Review of ALL DENTAL Subjects Neha

REVIEW OF
ALL DENTAL SUBJECTS

(ROADS)
Neha Sethi
BDS MDS MBA
Assistant Professor
BRS Dental College and Hospital
Panchkula, Haryana, India
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Review of All Dental Subjects

First Edition: 2015
ISBN 978-93-5152-732-9
Printed at
Dedicated
to
All My Students
and
Mentors, Who Sparked My Enthusiasm for Learning
Acknowledgments
I gladly utilize this opportunity to express my deep sense of gratitude and indebtedness to my parents and family, without whose
everlasting inspiration, incessant encouragement, constructive criticism and valuable suggestions for improvement, the comple-
tion of this study would not have been possible.
I am immensely indebted to Dr Pankaj Malhotra, MDS Periodontics and Implantoloy, Dr Akash Kasatwar, MDS Oral
and Maxillofacial Surgery, Dr Hitesh Chandra, MDS Pedodontics and Public Health Dentistry and all my colleagues for
their contribution toward the various chapters in the book. I am also thankful for their constant support and encouragement.
My sincere thanks to all my students and MDS aspirants whose continuous queries and suggestions help me make this book
better.
I am thankful to Ms Chetna Malhotra Vohra, Ms Shagufta Khan and others at Jaypee Group for their cooperation and
help whenever I needed.
My salutations to ALMIGHTY – A tangent between zero and infinity – for his divine grace bestowed when needed.
From the Publisher’s Desk

We request all the readers to provide us their
valuable suggestions/errors (if any)
at: jppgmee@gmail.com
so as to help us in further improvement of this book in the subsequent edition
A Few Words to Share
Time has gone when the questions were repeated in AIPGDEE from previous year question papers and the repeat questions
determined the results. Today almost 35–50 questions are totally new which have not appeared in any preparation books till
date. These questions actually determine the result of any exam.
All MDS aspirants read the previous papers and are able to solve the repeat. Important aspect here is the correct answers
and explanations of these questions. You do not want a repeat question to go wrong!
Also to get the edge above others, aspirants need to prepare for the new questions, which have not yet appeared in any
question banks.
AIPGDEE is well-devised to test the skills in and around various subjects comprehensively but if you are having good un-
derstanding of subjects and well updated, you can get through. It is not limited to the last moment preparation or the cramming
ability.
The trends been changing year by year, with emphasis more on clinically oriented and in-depth specialized topics like or-
thodontics, radiology, pharmacology, genetics, molecular biology, etc. The paper been tiresome which tests the tricky nature of
common topics.
Keeping these in mind, the concept of ROADS was laid. Eight hundred to one thousand pages give you an insight of the
topics commonly asked in entrance exams and ‘Good to Know’ points introduce several newer topics and sections to raise your
bar above the aspirants.
This book will help you crack various pre-PG entrance exams ranging from State entrances to All India level exams.
Neha Sethi
Road to MDS
AIPGDEE is conducted by AIIMS. The syllabus for AIPGDEE shall be that of the BDS standard. The syllabus shall cover all
the subjects taught during the BDS course.
Initial Preparation
• Earlier you start, better it is. As time lost is time gone
•
• Start with subjects and topics which interest you more, slowly move on to the less interesting subjects
•
• Plan and plan how to start preparation for each subject
•
• If preparing with ROADS, read the subject chapter first and then attempt 700–1000 questions of that subject
•
• Revise continuously
•
• Talk to friends, group study is helpful. Discussing important/difficult topics makes them easier to understand.
•
• Do not cut yourself from your life. Four to five hours per day for 8–10 months is usually sufficient.
•
• More than the number of hours you put in, important is the amount of concentration you put in those hours of study. So
•
practice meditation exercises regularly to improve your concentration skills
• Take a break, it is very helpful. Taking a evening off once or twice a month is not a bad idea at all.
•
Last Minute Preparation
The last 20–30 days are very crucial and stressful at the same time. These play an important role in how you will do in the
exam on D-day. Here are few tips for the last minute preparation.
• Firstly do not start a new book now
•
• Revise all your notes. Use ROADS to consolidate what you have learnt
•
• Go through last 2 years papers of NEET, AIIMS (Nov and May)
•
• Also go through AIPGMEE papers of at least last 3 years and surely of this year
•
• Last but not the least sleep well and eat well before the exams
•
Hope these will be helpful to you and will help to take a step closer to your dreams.
List of Entrance Exams in MDS
• All India Institute of Medical Science Entrance Exam
•
• All India Post Graduate Medical/ Dental Entrance Examination
•
• Annamalai University MDS Entrance Exam
•
• Avinashilingam Deemed University for Women MDS Entrance Exam
•
• Baba Farid University of Health Sciences MDS Entrance Exam
•
• Banaras Hindu University (BHU) MDS Entrance Test
•
• Bangalore University MDS Entrance Exam
•
• Barkatullah University MDS Entrance Exam
•
• Bharath University Chennai MDS Entrance Exam
•
• Bharati Vidyapeeth Dental College and Hospital (Pune) MDS Entrance Exam
•
• Bhavnagar University MDS Entrance Exam
•
• Calcutta University MDS Entrance Exam
•
• Calicut University MDS Entrance Exam
•
• Delhi University MDS Entrance Exam
•
• Department of Dental Surgery, All India Institute of Medical Sciences MDS Entrance Exam
•
• Dr NTR University of Health Sciences MDS Entrance Exam
•
• Dr. Ram Manohar Lohiya, Avadh University MDS Entrance Exam
•
• Gitam University MDS Entrance Exam
•
• Indira Gandhi National Open University (IGNOU) MDS Entrance Exam
•
• Institute of Medical Sciences - Banaras Hindu University MDS Entrance Exam
•
• JSS University MDS Entrance Exam
•
• Kannur University MDS Entrance Exam
•
• Kerala University MDS Entrance Exam
•
• KLE University MDS Entrance Exam
•
• Maharashtra University MDS Entrance Exam
•
• Maharishi Markandeshwar University MDS Entrance Exam
•
• Manipal College of Allied Health Sciences MDS Entrance Exam
•
• Manipal University MDS Entrance Exam
•
• NITTE University Mangalore MDS Entrance Exam
•
• Padmashree Dr DY Patil University MDS Entrance Exam
•
• Pondicherry University MDS Entrance Exam
•
• Pt BD Sharma University of Health Sciences MDS Entrance Exam
•
• Punjab University MDS Entrance Exam
•
• Rajasthan University of Health Sciences (RUHS) MDS Entrance Exam
•
• Rajiv Gandhi University of Health and Sciences MDS Entrance Exam
•
• Saveetha University MDS Entrance Exam
•
• Sri Ramachandra Medical College and Research Institute MDS Entrance Exam
•
• SRM University MDS Entrance Exam
•
viii Review of All Dental Subjects

• Tamil Nadu Dr MGR Medical University MDS Entrance Exam
•
• West Bengal University of Health Sciences MDS Entrance Exam
•
• Vinayaka Missions University MDS Entrance Exam
•
• West Bengal University of Health Sciences
•
All India Post Graduate Entrance Exam
• Conducted by AIIMS every year
•
• Exam date–January
•
• Exam center
•
• Online application forms are available from November/December of previous year
•
• Exam pattern
•
– There will be only one paper of 3 hours duration.
–
– The paper shall comprise of 200 MCQs, consisting of Basic Sciences, Para Clinical and Clinical Subjects.
–
– While each single correct shall be awarded 4 marks, each incorrect response is liable to deduction of one mark.
–
– Zero mark will be given to those questions which are left unanswered. However the question with one and more
–
response as answers will be treated as incorrect answer and mark shall be deducted.
• For details–check the website www.aiimsexams.org
•
AIIMS PG Exam
• Conducted by AIIMS Twice a year
•
• Exam date–first week of November and May every year
•
• Exam center–Delhi
•
• Online application forms are available
•
• Exam pattern
•
– Duration: 90 Minutes
–
– No. of questions: 90 Objective type questions
–
– Negative Marking: 1/3rd of the marks allocated for a right response will be deducted if the response is incorrect
–
• For details–check the website www.aiimsexams.org
•
PGIMER Entrance Exam
• Conducted by Post Graduate Institute of Medical Education and Research for admission to postgraduate and postdoctoral
•
programs in MD/MS/MHA/DM/MCh/House Jobs (Oral Health Science).
• Conducted twice a year, one for the session beginning in January and other in July.
•
• Exam pattern
•
– Duration–1.5 hours
–
– No. of Questions-100 Multiple Choice Questions
–
– 0.25 negative marking will be applicable for wrong answer.
–
• For details–check the website www.pgimer.edu.in
•
COMEDK PGET
• Exam date–first week of February
•
• Exam center–Bangalore (only)
•
• Online application forms are available from November/December of previous year
•
List of Entrance Exams in MDS ix

• Exam pattern
•
– Each test will have 180 Multiple-Choice Questions
–
– The time allotted for the test would be 180 minutes (3 hours). The test will begin at 10:00 AM and end at 01:00 PM.
–
– Each correct answer is awarded one mark.
–
– No Mark/s will be awarded for multiple marking (marking multiple responses) of any question.
–
– There will be no negative marking
–
• For details–check the website www.comedk.org
•
Reference Books
1. A Concise Textbook of Surgery – S Das

2. A Textbook of Operative Dentistry – Vimal K Sikri

3. BD Chaurasia’s Human Anatomy – BD Chaurasia

4. Boucher’s Complete Denture Prosthodontics – Zarb

5. Burkett’s Oral Medicine – M Glick

6. Carranza’s Clinical Periodontology

7. Clinical Neuroanatomy – Richard S Snell

8. Cohen’s Pathways of the Pulp – Kenneth M Hargreaves

9. Community Dentistry – Soben Peter

10. Concise Medical Physiology – Chaudhari

11. Contemporary Fixed Prosthodontics – Stephen F Rosenstiel

12. Endodontics – Ingle and Backland

13. Essentials of Medical Pharamcology – KD Tripathi

14. Fundamentals of Fixed Prosthodontics – Herbert T Shillingburg

15. Goodman and Gilman’s The Pharmacological Basis of Therapeutics

16. Graber’s Textbook of Orthodontics

17. Human Embryology – IB Singh

18. Handbook of Local Anesthesia – SF Malamed

19. Harper’s Biochemistry

20. Harrison’s Principles of Internal Medicine

21. Killey’s fractures of the mandible – Peter Banks, Homer Charles Killey

22. McCracken’s Removable Partial Prosthodontics

23. McDonald and Avery Dentistry for the Child and Adolescent – Jeffrey A Dean

24. Medicine – Davidson

25. Oral and Maxillofacial Pathology – Neville

26. Oral and Maxillofacial Surgery – Vinod Kapoor

27. Oral and Maxillofacial Surgery – Daniel M Laskin

28. Oral Radiology – SC White and MJ Pharaoh

29. Orban’s Oral Histology and Embryology – GS Kumar

30. Orthodontics – SI Balaji

31. Park’s Textbook of Preventive and Social Medicine

32. Peterson’s Principles of Oral and Maxillofacial Surgery

33. Phillip’s – Science of Dental Materials

34. Robbins Basic Pathology – Vinay Kumar

35. Shafer’s Textbook of Oral Pathology

36. Short Practice of Surgery – Bailley and Love’s

37. Sturdevant’s Art and Science of Operative Dentistry – Swift and Heymann

38. The Essentials of Forensic Medicine and Toxicology – N Reddy

39. Ten Cate’s Oral Histology: Development, Structure, and Function – Antonio Nanci

40. Textbook of Human Histology – Inderbir Singh

41. Textbook of Microbiology – Ananthanarayan and Paniker

42. Textbook of Medical Biochemistry – Chatterjea MN and Shinde Rana

43. Textbook of Pathology – Harsh Mohan

44. Textbook of Pediatric Dentistry – Nikhil Marwah

45. Wheeler’s Dental Anatomy, Physiology and Occlusion – Ash and Fausto

Contents
1. Anatomy ..................................................................................................................................1-58

.
2. Biochemistry .......................................................................................................................59-102

.
3. Physiology .........................................................................................................................103-152

.
4. General Pathology ............................................................................................................153-205

.
5. Microbiology .....................................................................................................................206-247

.
6. Pharmacology ...................................................................................................................248-290

.
7. General Medicine and Surgery .........................................................................................291-352

.
8. Dental Materials................................................................................................................353-389

.
9. Dental Anatomy and Histology ........................................................................................390-411

.
10. Oral Pathology and Oral Medicine ...................................................................................412-470

.
11. Complete Dentures ............................................................................................................471-500

.
12. Removable Partial Dentures .............................................................................................501-518

.
13. Fixed Partial Dentures.......................................................................................................519-533

.
14. Periodontics .......................................................................................................................534-593

.
15. Radiology ...........................................................................................................................594-621

.
16. Pedodontics .......................................................................................................................622-649

.
17. Conservative Dentistry......................................................................................................650-687

.
18. Endodontics .......................................................................................................................688-709

.
19. Oral Surgery ......................................................................................................................710-744

.
20. Orthodontics .....................................................................................................................745-783

.
21. Community Dentistry .......................................................................................................784-827

.
22. Miscellaneous Topics .........................................................................................................828-842

.
23. AIDS ..................................................................................................................................843-850

.
24. Recent Exams .................................................................................................................................. 851-855

.
CHAPTER 1
Anatomy
Objectives
• Embryology • Ear and nose

• Histology • Paranasal sinuses

• Osteology • Tonsil

• Face • Orbit

• Muscles of mastication • Lacrimal apparatus

• Salivary glands • Neck

• Tongue • Brain and spinal cord

• Palate • Thorax

• Pharynx • Abdomen

• Larynx • Miscellaneous

EMBRYOLOGY • Primitive knot (or primitive node) is the organizer
•
for gastrulation in vertebrates. (AIPG 2008)
• Merkel’s cartilage

– In birds it is known as “Hensen’s node”.
•
– Extends from the midline backward and dorsally and
–

(AIPG 2001)
–

terminates as the malleus. – In amphibians, it is knows as “Spemann’s organizer”.
–
– Articulates with the incal cartilage. • Prechordal plate.
•
–
– This primary jaw joint exists for about 4 months until – Formed by the slight enlargement of the ectodermal
–
–
the cartilages ossify and become incorporated in the and endodermal cells at the head (or rostral) end of
middle ear. (AIPG 2009, AIIMS MAY 2011) the embryo.
– At the prechordal plate there is firm union between

–
2 weeks Formation of prechordal plate the ectodermal and endodermal cells.

(NEET 2013)
3 months of gestation The secondary jaw joint, the TMJ
begins to form
• Primitive streak
•
10 weeks First indication of future joint
– Develops within along the midline of the floor of the

(AIIMS May 2013)
–
amniotic cavity which is formed by ectoderm.

2 Review of All Dental Subjects

– Narrow groove with slightly bulging areas on each – This differentiates the embryo into the germ layers-
–
–
side. (AIPG 1995) endoderm, mesoderm, and ectoderm.

– Rostral end finishes in primitive node. – This time period (3-4th week of IUL) is sometimes
–
– Posterior to the node is the primitive pit where the
–
called the trilaminar disk stage and at this time the
–
cells of the epiblast (the upper layer of embryonic
cells) initially begin to invaginate. embryo is called Trophoblast. (AIPG 2002)

Human cell types/listed derived primarily from ectoderm
Surface ectoderm Integumentary system Trichocyte . Keratinocyte
Nervous system Anterior pituitary (Gonadotrope, Corticotrope, Thyrotrope, Somatotrope, Lactotrope
Neural crest Endocrine system Chromaffin cell
(AIPG 2007,2010)
Integumentary system Melanoblast → Melanocyte (Nevus cell) Merkel cell
Teeth Odontoblast
Nervous System Glia: Schwann cell
ANATOMY
Eyes Corneal Keratocyte

Neural tube Nervous system Neuroblast Visual Photoreceptor cells (Cone cell, Rod cell) →
(Neural stem cell) (Horizontal cell)
Glioblast Bipolar cell → (Amacrine cell) Retinal
ganglion cell (Midget cell, Parasol cell,
Bistratified cell, Giant retinal ganglion cells,
Photosensitive ganglion cell) Diencephalon: P
Cell, M Cell, K-cell, Muller gila
Auditory Boettcher cell
Other Magnocellular neurosecretory cell. Stellate
cell
Glioblast Oligodendrocyte precursor cell →
Oligodendrocyte.
Astrocyte. Ependymal cell. Pinealocyte.
Neural crest cells leave neuroectoderm and enter mesoderm. • Adrenal medulla
•
Neural crest cells: give rise to heterogeneous array of tissues: • Schwann cells
(AIPG 2010)
•
• Glial cells

• Connective tissue and bones of the face and skull.
•
• Arachnoid and pia mater (leptomeninges)
•
• Cranial nerve ganglia
•
•
• C Cells of the thyroid. Derivatives of Neuroectoderm
•
• Odontoblasts • All neurons within brain and spinal cord
•
•
• Spinal ganglia • Retina
•
•
• Sympathetic chain and preaortic ganglion • Neurohypophysis
•
•
• Melanocytes • Astrocytes, oligodendrocytes
•
•
• Parasympathetic ganglia of GIT
•
Mesodermal derivatives • Paraxial mesoderm is organized into segments called “somitomeres”.
•
• They are arranged cephalocaudally from occipital region.
•
• Somitomeres arrange into somites.
•
• Each somite gives rise to:
•
- Sclerotome-cartilage and bone of axial and paraxial skeleton (remember neural crest cells give rise to
-
cartilage and bones of skull and face)
- Myotome-segmental muscle component
-
- Dermatome-segmental skin component (AIPG 2012)
-

• Each myotome and dermatome have their own segmental nerve component.
•
Anatomy 3

Intermediate mesoderm • Differentiates into excretory units of urinary system and the gonads (urogenital system)
•
Lateral plate mesoderm • Splits into parietal and visceral layers.
•
• Parietal mesoderm + overlying ectoderm gives rise to lateral and ventral body wall viscera.
•
• Mesoderm + embryonic endoderm give rise to wall of the gut.
•
• Cortical portion of suprarenal gland and spleen also develop from mesoderm.
•
Human cell types derived primarily from mesoderm
Paraxial Mesenchymal stem cell Osteochondro Bone: Osteoblast, Osteocyte cartilage: Chondroblast,
(MSC) Cartilage/ bone/ progenitor cell (OCP) Chondrocyte
muscle
Myofibroblast Fibroblast Fibrocyte

Muscle: Myoblast Myocyte. Satellite cell. Tendon cell.
Myocardiocyte
Digestive system Adipose: Lipoblast, Adipocyte Interstitial cell of kajal
Intermediate Renal Stem Cell (RSC) Angioblast, Endothelial cell. Mesangial cell Intraglomerular, Extraglomerular.
ANATOMY
Urinary system Juxtaglomerular cell . Macula densa cell
Stromal cell, Interstitial cell
Simple epithelial cell, Podocyte. Kidney proximal tubule brush border cell
Reproductive system Sertoli cell. Leydig cell. Peg cell (spermatozoon and ovum are germ cells)
Lateral plate Hematopoietic stem cell Lymphoid B Cell . T cell (Cytotoxic T cell, Natural Killar T cell,
hemangioblast (HSC) Blood/immune (CFU-L) Regulatory T cell, T helper cell) . Natural Killer cell
Myeloid (CFU- Granulocytes (Basophil granulocyte, Eosinophil
GEMM) granulocyte, Neutrophil granulocyte/Hypersegmented
neutrophil). Monocyte/Macrophage. Red blood cell
(reticulocyte). Thrombocyte/Megakaryocyte. Mast cell.
Dendritic cell
Circulatory system Endothelial progenitor cell. Endothelial stem cell.
Angioblast/Mesoangioblast Pericyte . Mural cell
Derivatives of Endoderm
Germ Layer Category System Products
Endoderm General Gastrointestinal tract The entire alimentary canal except part of the mouth, pharynx and the terminal
part of the rectum (ectoderm), the lining cells of all the glands.
Buccopharyngeal membrane is both ectodermal (towards future oral cavity) and
endoderm membrance (towards future GIT). This breaks open at 4th week to
communicate between foregut and amniotic cavity.
Endoderm General Respiratory tract Epithelial lining of respiratory tract, the trachea, bronchi, and alveoli of the lungs
Endoderm General Endocrine glands and Parenchyma of thyroid, parathyroid, liver and pancreas. Reticular stoma of the
organs tonsils and thymus (the lining of the follicles of the thyroid gland and thymus)
Endoderm Auditory system The epithelial lining of the auditory tube and tympanic cavity
Endoderm Urinary system The epithelial lining of urinary bladder and part of the urethra
Arch Skeletal element Nerve Muscle

I (Mandibular) • Meckel’s cartilage (AIPG 2000) Mandibular-third • Medial and lateral pterygoid
•

•
• Incus, malleus division of the V • Masseter (KAR 1997, NEET 2013)
cranial nerve
•
•

• Anterior mandible • Temporalis
•
•
• Zygomatic bone • Mylohyoid
•
•
• Palatine bone • Ant.belly of digastric
•
•
• Part of temporal bone • Tensor tympani
•
•
• Ligament of the malleus • Tensor palati
•
•

• Sphenomandibular ligament (KAR 2001) (KAR 1997, AIIMS Nov 2012)
•

• Also responsible for formation of maxilla
•

II Hyoid • Stapes Facial • Muscles of face
•
•

• Styloid process (COMEDK 2007) (COMEDK 2006)

•

• Smaller cornu of hyoid bone • Occipitofrontalis
•
•
• Superior part of body hyoid bone • Platysma, stylohyoid
•
•
• Post belly of digastric (PGI 2002)
•

• Stapedius (AIPG 2001)
•

• Auricular muscles
•
III • Greater cornu of hyoid bone Glosso-pharyngeal • Stylopharyngeus
•

•
• Lower part of the body of hyoid bone (PGI 1998)
•
IV • Cartilages of larynx are derived from both Superior • All The muscles of pharynx except
•
•
IV and VI Laryngeal stylopharyngeus
• All the muscles of palate except
•
tensor veli palate
• Cricothyroid muscle
•
Brachial arches and pouches
ANATOMY
Pouches Derivatives
1st Pouch • Pharyngotympanic tube
•
• Middle ear cavity (KAR 1999)
•

• Tympanic antrum
•
2nd Pouch • Tonsil (KCET 2009)
•

• Tubotympanic recess
•
3rd Pouch • Inferior parathyroid glands (APPSC 1999)
•

• Thymus
•
4th Pouch • Superior parathyroid glands
•
5th Pouch (ultimobranchial pouch) • Parafollicular cells of thyroid (KAR 2003)
•

HISTOLOGY
Squamous epithelium
Mesothelium Lungs and free surface of pericardium, pleura and peritoneum.
Endocardium Inside lining of heart
Endothelium Inside lining of blood vessels and lymphatics
Stratified squamous Lining of skin and mucosa subjected to friction such as oral cavity, oesophagus
Columnar epithelium
Simple columnar Lining of stomach and large intestine.
Ciliated columnar Respiratory tract, uterus, uterine tubes, auditory tube
Striated columnar Small intestine (regular microvilli)
Brush border columnar Gall bladder (regular microvilli)
Secretary columnar Stomach and intestine
Cuboidal
Simple cuboidal Thyroid gland follicles, ducts of glands, surface of ovary (germinal epithelium)
Brush border cuboidal Proximal convoluted tubule.
Pseudostratified epithelium
Simple pseudostratified Auditory tube, olfactory area of nose, male urethra (COMEDK 2008)

Ciliated pseudostratified Trachea and large bronchi.
Transitional epithelium (AIPG 2008) Ureter, urinary bladder, parts of urethra
Anatomy 5

Cartilage
• Modified connective tissue. It consists of intercellular material called matrix.
•
• Mesenchymal in original.
•
• Cartilage-forming cells are called chondroblasts.
•
• Cartilage grows by both interstitial and appositional growth.
•
• Some mesenchymal cells that surround the developing cartilage form the perichondrium.
•
Types of Cartilage
Hyaline cartilage Matrix consists of lacunar capsule containing individual Costal cartilage
chondrocytes. Articular cartilages of most synovial joints
Widely distributed in the body. Thyroid, cricoid and arytenoid cartilages, pharyngeal
Surface covered by perichondrium. cartilages, parts of nasal septum, epiphyseal plate
Type II collagen is found (AIPG 2008) essential for bone growth

Fibrous cartilage Also called white cartilage. It is found in symphysis.
Type I collagen is found. Intervertebral discs, public symphysis, articular disc of
ANATOMY
Perichondrium is absent. most of the joints and menisci of knee joint.
Highest tensile force.
Calcification may occur with age.
Elastic cartilage Yellow cartilage. It is found in auricle.
(AIPG 2002) This is similar to hyaline cartilage except that elastic fibres Wall of the medial part of the auditory tube.
are present instead of type II collagen fibres. Epiglottis, corniculate, cuneiform and apical part of the
calcification does not occur. arytenoids cartilages of larynx.
Types of Glands
Aprocrine Glands • Apical part of cell is shed off to discharge secretion (decapitation secretion)
•
• E.g. sweat glands in axilla, groin, mammary glands
•
Holocrine glands • Entire cell disintegrates discharges secretion
•
• E.g. sebaceous glands
•
Eccrine glands • Cell is intact, secretions are thrown out by exocytosis.
•
(merocrine) • E.g. sweat gland on palm
•
• Modified sweat glands are ceruminous glands, ciliary glands
•
• Meibomian glands, glands of Zeis are modified sebaceous glands
•
OSTEOLOGY
Bone
Epiphysis • Ends and tips of bone which ossify from secondary centres
•
• Following types:
•
- Pressure epiphysis is articular and takes part in transmission of the weight. Example: head of femur; lower and
-
of radius, etc.
- Traction epiphysis is nonarticular and does not take part in the transmission of the weight. It always provides
-
attachment to one or more tendons which exert a traction on the epiphysis. The traction epiphyses ossify later than
the pressure epiphyses. Examples: trochanters of femur and tubercles of humerus.
- Atavistic epiphysis is phylogenetically and independent bone which in man becomes fused to another bone.
-
Examples: coracoid process of scapula and os trigonum.
- Aberrant epiphysis is not always present. Examples: epiphysis at the head of the first metacarpal and at the
-
base of other metacarpal bones
Diaphysis • It is the elongated shaft of a long bone which ossifies from a primary centre
•
Metaphysis • The epiphysis ends of a diaphysis and called metaphysis.
•
• Each metaphysis is the zone of active growth
•
• Most common site for osteomyelitis (AIPG 2003)
•


Stages during growth of epiphyseal plate (AIPG 2005)
Growth

(proliferation of cells/interstitial and appositional growth)
↓
Transformation

(Hypertrophy/calcification of matrix)
↓
Ossification

(Chondrolysis/ Vascularization/ osteogenesis)
↓
Remodelling Stages during growth of epiphyseal plate (AIPG 2005)

Skull
ANATOMY
Skull is composed of 22 bones. (AP 2003, 1999)

It is composed of:
Neurocranium Viscerocranium
• Surrounds the brain, eyes, middle and inner ears. • The face and viscerocranium are formed from the neural crest
•
•
• Contains 8 bones derived membrane bones.
•
- 2 – bilateral (parietal and temporal bone) • Facial skeleton includes from forehead to chin
•
-
- 4 single bones - Frontal bones
-
-
* Frontal - Orbital bones
-

* Occipital - Nasal bones
-

* Sphenoid - Vomer
-

* Ethmoid - Maxilla
-

- Mandible
-
• The maxilla and mandible are included since they form from the
•
first brachial arch
• Also included are medial pterygoid plates of sphenoid bone
•
- Palatine bones
-
- Tympanic bones
-
Ethmoid Bone (AIIMS Nov 2013)

• The ethmoid bone consists of four parts
•
– Horizontal or cribriform part-forming part of base of cranium
–
– A perpendicular part-constituting part of nasal septum
–
– 2 lateral labryrinths
–
• Each ethmoidal labryinth consists of thin walled highly variable air cells arranged in three groups: anterior, middle and
•
posterior. These are referred to as anterior air cells (middle and anterior–2-8 in number)
• Inferior turbinates: Largest among the three. Responsible for the airflow direction, humidification, heating and filtering
•
of the inhaled air.
Lambda Junction of sagittal and lambdoid sutures

Junction of sagittal and coronal sutures
Bregma (AIPG 97, Man 94) Highest point on skull head in anatomic position
Most prominent point on external occipital protruberance
Vertex (PGI 2003) Junction of frontal, parietal, sphenoid and temporal bones
Inion
Pterion (AIPG 2006, Man 2000)
Anatomy 7

Cervical Vertebra
• Identified by the presence of foramen transversarium (transmits vertebral artery, vertebral veins and inferior cervical
•
ganglion) (AIIMS May 2009, AIPG 1996)

• There are 7 cervical vertebrae
•
– 3 to 6 are typical
–
– 1st, 2nd and 7th are atypical.
–
– 1st–Atlas-ring shaped without body and spine.
–
– 2nd-axis” (Epistropheus)- identified by the presence of dens (odontoid process), which is a strong tooth-like
–
structure; Its tip is bifid, terminating in two rough tubercles.
– 7th-“vertebra prominens” because of its long, most prominent spinous process.
–
• The anterior tubercle of 6th cervical vertebra is large and is called the “carotid tubercle” because the common carotid
•
artery can be compressed against it.
ANATOMY
Types of Bones
Sesamoid Pneumatic bones (having air filled spaces) Membranous bone
• Patella • Ethmoid • Skull vault bone
•
•
•
• Pisiform • Maxilla • Facial bones
•
•
•
• Fabella • Sphenoid
•
•
• Frontal
•
• Mastoid
•
Classification of Joints
Fibrous joints Sutures – Skull
Syndesmosis- Inferior tibiofibular joint (AIIMS 2007, AP 2008)

Gomphosis - Tooth in sockets
Cartilaginous joints • Primary cartilaginous joints
•
- Synchondrosis or hyaline cartilaginous joints (MCET 2010)
-

- Bones are united by a plate of hyaline cartilage so that joint is immovable
-
- Examples
-
* Joint between epiphysis and diaphysis

* Spheno-occipital joint

* First chondrosternal joint

* Costochondral joint (AIPG 2004)

• Secondary cartilaginous joint
•
- Symphysis or fibrocartilaginous joints
-
- Articular surfaces are covered by a thin layer of hyaline cartilage and united by a disc of fibrocartilage
-
- Typical these joints occur in median plane and allow limited movements
-
- Examples
-
* Symphysis pubis

* Manubriosternal joint

* Intervertebral joint between bodies


Synovial joint- freely
Hinge joint (only flexion and extension possible) Elbow, ankle, interphalangeal joints
movable joints

(AIPG 2010) Ellipsoidal joint Wrist, altanto – occipital

Pivot (trachoid) joint Altanto – axial, superior and inferior radioulnar joint
Condylar/bicondylar joint Knee, TMJ
Saddle joint (Sellar) Thumb, sternoclavicular calcaneocuboidal, incudo-

malleus joint
Ball and socket Shoulder, hip, incus- stapedial joint
Atlanto-axial joint • Joints move as one unit and permit rotation (right and left) of the atlas along with the entire skull.
•
• The atlas carrying the globe of the head rotates around the dens of the axis. (AIPG 2004, KCET 2010)
•

• The atlanto-axial joints are called the joints of ‘no’ or “negative” expression
•
Atlanto- occipital joints The movements permitted at these joints are flexion, extension (nodding), and lateral flexion.
ANATOMY
They are called joints of ‘yes’ or “positive” expression
A functional classification of joints is based on the degree of movement permitted within the joint. Using this type of
classification, the three kids of articulations are as follows:
• Synarthroses: Immovable joints.
•
• Amphiarthyroses: Slightly movable joints. (AIPG 2007)
•

• Diarthroses: Freely movable joints.
•
You should know
• Father of modern anatomy is Andreas Vesalius.
•
• Father of anatomy-Herophileus
•
• Total bones in human body are 206.
•
• Total vertebrae in human body are 33: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, 4 coccygeal.
•
Formina of Skull and Structures Passing Through Them
Norma verticals
Parietal foramen Transmits and emissary vein from superior sagittal sinus
Norma occipitalis
Mastoid foramen Transmits an emissary vein and meningeal branch of occipital artery. (MAN 1999)

Norma frontalis
Supraorbital foramen Transmits supraobital nerves and vessels
Infraorbital foramen Transmits infraobital nerve and vessels
Zygomaticofacial foramen Transmits the nerve of same name
Mental foramen on mandible
(AIPG 2004) Transmits mental nerve and vessels.
Norma lateralis
Tympanomastoid fissue Transmits auricular branch of vagus nerve
Mastoid foramen Transmits an emissary vein connecting the sigmoid sinus with posterior auricular vein, meningeal branch
of occipital artery
Zyogomaticotemporal Transmits the nerve of same name and a minute artery.
foramen
Norma basalis
Incisive foramen transmits • Terminal parts of greater palatine vessels from palate to nose.
•
• Terminal part of nasopalatine nerve from nose to palate.
•
Anatomy 9

Greater palatine foramen Greater palatine vessels, anterior palatine nerve
Lesser palatine foramen Transmits middle and posterior palatine nerves.
Palatovaginal canal transmits • Pharynegeal branch from pterygopalatine ganglion.
•
• Small pharynegeal branch of maxillary artery.
•
Vomerovaginal canal Branches of pharyngeal nerves and vessels.
Foramen ovale Mandibular nerve and accessory artery (COMEDK 2006, MAN 1999)

Foramen spinosum Middle meningeal artery (Br of internal maxillary Artery) (AIPG 2006, AIIMS 2002, KAR 1994)

Emissary sphenoidal Transmits and emissary vein connecting cavernous sinus with pterygoid plexus of veins.
foramen
Canalis innominatus Tansmits lesser petrosal nerve.
Carotid canal Transmits internal carotid artery, venous and sympathetic plexus around the artery.
ANATOMY
Foramen lacerum Meningeal branch of ascending pharyngeal artery and an emissary vein from cavernous sinus, internal
carotid artery with venous and sympathetic plexus around it. In the upper part of foramen the greater
petrosal nerve unites with the deep petrosal nerve to form nerve of pterygoid canal.
Petro tympanic fissure Transmits the chorda tympani nerve and anterior tympanic artery
Foramen magnum • Through wider posterior part

•
- Lower part of medulla
-
- Tonsils of cerebellum max
-
- Meninges
-
• Through subarachnoid space
•
- Spinal accessory nerve
-
- Vertebral arteries
-
- Sympathetic plexus around the vertebral arteries
-
- Anterior and posterior spinal arteries
-
• Through narrow anterior part
•
- Apical ligament of dens
-
- Membrana tectoria.
-
Hypoglossal canal (HAEM) Anterior condylar canal transmits the hypoglossal nerve, meningeal branch of ascending pharyngeal artery,
emissary vein connecting sigmoid sinus with the internal jugular, meningeal branch of hypoglossal nerve.
Posterior condylar canal Transmits an emissary vein connecting the sigmoid sinus with suboccipital venous plexus.
Jugular foramen (AIPG 2003) Through anterior part;

• Inferior petrosal sinus
•
• Meningeal branch of ascending pharyngeal artery.
•
Through Middle part 9th, 10th, 11th cranial nerves.
Through posterior part:
• Internal jugular vein.
•
• Meningeal branch of occipital artery.
•
Mastoid canailculus Transmits auricular branch of vagus nerve
Typmpanic canailculus Transmits tympanic branch of glossopharyngeal nerve to middle ear.

Stylomastoid foramen Facial nerve
Anterior and posterior Anterior and posterior ethmoidal canals
ethmoidal canals
Foramen caecum Blind in nature
Optic canal transmits Optic nerve and ophthalmic artery

Superior orbital fissure • Lateral part
•
- Lacrimal nerve
-
- Frontal nerve
-
- Trochlear nerve,
-
- Lacrimal and middle meningeal artery
-
• Middle part
•
- Occulomotor nerve (AIIMS May 2009)
-

- Nasocilliary nerve
-
- Abducent nerve
-
• Inferior Orbital Fisssure
•
- Maxillary nerve
-
- Zygomatic nerve
-
- Orbital branches of pterygopalatine ganglion
-
- Infraorbital nerve and vessel
-
- Communication between inferior ophthalmic vein and pterygoid plexus of veins
ANATOMY
-
Foramen rotundum Maxillary nerve (AIPG 2001)

Internal acoustic meatus Transmits the 7th and 8th cranial nerves and labyrinthine vessels.
Good to know points

• Maxilla articulates with nasal, lacrimal, frontal, palatine and zygomatic bones.
•
• Mental foramen is present on outer surface of body of mandible between the roots of two premolars
•

(AIIMS 1998, MAN 1995)

• Lingua is a sharp tongue shaped projection at the anterior margin of mandibular foramen. It gives attachment to
•
sphenomandibular ligament. (TNPSC 1999)

• The orbital plate of ethmoid is the thinnest and weakest part of the orbit and is k/a lamina papyracea
•
• The frontal process of maxilla, lacrimal bone, orbital plate of ethmoid and sphenoid make the medial wall of orbit.
•
• Mandibular fossa is a part of temporal bone. It along with articular tubercle forms the upper articular surface of
•
temporomandibular joint.
• Suprameatal triangle externally represents mastoid antrum. (KAR 2003)
•

• Foramen transversium is typically exclusive to the transverse process of cervical vertebra. It is not present in thoracic and
•
lumbar vertebra. (AIIMS 2009)

Face
Facial Muscles Origin Insertion Action
• Corrugator supercilli • Medial end of supercilliary • Skin of eye brow • Vertical wrinkling of forehead:
•
•
•
•
arch frowning
• Orbicularis oris: • Medial part of medial • Concentric rings return to • Closes lid tightly, wrinkling, protects
•
•
•
•
- Orbital part, on and palpebral ligament and the point of origin eye from bright light
adjoining bone
-
around the orbital
margin
- Palpebral part, in • Lateral part of medial • Lateral palpabral raphae • Closes lid gently
-
•
•
•
the lids palpebral ligament
- Lacrimal part, • Lacrimal fascia and • Upper and lower tarsi • Dilates lacrimal sac, directs lac.
-
•
•
•
lateral and deep to lacrimal bone Puncta into lacus lacrimalis;
the lacrimal sac supports the lower lid.
• Orbiularis oris • Superior incisivus, from • Angle of mouth • Closes and purses the mouth,
•
•
•
•
- Intrinsic part, maxilla, inferior incisivus, numerous extrinsic muscles make
from mandible it more versatile for various types of
-
deepest stratum,
very thin sheet grimaces
Anatomy 11

- Extrinsic part, two • Thickest middle stratum, • Lips and the angle of the
-
•
•
strata, formed by derived from buccinators, mouth
converging muscles thick superficial stratum,
derived from elevators and
depressors of lips and their
angles
• Buccinators, the • Upper fibres, from maxilla, • Upper fibres, straight to the • Flattens cheek against gums and
•
•
•
•
muscle of cheek opposite molar teeth upper lip teeth, prevents accumulation of food
in the vestibule
• Lower fibres, from • Lower fibres, straight to the
•
•
mandible opposite molar lower lip
teeth
• Middle fibres, from • Middle fibres decussate
•
•
pterygomandibular raphae before passing to the lips
(AIPG 2002)
• Platysma • Upper parts of pectoral and • Anterior fibres, to the base • Releases pressure of skin on
ANATOMY
•
•
•
•
deltoid fasciae of the mandible, posterior the subjacent veins, depresses
fibres, to the skin of the mandible, pulls the angle of the
lower face and lip, and mouth downwards as in horror or
may be continuous with the surprise. (AIPG 1994, MAN 1994)
risorius
Facial expressions Muscles involved

Smiling and laughing Zygomaticus major
Sadness Levator labli superioris and levator anguli oris
Grief Depressor anguli oris
Anger Dilator naris and depressor septi
Frowning (KAR 2000) Corrugator supercilii and procerus
Functional groups of facial muscles

Opening Sphincter Dilators
Palpebral fissure Orbicularis oculi • Levator palpebrae superioris
•
• Occipitofrontalis part.
•
Oral fissure Orbicularis oris All the muscles around the mouth, except the orbicularis oris the
sphincter, and the mentalis which does not mingle with orbicularis
oris.
Nostrils Compressor naris • Dilator naris.

•
• Depressor septi.
•
• Medial slip of levator labli superoris alaequae nasi.
•
Nerve Supply of Face
• Facial nerve (VII) the motor nerve of the face for all muscles, except levator palpebrae superious, which is supplied by
•
occulomotor nerve (III)
• Trigeminal nerve is the main sensory nerve of the face (V)
•
• The skin over angle of the jaw is supplied through great auricular nerve (PGI 2005)
•

Arch of Aorta
• Brachiocephalic artery
•
– Right common carotid artery
–

External carotid artery

Internal carotid artery

– Right subclavian artery
–
• Left common carotid
•
• Left subclavian artery
•
Arteries of the Face
External carotid Facial artery The anterior branches on the face are large and named.
Artery (ECA) They are (1) Inferior labial, (2) superior labial, and (3)

(AIPG 2001) Interal nasal to the ala and dorsum of the nose.
The posterior branches are small and unnamed.

Maxillary artery Inferior alveolar is The Buccal and mental

(MAN 2002, AIIMS 1991) Formed From the second artery from inferior
ANATOMY

part of maxillary artery alveolar.
(AIPG 1994, MAN 1994)
Superficial temporal artery Transverse facial is a small branch of superficial temporal.

It supplies the parotid gland and its duct, Masseter and
the overlying skin. and ends by anastomosing with
neighbouring arteries.
Internal carotid Ophthalmic artery arises from cerebral Supraobital, supratrochlear, dorsal nasal branches.
artery (ICA) part of ICA (AIPG 1998)

Lingual Artery
• Arises from the anterior surface of external carotid artery
•
• Supplies the tongue and floor of the mouth
•
• Branches
•
– Dorsal lingual artery
–
– Sublingual artery
–
– Supplies the hyoglossus, genioglossus
–
• Deep lingual artery
•
Right Subclavian Artery
• Principal artery of upper limb
•
Branches
– Vertebral artery (first and largest branch) – Internal thoracic

– Thyrocervical trunk – Inferior thyroid artery

– Supra scapular – Superficial cervical artery

– Costo cervical trunk – Dorsal scapular artery

Maxillary Artery
• Terminal branch of external carotid artery
•
• Divided into 3 by lateral pterygoid into 3 parts
•
Anatomy 13

First or mandibular • Deep auricular artery
•
part - Supplies TMJ, external acoustic meatus and tympanic membrane
-
• Anterior tympanic branch
•
- Supplies the middle ear
-
• Middle meningeal artery
•
- Supplies duramater, periosteum of bone and red bone marrow
-
- The frontal or anterior branch is the commonest source of extradural hemorrhage (AIIMS MAY 2013)
-
• Accessory meningeal artery
•
- Supplies meninges and infratemporal fossa
-
• Inferior alveolar artery
•
- Lingual branch to tongue
-
- Br to mylohyoid muscle
-
- Mental br to supply the chin
-
Second or • Branches to muscles of mastication
•
pterygoid part • Branches to buccinators
ANATOMY
•
Third or pterygoid • These are closely involved in Le Fort I, II, III fractures.
•
palatine part • Posterior superior alveolar
•
- Supplies molars and premolars
-
- Supplies maxillary sinus
-
• Infraorbital
•
- Supplies incisors and canines
-
- Lacrimal sac, nose, upper lip
-
• Greater palatine
•
- Supplies palate and gums
-
- Gives lesser palatine branch that supplies soft palate and tonsil
-
• Pharyngeal branch
•
- Supplies the nasopharynx, auditory tube, sphenoidal air sinus
-
• Artery of pterygoid canal
•
- Supplies the pharynx, auditory tube and tympanic cavity
-
• Sphenopalatine artery
•
- Postero lateral nasal branches to lateral wall of nose and paranasal sinuses
-
- Posterior septal branches to nasal septum
-
Venous Drainage of Head, Neck and Face
Retromandibular vein
• Formed by the junction of superficial temporal vein and maxillary vein.
•
• It lies in the substance of parotid gland
•
• Divides into 2 divisions: Anterior and posterior division
•
• Anterior branch joins facial vein to form common facial vein (drain into internal jugular vein)
•
• Posterior branch joins posterior auricular vein to form external jugular vein.
•
External Jugular Vein
• Site of origin:
•
– Union of posterior division of retromandibular vein and posterior auricular vein – just below the angle of the
–
mandible (KAR 2000)

– It is provided by two valves one at the termination and other at 4 cm above clavicle. Between these two valves the vein
–
is dilated to form a sinus.

• Tributaries:
•
– Posterior auricular
–
– Posterior division of retromandibular
–
– Transverse cervical
–
– Suprascapular
–
– Anterior jugular
–
– Occipital
–
– Oblique jugular
–
– Posterior external jugular vein
–
Anterior jugular vein:
• Site of origin:
•
– Just below the chin by the union of small tributaries from the submandibular region and runs down the anterior
–
median line. Terminates by going laterally deep to sternocleidomastoid and draining into external jugular vein.
– Sometimes vein of kocher replaces the external jugular vein and accompanies the anterior jugular vein.
–
ANATOMY
Dangerous area of Face

• Facial veins are devoid of valves and rests directly on muscles
•
• Infection from the upper lip and the lower part of nose may travel in retrograde direction to cavernous sinus, due to
•
communication between deep facial vein and angular vein. Deep facial vein drains into cavernous sinus. (AIPG 2002)

Cutaneous Nerves of the Face
Main nerve Branch Area of distribution
Ophthalmic division of Supratrochlear nerve Scalp up to vertex, forehead;
trigeminal nerve Supraorbital nerve Upper eyelid; conjunctiva, small part of lower eyelid.
Lacrimal nerve and root, dorsum and tip of nose.
External nasal nerve
Maxillary division of Infraorbital nerve Upper lip; side and ala of nose; most of the lower eyelid;
trigeminal nerve Zygomaticofacial nerve (AIPG 1998) upper part of cheek .Upper part of the cheek.
Zygomatico temporal nerve anterior part of temple.
Mandubular division of Auriculo temporal nerve Upper 2/3 of lateral surface of auricle; and side of head.
trigeminal nerve Buccal nerve Lower and major part of the cheek.
Mental nerve Lowe lip; chin; lower part of cheek; lower jaw except over the
angle.
Cervical plexus Anterior division of great auricular nerve Skin over the angle of the jaw and over the parotid gland.
Cutaneous nerve (C2,C3). Lower margin of the lower jaw. lower 1/3rd of both lateral
Upper division of transverse (anterior) and medial surface of pinna.
cutaneous nerve of neck (C 2, C3)
MUSCLES OF MASTICATION
Mainly four muscles: (AIPG 2003, AIIMS 1989)
• Masseter
•
• Temporalis
•
• Lateral pterygoid
•
• Medial pterygoid
•
Origin Insertion Nerve supply Actions
• Masseter Masseteric nerve, Elevation of mandible
•
It is quadrilateral; in shape and has 3 branch of the anterior
trunk of mandibular

layers:
nerve
Anatomy 15

- Superficial layer: Its fibres originate Downwards and backwards into
-
from the angle and lower half of the
* Zygomatic process of maxilla in lateral surface of mandible

the form of a thick aponeurosis
* Anterior 2/3rd of the lower border

of zygomatic arch (AIIMS 1992)

- Middle layer: From the following Into the middle part of ramus.
-
two places of zygomatic arch:
* Deep surface of anterior 2/3rd of

the arch
* Lower border of posterior 1/3rd of

the arch
- Deep layer: Into the upper part of the ramus

-
From the deep surface of zygomatic and coronoid process
ANATOMY

arch
• Temporalis: • The fibres converge By deep temporal • Elevates mandible
•
•
•
* From whole length of temporal downwards. The anterior branches of the • posterior fibres retract the
fibres descend vertically, anterior trunk of the

•
fossa mandible after protraction
intermediate obliquely and mandibular nerve

* From deep surface of temporalis (MAN 2002)
posterior fibres horizontally to (AP 2001)

fascia (AP 2000)
• Helps in lareral sliding of
get inserted into the coronoid

•
mandible during grinding
process and anterior margin
of ramus of mandible

(PGI 2005)

• Some fibres also join
•
masseter and pass on to the
mandible
• Lateral pterygoid: It is short thick • Fibres pass backwards and By a branch of It helps in opening the mouth by
•
•
muscle with origin by two heads laterally to get inserted into: mandibular nerve pulling the condylar process of
mandible forward (AIPG

2014, 2012, AIIMS May 2010)
* Upper head: Arises from • Depression in front of the Protrusion of mandible along

•
infra temporal surface and neck of mandible with medial pterygoid
infratemporal crest of greater wing
of sphenoid
* Lower head: Arises from the • Articular disc of

•
lateral surface of lateral pterygoid temporomandibular joint
plate of sphenoid (COMEDK 2006)
• Medial pterygoid: It is a thick Raises the mandible

•
quadrilateral muscle
* Superficial part: Into the lower and back part of By a branch of • Assists in protrusion of

•
From the medial surface of lateral the medial surface of angle and mandibular nerve mandible
ramus of mandible as high as

pterygoid plate. • Acting with lateral pterygoid
mandibular foramen above and
•
From the grooved surface of the alternatively, it produces a
nearly as forwards as mylohyoid movement

pyramidal surface of palatine bone
groove
* Deep part: small slip originates

from the lateral surface of palatine
bone and tuberosity of maxilla
Movement Muscles
Elevation Masseter, temporalis, medial pterygoid
(MAN 1994, AIIMS 1993)

Movement Muscles
Depression Lateral pterygoid
(AIPG 2012, AIIMS MAY 2013)
Depression of mandible Digastric, genohyoid, mylohyoid
against resistance
(Mouth is opened wide or
against resistance)
Protrusion (PGI 2001) Lateral and medial pterygoid

Retraction Posterior fibers of temporalis
Resistance of retraction Middle and deep fibres of masseter, digastric and genohyoid
Lateral movement (example Alternate contraction and relaxation of pterygoid muscles.
towards right) Ex. contraction of left lateral pterygoid and right medial pterygoid followed by relaxation of right lateral
(AIIMS Nov 2013) pterygoid
Chewing movements/side- Medial and lateral pterygoid of each side acting alternately.
ANATOMY
side movements
Structure present superficial to hyoglossus are: Structures present deep to hyoglossus are: (AIIMS 1998, AIPG 1999)
• Lingual nerve • Glossopharyngeal nerve
•
•
• Hypoglossal nerve • Lingual artery
•
•
• Submandibular ganglion • Stylohyoid ligament
•
•
• Submandibular gland • Genioglossus
•
•
- Submandibular duct • Intrinsic muscles of tongue
-
•
- Styloglossus
-
SALIVARY GLANDS
• The daily secretion of saliva: 500 and 1500 milliliters.

•
• Normal stimulated secretion rate in adults is 1 – 2 ml per minute.
•
• Circadian variation: Unstimulated flow peaks at approx 5pm in most individuals, with a minimum flow at night (0.05ml/
•
min) during sleep allowing populations of bacteria to build up in mouth - result is a dragon breath in morning
• Saliva is a merocrine secretion
•
• The viscosity of saliva is non-Newtonian. The ability to draw out a thread of saliva is known as ‘Spinnbarkelt’.
•
• Saliva has a pH between 6.0 and 7.4 (with the higher pH exhibited upon increased secretion).
•
Salivary Gland
Gland Situation Duct opening Secretion Innervation
Parotid Below the external Stensons duct Purely serous Parasympathetic Nerves: secretomotor. They reach
acoustic meatus ----after piercing the the gland through the auriculotemporal nerve. The
between the ramus buccinators opens preganglionic fibres begin in the inferior salivatory
of mandible and into the vestibule of nucleus, pass through the 9th nerve, its tympanic
sternocleidomastoid. mouth opposite the branch, tympanic plexus and lesser petrosal nerve
Largest of all crown of maxillary and relay in the otic ganglion. The post ganglionic
salivary glands 2nd molar fibres pass through the auriculotemporal nerve and
reach the gland. (PGI 2001, KCET 2007)

Sympathetic Nerves: Sympathetic nerves are
vasomotor. They are derived from the plexus around
the external carotid artery.
Sensory Nerves: Auriculotemporal nerve.
Anatomy 17

Gland Situation Duct opening Secretion Innervation
Submandibular Roughly J shaped Wharton’s duct--- Mixed and • Supplied by submandibular ganglia.
•
salivary gland, opens on the floor predominantly • Parasympathetic Fibres: Are secretomotor
•
situated in the of mouth, on the serous from chorda tympani. They begin in the superior
anterior part of the summit of the sub salivatory nucleus and pass through sensory root
digastrics triangle. lingual papilla, at of facial nerve, geniculate ganglion, facial nerve,
The gland is divided the side of frenulum chorda tympani, lingual nerve and submandibular
into larger superficial of tongue. ganglion where the preganglionic fibres relay.
and small deep The post ganglionic fibres emerge from the
parts by mylohyoid ganglion and soon enter the submandibular
muscle gland.

(AIIMS 1999)
• Sympathetic Fibres: Are vasomotor. They are

•
Sublingual Smallest of the three Bartholin’s Mixed and from the plexus around the facial artery.
salivary gland. It is duct—10 – 15 predominantly • Sensory Fibers: From lingual nerve
•
ANATOMY
situated above the ducts emerge mucous
mylohyoid, below from the gland.
the mucosa of the Most of them open
floor of the mouth. directly into the
(AIPG 2007, AIIMS floor of the mouth
Nov 2012) on the summit of
sublingual fold. A
few of them join
the submandibular
duct.
Parotid Duct (AIIMS May 2008) Labial and Glands of lips and cheeks are mixed
buccal glands consisting of mucous tubules with serous
• Thick walled and is about 5 cm long demilunes. Intercalated ducts are variable
•
• It emerges from the middle of the anterior border of the in length.
•
gland Glossopalatine Pure mucous glands. They are principally
glands localized to the region of the isthmus in
• At the anterior border of masseter it turns medially and glossopalatine fold.
•
pierces (AIIMS 1989, AIPG 2007)
Pure mucous in nature lying in the lamina

Palatal glands
– Buccal pad of fat propria of the posterior lateral region of the
–
– The buccopharyngeal fascia hard palate
–
– Buccinators (obliquely) Lingual glands The glands of tongue in the anterior region
–
called glands of Blandin and Nuhn are
• Orifice is located on the buccal surface near maxillary purely mucous in nature where as glands in
•
surface of 2nd molar (AIPG 2003) the posterior tongue are mixed.
The posterior lingual serous glands called
Von Ebner’s glands are located between
• Structures within the parotid gland: (COMEDK 2006, the muscle fibres of the tongue below the
•
PGI 1999, KAR 1998) circumvallate papilla
– Arteries:
–
External carotid artery TONGUE

Maxillary artery
Development of Tongue:

Superficial temporal vessel

(PGI 2000, AIIMS 1998, KAR 2000, 1999)

Posterior auricular artery

Epithelium

– Veins: Retromandibular vein •
•
– Anterior 2/3rd: First branchial arch: two lingual
–
– Nerve: Facial nerve
–
swellings and one tuberculum impar
–
• Minor salivary glands: small groups of secretory units – Posterior 1/3rd: Third branchial arch: cranial half of
•
–
opening via short ducts directly into the mouth. hypobranchial eminence (AIPG 2002)


– Posterior most: Fourth arch
–
• Muscle: occipital myotomes
•

(AIPG 2008, COMEDK 2006)

• Connective tissues: Local mesenchyme
•
• Pre sulcal mucosa: Tuberculum impar
•
• Post sulcal part: Hypobranchial eminence
•
Development of Genioglossus
• Motor nerves: (AIPG 1999, AIIMS 1994)
•

– All muscles except palatoglossus are supplied by hypoglossal nerve (AIPG 2009)
–

– Palatoglossus is supplied by cranial part of accessory nerve (AIPG 2012)
–

• Sensory: (AIIMS may 2013)
•

– Anterior 2/3rd
–
Lingual nerve: General sensory
ANATOMY

Chorda tympani: Special sensory

– Posterior 1/3rd: Glossopharyngeal nerve – general and special sensory
–

(AIIMS MAY 2013, AIPG 2002, 2007, KCET 2009)

– Posterior most part: Vagus (internal laryngeal)
–
Genioglossus is the only tongue muscle which protrudes it. It is used for testing the integrity of hypoglossal nerve. If the right
hypolglossal is paralysed, the tongue will deviate towards the right as the normal left hypoglossal will pull the base of tongue to left
and resultant deviation of the apex towards the right. (AIIMS Nov 2013)

Lymphatics: (AIPG 2014, AIIMS Nov 2013)

• Drain chiefly into the deep cervical lymph nodes.
•
• Lymph nodes situated at the bifurcation of common carotid artery is intimately associated with the lymph vessels from
•
tongue so also known as principal gland/node of the tongue.
• Lymph vessels from the tongue may be divided into:
•
• Apical: From the tip of the tongue. Drains bilaterally into the submental lymph nodes
•

(MAR 1998, MAN 2000)

• Lateral: From lateral margins of the tongue, these pierce the mylohyoid to drain in the submaxillary lymph nodes or
•
directly into the deep cervical nodes.
• Basal: From vallate papillae region. Drain into the upper deep cervical lymph nodes.
•
• Median
•
• Ultimately the whole lymph drains into the jugulo-omohyoid nodes.
•
• Arterial supply: Lingual artery (AIPG 1996)
•

• The base of the tongue is attached to the hyoid bone and mandible. (PGI 2006)
•

Muscles of Tongue
Extrinsic muscles (paired with a central raphae) Intrinsic muscles
• Genioglossus • Superior longitudinal
•
•
• Hyoglossus • Inferior longitudinal
•
•
• Chondroglossus • Transverse
•
•
• Styloglossus • Vertical
•
•
• Palatoglossus
•
Anatomy 19

• Genioglossus • Spreading in a fan shaped manner, • Hypoglossal • Protrudes tip of tongue
•
•
•
•
- From the upper genial tubercle the fibres are inserted as follows: nerve out of mouth (MAN 2002)
-
on inner surface of symphysis of • Inferior fibres: to the upper part • By pulling two parts of
•
•
mandible (COMEDK 2007, 2005) of anterior surface of body of hyoid tongue downwards,
bone just near the midline and it helps in making the
also with the middle constrictor of dorsum of tongue
pharynx concave
• Middle and superior fibres: these
•
fibres form the bulk of the tongue
intermingling with intrinsic muscles
of the tongue from the root to the
apex
• Hyoglossus • Lateral side of tongue • Hypoglossal • Depression of tongue

•
•

•
•
- From the whole length of greater (AIPG 2010) nerve (KAR 1997)

-
cornu of hyoid bone
ANATOMY
- From anterior surface of lateral part
-
of hyoid bone
• Chondroglossus: • Into the musculature of tongue • Hypoglossal • Aids hyoglossus

•
•
•
•
- At times it is considered a part of nerve
-
hyoglossus muscle.
- From medial side and base of lesser
-
cornu of hyoid bone and adjacent
part of body of hyoid bone
• Styloglossus: • It blends with the musculature • Hypoglossal • Upward and backward

•
•
•
•
- From the anterior and lateral aspect of tongue, few fibres running nerve movement of tongue
longitudinally and others obliquely (AIPG 2010)
-
of styloid process of temporal bone

near its apex from the upper end of (AIPG 2010)

stylomandibular ligament
• Palatoglossus: Oral surface of palatine • Descends in the palatoglossal • Cranial part • Pulls up the root of the
•
•
•
•
aponeurosis arch to the side of the tongue at of accessory tongue and approximates
the junction of oral and pharyngeal (11th) nerve the palatoglossal arch
parts and thus closes the
oropharyngeal isthmus
• Superior longitudinal: Fibres arise • These fibres run toward upto the • Hypoglossal • Together superior and
•
•
•
•
from the submucous layer of tongue edge of tongue, some getting nerve inferior longitudinal:
near epiglottis and from median fibrous inserted into the mucous membrane • Shorten the tongue
septum of tongue
•
• Superior longitudinal
•
• Inferior longitudinal: It is situated on • Hypoglossal elevates the side of
tongue, making the
•
•
the under surface of tongue between nerve
genioglossus and hyoglossus muscles dorsum concave.
• Inferior longitudinal
•
depresses the sides of
tongue, there by making it
dorsum convex.
• Transverse: • From root to apex of tongue • Hypoglossal • Narrows and elongates
•
•
•
•
- Arising from the median fibrous • Few fibres are connected with body nerve the tongue
-
•
septum the fibres run laterally to of hyoid posteriorly and styloglossus
get inserted into submucous fibrous anteriorly.
tissue at the side of tongue and into
the palatopharyngeus muscle
• Verticalis: Flattens and broadens the

•
- This muscle is seen at the free border tongue.
-
of tongue running from upper to
under surface of tongue

• Injury to the hypoglossal nerve produces paralysis Special sensory and • Carries taste sensation from the
•
•
of the muscles of the tongue of the same side. So the gustatory nerves oral surface are contained in the
lesser palatine nerves.
tongue will deviate to the same side of which the • The fibres travel through the greater
hypoglossal nerve is damaged.
•
petrosal nerve to the geniculate

(AIPG 2008, 2009, MAN 1999) ganglion of the facial nerve to the

nucleus of solitary tract.

(AIPG 2011, KAR 1997)
PALATE

Secretomotor • Derived from the superior salivatory
•
nerves nucleus and travel through the
Hard palate (bony) forms the anterior 4/5 of the palate. It is greater petrosal nerve.
formed by the maxillary and palatine bone. (KAR 1997)

Soft palate forms the posterior 1/5 of palate. Uvula hangs from Blood Supply
posterior border of soft palate in the midline. (AIIMS 1990)
• Greater palatine branch of maxillary artery (PGI 1999)

•

Soft Palate • Ascending palatine branch of facial artery (AIPG 1999)
•

• Palatine branch of ascending pharyngeal artery
ANATOMY
•
Anterior part • More horizontal in position Veins
•
• Less mobile • Pass to the pterygoid and tonsillar plexus of veins
•
•
• Made up of palatine aponeurosis
•
mainly
• Is the chief area acted upon by the Paralysis of Soft Palate Causes
•
tensor veli palatine • Nasal regurgitation of fluids

•
(AIPG 2005)
• Nasal twang in voice
• Has abundant mucous glands
•
• Flattening of palatal arch
•
• A complete denture should usually
•
•
be extended to cover this area
• More mobile
PHARYNX
Posterior part
•
• Palatine aponeurosis is thin here
Muscles of Pharynx
•
• Lies obliquely
•
• Abundant mucous glands are
The muscular coat of pharynx consists of an outer circular
•
present
muscle layer and an inner longitudinal muscle layer.
Muscles of the Soft Palate • The outer circular layer is made up of:
•
• Tensor veli palatine – Superior constrictor
–
•
• Levator veli palatine – Middle constrictor
–
– Inferior constrictor
•
• Musculus uvulae
–
• The inferior constrictor is made up of two parts, i.e.,
•
• Palatoglossus
•
the thyropharyngeus and the cricopharyngeus. The
•
• Palatopharyngeus thyropharyngeus arises from thyroid cartilage and the
•
cricopharyngeus arises from the cricoid cartilage.

(AIPG 2011, AIIMS 2011)
Nerve Supply

• All the constrictors of pharynx are inserted into a
•
Motor supply • All muscles of soft palate except median raphae on the posterior wall of the pharynx.
(PGI 2006)
•
tensor veli palatini are supplied by

the pharyngeal plexus.
• The fibres of this plexus are
Origin of Constrictors of Pharynx
•
derived from the cranial part of the
accessory nerve through vagus.
• The tensor veli palatini is supplied Superior constrictor • Pterygoid hamulus
•
takes origin from
•
by the mandibular nerve • Pterygomandibular raphae
•
the (from above • Medial surface of mandible at the
General sensory • The middle and posterior lesser
downwards)
•
•
nerves (AIPG 2002, palatine nerves which are branches posterior end of the mylohyoid line
AIIMS 2001, 1995) of maxillary nerve through the i.e. near the lower attachment of
pterygopalatine ganglion the pterygomandibular raphae
• From the glossopharyngeal nerve • Side of posterior part of tongue
•
•
Anatomy 21

Middle constrictor • Lower part of stylohyoid ligament • It is a weakness in wall of pharynx (KAR 2003)
•

•
takes origin from • Lesser cornua of hyoid bone • It lies between propulsive thyropharyngeus and sphincter
•
•

(AIIMS 2007) (AIPG 2010) cricopharyngeus. Its level is below the level of vocal folds.

• Upper border of greater cornua of
• Etiology: Neurovascular incoordination.
•
hyoid bone
•
Thyropharyngeus and cricopharyngeus are supplied by
Inferior constrictor • Thyropharyngeus arises from different nerves. When cricopharyngeus fails to relax
•
consists of two parts thyroid cartilage while thyropharyngeus contracts, pressure builds which
• Cricopharyngeus arises from the may lead to diverticular formation through Killian’s
•
cricoid cartilage dehiscence.
The longitudinal muscle coat consists of: Hypopharyngeal diverticula

• Stylopharyngeus • Usually left sided, more common in men
•
•
• Palatopharyngeus • Seen as a protrusion through Killian’s dehiscence
•
•
• Salpingopharyngeus • Complications include:
ANATOMY
•
•
– Regurgitation of food
–
Gaps Between Pharyngeal Muscles and Structures – Pooling of food
–
Related to Them – Aspiration, etc
–
Position Structures passing through
• Diagnosis is by radiology after a barium meal
•
it • Treatment: by surgical excision
•
The large gap between the upper • Auditory tube • Diagnosis is by radiology after a barium meal
•
•
concave border of the superior • Levator veli palatine muscle • Treatment: by surgical excision
constrictor and the base of the
•
•
• Ascending palatine artery
skull is semilunar and is known
•
as sinus of Morgagni
Palatoglossal Arch (AIIMS May 2008)
Gap between the superior and Stylopharyngeus and

middle constrictors glossopharyngeal nerve
• The anterior of the two folds of mucous membrane on
•
either side of oropharynx, enclosing the palatoglossal
Gap between the middle and The internal laryngeal nerve
inferior constrictors and superior laryngeal vessels muscle.
pierce the thyrohyoid • The palatoglossal arch (glossopalatine arch, anterior pillar
•
Gap between the lower border of of fauces) on either side runs downward, lateral ward and
the inferior constrictors and the
oesophagus forward to the side of the tongue and is formed by the
projection of the glossopalatine with its covering mucous
Suprahyoid muscles Infrahyoid muscles membrane.
• Digastric • Sternohyoid • The palatoglossal arch is created by the connection of the
•
•
•
• Stylohyoid • Sternothyroid palatoglossal muscle to the upper region of tongue and
rear of palate.
•
•
• Mylohyoid • Thyrohyoid
• Folds of the mucous membrane passes from the soft palate
•
•
•
• Geniohyoid • Omohyoid to the side of the tongue and encloses the palatoglossal
•
•
muscle.
Killians Dehiscence (AIPG 2001)
• Tongue movements affect the palatoglossal arch.

•

• Seen in posterior wall of pharynx (AIIMS May 2010, AIIMS 2007, AIPG 2007)
•

LARYNX
Location • Extends from the C3 to lower border of the C6 where it is continuous with the trachea
•
Cartilages • 9 cartilages
•
- 3 are paired (Arytenoid, Corniculate, Cuneiform)
-
- 3 are unpaired (Thyroid, Cricoid, Epiglottic)
-

• The thyroid and cricoid cartilages and the basal part of arytenoid cartilages are made up of hyaline cartilage. They
•
may ossify after the age of 25 years. The other cartilages of larynx are made of elastic cartilage and do not ossify.
• At the level of thyroid cartilage – carotid pulse is palpable, bifurcation of common carotid artery
•

(AIPG 2001,2007,2012, NEET 2013)

• At the level of cricoid cartilage – cricothroidotomy is done in the space between the cricoid and thyroid cartilage
•
Muscles • Cricothyroid Only intrinsic muscle lying on the external aspect of larynx; tensor of larynx; supplied by external
•
laryngeal nerve – all are unique features, remember.
• Posterior Cricoarytenoid Only ABDuctor of vocal cords (opens the glottis). (MAN 2000,AIPG 2000, AIIMS 2001)
•

• Lateral cricoarytenoid, ADDuctor of vocal cords (close the glottis)
•
 
• Transverse arytenoids
•
 
• Thyroarytenoid Upper part = thyroepiglotticus, lower part = vocalis
•
Motor Nerve • The Recurrent laryngeal N supplies all the intrinsic muscles of the larynx, except the Cricothyroid which is by the
ANATOMY
•
supply External laryngeal nerve. (AIPG 1999, AIIMS 1999, KCET 2012)

Sensory • Internal laryngeal N. supplies mucus membrane above level of vocal folds. RLN supplies it below the level of vocal
•
Nerve supply folds. (COMEDK 2010)

Also Note
• In high tracheostomy incision is given just above the isthmus of first tracheal ring
•
• In low tracheostomy, incision is given through 2nd and 4th tracheal rings
•
Action Muscles Involved
Muscles which open glottis or abductors of vocal cord Posterior cricoarytenoids
Muscles which close the glottis of adductors of vocal cord • Lateral cricoarytenoids
•
• Transverse arytenoids, cricoarytenoids
•
• Thyroarytenoids
•
Muscles which tense the vocal cord • Cricothyroids
•
Muscles which relax the vocal cord • Thyoarytenoids
•
• Vocalis
•
Muscles which open the inlet of larynx • Thyroepiglotticus
•
Muscles which close the inlet of larynx • Aryepiglotticus
•
• Oblique artytenoids.
•
EAR AND NOSE
• Nasal septum:
•
– Blood supply: Anteroposterior part:
–
Anterior ethmoidal artery
Superior labial branch of the facial artery
– Posteroinferior part by sphenopalatine artery
–
Little’s or Kiesselbach’s area: (AIPG 1998)

• Anastomoses between the septal ramus of the superior labial branch of the facial artery and the sphenopalatine artery,
•
apart from a large capillary network
• This is common site of bleeding from the nose
•
Anatomy 23

Nerve supply
(NEET 2013, AIPG 1999)
• Anterosuperior part of septum is supplied by the internal nasal branch of the anterior ethmoidal nerve
•
• Posteroinferior part: Nasopalatine branch of the pterygopalatine ganglion
•
• Olfactory nerves (special sensory nerves) supply the olfactory area.
•
Nasal Conchae
• Are curved bony projections directed downward and medially.
•
• 3 conchae are:
•
– Inferior concha: Independent bone
–
– Middle concha: Projection from medial surface of the ethmoidal labyrinth. (PGI 2008)
–

– Superior concha: Projection from the medial surface of the ethmoidal labyrinth. It is the smallest concha situated just
–
above the posterior part of middle concha.
ANATOMY
• Auditory ossicles. Three auditory ossicles (“ear bones”) are present in the middle-ear chamber of each ear and serve
•
to transmit sound impulses. From outer to inner, these bones are the malleus (“hammer”), incus (“anvil”) and stapes
(“stirrup”). Malleus is the largest, and the most laterally placed ossicle. Incus of Anvil resembles a molar teeth. Stapes is the
smallest, and the most medially placed ossicle of the ear. These develop early in fetal life and are of full size at birth.

(AIPG 2012)

• Joints of the ossicles.
•
– The articulations between ossicles include the malleus-incus- The incudomalleolar joint is a saddle joint. (AIPG 2009)
–

– Articulation and the incus-stapes-The incudostapedial joint is a ball and socket. Both of them are synovial joints.
–
Muscles of the middle Ear
• There are two muscles, the tensor tympani (first arch) and the stapedius (second arch). Both act simultaneously to damp
•
down the intensity of high-pitched sound waves and thus protect the internal ear.
• A child can withstand noisy sound better than an adult because the external ear is shorter and tympanic membrane is
•
softer.
Meatus Openings of
Superior meatus (smallest) Posterior ethmoidal sinus
Middle meatus Maxillary sinus (KCET 2010)
Frontal sinus
Middle ethmoidal sinus
Inferior meatus (largest) Nasolacrimal duct
• Posterior ethmoidal air sinus opens into: (COMEDK 2012)

•

– Superior meatus
–
– Middle meatus
–
– Inferior meatus
–
– Spheno ethmoidal recess
–
Pharyngotympanic tube/ Eustachian tube/ Auditory tube
• It is a trumpet shaped channel which connects middle ear cavity with the nasopharynx.
•
• It is about 4 cm long and is directed downward, forward and medially.
•
• It forms an angle of 45 degrees with the saggittal plane and 30 degrees with the horizontal plane.
•
• The tube is divided into bony and cartilaginous part
•

Bony part • Forms the posterior and lateral 1/3rd of the Sneezing (AIIMS May 2008)
•

tube and lies in the petrous temporal bone
near the tympanic plate Sneezing reflex is triggered by a variety of stimuli, the most
• Its lateral end is wide and opens on the
common of which is stimulation of nasal mucosa (trigeminal
nerve endings) by mechanical or chemical stimuli.
•
anterior wall of the middle ear cavity. The
medial end is narrow and is jagged for Sneezing reflex has 2 phases:
attachment of the cartilaginous part
• Nasal
• The lumen of the tube is oblong being
•
– The afferent limb of the nasal phase consists of
•
widest from side to side.
–
the ethmoidal (cranial nerve V) and olfactory (C
Cartilaginous • Forms anterior and medial 1/3rd of the N I) which projects to sneezing centre in medulla
•
part tube and lies in the sulcus tubae, a groove
between the greater wing of sphenoid and
oblongata
the apex of the petrous temporal – The efferent limb of nasal phase consists of
–
• It is made up of triangular plate of cartilage preganglionic fibres of greater petrosal nerve (CN
VII) and the sphenopalatine ganglia (CN VII)
•
which is curled to form the superior and
medial walls of the tube. which innervates the glands and the blood vessels
in the nose.
ANATOMY
• The lateral wall and the floor are completed

•
by a fibrous membrane • Respiratory
•
• The apex of the plate is attached to the
– Respiratory phase of the sneezing reflex
•
medial end of the bony part
–
commences when a critical number of inspiratory
• The base is free and forms the tubal
and expiratory neurons are recruited by sneezing
•
elevation in the nasopharynx
centre.
Vascular supply (AIPG 2012)

• Arterial supply is through • Ascending pharyngeal Sternutogenesis

• Middle meningeal arteries
• A sneeze involves dozens of muscles in the face, chest

• The artery of pterygoid canal
•
and abdomen, all operating in a correct sequence that has

• Venous drainage is into: • Pharyngeal and pterygoid been hard wired in the brain and spinal cord.

plexuses of vein
• The sequence is mediated by trigeminal nerve particularly

• Lymphatics pass into: • Retropharyngeal nodes
•
the anterior ethmoidal, posterior nasal and infraorbital

Nerve supply branches.
• At the pharyngeal end by the pharyngeal branch of the
PARANASAL SINUSES
•
pterygopalatine ganglion suspended by maxillary nerve
• Cartilaginous part by the nevus spinosus branch of • Air-filled bony cavities located in the face and skull
•
mandibular nerve
•
adjacent to the nose. (AIPG 2012)

• Bony part by tympanic plexus by the glossopharyngeal • Derive their nomenclature from the bones that they
•
nerve
•
pneumatize.
Functions • Occur as “paired” structures
•
• The tube provides a communication of the middle ear – Frontal sinuses
–
•
cavity with the exterior, thus ensuring the equal air – Maxillary sinuses
–
pressure on both sides of the tympanic membrane – Ethmoid sinuses
–
– The tube is usually closed. It opens during the – Sphenoid sinuses
–
• Each sinus is connected to the nose by a small opening
–
swallowing, yawning and sneezing, by the action of
•
the tensor and levator veli palatine muscles called an ostium.
• The sinuses form in utero as small pockets the size of a
Clinical importance
•
pea. At birth they are mostly rudimentary.
• Infection may pass through from the throat to auditory • Purpose
•
tube. This is more common in children because the tube is
•
– Lighten the skull
shorter and straighter in them.
–
– Improve vocal resonance
• Inflammation of the auditory tube is often secondary to an
–
– Prevent dehydration
•
attack of common cold or sore throat.
–
Anatomy 25

Frontal Sinus
• It lies in the frontal bone deep to superciliary arch
•
• Opens into middle meatus of nose (AIIMS 1999)
•

• e right and left sinuses are usually unequal in size
•
TH
• ey are rudimentary or absent at birth
•
TH
• Supraorbital arteries supply the frontal sinus.
•
Sphenoidal Sinus
• The right and left sphenoidal sinuses lie within the body of sphenoid bone
•
• They are separated by the septum
•
• Each sinus is related superiorly to the optic chiasma and hypophysis cerebri, and laterally to the internal carotid artery
•
and the cavernous sinus
• Arterial supply: Posterior ethmoidal and internal carotid artery (AIIMS 1998)
•

ANATOMY
• Supplied by posterior ethmoidal nerve (AIPG 1999)
•

Ethmoidal Sinus
• These are numerous small interconnecting spaces which lie within the labyrinth of the ethmoidal sinus
•
• The anterior ethmoidal sinus is made of 1 – 11 air cells
•
• The middle ethmoidal sinus consists of 1 – 7 air cells
•
• The posterior ethmoidal sinus consist of 1 – 7 air cells.
•
Maxillary Sinus
• Also known as antrum of Highmore.
•
• Largest and most constant of the paranasal sinuses. (KAR 2000)
•

• It is the first sinus to develop in utero (4th month). After birth, it undergoes two periods of rapid growth, between birth
•
and 3 years of life, then between ages 7 and 18 years
• At birth it forms an oblong cavity about 1cm long and 0.5 cm high and covers less than a third of length of lateral wall of
•
nose. It grows rapidly during 6 to 7 years of life.
• From one year to the adulthood, maxillary sinus grows and attains approximately 15 mm- of capacity. (AIPG 2002)
•

• The floor of the sinus does not extend below that of the nasal cavity until the eruption It grows vertically in size by about
•
2-3 mm a year, attaining its adult size after the full eruption of the permanent dentition.
• Occurs earlier in girls than boys
•
• Pyramidal shaped.
•
• The base of the maxillary sinus is directed medially and the apex superolaterally. Its anterior and posterior surface is
•
formed by the corresponding surfaces of the maxilla, its roof by the orbital surface and floor by the palatine and alveolar
processes of the maxilla. Occasionally, dehiscence may be present in the floor of the sinus (2%) wherein the roots of the teeth
come to lie in close relation to the mucosa facilitating spread of infection.
• Vertical growth of the sinus occurs in stages. In young children, the floor of the sinus is approximately 4 mm above the
•
level of the nasal floor, following which it subsequently extends 1 to 5.5 mm below the nasal floor after the age of 12 years.
• The anterior wall of the sinus corresponds to the anterior surface of the maxilla extending superiorly from the orbital
•
rim above to the teeth below. It is thinnest just above the root of the canine tooth and it is from this area that the sinus can
be approached via canine puncture techniques or through the classical Caldwell-Luc approach.
• The posterior wall is formed by the corresponding surface of the maxilla superiorly, and part of the palatine bone
•
inferiorly. It is related to pterigopalatine fossa making maxillary sinus one of the ways to approach the fossa.

• The medial wall of the sinus is shared with the nasal cavity and forms part of the lateral nasal wall within which is
•
present the nasolacrimal duct this can be damaged by surgical trauma
• The normal ostium of the sinus is 7-11 mm in length and 2-6 mm high. Oedema of mucosa surrounding it can markedly
•
block the ostium. Accessory ostia or Giraldes orifice are present in 28%.
• Ostium is obstructed by uncinate process.
•
• Thickness of the floor varies 2-3mm.
•
• The roof is the floor of the orbit.it is associated with orbit and its contents, thickness varies 2-5mm on roof.
•
• Opens into middle meatus at hiatus semilunaris (KCET 2007)
•

• Osteomeatal complex – it is formed by uncinate process, maxillary ostium, infundibulum, ethmoid bulla. These form
•
functional complex through which maxillary sinus drain.
• The accessory ostia may be found in middle nasal meatus and are rarely present in inferior nasal meatus.
•
• The most common anatomical variation in the maxillary sinus is the infraorbital ethmoid cell, or Haller cell; Haller cells
ANATOMY
•
are pneumatized ethmoid cells that project along the floor of the orbit, arising most often from the anterior ethmoids. They
can in some cases compromise the patency of the maxillary sinus infundibulum, and in other cases can be involved in the
chronic polypoid disease, which will mandate opening them.
– The sinuses are lined with pseudostratified ciliated columnar epithelium which is continuity with the mucosa of the
–
nasal cavities.
– Goblet cells produce glycoproteins which are responsible for the viscosity and elasticity of mucus. They are innervated
–
by the parasympathetic and sympathetic nervous system. Thus, parasympathetic stimulation induces thicker mucus
with sympathetic stimulation leading to more watery mucus secretion.
Blood, Nerve Supply and Lymphatic Drainage
• Internal and external carotid systems.

•
• The anterior ethmoidal artery: Supplies the upper part of the medial wall of the antral cavity and the ethmoidal sinus.
•
• Internal and external carotid systems.
•
• The anterior ethmoidal artery: Supplies the upper part of the medial wall of the antral cavity and the ethmoidal sinus.
•
• The sphenopalatine artery: To the lateral nasal wall, lining membrane of the maxillary sinus on its supramedial aspect.
•
• The posterolateral wall, alveolus and teeth are served by the posterosuperior dental vessels, and similarly the anterolateral
•
wall by the infraorbital artery.
• The lymphatic drainage broadly follows the blood supply.
•
• Anterior lymphatic channels from the anterolateral walls drain to the submandibular nodes. (COMEDK 2002)
•

• Branches of V2 innervate the maxillary sinus. Specifically, the greater palatine nerve and the branches of the infraorbital
•
nerve.
TONSIL
The tonsillar ring or Waldeyer’s ring consists of the following tonsils. (AIPG 1997)

Tonsil Location Features
Pharyngeal tonsils Nasopharynx Contains no lymph, sinuses, nor crypts. Surrounded in part by connective tissue
(adenoids) and in part by epithelium.
Palatine tonsils In isthmus of fauces Reach 200% of size by puberty and show regression. Surrounded in part by
(between palaotglossal and connective tissue and in part by epithelium. Contain crypts and lymphoid follicles
palatopharynegeal), Dorsum (No sinuses)
of tongue (posteriorly)

(KAR 2008)

Anatomy 27

Tonsil Location Features
Lingual tonsils Dorsum of tongue-posterior Lymphoid follicles, each with a single crypt
one-third
Tubal tonsils Behind the eustachian tube. Continuous with the lateral part of the pharyngeal tonsil.
The facial artery supplies the tonsils. (MAN 1994) under the control of the autonomic nervous system

(involuntary). They work in response to light, closeness
Orbit of an object (for focusing) etc.
• Ring of Zinn, gives attachment to muscles of orbit
•
(except inferior oblique) Muscles of Eye
• Eyeball is supported from below by lockwood
Muscle Action
•
suspensory ligament
• Eyeball has following layers: Superior rectus • Upward rotation
•
•
– Outer fibrous coat: Cornea, sclera (MAN 2002)
ANATOMY

–
– Middle vascular coat (also known as uveal tract) • Medial rotation
•
–
– Choroid, ciliary body, ciliary muscle • Intortion
•
–
– Inner nervous coat: Retina Inferior rectus • Downward rotation
–
• Supraorbital notch is present at the junction of: medial
•
• Medial rotation
•
and intermediate thirds of upper orbital margin
•
• Extortion
•
• The modified sebaceous glands in eyelid are :
Medial rectus • Medial rotation or
•
– Glands of Zeis
•
adduction
–
– Torsal glands
Lateral rectus • Lateral rotation or
–
• Superior oblique muscle arises from: Floor of orbit.
•
abduction
•
Inferior orbital Transmits the zygomatic nerve, orbital Superior oblique • Downward rotation
fissure branches of pterygopalatine ganglion,
•
• Lateral rotation
infraorbital vessels, communication
•
between the inferior ophthalmic vein and • Intortion
•
pterygoid plexus of veins.
Inferior oblique • Upward rotation
•
Infraorbital groove Transmits the corresponding nerve and (MAN 2002)

and canal vessels. • Lateral rotation
•
Zygomatic Transmits the zygomatic nerve • Intortion
•
foramen
Levator palpebral superioris • Elevation of upper eyelid
•
• Extraocular muscles: There are seven voluntary (somatic • Nerve supply: All muscles are supplied by third
•
•
innervation) and at least three involuntary (sympathetic cranial nerve except:
innervation) muscles. (Neet 2013) – SQ4: Fourth cranial nerve for superior oblique

–
– Voluntary muscles are: – LR6: Sixth cranial nerve for lateral rectus.
–
–
Four recti: Superior rectus, inferior rectus, medial

rectus, lateral rectus Good to Know
Two oblique: Superior oblique and inferior • Limen insulae lies in the lateral relation of anterior

•
oblique perforated substance (APS). (AIIMS May 2011)

One levator: Levator palpebra superioris • Uncus lies in the posterolateral relation of APS

•
Recti muscles arise from common annular tendon • Optic chiasma lies in the medial relation of APS

•
(tendinous ring) • APS lies on the base of the brain anterior to each optic
• The intrinsic muscles control the lens and pupil. The
•
tract, containing numerous perforations through which
•
intrinsic eye muscles, (including the iris sphincter, branches of anterior and middle cerebral arteries are
radial pupil dilator muscles and the ciliary muscle, are transmitted to the deeper structure. It is included under
olfactory area.

• Limen insulae, uncus, and the entorhinal area (anterior Middle layer: Sternohyoidomohyoid division,
•

part of parahippoampal gyrus) are collectively called as Sternothyroid, thyrohyoid division, Visceral
pyriform cortex and are connected to olfactory pathway. division (Buccopharyngeal, Pretracheal,
(MAN 2002, KAR 2001, AIPG 1993) Retropharyngeal)

• The insulae is important for gustatory sensation, motor Posterior layer: Alar division and prevertebral

division
•
speech control, vestibular function and sympathetic
control of cardiovascular tone. Carotid sheath

• The “investing layer of deep cervical fascia” splits to
•
enclose
LACRIMAL APPARATUS
– Two muscles: Trapezius, sternocleidomastoid
–
– Two glands: Parotid, submandibular
• Parts
–
– Two spaces: Suprasternal and supraclavicular
•
– Lacrimal gland: Orbital part and palpebral part
–
• The pretracheal fascia encloses and suspends the thyroid
–
•
– Conjuctival sac gland. (AIIMS 2010)
–

– Lacrimal canaliculi (10mm) • Carotid sheath
–
– Lacrimal sac (12mm)
•
– The carotid sheath is a condensation of fibroareolar
ANATOMY
–
– Nasolacrimal duct (18mm)
–
tissue around the main vessels of neck. It encloses
–
• Arterial supply: lacrimal branch of ophthalmic artery common and internal carotid arteries, internal jugular
•
• Nerve supply: vein and the vagus nerve.
– The ansa cervicalis is embedded in the anterior wall of
•
– Secretomotor fibres: –
the carotid sheath.
–
Lacrimatory nucleus – The cervical sympathetic chain lies behind the sheath,
↓
–
attached to prevertebral fascia.
Nervus intermedius – Parotid swellings are very painfully due to unyielding
↓
–
nature of parotid fascia.
Facial nerve • While excising the submandibular gland, the external
•
↓ carotid artery should be secured before dividing it;
Greater petrosal nerve (AIPG 2010, 2012, COMEDK otherwise it may retract through stylomandibular
2004, 2008) ligament and cause serious bleeding.

↓
Pretracheal spaces • Lies behind the pretracheal
Nerve to pterygoid canal
•
fascia and strap muscles and in
↓ front of oesophagus
Pterygoid canal • Radiologically the portion
↓
•
behind the strap fascia and the
Maxillary nerve thyroid fascia is referred to as
anterior cervical space
↓
• This space often provides
Zygomatic nerve
•
a symmetric landmark on
↓ transverse imaging
Zygomaticotemporal nerve Retrovisceral space • Continuous superiorly with
↓
•
retropharyngeal space
Gland • Situated between the posterior
•
wall of the esophagus and
prevertebral fascia
NECK Prevertebral fascia • Potential space between the
•
(AIIMS May 2013) prevertebral fascia and vertebral
Cervical Fascia column
• Also known as danger space
• Deep fascia is absent on face except over parotid gland
•

(AIIMS Nov 2011)
•

(parotid fascia) and buccinator (buccopharyngeal fascia). Carotid space • Layer of loose connective tissue
(AIIMS Nov 2012)
•
demarcated by adjacent portion

– The deep fascia covering the neck is condensed to of investing layer of deep
cervical fascia, the pretracheal
–
form fascia and the prevertebral
Anterior layer: Investing fascia (over the neck), fascia.

Parotidomasseteric, Temporal
Anatomy 29

• Cervical symapthetic ganglion
•
– Cervical parts of the right and left sympathetic trunks are situated one on each side of the cervical part of the vertebral
–
column.
– Origin: From fibres of T1 to T4 of spinal cord that ascent into the neck.
–
Due to fusion of 3 ganglia, superior, middle, inferior branches of superior ganglia:

To ventral rami of upper 4 cervical nerves

Plexus around internal carotid artery. Apart of this plexus supplies dilator pupillae.

Plexus around external carotid artery.

Pharyngeal branches form pharyngeal plexus.

Left superior cervical cardiac goes to superficial cardiac plexus while the right goes to deep cardiac plexus.

• Middle cervical ganglion: Formed by 5th and 6th cervical ganglia
•
– Branches: Branches to ventral rami of 5th and 6th cervical nerves, thyroid, parathyroid, tracheal, oesophageal and
–
to deep cardiac plexus.
– Largest ganglia of the neck
–
• Inferior cervical ganglia: Formed by fusion with first thoracic ganglion and 7 and 8 cervical ganglion is called stellate
ANATOMY
•
gangion.
– Branches: To ventral rami of C7 and C8 plexus around vertebral artery and Subclavian artery, deep cardiac plexus.
–

(KAR 2003)

• Stellate (cervicothoracic) ganglion-First thoracic ganglion fused with the inferior cervical ganglion. Damage to it can
•
lead to Horner’s syndrome.
• Nodose ganglion: (Ganglion of the trunk; inferior ganglion of the X nerve) is cylindrical in form, 2.5 cm in length. It is
•
chiefly visceral afferent in function carrying sensation of the heart, larynx, lungs and alimentary tract from the pharynx
to the transverse colon.
Anterior Triangles (AIPG 2003)

Important contents
Submental triangle Submental lymph nodes
Digastric triangle ANTERIOR PART

Submandibular salivary gland (AIPG 1995)
Submandibular lymph nodes
Facial vein and artery
Mylohyoid nerves and vessels
POSTERIOR PART
Parotid gland
Styloglossus, stylopharyngeus
IX and X nerves
ECA and ICA
Carotid triangles Arteries: ECA and ICA and CCA with carotid sinus and the carotid body at its termination.
Veins: Common facial vein and IJV
Nerves: IX, X superior laryngeal branch of X nerve dividing into the external and internal laryngeal nerves, spinal
branch of XI nerve and XII nerve
Lymph nodes: Jugulodigastric node and jugulo-omohyoid node
Carotid sheath and its contents
Muscular triangle INFRAHYOID MUSCLE

Sternohyoid
Sternothyoid
Thyrohyoid
Omohyoid
Posterior Triangles Important contents

Occipital triangle • Spinal accessory nerve
•
• Nerves-Lesser occipital (C2), Great auricular (C2,C3), anterior cutaneous (C2,C3) and Supraclavicular (C3,
•
C4)

Posterior Triangles Important contents
• Muscular branches-levator scapulae and trapezius (C3,C4) rhombodiues (C5)
•
• Upper part of brachial plexus
•
• Occipital artery
•
• Transverse cervical artery and vein
•
Supraclavicular or • Suprascapular nerve (C5, C6), nerve to subclavius (C5, C6) and serratus anterior (C5,C6, C7)
•
Subclavian Triangle • Third part of subclavian artery and subclavian vein
•
• Suprascapular artery and vein
•
• Lower part of external jugular vein
•
Infrahyoid Muscles
Muscle Origin Fibres tendon Insertion Nerve supply Actions
1. Sternohyoid a. Posterior surface of Converge Medial part of lower Ansa cervicalls Depresses hyoid bone

(SH) manubrium superiorly and border of hyoid following its elevation
b. Adjoining parts diverge inferiorly bone. during swallowing and
ANATOMY
vocal movements

of clavicle
and posterior
sternoclavicular
ligament
2 Sternothyroid a. Posterior surface of Diverge superiorly Oblique line on the Ansa cervicalls Depresses larynx after it

manubrium and converge lamina of thyroid has been elevated in the
b. Adjoining part inferiorly cartilage acts of swallowing and
vocal movements

of first costal
cartilage
3 Thyrohyoid Oblique line of thyroid Small quadrilateral Lower border of C1 through Depresses hyoid bone.

(TH), appears cartilage muscle body and greater hypoglossal nerve Elevates larynx when
part of ST lies cornu of hyoid hyoid is fixed by
deep to SH. bone. Suprahyoid muscles
4 Omohyoid a Upper border Central tendon Lower border of Superior belly by a Depresses hyoid

(OH) has an of scapula near lies on IJV at the body of hyoid bone superior root of bone following its
inferior belly, suprascapular level of cricoid, and lateral to the SH ansa cervicalis; elevation during
a common notch. bound to clavicle by inferior belly by swallowing or vocal
tendon and a b Adjoining part of a fascial Pulley ansa cervicalis movements.
superior belly

suprascapular b Possibly helps in
Arises by

ligament prolonged inspiratory
inferior belly; efforts.
inserted by
superior belly.
5 Digastric (DG) a Anterior belly a Anterior Both heads meet Anterior belly by a Depresses mandible

has two bellies (DGA) from belly runs at the intermediate mylohyoid nerve when mouth is
united by and digastric fossa of downwards tendon which Posterior belly by opened widely or
an intermediate mandible and backwards perforates SH and facial nerve against resistance to
tendon b Posterior belly b Posterior is held by a fibrous (Man 1994, AIIMS lateral pterygoid.
pulley May 2013)

(DGP) from belly runs b Elevates hyoid bone.

mastoid notch of downwards (BHU 2012, AIIMS
temporal bone and forwards. 1990)

(PGI 2003)

6 Stylohyoid Posterior surface of Tendon is Junction of body Facial nerve a Pulls hyoid bone

(SH) small styloid process perforated by DG and greater cornu upwards and
muscle, lies on tendon of hyoid bone backwards.
upper border of b With other hyoid
DGP

muscles, it fixes the
hyoid bone.
Anatomy 31

Muscle Origin Fibres tendon Insertion Nerve supply Actions
7 Mylohyoid Mylohyoid line of Fibres run medially a Posterior Mylohyoid Elevates, floor of

(MH) flat, mandible. and slightly fibres: Body of mouth in first stage of
triangular downwards hyoid bone. deglutition.
muscle; two b Middle and Helps in depression of
form floor of mandible and elevation of

anterior fibres;
mouth cavity median raphe. hyoid bone. (KAR 1998)
deep to DGA
8 Geniohyoid Inferior mental spine Runs backwards Anterior surface of C1 through a Elevates hyoid bone

(Gh) short and (genial tubercle) and downwards body of hyoid bone. hypoglossal nerve b May depress
narrow muscle;

mandible when hyoid
lies above is fixed
medial part of
MH
Sternocleidomastoid Muscle
ANATOMY
The sternocleidomastoid is enclosed in the investing layer of deep cervical fascia, and is pierced by the accessory nerve and by the
four-sternocleidomastoid arteries. It divides the neck into anterior and posterior triangles. (AIPG 1995, 1994)

Origin • The sternal head in tendinous and arises from the superolateral part of the front of the manubrium sterni.
•
• The clavicular head is musculotendinous and arises from the medial one-third of the superior surface of the
•
clavicle.
Insertion It is inserted (a) by a thick tendon into the lateral surface of the mastoid process from its tip to its superior border, and
(b) by a thin aponeurosis into the lateral half of the superior nuchal line of the occipital bone
Nerve supply The spinal accessory nerve provides the motor supply. It passes through the muscle.
Blood supply One branch each from superior thyroid artery and suprascapular artery and two branches from the occipital artery
Action a. When one muscle contracts:

* It turns the chin to the opposite side.

* It can also tilt the head towards the shoulder.

b. When both muscles contract together:

* They draw the head forwards as in eating and in lifting the head from a pillow.

* With the longus colli, they flex the neck against resistance.

* The reverse action helps in forced inspiration.

BRAIN AND SPINAL CORD
The scalp is a multilayered structure with layers:
• Skin
•
• Connective tissue
•
• Aponeurotic layer
•
• Loose connective tissue
•
• Pericranium
•
Astrocytes Astrocytes are the largest of the neuroglial cells. Astrocytes are important in controlling the microenvironment
of nerve cells and participate in the maintenance of the blood-brain barrier.
Oligodendrocytes Oligodendrocytes have small nuclei and contain abundant mitochondria, ribosomes, and microtubules.
Oligodendrocytes myelinate axons in the CNS.
Microglia Microglia are small, dense, elongated cells with nuclei .They originate from the mesoderm, unlike other neuroglial
cells, which originate from the neuroectoderm. Microglia are phagocyte and part of the mononuclear phagocyte
system.

Ependymal cells Ependymal cells line the ventricular cavities of the brain and the central canal of the spinal cord. They are
capable of mitosis and can develop long processes that cerebrospinal fluid through the ventricles.
Schwann cells Schwann cells contain elongated nuclei that lie parallel to the axons of peripheral neurons. Schwann cells
myelinate peripheral axons
• Brain is covered by
•
Dura mater Outermost and thickest of all the layers. It encloses cranial venous sinuses. It has distinict blood supply and so
also the nerve supply.
Arachnoid Middle layer arachnoid is separated from dura mater by subdural space; subarachnoid space contains CSF
and it separates arachnoid and pia mater. (COMEDK 2009)

Pia mater Innermost layer of brain.
• The different folds of dura mater are

ANATOMY
•
Falx cerebri Sickle-shaped fold of dura mater encloses straight sinus and inferior sagittal sinus in its posterior 2/3rd.
Tentorium cerebelli Tent shaped fold of dura mater encloses transverse and superior petrosal sinus. It also forms the trigeminal/
Meckel’s cave in which trigeminal or gasserian ganglion is present.
Falx cerbelli Sickle shaped, encloses occipital sinus
Diaphragm sellae Forms the roof of hypophyseal fossa
Venous Sinuses
• Duramater forms its wall
•
• Inner lining of endothelium
•
• Valveless
•
• Muscle less
•
• Superior sagittal sinus continues as right transverse sinus (IGNOU 2010)
•

• Inferior sagittal sinus ends by joining the great cerebral vein to form straight sinus
•
• Straight sinus continues as sigmoid sinus
•
• Sigmoid sinus becomes the superior bulb of internal jugular vein. Thrombosis of sigmoid sinus is always secondary to
•
infection in middle ear or in the mastoid process
• Sigmoid sinus grooves the mastoid part of temporal bone where it is separated anteriorly from the mastoid antrum and
•
mastoid air cells by a thin plate of bone.
• Venous sinuses of dura mater are:

•
Paired Unpaired
1 Cavernous sinus 1. Superior sagittal sinus

2 Superior petrosal sinus 2. Inferior sagittal sinus

3 Inferior petrosal sinus 3. Straight sinus

4 Transverse sinus 4. Occipital sinus

5 Sigmoid sinus 5. Anterior intercavernous sinus

6 Sphenoparietal sinus 6. Posterior intercavernous sinus

7 Petro squamous sinus 7. Basilar plexus of veins

8 Middle meningeal 8. Sinus sphenoid air sinus

Anatomy 33

Cerebrum
Brodmann Areas of Cerebral Cortex (47 Areas)
Area Function
1,2,3 Primary sensory cortex; lies in the postcentral gyrus
4 Primary voluntary motor cortex; lies along the posterior part of the precentral gyrus adjoining the central sulcus.
17 Primary visual cortex; lies in the calcarine fissure of the occipital pole
22 Wernicke’s area; lies in the posterior part of the superior temporal lobe
41 Primary auditory area; lies on the cephalic border of the superior temporal gyrus in the depths of the lateral fissure.
44,45 Broca’s area, lies in the posterior part of the inferior frontal gyrus
White Matter of Cerebral Hemispheres
ANATOMY
• Corpus callosum
•
– Is made up of a large mass of nerve fibres that connect the two cerebral hemispheres and it helps in coordinating
–
activity between the two hemispheres
• Internal capsule
•
– There are a large number of nerve fibres interconnecting the cerebral cortex with centres in the brainstem and spinal
–
cord, and the thalamus.
– Most of these fibres pass through the interval between the thalamus and caudate nucleus medially and the lentiform
–
nucleus laterally. This region is called the internal capsule.
– Lesions of the internal capsule are usually vascular due to involvement of the middle cerebral A. (which supplies this
–
part). They give rise to hemiplegia of the opposite half of the body with an UMN type of facial palsy..
Part Descending fibres Ascending fibres

Anterior limb Fronto pontine Anterior thalamic radiation
Genus Cortico nuclear Anterior part of superior thalamic radiation

Posterior limb Cortico-pontine, CST, CRT Superior thalamic radiation. Fibres radiate from
lobus pallidus to subthalamic nucleus
Retro lentiform part Parieto-, temporo, occipito to pontine fibres Post thalamic radiation
Sub lentiform part Connection between temporal lobe and thalamus Auditory radiation
• Basal ganglia:
•
– Lenticular nucleus (putamen + globus pallidus)
–
 
– Caudate nucleus
–
 
– Substantia nigra and subthalamic nucleus.
–
 
– Main function of basal ganglia is to modulate the motor outflow of cortex so smoothening voluntary actions. Damage
–
to basal ganglia leads to involuntary movements.
• Main functional areas of cerebral cortex

•
Auditory area Temporal lobe
Visual area Occipital tube
Sensory area (Body is represented upside down) Postcentral gyrus (Parietal lobe)
Motor area (body is represented upside down and stimulation of this Precentral gyrus (frontal tube)
area results in movements in the opposite half of the body)

Premotor area or psychomotor area (Patterns of movement are Frontal gyrus
remembered in this area)
Motor speech area of in Broca (Injury to this region results in loss Inferior frontal gyrus (left hemisphere in right handed persons)
of speech or aphasis) (AIIMS May 2010, May 2009)

Thalamus
• Major synaptic relay station and is concerned with processing of ascending sensory information to the cerebral cortex.
•

(AIPG 1998)

• Blood supply of thalamus: Posterior communicating, posterior cerebral and anterior choroidal arteries
•
Limbic System
• Includes cingulate gyrus, hippocampus, fornix and mamillary bodies.
•
• Limbic system is concerned with emotional behaviour, sexual behaviour and food habits. The famous 5 F’s: Feeling, Fighting,
•
 
ANATOMY
Fleeing, Feeding and sex.
Hypothalamus “Head ganglion of the autonomic nervous system”

• Functions of hypothalamus include:
•
– Endocrine control (by forming releasing hormones e.g. TRH, CRH etc)
–
– Neurosecretion: Oxytocin (paraventricular nucleus) and vasopressin (supraoptic nucleus) are secreted
–
by hypothalamus and transported to the posterior pituitary.
 
– General autonomic effects: Anterior hypothalamus mediates Parasympathetic activity and Posterior
–
hypothalamus mediates Sympathetic activity “APPS”
 
– Temperature regulation (posterior hypothalamus regulates heat conservation and production when cold;
–
Anterior hypothalamus coordinates cooling when hot).
 
– Appetite regulation (Hunger: lateral feeding centre – destruction anorexia and starvation); (Ventromedial
–
satiety centre–destruction hyperphagia and obesity)
 
– Thirst and water balance (supraoptic nucleus).
–
– Sexual behaviour, emotion, fear (Septal nucleus – destruction rage).
–
– Circadian rhythm maintenance (biological clocks – suprachaismatic nucleus).
–
Midbrain
• Connects the pons and cerebellum to the diencephalon.
•
• Contains the cerebral peduncles (corticobulbar, corticospinal tracts), red nucleus, substantia nigra and the cranial nerve
•
 
nuclei of III and IV and a portion of the large sensory nucleus of V.
• Ascending sensory fibres travel in the lateral and medial lemniscus.
•
• Descending motor fibres pass en route to pons and spinal cord
•
Pons (means “Bridge”)
• Lies between the medulla and midbrain and is connected to the cerebellum by the middle cerebellar peduncle.
•
• Upper pons: Most prominent features are the pontine nuclei and the pontocerebellar fibres anteriorly.
•
• Lower pons: Dorsal surface forms the upper part of the floor of the fourth ventricle.
•
• Contains the nuclei of the VI, VII and VIII cranial nerves. (The sensory nucleus of V is extensive, extending from
•
the midbrain to the upper cervical level, with the most important part in the pons and the medulla. The motor nucleus
 
of V is in the pons. The corticospinal tracts cross in the lower pons.)
 
Anatomy 35

Medulla Cerebellum
• Continuous through the foramen magnum with the spinal • It is situated in the posterior cranial fossa behind the pons
•
and medulla.
•
cord, and above with the pons.
• Connected to the cerebellum by the inferior cerebellar • Each hemisphere is divided into three lobes. The anterior
•
is separated from the middle lobe by fissura prima.
•
peduncle.
• The flocculnodular lobe is the smallest lobe.
• Contains the nucleus ambiguus (motor to IX, X and XI)
•
• The cerebellum has three major connections with rest of
•
and the nucleus solitarius (sensory VIII, IX and X).
•
central nervous system:
• Most prominent cranial nerve nuclei are IX, X, XI and
– Superior cerebellar peduncle-carries motor impulses
•
XII.
–
to thalamus.
• The dorsal column nuclei cross to form the medial
– Middle cerebellar peduncle-carries sensory impulses
•
lemniscus.
–
from cortex to cerebellum.
• Sensory decussation contains some uncrossed fibres. – Inferior cerebellar peduncle-carries sensory
•
–
impulses from spinal cord to cerebellum.
Spinal Cord
ANATOMY
• Phylogenetic divisions of the cerebellum
•
• 45 cm long, extends from the upper border of Atlas
Archicerebellum • Most primitive parts of the
•
(C1) to the lower border of L1 or upper border of L2.
•
(vestibulocerebelum) cerebellum.
Here it narrows to a sharp tip, the conus medullaris. • Consist of lingula and
Below this the nerve roots form the cauda equina.
•
flocculonodular lobe.
• In adults the cord ends at the junction between L1 and • Mainly concerned with
•
balance and maintaining
•
L2 (AIPG 2006)
equilibrium.

• In children the cord ends at the level of 3rd lumbar
Paleocerebellum • Consist of entire anterior
•
vertebra (L3)
•
(spinocerebellum) lobe except the – lingula, the
• The dural sheath ends at level of S2 vertebra pyramids and uvula of the
•
posterior lobe.
• Filum terminale extends from level S2vertebra to coccyx
• Mainly concerned with
•
• The conus is continuous below with the filum terminale, •
maintaining tone and posture
•
a fine connective tissue filament, which descends upto of the body
the dorsum of the first coccygeal segment. Neocerebellum • Most recent part of the
•
(cerebrocerebellum) cerebellum.
• Subarachnoid space extends upto the lower border of
• Consists of middle lobe
•
S2 where the dura fuses with the filum teminale and
•
• Mainly concerned with
obliterates the subarachnoid space.
•
planning and programming
• Spinal cord is made up of 31 spinal nerves—8 cervical. of voluntary movements
•
12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal. through its connections
with the highly developed
• For C1-C7, nerves exit via the intervertebral foramina neocortex.
•
above the corresponding vertebra; nerves C8 and below
exit below. • Cavities:
•
 
• Cervical enlargement of spinal cord extends from C3 to Part Cavity
•
T2 segments–source of spinal nerves supplying upper Forebrain (prosencephalon)
limbs
Telencephalon Lateral ventricle
• Lumbar enlargement extends from L1 to S3 (source of
Diencephalon Third ventricle
•
spinal nerves supplying the lower limbs).
Midbrain (mesencephalon) Aqueduct of sylvius
• Lumbar puncture is usually done at the L4-L5 (or L3-
Hindbrain (rhombencephalon)
•
L4) interspaces.
Metencephalon Upper half of 4th venticle
• Blood supply: Anterior spinal artery supplies the
Myelencephalon Caudal half of 4th Ventricle
•
anterior two-thirds of the cord (branch of the vertebral
artery) and two posterior arteries (branches of the • Cerebrellar cortex
•
 
vertebral or posterior cerebellar arteries) supply the – Cerebellar cortex has 3 layers, which contain five cell
–
remainder. types (does not include bipolar cells)

Outermost molecular layer: Stellate and basket
Association fibres • Represent ipsilateral cortico axons.

•
cells • They allow a very large degree of
Middle layer: Purkinje cells (AIPG 2010)
•
intrahemispheric interconnection

Inner (deeper/granular) layer: Granule and golgi between different parts of the
cerebral cortex.

cells
– The only output (efferent) fibres of cerebellar • They may be short or long and
•
diffused or arranged in bundles
–
cortex are Purkinge cells, which use GABA as their • Represent axons connecting cortical
Commissural fibres
neurotransmitter and are inhibitory to deep cerebellar
•
areas with these contralateral
nuclei homologous areas and may enter
– The remaining four cells are afferent in nature the corpus callosum, the anterior
–
– Mossy fibres excite: granule cells – excite the commissure, or the commissure of
the fornix.
–
remaining four cells via the parallel fibres.
• In addition there are further indirect
– Afferent cells which are basket cells (located in
•
connections between the cerebral
–
molecular layer). Stellate cells located in superficial hemispheres in the diencephalon
layer and golgi cells in granular layer are example of and the brain stem
inhibitory interneurons. Projection fibres • Connect the cerebral cortex with
ANATOMY
•
– Bipolar cells are present in the cerebral and NOT subcortical nuclei.
–
CEREBELLAR cortex and retina • They ascend from or descend to the
•
– In grey matter of CNS dendritic tree grows maximum subcortical nuclei in major tracts,
including the internal capsule and
–
in the postnatal life. the fornix.
Cerebral hemisphere fibres (AIIMS May 2008): 3 types of • The internal capsule serves the
•
tracts. The association fibres are intrahemispheric fibres and neocortex while fornix serves the
commissural fibres are interhemispheric. archicortex.
Cerebrospinal Fluid pathway

CSF is secreted at the choroid plexus
lateral ventricle
↓
Foramen Munro
↓
3rd ventricle
↓
Aqueduct of Sylvius
↓
4th ventricle
↓
Foramen of Magendie, Foramen of Luschka
↓
Basal Cisterns
Causes of Reduced CSF Protein
• CSF protein between 3 and 20 mg/dl is considered below normal range.

•
• CSF leaks
•
• Removal of large volumes of repeated lumbar punctures
•
• During pneumoencephalography
•
• Traumatic leaks
•
• Removal of CSF for cytologic studies
•
Anatomy 37

Blood Brain Barrier (BBB) • Carotid body has chemoreceptors and monitors the
•
oxygen partial pressure; Carotid sinus has baroreceptor
Definition Formed by foot processes of astrocytes
and endothelial cells of brain capillaries
and it monitors blood pressure. (AIPG 2012)
 

having tight junctions (AIPG 2010) • Brain is supplied by branches of the two internal carotid

•
Substances which • •
Lipid soluble substances can and two vertebral arteries.
cross BBB cross BBB (AIPG 2010)

• Anaesthetic gases
Branches of Internal Carotid Artery
•
• Carbon dioxide and oxygen
•
• Unconjugated bilirubin Cervical part No branches arise from the internal carotid
•
• Urea (AIPG 2003) artery in the neck
•
Substances which • Bile salts Petrous part • Cardiotympanic branch
•
•
do not cross BBB • Catecholamines Pterygoid branch
•

• Proteins/polypeptides
Cavernous part
•
• 5 HT Branches to trigeminal ganglion and
(AIPG 2009) hypophysis cerebri
•
ANATOMY
Areas which • Area postrema
Cerebral part • Opthalmic artery
•
lies outside • Neurohypophysis
•
• Anterior cerebral artery
•
BBB are called • Adjacent ventral median eminence
•
• Middle cerebral
•
circumventricular of hypothalamus
•
organs (AIIMS May • Posterior communicating (AIPG 2007)
•
2009) • Anterior choroidal
•
• Anoxia • Of these, ophthalmic artery supplies
Blood brain barrier
•
orbit while the others supply the brain.
•
can be damaged by • Ischemia
•
• Inflammation • Circle of Willis:
•
•
• Hyperosmolality – Posterior communicating artery anastomoses with
•
–
• Acidosis the posterior cerebral A. The internal carotid and
•
• Trauma vertebrobasilar system are connected by Posterior
•
Pituitary Gland communicating A., Ant.cerebral A. of two sides are
connected by the Ant. communicating A. As a result
• The anterior • The posterior of these anastomoses an arterial circle (Circle of
•
•
(adenohypophysis) and pituitary Willis) is formed. (AIIMS 1999)
intermediate pituitary are a (neurohypophysis

derivative of Rathke’s pouch or pars nervosa)
(oral ectoderm). develops from
• Berry aneurysms
•
• The anterior pituitary synthesizes a downgrowth – Berry aneurysms occur at the bifurcations in the
–
from the floor of circle of Willis.
•
and secretes FSH, LH, ACTH,
TSH, GH, melanotropin (MSH), the third ventricle
(diencephalon) –
– MC site is bifurcation of the anterior
prolactin. These hormones
–
are released from the anterior neurectoderm. communicating artery.
pituitary under the influence of • Vasopressin and – Rupture leads to hemorrhagic stroke/Subarachnoid
–
hemorrhage.
•
hypothalamus. Oxytocin, made in
• Acidophils secrete: GH, the hypothalamus – A/w adult polycystic kidney disease, Ehlers Danlos
and shipped to the
–
•
Prolcatin syn., Marfan’s syndrome. Other risk factors:
posterior pituitary.
• Basophils secrete FSH, LH, advancing age, hypertension, smoking race (higher
•
ACTH, TSH
 
risk in blacks)
 
Blood supply of Brain
• External carotid A.: Each common carotid A. divides at
• Right common carotid A. arises from the Brachiocephalic
•
the level of the upper border of the thyroid cartilage (C4
•
A. level) into internal carotid and external carotid A.
• Left common carotid A. arises from the Aortic arch
•
• Each common carotid A. divides at the level of the Branches of External Carotid Artery (AIPG 2001)

•
upper border of the thyroid cartilage (C4 level) into I. Anterior Superior thyroid
internal carotid and external carotid A. At this bifurcation
 
carotid body and carotid sinus are present. Lingual (AP 2001)


Facial (AIPG 1998) Palpating Positions of Various Arteries

II. Posterior Occipital Arteries Palpating position
Posterior auricular Common carotid (AIPG 2012, 2010) Against transverse process
of C6
III. Medial (AIPG 2003) Ascending pharyngeal
Superficial temporal Just in front of tragus of ear

IV. Terminal Kar 2001) Maxillary (AIPG 1995, 1994)
Subclavian Just above middle of clavicle

Superficial temporal
Branchial In front of elbow just medial
• Facial Artery to tendon of biceps
•
• Facial artery is the anterior branch of external carotid Femoral At groin just below inguinal
•
artery. It runs upwards first in the neck (cervical part) and ligament
then on face (facial part) Popliteal Behind knee in lower part of
popliteal fossa against tibial
• Branches of facial artery condyles with knee in 400
•
– Cervical part flexed positions
ANATOMY
–
Ascending palatine to roof of tongue and the tonsil
Cavernous Sinus

Tonsillar to tonsil
• A collection of venous sinuses on either side of the

Submental to submental triangle and sublingual •
pituitary.

salivary gland
• Blood from eye and superficial cortex cavernous sinus
Glandular to submandibular salivary gland and
•
internal jugular vein

submandibular lymph nodes
• CN III, IV, V1, V2 and VII and postganglionic
– Facial part
•
sympathetic fibres en route to orbit all pass through the
–
Superior labial to upper lip wall of cavernous sinus

 
Inferior labial to lower lip • CN VI is ‘free floating’ in cavernous sinus,.

•
Lateral nasal to dorsum of nose • Cavernous portion of internal carotid artery is also here.

Vertebral A.: Arises from first part of Subclavian.A. It runs
•
• Structures outside the sinus.
through the transverse foramina of the upper 6 cervical
•
vertebrae. It then enters the vertebral canal. • Superiorly • Optic tract, optic chiasma, Olfactory tract,
•
•
Internal carotid artery. Anterior perforated
 
– Branches of vertebral. A. substance.
–
Spinal, Muscular and meningeal branches. • Interiorly • Foramen lacerum, Junction of body and

Posterior Inferior Cerebellar A: largest branch. It
•
•
greater wing of sphenoid.

gives off the Posterior Spinal A. • Medially • Hypophysio cerebri, Sphenoidal air sinus
•
•
Anterior Spinal A.: Is a single artery; it is present
• Laterally • Temporal lobe with uncus.

in the anterior median fissure.
•
•
• Anteriorly • Superior orbital tissue apex of the orbit.
Posterior Spinal A.: There are two posterior
•
•

spinal arteries (one on each side); may sometimes • Posteriorly • Apex of the petrous, temporal and crus
•
•
cerebri of the mid brain.
arise from the vertebral A.
Basilar A.: At the lower border of the pons • Structures in the lateral wall of the sinus.

•
Vertebral A. unites with its fellow of the opposite – Oculomotor nerve
side to form the Basilar A. This artery in turn ends
–
– Ophthalmic nerve
at upper border of pons by dividing into the right
–
– Trochlear nerve
and left Posterior Cerebral A.
–
– Maxillary nerve
- Branches of Basilar A.
–
– Trigeminal ganglion

∗ Posterior cerebral A.: Terminal branches.
–
• Structures passing through the center of the sinus
∗
•

∗ Superior cerebellar A. (AIPG 2007)
∗

∗ Pontine A. – Internal carotial artery
∗
–
∗ Labyrinthine A.: More commonly this – Abducent nerve.
–
∗
arises from Ant. Inferior Cerebellar A. • Draining channels of cavernous sinus (valveless)
•

∗ Anterior inferior cerebellar A. (AIPG 2002, MAN 1998)

∗
Anatomy 39

Into Through • Tributaries (incoming channels) (AIPG 2009)
•

– From orbit
Transverse sinus Superior petrosal sinus
–
Superior ophthalmic vein
Internal jugular vein

Inferior petrosal sinus and venous
Inferior ophthalmic vein
plexus around internal carotid artery

Central vein of retina
Pterygoid plexus Emissary veins passing through

foramen ovale, foramen lacerum, – From brain
–
emissary sphenoid foramen Superior middle cerebral vein

Inferior cerebral vein
Facial vein Superior ophthalmic vein

– From meninges

(AIPG 1998)
–

Communication Anterior and posterior intercavernous Sphenoparietal sinus

between sinuses sinuses and basilar plexus of veins Middle meningeal vein

Cavernous Sinus Thrombosis
Etiology • Rare complication of common facial infections, most notably nasal furuncles (50%), sphenoidal or ethmoidal
ANATOMY
•
 
(AIPG 2014) sinusitis (30%), and dental infections (10%). MC pathogens are Staphylococcus aureus (70%), followed
by Streptococcus.
 
• The anterior route composed of ophthalmic veins and their anastomosis with the facial vein, the angular vein,
•
infraorbital vein and inferior palpebral vein, readily allows the invasion of the cavernous sinus.
• Spread of infection by this pathway presents the classic picture of a fulminating cavernous sinus thrombosis
•
and CST through this route is more common than posterior route. (NEET 2013)

• The pterygoid venous plexus, which constitutes the posterior route, provide a connection between cavernous
•
sinus and the retromandibular vein. (AIIMS May 2013)

Clinical features • Abrupt onset of unilateral periorbital edema, headache, photophobia, and proptosis. Other common signs and
•
symptoms include: Ptosis, Chemosis, Cranial nerve palsies (III, IV, V, VI). CN VI palsy is the MC.

(MCET 2007, AIIMS 2009)

• Sensory deficits of the ophthalmic and maxillary branch of the fifth nerve are common. Periorbital sensory loss
•
and impaired corneal reflex may be noted.
• Papilledema, retinal hemorrhages, and decreased visual acuity and blindness may occur from venous
•
congestion within the retina.
• Appearance of signs and symptoms in the contralateral eye is diagnostic of CST, although the process may
•
remain confined to one eye.
• Fever, tachycardia, sepsis may be present. Headache with nuchal rigidity may occur.
•
• Pupil may be dilated and sluggishly reactive.
•
• Infection can spread to contralateral cavernous sinus within 24–48 hr of initial presentation.
•
Treatment • Includes high dose IV antibiotics, sometimes corticosteroids.
•
• Surgical drainage is indicated if sphenoid sinus involvement present.
•
CRANIAL NERVES
• Cranial Nerve Nuclei
•
– Located in tegmentum portion of brainstem (between dorsal and ventral pons)
–
– Midbrain: Nuclei of CN III, IV :
–
 
– Pons: Nuclei of CN V, VI, VII, VIII
–
– Medulla: Nuclei of CN IX, X, XI, XII
–
• Good to know about cranial nerves
•
• Thinnest/most slender and smallest CN (AIPG 2011) • Trochlear N.
•

•
• Only CN. that emerges from the brainstem on its dorsal aspect
•

(AIPG 2010)

• CN with longest intracranial course
•
• Only CN to undergo complete internal decussation before
•
emerging, supplies contralateral superior oblique muscles.

• Thickest/Largest CN • Trigeminal N.
•
•
• Largest branch of trigeminal N is Mandibular.N.
•
• Passes through Meckel’s cave
•
• MC affected CN with raised intracranial pressure due to Abducent (“Abducens” refers to abduction of eye; supplies lateral
•
long intracranial course – false localizing sign rectus)
 
• MC CN affected in spinal anesthesia
•
• CN with longest intraosseus course Facial
•
• MC injured motor CN
•
• Cranial nerve nuclei in relation to the floor of the fourth Vagus, Abducent and Hypoglossal nucleus
•
ventricle
• CN carrying parsympathetic fibres (AIPG 2011, BHU 2012) III, VII, IX, X
•

• CN with both motor and sensory components V, VII, IX, X
•
• CN with purely motor III, IV, VI, XII (KCET 2010, AIIMS 1990, 1991, AIPG 1990)
ANATOMY
•

• CN with pure sensory I, II, VIII
•
• Tip of the nose is supplied by Trigeminal N. (through nasociliary branch of ophthalmic N.)
•
• Skin over angle of mandible is supplied by Greater auricular N.
•
 
• CN containing somatic efferents or general somatic efferents III,IV, VI, XII
•

(AIPG 2011, COMEDK 2011)

• CN containing bronchial efferent or special visceral efferents V,VII,IX,X,XI
•
• CN containing general visceral efferents III, VII, IX, X
•
Occulomotor Nerve
• Entirely motor in function
•
• Nuclei
•
– 2 motor
–
main motor nuclei

accessory parasympathetic nucleus

– Main motor nuclei
–
Situated in anterior part of grey matter that surrounds cerebral aqueduct of the midbrain

Lies at the level of superior colliculus

– Accessory parasympathetic nucleus (Edinger Westphal nucleus)
–
Situated posterior to the main occulomotor nuclei

Preganglionic axons, accompany the other occulomotor fibres to the orbit. Here the synapse in the ciliary ganglion

and post ganglionic fibres pass through the short ciliary nerves to the constrictor papillae of the iris and ciliary
muscles.
Paralysis of 3rd nerve will result in:

• Ptosis (drooping of upper eyelid) (NEET 2013)
•

• Lateral squint
•
• Dilation of pupil
•
• Loss of accomodation
•
• Slight proptosis (forward projection of eye)
•
• Diplopia (double vision)
•
Anatomy 41

Trigeminal Nerve
• Largest cranial nerve
•
• Contains both sensory and motor fibres
•
• Branches: 3
•
– Ophthalmic nerve
–
– Maxillary nerve
–
– Mandibular nerve
–
Ophthalmic nerve: (AIPG 1998)

Frontal Nasociliary Lacrimal
a. Supratrochlear: a. Posterior ethmoidal: Sphenoidal air sinus, posterior ethmoidal air Lateral part of upper eyelid; conveys

Upper eyelid, sinuses. (AIPG 2012) secretomotor fibres from zygomatic

conjunctiva, b. Long ciliary: Sensory to eyeball. nerve to lacrimal gland.
ANATOMY
lower part of

c. Nerve to ciliary ganglion
forehead.

d. Infratrochler: Both eyelids. side of nose, lacrimal sac.

(MAN 2000)

b. Supraorbital: e. Anterior ethmoidal: (AIPG 2011)

Frontal air sinus, 1. Middle and anterior ethmoidal sinuses.

upper eyelid, 2. Medial internal nasal.
forehead, scalp

3. Lateral internal nasal.
till vertex

4. External nasal.

Mandibular Nerve arises from the lateral part of trigeminal ganglion, and
leaves the cranial cavity through the foramen ovale.
• Largest of the three branches of trigeminal nerve – The motor root also passes through the foramen
•
–
• Has both sensory and motor fibres ovale to join the sensory root just below the foramen
(AIIMS 1995)
•
• Nerve of the first branchial arch forming the main trunk.

– The main trunk lies in the infratemporal fossa, on the
•
• Course
–
tensor palate deep to the lateral pterygoid.
•
– Begins in the middle cranial fossa through a large – After a short course the main trunk divides into a
–
–
sensory root and small motor root. Sensory root small anterior and a posterior trunk.
• Branches (NEET 2013, AIPG 1992, 2000)
•

From the main trunk • Meningeal branch
•
• Nerve to medial pterygoid (AIPG 2012)
•

From the anterior trunk (AIIMS 2000) • Buccal nerve (sensory branch)

•
• Massetric nerve
•
• Nerve to lateral pterygoid
•
From posterior trunk (AIPG 1999) • Auriculotemporal nerve

•
• Lingual nerve
•
• Inferior alveolar nerve
•
• Buccal Nerve
•
– Only sensory branch from anterior division
–
– Passes between two heads of lateral pterygoid (PGI 2006)
–

– Supplies skin and mucous membrane related to buccinators (AIPG 1999, KAR 2003)
–

• Masseteric nerve
•
– Passes laterally through the mandibular (sigmoid) notch (PGI 1999)
–


• Auriculotemporal nerve
•
– Arises from two roots and its 2 roots encircle the middle meningeal artery
–
– Auricular part supplies
–
Skin of tragus

External acoustic meatus

Tympanic membrane

Upper part of pinna

– Temporal part supplies
–
Skin of temple

Auriculotemporal nerve also supplies the sensory and secretomotor fibres to parotid gland and TMJ

(AIPG 2002,1994, KAR 2001)

• Lingual nerve (AIPG 2009, 2011)
•

– Supplies sensory fibres to anterior 2/3rds of tongue and floor of mouth
–
ANATOMY
– Fibres of chorda tympani are also distributed through it

–
– It runs between the lateral and medial pterygoid
–
– Then it lie medial to third molar between origin of superior constrictor and mylohyoid muscles.
–
– Within tongue it lies above the hyoglossus but deep to mylohyoid and winds around the submandibular gland.
–
• Inferior Alveolar nerve
•
– Enters the mandibular foramen and runs in the mandibular canal where it is accompanied by inferior alveolar artery
–

(AIIMS 1996)

– Branches
–
Mylohyoid branch (AIPG 2007)

- Contains all the motor fibres of posterior division

- It pierces the sphenomandibular ligament and supplies mylohyoid nerve and anterior belly of digastric

Branches to lower teeth and gums

Mental nerve to skin of chin and lower lip (AIPG 1994, MAN 1994)

Facial Nerve
• 7th cranial nerve (AIPG 1998)
•

• Nerve of 2nd branchial arch
•
• Nuclei: The fibres of the nerve arise from the four nuclei situated in the lower pons (AIPG 2008)
•

– Motor nucleus or braciomotor
–
– Superior salivatory nucleus or parasympathetic
–
– Lacrimatory nucleus is also parasympathetic
–
– Nucleus of tractus solitarius which is gustatory and also receives afferent fibres from the gland (AIPG 2014)
–

Functional components Associated nuclei Structures innervated
• Special visceral efferent Motor Facial muscles
•
Hyoid elevators
• General visceral efferent Lacrimatory nucleus Lacrimal gland

•
(parasympathetic) Superior salivatory nucleus Submandibular, sublingual gland, glands of pharynx, nose,
palate
• Special visceral afferent Nucleus of tractus solitarius Taste fibres from anterior 2/3rd of tongue and palate
•

(AIIMS 1999)

• General sensory afferent Mesencephalic nucleus of trigeminal A part of skin of ear, proprioceptive impulses from muscles
•
of face
Anatomy 43

Branches
Within the facial canal • Greater petrosal nerve
•
• The nerve to stapedius (AIPG 2001, 2012, KAR 1998)
•

• The chorda tympani
•
Exit of stylomastoid foramen
• Posterior auricle
•
(AIPG 2002) • Digastrics

•
• Nerve to Stylohyoid
•
Terminal branches •
•
Temporal
• Zygomatic
•
• Buccal
•
• Marginal mandibular
•
• Cervical
•
Communicating branches with
adjacent cranial and spinal nerves
ANATOMY
• Muscles of facial expression are supplied by facial nerve but levator palpebrae superioris is supplied by occulomotor
•
nerve (AIIMS 2003)

• Facial nerve is supplied by maxillary artery
•
• Greater superficial petrosal nerve is the first branch of facial nerve. It arises from geniculate ganglion.
•
• Involvement of “chorda tympanic nerve” near its point of origin in the facial canal is accompanied by paralysis of motor,
•
gustatory and autonomic functions of nerve. (AIIMS MAY 2013)

• Involvement of nerve after the level of stylomastoid foramen results in paralysis of facial muscles without dysguesia.
•
Lesions of the Facial Nerve (AIPG 2000)

Infranuclear lesion (AIPG 2008) Supranuclear lesions (COMEDK 2007)
• Whole of the face is paralyzed • Only the lower part of face of contralateral side is paralysed
•
•
• Face becomes asymmetrical and is drawn up to the normal • The upper part escapes due to its bilateral representation in the
•
•
side cerebral cortex
• Affected side is motionless
•
• Wrinkles disappear from forehead
•
• Eye cannot be closed
•
• Any attempts to smile will draw the mouth to normal side
•
• During mastication, food accumulates between the teeth and
•
the cheek
• Articulation of labials is impaired
•
Various Ganglia
• Trigeminal ganglion
•
– Crescentic or semilunar-shaped sensory ganglion of 5th cranial nerve.
–
– Lies on the trigeminal impression on the anterior surface of petrous part of temporal bone
–
– Occupies a special space of dura mater called the trigeminal meckel’s cave.
–
– The central process of the ganglion cells form the large sensory root while the peripheral process of the ganglion cells
–
forms the three divisions of the trigeminal nerve.
• Ciliary ganglion – It has sensory, motor, and sympathetic roots.

•
–
– Parasympathetic ganglion places in course of the The sensory root comes from nasociliary nerve. It

contains sensory fibres from the eyeball.
–
oculomotor nerve.
– It lies near apex of orbit between the optic nerve and The motor root arises oculomotor nerve. It carries

preganglionic fibres from Edinger-Westphal
–
tendon of the lateral rectus muscle.

nucleus to supply the sphincter pupillae and – Postganglionic fibres for the submandibular gland
–
ciliaris muscle. reach the gland through branches of the ganglion.
The sympathetic root carries postganglionic Post ganglionic fibres for the sublingual and anterior
lingual gland are supplied through lingual nerve.

fibres of superior cervical ganglion to supply the

blood vessels of eyeball and the dilator pupillae. (AIPG 1993)

– The symphathetic fibres carry the postganglionic
• Pterygopalatine ganglion (sphenopalatine ganglion)
–
fibres of superior cervical ganglion to supply to
•
– This is the largest parasympathetic peripheral submandibular and sublingual glands.
–
ganglion. – Symphatetic fibres pass through the submandibular
–
– It lies in the pterygopalatine fossa just below the ganglion without relay
–
maxillary nerve.
– Topographically it is related to the maxillary nerve, • Otic ganglion
•
–
but functionally it is connected to the facial nerve. – Topographically related to Mandibular nerve, but

(COMEDK 2006)
–
functionally it is a part of the Glossopharyngeal

– The motor or parasympathetic root is formed by the nerve.
–
nerve of pterygoid canal. – It is situated in the infratemporal fossa, just below
ANATOMY
Carries preganglionic fibres of superior salivary
–
the foramen ovale and surrounds the origin of

nucleus through the nervus intermedius, facial nerve to medial pterygoid. (AIIMS 1994)

nerve, geniculate ganglion, the greater petrosal – The preganglionic parasympathetic fibres from the
–
nerve and the nerve of pterygoid canal to reach inferior salivary nucleus are passed through the
the ganglion. glossopharyngeal nerve, its tympanic branch, the
The postganglionic fibres supply the lacrimal tympanic plexus and the lesser petrosal nerve to

glands, mucous glands of nose, paranasal sinuses, reach the ganglion.
the palate and the nasopharynx. – The postganglionic fibres reach the parotid gland
The sympathetic root is also derived from nerve
–
through auriculotemporal nerve.

of pterygoid canal. It carries postganglionic fibres (AIPG 2002, KAR 1997)

of superior cervical sympathetic ganglion to
supply the nose, the paranasal sinuses, the palate • Geniculate ganglion
•
and the nasopharynx. – The geniculate ganglion is located on the first bend of
• Submandibular ganglion
–
the facial nerve. It is a sensory ganglion.
•
– Topographically it is related to the Lingual nerve but – The taste fibres are present in the nerve area, peripheral
–
functionally it is connected to the Facial nerve.
–
process of pseudounipolar neurons present in the
– It is relay station for secretomotor fibres to the geniculate ganglion. (AIPG 2008, 2011)
–

submandibular and sublingual glands. – Fibres of GSPN arise here (in course of facial nerve)
– The parasympathetic preganglionic fibres that arise in
–
but they relay to lacrimal gland via spenopalatine
–
the superior salivatory nucleus pass through the facial ganglia. (PGI 2003)

nerve, the chorda tympani, and the lingual nerve to The three ganglions associated with facial nerve are geniculate,
reach the ganglion. (AIPG 2005) submandibular and pterygopalatine

THORAX
Thymus
Development • Endoderm of 3rd pharyngeal pouch
•
Histologically - • Cortex: lymphocytes (95% T cells) germinal centres appear in autoimmune diseases, normally absent.
•
there are two parts • Medulla: Hassal’s corpuscles, epithelial cells which secrete lymphopoietin (competence inducing factor) and
•
blood thymus barrier
Weight • At birth is 10-15grams

•
• At puberty – 30-40 grams
•
• Regresses after puberty
•
Anatomy 45

Function • Thymus is believed to produce T lymphocytes throughout life
•
Aging • Involution of thymus is
•
- Enhanced by – hypertrophy of adrenal cortex, injection of cortisone/testosterone
-
- Delayed by –castration/adrenalectomy
-
Blood supply • Inferior thoracic and inferior thyroid artery
•
Nerve supply • Vasomotor nerves derived from stellate ganglion. Capsule is supplied by phrenic nerve
•
Lymphatics • Thymus does not receive any lymph vessels, but gives off efferent vessels
•
Thyroid Gland
Development • Develops from a median endodermal thyroid diverticulum at caudal end of thyroglosaal duct
•
• Lateral thyroid develops from the 4th pharyngeal pouch
ANATOMY
•
• Position of upper end is marked by foramen caecum (COMEDK 2008)
•

• Parafollicular cells (C cells) develop from ultimobranchial body (5th pharyngeal pouch)
•
Arterial supply • Superior thyroid artery (branch of external carotid artery)
•
• Inferior TA (branch of thyrocervical trunk)
•
• Thyroidea ima (branch of brachiocephalic)
•
• Lowest TA ( trunk/arch of aorta)
•
• Parathyroid gland is by inferior thyroid artery
•
Venous drainage • Superior thyroid vein (drains into the common facial vein)
•
• Middle thyroid vein (drains into the inferior jugular vein)
•
• Inferior thyroid vein (drains into the left brachiocephalic vein)
•
• 4th thyroid vein of Kocher’s (drains into the inferior jugular vein)
•
Ribs
• Shortest, broadest and most curved 1st rib
•
• Typical ribs 3-9
•
• True ribs/ vertebrospinal ribs (cartilage connected to 1-7
•
sternum)
• Costal margin is formed by 7-10
•
• Typical vertebrae 2-8
•
• False ribs/vertebrochondral 8-12
•
• Floating ribs (vertebral ribs) 11,12
•
Trachea Trachealis muscle. This contracts reducing the size of the
 
• Length = 10-16 cm, inner diameter = 2-2.5 cm lumen of the trachea to increase the air flow rate during
coughing.
•
• It commences at the larynx (C6) and bifurcates into the
•
main bronchi (at lower border of T4). • The esophagus lies posteriorly to the trachea. The
•
• Lined with pseudostratified ciliated columnar epithelium. cartilaginous rings are incomplete because this allows the
•
• There are about 15 – 20 incomplete C-shaped cartilaginous trachea to collapse slightly to allow food to pass down the
 
esophagus.
•
rings, which reinforces the anterior and lateral sides of
the trachea to protect and maintain the airway open. • Isthmus of thyroid gland is extended between 2-4 tracheal
 
•
• There is a piece of smooth muscle connecting the rings.
•
ends off the incomplete cartilaginous rings called the • Tracheostomy is done through 2-4 tracheal rings.
•

• Trachea bifurcates at sternal angle (angle formed by Bronchopulmonary Segment
•
manubrium to body of sternum), cricoid at T5
• A bronchopulmonary segment (BPS) is a division of a lung
• Blood supply is by inferior thyroid artery (AIPG 2001)
•
that is separated from the rest of the lung by a connective
•

• Thyroid swellings are the main cause of compression of tissue septum.
•
trachea • This property allows a BPS to be surgically removed without
•
Bronchi affecting other segments.
• The trachea divides at the level of lower border of T4 • Anatomical, functional and surgical unit of the lung.
•
•
vertebra into two principal bronchi • Right lung has 10 segments; left lung has 8.
•
• Right bronchus: Wider, shorter, more vertical, 2cm in • Apical (superior) segment of lower lobe is related to
•
length
•
posterior parts of 4-8 ribs and can be examined in the
• Left bronchus: Narrower, longer, more horizontal, 5 cm triangle of auscultation.
•
in length.
• Each BPS has a tertiary (segmental) bronchus and 2
• Due to above facts, inhaled foreign body is more likely
•
arteries (bronchial and pulmonary) in the center; veins
•
to enter the right bronchus.
and lymphatics drain along the borders.
ANATOMY
• Right main bronchus divides into 2 lobar bronchi, while
 
• It does not have its own vein. Pulmonary vein is
•
the left main bronchus divides into 3 lobar bronchi.
•
intersegmental and it drains the bronchopulmonary
• The lobar bronchi divide into tertiary (segmental) segments
•
bronchi.
• It is aerated by tertiary bronchi
•
 
Lungs
Right lung Left lung

• Is divided into 3 lobes (superior, middle, inferior) by two • Is divided into 2 lobes (superior and inferior) by an oblique
•
•
fissures—horizontal and oblique. fissure. The tongue shaped projection of the superior lobe of left
 
• Weighs about 625 gm, 50 gm heavier than left lung lung below the cardiac notch is called lingula.
•
• Shorter and broader than left • Larger and narrower than right lung
•
•
• Anterior border is straight • Anterior border is interrupted by cardiac notch
•
•
Right Principal Bronchus
• Wider, shorter and more vertical than the left being about 2.5 cm long
•
• The greater width and more vertical course of the right principal bronchus explains why the foreign bodies enter it than the
•
left. (AIPG 2004)

• Inferior lobar bronchus is the terminal continuation of the principal bronchus
•
Heart
Development • Heart is the first organ to start functioning in human embryo
•
• Truncus arteriosus gives rise to ascending aorta, pulmonary trunk. Spiral septum is present in between them.
•
Development of • Muscular part–Develops from the floor of bulboventricular cavity
•
IVS • Membranous part–Develops from the bulbar ridge, and endocardial cushion proliferation
•
Arterial supply • Right Coronary A. • Right atrium
•
•
• (Two main branches are: posterior descending A. • Right ventricle and posterior 1/3 of interventricular
•
•
and marginal A.) septum
• SA Node
•
• AV node
•
• Left Coronary A. • Anterior part of right and left ventricle
•
•
• (Two main branches are: Left anterior • Lateral wall of left ventricle
•
•
descending A. and circumflex A..) • Anterior 2/3s of interventricular septum
•
• A-V groove.
•
• SA node (in 40% of cases)
•
Anatomy 47

Venous drainage • 90% drains into right atrium through coronary sinus via the great, middle and small cardiac veins.
•
• 10% drains into other chambers via the venae cordis minimis.
•
• The tributaries of coronary sinus are:
•
- Great, middle and small cardiac veins
-
- Posterior vein of left ventricle
-
- Oblique vein of left atrium (of Marshall)
-
- Right marginal vein
-
Nerve supply • Parasympathetic: Right vagus → SA node and atria; left vagus → AV node and conducting tissue.
•
• Sympathetic: Cervical and upper thoracic sympathetic ganglia
•
Valves • Tricuspid valve has 3 leaflets: Anterior (largest), septal (smallest) and posterior.
•
• Mitral valve has 2 leaflets: Anterior (larger), posterior (smaller)
•
• Pulmonary valve has 3 cusps: 1 Posterior and 2 anterior
•
• Aortic valve has 3 cusps: 1 Anterior and 2 posterior.
•
• Heart borders on Chest X ray
ANATOMY
•
Right border • Superior vena cava, right atrium and inferior vena cava.
•
Left border • Aortic arch, left pulmonary artery, aortic knuckle, left atrial appendage, left ventricle.
•
Some Importants Points About Heart
• Torus aorticus is the prominent region of the right atrial septum sited superiorly and anteriorly. It is superior to the
•
coronary sinus and anterior to the fossa ovalis. It represents the deeper and anterior surface of the posterior sinus and
cusp of the aortic valve.
• Valve of Viussens: venous valve dividing the great cardiac vein and coronary sinus.
•
• Leiden convention: is used in imaging of heart; the artery that arises from the observer’s left hand side is the left coronary
•
artery and the other is the right.
• Lymphatics drain into the tracheobronchial and mediastinal lymph nodes
•
• Left auricle forms the post-surface i.e. base of heart and lies behind the right auricle.
•
• Apex of the heart is formed by the left ventricle
•
• Membranous part of atrioventicular part of the IVS lies between the right auricle and left ventricle.
•
• Rough portion of right auricle interior forms a series of horizontal ridges called the pectinate muscles
•
• Tetralogy of Fallot is a common anmaly, accounting for about 8% of congenital heart defects. The embryological defect
•
is unequal division of the truncus arteriosus and conus cordis by the aorticopulmonary septum.
• Fossa ovalis
•
– Primary septum of fetal heart
–
– A saucer shaped depression in lower part of interarterial septum
–
– Failure of fusion of two septa (primary and secondary) gives persistent foramen ovale.
–
• Orifice of the coronary sinus is guarded by the thebesian valve while that of inferior vena cava by rudimentary Eustachian
•
valve.
• Superior vena cava doesnot have a valve
•
• Atrioventricular groove lodges the right coronary artery while left coronary artery lies in the interventricular groove.
•
Conduction System
SA node • Located at the junction of superior vena cava and right auricle subepicardially and superolaterally
•
• SA node is also known as the cardiac pacemaker as its rate of discharge determines the rate at which the heart
•
beats
• Whole conduction system including the SA node contains specialized nodal cardiac muscle
•
• SA node is supplied by right coronary artery in 60% cases and left coronary artery in 40% cases
•
AV node • Located in the right posterior portion of right atrium
•
• Koch’s triangle is a important landmark for AV node
•
Purkinje fibres • Conduction velocity is highest in Purkinje system. It is 4 m/s
•

Diaphragm
• Mesodermal in origin
•
• Develops from the fusion of septum transversum (central tendon), dorsal eosophageal mesentry and pleuroperitoneal
•
membranes
• Muscles of develop from 3,4,5 cervical myotomes and hence motor innervation is by phrenic nerve that arises from ventral
•
rami of C3, C4, and C5.
• Phrenic nerve gives sensory supply to central part. Lateral part receives it sensory supply from intercostal nerves
•
• The left phrenic nerve passes through the vena caval opening
•
• Level of diaphragm is highest in supine, and least in sitting position. It is intermediate in standing position.
•
Openings in the Diaphragm
IVC Opening Esophageal opening Aortic opening
Present in the central tendon Present in the muscular portion on the left Present in midline between diaphragmatic crura at T12
ANATOMY
portion on the right side of side at T10 vertebral level. vertebral level.
midline at T8 vertebral level.
Structures passing are: Structures passing are: Structures passing are:

 
 
• Inferior Vena cava (IVC) • Oesophagus • Aorta
•
 
•
 
•
 
• Branches of Right phrenic • Right and Left Vagus N. • Azygos V.
•
•
•
 
N. • Oesophageal branch of left gastric A. • Thoracic duct
•
 
•
 
• Accompanying veins and lymphatics. • Hemiazygos V . (passes through left crus)
•
•
 
• Sympathetic trunk (passes behind medial arcuate
•
ligament)
• Left phrenic N. (pierces the muscle of left dome)
•
 
• Subcostal N. and Vessels (pass behind lateral arcuate
•
ligament)
Thoracic duct
• Largest lymphatic channel in the body.
•
• Receives tributaries both from thorax and neck
•
• From the thorax
•
– Left intercostal lymph nodes
–
– Bilateral descending thoracic trunk
–
– Ascending lumbar trunk
–
– Posterior mediastinal nodes
–
• In neck
•
– Left jugular lymph trunk
–
– Left subclavian lymph trunk
–
– Left bronchomediastinal lymph trunk
–
ABDOMEN
• Eosophagus
•
– 25 cm long; Occupies the posterior mediastinum
–
– Extends from the cricopharyngeal sphincter to the cardia of the stomach (45 cm from teeth to cardia of stomach);
–
1.25 cm of this tube lies below the diaphragm
 
Anatomy 49

– Is the narrowest region of the alimentary tract – It has NO mesentery and is only partially covered with
–
peritoneum .
–
except for the vermiform appendix.
– Lined by stratified squamous nonkeratinising – Ligament of Trietz (LoT) – is a fibromuscular band,
–
–
epithelium which is replaced by specialised which suspends and supports the duodeo-jejunal
columnar epithelium (lower 3 cm) at the level of flexure.
 
the hiatus similar to gastric mucosa but without
– Upper GI bleed – from proximal to LoT; Lower GI
oxyntic and peptic cells
–
– Serosa is absent in esophagus bleed – from distal to LoT.
–
– Parasympathetic N. supply: Vagus through an
• Spleen
–
extrinsic and intrinsic plexus. The intrinsic plexus
•
has no Meissner’s network, which is present – Galen called it as “the organ full of mystery”
 
elsewhere through the alimentary canal, and only
–
– Spleen arises by mesenchymal differentiation along
Auerbach’s plexus is present.
–
the left side of the dorsal mesogastrium.
• Stomach (Gaster or Ventriculus) – Weight of normal adult spleen in 75-150g and is
–
situated posteriorly between the fundus of the
•
– It is the most dilated part of the alimentary canal.
ANATOMY
stomach and the diaphragm in the long axis of
–
– Mean capacity is about 30 ml at birth, 1000ml at
tenth rib.
–
puberty and about 1500ml in adults.
– The spleen is in contact with the adrenal gland,
–
• Small intestine upper pole of the kidney, the pancreas and splenic
•
– About 6m long and consists of: Short, fixed, flexure of the colon.
–
 
curved section, devoid of mesentery called – Accessory spleens or splenunculi – MC are found
–
duodenum Long mobile part attached to posterior near the hilum of the spleen.
 
abdominal wall by mesentery, and of which the – Splenic A. – branch of celiac trunk (foregut A.) –
proximal 40% constitutes the jejunum and distal
–
supplies spleen.
 
