption. Its action is probably related to its antibacterial properties.
Figure 8.172 shows both external inflammatory resorption (right lateral
incisor) and external replacement resorption (left central incisor); the latter
does not respond to calcium hydroxide treatment as demonstrated by the
case shown (Fig. 8.173). One recently raised concern is that, in common
with sodium hypochlorite, it may affect the physical properties of dentine
adversely, particularly when used long term. According to some early
studies, it does appear to make teeth more susceptible to fracture, although
the effect appears to be limited to the surface.
Despite these positive features, recent literature casts some doubt on
the predictability of the antimicrobial effect, based on the resistance of
Enterococcus faecalis to calcium hydroxide because of its proton pump
 218  Non-surgical root-canal treatment

A B C

Fig. 8.170  (a–c) Intracanal repair of perforation in the furcal aspect of the mesial root of lower molar

A B C
A
Fig. 8.171  (a–c) Treatment of horizontal fractures where apical fragment has vital pulp tissue

Fig. 8.172  (a) External inflammatory

resorption in mandibular right lateral
incisor and replacement resorption in
A B C left central incisor; (b) resolution of
inflammatory resorption following
Fig. 8.173  Non-resolution of replacement resorption, despite root-canal treatment. (a) Pre-operative radiograph of canal debridement and calcium
two central incisors; and (b–c) follow-up radiographs of the central incisors following chemo-mechanical hydroxide dressing in right lateral
debridement and dressing with calcium hydroxide paste incisor

Fig. 8.174  Calcium hydroxide preparations
Fig. 8.175  Preparation
of calcium hydroxide
paste with powder and
water
mechanism. Overall though, the merits of calcium hydroxide outweigh any
disadvantages and it remains the medicament of choice.
Calcium hydroxide preparations
Many commercially available products (e.g. Multical, Endocal, Hypocal,
Rootcal; Fig. 8.174) contain calcium hydroxide together with other ingre-
dients. The constituents of these commercial products vary widely: the
calcium hydroxide content is about 34–50%; barium sulphate 5–15%. The
remainder is water and methyl or hydroxyl-methyl cellulose. Other anti-
septic materials, such as chlorothymonol may be added.
The disadvantage of commercially available materials is that the most
important ingredient (calcium hydroxide) is diluted and the pastes may be
more difficult to place with any degree of control. Many clinicians prefer
to use the pure-grade calcium hydroxide powder, which can be mixed in
a ratio of 7 : 1 with barium sulphate powder for radiopacity. The resultant
mixture should be stored in an air-tight bottle. It may be mixed with water,
saline or local anaesthetic (without vasoconstrictor) to a paste of the pre-
ferred consistency (Fig. 8.175). The consistency of the paste can be
changed on demand even within the canal by simply absorbing water with
a paper point or adding more. It is therefore very versatile in placement
but it must be remembered that the agent must be in aqueous solution to
be active. The powder may also be added as a thickener to commercial
products but this may adversely affect their rheological properties.
Placement of calcium hydroxide
The method of placement of calcium hydroxide is usually a matter of
personal preference. A range of manual and automated techniques may be
used depending upon the consistency of the preparation. The more fluid,
Non-surgical root-canal treatment  219
Fig. 8.176  Messing gun
commercially available pastes may be applied with files or paper points
but the material is unlikely to reach all aspects of the root-canal system.
Some recommend the use of spiral fillers or an ultrasonically activated file
as the most effective means of placement.
The stiffer pastes mixed to requirement may be loaded using amalgam
carriers, such as the Messing Gun (Fig. 8.176). The paste can be packed
down to the position required using pluggers or files. As above, the consist-
ency is very easily modified as per the requirement of the case. Packing
large pellets of hard mix may cause periapical discomfort if air is trapped
apical to the calcium hydroxide. It is better to break up the dressing into
smaller portions within the canal before packing these apically. Having
placed such a mix, it is best to introduce water to ensure that the material
is in solution.
Removal and replacement of calcium hydroxide
Calcium hydroxide is relatively easily removed by washing and irrigating
with water or sodium hypochlorite. The latter is preferable because it will
allow further dissolution of residual organic debris. Sometimes, the
calcium hydroxide may become very well compacted in a narrow canal
giving the impression of a blockage. It is important then to use sufficient
water and a small file to negotiate past it. An ultrasonically activated file
is very effective at removing calcium hydroxide dressings. The use of
weak acids, such as EDTA or citric acid, significantly enhances its removal
leaving a cleaner canal wall as viewed by SEM, if this is considered
desirable.
The duration of dressing with calcium hydroxide is dependent upon the
objective of dressing. If used as a routine antibacterial dressing, then 7
days are sufficient. If the objective is to arrest a weeping canal, then it may
be necessary to dress with a stiffer paste for a period of at least 14 days.
If it is found that a substantial amount of the paste has been resorbed (Fig.
8.177) more frequent dressings with stiffer pastes may be required. Dress-
ing and irrigation are continued until weeping is stemmed.
The use of calcium hydroxide to induce calcific repair at the periapex
requires longer periods of dressing. In the first instance, the dressing is
changed at 2–4 weeks to evaluate the degree of loss or contamination of
the calcium hydroxide. It also allows a further opportunity to irrigate the
canal with sodium hypochlorite and reduce the bacterial and organic con-
tamination. The dressing may then be left in place and healing reassessed
at 3–4-monthly intervals. It has been shown that the frequency of change
may enhance the effectiveness in periapical resolution but the benefit may
be marginal.
Criteria for assessment of healing include absence of intracanal bleeding
or exudates, absence of symptoms, tactile evidence of a barrier and radio-
graphic evidence of bone resolution adjacent to the site of calcific repair
(Fig. 8.178). Incompletely formed apices can take up to 24 months before
a complete barrier forms, but most are complete by 9 months. The duration
of dressing should be balanced against the possible damage incurred on
the mechanical properties of dentine.
There is no definitive guidance on the duration of dressing in case of
dental trauma and root resorption. These should be gauged on the basis of
 220  Non-surgical root-canal treatment

Fig. 8.179  (a,b) Canal

debridement and
dressing with calcium
hydroxide may aid
diagnosis of a perio–
endo lesion

A B

Fig. 8.177  (a,b) Resorption of calcium hydroxide paste with time

B
Fig. 8.178  (a) Large
periapical lesion
associated with
incompletely formed outcome of treatment, e.g. perio–endo cases (Fig. 8.179) or orthodontic
maxillary lateral incisor; cases under treatment.
(b) periapical resolution It may be concluded that there are positive advantages to the routine
following canal
dressing of root canals with calcium hydroxide.
debridement and
calcium hydroxide
dressing TEMPORARY CORONAL ACCESS CAVITY SEAL
A
Following the completion of radicular access, irrigation and the chemical
dressing of the root-canal system, it is essential to ensure that the coronal
access cavity is sealed to exclude bacterial microleakage and saliva, which
may inactivate the medicament and allow regrowth of bacteria. Lack of
an adequate temporary access cavity seal has been implicated as one of
the sources of infection by E. faecalis that makes infection of the root-
canal system difficult to eradicate.
The integrity of the seal depends on the strength and durability of the
temporary restorative material and the marginal seal. Access cavities
should be designed to provide retention in both the apical, as well as
coronal directions. It is customary for the access cavity to be sealed in
a double layer by applying a layer of gutta-percha over some cotton
wool, prior to applying the definitive sealing material (Fig. 8.180a,b). This
enables the seal to be condensed against a relatively firm material that
is easily removed. Some clinicians recommend the use of polytetrafluor-
B
oethylene (PTFE or Teflon) tape because of its inertness. The benefit of
using cotton wool, particularly in teeth with restorations, is that it helps to
the requirement of the case. For further guidance see Andreasen & diagnose intervisit coronal leakage evident from its discoloration (see
Andreasen (1994). Chapter 6).
Calcium hydroxide may also be used as a long-term dressing or as a The materials available for temporary seal include, zinc oxide/eugenol
short-term root filling if treatment cannot be completed for logistical (preferably reinforced), glass ionomer cements, polycarboxylate cements,
reasons or if the tooth needs to be left on review to assess the possible zinc phosphate cement, composite resins and, lastly, Cavit.

ZnO/Eugenol A B = gutta-percha: C = cotton
dressing
B wool; (c) the IRM dressing
Gutta percha
C
Cotton wool
B C
Calcium
hydroxide
A B
Fig. 8.181  (a) Intact IRM dressing with a high powder : liquid ratio after 2 years; (b) degraded IRM
dressing with a low powder : liquid ratio after 3 months
ZINC OXIDE/EUGENOL CEMENT
The material of choice is zinc oxide/eugenol because it has proven ability
to seal against microorganisms. It is not very strong or durable and, there-
fore, reinforced cements (such as IRM or Kalzinol) should be used. These
materials are best used to restore a conventional access cavity rather than
a larger defect.
To effect a good seal, proper manipulation of this sticky material is
essential. It should be adapted with apical pressure from the centre of the
cavity outwards or it may pull away from the margin (see Fig. 8.180c).
When mixed to a high powder/liquid ratio the material is very durable
(Fig. 8.181a). In the case shown, the patient did not attend for 2 years after
placement but the IRM dressings were still intact. In the second case (Fig.
8.181b), a low powder/liquid ratio resulted in surface loss of material over
a period of 3 months.
The only disadvantage of using zinc oxide/eugenol is its incompatibility
with composite resins. If this is likely to be a problem, a non-eugenol
dressing may be used but would lack antibacterial effect.
GLASS IONOMER CEMENTS
Glass ionomer cements have been recommended because of their adhesive
properties. However, the need to use the material in bulk means that the
setting contraction may be significant and can cause the integrity of at least
part of its margin to be compromised. Resin reinforced glass ionomer
appears to have good antibacterial properties.
OTHER MATERIALS
Other cements, such as zinc phosphate and zinc polycarboxylate, provide
durable restorations and reasonable marginal integrity at high powder/
Non-surgical root-canal treatment  221
Fig. 8.180  (a) Retention and
resistance form of an access
cavity; (b) double-layered
dressing of access cavity: A =
zinc oxide/ eugenol dressing;  
tends to pull away (arrowed)
from the cavity wall opposite to
that being adapted unless
adapted with apical pressure
Fig. 8.182  Postoperative radiograph of non-
surgical root canal treatment on mandibular molar
tooth with well-designed and integrated coronal
restoration
liquid ratios but do not possess the same antimicrobial activity as zinc
oxide/eugenol.
Cavit is popular because it is available in a ready-to-use form. It is
essentially “plaster”, and can give a reasonable seal over periods of about
a week, but is not very durable. It does possess some antimicrobial effect
but is not as strong as zinc oxide/eugenol. Its so-called “self-repair” capac-
ity is related to its ability to absorb moisture and expand. Because of its
lack of physical strength it needs to be used in adequate depth, considered
to be about 3–4 mm. Restoration of large cavities with Cavit results in
cracks within it accompanied by leakage.
The most recent generation of access restorative materials consist of
resins. One example is TERM, which is a light-cured resin; it does undergo
curing shrinkage and is hygroscopic but may be useful for larger cavities.
It is not recommended for use over one month.
ROOT-CANAL SYSTEM OBTURATION
“Obturate” means to block, obstruct, cork, stopper or occlude; to obturate
is to occlude or fill a cavity. Historically, obturation of the root-canal
system was viewed as the most critical part of the whole treatment. As a
result, extensive efforts have been devoted to the development of the ideal
root-canal filling techniques and filling material. However, it must be
stated that the success of non-surgical root-canal treatment is more depend-
ent on the debridement of the root-canal system, with obturation playing
the secondary role of incarcerating residual bacteria and preventing recon-
tamination. The purpose is therefore to “seal” the entire root-canal system,
including the coronal entry. Therefore, obturation of the root-canal system
should begin with the root-canal filling and finish with an integrated, well
designed and executed coronal restoration (Fig. 8.182). The context of the
 222  Non-surgical root-canal treatment

seal remains ill defined. It is not as previously thought, a hermetic seal,

since micro- and nanoleakage at various levels are endemic; the critical
relevant threshold has not been defined. The aim is to achieve the best
permanent adaptation achievable with contemporary materials, since it is
clinically proven that this works.

WHEN SHOULD THE ROOT-CANAL SYSTEM

BE OBTURATED?
There is an on-going debate on whether root-canal treatments should be
completed in a single visit or multiple visits. There are numerous advan- A
tages to completing treatments in a single visit and it is generally accepted
A
that vital cases of pulpectomy may be best treated in a single visit. Many
endodontists believe that, given adequate time, most cases can be com-
pleted in a single visit. However, many are of the opinion that non-vital
cases should never be treated in a single visit. This may be due to the belief
that there is likely to be more postoperative pain and further complications
with single-visit management than with multiple-visit therapy. To date,
these beliefs have not been substantiated by research and, in the hands of
expert clinicians, single-visit treatment is equally successful. The case may
be different for general dental practitioners who do not perform root-canal
treatments as frequently or perhaps to the same standard.
Ideally, a number of conditions should be met before a root filling is
placed. These include: B B

• absence of pain and swelling Fig. 8.183  (a,b) Root Fig. 8.184  (a) Overfilling of the root canal system;
• absence of persistent exudate in the canal filling end at a point (b) overextension of the root filling – note the
• thoroughly debrided root-canal system (all canals identified, corresponding to the
canal terminus
voids alongside the silver cones (arrows)
prepared and irrigated for adequate time)
• adequate time to complete the procedure. Fig. 8.185  Arrested
Completion of the treatment in a single visit has a number of advantages root formation resulting
in an open apex
for both the patient and the clinician. These include the following:

• the root-canal system is in the most decontaminated state

immediately after shaping and debridement, while there is
potential for recontamination between visits
• single-visit treatment provides no opportunity for temporary
restorations to leak
• there is less opportunity for teeth to fracture as definitive
restorations can be placed earlier
• the clinician is most familiar with the root-canal morphology for
effective obturation at the completion of the preparation
• there are both financial and time savings
• single-visit treatments are particularly beneficial for medically-
compromised patients whose conditions necessitate antibiotic
premedication
• the patient is exposed to local anaesthesia, rubber dam and
postoperative discomfort only once.
WHERE SHOULD THE ROOT FILLING TERMINATE IN
RELATION TO THE APEX?
A second controversy has to do with the ideal apical extent of the root
filling. Prognostic studies published in the last 50 years all unanimously
agree that overfilling the canal results in reduced success rates. According
to these studies, the optimal result is to end the root filling one to two
millimetres short of the radiographic apex in teeth with apical periodonti-
tis, at a point corresponding to the terminus of the canal (Fig. 8.183).
However, it is important to remember that many factors other than the
obturating material influenced these results. Ideally, all root-filling material
should remain within the confines of the root-canal system; the location
of the terminal ends of which was discussed before.
In practice, the extrusion of small amounts of sealer beyond the confines
of the root-canal system can delay healing although it is actually viewed
by some endodontists as a desirable indication of the adequacy of obtura-
tion of the complete canal system. A distinction is often made between
overfilling (Fig. 8.184a) and overextension (Fig. 8.184b) of a root filling.
An overextended root filling is one that has been extruded beyond the
confines of the canal system but does not completely fill the canal system,
while an overfilled canal is completely obturated and has, in addition, been
extended beyond the confines of the root-canal system.
Technical difficulties frequently arise in obturation of root-canal systems
with incomplete apices (Fig. 8.185) or in cases where resorption (Fig.
8.186), or iatrogenic causes have destroyed the normal apical anatomy. In
these cases, modifications may have to be made during both the prepara-
tion and obturation of the canal system.
The ideal outcome of root-canal treatment should be periapical healing
with regeneration of the normal periodontal ligament and, in particular,
sealing of the apical foramina with the laying down of cementum
(Fig. 8.187).

Fig. 8.186  External apical root
resorption: resorbed root surface
arrowed
A B
Fig. 8.188  (a) Preoperative radiograph of symptomatic lower molar tooth with prior silver cone obturation; (b) corroded silver cones removed during the
retreatment – note the black corrosion products formed on the cones; (c) case immediately after retreatment with gutta-percha
THE IDEAL ROOT-FILLING MATERIAL
Concepts of the ideal root-filling material are changing as the role of
obturation is better appreciated. The root-filling material of the past was
inert but it is more conceived as a bioactive material now. The required
properties of an ideal root-filling material have been defined as follows:
• it should induce or at least support regeneration of damaged
tissues
• be antimicrobial
• not irritate periradicular tissues
• not be toxic either locally or systemically
• be easily adapted to the canal walls and have capacity for self-
adaptation and self-sealing with dimensional fluctuations over time
• have good flow characteristics
• not stain dentine
• have good handling characteristics
• be radiopaque
• be impermeable to tissue fluids
• be dimensionally stable
• be cheap and have a long shelf-life
• reinforce, support and strengthen the root structure.
Historically, a plethora of materials has been used to obturate the root-
canal system. Effective use requires an understanding of the properties of
the material and an appreciation of the anatomy and morphology of the
Non-surgical root-canal treatment  223
Fig. 8.187  (a) Low-power
view of healing by
cementum formation
when Sealapex is used.
(Black particles are residual
Sealapex and root filling
material) (courtesy of Prof.
M Tagger); (b) high-power
view of (a) (courtesy of
Prof. M Tagger)
A B
C
root-canal system. Many obturating techniques and materials were
designed and used based on misunderstandings of this morphology.
Solid cores
Solid obturators, such as silver, titanium or acrylic cones were designed
to fit snugly into a canal “machined” to an equivalent dimension. However,
the irregular nature of the root-canal system was not fully accounted for
and these solid cores fitted only where they touched the irregular canal
walls. The remaining spaces were filled with cement or sealer. Over time,
tissue fluids could percolate into the canal system as the sealer is gradually
washed out. In cases obturated with silver cones, this was deemed to
induce corrosion products (silver sulphites and chlorides) (Fig. 8.188),
which were thought to provoke an apical inflammatory response.
Pastes
Many “paste” materials have been formulated to “simplify” obturation and
have been recommended for use alone or in combination with a master
cone. As it is not possible to compact a paste, it is virtually impossible to
ensure complete obturation of the root-canal system with paste materials
unless they expand on setting (Fig. 8.189). Expanding materials though
may be difficult to confine to the root-canal system. Extrusion of obtura-
tion materials beyond the confines of the root-canal system is undesirable
and, in the case of some paste materials, can result in permanent damage
to adjacent structures, such as neural tissue.
 224  Non-surgical root-canal treatment

Fig. 8.189  Tooth

obturated with
Endomethasone paste Volume
60

50 Amorphous phase

40 Change to Amorphous phase

Alpha phase
30
Change to Alpha phase
20

10 Beta phase

0
0 20 40 60 80 100
Temperature (ºC)

Stereochemistry of polyisoprene Fig. 8.191  Volumetric and phase changes associated with heating
gutta-percha
CH3 CH2 Isoprene monomer
C C
CH2 H Table 8.3  Percentage composition of conventional gutta-percha points

CH2 CH3 H cis-polyisoprene = natural rubber Gutta-percha 20

CH2 CH2
C C C C CH2 Zinc oxide 60–75
CH2 CH2 C C
CH3 H CH3 H Metal sulphates 1.5–17
Waxes/resins 1–4

CH2 CH3 CH3 trans-polyisoprene = Alpha gutta-percha

CH2
C C C H
C C
CH3 CH2 CH2 H CH3
CH2 H CH2 H CH2
trans-polyisoprene = Beta gutta-percha
C C
CH3 CH2 C C C C
CH2 CH2 CH3
Fig. 8.190  Structural formulae for isoprene, rubber, gutta-percha (α and β
phases)
Gutta-percha
The most commonly used obturating material has been gutta-percha (trans-
polyisoprene) (Fig. 8.190). It has been used in endodontics as the core
filling material for well over 100 years. The gutta-percha used in dentistry
is composed of approximately 19–22% of trans-polyisoprene and 59–75%
zinc oxide filler with other additives (Table 8.3). The additives include
waxes or resins, which enhance the plasticity of the material and metal
salts, which are used to increase the radiodensity of the material. The exact
composition of the commercially available product varies from manufac-
turer to manufacturer.
The stereo-chemical formula of gutta-percha is the mirror image of
natural rubber (a transisomer of rubber) and exists in three different forms;
two crystalline forms (α and β) and an amorphous form. All three forms
play a part in root canal obturation. Gutta-percha harvested from the Pal-
aquium gutta tree is mainly the α-phase while that in gutta-percha cones
available commercially exists mainly as the β-phase. The β-phase is con-
verted to the α-phase by heating to 42–49°C. Further heating to between
53°C and 59°C results in loss of the crystalline form and formation of an
amorphous melt (Fig. 8.191). The relevance of these structural changes is
that they are associated with volumetric changes that in turn influence the
clinical procedures during obturation. Manufacturers of some thermoplas-
ticized obturating systems, such as Thermafil® stress the importance of
maintaining vertical compaction pressures on the molten gutta-percha in
the coronal portion of the canal system while the material cools and under-
goes contraction and shrinkage. This vertical pressure is necessary to
compensate for the volumetric contraction associated with cooling of the
gutta-percha in the root-canal system.
C
CH2
Commercially available dental gutta-percha demonstrates several of the
properties of the ideal root-filling material but does not fulfil all of the
H
properties by any means. It is not toxic and is cheap. It is possible to
CH2
encourage flow by thermoplasticizing it and it adapts fairly well to the
canal wall, but does not bond to dentine. It does not stain dentine; it is
radiopaque (due to added radiopaque agents) and has good handling char-
acteristics and has a relatively long shelf-life. Clinically, it is not very
irritating to periradicular tissues but histologically provokes a chronic
inflammatory response, particularly in smaller particulate form. In addi-
tion, it neither induces nor supports regeneration of damaged tissues.
Despite its many drawbacks, it remains the material of choice of those
commercially available. The following discussion on obturation tech-
niques relates to the use of gutta-percha as the obturation material.
Alternative materials
Resilon®
This relatively new material exhibits the properties of gutta-percha and
looks like it. It is composed of the polymer polycaprolactone. It is used
with an adhesive sealant, “epiphany” in an attempt to create what has been
described as a “monoblock”, however, the existence and survival of such
a physical entity is not proven. It exhibits similar thermoplastic and chemi-
cal properties to gutta-percha and is therefore relatively inert.
SmartSeal®
This is a relatively new material made of a synthetic polymer. SmartSeal
consists of a radiopaque polymer core coated with a hydrophilic polymer,
which expands laterally upon absorbing water. It is used with either an
epoxy resin sealer or, more recently a bioceramic sealer. The epoxy resin
sealer contains a polymer, which can swell on contact with water. As yet
there is little research on the use of this material for obturation of the root-
canal system.
Experimental materials
The trend is towards development of bioactive root filling materials that
may aid killing of residual bacteria, create an on-going seal despite
 Non-surgical root-canal treatment  225

Fig. 8.192  (a,b) Experimental root filling material A = conventional gutta-percha and sealer root
filling showing leakage (Black ink); B = experimental root filling without exposure to an aqueous
environment showing less leakage; C = experimental root filling material exposed to an aqueous
environment showing no apical leakage

A B C

disruption in an aqueous environment through precipitation of salts and
facilitate regeneration of apical tissues through release of growth factors.
Figure 8.192 shows an example of an experimental material that forms a
precipitate at the interface in an aqueous environment that enables a seal
without a conventional sealer that is better than conventional gutta-percha
and sealer (Alani et al., 2009).
Sealers
A root-canal sealer is radiopaque luting agent used, usually in combination
with a solid or semisolid core material, to fill voids and to seal root canals
during obturation. All current obturation techniques require the use of a
sealer to fill minor discrepancies and voids in the obturation and to improve
the seal between the core material and the walls of the canal. Sealers also
act as a lubricant during gutta-percha placement and reduce leakage.
Sealers (Fig. 8.193) can be divided into a number of main groups based
on their constituents:
• zinc-oxide/eugenol materials (Roths, Pulp canal sealer, Wachs,
Tubliseal, Procosol)
• calcium hydroxide-containing materials (Sealapex, Apexit, CRCS)
• glass ionomer (Ketac-Endo)
• resins (AH-26, AH Plus, Diaket, Lee Endo-Fill)
• flexible polymers (Epiphany)
• bioceramic (Smartpaste).
As with all obturating materials, the ideal sealer should be biocompat-
ible, adhere to canal walls, be radiopaque, impermeable to tissue fluids,
dimensionally stable, antiseptic, not discolour the tooth, and be easily
manipulated.
 226  Non-surgical root-canal treatment
Fig. 8.193  A variety of sealers currently used in endodontics
A B
Fig. 8.195  (a–c) Irregular nature of apical foramina
OBTURATION TECHNIQUES
Gutta-percha is available in many forms for use in combination with a
variety of obturating techniques. These include:
• lateral compaction
• warm vertical compaction
• thermocompaction and hybrid technique
• thermoplasticized gutta-percha supported on a solid core
• injectable thermoplasticized gutta-percha.
Comparisons have been made between the different gutta-percha obtu-
rating techniques but, despite a large body of research papers, there is no
definite evidence to support one technique in favour of another from the
perspective of clinical success. Historically, lateral compaction has been
used as a “gold-standard” to evaluate new obturating techniques; lateral
compaction remains the most widely taught and practised technique world-
wide. The term “compaction” is used throughout this chapter and is con-
sidered more accurate than “condensation” as examination of the physical
properties of gutta-percha demonstrates that the material cannot be
condensed.
PRINCIPLES OF OBTURATION
Preparation of canal surface
The smear layer is a surface accumulation of debris formed on dentine
during instrumentation (Fig. 8.194a). It is composed of organic and inor-
ganic components and forms both a superficial, loosely adherent, layer and
a deeper, tightly adherent, layer. There is some debate as to whether the
A B
Fig. 8.194  (a) SEM of smear layer formed during instrumentation of a canal
(×600); (b) SEM of canal wall following irrigation with 5.25% sodium
hypochlorite and 17% ethylenediaminetetraacetic acid showing exposure of
the dentinal tubules (×600)
C
smear layer should be removed or not. On the one hand, removal will
eliminate the bacteria contained within it and will expose the dentinal
tubules allowing closer adaptation of the obturating material. Sealer and
gutta-percha have been shown to flow into the tubules and bonding agents
can form tags in the dentine. On the other hand, opening the tubules may
provide a passage for microorganisms into the body of the dentine wall
(Fig. 8.194b). The use of EDTA irrigation provides the surface with a
negative energy that facilitates better adaptation of the root-filling
material.
Dry canal
Moisture in the canal or in the dentine will preclude effective obturation
but complete drying and dehydration are impossible. Some clinicians
prefer to use alcohol to dehydrate the surface but the benefit of this is
unknown. The crucial area that is difficult to dry predictably is the apical
anatomy and the best attempt possible remains with paper points.
Controlled apical placement
This is the single most important part of obturation. Given the variability
in the anatomy of apical canal systems, and the cross-sections of apical
termini (Fig. 8.195), cone-fit is unlikely to be sufficient to effect a primary
seal. Furthermore, apical resorption or iatrogenic alterations to the apical
anatomy present additional challenges. It may be necessary to create an
apical matrix or barrier in order to prevent extrusion of the obturating
material. The matrix may be calcium hydroxide, ProRoot MTA (mineral
trioxide aggregate) (Fig. 8.196) or collagen (Fig. 8.197), which can be
placed to the established working length. The obturating material can then
 Non-surgical root-canal treatment  227

Fig. 8.196  Mineral Fig. 8.197  Collagen

trioxide aggregate material, such as
(MTA) CollaPlug can be used
to form an apical matrix

Fig. 8.198  (a) Chloroform

dip technique; (b) impression
of apical foramen; (c,d)
filling apical canal
irregularities with chloroform
dip technique

B C D

A B C

Fig. 8.199  (a–c) Customizing master point

be packed against this matrix. An alternative is to allow healing with
longer-term calcium hydroxide dressing prior to obturation.
A better and easier option which should be adopted routinely in every
case, is the customization of the master gutta-percha cone, regardless of
the technique (Fig. 8.198). It consists of selecting a master point at least
two sizes larger than the apical preparation and should bind about 2 mm
from WL. The tip of the point (length by which it binds short of the WL)
is dipped into chloroform for 1 second only (Fig. 8.198a); the purpose is
to soften the outer aspect, retaining the rigidity of the core. In a regularly
tapered canal, a significant length of the apical canal could be custom
fitted. If the canal is wider and more of the outer aspect of the gutta-percha
is to be softened, the point is dipped for slightly longer. The softened
point is then placed into the canal noting its orientation with a mark; the
point is then firmly pushed to the WL; if it does not immediately sit to
WL, a pumping motion is used progressively to seat it with continual
pumping. The tip should be examined to reveal the impression of the apical
anatomy (Fig. 8.198b); this will give insight about the challenge that lies
ahead. The point is left on the instrument tray to dry out. The orientation
mark is crucial for reseating accurately with the sealer. Large canals can
also be obturated with custom rolled gutta-percha cones, which may also
be further customized by chloroform dipping (Fig. 8.199).
Apical control of root filling material also includes the placement of the
sealer, which being fluid, is obviously difficult to control. The control is
therefore a function of adequate viscosity, quantity and how it is delivered.
 228  Non-surgical root-canal treatment
Fig. 8.200  Desirable
consistency of sealer
Sealers may have predetermined mixing ratios if encapsulated but others
have set powder/liquid or paste/paste components with potential for vari-
ation in viscosity. Sealers should where possible be mixed to an optimal
viscosity judged clinically by evaluating its “stringiness” when raised from
the mixing surface (Fig. 8.200). The canal walls may be thinly and evenly
coated with a spreader (Fig. 8.201), file or paper point but excessive apical
loading should be avoided. An ultrasonically activated file is quite effec-
tive in spreading the sealer evenly but may stain the sealer and cause it to
set faster by heat generation.
Efficient and effective backfill
Once the apical placement is controlled by customization and a few
accessory points placed by cold lateral compaction, it becomes easier to
backfill into the entire root-canal system, using any thermoplasticized
technique of the operator’s choice. If a significant length of the apical canal
is customized (>3–4 mm), placement of accessory points may not be
necessary.
Coronal seal
Once the root filling has been placed, the coronal part should be neatly
finished and a subseal placed to protect it, preferably using an antibacterial
material, such as zinc oxide/eugenol. A semi-permanent plastic material
(amalgam, GIC, composite resin) should be used to cover this subseal.
LATERAL COMPACTION
There is no compaction technique that is exclusively lateral or vertical in
nature. All techniques will have both vertical and lateral components. The
specifically named “lateral compaction” technique involves placing tapered
gutta-percha cones in the canal and compacting them under pressure
against the walls of the canal with a metal spreader (Fig. 8.202). The first
gutta-percha cone, called the “master cone or point”, is ISO standardized
so that it matches ISO files sizes (Fig. 8.203) and should be chosen to
customize to the apical preparation size. Ideally, the customized master
cone (as previously described) should fit accurately in the apical few mil-
limetres at the predetermined length (Fig. 8.204a). The customized point
should not be easily forced beyond the final preparation point and may
demonstrate a slight resistance to removal called “tug-back”. The concept
of apical “tug-back” has been widely cited as a requirement for a well-
fitting master cone and should be valid as long as the taper of the point is
smaller than that of the prepared canal.
Once master point selection and customization is complete, the canal is
dried for sealer and master point placement. Subsequent gutta-percha
cones are called “accessory cones”, are non-standardized in taper and
match spreader tapers (Fig. 8.205). The metal spreaders can be either finger
or hand manipulated and are preselected by placing in the canal to reach
WL freely (Fig. 8.206) before the master cone is compacted. The spreader
should be left in place for a few seconds to allow the gutta-percha time to
Fig. 8.201  Application of sealer to Fig. 8.202  The taper of the canal
canal wall should be matched with spreader
and accessory points: A = spreader;
B = master point; C = accessory
points
Fig. 8.203  Standardized
gutta-percha points
match files
deform and flow under pressure (Fig. 8.204b). Following removal of the
spreader, the first accessory cone with a light coating of sealer is placed
and compacted into place. This process is repeated until the canal is filled
(Figs 8.204c, 8.207). The selection of the taper (of gutta-percha and
matched spreader) depends on the taper of the canal at any given segmental
level in the canal to maximize efficiency (Fig. 8.208). It is recommended
that finger spreaders be used as hand spreaders very easily generate forces
that may fracture roots (Fig. 8.209).
It is important that the spreader reaches at least to within 1 mm of the
working length in order to ensure adequate compaction of the gutta-percha
against the canal walls. In addition, a regularly tapered canal contributes
to adequate obturation (Fig. 8.210). Gutta-percha may, under the right
circumstances of matching tapers of gutta-percha, spreader and canal, be
compacted into lateral canals (Fig. 8.211). Teeth, such as premolars and
canines that are wide in the labiopalatal dimension will not be so well
filled without the aid of heat (Fig. 8.212). Apical canal morphology also
influences the management of the initial phase of the procedure. When two
canals join in the apical part, it is best to customize master points in each
simultaneously to prevent occlusion of the unfilled canal with sealer (Fig.
8.213). Accessory points are then placed alternately in each canal. If a
single canal divides into two, one canal should be obturated first up to the
division and then the second (Fig. 8.214).

A
A
C
Fig. 8.205  Non-standardized gutta-percha points Fig. 8.206  Radiograph showing
should be used with matching spreaders prefitting of spreader
Adaptation and compaction of gutta-percha to the walls of an irregular
root-canal system is facilitated by the use of heat to make the gutta-percha
more pliant. This can be done in a number of ways. Originally, instruments
were heated in an open flame and then rapidly applied to the gutta-percha
mass. More sophisticated heat-delivery systems have now been developed,
which allow heat to be safely and easily applied to the mass of gutta-percha
within a few millimetres of the working length. Touch n’ Heat has been a
popular choice (Fig. 8.215). Heat may also be applied using an ultrasoni-
cally activated spreader or file (Fig. 8.216). This is a clean and effective
way to introduce heat, which is switched off in an instant as the heat is
frictional. The factors affecting efficacy are the power setting, duration of
activation and rate and extent of apical advance. Care needs to be exercised
to prevent extrusion. The activation should be followed by further cold
Non-surgical root-canal treatment  229
Fig. 8.204  (a) Selection of master
gutta-percha point (A) to occlude apical
foramen; (b) compaction of gutta-percha
point with spreader: A = spreader;
B = gutta-percha; (c) longitudinal view
– three accessory points compacted into
the inner curve
B C
Fig. 8.207  (a) Cross-sectional view of apical part of
canal showing master point and one accessory point;  
(b) cross-sectional view of apical part of canal showing
master point and three accessory points ; (c) cross-
sectional view of apical part of canal showing master
point and multiple accessory points (multiple colours)
lateral compaction. The use of heat improves the homogeneity of the final
obturation in comparison to cold lateral compaction alone where the cones
may retain their integrity. In addition, heating the gutta-percha reduces the
compaction pressures necessary to ensure adaptation thereby reducing the
risk of root fracture.
 230  Non-surgical root-canal treatment

Fig. 8.209  Root end crack produced by Fig. 8.210  Quality of properly compacted
cold lateral compaction of gutta-percha gutta-percha removed from well-tapered canal

Fig. 8.208  The taper of the canal

should be matched with spreader and
accessory points: A = spreader; B = wide
accessory points; C = narrow accessory
points; D = master point; E = wide Fig. 8.211  Gutta-percha point deformed into lateral Fig. 8.212  Poor compaction
taper; F = narrow taper canal during cold lateral compaction (arrow) in irregularly tapered canal

Fig. 8.213  Obturation of Fig. 8.214  Obturation of canal that divides apically Fig. 8.215  Touch ‘n’ Heat (Analytic Technology)
canals that join apically

A B C D

Fig. 8.216  (a,b) Ultrasonic lateral compaction of gutta-percha in an extracted tooth model; (c,d) filling of accessory anatomy using ultrasonic lateral compaction
of gutta-percha (c) before; (d) after (arrowed)

Fig. 8.217  (a)
Magnified image of
finger plugger (Miller
Inc, York, PA, USA);  
A (b) double-ended
Dovgan Pluggers (Miltex
Inc, York, PA, USA)
Fig. 8.218  Premeasured
pluggers
Lateral compaction is by far the best technique for controlling apical
placement of root filing material and should form the basis of any hybrid-
ized technique.
WARM VERTICAL COMPACTION
Vertical compaction was first described many years ago but was made
popular in 1967 by Schilder. The original technique described involved
placement of a fitted non-standardized master cone in the canal with a
minimal amount of sealer. The master cone tip is adjusted to ensure a close
fit apically either by cutting off the tip or by using solvent to soften the
tip, which can then be more easily adapted to the apical portion of the
canal. The gutta-percha is warmed with heat carriers and a series of flat-
ended pluggers are used to compact the gutta-percha starting initially in
the apical portion. It is important that the pluggers, either finger or hand
(Fig. 8.217) are prefitted at 2-mm intervals (Fig. 8.218 ) so that at each
level of the canal the appropriate plugger captures the maximum cross-
sectional area of softened gutta-percha (Fig. 8.219a,b) without binding the
canal walls. Binding of the pluggers on the canal walls (Fig. 8.219c) could
cause fracture of the root, while too small a plugger (Fig. 8.219d) would
simply plunge through the gutta-percha. The smallest plugger should fit to
within 5 mm of the working length to achieve good apical compaction
without extrusion. The width and rigidity of the pluggers necessitated a
more widely tapered canal preparation than for lateral compaction but the
flexibility of modern pluggers allows narrower preparations.
The pre-fitted master cone is placed to the designated length in the canal,
the walls of which have been coated lightly with sealer (Fig. 8.220). The
cone is seared off at the canal-orifice level with a hot instrument. A cold
plugger dipped in sealer powder or wiped with alcohol is used to begin
the compaction process. The coronal-most few millimetres of warmed
gutta-percha are moved laterally and apically. The heat carrier is now
plunged 3–4 mm into the gutta-percha and quickly removed. Some gutta-
percha is removed with the heated instrument and immediately the remain-
ing gutta-percha is compacted with the next prefitted plugger. The body
of the gutta-percha is warmed 4–5 mm ahead of the heated instrument and
the compacting action of the cold plugger moves the gutta-percha apically
and laterally. This procedure is repeated until about 5 mm of well-
compacted gutta-percha remains in the apical portion of the canal. The
coronal portion is then back-filled by introducing 3–4 mm segments of
gutta-percha, which are then heated and compacted in sequence.
Non-surgical root-canal treatment  231
B C
Fig. 8.219  (a) Warm vertical compaction; (b) plugger should capture
maximum cross-sectional area of gutta-percha without apical binding;  
(c) plugger binding apically may split root; (d) small plugger is ineffective
The compaction of the heated gutta-percha encourages flow of the
obturating material into canal irregularities and accessory anatomical fea-
tures. Careful adherence to the step-by-step approach usually results in a
dense homogeneous fill (Fig. 8.221).
Variations on the warm vertical obturation procedure have been intro-
duced to improve and simplify the procedure. These include a variety of
electrically-operated heat carriers available on the market (Fig. 8.222).
These units allow for instant delivery of heat to the gutta-percha mass that
can then be compacted. The System-B heating element is contained within
specifically designed pluggers, the tips of which vary from 0.30 mm to
0.70 mm in diameter. The heat carriers or “Buchanan system B pluggers”
have shapes that closely approximate the shapes of tapered root-canal
preparations. These pluggers currently come in five sizes or tapers; extra-
fine (0.04), fine (0.06), fine-medium (0.08), medium (0.10), and medium-
large (0.12), which resemble the greater taper of master cones (Fig. 8.223).
In addition, these dead-soft stainless steel heat pluggers are quite flexible,
allowing for deeper compaction especially in narrow, curved canals. An
example of a technique recommended by the manufacturer for use with
the System-B is illustrated in Box 8.1.
The System-B “Continuous Wave” obturation technique is based on the
Schilder warm vertical compaction procedure. Before the master cone is
positioned, one of the five System-B pluggers is chosen. The plugger (ML,
M, FM, F, XF) is fitted to within 5–7 mm of the working length and the
position on the plugger noted. The heat source is set to 200°C. The canal
orifice is coated with a small amount of sealer and the cone is placed to
length. The tip of the plugger is placed into the canal orifice and activated.
It is driven through the gutta-percha to the predetermined length. The heat
is removed, the tip cools rapidly and the plugger’s position is maintained
for 5–10 seconds until the apical gutta-percha has set. This apical pressure
compensates for volumetric changes as the gutta-percha changes from the
amorphous melt form back to the crystalline α-form. The tip is reactivated
for 1 second in order to release the plugger and to remove excess gutta-
percha. At this stage, the apical portion has been obturated and the remain-
der of the canal can be backfilled or post-space can be formed.
The “backfill” can be completed as described by Schilder or using a
variety of injection delivery systems for thermoplasticized gutta-percha;
 232  Non-surgical root-canal treatment

HC
HC
HC

A B C D E F

HC HC

B
A

G H I J K L

Fig. 8.220  Procedure for warm vertical compaction: (a) fitting master point; (b) application of heat carrier (HC); (c) plugging heated gutta-percha;
(d) reapplication of heat carrier (HC); (e) reapplication of plugger; (f) reapplication of heat carrier (HC); (g) reapplication of plugger; (h) addition of new section
of gutta-percha (3–4 mm); (i) application of heat carrier (HC); (j) reapplication of plugger; (k) reapplication of heat carrier (HC) to new section of gutta-percha;  
(l) reapplication of plugger

A B C

Fig. 8.221  (a–c) Radiograph of case obturated with the warm vertical compaction technique

Fig. 8.222  Electrically-operated heat carriers
Fig. 8.223  Buchanan
system B pluggers
Box 8.1 Recommended technique for System-B compaction
1. Fit a non-standardized (fine, fine-medium, medium, or medium-large) gutta-
percha cone into a tapered root canal preparation. You can also use greater
taper gutta-percha points 0.04, 0.06, 0.08, 0.10, and 0.12
2. Choose a Buchanan plugger that matches the taper of the gutta-percha point
and place a rubber stop onto the plugger 5 mm short of the working length:
fine plugger = 0.04 + 0.06 taper; fine-medium plugger = 0.06 + 0.08 taper;
medium plugger = 0.08 + 0.10 taper; medium-large plugger = 0.10 + 0.12
taper
3. Prefit the Buchanan plugger to its binding point in the canal (usually 5–7 mm
short of length). Adjust the stop and remove the plugger
4. Dry the canal and cement the cone
5. Turn the System-B unit to “Use” position. Then, holding the button on
momentarily, drive the preheated plugger smoothly through the gutta percha
until it stops. Repeat this procedure until the plugger is within 0.5–1 mm of the
binding point
6. Maintain apical pressure without heat for a 10-second “sustained push” to take
up any shrinkage that might occur upon cooling
7. Still maintaining apical pressure, push the button again for 1.5 seconds.
Withdraw the plugger after cooling for 1 second. Because the Buchanan
pluggers heat from their tips back, the heat burst in this portion of the
procedure causes rapid severance of the instrument and the coronal surplus of
gutta-percha from the already condensed and set apical mass
8. The canal is now ready for back-filling using an injection system (Fig. 8.224)
Non-surgical root-canal treatment  233
Fig. 8.224  Injection delivery systems for thermoplasticized gutta-percha
some of which combine the heat carrier and injection functions
(Fig. 8.224).
INJECTION OF THERMOPLASTICIZED GUTTA-PERCHA
This technique involves injecting molten gutta-percha into the root-canal
system. Theoretically simple, this technique demands considerable care
and is associated with the disadvantages of any thermoplasticized material.
Even though it has been recommended for obturation of the complete
root-canal system, it is probably prudent to use the injectable heated gutta-
percha as a backfilling material as described above or in cases where apical
occlusion is already assured. As with all gutta-percha obturations, a sealer
must be used. A variety of systems are now available (see Fig. 8.224).
Commonly used systems include the Obtura® system (“high-heat”) and
the Ultrafil (“low-heat”) systems. Injectable gutta-percha allows for rapid
backfilling of the canal with material that demonstrates excellent flow
properties.
The Obtura® system consists of a control unit and a pistol-grip syringe
designed to accept gutta-percha pellets formulated for use with the system.
The gutta-percha is heated in the barrel of the syringe to 160–200°C. The
molten gutta-percha is extruded through silver needles that are supplied in
20, 23 and 25 gauge sizes (Fig. 8.225a). As the gutta-percha leaves the tip
of the needle, its temperature drops to between 62°C and 65°C. The
heating barrel reaches full operating temperature in less than two minutes
thereby eliminating the need to preheat the gutta-percha.
The “low-heat” Ultrafil system heats cannules (see Fig. 8.225b) contain-
ing gutta-percha to 70°C in a heating unit. The gutta-percha is supplied in
three different formulations; regular set; endoset; and firm set. The can-
nules must be placed in the heater at least 15 minutes before use and must
be discarded after 4 hours’ heating. The trigger is squeezed gently and
released and the gutta-percha is allowed to flow out at its own rate. It is
important to avoid excessive pressure in order to prevent extrusion of the
material from other channels (Fig. 8.226).
THERMOPLASTICIZED GUTTA-PERCHA CARRIERS
In 1978, Johnson described an ingenious technique for delivery of
gutta-percha to a root-canal system by coating an endodontic file with
 234  Non-surgical root-canal treatment

A Fig. 8.227  Thermafil equipment

B A B

Fig. 8.225  (a) Disposable silver needles for Fig. 8.226  (a) Fracture of cannule due to haste
Obtura; (b) prefilled gutta-percha cannules for or inadequate heating; (b) extrusion of Fig. 8.228  If carrier is too small it
Ultrafil gutta-percha through the back of cannule may be extruded

thermoplasticized α-phase gutta-percha. This concept is widely marketed
as the Thermafil system (Fig. 8.227). The original commercially available
metal carrier has now been replaced with a radiopaque plastic carrier and
is available in a series of ISO sizes from #20 to #140, as well as non-ISO
ProTaper shapes. Verifiers made of fluted tapered NiTi wire are used to
gauge and select the appropriate size for a given canal. If the selected
carrier is too small the carrier may be extruded (Fig. 8.228) and if it is too
large the root-canal filling may be short. The carriers must be heated in
a special oven at 115°C according to the manufacturer’s instructions.
Maximum and minimum times should be observed in order to ensure
adequate heating. However, if left in the oven longer than the designated
time, the obturators must be discarded. A very small amount of slow-
setting sealer is applied to the walls and the heated carriers are then placed
firmly and smoothly to full length in the canal. The length can be deter-
mined in advance using the rubber stoppers on the carriers. In teeth with
multiple canals, excess gutta-percha from the first carrier can be prevented
from blocking the orifices to the other canals by placing a temporary
obstruction, such as damp cotton pellet or paper points into these
orifices.
As with other thermoplasticized techniques, it is important to compen-
sate for the volumetric shrinkage that occurs when the gutta-percha cools
by maintaining apical pressure on the cooling material. This is done by
compacting the gutta-percha around the central carrier in an apical direc-
tion as it cools.
Thermoplasticized gutta-percha has been shown to obturate the canal
system effectively and to flow very well into accessory anatomical spaces
(Fig. 8.229). The apical seal provided by these techniques has also proven
to be as effective as any other obturation technique. However, apical
control of the flow of the thermoplasticized material is difficult and con-
stitutes a potential disadvantage of these techniques. In addition, a section
of the core carrier obturators, such as Thermafil (Dentsply) or Softcore
(SybronEndo) needs to be removed if the tooth has been treatment planned
for a post-retained restoration. Smooth round-ended burs specifically
designed to aid removal of the plastic core have been designed by the
manufacturer (Fig. 8.230).
A number of cone systems are also available on the market, including
a core carrier system called SimpliFill (SybronEndo), which has been
designed to overcome the problem of providing post space following
obturation (Fig. 8.231). In this technique, 5-mm plugs of gutta-percha are
carried to the apical portion of the preparation and sealed in place with an
endodontic sealer (AH Plus Epoxy Resin is recommended by the manu-
facturer). The carrier can then be removed leaving the apical 5 mm of
gutta-percha behind. The plugs are supplied in ISO sizes 35–130.
THERMOMECHANICAL COMPACTION TECHNIQUE
Thermomechanical compaction describes the plasticization of gutta-percha
by heat developed through mechanical friction. A well-adapted master
cone is placed in the canal with a suitable sealer. A mechanically activated
rotating compactor similar to a reverse Hedstroem file (thermocompactor)
(Fig. 8.232) is introduced into the canal, which heats up the gutta-percha
and thermoplasticizes it (Fig. 8.233). Accessory points may be added prior
to commencing compaction if necessary. Disadvantages of the thermo-
compaction technique include apical extrusion of obturation material (Fig.
8.234), as is common with all thermoplasticized techniques, gouging of
the wall by the compactor (Fig. 8.235), excessive heating of the supporting

tissues surrounding the root resulting in resorption (Fig. 8.236) and frac-
ture of the instrument.
HYBRID TECHNIQUE
Each technique offers its own characteristic advantages and disadvantages.
There is therefore considerable merit in devising hybrid techniques that
combine the best of all techniques for simple, safe, effective efficiency.
A B
Fig. 8.229  (a–c) Roots rendered transparent by clearing show good filling of
accessory anatomy using Thermafil obturators; (d) molars filled with Thermafil
obturators
A Fig. 8.231  (a) The SimpliFil carrier from Lightspeed Endodontics, TX, USA; (b) SimpliFil obturators (Lightspeed
Endodontics, TX, USA); (c) a SimpliFil obturator
Non-surgical root-canal treatment  235
Master cone customization provides the best apical control in conjunc-
tion with cold compaction, although if a sufficient length of the apical cone
(2–3 mm) is properly customized, cold compaction is not necessary. Cold
compaction helps ensure that the apical part is properly compacted in a
safe and controlled way. This can be followed by a warm vertical approach
to seal the apically placed gutta-percha, which would then allow any
rapid thermoplasticized technique to backfill with intermittent vertical
compaction.
CORONAL SEAL
POST-PREPARATION/RESTORATIVE
CONSIDERATIONS
It is absolutely essential that an adequate coronal restoration be placed
following obturation of the root-canal system (see Fig. 8.182). It has been
shown that the coronal restoration is as important as root-canal obturation.
Placement of a permanent core restoration at this time would appear to be
a sensible approach to the overall management of the case. Following
obturation of the root-canal system, the tooth will never be “cleaner” as it
Fig. 8.230  Post-space preparation when using Thermafil plastic carrier
obturators
 236  Non-surgical root-canal treatment

Fig. 8.234  Extrusion of root filling material

following thermocompaction

Fig. 8.232  (a) Maillefer gutta-condensor (SEM

view); (b) Maillefer gutta-condensor (SEM view)

Fig. 8.233  (a,b) Thermomechanical compaction

obturation (courtesy Dr J Woodson)

A B C D

Fig. 8.235  Gouging of canal walls in mandibular Fig. 8.236  (a) Normal periodontium; (b,c) various degrees of resorption seen on the root surface
first molar during thermocompaction (arrowed) following thermocompaction; (d) ankylosis (courtesy of Dr E Saunders)

has been soaking in sodium hypochlorite throughout the preparation stage
and the rubber dam remains in place. In addition, placing the core at this
appointment negates the need to place a temporary restoration and reduces
the number of dental appointments for the patient.
If a post space is required the root canal system should always be com-
pletely filled and then cut back. The space created may be filled with a
calcium hydroxide paste between visits in an attempt to reduce the chance
of bacterial recontamination.
FURTHER READING
European Society of Endodontology, 2006. Quality guidelines for endodontic treatment:
consensus report of the European Society of Endodontology. Int Endod J 39 (12),
921–930.
Gordon, M.P.J., Chandler, N.P., 2004. Electronic apex locators. Int Endod J 37,
425–437.
Gulabivala, K., Ng, Y.-L., Gilbertson, M., et al., 2010. The fluid mechanics of root canal
irrigation. Physiological measurement 31, R49–R84. http://stacks.iop.org/0967-
3334/31/R49.

Management of non-surgical root-canal treatment failure
The aim of this chapter is to outline the technical and clinical basis for
non-surgical or surgical management of root-canal treatment failure. The
foundational knowledge and principles for this chapter were laid previ-
ously as follows:
• the rationale for retreatment was established in Chapter 3
• the decision-making process and planning for retreatment were
discussed in Chapter 5
• non-surgical and surgical retreatment armamentaria were described
in Chapter 6
• the general principles of non-surgical root-canal treatment were
discussed in Chapter 8.
DIAGNOSIS OF NON-SURGICAL ROOT-CANAL
TREATMENT FAILURE
Non-surgical root-canal treatment failure is diagnosed based on the fol-
lowing clinical and radiographic criteria (Fig. 9.1):
• presence of clinical signs (swelling, sinus, tenderness to pressure
or percussion) and/or symptoms (pain of endodontic origin)
• enlargement of existing periradicular radiolucent lesion associated
with the tooth
• development of new periradicular radiolucent lesion associated
with the tooth
• persistence of periradicular radiolucent lesion associated with a
tooth that had root-canal treatment at least 4 years previously.
It is of the utmost importance to distinguish persistent pain of endodon-
tic origin from chronic non-odontogenic, neuropathic or neuromuscular
pain by adopting the assessment approaches described in Chapters 4 and
16. The two-dimensional limitations of conventional periapical radiogra-
phy may be overcome by three-dimensional cone-beam-computerized
tomography (CBCT) to increase sensitivity, if necessary, for confirmation
of the periapical status of root-treated teeth exhibiting no obvious periapi-
cal radiolucency but associated with persistent pain (Fig. 9.2).
DECISION-MAKING PROCESS
Once failure of non-surgical root-canal treatment has been diagnosed, a
number of important decisions need to be made between the dentist and
patient. A critical choice must be made between electing to retreat the
root-canal system non-surgically, perform surgical management or select-
ing extraction with or without a replacement prosthetic unit. The aspects
influencing the final decision will include:
1 Clinician factors:
i judgement about what is wrong with the tooth: factors to
decide on will include the presence of a crack, and whether
the infection is likely to be intraradicular or extraradicular or
whether some other pathosis is at play
ii judgement about treatment options and the correct choice:
factors to decide on will include whether the dentist can
improve upon previous root-canal treatment and, if so, in what
way; non-surgical retreatment may involve removal of
restorations, retention aids, root-filling material and correcting
iatrogenic problems
© 2014 Elsevier Ltd. All rights reserved.
9
Section 3 Delivery of endodontic treatment
Y-L Ng, K Gulabivala  
iii judgement about prognosis of different options in their hands: the
dentist will need to be sure that the tooth is predictably restorable
and a viable future unit, as well as determine how each treatment
option could be executed together with a realistic prognosis
iv judgement about prognosis in the hands of specialist(s): if the
dentist is unsure about the prognosis in their hands, they should
offer referral to a specialist who may be able to provide the
complex care with a better prognosis
v cost of different options: the dentist will need first to visualise
the procedures virtually, in the mind’s eye, to assess the
practical process, resource and time required. The better versed
and experienced they are the more precise their estimation.
2 Patient factors:
i understand what is wrong with the tooth
ii understand what can realistically be done and what their
preference may be
iii understand the chances of success depending upon what is
done and who does it
iv understand the relative costs, what is desirable and what is
affordable.
The dentist must ensure that the patient understands the nature of the
problem, the chances of resolving it and the means to be deployed to do
so. They must be clear about the dentist’s expertise to perform the tasks
and what other options may be available to them should they wish to take
them. An interactive process will need to have been followed and the final
decision preferably recorded in a mutually signed agreement. There may
be uncertainties at play in the process and these must be clearly recorded,
for example, it may not be certain without exploration whether a crack is
present, which may affect the direction of the decision-making pathway.
Under these circumstances, which are common, the treatment plan
path­way may be written as being subject to conditions being met upon
exploration.
NON-SURGICAL ROOT-CANAL RETREATMENT
INDICATIONS FOR NON-SURGICAL
ROOT-CANAL RETREATMENT
Non-surgical root-canal retreatment is indicated under the following three
circumstances:
1 when, having confirmed treatment failure, it is judged that the
residual infection is principally intraradicular and that it is
accessible through a conventional access, having negotiated any
obstructions. It is self-evident that this decision presupposes that
obstructions can be removed or bypassed without compromising
the remaining tooth structure; the purpose is to treat the residual
infection
2 when a new and complex restoration is required for a tooth with a
technically poor root filling (Fig. 9.3) but which exhibits no
evidence of pathoses or symptoms; the purpose is to correct the
technical quality of the root-canal treatment, as the ownership will
lie with the restoring dentist
3 when it is suspected that a tooth with an adequate or inadequate
root filling has been contaminated due to leakage or loss of its
restoration (Fig. 9.4); the purpose is to decontaminate the root-
canal system and place a new root filling and restoration.
 238  Management of non-surgical root-canal treatment failure

A
C

E F

Fig. 9.1  (a–f) Root-canal treatment failure diagnosed based on clinical and radiographic criteria

Fig. 9.3  Technically

inadequate root filling
in the maxillary first
molar

Fig. 9.4  Inadequate

root filling and coronal
restoration associated
with the mandibular
first molar

A B

Fig. 9.2  (a) Periapical radiograph, and (b) proximal view captured from
cone-beam CT scan of the root treated maxillary lateral incisor associated with
persistent pain with no obvious periapical radiolucency
 Management of non-surgical root-canal treatment failure  239
Fig. 9.5  Loupes Fig. 9.6  Microscope
PRINCIPLES OF ROOT-CANAL RETREATMENT
The principles of root-canal retreatment are identical to those for de novo
root-canal treatment, with the exception of certain additional conditions:
1 the resident infection is likely to have been altered through
artificial selection to one with a reduced diversity, dominated by
Gram-positive bacteria, and a microbiota that is more difficult to
eradicate
2 access to the residual infection may be compromised by the
presence of various types of obstructions, including dentine debris,
iatrogenic errors in preparation, root-filling material, radicular
dowel and restorative material
3 the tactile feel of the natural canal will have been altered through
changes in shape, packed organic/inorganic debris, iatrogenic
conditions, chemical treatment, impacted foreign materials.
The specific principles of root-canal retreatment are therefore to:
1 remove all restorative material as atraumatically as possible, where
possible sacrificing restorative material rather than tooth structure;
the exception will be when a new and sound restoration has
recently been placed and can be excluded as part of the aetiology
2 assess the restorability of the tooth and, if deemed so (see
Chapter 14), stabilize it for root-canal retreatment to prevent
recontamination during treatment
3 remove all root-filling material without sacrificing any additional
dentine, if possible; the exception will be only if the canals were
previously inadequately prepared but, even under those
circumstances, avoid instrumenting dentine at this stage; it will be
easier to determine iatrogenic errors as belonging to the previous
procedure
4 gauge the canal to understand its previous shaping and identify any
missed anatomy or root canals once all root-filling material has
been removed and apical patency and length of canal have been
determined
5 refine and modify the shape of the root-canal system as necessary
to deliver irrigant and root-filling material to the termini; the skills
of gauging come into their own in such cases
6 complete root-canal treatment at this stage as if it were a de novo
case; except if elements of obstruction could not be corrected.
The most common error in non-surgical root-canal retreatment is
removal of excessive dentine with the consequence of further weakening
Fig. 9.7  Leaking crown beneath buccal margin
the tooth and creating new iatrogenic problems. It is critical to use some
form of magnification when required; for example, for creating a trough
of dentine around a post or fractured instrument requires good magnifica-
tion (Figs 9.5, 9.6), good lighting, and a steady hand. Longer appointments
are required for retreatment cases, in particular for removal of foreign
material from root canals.
Removal of coronal restorations
All coronal restorations should be removed prior to treatment if they are
either leaking or if caries is present (Figs 9.7, 9.8). This also applies to
full coverage crowns. If the restoration is sound it is better to leave it in
place during treatment and access the pulp chamber through the restora-
tion. It is easier to place a rubber dam and to keep the operating field dry
by cutting through an existing restoration (Figs 9.9, 9.10).
It is difficult, or impossible, to remove a crown that is seated on a near
parallel preparation and is well fitting without damaging it beyond repair.
It is always well worth trying to ease off a crown by inserting a large
excavator under the margin and lightly twisting as it may be loose. As a
rule, the safest way to remove a cast restoration is to cut it off to prevent
damage to underlying tooth structure.
Removal of bridges
Any bridge that has become decemented must be removed. In most cases,
when an abutment tooth requires retreatment, the patient should be fore-
warned of the possible need for a new bridge. If a new bridge is already
planned then it is immaterial if it is damaged during its removal, providing
an adequate temporary bridge can be constructed and placed. The easiest
method for removing a bridge is to make a vertical cut through the retainer
on the buccal aspect and then to break the cement lute with an instrument,
such as a Mitchell’s trimmer by inserting it into the cut and twisting the
blade. There are, however, many devices (see Fig. 6.17) which can be used
to remove bridges – most of them causing both the operator and patient
varying degrees of aggravation.
Removal of posts
There are many different systems and gadgets on the market specifically
made for the removal of posts (see Fig. 6.18). The success and ease of
removal depends on the type, length, quality of fit of the posts and the
cement material. Posts can be broadly classified into prefabricated or
custom laboratory-made cast metal posts. Prefabricated posts include
screw or cemented wrought gold, stainless steel or titanium metal posts,
 240  Management of non-surgical root-canal treatment failure

Fig. 9.8  Poor marginal adaptation Fig. 9.9  Access through restoration with no caries Fig. 9.10  Access through well-fitting
on distal aspect of crown with signs crown
of leakage

Fig. 9.11  (a) Ultrasonic tips; (b) ultrasonic tip applied

to a post (predictable restorability may be
questionable)

A B

C
B

A Fig. 9.12  (a) Post fractured at canal orifice; (b) troughing cut around post with ultrasonic file; (c) loosened
post removed with fine-beaked forceps (predictble restorability may be questionable)

zirconia ceramic posts, or carbon or glass (quartz) fibre posts. Ceramic and
fibre posts are likely to be used with aesthetic ceramic crowns and have a Fig. 9.13  Post being removed using
the Ruddle post extractor
lower radiodensity than stainless steel or gold posts.
For metal posts, first attempts at removal are usually made by use of
ultrasonic vibration. The crown is first removed by cutting a vertical slot
to allow leverage and expansion of the margins. Excess cement is then
taken away. A solid curved tip is inserted in the ultrasonic hand-piece and
applied gently around the incisal edge of the core under water coolant (Fig.
9.11). The power is varied while the ultrasonic tip is in contact with the
core to achieve the desired effect. When the right power setting is reached,
cement particles may be observed vibrating at the base of the core. If this
does not loosen the post after a few minutes, a fine tip can be used to cut
a narrow trough around the post to reduce the retention (Fig. 9.12a,b). The
first step is then repeated with the blunt tip. This procedure will remove
the majority of posts (Fig. 9.12c). In the case of an excessively long, non-
threaded post, when ultrasonic vibration is not successful, one of the post-
extracting devices may have to be used (Fig. 9.13).
Ceramic posts are likely to be cemented with resin- or glass ionomer-
based cements. Well-fitting ceramic posts with resin cement are extremely
 Management of non-surgical root-canal treatment failure  241

Fig. 9.15  Nickel–titanium orifice

openers, Hedstroem files and
chloroform are useful for gutta-
percha removal

A B

Fig. 9.14  (a) D.T. Light post removal kit; (b) the fibre post in the palatal canal
of the maxillary right first molar was successfully removed

D E F G

Fig. 9.16  (a) Gutta-percha in distal canal; (b) orifice opener removing gutta-percha with hand-piece – speed at 700 rpm; (c) set hand-piece speed at 700 rpm
for gutta-percha removal; (d) apical portion of gutta-percha removed with Hedstroem file; (e) chloroform placed in canal entrance using a syringe; (f) file placed
in canal to mix chloroform and gutta-percha then wicked with paper points; (g) remaining gutta-percha dissolved in chloroform and wicked with paper points

difficult to remove. Fibre posts are much easier to remove than metal, they
can be disintegrated by applying ultrasonic tips, Piezo or Gates–Glidden
drills, a small stainless steel rosehead bur or specially designed drills (DT
Light-post removal kit, Bisco, Inc., Schaumburg, IL, USA) into the centre
of the post (Fig. 9.14).
Removing gutta-percha
Poorly condensed gutta-percha root fillings in teeth requiring retreatment
can be easily removed by threading Hedstroem files into existing spaces
to engage the gutta-percha, which may then be pulled out with the file.
Well-condensed gutta-percha is a different prospect and requires creation
of space to insert Hedstroem files to engage the bulk of the material. Space
creation is achieved by softening the gutta-percha using heat or solvent
and inserting the relevant file or instrument.
The first stage of removing well-condensed gutta-percha (GP) involves
gaining access to the pulp chamber and clearing it. This may be accomplished
with a high-speed bur and hand excavators. A GP root filling that has been in
place for many years tends to become vulcanized and can be brittle and hard,
making it more difficult to remove. Ultrasonic tips, nickel–titanium orifice
openers, Hedstroem files and chloroform are useful for removing gutta-percha
(Fig. 9.15). There are three stages to the procedure:
1 A simple way to remove the coronal bulk of the GP is to use a
narrow ultrasonic fine scaler tip or a nickel–titanium rotary
instrument (Fig. 9.16a–c)
2 Most of the remaining bulk of the GP can be removed with
Hedstroem files (Fig. 9.16d). The largest file that will not bind to
the canal wall is placed in the canal and rotated by hand to engage
the GP only. The depth of penetration required can be judged
from the preoperative radiograph but mostly by tactile feel
3 The final stage consists of “wicking” with paper points, once the
bulk of the gutta-percha has already been removed. The canal is
flooded with chloroform from a disposable dispenser (Fig. 9.16e)
 242  Management of non-surgical root-canal treatment failure
to dissolve remaining tags of gutta-percha adhering to the canal
walls. The chloroform should not overflow the pulp chamber
otherwise the rubber dam may be dissolved. The chloroform is
then stirred using a small hand file to ensure the solution dissolves
the GP completely (Fig. 9.16f). The largest paper points that fit
into the canal are then selected and used to soak up the dissolved
mass. Wicking is achieved by inserting several points one after the
other into the canal (Fig. 9.16g). The process is repeated until no
further pink discoloration is discerned on the paper points. The
canal is then thoroughly washed with irrigants.
Removing gutta-percha with a central core (Thermafil®)
As before, the gutta-percha is likely to fill the space well, therefore, there
will be a need to create some space first using the techniques already
described. The initial goal is to remove the plastic core, using a nickel–
titanium rotary instrument, or by braiding with Hedstroem files. The
nickel–titanium instruments are run at 600–700 rpm. The size selected is
small enough to allow the tip to engage the GP between the core and the
canal wall. Once the core is removed, the residual GP may be removed by
using the previously described Hedstroem and wicking technique. The
braiding technique consists of creating space to pass two or three Hed-
stroem files alongside the carrier distributed around its circumference.
Once these are in place, they are twisted around each other, the so-called
“braiding” and then used to pull the carrier out. It is worth noting how
long ago the original obturation was performed as the latest Thermafil®
carriers have a longitudinal slot to facilitate removal during retreatment,
while the original Thermafil® had metal carriers.
Removing cement material
Different types of cement may be found in previously treated canals. They
may be zinc oxide eugenol, resin or formaldehyde resin (N2, Russian Red
cement) -based materials. Specific solvents, including Endosolv E and
Endosolv R (Septodont, Cedex, France) are available for the former two
types of cements, respectively. There is no solvent for N2 and Russian Red
cements, attempts to remove them using small long shank round bur or
ultrasonic tip may result in a false canal leading to a perforation.
Negotiating a ledge
When the previous root filling is short of the apex, there may either be a
ledge or debris packed into the canal. It may be possible to detect a ledge
radiographically if the angle is favourable (Fig. 9.17). Deviation of the
apical extent of the root filling from the centre may be suggestive of a
ledge. Ledges may be negotiated once the coronal portion of the canal has
been cleaned out; a size 08 or 10 stainless steel file with a sharp precurve
at the tip may be used to explore for the canal opening. Once found it is
threaded in and is worked gently to file away the ledge (Fig. 9.18).
Packed dentine debris
The aetiogenesis of a ledge is usually preceded by blockage of the canal by
dentine debris (Fig. 9.19a). The first challenge is to detect and diagnose the
presence of blockage by dentine debris, which can only be achieved by tactile
sense. There is no easy method for unpicking the debris blockage except by
the patient use of a small file in a deliberate, controlled but firm picking
motion. This is facilitated by chemical dissolution with EDTA for the inor-
ganic component and sodium hypochlorite for the organic component; the two
should be used alternately in copious amounts and delivered by agitation with
a file or if necessary with a well-fitting gutta-percha point. Should these meas-
ures fail, it may be worth trying a small precurved ultrasonically energized
file to loosen the debris (Fig. 9.19b–d). The danger is that when the debris is
packed very tightly it may be as hard as the surrounding dentine and attempts
to remove it may result in a false canal leading to a perforation.
Sclerosed canals
Sometimes teeth requiring retreatment may have untreated canal systems
or only partially treated systems, not because of iatrogenic blockage but
because of pre-existing natural canal sclerosis that the previous operator
failed to negotiate. Natural canal sclerosis has varied aetiogenesis, including
in elderly teeth, those that have been traumatized, had multiple large restora-
tions or chronic marginal periodontitis. The calcification takes the form of:
1 additional, irregular tertiary dentine, which makes the canal
narrower and the surface more irregular but retains the canal
pathway for instrument negotiation
Fig. 9.17  Short root filling in curved
canal suggesting ledge present
(arrowed)
Fig. 9.18  Ledge bypassed placing a curve at the
tip of small file. Rubber stoppers with marking to
indicate orientation of the curve
 Management of non-surgical root-canal treatment failure  243