60% the ileum.
– Peyer’s patches are placed lengthwise in the
–
intestine, most distant from the attachment of the – The part of dorsal mesentery that extends between
–
mesentery. spleen and greater curvature of the stomach is
called Gastrosplenic ligament, the part of dorsal
• Duodenum
 
mesentery that extends between spleen and left
•
– It is 20-25 cm long, is the shortest, widest and most kidney is splenaorenal ligament
–
fixed part of the small intestine
Oesophagus Cobelli’s glands are present just above the cardia in the mucosa, secrete mucus. The oesophagus also contains submucosal
mucous glands.
Stomach Cardiac glands Cardiac glands are heavily branched tubular glands (similar to the
cardiac glands of the esophagus), which contain mainly mucus-
producing cells.
Small Principal (or Chief cells (of zymogenic Most numerous. Occur primarily in the body of the glands They
corpus fundic) cells) produce pepsinogen, which is a precursor of the proteolytic enzyme
Intestine glands in principal pepsin.
glands we find Parietal cells (or oxyntic
cells) Parietal cells secrete the hydrochloric acid of the gastric juice. HCI
four cell type: chief
activates pepsinogen. Parietal cell also secrete intrinsic factor, which
cells, parietal cells,
Mucous neck cells is necessary for the resorption of vitamin B12.
mucous neck cells
and endocrine Secrete mucin which protects the mucosa
cells. Endrocrine cells
Gastrin-producing cells (G cells) and somatostatin-producing cells (D
Pyloric glands cells)
Enteroendocrine glands may contain Argentaffin cells which secrete
Duodenum serotonin.
More coiled than principal glands, and they may be branched.
Endocrine cells, in particular gastrin-producing cells, are more
frequent than in principal glands. A chief cells are usually absent.
Submucosal glands of the duodenum are also called Brunner’s
glands.
Contains mucosal glands

Liver
• Largest gland in the body after the skin the largest organ of the body (AIIMS Nov 2010)
•

• Weighs 1.5 kg, covered by a fibrous capsule – Glisson’s capsule.
•
Anatomical lobes of liver • 4 lobes, right (largest), left, caudate, and quadrate.
•

(COMEDK 2005) • Reidel’s lobe is a tongue shaped projection from the Right lobe
•
Surgical lobes of the liver • (The right and left) are separated by a plane connecting the gall- bladder
•
••
and inferior vena cava.
Counaid’s segments • 8 Functional segments of liver are present, each demarcated by the vascular and biliary
•
drainage
Blood flow to the liver • Is 1500 ml/min.
•
• Of this 75% of afferent blood is conveyed by portal vein and 25% is conveyed by hepatic
•
artery.
Bare area of the liver • A triangular area devoid of peritoneal covering, it is limited by the upper and lower layers of
ANATOMY
•
the coronary ligament and the triangular ligament
• Clinically important because it represents a site where infection can spread from the
•
abdominal cavity to the thoracic cavity.
Morrison’s pouch (Hepatorenal • Commonest site of subphrenic abscess.
•
pouch, right subhepatic space)
Porta hepatis contains • Right and left hepatic ducts
•
• Right and left branches of hepatic artery
•
• Portal vein
•
• Hepatic lymph nodes
•
Sinusoids of liver • Irregular “capillaries” with fenestrated endothelium (pores 100- 200 nm in dia). NO basement
•
membrane.
• Allow macromolecules of plasma full access to basal surface of hepatocytes through
•
perinusoidal space (Space of Disse).
Space of Disse Contain cells of Ito (vitamin A synthesis) and Kupffer cells (liver macrophages)
Apical surface of hepatocytes facses bile canailiculi. Basolateral surface faces sinusoids.
Portal acnius • Zone 1 – periportal zone – affected 1st by viral hepatitis

•
• Zone 2 – intermediate zone
•
• Zone 3 – pericentral vein (centrilobular) zone: contains P 450 system, affected 1st by ischemia,
•
most susceptible to toxic injury, alcoholic hepatitis
Pancreas
• Duct of Wirsung: Main duct of pancreas
•
• Duct of Santorini: Accessory pancreatic duct
•
• Exocrine pancreas
•
– Functions: Digestive enzymes production in response to the small intestine hormones secretin and cholecystokinin. Acinar
–
 
cells secrete trypsin, chymotrypsin, pancreatic lipase, and pancreatic amylase
• Endocrine pancreas
•
– Functions: Hormone production and secretion by Islets of Langerhans.
–
– α cells secrete glucagon (AIPG 2008)
–

– β cells secrete insulin and amylin (amylin MAY act as inhibitor of insulin)
–
– δ cells secrete somatostatin
–
– PP cells secrete pancreatic polypeptide
–
– Epsilon cells secrete Ghrelin (stimulates appetite)
–
Anatomy 51

Kidney
• Right kidney is at a lower level than the left, due to the liver in the right side.
•
• Kidney has outer cortex and inner medulla (7 calyces)
•
• Structures at the hilum of kidney
•
– Renal Vein
–
– Renal Artery
–
– Renal Pelvis.
–
• Blood supply
•
– Renal A. from aorta divides into 5 segmental arteries (end arteries)
–
– Renal veins drain into IVC.
–
– The left renal V. receives the left testicular V. in the male and this may get blocked by kidney tumor producing left
–
 
varicocele.
MISCELLANEOUS – Basically G1 and G2 phase provide time for cell growth
ANATOMY
–
before and after DNA synthesis
Cell Cycle – Go phase: dormant phase
–
– The sequence is G0-G1–S–G2–M
• Cell cycle is defined as the interval between two successive
–
– Growth factors stimulate the progression of G1 into
•
mitotic divisions resulting in production of the daughter –
cells. S phase
– Two types of proteins regulate the cell cycle
• Cell cycle is divided into two major phases
–
Cyclin
•
– Interphase

Cyclin dependent protein kinases
–
– Mitotic phase

• M phase
–
• Interphase
•
•
– S phase: DNA replication (AIPG 2003) – Prophase
–
–

– G1 phase: S-phase is preceded by an interval or gap – Metaphase
–
–
– G2 phase: Precedes mitotic phase. It makes sure that – Anaphase
–
–
DNA replication is complete before starting of mitosis – Telophase
–
Prophase Chromosomes continue to condense, shorten and thicken.
Prometaphase Chromatids become distinguishable.
Metaphase Arranged along equatorial plane and double structure is clearly visible. Each is attached by
microtubule from centromere to the centriole forming the mitotic spindle.
Anaphase Beginning of anaphase marked by the division of chromosomes and migration of chromatids to
opposite poles of the spindle.
Telophase Chromosomes uncoil and lengthen. The nuclear envelope re-forms and the cytoplasm divides.
Meiosis
Takes place in exclusively in germ cells to generate sperm and oocyte with half the number of chromosomes. Meiosis has two
components
• Meiosis 1: At the beginning of meiosis I, germ cells replicate DNA so that each of 46 chromosomes is duplicated into
•
sister chromatids.. Homologous in pairs called “synapsis”. The point of attachment is called “chiasma”. After meiosis I, two
daughter cells are formed containing 23 double- structured chromosomes.
• Meiosis II: Is similar to mitosis. As a result at the end of meiosis a total of 4 daughter cells containing haploid number (23
•
single chromosomes) is formed.
Crossover
Interchange of chromatid segments between paired homologous chromosomes during meiosis I occurs.

• Genetic variability is enhanced. Third phase- 8-38 weeks The embryo grows and
•
• Each daughter cell contains haploid number which after period of matures, is now called a
•
fertilization, diploid number is restored. fetogenesis fetus. This is the period of
functional maturation.
One primary oocyte develops four daughter cells (22+X).
But only one develops into mature gamete-the “oocyte”. The Foetal Hormones and their Significance
other three develop into “polar bodies”, which degenerate
subsequently. Spermatocyte develops into 4 daughter cells: • Human chorionic gonadotropin (HCG) presence in the
•
Two with 22 plus X chromosomes and two with 22 plus Y urine of mother is used as indicator of pregnancy.
chromosomes. • Somatomammotropin (placental lactogen) is a growth
•
hormone-like substance that supplies foetus, priority on
Also Note maternal blood glucose and makes mother diabetogenic.
• Normal aminotic fluid produced is 800 ml, out of which
• Spindles are formed in the late prophase and
•
half of the amount (400 ml) is drunk by foetus itself.
•
chromosomes are attached to spindles in metaphase
• Alpha-fetoprotein is analysed in amniocentesis test.
• Genetic shuffling occurs in second meiotic division
•
ANATOMY
•
• G2, M phase cells are most susceptible to radiation • The zygote develops into blastula, morula and gastrula
•
•
injury in succession.
• Barr body is found in interphase of cell cycle • •
The formation of germinal embryonic mesoderm and
•
• Cell cycle regulators in cell growth are cyclins and endoderm is called as gastrulation.
•
kinases • The gastrula in humans is characterized by three germ
•
• Mitotic spindles are formed by microtubules which layers.
•
contain tubulins • The germ layers are the forerunners of all adult tissues
•
• Vincristine and vinblastine act by breaking and organs.
•
microtubules, while paclitaxel stabilizes them.
Colchicine is also a mitotic inhibitor. Cell Hormones
Somatotrophs Somatotropin (growth
hormone)
Radiation Injury
Mammotrophs Proclactin (Lactogenic
• In G1 phase – chromosomal aberrations may occur hormone, LTH)
•
• In G2 phase – chromatid aberrations may occur Corticotrophs Adrenocorticotropic hormone
•
• Cells are most radiosensitive in G2- M interface and most (ACTH
•
resistant towards the end of S phase. (M>G2> G1> S) Thyrotrophs Thyrotropin (TSH)
Gonadotrophs Follicle stimulating hormone,

First phase- First two weeks It involves largely celluar
leutinizing hormone, interstitial
Ovular or after fertilization proliferation and migration,
cell stimulating hormone
germinal period with some differentiation
of cell populations. Cells of pars intermedia Melanocyte stimulating
Few congenital defects hormone
result from this period of
Pars posterior Vasopressing (antidiuretic
development because, if
hormone), oxytocin
the perturbation is serve,
the embryo is lost itself Follicular cells T3 and T4
instead of teratogenesis.
High rates of lethality may Parafollicular cells (Cells) Thyrocalcitonin
occur.
Thyroid Calcitonin (AIPG 2006)

Second phase- The second Period of greatest
period of phase spans the sensitivity. This is also the Chief cell (principal cell Parathormone
embryogenesis next 4 (3-to 8) formative period of organs.
Cells of zona glomerulosa Aldosteroen,
weeks Each organ has peak
deoxycorticosterone
sensitivity. It is a particularly
vulnerable period for Cells of zona fasiculata Cortisol, cortisone
the embryo because it
involves many intricate this Cells of zona reticularis Oestrogne, androgens
period many recongnized
congenital defects develop. Medullary cells Epinephrine
Anatomy 53

Differences between infant and adult(AIPG 1999, AIIMS 1998)

• The oral cavity is small in the newborn and totally filled by the tongue due to small and slightly retracted lower jaw
•
• The newborn has a set of sucking pads in the cheeks which provide stability during sucking
•
• The soft palate and epiglottis are in contact at rest, providing an additional valve at the back of oral cavity
•
• The larynx and hyoid cartilage are higher in the neck and closer to the base of the epiglottis in an infant providing added
•
protection of the airway while feeding.
• The infant’s larynx differs markedly from its adult counterpart
•
– Although it is about one third size it is proportionally larger (AIPG 2012)
–

– Its lumen is short and funnel shaped and disproportionately narrower than that of adult
–
– It lies higher in the neck
–
Some Important Points
The receptors for specific mechanics of proprioception
ANATOMY
Ruffini endings Static mechanoreceptors which position the mandible
Pacinian corpuscles Dynamic mechanoreceptors which accelerate movement during reflexes
Golgi tendon organs Static mechanoreceptors for protection of ligaments around the temporomandibular joint
Free nerve endings Pain receptors for protection of the temporomandibular joint itself
• Parietal Pleura is Pain-sensitive.

•
• The costodiaphragmatic line of pleural reflection (inferior margin of pleura) crosses the 8th rib in the mid-clavicular line,
•
 
10th rib in the mid-axillary line, 12th rib at the lateral border of sacrospinalis muscle (8, 10, 12)
• The neurovascular bundle of the intercostal space is situated just below the upper rib. Hence in pleural tapping, the needle
•
 
is inserted just above the upper border of the rib (lower part of intercostal space) usually in midaxillary line.
• The relationship of structures in the costal groove (from above down is Vein, Artery, Nerve “VAN”.
•
• Clara cells, originally thought to be characteristic of the terminal bronchioles, are also found in more proximal levels of
•
 
the bronchial tree and even in the nasal mucosa. (AIPG 2007, 2010)

• Type 2 alveolar epithelial cells secrete surfactant.
•
• Better described as bat with extended wings–sphenoid bone (AIPG 1997, 1994)
•

Some Points about Arteries
• Highest mean velocity is seen in aorta
•
• Windkessel vessels: Distal portion of aorta and larger arteries. These have more recoil and elasticity.
•
• Maximum pressure drop occur in: Small arteries and arterioles
•
• Resistance vessels: Arterioles and small arteries
•
• Maximum total cross sectional area: Capillaries (lowest velocity)
•
• Veins contain 50% of the total circulating blood volume: capacitance vessels.
•
• Portal venous system is a valveless system
•
• Portal circulation is seen in liver and pituitary (hypophysis cerebri)
•
• Counter current multiplier system is seen in kidney and vasa recta of testis
•
• Veins which don’t have muscular tissues
•
– Dural sinuses and pial veins
–
– Veins of maternal part of placenta
–
– Retinal veins
–

– Veins of spongy bones
–
– Venous spaces of erectile tissue of penis
–
• Veins which don’t have valves
•
– Superior vena cava and inferior vena cava
–
– Very small veins having diameter less than 2mm
–
– Cerebral, emissary and pulmonary veins
–
– Hepatic, renal, ovarian and uterine veins
–
• End Arteries: Arteries which do not anastomose their neighbors
•
– Central artery of retina (absolute end artery)
–
– Central branches of cerebral artery
–
– Vasa recta of mesenteric artery
–
– Arteries of spleen, liver, kidneys, lungs
–
• Bronchial arteries supply blood for nutrition of the lung, are derived from descending thoracic aorta or upper posterior
ANATOMY
•
 
intercostal arteries.
• Right bronchial veins drain into the azygous vein, the left bronchial vein drain into the hemiazygous vein.
•
• Internal thoracic artery terminates in the sixth intercostal space by dividing into the superior epigastric and musculophrenic
•
 
arteries.
• Pulsations felt in the suprasternal space is due to inferior thyroid artery. (AIPG 1999)
•

• Capillaries: 3 types
•
– End to end–labial branches of facial artery, intercostal artery
–
– Convergent: Vertebral arteries to form basilar artery
–
– Transverse
–
• Arteriovenous shunts
•
– Rich arterio venous anastomosis are present in skin of nose, lips, ear lobule, thyroid mucosa.
–
– These are under autonomic control in skin. They regulate regional blood flow, blood pressure, temperature
–
(thermoregulation)
Some Points About Nerves

• Nerve supply of pinna is by mandibular nerve.
•
• Nervus intermedius of Wrisberg: Sensory component of facial nerve
•
• Jacobson’s nerve: tympanic branch of the ninth nerve. Forms the tympanic plexus in middle ear and enters the petrous
•
bone through tympanic canaliculus
• Arnold’s/A; derman’s nerve: Auricular branch of vagus
•
• Vidian nerve: Nerve to pterygoid canal. Formed in foramen lacerum. Gives the autonomic supply to nasal sinuses (nerve
•
of Hay fever)
– Vidian neurectomy is done in Vasomotor rhinitis
–
• Median nerve is also called the laborer’s nerve as it controls the coarse movements of hand.
•
• Ulnar nerve is also called Musician’s nerve as it controls the fine movement’s of hand
•
– Ulnar nerve has got the worst and radial nerve has the best prognosis in repair of nerve.
–
• Cubital Tunnel syndrome
•
– Commonly seen in guitarists
–
– A common problem among both acoustic and electric guitar players, as well as other stringed instrument player, is the
–
development of forearm pain, tingling and numbness, typically on the same side you fret the instrument. This type of
repetitive injury is called the cubital tunnel syndrome.
Anatomy 55

– It typically involves the ring and little fingers since these fingers receive their nerve supply from the ulnar nerve(
–
musician’s nerve) (AIIMS May 2008)

– The main cause is the compression of the ulnar nerve
–
– Since the ulnar nerve passes between the muscles that perform flexion of the wrist, bending of the fingertips and
–
stretching the little finger to reach the higher frets can irritate the muscles surrounding this nerve with constant overuse
of these muscles, they can become inflamed. This is especially evident in guitarists who have not developed strength in
the forearm musculature in preparartion of hours of practice time. This swelling starts squeezing down the ulnar nerve.
• Sluder’s neuralgia: Neuralgia of the sphenopalatine ganglion. There is sharp nasal pain in the distribution of anterior
•
ethmoidal nerve.
• Shy-Drager syndrome is a degenerative disorder of the nervous system. Multiple areas of the nervous system can be
•
affected, such as the parts that control motor and involuntary functions. The motor system controls movement and
balance. The involuntary, or autonomic, nervous system controls body functions (for example, blood pressure, bowel
and bladder function). Shy-Drager syndrome may cause postural hypotension. Postural hypotension is a drop in blood
pressure after changing position that can result in dizziness or fainting. (AIIMS Nov 2013)
ANATOMY

Some Points about Muscles
• Exceptions regarding nerve supply of muscles
•
– All the muscles of facial expression are supplied by facial nerve except for “levator palpebrae superiors” which is supplied
–
by oculomotor nerve.
– All the muscles of eye except superior oblique and lateral rectus are supplied by third or oculomotor nerve. The superior
–
oblique is supplied by 4th cranial or trochlear nerve (SO4). The lateral rectus is supplied by the 6th or abducent nerve
(LR6).
– All the muscles of tongue are supplied by hypoglossal nerve except for palatoglosus which is supplied by the cranial part
–
of accessory nerve through the pharyngeal plexus. (AIPG 2003, 1999, MAN 1999, AP 2006)

– All the muscles of larynx are supplied by the recurrent laryngeal nerve except for cricothyroid (only intrinsic muscle
–
lying on the external aspect of the larynx) which is supplied by the external laryngeal nerve.(NEET 2013, MAN 2000)

– All the muscles of pharynx are supplied by the cranial accessory nerve through branches of vagus except the
–
stylopharyngeus, which is supplied by the glossopharyngeal nerve. (AIPG 1996, 1999, AIIMS 1998, 2002, Nov 2012)

– All the muscles of the soft palate are supplied by the cranial accessory nerve through vagal branches except for tensor
–
palati which is supplied by the mandibular nerve. (AP 2009)

– All the infrahyoid muscles are supplied by ansa cervicalis (formed by superior and inferior roots. The superior root
–
of continuation of the descending branch of the hypoglossal nerve and its fibres are derived from the first cervical
nerve. The inferior root is derived from spinal nerves C2 and C3) except for thyroid, which is supplied by C1 through
hypoglossal nerve. (AIIMS 2006, MAN 1995)

• Masseteric notch (AIIMS May 2013)
•

– The buccinators muscle joins the superior constrictor at the pterygomandibular raphae distal to the retromolar pad
–
area. It is buccal to this area that the action of masseter muscle pushes the buccinators muscle towards the retromolar
pad. The impression is reflected superiorly and medially forming a notch/groove called the masseteric notch or
masseter groove. To record the action of the masseter muscle, the patient is asked to willfully close the mouth against
resistance. If the distobuccal flange of the mandibular denture base is not contoured to allow freedom for masseter
muscle action, the denture will be dislodged.
Good to know Points

• Azygos means unpaired.
•
• Sibson’s fascia (suprapleural membrane)= the diaphragm of the inlet of the thorax.
•
• Afferent fibres of cornea pass through trigeminal nerve while efferent come from by facial nerve (AIPG 2006)
•


• Genomic imprinting: Leads to preferential expression of an allele depending on its parental origin.
•

(AIPG 2006, 2005)

– Maternal genomic imprinting: Inactivation of the maternal allele
–
– Paternal genomic imprinting: Inactivation of gene on paternal allele
–
– Deletion of only functional allele results in genetic syndromes
–
– Prader willi syndrome: Deletion of paternally derived chromosome
–
– Angelmann syndrome: deletion of maternally derived chromosome
–
• Basal ganglia doesn’t contain thalamus
•
• Occulomotor nerve doesn’t forms the floor of the 3rd ventricle
•
• Ptosis may occur due to damage to occulomotor nerve (KAR 2000, AIPG 1998, MCET 2007)
•

• Not a branch of external carotid artery: Anterior ethmoidal artery
•
• Not a branch of intracavernous portion of internal carotid artery – ophthalmic artery (AIPG 2014)
•

Mandible is not a pneumatic bone (NEET 2013, AIPG 2012)
ANATOMY
•
•

• Prevertebral fascia is not in posterior relation to Scalenus anterior
•
• Vitelline vein does not form superior vena cava
•
• Structure which does not pass through the foramen magnum is spinal cord
•
• Lower articular surface is formed by head of mandible.
•
• Lymphatics are not found in brain, choroid, internal ear
•
• Trapezius is not inserted in the first rib
•
• Left phrenic nerve does not pass through esophageal hiatus
•
• Right bronchomediastinal lymph trunk does not supply the thoracic duct
•
• Stare cells, stellate cells and malpighian bodies are present in spleen
•
• Kupffer cells are present in liver
•
• Reticular cells, plasma cells, memory cells are present in lymph nodes.
•
• Ligaments: Fibrous bands which connects bone to bone. This is a position and movement sensor
•
• Tendon: Muscle to bone
•
• Synovial membrane lines the interior of the joint except the articular surfaces that are covered by hyaline cartilage. It has
•
poor nerve supply.
• Cartilage: Has no blood vessels, no nerve supply and no lymphatics. It contains anti-angiogenic factor.
•
• Capsule and Ligaments: Rich nerve supply and blood supply. Acutely sensitive to pain and stretches.
•
• Mosaicism: Genetically different cell types arise from single zygote. Usually present in mammals e.g. Turner syndrome
•

(AIPG 2010)

• Chimerism: Genetically different cell originate from more than one zygote.
•
Papillae of Tongue
Filliform papillae • Keratinized thread like and give the tongue a characterized velvety appearance
•
• Conical papillae
•
• Smallest and most numerous
•
• Do not contain taste buds (AIPG 2008)
•

Fungiform papillae • Mushroom shaped
•
• Numerous near the tip and margins of tongue
•
• Distinguished by their bright red colour
•
• Contain a few (one to three) taste buds found only on the dorsal surface. (AIIMS 1990)
•

Anatomy 57

Circumvallate • Present in front of the V shaped sulcus terminalis (AIPG 2000)
•

papillae • Large in size and 8-12 in number
•
• Contain the maximum taste buds. (AIIMS 1993)
•

• •
Von ebners salivary gland ducts open into its trough
Foliate papillae • Present on the lateral border of posterior parts of tongue

•
• Contains taste buds
•
Plexuses
• Coeliac plexus (Solar plexus)
•
– Largest major abdominopelvic autonomic plexus
–
– Situated on the aorta and surrounds coeliac trunk. It is anteromedial to sympathetic chain (AIPG 2011)
–

– It is posterior to the stomach and lesser sac, anterior to the crura of diaphragm at the level of T12 and L1
–
– Surrounds the coeliac trunk and the root of superior mesenteric artery
–
• Superior hypogastric plexus: Lies in front of bifurcation of aorta
ANATOMY
•
• Inferior hypogastric plexus: Contains pelvic splanchnic nerves
•
• Dangerous areas
•
– Of the scalp: Layer of loose areolar tissue of scalp as emissary veins open here which may transmit the infection to
–
venous sinuses (AIPG 2014, AIIMS May 2013)

– Of eye: Ciliary body
–
– Of nose: Olfactory area
–
– Of face: Infection of the lower part of nose and upper lip may be transmitted directly to cavernous sinus through
–
the facial vein and its communications i.e. superior ophthalmic vein and deep facial vein. Infection first enters the
brachiocephalic vein. (AIPG 2014, 2010, NEET 2013, AIIMS Nov 2013)

Lymphatic Drainage
• Tonsils: Jugulodigastric lymph nodes
•
• Tongue: Jugulo omohyoid
•
• Thyroid and parotid: Deep cervical lymph nodes
•
• Cervical part of esophagus: Paratracheal and deep cervical lymph nodes
•
Various Triangles
• Koch’s triangle
•
– Important landmark for AV node
–
– Boundaries includes – tendon of Todaro, Coronary sinus and base or septal leaflet ring of Tricuspid valve
–
• Triangle of auscultation
•
– Bounded by 2 muscles and scapula
–
Superiorly: Trapezius

Inferiorly: Latissimus dorsi

Laterally: Medial wall of scapula

– Rib 7 and rhomboideus major lie in the floor of triangle
–
• Calot’s triangle
•
– Bounded by cystic duct (right), common heaptic duct (left) and porta hepatis (base).
–
– Contains cystic srtery, right hepatic artey, accessory right hepatic artery and accessory bile ducts
–
– Important landmark during cholecystectomy
–

• Trautmann’s triangle
•
– Bounded by sigmoid sinus posteriorly, bony labyrinth anteriorly and superior petrosal sinus or dura above
–
Angles
• Sternal angle: Formed when second costal cartilage joins the sternum at this level. Also known as angle of Louis
•
• Renal angle: Formed between 12th rib and erector spinae
•
• Citelli’s angle: Also known as sinodural angle, situated between the sigmoid sinus and middle fossa.
•
• Solid angle: Area of intersection of three bony semicircular canals
•
• Alpha angle: Formed by the intersection of the visual axis with the optical axis at the nodal point
•
• Kappa angle: Angle between the pupillary axis
•
ANATOMY
CHAPTER 2
Biochemistry
Objectives
• Carbohydrates • Informational Macromolecules

• Lipids • Vitamins and Minerals

• Proteins • Miscellaneous

• Enzymes

CARBOHYDRATES
• Classification of carbohydrates

Monosaccharides Oligosaccharides Trisaccha- Polysaccharides
rides
Aldoses Ketoses Disaccharides E.g. raffinose Homopolys Hetreropolysaccharides /
accharides mucopolysaccharides
E.g. glucose E.g. fructose Reducing Nonreducing E.g. starch E.g. hyaluronic acid
E.g. maltose E.g. sucrose (cane Dextrin Keratin sulphate
(malt sugar) sugar) (KAR 1997,
AP 1998)
Lactose (milk Trehalose Inulin
sugar)
Glycogen Chondroitin sulphate
Cellulose Heparin sulphate
• Maltose: glucose + glucose AIPG 2012, AP 2006, AIIMS Nov 2013

•

• Lactose: glucose + galactose (MAN 1995)
•

• Sucrose: glucose + fructose (COMEDK 2005)
•

• Trihalose: glucose + glucose
•
• Starch: α-D-Glucose
•
• Amylase: (15 – 20%)–non branching structure (α 1-4)
•
• Amylopectin (80- 85%)–branched after 24-30 residues (α 1-6)
•
• Glycogen: α D-Glucose α 1-4 highly branched
•

• Inulin: fructosan
•
• Cellulose: β- D Glucopyranose (β 1-4 ) β- D Glucopyranose
•
Humans lack hydrolases which attacks β linkages
• Chitin: N acetyl glucosamine (β 1-4)
•
– Structural polysaccharide of invertebrates
–
Mucopolysaccharides
• Hyaluronic acid: glucoronic acid + N- acetyl glucosamine ( no sulphate)
•
• Chondroitin sulphate: glucoronic acid + N- acetyl galactosamine
•
• Dermatan sulphate: iduronic acid + N- acetyl galactosamine
•
• Keratin sulphate I + II: N-acetyl glucosamine + glucuronic acid (10%) or iduronic acid (90%)
BIOCHEMISTRY
•
• Heparin sulphate: glucosamine + glucoronic acid
•
• Isomers: have same molecular formula but different structure
•
• Enantiomers: stereoisomers that are mirror images of each other
•
• Epimers: Two sugars that differ in configuration at only one chiral centre. Eg galactose is epimer of glucose at position 4,
•
while mannose is a epimer of glucose at 2nd position.
• Anomers: isomers of monosaccharides that differ in configuration at the carbonyl carbon atom.
•
• Mutarotation: involves interconversion of α and β forms of the monosaccharide with intermediate formation of the linear
•
aldehyde or ketone which results in optical rotation of a sugar in solution.
• When sucrose is hydrolysed there is inversion of optical rotation from dextro rotatory to levo-rotatory. Hence the enzyme is
•
called invertase. The hydrolysed mixture of sucrose containing glucose and fructose is known as invert sugars.
• A method for synthesis of higher monosaccharides from lower one is called Killiani Synthesis.
•
• Starch and glycogen are the carbohydrate reserves of plants and animals respectively.
•
• Cellulose is not digested in humans (KCET 2007)
•

• Glucose–Energy currency among carbohydrates (ATP is the energy currency of the cell) (AIPG 2010)
•

– Shows stereo as well as optical isomerism
–
– Transport is mainly by active transport.
–
– Absorption of glucose from intestinal lumen into the intestinal cells is by Sodium dependent glucose transporter
–
(SGluT)
– Intestinal cells release glucose into the bloodstream by the carrier mechanism called glucose transporter type 2
–
(GluT2)
– The GluT 4 has been implicated in Type 2 diabetes mellitus.
–
Glucose Transporters
Name Distribution
GLUT - 1 • Is widely distributed in fetal tissues Levels in cell membranes are increased by reduced
•
• In adults: highest level in erythrocytes and endothelial glucose levels and decreased by increased glucose
levels
•
cells of blood brain barrier
• Responsible for the low level of basal glucose uptake
•
required to sustain respiration in all cells
GLUT - 2 • Expressed by renal tubular cells, intestinal epithelial cells, Is a high capacity and low affinity isoform
•
liver cells and pancreatic beta cells.
• All three monosaccharides are transported from the
•
intestinal mucosa cell into the portal circulation by GLUT-2
Biochemistry 61

Name Distribution
GLUT - 3 • Expressed mostly in neurons and in the placenta Is a high affinity isoform
•
GLUT - 4 (AIPG 2009) • Found in adipose tissue and skeletal muscle Is insulin regulated
•
Disease Accumulated product Deficient enzyme
Hunter Heparin sulphate, dermatan sulphate Iduronate sulfatase
Hurler + Scheie Heparin sulphate, dermatan sulphate α L iduronidase
Mucolipoidosis VII Heparin sulphate, dermatan sulphate β glucoronidase
San filippo A Heparin sulphate N- acetyl glucosaminidase
San filippo B Heparin sulphate N- acetyl glucosamine 6 sulphatase
BIOCHEMISTRY
• General appearance of Mucopolysaccharidosis
•
– Coarse facies – Corneal clouding
–

– Hepatitis – Splenomegaly
–

– Joint stiffness – Hernias
–

Identification of Unknown Solution
Unknown solution
↓
Molisch’s Test
(formation of furfural or furfural derivatives)
(molisch’s reagent – 10% solution of α-naphthol in ethanol)
↓
Carbohydrates present (+) Carbohydrates absent (-)

Reducing tests: fehling’s test
Benedict’s test
↓
Reducing sugars present (+) Reducing sugars absent(-)

(mono/disaccharides) Sucrose/ polysaccharides

↓ ↓

Barfoed’s test Iodine test

↓ ↓

(-) (+) (-)
disaccha- Polysaccharides sucrose
rides
Eg glucose Phenyl hydrazine test
Fructose(salvinoff’s test) Eg lactose
Galactose ( Tollen’s test) Maltose
Pentose (Orcinol test)
• All reducing sugars form characteristic osazone crystals.

•
– Glucose and fructose form needle shaped crystals
–
– Maltose forms sun flower shaped crystals
–
– Lactose forms hedge hog shaped crystals
–

Glycolysis
• Defined as sequence of reactions converting glucose to pyruvate ( in aerobic conditions) or lactate ( in anaerobic conditions)
•
with the production of ATP.
• Occurs in cytosol
•
• Glycolysis is the major pathway for ATP synthesis in tissues lacking mitochondria e.g. RBCs, cornea, lens etc.
•
• Glycolysis is essential for brain, which is dependent on glucose for energy.
•
• Products formed:
•
– During aerobic conditions: 2 Pyruvate + 8 moles of ATP per glucose
–
↓
Enters the citric acid cycle to produce CO2 +H2O + 30 ATP
– During anaerobic conditions: Lactate + 2 moles of ATP per glucose
–
Glycolysis/ EMP pathway
BIOCHEMISTRY
(Emberdon Meyerhof Pathway)
Fig.2.1 Glycolysis/EMP pathway
Points and Note

• Most of the reactions are reversible in glycolysis except the following 3, which are also the major sites of regulation of
•
glycolysis. These are:
hexokinase

– Glucose Glucose 6- phosphate
–
phosphofructokinse

– Fructose 6 phosphate Fructose 1,6 bisphosphate
–
Pyruvate kinase

– Phosphoenol pyruvate Pyruvate
–
Biochemistry 63

• Glucokinase is under the influence of insulin, but its isoenzyme hexokinase is not.
•
• Hexokinase is a key glycolytic enzyme, while glucose 6 phosphatase is a key gluconeogenic enzyme. (AIPG 1999)
•

• Phosphofructokinase is an important rate limiting enzyme in glycolysis.
•
• The inhibition of glycolysis by oxygen is known as Pasteur effect.
•
• Enolase enzyme is inihibited by fluoride. For blood glucose in laboratory, fluoride (usually NaF) is added to prevent
•
glycolysis by the cells, that blood glucose is correctly estimated. (AIPG 2005, 2007)

• Substrate level Phosphorylation: Synthesis of ATP without the involvement of electron transport chain. Examples of
•
substrate level phosphorylation in glycolysis are:
Phosphoglycerate kinase
– 1,3 bisphosphoglycerate 3-phosphoglycerate
–
Pyruvate kinase
– Phosphoenol pyruvate pyruvate
BIOCHEMISTRY
–
• In citric acid cycle: substrate level phosphorylation occurs at:
•
Succinate thiokinase (AIPG 2002)

– Succinyl CoA succinate
–
• Disorders associated with impaired glycolysis • Fate of Pyruvate
•
•
– Pyruvate kinase deficiency – hemolytic anaemia – To lactate –
–

–
– Hexokinase deficiency - leads to low concentration of pyruvate + NADH lactate dehydrogenase lactate + NAD

–
1, 3 BPG which is precursor of 2,3 BPG. Consequently CO2

the haemoglobin of these patients with low level of 2,3 – To acetyl CoA- (BHU 2012)
–

BPG have higher oxygen affinity, oxygen saturation Oxidative decarboxylation – takes place in mitochondrial

curve shifts to left. membrane (AIIMS 1991)

– During starvation, the levels of fructose 2, 6 Pyruvate dehydrogenase complex
–

bisphosphate decreases which decreases the activity of
PFK and increases that of phosphate thus determining ↓
whether synthesis or degradation of glucose occurs. Pyruvate acetyl CoA +CO2

Pyruvate Dehydrogenase Complex
Multienzyme complex containing 3 enzymes and 5 coenzymes
Enzymes Coenzymes
Pyruvate dehydrogenase TPP (AIPG 2009)

Dihydrolipoyl transacetylase FAD
Dihydrolipoyl dehydrogenase NAD
CoA-SH
Lipoic acid
Genetic Defect in pyruvate Dehydrogenase Complex

• Leads to - Lactic acidosis (AIPG 2012)
•

– Neurologic disorder
–
Cori’s cycle accumulated in the muscle tissues. the muscle cramps,
often associated with strenuous muscular exercise, are
• In an actively contracting muscle, only about 8% of
thought to be due to lactate accumulation.
•
the pyruvate is utilised by the citric acid cycle and the
• Lactate cycle or cori’s cycle was described by Carl Cori and
remaining molecules are therefore reduced to lactate.
•
Gerty Cori for which they were awarded Nobel Prize in
• The lactic acid thus generated should not be allowed to 1947.
•

Cori’s Cycle
Citric Acid Cycle

BIOCHEMISTRY
Fig.2.2 Citric acid/ kreb’s cycle
• Proposed by Sir Hans Krebs in 1937 for which he was awarded Nobel prize in 1953.
•
• Final common oxidative pathway that oxidizes acetyl CoA to CO2.
•
• Source of reduced co enzymes that provide the substrate for the respiratory chain.
•
• Acts as a link between catabolic and anabolic pathways (amphibolic role).
•
• It provides precursors for synthesis of amino acids and nucleotides.
•
• 12 high energy bonds are produced per turn of citric acid cycle.
•
• Fat cannot be converted to glucose
•
• TCA cycle is regulated by the need for ATP.
•
Gluconeogenesis
• Process by which new glucose is synthesized from non carbohydrate precursors like lactate and gluconeogenic amino
•
acids. (MAN 2002)

• Occurs mainly in liver
•
• Gluconeogenesis involves several enzymes of glycolysis. The irreversible steps in glycolysis are circumvented by four
•
enzymes which are designated as the key enzymes of gluconeogenesis.
Biochemistry 65

Irreversible steps in glycolysis Corresponding key gluconeogenic enzymes
• Pyruvate kinase • Pyruvate carboxylase; phosphoenol pyruvate- carboxy kinase
•
•
• Phosphofructokinase • Fructose 1,6- bisphosphatase
•
•
• Hexokinase • Glucose 6 – phosphatase
•
•
• The first reaction of gluconeogenesis, carboxylation of pyruvate to oxaloactetate is catalysed by a mitochondrial enzyme,
•
pyruvate carboxylase, occurs in mitochondria. (AIPG 1999)

• Rest of the reactions take place in cytosol. This is achieved by the malate shuttle.
•
• The reactions are catalysed by the iso-enzymes of malate dehydrogenase (MDH); one mitochondrial and other cytosolic.
•
• Energy requirement:
•
Glycolysis (generates 2 ATPs)
BIOCHEMISTRY
Glucose Lactate
Gluconeogenesis ( utilises 6 ATPs)
• Substrates for Gluconeogenesis: Glycogen

•
– Lactate: Most important substrate.
• Glycogen phosphorylase is activated by glycogen and
–
– Glucogenic Amino Acids: most important–alanine
•
adrenaline. Glycogen synthase is activated by insulin.
–
the glucogenic amino acids are transaminated to TCA

cycle intermediates so that they form oxaloacetate or (COMEDK 2005)

pyruvate. • Glycogen is the carbohydrate reserve of the body. The
•
– Glycerol: The glycerol part of fat is phosphorylated in degradation of stored glycogen in liver and skeletal muscle
–
the liver cytosol by ATP to glycerol 3 phosphate which (skeletal muscle contains highest glycogen content in the
is then oxidised to dihydroxy acetone phosphate by an body) constitutes glycogenolysis.
NAD+ dependent dehydrogenase.
• Because of absence of enzyme glucose 6 phosphatase in
– Propionyl CoA: Formed from odd chain fatty acids.
•
muscle, free glucose is not produced. Therefore liver is
–
Even chain fatty acids cannot be converted to
the major glycogen storage organ to provide glucose in
glucose. (AIIMS 2006)
circulation.

Chemiosmotic Hypothesis • Glycogen storage disorders are inborn metabolic
•
• Also known as Mitchelle hypothesis disorders. Term given by Garrod in 1908.
•
• Explains how the free energy generated by the transport
•
of electrons by the electron transport chains is used • Von – Gierke’s Disease:
•
to produce ATP from ADP +iP i.e. it links the ATP – Most common glycogen storage disorder
production and respiratory chain.
–
– Glu-6-Phosphatase is deficient
–
• Proton pump: – Fasting hypoglycaemia that does not respond to
•
–
– Electron transport is coupled by transport of stimulation by adrenaline
–
protons across the inner mitochondrial membrane – Hyperlipidemia, lactic acidosis and ketosis are also
–
from the matrix to the inter membrane space. This seen
process creates across the inner mitochondrial – Glu 6-P is accumulated which is channelled to
–
membrane an electrical gradient and a pH gradient HMP pathway producing more ribose and more
nucleotides.
– Purines are then catabolised to uric acid, leading to
• ATP synthesis
–
hyperuricemia.
•
– Synthesize ATP, utilizes the energy of the proton – As glycogen gets accumulated in liver, it may
–
–
gradient generated by the electron transport chain produce cirrhosis due to massive liver enlargement.

Disease Deficient enzyme Salient features
• Fasting
Type I:
•
Glucose 6-phosphatase • Hypoglycaemia
Von Gierke’s disease
•
• Hepatomegaly
•
Type II: • Liver, heart and muscle affected;
Lysosomal maltase(MCET 2007)
•
Generalised glycogenosis; Pompe’s Disease • Death before 2 years
•
Type III: • Highly branched dextrin accumulates;
Limit Dextrinosis; Debranching enzyme
•
Cori’s disease • Hepatomegaly
•
Type IV: • Glycogen with little branches
Amylopectinosis Branching enzyme
•
Anderson’s disease • Hepatomegaly
•
BIOCHEMISTRY
Type V:
Muscle phosphorylase • Exercise intolerance
McArdie’s disease
•
Type VI:
Liver phosphorylase • Hypoglycaemia
Hers disease
•
Type VII:
Muscle PFK • Accumulation of glycogen in muscles
Tarui’s disease
•
Type VIII Liver phosphorylase kinase
Type IX:
Glycogen synthase
Lewis disease
HMP Pathway
• Known as
•
– Hexose Mnophosphate Pathway (HMP)
–
– Pentose phosphate pathway
–
– Dickens- Horecker pathway
–
– Shunt pathway
–
– Phosphogluconate oxidative pathway
–
• Generates NADPH required for reductive biosynthesis of steroid, fatty acids and cholesterol. (AIPG 2010)
•

• Also provides pentose sugars ( ribose and deoxyribose) for nucleic acid synthesis.
•
• NADPH, glutathione and glutathione reductase are required to preserve the integrity of RBC membrane. (AIPG 2009)
•

• NADPH is also required for maintaining the transparency of the lens of the eye. (AIPG 2010)
•

• ATP is neither utilized nor produced by the HMP shunt pathway.
•
• Glucose 6 phosphate dehydrogenase (G6PD) is the rate limiting enzyme here.. In clinical practice, it is one of the most
•
common enzyme deficiency seen. It is a X- linked condition.
• G 6PD deficiency can lead to drug induced haemolytic anaemia. This deficiency is only manifested in the presence of
•
certain drugs or toxins such as: antimalarial drugs like primaquin and ingestion of fava beans ( favism). Sulpha drugs and
furadantin may also precipitate the hemolysis. (AIPG 2012)

– This is characterised by jaundice and severe anaemia.
–
– G 6PD deficient persons will show increased methemoglobin in circulation, even though cyanosis may not be manifested.
–
Rapport- Leubering Cycle
• It occurs in erythrocytes and is mainly concerned with production of 2,3- BPG (2,3 – biphosphoglycerate). In presence of
•
2,3- BPG, oxyhemoglobin unloads more oxygen to the tissues.
Biochemistry 67

• Increase in erythrocyte 2,3 BPG is seen in hypoxic conditions, high altitude, fetal tissues, and anaemic conditions. In all
•
these cases 2,3 BPG will enhance the supply of oxygen to tissues.
• It is supplemental pathway to glycolysis. It is mainly concerned with the synthesis of 2,3- BPG in the RBC.
•
Glycosaminoglycans (GAGs)
• The major GAGs are
•
– Hyaluronic aid
–
– Chondroitin sulphate
–
– Keratin sulfate I and II
–
– Heparin
–
– Heparan sulfate
–
– Dermatan sulfate
BIOCHEMISTRY
–
• GAGs are made of repeated disaccharides unit containing a uronic acid + hexosamine
•
• Hexosoamine may be either galactosamine or glucosamine
•
• Uronic acid is either glucoronic acid or iduronic acid
•
• GAGs are degraded by lysosomal hydrolases, the genetic deficiency of which results in MPS or hurler’s syndrome
•
• Heparin is an intracellular component of mast cells and functions predominantly as an anticoagulant and lipid clearing
•
agent, whereas heparin sulphate may be extracellular or an integral or ubiquitous component of the cell surface in many
tissues including blood vessel walls, amyloid and brain.
• Genetic deficiency of lysosomal hydrolases responsible for dermatan sulphate and/ or heparin sulphate metabolism lead
•
to Mucopolysaccharidoses.
Good to Know
• Normal fasting blood glucose value is 70-110 mg/dl.
•
• Major factors that cause entry of glucose into blood are: absorption from intestines, glycogenolysis and gluconeogenesis.
•
• Rate limiting step in glycolysis is catalyzed by phosphofructokinase (PFK-1).
•
• Glucose 6 phosphate is an important compound that joins several metabolic pathways viz. Glycolysis, glycogenolysis,
•
glycogenesis, gluconeogenesis and pentose phosphate pathway.
• Oxidase–peroxidase enzyme system is used to determine glucose in urine and blood.
•
• Major factors that cause depletion of glucose in blood are: utilization by tissues, glycogenesis and conversion to fat.
•
• Hyperglycemic hormones are Glucagon, Cortisol, Adrenaline and Growth hormone.
•
• Insulin is a hypoglycaemic hormone
•
• Reducing substances in urine other than glucose are fructose, lactose, galactose, pentoses, homogenistic acid, salicylates,
•
glucoronides and ascorbic acid.
• Hereditary fructose intolerance is due to deficiency of enzyme aldolase B
•
• Galactose is necessary for synthesis of lactose.
•
• Galactosemia is due to deficiency of galactose 1-phosphate uridyl transferase enzyme.
•
• Lactose free diet is the treatment for galactosemia.
•
• Alcohol is metabolised by alcohol dehydrogenase and aldehyde dehydrogenase. (AIPG 2008)
•

• HMP shunt and uronic acid pathway are considered as alternative pathways to glycolysis.
•
LIPIDS
• Lipids may be defined as compounds which are relatively insoluble in water, but freely soluble in nonpolar or organic
•
solvents like benzene, chloroform, ether, hot alcohol, acetone, etc.

• Lipids are classified into simple, compound, derived lipids.
•
– Compounds lipids are subclassified into phospholipids containing phosphoric acid, non-phosphorylated lipids and
–
sublipids.
– Compound lipids contain molecules other than fatty acids.
–
Phospholipids, containing phosphoric acid
• Nitrogen containing glycerophosphatides: • Lecithin – phosphatidyl choline
•
•
• Cephalin – phosphatidyl ethanol amine
•
• Phosphatidyl serine
•
• Non-nitrogen glycerophosphatides • Phosphatidyl glycerol
•
•
• Phosphotidyl inositol
•
• Diphosphotidyl glycerol (cardiolipin)
•
BIOCHEMISTRY
• Plasmalogens, having long chain alcohol • Choline plasmalogen

•
•
• Ethanocholine plasmalogen
•
• Phospho sphingosides with sphingosine • Sphingomyelin
•
•
Non- phosphorylated Lipids
• Cerebrosides (ceramide monohexosides)

•
• Glycosphingolipids (carbohydrates) • Globosides (ceramide oligosaccharides)
•
•
• Gangliosides (having N- acetyl neuramic acid)
•
• Sulphated cerebrosides
•
• Sulpholipids or sulphates • Sulphated globosides
•
•
• Sulphated gangliosides
•
• Fatty acids are classified as:
•
– Depending on the number of carbon atoms
–
– Depending on the length of hydrocarbon chain
–
– Depending on the nature of hydrocarbon chain
–
• Fatty acid with 4 to 6 carbon atoms are called short chain fatty acids ( SCFA) (e.g. Butyric acid) and those with 8 to 14
•
carbon atoms are called medium chain fatty acids (MCFA) (e.g. Lauric acid)
• MCFA digestion does not require pancreatic lipase and bile salts. They diffuse directly into portal circulation.
•
• Sphingomyelins are the only sphingolipids which contain phosphate and does not contain a sugar residue.
•
Disease Enzyme deficiency Metabolite
Goucher’s disease Glucocerbrosidase Glucocerebroside
Nieman pik disease Sphingo myelinase Sphinomylein
Fabry’s disese Alpha galactosidase Ceramide
Krabbe’s disease Galacto cerebrosidase Galacto cerebroside
Metachromatic leucodystrophy Aryl sulfatase A Sulfatide
• Deficiency of enzymes of sphingolipid metabolism results in sphingolipidosis, a group of inborn metabolic disorders
•
Sphingolipidosis resulting in accumulation of specific lipid residues.
• Mental retardation, neurologic deficit and skeletal abnormalities are common presenting symptoms.
•
Biochemistry 69

• Enzyme sphingomyelinase is deficient and sphingomyelin is accumulated in tissues. (AIPG 2011)
Niemann-Pick
•

• Salient features are severe mental retardation, hepatosplenomegaly and cherry red spot in macula of retina.
Disease:
•
•
•
Death usually occurs by the age of 2 years.
Gaucher’s death • Due to absence of the enzyme beta glucosidase. Glucocerebroside is accumulated.
•
Tay Sachs • Due to absence of hexosaminidase and ganglioside is accumulated.
•
disease • Death usually occurs by the age of 3 years.
•
• Essential fatty acids: (KAR 2000, MAN 1995, 1997, 1998)
•
– linoleic acid ( 2 double bonds)
–
– linolenic acid ( 3 double bonds) these both cannot be synthesized in the body.
–
– Arachidonic acid: synthesized in the body but not sufficient.
–
BIOCHEMISTRY
• Normal dietary allowance of PUFA (polyunsaturated fatty acid) is 2—3 % of total calories.
•
• Deficiency causes acanthosis, hyperkeratosis and hypercholesterolemia.
•
• PUFA form membrane lipids, influence fluidity of the plasma membrane and act as precursors for prostaglandin synthesis.
•
• Prostaglandins: Derivatives of prostanic acid.
•
– PGD2, PGE2, PGF2, PGI2, and TXA2 are the commonly occurring prostaglandins in the human body.
–
– Prostaglandins act as local hormones and function through G protein coupled receptors. In most cases PGE increases
–
cAMP. (AIPG 2009)

– PGF2 may be used for medical termination of pregnancy, since it stimulates uterine muscles.
–
• Waxes are esters of long chain fatty acids with high molecular weight monohydroxy aliphatic alcohols.
•
• Coconut oil: Conatins lauric acid: CH3(CH2)10COOH
•
• Peanut oil: Contains arachidonic acid CH3(CH2)18COOH
•
• Ricinolenic acid contains a hydroxyl group–found in castor oil
•
• Chaulmoogra oil–contains chaulmogric acid heterocyclic ring–is used for the treatment of leprosy.
•
• Steroids–have a steroid nucleus i.e. cyclopentanoperhy drophenathrene nucleus.
•
• Emulsification is a pre-requisite for digestion of lipids. The lipids are dispersed into smaller droplets is increased. This
•
process is favoured by:
– Bile salts (detergent action)
–
– Peristalsis (mechanical mixing)
–
– Phospholipids
–
• Digestion of lipids needs bile salts and pancreatic lipase. Digestion is partial.
•
• Long chain fatty acids are absorbed as micelles into the lymph vessels, then carried as chylomicrons in the blood from
•
intestine to liver and adipose tissue.
• Short chain fatty acids are absorbed directly into the blood stream.
•
• Carnithine helps in transport of Fatty acyl CoA through inner mitochondrial membrane.
•
• α- oxidation occurs in microsomes of liver and brain.
•
• Most important theory of fatty acid oxidation is β-oxidation, proposed by Knoop.
•
β-Oxidation
• Takes place in mitochondria. The entry of fatty acid into mitochondria needs carnithine.
•
• In it, 2 carbon units are successively removed.
•
• The first dehydrogenase needs FAD and the second dehydrogenase is dependent on NAD
•
• Palmitic acid( 16 carbons) on β-oxidation yields 129 ATPs.
•
• Odd chain fatty acids finally yield 3 carbon propionic acid.
•
• It is finally broken down into succinyl CoA with the help of enzymes requiring biotin and vitamin B12.
•

Fatty acid Synthesis
• Fatty acid synthesis takes place by a multienzyme complex.
•
• Acetyl CoA carboxylase, a biotin requiring enzyme is the rate limiting enzyme of the fatty acid synthesis.
•
• Require the coenzyme NADPH.
•
• Insulin favours lipogenesis and glucagon has the opposite effect. (KCET 2009)
•

• Diabetes mellitus and starvation are the important causes of ketogenesis.
•
• Glucagon stimulates ketogenesis, while insulin suppresses ketogenesis.
•
• Ketone bodies in urine is assessed by Rothera’s test. (AIPG 2011)
•

Ketone Bodies become more significant when glucose is in short supply to
• Acetoacetate is the primary ketone body while beta the tissues, as in cases of starvation and diabetes mellitus.
BIOCHEMISTRY
•
hydroxyl butyrate and acetone are secondary ketone • They are the major source of fuel for the brain and other
bodies. They are synthesized exclusively by the liver
•
parts of CNS.(AIPG 2008)
mitochondria. Normal level: 3 mg/100ml of blood.
• Ketone bodies are water soluble and energy yielding. • Diabetes mellitus is associated with insulin deficiency
•
and this results in impaired carbohydrate metabolism
•
However acetone is an exception, since it cannot be
metabolized. and increased lipolysis. Both of these ultimately results in
• The synthesis of ketone bodies occur in liver and the accumulation of acetyl CoA and its conversion to ketone
•
enzymes are located in the mitochondrial matrix. bodies. Diabetic ketoacidosis is dangerous and may result
• The production of ketone bodies and their utilization in coma, and even death, if not treated.
•
Cholesterol
• Cholesterol contains perhydro cyclopentano phenanthrene ring. Cholesterol has 27 carbon rings.
•
• Cholesterol is synthesized from acetyl CoA. The rate limiting enzyme is HMG CoA reductase.
•
• Excretion of cholesterol is through bile, either as cholesterol as such or as bile salts.
•
• Cholesterol is a useful substance, bile salts, and steroid hormones (estrogen, progesterone, testosterone) are produced
•
from cholesterol.
• Cholesterol plays a role in vitamin D synthesis: 7–dehydro cholesterol, an intermediate product in the synthesis of
•
cholesterol is converted to cholecalciferol (vitamin D3) by ultraviolet rays in the skin. (AIIMS 1989)

• High density lipoproteins (HDL) and the enzyme lecithin–cholesterol acyl transferase (LCAT) are responsible for the
•
transport and elimination of cholesterol from the body.
• The normal plasma cholesterol level is in the range of 150-250 mg/dl. (KAR 1998)
•

• Increase in plasma cholesterol (>250mg/dl) is known as hypercholesterolemia and is seen in diabetes mellitus,
•
hypothyroidism (myxoedema), obstructive jaundice and nephritic syndrome.
Lipoproteins tissues, LDL cholesterol is said to be a bad cholesterol.

• In the blood, lipoproteins are chylomicrons, VDL, LDL (AIPG 2006)

•
and HDL. These are separated either by electrophoresis or • HDL carry cholesterol from peripheral tissues to liver
•
by ultracentrifugation. and is later excreted. Hence, HDL cholesterol is said to be
• Chylomicrons carry dietary triglycerides from intestines good cholesterol. For this excretion, PUFA is required.
•
to liver and adipose tissue. (AIPG 2006) The enzyme LCAT helps in this reaction. (KAR 2002)

• VLDL carry endogenously produced triglycerides from • To prevent atherosclerosis and heart diseases, the aim is to
•
•
liver to peripheral tissues. reduce total cholesterol below 180mg/dl; to decrease LDL-
• LDL carry triglycerides and cholesterol from liver to cholesterol below 130 mg/dl and to keep HDL-cholesterol
•
peripheral tissues. since the cholesterol is deposited in above 35mg/dl.
Biochemistry 71

Synthesis of Brain Lipids
• Sphingosine is formed by condensation of palmitic acid with amino acid serine
•
• Palmitic acid + serine = Sphingosine (or sphingol)
•
• Sphingosine + Fatty acid = Ceramide
•
• Ceramide + glucose = glucocerebroside
•
• Ceramide + phosphocholine = Sphingomyelin
•
• Sphingolipid + neuramic acid = ganglioside
•
Phosphatides
• Contains glycerol as alcohol group
•
BIOCHEMISTRY
• E.g. cephalin (phosphatidyl ethanolamine)
•
– Lecithin (phosphatidyl choline)
–
– Cardiolipins
–
– Plasmalogens
–
Identification of Fats and Oils
• Saponification number – amount of detergent required for 100 gm of FA. high in short chain fatty acids
•
• Acid number – indicates degree of rancidity of fat
•
• Iodine number – indicates degree of unsaturation of fat
•
• Acetyl number – measure number of OH- group present used for detection of adulteration in fat.
•
Some Extra Points
• Lipoprotein which does not move in electrophoresis – chylomicron (least no. of proteins)
•
• Maximum concentration of exogenous triglycerides is seen in chylomicron
•
• Maximum concentration of endogenous triglycerides is seen in VLDL
•
• Major lipoprotein of blood is LDL
•
• Maximum content of cholesterol is seen in LDL
•
• Apo B 100 is major lipoprotein of VLDL, LDL and IDL
•
• Apolipoproteins are most strongly associated with coronary heart disease and HDL have protective role.
•
• Apolipoprotein B has highest predictive value in morbidity of coronary heart disease.
•
• Occurs after 2 or 3 days without food
•
• Initially increased gluconeogenesis is seen which reduces later
Metabolism in
•
• First liver glycogen is mobilized, then fats and lastly tissue protein
starvation
•
• Hypoglycemia depress insulin secretion and glucagon activity increases it.
•
• In starvation, alanine and glutamine are the most important source of gluconeogenesis.
•
• Insulin suppresses G 6 phosphatase activity resulting in G 6 P to enter glycogenesis to form glycogen
Metabolism
•
• In well fed state only heart utilizes fatty acids, while muscles, liver and brain utilize glucose as a substrate for energy
in well fed/
•
production
absorptive phase
• Malonyl CoA the intermediate in fatty acid synthesis is a potent inhibitor of CPT-1
•
• Increased NADH/NAD redox ratio which leads to accumulation of fats mainly in the form of triglycerides in liver
Metabolic
•
adaptations in • Fatty liver is caused by a combination of impaired fatty acid oxidation and increased lipogenesis
•
Alcoholics (fatty
liver)

NADPH
• Is produced by–pentose phosphate pathway
•
• Is required for
•
– Fatty acid synthesis
–
– Steroid synthesis
–
– Glutathione reductase
–
Sites of Various Metabolic Pathways
• Citric acid cycle
•
• Oxidative phosphorylation
•
• Fatty acid oxidation Mitochondria
•
• Electron transfer
BIOCHEMISTRY
•
• Synthesis of ketone bodies
•
• Protein synthesis Ribosomes
•
• Glycoprotein synthesis Golgi complex (AIPG 2005)
•

• RNA synthesis Nucleolus
•
• Cholesterol synthesis
•
• Glycolysis
•
• Fatty acid synthesis
•
• Glycogenesis Cytoplasm
•
• Glycogenolysis
•
• HMP shunt
•
• Glucogeneogenesis
•
• Urea cycle
In both mitochondria and cytosol
•
• Gluconeogenesis
•
PROTEINS
• Most amino acids in the body are alpha amino acids.
•
• Amino acids can be classified based on their:
•
– Structure
–
– Metabolic fate
–
– Nutritional requirements
–
Classification based on structure:
• Neutral aliphatic amino acids • Glycine
•
•
• Alanine
•
• Serine
•
• Threonine
•
• Valine
•
• Leucine
•
• Isoleucine
•
• Neutral aromatic amino acids • Phenyl alanine
•
•
• Tyrosine
•
• Tryptophan
•
• Neutral heterocyclic • Proline
•
•
Biochemistry 73

• Neutral sulphur containing amino acid • Cystine
•
•
• Cysteine
•
• Methionine
•
• Basic amino acids • Lysine
•
•
• Arginine
•
• Histidine
•
• Acidic amino acids • Asparagine
•
•
• Aspartic acid
•
• Glutamic acid
•
• Glutamine
•
• Amino acid with indole ring • Tryptophan
•
•
• Amino acid with imino group • Proline (AIPG 2005)
•
•

BIOCHEMISTRY
• Amino acid with imidazole ring • Histidine
•
•
• Amino acid with dicarboxylic group • Aspartic acid
•
•
• Glutamic acid
•
• Amino acid which is a methyl group donor • Methionine
•
•
• Optically inactive amino acid • Glycine
•
•
• Amino acid which is present in peptides and absent in • Ornithine
•
•
proteins
Classification based on nutritional requirement:

• Essential amino acids (that cannot be synthesized by the body) • Arginine
•
•
(KAR 1999) • Valine
•
• Histidine
•
• Isoleucine
•
• Leucine
•
• Lysine
•
• Methionine
•
• Phenyl alanine
•
• Threonine
•
• Tryptophan
•
• Non essential amino acids ( can be synthesized by the body) • Alanine
•
•
• Glycine
•
• Serine
•
• Tyrosine
•
• Proline
•
• Semi essential amino acids • Arginine
•
•
• Histidine
•
• Classification based on metabolic fate:
•
Ketogenic Glycogenic and ketogenic (AIIMS may 2013) Glycogenic
Leucine (COMEDK 2004, KAR 2000) Phenyl alanine All other amino acids
Lysine Isoleucine
Tyrosine
Tryptophan
• In solution, amino acids exist as ‘Zwitter ions’ or ‘ampholytes’ at their characteristic pH.
•
• Glycine has no asymmetric carbon atoms and therefore has no optical activity.
•
• Nitrogen content of ordinary proteins is on average 16% by weight. (COMEDK 2011)
•


Protein Structure can be Studied at four Levels
Primary • •
determines the biological activity of the protein. Stabilized by covalent bonds (strongest bonds). Alterations lead to loss
structure of functional capacity e.g. Sickle cell haemoglobin
Secondary • Could be alpha helix or beta pleated sheet.
•
structure – Alpha helix–intra chain hydrogen bonding e.g. hair, skin and nails are rich in keratin . proline is absent in alpha helix
–
– Beta pleated sheet structure – inter chain hydrogen bonding. Present in silk fibres. Proline is present that causes kinks.
–
– Triple helix – found in collagen. Inter chain hydrogen bonding is seen
–
Tertiary • Entire 3 D confirmation of a single polypeptide chain. Major interactions are hydrophobic. Other weak bonds are ionic/
•
salt/electrostatic vanderwaals, hydrogen bonds. Vibratory property is seen using X ray diffraction.
Quaternary • Arranged as homo or heterodimers. Defines the polypeptide composition and spatial relationship between subunits of
•
structure proteins that are assembled from more than one polypeptide units.(AIPG 2006) Examples include hemoglobin, DNA
polymerases, microtubules etc. Examples of oligomeric proteins with quaternary structure are haemoglobin, myoglobin,
and creatine kinase.
BIOCHEMISTRY
Analysis of Protein Structure

• Primary structure–Amino acid composition is determined by
•
– Hot acid hydrolysis
–
– Ion exchange chromatography (Edman reaction)
–
• Secondary and tertiary structure
•
– X ray crystallography (X ray diffraction method)
–
– UV spectroscopy
–
• Simple Proteins: classified into:
•
– Albumin: present in serum, milk and egg. Soluble in water and salt solution.
–
– Globulins: present in serum, milk and egg. Sparingly soluble in H2O but soluble in dilute neutral salt solutions.
–
– Protamines: gliadin of wheat. Soluble in 60-80% alcohol.
–
– Glutelins: present in wheat and soluble in dilute acids and alkalis.
–
– Scleroproteins: present in bones, cartilages, skin, hair,nail and horn. Insoluble.
–
– Histones: highly basic proteins e.g. nucleoproteins. Soluble in water.
–
• Solubility of a protein is dependent on the ionic concentration of the medium. Hence proteins may be ‘salted out’.
•
• Denaturation of proteins results in loss of biological activity but not the primary structure. Denaturation may be reversible.
•
• Methods of protein estimation include colorimetry (Biuret test and Lowry’s method), (TNPSC 1999) Turbidimetry,
•
Radial immunodiffusion, Radioimmunoassay (RIA) and enzyme immune assay ( EIA).
• Transamination: the transfer of amino group from an amino acid to keto acid is known as transanimation, this reaction
•
is mediated by transaminases, an enzyme that require pyridoxal phosphate, a coenzyme derived from Vitamin B6.
• Transamination reaction is a reversible process and responsible for the synthesis of non essential amino acids.
•
Transamination also diverts the excess amino acids towards energy generation. All the amino acids except lysine,
threonine, proline and hydroxyproline participate in transamination. (AIPG 2008)

• Michaelis Menten constant (Km) is the concentration of substrate required to produce exactly half of the maximum
•
velocity of the reaction.
• Induced fit hypothesis was proposed by Koshland.
•
Chaperones (AIPG 2004)
• Proteins that play a role in the assembly or proper folding of other proteins without themselves being components of the
•
latter (AIPG 2008, AIIMS 2006)

• Present in a wide range of species
•
Biochemistry 75

• Also called as heat shock proteins
•
• Bind predominantly to the hydrophobic regions of unfolded or aggregated proteins’, act in part as a quality control or editing
•
mechanism for detecting misfolded or otherwise defective proteins
• Most chaperones show ATPase actvity, with ATP or ADP being involved in the protein chaperone interaction.
•
• Found in cytoplasm, mitochondria and endoplasmic lumen
•
Amino Acids Required for Specific Products
• Carnithine: Formed from lysine + methionine
•
• Carnosine: Beta alanine+ histidine, dipeptide of skeletal and heart muscles
•
• Choline: Formed with the help of methionine, glycine, serine B6
•
• Creatine: Glycine + Arginine + methionine
•
• Glutathione: Glycine + Cysteine+ Glutamate
BIOCHEMISTRY
•
• Histone: Protein rich in arginine+ histidine
•
• Keratin: Histidine: arginine: lysine (1:12:4)
•
• Purine: Glycine + Aspartate + Glutamine + serine
•
• Pyrimidine: Asparate + glutamine
•
Nice to Know
• Amino acids which are glucogenic and ketogenic are lysine, phenylalanine, tyrosine, tryptophan, isoleucine.
•
• Only ketogenic (fat forming) amino acids–l–leucine
•
• Amino acid producing hypoglycemia–leucine (ketogenic) and arginine
•
• Aspartate and glutamate are monoamino dicarboxylic acid
•
• Glutamate is the precursor of arginine, proline, glutamine
•
• Hemoglobin can act as buffer at physiological pH because of high content of histidine
•
• All amino acids except glycine exists in D and L isomer. Glycine has no asymmetric carbon atom, so it does not show
•
stereoisomerism or optical isomerism
• There are not RNA for OH proline, gamma carboxy glutamate, OH lysine.
•
• Amino acid associated with atherosclerosis and increases the risk of CAD – homocystiene
•
• Zwitter ion are molecules with no net charge i.e. have positive ions = negative ions
•
• Isoelectric point is the pH at which an amino acid bears no net charge
•
• Glycine is the fundamental building unit (forms building blocks)
•
Tests for Proteins
Test Used for
Colour reactions Xanthoproteic (for aromatic Amino acids)
Millon’s (Tyrosine)
Sakaguchi (Arginine)
Sullivan (cysteine and cystine)
Lead acetate (cysteine and cystine and methionine)
Hopkins Kole aldehyde reaction (for tryptophan)
Quantitative Assay Ninhydrin reaction

Fluoroscarmine (can detect no. of amino acids)–better than Ninhydrin
NH2 detection Von-slyke method

Mass Spectrometry
Peptide chain sequencing Edmans (for N terminal)

Inborn Errors of Amino Acid Metabolism
Phenylketonuria • Phenylalanine accumulates in the blood (AIPG 2012)
•

••
Phenylalanine builds up toxic concentrations in body fluids, resulting in CNS damage with mental retardation.
• Elevated phenylalanine inhibits melanin synthesis, leading to hypopigmentation
•
• It is due to deficiency of enzyme phenylalanine hydroxylase or dihydropteridine reductase.
•
• Treatment involves restricting dietary protein
•
Albinism • Deficient enzyme: tyrosine kinase (APPSC 1999)
•

• Albinos have little or no melanin. They are more susceptible to sunburns, skin carcinomas and photophobias.
•
Homocystinuria • In this disorder, homocysteine, which accumulates in blood and body fluids appears in the urine.
•
• Homocytsinuria may result from the following reasons:
•
– Cystathionine synthase deficiency
–
– Reduced affinity of cystathionine synthase for its coenzyme, pyridoxal phosphate PLP)
BIOCHEMISTRY
–
– Vitamin B12 coenzyme deficiency.
–
• Pathologic changes include discoloration of optic lens,mental retardation, osteoporosis and other skeletal
•
abnormalities, artherosclerosis and thromboembolism.
• Patients may be treated with vitamin therapy or with synthetic diets low in methionine, and by administering betaine
•
as an alternative methyl group donor.
Maple syrup • In it, the branched chain keto acids derived from isoleucine, leucine and valine appear in the urine giving it a maple
•
urine disease syrup like disease.
• Deficiency of branched chain 2 keto acid decarboxylase enzyme is seen in it.
•
• The elevated keto acids cause severe brain damage and death in the first year of life.
•
• Megadoses of thiamine may be helpful in few cases.
•
Histidinemia • This is characterized by elevated histidine in the blood plasma and excessive histidine metabolites in the urine.
•
• Deficient enzyme is histidine α-deaminase. (KAR 2002)
•
• Mental retardation and speech defects may occur though rare.
•
• No treatment required.
•
Alkaptonuria • Most important clinical manifestation is the darkening of urine on standing.
•
• Also seen is generalized pigmentation of connective tissues and a form of arthritis.
•
• Deficient enzyme in this disease is homogentisate oxidase. (AIIMS 1995)
•

• The mechanism of the ochronosis involves oxidation of homogenistic acid by polyphenol oxidase, forming
•
benzoquinone acetate, which polymerizes and binds to connective tissue macromolecules.
• Homogentisate in the urine is then oxidized by O2 in air to a brownish black pigment.
•
Urea Ammonia transport

Urea cycle.
• Urea is mainly formed in liver and to some extent in brain

•
(among tissues it is skeletal muscle)
• Amino acids involved in the urea formation are ornithine, Urea cycle
•
arginine and citrulline. Steps in urea synthesis in liver • Also known as Kreb’s Henseleit cycle
•
are discovered by Krebs and Henseleit. So it is named as • Urea is the end product of protein metabolism
•
Krebs-Henseleit cycle (ornithine cycle). • it is formed from ammonia, carbon dioxide and
•
• Biosynthesis of urea aspartate. Carbamoyl phosphate synthase I is the
•
– Urea is the major end product of nitrogen catabolism pacemaker enzyme of urea cycle (hepatic mitochondrial
–
in humans. The synthesis takes place in liver and enzyme).
clearance is from kidney. Various steps involved in its • Carbamoyl phosphate synthase II, a cytosolic enzyme
•
synthesis are: (AIPG 2008) that uses glutamine rather than ammonia as the

Transamination (of alanine and glutamine) nitrogen donor, functions in pyrimidine biosynthesis.

Oxidative deamination (of glutamate)

Biochemistry 77

• Ammonia is produced form various sources such as On chromosome 16: • Three genes within the alpha gene
•
•
cluster
bacterial flora of intestine, glutamic acid dehydrogenase,
– Zeta geneζ
bacterial enzymes which attach foot proteins etc. Liver
–
– 2 alpha genes (α and)
converts ammonia into urea (ammonia is very toxic
–
On chromosome 11 • There are 5 genes within beta gene
whereas urea is not that much toxic).
•
cluster
• The brain can also remove ammonia with the help of – Epsilon ε
•
–
glutamine synthetase enzyme, whereas ammonia is – Deltaδ
–
– Betaβ
converted to glutamine.
–
– 2 gamma γ
–
• The number of ATP from one molecule of glutamic acid is
•
12. • After 8 weeks of fetal life (embryonic hemoglobin) is
•
formed
Good to know: • HbA–made up of 2 alpha chains and 2 beta chains.
BIOCHEMISTRY
•
• 1st nitrogen of urea cycle is suplied by free ammonia • HbF–made up of 2 alpha and 2 gamma chains.
•

•
• 2nd nitrogen of urea cycle is supplied by aspartate (AIPG 2012)

•
• First two steps occur in mitochondria • HbF–fetal haemoglobin has a higher affinity for O2,
•
lower affinity for BPG.
•
• Rest cycle occurs in cytosol
• HbA2–appears 12 weeks after birth
•
• Enzyme responsible for cleavage and direct release of
•
• Agents such as butyrate and histone deacetylate
•
urea is present in liver and is arginase and therfore
•
tissues can synthesize arginine but only liver can form inhibitors can also activate fetal hemoglobin genes
urea. partially after birth.
• In Hb iron is always in ferrous forms (AIPG 2008)
• Glutamate serves as ‘collection centre’ for amino
•

• Each gram of Hb contains 3.4mg of iron
•
groups in biological system. In presence of the enzyme
•
glutamate dehydrogenase, it rapidly undergoes • Heme is a derivative of porphyrin.
•
oxidative deamination, to liberate free ammonia for
urea synthesis. • The rate limiting step of heme synthesis is the ALA
•
synthesis; enzyme is ALA synthase which needs pyridoxal
• Calorific value (AIPG 2012)
phosphate as co-enzyme.
•

– Carbohydrate – 4 Kcal/g
• Acute intermittent porphyria is an inborn error of
–
– Fat – 9 Kcal/g (PGI 2006)
•
metabolism affecting porphyrin synthesis.
–

– Protein – 4 Kcal/g (COMEDK 2012)
• End products of heme catabolism are bile pigments.
–

•
• Bile pigments are bilirubin and biliverdin
•
Inborn Errors of the Urea Cycle • Bilirubin is produced in RE cells (AIPG 2005)
•

Deficient Enzyme Metabolic disorder • In Sickle cell haemoglobin, glutamic acid at the 6th
•
position of beta chain of HbA is replaced by valine. (mis
• Carbamoyl phosphate synthetase Hyperammonaemia type I
sense mutation) (AIPG 2010)
•

• Ornithine transcarbamoylase Hyperammonaemia type II • Thalassemia means normal haemoglobins in abnormal
•
•
proportions
• Argininosuccinic acid synthetase Citrullinaemia
• Most common cause of anaemia is iron deficiency.
•
•
• Argininosuccinase Argininosuccinicaciduria
Difference between HbF and HbA
•
• Arginase Hyperargininaemia • HbF binds O2 more avidly than does Hba and tends
•
•
to shift the ODC curve to the left As a result P50 is
Haemoglobin decreased
• Molecular weight: 67000 • During the first month after the birth, ODC begins to
•
shift to the right and between 4 to 6 months of age it is
•
• Tetramer consisting of 2 pairs of globin chains similar to that of adult
•
• Two hemoglobin clusters are involved in the production • Hbf is resistant to alkali denaturation. and has least
•
of hemoglobin and are located on the ends of the short
•
affinity for 2,3 BPG
arm of chromosome 16 and 11

Collagen
• Structural protein with unique amino acid composition glycine (33%), proline (10%) hydroxyl-proline (10%) and
•
hydroxylysine (1%). (AIPG 2001, AIIMS 2000, MAN 2001)

• Collagen has a triple helical structure. Lysine residues form intra molecular covalent cross links
•
• Two hydroxyl lysine residues along with one lysine residue form intermolecular covalent crosslinks.
•
Biosynthesis of Collagen
• Synthesis on endoplasmic reticulum
•
• Post translational processing in the lumen of ER, involves removal of signal peptide.
•
– Hydroxylation of proline and lysine by enzymes, propylhydroxylase and lysyl hydroxylase which require ferrous ion,
–
ascorbic acid, oxygen and α-ketoglutrate. (KAR 1999)

– Glycosylation, formation of disulfide bonds and triple helix.
BIOCHEMISTRY
–
• Collagen is released from fibroblast as procollagen
•
• Extracellular processing: involves formation of tropocollagen, collagen fibre formation and collagen maturation which
•
involves cross links between aldehyde of lysine and hydroxylysine formed by enzyme lysyl oxidase.
Disorders Related to Collagen Metabolism

• Scurvy: Vit C deficiency, hydroxylation of proline and lysine are absent.
•
• Ehlers-Danlos syndrome: Deficiency of lysyl hydroxylase is seen.
•
• Alport syndrome: Defect in gene coding for type IV collagen found in basement membrane of renal glomeruli.
•
• Osteogenesis imperfecta defect in genes coding for procollagen.
•
ENZYMES
• According to the International Union of Biochemistry and Molecular Biology (IUBMB) in 1964, the enzymes have been
•
classified as:
Classification of enzymes
Class 1 Oxidoreductases E.g. alcohol dehydrogenase
Class 2 Transferases Kinases (AIPG 2005, AIIMS 2001)

Class3 Hydrolases Acetyl choline esterase
Class 4 Lyase Hydratase
Class 5 Isomerase Triose phosphate isomerise
Class 6 Ligases Acetyl CoA carboxylase
• Enzymes may be simple or compound proteins.

•
– In case of compound proteins, the protein component is termed ‘apoenzyme’ and the prosthetic group is termed
–
‘coenzyme’. The combination produces a functional ‘holoenzyme’.
• Coenzymes are mainly constituted by the B complex group of vitamins.
•
• Zymogens: Inactive precursors of enzymes or proenzymes are called zymogens. (KCET 2008)
•

• Ribozymes: Catalytic RNAs e.g. RNA splicing-peptidyl transferase
•
• Abzymes: Catalytic antibodies.
•
• Enzymes requiring the presence certain metal ion for their activity are called Metallo-enzymes. Examples are carbonic
•
anhydrase (Zinc), catalase and peroxidase (iron), lipase (calcium), etc.
Biochemistry 79

• Michaelis Menton theory states that an enzyme (E) combines with a substrate (S) to form an enzyme –substrate (E-S)
•
complex, which breaks down to give the product (P).
• Theories proposed to explain the mechanism of enzyme action are:
•
– Fischer’s Template (lock and key) theory
–
– Koshland’s Induced fit theory
–
• Area of the enzyme where the catalysis occurs is called the ‘active site’.
•
• Isoenzymes are physically distinct forms of the same enzyme activity.
•
Enzyme Inhibition
Vmax Affinity Efficiency Km
Competitive inhibition Does not effect Decreases Remains the same K increases (MAN 1999)

Non-competitive 1/Vmax increases as Remain same Efficiency 1/Km remains the same as substrate
BIOCHEMISTRY
inhibition (or allosteric) Vmax is decreased decreases conc. has no effect on inhibition
Uncompetitive Vmax is lower Inhibitors combine only with Apparent Km<Km

inhibition the enzyme substrate forming
an irreversible complex.
Enzymes Present in Mitochondria

• Outer membrane • CPT-1, MAO
•
•
• Acetyl CoA synthatase
•
• Phospholipase A2
•
• Intermembrane space • Adenylate kinase, creatinine kinase
•
•
• Inner membrane • CPT II
•
•
• ETC/ respiratory chain
•
• Matrix • ATP synthase
•
•
• Oxidative phosphorylation
•
• KB synthesis
•
• Beta oxidation
•
• TCA cycle
•
• Urea cycle
•
• Alcohol dehydrogenase
•
• SGOT
•
• Secondary, tertiary and quaternary structure of proteins are stabilized by hydrogen bonds, ionic bonds, hydrophobic
•
interactions and van der waals forces.
• Cysteine forms disulfide linkages between two polypeptide chains in oligomeric proteins.
•
• Strength of different bonds–covalent bonds> disulfides>electrostatic >vanderwaal forces
•
• A carboxyl group makes a carbon based compound the least polar, while an amino acid group makes it a stronger acid.
•
Enzymes Profiles in Diseases
Hepatic diseases
• Alanine aminotransferase Marked increase in parenchymal liver diseases
•
• Alkaline phosphatase Marked increase in obstructive liver disease
•
Myocardial infarction
• Creatine kinase (CK-MB) (COMEDK 2007) First enzyme to rise following infarction, CK-MB isoenzyme is specific
•
• Aspartate amino-transferase (AST) Rises after the rise in CK and returns to normal in 4-5 days
Last enzyme to rise. LDH-1 becomes more than 2 (flipped pattern)
•
• Lactate dehydrogenase (LDH) (KCET 2011)
•

Muscle diseases Marked increase in muscle diseases. CK-MM function is elevated.
• Creatine kinase (CK-MM)
•
Bone diseases Marked elevation in osteoblastic bone activity as in rickets. Heat labile bone isoenzyme is
• Alkaline phosphatase (ALP) elevated. Also in Paget’s disease.
•
Prostate cancer Marked for prostate cancer. Mild increase in benign prostate enlargement.
• Prostate specific antigen (PSA) Marked for prostate cancer. Metastatic bone disease especially from a primary prostate.
•
• Acid phosphatase (ACP) Inhibited by L tartrate.
•
Amylase Acute pancreatitis
Acid phosphatse Osteopetrosis
Some Rate Limiting Enzymes

BIOCHEMISTRY
Metabolic Pathway Rate Limiting Enzyme

Glycolysis Phosphofructokinase
Glycogenesis Glycogen synthetase (MAN 2000)

Glycogenolysis Phosphorylase
Glyconeogenesis Fructose 1,6 bisphosphate
Cholesterol synthesis HMG CoA reductase
Fatty acid synthesis Acetyl CoA carboxylase
Urea synthesis Carbonyl phosphate synthetase (Arginase)
Citric acid cycle Isocitrate dehydrogenase
Ketone bodies HMG CoA synthase
Porphyrin synthesis Aminolevulinate synthase
Bile acids 7-alpha hydroxylase
Therapeutic use of Enzymes

Enzyme Therapeutic application
• Asparaginase • Acute lymphoid leukemia
•
•
• Streptokinase • To lyse intravascular clot
•
•
• Urokinase • To lyse intravascular clot
•
•
• Hyaluronidase • Enhance local anaesthesia
•
•
• Pancreatin • Pancreatic insufficiency
•
•
• Papain • Anti-inflammatory
•
•
INFORMATIONAL MOLECULES • Pol I is the most abundant replicating activity in E. coli but
•
has as its primary role to ensure the fidelity of replication
DNA AND RNA through the repair of damaged and mismatched DNA.
• DNA Replication: The mechanics of DNA replication was • Replication of the E. coli genome is the job of pol III. This
•
enzyme is much less abundant than pol I; however, its
•
originally characterized in the bacterium, E. coli which
contains 3 distinct enzymes capable of catalyzing the activity is nearly 100 times that of pol I.
replication of DNA. DNA polymerase (pol) I, II, and III. • There have been 5 distinct eukaryotic DNA polymerases
•
Biochemistry 81

identified, α, β, γ, δ and ε. The identity of the individual direction being copied continuously and one strand in
enzymes relates to its subcellular localization as well as its each direction being copied discontinuously.
primary replicative activity. The polymerase of eukaryotic • During the process of DNA polymerases incorporating
cells that is the equivalent of E. coli pol III is pol-α. The
•
dNTPs into DNA in the 5’—>3’ direction they are moving
pol I equivalent in eukaryotes is pol-β. Polymerase-γ is in the 3’—>5’ direction with respect to the template strand.
responsible for replication of mitochondrial DNA. In order for DNA synthesis to occur simultaneously
• The ability of DNA polymerases to replicate DNA on both template strands as well as bidirectionally one
•
requires a number of additional accessory proteins. strand appears to be synthesized in the 3’—>5’ direction.
The combination of polymerases with several of the In actuality one strand of newly synthesized DNA is
accessory proteins yields an activity identified as DNA produced discontinuously.
polymerase holoenzyme. These accessory proteins • The strand of DNA synthesized continuously is
•
include (not ordered with respect to importance): termed the leading strand and the discontinuous
strand is termed the lagging strand. The lagging strand
BIOCHEMISTRY
– Primase
of DNA is composed of short stretches of RNA primer
–
– Processivity accessory proteins
plus newly synthesized DNA approximately 100–200
–
– Single strand binding proteins
bases long (the approximate distance between adjacent
–
– Helicase nucleosomes). The lagging strands of DNA are also
–
– DNA ligase called Okazaki fragments.
–
– Topoisomerases
• This torsional stress is relieved by DNA topoisomerases.
–
– Uracil-DNA N-glycosylase
•
Topoisomerases relieve torsional stresses in duplexes of
–
DNA by introducing either double- (topoisomerases II)
• The process of DNA replication begins at specific sites in or single-stranded (topoisomerases I) breaks into the
•
the chromosomes termed origins of replication, requires backbone of the DNA. These breaks allow unwinding
a primer bearing a free 3’–OH, proceeds specifically in the of the duplex and removal of the replication-induced
5’—>3’ direction on both strands of DNA concurrently torsional strain. The nicks are then resealed by the
and results in the copying of the template strands in a topoisomerases.
semiconservative manner. The semiconservative nature • The RNA primers of the leading strands and Okazaki
•
of DNA replication means that the newly synthesized fragments are removed by the repair DNA polymerases
daughter strands remain associated with their respective simultaneously replacing the ribonucleotides with
parental template strands. deoxyribonucleotides. The gaps that exist between the
3’–OH of one leading strand and the 5’–phosphate of
• In order for DNA polymerases to synthesize DNA they another as well as between one Okazaki fragment and
•
must encounter a free 3’–OH which is the substrate another are repaired by DNA ligases thereby, completing
for attachment of the 5’–phosphate of the incoming the process of replication.
nucleotide.
• During repair of damaged DNA the 3’–OH can arise from RNA (AIPG 2007)
•
the hydrolysis of the backbone of one of the two strands.
The 3 RNA classes are:
• During replication the 3’–OH is supplied through the use
•
of an RNA primer, synthesized by the primase activity. Messenger This class of RNAs are the genetic coding
RNAs (mRNAs) templates used by the translational machinery
• The primase utilizes the DNA strands as templates and to determine the order of amino acids
•
synthesizes a short stretch of RNA generating a primer for incorporated into an elongating polypeptide in
the process of translation.
DNA polymerase.
• Synthesis of DNA proceeds in the 5’—>3’ direction through Transfer RNAs This class of small RNAs form covalent
(tRNAs) attachments to individual amino acids and
•
the attachment of the 5’–phosphate of an incoming dNTP recognize the encoded sequences of the
to the existing 3’–OH in the elongating DNA strands with mRNAs to allow correct insertion of amino acids
the concomitant release of pyrophosphate. into the elongating polypeptide chain. Contains
many modifications of the standard bases A,
• Initiation of synthesis, at origins of replication, occurs U G and C, including methylation, reduction,
•
simultaneously on both strands of DNA. Synthesis deamination and rearranged glycosidic bonds.

(AIPG 2006)
then proceeds bidirectionally, with one strand in each


Ribosomal This class of RNAs are assembled, together Posttranscriptional Processing of RNAs (AIIMS 2006)
RNAs (rRNAs) with numerous ribosomal proteins, to form the
ribosomes. Ribosomes engage the mRNAs • Capping and methylation of eukaryotic mRNA
•
and form a catalytic domain into which the • 3’ cleavage and polyadenylation
tRNAs enter with their attached amino acids.
•
The proteins of the ribosomes catalyze all of • Splicing
•
the functions of polypeptide synthesis.
CYTOGENETICS, MOLECULAR GENETICS AND

All RNA polymerases are dependent upon a DNA GENOMIC TECHNOLOGY
template in order to synthesize RNA. The resultant RNA
is, therefore, complimentary to the template strand of the Karotyping
DNA duplex and identical to the non-template strand. The • The study of chromosomes-karotyping- is the basic tool
•
non-template strand is called the coding strand because its’ of cytogenetics. The chromosome spread is produced by
sequences are identical to those of the mRNA. However, in use of mitotic spindle inhibitors (e.g. colcemid) to arrest
BIOCHEMISTRY
RNA, U is substituted for T. (AIPG 2006) mitosis in dividing cells in metaphase, and then to stain
the chromosome (AIIMS MAY 2013, AIPG 2014)

Classes of RNA Polymerases • A karotype is a photograph(image) of stained chromosome
•
• In prokaryotic cells, all 3 RNA classes are synthesized pairs arranged in order of decreasing length (in metaphase
•
by a single polymerase. spread stage).
• In eukaryotic cells there are 3 distinct classes of RNA • Idiogram is details of banding of chromosome.
•
•
polymerase, RNA polymerase (pol) I, II and III. • Chromosomes have characteristic banding patterns
•
• Each polymerase is responsible for the synthesis of a created by trypsin and Giemsa stain, hence known as G
banding. (AIPG 2014, 2010)
•
different class of RNA.
• RNA pol I is responsible for rRNA synthesis (excluding • Each chromosome arm is defined further by numbering
•
the bands, the higher the number, the further that area is
•
the 5S rRNA).
from the centromere.
• RNA pol II synthesizes the mRNAs and some of
• Every cell of the human body has 46 chromosomes occurring
•
the small nuclear RNAs (snRNAs) involved in RNA
•
splicing. in 23 pairs. Chromosomes are laid out in pairs, from largest
(#1) to the smallest (#22). The last pair are called the sex
• RNA pol III synthesizes the tRNAs, the 5S rRNA and
chromosomes labelled X or Y. Female have two X chromosomes
•
some snRNA
(XX) and males have an X and a Y chromosome (XY).
• There are 4 major rRNAs in eukaryotic cells designated • Human X chromosome is large submetacentric
•
by their sedimentation size. The 28S, 5S 5.8S RNAs are
•
chromosome with numerous genes
associated with the large ribosomal subunit and the 18S
rRNA is associated with the small ribosomal subunit. • Human Y chromosome is a small acrocentric
•
chromosome. (AIPG 2004)
• An additional feature of bacterial mRNAs is that most

• Each chromosome has a p and q arm. P (petit) is the
•
are polycistronic. This means that multiple polypeptides
•
short arm amd Q (next letter in alphabet) is the long
can be synthesized from a single primary transcript.
arm.
Mechanism by which ribosomes recognizes the nucleotide • The arms are separated by a region known as the centromere
•
sequence that initiates transation:
• Karotyping is applicable only to cells that are dividing
• Shine Dalgarno Sequence: (AIPG 2004)
•
or can be induced to divide in vitro. This limitation can
•

– Sequence of nucleotide base (5’ UAGGAGG-3’) be overcome with DNA probes labelled with fluorescent
–
located 6-10 bases upstream on AUG codon on dyes that recognizes chromosome specific sequences
mRNA molecule in bacteria like E coli – a technique known as FISH (fluorescence in situ
– The 16 S ribosomal RNA component of the 30 hybridization)
–
S ribosomal subumit has a nucleotide sequence
• FISH, chromosome painting and spectral
complementary to all or part of shine dalgrano sequence
•
karotyping (SKY) are rapid methods of chromosome
– Thus mRNA and 16 S ribosomal RNA can form
identification. (AIPG 2012)
–
complimentary base pairs thus facilitating the binding and

positioning of the mRNA on the 30 S ribosomal subunit.
Biochemistry 83

• The mobility of ds DNA in gel electrophoresis depends on strand size and length but is relatively independent of
•
nucleotide sequence. However, mobility of single stranded DNA is highly affected by a small change in nucleotide
sequence because relatively unstable ss DNA forms intrastrand base pairing, loop and folds that gives the single strand
a unique 3rd structure, regardless of its length. (AIPG 2007)

• Single stranded conformation polymorphism (SSCP) is electrophoretic separation of single stranded nucleic acids based
•
on their differences in nucleotide sequence that results in a different secondary structure and a measurable difference in
its mobility through gel. So the SSCP can detect point mutations
Chromosomal Mutations
Due to abnormal number of chromosomes Due to alteration in structure of chromosomes
• Euploid means any exact multiple of haploid number (23) and • Deletion: Loss of portion of chromosome and may be terminal or interstitial
•
•
aneuploidy means chromosomes not in exact multiples of 23. • Ring chromosome is a special form of deletion, produced when break
•
• The usual cause of aneuploidy are occurs at both ends of chromosomes with fusion of damaged ends.
BIOCHEMISTRY
•
• Inversion refers to re-arrangement that involves two breaks within single
Non disjunction Anaphase lag
•
chromosome with inverted reincorporation of segment.
– Occurs when a homologous pair – One homologous chro- • Paracentric inversion involves breaks on opposite side of centromere
•
–
–
fails to disjoin at the 1st meiotic mosome in meiosis or • Isochromosome results when one arm of chromosome is lost and the
division, or two chromatids fail to one chromatid in mitosis
•
other is duplicated resulting in a chromosome containing 2 short arms or
separate either at 2nd meiotic di- lags behind and is left 2 long arms only.
vision or mitosis resulting in 2 an- out of cell and one with
• Translocation refers to transfer of a segment of chromosome to another
euploid cells. monosomy
•
nonhomologous chromosome.
– If this occurs in gametogenesis, – All autosomal monoso-
• Reciprocal translocation is mutual swapping of ends between two non
–
–
gametes formed have either an mies are fatal.
•
extra (n+1) or one (n-1) chromo- – Monosomies and tri- homologous chromosomes. It may be balanced or unbalanced
–
some. somies of sex chromo- • Robertsonian translocation (or centric fusion ) is translocation between
•
– Fertilization of such gametes by somes and trisomy of 2 acrocentric chromosomes( 13, 14, 15, 21 and22). The break occurs close
–
normal gametes result in–trisomic 21 autosomal chromo- to centromere of each chromosome and transfer of segments leading to
( 2n+1) or monosomic (2n-1) zy- some are compatible one very long and one extremely small chromosome.
gotes. with life.
Point Mutations
Silent mutations • Codon containing the changed base pairs for amino acid with no detectable effects
•
Missense mutations • The changed base codes for different aa.
•
• E.g. UCA codes for serine while ACA codes for threonine
•
Nonsense mutation • Changed base becomes either a non sense codon or termination codon (COMEDK 2004)
•

• E.g. UCA may change to UAA
•
• UAA, UAG and UGA are stop codons
•
Transformation • Transfer of genetic information through the agency of free DNA
•
• E.g. pneumococci, bacillus
•
Transduction • Transfer of a portion of DNA from one bacterium to another by a bacteriophage
•
Transversion • Substitution of a purine for a pyramidine and vice versa in base pairing
•
Translation (AIPG 1998, AIIMS 1998) • Transfer of information from mRNA to proteins resulting in polypeptide formation
•
Transcription (COMEDK 2008, MAN 1995) • Replication of messenger RNA from the DNA. Mediated by RNA polymerase II
•
Reverse transcription • Formation of DNA from RNA and is mediated by reverse transcriptase
•
• Seen in oncogenic viruses. (AIPG 2004, KAR 2004)
•

Genomics • Study of organism’s entire genome
•

Proteomics • Quantitative and qualitative study of entire proteome (all expressed protein)
•
Glycomics • Deals with structure and function of chains of sugar (oligosaccharide)
•
Bioinformatics • Scientific discipline that combines the tools and techniques of mathematics, computer
•
science and biology with the aim of understanding the biologic significance of variety
of data.
Cytogenetics • Branch of genetics concern with structure and function of cell, especially the
•
chromosome
Pharmacogenomics • The study of genetically determined variations in responses to drugs in human or in
•
laboratory organisms.
BIOCHEMISTRY
Genomic Imprinting: Selective inactivation of a gene or set of genes on either the maternal or paternal chromosome. It
occurs in ovum or sperm before fertilization and is then transmitted to all somatic cells through mitosis and so is of 2 types:

(AIPG 2005, 2006)

• Maternal genomic imprinting: maternal allele is inactive. e.g. Angelmann syndrome
•
• Paternal genomic imprinting: paternal gene is inactive. e.g Prader Willi Syndrome
•
Genetic Code
• The genetic code is considered as universal, specific, non-overlapping and degenerate.
•
• The codon degeneracy is explained by Wobble Hypothesis, which was put forth by Crick.
•
• Wobble Hypothesis is a phenomenon in which a single tRNA can recognize more than one codon. Wobbling is attributed
•
to the difference in the spatial arrangement of the 5’ end of the anticodon.
• Wobbling hypothesis explains the degeneracy of the genetic code i.e. existence of multiple codons for a single amino acids.
•
• Although there are 61 codons for amino acids, the number of tRNAs are around 40, which is due to wobbling
•
• Clinical significance
•
– Abnormalities in the splicing process can lead to various disease states. Many defects in the β-globin genes are known
–
to exist leading to β-thalassemias. Some of these defects are caused by mutations in the sequences of the gene required
for intron recognition and, therefore, result in abnormal processing of the β-globin primary transcript.
– Patients suffering from a number of different connective tissue diseases exhibit humoral auto-antibodies that recognize
–
cellular RNA-protein complexes. Patients suffering from systemic lupus erythematosis have auto-antibodies that
recognize the U1 RNA of the spliceosome.
Lesh Nyhan Syndrome

• HGPRT deficiency sex linked, manifested in males. Characterised by hyperuricemia and severe neurologic problem
•
• Allopurinol does not ameliorate neurologic symptoms.
•
• The metabolic consequences of congenital HGPRT deficiency in Lesh Nyhan syndrome. Loss of HGPRT leads to PRPP
•
levels and stimulation of de novo purine synthesis. One ultimate consequence is increased production of uric acid.
SCID (Severe Combined Immunodeficiency Syndrome):
• Deficiency of enzyme adenosine deaminase (ADA). Intracellular accumulation of adenosine and deoxyadenosine interferes
•
with DNA synthesis, hence abortive lymphoid differentiation.
Biochemistry 85

Inhibitors of
Purine synthesis • 6- Mercaptopurine
•
• Thiopurines
•
• Tiazofurin
•
Pyrimidine nucleotide • N-(phosphonacetyl) L-asparate (PALA) – inhibitor of carbamoyl transferase reaction.
synthesis
•
• Pyrazofurin
•
• 5-fluorouracil
•
DNA synthesis • Methotrexate
•
Viral DNA synthesis • 3’Azido 3’deoxythymidine (AZT)
•
• Acyclovir
BIOCHEMISTRY
•
• Gancyclovir
•
• Cytosine arabinose
•
Polymerase Chain Reaction (PCR)
• Is a test tube method of amplifying a selected DNA sequence. It uses Mg++ ion and thermostable DNA polymerase enzyme.
•
Advantage of thermostability is that the enzyme itself is not denatured and therefore does not have to be added at each
successive cycle.
• Probes are required in blot ( southern, western, northern) tests but not in PCR. PCR uses Taq Man, molecular becon and
•
Syber Green dyes.
– Leber’s hereditary optic neuropathy is caused by a mitochondrial DNA anomaly. (AIPG 2004)
–

BIOCHEMISTRY
VITAMINS
86

Name Sources RDA Functions Deficiency Hypervitaminosis Oral manifestation of defi-
ciency
• • • •
Vitamin A Cod-liver oil, Approx. 1 - • Plays a role in • Night blindness • Impaired visions • Keratinising metaplasia

(Retinol) liver, kidney, milk 5mg rhodopsin cycle or (AIPG 2005) •
• Headache of epithelium resulting in

products, butter, (PGI 2003) Wald’s visual cycle •
• Xerophthalmia(AIIMS increased keratin formation
•
• Nausea

(Fat-soluble, yolk, as provitamin (AIIMS 1989) 1998) characterised by •
• Occlusion of salivary gland
•
A in carrots • Tiredness
•
light and oxy- • Rods are involved in dryness of conjunctiva & ducts with keratin
•
gen-sensitive) dim light vision and cornea • skin change
•
• Enamel hypoplasia,
(AIPG 2005) cones are involved •
• Bitot spots in the form atypical dentin formation
in bright light and of triangular plaques in and epithelial invasion
colour vision conjunctiva of pulpal tissue is a
•
• If xerophthalmia persists, characteristic feature
•
destruction of cornea • Enamel is affected more
occurs, leading to total than dentin
blindness. This condition is •
• Delayed eruption of teeth

known as keratomalacia.
(KAR 2000)
• • •
Vitamin B1 Wheat germs, Approx. 2mg • Thiamine • Dry beri beri or peripheral • None
(Thiamine) wholemeal cereals, pyrophosphate neuritis; (PGI 1998)
peas, heart, pork, (TPP) is a wet beri beri or cardiac
(Water-soluble, barn, oatmeal, liver, coenzyme of manifestations and
Thiamine gets brown rice thiamine and is cerebral or Wernickes
destroyed by mostly associated encephalopathy with
heat and long with carbohydrate Korsakoff’s psychosis
metabolism are seen. (AIPG 2010,
storage, but
not by freezing. •
• TPP is reqd for MAN 2000,MAN 1994)
•
Daily intake of acetyl choline • Also seen are Heavy
vitamin B1 is synthesis and ion muscle- and nerve
important, be- translocation of disturbances, tiredness,
cause the body neural tissue dyspepsias, dropsy,
•
• Plays important role cardiac insufficiency,
can´t store B1,
in transmission of cramps, paralyses, prickle
which comes
nerve impulses. in arms and legs
over the food)
• • • •
Vitamin B2 Milk products, Approx. 2 • FMN and FAD are • Nasolabial seborrhea or • Not known • Glossitis: the filiform
(Riboflavin) Meat, wholemeal mg two coenzyme forms dyssebacia papillae become atrophic
cereal, cheese, of riboflavin that •
• Vascularisation of cornea white the fungiform
(Water-soluble) eggs, liver, sea- participate in many papillae become engorge
•
• Scrotal dermatitis
fish, green leafy redox reactions and mushroom shaped,
•
vegetables, whey • skin inflammation, brittle resulting in magenta
•
• Responsible for
powder nails, anaemia, callus coloured tongue.
energy production.
attrition
•
FMN and FAD • Cheilosis, ocular lesions

are known as (KAR 1999)
Flavoproteins

ciency
•
• Assay of
glutathione
reductase in
erythrocytes will be
useful in assessing
the riboflavin
deficiency.
•
•
• •
Vitamin B3 Barn, peanuts, 13 - 16 mg • NAD and NADP+ are • Pellagra characterized • (with over 100mg • Bald tongue of sandwith
(Niacin, Nic- peas, liver, poultry, synthesized from by 3 Ds i.e. dermatitis, a day) pruritus, •
• Raw beefy tongue

otinc acid) fish, lean meat tryptophan. diarrhoea, dermatitis and nausea, allergies (AIPG 2010, AIPG 1995)
(KAR 2003) if left untreated may lead to
•
• The mucosa become fiery

(Water-solu- •
• Most enzyme 4th D i.e. death
red and painful

ble, effect is involving in redox (AIIMS 1994, MAN 2002,
•
APPSC 1999) • Salivation is profuse
outweighed reactions are
by sugar and dependent on
alcohol) NAD+and NADP+.
•
• Building and
degradation of
fat, protein and
carbohydrates, good
sleep
• • •
Vitamin B5 Liver, vegetable, Approx. 10 • Against turning • Burning feet syndrome • Excreted through
(Pantothenic wheat germs, mg grey, hair loss, •
• Nerve malfunctions, urine
acid) asparagus, hair and mucous bad healing of wounds,
crabs, meat, membrane illnesses,
Biochemistry

hair early turning grey,
(Water-soluble, sunflower cores, necessarily for weakened immune system
heat-sensitive) Pumpernickel the dismantling of
•
• Pantothenic acid is one of
fat, proteins and
the water soluble vitamins
carbohydrates
that is synthesized in body
(AIIMS May 2009)
•
• •
Vitamin B6 Bananas, nuts, Approx. 2 • PLP or pyridoxal • Peripheral neuropathy • With intake of this
(Pyridoxine) whole meal mg phosphate is a ( due to decreased for a longer time
AIPG 2012 products, yeast, coenzyme of B6 synthesis of serotonin in form of tablets
liver, potatoes, involved in various catecholamines) and it can deposit in
(Water-soluble, green beans, reactions like demyelination of neurons the body tissue
neither heat cauliflower, carrots transamination, •
• Isoniazid is an antagonist and lead to nerve
nor light-resist- decarboxylation, of vitamin B6. damages.
ing) deamination,
transsulfuaration,
etc
•
• Many biogenic
amines like
serotonin, serine
and catecholamines
are synthesized
from PLP.
87
BIOCHEMISTRY
BIOCHEMISTRY
88

ciency
• • •
Vitamin B7 Liver, cauliflower, approx. 0,5 • Participates in • States of exhaustion, skin • not known
(Biotin, Vitamin champignons, mg carboxylation inflammations, muscular
H) wholemeal reactions pains, hair loss, nausea
products, eggs, •
• It is involving in
(Water-soluble) avocado, spinach, gluconeogenesis,
milk citric acid cycle and
fatty acid synthesis.
• • • •
Vitamin B9 Liver, wheat germs, approx. 160 • Required for one • Macrocyctic anaemia • Allgergies, sleep • Glossitis: the filliform
(Folic acid, spinach µg carbon metabolism •
• Glossitis disturbances and papillae disappear first,
Vitamin M) •
• Reqd for synthesis bad moods (with but in advanced cases the
•
• Aminopterin and
of amino acids ( gly, more than 15 mg fungiform papillae are lost
methotrexate are structural
(Water-soluble, ser, )purines and a day) and the tongue become
analogue of folic acid used
do not tolerate pyrimidines smooth and fiery red in
in treatment of cancer.
with heat, light colour.
•
• Tetrahydrofolate
or oxygen) (THF or FH4) is the
active form of folic
acid.
• • • •
Vitamin B12 Liver, milk, yolk, approx. 5 µg • Building substance • Pernicious anaemia • Not possible, • Beefy red tongue with
(Cobalamin) fish, meat, oysters, of cytoblast and (AIIMS May 2010, because it will be glossopyrosis, glossitis
qurk, barn erythrocyte, 1996(AIPG 2007) excreted by the and glossdynia
(Water-soluble, nerve pains, skin •
• Neurological manifestation body •
• Hunter’s glossitis or
heatproof) and mucosa due to degeneration of moller’s glossitis which
inflammation, liver posterior and lateral tracts is similar to ‘bald tongue of
Also known damage of spinal cord sand with’ seen in pellagra.
as erythrocyte •
• Degeneration of myelin
growth factor sheath and peripheral
nerves occurs
•
•
• •
Vitamin C Citric fruits, black approx. 75 • Inflammation and • Deficiency may result in • In the case of • The pathognomic sign is
(ascorbic acid) currants, potatoes, mg - 200 mg bleeding-restraining, scurvy, characterized overdosing in form the swollen and spongy
paprika, tomatoes, (KAR 1998, assists the body’s by spongy & boggy of powder and pills gums, particularly the
(Water-soluble, collard, spinach, AP 1998, defences, protects gums, loose teeth nausea, vomiting interdental papillae is
oxygen and vegetables, radish AIIMS 2001) cells against anaemia swollen joints, and urine stones involved producing the
(KAR 1997) chemical destruction, delayed wound healing, can be the result. appearance of scurvy
dryness- activates enzymes,
•
sensitive, not • Man cannot haemorrhage, osteoporosis buds.
structure of
for a long time synthesize •
• Defective collagen •
• In severe cases,
connective tissue,
it due to synthesis haemorrhages to
stress) bones and dental
deficiency periodontal membrane
•
enamel, faster • Cork screw hair pattern
of L- healing of wounds, followed by loss of bone
with tiny bleeding points
glucolactone stabilisation of and loosening of teeth
around the orifice of a hair
oxidase psyche occurs.
follicle
enzyme.
•
• As it a strong •
• Woody legs with large
oxidant, it spares spontaneous bruises in
vit A, E and some lower extremities
B complex vitamins
•
from oxidation and • Trummer field zone is the
free radical injury. classic histologic picture of
bone in scurvy.

ciency
•
• • •
Vitamin D (Cal- Cod-liver oil, liver, approx. 5 µg • Regulation of • Rickets in children • (Only with man- • Delayed eruption of
ciferol) milk, yolk, butter, calcium- and •
• Osteomalacia in adults made Vitamin D) primary and permanent
sea fish, herring, phosphate Calcium deposits teeth
•
• Pigeon chest is an
(Fat-soluble, champignons, household, structure in bones, heart •
• Malalignment of teeth
important feature of rickets
light sensitive, avocado of bone, assist muscle, blood
•
•
• Bone curvature and • Developmental anomalies
heatproof) admission of vessels, stomach,
softening of dentin and enamel.
calcium headache,
•
•
• increased infection vomiting, swidle, • The teeth show wide
gastro-intestinal predentin zone with much
•
• renal osteodystrophy may
diseases interglobular dentin
be seen in patients with
•
chronic renal failure • The pulp horns are
elongated and extend high
reaching the DEJ
•
• •
Vitamin E (To- Sunflowers -corn 10 - 30 • By its antioxidant • Decreased male fertility • Particularly by
copherol)(AIPG -Soya and wheat mg (with property it protects •
• Impaired foetal maternal synthetically
1997) germ oil, nuts, fat-enrich the PUFA from per vascular relationship manufactured
flaxseed, salsify, nutrition oxidation reactions caps) bad healing
•
• Encephalomalacia
(Fat-soluble, it peperoni, collard, more) •
• Protect liver from of wounds,
•
• Nutritional muscular deficiency
is destroyed by avocado toxic compounds
dystrophy symptoms, swindle,
open storage, •
• Pressor and
deep-freezing nausea
maintains germinal
or cooking with epithelium of
much fat) gonads
•
• Prevents heart
disease by
Biochemistry

preventing the
oxidation of LDL
•
• Delays the onset
of cataract in
association of vit A
and C
•
• Protect RBCs from
haemolysis by
oxidising agents
• • • •
Vitamin K Eggs, liver, green approx. 2 mg • Necessary for • High doses of vitamin A • With intake for • Prothrombin levels below
(Phyllochinon) collard, green formation of the and E work against vitamin a longer time, 33% result in gingival
vegetable, bulbs, blood clotting factors K. it can become bleeding after tooth
(Fat-soluble, oatmeal, kiwi, •
• Brings about •
• Increased clotting time toxic, bleedings, brushing
food with Vita- tomatoes, cress post translational hot flashes, renal •
• Spontaneous gingival
•
• Deficiency uncommon
min K should modification of 2, diseases haemorrhages occur when
be stored in 7, 9,10 particularly prothrombin levels fall

dark) AIPG prothrombin (AIPG below 20 %
2002, AIIMS 2005, 2007, 2011,
2002 AIIMS May 2010,
KAR 1998, 1999)
89
BIOCHEMISTRY
BIOCHEMISTRY
90

ciency
• • •
Inositol • Green citrus fruits, • in man–not known • 4 -8 mg orally
grains, yeast •
• in animals – alopecia, •
• Uses:
dermatitis , fatty liver •
• Neuropathies
• •
Biotin • Liver, eggs, meal • Not known
• • •
Choline • Egg yolk, liver, meat • Fatty liver cirrhosis, • 3- 6 mg orally
hemorrhagic renal
lesions
Folic acid 0.05- 0.2 mg •

• Yeast, fresh green •
• Pernicious anaemia, •
• 15mg orally
vegetables, liver, glossitis, Megaloblastic

kidney, meat, cereals anemia
(AIPG 2006, 2011)
Cyanocobala- 1mcg •
• Liver, synthesized in •
• Pernicious anemia, •
• 100mcg orally or im
mine (vitamin colon but useful to host subacute degeneration
B12) of spinal cord, glossitis
• • • •
Vitamin C • Green vegetables, • Scurvy • 50–100mg/day • Oxalate and urate
(ascorbic acid) citrus fruits, •
• Uses: stones
(KAR 1999) strawberries, potato •• Iron overload in iron
•
• Scurvy, wound
healing, alkalosis, storage disease
alkaptonuria, prickly
heat
Biochemistry 91

Important Points About Vitamins
• Vitamins involved in tooth development and calcification (NEET 2013, AIPG 2012) • A, D
•

•
• Enamel hypoplasia is seen in deficiency of
•
• Hypervitaminosis is commonly seen in association with these vitamins
•
• Vitamin involved in collagen synthesis • Vitamin C
•
•
• In treatment of methemoglobinemia
•
• Acts as respiratory quotient
•
• Gingiva is most commonly affected by deficiency of
•
• Vitamins involved in electron transfer • Vitamin K and B12
•
•
• Heat stable and light sensitive vitamins
•
• Heat labile vitamins • Vit C, Folic acid and biotin
•
•
BIOCHEMISTRY
• Vitamin that cannot cross placenta • Vit D
•
•
• Vitamin which has action similar to hormone
•
• Vitamin stored in fat
•
• Vitamin stored in liver • A, D, K, B12, folate
•
•
• People consuming polished rice as staple food suffer from deficiency of • Vitamin B1
•
•
• People taking only maize as staple diet suffer from deficiency of • Niacin ( due to diets low in tryptophan)
•
•
• Vitamins associated with peripheral neuritis are • Vitamin B1, B12, B6,E
•
•
• Vitamins required for wound healing • A, C
•
•
• Toad skin (phrynoderma) is seen in deficiency of • Vitamin A and essential fatty acids
•
•
• Erythrocyte maturation factor • Vit B12
•
•
• Vitamin that inhibits lactation • Vitamin B6
•
•
• Schilling test is used to test the deficiency of • Vitamin B12
•
•
• Used in the treatment of homocysteinuria (AIPG 2006)
•
• Blue diaper syndrome is associated with • Tryptophan malabsorption
•
•
• Gusten • Zinc containing protein of saliva is important
•
•
for taste sensation
Vitamin involved in carboxylic group transfer Biotin

Coenzyme in transamination B6 (pyridoxine)
Megenta colour tongue is caused by deficiency of Riboflavin
Coenzyme A function depends on Pantothenic acid (KAR 2003, AIIMS 2001)
Vitamin involved in “one carbon” fragment or simple carbon units Tetrahydrofolate
Vitamin involved in collagen synthesis Vit. C
Vitamin involved in electron transfer Riboflavin, and Vit. K
Toxic if taken in excess dose Vit. A and D
Vitamin necessary for absorption of bile salts Vit. D and K
Vitamin necessary for coagulation Vit. K
Erythrocyte maturation factor Vit. B12 or cyanocobalamine
Vitamins stored in liver A,D,K,B12 , Folate
Vitamins stored in fat Vit. D
Vitamin present in cereals Thiamine
Vitamins which are present in animal food Vit B12 and D

Heat stable and light sensitive Vit. K and Riboflavin
Vitamins synthesized is gut B2, B12 and Vit. K
Vitamin synthesized by skin Vit. D
Vitamin which is anti-oxidant Vit. E
Vitamin used in treatment of methemogloninaemia Vit.C
Deficiency of which vitamin causes convulsions Pyridoxine
Vitamins required for wound healing Vit. A and C
Vitamins required for development of tooth and its maintenance Vit. A, C and D
Raw beef tongue or bald tongue of sandwith is caused by Niacin deficiency (KAR 1998)

Vitamin that causes neonatal jaundice Vit. K
BIOCHEMISTRY
Biochemical Function of Vitamins

Vitamin Classical Role More Recent Role
Vitamin C Hydroxylation Reaction In Vivo Antioxidant
Beta-carotene Provitamin A Antioxidant, Immune Function
Vitamin K Clotting Factors Calcium Metabolism
Vitamin D Calcium Absorption Mineralisation of Bone Differentiation and Growth, Immune Function
Vitamin B6 Coenzyme Steroid Regulation
Niacin Coenzyme Lipid Lowering
Folic Acid Production and Maintenance of new cells Protection Against Neural Tube Birth Defects
Folic Acid, B6 and B12 Energy Metabolism May Lower Risk of Heart Disease and Stroke*
Antioxidant vitamins Protection against Cancer and Heart Disease*
Dematitis is seen with deficiency of Pyridoxine

Biotin
B2, B3
Niacin
Dementia is seen in deficiency of Thiamine
Niacin
B 12
Angular stomatitis Riboflavin
Niacin
Pyridoxine / iron
Tongue changes in vitamin deficiency

• Riboflavin def.: Magenta tongue
•
• Niacin def.: Beefy/ fiery red tongue
•
• B12 DEF: Bald tongue
•
• Folic acid def.: painful tongue
•
VITAMIN ANTAGONIST
Vitamin K Dicoumarol, Heparin, Salicylates
Vitamin B1 Pyrithiamine and Oxythiamine
Pyridoxine Isoniazid
Biotin Biotin sulphonic acid, desthiobiotin
Folic acid Aminopterin, Methotrexate
Biochemistry 93

• Folic acid is associated with the metabolism of histidine. Formiminoglutamate (FIGLU) formed in histidine metabolism
•
accumulates and is excreted in urine. Histidine load test utilizing the excretion of FIGLU in urine is used to assess folic
acid deficiency.
Minerals
• Calcium • Required for bone mineralization

•
•
• Muscle contraction, cardiac function, digestive system function
•
• Also used for blood coagulation
•
• Known as ‘knitter’ as it promotes healing.
•
• Required for strength, power, tone, longevity, vitality, endurance and healing of wounds.
•
BIOCHEMISTRY
• Chlorine • To maintain function of numerous cellular pumps
•
•
• Iron • Heme moiety of haemoglobin
•
•
• Transport of oxygen
•
• Magnesium • Natural tranquilizer called the anti stress mineral.
•
•
• Aids in relaxing nerves, relieving tension, assisting digestion, activating enzymes important for protein and
•
carbohydrate metabolism
• Modulates the electrical potential across all cell membranes.
•
• Mineralization and proper functioning of ATP.
•
• Cofactor for various enzymes (AIIMS 2001)
•

• Important in the production and transfer of energy, muscle contraction and relaxation and nerve conduction.
•
• Phosphate • Acts as buffer in blood
•
•
• Reqd for bone mineralization and is necessary for energy utilization
•
• Potassium • Key circulating electrolyte
•
•
• Regulation of ATP-dependent channels along with sodium
•
• Also has role in the transmission of nerve impulses in the brain
•
• Sodium • Key circulating electrolyte
•
•
• Part of Na+/K+ ATPases and their primary function is in the transmission of nerve impulses in the brain.
•
• Sulphur • Primary function in amino acid metabolism
•
•
• Aids in elimination of toxic substances through agitation.
•
• Aids functions in enzyme reactions and protein synthesis and is important cellular respiration.
•
• Necessary for the modification of complex carbohydrates present in proteins and lipids.
•
• Copper • Formation of RBCs, synthesis of haemoglobin, and the formation of bone.
•
•
• Also reqd for energy production, wound healing, taste sensation, skin and hair colour.
•
• Involved in proper processing of collagen, and thus is important in skin, bone, and connective tissue production.
•
• Iodine • Also known as metabolizer.
•
•
• Reqd for synthesis of thyroid hormones
•
• Important role in regulation of energy metabolism via thyroid hormone functions.
•
• Helps protect brain by destroying harmful toxins.
•
• Manganese • Involved in reactions of protein and fat metabolism
•
•
• Promotes a healthy nervous system
•
• Necessary for digestive function, bone growth and immune function
•

• Necessary for the proper function of super oxide dismutase (SOD): enzyme reqd for preventing super oxide anions
•
from damaging cells.
•
•
Carpel tunnel syndrome: a painful condition in which arm tendons are weak or damaged, is a sign of manganese
deficiency.
• Molybdenum • Instrumental in regulating pH balance in the body.

•
•
• Co-factor in several oxidases such as xanthine oxidase (purine nucleotide catabolism), aldehyde oxidase, and
•
sulphite oxidase.
• Helps to eliminate toxic nitrogen waste by turning it into uric acid which can be excreted easily.
•
• Selenium • Modifier of activity of glutathione peroxidase
•
•
• Promotes normal body growth, enhances fertility, encourages tissue elasticity and is potent antioxidant that
•
naturally reduces the retention of toxic metals in body. (AIPG 2004)

BIOCHEMISTRY
• Zinc • Promotes wound healing

•
•
• Regulates immune function
•
• Serves as a cofactor for numerous anti oxidant enzymes (AIIMS 2006)
•

• Necessary for protein synthesis and processing of collagen.
•
• Chromium • Major factor in the development of heart disease.
•
•
• Helps regulate insulin and blood sugar levels.
•
• Plays an important role in the liver synthesis of fatty acids (burns fat).
•
• Part of glucose tolerance factor
•
• Cobalt • Stored in red blood cell
•
•
• Helps in repair of myelin sheath,
•
• Increases the effectiveness of glucose transport from the blood into body cells
•
• Increases the assimilation of iron and the building of red blood cells
•
• Agent of vitamin B12, it increases the ability to absorb it. (TNPSC 1999)
•

• Silver • Systemic disinfectant
•
•
• Neutralizes sodium fluoride poisoning beneficial for growing and thinning hair.
•
• Constituent of oxidase, cytochrome oxidase.
•
• Transported by albumin, bound to ceruloplasmin.
•
• Ceruloplasmin is copper dependent ferroxidase.
•
• Lithium • Trace element useful in treating alcoholism, maniac depression and mental instability.
•
•
Cofactor Enzyme
Zinc • Dehydrogenase
•
• Alkaline phosphatase
•
• Carbonic anhydrase
•
Copper • Tyrosinase
•
• Cytochrome oxidase
•
Magnesium • Hexokinase
•
• Glucokinase
•
• Phosphofructokinase
•
Potassium • Pyruvate kinase
•
Iron • Peroxidase
•
Manganese • phosphatase
•
• glycosyl transferase
•
Biochemistry 95

MISCELLANEOUS
CELL MEMBRANE
Characteristics of Bio-Membrane
• Basic or key structure is the lipid bilayer
•
• Membrane is asymmetric and dynamic structure
•
• Hydrophobic regions of the phospholipids are protected from the aqueous environment, while hydrophilic ends are
•
immersed in water. Lipids and certain proteins show rapid lateral diffusion. Phospholipids exhibit very slow Flip-Flop
movements but proteins do not show flip-flop
• Peripheral proteins do not interact with PL directly. They are loosely bound to membrane
•
• Protein composition differs in membranes. Most membrane proteins can be separated from each other by using SDS-
•
PAGE
BIOCHEMISTRY
The fluid mosaic model of Membrane
• Proposed by Singer and Nicholson in 1972
•
• The membrane consists of a bimolecular lipid layer with proteins inserted in it or bound to either surface
•
• Integral proteins are firmly embedded in lipid bilayers. Some of these proteins known as transmembrane proteins completely
•
span the bilayer.
• Integral proteins have two hydrophilic ends separated by an intervening hydrophobic region (transverse region). They are
•
most abundant, usually globular and are amphipathic. They interact with phospholipids and are asymmetrically distributed
across the membrane bilayer.
• All the glycolipids and many of the proteins have externally exposed oligosaccharide chains.
•
• Fluidity of membranes are largely dependent upon the lipid composition of the membrane
•
Structure of cell membrane
• Proteins
•
Type Description Examples
Integral proteins or Span the membrane and have a Ion channels,
transmembrane proteins • Hydrophilic cytosolic domain, which interacts with internal molecules. proton pumps, G
•
• A hydrophobic membrane-spanning domain that anchors it within the cell protein coupled
(AIPG 2004)
receptor
•
membrane and
• A hydrophilic extracellular domain that interacts with external molecules.
•
The hydrophobic domain consists of one, multiple, or a combination of a-helices
and b sheet protein motifs.
Lipid anchored proteins Covalently-bound to single or multiple lipid molecules; hydrophobically insert into G Proteins
the cell membrane and anchor the protein. The protein itself is not in contact with
the membrane.
Peripheral proteins Attached to integral membrane proteins, or associated with peripheral regions of the Some enzymes,
lipid bilayer. These proteins tend to have only temporary interactions with biological Some hormones
membranes, and, once reacted the molecule dissociates to carry on its work in the
cytoplasm.
• Lipids: The cell membrane consist of three classes of amphipathic lipids: phospholipids, glycolipids, and cholesterols.
•
Cardiolipin is an important component of the inner mitochondrial membrane, where it constitutes abut 20% of the total
lipid composition. (APPSC 1999)

• Carbohydrates:Plasma membranes also contain carbohydrates, predominantly glycoproteins, but the some glycolipids
•

(cerebrosides and gangliosides). For the most part, no glycosylation occurs on membranes within the cell; rather
generally glycosylation occurs on the extracellular surface of the plasma membrane. Proteoglycans are glycoproteins that
heavily glycosylated. They have a core protein with one or more covalently attached glycosaminoglycan (GAG) chain (s).
Proteoglycans occur in the connective tissue.

Buffering Systems
The three most important buffering systems in biological systems are proteins, bicarbonate, an phosphate. The major buffer
in plasma and interstitial fluid is bicarbonate, whereas and organic phosphate esters are the major buffers of intracellular fluid.
Protein buffering system Histidine is the only amino acid The imidazole side Histidine plays a key role in making
with good buffering capacity at chain of histidine has haemoglobin an excellent buffer in red blood
physiological pH. a pka that ranges from cells
5.6-7.0
Bicarbonate buffering Carbonic acid (H2CO3) is the That pka for this reaction The bicarbonate-CO2 system is the most
system proton donor, bicarbonate is 6.1 important buffer in maintain the pH of blood
anion (HCO3-) is the proton plasma and interstitial fluid at its normal value
acceptor. of 7-4.
The strength of this buffering To keep blood pH at 7.4 the HCO3: H2CO3
system lies in the ability of ratio should be: 20: 1
carbonic acid to be converted
BIOCHEMISTRY
to carbon dioxide.
Phosphate system: The phosphate buffering The pka 6.8 is The phosphate buffering systems of little
system consists of H2PO4– as sufficiently close to the importance in plasma and interstitial fluid
HPO42/H2PO4 - the portion donor and HPO32– normal intracellular pH because of the low concentrations of
as the proton acceptor. to make it an ideal phosphates in extracellular fluids. Ideal buffer
in those fluids that contain high concentrations
of phosphate, such as Red blood cells (not
whole blood) and kidney tubules.
Organic phosphate 6.5-7.5

esters
Pasteur effect: Availability of plenty of oxygen enhances the reactions of citric cycle and leads to a retardation of the
glycolytic reaction. The rate-limiting step in glycolysis, phosphofructokinase, is inhibited by citrate and ATP. A consequence
of the inhibition of phosphofructokinase-1 is an accumulation of glucose 6- phosphate that, in turn, inhbits further uptake of
glucose in extrahepatic tissues by allosteric inhibition of hexokinase.
Crabtree effect: This is reverse of Pasteur effect. High concentrations of glucose inhibit citric acid cycle and enhance glycolysis.
Bohr effect is related to oxygenation of haemoglobin.
Abnormal urine constituent Test

Albumins, globulins Heat coagulation test
Proteins Sulfosalicylic acid test
Blood Benzidine test
Glucose Benedict’s test
Specific test for glucose Glucose oxidase test
Ketone bodies Rothera’s test
Bile salts Hay’s test, Pattenkofer’s test
Bile pigments Fouchet’s test, Gmelin’s test
Xenobiotics
The purpose of metabolism of xenobiotics is to increase their water solubility (polarity) and thus facilitate their excretion
from the body. Very hydrophobic xenobiotics would persist in adipose tissue if not converted to more polar forms.
It occurs in two phases:
Phase 1: Major reaction involved is hydroxylation. Catalyzed by cytochrome P450 (AIPG 2003, KAR 1999)

Phase 2: Hydroxylated compounds converted to various polar metabolites by conjugation with glucoronic acid. Sulfate, acetate,
glutathione or certain amino acids, or by methylation.
Biochemistry 97

Hydroxylation is the chief reaction involved in phase I, in which the hydrophobic substrates are converted to hydrophilic
compounds. In phase II, these hydroxylated derivatives (already hydrophilic) are conjugated with molecules such as glucuronic
acid, sulfate, or glutathione, which renders them even more water-soluble, and they are eventually excreted in the urine or
bile.
Tissue-specific synthetic reactions

Include the following four types of reactions:
Hydroxylation Cortisol synthesis by the adrenal cortex Hydroxylation at carbons 11, 17 and 21
reactions
Aldosterone synthesis Hydroxylation at carbons 11, 18 and 21
Side chain cleavage C19 androgen 17, 20-desmolase removes the remainder of the side chain and
converts the steroid a C19 androgen
BIOCHEMISTRY
Reduction Dihydrotestosterone (DHT) 5- -reductase reduces the double bond in testosterone to form
a
dihydrotestosterone (DHT). This enzyme is present in tissues that use
DHT as the major androgen
Demethylation Convert androgens to estrogens Aromatase removes the methyl group that extend up between the A
and B rings of the steroid nucleus and makes the A-ring aromatic
Nutritive Value of certain common food (AIPG 2002)

• Both cereals and pulses contains essential amino acids
•
• Best measure of protein nutrition is serum albumin. (normal - >3.3gm/dl)
•
• Most essential fatty acid–Linoleic acid
•
• Copper deficiency
•
– Seen in infants fed on cow’s milk for prolonged time
–
– Causes neutropenia
–
• Rice
•
– 6-9% proteins, rich in lysine
–
– Milling removes thiamine, riboflavin and proteins
–
• Wheat
•
– 9-16% protein, less theorenine and lysine
–
• Maize
•
– Has significant amounts of carotenoid
–
• Pulses
•
– 20-25% proteins
–
– Rich in lysine
–
– Poor in methionine and cystein
–
– Soyabean – 40% protein
–
– Called poor man’s meat
–
• Green vegetables
•
– The darker the leaf, more the nutrition
–
– Rich in lysine
–
– Deficient in sulfur containing amino acids
–
– Low bioavailability of calcium, iron because of oxalates
–
• Egg
•
– All nutrients except carbohydrats and vitamin C
–
– 10% protein, iron,calcium and cholesterol (AIIMS Nov 2013)
–


– Egg protein has 100% bioavailability (milk protein – 75%)
–
– Serves as a standard to compare other proteins
–
– Have all the essential amino acids
–
– Raw egg white is not assimilated. Boiling destroys biotin which hampers the biotin utilization.
–
• Nuts
•
– Rich in protein, fats and cellulose
–
– Difficult to digest
–
– Increased vitamin B and minerals
–
– Maximum iron – pistachis
–
– Good source of essential fatty acids
–
– Peanuts must be dried to avoid aflatoxin
–
• Fish
•
BIOCHEMISTRY
– Liver oils rich in vitamin A and D

–
– Oyesters and lobster are rich in iodine
–
– No carbohydrates
–
• Vegetable oils are deficient in vitamin A and D
•
Reactive oxygen species (AIIMS Nov 2013, NEET 2013)
These are synthesized via the NADPH oxidase pathway and are releasd from neutrophils and macrophages activated by
microbes or immune complexes. Within the lysosomes, these function to digest the microbes and necrotic cells. ROS species
are responsible for tissue injury by several mechanisms such as
• Endothelial damage
•
• Protease activation and anti protease inactivation
•
• Direct injury to tumor cells, erythrocytes etc
•
Antioxidants
Antioxidants are those substances which when present in lower concentrations compared to those of an oxidisable substrate,
will significantly delay or inhibit oxidation of that substrate
Mechanism Of Action
• Prevention of formation of free radicals
•
• Interception of free radicals by scavenging the reactive metabolites and converting them to less reactive molecule
•
• Facilitating the repair of damage caused by free radicals
•
• Providing a favourable environment for effective functioning of other antioxidant.
•
Antioxidants can be categorized by several methods
Based on Mode A. Preventive Antioxidants

of Action • Suppress the formation of FR e.g., SOD, catalase, GSH-Px, transferrin
•
B. Radical Scavenging Antioxidants
• Scavenges radicals to inhibit chain initiation and break chain propagation.
•
– e.g., Vit A,Vit E,Vit C, Ubiquinol
–
C. Repair and denovo enzymes
• Repair the damage and reconstitute the membrane e.g., DNA repair enzymes, protease, transferase
•
Based on Loca- • Intracellular
•
tion – SOD 1 and 2, catalase, GSH-Px, GSH, ubiquinone (reduced form)
–
• Extracellular
•
– SOD-3, GSH, lactoferrin, transferrin, cartoenoids, ascorbate, haptoglobin, uric acid
–
• Membrane associated
•
– α-tocopherol
–
Biochemistry 99

Based on Solu- • Water soluble
•
bility – GSH, ascorbate, albumin, uric acid, haptoglobin, ceruloplasmin, polyphenolic flavenoids
–
• Lipid soluble
•
– α -Tocopherol, carotenoids, bilirubin, ubiquinone (reduced form)
–
Based on • DNA protective antioxidants
•
Structures they – SOD 1and2, GSH, GSH-Px, DNA repair enzymes
–
Protect • Protein protective antioxidants
•
• Sequestration of transition metal
•
• Scavenging by competing substrates
•
• Antioxidant enzymes
•
• Lipid protective antioxidants
•
– α -Tocopherol, ascorbate, carotenoids, bilirubin, reduced ubiquinone, GSH, GSH-Px
–
Based on their • Exogenous antioxidants (diet)
BIOCHEMISTRY
•
Origin – Carotenoids, ascorbic acid, tocopherols, folic acid, cysteine
–
• Endogenous antioxidants
•
– Catalase, SOD, GSH-Px, GSH, transferrin, ferritin, proteases
–
• Synthetic antioxidants
•
– N-acetylcysteine, penicillinamine, tetracyclines
–
Glutathione • Essential tripeptide synthesised within cell,
•
• It has central thiol containing cysteine aminoacid.
•
• It is pivotal molecule to immune system for regulation of IL-2 dependent T-lymhocyte proliferation.
•
• The increasing cytosolic cysteine concentration of monocytes and macrophages using synthetic form of cysteine
•
called N-acetyl cysteine blocks ROS mediated activation of NF-kB and pro-inflammatory cytokine production
• Role of Glutathione:
•
– One of the most vital intracellular antioxidant scavengers
–
– Maintains the intracellular redox balance –regulating the signalling pathways affected by oxidative stress.
–
– Acts as neurotransmitter governing neuro-immune- endocrine functions.
–
– Important to preservation of other antioxidant species (vit E and C)
–
– Regulates the activation of redox sensitive transcription factors, controlling pro-inflammatory cytokine pro-
–
duction- great importance in periodontal diseases.
Superoxide • Important defense mechanism against excess superoxide release within gingival fibroblasts.
•
Dismutases Types:
(Sod) • SOD 1- Cu 2+
2+
/ Zn2+dependent enzyme found in cytosol
•
• SOD 2- Mn dependent enzyme found in mitochondria
•
• SOD 3- extracellular enzyme - low levels
•
Activates the conversion 10,000 times faster than spontaneous dismutation

02.- + 02.- + 2H+ ‘02 + H202

Catalase Catalase contains heme bound iron and is mainly located in peroxisomes . With great efficacy, dismutases the H202 to
form H2O and O2 and it has very high turn over
Antioxidant A diet rich in FRUITS and VEGETABLES And Nutritional Supplements

Enzymes
Ascorbic Acid The activities of vitamin C includes

• Protection against ROS present in cigarette smoke
•
• A powerful scavenger of HOCL, OH, 02.- , ‘02
•
• Possesses the ability to regenerate á-tocopherol from radical that forms at membrane surfaces
•
• Prevents Fenton reaction by↓ heme breakdown
•
• Reduce CRP mediated expression of monocyte adhesion molecules
•
• Ability to ↓ pro-inflammatory gene expression
•
GCF levels of ascorbate three fold higher than plasma level (30-60 mµ) and has been shown to prevent activation
of neutrophil collagenase.
100
Alpha –To- • Most important and effective lipid soluble AO vital to maintain cell membrane integrity against lipid peroxidation by
•
copherols peroxyl radical scavenging.
(Vitamin E) ••
Located within cell membrane phospholipids and is a major chain breaking antioxidant but has limited mobility (cell
membranes) which restricts its efficacy.
Carotenoids • Lipophilic and higher plasma concentration protects against various inflammatory and malignant diseases.
•
(Vitamin A) • Includes
•
– Lycopene- predominates in plasma
–
– á carotene – scavenges peroxyl radical
–
– â carotene – scavenges singlet oxygen
–
– Retinol (vitamin A1)
–
– Dehydroretinol (vitamin A2)
–
It is derived only from diet. Vitamin A as an antioxidant is controversial as its behaviour depends upon oxygen tension of
the enviornment, at higher oxygen tension it has pro-oxidant behaviour, associated with substantial determental effects
upon surrounding tissues.
BIOCHEMISTRY
Polyphenols • There are 4000 flavenoids, most common are catechin, epigallocatechin gallate and quercetin
•
• Dietary intake– red wine, green tea, vegetables
•
• Mechanism
•
– Radical scavenging
–
– Terminates lipid peroxidation
–
– Iron chelation
–
– Sparing vitamin E
–
– restoration of Vitamin C
–
Uric Acid • Uric acid major (70%) antioxidant in saliva and is found in GCF also.
•
• Uric acid is a relatively powerful scavenging antioxidant of - HOCL, OH, ‘02.
•
• Protects alpha 1-antitrypsin when combined with ascorbate
•
• Binding with divalent metal ions prevents Fenton reaction
•
Ubiquinone • Vital component of mammalian cell mitochondria and performs an important function in hydrogen electron transfer
•
system. It has strong antioxidant properties in its reduced form.
• Co enzyme Q10 deficiency has been demonstrated in the gingival tissues of periodontitis subjects.
•
Antioxidant Capacity of Saliva Antioxidant Capacity of Gcf
• Uric acid dominant AO in saliva and display conc similar to • Reduced glutathionemajor AO in GCF
•
•
serum.
• Albumin and ascorbic acid – other AO, but conc less than serum • Repeated washing and centrifugation, results in oxidation of
•
•
several AO by time of assay.
• Stimulated saliva contains lower conc of AO but when flow rates • Storage of fluid samples at -20oc results in loss of AO capacity
•
•
are taken into account, AO capacity is higher than unstimulated (immersion in liquid nitrogen)
saliva
Good to Know Points

• Schilling test is used to detect vitamin B12 deficiency
•
• Salkowski test is a test for cholesterol
•
• Blue daper syndrome is associated with tryptophan malabsorption
•
• Glycemic index measures the time course of post prandial glucose concentrations from a graph.
•
• Foods like high fiber content and low glycemic index (e.g. grains, fruits and vegetables) should be preffered for
•
consumption.
• Gusten, a zinc containing protein of the saliva is important for taste sensation
•
• Zellweger syndrome is due to absence of peroxisomes in all most all tissues as a result of whichlong chain fatty acids are
•
not oxidized and accumulated in liver and brain. So this syndrome is also called as cerebrohepatorenal syndrome.
Biochemistry 101

Arginine
• Substrate for the production of nitric oxide, a wonder molecule with a wide range of functions like:
•
– Acts as a vasodilator and causes relaxation of smooth muscles
–
– Regulates blood flow and blood pressure
–
– Inhibits platelet aggregation and adhesion
–
– Functions as neurotransmitter
–
– Mediates bactericidal action of macrophages
–
– Involved in erection of penis
–
• These actions of nitric oxide are mediated through cGMP and protein kinase G
•
Somatomedin
• Growth factor secreted by liver that mediates growth promoting effects of growth hormone
•
BIOCHEMISTRY
• Actions
•
– Formation of chondroitin sulphate
–
– Belongs to insulin family and resembles insulin, hence elicits insulin like effects.
–
Biochemical Functions of Mature RBC
• Anaerobic glycolysis – end product is lactate
•
• Pentose phosphate shunt (synthesis of glutathione and NADPH)
•
• Methemoglobin reductase system (reduces heme iron from Fe+++ to Fe++)
•
• Synthesis of 2,3 DPG (causes right shift of ODC) (AIIMS may 2009)
•
RBC Metabolism
• RBC is highly dependent on glucose as its energy source. Membrane contains high affinity glucose transporters
•
• As there are no mitochondria there is no production of ATP by oxidative phosphorylation. Only anaerobic glycolysis is
•
possible, which produces lactate and ATP.
• RBC’s lack mitochondria (so no Kreb’ s cycle in RBCs), nuclei and class –I and II HLA antigens
•
• Synthesis of glycogen, fatty acids, protein and nucleic acids do not occur in RBCs.
•
• Non-heme iron is present in foods of vegetables origin (legumes, nuts, green leafy vegs, jaggery). It is in Fe+++ form.
•
• Foods rich in heme iron are liver, meat, poultry and fish (iron is in ferrous Fe++ form for better absorption)
•
• All cytochromes are dehydrogenases except cytoxidases.
•
• Large amount of iron inhibitors are present in vegetarian foods – like phytate in bran, phosphate in egg yolk, tannin in
•
tea and oxalates in vegetables
Points to note
• NOT true of lipoprotein lipase – does not require apo CII as a cofactor
•
• The concentration of 2,3 DPG in red cells does NOT increase in response to – Hypoxanthine
•
• In humans acetyl CoA can NOT directly give rise to formation of Glucose
•
• Insulin does NOT cause Ketogenesis
•
• Free radicals in lens are NOT held by Vitamin A
•
• cAMP is NOT a second messenger for Dopamine
•
• Amino acid which CANNOT be phosphyrylated by prokaryotic protein kinases – Asparagine
•
• NOT true of glutathione – Converts Hb to Met Hb
•
• Eukaryotic membrane does NOT contain– Triglycerides
•
• NOT a cause of fasting hypoglycemia – Glucagon excess
•
102
• Does NOT occur when liver glucose is short–Increase in fructose 2,6 biphosphonate
•
• NOT degraded by colonic flora–lignin
•
• TPN does not provide–Fibre
•
• NOT true about trace elements–Zinc deficiency causes pulmonary fibrosis
•
• NOT true about HDL–can oxidize LDL
•
• Free radical are not produced by–Glutathione Peroxidase
•
• NOT a method of total protein estimation – bromocresol green assay (BCG assay)
•
• NOT true about oxygenase enzyme–Involved in carboxylation of drugs
•
• Acetoacetic acid (KB) and fatty acids–are not substrate for glucose synthesis
•
• Sedoheptulose PO4 is not a product of Pentose pathway
BIOCHEMISTRY
•
• Phosphate is NOT a product of ganglioside
•
• HMG CoA is NOT involved in Isoleucine metabolism
•
• NOT a secondary messenger–guanyl cyclise
•
• Structure of protein CANNOT be determined by HPLC
•
• Phosphoenol pyruvate is NOT produced directly from pyruvate
•
• Enzyme NOT used in gluconeogenesis–Pyruvate dehydrogenase
•
• Hydrogen bond is NOT present in primary structure
•
• Covalent bond is NOT present in antigen antibody complex or enzyme substrate complex
•
• Pyridoxal phosphate is NOT required for hydroxylation of proline in collagen synthesis
•
• Tyrosine is NOT an essential amino acid (but it becomes essential in PKU)
•
• Glutamate is NOT a precursor of Histidine
•
• Reaction which does NOT occur in glycolysis– hydration
•
• Rothera’s test detects ketone bodies but it can NOT detect β-hydroxy butyrate
•
• Biotin is NOT required as a co-enzyme in Pyruvate dehydrogenase (it requires thiamine)
•
• Sphingomyelin does NOT contain Lecithin
•
• Cherry red spot is NOT seen in Gauchers disease
•
• Hepatomegaly is NOT seen in Hepatic porphyria
•
• Ligase chain reaction is NOT useful for detection of Mutation
•
• Tissue which can NOT catabolise Acetoacetate to CO2, H2O and usable energy – Brain and liver
•
– Skeletal muscle maintain large stores of glycogen which provide a source of glucose for energy during exertion
–
– In resting muscle preferred fuel is fatty acids
–
– Fatty acids are major fuel source for heart, renal cortex, adipose tissues
–
– Retina completely depends upon glucose as a fuel source
–
– Proteins that assist folding include – protein disulphide isomerase, proline cis – trans isomerase and chaperons
–
– Abnormal folding of proteins (β-amyloid), unassisted by chaperones, leads to Alzheimer’s disease.
–
CHAPTER 3
Physiology
Objectives
• Molecular Physiology • Excretory System and Water Ion Balance

• Nervous System • Regulation of Organic Metabolism

• Physiologic Muscle System • Endocrine System

• Cardiovascular System • Reproductive System

• Respiratory System • Miscellaneous

• GIT (Gastrointestinal Tract)

CELLULAR AND MOLECULAR PHYSIOLOGY
Extracellular Matrix (ECM)
• Cells are surrounded by ECM often known as connective tissue.
•
• ECM contains 3 major classes of molecules
•
Structural fibrous proteins Adhesive glycoproteins Glycans
• Collagen: Most abundant protein found in animal • Fibronectin: involved in cell adhesion and Hyaluronic acid, sulfates
•
•
world. It constitutes 25% of mammalian protein. It migration. (chondroitin, keratin, heparin,
has a triple helix structure. • Laminin: abundant in basal lamina dermatan).
•
• Elastin: provides extensibility and recoil in lung, (basement membrane) and glomerular
•
blood vessels and ligaments. basement membrane; they are cross shaped
 
• Fibrillin: Large glycoprotein present in microfibrils molecules. (AIPG 2004, 2008)

•
(in zonular fibres of lens, periosteum, elastin
fibres in aorta). Mutations in fibrillin-1 results in
 
Marfan’s syndrome; Mutations in fibrillin-2 result
in congenital contractural arachnodactyly .
 
• Fluidity is decreased by --- Saturated FA eg: stearic acid and palmitic acid
•
• Cholesterol modifies the fluidity of the membrane
•
• At temperature below Tm – it interferes with the interaction of the hydrocarbon tails of FA and thus increasing fluidity
•
• At temperatures above Tm it limits or decreases fluidity
•
• As membrane fluidity increases so its permeability to water and other small hydrophilic molecules
•
104
Transport Across Biomembrane

Mechanism Mode of transport Kinetic Examples
Active transport Carrier mediated Against concentration and electrical Na+ K+ ATPase (sodium pump)
(electrochemical) gradient, energy (ATP)
required
Facilitated diffusion Passive from high to low energy, Substance is moved in the direction of Glucose transporters, (GLUTS),
but carrier is required electro-chemical gradient hormones
Simple diffusion Passive carrier is not required Diffusion of lipid soluble drugs
Osmosis Passive Fluid shifts from hypo and hyper osmolar
compartment
Rough Endoplasmic Reticulum (RER) to serine by the enzyme glycosyltransferase); sulfation;

• A membranous organelle that contains ribosomes and phosphorylation. (AIPG 2005)
•

attached to its cytoplasmic surface. – Protein sorting and packaging: Secretory proteins (e.g.,
PHYSIOLOGY
–
• Functions of rER include: insulin) are packaged into clathrin-coated vesicles;
•
– Synthesis of proteins: secretory (exported) proteins cell- membrane proteins (e.g. hormone receptors)
are packaged into nonclathrin-coated vesicles; and
–
(e.g., insulin), cell membrane proteins (e.g., hormone
receptors), and lysosomal enzymes. lysosomal enzymes are packaged into clathrin coated
– Co-translational modification of proteins, including vesicles after phosphorylation of mannose to form
mannose-6-phospahte.
–
N-linked glycosylation (addition of sugars to
– Membrane recycling.

aspargine begins in the rER and is completed in
–
 
the Golgi complex) – Vesicular trafficking proteins: COPI: retrograde,
–
Hydroxylation of proline and lysine during Golgi ER COPII: anterograde, RER,cis-Golgi. Clathrin:
 
trans-Golgi lysosomes, plasma membrane endosomes

collagen synthesis
Cleavage of the signal sequence (receptor mediated endocytosis) (AIPG 2005)

Folding of the nascent protein into a 3-D Lysosomes

configuration
• Contains lytic enzymes e.g. ribonucleases,
Association of protein subunits into a multimeric
•
deoxyribonucleases, phosphatase, glycosidase

complex.
• Nissl bodies (in neurons): Synthesize enzymes (e.g., • Interior is more acidic due to proton pump
•
•
Chat) and peptide neurotransmitters • Vitamin A overdose causes injury to lysosomes
•
• Free ribosomes: Unattached to any membrane; site of • Processing/modification of oligosaccharides (AIPG 2001)
•
•
synthesis of cytosolic and organellar proteins.
Organelle Function
• Mucus secreting goblet cells of small intestine and Nucleolus Synthesis of rRNA
•
antibody-secreting plasma cells are rich in RER
Ribosomes Site of protein synthesis, translation of mRNA
Smooth Endoplasmic Reticulum (SER) RER Site of protein synthesis
SER Site of steroid synthesis/detoxification and
• SER is the site of steroid synthesis and detoxification of fatty acid elongation
•
drugs and poisons.
Golgi body Processing and packaging of proteins and
• Liver hepatocytes and steroid producing cells of the lysosome formation (AIPG 2005, 2003)
•

adrenal cortex are rich in SER. Lysosomes Suicidal bags of cell
Peroxisomes Contains oxidases
Golgi Complex
• Stack of membraneous cisternae that receives vesicles of Telomeres (AIPG 2009)
•
newly synthesized proteins from the rER. • After a fixed number of divisions, normal cells become
•
• Functions of Golgi complex include: arrested in a terminally non dividing state known as
replicative senescence.
•
– Posttranslational modification of proteins:
• As the cell divide there is shortening of some specialized
–
completion of N-linked glycosylation that began in
•
the RER; O- linked glycosylation (addition of sugars structures called telomeres at the end of the chromosomes
Physiology 105

that are responsible for complete replication of – Microtubules associated proteins are: Kinesin,
–
chromosomal ends and protecting chromosomal termini dynein, and dynamin
from fusion and degradation. – Centrosome is the organizing centre of cell for
–
• As the somatic cells divide, the telomeres keeps on assembly of microtubules
•
shortening and the chromosome is now unprotected and – Actin is the most abundant protein present in
–
cell replication is arrested. (AIPG 2006, 2009, 2013) mammalian cells

– Selectins play key roles in inflammation and in
Cytoskeleton
–
lymphocyte homing
Microfilament Microtubules Intermediate fila- • Cytoskeleton are essential for
ments
•
– Leukocyte movement
Actin and myosin Hollow slender • Resists external
–
– Constitute structure like cilia, spindles, centrioles
•
and their regulatory tubes made up of pressure
–
protein a protein called • Are not involved in process (dendrites) of neuron – microtubule
‘tubulin’
•
movement of cell/ – Sperm motility
PHYSIOLOGY
–
flagella – Ciliary mobility of respiratory epithelium
–
• Motility of the cell is due to tubulin proteins present in – Provides flexible intracellular scaffolding that
•
–
microtubules. Microcytes are essential for leucocyte helps resist extra oral pressure applied to the cell –
migration and phagocytosis intermediate filaments
• Coordinated dynein: Microtubule interactions within – Keratins, neurofilaments, desmin, vimentin, glial cells
•
–
the axoneme are the basis of ciliary and sperm movement are examples of intermediate filament. (AIPG 2005)

Cell Junctions
Zonula Occludens (Tight • Composed of claudins and occludins.
•
Junctions) • Extends around the entire perimeter of cells; outer leaflets of the cell membrane of two adjoining cells
•
fuse at various points.
 
• Prevents or retards the diffusion of material across an epithelium via the paracellular pathway (i.e.,
•
through intercellular space).
Zonula Adherens (Interme- • Completely encircles the cell; however, adjacent plasma membranes are separated by a gap of
diate Junctions)
•
approx. 20 nm; provides rigidity and stability.
Macula Adherens (Desmo- • Situated below zonula adherens; provides strong attachment between cells.
somes)
•
• Found in tissues subject to physical stress
•
Hemidesmosomes • Anchoring junctions for attachment of a cell to underlying extracellular matrix
•
Gap Junction • Occur at small discrete sites for metabolic and electrical coupling.
•
• Cell membranes of two adjoining cells are separated by an intercellular space bridged by connexons.
•
• Connexons contain central pores that allow passage of ions, steroids, amino acids, and small
•
molecules (< 1200 d) between cells.
 
Cell adhesion molecules • Integrins, Cadherins, Selectins, IgG superfamily molcules
•
Also note
• Largest organelle of eukaryotic cell is endoplasmic reticulum
•
• Nisse granules are are seen in cytoplasm of neurons – composed of rough endoplasmic reticulum and riboncueloproteins.
•
 
• Lipofuscin (lipochrome): “wear and tear” pigment; yellow brown intracellular lipid pigment found in old age; found in
•
 
senile dementia, brown atrophy of heart and in severe wasting due to malnutrition.
• Clara cells
•
– They are cuboidal non ciliated cells.
–
– It is also interesting that, like type 2 alveolar cells, they also give rise to other epithelial cells in epithelial regeneration
–
after damage. (AIPG 2007)

106
– In humans these cells are restricted mainly to the terminal and respiratory bronchioles; although in other species they
–
also occur at higher levels of the respiratory tract, and even in the nasal mucosa.
• Laws and Principles
•
Isohydric principle All buffer pairs in a homogenous solution are in equilibrium with the same [H+]
Henderson Hassel- When acids are placed in solution,
bach equation pH = pKa + log [A-/HA].
Ficks principle Deals with diffusion.

Gibbs Donnan In presence of a non diffusible ion, the diffusible ions distribute themselves so that at equilibrium, their concentration
 
effect ratios are equal
Nernst equation At equilibrium, the distribution of permanent ions across the membrane is asymmetric and an electric gradient
 
exists, whose magnitude can be determined.
Hagen Poiseuille Is the basis for thermodilution method used in measurement of cardiac output by pulmonary Catheter.
 
principle
PHYSIOLOGY
Plasma Proteins
Albumin Globulins Fibrinogen
 
• Most abundant plasma protein • Gamma globulins are • Large size
•
•
•
• Exerts 70-80% of colloidal osmotic pressure. concerned with antibody • Contributes to viscosity
function.
•
•
• Has low viscosity and high concentration in blood. of blood
• Antibodies are γ globulin
•
• Synthesized by liver (KAR 2003)
•
• Albumin: Globulin ratio = 2:1
•

• Oncotic pressure of plasma is mainly due to albumin (AIPG 2011)
•
•
Globulins
α1- globulin α2- globulin β-globulin
• α1 –acid glycoprotein (orosomucoid) • Ceruloplasmin: • b-lipoproteins (LDL)
•
•
•
– Binds progesterone – Binds and transports copper in plasma • Transferrin (siderophyllin)
–
–
•
– Indicator of acute inflammation – ↑in pregnancy, RA – Carrier of iron, bacterostatic
–
 
–
• Alpha Feto, Proetin α1-antitrypsin, • Haptoglobin
–
– ↑in iron deficiency anemia, and in
•
•
Trypsin. Plasmin, thrombin etc.
–
 
– Binds and transports free hemoglobin last month of pregnancy
–
 
• Hemopexin: binds heme – ↓in PEM, MI, cirrhosis, nephrotic
•
–
 
syndrome C-Reactive Protein
 
Good to Know
• Anti protease plasma proteins are
•
– Anti chymotrypsin
–
– α1 chymotrypsin
–
– Macroglobulin
–
– Antithrombin
–
• Beta 2 microglobulin levels are increased in patients with chronic dialysis
•
• Serum beta 2 microglobulin is the single most powerful predictor of survival in patients with multiple myeloma
•
• α 2 macroglobulin is a large plasma glycoprotein which has role in transport of zinc and acts as a pan proteinases
•
inhibitor
Transport/Binding Proteins
Ceruloplasmin Binds and transports copper ion
Transferrin Transports iron
Ferritin Storage form of iron in tissues
Transthyretin Binds and transports thyroxine
Physiology 107

Transcortin Binds cortisol
Haptoglobulin Binds extracorpuscular Hb
Hemopexin Binds heme
Acute Phase Proteins

• Proteins increased during inflammation or secondary to tissue damage
•
• Include
•
– C Reactive Protein
–
– Haptoglobulin
–
– Alpha 1 Antitrypsin
–
– Procalcitonin
–
PHYSIOLOGY
The factors which result in oedema formation Factors which prevent oedema formation
• Vascular Factors - Decreased plasma oncotic pressure • Increased blood oncotic pressure
•
•
(colloidal osmotic pressure) • Decreased capillary hydrostatic pressure
•
– Increased capillary hydrostatic pressure • Decreased capillary permeability
–
– Increased capillary permeability
•
• Decreased tissue hydrostatic pressure or tissue tension
–
• Tissue factors
•
• Increased lymphatic drainage
•
– Increased oncotic pressure of interstitial fluid
•
• Increased excretion of sodium and water
–
– Decreased tissue tension
•
–
– Lymphatic obstruction
–
– Increased sodium and water retention
–
Nice to know
Actin and myosin molecules are contractile proteins similar to those found in muscle cells
Thrombosthenin Another contractile protein that can cause the platelets to contract.
Maintains the shape of the cells.
Residuals of endoplasmic reticuium and the Golgi apparatus Store large quantities of calcium ions
Mitochondria Capable of forming adenosine triphosphate (ATP) and adenosine
diphosphate (ADP)
Enzyme systems Prostaglandins, Which are local hormones that cause many vascular
and other local tissue reactions
Fibrin-stabilizing factors, Cell membrane glycoproteins Blood Coagulation
Phospholipids Multiple stages in the blood-clotting process.
Calmodulin (AIPG 2004)

• Calcium dependent regulatory protein
•
• Has four calcium binding sites and full occupancy of these sites induces marked conformational changes that allow
•
calmodulin to activate enzymes and ion channels
• Action of calcium calmodulin complex
•
Enzymes and proteins regulated by this complex Regulation of activity of many structural elements in cells
• Adenylate cyclase • Actin myosin complex of smooth muscles
•
•
• Calcium dependent protein kinases • Various microfilament mediated processes in non contractile cells
•
•
• Ca2+ Mg++ ATPase including
•
• Ca2+ phospholipid dependent protein kinase – Cell motility
–
– Cell conformation changes
•
• Cyclic phosphodiestrase
–
– Mitosis
•
• Nitric oxide synthase
–
– Granule release
•
–
• Phosphorylase kinase – Endocytosis
–
•
• Some ion channels and receptors
•
108
Also Note
• The volumes of the various fluid compartments are measured by an indicator dilution method. Total body water is
•
 
measured using tritiated water or deuterium oxide. Extracellular fluid (ECF) volume: is measured using saccharides,
 
e.g. inulin, mannitol or ions like thiocyanate. (AIIMS Nov 2013)

 
• Plasma volume (PV): Is measured using dye like Evans blue, radioiodinated serum albumin or RBCs labelled with
•
Phosphorus 32 or Chromium 51.
• Osmolality: Solute or particle concentration of a fluid. 278 to 305 mOsm/kg serum water (AIPG 2006)
•

NERVOUS SYSTEM
Broca’s Area • Located in the inferior frontal gyrus

•
(AIIMS May 08, May 10) • Motor speech area
PHYSIOLOGY
•
• Associated with word formation
•
• Associated lesion is Broca’s aphasia
•
Wernicke’s area • Located in the supramarginal gyrus
•
• This is sensory speech area associate with the comprehension of sounds (sound recognition takes
•
place here)
• Associated lesion is wernicke’s aphasia
•
Arcuate fasciculus • Connects wernicke’s area to broca’s area
•
• This area plays an important role in repetition
•
• Associated lesion is conductive aphasia
•
Angular gyrus • Located behind the wernicke’s area
•
• This area is important in understanding written language or pictures that are visualized, information is
•
processed and transmitted to wernicke’s area
• Associated lesion is anomic aphasia(patient is unable to name visualized objects)
•
Component of Extra pyramidal tract. Location Main function
Red nucleus Mesencephalon Skeletal muscle tone
Cerebellar nuclei Cerebellum Primary control coordination of movements and integration of
sensory feedback
Cerebral nuclei Cerebral hemispheres Control coordination and preparation of limb movements
Superior colliculi Mosencephalon process Visual information
Vestibular nuclei Pons and medulla oblongata Concerned with equilibrium sensations.
Functions of
Basal Ganglia Planning and programming of voluntary movements, thought is converted into action
Involved in cognitive control of motor activity. Basal ganglia are important for timing the movements, and scaling the
intensity of movements.
Thalamus Sensory relay station
Hippocampus Short term memory
Frontal lobe Self stimulation reward
Cerebellum Coordination of Movements
3 biochemically distinct pathways in the basal ganglia and they operate in a balanced fashion.
i. The nigro-striatal dopaminergic system.

ii. The intrastriatal cholinergic system.

iii. Striatopaillidal and striatonigral system of GABA-secreting neurons.

Physiology 109

Good to Know • Astrocytes processes terminate as end feet at the basal
•
• Degeneration of the nigrostriatal dopaminergic system laminae of blood vessels and the pial surface where they
•
leads to Parkinson’s disease. are bound together by desmosomal junctions.
• Loss of the intrastriatal GABA-ergic and cholinergic • Ependymal cells (ependymocytes) line the ventricles and
•
neurons leads to Huntington’s disease.
•
central canal.
• Marked and characteristic abnormalities of motor • As intrafascicular cells in myelinated tracts, the major role
•
function are produced by disease processes affecting the
•
of oligodendrocytes is to lay down myelin around central
basal ganglia. The motor abnormalities may be either of
the hyperkinetic or hypokinetic type. nervous axons and thus they are the central counterpart of
peripheral myelinating Schwann’s cells. (AIPG 2007)
• Hyperkinetic conditions- chorea, athetosis, and ballism.

• B fibres (myelinated) – autonomic preganglionic fibres
•
• Hypokinetic conditions- akinesia, bradykinesia.
•
•
• Glutamate is the main excitatory transmitter in
• Glial cells
•
brain and spinal cord, responsible for 75% excitatory
•
– Derived from neuroectoderm or from bone marrow.
PHYSIOLOGY
transmission in brain. The neurotransmitters of CNS
–
– Have important structural and metabolic are:
–
interaction with neurons and their dendritic and
exonal processes. – Excitatory amino acids: Glutamate and Aspartate
–

– Have a primary role in wide range of normal (AIPG 2004)

– Inhibitory amino acids: Gama amino butyric acid
–
functions and reactions to injury, including
–
inflammation, repair, fluid balance and energy (GABA), Glycine
metabolism.T • β – endorphins are found in hypothalamus, thalamus,
•
– Heir role in axonal regeneration is not clear but its brainstem, retina
–
consider to have their inhibitory effect by secretion • Somatostatin is secreted from median eminence of
•
of neuroinhibitory substances. (AIPG 2008) hypothalamus, substantia gelatinosa, retina

Neurotransmitter Physiologic Anatomy Clinical Aspects
Acetylcholine Motor neurons in spinal cord neuromuscular Acetylcholinesterases (nerve gases) Myasthenia gravis
junction Basal forebrain wide spread cortex (antibodies to ACh receptor)
Interneurons in striatum Autonomic nervous system Congenital myasthenic syndrome. (mutations in Ach receptor
 
(preganglionic, and postganglionic sympathetic) subunits) Lambert-Eaton syndrome (antibodies to Ca
 
channels impairs ACh release)
Botulism toxin (disrupts ACh release by
exocytosis) Alzheimer’s disease (selective cell death) AD
 
frontal lobe epilepsy (mutations in CNS ACh receptor)
Parkinson’s disease (tremor)
Dopamine Substantia nigrastriatum (nigrostriatal pathway) Parkinson’s disease (selective cell death) MPTP
Substantia nigralimbic system and widespread cortex parkinsonism (toxin transported into neurons) Addiction,
 
Arcuate nucleus of hypothalamus anterior pituitary behavioral disorders Inhibits prolactin secretion
 
(via portal veins)
Norepinephrine Locus coeruleus (pons) limbic system, hypothalamus, Mood disorders (MAO inhibitors and tricyclics increase NE
(NE) cortex Medulla locus coeruleus, spinal cord and improve depression) Anxiety
 
Postganglionic sympathetic neurons Orthostatic tachycardia syndrome (mutations in NE
transporter)
Serotonin Pontine raphe nuclei widespread projections Medulla/ Mood disorders (SSRIs improve depression) Migraine pain
 
pons dorsal horn of spinal cord pathway Pain pathway
 
γ-Amino Butyric Major inhibitory neurotransmitter in brain; Widespread Stiff person syndrome (antibodies to glutamic acid
Acid (GABA) cortical interneurons and long projection pathways decarboxylase, the biosynthetic enzyme for GABA) Epilepsy

(AIPG 2007) (gabapentin and valproic acid increase GABA)

Glycine Major inhibitory neurotransmitter in spinal cord Spasticity Hyper-plexia (myoclonic startle syndrome) due to
 
mutations in glycine receptor
Glutamate Major excitatory neurotransmitter; located Seizures due to ingestion of domoic acid (a glutamate
 
throughout CNS, including cortical pyramidal cells analogue) Rasmussen’s encephalitis (antibody against
 
glutamate receptor 3)
Excitotoxic cell death
110
• Passage of impulses in a single direction, from Representation in Cerebral Cortex (AIIMS May 09)
•

synaptic junctions or receptors along exons to their • Vertical and upside down – sensory homunculus
termination is known as orthodromic conduction.
•
• There is detailed localization of fibres from the various
• Antidromic conduction takes place in the opposite
•
parts of the body in the postcentral gyrus.
•
direction. Though axons can conduct in either direction,
antidromic impulses die out at the synaptic junctions. • Size of the receiving area for impulses is proportionate
•
Synapses conduct impulses only in one direction due to the use of the part.
to the presence of vesicles containing neurotransmitters • The cortical areas for sensation from the trunk and back
•
only at the axonal end-feet. are small, whereas very larger areas are concerned with
hand, mouth .
Spatial summation Convergence of several afferent
impulses (whether inhibitory or • Lesions of the post central gyrus:
•
excitatory) on the same postsynaptic – Decreased sensations
nerve soma. The postsynaptic neuron
–
– Fine touch and proprioception are reduced
sums up all local synaptic potentials
–
PHYSIOLOGY
and together they will produce greater – Sensation of pain and temperature are affected to a
–
depolarization. lesser degree.
Temporal summation Occurs when two impulses arrive at • Upon recovery:
•
postsynaptic neuron in rapid succession.
– Pain sensation comes first
As a result, the resulting postsynaptic
–
depolarisations increase in step wise – Followed by temperature
–
fashion over time – And finally proprioception and fine touch.
–
Facilitation, augmen- Follows titanic stimulation of the
tation, post-tetanic presynaptic neuron. As a result more
potentiation amounts of neurotransmitter is released Light Reflex
due to accumulation of Ca2+ in the
presynaptic terminal. The resulting • When light is flashed into the eyes, pupil constricts. It is
•
depolarization at the postsynaptic known as light reflex. It is of two types:
terminal will be greater than expected – Direct: When light is thrown into one eye, the
–
Memory (long-term New protein synthesis constriction of pupil occurs in that eye
potentiation)
– Indirect: If the light is flashed in one eye, the
–
constriction of pupil of other eye takes place
Ascending tract Functions • Pathway for the light reflex
•
Anterior spinothalamic tract Crude touch sensations 1 Light rays on eye Pain Pathway
Lateral spinothalamic tract Pain and temperature 2 Optic nerve Sense organs for pain are free nerve

sensations (AIPG 2008) (AIIMS NOV 2012) ending found in almost every tissue of

the body
Spinothalamic tracts Subconscious kinesthetic
sensations 3 Optic chiasma Aδ (mylineated) → fast pain → DRG
Spinoreticular tract Consciousness and 4 Optic tract C (unmylineated) → Slow Pain →

awareness DRG
Spinovestibular tract Proprioception 5 Pretectal nucleus Substance P is the mediator of pain

6 Edinger – Westphal Afferent limb of autonomic/visceral
nucleus (III cranial nervous system carries sensory
Hunger centre of brain is Hypothalamus
nerve) information (pain) by sympathetic

(MAN-98)
Unmylineated C fibres. Relief
Breathing centre ceases upon Medulla oblongata mechanism of massage and counter
destruction of the (APPSC-99) irritants

7 Ciliary ganglion Hot water bag used for abdominal
Respiratory centre is situated in Medulla oblongata
pain works by stimulation of Aδ thus

(Kar-02, MAN-01)
inhibiting adrengenic receptors
Thermal regulating centers are Hypothalamus 8 Short ciliary nerve
present in (AIIMS, AIPG-94 (Kar-2k)

(Thermostat in brain) 9 Contraction of

(Kar-98, Manipal-09) constrictor papillae
Centre of activity of autonomic Hypothalamus and constriction of
nervous system is (AIIMS-89) pupil

Physiology 111

Pain Reflexes
Facial Pain Scale • Pain is the fifth vital sign
•
• To be most accurate, pain scales are best used as the pain is occurring (AIPG 2010)
•

• The most widely used scales are visual, verbal, and numerical or some combination of all three forms.
•
Visual Scale (e.g. Wong •
•
Designed for children aged 3 years and older, also helpful for elderly patients who may be cognitively
Baker Facial Scale) impaired.
• It offers a visual description for those who don’t have the verbal skills to explain how their symptoms make
•
them feel.
• The original version of scale consisted of seven faces but revised scale (FPS R) developed by Bieri et al
•
1990 consists of six faces.
• The Sydney Animated Facial Expressions (SAFE) Scale developed by Champion and collegeaues is
•
a version of the FPS.
• The SAFE scale is a computer animation in which a single face varies smoothly from ‘no pain to most pain
•
possible’ of the FPS (through 101 frames)
PHYSIOLOGY
H reflex • A refractory reaction of muscles after electrical stimulation of sensory fibres (Ia afferents stemming
•
from muscle spindles) in their innervating nerves
• H reflex test is performed using an electric stimulator which gives usually a square wave current of
•
short duration and small amplitude (higher stimulations might involve alpha fibres, causing M wave,
compromising the results), an EMG set, to record the muscle response.
• H reflex is analogous to the mechanically induced spinal stretch reflex (for example, knee jerk reflex)
•
because in both cases muscle spindle innervating fibres are activated.
• H reflex is used to assess fitness of astronauts
•
• H reflex was the first medical experiment completed on the International Space Station.
•
Knee Jerk Reflex (Patel- • Is a stretch reflex and is a myotactic reflex.
•
lar Reflex) • Striking the patellar tendon with a tendon hammer just below the patella stretches the quadriceps tendon
•
this stimulus stretch sensory receptors (most importantly, muscle spindles) that trigger an afferent
impulses in a sensory nerve fibre of the femoral nerve leading to the lumbar region of the spinal cord.
• There the sensory neuron synapses directly with a motor neuron that conducts an efferent impulse to the
•
quadriceps femoris muscle, triggering contraction. This contraction, coordinated with the relation of the
antagonistic flexor hamstring muscle causes the leg to kick.
• This reflex helps maintain posture and balance, allowing one to walk without consciously thinking about
•
each step
• It is a clinical and classic example of the monosynaptic reflex arc.
•
• There is no interneuron in the pathway leading to flexion of the quadriceps muscle. Instead the bipolar
•
sensory neuron synapses directly on a motor neuron in the spinal cord.
• However there is inhibitory interneuron used to relax the antagonistic hamstring muscle.
•
• Testing the patellar tendon reflex tests the function of the femoral nerve and spinal cord segments L2-L4
•
• The absence or decrease of this reflex is known as Westphal’s sign
•
• Reaction time is 19-24 mins
•
R III reflex • The R3 component of the electrically elicited blink reflex is present in patients with congenital insensitivity
•
to pain like in hereditary sensory and autonomic neuropathy (HSAN), a rare developmental disorder
characterized by severe decreased perception of pain and autonomic dysfunction.
• Electrical stimulation of the supraorbital branch of the trigeminal nerve evokes the blink reflex, a
•
polysynaptic reflex that closes the eyelids by contracting the orbicularis oculi muscle.
• The blink reflex can be recorded with EMG electrodes over the lower eyelid, and is widely used for the
•
functional evaluation of the trigeminal and facial nerves and their brainstem connections.
• Three components (R1, R2, R3) are usually identified in the electrically elicited blink reflex. Myelinated
•
Aβ fibres conduct the afferent impulses of the R1 and R2 responses. All synapses involved in the R1
response are in the pons. R2 response includes neuronal fibres that enter the pons and travel caudally
through the spinal trigeminal nucleus to synapse with the interneurons in the medulla oblongata.
• The neuronal synapses of the R3 response are less well known but are believed to be mediated by a
•
polysynaptic neuronal circuit in the medulla oblongata or in the rostral segments of the cervical spinal
cord.
112
The mammalian nerve fibres are divided into A, B and C types:

Fibre type Function Fibre diameter (µm) Conduction velocity (m/s)
A (myelinated
• α Proprioception, somatic motor 12-20 70-120
•
• β Touch, pressure 5-12 30-70
Motor to muscle spindle (AIPG 2012) 3-6 15-30
•
• π

Cold, pain and touch 2-5 12-30
•
• δ
•
B Preganglionic autonomic <3 3-15
Dorsal root Pain, temperature, reflex response and 0.4-1.2 0.5-2

some mechanoreception
Sympathetic Post ganglionic sympathetic 0.3-1.3 0.7-2.5

PHYSIOLOGY
A Delta Fibres
These have lower electrical thresholds than C fibres, and respond to a number of stimuli. These mediate acute, sharp pain
and are excited by hydromechanical events in dentinal tubules such as drilling or drying. Electric pulp tester detects pain by
stimulating these fibres.
C fibres mediate the dull aching or throbbing pain and the pulpal pain. (AIIMS NOV 2010, May 2013, Nov 2013)

Sleep
Different phases of sleep:
Stage 0 (awake) • From lying down to falling asleep and occasional nocturnal awakenings, 1-2 % of sleep time
•
• EEG shows α activity when eyes are closed and β activity when open
•
• Eye movements are irregular and slowly rolling
•
Stage 1 (dozing) • α- activity interspersed with θ waves. 3- 6%
•
• eye movements reduced but there may be bursts of rolling
•
Stage 2 (unequivocal sleep) • θ waves with interspersed spindles.
•
• K complexes can be evoked on evoked on sensory stimulation
•
• Eye movements few.
•
• Easily arousable. 40 – 50 %
•
Stage 3 (deep sleep transition) • EEG shows θ and δ waves and spindle activity, K complexes can be evoked with strong stimuli only
•
• Eye movements few
•
• Not easily arousable. 5 – 8%
•
Stage 4 (cerebral sleep) • δ- activity predominates
•
• K complexes cannot be evoked
•
• Eyes fixed
•
• Difficult to arouse 10-20%
•
REM sleep (paradoxical sleep) • EEG has waves of all frequencies, K complexes cannot be elicited. Marked, irregular and darting
•
eye movements, dreams and nightmares occur
• Heart rate and BP fluctuates respiration irregular
•
• Muscles relaxed
•
• Erection occurs in males
•
• 20 – 30 %
•
Physiology 113

Also Note
Alpha waves Frequency – 8 – 13 cycles/sec
Found in all normal adults when they are awake and in quiet, resting state of cerebration
Occur most intensely in occipital region
Voltage: 50 Vol
During deep sleep Alpha waves disappear
Beta Waves When the awake persons attention is directed towards some specific type of mental activity, alpha waves change
to beta ones
Frequency: 80 cycles/sec
Mainly in parietal and frontal regions
Theta Waves Frequency: 4 to 7 cycles/sec

Occur normally in parietal and temporal regions in children, but they also occur during emotional stress in some
adults
PHYSIOLOGY
Delta Waves Include all the waves of EEG with frequency less than 3.5 cycles/sec
Voltage 2-4 times greater than other waves
Differences between sympathetic and parasympathetic division of the autonomic nervous system
Sympathetic Parasympathetic
1. Origin Dorso lumbar (T1 to L2 or L3) Cranio sacral (III, VII, IX, X; S2-S4)

2. Distribution Wide Limited to head, neck and trunk

3. Ganglia Away from organs On or close to organs

4. Postganglionic fibres Long Short

5. Pre: Post ganglionic 1:20 to 1:100 1:1 to 1:2 (except in enteric plexuses)

6. Transmitter (neuroeffector) Noradrenaline (major) Acetyl choline

Acetylcholine (minor)
7. Stability of transmitter NA stable, diffuses for wider actions ACh rapidly destroyed locally

8. Important function Tackling stress and emergency Assimilation of food, conservation of energy

The vestibulocochlear nerve (auditory or acoustic nerve) is • Meissner’s corpuscles
•
the eight cranial nerves, and is responsible for transmitting – Glaborous (hairless) skin – 40% of fingertip receptors
sound and equilibrium (balance). (AIIMS May 09)
–
– Dynamic fine touch (e.g.,manipulation)

–
• Paccinian corpuscles
Sensory Corpuscles
•
– Deep skin layers, ligaments, joints
• Free nerve endings
–
• Merkel’s discs (Cup shaped)
•
– All skin (some viscera)
•
– Hair follicles
–
– Pain and temperature
–
– Static touch (e.g., shapes, edges, textures)
–
–
Lesions of Cerebellum (AIPG 2011)
Ataxia Lack of coordination of movement
Asynergia Lack of coordination between different group of muscles
Astasia Unsteady voluntary movement
Dysdiadochokinesia Inability to do rapid alternate successive movement
114
Seddon’s Classification of Nerve Injury

Features Neuropraxia Axontemesis Neurotemesis
Pathology • No anatomical disruption • Axons and myelin • Competitive division of nerve
•
•
•
• Both axon and sheath sheath disrupted but • Axon and neural tube (i.e. perineurium,
•
endoneural perineurium
•
intact epineurium and endoneural sheath) both
and epineurium sheath are divided.
• Physiological disruption of
(neural tube) is intact.
•
conduction only
Degeneration • No degeneration • Degeneration is present • Degeneration is present proximal and
•
•
•
proximal and distal distal (Wallerian)
(Wallerian)
Prognosis • Excellent • Good/fair/poor • Poor
•
•
•
• Recovery is complete • Occurs as regenerating
•
•
axons grow into intact
sheath
PHYSIOLOGY
Tinel’s sign • Absent • Advancing • Static

•
•
•
(NEET 2013)

PHYSIOLOGIC MUSCLE SYSTEM – The area between two adjacent Z lines is a sarcomere.
–
It is the basic unit of contraction. In each sarcomere,
Muscles I bands become narrower during the muscle
contraction.
Skeletal • Has cross striations
•
• But it is functionally syncitial and rhythmically – Actinin binds actin to the Z lines
–
•
contracts without external innervations owing to – Titin (giant protein) connects Z lines to the M lines
–
the presence in the myocardium of pacemaker and provides scaffolding to the sarcomere.
cells that discharge spontaneously
– Desmin binds the Z lines to the plasma membrane.

(AIIMS May 2009)
–
– Sarcotubular system: T tubules and sarcoplasmic

–
Smooth • Lack cross striations, reticulum.
Motor unit: Each single motor neuron and the
•
• Found in most hollow viscera and in the eye. –
–
•
muscle fibre it innervates is called a motor unit.
Muscle Fibre
• Each muscle fibre is a single cell that is long, multinucleated, – Rheobase: Minimum strength of current (stimulus)
–
to produce a response
•
cylindric and surrounded by a cell membrane, the
sarcolemma. The muscle fibre is in turn made up of – Utilization time: Time taken by a rheobase to
–
myofibrils inturn made up of individual filaments made produce a response
up of contractile proteins. – Chronaxie: Time taken by a twice of rheobase current
–
to produce a response
– Muscle contractile proteins are actin, myosin,
– Contractions
–
troponin (I, T, C) and tropomyosin.
–
Troponin: Present in skeletal and cardiac Isometric (same length): Contraction occurs

without change in length of muscle; no “work”

muscles but not smooth muscle. Has 3 subunits
Troponin T: Binds to Tropomyosin is done.

Troponin I: Inhibits myosin-actin interaction Isotonic (Same tension): Contraction against a

Troponin C: Binds Calcium and brings constant load with approximation of the ends of

about Contraction by removing effect of the muscle; “work” is done
tropomyosin. (AIPG 2010, AIIMS May 2009) Treppe or staircase phenomenon: When

a series of maximal stimuli is delivered to a
– Differences in the refractive indexes of the various skeletal muscle at sub-tetanising frequency,
–
parts of the skeletal muscle are responsible for the tension rises during each twitch. After several
cross striations seen. contraction, a uniform tension per contraction
– The lighter I band is divided by the dark Z line and the is reached – known as treppe.
–
darker A band is divided by the lighter H line.
Physiology 115

• Skeletal Muscle Contraction – The relaxation of the muscle. During relaxation, Ca2
•
–
– Action potential depolarization opens voltage gated is taken up by the SR, causing the release for action
–
Ca2+ channels, inducing neurotransmitter release from the myosin cross-bridges. Tropomyosin returns
– Postsynaptic ligand binding leads to muscle cell to its normal configuration, blocking this interaction.
–
depolarization in the motor end plate
• Circulating levels of chromogranin A appear to be a
– Depolarisation travels along muscle cell down T
•
better index of sympathetic activity.
–
tubule
– Depolarisation of the voltage sensitive • 5HT2A receptors mediate platelet aggregation and
•
smooth muscle contraction, 5HT3 receptors are present
–
dihydropyridine receptor, coupled to the ryanodine
receptor on the sarcoplasmic reticulum, induces a in GIT and area postrema and are related to vomiting.
5HT4 receptors are present in GIT and facilitate
 
conformational change causing Ca2+ release (calcium-
induced calcium release) secretion and peristalsis and in brain. 5HT6 and 5HT7
– Released calcium binds to Troponin C causing a receptors are present throughout the limbic system.
5HT7 – high affinity for antidepressant drugs
–
conformational change that moves tropomyosin out
PHYSIOLOGY
of the myosin binding groove on actin filaments • The thin filaments lack troponin in smooth muscles
•
 
– Myosin binds a new site on actin, which constitutes
• Golgi Tendon Organ: Is an encapsulated sensory receptor,
–
the ‘power stroke’; ADP is the released, returning
•
myosin to the rigor state. consisting of net like collection of knobby nerve endings
among the fascicles of a tendon. (AIIMS May 2011)
 
– Contraction results in H and I band shortening, but
–
the A band remains the same length. (A band Always – There are 3 to 25 (usually 10 to 15) muscle fibres, so
–
remains same length). they are stimulated by both passive stretch and active
 
contraction of muscle tension.
• Sliding filament model of muscle contraction: One
– The golgi organ (also called golgi tendon
•
motor neuron innervates several skeletal muscle fibers.
–
organ, tendon organ, neurotendinous organ or
When an action potential reaches the neuromuscular
neurotendinous spindle), is a proprioceptive sensory
junction, acetylcholine is released from vesicles within
receptor organ that is located at the insertion of
the axon terminus and binds to postsynaptic nicotinic
skeletal muscle fibres into the tendons of skeletal
receptors on the sarcolemma. This, in turn, increases the
muscle. It provides the sensory component of the
membrane permeability of Na+ and K+ and depolarizes
golgi tendon reflex. (AIPG 2009)
the muscle cell.

– It is a net like collection of knob by nerve endings
–
• Excitation-contraction Coupling is the process by which among the fascicles of a tendon that is located in series
with extrafusal muscle fibres and innervated by type
•
an action potential initiates the contractile process. It
involves four steps: Ib afferents.
– The propagation of the action potential into the T – Major difference between the function of the golgi
–
tendon organ and the muscle spindle is that the
–
tubule and release of Ca2+ from the terminal cisternae.
– Activation of the muscle proteins by Ca2: Calcium spindle detects changes in muscle length, while the
tendon organ detects changes in muscle tension.
–
released from the terminal cisternae of each
SR bind to troponin C, which is attached to the – They are stimulated by both passive stretch and active
–
tropomyosin molecule of thin filaments. This causes contraction of the muscle to relax the muscle (inverse
a conformational change in the shape of tropomyosin, stretch reflex) and function as a transducer to regulate
allowing the actin filament to interact with the myosin muscle force.
cross-bridge. – The threshold of golgi tendon is low. Since more
–
– The generation of tension by muscle proteins: The elastic muscle fibres take up much of the stretch, the
degree of stimulation by passive stretch is not great,
–
ATP molecule bound to myosin is hydrolyzed to ADP
+ Pi;. When the ADP + Pi is released from myosin, and strong stretch is required to produce relaxation.
the action filament is pulled closer toward the center However, contraction of muscle regularly stimulate
of the sarcomere, shortening its length. As long as golgi tendon. It is responsible for stretch reflex.
Ca2+ and ATP are available, this cycle continues, – This inhibitory negative feedback lengthening
–
further contracting the muscle. If more muscle force reaction prevents development of too much tension on
is needed, more motor units are activated. the muscle and protects tearing of muscle or avulsion
116
of tendon. Tendon organ equalizes contractile forces • The impulses originating from the spindle are transmitted
•
of different muscle fibres by inhibiting fibres exerting to the CNS by fast sensory fibres that pass directly to the
excess tension. motor neurons which supply the same muscle
• The neurotransmitter at the central synapse is glutamate
• Withdrawal reflex:
•
•
– Postsynaptic reflex occurring in response to noxious Structure of Muscle Spindles
–
or painful stimuli.
• Each muscle spindle has three essential elements:
– The response is flexor muscle contraction and
•
– A group of specialized intrafusal muscle fibres with
–
inhibition of extensor muscle, so that the part
–
contractile polar ends and a noncontractile center.
stimulated is flexed and withdrawn from stimuli. – Large diameter myelinated afferent nerves
– On application of strong stimuli, about 0.2 to
–
(types Ia) originating in the central portion of the
–
0.5 second after flexor and withdrawal response intrafusal fibres
n one limb, the opposite limb begins to extend, – Small diameter myelinated efferent nerves supplying
–
the polar contractile regions of the intrafusal fibres
PHYSIOLOGY
this is called cross extension reflex. It is a part of

the withdrawal reflex as extension of the opposite • It is important to understand the relationship of
•
limb can withdraw the entire body away from the these elements to each other and to the muscle itself
noxious stimuli. to appreciate the role of this sense organ in signaling
changes in the length of the muscle in which it is located.
• Reciprocal innervation: Changes in muscle spindle length are associated with
changes in joint angle, thus muscle spindles provide
•
– It is a phenomenon in which a relaxation of antagonist information on position; proprioception.
–
muscle occurs, when a stretch reflex excites one
muscle.
Innervations
– Neuronal circuit which causes this reciprocal
– The spindle have a motor nerve supply of their own.
–
inhibition is called reciprocal innervation
–
– Is fiber transmit impulse from protagonist muscle These nerves are 3 – 6m in diameter, constitute
about 30% of the fibres in the ventral roots, and are
–
and cause inhibition of motor neuron to antagonist
called gamma motor neurons (AIIMS NOV 2013)
muscle.
– There are two types of gamma motor neurons,
– Bisynaptic pathway, collateral from Ia fibre passing
–
dynamic, which supply the dynamic nuclear bag
–
through inhibitory of golgi bottle interneuron fibres, and static, which supply the static nuclear bag
fibres and nuclear chain fibres.
• Inverse stretch reflex:
– Activation of the static gamma motor neurons
•
It is sudden relaxation of muscle on development
–
– increases the tonic level of activity in both group I
–
of high magnitude of tension and II endings, decreases the dynamic sensitivity of
– It is autogenic inhibitory negative feedback group Ia afferents and prevent silencing of Ia afferents
–
lengthening reaction that protects against muscle during muscle stretch.
tear
• Fasciculations: Is visible or palpable twitch within
– Golgi tendon organ is receptor for inverse stretch
•
a single muscle due to spontaneous discharge of one
–
reflex. motor unit.
• Fibrillation: Fine, irregular contraction of individual
•
Muscle spindles (AIIMS May 2009, May 2011) fibres, they are not visible grossly
• When a skeletal muscle with an intact nerve supply is • Tremor: Rhythmic abnormal involuntary movement
•
•
stretched, it contracts. This response is called the stretch • Chorea: Rapid, jerky, semipurposive irregular
reflex.
•
movement more commonly occurring in the distal part.
• The stimulus that initiates the reflex is stretch of the
•
muscle, and the response is contraction of the muscle
Bezold-Jarisch Reflex (AIIMS May 2011)
being stretched.

• A cardiovascular decompressor reflex involving a marked
• The sense organ is a small encapsulated spindle like or
•
increase in vagal (parasympathetic) efferent discharge
•
fusiform shaped structure called the muscle spindle,
to the heart, elicited by stimulation of chemoreceptors,
located within the fleshy part of the muscle.
primarily in the left ventricle.
Physiology 117

• This causes slowing of the heart beat (bradycardia) and • Bundle of Kent is the aberrant conducting bundle in
•
dilatation of peripheral blood vessels with resulting
•
WPW syndrome.
lowering of the blood pressure.
• The liver receives about 1000 mL/min from the portal
• A German physiologist Albert von Bezold originated the
•
vein and 500 mL/min from the hepatic artery.
•
concept in 1867, later revised by an Austrian dermatologist
Adolf Jarisch in 1937. • Portal venous pressure is normally about 10 mmHg in
•
humans.
Accommoda- • It is a property of nerve, where a slowly
• The maximal heart rate achieved during exercise is in
•
tion rising (increasing) subthreshold stimulus
•
raises (increases) the threshold of nerve to children, it rises to 200 or more beats per minute; in
generate an action potential (AIPG 2009)
adults it rarely exceeds 195 beats per minute.

 
Adaptation (de- • It is a progressive decrease in sensory
• A good example of ‘warm shock’ is anaphylactic shock.
•
sensitization) receptor response despite the continued
•
presence of a stimulus. When a maintained
stimulus of constant strength is applied to a • Haematocrit of capillary blood is regularly about 25%
receptor, the frequency of action potential
•
lower than the whole body haematocrit.
PHYSIOLOGY
in its sensory nerve declines over time.
This is known as adaptation. • At rest, at least 50% of the circulating blood volume is in
•
Electronic • EC is direct spread of electrical current by systemic veins. When extra blood is administered by
transfusion, less than 1% of it is distributed in the arterial
•
conduction ion conduction within the fluids of dendrites
but without generation of action potential. It system (‘high pressure system’) and all the rest is found
is decremental conduction, as the dendritic
membrane is thin and partially permeable
n the systemic veins, pulmonary circulation, and heart
 
to K+ and Cl- ions, making them leaky to chambers other than the left ventricle (‘low-pressure
electric current. system’).
• Blood Flow
CIRCULATORY SYSTEM
•
– Resistance vessels=Arterioles (major sites
–
• The normal total circulating blood volume is about 8% of of resistance to blood flow); Capacitance
•
the total body weight. About 55% of this volume is plasma. vessels=Veins. (AIPG 2005)

• Fluid portion of blood is the plasma. If whole blood is – Distribution of blood flow is mainly regulated by
–
the arterioles.
•
allowed to clot and the clot is removed, the remaining
fluid is called serum. (NEET 2013) – The average velocity of fluid movement at any
–

• By the age of 20, the marrows in the cavities of the long point in a system of tubes is inversely proportional
to the cross- sectional area at that point, Therefore,
•
bones have become inactive, except for the upper humerus
 
and the femur. (AIPG 2008) the average velocity of blood is high in the aorta,
declines steadily in the smaller vessels and is lowest

• The average half-life of a neutrophil in the circulation is 6
 
in the capillaries,
•
hours.
– Flow through a vessel is doubled by an increase
• Average lifespan of an RBC is 120 days. When osmotic
–
in only 19% of its radius; and when the radius is
•
fragility is normal, red cells begin to haemolyse
doubled, resistance is reduced to 6% of its previous
when suspended in 0.48% saline and haemolysis is
 
value.
 
complete in 0.33% saline. (AIPG 2002, 2012)
– The total area of all the capillary walls in the adult

–
• Persons with type AB blood are ‘universal recipients’ exceeds about 6300 sq.m in the adult.
•
and type O individuals are ‘universal donors’. – Laminar flow occurs up to a certain critical
–
• Autologous transfusion: the patient’s own blood is velocity. At or above this velocity, flow is turbulent.
Streamline flow is silent, but turbulent flow creates
•
withdrawn in advance of elective surgery and then this
 
blood is infused back if a transfusion is needed during sounds.
 
the surgery. – Turbulence occurs more frequently in anemia
–
• Parahaemophilia is due to factor 5 deficiency. because the viscosity of the blood is lower. This may
be the explanation of the systolic murmurs that are
•
• There are 3 bundles of atrial fibres that contain purkinje
 
common in anemia. (AIPG 2009)
•
fibres and conduct impulses from the SA node to the

AV node: anterior internodal tract of Bachman, middle
• Circulation through Brain
 
internodal tract of Wenckebach and posterior internodal
•
tract of Thorel. – The brain capillaries are surrounded by the end feet
–
of astrocytes.
118
– The brain weighs about 1400g in air, but in the CSF it cranium at any time must be relatively constant
–
weighs only 50g. (Monro-Kellie doctrine).
 
– Kety method of measuring cerebral blood flow uses – In the brain autoregulation maintains a normal
–
–
nitrous oxide cerebral blood flow at arterial pressures of 65-140 mm
– The part of the brain with the largest blood flow is the Hg.
–
inferior colliculus. – Respiratory quotient (RQ), of cerebral tissue is 0.95-
–
– Blood flow in the grey matter is about 6 times that in 0.99 in normal individuals.
–
the white matter. – The vasodilatation produced by carbon dioxide is
–
– The volume of blood, spinal fluid and brain in the maximum in brain.
–
 
Compartment Substances used Normal volume
Total body fluid Deuterium oxide (D2O, heavy water) is most frequently TBW in a 70-kg adult averages about 40 litres, or
used. Tritium oxide and aminopyrine have also been 60% of the total body weight
used for this purpose.
PHYSIOLOGY
Extracellular fluid Radioactive sodium, radioactive chloride, radioactive 9 to 22 litres

bromide, thiosulfate ion, thiocyanate ion, thiocyanate Average - 15 litres
ion, inulin and sucrose.
Plasma volume Dyes like Evans blue (T-1824) which become bound to 3.6 liters on average*
plasma protein are used in measuring plasma volume.
Plasma volume can also be measured by injecting
serum albumin labelled with radioactive iodine.
Blood volume 5-6 liters on average
Red cell volume Chromium (51cr), Isotopes of iron and phosphorus
(59Fe and 32P)
Interstitial fluid volume The volume of the interstitial fluid can be calculated by About 10-12 liters
subtracting the plasma volume from the ECF volume.
RBC count Means number of RBC present in one cubic mm of Normal value is 5.5 to 4.8 million/cubic mm
blood.
Haemoglobin concentration Means amount of haemoglobin in grams in 100 mL of Normal value 15 g/100 mL of blood
whole blood
Haemotocrit value (packed cell The volume of the packed formed elements 45 mL/100 mL (45%) - Wintrobe tube haematrocit
volume)
Mean corpuscular volume Volume of an average of RBC. MCV = volume of RBC Normal value—80 to 90 cubic microns.
in 1 mL of blood/no of RBC in 1 mL of blood
Mean corpuscular haemoglobin Is the amount of haemoglobin present in an average Normal value is 30 pg (pictograms)
(MHC) RBC
Mean corpuscular haemoglobin Means the amount of haemoglobin present in 100 ml Normal Value 33/100 mL of packed cells
concentration (MCHC) MCHC of RBC.
= (haemogobin (in g/100 mL)/
packed cell volume) X 100.
Characteristics of WBC
Cells Percentages Important features
Composition
Neutrophils (60-70%) • Nucleus has 4-5 lobes.
•
• Contains neutrophilic granules, which take both acidic and basic stains. The granules appears
•
VIOLET after staining.
• Engulf bacteria by phagocytosis and help in opsonisation So,known as microscopic policeman or
•
frontline soldiers.
Eosinophil (2-4%) • Nucleus is bilobed. Contains eosinophilic large granules, which stain BRIGHT RED with eosin.
•
• The major function are detoxification, disintegration and removal of foreign proteins.
•
• They mainly act against the parasites. The eosinophil count is increased during parasitic infestations
•
and allergic conditions.
• Parasitic infestations and allergic conditions.
•
• Prevents hypersensitivity to antigen-antibody complexes (anti-allergic role)
•
Physiology 119

Basophils (0-1%) • Nucleus is bilobed.
•
• Contains basophilic granules, which stain purple blue with basic dyes like methylene blue.
•
• Prevents intravascular clotting by release of heparin.
•
• Plays an important role in healing process.
•
• Produces hypersensitivity reactions.
•
Lymphocytes (20-40%) • Nucleus is without any lobes.
•
••
Clear cytoplasm without granules.
• Depending on function, they are divided into:
•
– T-lymphocytes-concerned with cellular immunity
–
– B-lymphocytes-concerned with humoral immunity.
–
Monocytes (2-6%) • Largest leucocytes
•
• The cytoplasm is clear without granules and contain horse shoe or kidney shaped eccentrically
•
placed nucleus.
PHYSIOLOGY
• Forms tissue macrophages and acts as scavenger.
•
• Along with neutrophil, monocytes constitute the first line of defense.
•
Enzymes and Constituents of Neutrophil Granules (AIPG 2007)

Action of Constituent Primary granule Secondary Granule Tertiary granule
Microbicidal enzymes Myeloperoxidase, Lysozyme Lysozyme
Neutral proteinases Elastase, Cathepsin G, Proteinase Collagenase Gelatinase (MMP-9)

–3
Acid Hydrolases N-acetyl -

b-glucosaminidase
Cathepsin-B
Cathepsin-D
b-glycerophosphatase
b-mannosidase
Others Defensins Lactoferrin

Cationic proteins Cobaliphilin
Bactericidal or i C3b receptor (CR3)
Premeability increasing factors Cytochrome
b245
• The normal function of neutrophils may be divided into three phases:

•
a Chemotaxis and neutrophil activation

b Phagocytosis

c Killing and digestion of the pathogens

Erythropoiesis
Formation of blood starts in the third week of intrauterine life
Erythropoiesis in intrauterine life
3rd week to 3rd month • Erythropoiesis occurs in the mesoderm of yolk sac
•
(intravascular phase) • Only stage when erythropoiesis occurs within the blood vessels
•
3rd month to 5th month • Erythropoiesis occurs in liver and spleen
•
(hepatic phase)
5th month onwards • Erythropoiesis occurs in red bone marrow ( all marrow is red at this stage)
•
( myeloid phase)
120
Post natal erythropoiesis Occurs in the red bone marrow

From birth to 5 years All bones (flat + long bones)
During this period all marrow is red
5 years to 20 years (AIPG 2010) All bones (flat + long bones)

Flat bones> long bones
After 20 years (AIIMS May 08) Flat bones

Little from the proximal portions of humerus and tibia
• Haemolysis is seen in thalassaemia, sickle cell anaemia, methotrexate therapy and in haemolytic jaundice.
•
Intracorpuscular • Abnormalities of RBC interior Hereditary thalasaemia, sickle cell anaemia
•
– Enzyme defects
–
– Haemoglobinopathies
–
• RBC membrane abnormalities
•
– Hereditary spherocytosis
PHYSIOLOGY
–
Extracorpuscular Spur cell anaemia Acquired mismatchings, methotrexate therapy and haemolytic
Three extrinsic factors jaundice and some snake venoms
– Hypersplenism
–
– Antibody: Immune haemolysis
–
– Microangiopathic haemolysis
–
– Infections, toxins, etc.
–
Coagulation
• Platelet aggregation is stimulated by thromboxane and α2 receptor-activation, but inhibited by other inflammatory
•
products like PGI2 and PGD2. (AIPG 2010)

• The coagulation cascade of secondary hemostasis has two pathways
•
– The Contact Activation pathway (formerly known as the Intrinsic Pathway) and
–
– The Tissue Factor pathway (formerly known as the Extrinsic pathway) that lead to fibrin formation.
–
Cofactors
• Calcium and phospholipid
•
• Vitamin K
•
Inhibitors
• Protein C
•
• Antithrombin
•
Coagulation factors and related substances
Number and/or name Function
• Fibrinogen Forms clot (fibrin)

•
• Prothrombin Its active form (IIa) activates I, V, VIII, XI, XIII, protein C, platelets
•
• Tissue factor Co-factor of VIIa (formerly known as factor III)
•
• Calcium Required for coagulation factors to bind to phospholipid (formerly known as
•
factor IV)
• Proaccelerin, labile factor (AIPG 2007) Co-factor of X with which it forms the prothrombinase complex
•

Unassigned – old name of Factor Va
• Stable factor Activates IX, X
•
Physiology 121

• Antihemophilic factor Co-factor of IX with which it forms the tenase complex
•
• Christmas factor Activates X: forms tenase complex with factor VIII
•
• Stuart-Power factor Activates II: Forms prothrombinase complex with factor V
•
• Plasma thromboplastin antecedent Activates IX
•
• Hageman factor Activates factor XI and prekallikrein
•
• Fibrin-stabilizing factor Crosslinks fibrin
•
• Von Willebrand factor Binds to VIII, mediates platelet adhesion
•
• Prekallikrein Activates XII and prekallikrein; cleaves HMWK
•
• High molecular weight kininogen (HMWK) Supports reciprocal activation of XII, XI, and prekallikrein
•
• Fibronectin Mediates cell adhesion
PHYSIOLOGY
•
• Antithrombin III Inhibits IIa, Xa, and other proteases;
•
• Heparin cofactor II Inhibits IIa, cofactor for heparin and dermatan sulfate (“minor antithrombin”)
•
• Protein C Inactivates Va and VIIIa
•
• Protein S Cofactor for activated protein C (APC, inactive when bound to C4b-binding
•
protein)
• Protein Z Mediates thrombin adhesion to phospholipids and stimulates degradation of

•
factor X by ZPI
• Protein Z-related protease inhibitor (ZPI) Degrades factors X (in presence of protein Z) and XI (independently)
•
• Plasminogen Converts to plasmin, lyses fibrin and other proteins
•
• Alpha 2-antiplasmin Inhibits plasmin
•
• Tissue plasminogen activator (tPA) Activates plasminogen
•
• Urokinase Activates plasminogen
•
• Plasminogen activator inhibitor-1 (PAI1) Inactivates tPA and urokinase (endothelial PAI)
•
• Plasminogen activator inhibitor-2 (PAI2) Inactivates tPA and urokinase (placental PAI)
•
• Cancer procoagulant Pathological factor X activator linked to thrombosis in cancer
•
• Clotting factors that participate in extrinsic pathway • 3,4,5,7,10
•
•
(measured by the prothrobin time)
• Clotting factors that participate in intrinsic and common • 4,5,8,9,10,11,12

•
•
pathway (measured by partial thromboplastin time (PTT)
-
• Factors that are absent or reduced in stored blood • 5,8
•
•
• Cryoppt is rich source of clotting factor • 8
•
•
• Classical hemophilia (hem A) (AIPG 2011) • 8
•

•
• Christmas disease (AIPG 2014, 2008) • 9
•
•
• Hem C • 11
•
•
• Para hemophilia • 5
•
•
• Vascular hemophilia • Von willebrand’s factor
•
•
122
Nice to Know
• The skin and skeletal muscle blood vessels represent by far the most important site of peripheral resistance and offer
•
maximum resistance to blood flow.
• Marey’s law: HR is inversely related to systemic BP
•
• The best source for the hematopoietic stem cells is the umbilical cord blood
•
• Genes for granulocyte and macrophage colony stimulating factor (GM-CSF) are located together on the long arm of
•
chromosome 5
• Homeostasis: Term given by WB cannon--- termed as ‘Milieu Interieur’ by Claude Bernard in 19th century
•
• Due to high concentration of hemoglobin in blood than plasma proteins, Hb has about 6 times more buffering capacity
•
than plasma proteins. The deoxygenated Hb is more powerful buffer than oxygenated Hb because of its higher pK.
• In adults, during resting conditions both the kidneys receive 1300ml of blood per minute or about 26% of his cardiac
•
output.
PHYSIOLOGY
• Splenectomy causes increase in the platelet count (thrombocytosis)

•
– HbA1 – has a glucose attached to the terminal valine in attacks of paroxysmal atrial arrhythmias. In them
–
each β chain – increases in blood in poorly controlled an additional aberrant muscular or nodal tissue
diabetes mellitus (AIPG 2014) connection (bundle of Kent) is present between atria

– The anterior intermodal tract of Bachmann, the and ventricle
–
middle internodal tract of Wenckebach and the
posterior internodal tract of Thorel connects the SA • Tourniquet test (AIPG 2004)
•

node to AV node. – Also known as capillary fragility test, Hess test,
–
– SA node develops from structure on right side of Rumpel Leede test, bandage test
–
embryo–supplied by right vagus – Is positive in vitamin C deficiency and
–
– AV node develops from left side of embryo – supplied thrombocytopenic purpura
–
by left vagus – Capillary fragility tests are employed as a crude
–
– Disease processes affecting the sinus node lead to measure of endothelial cohesion, the strength of
–
marked bradycardia accompanied by dizziness and which is dependent on endothelial integrity, platelet
syncope–Sick Sinus Syndrome maintenance and subendothelial adhesives such as
– The incomplete heart block, there are repeated Von Willebrand factor, fibronectin and collagen.
–
sequences of beats in which PR interval lengthens • Arneth count is used to count the number of nuclear
•
until a ventricular beat is dropped – Wenckebach lobes in hundred neutrophils
phenomenon • Ion required insulin synthesis is zinc ions
– Wolff-Parkinson White syndrome–accelerated AV
•
–
conduction seen in normal individuals prone to
Screening Tests
Clot retraction time Platelets adhesiveness and platelets It is impaired in thrombocytopenic purpura and normal in
aggregation can be deterermined by clot heamophilia.
retraction time. Clot retraction usually sets
within 6 hours and completed by 24 hours.
Prothrombin time (PT) Normal prothrombin time is 15-19 seconds. It is prolonged in factors II,V,VII and X deficiency.
Prothrombin time of patient before surgery Prothrombin time is normal in haemophilia.
should be within 25% of normal.
Clotting time or coagulation Measured by Lee White tube method is 5-10 It is increased in haemophilia
time minutes
Bleeding time Measured by Duke bleeding time -1.5 to 3 It is increased in purpura and normal in haemophilia.
minutes,Ivy bleeding time 1-4 minutes
Capiliary fragility test (hess Appearance of more than 10 new petechiae is This signifies fall of thrombocyte count below 70,000 per
test or Torniquet test) a positive reaction cu.mm.
Physiology 123

Partial thromboplastin A prolonged clotting time is observed if plasma This test is used to diagnose and control in treatment of
generation test. is observed if plasma is deficient of factor VIII haemophilia.
and IX
International normalized PT of patient Most reliable for monitoring anticoagualant acitivity.

ratio (INR) PT of the standard
CARDIOVASCULAR SYSTEM
Stroke Volume and Cardiac Output

• Cardiac output (CO) = stroke volume (SV) X heart rate (HR); CO = SV x HR
•
• SV = End diastolic volume – End systolic volume (EDV – ESV).
•
• SV affected by contractility, afterload and preload
PHYSIOLOGY
•
Cardiac Ouput (COP)
Output of the heart per minute. COP is 5L/min in resting
supine man.
Pressure = Flow x Resistance
Systemic BP = Systemic Blood Flow x PR
Cardiac Work = Stroke work x HR = SV x MAP X HR
CO SV × HR
Cardiac index =
Body surface area BSA
⇒ 3.2L/min/sq.m of body surface
Contractility (and SV) ↑with Contractility (and SV) ↓with − β-blocker usage
• Catecholamine release (↑activity of Ca2+ pump in sarcoplasmic • Heart failure − Acidosis − Hypoxia/hypercapnea − Non-
•
•
 
 
 
reticulum) dihydropyridine Ca2+ channel blockers
• ↑intracellular calcium
•
• ↓intravascular sodium
•
• Digitalis (↑intracellular Na+ resulting in ↑ Ca2+)
•
 
• Stressful events (anxiety, exercise)
•
Preload and Afterload
– Preload = Ventricular end diastolic volume (the amount of stretching force on cardiac muscle fibres at the end of
–
diastole).
– Preload ↑with exercise (slightly), ↑ blood volume (overtransfusion) and excitement (sympathetics).
–
– Preload pumps up the heart.
–
– Venodilators (eg, nitroglycerine) ↓ preload.
–
– Afterload = The vascular resistance that ventricles must overcome to produce outflow.
–
– Vasodilators (eg, hydralazine) ↓afterload.
–
– Frank-Starling law: Increasing the end-diastolic ventricular volume causes an increased stretch on cardiac muscle
–
fibers; this leads to an increase in the force of contraction i.e., Force of contraction is proportional to the initial length
of cardiac muscle fiber (preload)
– Ejection fraction: Stroke Volume/End-Diastolic Volume; EF = SV/EDV; normally 55-75%. It is an index of ventricular
–
contractility
– Pulse pressure: Systolic BP – diastolic BP .
–
 
– Mean arterial pressure: diastolic BP + 1/3 pulse pressure
–
124
• Blood Pressure (BP) Myocardial Action Potential

•
– BP is high in Occurs in atrial and ventricular fibres and Purkinje fibres.
–
Rigid/ calcified vessels
Phase 0 Rapid upstroke: Voltage gated Na+ channels open,

Diabetics
this depolarizes the cell (makes inside more positive)

Elderly

Obesity Phase 1 Initial repolarisation: Inactivation of voltage gated

– Methods of BP recording Na+ channels (↓ Na+ conductance inward) and
voltage gated K+ channels begin to open (K+
–
NIBP (non invasive): Using sphygmomanometer
 
conductance outward

IBP or ABP (invasive): Most accurate method of

blood pressure. Artery is directly catheterized and Phase 2 Plateau: Ca2+ influx through voltage gated
connected to a manometer Ca2+ channels balances K+ efflux; inward and
– Korotkoff ’s sound: Produced by turbulent flow in outward currents are approx. equal. Ca2+ influx
 
triggers Ca2+ release from the sarcoplasmic reticulum
–
the brachial artery. Sounds again reappear at lower
and myocyte contraction.
pressure (auscultatory gap).
 
– Normal value of Bp is 120/80 mmHg
PHYSIOLOGY
Phase 3 Rapid repolarisation: Ca2+ conductance ↓, K+ efflux

–
– Pulse pressure: Difference between systolic and predominates; this hyperpolarizes the cell.
–
diastolic
– Determinants of pulse pressure Phase 4 Resting potential: High K+ permeability through K+
channels.
–
Stroke volume

Arterial compliance: Aorta and large arteries
Carotid and Aortic Bodies

are more compliant, so pulse pressure is less.
Maximum is seen in dorsalis pedis artery • There is a carotid body near the carotid bifurcation
•
on each side, and there are usually two or more aortic
Cardiac Cycle bodies near the arch of the aorta. (NEET 2013)

• Each carotid and aortic body (glomus) contains islands
• Duration: 0.8 seconds
•
of two types of cells, type I and type II cells, surrounded
•
• Phases: Left Ventricle by fenestrated sinusoid capillaries.
•
– Isovolumetric contraction: Period between mitral • The type I or glomus cells are closely associated with
–
valve closing and aortic valve opening; period of
•
cuplike endings of the afferent nerves.
highest oxygen consumption
• The glomus cell resemble adrenal chromaffin cells and
– Systolic ejection: Period between aortic valve
•
have dense core granules containing catecholamines
–
opening and closing
that are released upon exposure to hypoxia and cyanide.
– Isovolumetric relaxation: Period between aortic
• The cells are excited by hypoxia and the principal
–
valve closing and mitral valve opening
•
– Rapid ventricular filling: Period just after mitral transmitter appears to be dopamine, which excites the
nerve endings by way of D2 receptors.
–
valve opening
– Reduced ventricular filling: Period just before • The type II cells are glia like, and each surrounds four to
•
–
mitral valve closure. six type I cells. Their function is probably sustentacular.
• Phase of minimum motion of heart–mid diastole • Carotid bodies are positioned near a major arterial
•
•
• When heart rate is low – duration of diastole increases baroreceptor, the carotid sinus. Two aortic bodies are
•
and AV valves drift towards the closed position shown near the aortic arch.
• During exercise, diastole is shortened more than systole
Organization of Carotid Body
•
• 70% of ventricular filling occurs passively during atrial
•
diastole • Type I (glomus) cells contain catecholamines. When
•
• In mid diastole or isovolumetric relaxation phase, there exposed to hypoxia, they release their catecholamines,
which stimulate the cuplike endings of the carotid sinus
•
is maximum drop in pressure. Stroke volume and work
done are least nerve fibres in the glossopharyngeal nerve.
• The glia like type II cells surround the type I cells and
• Last to be depolarized are:
•
probably have a sustencular function
•
– Postero basal portion of left ventricle • Outside the capsule of each body, the nerve fibres acquire
–
– Pulmonary conus
•
a myelin sheath, however they are only 2 to 5 mm in
–
– Uppermost portion of septum diameter and conduct at relatively low rate of 7 to 12m/s
–
Physiology 125

• Afferents from the carotid bodies ascend to the medulla • In sufficient doses, nicotine and lobeline activate the
•
•
via the carotid sinus and glossopharyngeal nerves, and chemoreceptors. It has also been reported that infusion
fibres from the aortic bodies ascend in the vagi of K+ increases the discharge rate in chemoreceptor
• The blood flow in each 2mg carotid body is about 0.04ml/ afferents, and because the plasma K+ level is increased
•
min, or 2000ml/100g of tissue/min compared with a blood during exercise, the increase may contribute to exercise
flow of 54ml/100g of tissue/min in brain and kidneys. induced hyperapnea.
• Because the blood flow per unit of tissue is so enormous, – ECG:
•
the O2 needs of the cells can be met largely by dissolved
–
P wave: Atrial depolarization
O2 alone. Therefore the receptors are not stimulated

QRS complex: ventricular depolarization
in conditions such as anaemia or carbon monoxide

T wave: ventricular repolarization
poisoning, in which the amount of dissolved O2 in

– Chronotropic action–effect on heart rate
the blood reaching the receptors is generally normal
–
– Inotropic action–effect on force of contraction
even though the combined O2 in the blood is markedly
–
– Dromotropic action–effect on conduction of
decreased. (AIIMS May 2013)
–
impulse through heart
PHYSIOLOGY

• The receptors are stimulated when the arterial pO2 is low – Bathmotropic action: effect on excitability of
•
–
or when, because of vascular stasis, the amount of oxygen cardiac muscle
delivered to the receptors per unit time is decreased. – Heart receives its blood supply during diastolic
–
• Powerful stimulation is also produced by cyanide, which while other parts of the body receive blood during
•
prevents oxygen utilization at the tissue level. systole
Vasoconstrictor Vasodilators
• Angiotensin II – activates phospholipase C • Nitric oxide – activates guanylyl cyclase
•
•
• Endothelin I – activates phospholipase A2 • Bradykinin- activates phospholipase C
•
•
• VIP – activates protein kinase A
•
• Substance P – activates phospholipase C
•
Heart Sounds
Feature 1st Heart sound 2nd 3rd 4th
Character Low pitched (frequency) Shorter high pitched Soft low pitches weak Arterial heart sound
slightly prolonged ‘lub’ ‘dup’ (AIPG 2010) rumbling

Cause Sudden closure of mitral Closure of aortic and Rapid ventricular filling due Ventricular filling due to atrial
and tricuspid valve pulmonary valves to in thrusting of blood from contraction causing in thrusting of
atria blood
Timings Start of ventricular systole Just after end of Beginning of middle third of Immediately before 1st heart sound
ventricular systole diastole (presystolic)
RESPIRATORY SYSTEM – Lymphatic channels are more abundant in the lungs

–
than in any other organ.
Airways – There is a circadian rhythm in bronchial tone, with
–
maximal constriction at about 6 AM and maximal
– Between the trachea and alveolar sacs, the airways dilatation at 6 PM. That is why asthma attacks are
 
–
divide 23 times. The first 16 generations of passages more severe in the late night and early morning hours.
form the conducting zone of the airways. The • Dead Space
remaining 7 generations form the transitional and
•
– Anatomic dead space=150ml
respiratory zones where gas exchange occurs.
–
– When the alveolar dead space (ie all the air in the
– There are 300 million alveoli in humans and the total
–
alveoli that is not participating in gas exchange)
–
area of the alveolar walls in contact with capillaries in is included in the total measurement of the dead
both lungs is about 70 sq.m. space, this is known as physiologic dead space.
– Largest amount of smooth muscle relative to the – In a normal person, the anatomic and physiologic
–
–
thickness of the wall is present in the terminal dead spaces are nearly equal because all alveoli are
bronchioles. functional in the normal lung.
126
Dead space is decreased by Dead space increased by

• Supine position • Endotracheal intubation (artificial airway)
•
•
• Neck fully flexed with depressed chin • Standing position (due to hypoperfusion of apical alveoli)
•
•
• Low lung volumes • Emphysema
•
•
• Tracheostomy (artificial airway) (AIIMS May 09) • Neck extension
•

•
• Ipratropium (bronchial dilatation)
•
• Pulmonary Blood Flow
•
– It takes an RBC about 0.75 seconds to traverse the pulmonary capillaries at rest and 0.3 seconds or less during exercise.
–
– About 2% of blood in the systemic arteries is blood that has bypassed the pulmonary capillaries.
–
– There is an increase in pulmonary blood flow from the apices to the bases of the lungs, i.e., base has more blood flow
–
• Blood gases
•
Transport of oxygen in blood Transport of carbon dioxide in blood
PHYSIOLOGY
• Oxygen is transported mainly (97%) in chemical combination • CO2 is transported in blood mainly (70%) in the form of bicarbonates
•
•
with Hb in the form of oxyhemoglobin • Plasma HCO3-> carbamino compounds > dissolved CO2 plasma
•
• Only 3% oxygen is transported in dissolved state in plasma • It is 20 times more soluble in blood than oxygen and its dissociation
•
•
• Total oxygen content of arterial blood is 200 ml/l while that of curve is linear over physiological range.
•
mixed venous blood is 48 ml/l
• Ventilation Perfusion Ratio (V/Q ratio)
•
– The ratio of pulmonary ventilation (V) to pulmonary blood flow (Q) for the whole lung at rest is about 0.8 = ventilation
–
perfusion (V/Q) ratio.
– V/Q in different areas of the lungs
–
Blood flow is lowest at the apex and highest at the base (AIPG 2012)

Ventilation is lowest at the apex and highest at the base, but differences in ventilation are not as great as or perfusion.

 
V/Q at the apex > 1.0; at the base < 0.8.

V/Q is high at the apices of the lungs and this is said to account for the predilection of TB for this area.

Oxygen delivery to tissue depends on:
Lung • Amount of oxygen entering the lungs (ventilation)
•
• Adequacy of pulmonary gas exchange (diffusion)
•
Cardiovascular • Cardiac output
•
system • Peripheral vascular resistance i.e. degree of constriction of vascular bed in the tissue
•
Blood • Capacity of blood flow to carry oxygen, which depends on:
•
• Amount of dissolved oxygen in plasma
•
• Amount of hemoglobin
•
• Affinity of Hb for oxygen
•
• Which is represented by oxygen Hb dissociation curve and depends on 2,3 DPG, pH and temperature.
•
Compliance
• Compliance of lung is a measure of stretchability of lungs and hence its total capacity. It is the change in lung volume per
•
unit change in air way pressure (V/P).
• Lung compliance is increased in:
•
– Emphysema
–
• Lung compliance is decreased in:
•
– Deformities of thorax e.g. kyphosis, scoliosis
–
– Paralysis of respiratory muscles
–
– Pleural effusion
–
– Abnormal thorax e.g. pneumothorax, hydrothorax, hemothorax (AIPG 2011)
–

– Interstitial pulmonary fibrosis
–
– Interstitial lung disease
–
– Pulmonary congestion
–
Physiology 127

• Pulmonary arterioles have less smooth muscles and not more smooth muscles than systemic arterioles
•
Feature Systemic Pulmonary
• Structure • Thick walls • Thin walls
•
•
•
• Abundant smooth muscle • Less smooth muscles
•
•
• Mean pressure/ Resistance • High pressure/High resistance • Low pressure/ low resistance (25/8 mmHg)
•
•
•
(120/80mm Hg)
Non Respiratory Functions of Lungs (AIPG 2011)

Blood filtration The pulmonary capillary bed acts as a blood filter preventing particles like small clots,
detached cells or bubbles from reaching systemic circulation
Defence mechanisms • The lungs are involved in a number of functions related to defense by a variety of
•
mechanisms etc:
– Normal mechanical defenses (filtration/Epithelial barriers/ Mucociliary clearance
PHYSIOLOGY
–
etc)
– Natural phagocytic defenses (Macrophages, PMN, Microbicidal activities, eg
–
antiprotease
– Specific immune defense (humoral/cell mediated immunity)
–
Metabolic and endocrine function • Conversion of angiotensin I to Angiotensin II by angiotensin converting enzyme (helps
•
in regulation of sodium/ water balance and blood pressure) (AIPG 2007)

• Fibrinolytic function/ Heparin
•
– Lungs are believed to be capable of producing substances necessary to delay
–
clotting and/or dissolve small clots (fibrinolysis)
– Pulmonary endothelium is known to be rich in plasmin activator. This converts
–
plasminogen into plasmin which in turn promotes fibrinolysis
– The lung is rich in mast cells which secrete ‘heparin’ an anticoagulant
–
• Synthesis of surfactant
•
– Surfactant is synthesized by type II alveolar epithelial cells
–
• Reservoir of blood
•
– Pulmonary circulation may act as temporary reservoir of blood
–
• Acid base balance
•
– Lungs play an important role in acid base balance
–
• Cooling and water balance (sodium balance)
•
Synthesis/ Storage/Removal/Deactivation • Bradykinin, Serotonin, Histamine and certain prostaglandins are all produced and/or
•
of vasoactive substances stored in the lungs, and may be released into the greatest into the general circulation
under certain circumstances, e.g. anaphylactic shock,
• Bradykinin, Norepinephrine and certain prostaglandins are also removed/deactivated
•
in the lungs
The process of certain vasoactive substances by Lungs
Released by • Heparin
•
Endothelium • Lipoprotein Lipase
•
• Prostacycline
•
• Kallikerin
•
• Leukotriens
•
Metabolized by • Angiotensin
•
Luminal surface • Bradykinin
•
• Adenine neucleotide
•
Uptake by • Serotonin
•
endothelium and • Nor epinephrine
then metabolized
•
• Prostaglandin E and F
•
Generation • Endothelins
•
of vasoactive • Nitric oxide
substances by
•
• Prostacyclin
lungs
•
• Hyper polarizing factor
•
128
Unaffected in • Angiotensin II
•
traversing the • Epinephrine
lungs
•
• Dopamine
•
••
Vasopressin
• Prostaglandin
•
• VIP
•
• Oxytocin
•
Synthesis of • Certain peptides like substance Q and some opiates are synthesized in the lungs
•
certain peptides
• Kussumal breathing: Increase in rate and depth of • The bronchial system is more prominent in neonates and
•
young children, and it may play a greater role in bringing
•
respiration seen in diabetic ketoacidosis and anaemia.
nutrients to the developing lung.
• Cheyne-Stoke breathing: Periodic breathing –
PHYSIOLOGY
•
characterized by initial rapid and deep respiration Lung Volumes and Capacities
followed by complete cessation – 1 minute duration
Tidal volume (TV) It is the air that moves 500ml
– Seen in physiological condition such as deep sleep, into the lung with each
–
high altitude, new born babies and severe muscular normal inspiration or
exercises. the volume of air that
moves out of lung
– Pathological condition: Narcotic poisoning, with each expiration.
–
uremic condition, cardiac failure and increased
intracranial pressure. Inspiratory Reserve The air inspired with 3300ml
Volume (IRV) a maximal inspiratory
• Biots breathing: Periods of apnea and hyperapnea
effort in excess of
•
– Seen in lesions of brain, injuries to brain tidal volume
–
Bronchial Circulation Expiratory Reserve The air expelled with 1000ml
Volume (ERV) a maximal expiratory
• The existence of separate circulatory system in the lung effort in excess of
•
with oxygenated blood from the systemic circulation tidal volume
was first observed by Frederich Ruysch. This second
Residual Volume (RV) The amount of air 1200ml
circulation is the bronchial circulation. remaining in the lungs
• It provides systemic arterial perfusion to trachea, upper even after forced
expiration
•
airway, surface secretory cells, glands, nerves, visceral
pleural surface, lymph nodes, pulmonary arteries and Inspiratory Capacity Total amount of air 3800ml
veins. (AIPG 2010) (IC= TV+IRV) that can be breathed

in
• The bronchial circulation perfuses the upper respiratory
•
tract, it does not reach the terminal or respiratory Vital Capacity (VC= Maximal amount of air 4800ml
TV+IRV+ERV) that can be expelled
bronchioles or the alveolus. (AIPG 2011) out forcefully after a

• The bronchial circulation receives only about 1% of the deep inspiration
•
total cardiac output, compared to almost 100% for the
Functional Residual Ca- It is the volume 2200ml
pulmonary circulation. pacity (FRC= ERV+RV) of air remaining
• Bronchial circulation has angiogenesis capabilities. Such in the lung after
normal expiration
•
capabilities are particularly important for repair when (after normal tidal
tissues are damaged. expiration)
• The major pathway for tumour angiogenesis in the lung
Total Lung Capacity The amount of air 6000ml (4.2
•
via the bronchial circulation. (TLC=TV+IRV+ERV+RV) present in the lung to 6L)
• The physiological function of bronchial circulation remain after a maximal
inspiration. This is the
•
as enigma, because lung transplant studies have shown maximum volume to
that adult lungs can function normally in the absence of a which the lungs can
bronchial circulatory system be expanded.
Physiology 129

Alveolar ventilation 4.2l/min
Total lung capacity 4 to 6 ml

Respiratory minute volume (rest) 6l/min
Maximum voluntary ventilation 125 to 170 l/min
Timed vital capacity in 1 sec (FeV1) 83%
- in 3 sec 97%
Work of quiet breathing 0.5kg-m/min
Maximum work of breathing 10kg-ml/breath
Muscles of Respiration
PHYSIOLOGY
Primary inspiratory muscles are diaphragm, external intercostals muscles. Accessory inspiratory muscles are sternomastoid,
scalenii and anterior serratus.
Primary expiratory muscle is internal intercostals. Accessory expiratory muscles are muscles of abdomen.
I. The muscles of inspiration

I. The diaphragm It moves downward like a piston when it contracts and brings about an increase in the

vertical axis of the chest (pump-handle movement)
II. External intercostals Elevate the lower ribs and increase the anteroposterior diameter of the chest cavity

(bucket- handle movement).
III. Anterior Serrati Lift may of the ribs

VI The Scalene and Sternocleidomastiods Accessory inspiratory

II. The expiratory muscles
I. Internal intercostals Lower the chest cage by pulling the upper ribs backward in relation to the lower ribs.

II. The abdominal recti Pull the cage downward and inward. They also increase the intra-abdominal pressure

by compressing the abdominal contents toward the diaphragm.
Surfactant
• Lipid surface tension reducing agent
•
• Produced by:
•
– Type II alveolar epithelial cells (pneumocytes) at 20 weeks of life and peaks at 35 weeks gestation
–
– Secreted by exocytosis
–
• Composition:
•
– Phospholipids:
–
Dipalmitoylphosphatidyl choline -62%

Phosphotidyl glycine – 5%

Other phospholipids – 10%

– Neutral lipids – 13%
–
– Protein 8%
–
– Carbohydrate -2%
–
• Function:
•
– Reduces alveolar surface tension
–
– Prevent alveolar collapse
–
– Reduces effort of breathing
–
– Prevents pulmonary edema
–
130
Regulation of Respiration – Pre-Botzinger complex: An area just caudal to the
–
Botzinger comples – implicated as site of respiratory
Two separate neural mechanisms regulate respiration. rhythm generation. Note: Medullary lesions can lead
– Voluntary system = is located in the cerebral cortex.
 
 
to various type of abnormal breathing patterns which
–
– The automatic system = is located in the pons and include Cluster breathing, Ataxic breathing (Biot’s
–
medulla. breathing), Cheyne-Stokes respiration, Gasping.
• Medullary respiratory center: • Pontine respiratory center:
•
•
– Dorsal respiratory group: Primarily responsible – Apneustic center: In the lower pons, stimulates
–
–
for inspiration; input via cranial nerves (CN X, inspiration, producing deep and prolonged
peripheral chemoreceptors and mechanoreceptors inspiratory gasp.
 
in the lung) and CN IX (peripheral chemoreceptors)l – Pneumotaxic center: In the upper pons, inhibits
–
output via the phrenic nerve. inspiration; therefore regulates inspiratory volume
 
– Ventral group: primarily responsible for active and respiratory rate.
 
– Cerebral cortex: Controls the voluntary component
–
expiration during forceful breathing; not active during
–
normal breathing when expiration is passive. “DIVE of breathing (i.e., a person can voluntarily hold breath
PHYSIOLOGY
or hyperventilate)
 
 
= Dorsal Inspiration, Ventral Expiration”
Fick’s law Concentration of a gas that dissolves in a liquid is proportional to its partial pressure and its solubility
coefficient.
Dalton’s law That the partial pressure of a gas in a mixture is equal to the pressure that the gas would exert if it alone
occupied the total volume of the mixture.
Henry’s law Concentration of a gas that dissolves in a liquid is proportional to the pressure above the liquid.
The universal gas law States that PV = nRT, where P = pressure, V = volume, n = mol, R = gas constant, and T = absolute
temperature (measured in Kelvin).
This oxygen dissociation is effected by:

1 Haemoglobin concentration RBC

2 Temperature of body

3 Carbon dioxide tension of blood (normal 46 mm Hg) (AIPG 2011, 2010)

4 Acid metabolities, i.e., effect of 2,3-DPG (2-3 Diphosphoglycerate)

Any facts which shifts the curve to right helps in deoxy- Factors which favour dissociation curve to left are:
genation. Factors which help in deoxygenation are:
• Raised venous carbon dioxide tension (Bohr effect). • Decrease in 2,3 – DPG
•
•
• Decreased arterial oxygen tension • Increase pH
•
•
• Increase in 2,3- DPG levels (anaemia and hypoxia) • Increased arterial oxygen and decreased venous carbon dioxide
•
•
• Increase in temperature tension.
•
• Increase in acidity of plasma decrease in pH. • Fall in temperature
•
•
• Decrease in affinity of oxygen to haemoglobin. • Increase in affinity of oxygen to haemoglobin.
•
•
Hypoxia
• Hypoxia is oxygen deficiency at the tissue level.

•
• A normal individual is not conscious of respiration until ventilation is doubled and breathing is not uncomfortable (i.e.
•
 
the dyspnea point is not reached) until ventilation is tripled or quadrupled.
• Dyspneic index is the percentage of respiratory capacity not being used at a given respiratory minute volume. When the
•
 
dyspneic index is less than about 70%, dyspnea is usually present.
• The pulmonary vasculature is unique in that hypoxia causes vasoconstriction.
•
• In other organs, hypoxia causes vasodilation.
•
Normal arterial blood contains 19.5 mL of oxygen per 100 ml of blood. It is 97% saturated when oxygen tension of arterial
blood is 100 mm Hg. Capability and venous blood contains. 14.5 mL/100 mL oxygen, which the oxygen tension is 40 mm and
75% saturated. Remaining 5 ml is extracted by resting tissue. (NEET 2013)

Physiology 131

Hypoxia Oxygen tension (PO2) Oxygen saturation Oxygen carrying ca- Clinical conditions
of arterial blood of arterial blood pacity of blood
Hypoxic hypoxia Tension of oxygen in Normal Normal This kind of hypoxia is seen in
(or) arterial hypoxia arterial blood is lower than collapse of lungs, depression of
normal due to low oxygen respiratory center, tuberculosis,
content of blood pneumonia, emphysema
congestive cardiac failure,
asthma etc. Oxygen therapy is
useful
Anaemic Normal Oxygen saturation is Lower than normal It is seen in quantitative

hypoxia or normal. How much low and qualitative deficiency
hypohaemoglobin the haemoglobin it is of haemoglobin. Or carbon
hypoxia fully saturated. monoxide posisoning.
Stagnant hypoxia Normal Oxygen capacity is normal, It is seen in haemorrhage, loss

(Ischaemic but blood flow to the tissues of fluid due to vomiting, diarrhea,
PHYSIOLOGY
hypoxia) is deficient burns, congestive cardiac failure
etc.
Histoxic hypoxia Normal Normal Normal blood flow is also In spite of everything being
normal. normal, tissues fail to extract
oxygen from blood as seen
in cyanide poisoning. Venous
blood has higher O2 saturation
because of the inability of
tissues to extract the arterial O2.
Oxygen therapy is not effective
in this from of hypoxia.
Hypercapnea
• Increased carbon dioxide content of blood (AIPG 2010)
•

• Conditions causing it:
•
– Asphyxia (blockage of respiratory pathway)
–
– Breathing air rich in carbon dioxide
–
• Effects
•
– During hypercapnea respiratory centres are stimulated excessively. This leads to dyspnea
–
– pH of the blood reduces. (AIPG 2011)
–

– Tachycardia and increased blood pressure
–
– Flushing of skin due to peripheral vasodilation
–
– Headache, depression and laziness.
–
– Muscular rigidity, fine tremors and generalized convulsions and eventually coma k/a CO2 narcosis.
–
• In febrile patient there is 13% increase in CO2 production for each 10 rise in temperature and a high carbohydrate intake
•
increase CO2 production because of increase in RQ.
Oxygen-Hemoglobin Dissociation Curve

– The relationship between the percentage saturation of Hb and partial pressure of O2 in arterial blood.
–
– O2 binds to Fe2+ in haem to form oxyhaemoglobin
–
– Sigmoidal shaped curve due to positive co-operativity, i.e. the binding of one O2 molecule facilitates the binding of the
–
 
next. Similarly the release of one O2 molecule promotes the release of others.
– The effect of pH on the O2 binding of Hb is called the Bohr effect; the affinity of Hb for oxygen increases at higher
–
pH, and decreases with fall in pH.
 
– 2,3-BPG is synthesized in the RBCs from metabolites of the glycolytic pathway. It binds to Hb stabilizing the deoxy form,
–
 
and reduces the affinity of Hb for O2, causing the release of O2. Production is stimulated by hypoxia, e.g., anemia and
altitude
132
• Myoglobin Curve • Dilation is produced by sympathetic discharge and

•
•
– Myoglobin binds only one mole of oxygen per mole. VIP and constriction by parasympathetic discharge and
–
– It shows NO Bohr effect. substance P. Cool air causes bronchoconstriction.
–
– Its dissociation curve is a rectangular hyperbola.

(AIPG 2011)
–
• Chloride Shift

•
– The solubility of CO2in blood is 20 times that of O2 • Circadian rhythm in bronchial tone, with maximum
–
•
• Chloride shift: since the rise in HCO3– content of red constriction at 6 am and maximum dilation at 6pm
•
cell is much greater than that in the plasma as the blood • Patchy atelectasis is also associated with surfactant
passes through the capillaries, about 70% of the HCO3–
•
deficiency in patients who have undergone cardiac
 
formed in the red cells enters the plasma. The excess surgeries involving use of pump oxygenation and
HCO3– leaves the red cell in exchange for Cl–, the process interruption of pulmonary circulation
being mediated by band 3, a membrane protein. This
exchange is called chloride shift. • Cigarette smoking decreases lung surfactant
•
– The chloride content of venous blood is therefore • The quaternary structure of hemoglobin determines its
PHYSIOLOGY
•
affinity for oxygen
–
significantly greater than in arterial blood.
– The chloride shift occurs rapidly and is essentially • The receptors in the carotid and aortic bodies are
•
–
complete in 1 second. stimulated by a rise in the pCO2 or H+ ion concentration
of the arterial blood or decline in its pO2.
Good to Know
• The Hering Breur inflation reflex is an increase in the
• The bronchial veins drain into the azygous vein. The
•
duration of expiration produced by steady lung inflation
•
bronchial circulation nourishes the bronchi and pleura and HeringBreur deflation reflex is a decrease in duration
• Lymphatic channels are most abundant in lungs of expiration produced by marked deflation of lungs
•
• The presence in intrapleural space between the lungs • Since voluntary and automatic control of respiration
•
•
and chest wall is subatospheric (-2.5mmHg at 1 atm) are separate, automatic control is sometimes disrupted
• If the lungs lose their elasticity, the chest expands and without loss of voluntary control. This clinical condition
•
becomes barrel shaped is known as Ondine’s curse.
• Diffusing capacity for O2 is 400ml/minute/1mmHg. Thus
•
Diaphragm diffusing capacity for CO2 is 20 times more than that of
O2.
• Movement of the diaphragm accounts for 75% of
• Most effective method of assessing breathing is by
•
the change in the intrathoracic volume during quite
•
inspiration measuring tidal volume
• The distance between the diaphragm moves ranges from • The volume of air remaining in the lung after normal
•
expiration is functional Residual volume (FRV). The
•
1.5cm to as much as 7 cm with deep inspiration
volume of air remaining in the lungs after forced expiration
• Diaphragm has 3 parts–
is residual volume (RV)
•
– Costal portion–made up of muscle fibres that are
• Vital capacity and timed vital capacity (TVC) are
–
attached to the ribs and the bottom of thoracic cage
•
– The crural portion made up of fibres that are attached reduced greatly in the respiratory diseases like asthma,
emphysema, pneumonia, etc. in scoliosis, vital capacity is
–
to the ligaments along the vertebrae , and the
– Central tendon into which the costal and crural fibres reduced but TVC is normal.
–
insert. Inferior part of pericardium • Pulmonary ventilation = TV X respiratory rate
•
Also Note • Alveolar ventilation = (tidal volume TV – dead space) X
•
respiratory rate
• Transaction of the spinal cord above C3 is fatal without
• Mouth to mouth respiration provides 16% of O2. This is
•
artificial respiration but C5 is not, because it leaves the
•
phrenic nerve intact. Phrenic nerve arises from C3 to the amount of oxygen present in exhaled, expired air
C5. • O2 content of inspired air is 21%, alveolar air is 14%, and
•
• The scalene and sternocleidomastoid muscles in the neck that of expired air is 16%
•
are accessory inspiratory muscles that help to elevate • Room air or atmospheric air contain 78% N2 + 21% O2 +
•
the thoracic cage during deep labored respiration. 1% other gases
Physiology 133

GASTROINTESTINAL TRACT
• Composition of saliva - 99% Water + 1% solids
•
– Inorganic components (Electrolytes)
–
– Organic components (Mucus, enzymes)
–
Proteins of acinar cell origin Proteins of nonacinar cell origin
• Amylase–(found in highest concentration in saliva. Parotid • Lysozyme (helps in oral protective functions)
•
•
saliva: 60-120mg/100ml. Submand saliva: 25mg/100ml) – Secretary IgA (synthesized by plasma cells, neutralizes surface

(AIPG 2012)
–
charge of bacteria, inhibits bacterial adherence, prevents

• Lipase adverse effects of bacterial toxins and enzymes)
•
• Mucous glycoproteins (MG1 and MG2 found in submand and • Growth factors
•
•
subling saliva) • Regulatory peptides
•
• Proline rich glycoproteins (found in parotid saliva; stabilize • Other polypeptides
•
•
tooth surface +aid remineralization) (AIPG 2004)
PHYSIOLOGY
– Statherin: Is a small phosphoprotein which inhibits

–
– Basic glycoprotein (adsorbs to membranes) hydroxyapatite crystal growth. It also prevents precipitation of
–
– Acidic protein (attaches to tooth surface) calcium phosphates from supersaturated solutions and favors
–
• Tyrosine-rich protein (prevent Ca precipitation from saliva remineralization. It is important as an inhibitor of calculus
•
• Histadine-rich protein (help in pellicle formation) formation, both in the glands and on the teeth.
– Sialin: Is a tetrapeptide which helps to regulate the pH of
•
• Peroxidase (inhibits bacterial glycolysis and adherence of –
plaque.
•
S.mutans to saliva coated hydroxyapatite, reduces bacterial
aggregation)
Taste
• Primary taste (AIPG 2012)
•

– Sour
–
– Sweet
–
– Salty
–
– Bitter
–
– Umami
–
• Probable chemical receptors in taste cells
•
– 2 sodium receptor
–
– 2 potassium receptor
–
– 2 sweet receptor
–
– 2 bitter receptor
–
– 1 chloride receptor
–
– 1 adenosine receptor
–
– 1 glutamate receptor
–
– 1 inosine receptor
–
– 1 hydrogen ion receptor
–
Gastric glands can be divided into three groups on the basis of site
Gastric glands Cells Functions/secretions
• Principal gastric glands (body and • Mucous neck cells • Mucous
•
•
•
fundus) • Chief/peptic cells • Pepsinogen and lipase
•
•
• Parietal/ oxyntic cells • HCL and intrinsic factor
•
•
• Stem cells • Differentiation into other cell types
•
•
• Neuroendocrine/enetroendocrine • Gastrin
•
•
– G cells • Somatostatin
–
•
– D cells • Histamine
–
– ECL (enterochromattin like cells)
•
–
134
Gastric glands Cells Functions/secretions

• Cardiac glands ( near cardiac orifice) • Mucous secreting cells • Mucous
•
•
•
• Few parietal and chief cells • HCL, Intrinsic factor, pepsinogen, lipase
•
•
(AIIMS 2010, 2011, AIPG 2009)
• Pyloric glands (pyloric antrum) • Mucous secreting cells • Mucous
•
•
•
• G cells • Gastrin
•
•
Factors affecting gastrin secretion
• Any stimuli that affects gastrin secretion also affects acid secretion from the stomach
•
Stimuli that increase gastrin (and HCl) Stimuli that inhibit gastrin secretion
secretion
• Peptidase and amino acids Luminal • Acid
•
•
• Distention • Somatostatin
•
•
PHYSIOLOGY
• Ca++ Blood borne • Secretin, GIP, VIP, Glucagon, Calcitonin

•
•
• Epinephrine
•
• Increased vagal discharge via GRP Neural
•
(gastrin releasing polypeptide-
noncholinergic)
Hormones of GIT System

Source Function
Intrinsic factor (a Produced by the Necessary for the absorption of vitamin B12 in the terminal ileum
glycoprotein) (AIIMS parietal cells of

May 08 (AIPG 2008) stomach
Secretin S cells of duodenum, • Stimulates the secretion of watery, alkaline pancreatic secretion
•
jejunum, ileum • The secretion of large amount of watery juice with high bicarbonate ion protects
•
the intestinal mucosa from acid chyme by neutralizing it and provides an alkaline
pH for the activation of pancreatic enzyme
• Other actions are:
•
• Inhibition of gastric juice secretion and motility of stomach
•
• Causes contraction of pyloric sphincter
•
Motilin (polypeptide) M cells of small • It increases the migrating myoelectric complex component of gastrointestinal
•
intestine motility and stimulates the production of pepsin (AIPG 2008)

• At alkaline pH in duodenum stimulates its release
•
• At low pH it inhibits gastric motor activity, whereas at high pH it has a stimulatory
•
effect
GIP (gastric inhibitory K cells of duodenum • Inhibits secretion of gastric juice
•
peptide) and jejunum • Inhibits gastric motility
•
• Increases insulin secretion by stimulating β cells of pancreas
•
Bile
• Secreted by hepatocytes into the bile capillaries and from there into duodenum through ‘Sphincter of Oddi’
•
• Bile is concentrated and stored in GB. When food enters into the duodenum, secretin and CCK-PZ stimulate GB to contract
•
and bile is poured into duodenum
• Choleretics-substances that increase bile secretion. Bile salts are the most potent choleretics
•
• Cholagogues: Are the substances that increase GB contraction eg: fatty acids and amino acids in duodenum release CCK,
•
Ca++ ions.
• Rate of bile production is 500 ml/day and that of bile salts is 0.2-0.4 gm/day. Substance which increase bile production are
•
vagus stimulation, secretin (increase HCO3 and water content of bile)
Physiology 135

Bile Acids
Principal/primary Bile Acids- • Cholic acid
•
formed in liver from cholesterol • Chenodeoxycholic acid
•
Secondary Bile Acids – • Deoxycholic acid
•
Formed in the colon by bacterial action. Primary • Lithocholic acid
bile acids are converted into 2nd bile acids
•
Bile salts • Are sodium or potassium salts of bile acid conjugated with glycine or taurine eg: Na+
•
- Glyco/Tauro- cholate or K+ - Glyco/Tauro- cholate
• They decrease surface tension and responsible for emulsification of fat along with
•
phospholipid and monoglycerides
••
Bile salts are amphiphathic
• Increase bile salts excretion in urine is seen in obstructive jaundice
•
PHYSIOLOGY
Enterohepatic Circulation (AIPG 2011) – Bile salts and bile acids are recycled approximately 2
–
times during each meal, and about 6-8 times each day
• The enterohepatic circulation is a circuit in which solutes
via the enterohepatic circulation.
•
are secreted by the liver only to be returned to the liver via
– About 95% of the bile salts that arrive in the intestine
intenstinal reabsorption.
–
are reabsorbed.
• Molecules in the enterohepatic circulation are: – Bile salts that become deconjugated revert to bile acids,
•
–
– Secreted into bile by hepatocytes which are mostly undissociated and are reabsorbed by
–
– Delivered to the small intenstine via the biliary duct simple diffusion in the jejunum.
–
– Reabsorbed from the small intenstine – Most primary and secondary bile salts are reabsorbed
–
–
– Returned to the liver via the portal venous system to via Na+ bile salt co-transport when they reach distal
–
become available again for uptake and secretion by ileum.
hepatocytes – A small amount of bile acid (mostly as lithocholic
–
• Importance: acid) is lost in fecal excretion each day.
•
– Bile acid pool is not large enough to assimilate the – The rate of bile acid loss in feces is matched by the rate
–
–
lipid content of a typical meal. of hepatic bile acid synthesis, thereby maintaining the
bile acid pool.
Peristaltic Movements
• Tonic contractions • Tonic contraction. Constant, low-grade tone is maintained in the gut wall on which stronger contractions are
•
•
superimposed.
• Tonic contractions prevent the distention of gut.
•
• Loss of tone (loss of parasympathetic stimulation) results in retention of gut contents and constipation.
•
• They are also found at sphincter regions.
•
• Long duration of action (minutes to hours)
•
• Rhythmic • Consists of alternate bloat and narrow areas in an area of the small intestine. Common in small intestine
•
•
contraction and as the name suggests helps in mixing up of the contents with the digestive juices.
a. Segmentation • Increases the surface area for digestion and absorption by increasing the contact between gut wall and the

•
(Mixing) contents
• Stimulated by distension
•
• Occurs at a rate of 10-11 cycles/min at duodenum and slows down to 5-6 cycles at ileum.
•
b. Peistalisis • Consist of rhythmic coordinated contraction and relaxation of circular and longitudinal muscles, which create

•
(propulsion) and moving ring of constriction that moves food along the gut.
• Controlled by enteric nervous system-local reflexes stimulated by the distension.
•
• Propels the chime forwards.
•
136
Gastric Emptying (Enterogastric Emptying) (AIPG 2002)

Stimulated by • Gastrin
•
• Excitement
•
• Carbohydrate rich diet
•
Delayed by ••
Fatty meal
• Protein rich diet
•
• Acid bathing
•
• GIP
•
Hormones that inhibit • Cholecystokinin
•
gastric emptying • Secretin
•
• Gastric inhibitory peptide
•
Gastric Motility
PHYSIOLOGY
Increased by Decreased by
• Gastrin • Enterogastrone (CCK, secretin)
•
•
• Histamine • Epinephrine
•
•
• AcH • Norepinephrine
•
•
• Nicotine • Atropine
•
•
• K+ • Ca++
•
•
Factors Affecting Intestinal Motility
Mechanical • Distension of gut (the usual stimulus)
•
• Chemical or physical irritation of the gut
•
Hormonal • Cholecystokinin–Enhances motility of the small intestine and colon (inhibits gastric emptying)
•
• VIP–Relaxes intestinal smooth muscle include sphincters
•
• Motilin–Enhances gastric and intestinal motility
•
Neural • Parasympathetic cholinergic stimulation (acetyl choline) enhances intestinal gastric motility
•
• Sympathetic stimulation inhibits gastric and intestinal motility
•
Others • MMC
•
• Gastroileal reflex
•
Migratory motor In an empty stomach wave of depolarization starts at regular intervals (every 90 minutes approx) and proceeds caudally
complex until it reaches the terminal part of ileum where it dies
Gastroileal reflex Vigorous gastric secretion/ gastric peristalsis can cause ileal peristalsis – emptying of ileum in large intestine which in
turn may provoke a mass peristalsis in the colon and an urge to defecate may develop
Dietary Fibre
Definition All ingested food that reaches the large intestine in an essentially unchanged form
Components • Cellulose
•
• Hemicellulose
•
• Pectin
•
• Lignin
•
• Gums
•
• Pentose
•
Advantages • Contributes bulk by absorbing water 10 to 15 times of its own weight (provides a larger volume of indigestible materials
•
in colon) and thus hastens passage through the gut, decreasing the transit time.
• Soluble fiber lower total blood cholesterol levels by lowering LDL or bad cholesterol level. It also slows the absorption
•
of sugar and reduce the risk of developing type II diabetes
Physiology 137

Transit Time in Small Intestine and Colon hepatic flexure in 6 hours, the splenic flexure in 9 hours
and the pelvic colon in 12 hours
• The first part of the test meal reaches the caecum in about
• From the pelvic colon to the anus, transport is much
•
4 hours; all of the undigested portions have entered the
•
slower
colon in 8 to 9 hours.
• As much as 25% of the residues of the test meal can still be
• On average, the first remnants of the meal reach the
•
found in rectum after 72 hours.
•
Daily Water Turnover (ml) in GIT
Ingested 2000
Endogenous secretions
• Salivary glands 1500
•
• Stomach 2500
500
•
• Bile
1500
•
• Pancreas 1000
•
PHYSIOLOGY
• Intestine 7000
•
Total
Total Input 9000
Reabsorbed
• Jejunum 5500
•
• Ileum 2000
1300
•
• Colon
8800
•
Total
Balance in stool 200
Absorption Rate of Absorption from GIT

Proximal intestine is the site of absorption of iron, calcium, • Galactose >glucose>fructose> mannose
•
water soluble vitamins and long chain fatty acids • Absorption of glucose is increased by
•
Proximal and mid intestine – sugars – Thyroid hormone
–
Middle small intestine and jejunum–amino acids – Anterior pituitary hormone
–
Terminal ileum: Bile salts and vitamin B12 (AIPG 2001) – ACTH
–

Colon: Secretes mucous and absorbs water, electrolytes and – Vitamin B12
–
short chain fatty acids – Vitamin B6
–
Iron is absorbed from duodenum and proximal jejunum – Pantothenic acid
–
– Insulin has no effect on absorption of glucose in GIT
Calcium and folate is mainly absorbed from jejunum
–
Iron Absorption
Increased by: (AIPG 2012) Is decreased by
• Acids • Alkalies
•
•
• Ascorbic acid (Vitamin C) • Phosphates
•
•
• Amino acid containing SH- group • Phytates (in maize, wheat)
•
•
• Meat • Tetracycline
•
•
All of them reduces Fe3+ to Fe2+ • Present of other food in stomach
•
Pancreatic Cells in Humans
Pancreatic cells Secretion
α cells Glucagon
β cells Insulin
δ cells Somatostatin
F cells Pancreatic polypeptide
D 1 cells VIP
138
– Endocrine pancreas secretes hormones i.e. insulin, Calcium Absorption

–
glucagon and somatostatin
Decreased by: (AIPG Increased by
– Exocrine panceeas secretes digestive enzymes i.e. 2006)
–
trypsin, chymotrypsin
• Achlorhydria • Protein (also increases Mg
• The self digestion of pancreas is prevented by:
•
•
• Taking drugs that inhibits absorption)
•
– The majority of the enzymes are synthesized as
•
gastric acid secretion • Hypocalcemia
–
•
inactive proenzymes (with the exception of amylase • Pancreatic and biliary • Acidic pH in stomach
•
•

and lipase) non-sufficiency where (AIPG 2012)

ingested calcium remains
– The enzymes are sequestered in membrane bound bound to unabsorbed fatty
–
zymogen granules in the acinar cells acids etc.
– Activation of proenzymes requires conversion of • Phosphates and oxalates
–
•
inactive trypsinogen to active trypsin by duodenal • Alkalis
•
enteropeptidase (enterokinase) • Hypercalcemia
•
– Trypsin inhibitors including serine protease inhibitor
PHYSIOLOGY
–
Kazal type I are present within acinar and ductal Appetite
secretion.
– Pancreatic enzymes require alkaline medium for their Stimulated by Suppressed by
–
activity so bicarbonate secretion will help in their • •
Orexins A and • Serotonin
•
activity. B, b-endorphins, • CART
endocannabinoids
•
• Glucagon
Calcium homeostasis (AIPG 2012) • Agouti related
•
• MSH

•
• Calcitonin is a hypocalcemic hormone. It causes peptide
•
• Corticotropin releasing hormone
•
Hypocalcemia by inhibiting bone resorption by direct • GALP
•
•
action on osteoclasts. It inhibits the osteoclasts and also • Neuropeptide Y
•
increases calcium secretion (calciuric). It is useful in Pagets – acts as a
–
neurotransmitter
Disease, post menopausal osteoporosis, hypocalcemic in brain and
states (hyperparathyroidism), Hypervitaminosis D, ANS.
Osteolytic metastasis. – Secreted by
–
hypothalamus
• Parathormone activates vitamin D which in turn • GnRH
•
•
increases calcium absorption from proximal small
intestine thus it indirectly increases calcium absorption. • Ghrelin is a polypeptide of GI hormone secreted from
•
PTH also promotes reabsorption of of filtered calcium stomach and hypothalamus.
from proximal tubules of kidney – Involved in control of food intake by GH stimulation
–
• Calcium absorption is facilitated by proteins and inhibited activity
•
by phosphates, phytates, oxalates. – Stimulates appetite.
–
• Skin is involved in calcium homeostasis as a source of – Increased by fasting/starvation
–
•
vitamin D3 (cholecalciferol) with the help of UV rays of Also Note
sunlight.
• The salivary and pancreatic α amylase hydrolyze 1:4
The metabolic pathway of Vitamin D
•
αlinkages but space the 1:6 α linkages, 1:4 α linkages next
to branching points
• The maximal rate of glucose absorption from the intestine
•
is about 120g/hr
• Congenital defect in mechanism of transport of

•
neutral amino acids in intestine and renal tubules
---Hartnup’s disease
• Congenital defect in mechanism of transport of basic
•
amino acids in intestine and renal tubules----cystinuria
Physiology 139

• Absorption of protein antigens, particularly bacterial EXCRETORY SYSTEM AND WATER ION
•
and viral proteins takes place in large microfold cells or BALANCE
M cells, specialized intestinal epithelial cells that overlie
Peyer’s pathches. • Normal GFR is 125ml/min or 7.5 l/hour or 180l/day
•
• Lingual lipase is secretes by Ebner’s glands on the dorsal • Net filtration rate is 15 mmHg
•
surface of tongue.
•
• The GFR tends to be maintained when efferent arteriolar
• Histamine stimulate the secretion of HCl by stomach
•
constriction is greater than afferent constriction, but
•
• The caveolin coated pits on the cell membrane are either type of constriction decreases blood flow to the
•
concerned with transport of vitamins into the cells. tubules
• Intrinsic nerve supply of stomach – myenteric nerve • Factors affecting the GFR:
•
plexus (known as Auerbach’s plexus present in between
•
middle circular muscle and outer longitudinal muscle – Changes in the renal blood flow
–
layer) and submucous nerve plexus (Meissner’s plexus, – Changes in glomerular capillary hydrostatic pressure
PHYSIOLOGY
–
situated between muscular layer and submucosal layer) – Changes in systemic blood pressure
–
• In between the body of stomach and pyloric antrum, there – Afferent or efferent arteriolar constriction
–
– Changes in hydrostatic pressure in Bowman’s capsule
•
is an angular notch called the insisura angularis
–
• Accessory pancreatic duct–Duct of Satorini – Ureteral obstruction
–
– Edema of kidney inside tight renal capsule
•
• Wirsung’s duct and common bile duct forms the ampulla –
– Changes in concentration of plasma proteins:
•
of Vater.
–
dehydration, hypoproteinemia
• Trypsin accelerates blood clotting – Changes in Kf
•
–
• Trypsin–endopeptidase–breaks the interior bonds of – Changes in glomerular capillary permeability
•
–
protein molecules – Changes in effective filtration surface area
–
• Carboxypeptidase–exopeptidase–breaks the terminal
• Inulin and creatinine can be used to measure GFR.
•
bonds of protein molecules
•
Requirements of substances used to measure GFR:
• Secretin–first chemical messenger/hormone that was
– Filtered freely
•
demonstrated found by Bayliss and Starling in 1902.
–
– Neither reabsorbed, nor secreted by tubules
–
– Nontoxic
• Functions of cholecystokinin are:
–
– Not metabolized by body
•
– Secretion of pancreatic juice with more amounts of
–
• Proximal convoluted tubule reabsorbs approximately
–
enzymes
•
50 to 60% of water (bulk of water), which is secondary
– Causes contraction of gall bladder (obligatory) to Na+ reabsorption.
–
– Inhibits gastric motility and increases the motility
–
of intestine
– Accelerates the activity of secretin to produce more • Macula densa is a modified region of distal convoluted
•
tubule (DCT) epithelium at the point where afferent
–
alkaline pancreatic juice
arteriole enters glomerulus and efferent arteriole leaves
• APUD cells: Amine precursors uptake and decarboxylase it. This location marks the start of DCT. Macula densa
senses sodium chloride concentration. Rennin secretion
•
• The duodenum becomes jejunum at the ligament of Trietz.
is inversely proportional to the amount of sodium and
•
• Insulin binds with plasma protein, with anti- insulin chloride entering DCT from loop of Henle, where macula
•
activity called synalbumin cells are located.
• Gastric inhibitory peptide alone in very small • Lacis cells also known as extra glomerular mesangial
•
•
concentration can increase insulin secretion therefore it is cells. They are agranular cells, strategically located
known as physiologic GUT factor. between macula densa and juxta glomerular cells at
• Glucose transport across the brain, kidney, tubules, GIT junction between afferent and efferent arterioles. Mediates
•
and RBCs doesnot require insulin. signals between them. Also contain rennin.
140
Reabsorption of Water
Obligatory Reabsorption Facultative Reabsorption
• Absorption of water in proximal tubules secondary to Na+ • Absorption of water in distal tubules and collecting duct in
•
•
reabsorption presence of ADH
• Absorption of water in renal tubules independent of plasma • Absorption of water depends on variation in plasma osmolality
•
•
osmolality (irrespective of water balance) • Normally DCT and collecting ducts are not permeable to water but
•
• Filtered water is reabsorbed iso-osmotically and is in presence of ADH, these segments become permeable.
•
independent of ADH levels
Proximal Tubule Function fructose, amino acids, calcium, uric acid and vitamin C.
 
• “Workhorse of the nephron”. Contains brush border. • Passive reabsorption of urea and water due to the osmotic
•
•
• Iso-osmotic reabsorption of 2/3rds of the glomerular gradient generated by solute reabsorption.
 
•
filtrate. • Active secretion of organic acids (e.g. PAH, diuretics,
PHYSIOLOGY
• Active reabsorption of all of the glucose and amino acids
•
salicylates, penicillins and probenecid) and ammonia
•
and most of the sodium, potassium, glucose, galactose,
 
which acts as a buffer for secreted H+.
 
Loop of Henle:
Thin ascending limb This segment is highly permeable to water
As this segment passes through inner medullary interstitium (which is increasing hypertonic) more water is
reabsorbed
Thin ascending limb Fluid becomes more dilute in this segment because of movement of Na+ and Cl- out of tubular lumen
Thick ascending limb In this segment a carrier transports one Na+, one K+ and 2Cl- from the tubular lumen into the tubular cells.
Renal Autoregulation
• Two mechanisms account for renal autoregulation
•
Myogenic mechanism • An increase in pressure stretches blood vessels and open stretch activated cation channels in smooth
•
muscle cells.
• The macula densa is a specialized group of epithelial cells in the distal tubules that comes in close contact
•
with the afferent and efferent arterioles.
• It contains golgi apparatus directed towards the arterioles, suggesting that these cells may be secreting a
•
substance toward the arterioles.
• This is a negative feedback mechanism that stabilizes renal blood flow and GFR
•
• A large sodium chloride concentration is indicative of an elevated GFR, while low concentration indicates
•
depressed GFR. NaCl is sensed by macula densa by an apical Na-K-2Cl cotransporter.
Tubule glomerular • Feedback from renal tubules to the glomerulus to regulate the GFR in an attempt to ensure constant NaCl
•
feedback delivey to distal tubule. (AIPG 2010)

• The macula densa senses the changes in Na Cl concentration
•
Counter Current Multiplier
• The prime driving force for counter current multiplier is reabsorption of Na+ in thick ascending limb.
•
• Objective: to produce medullary hyperosmolality
•
• It is a mechanism for producing a hyperosmotic renal medulla
•
Good to Know
• The epithelium of the collecting ducts is made up of principal cells (P cells) and intercalated (I) cells
•
• P cells: Involved in sodium reabsorption and ADH stimulated water reabsorption
•
• I cells: Concerned with acid secretion and HCO3- transport
•
• Glomerular capillaries are the only capillaries in the body that drain into arterioles
•
• Glucose transport is inhibited by the plant glucoside phlorhizin, which competes with d-glucose for binding to carrier
•
Physiology 141

• Thin and thick ascending limb of henle, early distal tubules are impermeable to water
•
• More than 50% of potassium that appears in urine is derived from secretion by distal tubule
•
• Osmolality of urine depends on the action of vasopressin in collecting ducts
•
• Reabsorption of glucose is coupled with Na+ reabsorption in GIT also known as Glucose Na+ symport (basis of use of
•
ORS in diarrhea)
Renin Angiotensin System • Juxtaglomerular apparatus: Consists of
•
• Renin is released by the kidneys (juxtaglomerular cells) juxtaglomerular cells (renin secreting smooth muscle
cells in the afferent arteriolar walls), macula densa (Na+
•
upon sensing ↓ BP and cleaves angiotensionogen (from
the liver) to angiotensin I. Angiotensin I is then cleaved sensor, modified distal convoluted tubular epithelium)
by angiotensin converting enzyme (ACE), primarily in the and granulated lacis cells.
 
lung capillaries to angiotensin II. • Glomerular filtration barrier: Responsible for
PHYSIOLOGY
•
filtration of plasma according to size and net charge.
• Composed of
•
– Fenestrated capillary endothelium (size barrier)
–
– Fused basement membrane with heparan sulfate
–
(negative charge barrier)
– Epithelial layer consisting of podocyte foot
–
processes. The charge barrier is lost in nephrotic
 
syn. leading to albuminuria, hypoproteinemia,
generalized edema and hyperplipidemia.
 
(AIIMS Nov 2010, 2012)

• Glomerular filtration rate (GFR): Inulin can be used
• Actions of angiotensin II:
•
 
to calculate GFR because it is freely filtered and neither
•
− Powerful vasoconstrictor reabsorbed nor excreted. Creatinine clearance is an

 
− Release of aldosterone from adrenal cortex approximate measure of GFR. Normal GFR = 120 mL/

− Release of ADH from posterior pituitary min or 180 mL/day. (AIPG 2008)

 

− Stimulates hypothalamus – ↑ thirst. • Effective renal plasma flow (RPF): RPF can be estimated

• Overall angiotensin II serves to ↑ intravascular
•
 
using paraamino hippuric acid (PAH) because it is both
•
volume and ↑ BP. filtered and actively secreted in the proximal tubule. All
• Atrial natriuretic peptide released from atria (in PAH entering the kidney is excreted. RPF = 660 ml/min.
•
response to ↑ atrial pressure) may act as a ‘check’ on the Approximately 120 ml/min of the 660 ml/min is filtered
renin- angiotensin system (eg, in heart failure). ↓ renin at the glomerulus as ultrafiltrate, 65% is reabsorbed in
 
and ↑ GFR. the proximal tubule. Average urine output = 1.2 ml/
min, i.e. only 1% of 120 ml/min of ultrafiltrate filtered at
Endocrine Function of the Kidney glomerulus
• Synthesis of erythropoetin by endothelial cells of • Filtration fraction: GFR/RPF i.e., the fraction of RPF
•
peritubular capillaries under stimulus of hypoxia and
•
filtered across the glomerular capillaries. Normally
anaemia. about 0.2.
 
• Conversion of 25-OH vitamin D to • Glucose clearance :Glucose at a normal plasma level
•
1,25-dihydroxycholecalciferol (vitamin D) by
•
is completely reabsorbed in the proximal tubule. At
1-a-hydroxylase which is activated by parathormone. plasma glucose of 200 mg/dL, glucosuria begins
 
• Juxtaglomerular cells secrete renin in response to ↓ renal (threshold).
•
arterial pressure and ↑ renal sympathetic discharge. • There are approximately 1.3 million nephrons in each
•
• Secretion of prostaglandins that vasodilate the afferent human kidney.
•
arterioles to ↑ GFR.
142
• The epithelium of the collecting ducts is made up of Mechanism Activated by Heat (AIPG 2012)

•
principal cells (P cells) that respond to vasopressin
Increased heat loss Decreased heat production
and intercalated (I cells) that secrete acid.
• Cutaneous vasodilation • Anorexia, decreased
 
• The total length of nephrons including the collecting
•

•
(AIPG 2005) appetite
•

ducts ranges from 45-65 mm. • Sweating • Apathy and inertia
•
•
• Glomerular capillaries are the only capillaries in the • Increase respiration
•
•
body that drain into arterioles. Mechanism activated by cold
• In humans the total surface area of the renal capillaries
Decreased heat loss Increased heat production
•
is equal to the surface area of tubules, both being about
12 sq.m. • Cutaneous • Shivering
•
•
vasoconstriction
 
• Hunger
• The volume of blood in the renal capillaries at any given

(AIIMS May 2008)
•
• Increased voluntary activity
•

time is 30-40 ml. – By a reflex – in
•
• Increased secretion of
–
• Glomerular filtrate is an ultrafiltrate of plasma and of sympathetic output
•
PHYSIOLOGY
norepinephrine/epinephrine
– By a local direct action
•
identical composition except for a few proteins.
–
– Local direct action
–
• The renal function with which oxygen consumption increases the activity
•
correlates best is the rate of active transport of sodium. of the adrenergic
neurotransmitter NE
Renal Threshold • •
Piloerection
• Curling up
• Plasma level of glucose at which glucose first appears in
•
•
Urine is 80 mg% (venous) or 200 mg% (arterial) blood
glucose ENDOCRINE SYSTEM
• Transport Maximum of glucose (TMG) – 360 mg/min
• Endocrine glands (ductless glands) (AIPG 2012)
•
(Splay Phenomena is seen)
•

– Hypothalamus
• In renal glycosuria renal threshold for glucose is low
–
– Anterior pituitary
•
–
• Urea has no Tm (tubular maximum) value – Posterior pituitary (neurohypophysis)
•
–
• Maximum urine acidity 0.03, normal urinary pH = 5.85, – Islet of Langerhans in pancreas
–
– Adrenal cortex
•
specific gravity 1.015 – 1.025
–
– Adrenal medulla
• Daily loss of N2 in urine – 20 – 50gm
–
– Thyroid
•
–
– Parathyroid
Regulation of Organic Metabolism
–
– Kidney
–
• Osmolarity –is the number of osmoles per litre of – Ovary and testis
–
•
solution. Changes with temperature and pressure of • Pineal gland contains high amounts of serotonin,
other solutes
•
norepinephrine and melatonin. It also secretes some
• Osmolality – is the number of moles per kg of solvent. substance which may cause schizophrenia
•
Doesn’t change with temperature • Cushing’s disease: Due to pituitary cause
Tonicity – is the osmolality of a solution relative to
•
• • Cushing’s syndrome: Due to adrenal cause
•
plasma.
•
• Thyroxine binding globulin (TBG) increases in estrogen
• Osmolality of plasma is 280-290 mosm/l
•
treated patients, during pregnancy and some drugs.
•
• Contribution to osmolality of plasma
– Decreased by glucocorticoids, androgens, the weak
•
– Na+ and its associated anions which is 270 mosm/l
–
androgen damazol and L-asparaginase
–
– maximum
– Glucose 5mosm/l • Frolich’s syndrome (dystrophia adiposgenitalis) is due
•
to hyposecretion of both anterior and posterior pituitary
–
– Urea: 5mosm/l
hormones
–
– Proteins: 2mosm/l
–
– Potassium ions are intracellular – so no effect • Aldosterone: Llive saving hormone
–
•
• Colloidal osmotic pressure of plasma is also known as • Cortisol: Live protecting hormone
•
oncotic pressure and is mainly due to plasma proteins
•
• Thymopoietin: Inhibits Ach release, so hyperactivity of
especially albumin.
•
thymus causes myasthenia gravis
Physiology 143

Effects of Insulin on Various Tissues
On Adipose tissue • Increased glucose entry
•
• Increased fatty acid synthesis
•
••
Increased glycerol phosphate synthesis
• Increased triglyceride deposition
•
• Action of lipoprotein lipase
•
• Inhibition of hormone sensitive lipase
•
• Increased K+ uptake
•
On muscles • Increased glucose entry
•
• Increased glycogen synthesis
•
• Increased amino acid uptake
•
• Increased protein synthesis in ribosomes
•
• Decreased protein catabolism
•
PHYSIOLOGY
• Decreased release of gluconeogenic amino acid
•
• Increased ketone uptake
•
• Increased K+ uptake
•
On liver • Decreased ketogenesis
•
• Increased protein synthesis
•
• Increased lipid synthesis
•
• Decreased glucose output due to decreased gluconeogenesis (inhibits pyruvate carboxylase), increased
•
glycogen synthesis and increased glycolysis
In general • Increases cell growth
•
Pituitary Gland
Adenohypophysis (anterior pituitary) Neurohypophysis (posterior pituitary)
• Develops as an upward growth called Rathke’s • Develops a downward growth from the floor of diencephalon and connected to
•
•
pouch from ectodermal roof of the stomodeum hypothalamus by neural pathways
• Hormones secreted from anterior pituitary • Hormones secreted are:
•
•
– TSH – Oxytocin
–
–
– ACTH – vasopressin (ADH)
–
–
– FSH
–
– LH
–
– Prolactin
–
– Growth hormone
–
Also Note
• Oxytocin and vasopressin is synthesized in supraoptic and paraventricular nuclei of hypothalamus
•
• Melanocyte stimulating hormone (MSH) is secreted by intermediate pituitary gland. However, intermediate lobe is
•
rudimentary in humans and it appears that MSH is not secreted in adults.
• Tumours of somatotrophes of the anterior pituitary secrete large amount of growth hormone, leading in children to
•
gigantism and in adults to acromegaly. Hypersecretion of GH is accompanied by hypersecretion of prolactin in 20 to 40%
of patient with acromegaly.
• Somatomedin are polypeptide growth factors secreted by liver and other tissues. The effect of growth hormone on growth,
•
cartilage and protein metabolism depend on interaction between GH and somatomedin.
• Lorain dwarfism: The secretion of growth hormones is normal or high. But there is deficiency of somatomedin.
•
• Simmond’s disease: Pituitary cachexia –due to hyposecretion of all anterior pituitary hormones – characterized by
•
developing senile decay
• Increased GH and decreased somatomedin levels are seen in Kwashiokar
•
• Increased growth hormone during adolescence – Gigantism
•
• Increased growth hormone after epiphyseal fusion results in Acromegaly
•
144
Adrenal Cortex
• Adrenal cortex secretes 3 major steroids
•
• Glucocorticoids: From Zona Glomerulosa
•
• Mineralocorticoids: From Zona Fasciculata
•
• Sex Steroids (androgens): From zona Reticulata
•
Glucocorticoids • Cortisol (hydrocortisone) is the major glucocorticoid in humans
•
• Receptors are present predominantly in the cytoplasm. Inactive receptor binds with heat shock protein 90
•
Mineralocorti- • Aldosterone is the main mineralocorticoid
•
coids • Receptors are expressed principally in the kidney (DCT and collecting ducts of nephron) also in colon, salivary
•
glands, sweat glands, and hippocampus
• Mineralocorticoids receptors are not expressed in liver.
•
• Aldosterone regulates sodium and potassium homeostasis. It acts on the principal cells of DCT and collecting duct
PHYSIOLOGY
•
• It enhances the reabsorption of sodium ions and urinary excretion of K+ and H+.
•
• Causes diastolic hypertension without the accompanying edema
•
ADH
• ADH secretion is stimulated by either an increase in ECF osmolarity or decrease in effective blood volume. However ADH
•
secretion is considered more sensitive to small changes in osmolarity than to similar changes in blood volume.
• For example, 1% increase in osmolarity or 10% decrease in blood volume is required to increase ADH levels.
•
Factors causing increased ADH secretion Factors causing decreased ADH secretion
• Hyperosmolarity • Hypo-osmolarity
•
•
• Hypovolumia • Hypervolumia
•
•
• Hypotension • Hypertension
•
•
• Nausea (100 times increase in ADH) • Drugs–alcohol, clonidine, haloperidol
•
•
• Hypoxia
•
• Drugs – Morphine, nicotine, cyclophosphamide
•
Hormones
I. Hormones that bind to II. Hormones that bind to cell surface receptors
intracellular receptors
Androgens, Calcitriol (1,25 a. The Second Messenger Is cAMP:

[OH] 2-D3, Estrogens, 2-Adrenergic Catecholamines, b-Adrenergic Catecholamines, ACTH, ADH, Calcitonin, Parathyroid

Glucocorticoids, Hormone, Human Chorionic gonadotropin, Corticotropin-relasing hormone, FSH, LH, Glucagon,
Mineralocorticoids, Lipotropin, MSH, TSH, Somatostatin
Progestins, Retinoic acid,
Thyroid hormones (T3 and b. The second messenger is cGMP:

T4) Atrial natriuretic factor, nitric oxide

c. The second messenger is calcium or phosphatidyl inositols (or both):

Acetylcholine (muscarinic), a1- Adrenergic catecholamines, Angiotensin II, Antidiuretic hormone

(vasopressin),Cholecystokinin, Gastrin, Gonadotropin-releasing hormone, Oxytocin, Platelet-derived
growth factor, Substance P, Thyrotropin-releasing hormone
d. The second messenger is a kinase or phosphatase cascade:

Chorionic somatomammotropin, Epidermal growth factor, Erythropoietin, fibroblast growth factor, Growth

hormone, Insulin, Insulin-like growth factors I and II, Nerve growth factor, Platelet-derived growth factor
Physiology 145

Hormones
Organ Product secreted Site of action Biological effects
• Brain Oxytocin Ulterus Contraction of the uterus.

•
– Neurosecretory Myoepithelial cells of – To facilitate the assent of spermatozoa
–
mammany gland – Delivery of the fetus, ejection of milk
–
cells of
–
hypothalamus
Vasopressin or anti- Kidney Increase absorption of water

Diuretic hormone (ADH)
Release factors Anterior pituitary Stimulate or inhibit the secretion of anterior pituitary
hormones
PHYSIOLOGY
– Neurons Neurotransmitters Neuron synapses Transmission of nerve impulse
–
Acetylcholine Serotonin, Neuromuscular
GABA Adrenaline Junctions
Noradrenaline
Dopamine etc.
– Pineal body Melatonin (synthesis and Gonads Darkening of skin

–
secretion promoted by
darkness and inhibited
by light)
• Pituitary Growth hormone or Almost all organs of the body Growth of bones, cartilage, muscles and viscera;
•
– Anterior lobe somatotropic hormone promotes synthesis of proteins in tissues, influences
(STH) carbohydrate and fat metabolism; mobilized body
–
mechanisms in situations of nutritional scarcity.
ACTH Adrenal Synthesis and secretion of adrenal hormones,

Adipose tissue mobilization of fats
TSH Thyroid Synthesis and secretion of thyroid hormones
Gonadotrophins Ovaries in females Testes in Development of follicles, ovulation: secretion of

FSH, LH males estrogens and progesterone spermatogenesis,
development and function of testis, secretion of
testosterone.
Prolactin Mammary glands Development of mammary glands in combination

with other hormones, estrogens, progesterone,
STH, adrenal corticoids, lactation
• Thyroid Triiodothyronine (T3) Several organs Increase in basal metabolic rate and in
•
consumption of oxygen by cells; growth promotion
and development. About 4 times less potent than
T4.
Thyroxine (T4) Several organs Increase in basal metabolic rate and in

consumption of oxyzen by cells; growth promotion
and development.
Calcitonin - Lower the level of calcium in blood (AIPG 2005)

• Parathyroid Parathyroid hormone Bones Mobilizes calcium from bones to raise serum levels
•
Kidney of calcium; increases excretion of phosphate.
146
Hormones
• Thymus Partially from bone Stem cells Development of precursor cells to lymphocytes
•
characterized marrow eventually competent for cell-mediated (T-cell) and
– Humoral having role in production of antibodies (B-cell).
–
factors
• Pancreas Insulin Muscles, liver, Reduces blood glucose levels by promoting its
•
adipose tissue uptake by peripheral cells; increases utilization of
and many other carbohydrates; increases deposition of glycogen,
organs stimulates lipogenesis; anabolic effects on protein
synthesis
Glucagon Liver, adipose tissue Hyperglycaemic factor mobilizes liver glycogen

stores to replenish blood glucose level. Enhances
conversion of amino acids to carbohydrate.
PHYSIOLOGY
• Adrenal cortex Glucocorticoids Several organs Retention of sodium and excretion of potassium;
•
Principal member maintenance of extracelluar volume; cardiovascular
(Hydrocortisone) function; adaptation to stress (trauma, cold,
mineral corticoids heat , toxins, infections, fasting, forced exercise,
(adosterone) etc.), immunosuppressive action, promotion of
androgens gluconegenesis, anti-inflamamatory action.
• Adrenal Epinephrine Heart muscles, Increase the heart rate, raise systolic blood
•
– Medulla Norepinephrine liver and other pressure; mobilize glucose
–

Dopamine Organs From liver and muscles: anxiety
• Ovaries Estrogens Female reproductive organs Promotes growth of uterus, mammary glands an
•
and secondary sex organs, vaginal epithelium; feedback effect on secretion of
uterus, vagina, mammary gonadotrophins, influences behaviour and psychic
glands, pituitary, brain patterns.
Progesterone -do- Acts synergistically and in some cases

antagonistically to estrogens; preparation of
the uterus for implantation of the blastocyst;
maintenance of pregnancy; regulation of the
accessory organs.
• Testis Androgens Male reproductive and Sprematogenesis, seminal plasma secretions, hair
•
accessory organs, muscles patterns, skeletal configuration, voice changes;
regulation of sebaceous gland activity; general
anabolic hormone stimulates protein synthesis.
• Stomach Gasterin Gastric glands Stimulation of gastric secretions.

•
• Duodenum Secretin Pancreas Stimulates the secretion of pancreatic fluids.
•
• Intestines Cholecystokinin Gall bladder Release of bile
•
Pancreozymin Pancreas, stomach
Enterogastrone
• Kidney Erythropoetin Haematopoietic Stimulation of the formation of blood cells,

•
Renin, angiotensin Organs, vasoconstriction, elevation of blood pressure,
Cardiovascular increased cardiac output, autonomous system.
system, adrenals, kidney
Physiology 147

Hormones of the Gastrointestinal Tract
Hormone Source Chemistry Physiological Action

stimulus of release
• Gastrins Antral mucosa Polypeptides Protein breakdown Gastric acid, pepsins and intrinsic factor
•
and duodenal consisting o G14, products, distensin stimulation. Increases growth of gastric
bulb G17, G34 and a big of stomach, vagal mucosa.
gastrin with 45 amino stimulation, calcium, Stimulation of gastric motility. Closure of
acid residue ( in both Epinephrine gastroesophageal junction. Stimulates
sulfated and non- glucagons secretion.
sulfated forms)
• Cholecystokinin Mucosa of the Polypeptides with Secreting, products Secretion of enzyme rich pancreatic juice.
•
pancreozymin upper small 39 amino acids. Also of protein digestion, Trophic action on pancreas. Contraction
(CCK-PZ or intestine and present in various soaps and fats of gall bladder. Relaxation of sphincter
CCK) nerves of the froms (structure of Oddi. Inhibits gastric emptying and
PHYSIOLOGY
distal part of resembles gastrins) prevents regurgitation of duodenal contents
lieum and colon into the stomach. Stimulates glucagons
secretion.
• Secretin Cells present Linear polypeptide Acid chime in Copious bicarbonate rich pancreatic
•
in the deep structure similar to duodenum, vagal juice secretion. Increase bile secretion
seated glands glucagons, glicentin stimulation products (choleretics), decreases gastric acid
from the upper (GLI) VIP, GIP or protein digestion secretion. Causes contraction of pyloric,
intestine sphincter. Augments cholecystokinin action.
• Somatostatin Gastrointestinal 14 amino acid residue - Inhibits gastric secretion

•
mucosa with disulphide bridge
• VIP (Vasoactive Gland cells and 28 amino acid residue Fats and fatty acids Stimulates intestinal secretion of water and
•
intestinal peptide) nerves of the GI electrolytes, inhibits gastric acid secretion,
tract potentiates the action of acetylcholine on
salivary glands.
• Enterogastrone -do- -do- Inhibition of gastric secretion

•
• Substance Endocrine cells 11 amino acid residue - Stimulates intestinal motility
•
of the GI tract
• Motilin Duodenal 22 amino acid residue - Stimulates gastric acid secretion

•
mucosa
• Glucagon ‘A’ cells of the 29 amino acid residue - Plays a role in hyperglycaemla of diabates
•
(Intestinal mucosa of Functions in GIT are not known
glucagons) stomach and
duodenum
• Glicantin -do- Larger molecule than Acid chyme in the Exact mode of action in GIT is not known.
•
(Glucagon like Glucagon intestine
immunoreactivity)
GLI)
• Villikinin Mechanical Movements of the villi

•
distension of small
intestine, presence
of food
• Enterocrinin Increases secretion of sulcus entericus.

•
148
Hormones Which Bring about Physiological Responses by Increasing Cyclic AMP Formation
Hormone Tissue Principal responses
Adrenaline Liver Glycogenolysis
(Beta receptor) Muscle Glycogenolysis
Fat Lipolysis
Cardiac muscle Positive inotropism
Smooth muscle Relaxation
Parotid gland Amylase release
Pancreas Insulin release
Noradrenaline Brain Facilitation of neuromuscular transmission
(Beta receptors) Cerebellum Discharge frequency of purkinje cells
Pineal Melatonin synthesis
Histamine Cardiac muscles Positive inotropism
Gastric mucosa HCI secretion
PHYSIOLOGY
Glucagon Liver Glycogenolysis

Fat Lipolysis
Pancreas Insulin release
Adrenocorticotropic hormone Adrenal Steroidogenesis

cortex
Lutenizing hormone Ovary Steroidogenesis

(LH, ICSH) Corpus Steroidogenesis
Fat Lipolysis
Thyroid stimulating hormone Thyroid Thyroglobulin hydrolysis, iodination, glucose oxidation
Parathyroid hormone Renal cortex Phosphaturia,

Bone Calcium resorption
Vasopressin Renal-medulla Water reaabsorption
Some Important Points

• Pre optic nucleus is sexullay dimorphic nucleus, contains more neurons in males
•
• Thermoregulatory centre I situated in the pre optic area in anterior hypothalamus near the wall of the third ventricle
•
• Anti drop effect of temperature regulation is mediated by serotonin
•
• Injection of hypertonic saline in supra optic nucleus–intense thirst
•
• Injection of hypotonic saline in supra optic nucleus results in–diuresis
•
T3 Vs T4
• T3 is more active, more potent and has maximum affinity for albumin
•
• T4 is inactive and more tightly bound to plasma protein (T4 is the major circulating thyroid hormone)
•
• MIT + T3 → T4 (in periphery)→T3 (active form)
•
Somatomedins
• Polypeptide growth factors secreted by liver and other tissues
•
• Somatomedin C is also known as IGF – I mainly involved in skeletal and cartilage growth. It mediates chondroitin sulfate
•
deposition.
• MSA of IGF – II is mainly involved in growth during fetal development
•
• Hormones in stress
•
• Secretion of stress hormones increased --- Epinephrine, Norepinephrine, cortisol, glucagon
•
Physiology 149

• Decreased secretion of anabolic hormones --- Insulin, testosterone
•
• Stress induced hypoglycemia is mediated by – epinephrine, cortisol, glucagon (by stimulation of gluconeogenesis)
•
• Increased lipolysis
•
• Mild hemorrhage leads to – increased ACTH, increased aldosterone, increased sympathetic activity, increased TPR,
•
increased venoconstriction
REPRODUCTIVE SYSTEM
• Spermatids are attacked by Gossypol, a phenolic compound (cotton seed oil) that inhibits the lactate dehydrogenase found
•
in sperms and may prove to be of value as a male contraceptive.
• Progesterone antagonist, such as Mifepristone is helpful in producing abortion following conception. It acts by inhibiting
•
the progestational effects on uterus.
PHYSIOLOGY
Estrogen
• Estrogen induced growth requires continuous replenishment of energy, predominantly generated by glycolysis. Estrogen
•
induced changes in glycolysis appeared to be mediated via its regulation of GLUT 1 expression and glycolytic enzyme
induction.
• Estrogen is also shown to modulate insulin sensitivity possibly by altering insulin related gene expression.
•
• Ay physiological levels, testosterone and estradiol are thought to be involved in maintaining normal insulin sensitivity.
•
However outside this ‘physiological window’ these steroids may promote insulin resistance.
• Estradiol promotes the energetic capacity of mitochondria by maximizing aerobic glycolysis.
•
• Alterations in the composition of the plasma lipids caused by estrogens are characterized by an increase in the high
•
density lipoproteins, a slight reduction in the low density lipoproteins and a reduction in plasma cholesterol levels.
• Once ejaculated into the female, the spermatozoa move up the uterus to the isthmus of the uterine tubes, where they slow
•
down and capacitation.
• Capacitation involves the destabilization of the sperm head membrane rendering it more fusigenic. This change is facilitated
•
by the removal of sterols (eg cholesterol) and non covalently bound epididymal/seminal glycoproteins. The result is a more
fluid membrane with an increased permeability to Ca2+.
Action of Luteinizing Hormone

• Stimulates ovulation
•
• Formation and maintenance of corpus luteum
•
• Formation of progesterone in the corpus luteum from the lutein cells.
•
Fate of Corpus Luteum after Ovulation
• Fertilization occurs:
•
– Corpus luteum stays (maintained by LH) and produce hormones
–
– By 8th week, placenta grows sufficiently and starts producing hormones,
–
– So corpus luteum regresses
–
• No fertilization occurs:
•
– Corpus luteum begins to degenerate about 4 days before the next menses (24th day of cycle) and eventually replaced
–
by scar tissue.
150
MISCELLANEOUS
Decompression Sickness
– Also known as Caisson’s disease, Bends, Diver’s paralysis, dysbarism
–
– Form of gas embolism due to sudden lowering of atmospheric pressure
–
– Seen in deep sea divers, rapid ascent of scuba, unpressurized aircraft in rapid ascent
–
– Gas bubble within skeletal system is responsible for bends
–
– Chokes occur in lungs
–
• Changes seen in acclimatization to high altitudes (AIPG 2010)
•

– 10,000 feet above sea level is considered as high altitude. At these altitudes, barometric pressure decreases and there
–
is decrease in pO2 and decrease in pN2 while pCO2 and pH2O remains constant.
– Increase in 2,3 DPG of RBCs: Decreased affinity for oxygen
–
– Erythropoietin secretion: Polycythemia vera (increased RBC volume)
PHYSIOLOGY
–
– Increased number of mitochondria and tissue content of cytochrome oxidase, increased pulmonary ventilation
–
– Increase in myoglobin
–
– Barrel shaped chest
–
– Alkaline urine production
–
• Changes in athletes
•
– Maintains high cardiac output at lower heart rate
–
– Greater end systolic ventricular volume
–
– Greater stroke volume at rest
–
Changes during supine to prone position Changes during standing to supine
• Significant volume of blood pools in lower limbs due to high • Immediate increase in venous return (AIPG 2008)
•
•

compliance of lower limb veins this venous return decrease
• Decrease in venous return – decreases stroke volume and
•
cardiac output
Changes during Moderate Exercise (AIPG 2007, NEET 2013)

Cardiac output Quiet standing Exercise
5900 m/min 24000ml/min
Blood flow to
Heart 250 ml/min 1000 ml/min
Brain 750 ml/min 750 ml/min
Active skeletal muscle 650 ml/min 20850 ml/min
Inactive skeletal muscle 650 ml/min 300 ml/min
Skin 500 ml/min 500 ml/min
Kidney, liver, GIT etc 3100 ml/min 600 ml/min
Good to Know
• Microtubule assembly is prevented by colchicines and vinblastine. The anticancer drug paclitaxel (taxol) binds to
•
microtubules and makes them so stable that organelles cannot move. Mitotic spindle cannot form and cells die.
• X linked charcot-Marie–Tooth disease is a peripheral neuropathy associated with mutation of one particular connexin
•
(subunit of gap junction) gene.
• Bell–Magendie law–in the spinal cord the dorsal roots are sensory and ventral roots are motor
•
Physiology 151

• The prefrontal lobe forms a closed circuit connection with • Triple response of Lewis
•
thalamus known as Papez circuit–responsible for resting
•
– Develops when skin is stroked firmly
EEG and plays an important role in control and genesis of
–
– Mediated primarily by histamine
emotions. (AIIMS May 2010)
–
– There is

–
• The retinal vessels supply the bipolar and ganglion Red reaction: Flare - Wheal

•
cells, but the receptors are nourished for the most part, Red reaction is due to histamine mediated

by the capillary plexus in the choroid. This is why retinal relaxation of precapillary sphincters
detachment is so damaging to the receptor cells. Flare reaction (Flush): Axon reflex – is due to

• Receptors in the semicircular canals detect rotational substance P mediated arteriolar dilatation
•
acceleration, Wheal ( skin edema) is due to histamine

– Receptors in utricle: Linear acceleration in mediated increased capillary permeability
–
horizontal direction
– Receptors in saccule: Linear acceleration in vertical • Immune complexes are removed from blood by Kupffer’s
–
direction
•
PHYSIOLOGY
cell
• Ear: The processes of hair cells project into the
• Histiocytes are RE cells that help in phagocytosis. Fixed
•
endolymph whereas the bases are bathed in perilymph.
•
This arrangement is necessary for normal production of histiocytes are called as tissue macrophages while the free
generator potential histiocytes are called as wandering RE cells
• Endocrine glands that are not influenced by the pituitary
• Damage to the lateral corticospinal tract in humans
•
gland include the adrenal medulla, parathyroids and islets
•
produces the Babinski’s sign–dorsiflexion of the great toe of langerhans
and fanning of other toes when the lateral aspect of sole of
foot is scratched. • The cell bodies of the principal histaminergic neurons in
•
• The lewy bodies are inclusion bodies in neurons that the brain are located in the mediobasal hypothalamus
•
occur in all forms of Parkinson’s disease. Two proteins, • Perception of disgust appears to depend on the insular
α-synuclein and barkin, interact and are found in lewy
•
cortex on left side.
bodies
• Lesions of parietal lobe: The representational
• Brown fat, a special form of body fat that has extensive
•
hemisphere: unilateral inattention and neglect
•
sympathetic innervations may contribute to regulation of
body weights. • Loss of cholinergic neurons in the nucleus basalis of
•
• New neurons can form from stem cells throughout life in Meynert and related areas of forebrain – loss of recent
memory
•
two areas: the olfactory bulb and hippocampus
• Cytochrome: Directly involved in the regulation of • Lesions of mamillary bodies: Loss of recent memory
•
• The hippocampus is currently credited with being
•
apoptosis (AIPG 2007)
•
the area of the brain in which short term memory

• Types of Dichromatism is converted into long term memory. Long term
•
– Protanopia: No red, only green and blue potentiation has been used as cellular model responsible
for long term memory in hippocampus. (AIPG 2010)
–
– Deuteranopia: No green, only red and blue

–
– Tritanopia: No blue, only red and green • Hippocampus is not the site where long term memory is
•
(AIIMS May 2010)
–
• Ishihara’s chart is used to test colour blindness stored it is stored in neocortex.