Fig. 9.19  (a) Plastic block ledged and packed with debris;
(b) size 15 ultrasonic file used in wet canal to dislodge
debris; (c) size 10 K-file with curve at the tip bypasses the
ledge; (d) canal preparation completed using hand
instruments

B
C D
A

A B C D

Fig. 9.20  (a) Patient referred as canal could not be located (arrowed); (b) increasing resolution of radiograph showing canal is patent (arrowed); (c) canal located
and negotiated as described in text; (d) canal preparation completed and obturated

2 dentine tubule sclerosis, which makes the dentine harder to

instrument but retains the canal pathway
3 dystrophic calcification of the pulp, which also narrows the canal
irregularly but may be more prone to cause blockage.
All three of these may of course exist concurrently. Depending upon the
aetiogenesis, the canal width may vary in different portions. For example,
sclerosis due to irritation from coronal dentine may result in narrowing in
the coronal portion that widens out towards the apex. It is necessary to
diagnose the precise type of sclerosis, case by case.
The key is that the canal orifice should be located first. Once located, Fig. 9.21  Fractured instrument in Fig. 9.22  Fractured instrument in
coronal portion – often possible to middle portion – may be possible to
the challenge is patiently to negotiate it to its length by gentle stem-
remove remove
winding of size 06, 08, 10 hand files with lubricant containing EDTA.
When the file begins to meet resistance, a larger file is sensitively advanced
and the procedure repeated; the steps are size 10, 15, 20 and then back to the potential for a favourable outcome and should be removed, if techni-
size 06, 08, 10. The goal is to eliminate coronal binding likely to be the cally feasible without incurring further iatrogenic damage. A preoperative
cause of interrupted advancement. It is cases such as these that demand radiograph will show where the metallic object is located together with its
tactile skills, for which there is no technological substitute (Fig. 9.20). conjunction. The simple classification below will help the operator decide
how best to proceed. Examples are presented in Figures 9.21–9.23.
Removal of metal instruments and silver points
Class 1 lies in the canal but protrudes into the pulp chamber. These are
It should be emphasized that a fractured instrument in itself does not cause simple to remove using a Steiglitz or a small pair of locking forceps.
failure. It does not endanger the health of the patient nor itself produce any Class 2 lies within the straight part of the canal. An attempt is initially
symptoms, providing it lies entirely within the canal system. If, however, made to bypass the obstruction with a small hand file and lubricant. If the
it prevents access to the apical infection, then it will clearly compromise canal can be negotiated to the working length and prepared, it may not be
 244  Management of non-surgical root-canal treatment failure

A B C

Fig. 9.23  Fractured instrument in Fig. 9.24  (a–c) Separated instrument extruded into the apical tissue during attempts to remove it
apical portion – difficult to remove

A B

Fig. 9.25  (a) Fractured instrument embedded during retrograde amalgam placement in the 12; (b) Cancellier tube fitted
D over the exposed instrument; (c) Cancellier tube tapped out with artery forceps; (d) fractured instrument successfully
removed; (e) Hedstroem file securely glued in Cancellier tube; (f) canal prepared and obturated

necessary to remove the metallic object but simply to obturate the canal
so that the object is embedded within the filling material. However, care
should be taken not to push the bypassed material, which may have been
detached from the canal wall/niche, into the apical tissue and compromise
periapical healing (Fig. 9.24).
If the object cannot be bypassed, a narrow trough is cut around the
embedded object with an ultrasonic tip. When the coronal 2.0 mm is
exposed, it can be removed using an extractor or specifically designed
instrument removal system (Fig. 9.25).
Great care has to be taken when ultrasound is used to remove a silver
point or nickel–titanium instrument. Silver is soft and the ultrasonic tip,
rather than cutting a trough around the point will cut into it; in the case of
nickel–titanium, the ultrasonic tip will shatter small pieces from the
fractured instrument making it more difficult to remove. Avoiding the
silver point or nickel–titanium instrument with the ultrasonic tip requires
excellent vision and good magnification, as well as a steady hand.
Class 3 lies beyond a curve in the canal. The majority of these metallic
objects cannot be removed without excessive removal of dentine and risk
of canal perforation. An attempt is made to bypass the fragment using a
fine stainless steel file with a lubricant. A small curve is placed at the tip
of the instrument to help locate a passage past the object. Canals are not
round and, therefore, there should be a gap between the metal and the wall
of the canal. Alternatively, it may sometimes be possible to thread an
instrument into a spiral flute if it is large enough and not engaged into
dentine. Once the instrument can be bypassed, larger instruments are used
until the canal is prepared to the desired shape (Fig. 9.26).
 Management of non-surgical root-canal treatment failure  245

A B C

Fig. 9.26  (a) Fractured instrument lies beyond a curve in the canal; (b) fractured instrument bypassed using hand instruments and then dislodged with ultrasonic
15 K-file; (c) canal prepared and obturated

A B

Fig. 9.27  Silver point in mesial canal – perforation

in pulp chamber

Fig. 9.28  (a,b) ProRoot® material (MTA) both original grey and the white material
(Dentsply, Tulsa); (b) MTA and sterile water mixed; (c) MTA placed on floor of pulp
chamber to seal perforation

Perforations
Perforations may occur due to internal/external resorption or operator
error. The success of a repair will depend on the site and size of the per-
foration, and the risk or degree of contamination. Those perforations
enclosed within bone housing may be associated with a favourable outcome
if the infection is controlled (Fig. 9.27); one that communicates with the
oral cavity may be repaired as a normal tooth cavity with an unusual
morphology. The perforation should be repaired as soon as possible to
prevent ongoing contamination. Many different materials have been rec-
ommended for repair of perforations, including zinc oxide/eugenol-based
cements, such as IRM® and EBA®, selected for their antibacterial proper-
ties. The contemporary material of choice for enclosed perforations is
mineral trioxide aggregate (MTA) (Fig. 9.28) because of its biocompatibil-
ity and osteogenic properties. Its long setting time and, therefore, tendency
to be washed away in the presence of saliva, renders it inappropriate for
perforations exposed to the oral cavity. Under such circumstances, the
material of choice is glass ionomer cement (GIC). Figures 9.27 and 9.29
show perforation repair using GIC as a temporary measure to allow com-
pletion of chemomechanical debridement of the canal system. The GIC
was subsequently replaced with MTA prior to root filling. In some cases,
an iatrogenic perforation located in the apical third of the canal can be
treated as a separate canal and obturated with gutta-percha.
Surgical repair of a perforation is indicated when access through the
canal is impossible.
SURGICAL ROOT-CANAL RETREATMENT
INDICATIONS AND CLASSIFICATION OF ENDODONTIC
SURGICAL PROCEDURES
Dentistry, in its broader sense is considered a surgical discipline, so it is
useful to define the context of the term endodontic surgery. Endodontic
surgery refers to direct access to the periradicular tissues through incision
of the overlying mucogingival complex. Historically, numerous reasons
were cited as indications for surgical root-canal treatment. Advances
in understanding and knowledge of endodontic biology have crystallized
the main indications for surgery into procedures used to resolve, through
direct access to the root, that which could not be achieved intraradicularly.
Advances in the technical aspects of root-canal treatment and the success
 246  Management of non-surgical root-canal treatment failure

A B D
C

Fig. 9.29  (a) Perforation visible. Endodontic probe placing glass ionomer cement (GIC) at the perimeter
of the perforation; (b) building GIC bridge without touching periodontal tissue; (c) GIC bridge completed;
(d) additional GIC placed to prevent material being pushed into periodontal tissue; (e) postoperative
radiograph

rates of guideline-standard root-canal treatment have reduced surgery

indications substantially. As most objectives can be achieved through
non-surgical root-canal treatment, the frequency of endodontic surgery
in practice has declined. The costliness of the surgical intervention also
competes unfavourably with the alternative option of extraction and
replacement with a prosthetic unit. The reasons for performing endodontic
surgery may be classified as shown below:

• emergency surgery
▸ incision and drainage
▸ trephination
• biopsy
• periapical surgery for root-end management Fig. 9.30  Incision and drainage Fig. 9.31  Cellulitis is a symptomatic
• corrective surgery oedematous inflammatory process
▸ perforation repair that spreads diffusely through fascial
▸ root resection planes
▸ hemisection
• intentional replantation for root-end management or corrective
surgery Fig. 9.32  Radiograph
• regenerative procedures of a mandibular molar
• decompression. showing mishap
involving perforation of
the mesial root during a
EMERGENCY SURGERY trephination procedure.
GP cone placed in sinus
Incision and drainage tract originating at
mid-root level
This procedure consists of the creation of a surgical opening in the oral
mucosa for the purpose of releasing pus and exudate (Fig. 9.30) and is a
relatively minor procedure. However, when the swelling extends to the
tissue spaces with an extraoral component, this may result in life-
threatening situations, such as occlusion of the airway. Cellulitis (Fig.
9.31) is a symptomatic oedematous inflammatory process that spreads
diffusely through the fascial planes. This infection demands immediate drainage causing intense pain; the purpose of the procedure is to aid release
treatment with both antibiotic and analgesic medication and establishment of inflammatory exudate through perforation of the cortical plate. The
of drainage if at all possible (see Chapter 10 for further details). procedure may involve the use of trephine burs or be as simple as the
puncturing of the cortical plate with a sterile finger spreader. Mishaps can
Trephination
occur with the use of burs (Fig. 9.32) and damage to the tooth may require
This is the surgical perforation of the alveolar cortical plate to release surgical correction (Fig. 9.33). These procedures are performed when
accumulated periradicular tissue exudate. This procedure is used in cases drainage through the root canal is not possible or evident. Antibiotics are
where the absence of any obvious intra- or extraoral swelling prevents required only when there is systemic involvement.
 Management of non-surgical root-canal treatment failure  247

Fig. 9.33  Postoperative Fig. 9.36  Triangular

radiograph 2 months flap
following resection of
the mesial root to the
level of a clearly
outlined bur hole
formed by the
misdirected trephine

Fig. 9.37  Rectangular

flap

Fig. 9.38  Semilunar

flap

Fig. 9.34  Taking an excisional biopsy Fig. 9.35  Biopsy bottle containing
for histological examination during a 10% formalin and correctly
periradicular surgical procedure completed clinical biopsy request
form

BIOPSY
The purpose of taking a biopsy is to establish a definitive diagnosis by
histological examination. It involves the surgical removal of a soft and/or
hard tissue specimen for histological evaluation (Fig. 9.34). The value of
routine histopathological examination during endodontic surgical proce-
dures must not be underestimated. The taking of a routine biopsy during
periradicular surgical procedures has come to be accepted as the standard
of care, particularly given the reduced frequency of surgery and, therefore,
higher chance of non-endodontic pathoses. Correct handling of the
removed tissue is central to the formation of an accurate histological diag-
nosis. Recovered tissue must be placed immediately in a 10% formalin
solution and sent with complete relevant details to the pathology labora-
tory (Fig. 9.35). A biopsy request should include:
• a history of the case, including patient details
• a clinical description of the lesion
• a gross description of the biopsied tissue including size, location,
duration, colour, texture, consistency and radiographic appearance
• provisional diagnosis.
a surgery and differ from periodontal surgery flaps in only involving healthy
Biopsies are usually excisional or incisional. Excisional biopsy is used
to remove the lesion in its entirety and may, therefore also be therapeutic.
An incisional biopsy is only used to establish a diagnosis and would be
rarely used in endodontic procedures.
PERIAPICAL SURGERY AND
ROOT-END MANAGEMENT
The periapical surgery procedure includes curettage of the lesion, root-end
resection, root-end cavity preparation and root-end filling.
As a preliminary procedure for all periapical surgery, a tissue flap must
be reflected. Careful and considered soft tissue management greatly
enhances the prognosis of the surgical procedure and improves the post-
operative wound healing.
Flap design
The main considerations governing flap design are good access and vision,
while minimizing trauma to the soft tissues during retraction. The design
should ensure good blood supply to the flap, avoid damage to the surround-
ing structures and facilitate primary wound closure. The flap design should
include the tooth to be treated and, only if necessary, one or more teeth on
either side; a balance must be struck between the risk of postoperative
gingival recession and good surgical access. It is always preferable to
extend the flap further than to attempt to work in a restricted field. Factors
which influence the extent of the flap include position of the mental nerve,
muscle and fraenal attachments, root and bony eminences and large bony
defects. Full and limited mucoperiosteal flaps are used in endodontic
marginal tissue. Mucoperiosteal flaps consist of the periosteum along with
the overlying alveolar mucosa and gingival tissues. Flap names are desig-
nated according to their shape and include triangular (Fig. 9.36), rectan-
gular (Fig. 9.37), semilunar (Fig. 9.38), submarginal (Fig. 9.39),
papilla-base (Fig. 9.40) and palatal (Fig. 9.41). Flaps with vertical reliev-
ing incisions are less likely to produce excessive bleeding because of the
orientation of the submucosal vasculature (Fig. 9.42), although this only
confers a slight advantage. Incision lines should always be placed so that
wound closure is on sound bone. Buccal flaps are most commonly used to
gain access to the periradicular tissues; however, a palatal approach may
 248  Management of non-surgical root-canal treatment failure

Fig. 9.39  Submarginal Fig. 9.43  Palatal flap

flap

Initial shallow
incision to 1.5mm
Relieving incision line
Micro-surgical blade Fig. 9.44  Triangular mucoperiosteal
flap

Second angled
incision directed
at the crestal bone

(Fig. 9.46), where potential for recession associated with adjacent crowned
Papilla base incision
teeth is to be avoided. Rectangular and triangular flaps appear to be the
Fig. 9.40  Papilla-base flap (adapted from Velvart 2002 – Papilla base incision. most commonly taught, based on blood vessel alignment, but clinical
International Endodontic Journal, 35, 453–460) experience suggests no obvious difference in healing compared with trap-
ezoid flaps. The triangular flap has the advantage of flexibility as the flap
Fig. 9.41  Palatal flap may either be extended or converted into a rectangular one if necessary.
Incisive It is created by the use of an intrasulcular and relieving incision (Fig. 9.47).
foramen The relieving incision is started in alveolar mucosa, passes through the
attached and marginal gingivae and ends on the mesial or distal aspect of
the teeth. The gingival papillae should not be incised, this will facilitate
repositioning of the flap and prevent sloughing of the papillae. Elevation
Palatal of the flap should commence in the attached gingivae of the vertical inci-
ridges sion (Fig. 9.48). The advantages of the full flaps include provision of good
access to the root tissues (Fig. 9.49), ease of reflection and repositioning
and provision for excellent healing, usually without scarring, thereby mini-
mizing postoperative pain and swelling. The only disadvantage of these
Fig. 9.42  Vertical flaps is the possibility of postoperative gingival recession. This has been
orientation of blood shown to be minimal with the correct handling of the tissues and is more
vessels in oral mucosa likely to occur with thin marginal tissues.

Limited mucoperiosteal flaps

be indicated for gaining access to palatal roots or defects (Figs 9.41, 9.43).
The only indications for lingual flap reflection are crown lengthening
procedures or if repair of a coronal, lingually located defect is planned.
Full mucoperiosteal flaps
These may be triangular (Figs 9.36, 9.44), rectangular (Figs 9.37, 9.45),
or trapezoid. The vertical component of the trapezoid flap is angulated,
cutting across the vasculature (see Fig. 9.42) and was traditionally in
very common use; it is useful for reflecting a flap based on a single tooth
These flap designs eliminate the need to disturb the gingival margins
especially those around restorations where recession would be most notice-
able. They include the semilunar (see Fig. 9.38), submarginal (Figs 9.39,
9.50) and the papilla-base (Fig. 9.51) flaps. The semilunar flap is created
by cutting a semilunar shaped incision in the alveolar mucosa. The access
provided is limited and scarring is a frequent complication (Fig. 9.52). The
submarginal flap consists of two vertical and a scalloped horizontal inci-
sion in the attached gingivae, which follows the outline of the gingival
margin (Leubke-Ochsenbein). It must be noted that the required width of
the attached gingivae is 3–5 mm. The papilla-base flap involves vertical
releasing incision(s) along with a shallow incision in the base of the papilla
and a second incision directed to the crestal bone. This creates a split-
thickness flap in the area of the papilla base (Figs 9.40, 9.51).
These limited flap designs may be appropriate when recession may lead
to exposure of the crown margin.
 Management of non-surgical root-canal treatment failure  249

B C

Fig. 9.45  (a–c) Rectangular full mucoperiosteal tissue flaps

A B

Fig. 9.46  (a,b) Trapezoid full mucoperiosteal tissue flaps

Fig. 9.47  Intrasulcular

and vertical relieving
incision

Fig. 9.48  Elevation of tissue Fig. 9.49  Excellent access provided

commencing in the attached by full mucoperiosteal flaps; note
gingivae of the vertical incision placement of retractor firmly on
bone

A B C D

Fig. 9.50  (a–d) Submarginal full mucoperiosteal flaps with differently designed incision lines; NB in (c) the flap is reflected towards the crowns; (d) shows a
Leube-Ochsenbein approach
 250  Management of non-surgical root-canal treatment failure

Fig. 9.51  Papilla-based Fig. 9.53  Retained

flap tissue tags (arrows)  
on the cortical bone
enhance reattachment
and postoperative
healing

Fig. 9.52  Scarring of tissues Fig. 9.54  Retained tissue tags

subsequent to creation of a semilunar (arrowed) enhance wound repair
incision in the oral mucosa following repositioning of the tissue
flap

Incisions
A variety of incisions is used during creation of mucoperiosteal flaps.
These include:

• intrasulcular incision (see Fig. 9.47)

• vertical relieving incision (see Fig. 9.47)
• papilla-base incision (see Fig. 9.51).
Irrespective of the type, a number of basic principles apply when making
incisions. These include:

• avoid crossing underlying bony defects Fig. 9.55  Osteotomy. Location of the root surface during periradicular surgery
• create the incision with a single firm continuous stroke usually involves removal of overlying bone unless the lesion has already
• plan the start and finish points of the incision perforated the cortical plate (see Fig. 9.57) or a natural dehiscence or
• avoid bony eminences with vertical incisions. fenestration exists

Flap elevation Flap retraction

Elevation of the flap must be performed with care in order to avoid damage
to the tissues. As already indicated, elevation is commenced in the vertical
incision and away from the gingival margin, in the attached gingivae (see
Fig. 9.48). This minimizes damage to the delicate papillary tissues. The
flap should be gently undermined (see Figs 9.44, 9.48). All reflective
forces should be applied to the periosteum, which then allows for passive
reflection of the overlying alveolar mucosa and gingivae. The small tissue
tags which remain attached to the cervical regions of the teeth or the
underlying alveolar bone must be preserved in order to enhance reattach-
ment (Figs 9.53, 9.54). Scarring from previous surgery or the presence of
a sinus tract can complicate flap elevation.
Care for the reflected soft tissues is essential to good postoperative wound
healing. The operator must ensure that the retractor is placed firmly on the
bone avoiding pinching of any soft tissue (see Fig. 9.49). Frequent saline
irrigation of the surgical site prevents dehydration of the flap and the tissue
tags attached to the teeth, encouraging optimum healing. In the mandibular
premolar region, the mental nerve should be identified and protected with
a retractor.
Osteotomy
Access to the periapical tissues and root-end is gained by removing the
overlying alveolar bone (Fig. 9.55), unless the lesion has already breached
 Management of non-surgical root-canal treatment failure  251
Fig. 9.56  Preoperative view showing Fig. 9.57  Perforation of the cortical
existing sinus associated with tooth plate of bone over tooth 22 by the
22 periradicular lesion
A B C D
Fig. 9.60  (a–e) Traditional 45° resection angle
the cortical plate (Figs 9.56, 9.57). If the cortical plate is intact, measure-
ments from radiographs or from working lengths obtained during a non-
surgical treatment must be used to estimate the position of the root apices.
In conjunction with copious sterile irrigation a rear-venting surgical hand-
piece (see Figs 9.55, 6.21) is used to remove the bone with a gentle brush-
ing motion. Large round tungsten–carbide burs (Figs 9.58, 9.59) have been
shown to be most suitable for safe bone removal. Excessive heating of the
bone via the use of excessive pressure on the rotating instrument, excessive
depth of cutting, inadequate cooling or the use of the wrong cutting instru-
ment can result in stagnation of the local bone circulation and eventual
tissue necrosis. Caution must be exercised at all times not to damage
adjacent teeth and soft tissues.
Curettage
This has been defined as a surgical procedure to remove diseased or
reactive tissue and/or foreign material from the periradicular bone sur-
rounding the root of an endodontically treated tooth. Some clinicians
argue that resection of the root-end can facilitate curettage as access to
the palatal/lingual surfaces is improved, however, it is always better to
curette first and resect later so that clear sight of the root end is obtained
during resection. All curetted tissue must be removed and sent for
Fig. 9.58  Burs used
during periradicular
surgery for bone
removal
Fig. 9.59  SEM of a large round
surgical tungsten–carbide which
generates the least frictional heat
E
histopathological examination as sinister lesions have been identified in
the past.
Root-end resection
The level at which the root-end is resected and the angle of resection are
important considerations. The majority of the anatomical aberrations are
found in the apical region and resection at this level would eliminate a
large proportion of root-canal ramifications. As the residual infection is
most likely to reside in the anatomical complexities in the apical 3 mm of
the root, it is often recommended that the apical 3 mm of the root-end be
removed as a matter of routine. In the authors’view this may prove grossly
excessive because not all roots have complex anatomy in the apical 3 mm
and some short roots cannot survive such a heavy reduction. It is better
gradually to pare the apex down, while visualizing the apical canal anatomy
at the resected face; the shaving may be continued if complex anatomy is
revealed, otherwise aborted.
Ideally, the root should be resected perpendicular to its long axis. Such
a resection angle reduces the number of dentinal tubules exposed, decreas-
ing the communication pathways between the canal system and periradicu-
lar tissues. The 45° resection angle (Fig. 9.60) previously recommended
was to improve access and visibility when using traditional surgical
 252  Management of non-surgical root-canal treatment failure
A B
Fig. 9.62  (a) A 1% solution of methylene blue dye is used to stain the root
to facilitate visualization of vertical root fractures or to outline the resected
A root face; (b) application of dye with sterile sponge applicator; (c) resected
root face outlined with methylene blue
micro-hand-pieces (Fig. 9.61), however, with the introduction of micro-
surgical instruments, this problem has largely been overcome.
Visualization of the root-end outline can be enhanced by staining it with
a 1% solution of methylene blue dye (Fig. 9.62). The root-end should be
carefully inspected for anatomical details, fractures and incomplete resec-
tion. Identification of the canal anatomy and, in particular isthmi, facili-
tates the correct extension of the root-end preparation.
In certain circumstances, it is not possible to remove the recommended
3 mm. For instance, a long post or reduced bone support limit the amount
of root-end removal, and close proximity of the apex to neurovascular
bundles may demand a high level of resection. As iterated, root-end resec-
tion should be started from the root apex and advance gradually coronally
up to the point where the root canal or root-filling materials are visible in
order avoid over-shortening of the root.
Root-end cavity preparation
The rationale for preparation and filling of the root-end is to debride the
canal system and seal off any residual intracanal infection. The rationale
for placement of a root-end filling is to prevent egress of any residual
intracanal microorganisms and/or their products into the periradicular
tissues. The apical seal is all important in apical surgery, even more so
than in conventional root-canal treatment. A “double seal” consisting of
the physical barrier provided by the root-end filling material, as well as a
biological seal formed by regeneration of the periodontal apparatus over
the resected root face is the ideal outcome. This has been shown to be
achievable with the root-end filling materials available today, such as
Diaket (Fig. 9.63) and MTA (Fig. 9.64).
Fig. 9.61  (a,b) Surgical micro-hand-piece in use
Fig. 9.63  H&E of a Diaket section
Fig. 9.64  Masson’s
trichrome stained
section showing MTA  
as a root-end filling
associated with
regeneration of the
periodontal apparatus
The ideal root-end cavity should be prepared along the axis of the root,
have near parallel walls, be at least 3 mm deep and encompass the root-
canal anatomy. The introduction of ultrasonic root-end tips has revolution-
ized root-end preparation (Figs 9.65, 9.66). The smaller size of the
ultrasonic hand-piece and the angulation of the root-end tips allow better
access. A recognized complication of root-end preparation was perforation
of the lingual aspect of the root when conventional surgical hand-pieces
were used in conjunction with 45° bevels. This iatrogenic complication is
less likely when ultrasonically energized root-end preparation tips are used
instead.
It is possible to instrument the root-canal system from a retrograde
approach using conventional files (Fig 9.67). Bent hand files matching the
canal length and held in a pair of haemostat forceps may be used during
debridement of the canal. The recently introduced long (9–11 mm)
 Management of non-surgical root-canal treatment failure  253

Fig. 9.65  Use of an ultrasonically energized tip to

create a root-end preparation

A
B C

Fig. 9.67  Retrograde root canal treatment of a missed second canal

Fig. 9.66  Root-end preparation
created with ultrasonically energized
tips (courtsey Dr David Dickey)
(arrowed) in 13: (a) pre-operative radiograph shows unfilled canal alongside
that with a post, which has had a retrograde placed; (b, c) retrograde filing
with a hedstrom instrument; (d, e) cold lateral compaction to fill prepared
canal; (f) completed obturation of second canal and replaced amalgam F
retrograde in first canal showing periapical healing

ultrasonic root-end tips may also be used. The closer the retrograde root Fig. 9.68  Racellets®
filling can be placed to the post or the fractured instrument, the more suc-
cessful is the treatment outcome. In line with this approach, newer ultra-
sonic tips are longer but lack the flexibility of conventional files.

Haemostasis
Adequate haemostasis is central to periapical surgery and, in particular,
root-end management. Administration of adequate amounts of vasopressor
agents contained in the local analgesic carpules will usually ensure good
haemostasis, which will be maintained throughout the procedure provided
that the procedure is completed within a reasonable time frame. After this
“window of opportunity” control of the blood flow is lost and a massive
increase in bleeding occurs due to the “rebound phenomenon”.
A number of locally applied haemostatic agents are available for use
during the surgical procedure. These include Racellets® (adrenaline (nore- placed into the bony defect may also arrest bleeding. Complete removal
pinephrine) impregnated cotton pellets) (Fig. 9.68), ferric sulphate (Fig. of the haemostatic agents is usually recommended especially when using
9.69) (e.g. Cutrol), bone wax, oxidized cellulose (Surgicel®) (Fig. 9.70), bone wax or ferric sulphate. Any of these materials remaining in the bony
gelatine-based foam (Gelfoam) and bovine-derived collagen (Collacote® crypt will usually evoke an inflammatory foreign-body reaction, which
or Collaplug®) (Fig. 9.71). Application of pressure on plain cotton pellets may prevent or delay healing.
 254  Management of non-surgical root-canal treatment failure
A B
Fig. 9.69  (a) Ferric sulphate haemostatic agent; (b) ferric sulphate applicator
Fig. 9.72  Root resection without Fig. 9.73  Super ethoxybenzoic acid
retrograde filling
Root-end filling
Following root-end resection, it is usually recommended that a root-end
preparation and root-end filling be placed. However, this is not always
the case and there is some debate as to whether a better seal is achieved
by placement of a root-end filling where the canal has recently been
well obturated (Fig. 9.72). In all other cases root-end filling is
recommended.
The ideal root-end filling material should be biocompatible, antibacte-
rial, easy to place and remove, radiopaque, dimensionally stable, adhere
to the root canal wall, insoluble and induce regeneration of the periradicu-
lar tissues. Of the variety of root-end filling materials available, none fulfils
all the above criteria. The materials currently most commonly used are
Fig. 9.70  Surgicel®
Fig. 9.71  (a) Collagen agents Collaplug and Collacote
can be used to stem blood flow in the crypt both
physically and by contributing to the clotting cascade;
(b) Collaplug in a bone crypt over the maxillary lateral
incisor
Fig. 9.74  Intermediate restorative
material
MTA (see Fig. 9.28a), super ethoxybenzoic acid (EBA) (Fig. 9.73), inter-
mediate restorative material (IRM) (Fig. 9.74), gutta-percha, Diaket (Fig.
9.75), composite resin, and glass ionomer cement. Amalgam has been
widely used in the past but it can no longer be recommended as a root-end
filling material due to new evidence demonstrating the superiority of other
materials and due to the long-term failure of cases where amalgam was
used. This failure may be due to initial leakage, formation of corrosion
products and possible electrochemical reactions when in contact with a
metal post. An additional problem with the use of amalgam as a root-end
filling material is tattooing of the soft tissues (see Fig. 9.52). At present,
the most suitable material for use in root-end cavities appears to be MTA
(see Fig. 9.28a); the newer Biodentine® (Fig. 9.76) remains untested in
this scenario.
 Management of non-surgical root-canal treatment failure  255
Fig. 9.75  Diaket (ESPE, Germany) Fig. 9.76  Biodentine®
Fig. 9.79  Diaket root-end filling in Fig. 9.80  MTA root-end filling in tooth #36
tooth #22
Following its creation, the root-end cavity should be dried before the
root-end filling is placed. This can be achieved with cut sterile paper points
or with a short needle attached to high volume suction, such as the Stropko
device. The surgical crypt should be packed with adrenaline-containing
local anaesthetic solution impregnated cotton pellets or a collagen mate-
rial, such as Collaplug (see Fig. 9.71b) during the placement of the root-
end filling. This will help maintain a dry field and, in addition, will
facilitate removal of any excess filling material at the end of the procedure.
There are a number of instruments, devices and systems available to facili-
tate root-end filling placement (see Fig. 6.27a–e). Carriers, such as the
MAP kit or MTA block/Lee’s carver will help transport the material to the
surgical site and then surgical root-end pluggers, available in different
sizes and angulations, allow good condensation and adaptation of the
filling material to the canal walls. The root-end filling should be routinely
burnished or polished except when MTA is used. This finish is not possible
with grey or white ProRoot MTA as it does not set for approximately 4
hours. MTA-Angelus (Angelus, Londrina, PR, Brazil) (Fig. 9.77) which
is an alternative to ProRoot MTA contains 80% Portland cement and 20%
bismuth oxide, with no addition of calcium sulphate in an attempt to reduce
Fig. 9.77  Angelus® MTA Fig. 9.78  Amalgam root-end fillings
Fig. 9.81  Composite root-end filling
in tooth #21
setting time (10–15 minutes). The bony crypt should be cleared of all
foreign materials, such as root-end filling, haemostatic agents or cotton
pellets. The surgical site is then irrigated with sterile saline. Prior to wound
closure, a periapical radiograph should be exposed to confirm adequate
placement and compaction of the root-end filling, as well as the absence
of extraneous material in the periradicular tissues (Figs 9.78–9.81).
Through and through surgery
This treatment approach (Fig. 9.82) is indicated when exudation into the
root canal cannot be controlled by non-surgical chemomechanical debride-
ment. Following removal of the existing canal medicament and irrigation
of the canal system, the flap elevation, osteotomy and root-end resection
are carried out as previously described. The root canal is then obturated
with thermoplasticized injection gutta-percha and sealer. A flat plastic
instrument is placed at the apex to prevent gross extrusion of gutta-percha.
Any excess gutta-percha can be removed using a scalpel blade 11 and the
gutta-percha surface should be burnished. Alternatively, a root-end cavity
may be prepared and filled with MTA as previously described. The access
cavity should be sealed with a temporary restorative material and then a
 256  Management of non-surgical root-canal treatment failure
A B
Fig. 9.82  (a–c) Through and through surgery
A B
Fig. 9.83  (a,b) Extrusion of gutta-percha root filling during compaction of
temporary filling in an immature tooth
permanent filling subsequently. Exertion of excessive force during
compaction of the temporary filling in immature root with thin walls may
cause root fracture and apical extrusion of the gutta-percha root filling
(Fig. 9.83).
Wound closure
Optimal wound healing is dependent on correct flap replacement and
suturing. The flap should be repositioned and held in place under gentle
compression for a few minutes with damp gauze. Once all the sutures have
been placed, the flap should be compressed again with digital pressure for
approximately 5–10 minutes. The rationale for this procedure is to encour-
age formation of as thin a clot as possible. If this is not achieved, compli-
cations including infection, scar tissue formation, swelling and bruising
may occur. The importance of good oral hygiene must be emphasized to
the patient.
The choice of suture material used for wound closure depends on the
clinician who should be aware of the advantages and disadvantages of each
material (Fig. 9.84). Black silk and catgut sutures have been widely used
in oral surgery in the past and continue to be the suture of choice for many
C
Fig. 9.84  A variety
of suture material  
is available for use  
for wound closure
following endodontic
surgery
Fig. 9.85  Postoperative
closure of submarginal
flap with gut suture
material
surgeons. Good quality needle holders and scissors are recommended (see
Fig. 6.28). Black silk is strong, easy to use and is relatively cheap. However,
it is a braided suture and hence it encourages wicking – an undesirable
property, which allows microorganisms to track along the length of the
suture into the wound. This in turn delays healing of the suture tracks. In
addition, black silk is non-resorbable and needs to be removed. Catgut, on
the other hand is resorbable and is a monofilament. Unfortunately, it is
more difficult to handle. Monofilamentous sutures, such as nylon, polyes-
ter and expanded polytetrafluoroethylene have many advantages. They
tend to be strong, easy to handle and see, non-allergenic and available in
a number of sizes. Although animal studies indicate that the wound reaches
the major part of its strength after 36 hours, and it has been suggested that
sutures can be removed after 2–3 days postoperatively (Fig. 9.85), the
authors are cautious about this recommendation. In a clinical scenario, the
wound strength may not be sufficient to withstand stresses/tension induced
during function and may be displaced; furthermore, early removal of
 Management of non-surgical root-canal treatment failure  257

Fig. 9.86  Immediately postoperatively Fig. 9.87  Two days postoperatively Fig. 9.88  Two weeks postoperatively

sutures is also more uncomfortable for the patient due to residual postop- Fig. 9.89  (a,b) Surgical
erative pain and swelling. Therefore, suture removal is recommended at 7 repair of external
days when wound strength is assured and swelling and pain are reduced, resorptive defect on  
as has been traditionally practised for decades. the mandibular first
When suturing the tissues, it is important to ensure that the flap is not premolar
under tension. The horizontal incision is usually sutured first. The tech-
nique most commonly used in endodontic surgery involves the use of
interrupted sutures. The single sling suture, vertical mattress suture and
the anchor suture may also be used. Postoperative wound healing is dem-
onstrated (Figs 9.86–9.88).
A

Wound healing
Various tissues are wounded during periradicular surgery. These are muco-
periosteal tissues (gingivae, alveolar mucosa and periosteum), periradicu-
lar tissues (bone and periodontal ligament) and radicular tissues (dentine
and cementum). Harrison and Jurosky (1991a,b, 1992) give a detailed
account of the three different types of wound healing: incisional; dissec-
tional; and excisional. To promote optimum healing, the operator must
ensure close approximation of the wound edges, encouraging healing by
primary intention. Appropriate oral hygiene measures must be established
to prevent infection of the surgical site, which may lead to wound break-
down and healing by secondary intention (scarring).
The first event in wound healing is clot formation. The function of the
clot is to provide an initial seal and strength, attach the opposing wound
edges and thereby provide a pathway for the migration of inflammatory
and repair cells. Inflammatory cells, such as polymorphonuclear leuco-
cytes migrate to the wound site (chemotaxis) and are responsible for
removal of bacteria and cellular debris (phagocytosis). Activated macro- B
phages then invade and stimulate fibroblasts to form new collagen and
small blood vessels (angiogenesis). Once an epithelial barrier has been
formed, connective-tissue healing commences. With time, the connective Caries involves destruction of dental tissues as a result of microbial
tissue remodels and matures. action. An untreated carious lesion may invade the floor of the pulp
chamber or extend along the root resulting in perforation of the root. Treat-
CORRECTIVE SURGERY ment of these perforations may require a combination of crown lengthen-
ing, root extrusion or root resection in order to retain valuable radicular
Perforation repair
segments. In must be said that the pattern of tooth destruction leading to
A radicular perforation is an artificially created communication between perforation in most cases will render the tooth unrestorable.
the root-canal system and the supporting periodontal apparatus of the Perforations resulting from procedural errors are probably the second
tooth. Perforations compromise the health of the periradicular tissues most common cause of endodontic failure and account for close to 10%
and threaten the viability of the tooth. Perforations pose a number of of all endodontic failures.
diagnostic and management problems. They generally occur through three Irrespective of the factors involved in the creation of the perforation,
mechanisms: resorptive processes (Fig. 9.89); caries; and procedural errors the management and repair will depend on three factors: (1) the location
(Fig. 9.90). of the perforation; (2) the length of time since the perforation was created;
Resorptive processes, given sufficient time, will perforate the root struc- and (3) the size of the perforation. The most important of these is the
ture. The resorptive process may be internal or external in origin and it is location of the perforation. Perforations close to the height of the alveolar
important to distinguish between them so that appropriate treatment can crest are the most difficult to repair and generally have the least favourable
be rendered. prognosis due to their communication with the gingival sulcus and the
 258  Management of non-surgical root-canal treatment failure
A B
A B
Fig. 9.91  (a) Perforation of the distal aspect of the mesial root of tooth 36; (b) reflected tissue flap revealing extent of the bone loss associated with the
perforation; (c) surgical repair of the perforation with MTA
A
B
microorganisms contained within it. This location has been described as
the “critical crestal zone”. Coronal to this, a perforation can be repaired
with restorative material with or without crown lengthening. Apically, a
perforation can be viewed as a secondary foramen.
The treatment of a perforation affecting the mesial root of a mandibular
molar is illustrated (Fig. 9.91).
Root resection
A root resection or root amputation is defined as the removal of an entire
root leaving the crown of the tooth intact (Fig. 9.92). Root resections have
been performed for a multitude of reasons for many decades. Today, the
main indications for root resection include:
• treatment of a periodontal defect, e.g., furcation defect, class III
periodontal defect
• vertical root fracture of one root of a multirooted tooth
• caries, or a resorptive defect of one root of a multirooted tooth that
cannot be managed in other ways
• removal of a root that has undergone an irreparable perforation
Fig. 9.90  (a) Perforation on the mesiolingual aspect
of tooth 35 following a procedural error; (b) 2-year
follow-up of non-surgical repair of the perforation
C
Fig. 9.92  (a) Preoperative radiograph of the maxillary
first molar prior to resection of the mesiobuccal root,
which was associated with extensive bone loss. Note
the use of amalgam compacted into the orifice. The
amalgam acts as a permanent restoration and is easily
visualized during the surgical procedure; (b) 1-year
postoperative radiograph of the tooth
• treatment of one root of a multirooted tooth that is not amenable to
non-surgical or surgical treatment.
Contraindications to root resection include:
• fused roots
• unrestorable tooth
• paucity of support for or attachment to remaining root(s).
A case of root resection of the mesial root of a mandibular first molar
is presented to emphasize procedural aspects. Where possible, endodontic
treatment should be completed prior to root resection (Fig. 9.93a).
Amalgam has been placed in the root with the perforation that is due to
be resected. This will facilitate orientation during the surgical procedure
and will, more importantly, seal the remaining root-canal systems from the
oral cavity. Preservation of alveolar bone is important but, in many cases,
removal of some bone around the root to be resected will be necessary.
Following reflection of a soft-tissue flap, root resection is performed with
a high-speed, tapered tungsten carbide bur starting at the most accessible
coronal aspect of the root. The instrument is directed apically towards the
 Management of non-surgical root-canal treatment failure  259
A B
E F
Fig. 9.93  (a) Preoperative radiograph; (b) clinical view following root resection; (c) placement of bone substitute Bio-Oss; (d) Bio-Oss bovine bone graft;
(e) resorbable membrane in place; (f) 5-year follow-up radiograph
A B
furcation, stopping just short of the furcation in order to avoid damage to
the adjacent root surface. The root can then be completely sectioned gently
fracturing the remaining root material with a fine elevator placed in the
resection line. Having removed the resected root (Fig. 9.93b), the place-
ment of a bone substitute and membrane covering further enhance healing
and resolution (Fig. 9.93c–e). A 5-year follow-up radiograph shows a
favourable outcome (Fig. 9.93f). Root resection should be avoided prior
to non-surgical root-canal treatment (NSRCT) (Fig. 9.94a) and it is impor-
tant to confirm that no residual root spurs remain as they can lead to
localized periodontal breakdown (Fig. 9.94b). (For further discussion of
root resections, see Chapter 12.)
Hemisection
Hemisection is defined as the surgical separation of a multirooted tooth,
usually a mandibular molar, through the furcation in such a way that a
root and the associated portion of the crown may be removed (Fig. 9.95).
Fig. 9.94  (a) Root resection performed prior to
NSRCT is not recommended – note “spur” of dentine
remaining, which will complicate the periodontal
management of the case; (b) correction of the
problems by performing NSRCT and by removing the
dentine spur
The need for a mucoperiosteal flap is determined following each case
evaluation. Restoration of the remaining portions of the tooth is critical to
the long-term survival of the tooth (Fig. 9.96). (For further discussion, see
Chapter 14.)
When hemisection is performed prior to NSRCT (Fig. 9.97a), it is nec-
essary to isolate the remaining tooth and complete the treatment in the
normal way (Fig. 9.97b,c).
INTENTIONAL REPLANTATION
AND TRANSPLANTATION
Intentional replantation is defined as the replacement of a tooth in its
socket following deliberate surgical avulsion (Figs 9.98–9.100). Trans-
plantation of a tooth, involves replacement of a tooth in a socket other than
the one from which it had been extracted (Fig. 9.101). This is normally
limited to procedures within the same mouth.
 260  Management of non-surgical root-canal treatment failure
Fig. 9.95  Hemisected
mandibular molar
A B
Fig. 9.97  (a) Hemisection performed prior to NSRCT – note bleeding pulpal tissue; (b) isolated hemisected tooth; (c) completed NSRCT
Fig. 9.98  Replanted molar – note lack of NSRCT Fig. 9.99  Radiograph of intentional replantation
– preoperative
As a general rule, intentional replantation is considered a procedure of
last resort, although many successful cases have been reported in the lit-
erature. Much is now understood about the physiology of the periodontal
ligament surrounding the root of the extracted tooth and appropriate
handling of the root will enhance the chances of success following
replantation.
It is desirable to perform non-surgical root-canal treatment on the tooth
prior to replanting or transplanting. The ligament of the extracted tooth
should be protected in the same way as that of an avulsed tooth. The cells
of the periodontal ligament and the socket are very susceptible to damage
and must be protected from trauma and from desiccation. If the tooth is
out of the mouth for any time, it should be placed in a storage medium,
such as Hanks Balanced Salt Solution (HBSS) or Ringer’s solution. These
isotonic solutions provide the greatest chance of ensuring vitality of the
periodontal ligament which will, in turn, reduce the chance of resorption
Fig. 9.96  Restored
distal segment
C
Fig. 9.100  Radiograph of intentional replantation
– postoperative
of the root at a later date. Root-end preparation and root-end filling are
performed extraorally under a constant stream of isotonic saline or HBSS.
REGENERATIVE PROCEDURES
In 1793, John Hunter said that, “the only rational form of treatment is that
which calls forth the recuperative powers of the body …”. More recently,
Melcher (1976) wrote a paper entitled “On the repair potential of periodon-
tal tissues”, which resulted in a reappraisal of the processes involved in
periodontal regeneration. The emphasis following endodontic and perio-
dontal surgery has subsequently shifted towards regeneration of tissues as
opposed to repair alone.
Regeneration of the periradicular tissues subsequent to surgery or due
to the ravages of disease processes implies replacement of the various
components of the tissue in their appropriate locations, amounts and
 Management of non-surgical root-canal treatment failure  261

A B C

Fig. 9.101  (a) Transplantation case. Radiographic and clinical examination revealed a hopeless prognosis for the mandibular second molar tooth; (b) bitewing
radiograph indicating relationship of maxillary to mandibular teeth; (c) NSRCT completed on unopposed maxillary third molar; (d) maxillary third molar extracted
gently and the root-ends resected; (e) root-end preparations prepared and obturated with Diaket root-end filling material. The palatal root had to be extensively
resected in order to allow the tooth to be positioned in the recipient socket; (f) transplanted tooth in recipient site (courtesy of Dr JD Regan)

relationships to each other. Repair, on the other hand, is a biological
process by which continuity of disrupted tissue is restored by new tissues
that do not replicate the structure and function of the lost ones.
Melcher (1976) stated that the cells that repopulate the exposed root
surface determine the nature of the attachment that will form. If the rapidly
growing epithelium proliferates first, a long junctional epithelium (JE) will
form. If cells from the gingival connective tissue (CT) meet the root
surface, root resorption might be the sequela. If bone comes in direct
contact with the root, root resorption and ankylosis may occur. However,
if cells from the periodontal ligament (PDL) populate the root surface first,
new connective tissue attachment may develop.
Overall, guided tissue regeneration (GTR) procedures have been shown
to improve the levels of attachment. However, histometric assessment
reveals that incomplete regeneration frequently occurs. Aukhil et al. (1986)
described three different zones of healing after barrier therapy:
• junctional epithelium
• fibres parallel to the root surface
• new CT attachment (new bone, PDL, cementum).
A number of commercially available membranes are currently available.
The use of membranes in endodontic surgical cases became more wide-
spread following the development of bioabsorbable materials. Prior to this,
the non-resorbable material, such as the expanded polytetrafluoroethylene
(e-PTFE Gore-Tex) membrane (This product has been discontinued) had
Fig. 9.102  Biomend
absorbable collagen
membrane placed over
large through and
through defect with
2–3 mm extension over
the osseous margins of
the lesion
to be removed during a second follow-up surgical procedure some 6 weeks
after the initial procedure. Commercially available bioabsorbable mem-
branes include bovine collagen, and synthetic membranes (polylactic acid,
polyglycolic acid, polyurethane, Resolut XT/Resolut Adapt [synthetic bio-
absorbable glycolide and trimethylene carbonate copolymer fiber and an
occlusive membrane of synthetic bioabsorbable glycolide and lactide
copolymer], polyglactin-910 mesh with copolymer of glycolide and
lactide). The most common material is collagen, such as Biomend® (Fig.
9.102) and BioGide® (Fig. 9.103) (both collagen products). It is important
 262  Management of non-surgical root-canal treatment failure

Fig. 9.103  BioGide® Fig. 9.104  Bio-Oss®

bone graft

A B

Fig. 9.105  Perioglass® Fig. 9.106  (a,b) Capset calcium sulphate material

Fig. 9.107  (a–e) Decompression

procedures (courtesy of Dr MB Saunders)

B
A

to place the membrane so that its edges are fully supported by 2–3 mm of
bone away from the edge of the crypt. Many clinicians prescribe antibiot-
ics for their patients following placement of a membrane but there is no
evidence to support routine use of antibiotics.
Other substitute materials are also available as supports for membranes
or as regenerative materials aimed at supporting, if not inducing, bone
formation. These include Bio-Oss® (Fig. 9.104), Perioglass® (Fig. 9.105)
and calcium sulphate (Fig. 9.106).
At present, the evidence for routine use of GTR for apical surgery is
weak but it may be beneficial for large through-and-through lesions.
DECOMPRESSION
Decompression or marsupialization involves the surgical exteriorization
of a large periradicular lesion in order to facilitate healing of the lesion
(Fig. 9.107). The lesion is penetrated through the periosteum and cortical
 Management of non-surgical root-canal treatment failure  263
plate and the patency of the opening is maintained by inserting a flanged
cannula allowing for daily irrigation of the lesion by the patient. The
advantages of this procedure include reduction in the risk of damaging
either adjacent vital teeth or anatomical structures (Fig. 5.47).
REFERENCES AND FURTHER READING
Atmeh, A.R., Chong, E.Z., Richard, G., et al., 2012. Dentin-cement interfacial
interaction: calcium silicates and polyalkenoates. J Dent Res 91 (5), 454–459.
Aukhil, I., 1991. Biology of tooth-cell adhesion. Dent Clin North America 35, 459–467.
Aukhil, I., Pettersson, E., Suggs, C., 1986. Guided tissue regeneration. An experimental
procedure in beagle dogs. J Periodontal 57, 727–734.
Bashutski, J.D., Wang, H.L., 2009. Periodontal and endodontic regeneration. J Endod 35
(3), 321–328.
Harrison, J.W., Jurosky, K.A., 1991a. Wound healing in the tissue of the peridontium
following periradicular surgery. 1. The incissional wound. J Endod 17 (9), 425–435.
Harrison, J.W., Jurosky, K.A., 1991b. Wound healing in the tissue of the peridontium
following periradicular surgery. 2. The dissectional wound. J Endod 17 (11), 544–552.
Harrison, J.W., Jurosky, K.A., 1992. Wound healing in the tissues of the periodontium
following periradicular surgery. 3. The osseous excisional wound. J Endod 18, 76–81.
Laurent, P., Camps, J., About, I., 2012. Biodentine(TM) induces TGF-β1 release from
human pulp cells and early dental pulp mineralization. Int Endod J 45 (5), 439–448.
Melcher, A.H., 1976. On the repair potential of periodontal tissues. J Periodontal 47,
256–260.
Roberts, H.W., Toth, J.M., Berzins, D.W., et al., 2008. Mineral trioxide aggregate
material use in endodontic treatment: a review of the literature. Dent Mater 24 (2),
149–164.
Tsesis, I., Rosen, E., Tamse, A., et al., 2011. Effect of guided tissue regeneration on the
outcome of surgical endodontic treatment: a systematic review and meta-analysis. J
Endod 37 (8), 1039–1045.
Zanini, M., Sautier, J.M., Berdal, A., et al., 2012. Biodentine induces immortalized
murine pulp cell differentiation into odontoblast-like cells and stimulates
biomineralization. J Endod 38 (9), 1220–1226.
 10
Section 3  Delivery of endodontic treatment
Management of acute emergencies and traumatic dental injuries
  K Gulabivala, Y-L Ng
PRINCIPLES OF MANAGEMENT OF PAIN
The most fulfilling aspect of endodontic treatment is the opportunity to
care for the patient in pain. Acute dental pain is notoriously difficult to
cope with for most patients, particularly that of pulpal origin. They will
arrive in a distressed state, being anxious and irritable having had disturbed
sleep, eating patterns. Their psychological demeanor may be defensive,
aggressive, blaming or even dulled through fatigue and dosing on
medication.
Successful management of pain is:
1 preceded by sharp diagnostic and psychological insight
complemented by a confident manner
2 accompanied by effective and efficient treatment execution,
including adequate anaesthesia and analgesia
3 succeeded (hopefully) by patient gratitude and loyalty; and a
personally enhanced reputation for the dentist.
For effective practice development, there is no greater pathway than
caring for patients in acute pain. The investment required is a moral,
human, compassionate, patient and confident approach, coupled with
understanding of the biology of the problem, as well as insight about
pharmacological armamentaria.
The majority of patients attending the dentist in pain suffer from the
acute consequences of pulpal or periradicular disease (Table 10.1), but the
dentist must beware of confounding factors.
The clinician’s aim in providing emergency care is to control the infec-
tion and inflammation by removing the cause of the problem. However,
the response to the underlying injury will endure for the period of time it
takes for the triggered biological mechanisms to switch off. During this
latent period, pharmacological means may be intelligently employed to
help control the lingering pain until the unpleasant experience subsides
naturally through innate physiological mechanisms. There are strong psy-
chological elements to pain control as evidenced by placebo effects, hence,
a biologically robust strategy, accompanied by effective surgical execution
and a firm, confident manner is paramount.
DIAGNOSTIC ACCURACY
Patients presenting in a dental practice suffering from orofacial pain must
be viewed from a broad diagnostic perspective. The cognitive and material
tools possessed by dentists naturally sway their management towards
dental intervention but non-dental factors can mimic dental pain too. This
is due in part to convergence of peripheral neural pathways in the central
nervous system and in part to the patients’ inability to articulate their
experience in a meaningful way to the dentist. Dentists should therefore
be aware of the common causes of misdiagnosis. These include non-
odontogenic inflammation, vascular, musculoskeletal, neurological, and
systemic or psychogenic problems (see Chapter 16). Temporomandibular
joint (TMJ) and muscular pain from the masseter, lateral pterygoid and
temporalis muscles may refer pain to the maxillary or mandibular molars,
premolars or even anterior teeth on occasion. Such a condition may be
more appropriately managed with reassurance, explanation, reduction in
muscle and joint load, stretching exercises, heat/cold therapy and lastly,
the use of an occlusal acrylic splint may help (Figs 10.1, 10.2).
© 2014 Elsevier Ltd. All rights reserved.
It is also worth bearing in mind that patients who have been suffering
long-standing pain may have a reduced threshold of pain perception as a
result of central or peripheral sensitization. The zone of sensitization may
be restricted close to the origin of the problem or expanded to various
distances from it. It is worth, therefore, exploring and mapping zones of
hyperalgesia (heightened response to noxious stimuli) and allodynia
(heightened response to non-noxious stimuli), lest detected local tender-
ness is in fact part of this phenomenon. Sensitization may be evident in
patients with a history of chronic pain, TMJ dysfunction, fibromyalgia and
whiplash injury.
EFFECTIVE INTRAOPERATIVE PAIN CONTROL
LOCAL ANALGESIC AGENTS AND THEIR ACTIONS
Difficulties can often be encountered in trying to secure analgesia in
irreversibly inflamed pulps or where there is acute infection. Failure
of analgesia may be operator dependent (poor technique, choice of tech-
nique and/or solution) or patient dependent (anatomical, pathological or
psychological).
The most commonly used analgesic solution for most endodontic pro-
cedures is lignocaine with adrenaline (epinephrine) (Fig. 10.3). Providing
the analgesic solution is given slowly with an aspirating technique, then
the adrenaline (epinephrine) is not a problem in most patients.
The success rate for inferior alveolar block injections is over 90%. A
practitioner who regularly fails with this method should reassess their
technique. Although, it is generally considered that the sign of a successful
block is a numb lip, all that this indicates is that the nerves to the soft
tissues of the lip have been blocked; it does not necessarily infer pulpal
analgesia. The presence of infection and inflammation can reduce the
efficacy of analgesic solutions. In solution, the local analgesic exists in
two ionic forms, an uncharged anion (RN) and a positively charged cation
(RNH+). Both forms of the solution are required for analgesia.
RNH+ ⇌ RN + H+
Inflammation lowers the tissue pH and, correspondingly, the amount of
the base form of the analgesic available to penetrate the nerve membrane.
Consequently, there is less of the ionized form within the nerve to achieve
analgesia. In addition, nerves arising in inflamed tissue have altered resting
potentials and decreased excitability thresholds. These changes are not
restricted to the inflamed pulp but affect the entire neural membrane.
Articaine with adrenaline (epinephrine) (Fig. 10.4) has gained favour as
a local analgesic solution to use where lignocaine appears to have failed.
Articaine differs from lignocaine as it has a thiophene ring as its lipophilic
component rather than a substituted aromatic ring. Studies show that it is
no more effective as an analgesic agent than lignocaine. However, it does
have an increased propensity to diffuse widely, which may allow it to block
accessory innervations over a broader field. In addition, the different stere-
ochemical structure may also account for its apparently higher success
rate. Unfortunately, it is also associated with a higher frequency of persist-
ent paraesthesia.
The use of long-acting anaesthetics may provide the patient pain relief
while the postoperative analgesics start to act. Marcaine (0.5% bupi-
vacaine with 1 : 200 000 epinephrine) when used as a regional block can
give soft-tissue anaesthesia of 6–8 hours. Marcaine is not available in all
 Management of acute emergencies and traumatic dental injuries  265

countries in dental anaesthetic cartridges and, in some areas, is not licensed Akinosi techniques both attempt to anaesthetize the inferior alveolar nerve
for dental use. Dental practitioners should satisfy themselves as to the local at a higher level. Both these methods are best reserved for cases where the
rules before administering it. Other preparations of bupivacaine are avail- conventional block fails as they can produce more complications than the
able, such as carbostesin (Fig. 10.5). standard approach – the higher the needle, the closer it is to the maxillary
artery and the pterygoid plexus.
LOCAL ANALGESIC AGENT DELIVERY
Gow–Gates technique
If an inferior alveolar block fails and a repeat attempt also fails, then an
This is a true mandibular block injection that provides analgesia of all the
alternative technique should be considered. The Gow–Gates and the
sensory divisions of the mandibular nerve, including buccal, inferior alve-
olar, lingual and mylohyoid. The method relies upon the deposition of
analgesic solution adjacent to the head of the mandibular condyle
(Fig. 10.6). The patient has the mouth wide open and a line is imagined
Table 10.1  Prevalence of acute orofacial or dental pain
from the corner of the mouth to the intertragic notch; this is the plane of
Prevalence of acute approach. The needle is introduced from the direction of the contralateral
Population orofacial or dental pain Comments mandibular canine tooth and directed over the ipsilateral maxillary second
USA (National Health 14% (acute orofacial pain Most common molar (Fig. 10.7). The point of mucosal penetration is higher than for a
Interview Survey, 1989) in the past 6 months) causes: caries & conventional inferior dental block. The needle is advanced until bony
periodontal disease contact is made with the head of the condyle, withdrawn slightly, aspira-
UK (Adult Dental Health 26% (dental pain) Most cases were tion performed, and a full cartridge of analgesic is delivered.
Survey, 2009) associated with
gross caries & sepsis
Toronto, Canada (Locker & 29% (teeth with cold/hot); 50% of cases
Akinosi technique
Grushka, 1987) 14% (toothache) in the reported severe This is a simpler technique than the Gow–Gates method and is sometimes
past 4 weeks symptoms
Sao Paulo, Brazil (age 12, 26% (dental pain) Most cases were
known as the closed-mouth technique. The patient has the mouth closed
15 adolescents) (2010) associated with and a 35 mm needle is used. The syringe is advanced parallel to the maxil-
untreated caries lary occlusal plane at the level of the maxillary mucogingival junction.
or endodontic
treatment need
The needle is advanced until the hub is level with the distal surface of the
Hong Kong, China (1222 28% (tooth sensitivity);
maxillary second molar (Fig. 10.8). At this point, a cartridge of analgesic
18+ Chinese speaking 13% (toothache) solution is deposited. This technique does not rely on touching bone and
people in 2006) this can be a disadvantage. However, the Akinosi technique allows provi-
sion of analgesia in a situation where all other methods of giving an

Fig. 10.3  Xylocaine

Fig. 10.1  Splint therapy for TMJ dysfunction Fig. 10.2  Palatal view of occlusal splint

Fig. 10.4  Articaine

Fig. 10.5  Carbostesin

Fig. 10.6  Position of deposition of local
anaesthetic solution for Gow–Gates technique for
inferior dental block
 266  Management of acute emergencies and traumatic dental injuries
Fig. 10.7  Gow–Gates technique for inferior dental Fig. 10.8  Akinosi technique for inferior dental
block block
Fig. 10.10  Needle insertion for intraligamental Fig. 10.11  Intraosseous injection using X-Tips
injection
inferior dental block would fail. Both motor and sensory analgesia are
achieved allowing the patient to open the mouth.
INTRALIGAMENTAL INJECTIONS
Intraligamental injections are used to deposit analgesic directly into
the periodontal ligament space and a number of specialized syringes
(Fig. 10.9) and small needles have been developed to facilitate this. The
needle is inserted into the mesial gingival sulcus and in contact with the
tooth (Fig. 10.10). The needle is supported by fingers and positioned with
maximal penetration between the root and crestal alveolar bone. Pressure
is slowly applied to the syringe handle for 20–30 seconds. Backpressure
has to be developed for this technique to work and blanching of the soft
tissues would be a sign of probable success. If analgesic solution flows
readily out of the sulcus then analgesia will not be achieved. Pressure is
necessary to force the solution into the marrow spaces to contact and block
the dental nerves. The technique should be repeated on the distal and
lingual surfaces of the involved tooth.
INTRAPULPAL INJECTIONS
The major drawback of the intrapulpal injection is the need for the needle
to be inserted into a very sensitive and inflamed pulp. The injection can,
therefore, be painful. Additionally, the pulp has to be exposed to give the
injection and analgesic problems may have occurred prior to this being
achieved. The injection has to be given under strong backpressure. In the
absence of backpressure, it is difficult to achieve analgesia. The mecha-
nism of action is the intrapulpal pressure, as the technique can work even
with saline. One technique to create the backpressure is “stoppering” the
cavity with gutta-percha to allow the backpressure to build up. Alterna-
tively, a small hole can be made into the pulp chamber with a half-round
bur, through which the needle can be introduced. If the pulp chamber has
Fig. 10.9  Peripress for intraligamental injections
Fig. 10.12  Intraosseous guide sleeve left in situ
until the end of the procedure
already been opened, then the needle may be advanced further into the
canal until it is wedged in place to create the backpressure. The needle
may need to be supported to prevent it from buckling. If the backpressure
cannot be created, then a larger needle may be required. Buckling can be
overcome by using the shorter and finer intraligamental needles.
INTRAOSSEOUS TECHNIQUE
The intraosseous technique allows analgesic solution to be deposited
directly into the cancellous bone around the apices of the tooth. It has a
rapid onset and has shown extremely favourable results when used as a
supplemental analgesic for the “hot” mandibular molar. The mucosa over-
lying the injection site, either just mesial or distal of the tooth to be treated,
is anaesthetized with a small infiltration. Special kits have been developed
that facilitate drilling a small hole through the mucosa and cortical plate
to allow injection of the anaesthetic solution into the cancellous bone.
X-Tips (Prestige Dental, Bradford, UK) consist of a drill to perforate the
cortical plate combined with a guide sleeve. When the drill is withdrawn
the guide sleeve is left in situ. The analgesic solution can be injected
through the guide sleeve, which is designed to accept an ultra-short
27-gauge needle (Fig. 10.11). The guide sleeve can be left in place during
the procedure so that the anaesthetic can be “topped-up” if required
(Fig. 10.12). A small number of patients develop soreness at the injection
site and a transitory increased heart rate can occur depending on the anal-
gesic solution used.
MANAGEMENT OF THE “HOT” PULP
The presence of symptomatic irreversible pulpitis (“hot pulp”) may require
additional strategies to control pain and allow pulp extirpation. The
problem typically affects mandibular molars. The factors to consider are
accessory nerve supply and altered nerve function.
 Management of acute emergencies and traumatic dental injuries  267

Supplemental analgesia is often required when treating the “hot”