•
• Chromatolysis is disappearance of Nissle granules
• The coupling of monoiodotyrosine and DIT and
•
•
• Aphasia: Loss of speech iodination of thyroglobulin is blocked by thiourylenes
such as methimazole. These cause an increase in thyroid
•
• Dysarthria: Difficulty in articulation of speech size and decrease in plasma T4.
•
• Agnosia: Inability to understand the words or recognize • Thyroid hormone bind to DNA in form of heterodimer
•
a subject
•
with retinoid receptor.
• The signs and symptom which occur after hemisection • Ionophores are transmembrane proteins that control
•
•
of the spinal cord constitute Brown – Sequard Syndrome. transport of ions across the biological membrane
Crude touch, temperature and pain sensations are not • One of the major functional differences between the
•
affected on the opposite side. female and male sex chromosome is that the male
• The biological anticoagulant is hirudine chromosome has the SRY (sex determining region ‘Y’)
•
152
gene that encodes a protein called the testis determining • Hyperalgesia: Perception of mild pain as exaggerated
•
factor (also k/a SRY protein) (AIPG 2010) • Pallesthesia: Ability to feel mechanical vibrations

•
• Spirometry do not measure --- FRC, TLC, RV (through pacinian corpuscles/ touch receptors)
•
• Stereogenesis: Ability to perceive shape and size form and
• NOT seen in sympathetic stimulation – Increased
•
nature of a object
•
refractory period
– Ability to perceive shape and size is lost (asterogenesis)
• Collagen – is NOT present freely inside the cytoplasm
–
different to lesion of tractus cuneatus
•
• Iron absorption is NOT decreased by Vit. C – In Pavlov’s classical experiment salivation by dog
•
–
• NOT true in exercise – shifting of oxygen dissociation on seeing food is an innate reflex (unconditioned).
•
curve to the left And salivation by dog on ringing the bell is only
• Hematocrit – Value not changes with age conditioned reflex
•
• ABO antigens are NOT found in --- CSF • Blood Nerve barrier is formed by–Perineurium cells
•
•
• Calcitonin --- is NOT required for GI absorption of • Blood Brain barrier is formed by–Foot processes of
PHYSIOLOGY
•
•
calcium astrocytes
• Factor which is NOT responsible for venous return • Blood Testes barrier is formed by–Sertoli cells
•
•
during standing --- Arterial pulsation
• NOT an effect of insulin --- Gluconeogenesis
Green house effect/global warming
•
• NOT seen in Emphysema --- Increased FEV1 and
• It is because of the emission of greenhouse gases (CO most
•
decreased RV
•
common, Ozone, chloro-flourocarbons, Halons, methane
• NOT required for GI absorption of calcium - calcitonin and N2O) into the atmosphere
•
• Responsible for increase in average global surface
Disorders of Perception
•
temperature
• Allodynia: Perception of Non–painful stimulus (eg: • Not seen with N2
•
•
touch) as painful • Stratosphere of ozone protects from harmful UV rays
•
CHAPTER 4
General Pathology
Objectives
• General pathology • Immunology and genetics

• Wound healing and repair • Pathology of blood cells

• Inflammation • Cardiovascular pathology

• Fluid and hemodynamic pathology • Transfusion disorders

• Thrombosis, embolism, infarction and aneurysm • Respiratory pathology

• Neoplasia • Environmental pathology

• Various disorders and their important features • Miscellaneous
• Pathological deposits

GENERAL PATHOLOGY
• Adaptation: Is the cell’s response to prolonged stress
 
• Cell injury: Reversible (hydropic change) or irreversible (necrosis)
• Cell death: Necrosis (due to irreversible injury) and apoptosis (programmed cell death).
General Mechanisms of Cell Injury

• Oxygen derived free radicals.
• Increased intracellular calcium
• ATP depletion
• Defects in membrane permeability
Changes seen in both reversible and irrevers- Changes seen only in irreversible cell injury
ible cell injury(AIPG 2005)
• Cellular swelling • Cell membrane rupture, lysosomal rupture
•
•
• Mitochondrial swelling • Nuclear changes – pyknosis (nuclear condensation), karyolysis (loss of nuclear
•
•
• Dilatation and degranulation of RER chromatin, karyorrhexis (nuclear fragmentation). (AIPG 2007))

•
• Autophagocytsosis • Amorphous densities in mitochondria
•
 
•
• Ca2+ influx capase activation
•
154
Degeneration
• Reaction of cells to injury and represents retrograde change caused by a disturbance in cell metabolism.
• Degeneration is reversible cell injury while cell death is a state of irreversible cell disorganization.
• Seven types of degeneration are present
– Fatty – Albuminous
–
– Atheromatous, – Hyaline,
–
– Mucinous, – Calcerous
–
– Zenker.
–
Fibrinoid degeneration • Tissue accumulates deposits of acidophilic homogoneous material resembling fibrin.
GENERAL PATHOLOGY
•
• Seen in immunopathologic tissue injury, e.g., Autoimmune diseases, immune complex vasculitiis, Arthus
•
reaction.
Cloudy swelling • Most common degeneration (albuminous, hydropic).
•
• Reversible.
•
• Most common sites for cloudy swelling are kidneys, liver and myocardium
•
Hyaline degeneration • Non-specific degeneration mainly affecting the collagenous connective tissue and fibrous tissue is hyaline
•
degeneration.
Intracellular hyaline • Mallory stain is used in case of hyaline degeneration. Mallory’s hyaline seen in alcoholic liver cell injury.
•
degeneration
• Hyaline degeneration in voluntary muscle is called as Zenker degeneration.
•
• Zenker degeneration is seen in typhoid fever specifically in striated muscle.
•
• Russel bodies – Excess immunoglobulins in plasma cells
•
Extracellular hyaline • Hyalinised old scar, hyaline arteriosclerosis and hyalinised glomeruli
•
degeneration
Mucinous degeneration • Excessive production of mucus
•
• Two types
•
– Epithelial
–
– Mesenchymal
–
Fatty degeneration • Cholesterol crystals are seen in cells undergoing autolysis in lipoid degeneration.
•
Necrosis
Types of Necrosis
Coagulation • Most common type of necrosis.
•
necrosis
• Conversion of normal cells into their tombstones is hallmark of coagulative necrosis.
•
• General architecture is preserved except for some nuclear change.
•
• Most common results from interruption of blood supply, commonly seen in the end organs.
•
• E.g.: Infarct of heart, kidney and spleen etc
•
Liquefaction • Also known as colliquative necrosis.
•
necrosis
• There is enzymatic digestion of the tissue.
•
• Architecture is lost. Necrotic tissue is soft and liquefied.
•
• Tissue is softened/liquefied due to enzyme action (autolysis and heterolysis)
•
General Pathology 155

• It is commonly seen in CNS resulting from interruption of blood supply. It also occurs in area of bacterial infection.
•
• Seen in brain, abscesses
•
Caseous necro- • Induced by cell mediated immunity (T lymphocytes, macrophages, cytokines)
•
sis • Tissue appears cheesy; histologically consists of granular material surrounded by epithelioid cells and
•
multinucleated giant cells
• Seen in tuberculosis, fungal granulomas

•
Fat necrosis • Necrosis in adipose tissue induced by lipases (derived from injured pancreatic cells in acute pancreatitis) or
•
trauma to adipose tissue (breast trauma)
Fibrinoid necro- • Free fatty acids bind with calcium to form calcium soaps.
GENERAL PATHOLOGY
•
sis
• Typically seen in arteries, arterioles or glomerular capillaries damaged by autoimmune diseases
•
• Blood vessels are impregnated by fibrin and other serum proteins and appear magenta-red on histology
•
Gangrenous ne- • A clinical term for ischemic necrosis accompanied by bacterial infection, which leads to partial liquefaction of
•
crosis tissues.
• ‘Dry gangrene’ (mummification) refers to noninfected ischemic necrosis accompanied by drying of the tissues.
•
Apoptosis
Programmed cell death (NEET 2013, AIPG 2012)
• Mitochondria plays a central role-Increased mitochondrial outer-membrane permeability is the major trigger of the
•
 
intrinsic apoptosis pathway.
Morphological • Cell shrinkage
Changes
•
• Chromatin condensation
•
• Formation of cytoplasmic blebs and apoptotic bodie
•
• Phagocytosis of apoptotic cells or bodies
•
Biochemical • Protein cleavage
Feature
•
• DNA breakdown
•
• Phagocytic recognition
•
Pro-apoptotic • Bak, Bim, Bax
molecules
•
Anti-apoptotic • Bcl-2, Bcl-x (AIPG 2004)
molecules
•

Examples of • During embryogenesis (programmed destruction of cells)
Apoptosis
•
• Endometrium, prostate in adults (hormone dependent involution of tissues)
•
• Cell deletion in multiplying cell populations (intestinal crypt epithelium), tumours and lymphoid organs.
•
• Cell death by cytotoxic T cells, cell injury in certain viral diseases, atrophy in organs after duct obstruction.
•
Functions of • Elimination of cells in embryological development (e.g. motor neurones).
Apoptosis
•
• Induction of tolerance to self-antigens by removal of autoreactive T lymphocytes.
•
• Removal of virally infected cells.
•
• Removal of cells, which have undergone DNA damage.
•
156
Detection of • Terminal deoxynucleotidyl transferase biotin – dUTP nick end labeling (TUNEL) mostly used for in vivo apoptosis
apoptosis
•
 
detection
• DNA fragmentation assay – observed by electrophoresis of genomic DNA

•
• Annexin V/Propidium iodide assay by flow cytometry or fluorescent microscopy
•
• Caspase activity assay (AIPG 2008)
•

• The mechanisms by which Diabetes Mellitus enhances of CO2 in the lungs (e.g., chronic obstructive
•
apoptosis are: pulmonary disease).
– Ventilation defects, in which air does not reach the
GENERAL PATHOLOGY
– Activation of the polyol pathway
–
respiratory unit for gas exchange (e.g., atelectasis, or
–
– Formation of advanced glycation end products
the collapse of alveoli).
–
– Formation of reactive oxygen species
– Perfusion defects characterized by blockage of
–
– Higher levels of TNF-α expression
–
blood flow through the pulmonary capillaries (e.g.,
–
Differences between Apoptosis and Necrosis pulmonary embolus).
– Diffusion defects, which interfere with gas exchange at
–
NECROSIS APOPTOSIS the alveolar-capillary interface (e.g.. fluid in patients
Etiology Acute cell injury due to Various intracellular or with left heart failure}.
extracellular stimuli extracellular stimuli – As long as the capillary PO2 is higher than that in the
–
tissue, 0: will move into the tissue by the process of
Character Pathologic Physiologic/pathologic
diffusion. (AIPG 2012)
Distribution Groups of cells or Widely scattered isolated
patches of tissues cells • Hb-related abnormalities encompass those
•
associated with a reduction in Hb concentration;
Energy Passive (ATP Active (ATP dependant) decreased O; saturation (SaO:). representing the
requirement independent) percentage of heme groups occupied by O2; and
decreased release of 02 from Hb at the tissue level.
Cell size Enlarged (swelling) Reduced (shrinkage)
• The o2 content is the total amount of O2 carried in the
•
Nucleus Pyknosis karyohexis- Fragmentation into blood and is equal to 1.34 (Hb g/dL) X SaO2 + PaO2.
karyolysis nucleosome sized
fragments – In anemia, there is a reduction in the Hb
–
concentration, which reduces the total O2 content
Cellular Enzymatic digestion, Intact, maybe released as (1.34 Hb g/dL] x SaO2 + PaO2) without altering the
contents contents may leak out apoptotic bodies SaO2 or the PaO2, since there is normal O2 exchange
of the cell
in the lungs.
Plasma Disrupted Intact – altered structure
– Methemoglobin is heme iron in the ferric state,
–
membrane which is unable to bind with O2,iron must be in the
ferrous to bind with O2.
Adjacent Frequent Not present – Oxidizing agents such as nitrites (e g., nitroglycerin).
inflammation
–
nitrates converted into nitrites in the gut (e.g., from
DNA changes Random DNA Chromatin condensation nitrate-rich well water), and sulfur-containing
fragmentation with DNA fragmentation drugs increase the formation of metHb.
– Patients are cyanotic and do not respond to
–
administration of O2, since the heme iron is in the
Apoxemia ferrous state.
• Reduction in the amount of oxygen (O) dissolved in – Methylene blue is the treatment of choice, since
–
it enhances the conversion of iron to the ferrous
•
plasma (Pao2, where the lowercase letter “a” means
arterial). (NEET 2013) condition by acting as an artificial electron carrier
in the NADPH dependent metHb reductase system,

• It can be secondary to
white ascorbic acid, a reducing agent, assumes an
•
– Respiratory acidosis, which is secondary to retention ancillary role in treatment.
–

• In carbon monoxide (CO) poisoning, CO competes Free radicals
•
with 02 for binding sites on heme iron in place of oxygen,
• Unstable chemical species that have a single, unpaired
thereby decreasing the O2 content by decreasing the SaO2
•
electron in their outer orbit.
– The patient will have a cherry red discoloration of the • Produced by ionizing radiation, damaged mitochondria,
–
•
skin owing to the combination of CO with myoglobin. oxidase reactions, drugs (e.g., acetaminophen) and
– Administration of o2 is the treatment of choice in CO chemicals (e g. carbon tetrachloride [CCI4,]).
• Oxygen-derived FRs include superoxide, hydroxyl ions,
–
poisoning.
•
and peroxide.
– Factors moving the O, dissociation curve to the
• Cause cell injury by lipid peroxidation, in which lipid
–
left (high affinity of Hb for O2;), such as decreased
•
FRs combine with molecular oxygen
2,3-bisphosphoglycerate, CO, metHb, hypothermia,
GENERAL PATHOLOGY
• FRs are neutralized by superoxide dismutase: catalase;
and HbF (fetal Hb), decrease the release of 02 to tissue.
•
glutathione peroxidase (which generates glutathione),
and antioxidants, such as vitamin E, vitamin C, and
• Abnormalities in oxidative phosphorylation selenium
•
include [Those which block the oxidative pathway • Examples:
•
(e.g., inhibition of cytochrome oxidase by CO and – Retrolental fibroplasia and blindness in
–
cyanide) and those which produce abnormalities newborns secondary to o2. FR injury results from
In phosphorylation by damaging mitochondrial administration (damage occurs to tissue in Iron
membranes (e.g., uncoupling agents such as alcohol overload states (hemochromatosis), since iron
and aldehydes). helps generate FRs by fenton reaction)
– Acetaminophen hepatotoxicity is associated with
– The O2 content is normal, but ATP synthesis is
–
the formation of acetaminophen FRs in the-
–
decreased cytochrome P450 system, leading to liver necrosis
– O2 an electron acceptor, is the last reaction in the and failure.
–
electron transport chain, which underscores why – CCI4 hepatotoxicity is related to its conversion to
–
tissue hypoxia virtually shuts down ATP synthesis. CCI, FRs in the cytochrome system, leading to liver
cell necrosis and fatty change
Ultrastructural and biochemical alterations In hypoxic cell Cytoskeletal abnormalities

Injury • Microtubules are polymers composed of the protein
•
tubulin that are capable of undergoing rapid assembly and
Reversible conse- • Loss of the ATP-dependent sodium/ disassembly in the cytosol.
•
quences directly re- potassium pump
• The Chediak Higashi syndrome (CHS) is an autosomal
lated to a reduction • Cloudy swelling
•
recessive cytoskeletal abnormality in which the main
•
In ATP synthesis. • Increased Anaerobic glycolysis
defect is in the assembly (polymerization) of microtubules
•
• Intracellular lactic acidosis in the cytoplasm.
•
• Reduced protein synthesis
• Alterations occur in certain of the intermediate function
•
• EM findings -swelling of the
•
when damaging stimuli cause cells to release stress
•
smooth endoplasmic reticulum (first
alteration) and mitochondria.
proteins (also called heat shock proteins) that are vital to
survival of cell.
Irreversible conse- • Free radical damage – Ubiquitin aids in the removal of old or damaged
–
•
quences of hypoxic • Cell membranes are damaged proteins, such as intermediate filaments by first
binding to the protein and then delivering it to
•
cell injury. • Formation of large amorphous
proteases for degradation.
•
densities in mitochondria
• Increased cytosolic concentration of – Mallory’s bodies are masses of keratin Intermediate
–
filaments in hepatocytes of patients with alcoholic
•
calcium
• Nuclear abnormalities - pyknosis liver disease that have been “ubiquinated,” or marked
for destruction by proteases.
•
-(ink dot appearance), karyorrhexis
(nuclear fragmentation), and • The membrane skeleton provides structural integrity to
•
karyolysis (dissolution of nuclear the cell membrane. It is composed of spectrin, actin, and
chromatin – AIIMS May 2010). protein 4.1.
• Release of intracellular enzymes
• Congenital spherocytosis, an autosomal dominant disease,
•
from damaged cells is an excellent
•
marker of cell injury is an example of a defect in spectrin resulting in a hemolytic
anemia
158
Microscopic Examination of Cerebral Ischemia (AIPG 2012)
After the first 12 hours Upto 48 hours

• Both cytotoxic and vasogenic edema predominate • Neutrophilic emigration
•
•
• Endothelial and glial cells, mainly astrocytes swell and • Phagocytic cells, derived from circulating monocytes and
•
•
disintegrate activated microglia are evident.
• The macrophages become stuffed with the products of myelin
•
breakdown or blood and may persist in lesion for months to years
• Reactive astrocytes can be seen as early as 1 week after the insult.
•
GENERAL PATHOLOGY
Pathophysiology of growth alterations

Atrophy • Shrinkage in cell size (organ size and weight as well) with the loss of cell substance and reduction in metabolic
•
activity.
• May be a physiologic (e.g., involution of the thymus with advancing age) or a pathologic process (e.g., cerebral
•
atrophy in atherosclerosis of the carotid artery).
• In autophagy: cell organelles are encompassed by membranes to form vacuoles wherein they are progressively
•
degraded until only undigestable, lipid rich material, called lipofuschin remains behind in residual bodies.
• In H-and E-stained tissue, lipofuschin often‘ called the “wear and tear pigment, has yellow brown granular
•
appearance, Which If extensive enough, grossly discolors the tissue, producing a condition called brown atrophy.
• Clinical examples include skeletal muscle atrophy in a cast and atrophy of target organs in hypopituitarism as a result
•
of the loss of trophic hormone stimulation
Agenesis • Absence of an organ resulting from failure to develop any discernible primordial tissue (anlage) during embryonic
•
development (e.g., renal agenesis).
Aplasia • The primordium of life organ is present, but there Is no further development of the tissue (e.g , aplasia of the adrenal
•
cortex).
Hypoplasia • Incomplete or partial development ol an organ or tissue (e.g., hypoplastic left heart) and differs from atrophy In that
•
the latter begins with a normal-sized organ that subsequently becomes smaller as ceil mass is lost.
Hypertrophy • Increase in cell size due to an increase In the synthesis of structural components and organelles
•
• Examples of physiologic hypertrophy is hypertrophy of the heart in a well-trained athlete
•
Hyperplasia • Increase In the number of cells
•
• Both hyperplasia and hypertrophy are characterized by an increased expression of the protooncogenes, which are
•
growth-controlling genes (AIPG 2005)

• Same factors can stimulate both processes such as growth hormones, estrogen, protocooncogenes, growth factors
•

(AIPG 2005)

• Clinical examples of physiologic hyperplasia is hyperplasia of endometrial glands during the proliferative phase of
•
the menstrual cycle
• An example of approximately equal amounts of hypertrophy and hyperplasia is smooth muscle hypertrophy/
•
hyperplasia in the uterus in pregnancy.
Metaplasia • Reversible replacement of one adult cell type by another adult cell type, usually as an adaptive process instigated by
•
the host tissue as a response against chronic irritation (e.g., smoking, Infection).
• Clinical examples include the presence of increased goblet cells in the terminal bronchioles of a smoker
•
Dysplasia • Reversible atypical hyperplasia
•
• Disorderly proliferation of cells with nuclear variation in size and shape and increased mitotic activity with normal
•
mitotic spindles.
• Arises from a metaplastic or hyperplastic process and may progress to cancer through a series of steps if the irritating
•
stimulus is not removed. (AIPG 2001)

• Using the bronchial mucosa in a smoker as an example, the following progression occurs: normal pseudostratified
•
ciliated columnar epithelium—goblet cell hyperplasia and basal cell - hyperplasia— squamous metaplasia—>
squamous dysplasia (mild, moderate, severe)— squamous carcinoma in situ (limited to the full thickness of the
epithelium) —• invasive squamous carcinoma (invades through the basement membrane and has the ability to
metastasize)
Anaplasia • Lack of differentiation. The malignant cells resemble more primitive, undifferentiated cells than those from which they
•
arose. (AIPG 2007)


Also know
• In the cell division cycle, the main cell cycle regulators are kinases (e.g., p34 kinase), which regulate the progression front
•
one phase to the next, and small proteins called cyclins whose main function is to activate these kinases
• Cells in the G phase (G = gap), or resting phase of the cell cycle, enter the cycle when one or more of the above-mentioned
•
growth promoter mechanisms are invoked.
• In the G1 phase (most variable phase of the cycle) structural proteins are synthesized.
•
• Chromosomal replication occurs in S (synthetic) phase.
•
• In the G2 phase, the mitotic spindle (composed of microtubules) is assembled.
•
• Mitosis (M phase) results in division of the cell into two daughter cells; the latter then enter the G1, phase, which
•
GENERAL PATHOLOGY
determines whether the cells enter the G1„ phase, remain in the cycle to divide again, or become terminally differentiated
and unable to divide again.
• Cell growth by paracrine stimulation refers to the production of a growth peptide in one cell that attaches to peptide receptors
•
on nearby cells without having to enter the blood stream.
• Cell growth by autocrine stimulation occurs when the same cell produces growth factors and receptors.
•
“Wound Healing and Repair
The healing process may be of three types

• Healing by first intention (primary healing)
•
• Healing by second intention (secondary healing)
•
• Healing by third intention (delayed primary closure)
•
Fig.4.1 Healing by first intention
160
“DIFFERENCE BETWEEN HEALING BY PRIMARY AND SECONDARY INTENTION

Primary Intention Secondary Intention Third intention
Wound is clean, uninfected and Wound is open with a large tissue defect, at Delayed primary closure
surgically incised times infected
No much loss of tissues and Extensive loss of tissues and cells

cells
Edges of wounds are Wound is not approximately by surgical Wound is left open to be closed at a later day (4 – 7
approximated by surgical sutures. days) using a primary closure technique
sutures
GENERAL PATHOLOGY
Healing is rapid Healing is slow Slow
Large scar is formed Neat scar of primary union is not formed
Less granulation tissue More granulation tissue
Wound contraction is not present Wound contraction present Is less
Wound Healing
– By 24-48 hour: Epithelial closure takes place.
–
– On day 3: Neutrophils are replaced by macrophages.
–
– By Day 5: Collagen fibrils begin to appear and epithelial proliferation is maximal.
–
– At the end of first week: Wound strength is approximately 10%.
–
– By 3 months: Recovery of tensile strength is 70-80%.
–
Recovery of Tensile Strength Results from
• Increased collagen synthesis exceeding collagen degradation during the first 2 months.
•
• Structural modifications of collagen fibres when collagen synthesis ceases at late times.
•
Cells involved in wound healing may be classified into three types on the basis of their potential to divide
Labile cells • These cells divide continually and have considerable division potential throughout postnatal life.
•
• They are necessary for regeneration as these cells can populate the wound, divide, differentiate and restore
•
the original tissue architecture and composition.
• Eg. Surface epithelial cells of epidermis, alimentary tract, respiratory tract urinary tract, hemopoietic cells of
•
bone marrow and cells of lymph node and spleen.
Stable cells • These cells can populate the wound site and produce a scar, which is a repair tissue.
•
• They have limited division potential
•
• Eg. Fibroblasts, Endothelial cells, osteoblasts and chondrocytes
•
Permanent cells • These cells have exited the cell cycle, differentiated and do not divide.
•
• Injuries to tissues containing permanent cells can only heal by repair because these cells cannot divide and
•
are replaced by cells that produce only scar tissue
• Eg. Neurons of the nervous system, skeletal muscle and cardiac muscle cells
•

Mechanical Physical Factors
Cell-To-Cell Interaction • Cell movement and differentiation are related to cell-to-cell interactions as has been noted in the
•
healing of a wound in which epidermis and connective tissue have a complex interaction.
Cell-To-Matrix Interaction • Cell migration and differentiation are influenced by the surrounding matrix. The presence of fibrin
•
appears to stimulate fibroblast activity as well as angiogenesis.
• LAMININ inhibits epidermal cell migration.
•
• INTEGRINS are the transmembrane glycoproteins on the cells that acts as receptors for matrix proteins.
•
Growth Stimulators And • Growth factors are a class of natural biologic mediators that regulate crucial cellular events involved in
•
Inhibitors tissue repair such as
• DNA synthesis
GENERAL PATHOLOGY
•
• Chemotaxis
•
• Differentiation
•
• Matrix synthesis
•
Cells in tissue culture continue to move on a surface until they establish contact with similar cells, at which point movement
stops. This is termed ‘contact inhibition’. This appears to be dependent on the density of cells pressed and has been termed
‘density dependent regulation of growth’.
INFLAMMATION
Vascular Events Leukocyte Events (Cellular Events)
• Increased Blood Flow • Margination
•
•
• From relaxation of terminal arterioles in the inflammatory lesion • Diapedesis
•
•
• Produces local erythema (rubor) and heat (calor) • Chemotaxis
•
•
• Increased Vascular Permeability • Phagocytosis
•
•
• From contraction of capillary endothelial cells • Degranulation
•
•
• Extravasation of water, low and high molecular weight solutes
•
and blood cells
• Leads to local swelling (tumor)
•
Chemical mediators of inflammation
Vasodilation Histamine, serotonin, bradykinin
Increased vascular permeability Vasoactive amines, C3a and C5a, bradykinin, leukotriene C4
Chemotaxis, leucocyte recruitment and activation C5a, leucotriene B4, IL-1, TNF
Fever IL-1, TNF, prostaglandin
Pain Prostaglandin (PGE2)

Tissue damage Neutrophil and macrophage lysomal enzymes, oxygen Metabolites

(NEET 2013)

Opsonins and Opsonic Receptors
Target Opsonin Opsonic receptor Cells possessing Opsonic Receptors

Gram negative LPS-binding protein (LBP) or CD14 Neutrophils (if primed with TNF- a),
bacteria septin Macrophages
162
Target Opsonin Opsonic receptor Cells possessing Opsonic Receptors

Any particle or cell C3b CR3 (Mac l) Neutrophils
Any Particle or cell IgG1, IgG2, IgG3 Fcg RII Neutrophils Macrophages
Acute Phase Reactants
Positive Negative
CRP Albumin
Mannose binding protein (MAH 2012) Transferrin

GENERAL PATHOLOGY
Complement factors Transthyretin
Ferritin Transcortin
Cerruloplasmin Retinol Binding Protein
Serum amyloid A
Haptoglobin (MAH 2012)

Alpha 1 antitrypsin
Alpha2 macroglobulin
Cytokines
• Soluble proteins produced by a wide variety of hematopoietic and non hematopoietic cell types
•
• Involved in the regulation of the growth, development, and activation of immune system cells and in the mediation of
•
the inflammatory response.
– Immunoregulatory cytokines involved in the activation, growth, and differentiation of lymphocytes and monocytes,
–
e.g., IL-2, IL-4, IL-10, , and transforming growth factor (TGF)
– Proinflammatory cytokines --IL-1, TNFa and IL-6 and the chemokine family of inflammatory cytokines, within
–
which are included IL-8, monocyte chemotactic protein (MCP)-1, MCP-2, MCP-3, macrophage inflammatory
protein and regulation-upon-activation, normal T expressed and secreted (RANTES)
– Cytokines that regulate immature leukocyte growth and differentiation, e.g., IL-3, IL-7, and GM-CSF.
–
Prostaglandins
LTA4 Produced in leucocytes, platelets, mast cells, vascular tissue.
LTC4, LTD4, LTE4 • Contraction of smooth muscle

•
• Bronchoconstriction
•
• Vasoconstriction
•
• ↑vascular permeability
•
• Components of SRSA. (PGI 1995)
•

LTB4 • ↑Chemotaxis
•
• Adhesion of WBC (COMED 2006)
•

• Release of lysosomal enzymes
•
Thromboxanes • Produced mainly in platelets
•
• Promotes platelet aggregation
•
• Vasoconstriction
•
• Smooth muscle contraction
•
Prostacyclins • Produced by endothelium of vessels
•
 
• Vasodilation
•
• Inhibits platelet aggregation (PGI 1992)
•


FLUID AND HEMODYNAMIC PATHOLOGY
Oedema
Factors which cause oedema Factors which prevent oedema formation

formation
Vascular factors Tissue factors
• Decreased plasma oncotic pressure • Increased oncotic pressure of • Increased blood colloidal osmotic pressure
•
•
•
of intestinal fluid interstitial fluid
• Increased capillary hydrostatic • Decreased tissue tension • Decreased capillary hydrostatic pressure
•
•
•
pressure
GENERAL PATHOLOGY
• Increased capillary permeability • Lymphatic obstruction (or) decreased • Decreased capillary permeability
•
•
•
lymphatic drainage
• Increased sodium and water • Decreased tissue oncotic pressure

•
•
retention
• Increased tissue hydrostatic pressure (or)
•
tissue tension
• Increased lymphatic drainage
•
Shock
• Shock results in the hypoperfusion of tissue with subsequent impaired tissue oxygenation (NEET 2013)
•
• The four types are
•
– Hypovolemic shock (e.g.. due to hemorrhage or excessive sweating).
–
– Cardiogenic shock (e.g.. pump failure secondary to an acute myocardial infarction),
–
– Septic shock (gram-negative endotoxic shock), and
–
– Neurogenic shock (loss of vasomotor tone in venules and small veins as In fainting, spinal cord injury or use of autonomic
–
blocking agents).
• Loss of 20% of the blood volume (about 1000 mL) results in hypovolemic shock.
•
– In blood loss, the hemoglobin (Hb) and hematocrit (Hct) may remain normal for 1-3 days owing to the equal loss of
–
plasma and RBCs and to vascular contraction around the reduced volume of blood.
– Laboratory abnormalities include metabolic acidosis secondary to retention of lactate from tissue hypoxia and
–
hyperglycemia due to glycogenolysis from the release of cortisol, glucagon, and catecholamine.
• Cardiogenic shock can arise from an acute myocardial infarction, valvular disease, and cardiomyopathies.
•
• Septic (endotoxic) shock may be associated with endotoxin-containing gram-negative bacteria (e.g.. Escherichia coli),
•
exotoxin-producing gram-positive organisms, and fungi.
– The acute phase is characterized by
–
Peripheral arteriolar vasodilatation (warm skin, reduced oxygen exchange in tissue leading to tissue hypoxia and

then to lactic acidosis and hypotension).
High-output cardiac failure (dilated arterioles shunt more blood through the microcirculation back to the heart),

and
Sinus tachycardia

• Endotoxins primarily bind to CD14 receptors on leukocytes, endothelial cells, and other cells, resulting in direct injury
•
or the release of the following chemical mediators.
– Interleukin 1 (IL-1) and tumor necrosis factor (TNF) are released from macrophage activation (the increased
–
neutrophil adhesion to vessels leads to vessel damage). (AIIMS May 2013)

164
– Nitric oxide (endothelium -derived relaxing factor) is potent vasodilator derived from endothelial cells and
–
activated macrophages.
– Anaphylatoxins C3a and C5a (Vasodilators) are released from endotoxin activation of the alternative pathway
–
– Prostaglandins (vasodilators), leukotrienes (vasoconstrictors) and myocardial depressant factor (which reduces
–
ventricular contractility) are additional mediators Involved In endotoxic shock.
– Multi-organ dysfunction is the most common cause of death
–
– Cardiac abnormalities consist of muscle necrosis (Infarction, contraction band necrosis), decreased cardiac
–
contractility (depressant factor), increased left ventricular end-diastolic volume (LVEDV), decreased ejection
fraction (stroke volume/LVEDV), normal stroke volume, and increased cardiac output (increased venous return
plus sinus tachycardia)
GENERAL PATHOLOGY
– Microvascular injury often precipitates disseminated Intravascular coagulation

–
– Neutrophil-related injury in the lungs predisposes to the adult respiratory distress syndrome.
–
– Hypotension and tissue hypoxia commonly produce Ischemic acute tubular necrosis (the kidney Is the organ most
–
frequently affected In shock).
– The mortality rate in septic shock is 20- 80%.
–
• Differences between endotoxic shock and cardiogenic/hypovolemic shock include warm skin (In the former) rather than
•
cold, clammy skin (peripheral vasoconstriction) and an increased (in the former) rather than a decreased cardiac output.
Hyperemia and Congestion
Hyperemia Congestion
Active hyperemia refers to arteriolar dilatation of sympathetic or Passive hyeperemia (Congestion) results from impaired venous
humoral origin, eg. Usually a physiologic response to increased drainage and engorgement of organ with venous blood.
functional demand as after exercise or in inflammation.
CVC liver CVC of lungs

• Seen in right ventricular failure – leads to ‘Nutmeg’ liver; • Seen in left ventricular failure; if chronic leads to – edematous
•
•
hemosiderin laden septa become fibrotic – ‘brown induration of
lungs’
• With severe CVC of liver, fibrous thickening of the walls of the • ‘Heart failure cells’ hemosiderin laden intra- alveolar macrophages.
•
•
veins and central sinusoids leads to ‘cardiac sclerosis’ (‘cardiac
cirrhosis’).
THROMBOSIS, EMBOLISM, INFARCTION AND ANEURYSM

Thrombosis
• A thrombus is an adherent intravascular masscomposed of varying proportions of coagulation factors, RBCs, and
•
platelets.
Types
Arterial thrombi Venous thrombi
• Thrombi are grey-red, non-occlusive (mural), with pale layers • Thrombi are red-blue, lines of Zahn only rarely evident.
•
•
of platelets and fibrin alternating with darker layers containing
more abundant RBCs (lines of Zahn).
• Common in coronary, cerebral, iliac and femoral arteries. • Common in deep leg veins, femoral and iliac veins and rarely
•
•
superficial varicose veins.

Risk Factor
For venous thrombosis (AIIMS Nov 2010) For arterial thrombosis
• Surgery (general and orthopedic), • Atherosclerosis (most common),
•
•
• Immobility (postoperative state), • Smoking
•
•
• Obesity, • Hypertension,
•
•
• Congestive heart failure. • Dlabetes mellitus,
•
•
• Malignancy, and • LDL > 100 mg/dL,
•
•
GENERAL PATHOLOGY
• Use of oral contraceptives • HDL < 35 mg/dl
•
•
• A family history of premature acute myocardlal infarction or Stroke.
•
• Thrombogenesis is influenced by Virchow’s triad which • Possible sequelae of thrombus formation include
•
consists of:
•
the following
– Endothelial injury (most important), alone can induce
– Thromboembolism with the potential for infarction
–
thrombosis
–
– Normal blood flow disturbances (stasis and turbulence – Dissolution of the clot by the fibrinolytic system
–
– Organization and possible recanalization of the clot
–
of blood) –
– Hypercoagulability with restoration of blood flow
–
– Infection of the thrombus
• Hypercoagulable states usually predispose to red
–
•
thrombi in venous thrombosis. Types of Embolism
– They may be hereditary (uncommon) or acquired
• Thromboembolism (MC): embolism of thrombus or
–
•
blood clot
Acquired conditions Hereditary AT III defi- • Cholesterol embolism: embolism of cholesterol, often
ciency
•
from atherosclerotic plaque inside a vessel
• D i s s e m i n a t e d • Patients present at a
• Fat embolism: embolism of fat droplets; intravascular fat
•
•
cancer, which cause young age with a history
•
thrombocytosis and of recurrent deep venous globules in microvessels, especially in lungs, kidneys, and
elevation of coagulation thrombosis with or without brain. Requires special fat stains (oil-red O) and avoidance
factors such as fibrinogen, recurrent pulmonary
V, and VIII emboli
of fat solvent fixatives
• Oral contraceptive use • Functional and • Air embolism (gas): embolism of air bubbles
•
•
•
(estrogen increases immunologic (Is ATIII • Septic embolism: embolism of pus-containing bacteria
the concentration of present’’) assays
•
coagulation factors • Tissue embolism: embolism of small fragments of tissue
•
and decreases ATIII • Foreign body embolism: embolism of foreign materials
concentration)
•
such as talc and other small objects
• Hyperviscosity of blood • Hereditary deficiencies of
• Amniotic fluid embolism: Embolism of amniotic fluid,
•
•
secondary to polycythemla either protein C or protein
•
 
(in which there is an excess S follow an autosomal foetal cells, hair, or other debris that enters the mother’s
number of RBCs) or dominant inheritance bloodstream via the placental bed of the uterus and
hypergammaglobulinemia, pattern
particularly an increase in triggers an allergic reaction; diagnostic
IgM.
Fate of pulmonary emboli
• 60-80% are clinically silent
• Treatment during active thrombosis is with very high
•
• Sudden death, cor pulmonale or CVS collapse if >60%
•
doses of heparin while coumarin derivatives (e.g.
•
warfarin) are used for prophylaxis of pulmonary circulation is embolized.
– Heparin is employed in acute thrombosis, and • Pulmonary hemorrhage: when medium sized arteries
•
–
coumarin derivative are used for long term are affected, no infarct seen.
maintenance (started at low levels to prevent skin • Pulmonary hypertension with right sided heart failure.
necrosis)
•
166
Good to know venous thrombosis due to gravid uterus compressing the

inferior vena cava causing venous stasis in the legs.
• ‘Currant-jelly’ clots: Post-mortem clots which are not
• Phlegmasia cerulea dolens (painful blue leg): Swollen
•
attached to the vessel wall; helps to differentiate from
•
ante-mortem thrombi bluish skin with superficial gangrene, occurring as
• Trosseau’s phenomenon: (migratory thrombophlebitis) a complication of ileofemoral venous thrombosis and
decreased arterial blood flow
•
seen in disseminated visceral cancers (most often in
Ca pancreas and GIT cancers, also lungs, prostate, female • Paradoxical embolism: A venous embolism that passes
•
reproductive tract, breast) into the systemic circulation through interatrial or
• Phlegmasia alba dolens (painful white leg): Ileofemoral interventricular defect.
•
 
GENERAL PATHOLOGY
Atherosclerosis
• Characterized by intimal lesions called atheromas (also called atheromatous or atherosclerotic plaques) that protrude
•
into vessel lumens.
• An atheromatous plaque consists of a raised lesion with a soft, yellow, grumous core of lipid (mainly cholesterol and
•
cholesterol esters) covered by a white fibrous cap.
• Atherosclerosis is produced by the following pathologic events:
•
– Endothelial injury causes (among other things) increased vascular permeability, leukocyte adhesion, and
–
thrombosis.
– Accumulation of lipoproteins (mainly LDL and its oxidized forms) in the vessel wall.
–
– Monocyte adhesion to the endothelium followed by migration into the intima and transformation into macrophages
–
and foam cells.
– Platelet adhesion
–
– Factor release from activated platelets, macrophages and vascular wall cells, inducing smooth muscle cell recruitment,
–
either from the media or from circulating precursors.
– Smooth muscle cell proliferation and ECM production
–
– Lipid accumulation both extracellularly and within cells (macrophages and smooth muscle cells)
–
Infarction
• Infarction, MC (97%) results from occlusion of arterial supply; rarely caused by obstruction of venous drainage, usually in
•
organs having no bypass channels (ovary, testis). (AIPG 2012)
• Common to all infarctions is ischaemic coagulative necrosis, but an important exception is encephalomalacia (infarcts in
•
brain), which is marked by liquefactive necrosis.
Haemorrhagic (Red) Infarcts Pale (white) Infarcts

Seen in venous occlusion (e.g. torsion of ovary, testis) and in Occur in solid organs with end arteries (having few anastomoses) such
tissues that are loose (e.g., lung) or have a double innervation as kidneys and spleen
(small intestine, lung).
Amyloidosis
Category Major fibril protein
• Primary amyloidosis (multiple myeloma) • AL = Light chain
•
•
• Secondary amyloidosis • AA = 2A’s = 20; AA = Acute phase reactant
•
•
• Hemodialysis associated • Aβ2 microglobulin (MHC class I protein)
•
•
• Senile cardiac • ATTR/AF = Transthyretin
•
•
• Medullary thyroid Ca • A-Cal = Calcitonin
•
•

Category Major fibril protein
• Alzheimer’s disease • Amyloid precursor protein (APP)
•
•
• Diabetes mellitus • AE = Endocrine, Amylin
•
•
Type of Amyloidosis Amyloid protein
• Primary Amyloidosis, Myeloma • AL, (AIPG 2007, PGI 1989)
•
•

• Secondary Amyloidosis, Tuberculosis, Rheumatoid arthritis, • AA, TN 1990
•
•

Hodgkins lymphoma
• Familial Medittarean Fever • AA

•
•
GENERAL PATHOLOGY
• Hemodialysis associated Amyloidosis • Aβ2M
•
•
• Cerebral (Alzhiemers) Amyloidosis • Aβ
•
•
• Cardiac Amyloidosis • ATTR (AIIMS 2007)
•
•

Also note
• Amyloidosis is deposition of an “extracellular protein”.
•
• Individual subunits form “β pleated sheets.” (AIPG 2007)
•

• Kidney followed by liver is the commonest sites involved. (PGI 1988)
•
• Deposits stain “red” with Congo red.
•
• “Apple green birefrigerence” is seen on Congo red stain under polarized light.
•
• Amyloid is composed of “fibrillary protein, amyloid P Component and Glycosaminoglycans”.
•
• Thyroid cancer with amyloid stroma: MTC (Medullary Ca thyroid) (PGI 1988)
•
• Rectal biopsy is the best diagnostic method. (AIPG 2007)
•

• On light microscopy: Eosinophilic amorphous substance
•
• Congo red in ordinary light: Pink color (AIIMS 1983)
•
• Congo red on polarizing microscope: Yellow green birefringence
•
• Electron microscopy: Non branching fibrils
•
• X ray crystallography: Crossed β pleated configuration
•
NEOPLASIA
• Both benign and malignant tumors are composed of parenchyma consisting of proliferating cells and supporting connective
•
tissue stroma. The parenchymal component of a tumor determines its biologic behavior
– Most tumors are of epithelial origin (ecto- endo- mesoderm), while the remainder are of connective tissue origin
–
• Terminology
•
Benign tumors Malignant tumors
• Add ‘oma’ to cell type e.g. lipoma • Epithelial origin - carcinomas
•
•
• The suffix “oma” does not always indicate a benign tumor,
•
e.g., melanoma, lymphoma, astrocytoma, and hepatoma are
malignant tumors.
• Arising from gland – adenoma • Glandular epithelium - adenocarcinoma
•
•
• From epithelial surface – polyps or papilloma • Those arising from transitional epithelium in the urinary system
•
•
(e.g. bladder, renal pelvis) are designated transitional cell
carcinomas
168
Benign tumors Malignant tumors

• Features • Connective tissue origin – sarcomas
•
•
– Encapsulated
• Features

– Grow slowly
•

– Non invading, – Capacity of malignant tumors to invade

– Have minimal mitotic activity, normal spindles, – Metastasis

– Resemble the parent tissue. – On encapsulated

– Rapidly growing

– Atypical mitotic spindles

• APUD (amine precursor uptake and decarboxylation) tumors are neuroendocrine tumours having dense-core
GENERAL PATHOLOGY
•
neurosecretory granules on electron microscopy that most commonly develop from neural crest and neural ectoderm.
(e.g.. small-cell carcinoma of lung, carcinoid tumors).
• Teratomas derive from all three germ cell layers (e.g. teratoma of the ovary or testis).
•
– They commonly have teeth and bone, which are visible on x-ray.
–
– They are the most common germ cell tumors, which are lot (potential tumors that may differentiate in any direction.
–
Oncogenes
• Involves only single allele because they are gained from functional mutations
•
• Are dominant
•
• RAS oncogene is a single transduction protein which means that it communicates signal to other cells. Sometimes DNA
•
mutation turns the signal to other cells. Sometimes DNA mutation turns the signal permanently on; which leads to
unlimited cell growth and cancer. The RAS superfamily of small GTPases includes the RAS, Rho,Arf, Rab, Ran families.
(AIIMS May 08)

Inherited carcinoma (Ca) Abnormal gene Other non-inherited Ca seen with this gene
1. Retinoblastoma RB1 Many

2. Li fraumeri syndrome P53 Many

3. Melanoma INK 7a Many

4. Colorectal Ca MCH1, MSH2, MSH6 Most colorectal Ca

5. Breast and ovarian Ca BRCA1, BRCA2 Only rare ovarian Ca

6. Wilm tumor (nephroblastoma) WT1 Wilms tumour

(AIPG 2012)

7. Nerve tumour including brain NF1, NF2 Small number of colon Ca, melanoma, neuroblastoma

(AIPG 2006)
8. Kidney Ca VHL Certain type of kidney Ca

Tumour Suppressor Gene/ Anti Oncogene
• Follow the two hit hypothesis i.e. both alleles that code for a particular genes must be affected… recessive
•
• 1st tumour suppressor gene detected was the human retinoblastoma protein (PRb protein).
•
• Other is p53- stimulates apoptosis and has been called as ‘Guardian of genome’ or ‘Guardian angel gene’ or ‘master
•
watchman’ because of its role in conserving stability by preventing genome mutation.
• Examples are APC, CD95, BRCA1, BRCA2
•

Tumour suppressor gene Function Cancer
• APC Control the function of specific transcription factors Familial adenomatous and non inherites colorectal Ca
•
• BRACA 1, 2 DNA damage repair Inherited breast cancers, ovarian Ca
•
• CDKN2A Gene locus that encodes P16 and P14 ARF Brain tumours
•
• DCC Unknown Colorectal Ca
•
• DPC4 (SMAD4) Mediates signaling from growth face receptors Colorectal tumours
•
• MEN I Codes for menin protein that interacts with MEN I syndrome
•
transcription factors and prevents transcription of
GENERAL PATHOLOGY
certain genes
• MTS 1 Inhibitor of cyclin dependent kinases Melanoma

•
• NF1 RAS GTPase activating protein Neurofibromatosis type 1
•
• NF2 RAS GTPase activating protein Neurofibromatosis type 2
•
• P 53 Encodes a transcription factor for p21 that arrests Bladder, breast, colorectal, esophageal, liver, lung
•
the cell cycle in G phase prostate and ovarian Ca, brain tumours, sarcomas,
lymphomas and leukemias
• PTEN Lipid phosphatase that regulates cell survival Cawden syndrome, increased risk of breast Ca with
•
thyroid Ca
• Rb Alters activity of certain transcription factors that play Retinoblastoma, sarcomas, bladder, breast, esophageal,
•
a role in the control of cell division prostate, lung Ca
• VHL May target protein for degradation Renal cell Ca

•
• Premalignant Lesions
•
– Leucoplakia
–
– Erythroplakia
–
– Chronic hyperplastic candidiasis.
–
– Oral submucous fibrosis
–
– Syphilitic glossitis;
–
– Sideropenic dysphagia
–
• Premalignant Forms of SCC
•
– Actinic keratosis, or solar keratosis
–
– Actinic cheilitis
–
– Bowen’s disease
–
– Erythroplasia of Queyrat
–
– DLE
–
– Xeroderma Pigmentosa (due to single defect in DNA repair gene) (AIPG 2011)
–
– UV Radiation –UV B
–
– Hypertrophic lichen planus
–
• Actinic keratoses and cheilitis are hyperkeratotic papules and plaques that occur on sun-exposed areas. While the
•
potential for malignant degeneration is low in any individual lesion, the risk of SCC increases with larger numbers of
lesions.
170
• Bowen’s disease presents as a scaling, erythematous plaque, which may develop into invasive SCC in up to 20% of cases.
•
Treatment of premalignant and in situ lesions reduces the subsequent risk of invasive disease
• Invasion of Extracellular Matrix

•
– Both cancer cells that merely invade surrounding tissues and those that metastasize have to take this first essential step.
–
In this process there is:
Loss of adhesion molecules on the cancer cells (E-cadherin or catenin mutations)

High density expression of laminin and fibronectin receptors on all the surfaces of the detached malignant cells

(instead of only on the basal surface, as in normal epithelial cells)
Expression of integrin receptors that facilitate interaction with other ECM proteins and glycoproteins.
GENERAL PATHOLOGY

Generation of many types of proteases that digest all that obstructs the passage of tumor cells.

Perhaps active suppression of anti-proteases secreted by the other tissue cells.

Increased expression of certain tumor-cell motility factors like beta- 15 thymosin

Increased responsiveness to mitogen molecules derived from tissue proteins.

Diagnosis of Bone Tumours
Tumours arising from
Epiphysis • Osteoclastoma (AIPG 2002)

•

• Chondroblastoma
•
Diaphysis • Ewing’s sarcoma
•
• Osteoid osteoma
•
• Multiple myeloma
•
Metaphysis • Osteogenic sarcoma
•
• Bone cysts
•
• Chondroma
•
• Chondrosarcoma
•
• Brodie’s abscess
•
Age Groups
• Ewing’s sarcoma – 5-15 years
•
• Osteosarcoma–primary–10-20yrs, secondary–40yrs
•
• Osteoclastoma–20-40years
•
• Chondrosarcoma–30-60years
•
• Multiple myeloma–7th decade
•
• Osteoid ostema–5-25 years
•
Important Points
Commonest bone tumor Secondaries
Commonest primary malignant tumor Multiple myeloma (AIPG 2010)

Commonest primary malignant tumor of long bones Osteosarcoma (AIIMS May 2010)

Commonest benign tumor Osteochondroma (not a true neoplasm)
Commonest true benign tumor of bone Osteoid osteoma

Commonest Site
Ivory osteoma Frontal sinus
• Osteoid osteoma • Tibia

•
•
• Ameloblastoma/adamtinoma (AIPG 2001) • Mandible
•

•
• Chondroma • Sacrum and cervical spine
•
•
• Osteoclastoma • Lower end of femur
•
•
• Osteosarcoma • Tibia
•
•
GENERAL PATHOLOGY
• Ewing’s • Tibia
•
•
• Multiple myeloma • Vertebra
•
•
• Osteochondroma • Metaphysis
•
•
VARIOUS DISORDERS AND THEIR IMPORTANT FEATURES
Anterior pituitary HYPERfunction • Most cases caused by adenoma in the anterior lobe
•
• Produces excess of a single hormone usually
•
• Peak ages 20’s—60’s
•
• Prolactinoma-Most common type, causes amenorrhea, infertility, loss of libido,
•
galactorrhea
• Somatotroph (growth hormone) - If occuring before puberty= gigantism; If occurring
•
after puberty= acromegaly
• Corticotroph adenoma - Increased ACTH production—can cause Cushings disease
•
Anterior pituitary HYPOfunction • Most often due to a non-secretory adenoma or less commonly ischemic necrosis of the
•
pituitary
• Sheehan’s syndrome—postpartum ischemic necrosis
•
• Empty sella syndrome—herniation of CSF into the sella tursica compressing the
•
pituitary
Posterior Pituitary ADH Hypersecretion • (Inappropriate ADH secretion) due to ADH producing tumor such as oat cell lung
•
carcinoma
• Results in water retention and inability to dilute urine
•
• Hyponatremia excess secretion of sodium leading to low levels of sodium in the blood
•
Posterior Pituitary ADH Hyposecretion • Promotes resorption of free water
•

• Due to post pituitary destruction—neoplasm, trauma, inflammation
•
• Can cause diabetes insipidus characterized by excess urination, dilute urine, and
•
extreme thirst (AIPG 2011)

Hyperthyroidism (thyrotoxicosis) • Most common cause= Graves disease
•

• Increased circulating T3 and T4, increased I-131 uptake, decreased TSH
•
• Clinical manifestations - sweating, warm skin, heat intolerance, tachycardia, muscle
•
weakness, exopthalmos, diarrhea, weight loss (AIPG 2001)

• Thyroid storm—abrupt onset hyperthyroidism
•
• Graves disease: Affects 1-2 % of US women; Thyrotoxicosis, exopthalmos, pretibial
•
myxedema; Autoimmune process—autoantibodies to TSH receptor, microsomes,
thyroglobulin, and thyroid hormones
172
Hypothyroidism • Decreased T3 and T4, increased TSH
•

• Hypothyroidism is manifest as myxedema in adults and cretinism in children (in children
•
usually due to iodine deficiency)
• Clinical manifestations: Lethargy, mental slowness, rough skin, cardiac enlargement,
•
obesity, cold intolerance, constipation
• Causes: Radiation, surgery, Hashimoto’s
•
• Hashimoto’s thyroiditis: Autoimmune disorder; Massive infiltrates of lymphocytes
•
with germinal centers; Hurtle cells prominent (epithelial cells with eosinophilic granular
cytoplasm); Gland enlarges but is hypofunctional; Increased risk of lymphoma;
Females 12:1; Can have intermittent periods of hyperthyroidism (thyrotoxicosis)
Subacute granulomatous thyroiditis • Acute onset, often preceded by URI

GENERAL PATHOLOGY
•
(deQuervain’s) • Granulomatous inflammation
•
• Self limiting
•
• Transient thyrotoxicosis
•
Reidels’s thyroiditis • Fibrous replacement of thyroid, rare, unknown origin
•
Hyperparathyroidism • Most often due to a parathyroid adenoma
•
• Also can be caused by gland hyperplasia, or PTH secreting malignant tumor
•
• Symptoms: Stones, Moans, bones, groans
•
• Increased serum calcium, increased alkaline phosphatase; decreased phosphorus
•

(AIPG 2001,2012)

• Excessive bone resorption, seizures, pancreatitis, osteoporosis, kidney stones, peptic
•
ulcers
• Renal failure= most common cause of secondary hyperparathyroidism
•
• Aggregates of osteoclasts, reactive giant cells and hemorrhagic debris occasionally
•
form masses that may be mistaken for neoplasms – brown tumours of
hyperparathyroidism (NEET 2013,AIPG 2006)

• The brown colour is the result of vascularity, hemorrhage andd hemosiderin deposition.
•
Hypoparathyroidism • Caused mainly by surgical misadventure
•
William syndrome • Chvostek’s and Troussau’s sign
•
• Neuromuscular irritability, carpopedal spasms, occasional seizures
•
• Autosomal dominant idiopathic hypercalcemia of infancy
•
Hypocalcemia • Numbness and tingling of circumoral region and the tips of fingers and toes
•
• Extensive spasm of skeletal muscle with cramps and tetany
•
• Carpopedal spasm
•
• Laryngospasm with stridor
•
• Hyperactive tendon reflex
•
• Prolongation of QT interval
•
• Increased intracranial pressure in some patients with long standing hypocalcemia.
•
• Papilloedema is associated with these cases
•
• Signs
•
– Chovstek’s: Contraction of facial muscles in response to tapping the facial nerve
–
anterior to ear.
– Trousseu’s: Carpal spams occurring after occlusion of brachial artery with a blood-
–
pressure cuff for 3 mins.
– Erb’s: Muscle contraction can be produced by application of subthreshold electrical
–
stimulation
– Perronial’s sign: Trapping over the peroneal nerve at the neck of the fibula will
–
produce planter flexion adduction of the foot (pedal spasm).

Adrenal cortex HYPERfunction • Cushings syndrome: Most frequent cause=exogenous steroids; Other causes;
•
pituitary adenoma, oat cell carcinoma; Clinical: Buffalo hump, moon face, truncal weight
gain, muscle wasting, abdominal striae, hypertension, mental disturbances, hirsutism
• Hyperaldosteronism: Conn’s syndrome (primary hyperaldosteronism) - Usually
•

from adrenal adenoma, hypertension, sodium/water retention, Decreased potassium;
decreased renin. Secondary aldosteronism - Due to renal ischemia; increased rennin

• Adrenal virulism: Virulism in females; precocious puberty in males; Caused by
•
enzyme defects—hydroxylase deficiency or caused by adrenal cortex tumor
Adrenal Cortex HYPOfunction • Addison’s disease: Hypotension, increased skin pigmentation, increased potassium,
•
weight loss, somnolence, personality changes; Most often caused by idiopathic adrenal
atrophy; Can also be caused by tuberculosis or metastatic tumors
• Waterhouse-Friedrichsen syndrome: Castastrophic adrenal insufficiency caused by
GENERAL PATHOLOGY
•
hemorrhagic necrosis of adrenal cortex; Often associated with DIC; Characteristically
due to meningococcal meningitis
Pheochromocytomas • Adrenal tumor

•
• Clinical: tachycardia, headache, sweating, tremors, elevated VMA
•
• Important cause of surgically correctable paroxysmal hypertension
•

• Rule of tens =10% bilateral, 10% children, 10% malignant
•
• Can occur as part of MEN syndrome
•
Neuroblastoma • Adrenal cortex tumor
•
• Highly malignant tumor of early childhood (0-3 years of age)
•
• Catacholamine producing tumor presenting as an abdominal mass
•
• Produces hypertension
•
• Characterized by one or more of the following: Amplification of N-myc oncogene, Deletion
•
short arm chromosome 1, Loss of alleles chromosome 14
Multiple endocrine neoplasia syn- • Autosomal dominant syndromes in which more than one endocrine organ is
•
dromes hyperfunctional
• MEN I (Wermer)
•
• MEN II (Sipple)
•
• MEN IIB (MEN III)
•
MEN I (Wermer) • Hyperplasias or tumors of pituitary, parathyroid, or pancreatic islands (3Ps)
•

• Hyperparthyroidism is most common manifestation
•
• Mutations of MEN I gene
•
MEN II (Sipple) • Pheochromocytoma, medullary carcinoma of the thyroid, and hyperplasia or tumor of
•
parathyroid producing hyperparathyroidism
• Mutations of rat oncogene
•

MEN IIB (MEN III) • Pheochromcytomas, medullary carcinoma of thyroid, and multiple mucosal neuromas
•
• Does NOT cause hyperparathyroidism
•
• Linked to different mutations of rat oncogene
•
Acute leukemias • Most often in children with a second peak over 60 (AML)
•

• Death within 6-12 months if no intervention
•
Acute lymphoblastic leukemia (ALL) • Most common malignancy of children
•

• Predominance of lymphoblasts in blood and marrow
•
• Most responsive to therapy
•
Acute myeloblastic leukemia (AML) • Predominance of myeloblasts
•

(AIPG 2012) • Most often in adults >60
•
• Responds more poorly to therapy than ALL
•
Chronic leukemia • Proliferation of cells more mature than in acute leukemias; longer less devastating
•
course than acute leukemias; generally less responsive to therapy than acute leukemia
174
Chronic lymphoblastic leukemia (CLL) • Usually a B-cell proliferation
•

• Lymphadenopathy and spleenomegaly frequently
•
• Complications: Warm antibody autoimmune hemolytic anemia and
•
hypogammaglobulinemia; increased susceptibility to infections
• Average survival 3-6 years after diagnosis
•
Chronic myelogenous leukemia (CML) • Part of the myeloproliferative syndrome
•

• Philadelphia chromosome (translocation 9-22)
•
• Marked leukocytosis
•
• Prominent spleenomegaly
•
• Peak incidence ages 35-50
•
GENERAL PATHOLOGY
Hairy cell leukemia ••

Middle age men/ pancytopenia and splenomegaly/hepatomegaly, lymphadenopathy

• Dramatic response to therapeutic medications
•
• Positive staining of cells for tartrate resistant acid phosphatase (TRAP)
•
Multiple myeloma (AIPG 2006) • Malignant monoclonal plasma cell proliferation affecting older (>50) individuals
•

• Punched out (lytic) radioluciencies in bone
•
• Demineralization of bone (osteopenia)
•
• Severe bone pain and spontaneous fractures M protein spike (usually IgG or IgA (either
•
kappa or lambda light chain))
• Urine contains Bence Jones protein (AIIMS May 2009, AIPG 2006, 2001)
•

• Increased susceptibility to infection
•
• Hypercalcemia due to bone destruction
•
• Renal insufficiency with azotemia
•
• Amyloidosis
•
• Plasma cell disorder
•
Burkitt’s lymphoma • Aggressive B cell lymphoma
•

• Linked to EBV (Epstein Barr) infection
•
• Associated with cytogenic change-- translocation (8, 14)
•
• African form often involves the mandible or maxilla Microscopically: “starry sky”
•
appearance
Mycosis fungoides • Low grade T-cell lymphoma involving the skin

•
Sezary syndrome • T-cell proliferation similar to mycosis fungoides but also has malignant T cells in
•
the peripheral blood

Wilson’s disease (AIPG 2010) • Wilson’s disease is an autosomal recessive disorder caused by mutations in the ATP7B
•
gene
• Pathogenesis: ATP7B protein deficiency impairs biliary copper excretion, resulting in
•
positive copper balance, hepatic copper accumulation and copper toxicity from oxidant
damage
Hepato lenticular disease • Increased urinary excretion of copper (AIPG 2010)
•

Useful Tests For Wilson’s Disease
Test Normal value Heteroxygous carriers Wilson’s disease
Serum 180-350 mg/l Low in 20% Low in 90%
ceruloplasmin
KF rings Absent Absent Present in 99% and if neurologic or psychiatric symptoms present
in 30-50% in hepatic presentation and presymptomatic state
24 hour urine 0.3 -0.8 mmol Normal to 1.3 mmol >1.6 mmol in symptomatic patients
copper (20-50 mg)
Liver copper 0.3 – 0.8 mmol/g Normal to 2.0 mmol

Test Normal value Heteroxygous carriers Wilson’s disease
>3.1 mmol (>200mg) obstructive liver disease can cause false
positive results
Haplotype analysis 0 matches 1 match
Important Translocations
• t(8;14) Burkitts Lymphoma
•
• t(9;22) CML
•
• t(15;17) AML
•
GENERAL PATHOLOGY
• t(11;22) Ewings sarcomaUPSC 01
•
• t(X;18) Synovial cell Ca
•
PATHOLOGICAL DEPOSITS Serum Alkaline Phosphatase (ALP)
• Derived from (BLIP), Bone; Liver; Intestine; Placenta.
•
Dystrophic calcification Metastatic calcification • Raised levels are seen in ( remember all these conditions)_
•
• Occurs in nonviable • Occurs in Normal – Increased Osteoblastic Bone conditions: Paget’s
•
•
or Dying tissues in the tissues and results from –
disease (Osteitis deformans), Osteogenic sarcoma,
presence of NORMAL hypercalcemia
serum calcium levels
Metastatic bone tumour, Metabolic bone disease
(Rickets; Osteomalacia), Hyperparathyroidism.
• Seen in areas of • Seen in the interstitial – Biliary obstruction: intra/extra hepatic; Biliary
•
•
–
caseous necrosis (TB), tissues of the vasculature, cirrhosis
liquefactive necrosis kidneys, lungs, and gastric
– Intestine: ulcerative colitis, Crohn’s disease
(abscess), fat necrosis, mucosa.
–
atherosclerosis,
– Placenta: late pregnancy
–
damaged heart valves, – Others: Infectious mononucleosis, Temporal arteritis,
–
stroma of some tumours, carcoidosis, amyloidosis, RA.
psammoma bodies • Alkaline phosphatase from liver and bone is distinguished
•
by heat stability at 56 deg centigrade; ALP from bone is
heat labile (“Bone burns, Liver lasts”).
Raised Serum Acid Phosphatase
• Metastatic Cancer of Prostate – In prostate acid phosphatase activity is 100 times more than in any other tissue.
•
• Prostatitis, urinary retention
•
• Gaucher’s disease, Niemann Pick’s disease
•
• Metabolic bone disease (Paget’s, osteomalacia)
•
• Haemolytic anaemia
•
• Any cancer that has metastasized to bone.
•
Creatine Phosphokinase (Creatine Kinase, CK) (AIPG 2008)
CK-MM: skeletal Muscle Increased CK
CK-MB: Heart
CK-BB: Brain (also bowel infarction, neoplasms) • Cardiac muscle damage: Myocardial Infarction, Myocarditis
•
• Skeletal muscle damage: Rhabdomyolysis, Myositis, Crush
•
injury or trauma, Dermatomyositis or Polymyositis, Vigorous
Exercise, Muscular Dystrophy, Malignant hyperthermia,
Intramuscular injections
• Brain damage: Seizure, Cerebrovascular Accident, Delirium
•
tremens
• Others: Acute renal failure, Myxedema, Pulmonary infarction,
•
Pulmonary Embolus, Acute Aortic Dissection, Statins
176
IMMUNOLOGY AND GENETICS

• Immune system
•
– The immune system consists of B, T, natural killer and phagocytic cells and the complement system.
–
– Factors predisposing to immune disorders include prematurity, autoimmune disease, lymphoproliferative disorders
–
infections (AIDS) and immunosuppressive disorders.
– Flow cytometry is useful in identifying B and T cell markers (proteins) by means of fluorescent antibodies
–
(AIPG 2007)

– Quantitative measurement of serum immunoglobulin (Igs) and detection of isohemagluttinins against blood group
–
antigens are used to evaluate B cell function.
• Igs in decreasing order of concentration are IgG, IgA, IgM, IgD and IgE.
GENERAL PATHOLOGY
•
• Since IgM synthesis begins at birth, the presence of IgM in the newborn indicates a fetal intrauterine infection (e.g.
•
cytomegalovirus infection)
• IgG synthesis begins at 2 months of age, hence the presence of IgG in cord blood is maternally derived.
•
• ISO hemagglutinins are present in patients with blood specific mitogens with patient lymphocytes (eg,
•
group A (anti – B IgM), group B (anti-A IgG), and phytohemogluttinin for T cells and staphylococcus A
group ‘O’ (anti-A IgM. anti-B IgM, and antl-A. IgG). for B cells), which are stimulated to divide (increased
Isohemagglutinins are absent in blood group AB uptake of titrated thymidine) if they are functional.
individuals and in newborns. – Skin testing with common antigens (e.g. mumps)
–
• Functional assays are available for B and T cells. produces an inflammatory reaction in the presence of
normal T-cell function (the absence of a response is
•
– Mitogen assays involve the in vitro interaction of
called allergy).
–
B-cell immunodeficiency (ID) disorders
Bruton’s agammaglobulin- • Sex-linked recessive (SXR) disease whose pathogenesis involves the failure of pre-B cells to
•
emia differentiate into mature B cells.
• Maternally derived IgG protects the newborn for a few months before affected infants begin
•
to develop sinopulmonary disease associated with Streptococcus pneumoniae, Haemophilus
influenzae, and Staphylococcus aureus.
• Since cell-mediated Immunity (CMI) is intact, there is an effective host defense against most
•
viruses and fungi,
Common variable immune • First presents between 15 and 35 years of age with recurrent sinopulmonary infections due to
•
deficiency (CVID) decreased Ig production.
• There is an intrinsic defect in the maturation of B cells into antibody-producing plasma cells.
•
• CVID patients are also prone to giardiasis, malabsorption (e g . celiac sprue), and autoimmune
•
disease (e.g, pernicious anemia).
Selective IgA deficiency • The most common hereditary immunodeficiency. Is due to an intrinsic defect in the differentiation
•
of B cells committed to synthesizing IgA or to a defect in T cells that prevents B cells from
synthesizing IgA.
• Symptomatic patients usually have recurrent problems with sinopulmonary infections (owing to lack
•
of secretory IgA) and an increased incidence of giardiasis, autoimmune disease, and allergies
• Both serum and secretory IgA levels are decreased.
•
Sex-linked lympho-prolifer- • Epsteln–Barr virus (EBV)- related disease associated with hypogammaglobulinemia and an
•
ative (LP) syndrome increased incidence of malignant LP disorders.

T cell and combined B and T cell immunodeficiency disorders
DiGeorge syndrome (thymic • Marked by the failure of the third and fourth pharyngeal pouches to develop, with subsequent
•
hypoplasia) absence of all four parathyroid glands (causing hypocalcemia and tetany) and the thymus (absent
thymic shadow on chest x-ray)
• Patients have abnormal facies and an increased incidence of truncus arteriosus, in which the
•
aorta and pulmonary artery share a common trunk (causing cyanosis).
• Defective CMl results in chronic candidiasis and Pneumocystis carinii (PC) pneumonitis.
•
••
As with all T-cell immunodeficiencies, blood transfusions containing immunocompetent donor cells
may result in a graft-versus-host (GVH) reaction or transmission of CMV in lymphocytes, hence
the importance of irradiating blood before transfusion.
Severe combined Immuno- • Characterized by deficiencies in both B and T cells inherited in either an autosomal or an SXR
GENERAL PATHOLOGY
•
deficiency (SCID) pattern.
• Approximately 50% of children with the autosomal recessive (AR) pattern have a deficiency of
•
adenosine deaminase, which leads to an accumulation of adenine that is toxic to both B and T
lymphocytes.
• Children with SCID present with life-threatening infections often associated with pneumonia
•
secondary to P carinii pneumonitis.
• SCID is the first genetic disease for which gene therapy has been used to replace the missing
•
enzyme—adenosine deaminase—in the host’s DNA.
Wiskott-Aldrich syndrome • SXR disease with a triad of thrombocytopenia, eczema, and recurrent sinopulmonary infections
•
complicated by an increased risk for development of malignant lymphomas.
• Laboratory studies reveal low IgM levels and increased concentrations of IgG, IgA, and IgE.
•
Defects in CMI develop later in the course of the disease
Ataxia telangiectasia (AT) • Autosomal recessive disease consisting of cerebellar ataxia, prominent arteriolar telengectasia
•
(small collections of dilated blood vessels) around the eyes and on the skin, and severe
slnopulmonary disease.
• Chromosome instability syndrome.
•
• Increased susceptibility for chromosomal mutations owing to DNA enzyme repair defects, leading
•
to an increased risk for development of lymphomas or leukemias.
Disorders of the Complement System
• The complement system consists of proteins primarily synthesized by the liver as acute phase reactants. Complement
•
components augment vascular and cellular events in acute inflammation, lyse cells (bacteria), and participate in cytotoxic
immunity and immune complex hypersensitivity reactions.
• When activated, the classical and alternative pathways both converge on C3 and, along with C5 convertase, activate the
•
membrane attack complex (MAC), which is cytolytic.
• Decay accelerating factor (DAF) located on cell membranes enhances the degradation of C3 and C5 convertase, thereby
•
protecting the cell against MAC destruction.
• C1 esterase inhibitor exerts a negative control on the activation of Cl in the classical pathway.
•
– The concentration of C4 is used to evaluate the classical pathway, factor B the alternative pathway, and C3 either
–
system.
• Complement Disorders are Either Acquired (More leaves the hematopoietic cells (neutrophils. RBCs,
•
Common) or Inherited and platelets) susceptible to intravascular destruction
– Low complement levels are most commonly due to (pancytopenia) by MAC.
– C1 esterase inhibitor deficiency (e.g. hereditary
–
their utilization in antibody-complement reactions
–
angioedema) is an autosomal dominant disease that
(e.g., immune complex diseases). results in the excessive release of C2-derived kinins
– Paroxysmal nocturnal hemoglobinuria (PNH) (causing increased vessel permeability), leading to
–
is an acquired stem cell disorder associated with a swelling of the face and oropharynx (respiratory
membrane defect involving the loss of DAF, which embarrassment)
178
– C2 deficiency is the most common hereditary Successful transplantation requires

–
deficiency and is associated with an increased

compatibility of ABO blood groups, absence of
incidence of autoimmune disease (e.g, systemic lupus preformed anti- HLA cytotoxic antibodies In
erythematosus [SLE]). the recipient’s serum, and as close a match of
– C5-C8 deficiency is associated with disseminated III-A-A, -B, and -f) loci between recipient and
–
gonococcemia donor as possible
A lymphocyte crossmatch screens (or anti-HLA
• Major histocompatibility complex (MHC)

antibodies directed against donor lymphocytes.
•
– The MHC, known collectively as the HLA The HLA-A and-B derived class I antigens
–
(human leukocyte antigen) system, is located on on lymphocytes are Identified by serologic
chromosome 6 testing using known test sera (e.g., anti-HbVA3
GENERAL PATHOLOGY
– The gene products (class I and class II antigens) antibodies) and reacting individual antibodies
–
are membrane-associated glycoproteins that are against recipient and donor lymphocytes
located on all nucleated cells, where they serve as a (lymphocyte microcytotoxicity test)
marker of identity
– The HLA-A.-B. and-C gene loci code for class I Class II antigen (D loci) matching requires a mixed
–
antigens (recognized by CD8 cytotoxic T cells) that

lymphocyte reaction (MLR) whereby functional
are located on all nucleated cells (not mature RBCs) lymphocytes from (live recipient and previously
– The HLA-D,-DR.-DP. –DQ and -DO gene loci code irradiated (killed) donor lymphocytes are mixed
–
for class II antigens (recognized by CD4 helper T together with tritiated thymidine to detect the
cells) that are located on antigen-presenting cells degree of compatibility between their D loci
(macrophages, Langerhans’ cells in the skin, B cells, (increased radioactivity indicates Incompatibility)
and activated T cells).
To check for a graft-versus-host reaction the

recipient’s lymphocytes are irradiated (killed) and
– Class I MHC functional donor lymphocytes are reacted against
–
They are glycoproteins the host’s HLA- D loci

 
present on surface of all nucleated cells • Transplantation and transplantation rejection
•

Presents antigen to CD 8 positive cells • An autograft is a transplant of tissue from self to self, a
•

Have only one chain encoded by MHC locus. syngenic graft (isograft) is between identical twins, an

Antigen binding site on MHC I is proximal end of allograft is between unrelated Individuals, and a xenograft
is from one species to another (e. g. pig heart transplant)

alpha subunit of 1 and 2 (AIPG 2010)
– Class II MHC • The chance of a sibling having another sibling with a 0, 1,
•
–
They are glycoproteins present on the surface of or 2 haplotype match is 25%, 50%, and 25%, respectively

Macrophages, B cells, Dendritic cells of spleen (parents are a one haplotype match)
andLangerhans cells. • The three types of transplant rejection of an allograft are
Presents antigen to CD 4 positive cells
•
designated hyper acute, acute, and chronic rejection

Not Present on surface of nucleated cells

Have both chains encoded by MHC locus. Hyper acute • Usually occurs within minutes of

•
– Individuals inherit one HLA haplotype from each parent rejection vascular attachment of the allograft
–
in codominant fashion (both haplotypes are capable of (e g. kidney) owing to the presence
of ABO incompatibility or preformed
expressing themselves), which when combined, become cytotoxic antibodies directed against
the HLA genotype of the individual donor antigens, both of which produce
vessel injury and thrombosis (type II
hypersensitivity)
– Laboratory assessment In transplantation
–
HLA testing is useful in transplantation workups, Acute rejection • Most common type and usually surfaces

•
paternity suits, crossmatches for compatible within the first 3 months following
transplantation
platelets, and identification of patients who are
at risk for certain disorders (e.g., the association • Both cell-mediated (more important)
•
between HLA B-27 and ankylosing spondylitis). and antibody-mediated reactions occur
in the graft

• The antibody (humoral) component
LAKs produce extensive epithelial cell necrosis

in the biliary tract (jaundice), the skin (maculo-
•
produces a necrotizing vasculitis
with subsequent vessel damage papular rash), and the gastrointestinal tract
and intravascular thrombosis (type II (diarrhea).
antibody-mediated hypersensitivity Immunosuppressive therapy has increased the
reaction) or Intimal thickening with

obliteration of the vessel lumen “if the
incidence of cervical cancer, malignant lymphomas
graft is in place for a longer period of (immunoblastic), and basal and squamous cell
time. carcinomas of the skin (most common overall
malignancy).
• The CMI component is an interaction
•
between donor macrophages and host • Types of transplants
cytotoxic and helper T-cell that results
•
GENERAL PATHOLOGY
in an extensive interstitial infiltrate in – Corneal transplants have the best overall graft
–
the graft, edema, and cytokine damage survival rate.
to the tissue (type IV cell-mediated – Living donor renal transplants with a two
hypersensitivity reaction).
–
haplotype match have a >30% 5-year survival rate
• Acute rejection is potentially reversible that drops to 80% with a one haplotype match.
•
with the use of immunosuppressive – Cadaver transplants between unrelated donors
–
drugs as cyclosporin A (which blocks CD are the most common renal transplants and have
4 helper cell release of interleukln-2 [IL
2]), corticosteroids (lymphotoxic), and a survival rate similar to a one haplotype match,
OKT, a monoclonal antibody directed particularly If the patient receives multiple blood
against the CD3 antigen receptor) transfusions prior to the surgery (which possibly
Induces tolerance to the allograft)
Chronic rejec- • Irreversible and generally occurs over
– Bone marrow transplants are primarily used in the
•
tion months to years. Extensive fibrosis and
–
chronic ischemia due to vessel damage treatment of aplastic anemia, leukemia, and certain
with intima thickening and luminal types of immunodeficiencies.
obliteration mark the histologic findings.
– Donor marrow contains pluripotential hematopoietic
–
• The pathogenesis is not well stem cells that repopulate the lymphoid, erythroid,
myeloid, and megakaryocytic series in the recipient
•
characterized but involves the release
of growth factors from activated – The recipient assumes the ABO group of the donor.
macrophages.
–
• HLA haplotypes and disease relationships and risk
The GVH reaction is a potential complication in
•

– Patients with HLA-associated diseases have a familial

bone marrow and liver transplants and in blood
–
transfusions administered to patients with T-celI predisposition to the disease, weak penetrance (it does
not have to occur), and abnormalities in their immune
immunodeficiency conditions.
system that predispose to autoimmune diseases.
- The reaction is initiated when donor lympho-
– B Important HLA-disease relationships include

cytes produce IL-2, which activates host NK
–
hemochromatosis with HLA-A3 (risk 7%), celiac
cells (designated lymphokine-activated NK-
disease with HLA-B8 and-DR3 (risk 13%), ankylosing
cells, or LAKs), the primary effector cells in
spondylitis with IIU-B27 (risk 80%), multiple sclerosis
acute GVH reactions.
with HLA-DR2 (risk 3%).
Inheritance
Autosomal dominant (AD) inheritance Autosomal recessive (AR) disorder
• Vertical transmission through males and females • Are clinically expressed only in the homozygous state.
•
•
• Unless it is a new mutation, an affected person will have an • Offspring must inherit a copy of the disease causing allele from
•
•
affected parent each parent
• Either sex may be affected
•
• An affected parent has a 1 in 2 or 50% chance of having an
•
affected child
• In AD condition, obligate carrier is a person with affected parent
•
and child
180
PATHOLOGY OF BLOOD CELLS

GENERAL PATHOLOGY
Fig.4.2 Erythropoiesis
LUEKOCYTOSIS
Fig.4.3 Leukocytosis

Differential Count of Leukocytes and Normal Wbc Values (Dacie and Lewis 1984)
Normal WBC values Absolute count x 109/l
TOTAL LEUKOCYTE COUNT

• Infants (full term, at high) 10 – 25
•
• Infants (1 year) 6 – 18
•
• Childhood (4-7 years) 5 – 15
•
• Childhood (8-10 years) 4.5 – 13.5
•
• Adults 4 – 11
•
GENERAL PATHOLOGY
DIFFERENTIAL COUNT IN ADULTS (x 109/l)
• Neutrophils 2 – 7.5 (40 – 75%)

•
• Lymphocytes 1.5 – 4 (20 – 50%)
•
• Monocytes 0.2 – 0.8 (2 – 10%)
•
• Eosinophils 0.04 – 0.4 (1 – 6%)
•
• Basophils 0.01 – 0.1 (<1%)
•
Biochemical Characteristics of Neutrophils
• Active glycolysis
•
• Active HMP shunt
•
• Moderate oxidative phosphorylation
•
• Rich in lysosomes and their enzymes
•
• Contain unique enzymes like NADPH oxidase
•
• Contain CD11/CD18 integrins
•
Causes for leucocytosis
Malignant Acute and chronic lymphatic leukemia, non hodgkins lym-

phomas
Infections Epstein barr virus infections
Cytomegalovirus

HIV, hepatitis

Herpes simplex

Measles ,mumps, chickenpox,

Miscellaneous Thyrotoxicosis
Causes of Neutrophilia
• Infection • Bacterial
•
•
• Inflammation • Rheumatoid arthritis
•
•
• Trauma
•

• Drugs • Steroids
•
•
• Malignant diseases • Gastric, bronchogenic , breast
•
•
• Metabolic diseases • Renal failure and acidosis
•
•
182
Causes for Eosinophila

• Parasitic infections • Hookworm diseases, scabies
•
•
• Allergic disorders • Hay fever, asthma
•
•
• Skin disorder • Dermatitis herpetiformis, psoriasis
•
•
• Tumours • Lymphoma, carcinomatosis
•
•
• Sarcoidosis
•

• Polyartheritis nodosa
GENERAL PATHOLOGY
•

• Respiratory tract infections • Eosinophilic pneumonia
•
•
• ASPA
•
• Cystic fibrosis
•
• GIT disease • Coeliac disease
•
•
• Inflammatory bowel disease
•
• Neoplastic • Eosinophil leukemia
•
•
• Lymphoma
•
• CML
•
• Vascular • Polycythemia (AIPG 2001)
•
•

Causes of Eosinopenia
• Adrenal steroids
•
• ACTH induced eosinopenia
•
Causes for Basophilia
• Myeloproliferative Diseases
•

• Carcinoma
•

• Hypothyroidism
•

• Ulcerative Colitis
•

• Infections Influenza, Chicken Pox, Tuberculosis
•
Causes For Luecopenia
Drugs Phenylbutazone Oxyphenylbutazone, Penicillamine, Antithyroid Drugs, Antiarrhythmic Drugs,
Antidepressants, Sulphonamides Cephalosporins
Infections Viral: Hepatitis
Bacterial: Mililary TB, typhoid,
Systemic Lupus Erythematosus
Megaloblastic Anemia

Causes For Leukemia
Factors associated with the development of leukemia
• Ionizing Radiation: Atomic bombs explosion, repeated x ray exposure.

•
• Cytotoxic Drugs
•
• Exposure To Benzene In Industry
•
• Retroviruses
•
• Immunological Diseases
•
GENERAL PATHOLOGY
Causes For Thrombocytosis
Reactive thrombocytosis Malignant thrombocytosis
• Chronic inflammatory disorders Essential thrombocythaemia

•
• Malignant disease Polycythaemia rubra vera
•
• Tissue damage Myelofibrosis
•
• Heamolytic anemias Chronic myeloid leukemia
•
• Post splenectomy
•

• Post heamorrhage
•
Monocytes are increased in (AIIMS Nov 2010) Monocytes are decreased in
• Tuberculosis Acute infection

•
• Brucellosis Stress
•
• SABE Glucocorticoid therapy
•
• Rocky Mountain fever Aplastic anemia
•
• Malaria Hairy cell leukemia
•
• Kala azar Treatment with myelotoxic drugs
•
• Granulamatous disease – Sarcoidosis and Regional enteritis
•
• Some collagen vascular disease
•
• Malignancies – Leukemias (AML, CML)
•
• Myeloproliferative disorders (monocytic, Myelomonocytic
•
leukemia)
• Lymphocytic tumors (Hodgkins, Multiple Myeloma etc)

•
• Hemolytic anemia
•
• Chronic idiopathic neutropenia
•
• Post splenectomy
•
184
Neutrophil functional disorders can be classified as:

GENERAL PATHOLOGY
Neutrophil defects: Qualitative Functional Disorders

Disease Entity Neutrophil Deficit Lab Test Clinical features
1 Chediak – Higashi Altered migration, Peripheral blood smear, NBT Aggressive periodontitis, oral
Syndrome degranulation and Test ulceration, Oculocutaneous albinism,
phagocytosis, secondary to recurrent infection, bleeding
megabodies tendencies.
2. Chronic Defective NADPH oxidase, NBT Test, Flow cytometry Recurrent bacterial and fungal
granulomatous with impaired intracellular infection, gingivitis, / periodontitis
disease killing
3. Hyperimmunoglobulin Reduced chemotaxis Elevated serum IgE, Rebuck Cold abscesses, deep set eyes,
E (Job) syndrome skin window, Boyden Chamber gingivitis, oral ulcerations
4. LAD – I Impaired adherence, Rebuck skin window, Boyden Severe periodontitis, fiery red mucosa
phagocytosis, deficiency in chamber, Flow cytometry
CD18 or CD11b integrin
LAD – II Impaired rolling, selectin Rebuck skin window, Boyden Short stature, mental retardation,
deficiency chamber, Flow cytometry periodontitis
5. Papillon Lefevre Defects in chemotaxis, killing Chemotactic tests, Phagocytic Aggressive periodontitis, palmoplantar
syndrome and phagocytosis tests keratosis
6. Down’s Syndrome Defects in chemotaxis, Killing Chemotactic tests, Phagocytic Mental retardation, increased
and phagocytosis tests susceptibility to infection
7. Lazy Leukocyte Neutropenia, depressed Absolute neutrophil count Recurrent infection, gingivitis,
Syndrome chemotaxis periodontitis
8. Myeloperoxidase Unable to oxidise Cl- ions, Peroxidase staining of blood Generally benign, with increased
deficiency unable to produce HOCl with films, Flow cytometry , Enzyme susceptibility to fungal infections.
impaired intracellular killing assay
9. Glycogen storage Neutropenia, defective Absolute neutrophil count, NBT “Doll like” Facial features, bleeding
disorder type 1b migration and chemotaxis, tests chemotaxis test episodes
altered respiratory burst

Disease Entity Neutrophil Deficit Lab Test Clinical features
10. Acatalasia Catalase deficiency Catalase assay Oral ulceration, increased risk from
type II diabetes
11. Diabetes mellitus Decreased chemotaxis, Blood sugar level, Glucose Increase prevalence and severity
adherence and phagocytosis Tolerance Test, Glycosylated of gingivitis, increased periodontal
hemoglobin level destruction.
Drugs Associated with Neutropenia

1. Antipyretic and NSAIDS
Aminopyrine
GENERAL PATHOLOGY
Phenylbutazone
Indomethacin
2. Tanquilizers
Chlorpromazine
Promazine
Other Phenothiazines
3. Anticonvulsants
Carbamazepine
4. Antithyroid drugs
Propthiouracil
Carbimazole
Methimazole
5. Antibiotics and Antimalarials

Dapsone
Sulphonamides
Methicillin
6. Diuretics and Antihypertensives

Thiazides
Captopril
HEMOPOIETIC GROWTH FACTORS

Growth factors Site of action
• Interleukin-1 (IL), Tumor Stromal cells and bone marrow

•
necrosis factor
• SCF Pleuripotent cells
•
186
Growth factors Site of action
• IL-3, IL-6, GM-CSF Early multipotent cells

•
• G-CSF, M-CSF, IL-5 ,EO Late cells committed to one or two lineages
•
– CSF, Erythropoietin,
Thrombopoietin
Hemopoietic Growth Factors are Mainly Produced by the following cells

• Endothelial cells
•
• Fibroblasts
GENERAL PATHOLOGY
•
• Monocytes and macrophages
•
• T lymphocytes
•
• Kidney (produces 90% of erythropoietin).
•
Functions of Hemopoietic Growth Factors
• Stimulate differentiation and proliferation of committed marrow precursors

•
• Affects the function of mature cells on which they act by phagocytosis, superoxide generation and cytotoxicity (in the
•
case of neutrophils).
• Affect membrane integrity and surface adhesion properties of their target cells
•
• GM-CSF immobilise phagocytes causing their accumulation at local sites of inflammation
•
• Non–specific growth factors like IL–08 stimulates neutrophil chemotaxis and migration across endothelial membrane
•
• GM–CSF potentiates viability and microbial killing and the production of cytokines by mature neutrophils monocytes
•
and eosinophils
• Inhibit apoptosis of target cells
•
Also note
(Thalassemias–Hypochro- Sickle cell anaemia–Normochromic and noromcytic
mic microcytic)
Tear drop cells (macro- Thalassaemia and myelofibrosis

cytes)
Sickle cells (drepano- Sickle cell anaemia

cytes)
Rouleaux (“stack of Refers to RBCs lining up in a row. Rouleaux are characteristic of multiple myeloma
coins”)
Bite cells RBCs with ‘bites’ of cytoplasm being removed by splenicmacrophages. Bite cells may be seen in G6PD
deficiency.
Target cells Is a form of leptocyte seen in iron deficiency anaemia and thalassaemia, and severe liver diseases
Anisocytosis • Increased variation in size of the red cell is termed as anisocytosis

•
• Production of large cells is called macrocytosis, Eg: Megaloblastic Anaemia
•
• Production of small cells is called microcytosis. E.g.: Iron deficiency anaemia, thalassaemia,
•
spherocytosis.
Poikolocytosis Increased variation in shape of RBC. E.g.: Megaloblastic anaemia, Iron deficiency anaemia, thalassaemia

Spherocytosis • Presence of spheroidal rather than bi-concave disc- shaped red blood cells.
•
• Seen in hereditary spherocytosis.
•
Schistocytosis • Fragmentation of erythrocytes
•
• Seen in thalassaemia, megaloblastic anaemia, iron deficiency anaemia.
•
Leptocytosis • Presence of unusually thin red cells. E.g.: Severe iron deficiency anaemia and thalassaemia.
•
Stomatocytosis • Presence of stomatocytes, which have central area having slit-like or mouth-like appearance.
•
• Found in alcoholism or as an artifact
•
GENERAL PATHOLOGY
Red Cell Inclusions
Basophilic stippling • Results from cytoplasmic remnants of RNA. May indicate Reticulocytosis or lead poisoning.
•
Howell-Jolly bodies • Are remnants of nuclear chromatin. May occur in severe anaemias or patients without spleens.
•
Pappenheimer bodies • Are composed of iron. May be found in the peripheral blood following splenectomy.
•
Ring sideroblast • Iron trapped abnormally in mitochondria, forming a ring around nucleus. can be seen in sideroblastic
•
anaemia.
Heinz bodies • Denatured haemoglobin. Can be seen with G6PD (glucose-6- phosphate dehydrogenase) deficiency.
•
Procoagulant States: Anti coagulant factors Hyperviscosity
• Factor V (Leidein mutation) • Antithrombin III • Multiple myeloma (PGI 2004)

•

•
•

(AIIMS 2003)

• Protein C deficiency • Protein C • Cryoglobinemia (PGI 2003)
•

•
•

(PGI 2003, AIIMS May 2013)

• Protein S deficiency (PGI 2003) • Protein S • Myeloproliferative disorders
•

•
•
• Homocystenemia • Prostacyclin
•
•
• Antiphospholipid antibody • Nitric oxide
•
•
CARDIOVASCULAR PATHOLOGY
• Normal hemostasis
•
– Endothelial cells provide an anticoagulant function in the uninjured state and a procoagulant role when injured.
–
They synthesize anticoagulants such as tissue plasminogen activator (tPA), which activates plasminogen to

produce plasmin, a fibrinolytic agent, and prostacyclin (PGI2; a vasodilator and inhibitor of platelet aggregation),
which derives from the action of cyclooxygenase on arachidonic acid.
They synthesize von Willebrand’s factor (Vlll:vWF). a procoagulant that binds to glycoprotein receptor Ib

(GP1b) on the platelet membrane producing platelet adhesion in areas of endothelial injury.
Exposure of subendothelial tissue after injury not only produces platelet adhesion but also leads to activation of

factors XII and XI (by exposure of collagen) in the intrinsic coagulation system and factor VII in the extrinsic
system by tissue thromboplastin released by the injured endothelial cells.
– Platelets derived from cytoplasmic fragmentation of megakaryocytes are released into the circulation (150,000-400,000
–
ceIIs/m-L), where they live for 9-10 days.
One third of the total platelet pool is stored in the spleen and exchanges freely with the circulating pool.

GP1b and fibrinogen (GPlIb/llla) receptors are present on the platelet surface.

188
The platelet membrane contains platelet factor – Vascular disease (e g. scurvy)

–
3 (PF3), which is the phospholipid substrate – Thrombocytopenia (fewer platelets available for
–
upon which the clotting sequence must occur. aggregation)
Platelet adhesion is a stimulus for the conversion – Von Willebrand’s disease (VWD) (absence of
–
of arachidonic acid to thromboxane A2 (TXA2; a factor VIII antigen, clot promoting factor and von
platelet aggregator and vasoconstrictor) and the willebrand’s factor) (AIPG 2005)
release of chemicals (release reaction) from alpha – For patients on aspirin or other NSAIDs (which
–
granules (e g., VIIl:vWF. Fibrinogen) and from inhibit TXA formation), this being main cause of
dense bodies (e.g., ADP, calcium). prolonged BT.
Platelet cyclooxygenase is more susceptible to
• Platelet aggregation studies evaluate the in vitro

inactivation by aspirin (Irreversible) and NSAIDs
GENERAL PATHOLOGY
•
(reversible) than is endothelial cell cyclooxygenase, response of platelet-rich plasma to aggregating agents
underscoring the role of the former in inhibiting (e g. ADP)
platelet aggregation. – The ristocetin aggregation test evaluates the
–
After platelets aggregate in the vessel lumen interaction of circulating VII vVWF (derived from

(induced by TXA, and ADP), fibrinogen molecules endothelial cells) with the antibiotic ristocetin, which
attach to GPIIb/llIa, leading to the formation of a facilitates binding of the factor to platelets, leading
primary hemostatic plug, which stops small vessel to aggregation, hence providing documentation of
bleeding an intact VIII vWF/GPlb receptor system
– The ristocetin cofactor assay is the single best test
– Plasma proteins provide procoagulants
–
for diagnosing von Willebrand’s disease.
–
(coagulation factors, tissue thromboplastin),
anticoagulants (antithrombin III, proteins C and S),
fibrinolytic proteins (plasmin), and complement. Coagulation System Tests
Anticoagulants Include antithrombin III
• The prothrombin time (PT, 11-15 seconds) evaluates the

(ATIII), protein C, and protein S.
•
integrity of theextrinsic system down to the formation
Heparin markedly enhances AT111 activity,
of a clot.

which has an inhibitory effect on serine
proteoses (particularly thrombin and factor X). • The international normalized ratio (INR) is employed
•
Proteins C and S inactivate factors V and VIII to standardize the reporting of PT results in patients

and enhance fibrinolytic activity. taking warfarin owing to different reagents used.
– The fibrinolytic system breaks down the stable clot • The PT is the most sensitive test for the following
–
in order to restore blood flow.
•
measurements:
It is activated primarily by the action of
– Detecting final common pathway deficiencies

tPA on plasminogen to form the enzyme
–
plasmin. Plasmin acts on clot-associated fibrin (factor X – clot)
monomers as well as circulating fibrinogen and – Confirming factor VII deficiency
–
clot associated fibrinogen to produce fibrinogen – Following patients on warfarin therapy
–
degradation products X, Y, D and E. – Evaluating severity of liver disease.
–
• The activated partial thromboplastin time (aPTT; 25 –
•
Laboratory Evaluation of Hemostasis 35 seconds) evaluates the intrinsic system down to the
formation of clot (XII – XI-IX-VIII-X-V-II-I-clot) and
• Platelets tests are quantitative (e.g. platelet count) or test is also the test of choice for monitoring heparin therapy.
•
platelet function (e g . bleeding time).The bleeding time
• Factor assays are available for most coagulation factors:
(BT; < 10 minutes), evaluates vessel integrity and platelet
•
function up to the formation of the primary hemostatic – In addition to VIII vWF, other factor VIII assays
–
plug, which coincides with the cessation of bleeding in the are available to help distinguish von Willebrand’s
test. disease and hemophilia A.
• It is normal in coagulation factor deficiencies (e.g., – Immunologic assays measure the concentration of
–
VIII: antigen (VIII: Ag), which is a carrier protein
•
hemophilia A), since the coagulation system is most
responsible for the stable clot. for circulating VIII: vWF, and VIII: Coagulant
(VIII:C) in the intrinsic system.
• It is prolonged in the following disorders:
•

• Mixing studies differentiate true factor deficiencies or qualitative (functional) abnormalities (e.g., aspirin
inhibition of platelet aggregation).
•
from factor deficiencies secondary to destruction by
antibodies (inhibitors). • Thrombocytopenia (too few platelets) may result from
•
decreased production, increased destruction, or abnormal
• Fibrinolytic system tests
distribution (e.g., splenomegaly).
•
– Degradation products (FDPs) X, V, D), and E
– Production disorders are those which interfere with
–
ofplasmin-mediated cleavage of fibrinogen clot-
–
thrombopoiesis (e.g., aplastic anemia due to a drug,
associated fibrinogen, or clot-associated fibrin
leukemia).
monomers are detected by agglutination tests.
– Destruction disorders are broadly subclassified as
– The D-dimer assay specifically detects clot associated
–
Immune or nonimmune
–
fibrin degradation products that have been cross
Idiopathic thrombocytopenic purpura (ITP)
GENERAL PATHOLOGY
linked by factor XIII, hence distinguishing them

is an autoimmune disease characterized by the
from the X, Y, D and E fragments, which derive
development of IgG antibodies against GPIIb/IIIa
from breakdown of circulating fibrinogen. receptor on platelets with subsequent removal of
thesensitized platelets by splenic macrophages (a
• Physical findings in hemostasis disorders:
type II hypersensitivity reaction).
•
– Vascular and platelet abnormalities are characterized - Megakaryocytes are present in the marrow,
–
by the following signs: but the platelets are peripherally destroyed by
Epistaxis (nose bleeds, the most common
the spleen (which usually is normal In size).

manifestation) - High-dose corticosteroids are used to treat
Easy bruising
symptomatic patients, and recovery is the rule

Cutaneous bleeding
within 4 to 6 weeks

- Petechiae ( 1 to 3 mm pinpoint hemorrhages) Autoimmune thrombocytopenias associated with
- Ecchymosis (purpuric lesions about the size of

systemic lgG-mediated immune disease (e.g..
a quarter) systemic lupus erythematosus) are insidious in
Prolonged bleeding from superficial scratches
onset and tend to persist in spite of corticosteroid

– Coagulopathies are associated with the following therapy, splenectomy or immunosuppressive
–
conditions: therapy.
Bleeding after molar extraction
Virus-associated Immune thrombocytopenia

Delayed bleeding after surgery

(immunocomplex or antibody destruction of

Hematuria or gastrointestinal bleeding
platelets) may accompany cytomegalovirus,

Bleeding into tissues (muscle) or spaces (joints)
Infectious mononucleosis, and HIV Infection

Drug-Induced autoimmune thrombocytopenia
• Vascular disorders

(most commonly due to drug-dependent
•
– Hereditary hemorrhagic telangiectasia (Osler- IgG antibodies) may occur with exposure to
–
Weber Rendu disease) I an autosomal dominant quinidine, sulfa compounds, penicillin, heparin,
disease that presents with epistaxis and and thiazides.
telangiectasisas (dilated vascular channels) in the Autoimmune thrombocytopenias are a group
mouth and gastrointestinal tract (bleeding with

of disorders in which the host develops IgG
iron deficiency) antibodies after exposure to foreign antigens (e.g.,
– Acquired vascular disorders include the following; platelet HLA or PLA1 antigens) from another
–
Scurvy, with defects in collagen synthesis. individual (e.g., a fetus or blood product).

Hypercortisol states, with defective collagen Thrombotic thrombocytopenic purpura (TTP) a

synthesis.

nonimmune thrombocytopenia, occurs mainly
Senile purpura (atrophy of perivascular in young women and is characterized by the

support). following pentad:
Henoch-Schonlein purpura, an immune - Severe thrombocytopenia;

complex vasculitis with palpable purpura (due - Microangiopathic hemolytic anemia, in which
to Inflammation). schistocytes (fragmented RBCs) are present;
- Neurologic abnormalities (often severe):

• Platelet disorders: Platelet disorders are quantitative - Renal failure (usually mild); and
•
abnormalities (e.g., thrombocytopenia, thrombocytosis) - Fever.

190
It is secondary to endothelial damage small Normal PT

vessels by an unknown circulating factor in Normal BT (no platelet defects).

plasma, leading to widespread platelet thrombus Immediate increase in the synthesis of new VIII:

formation (not a fibrin clot as in DIC) and C after infusion of products containing factor VIII
thrombocytopenia (platelet consumption) that is not in excess of amount of factor VIII
Obstruction of the microvasculature by platelet infused.

thrombi damages RBCs (intravascular hemolysis) – Depending on the severity of disease, treatment
–
and produces widespread organ injury includes replacement therapy (lyophilized factor VIII
– The hemolytic uremic syndrome (HUS), a concentrate, which has a small risk of transmitting
–
nonimmune thrombocytopenia, occurs primarily In HIV infection; recombinant factor Vlll, which carries
infants and young children and is clinically similar no risk of HIV infection; or desmopressin in mild
GENERAL PATHOLOGY
to TTP except for milder neurologic abnormalities, cases to increase the synthesis of all the factor VIII
more severe renal disease, and in some cases a history components).
of exposure to a toxin produced by E coli serotype
0157:H7 consumed in raw ground beef. • VWD is the most common hereditary bleeding
•
disorder.
• Thrombocytosis (too many platelets; >100,000 cells/ – Classical type 1 VWD (75-90% of cases) is inherited
•
–
uL) may be associated with chronic iron deficiency as an autosomal dominant disease.
anemia, splenectomy, tuberculosis, or an underlying – VWD presents with signs related to a platelet
–
malignancy. adhesion defect (epistaxis, Increased bruising,
• Qualitative (functional) platelet disorders can be menorrhagia) or coagulation deficiency
•
hereditary or acquired (more common). (gastrointestinal bleeding often associated with
– The BT is prolonged regardless of the platelet count. angiodysplasia).
– Laboratory findings Include the following;
–
– Drugs that Inhibit platelet function (e.g., aspirin)
–
Prolonged BT.
–
are the most common cause of platelet dysfunction.

– Platelet dysfunction (prolonged BT) is the most Prolonged aPTT with a normal PT

Low percent activity for factors VIII:vWF,
–
common acquired defect in uremia and frequently

complicates liver failure(FDPs inhibit platelet VIII:C (< 40% of normal), and VIII:Ag.
aggregation), multiple myeloma (excessive Slow but sustained Increase in new factor VIII

immunoglobulins inhibit platelet aggregation), synthesis that is greater than the amount of
vWD and the myeloproliferative diseases (.e.g.. factor VIII infused.
polycythemia rubra vera). – Cryoprecipitate (a single donor component
–
– Hereditary disorders affect either platelet adhesion containing factors VIII:vWF, VIII:C) is the
mainstay of treatment, while desmopressin and
–
(e.g.. vWD) or platelet aggregation (e.g. storage
pool defects, with deficiency of ADP). estrogen/progestrin compounds are useful in mild
cases (estrogen increases factor VIII synthesis)
(AIIMS May 2013)
Coagulation disorders

• Coagulation disorders can be either hereditary (usually
• Hemophilia B (factor IX deficiency, Christmas disease)
•
single deficiencies) or acquired (e g., defective production,
•
has an SXR inheritance pattern, a prolonged aPTT and a
pathologic inhibition, or consumption).
similar clinical presentation to hemophilia A.
• Hemophilia A is a sex linked recessive (SXR) disease
• Circulating anticoagulants are antibodies (inhibitors)
•
transferred to males from female carriers who transmit
•
against certain coagulation factors that render those
the disease to 50% of their sons and to 50% of their
factors inactive, hence the confusion with a coagulation
daughters (who will be carriers).
deficiency.
– The abnormal site on the X chromosome can be
– Factor VIII inhibitors are the most common
–
detected prenatally using restriction fragments length
–
inhibitors and are associated with postpartum state,
polymorphism (RFLP)
chlorpromazine therapy, and factor VIII treatment of
– Laboratory findings include: (AIIMS May 10)
hemophilia A patients.
–

Deficiency of factor VIII:C (coagulant factor)
– Factor V inhibitors are encountered with streptomycin

Normal VIII:vWF levels
–
or aminoglycoside therapy, while factor XIII inhibitors

Prolonged aPTT


are sometimes noted in patients taking isoniazid. by laboratory evidence of activation of the procoagulant
– Mixing studies do not correct the prolong PT or aPTT and fibrinolytic systems, resulting in end organ damage
–
– The lupus anticoagulant (LA) and anticard lipin or failure.
–
antibodies (ACA) are associated with antiphospholipid – Precipitating factors include the following:
(APL) syndrome.
–
Septicemia
They belong to a family of antibodies that react

Obstetrical problems

to phospholipids bound to plasma proteins (e.g.

Hemolytic transfusion reactions
coagulation factors)

Massive trauma (e.g., release of tissue
APLs occur in about 25% patients with SLE, but

thromboplastin).

they are also present in AIDS, other autoimmune
Malignancy (e.g., acute progranulocytic leukemia,
diseases, malignancy, old age, patients taking

metastatic carcinoma).
GENERAL PATHOLOGY
drugs such as chlorpromazine and procainamide.
APLs damage endothelial cells, predisposing the
– The pathophysiology of DIC initially involves
–
activation of the coagulation and fibrinolytic systems

patient to vessel thrombosis
LA act against PF3 in the prothrombin complex, by one of the above precipitating factors.
– The coagulation system is responsible for the

causing a prolongation of the aPTT (90%) and PT
–
(20%) following:
ACA reacts against the cardiolipin in the RPR Activating the kinin system (to increase vessel

and VDRL test system, producing a biologic false permeability and vessel dilation, leading to shock)
positive syphilis serology (FTA-Abs is negative) Generating massive quantities of thrombin

to form fibrin clots (thrombin deposits in the
• Vitamin K deficiency produces a hemorrhagic microcirculation and consumes platelets and
•
diathesis as a result of multiple coagulation defects. coagulation factors).
Vitamin K is a fat soluble vitamin that converts the Activating the fibrinolytic system (factor XII,
precursor vitamin K dependent factors II, VII, IX, X,

kinins) leading to the formation of plasmin
protein C, and protein S into functional coagulation – Plasmin does the following:
factors by posttranslational γ carboxylation of glutamyl
–
Activates the complement system (anaphylatoxins
residues in the N terminal portion of the proteins.

C3a and C5a cause mast cell release of vasoactive
– Epoxide reductase catalyzes the conversion of the amines that produce increased vessel permeability
–
relatively inactive K2 to the more active vitamin K1, and vasodilatation, leading to shock)
which is responsible for γ carboxylation process. Cleaves fibrinogen and fibrin clot Into X, Y, D
– The activated factors have the following biological

and E degradation products (which interfere with
–
half lives: factor VII and protein C, 6 hours; factors normal clot formation and platelet function)
IX and X, 24 hours; ad factor II (prothrombin), 60 Degrades clotting factors (causing multiple factor
hours.

deficiencies).
– Vitamin K is obtained from the diet and also Cleaves fibrin clots to form D-dimers
–
synthesized by colonic bacteria

– The result of all these interacting events Is a
– Causes of vitamin K deficiency include the
–
combination of thrombosis and bleeding.
–
following: – Patients present with the following signs:
Fat malabsorption (e.g. due to celiac disease,
–
Widespread oozing of blood from wounds and

bile salt deficiency or pancreatic disease)

venipuncture sites.
Use of broad spectrum antibiotics, which Subcutaneous bleeds and ecchymosis.

destroy colonic bacteria.

Anemia secondary to damage of circulating
The newborn state (bacterial colonization

RBCs by fibrin clots (microangiopathic hemolytic

is lacking at birth and there is a danger of anemia with schistocytes) and blood loss.
hemorrhagic disease unless the newborn is Widespread organ dysfunction Involving the
treated with intramuscular vitamin K)

kidneys (renal failure), lungs (adult respiratory
– Coumarin derivatives, which inhibit epoxide distress syndrome), and CNS (stroke).
–
reductase. – Laboratory abnormalities include the following:
–
(AIIMS May 2013)
• Disseminated intravascular coagulation (DIC) is an

Prolonged PT and aPTT (due to clot consumption
•
intravascular thrombohemorrhagc disorder characterized

of fibrinogen. V, VIII, and prothrombin)
192
Elevation of fibrinopeptide A (a cleavage product A forward type does not determine the genotype

of fibrinogen). (true genetic makeup) of the patient’s blood
Increased PF4 (an indicator of platelet group; for example, an AA or an AO individual

activation). is phenotypically (thephenotype is the physical

Presence of D-dimers and fibrinogen degradation
expression of the genotype) blood group A.

products.
The genotype can be derived in families where the
Decreased ATIII concentration (ATIII Is used In

AB0 status is available for parents and children;

the neutralization of serine proteases)
Thrombocytopenia (due to platelets consumed In for example, if an A mother and a B father have
an O child, then the parents must be genotypically

the clots).
– The sine-quo-non for the treatment of DIC Is to treat AO and BO.
–
the underlying disease in conjunction with ancillary
GENERAL PATHOLOGY
treatment consisting of the following: – In transfusion therapy, the ABO system must
–
Subcutaneous low-dose heparin which blocks be appropriately matched between recipient and

thrombin and other serine proteases, hence donor.
reducing clot formation. For example, a blood group A person, who has
Blood component therapy (plasma, platelets, fresh

anti B IgM isohemagglutinins can receive only

frozen plasma concentrate)
A or O blood.
Individuals with blood group O can receive
TRANSFUSION DISORDERS

only O blood owing to the presence of anti A
IgM and anti A,B IgG in their serum, which
• ABO blood group system (NEET 2013) would destroy cells with A or B antigen on their
•
– The ABO system is the product of one gene locus surface.
–
having specific genes which code for transferases Blood group O (universal donor) packed RBCs

that attach antigenically different carbohydrate may be transfused into patients of any blood
moieties to the terminal end of H antigen protruding group owing to lack of A and B antigens on the
from the surface of the RBC membrane RBCs.
The H gene codes for a transferase that attaches

fucose to the terminal end of a glycolipid to • ABO incompatibility and Rh hemolytic disease of the
•
produce H antigen. newborn ABO incompatibility is the most common cause
The A gene codes for a transferase that attaches of HDN, anemia in the newborn, and jaundice in the first

N-acetylgalactosamine to the H antigen, 24 hours after birth.
thereby producing A antigen (blood group A)
– It occurs in <25% of normal pregnancies and
The B gene codes for a transferase that attaches
–
invariably involves an 0 mother with an A or B baby,

galactose to H antigen to produce B antigen
(blood group B) since O individuals already have anti-A,B IgG in their
The O gene is inactive, hence neither A nor B plasma that is capable of crossing the placenta and

antigens are on the surface of blood group O attaching to fetal RBCs surfaced by A or B antigen.
RBCs. – The sensitized fetal RBCs are removed extravascularly
–
Group AB individuals have H antigen that by macrophages in the fetal spleen, liver, and bone

carries either A or B active sugars marrow, resulting in anemia and an increase in
The A and B antigens are also located on cells unconjugated bilirubin, the latter metabolized by the

other than RBCs (e.g. sperm, squamous cells, mother’s liver.
and neoplastic cells). – After delivery, the baby’s immature liver enzymes are
An individual receives one blood group antigen
–
unable to handle the increased unconjugated bilirubin

from the mother and one from the father
load, resulting in jaundice shortly after birth (not at
– In the laboratory, a forward type identifies the blood birth).
– ABO incompatibility may occur during the first or
–
group antigen on the surface of RBCs by using anti-A
–
and anti-B test serum, while a back type reacts A any other pregnancy involving a baby with blood
and B test RBCs against patient serum lo identify the group A or B antigens on its RBCs.
isohemagglutinins that correspond with the blood – ABO incompatibility protects against Rh sensitization,
–
group. since any fetal Rh-positive cells entering the maternal

circulation are immediately destroyed by the O derived anti-A,B IgG antibodies in the newborn’s
mother’s anti-A IgM and anti-B IgM antibodies. serum.
– Abnormal laboratory tests in newborns with ABO – Treatment usually utilizes phototherapy, with
–
ultraviolet light oxidizing unconjugated bilirubin in
–
incompatibility include spherocytes in the peripheral the skin to harmless w.ater-soluble dipyrroles that are
blood, a weakly positive direct Coombs’ test, and a eliminated in the urine.
positive indirect Coombs’ test secondary to maternally – Exchange transfusions are not usually required.
–
• Rh hemolytic disease of the newborn is most commonly due to anti-D antibodies that have developed in a woman from
•
exposure to Rh-positive RBCs in a previous pregnancy or blood transfusion.
– An Rh-negative woman who is carrying an Rh-positive infant for the first time does not haveto worry about her
GENERAL PATHOLOGY
–
newborn developing HDN, however, if she becomes sensitized (develop anti-D) in that pregnancy, the risk for HDN
and the severity of HDN increase withsubsequent pregnancies.
– Anti-D lgG antibodies in the mother in subsequent pregnancies will cross the placenta and attach to fetal Rh-
–
positiveRBCs when they are removed by macrophages, leading to anemia. and unconjugated hyperbilirubinemia.
– If the degree of anemia is severe, extramedullarly hematopoiesis (RBC production in the spleen, liver, etc.) may occur
–
as compensation, as well as cardiac failure, resulting in generalized edema in the fetus (hydrops fetalis)
– After delivery, the immature liver conjugation systems are overwhelmed, producing a rapid increase in unconjugated
–
bilirubin in the blood.
– Fetal albumin binding sites become fully saturated by the unconjugated bilirubin, hence increasing the free (unbound)
–
lipid-soluble unconjugated bilirubin, which crosses the immature blood-brain barrier and deposits in the lipid-
soluble brain to produce a condition called kernicterus.
– During pregnancy. Rh-negative women without anti-D antibodies are given a standard dose of Rh immunoglobulin
–
(RhIg) containing purified IgG anti-D antibodies at 28 weeks’ gestation, thereby reducing the chance for sensitization
by 90%.
– Rh-negative and anti-D-negative women who have not received RhIg during their pregnancy and who deliver Rh-
–
positive babies are still (Modulates for RhIg immunization (passive immunization).
– The amount of fetal blood in the mother’s circulation is determined by the Kleihauer-Betke test, which detects fetal
–
Hb in fetal RBCs.
– An estimate of the amount of fetal RBCs in the mother’s circulation is calculated so that the appropriate amount of
–
RhIg is administered intramuscularly within 72 hours following delivery.
– RhIg may work because the anti-D antibodies attach to fetal Rh-positive cells, resulting in their premature destruction,
–
or the antibody may cover the antigen, preventing its exposure to the mother’s immune system
RESPIRATORY PATHOLOGY Hyaline Membrane Disease

Cheyne-Stokes Respiration/Periodic Respiration/ • Due to deficiency of surfactant secreted by type 2
•
Cyclic Respiration pneumocytes.
• This is common in advanced Heart Failure and is usually • There is a formation of hyaline membrane composed
•
of fibrin, necrotic epithelial debris and exudative
•
a/w low cardiac output.
• It is caused by a ↓sensitivity of the respiratory center to proteins in alveolar ducts and airspaces. Hence also
 
called hyaline membrane disease
•
arterial PCO2.
• There is an apneic phase, during which the arterial
•
PO2 falls and the arterial PCO2 rises. These changes in
the arterial blood gas content stimulate the depressed Emphysema (Pink Puffer)
 
respiratory center, resulting in hyperventilation and
hypocapnia, followed in turn by recurrence of apnea. • Emphysema is the abnormal permanent enlargement of
•
 
• It may be perceived by the patient or the patient’s family air spaces distal to the terminal bronchioles, with alveolar
wall destruction and minimal fibrosis.
•
as severe dyspnea or as a transient cessation of breathing.
194
Types of emphysema Pathology Clinical features

Centriacinar emphysema – Excess activity of protease and elas- – Dyspnea,
–
–
tase resulting in permanent enlarge-
ment of distal airspaces with de-
struction of alveolar walls; smoking
inactivates α-1-AT.
– Dilatation of respiratory bronchioles –– ↓FEV1
–
– Involves upper lobes and apices –– ↓FVC
–
– Seen in male smokers. Panacinar –– ↑TLC
–
 
emphysema
GENERAL PATHOLOGY
– Uniform destruction and enlargement – Barrel chest, hypoxia,

–
–
of acinus
– More common in lower basal zones – respiratory acidosis, pulmonary hy-
–
–
 
pertension, cor pulmonale.
– Strong a/w α-1-AT deficiency. Para-
–
 
septal emphysema
– Involves the distal acinus, sparing the

–
proximal
– Common adjacent to the pleura and

–
adjacent to fibrosis or scars resulting
in bullae and blebs which may lead to
spontaneous pneumothorax.
Chronic Bronchitis (Blue Bloater)
Definition • Persistent cough with sputum production for at least 3 months in at least 2 consecutive years.
•
Pathology • Chronic airway irritation by tobacco smoke, mucus hypersecretion with mucus gland hypertrophy; goblet cell
•
metaplasia in bronchiolar epithelium, bronchiolitis
Clinical features • Productive cough, wheezing, cyanosis, rales, cor pulmonale
•
Reid index • is the ratio of thickness of submucosal glands to that of bronchial wall. In persons without a history of chronic
•
bronchitis this ratio is 0.44 ± 0.09, whereas in those with such a history the mean ratio is 0.52 ± 0.08
Asthma
Two types • Extrinsic asthma: type 1 hypersensitivity reaction.
•
• Intrinsic asthma: trigger is nonimmune and may include aspirin, cold, exercise, psychogenic or infection.
•
 
Pathology – Bronchial wall edema and development of inflammatory infiltrate with increased number of eosinophils,
–
thickening of basement membrane, bronchial smooth muscle hypertrophy and hyperplasia, and hyper-
trophy of submucosal mucus glands.
Microscopically Whorled mucus plugs (Curschmann’s spirals) and crystalloid debris of eosinophil membranes (Charcot-
Leyden crystals) are seen within airways.
Management of Acute Severe Asthma Includes

• High flow oxygen
•
 
• Nebulised short acting β-2 agonist (salbutamol or terbutaline)
•
 
• High dose corticosteroids (prednisolone oral or IV hydrocortisone)
•
• Nebulised ipratropium bromide
•
 
• IV aminophylline/theophylline.
•

Bronchiectasis
• Chronic necrostising infection of bronchi permanently dilated bronchi, purulent sputum, recurrent infections,
•
hemoptysis
• A/w cystic fibrosis, poor ciliary motility.
•
• Kartagener’s syndrome (bronchectasis, sinusitis, situs inversus).
•
• Patients can develop Aspergillosis.
•
• Gold standard investigation–HRCT (High Resolution CT)
•
Pneumonia
GENERAL PATHOLOGY
• Definition: Pneumonia is an infection of the pulmonary parenchyma.
•
• Classification:
•
– Community-acquired pneumonia (CAP) or
–
– Health care–associated pneumonia (HCAP),
–
Hospital-acquired pneumonia (HAP) and

Ventilator-associated pneumonia (VAP).

D/D of Community Acquired Pneumonias
Common organisms
Streptococcus • MC cause; MC in winter; young to middle aged patients; rapid onset high fever, pleuritic chest pain, herpes
•
pneumoniae labialis, ‘rusty sputum’
Mycoplasma • Atypical pneumonia, children and young adults; epidemics occur every 3-4 years, rare complications –
•
pneumoniae hemolytic anemia (cold agglutinins), erythema nodosum, Steven Johnson syndrome, myocarditis, pericarditis,
Gullain Barre syndrome
Chlamydia • Large scale epidemics or sporadic, often self limiting mild illness, headaches, usually diagnosed on serology
•
pneumoniae
Legionella • Recent foreign travel; atypical pneumonia, local epidemics around point source (ex: cooling tower, aerosolized
•
pneumophilia water); variety of clinical features such as headache, confusion, malaise, myalgia, high fever, diarrhea; Labs –
hyponatremia, elevated liver enzymes, hypoalbuminemia, elevated creatine kinase, CXR appearances may be
slow to resolve
Uncommon Organisms
Hemophilus influenzae • Often underlying lung disease (COPD, bronchiectasis)

•
Klebsiella • MC in men and alcoholics, ‘currant jelly’ sputum, upper lobe involvement typical, low platelet count and
•
leucopenia
Staphylococcus aureus • Coexistent debilitating illness and often preceded by influenza (postviral); CXR – multilobar shadowing,
•
cavitation, pneumatoceles, abscesses; dissemination – brain abscess or endocarditis; mortality -30%
Chlamydia psittaci • Contact with birds/imported birds/parrots/ducks/turkeys; low grade fever, long illness, hepatosplenomegaly
•
Coxiella burnetti (Q • Male sex, farm or abattoir contact; chronic course; influenza like illness
•
fever)
Nosocomial (hospital • Gram negative rods, staphylococcus
•
acquired)
Aspiration pneumonia • Anaerobes
•
196
• MC cause of Pneumonia in children Viral

•

• MC cause of hospital acquired pneumonia Enteric gram neg. bacilli
•

• Cystic fibrosis, Immunocompromised/ chronically ill Pseudomonas aeruginosa
•

patients, (AIPG 2014)

• Exposure to bats or birds H. capsulatum
•

• Exposure to rabbits Francisella tularensis
•

• Exposure to sheep, goats, parturient cats Coxiella burnetii
•

• Dementia, stroke, decreased level of consciousness Oral anaerobes, gram- negative enteric bacteria
•

Natural Course of Uncomplicated Lobar Pneumonia
GENERAL PATHOLOGY
• Congestion predominates in the first 24 hours

•
• Red hepatization (consolidation) is a picture of lung tissue with confluent acute exudation containing neutrophils and
•
 
red cells, giving a red, firm liver-like gross appearance.
• Grey hepatisation follows as the red cells disintegrate and the remaining fibrinosuppurative exudate persists, giving a
•
 
grey brown gross appearance; neutrophils predominate.
• Resolution is the favourable final stage in which consolidated exudate undergoes enzymatic and cellular degradation and
•
 
clearance’ macrophage is predominant cell type. Normal structure is restored.
Risk Factors for Pneumococcal Pneumonia

• Dementia,
•
• Seizure disorders,
•
• Heart failure,
•
• Cerebrovascular disease,
•
• Alcoholism,
•
• Tobacco smoking,
•
• Chronic obstructive pulmonary disease, and
•
• HIV infection.
•
Indications for Pneumococcal Capsular Polysaccharide Vaccine
 
• Asplenia (anatomic or functional)
•
• Age>65
•
• Patients with CSF leak, diabetes, mellitus, alcoholism, cirrhosis, chronic renal insufficiency, chronic pulmonary disease, or
•
 
advanced cardiovascular disease
• Immunocompromised conditions (e.g., multiple myeloma, lymphoma, Hodgkin’s disease, HIV infection, organ
•
transplantation, or chronic glucocorticoid use)
• Genetically at risk (e.g., Native Americans, and Native Alaskans)
•

• Patients living in environments where outbreaks are particularly likely to occur (e.g., nursing homes).
•
Mycobacterium Tuberculosis (Koch’s bacillus)
• Gram + rod, acid fast.
•
• High cell wall content of mycolic acid – leads to acid fastness and also Stains red on Zeihl Neelsen stain..
•
• Obligate aerobe - requires Lowenstein Jensen (L-J) medium for growth
•
• Doubling time = 18 hours (vs 20 minutes for E.coli), hence can take upto 8 weeks for cultures to grow
•

• Produces niacin.
•
• Virulence factors: Cord factor allows growth in extended chains.
•
• Mycolic acids are linked to underlying arabinogalactan and peptidoglycan – confers very low permeability of the
•
cell wall, thus reducing the effectiveness of most antibiotics.
 
• Cell wall lipoarabinomannan, is involved in the pathogen-host interaction and facilitates the survival of M. tuberculosis
•
 
within macrophages.
Differences between Primary (Childhood) TB and Secondary TB (Adult TB)
GENERAL PATHOLOGY
Primary TB (Childhood TB)
• Soon after initial infection with TB bacilli Often seen in children Involves middle and lower lung zones
•
 
• Primary subpleural granuloma in the inferior upper lobe/superior lower lobe region (Ghon focus) + draining hilar/bronchial
•
lymph nodes = Ghon complex.
• In severe cases, the primary site rapidly enlarges, its central portion undergoes necrosis, and cavitation develops (progressive
•
primary TB).
• Mostly non-infectious Sputum positivity rare
•
• Lymphadenopathy is significant (mediastinal or hilar)
•
• Cavity rare or thin walled
•
• Healing mainly by dystrophic calcification
•
• Extrapulmonary complication is very common
•
• Spread by hematogenous, lymphatic and parenchymatous route
•
Secondary TB (Adult-type, Reactivation, Postprimary Disease)
• Endogenous reactivation of latent infection
•
• Often seen in adults
•
• Involves apical and posterior segments of the upper lobes and superior segments of the lower lobes
•
• Leads to caseous necrosis and formation of
•
– Cavitations (mainly)
–
– Fibrosis
–
– Calcifications
–
 
• Highly infectious
•
• Sputum for AFB common
•
• No significant lymphadenopathy
•
• Cavity common (thick walled)
•
• Healing by fibrosis
•
• Lesion is mainly localised to lungs
•
• Spread is mainly bronchogenic inside the parenchyma. Extrathoracic spread is not documented
•
Pneumoconiosis
• Particles > 5μ are filtered in upper airways and < 1μ can remain suspended and are exhaled.
•
• Particles 1-5μ settle in the alveoli as the most potentially dangerous particles.
•
198
Inorganic Dusts Transudative Pleural Exudative Pleural Effusion

Effusion
Type of pneumoconiosis
– Pulmonary infacrtion/em-
• Coal dust : Anthracosis
–
bolism
•
• Silica : Silicosis
•
– Subdiaphragmatic disor-
• Asbestos : Asbestosis
–
ders (subphrenic abscess,
•
• Iron : Siderosis
 
pancreatitis etc.)
•
Organic Dusts Uncommon Causes of Pleural Effusion
• Sugarcane fibre (Bagasse) : Bagassosis • Connective tissue diseases (SLE, RA)
GENERAL PATHOLOGY
•
•
• Cotton dust : Byssinosis (‘Monday • Acute rheumatic fever
•
•
chest tightness’) • Post myocardial infarction syndrome
•
• Tobacco : Tobaccosis • Meig’s syndrome (benign ovarian tumor plus pleural
•
•
• Hay or grain dust : Farmer’s lung effusion)
•
(a/w thermophilic • Myxedema
•
actinomycetes) • Uremia
•
• Asbestos related benign pleural effusion
Silicosis
•
• Prolonged inhalation of silica (SiO2 or crystalline Dyspnea
•
quartz) produces a chronic, nodular, dense pulmonary • Orthopnea (dyspnea on recumbency) and nocturnal
fibrosis.
•
dyspnea are seen in asthma, LVF, GERD (gastroesophageal
• CXR shows reflux disease), obstructive sleep apnea.
•
– ‘Snow-storm’ appearance; • Platypnea (dyspnea that worsens in upright position) is
–
•
– “Egg shell” calcification of hilar nodes seen (in 20% a/w deficient abdominal musculature, AV malformations
–
of cases). (AIPG 2003) at lung bases
• Silicotics have greater risk of acquiring pulmonary TB • Trpeopnea: dyspnea that occurs only in lateral decubitus
•
(silicotuberculosis)
•
position most often in patients with heart disease
• Constant dyspnea is mostly due to COPD but also seen in
•
ILD (pulm. fibrosis).
Pleural Effusion: 2 Types
Transudative Pleural Exudative Pleural Effusion Caisson’s Disease: (Also Called Hyperbaric
Effusion
Decompression Sickness, the ‘Bends’, Diver’s palsy)
• Mechanism: Due • Increased microvascular
• A specialised form of gas embolism.
•
•
to either increased pressure due to disease of
•
hydrostatic pressure the pleura itself or injury in the • In divers who descend to high atmospheric pressures
or decreased osmotic adjacent lung – local factors.
•
pressure – due to
underwater, increased amounts of atmospheric gases
systemic factors. (mainly nitrogen) are dissolved in blood and tissue fluids.
 
• When such a person ascends too rapidly, nitrogen
• Causes • Causes:
•
comes out of solution as minute bubbles, particularly in
•
•
– Left ventricular – TB fatty tissues which have high affinity for nitrogen. These
 
–
–
failure (MC cause) bubbles may coalesce together to form large emboli.
– Cirrhosis – Pneumonia (para-pneu- • Bends: acute pain in joints, ligaments and tendons
–
–
•
monic)
• Chokes: respiratory distress.
•
– Nephrotic syn- – Viral infection • Treatment is immediate hyperbaric oxygen therapy.
–
–
•
drome
Acute Rheumatic Fever
– Malnutrition – Malignancy • Usually affects children
•
–
–
• Age 5-15 years
•

• Triggered by immune mediated delayed response to • Subcutaneous nodule
•
infections
•
Minor manifestations
• Group A Streptococci which have antigens that may cross

• Fever
•
react with cardiac myosin and sarcolemmal membrane
•
protein • Arthralgia
•
• Antibodies produced against streptococcal antigen • Previous RF
•
•
causes inflammation in the endocardium, myocardium, • Raised ESR or CRF
•
pericardium as well joints and skin • Leucocytosis
•
• Histologically fibrinoid degeneration is seen in skin • First degree AV block
•
•
Treatment Plus
GENERAL PATHOLOGY
• Bed rest and supportive therapy • Supporting evidence of streptococcal infection, recent
•
• Aspirin
•
scarlet fever, raised antitrypsin O or streptococcal
•
• Corticosteroid antibody
•
• Titre, positive throat culture
•
Aschoff Nodules are Pathognomic and Occur Only
in Heart ENVIRONMENTAL PATHOLOGY
• They are composed of multinucleated giant cells
• Mechanical injuries
•
surrounded by macrophages and T–lymphocytes
•
• They are not seen until the subacute or chronic phase of – Fractures are breaks in the continuity of previously
–
normal bone (e.g. a comminuted fracture with more
•
rheumatic carditis
than three bone fragments) or diseased bone (e.g.
pathologic fracture due to a metastatic lesion).
Clinical Features
– Contusions (bruises) are a blunt-force injury to the
–
• Sydenham chorea skin with subsequent escape of blood into tissue
•
• Prior sore throat – Abrasions are superficial excoriations of the epidermis
•
–
• Carditits that are inflicted by a direct or tangential blow to the
•
• Dysponea (CCF) skin
•
• Syncope – A laceration Is a blunt-force injury that overstretches
–
the skin, resulting In a tear that is bridged by vessels,
•
• Pancarditis
nerves, and connective.
•
• Cary comb murmur
– Incisions are wounds with sharp margins (e.g. a
•
• Aortic or mitral regurgitation
–
surgical wound) that do not have vessels, nerves, or
•
• Heart block connective tissue bridging the defect,
•
• Flitting polyarthritits – Motor vehicle accidents are the most common cause
•
–
• Edema (heart failure) of accidental death between 18 and 24 years of age.
•
• Erythema marginatum Gunshot wounds are either penetrating
•

• Subcutaneous node (over bone or tendons) (which do not exit the body) or perforating
•
(which do exit the body)
Jones Criteria for Diagnosis Contact wounds contain soot and gunpowder
in the wound (called fouling)
- Intermediate wounds have powder tattooing
Major Manifestations

(stippling) of the skin around the entrance
• Carditis site but no fouling.
•
• Polyarthritis - Distant wounds do not have powder tattoo-
ing
•
• Chorea
- Exit wounds are larger and more irregular
•
• Erythema marginatum than entrance wounds.
•
200
Drowning is the third most common cause of Frostbite is a form of localized tissue injury

death from 1 to 14 years of age. secondary to both direct (ice crystallization in
- Near drowning is defined as survival following cells) and indirect (vasodilatation and thrombosis)
asphyxia secondary to submersion damage
- In wet drowning (90% of cases), there is an ini- Generalized hypothermia (core body temperature
tial laryngospasm on contact with water, fol-

<35°C) occurs when the whole body is exposed
lowed by relaxation and aspiration of water.
to freezing temperatures for a prolonged period of
- In dry drowning (10%) there is intense laryn-
gospasm without significant relaxation. time and may progress to circulatory failure and
- Water (fresh or salt water) in the lungs de- death.
stroys surfactant (produces atelectasis with • Electrical Injuries
intrapulmonary shunting) causes diffuse alve-
•
GENERAL PATHOLOGY
olar damage and initiates spasm in the bron- – Ohm’s Law states that the current (I, expressed in
–
chioles. amps) is equal to the voltage (E) divided by the
- The immediate cause of death in drowning is resistance (R, expressed in ohms) to the flow of

cardiac arrhythmias. current: I (amps) - E (volts)/R (ohms)
– Current is the most important factor in electrocution
• Thermal injuries
–
AC is more dangerous than DC,
•
– First-degree burns are painful partial thickness

Dry skin has higher tissue resistance to current
–
burns (e.g. sunburn) that primarily produce cell

(particularly the hands and feet).
necrosis limited to the epidermis and heal without Wet skin lowers the resistance lo current
scarring.

(voltage is constant), hence increasing current,
– Second-degree burns are painful partial thickness which may produce cardiorespiratory arrest.
–
burns that involve the entire epidermis, form
blisters within the epidermis, and heal without
• Radiation injuries
scarring.
•
–– g-Rays, x-rays, and particulate radiation emitted by
– Third degree burns are painless full thickness
radioactive substances (e.g., a- and β-particles) are
–
burns with extensive necrosis of the epidermis and
examples of ionizing radiation, since they produce
adnexa and commonly heal with extensive scarring transient ionization alter tissue absorption.
complicated by keloid formation The shorter the wavelength of radiation, the
– Infection is the most common overall cause of

greater the penetration (e.g., a- and β particles
–
death (Pseudomonas aeruginosa Is the most have low penetration, whereas γ -rays have high
frequentcause. penetration).
– Hyperthermia is defined as a core body temperature The type of radiation, its cumulative dose, and
–

that is >37.2 0C the surface area of tissue exposed to that dose
Heat cramps are seen in untrained athletes or determine radiation effect on tissue.

laborers who become volume depleted, lose Radiation produces both direct and indirect injury

excessive amounts of salt and water, and develop to DNA (most susceptible protein), the latter type
muscle spasms a few hours later (no fever) by producing free radicals (e.g., hydroxyl radicals)
Heat exhaustion is noted in athletes who are
from hydrolysis of water in the tissue.
Tissue susceptibility to radiation is directly related

training in a hot and humid environment and

to the degree of mitotic activity and indirectly to
who develop severe volume depletion with mild
the degree of specialization of the tissue.
elevation in core body temperature
The peak sensitivity of proliferating cells to
Heat stroke is characterized by core body

radiating is in G2 (synthesis of mitotic spindle)

temperatures> 41 0C with associated CNS
and mitosis.
depression and hypohidrosis (lack of sweating)
Tissues with a high radio sensitivity are
Malignant hyperthermia is an AD disease

hematopoietic cells (e.g., lymphocytes) and

with a defect in calcium release channels in the
germinal cells; tissues with low radio sensitivity
muscle sarcoplasmic reticulum that produces include bone, mature cartilage, and muscle.
massive muscle contractions and extremely Total body irradiation has its greatest effect on the
high temperatures after induction of anesthesia

hematopoietic system, resulting in lymphopenia,
by halothane and succinylcholine thrombocytopenia, and bone marrow hypoplasia.

Nonionizing radiation injuries are due to ultraviolet (UV) light, lasers, microwaves, or infrared.

- The UVB portion of ultraviolet light is most responsible for sunburn (first and second-degree burns) and skin
cancer (e.g., basal cell carcinoma [most common], squamous cell carcinoma, and malignant melanoma).
- Laser radiation produces an Intense area of localized heat that is equivalent to a third-degree burn.
• High-altitude Injuries: The oxygen concentration is the same at high altitude (21%) as at sea level; however, the barometric
•
pressure is decreased
– Hyperventilation is a useful response to high- altitude sickness, since lowering alveolar CO2, (respiratory alkalosis)
–
automatically increases PAO2, which leads to an increase in arterial PO2.
– Acute mountain sickness occurs within the first 24-36 hours of an ascent above 8000-10.000 feet (2400-3000 m) and
–
GENERAL PATHOLOGY
may be prevented or ameliorated by taking acetazolamide (carbonic anhydrase Inhibitor) a few days before and during
ascent.
Sudden Infant Death Syndrome (SIDS)
• SIDS, or crib death, is the sudden death of an infant under 1 year of age that remains unexplained alter a complete
•
postmortem examination.
• The peak incidence Is between 2 and 3 months after birth.
•
• Sleeping in a supine position is most responsible for the decline in deaths due to SIDS. Maternal risk factors Include low
•
socioeconomic status, smoking, and drug abuse, while infant risk factors consist of prematurity and a history of previous
SIDS victims in the family.
• The apnea hypothesis (respiratory center abnormality and/or obstruction 10 air flow) is favored as the terminal event in
•
SIDS.
• Autopsy findings primarily exhibit signs of hypoxia (e.g., thickened pulmonary arteries, petechiae on the pleura and
•
epicardium) and mild inflammation in the lungs.
MISCELLANEOUS
• Synaptic Stripping: phenomenon first noticed in spinal lesion by Blinzinger and Kreutzberg, post inflammation microglia
•
remove the branch from nerves near damaged tissues, thus helps promote regrowth and remapping of damaged neural
circuit. Occurrence of synaptic stripping is likely to explain nuclear hyperexcitability and failure of recovery of complex five
motor movements that are commonly observed following peripheral injury to the facial nerve. (AIPG 2010)
Common Stains used in Surgical Pathology
Stain Component/tissue Dyes Interpretation

A. MYLOID

1. Congo red with polarizing Amyloid Congo red Green birefringence – amyloid
light
2. Toluidine blue Amyloid Toluidine blue Orthochromatic blue – amyloid

B. CARBOHYDRATES

3. Periodic acid schiff (PAS) Carbohydrates (mainly Periodic acid-Schiff reagent Glycogen and other carbohydrates:

glycogen) (basic fuschin magenta
Nuclei: Blue
4. Mucicarmine/ Best’s carmine Acidic mucin Carmine Mucin: red

Nuclei: Blue
202

5. Alcian blue (AB) Acidic mucin Alcian blue (pH 2.5) Acid mucin: Blue

Nuclei: Red
6. Combined AB- PAS Neutral mucin Alcian blue Acid mucin: Blue Neutral mucin:

magenta
Nuclei: Pale blue
C. CONNECTIVE TISSUE

7. Van Gieson’s Extracellular collagen Picric acid, acid fuschin, Nuclei: Blue/black

Celestin blue haemalum Collagen: Red
Other tissues: Yellow
GENERAL PATHOLOGY
8. Masson’s trachoma Extracellular collagen Acid fuschin, phosphomolybdic Nuclei: blue/black

acid, methyl blue, Celestin blue Cytoplasm, muscle, red cells: Red
haemalum Collagen: Blue
9. Phosphotungstic Muscle and glial Haematoxylin, phosphotungstic Muscle striatation, neuroglial fibres,
haematoxylin (PTAH) filaments acid, permananganate, oxalic fibrin: Dark blue
acid Nuclei: Blue
Cytoplasm: Pale pink
10. Verhoff’s elastic Elastic fibres Haematoxylin, ferric chloride, Elastic fibres: black
iodine, potassium iodide Other tissues: Counter-stained
11. Gordon and sweet’s Reticular fibres Silver nitrate Reticular fibres: Black
Nuclei: Black or counter stained
D. LIPIDS

12. Oil Red O Fats (unfixed cryostat) Oil red O Minerals oils: Red Unsaturated fats and
Phospholipids: Pink
13. Sudan black B Fats (unfixed cryostat) Sudan black B Unsaturated fats: Blue black
14. Osmium tetroxide Fats Osmium tetroxide Unsaturated lipids: Brown black
Saturated lipids: Unstained
E. MICRO-ORGANISMS

15. Gram’s Bacteria Crystal violet, Lugol’s iodine, Gram’s positive, keratinin, fibrin: Blue
neutral red Gram negative: Red
16. Ziehl-Neelson’s (acid fast) Tubercle bacilli Carbol fuschin, methylene blue Tubercle bacilli, hair shaft, actinomyces:
Red
Background: Pale blue
17. Fite Wade Leprosy bacilli Carbol Fuschin, methylene blue Lepra bacilli: Red
(decolorize in 10% sulfuric acid Background: Blue
18. Grocott’s silver Fungi Sodium tetraborate, silver Fungi, pneumocystitis: Black
methanamine nitrate, methanamine Red cells: Yellow
Background: Pale green
19. Giemsa Parasites Giemsa powder Protozoa: Dark blue

Nuclei: Blue
20. Shikata’s orcein Hepatitis B surface Acid permanganate, orcein, HBsAg positive: Brown to black

antigen tetrazine Background: Yellow
F. NEURAL TISSUES

21. Luxol fast blue Myelin Luxol fast blue, cresyl violet Myelin: Blue/green
Cells: Violet/pink

22. Bielschowsky’s silver Axons Silver nitrate Axon and neurofibrils:black

G. PIGMENTS AND MINERALS

23. Perl’s Prussian blue Haemosiderin, iron Potassium ferrocyanide Ferric iron: Blue

Nuclei: Red
24. Masson-fontana Melanin, argentaffin Silver nitrate Melanin, argentaffin, chromaffin

cells Lipofuscin: Black
Nuclei: Red
25. Alizarin red S Calcium Alizarin red S Calcium deposits: Orange red
GENERAL PATHOLOGY

(AIIMS May 08) (AIPG 2007)
26. Von Korsa Mineralized bone Silver nitrate, sarfranin O Mineralized bone: Black

Osteoid: Red
27. Rubeanic acid Copper Rubeanic acid Copper: Greenish black

Nuclei: Pale red
28. Grimelius Argyrophil cells Silver nitrate Argyrophil granules: Brown black

H. PROTEINS AND NUCLEIC

ACID
29. Fuelgen Reaction DNA Potssium Metabisulphite DNA: Red purple

Cytoplasm: Green
30. Methyl green pyronin DNA, RNA Methyl green, pyronin Y DNA: Green blue RNA red

Good to Know
• Germline mutation of STK11 (serine threonine kinase) is a tumour suppressor gene located on band 19p.13.3 results
•
in hereditary intestinal polyposis. In cancer, inactivation of the gene followed by APC/B – catenin and p55 pathways
occur. (AIIMS May 2011)

• Cells involved first in tissue injury are neutrophils. (AIIMS MAY 2009, AIPG 2007, (AIPG 2008))
•

• Heart failure cells are seen in: lung.
•
• Lines of Zahn are found in thrombus. (JKHD 2005)
•

• Shock lung is other name for ARDS.(Diffuse alveolar damage) (AIIMS 2008)
•
• Epitheliod and multi nucleated giant cells are derived from monocyte –macrophages. (AI 2002)
•

• Wound contraction is mediated by myofibroblasts. (JKHD 2005)
•

• C5a is the most important mediator of chemotaxis. (Delhi 2005)
•

• Ames test − Exfoliative cytology (AIPG 2005)
•

– Diseases due to defects −
–
– A simple in vitro test for carcinogenecity utilising the ability of potential carcinogens to induce mutation in selected
–
strains of the bacterium Salmonellla typhimurium is MC used in diagnosis of dysplasia, Ca in situ, and invasive
 
cancer of the cervix and also tumours of the stomach, bronchus and urinary bladder Xeroderma pigmentosum
Mitochondrial DNA
• Mutation rate about ten times greater than nuclear DNA.
•
• This is because there are no introns and a mutation invaribly strikes a coding sequence (axon).
•
• Tissues with greatest ATP requirement (CNS, Skeletal muscle, Heart muscle, Kidney, Liver) are most affected.
•
204
• Mitochondrial DNA is maternally inherited because mitochondria from sperms do not enter the fertilized egg.
•
• Mitochondrial DNA is Closed and circular and 16.5 kb in length. (AIPG 2006)
•

Nephrotic Syndrome (NEET 2013)
• Hypoalbuminemia due to proteinuria.
•
• Hypercoagulability due to increased urinary loss of AT III, decreased levels of protein C and protein S and increased platelet
•
aggregation.
• Hyperlipidemia and hypercholestremia due to loss of transferring
•
• Increased susceptibility to infection due to loss of IgG
•
• Microcytic hypochromic anemia due to loss of transferring
GENERAL PATHOLOGY
•
• Hypocalcemia and secondary increased PTH due to increased loss of cholecalciferol binding protein which leads to
•
increased vitamin D deficiency and hence secondary parathyroid hormone release.
• Hypothyroidism
•
Nice to Know
Hunner’s ulcer • Ulcerative interstitial cystitis; MC in women
•
Malakoplakia • A/w E.coli; affects urinary bladder (chronic cystitis); foamy histiocytes with intracytoplasmic
•
inclusions called Michaelis-Gutmann bodies are seen - pathognomonic.
Koilocytosis • vacuolation of superficial epithelial cells (ballooning degeneration) is characteristic of human

•
papilloma virus (HPV) types and 11.
Giantcondyloma • (Buschke-Lowenstein tumour, verrucuous carcinoma) solitary exophytic lesion that may
•
destroy much of the penis, it is generally larger than condyloma cuminatum.
• A/w HPV 6 and 11 infection. Locally invasive and recurrent but No metastasis. Surgical
•
excision required.
Erythroplasia of Queyrat • Paget’s disease of penis; Persistent rawness of the glans followed by cancer of the penis.
•
Crooke’s hyaline change • Occurs within pituitary basophils, caused by the presence of elevated cortisol levels
•
Sheehan’s syndrome • Hypopituitarism usuallycaused by infarction of the anterior pituitary; classically a/w
•
obstetric/haemorrhagic shock; post partum pituitary necrosis.
‘Hurthle cells’ • (Ashkanazy cells, oxyphil cells, oroncocytes) seen in Hashimoto’s thyroiditis–large
•
granular eosinophilic cell derived from thyroid follicular epithelium by accumulation of
mitochondria.
Plummer’sdisease • Toxic multi nodular goiter, usually not a/w With exophthalmos.
•
“Orphan annieeyes”. • Hypochromatic empty nuclei devoid of nucleoli seen in Papillary Ca. of thyroid.
•
Waterhouse- Friedrichson syndrome • Over whelming septicaemic infection seen in meningococcal meningitis. There is bilateral
•
 
adrenal haemorrhage beginning in the medulla.
Zellbalen • Well differentiated neuroendocrine cells arranged in nests, seen in carotid body tumour
•
(chemodectoma).
Duret haemorrhages • Seen in transtentorial herniations due to tearing of feeding vessels.

•
Capillary telangiectasias • In the brain occur MC in the pons.
•
Pathologic findingsin. TB meningitis • Arachnoidfibrosis, hydrocephalus and obliterative endarteritis
•
AIDS neuropathy • MC is a distal symmetric painful sensory neuropathy
•

Alzheimer’sdisease • Neuro fibrillary tangles, neuritic plaques, amyloid angiopathy, granulovacuolar degeneration
•
in pyramidal cells of hippocampus
Pick disease • Cortical atrophy in frontal and temporal lobes, Pick bodies (intracytoplasmic).
•
Lewy bodies • Intracytoplasmic inclusions in Parkinson’s disease.
•
Krabbe’s disease. • Deficiency of β-galactosidase, globoid cells may be seen
•
Reye’s syndrome • Jaundiceischaracteristicallyabsentorminimal.
•
Primarybiliary. cirrhosis • Most important auto antibody in is IgG antimitochondrial antibody (AMA) in 90% cases Often
•
the earliest symptom is pruritus.
GENERAL PATHOLOGY
Gaucher’scell • Foamy macrophage distended with PAS-positive material that has afibrillary appearance
•
resembling crumpled tissue paper.
Spleen in SLE • Marked perivascular fibrosis around penicilliary arteries is characteristic producing an onion-
•
skin appearance.
Sagospleen • Amyloid deposits limited to the splenic follicles giving rise to “tapioca-like”granules on
•
gross inspection.
CHAPTER 5
Microbiology
Objectives
• Sterilization and disinfection • Mycology

• Immunology • Parasitology

• Bacteriology • Miscellaneous

• Virology

STERILIZATION AND DISINFECTION
Terminology
Sterilization • Process by which an article, surface or medium is freed from all living microorganisms either in vegetative or spore
•
state. (NEET 2013, AIPG 2012, AIIMS MAY 2009)

Disinfection • Destruction or removal of all pathogenic organisms, or organisms capable of giving rise to infection
•
Disinfectants • Normally applied to inanimate objects, as most are ordinarily too toxic to be applied to living tissues
•
Antiseptics • Chemical disinfectants, which can be safely applied to skin or mucous membrane and are used to prevent
•
infection by inhibiting the growth of bacteria are called antiseptics.
Germicides • Agents that kill most vegetative bacteria, especially pathogens but not all spore forms are called germicides. The
•
terms virucide, sporicide and fungicide refer to substances that kill viruses, spores and fungi respectively
Asepsis • A term used to denote the avoidance of infection or microbial contamination.

•
Sanitation • This means reducing microbial populations to level judged safe by public health requirements
•
Decontamination • Process of rendering an article or an area free of danger from contaminants, including microbial, chemical,
•
radioactive and other hazards.
Disinfectants for Hospital Use

Group Examples Advantages and disadvantages
Phenolics Clear soluble phenolic compounds, Good general purpose disinfectants, not readily inactivated by organic
chloroxylenols matter, active agents, wide range of organisms including mycobacteria not
sporicidal inactivated by hard water and organic matter, pseudomonas
grows readily chloroxylenol solutions, limited activity against other gram
negatives
Microbiology 207

Group Examples Advantages and disadvantages
Halogens Hypochlorites (chloramines) iodine and Cheap, effective, act by release of free chlorine, active against viruses and
Other heavy iodophors mercuric chloride therefore recommended for disinfection of equipment soiled with blood

metals (AIPG 2007) (because of hepatitis risk), inactivated by organic material, corrode metals.

Useful skin disinfections, sporicidal. Used as topical skin preparations
Quaternary Benzalkonium chloride, cetavlon Have detergent properties, activity against gram negative << gram positive
ammonium improved by combination with diguanide, e.g. chlorhexidine, useful as skin
compounds disinfections, inactivated by hard water and organic materials, contamination
of stock solutions with gram negative rods can be a problem
Diguanides Chlorhexidine Useful disinfectant for skin and mucous membranes, inactivated by any
materials and too expensive for environmental use, alcoholic solutions are
less easily contaminated, combinations of chlorhexidine and detergent highly
effective for disinfection of hands
MICROBOLOGY
Alcohols Ethyl alcohol, isopropyl alcohol Good choice for skin disinfection and for clean surfaces, sometimes used in
combination with iodine or chlorhexidine, water must be present for bacterial
killing (i.e. 70% ethanol best), isopropyl preferred for skin and articles in
contact with patient (AIIMS May 2010)

Aldehydes Formaldehyde/formalin glutaraldehyde General disinfectant, kills vegetative organisms including mycobacteria,
slowly but effectively more active.
Hexachlorophene Activity against gram positive >> gram negative, used in soap or dusting
powder as skin disinfectant
• Heat-Based Sterilization: There are three types of heat sterilization methods commonly used in dentistry.
•
– Steam under pressure (autoclaving) :The lethal effect of moist heat is due to denaturation and coagulation of proteins.
–
– Dry heat sterilizers are either static air (convection or FDA-approved oven type) or forced air (rapid heat-transfer).
–
The killing effect of dry heat is due to protein denaturation, oxidative damage and the toxic effects of elevated levels
of electrolysis.
– Unsaturated chemical vapor sterilizers use a proprietary formula of alcohol/formaldehyde.
–
• Moist heat is superior to dry heat as:
•
– Moist heat kills at a much lower temperature than dry heat.
–
– Moist heat penetrates better; this is partly due to its density and partly due to negative pressure.
–
– Results are consistently good.
–
• Main disadvantages of moist heat are:
•
– Blunting and corrosion of sharp instruments.
–
– Damage to certain rubber goods.
–
Autoclave Hot air oven
Time and temperature • 121° C for 15 minutes at 15 lbs per sq inch 160° C for 120 minutes
•
• 134° C for 3 minutes at 15 lbs per sq inch. 170° C for 70 minutes
•
• To minimize the corrosive effect of steam on metal, ammonia, or 2% sodium nitrate can be used.
•
– Proper monitoring of sterilization procedures should include a combination of process indicators, including the
–
following:
– Mechanical—involves assessment of cycle time, temperature, and pressure by observing the gauges or displays on
–
the sterilizer.
– Chemical—uses sensitive chemicals that change color when a given parameter is reached (e.g., heat-sensitive external
–
tape, internal chemical indicator strip).
208
• Biological—this method is the most valid method for monitoring the sterilization process because it assesses the
•
process directly. Sterilization control. (AIPG 2008)

– Hot air oven–clostridium tetani
–
– Autoclave–bacillus stearothermophilus (NEET 2013)
–

• Filtration helps to remove bacteria from heat labile liquids. The following types of filters are used:
•
Candle filters • They are of 2 types
•
– Unglazed ceramic filters (Chamberland and Doultons filter)
–
– Diatomaceous earth filters (Berkefeld and Mandler filters)
–
Asbestos filters
MICROBIOLOGY
• Sietz and Sterimat filters-their carcinogenic potential has discouraged their use.
•
Sintered glass filters • Prepared by heat fusing finely powdered glass particles of graded size. They have low absorptive property
•
and is expensive
Membrane filters • Made of cellulose ester and other polymers

•
New disinfection methods include: New sterilization methods include
• A persistent antimicrobial coating that can be applied to • A chemical sterilization process for endoscopes that integrates
•
•
inanimate and animate objects (Surfacine) cleaning (Endoclens)
• A high-level disinfectant with reduced exposure time • A rapid (4-hour) readout biological indicator for ethylene oxide
•
•
(orthophthalaldehyde) sterilization (Attest)
• And an antimicrobial agent that can be applied to animate and • And a hydrogen peroxide plasma sterilizer that has a shorter cycle
•
•
inanimate objects (super-oxidized water). time and improved efficacy (Sterrad 50).
Test of pasteurized milk
Phosphatase test • Widely used to test the efficacy of pasteurization

•
• Tests for phosphatase in milk which is normally destroyed on heating milk at temperatures required for
•
pasteurization
• Presence of phosphatase in pasteurized milk indicates inadequate pasteurization of milk.

•
Standard plate count • Determines the bacteriological quality of pasteurized milk
•
• A limit of 30,000 bacteria per ml of pasteurized milk is the criteria
•
Coliform count • Tests for the presence of coliform in pasteurized milk.
•
• Coliforms are usually completely destroyed by pasteurization and therefore their presence indicates
•
incomplete pasteurization
• Standard is coliform be absent in 1ml of milk.

•
Methylene blue test • This test is carried on milk accepted for pasteurization.
•
• Indirect method for the detection of micro-organisms in milk and serves as a confirmation for heavy
•
contamination. (AIPG 2005)

• Coxiella burnetti survives the holder method of pasteurization
•
• Simple and Grieg proved the bactericidal activity of sunlight by using Typhoid bacilli. (AIPG 2012)
•

Microbiology 209

Comparison of New with Standard Technology
New Standard Advantages Disadvantages
Orthophthalaldehyde Glutaraldehyde – Shorter process time – Stains protein gray.
–
–
– No activation – Higher cost
–
–
– Not a known irritant to eyes and nasal
–
passages
– No vapour ceiling limit.
–
– Weak odor.
–
Surfacine Disinfectants (phenolic – Antimicrobial persistence (>13 days) – Cost
–
–
Quaternary ammonium); – May be used on animate and inani-
MICROBOLOGY
–
mate surfaces.
Antiseptics (alcohol, – Broad antimicrobial spectrum.

–
Iodophore, Chlorhexidine
Gluconate – Transfers active agent (silver) to mi-

–
crobes on demand without elution
– Resistant to forming biofilms.

–
– No toxicity to mammalian cells.
–
Super – oxidized High- or low-level – Basic materials (saline and electricity) – Production equipment
–
–
water disinfectants; antiseptics inexpensive expensive due to monitor-
ing.
– End product not damaging to environ- – Endoscope compatibility

–
–
ment. unknown.
– Nontoxic to biological tissues. – Decreased efficacy in
–
–
presence of organic
matter.
– Limited-use life (must be

–
freshly generated).
Endoclens None – Device automatically cleans and steril- – Cost

–
–
izes.
– Rapid cycle time (<30 min )

–
– Tests endoscope for channel blockage – Point-of-use system, no
–
–
and leaks. long-term storage activity.
– Advantages of automated processes

–
(e.g., consistent exposure to sterilant,
filtered water rinse, operator conve-
nience).
– Use for immersible instruments only.

–
EO rapid Read out. 48-hr spore readout – Rapid (4-hr), reliable assessment of – Cost
–
–
biological indicator. sterilization efficacy.
– Prevents recall of released sterilization – Not tested with EO and

–
–
loads. CO2 mixtures.
Plasma Sterilizer. Hydrogen peroxide gas – Use of two hydrogen peroxide diffu- – Cost
–
–
sion-plasma stage cycles is a more
effective sterilization process.
210
New Standard Advantages Disadvantages

– Reduced cycle time (45 min) – Endoscopes with
–
–
lengths>40 cm or a diam-
eter of <3 mm cannot be
processed.
– Various sized units available
–
– Leaves no toxic residues.
–
IMMUNOLOGY
Historical background
• Chinese physicians in the eleventh century observed that the inhalation of small pox crusts presented the subsequent
•
occurrence of the disease.
MICROBIOLOGY
• Edward Jenner (1798), the discovery that inoculation with cowpox crusts protected humans from smallpox.
•
• Further development of preventive immunization were made possible by Louis Pasteur (1881), who coined the term
•
“vaccine”.
• Later Robert Koch discovered the tubercle bacillus and developed his studies of bacterial etiology of infectious diseases.
•

(AIIMS May 2010)

• Koch’s postulates: microorganisms can be accepted as the causative agent of an infectious disease only if the following
•
conditions are satisfied:
– The bacterium should be constantly associated with the lesion of the disease.
–
– It should be possible to isolate the bacterium in pure culture from the lesion.
–
– Inoculation of such pure culture into suitable laboratory animals should reproduce the lesion of the disease.
–
– It should be possible to reisolate the bacterium in pure culture from the lesion produced in the experimental animals.
–
– An additional criteria subsequently requires the specific antibodies to the bacterium should be demonstrable in the
–
serum of patients suffering from the disease.
• E. Metchin Koff (1880’s) elucidated the importance of phagocytosis by leukocytes natural immunity and developed the first
•
theory of cell mediated immunity.
• Paul Ehrlich (1908) proposed the humoral theory of antibody formation.
•
Immunity
Innate immunity (AIIMS May 08) Acquired/ adaptive immunity
This is the first line of defence against infectious agents Second line of defense against infectious agents and is called into
play when innate immunity is breached
It is present from birth Acquired
Natural and does not depend on prior exposure to any antigen Initial exposure causes immunogenic priming
Nonspecific Specific
Has no memory Repeated exposures elicit memory (adaptive)
Components Components
Humoral: Humoral:
• Acute phase proteins • Bone marrow derived B lymphocytes: and secreted antibodies
•
•

(AIPG 2005)

• Interferons
•
Microbiology 211

Innate immunity (AIIMS May 08) Acquired/ adaptive immunity
• Lysozymes
•
• Complement system
•
Cellular: Cellular:
• Macrophages • Thymus derived T lymphocytes
•
•
• Dendritic cells, • Cytotoxic T lymphocytes
•
•
• NK cells (AIPG 2008)
•

• Neutrophils
•
• Eosinophils
•
MICROBOLOGY
• Basophils
•
• Mast cells
•
• Epithelial cells
•
Cytokines: Cytokine:
Cytokines that mediate host defence and inflammation as well as those Cytokines that regulate specific T versus B lymphocytic immune
that regulate adaptive immune response responses
Cells of immune responses

• Lymphocytes: Lymphocytes includes three types of cells.
•
– T-lymphocytes or T cells, which are derived from the thymus and play a role in cell-mediated immunity.
–
T helper cells. (AIPG 2011)

T-inducer cells

T-suppressor cells :

T-Cytotoxic cells :

T-contrasuppressor cells: These cells present the inactivation of T-helper and T-inducer cells by the action of

suppressor effector T-cells. They are antigen specific and may be important in immunologic memory.
– B-lymphocytes or B-cells which are derived from liver, spleen and bone marrow are the precursors of plasma cells and
–
play a role in humoral immunity. B lymphocytes represents 3 to 15% of circulating lymphoid cells and are primarily
defined by surface immunoglobulins S(Ig).
– Natural killer (NK) and killer (K) cells.
–
• Major components of the innate immune system
•
212
Pattern recognition receptors • C type lectins, leucine, leucine-rich proteins, scavenger receptors, pentraxins, lipid transferases,
•
(PRR) integrins (AIPG 2014)

Antimicrobial peptides • Alfa Defensins, beta defensins, cathelin, protegrin, granulosyin, lysozymes, histatin, secretory
•
leukoprotease inhibitor, and probiotics
Cells • Macrophages, dendritic cells, NK (natural Killer) cells, NK-T cells, neutrophils, eosinophils,mast
•
cells, basophils and epithelial cells
Complement components • Classic and alternative complement pathway, and proteins that bind complement components
•
Cytokines • Mediate host defense and inflammation, as well as modify adaptive immune responses
•
Cells of the Innate Immune System and their Major Roles in Triggering Adaptive Immunity
MICROBIOLOGY
Cell type Major role in innate immunity Major role in adaptive immunity
• Macrophages and Phagocytose and kill bacteria; produce Interleukin (IL-1)-1 and tumour necrosis factor (TNF)
•
monocytes inflammatory cytokines to upregulate lymphocytes adhesion molecule and
chemokines to attract antigen-specific lymphocytes;
Produce IL-2 to recruit TH1 helper T cell responses
• Precursors of dendritic Produce large amount of interferon IFN-alfa is a potent activator of macrophage and mature
•
cells or immature (IFN),which has antitumor and antiviral dendritic cells to phagocytose invading pathogens and
dendritic cells activity. They are the most important present pathogen antigens to T and B cells. (AIPG 2010)

antigen presenting cells (APC)
• Natural killer (NK) cells Kill foreign and host cells that have low Produce TNF-a and IFN-y that recruit Th-1 helper T cell
•
levels of MHC+self peptides. responses
• NK-T cells Lymphocytes with both T cell and NK Produce IL-4 to recruit TH2 helper T cell response, IgG1
•
surface markers kill host cells infected with and IgE production
intracellular bacteria
• Neutrophils Phagocytes and kill bacteria, produce Produce nitric oxide synthase and nitric oxide that inhibit
•
antimicrobial peptides apoptosis in lymphocytes and can prolong adaptive
immune responses
• Eosinophils Kill invading parasites Produce IL-5 that recruit Ig-specific antibody responses
•
• Natural Killer Cells:
•
– Are part of “innate” immunity (AIPG 2007)
–

– Are “large granular lymphocytes”
–
– Lack T cell receptor, surface IgM and IgD.
–
– Express CD 16 and CD 56. (Delhi 2009)
–

– The classic NK cells are CD2+, CD3+, CD4+, CD56+, and CD16+.
–
– Thymus is not required for their development
–
– Activity not enhanced by prior sensitization. NK cells do not require sensitization to express the killer function.
–
– NK cells constitute 2 to 10% of normal peripheral blood lymphocytes.
–
– Contain Azurophilic granules.
–
– Kill virus infected cells and cancer cells
–
– Kill by producing perforins, granzymes.
–
– Killing is non specific.
–
– NK cells are not MHC-restricted--they will kill certain autologous, allogeneic, and even xenogeneic tumor cells
–
whether or not these targets express MHC. (AIIMS NOV 2012)

– NK cells do not use the TCR, CD3 complex to recognize target cells.
–
– Killing is not dependent on foreign antigen presentation.(MHC Independent)
–
Microbiology 213

MICROBOLOGY
Fig.5.1 Recognition of antigen by b cells
Mediators released from Human Mast Cells and Basophils

Mediator Actions
• Histamine Smooth-muscle contraction, increased vascular permeability.
•
• Eosinophil chemotactic factor of anaphylaxis (ECF-A) Chemotactic attraction of eosinophils
•
• Platelet-activating factor Activates platelets to secrete serotonin and other mediators smooth
•
muscle contraction ; induces vascular permeability
• Neutrophil chemotactic factor (NCF) Chemotactic attraction of neutrophils
•
• Leukotactic activity (leukotriene B4) Chemotatic attraction of neutrophils
•
• Heparin Anticoagulant
•
• Slow-reacting substance of anaphylaxis (SRSA) (leukotriene C4, Smooth muscle contraction
•
D4, E4)
• Interleukins are a diverse group of cytokines. Most are produced by and act on other cells in the immune/inflammatory
•
response and have intertwining biologic activity. (AIPG 2008)

– Lymphocytes, fibroblasts and macrophages produce IL-1. (AIPG 2002)
–

– Its functions are:
–
Stimulation of the production of endothelial adhesion molecules such as selections to begin the inflammatory

process
Production of prostaglandins by fibroblasts and osteoclasts

Activation of phagocytes that makes T cell surfaces more receptive to antigens (AIPG 2002)

Stimulation of the release of IL-2 by T cells and NK cells

– IL-2 enhances T cell and NK cell growth and activation.
–
– IL-4 causes B cells to activate and divide. It promotes immunoglobulin and is also a growth factor for mast cells.
–
– IL-6 is produced by macrophages and CD4+T cells and stimulates the production of B cells and mast cells.
–
214
– IL-8 is produced by fibroblasts, endothelial cells and monocytes and stimulates activation and chemotaxis by
–
macrophages, PMNs and T cells.
– IL-10 is produced by CD4+ T cells and inhibits the production of cytokines by CD8+T cells. (NEET 2013)
–

– Proinflammatory cytokines E.g. IL-1, IL-6 and TNF
–
– Chemotactic cytokines E.g. IL-8
–
– Lymphocytes signaling cytokines
–
E.g. Cytokines released by Th1- IL-2, IFN.

Cytokines released by Th2- IL-4,IL-5,IL-10 and IL-13.

• Interferons are cytokines usually associated with antiviral activity. Interferon-gamma plays an important role in periodontal
•
disease. It is released by the CD4+T cells and enhances phagocytosis via a number of pathways. They are antiviral agents and
can fight tumors. (AIPG 2007) (AIIMS May 08)

– Induce resistance to viral replication by activating cellular genes that:
MICROBIOLOGY
–
– Destroy viral mRNA
–
– Inhibit translation of viral proteins
–
• Migration inhibitory factor (MIF) is produced by activated T cells and prevents the migration of macrophages from an
•
area of inflammation or infection, thereby increasing the population of macrophages in that area.
• Tumor necrosis factor (TNF) aids in the formation of selectins and ICBMs on endothelial walls, thus aiding in migration
•
of leukocytes.
• Lymphotoxin (LT) is produced by activated T cells. It works together with IFN-g to activate leukocytes
•
• Transforming growth factor-beta TGF-beta) is a group of cytokines produced by macrophages and platelets. Its primary
•
role appears to be the inhibition of the immune system.
• Matrix metalloproteins (MMPs) are a group of enzymes that degrade collagen, the ground substance and other structures.
•
• Elastase, glucoronidase and hyaluronidase are lysosomal enzymes produced by the destruction of PMNs and fibroblasts.
•
• Colony stimulating factors (CSFs) exist for granulocytes, lymphocytes and macrophages. They are cytokines derived from
•
T cells that control hematopoiesis.
• Immunoglobulins provide a structural and chemical concept while antibody is a biological and functional concept.
•
Ig class H chain
• IgG (gamma)
•
γ
• IgA (alpha)
•
α
• IgM µ (mu)
•
• IgD δ (delta)
•
• IgE € (epsilon)
•
• The highly variable zones numbering 3 in L and 4 in H chains are known as hypervariable regions (or hot spots) and
•
involved with the formation of antigen binding sites. (AIPG 2008)

IgG – 80%, molecular weight 150,000 (7S)
warm Ig Half life – 23 days
Increases in chronic malaria, kala-azar or myeloma
Crosses the placental barrier – natural passive immunity in newborn (AIPG 2001)

Ig G binds to micro-organisms and increases their phagocytosis
Microbiology 215

Extracellular killing of target cells coated with IgG is mediated through recognition of surface Fc fragment by K cells bearing
the appropriate receptors.
Ig G complexes with platelet Fc receptors – aggregation and vasoactive amine release
Passively administered IgG suppresses the homologous antibody synthesis by feedback mechanism – property utilized in
isoimmunization of women by administration of anti Rh(D) IgG during delivery
IgG is a late Ab and makes its appearance after the initial immune response which is IgM in nature
4 subclasses of IgG – IgG1 (65%), IgG2(23%), IgG3(8%), IgG4(4%) (AIPG 2005)

IgA 10-13%, 0.6 – 4.2 mg/ml, molecular weight – 160,000 (7S)
Contains an additional structural unit called the transport (T) or secretory (S) piece.
Synthesized not in the lymphoid cells but in the epithelial cells of glands, intestines and respiratory tract. And Is attached to
IgA during transport across cells.
MICROBOLOGY
Present in saliva (NEET 2013)

Synthesized by plasma cells
Dimeric cells – across hepatic parenchyma into bile.
Concentration in secretions and on mucous surfaces – local immunity
Inhibits adherence of micro-organisms to the surface of mucosal cells
Does not fix complement but activate alternate complement pathway
IgA – Ig A1 and Ig A2 (lacks interchain disulphide bonds)
IgM – cold Ig 5 – 8%, 0.5 – 2 mg/ml
Half life – 5 days, mol wt – 900,000 (19S)
Known as millionaire molecule

Pentamer, ca also exist as a monomer. has an extra domain on the mu chain (CH4) and another protein covalently bound
via a S-S bond called the J chain
80% intravascular.
Earliest Ig to be synthesized by foetus (20 weeks of age)
It is transported across placenta, presence of IgM in foetus indicates intrauterine infection and its detection suggests
diagnosis of congenital syphilis, rubella and toxoplasmosis (AIPG 2002)

Treatment of serum with 0.12M – 2 mercapto ethanol selectively destroys IgM without affecting IgG antibodies
IgM–IgM1 and IgM2 characterized by µ1 and µ2 H chains respectively
Its deficiency is associated with septicaemia
IgD 0.3 mg/ml intravascular.

Half life – 3 days
IgD and IgM occur on surface of unstimulated B lymphocytes and serve as recognition receptors for antigen.
IgD1 and IgD2
IgE Discovered by Ishizaka in 1966
8S (190000), half life – 2days
Thermolabile, homocytotropism
Mediates the Prausnitz – Kustner reaction – susceptible to mercaptoethanol doesn’t cross placenta or fix complement
extravascular
216
• Heterophil antigen is an antigen common to more than one species and whose species distribution is unrelated to its
•
phylogenetic distribution (viz., Forssman antigen, lens protein, certain caseins, etc.). These heterophile antigens in the
diagnosis of infectious mononucleosis.
• Infectious Mononucleosis Tests (synonyms: Heterophil agglutination test, Paul-Bunnell-Davidsohn test; Forssman
•
antibody test; Monospot test). Following infection with Epstein-Barr virus (EBV) in infectious mononucleosis (IM), 85-
90% of patients produce specific IM heterophile antibodies. These antibodies can be detected by following tests:
– Paul-Bunnell test: Sera of infectious mononucleosis patients, there are agglutinations to sheep erythrocytes, which
–
are adsorbed by ox red cells but no guinea pig cells.
– Monospot test: Horse red cells agglutinate on exposure to heterophile antibodies. The Monospot uses this in conjunction
–
with the principle of the Davidsohn differential test. Sensitivity and specificity for monospot are 94% and 98%
respectively.
– Forssman antigen-antibody reaction: The combination of Forssman antibody with heterogenetic antigen of the
–
MICROBIOLOGY
Forssman type, as in the agglutination of sleep erythrocytes (which contain Forssman antigen) by serum from a person
with infectious mononucleosis that contains Forssman antibody.
• Davidsohn differential test: Agglutination of the sheep or horse red cells is not specific and only determines the presence
•
or absence of heterophile antibodies including non EBV Forssman hetrophile antibodies.
– Guinea pig kidney cells contain the Forssman antigen, therefore absorbing serum with cells removes the Forssman
–
antibodies – Serum I
– Ox (beef) erythrocytes contain the IM antigen, therefore absorbing serum with erythrocytes removes the specific EBV
–
antibodies – Serum II
– When the two absorbed serums are mixed with sheep/horse red cells, a positive result is indicated by stronger
–
agglutination with serum 1.
Other heterophile reactions are
Well-Felix reaction • Serodiagnosis of typhus fevers, sharing of a common antigen between typhus rickettsiae and some
•
strains of Proteus bacilli. Proteus bacilli is used as antigen
Streptococcus MG agglutina- • Another example of heterophile agglutination test is the Streptococcus MG agglutination test for
•
tion diagnosis of primary atypical pneumonia.
Hypersensitivity Reactions
Type Clinical syndrome Time required for Mediators Examples
manifestation
Type I (IgE type) 1. Anaphylaxis Minutes IgE, histamine and other • Reactions due to administration

•
Anaphylactic vasoactive amines of penicillin

reaction (NEET 2013) (AIPG 2005)
2. Atopy Minutes -do- • Bronchial asthma

•
• Allergic dermatitis
•
• Angioneurotic oedema
•
• Hay fever (seasonal allergic
•
rhinitis) (AIPG 2008)

Type II Cytoxic Antibody mediated Hours to days IgG, IgM, C • Reactions in dental pulp and
•
reaction damage periapical infections
• Autoimmune haemolytic
•
anaemia
• Idiopathic thrombocytic purpura
•
• Blood transfusion reactions
•
Microbiology 217

Type Clinical syndrome Time required for Mediators Examples
manifestation
• Erythroblastosis fetalis
•
• Myasthenia gravis
•
Type III Immune 1. Arthus Hours to days IgG, IgM, C leucocytes Intrapulmonary arthus like reaction

complex reaction reaction (local to inhaled antigen
manifestation)
(AIIMS May 2010)
Farmers lung response to bacterial

antigen from mould hay
2. Serum sickness -do- -do- Stevens Johnson syndrome

(Generalized
manifestation)
MICROBOLOGY
(AIPG 2003)
SLE; polyarteritis nodosa, Sjogren’s
syndrome.
Skin disease
Various forms of glomerulonephiritis
Type IV cell mediated 1. Tuberculin or T cells, macrophages, Mantoux test

immunity infection type lymphokines
2. Contact dermatitis Hours to days Generally all fungal, viral and other

intercellular infections.
Contact dermatitis due to allergic

response to a number of chemicals
(E.g.: Acylic)
Good to know • Fever stimulates production of interferon and helps in

•
recovery from viral infection.
• The earliest description of an abnormal Ig was • Concept of local immunity–Besredka (1919-1924)
•
Bence–Jones proteins by Bence Jones in 1847. It is
•
• Haptens are substances which are incapable of inducing
found in multiple myeloma. Identified in urine by its
•
antibody formation by themselves, but can react
characteristic properties of coagulating when heated to specifically with antibodies. They become immunogenic
600C but redissolving at 800C. contains only light chains (capable of inducing antibodies) on combining with larger
(λ or κ) – monoclonal antibodies. molecule carrier.
• Morrack proposed the lattice hypothesis to explain the • Globulins: water insoluble euglobulins, water soluble
•
•
mechanism of precipitation pseudoglobulins
• Immunoelectrophoresis devised by Grabar and • Most antibodies are euglobulins
•
•
Williams (1953), Race (1945) for detection of anti RH • Both C3a and C5a are anaphylatoxic and chemotactic in
•
antibodies that do not agglutinate RH positive RBCs in nature
saline • Synthesis of the Ig in plasma cells occurs in endoplasmic
•
reticulum (AIIMS May 2010)
• Pillemer (1954) described properdin, a euglobulin

• Graft versus host reaction is caused by T lymphocytes
•
present in normal serum which along with complement
•
and magnesium ions causes lysis of gram negative • Opsonization is by IgG, IgM, C3b
•
bacteria and some viruses. • The exact part of the antigen that reacts with the immune
•
system is epitope.
• Therapeutic induction of fever was employed for
• Antigen combining site of antibody is paratope.
•
the destruction of Treponema pallidum in tissues of
•
syphilitic patients before penicillin was available. • Tiselius and Kabat (1938) showed that the antibodies
•
activity was associated with gamma globulin fraction.
218
• Synthesis of complement
•
– C1 – intestinal epithelium
–
– C2 and C4 - macrophages
–
– C5, C8 – spleen
–
– C3, C6, C9 - liver
–
– C7 – not known
–
• Biologic activities of some complement components
•
Component Activity
• C4a weak Histamine release from basophils and mast cells
•
anaphylatoxin
• C3a anaphylatoxin Evokes histamine release from basophils and mast cells
MICROBIOLOGY
•
• C5a anaphylatoxin Evokes histamine release from basophils and mast cells, potent chemotactic for monocytes and neutrophils
•
• C3b, C3bi Opsonization factor: Phagocytosis by neutrophils and monocytes; promotes immune complex binding to
•
cells within monocyte-macrophage system, as well as neutrophils.
• C5-9 Membrane attack complex leading to cell destruction

•
Clinical syndromes associated with genetic deficiency of complement components
Group Deficiency Syndrome
I C1 inhibitor Hereditary angioneurotic oedema
II Early components of classical pathway C1, SLE and other collagen vascular diseases
C2, C4
III C3 and its regulatory protein C3b inactivator Severe recurrent pyogenic infections
IV C5 to C8 Bacteremia mainly with gram negative diplococci, toxoplasmosis
V C9 No particular disease
Theories of Immune Response

• Side chain theory–Ehrlich (1900)
•
• Direct template theories–Brent and Haurowitz (1930), Mudd (1932)
•
• Indirect template theories–Burnet and Fenner (1949)
•
• Natural selection theory–Jerne (1955)
•
• Clonal selection theory–Burnet (1957)
•
Primary mediators of anaphylaxis
• Histamine
•
• Serotonin
•
• Chemotactic factors
•
Secondary mediators of anaphylaxis
– Slow reacting substance of anaphylaxis (SRS- A)
–
– Prostaglandin
–
– Leukotriene
–
– Platelet activating factors
–
• Phagocytic macrophages
•
– Epitheliod cells, found in granulomas, arise from antigen-activated blood monocytes
–
Microbiology 219

– Multinucleated giant cells are formed by the fusion of macrophages and have been characterized by either Langerhans
–
types with relatively few nuclei or foreign body types with many nuclei dispersed throughout the cytoplasm.
– Kuffer cells are long lived resident liver macrophages situated at the interface with the blood stream. Alveolar
–
macrophages line the alveoli and encounter inhaled pathogens.
– Dendritic cells are characterized by numerous long, slender processes and by irregularly shaped nuclei. Show little or no
–
phagocytic activity but very effective in antigen presentation of T and / or B lymphocytes types of dendritic cells include
lymphoid, follicular, and interdigitating cells.
• The compound that sensitizes bacteria and viruses to UV radiation is nucleic acid
•
• Rideal Walker test is used to test the efficiency of a disinfectant. It is also known as ‘phenol coeffecient’ test. Salmonella
•
typhosa is the test organism
• Detergents act on the phosphate groups of cell membrane. As a result the membrane looses its semipermeability and cell
•
proteins are denatured
MICROBOLOGY
• Vaccines are sterilized by moist heat below 1000C. vaccines of non sporing bacteria are heat inactivated in special vaccine
•
baths at 600 C for 1 hour.
Diagnosis of syphilis
Non specific serological tests for diagnosis of syphilis using • Wasserman test (Complement fixation test)
•
cardiolipin antigen are • VDRL test (slide flocculation )
•
• Kahn test (tube flocculation)
•
Specific tests using pathogenic treponemas are • TPI (complement fixation test)
•
• FTA – Abs test (functional treponemal antibody absorption test)
•
• TPHA (treponema pallidum haemagluttination assay)
•
• The presence of a protein coat in viruses makes protective vaccines a possibility
•
• Southern blotting is a technique for identifying DNA fragments
•
• Nouthern blotting–RNA (AIPG 2008)
•

• Western/immune blotting–proteins (antigens) (AIPG 2014)
•

• PCR is the most sensitive and specific test and is the gold standard for diagnosis in all stages of HIV infection
•

(AIPG 2010)

BACTERIOLOGY
Prokaryotes: (AIPG 2011-2012) Eukaryotes: (2008, 2009, 2010)

• Absence of nuclear membrane (AIPG 1999) Presence of nuclear membrane. (TWO SEPARATE BILAYERS)
•

• Absence of nucleolus Presence of nucleolus
•
• Absence of organized DNA (no histones) Presence of DNA
•
• Absence of cytoplasmic organalles Presence of cytoplasmic organalles
•
• Absence of sterols/ muramic acid Presence of sterols/ muramic acid
•
• Bacteria are prokaryotes.
•
Bacteria and their Alternate Names
• Bordetella Bordet gengou bacillus
•
• Clostridium tetani Nicolaire’s bacillus
•
220
• Corynebacterium diphtheriae Klebs Loeffler’s bacillus

•
• Corynebacterium pseudotuberculosis Priesz Nocard bacillus
•
• Corynebacterium pseudodiphtheriticum Hoffman’s bacillus
•
• Haemophilus aegypticus Koch weeks bacillus
•
• Haemophilus influenzae Pfeiffer’s bacillus
•
• Klebsiella pneumoniae Friedlander’s bacillus
•
• Klebsiella ozaenae Abel’s bacillus
•
• Klebsiella rhinoscleromatosis Frisch bacillus
•
MICROBIOLOGY
• Mycobacterium tuberculosis Koch’s bacillus

•
• Mycobacterium intracellulare Battey’s bacillus
•
• Mycobacterium paratuberculosis Johne’s bacillus
•
• Mycoplasma Eaton agent
•
• Pseudomonas pseudomallei Whitmore’s bacillus
•
Bacteria and their shape, appearance
Bacteria Shape and Arrangement

• Meningococci, Gonococci, Pneumococci In pairs
•
• Clostridium tetani Drumstick appearance
•
• Diphtheria bacilli Cuneiform or Chinese letter pattern
•
• Anthrax Bamboo stick appearance
•
• Staphylococci Grape bunch
•
• Streptococci Chains
•
• Leprosy bacilli Cigar bundle appearance
•
• Actinomyces Branched filamentous forms
•
• All cocci expect Neisseria are Gram-positive.
•
• All bacilli except DATTA are Gram-negative
•
D-Diphtheria

A-Actinomycosis

T-Tetani

T-Tuberculosis

A-Anthrax

Identification Tests
Tests Bacteria
• Naggler’s reaction • Clostridia
•
•
• Satellitism • H.influenza
•
•
Microbiology 221

Tests Bacteria
• Dick test, Schueltz–Charlton reaction • Streptococci
•
•
• Elek’s test, Schick test • Diphtheria
•
•
• Milk ring test • Brucellosis
•
•
• Koch’s phenomenon, Montoux test • Tuberculosis
•
•
• String test • Vibrio cholera
•
•
Cultural Characteristics of Bacteria
Bacteria Cultural Characteristics
MICROBOLOGY
• Staphylococcus Oil paint appearance
•
• Bordertella pertusis Thumb print appearance/ bisected pearls/ mercury drops
•
• Corneybacterium diphtheria Daisy head/frog’s egg/poached egg colony (grasis/ inlesmediux/ mitisrespy)
•
• Mycoplasma Fried egg appearances
•
• Hemophilus influenzae Satellitism
•
• Neiserria meningitidis Lenticular shaped
•
• Pneumococcus Draughtsman ( concentric ring) appearance
•
• Bacillus anthracis Bamboo stick/medusa head
•
• Yersinia pestis Stalactite growth
•
Bacterial Culture
Simple media or basal media Provides essential substances for growth of micro organisms
Example – nutrient broth
Enriched medium Substances such as blood, serum or egg are added to the basal medium
• E.g. –
•
– Blood agar
–
– Chocolate agar
–
• Egg media
•
Selective media • Substances that inhibit or poison all but a few micro-organisms are added to a
•
solid media
• Facilitates the isolation of a particular species

•
• E.g. deoxycholate citrate medium for dysentery bacilli
•
Enrichment media • Addition of certain substances to a liquid medium that have stimulatory effects on
•
bacteria of interest and inhibitory effect on other
• E.g.
•
– Tetrathionate broth
–
– Selenite F broth
–
222
Agar has no nutrient value and is not affected by growth of bacteria

• It is used to solidify culture media
•
• Not a culture media in itself
•
• Obtained from sea weeds
•
• Chief constituent is a long chain polysaccharide
•
Various Culture Media
• Smith noguchi medium: Spirochetes
•
• Selenite F Broth: Salmonella, shigella
•
• Dorset egg medium: Mycobacterium Noguchi medium: Borellia
MICROBIOLOGY
•
• BYCE Medium: Legionella
•
• Lofflers serum slope: Cornyebacterium diphtheria
•
• Tellurite Media: Cornyebacterium diphtheria
•
• Thayer martin media: N. gonorrhea
•
• Korthoff media: Leptospira
•
• Staurts media: Leptospira
•
• Fletcher media: Leptospira
•
• Choclate agar: H. influenza
•
• Bordet gengou: B. pertussis
•
• Lownstein Johnson: M. tuberculosis
•
• Sabourdars media: Fungi (AIPG 2008)
•

• Skirrows media: Campylobacter jujeni
•
• Mc Coy cell culture: Chlamydia (AIIMS May 2010)
•

Bacterial growth factors
– Tryptophan–Salmonella typhi
–
– Glutathione–Gonococci
–
– Niacin test–to differentiate human tubercle bacilli from atypical mycobacterium (AIPG 2009)
–

• Bacterial capsule is a thick gelatinous, circumscribed envelope situated just outside the cell wall of some bacteria,
•
formed by active secretion of bacteria itself. (AIPG 2012)

– Constituents:
–
98% water

2% includes :

- Polypeptides

- Polysaccharides

- Lipoproteins

- Hyaluronic acid

– Demonstration of capsule:
–
Ordinary stains: methylene blue, Gram stain

Special stains: India Ink, Congo red

Capsule swelling reaction.

Microbiology 223

Organisms That Do Not Gram Stain Well
– Treponema (too thin to be visualized). Require darkfield microscopy and fluorescent antibody staining.
–
– Rickettsia (intracellular parasite).
–
– Mycobacteria (high-lipid-content cell wall) require acid-fast stain.
–
– Mycoplasma (no cell wall).
–
– Legionella pneumophila (primarily intracellular), silver stain
–
– Chlamydia (intracellular parasite; lacks muramic acid in cell wall).
–
• Flagella
•
– Types:
–
Montrichous: Single flagella at one pole. e.g. Vibrio

Amphitrichous: at both poles e.g. Listeria, Monocytogens

Lophotrichous: Tuft of flagella at one/both poles e.g. spirilla pseudomonas
MICROBOLOGY

Peritrichous: flagella is present all around the periphery e.g. Salmonella, E.coli

• The lipopolysaccharides (LPS) present on the cell walls of gram negative bacteria consists of 3 regions. LPS formerly
•
known as Boivin antigen
– Region I–polysaccharides portion determining ‘O’ antigen specificity
–
– Region II–core polysaccharide
–
– Region III–glycolipid portion (lipid A) responsible for endotoxic activities such as pyrogenicity, tissue necrosis, etc.
–
When lysozyme acts on gram positive bacteria in hypertonic solution: Protoplast is formed. (AIPG 2003)

When lysozyme acts on gram negative bacteria in hypertonic solution: Spheroplast is formed.

Difference between protoplast and spheroplast: In spheroplast some cell wall material is retained.

Mesosomes (chondroids): Analogous to mitochondria

Volutin granules: Metachromatic or Babes- Ernst Granules, common in diphtheria bacilli

Quellung reaction: Neufeld in 1902

Flagellar antibodies are not protective but useful in serodiagnosis.

Fimbriae: Specifically inhibited by D-mannose

SABE: Streptococcus sanguis (streptococcus viridians group) (AIPG 2009, 2011)

Acute endocarditis: Staph aureus or pyogenes

Post operative endocarditis: Staph albus or epidermis

Neurotoxin of tetanus acts on spinal cord

Transport media for cholera: Cary blair medium or Venkatraman Ramakrishnan medium

Difference Between Extoxins and Endotoxins
Exotoxins Endotoxins
Source Secreted by both Gram-negative and Cell wall from most Gram-negative bacteria
Gram-positive bacteria
Nature Proteins (polypeptide) Lipopolysaccharides
Stability Heat labile Heat stable

Antigenicity Highly antigenic Poorly antigenic
Toxicity Highly fatal Low fatal
Vaccines Toxoid can be used as vaccines No
Tissue specificity Highly specific No specificity
224
Differential Diagnosis of Gram-positive Bacteria

Catalase test Between streptococci and staphylococci. It is positive for staphylococci. Negative for streptococci
Haemolytic test Its is based on the specific haemolytic ability of streptococci:

– Beta-haemolytic streptococci completely lyse the RBCs, leaving a clear zone of hermolysis
–
around the colony
– Alpha-haemolytic streptococci only partially lyse the RBCs, leaving a greenish discolouration
–
of the culture medium surrounding the colony.
– Gamma-haemolytic streptococci are unable to haemolyze the RBCs, and therefore we should
–
really not use the word “haemolytic” in this situation-non-haemolytic
Streptolysin test Between alpha-haemolytic and beta-haemolytic. Production of streptolysin ‘A’ and streptolysis “s” by beta-
hemolytic bacteria
C-antigen test To differentiate between lancefield and non-lancefield (Strepto. Viridians group and S. pneumoniae).
Presence of carbohydrate indicates Lancefield group (AIPG 2007)
MICROBIOLOGY

Bile test/Optochin sensi- Differentiates between the strepto. viridans group and S. pnuemoniae of alphahaemolysis
tivity test Viridans group are not bile soluble and not inhibited by optochin.
Pneumoniae, which is bile soluble and is inhibited by optochin
Insulin fermentation test With insulin streptococci is non-ferementer and pheumococci produces acid fermentation
Fermentation of mannitol To differentiate between streptococcus mutans and other oral streptococci (AIPG 2008)

and sorbital
Bacitracin test (AIIMS May Inhibition of bacitracin disk. Identification of group A sptreptococci from other group of streptococci.

2009) (AIIMS May 2009)

6.5% NaCl and pencillin G To differentiate between enterococci (Strep. feacalis) and non-enterococci (Strep. bovis): Enterococci
grow in 6.5% NaCl and not killed by penicillin G. Non-enterococci are inhibited by 6.5% NaCl and pencillin
G.
Coagulation test To differentiate between Staphylococcus aureus and other staphylococci. Coagulation test +ve -
Staphylococcus aureus
Phases of Bacterial Growth Cycle
Lag Phase • Nutrients incorporated

•
Log Phase • Rapid cell division uniform staining occurs (AIPG 2003) UPSC 2000
•

Stationary Phase • Cell Death=Cell formation (sporulation occurs) (JK BOPEE 2011)
•

Death Phase • Cell death > Cell formation (JK BOPEE 2012)
•

• The toxin molecule of vibrio cholera consists of A (A1 and A2) and B (5) subunits.
•
– The A1 fragment causes prolonged activation of cellular adenylate cyclate and accumulation of cAMP, leading to
–
outpouring into the small intestinal lumen,of large quantities of water and consequently watery diarrhea. The toxin
also inhibits intestinal absorption of Na+and Cl-. (AIIMS May 2010, Nov 2013)

Pathogenic Bacteria
Bacteria Disease Source
• Vibrio cholera • Watery diarrhea • Shell fish

•
•
•
• Enterotoxigenic E. coli • Watery diarrhea • Salads, cheese, meat,water
•
•
•
Microbiology 225

Bacteria Disease Source
• Enterohemorrhagic • Bloody diarrhea • Groud beef, roast beef, salami, raw milk, raw
•
•
•
vegetables, apple juice, beef, poultry, eggs, diary
products, potato or eggs, diary products, potato
• Salmonella spp • Inflammatory diarrhea
•
•
• Shigella spp • Dysentery
•
•
• Vibrio parahemolyticus • Dysentery
•
•
The Various Methods of Gene Transfer in Bacteria are
Transformation • Transfer of genetic material through agency of free DNA
•
• 10-50 genes are usually transferred
MICROBOLOGY
•
• Have one bacteria (drug resistant bacteria) releases the DNA into the medium which is taken up by another
•
bacteria
• Identified 1st by Avery, McLeod, and McCarty in 1944 in S - R transformation of pneumococci
•
• This has been seen in Bacillus, Pneumococcus, Haemophillus.
•
Transduction • Transfer of genetic material via bacteriophage
•
• Chromosomal DNA, episomes and plasmids: all can be transferred by transduction
•
• Is the most widespread mechanism of gene transfer among prokaryotes and provides an excellent tool
•
for gene mapping
• Eg: penicillin resistance in staphylococcus
•
• Has been proposed as a method of genetic engineering in treatment of some inborn errors of metabolism
•
Lysogenic conversion • Herein the bacteriophage infects the bacterial cell instead of causing its lysis (as it happens in virulent or
•
lytic cycle), incorporates its own DNA into the chromosome of bacteria. This is called the temperate or non
lytic cycle. The phage DNA that gets incorporated into the bacterial DNA is called prophage. This process
is called lysogeny.
• Here the host remains unharmed and is quite frequent in nature
•
• Eg: lysogenic conversion in diphtheria bacilli by β phage. This phage conversion is necessary for toxin
•
production by these bacteria.
Conjugation • Sexual contact through formation of a bridge or sex pilus
•
• Is common in gm –ve bacilli
•
• Both chromosomal and extrachromosomal DNA can be transferred
•
• Is the commonest mode of drug resistance transfer in bacteria
•
• ‘F’ factor: it is necessary for sex pilus formation: F +ve cells mate with F –ve cells and render them F +ve
•
along with transfer of chromosomes.
Other Important complete thing Points

• Mutational drug resistance is of great importance in tuberculosis
•
• Transferable drug resistance mediated by R factor is the most important method of drug resistance transfer in bacteria
•
• Transposons: Segments of DNA that can move around between chromosomal and extrachromosomal DNA with the cell.
•
It is method of amplifying genetic transfer in nature
Comparison of Mutational and Transferable Types of Drug Resistance in Bacteria

Mutational drug resistance Transferable drug resistance
• Involves resistance to one drug at a time • Simultaneous resistance to multiple drugs. May involve all drugs used in
•
•
clinical treatment
226
Mutational drug resistance Transferable drug resistance

• Degree of resistance is usually Low • Degree of resistance is usually High
•
•
• May be overcome by high drug usage • High drug usage ineffective
•
•
• Can be prevented by treatment with combination • Combination of drugs cannot prevent it
•
•
drugs
• Resistance does not spread • Resistance spreads to other cells of same or different species of the genus
•
•
• Resistant mutants are usually metabolically defective • Metabolically normal
•
•
• Virulence may be low • Virulence not decreased
•
•
Good to know
• Clostridium difficile is associated with antibiotic associated pseudomembranous colitis.
•
• Phage conversion is required for diphtheria.
MICROBIOLOGY
•
• The only gram negative organism having pili is Corneybacterium diphtheria
•
• Malignant pustule is cutaneous anthrax
•
• Vincent’s angina is caused by Borrelia vincentii and fusobacterium fusiform
•
Stains in bacteriology
• Acid fastness of tuberculus bacilli is due to presence of mycolic acid in cell wall
•
• Pneumococci: Indian ink
•
• C. diphtheria: Methylene blue, Albert’s, Neisseria staining
•
• Spirochaetes: Giemsa stain, Levaditis
•
• Noacrdia, TB , Leprosy: Acid fast (zeil nelson)
•
• For rapid diagnosis of Tb: Auramine and Rhodamine
•
• Anthrax, brucella, leptospira, Rickettisia, Borrelia and coxiella burnetti are common examples of zoonotic diseases.
•
• Diphtheria is pathogenic only when infected with betaphage
•
• E. coli is pathogenic only when infected with lambda k12
•
• The emetic syndrome is caused by ingestion of heat stable emetic toxin (cerulide, acrylic peptide) produced in food
•
• Diarrheal syndrome is mainly caused due to ingestion of B. cereus cells in foods, followed by toxin production in small
•
intestine
• Naggler’s reaction is given by alpha toxin of Clostridium perfringens, Clostridium botulinum causes constipation and
•
occurs after 16 – 24 hours
B.cereus
– The illness is characterized by acute nausea and vomiting 1–5 hours after the meal
–
– Diarrhea is not common
–
– B. cereus is present in large numbers in cooked rice and faecal samples from these patients
–
– Both types are mild and self limited, requiring no specific treatment
–
– Isolates from diarrheal type of disease produce an enterotoxin which causes fluid accumulation in ligated rabbit ileal
–
loop, resembling the heat stable enterotoxin of escherichia coli
– The emetic toxin was produced only when B.cereus was grown in rice and not any other meal
–
– Two mechanism of action have been described for the enterotoxin of B.cereus, one involving stimulation of CAMP
–
system and other independent of it.
– A special mannitol egg yolk – phenol red polymyxin agar (MYPA) medium is useful in isolating B.cereus from faeces
–
and other sources
– B.cereus produces lecithinase and ferments glucose but not mannitol
–
Microbiology 227

Food Poisoning
Incubation period Symptoms Common food sources
1 to 6 hour – Nausea, vomiting, diarrhea Ham, poultry, potato or egg, salad, mayonnaise, cream pasteries, fried
–
rice
– Staphylococcus – NVD
–
–
aureus
– Bacillus cereus
–
8 to 16 hr
– Clostridium per- – Abdominal cramps, diarrhea Beef, poultry, legumes, gravies, meat, vegetables. Dried beans, cereals
–
–
finges (vomiting rare)
– B. cereus – Abdominal cramps, diarrhea,
–
–
(AIIMS May 08) (vomiting rare)

MICROBOLOGY
Nice to Know
• The most important complications of typhoid fever are intestinal perforation, hemorrhage and circulatory collapse.
•
Osteomyelitis is a rare sequel.
• Hydrolysis of pyrrolidonyl napthylglamide (PVR test) and failure to ferment ribose and sensitivity to bacterium are useful
•
in differentiating streptococcus pyogenes from other streptococci
• Schultz Charlton reaction: Blanching of the erythematous rash on local injection, convalescent serum is used as diagnostic
•
test for scarlet fever
• The Dansyz phenomenon and Ehrlich phenomenon which are seen during preparation of diphtheria vaccine is due to the
•
ability of toxins and anti toxins to combine in varying proportions
• The lab test used to differentiate between micrococci and staphylococci is Hugh and Leifson’s oxidation–fermentation
•
test in which micrococci show oxidative and staphylococci show fermentive patterns
• Organisms that cause gangrene have a proteolytic metabolism predominantly Inductive microbial enzymes can be
•
detected only in the presence of their specific substrates
• Pathogenic treponemas can be maintained in rabbit testis only

•
• Salmonella, Shigella–Non lactose fermenters
•
• Escherichia, Klebsiella–Lactose fermenters
•
• Parcolons–Late fermenters
•
• Citron bodies and boat or leaf shaped pleomorphic bacilli with irregular staining suggest clostridium septicum
•
• All members of Salmonella genus are motile with peritrichate flagella except S. gallinaum – pullorum which is always non
•
motile.
• Salmonella typhii–also known as Eberth- Gaffkey bacillis or Eberthella typhii
•
• The screening techniques for identifying bacteriuria are:
•
– Griess nitrite test
–
– Catalase test
–
– Triphenyl tetrazolium chloride (TTC) test
–
– Dip slide culture methods
–
• Pseudomonas aeruginosa–causes blue pus or pyocyanea
•
• Yersinia pestis–causes plague or black death
•
– Gives safety pin appearance in stained smears
–
– Shows stalactite growth in ghee broth culture (AIPG 2007)
–

• Because of its devastating morbidity and massive mortility, TB is also called as ‘the white plague’ and ‘the captain of all
•
men of death’
• Campylobacter jejuni is medically most important as it causes attacks of diarrhea world wide
•
• Klebsiella rhinoscleromatis causes rhinoscleroma which includes hebra nose, paralysis of soft palate with enlargement
•
of uvula
• In cholera, copro antibodies develop in the intestine appear in faeces. They consist of IgG, IgM, IgA
•
228
Zoonotic Bacteria
Species Disease Transmission and source
Bartonella henselae Cat scratch fever–lymphoadenopathy; Bacillary Cat scratch
angiomatosis causes diffuse skin hemangiomas
typically seen in AIDS patients; also peliosis hepatis
Bartonella quintana Trench fever with abrupt onset fever Seen in crowded unsanitary conditions
Brucella spp. Undulant (Malta) fever = fever waxes and wanes Diary products; contact with sheep/

(AIIMS Nov 2013, AIPG 2006) over months, hepatosplenomegaly cattle. Unpasterurised dairy products

 
give you Undulant fever
Fransiscella tularensis Tularemia, ulceroglandular i.e. ulcer with adenopathy Tick bite; rabbits, deer
Yersinia pestis Plague, buboes and rapid sepsis Flea bite; rodents
MICROBIOLOGY
Pasteurella multicoda Cellulitis From dog or cat bites.
Staphylococcus Aureus (AIIMS May 2010)
Properties • Gram +ve cocci in grape like clusters; coagulase +, Catalase +, beta hemolytic, colonies have golden colour
•
and oil paint appearance; sensitive to Lysostaphin.
• It is normal human skin flora colonizing anterior nose and intertriginous areas.
•
Virulence factors • Enterotoxin: preformed exotoxin secreted in the intestines, heat resistant. Causes food poisoning typified by
•
vomiting and diarrhea within 8 hours of food consumption.
• Toxic shock syndrome toxin 1 (TSST 1): A superantigen binds to a constant region of the T cell receptor,
•
non- specifically activating T lymphocytes resulting in unregulated inflammation; acquired from contaminated
tampons in menstruating women or from infected wounds; leads to systemic hypotension, tachycardia.
• Exfoliatin: another superantigen causes Staphylococcal Scalded Skin Syndrome (SSSS) in children
•
under 4 years; SSSS in neonates is called Ritter’s disease and in older individuals is called toxic epidermal
necrolysis. Diffuse tender erythema often with bullae and desquamation. Nikolsky’s sign is present
(sloughing of the epidermis can be provoked by gentle stroking of the skin). Milder and more common forms of
SSSS include pemphigus neonatorum and bullous impetigo
• Others are Protein A, Alpha toxin (hemolysin), Panton-Valentine leukocidin
•
Diseases • Skin infection: furuncles, boils, abcesses, carbuncles, impetigo, acute paronychia, folliculitis.
•
• Pneumonia classically seen during resolution phase of a prior viral pneumonia; pneumatoceles seen in
•
children; also follows tracheal intubation of a hospitalized patient (AIPG 2005)
 

• Bacteremia commonly due to IV drug abuse, post-surgical via wounds or nosocomial via intravenous catheters.
•
• Acute severe bacterial endocarditis of both native and prosthetic valves
•
• Osteomyelitis, sphenoid sinusitis.spinal epidural abscess; septic intracranial thrombophlebitis; septic bursitis,
•
postoperative wound infections
• MRSA (methicillin-resistant S. aureus) infection – important cause of serious nosocomial and community-
•
acquired infections. Resistant to beta-lactams due to altered penicillin-binding protein.,
DOC • For MSSA (methicillin sensitive S. aureus penicillinase resistant penicillin (oxacillin, nafcillin) with 1st generation
•
 
cephaolosporin as second line. (Methicillin caused interstitial nephritis and no longer available).
• For MRSA – vancomycin, linezolid (bacteriostatic, oral, hematotoxicity) and daptomycin (bactericidal, IV only),
•
clindamycin and TMP-SMZ.
Microbiology 229

HEMOLYTIC BACTERIA
α-hemolytic bacteria β-hemoIytic bacteria
• Form green ring around colonies on blood agar. Includes: • Form clear area of hemolysis on blood agar. Includes:
•
•
– Streptococcus pneumoniae (catalase -ve and optochin sen- – Staphylococcus aureus (catalase and coagulase +ve)
–
–
sitive)
• Streptococcus viridans (catalase -ve and optochin resistant) • Streptococcus pyogenes–group A strep (catalase -ve and
•
•
bacitracin sensitive) (AIIMS May 2010)

• Streptococcus agalactiae–group B strep (catalase -ve and
•
bacitracin resistant)
• Listeria monocytogenes (tumbling motility, meningitis in
•
newborns unpasteurized milk)
MICROBOLOGY
Streptococci (AIPG 2010)
• C carbohydrate is used for Lancfield classification. (AIIMS 2007 May 08)
•

• M protein is mainly responsible for pathogenecity. (AIIMS 1995)
•

• MC organism causing cellulitis: streptococcus pyogenes
•
• Pikes medium is used.
•
Fig.5.2 Classification of streptococci
Species or com- Lance field group Hemolysis in hu- Habitat in dis- Laboratory test Common diseases
mon name man hosts eases caused
Str. Pyogenes A Beta Throat, skin Bacitracin Neonatal meningitis,
sensitive, PYR test septicaemia
positive, ribose not
fermented
230
Species or com- Lance field group Hemolysis in hu- Habitat in dis- Laboratory test Common diseases
mon name man hosts eases caused
Str. Agalactiae B Beta Female genital CAMP test, Neonatal meningitis,
tract, rectum hippurate hydrolysis septicaemia
Str. Equisimilis C Beta Throat Ribose and Pharyngitis, endocarditis

trehalose
fermentation
Str. Anginosus A,C,F,G untypable Beta (alpha, Throat, colon, Group A strains Pyogenic infections
gamma) female genital tract bacitracin resistant,
PYR negative,
minute colony of
variants of other
groups
Enterococcus sp. D Gamma (alpha, Colon Growth in 6.5% Urinary tract infections,
MICROBIOLOGY
(str. Faecalis and beta) NaCl, PYR positive endocarditis, suppurative

other enterococci) infections
Nonentrococcal D Gamma Colon No growth in 6.5% Endocarditis
group D species NaCl
(str. Bovis)
Viridians Not typed Alpha Mouth, colon, Optochin Endocarditis (Str. Sanguis),
streptococci female genital tract resistant, species dental caries (Str. Mutans)
classification
on biochemical
properties
Good to know
• Cell wall peptidoglycan is a virulence factor that confers rigidity and structural integrity to the bacterial cell. It activates
•
complement and induces release of inflammatory cytokines.
• Streptococcus pyogenes are typed based on surface protein M, T and R.
•
M protein • Acts as a virulence factor by inhibiting phagocytosis
•
Antigenic • It is heat and acid stable, but susceptible to tryptic digestion. Extraction by Lancefield acid extraction method. Typing
•
is done by type specific sera. 80 M types have been identified.
T protein • Acid labile, trypsin resistant. Antigen is present in many serotypes of Strept. pyogenes. It may be type specific, but
•
many different types possess same T antigen. It is demonstrated by slide agglutination test using trypsin treated whole
streptoctocci. T and R proteins have no relation to virulence.
• Facultative streptococci form the most numerous single group in the oral cavity. Averaging in most surveys nearly ½ the
•
viable counts of saliva and dorsum of tongue and about 1/4th of viable counts of plaque and gingival sulcus

(AIIMS May 2008, AIPG 2007)

• The pyogenic (hemolytic) varieties are usually scarce in the oral cavity this has been attributed to a salivary inhibitory factor
•
distinct from lysozyme or hydrogen peroxide
• The pyogenic streptococci isolated occasionally from the oral cavity probably derived from the oronasopharynx and should
•
not be regarded as resident flora.
• By far the most abundant of oral streptococci are those considered in viridians group. These are divided into two broad
•
groups:
– Strept. Salivarius
–
– Strept. mitis
–
• Streptococcus salivarius average about half the viable count of facultative streptococci from the saliva or tongue
•
scrapings. This organism ordinarily numbers less than 1% of viable count in plaque.
• Majority of other oral facultative streptococci are strept. Mitis, mutans and sanguis.
•
– S. sanguis–makes up about ½ of the count of facultative streptococci in plaque, which seems to be their primary
–
habitat–causes SABE (AIIMS May 2010)

Microbiology 231

Enzymes Produced by Streptococci
Streptokinase (fibri- • Dissolves fibrin clot
•
nolysin)
Erythrogenic toxin •
•
Causes scarlet fever
Streptodornase • Produces exudative inflammation

•
Hyaluronidase • Dissolves ground substance and spreads the infection
•
Streptolysin • ASO titres increased in rheumatic fever
•
Streptococcus Pneumoniae
Properties • Gram + cocci; Flame-shaped or lanceolate diplococci; ‘Draughtsman appearance’ on blood agar; Capsule
MICROBOLOGY
•
demonstrated with India ink; Quellung reaction (Neufeld’s capsule swelling reaction) seen; Optochnin
sensitive (differentiates from S.viridans); Bile soluble; Alpha hemolytic
Virulence factors • Polysaccharide capsule: inhibits phagocytosis; forms basis of antigenic serotyping, antipneumococcal vaccine.
•
 
• IgA protease: degrades IgA in mucosal secretions.
•
• Pneumolysin(hemolysin): acts as a cytotoxin and activates the complement system, causes a release of
•
TNF- α and IL-1
 
• Cell surface proteins: surface protein A, surface adhesin A
•
• Enzymes: autolysin, neuraminidase, and hyaluronidase
•
Diseases • Community acquired pneumonia (No cavitation; in adults–lobar consolidation; in children–
•
parenchymal consolidation with bronchopneumonia; sputum contains blood)
 
• Acute otitis media
•
• Meningitis (in adults over 30), (including meningitis due to head trauma, CSF leak)
•
• Sinusitis, Bronchitis
•
High Risk Groups • Elderly (> 60 yrs), children (<2 years), Blacks.
•
(requiring pneumo- • Immunodeficiencies: HIV infection, malignancy, diabetes mellitus, after splenectomy (surgical
•
coccal vaccine) or autosplenectomy in sickle cell disease), humoral immunity defects, complement deficiencies, and
 
neutrophil dysfunction
 
• Decreased pulmonary clearance functions: asthma, chronic bronchitis, chronic obstructive pulmonary disease
•
 
(COPD), viral infections, and active/passive cigarette smoke exposure.
DOC • Penicillins, Cephalosporins

•
Prophylaxis • Polyvalent polysaccharide vaccine against 23 different S.pneumoniae serotypes. For children diphtheria toxoid-
•
conjugated vaccine against 7 serotypes.
Neisseria Meningitidis
Properties • Gram-negative; diplococcus arranged like 2 kidney beans facing each other; Catalase and oxidase positive;
•
ferments maltose; grows on chocolate agar
• Transmitted via respiratory droplets, colonise nasopharynx, Carriers are the most important source of infection;
•
outbreaks occur in military barracks or communal settings.
Virulence factors • IgA protease, antiphagocytic capsule. People with defects in late complement pathway (C6-C9) are prone to
•
Neisseria infections.
Diseases • Meningitis, in CSF meningococci are seen inside neutrophil
•
• Waterhouse-Friderichson syndrome–sepsis resulting in DIC and adrenal gland failure due to adrenal infarction
•
 
DOC • Penicillin.
•
Vaccines • Available against strains A and C, Y, W135. The vaccine is not recommended for pregnant women and children
•
< 2 years.
• Chemoprophylaxis is with Rifampicin
•
232
Neisseria Gonorrheae
Properties • Gram-negative, diplococci inside neutrophils; catalase and oxidase positive, does not ferment maltose; grows on
•
Thayer martin medium (chocolate agar with antibiotics to suppress genitourinary colonizers)
• Sexually transmitted.
•
Virulence factors • IgA protease, Pili. People with defects in late complement pathway (C6-C9) are prone to Neisseria infections
•
Causes • Chronic urethritis (‘clap’) with stricture formation MC in bulbar urethra.
•
• PID, salpingitis, vulvovaginitis (only in prepubertal since adult vagina resistant to infection due to acid pH of
•
 
vaginal secretions), proctitis (‘watercan’ perineum)
• Pharyngitis, conjunctivitis, ophthalmia neonatorum.
•
DOC • Penicillin
•
MICROBIOLOGY
Meningococci (N. meningitides) Gonococci (N.gonorrheae)

• Polysaccharide capsule • No Polysaccharide capsule
•
•
• Maltose and Glucose fermentation • No maltose fermentation
•
•
• Vaccine present • No vaccine
•
•
• Respiratory and oral secretions • Sexually transmitted
•
•
• Plasmids rare • Plasmids frequent
•
•
Haemophilus Influenzae
Properties • The first free-living organism whose entire genome has been sequenced.
•
• Gram-negative; variable shape (pleomorphic coccobacillus).
•
• Aerosol transmission; culture on chocolate agar requires factor V (NAD) and X (hematin) for growth.
•
Virulence factor • Type b polysaccharide capsule; IgA protease
•
Haemophilus. Influ- – Acute Epiglottitis (HiB MC cause)
–
enzae causes – Meningitis in children < 2years of age.
–
– Otitis media
Pneumonia (community acquired) - Nontypable H. influenzae is the 2nd MC cause; common among pa-
–
–
–
tients with COPD or AIDS.
 
DOC – Treat meningitis with ceftriaxone; rifampicin prophylaxis in close contacts
–
– Vaccine contains type B capsular polysaccharide conjugated to diphtheria toxoid or other protein. Hib
–
conjugate vaccine given between 2 and 18 months of age.
 
Corynebacterium
Properties • Gram + Rod, thin, club shaped, arranged in palisades, V or L shaped formations, cuneiform (Chinese letter)
•
pattern.
• Metachromatic granules composed of polymetaphosphate (volutin, Babes-Ernst, polar granules) are
•
stained by special stains - Albert’s, Neisser’s, Ponder’s.
 
• Form black colonies on tellurite agar (in 2 days); grow very rapidly on Loeffler’s serum slope (in 6-8
•
hours); Respiratory droplet transmission.
 
Virulence factors • Diphtheria toxin (exotoxin encoded by β prophage) ADP-ribosylates EF2 thereby inhibiting protein synthesis
•
in the cell. Similar to pseudomonas exotoxin A.
• Shick test is the injection of pure diphtheria toxinintradermally into a patient, if no inflammation occurs the
•
patient is immune (AIPG 2002)

• Elek’s gel precipitation test is an in vitro test for finding toxigenicity of diphtheria
•
Microbiology 233

Causes • Pseudomembranous pharyngitis (grayish-white membrane) – faucial diphtheria is MC.
•
• Cervical Lymphadenopathy – Bull neck
•
• Toxin has special affinity for Myocardium, Adrenals and Nerve endings (MAN). Also kidneys and liver can be
•
 
involved.
DOC •
•
Penicillin; but for treatment of carriers and for prophylaxis erythromycin is more effective.
Clostridium
• Gram-positive rods, obligate anaerobes, spore forming, highly pleomorphic.
•
• Clostridia are motile (stately) with peritrichate flagella except Cl.welchii and Cl.tetani type VI.
•
• Capsulated clostridia are Cl.welchii and Cl.butyricum ONLY.
•
• Cl.histiolyticum is aerotolerant and may even grow aerobically. For anaerobic growth, more important than the absence
MICROBOLOGY
•
 
of oxygen, is the presence of a sufficiently low Redox potential in the medium.
• In humans, clostridia normally reside in the gastrointestinal tract and in the female genital tract.
•
• Of the 30 or more species that normally colonize humans, Clostridium ramosum is the most common.
•
• C. perfringensis the most common of the clostridial species isolated from tissue infections and bacteremias.
•
Classification
Proteolytic Predominating Saccharolytic Predominating (AIPG 2012)

• Cl.bifermentans • Cl.welchii
•
•
• Cl.botulinum A, B, F • Cl.septicum
•
•
• Cl.chauvoei
• Cl.histiolyticum
•
•
• Cl.oedematiens
• Cl.sordelli
•
•
• Cl.sporogenes
•
Slightly proteolytic but not saccharolytic
Cl.difficle; Cl.tetani.
Neither proteolytic nor saccharolytic

Cl.cochlearum
Cl. Tetani
Properties Gram + rod, terminal spores give ‘drumstick’ appearance.
Toxins • Haemolysin (tetanolysin) and neurotoxin (tetanospasmin).

•
– Tetanospasmin is an exotoxin produced at site of inoculation, carried by bloodstream to peripheral nerves, trans-
–
 
ported retrograde up the axon to the proximal synapse (i.e. acts presynaptically, unlike strychnine, which acts post-
synaptically) where it inhibits the release of inhibitory signals like glycine, thereby causing unopposed stimulation of
the nerve.
Diseases • Tetanus
•
– Infects dirty wounds, causing permanent neuromuscular stimulation, classically lockjaw from inability to relax jaw
–
muscles, and risus sardonicus (sardonic smile), death is ultimately secondary to respiratory failure
DOC • Antitetanus immunoglobulin. Prophylaxis: vaccination with tetanus toxoid

•
Cl. Botulinum
Properties • Gram + rod with subterminal spores, obligate anaerobe
•
Virulence • Botulinum toxin is preformed, heat-labile, absorbed in gut, carried by blood to nerve endings where it blocks the release
•
 
factors of acetylcholine into the nerve synapse.
• Botulinum toxin is being used as therapy for blepharospasm, strabismus, and other dystonias.
•
234
Diseases • Classic Botulism: Symptoms begin within 12-36 hours after ingestion of food. Classic “descending paralysis” with
•
significant bulbar effects (ocular paresis, diplopia, dysarthria, dysphagia, carnial neuropathy) ultimately causing respiratory
collapse in 1-7 days after onset.
• Wound botulism: Caused by contamination of wounds by spores in soil, features same as classic botulism.
•
• Infant botulism: Seen after ingestion of bacterial spores in honey; disease usually not fatal in infants.
•
DOC • Antitoxin
•
Pseudomonas (AIIMS May 2010)
Properties • Gram (-) ve aerobic motile tacilli with polar flagella
•
• Pseudomonas aeruginosa the most common in this group
•
• P.aeruginosa (P.pyocyanea)
•
• Obligate aerobic bacilli which is differentiated from enteric Gram (-)ve bacilli by its abillllity to oxidize
•
MICROBIOLOGY
indophenols and inability to ferment lactose.

• Non capsulated but many stains have mucoid slime layer of alginate. Particularly from patient of cystic
•
fibrosis.
Culture and growth • Selective media- Cetrimide agar

•
characteristics
Pigment • Pyocyanin- Bluish green produced only by P. aeruginosa inhibits growth of many other bacteria.
•
• Fluorescin-Greenish yellow, produced by all species of pseudomonas
•
Classification • On the basis of difference of lipopolysaccharide
•
• Restriction endonuclease typing with pulsed gel electrophoresis is most reliable method.
•
Pathogenicity and resis- • Most common and most serious cause of infection in burns
•
tance • Most common infection outside hospital is suppurative otitis
•
• Causative agent for Shanghai fever
•
• Blue pus with characteristic fruity odor
•
• Resistant to common antiseptic and disinfectant such as dettol, even may grow profusely in bottle of these
•
antiseptic
Virulence factor • Pilli or fimbriac

•
• Mucoid exopolysaccharide/ alginate
•
• Lipopolysaccharide or endotoxin
•
• Alkaline protease
•
• Elastase
•
• Exotoxin (A,S,T,U,Y)
•
• Phospholipased hemolysin
•
• Exotoxin A- Acts as NADase, protein synthesis
•
• Exotoxin B- ribosylation of GTP finding protein, disruption of cellular actin cytoskeleton
•
Bacteroides (AIIMS May 2010, Nov 2012, AIPG 2001)
• Bacteroides species are the most predominant flora in the intestine far out numbering the Escherichia coli.
•
• Strictly anaerobic,
•
• Gram negative,
•
• non-motile,
•
• non sporing bacilli, but may appear pleomorphic.
•
• Virulence factors:
•
– Capsular polysaccharide
–
– Have LPS but lack the lipo-polysaccharide structure with endotoxic activity
–
– Produces superoxide dismutase and can survive in absence of oxygen for days
–
Microbiology 235

Legionella (AIIMS May 2009) – S. typhi(H and O)
–
– S. paratyphi (H)
• Morphology
–
• In case of Salmonella infections, it is a demonstration of
•
•
– Gram negative agglutinating antibodies against antigens O-somatic and
–
– Coccobacilli H-flagellar in the blood.
–
– Non capsulated • For brucellosis, only O-somatic antigen is used.
•
–
– Motile by polar or subpolar flagella • The highest dilution of the patients serum in which
–
•
– Best visualized by direct fluorescent antibody agglutinations occurs is noted, e.g. if the dilution is 1
in160 then the titer is 169.
–
• Transmission
•
– The natural habitat is aquatic bodies • A single test of O titer of 1:100 or more and of H titer of
•
1:200 or more is significant.
–
– Multiply and survive inside free living amoeba and
• A rising titer of four fold or higher in an interval of 7–10
–
protozoa
•
– Man to man transmission does not occur. days is more meaningful than one test
MICROBOLOGY
–

(AIIMS May 2012)
VIROLOGY

Anthrax
• Cutaneous anthrax • Viruses: Smallest infectious agent containing only
•
•
– Hide porter’s disease one kind of nucleic acid as their genome. A
• Virion: Extracellular infectious particle. (AIPG 1990)
–
– As it used to be common in dock workers carrying
•

–
loads of hides and skin on their bare backs. • Largest virus: Pox Virus (300 nm).
•
• Smallest Virus: Foot and Mouth Disease Virus (20
• Pulmonary anthrax
•
nm).
•
– Wool sorter’s disease because it is used to be common • Capsid is a protein coat surrounding nucleic acids.
–
in worker’s in wool factories due to inhalation of dust
•
from infected wool. • Capsid+nucleic acid is Nucleocapsid.
Prophylaxis of Anthrax–The Sterne vaccine contained
•
• • Virusoids are nucleic acids that depend on helper viruses
•
spores of noncapsulated avirulent mutant strain. The
•
to package the nucleic acids into virus-like particles.
Mazucchi vaccine contained spores of stable attenuated
carbazoo strain in 2% saponin • Viroids are simply molecules of naked, cyclical, mostly
•
double-stranded, small RNAs and appear to be restricted
• Anthrax bacilli can be stained by trichome methylene to plants, in which they spread from cell to cell and are
•
blue stain (AIIMS May 2009) replicated by cellular RNA polymerase II.

Widal Test: (AIIMS May 2010, AIPG 2002) • Prions are protein molecules that can spread from
•
cell to cell and effect changes in the structure of their
• The Widal test is a presumptive serological test for normal counterparts (cellular proteins). Prions have
•
Enteric fever or Undulant fever/ typhoid fever been implicated in neurodegenerative conditions such
• Test for measurement of H and O agglutinins as Creutzfeldt-Jakob disease, Kuru, and Gerstmann-
•
• Two tubes are used Straussler disease. Prions have also been implicated in
neurodegeneration associated with human infection with
•
– Dreyer’s tube (conical bottom for H)
bovine spongiform encephalopathy (“mad cow disease”).
–
– Felix tube (round bottom for O)

(NEET 2013, AIIMS Nov 2013, Nov 2012, May 2012)
–
• Antigens used:

•
Classification of DNA Viruses
Capsid symmetry Virion: Enveloped or Naked Physical type of Nucleic acid Virus family
Icosahedral Naked SS Parvoviridae
DS circular Papovaviridae
DS Adenoviridae
Enveloped DS Herpesviridae
Complex Complex coats DS Poxviridae
DS circular HepaDNA viridae
236
Classification of RNA Viruses

Capsid symmetry Virion: Enveloped or Naked Physical type of Nucleic acid Virus family
Icosahedral Naked SS PicoRNA viridae
DS segmented Reoviridae
Enveloped SS Togaviridae
Unknown or complex Enveloped SS Flaviviridae
SS segmented Arenaviridae
SS Coronaviridae
SS Retroviridae
MICROBIOLOGY
Helical Enveloped SS segmented Bunyaviridae

SS segmented Orthomyxoviridae
Paramyxoviridae
Rhabdoviridae
Cell Cultures for Viruses (AIPG 2012)

Primay cell • Rhesus monkey kidney cell culture
•
culture • Human amnion cell culture
•
• Chick embryo fibroblast cell culture (AIIMS May 2013)
•

Diploid cell • WL38 Human embryonic lung cell strain
•
strains • HL8 Rhesus embryo cell strain
•
Continuous cell • HeLA Human carcinova of cervix cell line
•
lines. • HEP-2 Human epithelium of larynx
•
• KB Human carcinoma of nasopharynx cell line
•
• McCoy Human synovial carcinoma cell line
•
• Detroit-6 Sternal marrow cell line
•
• Chage C/I/L/K Human conjunctiva(c) Intestine (I), liver ( L) kidney (K)
•
• Vero vervet monkey kidney cell line
•
• BHK -21 Baby hamster kidney cell line.
•
Good to Know • Koplick’s spots are pathognomic intraoral spots that
•
appear 2-3 days before the onset of cutaneous rash in
• The first human disease proved to have viral etiology was measles (Rubeola virus). They are bluish white ulcerations
•
yellow fever on the buccal mucosa.
• Though HIV is present in saliva, it is not transmitted • Parvovirus B19 induces aplastic crisis in children with
•
through saliva because of presence of anti HIV salivary
•
the hemolytic anemias
protein called ‘secretory leucocyte protease inhibitors’.
• Incomplete viruses seen in influenza infection, show high
• Pigs are important source of Japenese encephalitis
•
haemagglutination titre and low infectivity. This is known
•
• The only grp A arbovirus causing epidemic disease in as Von Magnus phenomenon
•
India is Chikungunya, vector is Aedes aegypti • Fever acts as natural defense mechanism against viral
•
• Inclusion bodies–demonstrated in viruse infected cells infection. An exception is herpes simplex which gets
activated by fever to produce fever blisters
•
histologically. They may be intracytoplasmic (Rabdo
virus, pox virus), intranuclear (Herpes viruses) or both • Vaccinia virus is unique in that it is an artificial virus and
•
(Measles virus). The intracytoplasmic inclusion bodies in does not occur in nature
rabies (Rhabdo virus) are known as Negri bodies • Adenoviruses have the appearance of a space vehicle
•
Microbiology 237

Hepatitis Virus
Hepatitis A virus • Is a nonenveloped 27-nm, heat, acid-, and ether-resistant RNA virus in the hepatovirus genus of the
•
KERALA 1999 picornavirus family,
AIIMS 19910 ••
Previously called enterovirus 72 No chronic course.
• Inactivated by boiling, formalin, UV radiation.
•
Hepatitis B virus • Is a DNA virus, Hepadenavirus Contains DNA dependent DNA polymerase and RNA dependent reverse
•
(AI 2000 PGI 1987 transcriptase. (AIPG 2010)

Manipal 2006 AI • Reverse transcriptase is coded by P gene.
•
2003
• Dane particle is HBV.
•
• HBV strain in India is Ayw, Adr
•
• HBV has maximum perinatal transmission risk.
•
• Oncogenicity present in Hepatitis B especially after neonatal infection.
MICROBOLOGY
•
• Carrier state present in Hepatitis B
•
• Hepatitis B virus may present in blood and other body fluids and excretions such as saliva, breast milk, semen,
•
vaginal secretions, urine, bile etc.
• Feaces not known to be infectious
•
Hepatitis C virus • “Non-A, non-B hepatitis,” is a linear, single-stranded, positive-sense, RNA virus; (Enveloped) HCV belongs
•
to family Flaviviridae.Major cause of post transfusion hepatitis Causes chronic hepatitis.

(PGI 2005 AIIMS 2004 AIIMS 1998 JIPMER 1999)

Hepatitis D • The delta hepatitis agent, or HDV, is a defective RNA virus. Coinfects with and requires the helper function of
•
HBV (or other hepadnaviruses) for its replication and expression.Resembles plant viruses
Hepatitis E • Previously labeled “epidemic or enterically transmitted non-A, non-B hepatitis”, HEV is an enterically
•
transmitted virus. Is a Calci virus.
 
• Mortality in pregnancy is a feature of Hep E virus.
•
• Hepatic encephalopathy in pregnancy is seen.
•
• Fulminant hepatic failure can occur with Hep C in pregnancy.
•
Hepatitis G • Also called GB virus RNA virus. Blood borne virus Resembles Hep C virus. Lamuvudine responsive
•
 
 
Also note
• Spreads by faeco oral route-Hepatitis A and E (AIIMS 2003)
•

• Spreads by percutaneous route-Hepatitis B,C and D
•
– As we can prevent HBV hepatitis by vaccine, hepatocellular carcinoma becomes the only human cancer which is
–
vaccine preventable
– Antibody to HbsAg have little role in the diagnosis of acute hepatitis as it indicates good immunity after treatment
–
of the patient is protected.
– HbsAg may be the earliest virological marker for viral hepatitis but it is not confirmatory evidence for the diagnosis
–
of acute viral hepatitis
– Presence of HbsAg alone may also be seen in carrier state and in cases of chronic hepatitis.
–
– So presence of HbsAg alone in serum indicates three possible diagnosis, ie either
–
Acute hepatitis B or

Chronic hepatitis B or

Carrier state of hepatitis B

– To establish a diagnosis of hepatitis B confirmly, the presence of IgM anti Hbc is required along with HbsAg.
–
238
Serological Markers for Diagnosis of Viral Hepatitis

Hbs Ag • Hbs Ag with or without IgM anti Hbc represents HBV infection
•
IgM anti Hbc • If IgM anti HBc is present, HBV infection is considered acute
•
• •
If IgM anti HBc is absent, then HBV infection is considered chronic
• Diagnosis of acute hepatitis B can be confirmed even in the absence of Hbs Ag when IgM anti Hbc is detectable
•
IgM anti HAV • Presence of IgM anti HAV confirms acute hepatitis A infection
•
Anti HCV • Presence of anti HCV confirms acute hepatitis C infection.
•
• Antibodies to core antigen are of two types: IgM anti HBc and IgG anti Hbc. These antibodies are not protective
•
• Presence of IgM anti HBc indicates – acute infection
•
• Presence of IgG anti Hbc indicate – chronic infection
•
MICROBIOLOGY
Hepatitis B surface • With the development of antibody to HbsAg i.e. anti HbsAg the HbsAg disappears
•
antibody (anti – HBs): • Patient is protected
•
• Anti HbsAg indicates good immunity
•
• Anti HbsAg indicates protection against hepatitis B
•
HbcAg • Hidden component of viral core and is not detectable at all (AIPG 2008)
•

Anti HBcAg • Antibodies to HBcAg develops early in the course of disease
•
• This is the first antibody to appear after an acute infection and persists in serum even during the recovery
•
phase
• When acute, antibody is of IgM type
•
• When chronic antibody is of IgG type
•
Hbe Ag • Is a soluble protein found only in HbsAg positive serum
•
• It appears shortly after the appearance of HbsAg
•
• Its principal clinical usefulness is an indicator of relative infectivity
•
• It denotes viral replication
•
Anti HbeAg:(AIPG • Anti HbeAg appears after the disappearance of HbeAg
•
2007) • It indicates diminished viral replication and decreased infectivity
•
• Hepatitis B immune globulin (HbIG) – a product available for prophylaxis against HBV infection. HBIG is
•
prepared from plasma containing high titres of anti- Hbs and provides short term protection (3 to 6 months)
Role of HBV DNA in the Diagnosis of Hepatitis B

• HBV DNA has a same role as the HBeAg is like HbeAg it is an indicator of viral replication
•
• But the test for detection of HBV DNA are more quantitative and sensitive.
•
• HBV DNA is detected by;
•
– Hybridization assays
–
– PCR
–
Measles (Rubeola)
A highly communicable disease, is spread by droplet infection and the period of infectivity is from 4 days before until 2 days
after the onset of the rash. The incubation period is 8-14 days. Two distinct phases of the disease can be recognized.
The pre-eruptive and ca- • This is the stage of viraemia and viral dissemination. Malaise, fever, rhinorrhoea, cough, conjunctival
•
tarrhal stage suffusion.
• Pathognomonic Koplik’s spots are small, grayish, irregular lesions surrounded by an erythematous
•
base are found in greatest numbers on the buccal mucous membrane opposite to the second molar
tooth. They occur a day or two before the onset of the rash.
The eruptive or exanthem- • This is characterized by the presence of a maculopapular rash that initially occurs on the face,
•
atous stage chiefly the forehead, and then spread rapidly to involve the rest of the body.
Microbiology 239

Herpes Viruses
• Virus Varicella zoster virus (VZV), α herpes virus • Chickenpox
•
 

•
(NEET 2013) • Shingles (herpes zoster)

•
• Cytomegalovirus (CMV), β herpes virus • Congenital infection In AIDS: pneumonitis, retinitis (cottage cheese or tomato
•
•
 
ketchup retinopathy, Pizza pie retinopathy), enteritis, generalised infection
• Epstein-Barr virus (EBV), γ herpes virus • Infectious mononucleosis Burkitt’s lymphoma Nasopharyngeal carcinoma Oral
•

•
 
 
 
(AIPG 2001) hairy leukoplakia (AIDS patients)
• Herpes simplex virus 1 (HSV 1) • Herpes labialis (cold sores) keratoconjuctivitis Finger infections (whitlow)
•
 
•
Encephalitis Gingivostomatitis
• Genital infections
•
• HSV 2 • Genital infections Neonatal infections (acquired during vaginal delivery)
•
•
 
• Human herpes virus 6 (HHV- 6) and HHV-7 • Exanthem subitum disease in immuncompromised patients
•
•
 
 
MICROBOLOGY
• HHV-8 • A/w Kaposi’s sarcoma
•
•
Polio Virus Infection May follow One of the Several Courses
Inapparent infection • It occurs in 80-95% of cases and causes no diseases
•
Abortive poliomyelitis • It occurs in about 5% of patients
•
• It is a non specific influenza like syndrome which occurs 1- 2 week after infection.
•
• Fever, malaria, anorexia and headache are prominent features and there may be sore throat and abdominal
•
or muscular pain.
• The illness is short lived for upto 2-3 days
•
• The physical examination may be normal or may reveal nonspecific pharyngitis abdominal or muscular
•
tenderness and weakness.
• Recovery is complete and no neurological sign or sequence develop
•
Nonparalytic polio- • It occurs in 1% of patients infected with poliovirus
•
myelitis • They present as soreness and softness of the posterior muscles of the neck, trunk and limbs
•
Paralytic poliomy- • Paralytic poliomyelitis develops in about 1% patients causing three clinically recognizable syndroms which are:
•
elitis – Spinal paralytic poliomyelitis
–
– Bulbar poliomyelitis
–
– Polioencephalitis
–
The risk factors found to precipitate an attack of paralytic polio in individuals infected with polio include:
• Fatigue
•
• Trauma
•
• I.M injections
•
• Operative procedure like tonsillectomy syndromes especially during epidemics of polio and
•
• Administration of immunizing agents particularly alum containing DPT
•
Viral Zoonotic Infections
Disease Pathogen Animal reservoir Mode of transmission
Prions (Kuru)
vCJD Prion protein Cattle Ingestion (CNS tissue)
Viral
Lessa fever Flavivirus Multimammate rat Direct contact
Japanese encephalitis Rhabdovirus Pigs Mosquito bite
Flavivirus Dog and other mammals Saliva, faeces (bats)
Rabies Corona virus Primates Mosquito bite
Yellow fever Civet cats and small mammals Droplet
SARS
240
MYCOLOGY
• Phycomycetes: are lower fungi with nonseptate hyphae and form endogenous asexual spores called “sporangiospores”
•
contained within swollen sack like structures called “sporangia”.
• The higher fungi given have septate hyphae and make exogenous asexual spores called “conidia”
•
• Ascomycetes form sexual spores (ascospores)
•
• Basidiomycetes form sexual spores (basidiospores)
•
• Fungi imperfecti (deuteromycetes or hyphomycetes) contain fungi whose sexual phases have not been distinguished.
•
• Fungi are cultured in Saboubards medium.
•
• NON Culturable fungus: Rhinosporodium
•
• Common culture media used in mycology are Saboraud’s dextrose agar, Cornmeal agar and Czapek-Dox medium.
MICROBIOLOGY
•

(AIPG 2003, AIIMS Nov 2006)

• Fungi are Eukaryotic organisms.
•
• Fungal cell wall contains Chitin. (Chitin is a polysaccharide of long chains of N acetyl glucosamine.)
•
• Fungal Cell membrane contains Ergosterol in contrast to human cell membrane which contains cholesterol.
•
• STAINED by PAS
•
• Most fungi reproduce asexually by forming asexual spore’s conidia.
•
• Fungi without sexual stage: fungi imperfectii
•
• Sporangiospores, blastospores, arthrospores and chlamydospores are asexual spores. Zygospores, ascospores and
•
basidiospores are sexual spores
• Candida species other than Candida glabrata appear in tissue as both budding yeasts and tubular elements called
•
 
pseudohyphae. (Delhi 1987)

• Pneumocystis carinii is closer to fungi than to parasites by ribosomal sequences
•
• Only pathogenic yeast–Cryptococcus neoformes
•
• Non pathogenic yeast–Saccharomyces cerevisae
•
• The mechanism by which most fungi cause disease is hypersensitivity
•
• Aflatoxicosis is produced by Aspergillus flavus while ergotoxicosis is produced by fungus Claviceps purpuria
•
• Reynold’s Braude phenomenon–rapid method of identifying C ablicans is based on its ability to form germ tubes within
•
2 hours when incubated in human serum at 370C.
• Sclerotic bodies measuring 3–5 mm in size multiseptate, chestnut, brown colour is characteristic of Chromoblastomycosis
•
Candidiasis (Candida Albicans)
Properties • Common normal flora but opportunistic pathogen; budding yeast with pseudohyphae in culture at 20°C; germ tube
•
formation at 37°C diagnostic - Reynolds-Braude phenomenon
• Transmission occurs by inhalation of spores. No person-to-person spread.
•
Causes • Oral Thrush, perleche (at angle of mouth), esophagitis in immunocompromised (neonates, steroids, diabetes,
•
AIDS)
• Vulvovaginitis (high pH, pregnancy, diabetes, use of antibiotics)
•
• Chronic mucocutaneous candidiasis (a/w T-cell deficiency)
•
• Endocarditis in IV drug users (caused by Candida parapsilosis and Candida tropicalis), paronychia
•
• Disseminated candidiasis (to any organ),
•
• Intertrigo in skin folds
•
Treatment • Nystatin for superficial infection; amphotericin B for serious systemic infection.
•
Microbiology 241

Cryptococcosis (Cryptococcus Neoformans)
Properties • Yeast with large capsule seen on India ink stain; mucicarmine stain in tissues; Culture on Sabouraud’s agar;
•
Latex agglutination test detects polysaccharide capsular antigen Acquired by inhalation of fungus into the lungs;
Found in soil, pigeon droppings.
Causes • Cryptococcal meningitis in immunosuppressed, MC in AIDS; small cysts in gray matter of brain - “Soap bubble”
•
lesions
• Other lesions are pulmonary, skin, osteolytic (presenting as cold abscess), prostatitis, endophthalmitis, hepatitis,
•
pericarditis, endocarditis and renal abscess.
Treatment • Amphotericin, then fluconazole for life for prophylaxis.
•
Sporotrichosis (Sporothrix Schenckii)
• Dimorphic fungus that lives on vegetation; Cigar-shaped budding yeast visible in pus; “asteroid bodies” are seen on
MICROBOLOGY
•
histology of the lesion.
• Infection is acquired through thorn pricks (“rose gardener’s” disease) or other minor skin trauma.
•
• Causes
•
– Plaque sporotrichosis: Infection limited to the site of inoculation
–
– Lymphangitic sporotrichosis: More common, infections extends along proximal lymphatic channels, skip areas seen,
–
 
spread beyond the regional lymph nodes is uncommon. Most cases occur in the upper limb.
 
• Treat with itraconazole or potassium iodide.
•
Darling’s Disease
• Acquired via inhalation of spores in bat guano or bird droppings.
•
• Causes
•
– Pneumonia, chronic pulmonary histoplasmosis. -Sputum culture is the preferred method for diagnosis
–
– Ocular histoplasmosis syndrome is a distinct clinical form of uveitis, although a positive histoplasmin skin test is a
–
requisite for diagnosis, none of the patients involved has had active histoplasmosis.
• Treatment: Itraconazole for pneumonia, amphotericin for disseminated disease
•
Pneumocystis Jiroveci (formerly pneumocystis carinii)
• Clumps of cysts best seen on methenamine silver staining and culture of bronchoscopic washings;
•
• Causes disease in AIDS patients or immunosuppressed.
•
• Causes
•
– PneumoCystis jiroveci Pneumonia (PCP) is characterized by fever, dyspnea and nonproductive cough; severe hypoxia
–
and dyspnea out of proportion to unimpressive lung exam; CXR shows ground-glass haziness in bilateral lower lobes,
no hilar adenopathy, and pleural effusions are rare.
– Extrapulmonary manifestations of Pneumocystis carinii infection in patients with HIV infection are – Acute otitis,
–
retinitis, visceral cystic calcifications, necrotising vasculitis, intestinal obstruction, lymphadenopathy, bone marrow
involvement, ascites, thyroiditis.
• Treatment: Trimethorpim-sulfamethoxazole (TMP-SMX); Prednisolone is given when PaO2 is < 70 mm Hg;
•
combination of clindamycin and primaquine is likely to be more effective than intravenous pentamidine in the treatment
of infections that are resistant to TMP-SMX.
 
Mucormycosis
• Mold with irregular nonseptate hyphae branching at wide angles (>90 deg).
•
• Frequent causes are Mucor, Rhizopus, Absidia and Cunning hamella.
•
• Fungi also proliferate in the walls of blood vessels and cause infarction and necrosis of distal tissue.
•
• Disease mostly in ketoacidotic diabetics, organ transplantation patients, and leukemic patients.
•
242
• Types:
•
– Rhinocerebral: Can start as headache or visual loss, starts in paranasal sinuses, spreads to orbit (proptosis, CN III palsy,
–
hard palate, brain (frontal lobe abscess).
– Pulmonary and cutaneous mucormycosis
–
• Treatment: Surgical debridement plus amphotericin B.
•
Coccidiodomycosis
• Coccidioides imnitis reproduces in host tissue by forming small endospores within mature spherules. It forms thick-walled,
•
barrel-shaped spores called arthrospore; Infection results from inhalation of arthrospores.
• Causes
•
– A self-limited influenza like fever (valley fever) with arthralgia (desert rheumatism), and erythema nodosum
–
 
– Disseminated disease - pneumonia and meningitis may occur.
–
• Treatment: amphoptericin B, fluconazole, itraconazole.
MICROBIOLOGY
•
Aspergillosis
• Aspergillus fumigatus (MC), A.niger, A.flavus; mold with septate hyphae that branch at a V-shaped (45°) angle.
•
• Causes
•
– Allergic bronchopulmonary aspergillosis (ABPA); a hypersensitivity reaction to fungus in large airways, similar to
–
 
asthma (high IgE)
– Aspergilloma (“fungus ball”) in an old (usually tuberculous) lung cavity, causes hemoptysis, rarely becomes invasive.
–
 
– Invasive pulmonary aspergillosis, (in neutropenic patients, leukemics, and chronic granulomatous disease)
–
 
– Disseminated disease: in patients on chronic steroids, neutropenics.
–
– Otomycosis, Corneal ulcers.
–
• Treatment: Amphotericin B, itraconazole, voriconazole.
•
PARASITOLOGY
Pathogenic lesions produced by Entamoeba histolytica
Intestinal lesions Extraintestinal or metastatic lesions
• Acute amoebic dysentery • Liver: Amoebic liver abscess
•
•
– Complication: – Multiple small abscesses involving whole liver
–
–
- Multiple ulcer – A large solitary abscess in the right lobe

–
- Pericaecal and pericolic abscess • Lung: Primary: small multiple abscess

•
- Amoebic appendicitis – Secondary–single abscess in lower lobe of right lung

- Peritonitis
–
• Brain: A brain abscess in one of the cerebral hemisphere

- Perforation
•
• Spleen: Splenic abscess

- Gangrene and fistula of gut
•
• Skin: Granulomatous inflammation of skin

• Chronic intestinal amoebiasis
•
•
– Single latent-ulcer in the caecum • Urogenital tract: Amoeba enters through recto-vesicle fistula and
•
recto vaginal fistula
–
– Multiple small superficial ulcers scattered throughout
–
– Thickened caecum and colour
–
– Pigmented/ non-pigmented scar
–
Laboratory Diagnosis of Kala azar
Examination of blood smear by Shortt’s Method Leishmania skin test – Montenegro test
• For this, blood smear is dried as quickly as possible to prevent • Principle: Delayed hypersensitivity
•
•
rouleaux formation. • 0.1 ml (10%) antigen suspension is injected intradermally on
•
• Smear is fixed with methanol forearm
•
• Then washing is done with distilled water • Indurations are considered positive.
•
•
• Finally staining is done with dilute Giemsa stain, again • Skin test is negative in Indian kala azar.
•
•
washing is done in distilled water and film is dried and
examined.
• LD bodies are seen in neutrophils and monocytes (Leishmani
•
donovani –LD)
Microbiology 243

Clinical Features of Malaria
• Incubation period is about 10 days
•
• The symptoms are divided into three stages:
•
– Cold stage: In this stage there is fever for 1 -2 hours followed by cold hands and feet, bodyache and shivering.
–
– Hot stage: lasts for about 4 hours during which there is high fever (upto 1050 C) vomiting and headache.
–
– Swearing stage: It lasts for 1-2 hours during which there is lot of sweating and fever comes to normal.
–
– In benign form, fever develops on every third day ( tertian fever) or fourth day (quatrain fever)
–
– In malignant form, fever develop more often (less than three days) and there may be vomiting and jaundice.
–
Species Disease Important features Blood smears Liver stages Treatment
Plasmodium vivax Benign tertian 48 – Hour fever spikes Enlarged host cells and Persistent Chloroquine
MICROBOLOGY
fever trophozoites hypnozoites
Plasmodium ovale Bengin tertian 48 – Hour fever spikes Oval, jagged, RBCs Persistent Chloroquine
Plasmodium malariae* Quartan or 72-hour fever spikes Bar and band forms; No persistent Chloroquine
malarial rosette schizonts stage
Plasmodium Malignant tertian Irregular fever spikes; Multiple ring forms*; No persistent Reistant to choloroquine
falciparum causes cerebral crescent shaped stage

(AIPG 2010) malaria gametes

• Malaria
•
– Sporozoites or infective stages to man where as gametocytes are infective stages to mosquito. So gametogamy occurs in
–
man and sporogamy occurs in mosquito. (AIIMS May 2010)

– Sporozoites are sickle shaped and merozoites are banana shaped
–
– Malaria pigment in Haematin–globin pigment
–
• P. vivax: Benign tertian malaria
•
– Infected erythrocytes shows Schuffner’s dots
–
• P. falciparum: Malignant tertian malaria or Black water fever
•
– Tropical splenomegaly syndrome
–
– Cerebral malaria
–
– Infected RBC show Maurer’s dots
–
• P. malaria: Quartan malaria
•
– Infected RBCs shows Zeimann’s dots
–
• P. ovale: Ovale tertian malaria
•
– Infected RBC show Schuffner’s dots
–
Taenia solumn Pork tapeworm
Taenia saginata Beef tapeworm
Diphyllobothrium latum Fish tapeworm

Echinococcus granulosus Dog tapeworm
Hymenolepsis nana Dwarf tapeworm
Entrobius Pin worm, thread worm, seat worm
Ancylostoma Hook worm

Trichuris trichura Whip worm
Ascaris Round worm
244
GROUP SPECIES DISEASE VECTOR VERTEBRATE RESERVOIR

Typhus R. prowazeki Epidemic typhus – Bril – Zinsser Louse Human beings
R. typhi Endemic typhus Rat flea Rat
R. felis Endemic typhus Cat flea Opossum
Spotted fever R. rickettsii Rocky mountain spotted fever Tick Rabbit, dog, small rodents
R. siberica Siberian tick typhus Tick Wild animal cattle
R. conori • Boutonneus fever Tick Dogs, rodents
•
• S. African tick typhus
•
• Kenyan tick typhus
•
• Indian tick typhus
•
MICROBIOLOGY
R. australis Queen land tick typhus Tick Brush rodents
R. japonica Oriental spotted fever Tick -----------------
R. akari Ricketssial pox Gambarid mite Mouse
Scrub typhus O. tsutsu gamushi Scrum typhus Tromboculid mite Small rodents, birds
Lyme disease Borrelia burgdorferi Lyme disease Ixodid tick -------------

(AIIMS May 08)
• Ascaris pneumonia is characterized by the presence of Charcoal–Leyden crystals in the sputum.

•
• Megaloblastic anaemia is caused by fish tapeworm (Diphyllobothrium latum)
•
• Kala azar or leishmaniasis or Dum Dum fever or topical splenomegaly is caused by Leishmania donovani
•
• Autoinfection is seen with Entrobius
•
• Medusa lock appearance in Xray is seen in Ascaris
•
• The inflammatory type of tinea capitis with superadded secondary bacterial infection leading to a painful, circumscribed,
•
boggy and indurated lesion is called Kerion
• Ceiling temperature–is the temperature above which ‘Pocks’ are not produced in chick embryos.
•
Leptospirosis
• Leptospirosis is Zoonosis.
•
• Transmission of leptospires may follow direct contact with urine, blood or tissue from an infected animal or exposed to a
•
contaminated environment.
• Leptospires are spirochaetes and causative agents for weil’s disease named ‘Ictohaemorrhagicus fever’.
•
• Leptospires are found in the urine of rats, dogs and other wild animals. Rodents especially rats are the most important
•
reservoirs. (AIPG 2014, 2005)

• Transmission: Human beings are infected when leptospires in water contaminated but urine of carrier animals enters the
•
body through cuts or abrasions or through intact mucosa of mouth, nose or conjunctiva.
WHO Criteria for Diagnosis of Chikungunya

Clinical criteria Laboratory criteria
• Acute onset of fever > 38.5 C and severe • At lease on the following tests in the acute phase:
•
•
• Arthralgia/arthritis not explained by other medical conditions – Virus isolation
•
–
– Presence of viral RNA by RT-PCR
Epidemiological criteria
–
– Presence of virus specific IgM antibodies in single serum
• Residing or having visited epidemic areas, having reported
–
sample collected in acute or convalescent stage
•
transmission within 15 days prior to the onset of symptoms. – Four-fold rising of IgM titers in samples collected at least three
–
weeks apart
Microbiology 245

MISCELLANEOUS
Incubation • The period elapsed from invasion of the tissues by pathogens and appearance of clinical features
•
Prodromal stage • Signs and symptoms are not specific for diseases. Antibody titre is rising
•
Fastigium • Disease is easily recognized. In this phase high titres (Peak) of antibodies are found.
•
Defervescence stage • Body’s defense mechanisms dominate and patient feels better,
•
Convalescence (recovery stage) • In convalescence the antibody titres decrease. The patient may act as carrier also decrease in
•
body temperature.
Probiotics
• Live microorganisms thought to be healthy for the host organism.
•
• Lactic acid bacteria (LAB) and bifidobacteria are the most common types of microbes and as probiotics; but certain yeasts
MICROBOLOGY
•
and bacilli may also be helpful.
• Consumed as part of fermented foods with specially added active live cultures; such as in yogurt, soy yogurt, or as dietary
•
supplements.
• Affect the host by improving its intestinal microbial balance, thus inhibiting pathogens and toxin-producing bacteria.
•

(AIPG 2010)

Flora of the Intestine
Health promoting Mild virulent and pathogenic as well Pathogenic and virulent
as health promoting
• Bifidobacteria Bacteriodaceae Veillonella organisms
•
• Lactobacillus organisms Peptococcacea Clostridium perfringens
Escherichia coli Staphylococci
•
• Eubacterium organisms
Proteus organisms
•
Amoebic Meningoencephalitis
Etiology • Amoebic meningoencephalitis is caused by free living amoebas
•
• The free living amoebas which have been implicated are:
•
• Nageleria fowleri
•
• Acanthamoeba casteltani
•
• Hartmengella
•
Causes • Nageteria foweri are responsible for acute cases of meningoencephalitis while acanathamoeba cause chronic
•
meningoencephalitis
• Nageteria foweri enters via the nose and cribrifom plate of the ethmoid passing directly into the brain tissue where
•
they form nests of amoebas that cause extensive haemorrhage and damage chiefly in the basilar portion of the
cerebrum and cerebellum
• In most cases death ensures in less than a week
•
• In contrast Acenthamoeba causes subacute and chronic amoebic meningoencephalitis.
•
Diagnosis • Microscopic examination of the cerebrospinal fluid which contains the trophozoite and red cells but no bacteria.
•
Treatment: • Antiprotozoal agents is largely ineffective
•
• N foweri has an invitro sensitivity to amphotericin B (antifungal drug) therefore this drug is used in the same
•
schedule as in the fungal diseases.
Also know
• Metchnik off gave the cellular concepts of immunity, discovered phagocytic cells
•
• Bennet 1967–immunologically surveillance
•
• Lord Lister–father of antiseptic surgery
•
• Ehrlich (1906)–father of chemotherapy
•
• Walksmann (1944)–discovered streptomycin
•
246
• Brucella abortus requires high levels of CO2 for growth (Capnophilic)

•
• Most of the drug resistance occurs due to conjugation.
•
• Half life of free HIV in plasma is 6 hours
•
• Both dendritic cells and macrophages act as antigen presenting cells
•
• The tracing of carriers in cities may be accomplished by the Sewer- Swab technique
•
• Enteroinvasive E coli–Sereny test is used in laboratory diagnosis.
•
• Ito’s test: Chancroid
•
• Frei’s test: Lymphogranuloma venerium
•
• Napier’s aldehyde or Formol gel test/ Chopra’s antimony test: Leishmania donovani
•
• Paget’s test: For small swelling
•
• Rosewaller’s test: Rheumatoid arthritis
MICROBIOLOGY
•
• Schiller’s test: CA cervix
•
• Figlu’s excretion test: Folic acid absorption test
•
• Gordon’s biological test: Hodgkin’s disease
•
• Coomb’s test: For identification of Rh antigen of fetus (AIIMS May 2010)
•

• Ame’s test: For mutagenic carcinoma (bacterial test)
•
• HLA B27: Ankylosing spondylytis
•
• HLA DR 4: Rheumatoid arthritis
•
• HLA DR3: Many autoimmune conditions
•
• Adenosine deamine (ADA) deficiency is the first immunodeficiency disease associated with enzyme deficiency
•
(SCID) (AIPG 2001)

• Stormy fermentation–lactose fermentation in litmus milk by Clostridium perfringens
•
• Lepra bacillus: Hansen (1874)
•
• Gonococcus: Neisser (1881)
•
• Diphtheria bacillus: Klebs(1883), Loeffler (1884)
•
• Pneumococcus: Frankel (1886)
•
• Meningococcus: Weichselbum (1887)
•
• Diphtheria toxin: Rocus and Yesin (1888)
•
• Tetanus bacillus: Kitasato (1889) and Nicotrien (1884)
•
• Plaque bacillus: Yersin (1890)
•
• Staphylococcus: Ojston (1881)
•
• Pneumoniae after exposure to parrots: • Chlamydiae Psittaci
•
•
• Pregnant women with cats: • Toxoplasmosis gondii (JK 2012)
•
•

• Muscle pain and eosinophilia: • Trichinosis (Trichinella spiralis)
•
•
• Slaughter house worker with fever: • Brucellosis
•
•
• Gardener stuck with a thorn: • Sporothrix schenckii
•
•
• Aplastic anemia in Sickle cell Disease: • Parvo virus B 19
•
•
• Fungus Ball: • Aspergillus
•
•
Microbiology 247

• Swollen jaw with sulfur granules: • Actinomyces israelii
•
•
• Necrotizing fasciitis: • Streptococcus pyogenes
•
•
• Diaper rash with hyphae and yeast on microscopy: • Candida
•
•
• Burnt tissue with blue green pus, grape like odour: • Pseudomonas aeruginosa
•
•
• Denuded superficial area of large skin area: • Staph aureus
•
•
• Pink umblicate warts with central debris: • Molluscum contagiosum
•
•
• Virus latent in sensory ganglia with unilateral reactivation: • Varicella zoster virus
•
•
• Virus latent in trigeminal ganglia: • Herpes simplex virus 1, VZV
•
•
• Virus latent in S2, S3: • Herpes simplex virus 2
MICROBOLOGY
•
•
• Man is the definitive host in most of the parasitic infection except the following parasites where it is an intermediate
•
host.
– Echinococcus granulosus (Hydatid worm)
–
 
– Plasmodium (Malaria)
–
 
– Taenia solium (Man is both definitive an intermediate host)
–
– Toxoplasma gondii
–
 
– Sarocysts lindemanii
–
CHAPTER 6
Pharmacology
Objectives
• General Pharmacology • Drug acting on CVS, GIT, Respiratory System

• ANS and CNS drugs • Chemotherapy

• NSAIDs • Dental Pharmacology

• Blood and Endocrinal Drugs • Miscellaneous

GENERAL PHARMACOLOGY
Pharmacokinetics • Is quantitative study of drug movement in through and out of the body.What the body does to a drug.
•

(PGI 1995)
Pharmacodynamics • Is what the drug does to a body.

•
Pharmacogenetics • Study of genetic basis for variability in drug response.
•
Pharmacogenomics • Use of genetic information to guide choice of drug and dose on individual basis.
•
Pharmacovigilance • Science and activities related to detection, assessment, understanding and prevention of adverse effects of
•
drug or other drug related problems.
The plasma life of a drug is the time taken for its plasma concentration to be reduced to half of its original value.
• Types:
•
– Alpha phase: This is due to distribution of drug. It is further divided into:
–
Alpha 1 is due to distribution of drug into highly vascular organ.

Alpha 2 is due to distribution of drug into less vascular organ.

– Beta phase: This is due to elimination of drug.
–
• t½ can determine: (AIIMS 1992)
•

– Elimination time
–
– Steady state plasma concentration
–
– Dosing rate
–
– Maintainance dose
–
Pharmacology 249

• Clearance: Measure of the rate at which the organs that eliminate drug from the body remove drug from the blood.
•

(KAR 2006)

• Volume of distribution, an indication of the extent to which the drug is distributed outside of the blood compartment
•
• Bioavailability, the fraction of the administered dose that reaches the systemic circulation.
•
• Steady state is achieved when the rate of drug elimination equals the rate of drug delivery into the systemic circulation,
•
which, if bioavailability is complete, corresponds to the rate at which the drug dose is administered
• Therapeutic index: The ratio of the toxic dose to the therapeutic dose. LD50/ED50 (AIPG 2008, UP 2007)
•

• Drug Potency: Refers to amount of drug needed to produce a certain response.
•
• Drug Efficacy: Maximal effect that a particular drug may elicit. (PGI 1998)
•

• Therapeutic window phenomenon: Optimal therapeutic response of drug is exerted only over a narrow range of plasma
PHARMACOLOGY
•
drug concentration. e.g.: TCA, clonidine, glipize
(PGI 1995)
• First pass metabolism is seen with oral route and rectal route. (AIPG 1994)
•

• More first pass metabolism is seen with oral route.
•
• Bioavailability by IV route is 100%.
•
• Sublingual route bypasses first pass metabolism.
•
• Efficacy: Maximal response that can be elicited by drug
•
• Potency: Amount of drug needed to produce a certain response.
•
• Intrinsic activity (efficacy): Ability of drug to activate receptor
•
• Agonist: Have affinity and maximal efficacy (Delhi 1987)
•

• Antagonist: Have affinity and no maximal efficacy (Delhi 1990)
•

• Partial agonist: Have affinity and sub maximal efficacy
•
• Inverse agonist: Have affinity and opposite efficacy
•
• Inverse agonists have affinity but intrinsic activity with a minus sign
•
• Agonists have both affinity and maximum intrinsic activity (IA = 1)
•
• A drug with preferential affinity for inactive receptor will actually produce an effect opposite to that of an agonist and is
•
known as inverse agonist.
Drugs undergoing zero Drugs undergoing first order Drugs Undergoing Enterohepatic Hit and run drugs
order kinetics kinetics Circulation
• A “constant amount “of • the time required to achieve • Drugs whose effects
•
•
•
drug is eliminated per unit steady-state levels can be last much longer than
time. predicted from the half-life, the drug itself.
• Rate of elimination is because accumulation is
a first-order process with a
•
independent of plasma
concentration. half-life identical to that for
elimination.
• Drugs with zero order
• Thus, accumulation reaches
•
elimination have no fixed
•
half life. (t ½ is variable) 90% of steady-state levels at
the end of three to four half-live
• A “Constant fraction “of
•
drug is eliminated per unit
time. Rate of elimination is
directly dependent on plasma
concentration. (COMED 2008)
• Drugs with first order
•
elimination have fixed half life.
(t ½ is constant)
250
• Phenytoin • Most drugs show first order • Erythromycin • Reserpine

•
•
•
•
• Aspirin kinetics. • Ampicillin • Guanethedine
•
•
•
• Ethanol • Rifampicin • MAO inhibitors
•
•
•
• Theophylline • Tetracycline • Omeprazole
•
•
•
• Propafenone • OCPs
•
•
• Warfarin • Phenopthalein
•
•
• Tolbutamide
•
• Placebo: Inert substance given in the form of medicine with no pharmacological effect but psychological effect.
•
• Nacebo: Is reverse of placebo: refers to negative psychodynamic effect evoked by loss of faith in medication or physician
•
prescribing medication.
PHARMACOLOGY
• Pseudo zero order: Drugs that follow first order kinetics but at higher doses follow zero order kinetics. E.g. Phenytoin,
•
Tolbutamide, Warfarin and Theophylline follows both zero as well as first-order kinetics.
Good to Know points

– In 1st t1/2 E50% drug eliminated
–
– In 2 nd t1/2 E75% drug eliminated
–
– In 3 rd t1/2 E87.5% drug eliminated
–
– In 4 th t1/2 E93.7% drug eliminated (COMED 2003)
–

– In 5 th t1/2 E97% drug eliminated
–
– Loading dose is governed by volume of distribution. (AIIMS May 2010)
–

– Maintainance dose is governed by clearance of drug and half life (t ½).
–
• Loading dose (LD) = Vd x Css Css = plasma concentration at steady state
•
• Clearance (Cl) = k x Vd k= elimination rate constant
•
• Infusion rate (Ko) = CL x CssCl = total body clearance
•
07xvd 0.7
• Maintenance dose (MD) = t1/2 = CL = k
•
• Apparent volume of distribution (Vd) = dose / C0 C0= plasma level at zero time
•
• Approximate Vd (weight 70kg)
•
– Plasma volume – 3L
–
– Blood volume – 5L
–
– ECF – 12-14 L
–
– Total body water – 40-42 L
–
• Factors governing volume of distribution of a drug are:
•
– Lipid: water coefficient of drug. (UP 2007)
–

– pKa: value of a drug.
–
– Degree of Plasma protein binding (UP 2007)
–

– Degree of blood flow.
–
– Affinity for different tissues. (UP 2007)
–

– Fat: Lean body mass ratio
–
– Diseases like CHF, Uremia, Cirrhosis
–
– Pregnancy
–
Pharmacology 251

Drugs that should not be given by IV route • The substrates of CYP enzymes include metabolic
•
intermediates such as lipids and steroidal hormones, as
• Paracetamol
well as xenobiotic substances such as drugs and other
•
• Diclofenac toxic chemicals.
•
• Chloroquine • CYPs are the major enzymes involved in drug metabolism
•
• Adrenaline
•
and bioactivation, accounting for 75% of the total
•
metabolism.
• Lipid soluble drugs diffuse by dissolving in the lipoidal
• The most common reaction catalyzed by cytochromes
•
matrix of the membrane, the rate of transport being
•
proportional to lipid: water partition coefficient of the P450 is a monooxygenase reaction.
drug • P450 enzymes absorb light at wavelengths near 450 nm,
For weak acids and bases
•
• identifiable as a characteristic Soret peak.
•
– Ionized: Water soluble • CYP enzymes have been identified in all kingdoms of life,
–
– Non ionized: Lipid soluble
PHARMACOLOGY
•
i.e. in animals, plants, fungi, bacteria, and viruses.
–
• Acidic drugs: Largely unionized at gastric pH absorbed
•
from stomach
• Both microsomal and nonmicrosomal enzymes
• Basic drugs: Absorbed from duodenum and intestine
•
are deficient in the newborn specially premature,
•
Plasma Protein Binding making them more susceptible to many drugs eg
chloramphenicol, opoids etc.
• Basic–α1 acid glycoprotein • Hofmann elimination: Refers to inactivation of
•
Acidic– albumin
•
• drug in the body fluids by spontaneous molecular
•
Drugs bound to albumin Drugs bound to α acid rearrangement without the agency of any enzyme. Eg
glycoprotein atracurium
• Barbiturates • Prazosin • Drugs with zero order elimination include ethanol
•
•
•
• Benzodiazepenes • Methadone (except low blood levels), phenytoin (high therapeutic
•
•
• Phenytoin (PGI 1986) • Lidocaine doses) and salicylates (toxic doses)
•
•
Penicillin • Verapamil • Emotional stress reduces the rate of absorption of an
•
• Sulfonamides
•
• Bupivacaine orally administered drug
•
•
• Tetracycline • Quinidine
• Inunction–drugs when rubbed into the skin can get
•
•
• Tolbutamide
•
absorbed and produce systemic effects. Eg nitroglycerine
•
• Warfarin (PGI 1986)
ointment.
•
• Bound fraction is not available for action.
•
• In hypoalbumenemia binding may be reduced and high Prodrugs (inactive/latent drug that is converted to active form
•
concentration of free drug may be available in body)
• Binding sites are non specific and one drug can displace • Enalapril • Enalaprilate (AIIMS 2006)
•
•
•
other. (AIPG 2000)
• Sulfasalazine • 5 Aminosalicyclic acid

•
•
– In addition to crossing the blood brain barrier, • Flourouracil • Flourouracil monophosphate
–
the lipid soluble drugs redistribute into fat tissues
•
•
prior to elimination. • Dipivefrine • Epinephrine
•
•
– The BBB is deficient at the CTZ in the medulla
• Prednisolone • Prednisolone
–
oblongata (even lipid insoluble drugs are emetic)
•
•
and certain periventricular sites (anterior • Levodopa • Dopamine
•
•
hypothalamus) • Methyl dopa
– The placental efflux P glycoprotein serves to limit
•
• Terfenadine
–
foetal exposure to maternally administered drugs
•
• Zidovudine
•
The Cytochrome P450 Superfamily (CYP)
• Orphan Drugs: a drug not developed into usuable
• Is a large and diverse group of enzymes.
•
medicine as the costs will not be recovered by the
•
• The function of most CYP enzymes is to catalyze the developer and the disease as orphan disease and sufferer
•
oxidation of organic substances. as health orphan
252
Drug Metabolism
Drug interference by food
• Proton pump inhibitors (omeprazole) should be taken at least 30 min before meal
•
• Unionized drugs are well absorbed orally while highly ionized drugs (e.g streptomycin and Neostigmine) are absorbed
•
poorly when given orally
• Acidic drugs are unionized in stomach (salicylates/salicylic acid and barbituric acids) and absorbed in stomach
•
Drugs not Metabolized in Liver
• Penicillin G (given parentrally it bypasses GIT and first pass metabolism)
•
• Synthetic estrogens (ethinyl derivative of estradiol)
•
PHARMACOLOGY
• Natural estrogens when given orally are inactivated in liver before reaching general circulation
•
• Digoxin (safely given in liver diseases)
•
Drugs Excreted unchanged in Urine
• Digitalis • Phenformin/Metformin/Chlorpropamide

• Bretylium • Gonadotropin
•

• Methotrexate • Thiacetazone
•

• Sodium stibolgluconate • Aminoglycoside
•

• Acyclovir • Neomycin
•

• Gallamine • Norfloxacin
•

Clinical Trials
Phases Trial Study is conducted on Establish Remark
I Non therapeutic Healthy human volunteers Safety Pharmalogical studies
II Therapeutic exploratory Patients Efficacy
III Therapeutic Confirmatory RCT are done, compared with standard drugs
IV Post – Marketing surveillance

studies
Drug Metabolism
• Phase I: (Non Synthetic) reactions–To attach functional group to drug molecule. Use cytochrome P450 monoxygenases
•
• Phase II: (synthetic): To attach a conjugate to the drug molecule
•
– Non synthetic or Phase I reaction
–
Oxidation ( mostly)

- N- or O- dealkylations

- Oxidative deamination

Reduction

Hydrolysis

Decyclization

– Synthetic or phase II reactions
–
Glucoronidation, Conjugation

Acetylation

Methylation

Sulfation

→ Oxidation involves maximum drug metabolizing reactions, 50% of these use cytochrome CYP3a4/5
Pharmacology 253

ANS AND CNS DRUGS
Cholinergic Drugs
Cholinergic agonist Anticholinestrases
• Choline esters • Reversible:
•
•
– Acetyl choline – Carbamates:
–
–
– Methacholine - Physostigmine
–
-
– Carbachol - Neostigimine
–
-
– Bethanechol - Pyridostigmine
–
-
• Alkaloids - Edrophonium
•
-
– Muscarine - Rivastigmine
-
– Acridine
–
– Pilocarpine (AIPG 1999)
–
- Tacrine
–
– Arecoline
-
• Irreversible:
PHARMACOLOGY
–
•
– Organophosphates
–
- Dyflos
-
- Echothiophate
-
- Parathion
-
- Malathion
-
– Carbamates
–
- Carbaryl
-
- Proponur
-
Anticholinergic Drugs
Natural alkaloids • Atropine
•
• Hyoscine
•
Semisynthetic derivatives • Homatropine
•
• Hyoscine butyl bromide
•
• Ipratropium bromide
•
Synthetic compounds • Mydriatics: Tropicamide
•
• Antisecretory: Antispasmodics
•
– Quaternary compound:
–
- Oxyphenonium
-
- Clinidium
-
- Isopropamide
-
– Tertiary amines
–
- Dicyclomine
-
- Piernzepine
-
- Telenzepine
-
• Anti parkinsonism
•
- Benzhexol
-
- Procyclidine
-
- Bisperiden
-
- Benzodropine
-
Uses of Cholinergic drugs
• As mitotic
•
– In glaucoma
–
Open angle (wide angle, chronic simple) Angle closure (narrow angle, acute congestive
• β- adrenergic blockers • Topical β blockers
•
•
• mitotic • Mitotic
•
•
• α- adrenergic agonists • Hypertonic mannitol (20%) or glycerol (10%)
•
•
• Carbonic anhydrase inhibitor • Acetazolamide
•
•
• Prostaglandins • Apraclonidine
•
•
254
– To counteract the effects of mydriatics after refraction testing

–
– To prevent formation of adhesions between iris and cornea and iris and lens
–
• Myasthenia gravis
•
• Post operative paralytic ileus/ urinary retention
•
• Post operative decuriarization
•
• Cobra bite
•
• Belladonna posoining
•
• Other drug over dosages–tricyclic antidepressants, phenothiazines, antihistaminics
•
• Alzeheimer’s disease
•
Atropine
PHARMACOLOGY
Pharmacology • Anticholinergic drug

•
• Blocks the actions of acetyl choline on autonomic effectors and in the CNS exerted through muscarinic
•
receptors
Pharmacological ac- • CNS:

tion
•
– Stimulates medullary centres – vagal, respiratory and motor
–
– Has anti motion sickness property
–
– Suppresses tremor and rigidity of parkinsonism
–
• CVS:
•
– Tachycardia
–
– Decreases heart rate
–
– Blocks M2 receptors on SA node
–
• Eye:
•
– Mydriasis
–
– Cycloplegia
–
– Photophobia
–
– Blurring of near vision
–
• Smooth muscles
•
– Causes relaxation
–
– Bronchodilatation
–
– Reduces airway resistance
–
– Relaxes urinary bladder
–
• Glands:
•
– Decreases secretion of sweat, saliva, tracheobronchial and lacrimal glands (Man 1994)
–

– Decreases secretion of acid, pepsin and mucus
–
Pharmacokinetics: • T ½ = 3-4 hours
•
Therapeutic uses • Antisecretory
•
– Preanaesthetic mediaction
–
– Peptic ulcer
–
– Pulmonary embolism
–
• As antispasmodic
•
– Intestinal and renal colic, abdominal cramps
–
– Nervous and drug induced diarrhea
–
– Spastic constipation
–
– Pylorospasm
–
• Bronchial asthma, asthmatic bronchitis, COPD
•
• As mydraiatic and cycloplegic – for use in uveitis and during refraction
•
– Iritis, iridocystitis, choroditis, keratitis, corneal ulcer
–
• As cardiac vagolytic
•
• To antagonize muscarinic effects of drugs and poisons
•
Pharmacology 255

Side effects • Dry mouth
•
• Dry, flushed and hot skin
•
• Ataxia, delirium, hallucination
•
• Hypotension
•
• Dilated pupil, photophobia, blurring of vision
•
Contraindications • Narrow iridocorneal angle –may precipitate congestive glaucoma
•
Interactions • Atropine delays gastric emptying – so absorption of drugs is slowed
•
• Antacids interfere with absorption
•
• MAO inhibitors interfere with its metabolism
•
Anti Cholinesterase Poisoning
PHARMACOLOGY
Reversible • Carbamates–Physiostigmine, neostigmine, pyridostigmine, ambenonium, edrophonium, demecarium
•
Irreversible • Organophosphates: Dyflos (DFP), echothiophate, parathion, malathion, diazinon (all insectides); tabun, sarin, soman
•
(nerve gases for chemical warfare); carbamates: carbaryl, propoxur (both are insectides).
Symptoms • Increased secretions (diarrohea, urination, lacrimation, sweating, salivation);

•
• Miosis,
•
• Bronchospasm,
•
• Bradycardia,
•
• Excitation of skeletal muscle and CNS
•
Treatment • Atropine IV (muscarine antagonist) and cholinesterase reactivators (Pralidoxime, 2 –PAM) is a specific antidote that
•
reverses organophosphate binding to the cholinesterase enzyme
• Organophosphate Poisoning: Symptoms

•
– Diarrhoea
–
– Urination
–
– Pin point pupils (TN 1989)
–

– Miosis
–
– Bradycardia
–
– Bronchoconstriction
–
– Excitation of muscles and CNS (Nicotinic)
–
– Lacrimation
–
– Salivation
–
– Sweating
–
• Atropine is used in OP Poisoning.(Antidote) (KERALA 1995)
•

• Pralidoxime is used in conjuction and reactivates cholinesterase. (AIPG 2007, 2008)
•

Adrenergic Drugs
• Therapeutic uses:
•
– Vascular uses:
–
Hypotensive states: Dopamine/Dobutamine/Adrenaline

Along with LA: Adrenaline

Control of local bleeding–Adrenaline

Nasal decongestant–α- agonists

Peripheral vascular diseases like Buerger’s disease, Raynaud’s phenomenon, diabetic vascular insufficiency,

gangrene, frost bites
256
– Cardiac uses
–
Cardiac arrest: Adrenaline

Stokes–Adams Syndrome–Adrenaline/Isoprenaline

Partial or complete A V block–Isoprenaline

Congestive heart failure–Dopamine/Dobutamine

– Bronchial Asthma–especially β2 stimulants
–
– Allergic disorders–Adrenaline
–
– Mydriatic–phenylephrine
–
– Central uses:
–
Narcolepsy

Epilepsy–Amphetamines

PHARMACOLOGY
Parkinsonism–Amphetamines

Hyperkinetic children-Amphetamines

Obesity–Anorectic drugs

– Nocturnal enuresis in children and urinary incontinence – Amphetamines
–
– Uterine relaxant–isoxsuprine, ritodrine (β2 stimulants)
–
– Insulin hypoglycaemia–Adrenaline
–
• Adverse effects and Contraindications:
•
– Transient restlessness, palpitation, anxiety, tremor, pallor may occur after sc/im injection of Adrenaline
–
– Marked rise in BP leading to cerebral haemorrhage, ventricular tachycardia/ fibrillation–on large doses by IV
–
– Adrenaline is contraindicated in hypertensive, hyperthyroid and angina patients
–
– Adrenaline should not be given during anaesthesia with halothane (risk of arrhythmias) and to patients receiving
–
β-blockers (marked rise in BP)
Therapeutic uses of α-blockers

• Pheochromocytoma
•
• Hypertension
•
• Secondary shock
•
• Peripheral vascular disease
•
• Congestive heart failure-prazosin
•
• Benign hypertrophy of prostate–prazosin
•
• Migraine–Ergotamine
•
• Papaverine/Phentolamine induced penile erection (PIPE)–therapy for impotence
•
Therapeutic uses of β-blockers
• Hypertension
•
• Angina pectoris
•
• Cardiac arrhythmias
•
• MI
•
• CHF
•
• Dissecting aortic aneurysms
•
•
• Thyrotoxicosis
•
• Migraine
•
Pharmacology 257

• Anxiety
•
• Essential tremor
•
• Glaucoma
•
• Hypertrophic cardiomyopathy
•
Norepinehrine
• Used as a vasopressor medication for patients with critical hypotension.
•
• Act on both α1 and α2 receptors with resultant increase in peripheral vascular resistance. (AIIMS May 08)
•

• NE is called the general vasoconstrictor as it causes constriction of blood vessels throughout the body via alpha-receptors.
•
Total peripheral resistance is increased diastolic blood pressure.
Mechanism of action of NE: stimulates β1 adrenergic receptors and α adrenergic receptors causing increased contractility
PHARMACOLOGY
•
•
and HR as well as vasoconstriction, thereby increasing systemic BP and coronary blood flow, clinically alpha effects
(vasoconstriction) are greater than β effects (inotropic and chronotropic effects).
Types of Receptors
β1 β2 β3
Location Heart, juxtaglomerular cells in kidney Bronchi, BV, uterus, GIT, urinary Adipose tissue
tract, eye
Selective agonist Dobutamine Salbutamol, terbutaline -
Selective antagonist Metoprolol, atenolol α-methyl propranolol -
α-1 α-2
Location Postjunctional on effector organs Pre junctional on nerve endings, also post junc. In brain, pancreatic beta cells,
platelets.
Functions GIT Smooth muscle – contraction Inhibition of transmitter release
Vasoconstriction Vasoconstriction
Gland – secretion Platelet aggregation
Gut – relaxation Decreased insulin release
Heart – arrhythmia
Selective agonist Phenylephrine, methoxamine Clonidine
Selective antagonist Prazosin Yohimbine, rauwolscine
Effector pathway 7 IP3/DAG – increased Decreased cAMP, K+ channel increased, IP3/DAG increased
Phospholipase A2- increased PG
Muscurinic
Type of receptors Function Agonists Antagonistic
M1 (MAN 1999) • Depolarisation in autonomic ganglia Non-specific Non-Specific and
•
• Secretion from salivary glands and • Pirenzepine
•
•
stomach • Telezepine
•
• In CNS (memory)
•
M2 • Slowed heart rate Non-specific Non-specific and
•
• Reduced contractile forces of atrium Gallamine
Methoctramine
•
• Reduce conduction velocity of AV
Triptamine
•
node
• In CNS Homotropic inhibition
•
258
Type of receptors Function Agonists Antagonistic

M3 • Smooth muscle contraction Non-specific Non-specific and
•
• Increased intracellular calcium in Bethanechol Darifenacin
•
vascular endothelium Carbachol Titoropium
Pilocarpine (in eye)
• Increased endocrine and exocrine
•
gland secretions, e.g., salivary
glands and stomach
• In CNS Eye accommodation
•
Vasodilation Induced emesis
M4 • Activation of M4 causes decreased Non-specific Non-specific
•
locomotion In CNS
M5 • In CNS Non-specific Non-specific

•
PHARMACOLOGY
Nicotinic Receptor
Nm Nn
Neuromuscular junction, depolarisation of muscle endplate. Contraction Autonomic ganglia depolarization; adrenal medulla,
of skeletal muscle catecholamine release
Stimulated by phenyltrimethylammonium (PTMA) Stimulated by dimethyl phenyl piperazinium (DMPP)
Tubocurarine is antagonist of skeletal muscles Hexamethonium is antagonist.
Differences Between Sympathetic and Parasympathetic Division of the Autonomic Nervous System
Sympathetic Parasympathetic
• Origin Dorso lumbar (T1 to L2 or L3) Cranio sacral (III, VII, IX, X; S2-S4)
•
• Distribution Wide Limited to head, neck and trunk
•
• Ganglia Away from organs On or close to organs
•
• Postganglionic fibres Long Short
•
• Pre:Post ganglionic 1:20 to 1:100 1:1 to 1:2 (except in enteric plexuses)
•
• Transmitter (neuroeffector) Noradrenaline (major) Acetyl choline
•
Acetylcholine (minor)
• Stability of transmitter NA stable, diffuses for wider actions ACh rapidly destroyed locally
•
• Important function Tackling stress and emergency Assimilation of food, conservation of energy
•
Effect on organ Sympathetic Parasympathetic
– Iris muscle Contracts radial muscle (dilates pupil) Contracts sphincter muscle
–
– Ciliary muscle Relaxes β2 Contracts
–
– Heart Decreases
–
• SA node Increases heart rate via β1, β2
•
• Atria Increases contractility and conduction velocity Decrease
•
via β1and β2
• AV node and conduction velocity Increases conduction velocity via β1 and β2 Decreases
•
• Ventricles Increases contractility and conduction via β1, β2 Decreases
•
– Arterioles Constricts via α1, α2 or dilates via β2 Dilates
–
• Coronary
•
Pharmacology 259

Effect on organ Sympathetic Parasympathetic
• Skin Constricts via α1, α2 Dilates
•
• Skeletal muscle Constricts via α1, α2 or dilates via β2 Dilates
•
• Abdominal viscera and kidney Constricts via α1 Dilates
•
• Salivary gland Constricts via α1, α2 Dilates
•
• Penis or clitoris Constricts via α1, α2 Dilates (produces erection)
•
– Veins Constricts via α1, α2 or dilates via β2 Dilates
–
– Lungs
–
• Bronchial muscles Relaxes via β2 Constricts
•
• Bronchial glands Inhibits secretion via α1 or stimulates via β2 Stimulates secretion
•
– Salivary glands Stimulates secretion (thick secretion via α1) Stimulates watery secretion
–
– Stomach Increases
–
• Motility, tone Decreases via α1, α2, β2
PHARMACOLOGY
•
• Sphincters Constricts via α1 Relaxes
•
• Secretion Inhibits via α2 Stimulates
•
– Gall bladder Relaxes via β2 Contracts
–
– Liver Glycogenolysis via α1, β2 gluconeogenesis Glycogen synthesis
–
– Pancreas
–
• Exocrine glands Inhibits secretion via α1 Stimulates
•
• Endocrine glands Inhibits insulin secretion via α2 and stimulates …………….
•
glucagon secretion via β2
• Fat cells Increases fat breakdown, causes release of ……………..
•
FFA via α1, β1
– Urinary bladder
–
• Detrusor muscle Relaxes via β2 Contracts
•
• Sphincter Constricts via α1 Relaxes
•
– Uterus Pregnant uterus contracts via α1; non pregnant Variable
–
relaxes via β2
– Male reproductive tract Ejaculation via α1 Erection
–
– Skin ……..
–
• Pilomotor muscle Contracts via α1
•
• Sweat glands Localized (adrenergic) sweating via α1 Generalized (cholinergic sweating)
•
• Lacrimal glands ………. Secretion
•
Skeletal Muscle Relaxants
Peripherally acting MR (MAN 1998) Centrally acting MR
• Neuromuscular blocking agents (MAN 1995) • Mephensin group
•
•
– Non depolarizing (competitive) blockers – Mephenesin
–

–
(MAN 2002, BHU 2007) – Carisoprodol

–
- Long acting – Chlorzoxazone
-
–
∗ D tubocurarine (MAN 2001) – Methocarbamol
∗

–
∗ Pancuronium • Benzodiazepines
∗
•
∗ Doxacurium – Diazepam and others
∗
∗ Pipecuronium
–
• GABA derivatives
∗
- Intermediate acting
•
– Baclofen (AIPG 1993)
-
∗ Vecuronium
–

• Central α2 agonist
∗
∗ Atracurium
•
– Tizanidine
∗
- Short acting
–
-
∗ Mivacurium (AIIMS 1999)
∗

– Depolarizing blockers:
–
- Succinyl choline
-

(AIPG 1999, AIIMS 19998, MAN 1994)

- Decamethonium
-
• Directly acting
•
– Dantrolene sodium
–
– Quinine
–
260
Sedative–Hypnotics
Barbiturates • Long acting: phenobarbitone, Mephobarbitone
•
• Short acting: Butobarbitone, Pentobarbitone
•
• Ultrashort acting: Thiopentone, Hexobarbitone
•
Benzodiazepines • Hypnotic
•
– Diazapem
–
– Flurazepam
–
– Nitrazepam
–
– Temazepam
–
– Triazolam
–
– Midazolam
–
• Antianxiety
•
- Diazepam
PHARMACOLOGY
-
- Chlordiazepoxide
-
- Oxezapam
-
- Lorazepam
-
• Anticonvulsant
•
- Diazepam
-
- Clonazepam
-
- Clobazam
-
Newer nonbenzodiazepine • Zopiclone
•
hypnotic • Zolpiden
•
• Zaleplon (Sonata), indiplon
•
Benzodiazepines • Pharmacological actions
•
• Mechanism of action: – CNS: has specific depressant and stimulant actions:
•
–
– Act preferentially on midbrain ascending reticular – Depressant actions are:
–
–
formation and on limbic system. Analgesia:

– Muscle relaxation is produced by primary medullary - Acts on substantia gelatinosa of dorsal horn to
–

site of action and ataxia is due to action on cerebellum inhibit release of excitatory transmitters from
– Act by enhancing presynaptic/ postsynaptic inhibition primary afferents carrying impulses.
–
through a specific BZD receptor which is an integral - Release of substance P from primary pain af-
part of GABAA receptor Cl- channel complex

ferents in the spinal cord and its post synaptic
– The modulatory BZD receptors increases the action on dorsal horn neurons is inhibited by
–
frequency of Cl- channel opening induced by morphine.
submaximal concentration of GABA - Action at supraspinal sites in medulla, mid
– BZDs don’t themselves increase Cl- conductance, have

brain, limbic and cortical areas may alter pro-
–
only GABA facilitatory but no GABA mimetic action cessing and interpretation of pain impulses as
– low ceiling CNS depressor
well as send inhibitory impulses through de-
– BZDs agonists enhance GABA induced
scending pathways to spinal cord
–
hyperpolarization (due to influx of Cl- ions) and
Sedation:
decrease firing rate of neurons

- Drowsiness and indifference to surroundings

Hypnotics that are structurally dissimilar to as well as to own body occurs without motor
benzodiazepines, presumably, their therapeutic efficacies incoordination
are due to Hypnotics that are structurally dissimilar to Mood and subjective changes:

benzodiazepines, presumably, their therapeutic effective in - Mediated by don’t release in nucleus accum-

relieving sleep onset insomnia. The two drugs have similar bens
efficacies and both display sustained hypnotic efficacy without - Inhibition of nor adrenaline release in locus

occurrence of rebound insomnia on abrupt discontinuation. erulean by opiods is implicated in their action
to allay apprehension and fear
Depresses respiratory centre, cough centre,
Morphine (opoid Alkaloid)

temperature regulatory centre and vasomotor
• Principal alkaloid in opium
centre
•
Pharmacology 261

– Stimulant actions: Anaesthesia
–
CTZ: Nausea, vomiting–sensitizes CTZ to
• The anaesthetic injected in the paravertebral block

vestibular and other impulses
•
may diffuse laterally in the intercostals space or up and
Edinger–Westphal nucleus–of III nerve is
down the ipsilateral paravertebral spaces.

stimulated producing miosis
Vagal centre: Stimulated – can cause bradycardia
• First LA introduced by Niemann in 1860–cocaine
•
Lofgren developed lidocaine in 1943.

Inhibition of GABA release by hippocampal •
•

interneurons • Local anaesthetic injection with contaminated alcohol
•
– Neuro-endocrine: or sterilizing solution near the nerve causes irritation,
–
Hypothalamic activation by afferent collaterals is which results in edema and increased pressure on

dampened. Its influence on pituitary is reduced. nerve, leading to its paraesthesia.
As a result FSH, LH, ACTH levels are reduced, • Neuraxial adjuvants are used to improve or prolong
•
PHARMACOLOGY
while prolactin and GH are increased. analgesia and at the same time decrease the adverse
– CVS: effects associated with high doses of a single local
–
Vasodilatation anaesthetic agent. This is called dose-sparing effect.

- Direct action decreasing tone of blood vessels • Their secondary use:

•
- Histamine release – To increase the speed of onset of neural blockade

- Depression of vasomotor centre
–
(reduce latency)

– GIT: Decreases propulsive movements–causes – To improve the quality of neural blockade
–
–
constipation – To prolong the duration of neural blockade
–
• Neuraxial adjuvants: opoids, sodium bicarbonate,
• Is contraindicated in head injury, as
•
vasoconstrictors, alpha 2 adrenoceptor agonists.
•
– By retaining CO2 it increases the intracranial
• Cholinergic agonists, N methyl D aspartate antagonists,
–
tension, which will add to that already caused by
•
γ aminobutyric acid (GABA) receptor agonists.
head injury itself.
– Even therapeutic doses can cause marked • The addition of 8.4% sodium bicarbonate to lidocaine
•
increases the pH, this alkalinity favours the diffusion of
–
respiratory depression
– Vomiting, miosis and altered mental ability a greater proportion of LA across the neural membrane,
more rapid onset of neural blockade
–
produced by morphine interfere with assessment of
progress in head injury.
• Drugs used in day care anaesthesia are:
•
Signs and Symptoms of Opioid Withdrawl (BHU 08, KCET – Midazolam
–
2011) – Sevoflurane
–
• Marked drug seeking behavior – Fentanyl
–
– Propofol
•
• Lacrimation
–
– Mivacurium
•
• Sweating
–
• The cerebral blood flow increase normally by N2O is
•
•
• Anxiety and fear attenuated when used with barbiturates, benzodiazepines,
•
• Restlessness narcotics and propofol.
•
• Gooseflesh • Amide type anaesthetics should be used with care in
•
•
• Mydriasis patients with severe liver disease
•
• Insomnia
Stages of Anaesthesia
•
• Abdominal colic
• General anesthesia causes an irregularly descending
•
• Diarrhea
•
depression of CNS i.e. the higher function is lost first
•
• Dehydration and progressively lower areas of brain are involved. The
•
• Hypertension vital centres located in the medulla are paralysed last as
•
• Palpitations and rapid weight loss the depth of anaesthesia increases.
•
• Guedel described 4 stages with ether anaesthesia,
Delirium and convulsions are a feature of barbiturate
•
dividing the stage 3 into 4 phases:
withdrawl.
262
I stage of anaesthesia • Starts from beginning of anesthetic inhalation and lasts upto the loss of consciousness.
•
• Pain is progressively abolished
•
• Patient is conscious
•
• Reflexes and respiration are normal
•
•
•
Difficult to maintain
II stage of delirium • Loss of consciousness to beginning of regular respiration

•
• Muscle tone increases
•
• Apparent excitement is seen
•
• Breathing is jerky
•
• Vomiting, involuntary micturation
•
• Heart rate increases and pupil dilate
•
• BP increases
PHARMACOLOGY
•
III stage of Surgical • Onset of regular respiration to cessation of spontaneous breathing. Divided into 4 planes:
Anaesthesia
•
– Plane 1: roving eyeballs. Ends when eyes become fixed
–
– Plane 2: loss of corneal and laryngeal reflexes
–
– Plane 3: pupil starts dilating and light reflex is lost
–
– Plane 4: intercostals paralysis, shallow abdominal respiration, dilated pupil, weak muscle tone, BP falls,
–
HR increases with weak pulse, respiration decreases.
IV medullary paralysis • Cessation of breathing to failure of circulation and death.

•
• Pupil is widely dilated
•
• Muscles are totally flabby
•
• Pulse is thread and imperceptible
•
• Decreases blood pressure
•
• Minor surgeries like extractions are carried out in Stage I or Stage of analgesia. Major surgeries are carried on stage III
•
and plane III of general anaesthesia or stage of surgical anaesthesia (AIPG 1994)

Preanaesthetic Medications
• Opoids: Morphine (10mg) or pethidine (50-100mg)
•
• Sedative–antianxiety drugs: Benzodiazepines like diazepine or lorazepam
•
• Anticholinergics: Atropine or hyoscine (0.6mg)
•
• Neuroleptics: Chlorpromazine im
•
• H2 blockers: Cimetidine, famotidine
•
• Antiemetics: metoclopropamide, odansteron
•
Local Anaesthetics
Injectable Surface anaesthetic
• Low potency, short duration • Soluble
•
•
– Procaine – Cocaine
–
–
– Chloroprocaine – Lignocaine
–
–
• Intermediate potency and duration – Tetracaine
–
– Benoninate
•
– Lignocaine (lidocaine)
–
• Insoluble
–
– Prilocaine
•
– Benzocaine
–
• High potency, long duration
–
– Butamen
•
– Tetracaine
–
– Onethazaine
–
– Bupivacaine
–
–
– Ropicaine
–
– Dibucaine
–
Pharmacology 263

Lignocaine
• Most commonly used local anaesthetic
•
• Popular antiarrhythmic in intensive care units
•
Pharmacological • Suppression of automaticity in ectopic foci–cardiac action
•
action • Improves condition in depolarized or stretched fibres by increasing RMP to near normal values
•
Pharmacokinetics • Inactive by oral route due to high first pass metabolism
•
• Action by IV bolus dose lasts 10-20 minutes only because of rapid redistribution
•
• It is hydrolysed, deethylated and conjugated, excreted in urine
•
• Its metabolism is hepatic blood flow dependent
•
• T ½ of early distribution phase is 8 min
•
• T ½ of later elimination phase is 2 hour
•
PHARMACOLOGY
• Therapeutic plasma concentration is 2 – 5 µg/ml
•
Indication • Ventricular tacharrhythmias
•
• Useful in digitalis toxicity
•
Adverse effects • Drowsiness
•
• Nausea
•
• Paraesthesis
•
• Blurred vision
•
• Disorientation
•
• Twitching
•
• Fits
•
Contraindications • Hypersensitivity to amide group of LA
•
• AV block
•
• Cardiac decompensation
•
• Bradycardia
•
Uses • Surface application
•
• Infiltration
•
• Nerve block
•
• Epidural, spinal and iv regional block anaesthesia
•
Addition of a Vasoconstrictor (eg. Adrenaline 1:50000 to 1:200000)
• Prolongs the duration of action of LA by decreasing their rate of removal from the site into circulation
•
• Reduces systemic toxicity of LA
•
• Makes injection more painful
•
• Provides a bloodless field for surgery
•
• Increases chances of subsequent local tissue edema and necrosis, delays wound healing
•
• Raise BP and promote arrhythmias
•
General Anaesthetics
Inhalational • Gas
•
– Nitrous oxide
–
• Liquid
•
– Ether
–
– Halothane
–
– Enflurane
–
– Isoflurane
–
– Desflurane
–
– Sevoflurane
–
264
Intravenous • Inducing agents
•
– Thiopentone sodium
–
– Propofol
–
– Etomidate
–
Slower acting • Benzodiazepines
•
– Diazepam
–
– Lorazepam
–
– Midazolam
–
• Dissociative anaesthesia
•
– Ketamine
–
• Opoid analgesia
•
• Fentanyl
•
PHARMACOLOGY
Antidepressants • Atypical antidepressants
•
• Reversible inhibitors of MAO–A (RIMAs) – Trazodone
–
•
– Moclobemide – Mianserin
–
– Bupropion
–
– Clorgyline
–
–
• Tricyclic antidepressants (TCAs)
CNS Stimulants
•
– NA and 5 HT reuptake inhibitors
• Convulsants:
–
Imipramine
•
– Strychnine

Amitriptyline
–
– Picrotoxin

Clomipramine
–
– Bicucculline

– Predominantly NA reuptake inhibitors
–
• Analeptics
–
Desipramine
•
– Doxapram

Nortriptyline
–
– Prethcamide

Amoxapine
–
• Psychostimulants

• Selective serotonin reuptake inhibitors (SSRIs)
•
– Amphetamines
•
– Fluoxetine
–
– Pemoline
–
–
– Fluvoxamine – Cocaine
–
–
– Citalopram – Caffeine
–
–
Anti Histmanics
Location Agonist Antagonist
H1 SM, CNS, Endothelial cells Histamine, Promethazine Chlorphenaramine
H2 Gastric, Parietal cells, Cardian m/s Dimaprit Ranitidine
H3 CNS Origin cells (R) histamine Thioperamide Clobenpropit
H4 Hemopoietic Clobenpropit Thioperamide
Drugs used in the Treatment of Parkinsonism the oxidative deamination of dopamine in the brain. It is
used as an adjunct to leovodopa.
• Precursor of dopamine: Levodopa is the precursor of
•
dopamine. It is the main treatment for Parkinson’s disease. • Potentiate dopaminergic responses: Amanatadine,
•
It is given with carbidopa to increase effectiveness and an antiviral, potentiates dopaminergic responses.
reduce side effects. Antiparkinosonian actions are unrelated to the antiviral
• Dopamine agonists: Bromocriptine or pergolide. These effects.
•
are given in addition to levodopa early in the treatment
to enhance levodopa’s action, or may be given when • Anticholinergic drugs (benztropine and trihexyphendiyl,
•
levodopa’s side effects become more of a problem certain antidepressants and anthistamines such as
diphenhydramine) may be given without levodopa in the
• Inhibitor of MAO Type B: Selegiline is a selective
early stages of disease, with levodopa in later stages.
•
inhibitor of MAO Type B. This enzyme is responsible for
Pharmacology 265

NSAIDS
Non selective • Ibuprofen

•
COX 2 inhibitors ••
Naproxen
• Indomethacin
•
• Ketorolac
•
• Sulindac
•
Selective COX 2 • Celecoxib,
•
inhibitors: • Etorocoxib,
•
• Valdecoxib,
•
• lumiracoxib,
•
• Rofecoxib (PGI 2002)
•

PHARMACOLOGY
Preferential COX • Nimesulide, (JK 2001)
•

2 inhibitors: • Meloxicam,
•
• Namebutone (AIIMS 1998)
•

• Selective COX 2 inhibitors don’t have antiplatelet action. (PGI 2007)
•

• NSAID with good tissue penetration/good concentration in synovial fluid: Ketorolac (UP 2007)
•

• Ketorolac is non narcotic, non steroidal but acting on opoid receptors. (MP 1998)
•

• Misoprostol is effective in NSAID induced Gastric ulcer. (AIPG 1997)
•

• Nefopam doers not inhibit prostaglandins. (Manipal 2006)
•

• Beneficial actions due to prostaglandin synthesis inhibition
•
– Analgesia: Prevention of pain, nerve ending sensitization induced by bradykinin, TNFα, ILs. More effective against
–
inflammation associated pain.
– Antipyresis: Blocks the action of pyrogen through COX-2 inhibition
–
– Anti-inflammatory: Inhibition of PG synthesis at the site of injury
–
– Anti–thrombotic: Inhibits synthesis of both pro-aggregatory (TXA2) and anti-aggregatory (PGI2) prostanoids.
–
(increases bleeding time)
– Closure of ductus arteriosus: Inhibition of PGE2 and PGI2
–
– Dysmenorrhoea: Lowers uterine PGs levels
–
– Partuirition: Delays and retards labour
–
• Aspirin:
•
– Irreversible COX inhibitor: (PGI 2002, AIPG 2001)
–

– Antiplatelet
–
– Analgesia
–
– Antipyretic
–
– Anti-inflammatory
–
– Anti thrombotic effect.: It inhibits TXA2 synthesis in platelets by irreversible acetylation and inhibition of COX 1.
–
Platelets are annucleate and can’t overcome this inhibition but endothelial cells are nucleate and can overcome

this acetylation by regenerating more enzyme
This is a theraupatic effect finding use of aspirn in prophylaxis for stroke and MI management.