Table 10.2  The 2007 Oxford league table of analgesic efficacy
pulp to account for accessory nerve supply infiltrations; while not a
replacement for inferior dental blocks, it may be required to block input Number of Percent with
from the cervical plexus, together with the mylohyoid and lingual nerves. patients in at least 50%
Analgesic comparison pain relief NNT*
Cross-innervation from the contralateral inferior alveolar nerve should also
be considered. In the maxillary arch, the posterior superior alveolar block Ibuprofen 600/800 165 86 1.7
to the maxillary molars can be considered while anterior superior alveolar Diclofenac 100 545 69 1.8
Ketorolac 20 69 57 1.8
nerve block can deposit analgesic at the opening of the infraorbital foramen
Oxycodone IR 5 + paracetamol 500 150 60 2.2
– decussation of the fibres of the anterior superior dental nerve can provide
Paracetamol 1000 + codeine 60 197 57 2.2
innervation to the premolar teeth. When treating vital molar teeth, palatal
Oxycodone IR 15 60 73 2.3
infiltrations to block innervation from the greater palatine or nasopalatine
Aspirin 1200 279 61 2.4
nerve should be considered mandatory. Ibuprofen 400 5456 55 2.5
There are two main classes of sodium channels in neural function, Diclofenac 25 502 53 2.6
divided on the basis of their sensitivity or resistance to tetrodotoxin. The Ketorolac 10 790 50 2.6
sensitive channels are found on most neurons, while the resistant channels Oxycodone IR 10 + paracetamol 650 315 66 2.6
are found mainly on Aδ and C fibres, which are the main nociceptive fibres Paracetamol 650 + tramadol 75 679 43 2.6
in the pulp. Their activity increases in the presence of inflammation Diclofenac 50 1296 57 2.7
through an increase in the number of channels, as well as reduction in the Ibuprofen 200 3248 48 2.7
threshold due to the presence of mediators, such as prostaglandin E2 Naproxen 400/440 197 51 2.7
(PGE2) and nerve growth factor (NGF). Such channels are relatively resist- Naproxen 500/550 784 52 2.7
ant to lignocaine but its effect may be enhanced by increasing the dose Oxycodone IR 10+ paracetamol 1000 83 67 2.7
and by premedicating with ibuprofen (400 mg) about one hour before Dextropropoxyphene 130 50 40 2.8
Paracetamol 650 + tramadol 112 201 60 2.8
administration of the local anaesthetic. Alternatively, the channels are
Tramadol 150 561 48 2.9
more susceptible to bupivacaine and mepivacaine.
Naproxen 200/220 202 45 3.4
Paracetamol 500 561 61 3.5
Ibuprofen 100 495 36 3.7
EFFECTIVE POSTOPERATIVE PAIN CONTROL Paracetamol 1500 138 65 3.7
Oxycodone IR 5 + paracetamol 1000 78 55 3.8
Following the option of long-acting local anaesthetics, the next option is Paracetamol 1000 2759 46 3.8
the use of systemically administered centrally or peripherally acting anal- Paracetamol 600/650 + codeine 60 1123 42 4.2
gesics. A medical history needs to be taken to rule out possible drug Aspirin 600/650 5061 38 4.4
hypersensitivity. Dental pain is generally of short duration with analgesics Paracetamol 650 + 963 38 4.4
only being taken for 24–48 hours and it is unlikely, therefore, that unwanted dextropropoxyphene (65 mg
hydrochloride or 100 mg napsylate)
effects would occur.
Paracetamol 600/650 1886 38 4.6
The relative efficacy of different analgesics is provided by the Oxford
Ibuprofen 50 316 32 4.7
league table (Table 10.2). Aspirin is widely used. However, its efficacy Tramadol 100 882 30 4.8
is dose related, 1000–1200 mg four times per day providing greater Aspirin 650 + codeine 60 598 25 5.3
analgesia than 500–600 mg four times per day. Non-steroidal anti- Tramadol 75 563 32 5.3
inflammatory drugs (NSAIDs), such as ibuprofen, can also be used. Ibu- Oxycodone IR 5 + paracetamol 325 149 24 5.5
profen has been shown to be one of the most effective analgesics at Paracetamol 300 + codeine 30 379 26 5.7
reducing acute pain and its efficacy is also dose related; 400 mg four Tramadol 50 770 19 8.3
times per day appears to be the optimal dose but up to 800 mg delivers Codeine 60 1305 15 16.7
100% efficacy, if there are no side effects. Paracetamol is often used
by patients with sensitivity to aspirin and the other NSAIDs and can *Numbers needed to treat (NNT) are calculated for the proportion of patients
with at least 50% pain relief over 4–6 hours compared with placebo in
be efficacious in high dosage, but it does not have the same anti- randomized, double-blind, single-dose studies in patients with moderate to severe
inflammatory properties. pain. Drugs were oral, unless specified, and doses are milligrams.
Peripherally acting analgesics are often provided in combination with a (www.jr2.ox.ac.uk/bandolier/booth/painpag/)

centrally acting analgesic, such as codeine. Evidence suggests that com-

bined analgesics are more effective than the individual constituents alone.
Severe pain may be treated by the use of a NSAID and paracetamol in
tandem. An initial dose of the NSAID can be given with paracetamol being
taken 2–3 hours later. The NSAID can again be given 2 hours following
this. The obvious risks are patients not understanding the drug regimen or
using a proprietary analgesic with both an NSAID and paracetamol, and
therefore possibly overdosing on the paracetamol.
Analgesics have been shown to be more beneficial if they are taken
before severe pain occurs. Patients should be advised that the analgesics
should be taken if they feel the onset of pain and possibly to continue with
a regular dose after the pain has subsided for a period of time.
The mechanism of action of NSAID-like drugs is through the inhibition
of cyclo-oxygenase, of which there are two types, COX1 and COX2. The
former are constitutive and are present in stomach, kidneys and platelets;
they are inhibited by the traditional NSAIDs. The latter are inducible and
are synthesized in inflamed tissues. Side effects include cardiovascular or
gastrointestinal problems. COX2 inhibitors should have fewer side effects,
such as gastrointestinal of kidney problems.
Contraindications for aspirin include ulcers, asthma, diabetes, gout,
influenza (Reye’s syndrome) and liver dysfunction. It is well to remember
the possibility of drug interactions of NSAID-like drugs, which include:
reduction of anti-high blood pressure effectiveness with ACE inhibitors,
beta blockers, thiazide and loop diuretics; increased nephrotoxicity with
 268  Management of acute emergencies and traumatic dental injuries
cyclosporins; increased serum concentrations with hydantins and lithium;
increased toxicity with methotrexate, increased blood pressure with sym-
pathomimetics; and increased prothrombin time with anticoagulants.
EMERGENCY SCENARIOS
Endodontic emergencies may be divided by temporal association into
preoperative, intraoperative and postoperative events, although the bound-
aries of this classification are not sacrosanct. Preoperative pain often pre-
dicts intraoperative and postoperative pain but other factors may also be
involved.
PREOPERATIVE EMERGENCIES
Patients fall into two broad categories, those who are part of the practice
and under regular or irregular review and those who have never attended
the practice before and merely seek resolution of an urgent problem. The
former group of patients will have available details of dental status and
previous treatment, albeit with their recent history requiring updating;
whereas the latter group requires a thorough investigation to determine the
nature of the problem, as well as the level and type of service appropriate
for their needs.
Inevitably, patients arrive seeking emergency treatment at a time incon-
venient to the busy practitioner. However, it is essential that time is made
to reach a proper diagnosis. Apart from the patient often not being able to
locate the specific tooth causing the problem, there are a number of patho-
logical entities that will mimic pain of odontogenic origin and, in these
cases, endodontic procedures are obviously not indicated.
Identifiable endodontic emergencies fall into the following categories:
 painof pulpal origin
 emergencies of periradicular origin
 emergencies resulting from traumatic injuries.
EMERGENCIES OF PULPAL ORIGIN
Diagnosis
The innervation of the dental pulp consists of myelinated Aδ fibres and
unmyelinated C fibres, which give rise to distinct types of pain sensations
as discussed in Chapter 4. Pulpal pain is typically stimulated by hot or
cold stimuli, however, it is important to be clear whether the pain has the
sharp quality attributable to Aδ fibre stimulation or the dull aching,
throbbing quality associated with pulpitis and C fibres. Many dentists
confuse localizable dentine sensitivity with the unlocalizable pain of
pulpal origin. Identification of the tooth is not helped by the perception of
A
B
the patient, as to which tooth is the culprit; even dentists with toothache
get it wrong. Pulpal pain only becomes localizable when the inflammation
is advanced enough to involve the periapical tissues and the tooth becomes
tender to touch or tap.
The dentist should seek all historical, clinical and radiographic clues to
identify the cause. Sometimes, this will be obvious, such as secondary
caries or crack (Figs 10.13, 10.14a) and, at other times, the patient may
present with a quadrant of teeth with deep restorations (Fig. 10.15), all
posing as potential candidates. It is not unheard of that, under such cir-
cumstances, several teeth end up with pulp extirpations. It is important to
differentiate the causative tooth by using a combination of pulpal stimula-
tion (uncomfortable as that may be) and selective, diagnostic local anaes-
thesia. There is no local anaesthetic technique that can be completely
confined to one tooth but intraligamental anaesthesia affords a close pos-
sibility. The principle is to choose the most likely candidate but to anaes-
thetize from the mesial to distal and maxillary to mandibular. When the
pain is abolished, the tooth is identified; effectiveness of anaesthesia may
be tested by pulp testing.
The distinction between reversible and irreversible pulpitis is not clear-
cut. In both cases, there may be pain stimulated by hot, cold or sweet
stimuli, lingering for various periods of time as a dull ache, sometimes
arising spontaneously and sometimes keeping the patient awake at night.
At times, the pain may be so severe that the patient will find it intolerable,
described as the worst imaginable pain and likened to being stabbed in the
jaw with a red-hot poker or knife. The longer the episodes of lingering
pain, the more spontaneous the episodes, the greater the frequency of sleep
loss, the more severe the pain, the greater the response to hot rather than
cold (indeed sometimes cold may relieve), the more likely it is that the
pain will be judged irreversible. Indeed, severe pulpal pain of the sort
described may sometimes be associated with a relatively normal pulp
(Seltzer et al., 1963; Dummer et al., 1980). In the case shown, placement
of cast onlays resulted in pain characteristic of irreversible pulpitis,
Fig. 10.13  Irreversible
pulpitis in mandibular
first molar showing a
widened periodontal
ligament space around
both apices
Fig. 10.14  (a) Vertical unrestorable fracture in maxillary
molar (arrowed); (b) maxillary molar following extraction;
(c) maxillary molar with separated fractured segment
 Management of acute emergencies and traumatic dental injuries  269

A B

Fig. 10.16  (a) Symptoms consistent with irreversible pulpitis were triggered following placement of cast
Fig. 10.15  Teeth with deep restorations onlays on the mandibular molars; (b) symptoms resolved spontaneously after 2–3 months, whilst the teeth
continued to respond normally to pulp tests, remaining free of apical disease many years afterwards

Fig. 10.17  Use of fibreoptic light to Fig. 10.18  Dressed molar tooth Fig. 10.19  Mandibular molar with thickening of
illustrate the extent of an incomplete PDL space and condensing osteitis
fracture (courtesy of Dr CC
Youngson, Liverpool Dental Institute)

however, the patient was able to tolerate the pain and in time, the pain
resolved. Many years on, the teeth respond normally to pulp tests and
remain free of apical disease (Fig. 10.16). Patients unable to tolerate the
pain would opt to have the pulps extirpated, therefore, the correct term for
the diagnosis is pulpalgia rather than pulpitis.
Cracked tooth syndrome (CTS) may also result in pulpitis and the crack
may need additional management by placement of an orthodontic band to
prevent cuspal flexure and catastrophic fracture. The degree of pain may
vary considerably, from momentary pain on encountering heat and cold to
spontaneous pain or pain on biting. The pain on biting will have a sharp
quality, while the pain on hot and cold may vary from sharp to a dull aching
quality. A fibreoptic light may be useful in locating and determining the
extent of the cracks (Fig. 10.17) but they are not always visible in the early
stages of CTS.
Treatment
If it is judged that the pain is due to reversible pulpitis, treatment involves
removing the source of dentinal or pulpal irritation. In the case of sensitive
dentine, patent dentinal tubules may be treated using fluoride or desensitiz-
ing agents. Dental caries and faulty restorations should be removed and
replaced with a sedative dressing, typically containing zinc-oxide/eugenol
(Fig. 10.18).
If it is judged that the pain is due to irreversible pulpitis, the pulp should
be extirpated (Fig. 10.19). The ideal emergency treatment for irreversible
pulpitis is to remove the diseased pulp completely and to clean and prepare
the pulp canal system. Irrigating the pulp chamber with a 2.5–5.0% solu-
tion of sodium hypochlorite ensures disinfection before canal instrumenta-
tion. If time does not allow this, removal of pulp tissue from the pulp
chamber and coronal part of the root canals is often effective. The use of
corticosteroid preparations in vital root canals has been advocated in situ-
ations where complete instrumentation is inconvenient or impossible
because profound anaesthesia cannot be secured. In the presence of severe
pulpal inflammation, the effectiveness of local anaesthesia is reduced as
discussed above.
In cracked teeth, dentine bonded materials may prove useful in small
cavities as an interim restoration before constructing a restoration giving
occlusal protection (Fig. 10.20). Once a vertical crack is initiated, the
treatment goal is to prevent catastrophic propagation and retain the tooth
for as long as possible; some teeth can last up to 10 years with cuspal
protection.
Where a crack involves the pulp and symptoms suggest an irreversible
pulpitis, all restorations should be removed from the tooth and the extent
of the crack determined. If the crack has propagated to a fracture and a
portion of the tooth is mobile it should be removed, examined, and
the possibility of restoring the remaining tooth substance established (see
Fig. 10.14a). Examination of the extracted fragment allows accurate
assessment of the restorability of the tooth. Where the fracture runs into
the apical periodontal attachment apparatus, as in this case, then extraction
is the only option (see Fig. 10.14b,c). If the tooth is restorable, root canal
 270  Management of acute emergencies and traumatic dental injuries

Fig. 10.20  Gold partial coverage Fig. 10.21  Molar tooth supported Fig. 10.22  Vertical fractures involving
restoration giving occlusal protection by an orthodontic band the floor of the chamber

treatment may commence. Should the fracture line run through the floor Camphorated Phenol Cresatin
of the pulp chamber, then it is unlikely that the tooth will respond to treat- 15 15
ment in the long term.
In cases where the tooth is cracked but is incomplete, the crown should **

Number of cases
10 10 **
be supported with a metal band (Fig. 10.21) and root canal treatment com-
menced. The long-term prognosis of posterior teeth with oblique fractures
above the alveolar crest and involving only the roof of the pulp chamber 5 5
is higher than vertical fractures involving the floor of the chamber
(Fig. 10.22). 0 0
Whether the treatment consists of a pulpotomy or pulpectomy, there 0 1 7 30 0 1 7 30
Day
should be 50–75% reduction in the severity of the pain within one day but
Eugenol Zoe
the residual pain may linger for 24–48 hours gradually reducing over the 15 15
following 24 hours (total 72 hours). It may take a further 7–28 days gradu-
ally to subside completely (Fig. 10.23). The lingering pain may be worse
10 * 10
when a complete pulpectomy with cleaning and shaping is performed. If
symptoms continue beyond this time, the presence of residual inflamed
pulpal tissue should be investigated in the root canal system in the form 5 5
of an undiagnosed canal.
If the tooth is extracted, the pain may gradually subside over the next
0 0
3 days, albeit with a changed character. 0 1 7 30 0 1 7 30
Some clinicians recommend occlusal reduction, but such an approach
should only be adopted following a proper occlusal assessment. The tooth Saline Dry Pellet
15 15
will not stay out of contact for long because of continued eruption. Occlu- **
sal reduction works when there had been previous presence of percussion
sensitivity, in vital cases and in the absence of a periapical radiolucency. 10 10
The authors do not recommend it as a routine procedure.
5 5
Medication
Antibiotics have commonly been prescribed for irreversible pulpitis but
0 0
such medication will have no effect on the inflamed pulp and is contrain- 0 1 7 30 0 1 7 30
dicated. Analgesics are a useful adjunct to manage the residual pain as Fig. 10.23  Number of cases presenting with symptoms over a 30-day period
discussed above. following root canal dressing using various materials (darkest shade = pain,
intermediate shade = discomfort, lightest shade = no symptoms; * patient did
EMERGENCIES OF PERIRADICULAR ORIGIN not attend for the 30 day clinical examination; ** patients needed further
emergency treatment) (Hasselgren, G., Reit, C.,1989. Emergency pulpotomy:
Diagnosis pain relieving effect with and without the use of sedative dressings. J Endod
15 (6), 254–256)
Inflammation and infection of the periodontal tissues may cause severe
pain. The purpose of the periapical inflammatory lesion is to restrict infec-
tion to the tooth; therefore, the seriousness of the problem escalates when Acute apical periodontitis is an acute inflammation of the periodontal
it has failed in this remit and infection is spreading to subjacent tissues ligament, generally related to pulpal inflammation but occasionally result-
and other parts of the body. ing from acute or chronic trauma.
It is important to establish whether the pain and swelling involving the An acute apical abscess (Fig. 10.24a) may develop as incipient apical
supporting tissues is of periodontal or pulpal origin. Classically, pulp tests periodontitis or from a pre-existing chronic lesion. In the incipient lesion,
will help to differentiate the origin unless, of course, there is partial necro- the tooth involved does not exhibit an apical radiolucency and will be
sis. Careful periodontal probing should supplement the examination. exquisitely painful to touch.
 Management of acute emergencies and traumatic dental injuries  271

A B C D

Fig. 10.24  (a) Acute apical abscess with facial swelling; (b,c) swelling of chin associated with mandibular anterior teeth; (d) large mandibular radiolucency
related to the incisor teeth

In acute exacerbation of a chronic lesion, the tooth may be extruded

from the socket and in later stages become mobile; the pus collects locally
(Fig. 10.24b–d).
Depending upon the nature of infection, host response and effectiveness
of initial treatment, pus may spread by direct continuity through tissues
planes or spaces, through the bloodstream or through the lymphatics.
Spread through the bloodstream may cause thrombophlebitis, which may
propagate along veins, for example, entering the cranial cavity via emis-
sary veins to cause cavernous sinus thrombophlebitis. Lymphatic spread
may reach lymph nodes and eventually the bloodstream. Organisms or
infected emboli may lead to bacteraemia, septicaemia and pyaemia, with
embolic abscesses. Although, the advent of antibiotics had made these a A B
thing of the past, the increase in resistance to antibiotics and increasing
occurrence of malnutrition among drug and alcohol addicts, viral infec- Fig. 10.25  (a) Lateral and (b) frontal photographic views showing drainage
tions, diabetes and immunosuppression may lead to susceptibility. inserts for treatment of Ludwig’s angina
The spaces are not normally apparent and contain loose connective
tissue but tissue planes separate into such through the force of spreading
fluid or pus. The direction of spread is dictated by the site of source, the
develops rapidly involving the sublingual tissues and distends the
initial direction of spread (buccal or lingual), and tissue attachments (Fig.
floor of the mouth and forces the tongue up against the palate. The
3.19e–g). Muscle attachments, such as those of the mylohyoid, buccina-
patient is very ill with marked pyrexia. There is difficulty in
tors, masseter, medial and lateral pterygoids, temporalis and the superior
swallowing and speech, with progressive dyspnoea, leading to
constrictor of the pharynx play important roles. Also important, although
oedema of the glottis and complete respiratory obstruction.
to a slightly lesser extent, are fascial layers, such as the investing layer of
Untreated, the condition can be fatal in 12–24 hours. Management
deep cervical fascia, the prevertebral fascia, the pretracheal fascia and the
involves intravenous antibiotic therapy, rehydration, analgesics and
carotid sheath. The potential spaces in relation to the mandible are the:
antipyretics under medical care, draining the abscess and tooth
 Submental space – via lymphatic spread from lower incisors; extraction. Drainage may require extra-oral skin incision, blunt
distinct firm swelling under the chin with discomfort on dissection to open the abscess locules and insertion of bilateral
swallowing drains to permit continuous drainage from the sublingual spaces for
 Submandibular space – via lingual spread from second or third 24–48 hours (Fig. 10.25). The purulent collection should be sent
molars; firm swelling of the submandibular region, with some for microbiology investigation to determine antibiotic sensitivity, in
bulging over the lower border case of resistance
 Sublingual space – via spread from premolars but also occasionally  Buccal space – via mandibular molars draining buccally; firm
from canines and incisors; firm swelling in anterior part of the floor swelling just behind the angle of the mouth reaching to the lower
of the mouth, which raises the tongue. There is pain on swelling. border of the mandible
Ludwig’s angina – is a firm cellulitis simultaneously affecting the  Submasseteric interval – via third molar or other mandibular
submandibular, submental and sublingual spaces bilaterally. This molars draining backwards and buccally subperiosteally. External
usually arises from infection of the third molar. There is a massive facial swelling limited to masseter boundary and acutely tender
firm bilateral submandibular swelling, which extends down the limiting opening. Untreated, can become chronic with osteomyelitis
anterior part of the neck to the clavicles. Intraorally, a swelling of the cortical plate
272  Management of acute emergencies and traumatic dental injuries
 Pterygomandibular space – via third molars or infection spread by
injection upon inferior dental nerve block posterior superior block.
There is limited external swelling but there is severe limitation of
opening and dysphagia
 Lateral (para)pharyngeal space – via third molars; there is extreme
pain on swelling with limitation of opening and considerable
pyrexia and malaise. The tonsil and lateral pharyngeal wall are
pushed inwards but there is little external facial swelling. This is a
serious infection and complications include thrombophlebitis of the
internal jugular vein, erosion of the carotid artery may be fatal; this
may be presaged by inequality of the pupils because of
involvement of the cervical sympathetic chain.
The spaces in relation to the maxilla are:
 Within the lip – via upper incisors or canines; infection remains
behind the orbicularis oris which, as they take origin at the anterior
nasal spine, results in the swelling pointing over the lateral
incisors. Rarely, infection may spread to the cavernous sinus
because the veins have no valves
 Within the canine fossa – via the canine or premolar draining
buccally. If the root is short, pus may drain below the levator
anguli oris and point to the buccal sulcus. Otherwise, the pus may
travel up between the levator labii superioris and levator superioris
alaeque nasi to point below the medial corner of the eye. There
may be considerable swelling of the cheek and upper lip;
nasolabial fold may be obliterated and there may be oedema of the
Fig. 10.26  Closure of
eye associated with
infection thought to
arise from maxillary
canine
B C
lower eyelid (Fig. 10.26). There is risk of cavernous sinus
thrombosis
 Palatal subperiosteal interval – the palatal mucosa is closely
tethered to the periosteum, particularly at the gingival margin and
median suture. Infections associated with the maxillary lateral
incisor are closer to the palate and drain into the palatal aspect
separating the periosteum and producing a circumscribed fluctuant
swelling; it rarely crosses the midline but may track backwards to
the soft palate (Fig. 10.27)
 Maxillary antrum – the relationship between the antrum and apices
of maxillary teeth varies but most commonly second and first
molars may be close, followed by the third molar, premolars, or
even the canine. Infections arising from these generally drain
buccally or even palatally but may rarely drain into the antrum.
Usually, proximity of the apices may cause mucosal thickening in
the overlying antrum. Pus draining into the antrum may result in
acute sinusitis
 Infratemporal fossa space – this space is continuous with the upper
part of the pterygomandibular space and, in contrast to the lower
space, is infected by the maxillary molars or contaminated needles
during injection. Infection may spread deep to and lateral to the
temporalis muscle. There may be marked limitation of opening.
The swelling is subtly evident as a filling out of the hollow behind
the zygomatic process of the frontal bone. Infection of this space is
serious because of the presence of pterygoid plexus of veins, which
communicate with the cavernous sinus
 Subtemporalis muscle interval – the above infection may track
further upwards to produce this infection.
Treatment
Emergency treatment of a periodontal abscess will involve institution of
drainage, debridement of the pocket and, when required, antibiotic pre-
scription. Root canal treatment of a tooth with acute apical periodontitis
should aim to ensure that the canal system is thoroughly debrided without
inflicting further insult to the apical tissues by over-instrumentation or
extrusion. Occlusal adjustment to relieve contacts may initially be helpful.
The priority for pain relief in an acute apical abscess is to establish
drainage through the root canal system (Fig. 10.28); incision and drainage
are not productive. The tooth, if tender, should be stabilized while the
Fig. 10.27  (a) Palatal
swelling associated with
maxillary lateral incisor; (b,c)
aspiration from the palatal
swelling using a wide-bore
needle and syringe
 Management of acute emergencies and traumatic dental injuries  273
Fig. 10.28  Tooth
drainage of an apical
abscess
access cavity is being cut as the vibration from the hand-piece will induce
extreme pain, despite anaesthesia.
In acute exacerbation of a chronic lesion, any fluctuant swelling should
be incised to establish drainage. Under local anaesthesia, an incision
should be made using a No. 11 blade through the point of maximum fluctu-
ance, parallel to the surface of the alveolar bone in the labial sulcus or
anteroposteriorly parallel to the nerves and blood-vessels in the palate, to
liberate the contained pus. If pus has not been found, a closed blade mos-
quito artery forceps can be used to thrust through the incision and advance
deeper into the abscess and then open to liberate the pus. The space can
then be irrigated with saline using a wide-bore irrigation needle. The canal
system should then be thoroughly debrided and irrigated, preferably using
ultrasonic agitation, the access is sealed with calcium hydroxide to prevent
recontamination. Only when there is profuse, uncontrollable drainage
should a tooth be left open to drain for a maximum period of 24 hours.
This normally occurs when the problem is caused by an infected cyst; the
exudate being clear, yellowish, and sometimes mixed with blood or pus.
Management of a spreading infection and cellulitis with raised body
temperature must involve establishment of local drainage through soft
tissues and/or root canal system and prescription of antibiotics. The age-old
adage, “do not let the sun set on accumulated pus” still holds true and
should be complied with wherever possible to achieve drainage.
Incision and drainage requires knowledge of tissue spaces, where pus
may accumulate, and knowledge and confidence to deal with the anatomi-
cal structures. Incision and drainage are indicated where evidence of pus
is indicated by dusky redness in the general redness of a firm swelling (see
Fig. 10.24c), where there is localized tenderness over the centre of a swell-
ing, where there is pitting oedema in the middle of a previously firm
swelling. Where the clinician feels they lack adequate skill, the patient
should be promptly referred for appropriate care. Adequate anaesthesia is
paramount and the presence of the pus and infection dictates that anaes-
thetic is deposited proximally or regionally for effectiveness. The incision
is made intra-orally wherever possible, directly over the most fluctuant
part, firmly and down to the periosoteum and should be wide enough to
drain the whole cavity. In general, knowledge of surgical anatomy will
help avoid important vessels and nerves, for example, incision of a palatal
abscess should be performed in an anteroposterior direction to avoid divid-
ing the greater palatine vessels. Once incised, the scalpel blade is not
required and is replaced with a pair of mosquito artery forceps to explore
and open up locules of pus, which may be aspirated away. The site
and incision may be washed with saline. A drain, consisting of a radio-
paque non-resorbable material, such as plastic is secured with a suture for
2–3 days.
Fig. 10.29  Extraoral drainage of a
tooth abscess
If ever an extra-oral incision is called for, it should ideally be undertaken
by a surgeon with insight about anatomical structures and management of
such incisions. They should follow the lines of Langer and skin creases,
otherwise the principles are the same. Particular care is also required for
drainage of pus from tissue compartments that are inaccessible (pterygo-
mandibular, lateral pharyngeal, submasseteric, infratemporal) and where
it may be impossible to elicit classic signs of suppuration.
Management of an unresponding spreading infection and cellulitis that
appears to begin to involve the floor of the mouth and upper neck or
towards the cavernous sinus, must involve prompt referral to a hospital
for emergency care involving immediate drainage of the relevant tissue
compartments, tooth extraction if necessary and intravenous antibiotics
(Fig. 10.29). These patients need constant monitoring, if necessary in
intensive care, to control respiratory difficulty. Maintaining airway patency
is of the highest priority because swelling makes oral endotracheal intuba-
tion difficult. Fibreoptic nasotracheal intubation performed under topical
anaesthesia in the operating room or intensive care unit with the patient
awake is preferable. Some patients require a tracheotomy. Patients without
immediate need for intubation require intense observation and may benefit
temporarily from a nasal trumpet.
Pus samples should be obtained, where possible, using a wide-bore
needle enables anaerobic culturing. Both aerobic and anaerobic culture and
antibiotic sensitivity tests should be performed to inform any required
subsequent therapy. The approach also enables drainage of an abscess (see
Fig. 10.27b, c).
Successfully controlled infection is apparent in the drop in the patient’s
body temperature, a reduction in malaise and toxaemia, relief of pain and
a reduction in the swelling. Initial signs include the appearance of fine
wrinkles where the skin may have been tense, red and shiny.
Medication
Antibiotics are indicated when patients have toxic systemic effects and a
raised temperature. There is currently insufficient evidence to advocate the
use of one regimen over another. Increasingly, short-term antibiotics are
being used. For patients who are not allergic to penicillin, a two-dose
regimen of 3G amoxicillin can be used. Alternatively, for most patients,
where drainage has been instigated, 2 or 3 days of oral antibiotics, given
in a high dose, will suffice for acute dentoalveolar infections; amoxicillin
250 mg every 8 hours. Metronidazole is active against anaerobic organ-
isms, which are commonly found in acute dental infections. It is often
given in combination with amoxicillin with good effect. However, it has
also been shown to have good efficacy in isolation, possibly because the
true nature of dental infections is not properly appreciated. If local patterns
 274  Management of acute emergencies and traumatic dental injuries

Table 10.3  Combinations of possible injuries

Hard dental tissue injury

No other + Periodontal ligament + Alveolar fracture + Facial skeleton + General + Head
Supporting tissue injury injuries injury (crushing/tearing) (single/multiple) injury injuries injury
Enamel fracture √ √ √ √ √ √
Enamel & dentine fracture √ √ √ √ √ √
Enamel/dentine fracture and pulp exposure √ √ √ √ √ √
Crown/root fracture √ √ √ √ √ √
Root fracture √ √ √ √ √ √

of antimicrobial resistance indicate a high prevalence of resistance to Fig. 10.30  Young patient with facial
amoxicillin then the use of either metronidazole (400 mg 2–3 times daily) and possible head injuries
or amoxicillin in combination with clavulanic acid should be considered
as alternatives. Clindamycin remains an alternative in individuals who are
allergic to the penicillin group of antibiotics. It is advisable to review all
patients within 24 hours.
Analgesic regimens should be employed as discussed above, titrated
against the patient’s needs.

EMERGENCIES RESULTING FROM ACUTE

DENTOALVEOLAR TRAUMA
Triage
Acute traumatic injuries to the dentoalveolus may occur at any age but
presentation in a practice environment is likely to be dictated by the seri-
ousness of the overall injuries and the nature of the healthcare system.
Dentoalveolar injuries are often accompanied by other injuries, the seri-
ousness of which may sometimes reduce the relative importance of the
dental injuries, in priority. Injuries may consist of any combination depicted
treatment instigated in timely fashion. Traumatic incidents may result in
in Table 10.3.
either displacement (luxation/avulsion) or breakage (fractures of crowns/
A triage process is necessary to decide on such priorities and will be
roots) of teeth, with or without damage to the supporting tissues. Although
routine practice in a hospital environment, where serious injuries are gen-
it is convenient to describe individual injuries and their management in
erally directed. Road traffic accidents, serious assaults and industrial acci-
isolation for books, guidelines (Flores et al., 2007a–c) or for instruction,
dents, often involving adults are directed to hospitals, where airway and
the reality is that traumatic injuries are unpredictable and occur in diverse
breathing, bleeding, head injuries, cardiovascular problems and serious
combinations in different patients. Therefore, treatment need must be
skeletal and life-threatening injuries will be dealt with first.
determined and prescribed on an individual basis; the guidelines merely
Somewhat less severe injuries may present directly to a dental practice
serving to form the building blocks for a definitive plan. Before an endo-
where, nevertheless, a triage system should be employed to ensure that a
dontic plan can be implemented, a number of judgements must be made:
serious injury has not been missed. The cause and nature of the injury
should be established by questioning the patient and the accompanying  Determine the nature and extent of the injuries: it is important to
adult. The conversation should be meticulously recorded for potential assess the nature and extent of both bony and soft-tissue injuries.
future medico-legal enquiries. Identify any episodes of loss of conscious- Examination of facial lacerations and skeletal fractures should take
ness, headache, amnesia, nausea and vomiting. The precise details of the precedence over the dental examination. Characterize the nature and
injury, including mechanics, location and timing should be ascertained. extent of the dental and supporting tissue injuries after thorough but
Patients recently involved in traumatic injuries may be in a stunned gentle cleansing and washing of any wounds. Displacement
condition, possibly in shock, anxious and perhaps still trying to adjust to (luxation) of teeth may be minimal (subluxation), lateral
their suddenly changed dental or physical status. Therefore, they may not (combination of crushing, stretching and tearing injuries in
be the most cooperative, for which allowance must be made. A calm, periodontal ligament), extrusive (dominated by stretching and
relaxed, confident manner is essential to reassure the patient that any tearing), intrusive (dominated by crushing) and complete avulsion
further intervention is not going to incur more pain or further damage to (with complete tearing). Any history of previous injury or periodontal
their teeth or face. Patients gain confidence from a confident, systematic disease is pertinent. An assessment should be made of disturbances to
and thorough approach. the appearance, occlusion and the patient’s perception of sensations
Trauma to young patients (Fig. 10.30) and immature teeth are a common in the mouth. Any changes to the integrity, mobility and percussion
cause of dental emergencies and often arise from sport and play; those sound of teeth should be noted. The nature of observed injures should
with class 2 division 1 malocclusions being more susceptible. These inju- be consistent with the described version of events. Soft and hard
ries can leave patients requiring dental treatment for many years, espe- tissue radiographs should be taken as required determining soft tissue
cially if the extent of the injury is not properly diagnosed and the correct impregnation and alveolar fractures
 Management of acute emergencies and traumatic dental injuries  275
 Determine those teeth that can and those that cannot be saved: the
extent of dental damage (nature and extent of coronal/radicular
fractures) should be assessed and their prognoses established.
Efforts required to retain the teeth should be considered, in the
light of the patient’s overall treatment needs (including any
relevant medical conditions), in order to reach a balanced decision
regarding the future of the teeth
 Determine the priorities of treatment, divided into short-, medium-
and long-term plans: a sequence will be agreed with the patient for
the order, in which hopeless teeth may be extracted, painful teeth
stabilized and managed to alleviate pain (coverage of exposed
dentine or pulp extirpation), soft- and hard-tissue radiographs
taken, antitetanus and antibiotic cover provided, temporary
restorative solutions implemented to preserve aesthetics, space,
function and speech (temporary dentures, resin-retained or Essix-
retained teeth), vital pulp therapy, root canal treatment, restorative
work provided, regular review protocol established, and
contingency for longer term failure and the need for, and referral to
specialist colleagues established.
ACUTE MANAGEMENT
The principles of acute management of traumatic dentoalveolar injuries
are as those for the management of any acute injury. They are to:
 replace or approximate displaced parts
 stabilize repositioned parts to allow optimal primary healing
 dress or cover exposed part(s)
 rest the injured part(s) or allow only physiologic movement to
allow optimal healing.
These principles are applied below to facilitate immediate management
of dentoalveolar injuries.
Crown fractures
Crown fractures may involve only the enamel or both the enamel and the
dentine (Fig. 10.31a). The damaged tooth should be assessed (clinically,
radiographically and through pulp testing) before deciding on the nature
of stabilization and protection required. Enamel may be smoothened or
rebuilt with composite to stabilize the tooth position. Exposed dentine is
protected with a liner and a bonded composite. It may be possible to reat-
tach the fractured portion of the tooth as the restoration (Fig. 10.31b).
Fracture resulting in pulpal exposure requires the additional and prior
consideration of vital pulp therapy to protect the pulp through dentine
regeneration. The emphasis on such a conservative approach is even
greater for teeth with immature roots, in order to encourage continued root
development. If the exposed pulp is judged to be superficially infected and
necrotic, partial removal of the pulp may be considered. Alternatively,
if the pulp is judged to be beyond regeneration, pulpectomy may be con-
sidered. Details of the vital pulp therapy procedures are provided in
Chapter 7.
Crown–root fractures
The treatment of crown–root fractures depends largely on their location,
orientation and the degree of mobility of the coronal portion. To embark
on a complex and costly treatment plan, the longevity of the planned
restorative strategy must be assured without the risk of incurring damage
to the structures that may facilitate future restorative options, such as
implants. The need for surgery to expose the margins of the fracture,
orthodontic extrusion of the root to facilitate restorative procedures, and
space maintenance to avoid later restorative problems should be borne
in mind.
Fig. 10.31  (a) Maxillary
incisor with complicated
crown fracture (courtesy
of Department of Child
Dental Health, Leeds
Dental Institute). (b)
Subsequent restoration
of maxillary incisor
using fractured section
(courtesy of Department
of Child Dental Health,
A
Leeds Dental Institute)
B
Root fractures
Traumatic impact injuries may cause a variety of patterns of root fractures
which, because of the nature and direction of force, will generally tend to
be transverse or oblique but may also be vertically oriented. Transverse
root fractures may occur in any third of the root and in conjunction with
the level of injury to the alveolar housing will dictate the level of mobility.
Traditionally, root fractures below the level of the alveolar crest, unex-
posed to the oral environment, have been splinted for long periods, up to
12 weeks, to secure union of the fragments. Although, this length of time
for splinting may only be necessary in situations where there has been
displacement and considerable mobility of the coronal fragment. Where
there is no increased mobility, splinting may not be required and the tooth
should then be reviewed clinically and radiographically at 3, 6 and 12
months.
The degree of displacement of the coronal root fragment may also
determine the extent of damage to the pulp. Pulp testing may be unreliable
for a period of 2 to 6 months, although recovery up to 12 months is also
possible.
If the tooth remains firm and the pulp remains responsive, no further
treatment is necessary. Many undiagnosed fractures remain symptomless
and cause no problems (Figs 10.32, 10.33). Sometimes, a coronal level
root fracture, although having increased but not increasing mobility, may
survive if allowed to for years; in the cases shown, one tooth has survived
for 30 years (Fig. 10.34) and another for 20 years (Fig. 10.35).
If the pulp response is not regained, generally (in about 25% of cases),
the coronal segment may become necrotic with evidence of pulp infection
indicated by a developing radiolucency at the fracture line (Fig. 10.36b).
In others, the pulp may become symptomatic (Fig. 10.37a). In either case,
root canal treatment may then be performed to the fracture line. Calcium
hydroxide is used as a long-term medicament to encourage calcification
(Fig. 10.36b) and formation of a hard-tissue barrier, against which the
obturating material can be compacted (Figs 10.36c, 10.37b). Sometimes,
the calcium hydroxide may not be effective in inducing an effective calcific
 276  Management of acute emergencies and traumatic dental injuries

Fig. 10.34  (a) Incisor

with longstanding
(30 yrs) horizontal
fracture. (b) radiograph
of the same tooth
confirming an absence
of previous interventive
treatment

Fig. 10.32  Symptomless, healed Fig. 10.33  Symptomless,

root fracture undiagnosed root fracture

A B C

Fig. 10.36  (a) Horizontal middle third fracture of maxillary incisor; (b) calcium hydroxide dressing to fracture line;
(c) obturation of fractured incisor to fracture line

Fig. 10.35  Incisor with longstanding

horizontal fracture survived for 20
years

barrier (Fig. 10.38a–c) and allow some extrusion of root filling material,
however, the apical fragment may survive with pulp obliteration
(Fig. 10.38d). In fact, it should be noted that pulp obliteration is the general
outcome in the apical fragment (Figs 10.36c, 10.37b, 10.38d). Alterna-
tively, MTA can be placed apically to act as a hard tissue barrier or, indeed,
to act as the entire root-filling material, although the long-term effects of
this latter approach are not known. Root canal treatment of both fragments
is only necessary in the case of apical changes (very rare) or if it is impos-
sible to control file length adequately during the procedure (Fig. 10.39).
When the whole pulp becomes necrotic, surgical removal of the apical
portion may be a more manageable option.
Roots of molar teeth may also be fractured through trauma, such as in
this case where the patient was struck by a cricket ball, fracturing the
mesiobuccal root (Fig. 10.40a). The root was removed and, as the pulp
presented a clinically healthy looking surface, it was pulp capped and
restored with glass ionomer cement (Fig. 10.40b,c). After 2 years, unfor-
tunately, the glass ionomer cap became loose, the pulp was in the early
stages of necrosis, requiring extirpation (Fig. 10.40d). The problem was
that there was no secure means of restoring the pulp cap as there was no
cavity; the reliance being on adhesion, which failed after a time.
Sometimes, teeth with pre-existing root fillings and posts may also be
traumatized and present with a fracture. The stress concentration, whether
 Management of acute emergencies and traumatic dental injuries  277
due to chronic fatigue or impact injury, occurs at the apex of the post,
where the fracture line is or, in due course, radiolucencies may present
(Fig. 10.41).
Treatment of luxated teeth
The nature of luxation or tooth displacement is categorized as subluxation
(minimal), lateral luxation, extrusive luxation, intrusive luxation and avul-
sion. These terms define both the nature and extent of crushing or stretching/
tearing injuries inflicted on the periodontal ligament. They may further be
accompanied by injuries to the alveolar housing, as well as the tooth
structure and neurovascular supply to the pulp. Displaced teeth should be
repositioned and stabilized. The original position of the teeth may be dif-
ficult to determine sometimes if the teeth were previously irregularly
arranged. Clues may be obtained from occlusal faceting caused by
parafunction and from pre-injury photos of the patient smiling (which are
not always available when needed).
A B
Fig. 10.37  (a) Maxillary incisor with middle-third horizontal fracture;
(b) fractured incisor following root canal treatment to the fracture line
A B
C
Fig. 10.38  (a–c) Calcium hydroxide failed to induce an effective calcific barrier at the apical end of the coronal fragment; (d) apical fragment survived with pulp
obliteration
Many types of splint are available for stabilizing repositioned, replanted
and fractured teeth. The requirement of the splint may be to achieve rigid
fixation if there is extensive root and alveolar bone fracture or semi-rigid
fixation if the purpose is simply to provide stability with physiological
mobility, that is, avoid accidental redisplacement. As a guide, when mul-
tiple teeth have been displaced with alveolar bone and root fractures, rigid
fixation may be appropriate, involving several uninjured teeth on either
side. The recommended duration of splinting is 1 month but may be
extended up to 4 months if the root fracture is near the cervical region,
while localized avulsion of a single tooth may simply merit a twist-flex
wire attached to the avulsed tooth and one tooth on either side with com-
posite (Fig. 10.42). The use of etched enamel retained composite and
polymethacrylate reinforced with wire or nylon has also been advocated.
Reimplanted teeth are generally splinted up to 14 days.
If there is evidence to suggest that the pulp of a luxated tooth has
become necrotic and infected, root canal treatment should be initiated.
Completely avulsed teeth that have been replanted should undergo
root canal treatment 7–10 days following replantation. The possibility
of replacement resorption (Fig. 10.43) can neither be predicted nor
treated.
INTRAOPERATIVE EMERGENCIES
True intraoperative emergencies should be few if planning and preparation
have been effective. They can be divided into medical problems and the
hypochlorite accident.
MEDICAL EMERGENCIES
It is every dental professional’s ethical and moral responsibility to ensure
that they have knowledge and skills to deal with any medical emergency
that may arise in their practice. Although rare, it is estimated that the
average dentist can encounter a medical emergency every 16 months; a
problem more likely in an ageing population. Dentists are now required
to have training in cardiopulmonary resuscitation (CPR), basic airway
management and the use of an automatic external defibrillator (AED),
which is updated annually.
Hopefully, a good medical history will have identified those patients
who may be at risk from a medical emergency. There are very few, if any,
D
 278  Management of acute emergencies and traumatic dental injuries
medical conditions that preclude the possibility of endodontic treatment,
especially as the alternative is often a tooth extraction with the entire
attendant trauma. However, special arrangements may have to be in place
to guard against possible problems. Diabetics may wish to be seen at a
certain time of day so that their routines are not disturbed with the pos-
sibility of a hypoglycaemic attack occurring. Consultation with other spe-
cialists is often of benefit where the use of corticosteroids may be involved
for those patients who have adrenal insufficiency. The prepositioning of
intravenous access would allow a quicker and possibly less-panicked
response in the case of an emergency.
A B
Fig. 10.39  (a) Maxillary incisor with horizontal fracture; (b) root canal
treatment of fractured incisor because of pulpal symptoms
A B
Fig. 10.40  (a) Mesio-buccal root of the maxillary first molar with horizontal fracture. (b,c) The mesio-
buccal root in (a) was amputated and exposed pulp capped and restored with glass ionomer cement. (d)
D
The glass ionomer cap in (c) debonded after 2 years
While the treatment for vaso-vagal syncopy is to lay the patient flat,
during pregnancy, laying the patient flat can induce syncopy. Treatment is
to remove the pressure of the fetus on the vena cavae by raising the patient
forward.
Cardiovascular conditions in the mildest form would present as angina
attack, for which the patient should be able to self-medicate, although
having a glyceryl trinitrate inhaler in the practice is advised, ideally with
blood pressure monitoring. Patients exhibiting signs of a myocardial inf-
arction should be given oxygen and the emergency services called promptly.
CPR training should be engaged as required.
One of the most serious medical emergencies in the practice is anaphy-
laxis. A patient can have an anaphylactic reaction to many materials. There
has been a reported increase in reactions to latex. The use of rubber dam
in endodontics makes this occurrence particularly important. A medical
history showing food intolerance to bananas and avocados may show a
cross-reaction to latex. Patients can develop a reaction to latex with a
number of exposures. Where patients show possible early signs, such as
tingling of the lips, then latex-free rubber dam and gloves should be con-
sidered. Where there are the signs of an anaphylactic reaction, adrenaline
(epinephrine) (0.5–1 ml 1 : 1000 intramuscularly in adults) and oxygen
should be administered as a first line of management. The emergency
services should be called immediately.
SODIUM HYPOCHLORITE
Ironically, although the chief problem of irrigation is irrigant delivery to
the apical part of the canal, it is suspected that, in most cases, there may
be some seepage or diffusion of the irrigant into the periapical tissues,
which probably causes little harm. Very occasionally, extrusion of a suf-
ficient bolus of irrigant may cause adverse reactions, particularly when
using sodium hypochlorite (NaOCl) (Hülsmann & Hahn, 2000). Acciden-
tal injection of NaOCl into the periapical tissues via the apical terminus
or root perforations can cause sudden sharp severe pain, immediate swell-
ing (Fig. 10.44) and profuse bleeding. A NaOCl accident would more
 Management of acute emergencies and traumatic dental injuries  279

likely occur when NaOCl had direct access to a soft-tissue space, such as alveolar bone had been perforated by the disease process. Extrusion of
the buccal or infraorbital, cyst or maxillary sinus rather than simply con- high concentration (5%) NaOCl may cause extensive tissue damage result-
tacting periapical tissue. This is more commonly reported in the maxilla ing in tissue necrosis. Lower concentration may increase vascular perme-
than in the mandible and might happen when the anatomic apex of a tooth ability, probably as a result of damage to the blood vessels, as well as the
naturally fenestrated through the overlying alveolar bone or when the release of chemical mediators, such as histamine, from involved tissue.
This characteristic causes immediate swelling and often profuse bleeding
through the root canal.
It must be stressed that great care should be taken when using NaOCl.
Fig. 10.41  Maxillary The bore of any needle used should be large enough to allow the free flow
incisor with an oblique of the disinfectant without the application of undue pressure. A “side-
root fracture apical to venting” needle is less prone to apical extrusion. It is always wise to check
the post and associated that it is securely fastened to the syringe and it is worth considering the
with a periradicular
placement of a rubber stop on the needle short of the working length. The
radiolucency
needle should not bind in the canal and it should be possible to keep the
needle moving within the canal. The irrigant should be expressed slowly
and irrigation should be stopped if any resistance to the plunger is felt.
The potential for extrusion when using negative pressure, sonic or
ultrasonic systems has been investigated using extracted tooth models with
pre-prepared canals. No evidence of extrusion of irrigant was found using
the negative pressure EndoVac® system but a minimal amount was
extruded using the sonic EndoActivator™. Both these techniques had
significantly less extrusion than manual dynamic irrigation (pumping of
irrigant using a matching gutta-percha point), automated dynamic irriga-
tion (RinsEndo handpiece) or ultrasonic active irrigation. There is,
however, a higher risk of apical extrusion of irrigant delivered through the
RinsEndo handpiece than irrigant delivered manually through syringe
Fig. 10.42  Twist-flex
irrigation. Ultrasonic irrigation during canal preparation was found to
wire splint (courtesy of result in significantly more extrusion than dynamic syringe irrigation.
Department of Child Limiting the extension of the needle or ultrasonic file 1 mm short of canal
Dental Health, Leeds terminus could reduce extrusion.
Dental Institute) When a hypochlorite accident occurs, the patient will report a sudden
sharp pain despite effective dental anaesthesia. The patient will be clearly
alarmed as often will the dentist. It is important for the clinician to stay
calm and reassure the patient. The canal benefits from being washed with
sterile water. Further analgesic may be administered to relieve pain. The
tooth should be monitored over the next half an hour; there may be a
bloody exudate. Drainage should be encouraged. Antibiotics should be
considered in serious cases if there is a risk of infection.
Corticosteroids assist in limiting the swelling. The use of cold com-
presses for 6 hours will help to reduce pain and swelling. Following this,
warm compresses will help to encourage healthy healing. The patient
should be warned of swelling and consequent bruising.
In the case of maxillary teeth, injection into the maxillary antrum is a
risk; the patient may report the smell and taste of bleach, in addition to
sudden pain. Likewise, in mandibular teeth, injection into the inferior
dental nerve canal is a risk, with consequent neural damage. Extrusion into
the muscle mass may lead to scarring and facial asymmetry in rare cases.

INTERAPPOINTMENT AND
POSTOPERATIVE EMERGENCIES

Patients may experience pain after canal preparation and cleaning or fol-
lowing obturation of the root canal system; it is a normal finding in almost
half of all patients. The presence of preoperative pain guarantees postop-
erative pain owing to pre-existing hyperalgesia. This can take 3–4 days to
Fig. 10.43  Replacement
subside but will be maximal over the first 24–48 hours. Other predictors
resorption affecting
maxillary incisor Fig. 10.44  Soft tissue swelling of postoperative pain are female gender, presence of necrotic pulp tissue
(courtesy of Department following a sodium hypochlorite and apical periodontitis, presence of allergies, previous history of painful
of Child Dental Health, accident treatment and manual dynamic irrigation. It is as well to forewarn the
Leeds Dental Institute) patient and give medication advice.
 280  Management of acute emergencies and traumatic dental injuries
Acute apical periodontitis is common following root canal preparation
and is due to over-instrumentation, extrusion of medicaments, and
incomplete canal preparation (due to inadequate length or irrigant penetra-
tion) and traumatic occlusion. Teeth with pre-existing chronic lesions
without sinus formation or symptoms are more prone to interappointment
exacerbation. It is thought that this may be explained by the altered adapta-
tion syndrome, where a change in the chronic balance between the micro-
biota and host is altered; the response may be dominated by exudate rather
than pus. A patient who is allergic to various substances, or is atopic, may
be more susceptible; readiness with their usual antihistamine medication
may prove helpful.
Management of interappointment problems depends on the preoperative
diagnosis and the presenting symptoms. A tooth with a previously vital
pulp, treated by complete cleaning and shaping generally does not require
emergency attention, only reassurance. Teeth undergoing incomplete vital
pulpectomy because of shortness of time may benefit from dressing with
a corticosteroid medicament; completion of root canal treatment should
follow swiftly afterwards.
Teeth with previously necrotic pulps and an absence of swelling at
presentation should be reopened and irrigated to allow any exudate to
Fig. 10.45  Carious
maxillary premolar
Fig. 10.46  Root canal over-filling in
mandibular molar
B
A
C
drain, after which the canals should be gently instrumented and irrigated
with sodium hypochlorite. A calcium hydroxide dressing should be placed
and the access sealed. In contrast, teeth with previously necrotic pulps and
presence of a swelling at presentation should have incision and drainage
performed and the canal system re-irrigated. This process should also
involve a search for any missed canals and their appropriate management.
The access should be sealed; there are few indications for leaving teeth on
open drainage.
Interappointment discomfort is also encountered with leaking restora-
tions, which allow recontamination of the canal system. The area of
leakage must be found and the problem dealt with. Where a pre-existing
crown has been retained and access gained through it to complete an
endodontic procedure, its marginal integrity should be critically assessed
(Fig. 10.45).
The probable causes of pain following obturation of the root canal
system are inadequate cleaning of the root canal system, extrusion of
irritant materials (Fig. 10.46), root fracture precipitated by the filling pro-
cedure (Fig. 10.47) and traumatic occlusion.
Pre-informing patients about possible discomfort in the first few days
following root canal treatment and advice regarding analgesics will reduce
the patient’s anxiety regarding postoperative pain. Where patients do
require follow-up treatment, this may involve reassurance, advice on the
use of analgesics (and possibly antibiotics), removal of the root filling and
repreparation of the root canals, and surgical endodontic treatment to
remove extruded material or resection of the root. There are a few cases
where the symptoms do not respond to further therapy, in which case
extraction may need to be considered.
MEDIUM- TO LONG-TERM MANAGEMENT OF
DENTOALVEOLAR INJURIES
Emergency treatment of patients with traumatic injuries is only the begin-
ning of a long journey, if the patient is compliant enough to stay the course.
The problem with a proportion of adult dentoalveolar trauma patients
is that the precipitating factor (drug or alcohol addiction, violent behav-
iour) also selects non-compliance. Given the nature of circumstances in
which the injuries are incurred, often there may be accident or criminal
compensation queries to deal with either from insurance or law agencies.
Medical records will therefore inevitably come under external scrutiny,
placing added pressure to ensure comprehensive, accurate and legible
recording.
The dentist may also be asked to contribute to prognostication and
estimation of the patient’s needs for future aesthetic and functional
Fig. 10.47  (a) Radiographic appearance of root with
vertical bone loss; (b) further bone loss – suspected
vertical fracture precipitated by the obturation procedure;
(c) extracted root with fracture (all courtesy of Mr AF
Speirs, Leeds Dental Institute)
 Management of acute emergencies and traumatic dental injuries  281
demands to calculate the costs, although this is likely to have been an
exercise the dentist will have entered into with the patient. The difference
is that the patient’s requirements will be spread over many years and the
costs are therefore difficult to estimate, yet the compensation boards will
require those estimates at the outset, not many years later. The dentist
should therefore become familiar with the literature on the natural history
of outcomes of injuries and the outcomes of management approaches. This
may be made somewhat challenging by the relatively limited amount of
such data available, although it must be said that it is fortunate that some
groups have focused on gathering such data very well.
The dentist should understand the nature and timing of healing and
complications associated with various types of injuries, which should have
a biological foundation, confirmed by clinical data. The factors to consider
are injuries to and healing of the dental hard tissues, dental pulp, perio-
dontal ligament and alveolar bone.
HEALING PATTERNS, TRENDS AND
SALIENT FEATURES
Template for wound healing, repair and regeneration
The process of wound healing follows a standard pattern dictated by
molecular signalling from various cell lines. It initially involves a clearing
of the dead tissue by polymorphonuclear lymphocytes (PMNs) and mac-
rophages, which are attracted to the site by release of factors signalling
cell death and foreign matter. The PMNs dominate initially as they are
important in helping to control incipient infection to be replaced by the
macrophages, which play an active role in coordinating the healing process.
As the clearance by phagocytosis and digestion gets under way, the mac-
rophages signal the influx of nutritive elements to the site by the ingrowth
of budding capillary vessels (angiogenesis). Circulating proteins and
immune cells will be attracted by foreign material and bacterial factors.
Following closely behind are undifferentiated mesenchymal cells and
fibroblasts from the perivascular tissues, which slowly but gradually come
to dominate the cell population. The former, depending upon the extent to
which they are able to differentiate into local tissue cells upon chemical
attraction and stimulation, will dictate the regenerative process, while the
latter will aid and support healing and repair.
The balance between regeneration (replacement with original tissue) or
repair (replacement with fibrous tissue) will be dictated by the relative
extent of tissue damage and availability and stimulation of pluripotential
cells. The greater the damage and the more compromised the local pres-
ence of mesenchymal cells, the more likely it is that healing will occur by
fibrous tissue formation.
Pulp
Depending upon the nature of injury, pulp death may be almost instantane-
ous or drawn out over several days to weeks. The peripheral parts, coronal
pulp horns would succumb first and may be found to be dying at about 3
days. The wound healing process described above may enable new blood
vessels to invade at the apical foramen by 4 days, by 10 days these will
have advanced to mid-root and by 30–40 days will have become estab-
lished in the coronal part. Nerve growth lags behind and will have advanced
into the apical portion only by day 14, slowly progressing coronally there-
after. Residual populations of undifferentiated mesenchymal cells in the
pulp or in the apical papilla region may help to reinvigorate the regenera-
tive potential of the pulp in the immature tooth.
Periodontal ligament
Damage to the periodontal attachment may be considered in relation to
both the epithelial attachment and the rest of the fibre attachment. The
initial priority is the epithelial seal, which occurs by mitosis and migration
of basal and prickle cells from adjacent intact tissue. The seal is formed
as early as within 24 hours on the foundation of a fibrin clot. By rapid cell
division, the multiple layers of the epithelium are re-established within 3
days and an intact barrier is evident at 7 days.
The initial coagulum in the periodontal ligament is replaced by a young
connective tissue by 3–4 days. The cells for this process, consisting
of pluripotential undifferentiated mesenchymal cells, originate from the
adjacent periodontal ligament and the endosteum. The cells differentiate
into fibroblasts synthesizing ground substance and collagen, as well as
cementoblasts and osteoblasts that initiate new cementum and bone forma-
tion. Cementoblasts begin to deposit cementoid by 10–12 days, while
osteoblasts deposit osteoid within 10–14 days; new collagen fibres will be
evident at 14 days. By 21–28 days, the full periodontal apparatus, consist-
ing of functional cementum, bone and periodontal ligament fibres will
be established.
Where the damage to the periodontal ligament is excessive, clastic cells
may dominate resulting in resorption of the unprotected hard tissue surface.
In the absence of inflammation, the root surface is recognized as a mineral-
ized surface, which is then modified by resorption and redeposition of
osteoid. This, replacement resorption, may be evident as early as 2 months.
Where excessive periodontal ligament damage is superimposed by
infection either from an inadequate or incomplete epithelial seal or from
infection of the root canal system, the healing process becomes superim-
posed by inflammation. This may fuel a much more aggressive resorptive
process, known as inflammatory resorption, which may be evident at 2
weeks.
Root fracture and apical development
Root fractures may or may not heal depending upon the presence of
optimal conditions; lack of approximation, infection and severe inflamma-
tion may preclude it. Healing may be dominated by connective tissue from
the pulp or periodontal ligament. If the pulp has survived the injury or is
revascularized rapidly enough, pulpal cells can contribute to healing by
forming a dentine callus intrapulpally and cementum callus externally. By
definition, this is only likely if the two fragments are optimally approxi-
mated by repositioning and maintained in such position (by splinting) for
a period of up to 3 months.
The pulp and the apical residue of the dental papilla are responsible for
the ongoing development of the root. Pulp death or damage to the apical
region of the root may arrest root development. Much effort has been
recently spent on devising ways to encourage continued root growth when
the pulp has been compromised. This includes efforts to regenerate the
pulp by inducing apical bleeding to invite mesenchymal pulpal stem cells
into the pulp space. Protection of the apical tissues by eliminating infection
and inflammation appears to encourage continued root growth (apexogen-
esis) (Fig. 10.48). In the absence of such continued root growth, the clini-
cal effort is spent on inducing a calcific barrier (apexification) to prevent
apical extrusion during root canal obturation.
Other ways to prevent apical extrusion includes the use of MTA plug
apically (Fig. 10.49).
Alveolar bone
The healing progression will depend upon the extent of injury to the over-
lying mucosa, epithelial attachment, the bone itself and periosteum. As
for any injury, the immediate aftermath is followed by the formation
of a coagulum. PMNs and macrophages will begin the clearing process by
migrating into the coagulum from the mucosal and endosteal surfaces
and be established by the day 4. Undifferentiated mesenchymal cells and
fibroblasts will migrate into the coagulum by days 4–7; these will
 282  Management of acute emergencies and traumatic dental injuries

Fig. 10.48  (a,b) Continued root growth following

dressing with calcium hydroxide

A B

Fig. 10.49  (a–c) Use of MTA plug for obturating the

maxillary central incisor with immature apex

A C

Table 10.4  Percentage of teeth with pulp survival after various types of injury

1 month 2 months 3 months 6 months 12 months 24 months 36 months 48 months 60 months 10 years
Concussion Closed apex 100 100 97 97 97 97 97 97 97 97
Open apex 100 100 100 100 100 100 100 100 100 100
Subluxation Closed apex 100 100 90 85 85 85 85 85 85 85
Open apex 100 100 100 100 100 100 100 100 100 100
Extrusive Closed apex 100 87 50 50 45 45 45 45 45 45
luxation Open apex 100 99 97 97 95 95 95 95 95 95
Lateral Closed apex 100 90 50 35 25 25 25 25 22 22
luxation Open apex 100 98 97 96 96 94 94 94 94 94
Intrusive Closed apex 100 60 30 3 1 1 1 1 1 1
luxation Open apex 100 90 77 55 48 48 48 48 38 38
Replantation Closed apex – 38 3 1 0 0 0 0 0 0
Open apex – 60 42 35 35 35 35 35 35 35

After Andreasen & Pedersen, 1985; Andreasen et al., 1989

contain osteoprogenitor cells, pre-osteoblasts and osteoblasts. Under

optimal conditions, woven bone will have begun to form between 12 and
14 days. During this healing phase, reorganization of the marginal bone
may occur and result in temporary loosening of the tooth, which may be
evident at 2–3 weeks. Within 3–4 weeks, definitive trabeculae with osteo-
cytes will be evident. Maturation of the initial trabeculae into functional
bone may take between 2 and 4 months. The teeth and, therefore, the bone
may need to be stabilized to facilitate bone regeneration by splinting for
up to 2 months.
CLINICAL DATA FOR PROGNOSTICATION ON
OUTCOMES OF TRAUMATIC INJURIES
It is useful to have clinical data on the outcomes of traumatic injuries and
approaches to their management. A number of groups have taken the
trouble to gather such data meticulously. The tables provide summary
estimates for various sequelae following traumatic injuries.
Table 10.4 shows that regardless of the type of luxation injury, the
presence of an open apex provides the best chance of pulp survival, even
 Management of acute emergencies and traumatic dental injuries  283

in intrusive injuries, which overall have the poorest prognosis. This is

Table 10.5  Percentage of teeth with different types of periodontal healing
probably a reflection of good blood supply via a thick neurovascular after various injuries
bundle that is less susceptible to crushing. Mild luxation (concussion/
subluxation) has minimal effect on the pulp, while crushing injuries Normal Surface Inflammatory
PDL resorption resorption Ankylosis
(lateral and intrusive luxation) inflict the greatest damage on the pulp. It
is evident that there are early and late manifestations of pulp demise; Concussion Closed 90 10 0 0
apex
the early may reflect initial overt or direct damage to the pulp or its
Open 98 2 0 0
blood supply, while the late may reflect gradual damage due to cracks apex
or breaches in the external covering layer, which perhaps propagate Subluxation Closed 90 8 2 0
with time. apex
When luxated teeth are repositioned after alveolar fracture within 1 Open 99 1 0 0
hour, pulp survival is 65%; if repositioned within 24 hours, the pulp sur- apex

vival drops to 20% and if repositioned after 24 hours, pulp survival drops Extrusive Closed 80 15 5 0
luxation apex
to 10%.
Open 86 7 7 0
Table 10.5 depicts the data for periodontal ligament damage after apex
luxation injuries. Once again, teeth with open apices seem to fare Lateral Closed 67 30 3 1
better, presumably because such teeth will be socketed in alveolar luxation apex
bone that is thinner and more resilient. Young bone of such patients Open 90 7 3 0
apex
may be more prone to “green-stick” fracture. Once again, the crush-
ing injuries of lateral and intrusive luxation result in the most unfa- Intrusive Closed 0 30 40 30
luxation apex
vourable healing outcomes, with intrusive injuries being by far the Open 30 20 40 10
worst. apex
When teeth are repositioned after alveolar fracture, 10% may develop
resorption. After Andreasen & Pedersen, 1985; Andreasen et al., 1989
Table 10.6 shows the pulpal effects of superimposition of an uncompli-
cated crown fracture on various luxation injuries. Once again, teeth with
open apices fare the best for reasons already cited. However, additional
crushing injuries on top of a crown fracture inflicts progressively worse
damage on the pulp. Table 10.6  Percentage of teeth with pulp survival after various types of
injury plus uncomplicated crown fracture
Table 10.7 shows the data on root fracture healing when associ-
ated with different types of luxation injuries. Teeth with open apices Pulp survival Pulp necrosis
again show the best healing outcomes, 100% hard tissue union in
No luxation Closed apex 98 2
lateral and mild luxation injuries. In this case, in contrast to the pre-
Open apex 99 1
vious pattern, extrusive luxation fares the worst, presumably because
Concussion Closed apex 88 12
of separation between the fragments. In addition, in mature roots, Open apex 98 2
displacement of the coronal fragment resulted in pulp necrosis in
Subluxation Closed apex 50 50
25% of teeth. Open apex 80 20
Outcome data on pulp survival and periodontal ligament healing fol-
Extrusive luxation Closed apex 20 80
lowing replantation of avulsed teeth are depicted in Tables 10.8 and 10.9. Open apex 60 40
It is unsurprising that the response to complete severance of the blood
Lateral luxation Closed apex 15 85
supply during avulsion is total pulp necrosis in the mature tooth. It Open apex 70 30
is even surprising that there is some evidence of a pulp response up
Intrusive luxation Closed apex 0 100
to 6 months in such teeth. The periodontal healing response following Open apex 0 100
replantation is similar for mature and immature teeth up to 6 months, after
which differences become evident with immature teeth faring better pre- After Andreasen et al., 1989
sumably because of lesser damage to the alveolar housing and root surface
during avulsion.
Table 10.9 depicts the data on pulp survival and periodontal healing
as a function of the amount of time, for which the avulsed teeth were
stored dry prior to replantation. Mature teeth show no chance of Table 10.7  Percentage of teeth with different types of root fracture
healing in various luxation injuries
pulp survival regardless of how minimal the storage time is, while imma-
ture teeth, on the contrary, show potential for revascularization and Granulation Connective Hard tissue
regeneration, which diminishes with extra-oral time from 5 minutes to tissue tissue union
120 minutes. Concussion/ Closed apex 5 20 75
The periodontal healing is again better for immature teeth but only subluxation Open apex 0 0 100
significantly during the first 40 minutes, thereafter (40–120 minutes extra- Extrusive Closed apex 40 45 5
oral storage), the differences between mature and immature teeth diminish luxation Open apex 0 50 50
to a negligible level. Lateral Closed apex 30 55 15
These data may be used to good advantage in predicting the prognosis luxation Open apex 0 0 100
of traumatically injured teeth and formulating long-term treatment plans
and cost estimates. After Andreasen et al., 1989
 284  Management of acute emergencies and traumatic dental injuries

Table 10.8  Percentage of teeth with pulp survival and periodontal ligament (PDL) healing after replantation in permanent dentition

1 month 2 months 3 months 6 months 12 months 24 months 36 months 48 months 60 months 10 years
Pulp survival Closed apex 100 38 5 2 0 0 0 0 0 0
Open apex 100 57 38 30 30 30 30 30 30 30
PDL healing Closed apex 100 90 60 48 25 25 25 25 15 15
Open apex 100 88 60 48 42 42 42 42 38 38

After Andreasen et al., 1989

Flores, M.T., Andersson, L., Andreasen, J.O., et al., 2007b. International Association of
Table 10.9  Percentage of teeth with pulp survival and periodontal Dental Traumatology. Guidelines for the management of traumatic dental injuries. II.
ligament (PDL) healing after replantation following dry storage of Avulsion of permanent teeth. Dent Traumatol 23 (3), 130–136.
different durations Flores, M.T., Malmgren, B., Andersson, L., et al., 2007c. International Association of
Dental Traumatology. Guidelines for the management of traumatic dental injuries. III.
5 mins 20 mins 40 mins 60 mins 120 mins Primary teeth. Dent Traumatol 23 (4), 196–202.
Hasselgren, G., Reit, C., 1989. Emergency pulpotomy: pain relieving effect with and
Pulp Closed 0 0 0 0 0 without the use of sedative dressings. J Endod 15 (6), 254–256.
survival apex Hülsmann, M., Hahn, W., 2000. Complications during root canal irrigation – literature
Open 55 35 25 20 10 review and case reports. Int Endod J 33 (3), 186–193.
apex Khan, A.A., McCreary, B., Owatz, C.B., et al., 2007a. The development of a diagnostic
instrument for the measurement of mechanical allodynia. J Endod 33 (6), 663–666.
PDL Closed 50 28 10 10 10 Khan, A.A., Owatz, C.B., Schindler, W.G., et al., 2007b. Measurement of mechanical
healing apex allodynia and local anesthetic efficacy in patients with irreversible pulpitis and acute
Open 65 65 40 15 12 periradicular periodontitis. J Endod 33 (7), 796–799.
apex Locker, D., Grushka, M., 1987. Prevalence of oral and facial pain and discomfort:
preliminary results of a mail survey. Community Dent Oral Epidemiol 15 (3), 169–172.
After Andreasen et al., 1989 McMillan, A.S., Wong, M.C., Zheng, J., et al., 2006. Prevalence of orofacial pain and
treatment seeking in Hong Kong Chinese. J Orofac Pain 20 (3), 218–225.
Owatz, C.B., Khan, A.A., Schindler, W.G., et al., 2007. The incidence of mechanical
allodynia in patients with irreversible pulpitis. J Endod 33 (5), 552–556.
Peres, M.A., Peres, K.G., Frias, A.C., et al., 2010. Contextual and individual assessment
of dental pain period prevalence in adolescents: a multilevel approach. BMC Oral
Health 10, 20.
REFERENCES AND FURTHER READING Seltzer, S., Bender, I.B., Ziontz, M., 1963. The dynamics of pulp inflammation:
Andreasen, F.M., Pedersen, B.V., 1985. Prognosis of luxated permanent teeth – the correlations between diagnostic data and actual histologic findings in the pulp. Oral
development of pulp necrosis. Endod Dent Traumatol 1 (6), 207–220. Surg Oral Med Oral Pathol 16, 969–977.
Andreasen, F.M., 1989. Pulpal healing after luxation injuries and root fracture in the Steele, J., O’Sullivan, I., 2011. Executive summary: Adult Dental Health Survey (2009)
permanent dentition. Endod Dent Traumatol 5 (3), 111–131. The Health and Social Care Information Centre. www.ic.nhs.uk/webfiles/
Andreasen, J.O., Andreasen, F.M., Andersson, L., 2007. Textbook and color atlas of publications/007_Primary_Care/Dentistry/dentalsurvey09/
traumatic injuries to the teeth, 4th ed. Wiley-Blackwell. AdultDentalHealthSurvey_2009_ExecutiveSummary.pdf (accessed Aug, 2013).
Dummer, P.M., Hicks, R., Huws, D., 1980. Clinical signs and symptoms in pulp disease. Vargas, C.M., Macek, M.D., Marcus, S.E., 2000. Sociodemographic correlates of tooth
Int Endod J 13 (1), 27–35. pain among adults: United States, 1989. Pain 85 (1–2), 87–92.
Flores, M.T., Andersson, L., Andreasen, J.O., et al., 2007a. International Association of White, D.A., Tsakos, G., Pitts, N.B., et al., 2012. Adult Dental Health Survey 2009:
Dental Traumatology. Guidelines for the management of traumatic dental injuries. I. common oral health conditions and their impact on the population. Br Dent J 213
Fractures and luxations of permanent teeth. Dent Traumatol 23 (2), 66–71. (11), 567–572.

Management of tooth resorption
Dental resorption is a physiological or pathological process, which involves
loss of dentine and/or cementum by hard tissue resorbing cells. As a physi-
ological process on the root surface, it is dynamic and continual but is not
clinically detectable. Occasionally, such resorption may be triggered to
become transiently pathological but leaving no long-term consequences;
it is usually detected only by chance. Progressive pathological resorption
may also remain asymptomatic until it reaches an advanced stage. Early
diagnosis and appropriate management is necessary if tooth loss is to be
avoided or delayed. Depending on whether resorption is internal or exter-
nal in nature, different treatment modalities are recommended. Under-
standing the aetiology and pathogenesis of the disease process is essential
for appropriate management of teeth undergoing resorption.
AETIOLOGY AND PATHOGENESIS
Dentine and cementum are protected from resorption by their non-
mineralized structural components (predentine and precementum) and
cells (odontoblasts and cementoblasts). Secretion of an anti-invasion
factor by predentine, precementum and intact periodontal ligament is
thought to prevent attachment of multinucleated resorbing dentinoclasts to
dental hard tissues. Anti-invasion factor has also been found in cartilage
and blood vessel walls. It is believed that the highly mineralized intermedi-
ate cementum layer (hyaline layer of Hopewell-Smith) further prevents
external root resorption by covering the dentinal tubules, acting as a pro-
tective barrier between root-canal irritants and the periodontal ligament.
The cells responsible for resorption of dental hard tissues are multinu-
cleated giant cells classified as clasts (Fig. 11.1). These cells attach them-
selves to the mineralized tissues by the cell membrane adjacent to the part
of the cytoplasm called the “clear zone”. Resorption takes place under the
highly folded cell membrane, known as the ruffled border (Fig. 11.2) in
this zone. The membrane releases a cocktail of enzymes capable of dis-
solving both organic and inorganic components of hard tissues. Osteoclasts
are involved in resorption of bone and dentinoclasts resorb dentine and
cementum. The latter are smaller, have fewer nuclei and their clear zone
is minimal or non-existent.
For dental resorption to occur, there must be damage to the non-
mineralized components (predentine and periodontal ligaments) and inter-
ference with the normal protection afforded by blast cells (odontoblasts,
cementoblasts and fibroblasts), which allows colonization of the denuded
surfaces by dentinoclasts. The causes of such damage are listed in Table
11.1. The concomitant acute inflammation during injury activates the den-
tinoclasts and initiates resorption. However, this process may be transient
in the absence of a perpetuating or persistent stimulus for the dentinoclasts,
allowing repair by hard tissue deposition to occur. Resorption becomes
progressive if it is sustained by chronic inflammation, whether in the pulp
or periodontium. The causes of persistent chronic inflammation are listed
in Table 11.2.
Pathological resorption has been classified by site, aetiology and patho-
genesis. The classification system presented below is based on all three
aspects to facilitate diagnosis and treatment planning.
1 Internal resorption
1 Transient internal resorption
2 Progressive internal resorption
i Sustained by bacteria or their products invading the pulp
ii Sustained by cytotoxic materials used in pulp therapy
© 2014 Elsevier Ltd. All rights reserved.
11
Section 3 Delivery of endodontic treatment
Y-L Ng, K Gulabivala  
2 External resorption
1 Transient external resorption
2 Progressive external resorption without persistent inflammation of
periodontal tissue (replacement resorption)
3 Progressive external resorption associated with persistent localized
inflammation of periodontal tissue
i Sustained by root-canal infection
ii Sustained by “pressure effect”
iii Sustained by foreign material
iv Sustained by subgingival plaque
4 Progressive external resorption associated with identified systemic
disease process
5 Progressive external resorption associated with no obvious local or
systemic disease process (idiopathic).
INTERNAL RESORPTION
This type of resorption has a prevalence of 0.1–1.6% in permanent teeth.
It is initiated by damage to or loss of the predentine and odontoblast layer
(see Table 11.1) and sustained by pulpal inflammation (see Table 11.2).
Dental trauma, overheating and dehydration during restorative procedures,
use of cytotoxic restorative materials or dressing materials in pulpotomies,
and orthodontic tooth movement are factors that may injure the protective
predentine and odontoblast cells.
Transient internal resorption
In the absence of persistent pulpal inflammation, initial resorption of
dentine from the pulpal aspect is self-limiting with no clinical consequence
(Fig. 11.3). It has been detected, for example, in boxers sustaining repeti-
tive injury to anterior teeth.
Progressive internal resorption
In the early stages of internal resorption, microleakage of bacteria and their
products via dentinal tubules and cracks sustain the inflammatory process.
Eventually, the coronal pulp is invaded by bacteria and becomes necrotic.
The former provides ongoing stimulus for resorption. The pulpal tissue
in the resorptive defect and apical to it is vital and provides blood supply
to the resorption area. The rate of progression of resorptive activity may
be related to the strength of inflammatory stimulus. In the case of total
pulp necrosis where the blood supply is cut off, the resorption ceases.
Calcified substance (osteo-dentine) similar to bone may be present
within the inflammatory tissue in the resorptive defect and this type of
presentation has been classified separately as “internal replacement resorp-
tion”, “root-canal replacement resorption”, or “metaplastic resorption”.
Clinically, the early stages of internal resorption are usually asympto-
matic. A pink spot may be present on the crown if resorption takes place
in the pulp chamber (Fig. 11.4). The pink discoloration associated with
internal resorption is caused by the highly vascularized inflammatory
tissue undermining the coronal enamel. Vital pulp tissue is required for
internal resorption to progress, therefore, such teeth will give positive
responses to pulp tests. However, a negative response could not rule out
the progression of resorption because only the pulp tissue coronal to the
lesion may be necrotic. Progression of inflammation fuelling the resorption
may result in total necrosis of the pulp and, therefore, cessation of internal
resorption. The necrotic pulp may then become infected and symptomatic,
discoloured and give negative responses to pulp tests (Fig. 11.5).
 286  Management of tooth resorption
Fig. 11.1  Multinucleated cells lying
in lacunae
Table 11.1  Factors interfering with protective mechanisms
preventing resorption
Predentine/odontoblasts
Trauma
Restorative procedures
Use of cytotoxic materials in pulp
therapy
Vital bleaching
Pathological and non-pathological
tooth surface loss
Orthodontic therapy
Periodontal disease
(Developmental defects of dentine)
Table 11.2  Causes of persistent chronic inflammation in pulp/periodontium
Chronic inflammation of the pulp
Microbial leakage around
restorations and via tubules
or cracks
Irritation by cytotoxic restorative
materials
B B
D
A D B
Fig. 11.2  (a) Light micrograph of an osteoclast-like cell in close
apposition to dentine, cementum and alveolar bone (×100);  
(b) electron micrograph of the osteooclast-like cell in (a) with
its ruffled border along dentine, cementum, and alveolar bone
(×5000); (c) electron micrograph showing the ruffled border of
the osteoclast-like cell in (a) along dentine, cementum, and
alveolar bone (×19 000). B = alveolar bone, C = cementum,
D = dentine
D C C B
Precementum/cementoblasts
Trauma
Orthodontic therapy
Orthognathic surgery
Periodontal therapy
Dento-alveolar surgery
Bruxism
Root-canal obturation using heated
gutta-percha techniques or
post-space preparation
(Developmental defects of cementum)
Chronic inflammation of the periodontium
Fig. 11.3  Transient internal resorption in a maxillary incisor, the pulp
Root-canal infection
subsequently became necrotic and apical periodontitis developed
Subgingival plaque
Pathosis adjacent to roots caused by
growing cysts and tumours, impacted
teeth and orthodontic forces
Irritation by internal bleaching agent
Altered biological dynamics, due to
regenerative technique or grafting
material

Fig. 11.4  Internal
resorption affecting the
pulp chamber of the
maxillary second molar,
the crown exhibited a
pinkish discoloration
(arrowed)
A B
Fig. 11.7  The right maxillary lateral Fig. 11.8  (a–c) Internal resorption affecting the left maxillary incisor with similar presentation as external resorption
incisor associated with extensive
internal resorption and associated
periradicular radiolucency where it
breached the distal surface (arrowed)
Radiographically, the appearance of internal resorption has been classi-
cally described as a well-circumscribed, symmetrical, oval or circular
shaped radiolucency continuous with the root canal (Fig. 11.6). The radi-
olucency has a uniform density and the pulp chamber or canal cannot be
followed through the lesion. The position of the radiolucency remains the
same in mesial or distal angled radiographic views. However, a radiopaque
mass resembling calcification may be present within the lesion or in the
canal space apical to the internal resorption. A periradicular radiolucency
may be associated with perforation of the root or total necrosis of the pulp
in advanced cases (Fig. 11.7). This may pose difficulty in differentiation
from external inflammatory resorption associated with root-canal infection
(Fig. 11.8). Occasionally, internal resorptive lesions remain undetected and
may only appear incidentally on a post-obturation radiograph (Fig. 11.9).
Management of tooth resorption  287
Fig. 11.5  Internal resorption affecting Fig. 11.6  Internal resorption affecting
the maxillary lateral incisor, the pulp the right maxillary central incisor
became infected and apical
periodontitis developed
C
Management of progressive internal resorption varies according to the
extent of the lesion, presence of calcification and perforation. Root-canal
treatment should be carried out immediately after detection in order to
prevent further disease progression leading to root perforation.
It may be difficult to control haemorrhage and to remove completely
the severely inflamed tissue from the resorptive defect. Therefore, debride-
ment should be carried out using copious amounts of sodium hypochlorite
irrigant. In addition to its antibacterial properties, sodium hypochlorite
also possesses tissue-dissolving ability. Use of higher concentration (5%)
of sodium hypochlorite in combination with ultrasonic agitation has been
recommended and may enhance debridement. The canal should be checked
for perforation by exploring with a curved file attached to an apex locator.
Care should be taken to prevent extrusion of sodium hypochlorite irrigant
 288  Management of tooth resorption
A B
A B
through any perforation. An extensive lesion with calcification may render
canal location and complete debridement of the resorptive defect impos-
sible (Figs 11.4, 11.10). Calcium hydroxide dressing should be used
between appointments to prevent recolonization by bacteria and to facili-
tate removal of any residual inflamed tissue within the irregular resorptive
defect. Long-term dressing with calcium hydroxide is indicated to induce
hard tissue repair if a perforation is present (see Figs 11.7, 11.11). It may
be prudent to delay root-canal obturation until complete bone healing has
occurred to ensure minimum extrusion of filling material.
Complete obturation of the defect may be achieved by using a
thermoplasticized root-filling technique, such as injection of molten gutta-
percha using an Obtura II system (see Chapter 8) after filling the
canal apical to the defect using lateral or vertical compaction technique
(Fig. 11.11).
A surgical approach is indicated when a large perforation is present and
or excess root-filling material has been extruded into the periodontal tissue.
However, these cases have compromised prognosis and are prone to root
fracture.
EXTERNAL RESORPTION
Resorption of the root surface is commonly seen in association with severe
dental trauma, apical periodontitis or orthodontic treatment. The apical
region is generally affected but lateral and cervical aspects of the root may
also be involved.
Transient external resorption
Injury to precementum and cementoblasts initiates this type of resorption
(see Table 11.1). Where trauma is not severe, external inflammatory
resorption is transient and repair may follow. This has also been called
“external surface resorption” (Fig. 11.12).
Fig. 11.9  (a,b) Internal resorption affecting the right
mandibular first molar
Fig. 11.10  (a,b) Extensive internal resorption defect
with calcification of the tooth in Figure 11.4 rendered
complete debridement impossible
Clinically, the involved tooth is usually asymptomatic and the small
resorptive defects are not usually visible on radiographs. Occasionally,
they may appear as small excavations of the root surface delineated by an
intact periodontal ligament space (Fig. 11.12b). This condition is self-
limiting and no active treatment is required.
Progressive external resorption without persistent
inflammation of the periodontal tissue
This type of resorption has traditionally been described as “external
replacement resorption”. It is usually a consequence of luxation injuries
or is frequently observed following replantation of avulsed teeth when
extensive loss of viability of periodontal ligament and damage of cemen-
tum of at least 20% of root surface has occurred. Synthesis of anti-invasion
factor and collagenase inhibitor may be affected, providing an opportunity
for resorbing osteoclasts to populate the denuded root surface. It is believed
that the osteoclasts cannot differentiate between cementum, which is
usually protected by periodontal ligament, and bone. The osteoblasts
deposit bone where dentine and cementum have been resorbed. The
process seems akin to bone remodelling.
Often in the dental literature, the terms “ankylosis” and “replacement
resorption” are used synonymously. However, in “ankylosis”, there is no
loss of root dentine and cementum, merely fusion or close proximity of
the root and bone. In “replacement resorption”, dentine and cementum are
lost to be replaced with bone (Fig. 11.13).
Clinically, the involved tooth is asymptomatic. Similar to ankylosis, the
high-pitched metallic sound on percussion and absence of physiological
tooth movement are the typical characteristic features. The tooth may be
in infra-occlusion in a growing child.
Radiographically, the root appears to be gradually replaced by bone.
The junction of bone and cementum has a mottled appearance and the
periodontal ligament space is not evident (Fig. 11.14).
 Management of tooth resorption  289

A B

C D

Fig. 11.11  (a) Internal resorption in a maxillary central incisor; (b) calcium hydroxide dressing filling the defect incompletely and inadequately; (c) apical part of
the root canal obturated with laterally compacted gutta-percha and sealer; (d) the resorption cavity and coronal part of the canal obturated with warm gutta-
percha and sealer

Fig. 11.13  Replacement resorption

affecting the mandibular central
incisors (arrowed)

A B

Fig. 11.12  Surface resorption: (a) diagram; (b) radiograph (arrowed)

Management strategies should be directed towards prevention as this
type of resorption is not treatable. An avulsed tooth should be immediately
replanted or stored in milk/transplant medium to preserve the vitality of
periodontal ligaments.
Progressive external resorption with persistent
inflammation of the periodontal tissue sustained by
1.  Root-canal infection
In progressive external resorption with persistent inflammation of the peri-
odontium, the most common sustaining factor is thought to be root-canal
infection, causing inflammation in the periodontal ligament adjacent to
the denuded area of root surface. Resorption may be found around the
apical or lateral root-canal foramina in 87.3% of teeth associated with
periradicular periodontitis (Fig. 11.15). It has been hypothesized that the
cementum at the cemento–dentinal junction apically may be too thin or
even non-existent to afford effective protection against dentine resorption.
When inflammation is confined to a small area at the apex of the root, the
concentration of resorbing factors may be high enough to overcome resist-
ance of the root (perhaps due to hyper-mineralisation) to resorption.
In traumatized teeth, damage to the periodontal tissues may lead to
resorption of the cementum exposing the underlying dentine. If the pulp
is necrotic and infected, microbial products are enabled to diffuse through
the dentinal tubules into the periradicular tissues (Fig. 11.16a,b) and
fuel an aggressive form of inflammatory resorption (Fig. 11.16c). Root-
canal debridement and dressing with calcium hydroxide may remove the
inflammatory component, reducing the resorption to a replacement variety
(Fig. 11.16d).
 290  Management of tooth resorption
A B
C
D E
Fig. 11.14  (a) Inflammatory resorption affecting the right maxillary incisors and
canine, which were replanted after avulsion and initially exhibited the high
percussion tone of ankylosed teeth; (b) inflammatory component resolved by
root canal treatment as evidenced by bone healing; with minimal replacement
resorption at 1 year; and (c) 8 years following root-canal treatment further
progress in replacement resorption is evident; (d) the maxillary lateral incisor in a
separate case associated with almost complete root resorption with gutta-
percha remaining in bone tissue after ankylosis; (e) almost complete replacement
resorption of a root in a separate case, 13 years after traumatic luxation
Fig. 11.15  Apical resorption: (a) histological section; (b) electron micrograph
Clinically, the involved tooth presents with signs and symptoms of
chronic apical periodontitis. Extensive resorption can lead to increased
mobility of the tooth. Pulp tests usually yield negative responses.
Radiographically, radiolucent resorptive lesion(s) may be present at any
level of the root (Fig. 11.17). Progressive external resorption associated
with periradicular periodontitis with no previous luxation injuries may not
be noticeable or may present as irregular shortening of the root with an
associated radiolucent lesion (Fig. 11.17a). On the other hand, multiple
radiolucent resorption cavities (Fig. 11.18) may appear along any part of
the root in conjunction with periradicular radiolucent lesions a few months
after luxation injuries. These resorptive lesions exhibit ill-defined borders,
asymmetrical distribution and variations in the radiodensity (Fig. 11.18).
The outline of the root canal remains unaltered within the superimposed
resorptive lesion. The position of the lesion changes with respect to the
angulation of X-ray beam (Fig. 11.17).
Management of this type of resorption includes thorough chemome-
chanical debridement of the root canal using sodium hypochlorite for
irrigation and calcium hydroxide for interappointment dressing. Long-term
dressing with calcium hydroxide is indicated in case of extensive resorp-
tion. Prognosis is generally good and the only problem encountered may
be prevention of root-filling material extrusion when resorption is present
at the canal foramen (Fig. 11.19). This could be minimised by customizing
the master gutta-percha cone (see Chapter 8) or delaying root filling until
complete bone healing has been achieved.
Timely elective root-canal treatment after severe luxation injury could
prevent this type of progressive external resorption.
2.  Pressure
The second factor, which can sustain resorption in the periradicular tissues,
as well as cause damage to the periodontal ligament and cementum, is
apparent pressure. Also called “pressure resorption”, this type of external
resorption may be associated with, and possibly mediated through inflam-
mation in situations such as: impacted teeth (Fig. 11.20), orthodontic
treatment (Fig. 11.21), occlusal trauma, and growing cysts and tumours.
 Management of tooth resorption  291

Pulp Periodontal
necrosis space

B
Inflammatory
A resorption

Fig. 11.16  (a) Diagram illustrating that microorganisms or microbial products pass through dentinal tubules
into surrounding tissues after loss of cementum; (b) light micrograph showing multinucleated cells together
with neutrophilic granulocytes at resorbed external dentine surface with microorganisms extending into
dentinal tubules on the pulpal side; (c) external root resorption after luxation and pulp necrosis; (d) 3
D months after root canal debridement of the teeth in (c). The inflammatory component removed has
reduced the aggressive inflammatory process to a slower resorption by replacement resorption

A B C

Fig. 11.17  (a) A mandibular first molar associated with apical progressive external resorption and apical periodontitis; (b,c) progressive external resorptive defect
present at the apex and mid-root level of the maxillary left central incisor

It is not known whether there is in fact a localized increase in pressure
that stimulates this type of resorption; it is likely that it is mediated by a
molecular mechanism. In any case, the conceptual model seems to fit.
Resorption associated with orthodontic treatment has also been classified
as “periapical replacement resorption” by Bender et al. (1997) who sug-
gested that pulpal inflammation might also be involved in this phenome-
non. However, this type of resorption could only be arrested by removal
of pressure from orthodontic movement of teeth but not by root-canal
treatment.
Clinically, the involved tooth is usually asymptomatic and the pulp is
vital. Increase in mobility may be associated with a severely shortened
root.
Radiographically, the periodontal ligaments and the surrounding bone
adjacent to the resorptive defect appear normal (see Fig. 11.21a,f).
 292  Management of tooth resorption
A B
Fig. 11.18  (a) Lateral inflammatory root resorption following luxation injury; (b) two years after chemomechanical debridement and calcium hydroxide dressing;
(c) obturation of the root canal system of the tooth in (a); (d) slow resolution of the periradicular radiolucencies
Fig. 11.19  The maxillary central
incisor associated with apical
resorption and root filling material
extruded into apical tissue
Management consists of removal of the cause which arrests the
resorption.
3.  Irritation by foreign material
The third sustaining factor, irritation by foreign materials may also provide
an ongoing stimulus for the resorbing cells. This type of resorption has
been observed in relation to connective tissue grafting, bone grafting and
tissue regenerative procedures (Fig. 11.22). Root planing prior to use of
regenerative techniques damages cementum, allowing dentinoclasts to
adhere to the root surface. The host defensive mechanisms that come into
play in the presence of the grafting or regenerative materials, perhaps
together with any persistent marginal periodontitis, sustain inflammation
in the periodontal tissue.
Clinical presentation, radiographic appearance and management of this
type of resorption are similar to the progressive external resorption sus-
tained by subgingival plaque.
C D
4.  Subgingival plaque
Progressive external resorption with persistent inflammation may be local-
ized at the cervical level and is commonly known as “cervical resorption”
(Fig. 11.23). Due to the wide variations in its clinical presentation and
poorly defined aetiology in the past, numerous terms have been used to
describe this phenomenon (Table 11.3). It is initiated by damage to the
cervical attachment apparatus (cementum or periodontal ligament) below
the epithelial attachment. Orthodontic tooth movement, subgingival scaling
and root planing, orthognathic and dentoalveolar surgery, and internal
bleaching agents may damage the cementum and initiate resorption. In
10% of the population, dentine is not covered by cementum at the cemento–
enamel junction and may be susceptible to resorption. In addition, the
exposed dentinal tubules provide a pathway between the pulp and gingival
sulcus/periodontal ligament in these cases. The resorptive process is then
sustained by subgingival plaque. The multinucleated osteoclastic cells gain
entry onto the tooth surface and cause resorption of dentine. The pulpal
space is not invaded even in advanced cases (Fig. 11.24), due to the protec-
tive predentine layer and resorption spreads circumferentially around the
root canal (Fig. 11.25). The pulp is only invaded if the predentine is min-
eralized and no longer functioning as predentine. In this case, the resorbing
tissue may establish vascular communication with the pulp in some cases,
otherwise the tissues remain adjacent but separate. A classification of inva-
sive cervical resorption is given by Heithersay (1999) (Fig. 11.26).
Clinically, the tooth is asymptomatic early on but will develop symp-
toms of pulpitis in the advanced stages. On exploration with a probe, a
subgingival, supracrestal non-carious cavity may be detected. A pink spot
will be present when the inflammatory tissue undermines the enamel of
the crown (Fig. 11.27). The pulp remains vital in most cases.
Radiographically, the resorptive lesion may present as a well-
circumscribed (Figs 11.24b, 11.28) or an irregular mottled (Fig. 11.29)
radiolucency involving the buccal, lingual or proximal surface of the tooth.
Nevertheless, the outline of the pulp and root canal can be distinguished
through the resorptive lesion. Adjacent angular alveolar bone loss may be
noticed when the lesion involves proximal surfaces.
Management and prognosis vary according to the extent and accessibil-
ity of the lesion, in particular the size of the exposure on the root surface
and its distribution around the circumference of the root (see Figs 11.23a,b,
11.30 = good prognosis, 11.28 = questionable prognosis, 11.24a,b, 11.27,
 Management of tooth resorption  293

A B

C D

D E

Fig. 11.20  Progressive external resorption associated with impacted teeth

arrested following extraction of the impacted teeth, shown for two cases (a–c)
and (d–e)
E F

Fig. 11.21  (a–f) Progressive external resorption associated with orthodontic

treatment
 294  Management of tooth resorption

Fig. 11.23  (a,b) Class 1

(see Fig. 11.26 for
classification)
progressive cervical
inflammatory resorption
affecting the maxillary
right central incisor

A B

Fig. 11.22  (a,b) Progressive external resorption (arrowed) associated with

previous periodontal disease, surgical periodontal debridement and
regenerative procedure using Emdogain (from St George G, Darbar U, Thomas
G (2006). Inflammatory external root resorption following surgical treatment
for intra-bony defects: a report of two cases involving Emdogain and a review
of the literature. J Clin Periodontal 33, 449–454)

B
Table 11.3  Terms used to describe progressive external resorption
sustained by subgingival plaque

1. Asymmetric internal resorption

2. Burrowing resorption
3. Cervical resorption
4. Extracanal invasive resorption
5. Internal–external resorption
6. Invasive cervical resorption
7. Peripheral inflammatory root resorption
8. Progressive intradental resorption
9. Spontaneous intermittent resorption
10. Subepithelial inflammatory root resorption
11. Supraosseous extracanal invasive resorption
A

11.29 = poor prognosis cases) as well as vitality of the pulp. A shallow

localized lesion on a readily accessible buccal or lingual surface of the
tooth with a vital pulp has good prognosis. Management should involve
surgical exposure of the lesion and curettage of inflammatory tissue fol-
lowed by sealing the defect with glass ionomer cement (GIC) (Fig. 11.31).
The vitality of the pulp should be monitored periodically after treatment.
A proximal lesion may have poor accessibility and require raising of both
buccal and lingual/palatal flaps to expose the lesion. An example of a case C
is shown in Figure 11.30. Insertion of GIC into the proximal cavity and
ensuring a good marginal seal may be difficult. In either case, the unsup-
ported enamel or dentine at the cavity margin should be spared to provide
retention for the restoration. It is important to remove completely the
inflammatory tissue from the resorptive defect. Its removal could be facili-
tated by topical application of 90% trichloracetic acid solution. Pulpal
exposure after curettage of inflammatory tissue requires immediate elec-
tive pulpectomy, complete cleaning, shaping and obturation of the root-
canal system at the same appointment prior to restoring the cavity
B
permanently. If root-canal treatment is not carried out at the same visit,
the prognosis may be compromised as the pulp will most likely lose vital- Fig. 11.24  (a,b) Probable class 3 (see Fig. 11.26 for classification) progressive
ity, and the chances of success will be reduced. There is also the risk of cervical inflammatory resorption affecting the mandibular canine
 Management of tooth resorption  295

Class 1

Class 2

Class 3

Class 4

A B

Fig. 11.25  Burrowing external tooth resorption: (a) radiograph; (b) histological
section – note that the pulp cavity is not involved

Fig. 11.26  A classification of invasive cervical resorption (adapted from

Heithersay, 1999)

A B C

Fig. 11.27  (a–c) Pink discoloration in the cervical third of the crown of maxillary central incisor associated with Class 2 or 3 progressive cervical inflammatory
resorption

Fig. 11.28  Class 3 progressive Fig. 11.29  Class 4 progressive

cervical inflammatory resorption cervical inflammatory resorption
affecting the maxillary lateral incisor affecting the mandibular central
following placement of an implant incisor
replacing the central incisor
 296  Management of tooth resorption

A B C

Fig. 11.30  (a–e) Cone-beam computed tomography

images showing Class 4 progressive cervical
inflammatory resorption affecting the mandibular  
first molar, the resorption has invaded laterally to a
considerable extent from a minute external opening
on the disto-lingual surface. The lesion did not appear
to have any communication with the pulp or the
periodontal ligament; (f) external repair of the entry
point; (g) completed root canal treatment with good
final prognosis. The good prognosis is due to the fact
that the entry point remained confined and the
resorptive lesion did not tap blood supply from either
the pulpal or other contacts with the periodontal
ligament. Either a large area of resorption on the root
D E surface (compromising restoration) or additional
points of blood supply (making it difficult to
completely excise and control the resorptive tissue)
would reduce prognosis

F G

A B C

Fig. 11.31  (a) Pink spot in cervical region of maxillary lateral incisor; (b) extent of defect with flap reflected; (c) defect repaired with glass ionomer cement
 Management of tooth resorption  297

dislodgement of the restoration during root-canal treatment. An extensive condition is suspected, the patient should be referred to a specialist for
or irregular mottled lesion with a large surface area of loss has extremely further management. No local dental treatment is indicated.
poor prognosis and no treatment is recommended (Fig. 11.32).

Progressive external resorption associated with
systemic disease
Shortening of roots or dental resorption has been associated with some
systemic diseases (Table 11.4) and is known as “systemic resorption”. The
evidence though consists mainly of retrospective case reports. The role of
systemic diseases in dental resorption is poorly understood.
The clinical presentation of resorption related to systemic diseases
usually involves multiple teeth and is presented in Table 11.4. When this
Progressive external resorption associated with no
obvious local or systemic disease (idiopathic)
Cases of resorption where no local or systemic factors can be identified
are classified as “idiopathic resorption”. There may be a wide range of
different presentations (Figs 11.33–11.37).
When no systemic disease can be detected, the condition can only be
monitored to provide palliative care to elongate the life of the teeth while
a definitive prosthodontics plan is made.

Fig. 11.32  Type IV progressive cervical Fig. 11.33  Progressive idiopathic external resorption affecting the right maxillary and mandibular teeth only
inflammatory resorption affecting the
mandibular incisors

Table 11.4  List of systemic diseases associated with shortening of root or dental resorption

Systemic disease Type of defect Possible role in dental resorption

Herpes zoster involving maxillary
or mandibular branches of
trigerminal nerve
Hyperoxaluria and oxalosis
Hypophosphatasia
Radiotherapy
Hypoparathyroidism
Hereditary fibrous osteodysplasia
(osteogensis imperfecta)
Paget’s disease (osteitis
deformans)
Hyperparathyroidism
Progressive internal resorption Viral infection affecting the nerve endings within the pulp
causes damage to protective layer and persistent
inflammation of the pulp
Progressive internal or external resorption Foreign body reaction to calcium oxalate crystals deposited
within the pulp and periodontium causing damage and
persistent inflammation at both sites
Progressive external resorption Developmental defects of dentine and cementum
(hypomineralized or hypolplasia) render the root more
susceptible to resorption by other causes
Root dwarfism Damaged developing teeth results in various developmental
Root shortening anomalies depending on the stage of development at the
time of therapy
Incomplete root development Associated enamel hypoplasia, hypomineralized dentine render
Progressive external resorption the teeth more susceptible to resorption by other causes
Progressive replacement of dentine at pulpal and periodontal Altered metabolism affects the viability of the protective
aspects by osteo-dentine and osteo-cementum. components; odontoblasts and cementoblasts and renders
The involved tooth is separated by a layer of connective the teeth more susceptible to resorption by other causes
tissues from the adjacent bone
Progressive replacement of dentine and cementum by Unknown
coarse-fibred bone
Root shortening Unknown
 298  Management of tooth resorption

A B

Fig. 11.34  (a–c) Progressive idiopathic external cervical resorption affecting the right maxillary and
mandibular teeth in a patient who also exhibits a lack of any occlusal contacts on the right side. C
There is therefore a co-existing tooth eruption disorder

Fig. 11.35  Progressive idiopathic

external cervical resorption affecting
the maxillary canine only

Fig. 11.36  Progressive idiopathic external cervical resorption affecting the

maxillary and mandibular molars. The extracted first and second molars were
also affected

A B C

Fig. 11.37  (a–c) Progressive idiopathic external cervical resorption affecting the mandibular right premolars and molars only

REFERENCES AND FURTHER READING
Bender, I.B., Byers, M.R., Mori, K., 1997. Periapical replacement resorption of
permanent, vital, endodontically treated incisors after orthodontic movement: report
of two cases. J Endod 23 (12), 768–773.
Hammarström, L., Blomlöf, L., Lindskog, S., 1989. Dynamics of dentoalveolar
ankylosis and associated root resorption. Endod Dent Traumatol 5 (4), 163–175.
Heithersay, G.S., 1999. Treatment of invasive cervical resorption: an analysis of results
using topical application of trichloracetic acid, curettage, and restoration.
Quintessence lnt 30, 96–110.
Lindskog, S., Hammarström, L., 1980. Evidence in favour of anti-invasion factor in
cementum or periodontal membrane of human teeth. Scand J Dent Res 88, 161–163.
Lindskog, S., Pierce, A.M., Blomlof, L., et al., 1985. The role of the necrotic periodontal
membrane in cementum resorption and ankylosis. Endod Dent Traumatol 1 (3),
96–101.
Ne, R.F., Witherspoon, D.E., Gutmann, J.L., 1999. Tooth resorption. Quintessence lnt
30, 9–25.
Tronstad, L., 1988. Root resorption – etiology, terminology and clinical manifestations.
Endod Dent Traumatol 4, 241–252.
Trope, M., 2002. Root resorption due to dental trauma. Endod Topics 1, 79–100.
Wedenberg, C., Lindskog, S., 1985. Experimental internal resorption in monkey teeth.
Endod Dent Traumatol 1 (6), 221–227.
Wedenberg, C., 1987. Evidence for a dentin-derived inhibitor of macrophage spreading.
Scand J Dent Res 95 (5), 381–388.

Section 4 Multidisciplinary aspects of endodontic management
COMPARISON OF APICAL AND
MARGINAL PERIODONTITIS
It is a curious and clinically relevant fact that both pulpal and periodontal
diseases have their terminal effects in the periodontal tissues (cementum,
periodontal ligament, alveolar bone). The difference is that the initial
manifestation in periapical disease is at the apex of the root whereas, in
periodontal disease, it is at the cervical (marginal) aspect of the tooth (Fig.
12.1). In both cases, the periodontal tissues become chronically inflamed
as a result of an anaerobically and Gram-negative dominated microbiota
in or on the adjacent root surface.
PRECEDING DISEASE STATES IN APICAL OR
MARGINAL PERIODONTITIS
Marginal inflammation of the gingival tissues, called gingivitis, is pre-
ceded by the accumulation of plaque around the gingival margin of the
tooth. If the plaque is allowed to be sustained, the associated inflammation
of the gingival tissues is described to progress through the so-called initial,
early, established and advanced lesions. Two types of established lesions
are recognized: that which can remain stable for months to years and that
which progresses to periodontitis in the susceptible host. The initial
defence is mediated at the level of the marginal attachment of the gingival
(epithelial and connective) tissues through polymorphonuclear leucocytes
(PMNs) and macrophages, as well as inflammation of the underlying con-
nective tissue (Fig. 12.2). In contrast, apical periodontitis is preceded by
persistent pulpal inflammation, which follows bacterial colonization of
dentine. The initial defence is mediated at the level of the pulp–dentine
complex with the odontoblastic layer the key player, together with inflam-
mation of the underlying pulp tissue (see Chapter 1).
PROGRESSION, CLINICAL MANIFESTATION
AND MEASUREMENT OF APICAL AND
MARGINAL PERIODONTITIS
In marginal periodontitis, supragingival plaque sets the stage for subgin-
gival microbial colonization of the root surface. Following the initial signs
of gingivitis, which include change in colour of the gingival tissues and
bleeding, there is breakdown of the connective tissue attachment and
progressive loss of bone when the responsible microbiota are not removed
by effective tooth brushing (Figs 12.3–12.5). The degree to which this
occurs is determined by modifying or risk factors which affect host sus-
ceptibility. Once this process becomes established, the disease progresses
apically by periodic exacerbation that may mirror variations in the host
immune response. The apical progression involves migration of the junc-
tional epithelium, loss of connective tissue attachment and, ultimately, loss
of bone. The pattern of attachment and bone loss can be site specific,
varying around the circumference of the same tooth, and/or tooth specific
varying around different teeth in the same mouth. The pattern of attach-
ment loss may be relatively constant around all teeth in the mouth resulting
in a horizontal pattern of marginal bone loss where the alveolar crest lies
more than 2 mm below the cemento–enamel junction but parallel to the
occlusal plane (Fig. 12.6). In other cases, the attachment loss may be
irregular and localized to specific teeth with angular bone defects (also
© 2014 Elsevier Ltd. All rights reserved.
12
The perio–endo interface
K Gulabivala, UR Darbar, Y-L Ng  
called vertical defects), in which the pattern of bone destruction progresses
vertically along the root creating an oblique orientation of the alveolar
crest with the tooth, the crest and root comprising opposite sides of the
defect (Fig. 12.7). Although, the exact determinants of the patterns of bone
loss remain unclear, this type of attachment loss may be associated with:
• nature of specific pathogenic microbiota on the root
• host susceptibility and modifying risk factors
• gingival tissue type
• anatomical root defects (grooves, enamel pearls)
• anatomy of alveolar bone (thickness and quality)
• pulp infection
• root fracture.
The resulting bony defects take different morphological forms, defined
as 1-walled, 2-walled, 3-walled or crater defects. Sites with thin gingival
tissue biotype often present with horizontal bone loss and thick biotype
with irregular bone loss. Any of these localized forms of attachment loss
may eventually encroach on (Fig. 12.8) and envelop the apex of the tooth
root (Fig. 12.9) resulting in secondary involvement of the pulp, although
this process may take years. Very rarely, periodontal involvement of a
lateral canal may cause the demise of the pulp.
Patients in the early stages of periodontal disease will complain of
bleeding gums but pain is rarely reported. Soreness of the gums is more
common and is frequently described as a dull gnawing discomfort. Severe
pain is only associated with acute exacerbation of the condition and
patients are usually oblivious to periodontal problems, which may first
manifest in tooth mobility or, rarely, even loss.
The diagnostic process includes history, clinical examination of the
involved tissues and radiography. In the early stages of the disease, there
is loss of stippling of the gingival tissues with associated redness and
swelling. The gingival tissues are examined for degree of bleeding by
running a periodontal probe in the marginal sulcular tissues; inflamed
tissues exhibiting immediate bleeding. The extent and severity of perio-
dontal disease is measured by characterizing the attachment loss, taking
account of any recession, periodontal probing defects (signifying separa-
tion between soft and hard tissue) and radiographic assessment of the
pattern of bone loss. Where there is sufficient thickness of bone, the attach-
ment loss may overtake total marginal loss of bone, creating an infra-bony
defect (see Fig. 12.3).
In health, the probing depths may measure up to 3 mm but inflamed
tissues may yield 5 mm (moderate disease) or more (severe disease), even
up to 15 mm if the attachment loss extends to the root apex. The clinical
assessment of soft tissues is complemented by radiographic assessment of
the bone levels. The radiographic views of choice, accepting their
2-dimensional limitations, are parallel view (long-cone) periapicals, as
they provide an optimal indication of the relationship between bone levels
and root length. Cone-beam computed tomography offers a better
3-dimensional option but often at the cost of resolution.
In apical periodontitis, pulp infection commences in the crown of the
tooth and progresses apically. If, as on relatively rare occasions, the pulp
tissue in a lateral canal becomes necrotic and infected, a lateral periradicu-
lar radiolucency (usually enclosed by intact marginal bone) will arise,
representing a localized site of inflammation (Fig. 12.10). As the infection
in the pulp progresses further apically, the pulp tissue in the apical part of
 300  The perio–endo interface

Fig. 12.1  Initial manifestation of periodontal Fig. 12.2  Junctional epithelium Fig. 12.3  Section showing loss of
disease at the cervical aspect of the tooth marginal attachment and
(arrowed) periodontal destruction

Fig. 12.4  Early Fig. 12.5  Advanced

periodontal destruction periodontal destruction

A B C

Fig. 12.6  (a) Horizontal bone loss; (b) horizontal bone loss – 4 years later; (c) horizontal bone loss – 12 years later

Fig. 12.7  Vertical bone Fig. 12.8  Periodontal

loss bone loss encroaching
on the apices of teeth
in the maxillary arch

B A
Fig. 12.9  (a) Periodontal bone loss involving the mesial root of 36;
(b) periapical radiograph of the same as in (a)
A B
Fig. 12.11  (a) Early periradicular bone loss in 32 (arrowed); (b) further apical
and marginal bone loss over a 10-year period in the tooth shown in (a)
the root succumbs and further lateral and apical foramina may become
associated with adjacent bone loss (Fig. 12.11). The size and distribution
of apical periodontitis (and thus apical radiolucency) is dictated by:
• the distribution of the lateral and apical foramina
• the nature and extent of the infecting microbiota
• the nature of the periradicular host defence.
Periapical disease may manifest asymptomatically or symptomatically,
depending upon the nature of host and microbial factors involved (see
Chapter 3 for details). Periapical lesions can remain asymptomatic and
stable in size for years. The presence and extent of periapical disease is
mainly measured radiographically (as it is not directly visible or probea-
ble) and also requires standardized radiography. The lesions of chronic
apical periodontitis seldom result in retrograde marginal periodontitis with
attachment loss. However, when this does occur, the probing depth and
bone defect is usually deep and very localized. Long-standing, untreated,
marginal loss of attachment caused by root-canal infection may secondar-
ily become established as true marginal periodontitis requiring endodontic
The perio–endo interface  301
B
Fig. 12.10  (a) Lateral periodontal bone loss of pulpal origin (arrowed);
(b) resolution following root-canal treatment
and periodontal treatment. It has been suggested through classifications
that such periodontal lesions caused by root-canal infection may progres-
sively widen with time. If true, characterization of such loss of attachment
requires the recording of the continuous probing profile around the tooth
(Fig. 12.12), which defines both the width and the depth of the defect.
Following root-canal treatment, the chances of resolution of this type of
localized marginal loss of attachment are high, because the infection is
“closed” and “contained” within the tooth. The true prevalence of this type
of presentation and its susceptibility to treatment is unknown.
In contrast, marginal loss of attachment due to periodontal disease, is
seldom recovered in full, due to “the open” nature of the lesion, the imme-
diate proximity of the infection to the marginal tissues and the role of host
susceptibility and modifying factors in the initial progression of the lesion.
There may be greater chance of attachment recovery in infra-bony defects
with multiple walls.
CELL PROFILES IN APICAL AND
MARGINAL PERIODONTITIS
Both disease processes are characterized by transition from innate to adap-
tive immune responses. The precise distribution of cell proportions varies
with time according to the nature of host–microbial interaction. The cell
types for apical periodontitis were reported in Chapter 3, and include,
PMNs, macrophages, fibroblasts, B and T lymphocytes, mast cells, plasma
cells and epithelioid cells. The same cell types are found in the developing
lesions of marginal periodontitis, however, the dominant cell type in the
advanced periodontal lesion is the plasma cell. Epithelial proliferation is
evident in both disease processes, the junctional epithelium in periodontal
disease, and the rests of Malassez in apical periodontitis, which may lead
to cyst formation in apical but not marginal periodontitis.
MICROBIOTA ASSOCIATED WITH APICAL OR
MARGINAL PERIODONTITIS
The details of the microbiota involved in apical periodontitis were dis-
cussed in Chapter 3. Both disease processes show the classical progression
from an initial Gram-positive, aerobic/facultative colonizing flora, replaced
by an increasingly diverse and complex facultatively anaerobic flora, to
 302  The perio–endo interface

Fig. 12.12  (a–c) Continuous periodontal

probing around maxillary molar showing
sudden changes in probing depths

A B C

be succeeded by a progressively strictly anaerobic and Gram-negative

Table 12.1  Risk factors
dominated microbiota. The diversity of the microbiota in apical periodon-
titis is more selective and restricted because of the nature of the niche. The Periodontal disease Periapical disease
dominant strains may be similar in general terms but the species associated
Non-modifiable Non-modifiable
with disease progression may be different by virtue of ecological differ-
• Age • Age
ences. Perio–endo cases show a similarity in the general profile of species • Gender • Gender
recovered from the root canal versus the periodontal pocket but there may • Race/ethnicity • Tooth type; 1st molars
be subtle differences at a strain level, even if the same species may appear • Gene polymorphisms • Race/ethnicity?
Environmental, acquired • Gene polymorphisms?
to be present. The differences may reflect the “open” versus “closed” • Allergies
• Specific microbiota
nature of the niches. Abscesses of apical or marginal origin may have a Environmental, acquired
• Smoking
distinct proportion of spirochaetes according to one source (up to 10% in • Diabetes • Caries; 1° & 2° (↑)
periapical and up to 60% in lateral periodontal). Research on marginal • Obesity • Trauma
• Osteopenia/osteoporosity • Restorations; inadequate
periodontitis has focused on identifying key species associated with
• HIV • Root fillings; inadequate
disease progression but equivalent research on apical periodontitis is • Psychosocial • Usage of dental service
missing. • Diabetes
• Smoking

RISK FACTORS FOR PROGRESSION OF APICAL OR

MARGINAL PERIODONTITIS
Epidemiological studies on these diseases have allowed various associa-
tions to be measured in populations. These yield interesting links between
various factors and prevalence or progression of the disease. The types of
associations have been divided into non-modifiable and environmental
(Table 12.1); although some common factors have been investigated, dif-
ferences emerge in the pattern of factors that may predispose to each
disease’s prevalence or its respective progression. The differences may
also reflect the different pathways of exposure to the oral environment.
NATURAL HISTORY OF APICAL AND
MARGINAL PERIODONTITIS
The natural history of the disease process, that is, the manner in which
disease progresses when untreated, has been measured for marginal peri-
odontitis with interesting outcomes. Such studies helped to determine that
not all patients progressed from gingivitis to periodontitis, that the progres-
sion in chronic marginal periodontitis occurred in episodic bursts and that
another group suffered from aggressive progression despite minimal
plaque. This insight reshaped the approach to management of periodontal
disease. A similar type of insight is lacking for apical periodontitis. It is
not known precisely what proportion of periapical lesions are chronic
asymptomatic, the proportion that develop acute symptoms or sinuses and
why some form large lesions that fail to respond well to treatment. It is
likely that both diseases share a common genetic predisposition in the
manner in which the host responds to specific types of microbiota.
ASSOCIATION OF APICAL AND MARGINAL
PERIODONTITIS WITH SYSTEMIC DISEASES
The implication of periapical disease in the “focal infection theory” at the
turn of the last century nearly wiped endodontic practice from the face of
dental curricula, despite the fact that the original assertion by Hunter
alluded to periodontal disease in “mausoleums of gold”. Over the last
couple of decades, suggested links between marginal periodontitis and a
number of systemic conditions (cardiovascular disease, diabetes, preg-
nancy complications) have steered the discipline towards an area of
research called “periodontal medicine”.
Emergent evidence suggests that the vast area of exposure of the host
blood stream to the oral microbiota, via the inflamed and ulcerated peri-
odontal sulcus, leads to a marked systemic host response that is manifest
in circulating biomarkers of inflammation. Such pro-inflammatory media-
tors are found in atheromatous lesions. Among the many factors implicated
in preterm births, periodontal disease is a frequently investigated putative
cause; although the evidence is equivocal and contradictory at the time of
writing. Periodontal disease has been implicated in a two-way relationship
with diabetes, where each may affect the control and progression of
the other.
 The perio–endo interface  303

In contrast, the number of investigations on the relationship between
apical periodontitis and systemic diseases is sparse and without any sig-
nificant associations. Investigations on the effect of smoking, diabetes and
on cardiovascular disease have failed to note significant findings. This may
also be explained by the fact that the likely surface area of exposure,
between an ulcerated periapical lesion and the resident microbiota in the
root canal, is probably limited. It may, however, be argued that the selec-
tive and protective sanctuary of the root-canal system may allow privi-
leged entry for uniquely adapted strains, capable of colonizing and invading
body tissues; but this remains to be shown.
PATHWAYS OF COMMUNICATION BETWEEN PULP
AND PERIODONTIUM
The pulpal and periodontal tissues may communicate via natural anatomi-
cal features (lateral or accessory canals, apical foramina, exposed dentinal
tubules, developmental and cementum defects) or via acquired defects
(perforations or root fractures caused by iatrogenic factors and parafunc-
tional wear and tear). The patency or permeability of the communication
is determined by its morphology and dimension, as well as its content and
fluid dynamic characteristics.
LATERAL AND ACCESSORY CANALS
Lateral canals are considered to be rare in the coronal third of the root and
arise with a frequency of ≈10% in the middle third (Fig. 12.13) and
≈25–35% in the apical third (Figs 12.14, 12.15) of the root. The mean
prevalence of lateral canals, derived from a number of studies as shown
in Table 12.2, is ≈45%.
The prevalence of accessory or furcal canals in the furcation varies
between 30 and 60%. The wide range reflects the outcome of methods
used to detect them, since not all openings pass through as continuous
channels.
DENTINAL TUBULES
Under normal circumstances, dentinal tubules do not provide a communi-
cation between the pulp and periodontium but may do so if, under condi-
tions of gingival recession or loss of attachment, the cementum is worn
away by professional or home root debridement (Fig. 12.16). Dentinal
tubules provide long and extremely narrow channels of communication
(see Chapter 1) but are perfectly capable of conveying PMNs, bacteria and
their products, as well as molecular mediators of inflammation (Fig. 12.17)
(see Cementum defects).
DEVELOPMENT DEFECTS
Various defects, such as invaginations of the coronal or radicular tissues
may occur during the development of teeth (see Chapter 1). In the majority
of cases, the invaginations do not allow communication between the
tissues but, occasionally, developmental grooves, e.g. palato-gingival
groove may be deep enough to communicate with the pulp (Fig. 12.18).
Fig. 12.15  Lateral
canals containing blood
vessels in the apical
third of the root
(courtesy of Prof.  
I Kramer)

Table 12.2  Prevalence of lateral canals

Studies Year No. of teeth % with lateral canals

Rubach & Mitchell 1965 74 45
Lowman et al. 1973 46 59
Vertucci & Williams 1974 100 46
Kirkham 1975 100 23 Fig. 12.16  (a,b)
Vertucci & Gegauff 1979 400 49 Cementum and dentine
Total & mean 720 44.4 worn away by
professional or home
root debridement; note
the reduction in the
apparent periapical
lesion solely through
oral hygiene measures –  
this was not a true
periapical lesion (a) but
A periodontal bone loss
superimposed on the
periapex (courtesy of Dr
Graham Bailey)

Fig. 12.13  Lateral canal in middle Fig. 12.14  Lateral canals in the apical B
third of mandibular incisor third of a mandibular premolar
 304  The perio–endo interface

CEMENTUM COVERAGE DEFECTS Another recognized condition is the cemental tear. These occur mainly
in men and may be associated with acute or chronic trauma. They can
In 10% of teeth (see Chapter 1), the cementum does not abut or overlap result in periodontal inflammation, abscess formation and deep probing
the enamel, leaving dentinal tubules open at the cervical margin of teeth. defects. The majority of involved teeth give positive pulp responses but
Equally, such defects may sometimes arise on the root surface through they may also be found in root-treated teeth with posts. Stress concentra-
abrasion or as a result of resorption. tion related to the apical extent of the post may result in a crack within
the cementum (Fig. 12.19a), as in the shown case, with associated lateral
Fig. 12.17  radiolucency that resolved upon surgical cleaning of the crack and filling
Microorganisms within with EBA cement (Fig. 12.19b,c). The tooth also had apical retrograde
dentinal tubules of root-canal treatment.
infected tooth

IATROGENIC PERFORATIONS AND ROOT FRACTURE

Iatrogenic perforations may occur in lateral walls of the roots or through
the pulpal floor in a multirooted tooth as a result of faulty root-canal treat-
ment (furcal strip perforation, apical transportation, lateral perforation) or
restorative procedures (post or pin perforations). In addition, root fractures,
both vertical and horizontal, create an artificial communication between

A B C D

Fig. 12.18  (a) Palato-gingival groove in maxillary central incisor; (b) radiograph of the tooth showing bone loss; (c) diagnostic endodontic instrument in canal
and gutta-percha points in sinus tract and periodontal pocket, respectively; (d) radiograph demonstrating some infilling of bony defect but failure due to
communication between groove and root canal system

Fig. 12.19  (a) Crack within cementum

associated with the apical extent of a
post; (b,c) lateral radiolucency in (a)
resolved upon surgical cleaning of the
crack and filling with EBA cement

A C

the pulp space and the periodontal ligament, which may be associated with
healthy or root-treated teeth.
EFFECT OF PULP DISEASE AND ITS TREATMENT
ON THE PERIODONTIUM
PULPO-PERIAPICAL INFLAMMATION AND BONE LOSS
It is well known that pulp inflammation can be transmitted through lateral
communications to the periodontium, both in the furcation and apically;
when severe, it can manifest in submarginal bone loss, especially in
younger patients (Fig. 12.20). Pulpitis is succeeded by pulp necrosis, root-
canal infection, and apical periodontitis; the latter may manifest in a
number of ways in the periodontium. It may contribute to horizontal mar-
ginal bone loss (see Fig. 12.13), vertical intra-bony defects (see Fig.
12.11b), or furcation involvement in multirooted teeth (Fig. 12.21).
PULPO-PERIAPICAL INFLAMMATION AND
PERIODONTAL WOUND HEALING
Teeth subjected to acute dentoalveolar trauma followed by pulp necrosis
exhibit compromised periodontal healing with marginal epithelial down-
growth on their roots. Likewise, wound healing after periodontal or apical
A B
Fig. 12.20  (a) Pulpal inflammation in 16 leading to thickening of the periodontal
ligament space on the palatal root; (b) pulpal inflammation evident on opening the pulp
chamber
A B
Fig. 12.22  (a) Extrusion of root-filling material in mandibular molar; (b) delayed apical healing
associated with the extrusion
The perio–endo interface  305
surgery may also be compromised in the presence of root-canal infection,
resulting in attachment loss or recession. Many factors influence this,
including gingival tissue thickness (gingival biotype), alveolar bone level,
surgical trauma to the flap (or alternatively, the quality of flap protection),
effectiveness of flap repositioning and adequacy of suturing. Mean attach-
ment loss after periapical surgery is greater in the absence of periapical
healing (being indicative of persistent root-canal infection).
Some periodontists may request root-canal treatment on teeth with
“doubtful” pulp status when regenerative surgery is planned in the site.
The rationale is to eliminate possible sources of infection to maximize the
potential for successful periodontal outcome. The desire to eliminate
potential, unconfirmed root-canal infection must be tempered by the
knowledge that extrusion of root-canal treatment materials may have an
equally negative impact on periradicular healing (Fig. 12.22) and, there-
fore, the prognosis of subsequent periodontal surgery. Equally, some peri-
odontists may request root-canal treatment on teeth with “doubtful” pulp
status when implant fixture placement is planned in an adjacent site.
EFFECT OF IATROGENIC PROBLEMS
Iatrogenic perforations create additional, and usually larger, channels of
communication between the pulp space and periodontium. If previously
infected, these may cause insurmountable inflammation that may be treated
only by root amputation or tooth extraction. The larger is the communica-
tion, the more difficult, the management (Figs 12.23, 12.24).
Fig. 12.21  Furcal and apical bone loss in a
mandibular molar
Fig. 12.23  Perforation in central incisor
 306  The perio–endo interface

Fig. 12.26  (a) Pulpal

and periodontal
involvement of  
maxillary premolar;  
(b) progression of the
two separate processes
gives a combined lesion

Fig. 12.24  Perforation in the Fig. 12.25  Reparative dentine

floor of the pulp chamber of a defending the pulp space
mandibular molar

EFFECT OF PERIODONTAL DISEASE AND ITS

TREATMENT ON THE PULP
Fig. 12.27  Pulp inflammation
adjacent to open dentinal tubules
EFFECT OF PERIODONTAL DISEASE ON THE PULP
Biofilm contamination of the root surface and infection of the periodon-
tium appears to have only a limited effect on the pulp. This is probably
because the pulp–dentine complex response tends to close off channels of
communication by sclerosis of dentinal tubules (Fig. 12.25) and by laying
down secondary dentine. A chronic pulp response may be reflected in a
greater prevalence of dystrophic pulp calcification and canal narrowing in
periodontally involved teeth, which can lead to technical problems during
root-canal treatment. Occasionally, the bacterial stimulus from exposed
lateral canals may be sufficient to cause localized pulp necrosis and infec-
tion, adding to the periodontal problem. The pulp may eventually succumb
either because the periodontal disease reaches the root apex or the infection
in the pulp spreads (Fig. 12.26). In either case, the long-term prognosis of
the tooth is likely to be poor at this point and it should be extracted or, if
a single root of a multirooted tooth is involved, root amputation may be
considered.

EFFECT OF PERIODONTAL TREATMENT ON THE PULP

The treatment of marginal periodontitis involves patient education and oral
hygiene instruction followed by a course of non-surgical debridement.
Previously, the term root planing was used to describe this non-surgical
phase of treatment as the aim was to remove the infected cementum layer
on the root surface to encourage healing and attachment. The contempo-
rary aim of root surface debridement is to disturb the bacterial biofilm and
remove any plaque-retaining factors, such as calculus. However, this in
itself inevitably may result in some removal of the cementum layer, pos-
sibly exposing dentinal tubules. Microbial colonization of exposed tubules
can lead to localized pulp inflammation (Fig. 12.27) that would usually
resolve if the pulp is not already compromised by restorative procedures.
If compromised, then the microbial insult may be sufficient to tip the
balance towards pulp necrosis and infection. Exposure of dentinal tubules
leads to dentine sensitivity and with plaque accumulation to hypersensitiv-
ity, which is a hyperalgesic state of the former.
DEFINITION AND CLASSIFICATION
OF PERIO–ENDO LESIONS
Apical and marginal periodontitis, via their unique and different incipient
natural histories, both ultimately manifest in their common borderland, the
periodontal tissues. Despite the common manifestation, in the vast major-
ity of patients, these two disease processes are easily differentiated but, in
a small proportion, each disease process has the potential to mimic the
other and, in some, the two disease processes may be coexistent. The
importance of discrimination between the two lies in the fact that each
disease requires entirely different clinical treatment regimens, periodontal
surface debridement versus root-canal treatment, albeit with identical
goals of surface microbial decontamination. If the disease in one tissue is
either left untreated or is inadequately treated, it may secondarily progress
to involve the other tissue.

DEFINITION OF PERIO–ENDO LESIONS
The relatively small and unique group of clinical cases in which the origin
of the disease process cannot be clearly discriminated, has been loosely
termed “ ‘perio–endo” lesions. Precise definitions are elusive but may
include:
• an isolated, usually narrow, deep probing depth of pulpal or
periodontal origin, in an otherwise periodontal disease-free mouth
• lesion with submarginal or intra-bony periradicular bone loss of
pulpal and/or periodontal origin that communicates with the oral
cavity via a periodontal probing defect
• localized deep periodontal probing defect of pulpal or
a down and will also help differentiate and distinguish problems associated
periodontal origin, in a mouth with other sites of periodontal
disease, which may or may not be extensive.
These definitions do not specify the apical or marginal origin of the
lesions, as by their nature, the origin is unknown at the time of presenta-
tion. The key aspect of the definitions is that they represent a potentially
broad range of clinical presentations with a common feature, an isolated
“deep” probing defect with an uncertain (endo or perio) origin.
CLASSIFICATION OF PERIO–ENDO LESIONS
Several classifications of perio–endo lesions have been proposed but none
of them especially contributes to diagnosis or treatment. They do, however,
serve to delineate the categories possible to encounter in practice. A simple
classification is adopted here:
1 Primary endodontic lesion (with potential for secondary
periodontal involvement)
2 Primary periodontal lesion (with potential for secondary pulpal
involvement)
3 True combined lesion of dual origin.
DIAGNOSIS OF PERIO–ENDO LESIONS
Isolated “perio–endo” lesions in patients without generalized periodontal
disease are easily identified as such, despite their variable presentation.
The precise presentation features depend on the aetiology and its duration
of existence. Localized, marked areas of attachment loss (often categorized
as perio–endo lesions) also arise in patients with generalized periodontal
disease but the number of sites involved and their presentation are more
variable and complex. Many of these may simply reflect locally advanced
periodontal breakdown, defects with true uncertainty about origin are rarer
and more difficult to diagnose.
Regardless of their location and number, “perio–endo” lesions continue
to challenge clinicians in arriving at a definitive diagnosis of origin because
of the difficulty in ascertaining the pulp status, as the tissues are invisible.
Total pulp necrosis is relatively easy to diagnose (because of the high
sensitivity and specificity of pulp tests under those conditions) but partial
pulp necrosis and the presence of infection pose a problem, particularly in
multirooted teeth.
Diagnosis is based on taking a systematic and careful history and on
clinical examination; encompassing both endodontic and periodontal com-
ponents. The key elements, which should be considered together, include:
• history of dentinal, pulpal or periapical pain
• history of periodontal symptoms (gum bleeding, tooth mobility
and drifting, abscesses)
• signs of pulpal/periapical disease (including pulp tests)
• periodontal charting, including the probing profile around the tooth
• radiographic pattern of marginal and periradicular bone loss.
The perio–endo interface  307
HISTORY OF DENTINAL, PULPAL AND
PERIAPICAL PAIN
This may give clues about the pulpal history of the tooth and the likelihood
of partial pulp necrosis as the cause of the presenting findings.
HISTORY OF PERIODONTAL SYMPTOMS
The duration and nature of the periodontal symptoms will help to charac-
terize the general periodontal status and should include an assessment of
risk factors, such as smoking, stress and diabetes. The information will
give an indication of the individual’s susceptibility to periodontal break-
with generalized periodontal problems as opposed to those associated with
localized periodontal breakdown. This aspect of the examination is par-
ticularly important in patients with generalized periodontal breakdown to
assess the prognosis of the teeth in relation to the patient’s motivation and
compliance, which will affect the response to treatment.
As a rule, acute pain is not a common presenting feature of “perio–
endo” lesions because of their “open” nature. However, acute exacerba-
tions do occur and are then frequently attributed to endodontic origin but
such symptoms can arise equally commonly from either source. It has been
suggested that dentoalveolar abscesses with 30–60% spirochaetes on dark-
field microscopy are more likely to be of periodontal origin and those with
0–10% spirochaetes to be of endodontic origin.
SIGNS OF PULPAL OR PERIAPICAL DISEASE
The involved and adjacent teeth should be examined carefully for evidence
of pulpal or periapical disease. This includes performing pulp tests on the
teeth using cold, heat and electrical stimulation, as each of these tests gives
different clues. Each root or cusp of a multirooted tooth should be tested
separately to elicit unique responses from each part of the tooth. Although,
it may be thought that pulp-test responses from a tooth would be uniform
when applied to different parts of its surface, local variations in thickness
of enamel and dentine, as well as partial pulp necrosis can contribute to
different responses.
Root-filled teeth may also be associated with perio–endo lesions. The
technical quality of the root filling, how long ago it was performed,
whether it was performed under rubber dam using bleach and by whom,
should be determined. The quality of the root filling (poor or good) does
not necessarily correlate with the presence or absence of residual root-
canal infection. This must be gauged from other clinical signs of infection,
namely changes in the periodontal ligament space at canal termini (apical
or lateral).
PERIODONTAL CHARTING INCLUDING THE PROBING
PROFILE OF THE TOOTH
A full periodontal assessment must be performed if the patient gives a
history of periodontal disease. It should include a record of the recession,
mobility and furcation involvement. The nature of the restorations should
also be noted, especially on teeth designated as having combined prob-
lems. Teeth suspected of having perio–endo lesions should have their
periodontal probing profile recorded in detail using continuous probing
(Figs 12.28, 12.29).
Clinically, attachment loss is measured by probing the pocket from a
fixed reference point. Ideally, this should be the cemento–enamel junction
(CEJ), however, due to difficulties of ascertaining the position of the CEJ,
the gingival margin is often used as the reference point. The probing depth,
described as the distance between the gingival margin and the apical depth
of probe penetration, is used to characterize the distribution of the
 308  The perio–endo interface
attachment and bone loss. The accuracy and reproducibility of probing is
dependent upon the type of probe, applied force and position and orienta-
tion of the probe in relation to the tooth. The findings are denoted by a
6-point charting (3 points buccally and 3 points palatally or lingually) (Fig.
12.30) of the whole mouth and is used in conjunction with standardized
accurate full-mouth, parallel-view periapical radiographs.
A B
Fig. 12.28  (a) Three-point probing
depths palatally – distopalatal
C probing; (b) midpalatal probing;  
(c) mesiopalatal probing
BUCCAL
P
P.D 8 11 2 7 9 32 3 7 2 7 322
R 2 0 56 32 0 057 0 30
FI
M II
E E
PALATAL
P.D 4 2 3 12 10 8 5 2 2
R 0 0 24 0
FI – –
M II
M M
In contrast to this, a continuous probing profile is obtained by probing
gently along the entire circumference of the gingival sulcus of the tooth
suspected to be associated with a perio–endo lesion (see Fig. 12.12). An
accurate record of the continuous probing profile is maintained by dividing
the tooth into sections, as shown in Figure 12.29. The probing profile will
help define the nature of the pocket, i.e. whether it is long and narrow or
broad and wide, and also aid monitoring of its response to treatment.
Long, narrow pockets are classically considered to be of endodontic
origin (Fig. 12.31). However, lateral endodontic abscesses may result in
“blow-out” lesions that exhibit extremely wide, as well as deep, probing
profiles (Fig. 12.32), yet respond favourably to endodontic treatment
alone. The so-called endodontic lesions with secondary periodontal
involvement should, by definition, have deep but narrower probing profiles
BUCCAL
2 2 2
2 2 2
2
2 2
3 2
6 2
7
7 7
MESIAL DISTAL
7 8
12 8
12 9
12 10
9 10
10 10 10 10
LINGUAL
Fig. 12.29  Charting continuous probing profile of the tooth
Fig. 12.30  Six-point probing chart
produced for the maxillary incisor in  
Fig. 12.29. P = pus; PD = probing depth
in millimetres (mm); R = recession in mm;
FI = furcation involvement; M = mobility
(11 = grade of mobility)
–
 The perio–endo interface  309

A B

Fig. 12.31  (a) Probing on the distal aspect of an endodontically compromised molar; (b) radiograph of Fig. 12.32  Probing lateral endodontic abscess
involved molar

Fig. 12.33  Bone loss involving the Fig. 12.34  Bone loss
apical third encroaching on the
periapices of 15 and 17

Fig. 12.35  (a) Bone loss

between 15 and 16;  
(b) probing the bone
defect

and should respond favourably to endodontic treatment. They may also

require adjunctive periodontal management. There are, however, few
recorded cases that demonstrate such true natural progression of endodon- A
tic to periodontal disease.