– Causes respiratory alkalosis and metabolic acidosis in high doses.
–
– GIT ulceration, bleeding, salicylism: tinnitus vertigo
–
• Acetaminophen
•
– No antiplatelet action
–
– No Reyes syndrome
–
– No bronchospasm
–
– Lesser GIT effects
–
266
– Increased doses cause hepatotoxicity due to depletion of glutathione

–
– N acetyl cysteine is used in acetaminophen toxicity (AIPG 1996)
–

• Drug interactions with NSAIDs (pharmacodynamics)
•
– Diuretics: Decreases diuresis
–
– β- blockers: Decreases antihypertensive effect
–
– Anticoagulants: Increases risk of GI bleed
–
– Alcohol: Increases risk of GI bleed
–
– Sulfonylureas: Increases risk of hypoglycaemia
–
– Corticosteroids: Increases risk of GI bleed
–
• Most asthmatics and patients who develop bronchospasm or intolerance to aspirin and ibuprofen or other NSAIDs donot
•
cross react with nimesulide. Its specific usefulness appears to be in such patients.
PHARMACOLOGY
Corticosteroids
• Uses: (AIIMS 1992)
•
– Replacement Therapy:
–
Acute adrenal insufficiency

Chronic adrenal insufficiency (Addisons disease)

Congenital adrenal hyperplasia (Adrenogenital syndrome)

– Pharmacotherapy
–
Arthritis

- Rheumatoid arthritis

- Osteoarthritis

- Rheumatic fever

- Gout

Collagen diseases: Lupus erythematosus, polyarteritis nodosa, glomerulonephritis, nephritic syndrome

Severe allergic reactions: Edema, urticaria, serum sickness

Autoimmune diseases: Hemolytic anaemia, thrombocytopenia

Bronchial asthma

Other: Infective diseases, eye diseases, malignancies, organ transplantation, cerebral edema.

• Adverse effects (with prolonged therapy)
•
– Mineralocorticoid
–
Na+and water retention, edema, hypokalemic alkalosis, progressive rise in BP

– Glucocorticoid
–
Cushing’s disease–rounded face, narrow mouth, supraclavicular hump, obesity of trunk with thin limbs

Fragile skin, purple striae

Hyperglycaemia

Muscular weakness

Susceptibility to infection

Drug Therapy for Migraine
Severity Drug therapy
Mild Simple analgesics (paracetamol)/NSAIDs (ibuprofen/diclofenac) or their combinations
+/- antiemetic (metoclopramide)
Moderate NSAIDs combo/ ergot alkaloids/ sumatriptan + antiemetic
Severe Ergot alkaloid/ sumatriptan + antiemetic + prophylaxis (for 6 months)

• Propanolol/β-blockers
•
• Amitriptyline/other tricyclic depressants
•
• Flunarizine/other Ca2+ channel blockers
•
• Methysergide/ cyproloptadine
•
Pharmacology 267

BLOOD AND ENDOCRINAL DRUGS
Coagulants Anticoagulants
• Vitamin K • Drugs used in vitro: these include:
•
•
– K1 (from plants, fat soluble): Phytonadione – Heparin: 150 units to prevent clotting of 100ml of blood
–
–
– K2 (produced by bacterial, fat soluble): Menaquinone – Calcium complexing agents: these include:
–
–
– K3 (synthetic) - Na citrate: 1.6g for 350ml of blood used to keep blood in
–
-
- Fat soluble: Menadione fluid transfusion
-
- Water soluble: menadione sodium diphosphate - Na oxalate: 10mg per ml of blood
-
-
• Miscellaneous - Na edetate: 2mg per ml
•
-
– Fibrinogen • Drugs used in vivo:
•
–
– Anti-hemophilic factor – Heparin and low molecular weight heparin
–
–
– Ethamsylate – Heparinoids: Include heparin sulfate and dextran sulfate
–
–
– Oral anticoagulants
PHARMACOLOGY
–
- Coumarin derivative: warfarin sodium, bishydroxy
-
coumarin
- Inarandione derivative: Phenondione
-
Heparin vs Warfarin
Heparin Warfarin
Structure Large anionic polymer, acidic Small lipid soluble molecule
Route given Prenatal Oral
Site of action Blood Liver
Mechanism of action Activates antithrombin III which decreases Impairs synthesis of vitamin K dependent factors II, VIII, IX
the action of thrombin IIa and Xa and X, protein C and protein S

(AIPG 1997)

Onset Rapid Slow
Duration of action Acute (hours) -
Treatment of overdose Protamine sulfate IV vitamin K and fresh frozen plasma

(AIIMS 1998, 1996, AIPG 1997)

Monitoring PT/INR PT/IN
Antiplatelet Drugs
Acetyl salicylates Aspirin Thienopyridines Clopidogrel Glycoprotein (GP)IIa/IIIb receptor antagonists
• Aspirin causes irreversible • These inhibit the ADP receptors in the • These agents inhibit the Gp IIa /IIIb receptor complex,
•
•
•
inhibition of cyclo oxygenase surface of platelets a key receptor involved in platelet aggregation (Gp IIa/
and thromboxane synthesis IIIb is an adhesive receptor for fibrinogen and WF and
is required for platelet aggregation)
• This leads to the prevention • They thus selectively inhibit ADP – • These agents are also called ‘disintegrins’
•
•
•
of thromboxane – A synthesis induced platelet aggregation and
and impairment of platelet likely ADP mediated amplification of
secretion and aggregation platelets response to other agonists
Thrombolytics
Examples • Streptokinase, urokinase, tPA (tissue plasminogen activator)
•
Mechanism of action • Directly or indirectly aid in conversion of plasminogen to plasmin, the major fibriolytic enzyme which cleaves
•
thrombin and fibrin clots
• Increases PT, PTT
•
• Low platelet count
•
268
Indication • Early MI, Early ischemic stroke
•
Adverse effects • Bleeding
•
Management of over- • Aminocaproic acid, an inhibitor of fibrinolysis
•
dose
Effect of drugs and metabolic changes on oral anticoagulant potency

Factors leading to enhanced potency and increased prothrombin time (AIPG 2000)
Reduced coumarin clearance • Disulfiram
•
• Metronidazole
•
• Trimethoprim-sulfamethoxazole
•
PHARMACOLOGY
Reduced albumin binding • Phenylbutazone
•
Additive haemostatic effect (negative effect) of certain • •
Aspirin
drugs or disorders • Heparin
•
• Liver disease
•
• Thrombocytopenia
•
• Vitamin K deficiency as seen with antibiotics
•
Increased turnover of vitamin K • Clorifibrate
•
• Hypermetabolism (e.g., hyperthyroidism)
•
Factors leading to diminished potency and decreased prothrombin time
Accelerated coumarin clearance induction of hepatic • Barbiturates
•
metabolizing enzymes • Rifampin
•
• Oral contraceptives (remember RBC—rifampicin, barbiturates, contraceptive)
•
Reduced absorption • Cholestyramine
•
Impaired metabolism • Genetic coumarin resistance
•
Oral Hypoglycaemic Drugs
Sulphonyl ureas • First generation
•
• Tolbutamide
•
• Chlorpropamide
•
• Second generation
•
• Gilbenclamide
•
• Glipizide
•
• Gliclazide
•
• Glimepiride
•
Biguanides • Phenformin
•
• Metformin
•
Meglitinide analogues • Repaglinide
•
• Nateglinide
•
Thiazolidinediones • Rosiglitazone
•
• Pioglitazone
•
α-Glucosidase Inhibitors • Acarbose
•
• Migitol
•
Pharmacology 269

Pioglitazone (AIIMS May 2011, AIPG 2010)
• It acts on insulin gene and even in the absence of insulin helps in metabolism of carbohydrates
•
• It is thiazolidione derivative
•
• Pioglitazone and rosiglitazone are selective agonists for nuclear peroxisome proliferator-activated receptor-γ (PPAR γ)
•
and activates insulin responsive genes that regulate carbohydrate and lipid metabolism. It exerts its principal effects by
increasing insulin sensitivity in peripheral tissue.
• It can also activate genes that regulate fatty acid metabolism in peripheral tissue. It increases glucose transport into
•
muscle and adipose tissue by enhancing the synthesis and translocation of specific forms of the glucose transporters.
Although muscle is an insulin sensitive tissue, PPAR γ is virtually absent in skeletal muscle.
• This drug causes activation of adiocyte hormones and/or adipokines, the most promising of which is adiponectin.
•
• Adiponectin is associated with increased insulin sensitivity and stimulates glucose transport into muscle and increases
PHARMACOLOGY
•
fatty acid oxidation-adipogenic-patients may become fat.
• It is metabolized by the liver and may be administered to patients with renal insufficiency, but should not be used if there
•
is active hepatic disease or significant elevations of serum liver transaminases.
Acarbose (AIIMS May 2011)

• Inhibits glycoside hydrolases, needed to digest carbohydrates, to be specific, α-glucosidase enzymes in the brush border of
•
the small intestines and pancreatic α amylase.
• Pancreatic α amylase hydrolyzes complex starches to oligosaccharides in the lumen of the small intestine; whereas
•
the membrane bound intestinal α-glucosidases hydrolyse oligosaccharides, and dissacharides to glucose and other
monosaccharides in the small intestine.
• Inhibition of these enzyme systems reduces the rate of digestion of complex carbohydrates. Less glucose is absorbed because
•
the carbohydrates are not broken down into glucose molecules. In diabetic patients, the short term effect of these drug
therapies is to decrease current blood glucose levels and long term effect is a reduction in HbA1c levels.
• Acarbose does not enhance insulin secretion and when used as monotherapy does not cause hypoglycemia at normal
•
glucose levels.
Also note
• Tamoxifen (AIPG 2008, 2009, 2010)
•

– Oral selective estrogen receptor modulator”. (PGI 2002)
–

– ↓FSH. (PGI 2000)
–

– It is used for the treatment of early and advanced breast cancer in both pre- and post-menopausal women.
–
• Exemastine, latrazole are other hormonal agents used for breast cancer. (AIPG 2004)
•

• Latrazole is an aromatase inhibitor. (AIIMS 2006)
•

• Dopamine decreases Prolactin levels, so DA agonists cause hypoprolactemia and v/v
•
• Estrogen and thyroid hormones increase prolactin levels
•
• Hyperprolactinemia (increases prolactin levels) has negative feedback on estrogen so increase prolactin level causes
•
decreases estrogens
DRUGS ACTING ON CVS, GIT, RESPIRATORY SYSTEM
Condition First choice Alternative

• Artial flutter Quinidine Procainamide, Verpamil, phenytoin
•
Amiodarone, Digitalis
• Ventricular tachycardia Acute: Lignocaine Acute: Procaine
•
Chronic: Procaine, quinidine Chronic: Amiodarone
270
Condition First choice Alternative

• Ventricular fibrillation Acute: Electrical defibrillation Acute: Lignocaine, procainamide,
•
Chronic: Amiodarone Disopyramide
• Atrial fibrillation Acute: Verapamil, Acute: Quinidine,
•
Chronic: Digitalis, Quinidine Chronic: Procaine, Verapamil
• Ventricular extrasystoles
•
• Mi Acute: Lidnocaine Procainamide, phenytoin
Acute: Lidnocaine Proparonolol
•
• Digitalis induced
Chronic: Quinidine Amiodarone
•
• Atrial extrasystole Quinidine Propranolol
•
• Paroxysmal supraventicular Acute: Adenosine, digoxin Acute: Digoxin, beta-blockers
•
tachycardia Chronic: Verapamil, Chronic – quinidine, propranolol
PHARMACOLOGY
Isosorbide Dinitrate
• Sublingual administration produces maximal plasma concentrations of the drug by 6 minutes.
•
• The primary initial metabolites, isosorbide – 2 – mononitrate and isosorbide-5-mononitrate, have longer half live (3 to 6
•
hours) and are presumed to contribute to the therapeutic efficacy of the drug.
Nitroglycerin
• In humans, peak concentrations of nitroglycerin are found in plasma within 4 minutes of sublingual administration; the
•
drug has a halflife of 1 to 3 minutes.
• The onset of action of nitroglycerin may be even more rapid if it is delivered as a sublingual spray rather than as a
•
sublingual tablet.
• This is preferred in acute attack
•
Isosorbide 5-mononitrate
• Available in tablet form.
•
• It does not undergo significant first-pass metabolism
•
The mononitrate has a significantly longer half-life than does isosorbide dinitrate and has been formulated as a plain tablet and as
a sustained release preparation; both have longer durations of action than the corresponding dosage forms of isosorbide dinitrate.
Antihypertensive Drugs
ACE inhibitors • Captopril
•
• Enalapril
•
• Ramipril
•
Angiotensin (AT1) • Losartan
•
antagonist • Candesartan
•
Calcium channel • Verapamil
•
blockers • Nifedipine
•
• Amlodipine
•
Diuretics • Thiazides
•
• Hydrochlorothizide
•
• Chlorthalidone
•
• High ceiling
•
• Furosemide
•
• K sparing
•
• Spironolactone
•
• Triametrene
•
• Metoprolol
•
Pharmacology 271

β- adrenergic block- • Propanolol
•
ers • Atenolol
•
• Metoprolol
•
β + α adrenergic •
•
Labetalol
blockers • Carvedilol
•
α- adrenergic block- • Prazosin
•
ers • Terazosin
•
• Doxazosin
•
• Phentolamine
•
• Phenoxybenzamine
•
Central sympatho- • Clonidine
•
lytics • Methyl dopa
PHARMACOLOGY
•
Vasodilators • Arteriolar
•
• Hydralazine
•
• Minoxidil
•
• Diazoxide
•
• Arteriolar and venous
•
• Sodium nitroprusside
•
Anti Asthmatics
Theophylline and Doxophylline
• MOA
•
– Inhibits phosphodiesterase 4 and increases cAMP concentration. (AIPG 2006)
–

– Blocks adenosine receptors (AIPG 2005)
–

– Releases calcium from Sarcoplasm
–
– BETA 2 Agonist (AIPG 2010)
–

– Stimulates Mucociliary movement (AIPG 2010)
–

• Pharmacokinetics and dynamics
•
– It has low therapeutic index
–
– At high doses kinetics changes from First order to zero order.
–
– Erythromycin inhibits metabolism of Theophylline (Increases Theophylline levels)
–
– Crosses placenta and is sereted in milk.
–
Drugs used for Peptic Ulcer
Reduction of gastric • H2 antihistaminics:
•
acid secretion – Cimetidine
–
– Ranitidine
–
– Famotidine
–
– Roxatidine
–
– Loxatidine
–
• Proton pump inhibitors:
•
– Omeprazole
–
– Lansoprazole
–
• Anticholinergics:
•
– Pirenzepine
–
– Oxyphenonium
–
• Prostaglandin analogues:
•
– Misoprostol
–
– Enprostil
–
272
Neutralization of • Systemic:
•
gastric acids (ant- – Sodium bicarbonate
acids)
–
– Sodium citrate
–
• Non systemic:
•
– Magnesium hydroxide
–
– Magnesium trisilicate
–
––
Al hydroxide gel
– Calcium carbonate
–
Ulcer protective • Sucrafalte
•
• Colloidal bismuth subcitrate (CBS)
•
Ulcer healing drugs • Carbenoxolone sodium
•
Anti – H pylori drugs • Amoxicillin
PHARMACOLOGY
•
• Clarithromycin
•
• Metronidazole
•
• Tinidazole
•
• Tetracycline
•
Anti Emetics
• Anticholinergics: Hyoscine, Dicyclomine
•
• H1 antihistaminics: Promethazine, Dimenhydrinate, Cyclizine, Meclozine, Cinnarizine
•
• Neuroleptics: Chlorpromazine, Prochlorperazine
•
• Prokinetic drugs: Metoclopramide, Domperidone, Cisapride
•
• 5 HT3 antagonists: Ondansterone (AIPG 2001)
•

• Adjuvant antiemetics: Dexamethasone, benzodiazepines
•
Laxatives and Purgatives
• Bulk forming drugs
•
– Dietary fibre
–
– Isabgol
–
– Agar agar
–
– Plantago seeds
–
– Methyl cellulose
–
• Stool softener (Emolluients)
•
– Decussate sodium
–
– Liquid paraffin
–
• Stimulant purgatives (contact laxatives)
•
– Diphenyl methane
–
Phenolphthalein

Bisacodyl

– Anthraquinone
–
Senna

Cascara

– Fixed oil
–
Castor oil

• Osmotic laxatives (saline purgatives)
•
– Magnesium sulfate
–
– Milk of magnesia
–
Pharmacology 273

– Magnesium citrate
–
– Sodium potassium tartarate
–
– Lactulose
–
– Polyethylene glycol
–
Antidiaarrhoeal Agents
• Adsorbants:
•
– Psyllium
–
– Ispaghula
–
– Methyl cellulose
–
• Antisecretory
•
– Sulfasalazine
–
PHARMACOLOGY
– Mesalazine
–
– Bismuth subsalicylate
–
– Corticosteroids (prednisolone)
–
– Anticholinergics (atropine)
–
– Octreotide
–
– Opoids (loperamide) (AIPG 2001)
–

• Antimotility drugs
•
– Codeine
–
– Diphenoxylate
–
– Loperamide
–
Diuretics
High efficacy diuretics • Sulphamoyl derivatives
•
(inhibitors of Na+ K+ 2Cl-
cotransport)
– Furosemide
–
– Bumetanide
–
• Phenoxyacetic acid derivative
•
– Ethacrynic acid
–
• Organomercurials
•
– Mersalyl
–
Medium efficacy diuret- • Benzothiadiazines (Thiazides)
•
ics (Inhibitors of Na+ Cl-
symport)
– Chlorothiazide
–
– Hydrochlorothiazide
–
– Clopamide
–
• Thiazide like (related heterocyclics)
•
– Chlorthalidone
–
– Xipamide
–
Weak or adjuvant diuret- • Carbonic anhydrase inhibitors
•
ics
– Acetazolamide
–
• Potassium sparing diuretics
•
– Aldosterone antagonist – spironolactone
–
– Directly acting (inhibitors of renal epithelial Na+ channel)–Triameterene, Amiloride
–
• Osmotic Diuretics–Mannitol
•
• Xanthenes–Theophylline
•
274
Diuretic Site of action MOA Indication Adverse effects

Carbonic anhydrase Proximal convulated Inhibits carbonic anhydrase Glaucoma Hypokalemia
inhibitor tubule Mild diuresis Epilepsy Renal stones
Prevents bicarbonate reabsorption Metabolic alkalosis
Altitude sickness
Thiazides DCT Inhibits Na/Cl cotransporter HTN Hypokalemic metabolic

Increases Ca+ reabsorption Chronic heart failure alkalosis
Diabetes insipidus Hyperglycemia
Hyperuricemia
Osmotic agents PCT loop of henle Increased tubular fluid osmolarity Acute glaucoma Pulmonary edema
Increased urinary flow Shock Dehydration
Drug toxicity CHF
PHARMACOLOGY
Loop diuretics Ascending loop of Inhibits Na/K/Cl cotransporter CHF Ototoxicity

Henle to decrease reabsorption and Pulmonary edema Gout
indirectly inhibit Ca reabsorption Hypercalcemia Hypokalemia
Rapid onset Hypocalcemia
K–sparing Collecting tubules Aldosterone receptor antagonist Secondary Gynaecomastia,

hyperaldosteronism, hyperkalemia, menstrual
CHF irregularity
CHEMOTHERAPY
Classifications
Chemical Structure
• Sulfonamides and related drugs: Sulfadizine and others, Sulfones–Dapsone (DDS), Paraaminosalicylic acid (PAS).
•
• Diaminophyrimidines: Trimethoprim, Pyrimethamine.
•
• Quinolones: Nalidixic Acid, Norfloxacin, Ciprofloxacin, etc.
•
• B-lactam antibiotics: Penicillins, Cephalosporins, Monobactams, Carbapenems.
•
• Tetracyclines: Oxytetracycline, Doxycycline, etc.
•
• Notribenzene derivative: Chloramphenicol.
•
• Aminoflycosides: Streptomycin, Gentamycin, Neomycin etc.
•
• Macrolide antibiotics: Erythromycin, Roxithromycin, Azithromycin etc.
•
• Polypeptide antibiotics: Polymyxin–B, Colistin, Bacitracin, Tyrothricin.
•
• Glycopeptidies: Vancomycin, Teicoplanin.
•
• Oxazolidinone: Linezolid
•
• Nitrofuran derivatives: Nitrofurantoin, Furazolidone.
•
• Nitroimidazoles: Metronidazole, Tinidazole. (AIPG 1993)
•

• Nicotinic Acid derivatives: isoniazid, Pyrazinamide, Ethionamide.
•
• Polyene Antibiotics: Nystatin, Amphotericin–B, Hamycin.
•
• Azole Derivatives: Miconazole, Clotrimazole, Ketoconazole, Fluconazole. (MAN 2001)
•

• Others: Rifampin, Lincomycin, Clindamycin, Spectinomycin, Sod. Fusidate, Cycloserin, Viomycin, Ethambutol,
•
Thiacetazone, Clofazimine, Griseofulvin.
Pharmacology 275

Mechanism Of Action
Inhibit cell wall synthesis Cause leakage from cell Inhibit protein synthesis Inhibition of Peptidoglycan
(AIPG 2006, 1997) membranes • Tetracyclines–30S ribosomes synthesis
•
• Penicillins • Polymyxins (MCET 2007, AIIMS 1992) • Cycloserin
•
•
•
• Cephalosporins • Colistin • Chloramphenicol • Bacitracin
•
•
•
•
• Cycloserine • Bacitracin • Erythromycin
•
•
•
• Vancomycin • Clindamycin
• Polyenes
•
•
•
• Bacitracin • Amphotericin B
•
•
• Nystatin
•
• Hamycin
•
Inhibit DNA gyrase Interfere with DNA function Interfere with DNA synthesis

PHARMACOLOGY
• Fluoroquinolones: (AIIMS 2000) • Acyclovir
•

•
Ciprofloxacin. (MAN • Rifampin • Zidovudine
•
2000, AIPG 2000)
•
• Metronidazole
•
Type Of Organisms Against Which Primarily Active
Antibacterial Antifungal (MAN 2000) Antiviral
• Penicillin • Griseofulvin • Acyclovir
•
•
•
• Amino glycosides, • Amphotericin B (AIPG 2012) • Amantadine
•
•
•
• Erythromycin • Ketoconazole • Zidovudine
•
•
•
Antiprotozoal Antihelminthic
• Chloroquine • Mebendazole
•
•
• Pyrimenthamin • Pyrantel
•
•
• Metronidazole • Niclosamide
•
•
• Diloxanide • Diethyl Carbamazepine
•
•
Narrow spectrum Broad spectrum (AP 2006, AIIMS 2000)

• Penicillin • Tetracycline
•
•
• Streptomycin • Chloramphenicol
•
•
• Erythromycin
•
Bacteriostatic Bactericidal (MAN 1995)

• Sulfonamides • Penicillins
•
•
• Erythromycin • Cephalosporins
•
•
• Penicillin G • Aminoglycosides
•
•
• Tetracyclines • Vancomycin
•
•
• Chloramphenicol
• Polypeptides
•
• Clindamycin
•
• Ciprofloxacin
•
•
Antibiotics Are Obtained From
Fungi • Penicillin
•
• Griseofulvin
•
• Cephalosporin
•
Bacteria • Polymyxin B
•
• Tyrothricin
•
• Colistin
•
• Aztreonam
•
• Bacitracin
•
276
Actinomycetes • Aminoglycosides
•
• Macrolides
•
• Tetracyclines
•
• Polyenes
•
• Chloramphenicol
•
Penicillin (AIIMS 2008)
• Has a wide therapeutic range and safest drug.
•
• The form most commonly used is benzyl penicillin
•
• Benzyl penicillin is effective against Gram-Positive bacilli and cocci and Gram negative cocci, Highly effective for syphilis
•
and actinomycosis and gonorrhea
• Acts by causing defective synthesis of cell wall glycoprotein
PHARMACOLOGY
•
• Absorption is rapid following intramuscular injection.
•
• Adverse effects
•
– Anaphylaxis
–
– Angioedema
–
– Super infection
–
– Jarisch-Herxheimer reaction
–
• Therapeautic uses: (AIPG 2006)
•

– Streptococcal infections
–
– Syphilis
–
– Gonorrhoea (MAN 1995)
–

– Actinomycosis
–
– Clostridial infections
–
– Abscess
–
– Cellulitis
–
• Route of administration
•
– Procaine penicillin, benzathine penicillin–Deep IM
–
– Crystalline penicillin – IM/IV (MAN 1999)
–

– Phenoxy methyl penicillin or penicillin V – Oral (AIPG 1995, KAR 1997)
–

Semi-synthetic penicillins
Sub class I Sub-class II Subclass III
• Acid resistant (oral) • penicillinase resistant • Wide spectrum
•
•
•
Penicillin V (PHENOXY METHYL Methicillin Ampicillin
PENCILLIN) Cloxacillin Amoxycillin
Phenoxy ethyl penicillin Carbenicillin
Penicillinase-Resistant Penicillins are able to Resist Degradation by Staphylococcal Penicillinase

• Methicillin, (Acid labile) (JIPMER 1991)
•

• Naficillin,
•
• Oxacillin,
•
• Cloxacillin (PGI 2004, AIIMS 2000, AIPG 1996)
•

• Dicloxacillin
•
• Flucloxacillin
•
• Cephalosporins
•
Pharmacology 277

Macrolides
• So called because they have a large lactone ring in their structure.
•
• Macrolides stimulate motilin receptors and cause GIT distress. (AIPG 2014, MP 2000 AIPG 1999)
•

• Three important macrolides are:
•
– Erythromycin,
–
Erythromycin estolate causes cholestatic jaundice.

Erythromycin is used in penicillin allergics. (AIPG 2010, MAN 1998, KAR 2003)

– Azithromycin: Effective against Chlamydia, Mycoplasma, Ureaplasma. Legionella (PGI 1997)
–

Safe in pregnancy

– Clarithromycin
–
Effective against H. Pylori
PHARMACOLOGY

Aminoglycosides (AIPG 2010)
• So called because they contain aminocarbohydrate complexes with glycoside bonding.
•
• These drugs are the mainstay in the treatment of Gram-negative infections.
•
• Streptomycin
•
– Derivative from Streptomyces grieseus.
–
– Mainstay in the treatment of gram-negative bacteria like E.coli, Proteus, Shigella, Pseudomonas, Yersinia, Brucella
–
and Listeria.
– It is widely active against some Gram positive cocci also
–
Adverse effects
• Ototoxicity (AIIMS 1998)
•

• Nephrotoxicity
•
• Superinfection
•
• Neuromuscular blockade.
•
Therapeutic uses
• Septicaemia
•
• Gram-negative meningitis
•
• Tuberculosis
•
• Plague
•
• Bacterial endocarditis
•
Cephalosporins
• Extracted from Cephalosporeum actromonium. Resembles penicillin in structure.
•
• Active against:
•
– Gram-positive: C. diphteriae, Pneumococcus, streptococci
–
– Gram-negative: E. coli, Proteus, Klebsiella, Neisseiria
–
• MOA: (AIIMS 1995)
•
– They inhibit the bacterial cell wall synthesis
–
– Does not undergo any metabolism in the body.
–
– One exception to this rule, cefotaxime is partly metabilised by the liver
–
– Excretion is by the kidney. There is one expection-cefaperazone, in which biliary excretion is significant
–
278
Major generations of Cephalosporins

First generation Second generation Third generation (AIIMS 2006) Fourth generation
• Parenteral • Parenteral • Parenteral Cefepine
•
•
•
– Cephalothin – Cefamandole – Cefotaxime Cefpirome (AIIMS 2004)

–
–
–
– Cephaloprin – Cefuroxime – Ceftriaxone
–
–
–
– Cefazolin – Cefonicid – Ceftazdime
–
–
–
• Oral – Ceforanide – Cefoperazone
•
–
–
– Cephalexin – Cefoxitin • Oral
–
•
– Cefotetan
–
– Cephadrine –
– Cefixime
• Oral
–

–
(APPSC 1999) – Cefpodoxime proxetil
•

–
– Cefprozil – Ceftibuten
–
–
– Cefuroxime axetil – Cefdinir
–
–
– Cefaclor
–
PHARMACOLOGY
Sulfonamides
• Short acting (4–8 hr) Sulfadiazine.
•
• Intermediate acting (8–12 hr) Sulfonamethoxazole, Sulfonamozole.
•
• Long acting ( - 7 dyas) Sulfonadoxine, Sulfamethopyrazine.
•
• Special purpose sulfonamides, Mafenide, silver sulfadiazine.
•
• Mechanism of action
•
Anti Pseudomonas Antibiotics (AIIMS May 08, 1992)
1. Penicillins • Pipercillin (AIPG 2006)

•

• Mezlocillin
•
• Ticarcillin
•
• Carbenicillin
•
2. Cephalosporin • Ceftazidime

•
• Cefepime (AIIMS 2009, AIPG 2011)
•

• Cefoperazone
•
3. Carbapenam • Imipenam

•
• Meropenam
•
4. Monobactum • Aztrenam

•
5. Aminoglycopide • Gentamycin

•
• Amikacin
•
• Tobramycin
•
Pharmacology 279

6. Fluoroquinolone • Ciprofloxacin

•
• Levofloxacin
•
7. Other agents • Polymyxin B

•
• Colistin
•
Adverse effects of Tetracycline • Pencillin group antibiotics acquired plasmid mediated
•
• Hepatotoxicity resistance by producing pencillinase/β – Lactamase
•
• Renal toxicity and fanconi syndrome • To overcome the problem of β – Lactamases broad-
•
spectrum cephalosporins were developed, which
•
• Phototoxicity (MAN 1999) contained oxy amino side chain. Cefotaxime, cefazidime,
•

• Staining of teeth due to formation of chelates with calcium cefitizoxome and ceftriaxone. (KAR 1998)
•

ions (AIIMS 1995, 2001, AIPG 1993, 2004,
PHARMACOLOGY

MAN 1999, KAR 2000) Resistance Mechanism

• Suppression of bone marrow growth
Drugs Mechanism
•
Adverse effects of antibiotics Penicillin/ • b lactamase cleavage of b- lactam
•
Cephalosporin ring, or altered PBP in MRSA
• Aminoglycosides: 8th cranial nerve and kidney toxicity
•

(MAN 1994) Aminoglycosides • Modification via acetylation, or

•
• Tetracyclines: Liver and kidney damage, antianabolic phosphorylation
•
effect. Vancomycin • Replacement of terminal d-ALA with
•
• Chloramphenicol: Bone marrow depression, Grey baby d-LAC
•
syndrome, aplastic anemia, hypersensitivity reaction Macrolides • Methylation of rRNA near ribosome

•
(AIPG 1996, MAN 1999) binding site uptake

• Polymyxin B: Neurological and renal toxicity. Sulfonamides • Altered enzyme, PABA synthesis
•
•
• Vancomycin: Hearing loss, kidney damage. Quinolones • Altered gyrase or reduced uptake
•
•
• Amphotericin B: Kidney, bone marrow and neurological
Chloramphenicol • Modification via acetylation
•
toxicity. (AIIMS 2004)
•

Tetracycline • Plasma mediated synthesis of protein
•
that prevents ribosomal binding site
Antibiotic Resistance
• Elaboration of tetracycline inactivating
•
• First antibiotic resistance was observed among penicillin. enzyme (MAN 2000, AIPG 1993)

•
Dose reduction needed in renal failure: (AP 2007)
Even in mild failure Only in moderate-severe failure Drugs to be avoided
• Aminoglycoside • Metronidazole • Cephalothin
•
•
•
• Amphotericin B • Carbenicillin • Nitrofuratoin
•
•
•
• Cephalosporins • Cotrimoxazole • Nalidixic acid
•
•
•
• Ethambutol • Fluoroquinolones • Tetracyclins (except doxycycline)
•
•
•
• Vancomycin
•
Dose reduction needed in hepatic failure
Drugs to be avoided Dose reduction needed
• Erythromycin estolate • Chloramphenicol
•
•
• Tetracyclines (MAN 1999) • Isoniazid
•
•
• Pyrazinamide • Metronidazole
•
•
• Nalidixic acid • Rifampin
•
•
• Clindamycin
•
280
Cardiac Conditions considered for prophylaxis

High risk Moderate risk Negligible risk
• Prosthetic cardiac valves • Most other congenital cardiac • Isolated secundum atrial septal defect
•
•
•
• Previous bacterial endocarditis malformations • Surgical repair of atrial septal defect, ventricular septal
•
•
• Complex, cyanotic congenital • Acquired valvular dysfunction defect
•
•
heart disease • Hypertrophic cardiomyopathy • Previous coronary artery bypass graft surgery
•
•
• Surgically constructed systemic • Mitral valve prolapse with • Physiologic or functional murmur
•
•
•
pulmonary shunts regurgitation • Previous Kawasaki disease/rheumatic disease without
•
valvular dysfunction
• Cardiac pacemaker
•
• Implanted defibrillators
•
Antibiotic Prophylactic Regimes for certain Dental Procedures
PHARMACOLOGY
Standard prophylaxis • Amoxicillin: 2g (Adults), 50mg/kg (Child) 1 hr before procedure

•
If oral route not possible • Ampicillin: 2g IM/IV (Adults), 50mg/kg IM/IV (child) within 30 mins before procedure
•
Allergic to penicillin • Clindamycin: 600mg (Adults), 20mg/kg (Child) orally 1hr before procedure
•
• Cephalexin/cefadroxil: 2g (Adult), 50mg/kg (Child) 1hr before procedure
•
• Azithromycin/ clathrimycin: 500mg (Adults), 15mg/kg (child) 1hr before procedure
•
Allergic to penicillin and oral route • Clindamycin: 600mg (Adults), 15mg/kg (Child) IV 1hr before procedure
•
not possible
• Cefazolin: 1g (adult) 25mg/kg (Child) IM/IV within 30 minutes before procedure

•
Dental Conditions considered for prophylaxis in susceptible patients
High risk Negligible risk
• Dental extractions • Restorative dental procedures with or without retraction cord
•
•
• Periodontal surgeries • LA injection
•
•
• Dental implant placement • Intracanal endodontic procedures
•
•
• Endodontic instrumentation or surgery beyond apex • Placement of rubber dams
•
•
• Subgingival placement of antibiotic fibres or strips • Removable appliance placement
•
•
• Initial placement of orthodontic bands • Making impressions
•
•
• Intraligamentary local anaesthetic injections • Taking radiographs
•
•
• Prophylactic cleaning of teeth with anticipated bleeding
•
Anti – Tubercular Drugs
• Safe in liver disease: Azithromycin, Clarithromycin, Ethambutol, Rifabutin, Streptomycin
•
– Patient with hepatic disease should be treated with–Etham + Streptomycin (if required INH + Rmp cautiously)
–
• Safe in renal Disease: Rifabutin, Rmp – Absolutely safe
•
– Azithro, Clairthro, Ethambutol, INH, Pzm, Rifabutin, Rmp–Relatively safe (use when CCL > 30ml/min)
–
• ATT regimen in CRF patient: INH + Rmp + Pzm + Etham for 1st 2 months
•
• Safe in Pregnancy: INH, Rmp, ethm, Azithromycin, Rifabutin (streptomycin is contraindicated) (AIPG 1998)
•

– ATT regimen in Pregnancy: INH + Rmp for 9 months and ethambutol for first 2 months
–
• Regimen in HIV Infected patients: 4 drugs -- INH + Rifabutin + Pzm + E/S for 6 months (Avoided in HIV infected
•
patients – Thiacetazone (Amithiozone) because of serious skin and GI toxicity.
• Prolonged INH therapy can lead to pyridoxine deficiency → Peripheral neuritis is the most important dose dependent
•
ad/e of INH therapy. Pyridoxine is given prophylactically with INH to prevent neurotoxicity (AIPG 2003, KAR 2001)

• ATT which cross BBB:Pzm, Ethionamide, cycloserine
•
Pharmacology 281

Parasitology
Antimalarials
• Treatment of (COMEDK 2008)
•

– Chloroquine sensitive malaria: chloroquine
–
– Chloroquine resistant malaria: mefloquine (Manipal 2006)
–

– Mefloquine resistant malaria: sulfadoxine+pyremethamine
–
• Quinine
•
– It is the DOC for cerebral malaria. (PGI 1993)
–

– Causes hypoglycemia (PGI 1999)
–

– Can be given safely in pregnancy along with chloroquine (PGI 2002)
–

• Primaquine
•
PHARMACOLOGY
– It is the only anti malarial active in exoerythrocytic stage
–
– Primaquine is ineffective against p. falciparum (UPSC 1984)
–

– Primaquine is effective for radical cure of pl. vivax (PGI 1986)
–

– Can cause G6PD deficiency. (AP 1988)
–

• Halofantrine
•
– Is effective against Chloroquine resistant p. falciparum and p. vivax. (AIIMS 1997)
–

– Causes prolonged QT
–
• Chloroquine
•
– Chloroquine is an antimalarial drug.
–
– Chloroquine is also an immunosuppressant drug.
–
– Chloroquine is lysomotrophic (accumulates in lysosomes)
–
– It is widely distributed in adipose tissue.
–
– It also has
–
Anti tumor,

Anti viral,

Disease-modifying antirheumatic drug (DMARD) properties.

– It is used in treatment of SLE, Rheumatoid arthritis
–
– Chloroquine is known to cause lots of side effects.
–
Classification Of Antiviral Drugs
Anti-Herpes Agents • Idoxuridine.
•
• Acyclovir.
•
• Famciclovir.
•
• Vidarabine.
•
• Trifluridine.
•
• Foscarnet.
•
• Ganciclovir.
•
Anti-Retroviral • Reverse transcriptase inhibitors (RTIs):
•
Agents – Nucleoside reverse transcriptase inhibitor:
–
- Zidovudine (AZT)
-
- Didanosine.
-
- Zalcitabine.
-
- Stavudine.
-
- Lamivudine.
-
- Abacavir.
-
– Non-nucleoside reverse transcriptase inhibitor:
–
- Nevirapine.
-
- Efavirenz (COMEDK 2008)
-

- Delavirdine.
-
282
• Protease inhibitors: (COMEDK 2011)
•

– Ritonavir.
–
– Saquinavir.
–
– Indinavir.
–
– Nelfinavir.
–
– Amprenavir.
–
– Lopinavir
–
Anti-Influenza Agents • Amantadine.
•
• Rimantadine
•
Nonselective Agents • Ribavirin.
•
• Lamivudine.
•
• Interferon-α.
•
PHARMACOLOGY
Good to know
• Lamivudine and Emtricitabine are best tolerated NRTIs
•
• Stavudine has maximum chances of causing lactic acidosis and it is most strongly a/w lipodystrophy among all NRTIs
•
• All PIs (-virs) are metabolized by liver and can cause lipodystrophy
•
• Skin Rashes are seen with NNRTIs. Nevirapine can cause SJS and TEN
•
• Not effective against HIV–2: Nevirapine, efavirenz, enfuvirtide
•
• Newer Art
•
– Maraviroc is a CCR5 (chemochine receptor 5) inhibitor for HIV–1
–
– Raltegravir is an integrase inhibitor against HIV
–
• HAART
– Includes 3 or more drugs of which 1 or 2 are NRTIs
–
– May be 2 NRTIs + 1 PI or 1 NNRTI + 1 PI
–
– For post exposure prophylaxis: 2 NRTI (routine exposure) or 2 NRTI + 1 additional drug for high risk exposure
–
DENTAL PHARMACOLOGY
• Astringents: Those substances that cause precipitation and do not cause penetration to cells, thus affect superficial layer
•
only. The astringents are divided into:
– Vegetable astringents:
–
Catechu: It is used for mouthwash

Tannic acid: At concentration of 3.5% it is used as mummifying agents, obtundent and mouth wash

– Alcohol: At 50% to 90% concentration, ethanol and methanol are perfect astringents.
–
– Mineral astringents: These are the heavy metal ions which are used as antiseptics and astringents. They are:
–
Copper sulphate: At a conc of 0.5% - 2%, used to treat gum ulcers and mouthwash

Alum: Used for hardening gums in case of inflamed and ulcerated gums

– Actions:
–
Toughen the tissue surfaces making it mechanically stronger and decrease exudation.

It causes hemostasis and reduces blood flow

They resist penetration of bacteria and form protective covering over underlying tissues.

• Mummifying agents:
•
– Used for drying and hardening of tissues of root canal and pulp to protect it from infection and to maintain aseptic
–
condition.
– The mummifying agents are:
–
Pharmacology 283

Iodoform: It is used in combination with tannic as well as the mineralization of the bone newly formed

acid, glycerine and eugenol. It produces its action by osteoblasts. Alendronate and the other potent
by slow liberation of iodine. N containing bisphosphonates such as risedronate,
Paraform: Its combination is with ZnO and ibandronate and zoledronate specifically inhibit bone

glycerine. It produces its action by slow liberation resorption without any effect on mineralization at
of formaldehyde. pharmacologically achievable doses.
Liquid formaldehyde: It is combined with ZnO,
Vaccines

glycerine and local anaesthetic.
Some astringents such as tannic acid and cresol
Killed vaccines (inacti- Live attenuated vaccines

are also used as mummifying agents.
vated)
• Obtundents: Drugs that reduce the sensitivity of Bacterial
•
dentin and hence cause excavation without causing • TAB • BCG
pain.
•
•
PHARMACOLOGY
• Cholera • Typhoid
– Classification:
•
•
• Whooping cough
–
Drugs which cause action by paralysis of
•
• Meningococcal

sensory nerve endings i.e. camphor, thymol and
•
• Haemophilus type B
menthol, etc
•
• Plague
Drugs which cause action by degrading nervous
•

tissue, for example absolute alcohol Viral
– Drugs which cause action by precipitation of
• Poliomyelitis inactivated • Poliomyelitis oral live (Sabin)
–
surface proteins, for example ethyl alcohol, zinc
•
•
(salk) • Mumps
chloride etc.
•
• Rabies (Brain substance) • Measles
•
•
• Rabies (chick embryo cell) • Rubella
•
MISCELLANEOUS
•
• Rabies (human diploid cell) • Varicella
•
•
• Rabies (vero cell)
•
Drugs for the Treatment of Bone Diseases • Influenza
•
• Hepatitis B
• Bisphosphonates: (AIPG 2011)
•
• Hepatitis A
•

– Nitrogeneous (alendronic acid, ibandronic acid,
•
–
incadronic acid, pamidronic acid, risedronic acid, Toxoids
zoledronic acid) Tetanus (fluid/adsorbed)
Diphtheria (adsorbed)
– Non nitrogeneous (etidronic acid, clodronic acid,
–
tiludronic acid) Combined vaccines
• Bone morphogenetc proteins: Dibotermin alfa, Double antigen (DT-DA)
•
Eptotermin alfa Triple antigen (DPT)
Typhoid paratyphoid cholera (TABC)
– Other resorption inhibitor (ipriflavone), Aluminium Measles – mumps – rubella (MMR)
–
chlorohydrate, dual action bone agent (strontium
ranelate) Reverse steal phenomenon (Robin hood phenomenon )
– RANKL inhibitor (Denosuab), cathepsin K inhibitor (AIIMS Nov 2010)
–
(odonacatib)
• Effect of hypocapnea producing increased blood flow to
– Strontium ranelate, a strontium (II) salt of ranelic
•
the brain.
–
acid, is a medication for osteoporosis marketed as
protelos or Protos by Servier. It increases deposition • Vasoconstriction occurs in the adjacent, normal arterioles,
•
of new bone osteoblasts and reduces the resorption of thereby causing a local increase in perfusion pressure and
bone by osteoclasts. It is therefore, promoted as a dual augmenting collateral flow to the ischemic, unreactive
action bone agent (DABA) maximally vasodilated area of the brain
– Teriparatide increases both be formation and bone • Conversely to above, a vasoconstriction caused by
•
–
resorption. (AIIMS May 2011) hypocapnea or a suitable anesthetic agent, such as

– Alendronate inhibits osteomediated bone resorption. thiopentone will cause a reduced blood flow to the
–
Whereas pyrophosphates and the first bisphosphonate, normal responsive regions of the brain resulting into
etidronate, are capable of inhibiting bone resorption redistribution of blood to ischemic regions.
284
• Thus the Inverse Steal redistributes more CBF to ischemic thus an inverse steal phenomenon occurs which can
•
areas. improve the overall circulatory condition.
• The vasoconstriction induced by barbiturates concerns the • Furthermore, barbiturates can decrease CBF in the non
•
ischemic brain by increasing the vascular resistance,
•
normal brain capillary bed and not the microvasculature which may actually improve flow in focal ischemia by
more or less altered by acidosis in ischemic brain areas, producing a Reverse Steal phenomenon.
Ifosfamide (IFO) (AIIMS May 2011)

• Nitrogen ustard alkylating agent
•
• It is an analogue of other nitrogen mustard cyclophosphamide.
•
• Both of them are given as prodrug and activated by ring hydroxylation in the liver.
•
• Ifosfamide is the most neurotoxic among all alkylating agents, producing altered mental status, coma, generalized
•
seizures, and cerebellar ataxia.
PHARMACOLOGY
• These side effects have been linked to the release of chloroacetaldehyde from the phosphate-linked chloroethyl side chain
•
of ifosfamide.
• Ifosfamide has virtually the same toxicity profile as cyclophosphamide although it causes greater platelet suppression,
•
neurotoxicity, nephrotoxicity, and in the absence of mensa urothelial damage.
Antiseptics
• Phenol derivatives • Phenol, cresol
•
•
• Oxidizing agents • Potassium permanganate, H2O2
•
•
• Halogens • Iodine, chlorine
•
•
• Biguanide • Chlorhexidine
•
•
• Quaternary ammonium (cationic) • Cetrimide
•
•
• Soaps • Of potassium and sodium
•
•
• Alcohols • Ethanol, isopropanol
•
•
• Aldehydes • Formaldehyde, Glutaraldehyde
•
•
• Acids • Boric acid, acetic acid
•
•
• Metallic salts • Silver nitrate, silver sulfadiazine
•
•
• Dyes • Gentian violet, brilliant green
•
•
• Furan derivatives • Nitrofurazone
•
•
Side Effects of Drugs
Altered Taste Dry Mouth Salivation
• Calcium channel blockers • Thiazide diuretics • Anti Parkinson, anticholinergic
•
•
•
• Angiotensin II antagonists • Potassium sparing diuretics (Aldactone) (Cogentin) increased salivation
•
•
• Theophylline derivative • Beta blockers • Antihistamines increased thickness
•
of secretions
•
•
• Antihistamine • Beta 2 adrenergic agonists
• Cholinergic Agent - excessive
•
•
• Anticonvulsant – (Dilantin) • Theophylline derivatives
•
salivation
•
•
• Anti-Parkinson agent • Corticosteroids
•
•
• CNS Stimulant- amphetamine • Anticonvulsant
•
•
• Proton pump inhibitors • AntiParkinson agent
•
•
• Laxative – bitter taste • Calcitonin
•
•
• Biguanides
•
• Biphosphonate derivatives
•
Pharmacology 285

Drug Toxicity
Nephrotoxicity Hepatotoxicity Cardiotoxic drugs
• Most nephrotoxic • Acetaminophen hepatotoxicity (direct toxin) • Doxarubicin
•
•
•
cephalosporine: cephaloridine • Halothane hepatotoxicity (idiosyncratic reaction) • Daunorubicin
•
•
• Most nephrotoxic • Methyldopa hepatotoxicity (toxic and idiosyncratic reaction) • VincristineE
•
aminoglycoside: gentamycin.
•
•
• Isoniazid hepatotoxicity (toxic and idiosyncratic reaction) • HalothaneE
• Least nephrotoxic
•
•
• Sodium valproate hepatotoxicity (toxic and idiosyncratic reaction) • Alcohol?
•
antitubercular: rifampicin
•
•
• Phenytoin hepatotoxicity (idiosyncratic reaction)
• Least nephrotoxic •
• Chlorpromazine hepatotoxicity (cholestatic idiosyncratic reaction)
•
aminoglycoside: tobramycin.
•
• Tetracycline safe in renal • Amiodarone hepatotoxicity (toxic and idiosyncratic reaction)
•
•
failure: doxycycline • Erythromycin hepatotoxicity (cholestatic idiosyncratic reaction)
•
• Oral contraceptive hepatotoxicity (cholestatic reaction)
PHARMACOLOGY
•
• 17, a-alkyl-substituted anabolic steroids (cholestatic reaction)
•
• Trimethoprim-sulfamethoxazole hepatotoxicity (idiosyncratic
•
reaction)
• Hydroxymethylglutaryl-coenzyme (HMG-CoA) reductase
•
inhibitors (“statins”) (idiosyncratic mixed hepatocellular and
cholestatic reaction)
• Total parenteral nutrition (steatosis, cholestasis)
•
• Drugs Causing Osteoporosis
•
– Glucocorticoids
–
– Anticonvulsants
–
– Cytotoxic drugs
–
– Cyclosporine
–
– Lithium
–
– Heparin
–
– GnRH analouges
–
– Almunium
–
– Throxine in increased doses
–
• Drugs with Low Safety Margin
•
– Digoxin
–
– Antiarrhythmics
–
– Anticonvulsants

– TCA (tricyclic antidepressants)

– Lithium (AIIMS 1982)

– Aminoglycosides

Adverse Effects of Some Drugs
Pseudotumor Cerebri • Glucocorticoids/ Mineralocorticoids
•
• OCPs
•
• Tetracycline
•
• Amiodarone
•
• Nalidixic acid
•
Alopecia • Ethionamide
•
• Cytotoxic drugs
•
• Heparin
•
• OCP withdrawl
•
• Li
•
• Valproate
•
286
Pancreatitis • Thiazides
•
• Steroids
•
• Melphalan
•
• L-asparginane
•
Pigmentation of skin • Clofazimine,
•
• Nicotinamide
•
• OCP
•
• ACTH
•
• Serusa
•
• Amiodarone
•
• Zidovudine
•
• Mepacrine
PHARMACOLOGY
•
• Phenothiazine
•
• Chloroquine
•
Flu like Syndrome • MethylDopa
•
• Rmp
•
• Interferon
•
• Clofibrate
•
• Hydralazine
•
Fibrous Gingival Hyper- • Nifedipine
•
plasia • Phenytoin
•
Livido reticularis • Amantadine
•
• Bromocriptine
•
Pure Red cell Aplasia • Chlorpropamide
•
• Azathioprine
•
• Phenytoin, INH
•
Drugs precipitating • Pzm, Ethambutol
•
Gout (Hyperuricemic) • Thiazide
•
• Frusemide
•
• Ethacrynic acid
•
• Diazoxide
•
• Clofibrate
•
• Cytotoxic drugs
•
• L-Dopa
•
Nephrotic Syndrome • Gold
•
• Captopril
•
• Probenecid
•
• Pencillamine
•
• NSAIDs
•
• Trimethadione
•
Teratogens
• Carbamezapine • Cleft Lip, cleft palate.
•
•
• Valproic acid • Neural tube defects.
•
•
• Warfarin • Chondrodysplasia punctata
•
•
• Carbimazole • Fetal cutis Aplasia
•
•
• Lithium • Ebsteins Anomaly
•
•
• Thalidomide • Phocomelia
•
•
• Chloramphenicol • Grey baby syndrome
•
•
Pharmacology 287

Drugs Produced by DNA Recombinant Technology: Also Note
• Human insulin • For treatment of seizures in pregnancy Phenobarbital is
•
considered drug of choice
•
• Growth hormone
• Among anti-thyroid drugs: Thyroid drugs propylthiouracil
•
•
• Interferons is DOC, however it may cause aplasia cutis. Radioactive
•
• Interleukins isotopes are absolutely contraindicated in pregnancy
• For treatment of UTI in pregnancy nitrofurantoin,
•
• Monoclonal antibodies
•
ampicillin and cephalexin are safe (flouroquinolones are
•
• Vaccines contraindicated)
•
• DOC for prophylaxis of malaria in endemic area is
•
proguanil and for treatment is chloroquine
Good to Know • For anticoagulation in pregnancy: Heparin (for 1st 12
•
weeks) → Warfarin up to 36 week → Heparin 1 week
PHARMACOLOGY
• Hyperthyroid patients are relatively resistant to
before delivery and after 2 days → restart warfarin in
•
inotropic action but more prone to arrhythmic action
purpereum
of digoxin. (AIPG 2003)
• Heparin does not cross placenta. It is anticoagulant of

•
• Head injury patients are prone to go into respiratory choice in pregnancy. While unfractioned heparin is safe
•
failure with normal doses of morphine. in pregnancy, LMW heparin can cross placental barrier
• Adrenaline followed by a short course of glucocorticoids • Lidocaine is safe first line IV drug for ventricular
•
arrhythmias in pregnancy. Among oral drugs qunidine
•
is indicated for bronchospasm attending drug has been found to be safe. Adenosine > verapalmil for
hypersensitivity. Glucocorticoids are the only drug treatment of SVT
effective in type II, III and IV reactions. • For treatment of eclampsia, Magsulph is the drug of choice
•
• Active components in grapefruit juice include • For treatment of Hypertension oral drugs of preference are
•
•
furanocoumarins capable of inhibiting the metabolism methyldopa > hydralazine > CCBs > atenolol > labetolol
of many drugs, including alprazolam, atorvastin, in that order
cisapride, cyclosporine and midazolam • For hypertensive crisis labetolol, hydralazine,
•
nitroglycerine can be used
• Cats are deficient in glucuronyl transferase and dogs
• Drug of choice for chlamydial infection in pregnancy ----
•
are deficient in acetyl transferase.
•
Azithromycin (erythromycin is alternative)
• Drug of choice for listerosis in pregnancy – Ampicillin
•
Drugs Safe In
Hepatic Disease Renal Disease Porphyria
• Digoxin • Doxycycline • Glucocorticoid
•
•
•
• Ethambutol • Polymyxin – B • Clonazepam
•
•
•
• Streptomycin • Penicillin • Streptomycin
•
•
•
• Chloroquine • Adriamycin • Pencillin
•
•
•
• ANTIBIOTICS – • Ceftriaxone • Aspirin, Acetaminophen
•
•
•
• Ampicillin • CPZ • Atropine
•
•
•
• Cloxacillin • Pefloxin • Insulin
•
•
•
• IIIrd generation cephalosporins • Chloramphenicol • Pefloxacin
•
•
•
• Aminoglycosides (CACA) • Erythromycyin • Opiates
•
•
•
• Omeraprazole • Narcotic analgesics
•
•
• Dicloxacillin
•
• Naficillin
•
• Clindamycin
•
• Metronidazole
•
288
Safe in Pregnancy (drugs which do not cross placental bar- Drugs contraindicated in Pregnancy (teratogenic)
rier)
• Heparin • LMW Heparin can cross placenta but safety ±
•
•
• Insulin • Iodine/Iodides
•
•
• TSH, ACTH • Lithium
•
•
• INH, Rmp, Ethambutol • ACE inhibitors, β Blockers
•
•
• Vasodilator: Methyldopa, Hydralazine • Atropine
•
•
• CCB (nifedipine) • Diazepam, chloral hydrate
•
•
• Anti Arrythmic: Quinidine, Dispyramide and Procainamide are • Corticosteroid
•
•
PHARMACOLOGY
relatively safe
• Lidocaine can be given • Phenytoin, valproate

•
•
• Antihelmenthic: Piperazine • Bisulfan
•
•
• Niclosamide • Cocaine, Heroine, Ethanol
•
•
• Desmopressin (For DI in pregnancy) • Progestrins
•
•
• Chloroquine (DOC for Rx of Malaria) • Retinoids
•
•
• Proguanil ( DOC for Px of malaria) • Tamoxifen
•
•
• Acyclovir • Ciprofloxacin
•
•
• Antibiotics: Pencillin, Macrolides, Most cephalosporins, • Chloramphenicol
•
•
Amoxicillin, ampicillin
• Among immunosuppressive drugs: Azathioprine, and • Tetracycline

•
•
Cyclosporin (Cat C) relatively safe
• Warfarin (can be given in 2nd trimester) • Aminoglycosides (eg. Streptomycin)

•
•
• Prophylthiouracil) • Allopurinol
•
•
• Live Vaccines
•
• Metronidazole (in 1st trimester)
•
• Theophylline
•
• Other Immunosuppresive drugs
•
• Warfarin ( Ist and IIIrd trimester)
•
Drugs Causing Important Syndromes
• Gray Baby Syndrome: Chloramphenicol (In preterm babies)
•
• Fanconi Syndrome: Tetracyclines (outdated tetracyclines can cause PCT damage)
•
• Reye’s Syndrome: Salicylates (Aspirin)
•
• Red Man Syndrome: Vancomycin (KCET 2012)
•

• Hemolytic Uremic Syndrome: Mistomycin–C (m/c Drug), Cisplatin, Bleomycin
•
• Tumor Lysis Syndrome: Fludarabine Rx in pt of CLL
•
• Hand Foot Syndrome: Capecitabine
•
• Mobius Syndrome: Misoprostol
•
Pharmacology 289

Drugs that Impair DNA Metabolism also Causes Megaloblastic Anemia
• Purine antagonist: 6MP, azathioprine
•
• Pyrimidine: 5 – FU, cytosine arbanoside
•
• Others: Procarbazine, Hydroxyurea, Zidovudine, Acyclovir and Primidone
•
Drugs Inhibiting Nucleic Acids Enzymes
Enzymes Inhibited by

DNA Polymerase ( DNA dependent DNA Polymerase) Cytarabine, Vidarabine, acyclovir

DNA dependent RNA Polymerase Rifampicin

Reverse Transcriptase (RNA dependent DNA Polymerase Zidovudine

Thymidylate synthetase 5 FU

DNA Gyrase Quniolones, novobiocin, nalidixic acid
PHARMACOLOGY

DNA Topoisomerase I Camptothecin, Irinothecan

DNA Topoisomerase II Anthracyclines (Daxorubicin, daunorubicin, epirubicin, idarubicin),

Epipodophyllotoxin (Etoposide, Teniposide)

Also Know
• Artificial RBCs/ Blood Substitutes–Perfluoro carbons (Fusol–DA)
•
• Artificial Tears-Methycellulose drops
•
• Artificial Cement Substance–Hydroxyapatite
•
• Cisapride should not be coadministered with enzyme inhibitors like ketoconazole and erythromycin. May precipitate
•
Torsades de Pointes
• Dipyramidole worsens angina and causes coronary steal phenomenon
•
Pseudomembranous Enterocolitis
• Clindamycin (COMEDK 2011)
•

• Tetracycline
•
• Ampicillin (MAN 1994, AIIMS 1993)
•

• Cephalosporin (AIIMS 1995, AP 2008)
•

• DOC – Metronidazole > Vancomycin (AIPG 1999)
•

Post Antibiotic Effect is seen with
• Flouroquinolones
•
• Aminoglycosides
•
• Betalactamase Inhibitor
•
Drugs Causing Disulfiram like Reaction/Alcohol Intolerance (Deterrents)
• Procarbazipine
•
• Metronidazole
•
• Sulfonamides
•
• Griesofulvin
•
• Furazolidone
•
• Cephalosporins (cefoperazone, Cefamandole, Cefotetan)
•
• Moxalactam
•
• Chlorpropamide
•
• Nitrafezole
•
290
Jerish – Herxheimer Reaction (MAN 2000, AP 2010)

• Occurs when penicillin is injected in syphilitic patients
•
• Occurs due to sudden release of spirochaetal lytic products
•
• Reaction lasts for 12–72 hours
•
• Symptoms
•
– Shivering
–
– Fever
–
– Myalgiaexacerbation of lesion
–
• This does not recur and does not need interruption of therapy.
•
PHARMACOLOGY
Chelating Agents
• BAL (British Antileusite): For heavy metal poisoning
•
• Dimercapto succinic acid (DMSA): For lead poisoning
•
• EDTA: For heavy metal poisoning
•
• Penicillamine: For copper poisoning
•
• Desferrioxamine: For acute iron poisoning and transfusion siderosis, which occurs in thalassemia patients receiving
•
repeated blood transfusion (AIPG 1995)

Oncotoxic Combinations • Pomp
•
• Mopp–used in Hodgkin’s disease (COMEDK 2005) – Prednisolone
–
– Oncovin
•

– Mechorethamine
–
– MTX
–
– Oncovin (Vincristine)
–
– Purinethol
–
– Procarbazine
–
• Cart
–
– Prednisolone
•
– Cytarabine
–
• Vamp
–
•
– Vincristine – Asparaginase
–
– Rubdomycin
–
– Amethopterine
–
– 6-TG
–
– 6-MP
–
• Bacop
–
– prednisolone
•
–
• Coap – Bleomycin
•
–
– Cyclophosphamide – Adriamycin
–
–
– Oncovin – Cyclophosphamide
–
– Oncovin
–
– Ara-C
–
– Prednisolone
–
– Prednisolone
–
–
CHAPTER 7
General Medicine and Surgery
Objectives
• Cardiovascular system • Electrolyte and Fluid Balance

• Respiratory system • Wound Tissue and Repair

• GIT and Liver • Burns

• Excretory System • Trauma

• Endocrine System • Cysts, Ulcers and Swellings

• Neuromuscular System • Arteriovenous Disease

• Central Nervous System • Lymphatic System

• Infections • Miscellaneous

CARDIOVASCULAR SYSTEM – SV = End diastolic volume – End systolic volume
–
(EDV – ESV).
• Heart-Valves – SV affected by contractility, afterload and preload.
•
–
– Tricuspid valve has 3 leaflets: anterior (largest), septal
–
(smallest) and posterior. • Contractility (and SV) ↑ with
•
– Mitral valve has 2 leaflets: anterior (larger), posterior – Catecholamine release (↑ activity of Ca2+ pump in
–
–
(smaller) sarcoplasmic reticulum)
– Pulmonary valve has 3cusps: 1 posterior and 2 –– ↑ intracellular calcium
–
anterior –– ↓ intravascular sodium
– Aortic valve has 3 cusps: 1 anterior and 2 posterior. – Digitalis (↑ intracellular Na+ resulting in ↑ Ca2+)
–
–
 
• Heart borders on Chest X ray – Stressful events (anxiety, exercise)
•
–
Right border • Superior vena cava, right atrium and inferior
•
vena cava. • Contractility (and SV) ↓ with
•
Left border • Aortic arch, left pulmonary artery, aortic – β-blocker usage
•
–
knuckle, left atrial appendage, left ventricle. – Heart failure
–
 
• Stroke volume and cardiac output – Acidosis
–
•
– Cardiac output (CO) = stroke volume (SV) X heart – Hypoxia/hypercapnea
–
– Non-dihydropyridine Ca2+ channel blockers
–
rate (HR); CO = SV x HR
–
292
• Afterload: The vascular resistance that ventricles must overcome to produce outflow. Vasodilators (eg, hydralazine) ↓
•
afterload.
• Preload = ventricular end diastolic volume (the amount of stretching force on cardiac muscle fibres at the end of diastole).
•
• Preload increases with
•
– Exercise (slightly)
–
–– ↑ Blood volume (overtransfusion)
GENERAL MEDICINE AND SURGERY
– Excitement (sympathetics).
–
• Preload pumps up the heart.
•
• Venodilators (eg, nitroglycerine) decreases preload.
•
Good to Know
• Torus aorticus
•
– Prominent region of the right atrial septum sited superiorly and anteriorly.
–
– Superior to the coronary sinus and anterior to the fossa ovalis.
–
– Represents the deeper and anterior surface of the posterior sinus and cusp of the aortic valve.
–
• Valve of Vieussens: Venous valve dividing the great cardiac vein and coronary sinus.
•
• Leiden convention: Is used in imaging of heart; the artery that arises from the observer’s left hand side is the left coronary
•
artery and the other is the right.
• Pacemaker Action Potential Occurs in the SA node and AV node.
•
 
 
Myocardial Action Potential
Occurs in atrial and ventricular fibres and Purkinje fibres.
Phase 0 • Rapid upstroke: Voltage gated Na+ channels open, this depolarizes the cell (makes inside more positive)
•
Phase 1 • Initial repolarisation: Inactivation of voltage gated Na+ channels (↓ Na+ conductance inward) and voltage gated K+
•
 
channels begin to open (K+ conductance outward)
Phase 2 • Plateau: Ca2+ influx through voltage gated Ca2+ channels balances K+ efflux; inward and outward currents are
•
 
approx. equal. Ca2+ influx triggers Ca2+ release from the sarcoplasmic reticulum and myocyte contraction
 
Phase 3 • Rapid repolarisation: Ca2+ conductance ↓, K+ efflux predominates; this hyperpolarizes the cell.
•
Phase 4 • Resting potential: High K+ permeability through K+ channels
•
Cardiac Cycle – Phases
Isovolumetric contraction • Period between mitral valve closing and aortic valve opening; period of highest oxygen consumption
•
Systolic ejection • Period between aortic valve opening and closing
•
Isovolumetric relaxation • Period between aortic valve closing and mitral valve opening
•
Rapid ventricular filling • Period just after mitral valve opening
•
Reduced ventricular filling • Period just before mitral valve closure
•
Conduction speeds
Tissue Conduction rate

SA node, Av node 0.05 m/s

Atrial pathways, bundle 1m/s

of His, Ventricular muscle

Purkinje system 4m/s

General Medicine and Surgery 293

Heart Sounds
Sound Mechanism Other features
S1 Due to mitral and tricuspid valve closure Load S1 in hyperdynamic circulation (anemia, pregnancy, thyrotoxicosis),
Occurs at onset of systole Mitral stenosis
Loudest at mitral area Soft S1 in heart failure, mitral regurgitation
S2 Due to aortic and pulmonary valve closure

Occurs at end of systole
Loudest at left sterna border
S3 From ventricular wall due to abrupt cessation Maybe physiological in young people pregnancy
of rapid filling Pathological in heart failure, mitral regurgitation
Occurs early in diastole
Low pitched, often heard as gallop
S4 Due to high atrial pressure S4 = ‘atrial kick’

Occurs at end of diastole Always pathological – a/w severe LV hypertrophy (eg: HOCM)
Absent in atrial fibrillation
Pulse
• Normal pulse: has a small anarcrotic wave on the upstroke which is not felt. This is followed by a big tidal or percussion
•
wave which is felt by the palpating finger. On the following downstroke there is a notch (dicrotic notches) followed by
wave (diacritic wave) both of which are not normally palpable.
• Anacrotic pulse: Slow rising twice beating both waves felt during systole. Felt in carotids in aortic stenosis
•
• Pulsus Biferiens: Rapid rising, twice beating. Felt during systole. Here the percussion wave is felt first followed by small
•
wave. This is seen in:
– Idiopathic hypertrophic subaortic stenosis
–
– Severe AI with mild AS
–
• Dicrotic pulse: Twice beating pulse where the first percussion wave is felt during systole and second dicrotic wave is felt
•
during diastole. It is seen when the peripheral resistance and diastolic pressures are low as in:
– Fevers like typhoid fever
–
– Congestive cardiac failure
–
– Cardiac tamponade
–
– Following open heart surgery
–
• Pulsus parvus et tardus: Is a slow rising pulse like the anacrotic pulse but the anacrotic wave is not felt. Seen in aortic
•
stenosis.
• Pulsus alternans: Is characterized by a strong and weak beat occurring alternately, probably due to alternate rather than
•
the regular contraction of the muscle fibres of the left ventricle. Seen in:
– Left ventricular failure
–
– Toxic myocarditis
–
– Paroxysmal tachycardias
–
– For severe beats following a premature beat (KAR 2000)
–

• Pulsus paradoxus: In some cases the peripheral pulse can disappear on inspiration while, paradoxically, heart sounds
•
remain audible during the ‘missed beats’.
– A reverse pulsus paradoxus may occur in patients receiving continuous airway pressure on a mechanical ventilator.
–
– Causes include:
–
Superior vena cava obstruction

Lung conditions like asthma, emphysema, airway obstruction

Cardiac conditions like pericardial effusion, constrictive pericarditis and severe congestive cardiac failure.

(COMEDK 2011)

294
If the thoracic cage is immobile as in ankylosing spondylitis, pulsus paradoxus does not occur.

Alternate premature beats

AV block every third sinus impulse being blocked.

Sinoartrial block with ventricular escape

• Thready pulse: the pulse rate is rapid and the pulse wave is small and disaapears quickly. This is seen in shock especially
•
cardiogenic.
• Waterhammer pulse: is alarge bounding pulse associated with increased stroke volume of the left ventricle and decrease
•
in the peripheral resistance, leading to a wide pulse pressure. The forceful jerk and quickly disappear. Causes are:
– Physiological
–
Fever

Chronic alcoholism

Pregnancy

– High output states or syndromes
–
Anemia
�

Beriberi

Cor pulmonale

Cirrhosis of liver

Paget’s disease

Arteriovenous fistula

Thyrotoxicosis (MAN 1998)

– Cardiac lesions
–
Aortic regurgitation

Rupture of sinus of Valsalva into the heart chambers

Patent ductus arteriosus

Aortopulmonary window

Bradycardia (MAHE 2007)

Systolic hypertension

Jugular Venous Pressure
• Normal consists of three positive waves (a, c and v) and two negative waves (x and y)
•
Element Event
Positive waves
‘a’ wave • Due to right atrial contraction. Its height reflects the rate of filling and elasticity of the right atrium
•
‘c’ wave • Transmitted carotid impulse at onset of systole i.e. onset of ventricular contraction
•
‘v’ wave • Seen immediately after ‘x’ descent. Passive atrial filling against closed tricuspid valve in systole. It reflects the
•
volume of blood entering. Pressure peak immediately to opening of tricuspid valve. (COMEDK 2010)

Negative waves
‘x’ descent • Seen during right atrial relaxation. The ‘x’ descent results from right atrial filling and descent of tricuspid valve in
•
systole. Pulling of the base of the atrium caused by ventricular contraction.
‘y’ descent • Reflects passive filling of the right ventricle at start of diastole. Fall in right ventricular pressure as tricuspid valve
•
opens.
• Abnormalities of ‘a’ waves

•
– ‘a’ wave is absent in atrial fibrillation
–
– ‘a’ wave is diminished in
–
Tachycardia

Prolonged PR interval


– Large or giant ‘a’ waves are present in
–
Tricuspid stenosis

Tricuspid atresia

Right atrial myxoma

Pulmonary stenosis

Pulmonary hypertension

– Cannon ‘a’ waves occurs in:
–
Complete heart block

Ventricular tachycardia

Ectopic beats

– Raised JVP with normal waveform
–
Fluid overload

Right heart failure

– Raised JVP with absent pulsation
–
SVC obstruction

– Deep x and y descents
–
Constrictive pericarditis

Pericardial tamponade

Murmurs
• Abnormal heart sounds caused by vibration of the valves or the wall of the heart or great vessels.
•
• Murmurs may be systolic (if it is between first and second heart sound) or diastolic (if between the second and first heart
•
sound) or continuous (present throughout systole and diastole)
• Systolic murmurs are graded by Levine as:

•
– Grade I: Very faint murmur only audible with effort
–
– Grade II: Faint murmur but clearly and definitely audible
–
– Grade III: Moderately loud murmur but no thrill
–
– Grade IV: Loud murmur with thrill
–
– Grade V: Louder with thrill and can be heard away from the involved site
–
– Grade VI: Murmur with thrill heard even if the stethoscope is lifted up from the chest wall
–
• Innocent murmurs:
•
– Characteristics:
–
More commonly heard in children

Usually heard in pulmonary area

Usually not a loud murmur

No thrill

Variation of murmur on posture or respiration

Usually systolic, but may be continuous

Soft, short and blowing in nature

Usually localized

– Differential Diagnosis
–
Pulmonary ejection murmur

Vibratory murmur

Supraclavicular arterial bruit

Venous hum

Mammary soufflé

296
Organic Murmur
Systolic murmur
• Midsystolic ejection murmurs • Aortic:
•
•
– Aortic stenosis
–
– Coarctation
–
– Aneurysm
–
– Patent ductus arteriosus
–
– Aortic insufficiency
–
– High output states
–
• Pulmonary:
•
– Pulmonary stenosis
–
– Fallot’s tetrad
–
– Pulmonary artery dilatation
–
– Pulmonary hypertension
–
– Atrial septal defect
–
– High output state
–
– Innocent
–
• Pansystolic Murmur • Myocardial infarction
•
•
• Tricuspid insufficiency
•
• Ventricular septal defect
•
• Late systolic murmur • Mitral valve prolapsed
•
•
• Coarctation of aorta
•
• Pulmonary stenosis
•
• Hypertrophic cardiomyopathy (HOCM)
•
• Papillary muscle dysfunction (PMD)
•
Diastolic murmurs: (Man 2001)
• Early diatolic murmurs: • Atrial regurgitation

•
•
• PI
•
• Graham Steell’s murmur: this is functional, diastolic murmur best heard in the
•
pulmonary area due to pulmonary hypertension.
• Mid diastolic murmurs • MS
•
•
• TS
•
• Carey Coomb’s murmur: This is the functional, apical, mid diastolic murmur
•
of mitral valvulitis.
• Austin Flint murmur: This is the functional, apical, diastolic murmur of free
•
AI, without any lesion of the mitral valve.
• Flow murmurs: Occur because of increased blood flow, in diastole, across
•
the mitral or tricuspid valves as in:
– Atrial septal defect
–
– Ventricular septal defect
–
– Patent ductus arteriosus
–
– Myocardial infarction
–
– Tricuspid insufficiency
–
– Aortopulmonary septal defect
–
– Complete heart block
–
• Late diastolic or presystolic murmurs • MS
•
•
• TS
•
• Left atrial myxoma
•
• Right atrial myxoma
•
Types of murmurs
• Austin Flint Murmur • Mid diastolic murmur in AR
•
•
• Carry’s Coomb’s Murmur • Mid diastolic murmur in acute rheumatic fever
•
•

• Gibson’s Murmur • ‘Train in Tunnel’ murmur in PDA
•
•
• Graham Steel Murmur • Early diastolic murmur of pulmonary regurgitation
•
•
• Still’s Murmur • Vibratory systolic innocent MI
•
•
• Musical or seagull Murmur • Aortic Regurgitation
•
•
• Mean’s murmur • Harsh pulmonary systolic murmur in thyrotoxicosis
•
•
Waves of Normal ECG
Wave/segment From – To Cause Duration
P wave Atrial depolarization 0.1
QRS complex Ventricular Depolarization 0.08-0.10

(UP 2007, AlPG 1998)
T Wave Ventricular Repolarisation 0.2
P-R interval Onset of P wave to onset of (0.12-0.2)

Q wave
Q – T Interval Onset of Q wave and end of 0.4 – 0.42

T wave
PR interval
• This is measured from the beginning of the P wave to the beginning of the QRS complex, i.e. it includes the P wave plus
•
the PR segment
• It is usually 120 to 200ms long
•
• A long PR interval (of over 200 ms) may indicate a first-degree heart block. (KAR 2010)
•

• Prolongation can be associated with hyperkalemia or acute rheumatic fever. A variable PR interval may indicate other
•
types of heart block.
• A short PR interval may indicate a pre-excitation syndrome via an accessory pathway that leads to early activation of the
•
ventricles, such as seen in Wolff-Parkinson White Syndrome.
ECG Changes seen in Acute Myocardial Infarction (AIIMS 1995)

• Hyperacute phase:
•
• ST Elevation
•
• Tall T wave
•
• Increased ventricular activation time
•
Fully Evolved Phase
• Pathological Q wave
•
• Elevated ST segment
•
• Inverted T waves
•
Old Infarct
• Pathological Q waves
•
Osborn Waves
• Also known as camel-hump sign, late delta wave or current of injury
•
• Osborn waves are positive deflections occurring at the junction between the QRS complex and the ST segment, where the
•
S point, also known as the J joint, has a myocardial infarction like elevation
298
• QT INTERVAL PROLONGED. AIPG 2007

•

• Observed in
•
– Hypothermia
–
– Hypercalcemia
–
– Brain injury
–
– Vasospastic angina
–
– Ventricular fibrillation.
–
Hypokalemia Hyperkalemia
 
• Severe hypokalemia (serum K <3 mEq/L) may produce • The ECG Changes are:
•
•
Muscular weakness and lead to paralysis and respiratory – Shortening of the QT interval (AIIMS 2004, 2006)
failure. Muscular malfunction may result in respiratory
–

– Tall, peaked T waves (serum K >5.5 mEq/L).
hypoventilation, paralytic ileus
–
• Progressive hyperkalemia produces nodal and ventricular
•
• The characteristic ECG changes: (AIIMS 97) arrhythmias, widening of the QRS complex (serum K >6.5
•

– ST segment depression (AIIMS 2007) mEq/L),
–

– Increased U wave amplitude, and – PR interval prolongation and disappearance of the P wave,
–
–
– T wave amplitude <U wave amplitude. and, finally, (AIIMS 2004, 2006)
–

• Severe hypokalemia may produce premature ventricular and – Degeneration of the QRS complex to a sine wave pattern
•
–
atrial contractions and ventricular and atrial tachyarrhythmias and ventricular asystole or fibrillation. (AIIMS 2004)
 
Valvular Disease
Valvular disease Symptoms Signs Pathophysiology/important features
Mitral stenosis • Dyspnoea • Atrial fibrillation • It is mostly of rheumatic origin.
•
•
•
(MS) • Oedema, ascites • Mitral fascies (Man 1996, 1997) • Due to mitral valve stenosis blood from the
•
•
•
(Right heart failure) – Auscultation left atrium to left ventricle is restricted, left
atrial pressure rises (atrial fibrillation) leading
–
• Palpitation (Atrial – Loud first heart sound
to elevated pulmonary venous and capillary
•
–

fibrillation) (Man 1998) (KAR 2009)
pressure, with resultant increase in right

• Haemoptysis – Opening snap
ventricular after load and RV hypertrophy and
–
– Mid diastolic murmur
•
(pulmonary
failure.
–
congestion) • Signs of pulmonary congestion –
•
crepitations, pulmonary oedema • The left ventricular diastolic pressure is normal
• Chest pain (pulmonary
•
• Pulmonary hypertension in isolated MS
•
hypertension)
•
• Stroke • Right heart failure
•
•
• Kerley B lines in chest
•
MR or mitral • Dyspnoea (pulmonary • Atrial fibrillation • Rheumatic heart disease, endocarditis and
•
•
•
incompetence venous congestion) • Displaced hyperdynamic apex myocardial infarction are the most common
causes of MR. MR is a common feature of
•
• Fatigue (low cardiac beat
Marfan’s syndrome
•
output) • Apical pansystolic murmur
• MR produces symptom complex that is similar
•
• Oedema, ascites (right radiating to axilla
•
to that of MS
•
heart failure) • Signs of pulmonary venous
• There is dilation of left atrium and ventricle
•
congestion–crepitations,
•
pulmonary edema • MR causes dilatation of left atrium, pulmonary
•
• Pulmonary hypertension venous and capillary congestion with resultant
increase in right ventricular after load and right
•
• Right heart failure
heart failure.
•
• There is also left ventricular dilatation and the
•
apex beat is displaced to the left as a result of it.
Aortic stenosis • Dyspnoea • Ejection cystolic murmur • Sudden death is seen in AS
•
•
•
(AS) • Angina • Slow rising carotid pulse • Blood does not enter the aorta due to AS and
•
•
•
• Syncope death • Thrusting apex beat (LV pressure the left ventricle becomes hypertrophied
•
•
overload) • Coronary blood flow is inadequate and the
•
patients may develop angina, syncope.
• Eventually LV can no longer overcome the
•
outflow obstruction and pulmonary edema
ensues.

Valvular disease Symptoms Signs Pathophysiology/important features
Aortic • Awareness of heart • Murmurs • The aorta dilates
•
•
•
regurgitation beat – Early diastolic murmur • The left ventricle also dilates and hypertrophies
(AR)
–
•
• Palpitations – Austin flint murmur to compensate for the regurgitation
•
–

• Angina (AIPG 2001) • The stroke output of the left ventricle is

– Systolic murmur
•
•
• Breathlessness doubled or tripled. This leads to awareness of
–
• Pulses heart beat and pulsatile major arteries.
•
•
– Collapsing pulse
–
– Bounding peripheral pulses
–
• Femoral bruit (Piston shot) –
•
Duroziez’s sign
• Head nodding with pulse
•
(demusset’s sign)
• Displaced apex beat
•
• Fourth heart sound
•
• Pulmonary venous congestion
•
• Protruded forehead – light house
•
sign
• Pultrations of ovule – Muller’s
•
sign
• Dancing carotids
•
• Lower limb systole >20 Hill’s
•
sign
Rheumatic Fever
Jones criteria for the rheumatic fever
Major manifestations Minor manifestations
• Carditis • Fever
•
•
• Polyarteritis (Migratory and painful) • Arthralgia
•
•
• Chorea (Sydenham’s chorea) • Previous h/o rheumatic fever
•
•
• Erythema marginatum • Raised ESR or C reactive protein
•
•
• Subcutaneous nodules over bones or tendons • Leukocytosis
•
•
• First or second degree AV block PLUS
•
• Supporting evidence of preceding streptococcal infection like recent
•
scarlet fever, raised anti streptolysin O (ASO) positive throat culture.
Subcutaneous Nodules – Subendocardial McCallums patches are present

–

(AIPG 1995)
• Painless

– MC cause of mitral stenosis
•
• Firm collections of collagen fibers over bones or
–
•
tendons. Infective Endocarditis
• They commonly appear on the back of the wrist, the
• Infective endocarditis is due to microbial infection of
•
outside elbow, and the front of the knees (AIPG 2007)
•
a heart valve, chamber or blood vessel or a congenital
anomaly (e.g. septal defect)
Rheumatic Heart Disease
• It mostly affects jet lesions i.e. areas of endocardial damage
•
• Preceded by Streptococcal pharyngitis caused by high pressure jet of blood such as VSD, MR and
•
• Characteristic Features AR. Risk of endocarditis is less in low pressure like atrial
•
– Aschoff bodies (PGI 2007) septal defect.
–

– Antischowk cells/caterpillar cells • When the infection is established, vegetations composed
•
–
– Pancarditis (AIPG 1999) of organisms, fibrin and platelets grow to become large
–

– Bread and butter pericarditis enough to cause obstruction and also break away as
–
– Vegetation along closure of valves emboli.
–
300
• Clinical features of infective endocarditis

•
– Roth spots in fundi
–
– Cerebral emboli
–
– Petechial hemorrhages of skin and mucous membranes
–
– Splinter hemorrhage of skin and mucous membranes
–
– Osler’s nodes which are painful tender swellings
–
– Splenomegaly
–
– Haematuria
–
– Murmurs, arrhythmias and cardiac failure
–
• Risk of I.E. in various lesions (MAN 1998)
•
High risk Moderate risk Low risk
• MR • Mitral valve prolapse + MR • ASD
•
•
•
• Prosthetic heart valve • Mitral stenosis
•
•
• Tetralogy of fallot
•
• VSD
•
• Coarctation of aorta
•
• Patent ductus arteriosus
•
Prior native valve endocarditis poses a significant risk factor for subsequent episodes as a consequence of both the continued
presence of the risk factors that contributed to the initial episode (e.g., intravenous drug use or periodontitis) and the additional
risk posed by the damage to the valve sustained in the initial episode. (PGI 2008, AIPG 2010)

Endocarditis Organism
• Subacute endocarditis • Strept viridans group (Strep sanguis, Strep. Mitis, Hemolytic Streptococci)
•
•

(PGI 1998, AIPG 2003, AIIMS 2004)

• Acute endocarditis • Staph. Aureus, Strep pneumoniae
•
•
• Post operative endocarditis • Staph epidermis
•
•
Atherosclerosis • Diabetes mellitus
•
• Family history
Risk Factor for atherosclerosis
•
• Obesity
• Smoking
•
• Physical Inactivity
•
• Hypertension
•
•
• Low HDL, Raised Apolipoprotein (AIPG 2006) Micro-organisms associated with Artherosclerosis
•
• Familial hypercholestolemia • CMV
•
•
• Familial hypertryglyceredemia • Chlamydiae
•
•
• Familial dysbetalipoproteinemia • H. Pylori
•
•
Amino Acid Associated with Atherosclerosis: Homocysteine (AIIMS 2006)

Management
• Antiplatelet therapy is indicated in all patients with coronary artery disease. Aspirin is the most common first choice, but
•
clopidogrel, a thienopyridine derivative closely related to ticlopidine, is an alternative. (KAR 2009)

• Streptokinase is a generation I plasminogen activator for lysis of clots during management of attacks of myocardial
•
infarction.
• Nifedipine is used for cardiac arrhythmias and hypertension
•
• Calcium channel blockers are potent vasodilators to relieve coronary artery spasm.
•

• Digoxin is used in cardiac failures
•
• Nitrates
•
– Are not commonly used in the management of renal colic though they are capable of relieving spasm
–
– Nitrates relax all types of smooth muscle irrespective of the state of pre existing muscle tone.
–
– Commonly used in the therapy of congestive heart failure (CHF) (AIPG 2011)
–

– Amyl nitrite is an antidote used to treat cyanide poisoning. Amyl nitrate oxidizes hemoglobin to methhemoglobin.

–
This is normally undesirable because this form of hemoglobin binds oxygen less avidly. However, methemoglobin
strongly binds cyanide and prevents further degradation of electron transport system.
– Nitrates also have been used with some success in oesophageal spasm. It decreases the vasospam in the brainstem,
–
similar to calcium channel blockers.
– The nitrates are occasionally used to relax the ureter in renal colic and the common duct in biliary colic, efficacy is
–
very low.
Good to know
• In stable angina enzyme levels are normal. (AIIMS 2003)
•

• Myoglobin is the first to rise
•
• CK-MB is useful to look for reinfarction as it returns to normal after 2-3 days (troponin T remains elevated for up to 10
•
days)
• CK-MB is raised earlier than other enzymes.
•
• Troponin is a marker of cardiac infarction. (AIIMS 2004)
•

• Troponin is also a better marker of cardiac infarction in athletes. (AIIMS 2011)
•

• Sensitive marker for myocardial infarction is Troponin T (TN 2008)
•

Biochemical Markers (AIPG 1995)
Enzymes that are • CPK-MB

•
elevated in the • SGOT (AST) (AIIMS 1992)
•

plasma in myocar- • LDH
dial infarction
•
Proteins elevated • Troponin T and I
•
in the plasma in
myocardial infarc-
tion
The best preferred • Troponins

•
bio chemical mark- • CPK-MB
•
ers for MI
Marker appearing • LDH

•
last in MI
Begins to rise Peak value Returns to Normal

Myoglobin 1-2 Hours 6-8 hours 1-2 days
CK-MB 2-6 hours 16-20 hours 1-2 days
CK 4-8 hours 16-24 hours 3-4 days (AIIMS 2006)

Trop T 4-6 hours 12-24 hours 7-10 days (AIIMS 1998)

AST 12-24 hours 36-48 hours 3-4 days
LDH 24-48 hours 72 hours 8-10 days
302
Eisenmenger’s Syndrome
• Describes the reversal of a left to right shunt in a congenital heart defect due to pulmonary hypertension
•
• Associated with
•
– VSD
–
– ASD
–
– PDA
–
• Features
•
– Original murmur may disappear
–
– Cyanosis
–
– Clubbing
–
– Right ventricular failure
–
– Haemoptysis, Embolism
–
Cardiac Tamponade
• The accumulation of fluid in the pericardium in an amount sufficient to cause serious obstruction to the inflow of blood
•
to the ventricles results in cardiac tamponade
• Common causes
•
– Neoplastic disease
–
– idiopathic pericarditis
–
– uremia.
–
• Tamponade may also result from bleeding into the pericardial space either following cardiac operations and trauma
•
(including cardiac perforation during diagnostic procedures) or from tuberculosis and hemopericardium.
• Features
•
– Elevation of intracardiac pressures
–
– Limitations of ventricular filling, and
–
– Reduction of cardiac output
–
– Electrical alternans (AIPG 2004)
–

– Pulsus paradoxus (AIPG 2006)
–

– JVP (AIIMS 1995)
–

– Prominent X descent
–
– Absent Y descent
–
– Becks triad: Hypotension, Silent heart, Inc JVP (PGI 2003)
–

– Absent kussumals sign
–
Constrictive Pericarditis
• Right heart failure occurs
•
• Raised JVP seen
•
• Ascites precox seen
•
• Prominent X descent
•
• Prominent Y descent
•
• Thickened Pericardium
•
• Kussumals sign
•
• Square root sign +ve
•

Key Points • Cor pulmonale or pulmonary heart disease is enlargement
•
of the right ventricle of the heart as a response to increased
• Risk of endocarditis is less in low pressure lesions like
resistance or high blood pressure in the lungs. It is a
•
atrial septal defect (ASD) while it is more in high pressure
condition where there is right ventricular hypertrophy
lesions like ventricular septal defect (VSD), mitral
with or without failure resulting from diseases affecting
regurgitation and aortic regurgitation.
structure or function of the lung.
• Markers that arise first in MI–tropinins T and I, CPK-

(MAHE 2010,APPSC 1999)

•
MB

• Splinter hemorrhages:
• Commonest congenital heart disease: VSD
•
– Flame shaped or linear hemorrhages under the nail
•

(KAR 1997)
–
bed,

• Commonest cyanotic heart disease: Tetralogy of
– seen in infective endocarditis
•
Fallot (COMEDK 2008)
–
• Corrigan’s Sign or dancing carotids:

• Commonest cause of MS, MR, AR, TR: Rheumatic
•
– Increased pulsation of neck vessels occurs with
•
valvulitis
–
collapsing radial pulse.
• Commonest cause complicated by SABE: Rheumatic – Due to wide pulse pressure
•
MR
–
– Seen in aortic regurgitation
–
• Rheumatic activity mostly involves mitral and aortic
•
valves • Kussumaul’s sign:
• Rheumatic fever mostly results in MR
•
– Is an increase rather than the normal decrease of the
•
–
• Commonest valvular lesion following MI–MR jugular venous pressure during inspiration
– Frequently seen in constrictive pericarditis
•
• Commonest cause of high output failure–chronic severe
–
• Atrial flutter: P waves assume saw toothed appearance
•
anemia
•
seen in ECG
• Valve affected in infective endocarditis due to IV drug
• Normal cardiac output varies from 2.5–3.8 L/min/m2
•
abuse–tricuspid
•
• Commonest valve involved in Ebstein anomaly–tricuspid • Site of lesion in Bell’s palsy is labyrinthine portion of
•
facial nerve within the facial canal or the stylomastoid
•
• Ventricular asystole may complicate complete heart block
foramen
•
or Mobitz type II second degree AV block and may cause
recurrent syncope or Strokes Adams attack. • Cardiopulmonary resuscitation: (TNPSC 1999)
Myocardial infarcts–
•
• – Rescue breathing in adult is 12 times/min
•
– Transmural (full thickness)
–
– Compression to ventilation ratio in two person
–
– Subendocardial (partial thickness)
–
CPR is 5:1
–
• Pacemaker of the heart is SA node (AIPG 1996) – Compression to ventilation ratio in one person
•

• The most common cause of mitral regurgitation in a
–
CPR is 15:2
•
patient who has no evidence of mitral stenosis is mitral – Compression should be 60-80/minute in adults.
valve prolapse. (KAR 2006)
–
Compressions should be 100/minute in children

• The most common cause of death in the sophisticated – Depth of compression should be 1-½ -2 inches
•
world is ischemic heart disease.
–
at the lower half of sternum at an average of each
• Torsade de pointes (TDP) also called as torsade, second.
•
variant of ventricular tachycardia.
• Starling’s law (MAHE 2007)
– It’s a complication of prolonged ventricular
•
– Starling’s law of heart states that increase in force of
–
repolarization (long QT interval).
–
– Also known as twisting points. contraction is directly related to cardiac output.
– Starling’s law of heart states that the force of
–
– More common in women.
–
ventricular contraction is directly related to the end
–
– Treatment:
diastolic volume.
–
Identification of cause.
– Preload is the end diastolic filling pressure of the

Intravenous magnesium in all cases–8mmol
–
ventricle just before contraction.

over 15min then 72 mmol over 24 hours.
– The force against which the ventricular contracts is

(COMEDK 2011)
–
termed the afterload.

304
• Orthostatic hypotension (MAHE 2007)

•
– A drop in systolic blood pressure of 20 mm Hg or more on standing from a sitting or lying position
–
– This occurs as blood pools in the legs because of gravity. Usually, reflex vasoconstriction prevents a drop in pressure
–
but if this is absent or the patient is fluid depleted, postural hypotension can occur.
– This condition is more prevalent in the elderly because of age related autonomic dysfunction.
–
• SIRS (Systemic Inflammatory Response Syndrome)

•
– Denotes a generalized inflammatory response to a medley of severe clinical insults usually resulting from infection and
–
necessarily not so in all cases.
– Clinical features: (PGI 2009)
–

Temperature > 370C or <360C

Respiration rate greater than 20/min and carbon dioxide pressure in arterial blood is greater than 36mm of Hg

Heart rate is greater than 90 beats per minute

WBC count less than 4000/cc or greater than 12000/cc or greater than 10% bands (Immature WBCs).

General Features of Shock Common to Most Types of Shock
• Hypotension (systolic BP < 100 mm Hg)
•
• Tachycardia with low volume pulse (pulse > 100/min)
•
• Sweating
•
• Cold, Clammy skin (cyanoses peripheries)
•
• Rapid shallow respiration
•
• Drowsiness, confusion, irritability
•
• Oligouria (urine output < 30ml/hr)
•
• Elevated or reduced CVP
•
• Multi organ failure
•
Abnormal Shapes of Chest
Pigeon chest/ heeled chest/ • Rickets

•
pectus carinatum • Severe asthma during childhood
•
Funnel chest/pectus exca- • Lobbler’s chest
•
vatum
Barrel shaped chest • Emphysema

•
• COPD
•
• In this the A-P diameter is increased relative to the lateral diameter.
•
Bulging • Pleural effusion
•
• Pneumothorax
•
• Aneurysms
•
Depression/flattening • Fibrosis
•
• Pleural adhesions
•
• Unilateral muscle wasting
•
Flale chest/phthinoid chest/ • Tuberculosis
•
alar chest

Clubbing
Definition: bulbous enlargement of soft parts of terminal phalanges with both transverse and longitudinal curving of the nails.
Causes (AIPG 1995, AIIMS 1993)

• Pulmonary
•
– Bronchogenic carcinoma

–
– Lung abscess
–
– Bronchiectasis
–
• Cardiac
•
– Infective endocarditis
–
– Cyanotic congenital heart disease
–
• Alimentary
•
– Ulcerative colitis
–
– Crohn’s disease
–
– Biliary cirrhosis
–
• Endocrine
•
– Myxedema
–
– Grave’s disease
–
– Acromegaly
–
• Miscellaneous
•
– Hereditary
–
– Heroine addicts – only in upper limbs due to chronic obstructive phlebitis
–
Grades Of Clubbing
I Softening of the nail bed
II Obliteration of angle of the nail bed
III Swelling of the base of the nail causing overlying skin to become tense, shiny and wet and increasing the curvature of the nail.
IV Swelling of the fingers in all dimensions with hypertrophic pulmonary osteoarthropathy.
Pseudoclubbing
In hyperparathyroidism, excessive bone resorption may result in disappearance of the terminal phalanges with telescoping of
soft tissues and a ‘drumstick’ appearance f the fingers resembling clubbing. However the curvature of the nail is not present.
Schamroth’s Sign
• Normally when two fingers are held together with nails facing each other, a space is seen at the level of proximal nail fold.
•
This is lost in case of clubbing.
Sputum Pathology
• Purulent sputum • Bronchiectasis
•
•
• Lung abscess
•
• Mucopurulent • Active bronchopulmonary infections
•
•
• Pink frothy • Pulmonary oedema
•
•
• Black sputum • Pneumonia
•
•
• Rusty sputum • Pneumonia
•
•
• Red • Bronchial carcinoma
•
•
• Foul smell of sputum • Lung abscess
•
•
• Bronchiectasis
•
306
Kussmaul breathing • Increase in rate and depth of respiration seen in diabetic ketoacidosis
•
Cheyne- Stokes breathing • Most common type of periodic breathing characterized by initial rapid and deep respiration
•
followed by complete cessation of respiration.
E.g.:
– Physiological conditions:
–
– During sleep
–
– High altitude
–
– New born babies
–
– After severe muscular exercise
–
– Pathological conditions:
–
– Narcotic poisoning
–
– Uremic conditions
–
– Cardiac failure
–
Biots breathing • Another form of periodic breathing characterized by period of apnea and hyperapnea
•
• Rhythm and depth of respiration are irregular with occasional signs and irregular pauses
•
• E.g. lesion of brain, injuries to brain
•
Breathing Sounds collapse, or intraluminal obstruction by the neoplasm or
secretions
• The primary adventitious (abnormal) sounds that can be
• Rhonchi is the term applied to the sounds created when
•
heard include crackles (rales), wheezes, and rhonchi.
•
there is free liquid in the airway lumen, the viscous
• Crackles represent the typically inspiratory sound created interaction between the free liquid and the moving air
•
when alveoli and small airways open and close with creates a low-pitched vibratory sound.

respiration and they are often associated with interstitial (MAN 1994, AIPG 1993)

lung disease, micro-atelectasis, or filling of alveoli by • Other adventitious sounds include pleural friction rubs
•
liquid. and stridor. The gritty sound of a pleural friction rub
• Wheezes, which are generally more prominent during indicates inflamed pleural surfaces rubbing against each
other, often during inspiratory and expiratory phases
•
expiration than inspiration, reflect the oscillation of the
of the respiratory cycle. Stridor, which occurs primarily
airway walls that occurs when there is airflow limitation,
during inspiration, represents flow through a narrowed
as may be produced by bronchospasm, airway edema or
upper airway, as occurs in an infant with croup.
Cyanosis
• This is a dusky blue discoloration of the skin (particularly at the extremities) or of the mucous membranes when the
•
capillary oxygen saturation is less than 85%.
• Types of cyanosis:
•
– Central
–
– Peripheral
–
– Cyanosis due to abnormal pigments (methemoglobin, sulfhemoglobin)
–
– Mixed
–
Central cyanosis Peripheral cyanosis
Mechanism Diminished arterial oxygen saturation. Diminished flow of blood to the local part is seen in the
This occurs in cardiac and respiratory hands and feet, which are cold.
disorders associated venous blood
into the systemic circulation, as in the
presence of a right to left heart shunt.
Sites On skin and mucous membranes. E.g. On skin only

tongue, lips, cheeks
Temperature of the limb Warm Cold

Disease Colour of pleural fluid Other characteristic features
Tuberculosis Amber • Predominant cells are lymphocytes
•
• Low glucose level
•
Malignant disease Blood stained • Predominance of serosal cell, malignant cells
•
• Evidence of malignant disease elsewhere
•
• Increased levels of amylase in pleural fluid

•
Rheumatoid disease Turbid • Very low glucose content
•
• Presence of cholesterol crystals in chronic effusion
•
Acute pancreatitis Blood stained • Very high amylase levels in pleural fluid than in
•
serum
Obstruction of thoracic outlet Milky • It is chyle type of pleural fluid
•
Obstructive disease (COPD) Restrictive diseases
• Asthma • Interstitial lung diseases
•
•
• Chronic bronchitis – Sarcoidosis
–
•
• Emphysema – Fibrosing alveolitis, etc
–
• Neuromuscular diseases
•
• Cystic fibrosis
•
• Chest wall
•
• Bronchiectasis
•
– Kyphoscoliosis
•
–
– Ankylosing spondylitis
–
Good to Know
• A total lung capacity of less than 80% of predicted values indicate restrictive pulmonary disease.
•
• The spirometer measures the FEV1 and forced vital capacity (FVC)
•
• The FEV1expressed as a percentage of the FVC is an excellent measure of airflow limitation. In normal subjects it is
•
around 75%.
• With increasing airflow limitation, the FEV1falls proportionally more than the FVC, so that the FEV1/FVC ratio is reduced.
•
• With restrictive lung disease, the FEV1 and the FVC are reduced in the same proportion and the FEV1/FVC ratio remains
•
normal or may even increase because of the enhanced elastic recoil.
• The hallmark of the restrictive lung diseases is a decrease in total lung capacity and vital capacity and increase in FEV1/
•
FVC and lung compliance.
• Decreased expiratory flow rate is hallmark of obstructive lung disease. Decrease in forced expiratory volume in 1 second
•
(decreased FEV1) and decreased FEV1/FVC are characteristic of obstructive lung disease. (AIIMS 1997)

• In chronic airflow limitation (particularly in emphysema and asthma), the total lung capacity (TLC) is usually increased,
•
yet there is nearly always some reduction in the FVC. This is the result of disease in the small airways causing obstruction
to airflow before the normal RV is reached. The trapping of air within the lung (giving an increased RV) is a characteristic
feature of these diseases. (AIPG 2009, 2011, AIIMS 2010, PGI 2009)

Obstructive Restrictive
Total lung capacity (TLC) Normal to increase Decrease
Residual volume (RV) Increase Decrease
Vital capacity (VC) Decrease Decrease
FEV1/FVC Decrease Increase
Diffusion capacity Normal (decrease in emphysema) Decrease
Lung compliance Unaffected (increase in emphysema) Decrease
308
Chronic Obstructive Pulmonary Disease Asthma

COPD is a disease state characterized by airflow limitation that
is not fully reversible. The airflow limitation is usually both • Asthma is a disorder characterized by chronic airway
•
progressive and associate with an abnormal inflammatory obstruction and increased airway responsiveness. This
response of the lungs to noxious particles or gases. Chronic results in wheeze (inspiratory), breathlessness, cough
bronchitis and emphysema constitute COPD. and sensation of chest tightness.
• The symptoms become worse in mornings.

Emphysema
•
• Pectus carinatum or pigeon chest or keel breast
• A pathological process of permanent destructive
•
deformity is caused by severe asthma during childhood.
•
enlargement of the spaces distal to the terminal bronchioles
• The concept of step up and step down is followed in
• Pink puffers–predominantly emphysema
•
the treatment of asthma, where low dosage are given
•
as starting drugs and increased sequentially depending
Panacinar emphysema Centriacinar emphysema
upon the severity. If there has been good symptomatic
Acini are uniformly involved Distended and damage of lung control a step down schedule should be made.
from level of respiratory tissue is concentrated around
bronchiole to terminal blind the respiratory bronchioles, • Features of acute severe asthma (earlier known as status
•
alveoli whilst the more distal alveolar asthmaticus) (Kar 2009)
ducts and alveoli tend to be well

preserved. – Silent chest
–
Lesions are more common in Lesions are more common in – Bradycardia
–
lower zone and bases upper lobes – Pulsus paradoxus
–
Severe airflow limitation and Severe centri acinar – Exhaustion, confusion and reduced conscious level
–
[Vdot]/[Qdot] mismatch occur. emphysema is associated with
(ventilation /perfusion) substantial airflow limitation. Bronchial Carcinoma
Occurs in association with α1 Occurs predominantly
antitrypsin deficiency. This is in smokers. This form of Bronchial asthma is associated with raised levels of
less common emphysema is extremely leukotrienes
common.
• The hallmark of obstructive pattern of disease is decreased
•
expiratory flow rate and decreased FEV1/FVC
• Irregular emphysema: There is scarring and damage
• The hallmark of restrictive lung diseases is a decrease in
•
affecting the lung parenchyma patchily without particular
•
regard for acinar structure. total lung capacity and vital capacity and increase in FEV
1 / FVC and lung compliance
• Emphysema leads to expiratory airflow limitation and
• Features of acute severe asthma
•
air trapping. The loss of lung elastic recoil results in an
•
increase in TLC while the loss of alveoli with emphysema – Silent chest
–
results in decreased gas transfer. – Bradycardia
–
• Clinical features of emphysema/COPD: – Pulsus paradoxus
–
– Exhaustion, confusion and reduced conscious level
•
– Rhonchi especially on forced expiration
–
• Bronchial carcinoma arises from the bronchial epithelium
–
– Hyper inflation of alveoli
•
or mucous glands. It is the most common malignant
–
– Barrel shaped chest tumour in the west. Bronchial carcinoma accounts for
–
– Tracheal descent during inspiration [tracheal ‘tug’] 95% of all primary tumours of the lung.
–
– Contraction of accessory muscles of respiration
• Cigarette smoking is by far the most important single
–
– Reduction in length of trachea palpable above the
•
factor in the causation of lung cancer.
–
sternal notch
– Intercostal indrawing reduced circo sternal distance • The most common type of bronchial carcinoma is
•
–
squamous cell carcinoma followed by adenocarcinoma in
non-smokers.
Chronic Bronchitis
• Adenocarcinoma accounts for approximately 10% of all
• Any patient who coughed up sputum on most days for
•
bronchial carcinomas. It is the most common bronchial
•
at least 3 consecutive months for more than 2 successive carcinoma associated with asbestos and is proportionally
years. more common in non-smokers, in women, in the elderly
• Blue bloaters–predominantly bronchitis and in the Far East.
•

• Small cell carcinoma, often called oat-cell carcinoma, polypeptide hormones are secreted by these tumours.
•
accounts for 20-30% of all lung cancers. It arises from The tumour is rapidly growing and highly malignant. It
endocrine cells (Kutchitsky cells). These cells are responds to chemotherapy but prognosis remains poor.
members of the APUD system, which explains why many
Bronchiectasis (AIPG 1996, MAN 1999, 2002)

Bronchiectasis describes a permanent dilatation of the airways secondary to chronic infection or Inflammation
• Cylindrical Bronchiectasis: The bronchi appear as uniformly dilated tubes that abruptly end at a point that smaller
•
airways are obstructed by secretions.
• Varicose Bronchiectasis: The affected bronchi have an irregular or beaded pattern of dilatation resembling varicose veins
•
• Saccular (cystic) bronchiectasis: The bronchi have a ballooned appearance at the periphery, ending in blind sacs without
•
recognizable bronchial structures distal to the sacs
• Nodular bronchiectasis: Is seen in infection with mycobacterium avium (Delhi 2008)
•

• Feature of Kartageners syndrome
•
– Tram track lines on CXR
–
– Commonest in left lower lobe (AIIMS 1995)
–

– Clubbing is a feature (AP 2005)
–

• Amphoric breathing is a feature of Cavity and Persistant coarse crepitations are a feature of Bronchiectasis
•
• Does not predispose to lung cancer (AIPG 1998)
•

• HRCT is the diagnostic technique of choice
•

(AIIMS 2001)
Causes
• Post infective: Tuberculosis, measles, pertusis, pneumonia
•
• Cystic fibrosis
•
• Bronchial obstruction. Eg: Lung cancer/foreign body
•
• Immune deficiency: Selective IgA, Hypogammaglobulinaemia
•
• Allergic bronchopulmonary aspergillosis (ABPA)
•
• Ciliary dyskinetic syndromes: Kartagener’s syndrome, Young’s Syndrome
•
• Yellow nail syndrome
•
Pneumonia – Bronchopneumonia
–
– Lobar pneumonia
• Pneumonia is an inflammatory process involving alveolar
–
– Interstitial pneumonia
•
tissue of lungs.
–
• Histologically it is divided into 4 stages: (COMEDK 2010)
• Clinically there are mainly three types:
•
•
Acute congestion • Local vasodilation, congestion
(1 day)
•
• Capillaries engorged, alveoli oedematous (eosinophils, bacteria, few neutrophils)
•
Red hepatisation • Capillary engorgement persists
(1 day)
•
• Exudate has fibrin accumulation of RBCs, neutrophils together with some lymphocytes and macrophages
•
Grey hepatisation: • Decreased vasodilation and congestion
(8 days)
•
• There is accumulation of fibrin and characterized by destruction of red and white cells. Macrophages
•
recruited to alveoli, which are distented and consolidated (due to fibrin and dead cells)
Resolution after 3 • Exudate liquefied by fibrinolytics from plasma and macrophages

weeks
•
• If there is no tissue destruction, parenchyma returns to normal
•
• Rare with some virulent organisms (Klebsiella pneumonia)
•
310
• Lobar pneumonia is a radiological and pathological term referring to homogenous consolidation of one or more lung lobes.
•
• Bronchopneumonia refers to patchy alveolar consolidation associated with bronchial and bronchiolar inflammation often
•
affecting both lower lobes. (MAN 1998)

Atypical Pneumonia Syndrome
• Characterized by a more gradual onset, a dry cough, shortness of breath, a prominence of extrapulmonary symptoms
•
(such as headache, myalgias, fatigue, sore throat, nausea, vomiting and diarrhea), and abnormalities on chest radiographs
despite minimal signs of pulmonary involvement on physical examination.

• Atypical pneumonia is classically produced by:
•
– M.pneumoniae (AIPG 2005)
–

– L.pneumophilia (AIPG 2005)
–

– C.pneumoniae
–
– Oral anaerobes
–
– P. carinii
–
– Less frequent encountered pathogens C. psittaci, Coxiella burnetii, Francisella tularensis, H. capsulatum, and
–
Coccidiodes immitis
Also know
• Mycoplasma pneumonia: May be complicated by erythema multiforme, hemolytic anemia, bullous myringitis,
•
encephalitis and transverse myelitis
• Staph aureus: Post influenza and pneumatocele formation (AIPG 2014)
•

• Klibessela pneumonia: Is characterized by red current jelly sputum. Bulging fissure sign is seen
•
• Legionella pneumonia: Is frequently associated with diarrohea, deterioration in mental status (delirium), renal and
•
hepatic abnormalities, and marked hyponatremia; (walking pneumonia), failure to respond to beta lactam antibiotics
• Self limiting form of legionella infection is called pontaic fever (Flu like illness without pneumonia)
•
• C. pneumonia: Pneumonia sore throat, hoarseness, and wheezing are relatively common
•
• The atypical pneumonia syndrome in patients whose HIV infection suggests pneumocystis infection
•
• Pneumonia alba is due to treponema palladium
•
• Bronchopneumonia in measles is due to immunosuppression
•
• Plasma cell penumoniae is caused by: Pneumocystis carnii (PGI 2008)
•

• Nosocomial Pneumonia: Hospital induced pneumonia
•
Aspiration Pneumonia and anaerobic Lung Abscess
• Aspiration of a sufficient volume of gastric acid produces a chemical pneumonitis characterized by acute dyspnea and
•
wheezing with hypoxia and infiltrates on chest radiographs in one or both lower lobes.
• Clinical findings following aspiration of particulate matter depend on the extent of endobronchial obstruction and range
•
from acute apnea to persistent cough with or without recurrent infection.
• Although the aspiration of oral anaerobes can initially lead to an infiltrative process, it ultimately results in putrid sputum,
•
tissue necrosis, and pulmonary cavities. In about three-quarters of cases, the clinical course of an abcess of anaerobic
polymicrobial etiology is indolent.
• Patients with anaerobic abscesses are usually prone to aspiration of oropharyngeal contents and have periodontal disease.
•
Occupational Lung Disease
Anthracosis Caused by deposition of carbon particles
Bagassosis (COMEDK 2005) Caused by inhalation of sugar cane dust


Byssinosis (Monday fever) Caused by deposition of cotton fibre particle
Farmers lung Lung disease caused by mouldy hay
Asbestosis (AIIMS 2003) Deposition of asbestos particles in lung. It is the most common

pneumoconiosis which undergoes malignant change

Cystic Fibrosis (AIPG 2003, MAH 2011) Pleural Effusion
• It is an autosomal recessive inherited disorder with a • Pleural effusion is excess fluid that accumulates in the
•
pleural cavity, that surrounds the lungs. Excessive
•
carrier frequency in Caucasians of 1 in 22. Resulting from
mutations in a gene located on chromosome 7 amounts of such fluid can impair breathing by mass effect,
limiting the expansion of the lungs during ventilation.
• This disease is characterized by chronic airways infection
•
that ultimately leads to bronchiectasis, exocrine pancreatic • Various kinds of pleural effusion, depending upon the
•
insufficiency and intestinal dysfunction, abnormal sweat nature of the fluid and what caused its entry into the
gland function, and urogenital dysfunction. pleural space, are hydrothorax (serous fluid), hemothorax
• The classical form of the syndrome includes (blood), chylothorax (chyle), or pyothorax (pus).
•
bronchopulmonary infection and pancreatic insufficiency,
with a high sweat sodium and chloride concentration. Transudate Exudate
• Protein < 3gm/100ml • Protein > 3gm/100ml
• Increased viscosity of secretions in the lung and other
•
•
• LDH < 200 IU • LDH > 200 IU
•
organs, which causes ciliary dysfunction and chronic
•
•
• LDH ratio < 0.6 • LDH ratio > 0.6
bronchial infections
•
•
• Pleural fluid/serum protein • Pleural fluid/serum protein >
• Generalized calculus formation
•
•
< 0.5 0.5
•
• Malabsorption about 85% of patients has symptomatic
• CHF • Pneumoniae
•
steatorrhoea owing to pancreatic dysfunction.
•
•
• Cirrohosis • Pulmonary infarction
• Cavitation is usually seen with Staph infections
•
•
• Nephrotic syndrome • Tuberculosis
•

(AIPG 2010)
•
•
• Meigs Syndrome • Rheumatoid Arthritis

•
•

• Pulmonary Embolism (PGI 2002)
Interstitial Lung Diseases
•
• Myxedema
•
• Represent a large number of conditions that involve • Lupus erythematosus
•
•
the parenchyma of the lung, the alveoli, the alveolar • Pulmonary embolism
•
epithelium, the capillary endothelium as well as the • Bronchogenic cancer
•

(AIPG 2003)
perivascular and the lymphatic tissues

• Sarcoidosis, Idiopathic Pulmonary Fibrosis, and
•
Pulmonary fibrosis associated with CTDs are the Pulmonary Tuberculosis
most common ILDs of the unknown etiology
• Features • Ghon Complex: Primary subpleural granuloma in the
•
inferior upper lobe/superior lower lobe region (Ghon
•
– Onset of progressive exertional dyspnea or a
Focus) along with draining Hilar nodes
–
persistant,
– Non productive cough. • Puhls Lesion: Isolated lesion of chronic pulmonary TB in
•
apex of lung.
–
– Hemoptysis
–
– Wheezing • Assmans Focus (NEET 2012): Infraclavicular lesion of
•
–
– Chest pain may be present. chronic pulmonary TB
–
• Therapy • Rancke Complex: Combination of calcified peripheral
•
•
– Glucocorticoids are the mainstay of therapy for lesion (ghon complex) and calcified Hilar nodes seen in
–
suppression of the alveolitis present in ILD Primary TB
– Lung transplantation may be considered. • Kochs phenomenon is seen in Tuberculosis
–
•
312
Good to know
• Most common cause of community acquired pneumonia Streptococcus pneumonia/ Pneumonococcus pneumonia
•

• Causes of atypical pneumonia Mycoplasma, chlamydia, pneumocystitis carinii and viral
•

infections
• Pneumonia in association with high fever, confusion and Legionnaire’s pneumonia

•

diarrhea
• Most common micro organisms isolated from the patients with Gram negative bacilli
•

nosocomial pneumonias
• Drug of choice for atypical pneumonia caused by Clotrimoxazole, clindamycin

•

pneumocystitis
• Drug of choice for community acquired pneumonia Clarithromycin, flucloxacillin

•

• Drug of choice for atypical pneumonia caused by mycoplasma Erythromycin, clarithromycin
•

• Drugs used for treatment of atypical pneumonia caused by Doxycycline, erythromycin
•

chlamydia
Most Common
• Most common cause of hemoptysis • Bronchitis
•
•
• Most common cause of hemoptysis in India • Tuberculosis
•
•
• Most common cause of massive hemoptysis • Bronchiectasis
•
•
• Most common cause of massive hemoptysis in India • Tuberculosis
•
•
• Most common site for presenting symptom of lung cancer • Cough
•
•
• Most common cause of bronchogenic cysts • Middle Mediastinum
•
•
• Most common cause of stridor in children • Foreign body
•
•
GIT AND LIVER a somatic source than visceral. This type of pain is
characteristically aching and perceived to be near the
Epigastric pain surface of the body. For example, referred pain from
• Right hypochondrium is the most common site of pain gallstones is sometimes perceived in the right shoulder
because some of the afferent pain fibres run in the right
•
due to presence of gall stones. (AIIMS 2011)
phrenic nerve (C3-5)

• Epigastric pain is commonly caused by pancreatitis. But
•
gallstones can also cause less frequency of pain to its seat, Causes of GI Bleeding
i.e. two inches to the right of epigastrium. Often felt in the
Upper GI bleed- Lower GI bleeding Obscure GIB
epigastrium with radiation to the upper part of the lumbar
ing (UGIB) (LGIB)
region.
• Peptic ulcer • Meckel’s • Small intestine
• Gall stones pain is present in every part of abdomen
•
•
•
(most common) diverticulum is the bleeding
•
(COMEDK 2003) common cause
Referred pain • Small intestine
•
• Gastric erosion • Vascular ectasis tumours
• Perception of pain at a site distant from the origin of
•
•
•
the stimulus. One possible explanation for this is that • Varices • Neoplasms
•
•
the visceral and the somatic afferent nerve fibres share • Oesophagitis (adenomatous
polyps and
•
a common pathway at the level of the cord, which is • Cancer of adenocarcinoma)
spinothalamic tract.
•
stomach or
oesophagus • Colitis
• The brain tends to associate the stimulation more with
•
•

Dysphagia
• Is defined as a sensation of ‘sticking’ or obstruction of the passage of food through the mouth, pharynx, or oesophagus
•
• Aphagia signifies complete esophageal obstruction
•
• Odynophagia–painful swallowing
•
• Phagophobia–fear of swallowing and refusal to swallow may occur in hysteria, rabies, tetanus, and pharyngeal paralysis due
•
to fear of aspiration.

• Globus pharyngeus is the sensation of a lump lodged in the throat.
•
Etiology of Dysphagia
Mechanical dysphagia Neuromuscular dysphagia
• Disease of mouth and tongue (e.g. tonsillitis) • Neuromuscular disorders
•
•
• Extrinsic pressure – Pharyngeal disorders
•
–
– Mediastinal glands – Bulbar palsy (e.g. motor neuron disease)
–
– Myasthenia gravis
–
– Goiter
–
• Oesophageal motility disorders
–
– Enlarged left atrium
•
–
• Intrinsic lesion: – Achalasia
•
–
– Foreign body – Scleroderma
–
– Diffuse oesophageal spasm
–
– Stricture: –
– Presbyoesophagus
–
- Benign – peptic, corrosive
–
– Diabetes mellitus
-
- Malignant – carcinoma
–
– Chaga’s disease
-
– Lower oesophageal rings
–
–
– Oesophageal web
–
– Pharyngeal pouch
–
You should know
Hemoptysis Coughing of frank blood. Usually a respiratory symptom
Hematemesis Vomitus of red blood (altered blood) or ‘coffee ground’ (associated with food particles) usually a upper GIT symptom
(above the ligament of Treitz)
Hematochezia Is the passage of bright red or maroon blood from the rectum. Lower GIT lesion.
Melena Black, (dark) tarry, foul smelling coloured stools suggestive of upper gastro intestinal bleeding mainly oesophageal varices
bleeding.
Epistaxis Bleeding from nose
Cholecystitis Also note

• Is usually diagnosed by a history of the symptoms, as well
• Circulatory changes: Spider telangiectasis, palmar
•
as examination findings:
•
erythema, cyanosis
– Tender right upper quadrant with or without
• Endocrine changes: loss of libido, hair loss
–
Murphy’s sign
•
– Ortner’s sign: Tenderness when hand taps the edge of – Men: Gynaecomastia, testicular atrophy, impotence
–
–
the right costal arch. – Women: Breast atrophy, irregular menses,
–
– Georgievskiy: Myussi’s sign (phrenic nerve sign)- pain amennorhoea
–
when press between edges of sternocleidomastoid. • Haemorrhagic tendency: Bruises, purpura, epistaxis
– Boas sign: Increased sensitivity below the right
•
• Portal hypertension: Splenomegaly, collateral vessels,
–
scapula (also due to phrenic nerve irritation)
•
variceal bleeding, fetor hepaticus
Clinical features of hepatic cirrhosis: (MAN 2001) • Hepatic (portasystemic) encephalopathy
•
• Hepatomegaly • Other features: Pigmentation, digital clubbing, low
•
•
• Jaundice grade fever
•
• Ascites
•
314
Cholestasis (KAR 2006)

Early features Late features
• Jaundice • Xanthelasma and xanthomata
•
•
• Dark urine • Malabsorption
•
•
• Pale stools • Weight loss
•
•
• Pruritus • Osteomalacia
•
•
• Bleeding tendency
•
Characteristics of Hepatic Diseases
Parameter Hemolytic disease Hepato cellular Obstructive
• Blood hemoglobin Decrease Normal Normal
•
• Unconjugated bilirubin Increase Normal Normal
•
• Conjugated bilirubin Normal Increase Increase
•
• Alkaline phosphatase Normal Normal Increase
•
• Stool
•
– Colour Normal Normal Pale
–
• Urine
•
– Bilirubin Absent Increase Increase
–
– Urobilinogen Increase Increase Decrease
–
• Increase in serum bilirubin is best detected by examining Constipation: Is a very common symptom, defined it as
•
the sclerae which have a particular affinity to bilirubin having two or more of the following for atleast 12 weeks:
due to their elastin content. The presence of scleral icterus infrequent passage stools (<3/week), straining >25% of time,
indicates a serum bilirubin of atleast 51 mol/L (3.0 mg/dl). passage of hard stools, incomplete evacuation and sensation of
anorectal blockage.
Vomiting Reflux oesophagagitis: Inflammation of the lower esophagus
produced by persistent episodes of reflux. Patients may be
• The vomiting centres are located in the lateral reticular asymptomatic. Gastro-esophageal reflux occurs as a normal
•
formation of the medulla and are stimulated by the event, and the clinical features of GERD occur only when the
chemoreceptor trigger zones (CTZs) in the floor of the antireflex mechanisms fail sufficiently to allow gastric contents
fourth ventricle, and also by vagal afferents from the gut. to make prolonged contact with the lower esophageal mucosa.
These zones are directly by drugs, motion sickness and Regurgitation of food and ‘acid’ into the mouth occurs,
metabolic causes. particularly when the patient is bending or lying flat.
• Large volumes of vomit suggest intestinal obstruction.
Heartburn is a major feature of GERD. The differential
•
• Feculent vomit suggests low intestinal obstruction or the
diagnosis of the retrosternal pain from angina can be
•
presence of gastrocolic fistula
difficult; 20% of cases admitted to coronary care unit have
• Projectile vomiting is due to gastric outflow obstruction GERD.
•
• Many gastro intestinal conditions are associated with
•
vomiting, but nausea and vomiting without pain is Gastro – oesophageal Myocardial ischaemia
frequently non gastrointestinal in origin. reflux
• Chronic nausea-vomiting with no other abdominal • Burning pain produced by • Gripping or crushing pain
•
•
•
symptoms is usually due to a psychological cause. bending, stooping or lying • Pain radiates into neck,
down
•
shoulders and both arms
• Early morning vomiting is seen in pregnancy, alcohol • Pain seldom radiates to • Pain produced by exercise
•
dependence and some metabolic disorders (e.g. uraemia)
•
arm
•
• Accompanied by dyspnea
Flatulence: The term used to describe excessive wind. It • Pain precipitated by
•
•
includes belching, abdominal distension, ‘wind’ or the passage drinking hot liquids or
alcohols
of flatus per rectum. Swallowing air (aerophagia) is the
• Relieved by antacids
common cause.
•

Ulcers
• Ulcers are defined as a break in the mucosal surface 75mm in size, with depth to the submucosa. Peptic ulcer disease (PUD)
•
encompasses both duodenal and gastric ulcers.
Duodenal ulcer Gastric ulcer
• Very common and are 2-3 times more common than gastric • Less common
•
•
ulcers

• Most duodenal ulcers are found in the duodenal cap • Gastric ulcers are found in any part of the stomach, (antrum) but
•
•
are most commonly seen on the lesser curve.
• H. pylori infection may be present • H. pylori infection may be present

•
•
• Abdominal and epigastric pain as a burning or gnawing • Abdominal and epigastric pain present.
•
•
discomfort can be present in both.
• The typical pain pattern occurs 90mins to 3 hours after a meal • The pain pattern in these patients may be different from that in DU
•
•
when the patient is hungry again and is frequently relieved by patients, where discomfort may actually be precipitated by food
antacids or food. Pain that awakes a patient from sleep (between
midnight and 3 am) is the most discriminating symptom, with
two –thirds of DU patients describing this complaint.
• Nausea may accompany the pain, vomiting is infrequent but • Nausea and weight loss occur more commonly
•
•
often relieves the pain. Heart burn may be present.
• Both are relieved by antacids

•
• Stress ulcers: elevated gastric acid secretion may be noted in patients with stress ulceration after a head trauma
•
(Cushing’s ulcer) and severe burns (Curling’s ulcer). Patients suffering from shock, sepsis, massive burns, severe trauma,
or head injury can develop acute erosive gastric mucosal changes or frank ulceration with bleeding. Classified as stress
induced gastritis or ulcers, injury is most commonly observed in the acid producing (fundus and body) portions of the
stomach. Histologically stress injury does not contain inflammation or H. pylori, thus ‘gastritis’ is a misnomer.
H. Pylori Tests • Histology

•
• Culture
Features • H. pylori accounts for most of the peptic ulcer
•
• Urea breath test (documenting eradication)
•
cases
•

(AIPG 2007)
• More prevalent in developing countries

• Serological test (AIPG 1991, 1999))
•

(AIIMS 1997)
•

• Stool antigen test

• It is a gram negative bacillus
•
•
• Microaerophilic Treatment • Clarithromycin
•
•
• Urease producing • Bismuth subsalicylate
•
•
• pH- gated urea channel in H. pylori bacterium • Metronidazole
•
•
is called: Urel
Causes • Gastritis
Viral Hepatitis
•
• Gastric Ca
Incubation Periods
•
• Gastric lymphoma
•
• Peptic ulcer disease • Hepatitis A – 2-6 Weeks
•
•
Extra gastric • Ischemic heart disease • Hepatitis B – 4-8 Weeks
•
• Hepatitis C – 2- 22 Weeks
•
disease in • Coronary artherosclerosis (TN 2008)
•
•

which H.Pylori • Idiopathic thrombocytopenic purpura • Hepatitis D – 4-8 Weeks
is supposed
•
•
to play a role
• Iron deficiency anemia (AP 2006) • Hepatitis E – 2- 9 Weeks
•

•
AIIMS 2003, • Hepato cellular carcinoma
Hepatitis B:
•
AIPG 1999 • Cholangiocarcinoma
•
• Inflammatory bowel disease • Hepatitis B is a DNA virus; all others are RNA virus
•
•
• Raynaud’s Phenomenon • P Gene codes reverse transcriptase of hep B virus
•
•

(AIPG 2000)
316
• Spreads by feco-oral route–Hepatitis A and E • As a result of injury to the glomerular capillary wall,
•

•
(AIPG 2000) urinalysis typically reveals red blood cell casts, dysmorphic
• Spreads by percutaneous route–Hepatits B,C and D red blood cells, leukocytes and sub nephritic proteinuria
•
• Hepatitis B also spreads by vertical and sexual route, most of <3.5 gm per 24 hr (nephritic urinary settlement)
•
•
common (AIPG 2003) Hematuria is often macroscopic
•

• Oncogenicity present in Hepatitis B especially after Nephrotic Syndrome: (AIIMS May 2013)
•
neonatal infection
• Nephrotic syndrome is characterized by protein loss in
• Carrier state present in Hepatitis B
•
urine of more than 3.5g proteinuria/day, fluid retention
•
• Hepatitis B virus may be present in blood and other body or oedema, hypercoagulability, hyper cholesteremia
•
fluids and excretions such as saliva, breast milk, semen, and infections. (KCET 2010)

vaginal secretions, urine, bile, etc • Albumin is the dominant serum protein. Presence
•
• Feces not known to be infectious of albumin in the urine is a sure sign of glomerular
•
abnormality.
EXCRETORY SYSTEM • The diseases that cause nephritic syndrome always
•
affect the glomerulus.
• In diabetic nephropathy, histologically there is: • The acute nephritic syndrome is the clinical correlate
•
•
– Thickening of basement membrane of acute glomerular inflammation. In its most dramatic
–
– Mesangial proliferation form, the acute nephritic syndrome is characterized by
–
– Kimmelstein–Wlison bodies sudden onset (i.e. over days to weeks) of acute renal failure
–
• Renin and erythropoietin are the hormones released and oliguria (<400ml of urine per day) (AIPG 2007)
•

from the juxtaglomerular apparatus of kidney. • Renal blood flow and glomerular filtration rate (GFR)
•
• Renin stimulates the conversion of angiotensinogen fall as a result of obstruction of the glomerular capillary
•
to angiotensin II, which further stimulates the adrenal lumen by infiltrating inflammatory cells and proliferating
cortex to secrete aldosterone. This is called the Renin- resident glomerular cells.
Angiotensin-Aldosterone axis. • Renal blood flow and GFR are further compromised
•
• Rennin is an enzyme released from the chief cells of by intra renal vasoconstriction and mesangial cell
•
fundic glands of stomach. It is a milk-curdling enzyme. contraction that result from local imbalances of
It is absent in man. (AIPG 1998) vasoconstrictor (e.g., nitric oxide, prostacyclin) within the

renal microcirculation.
Acute Nephritic Syndrome • Extracellular fluid volume expansion, edema and
•
hypotension develop because of impaired GFR and
• Is characterized by sudden onset (i.e. over days to weeks) enhanced tubular reabsorption of salt and water.
•
of renal failure and oligouria (<400 ml of urine per day) • As a result of injury to the glomerular capillary wall,
• Renal blood flow and glomerular filtration rate (GFR) fall
•
urinalysis typically reveals red blood cell casts, dysmorphic
•
• Extracelllular fluid volume expansion, edema and red blood cells, leukocytes and subnephrotic proteinuria
•
• Hypertension develop because of impaired GFR and of upto 3.5 g per 24 h (nephritic urinary sediment).
Hematuria is often macroscopic.
•
enhanced tubular reabsorption of salt and water
Good to Know
• Glomerular filtration ceases when systolic blood pressure falls below 70mm of Hg.
•
• Azotemia occurs due to cardiac failure, pancreatitis, and burns. (MAHE 2009)
•

• Renal papillary necrosis is seen in sickle cell anemia. (KAR 2008)
•

• Magnesium excess mainly occurs in acute or chronic renal failure and may contribute to CNS disturbance associated with
•
severe uremia. It is rare because of the renal capacity to excrete excess ion. Magnesium exerts an effect on neuromuscular
irritability similar to that of calcium ions. (COMEDK 2009)


Difference between Nephritic and Nephrotic Syndrome
Nephritic Syndrome Nephrotic Syndrome
Hematuria (PGI 1997) Severe proteinuria (AIPG 2000)

Hypertension Hypoalbuminemia
Oligouria Hyperlipidemia
Proteinuria Fibrinogen increased (AIIMS 1998)

Lipoproteins increased
Low serum Calcium
Platelet activation (PGI 1999)

Decreased HDL (PGI 2000)

Causes of Red Coloured Urine
• Hematuria: Microscopic examination of urine will demonstrate the present of RBCs
•
• Myoglobinuria: Brownish red colour, associated with ischemic muscle damage, crush injuries, and after vigorous exercise
•
• Hemoglobinuria: With intravascular hemolysis
•
• Drugs
•
– Phenytoin
–
– Phenothiazines
–
– Adriamycin
–
• Foods
•
– Berries
–
– Beets
–
– Food colouring
–
Green Colored Urine
• Food Colourings
•
• Pseudomonas aeruginosa infection
•
• Oxalate poisoning
•
• Oxaluria
•
• Phenol poisoning can lead to green or black urine due to carboluria
•
Brown/Black Colored Urine
• Hemoglobin
•
• Nitrofurnas
•
• Alkaptonuria – on standing the urine shall turn into dark colour
•
• Renal Failure
•
Orange coloured urine: Rifampicin (AIIMS 1998)
• Pre-Renal Uraemia: Kidneys hold on to sodium to preserve volume
•
Pre-renal uraemia Acute tubular necrosis
• Urine sodium < 20 mmol/L >30 mmol/L (AIIMS 2000)
•

• Fractional sodium excretion <1% >1% (AIIMS 2007)
•

• Fractional urea excretion <35% >35% (PGI 2005)
•

318
• Urine: Plasma osmolality >1.5 <1.1

•
• Urine: Plasma urea >10.1 <8.1
•
• Specific gravity >1020 <1010 (PGI 2002)
•

• Urine Bland sediment Brown granular casts
•
• Response to fluid challenge Yes No

•
Glomerulonephritis
Membranous Glomerulo- • Presentation: Proteinuria/nephritic syndrome/CRF

•
nephritis • Cause: Infections,rheumatoid drugs,malignancy
•
• Gold, pencillamine
•
• 1/3rd resolve, 1/3rd respond to cytotoxics, 1/3rd develop CRF
•
IgA nephropathy (Berger’s • Typically young adult with hematuria following an URTI
•
disease mesangioprolif- • Patients present with gross hematuria often 24 to 48 hrs after a pharyngeal or GIT infection as compared
•
erative GN) to Post streptococcal glomerulonephritis which develops 10 days after pharyngitis and 2 weeks after
skin infection
Diffuse proliferative Glo- • Classical post streptococcal Glomerulonephritis in child

•
merulonephritis • Presents as nephritic syndrome/ARF
•
Minimal Change disease • Typically a child with nephritic syndrome (Accounts for 80%)
•
(MCD) • Causes: Idiopathic, HIV, Hodgkin’s, NSAIDs, Rifampicin, interferon alpha
•
• Good response to steroids
•
• IgA deposits
•
• Fusion of foot processes on EM
•
• No change in light microscopy
•
• Polyanions contribute to damage
•
• Hypertension is not common in MCD
•
Focal segmental Glomeru- • May be idiopathic or secondary to HIV, Heroin
•
losclerosis • Presentation: Proteinuria/nephritic syndrome/CRF
•
Rapidly progressive glo- • Rapid onset, often presenting as ARF, crescent formation, non selective proteinuria
•
merulonephritis (cresentic • Causes include
•
glomerulonephritis) – Post Streptococcal GN
–
– Goodpasture’s
–
– ANCA positive vasculitis
–
– SLE
–
– Infective Endocarditis
–
– HS Purpura
–
– Bergers disease
–
Mesangiocapillary Glo- • Type 1: cryoglobulinaemia, Hepatitis C
•
merulonephritis (membra- • Type 2: partial lipodystrophy
•
noproliferative)
Wegener’s Granuloma- • Necrotizing vasculitis of small arteries and veins together with granuloma formation that can be either
•
tosis intravascular or extravascular
• Lung involvement: Bilateral nodular cavitary infiltrates, demonstrate necrotizing granulomatous vasculitis
•
• The renal biopsy lesion is that of a pauci-immune necrotizing and crescentic GN
•

Goodpastures Syndrome
• Autoimmune disease in which autoantibodies directed against type IV collagen the clinical complex of anti-GBM nephritis
•
and lung hemorrhage is referred to Good Pastures Syndrome. Patients with Goodpastures syndrome are basically young
males (5-40 years; Male:female ratio 6:1)
• The target antigen is a component of the noncollagenous (NCI) domain of the α3 chain of type IV collagen, the α3 chain
•
being preferentially expressed in glomerular and pulmonary alveolar basement membrane.

• Anti-GBM disease commonly presents with hematuria, nephritic urinary sediment, subnephrotic proteinuria and
•
• Rapidly progressive renal failure over weeks, with or without pulmonary hemorrhage (AIPG 1997)
•

• About 20% of the patients have low titres of ANCA, usually a perinuclear (pANCA)
•
• Renal biopsy is the gold standard for diagnosis of anti-GBM nephritis
•
• The typical morphologic pattern on light microscopy is diffuse proliferative glomerulonephritis, with focal necrotizing
•
lesions and crescents in > 50% of glomeruli (crescentic glomerulonephritis)
• Immunofluroescence microscopy reveals linear ribbon like deposition of IgG along the GBM
•
• C3 is present in the same distribution in 70% of patients. Prominent IgG deposition along the tubule basement membrane
•
and tubulointerstitial inflammation is found occasionally
• Electron microscopy reveals nonspecific inflammatory changes without immune deposits. Typical features on lung biopsy
•
include alveolar hemorrhage.
Alport’s Syndrome (Hereditary Nephritis)

• Nephritis
•
• Nerve deafness
•
• Electron microscopy characteristically reveals both thinning and irregular thickening of the glomerular tubular basement
•
membranes, with splitting of the lamina densa into several lamellae separated by lucent zones containing electron dense
round granulations (“basketweave” appearance) (AIPG 2010)

• The etiology of Alports syndrome appears to be the absence of a 28kD peptide component of the noncollagenous (NC1)
•
domain of the α3 chain of type IV collagen in glomerular basement membrane (GBM). This peptide is known as the
‘Goodpasture antigen’. (AIIMS 2006)

• Eye disorders (Lens dislocation, coronal dystrophy, Posterior cataracts)
•
• Foamy cells in interstitium (PGI 2005)
•

Diabetes Insipidus
Types 1. Cranial

2. Nephrogenic

Causes • Cranial DI
•
– Idiopathic
–
– Post head injury
–
– Pituitary surgery
–
– Craniopharyngiomas
–
– Histiocytosis X
–
• Nephrogenic DI
•
– Genetic (Primary)
–
– Electrolytes: Hypercalcemia, Hypokalemia
–
– Drugs: Demeclocycline, lithium
–
– Tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
–
Investigation • High plasma osmolarity
•
• Low urine osmolarity
•
• Water deprivation test
•
320
Wolfram’s Syndrome (Didmoad) – Large hands and feet
–
– Prognathic lower jaw
• Cranial Diabetes Insipidus
–
•
• Diabetes Mellitus
–
– Hypertension
•
–
• Optic atrophy Cretin Pituitary dwarf
•
• Deafness • Hypothyroidism in • Growth hormone deficiency
•
•
•
children causes cretinism caused dwarfism(AIIMS 2004)

ENDOCRINE SYSTEM

• Stunted skeletal growth • Stunted but well proportionate
•
•
with disproportionate body parts
• Growth hormone hypersecretion occurring before body parts • No mental retardation
•
epiphysis have fused, results in gigantism while GH excess
•
• Mentally retarded • Reproductive function is normal
•
after epiphyseal closure results in acromegaly.
•
• Reproductive function is if there is only GH deficiency
•
• Clinical features of acromegaly (AIPG 1995, 97, 98) affected • Panhypopituitarism may cause
•
•
hypogonadism
– Skin thickening
–
– Enlarged nose and tongue • Macroglossia, glutteral • Fine sparse hair and wrinkled
•
•
–
– Macroglossia breathing and croaking atrophic skin is present
voice are present
–
– Carpal tunnel syndrome
–
Hyperthyroidism Hypothyroidism
• Palpitations and tachycardia, hypertension, dyspnea, atrial • Bradycardia, hypotension, congestive heart failure
•
•
fibrillation
• Weight loss despite normal, goiter, diffuse bruit • Weight gain, goiter, hoarseness and tiredness
•
•
• Heat intolerance • Cold intolerance
•
•
• Amenorrhea/oligomenorrhea • Menorrhagia
•
•
• Nervousness, irritability, emotional liability, tremor • Carpal tunnel syndrome, depression, aches and pains
•
•
• Increased sweating, pigmentation, pretibial myxedema • Dry flaky skin, alopecia, myxedema
•
•
• Lid lag, lid retraction, exophthalmos, diplopia, papilloedema • Macrocytosis, iron deficiency anaemia
•
•
Thyroid Storm (AIPG 1995, KAR 2009, MAHE 2007)
• Also referred to as thyrotoxic crisis, thyrotoxicosis
•
• An acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones (THs) in individuals with
•
thyrotoxicosis.
• Thyroid storm may be the initial presentation of thyrotoxicosis in undiagnosed children, particularly in neonates.
•
• Clinical presentation includes:
•
– Fever,
–
– Tachycardia,
–
– Hypertension, and
–
– Neurological and gastrointestinal abnormalities.
–
• Hypertension may be followed by congestive heart failure that is associated with hypotension and shock.
•
• Thyrotoxicosis is 3-5 times more common in females than in males, especially among pubertal children.
•
• Neonatal thyrotoxicosis occurs in 1-2% of neonates born to mothers with Graves disease. Infants younger than 1 year
•
constitute only 1% of childhood thyrotoxicosis.
• More than two thirds of all cases of thyrotoxicosis occur in children aged 10-15 years. Overall, thyrotoxicosis occurs most
•
commonly during the third and fourth decades of life.

• Because childhood thyrotoxicosis is more likely to occur in adolescents, thyroid storm is more common in this age group,
•
although it can occur in patients of all ages.
Causes
• Thyroid storm is precipitated by the following factors in individuals with thyrotoxicosis:
•
– Sepsis
–
– Surgery

–
– Anesthesia induction
–
– Radioactive iodine (RAI) therapy
–
– Drugs (anticholinergic and adrenergic drugs such as pseudoephedrine; salicylates; nonsteroidal anti-inflammatory
–
drugs [NSAIDs]; chemotherapy)
– Excessive TH ingestion
–
– Withdrawal of or noncompliance with antithyroid medications
–
– Diabetic ketoacidosis
–
– Direct trauma to the thyroid gland
–
– Vigorous palpation of an enlarged thyroid
–
– Toxemia of pregnancy and labor in older adolescents; molar pregnancy
–
• Thyroid storm can occur in children with thyrotoxicosis – Pheochromocytoma
•
–
due to any cause but is most commonly associated with – Supraventricular Tachycardia, Atrial Ectopic
–
Graves disease. Other reported causes of thyrotoxicosis Tachycardia
associated with thyroid storm include the following:
– Transplacental passage of maternal thyroid- • Therapy is aimed at
•
–
stimulating immunoglobulins in neonates – Ameliorating hyperadrenergic effects of TH on
– McCune-Albright syndrome with autonomous
–
peripheral tissues with use of beta-blockers (eg,
–
thyroid function propranolol, labetalol);
– Hyperfunctioning thyroid nodule
– Decreasing further synthesis of THs with
–
– Hyperfunctioning multinodular goiter
–
antithyroid medications (eg, propylthiouracil
–
– Thyroid-stimulating hormone (TSH)–secreting
[PTU], methimazole);
–
tumor
– Decreasing hormonal release from the thyroid,
–
• Graves disease may also occur in children with Down using iodides; and
•
or Turner syndromes and in association with other – Preventing further TH secretion and peripheral
autoimmune conditions, including the following:
–
conversion of T4 to T3, using glucocorticoids or
– Juvenile rheumatoid arthritis iodinated radiocontrast dyes when available.
–
– Addison disease
Pseudohypoparathyroidism is a group of disorders
–
– Type I diabetes
characterized by hypocalcemia due to renal resistance
–
– Myasthenia gravis
to PTH. PTH levels are high. Various phenotypic
–
– Chronic lymphocytic (Hashimoto) thyroiditis
abnormalities may be associated-classically, short stature,
–
– Systemic lupus erythematosus
round face, obesity, short fourth metacarpals, ectopic bone
–
– Chronic active hepatitis
–
– Nephrotic syndrome formation and mental retardation. Treatment is same as
–
primary.
• Differential Diagnosis: ‘Pseudohypoparathyroidism’ patients without
•
– Anxiety Disorder: Panic Disorder hypocalcemia but sharing the phenotypic abnormalities.
–
– Heart Failure, These patients have normal serum calcium and high serum
–
– Congestive Hypertension PTH.
–
– Hyperthyroidism
–
322
Disease Serum calcium Serum phosphorus Alkaline phosphorus

• Rickets (Vit D def) • Decreased • Decreased • Increased
•
•
•
•
• Osteomalacia • Decreased • Decreased • Increased
•
•
•
•
• Chronic renal failure • Decreased • Increased • Normal
•
•
•
•
• Hyper parathyroidism • Increased • Decreased • Increased
•
•
•
•
• Hypo parathyroidism • Decreased • Increased • Normal

•
•
•
•
• Osteoporosis • Normal • Normal • Normal
•
•
•
•
The term ‘renal osteodystrophy’ embraces the various forms of bone disease that may develop alone or in combination in
chronic renal failure–hyperparathyroid bone disease, osteomalacia, osteoporosis, osteosclerosis and adynamic bone disease.