RADIOGRAPHIC PATTERN OF BONE LOSS

The radiographic pattern of bone loss further helps characterize the nature
and extent of the periodontal breakdown and is read in conjunction with
the probing profile. The apical extent of bone loss (Figs 12.33, 12.34),
absence of definition of the periodontal ligament space around the per-
iradicular aspect and the general shape of the bone defect (angularity,
crater and presence of marginal bone) (Fig. 12.35), all help to characterize
the lesion. In patients with generalized periodontal disease, intra-bony
defects or horizontal bone loss affecting more than two-thirds of the root
length are more likely to have been influenced by pulp infection in the
associated tooth. B
The chance of pulp involvement is further enhanced by the presence of:

• large restorations with marked changes in contour of the pulp

chamber
• negative, delayed or exaggerated responses to pulp tests
• technically poor root filling(s).
 310  The perio–endo interface

lesion (Fig. 12.37a) is suppurative, then it may drain through a sinus tract
CAUSES OF PERIO–ENDO LESIONS AND THEIR
in the oral mucosa (Fig. 12.37b) or the periodontal ligament (Fig. 12.37c),
AETIOLOGY-BASED MANAGEMENT
as illustrated schematically (Fig. 12.38). Generally, endodontic resolution
will eliminate the pocketing (Fig. 12.37d). A lateral abscess may result in
Lesions with a higher chance of primary periodontal aetiology exhibit the
a much larger width of periodontal attachment loss. Diagnosis is straight-
following features:
forward when pulp tests are negative. When they are equivocal, because
• generalized periodontal disease of partial pulp necrosis, the diagnosis is difficult and other clues have to
• poor oral hygiene and presence of calculus be sought to arrive at a definitive diagnosis. In pure endodontic lesions,
• periodontal probing defects that are generally broad rather than even with severe bone loss, root-canal treatment alone will usually result
narrow. in complete resolution (Fig. 12.39). In cases of preoperative doubt about
the diagnosis, such a definitive response acts as a retrospective diagnostic
Lesions with a primary endodontic aetiology generally exhibit the fol-
lowing features:

• absence of generalized periodontal disease

• adequate oral hygiene
• narrow, deep, isolated, periodontal probing defect.
There are numerous causes of lesions with the latter presenting features
but the exact presentation depends upon the cause, history, duration and
episodes of acute exacerbation. The different causes, their presenting fea-
tures and selected approaches to management are described on a case basis
below to illustrate their aetiology-based treatment.

SINGLE ISOLATED PERIO–ENDO LESION

Root-canal infection
The infection of lateral canals may result in lateral areas of bone loss B
A
without always involving the root apices as a result of partial necrosis of
the pulp (see Fig. 12.10). In some cases, the periradicular area may extend Fig. 12.36  (a) Bone loss involving mesial side of mandibular premolar; (b)
around the whole of one side of the root (Fig. 12.36). In addition, if the resolution following root-canal treatment

Pulp

Sinus tract
through gingival
A B margin

Gingiva

Sinus tract
opening

Alveolar
bone
Periodontal
ligament

Mucosa

Sinus tract
opening

Periapical
lesion
C D

Fig. 12.37  (a) Furcal and apical bone loss associated with mandibular molar; (b) sinus tract Fig. 12.38  Pathways of suppuration spread
demonstrated in the same tooth; (c) periodontal probing before endodontic treatment; (d) periodontal
probing after endodontic treatment

A B
A B
Fig. 12.40  (a–b) Persistence of sinus tract following conventional root canal treatment; (c) surgical exposure reveals a labial mid-root lateral canal (arrowed); (d)
sinus resolution after cleaning and filling of lateral canal
tool. It is evident that in such a case, the wrongful selection of periodontal
root debridement as the treatment of choice may compromise subsequent
successful reattachment/regeneration of periodontal tissues. It is only on
rare occasions that conventional root-canal treatment is insufficient to
resolve a lateral lesion caused by a lateral canal, as illustrated in this case
(Fig. 12.40), where the lateral canal was fortuitously accessible on the
labial surface of an incisor for direct cleaning and filling.
Root cracks or fractures
Surprisingly, teeth with cracked roots can survive for several years without
catastrophic fracture. In the meantime, they produce periodontal break-
down with pathognomonic probing (Fig. 12.41) and bone loss (Fig. 12.42)
patterns. In Figure 12.41, the long-standing crack survived with two local-
ized deep probing defects on opposite surfaces of the root with mild
symptoms and without post-crown decementation until the extraction of
the teeth. The staining inside the root fragments shows the extent and
duration of the crack (Fig. 12.41d). The J-shaped radiographic lesion is
the classical sign of a long-standing root fracture, usually in the mesiodis-
tal plane (Fig. 12.42b). However, the precise presentation depends upon
the direction, extent and duration of the crack. A crack in the mesiodistal
plane that is prevented from progressing further apically by a crown, may
result in an associated bone defect that is limited to the coronal part of the
root (Fig. 12.43). The presence of a radicular post may mask radiographic
signs of a buccopalatal crack (Fig. 12.44). In general, cracks or fractures
will not be visible unless their plane is within 5° of that of the X-ray beam.
The perio–endo interface  311
Fig. 12.39  (a) Suppurating defect associated with
mandibular molar; (b) complete healing following
root-canal treatment and restoration
C D
Cracks can arise either in the crown (vital or non-vital teeth) or in the root
(vital or non-vital teeth; mid or apical level). Sometimes they can only be
confirmed by surgical exploration. Ultimately, the management of cracks
will involve extraction of tooth or root and may involve a judgement about
how long the unit may be left in situ, if it is asymptomatic and functional.
Such a decision would always need to be balanced against any potential
damage to a future restorative option, such as an implant through chronic
bone loss and healing by repair rather than regeneration.
Cracks arising in crowns of teeth with vital pulps seldom reach a point
of established periodontal pocketing as the tooth is extremely painful on
biting (often in a specific way) and the patient will seek advice earlier (e.g.
cracked-tooth syndrome). The crack line is often invisible in these cases.
By the time the crack line has become stained and visible, the pain on
biting is likely to have become less acute or altered in character because
of pulpal involvement. Diagnosis is confirmed by cementing a well-fitting
orthodontic band that should prevent relative movement of the tooth frag-
ments and stop or reduce the pain (Fig. 12.45a). Definitive treatment
involves placement of a cusp-covered cast restoration (Fig. 12.45b,c).
Cracks or fractures may arise in the roots of vital teeth (Fig. 12.46a,b)
and diagnosis may initially be problematic (Fig. 12.46c,d). In this case,
pulp involvement was suspected and a fracture was only noticed later
during treatment when bleeding into the canal could not be controlled. The
tooth required surgical treatment.
Cracks and fractures more commonly arise in non-vital teeth; those
with root-canal infection usually progress to extensive inflammation of
 312  The perio–endo interface

A B

C B

Fig. 12.41  (a,b) Gutta-percha points used to trace localized deep probing defects on opposite sides Fig. 12.42  (a) Root-filled mandibular incisors,
of premolars; (c) periapical radiograph of the premolars in (a,b); (d) root fragments of premolars in   one of which is fractured; note the widened
(c) following extraction periodontal ligament space; (b) over time, the
zone of widened PDL space developed into the
J-shaped pattern of bone loss around the
fractured incisor

A B

Fig. 12.43  Pattern of bone loss associated with Fig. 12.44  (a) Buccopalatal fracture in maxillary premolar; (b) appearance following removal of the
mesiodistal fracture in crowned mandibular molar fractured portion of root

the periodontium (Fig. 12.47), together with matching bone loss (Fig.
12.48). Symptoms may be mild, unless there are acute exacerbations.
Patients may report a bad taste and odour in the mouth. Cracks commenc-
ing in the crown (Fig. 12.49) may be visible with good lighting and
will often respond to biting tests on individual pairs of cusps. It is impor-
tant to protect such teeth from progression of the crack by placing a band
while endodontic treatment is carried out (Fig. 12.49c) and subsequently
by placing a permanent cast restoration with full cuspal coverage
(Fig. 12.49d,e). Cracks extending to the roots usually have a compromised
long-term prognosis but, with careful and skillful restorative management,
may offer up to 10 years’ service. As mentioned before, there is a fine
balance between choosing extraction or restoration; functional preser­
vation of the tooth has to be balanced against compromise of a future
implant site.
 The perio–endo interface  313

A B C

Fig. 12.45  (a) Banded vital premolar displaying cracked tooth syndrome; (b) preparation for a MOD onlay to provide occlusal protection; (c) MOD onlay
restoration in place

A B
Fig. 12.47  Fractured premolar with post-retained
restoration

Fig. 12.46  (a) Fracture of mesial root of vital mandibular first molar; (b) root fracture (arrowed) in Fig. 12.48  Bone loss related to fracture of the
mandibular second molar; (c) surgical exposure of root fragment (arrowed) in mandibular second mesial root of a mandibular molar
molar; (d) tooth in (b) following endodontic and surgical treatment

Teeth with cracks commencing in the root may also be tender to bite on
but display no differential discomfort on exerting pressure on individual
cusps. Such a fracture only results in a probing defect once the crack line
progresses to and beyond the gingival margin. Until then, if the crack line
is superimposed on a root filling or intraradicular post, diagnosis may be
reliant upon surgical exploration (Fig. 12.50). The degree of pocketing and
its width varies from a localized, narrow deep defect in an incipient frac-
ture to a wider defect in a more established and long-standing fracture.
The treatment will usually consist of root amputation in a multirooted tooth
or tooth extraction depending on the extent of the fracture.
All in all, the presentation of cracks and fractures is enormously diverse
in terms of pain, clinical presentation of swelling, sinus, mobility, percus-
sion sensitivity, drainage, abscess and radiographic appearance.
Root perforation
During root-canal treatment or restorative procedures, root perforation will
expose any residual infection within the root-canal system to the periodon-
tium and consequently lay the tooth open to the development of a perio–
endo lesion (Fig. 12.51). Coronal root perforations that traumatize the
marginal attachment may present with wider probing defects and are
 314  The perio–endo interface

A B C

Fig. 12.49  (a) Mandibular first molar with mesiodistal crack (arrowed); (b) periapical radiograph of tooth in (a) showing periradicular bone loss; (c) periapical
radiograph following root-canal treatment and the placement of a supporting orthodontic band; (d) tooth restored with a gold veneer crown to provide occlusal
protection; (e) radiograph of the tooth 15 months after commencement of treatment showing evidence of periradicular healing

Fig. 12.50  (a) Root-filled mandibular incisor with suspected fracture; note the
characteristically widened periodontal ligament space; (b) surgical exposure of the root Fig. 12.51  Mandibular molar with a perforation
showing an open incomplete fracture not yet communicating with the oral cavity and furcal and periradicular bone loss

difficult to manage without crown lengthening procedures (Fig. 12.52).
Perforations that are more apical have a better prognosis as they can be
treated as “iatrogenic canals” (Fig. 12.53). Immediate repair of the perfora-
tion without allowing it to become infected gives the best outcome. Furca-
tion perforations stand the best chance of success in the absence of a
periodontal communication (Fig. 12.54). The use of amalgam for repair
of perforations has been superseded by MTA (ProRoot®). Used in com-
bination with regenerative techniques in the appropriate situation it may
enhance the prognosis. Exposure of the perforation to the oral environment
(coronally or through a periodontal communication) decreases chances of
success (Fig. 12.55a). In the case shown (Fig. 12.55), a highly motivated
patient was nevertheless treated at his insistence with informed consent.
Following root-canal treatment, a flap was raised and tin foil placed as a
matrix (Fig. 12.55d) to repair the perforation surgically (Fig. 12.55e). As
the teeth appeared to have poor long-term prognosis, they were restored
with amalgam overlay restorations (Fig. 12.55g). The furcation defect
never healed and a through-and-through furcation morphology became
established following surgery but the patient was able to maintain it with
 The perio–endo interface  315

A B A B

Fig. 12.52  (a) Mandibular incisor with radiographic evidence of coronal-third Fig. 12.53  (a) Maxillary incisor with established lateral perforation; (b)
root perforation (arrowed) and a need for root-canal treatment; (b) radiographic appearance of the maxillary incisor following root-canal
mandibular incisor in (a) following crown-lengthening procedures, endodontic retreatment
treatment and new post-retained restorations

Fig. 12.54  (a) Furcal bone loss without periodontal

communication in a mandibular molar with long-
standing perforation; (b) tooth with evidence of some
healing following root-canal treatment and new
post-retained restoration

A B

Fig. 12.55  (a) Furcal bone

loss with periodontal
communication in a root-
treated mandibular molar;  
(b) periodontal probing of
the furcal bone defect of
tooth in (a); (c) surgical
exposure of the furcal
perforation; (d) tinfoil placed
below perforation to act as  
a matrix; (e) placement of
EBA cement; (f) radiograph
A B C following the sealing of the
perforation;

F
D E
 316  The perio–endo interface

Fig. 12.55 Continued  (g) the restored mandibular

molars; (h) radiograph of the mandibular molars  
10 years later

G H

D E

Fig. 12.56  (a) Radiograph of mandibular canine with external root resorption; (b) surgical exposure and removal of the granulomatous resorbing tissue;
(c) radiograph taken during root canal treatment; (d) radiograph of completed root canal treatment and coronal restoration; (e) minimal postoperative
periodontal probing of the restored defect

“bottle cleaner-type” brushes and the tooth has been functional for over Fig. 12.57  Class 4
10 years (Fig. 12.55h). Today, regenerative techniques may offer better progressive cervical
hope for such teeth. external inflammatory
resorption (arrowed)
Root resorption affecting the
mandibular first molar
Root resorption may arise anywhere on the root surface or even begin from
the crown. It can be classified into many types but most do not communi-
cate with the oral environment.
External cervical root resorption arises at the cervical margin as a result
of various insults to the periodontium (periodontal disease, trauma, tooth
bleaching, orthodontic treatment, surgery). The pattern of resorption may
vary according to the aetiology, type and severity. The entry point of
resorption may be confined and deep (with regular advancing front) (Fig.
12.56), confined and invasive (with irregular advancing front) (Fig. 12.57),

A B
Fig. 12.58  (a) Central incisor with broad shallow cervical defect; (b) surgical exposure and removal of
granulomatous resorbing tissue. The pulp is not exposed in this case and the tooth does not require
root-canal treatment
A B
Fig. 12.60  (a) Lateral incisor with large resorptive defect involving the
periodontal tissues. The central incisor also requires endodontic treatment;   f). Alternatively, or adjunctively, the groove may be filled with glass
(b) central and lateral incisors following endodontic treatment and surgical
removal of the apical portion of the lateral incisor root
and broad and shallow (with regular advancing front) (Fig. 12.58). Such
resorptive defects may be associated with a localized periodontal probing
defect, which is likely to be broader than those originating from root-canal
infections or root fractures. Management requires periodontal flap surgery
to expose and repair the defect but root-canal treatment may also be
required if the pulp is involved. The sequence of endodontic and periodon-
tal treatment depends on the nature of the problem. Sometimes both have
to be performed at the same operation for an optimal outcome (Fig. 12.56).
Internal root resorption may also lead to a communication between the
pulp and the periodontium and, if infected, may result in a perio–endo
communication. By definition, at the time of the perforation, the pulp is
likely to have been inflamed but vital. Since the process is driven by infec-
tion, the pulp may become necrotic and infected (Figs 12.59, 12.60a).
Treatment involves root-canal treatment and, if necessary, surgery (Fig.
12.60b). For differential diagnosis of these lesions see Chapter 4.
The perio–endo interface  317
Fig. 12.59  Large defect in maxillary incisor,
due to internal resorption
Anatomical tooth anomalies
These were classified in Chapter 1 and can present in a variety of ways;
the presentation is entirely dependent upon the nature of the anomaly. The
commonest perio–endo defect associated with an anomaly is due to devel-
opmental grooves on the palatal aspects of maxillary central or lateral
incisors (Fig. 12.61). They give the classical narrow, deep, localized
probing defect associated with periradicular bone loss. Identification of the
aetiology is generally easy as the groove often extends across the palatal
marginal ridge and into the cingulum pit (Fig. 12.62). The groove may
also occur bilaterally, though curiously, both teeth seldom develop perio–
endo lesions.
Sometimes the groove may be deep enough to communicate with the
pulp, which may become non-vital (see Fig. 12.18). Frequently though,
the tooth presents with a root filling. It may be that the pulp had indeed
become non-vital or that the previous operator had missed the localized
periodontal pocket and had assumed the problem to be of endodontic
origin. These teeth respond surprisingly well to surgical correction involv-
ing widening or flattening of the groove by judicious drilling (Fig. 12.62d–
ionomer cement if it is very deep. Flap adaptation and attachment is
favourable with or without guided tissue regeneration, giving successful
outcomes.
Other anatomical anomalies include root divisions (Fig. 12.63), fused
teeth (Fig. 12.64) and invaginations (Type 3) that communicate directly
with the periodontium rather than the pulp (Fig. 12.65). Consequently, the
pulp may remain vital and normal while the tooth is associated with a
periradicular radiolucency (Fig. 12.66). Some of these type 3 invaginations
may be treated by performing “root-canal treatment” on the invaginations,
while maintaining the pulp vitality; Figure 12.67 shows management of a
type 3a invagination and Figure 12.68, a type 3b invagination.
Another developmental anomaly that may lead to localized periodontal
breakdown is the presence of enamel “pearl(s)” in the furcation or proxi-
mal areas (Fig. 12.69), more common in maxillary than mandibular teeth.
These arise from a cluster of misplaced ameloblasts and vary in size. The
enamel sometimes contains a small core of dentine and, rarely, a strand of
pulp tissue. When small and confined these may be manageable but larger
pearls may need to be surgically managed by grinding, although pulp
exposure may need to be considered.
318  The perio–endo interface

Fig. 12.61  (a) Radiograph of non-vital

central incisor with periradicular bone loss;
(b) probing the developmental groove
present in the central incisor in (a);  
(c) exposure of the groove prior to
debriding and flattening the groove;  
(d) minimal postoperative probing
following surgery

B C

A B

C D

Fig. 12.62  (a) Palato-gingival groove in maxillary lateral incisor; (b) probing the
developmental defect; (c) radiograph of the lateral incisor prior to treatment;  
E F (d) surgical exposure of the defect; (e) groove flattened and debrided;  
(f) postoperative radiograph of the lateral incisor
 The perio–endo interface  319

A B A B C

Fig. 12.63  (a) Radiograph of maxillary lateral incisor with Fig. 12.64  (a) Fused central and lateral maxillary incisors (buccal view); (b) radiograph
two roots and a palato-gingival groove; (b) extracted of the fused teeth prior to extraction; (c) extracted fused teeth (palatal view)
specimen of maxillary lateral incisor with root division and
grooving; attempted endodontic treatment failed

Fig. 12.65  (a) Radiograph

of lateral incisor with
anatomical defect and bone
loss; (b) clinical appearance
of the lateral incisor with a
sinus tract (arrowed);  
(c) radiograph of the lateral
incisor following root-canal
treatment, debridement and
sealing of the defect

A
C

Fig. 12.66  Vital lateral incisor with

gingivo-palatal groove and large
periradicular radiolucency

A B

Fig. 12.67  (a) Root canal treatment of type 3a invagination;

(b) decontamination and calcium hydroxide dressing results in periradicular
resolution with maintained pulp vitality
 320  The perio–endo interface
A B
Fig. 12.68  (a) Lateral incisor with type 3b invagination; (b) root-filled
invagination shows complete periradicular healing with maintained pulp vitality
Fig. 12.69  Enamel “pearl(s)” in the furcation or proximal areas
Fig. 12.70  Loss of
periodontal attachment
on the distal side of   Poorly designed restorations
a maxillary canine
following orthodontic
treatment
Orthodontic treatment
Rarely, orthodontic treatment may result in localized periodontal break-
down, due to an adverse combination of factors, such as poor plaque
control, unfavourable soft tissue anatomy (thin quality tissues), tooth
spacing and bone morphology. Such a situation may arise, for example,
when an impacted maxillary canine is orthodontically moved into position
(Fig. 12.70). Management is based on correction of local factors and relies
on periodontal expertise.
Fig. 12.71  Localized
periodontal breakdown
related to a poorly
placed restoration;
although there is
periodontal involvement
of adjacent teeth as
well
Fig. 12.72  Localized periodontal
breakdown related to splinted
restorations (premolar is also
endodontically involved)
Tooth transplantation and replantation
These have traumatic impact on the periodontal attachment whether the
procedure is elective or accidental. Both can result in localized permanent
damage to the attachment apparatus leading to a periodontal probing
profile that varies according to the extent of injury. Prevention of the
problem by care during the primary procedure is always the optimal
approach but, once compromised, management is by correction of local
factors and relies on periodontal expertise.
Although poor oral hygiene, related to poorly designed restorations rarely
results in a classical perio–endo lesion, localized breakdown of the peri-
odontal attachment (Fig. 12.71) is possible. Overhanging restorations,
over-contoured crowns and poor embrasure contours all contribute to peri-
odontal breakdown either by compromising the oral hygiene or by
encroaching on the biological width. The linking of adjacent crowns to
provide splinting is occasionally employed but the design must ensure
adequate access for cleaning (Fig. 12.72). In addition to design, compli-
ance from the patient in maintaining cleanliness is essential to avoid
secondary periodontal problems (Fig. 12.73). The probing profile in these
situations is localized to the site of restorations but is usually of the broad
type. Replacing the restorations with those of acceptable contours and
access for improvement of oral hygiene usually stabilizes the situation.
Localized periodontal disease
Although, relatively rare, very localized periodontal breakdown can occur
around a single tooth in an otherwise periodontally intact dentition (Figs
12.74, 12.75). In the cases shown, only one tooth was involved and each
had a unique probing profile that was deep, although not strictly narrow.
 The perio–endo interface  321

A B

Fig. 12.73  Failure to maintain the cleanliness of Fig. 12.74  (a) OPG showing localized periodontal disease distal to 36; (b) close-up radiograph of the
a fixed prosthesis has led to localized periodontal area affected
destruction

B A B

Fig. 12.75  (a) OPG showing localized periodontal Fig. 12.76  (a) Localized gingival recession related to a mandibular incisor; (b) extensive
disease around distal root of 37; (b) periapical localized recession related to a mandibular molar with absence of probing at the gingival
radiograph of the localized destruction margin

The profiles were broad but, at least initially, restricted to one surface.
Presentation of similar localized breakdown on the buccal surface usually
leads to extensive localized recession (Fig. 12.76).
MULTIPLE PERIO–ENDO LESIONS
Isolated lesion(s) superimposed upon
generalized periodontitis
Any of the above isolated lesions can be found presenting as part of a
generalized periodontal problem. The identification of some of these
lesions becomes more challenging because of their occurrence together
with multiple localized sites of periodontal breakdown (see Fig. 12.7).
However, careful evaluation of the presenting features along with the clini-
cal examination may help locate those lesions with a pure endodontic
aetiology, which have a better outlook as opposed to those with a primary
periodontal aetiology (Fig. 12.77), which do not respond to root-canal
treatment (Fig. 12.78) and may even accelerate their loss. The most
common categories of periodontitis affecting adults are chronic periodon-
titis and aggressive periodontitis.
Chronic periodontitis
Previously termed “adult periodontitis”, this group embraces the constel-
lation of destructive periodontal diseases, which are slowly progressive
and can be categorized as mild, moderate or severe. Disease progression
is intermittent with periods of activity and remission influenced by bacte-
rial profile and risk factors. Individuals in this group will usually have poor
levels of plaque control and multiple deposits of calculus, both supra- and
subgingival. The role of general and local modifying factors should be
considered and both smoking and diabetes (uncontrolled) are positive risk
factors for periodontitis. Within this group, bone loss can be characterized
as either irregular (vertical) or horizontal. The involved teeth normally
give positive responses to pulp testing, indicating vital but not undiseased
pulp status. Teeth with extensive attachment loss of periodontal origin
have poor prognosis and should be extracted (Fig. 12.79). If such teeth
give a negative response to pulp testing, it will not be clear without good
insight into the clinical and radiographic history whether pulp necrosis is
primary or secondary to periodontal disease. In cases of uncertainty, per-
formance of first stage root-canal treatment followed by review of response
will indicate endodontic origin if there is a good response (Fig. 12.80).
 322  The perio–endo interface

B C

Fig. 12.77  (a) OPG of patient with a long-span mandibular fixed prosthesis; (b) OPG Fig. 12.78  Bone loss around a non-vital mandibular
taken 5 years later with a developing primary periodontal lesion related to the mesial premolar with a localized probing defect which had
abutment; (c) surgical exposure of the periodontal defect demonstrating extensive   not responded to endodontic treatment – lesion
bone loss was of primary periodontal origin

Fig. 12.79  (a) Radiographs

of patient with advanced
periodontal disease and
teeth with poor prognosis;
(b) clinical view of the
same patient as in (a)
A
B

A B C

Fig. 12.80  (a) Radiograph of mandibular molar with bone loss of uncertain aetiology (courtesy of Imran Azam); (b,c) radiographs of mandibular molar indicating
the response to root-canal treatment (courtesy of Imran Azam)

Aggressive periodontitis (juvenile periodontitis [JP]; Fig. 12.81  Case of

rapidly progressive periodontitis [RPP]) prepubertal periodontitis

This category comprises a group of severe, rapidly destructive and pro-

gressive form of periodontitis (previously embracing prepubertal perio-
dontitis (Fig. 12. 81), juvenile periodontitis (JP) (Fig. 12.82) and rapidly
progressive periodontitis (RPP) (Fig. 12.83). The time of onset of the
diseases is usually not known at presentation and has an underlying genetic
predisposition with a family history. Although host susceptibility (defects
in the polymorphonuclear leucocytes) in these groups has been identified
to play a significant role in disease progression, high proportions of spe-
cific bacteria, e.g. Actinomyces actinomycetemcomitans (AA) have also
been associated with these diseases. In contrast to the previous group,
clinical features normally include good oral hygiene with extensive
 The perio–endo interface  323

A B

Fig. 12.82  Radiographs of patient with juvenile Fig. 12.83  (a) Rapidly progressive periodontitis at 29 years of age; (b) same patient at 34 years of age
periodontitis

inflammation and severe periodontal breakdown (attachment and bone

loss) that is not consistent with the low level of plaque accumulation.
Within this group, isolated vertical bone-loss patterns may be superim-
posed upon the generalized horizontal bone-loss pattern affecting more
than two-thirds of the root length. In patients with localized aggressive
disease (previously called localized juvenile periodontitis), bone loss to
the root-end of the first molars and incisors is common. Given the rapid
nature of periodontal destruction, there is usually insufficient time for
irreversible pulp damage to occur, consequently, such periodontal lesions
rarely have an endodontic component. Therefore, although the lesions may
resemble perio–endo lesions and are often categorized as such, they rarely
benefit from root-canal treatment. These lesions often “burnout” in the
later stages and may remain as slowly progressing lesions.

MANAGEMENT OF PERIO–ENDO LESIONS

ESTIMATION OF PROGNOSIS
The management of any clinical condition depends upon a diagnosis and
A
the nature of the presenting problem. The previous section illustrated the
problem-based management of the aetiological factors, where the cause is
clearly evident. The clinical notion of the term “perio–endo lesion”,
however, by definition often implies a lack of definitive diagnosis at the
outset. In many cases, the true origin is not confirmed until either endo-
dontic or periodontal treatment or, sometimes, both treatments have been
completed. Progress in management is, therefore, based on an initial pro-
visional diagnosis derived on the basis of an educated guess about the
endodontic contribution to the problem. The decision to embark on a
course of treatment is usually based on estimating the prognoses of the
teeth and the strategic value of each in the dental arch. In perio–endo cases,
B
it is unique that the prognosis cannot be ascertained until the origin is
known, that is, until either endodontic or periodontal intervention has been Fig. 12.84  (a) Radiograph of infected lateral periodontal cyst; (b) confirmation
completed. In some cases, both types of intervention may fail to resolve of communication with the mouth
the problem. This is classically the difficulty in the case of infected lateral
periodontal cysts that communicate with the mouth (Fig. 12.84). Lesions
presenting within a generalized periodontal problem with bone loss to the centres on whether the primary therapy should be periodontal or endodon-
root-end, grade 3 mobility, and positive pulp response, are deemed to have tic. In cases of uncertainty (even where there may be partially necrotic and
a poor prognosis. infected pulp tissue but this cannot be confirmed), the simplest and least
damaging therapy should be undertaken first; that is periodontal debride-
ment. However, it is crucial that caution is exercised in root debridement
TREATMENT OF PERIO–ENDO CASES lest the lesion is of endodontic origin and viable cells on the root surface
Figure 12.85 shows a decision-tree for aiding the planning of treatment are destroyed. In the absence of any sign of resolution after a short review
of isolated perio–endo lesions. Any acute problems (pain and infection) period (6–8 weeks) following the initial periodontal debridement, the deci-
should be dealt with first. Primarily, gentle debridement of the pocket is sion to intervene endodontically may be taken. The first stage of root-canal
the main form of treatment when present and only used in conjunction treatment may be carried out (noting the contents of the canal as healthy,
with antibiotics if there is spreading infection and fever. The issue usually inflamed or necrotic pulp) and the tooth dressed with non-setting calcium
 324  The perio–endo interface

Treatment of Isolated Perio-Endo Lesions

Perio-endo lesion possible causes:
usually isolated, narrow localized pocket endo
perio
fracture
resorption
check endodontic status restorations
anatomy

root treated not root treated

evaluate adequacy vitality tests

preparation:
underprepared obturation:
overprepared underfilled
perforation overfilled positive negative
zipping poor adaptation
ledges
Fig. 12.86  The shapes of the roots Fig. 12.87  Naber’s probe
of maxillary first and second molars
root canal
is root canal retreatment feasible? perio treatment treatment
• Degree II – horizontal loss of periodontal support greater than
one-third but not encompassing the total width of the tooth
•
yes no resolution? resolution? Degree III – horizontal through and through destruction of the
OHI try OHI + debridement periodontal tissues in the furcal area.
yes no yes no Classifications based on vertical loss of bone are not in common use
resolution? resolution? due to the difficulty in assessing the level of the bone. In maxillary teeth,
check vitality again; check
if doubt, do root OHI furcation involvement is evaluated from midbuccal, mesiopalatal and dis-
yes no yes no
canal treatment and perio topalatal aspects. While in mandibular teeth, they are evaluated from the
mid-buccal and mid-lingual aspects. Furcation probing is performed with
do first stage endo,
clean and shape canals,
extract special probes, such as the Naber’s probe, which is curved to allow access
still no resolution
dress with Calcium Hydroxide into the furcation (Fig. 12.87). These clinical findings are used in conjunc-
tion with radiographic findings.
resolution? no look for other causes mentioned above Root amputations are considered when the furcation is compromised by
endodontic complications or Degree II or III involvement. Factors to be
yes final treatment options: extract, resect, hemisect
considered when deciding on root amputation are:
• Tooth-related factors
▸ restorability of the tooth
Fig. 12.85  Decision-tree for management of perio–endo lesions

▸ strategic value of the tooth

hydroxide to gauge the response. By this stage, a definitive diagnosis will
be possible but some cases will fail to respond after both measures and
may need either further evaluation to determine the causative factor or • Root-related
extraction.
Only when the pulp is clearly necrotic and infected should root-canal
treatment be initiated first and the tooth dressed with calcium hydroxide.
Periodontal treatment should follow in quick succession in the absence of
a lack of immediate healing after root-canal treatment.
Where the patient motivation or compliance is poor or extensive primary
dental disease prevails, the alternative of extraction should be considered
as a first option.
• Bone-related
ROOT AMPUTATION
▸ feasibility of root canal treatment
▸ post-treatment occlusal stability
factors
▸ length of the root trunk – ideally, a tooth with a short root trunk
is a better candidate for resection. Teeth with long trunks will
have a low furcation entrance and, once established, the amount
of periodontal support remaining around the roots will be poor
▸ divergence of the roots – the smaller the divergence (closely
approximated roots), the smaller the interradicular space; these
teeth are poor candidates for resection
▸ length and shape of roots – short and small roots may exhibit
increased mobility after resection
factors
▸ the residual bone around the remaining roots should be assessed

Root amputation is the sectioning and removal of one or two roots of

multirooted teeth. This option may be considered for molar teeth where
loss of periodontal attachment has involved the furcation. A detailed under-
standing of the anatomy and morphology of molar teeth is critical and the
differences between the root shape and size in relation to the different
molars must be appreciated (Fig. 12.86). The degree of furcation involve-
ment is classified on the basis of the amount of periodontal tissue destruc-
tion in the interradicular area:
• Degree I – horizontal loss of periodontal support less than
one-third of the width of the tooth
▸ localized deep-attachment loss at one surface of the remaining
roots may compromise the long-term prognosis of an otherwise
ideal abutment.
If the tooth has poor restorative or endodontic prognoses then extraction
is the treatment of choice. The coronal and radicular access cavities for
endodontic treatment should be conservative and compatible with the
requirement of debridement to achieve the goals of infection elimination,
as well as maintaining restorability. The roots to be retained should exhibit
both good endodontic and restorative prognoses. The root(s) to be sacri-
ficed do not require root-canal treatment unless it is suspected that pulp
necrosis is contributing to the periodontal lesion (Fig. 12.88). The canals

B
A
in the root to be amputated should be dressed and sealed with amalgam
(Fig. 12.89). Some operators prefer glass ionomer cement but this can
disintegrate in the mouth and, therefore, is not the preferred choice. It is
preferred practice to complete root-canal treatment first followed by the
resective surgery. The flap design is dictated by the extent of periodontal
breakdown. Although some operators use “buccal” flaps only, it is impor-
tant that both a buccal and palatal (or lingual) flap is raised to allow access
to all the furcal entrances. Relieving incisions are only used when visibility
into the furcation and periodontal defect is poor. Intracrevicular incisions
are normally used and it is important that a full thickness flap is elevated
to allow access to both the furcal entrances from a buccal and palatal aspect
(Fig. 12.90). Following resection, the undersurface of the crown should be
bevelled to eliminate the natural concave curvature in the apico-coronal
direction. The root resection in Figure 12.91 shows poor contouring.
On rare occasions where a vital resection becomes necessary, it is
important that endodontic treatment is initiated within 2 weeks of the
surgery to reduce the risk of any postsurgical infection. Such cases are
difficult to manage endodontically because of the potential for microbial
leakage into the root-canal system that may compromise outcome – a fact
that should be pointed out to patient and periodontist alike.
A study at the Eastman on periodontally involved molars with furcation
involvement, requiring root-canal treatment (n=40) were followed with
or without root resection; the outcomes are depicted in Figure 12.92.
The teeth with root resection had a 5-year survival of 93%, while those
without root resection had a survival rate of 47%. Based on this experi-
ence, the algorithm depicted in Figure 12.93 is presented to aid the deci-
sion making for optimal management of molars with degree III furcation
involvement.
The perio–endo interface  325
Fig. 12.88  (a) Pulp necrosis may have contributed
to the periodontal lesion associated with the
mesiobuccal root of the maxillary first molar; hence  
it has been root canal treated in addition to an
amalgam plug if resection is required (b)
Fig. 12.89  (a,b) The canals of the mesial root to be amputated
were dressed with calcium hydroxide and sealed with amalgam
ROLE OF REGENERATIVE TECHNIQUES IN TREATMENT
OF PERIO–ENDO LESIONS
Guided tissue regeneration refers to procedures that are used to regenerate
the lost periodontal structures through differential tissue development.
A number of methods have been adopted to achieve this and can be clas-
sified into:
• barriers
• enamel matrix derived proteins.
In the management of perio–endo lesions, barriers have been used with
a degree of success. Barriers function on the principle of selective exclu-
sion of cells to enable the desired cells (in this case the periodontal liga-
ment cells) to repopulate the wound thus enabling new attachment
formation to the root surface (Fig. 12.94). The first barriers used were
non-resorbable, however, due to problems with their exposure, infection
and the need for surgical re-entry to remove the barrier 6 weeks later, these
have been superseded by bioabsorbable barriers. The latter group fall into
two types:
• collagen-based (usually derived from bovine or porcine source)
• synthetic-based (copolymers of polylactic or polyglycolic acid).
A successful outcome requires that the barrier is stiff enough to preserve
the space into which cells can proliferate, but also allow the wound to
remain stable. After surgery, it is important to obtain primary closure,
although exposure of the barrier a few weeks later is a common complica-
tion. This does not appear to cause significant problems as the barrier does
not become infected but instead begins to absorb sooner.
326  The perio–endo interface

Kaplan-Meier survival estimates

1.00

0.75
root_resect = Yes
root_resect = No

0.50

0.25
A B

0.0
0 1000 2000 3000
Analysis time (day)

Fig. 12.92  Five-year survival of root treated periodontally involved teeth with
or without subsequent root amputation

Algorithm for management of furcation involved molars requiring

root canal treatment and root resection
C
Primary phase therapy, diagnoses and treatment planning MUST have been
completed before acceptance of any patients for Root Canal Treatment.
Joint treatment planning is essential in all multi-disciplinary cases.
D
Periodontal Origin Endodontic Origin
Uncertain Origin Diagnosis
Vital Pulp Non-Vital or Dying Pulp

Elective Root Elective Root Canal

Root Canal Treatment
Canal Treatment Treatment Treatment
and
Record individual root Record individual recording
Record individual
canal contents and root canal contents
root canal contents
record probing profile and probing profile

Access, clean, and shape

all canals; in the root
Fig. 12.90  (a) Surgical to be resected, maintain Access, clean and Access, clean and
Treatment
exposure of furcation WL at least 1mm short shape all canals and shape all canals
E Details
prior to sectioning   of EAL “0” reading to dress with calcium and dress with
the distobuccal root;   prevent extrusion. Dress hydroxide calcium hydroxide
(b) initial cut with with calcium hydroxide
diamond instrument;  
In root to be resected, Review symptoms, Review symptoms,
(c) widened cut to  
RF to WL but in coronal check probing profile check probing profile
allow instrumentation;  
third of canal, place If pocketing reduced or If pocketing reduced
(d) elevation of an amalgam seal of eliminated, complete or eliminated, complete
disto-buccal root;   root canal treatment root canal treatment
(e) appearance of the
tooth following removal Obturate other canals If no improvement, If no improvement
of the distobuccal root; as normal with a redress with redress with
F (f) suturing following coronal IRM plug calcium hydroxide calcium hydroxide
the surgery and advise extraction
Refer back to
Fig. 12.91  Poor Complete root Periodontist for further
contouring (arrowed) resection within one management/
associated with root month of RF treatment planning
resection
If the periodontal defect presented as breakdown of the mucosa over the root-tip,
complete root canal treatment and refer to the periodontist for mucogingival surgery
(+/– apical resection and retrograde filling by endodontist).

Fig. 12.93  Algorithm for management of furcation involved molars requiring

root canal treatment and root resection
 The perio–endo interface  327

Radicular groove

A 04.12.00 05.03.01 10.03.01

B

C D

Fig. 12.94  Histological section Fig. 12.95  (a) The three radiographs show the retreatment of the left maxillary lateral incisor with a radiolucency
showing new attachment formation and palatal periodontal breakdown related to a palato-gingival groove; (b) surgical exposure of the developmental
using a barrier (courtesy of Lars groove; (c) groove sealed with glass ionomer cement; (d) synthetic bioaborbable barrier placed; (e) complete
Laurell) resolution of the bone defect after treatment

The following case shows the use of a barrier in the management of
localized perio–endo lesion associated with a deep palato-gingival groove.
The patient in Figure 12.95 presented with a localized palatal break-
down associated with the maxillary left lateral incisor. The tooth had been
root treated twice before, however, there was no resolution of the residual
probing defect, which tracked along the line of the palato-gingival groove
(originally undiagnosed). Following referral, careful assessment and plan-
ning, the patient underwent root-canal retreatment and regenerative
surgery. At surgery, it was noted that the groove, which was deep, gave
the root a bifid appearance, tracked along the palatal aspect and terminated
in the apical third (Fig. 12.95b). The groove was cleaned and opened
slightly with a narrow ultrasonic tip. The residual bone defect, which had
a narrow three-walled morphology, was debrided and all the granulation
tissue removed. The palato-gingival groove was filled with glass ionomer
cement (Fig. 12.95c) and a bioabsorbable barrier was placed (Fig. 12.95d).
At follow up, healing had been uneventful with no persistent probing depths
and complete resolution of the bone defect as shown in Figure 12.95e.
Successful outcomes with barriers require good case and site selection
(including the soft tissue assessment and the defect anatomy), as well as
close postoperative follow up. Early follow up helps to identify complica-
tions, such as infection, which should be managed promptly. Although
enamel matrix derived proteins have been extensively used in periodontal
regeneration for periodontitis patients, they have not yet been applied to
the combined perio–endo lesion.
 328  The perio–endo interface
REFERENCES AND FURTHER READING
Bender, I.B., Seltzer, S., 1972. The effect of periodontal disease on the pulp. Oral Surg
Oral Med Oral Pathol 33 (3), 458–474.
Bergenholtz, G., Lindhe, J., 1978. Effect of experimentally induced marginal
periodontitis and periodontal scaling on the dental pulp. J Clin Periodontol 5 (1),
59–73.
Kirkham, D.B., 1975. The location and incidence of accessory pulpal canals in
periodontal pockets. J Am Dent Assoc 91, 353–356.
Lin, H.J., Chan, C.P., Yang, C.Y., et al., 2011. Cemental tear: clinical characteristics and
its predisposing factors. J Endod 37 (5), 611–618.
Lindhe, I., Lang, N.P., 2008. Clinical periodontology and implant dentistry, 5th ed.
Blackwell Munksgaard, Oxford.
Lowman, J.V., Burke, R.S., Pellu, G.B., 1973. Patent accessory canals: incidence in
molar furcation region. Oral Surg Oral Med Oral Pathol 36, 580–584.
Rubach, W.C., Mitchell, D.F., 1965. Periodontal disease, age, and pulp status. Oral Surg
Oral Med Oral Pathol 19, 483–493.
Seltzer, S., Bender, I.B., Ziontz, M., 1963. The interrelationship of pulp and periodontal
disease. Oral Surg Oral Med Oral Pathol 16, 1474–1490.
Seltzer, S., Bender, I.B., Nazimov, H., et al., 1967. Pulpitis-induced interradicular
periodontal changes in experimental animals. J Periodontol 38 (2), 124–129.
Tamse, A., Fuss, Z., Lustig, J., et al., 1999. An evaluation of endodontically treated
vertically fractured teeth. J Endod 25 (7), 506–508.
Vertucci, F.J., Gegauff, A., 1979. Root canal morphology of the maxillary first premolar.
J Am Dent Assoc 99, 194.
Vertucci, F.J., Williams, R., 1974. Furcation canals in the mandibular first molar. Oral
Surg Oral Med Oral Pathol 38, 308–314.

Section 4 Multidisciplinary aspects of endodontic management
THE NATURE OF CONTEMPORARY
ORTHODONTIC MANAGEMENT
Orthodontics is the speciality of dentistry concerned with the growth and
development of the dentofacial complex, and the diagnosis, prevention and
correction of dental and facial irregularities and/or abnormalities. Ortho-
dontic treatment is commonly undertaken for the management of maloc-
clusion, which refers to any deviation from normal or “ideal” occlusion.
As well as the management of malocclusion, orthodontic treatment is
increasingly being undertaken to enhance the results of other forms of
dental and surgical treatment, with a multidisciplinary approach. These
include the management of severe skeletal discrepancies in combination
with corrective jaw surgery, termed orthognathic surgery, the management
of clefts of the lip and palate, severe craniofacial deformities, hypodontia
and obstructive sleep apnoea. In addition, with greater numbers of adults
with more compromised dentitions requesting orthodontic treatment, the
orthodontic–restorative dentistry interface is more important than ever. As
such, it is imperative for endodontists and orthodontists to have an under-
standing of each others’ specialities, as well as recognizing the situations
when they must rely on one another’s expertise.
The application of a continuous force to a tooth results in remodelling
of alveolar bone, reorganization of the periodontal ligament and tooth
movement. Orthodontic tooth movement is a complex process involving
the coordinated activity of many cell types and numerous chemical media-
tors. The application of a continuous force to a tooth surface results in the
development of areas of compression and tension within the periodontal
ligament. Tipping forces, resulting from single point contact on a tooth
surface, such as those resulting from springs on removable orthodontic
appliances, produce loads that are greatest at the alveolar crest and root
apex on diagonally opposing sides. Bodily tooth movement results from
even compressive loads along one side of the periodontal ligament, result-
ing from a force couple from a fixed orthodontic appliance. The magnitude
of the force delivered is important in determining the tissue response.
Ideally, orthodontic forces should not exceed the capillary pressure within
the periodontal ligament, in order to prevent ischaemia and tissue necrosis.
The optimal force for tooth movement also depends on the type of tooth
movement required and the root surface area of the teeth to be moved
(Table 13.1); teeth with smaller roots require reduced forces for movement.
The forces for intrusion are the lightest as the forces are concentrated at
the root apices, which have a small surface area.
Light orthodontic forces that do not exceed capillary pressure result in
frontal bone resorption in areas of periodontal ligament compression and
bone deposition in areas of periodontal ligament tension. Forces that
exceed capillary pressure result in sterile necrosis in the area of the peri-
odontal ligament affected. As such, tooth movement is delayed and bone
resorption commences from beneath the area of necrosis within a few days.
This is termed undermining resorption because the cellular response occurs
by cell populations derived from the marrow spaces of the alveolar bone
on the undersurface of the area of necrosis. Resorption of the necrotic
tissue also leads to resorption of root surface cementum adjacent to these
areas, by cells termed “cementoclasts”. This may be the mechanism
causing orthodontically-related root resorption. Areas of resorbed cemen-
tum may undergo repair if the defects are small. With prolonged heavy
© 2014 Elsevier Ltd. All rights reserved.
13
The ortho–endo interface
K Gulabivala, FB Naini  
forces, root resorption may outstrip deposition resulting in significant root
shortening.
On the whole, the orthodontic discipline does not perceive that well-
managed movement of teeth compromises the pulp–dentine complex or
tooth roots. This perception may either be generally true or the effects are
such that they do not manifest until they are beyond the care of the
orthodontist.
EFFECT OF ORTHODONTIC TOOTH MOVEMENT
ON THE PULP
Orthodontic tooth movement by virtue of direct interruption and interfer-
ence with the neurovascular supply and, to a lesser extent, indirectly by
tooth flexure, may affect the pulp physiology and status. Although the
literature is relatively restricted, studies have been performed on animal
and human teeth, which were thoroughly reviewed by Hamilton &
Gutmann (1999). The nature, direction and extent of forces exerted (type
of orthodontic technique and its execution) during tooth movement, their
intermittent or continuous nature, the apical root maturity and age of
patient may all influence pulp changes. A variety of outcome measures
have been used to determine the effect of orthodontic tooth movement on
the pulp, including effects at a tissue level (pulpal inflammation, pulpal
degeneration, cellularity, fibrotic changes, predentine width, reparative
dentine formation, pulpal space obliteration, Hertwig’s epithelial root
sheath), cellular level (pulp cell metabolism and cell respiration rate, sur-
vival or degeneration of odontoblasts), vascular level (vascularity, blood
flow, circulatory disturbances, angiogenesis), neural level (neuronal cell
density, distribution of myelinated versus non-myelinated cells), molecular
level (expression of various molecular factors including calcitonin-gene-
related neuropeptide [CGRP], methionine encephalin, β-endorphin, sub-
stance P, neurokinin A, vasoactive intestinal polypeptide, neuropeptide Y)
and clinical level (pulp response to pulp testing, signs and symptoms,
discoloration, pulpitis, pulp necrosis).
Although the results were sometimes conflicting and contradictory, the
overall findings suggest that orthodontic tooth movement can cause neu-
rovascular disturbances, which result first in inflammatory and then degen-
erative changes in the pulp, particularly in teeth with mature root apices.
The effects are likely to be mediated through variations in the expression
of a variety of controlling molecular signalling systems, which would exert
their effects at vascular, neural, metabolic, cellular, and tissue levels. The
rate and pattern of dentinogenic activity may be altered or affected result-
ing in tertiary dentine and, rarely, even pulp obliteration (Fig. 13.1). The
prevalence and severity of the effects may be affected by the magnitude,
direction, continuous or intermittent nature and duration of forces exerted,
as well as any previous history of pulpal stimulation, such as through
caries, restorations, trauma or periodontal disease. Teeth with immature
roots are likely to be less affected because of a richer, thicker and less
constrained (apical foramen size) neurovascular bundle.
Clinically evident effects are generally minimal and may include altered
sensations to stimuli, such as pulp tests, pulpitis, dentinal pain due to
distortions caused by uneven cementing resin polymerization during
bracket attachment, pulpal haemorrhage and pulp necrosis. Sensation
 330  The ortho–endo interface

A B A

D
C B

Fig. 13.1  Premolar undergoing orthodontic tooth movement showing progressive pulpal sclerosis Fig. 13.2  Blunt root apices, particularly affecting
maxillary incisors

Table 13.1  Optimal force levels for different types of tooth movement Table 13.2  Risk factors for orthodontically-induced root resorption

Type of tooth movement Force level (g) Risk factor

Bodily movement 60–120 ROOT MORPHOLOGY
Tipping 30–60 Blunt roots (Fig. 13.2)
Rotation 30–60 Pipette-shaped roots
Extrusion 30–60 PREVIOUS TRAUMA
Intrusion 10–20 HABITS
Nail biting
Digit sucking
IATROGENIC (TREATMENT) FACTORS
originating from the pulp may be blended with or masked by those emerg-
Prolonged duration of treatment
ing from the stressed periodontal ligament.
Excessively high force levels
Intrusion
EFFECT OF ORTHODONTIC TOOTH MOVEMENT Extrusion
Increased amount/distance of tooth movement
ON ROOT RESORPTION
Torquing movements, particularly moving roots towards cortical bone (use of
rectangular archwires)
Resorption of roots associated with orthodontic tooth movement is well Intermaxillary elastic traction
established and has a logical biological basis. Yet it does not occur consist-
ently and may be affected by pulpal status, root morphology and nature
and magnitude of orthodontic forces. Small amounts of root resorption, up and duration of the force; heavy intrusive or tipping forces may be the
to 1–2 mm, occur in the majority of patients undergoing fixed appliance worst. Use of fewer teeth for anchorage or loss of anchorage is an impor-
orthodontic treatment, with little known long-term implications. Approxi- tant predictor of root resorption. Light intermittent forces allow the bone
mately 15% of patients may be affected by greater than 2.5 mm loss of to resorb instead of cementum. In reality, probably both tissues undergo
root length, which may have long-term implications, particularly if it resorption but that of the more labile bone tissue may dominate, allowing
occurs in conjunction with periodontal bone loss. Potential risk factors for the tooth to move.
orthodontically-induced root resorption are listed in Table 13.2. Resorption due to orthodontic tooth movement is regarded to be either
Orthodontic tooth movement is possible because of the mechano- of the surface type or the transient inflammatory type; the former being a
responsive adaptation of alveolar bone, that is, when mechanically stressed, physiologically adaptive variety and the latter the same type with super-
the bone resorbs and adapts. Likewise, cementum, the hard tissue covering imposed inflammation mediated by minor injury. Such resorption has been
dentine, is also labile, though to a lesser extent, otherwise the root would said to affect about 40% of maxillary incisors and almost 20% of man-
resorb instead of bone. The resorptive mechanism is similarly mediated dibular incisors. The classical radiographic pattern is slight blunting or
by blastic and clastic cells of the cementum type. It is supposed that the rounding of the root apex, sometimes extending to gross resorption (Fig.
primary factor influencing the resorption of cementum is the magnitude 13.2). The change in root shape is accompanied by maintenance of the

B
A
periodontal ligament space and its width. Apical root resorption is said to
be evident four times more commonly than lateral root resorption but it is
likely that histologically, such resorption affects those surfaces under
excessive pressure. Apical root resorption is more commonly manifest on
radiographs because the relative thinness of the roots makes the resorption
more evident. Theoretically, it could also be because the apical cementum
is more labile, although this is not consistent with the fact that root apices
are covered by cellular cementum, which is less prone to resorption than
the acellular cementum, which covers most of the root. Roots with pipette
shaped or blunt roots may be more susceptible to apical resorption.
The risk of severe localized root resorption during orthodontic treatment
appears to be greater for maxillary incisors (Fig. 13.3), with 3% of teeth
affected compared to less than 1% for all other teeth. This risk is increased
even further, up to a 20-fold, if the roots are forced against the palatal
cortical plate during treatment.
EFFECT OF ORTHODONTIC TOOTH MOVEMENT
ON RESORPTION OF VITAL, NON-VITAL OR
ROOT-TREATED TEETH
Once the cementum has been resorbed due to orthodontic forces, it was
supposed that the response of the dentine may potentially vary according
to the pulpal status. The responses to exposure of the dentine may be
predicted from a knowledge of pulpal and periapical aetiopathogenesis.
It may be speculated that exposure of vital healthy dentine may have an
exacerbating, reducing or neutral effect on resorption. It may be surmised
that the odontoblasts may remain neutral towards resorption because it is
a process external to the pulp and unconnected to it. An inhibitory effect
is only manifested by the unmineralized predentine if and when this
becomes involved. Alternatively, it may be supposed that the odontoblastic
process is able to sense peripheral damage and respond with a defensive
reaction through molecular release, although there is no evidence for
such a response. Lastly, the possible initiation of pulpal inflammation
through noxious stimuli or a neurogenic response (CGRP) may result in
an increase in resorption. The latter speculation is strongly believed in
some quarters.
In contrast, exposure of dentine associated with a necrotic and infected
pulp is likely to lead to a source of inflammation in the resorptively active
periodontal ligament, which in turn, would fuel a rapid acceleration in the
rate and extent of resorption. This would be similar to the aggressive
inflammatory resorption associated with traumatic injuries but is not
widely seen or reported, presumably because such teeth would normally
be root treated before embarking on orthodontic treatment.
Exposure of root-treated dentine is liable to lead to a variety of responses,
depending upon the inner state of the pulp space. It is evident that in
a tooth with well-performed root-canal treatment (biologically and
The ortho–endo interface  331
Fig. 13.3  Marked root resorption of the maxillary
central incisor teeth during fixed appliance
orthodontic treatment: (a) pretreatment; (b) during
treatment
technically with an absence of apical pathosis) and an inert root-filling
material, exposure of dentine or root-filled pulp space would elicit a
neutral response with a maintained periodontal ligament space. Likewise,
in a tooth with a technically inadequate root filling but absence of apical
pathosis (because the treatment had involved vital extirpation without root
canal infection), it is likely that the response would be neutral. In contrast,
where the treatment had been biologically inadequate (residual root-canal
infection) but technically sound (absence of periapical pathoses, techni-
cally adequate root filling), root resorption may expose the underlying
residual infection, leading to the development of periradicular inflamma-
tion and enhanced root resorption. In the case of a technically inadequate
root-canal treatment with a residual root-canal infection (associated apical
pathosis), the response to resorption would be expected to be similar to
that of a tooth with an infected root-canal system with apical pathosis, that
is, aggressive root resorption. Exposure of root-filling material that is not
biologically compatible may also result in some sort of inflammation-
fuelled exacerbation of the resorption. The exposed root-filling material
may or may not be resorbed depending upon its properties and the
host response. The scenarios clearly do not cover all eventualities and a
variety of responses would be expected from the continuous spectrum of
scenarios likely to exist in reality.
The literature mainly focuses on the comparison between vital and root-
treated teeth, the effect on non-vital teeth with or without periapical lesions
is ignored; the available studies on animals or humans either use radio-
graphic or histological outcome measures. The findings from these studies
have been conflicting. The majority of studies (n = 4) suggest there is no
difference in response between root-treated and vital teeth, a slightly
smaller number of studies (n = 3) suggest that vital teeth may resorb to a
greater extent than root-treated teeth, while a smaller number of studies
(n = 2) still suggest that root-treated teeth resorb to a greater extent than
vital teeth. These apparently conflicting findings may be explained by the
speculative proposals above.
EFFECT OF PREVIOUS TRAUMATIC INJURIES ON
ORTHODONTICALLY-MEDIATED RESORPTION AND
TOOTH MOVEMENT
Traumatic injuries may leave teeth with compromised but vital pulps,
repaired or unrepaired crown and root fractures, repaired or regenerated
periodontal support apparatus, ankylosis, arrested or on-going resorption
and arrested or on-going root development. Orthodontic movement of
traumatized teeth may be associated with modified responses. It may
become necessary orthodontically to move such teeth, either because of a
pre-existing malocclusion or because tooth displacement caused by the
trauma could not be corrected manually at the time. A further cause for
the need of orthodontic treatment precipitated by traumatic injury is that
 332  The ortho–endo interface
Fig. 13.4  Ankylosis
of the maxillary   by fixation with wires or screwed plates. During these procedures, it is
right canine during
orthodontic alignment
with fixed appliances
and consequent severe
disruption of the
occlusal plane, due to
unintentional intrusion
of maxillary dentition
tooth space is not protected by some means following avulsion or loss of
teeth. The consequent compensatory movement of teeth may then need to
be corrected before restorative treatment.
It is evident from the literature that traumatized teeth exhibit a range of
pulpal responses, including rapid pulp necrosis, delayed pulp necrosis or
pulp survival. In the case of teeth with compromised pulps that do not
manifest clinically, there is a higher chance that orthodontic tooth move-
ment may precipitate pulp necrosis. It is important to monitor for signs of
such changes through altered tooth discomfort or discoloration.
Teeth with repaired root fractures may be moved orthodontically without
risk of problems, even if the fragments were previously dislocated.
However, in those cases where the repair has not occurred or is poor, root
fragment separation may occur as a result. It has been suggested that teeth
that had displayed root separation at injury, albeit repositioned adequately
afterwards, should be observed for at least 2 years before initiating ortho-
dontic tooth movement.
Teeth with ankylosed roots may be moved if the area of ankylosis is
relatively small, otherwise there is likely to be no movement and, what is
more, the teeth providing anchorage could move in the opposite direction
(Fig. 13.4).
Traumatized teeth do not all show a higher propensity for root resorption
following orthodontic tooth movement, however, the likelihood is greater
if there is pre-existing resorption and if the degree of trauma was greater.
A classic dilemma regarding tooth repositioning arises when deciding
upon repositioning of an intruded tooth. Such teeth may either be allowed
to re-erupt spontaneously, be repositioned immediately using forceps or
be orthodontically repositioned once periodontal support healing is com-
plete. Immature teeth may be more amenable to spontaneous re-eruption.
If a mature tooth, which has experienced severe intrusive trauma and
required pulp therapy for that reason, must be repositioned orthodontically,
resorption appears to be less likely if a calcium hydroxide dressing is
maintained until the tooth movement is completed prior to definitive root-
canal filling placement.
EFFECT OF ORTHOGNATHIC/ORTHODONTIC TREATMENT
ON TEETH AND THEIR PULPS
When the malocclusion is based mainly on a skeletal discrepancy, it may
be necessary to correct it by orthognathic surgery, which is almost always
combined with some orthodontic tooth movement. A range of established
procedures are used for maxillary and mandibular skeletal correction.
These display characteristic prevalences for pulpal and periradicular alter-
ations. These are all brought about by direct or indirect interference with
the blood supply for variable periods of time during and after the surgery.
The surgical procedures in general demand the raising of large muco-
periosteal flaps, the sectioning of the alveolar and/or basal bone distal or
apical to the tooth apices before repositioning of the entire tooth-containing
block of bone into a new and more favourable position. This is followed
possible that the blood supply to teeth may be directly severed, sometimes
including the root apices. Otherwise, during longer procedures, blood
supply may be restricted to the teeth. The consequence is that the neurov-
ascular bundle would be affected, leading to loss of pulp sensitivity, rarely
pulp necrosis (see Fig. 14.15), and sometimes root resorption. Pulp revas-
cularization may be evident but regrowth of nerve supply is less likely.
There appear to be few permanent effects from orthognathic surgery on
pulpal tissues, which may be surprising considering the proximity of oste-
otomy cuts to the teeth. This is likely to be explained by the excellent
neurovascular supply of the maxillofacial region. Research after segmental
surgery has indicated that the vascular supply of the teeth in the mobilized
segment remained intact, although unresponsive to electrical pulp testing.
In a landmark study, Bell et al. (1975) demonstrated the biological basis
for this phenomenon, using microangiography, which showed that dental
and osseous components receive blood from a number of sources, includ-
ing the labial arteries, apical vessels, intra-alveolar vessels, the periodontal
plexus and the gingival plexus. It does appear, however, that the supporting
structures of the teeth fare better than pulps following surgery.
EFFECT OF ORTHODONTIC TOOTH MOVEMENT ON
ENDODONTIC TREATMENT AND ITS OUTCOME
Teeth undergoing orthodontic tooth movement may occasionally require
endodontic treatment although, wherever possible, the need should be
predicted beforehand during treatment planning. Root-canal treatment
during orthodontic treatment poses a number of difficulties, not least
during the diagnosis and treatment planning because of the problem of
pulpal or periradicular pain, being confounded by discomfort due to tooth
movement. Isolation of teeth could be complicated and novel methods can
be used to apply rubber dam, however, it is always better, if at all possible,
to remove wires to allow proper application of the rubber dam. Access
cavity preparation should not be compromised but it is worth remembering
that the tooth axis should be used for alignment, which may become con-
fused during tooth movement. Determination of the canal terminus and
working length could be compromised by the apical root resorption, which
may be altered further by the following visit. Under the circumstances, it
may be prudent to complete chemomechanical debridement but delay final
obturation until after completion of orthodontic treatment, with calcium
hydroxide dressing in the interim. If the dressing would be required long
term, the access should be sealed with a permanent filling material to avoid
seal breakdown. It is also a further consideration that long-term calcium
hydroxide dressing may cause tooth weakening. Apical root resorption
may complicate control of placement of root-filling material to the canal
terminus. Customization of the master gutta-percha cone is therefore
mandatory.
Should teeth require caries management or replacement of fillings, it
should be borne in mind that the pulpal response may be modified after
orthodontic tooth movement. There may be a greater propensity for unfa-
vourable pulpal responses. There is no definitive evidence that the prob-
ability of success of root-canal treatment is altered, however, the issue of
apical resorption and control of root filling extension may reduce success
rates indirectly.
ROLE OF ORTHODONTICS IN ENDODONTIC-RESTORATIVE
TREATMENT PLANNING
Orthodontic tooth movement may be used to facilitate or enhance endo-
dontic or restorative care. The most common scenario described is that of

the tooth with a crown compromised by tooth structure loss due to fracture,
caries, resorption (internal or external) or tooth surface loss. Under the
circumstances, in the presence of adequate root length and attached
gingiva, the root may be extruded using controlled orthodontic forces (See
Fig. 14.11). This process is sometimes termed forced eruption. In some
cases, subgingival fractures may extend to the level of the alveolar ridge,
making restoration of the fractured crown impossible, as any overexten-
sion of a crown margin would impinge on the biological width of the tooth
and lead to persistent gingival inflammation. As such, orthodontic extru-
sion of the fractured root coronally, out of the alveolar bone, would move
the fracture margin coronally in order that the tooth may be restored. If
enough of the tooth crown is present, it may be possible to bond an ortho-
dontic bracket and place extrusive forces via elastic traction to the root.
However, if the entire crown has fractured, leaving only the root, an attach-
ment may be temporarily cemented into the root canal, such as a thin piece
of wire with its occlusal aspect bent into a loop, to provide attachment for
the elastic traction.
Orthodontic tooth movement may also aid tooth alignment to facilitate
restorative treatment by distributing space adequately allowing properly
sized and contoured crowns or by achieving adequate tooth alignment for
bridge, denture or implant placement. Divergence of roots prior to implant
placement is often required, as otherwise implant placement may damage
the roots of the teeth. Correcting the angulation of the teeth adjacent to a
potential implant site by moving the roots away from one another will aid
the implantologist.
Implant placement may also be facilitated by moving teeth through bony
defects. This may help create adequate bone thickness in extraction sites.
It is possible, within limits, to move a tooth into a narrower edentulous
ridge, in order to develop a potential implant site. The alveolar bone that
is created behind a moving tooth will be approximately the width of the
The ortho–endo interface  333
Fig. 13.5  Alveolar ridge
created by movement  
of mandibular incisor
tooth, prior to implant
placement
root of the tooth that has been moved (Fig. 13.5). Such orthodontic implant
site development may eliminate or reduce the need for a bone graft in the
edentulous site prior to implant placement.
REFERENCES AND FURTHER READING
Bell, W.H., Fonseca, R.J., Kenneky, J.W., et al., 1975. Bone healing and
revascularization after total maxillary osteotomy. J Oral Surg 33 (4), 253–260.
Burnside, R.R., Sorenson, F.M., Buck, D.L., 1974. Electric vitality testing in orthodontic
patients. Angle Orthod 44 (3), 213–217.
Chaushu, S., Shapira, J., Heling, I., et al., 2004. Emergency orthodontic treatment after
the traumatic intrusive luxation of maxillary incisors. Am J Orthod Dentofacial
Orthop 126 (2), 162–172.
Hamilton, R.S., Gutmann, J.L., 1999. Endodontic-orthodontic relationships: a review of
integrated treatment planning challenges. Int Endod J 32 (5), 343–360.
Kaley, J., Phillips, C., 1991. Factors related to root resorption in edgewise practice.
Angle Orthod 61 (2), 125–132.
Llamas-Carreras, J.M., Amarilla, A., Solano, E., et al., 2010. Study of external root
resorption during orthodontic treatment in root filled teeth compared with their
contralateral teeth with vital pulps. Int Endod J 43 (8), 654–662.
 14
Section 4 Multidisciplinary aspects of endodontic management
The restorative–endo interface
  K Gulabivala, Y-L Ng
Much has been written about restoration of the root-treated tooth, in part
because such teeth are often lacking in sufficient coronal tooth structure
and what is remaining may be compromised by cracks or altered physical
properties. They therefore, require novel and ingenious methods of restora-
tion that account for their inherent weakness. The spectrum encompassed
by the pattern of distribution of remaining tooth structure is broad; attempts
have been made to devise an index to characterize it (Fig. 14.1). The dis-
tribution of the remaining tooth structure may enable it to be sculpted into
a preparation with adequate retention and resistance form for a restoration
or it may not (Fig. 14.2). In the latter situation, various dowel systems
have been used to supplement retention and resistance form by utilizing
the root structure. A wide range of dowel or retention systems is available
to aid restoration but significant research to support all the claims of
manufacturers is lacking. That root-treated teeth are more susceptible to
fracture is a widely held clinical impression and they may, therefore,
require different considerations when restoring them compared to vital
teeth. The high fracture rate of endodontically-treated teeth, especially
immature anterior teeth (Fig. 14.3) and those restored with mesio-occlusal-
distal (MOD) plastic restorations (Fig. 14.4) has been documented. Unre-
stored teeth, particularly mandibular molars, may develop mesiodistal
cracks across the marginal ridges in patients with heavy occlusal loading
(Fig. 14.5); but maxillary molars are not immune to such damage either
(Fig. 14.6). The three main reasons advanced to explain the possible high
fracture rate are:
1 Altered physical properties of tooth tissue The idea that root-
treated teeth are brittle has long been propagated as an explanation
for the apparently higher fracture rate of such teeth but no
convincing evidence has been found to support the theory.
Dehydrated dentine is brittle and hydrated or rehydrated dentine is
viscoelastic. The water in the dentinal tubules that confers on the
tooth its resilience. Measures to dehydrate teeth may be
counterproductive. Given that cementum is permeable to moisture,
it is difficult to envisage permanently dehydrated dentine in the
moisture-saturated mouth
2 Weakening due to loss of tooth tissue Many studies have evaluated
the effect of pattern of tooth-tissue loss as a cause of tooth
weakening. The loss of marginal ridge integrity is probably one
of the most important factors. The width of occlusal isthmus and
depth of cavities compound the situation. Loss of roof of the pulp
chamber has been considered to be an important contributory
factor in the weakening effect; its importance probably lies in
its contribution to the increased depth of the cavity, making the
cusps “longer” and more susceptible to flexure (Fig. 14.7a,b).
Loading of such cusps may lead to unfavourable stress
concentration at the cervical region making the cusps prone to
fracture (Fig. 14.7c,d)
3 Loss of proprioception Loss of the dental pulp may deprive the
tooth of some of its mechanoreceptive properties. Teeth without
pulps have a higher “load perception” threshold and may take up
to twice the load of a tooth with a vital pulp before registering
discomfort. Although proprioceptors have not been identified in
the dental pulp, there is evidence for Aβ nerve fibres which are
reputed to serve a proprioceptive function. Despite lack of clear
evidence, this concept is plausible and, together with tooth
© 2014 Elsevier Ltd. All rights reserved.
weakening, offers an attractive explanation for the apparently
higher rate of mechanical failure of root-treated teeth.
PRINCIPLES OF RESTORATION OF ROOT-TREATED TEETH
The same principles which govern the restoration of all teeth also apply
to root-treated teeth. However, it is important to pay special attention to
two factors to extend the longevity of tooth survival:
• preservation of remaining tooth tissue
• reduction of occlusal stress and its favourable distribution within
the remaining tooth tissue.
The most conservative restoration design compatible with acceptable
aesthetics and function should, therefore, be selected in conjunction with
patient consent. Occlusal loads can only be assessed subjectively from the
history: breaking restorations or teeth; occlusal tooth-tissue loss due to
attrition; abfraction lesions, mobility and drifting; and the size and activity
of the muscles of mastication are indicators of high loads. A young indi-
vidual with a thickset jaw, well-developed muscles of mastication and
marked faceting on occlusal contact areas is likely to exert greater occlusal
loads. Restoration design is dictated not only by the pattern of residual
tooth tissue but also by the properties of the restorative materials used.
Consideration of these and the occlusal demands of the individual case
together with meticulous execution of the clinical procedures should lead
to a successful and predictable restoration.
RESTORABILITY OF THE TOOTH
The restorability of the tooth should always be determined before endo-
dontic treatment as part of a general restorative and oral treatment plan.
Space available should be sufficient to place an aesthetic, functional res-
toration with cleansable contours, which will optimize the health of the
periodontal tissues and adjacent teeth. Often the tooth requiring endodontic
treatment is severely broken down and movement of neighbouring teeth
may result in occlusal (Fig. 14.8a) and proximal (Fig. 14.8b,c) loss of
space, which may occasionally be corrected by orthodontic movement but
this is not always a practical solution. Even when the tooth is not to be
restored but used as an overdenture abutment, an assessment of the space
for a denture is important (Fig. 14.9a,b). A denture with thin metal frame-
work may fracture (Fig. 14.9c).
An adequate amount of remaining tooth tissue is necessary in addition
to space. Although it is difficult to describe strict limits, a cast restoration
encompassing at least 2 mm of sound dentine around the circumference
would make the longevity of the restoration more predictable (Fig. 14.10).
In the absence of sufficient coronal tooth tissue, it may be possible to
gain retention from the root. Under such circumstances, it is critical to
evaluate the length, width, shape and curvature of the root, to assess the
potential use of a dowel. In the absence of sufficient coronal dentine, under
exceptional circumstances, it may be possible to extrude the tooth ortho-
dontically. In some procedures, the supporting alveolar and periodontal
tissues are extruded with it, which must then be recontoured surgically
prior to restoration (Fig. 14.11). Rapid extrusion may allow the tooth to
be extruded without the periodontal supporting tissues, circumventing the
 The restorative–endo interface  335