• Acetone breath (AIIMS 1998) • Diabetes mellitus
•

•
• Musty breath • Hepatic coma
•
•
• Uremic breath • Renal disease
•
•
• Alcoholic breath • Alcoholics
•
•
Diabetes Mellitus
• Diabetes mellitus is characterized by: (Man 1994, 2002, Mahe 2007)
•
– Polyuria, polyphagia and polydypsia
–
– Glucosuria
–
– Ketoacidosis
–
– Kussmaul breathing
–
– Bone resorption, loosening of teeth
–
– Multiple fleeting periodontal abscesses
–
– Acetone breath
–
Type I [Insulin dependent Diabetes Mellitus or IDDM) Type II (Non insulin dependent diabetes mellitus or NIDDM)
• It is due to the deficiency of insulin. It occurs due to: • Diabetes develops due to reduced number of insulin receptors. The
•
•
– Destruction of beta cells during auto immune diseases. structure, function of beta cells in normal.
–
– Destruction of beta cells by viral infection.
–
– Congenital disorder of beta cells
–
• It is not associated with obesity and is not hereditary • It is associated with obesity and is hereditary
•
•
• It is usually occurs in young age groups • It usually occurs after the age of 40 years
•
•
• Childhood diabetes is called ‘juvenile diabetes’ • It is also called as maturity onset diabetes
•
•
• It is commonly associated with acidosis or ketosis or coma • It is very rarely associated with ketosis
•
•
Tests for Diabetes Mellitus
• Prescreening tests:
•
– Fasting blood glucose (FBG)
–
– Random blood glucose (RBG)
–
• Routine screening:
•
Oral glucose tolerance test (OGTT) Is commonly used for the diagnosis of DM. lengthy procedure

Glucose challenge test (GCT): Mini version of OGTT


• Glucose control tests:
•
– Glycated hemoglobin (HbA1c): Measurement that indicates average glucose levels over the preceding 12 weeks.
–
– Glycolated proteins: Glycohaemoglobin, glycoalbumin and glycated total protein.
–
Fructosamine is a term that has come into acceptance and refers to both glycoalbumin and glycated total protein.

Average life span of these proteins is about 2-3 weeks. A reflection of the average glucose concentration over that
time.

The determination of fructosamine is the most commonly performed for the evaluation of glycemic control in

diabetes. Fructosamine values provide an indication of glucose levels over the preceeding 2-3 weeks, whereas for
glycated hemoglobin (HbA1c) it is 4-8 weeks.
Fructosamine is used as a method of evaluating the longer control therapies in diabetes and glucose levels in

conditions such as pregnancy.
Normal Levels
– Adults
–
Diabetic patients: greater than 2-5mmol/L

Nondiabetic patients: 1.5-2.7 mmol/l

– Child: 5% below adult levels
–
• A higher fructosamine value indicates poorer glycemic control.
•
• Fructosamine: Many proteins other than hemoglobin also undergo nonenzymatic glycation, leading to the formation
•
of advanced glycosylation end products, which may play a direct role in the development of diabetic microvascular
complications. The serum concentration of some of these proteins can also be used to estimate glycemic control. The term
fructosamine has been applied to the ketoamines formed in this process.
• Several methods are available for measuring serum fructosamine. Some of the assays are cheaper and easier to perform than
•
HBA1c assay
Glucose Sensitive Insulin Receptors (MAHE 2007)

• GLUT-1: Enables basal non insulin stimulated glucose uptake into many cells
•
• GLUT-2: Transports glucose into the beta cell: a prerequisite for glucose sensing
•
• GLUT-3: Enables non insulin mediated glucose uptake into brain neurons and placenta
•
• GLUT-4: Enables much of the peripheral action of insulin. It is the channel through which glucose is taken up into muscle
•
and adipose tissue cells following stimulation of the insulin receptor.
Diabetic Ketoacidosis: (MAN 2001)

• Hyperglycemia
•
• Hyperketonaemia
•
• Metabolic acidosis
•
• Hyperglycemia causes a profound osmotic diuresis leading to dehydration and electrolyte loss, particularly sodium and
•
potassium. Metabolic acidosis forces hydrogen ions into cells, displacing potassium ions.
• Insulin promotes movement of potassium into cells. Management of diabetic ketoacidosis includes IV infusion of soluble
•
insulin, IV 0.9% saline infusion and IV potassium supplements.
Cushing Syndrome/Hypercortisolism
Hypercortisolism should be suspected in the presence of:
• Hypertension of recent onset
•
• Dermal striae
•
• Easy bruisability
•
• Evidence of glucose intolerance (glycosuria)
•
324
Other manifestations of hypercortisolism include:

• Osteoporosis
•
• Muscle wasting
•
• Psychologic alterations
•
• Hirsuitism
•
• Granulocytic leukocytosis with lymphopenia

•
Conns Syndrome
• Hyperaldosteronism (COMED 2007, PGI 2005)
•

• Aldosterone increased
•
• Hypertension (PGI 2005)
•

• Sodium increased
•
• Potassium decreased (PGI 2005)
•

• Polyuria, polydypsia (PGI 2005)
•

• Weakness
•
• Proximal myopathy (PGI 2002)
•

Addison’s Disease NEUROMUSCULAR SYSTEM
Addisons disease is primary adrenocortical insufficiency.
Associated electrolyte abnormalities Mechanism of Pain Transmission
• Hyperkalaemia, hyponatraemia (PGI 1987)
•

• Hypoglycaemia occurs (AIPG 1990)
•

• Metabolic acidosis
•
Other Features
• 90% gland must be destroyed to manifest the disease
•
• Autoimmune cases are responsible for most cases
•
• Clinical signs include: fatigability, weakness, anorexia,
•
weight loss, cutaneous and mucosal pigmentation,
hypotension and hypoglycemia
• Most common cause in India is Tuberculosis of the gland
•

(AIIMS 2011)

• Pigmentation is usually increased except in adrenal
•
insufficiency secondary to pituitary failure. Increased
pigmentation is characterized by diffuse tanning of both
exposed and non exposed surface of the body, especially
on pressure points (bony prominence), skin folds, scars,
and extensor surfaces (PGI 1987) Nociceptors are activated by Nociceptors sensitized by

• Black freckles over the forehead, face, neck and shoulders; Potassium ions Prostaglandins
•
areas of vitiligo; and bluish black discolorations of the
Proteolytic enzymes Leukotrienes
areolae and of the mucous membranes of the lips, mouth,
rectum and vagina are common Serotonin NGF (never growth factor)
• In a patient with suspect Addisons disease, the definite
Bradykinin Substance P
•
investigation is a short ACTH test. Plasma cortisol is
measured before and 30 minutes after giving Synacthen Histamine Interleukin 1
250 µg IM. Adrenal autoantibodies such as anti – 21 TNF - α
hydroxylase may also be demonstrated. (MAHE 2007)

Acetylcholine
• Busulfan causes addisonian like features (PGI 1980)
•


Subdural Hematoma
Acute Chronic
• Duration Hematoma age is ≤ 3 years Hematoma is ≥ 3 weeks and a/w encapsulating membrane
•
• Age affected < 60 years; infrequent in children > 50 years, occurs in children of all ages
•
• Etiology High velocity acceleration deceleration head Adults: often from trivial head injury, may be forgotten Children:

•
 
injuries resulting in tearing of bridging veins unknown trauma, abuse or birth injury Balance between
between cerebral cortex and dural venous recurrent bleeding from hematoma membrane and resoprtion
sinuses; injury to surface of brain with bleeding determines ultimate size of hematoma
from injured cortical veins
• Associated Multisystem trauma Cervical spinal cord Alcoholism, Epilepsy, Coagulopathy, CSF shunt, Birth trauma,
•
 
conditions injury. Injury to thoracic, lumbar or cervical Child abuse
 
spine DIC
 
• Signs and Altered consciousness (99%), 1/3 may have a Slowed thinking, vague change in personality, headache
•
symptoms lucid interval; pupillary irregularity (ipsilateral (fluctuating in severity with changes in head position), mild
to hematoma); hemiparesis (contralateral to hemiparesis
hematoma); decerbrate posturing or flaccid
motor exam
• Imaging CT scan (with contrast if Hb< 9 mg%) Crescent CT scan (resolve from isodense to hypodense by 3 weeks)
•
shaped mass
• Treatment IV Mannitol to reduce ICP Emergency craniotomy IV Mannitol to reduce ICP Burr hole drainage
•
Types of Seizures
Type Clinical Involvement/EEG
• Simple partial Focal sensory (e.g., parasthesias, hallucinations) or motor Focal cortical region of brain
•
(e.g., repetitive or purposeless movement) activity, no loss of
consciousness; possible focal neurologic deficits lasting minutes
to hours after seizure (i.e., Todd paralysis) are common;
Jacksonian march; epilepsia partialis continua.
• Complex partial Hallucinations (e.g., auditory, visual, olfactory), automatisms Focal abnormalities in temporal lobe
•
(i.e., repeated coordinated movement), impaired consciousness,
postictal confusion
• Generalised convulsive Sutained contraction of extremities and back (tonic); repetitive Bilateral cerebral cortex involved;
•
• (Tonic-clonic, myoclonic, muscle contraction and relaxation (clonic); brief contraction period generalized EEG abnormalities
followed by repetitive contraction- relaxation (tonic-clonic); brief
•
atonic)
repetitive contractions (myoclonic); loss of tone (atonic); loss of
consciousness, incontinence, significant postictal confusion,
Bell’s Palsy
Most common form of • Idiopathic, i.e. Bell’s palsy.
•
facial paralysis
Clinically • Abrupt onset; maximal weakness being attained by 48 h as a general rule.
•
• Pain behind the ear may precede the paralysis for a day or two.
•
• Taste sensation may be lost unilaterally, and hyperacusis may be present.
•
• In some cases there is mild CSF lymphocytosis.
•
Pathophysiology • Bell’s palsy is a/w presence of HSV type 1 DNA in endoneurial fluid and posterior auricular muscle,
•
suggesting that a reactivation of this virus in the geniculate ganglion may be responsible. However, a
causal role for HSV in Bell’s palsy is unproven.
• An increased incidence of Bell’s palsy was also reported among recipients of inactivated intranasal
•
influenza vaccine, and it was hypothesized that this could have resulted from the Escherichia coli
enterotoxin used as adjuvant or to reactivation of latent virus.
326
Diagnosis • MRI may reveal swelling and uniform enhancement of the geniculate ganglion and facial nerve and, in
•
some cases, entrapment of the swollen nerve in the temporal bone.
• Approximately 80% of patients recover within a few weeks or months.
•
• Electromyography may be of some prognostic value; evidence of denervation after 10 days indicates
•
there has been axonal degeneration, that there will be a long delay (3 months as a rule) before
 
regeneration occurs, and that it may be incomplete.
 
D/D of facial palsy ••

Ramsay Hunt syndrome
• Leprosy
•
• Diabetes mellitus
•
• Connective tissue diseases including Sjögren’s syndrome
•
• Amyloidosis.
•
• Acoustic neuroma
•
• Lyme disease (uni or bilateral)
•
• Sarcoidosis and Gullain barre syndrome (bilateral)
•
• Melkersson-Rosenthal syndrome consists of recurrent facial paralysis; recurrent—and
•
eventually permanent facial (particularly labial) edema; and, less constantly, plication of the tongue.
 
Prognosis • The presence of incomplete paralysis in the first week is the most favorable prognostic sign.
•
Treatment • A course of glucocorticoids, given as prednisolone 60–80 mg daily during the first 5 days and then
•
tapered over the next 5 days, appears to shorten the recovery period and modestly improve the
functional outcome.
• A recently published randomized trial found no added benefit of acyclovir (400 mg five times daily for
•
10 days) compared to prednisolone alone for treatment of acute Bell’s palsy
Motor Neuron Lesions

Lower motor neuron Upper motor neuron
Lesions of facial nerve or its nucleus in the pons Lesion of intracranial portion proximal to pontine nucleus
Common causes Common causes

• Bell’s palsy • Cereberovascular accidents
•
•
• Herpes zoster infection (Ramsay Hunt Syndrome) • Tumours
•
•
• Parotid tumours • Demyelination
•
•
• Lesion in cerebellopontine angle
•
Presentation Presentation
• One half of the face is involved on the same side • Contralateral is involved.
•
•
(ipsilateral) of the lesion • The lower half of the face is involved as in lower motor neuron palsy whereas
•
• There is loss of muscles of facial expression the upper half of the face is spared as it has bilateral innervation.
•

• Absence of furrowing of face on the same side (COMEDK 2007)

•
• Inability to close ipsilateral eye
•
• Flattening of the angle of the mouth
•
• Deviation of mouth towards opposite side.
•
Clinical Sign Upper motor (pyrami- Lower motor lesion Extra pyramidal lesion Cerebellar lesion
dal lesion)
Power Weak Weak Normal Normal
Tone Spasticity (hypertonia) Flaccidity (hypotonia) Rigidity (cog wheel, lead Normal
pipe)
Wasting/Atrophy None Marked (cardinal feature) None None
Superficial reflexes Absent Absent Normal Normal

Clinical Sign Upper motor (pyrami- Lower motor lesion Extra pyramidal lesion Cerebellar lesion
dal lesion)
Deep tendon reflexes Exaggerated (KAR 1997) Absent/reduced Normal Normal
Plantar response Extensor (+ve Babsinki’s Flexor (normal or –ve Flexor Flexor
sign) Babsinki’s sign)

• Cerebellar lesions are characterized by: (AIIMS 2002) CENTRAL NERVOUS SYSTEM
•
– Intentional tremors
–
– Distance of targets misjudged resulting in past- CSF with raised protein and low glucose is seen in
–
pointing • Tuberculosis meningitis ( also lymphocytic)
•
– Impairment to produce rapid, accurate, regularly • Bacterial meningitis
–
alternating movements (dysdiadochokinesia)
•
• Malignant meningitis
– Ataxic gait
•
–
• Lewy body dementia is characterized by: (MP 2009) • In viral meningitis – glucose + protein content of CSF
•
•
• Progressive loss of ability to learn, retain and process is normal
•
new information (memory loss) • Herpes zoster most commonly affects the dorsal root
• Decline in language–difficulty in naming and in •
ganglion
•
understanding what is being said (various aphasia)
• Hypochondrial disorder is an anxious pre occupation
• Apraxia: Impaired ability to carry out skilled motor
•
with the possibility of having a serious physical illness
•
activities
• Agnosia: Failure to recognize objects (e.g. clothing), • With somatisation disorder, patients complains of
•
vomiting, pain, dizziness, headache which have no
•
placing or people
• Progressive loss of executive function–organizing, organic basis in disease
•
planning and sequencing • Somatoform pain disorder is used to describe severe,
•
• Behavioral change: Agitation, aggression, wandering persistent pain which cannot be explained by pathology
•
and persecutory delusions
• Loss of insight, relative or complete • Delusions are seen in:
•
•
• Depression: Though severe depression is unusual – Schizophrenia
•
–
because of loss of insight – Depressive illness
–
– Maniac depression
• Wernicke’s encephalopathy: There is involvement of
–
• Syringomyelia: Fluid filled cavities develops near the
•
brain characterized by ataxia, opthalmoplegia, confusion
•
centre of the spinal cord, slit like cavities may appear in
and disorientation
the medulla in association with syringomyelia, producing
• Korsakoff ’s psychosis: Develops due to involvement of
brain stem dysfunction (syringobulbia)
•
mammillary bodies and patient confabulates with loss of
memory • Lesions affecting the cord centrally: Syringomyelia
• Tongue deviation:
•
• Lesions affecting the posterior column: Tabes dorsalis,
•
– Affected side: Hypoglossal nerve paralysis
•
diabetic pseudotabes
–
– Opposite side: Facial nerve paralysis
• Lesions affecting the posterolateral columns:
–
• Lambert Eaton Myasthenic Syndrome (COMEDK
•
Subacute degeneration of spinal cord, subacute myelo
•
2008) optic neuropathy
– Characterized by muscle weakness due to impaired • Lesions affecting the complete cord transaction
–
transmission across the neuromuscular junction
•
(transverse myelopathy): Trauma, multiple sclerosis,
– Transmitter release is impaired with associated viral, Tb, transverse myelitis
–
antibodies to prejunctional voltage-gated calcium
• Parkinsonism is caused by depletion of the pigmented
channels
•
– Patients may have autonomic dysfunction (dry dopaminonergic neurons in the substantia nigra,
hyaline inclusions in the nigral cells (Lewy bodies) and
–
mouth) in addition to muscle weakness
– Cardinal clinical sign is absence of tendon reflexes atrophic changes in substantia nigra treated by DOPA
2 agonist.
–
– Treatment is done with 3-4 diaminopyridine.
–
328
• Triad of Parkinsonism: • Nucleus basalis of Meynert is effected (AIIMS 2011)
•
•
– Rigidity: – Features
–
–
Cogwheel type of rigidity in upper limbs – Aphasia

–
Lead pipe type of rigidity in lower limbs – Amnesia

–
– Bradykinesia – Agnosia
–
–
– Tremor at rest – Acalculia
–
–
• Intracerebral/Parenchymal hemorrhage–due to – Alexia
–
• There is reduction in Acetylcholine concentration
•
hypertension causing rupture of small arteries or
•
arterioles. Most common site is putamen (basal ganglia) • Presenile dementia occurs before 60 yrs of age
•

• Subarachnoid hemorrhage – due to spontaneous rupture (PGI 1991)
•

of berry aneurysm. Most common of berry aneurysm is • Associations with
anterior circulation of circle of Wills.
•
– Downs Syndrome, APP (Amyloid precursor
• Epilepsy, mental retardation and cutaneous angiofibromas
–
protein gene on chromosome 21)
•
are characteristics of tuberous sclerosis
• The sensory motor cortex is located on the labial surface – Presinilin 1 on chromosome 14
–
– Presinilin 2 on chromosome 1
•
of the cerebral hemisphere and is supplied by middle
–
cerebral artery. Occlusion of the middle cerebral artery • Treatment is by Tacrine, Donepezil, Memantine
•
thus produces contralateral hemiplegia and contralateral • •
Neurofibrillary tangles are intracytoplasmic
hemisensory loss filamentous inclusion found in Alzheimer disease and,
to a lesser extent, in normal aging brains. They usually
• Areas of the cerebral cortex involved in the generation
appear Intracellularly first (AIIMS 2011)
•
of the spoken language are Broca’s and Wernicke’s area

• Lesion in the Broca’s area (inferior frontal gyrus):
•
Causes motor aphasia Bulbar Palsy
• Lesion in the Wernicke’s area (supramarginal gyrus): • B/L LMNL of 9,10,11,12 Cranial nerves
•
•
Causes receptive, sensory aphasia • Features:
•
• Motor aphasia is a disorder of thought and word finding – Dysarthia
•
resulting in inadequate verbal expression
–
– Dysphagia
–
– Dysphonia
Five anatomically defined large scale networks are
–
most relevant: Pseudo Bulbar palsy
• A perisylvian network for language • B/L UMNL of 9,10,11,12 Cranial Nerves
•
•
• A parietofrontal network for spatial cognition Syringobulbia
•
• An occipitotemporal network for face and object • Facial pain/sensory loss
•
recognition
•
• Facial palsy
• A limbic network for retentive memory
•
• Vertigo, Nystagmus, Horner’s syndrome
•
• A prefrontal network for attention and behavior
•
•
Characterstic disturbance of gait and posture
Alzhiemers Disease
Associated with:
• Most common cause of dementia in elderly • On – Off phenomenon
•
• Cortical Dementia not subcortical dementia
•
• Decreased blinking
•
•
•
Causes brain atrophy in advanced cases • Symptoms of parkinson’s disease are caused by loss of
•
• Atrophy usually involves frontal, temporal and
•
nerve cells in the pigmented substantia nigra pars
•
parietal lobes compacta and the locus coeruleus in the midbrain
• Neurofibriallary tangles, Neuritic plaques, Parkinsonism can be induced by primates by exposure
•
Granulovascular degeneration, Hirano bodies are to 1-methyl-4-phenyl-1,2,3,6, - tetrahydropyridine
pathological features (MPTP)

INFECTIONS
• The serum of a patient who has received recombinant hepatitis B vaccine is positive for Hepatitis B surface antibody (anti
•
HBs)
• Best means of giving hepatitis B vaccine is intramuscular deltoid.
•
• In serological tests for detection of HIV an early positive ELISA is due to p24 antigen
•
• First sensation to be lost in leprosy is temperature.
•
• Group of viruses that inhibit the alimentary tract of children below 2 years of age is Coxsackie virus
•
• Pastia’s lines are transverse red streaks in skin folds seen in scarlet fever
•
• Minimum period required for post exposure chemo prophylaxis for HIV is 4 weeks
•
• Rubella (german measles)(AIPG 2001)
•
– in early pregnancy causes congenital deformities,
–
– transmitted by aerosol infection
–
– complications include pneumonia, encephalitis and otitis media
–
• Hepatitis E virus:
•
– Epidemics are exclusively caused by it
–
– Pregnant women are particularly liable to acute hepatic failure
–
• Bacterial infections causes neutrophilia
•
• Viral infections–lymphocytosis
•
• Parasitic infestations–eosinophilia
•
• Neutropenia is seen in
•
– Typhoid,
–
– Viral infections,
–
– Protozoal infestions,
–
– Agranulocytosis,
–
– Drugs
–
Incubation Period
Disease Incubation period
Short Anthrax 2 – 5 days
Diphtheria 2 – 5 days
Scarlet fever 1 -3 days
Typhoid 5 days
Cholera 2- 3 hours
Intermediate Measles 7 – 14 days (10days)
Mumps 2-3 weeks (18days)
Rubella 2 – 3 weeks (18days)
Chicken pox 14 – 21 days
Long Hepatitis A 2 – 6 weeks (4 weeks)

Hepatitis B 6 weeks – 6 months (12 weeks)
Tuberculosis Months – years
Leprosy 2 – 5 years
330
Surgical Infections • Chlorambucil is the drug of choice in chronic lymphocytic
•
leukemia whereas Busulfan, hydroxyl carbamide are drugs
• Cellulitis: Non suppurative spreading inflammation of choice in chronic myelocytic leukemia. (AIPG 1996)
•
of subcutaneous and fascial planes mainly due to • The gold standard for the diagnosis of osteoporosis is dual
•
Streptococcus pyogens energy X-ray absorptiometry (DXA) and the preferred
• Impetigo (Pyoderma): Is a superficial infection of the sites are the lumbar spine and lips.
•
skin caused mainly by group A streptococci
• Courvoisier’s sign: A palpable gall bladder in jaundiced
•
• Erysipelas: Is spreading inflammation of skin and patient usually is the consequence of distal biliary
•
subcutaneous tissue due to streptococcus pyogenes. obstruction by a pancreatic cancer.
• Boil (Furuncle), Folliculitis: Is an acute staphylococcal
• Conditions with decreased LAP (leukocyte alkaline
•
infection of hair follicle with perifolliculitis
•
• Hidradentis suppurativa: Is chronic infection of the phosphatase) scores are:
•
apocrine sweat glands involving group of follicle – Paroxysmal nocturnal hemoglobin
–
• Carbuncle: Infective gangrene of the skin and – Chronic myeloid leukemia
–
•
subcutaneous tissue mainly due to staphylococcal • Conditions with increased LAP scores are:
infection. Commonly seen in diabetic and
•
immunocompromised patients. – Polycythemia
–
– Leukamoid reaction
–
• Eczema or atopic dermatitis: ‘Monk’s cow rash’ over face – Infection
–
•
and neck – Myelofibrosis
–
• Pellagra: Sunburn rash or necklace rash
•
• Bromide poisoning: Acne form rash Most Common Complication of
•
• Forcheimer spots: Rubella (soft palate) In children In adults
•
• Herbedens nodes: Osteoarthritis
Measles Acute suppurative Bronchopneumonia
•
• Scrofula: Direct extension of the tuberculosis from otitis media
•
underlying focus like lymph node, bone or muscle. (JIPMER 1986)
• Pott’s disease: Tb spine
Mumps Aseptic Meningitis Orchitis, oophorotis
•
• Most common nerve involved in intracranial aneurysm
•
– III CN Rubella Arthalgia
• Bilateral facial palsy is seen in Gullian Barre Syndrome, Chicken pox CNS Complications Interstitial Pneumonia
•
Sarcoidosis and Melkerson–Rosenthal syndrome Secondary bacterial
• Neuropathic joint is seen in Diabetes mellitus, infections of skin
•
syringomyelia, Tabes dorsalis
Meningococcal Water house
• Osteosclerosis of the vertebral bodies is known as ‘Rugger Meningitis Fredickson
•
Jersey Spine’ seen in renal osteodystrophy
Pertussis Pneumonia Bronchopneumonia
• Cysts in polycystic kidney disease may be seen in:
•
– Liver Not a Complication of
–
– Spleen
–
– Pancreas Measles • Aspetic Meningitis
–
•
– Ovaries • Optic neuritis
–
• Important enzymes reflecting cholestasis:
•
• Pancreatitis
•
•
– alkaline phosphatase • Pneumonia
Mumps
–
– 5’ nucleotidase
•
• Appendicitis
–
– Gamma glutamyl transpeptidase
•
–
Chickenpox • Enteritis
•
• Thalassemia major: Anemia, splenomegaly, and • Pancreatitis
•
structural defects
•
Diptheria • Vertigo
• Aleukemic leukemia: The condition in which patient
•
• Myocarditis
•
present with normal and WBC in the peripheral blood. Pertussis
•
• Bacterial Endocarditis
• Addison’s disease is due to hemorrhage in adrenal cortex.
•
•
• Acid phosphatase is associated with monocyte. Pneumonia • Amyloidosis
•
•

Prion Diseases
• Prions are a unique class of infectious proteins associated with a group of neurodegenerative diseases, the transmissible
•
spongioform encephalopathies
• In humans, these diseases include
•
– Kuru
–
– Creutzfeldt-jakob disease

–
– Gerstmann-Straussler-Scheinker syndrome and
–
– Fatal familial insomnia
–
• In animals
•
– Scrapie and
–
– Bovine Spongioform encephalopathy (mad cow Disease)
–
ELECTROLYTE AND FLUID BALANCE
Unilateral Edema
• Painless
•
– Onset
–
From birth: Milroy’s disease

Late onset: Filariasis

• Painful
•
– Involves only big toe with Tophi: Gout
–
– Part of the limb affected and painful: Cellulitis
–
– Involves the whole limb
–
Linear and streaks

- Present: Filariasis

- Absent: Venous thrombosis

• Hereditary spherocytosis is associated with defect in reduced cell membrane protein ‘spectrin’ or ankyrin resulting in
•
hemolytic anemia. Osmotic fragility is increased in spherocytosis.
• Cardinal signs of respiratory arrest is apnea
•
• Tracheal shift to opposite side is seen in pleural effusion
•
• Ectopic ACTH is most commonly produced by CA lung
•
• Uveoparotitis is seen in Sarcoidosis
•
• Non caseating granuloma with bilateral hilar lymhadenopathy: Sarcoidosis
•
• Cytosolic cytochrome C is associated with apoptosis
•
• Angina lasts only for 3 -4 minutes, longer is myocardial infarction
•
• MI usually due to thrombus and often results in mitral regurgitation
•
• Piecemeal necrosis is seen in chronic active hepatitis
•
• α-hydroxylase deficiency affects the release of glucocorticoids
•
• Mee’s lines in the nails are characteristic of arsenic poisoning
•
• Enteropathy refers to the inflammation of ligamentous attachments of adjacent erosion of bone.
•
Causes of Elevated Alkaline Phosphatase
Bone derived ALP Liver derived ALP Miscellaneous conditions
Elevation suggests increased bone • Cholestric liver disease • Hodgkin’s disease
•
•
turnover/increased osteoblastic activity • Infiltrative liver disease • Hyperthyroidism
such as:
•
•
• E.g. cancer • Congestive heart failure
• Paget’s disease
•
•
• Diabetes
•
• Rickets and osteomalacia
•
•
332
Acid–Base Disorders (MAN 1994, 1995)

Condition pH Pa CO2 Bicarbonate Compensation
Metabolic acidosis Reduced -- Reduced Hyperventilation – reduction PaCO2
Metabolic alkalosis Increased -- Increased Hypoventilation – increase in PaCO2
Respiratory acidosis Reduced Increased -- Renal retention bicarbonation increases

Respiratory alkalosis Increased Reduced --- Renal excretion – bicarbonate increased
Causes of metabolic acidosis Causes of metabolic alkalosis

• Diarrhea • Vomiting
•
•
• Hypovolemic shock • Diuretics
•
•
• Starvation • Chronic respiratory failure
•
•
• Alcoholism • Aldosteronism
•
•
• Diabetic ketoacidosis • Cushings syndrome
•
•
• Lactic acidosis
•
• Chronic renal failure
•
• In edema fluid: Sp. Gravity < 1.012 (in transudate), > 1.020 (in exudates)
•
• In effusion fluid: Sp. Gravity < 1.016 (in transudate)
•
• In hydatid fluid: Sp. Gravity is 1.005 – 1.009
•
• Hallmark of an exudative fluid are: Proteins > 50% of serum level (3.0g/dl), LDH > 2/3rd of Serum level
•
• Ascites due to portal hypertension can be diagnosed with 95% certainity by calculating SAAG ie Serum ascetic albumin
•
gradient. Value greater than 1.1 is indicative of portal hypertension as cause of ascites
Mineral Associated Diseases

Zinc
• Integral component of many metalloenzymes in body
•
• Involved in the synthesis and stabilization of proteins, DNA and RNA and plays a structural role in ribosomes and
•
membranes
• Necessary for the binding of steroid harmone receptors and several other transcription factors to DNA and thereby plays
•
an important role in the regulation of gene transcription
• Absolutely required for spermatogenesis, Fetal growth and embryonic development
•
Deficiency of Zinc
Mild Chronic Severe Chronic
• Diabetes • Stunted growth in children Acrodermatitis Enteropathica Syndrome
•
•
• AIDS • Decreased taste sensation • Hypogonadism
•
•
•
• Cirrhosis • Impaired immune function • Dwarfism
•
•
•
• Alcoholism • Night blindness • Hypopigmented hair
•
•
•
• Inflammatory Bowel Disease
•
• Malabsorption Syndrome
•
• Sickle Cell anemia
•
• Ocular manifestations
•
– Photophobia
–
– Conjunctivitis
–
– Blepharitis
–
– Corneal dystrophy
–

• Associated symptoms
•
– Chronic Diarrohea
–
– Stomatitis
–
– Glossitis
–
– Paronychia
–
– Nail Dystrophy

–
– Growth retardation
–
– Irritability
–
– Delayed wound healing
–
• The diagnosis of zinc deficiency is usually made by decreased serum zinc level
•
• Pregnancy and birth control pills may slightly cause a slight depression in serum zinc levels, and hypoalbuminemia from
•
any cause can result in hypozincemia
Copper
• Dietary copper deficiency is relatively rare, although it has been described in premature infants fed milk diets and in infants
•
with malabsorption
• Signs and symptoms of Copper deficiency include
•
– A hypochromic–normocytic anemia
–
– Osteopenia
–
– Depigmentation
–
– Mental retardation and
–
– Psychomotor abnormalities
–
Selenium
Keshan’s disease is an endemic cardiomyopathy found in children and young women residing in regions of china where
dietary intake of selenium is low. Low blood levels of selenium in various populations have been correlated with an increase
in coronary artery disease and certain cancers.
Chromium
• Chromium potentiates the action of insulin in patients with impaired glucose tolerance, presumably by increasing insulin
•
receptor mediated signaling.
• Chromium deficiency has been reported to cause glucose intolerance, peripheral neuropathy, and confusion
•
Magnesium
Magnesium deficiency is a common clinical problem
• Reduced renal reabsorpation due to loop diuretics and alcohol use is a common cause of hypomagnesemia
•
• Vomiting and nasogastric suctioning, fluid loss from diarrohea.
•
• Hypomagnesemia is prevalent in alcoholics
•
• The clinical manifestations of hypomagnesemia are similar to those of severe hypocalcemia
•
The signs and symptoms of hypomagnesemia include
• Muscle weakness
•
• Prolonged PR and QT intervals
•
• Cardiac arrhythmias
•
• Positive Chvosteks sign and trousseau’s sign
•
• Carpopedal spasm can also occur with hypomagnesemia
•
334
Deficiency of Minerals
Iron deficiency Microcytic anemia
• Iodine • Goitre
•
•
• Zinc • Acrodermatitis Enteropathica
•
•
• Copper • Menkes disease
•
•
• Selenium • Cardiomyopathy
•
•
• Chromium • Impaired glucose tolerance
•
•
Arsenic Related Disease
Chronic arsenic exposure has been linked to many cancers. Most common are
• Basal Cell carcinoma
•
• Squamous cell carcinoma
•
• Angiosarcoma of liver
•
• Lung Ca
•
• Kidney Ca
•
• Colon Ca
•
• Non cirrohotic portal fibrosis is a medical condition associated with Arsenic exposure
•
Good to Know
• Wadding gait is seen in muscular dystrophy
•
• Hutchinson’s pupil is unilateral constricted pupil
•
• Globus pharyngeus is the sensation of a lump lodged in the throat
•
• Cysts in the polypeptide disease may be seen in:
•
– Liver
–
– Spleen
–
– Pancreas
–
– Ovaries
–
• Torres inclusion body may be found in yellow fever
•
• A characteristic feature of organic laryngeal paralysis is cow like cough
•
• Malignant disease + acute pancreatitis–increased levels of amylase in the pleural fluid than in serum
•
• Liver is most likely to be injured if excessive pressure is applied directly over xiphoid process during cardiac massage
•
• Severity of mitral stenosis is assessed by the length of murmur
•
• Leukocyte adhesion deficiency type I is seen in chromosome 1.
•
• The terminology of cytoplasmic ANCA (cANCA) refers to the diffuse, granular cytoplasmic staining pattern observed
•
by immunofluorescence microscopy when serum antibodies bind to indicator neutrophils. Proteinase 3, 29 kDa neutral
serine proteinase present in neutrophil azurophilic granules, is the major c-ANCA antigen.
• The most potent stimulator of native T cells is mature dendritic cell.
•
• Notching in ribs in Xrays–coarctation of aorta
•
• The most common site of cerebral hemorrhage in hypertension–cerebrum
•
• Polycythemia is seen in cor pulmonale
•
• Severe metabolic acidosis is clinically manifestated as hyperventilation or Kussmaul’s breathing – due to presence of H+ ions.
•
• Infection of terminal pulp is called as felon
•

• The technique where irradiation is from outside the patient is called as Tele therapy
•
• Saddle back type of temperature is seen in dengue fever
•
• Bradycardia is a resting pulse less than 60 per minute
•
• The cardinal symptom of MI is pain
•
• Progressive lengthening of successive PR interval followed by a dropped beat is called as Wenkebach’s phenomenon.
•
• Left anterior descending coronary artery is called widow’s artery
•
• Breathing accompanied by conscious effort is known as Dyspnoea
•
• Drug of choice in tropical pulmonary eosinophilia is diethyl carbamazine
•
• Normal pulse respiration ratio is 4:1
•
• The most common early symptom of bronchial carcinoma is cough
•
• Most common lymph nodes involved in Tb lymphadenitis is cervical
•
• Abrupt loss of consciousness associated with persistent bradycardia, ventricular asystole secondary to atherosclerosis is
•
called as Stokes Adams syncope.
• In status epilepticus the drug of choice is IV diazepam
•
• Vomiting centre and chemo receptor trigger zone (CTZ) are situated in medulla.
•
• The first symptom of tetanus is trismus
•
• In immunization schedule recommended by WHO for developing countries, the no. of oral polio vaccination doses for
•
infant is four
• Normal iron requirement per day in pregnancy is 3.5g (AIPG 2014)

•

• A healthy mother with a healthy child should start artificial feeding by 5-6 months
•
• A person is obese if he is overweight by 10% above the accepted standards.
•
• One litre of cow’s milk provides 1200 mg of calcium.
•
• The ratio of casein to albumin in human milk is 1:1
•
• Total number of tablets of iron with folic acid is given to pregnant women by a health worker is 100
•
• Commonest STD in India is gonorrhea
•
• The percentage of polymorphonuclear leukocytes which shows barr body in females is 3%.
•
• Commonest autosomal recessive disorder is cystic fibrosis.
•
• The first symptom of heart failure–Dyspnoea
•
• Both central and peripheral cyanosis occurs in congestive cardiac failure.
•
• Normal cardio thoracic ratio should be less than 0.5 in radiographic examination.
•
• Commonest cause of ventricular tachycardia is acute myocardial infarction. Treatment is by IV lignocaine.
•
• Saphenous vein is used in coronal by pass grafting.
•
• Calcification of ascending aorta is seen in cardiovascular syphilis
•
• Egg shell calcification in the hilar lymph nodes is a distinctive feature of silicosis
•
Commonest causative organism
• Boil • Staphylococcus
•
•
• Carbuncle • Staphylococcus
•
•
• Sinusitis • Pneumococcus
•
•
• UTI • E.coli
•
•
• Infection in burns • Pseudomonas
•
•
336
• Croup • Parainfluenza virus

•
•
• Pathogenic yeast • Cryptococcus
•
•
• Spread by auto infection • Tapeworm and Enterobiasis
•
•
• Acne • Corneybacterium acnes
•
•
• Commonest STD • Non gonococcal urethritis
•
•
• Common infective disease • Common cold
•
•
• Glandular fever • Epstein barr virus
•
•
• Scarlet fever • Streptococcus
•
•
• Colour blindness:
•
– Protanopes–Red blindness
–
– Deutanopes–Green blindness
–
– Tritanopes–Blue blindness
–
• Universal antidotes:
•
– Charcoal (powdered)
–
– Tannic acid (precipitate)
–
– Magnesium oxide (adsorbs toxin)
–
– Alkaloids, metal and glucosides
–
WOUND TISSUE AND REPAIR
Thrill
• Three fingers are placed on a swelling, the middle one being pressed firmly and the lateral ones lightly. The middle one is
•
percussed firmly, and after each stroke, the percussing finger is allowed to rest momentarily. The thrill felt by the adjacent
fingers confirms the presence of fluid under pressure.
– Sign of compression: When the swelling is compressed, it diminishes in size considerably or disappears. When the
–
pressure is released it refills slowly. Characteristically the sign is related to vascular swellings.
– Sign of indentation: Certain cysts containing putty like material can be moulded – thus the finger indents the
–
swelling.
– Sign of an aneurysm: Difficulty can be encountered in deciding whether the pulsation of a swelling is transmitted
–
or whether the swelling itself is pulsating. If the swelling is expansile and pushes the fingers apart, then it is an
aneurysmal swelling, while if the swelling is deflected by the pulsation, it is transmitted.
Crepitus • Crepitus of subcutaneous emphysema

•
• Term used in a variety of conditions but in each having a – It is due to gas in tissues
–
– Here a peculiar crackling sensation is imparted to the
•
fundamental diagnostic importance.
–
examining fingers
• Bone crepitus is noted as a coarse grating on the
– It is due to the trauma when gas is released into the
•
movement of a bone- it is very painful to the patient, and
–
an unmistakable diagnosis of a fracture of bone. tissues after a rib fracture or damage to the esophagus,
or due to gas forming organisms as in gas gangrene.
• Placing one hand on a joint and passively moving the joint
•
with the other hand elucidate joint crepitus: fine, evenly Types of Wound
spaced crepitations are present in many subacute and
chronic joint conditions. Wound may be closed or open
• Coarse, irregular crepitations signify osteoarthritis. • Closed: Bruise or contusion (AP 2000)
•

•
• Crepitus of tenosynovitis: found over an inflamed tendon • Open: Laceration, abrasion, avulsion
•
•
sheath when effusion has occurred into the sheath. • Combination: Crush
•

Contusion or bruise or • Produced by impact from blunt Skin grafts may be
•
hematoma object
• Full thickness: Consists of epidermis as well as full
•
Abrasion (AIIMS 2008) • Injury of skin in which the surface thickness of dermis
•
is rubbed off. Most are superficial
and will heal by epithelialization. • Split/partial thickness: Consists of epidermis and a
•
varying thickness of dermis. Types of split thickness
Laceration • Shallow or deep wound in the
grafts (KAR 2008)

•
mucosa caused by a sharp object

Avulsion • Avulsion injuries are open injuries – Thin: 0.008 to 0.012 inches or 0.2 to 0.3 mm
–
– Medium: 0.012 to 0.018 inches or 0.3 to 0.45 mm
•
where there has been a severe
–
degree of tissue damage – Thick: 0.018 to 0.030 inches or 0.45 to 0.75 mm
–
• Such injuries occur when hands • Split /partial thickness are also called as Thiersch
•
or limbs are trapped in moving
•
machinery, such as in rollers, grafts.
producing a degloving injury
Crush injuries • Further variant of blunt injury Keloid Scars

•
and are often accompanied by
degloving and compartment • A scar is the inevitable consequence of wound repair. Also
•
syndrome known as keloid. (AIPG 1993)

• Biologically identical to hypertrophic scars that in turn is
The most useful classification from the practical point
•
an extension of normal scar behavior.
of view is by Rank and Wakerfield into tidy and untidy
wounds. • More frequent in Afro-Caribbean and oriental racial
•
groups.
Tidy wounds Untidy wounds • Occur in wounds that healed perfectly without
•
• Tidy wounds are inflicted • Untidy wounds result from complications.
•
•
by sharp instruments and crushing, tearing, avulsion, • More common in certain sites such as the central chest,
contain no devitalized vascular injury or burns and
•
tissue contain devitalized tissue. the back and shoulders and the ear lobes.
• Such wounds can be • Such wounds must not be • Many keloid scars are untreatable and surgical treatment,
•
•
•
closed primarily with closed primarily as a single modality will usually be met with recurrence.

the expectation of quiet
(COMEDK 2005)
primary healing.

• Examples: surgical • Some keloid scars will improve with the application of
•
•
incisions, cuts from glass pressure.
and knife wounds
• Treatment:
• Skin wounds will usually
•
– Intralesional injections of steroids such as
•
be single and clean cut
–
• Fractures are uncommon • Usually associated with open triamcinolone can be helpful
•
•
in tidy wounds fractures – The best cure rates are achieved with a combination of
–
• The correct management of untidy wounds is wound surgery and post-operative interstitial radiotherapy.
•
excision, which means excision of all devitalized tissue
to create a tidy wound. Once the untidy wound has Fluid Replacement
been converted to a tidy wound by the process of wound
• Hypotension manifests when blood loss exceeds 30%
excision, it can be safely closed (or allowed to heal by
•

(COMEDK 2007)
second intention)

• Burri and coworkers reported a correlation between the
• The most important step in the management of any untidy
•
magnitude of blood loss and systolic blood pressure.
•
wound is wound excision. This process is sometimes
called ‘wound toilet or debridement’ • Most patients who lost less than 25% of blood volume
•
had systolic pressures approximately 110 mmHg
• The former implies washing and the latter laying open
• Subjects with estimated blood loss of 25% to 33% had
•
or fasciotomy, all of which may be important in wound
•
management. systolic pressures under 100mm Hg, cellular perfusion
restored before irreversible damage to cell biochemical
• Golden period for the treatment of open wounds is first
pathway occurs.
•
6 hours.
338
• Patients who lose over 40% of their blood volume develop profound hypotension, without blood flow to the brain,
•
syncope occurs, followed within minutesby cardiopulmonary arrest.
• The rate of transfusion depends upon the patent’s status. Usually 5ml/min is administered for the first minute, after which
•
10 to 20 ml/min is given.
• Where there is marked oligemia, 500ml can be given within 10 minutes and a second 500ml also can be given 10 minutes.
•
As much as 1500ml/min can be given through two 7.5 F catheters.
• Massive transfusion usually defined as the transfusion of blood products that are greater in volume than a patient’s
•
normal blood volume in less than 24 hours.
• The term massive transfusion implies a single transfusion greater than 2500 ml or 5000ml transfused over a period of 24
•
hours.
• Best indicator of fluid replacement following acute blood loss is pulmonary capillary wedge pressure (PCWP) and next is
•
central venous pressure (CVP) (KAR 1997)

– The PCWP is a better indicator of both circulating blood volume and left ventricular function
–
– It is obtained by a pulmonary artery floatation balloon catheter (Swan- Ganz)
–
– Pulmonary artery catheters determine central venous pressure (CVP) and pulmonary artery wedge pressure (PCWP).
–
– The internal jugular and subclavian veins are usually cannulated.
–
– Central venous pressure monitoring is used as one criterion for assessing fluid management in patients with unclear
–
volume status.
• Blood is stored in blood banks at 4oC ± 20C
•
• Cold citrate – containing blood undergoes changes during storage
•
• When blood is stored, changes occur over time, including leakage of intracellular potassium, decrease in pH, reduced
•
levels of intracellular adenosine triphosphate and 2,3 DPG in the RBCs with increased affinity of hemoglobin for oxygen,
degeneration of functional granulocytes and platelets, and deterioration of factors V and VIII. As a result blood is acidic
with decreased oxygen carrying capacity and poor red cell deformity.
– WBC – rapidly destroyed
–
– Platelets – survive upto 24 hours
–
– The shelf life of stored blood is 3 weeks
–
Preparation of Blood Components
• Component therapy is the accepted standard for the optimal management of the blood supply
•
• Blood is separated into its individual components (packed RBCs, plasma, and platelets) to optimize therapeutic potency.
•
• Blood is withdrawn from the donor and mixed with a citrate solution to prevent coagulation by binding calcium.
•
• Commonly used solutions for this purpose:
•
– Citrate phosphate dextrose (CPD)
–
– Citrate phosphate double dextrose (CP2D)
–
– Citrate phosphate dextrose adenine (CPDA-1)
–
• Solutions to extend storage life of cells contain some combination of dextrose, adenine, sodium chloride, and either
•
phosphate (AS-3) or mannitol (AS-1 and AS -5)
– The unit is gently centrifuged to pack the RBCs and leave about 70% of the platelets suspended in plasma.
–
– The platelet rich plasma is removed and centrifuged again at a faster speed to precipitate the platelets. All but 50ml
–
of supernatant plasma is removed and rapidly frozen at less than -300C. the platelets are resuspended to yield platelet
concentrate.
– Frozen plasma that is stored at less than -180C is termed as fresh frozen plasma.
–
– If the frozen plasma is allowed to thaw at 40C, the precipitate that remains can be collected to yield cryoprecipitate.
–

Blood Components
Components Properties Indications
• Red cell components Red cell components must be compatible with To increase circulating red cell mass to relieve clinical
•
the patient’s ABO blood groups features caused by insufficient oxygen delivery in
patients with low Hb levels
• Whole blood 450ml donor blood collected into 63 ml Stored at 2-6°C. shelf life upto 5 weeks. Contains

•
anticoagulant/preservative solution fibrinogen, other coagulation factors and plasma as
a colloid volume expander. Whole blood is suitable
for replacement of acute blood loss but red cell
concentrates plus colloid or crystalloid are acceptable
alternatives.
• Red cell concentrate Most of the plasma removed and replaced with a Some restrictions on use in infants, otherwise suitable
•
solution to optimize preservation of red cells for any patient requiring red cell replacement.
• Platelet concentrate One adult dose is made from four or five Treatment of bleeding due to thrombocytopenia and
•
donations of whole blood, or from a single some forms of platelet dysfunction. Prevention of
platelet apheresis procedure. Stored at 20-24°C bleeding due to thrombocytopenia in bone marrow
and must be agitated. Shelf life upto 5 days from failure.
collection. Platelets more effective if compatible
with patient’s ABO type. Plasma in group O
platelets can hemolyse red cells of group A
patient.
• Plasma (Fresh frozen 150-300 ml plasma obtained from one donation Replacement of coagulation factor deficiency if a
•
plasma, FFP) of whole blood. Shelf life upto 1 year. Should suitable licensed virus inactivated product is not
be compatible with patient’s ABO type. Group available, e.g. multiple coagulation deficiencies in
O plasma particularly is at risk of causing major haemorrhage.
haemolysis in a group A patient. Therapy of thrombotic thrombocytopenic purpura: by
infusion or plasma exchange.
• Virus inactivated plasma Obtained from a pool of donors’ plasma treated Indications as for FFP
•
with solvent and detergent, or from single
donations treated with methylene blue and light.
• Cryoprecipitate High molecular weight proteins are modestly Replacement of fibrinogen if a suitable licensed virus-
•
concentrated from plasma by precipitation near inactivated plasma derivative is not available. Used
freezing point. Each 10-20ml pack of precipitate for von willebrand disease and hemophilia if virus
contains fibrinogen, factor VIII and von Willebrand inactivated or replacement products not available.
factor.
Styptics
• Local hemostatic agents used to stop bleeding from a local approachable site. Styptics are particularly effective on oozing
•
surface. E.g. tooth socket, open wounds. (AP 2001)

• Examples
•
– Thrombin
–
– Fibrin
–
– Gelatin form
–
– Russels viper venom
–
– Vasoconstrictors like adrenaline
–
– Astringents like tannic acid.
–
BURNS – In adults:
–
Each upper extremity and the head and neck are

• Rule of nines 9% of the total body surface area (TBSA)
•
The lower extremities and the anterior and
– Alexander Wallace introduced ‘rule of nines’ for the

posterior trunk are 18% each.
–
determination of burn size and estimate the extent of The perineum and genitalia are assumed to be 1%
injury. (KAR 2007)

of the TBSA

340
– The berkow formula is used to accurately determine (which heal spontaneously) and full – thickness burns
–
burn sizes in children. requiring skin grafting.
Children have a relatively larger portion of the
• Survival after burn depends on the patients age and

body surface area in the head and neck, which is
•
percentage of burn
compensated for by a relatively smaller surface
area in the lower extremities. • A rapid loss of Intravascular fluid and proteins occurs
•
Infants have 21% of TBSA in the head and neck and through the heat injured capillaries. The volume loss

13% in each leg, which incrementally approaches is greatest in 6-8 hr, with capillary integrity returning
the adult proportions with increasing age. towards normal by 36-48 hrs.
Burns • The inflammatory response is cytokine mediated.
•
• Classification and outcomes after burn are based on Secretion of stress hormones ie catecholamines, cortisol,
glucagons, rennin – angiotensin and ADH is increased.
•
the Depth of burn. Classified as partial thickness burns
Classification
Class Depth of burn Characterstic Treatment and outcome
• Superficial Epidermis Erythema Heals spontaneously without scarring
•
• Partial thickness Epidermis + upper dermis Blisters Heals spontaneously with minimum scarring
•
Epidermis + Lower Dermis Require excision and grafting
• Full thickness Destruction of Epidermis + Leathery, painless (loss of Require excision and grafting, some scarring and loss
•
dermis sensation) of function
• Deep Skeletal muscle, fascia, bone Complete excision, limited function

•
• Split thickness grafts are used when the burns are extensive and split thickness graft can be extended 1.5 to 9 times the
•
original donor site by process of meshing.
• Full thickness grafts are particularly important to cover small areas like tip of nose, lips, eyelids where aesthetics is important.
•
• Lactated Ringer’s solution without dextrose is the fluid of choice except in children younger than 2 years, who should receive
•
5% dextrose Ringer’s lactate.
• The initial rate can be rapidly estimated by multiplying the TBSA burned by the patient’s weight in kilogram and then
•
dividing by 8. Thus the rate of infusion for an 80kg man with a 40% TBSA burn would be 80 kg X 40% TBSA/8 = 400ml /hr.
• Resuscitation formula:
•
Method Crystalloid Colloid Free water
• Parkland 4ml/kg/% TBSA burn None None
•
• Brooke 1.5ml/kg/% of TBSA burn 0.5ml/kg/% of TBSA burn 2.0 l
•
• Galveston 5000ml/m2 burned = 1500 None None
•
ml/m2 total for maintenance
in the first 24 hr
• Parenteral fluid
•
Parenteral fluid Constituents Use
• Plasma, albumin 4.5% Albumin, Na, K, Cl, bicarbonate Severe burns
•
• Dextrose 5% Low Na and K concentration Post operative period when sodium excretion is reduced
•
• Isotonic saline 0.9% High concentration of Na and Cl Vomiting, gastric or duodenal aspiration
•
• Ringer’s lactate (Hartmann’s Contains Na, K, Cl in the Hypovolemic shock
•
solution) (MAN 1995) concentration similar to plasma


• Depth of burns: the depth of burn varies depending upon the degree of tissue damage. Burn depth is classified into degree
•
of injury in the epidermis, dermis, subcutaneous fat and underlying structures.
– First degree burns are by definition, injuries confined to the epidermis. These burns are painful, erythematous, and
–
blanch to the touch with an intact epidermal barrier.
– Second degree burns are divided into two types: superficial and deep. All second degree burns have some degree of
–
dermal damage, and the division is based on the depth of injury into this structure.
– Third degree burns are full thickness through the epidermis and dermis and are characterized by a hard, leathery eschar

–
that is painless (due to nerve damage) and black, white, or cherry red. No epidermal or dermal appendages remain,
thus these wounds must heal by re-epithelization from the wound edges. Deep dermal and full thickness burns require
excision with skin grafting. (KAR 2007)

– Fourth degree burns involve other organs beneath the skin, such as muscle, bone and brain.
–
• Electrical Burns: (COMEDK 2008)
•
– Electrical injury is unlike other burn injuries in that the visible areas of tissue necrosis represent only a small portion of
–
destroyed tissue. Electrical current enters a part of the body, such as the fingers or hand and proceeds through tissues
with the lowest resistance to current, generally the nerves, blood vessels, and muscles.
– The skin has a relatively high resistance to electrical current and is therefore mostly spared. The current then leaves
–
the body at a ‘grounded’ area, typically the foot. Heat generated by the transfer of electrical current and passage of the
current itself then injures the tissue. During this exchange, the muscle is the major tissue through which the current
flows, and thus it sustains the most damage.
– The most serious derangements occur in the first 24 hours after injury. The patients with electrical burns may develop
–
cardiac dysrhythmias. Muscle damage results in release of hemochromogens (myoglobin), which are filtered in the
glomeruli and may result in obstructive nephropathy. So ‘port wine’ colored urine may be present.
– Large amount of blood pigment may be deposited in the collecting tubules of kidney as a result of hemolysis.
–
Hemoglobinuria will be gradually followed by oliguria, anuria and the patient may die of uraemia.
TRAUMA
• Golden Hour: The first one-hour is called as ‘golden hour’. After first 60 min (1 hour) body has difficulty in compensating
•
shock and trauma. The golden hour refers to the time from injury to the start of definite treatment in hospital.
– First 20 minutes: Discovery of trauma site and information to EMS
–
– Platinum 10 minutes: The aim is to assess, intervene and package at the site of trauma.
–
– Last 30 minutes: EMS attendant, transport to nearby hospital and stabilization.
–
– Golden hour is commonly associated with the first peak of trimodal distribution of death in trauma patients.
–
– Golden hour aims at breaking the vicious triad of trauma: Acidosis, coagulopathy and hypothermia.
–
• Elements of primary survey are: (MAHE 1995)
•
– A- Airway management
–
– B – Breathing and ventilation
–
– C – Circulation and haemorrhage control
–
– D – Dysfunction of the central nervous system
–
– E – Exposure in a controlled environment
–
Glasgow Coma Scale
Eye opening Verbal response Motor response
4. Spontaneous 5. Oriented and talks 6. Verbal command
3. Verbal stimuli 4. Disoriented and talks 5. Localizes pain
2. Painful stimuli 3. Inappropriate words 4. Withdraws to pain
1. No response 2. Incomprehensible sounds 3. Decorticate
1. No response 2. Decerebrate
1. No response
342
Maximum score: 15 (best score )

Minimum score: 3
Revised Trauma Score

Glasgow Coma Scale Systolic blood pressure Respiratory rate Points
13-15 >89 10-19 4
9-12 76-89 >29 3

6-8 50-75 6-9 2
4-5 1-5 1 1
3 0 0 0
CYSTS, ULCERS AND SWELLINGS CONGENITAL CYSTS: (KAR 2003, MAN 2001)
Dermoid
Teratomatous dermoids • Found in ovary, testis and superior mediastinum etc. they arise from stem cells containing all three
•
embryonic layers.
Sequestration dermoid • Formed by the inclusion of epithelial nests of lines of embryonic fusion. Found in the midline, external
•
angular process, on the skull and behind the ear.
Implantation dermoid • Due to implanted epithelial cells in the puncture wounds of fingers
•
Tubule dermoid • Thyroglossal cyst and ependymal cyst in the brain are examples
•
– Brachial cyst
–
• Acquired cysts:
•
– Sebaceous cyst
–
– Implantation dermoids
–
– Retention cysts
–
– Cystic tumours
–
• Parasitic cysts
•
– Hydatid
–
– Cysticercosis
–
Tumor Synonym Location
• Carotid body tumor Potato tumor, Chemodectoma (MAN 1997) Beneath the anterior edge of sternomastoid
•
• Infected, ulcerated sebaceous cyst Cock’s peculiar tumor Scalp
•
• Extra dural abscess Pott’s puffy tumor (AIIMS 2002) Skull
•

• Lipoma Ubiquitous tumor Universal
•
• Cylindroma Turban tumor Scalp
•
• Sternomastoid tumor (KAR 2000) Congenital torticollis Middle of the sternomastoid muscle
•
ARTERIOVENOUS DISEASE
Thromboangitis Obliterans (Buerger’s Disease)
– Usually one or two of the below three manifestations are present and occasionally all three
–
This is a condition characterized by occlusive disease of the small and medium sized arteries (planters, tibias, radial,

etc.)

Thrombophlebitis of superficial or deep veins The peripheral pulses are normal

Raynaud’s syndrome occurring in male patients The condition is attributable to abnormal

in a young age (usually under the age of 30 years)

sensitivity in the direct response of the arterioles
who are chronic smokers. to cold.
– The condition does not occur in women or non The condition is recognized by the characteristic
–
smokers. Gangrene of the toes and fingers is

sequence of blanching, dusky cyanosis and red
common and progressive. Arteriography sometimes
engorgement, often accompanied by pain.

shows a characteristic ‘corrugation’ of the femoral
Treatment:
arteries as well as the distal arterial occlusions and

helps to distinguish the condition from presenile - Calcium antagonists, such as nifedipine

artherosclerosis. Other forms of arteritis, e.g. - Electrically heated gloves in winter

polyarteritis nodosa, must be excluded. - Sympathectomy

– The treatment is total abstinence from smoking. - Protection from cold and avoidance of pulp
–

Established arterial occlusions may be treated along and nail bed infections are a part of the con-
the usual lines and sympathectomy may be useful servative regimen that is advised for mild cas-
adjunctive procedure. Nevertheless, amputation, es.+
conservative if possible may be required. – Secondary form: Although peripheral vasospasm may
–
be noted in artherosclerosis, thoracic outlet syndrome,
Raynaud’s Disease carpal tunnel, etc, the term secondary Raynaud’s
– May be primary or secondary syndrome is most often used for a peripheral arterial
manifestation of the collagen diseases, especially
–
– The primary idiopathic form:
progressive systemic sclerosis (scleroderma) and
–
Usually occurs in young women and affects the
systemic lupus erythematosis.

upper extremities more than the lower.
Buerger’s Disease Raynaud’s Disease

• Arterial occlusive disease mainly affecting lower limbs • Vasospastic condition affecting upper limbs
•
•
• Occurs in men from 20-40years and in smokers • Usually occurs in young women
•
•
• Characterized by gangrene of the toes and fingers and • Characterized by blanching of digits when exposed to cold and
•
•
corrugation of femoral arteries turning to red when attack passes off
• Abstinence from smoking and sympathectomy are useful in • Protection from cold and use of calcium anatgonists is the
•
•
treating this disease conservative treatment.
• Venous Incompetence – Varicose Veins – Often develop during pregnancy under the influence
•
–
– One of the most common problems with the veins of of estrogen and progesterone, which cause the smooth
muscle in the vein wall to relax.
–
the legs is failure of the valves
– This occurs frequently in the superficial venous – Complications of varicose veins:
–
Thrombosis, which is referred to as superficial
–
system resulting in varicose veins

– Varicose veins develop in the calf when the veins thrombophlebitis.
Deep vein thrombosis
–
above are normal

– More frequent in people who stand during their work Venous ulceration

–
LYMPHATIC SYSTEM
Right Drainage Area removes lymph from the Left Drainage Area removes lymph from the
• Right side of the head and neck • Left side of the head and neck
•
•
• Right arm • Left arm and the left upper quadrant
•
•
• Upper right quadrant of the body • Lower trunk
•
•
• Both legs
•
344
Lymphatic System Of Deep Head And Neck Middle ear • The mucosa of the tympanic
•
membrane and the antrum drain to
Deep nodes • Superior deep cervical nodes the parotid or upper deep cervical
lymph nodes.
•
• Inferior deep cervical nodes
•
• The tympanic end of the auditory
• Retropharyngeal nodes
•
tube drain to the deep cervical lymph
•
• Paratracheal nodes nodes
•
• Infrahyoid, prelaryngeal and
•
pretracheal nodes. Larynx • Laryngeal lymphatic vessels:
•
• Lingual nodes. • Form superior and inferior groups, at
•
•
the level of the vocal fold,
Retropharyngeal • Are formed by a median and 2 lateral
• Anastomose on the posterior wall.
•
nodes groups. The lateral group is found
•
bilaterally, anterior to the lateral – Superior vessels run with the
–
process of the atlas, along the border superior laryngeal vessels to the
of the longus capitis muscle. upper deep cervical nodes.
• Lie between the pharyngeal and – Inferior vessels run:
–
• Between the cricoid cartilage and the
•
prevertebral fasciae.
•
first tracheal ring to the inferior deep
• Receive afferents from the cervical nodes.
•
nasopharynx, eustachian tube and
joints between the occipital bone, C1 • Or through the cricothyroid ligament
•
and C2 vertebrae. to the pretracheal and prelaryngeal
nodes
• drain to the upper deep cervical
•
nodes Trachea • The tracheal plexus drains to:
•
– The pretracheal nodes
Paratracheal nodes • Lie on either side of the trachea
–
– The paratracheal nodes
•
and esophagus, along the recurrent
–
– Or directly to the inferior deep
laryngeal nerves.
–
cervical nodes
• Drain to the upper and lower deep
•
cervical nodes. Thyroid gland • Prelaryngeal nodes (above thyroid
•
isthmus) via the tracheal plexus,
Infrahoid, prelaryn- • Infrahyoid nodes are anterior to the
• Pretracheal nodes,
•
geal and pretra- thyrohyoid membrane.
•
cheal nodes are • Prelaryngeal nodes are on the conus • Paratracheal nodes,
•
•
located deep to the elasticus and cricothryoid ligament. • Brachiocephalic nodes (in superior
•
cervical fascia • Pretracheal nodes are anterior to the mediastinum),
•
trachea near the inferior thyroid veins • Deep cervical nodes via the superior
•
thyroid vessels,
The infrahyoid • Drain afferents from the anterior • And directly to the thoracic duct.
•
nodes cervical nodes.
•
• drain to the deep cervical nodes Mouth • Gingiva drain to the submandibular
•
nodes.
•
Lingual nodes • Form an inconstant group. • Soft and hard palate drain to the
•
•
• are found on the external surface superior deep cervical nodes and the
retropharyngeal nodes.
•
of the hyoglossus, and between the
genioglossi. • Anterior part of the floor of the mouth
•
• Drain to the upper cervical nodes. drains via the submental nodes or
directly to the superior deep cervical
•
nodes.
Lymphatic Drainage • Rest of the floor of the mouth drains to
•
the submandibular and superior deep
Nasal cavity and • The anterior region of the nasal cervical nodes.
•
nasopharynx cavity drains superficially to the
submandibular nodes. Teeth • Submandibular and deep cervical
•
• Rest of nasal cavity, paranasal nodes
•
sinuses, nasopharynx and pharyngeal
end of the auditory tube drain via the Tonsil • Drains to the superior deep cervical
•
retropharyngeal nodes or directly to nodes:
the upper deep cervical nodes. • Most to the jugulodigastric node.
•
• The posterior nasal floor drains to the • Some to the small nodes on the lateral
•
•
parotid nodes. aspect of the internal jugular vein

Tongue • The lingual mucosal plexus is MISCELLANEOUS
•
continuous with the intramuscular
plexus.
Meleny’s ulcer • Arises from post operative infected
• The anterior 2/3 of the tongue drains
•
wounds
•
into the marginal and central vessels.
• The posterior 1/3 of the tongue drains
Marjolin’s ulcer • Malignant ulcer that develops from a
•
scar (burn)
•
into the dorsal lymph vessels.
Brazin’s ulcer

• Marginal vessels of the tongue • Found in young adolescent girls,
•
(erythrouyonoid common on calves
•
– Arise from the tip of the tongue
ulcer)
–
and frenulum.
– Drain bilaterally to the: Martorell ulcer • Found in patients suffering with
–
•
– Submental nodes, hypertension, seen with old age.
–
– Jugulo-omohyoid node, Atherosclerosis on back of the calf.
–
– Anterior or middle submandibu-
–
lar node, Painless ulcer Painful ulcer
– Jugulo-digastric nodes.
• TB ulcer • Syphilis
–
• Central vessels of the tongue follow
•
•
• Terminal stages of • Initial stages of malignant
•
the lingual vein to drain to:
•
•
malignant diseases ulcers
– Deep cervical nodes (jugu-
• Tabes dorsalis, • Tropic ulcers
–
lodigastric and juguloomohyoid
•
•
nodes). • Peripheral neuritis
•
– Submandibular nodes.
–
• Dorsal vessels of the tongue • Edge of ulcer:
•
•
– Join with the marginal vessels – Undermined edge: Tuberculosis
–
– Drain into the jugulodigastric
–
– Punched out edge: Gummatous ulcer or deep
–
node or juguloomohyoid node
–
tropic ulcer
Pharynx and • Through the retropharyngeal or – Sloping edge: Healing traumatic or venous ulcer
–
– Raised and pearly white beaded edge: Rodent
•
cervical part of the paratracheal nodes
–
esophagus • Or directly to the deep cervical nodes. ulcer
•
• The epiglottis drains to the infrahyoid – Rolled and everted edge: Squamous cell carcinoma
–
•
nodes.
• Sinus: A blind track leading from the surface down to the
Abnormal Finding
•
tissues. The sinus is lined by granulation tissue, which may
• When the nodes are palpable describe the location, size, be epithelialized.
•
consistency, matting, mobility and tenderness. • Fistula: Communicating track between two epithelial
•
• Drainage sites for each group of nodes should be surfaces commonly between hollow viscera and the skin
•
evaluated. (external fistula) or between two hollow viscera (internal
– Anterior cervical adenitis: (Tonsillitis, Pharyngitis) fistula)
–
– Acute posterior lymphadenitis: (Acute otitis • Multiple fistula and Sinuses:
–
externa, scalp infections)
•
– ‘Watering can’ perineum: Multiple perianal fistulae
– Pre-auricular: (Acute otitis externa)
–
– Crohn’s disease: Multiple anal fistulae
–
– Deep Cervical: (Thyroid, Laryngeal CA, Systemic
–
– Actinomycosis: Multiple sinuses
–
diseases)
–
– Ulcerative colitis: Multiple fistulae
– Supraclavicular: ( Virchow’s node, Lung CA)
–
–
– Generalized: (Sarcoidosis, Tb, Lymphoma, CLL, • Commonest type of lymphoma is Hodgkin’s lymphoma.
•
–
Mono, HIV) The basic malignant cell of the Hodgkin’s lymphoma
• Lymph glands: is reticular cell. Best prognosis is for lymphocyte
•
– Hodgkin’s disease: Soft (fluctuating) elastic and predominant type.
–
rubbery • Capillary hemangioma
•
– Syphilis: Firm, discrete and shotty – Salmon patch: Present at birth, disappears by the age
–
–
– Secondary carcinoma: Stony hard of one year
–
– Tuberculosis: Matted lymph nodes – Portwine stain (nevus flammues): Present at birth,
–
–
– Milroy’s disease: Congenital lymphedema persists throughout life
–
– Strawberry angioma: It is not present at birth
–
346
• IV Fluids: Port wine stain • Naevus flammeus
•
•
– Bicarbonate is absent in: Rodent ulcer • Basal cell carcinoma
–
•
Darrow’s solution

Ringer’s lactate Turban tumor • Cylindroma
•

– Fluid rich in potassium: Darrow’s solution
Buerger’s disease • Thromboangitis obliterans
–
– IV fluid resembling plasma: Ringer lactate solution
•
–
– IV fluid that decrease cerebral oedema and Bedsores • Decubitus ulcers
–
prevents renal failure: Mannitol
•
– IV fluid of choice in cholera: Ringer’s lactate Brittle bones • Osteogenesis imperfecta
–
•
• Wound tensile strength approaches that of normal tissue Marble bones • Osteopetrosis (Alber’s
•
•
by 6 months but 100% normal after 2 years only. Schonberg disease)
• Graft rejection: Inflammation appears by 4th day (first Gargoylism • Hurler’s syndrome
•
•
set response). Slough appears by 10th day. If again grafted
from same donor (second set response) sloughs by 6th Anosteoplasia • Cleido cranial dysostosis
•
day.
Wilson disease • Hepatolenticular degeneration
•
Commonest Site of Lesion Amaurotic family idiocy • Tay-Sach’s disease
•
Erysipelas • Face and scrotum
Paget’s disease • Osteitis deformans
•
•
Cellulitis • Scrotum and scalp
•
Wry neck • Torticollis
•
Sebaceous cyst • Scalp, face and neck
•
Keloid • Sternum, face, neck
• Nerves injured in surgery
•
•
Lymphangioma and hem- • Tongue, lip – Submandibular gland: Lingual nerve
•
angioma
–
– Parotid gland: Facial nerve
–
Carbuncle • Back, nape of neck and
– Branchial cyst: Hypoglossal and Accessory N
–
– Cervical lymph node dissection
•
shoulders
–
Spinal accessory N
Impantation dermoid • Hand and finger

Mandibular branch of facial N
•

Dermoid cyst • External angle of eye Hypoglossal N

•
Kaposi sarcoma • Limbs • Frog’s face: Nasopharyngeal carcinoma
•
•
Granuloma pyogenicum • Face, fingers and toes • Countryman’s lip: Carcinoma of lip
•
•
• Madurai foot: Mycetoma foot
Corn • Toes and feet
•
• Trench foot: Frost bite
•
•
Malignant melanoma • Males: trunk
• Arthrotopic: Transplant being positioned in its
•
• Females: leg
•
anatomical site
•
Pregnancy tumor • Gums and tongue • Heterotopic: Transplant being positioned in a different
•
•
site.
Alternate Names
Tumors Causing Hypercalcemia
Corn • Grain
• Parathyroid adenoma
•
•
Boil • Furuncle
• Multiple endocrine neoplasias
•
•
Sebaceous cyst • Wen • Solid tumor with metastasis (breast)
•
•
• Non small cell carcinoma, renal cell carcinoma
Keratoacanthoma
•
• Molluscus sebaceum
• Hematological malignanicies (multiple myeloma,
•
•
Malherbe’s epithelioma • Benign calcifying epithelioma lymphoma, leukemia
•

Commonest type of • Squamous cell carcinoma Hairy cell leukemia • CD 103 +
•
•

Esophageal carcinoma (AIPG 1991)

Mantle cell lymphoma • CD 5+, CD 103-
Commonest site of squa- • Lower end of esophagus
•
•

mous cell carcinoma (AIIMS 1997) CLL • CD 23+

•
Commonest feature of • Dysphagia Apoptosis • CD 95+
•
•
achlasia cardia

Commonest feature of • Progressive dysphagia • Mycotic aneurysm is due to bacteria
•
Cancer esophagus
•
• Mycotic abscess is due to fungal infection (AIPG 2006)
•
Difficulty in swallowing • Dysphagia
– Brain stem lesion: cranial nerve involvement +
•
–
Pain during swallowing • Odynophagia sensory loss of ½ of face + contralateral ½ of body
•
– Thalamic lesion: sensory loss of ½ of face + same
–
Mitochondrial Ataxias ½ of body
– Internal capsule lesion: loss of face, arm, leg without
• Spinocerebellar syndromes have been identified with
–
higher cortical dysfunction
•
mutations in mitochondrial DNA (mt DNA)
Xeroderma Pigmentosum – Renkies edema: Is edema of vocal cords
–
– Reinke’s edema: Blunt trauma to eyes

• Xeroderma pigmentosum is a rare autosomal recessive
–
– Berlin’s edema: Generalized anasacra
•
neurocutaneous disorder –
– Solitary weakly ring enhancing lesion: CNS
• Caused by the inability to repair damage to DNA, such
–
lymphoma
•
as that produced by Ultraviolet radiation – Multiple ring enhancing lesion: Toxoplasmosis
–
• In addition to skin lesions, patients may show – Potts puffy tumor: Osteomyletis of the skull
•
–
progressive mental deterioration, Microcephaly, – Cocks peculiar tumor: Complicated infected
–
ataxia, spasticity, choreoathetosis, and hypogonadism sebaceous cyst
• Nerve deafness, peripheral neuropathy (predominantly – Hemoptysis normally is due to bronchial artery
–
•
axonal), electroencephalographic abnormalities, and – Hemoptysis in mitral stenosis is due to pulmonary
–
seizures are reported artery
– Familial breast cancer: BRCA 1
–
Hutchinsons Freckle
– Sporadiac breast cancer: p53
• Lentigo Maligna (melanoma
–
– HTLV 1: Adult T cell leukemia/ lymphoma, tropical
•
variant)
–
spastic paraplegia
Hutchinsons pupil • Blown pupil in uncal herniation – HTLV 2: Hairy T cell leukemia
•
–
– HTLV 3: HIV/AIDS
Hutchinsons sign • Herpes zoster opthalmicus,
–
– Rebound hypertension: Clonidine
•
vesicles at tip of nose
–
– Postural Hypotension: Prazosin
–
Hutchinsons teeth • Small widely spaced teeth in WHO criteria for the diagnosis of Multiple Myeloma
•
congenital syphilis
Major Criteria Minor Criteria
Hutchinsons triad • Interstitial keratitis, notched • Bone marrow • Bone marrow plasmacytosis
•
incisors, VIII nerve deafness
•
•
plasmacytosis > 30% of 10 to 30%
Hutchinsons Fracture • Fractured radial styloid process • Plasmacytoma on biopsy • Monoclonal protein present
•
•
•
but less than above
Charcot’s crystals • In bronchial asthma concentrations
•
Charcots disease • ALS • Presence of a monoclonal • Presence of lytic bone
•
•
protein (m-component) in lesions
•
Charcot’s joint • Neuropathic joints in leprosy, serum or urine
•
syphilis
• Serum IgG> 3.5gm/dl • Reduced normal
•
•
Charcots triad • Seen in multiple sclerosis, immunoglobulins to < 50% of
normal
•
cholangitis
Charcots aneurysm • Brain aneurysm • Serum IgA > 2gm/dl • IgG < 600 mg/dl
•
•
•
348
• Urine Bence-Jones protein • IgA < 100 mg/dl • Dyskeratosis: Abnormal development of epidermal
•
•
> 1gm/24 hrs
•
cells (feature of Premalignant lesions)
• IgM < 50 mg/dl
• Hyperkeratosis: Increased thickness of Stratum
•
•
Corneum
Diagnostic requirements: The diagnosis of multiple myeloma
requires a minimum of one major criteria and one minor • Parakeratoses: Presence of immature nucleated cells in
•
criteria or three minor criteria which must include bone Stratum Corneum
marrow plasmacytosis of 10-30% and the presence of a
monoclonal protein. These criteria must be manifest in a Important Skin tests
symptomatic patient with progressive disease
• Transillumination: Simply lighting a Dark room can
•
Primary skin lesions help to detect slight degrees of elevation and depression
of lesions as well as fine wrinkling or atrophy of the
• Macule: A flat coloured lesion < 2cm in diameter, not
epidermis. Cystic lesions allow transmission of some light,
•
raised above the surface of the surrounding skin. A
whereas nodules composed of cellular infiltrates do not.
freckle or ephelid, is a prototype pigmented macule.
• Diascopy: Firm pressure with a microscope slide against
• Patch: A large (<2 cm), flat lesion with a color different
•
skin lesions differentiates erythema of capillary dilatation
•
from the surrounding skin. This differs from a macule
only in size. from that of extravasated blood. Sarcoidosis, tuberculosis,
and other granulomatous inflammatory reactions in
• Papule: A small, solid lesion, < 1 cm in diameter, raised
the skin are suggested if diascopy of the lesions shows
•
above the surface of the surrounding skin and hence
a characterstic “apple-jelly” or glassy, fawn coloured
palpable (eg: a closed comedone, or whitehead, in acne
appearance.
• Nodule: A larger (1-5 cm), firm lesion raised above the
•
surface of the surrounding skin Wood’s Light Examination
• Tumor: A solid, raised growth > 5cm in diameter
“Long-Wave Ultraviolet (UVA) (360nm)” is useful in
•
• Plaque: A large (>1 cm), flat topped, raised lesion; edges evaluating several conditions of the skin. Wood’s Light
•
may be either be distinct (eg: in psoriasis) or gradually exaggerates the differences in the degree of pigmentation
blend with surrounding skin (eg: in eczematous
when the skin is examined with the lamp in a dark room.
dermatitis)
Melanin is a universal absorber of UV light, so decreased
• Vesicle: A small, fluid filled lesion, < 1 cm in diameter, melanin shows more reflection (light color) and increased
•
raised above the plane of surrounding skin. Fluid is melanin shows less reflection (darker color). Wood’s light
often visible, and the lesions are often translucent helps in recognizing the hypomelanotic ash leaf-shaped
• Pustule: A vesicle filled with leukocytes. Note: the macules of tuberous sclerosis, the extent of vitiligo and
•
presence of pustules does not necessarily signify the melanotic nevi. Some superficial fungal infections of
existence of an infection the scalp fluoresce blue-green; erythrasma, a superficial
• Bulla: A fluid filled, raised, often translucent lesion> intertriginous bacterial infection that produces a porphyrin,
•
1cm in diameter fluoresces a brilliant coral red; Pseudomonas infections may
• Cyst: A soft, raised, encapsulated lesion filled with give off yellow-green color under a Woods light.
•
semisolid or liquid contents
• Wheal: A raised, erythematous papule or plaque,
Physical Contact Testing
•
usually representing short-lived dermal edema
• The Koebner phenomenon: Occurs in certain skin
• Telangiectasia: Dilated, superficial blood vessels.
•
diseases that tend to evolve new skin lesions after
•
• Acanthosis: Increase in thickness of prickle cell layer traumatic injury in areas of apparently normal skin.
•
• Acantholysis: Loss of coherence between epidermal Seen in psoriasis and Lichen planus
•
cells. Seen in pemphigus (AIIMS 1991)
• Pathergy: Is the development of putular and ulcerative

• Corps Grains: Acantholytic, Dyskeratotic, basophilic
•
lesions at the site of the needle puncture, is suggestive
•
cells with rounded nuclei and perinuclear halo. Seen in
of Bechet’s syndrome and pyoderma gangrenosum.
Dariers disease

Disease Basement membrane molecule involved
• Bullous pemphigoid • BP antigen 1 and 2
•
•
• Herpes gestationis • BP antigen 2
•
•
• Epidermolysis bullosa • Type VII Dermal collagen
•
•
• Bullous lupus erythematosus • Type VII Dermal collagen
•
•
• Linear IgA Bullous disease • BP antigen 2

•
•
Pemphigus Pemphigoid
• Common in age group 40-60 yrs • Common in greater than 60 yrs
•
•
• Nikolskys sign present • Nikolskys sign absent (JK 2011)
•
•

• Intraepidermal bullae • Sub-epidermal bullae (AIIMS 1995)
•
•

• Flaccid bullae • Tense bullae
•
•
• Mucosal involvement common • Mucosal involvement Uncommon
•
•
• Acantholysis present • Acantholysis absent
•
•
Leprosy
• Leprosy is also called Hansens disease
•
• Virchows cells seen (UP 1995)
•

• The sensation to be lost earliest is the touch
•
• Rifampicin is the drug most rapidly acting and most potent against Leprosy bacillus
•
• Dapsone is the drug of choice. Dose is 1-2 mg/kg. half life is 24 hrs (AIPG 2002)
•

• 1st line of drugs – rifampicin, dapsone, clofazamine (Delhi 1983)
•

• DOC in neuritis is steroids (AIPG 1995)
•

• Nerve abscess treated by incison and drainage (AIIMS 1996)
•

• Leprosy bacillus is a gram positive, acid fast bacillus
•
• Lepra cells are also called foamy cells are actually histiocytes within which globi are found
•
• Generation time of Lepra bacillus is 12 days
•
• Only source of infection is the patient
•
• Incubation period of leprosy is 2-5 years
•
• Most common nerve involved is Ulnar nerve followed by post auricular nerve (PGI 1997)
•

• Schwann cells are involved first of all
•
• CNS, ovaries, lungs are not commonly invovled in leprosy (PGI 1998)
•

• TT is the most common type of leprosy in India (PGI 1997)
•

M. Leprae Grows Best in Cooler Tissues
• Skin
•
• Peripheral nerves
•
• Anterior chamber of eye
•
• Upper respiratory tract
•
• Testes
•
Tuberculoid Leprosy
• The initial lesion of tuberculoid leprosy is often a hypopigmented macule that is sharply demarcated and hypoesthetic
•
• Ineffective form
•
• Fully developed lesions are densely asthetic and devoid of the normal skin organs (sweat glands and the hair follicles)
•
350
• Patients eventually have one or more asymmetrically distributed, hypopigmented, anaethetic, nonpurutic, well defined
•
macules, often with erythematous and raised border
• Tuberculoid leprosy patients may also have asymmetric enlargement of one or a few peripheral nerves.
•
• Although any peripheral nerves may be enlarged (including small digital and supraclavicular nerves), those most commonly
•
affected are the ulnar, posterior auricular, peroneal, and post tibial nerves, with associated hypesthesia and myopathy
• At times, tuberculoid leprosy may be present with only nerve trunk involvement with no skin lesions; in such cases it is
•
termed as neural leprosy
• In TT leprosy the epidermis may be involved histologically
•
• On hematoxylin and eosin staining, TT and BT lesions appear as well defined non caseating granulomas with many
•
lymphocytes and langerhans giant cells.
• In tuberculoid leprosy, T cells breach the perineurium, and destruction of Schwann cells and axons may be evident, resulting
•
in fibrosis of the epineurium, replacement of the endoneurium with epithelial granulomas, and occasionally caseous necrosis
• AFB are generally absent or few in number
•
• Invasion and destruction of nerves in the dermis by T cells are pathognomic for Leprosy
•
Lepromatous Leprosy
• At the more severe end of the leprosy spectrum is lepromatous disease, which encompasses the LL and BL forms
•
• The initial skin lesions of lepromatous are skin coloured or slightly erythematous papules or nodules. In time the
•
individual lesions grow in diameter upto 2 cm; new papules and nodules then appear and may coalesce
• Patients later present with symmetrically distributed skin nodules, raised plaques, or diffuse dermal infiltration which
•
when on face, results in leonine facies.
• Late manifestations include loss of eyebrows, eyelashes, pendulous earlobes, and dry scaling skin, particularly on the feet
•
• Gyancomastia, madriosis, collapse of nasal bridge (TN 1996)
•

• Dermatopathology in lepromatous leprosy is confined to the dermis and particularly affects dermal appendages
•
• Histologically, the dermis characteristically contains highly vacuolated cells (foam cells) and fewer or absent non caseating
•
granuloma
• The dermis in lepramatous leprosy contains few lymphocytes and giant cells, and granulomas are absent
•
• In LL leprosy, bacilli are numerous in skin (as many as 109 /gm) where they are often found in large clumps (globi), and
•
in peripheral nerves, where they initially invade Schwann cells, resulting in foamy degenerative myelination and axonal
degeneration and later in Wallerian degeneration
Lepra Reactions
Type 1 reaction is also called as ‘Downgrading’ or ‘reversal’ reaction
• It occurs in borderline leprosy
•
• It is type IV delayed hypersensitivity reaction
•
• Signs of inflammation in previous lesions, neuritis and fever are characterstic
•
Treatment
• Continue antileprotics
•
• Use analgesics
•
• Corticosteroids are the drug of choice (AIPG 1995)
•

• Unresponsive to thalidomide (JIPMER 1995)
•

Type II reaction is called as ‘Erythema Nodusum Laprosum’
• It occurs in Lepramatous Leprosy (PGI 2004)
•

• It is type III Hypersensitivity reaction
•

Treatment
• Corticosteroids are the initially used drugs
•
• Thalidomide is effective
•
Lepromin Test is Positive in Patients Having Cell Mediated Immunity

• Cell mediated immunity is present in Tuberculosis. Hence Lepromin test is positive. As the spectrum of leprosy passes
•
from tuberculoid to lepromatous type the Lepromin test gets weaker
• Lepromin test is not a diagnostic test
•
• Lepromin test is a prognostic test
•
• Positive test suggests good prognosis
•
• Negative test suggests poor prognosis
•
• Lepromin test is negative in most children in first 6 months of life
•
• BCG vaccination may convert Lepra reaction from negative to positive
•
Autism
• Autism is characterized by onset of symptoms before 3 yrs of age
•
• Difficulty in concentration and communication is typical
•
• Lesion in frontal lobe, temporal lobe, cerebellum (JIPMER 1998)
•

• Delayed speech and language development (absence of blabbling, presence of echolia) (AIIMS 2006)
•

• Problems in forming social relationships in early childhood. (aloofness, absent social smile, lack of eye contact)
•
• Males are more affected in autism
•
• Features (AIPG 2010)
•

– Stereotyped movements
–
– Poor speech
–
– Lack of social interaction
–
• Some autistic children develop well developed isolated skills atypically such as remote memory, calculating abilities and
•
musical abilities. This atypical presentation is called ‘Idiot savant syndrome’
• Children develop
•
– Mental retardation
–
– Epilepsy
–
– EEG abnormalities
–
Illusion Hallucination Delusion Depersonalization Derealization
Misinterpretation of Perception without False unshakeable An alteration in perception An alteration in perception to
stimuli arising from stimuli belief not amenable to to self external world
external object reasoning
Alcohol Withdrawl
• Hangover
•
• Visual or tactile hallucinations
•
• Alcoholic Hallucinosis: Hallucinations usually auditory
•
• Alcoholic seizures (rum fits)
•
• Multiple seizures occuring during absistence usually 12-48 hrs after heavy drinks
•
352
Delerium Tremors
• Occur within 5 days of abstinence
•
• Clouding of consciousness
•
• Disorientation, anxiety, perceptual defect
•
• Hallucinations
•
• Autonomic disturbance
•
• Agitation, insomnia
•
• MC symptom of withdrawl
•
• Chlordiazepoxide is used for treatment
•
Alcohol withdrawl Opoid withdrawl Cocaine withdrawl
• Hangover Yawning Hypersomnia/insomnia
•
• Hallucinations/illusions Insomnia, disphoric mood Vivid unpleasant dreams
•
• Hyperactivity Inc BP, RR, Temp Inc appetite
•
• Insomnia Pupilary dilatation
•
• Seizures
•
• Symptoms appear commonly on
•
2nd day (KAR 2007)

Also Note
• Excessive sexual desire in male: Satyriasis (AIIMS 2008)
•

• Excessive sexual desire in female: nymphomania
•
• Transsexualism is change to opposite sex by surgery (AIIMS 2009)
•

CHAPTER 8
Dental Materials
Objectives
• Properties of Dental materials • Ceramics

• Impression Materials • Wrought Alloys

• Gypsum Products • Casting Alloys and Casting Properties

• Amalgam • Casting Procedure

• Direct Filling Gold • Abrasion and Polishing

• Restorative Resins • Tarnish and Corrosion

• Cements • Soldering, Welding and Brazing

• Denture Resins and Polymers • Miscellaneous

• Liners, Varnish and Waxes

PROPERTIES OF DENTAL MATERIALS
Important Terms and Terminologies
Stress
Internal resistance of the body to deformation is known as stress (AP 2013)

– Types:
–
Compressive Tensile Shear
Internal resistance to load placed on Any resistance to deformation of a body Stress that tends to resist twisting motion or a sliding
body, which tends to compress or by load that tends to stretch / elongate it of one portion of a body over another. Also known as
shorten it torsional stress (AIPG 2005)

• Impact: It is the stress that is induced by one/both bodies in motion when they meet
•
• Strain: Deformation produced as a result of external force is known as strain. it is measured in terms of deformation of
•
structure per unit dimension.
• Strain may be elastic/plastic: Elastic strain is reversible and disappears after stress is removed —plastic strain is the
•
permanent deformation.
354
• Malleability: Ability of a material to withstand rupture under compression

•
– Does not depend on length
–
– Increases with increase in temperature
–
• Ductility: ability of a material to withstand permanent deformation under a tensile load without rupture.
•
– Ductility decreases with increase in temperature, Malleability increase in temperature
–
– Gold is the most ductile and malleable metal, followed by silver, platinum and copper
–
– Ductility is measured in percent elongation and it is measure of brittleness.
–
– Cold bend test is used to measure ductility of material. (AIIMS Nov 2013, NEET 2013)
–

Creep
• Time dependent plastic deformation under a constant load.
DENTAL MATERIALS
•
– Types
–
Static Dynamic
• Time dependent deformation produced in a completely set • Produced when applied stress is fluctuating
•
•
solid subjected to a constant stress
• Resilience: Usually associated with springiness. Usually measured in terms of its modiolus of resilience which is the
•
amount of energy stored in a body, when one unit volume of a material is stressed to its proportional limit.
– Resilience is also measured by the area under the straight line portion of the stress strain curve.
–
• Elastic limit: Greatest stress to which material can be subjected such that it will return to its original dimension when
•
forces are released.
• Proportional limit: Maximum stress that may be produced in a structure with the stress remaining proportional to the
•
strain (Hooke’s law) (AIPG 2002)

• Hooke’s law: Stress is directly proportional to strain in elastic deformation.
•
• Yield strength: Strength required to produce particular offset (plastic strain) chosen.
•
• Modulus of elasticity: (Young’s modulus) - property found by dividing stress by corresponding strain at given load below
•
the proportional limit .It is equal to rigidity or stiffness of material. (AIPG 2003)

• Flexibility: Defined as the strain that occurs when the material is stressed to its proportional limit.
•
• Diametric compression test: Is used to measure tensile strength for only materials that exhibit very limited plastic
•
deformation.
• Toughness: Energy required to fracture a material.
•
Hardness
– Hardness is defined as the ability of a material to resist scratching.
–
– Can be divided into microhardness and macrohardness
–
Tests for microhardness: AIIMS May 2010 Tests for macrohardness
• Knoop hardness test • Brinell hardness
•
•
• Vickers hardness test (AIPG 2007) • Rockwell hardness
•

•
Brinell Hardness • Oldest test employed for determining the hardness of metals
•
Test • A hardened steel ball is pressed under a specified load into the polished surface of a material. The load is divided
•
by the area of the projected surface of the indentation, and the quotient is referred to as the Brinell hardness
number, usually abbreviated as BHN.
• For a given load, the smaller the indentation, the larger is the number and the harder is the material.
•
• Used extensively for determining the hardness of metals and metallic materials used in dentistry
•
• It is related to the proportional limit and ultimate tensile strength of dental gold alloys.
•
Dental Materials 355

Rockwell Hardness • Is somewhat similar to Brinell test in that a steel ball or a conical diamond point is used
•
Number • Instead of measuring the diameter of the impression, the depth of penetration is measured directly by a dial
•
gauge on the instrument
• Neither the brinell test for the Rockwell test is suitable for brittle materials.
•
Vickers Hardness • Employs the same principle of hardness testing as brinell test
•
Test: (AIIMS May 08) • Instead of a steel ball, a diamond in the shape of a square based pyramidal is used
•
• The lengths of the diagonals of the indentation are measured and averaged
•
• The Vickers test is employed in the ADA specifications for dental casting gold alloys
•
• Suitable for determining the hardness of brittle materials
•
• Used for measuring the hardness of tooth structure
•
DENTAL MATERIALS
Knoop Hardness • Employs a diamond indenting tool that is cut in the geometric configuration
•
Test • The impression is rhombic in outline, and the length of the largest diagonal is measured
•
• The hardness value is virtually independent of the ductility of the material tested.
•
Shore and Barcol • Are employed for measuring the hardness of dental materials, particularly rubbers and plastics
•
Test
• Three dimensions of colour: Quantitatively colour has been described in three variables
•
Hue Value Chroma
Refers to basic The lightness or darkness which can be measured The degree of saturation of the particular colour. Chroma
colour of the object independently of the colour hue cannot exist by itself and is always associated with hue and
value
• Munsell System: (AIIMS May 08, May 2010, AIPG 2007)

•
– It is a co-ordinate system which can be viewed as a cylinder. The lines are arranged sequentially around the perimeter
–
of the cylinder, while the chroma increases along a radius from the axis.
– The value coordinate varies along the length of the cylinder from black at the bottom to neutral grey at the centre to
–
white at the top.
– Munsel system is the most common method of measuring colour quantitatively
–
• Translucency: Property of an object that permits the passage of light through it but does not give any distinguishable image
•
• Fluorescence: Phenomenon in which energy is converted light with longer wavelength
•
• Benzold: Brucke Effect: change in colour due to change in brightness
•
• The human eye is sensitive to wave lengths of approximately 400 nanometers to 700 nanometers (violet-dark red).
•
• Metamerism: Objects that appear to be colour matched under one type light may appear very different under another light
•
source.
• The study of flow matter is rheology

•
• Newtonian fluid: Fluid that demonstrates a shear stress proportional to strain rate (n=1) (where n = flow index)
•
• Pseudoplastic: The viscosity decreases with increasing shear rate (examples are most of the dental materials) ( N = lesser
•
than 1)
• Dilatant: Rigidity increases as rate of deformation increases ( n = more than 1)
•
• Plastic: There are materials which behave like rigid body until some minimum value of shear stress is reached
•
• Thixotropic: Viscosity decreasing due to increasing temperature
•
356
• Linear coefficient of thermal expansion change in length of material when its temperature is raised/ lowered by 1
•
degree C
– Material LCTE- Alpha ( K* 10 raised to power-6)
–

– Tooth(crown) 11.4
–

– Dental Amalgam 25
–

– Denture Resin 81.1
–

– Composite Restorative Resin 35
–

– Pure Gold 14
–

– Gold Alloy 15
–

– Aluminous Porcelain 6.6
–

– Silicone Impression Material 210
DENTAL MATERIALS
–

• Acrylic Resin has highest coefficient of thermal expansion
•
• Thermal Conductivity is measured by determining quantity of heat in calories per second that passes through a 1cm
•
thick specimen having a cross sectional area of 1 sqcm keeping the temperature differential between under of specimen
as 1*C
• Latent Heat of fusion– Amount of heat required to change 1g of substance from solid to liquid
•
• Adhesion: The force that causes two substances to attach • Contact angle measurement is the test for measuring
•
•
when brought into intimate contact – the molecules are wettability of an adhesive to adherend.
different • Bonds
•
• Cohesion: The molecules are of the same kind – Vanderwaals forces: Physical forces
•
–
• The material/ film added to produce adhesion is ‘adhesive’. – Ionic bond: e.g. gypsum, phosphate cements
•
–
• The material to which the adhesive applied is ‘adherend’. – Covalent bonds: e.g. dental resins
–
– Metallic bonds: e.g. pure gold
•
• The point of apposition of adherend and adhesive is called
–
– Hydrogen bonds: Water
•
interface.
–
• Sublimation: Process by which some solids directly
• Surface energy is the reactivity of surface of material and
•
transform to gas phase
•
may vary with factors such as cleanliness of surface, type
• Glass Transition Temperature: Temperature at which
of space lattice etc.
•
there is an abrupt increase in the thermal expansion
• Contact angle is the angle formed when drop of adhesive coefficient, indicating increased molecular mobility.
•
is placed on the adherend.

(AIIMS May 2010)

IMPRESSION MATERIAL
• Classification
•
Mode of setting Rigid Elastic (AIPG 2003)
• Set by chemical reaction • Impression plaster • Alginate hydrocolloids (AIPG 2007)
•
•
•
(irreversible or thermoset) • Zinc oxide eugenol • Non aqueous elastomers – polysulphides, polyether, silicone
•
•
• Set by temperature change • Compound • Agar hydrocolloid
•
•
•
• Waxes
•
Impression Compound
• Classification (ADA no 3 )
•
Type I – Impression Compound Type ll-tray Compound
• Preliminary impressions in edentulous mouth • To check undercuts in inlay preparation
•
•
• For individual tooth impression • To make special tray
•
•
• Peripheral tracing or border moulding
•

• Composition – Accelerator: Adding accelerator decreases the setting
–
time.
•
– Copal resin
• Compressive strength of hardened ZnO E is 7 mpa after 2
–
– Bees wax/carnuaba wax,
•
hours of mixing.
–
– Plasticizer (like stearic acid or gutta percha)
–
– Filler (chalk/kaolin), • Dimensional stability is very good and shrinkage is less
–
•
– Colouring agents than 0.1%.
–
• Impression compounds contract approximately 0.3%- • Applications of ZnO E
•
0.4%from passing mouth to temperature.
•
– Cementing and insulating media,
• Glass transition temperature is 390C (AIPG 2007)
–
– Temporary filling,
•

• Impression compound should be placed at a temperature
–
– Root canal filling material,
•
of 450C in mouth.
–
DENTAL MATERIALS
– Surgical pack,
• Kneading of impression compound is done to obtain
–
– Bite registration paste,
•
uniform plasticity throughout the Mass.
–
– Edentulous impressions.
–
• Colloid state of matter in which matter is distributed
Zinc Oxide Eugenol
•
throughout the medium in particles so small dimension
Impression paste produces a rigid impression with high degree so that they will not settle out from liquid.
accuracy and good reproduction of surface detail.
• Colloid emulsion is formed by dispersion of droplets of a
• Available In paste form In two tubes
•
liquid in another liquid: oil in water
•
Base paste (white) Accelerator paste (red) • Colloid suspension: Colloid suspension is formed by
•
• Zinc oxlde-87% • Eugenol -12% particles of a solid dispersed in water.
•
•
• Ve g e t a b l e / m i n e r a l • Gum resin—50% Reversible Hydrocolloids (Agar)
•
•
oil—13% • Filler—20%
• Contain approximately 80 % of water and agar is the
•
• Lanolin—3%
•
main base.
•
• Coloring agent/ accelerator—5%
• Two forms ‘sol’ and ‘gel’.
•
• Resinous balsam ,-- 10%
•
•
• Accelerators used are glacial • ‘Sol’ has appearance and many characteristics of liquid
•
•
acid, zinc acetate, primary and is obtained by placing In boiling water.
alcohols. (AIPG 2007)
• ‘Gel’ is a semi solid brought on cooling, thus both

•
• According to ADA specification no. 16 ZnO E is of two liquefaction/gelation are the primarily reversible
changes regulated by application of heat.
•
types
– Type l: Hard (flow 30—50mm) • Gelation is thus conversion of sol to gel and occurs at a
•
temperature called gelation temperature (18—20).
–
– Type 2: Soft (flow 20—45mm)
–
• Setting reaction of zinc oxide and eugenol is typically • The liquefaction temperature is considerably higher
•
•
an acid-base reaction comprising of chelation reaction than gelation temperature and this difference is called
product called as zinc eugenolate as hysteresis. (AIPG 2007)

ZnO+H2 ---> Zn (OH)2 • Composition of agar
•
Zn (OH)2 + 2HE → ZnE2 + 2 H2O Agar 13-17% Basic constituent
• Initial setting time of ZnOE is 3-6 min. Final setting time • Borates 0.2 – 0.5% Strength
•
•
of ZnOE is 10-15 mins • Potassium 1-2% Proper setting of gypsum
•
• Factors controlling setting time are • Sulphate Model
•
•
– Particle size of ZnO powder: Smaller the size, lesser • Wax (hard). 0.5 – 1.0% Filler
–
•
the setting time • water balance Dispersion medium
•
– Temperature: Cooling the glass slab increases setting
–
time • Steps In manipulation of agar hydrocolloid
•

– Mixing time: Longer the mixing time shorter the (AIPG 2006)

–
setting time – Liquefying of gel by boiling for 10 minutes
–
358
– The sol form is stored at a temperature of 63*C (AIPG 2008)

–

– The tray material should be conditioned at a temperature of 43*C
–
– The gelling in the mouth by use of water cooled trays for 5 minutes
–
• Syneresis–loss of water by evaporation from the surface or by exuding the fluid
•
• Imbibition–the absorption of water, when immersed in water by the surface of the gel.
•
• Working time ranges between 7-15 minutes where as setting time is about 5 minutes.
•
• Storage media for agar impression can be 2% potassium sulphate or 100% relative humidity
•
DENTAL MATERIALS
Irreversible Hydrocolloids
They gel by a definite chemical reaction that is irreversible
Alginate
– Composition
–
Sodium/Potassium alginate/Ester salts of alginic acid 15%

Calcium sulphate 16%

Zinc oxide 4%

Potassium Titanium fluoride 3%

Diatomaceous Earth(filler) (AIIMS Nov 2013) 60

Sodium Phosphate 2%

– Water powder ratio of alginate is approximately 15g of powder mixed with 40 ml of water
–
– Optimal gelation time at room temporature is 2O*C and is between 3-4min (fast setting 1-2 min normal setting @ 4-5
–
min).
– Setting reaction of alginate
–
2 Na3Po4 + 3 CaSo4 → Ca3(Po4)2 + 3 Na2So4 + H2O → Calcium alginate + Na2SO4
Type Agar Alginate

• Grainy Material • Inadequate boiling, • Improper mixing, prolonged mixing, too low water
•
•
•
• Low storage temperature powder ratio
•
• Too long strorage time
•
• Tearing • Inadequate bulk, Premature • Inadequate bulk, Moisture contamination, Premature
•
•
•
Removal removal, Prolonged mixing
• Bubbles • Gelation of syringe material, air • Under gelation, preventing flow

•
•
•
incorporated during mixing
• Irregular Shaped • Material too cool/grainy • Moisture/debris on tissue

•
•
•
• Distortion • Impression not poured immediately, • Impression not poured immediately, Premature
•
•
•
Premature removal from tooth, removal from tooth, improper removal from tooth, tray
improper removal from tooth, tray held in mouth for too long
held in mouth for too long
• Rough/ Chalky stone cast • Inadequate cleaning of Impression • Premature removal
•
•
•
• Gelation time can be controlled by altering the temperature of water
•
– Colder the water: Longer the gelation time
–
– Warmer the water: Shorter the gelation time
–

• Compressive strength of alginate gels range from 5000-8000g/cm2
•
• The thickness of gel between the tray and tissues should be atleast 3 mm (1/8 inch).
•
Elastomeric Impression Materials (Rubber Base Impression Material) (AIPG 2006)

– Polysulfide
–
– Condensation polymerising silicone
–
– Addition polymerising silicone and
–
– Polyether
–
– Recently a fifth class is added that is light-curable polyether urethane dimethacrylate.
–
• The process of changing rubber base product or liquid polymer to rubber like material is generally known as vulcanization/
•
curing.
DENTAL MATERIALS
Polysulfides – First elastomeric Impression material to be introduced
–
– Composition
–
(also known as
Base Paste Accelerator Paste

mercaptan • Polysulfide polymer → 80 – 85% • Lead Dioxide → 60-68%
•
•
• Inert Filler → 16-18% • Dibutylpthalate → 30-35%
Thiokol
•
•
• Sulfur → 3%
•
Vulcanizing impres- • Magnesium Sterate → 2%
sion materials)
•
• Lead dioxide gives it its characteristic brown colour
•
• Polymerization reaction is exothermic in nature
•
• Setting time is 8-12 minutes → curing shrinkage (0.4%) is also high.
•
• It has highest permanent deformation 3-5% among elastomers. For maximal accuracy the cast should be
•
poured within the first 30 minutes.
• Polymerization shrinkage is high due to loss of by product i.e. water
•
• Polymerization shrinkage and permanent deformation can be minimized by taking minimum quality of impression
•
and custom tray
• Polysulfide has good flexibility (7%) and low hardness and 2mm spacing is necessary for making impression.
•
• Has unpleasant odour (AIPG 2007, 2010)
•

• Messy and stains clothes
•
• Highest tear strength (AIPG 2004 (AIPG 2008))
•

• Hydrophobic
•
• Biocompatible (AIPG 2004)
•

• Only impression materials that can be electroplated (AIPG 2003)
•

Condensation • Composition
•
silicone
Base Accelerator
Also known as • Polydimethyl • Orthoethyl silicate
•
•
room temperature
• Siloxane • Cross- Linking Agent
silicones
•
•
• Colloidal silica • Stannous Octate
•
•
• Colour pigments
•
• Setting reaction–it is a condensation reaction with a by product of ethyl alcohol. (AIPG 2007, 2010)
•
• Stannous Dimethyl siloxane → silicone rubber + orthoethyl silicate octate ethyl alcohol
•
• Setting time 6-12 minutes, mixing time 45 seconds.
•
• Spacing of impression tray for condensation silicones should be 3 mm.
•
• Highest curing shrinkage due to evaporation of ethyl alcohol byproduct. Pour the impression within 30 minutes
•
• Less permanent deformation than polysulfides
•
• Pleasant odor and colour
•
• Low tear strength
•
• Hydrophobic in nature
•
360
• Flexibility is higher than polysulfides
•
• Has limited shelf life (due to oxidation of tin component)
•
• Latex gloves are contraindicated with condensation silicones
•
Addition silicones • Composition:
•
also called polyvi- Base Accelerator

nyl siloxanes • Polymethyl hydrogen siloxane • Divinyl polysiloxane platinum salt - catalyst
•
•
• Fillers • Palladium–Hydrogen absorber
•
•
• Optimum filler size is between 5 -10 nanometer.
•
• (Vinyl siloxane+ Silane siloxane) + Platinum Salt and silicone rubber
•
• Addition silicones has the best dimensional stability among elastomers—lowest permanent deformation 0.05-
•
DENTAL MATERIALS
0.3% and low curing shrinkage 0.17%

• Setting time is 4-7 minutes and mixing and mixing time is 45 seconds.
•
• Extremely hydrophobic
•
• Handling with latex gloves is contraindicated because the sulfur present in the natural latex gloves inhibit the
•
setting of the addition silicone impression materials
• Good shelf life than condensation silicones
•
• Can be disinfected by immersing in 10% hypochlorite or 2% glutaraldehyde solutions
•
• Sometimes hydrogen may be evolved leading to pinpoint voids in stone casts.
•
• The low viscosity silicone materials are preferred for the patients with dry mouth and in those patients with
•
reduced mouth opening. (AIPG 2008)

Polyethers • Primarily function as an impression material.
•
• Composition
•
Base Accelerator

• Polyether • Aromatic sulfonate ester
•
•
• Colloidal silica phthalate • Colloidal silica phthalate
•
•
• Setting time 3—4 minutes and mixing time Is 30 sec.
•
• Stiffest of all elastomers
•
• High tear strength
•
• Dimensionally more stable
•
• Highest cell toxicity. Least biocompatible
•
• Polyethers are hydrophilic and so absorb water and change dimension.
•
• Spacing of 4 mm should be given in the tray.
•
• Polythers have more shelf-life compound to more than two years.
•
• Hydrophilic (KAR 2013)
•

Dust free Alginate
– Dust free alginate is the newer alginate without the silica particles
–
– It is coated with the glycol which makes the particles so heavy that on puffing or manipulation the alginate particles
–
do not blow in the air
– No health hazards as no silica
–
– Less shrinkage
–
– Produce good surface details
–
– Less Water/powder ratio
–
– More elastic and have higher tensile strength as compared to the older counterparts.
–
GYPSUM PRODUCTS
• Chemical from of Gypsum is CaSO4 2H2O {calcium sulphate dihydrate)
•

Classification of Gypsum products
Type I •
•
Impression plaster
Type II • Dental plaster

•
Type III • Dental stone or medium strength stone
•
Type IV • Improved stone or high strength stone
•
Type V • Dental stone, high strength, high expansion
•
Difference between Alpha and Beta Hemihydrate
DENTAL MATERIALS
Alpha hemihydrates Beta hemihydrates
• Manufacture Wet calcination Dry calcinations
•
• Microscopic appearance Cleavage fragments and crystal in form of rods and prisms Needle like crystals
•
• Particle size and shape Smaller, regular and dense Larger, irregular and porous
•
• W/P ratio 0.3 0.5
•
• Porosity Less porous More porous
•
• Mechanical properties Strength and hardness – more Less
•
• Application Dies, master casts Diagnostic casts
•
The principal constituents of dental plaster and stones is calcium sulphate hemihydrate (CaSO4)2.H2O
• Dihydrate 110---130*C hemihydrate 130—200*C anhydrite (AIPG 2008)
•

• CaSO4,2H2O-HCasO4)2.H2O -arrow CaSO4. This reaction drives water of crystallisation.
•
Types of Gypsum Products
Type 1 Type2 Type3 Type4 Type5

• Synonym Impression Model Dental Hydrocal, improved Densite, Improved Dental Extra hard
•
Plaster Stone, Class 1 Dental Stone, Class Stone
Dental Stone II Dental Stone, high
strength dental
• Setting 4-5 mins 12-15 mins 12-15 12-15 12-15

•
• Water powder 0.5-0.75 0.45-0.50 0.28-0.30 0.22-0.24 (AIIMS Nov 0.18-0.22
•

ratio 2013)
• Uses Final/Wash Fill the flasking Construction of As a die material Improved die Material
•
Impressions for denture casts in denture
complete dentures construction constructions
• Setting 0.15 0.30 0.20 (AIPG 2004) 0.10 0.30

•

Expansion
• Compressive 800 1300 3000 5000 7000

•
Strength (psi
units)
362
• Setting time: The time elapses from beginning of • Penetration test:
•
•
mixing until material hardens is known as setting time. – Types of penetrometers:
–
• Mixing time: Time from addition of powder to water Vicat needle Gilmore needle
•
until mixing is completed (mechanical 20-30 sec / hand
• Used for measuring • Two types: small and large
less than minute).
•
•
initial setting time • The small Gilmore needle is 1/4
• Working time: Time available to use a workable mix
•
• Weighs about 300gm, lb heavy and 1/12” in diameter,
•
(3min).
•
and needle diameter – while the large is 1lb and 1/24”
1mm respectively.
• Initial setting time can be tested by initial gilmore.
• The time elapsing from • The time elapsing from the
•
Final setting time can be tested by final Gilmore.
•
•
the start of mixing till start of mixing till the point of
the needle does not the 1lb Gilmore needle leaves
• Setting time can be controlled by is the (NEET 2013, penetrate to the bottom only a barely visible mark on
DENTAL MATERIALS
•
AIPG 2010) of the plaster is the the surface of the set plaster is
‘initial setting time’ known as ‘final setting time’.
– Water powder ratio: The more Water powder ratio,
–
the more setting time.
– Mixing time: The more longer and rapid is the mixing • Die hardeners (AIPG 2005)
–
•

time, the shorter is the setting time. – Improve the abrasion resistance of the gypsum.
– Temperature: Increase In temperature causes
–
– Examples are
–
retardation of reaction (more than 50*C)
–
Cyanoacrylates (AIPG 2007)
– Retarders/accelerators: These are chemical modifiers

Acrylic resin lacquers
–
to regulate the setting time

Polystyrene solution

• Setting expansion can be controlled by water powder
•
ratio, mixing time and by addition of chemicals.
Less water powder ratio and prolonged mixing time AMALGAM
produces greater setting expansion.
• An amalgam is defined as special types of alloy in which
•
mercury is one of the components
Chemicals that decrease the • K2SO4 – 4% • Dental amalgam is the most widely used filling material
•
setting expansion: (AIPG
•
• Borax for posterior teeth
2004, 2007, AIIMS May 2010)
•
Chemicals that increase set- • NaCl, KCl, LiCl
Composition of Amalgam
•
ting expansion • Pre existing set gypsum – Silver: 65%--increases expansion, increases
•
–
particles
strength, whiten the alloy
Accelerators • NaCl – upto 2% – Tin: 29%--reduces strength, hardness, reduces
•
–
• Na2SO4 – 3.4% resistance tarnish and corrosion
•
• KNO3 – Copper: 6%-Increases hardness, strength and
•
–
• K2SO4 >2% expansion
•
• KCl – most commonly used – Zinc: <1%--Scavenger/ deoxidiser
•
–
• Particles of set gypsum
•
• KCl
• Amalgam alloys can be classified into many ways
•
•
Retarder of gypsum prod- • Acetates • Low copper (less than 6%)
Depending upon
•
ucts
•
• Borates Copper content • High copper (more than 6%)
•
•
• Citrates – Admixed – 9-12%
•
–
– Single composition – 13 – 30%
–
Measurement of setting time of gypsum Based on Zinc • Zinc Containing – more than 0.1% Zn
•
content • Zinc free – less than 0.1% Zn
• By loss of gloss method: As the reaction proceeds, the
•
•
gloss disappears from the surface of plaster mix Based on Shape • Lathe cut,
•
• Spherical and
• Exothermic reaction: Rise in temperature can be used as
•
• Admixed
•
guide to measure setting time
•

Lathe cut (AIPG • Produced by milling or lathe cutting a Cu6Sn5 (η) Replaces the (γ2) phase in high copper amalgams
•
2006) cast ingot of amalgam alloy.
• Particles are irregular in shape Cu3Sn (ε) Present in some high copper single composition
•
• Inferior properties due to high mercury amalgams
•
content
• Less plastic • Increasing order of strength
•
– Low copper < admix alloy < single composition
•
• The recommended mercury alloy ratio
–
• High copper alloys are superior to low copper alloys in the
•
- 1:1
•
following respects
Spherical alloys • Produced by atomizing the liquid alloy.
– High resistance to tarnish and corrosion
•
• Spherical shaped alloy
–

(AIPG 2007, 2010)
•
• Require less mercury due to its smaller

– Decreased creep (AIPG 2006)
•
surface area. –so better properties
–

– High strength
DENTAL MATERIALS
• Requires less amalgamation time
–
– This all is due to elimination of gamma 2 phase in high
•
• More plastic and gains good strength
–
copper alloys
•
with lighter condensation forces
• Recommended mercury content is • During setting, amalgam undergoes 3 distinct
•
•
42% dimensional changes:
– Initial contraction due to dissolution of alloys
Generations of Amalgam
–
particles and formation of gamma 1 phase
– Expansion due to impingement of gamma 1 crystals
I Ag + Sn (Binary) –
– Delayed contraction due to absorption of unreacted
–
II Ag + S + Zn + Cu mercury
Net result --- Contraction
III Ag-Sn + Ag-Cu (eutectic alloy), Ag-Cu particles act as strong

fillers and increase the strength of amalgam
• According to ADA-specification: Amalgam should
IV High copper alloys (Cu–29%)
•
not expand/contract more than 20 micrometer/cm at
V Alloy + Indium (Indium–scavenger) 37°C between 5 minutes to 24 hours after beginning of
VI Alloy + Palladium/gold/platinum trituration.
• Secondary/delayed expansion may occur when amalgam
• Setting reaction
•
is contaminated by moisture during trituration/
•
– Low Copper-- condensation: May reach up to 400 micrometers (4%).
–
Ag3 Sn + Hg à Ag2Hg3 + Sn8 Hg • Amalgam may expand due to high mercury content—so
•
Gamma less mercury/alloy ratio and higher condensation pressure
– High Copper (admixed) may eliminate excess mercury.
• Delayed expansion is due to formation of hydrogen gas by
–
Ag3Sn +Ag-Cu +Hg → Ag2Hg3 + Sn8Hg + Ag3 Sn
•
electrolytic action H2O + Zn → ZnOH+H2.
Gamma 1 Gamma2 Gamma (unreacted)
– Occurs usually after 3 -4 days after insertion of
Sn8Hg+Ag—Cu ---→ Cu6Sn5 + Ag Hg3
–
amalgam (AIPG 2006)

Gamma2 (n) Gamma 1 • Mercuroscopic expansion occurs when mercury from
•
• Single Composition gamma 2 phase reacts with gamma phase particles.
•
Ag3 Sn+Cu3- Hg ------→ n + Gamma 1 + Ag2 Hg3 • EAMES Technique: Acc to this, mercury alloy ratio
•
• Importance of different Phases of Amalgam is 1:1. Also known as minimum mercury technique.
The mercury content of the final restoration should be
•
Phase Importance approx. 50% by weight. For spherical alloys it should be
Ag3Sn (γ) Strongest–more this phase in set amalgam, approx. 42% by weight,
more will be its strength
• Increased dryness technique: Another technique for
•
Ag2Hg3 (γ1) Base centered cubic lattice that increases the proportioning mercury and alloys.
tarnish and corrosion resistance of the final • Reduced residual mercury content can occur in
product
•
– Low mercury alloy ratio
–
Sn8Hg (γ2) Weakest phase (AIPG 2002) – Higher condensation pressure

–
Decreases the tarnish and corrosion resistance – Longer trituration time
and also increases the creep
–
– Smaller particle size.
–
364
• Compressive strength of amalgam should be minimum – Condensers have serrated nibs
–
•
310 mpa its tensile strength is between 48—70 mpa. – Larger condensers should be used for condensing
–
• Amalgam achieves 70% strength by 8 hours (AIPG 2005) spherical amalgams as their resistance to condensation
forces is less
•
• Strength can be affected by factors such as • Burnishing of slow setting alloys is contraindicated as
•
•
– Mercury content it can damage the margins of the restoration. Release
–
– Condensation of the free mercury occurs if burnishing increases the
–
– Porosity temperature above 600C
–
– Trituration
• Polishing should be done at least 24 hours after
–
•
• Creep is defined as a time dependent plastic condensation.
•
deformation. Creep values for low copper 0.8-8% high – Use of dry polishing powders are contraindicated as
copper - 0.05-0.9%
–
DENTAL MATERIALS
they can raise the temperature above 600C causing

• The main objective of trituration is to wet the alloy pulpal damage.
•
particles with mercury. – Wet abrasives in the form of paste should be used
–
• Trituration can be done either by hand mixing/ – Tin oxide, zinc oxide, pumice flour and precipitated
–
•
mechanical method. chalk are commonly used for finishing and
– Spherical alloys are usually triturated at low speeds polishing amalgams
• Decreased microleakage found in amalgam is due to
–
while high copper alloys at high speeds •
• Factors affecting trituration formation of corrosion products such as tin oxide and
tin hydroxide at interface between tooth and restoration.
•
– Duration
• Marginal defects are most common in amalgam
–
– Speed
•
restorations
–
• Effect of trituration
•
– Overtrituration reduced working time of all types • Mahler scale is used to describe the severity of marginal
•
defect
–
of amlgam
– Overtrituration favours net contraction • Depth of corrosion for most amalgam alloys can extend
•
–
Overtrituration increases the compressive and upto 100 – 500um (AIPG 2006)

tensile strength of lathe cut alloys (AIPG 2006)
Overtrituration reduced the compressive and • Mercury toxicity
•

tensile strength of spherical and admixed alloys – Less than 0.01% of elemental mercury is absorbed.
–
Overtrituration increases creep while – About of 65-85% of methyl vapour that is inhaled is
–

undertrituration decreases it. retained in the body. (AIPG 2006)

(AIIMS Nov 2013) – Almost 100% of methyl mercury is absorbed in gut.
–

(AIPG 2006)
• Amalgamtors are 3 types: – The lowest level of total blood mercury at which non
–
•
– Low speed: 3200-3400cycles/min specific symptoms start to occur is 35ng/ml.
– Minamata disease in Japan was due to methyl mercury
–
– Medium speed: 3700-3800cycles/min
–
poisoning.
–
– High speed: 4000-4400 cycles/min
– Blood level of mercury in patients of amalgam
–
–
• Appearance of mixed amalgam restorations is 0.7ng/ml while 0.3ng/ml in those
without amalgam restorations
•
– Under mixed: dull grainy, crumbly appearance
– One saltwater seafood meal per week raises blood
–
– Normal: shinning and separates from capsule in a
–
mercury level by 3ng/ml
–
single mass. Mix is warm – Symptoms of mercury poisoning
– Over mixed: soupy and sticks to inside of capsule.
–
Weakness, fatigue, anorexia
–
Hot to touch

Insomnia, irritability, weight loss

Tremors in extremities
• Condensers are instruments with serrated tips of different

– Symptoms of methyl mercury poisoning
•
shapes and sizes, shapes are oval, crescent, trapezoidal,
–
Paraesthesia of extremities, lips and tongue
triangular, circular or square point.

Ataxia

– Condensation is started at the centre and condenser Tunnel vision
–

point is stepped by little towards the cavity walls • Safe disposal of mercury (NEET 2013)
•

normally condensed force is 2-3 kg applied to each – It should never be poured down a drain or sewer,
increment.
–
flushed down a toilet.

– Some studies have shown that no solution (fixing • Condensation: process of cold working–increases the
–
solution in air-tight unbreakable container,
•
hardness, strength and results in fibrous grain structure.
completely prevents the passage of mercury vapour
into environment, so it is recommended sending of – Force of condensation is inversely proportion to
–
mercury containing articles to a recycling laboratory square of diameter of nib
– Force must be 450 to cavity wall and floor
–
– Stepping is a process of condensation whereby
DIRECT FILLING GOLD
–
each time condenser overlaps the preceding
• 100% gold or 24 karat gold is used. compactions.
• Bridging is the creation of void spaces due to failure to
•
• Directly compacted into the cavity
•
completely compact each increment of gold.
•
• Ideal for class V cavities.
•
DENTAL MATERIALS
Forms of Direct Filling Gold RESTORATIVE RESINS
Gold foil • Manufactured by beating pure gold into • Composites were developed in late 1950s and early 1960s
•
•
thin sheets composite is system composed of mixture of two or more
• Size – 4 x 4 inches macro molecules which are essentially insoluble in each
•
• Weight – 4gms – No. – 4 foils other and differ in from.
•
• Highly cohesive • Dental composites contain a high concentration of filler
•
•
• Surface impurities and foil treated with bonded to resin matrix by a coating-coupling agent.
•
ammonia makes it non cohesive
• Used generally for the external surface Chemically Activated Composites
•
veneering of the restorations
– Supplied as two pastes system (base and catalyst)
–
Electrolytic precipitate Powder: Conatins initiator Benzoyl peroxide

Mat Gold • Bulk filler Liquid form: Conatins tertiary amine as

activator
•
• Available as strips and cakes
– Shrinkage occurs towards center of the material
•
–
Mat foil • Mat gold wrapped in gold foil – Manipulation
•
–
• Also used for veneering the external Correct proportion of base and catalyst are
•
surface of the restoration like gold foil

taken on-a mixing pad.
Electralloy • Electrolytic precipitate alloyed with 0.1% Mixed up to 30 seconds by a agate spatula

•
calcium (metal spatula may discolor material)
• Calcium increases the strength and Insert into cavity walls where it is in plastic form
•

hardness Cavity should be overfilled slightly

Powdered Gold • Chemically precipitated gold powder Finishing can be done after 5 mins of mixing

– Chemical activated resin contains chemical
•
with an average particle size of 15um
–
• Goldent: powdered gold wrapped into activator-n dimethyl p-toludene which will react
•
cohesive gold foil creating balls with the initiator (benzyl peroxide) to form free
radicals and Initiate polymerisation.
• Cohesion of gold foil: An example of atomic
•
attraction and welding (AIIMS MAY 2013)
Light Activated Composites

• Non cohesive gold: Made cohesive by heating it before
•
insertion into the cavity. This is known as Degassing/ – Available as single paste system in dark syringes
–
Annealing/ Desorption. Initiator–camphoroquinone

– Gold foil: Bulk annealing or mica tray is the method Activator–diketone

–
of choice of annealing – Activated at 400–500nm i.e. blue region of visible
–
– Goldent: Ethanol flame light spectrum
–
– Electralloy: Electric annealing – UV light curing is not indicated because of its limited
–
•
–
The cavity preparations for DFG restorations should be depth of penetration through tooth structure.
•
with sharp internal line angles and point angles which – Source of light – tungsten halogen bulb
allows a convenient starting
–
– Exposure time–40–60 seconds
–
366
– Darker shades require longer exposure time. must be built up in increments and each increment
–
– Shrinkage occurs towards the light source must be cured
–
– Light emitted may cause retinal damage. So use of – High intensity light may be used; tip should be kept as
–
–
protective eyeglasses is mandatory close as possible to the restoration
– As depth of curing is limited so in deep cavities they – Resin thickness should not be greater than 2-2.5 mm
–
–
Visible light cure UV light cure
• Min 20sec for curing • 60sec
•
•
• Cure upto depth of 2mm • 1.5mm
•
•
• Camphoroquinone --474λ • Benzoin methyl ether
•
•
DENTAL MATERIALS
Composition
Resin matrix Bisphenol A glycidyl methacrylate (BisGMA) + TEGDMA acts as viscosity controller
Triethylene glycol dimethacrylate (TEGDMA)
Filler Silica Increases the strength, hardness, abrasion resistance and

decreases the polymerization shrinkage and water sorption
Coupling Organosilane, Zirconates or Titanates Bond the filler particles to the resin matrix
agent--
Inhibitor Hydroquinone Prevents premature polymerization
Opacifiers Titanium dioxide/aluminium oxide

and coloring
agents
• Polymerisation shrinkage may be same for chemical activators and light cured but pattern is different
•
• Composites can be classified depending upon particle size of fillers into four classes
•
Conventional Small Particle Hybrid
• Particle Size • 8-12 • 1-5 • 0.6-1
•
•
•
•
• Filler • 70-80% • 80-90% • 75-80%
•
•
•
•
• Compressive Strength • 250-300 Mpa • 350-400 Mpa • 300-350 Mpa
•
•
•
•
• Tensile Strength • 50-65 Mpa • 75-90 Mpa • 70-90 Mpa
•
•
•
•
• Modulus of Elasticity • 8-15 Gpa • 15-20 Gpa • 7-12 Gpa
•
•
•
•
• Hardness • 55 KHN • 50-60KHN • 50-60KHN
•
•
•
•
• Water Sorption • 0.5-0.7 Mg/cm2 • 0.5-0.6 Mg/cm2 • 0.5-0.7 Mg/cm2
•
•
•
•
Aesthestics
Good to know
• Microfilled composites is the resin of choice for aesthetic restoration of anterior teeth in non stress bearing areas. They
•
can be attained a smooth polishing on that of the unfilled resin.
• Small particles and hybrid composites can be used for restoration in stress bearing areas.
•
• Composites can be indicated in conditions where the aesthetics is a primary concern and if the patient is allergic to
•
mercury

• The most commonly used etchant is 37% phosphoric acid (30-50%). Concentration greater than the 50% result in
•
formation of monocalcium phosphate monohydrate which prevents further dissolution
• Length of application of etchant is about 60 sec (long for fluoride treated teeth)
•
• Bond strength to etched enamel range from 16-22 Mpa.
•
CEMENTS
• Dental cements is materials of comparatively low strength and are used extensively where strength is not a consideration
•
• Cements can be classified into many ways:
•
– Depending upon the function —Craig
DENTAL MATERIALS
–
– Depending upon the use-— Skinner
–
– Depending upon the setting reaction—EC Combe
–
• Restorative cements can be classified as
•
– Temporary or short term–for days to weeks
–
– Intermediate term–for weeks to months
–
– Permanent or long term–for years
–
• Most dental cements set by acid base reaction except calcium hydroxide and resin cement. Resins set by polymerization
•
reactions
Classification based on composition
• Based on Zinc oxide powder ZOE,
•
• Zinc polycarboxylate, Zinc phosphate
•
• Based on aluminosilicate powder
•
• Glass ionomer and silicates
•
• Based on phosphoric acid liquid
•
• Zinc phosphate,silicophosphates,silicates
•
• Based on polyacrylic liquid
•
• Glass Ionomer and polycarboxylate
•
• Fluoride releasing cements are:
•
– Silicate
–
– GIC (max)
–
– Silicophosphate
–
– Polycarboxylate (least)
–
• Among cements:
•
– Most soluble: ZOE
–
– Least soluble: Resin cements
–
– Most irritant effect on pulp: Silicate cement
–
– Least irritant: ZOE cement
–
– Chemical or true bond: GIC or polycarboxylate (AIPG 2006)
–

• Micro mechanical retention: Resin cements
•
• Factors increasing setting time
•
– Cooling the mixing slab
–
– Decreased P/L ratio
–
– Prolonged mixing time
–
– Loss of water from liquid
–
368
Silicate Cements Other oxides: 2%

• Composition Improves smoothness of mix
•

Powder Liquid Aluminium phosphate:16.2%

Silica–40% Phosphoric Acid–52% Aluminium: 2.5%

Alumina–30% Aluminium phosphate–4% Zinc: 7.1%

Sodium chloride Zinc/Magnesium

Calcium Chloride–19% Phosphate–6% • Setting time is 5—9 minutes.
•

Calcium Phosphate–7% Water–40% • The set cement is a cared structure consisting primarily
•

of unreacted zinc oxide particles embedded in a
• Setting time is 3-8 minutes.
cohesive amorphous matrix of zinc alumino sulphate.
•
• Silicate is the strongest of all dental cements and its
DENTAL MATERIALS
• Cooling the mixing slab markedly increases the setting

•
compressive strength 180 mpa
•
• Tensile strength -- is low which is 3.5 mpa time. It is the most effective method of controlling the
setting time.
•
• Hardness similar to that of dentine (70 KHN).
•
• Powder/liquid ratio is 1.6 gm/4 ml. • Prolonged spatulation retards the setting reaction as the
•
formed matrix is effectively destroyed and more time is
•
• Coefficient of thermal expansion is lower than any
needed to rebuild the bulk of the matrix.
•
other restorative material, which is dose to enamel and
dentine. • Compressive strength of phoshate is 103.5 mpa
•
• pH of cement at time of insertion is 2.8 and it is a severe • Tensile strength of cement is 5.5 mpa
•
irritant to the pulp.
•
• Modulus of elasticity is 13.5 Gpa
• Mixing time is one minute and is mixing is done by
•
• According ADA specification No.8
•
agate/plastic/cobalt-chromium spatula.
•
– (Fine luting) type 1: Film thickness not more than
–
• Anticariogenic property of silicates is due to flouride ions 25 micrometres
•
that are released which react with adjacent tooth structure – (Luting/filling) type 2: Film thickness not more
–
surrounding the restoration - making tooth surface more than 40 micrometres.
resistant to decalcification. • Acidity is quite high at time when they are inserted
•
• Flouride salts melt at lower temperature and dissolve in tooth after start of mixing pH is 3.5 and rapidly
approaches neutrality within 24—48 hr.
•
other ingredients. Thus they are called as ceramic fluxes

(AIPG 2003, 2007, AIIMS May 2010) • Recommended water/powder ratio is 1.5 mg/0.5 ml.
•

• Silicate cements are contraindicated in mouth breathers. • Mixing time of zinc phosphate is 75 seconds.
•
•
• Polishing should be delayed in silicate cements.
•
• Silicates are used in anterior restorations (meant for Zinc Oxide Eugenol Cement
•
aesthetics)
• Zinc oxide when mixed with eugenol sets to hard cement
•
Zinc Phosphate Cements that is compatible with hard and soft tissues of mouth.
• Zinc phosphate is the oldest of luting cements-it is also • According to ADA—4 types of ZnOE cement
•
•
called crown and bridge, zinc phosphate cement – Type I—for temporary cementation
–
• Composition – Type II—permanent cementation
–
– Type III—temporary filling material
•
Powder Liquid
–
– Type IV—Cavity Liners

Zinc Oxide: 90.2% Phosphoric: 38.2%
–
• Composition (AIPG 2008)

•
Principal constituent
Powder Liquid
Magnesium oxide: 8.2% aids Reacts with ZnO

in sintering • ZnO – 69% • Eugenol – 85%
•
•

Silica: 1.4% Water: 36% Controls • Ingredient • Reacts with ZnO
•
•

Rate of reaction • White resin – 29.7%
•


• Zinc Sterate – 1% • Olive oil – 15% plasticizer • Alumina fluoride: 1.6% • Water: Reaction medium
•
•
•
•
• Accelerator Plasticizer • Calcium Flouride: 15.7%
•
•
• Zinc acetate – 0.7% • Sodium Flouride: 9.3%
•
•
• Accelerator improves
•
• Aluminium phosphate: 3.8%
•
Properties
• The set cement consists of zinc oxide embedded in a • The powder contains initiators for light curing and
•
•
matrix of particles of zinc eugenolate. liquid component is modified with hydroxyl ethyl
• Setting time is 4-10 minutes. methacrylate (HEMA)
•
• Addition of drop of water, alcohol and acetic acid • The polymerization starts when exposed to light and
•
•
accelerates the setting reaction while addition of glycerin
DENTAL MATERIALS
subsequently followed by acid base reactions. This is
retards the reaction called ‘Dual Cure’ GIC
• Compressive strength may range from 4—55 mpa. • The structure of set cement consists, of agglomerates of
•
•
• Tensile strength ranges from 0.32—5.8 mpa unreacted powder particles surrounded by silica gel and
•
• Modulus of elasticity ranges from 0.22—5.4 mpa embedded In amorphous matrix of hydrated Ca and Al
•
• Powder/liquid ratio is 4:1 or 6:1 by Weight. poly salts.
•
• Highest solubility among dental cements
Properties
•
• Least irritating cement–pulp friendly cement •
•
•

(AIPG 2001) – Setting time for

–
• Has obtundant or soothing effect on the pulp in deep Type I–4--5 minutes;

•
cavities. Type II--7 minutes

– Compressive strength--150 mpa
Modified ZnOE
–
– Tensile strength--6.6 mpa
–
• ZnOE cements with improved mechanical properties— – Hardness--48 KHN
•
by adding ethoxy benzoic acid (EBA—62.5%)
–
– Glass ionomers bond chemically to tooth surface--
• Resin reinforced ZOE cement
–
bonding may be due to reaction between carboxyl
•
• Cements containing vanillate esters groups of polyacids and calcium in apatite of enamel
•
and dentine.
Glass Ionomer Cements – Glass ionomers posses anticariogenic properties--
–
• Glass ionomers are adhesive tooth coloured restorations (similar to silicates)
•
which were originally used for restoration of eroded areas. – Powder liquid ratio of glass ionomers is 3:1.
–
– Relatively biocompatible
• Classification of glass ionomers:
–
• Among the first three types i.e. type I, type II and type III
•
– Type I: For luting
•
(conventional and light cure) types the highest cumulative
–
– Type ll: For restorations release of fluoride after 30 days is from glass ionomer
–
– Type III: Liners and bases
liner (KCET 08)
–
– Type Iv: Fissure sealant

–
– Type V: Orthodontic cement GIC Modifications
–
– Type VI and VII: Core build up
Metal modi- • Introduced to improve the strength, fracture
–
– Type VIII and IX: Posterior packable GIC for
•
fied GIC toughness and resistance to wear and yet
–
atraumatic restorations maintain the potential for adhesion and
anticariogenic property.
• Composition • Types:
•
•
– Silver alloy admixed: Spherical amal-
Powder Liquid
–
gam alloy powder is mixed with type II
• Silica: 41.9% • Polyacrylic acid: With GIC powder (miracle mix)
•
•
copolymers – Cermet: Silver particles are bonded to
–
glass particles. This is done by sintering
• Alumina: 28.6% characterstics • Tartaric acid: Improves
of a mixture of the powders at a high tem-
•

•
(AIPG 2007) handing
perature.
370
Resin modi- • The two drawbacks of conventional GIC, ie • Properties
•
•
fied GIC moisture sensitivity and low early strength – Setting time is 7 to 9 minutes.
which occur due to slow acid base reaction
–
are overcome by adding some polymerizable – Compressive strength is 55 mpa.
–
functional group for additional curing process – Tensile strength is 6.2 mpa.
–

(AIPG 2008) – The pH of the liquid is 1.0-1.7 and freshly mixed

–
• Other names are: Light cure GIC, Dual core, cement is 3.0-4.0 after 24 hours pH of the cement is
•
Tricure, Resin ionomer, Compomer, Hybrid 5.0-6.0
ionomer
– Because of the larger size of the polyacrylic acid
• Properties:
–
molecules, it is less irritant to pulp than zinc phosphate
•
– Strength: Tensile strength is higher than
cement.
–
conventional GIC
– Adhesion – Binds chemically to the tooth due to chelation of the
–
–
– Adhesion with tooth is similar to conven- carboxyl group with calcium in the tooth structure
DENTAL MATERIALS
–
tional GIC – Provide good thermal insulation, so can be used as
– Adhesion with composite resin is better
–
base material
–
than conventional GIC.
Compomer • Combination of composite and GIC Zinc Silicophosphate Cement

•
(Polyacid • Is result of combination of zinc phosphate and silicate
modified
•
powders.
composite
resin) • Three types of silicophosphate are present according to
•
ADA
Bilayered or • GIC is used as liner under composite – Type l: Cementing medium
•
–
Sandwich restorations. – Type ll: Temporary posterior filling material
–
Restorations • Increases the retention form as GIC bonds – Type lll: Used as a dual purpose – cementing
•
–
both the tooth and composite medium and a temporary filling material
• Fluoride content reduces secondary caries. • Composition
•
•
Tunneling • Joining the occlusal lesion with the proximal Powder Liquid

•
restorations lesion by means of prepared tunnel under the Silicate Phosphoric acid
marginal ridge.

Zinc and aluminium salts
• GIC is the material of choice in this technique

Zinc oxide water
•

Atruamatic • Involves removal of affected tooth structure Magnesium oxide
•
Restoration with hand instruments followed by restoring

(ART) with GIC. • Properties
•
– Setting time is 3-5 minutes
–
– Compressive strength is 165 Mpa
Zinc Polycarboxylate
–
– Powder is incorporated into liquid in 2 or 3 large
–
• First cement system developed with a potential for increments
•
adhesion to tooth structure.
• It is primarily used for cementation of restoration, thermal Calcium Hydroxide Cement
•
insulating base and also used for intermediate restoration • Relatively weak cement
•
and luting agent for orthodontic purposes. • Applications
•
• Composition – For direct and indirect pulp capping
•
–
Powder Liquid – In apexification technique
–
• ZnO: Basic ingredient • Polyacrylic acid copolymer – In pulpotomy (apexogenesis)
–
– As a root canal disinfectant
•
•
–
• MgO: Principal modifier – As a cavity liner and base
•
–
• Properties
• Bismuth oxide: Small
•
– Water solubility is high
•
amounts
–
• Stannous flouride:
– Is alkaline in nature. It has a pH of 11. The high
–
alkalinity and its consequent antibacterial and protein
•
Increases strength,
modifies setting time. lysing effect helps in formation of reparative dentin.
– Effective antibacterial agent.
–

Uses of Cements
Cement Principal use Secondary use

• Zinc Phosphate Luting agent for Restoration and Orthodontic Intermediate Restoration. Thermal insulating bases.
•
appliances Canal restoration.
• Zinc Phosphate Intermediate Restoration

•
• With Silver or Copper Salts
•
• Copper phosphate (red or intermediate Restoration Root canal
•
black) Restorations
• Zinc oxide Eugenol Temporary and Intermediate
DENTAL MATERIALS
•
Restoration. Temporary and permanent luting
agent for restorations. Thermal insulation bases.
Pulp capping agent
• Poly Carboxy!ate Luting agent For restoration. Thermal insulating Luting agent for restoration for orthodontic appliances.
•
bases.
• Silicate Anterior Restoration.

•
• Sllico Phosphate Luting agent For orthodontic appliances Intermediate Restoration
•
Luting agent
• Glass Ionomer Coating for eroded areas, Luting agent for Pit and fissure Sealant, Anterior restorations
•
restoration bases
• Resin Luting agent or restoration Temporary Restoration

•
• Calcium hydroxide Pulp Capping agents, Thermal insulating bases
•

(AIPG 2007)

Nice to Know Points-Cements
• Cement that has highest strength • Silicophosphate GIC
•
•
• Truly (chemically) adhesive to tooth structure (AIIMS-96)
•

• Bond both to enamel and dentin • Polycarboxylate
•
•
• That bonds to enamel but not to dentin (AIIMS01) • Zinc phosphate
•

•
• Least thickness of luting film • 18 microns
•
•
• That is used as orthodontic adhesive (Man 97, Ka 2k) • ZOE
•

•
• Luting all ceramic restorations • GIC + Resin cement
•
•
• Chief constituent of root canal filling and periodontal dressings • ZOE
•
•
• Intermediate restorative • ZOE
•
•
• Most alkaline • Calcium hydroxide
•
•
• Most acidic • Zinc phosphate
•
•
• Commonly used pulp capping agent and liner • Calcium hydroxide
•
•
• Contraindicated in mouth breathers • Silicophosphate
•
•
• Cements that set by chelation • ZOE and polycarboxylate
•
•
372
Most stable (AIPG-97) ZOE (main drawback is it has least strength and hence used as temporary restoration)
Least Irritating to the ZOE,polycarboxylate and glass Ionomer

pulp
Most Irritating to pulp Sillico phosphates, silicates and Ionomer
(AIIMS-2k, Kar-98)
Least soluble in oral Silico phosphates, silicates and zincphosphate in order
cavity (Kar-97, PGI-95)
Thinnest film thick- Resin cement followed by glass Ionomer

ness (AIPG 97)
Most soluble In oral
DENTAL MATERIALS
Zinc phosphate
cavity (AP-04, AIPG
2014)
Most irritating to the Silicate cement
pulp
Most anticariogenic Silicate, silicophosphate and zinc phosphate silicate cement
Anticariogenic activity Silicate silicophosphate, GIC and polycarboxylate
Thermal expansion Silicate cement

close to tooth struc-
ture
Bacteriostatic Copper oxide
That Is commonly ZOE

used as temporary
filling
Commonly used as Zinc phosphate
temporary luting
(TNPSC-99]
DENTURE RESINS AND POLYMERS

• Synthetic resin—these are non - metallic compound, which have plastic like characteristics and are capable of changing to
•
material of higher molecular weights
• Based on behaviour resins can be classified as “thermoset” and “thermoplastic*
•
Thermoset Become permanently hard when heated above a E.g. vulcanite
resins critical temperature and they do not soften again
on heating.
Thermoplastic Softens under heat, becomes sufficiently plastic Impression compound and acrylic resin
to mold into any shape and on cooling will
harden into that particular shape.
• Condensation polymerization: Involves combining two dissimilar molecules into a third product that is entirely different
•
• Additive polymerization: both reactants are combined to form the product
•

Heat-Activated Denture Base Resins The degree of polymerization achieved using

chemically activated resins is not as complete. This
– Composition indicates there is a greater amount of unreacted
monomer in denture bases fabricated via chemical
–
Powder Liquid activation.
• Prepolymerized spheres of • Non-polymerized methyl First it acts as a plasticizer that results in decreased

•
•
poly (methyl methacrylate) methacrylate transverse strength of the denture resin.
• Benzoyl peroxide(initiator). • Hydroquinone(inhibitor) Second the residual monomer serves as a
•
•

• Glycol dimethacrylate potential tissue irritant thereby compromising the
•
(cross-linking agent) biocompatibility of the denture base.
• Initial hardening of the resin generally will occur within
•
30min of final flask closure. The flask should be held
DENTAL MATERIALS
Technique used
under pressure for a minimum of 3 hrs.
COMPRESSION • Polymer-to-Monomer Ratio: • Fluid Resin-Technique
•
•
MOLDING TECH- 3:1 (volumetric shrinkage may be
NIQUE limited to approximately 6%(0.5% Advantages Disadvantages
linear shrinkage) • Improved adaptation to • Noticeable shifting of
•
•
• Polymer-Monomer Interaction: underlying soft tissues, prosthetic teeth during
processing
•
These stages may be described as • •
Decreased probability of
– Sandy damage to prosthetic teeth • Air entrapments within the
•
and denture bases during denture base material
–
– Stringy
deflasking,
–
– Dough like • Poor bonding between the
–
•
– Rubbery or elastic and • Reduced material costs, and denture base material and
–
•
– Stiff. • Simplification of the flasking, acrylic resin teeth,
–
• Dough-Forming Time: Less
•
deflasking, and finishing • Technique sensitive
•
than 40 min from the start of the
•
procedures.
mixing process. In clinical use the
majority of resins reach dough like
consistency in less than10 min. Light-Activated Denture Base Resins
• Working Time: 5 min, can be • The single-component denture base resin is supplied
•
increased by refrigeration.
•
in sheet and rope forms and is packed in lightproof
• Most commonly used technique
pouched to prevent inadvertent polymerization
•
Injection Molding • The polymerization process is • Polymerization Shrinkage: Less than 1%. assembly
•
•
Technique exothermic. These components causes the resin to contract at approximately the same
may boil. rate as the surrounding dental stone.
Polymerization Via • This technique employs a specially • Comparison of heat and self-cured
•
•
Microwave Energy formulated resin and a nonmetallic
flask • Property • Self-cured • Heat-cured
•
•
•
• Results in less porosity
• Composition • Activator present • Activator absent
•
•
•
•
• Heat • Not necessary • Necessary
•
•
•
Chemially Activated Denture Base Resins • Porosity • Greater • Lesser
•
•
•
– Cold curing, self-curing, or auto polymerizing resins. • Molecular • Less • More
–
•
•
•
– Composition weight
–
A tertiary amine • Residual • More (4-5%) • Less (0.5%)

Dimethyl-para-toluidine, is added to the denture
•
•
•
Monomer

base liquid (i.e. monomer) activator • Strength • Less • More

(AIIMS May 2012)
•
•
•
• Flasking • Easy to deflask • Difficult to deflask

The fundamental difference between heat-
•
•
•

activated resins and chemically activated resins is • Colour • Poor • Greater
•
•
•
the method by which benzoyl peroxide is divided stability
to yield free radicals. • Distortion • Greater • Lesser
•
•
•
374
• Crazing • Cross Linkage: Formation of Three Dimensional
•
Molecules by interaction between individual linear chains
•
– Dimensional changes may occur during relaxation
– It increases strength and reduces water resorption
–
of processing stresses; these changes generally do
not cause clinical difficulties.
Stages of Polymerization
– In contrast, stress relaxation may produce small
–
surface flows that can adversely affect the aesthetic Inititation/ Induc- • Time during which the molecules of
and physical properties of a denture.
•
tion period initiator become activated and start to
– The production of such flows, or microcracks, is transfer energy to monomer. Initiation
may be brought by heat, chemical
–
termed crazing, by small linear cracks, imparts
(benzoyl peroxide) and light activated
“ hazy” or “Foggy” appearance surface cracks (camphoroquinone-VLC)
predispose a denture resin to fracture
DENTAL MATERIALS
– Crazing generally begins at the surface of a resin Propogation • The bulk of polymerisation occurs and
•
is usually accomplished by employing
–
and is oriented at right angles to tensile forces. external heat
Micro cracks formed in this manner subsequently
progress internally. Chain transfer • The chain termination can also result
•
from chain transfer. It differs from
termination in that the active state is
• Denture resins display viscose elastic behavior. The rate transferred from an activated radical to
•
at which this progressive deformation occurs is termed an inactive molecule
the creep rate. This rate may be elevated by increases in
temperature, applied load, residual monomer and the Termination • The chain reaction can be terminated
•
presence of plasticizers. either by direct coupling or by exchange
of hydrogen atom from one growing
• The Charpy impact strength for a heat-activated denture chain to another
•
resin may range from 0.98 to 1.27 joules. Values for high-
impact resins such as Lucitone 199 can be twice as high • Inhibition: A chemical added to monomer to inhibit the
as the values reported for conventional poly (methyl
•
polymerisation at room temperature (inhibitor)
methacrylate) resins. The knoop hardness values for heat-
activated resins may be as high as 20, whereas chemically • Various types of resins used in dentistry are acrylic, vinyl,
•
activated resins values of 16 to 18. polyterene, epoxy and other resin systems etc.
• Clinical applications • Separation media is applied to protect resin from

•
•
– Monomer is toxic when inhaled contacting with gypsum surface
–
– The advantage of cross-linked polymer is that it – To prevent water from mould entering into the
–
is more resistant to organic solvents (acetone in
–
acrylic resin as it may affect rate of polymerization
diabetics) to surface cracking and yields a polymer – To prevent monomer penetrating into mould
that is easier to grind
–
material causing plasters to adhere to acrylic resin
– Addition of butadiene-styrene rubber to resin as a and produce a rough surface. (AIPG 2010)
–
plasticizer is used for patients who have a history of

– Types of separation media are tin foil, soap, starches,
breaking dentures.
–
sodium silicate, alginate compound solution etc
– Light: Curable resins are used to make impression
– The most popular separation medium used is
–
trays
–
– Vinyl acetate ethylene co polymer is used to make sodium alginate solution which is water soluble
when applied they react with calcium of plaster/
–
mouth guards and fluoride application trays.
– All dentures are radiolucent and cannot be located, stone mould material to from a film of insoluble
Calcium alginate.
–
radiographically becomes a problem, the risk of
aspiration during accidents. Hence 10-15%bismuth
is added to incorporate opacity but bismuth • Proportion of polymer-monomer= 3:1 by volume and 2:1
•
increases the water sorption of dentures by weight.
– Due to low thermal conductivity dentures patients – Too much monomer (lower p/m ratio) will cause
–
–
notice low thermal stimulation. greater polymerisation shrinkage, extra time and
tendency for porosity to occur.
• CoPolymer: Copolymer is a resin formed by combining – Too little monomer (higher p/m ratio) will result in
•
–
of monomers that are chemically different (AIPG 2001) granular porosity and difficulty in working


• After final closure of flask: They should be kept at Cavity Varnish
•
room temperature for 30 to 60 minutes–this is called • Cavity varnish is a solution of one or more resins
Bench curing
•
which when applied on cavity walls evaporates leaving
– Heat the flask in water at 60-70*C for 9 hrs restoration and dentinal tubules.
–
– Heat the flask at 65*C for 90 mins, then boil water
– The film thickness ranges from 0.25 mm (2-40
–
for 1 hour for adequate polymerising in thinner
–
portions. micrometres)
• Thermal expansion, polymerisation contraction and – Composition of varnish is natural gum such as copal
–
•
thermal contraction occur during curing cycle resin/synthetic resin dissolved in an organic solvent
• When temperature of dough increases above 60*C the such as alcohol/acetone/other.
– Cavity varnish reduces microleakage around margins
•
molecules of benzyl peroxide decompose to free radicals
–
-- a free radical reacts with monomer and a new free of restoration prevents entry of corrosion products
DENTAL MATERIALS
radical is formed which in turn gets attached to another (thus prevents discolouration) etc.
monomer molecule. – Cavity varnishes are contraindicated in the following:
–
• The proportion of polymer/monomer used in fluid resin Composite—because it may react with resin
•
technique is 2:1–2.5:1 GIC: Because it will interfere with adhesion in

condition where therapeutic effect is needed such
Properties of Acrylic Resins as ZnOE, CaOH etc.
– Cavity base is selected on basis of design of cavity,
Melting point of monomer -48°C
–
type of permanent restorative material, proximity of

Boiling point of Monomer 100.8°C
pulp etc.