ML ML
3 0

DL
1

MB
0
A

D B
0 DB
2

Fig. 14.1  Restorability index (from McDonald A, Setchell D

(2005). Developing a tooth restorability index. Dent Update
32(6), 343–4, 346–8)

Fig. 14.2  (a–c) Distribution of remaining tooth

C structure with inadequate retention and
resistance form

A B

A B Fig. 14.4  (a) Radiograph of fractured root-treated maxillary

premolar; (b) clinical view of a fractured premolar; (c) fracture
Fig. 14.3  (a) Root-filled maxillary central incisor; through floor of the pulp chamber of molar
(b) middle third root fracture of the same tooth

C
 336  The restorative–endo interface

Fig. 14.5  (a–f) Mesiodistal

crack (arrowed) developed
in the mandibular second
molar in a patient with
heavy occlusal loading; Pulp
extirpation and crack
exploration (c); root canal
treatment of the
orthodontic band-protected
tooth (d); MOD onlay
preparation (e); and
cemented gold casting (f)

A
B C

E F

Fig. 14.6  Mesiodistal fracture

(arrowed) of maxillary molar
D

A B C D

Fig. 14.7  (a,b) Deeper proximal boxes and lack of roof of pulp chamber render cusps more prone to flexure; (c,d) photoelastic model (courtesy of Mr P O’Neilly)
showing concentration of stress increases at the base of the cusps (arrowed) when the roof of the pulp chamber is removed
 The restorative–endo interface  337

A B C

Fig. 14.8  (a) Occlusal loss of space (arrowed); (b,c) proximal loss of space (arrowed)

A B C

Fig. 14.9  (a,b) Occlusal space considerations for overdenture situation; (c) fracture of denture due to thinness of framework

A B
Fig. 14.10  The margins should be
finished on sound tooth tissue
(arrowed)

C D

Fig. 14.11  (a–d) Orthodontic extrusion and periodontal surgery are necessary to make tooth tissue
supragingival for restoration
 338  The restorative–endo interface
need for surgery. The long-term predictability of such teeth is not high and
such a plan must be agreed with informed consent about the cost–benefit
ratio.
WHEN TO RESTORE AFTER ENDODONTIC TREATMENT
The decision to place expensive coronal restorations on teeth immediately
following completion of root-canal treatment may sometimes be difficult
because of any uncertainty about success of root-canal treatment. It may
take at least one year, if not several years for a periapical lesion to heal
but it is not practical to wait this long before a permanent restoration is
placed; indeed, an early permanent coronal seal is an important final stage
in the completion of root-canal treatment so as to protect and seal the
root-canal system from recontamination and ensure success. Fortunately,
the mean success rate of root-canal treatment is relatively high (85%),
therefore, it remains only for the clinician to judge whether the tooth is
likely to fall into the 15% failure group. Persistent symptoms and signs of
infection, lack of apical patency during treatment, large periapical lesions,
extruded root-filling material, superimposed periodontal involvement and
tooth resorption may signal the teeth that may fall into this group. A small
proportion of asymptomatic teeth with the probability to fail may be
missed. It is therefore, not necessary to review the tooth for an arbitrary
period of longer than one month before providing the permanent restora-
tion. During this time, there should be no sinus, no tenderness to palpation
of the adjacent soft tissues and apices or to pressure and percussion of the
tooth. Any tooth with an uncertain postoperative endodontic status may
require a longer review period prior to restoration.
HOW TO RESTORE TEETH AFTER
ENDODONTIC TREATMENT
Restoration of the root-treated tooth should achieve satisfactory aesthetics,
form and function while preserving and protecting the maximum amount
of tooth tissue. In any given situation, a number of design options are
available. The choice depends on the structural integrity of tooth, aesthetic
and protective requirements. In order to place these in perspective, a
number of clinical cases have been used to illustrate the application of
these principles.
The biomechanics of anterior and posterior teeth are fundamentally dif-
ferent (Fig. 14.12). The anterior teeth serve an incising and tearing function
Fig. 14.12  (a,b) Line
diagrams showing
biomechanics of
anterior and posterior
teeth
A B
and, in parafunction, serve as the guiding surfaces for mandibular excur-
sions; they are generally not loaded axially except in class 3 malocclu-
sions. The teeth are broader in the labiolingual plane to provide greater
bulk and strength in this direction of loading (Fig. 14.13) and, therefore,
have long roots that are bulky labiolingually. Posterior teeth, in contrast,
serve a crushing, grinding function and have a broad rectangular base with
multiple roots, which are likely to be broad buccolingually. They are
loaded axially, except in mandibular excursive movements when lateral
forces may jar teeth in interference. Such interfering contacts, therefore
incur the worst damage on posterior teeth, resulting in cracks and fractures.
Anterior and posterior teeth therefore, merit separate consideration in
restorative options, not least because of their fundamentally different struc-
tures and loading considerations.
RESTORATION OF ANTERIOR TEETH
Tooth-coloured composite restorative material may provide an adequate
means to restore anterior teeth that have sufficient coronal tooth tissue for
adequate retention and resistance form.
Relatively intact teeth
Unrestored anterior teeth may require endodontic treatment because of
pulp necrosis caused by traumatic injury (Fig. 14.14), severance of blood
supply during surgery (Fig. 14.15), periodontal involvement (Fig. 14.16)
or tooth transplantation (Fig. 14.17). Restoration of such teeth would
normally be confined to the access cavities (Fig. 14.18) and may be
achieved satisfactorily with composite restorative material. In such cases,
“reinforcement” of the tooth by placement of a post or dowel remains
controversial (Fig. 14.19). The rationale for post placement is based on the
belief that the root-treated tooth is inherently weak and that the post would
provide a degree of reinforcement by distributing some of the stresses to
the root. The scientific support for this is equivocal. It appears that whether
a tooth is made more resistant to fracture by placement of a dowel is
dependent on the type of loading. It is widely accepted that where a post
is not required to aid retention then it should not be placed. If one is placed
then it should be at the expense of the minimal amount of tooth tissue. The
need for a post is a subjective clinical assessment based on the amount
and distribution of remaining dentine after preparation of the tooth for the
selected restoration. In Figure 14.20, sufficient dentine cores remained
after crown preparation to render post/cores unnecessary whereas, in
Figure 14.21, loss of tooth tissue in the three teeth was variable. The gold
posts and cores supplemented residual dentine cores. The idea of “rein-
forcement” has recently been resurrected with the possibility of using
adhesive luting cements to bond posts made of materials similar in physi-
cal properties to dentine (carbon-fibre or glass-fibre posts). There is, as
yet, no long-term clinical evidence to support this concept.
Previously unrestored, root-treated teeth sometimes require more exten-
sive restoration than simple access filling, for example, if the crown
requires realignment or if its discoloration cannot be dealt with by bleach-
ing alone. The most conservative restoration likely to satisfy aesthetic
and functional requirements should be selected so as not to weaken
the tooth further. Such restorations may include composite or porcelain
veneers (Fig. 14.22), with or without tooth preparation, according to the
prevailing preoperative condition. The least conservative preparation is for
a ceramometal or pure ceramic crown but, even using this design, the tooth
should be prepared to review the need for supplementation of retention by
a dowel.
Teeth with proximal cavities
A common clinical situation is one in which an anterior tooth has mesial
and distal cavities or restorations (Fig. 14.23). The addition of an access
 The restorative–endo interface  339

Fig. 14.14  Pulp necrosis following

trauma

Fig. 14.13  (a,b) Cross-sections and labio-lingual longitudinal sections of teeth

Fig. 14.15  Pulp necrosis Fig. 14.17  Pulp in

caused by orthognathic 3 damaged by
surgery transplantation

Fig. 14.16  Bone loss

around a non-vital
mandibular premolar,
which has not
responded to Fig. 14.18  Intact teeth
endodontic treatment requiring root-canal
– lesion of primary treatment may be
periodontal origin restored with composite
material
 340  The restorative–endo interface

A B

Fig. 14.19  “Reinforcement” of intact root-filled Fig. 14.20  (a) Adequate dentine cores remaining after crown preparation of root-filled canines render
teeth prepared for crowns is unnecessary posts or cores unnecessary; (b) buccal view of prepared left canine

A B

Fig. 14.21  As much tooth tissue should be Fig. 14.22  (a) Porcelain veneers – buccal view; (b) porcelain veneers – palatal view
retained as possible, supplemented with a metal
core as necessary

cavity leaves such a tooth with a “band” of missing tooth tissue across the
middle of its crown (Fig. 14.24). Provided that the labial enamel plate is
intact, relatively strong and unblemished by discoloration or surface
deformities, such as pitting, the tooth may be satisfactorily restored with
composite restorative materials. A crown may give a better aesthetic result,
particularly if adjacent teeth also need to be crowned, but will not neces-
sarily confer greater strength or durability on the tooth. The presence of
additional cavities/restorations or tooth-tissue loss would strengthen the
case for full coverage cast restorations.

Teeth with inadequate tissue for retention without

auxiliary aids
A full coverage cast restoration may be desirable if extensive tooth surface
has been lost due to caries, erosion, abrasion, attrition or previous restora-
tions. Poor aesthetics due to large restorations and severe discoloration
may also make a full crown more desirable. In such circumstances, the
“rooftop” preparations (Fig. 14.25), once recommended, are now consid-
ered too destructive. It is considered better to prepare the tooth for the
required restoration according to the requisite space demands and make
good the tooth-tissue deficit for retention and resistance form with a core Fig. 14.23  Mesial, distal and access Fig. 14.24  Loss of palatal tooth
retained by a dowel (Fig. 14.26). Spicules of tooth tissue that would not cavities leave a band of tooth tissue tissue when mesial, distal and
contribute to the strength of the tooth and may jeopardize uncomplicated missing palatally access cavities co-exist
 The restorative–endo interface  341

B B

Fig. 14.25  “Rooftop” preparation Fig. 14.26  (a,b) Use of post cores to supplement Fig. 14.27  (a) Following preparation for a crown,
dentine cores and retention spicules of tooth tissue that do not contribute to
the strength of the tooth should be sacrificed;  
(b) this also makes post/core construction easier

A B
D

Fig. 14.28  (a) The use of temporary post crowns may be complicated by recontamination of the root-canal system; (b) permanently cemented post, core and
temporary crown; (c,d) if surgery is required, the preparation margins may be modified after healing to avoid exposure of the crown/tooth junction

construction of a core may be sacrificed at this stage (Fig. 14.27). In this
way, a more conservative restoration may be constructed.
Severely broken down anterior teeth require expeditious restoration of
aesthetics and provision of predictable function. Three approaches may be
considered to achieve this during endodontic treatment:
1 A temporary post crown may be suitable if the post has adequate
length and is well fitting. Otherwise, its decementation may not
only cause inconvenience but also allow coronal leakage, further
compromising the prognosis of the tooth
2 A permanent post and core may be cemented permanently
following root canal treatment if there is a risk of losing the
temporary post-crown (Fig. 14.28a), followed by placement of a
temporary crown (Fig. 14.28b). This reduces the chances of
coronal leakage and, should periapical surgery be required (Fig.
14.28c), allows modification of the margin for a permanent crown
once the gingival margin has stabilized (Fig. 14.28d)
3 A temporary overdenture instead of post-crowns allows the
temporary seal to remain intact (Fig. 14.29). If the roots ultimately
need extraction, the overdenture also serves as an immediate
 342  The restorative–endo interface

Fig. 14.29  (a,b) Use of temporary overdenture Fig. 14.30  Prefabricated dowels
over abutments

replacement. The disadvantages include additional cost, time and

acceptability to the patient.

CHARACTERISTICS OF DOWELS OR POSTS

Dowels may be selected from a range of prefabricated designs (Fig. 14.30)
or may be custom-made (Fig. 14.31). Dowels are selected on their proper-
ties of retention, stress distribution, ease of application and cost. The
characteristics determining retention and stress distribution include mate-
rial of composition, shape, length, diameter, surface configuration and the
presence of a diaphragm.

Material of composition
The traditional material of construction was cast gold, which was sup-
plemented with wrought gold when conditions of stress or post dimensions
demanded. Soon, posts made of stainless steel and base metal alloys were
also available. The most recent additions include carbon or glass fibre posts
and ceramic posts, usually made of zirconia. The rationale for these is that
they may provide physical properties better matched to teeth and are also
deemed to be better aesthetically matched to teeth. Unfortunately, there is
a dearth of clinical evidence to support the later additions. The best evi-
dence for clinical survival exists for custom-made gold posts.
Shape
Dowels may be parallel-sided or tapering (Fig. 14.32). The parallel-
sided dowels provide better retention per unit length than the tapered
dowels. An increase in taper reduces retention. The stress-distributing
Fig. 14.31  Custom-made post and Fig. 14.32  Parallel-sided
cores or tapering dowels
characteristics of the two designs differ during installation and functional
loading. Tapered dowels generate the least stress during cementation (Fig.
14.33a), parallel-sided dowels generate greater stress by virtue of the
hydraulic pressure developed (Fig. 14.33b). However, the parallel-sided
posts perform better in function (Fig. 14.33c) because tapered posts gener-
ate a wedging force (Fig. 14.33d). This may be alleviated if the shoulder
rest is firm but this would concentrate stress at the shoulder.
Although parallel-sided dowels are considered more desirable, the
natural tapering shape of roots and prepared root canals mitigate against

A B C D
Fig. 14.33  (a) Tapered dowels generate least stress during cementation; (b) parallel dowels generate
greater stress during cementation; (c) parallel dowels provide better stress distribution in function;
(d) tapered dowels generate a wedging force during function (all courtesy of Mr P O’Neilly)
Fig. 14.35  Root perforation caused
by the parallel post in a mandibular
incisor (arrowed)
Fig. 14.36  Dentatus
Classic Post System
a dowel parallel along its entire length. Inevitably, the dowel will be
tapered in the coronal portion and be parallel-sided apically (Fig. 14.34)
but this carries a danger of apical root perforation (Fig. 14.35). One solu-
tion to this problem has been to taper the apical portion (Fig. 14.36).
Despite the relatively poorer retention and stress distribution characteris-
tics of the tapered post, it has been used successfully in many cases, which
often makes it a more conservative choice. Parallel-sided posts require
The restorative–endo interface  343
 
Fig. 14.34  Dowel tapered
coronally but parallel apically
A B C
Fig. 14.37  Selection of appropriate diameter of parallel-sided post:
B = optimum for retention and root strength
preparation of the canal to a matching shape, which can render their use
less conservative. A compromise is to select the narrowest parallel-sided
post compatible with adequate retention and strength of post and root
(Fig. 14.37).
Length
Length is as important a determinant of post retention as it is for crown
preparations. Longer posts provide better retention and stress distribution
for all types of posts in function. Unfortunately, an increase in length also
leads to greater stresses during installation, particularly of the parallel-
sided dowels. This can be eased to an extent by ensuring that the post is
vented (Fig. 14.38).
Determinants of dowel length
1 Root filling length The need for a minimum length of root filling may
limit the achievement of optimal post length in cases where the root
is of insufficient length to satisfy both requirements. There is no
 344  The restorative–endo interface
Fig. 14.38  Vented post (vent of surface – arrowed)
A B
Fig. 14.39  (a) Curved mandibular premolar prior to restoration; (b) post-
restoration radiograph indicating the influence of the position of curvature of
the root on the length of the post
common agreement about the minimum length of root filling that
should remain in the apical portion of the root: lengths from 3 to
7 mm have been suggested. There is little firm clinical evidence
to provide guidance, but what there is indicates that apical filling
material of less than 3 mm is more likely to be associated with
persistent periapical disease. The remaining root filling should be at
least 3 mm long and preferably as long as the minimum length of
post consistent with retention will allow it to be.
2 Root morphology This also influences dowel length. The degree and
position of root curvature (Fig. 14.39) and the cross-sectional size
and shape of the root will limit the length and diameter of the post
(Fig. 14.40).
3 Clinical yardsticks These have been advocated for determining post
length, including “various fractions of root length, 1 3 , 1 2 and 2 3 ”
(Fig. 14.41), “of similar length to the crown”, “in teeth with loss of
periodontal support the post should extend apical to the alveolar
bone”. Of these guidelines, the last two are widely accepted. The
required length of post for retention has to be weighed against
occlusal loading. If the loading is unfavourable, restorations retained
even by long posts may become uncemented (Fig. 14.42) but if
occlusal loading is minimal, extremely short posts may suffice
A B
Fig. 14.40  (a) Lack of appreciation of the cross-sectional profile of the root
leads to perforation; (b) extracted tooth showing the relationship between the
post and the cross-sectional shape of the root
Fig. 14.41  Over-long posts
(Fig. 14.43). It is sometimes argued that many roots are not long
enough to accommodate optimum lengths of both post and root filling
and that the length of one or the other needs to be compromised. The
choice is a matter of clinical judgement but is likely to favour post
retention.
Diameter
Posts must be of a minimum diameter to be strong enough to resist defor-
mation (Fig. 14.44) but the design of the restoration also contributes to the
fatiguing of the post and even a wide post will fracture if poorly designed
(Fig. 14.45). The diameter of a cast post should be greater than that of a
wrought post made of the same alloy if it is to be as strong. In narrow
roots, posts made of wrought metal should, therefore, be considered. Wider
posts provide only slightly better retention and their use also means thinner
and weaker residual root dentine, which may be prone to fracture (Fig.
14.46a). If the restoration is badly designed, the chances of root fracture
 The restorative–endo interface  345

A B

Fig. 14.42  (a) Decementation of unfavourably loaded long posts – note fractured porcelain on upper Fig. 14.43  Survival of favourably
right central incisor; (b) the displaced fixed prosthesis loaded short posts

B
C

Fig. 14.45  (a) Fracture of post (courtesy of Mr P King); (b) fractured post in
Fig. 14.44  Deformation of post central incisor with “roof-top” preparation; (c) displaced portion of crown
A
(courtesy of Mr P King) and fractured post

Fig. 14.46  (a) Wide posts may cause root fracture because of the
amount of dentine sacrificed; (b) unfavourable restoration designs
(such as this cantilever bridge with very wide intra-radicular post)
increase the risk of root fracture

increase (Fig. 14.46b). The minimum post diameter compatible with ade-
quate strength and retention should be considered.
Surface configuration
The surface of posts may be smooth, roughened, serrated or threaded and,
in addition, may be modified for venting. Surface characteristics influence
seating and retention. Rough or uneven surfaces increase retentive capac-
ity. Threaded posts have the best retentive properties. Prefabricated posts
with a variety of thread designs are available. They may be threaded along
their entire length or only on a restricted portion. Threaded posts generate
the greatest stresses, as demonstrated by the concentration of stresses
around the threaded portion of the post shown in Figure 14.47a. The
stresses increase when the post is loaded (Fig. 14.47b). The manner of
 346  The restorative–endo interface

A B C

E F
Fig. 14.47  (a) Higher stresses are associated with threads; (b) further increase in
stresses upon loading; (c) stresses caused by placement of a threaded parallel
post; (d) increase in stresses if the post is tightened by a quarter turn; (e)
loosening the post by tapping and cementing in place also reduces stresses; (f)
upon loading the stresses are considerably reduced (all courtesy of Mr P O’Neilly)

placement of the post also influences the stress generated. The stress asso-
ciated with the threads upon conventional placement is shown in Figure
14.47c. If the post is tightened by an extra quarter turn, the stress increases
tremendously (Fig. 14.47d). Upon loading, the stresses increase further,
but are proportionately much lower than those, due to over-tightening.
Removing the post and tapping the threads before replacement decreases
the stresses considerably. Loosening the fit of the post by removing and
replacing it and then cementing it in place also reduces the stress (Fig.
14.47e,f). Serrations on the posts are also associated with increased stresses
but not to the same extent as threads. Loading once again increases stresses.
The improved retention due to serrations and threads should, therefore, be
weighed against the disadvantages of increased stress concentration. The
surface of the post may also be modified with cutaway portions or chan-
nels, which act as escape routes for luting cement during installation and
allow better seating and improved retention. Fig. 14.48  Diaphragm built into Fig. 14.49  Root fracture associated
post/core (arrowed) with the tip of the post (arrowed)
Diaphragm
A diaphragm or an apron, usually placed on the palatal aspect, may help
to brace the tooth and distribute stresses more favourably (Fig. 14.48). It Relatively intact teeth
is also useful for making good lost tooth tissue. When there is inadequate Endodontic treatment is sometimes necessary on a tooth that has not previ-
coronal tooth tissue, a correctly designed and placed diaphragm prevents ously been restored or affected by caries. The pulp may become compro-
concentration of stresses around the apical portion of a post, which can mised by periodontal disease (Fig. 14.51), trauma (Fig. 14.52) or accidental
lead to horizontal or oblique fractures of the root (Fig. 14.49). severance of the blood supply during orthognathic surgery (Fig. 14.53).
Following root-canal treatment, the access cavity may be restored with a
plastic restorative material, such as amalgam or posterior composite, pro-
RESTORATION OF POSTERIOR TEETH vided there is no evidence of cracks in the tooth or signs of heavy occlusal
In posterior teeth, the plastic restorative material can serve as the tempo- loading (Fig. 14.54).
rary occlusal surface. The cores should have adequate proximal and occlu- The presence of cracks across marginal ridges or cusps (Fig. 14.55a,b),
sal contacts (Fig. 14.50). together with signs of heavy occlusal loading, indicates the need for cuspal
 The restorative–endo interface  347

Fig. 14.50  (a,b) Use of amalgam cores as interim Fig. 14.51  Pulp death caused by Fig. 14.52  Trauma to the first molar
restorations periodontal disease caused by a cricket ball resulting in
root fracture

A B

Fig. 14.53  Pulp compromised by orthognathic Fig. 14.54  (a,b) Simple plastic restoration of access cavity in the absence
surgery of occlusal cracks or faceting

protection – in the short term with a cemented orthodontic band (Fig.
14.55c) and in the long term preferably using a cast partial veneer gold
restoration (Fig. 14.55d,e). The design and execution of such a restoration
may be technically demanding because of the skills required. The problem
is to provide adequate retention and resistance form and to maintain the
margins in the proximal areas away from contact points to enable their
direct examination and access for cleaning. The nature of proximal contact
dictates whether it is possible to maintain the margin above the contact
or below it: the latter effectively means cutting a minimal proximal box
(Fig. 14.56).
Provided that a sufficient wrap-around effect is achieved and the prepa-
ration is minimally tapered, a satisfactory degree of retention and resist-
ance form may be obtained. Where it is considered to be insufficient, cast
pins may be employed to increase retention (Fig. 14.57).
Recent suggestions include the use of adhesive techniques, retaining the
composite materials by acid-etching enamel and dentine-bonding agents
to increase the strength of the tooth. Although supported by laboratory
studies, the durability of such bonding remains to be clinically proven. The
technique has been recommended as a temporary means of reinforcing a
tooth after endodontic treatment. Caution should be exercised in restoring
large cavities with this technique because of the potential for cusp defor-
mation and fracture caused by curing shrinkage of the composite material
(Fig. 14.58). Where cuspal coverage is required, it may be possible to bond
a base-metal alloy occlusal restoration to the prepared occlusal surface.
The use of a precious metal alloy is made possible by plating or heat treat-
ment (Fig. 14.59). In the case shown, occlusal surfaces eroded by acid and
attrition were restored by bonding heat-treated gold castings to the occlusal
surfaces. Minimal tooth preparation consisted of a bevelled margin of
1 mm depth around the circumference. This is a conservative and preferred
method for restoring relatively intact root-filled teeth.
Teeth with proximo-occlusal cavity
The case of a root-treated tooth with an existing proximal box needs dif-
ferent consideration (Fig. 14.60a). The restoration in this case will depend
on the width and depth of the box and the occlusal loading. In a tooth with
a moderately wide, shallow proximal box and no signs of severe occlusal
loading, a plastic restorative material may suffice (Fig. 14.60b). A tooth
 348  The restorative–endo interface

A
B C

Fig. 14.55  (a) Fracture line – mesiolingual cusp; (b) radiograph of molar in (a); (c) cemented orthodontic band; (d) modified onlay preparation; (e) radiograph of
tooth with root-canal treatment completed and a restoration with occlusal coverage

Fig. 14.56  (a,b) Effect of location of proximal contacts on preparation design

– mesial margin above and distal margin below contact point

Fig. 14.57  (a,b) The use of cast pins to aid retention of cast onlay
 The restorative–endo interface  349

A A

600
Disp. (µm ¥ 10)

500
Buccal Cusp Strain
400

300 Lingual Cusp Strain

Strain (µm/m)

200
Buccal Cusp Disp.

100
Composite Cure B
0
248 348 448 548 648 748 848
Fig. 14.60  (a) Root-filled tooth with moderately sized mesio-occlusal amalgam
B Time (s)
restoration and absence of faceting, cracks or history of restoration fracture;
Fig. 14.58  (a) Experimental measurement of cusp deformation caused by (b) restoration of tooth in (a) using amalgam
curing composite material in a mesio-occlusal distal cavity, using an adhesive
technique; (b) strain in buccal and lingual cusps with time after curing and
displacement of the cusps (all courtesy of Prof. N Meredith)
with a similar-sized cavity but signs of heavy occlusal loading, or which
provides lateral excursive guidance that cannot be eliminated, may benefit
more from a cast partial veneer metal restoration (Fig. 14.61). A plastic
restoration would be inadequate in a terminal tooth with a wide, deep box
with signs of heavy occlusal loading but a cast metal cuspal coverage
restoration would help to reduce such stresses and protect the tooth from
fracture (Fig. 14.62, a photoelastic model representation of the situation
shown in Figure 14.7d, under identical conditions but with a cuspal cover-
age restoration). The model remains relatively stress-free even when the
load is doubled. Figure 14.63 illustrates restoration of a case with a plastic
restorative material core followed by cuspal coverage restoration. The
premolar has been restored initially using composite on the buccal wall of
the undermined cusp to prevent discoloration by amalgam and the rest was
filled with amalgam (Fig. 14.63b). The tooth was then prepared for a
partial coverage cast onlay.

Teeth with MOD (mesio-occluso-distal) cavities

The presence of two proximal boxes almost makes it mandatory that cuspal
A protection is used, unless there is no opposing tooth or if the tooth occludes
against a tissue-born denture. Treatment options include plastic restorative
materials or cast restorations.
Amalgam may be used to provide cuspal protection by reducing cusp
height and rebuilding the entire occlusal surface. Although this is a rela-
tively cheap method of restoring a compromised tooth, it is a method that
takes considerable practice to develop correct occlusal contacts and more
occlusal reduction is required to provide adequate strength for the amalgam.
The method is suitable for those teeth already lacking considerable tooth
tissue (Figs 14.64, 14.65, 14.66).
Composite resin materials suffer from the disadvantages discussed
above, particularly when the cavity is large (Fig. 14.67). The problem
B
of curing shrinkage and its unfavourable stressing of residual tooth
Fig. 14.59  (a) Bonded heat-treated gold castings – buccal view; (b) bonded tissue may be partly overcome by using indirect composite or porcelain
heat-treated gold castings – occlusal view inlays/onlays (Fig. 14.68). The problem with these is that the cement
 350  The restorative–endo interface

A B

Fig. 14.61  (a,b) Restoration of a tooth with moderately sized mesio-occlusal amalgam with cast onlay Fig. 14.62  Photoelastic demonstration of
restoration absence of cervical stress concentration, due to
capped cusp cast onlay restoration (courtesy of
Mr P O’Neilly)

A B
C

Fig. 14.63  Restoration of root-filled mandibular premolar with capped cusp cast onlay restoration:
D (a) unrestored tooth with cavity; (b) tooth restored with core and prepared for casting; (c) cast onlay
restoration; (d) cemented onlay

A B C

Fig. 14.64  (a–c) Restoration of a severely damaged premolar and molar using capped cusp amalgam restorations

bond between the restoration and luting agent may fail allowing
microleakage.
The most conservative option is to consider (where appropriate) is the
use of partial veneer onlays (Fig. 14.69a–c), which help to minimize sac-
rifice of tooth tissue and provide adequate cuspal protection with proper
design. On a mandibular tooth, the need for a functional cusp bevel and
occlusal shoulder on the buccal aspect means greater metal coverage of
the buccal surface (Fig. 14.69d). On a maxillary tooth, the extent of metal
coverage of the buccal cusp may be minimized (Fig. 14.70). Aesthetics
may be improved by sandblasting the surface to reduce shine. The design
may be modified to suit the situation if additional tooth tissue is missing
(Fig. 14.71). However, if the preparation is executed inadequately, the
restoration will be retained poorly, resistance form will be reduced and the
aesthetics compromised.
 The restorative–endo interface  351

A A

B B

Fig. 14.65  (a,b) Clinical views of broken down Fig. 14.66  (a,b) Maxillary molar in 14.65 restored Fig. 14.67  Composite used to restore mesio-
maxillary molar with amalgam occlusal distal cavity in a root-filled premolar

A B C

Fig. 14.68  (a,b) Preparation of mandibular premolar for porcelain onlay; (c) restoration in place

A B C

Fig. 14.69  (a) Mandibular second premolar with an MOD amalgam requiring occlusal protection;
(b) preparation for partial veneer onlay; (c) gold onlay in place; (d) restoration covering the functional cusp
of the premolar

D
 352  The restorative–endo interface

Fig. 14.70  (a) Silver die of preparation for restoration of a maxillary

premolar with a capped cusp cast onlay; (b) buccal view of the
cemented cast restorations

A B

Fig. 14.71  (a) Die for modified cast onlay preparation; (b) cast
onlay preparation on the die

Fig. 14.72  Following access for Fig. 14.73  (a) Pulp

root-canal treatment and preparation exposure (arrowed)
for a ceramometal restoration, following preparation
remaining tooth tissue must be for a ceramometal
adequate for retention and resistance crown; (b) adequate
form tooth tissue remains
after access for root
canal treatment

The aesthetics of an extensive gold restoration may not be acceptable

to some patients who may prefer a full coverage ceramometal restoration.
However, before considering such a restoration the amount of tooth tissue
likely to be lost in providing space for the dual thickness of metal and
porcelain should be considered. The minimum thickness required is
1.3 mm. This may weaken the tooth further but may be an acceptable risk
in order to secure the aesthetic requirements. As long as extracoronal
tooth-tissue loss is minimal the preparation of an access cavity in addition
to sacrifice of dentine for a ceramometal restoration may leave enough
B
tooth tissue for retention and resistance form (Fig. 14.72). The preparation
of the maxillary premolar shown in Figure 14.73a for a ceramometal
crown resulted in a pulp exposure but root-canal treatment through a
coronal access cavity left enough tooth tissue (Fig. 14.73b) for retention
and resistance form without resorting to a post/core.
Retention for the core may be achieved in a number of ways, including
Teeth with inadequate tissue for retention without
the use of grooves and slots, dentine pins and dowels. Slots and grooves
auxiliary aids
cut into residual dentine require favourable distribution of the remaining
Teeth requiring root-canal treatment are often broken down to the extent dentine. The depth and size of these retentive devices depend on the physi-
that retention for a restoration is compromised (Fig. 14.74a). Restoration cal properties of the core material. Most of the currently available plastic
then requires installation of a core to replace the lost dentine before a full materials require reasonable bulk to provide strength, which limits their
or partial coverage cast restoration can be placed on the tooth (Fig. 14.74b). clinical application.

A B
A
2 mm
2 mm B
2 mm C
D
E
A B
D
E F
Fig. 14.75  (a) Use of dentine pins to retain an interim restoration: A = amalgam; B = access restoration; C = gutta percha; D = cotton wool; E = pin; (b) pin
perforation; (c) stress-induced dentinal fractures; (d) threaded pins generated the greatest stress (courtesy of Mr P O’Neilly); (e) hand-wrench for the insertion of
pins; (f) pins placed close together cause stresses to accumulate (courtesy of Mr P O’Neilly)
The use of dentine pins is not generally recommended in root-treated
teeth. The presence of a pulp chamber and root canals should provide
adequate opportunities for retention. Rarely, a pin may be useful to help
retain an interim amalgam restoration while root-canal treatment is being
performed (Fig. 14.75a). Placement of dentine pins is associated with
complications, such as perforation (Fig. 14.75b) and induction of stresses
in the dentine leading to cracks (Fig. 14.75c) and fractures. Induced
stresses are greatest with threaded (Fig. 14.75d) and friction-grip pins and
least with cemented pins but the latter require greater length for equivalent
retention. Stresses due to pins may be reduced by:
• preparing the pinhole with a sharp drill in a speed-reducing
hand-piece and minimum number of passes so as not to cut the
hole eccentrically
• using pins with minimal mismatch between size of pinhole
and pin
The restorative–endo interface  353
Fig. 14.74  (a) Tooth requiring a core to retain a cast
restoration; (b) amalgam core in place
Hairline
cracks
C
• inserting the pin using a hand-wrench (Fig. 14.75e) and unwinding
it by at least a quarter turn so as not to engage the bottom of the
pinhole
• using a threaded pin at least 4 mm long with 2 mm in dentine,
2 mm in restorative material and with 2 mm of restorative material
above the tip of the pin (Fig. 14.75a)
• using pins with sharper threads minimizes stresses during
installation (but these potentially increase stresses in function)
• using pins made of alloys softer than dentine, such as titanium,
which may induce less stress
• using only one pin per cusp because pins placed close together
result in interaction of stresses and an increased potential for
fracture (Fig. 14.75f).
The pulp space may be used for retention in a number of ways. The
most conservative is the Nayyar amalgam dowel core (Fig. 14.76). This
 354  The restorative–endo interface
A B
Fig. 14.76  (a) Nayyar amalgam core; (b) radiograph of the Nayyar amalgam
core
A B
Fig. 14.78  (a) Mandibular molar with Nayyar core; (b) mandibular molar restored with cast restoration; (c) radiograph
of the molar showing the extent of the core and cast restoration
involves placing amalgam in the pulp chamber. It was originally believed
that the amalgam should extend into the root canals to a depth of about
3 mm to retain the amalgam but it is better to seal the coronal aspect of
the root canals with zinc oxide/eugenol and use only the pulp chamber.
The coronal amalgam may be designed to act as the final capped-cusp
restoration (Fig. 14.77) or the core may be cut down for placement of a
cast restoration (Fig. 14.78). The shortness of the dowel reduces the dis-
turbance of the root filling. Adequate remaining tooth tissue is essential
and should be judged in terms of:
• depth of pulp chamber (Figs 14.76b, 14.79)
• distance from floor of pulp chamber to furcation (Fig. 14.79), floor
to amelo–cemental junction (Fig. 14.79), floor to alveolar crest
(Fig. 14.76b) and the projected margin of the crown (Fig. 14.78)
• thickness of dentine at the level of the crown margin (see
Fig. 14.10).
Nayyar cores are more rarely placed in premolars. When the remaining
coronal dentine is inadequate to support such a core, retention may be
gained by placing a dowel into one of the canals, usually the one with the
largest and straightest root and canal; for instance, the palatal canal of a
maxillary molar and the distal canal of a mandibular molar) (Fig. 14.80).
The dowel and the residual coronal dentine can then provide the retention
Fig. 14.77  (a) Root-
treated maxillary molar;
(b) molar restored with
Nayyar-based amalgam
restoration
C
Fig. 14.79  Sectioned molar
with Nayyar core in place
for the core. Multiple roots make it possible to place multiple posts, which
do not have to be as long as in single-rooted teeth.
CORE MATERIALS
AMALGAM
Amalgam remains the material of choice for cores because of its strength,
versatility, availability and dimensional stability. Its one drawback was the
slowness of set, making it difficult to prepare the core for a cast restoration
at the same visit. However, new faster- setting alloys have largely over-
come this disadvantage. Reports of systemic problems caused by amalgam
seem to be unfounded but environmental pollution caused by mercury is
raising further concerns.
COMPOSITE
Composite cores became popular because they could be command-set
and were strong. However, they tend to absorb moisture and are dimen-
sionally unstable, eugenol temporary cements tend to soften the core,
and moisture in the core may then affect the physical properties of acid-
based permanent luting cements, such as zinc phosphate, glass ionomer or
polycarboxylate.

A B
Fig. 14.80  (a–c) Stainless steel post-retained amalgam core in mandibular molar
A B
Fig. 14.81  (a) Partial veneer preparation in a maxillary premolar; (b) partial
veneer preparation in a mandibular molar; note that margins are prepared on
sound tooth structure
CERMETS
Cermets or metal reinforced glass ionomers have also been recommended
as core materials, but their strength does not compare with that of amalgam
or composites. They are suitable only for use as a space-filler to reduce
the amount of metal in the cast restoration. They should not be used as a
structural core that provides the principal retention and resistance form.
Once placed, the cores may serve as interim restorations before being
prepared for cast restorations. If aesthetic requirements allow, a conserva-
tive partial veneer restoration, such as a three-quarter crown is preferable
(Fig. 14.81). The margins of the casting should always be placed on sound
tooth tissue.
CAST CORES
Cast multiple posts or cores may be used in multirooted teeth with little
remaining coronal tooth tissue by constructing only one of the posts inte-
gral with the core and cementing the remaining post(s) into their respective
canals through the core. This method can be applied using either indirect
or direct techniques.
In the indirect technique, an impression of the tooth (Fig. 14.82a) and
post canals (Fig. 14.82b) is taken using preformed plastic patterns and
rubber-base impression material (Fig. 14.82c). A model is constructed with
a die (Fig. 14.82d), on which the post and core is waxed with drawable
posts in two canals (Fig. 14.82e,f). The cast post and core is tried in the
mouth for fit (Fig. 14.82g) and the removable posts are inserted through
their respective channels (Fig. 14.82h). The post and core system is
cemented with a luting agent, such as zinc phosphate (Fig. 14.82i,j). The
final crown is constructed with margins on sound tooth tissue (Fig. 14.82k).
The restorative–endo interface  355
C
Where some coronal tooth tissue remains, it may interfere with the path
of insertion of the core. The canal providing the path of least resistance
may be selected for the principal post to help preserve tooth tissue and
place a partial veneer cast restoration. If a substantial amount of tooth
tissue needs to be sacrificed to provide a path of insertion for the core, it
may be better to cement preformed posts into the canals and build up a
core with plastic restorative materials.
The direct technique may also be used to construct a multiple post and
core system using preformed plastic patterns and acrylic resin (Fig. 14.83).
The method is more difficult to perform than the indirect technique but is
more suitable in some circumstances.
ROOT-TREATED TEETH AS ABUTMENTS
It is generally accepted that the stresses on an abutment tooth are different
from and likely to be more severe than those on a single unit (Fig. 14.84).
There may be a higher tendency for root-treated (Fig. 14.85) abutment
teeth and their restorations to fail mechanically than vital abutments. For
this reason, many operators avoid using root-treated teeth as abutments.
However, it is also documented that such teeth can survive despite acting
as abutments (Fig. 14.86). The truth probably lies somewhere in between.
The potential for failure is a function not only of endodontic status but
also of the amount of remaining dentine, restoration design and occlusal
loading. The bridge shown in Figure 14.86 would not be expected to
survive, yet it has been in place for at least 10 years. Different bridge and
denture designs impose different stresses on the teeth and it is important
to select a design likely to reduce such stresses. Fixed–fixed bridge designs
distribute stresses equally between abutments whereas the minor retainer
in a fixed–movable design takes the lower load. The terminal abutment for
a free-end saddle design is likely to take greater loads than an abutment
for a bounded saddle. Crown to root ratios, bracing, type of retention and
rest seat design all influence lateral loading of abutment teeth. The number
of remaining teeth and potential for bracing from other teeth and soft
tissues may also dictate overall loading. The denture design selected
should attempt to minimize stresses on root-treated teeth.
OCCLUSAL LOADING
Occlusal loading is difficult to control. It is dependent not only on the
occlusal contacts but also on eating and chewing habits, parafunctional
activity and the state of the masticatory musculature. There is only limited
scope for influencing the nature and magnitude of occlusal forces. Ade-
quately designing and controlling the closure contact, intercuspal and
excursive relationships of teeth can achieve this. Lateral forces are often
regarded as being the most damaging and, therefore, designing excursive
occlusal contacts preferentially to load adjacent vital and more robust teeth
may be useful.
356  The restorative–endo interface

A B

D E

G H

K
J Fig. 14.82  (a–k) Indirect technique for the
construction of cast multipost/core

Fig. 14.83  (a,b) Direct technique for the construction

of multipost core

A B
 The restorative–endo interface  357

A B

Fig. 14.84  Stresses are likely to be more severe on Fig. 14.85  (a) Failed anterior cantilever bridge carried by a non-vital abutment; (b) displaced
an abutment tooth fixed prosthesis with fractured dentine core (arrowed)

Fig. 14.87  (a) Molar

requiring root resection;
(b) tooth post-resection

A B

Fig. 14.86  (a,b) Survival of severely weakened tooth as a bridge abutment

RESTORATION OF A TOOTH WITH A RESECTED ROOT B

If the crown of a tooth scheduled for root resection is intact, the only
restorations required are the amalgam seal in the canal of the root to be
resected and the access restoration (Fig. 14.87). If the tooth already has
a restoration with stable interproximal and occlusal contacts, no further
restoration should be required. In the absence of stable contacts, a suitable
restoration should be constructed (Fig. 14.88).
RESTORATION OF A HEMISECTED TOOTH
Teeth may be hemisected for various reasons, such as tooth fracture or
furcal involvement. The procedure may be followed by extraction of one
of the roots and restoration of the remaining one as a premolar. Restoration
is made difficult by the root morphology in the furcation (Fig. 14.89a).
Rarely, both roots may be restored as independent premolar units, but the
procedure is fraught with difficulties mainly related to controlling the
margin placement in the furcation (Fig. 14.89b). Successful restoration of
such teeth requires a high level of skill and insight about the problems to
overcome.
by blood or food products. Removal of the cause usually removes the
discoloration except in the case of severe secondary calcification, which
gives a dense, opaque yellow discoloration (Fig. 14.90). Options for treat-
ment include:
• vital bleaching
• non-vital bleaching
• labial/buccal veneers
• crowns.
VITAL BLEACHING
Vital bleaching may be considered for vital teeth sclerosed by secondary
calcification. Use of home-bleaching products is regarded by some as
potentially harmful and has been the subject of legal review in the Euro-
pean Union. Within the law at time of writing, dentists are able to use and
prescribe tooth whitening products containing or releasing 0.1% to 6%
hydrogen peroxide.

TREATMENT OF TOOTH DISCOLORATION

NON-VITAL BLEACHING
Non-vital teeth may be discoloured by various factors including caries, The use of bleaching agents in the access cavity under rubber dam isolation
restorations, secondary calcification and contamination of dentinal tubules is quite effective (Fig. 14.91a–c). Bleaching may be performed at the
358  The restorative–endo interface

A B

Fig. 14.88  (a–e) Restoration of hemisected

mandibular second molar and first molar

D E

Fig. 14.89  (a) Margin placement and contouring

difficulties caused by the shape of the tooth in the
furcal region (arrowed); (b) difficulties of contouring
restorations in the furcation

A
B

Fig. 14.90  (a) Obliteration of the pulp; (b) dense opaque

discoloration, due to the obliteration of the pulp

A

A B
D E
Fig. 14.91  (a) Preoperative view; (b) mild improvement at the end of visit; (c) more significant improvement after one week; (d) removal of root-filling material;
(e) zinc phosphate base; (f) 30-second etching of dentine; (g) hydrogen peroxide placed with cotton pledget; (h) mixing paste of sodium perborate
chair-side by placing hydrogen peroxide in the pulp chamber. Bleaching
is usually performed after the pulp chamber has been prepared by remov-
ing all restorative and root-filling material to the cervical level (Fig.
14.91d) and covering it with a layer of zinc phosphate (Fig. 14.91e). The
dentine is then etched for 30 seconds with phosphoric acid (Fig. 14.91f),
washed away and the cavity dried. Hydrogen peroxide is flooded into the
canal, taking care to ensure that there is no overflow (Fig. 14.91g). After
5–10 minutes, the access cavity is gently dried and a paste of sodium
perborate mixed with water (Fig. 14.91h) is applied. The access cavity is
properly sealed to prevent loss of dressing between appointments. There
may be some improvement at this stage (Fig. 14.91b). One week later,
further improvement is seen, due to the “walking bleach” technique
(Fig. 14.91c).
COMPOSITE OR PORCELAIN VENEERS
These can effectively mask discoloration provided that it is not severe and
that an adequate thickness of masking material is used. A combination of
bleaching and veneering may help if neither method alone is sufficient to
eliminate discoloration.
The restorative–endo interface  359
C
F
CERAMOMETAL OR CERAMIC CROWNS
These are capable of providing excellent aesthetics but require an adequate
thickness of porcelain, which means sacrificing more tissue in an already
weakened tooth.
EXTRACTION OF ROOT-TREATED TEETH AND
REPLACEMENT WITH IMPLANT-RETAINED CROWNS
It is inevitable that root-treated teeth and sometimes even those that have
not had the benefit of endodontic treatment may, at some stage, require
extraction and replacement with prosthesis. As discussed in Chapter 5,
there exist a number of options but the contemporary focus is on implant-
retained crowns because they avoid damage to and interference with adja-
cent teeth.
Teeth may require extraction because of extensive loss of tooth structure
(through tooth surface loss, caries or resorption) or cracks and fractures.
Under the circumstances and if the option of implants is to be considered,
the first priority is to maintain the periradicular alveolar bone. In this
context, it may be worth considering whether this is best achieved by tooth
 360  The restorative–endo interface
extraction and socket preservation/augmentation or by first providing first
stage root-canal treatment to allow periapical healing. Immediate place-
ment of an implant fixture into a site with previous symptomatic large
periapical lesion is not considered an optimal scenario.
The requirements of a successful implant-retained tooth, particularly in
the aesthetic zone, are adequate height, width and breadth of good quality
bone and a favourable gingival biotype. It is paramount that the implant
fixture has good primary stability on placement, demanding adequate
apical and palatal bone at the very least. For an aesthetic restoration, in
addition, there should be a good labial cortical plate supporting healthy
and thick biotype soft tissue. The factors influencing a favourable outcome
are many and, therefore, demand a good interface with the prosthodontic
and periodontal colleagues and specialists. The role of the endodontist
would be to participate in helping to control the periapical infection and
assist in bone regeneration prior to tooth extraction.
Once periapical healing is achieved, tooth extraction should be per-
formed gently with minimal trauma to the socket walls. Bone and soft
tissue grafting, as well as various substitutes may be used to augment the
socket site to help maintain the height and width of the ridge. Interdental
space maintenance is crucial and so an effective temporary restoration that
does not impinge on the socket and prevent healing is essential.
An implant restoration is prosthodontically driven and planning of
fixture placement should be based on optimal tooth position, aesthetics and
phonetics. These will dictate the optimal location, angulation and extent
of the fixture. Around these considerations are built the surgical demands
of grafting and regenerative approaches to ensure optimal integration and
aesthetic conditions.
REFERENCES AND FURTHER READING
Bergman, B., Lundqvist, P., Sjögren, U., et al., 1989. Restorative and endodontic results
after treatment with cast posts and cores. J Prosthet Dent 61 (1), 10–15.
Burke, F.J.T., 1992. Tooth fracture in vivo and in vitro. J Dent 20, 131–139.
Carter, J.M., Sorensen, S.E., Johnson, R.R., et al., 1983. Punch shear testing of extracted
vital and endodontically treated teeth. J Biomechanics 16, 841–848.
Cavel, W.T., Kelsey, W.P., Blankenall, R.J., 1985. An in vivo study of cuspal fracture.
J Prosthet Dent 53 (1), 38–41.
Dental Defence Union, 2002. Legal position with regard to teeth bleaching. Advice
leaflet GDP/014/1002.
Eakle, W.S., Maxwell, E.H., Braly, B.V., 1986. Fractures of posterior teeth in adults.
J Am Dent Assoc 112, 215–218.
Gher, M.E., Dunlap, R.M., Anderson, M.H., et al., 1987. Clinical survey of fractured
teeth. J Am Dent Assoc 114, 174–177.
Guzy, G.E., Nicholls, J.I., 1979. In vitro comparison of intact endodontically treated
teeth with and without endopost reinforcement. J Prosthet Dent 42 (1), 39–44.
Hansen, E.K., 1988. In vivo cusp fracture of endodontically treated premolars restored
with MOD amalgam or MOD resin fillings. Dent Mater 4, 169–173.
Hansen, E.K., Asmussen, E., 1990. In vivo fractures of endodontically treated posterior
teeth restored with enamel-bonded resin. Endod Dent Traumatol 6, 218–225.
Hansen, E.K., Asmussen, E., 1993. Cusp fracture of endodontically treated posterior
teeth restored with amalgam. Teeth restored in Denmark before 1975 versus after
1979. Acta Odontol Scand 51, 73–77.
Hansen, E.K., Asmussen, E., Christiansen, N.C., 1990. In vivo fractures of
endodontically treated posterior teeth restored with amalgam. Endod Dent Traumatol
6, 49–55.
Hatzikyriakeos, A.M., Reisis, G.I., Tsingos, N., 1992. A 3-year postoperative clinical
evaluation of posts and cores beneath existing crowns. J Prosthet Dent 67, 454–458.
Helfer, A.R., Melnick, S., Schilder, H., 1972. Determination of the moisture content of
vital and pulpless teeth. Oral Surg 34 (4), 661–670.
Heling, I., Gorfil, C., Slutzky, H., et al., 2002. Endodontic failure caused by inadequate
restorative procedures, review and treatment recommendations. J Prosthet Dent 87,
674–678.
Hommez, G.M., Coppens, C.R., De Moor, R.J., 2002. Periapical health related to the
quality of coronal restorations and root fillings. Int Endod J 35, 680–689.
Howe, C.A., McKendry, D.J., 1990. Effect of endodontic access preparation on
resistance to crown-root fracture. J Am Dent Assoc 121, 712–715.
Huang, T.G., Schilder, H., Nathanson, D., 1991. Effects of moisture content and
endodontic treatment on some mechanical properties of human dentine. J Endod 189
(5), 209–215.
Kantor, M.E., Pines, M.S., 1977. A comparative study of restorative techniques in
pulpless teeth. J Prosthet Dent 34, 405–412.
Kvist, T., Rydin, E., Reit, C., 1989. The relative frequency of periapical lesions in teeth
with root canal-retained posts. J Endod 15 (12), 578–580.
Lagouvardos, P., Souvai, P., Douvitasas, G., 1989. Coronal fractures in posterior teeth.
Op Dent 14, 28–32.
Lawson, T.D., Douglas, W.H., Geistfeld, R.E., 1981. Effect of prepared cavities on the
strength of teeth. Op Dent 6, 2–5.
Lewinstein, I., Grajower, R., 1981. Root dentine hardness of endodontically treated
teeth. J Endod 7, 421–422.
Nayyar, A., Walton, R.E., Leonard, L.A., 1980. An amalgam coronal-radicular dowel
and core technique for endodontically treated posterior teeth. J Prosthet Dent 43 (5),
511–515.
Panitvisai, P., Messer, H.H., 1995. Cuspal deflection in molars in relation to endodontic
and restorative procedures. J Endod 21, 57–61.
Papa, J., Cain, C., Messer, H.H., 1994. Moisture content of vital vs endodontically
treated teeth. Endod Dent Traumatol 10, 91–93.
Petelin, M., Skaleric, U., Cevc, P., et al., 1999. The permeability of human cementum in
vitro measured by electron paramagnetic resonance. Arch Oral Biol 44 (3), 259–267.
Randow, K., Glantz, P.O., 1986. On cantilever loading of vital and non-vital teeth – an
experimental clinical study. Acta Odontol Scand 44, 271–277.
Reeh, E.S., Messer, H.H., Douglas, W.H., 1989. Reduction in tooth stiffness as a result
of endodontic and restorative procedures. J Endod 15 (11), 512–516.
Sedgeley, C.M., Messer, H.H., 1992. Are endodontically treated teeth more brittle?
J Endod 18 (7), 332–335.
Sorensen, J.A., Martinoff, J.T., 1984. Intracoronal reinforcement and coronal coverage.
A study of endodontically treated teeth. J Prosthet Dent 51, 780–784.
Sorensen, J.A., Martinoff, J.T., 1984. Clinically significant factors in dowl design.
J Prosthet Dent 52, 28–35.
Trabert, K.C., Caputo, A.A., Abou-Rass, M., 1978. A comparison of endodontic and
restorative treatment. J Endod 4 (11), 341–345.

Section 4 Multidisciplinary aspects of endodontic management
The medical–endo interface and patients with special needs
OVERALL PATIENT CARE AND THE ROLE
OF ENDODONTICS
The health and well-being of an individual is influenced by factors as
diverse as their genetic make-up, environment, nutrition and interaction
with society. These factors all play a part in the physical, psychological,
social, cultural and spiritual aspects of the well-being of the individual.
Healthcare workers in general should have an awareness of the complex
interplay between such factors and their potential influence on the outcome
of any health-improving measure. Those involved in the direct delivery of
any intervention that may impinge on these factors should understand the
nature of the broadest effect of that intervention. Oral healthcare is per-
ceived by many in the general healthcare profession to play only a small
part in the overall well-being of the individual. The truth, however, is that
oral and dental problems may influence and, in turn, be influenced by the
overall well-being of the individual. Management of oral and dental health
is therefore, no less important than management of the overall health of
people. It requires a broad-based appreciation of life (including, social,
cultural, individual, psychological and spiritual contexts) in parallel with
the biological and clinical knowledge and skills necessary to deal with
diseases of the pulp and periradicular tissues. The dentist must, therefore,
be both an oral physician and surgeon.
The western world has experienced a dramatic improvement in living
standards and conditions over the last 50 years to the point that life spans
have increased to between 80 and 100 years. Such individuals are also
maintaining their dentitions for longer into their old age with the conse-
quence of increasing wear and tear problems associated with their teeth.
Paradoxically, these figures are juxtaposed with those indicating an
increase in life-style dependent diseases, such as obesity, diabetes, cardio-
vascular disease and cancer.
The dentist must therefore, be cognizant of the patient’s overall and
endodontic needs, where appropriate care is provided. The dentist must
know how to make an overall assessment of the patient and understand
how endodontic care may need to be modified or adjusted to meet the
patient’s needs. Endodontic care must be delivered within the confines of
a specific treatment plan which is patient centred, realistic and flexible.
Careful assessment and treatment planning will take account of factors,
such as patient access, general health, medical conditions and prognosis,
medication and therapeutics, previous standards of oral hygiene and
includes the skills of the dental team required to deliver care. Treatment
plans should be modified by an individual’s ability to cooperate with treat-
ment, which may fluctuate, but should retain the overall physical and
psychological well-being of the patient as the prime consideration.
The majority of patients have treatment under local anaesthesia within
a general dental practice setting, with a smaller group requiring more
specialized services, particularly for more complex treatment or manage-
ment. Inhalation sedation and intravenous sedation are indicated as the
next line of treatment when an individual is unable to cooperate for care
with local analgesia because of anxiety, learning or physical disability. For
some patients, sedation will be insufficient to manage necessary care and
treatment under general anaesthesia is indicated.
© 2014 Elsevier Ltd. All rights reserved.
15
A Mustard, K Gulabivala  
PATIENT ASSESSMENT
The completion of an up-to-date and accurate medical history is an essen-
tial prerequisite to both treatment planning and the delivery of dental care.
It should be remembered that “a good history is taken, not given” and the
dentist should actively engage with the patient, or those who care for the
patient, rather than simply request for a medical history form to be com-
pleted. It is not unusual for patients to be reluctant to divulge aspects of
their medical condition, i.e. the presence of blood-borne viruses, until trust
is established between the patient and the dental team. It is therefore, in
everyone’s best interest that relationship building between patient and
clinician is established as quickly as possible.
History taking also allows the dental team to examine the patient’s
physical appearance, behaviour and speech. The patient’s physical appear-
ance can not only provide an indication of any underlying medical condi-
tion and its severity, but also provides important information regarding
their self-esteem, ability to self-care or the level of care they are receiving.
The ability to cooperate for the dental examination can often be accurately
assessed by their behaviour but may give sufficient time for an apprehen-
sive patient to relax sufficiently to proceed. The patient’s capacity to
consent for dental treatment can be also assessed. If another person attends
with the patient, it is important to establish their relationship to the patient.
In those patients who have a visual or hearing disability, every opportunity
should be given to assure an effective means of communication is estab-
lished via additional techniques, such as bold text, braille, lip reading, sign
language and the block alphabet. Patients who have difficulty speaking,
often as a result of an underlying neurological condition, should be given
the necessary time to respond to the questions being asked if frustration
is to be avoided.
Particularly with patients who have special needs, or patients who are
being considered for treatment under conscious sedation or general anaes-
thesia, a significant amount of information needs to be gathered out-with
the confines of a pretyped medical history form or consultation. The dental
team needs to establish where the patient lives and who provides care for
the patient, the nature of the care (i.e. tooth brushing, personal hygiene)
and when is the care provided. Does the patient have any contact with
friends or relatives? Are their contact details available? Does the patient
have a support group, social worker or an Independent Mental Capacity
Advocate (IMCA).
If medical or dental treatment has been provided previously, then this
can provide important information for future care. Where and how did the
patient access their care? Was transportation required and of what type?
Were specific appointment times scheduled and how was the care deliv-
ered? Was postoperative care required? Who provided that care and in
what setting? Was the treatment successful and would that method be suit-
able for the current treatment planned?
It is highly desirable that all medical colleagues are actively aware of
any planned treatment under general anaesthesia for patients with a pro-
found learning disability. Often, additional examinations and invasive pro-
cedures, such as blood tests (which could otherwise prove impossible), can
be completed at the same time as the dental treatment.
 362  The medical–endo interface and patients with special needs
For those patients with conditions that may become progressively debil-
itating, treatment planning will need to take into account the likely nature
and time-frame of any deterioration. This may be unpredictable or impos-
sible for some conditions and can present the dental team with difficult
long-term treatment planning decisions.
MANAGEMENT OF THE
MEDICALLY-COMPROMISED PATIENT
CARDIOVASCULAR DISEASE
Cardiovascular disease (CVD) is the commonest cause of adult death in
the developed world. Hypertension is persistently raised blood pressure of
>140/90 mmHg. Ninety per cent of cases are “essential” with no non-
lifestyle causes. A significant number of the population are prescribed
antihypertensive medication via the use of diuretics, beta blockers, calcium
channel blockers, ACE inhibitors, sympatholytics and vasodilators. Stress,
including as a result of dental treatment, may further increase blood pres-
sure leading to a risk of stroke or cardiac arrest. Angina presents as a
severe, crushing chest pain. It is the result of impaired blood flow and
oxygenation of the heart muscle, usually due to atherosclerosis. Stable
angina is usually precipitated by effort and resolves with rest. Unstable
angina occurs at rest, with minimal exertion or rapidly increasing
severity.
Dental treatment for both conditions can safely be provided under local
anaesthesia. However, unstable angina carries a serious risk of myocardial
infarction and elective dental treatment should not be carried out. Care
should be given to ensure anxiety levels during treatment are minimized
and treatment under sedation may be a prudent option for the nervous
patient. Intravascular injection of epinephrine-containing local anaesthetic
should be avoided and the management of patient on anticoagulants is
discussed later in this chapter. Prophylactic glyceryl trinitrate spray has
been shown to be effective in the prevention of both hypertension and
angina during dental treatment. Routine dental treatment should be avoided
where appropriate for at least 6 months following a myocardial infarct with
some authors suggesting treatment should be postponed for 1 year, due to
the risk of further infarct within this period. Acute dental problems within
this timeframe should be managed in close consultation with the cardiolo-
gist responsible for the patient’s care.
INFECTIVE ENDOCARDITIS
Infective endocarditis is an infection of the endocardial surface of the
heart, which may include damaged heart valves, prosthetic heart valves or
ventricular septal defects. In the UK, current guidelines from the National
Institute of Clinical Excellence (NICE) recommend that antibiotic prophy-
laxis is not required for at risk groups as there was insufficient evidence
regarding the efficacy of the antibiotic regimen. The updated American
Heart Association guidelines (2007), on the other hand, recommend that
antibiotic prophylaxis prior to dental procedures be administered to patients
with previous infective endocarditis, prosthetic heart valve, cardiac trans-
plantation recipients with cardiac valvulopathy and some patients with
congenital heart disease (CHD). Patients with CHD are defined as those
with unrepaired cyanotic CHD (including conduits and palliative shunts),
repaired CHD with residual defects at or adjacent to the site of a prosthetic
patch or device, and completely repaired CHD with device or with pros-
thetic material in the first 6 months following the procedure. This is
because endothelialization of the prosthetic material generally occurs in
the 6 months following the procedure. Antibiotic prophylaxis is no longer
recommended for any other form of CHD.
STROKE
Stroke is a generic term for cerebrovascular accident (CVA) resulting in a
sudden or rapidly progressing neurological defect, which does not resolve
within 24 hours. Stroke is the third highest cause of death in the UK, after
ischaemic heart disease and all cancer types combined, with around
150 000 people having a stroke per year.
The effects of stroke principally result in unilateral numbness, weakness
and partial or complete paralysis of the arm, leg or face on the contralateral
side of the brain. The effects, severity and recovery can be varied. Mobility
may become impossible requiring the provision of domiciliary care for
dental treatment.
Endodontic treatment may be affected by the provision of anticoagu-
lants. The patient may have difficulty accessing care, particularly if they
are wheelchair bound. Communication may be challenging and anxiety,
fear or frustration are common emotions for patients who have undergone
stroke. Blood pressure should be monitored during treatment and attention
given to vasoconstrictor usage in patients who have reduced resiliency of
the cardiovascular system. Patients taking antihypertensive medication are
at increased risk of postural hypertension and this should be taken into
account following prolonged periods in the dental chair.
BLEEDING DISORDERS
A bleeding disorder arises if there is a problem in any part of the haemo-
static and clotting pathway, and can be congenital or acquired.
Acquired bleeding conditions occur as a result of liver disease and
platelet disorders or as the result of anticoagulant therapy. Patients with
liver failure, alcoholism, renal failure, thrombocytopenia, and chemo-
therapy will have coagulation and clotting disorders and should not
undergo a surgical intervention without liaising with the physician respon-
sible for their care.
Antiplatelet therapy, such as aspirin and clopidogrel, when used in
combination, have a synergistic effect impairing platelet function. However,
local measures should be adequate to achieve coagulation and the medica-
tion should not be stopped prior to a surgical procedure.
Coumarin therapy is most commonly prescribed in the form of the
vitamin K antagonist warfarin. Used for the prophylaxis or treatment of
deep vein thrombosis, prosthetic heart valves, and people with atrial fibril-
lation, it prolongs both prothrombin and the activated partial thromboplas-
tin time. The International Normalized Ratio (INR) is used to monitor its
effect with a therapeutic range of 2–3 for deep vein thrombosis (DVT) and
up to 4.5 for patients with prosthetic heart valves. Patients with an INR of
less than 4 can undergo surgery in general dental practice without any
warfarin dose adjustment. The patient may bleed more than normal but
this should be controlled via local measures. Ideally, the INR should be
checked on the day of the procedure.
Special precautions are not required for non-surgical endodontic treat-
ment. However, there is a theoretical risk of bleeding into the fascial planes
following an inferior alveolar nerve block and, where possible, this should
be avoided. If it is unavoidable, an aspirating technique should be used
with the injection given slowly to minimize tissue damage. Currently, there
are no specific published guidelines regarding the surgical endodontic
management of patients undergoing coumarin therapy. Therefore, if there
is doubt regarding the management of such a patient then it would be
prudent to seek advice from the patient’s haematologist prior to treatment.
Patients who have a poorly controlled INR or an INR>4 and require
multiple extractions should be treated in a hospital setting. Non-surgical
endodontic treatment should not present a significant bleeding risk.
However, the clinician should maintain the highest standards of atraumatic
technique, especially with regards to soft-tissue management, apical
 The medical–endo interface and patients with special needs  363
control (of instruments, as well as irrigants, particularly sodium hypochlo-
rite) and delivery of local anaesthesia. If there is any doubt with regards
to patient management, then the advice of the patient’s haematologist
should be sought prior to treatment.
Hereditary or congenital bleeding disorders have the potential to cause
severe bleeding tendencies. The most common congenital bleeding disor-
der is von Willebrand’s disease, followed by haemophilia A and haemo-
philia B.
Patients with von Willebrand’s disease (vWD) have an extended bleed-
ing time, due to poor platelet function and low levels of von Willebrand
factor and factor VIII activity.
Haemophilia A is characterized by a normal bleeding time but a pro-
longed activated partial thromboplastin time and low levels of factor VIII.
The rarer haemophilia B is the result of a genetic mutation leading to a
deficiency in factor IX. Both types of haemophilia typically manifest in
childhood as easy bruising and prolonged bleeding following injury.
Most patients should be able to be managed within a primary care
setting in coordination with the patient’s haemophilia with each haemato-
logical disorder and individual patient requiring an individual approach.
The goal of treatment is to minimize the challenge to the patient by restor-
ing the haemostatic system to acceptable levels and maintaining haemos-
tasis by local and adjunctive levels. This is normally achieved through the
delivery of coagulation therapy to raise coagulation factors to near normal
levels within 10–12 hours of factor VIII cover and on consecutive days
for factor IX.
It has been reported that patients with congenital bleeding disorders are
often highly anxious about dental treatment and often delay treatment until
they develop significant dental problems. In addition, patients with con-
genital bleeding disorders may have been exposed to the hepatitis C virus
(HCV) from the use of non-inactivated replacement factor concentrates
from pooled human blood until 1986, with the presence of HCV having
been reported in up to 70% of haemophilia patients.
During endodontic treatment, whether the patient has received prophy-
lactic coagulant cover or not, care must be taken to avoid trauma. As for
patients on anticoagulant therapy, apical control via the use of apex loca-
tors and careful instrumentation is required. Rubber dam application
should be as atraumatic as possible, otherwise it can lead to gingival bleed-
ing, which can be particularly troublesome in patients with vWD.
Local anaesthesia represents a more significant challenge. An inferior
alveolar nerve block must only be given after raising the appropriate clot-
ting factors levels via appropriate therapy as there is a risk of haematoma
in the retromolar or pterygoid space potentially compromising the airway.
Similarly, lingual infiltrations should be avoided without the appropriate
factor cover as it risks a significant haematoma. Therefore, alternative
anaesthesia via intraligamental or intraosseous techniques should be con-
sidered. Buccal infiltration with Articaine may provide sufficient anaesthe-
sia for mandibular molars though not for patients with pulpitis.
Any surgical procedure should be carried out with minimal trauma and
the use of both resorbable and non-resorbable sutures has been advocated.
Topical haemostatic agents such as tranexamic acid may provide rapid
haemostasis. Careful postoperative instructions should include a soft or
liquidized diet and the use of a tranexamic acid mouthwash regimen.
Despite all measures, postoperative haemorrhage may still occur occa-
sionally and patients should be instructed to contact their local haemo-
philia centre in the first instance for further clotting factor infusions.
RESPIRATORY DISEASE
Chronic obstructive pulmonary disease (COPD) and asthma are the most
likely respiratory diseases to be encountered in the dental surgery. COPD
encompasses a collection of diseases, including chronic bronchitis,
emphysema and chronic airways disease. There are in the region of 900 000
sufferers in England and Wales varying from mild disease through to severe
disease with respiratory failure. The majority of disease is smoking related.
Diagnosis is based on history, physical examination and spirometry tests
with treatment ranging from inhaled bronchodilators or corticosteroids,
through to confinement at home with constant nebulization.
Most patients can cope with dental treatment safely with only minor
adjustments to procedures in general dental practice. Where possible, treat-
ment should be delivered under local anaesthetic, due to the risk of respira-
tory depression during treatment under sedation. It is likely that the patient
will have to be treated in an upright position compromising access for
endodontic care. Patients who require oxygen therapy should bring suffi-
cient oxygen for the duration of treatment and this should be checked prior
to the initiation of care.
Asthma is common, affecting up to 5.4 million people in the UK in 2008.
It is a generalized airway obstruction, which is paroxysmal and reversible
in the early stages. The obstruction is the result of bronchial muscle con-
traction, mucosal swelling and increased mucus production leading to
coughing and wheezing, and/or shortness of breath. The use of salbutamol
or beclomethasone inhalers can lead to increased caries and periodontal
disease and patients should undergo regular dental reviews.
Before dental treatment, the severity of the condition should be ascer-
tained from the patient’s history with particular attention given to any
episodes of hospital admission. The patient should be instructed to use
their inhaler prior to treatment and it should be present for the duration of
the appointment. Again, local anaesthesia is the treatment modality of
choice with inhalation sedation an alternative for particularly anxious
patients, due to its ability to be rapidly controlled. Care should be taken
when prescribing non-steroidal anti-inflammatories, due to an increased
risk of allergy to aspirin, or precipitation of an asthma attack.
LATEX ALLERGY
Latex allergy occurs in 1–5% of the general population. Workers in the
rubber industry and healthcare professionals are at increased risk of devel-
oping a latex allergy as a result of occupational exposure. Patients with a
history of urogenital abnormalities and patients who have undergone mul-
tiple surgical procedures are at increased risk. Atopic individuals are also
a risk group. However, the highest risk group are patients with spina bifida
with reports of up to 67% of patients having a latex allergy.
Patients can be classified into three groups of latex allergy risk: Group
1: people with a previous history of anaphylaxis to latex; Group 2: people
with a history of type IV contact dermatitis to latex or signs and symptoms,
including rhinitis, urticaria or conjunctivitis; Group 3: no previous symp-
toms but fall into one of the “at risk” groups.
Dental management of Group 1 patients should only be undertaken in
a “latex screened” specialist setting with the appropriately trained staff and
equipment to manage an anaphylactic reaction. Group 2 patients can be
managed in coordination with a latex-modified environment via nitrile
gloves, latex-free rubber dam and local anaesthetic in plastic cartridges.
Care needs to be taken with the use of latex-free rubber dam in endodontic
retreatment cases, due to the potential of chloroform instantly to dissolve
the rubber dam on contact. Group 3 patients require no special measures
but the dental team should be alert to the patients’ increased risk. To date,
there have been no proven cases of hypersensitivity to gutta-percha root-
filling material.
DIABETES
Diabetes mellitus (DM) develops from either a deficiency in insulin pro-
duction or an impaired utilization of insulin, resulting in altered glucose
 364  The medical–endo interface and patients with special needs
tolerance or impaired lipid and carbohydrate metabolism. There are two
types: Type 1 and Type 2, with Type 2 being the most common and affect-
ing 85–95% of the diabetic population. Diabetes classically presents with
polyuria, polydipsia and polyphagia alongside fatigue, weakness, pruritus
and blurred vision. In Type 2 diabetes, the symptoms develop slowly and
the individual may be unaware of them at the time of diagnosis. Complica-
tions are a result of long-term exposure to raised glucose levels leading to
microvascular complications, such as retinopathy, neuropathies, renal
disease and loss of peripheral sensation resulting in poor wound healing.
Macrovascular complications result in coronary heart disease, cerebrovas-
cular disease and hypertension.
Management of Type 1 diabetes centres on subcutaneous infusion of
insulin with careful monitoring of blood glucose levels. Type 2 diabetes
is controlled by diet and oral hypoglycaemic medication, which stimulates
the release of insulin from the pancreas.
Oral manifestations of diabetes include xerostomia, burning mouth,
candidiasis, oral neuropathies and sialosis. Dental caries and advancing
periodontal disease generally occur in direct correlation with diabetic
control. Delayed healing presents an increased risk of oral infection and
DM has also been suggested as a risk factor for bisphosphonate-related
osteonecrosis.
Dental care should have a strong preventative ethos, particularly with
regards to diagnosis and effective management of caries and periodontal
disease. Patients with well-controlled Type 1 or 2 diabetes can be treated
similarly to non-diabetic patients provided the normal routine of diet,
medication and insulin is not disturbed. A blood glucose monitoring
machine should be used where possible to monitor blood glucose levels
before and during treatment. The dental team should pay close attention
to clinical signs of hypoglycaemia. Poorly controlled patients should be
referred to a specialist setting for dental care and treatment may have to
be delayed until diabetic control is improved.
The diabetic patient requiring endodontic treatment should be scheduled
first thing in the morning or immediately following lunch to minimize
disturbance to glucose levels. Particularly when long appointments are
scheduled, the patient should be encouraged at all times to report any
perceived changes in their condition during treatment. Anxiety levels
should be minimized whenever possible. However, sedation may mask the
signs of hypoglycaemia and should only be given by experienced
operators.
A small number of authors have reported that diabetic patients have
reduced periapical healing following root-canal treatment, especially in
insulin-dependent patients. The increased presence of periodontal disease
in diabetic patients may be a confounding factor for tooth loss following
root canal treatment. It has also been reported that persistent pain follow-
ing root-canal treatment may be a significant factor resulting in tooth loss
possibly as a consequence of diabetic neuropathy.
Collapse due to hypoglycaemia may be related to anxiety, missed meals
or inconvenient appointment times. Early signs of hypoglycaemia include
pallor, sweating, facial and lingual paraesthesia, hunger, confusion, agita-
tion and poor coordination. The dental team should be suspicious of mood
changes, anger or poor cooperation in a previously tolerant patient, espe-
cially under rubber dam. Left untreated, a hypoglycaemic episode may
progress from drowsiness to collapse and even coma. Management centres
on prevention via the timely delivery of oral glucose or Hypostop®. If
consciousness is lost, then the delivery of intramuscular glucagon (1 mg)
should restore consciousness within 15 minutes and the emergency serv-
ices should always be called if recovery is delayed. Collapse due to hyper-
glycaemia in the dental setting is unlikely due to the slow, progressive
nature of onset. If there is any doubt on the cause of the impending col-
lapse, then oral glucose should always be given as it will do no harm to
the hyperglycaemic patient.
BISPHOSPHONATE-RELATED OSTEONECROSIS
Bisphosphonates are a class of drugs used increasingly to treat osteoporo-
sis, multiple myeloma, Paget’s disease, osteogenesis imperfecta and malig-
nant bone metastases. Their efficacy in treating and preventing these
conditions has had a significant, positive impact for patients. However,
there is now a significant association between their use (particularly intra-
venous preparations) and osteonecrosis of the jaws.
The pathogenesis of bisphosphonate-related osteonecrosis is not yet
fully understood and, to date, there are no reported cases occurring out-
with the facial skeleton. Patients most commonly present with absent or
delayed hard or soft tissue healing after dental extractions or surgery. The
patient must have no history of radiation to the head and neck and a posi-
tive history for bisphosphonate medication. Patients with bisphosphonate-
related osteonecrosis are usually asymptomatic but may develop severe
pain as a result of secondary infection.
In patients who are currently undergoing intravenous bisphosphonate
therapy, any dental alveolar surgery, including extractions, implant place-
ment, periapical and periodontal surgery should be avoided as these
patients are seven times more likely to develop osteonecrosis than patients
not undergoing surgery. The relative risk of complications increases
with increased time of use for both oral and intravenous bisphosphonates,
and for co-morbidities such as diabetes. For unrestorable teeth, decorona-
tion and endodontic treatment of the remaining roots has been advocated.
It is likely that the increased use of intravenous bisphosphonates in
an ageing population will increase the demand for non-surgical endo­
dontic treatment, to avoid the risk of osteonecrosis following dental
extractions.
MULTIPLE SCLEROSIS
Multiple sclerosis (MS) is a complex neurological condition caused by
damage to the myelin sheath of the nervous system and results in interfer-
ence with both sensory and motor nerve transmission. MS is the most
common neurological disorder among young and middle-aged adults and
is more common in women than men. Its aetiology is not understood and,
although a number of probable causes have been postulated, no single
causative agent has been identified.
There are several different types of MS with different disease patterns.
One in five people with MS have benign disease with no permanent
disability, whereas 15% have progressive disease that steadily worsens
leading to profound disability. Symptoms are highly variable between
individuals but often include visual disturbance, neuralgias and paraes­
thesia, spasticity, tremor, fatigue and depression leading to progressive
disability. There are no specific tests for MS and diagnosis is based
on neurological history and examination. There is no cure and treat-
ment focuses on the prevention of disability and maintenance of quality
of life.
Endodontic management depends on the severity of any disability and
it is important that treatment planning includes the history of disease pro-
gression and takes into account the likelihood of future problems with both
accessing and delivering dental care. Appointment scheduling should take
place during phases of good health or at the patient’s best time of day to
minimize stress and fatigue. Extreme fatigue is common following dental
treatment and multiple short appointments may be necessary for root-canal
treatment. The use of a mouth prop may help reduce muscle fatigue during
the appointment.
The diagnosing clinician should also be aware that chronic pain is
common in up to 50% of patients with MS and may present as paraesthe-
sia, hyperalgesia or allodynia. Trigeminal neuralgia occurs in up to 32%
of patients with MS and, crucially, may be the presenting symptom in
 The medical–endo interface and patients with special needs  365
previously undiagnosed patients under 40 years of age. From the authors’
experience, patients with MS are often highly concerned about the pres-
ence or future placement of amalgam restorations. Case-control studies
have failed to demonstrate an association between mercury amalgam res-
torations and MS. In those patients who no longer wish to have amalgam
placed, the root-filled tooth should be restored with a gold restoration to
maximize longevity, especially in those patients where the replacement of
restorations may become extremely difficult in the future.
CEREBRAL PALSY
Cerebral palsy encompasses a group of non-progressive neurological and
physical disabilities developed in utero, at birth or in the first few months
of infancy. The damage to the brain is mainly caused by hypoxia, trauma
and infection. It is the most common congenital cause of physical disabil-
ity and primarily is a disorder of voluntary movement.
Diagnosis is made from clinical signs and there may be other impair-
ments of function, including vision, hearing and speech; epilepsy may also
be a feature. Learning disability is present in less than 50% of people with
cerebral palsy. Although non-progressive, secondary complications such
as respiratory infection can cause significant morbidity.
Dental features include a tapered maxillary arch, proclined incisors and
a high incidence of malocclusion. Facial grimacing, dysphagia and swal-
lowing difficulties are common, as is temporomandibular joint (TMJ)
spasticity and the occurrence of spontaneous subluxation. Bruxism and
non-carious tooth surface loss are also common. Patients are at increased
risk of periodontal disease and caries, due to difficulty in delivering effec-
tive oral hygiene.
Endodontic management may be extremely challenging due to uncon-
trolled movements, including muscle spasm or bite reflex. Anxiety man-
agement or treatment under inhalation sedation can aid access. Intravenous
sedation or general anaesthesia may be required for those patients with
profound disability.
PARKINSON’S DISEASE
Parkinson’s disease is a progressive neurological disorder caused by
degeneration of dopaminergic neurons in the substantia nigra of the basal
ganglia in the brain. The resulting dopamine depletion impairs the function
of those parts of the brain which control movement.
The aetiology is unknown and the risk of developing Parkison’s disease
increases with age. It affects men and women equally; with a prevalence
of 1 in 100 people over 60 years of age. Symptoms are classified into
motor and non-motor. The classical motor symptoms are dyskinesia
(tremor or involuntary movement), bradykinesia (slow movement) and
akinesia (muscular rigidity). Combined, these produce a characteristic
“mask-like” facial expression and a slow, shuffling gait.
Non-motor symptoms include sleep disturbance, psychoses and depres-
sion. Alzheimer’s disease has been reported in up to 30% of patients
with Parkinson’s disease as opposed to 10% of the equivalent general
population.
Diagnosis is based on clinical symptoms and, currently, there is no
known cure. Treatment is aimed at controlling symptoms and consists
of medication to increase the level or efficacy of dopamine within the
brain. Patients with Parkinson’s disease may have difficulty accessing
dental care. They are at increased risk of xerostomia, resulting in burning
mouth and root caries. Oral hygiene may become poor and patients may
become increasingly unable to wear partial or complete dentures, due to
poor retention as a result of xerostomia and uncoordinated or rigid facial
muscles.
Challenges in endodontic management relate to patient access, com-
munication and delivery of treatment. Appointments should be scheduled
for the individual’s best time of day, or when their medication has maximum
therapeutic effect, to try and reduce tremors and random movements
during treatment. It is critical that the dental team take the time to com-
municate with the patient in an effective manner. Namely, sufficient time
should be given to allow a patient to reply to a question without feeling
rushed or pressured as this will lead to frustration on both sides. The use
of yes/no questions can facilitate this process.
Tremor and random movements are the most significant physical barri-
ers to delivering care. Anxiety often increases both movements, and rela-
tionship building between the clinician and the patient can significantly
improve cooperation. Treatment under conscious sedation or rescheduling
to another session may also be required. Airway protection is critical, due
to impaired swallowing reflex and the risk of pulmonary aspiration. The
patient should not be reclined greater than 45° and the use of rubber dam
with effective saliva ejection is recommended.
DEMENTIA
Dementia is a progressive, neurodegenerative disease that affects the
ability to perform daily living activities. It encompasses a variety of syn-
dromes and can be both reversible and irreversible.
Dementia currently affects in the region of 700 000 people in the UK
and predominately presents in the over 65 age group. Two-thirds of people
with dementia are women and up to 64% of patients in care homes have
some form of dementia. Alzheimer’s disease is one of the most protracted
forms of the disease and is caused by the loss of cerebral neurons. Its
prevalence increases from 5 to 10 in 100 over the age of 65 to 1 in 5 80
year olds.
Diagnosis is based on recording symptoms over time and the result of
cognitive/memory tests. Clinical features include memory loss, language
deterioration, impaired visual–spatial skills, poor judgement, indifferent
attitude but preserved motor function. The type, severity, sequence, and
progression of mental changes vary widely, although Alzheimer’s disease
is usually progressive, resulting in severe brain damage over a period of
10 years from diagnosis.
Management is aimed at maintaining quality of life with medication
used to alleviate depression, agitation and challenging behaviour. Dental
treatment should be carried out with a realistic approach to decision
making and treatment planning. The ability to cope with dental treatment
varies hugely between patients, and may be hugely distressing for some
patients. In the early stages of dementia, dental treatment should plan for
the patient being unable to maintain their own teeth in the future and rigor-
ous preventive and oral hygiene measures should be instilled in those
involved in the patient’s long-term care.
ENDODONTICS AND PATIENTS WITH
LEARNING DISABILITY
A learning disability is a significant impairment of intelligence and social
functioning acquired before adulthood. Its cause may be genetic, congeni-
tal or acquired.
Learning disability affects the way an individual learns, communicates
and carries out everyday activities. The amount of support a person requires
throughout life varies according to the severity of their learning disability
and whether or not they have an additional physical disability. In most
developed countries, around 2.5% of the population have a learning dis-
ability equating to 1.5–2 million people in the UK. The most common
cause of learning disability is Down’s syndrome.
 366  The medical–endo interface and patients with special needs
DOWN’S SYNDROME
Down’s syndrome is a genetic condition caused by a chromosomal abnor-
mality (usually trisomy of chromosome 21) resulting in a characteristic
appearance, orodental features and cardiac anomalies (40%). In addition,
visual impairment (50%), hearing (up to 50%) impairment and a compro-
mised immune syndrome are commonplace.
Endodontic management may be impacted by a number of factors.
Depending on the severity of the learning disability, the patient may lack
the capacity to consent for the procedure. The consent process (discussed
later in this chapter) must be followed prior to the initiation of treatment.
Patients with Down’s syndrome are at increased risk of early onset peri-
odontal disease. Therefore, an integrated treatment plan with periodontal
colleagues is essential in the management of periodontally involved teeth
with an endodontic problem. Although gingival inflammation as a result
of mouth breathing may be common place, widespread gingival inflam-
mation may be a presenting factor for leukaemia in patients with Down’s
syndrome.
Congenital heart defects or mitral valve prolapse are common in adult
patients with Down’s syndrome. Although the prescription of antibiotic
cover for dental procedures considered high risk for inducing bacteraemia
is no longer recommended in the UK under NICE Guidelines, it is good
practice to minimize any potential bacteraemia by careful delivery of care.
The delivery of care may be influenced by the presence of atlanto-axial
joint instability affecting the ability of the patient to recline in the dental
chair, necessitating careful positioning, especially if dental treatment is to
be provided under general anaesthetic.
AUTISTIC SPECTRUM DISORDERS
Autistic spectrum disorders (ASD) are developmental disabilities affecting
social interaction, communication and imagination. They are usually diag-
nosed in the first 3 years of life and persist throughout life, with manage-
ment centring on achieving independence and self-care through creating a
highly structured environment. Patients with Asperger’s syndrome will
have normal intellect and language skills but poor social skills and a
reduced ability to show empathy. The more severe diagnosis of classical
autism will encompass patients who have a cognitive impairment, which
will be severe in 40% of patients. Patients with ASD are at increased risk
of dental caries, they may have a very restricted diet and attendance for
dental treatment may be a major challenge.
Despite looking calm, most patients with ASD have high anxiety levels
and combined with the sensitivity to external stimuli resulting in sensory
overload and withdrawal. Reaction to pain can be highly variable, from
complete insensitivity to over-reaction to the slightest touch. The dental
light, smell, taste and noise from the suction can result in an exuberant or
even painful reaction.
Endodontic treatment will require careful behavioural management cen-
tring on careful preparation for each dental visit taking communication
and behavioural factors into account. The use of clear, simple language
with short sentences and direct requests can help. Gestures or facial expres-
sions will not be understood and it is important the dental team asks the
patient for the information they need as it is unlikely to be volunteered.
Routine, both before and during the appointment, can help build structure
to each visit and facilitate treatment with the expectation that compliance
may be varied and inconsistent. A quiet waiting room with no background
noise and minimizing waiting time may help reduce anxiety.
EPILEPSY
Epilepsy, which occurs in less than 1% of the general population, affects
in the region of 30% of patients with a learning disability, increasing to
>50% of patients with a severe learning disability. Petit mal seizures are
brief periods of unresponsiveness or “absences”, which do not effect dental
treatment. Grand mal seizures result in loss of consciousness followed by
a tonic–clonic phase of body spasm followed by repetitive jerking of trunk
and limbs. Trauma from falls during grand mal seizures can cause dental
injury resulting in subluxation and avulsion of teeth, fracture and loss of
vitality.
Endodontic management requires no additional measures other than
those required for the conventional dental management of the epileptic
patient. The clinician should seek to attain as much information as possible
at the time of diagnosis regarding seizure history. Particular attention
should be given to establishing the presence of any triggers, the nature of
the seizures, including auras, frequency, duration, management and any
history of status epilepticus.
The information received should allow the dental team to avoid
any specific triggers (i.e. minimizing use of the dental light in photosensi-
tive patients) and in the event of the patient undergoing a seizure, recogniz-
ing what is normal for that patient, as well as abnormal. Prior to the
initiation of dental treatment, it is advisable that the patient has taken their
routine anti-epilepsy medication, has their emergency medication with
them, has eaten according to normal routine and is not excessively tired.
It is prudent to cancel the visit if the patient feels that their seizures are
poorly controlled on the day of treatment, as the additional stress may
trigger a seizure.
During dental treatment, the use of a mouth prop (regardless of whether
this would usually be required) can provide stability and a few additional
moments to remove dental instruments, including the rubber dam clamp if
the patient was unfortunate enough to undergo a seizure during treatment.
Following the completion of endodontic treatment, large posterior restora-
tions are at risk of fracture during the tonic–clonic seizures. The provision
of cast restorations has been suggested as being preferable, particularly
cast metal crowns thereby avoiding the risk of porcelain fracture.
In the poorly controlled epileptic patient, dental treatment may be
delayed until the seizures become controlled, or completed under inhala-
tion or intravenous sedation within a specialist setting to reduce the risk
of the patient undergoing a seizure during dental treatment.
CONSENT
Consent is a patient’s agreement for a healthcare professional to carry out
treatment. Informed consent is central to all forms of healthcare and a
patient’s legal and ethical right. It is a key component of high quality
services and promotes patients’ experience and provides autonomy. It is
essential for informed risk management and is one of the pillars of clinical
governance.
For the consent to be valid, the individual must have the capacity to
consent and be given sufficient information on the procedure (including
benefits, risks, additional procedures and alternatives). The individual
must not be acting under duress and should feel they have the option to
change their mind in the future.
Only a court or a proxy can give consent for a child under 16. The proxy
is normally a parent but can be another individual given parental respon-
sibility via a court order. Parental responsibility is conferred automatically
on the mother of a child irrespective of marital status. The father has
consent if he is married to the mother or on the child’s birth certificate. If
not, responsibility can be appointed by the mother or the court. Children
who are able to understand information and make a decision in their own
best interest are deemed as “Gillick competent” and can consent for
themselves.
Once a patient is above the age of 18, no other person can consent for
them regardless of their mental capacity. The Mental Capacity Act of 2005
 The medical–endo interface and patients with special needs  367
provides a statutory framework to empower and protect vulnerable people
who are not able to make their own decisions. It provides guidelines for
carers and health professionals to make clear who can take decisions, in
which situations and how they should proceed.
Where a decision needs to be made to provide medical or dental treat-
ment in an individual who does not have the capacity to consent, the
healthcare professional responsible for carrying out the particular treat-
ment or procedure is the decision maker. It is the decision-maker’s respon-
sibility to work out what would be in the best interest of that individual.
It is a criminal offence of neglect and ill treatment if the code of practice
is not followed.
Under the Mental Capacity Act, all individuals should be presumed to
be able to consent for themselves until proven not by a mental capacity
act assessment. Individuals should be fully supported to make their own
decisions, including investigating all possible methods of communication,
for example, the use of an interpreter or British Sign Language. Individuals
must retain the right to make what may seem an unwise decision. The
treatment must be within the patient’s best interest and be the least restric-
tive method.
Deciding if an individual has the capacity to consent is a two-stage
process. First, does the individual have a physical impairment of the mind
or brain? Or is there a psychological disturbance affecting the way the
individual’s mind or brain works? If so, does that impairment or distur-
bance mean that the person is unable to make the decision in question at
the time it needs to be made? Individuals need to demonstrate the ability
to understand the information, retain it and use it to communicate a deci-
sion. The decision is time-specific and therefore, it does not matter if the
impairment is temporary or permanent. It is also decision-specific and the
process must be repeated if the decision changes or a new decision needs
to be made. The act provides a checklist of factors that decision makers
must work through in deciding what is in the person’s best interest.
BEST INTEREST MEETINGS
Once the decision maker has decided that the patient lacks the capacity to
consent for themselves at that moment in time, a decision has to be made
in their best interest. Along with health professionals and carers, non-paid
carers and family members have a right to be consulted and should be
included in any decisions. Consideration should be given if the patient’s
incapacity is temporary; can the decision to provide treatment be delayed?
Assumptions should not be based upon age, appearance, condition or
behaviour. Consideration must be given to the patient’s past and present
wishes, feelings, beliefs and values. The views of family, friends, informal
carers and anyone with an interest in the individual’s welfare should also
be taken into account.
Information regarding the procedure, benefits, risks, additional proce-
dures and any alternatives should be provided, with clear objectives as to
how the clinician is acting in the patient’s best interest.
INDEPENDENT MENTAL CAPACITY
ADVOCATES (IMCA)
In cases of serious medical treatment, such as general anaesthesia and
conscious sedation, if the patient has no family members or unpaid carers,
they are deemed as un-befriended. An IMCA should be appointed to
provide an independent opinion to ensure that the decision maker is acting
within the patient’s best interest.
An IMCA will attend best interest meetings to ensure that all options
have been considered, the individual’s own opinions have been addressed,
no agendas are being pursued and, finally, the individual’s civil, human
and welfare rights are being respected.
ENDODONTICS AND THE MANAGEMENT OF ANXIETY
THE GAG REFLEX
Patients who present with a severe gag reflex preventing the delivery of
endodontic care are often referred to specialist endodontic practice or
secondary care for management. The gag reflex can be defined as “a pro-
tective reflex to prevent unwanted entry to mouth and oropharynx”. Retch-
ing is defined as a “process of attempting to eliminate noxious substances
from the upper GI tract”. However, these are both complex reflexes which
are influenced by higher centres of control and can therefore, be initiated
by sight, sound, smell and psychological stimuli.
Patients with a severe gag reflex can be classified into psychogenic
(where the reflex is triggered without direct physical contact) and soma-
togenic (where a specific area, i.e. posterior border of the palate triggers
the reflex). However, patients rarely fall wholly into one group and psy-
chogenic factors often predominate. This is no more apparent than in the
patient who gag’s spontaneously in the dental waiting room.
As with any other medical or dental condition, it is important that the
patient undergoes careful assessment of their condition prior to the initia-
tion of any diagnostic tests, which could initiate the reflex. The clinician
should be aware that often patients are highly embarrassed and it is not
unusual for the reflex to be linked to a major, traumatic life event. There-
fore, it is important that history taking is delivered in an empathetic manner
via open questions and a non-dental environment may be more suitable
for patients where specific dental stimuli (i.e. the smell of eugenol) can
trigger the reflex.
Relationship building and establishing trust between the clinician
and the patient is crucial to the effective delivery of care, with clinician
experience having been shown to be a significant factor in successful
management.
The management of patients with a severe gag reflex can broadly be
divided into a non-pharmacological and pharmacological approach, which
may be required in combination. Often through effective management of
the patient’s anxiety level, the gag reflex can be controlled sufficiently to
deliver the appropriate care. A traffic light system can be particularly
useful for managing the reflex with the red (stop) command being initiated
before the reflex begins. This gives the patient control regarding the
level of potential stimulation they undergo. It is critical that, for this tech-
nique to work, the clinician respects the red (stop) command on every
occasion.
During the delivery of endodontic care, the taking of radiographs is
often a significant challenge for patients with a severe gag reflex. If the
patient has a mouth-breathing habit, retraining the patient to breathe slowly
through their nose can help control the gag reflex. In patients where anxiety
levels are relatively controlled, the use of distraction techniques can be
particularly useful in helping the patient through the specific procedure.
Leg raising, temporal tapping and stimulation of acupuncture point CV24
have all been reported to aid reduction of the gag refex during dental treat-
ment. Adopting these techniques in combination with the traffic light
system may facilitate the completion of intraoperative radiographs. In
patients where the use of an endodontic film holder initiates the reflex,
using artery forceps combined with a bisecting angle radiographic tech-
nique may aid the process often by returning an element of control to the
patient.
Unfortunately, in some patients, particularly where anxiety levels are
unable to be controlled, behavioural techniques may not be successful and
a pharmacological approach may be required. The specific delivery of
local anaesthetic to the posterior margin of the palate has been reported to
aid reduction of the gag reflex. However, this is not an approach the author
has had success with and can significantly add to patient anxiety.
 368  The medical–endo interface and patients with special needs
The delivery of care via oral sedation, inhalation sedation or intravenous
sedation with midazolam may be successful in controlling anxiety levels
and the gag reflex sufficiently to deliver endodontic care. However, in a
small group of patients, intravenous sedation via propofol or general
anaesthesia (delivered in an appropriate environment via a consultant
anaesthetist) may be the only method guaranteed successfully to manage
the reflex.
ENDODONTICS AND CONSCIOUS SEDATION
The principle role of conscious sedation is to allay apprehension, anxiety
or fear. It is also used to reduce the stress of a prolonged surgical procedure
or to control gagging. Additionally, conscious sedation may be used to
stabilize blood pressure in patients with a history of hypertension, cardio-
vascular or cerebrovascular disease. The commonest forms of conscious
sedation are inhalation sedation, intravenous sedation with midazolam and
oral sedation.
Assessment
A detailed discussion of every aspect of the assessment of a dental patient
prior to sedation is beyond the scope of this chapter. Essentially, the clini-
cian is recording sufficient information to assess the patient’s level of
anxiety, and their medical status and suitability to undergo the sedative
treatment options available. Anxiety can be assessed via a detailed history
taking, communication and observation with additional measures, such as
the Modified Dental Anxiety Scale or Venham Scale proving useful. A
detailed medical history is essential with attention given to respiratory,
cardiovascular, liver and kidney diseases. Pregnancy, drug interactions and
a previous history of drug or alcohol abuse are also important factors to
be taken into account. In addition to a comprehensive medical history,
baseline recordings of heart rate and arterial blood pressure should be
noted. From these findings the patient’s fitness for sedation or general
anaesthesia can be classified according to the American Society of Anesthe-
siologists (ASA) fitness scale.
Written consent for both the dental procedure and the sedation to be
provided is essential and, for endodontic treatment, should include a treat-
ment plan for extraction should the tooth be deemed to be unrestorable
once treatment under sedation is commenced.
Inhalation sedation
The use of inhalation sedation in the delivery of dental care is a safe, reli-
able technique, which is well documented in the dental literature. Nitrous
oxide has excellent anxiolytic, sedative and analgesic properties with little
or no depression of myocardial or respiratory function. It has a wide
margin of safety and the dose can be titrated according to patient response.
The use of a nasal mask alongside a rubber dam can restrict access for
endodontics and a good level of patient cooperation is required for both
the sedation and endodontic care. However, this can be an excellent
technique for the management of a specific anxiety, i.e. needle phobia,
where the inhalation sedation can be utilized only during the delivery of
anaesthesia and then conventional endodontic treatment can be com-
menced once the patient’s initial anxiety has been controlled.
Intravenous sedation with midazolam
Midazolam is a water-soluble benzodiazepine with a short half-life provid-
ing a rapid onset of sedation with anxiolysis, anterograde amnesia and a
rapid recovery (within 1 or 2 hours). It has the disadvantage of requiring
venous access and must be delivered in an appropriate setting with con-
tinuous monitoring of oxygen saturation via pulse oximetry. It can be
extremely useful in the management of both dental anxiety and patients
with a severe gag reflex. However, midazolam produces a period of seda-
tion of 20–30 minutes followed by a state or relaxation for a further hour.
In a prolonged procedure, the patient may require careful titration of sup-
plemental doses of midazolam. Therefore, at the point of treatment plan-
ning, the clinicians delivering the sedation and endodontic care must
ensure that the endodontic treatment can be completed efficiently in the
appropriate time-frame for this to be an effective technique.
Oral and intranasal sedation
The use of oral sedation prior to the delivery of endodontic care can be
particularly useful in patients suffering from mild anxiety. However, the
patient will still need to be able to provide a reasonable level of coopera-
tion throughout the procedure to facilitate treatment. It is important that
the dose of oral sedation delivered is commensurate with the patient’s
ability to maintain cooperation particularly for the taking of intraoral
radiographs. However, the effect of oral sedation can be unpredictable, due
to the nature of a fixed dose.
Intranasal delivery of midazolam has a more predictable dose response
and quicker onset than oral sedation. For effective delivery, the patient
should have an unobstructed nasal airway. It is particularly useful in
patients with a learning disability to allow sufficient cooperation for can-
nulation prior to intravenous sedation. For both oral and intranasal seda-
tion the risk of respiratory depression is just as great as for intravenous
sedation with midazolam. Therefore, the clinical monitoring, use of pulse
oximetry and discharge criteria are identical to those of intravenous
sedation.
REFERENCES AND FURTHER READING
American Heart Association; American Dental Association Division of Communications,
2007. For the dental patient…: antibiotics and your heart: new guidelines from the
American Heart Association. J Am Dent Assoc 138 (6), 920.
Centre for Clinical Practice at NICE (UK), 2008. Prophylaxis against infective
endocarditis: antimicrobial prophylaxis against infective endocarditis in adults and
children undergoing interventional procedures. NICE Clinical Guidelines, No. 64,
London. Available from http://www.ncbi.nlm.nih.gov/books/NBK51789/ (accessed
Aug 2013).
Scully, C., 2010. Medical problems in dentistry, 6th ed. Church Livingstone.

Section 4 Multidisciplinary aspects of endodontic management
The orofacial pain–endo interface
DEFINITION OF PAIN
Pain is defined as an unpleasant sensory and emotional experience associ­
ated with actual or potential tissue damage. Pain has a strong motivational
input to behaviour, yet the link between tissue damage, pain and behaviour
is not always proportionate or direct. Pain from an accidental burn, such
as a hot iron, elicits sharp, transient pain causing a withdrawal reflex; this
is acute pain, which is protective in its behavioural drive. A stimulus that
is potentially damaging to tissues is considered noxious. The endodontic
equivalent of acute pain is that of dentinal, pulpal or periapical origin. Pain
that lasts for a few days or a few weeks can follow musculoskeletal or
sports injuries; this is prolonged pain, which can also be protective in its
behavioural drive. In a proportion of cases, the prolonged pain becomes
persistent or chronic, lasting beyond the period of injury and its healing;
this no longer has a protective value but it may continue to affect behav­
iour. The endodontic equivalent is neurogenic pain or pain from other
structures that appears to arise from teeth and its associated structures.
Although there are relatively few conditions to diagnose for the endo­
dontist, their overlapping presentation and innate subtleties complicate
straightforward identification (see Chapter 4). The problem is similar and
even more complicated when considering the overlapping presentation of
pain from other orofacial structures.
Orofacial pain may arise from or be associated with teeth, periodontium,
oral mucosa, temporomandibular joints (TMJ) and associated musculature,
cervical spine and associated musculature, maxillary sinuses, nose, eyes,
throat, salivary glands, nerve supply, vascular supply, and confounding
with headaches. Pain from these different structures and sources may have
distinctive characteristics, which aids their identification through knowl­
edge, practice and experience.
OROFACIAL PAIN PREVALENCE
It is difficult to determine accurately the true prevalence and incidence of
pain, both in general and in the orofacial region. Nevertheless, it is esti­
mated that a quarter of the adult population have suffered from orofacial
pain (MacFarlane et al., 2001). In children, toothache is the most common
orofacial pain, 12% experiencing an episode before the age of 5 and 32%
by the age of 12. Meanwhile, two recent UK studies of adults showed
12–19% of the population reported orofacial pain within the previous
month (Drangsholt & LeResche, 2009).
The prevalence of chronic pain is reputed to be 35.5% in the general
population (Raferty et al., 2011). In another large scale survey of 15 Euro­
pean countries, 19% of adults reported suffering from chronic pain, which
seriously affected the quality of their lives (Breivik et al., 2006). Further­
more, the overall incidence of chronic orofacial pain has been given as
38.7 per 100 000 per year (Koopman et al., 2009). In referred endodontic
patients, about 12% may have some form of chronic pain, either as a result
of endodontic treatment or because of initial misdiagnosis (Polycarpou
et al., 2005).
NEUROPHYSIOLOGICAL BASIS OF OROFACIAL PAIN
The sensory transmission of orofacial pain is conveyed predominantly by
Aδ and C fibres of the trigeminal nerve, which project to the nucleus
caudalis in the medulla. The latter is sometimes referred to as the
© 2014 Elsevier Ltd. All rights reserved.
16
R Leeson, K Gulabivala, Y-L Ng  
medullary dorsal horn as it is the functional equivalent of the spinal dorsal
horn. Pain input is modulated at this site in the brain stem before fibres
then project via the spinothalamic tract to the thalamus and thence to the
cerebral cortex. The sensory-discriminative component of pain and activa­
tion of the endogenous analgesic system are believed to originate within
the cortex. A schematic diagram illustrating the trigeminal pain pathway
is presented in Figure 16.1.
Convergence, inflammation and development of central sensitization
may collectively serve to intensify and confuse the pain experienced.
Convergence to the nucleus caudalis accounts for poor localization, spread
and referral of pain as seen in deep pain conditions involving the dental
pulp, the TMJ and associated musculature. Deep tissues have fewer noci­
ceptive nerve endings than cutaneous or mucosal tissues, which are more
clearly recognized as the source.
Sensitization and neuroplasticity may develop, first peripherally then
centrally, when persistent nociceptive facilitation exceeds inhibition. It
involves enlargement of the receptive field, decreased activation threshold,
wind-up with increased transmission of stimuli perceived as pain, altered
gene expression leading to prolonged functional change and, finally, per­
sistent pain and central sensitization. Allodynia and/or hyperalgesia are
common clinical presentations. Allodynia represents pain elicited by a
normally innocuous stimulus, while hyperalgesia represents pain of an
increased or prolonged nature, due to a noxious stimulus. Allodynia may
be observed when carefully examining a patient using a wisp of cotton
wool on the gingivae and discovering this initiates severe pain. Similarly
for hypersensitivity, gentle application of pressure to the apical area can
be perceived as intense pain.
Blocking peripheral inflammatory mechanisms by anti-inflammatory
drugs or blocking the conduction of nerve impulses with local anaesthetics
can reduce nociceptive input and potentially prevent the development of
central sensitization.
CLASSIFICATION OF OROFACIAL PAIN
Orofacial pain (OFP) is defined as pain whose origin is below the orbito-
meatal line, above the neck and anterior to the ears, including pain within
the mouth (Zakrzewska & Hamlyn, 1999).
Chronic OFP can be defined as pain in the face, mouth or jaws that has
been present intermittently or continuously for 3 months or longer. In
addition, chronic orofacial pain has also been defined by a persistence of
pain combined with signs of “chronification”, such as a strong association
with psychosocial problems, frequent changes of physicians, and multiple
further areas of pain.
Numerous classification systems based on the structures, symptoms or
treatment (Table 16.1) have been proposed for the orofacial region, the
more detailed assigning individuals to multiple categories, which ideally
incorporate both the physical component and the psychological impact of
pain. The number of classifications reflects the fact that the discipline is
still developing and there is still uncertainty about aetiopathogenesis, in
turn reflected in a rich field of research.
DIAGNOSIS OF OROFACIAL PAIN
A careful history is obtained to determine the characteristics of the orofa­
cial pain, as well as any history of other generalized chronic pain condi­
tions. Information on co-morbid anxiety, depression, sleep problems,
 370  The orofacial pain–endo interface

Fig. 16.2  The

associations and  
Vascular Neuropathic
overlap of various pain
Dura Convergence of primary Cerebral cortex categories

Eyes
Thalamus
Sinus Idiopathic

Muscle Spinal tract nucleus of

the Trigeminal nerve
Tooth
Inflammatory Musculoskeletal
Trigeminal
thalamic tract
Temporomandibular
joint Trigeminal ganglion

Nucleus caudalis Table 16.2  Factors determining the characteristics of orofacial pain
"Medullary dorsal horn"
Characteristics of orofacial pain
Duration and frequency – Acute/chronic
Anatomical location – Source/site
Trigeminal nerve
Symptoms and signs
Aetiology and pathophysiology
Aggravating and relieving factors
Fig. 16.1  A schematic diagram illustrating the trigeminal pain pathway
Mechanisms of pain

Table 16.1  Origin of some classification systems

Some of the classification systems available for orofacial pain

Table 16.3  Character and associated features of various types of
RDC/TMD (Research Diagnostic Criteria for Temporomandibular Disorders) 1992 orofacial pain
IASP (International Association for the Study of Pain) 1994
AAOP (American Academy of Orofacial Pain) 2008 Character of pain – an aid to orofacial pain differential diagnosis
ICHD (International Classification of Headache Disorders) 2nd edn 2004 Pain categories Character Associated features
Inflammatory Dull, aching, throbbing, Redness, swelling, heat, loss of
pounding, burning, function, hyperalgesia,
pressure, sharp, stabbing allodynia
social and family history should all be recorded. Pre-consultation question­ Musculoskeletal Dull, aching, pressure, Can be referred pain, often
naires may be useful when managing chronic pain to assess the behav­ occasionally sharp worse on function,
hyperalgesia, allodynia
ioural impact of pain and in establishing the patient’s goals and expectations. Neuropathic Continuous burning, Hyperalgesia, allodynia,
Clinical examination, together with special tests if required, is used to episodic electric shock, numbness, paraesthesia,
confirm diagnosis. The differential diagnoses of orofacial pain constitute stabbing. dysaesthesia
a vast list but a broad assessment is essential to exclude rare presentations (Neuro)Vascular Throbbing, pounding, Worse on increased intracranial
pulsating, sometimes pressure: head movement,
of intra- or extracranial malignant neoplasia, severe infective inflammatory stabbing physical activity, Valsalva
conditions before considering the more commonly encountered presenta­ manoeuvre, light and sound
tions of pain. The main causes of chronic orofacial pain are then often sensitivity, nausea, vomiting
classified into inflammatory, vascular, musculoskeletal, neuropathic and Idiopathic Range of character, often Anatomical distribution may not
dull aching with sharp be consistent with sensory
idiopathic (Fig. 16.2). episodes nerve distribution, may be
alleviated by eating, drinking
and distraction
CHARACTERISTICS OF OROFACIAL PAIN

The characteristics of the pain may assist in differentiating pain categories

but is not necessarily diagnostic (Table 16.2). There is much variation and
overlap in the presentation of pain (Fig. 16.2) and the clinician must
always rely on integration of history and examination findings to establish
the correct diagnosis (Table 16.3).
The anatomical location can sometimes be difficult to ascertain since
the source may not correspond to the site of pain. In addition, the pain
may be diffuse and difficult to localize. This is particularly evident
when there is convergence of nociceptive input to the caudal nucleus.
Descriptive terms for the character of pain vary considerably and include
the terms, sharp, dull, aching, burning, and throbbing. Together with fre­
quency (continuous, intermittent or paroxysmal), they may provide clues
as to the pathophysiology. Lancinating, electric shock-like, paroxysmal
pain is often used to describe trigeminal neuralgia, while a constant burning
sensation may be used to describe neuropathic pain.
Assessment of signs and symptoms, aggravating and relieving factors
are another important step in establishing a diagnosis. Acute inflammatory
conditions of non-odontogenic origin may commonly include sinusitis,
characterized as blockage, obstruction, congestion or nasal discharge with
or without loss or reduction in sense of smell causing pain in maxillary
teeth and face particularly on head movement. Sialadenitis or blockage of
salivary glands can cause swelling or pain on swallowing or salivation on
the thought of food. Temporomandibular joint disorder pain is often dull
 The orofacial pain–endo interface  371

Table 16.4  Characteristics of some commonly encountered orofacial pain conditions

Tension-type Migraine without or Trigeminal

Characteristics Atypical odontagia TMD/myofacial pain headache with aura Cluster headache neuralgia
Frequency Continuous Continuous or Episodic or chronic Intermittent Episodic or chronic Intermittent
intermittent
Duration Months or years Variable 30 minutes to 72 4–72 hours 15–180 minutes Brief; seconds
hours
Location Unilateral/bilateral; Unilateral/bilateral; Bilateral; Unilateral; Unilateral; Unilateral;
poorly localized around TMJ jaw occipital, parietal, frontal, temporal orbital, one or more
around a tooth/teeth musculature temporal, frontal supraorbital, divisions of the
often undergone temporal trigeminal nerve
multiple procedures
Quality of pain Dull, aching, Dull, aching, throbbing, Dull, non-pulsing, Pulsating, throbbing Hot searing, Electric shock-like,
throbbing, burning occasional sharp pain tightness, pricking, drilling lancinating
pressure, soreness
Intensity of pain Mild to moderate Mild to moderate Mild to moderate Moderate to severe Severe Severe
Aggravating Spontaneous or history Stress, mechanical jaw Stress, posture and Stress, routine physical Smoking, alcohol Washing, light
factors of trauma or movements muscle strain, activities, food, touch, shaving,
deafferentation missed meals, odour, loud noise, smoking, talking,
(pulpectomy/ weather changes, bright light, missed tooth brushing
extraction) menstruation, meals, alcohol,
fatigue menstruation, fatigue
Relieving factors Topical lidocaine, Systemic medication, Systemic Systemic medications, Systemic Systemic medication
systemic medication hot/cold pack, jaw medication, supine in a dark medication
exercises, hard/soft exercise, room, sleep
occlusal splint, stretching, fresh
acupuncture air
Associated May develop atypical Sense of fullness, May report neck, Nausea, photophobia, Conjunctival Severly debilitating.
symptoms facial pain buzzing or popping shoulder and phonophobia infection, Many patients
in the ears, limitation TMD pain Aura may occur prior to lacrimation, unable to eat,
in mouth opening or headache onset with nasal congestion, drink, clean the
restricted jaw visual disturbance, rhinorrhea, teeth, wash or
movment, noise on paraesthesia of forehead & shave the face
jaw movement hand,arm,face and facial sweating, due to pain
dysphasia miosis, ptosis,
eyelid oedema

Table 16.5  Four primary types of pain OROFACIAL PAIN AND ENDODONTICS

Nociceptive Transient pain Endodontic patients often present because of pain, which may or may not
In response to a noxious stimulus
be associated with previous treatment interventions. The topic of endodon­
Inflammatory Spontaneous pain and hypersensitivity
In response to tissue damage and inflammation
tic pain prior to any treatment intervention has been covered in Chapters
Neuropathic Spontaneous pain and hypersensitivity 4 (Diagnosis of endodontic problems) and 10 (Management of emergen­
In association with damage to or a lesion of the cies and traumatic injuries). Persistent pain associated with teeth after
nervous system non-surgical or surgical endodontic treatment has been used as an indicator
Functional Hypersensitivity to pain of treatment failure. However, pain may be experienced in a tooth or
Resulting from abnormal central processing of
normal input adjacent site in the absence of clinical or radiographic signs of dental
disease. Such diagnostic dilemmas in decision making during treatment
Woolf, 2004 planning were highlighted by Hunter as early as 1778. Failure to detect
pathological change on periapical radiographs may reflect limitations of
the diagnostic method rather than an absence of an osteolytic lesion.
Superimposition of adjacent anatomical structures over the suspect tooth
may further obscure the view. Conversely, residual periapical disease may
with sharp episodes; there may be pain on jaw movement originating either be truly absent and the pain may be non-odontogenic.
from the joints or muscles (masseter, temporalis, pterygoids and anterior Pain in a tooth site of neurogenic origin has been reported in the litera­
digastric), which can be referred to the maxillary molars. Conversely, ture but only a few published studies have investigated the occurrence
muscular pain may arise from painful dental conditions and can then of neuropathic pain after dental treatment. Evidence of the association
persist as an independent entity. Characteristics of some common chronic between dental treatment and chronic neuropathic pain has been presented
non-odontogenic orofacial pain problems are presented in Table 16.4. by Marbach (1978), Schnurr & Broke (1992) and Vicker et al. (1998), who
A mechanism-based approach to pain diagnosis can be useful when reported that most patients diagnosed with atypical odontalgia related the
considering appropriate treatments. The four primary types of pain (Table onset of the pain to dental treatment, dental infection or dental trauma.
16.5) are often considered to be the acute nociceptive and inflammatory Only four epidemiological studies (Marbach et al., 1982; Campbell
pains as opposed to the maladaptive neuropathic and functional pains et al., 1990; Berge, 2002; Oshima et al., 2009) have investigated the preva­
(Woolf, 2004). lence of chronic neuropathic pain after dental treatment. The study by
 372  The orofacial pain–endo interface
Marbach et al. (1982) was conducted by a single endodontist, who mailed
questionnaires to patients one month following non-surgical endodontic
treatment. Only female patients were included in their analyses because
the male sample was considered too small. Out of the 256 female patients
assessed, 20 (9%) reported persistent pain during the period of survey but
only 11 female patients attended for clinical and radiographic examination
to exclude an odontogenic cause of pain. Out of the 11 patients, 8 (3% of
256 female patients) were diagnosed with “phantom toothache”. Campbell
et al. (1990) carried out a similar survey of patients who had undergone
surgical endodontic treatment 2 years previously and found that 59 (50%)
of the 118 patients suffered from chronic pain that divided equally into
two groups; post-traumatic stress dysaesthesia (absence of pain preopera­
tively) (PTD) and phantom tooth pain (PTP) (presence of pain preopera­
tively). Oshima et al. (2009) reported 5.9% of 271 patients who had
chronic persistent pain that did not respond to previous endodontic proce­
dures were diagnosed with neuropathic tooth pain. In contrast, Berge
(2002) found none of the 1035 patients in their survey suffered from
chronic neuropathic pain following surgical removal of third molars 5–6
years previously. None of these studies extended their investigation to
include risk factors affecting prevalence of persistent pain after dental
treatment.
CASE HISTORIES OF TYPICAL OROFACIAL/ENDODONTIC
PAIN DILLEMAS
Scenario 1 
A 69-year-old male presents with a severe toothache in the maxillary left
canine, for which he requests endodontic treatment.
The pain is described as stabbing in character, “like an electric shock”,
lasting seconds in duration. He is unable to shave or wash the face on the
left or even to clean the teeth, eat, drink or allow cold air to touch this area
without triggering pain. However, pain does not disturb the patient from
sleep at night. Clinically, the canine is heavily restored and there are
extensive plaque deposits and inflammation of the gingivae in the upper
and lower dental arches.
• Question: What non-odontogenic condition may the patient be suffering
from?
• Answer: Trigeminal neuralgia. (Maxillary division V2).
• Question: What investigations would you consider?
• Answer: Radiograph to exclude endodontic problems with the canine.
Baseline blood tests prior to commencing medication. MRI to assess
trigeminal nerve.
• Question: What treatment might you consider and to whom would you
refer?
• Answer: Carbamezapine medication, referral to their General Medical
Practionner, an Orofacial Specialist or Neurologist.
Scenario 2 
A 49-year-old female presents with a dull, burning, continuous pain in the
upper right first premolar, with signs of allodynia and hypersensitivity in
the maxillary right maxilla. The tooth was restored then root-canal treated
6 months ago but the pain never subsided. Clinically and radiographically
the tooth in question appears to have an excellent non-surgical root-canal
treatment with good apical seal. However, the patient is adamant that the
tooth should be extracted.
Previously, a similar pain was present in the maxillary right second
premolar tooth which was restored, root-canal treated and subsequently
extracted. Unfortunately, maxillary right first and second molars underwent
a similar fate of restoration, root-canal treatment and extraction.
• Question: What is your advice to the patient with regards to the
extraction?
• Answer: Advise against extraction.
• Question: What is the most likely condition?
• Answer: Neuropathic pain (atypical odontalgia).
Scenario 3 
A 32-year-old male smoker presents with a 3-month history of a toothache
in the left maxilla possibly from a molar tooth, which wakes the patient
from sleep. On questioning, the pain occurs regularly at night, 1–2 hours
after falling asleep. When the patient awakes, he is experiencing an intense
pain which lasts from half an hour to 2 hours. He is unable to lie in bed but
agitation causes him to pace the room and seek distraction. Pain is located
in the eye, supraorbital and temporal region with associated features,
including ipsilateral conjunctival injection and lacrimation, rhinorrhea, nasal
blockage and ptosis.
• Question: What is the most probable non-odontogenic diagnosis?
• Answer: Cluster headache (Migranous neuralgia).
CONCLUDING REMARKS
If endodontic pain diagnosis is challenging, diagnosis of orofacial pain
mimicking endodontic pain is even more complex. It requires a systematic
gathering of relevant information and its appropriate processing through a
surgical sieve to identify likely causes. The responsibility lies with the
endodontist to exclude pain of dental and endodontic origin and then to
refer appropriately to specialists with the relevant knowledge and skills.
Depending on the country of residence, the relevant speciality may include
orofacial pain or oral medicine.
REFERENCES AND FURTHER READING
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Berge, T.I., 2002. Incidence of chronic neuropathic pain subsequent to surgical removal
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Breivik, H., Collett, B., Ventafridda, V., et al., 2006. Survey of chronic pain in Europe;
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The orofacial pain–endo interface  373
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 17
Section 4 Multidisciplinary aspects of endodontic management
The oral medicine and oral surgery–endo interface
  R Leeson, K Gulabivala

Periapical disease presents with swellings and radiographic changes (oste-

olytic or osteosclerotic). It is therefore, essential for dentists to be aware
DIFFERENTIAL DIAGNOSIS OF RADIOLUCENT AND
of any non-endodontic lesions that may mimic periapical pathosis.
RADIOPAQUE LESIONS
Although many of the lesions presented in this chapter appear to have such
Radiography remains the standard investigation for assessing lesions
distinct appearance that it may seem unlikely they would be confused with
within the bone. Periapical radiographs are ideal for endodontic cases in
apical pathosis, hospital records and journals are full of cases where just
assessing radiolucency and increased periodontal ligament space, particu-
that has happened. At best, this may be embarrassing and, at worst, it could
larly around the apex of a tooth. However, an OPG provides a useful screen
cost a life. Such confusion need not represent incompetence since all
for assessing more extensive lesions or when there is involvement of
dentists are taught the features of central tendency of any condition, as the
several teeth in more than one dental quadrant or region of the dentofacial
commonest presenting characteristics. Only experience and further train-
skeleton.
ing will enable the full spectrum of normal distribution of disease presenta-
The causes of radiolucent/opaque lesions are vast but summaries have
tion to be grasped. The problem is that presentations of many diseases can
been provided to highlight the most likely candidates. These are not
have overlapping features when the full spectrum of disease presentation
exhaustive lists but provide an overview of lesions which may be encoun-
is taken into account; the overlap is greater for some diseases than others,
tered in clinical practice. Before considering specific diagnostic character-
particularly when the time-line or natural history is considered. There may
istics, one should first consider the general radiographic (Table 17.9) and
be greater overlap at the incipient stages.
associated clinical (Table 17.10) features.
Endodontists and dentists should therefore, remain familiar with alterna-
tive diagnoses and retain a broad surgical sieve at their finger-tips. The
purpose of this chapter is not to provide encyclopaedic information about CYSTS
alternative disease states but to provide an organized summary listing of
the factors to consider. Where suspicions are aroused by a disease presenta- A number of cystic conditions may also present in the orofacial
tion, an appropriate referral to a specialist should be sought. region, the radiographic features of which are presented in Tables 17.11
and 17.12.

DIFFERENTIAL DIAGNOSIS OF OROFACIAL LUMPS

AND BUMPS
When examining any lesion whether obviously related to a tooth or adja-
cent to a tooth, a standard description (Table 17.1) is undertaken in order
to establish diagnosis or enable differential diagnosis.
Hard and soft tissue swellings are often encountered in the orofacial
region and are most frequently hyperplastic, reactive proliferations of
epithelium and connective tissue, due to irritation, chronic injury or infec-
tion. Self-limiting growths or benign neoplasms of connective tissue
develop from fibrous tissue, endothelia, skeletal and smooth muscle,
lipocytes, nerve sheaths and osteoprogenitor cells. Although usually slow
growing some may be aggressive and cause local destruction. Malignant
connective tissue sarcomas with their metastatic potential and rapid spread
are rare but early detection is important before haematogenous spread
occurs. Epithelial derived squamous cell carcinomas are however, the most
common malignant neoplasm of the oral cavity.
SOFT TISSUE SWELLINGS
Various tissue elements may give rise to soft tissue lesions that are hyper-
plasias or neoplasms, either benign or malignant. Connective tissue lesions
presenting as swellings are shown in Table 17.2.
Other tissues involved in orofacial soft tissue swellings may be epithe-
lial (Table 17.3) in origin or related to the salivary glands (Table 17.4),
haematological (Table 17.5) tissues or cysts (Table 17.6).
HARD TISSUE SWELLINGS
Hard tissue swellings in the mouth most commonly arise from bone (Table
17.7) or odontogenic (Table 17.8) origin and can be classified broadly into
the categories shown in Tables 17.7 and 17.8.
BONE LESIONS
A variety of bone lesions may present in the orofacial area and may be
classified into benign fibro-osseous lesions (Table 17.13), metabolic bone
conditions (Table 17.14), benign bone tumours (Table 17.15), and malig-
nant bone tumours (Table 17.16).
Idiopathic osteosclerosis
Areas of dense bone may frequently be encountered within the trabecular
spaces and may represent a developmental anomaly or, occasionally, a
compensatory response to abnormal stress. The radiographic appearance
may closely resemble that of sclerosing or condensing osteitis. However,
the tooth reacts normally to pulp testing (Fig. 17.9).
Fibro-cemento-osseous dysplasia
Fibro-cemento-osseous lesions present in their early stages as radiolucent
areas, commonly in relation to the apices of the mandibular incisors known
here as periapical fibro-cemento-osseous dysplasia (Fig. 17.10). These
lesions mature over a 5- to 10-year period with gradual infill of dense
cemento-osseous material to create radiopacities. The teeth remain respon-
sive to pulp tests and endodontic treatment is not required.
ODONTOGENIC TUMOURS
A range of different odontogenic tumours may arise in the jaws, and may
be classified into epithelial odontogenic tumours (Table 17.17), connective
tissue odontogenic tumours (Table 17.18), mixed connective tissue and
epithelial odontogenic tumours (Table 17.19) and malignant odontogenic
tumours (Table 17.20).

© 2014 Elsevier Ltd. All rights reserved.

 The oral medicine and oral surgery–endo interface  375

Table 17.1  Description of lesion METASTASES TO THE JAWS

It must be borne in mind that malignant tumours may also metastasize to
Site
the jaws from various sites including the breast, lungs, kidney, prostate,
Size
Shape
thyroid, stomach, colon and skin (Table 17.21).
Colour
Consistency DIFFERENTIAL DIAGNOSIS OF MUCOSAL LESIONS
Contour
Attachment Mucosal lesions (Table 17.22) may complicate or affect endodontic man-
agement in a number of ways. First, a mucosal lesion may be mistaken
for an odontogenic condition. Alternatively, it may aggravate and exacer-
bate an endodontic problem or management of an endodontic case may be
affected, for example, in allergic conditions with regards to the use of
materials and medicaments.

Table 17.2  Soft tissue swellings derived from connective tissue

Tissue Hyperplasia Benign neoplasm Malignant neoplasm

Fibrous Focal fibrous hyperplasia Fibromatosis Fibrosarcoma
Peripheral ossifying fibroma Myofibromatosis Malignant fibrous histiocytoma
Peripheral giant cell granuloma Myofibroma Malignant solitary fibrous tumour
Inflammatory fibrous hyperplasia Desmoplastic fibroma
Inflammatory papillary hyperplasia Nodular fascitis
Hyperplastic gingivitis Benign fibrous histiocytoma
Hereditary gingival fibromatosis Benign solitary fibrous tumour
Drug-induced gingival hyperplasia
Neural Traumatic neuroma Neurilemoma Neurogenic sarcoma
Palisaded encapsulated neuroma Neurofibroma
Granular cell tumour
Congenital gingival granular cell tumour
Neuroectodermal tumour of infancy
Muscle Leiomyoma Rhabdomyosarcoma
Adipose Lipoma Liposarcoma
Vascular Pyogenic granuloma (Fig. 17.1) Haemangioma Angiosarcoma
Lymphangioma Kaposi sarcoma
Osseous and cartilagenous Myositis ossificans Soft tissue osteoma
Osseous and cartilaginous choristoma

Fig. 17.1  Pyogenic granuloma

Table 17.3  Soft tissue swellings derived from epithelial tissue

Benign epithelial lesions Squamous papilloma, epithelial polyp

Benign pigmented lesions
Leukoplakia
Epithelial hyperplasia
Epithelial atrophy
Epithelial dysplasia
Erythroplakia
Malignant epithelial
neoplasms
Melanoma
(Fig. 17.2)
Keratocanthoma, verrucous papilloma
(Fig. 17.3a)
Leaflet papilloma (Fig. 17.3b,c)
Melanotic macule, naevi, seborrheic keratosis,
actinic lentigo, Peutz–Jeghers syndrome,
melasma, acanthosis nigricans
Hyperkeratosis, acanthosis, nicotinic stomatitis,
proliferative verrucous leukoplakia
Oral submucous fibrosis
Carcinoma in situ
Squamous cell carcinoma (Fig. 17.4), verrucous
carcinoma (Fig. 17.5)
376  The oral medicine and oral surgery–endo interface

Fig. 17.2  (a) Fibroepithelial polyp; (b) keratinized

fibroepithelial polyp

A B

C
B

A
Fig. 17.3  (a) Verrucous papilloma; (b,c) leaflet papilloma

Fig. 17.4  Squamous

Table 17.4  Soft tissue swellings derived from salivary gland tissue
cell carcinoma
Reactive lesions
Infections
Immune mediated diseases
Benign salivary gland
tumours (adenomas)
Malignant salivary gland
tumours
Fig. 17.5  Verrucous cell (adenocarcinomas)
carcinoma
Mucous extravasation cyst (mucocoele) (Fig. 17.6)
Mucous retention cyst
Sialolithiasis (salivary stone)
Chronic sclerosing sialadenitis
Necrotizing sialometaplasia
Acute parotitis
Viral endemic parotitis (mumps)
Bacterial sialadenitis
Lymphoepithelial sialadentitis
Sjögren’s syndrome
Pleomorphic adenoma
Monomorphic adenoma
Papillary cystadenoma lymphomatosa
Oncocytoma
Other adenomas
Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Acinic cell carcinoma
Polymorphous low-grade adenocarcinoma
Other adenocarcinomas

A B
Table 17.5  Soft tissue swellings derived from haematological tissue
Lymphoma
Leukaemia
Table 17.6  Soft and hard tissue swellings derived from odontogenic and
non-odontogenic cysts
Odontogenic cysts
Derived from rests of Malassez
Derived from reduced enamel
epithelium
Derived from dental lamina (rests of
Serres)
Developmental cysts
Cysts of vestigial ducts
Lymphoepithelial cysts
Cyst of vestigial tract
Cyst of embryonic skin
Cyst of mucosal epithelium
The oral medicine and oral surgery–endo interface  377
Fig. 17.6  (a,b) Mucocoele
Fig. 17.7  (a,b) Lateral periodontal cyst
Table 17.7  Hard tissue swellings derived from bone
Benign fibro-osseous lesions Cemento-osseous lesions
Fibrous dysplasia
Cherubism
Metabolic and endocrine conditions Paget’s disease
Hyperparathyroidism
Osteopetrosis
Osteogenesis iImperfecta
Benign bone tumours Torus (Fig. 17.8), exostosis, osteoma
Oseoid osteoma and osteoblastoma
Cemento-ossifying fibroma
Giant cell lesions
Traumatic bone cyst
Periapical/radicular/apical cyst Langerhans cell histiocytosis
Dentigerous cyst Malignant bone tumours Osteogenic sarcoma
Eruption cyst Chondrosarcoma
Paradental cyst Ewing sarcoma
Odontogenic keratocyst
Lateral periodontal cyst (Fig. 17.7)
Gingival cyst of adult
Dental lamina cyst of newborn
Glandular odontogenic cyst
(sialo-odontogenic cyst)
Nasopalatine duct cyst
Nasolabial cyst
Oral lymphoepithelial cysts
Cervical lymphoepithelial cysts
Thyroglossal tract cyst
Dermoid cyst
Epidermoid cyst
Heterotopic oral gastrointestinal cyst
Surgical ciliated cyst of the maxilla
378  The oral medicine and oral surgery–endo interface

Fig. 17.8  (a) Palatine torus; (b) mandibular tori

B
A

Table 17.8  Hard tissue swellings derived from odontogenic origin Table 17.11  Cysts

Epithelial odontogenic tumours Ameloblastoma Condition Radiographic features

Connective tissue odontogenic
tumours
Mixed odontogenic tumours
Malignant odontogenic tumours
Table 17.9  Radiographic considerations when investigating radiopaque
and radiolucent features
Position
Shape
Outline
Relationship with teeth
Relationship with anatomical structures
Calcifying epithelial odontogenic tumour
Adenomatoid odontogenic tumour
Calcifying odontogenic cyst
Squamous odontogenic tumour
Odontogenic fibroma
Odontogenic myxoma
Cementoblastoma
Ameloblastic fibroma
Odontoma
Ameloblastic fibro-odontoma
Malignant ameloblastoma
Ameloblastic carcinoma
Odontogenic carcinoma
Primary intra-osseous carcinoma
Maxilla, mandible, anterior, posterior
Unilocular, multilocular
Well defined, diffuse
Displacement, resorption
Inferior alveolar nerve, maxillary
antrum
Periapical cyst
Dentigerous cyst
Paradental cyst
Odontogenic keratocyst
Lateral periodontal cyst
Gingival cyst
Glandular odontogenic
cyst
Rounded well-circumscribed, often corticated,
located at the apex of a non-vital tooth. If
lateral, aspect of tooth appears as semicircular
radiolucency against the root surface
Well-circumscribed, surrounding crown of an
unerupted tooth attached at amelo–cemental
junction. Corticated interface with bone
indicating slow, uniform growth
Well-circumscribed cyst involving distal aspect of
third molars. Those which develop on the buccal
aspect of mandibular molars may not be visible
on routine radiograph, due to superimposed
image on adjacent tooth
Well-defined, solitary lesion, smooth or scalloped
margins, mutilocular, polycystic with thin
corticated margin. In inflamed cysts or those that
have perforated the cortex of the bone, the
corticated appearance may be unclear
Well-defined, small <1 cm, unilocular lesion,
delicately corticated, between the roots of vital
teeth. Common mandibular premolar region or
anterior maxilla or mandible
Rare polycystic botryoid variant is multilocular
(see Fig. 17.7)
Occasional pressure-induced saucerization in the
underlying alveolar bone but otherwise not
apparent on radiograph as confined to the
gingiva
Not specific appearance but often large, well-
defined, uni- or multilocular lesions of the
mandible

Table 17.10  Clinical features to consider associated with radiopaque and Table 17.12  Developmental cysts
radiolucent lesions
Condition Radiographic features
Associated swelling Hard-bony, smooth/irregular.
Nasopalatine duct cyst Well-circumscribed oval or heart-
Soft- fluctuant, fluid filled, bluish colour shaped radiolucency. Located
Teeth Displacement or increased mobility anterior maxilla, mid-line, between
Non-vital/vital, infection, resorption, missing roots of central incisors
Associated pathology Sinus tract, fistula, pus exudate, pathological fracture Cysts of mucosal epithelium Well-circumscribed radiolucency, in
close proximity to but separate from
the maxillary sinus

Table 17.13  Benign fibro-osseous lesions
Condition
Cemento-osseous lesions
Periapical cemental dysplasia
Florid cemento-osseous dysplasia
Juvenile fibrous dysplasia
Adult fibrous dysplasia
Cherubism
Table 17.14  Metabolic bone conditions
Condition
Paget’s disease
Hyperparathyroidism
Osteopetrosis
Osteogenesis imperfecta
Table 17.15  Benign bone tumours
Condition
Torus, exostosis, osteoma
Osteoid osteoma and osteoblastoma
Cemento-ossifying fibroma
Peripheral giant cell granuloma
Central giant cell lesion (granuloma)
Aneurysmal bone cyst
Traumatic bone cyst
Langerhans cell histiocytosis
(eosinophilic granuloma)
The oral medicine and oral surgery–endo interface  379
Clinical features Radiographic features
Vital teeth, often anterior mandible Three radiographic stages:
Non-expansile osteolytic (lucent); cementoblastic (lucent/opaque);
Non symptomatic lesion mature (opaque)
Non- expansile Mixed lucent and opaque lesions, multiple lesions diffusely
Non symptomatic distributed in the bone from alveolar crest to inferior border
Affects 1–-4 quadrants “Cotton wool” or “cloud” appearance
FIBROUS DYSPLASIA
Displacement of teeth Varies with stage of maturity of lesion
Expansion of cortices Early – lucent becoming opaque with more bone formation
Affects one or more bones usually self-limiting “Ground glass” or “orange peel” appearance.
Lamina dura obscured
Cortical plates thinned
As above Usually less homogeneous than juvenile appearance may exhibit
mixed radiolucent, radiopaque cotton wool appearance
CHERUBISM
Hereditary, typical cherub face Early – cystic lesions
Severe malocclusion. Late gradually changes to more radiopaque structures “ground
Displaced erupted and unerupted teeth, expanded arches glass” appearance similar to stabilized fibrous dysplasia
Radiographic features
Early, osteolytic stage, diffuse radiolucency
Late or less active stage, diffuse areas of increased bone density
Most commonly a combination of radiolucent and radiopaque lesions resembling “cotton-wool balls” in diffusely defined
radiolucency contained in a region of enlarged bone with thicker, less dense cortices. Maxilla and mandible are often greatly
enlarged and cranial cortical plates thickened.
Teeth may exhibit loss of lamina dura and hypercementosis of roots
Decreased bone density (osteoporosis) or mottled areas of radiolucency with thinning of cortical plates and medullary bone (osteitis
fibrosa cystic). In chronic or late stages, loss of normal trabecular pattern in the jaw bones and lack of distinctiveness in lamina
dura may occur
Occasionally large destructive radiolucency may occur indicative of “brown tumour”, a giant cell tumour of hypoparathyroidism.
Lesions are reversible if the hypoparathyroidism can be corrected
Increased bone density. Sinus cavities reduced in size, unerupted teeth common in severe forms of the disease
Unilocular radiolucences, both sides of the mandible. Dentinogenesis imperfecta, bulbous crowns, shortened roots and obliteration
of pulp chambers
Radiographic features
Well-demarcated overgrowth of bone (see Fig. 17.8)
Well-defined, rounded radiolucency with a surrounding zone of increased radiopacity
Unilocular or multilocular
Early, small lesions are usually radiolucent.
Enlarging lesions acquire irregular shaped radiopacities within the radiolucency
Late, mature lesions may be radiopaque with a margin of radiolucency, due to enlargement and coalescence of the
radiopaque elements
Root resorption and displacement of teeth often observed
GIANT CELL LESIONS
Small lesions – primarily in soft tissues
Larger lesions – superficial erosion of the cortical bone with widening of adjacent periodontal space sometimes
observed. In edentulous areas, erosion beneath the lesion is referred to as saucerization. Small spicules of bone may
extend vertically into the base of the lesion
Large radiolucency, indistinct line of demarcation with adjacent normal bone
Buccal and lingual expansion with complete cortical bone loss, teeth displacement and root resorption often observed
Unilocular, expansile, variable oval or fusiform radiolucency, sometimes trabeculated, thin or eroded cortex. Teeth may
be displaced and roots resorbed
Solitary, well-circumscribed radiolucency of variable size. A “scalloped” appearance is characteristic of larger lesions
which often extend between the roots of associated teeth. Occasional buccal or lingual cortical expansion
Solitary, intraosseous punched-out lesion, beneath and around tooth roots. May appear as focal areas of advanced
periodontal disease when several teeth are involved. Lack of bone around the teeth, gives the appearance of “teeth
floating in space”
380  The oral medicine and oral surgery–endo interface

Fig. 17.9  Dense bony trabecular

Table 17.16  Malignant bone tumours
pattern around the roots of vital
Condition Radiographic features
teeth

Osteogenic sarcoma Variable, dependent on specific histological type.

Features range from radiolucency to large areas of
radiopacity with a diffuse, poorly defined radiolucent
background
Widening of the periodontal membrane in adjacent
teeth and “sunburst” appearance of radiopacity from
the periosteum, may assist in diagnosis but are not
exclusive features to osteogenic sarcoma
Chondrosarcoma “Moth eaten” radiolucency with indistinct boundaries. In
addition, depending on the extent of calcification of
the cartilaginous component, flecks of blotchy
radiopacity. Commonly associated teeth have widening
of the periodontal membrane
Ewing sarcoma “Moth eaten” appearance of involved bone with
indistinct margins similar to osteomyelitis
“Onion skin” reaction or lamellar layering may be seen
in the periosteum

Table 17.17  Epithelial odontogenic tumours

Condition Radiographic features

Ameloblastoma
Common ameloblastoma
Unicystic ameloblastoma
Peripheral ameloblastoma
CEOT (calcifying epithelial
odontogenic tumour)
AOT (adenomatoid
odontogenic tumour)
Calcifying odontogenic cyst
Squamous odontogenic cyst
“Soap bubble”, multilocular, appearance
Size may be difficult to determine, due to lack of
demarcation with normal bone
Root resorption occasionally observed in rapidly
growing lesions
Unilocular, well demarcated and may even be
corticated. Tooth often present within the
radiolucency. If located in the premolar region,
displacement of adjacent tooth roots may
occur
Primarily extra-osseous but occasional
A
radiolucency visible beneath the lesion, due to
pressure exerted on the bone presenting as a
superficial saucerization of the cortical bone
Tooth separation may occur when located in the
interdental papilla
Small calcifications occur within diffuse
radiolucency. Radiopacity appears faint or as
discrete rounded structures
Small lesions are often unilocular radiolucencies
with indistinct demarcation from surrounding
bone similar to ameloblastoma
The frequent presentation over unerupted or
displaced teeth leads to a differential diagnosis
which includes dentigerous cyst, AOT (see
below) and ameloblastic fibro-odontoma
Peripheral lesions may present as superficial
cortical erosion
Unilocular, well-corticated and circumscribed
radiolucency that contains a tooth. The crown
of an impacted tooth is often surrounded but
this lesion extends apically beyond the
amelo–cemental junction and hence is
distinguishable from a dentigerous cyst B
Unilocular, well-circumscribed radiolucencies
containing flecks of radiopacity. Sometimes C
large tooth-like structures are located centrally
while small nodular radio-opacities are located Fig. 17.10  (a) Fibro-cemento-osseous-dysplasia related to a mandibular molar;
peripherally. Lesions may resemble a (b,c) cemental dysplasia
developing odontoma or ameloblastic
fibro-odontoma
Unilocular radiolucency for small lesions
When located in the bone coronal to the root
apices, tooth separation may occur
Multilocular large lesions with indistinct border
 The oral medicine and oral surgery–endo interface  381

Table 17.18  Connective tissue odontogenic tumours Table 17.20  Malignant odontogenic tumours

Condition Radiographic features Condition Radiographic features

Peripheral odontogenic
fibroma
Central odontogenic
fibroma
Odontogenic myxoma
Cementoblastoma
ODONTOGENIC FIBROMA Malignant ameloblastoma Similar to ameloblastoma with malignant
features
Small lesions are usually located within the gingiva
with no radiographic features Ameloblastic carcinoma Similar to ameloblastoma with malignant
Large lesions may cause saucerization of the cortical features
bone or widening of the cervical portion of the Odontogenic carcinoma Aggressive, destructive, intraosseous lesion
periodontal space characterized as a “diffuse honeycomb”
Small radiopaque flecks may be visible if lesions radiolucency
contain calcifications within the cellular connective Primary intraosseous carcinoma Poorly defined features
tissue
Well-circumscribed, unilocular or multilocular
Radiopaque flecks sometimes observed
Large lesions – multilocular radiolucencies, “soap
bubble” or “honeycomb” pattern. Trabeculations
angular or coarse may be noted. No distinct Table 17.21  Metastases to the jaws
demarcation with uninvolved bone similar to
ameloblastoma. No root resorption but tooth Condition Radiographic features
displacement may occur
Adenocarcinoma from Variable, mixed radiolucent/radiopaque lesions
Small lesions – unilocular non-specific radiolucencies
the breast
Unilocular, well-defined, radiolucent, radiopaque or
mixed lesions. Radiopaque lesions exhibit a zone
of peripheral radiolucency continuous with the
periodontal ligament space of unaffected areas of
the tooth. Adjacent roots may show apical third
resorption
Table 17.22  Mucosal lesions

Physical and chemical trauma Toothbrush trauma, denture trauma and

Table 17.19  Mixed connective tissue and epithelial odontogenic tumours
Condition
Ameloblastic fibroma
Odontoma
 Compound odontoma
 Complex odontoma
Ameloblastic fibro-
odontoma
Radiographic features
Unilocular or multilocular radiolucency
Well corticated, variable size
Often unilocular containing multiple (2–30)
radiopaque miniature teeth-like structures.
Located anteriorly in the jaws, between roots or
overlying crowns of unerupted teeth
Unilocular with distinct line of cortication and
absence of teeth–like structures. Located in the
posterior mandible over an impacted tooth most
commonly as a radiopaque, nodular mass
surrounded by radiolucency. Sometimes several
cms in diameter
Soft and hard tissue components vary
Often unilocular, well-circumscribed, large, mixed
radiolucent and radiopaque lesions containing an
impacted tooth
Occasionally multilocular. Opacities are usually
nodular and diffuse presenting as one large
isolated deposit or smaller dispersed areas
Recurrent aphthous stomatitis
(RAS)
Mucosal and skin conditions
Infective conditions
Allergic reactions
Possible immune-mediated
reactions
iatrogenic trauma. Thermal burns, radiation
mucositis and xerostomia, chemical burns
such as an asprin burn to the mucosa,
foreign bodies embedded in the tissues;
amalgam, graphite and food debris,
medication use resulting in gingival
hyperplasia (e.g. phenytoin, cyclosporine
and nifedipine)
Minor, major and herpetiform
Including conditions such as lichen planus,
lichenoid reactions, mucous membrane
pemphigoid, pemphigus vulgaris,
epidermolysis bullosa, erythema multiforma,
lupus erythematosus, progressive systemic
sclerosis
Bacterial, viral, fungal
Contact stomatitis, angioedema, Stevens-
Johnson syndrome
Orofacial granulomatosis (e.g. oral Crohn’s
disease
Melkerson-Rosenthal syndrome, cheilitis
granulomatosa)
Chronic granulomatous disease (e.g.
sarcoidosis, Wegner’s granulomatosis)

FURTHER READING
Scully, C., 2010. Oral medicine at a glance. Wiley-Blackwell, Oxford.
Whaites, E., 2007. Essentials of dental radiography and radiology, 4th ed. Churchill
Livingstone.
 Index

Page numbers followed by “f” indicate figures, “t” indicate tables, and “b” indicate boxes.

microbiota, 301–302
A natural history, 302 C
preceding disease states in, 299
Abscess progression, 299–301, 301f–302f Calcific bridge formation, 40f
acute apical, 117, 117f, 270, 271f, 272–273, 273f risk factors, 302, 302t Calcitonin gene-related peptide (CGRP), 47
acute periapical, 53–55, 56f–57f systemic diseases associated with, 302–303 Calcium hydroxide, 217–220, 217f–218f, 226–227
drainage, 273f Apical seal, 178, 178f paste, 39
and failed root canal treatment, 85 Arachidonic acid, 47 placement, 219, 219f
treatment, 272, 273f Archaea in periapical disease, 43 preparations, 216, 216f, 219, 219f
Abutments, 355, 357f Armamentarium, surgical, 148, 148f–149f removal and replacement, 219–220, 220f
Access cavities, coronal see Coronal access cavities Arterioles, 24, 25f tooth resorption, 287–288
Accessory canals, 13–14, 20, 303 Articaine, 264, 265f Calcium sulphate material, 262, 262f
Acellular cementum, 28, 29f Aspirin, 267–268 Calcospherites, 21–22, 22f
Acoustic microstreaming, 214–215, 214f Asthma, 363 Calculus removal, 157
Actinomyces species, 85 Atraumatic restorative therapy (ART), 38, 40, 168, Camphorated monochlorophenol (CMCP), 215, 216f
Adhesion molecules, 47 168f Canal probe, 145
Adrenaline (epinephrine), 156, 264 Autistic spectrum disorders (ASD), 366 Cancellier tubes, 147f
Akinosi technique, 265–266, 266f Autoclaves, 150–151 Cancellous bone, 112
Aldehydes, 216 Axons, 26, 26f–27f Canine fossa, 272, 272f
Alphaseal, 183f Canines
Alveolar bone, 31, 31f, 281–282 mandibular, 15–16, 16f
Alveolar crest fibres, 29–30, 29f B maxillary, 15–16, 15f–16f
Alzheimer’s disease, 365 Capillaries, 24, 25f
Amalgam, 255f, 349, 354 B lymphocytes, 45 Capset calcium sulphate material, 262, 262f
Ameloblasts, 5–6 Bacteria Carbon dioxide probes, 101, 115f
Amelogenesis imperfecta, 7t–8t biofilm and planktonic physiology, 75–76, 75f Carbostesin, 264–265, 265f
Anaesthesia, 156–157 culture studies, 67 Cardiovascular disease (CVD), 362
Analgesia, 156–157 ecology, 70–75, 74f Caries
efficacy of, 267, 267t and failed root canal treatment, 84–85, 85t, 86f, conservative management, 38, 40
intraoperative, 264–267 87t fissure sealing of occlusal, 40
local agents, 264–265 intraradicular, distribution, 67–70 optimal management, 166
actions, 264–265, 265f microscopy studies, 67–68, 68f–73f practical management approaches, 168–169,
delivery, 265–266 in periapical disease, 43 168f–169f
postoperative, 267–268, 267t persistent, effect on treatment outcome, 81–83 prevention, 38
relative, 156 root canal, 58f removal, 157–158, 158f
Anaphylaxis, 278 in situ hybridization microscopy studies, 68–70, Carts, 142–143, 143f
Angelus, 255f 74f Cast cores, 355, 356f
Angina, 362 Bacterial products, 43 Cavernous sinus thrombosis, 53–55
Ankylosis, 288, 332, 332f Balanced force technique, 193–194 Cavit, 221
Anodontia, 7t–8t Bayer Hedstroem, 195f Cavities
Anterior teeth restoration, 338–342, 339f–341f Benzodiazepines, 157, 368 deep, 169–172
Anti-invasion factor, 285 Best interest meetings, 367 principles of restoration, 166–167
Antibiotics, 157, 216–217 Bio-Oss, 262, 262f Cell-free zone, 21f, 22
periradicular origin emergencies, 273–274 Biodentine, 164t, 254, 255f Cell surface markers, 45
prophylactic, 362 Biofilms, 174–177, 175f Cellular cementum, 28, 28f
regenerative pulp therapy, 39 degradation, 207 Cellulitis, 53–55, 56f–57f, 246, 246f, 273
Anticipation, 152 physiology, 75–76, 75f Cement removal, 242
Anticurvature filing, 201 BioGide, 261–262, 262f Cementocytes, 28, 28f
Antigen-presenting cells (APCs), 49 Biomend, 261–262, 261f Cementum, 5–6, 28, 28f–29f, 303f–304f, 304
Antiplatelet therapy, 362 Biopsy, 247, 247f radiographic appearance, 112, 112f
Anxious patients, 156–157, 367–368 Bisecting angle periapical projections, 108, 108f Central tendency, 93
Apex locators, electronic, 184–187, 185f–186f Bisphosphonate-related osteonecrosis, 364 Ceramic crowns, 359
Apical abscess, 117, 117f, 270, 271f, 272–273, 273f Bleaching, 357–359, 359f Ceramometal crowns, 359
Apical constriction, 13, 13f Bleeding disorders, 362–363 Cerebral palsy, 365
Apical development, 281 Bone lesions, 374, 377t, 379t–380t, 380f Cermets, 355, 355f
Apical fibres, 29–30 Bone loss, 305, 305f, 309, 309f Cervical resorption, 292–297
Apical foramina, 13, 14t, 198–199, 199f Bone morphogenic proteins, 165 Cervical tray, 142
Apical periodontitis, 43, 61f, 63t Bone wax, 253 Chemomechanical procedure
acute, 270, 272 Briault probe, 145 biological and clinical perspective, 76–78, 77f–82f
cell profiles, 301 Bridges, removal, 146, 147f, 239 effects on biological events, 80–81
chronic, 117, 118f Broken-down teeth, 158–159, 159f technical aspects, 78–80
clinical manifestation, 299–301 Buccal space, 271 Chlorhexidine, 150, 157
measurement, 299–301 Burs, 250–251, 251f Chloroform clip technique, 227, 227f
 Index  383

Cholesterol clefts, 62f–63f, 85–86 Dentinal pain, 307 imaging, 102–116

Chronic obstructive pulmonary disease (COPD), 363 Dentinal tubules, 21–23, 22f–24f, 303, 303f–304f nature of, 93, 94t
Clamps, 159–160 bacteria in, 68, 72f–73f nature of endodontic problems, 93, 94t
Cleaning, 148–152, 150f nerve supply, 26 patient assessment, 94–102, 94t
Clinical area, 142–148, 142f–143f open, 36 Endodontic locking tweezers, 145, 145f
Clinical examination, 96–97 Dentine, 5–6, 22f Endodontic treatment
ease of oral access, 96, 97f aplasia, 7t–8t complications, 155
extraoral, 96, 96f, 97t hypocalcification, 7t–8t delivery sequence, 128–135
intraoral, 97f–98f intertubular, 23–24 effect of orthodontic tooth movement on, 332
Clinical interpretation, 20–21 peritubular, 23–24 immediate relief of symptoms, 128
Close support, 152–153, 153f primary, 23 multiple visit, 132–133
Clotting cascade, 48 radiographic appearance, 112, 112f planned review, 140, 140f–141f
Coagulation system, 48 reparative, 33 planning, 120–141
Collagen, 226–227, 227f, 255, 261–262 sclerosis, 22f, 23–24, 24f decision-making process, 135–140
Collaplug, 255 secondary, 23, 23f definitive treatment, 129–135
Complement system, 47–48 sensitivity, 26–27 factors influencing, 123–128, 123t
Composite, 255f, 349–350, 354 Dentine debris, 242, 243f ideal scenario, 120, 121b–122b
Composite veneers, 359 Dentine mud, 209–210 informed consent, 122–123
Concrescence, 7t–8t Dentine pins, 353, 353f initial treatment, 128–129
Condensing osteitis, 55, 58f Dentinogenesis imperfecta, 7t–8t medical records, 122–123
Cone-beam computed tomography (CBCT), 109–111, Dentoalveolar trauma, acute, 274–275 option selection, 120–121
110f, 111t acute management, 275–277 patient care, 120
Congenital heart disease (CHD), 362 medium- to long-term management, 280–283 reality of practice, 122–123, 122f
Conscious sedation, 368 triage, 274–275, 274f sequence, 128–135
Consent, 94, 122–123, 154–155, 366–367 Dentsply Tulsa Dental ProUltra™ tips, 148f referral, 155
Contamination zones, 143–144, 144f Development defects, 303, 304f role of, 361
Core materials, 354–355 Developmental grooves, 317, 318f–319f role of orthodontics in, 332–333
Coronal access cavities, 179–181 DG 16, 145 single visit, 132–133
cutting, 180, 180f–181f Diabetes mellitus, 363–364 Endomethasone paste, 224f
cutting principles, 179–180, 179f–180f Diagnosis see Endodontic diagnosis Endoring, 151, 151f
outline shape, 181, 181f–182f Diaket, 254, 255f EndoVac, 215, 215f
temporary seal, 220–221 Digital radiology, 103–104, 104f–105f Eosinophils, 44–45
Coronal seal, 235–236 Dilacerations, 6, 7f, 7t–8t Epilepsy, 366
Corrective surgery, 257–259 Discoloured teeth, 357–359, 358f–359f Epinephrine (adrenaline), 156, 264
Cortical bone, 31 Dopamine hydrolase, 47 Epithelial cells, 44–45
Coumarin therapy, 362 Dowels see Posts/dowels Epithelial polyp, 376f
Cracked tooth syndrome, 118, 269, 269f Dowgan carrier, 149f Epstein-Barr virus (EBV), 47
Cranial nerve injury, 97t Down’s syndrome, 366 Equipment, 142–143
Cresatin, 216 non-surgical retreatment, 146
Cresophene, 215, 216f surgical, 148, 148f–149f
Creutzfeld–Jakob disease (CJD), 152 E see also Instrumentation; specific items
Crown-root fractures, 275 Eruption times, 10, 10f–11f, 10t
Crowns Ectoderm, 2 Ethylenediaminetetraacetic acid (EDTA), 207
ceramic, 359 EDTA (ethylenediaminetetraacetic acid), 207 Evagination, 6, 7f, 7t–8t, 9f
ceramometal, 359 Electric pulp tester, 100–101, 100f Experimental root filling materials, 224–225, 225f
fractured, 118, 275, 275f, 283, 283t Electronic apex locators (EALs), 184–187, 185f–186f Explorer EXD3CH, 145, 145f
implant-retained, 359–360 Elevators, 148f External resorption, 118, 285, 288–297, 289f–298f
removal equipment, 146, 147f Emergencies, 268 Extracellular matrix (ECM), 75–76
Curettage, 251 acute dentoalveolar trauma, 274–275 Extraction
Cyclo-oxygenase, 267 interappointment, 279–280 decision-making process, 135–140
Cysts, 374, 377f, 378t intraoperative, 277–279 of root-treated teeth, 359–360
and failed root canal treatment, 85–86 involving sodium hypochlorite, 278–279
management, 85–86 medical, 277–278
periapical, 51–53, 53f–54f of periradicular origin, 270–274 F
Cytokines, 47, 50 postoperative, 279–280, 280f
Cytomegalovirus (CMV), 47 preoperative, 268–277 F-Met-Leu-Phe, 48–49
of pulpal origin, 268–270 Ferric sulphate, 253, 254f
surgical, 246 Fibreoptic light, 269, 269f
D Enamel Fibrinolysis system, 48
aplasia, 7t–8t Fibrinolytic peptides, 47
Decompression, 262–263, 262f hypoplasia, 7t–8t Fibro-cemento-osseous dysplasia, 115, 116f, 374,
Dementia, 365 radiographic appearance, 112, 112f 380f
Dendritic cells, 48–49 Enamel cord, 2–3 Fibrous healing, 88, 89f
Dental follicle, differentiation of, 5 Enamel-dentine junction development, 5–6 File holders/stands, 151, 151f
Dental lamina Enamel knot, 2–3, 4f Files
changes for permanent molars, 3–4 Enamel organs flexible, 200, 201f
development, 2, 3f development, 2, 3f–4f intermediate, 200, 201f
Dental nurses, 152–153, 152f differentiation of, 4–5, 5f precurved, 199–200, 200f
Dental papilla Enamel pearls, 317, 320f small, 200, 201f
development, 2–3, 3f Endocarditis, infective, 157, 157t, 362 Fish’s zones, 76–78
differentiation of, 5 Endodontic diagnosis, 93–119 Flaps
Dental records, 154 accuracy, 264 design, 247–257, 247f–248f
Dentinal dysplasia, 7t–8t diagnostic categories, 116–119 elevation, 248f–250f, 250
 384  Index

full mucoperiosteal, 248, 248f–249f Howship’s lacunae, 31, 31f Invagination, 6, 7f, 7t–9t, 10f, 317, 319f–320f
incisions, 249f–250f, 250 HPVs (human papilloma viruses), 47 Iodine-potassium iodide, 216
limited mucoperiosteal, 248, 249f–250f Human herpes virus-6 (HHV-6), 47 Iodoform, 216, 216f
retraction, 249f, 250 Human herpes virus-7 (HHV-7), 47
Flat plastic, 145 Human herpes virus-8 (HHV-8), 47
Flexible files, 200, 201f Human immunodeficiency virus (HIV), 151–152, J
Flutes, 196 157
Forceps, 147f Human papilloma viruses (HPVs), 47 Jaws, metastases to the, 375, 381t
Foreign body response, 86–87, 87f–88f Hydrodynamic theory, 26–27, 27f Juvenile periodontitis, 322–323, 323f
Foreign material irritation, 292, 294f Hydrogen peroxide, 357–359, 359f
Formocresol, 163 Hyperdontia, 7t–8t
Fractures Hypertension, 362 K
crown, 118, 275, 275f, 283, 283t Hypodontia, 7t–8t
crown-root, 275 Hypoglycaemia, 364 K3, 197f
instruments, 146, 147f Hypophosphataemia, 7t–8t Kerr Hedstroem, 195f
root see Root fractures Hypophosphatasia, 7t–8t Kerr K-file, 195f
teeth, 118, 118f, 268f Kerr K-Flex file, 193f, 195f
Front surface mirror, 145 Kerr K-reamer, 193f, 195f
Fungi I Kinins, 47–48
in periapical disease, 43
root canal, 59f–60f Iatrogenic problems, 305
Furcation probe, 145 Ibuprofen, 267 L
Fusion, 7t–8t, 9f, 317, 319f Idiopathic osteosclerosis, 115, 116f, 374
Idiopathic resorption, 297, 297f–298f Lamina dura, 112
Imaging techniques, 102–116 Lateral canals, 13–14, 14f, 20, 21f, 303, 303f
G see also specific techniques Lateral (para)pharyngeal space, 272
Implants, 130–131, 130f Lateral periodontal cyst, 377f
Gag reflex, 156, 367–368 Incandescence, 36f Latex allergy, 363
Germination, 6, 7f, 7t–8t Incision and drainage, 246, 246f, 273 Leaflet papilloma, 376f
Gingival fibres, 29–30, 29f Incisive foramen, 113, 113f Learning disability patients, 365–367
Gingivitis, 299 Incisors Ledermix, 217, 217f
Girofile, 201f mandibular, 15, 15f Ledge negotiation, 242, 242f
Glass ionomer cements, 221, 245 maxillary, 14–15, 15f Ledging, 198–199, 199f
Gluteraldehyde, 216 Independent mental capacity advocates (IMCA), Lee’s carver, 149f
Golden Medium, 201f 367 Legal considerations, 153–155
Gow-Gates technique, 265, 265f–266f Infection control, 151–152 Leukotrienes, 47, 50
Grand mal seizures, 366 Infective endocarditis, 157, 157t, 362 Light Speed, 202, 202f
Ground substance, 22–23, 23f Inferior dental artery, 30 Lignocaine, 264
Growth factors, 33 Inferior dental canal, 113, 113f Lips, 272
Guided tissue regeneration (GTR), 261 Inflammation Long-shanked excavators, 145, 145f
Gulabivala’s additional canal morphological groups, acute periapical, 50–51, 53f, 117, 117f Ludwig’s angina, 53–55, 56f–57f, 271, 271f
11f chronic, 44–45 Lumps and bumps, orofacial, 374, 375t
Gumboil, 53, 55f chronic periapical, 51, 53f Luxated teeth, 277, 282–283, 282t
Gutta-percha, 224, 224f, 224t, 254 chronic suppurative periapical, 53, 55f Lymphadenitis, 53–55
removal, 241–242, 241f pulp, 33, 36–37, 36f–37f Lymphangitis, 53–55
thermoplasticized Inflammatory resorption, 281 Lymphatic vessels, 25–26, 26f
carriers, 233–234, 234f–235f Informed consent, 94, 122–123, 366–367 Lymphocytes, 49
injection, 233, 234f Infratemporal fossa space, 272 Lysosomal enzymes, 47
Inhalation sedation, 368
Instrument removal system (IRS), 147f
H Instrumentation, 144–146 M
basic pack, 145, 145f
Haemophilia A, 363 hand, 192–195, 193f–195f Macrodontia, 7t–8t
Haemophilia B, 363 machined, 195–198, 195f Macrophages, 43–45, 48–50, 281
Haemostasis, 253, 253f–254f removal, 243–244, 243f–245f McSpadden engine-driven nickel–titanium file,
Halides, 216 transfer, 153, 153f 195f
Hand instrumentation, 192–195, 193f–195f twisted, 195 Magnetostrictive transducers, 214–215
Hard tissue swellings, 374, 377t–378t, 378f see also specific items Maillefer gutta-condensor, 236f
Healing Intentional replantation, 259–260, 260f Major histocompatibility complex (MHC), 49
fibrous, 88, 89f Interferons, 47 Mandible, spaces in relation to, 271–272
root fractures, 281, 282f Interleukins, 50 Mandibular processes, 2, 3f
wound, 257, 281, 305, 305f Intermediate cementum, 28 Mandibular teeth
Heart valves, prosthetic, 362 Intermediate plexus, 29–30, 29f canines, 15–16, 16f
Hedstroem file, 234–235 Intermediate restorative material (IRM), 254, first molars, 18–19, 18f–19f
Hemisection, 259, 260f, 357, 358f 254f incisors, 15, 15f
Hepatitis B, 151–152, 157 Internal resorption, 118, 285–288, 286f–289f, 286t premolars, 16–17, 17f
Hepatitis C, 363 International Normalised Ratio (INR), 362–363 second molars, 19, 19f–20f
Hero, 197f Interpretation, clinical, 20–21 third molars, 19–20, 20f
Herpes simplex (HSV-1/2), 47 Intraligamental injections, 266, 266f Mandibular tori, 378f
HIV (human immunodeficiency virus), 151–152, Intranasal sedation, 368 Manual agitation, 213, 213f
157 Intraosseous technique, 266, 266f Marcaine, 264–265
Horizontal fibres, 29–30 Intrapulpal injections, 266 Marginal periodontitis
Hot pulp, 266–267 Intravenous sedation, 157, 368 cell profiles, 301
 Index  385

clinical manifestation, 299–301, 300f Mucosal lesions, 375, 381t Osteotomy, 250–251, 250f–251f
measurement, 299–301 Multiple sclerosis (MS), 364–365 Overdenture, temporary, 341–342, 342f
microbiota, 301–302 Oxytalan fibre, 29–30
natural history, 302
preceding disease states in, 299, 300f N
progression, 299–301, 300f–301f P
risk factors, 302, 302t Naber’s probe, 324, 324f
systemic diseases associated with, 302–303 Nasal sedation, 157 Pain
Masserann kit, 147f Natural killer (NK) cells, 48–49 definition, 369
Mast cells, 44–45 Nayyar amalgam dowel core, 353–354, 354f diagnostic accuracy, 264
Matrix metalloproteinases, 47 Necrotic pulp tissue, 43 history, 307
Maxilla Needle holders, 149f immediate relief, 128
radiographic appearance, 112, 112f Negligence, 154 management principles, 264
spaces in relation to, 272 Nerve fibres, 26–28, 27f non-odontogenic, 119
Maxillary antrum, 272 Neuropeptide Y, 47 periodontal, 118–119
radiographic appearance, 112, 112f Neuropeptides, 47 postoperative, 279
radiographic interpretation errors, 112, 113f Nickel–titanium rotary instruments, 196–198, prevalence, 265t
Maxillary processes, 2, 3f 196f–198f pulpal, 268
Maxillary teeth Non-steroidal anti-inflammatory drugs (NSAIDs), relief see Analgesia
canines, 15–16, 15f–16f 267 source location, 101–102, 102f
first molars, 17–18, 17f Nuclear factor kappa B ligand (RANKL), 45 Palatal flap, 247–248, 248f
incisors, 14–15, 15f Nuclear factor kappa B (NF-κβ or RANK), 45 Palatal subperiosteal interval, 272, 272f
premolars, 16, 16f Palatine torus, 378f
second molars, 18, 18f Papilla-base flap, 247–248, 248f
third molars, 19–20, 20f O Paracetamol, 267
Medical emergencies, 277–278 Parallax techniques, 108–109, 108f–109f
Medical history, 95–96, 96f, 96t, 154, 361 Oblique fibres, 29–30, 29f Paralleling periapical projections, 107–108, 107f–108f
Medical records, 154 Occlusal examination, 102 Parkinson’s disease, 365
Medicaments, 151, 151f Occlusal loading, 355 Pastes, 151f, 223, 224f
Medication, 157 Odontoblastic processes, 21–22 Patency filing, 210–212
see also specific medication Odontoblasts, 5–6, 21–22, 21f Pathogen-associated molecular patterns (PAMPs),
Medico-legal considerations, 153–155 injury, 35–36, 35f 48–49
Membranes, 261–262, 261f–262f Odontogenic tumours, 374, 381t Patient assessment, 94–102, 361–362
Mental foramen, 113, 113f Odontome, 7t–8t, 9f clinical examination, 96–97, 96f, 97t
Mental imaging, 20–21 Odontopaste, 217 dental history, 96
Mesio-occlusal-distal (MOD) cavities, 349–352, Operation microscope, 145, 145f history taking, 95, 361
350f–352f Operative emergencies, 277–279 informed consent, 94
Messing gun, 149f, 219, 219f Oral sedation, 157, 368 medical history, 95–96, 96f, 96t, 154, 361
Metabolites, 47 Orofacial lumps and bumps, 374, 375t nature of presenting complaint, 94, 94t–95t
Metacresyl acetate, 216, 216f Orofacial pain, 369–373 occlusal examination, 102
Metastases to the jaws, 375, 381t case histories, 372 pain source location, 101–102, 102f
Micro-Apical Placement (MAP) System, 149f characteristics, 370–371, 370f, 370t–371t periodontal examination, 98–99, 98f–99f, 99t
Micro Mega Hedstroem, 193f classification, 369, 370t pulp testing, 100–101, 100f–102f
Microbes definition, 369 record keeping, 94
ecology, 70–75, 74f diagnosis, 369–370 social history, 96
and failed root canal treatment, 84–85, 85t and endodontics, 371–372 soft tissue examination, 98, 98f
Microbiota neurophysiological basis of, 369, 370f tooth examination, 99–100, 99f–100f
in apical/marginal periodontitis, 301–302 prevalence, 369 Patient(s)
root canal see Root canal microbiota Orthodontic band, 311, 346–347, 348f anaesthesia and analgesia, 156–157, 156f
Microcirculation, 25–26 Orthodontic tooth movement antibiotic cover, 157
Microdontia, 7t–8t effect of trauma on, 331–332 anxious, 156–157, 367–368
Microleakage, 36, 36f, 167, 170f effect on endodontic treatment, 332 care, 361
Microscope, operation, 145, 145f effect on pulp, 329–330, 330f, 330t education/information, 155–156, 155f–156f
Midazolam, 368 effect on root resorption, 330–331, 330f–331f, with HIV/HBV, 157
Miller classification of tooth mobility, 99, 99t 330t with learning disability, 365–367
Mineral trioxide aggregate (MTA), 39, 41, 41f, 164t, effect on tooth resorption, 331 medically compromised, 362–365
226–227, 227f, 245, 254, 255f Orthodontic treatment, 320, 320f medication, 157
Misdiagnosis, 88 definition, 329 oral care, 120
Mitchell’s trimmer, 145 effect on teeth and pulp, 332 protection, 155
Mobile cabinet, 142, 142f nature of contemporary, 329 with special needs, 361, 365–367
MOD (mesio-occlusal-distal cavities), 349–352, role in endodontic-restorative treatment planning, Pattern recognition, 93
350f–352f 332–333 Pattern recognition receptors (PRR), 48–49
Molars Osteitis, condensing, 55, 58f Perforations, 114, 115f, 198–199, 200f
mandibular Osteitis, sclerosing, 114, 115f iatrogenic, 304–305, 305f–306f
first, 18–19, 18f–19f Osteoblasts, 31 repair, 257–258, 257f–258f
second, 19, 19f Osteoclasts, 31 repair instruments, 146
third, 19–20, 20f Osteocytes, 31 root, 313–316, 314f–316f
maxillary Osteomyelitis, periapical, 55 in root canal retreatment, 245, 245f–246f
first, 17–18, 17f–18f Osteonecrosis, bisphosphonate-related, 364 Periapical abscess, 53–55, 56f–57f
second, 18, 18f Osteoprotegerin (OPG), 45 Periapical disease, 44f
third, 19–20, 20f Osteosclerosis acute abscess/cellulitis, 53–55, 56f–57f
MTA block, 149f idiopathic, 115, 116f, 374 acute inflammation, 50–51, 53f, 117, 117f
Mucocoele, 377f periapical, 55 aetiological factors, 43
 386  Index

chronic inflammation, 51, 53f Pocket measuring probe, 145 Pulp regeneration, 41
chronic suppurative inflammation, 53, 55f Points removal, silver, 243–244 Pulp space, 10–14
condensing osteitis, 55, 58f Polymorphonuclear leucocytes (PMNs), 34, 35f, characteristics, 11–14, 12f–13f
epithelial proliferation and cysts, 51–53, 53f–54f 43–45, 48–50, 281 classification of pulp systems, 10–11, 11f
host factors, 43–47, 46f, 48f Porcelain veneers, 359 dimensions, 14, 14t
osteomyelitis, 55 Post crown, temporary, 341–342 radiographic appearance, 112
osteosclerosis, 55 Posterior teeth restoration, 346–354, 347f–349f see also Root canals
pathogenesis and natural history, 48–55, 49f–52f Postoperative emergencies, 279–280, 280f Pulp testing, 100–101
prevention, 76–83 Posts/dowels electric pulp tester, 100–101, 100f
root canal microbiota, 59–62 characteristics, 342–346, 342f thermal, 101, 101f–102f
signs of, 307 composition material, 342 Pulp therapy, 163–173
treated teeth, 55–57, 58f–63f diameter, 344–345, 345f compromised pulp, 169–172
treatment, 76–83 diaphragm, 346, 346f deep cavities, 169–172
chemomechanical procedure, 76–81, 77f–82f length, 343–344, 344f–345f factors affecting outcome, 41
Periapical osteomyelitis, 55 permanent, 341, 341f future approaches, 41
Periapical pain, 307 removal, 239–241, 240f–241f primary dentition, 163
Periapical surgery, 89, 247–257 removal equipment, 146, 147f complications, 166
Perio-endo lesions shape, 342–343, 342f–343f follow up, 166
causes of, 310–323 surface configuration, 345–346, 346f pulp disease, 163, 164f
classification, 307 Pre-ameloblasts, 5–6 techniques, 163–166
definition, 307 Precurved files, 199–200, 200f tooth morphology, 163, 164f
diagnosis, 307–309 Predentine, 21–22, 21f rationale for, 38–39, 39f
management, 310–324, 324f Premolars regenerative, 39, 172, 173f
multiple, 321–323 mandibular, 16–17, 17f secondary/permanent dentition, 166–172
prognosis estimation, 323, 323f maxillary, 16, 16f caries, 166, 168–169
regenerative techniques, 325–327, 327f Preoperative emergencies, 268–277 cavity restoration, 166–169
single isolated, 310–321 Prepubertal periodontitis, 322–323, 322f smear layer, 164f, 167–168
Periodontal charting, 307–309 Presenting complaint, 94, 94t–95t success assessment, 39–40, 40f
Periodontal disease, localized, 320–321, 321f Pressure resorption, 290–292, 293f success probability, 40–41
Periodontal examination, 98–99, 98f–99f, 99t Pressure/vacuum agitation, 213, 214f Pulp tissue
Periodontal lesions, 114, 115f Prevention, 129 degrading, 206–207
Periodontal ligament, 28f–31f, 29–31 Primary dentition, 163, 164f necrosis, 43, 116–117, 117f
damage, 281, 283, 283t Primary epithelial band development, 2 Pulpal origin emergencies, 268–270
radiographic appearance, 112 Prion diseases, 152 diagnosis, 268–269, 268f–269f
radiographic interpretation errors, 112, 112f–113f Probes, 145 medication, 270
Periodontal ligament space Profile GT, 197f treatment, 269–270, 269f–270f
lesions, 114, 114f–115f Prostaglandins, 47, 50 Pulpal pain, 307
widening, 112 Pterygomandibular space, 272 Pulpectomy, 270
Periodontal pain, 118–119 Pulp Pulpitis
Periodontal support, 130, 130f anatomy and physiology of, 21–24, 21f irreversible, 116, 117f, 266–269, 268f
Periodontal symptoms history, 307 compromised, 169–172 reversible, 116, 268–269
Periodontal tissues, pre-endodontic management, 159 concussed, 116 Pulpo-periapical inflammation
Periodontitis death, 281 and bone loss, 305, 305f
aggressive, 322–323, 322f defence reactions, 33, 34f and periodontal wound healing, 305, 305f
apical see Apical periodontitis disease, 305, 307 Pulpotomy, 38–40, 40f, 163–165, 164f–165f,
chronic, 321, 322f prevention and treatment, 38 171–172, 172f, 270
initial manifestation, 299, 300f in primary teeth, 163 alternatives to, 165–166
isolated lesions superimposed upon, 321, 322f dystrophic calcification (stones), 37–38, 37f–38f Pyogenic granuloma, 375f
marginal see Marginal periodontitis effect of orthodontic tooth movement on, 329–330,
Periodontium, 136, 137f 330f, 330t
effect of pulp disease on, 305 effect of orthodontic treatment on, 332 Q
pulp communication with, 303–305 effect of periodontal disease on, 306, 306f
Perioglass, 262, 262f effect of periodontal treatment on, 306, 306f Quantec, 196, 196f–197f
Periradicular lesions, 114, 114f–115f functions of, 33, 34f Quorum sensing, 75
Periradicular origin emergencies, 270–274 hot, 266–267
diagnosis, 270–272, 271f–272f hyperaemic, 156
medication, 273–274 infection, 28 R
treatment, 272–273, 273f inflammation, spread of, 36–37, 36f–37f
Periradicular tissues, 28–31 inflammatory response, 33, 34f RaCe, 196, 196f
see also Alveolar bone; Cementum; Periodontal injury, 33–36, 34f–36f, 35t, 38–39 Race variations, 6–9, 10t
ligament nerve supply, 26–28, 26f–27f Radial lands, 196, 196f
Petit mal seizures, 366 normal, 116 Radiation safety, 106–107, 106f
Phagocytosis, 49 periodontium communication with, 303–305 Radicular access, 174, 175f, 189–190
Phenol, 215 regeneration, 281 apical-coronal techniques, 204, 205f
Phenol-based agents, 215–216 vascular supply, 24–26, 24f–26f apical enlargement, 205
Phosphoric acid, 357–359 Pulp capping, 39–40 automated devices, 195–198, 196f–198f, 196t
Photoactivated disinfection, 215, 215f direct, 38–40, 163, 164f, 170–171, 171f chemical treatment, 206–208, 211f–212f
Piezoelectric transducers, 214–215 indirect, 38–40, 163, 169–170, 170f–171f coronal-apical techniques, 204, 205f
Pink spot, 285, 292, 295f Pulp-dentine complex, 10–11 coronal preflaring, 204–205, 206f–207f
Planktonic physiology, 75–76, 75f anatomy and physiology of, 21–28, 21f in curved canals, 198–204, 199f–204f
Plaque removal, 157 reparative processes, 33 double curves, 202–203, 203f–204f
Plasma cells, 45 as a warning system, 33 full length, negotiation to, 205, 208f
Plexus of Raschkow, 26, 27f see also Dentine; Pulp hand instrumentation, 192–195, 193f–195f

length verification, 205
mechanical preparation, 192–215
by automated devices, 195–198, 196f–198f, 196t
and chemical treatment and irrigation, 206–208,
211f–212f
in curved canals, 198–204, 199f–204f
dynamic irrigation after, 212–215, 213f–215f
by hand instrumentation, 192–195, 193f–195f
irrigant delivery and actions, 208–212,
212f–213f
photoactivated disinfection, 215, 215f
recommended approach, 204–205, 205f–211f
push-pull filing, 194, 198–202
rotary motion, 193–194, 193f–194f
shaping, final, 205
taper gauging, 203–204
Radiography, conventional, 20–21
bisecting angle periapical projections, 108, 108f
comparison of technologies, 104, 105f
conventional films versus digital image, 103–104,
104f–105f
in diagnosis, 103–109, 103f–104f
errors in interpretation, 112–113
film holders, 104, 105f–106f
interpretation, 111–112
landmarks, 112, 112f
operator safety, 106–107
parallax techniques, 108–109, 109f
paralleling periapical projections, 107–108,
107f–108f
patient safety, 106
quality assurance, 111
radiation safety, 106–107, 106f
root canal terminus location, 183–184, 183f–185f
techniques, 107–109
viewing and storage equipment, 107, 107f
Radiolucent lesions, 374–375, 378t
Radiopaque lesions, 374–375, 378t
Rapidly progressive periodontitis, 322–323, 323f
Rebound phenomenon, 253
Recapitulation, 209–210
Record-keeping, 94, 122–123, 154
Rectangular flap, 247–248, 247f
Referral, 155
Regeneration, 281
Regenerative procedures, 260–262, 325–327, 327f
Regional odontodysplasia, 7t–8t
Relative analgesia, 156
Replacement resorption, 281, 288
Replantation, 320
intentional, 259–260, 260f
Resilon, 224
Resolut absorbable membrane, 261–262
Resorption
root, 316–317, 316f–317f, 330–331, 330f–331f, 330t
tooth, 118, 285–298
aetiology, 285–297
effect of orthodontic tooth movement on, 331
external, 118, 285, 288–297, 289f–298f
inflammatory, 281
internal, 118, 285–288, 286f–289f, 286t
pathogenesis, 285–297, 286f
replacement, 281
Respiratory disease, 363
Restorations, 334, 335f–336f, 338f–339f
anterior teeth, 338–342, 339f–341f
general considerations, 129, 129f–130f
hemisected teeth, 357
intact anterior teeth, 338, 339f–340f
intact posterior teeth, 346–347, 347f–349f
MOD (mesio-occlusal-distal cavities), 349–352,
350f–352f
poorly designed, 320, 320f–321f
posterior teeth, 346–354, 347f–349f
practical management approaches, 168–169
principles, 334
provisional, broken-down teeth, 158–159, 159f
proximal cavities, 338–340, 340f
proximo-occlusal cavities, 347–349, 349f–350f
removal, 157–158, 239, 239f–240f
restorability, 334–338, 337f
role of orthodontics in, 332–333
teeth with inadequate tissue, 340–342, 341f–342f,
352–354, 353f–355f
teeth with resected roots, 357, 357f–358f
timing after endodontic treatment, 338
of treated primary teeth, 166, 166f
Restoring force reduction, 199–200
Rests of Malassez, 29–30, 30f
Retractors, 149f
Retrograde pluggers, 149f
Retrograde seal, 89
RinsEndo, 215
Rooftop preparations, 340–341, 341f
Root amputation, 324–325, 324f–326f
Root canal infection, 310–311, 310f–311f
biofilm and planktonic physiology, 75–76, 75f
microbial ecology, 70–75, 74f
tooth resorption, 289–290, 290f–291f
Root canal microbiota
antibacterial action against, 208
culture studies, 67
distribution, 67–70
and failed root canal treatment, 84–85, 85t
microscopy studies, 67–68, 68f–73f
nature of, 62–67, 64f
periapical lesion development and, 59–62
physiological status, 67–70
in situ hybridization microscopy studies, 68–70,
73f–74f
species evenness/quantitative analysis, 65–67, 66f,
67t
species richness/qualitative analysis, 64–65, 65t, 66f
Root canal obturation, 178–179, 178f–179f, 221–235
advantages, 222
backfill, 228
canal surface preparation, 226, 226f
controlled apical placement, 226–228, 226f–228f
coronal seal, 228
definition, 221–222
dry canal, 226
filling termination, 222, 222f–223f
hybrid technique, 235
ideal filling material, 223–225, 223f
lateral compaction, 228, 228f–230f
pain following, 280
principles, 226–228
techniques, 226
thermomechanical compaction technique, 236f
thermoplasticized gutta-percha
carriers, 233–234, 234f–235f
injection, 233, 234f
warm vertical compaction, 231–233, 231f–233f, 233b
Root canal retreatment, 88–89, 89f, 237–245
anatomical considerations, 136, 137f–138f
bridge removal, 239
coronal restoration removal, 239, 239f–240f
decision-making process, 135–140, 137f
gutta-percha removal, 241–242, 241f
indications, 237, 238f
instrument and points removal, 243–244, 243f–245f
ledge negotiation, 242, 242f
packed dentine debris, 242, 243f
perforations, 245, 245f–246f
post removal, 239–241, 240f–241f
principles, 239–245, 239f
Index  387
sclerosed canals, 242–243
surgical, 245–263
systemic considerations, 138f–140f
Root canal treatment
alternative approaches, 90, 90f
analgesia/anaesthesia, 156
biological and clinical perspective, 76–78, 77f–82f
chemical intraradicular preparation, 174–178,
177f–178f
coronal access cavities, 179–181
temporary seal, 220–221
coronal seal, 235–236
effect of persistent bacteria on outcome, 81–83
effects on biological events, 80–81
factors affecting outcome, 83, 83f
failure, 83–89, 84f, 86f–89f, 87t, 237, 238f
instrumentation, 188, 189f
intracanal medication, interappointment, 178,
215–220
mechanical intraradicular preparation, 174,
175f–177f
point of termination of canal preparation, 181–183
previous, 134–135, 134f–136f
principles, 174–179
radicular access see radicular access
root-canal system obturation, 178–179, 178f–179f
technical aspects, 78–80
terminus location, 183–187, 183f–187f
working length determination, 187–188, 188f
Root canals
access to, 131–132, 131f–132f
accessory, 13–14, 20
anatomy, 132, 133f
bacteria in, 58f
characteristics, 12–13, 12t
combined method of determination of, 187
complex systems, 191f–192f
division, 20, 20f
dynamic irrigation after mechanical preparation,
212–215, 213f–215f
electronic apex locator determination of, 184–187,
185f–186f
fungi in, 59f–60f
irrigation, 206–208, 211f–212f
delivery, mechanics of, 208–212
intra-appointment, 174–178
lateral, 13–14, 20, 21f
paper-point determination of, 187
radiographic determination of, 183–184, 183f–185f
sclerosed, 132, 133f–134f, 242–243, 243f
secondary, 13–14
shape of, 11–12, 12f
simple systems, 189, 189f–191f
tactile determination of, 187, 187f
terminus location, 183–187, 183f–187f
working length determination, 187–188, 188f
Root division, 317, 319f
Root-end cavity preparation, 252–253, 252f–253f
Root-end filling, 254–255, 254f–255f
Root-end management, 247–257
Root-end resection, 251–252, 251f–252f
Root fractures, 114, 115f, 118, 118f, 304–305,
311–313, 313f–314f
healing, 281, 282f
traumatic, 275–277, 276f–279f
treatment planning, 136–139, 138f–139f
Root perforation, 313–316, 314f–316f
Root planing, 306
Root resection, 258–259, 258f–259f
Root resorption, 139–140, 139f–140f, 316–317,
316f–317f, 330–331, 330f–331f, 330t
Root sheath of Hertwig, 29–30
Root ZX, 184–186
 388  Index

Roots Super ethoxybenzoic acid (EBA), 254, 254f Thermafil removal, 242
characteristics, 11–13, 12t Supernumerary roots, 7t–8t Thermocompactor, 234–235
cracks, 311–313, 312f–313f Surgery Thermomechanical compaction technique, 236f
extra, 20 decision-making process, 135–140 Through and through surgery, 255–256, 256f
fractured, 114, 115f, 118, 118f Surgical armamentarium, 148, 148f–149f Tissue fluid, stagnant, 43
incompletely formed, 169, 169f Surgical endodontic procedures Tooth germ, 2–3, 3f, 5–6, 21f
shapes, 6–10 biopsy, 247, 247f Touch n’ Heat, 229
supernumerary, 7t–8t classification, 245–246 Trans-septal fibres, 29–30, 29f
Rotary motion, 193–194, 193f–194f corrective surgery, 257–259 Transforming growth factor-beta (TGF-β), 33
Rubber dams decompression, 262–263, 262f Transplantation, 320
advantages, 159–160, 160f emergency, 246 intentional, 259–260, 261f
application, 160–161, 161f indications, 245–246 Trauma
kits, 160f intentional replantation and transplantation, acute dentoalveolar, 274–275
Ruler, 145 259–260, 260f–261f clinical data for prognosis, 282–283, 282t
periapical surgery, 247–257 effect on orthodontic tooth movement, 331–332
regenerative procedures, 260–262 Trephination, 246, 246f–247f
S root-end management, 247–257 Triangular flap, 247–248, 247f–248f
Surgical retreatment, analgesia/anaesthesia, 156 Trigeminal pain pathway, 369, 370f
Safety tip, 197, 197f–198f Surgical tray, 148f Tug-back, 228
Scalpel blades, 148f Suture materials, 256–257, 256f Tumour necrosis factor (TNF), 45, 50
Sclerosed canals, 132, 133f–134f, 242–243, 243f Suture scissors, 149f Turner tooth, 166, 166f
Sclerosing osteitis, 114, 115f Swellings, 374
Sealers, 225, 226f System-B “Continuous Wave” obturation technique,
Sedation 231, 233b U
conscious, 368 Systemic resorption, 297, 297t
inhalation, 368 Ultradent tubes, 147f
intranasal, 368 Ultrafil system, 233
intravenous, 157, 368 T Ultrasonic agitation, 213, 214f
nasal, 157 Ultrasonic baths, 150
oral, 157, 368 T lymphocytes, 45 Ultrasonic units, 146, 146f
Seizures, 366 Talon cusps, 6, 7f, 7t–8t, 9f
Self-adjusting file, 197–198, 198f Taurodontism, 7t–8t
Semilunar flap, 247–248, 247f Teeth V
Sensibility testing, 100 access to, 131–132, 131f–132f
Sensitivity testing, 100 anatomical anomalies, 6, 7f, 7t–8t, 317 Varicella zoster virus (VZV), 47
Sharpey’s fibres, 28, 28f anatomy, 132 Vasoactive amines, 47
Sheath of Hertwig, 5 average lengths, 14t Vasoactive intestinal polypeptides, 47
Shell teeth, 7t–8t broken-down, 158–159, 159f Vasopressors, 156
Silver cone obturation, 223 cracked, 118, 118f Veneers, 359
Silver points removal, 243–244 development, 2–6, 3f Venules, 24, 25f
SimpliFill, 234, 235f dental follicle, 5 Verrucous cell carcinoma, 376f
SmartSeal, 224 dental lamina, 2–4, 3f Verrucous papilloma, 376f
Smear layer, 164f, 167–168 dental papilla, 2–3, 3f, 5 Vertucci’s classification of canal morphology, 11f
degradation, 207 early, 2, 3f Vestibular band development, 2
Sodium hypochlorite, 206–207, 216, 278–279 enamel organs, 2, 3f–5f, 4–5 Vestibule formation, 3, 4f
regenerative pulp therapy, 39 molecular regulation, 6 Viruses in periapical disease, 47
tooth resorption, 287–288 primary epithelial band, 2 Von Willebrand’s disease (vWD), 363
Sodium perborate, 357–359 sheath of Hertwig, 5
Soft tissue examination, 98, 98f successional permanent teeth, 4, 5f
Soft tissue swellings, 374, 375f–376f, 375t–377t tooth germ, 5–6 W
Solid obturators, 223, 223f vestibular band, 2
Sonic agitation, 213, 214f vestibule formation, 3, 4f Water supplies, 144, 144f
Splint therapy, 264, 265f discolored, 357–359, 358f–359f Weine’s classification of canal morphology, 11f
Spongy bone, 31 effect of orthodontic treatment on, 332 Work surface organization, 143–144, 144f
Squamous cell carcinoma, 376f eruption times, 10, 10t Working length determination, 187–188, 188f
Stabilization, 129 evagination, 6, 7f, 7t–8t, 9f Wound closure, 256–257, 256f–257f
Stagnant tissue fluid, 43 examination, 99–100, 99f–100f Wound healing, 257, 281, 305, 305f
Stagnation plane, 209–210 fractures, 99, 99f, 118, 118f, 268f
Stellate reticulum, 4–5 fused, 317, 319f
Sterilization, 148–152, 150f invagination, 6, 7f, 7t–9t, 10f X
Steroids, 217, 217f luxated, 277, 279f, 282–283, 282t
Storage, 151 mobility, 99, 99f, 99t X-ray machine, 145–146, 146f
Stratum intermedium, 4–5 morphology, 6 X-ray viewer, 146, 146f
Streptococci, 68–69 orientation, 132, 133f Xylocaine, 265f
Stroke, 362 pre-endodontic management, 157–162
Subgingival plaque, 292–297, 294f–297f probing profile, 307–309, 308f–309f
Sublingual space, 271 resorption see Resorption Z
Submandibular space, 271 restorability of, 131, 131f, 334–338, 337f
Submarginal flap, 247–248, 248f assessment of, 158, 158f Zinc oxide/eugenol cement, 221, 221f
Submasseteric interval, 271 shapes, 6–10 Zinc phosphate, 221, 357–359
Submental space, 271–272 strategic importance, treatment planning, 129, 130f Zinc polycarboxylate, 221
Substance P, 47 TERM, 221 Zipping, 198–199, 199f
Subtemporalis muscle interval, 272 Test cavity cutting, 102 Zones of Fish, 76–78