Density 0.945 g/ml at 20°C – For amalgam: CaOH, ZnOE can be used as bases for

–
Polymerisation heat 12.9 kcal/mol DFG-zinc polycaboxylate.

Volume shrinkage 21% (linear – 0.53%) – For resin: CaOH (eugenol may interfere with

–
Density of Polymer 1.19 gm/cm3 polymerisation)

Compression strength 75 Mpa
Dental Waxes

Tensile strength 52 Mpa

Hardness (H and S) 18-20/16-18 Khn • Waxes are solid substances made up of esters plate wax,
•

Modulus of Elasticity 2400 Mpa inlay wax, sticky wax, boxing wax.

• Classification:
LINERS, VARNISH AND WAXES
•
According to use • Pattern wax
•
– Inlay casting
• Cavity liners are used like cavity varnish to provide
–
– RPD casting
•
a barrier against the passage of irritants from cement
–
– Base plate
restorative materials and to reduce sensitivity of freshly
–
• Processing wax
•
cut dentine. – Boxing wax
–
• Composition of cavity liner is suspension of CaOH in – Utility wax
–
– Sticky wax
•
organic fluid such as ethylketone, ethyl alcohol
–
• Impression wax
• Cavity liners neither possess mechanical strength nor
•
– Corrective wax
•
provide any significant thermal insulation
–
– Bite registration wax
–
• Cement base is a layer of cement place under the
According to origin • Mineral waxes:
•
permanent restoration to encourage of pulp and to
•
protect against numerous types of insult to which it is – Paraffin wax and microcrystal-
–
line waxes
subjected • Plant waxes:
– Cement based may be of low strength and and high
•
– Carnauba wax, Candellila
–
strength.
–
wax, Japan wax, cocoa butter
– High Strength bases provide thermal protection, eg. • Insect waxes:
–
•
ZNPO4- GIC reinforced ZnOE etc. – Bee wax
– Low strength bases act as a barrier for irritating
–
• Animal waxes:
–
•
chemicals. Eg. CaOH, ZnOE etc. – Spermaceti (dental floss coat-
• Thickness of cavity base should be 0.75 mm.
–
ing) (AIPG 2004)

•
376
• Composition
•
Paraffin wax 60-70% Main ingredient of the wax. Disadvantage is high melting point
Carnuba or Cande- 25-30% a. Increases melting range of paraffin temperature

lilla b. lncreases hardness

c. Decreases flow paraffin at oral temperature

d. lmparts glossiness to the wax

Rosin 5-10% a. Increases the hardness

b. More flake-resistant

or Gum Dammer c. Enhances smoothness and lustre may replace part of paraffin

Ceresin
DENTAL MATERIALS
Added colours
• Uses of Waxes
•
Types of wax Uses
• Base plate • Used as base plate tray to establish Vertical dimension, plane of occlusion, and initial arch form (complete denture
•
•
construction)
• Boxing • Build up vertical walls around impression to produce desired size and form of base of cast
•
•
• Utility • A desirable contour to a perforated tray for use with hydrocolloids
•
•
• Sticky • Used for joining metal parts before soldering and for joining fragments of broken dentures before repair procedure
•
•
• Bite • Articulate correctly certain modes of opposing quadrants
•
•
registration
• Impression • Used to record non-undercut edentulous portion of the teeth
•
•
• Casting • Pattern for metallic framework of rpd and other similar structures
•
•
• Thermal contraction of wax from mouth temperature to room temperature is about 0.3%
•
• Waxes have low thermal conductivity and high coefficient of thermal expansion (350 x 10-6/0C) (BHU -07)
•

• Glass transition temperature of inlay wax is 35 C
0
•
• Working range of inlay waxes is the temperature at which a flow of 50-60% occurs and must remain at or below 43%
•
• Dental Inlay casting wax was divided Into 2 types
•
– Types I--medium wax-direct technique
–
– Types II--soft wax-indirect technique for inlays/ crowns
–
• Inlay wax has highest thermal expansion that is linear expansion of 0.7% with increase in temperature of 20*C
•
• Smoothening of inlay wax is improved by addition of Gum dammar. (flake resistant)
•
• The main ingredient of inlay wax is paraffin (40—50%)
•
• Distortion is the most serious problem, which is due to release of stresses inherent in pattern and are caused due to
•
– Contraction on cooling
–
– Occluded gas bubbles
–
– Change of shape of wax during moulding etc. (AIPG 2008)
–

Mouth Temperature Waxes (AIPG 2004)
• These are designed to flow at mouth temperature but do not flow at room temperature
•
• Uses
•
– To record posterior palatal seal in complete denture patients
–
– To record functional impression of tissues in a distal extension RPD via fluid wax functional impression technique
–
• Examples
•
– Iowa wax
–
– Koreecta wax no. 4
–

– H-L physiologic paste
–
– Adaptol
–
• Korecta No. 1 wax is a hard wax that is used to reinforce the impressions taken by softer waxes like Iowa or Korecta No 4 wax.
•
It is not a mouth temperature wax.
CERAMICS
• Ceramic is a compound of metallic and non-metallic compounds. Porcelains are glass ceramics
•
• All porcelains are ceramics but all ceramics are not porcelain
•
• Dental ceramics are the most suitable tooth coloured restorative materials used to make denture teeth, single unit crowns,
•
fixed partial dentures and labial veeners
• Feldspathic porcelain- A ceramic composed of a glass matrix phase and one or more crystalline phases such a leucite, K2O.
DENTAL MATERIALS
•
Al2O3.4SiO2)
Classification
Classification based • Denture teeth porcelain
•
on use • Metal ceramics
•
• Veneers
•
• Inlays Crowns Bridges
•
According to applica- • For porcelain teeth
•
tion • For Ceramo-metal restorations (Metal-Ceramic Systems)
•
• For All-ceramic restorations (All-Ceramic System)
•
According to micro- • Non-Crystalline Ceramics e.g.: Feldspathic porcelain
•

structure • Crystalline Ceramics e.g.: Aluminous porcelain, Glass-Ceramics
•

Dental porcelains are • High fusing 1300°C (2372°F)
•

classified according • Medium fusing 1101 – 1300°C (2013 – 2372° F)
to the firing tempera-
•

• Low fusing 850 – 1100°C (1562 – 2012°F)
tures as
•

• Ultra-low fusing <850°C (1562°F)
•

According to applica- • Core porcelain
•
tion • Body porcelain
•
• Enamel porcelain
•
According to method • Air fired (i.e., at atmospheric pressure)
•
of firing • Vacuum fired (i.e., below atmospheric pressure
•
• Composition of porcelain – Titanium, Zirconium: Opacity
–
– Manganese oxide: Lavender
•
Feldspar 60-80% (flux matrix, surface glaze)
–

Kaolin 3-5% (binder) • Stages in firing:
•

Quartz 15-25% (filler) Low bisque • Material becomes rigid, very

•
Alumina 8-20% (glass former) little shrinkage

Boric Oxide 2-7% (glass former) Medium bisque • Complete cohesion of powder
•

particles, lacks translucency and
Metallic Pigments 1% (Colouring)
high glaze-definite shrinkage

(AIPG 2007)
• Metallic oxides: Colouring agents to obtain various

•
shades simulating natural shades (AIPG 2014) High Bisque • Shrinkage is complete and mass
•

exhibits smooth surface light
– Iron oxide or Nickel oxide: Brown porosity
–
– Copper oxide: Green
–
– Cobalt Oxide: Blue
–
378
• Firing shrinkage is 40% by volume. – Metal oxide
–
•
• Aluminous porcelain: 40-50% alumina is added to core – Metaloxide-metaloxide
–
– Cohesive within metal
•
porcelain. The dispersed alumina crystals strengthen the
–
porcelain by interruption of crack propagation. – Cohesive within porcelain
–
• Porcelains are glazed to give smooth and glossy surface, CAD CAM (Computer Aided • Used to prepare metal and
•
•
enhance aesthetics and help in hygiene. Glazed porcelain Design and Computer crown inlays and crowns
is much stronger than unglazed porcelain. Aided Machining) without need for impressions
in casting procedure
– Self glaze is more permanent than applied glaze.
Copy-milling • The process of cutting a
–
– Pyroplastic flow of material occurs due to high
•
grinding a structure using
–
glazing temperature, which causes rounding of sharp a device that traces the
line angles and edges of restoration. surface of a master metal,
DENTAL MATERIALS
ceramic, or polymer pattern

• Properties and transfers the traced a
spatial positions to a cutting
•
– Compressive strength of porcelain is 331 mpa. station where a blank is
–
– Tensile strength is very low so brittle and results in cut or ground in a manner
–
fracture-34 mpa. similar to a key-cutting
– Shearing strength is low and is 110 mpa. procedure.
–
– Modulus of elasticity is high and is 69 GPA. Core ceramic • An opaque dental ceramic
–
– Surface hardness is more than natural teeth—460
•
material that provides
–
KHN. sufficient strength,
– Specific gravity varies from 2.2—2.3. toughness and stiffness to
support overlying layers of
–
– It is insoluble and impermeable to oral fluids—
veneering ceramics.
–
however flourides can stain the porcelain
• Composites, ceramics and
restoration.
•
titanium can be copy milled.
• The first commercially castable glass ceramic is dicor • Glass-ceramic: A ceramic consisting of a glass matrix
•
which was developed by carning glass works.
•
phase and at least one crystal phases that is produced by
• Cerestone is another type of ceramic which is shrinkage the controlled crystallization of the glass.
•
free and has Al2O3 (aluminium oxide) as principal • Green-state: A term referring to an pressed condition
component (70%)
•
before sintering.
– Radiopaque porcelain is cerestore. • Slip casting: A process used to form” green” ceramic
–
• Ceramming-glass ceramic material that is formed in
•
shapes by applying a slurry of ceramic particles and
•
desired shape as a glass then subjected to heat treatment water or a special liquid to a porous
to induce partial devitrification of glass. (AP 2013)

• Castable ceramic: A glass or other ceramic specially • Substrates (such as a die material) allowing capillary action
•
to remove water and the mass to deposited particles.
•
formulated to be cast into a refractory mold to produce
a core coping or core framework for a ceramic prosthesis. • Sag resistance: The resistance of alloys to creep when
•
• To overcome the disadvantage of porcelain – that is heated to high temperature during firing of porcelain
•
low tensile strength, the porcelain is bonded to an alloy
Ceramic Processing Methods
substructure–metal fused porcelain
Machining or grinding of the core structure is of
• The alloy used for bonding should have

particular importance since flows or minute cracks can be
•
– Coefficient of thermal expansion similar to porcelain introduced that can possibly be propagated to the point of
–
(AIPG 2004) fracture during subsequent initial forming
– Fusion temperature higher than that of porcelain Method Examples
–
– Should be capable of forming a good bond with

Powder Condensation (Vitadur-N, JPS empress,
–
porcelain

duceram LFC)
– Should have high proportional limit
Hot-pressing IPS Empress 2,finess,
–

• Bond failures in metals ceramics are classified by O Brien Slip Casting Dicor, In-ceram

•
– Metal-porcelain Slip-casting In-Ceram Cerec Vitablocs

–

(CAD-CAM) Procera AllCeram • Eutectic: It is a combination of two or more metals that

•
Cercon Lava, are mutually soluble in molten state but form into separate

Densely sintered Digizon,proCAD,Zircon. grains when the alloy solidifies. It has a definite melting
point lower than constituent metals. (AIPG 2001)

Glass infiltered In-ceram spinell,In-ceram

• Solid Solutions: An alloy in which the constituents freeze

alumina
•
without segregation of pure metals–most dental alloys are
• Clinical considerations of this type
•
– Uses
• Alloys can be classified depending upon the elements
–
To fabricate denture teeth
•
present such as binary–two constituents, tertiary–three,

Orthodontic brackets
quartenerary-four, quinary–five etc

Endodontic posts
• Examples of different types of alloys are:

Implants
DENTAL MATERIALS
•

Veneers – Eutectic: Copper and silver

–
Inlays – Solid solutions: Gold and silver

–
Single crowns – Chemical compounds: Silver and tin (Ag3Sn)

–
Bridges
• Constitutional Phase Diagram: A diagram that

• Criteria’s for selection of ceramics
•
•
Tooth vitality
depicts the phase of metal and composition as plotted
against temperature

Tensile strength

Selection of material • Dislocation: A defect within the crystals and along
•

Selection of method of fabrication these lines of dislocation weakness within the metal is

Shade selection created

• Coring: Is the induction of a non homogenous structure
•
WROUGHT ALLOYS such as a solid solution alloy solidifies
• Metallurgy-is the science of economically extracting

Steels
•
metals from their ores applying them to useful purposes.
• Metal-chemical element that Ionises positively when in – Steels are iron based alloys
•
–
solution. – In wrought metal alloys carbon content is less than
–
• Metalloids-there are elements that behave like metals 0.25%.
Cast iron-carbon content is 4—5%
•
under certain conditions and do not ionize positively in

solution. Examples of metalloids are carbon and silica. Stainless steel it is less than 1.7%.

• Metals have a melting point and alloys have a melting • Composition
•
•
range. Carbon steel Stainless steel
• A crystalline material has a definite melting point and • Composition Fe – 98% Fe – 81%
•
orientation of atoms called space
•
C – 1-1.2% Cr – 18%
Mn – 0.2% C – 0.61%
• Metals can be classified into a) noble metals b) Base Si -0.2%
•
metals
• Corrosion Very low High
• Base Metals–are those whose compounds with oxygen
•
resistance
•
are not decomposable by heat alone, retaining oxygen at
• Cutting High Less than carbon steel
high temperature
•
efficiency and dulls rapidly with
• Noble Metals-are those whose compounds with oxygen use
•
are not decomposable by heat alone at a temperature
not exceeding that of redness (AIPG 2008) • Physical Stiffer, stronger, Less harder and is not
•
properties harder, more brittle brittle

• The two metals that expand on solidifying from molten
•
state are bismuth and antimony • Efficiency Superior at high Superior at low speed
•
speeds and used and used for cutting
• Recrystallisation of metal: After the metal has been for cutting enamel dentin
•
working cold state, it may be heated to temperature
380
• Types/forms of steel
•
Ferrite Martensite Austenite
• Pure iron at room temperature Formed when austenite is cooled quickly Iron at temperature between 922 – 1394°C
•
(Quenched)
• Least strength Highest Moderate

•
• Good corrosion resistance Least Highest
•
• Least used in dentistry Used for making surgical and cutting 18-8 (18% - Cr, 8% Al) wires – used for making
•
instruments orthodontic wires greater ease of welding
• Cutting edge of stainless steel instruments is made up of martensite form

DENTAL MATERIALS
•
• Stainless steel with less strength is ferrite.
•
• Memory of stainless steel can be attributed to change in form i.e austentite to marsentite
•
CASTING ALLOYS AND CASTING PROPERTIES
• Noble metal alloys and base metal alloys are the common dental casting alloys
•
• As the Puregold is soft and ductile –they are allocated commonly with copper silver, Palladium, nickel and zinc etc.
•
• Gold content of dental casting gold alloys have been referred in terms of
•
1. Karat

2. Fineness.

• Karat is the part of pure gold in 24 parts of alloys.
•
• Fineness of a gold alloy is the parts per thousand of pure gold. Pure gold is thousand fine.
•
• Classification of Casting gold alloys
•
• Type I (Soft) Small inlays
•
• Type II (medium) Inlays, 3/4th crowns, pontics
•
• Type III (hard) Full crowns, short span bridges
•
• Type IV (extra hard) Long span bridges, clasps, partial denture frame work
•
• Composition of gold alloys
•
Type %Au %Cu %Ag %Pd %Pt
I. 83 6 10 0.5
II. 77 7 14 1 __
III. 75 9 11 3.5
IV. 69 10 12.5 3.5 3
– Gold: Provides tarnish and corrosion resistance, ductility and malleability

–
– Copper: Reduces melting point, hardener, helps to age harden alloy.
–
– Silver: Increases strength and hardness, imparts white colour.
–
– Platinum: Increases strength and corrosion.
–
– Zinc: Scavenger for oxygen.
–
• Properties of type III and type IV
•
– Density: 15.5g/cm3- 15.2 g/cm3
–
– Melting Range: 930 – 945*C
–

– Yield strength: 207-275mpa
–
– Hardness: 121-140 VHN
–
– Casting shrinkage: 1.4%
–
Hardening Treatments
Hardening heat treat- •
•
In order to improve physical properties-gold alloys are heat hardened.
ment/age hardening ––
It is done by soaking the casting at a specific temperature for a definite time usually 15—30 minutes
(temperature is usually 200-400*C)
– Before it is heat hardened it should undergo softening heat treatment.
–
– Heat hardening improves properties such as proportional limit, strength and hardness but decreases
–
ductility.
DENTAL MATERIALS
Softening heat treatment • Is indicated for structures that are to be ground, shaped or cold worked.
•
– Method— casting is placed in an electric furnace for 10 min at a temperature of 700*C and then
–
quenched in water. All properties such as proportional limit, hardness, tensile strength are reduced
but ductility is increased.
Tempering treatment • Reduces hardness but increases toughness.

•
Cold working/work hard- • Increases hardness, strength but decreases ductility
•
ening/strain hardening • The effects of cold working can be reversed by simply heating the metal. It is called as Annealing.
•
• Stainless steel can be hardened by both age hardening • Properties
•
•
and cold working (AIPG 2003) – Density: 8—9gm/cm3

–
• Application of ‘Lost wax Technique’ for the fabrication of – Fusion temperature: 1250-1450*C
–
•
cast inlay was first reported by Taggart (BHU 07) – Yield strength: 710 mpa

–
Cobalt—chromium alloys are also known as stellites because – Modulus of elasticity: 225x10 raised to power-3 mpa
–
they maintain their stringes, star like appearance under – Hardness: 432 VHN
–
different conditions. – Casting shrinkage: 2.3%
–
• Composition of cobalt-chromium alloys (BMA) – Tarnish and corrosion: Resistant
–
• Base metal alloys have low density, high stiffness (modulus
•

(AIPG 2003)
•
of elasticity), more passivity, low proportional limit and
– Cobalt 55-65%
less cost when compared to gold alloys.
–

– Chromium 23-30%
Casting shrinkage: Thermal shrinkage + solidification
–

– Nickel 0-20%

–

– Carbon 0.4% shrinkage
–

– Iron 0.5% • Base metal alloys have higher casting shrinkage (2.3%)
–

• Cobalt: Hardness, strength, rigidity, high melting point
•
than gold alloys (1.5%)
•
• Chromium: Corrosion resistance reduces melting point, • Among aluminium, chromium and titanium, titanium is
•
Eases strength, hardness, modulus of elasticity, fusion
•
the most corrosion resistant. For passivation, atleast 12%
temperature (AIIMS Nov 2013) of the chromium should be present.

• Carbon: It is more critical, small amounts may have effect • Ni Ti alloys exhibit shape memory and super elasticity
•
on strength, hardness, ductility
•

(AIPG 2007) (NEET 2013, AIPG 2003)

Alloys Composition
Elgiloy Cobalt – chromium – nickel
Nitinol Nickel – titanium
Beta titanium Titanium – Molybedenum – Aluminium
Titanium alloys Titanium – Aluminium – Vanadium (Ti- 6Al-4V)
382
CASTING PROCEDURE
• Wax pattern is made up type II Inlay casting wax.
•
• Sprue former – is made up of wax, plastic or metal-thickness should be in proportion to wax pattern
•
Purpose • To form a mount for wax pattern to create a channel for elimination of wax during burn out to compensate for alloy
•
shrinkage during solidification
Diameter • If the diameter of a sprue former is large and the wax pattern is thin, it may lead to a distortion of the wax pattern
(AIPG 2012)
•
• If the diameter of sprue former is smaller, it may lead a localized shrinkage. Porosity or suck back porosity because
•
this area solidifies the casting itself
Length • Length of sprue is 3/8’ to 1/2’ so that wax pattern will be approximately 1/4’ form top of ring
DENTAL MATERIALS
•
• However too short a sprue places the wax pattern far away from the end of casting ring as a result gases formed
•
during casting cannot be adequately vented so as to permit the molten alloy to fill the ring completely. This may lead
to porosity.
Placement • Should be attached to the thickest portion of the wax pattern to prevent turbulence
•
• Should be sprued at 45°C angle to the proximal area
•
A ring liner (asbestos/non-asbestos) is placed inside the casting ring-which will allow for mould expansion, acts as a
thermal insulator
• Wax elimination: The purpose of burnout is the elimination of wax from mould cavity and achieving thermal expansion
•
• Burnout temperature
•
– Gypsum investments: 400*C in 20 minutes and maintains it for 30 minutes, raise the temperature to 700*C and
–
maintain it for 30 minutes
– Phosphate investments: Temperature range from 750 – 9000C and maintaining it for 30 min
–
• Casting machines can be divided into two general types.
•
– Centrifugal force type
–
– Air pressure type.
–
• The various modes of fusing alloys are:
•
– By blow torch
–
– Electrical induction.
–
• Pickling—surface oxides from casting are removed by pickling in 50% hydrochloric acid. (NEET 2013)
•

• The fuel used is a combination of natural/artificial gas in air–oxygen and acetylene gas (high fusion alloys)
•
• The flame has four zones
•
Mixing zone Air and gas mix here
Combustion zone Surrounds inner zone: Green in colour - zone of partial combustion
Reducing zone Blue in colour: Just beyond green zone--hottest past - fusion of casting
alloy (AIPG 2007, 2010)

Oxidising zone Outer most zone: Complete combustion occurs, hottest zone
Die Materials
Gypsum (die stone) • Greatest accuracy with very slight expansion during setting
•
• Have least resistance to abrasion
•
• Die material of choice with hydrocolloid impression
•

Epoxy resins • Shrink on setting
•
• High resistance to abrasion
•
• Most commonly used die material
•
Electro plated silver • Have lethal potential due to the usuage of silver cyanide
•
• Polysulphide impressions can be easily electroplated
•
• Acrylic polyester and epoxy Elastomeric impressions are: used with these materials The dies prepared from these materials do
•
resins since water in alginate and agar impressions retard not have accuracy due to curing contraction
polymerisation of resin of 0.6%.
Metals

DENTAL MATERIALS
• Electroplated dies They are formed from impression compound and Electro formed dies possess greater
•
silicone impression materials. resistance to abrasion and a higher surface
hardness then the gypsum dies
• Amalgam dies Amalgam is used for preparing dies with the The disadvantage is that it results in
•
impression made of impression compound distortion
advantage of amalgam dies is greater hardness and
reproduction of surface details.
• Metal sprayed dies Alloys such as bismuth tin alloy melted at 138*C and It has a disadvantage of less surface hardness
•
sprayed into the impression in which dental stone is
poured the advantage is that
• Silicophosphate cement dies Sillicophosphate cement is used for preparing dies. It Disadvantage is setting shrinkage and loss of
•
has the advantage of greater hardness than die stone water on standing
Ceramic Die Materials

Refractory • A material that remains stable without decomposing at higher temperatures it is in the form of silica. Provides mould
•
expansion by thermal expansion and inversion
Binder • A material that binds together the particles of the refractory substance. E.g. a calcium sulfate hemihydrates, sodium
•
silicate be present in the investment to prevent shrinkage. Binder gives strength to the investment. To contribute to
mold expansion by setting expansion
Modifiers • E.g: ethyl silicate ammonium sulphate, sodium phosphate sodium chloride boric acid potassium, Chloride or boric acid
•
will enhance thermal expansion of gypsum
• Casting crucible (AIPG 2004)

•

– These are cup shaped structures which are used to melt alloys/metal prior to casting. The alloy to be melted is kept in
–
it and heated to liquidus temperature via an appropriate heat sorce.
– They are of 3 types:
–
Clay crucibles: Used for many types of crown and bridge alloys such as high noble and noble types

Carbon crucible: Can be used for higher fusing gold based metal ceramic alloys

- Base metal alloys cant be melted as at their higher fusion temperature, carbon contamination can occur

Quartz crucible: Used for melting higher fusing alloys

- Suited for alloys that are sensitive to carbon contamination

- Alloys with high palladium content, nickel based or cobalt based alloys

Casting Investment Materials
– Investment can be described as a ceramic material, which is suitable for forming a mould into which a metal/alloy is
–
approximately cast.
– Three types of investment materials are commonly used;
–
384
Gypsum -bonded(AIPG 2004, Phosphate-bonded Silica-bonded

2003,2007)
Composition •
•
Silica: 60 -65%-acts as a • Ammonium di-acid • Silica is the binder
•
•
refractory during heating, phosphate: Strength,
regulates thermal expansion, solubility
provides mold expansion. • Silica: Refractory
•
• Alpha hemihydrates: 30- • Magnesium oxide: Reacts
•
35% -acts as a binder, Imparts
•
with Phosphate ions- the binder
strength, contributes to mold
expansion
• Modifiers: 5%—reducing
•
agents Eg: carbon/copper
powder - modify setting
DENTAL MATERIALS
expansion and setting time Eg

boric acid
Properties • Type I: Casting shrinkage • Colloidal silica suspensions are • In addition to setting shrinkage, green
•
•
•
compensated by thermal used in place of water which shrinkage occurs due to loss of alcohol
expansion helps in greater expansion of and water from the gel (AIPG 2002)

• Type II: casting shrinkage the investment • Can be heated upto 1200°C
•
•
compensated by hygroscopic • With carbon: When casting
•
expansion alloy is gold
• Type III: for partial denture • Without carbon: For carbon
•
•
construction with gold alloys sensitive alloys such as base
• Normal setting expansion: metal, silver palladium alloys
•
0.5%
• Hygroscopic expansion: 1.2
•
– 2%
• Thermal expansion: 1-2%
•
Uses • Used in casting gold alloys • Used for high melting alloys • Used for high fusing base metal partial
•
•
•
like cobalt/chromium and metal denture alloys
ceramic restorations
• Factors which may alter hygroscopic setting expansion are

•
– Water powder ratio: Higher the water powder ratio- lesser hydroscopic setting expansion
–
– Temperature: Higher the temperature of Immersion of water - higher the expansion
–
• Setting expansion of casting investment is 0.1-0.5%
•
Normal setting expansion • ADA specification no.2 for type I investments permit the maximum setting expansion in air of only
•
0.6% the setting expansion of modern investment is 0.4%
Hygroscopic setting ex- • ADA specification no. 2 for type II investment require a minimal 1.2% and a maximum 2.2% expansion
•
pansion
Thermal expansion • ADA specification no.2 requires that the thermal expansion should be between 0 and 0.6% at 500*C
•
for type-l investments which rely mainly on thermal expansion for compensation, minimum thermal
expansion should not be less than 1% nor greater than 1.6%
Porosity
– Classification:
–
Those caused by solidification shrinkage

- Localized shrinkage porosity

- Suck back porosity

- Micro porosity


Those caused by gas:

- Pin hole porosity

- Gas inclusions porosity

- Sub surface porosity

Those caused by air trapped in mould

- Back pressure porosity

Porosity Cause Elimination
• Shrink spot porosity (localised • Irregular voids • Sprue of correct thickness, attaching sprue
•
•
•
shrinkage, suck back porosity) • Due to shrinkage of molten alloy on cooling at thickest portion of wax, flaring or placing a

(AIPG 2001) reservoir close to the wax pattern
•

(KCET -08)

• Back Pressure • Escape of air Is prevented Due to bulk of • Adjusting sprue pattern so that thickness
DENTAL MATERIALS
•
•
•
investment will not be more than 1/4th of the investment
between the bottom of casting ring and nearest
part of the wax pattern (AIPG 2009, 2011)

• Occluded Gas (pin hole) sub- • Spherical voids in casting, simultaneous • Avoid overheating and prolonged heat of alloy.
•
•
•
surface nucleation of solid grains and gas bubbles Controlling the rate entry if molten metal into
at first moment that the metal freezes at the the mould
mould at the mould wall
• Micro porosity • Due to rapid solidification shrinkage

•
•
Dimensional Errors in Casting
Problem Cause Precaution
• Casting too large Excessive Expansion Use correct temperature, use correct investment
•
• Casting too small Too little mould expansion Heat the mould sufficiently
•
• Distorted casting Distorted wax pattern Correct handling of wax
•
• Rough surface Investment breaks down, air bubbles on wax Avoid overheating of mould and alloy, Correct use of wetting agent,
•
(noduled on casting), weak investment correct vacuum investing, Avoid too high water powder ratio, avoid
dilution of investment from application of too much wetting agent,
fins on casting, cracking of investment, avoid too rapid heating of
investment (AIPG 2010)

Role of Carbon in Casting Procedures
Uses • As a reducing agent for alloys
•
• Facilitating de-investing of gold based alloys
•
Addition • Added to investment – both gypsum and phosphate based investment
•
• Added directly to fused alloy in crucible as a reducing flux
•
Advantages • Provides a reducing atmosphere to the alloy being cast
•
• Facilitates devesting of gold alloys and produces a cleaner casting
•
• Increases fluidity of the melted alloy when added as flux
•
• Minimizes porosity (used as flux)
•
Disadvantages • Carbon contamination can occur when investment is heated above recommended temperature. Hence gypsum
•
based investments for gold alloys without carbon can be heated to upto 700° C but those with carbon cant be
heated above 650°C else contamination will occur
• When casting temperature are high as seen in melting of high noble alloys for metal ceramic or base metals alloys,
•
carbon contamination from investment can easily occur. Such contamination embricates the alloy.
• Also contamination can occur when carbon crucibles are used.
•
• Carbon fluxes should be avoided when casting gold based metal cerami alloys as this added carbon may remove
•
the trace elements from the gold alloys, which are very important to provide the strength to alloys and bonding
porcelain.
386
Abrasion and Polishing

• Abrasion is smoothening of rough surface before polishing it.
•
• Abrasives may be classified as:
•
– Finishing
–
– polishing
–
– Cleansing
–
• Diamond particle size
•
• Coarse • 125 – 150 micro meter
•
•
• Medium • 88 – 125 micrometer
•
•
• Fine • 60 – 74 micrometer
DENTAL MATERIALS
•
•
• Very fine • 38 – 44 micrometer
•
•
• The clinical performance of diamond abrasive instruments depends on the size, spacing, uniformity, exposure and
•
bonding of the diamond particles.
• Increased pressure causes the particles to dig into surface more deeply leaving deeper scratches and removing more tooth
•
structure.
• Polishing is production of smooth mirror like surface without use of any external form.
•
• Polishing Agents
•
a. Pumice Smoothening dentures.

b. Rouge (crocus cloth) Polishing teeth

c. Tin oxide Noble metal alloys (AIPG 2001)

d. Chromic oxide Metallic restorations

e. Zinc oxide Stainless steel

f. Zirconium silicate Polishing amalgam

Dental prophylactic
Pastes/polishing strips
TARNISH AND CORROSION

• Tarnish: a surface discolouration on a metal or even a slightly loss of alteration of surface finish/lustre.
•
– Generally occurs due to formation calculus plaque on the surface of the metal.
–
– Occurs due to formation of oxides, sulfides and chlorides
–
– It is the forerunner of corrosion.
–
• Corrosion: It is actual deterioration of metal by reaction with environment.
•
Classification
Chemical or dry corrosion Electrolytic or wet corrosion
Chemical/dry corrosion in which metals react to from oxides, Electrolytic/electrochemical: This requires presence of water/
sulphides in absence of electrolytes. e.g., formation of silver tin other fluid electrolytes (the metal with the lowest electrode potential
system in dental alloys containing silver, oxidation of alloys in corrodes)
dental amalgam.

• Certain metals such as chromium, aluminium and titanium will from strong adherent oxide films on their surface to protect
•
from corrosion (passivating effect). (AIPG 2002)

• Noble metal alloys resist corrosion because they have positive EMF.
•
• Types of corrosion
•
Galvanic corrosion Stress corrosion Crevice or concentration cell corrosion
• Occurs between dissimilar metals • Metal at the site of maximum • Accumulation of food debris in crevices produces
•
•
•
in contact stress become more reactive one type of electrolyte and normal saliva produces
• Anode- The metal with low EMF (anode) than the unstressed metal another type of electrolyte
(cathode)
•
• Cathode – metal with high EMF • The oxygen tension in the bottom of the pit is less
•
• The stressed metal undergoes than the periphery of the pit
•
• E.g. amalgam (anode) undergoes
•
corrosion
•
corrosion and liberates mercury
DENTAL MATERIALS
and weakens the gold restoration • E.g. orthodontic wire, amalgam
•
(cathode) when in contact.
SOLDERING, WELDING AND BRAZING
Soldering • A process of uniting surfaces or edges of metals of alloys by use of 3 fused metal or alloy.
•
• Pre soldering: Joining of metals before porcelain veneering
•
• Post soldering: Joining of metals after porcelain veneering
•
Welding • The process of joining two clean surfaces of metals together by the use of heat and pressure.
•
• Cold welding: By applying pressure
•
• Hot welding: By applying heat
•
• Spot welding: used to join orthodontic wires
•
Brazing • Is joining of metal parts by a filler metal between them at a temperature below solidus temperature of the metal
•
being joined and below 450*C
• Solder is an alloy or metal used in joining metallic sections.

•
– Two types: Soft and hard
–
Soft solders have melting range of about 260 they lack corrosion resistance and not used for dental purposes

Hard solders have high melting temperatures Eg: Gold and silver solders

– Composition
–
Gold solder Silver solder
• Gold: 45-80%, • Silver: 10-80%
•
•
• Silver: 8-30%, • Copper: 15-50%
•
•
• Copper: 7-20%, • Zinc: 4-30%
•
•
• Tin: 2-4%,
•
• Zinc: 2-4%
•
• Fusion temperature is approximately 100* below the fusion temperature of alloy being soldered
•
• The optimum gap width between two soldered units should be 0.13 – 0.3mm.
•
• Fluxes: Flux is a fusible substance that when heated with metallic materials assist in fusion/soldering operation by cleaning
•
and protecting metals from oxidation of foreign matter (NEET 2013)

– Boric/Borate fluxes are used with noble metal alloys
–
– Flourides are used with Base metal alloys: borax compound + fluoride compounds dissolve high stability oxides like
–
those of chromium, nickel and cobalt (AIPG 2001)

– Borax fluxes are too fluid to be used for presoldering
–
– Fluorides fluxes cant be used for post-soldering because:
–
388
They are inactive at the low postsoldering • Decreased temperature of mixing jar of self cure resin

temperatures
•
causes prolonged initiation period and dough forming
They are likely to attack porcelain. time.

Reducing flux Oxidizing flux • Pyroplastic flow is decreased by addition of potash
•
• Is one that reduces to a • Composition: form of feldspar.
•
•
metallic state. Such oxides – Soldering flux: 60, • Butyl rubber dissolved in chloroform is used as
are dissolved in molten
–
•
– Potassium chlorate: an adhesive when making an impression with
metal. (Aiims Nov 2012) –
20,
– Composition – Sodium perborate: 20 polysulphides.
–
–
- Borax glass: 55 • Level II tests are the biological tests of materials which
-
parts,
•
are evaluated in experimental animals under conditions
- Boric acid: 35
that simulate clinical use of materials.
-
DENTAL MATERIALS
parts
- Silica: 10 parts.
• The less the grain size, the more the ductility and strength
-
•
• Anti: flux is any material that may be placed on surface of the alloy.
•
of metal to confine the flow of a solder and prevent it • The more the grain size more the brittleness and less the
•
from spreading beyond define limits. Eg: Graphite, rouge, strength of the alloy.
whiting suspended in alcohol. (AIPG 2014, AIIMS 2012) • Expansion of quartz is about 0.75% whereas cristoballite

•
expands 1.4%.
MISCELLANEOUS • Specific gravity is higher for noble metal alloys than base
•
metal alloys.
• Composition of Cold Mould Seal (NEET 2013) • Wax pattern should be refrigerated In case of
•

•
– Sodium alginate – 0.2% postponement of casting
–
– Disodium phosphate – 0.2 to 0.4% • Ceramic liners have thickness of 1 mm
•
–
– Glycerine – 4% • Silicate is called as synthetic porcelain.
–
•
– Preservative – 0.7%
• Enamel tags are formed to a depth of 30 micromotors.
–
– Alcohol – 7%
•
–
– Water – 86% • Iridium is used as a grain refiner in noble metal alloys.
•
–
• 50 µg of mercury per week is the maximum level of
• Quartz present in porcelain acts as a strengtheners.
•
occupational exposure.
•

(AIPG 2007)
• Cross bend test is used to measure the compressive/
• The metal having the highest melting point of all metals is
•
shear of dental porcelain,
•
carbon—3,700*C
• Beillby layer is the microcrystalline layer formed on a
• The metal having the lowest melting point of all metal is
•
metal surface.
•
silver—960*C
• Casting pressure is approximately 20 psi.
• Invariant transformation is a property of eutectic and
•
• Type C wax is soft wax used for construction of Inlay/
•
peritectic systems.
•
crowns,
• Sticky wax is also called model cement.
• Bakelite is the resin polymerising by condensation
•
• The setting reaction of dental plaster is basically a
•
reaction,
•
precipitation reaction.
• Dicor is composed of crystalline mica particle.
• Acrylic resin is softened by heat and introduced into flasks
•
• Indium improves the bonding property. (AIPG 2009)
•
in injection moulding technique.
•

• 540 calories are required to vapourise 1 g of H2O at 100*C.
Greening • Greenish discolouration of porcelain
•
•
• Biodegradable resins are cyanoacrylates.it is a single due to silver vapour escaping from
alloy surface into porcelain during firing
•
component, moisture activated, thermoplastic, group
of adhesives characterized by rapid polymerization and Green Strength • Also called wet strength of gypsum
•
excellent bond strength. (AIPG 2010) product. The wet strength is two or
more times less than the dry strength

• Buffering agent in liquid of silicate cements is
Greening Shrink- • observed in silica bonded investments
•
aluminium phosphate.
•
age due to drying of colloidal silica gel

Denture Cleaners • This bond is called “ionic”: Na is positively charged
•
• The most common commercial denture cleansers are and Cl negatively, because the outermost electron of
•
based upon or require immersion techniques. Immersion Na (sodium) is so weakly bound that Cl (chlorine) can
agents contain alkaline compounds, detergents, sodium “steal” it when they separate.
per borate, and flavoring agents.
• The dipole nature of water molecules enables it to
• Bleaches and bleach solutions should not be used for
•
pull the NaCl molecules apart and to surround each
•
cleaning metal prostheses, such as removable partial
denture frameworks. component with a water coating - so the substance is
dissolved.
• Prolonged use of such cleansers may cause noticeable wear
•
of resin surfaces and may adversely affect the function and
aesthetics of these prostheses. • Most commonly used heat source for melting solder–Gas
•
torch or gas oxygen torch
DENTAL MATERIALS
Water Dipole (AIIMS Nov 2013) • Various fuels are
•
• The water molecule has asymmetrical shape, with – Hydrogen
–
•
the hydrogen atoms sitting like two ears on the larger – Natural gas
–
oxygen atom. – Acetylene: Has highest flame temperature but is
–
• This leads to the molecule’s having an asymmetrically unstable
•
distributed electric charge, with the ears charged – Propane: Best (has highest flame temperature and
–
positively and the other end negatively. flame heat)
• This “dipole” is what makes water such a good solvent. • There should be optimum gap between metal parts to be
•
•
Many substances, such as ordinary salt (NaCl) are joined. If the gap is too narrow, strength is limited and if
held together not by covalent bonds but by electrical the gap is too wide, the joint strength will be controlled by
attraction “at a distance”, without significant electron- the strength of the solder.
sharing.
• Pure titanium can be laser welded in argon atmosphere.
•
CHAPTER 9
Dental Anatomy and Histology
Objectives
Dental Anatomy Dental Histology
• Tooth notation systems • Development of teeth

• Calcification and eruption of teeth • Enamel

• Physiological form of tooth • Dentin

• Morphological characteristics of primary and • Cementum

permanent dentition • Pulp

• Pulp chamber and root canals • Oral mucous membrane

• Occlusion • Periodontium

• Bone

• TMJ

DENTAL ANATOMY
TOOTH NOTATION SYSTEMS
Zsigmondy-Palmer system Universal (National) system FDI system

• Introduced by Zsigmondy • Given by American dental association • Introduced in 1971
•
•
•
in 1861 in 1968 • Also known as two digit notation
•
• Each quadrant is • Uses a unique number/letter for each • In two-digit system, first number represents
•
•
designated by symbol tooth.
•
tooth’s quadrant while second number is
• Permanent teeth are • Permanent teeth are numbered 1 to the number of tooth from midline.
•
•
numbered 1 to 8 32 starting from upper right molar • Permanent upper right central incisor is
•
• Primary teeth are indicated • Deciduous teeth are designated as designated as 11
•
•
by A to E A to T, in this A is upper right second • Deciduous upper right central incisor is
molar.
•
designated as 51
Advantages • Simple and easy to use • Unique letter or number for each tooth • Simple to understand and teach
•
•
•
• Less chances of confusion avoiding confusions • No confusion
•
•
between primary and • Easy to record on computer
•
permanent tooth • Easy for charting
•
Dental Anatomy and Histology 391

Zsigmondy-Palmer system Universal (National) system FDI system
Disadvantages • •
Difficulty in communication • Difficult to remember each letter or • May be confused with universal tooth
•
•
• Confusion between upper number of tooth numbering system
•
and lower quadrants,
while communication and
transferring a data.
DENTAL ANATOMY AND HISTOLOGY

CALCIFICATION AND ERUPTION OF TEETH
PRIMARY DENTITION
Maxilla
Tooth Hard tissue formation begins Crown completed Eruption
• Central incisor 4 months in utero (AIPG 2005) 4 months 7 ½ months
•
• Lateral incisor 4 ½ months in utero 5 months 9 months
•
• Canine 5 months in utero 9 months 18 months
•
• 1st molar 5 months in utero 6 months 14 months
•
• 2nd molar 6 months in utero 11 months 24 months
•
Mandible

• Central incisor 4 ½ months in utero 4 ½ months 6 months
•
• Lateral incisor 4 ½ months in utero 4 months 7 months
•
• Canine 5 months in utero 9 months 16 months
•
• 1st molar 5 months in utero 5 ½ months 12 months
•
• 2nd molar 6 months in utero 10 months 20 months
•
PERMANENT DENTITION
Maxilla

• Central incisor 3-4 months 4-5 years 7-8 years
•
• Lateral incisor 10-12 months 4-5 years 8-9 years
•
• Canine 4-5 months 6-7 years 11-12 years
•
• 1st premolar 1 ½ - 1 ¾ years 5-6 years 10-11 years
•
• 2nd premolar 2 – 2 ¼ years 6-7 years 10-12 years
•
• 1st Molar Birth 2 ½ - 3 years 6-7 years
•
• 2nd Molar 2 ½ - 3 years 7-8 years 12-15 years
•
• 3rd Molar 7-9 years 12-16 years 17-24 years
•
392
Mandible
• Central incisor 3-4 months 4-5 years 6-7 years
•
• Lateral incisor 3-4 months 4-5 years 7-8 years
•
• Canine 4-5 months 6-7 years 9-10 years

•
• 1st premolar 1 ½ - 2 years 5-6 years 10-11 years
•
• 2nd premolar 2 ¼ - 2 ½ years 6-7 years 11-12 years
•
• 1st Molar Birth 2 ½ - 3 years 6-7 years
•
• 2nd Molar 2 ½ - 3 years 7-8 years 11-13 years
•
• 3rd Molar 8-10 years 12-16 years 17-21 years
•
• A primary tooth generally takes from 1.5 to 2.5 months erupting permanent tooth comes to lie directly apical
•
from the beginning of clinical eruption until it reaches the to the primary teeth
occlusal plane. Canines usually takes the longest time to – Resorption then proceeds horizontally in an incisal
–
erupt. direction, causing the primary root to exfoliate and
• In the primary dentition, eruption occurs earlier in boys permanent one to erupt in place.
– In retained deciduous teeth, permanent incisors may
•
than in girls
–
erupt lingually. Maxillary permanent canines usually
• In permanent dentition, eruption in girls usually preceeds
erupt labial to retained canine.
•
that in boys
• Posterior teeth
•
• The rule of fours applies to the permanent tooth – The growing premolar crowns are initially located
•
development.
–
between the roots of primary molar teeth
– At birth, four first molars have initiated – The first sign of resorption around these crowns occur
–
–
calcifications (AIPG 2014) in the supporting interradicular bone.

– At 4 years of all crown have initiated calcification • The most common cause of retained primary teeth are
•
–
– At 8 years of age, all crowns are complete absence or impaction of permanent successors.
–
– At 12 years, all crowns emerge
PHYSIOLOGICAL FORM OF TOOTH AND
–
– At 16 years, all roots are complete
–

PERIODONTIUM
Resorption Pattern Anthropologic Nomenclature of Cusps of Molar
• Anterior Teeth Teeth
•
– With the onset of eruptive movement of the
Cusp Upper molar Lower Molar
–
permanent teeth, which precedes in the incisal and
labial direction, pressure is first directed at the bone • Mesiobuccal • Paracone • Protocone
•
•
•
separating the crypts of the permanent successors and • Mesiolingual • Protocone • Metacone
the alveolus of the primary roots. (NEET 2013)
•
•
•

– With the loss of separating bone, pressure is then • Distolingual • Hypocone • Entoconid
•
•
•
–
directed at the primary roots, therefore resorption
• Distobuccal • Methacone • Hypoconid
of the primary anterior teeth first occurs along the
•
•
•
lingual surface of the apical third of the root • Distal • Hypoconid
– It then proceeds labially until the crown of the
•
•
–
Shapes of the occlusal surfaces of some teeth
• Permanent maxillary 1st premolar Hexagonal
•
• Permanent mandibular 1st premolar Diamond (Y shaped) (AIPG 2007)
•

• Permanent mandibular 2nd premolar Square
•
• Permanent maxillary Ist molar Primary maxillary 2nd molar Rhomboidal
•
• Permanent maxillary 2nd molar Rhomboidal with more obtuse angles
•
• Permanent maxillary 3rd molar Heart shape
•
• Permanent mandibular 1st molar Hexagonal/trapezoidal

•
• Primary maxillary 1st molar Rectangular
•
Marginal Ridges
• Marginal ridges are defined as rounded borders of enamel which form the mesial and distal margins of occlusal surfaces
•
of premolars and molars and mesial and distal margins of lingual surfaces of the incisors and canines
Significance
• Help in balancing of teeth in both the arches
•
• Improve the efficiency of mastication
•
• Prevent food impaction in interproximal areas
•
• During restoration, marginal ridges should be restored in two planes, i.e. buccolingual and cervico-occlusally and also
•
restore adjacent marginal ridges at the same height One should always try to the level best to avoid common faults in
restoration of marginal ridges.
Embrasures
• When two teeth are in contact with each other, their curvatures adjacent to contact areas form spillway spaces called
•
embrasures . In other words, embrasures can be defined as V-shaped spaces that originate at proximal contact areas between
adjacent teeth and are named for the direction towards which they radiate. These are:
• Labial/buccal ana Lingual embrasures: These are spaces that widen out from the area of contact labially or buccally and
•
lingually.
• Incisal/occlusal embrasures: These are spaces that widen out from area of contact incisally/occlusally.
•
Proximal Contacts
Viewed from the facial Viewed from the occlusal Proximal surfaces
• Generally located increasingly • All are located in the middle 1/3 of the • Triangular: All anterior teeth.
•
•
•
more incisally (occlusally) from the crown. • Trapezoidal: All maxillary posterior teeth.
posterior to the anterior.
•
• Posterior contacts are positioned • Rhomboidal: All mandibular posterior teeth.
•
• The mesial contact is always located slightly buccal
•
•
more incisally than the distal.
• Proximal contacts prevent rotation,
•
mesial drift, and food impaction.
Importance of proper contact relation Improper proximal contact area can result in
• Stabilize the dental arches by combined anchorage effect • Food impaction
•
•
of the teeth • Periodontal disease
•
• Serves to keep food away from packing between the teeth • Carious lesions
•
•
• Protect interdental papillae • Mobility of teeth
•
•
Contact Areas
Maxillary Teeth Mandibular Teeth
• Central incisor • Incisal third • Incisal third very near to incisal edge
•
•
•
394
Maxillary Teeth Mandibular Teeth

• Central and lateral incisor • Junction of incisal and middle thirds • Incisal third
•
•
•
• Lateral incisor and canine • Middle third (LI), junction of incisal and middle • incisal third
•
•
•
third (canine)
• Canine and 1st premolar • Middle of middle 1/3rd (canine), junction of • Middle third, junction of incisal and middle third
•
•
•
middle and occlusal 1/3rd (1st premolar)
• 1st and 2nd premolar • Cervical to junction of middle and occlusal • Middle third, junction of middle and occlusal
•
•
•
1/3rds 1/3rds
• 2nd premolar and 1st molar • Cervical to junction of middle and occlusal • Middle third, junction of middle and occlusal
•
•
•
1/3rds 1/3rds
• 1st and 2nd molar • Middle of middle 1/3rd • Middle of middle 1/3rd
•
•
•
• 2nd and 3rd molar • Middle of middle 1/3rd • Middle of middle 1/3rd
•
•
•
Heights of Contour (HOC)
• Help form the mesial and distal contact areas.
•
• Allow for adequate gingival health.
•
Facial HOC’s: Lingual HOC’s:
• Located in the cervical third, except mandibular molars • Anterior teeth: Located in the cervical third (cingulum).
•
•
(junction of cervical and middle thirds). • Posterior teeth: Located in middle third, except mandibular
 
•
• Most prominent on mandibular posterior teeth. PM2 (occlusal third).
•
 
• Least prominent on mandibular anterior teeth.
•
CEJ Contours
• The maximum height of the proximal CEJ contour increases anteriorly.
•
• The mesial CEJ contour is always greater than the distal contour.
•
• The greatest CEJ contour is on the maxillary central incisor (mesial surface).
•
• Facial and lingual CEJs curve apically.
•
• Mesial and distal CEJs curve coronally.
•
Lobes
• Incisors and canines: 4 lobes (3 labial [mamelons], 1 lingual [cingulum]).
•
• Premolars: 4 lobes (3 buccal, 1 lingual) except mand PM2, which has 5 lobes (3 buccal, 2 lingual).
•
 
• First molars: 5 lobes (one for each cusp).
•
• Second molars: 4 lobes (one for each cusp).
•
• Third molars: 4 or 5 lobes (one for each cusp, depending on variation)
•
Arch Lenghts
• Maxillary: 128 mm (slightly longer).
•
• Mandibular: 126 mm.
•
Cuspal Slopes
Mesial cusp ridge • Primary maxillary canine
•
is longer than distal • Permanent maxillary first premolar facial cusp
•
cusp ridge in:

Distal cusp ridge is • Permanent maxillary canine cusp ridge
•
longer than mesial • Primary mandibular canine
•
in: • Permanent mandibular canine
•
• Permanent mandibular first premolar
•
••
Permanent maxillary second premolar

Blood Supply
ARTERIAL SUPPLY VENOUS RETURN
• All dental and periodontal arterial supply arises from the • All dental and periodontal venous return drains to the pterygoid
•
•
maxillary artery. plexus of veins, which eventually forms as the maxillary vein.
• The arterial supply generally parallels the corresponding
•
nerves.
MORPHOLOGICAL CHARACTERISTICS OF PRIMARY AND PERMANENT DENTITION
• Primary tooth which resembles permanent maxillary first molar Maxillary primary second molar
•
• Primary tooth which resembles permanent mandibular first molar7 Mandibular primary second molar
•
• Primary molar which does not resemble any tooth in permanent Mandibular first molar (AIPG 2002)
•
dentition
• Primary molar with prominent mesiofacial cervical ridge. Mandibular first molar
•
• Primary molar which resembles premolars Mandibular first molar
•
• Teeth having longest and largest root Permanent maxillary canine
•
• Posterior teeth having largest root Palatal root of maxillary first molar
•
• Tooth most commonly in abnormal relation with the other teeth in Maxillary lateral incisor (AIIMS May 2010, AIPG 2007)
•
the jaws
• Tooth with largest mesiodistal dimension Permanent mandibular first molar

•
• Tooth with largest buccolingual diameter Permanent maxillary first molar
•
• Tooth with longest crown Permanent mandibular canine
•
• Longest tooth in the dentition Permanent upper/lower canines
•
• Tooth which has cusp of Carabelli on mesiolingual cusps and Maxillary first permanent molar
•
maxillary deciduous second molar
• Tooth which is blocked out commonly due to lack of space Permanent maxillary canine
•
• Tooth which shows greatest variation in erupton timing Mandibular second premolar
•
(NEET 2013)

• The smallest tooth in human dentition Primary lower central incisor
•
• The largest tooth in human dentition Permanent maxillary first molar
•
• Most congenitally missing tooth next to third molars Upper lateral incisor (AIPG 2005)
•
• Permanent upper incisor teeth demonstrating greatest variation in Maxillary laterals (AIPG 2005)
•
tooth mass, size and shape next to third molar
• Tooth with most variable occlusal anatomy Upper third molars

•
• Smallest permanent tooth Mandibular central incisor
•
396
• Largest permanent tooth Maxillary first molar

•
• Tooth most frequently lost from arch due to caries Mandibular first molar
•
• Most common supernumerary tooth Mesiodens between incisors
•
• First permanent tooth to erupt Mandibular central incisor (AIPG 2002)
•
• First permanent tooth to calcify Mandibular first molar
•
• First primary tooth to erupt Mandibular central incisor
•
• Tooth with the largest cusp in the dentition Mesiolingual cusp of permanent maxillary first molar
•
(AIIMS May 2010)

• Tooth with the largest variation in root morphology Third molars
•
• Cornerstones of dentition Mandibular molars
•
• Corner tooth of dentition Maxillary canine
•
• Step-child of dentition Third molars
•
• Most commonly submerged tooth Deciduous mandibular II molar
•
• Most commonly missing deciduous teeth Maxillary lateral incisors
•
• Primary teeth with greatest buccolingual dimensions Maxillary second molar
•
• Primary teeth with greatest mesiodistal dimension Mandibular second molar
•
• The permanent tooth that shows greatest variation in occlusal form Mandibular second premolar
•
next to maxillary third molar
• Permanent teeth with steepest cuspal inclines Maxillary first premolar
•
• Permanent posterior teeth with three cusps most frequently Maxillary second molar
•
• Premolar with three cusps frequently Mandibular second premolar
•
• The anterior teeth most often shows a bifurcated root (facial and Mandibular canine
•
lingual)
• The teeth to show great variation in root morphology Third molar
•
• Largest root Maxillary canine
•
• Largest root which shows facial and lingual concavities Palatal of maxillary first molar
•
• Tooth with its roots in close proximity to maxillary sinus Maxillary permanent first molar
•
• Tooth with maximum incidience of a distolingual groove (or) shavel Maxillary lateral incisor
•
(or) palatogingival groove
• Tooth which has trifurcated roots Maxillary permanent first molar

•
• Tooth with maximum incidence of Talon’s cusp Mandibular central incisor
•
• Tooth with maximum incidence of dens in dent Maxillary lateral incisor
•
• Tooth with maximum incidence of dens evatinatus Mandibular premolar
•
• Tooth with maximum incidence of taurodontism Mandibular molars
•
• Most common natal and neonatal teeth Mandibular primary central incisors
•
Root Morphology
• The teeth with round blunt roots easy for extraction • Maxillary central incisors and mandibular second premolars
•
•
• The teeth with roots that are thin mesiodistally, wider – Mandibular central incisors
•
–
faciolingually and with mesial and distal concavities – Distobuccal root maxillary first molar
–
– Roots of mandibular molars
–

• The premolar with two roots and two root canals • Maxillary first premolars
•
•
• The anterior teeth which is least likely to variation in root • Maxillary canines
•
•
morphology
Important Development Grooves

• Palatogingival groove that extends from enamel to cementum • Maxillary lateral incisor

•
•
of root is present in
• Mesiolingual developmental groove is present in • Mandibular Ist premolar
•
•
• Mesial marginal development groove • Maxillary Ist premolar
•
•
• Maximum number of development grooves are present on • Mandibular central incisor
•
•
cingulum of
• Deep concavities on distal surface are present in • Maxillary Ist premolar

•
•
• Deep concavities on distal surface are present in • Maxillary Ist molar
•
•
• Developmental depressions on booth mesial and distal sides • Mandibular central incisors, Upper canines Mesial root of
•
•
of roots are seen in mandibular Ist molar
• Largest root with facial and lingual concavities • Palatal root of upper Ist molar
•
•
PULP CHAMBER AND ROOT CANALS
• Morphology of the pulp chamber
•
– Size of pulp cavity is dictated by:
–
Age

Parafunctional activity

Trauma history (caries, abrasion, erosion, etc)

• There are as many pulp horns as there are cusps. In permanent teeth, the size of a pulp horn is directly proportional to
•
the size of its associated cusp.
• Accessory Pulp Canals
•
– Found in cervical 1/3 of root and furcations.
–
– Allow pulp to communicate with PDL space.
–
– Contains pulpal nervous and vascular tissue.
–
Maxillary teeth Mandibular Teeth
• Central incisor Shovel shaped Smallest pulp in dentition
•
long and narrow with a flattened elliptical shape in cross
section buccolingually
• Lateral incisor Small and spoon shaped Similar to CI

•
• Cuspid Longest pulp with an elliptical cross section Similar but shorter than maxillary canine
•
buccolingually and distally inclined apex
• First premolar Large occluso cervical pulp chamber. 2 root Looks like a small mandibular canine with an insignificant or
•
missing lingual pulp horn
• Second premolar Same as first premolar but 1 root Lingual horn is smaller than the buccal horn
•
Roughly triangular or sometimes rectangular in cross section
• Molars Roughly rectangular cervical cross section The coronal cross section is rectangular with the mesiodistal
•
with greatest dimension buccolingually and dimension greatest
demonstrating a mesiobuccal prominence. Displays a mesiobuccal prominence
From the first to third molar, the coronal pulp The horn heights from highest to lowest are mesiobuccal,
chamber gets smaller and roots get closer together. mesiolingual distobuccal and distolingual
There are two roots:
Distal is shorter and strainghter
Mesial is longer, curved and often double.
398
OCCLUSION
• Occlusion: Any contact between the incising or masticating surfaces of the upper and lower teeth.
•
• Static occlusion: It Is defined as contact of teeth when jaws closed
•
• Dynamic occlusion: It Is defined is tooth contact during mandibular movements.
•
• Malocclusion: Any deviation from a physiologically acceptable contact of opposing dentition is called “malocclusion “
•
• Occlusal contact: Any contacting or touching of tooth surface is called occlusal contact. Unmodified, contact should
•
involve a normal, nonpathologic touching of tooth surfaces. Harmful occlusal contacts can occur in following forms:
– Parafunctional (nonfunctional) contacts: Normal tooth contacts that have been subjected to excessive use
–
through bruxism, clenching, etc.
– Interferences: Abnormal contacts that may occur in functional or parafunctional activity. Following occlusal
–
interferences are usually present:
Occlusal prematurity • Occlusal contact that interrupts the harmonious closure of the teeth along the centric relation arc. It can
•
result in damage to periodontium, masticatory muscles, and temporomandibular joint
Occlusal interfer- • Occlusal contact that disrupts the smooth excursive movements of teeth against each other. Presence of
•
ence occlusal interference can result in disclusion of the anterior guidance
Working side inter- • Interference present between posterior teeth on the side of the dental arches to which the mandible is
•
ference moving laterally in excursion. It usually occurs when stamp cusp moves against a shear cusp
Nonworking side • Occurs between posterior teeth on the side of the dental arches away from which the mandible is moving
•
interference laterally in excursion. It occurs when stamp cusp moves against shear cusp.
Protrusive interfer- • Caused by protrusive movement the mandible is called protrusive interference
•
ence
• Maximum intercuspation: It is the maximum occlusal contact or intercuspation irrespective of the condylar position.
•
This type of contact may or may not occur on the path of centric relation closure.
Types of Cusps
Functional Cups or Centric holding cusps or stamp cusps Non-functional cusps or Non-supporting cusps or guiding
cusps
Palatal cusps of maxillary posterior teeth and buccal cusps of Buccal cusps of maxillary posterior teeth and lingual cusps of mandibular
mandibular posterior teeth that come into occlusal contact in posterior teeth that do not directly contact the opposing teeth in
intercuspal position maintaining occlusal vertical dimension. They intercuspal position. They contact and guide the mandible during lateral
occlude into the central fossae and marginal ridges of opposing excursions and shear food during mastication. Hence they are also
teeth. called shearing or guiding cusps. They prevent food from escaping the
occlusal table and also protect tongue and buccal mocusa by keeping
them away from functional cusps.
• Plunger Cusp: A cusp that tends forcibly wedge food into inter proximal area of teeth of the opposing arch.
•
• Guiding inclines: The inclines or slopes of the guiding cusps from the guiding cusp tip towards the center of the tooth.
•
Occlusal Arrangement
There are two types of occlusal relationships, namely
Cusp-to-fossa • The stamp cusp of one tooth occludes in a single fossa of single opponent.
•
• Single tooth to tooth contact
•
Cusp-to-marginal ridge • Each tooth occludes with two opposing teeth
•
• Both the marginal ridge and fossa will come in contact with the opposite cusp.
•

CURVATURES OF OCCLUSAL PLANES
Curve of Spee (Anterio- • It is an imaginary line touching the buccal cusps of all the lower teeth from lower canine backwards and
•
posterior curve) approximates to the arc of a circle of radius 4’ inches or 10 cm.
• A continuation of this curve backwards in natural dentition with nearly pass through the head of condyle
•
Curve of Monson (Lat- • •
The curve of occlusion in which each cusp and incisal edge conforms to a segment of sphere of 8 inch in
diameter with its center in the region of glabella.

eral curve)
• The curve usually does not exceed 5 to 10 degrees from the horizontal plane of orientation when viewed
•
in frontal plane.
• It involves molar teeth and has its concavity facing upwards
•
Anti-Monson curve (Lat- • A curve of occlusion, which involves the teeth anterior to second premolars
•
eral curve) • It has its convexity facing upwards
•
• The 2nd premolars are not involved in any curve as they lie on a horizontal plane
•
Pleasure curve – The combination of Monson and antimonsoon curves in posterior occlusion is often referred to as
–
pleasure curve
Curve of Wilson – The curve of Wilson is concave for mandibular teeth and convex for maxillary teeth.
–
– It is a cross-arch, cross-tooth curve and indicates the difference between supporting and non-sup-
–
porting cusps in occlusion.
Developmental Anomalies
Size • Microdontia • Having one or more teeth that are smaller than normal
•
•
• Macrodontia • Having one or more teeth that are larger than normal.
•
•
Number • Complete anodontia • Congenital absence of teeth; generally due to developmental abnormalities such as
•
•
ectodermal dysplasia.
• Partial anodontia • Congenital absence of one or more teeth
•
•
• Hypodontia: Congenital absence of a few teeth
•
• Oligodontia: Congenital absence of a large number of teeth
•
• Supernumerary teeth • Teeth in excess of the normal number. Most common in maxilla.
•
•
• Mesiodens • A supernumerary tooth located between the maxillary central incisors
•
•
Morphology • Ankylosis • Fusion of the tooth and alveolar bone
•
•
• Dilaceration • A bend in the root of a tooth
•
•
• Taurodontism • A molar with an elongated root trunk. Generally occurs in patients with amelogenesis
•
•
 
imperfecta, Klinefelter’s syndrome, or Down’s syndrome
 
• Dens invaginatus • Developmental abnormality of maxillary lateral incisors in which the focal crown is
•
•
(dens in dente) invaginated for various distances. (AIPG 2003)
 
• Dens evaginatus • Developmental abnormality in which a focal portion of the crown projects outward,
•
•
 
creating an extra cusp. A prominent dens evaginatus often seen on maxillary lateral
incisors is called a talon cusp.
• Hypercementosis • Excessive deposition of cementum
•
•
• Cervical enamel • An apical extension of enamel usually located at furcation entrances on molar teeth
•
•
projection
• Enamel pearl • A small, focal mass of enamel formed apical to the CEJ
•
•
• Concrescence • Fusion of two completely formed teeth at their roots; must have confluent cementum.
•
•
 
• Fusion • Fusion of two unique tooth buds; must have confluent dentin. Its severity depends on
•
•
 
the stage of tooth development at which the fusion occurs
 
• Gemination • Development of two crowns from one tooth bud; share a single root and root canal
•
•
400
Development • Initiation • Congenitally missing teeth or supernumerary teeth
•
•
• Histo differentiation • Dentinogeneis imperfecta, amelogenesis imperfecta (AIPG 2003)
•
•
• Morphodifferentiation • Abnormal shape of tooth, e.g. peg laterals, extra cusp or root, mulberry molars
•
•
DENTAL HISTOLOGY
DEVELOPMENT OF TEETH
Thecondont • Periodontal membrane do not undergo significant changes.

•
Monophyodont • Presence of only one set of dentition for entire life
•
Diphyodont • Presence of two sets of dentition
•
Polyphydodont • Presence of more than two sets of dentition
•
Homodont • All the teeth have same shape without distinction such as incisors, canines, premolars and molars.
•
Heterodont • Presence of different groups of teeth.
•
• Molars—shapes
•
Bunodont – Primitive type of teeth seen in primates like cats, dogs, etc. and in Humans.
–
– Contains simple conical cusps with rounded edges.
–
Haplodont (AIIMS may – Seen in reptiles like crocodiles
–
2010, AIPG 2007) – Simplest cone from teeth with out any ridges on the occlusal surface
–
– Only simple hinge movements of jaws are seen.
–
Triconodont – Seen in early mammals
–
– Three cusps are arranged in line with the largest cusp in the center.
–
Tritubercular stage – Three cusps are arranged in triangle form.
–
Quadritubercular – 4th cusp is formed and an occlusal contact relationship between the upper and lower jaws is estab-
–
lished. Seen in human beings.
Tooth Attachment
Fusion of tooth to the Ankylosis
bone
Attachment through socket
• Direct attachment • Pluerodont: Tooth is attached to inner margins of bone. These teeth can be replaced.
•
•
without PDL ligament • Acrodont: Tooth is attached to crest of bone. They are not usually replaced.
•
• Attachment through • Gomphosis: Attachment by periodontal membrane which undergoes significant changes (human beings)
•
•
socket
Development of teeth: The following are important points to be noted.

• Initiation of primary teeth begins around 4-6 weeks I.U (first trimester of pregnancy)
•
• Initiation of permanent teeth and initiation of calcification of primary teeth is in second trimester or pregnancy.
•
• In primary dentition average range of time for initiation of calcification to completion of calcification is 10 weeks
•
prenatally to 12 months post natally. (AIPG 2014)

• The last primary tooth to be replaced by a permanent tooth is maxillary canine. (AIPG 2005)
•


• The range of time for the crowns of primary dentition to fully erupt is between 7 to 30 months, whereas crown formation
•
of all primary teeth is completed by 12 months of age.
• The range of time for the crowns of permanent dentition to fully erupt is between 6 to 13 year. (except for third molar)
•
• Root end completion in primary dentition is usually 1½ (one and half years) after eruption, whereas in permanent
•
dentition it is 3 years after eruption, ie. By 16 years. Root of all permanent first teeth are formed excluding third molar.
• First evidence of calcification of permanent teeth appears at birth and is permanent first molar.

•
• Maxillary canines show first evidence of calcification much earlier compared to lateral incisors.
•
• The only teeth initiated after birth are permanent second molars, third molars and premolars.
•
• In permanent dentition: Average range of time for initiation of calcification to completion of calcification is birth to 8
•
years of age excluding third molars.
Amelogenesis
Organization • The ameloblasts become elongated and the organelles become polarized before the same occurs to odontoblasts
•
Formation • The enamel matrix produced by ameloblasts starts virtually perpendicularly to the DEJ and progresses outward
•
toward the eventual tooth surface. The oldest enamel is located at the DEJ underlying a cusp or cingulum.
• Ameloblastic activity starts immediately after mantle dentin formation.
•
• As ameloblasts retreat, Tomes’ processes are formed around which enamel matrix proteins are secreted, most of
•
which are almost instantly partially mineralized to form enamel matrix. This determines the structure and morphology
of the tooth. (AIIMS Nov 2013)
Maturation • Final mineralization occurs with inorganic ion influx and removal of protein and water by cyclic ameloblastic activity,
•
 
forming hydroxyapatite (HA) crystals.
• As the HA crystals accumulate, they are tightly stacked in elongated units called enamel rods (prisms). The rods
•
 
are surrounded by a rod sheath and separated by an inter-rod substance that consists of HA crystals aligned in a
different direction than the rods themselves.
• Each keyhole-shaped enamel rod is formed by four ameloblasts (one for the head and three for the tail).
•
• At cusp tips, the enamel rods appear twisted and intertwined in a formation known as gnarled enamel.
•
• An additional two years period is required for complete calcification or maturation of enamel following eruption of
•
tooth into oral cavity following its contact with saliva. (AIIMS MAY 2013)
Enamel Knot (AIPG 2012)

• Enamel knot precursor cells can be detected first at the tip of the tooth buds by expression of p21 gene, followed shortly
•
by Shh
• By the cap stage, when the enamel knot is visible histologically, it expresses gene for many signaling molecules including
•
bmp2, bmp4, bmp 7, fgf 4, fgf 9
• The enamel knot represents the organizational centre which orchestrates cuspal morphogenesis
•
ENAMEL
Hardest and most highly mineralized substance of the body which covers the crown of the tooth.
Composition: • Inorganic content (by volume)
•
– Hydroxyapatite – 90-92%
–
– Other minerals and trace elements – 3-5%
–
• Organic content (by volume)
•
– Proteins and lipids – 1-2%
–
– Water – 4% (AIIMS NOV 2013)
–
402
Enamel proteins • Amelogenin
•
– Heterogenous group of low molecular weight proteins, accounting for about 90% of enamel proteins
–
– Hydrophobic in nature
–
– Rich in proline, histidine, glutamate, leucine
–
• Non amelogenns
•
– Constitute about 10% of enamel matrix protein
–
– Includes:
–
- Enamelin
-
- Ameloblastin
-
- Tuftelin (AIPG 2012)
-
Structure • Composed of millions of rods and prisms
•
• Diameter of enamel rod increases from dentin enamel junction towards outer surface of enamel in 1:2
•
• Enamel rod lie perpendicular to dentino enamel junction
•
• In cervical region, direction of enamel rod is incisally/occlusally in deciduous while in permanent, it is atypical.
•
• This change in direction of enamel rods should be kept in mind during tooth preparation so as to avoid unsupported
•
enamel rods.
Strength • Brittle
•
• Has high modulus of elasticity and low tensile strength
•
• Specific gravity of enamel is 2.8
•
• Hardness decreases from outer surface of the enamel to its inner surface.
•
• Density of enamel increases from DEJ to the outer surface.
•
• When compared, dentin has high compressive strength than enamel.
•
• Because of high compressive strength of dentin than enamel, the dentin acts as a cushion for enamel when
•
masticatory forces are applied on it.
Functions of • Hardest structure of tooth supporting the masticatory forces.

enamel
•
• Responsible for colour and esthetics
•
• Responsible for surface texture and translucency of tooth
•
• Supports underlying dentin and pulp.
•
Thickness of Enamel
Tooth type Thickness
• Anterior tooth (incisal edges) • 2.0 mm
•
•
• Premolar tooth (cusp) • 2.3 to 2.5 mm
•
•
• Molar tooth (cusp) • 2.5 to 3.0 mm
•
•
Colour of enamel depends on
• Colour of underlying dentin
•
• Thickness of enamel
•
• Amount of stains in enamel
•
• Anomalies occurring during developmental and mineralization stage like antibiotic usage and excess fluoride intake
•
affects the color.
Structures Present in Enamel

Gnarled enamel • Irregular enamel that is resistant to cleavage and cutting while tooth preparation
•
Bands of hunter • Usually occur because of alteration of light reflection (optical phenomenon) due to changes in rod direction.
•
schreger • Best seen in longitudinal ground sections seen in reflected light.
•
• They are considered to resist and disperse the strong forces.
•

Enamel tufts • Ribbon like structures which run from dentin to enamel
•
• Resemble tufts of grass
•
• Contain greater concentration of enamel proteins
•
• They are hypomineralized structure in the enamel, thus play role in spread of dental infection
•
Enamel lamellae • Leaf like defects present in enamel and may extend to DEJ (AIIMS Nov 2013)
•

• Contain organic substances (AIPG 2008)
•
• Commonly found at the base of occlusal pits and fissures.
•
• Caused by imperfect calcification of enamel tissue.
•
• Three types of lamellae are commonly seen:
•
– Type A composed of poorly calcified rod segments
–
– Type B composed of degenerated cells
–
– Type C arising after eruption where the crack is filled with mucoproteins from the oral preparartion.
–
• Type A lamellae is confined to enamel while type B and C may extend into dentin
•
Enamel Spindles • Odontoblastic processes cross DEJ and their ends are thickened, called enamel spindles
•
• Spindles serve as pain receptors, that is why when we cut in the enamel patient complains of pain
•
Striae of Retzius • Appear as brownish bands in the ground sections and illustrate the incremental pattern of enamel
•
Prismless Layer • Structureless layer of enamel near cervical line and to a lesser extent on the cusp tip which is more mineralized.
•
Usually 30 microns thick in primary teeth. (AIIMS Nov 2010, AIPG 2005, 2007)
Dentino-enamel • Scalloped/pitted in which crests are toward enamel and shallow depressions are in dentin.
•
junction • Helps in better interlocking between enamel and dentin. Prevents tearing of enamel during function.
•
• Hypomineralized zone
•
• About 30 microns thick
•
Occlusal pits and • Formed by the faulty coalescence of developmental lobes of premolars and molars.
•
fissures • Formed at the junction of the developmental lobes of the enamel organ.
•
• Grooves are developed by smooth coalescence of developmental lobes.
•
DENTIN
• Specialized connective tissue which is mesodermal in origin, formed from dental papilla.
•
• The unity of dentin-pulp is responsible for dentin formation and protection of the tooth.
•
Composition • Inorganic material: 70 percent
•
• Organic material: 20 percent (AIPG 2001)
•
• Water: 10 percent
•
Colour • Slightly darker than enamel and generally light yellowish
•
• Becomes darker with age
•
• On constant exposure to oral fluids and other irritants, the colour becomes light brown or black
•
Thickness • Usually more cuspal heights and incisal edges.
•
• Around 3 to 3.5 mm on the coronal surface
•
• With advancing age, thickness of secondary and tertiary dentin increases
•
Hardness • 1/5th of enamel
•
• Compressive hardness is 266 MPa
•
• Tensile strength–40 to 60 MPa
•
• Hardness increases with age
•
Functions • Provide strength to tooth
•
• Offers protection to pulp
•
• Provides flexibility to the tooth
•
• Affects the color of enamel
•
• Defensive in action
•
404
Structure of Dentin
Dentinal tubules • Follow a ‘S’ shaped curve in the tooth crown and are straighter in the incisal edges, cusps and root areas
•
• The ends of the tubules are perpendicular to dentin enamel and dentino cemental junctions
•
• Lateral branches, termed as canaliculi or microtubules are present throughout the dentin
•
•
•
Each dentinal tubule is lined with a layer of peritubular dentin, which is more mineralized than the
surrounding intertubular dentin
• Number of tubules increase fro 15,000 – 20,000/mm2 at DEJ to 45,000-65,000/mm2 toward the pulp.
•
• Diameter is 2-3 μm near pulp to 0.5 – 0.9μm near DEJ (AIPG 2005)
•
• Dentin tubules may extend from the odontoblastic layer to the dentino enamel junction and give high
•
permeability to the dentin.
• Contents of dentinal tubule:
•
– Odontoblastic process
–
– Dentinal fluid, a complex mixture of proteins such as albumin, transferrin, tenascin and proteoglycans.
–
Predentin • First formed dentin
•
• Unmineralized zone between the mineralized dentin and odontoblasts
•
• 10 to 30 μm thick
•
• Lies closest to pulp
•
Peritubular dentin • Lines the dentinal tubules and is more mineralized than intertubular dentin.
•
Intertubular dentin • Present between the tubules which is less mineralized than peritubular dentin
•
• Determines the elasticity of dentinal matrix
•
Primary dentin • This type of dentin is formed before root completion, gives initial shape of the tooth. It continues to grow
•
until 3 years after tooth eruption.
• Mantle dentin:
•
– At the outermost layer of the primary dentin, just under the enamel, a narrow zone called mantle dentin
–
exists.
– Formed as a result of initial mineralization reaction by newly differentiated odontoblasts.
–
– First formed dentin in the crown underlying the DEJ
–
• Circumpulpal dentin:
•
– Forms the remaining primary dentin and is more mineralized than mantle dentin. This dentin outlines
–
the pulp chamber and therefore it may be referred to as circumpulpal dentin.
– Formed before root completion.
–
Secondary dentin • Formed after completion of root formation.
•
• Direction of tubules is more asymmetrical and complicated as compared to primary dentin.
•
• Forms at a slower rate than primary.
•
Reparative dentin/ Ter- • Tertiary dentin frequently formed in response to external stimui such as dental caries, attrition and trauma.
tiary dentin
•
• Is the injury is severe and causes odontoblast cell death, odontoblast like cells synthesize specific reparative
•
dentin just beneath the site of injury to protect the pulp tissue.
• The tubular pattern ranges from irregular to an atubular pattern
•
• Reparative dentin matrix is less permeable; this prevents the diffusion of noxious agents from the tubules.
•
Sclerotic dentin • Occurs due to aging or chronic and mild irritation which causes a change in the composition of the primary
•
dentin. (AIPG 2007)
• In sclerotic dentin, peritubular dentin becomes wider due to deposition of calcified materials, which progress
•
from enamel to pulp.
• This area becomes harder, denser, less sensitive and more protrective of pulp against irritants.
•
• Type:
•
– Physiologic sclerotic dentin: occurs due to aging
–
– Reactive sclerotic dentin: occurs due to irritants
–
– Eburnated dentin: formed due to destruction by slow caries process or mild irritation and results in
–
hard, darkened cleanable surface on outward portion of reactive dentin.

Dead tracts • Results due to moderate type of stimuli such as moderate rate of caries or attrition.
•
• In this case, both affected and associated odontoblasts die, resulting in empty dental tubules which appear
•
black when ground sections of dentin are viewed under transmitted light.
CEMENTUM (Discussed In Detail In Periodontology)

Origin • Differentiated ectomesenchymal cells of the dental follicle.
•
Functions of Cemen- • Support: Provides attachment for teeth (Sharpey’s fibers).
•
tum • Protection: Helps prevent root resorption during tooth movement.
•
• Formative: Continual apical cementum deposition accounts for continual tooth eruption and movement
•
 
Cementogenesis • During root formation, ectomesenchymal cells of the dental follicle migrate through gaps in Hertwig’s epithelial
 
•
root sheath and orient themselves along radicular dentin. Here, they differentiate to cementoblasts and
secrete cementum (cementum matrix).
• As the cementoblasts retreat away from the dentin, the matrix is calcified and a new layer of cementum
•
matrix is secreted. These layers form resting lines, which can be seen microscopically.
• Cementoblasts may be trapped in their own matrix. When this occurs, they are known as cementocytes,
•
which reside in lacunae. They receive nutrients via canaliculi that extend to the periodontal ligament.
• Cementum is constantly produced at the apical portion of the root to account for the continual eruption of
•
teeth. Deposition of excessive cementoid is known as hypercementosis
Effects Of Aging On • ↑ cementum deposition

•
Cementum
Clinical Implications • Cementum enables orthodontic tooth movement because it is more resistant to resorption than
•
alveolar bone.
DENTAL PULP
• Basically the pulp is divided into the central and the peripheral region. The central region of both coronal region of both
•
coronal and radicular pulp contains nerves and blood vessels. (AIIMS Nov 2010)

The peripheral region contains the following zones
Odontoblatic layer • Odontoblasts consist of cell bodies and their cytoplasmic process. The odontoblastic cell bodies form the
•
odontoblastic zone whereas the odontoblastic processes are located within predentin matrix. Capillaries,
nerve fibres and dendritic cells may be found around the odontoblasts in this zone
Cell free zone of weil • Central to odontoblasts is subodontoblastic layer, termed as cell free zone of Weil. It contains plexuses of
•
capillaries and fibres ramification of small nerve
Cell rich zone • This zone lies next to subodotoblastic layer. It contains fibroblasts, undifferentiated cells which maintain
•
number of odontoblasts by proliferation and differentiation
Contents of Pulp
Cells Matrix
• Odontoblasts • Collagen fibres
•
•
• Fibroblasts • Ground substance
•
•
• Undifferentiated cells • Blood vesssels
•
•
• Defense cells • Lymphatics
•
•
• Mesenchymal cells • Nerves
•
•
• Macrophages, plasma and mast cells
•
406
Structural or Cellular Elements

• Odontoblasts
•
• They are first type of cells encountered as pulp approached from dentin.
•
• Undifferentiated mesenchymal cells
•
– Undifferentiated mesenchymall cells are descendents of undifferentiated cells of dental papilla which can
–
dedifferentiate and then redifferentiate into many cell types.
• Defence cells
•
– Histiocytes and macrophages: They originate from undifferentiated mesenchymal cells or monocytes. They appear
–
as large oval or spindle shaped cells which are involved in the elimination of dead cells, debris, bacteria and foreign
bodies, etc.
– Polymorphonuclear leukocytes: Most common from of leukocytes is neutrophil, though it is not present in healthy
–
pulp. They are major cell types in micro abscesses formation and are effective at destroying and phagocytosing
bacteria and dead cells.
– Lymphocytes: In normal pulps, mainly T lymphocytes are found. They are associated with injury and resultant
–
immune response.
– Mast cells: On stimulation, degranulation of mast cells release histamine which causes vasodilatation, increased
–
vessel permeability and thus allowing fluids and leukocytes to escape.
• Extracellular components
•
– The extracellular components include fibres and the ground substance of pulp.
–
– Fibres: The fibres are principally type I and III collagen. Collagen is synthesized and secreted by odontoblasts and
–
fibroblasts.
– Ground substance: It is a structureless mass with gel like consistency forming bulk of pulp.
–
– Odontoblasts form dentin in response to injury particularly when original dentin thickness has been compromised
–
as in caries, attrition, trauma or restorative procedure.
Age Changes in Pulp

Pukp like connective tissues, undergoes changes with time. Pulp can show changes in appearance (morphogenic) and in function
(physiologic)
Morphologic changes Physiologic changes
• Continued deposition of intratubular dentin – reduction in • Decrease in dentin permeability provides protected environment for
•
•
tubule diameter pulp reduced effect of iritants
• Reduction in pulp volume due to increase in secondary dentin • Possibility of reduced ability of pulp to react to irritants
•
•
deposition. • Possibility of reduced ability of pulp to react to irritants and repair
•
• Presence of dystrophic calcification and pulp stones itself.
•
• Decrease in sensitivity
•
• Reduction in number of blood vessels
•
ORAL MUCOUS MEMBRANE
Thickness of the mucosa
• Labial and buccal mucosa: 500 microns
•
• Soft palate: 150 microns
•
• Floor of mouth (thinnest): 100 microns (AIPG 2005)
•

• Gingiva: 250 microns
•
Region Mucosa
Lining mucosa Covering epithelium Lamina propria Submucosa

Region Mucosa
• Soft palate Thin–150 microns, non Thick with numerous short Diffuse tissue containing numerous minor salivary
•
keratinized stratified sq papillae, elastic fibres glands
epithelium, taste buds are forming an elastic lamina,
present highly vascular with well
developed capillary network
• Ventral surface of Thin non keratinized str sq Thin with numerous short Thin and irregular, may contain fat and small

•
tongue epithelium papillae and some elastic vessels, where absent, mucosa is bound
fibres, a few minor salivary to connective tissue surrounding tongue
glands, capillary network in musculature.
subpapillary layer, reticular
layer relatively avascular.
• Floor of the mouth Non keratinized, str sq Short papillae,some Loose fibrous connective tissue containing fat and
•
epithelium elastic fibres, extensive minor salivary glands
vascular supply with short
anastomosing capillary
loops
• Alveolar mucosa Thin, nonkeratinized str sq epi Short papillae, connective Loose connective tissue, containing thick elastic
•
tissue containing many fibres attaching it to periosteum of alveolar
elastic fibres, capillary loops process, minor salivary glands
close to the surface
• Labial and buccal Very thick–500 microns. Long slender papillae, Mucosa firmly attached to the underlying muscle
•
mucosa Nonkeratinized, stratified sq dense fibrous rich fibres by collagen and elastin, dense collagenous
epithelium vascular supply giving off connective tissue with fat, minor salivary glands
anastomosing capillary and sebaceous glands
loops to papillae
• Lips – vermilion zone Thin, orthokeratinized str sq Numerous narrow papillae, Mucosa firmly attached to underlying muscle;
•
epithelium capillary loops close to some sebaceous glands in vermillion border,
surface in papillary layer
• Lips – intermediate Thin paarakeratinized str sq Long irregular papillae, Minor salivary glands and fat
•
zone epithelium elastic and collagen fibres in
connective tissue
Masticatory mucosa
• Gingiva Ortho or para keratinized str Long narrow papillae dense No distinct layer
•
sq epithelium, usually stippling collagenous connective
present tissue
• Hard palate Thick ortho keratinized str sq Long papillae thick dense Dense collagenous connective tissue attaching
•
epithelium. collagenous tissue, esply mucosa to periosteum, fat and minor salivary
under rugae, moderate glands
vascular supply with short
capillary loops
Specialized mucosa
• Dorsal surface of Thick keratinized and non Long papillae minor salivary No distinct layer
•
tongue keratinized str sq epithelium glands in posterior portion,
forming 3 types of lingual rich innervation, capillary
papillae and taste buds plexus in papillary layer,
large vessels in deeper
layers
Sensitivity to Pain
Sensation Greatest Moderate Least

• Pain Lips, Pharynx, Base of tongue, Teeth Anterior Tongue, Gingiva Buccal Mucosa (AIPG 2012, AIIMS Nov
•
2013, NEET 2013)

• Heat Lips Anterior Teeth Ventral Tongue, Palate
•
• Cold Lips, Posterior Palate Base and Ventral Tongue Dorsum of Tongue, Buccal mucosa
•
• Touch Lips, Tip of tongue, Anterior Palate Gingiva Base of Tongue, Buccal Mucosa
•
408
PERIODONTAL LIGAMENT
• A soft connective tissue located between the tooth and alveolar bone.
•
• Approximately 0.2 mm wide but varies with tooth function and age.
•
Origin Differentiated ectomesenchymal cells of the dental follicle
Contents of The PDL • Cells and cellular elements
•
– Fibroblasts: Most common cell of the PDL.
–
– Cementoblasts and cementoclasts.
–
– Osteoblasts and osteoclasts.
–
– Macrophages, mast cells, and eosinophils.
–
– Undifferentiated mesenchymal cells.
–
• Ground substance: Proteoglycans, glycosaminoglycans, glycoproteins, and water (70%).
•
 
• Epithelial rests of Malassez: Remnants of HERS. Found closer to cementum than alveolar bone.
•
 
• Cementicles: Calcified masses either attached or unattached to root surfaces.
•
 
• Fibers
•
– Principal collagen fibers:
–
– Composed mostly of type I collagen, but also type III collagen
–
Blood vessels • The vasculature of the PDL arises from the maxillary artery. Vessels can reach the PDL from various sources:
•
• Periosteal vessels: Branches from the periosteum. This is the primary source of PDL vasculature.
•
 
• Apical vessels: Branches of the dental vessels that supply the apical regions of the PDL.
•
 
• Transalveolar vessels: Branches of transseptal vessels that perforate the alveolar bone proper.
•
 
• Anastomosing vessels of the gingiva.
•
Nerve fibers • Arise from branches of the trigeminal nerve (CN V)
 
•
• Free nerve endings: Transmit pain. Most abundant.
•
• Ruffini corpuscles: Provide mechanoreception.
•
• Coiled endings.
•
• Spindle endings.
•
Lymphatics • All drain to the submandibular lymph nodes, except mandibular incisors which drain to the submental nodes
 
•
Effects of Aging On The – ↓ PDL width.
–
Pdl – ↓ cellularity and fiber content.
–
Clinical Implications – Teeth in hypofunction have a decreased PDL width with fibers arranged parallel to the root.
–
– Teeth in hyperfunction have an increased PDL width.
–
Collagen
• Contains one or more triple helical domains.
•
• Collagen is a rigid, rod like structure that resists stretching and fibres made of it have high tensile strength.
•
• The collagen molecule consists of 3 distinct polypeptide chains called x chains. The formation of the triple helix depends on
•
the amino acid composition of the protein and the winding of the polypeptide chains.
• The amino acid sequence of the triple helix is Glycine–x–y.
•
• X–Y represents imino acids proline and hydroxyl proline 30% of the time.
•
Fibrillar • Type I, Type II, Type III, Type IV and Type XI collagen.
•
Fibril: Associated collagens • Type IX, Type XII and Type XIV collagen belong to this class
•
with interrupted triple helices
Collagen forming sheets • Type IV and VIII collagens belong to this group
•
Collagen forming sheets • Type IV and VIII collagen belong to this group
•
Collagen forming beaded fila- • Type V collagen
•
ments

Collagen forming anchoring • Type VII collagen
•
fibrils
Growth: Plate specific col- • Type X collagen
•
lagen
Miscellaneous • Type XIII
•
Important Periodontal Proteoglycan
Proteoglycan Glycosaminoglycans Proposed function
• Versican • Chondrotin sulfate • Influences cell migration and cell attachment
•
•
•
• Decorin • Dermatan sulfate or chondroitin sulfate • Control fibril formation and influences elasticity of connective
•
•
•
tissue.
• Biglycan • Dermatan sulfate or chondroitin sulfate • Influences organization of ECM
•
•
•
• Syndecan • Heparin sulfate and chondroitin sulfate • Attaches epithelial cells to extracellular matrix
•
•
•
Non Collagenous Proteins of Periodontal Ligament
Protein Functions
• Elastin • Facilitates stretching compression or distortion of tissue by applied forces.

•
•
• Fibronectin • Cellular adhesion, cytoskeletal organization, cell migration, phagocytosis, hemostasis, thrombosis
•
•
• Laminin • Mediates attachment of and differentiated state of epithelial cells to type IV collagen
•
•
• Osteocalcin • Inhibitor of hydroxyapatite precipitation chemoattractant for monocytes inhibitor of leukocyte release.
•
•
• Osteopontin • Promotes attachment and spreading of bone cells.
•
•
• Bone sailoprotein • Attachment factor for bone cells
•
•
• Osteonectin • Involved in mineralization process, modulates cells proliferation and phenotype, inhibitor of cell spreading
•
•
• Tenascin • Facilitates epithelial – mesenchymal interactions, destabilizes cell matrix adhesions
•
•
BONE (ALVEOLAR BONE)
• A general term to describe the bone in the maxilla and mandible which houses the teeth.
•
Interalveolar • The bony projection separating two alveoli
•
septum
Interradicular • Alveolar bone between the roots of multirooted teeth
•
septum
Origin • Differentiated ectomesenchymal cells of the dental follicle
•
Components of • Alveolar bone proper: The thin layer of cortical bone that immediately surrounds the teeth and into which PDL
•
alveolar bone fibers (Sharpey’s fibers) are embedded. It is also called bundle bone, lamina dura, or cribriform plate.
• Supporting alveolar bone: The part of the alveolus that surrounds the alveolar bone proper. It consists of the
•
following:
– Cortical bone (cortical plate): Forms the buccal and lingual outer surfaces of the maxilla and mandible. It
–
 
is generally thicker in the mandible and in posterior (molar) regions.
 
– Cancellous bone (spongy bone, trabecular bone): Fills the area between the cortical plates. It makes up
–
 
the majority of alveolar bone.
 
CLINICAL IMPLI- • The radiographic appearance of the lamina dura is determined as much by the x-ray beam angulation as it is by
•
CATIONS its integrity.
• The radiographic presence (or absence) of the crestal lamina dura has no correlation with periodontal attachment
•
loss
410
TEMPOROMANDIBULAR JOINT
• TMJ:
•
– Diarticular
–
– Diarthroidal
–
– Synovial
–
– Compound
–
– Ginglymoarthroidal
–
• Meniscus: Non-innervated and non-vascularized
•
• Components:
•
– Moving from superior to inferior:
–
Glenoid/ mandibular fossa (of temporal bone)

Articular cartilage

Disc/meniscus

Condylar cartilage cap

Condyle of mandible

– Articular capsule surrounds joint, with synovium internally
–
Ligaments stabilize

Bony Components
– Condyle of the mandible
–
Elliptically shaped with long axis oriented mediolaterally.

Posterior condyle is rounded and convex.

Anteroinferior aspect is concave.

– Glenoid/mandibular fossa (of temporal bone)
–
Concave

– Articular eminence
–
Anterior part of glenoid fossa (squamous temporal bone).

Articular eminence (tubercle) is convex.

– Articular sufaces
–
Glenoid fossa and condyle are lined with dense fibrocartilage.

Not hyaline cartilage like most synovial joints.

– Articular Disc (Meniscus)
–
Fibrocartilaginous biconcave disc. (AIPG 1993)

- Lies between articular surfaces of condyle and mandibular fossa.

- Divides disc space into superior and inferior compartments.

- Attaches peripherally to the capsule and anteriorly to the lateral pterygoid muscle.

 
- Attaches to medial and lateral poles of the condyle via collateral ligaments.

Regions

- Thin intermediate zone.

- Thick anterior and posterior bands.

- Posterior band is contiguous with the posterior attachment tissues (bilaminar zone).

- Bilaminar zone is vascular, innervated tissue (role in allowing condyle to move forward).

 
 
– Articular Capsule
–
Fibrous capsule that surrounds the TMJ.

Attaches superiorly to the glenoid fossa (tubercle of articular eminence).

Attaches inferiorly to the condylar neck.


– Synovium
–
Lines the internal surface of the joint capsule.

Secretes synovial fluid for joint lubrication.

Does not cover the articular surfaces or articular disc.

• Nerve supply
•
– Auriculotemporal nerve(AIIMS Nov 2010, AIIMS 1990) AIPG 2009, 1992)
–

– Massetric nerve

–
• Blood supply
•
– Branches from superficial temporal and maxillary arteries.
–
The Ligaments of TMJ Are:
Capsular ligament • Completely surrounds the condyle
•
Temporomandibular ligament • This is the external (lateral) portion of capsular ligament, which is attached to the zygomatic process
•
of temporal bone above and lateral, posterior margin of the neck of condyle below
Sphenomandibular ligament • It is attached above to the sphenoid bone and below to lingual of the mandible on medial side.
•
Stylomandibular ligament • Extends from the styloid process to the posterior border of the ramus of the mandible just above
•
the angle.
Acton Type of movement

• Protrusion • Gliding movement
•
•
• Slight opening of mouth • Hinge movements
•
•
• Wide opening of mouth • Hinge followed by gliding
•
•
• During opening of mandible from reduced contact position • Hinge followed by gliding
•
•
• Chewing movements • The head of one side glides forward, but the head of opposite
•
•
side rotates in a vertical axis
• Movement from retruded contact position unto terminal hinge axis • Only hinge movements
•
•
CHAPTER 10
Oral Pathology and Oral Medicine
Objectives
• Developmental Disorders • Blood Disorders

• Benign and Malignant tumours • Bleeding Disorders

• Odontogenic Cysts and Tumours • Skin Disorders

• Salivary Gland Disorders • Disease of Nerve and Muscle

• Bacterial, Viral and Mycotic Infections • Hereditary Conditions

• Pulp and Periapical Tissues • Important Points

• Bone and Joint • Miscellaneous

DEVELOPMENTAL DISORDERS AND CONDITIONS
Soft-tissue and/or hard-tissue defects that occur during the development of the individual, either before or after birth.
Oral-facial clefts • Cleft lip
•
– Unilateral (80%) or bilateral (20%) clefts of the lip.
–
– Defect between medial nasal process and maxillary process. (AIPG 2002)
–

– Approximately 1 in 1000 births, but varies with race.
–
• Cleft palate
•
– Lack of fusion between palatal shelves; approximately 1 in 2000 births.
–
– Cleft lip (25%), cleft palate (25%), cleft lip and palate (50%).
–
 
– In india, cleft palate has less frequency in those with blood group A. cleft lip occurs in more in those with
–
group O + AB
• Vander Woude syndrome: Paramedian lip pits + cleft lip +/- cleft palate, autosomal dominant
•
Lip pits • Invaginations at the commissures or near the midline.
•
• Commissural lip pits: failure of normal fusion of embryonal maxillary and mandibular processes. Autosomal
•
dominant
Fordyce granules • Ectopic sebaceous glands. (AIPG 2004, 2008, AIIMS MAY 2009)
•
 
 
• Commonly seen in buccal mucosa and/or lip.
•
• Clinically yellow spots on cheek mucosa lateral to angle of mouth bilaterally symmetrical
•
Leukoedema • Bilateral opacification of the buccal mucosa.
•
 
• Characterized by a milky white translucent coloration of the mucosa with minute ‘hanging’ folds of tissues.
•
• Common; no significance.
•
Oral Pathology and Oral Medicine 413

Cheilitis glandu- • Of three types:
•
laris – Simple
–
– Superficial suppurative type or Baetz’s disease
–
– Deep suppurative type or cheilitis glandularis apostemastosa
–
Cheilitis granulo- • Also known as Mischener’s disease
ORAL PATHOLOGY AND ORAL MEDICINE

•
matoses
Thyroid congenital • Lingual thyroid

•
 
abnormalities – Thyroid tissue mass, midline tongue base.
–
– Caused by incomplete decent of thyroid anlage.
–
– May be patient’s only thyroid.
–
• Thyroglossal tract cyst
•
– Midline neck swelling due to cystic change of remnants of thyroid tissue.
–
 
– Located along embryonic path of thyroid descent.
–
Exostoses – Excessive cortical bone growth of unknown cause.
–
– Buccal exostoses, torus palatinus, torus mandibularis.
–
Developmental soft • Dermoid cyst
•
tissue cysts - Mass in midline floor of mouth if above myolohyoid muscle.
-
- Mass in upper neck if below mylohyoid muscle.
-
• Branchial cyst
•
- Epithelial cyst within lymph node of the neck.
-
• Oral lymphoepithelial cyst
•
- Cyst within lymphoid tissue that is the counterpart of the neck.
-
- Nodule commonly in soft palate, oral floor, or lateral tongue.
-
Developmental Conditions of Tongue
Macroglossia • Causes:
•
– Congenital hyperplasia/hypertrophy Tumors
–
– Lymphangioma,
–
– Vascular malformation,
–
– Neurofibroma,
–
– Multiple granular cell tumors,
–
– Salivary gland tumors
–
– Endocrine abnormality
–
- Acromegaly,
-
- Cretinism
-
 
– Infections obstructing lymphatics
–
– Beckwith-Wiedemann syndrome
–
– Gigantism
–
– Amyloidosis
–
• Beckwith hypoglycaemic or Beckwith Wiedemn Syndrome – macroglossia + neonatal hypoglycemia +
•
microcephaly + featal visceromegaly
Geographic tongue (be- • Relatively common (2% of population) benign condition of the tongue of unknown cause.
•
nign migratory glossitis, • Appears as white annular lesions surrounding atrophic red central zones that migrate with time.
•
 
erythema migrans) (AIPG • In erythema migrans/benign migratory glossitis, filliform papilla are absent. (AIPG 2004)
2002) (AIPG 2008)
•

• Its histological features have been described to be reminiscent of Psoriasis as both show degeneration
•
of epithelium, with migration of lymphocytes, thereby producing an abscess.
• Occasionally symptomatic (mild pain or burning).
•
• No treatment necessary. (AIPG 2004)
•

Fissured tongue • Fissuring of tongue dorsum.
•
• Relatively common (3% of population), and usually asymptomatic.
•
 
• A component of Melkerson–Rosenthal syndrome. Fissured tongue, granulomatous cheilitis, and
•
 
facial paralysis.
414
Hemangioma • Congenital hemangioma
•
– Focal proliferation of capillaries.
–
– Most lesions undergo involution; persistent lesions are excised.
–
 
• Vascular malformation
•
– A persistent malformation of capillaries, veins, and arteries.
–
– Exhibits a thrill (palpate a pulse) and bruit (hear a pulse).
–
– Port wine stains are seen in hemangioma
–
– Micro – cherry or venous lakes refer to tiny vascular hemangioma of lip
–
– A type of vascular malformation is known as Sturge–Weber syndrome (encephalotrigeminal an-
–
giomatosis).
- Lesions involve skin along one of the branches of the trigeminal nerve.
-
- The leptomeninges of the cerebral cortex may be involved by the malformations, leading to
-
mental retardation and seizures.
– Hemangioma – vascular naevus
–
– Capillary hemangioma – protrusive naevus
–
Lymphangioma • This is a congenital focal proliferation of lymphatic channels.
•
 
• When occurring in the neck, it is called hygroma coli.
•
• Papillomatous tongue is seen in lymphangioma
•
• Tongue: Most common site for both lymphangioma and granular cell myoblastoma
•
Disease/disorder Papillae affected
• Benign migratory glossitis or geographic tongue • Multiple areas of desquamation of filiform papillae
•

•
(HP 2010, AIPG 2002)
• Riboflavin deficiency (KAR 2000) • Atrophy of filliform papillae with normal or engorged
•

•
• Black hairy tongue (lingua villosa) (AIIMS 1996, KAR 2002, • Hypertrophy of filiform papillae from 1mm to 15mm
•

•
AIPG 2004, AP 2008)
• Strawberry tongue (scarlet fever) • Swollen hyperemic fungiform papillae

•
•
• Familial dysantonomia • Absence of fungiform + circumvallate papillae
•
•
• Median rhomboid glossitis (central papillary atrophy of • Congenital abnormality resulting from failure of tuberculum impar
•
•
tongue) to retract before two halves of tongue fuses. Filliform papillae are
absent. (AIIMS 19991, 1998, 1999, 2001) (AIPG 2010)

Other Disorders of Tongue
• Glossodynia: Painful tongue • Glossopyrosis: Burning tongue

• Glossoplegia: Paralysis of tongue • Strawberry tongue: Early tongue change in scarlet
•

fever
• Raspberry: Late tongue change scarlet fever • Stomatitis scalatina: Mucosal change
•

• Geographical tongue: Migratory glossistis • Scrotal tongue: Fissured tongue
•

• Raw beefy tongue: Acrodynia (pink disease or swifts disease) • Black hairy tongue: Oral use of antibiotics
•

• Magenta red tongue: Vit. B12 deficiency (Riboflavin) • Moell’s/Hunter’s Glossitis: Vit. B2 deficiency
•

• Bald tongue of sandwith: Pellagra
•
Developmental Disturbances
Concrescence:(NEET 2013, • Form of fusion which occurs, after root formation has been completed.
•
AIPG 2004, 2005, 2007, AP • Teeth are united by cementum only
1998, PGI 2002, MAHE 2010,
•
• It is thought to arise as a result of traumatic injury or crowding of teeth with resorption of the interdental
AIIMS May 08, May 10, Nov 10)
•
bone so that the two roots are in approximate contact and become fused by the deposition of
cementum between them.
• The diagnosis can frequently by made by X ray
•

Gemination: (AIIMS nov 2012, • Anomalies which arise from an attempt at division of a single tooth germ by an invagination with the
•
MAN 2001) resultant incomplete formation of two teeth
• The structure is usually one with two completely or incompletely separated crowns that have a
•
single root and root canal
• Seen in both deciduous and permanent dentition

•
• Exhibit a hereditary tendency
•
• The term fusion and concrescence have been discussed by Levitas.
•
Fusion •
•
Occurs through union of two normally separated tooth germs
• May be complete or incomplete
•
• Occurs due to contacts produced by physical force or physical pressure
•
• Occurs before calcification begins
•
• Common in both dentitions
•
Twinning • The division of a single tooth resulting in one normal and one supernumerary tooth
•
• Number of teeth will be more than normal.
•
Torus mandibularis (AIIMS may • Exostosis or outgrowth of bone found on the lingual surfaces of the mandible
•
08, AIPG 2004, MAHE 2010) • More common in mongoloids and less in Caucasoid
•
• Usually occurs on the lingual surface of the mandible above the mylohyoid line usually opposite the
•
bicuspid teeth (AIPG 2007)

• Usually bilateral
•
• May be lobed or multiple
•
• Surgical removal may be required if it interferes with the denture placement
•
Dilacerations: (AIIMS 2007, • Abnormal curvature or bent in root common in maxillary incisors followed by mandibular anterior
•
AIPG 1991, 2007, 2010, AIPG teeth.
2006, 2010)
Taurodontism: (AIPG 2014, • Abnormal enlargement of the pulp chambers and body at the cost of root in multirooted teeth.
•
AIPG 2006, 2010, AIIMS 1995, • Mandibular teeth are involved. (AIPG 2006)(AIPG 2008)
2007)
•

• Associated with Klinefelters syndrome (AIPG 1994, 2010)
•

• Mostly due to failure of Hertwig’s sheath to invaginate at proper horizontal level.
•
• Mostly molars are involved and body of tooth is enlarged at expense of roots resulting in rectangular
•
teeth.
• Pulp chambers are large and lack the cervical constriction.
•
Talon cusp • Accessory cuspal structure projecting from cingulum area of anterior teeth.
•
• Commonly involved are maxillary anteriors.
•
• Also present in Rubinstein Taybi syndrome (mental retardation, incomplete descent of testes,
•
incomplete development of head structure) (KAR 2008)

Dens evaginatus (leong’s • Protuberance from occlusal surface of mandibular premolar.
•
premolar)
Dens invaginatus/ dens in • Invagination in crown before calcification of maxillary lateral incisor
•
dente (AIPG 2006, 2003, AIIMS • Permanent teeth more commonly involved, maxillary LI.
2007, AP 2010)
•
Supernumerary Teeth: (AIIMS • Most common is mesiodens occurring between maxillary CI (AP 2000)
•

1993, MAN 1994, 2001, KAR • Maxillary fourth molar – 2nd most common (PGI 1991)
2010, AIPG 2002)
•

• 90% of supernumerary teeth occur in maxilla
•
• Seen in:
•
– Cleidocranial dysplasia (AIPG 2001)
–

– Gardener’s syndrome
–
– Cleft lip and palate
–
416
Syndromes associated with Taurodontism Syndromes associated with talon cusp

• Amelogenesis imperfecta, hypoplastic type IE • Rubinstein Taybi syndrome
•
•
• Amelogenesis imperfecta: SyndromeTaurodontism, type IV • Mohr syndrome
•
•
• Cranioectodermal • Sturge Weber syndrome
•
•
• Ectodermal dysplasia • Ellis-van Creveld syndrome
•
•
• Hyperphosphatasia: Oligophrenia–taurodontism • Bloch-Sulzberger syndrome
•
•
• Hypophosphatasia
•
• Klinefelter syndrome
•
• Microdontia: Taurodontia–dens invaginatus
•
• Microcephalic: Dwarfism–taurodontism
•
• Oculo: Dento–digital dysplasia
•
• Oro: Facial–digital, type II
•
• Hodgkin’s syndrome
•
• Scanty hair oligodontia: Taurodontia
•
• Sex chromosomal aberrations (eg XXX, XYY)
•
• Down’s syndrome
•
• Trico: Dento–osseous, types I, II and III
•
• Iricho: Onycho-dental syndrome
•
Enamel Hypolplasia
• Hypoplastic type • Defective formation of matrix
•
•
• Formative stage is affected and enamel is not formed completely.
•

(KAR 2006)

• Hypocalcification/ Hypomineralisation • Defective mineralization of the matrix
•
•
• Enamel is so soft and can be pulled by instrument
•
• Hypomaturation • Crystals formed are immature
•
•
• Enamel is chipped off.
•
Causes of enamel hypoplasia: (AIPG 2005, AIIMS 1996, MAY 2009)

Hereditary type Environmental type
• In this type dentitions are affected. • Both enamel and dentin are involved.
•
•
• Only enamel is affected. • Environmental factors that affect ameloblasts are:
•
•
• E.g. Amelogenesis imperfecta – Nutritional deficiencies
•
–
• Either dentition may be involved and only a single tooth is – Exanthematous diseases
–
– Congenital syphilis
•
involved. (NEET 2013)
–
– Hypocalcemia

–
– Local infection or trauma (Turner’s tooth) commonly seen in
–
maxillary incisors and premolars (AIPG 2009, 2011,
KAR 2008, MAN 2001, PGI 1995,

– Fluorosis AIPG 1997, 1999, MAN 2000)
–

Genes with mutations in Amelogenesis imperfecta (MAHE 2009)
Gene Chromosome Proteins affected Inheritance
1. AMELX gene Xp 22.3 – p22.1 Amelogenesis essential for matrix formation X- linked
Yp 11
2. ENAM gene W Enamelin: Structural protein Autosomal dominant
3. MMP 20 Enamelysin: MMP protein involved in Autosomal recessive

development of enamel

Gene Chromosome Proteins affected Inheritance
4. Kallikrein four KLK4 Protease: Development of enamel Autosomal recessive
Dentinogenesis Imperfecta

(Differentiated from amelogenesis imperfecta by radiographic appearance only-obliterated pulp chambers
Type I Type II
• DI is seen without osteogenesis imperfecta • Bradywine type or Shell teeth (shield’s type III)
•
•
• Caused by mutation in dentin sialophosphoprotein (DSSP) • Apart from DSSP, 3 other genes DMP-1, BSP and SPP1 are also
•
•
gene that maps to chromosome 4 (autosomal dominant) involved

(AIPG 1995, 1999, 2009) • The dentin is extremely thin and the pulp chambers are
•
• Affected teeth are amber brown and opalescent and have broad enormous. (COMEDK 2006)
•

crowns with constriction of cervical area – TULIP shape • The most striking feature is the partial or total precocious
•
• Teeth have bulbous crowns, with narrow roots and root canals. obliteration of pulp chambers by continuous deposition of dentin.
•

The pulp chambers are smaller than normal. Dentin tubules are (MAN 1997)

irregular, larger in diameter and less numerous. Due to limited • Radiographically–shell teeth (KAR 2001)
ability of odontoblasts to form well organized dentinal matrix.
•

(AIPG 1994, 2009, AIIMS 1992, 1999, 2003, AP 2008)

• Water content – 60%
•
• Increased glycosaminoglycans
•
• Microhardness of dentin = cementum
•
Clinical Features
• DI usually exhibits a characteristic unusual translucent or opalescent hue. The usual scalloping of DEJ is absent. Rapid
•
attrition of enamel + dentin (AIPG 2009)

Dentin Dysplasia (Rootless Teeth)
• Characterized by normal enamel but atypical dentin formation with abnormal pulpal morphology
•
Type I or radicular dentin dysplasia: Type II or coronal dentin dysplasia:
• Both dentitions are involved • Permanent teeth appear normal
•
•
• Teeth exhibit extreme mobility and are exfoliated prematurely as • The permanent teeth contain multiple pulp stones.
•
•
result of their abnormally short roots
• In primary teeth – pulp chambers and root canals are completely • Deciduous teeth show brown, opalescent hue as in dentinogenesis
•
•
obliterated while in permanent teeth – a crescent shaped imperfecta.
pulpal remnant may be seen in pulp.
• The pulp is obliterated with calcified tubular dentin, osteodentin • The pulp chambers are obliterated
•
•
and fused denticles
• Normal dentinal tubule formation appears to be blocked, so that • The permanent teeth exhibit abnormally large pulp chambers in
•
•
new dentin forms around obstacles and takes characteristic the coronal portion often described as ‘thistle tube’ in shape.

appearance described as ‘lava flowing around boulders’ (COMEDK 2003, HP 2010, AIPG 2004)

and this pattern of ‘cascades of dentin’ results from repetitive • The deciduous teeth exhibits amorphous and atubular dentin in
attempts to form root structure. (AP 2011)
•
radicular portion, while the coronal dentin is normal.

Regional Odontodysplasia (Ghost Teeth)
• Imperfecta or odontodysplasia.
•
• Etiology is thought to be somatic mutation or a latent virus residing in the odontogenic epithelium.
•
• There is delay or total failure of eruption.
•
418
• Both dentitions are affected.

•
• Due to defective mineralization. Thin enamel + dentin + large pulp chambers.
•
• Abnormally large pulp chambers are seen. (APPSC 1999, MAN 2002, AP 2008)
•

• Radiographically, enamel and dentin are thin with large pulp chambers, giving ghost appearances. (AIPG 2008)
•

• Both permanent and deciduous dentition are involved.
•
• Maxillary permanent central, lateral and canine are affected (AIIMS 1996)
•

• Maxilla is more involved than mandible.
•
Osteogenesis Imperfecta
• Also known as brittle bones, fragilitis ossium, osteopsathyrosis, lobstein disease (AIIMS Nov 2012)
•

• Characterized by extreme fragility and porosity of bones leading to multiple fractures.
•
• The basic defect lies in the organic matrix because of failure in transformation of fetal collagen into mature
•
collagen.
• Osteogenesis imperfecta may be congenital (Vrolik’s type) or acquired later. In childhood (Torden or lobstein
type or osteopsathyrosis)
•
• Osteogenesis imperfecta (OI), disorder of congenital bone fragility caused mutations in the genes that codify for type I
•
procollagen (ie, COL1A1 and COL1A2).
• Glycine is substituted by another amino acid, usually a bulky R group, can be cysteine.
•
• Blue sclera is present (also present in osteopetrosis, fetal rickets, marfan syndrome and Ehlers danlos syndrome).
•

(AIPG 2008)

• There is abnormal bone turn over leading to increase in alkaline phosphate.
•
• Bisphosphonates decrease osteoclastic resorption of bone, leading to increased bone mass and bone strength.
•
Partial or complete obliteration of pulp chamber
Deciduous dentition • Dentinogenesis imperfecta type I
•
more affected • Coronal dentin dysplasia or dentin dysplasia type II
•
Both the dentitions • Dentigenesis imperfecta type I and II, nonbradywine type III
•
• Dentin dysplasia type I (radicular dentin dysplasia)
•
• Heck’s disease: or focal epithelial dysplasia occurs predominantly in children, presents as multiple nodular lesion
•
occurring most commonly on lower lip. The lesion contains virus particles, which are similar to human oral papilloma.
Highly contagious HPV induced epithelial proliferation. Cobblestone or fissured appearance – due to hyperplastic lesions.
• Bohn’s nodules are seen at junction of hard and soft palate whereas Epstein pearls are seen along the median raphae of
•
hard palate and dental lamina cysts of the new born are seen on the alveolar ridges. (AIPG 2014, 2003)

• Hereditary hemorrhagic telangietasia is seen commonly on lips.
•
– Characterized by angiomatous areas
–
– Early signs are epistaxis and bleeding from oral cavity
–
Delayed Eruption is seen in:
• Rickets
•
• Down syndrome
•
• Hypopituitarism
•
• Cleidocranial dysplasia
•
• Achondroplasia
•
• Cretinism
•
• Fibromatosis gingiva
•
• Cherubism
•

Mode of Inheritance
Mode of inheritance Disease
• Autosomal dominant • Dentinogenesis imperfecta (AIPG 1995, 2009)
•
•

• Dentin dysplasia

•
••
Amelogenesis imperfecta hypocalcification type
• Darrier’s disease
•
• White sponge disease
•
• Fibrous dysplasia
•
• Gingival fibromatosis
•
• Germination, fusion
•
• Scrotal tongue
•
• Torus mandibularis
•
• Autosomal recessive • Ectodermal anhydrotic dysplasia (AIPG 2005)
•
•

• Gingival fibromatosis (rare)
•
• Sex linked recessive • Ectodermal anhydrotic dysplasia
•
•
• X linked dominant • Vitamin D resistant rickets
•
•
Alterations in Teeth
Anodontia • Complete absence of teeth (AIIMS 2000, AIPG 2002)
•

Oligodontia • Multiple missing teeth (AIPG 1998, 2003)
•

False anodontia/ Induced • Multiple extracted teeth
•
anodontia
Pseudo anodontia • Multiple unerupted teeth
•
Microdontia • Size of tooth smaller than normal (MAN 2001)
•

Macrodontia • Size larger than normal
•
Natal teeth (dentitia • Teeth present in the oral cavity at the time of birth
•
praecox, congenital teeth,
premature teeth etc,)
Neonatal teeth (NEET • Those that erupt within 30 days
•

2013, MAN 1998, AIPG 2009,
2011)
Early infancy teeth • Teeth erupting after 30 days but erupting early
•
Most commonly ankylosed/ • Deciduous mandibular second molar (AIPG 2012)
•

submerged teeth (AP 1999)
Most commonly missing • Maxillary and mandibular lateral incisors
•
deciduous teeth
Most commonly missing • Third molars followed by maxillary laterals (KAR 2001)
•

permanent teeth
Teeth commonly affected • Maxillary lateral incisors followed by third molars (MAHE 2010, AIIMS may 2010, 1995)
•

by microdontia
• Severe illness before 1 year of age–hypoplastic defects occur in CI, LI, 1st molar and tip of cuspid
•
• After 3 years of age–premolars, 2ndand 3rd molars
•
• Satellite lesion with locally invasive property is seen in hemangioma
•
• Common mole is intra dermal nevus
•
• In junctional nevus, the epithelium is thin and shows cells crossing the junction and growing down into the connective
•
tissue. This is called ‘abtropfung or dropping off ’ effect. Because of this junctional activity it undergoes transformation
into malignant melanoma
420
BENIGN AND MALIGNANT LESIONS OF ORAL CAVITY

Premalignant Conditions
Premalignant Conditions Premalignant Lesions
• Erosive lichen planus • Leukoplakia (AIPG 2006)
•
•

• Actinic or solar keratosis • Erythroplakia
•
•
• Sideropenic dysphagia
•
• Bowen’s disease or carcinoma in situ
•
• Syphilitic glossitis
•
• DLE
•
• Dyskeratosis congenital
•
• Hyperplastic Candidiasis
•
• Peutz-Jegher’s syndrome
•
• Oral Submucous Fibrosis
•
• Oral lichen planus
•
Idiopathic Leukoplakia
• This designation refers to white/opaque oral mucosa lesions that do not rub off and are not clinically diagnostic for any
•
other white lesion.
• Cause is unknown, although tobacco and alcohol may be contributing factors.
•
• Biopsy is mandatory since diagnosis cannot be made clinically.
•
• The hallmarks of histological features of leukoplakia are epithelial dysplasia and surface hyperkeratosis. Dysplasia is
•
present more frequently in leukoplakia involving floor of the mouth.
• Transformation of benign lesions to squamous cell carcinoma is 5% to 15%.
•
• Treatment: excision; recurrence not uncommon.
•
Homogeneous or thick • Well-defined white patch, translucent localized of extensive, that is slightly elevated and that has a
•
leukoplakia fissured, wrinkled, or corrugated surface,
• It is non-palpable i.e., same as surrounding mucous membrane. Some times on palpation, these lesions
•
may feel leathery to “dry, or cracked mud-like”
• Different diagnosis is hyperplastic lichen planus
•
Speckled or nodular • Granular or non homogeneous. Raised mixed red-and-white lesion in which keratotic white nodules or
•
patches are distributed over an atrophic erythematous background
• Mostly seen at the angle of mouth and commisures of lips in chronic smokers. Indurations, fissuring and
•
ulcer formation is seen.
• Associated with a higher malignant transformation rate, with up to two-thirds of the cases epithelial
•
dysplasia or carcinoma
Verrucous or verruci- • Seen as white papilliferous or cauliflower like exophytic growth pattern.
•
form leukoplakia • These lesions are usually heavily keratinized and are most often seen in older, adults in the sixth to eight
•
decades of life. Commonly seen in the region, where the quid is kept for long time.
• Differential diagnosis is verrucous carcinoma
•
Proliferative verrucous • Was first described in 1985.
•
leukoplakia • Extensive papillary or verrucoid white plaques that tend to slowly involve multiple mucosal sites in the
•
oral cavity
• Transform into squamous cell carcinoma over a period of many years.
•
• PVL has a very high risk for transformation to dysplasia, squamous cell carcinoma or verrucous.
•
Erythroplakia (Erythroplasia) (AIPG 2002) • Biopsy mandatory.
•
• Erythroplakia: Erythroplasia of Queyrat • Term erythroplakia is applied to any area of reddened,
•
velvety textured mucosa that cannot be identified on the
•
• A high-risk, idiopathic red patch of mucosa.
basis of clinical and histopathological examinations as
•
• Most represent dysplasia or malignancy. being caused by inflammation or any other disease process
•

• Clinical features: Three clinical types are described in
Smokeless Tobacco-associated White Lesion
•
oral cavity
• Appears as bright red, soft, velvety lesion
• White mucosal change due to direct effects of smokeless
Homogenous
•
form
•
with straight or scalloped well demarcated tobacco and additives.
margins often quite extensive in size • By definition, not idiopathic leukoplakia, since cause is

•
• Common on buccal mucosa and soft known and lesion is clinically diagnostic (however, it
•
palate
could be classified under a more generic designation of
Irregular form • Erythroplakia interspersed with patches leukoplakia or white patch).
•
of leukoplakia in which erythematous
areas are irregular • Seen in labial and buccal vestibules where tobacco is
•
• Not as bright red as homogenous form held.
•
• Most frequently seen on the tongue and • May cause focal periodontal destruction, tooth abra-
•
•
floor of the mouth sion, and/or hypertension. Malignant transformation
Speckled type • Soft red lesions, slightly elevated with is rare.
•
an irregular outline and a granular and
finely nodular surface speckled with tiny
• Xeroderma pigmentosum: Facial pigmentation +
white plaques. It may be called speckled
•
erythroplakia or speckled leukoplakia carcinoma lip
• It may occur anywhere in oral cavity • Bowen’s disease: Intraepithelial CA in patients who had
•
•
• Erythroplakia commonly occurs most frequently in 6-7th arsenical therapy and is often associated with internal or
external cutaneous cancer.
•
decades of life
• The reason for the red appearance of these lesions is • Leukokeratosis Nicotina Palati/Stomatitis Nicotiana/
•
Pipe Smoker’s Palate: Seen in heavy smokers. The palate
•
that connective tissue pegs extend very high into the
epithelium and epithelium over these pegs is often very develops multinodular appearance with small red spot
thin. Capillaries in these superficial pegs are frequently in centre of each nodule representing dilated or partially
quite dilated. Further absence of any significant amount occluded orifice of accessory palatal salivary gland duct
of surface orthokeratin or parakeratin also contributes to around which inflammatory cell infiltration is present.
the red hue of the lesion • Pseudoepitheliomatous hyperplasia is seen in:
•
• Unlike leukoplakia, erythroplakia has no apparent sex – Granular cell myoblastoma
•
–
predilection – Blastomycosis
–
• Etiology of erythroplakia is unknown although it – Papillary hyperplasia
–
•
seems like that smoking and alcohol abuse is important – DLE
–
predisposing factors
• Malignant potential of erythroplakia is 17 fold higher
Malignant Conditions
•
than leukoplakia
Verrucous carcinoma
Actinic (Solar) Cheilitis
• A well-differentiated and slow-growing form of carcinoma
 
•
• Cause: ultraviolet light, especially UVB, 2900 to 3200 that infrequently metastasizes.
•
nm. • Tobacco and human papillomavirus (subtypes 16 and 18)
• The lower lip shows epithelial atrophy and focal
•
 
may have etiologic roles.
•
keratosis. The upper lip is minimally affected because it
is more protected from UV light. • Exhibits a broad-based verruciform architecture.
•
• The junction of vermilion and skin becomes indistinct. • Treated by surgical excision; good prognosis.
•

(NEET 2013)
•
• May progress to squamous cell carcinoma.

•
Squamous Cell Carcinoma
Oral Submucous Fibrosis
• The most common carcinoma of oral cavity. Over all
• Irreversible mucosal change thought to be due to
•
lower lip is the most affected site (38%)(MAHE 2011)
•
hypersensitivity to dietary substances, especially betel
nut. • Intraorally posterior lateral border of the tongue
•
• Mucosa becomes opaque due to submucosal scarring. (22%) is the most affected followed by floor of the
mouth (17%) worldwide.
•
• May progress to squamous cell carcinoma.
•
422
• In India the most common oral cancer is that of buccal mucosa i.e., alveolo buccal complex (38%) compared to
•
tongue (16%) may be due to abnormal tobacco habits.
• Major genes involved in head and neck squamous cell carcinoma (hnscc) include protooncogenes and tumor
•
suppressor genes (tsgs).
• Proto-oncogenes associated with hnscc include ras (rat sarcoma), cyclin-d1, myc, erb-b erythroblastosis), bcl-1,bcl-2
•
(b-cell lymphoma), int-2, ck8, and ck19,tsgs negatively regulate cell growth and differentiation.
• Both copies of a tsg must be inactivated or lost (loss of heterozygosity [loh] for loss of function (the “two-hit” hypothesis).
•
• Etiology
•
– Caused by mutation, amplification, or inactivation of oncogenes and tumor suppressor genes.
–
– Accumulation of genetic alterations results in loss of cell cycle control, abnormal signaling, increased cell survival,
–
and cell motility.
– Causes of the genetic alterations include tobacco, human papillomavirus (subtypes 16 and 18), and heredity.
–
– Increased risk of oral cancer in patients with Plummer–Vinson syndrome (mucosal atrophy, dysphagia, iron deficiency
–
syndrome). (AIPG 2006, AIPG 2008)

• Clinical features
•
 
– May present as chronic, nonhealing ulcer, Red/white patch, or mass.
–
– Most commonly seen in posterior-lateral tongue and floor of mouth.
–
 
– Clinical stage is more important than microscopic classification relative to patient prognosis.
–
• Treatment with excision and/or radiation; prognosis dependent mostly on stage
•
– Overall 5-year survival rate is 45% to 50%; with neck metastasis, 25%.
–
Basal Cell Carcinoma
– Also known as rodent ulcer (AIPG 2008)
–

– Common low-grade skin cancer that rarely metastasizes. (AIIMS May 2009)
–

– Usually in sun-damaged skin; very rare in mucosa. (AIPG 2001)
–

– Usually presents as nonhealing, indurated chronic ulcer.
–
 
– Treated with surgery; very good to excellent prognosis.
–
Oral Melanoma
– Malignancy of melanocytes.
–
– High-risk sites are palate and gingiva.
–
– Some lesions have prolonged in situ preceding vertical (invasive) growth.
–
– Common site of melanoma on orofacial skin – malar area
–
– Occurs almost always in adults; rarely seen in children.
–
 
– 5-year survival is < 20% for oral mucosal lesions (> 65% for skin lesions).
–
 
DERMAL NEVI
Congenital Nevus Acquired Nevus

• Small nevi -3.5 • Intradermal nevi: Common mole. Nevus cells are totally in dermis
•
•
cm or more • Junctional nevi: Clinically appears as intradermal nevi. Histologically the differentiation is important because it
•
• Garment nevi is prone for malignancy. Nevus cells are limited to basal layer of epithelium
•
– 10 cm more • Compound: Mixture of both of the above in dermis as well as epidermis
•
• Spindle cell (or) epitheloid cell: Commonly in children, clinically benign, histologically exhibits malignant
•
features.
• Blue nevus: A true mesodermal structure which rarely undergoes malignant transformation. It is 2nd most
•
common intra oral nevus.
The most common type of intraoral nevi is intramucosal nevus (>50%) followed by blue nevus

Connective Tissue Tumors—Benign
These tumors present as masses (lumps or bumps) within the submucosa. Overlying epithelium is generally intact, unless
ulceration occurs because of trauma to the lesion. These tumors generally fall into one of two groups: reactive or neoplastic.
Reactive

Fibrous lesions
Peripheral fibroma • Fibrous hyperplasia of the gingiva
•
• Most common benign tumor of oral cavity (AIPG 2005)
•

• Clinical features
•
– Elevated lesion of normal colour and smooth surface
–
– Sessile or occasionally pedunculated
–
– Most common in 3rd–5th decade
–
– Most frequent location–gingiva, buccal mucosa, tongue, lips and palate
–
– Surface may become inflamed due to repeated trauma
–
– Caused by trauma or chronic irritation.
–
• Treatment – conservative surgical excision
•
Generalized gingival • Fibrous hyperplasia caused by local factors and modified by systemic conditions
•
 
hyperplasia • Dilantin for seizures may contribute to gingival hyperplasia
•
Focal fibrous hyperplasia • Fibrous hyperplasia of oral mucosa.
•
• Caused by chronic trauma or chronic irritation.
•
• Also known as traumatic fibroma, irritation fibroma, and hyperplastic scar.
•
 
Denture-induced fibrous • Fibrous hyperplasia associated with ill-fitting dentures.
•
 
hyperplasia • Usually seen in anterior labial vestibules.
•
• Papillary hyperplasia (palatal papillomatosis) of the palate is another type of fibrous hyperplasia associated
•
with ill-fitting dentures. (AIPG 2004)

• No malignant potential to any of the fibrous hyperplasias.
•
Peripheral Giant cell • Also known as giant cell epulis, osteoclastoma, giant cell reparative granuloma
•
Granuloma • Clinical features:
•
– Always occur on gingiva or alveolar mucosa usually anterior to molars
–
– Sessile or pedunculated
–
– Dark red, vascular and has surface ulcerations
–
– More common in mandible (55%)
–
– More common in females
–
– Mean age – 30 years
–
• Histological features
•
– Stroma made of large no of capillaries and numerous giant cells (AIPG 2006)
–

– Non encapsulated
–
– Foci of hemorrhage and hemosiderin pigment seen
–
– Newly formed osteoid may be present
–
• Radiological features
•
– Edentulous areas show peripheral cuffing of bone
–
Central giant cell • Seen in all age groups
•
granuloma (AIIMS Nov 11) • More common in females
•
• Either jaw may be involved, though mandible is more common
•
• More common in anteriors. Doesn’t cross midline
•
• Characterized by large lesions that expand the cortical plate and can resorb roots and move teeth
•
• Composed of multi nucleated giant cells
•
• Ragiographically appear as multilocular radiolucencies of bone
•
Neural: traumatic • Entangled submucosal mass of neural tissue and scar
•
 
neuroma • Caused by injury to nerve.
•
• Most commonly seen at mental foramen in oral cavity.
•
• Oral mucous neuromas are seen in Schmidt syndrome
•
424
Fibrous lesions
Vascular: pyogenic • Hyperplasia of capillaries and fibroblasts.
•
granuloma • Caused by trauma or chronic irritation.
•
• Common in gingiva but can be seen anywhere there is mucosal (or skin) trauma.
•
 
Neoplastic–Benign
Fibrous
Nodular fasciitis • Rare submucosal proliferation of fibroblasts.
•
• A reactive lesion that exhibits rapid growth.
•
• Treated with surgical excision, rare recurrence
•
Fibromatosis • Although benign, this troublesome fibroblastic neoplasm is locally aggressive and infiltrative.
•
• Difficult to eradicate and often recurs.
•
• Behavior similar to low-grade fibrosarcoma.
•
Neural
Granular cell tumor • Benign, nonrecurring submucosal neoplasm of Schwann cells.

•
 
• Tumor cells have granular or grainy cytoplasm.
•
• Overlying epithelium may exhibit pseudoepitheliomatous hyperplasia (microscopically mimics
•
 
carcinoma).
• Most commonly seen in tongue.
•
• Infant counterpart is known as congenital granular cell tumor (congenital epulis).
•
 
– Occurs on gingiva only as pedunculated mass.
–
– No pseudoepitheliomatous hyperplasia.
–
– Surgical excision, no recurrence.
–
Schwannoma (neurilemmoma) • Also known as neurilemoma, perineural fibroblastoma, schwannoma, neurinoma, lemmoma.
 
•
• Benign neoplasm of Schwann cells.
•
• Any site; tongue favored.
•
• Solitary; not syndrome-related.
•
• The hallmark of neurilemoma is the pattern of alternating Antoni A and B areas, with varying relative
•
amounts.
• Antoni type A-characteristic palisading pattern of cells. It is hyper cellular area.
•
• Antoni type B-tissue does not exhibit characteristic palisading, but rather a disorderly arrangement of
•
cells and fibers. These are areas of hypocellularity.
• Verrucay bodies, small hyaline structures, are also characteristically present in this tumour
•

(MP 2006)

Neurofibroma/ • Benign neoplasm of Schwann cells and perineural fibroblasts.
•
Neurofibromatosis/Von • Any site, especially tongue and buccal mucosa.
Recklinghausen’s Disease
•
 
• Solitary to multiple.

(BHU 2008)
•
• Etiology: Most widely accepted view according to Holt, based on electron microscopy is that it arises
•
from Schwann cell, fibroblast and occasional Perineural cell
• Clinical features: exceedingly uncommon hereditary transmission as autosomal dominant trait
•
occurrence is 1 in 3000 births
• First variety include numerous sessile pedunculated elevated smooth surfaced nodules of variable
•
size are scattered over the skin surface chiefly the trunk, face and extremities.
• In the second form there are deeper, more diffuse lesions which are of greater proportions than the
•
superficial nature and are some time referred to as “Elephantiasis Neuromatosa” in addition the
majority of patient exhibit asymmetric area of cutaneous melanin pigmentation, often described as
Café Au Lait spots (AIPG 2005)

• Syndrome of neurofibromatosis I
•
– Multiple neurofibromas.
–
– Six or more café-au-lait macules (each > 1.5 cm diameter).
–
 
– Axillary freckling (Crowe’s sign), and iris freckling (Lisch spots).
–
 
– Malignant transformation of neurofibromas in 5% to 15% of patients.
–

Fibrous
• The greater clinical significance of neurofibromatosis aside from the cosmetic problem lies in the fact
•
that in some patient malignant transformation subsequently occurs in one or more of their lesion (15%
incidence). The type of sarcoma has been variously described as fibrosarcoma, Spindle cell sarcoma
and neurogenic sarcoma. Multiple fibromas gave much greater incidence of malignant transformation

than solitary neurofibroma.
• Von Recklinghausen • Von Recklinghausen disease(osteitis fibrosa cystica) of bone is hyperparathyroidism. (AIPG 2010)
•
•

disease of skin is • Café au lait spot–present in Neurofibromatosis, polystotic type of fibrous dysplasia
neurofibroma
•
Muscle

• Leiomyoma • Relatively rare, benign neoplasm of smooth muscle origin.
•
•
• Rhabdomyoma • Very rare, benign neoplasm of skeletal muscle origin.
•
•
Fat

• lipoma • Uncommon benign neoplasm of fat cell origin.
•
 
•
• Buccal mucosa is characteristic site.
•
• This group of rare tumors arises from malignant conversion of connective tissue cells within the
•
submucosa. They present as masses or ulcerated masses
Neoplastic Lesions–Malignant
Fibrous
– Fibrosarcoma Rare sarcoma showing microscopic evidence of fibroblast differentiation.
–
• Neural • Malignant peripheral nerve sheath tumor (neurosarcoma)
•
•
• Rare sarcoma showing microscopic evidence of neural differentiation.
•
 
• May arise from pre-existing neurofibroma or de novo (no pre-existing lesion).
•
 
• Vascular
•
– Kaposi’s sarcoma • Malignant proliferation of endothelial cells.
–
•
• Human herpes virus 8 has etiologic role.
•
• Most commonly seen as a complication of AIDS; incidence markedly reduced by new antiretroviral
•
 
therapies.
• May also be seen as endemic African type or classic Mediterranean type.
•
• A multicentric neoplastic proliferation of endothelial cells.
•
• Kaposis sarcoma (KS) usually occurs when CD4 lymphocyte counts are (COMEDK 2009)
•

• Muscle
•
– Leiomyosarcoma • Rare sarcoma showing microscopic evidence of smooth muscle differentiation.
–
 
•
 
– Rhabdom y os ar- • Rare sarcoma showing microscopic evidence of skeletal muscle differentiation. (AIPG 2009)
–
•

coma
 
• Fat
•
– Liposarcoma • Rare sarcoma showing microscopic evidence of fat cell differentiation.
–
 
•
 
Malignant Fibrous Histiocyiomas
• Are group of aggressive malignant neoplasms, arising from undifferentiated mesenchymal cells that differentiate along
•
both fibroblastic and histiocyte pathways.
• Histologically the neoplasm reveals actively proliferating, numerous polyhedral or oval shaped, malignant histiocytes and
•
many spindle-shaped malignant fibrous cells.
426
• These malignant cells are often arranged in a typical “cart-wheel” or “storiform” pattern.
•
• Benign tumour of smooth muscle • Leiomyoma, Angiomyoma
•
•
• Malignant tumour of smooth muscle • Leiomyosarcoma
•
•
• Benign tumour of striated (voluntary) muscle • Rhabdomyoma

•
•
• Malignant tumour of striated muscle • Rhabdomyosarcoma
•
•
• Benign tumour of nerve tissue • Traumatic neuroma, neurofibroma, neurilemmoma
•
•
• Malignant tumour of nerve tissue • Malignant schwannoma, Olfactory neuroblastoma
•
•
You Should Know
• Most common bone tumours:
•
– Osteochondroma is the most common benign bone tumor (AIPG 2002)
–

– Osteosarcoma is the 2nd most common malignant bone tumour
–
– Osteosarcoma is the 1st most common malignant bone tumour in children (AIPG 2001)
–

• About 88% of the lip cancers occur on lower lip.
•
• Most lip carcinoma are well differentiated–Grade I carcinomatous lesions. So metastasis late–good prognosis
•
• The sarcoma differ from carcinoma by their typical occurrence in young person and their tendency to metastasize through
•
blood stream rather lymphocytes.
• All carcinoma metastasize by lymph nodes except renal cell carcinoma (occurs by hematogenous route).
•
• Sarcoma that spreads through lymphatics- Rhabdomyosarcoma
•
• HPV type 6, 11 are commonly associated with squamous papillomas. Multiple papillomatous lesions are seen in Cowden’s
•
syndrome. Cutaneous marker of breast cancer
• Hemangiopericytoma resembles Glomus tumour. Staghorn pattern is an important histological feature of
•
hemangiopericytoma
• Metastasis from carcinoma of oral cavity chiefly involve the submaxillary and cervical lymph nodes followed by pre-
•
auricular and post – auricular lymph nodes.
• Storiform pattern of fibrous tissue is seen in malignant fibrous histiocytoma
•
• Presence of epithelial pearls in spinous layer of epithelium is characteristic of carcinoma.
•
TREATMENT MODALITY INDICATION

Surgery • For T1 and T2 lesions
•
• For tumors involving bone
•
• For tumors that lack sensitivity to radiation
•
• For tumors showing recurrence after maximum dose of radiotherapy
•
• In case of clinically positive cervical lymphnode involvement
•
Radiation • For T1 and T2 lesion
•
• Exophytic and well oxygenated tumors
•
• Tumors with small cervical metastasis
•
Brachy Therapy • Primary treatment modality for localized tumors in anterior 2/3rds of oral cavity, for boosted doses of radiation
•
(Interstitial And Intra to a specific site and for treatment following recurrence.
Cavitary Implants)
External Beam Therapy • Indicated for primary tumors of posterior third of tongue, oropharynx and tonsillar pillar, are best treated by
•
(Tele Therapy) external beam therapy.
• External beam therapy with wedged – pair field allows a therapeutic dose to unilateral dose while sparing a high
•
dose to opposite dose.
• External beam therapy with a parallel opposed –field set or three- field set –up is used for the tumors present
•
in midline.

TREATMENT MODALITY INDICATION

Chemotherapy • Used as adjunct to other treatment modalities to promote initial tumor reduction and to provide early treatment
•
of micrometastasis.
Combined Radiation • Larger T2, T3 and T4 lesions.

•
and Surgery
Commando Operation • Is done when carcinoma is fixed to mandible with infiltration of floor of the mouth.
•
• It consists of hemimandibulectomy and removal of the floor of the radical neck dissection.
•
Lymphoid Neoplasms
• Lymphoid neoplasms are all malignant.
•
• Hodgkin’s lymphoma, characterized by Reed–Sternberg cells, is part of this group but is very rare in the oral cavity.
•
• Most lymphoid neoplasms occur in lymph nodes, although they occassionally arise in extranodal tissues, such as mucosa-
•
associated lymphoid tissue (MALT). Oral presentation is as a mass, ulcerated mass, or radiolucency. (NEET 2013)

• Lymphomas
•
Cause • Undetermined for most lymphomas Epstein-Barr virus is important causative factor inimmunodeficiency and in some
•
 
Burkitt’s lymphomas.
• Chromosome translocations are factors in some lymphomas, including Burkitt’s lymphoma.
•
Classification • Microscopic criteria used to separate the various types of lymphoma
•
• Important for predicting behavior and prescribing treatment
•
• Most are B-cell type; T-cell lymphomas very rare in the mouth
•
Staging • Determination of the clinical extent of the disease
•
• An important factor for deciding type and intensity of therapy
•
 
• Helps determine prognosis
•
Clinical fea- • Lymphoma behavior patterns range from indolent to highly aggressive. Most head and neck tumors start in lymph
•
 
tures nodes or in mucosa-associated lymphoid tissues (MALT lymphomas). Tonsils and palate are most common intra oral
 
sites.
• Bone involvement, especially in Burkitt’s lymphoma,often results in swelling, pain, tooth mobility, and lip paresthesia. AIDS-
•
 
associated lymphomas are typically high-grade B-cell tumors.
Treatment • Dependent upon lymphoma classification and stage

•
• Typically, radiation is used for localized disease, and chemotherapy for extensive disease; combination radiation-
•
chemotherapy is also used.
• Some indolent low-grade lymphomas, known to respond poorly to therapeutic regimens, are not treated
•
• Infiltration of gingival tissues by leukemic cells is common to chronic monocytic leukemia. Gingiva is red, boggy, and
•
hemorrhagic.
• Treatment with chemotherapy is quite successful for acute leukemias but is less so for chronic leukemias.
•
• Types of hodgkin’s disease
•
Nodular sclero- • Broad bands divide into node into nodules.
•
sis: 60 – 80% • Cell – lacunar type Reed- Sternberg (RS)cell which has multilobulated/ monolobated nucleus
•
• Involves mediastinum + supra diaphragmatic sites
•
Mixed Cellular- • RS cells are of classic type – large with bilobate, double or multiple nuclei and large eosinophilic inclusion like
•
ity: 15- 30% nucleolus
• Involves abdominal lymph nodes and spleen
•
Lymphocyte • Associated with old age and HIV positive patients
•
depleted - < 1% • Large number of RS cells and bizarre sarcomatous variants are present
•
of cases
lymphocyte • RS cells are classic or lacunar with lymphocytic infiltration
•
rich: 5%
428
Nodular • RS cells appear infrequently instead popcorn cells :a variety of lymphocytic and histiocytic cells are seen.
•
lymphocyte
predominant:
5%
• Non-Hodgkin’s lymphoma
•
– Malignancy of one of the cells making up lymphoid tissue.
–
– Microscopic classification of the various types of lymphomas currently follows the Revised European American Lymphoma
–
 
(REAL) scheme.
– Multiple myeloma/plasma cell myeloma
–
– Represents a monoclonal neoplastic expansion of immunoglobulin-secreting B cells (plasma cells) in what could be
–
termed a monoclonal gammopathy.
– Clinical features
–
Multiple “punched-out” bone lucencies (solitary plasmacytoma invariably becomes multiple myeloma) in

 
 
patients >50 years. (AIPG 2008)

Abnormal immunoglobulin protein peak (M protein) on serum electrophoresis.

Urinary monoclonal light chains (Bence–Jones protein). (AIPG 2012,2008,2002)

 

Pain, swelling, and numbness.

Anemia, bleeding, infection, fracture associated with extensive marrow involvement.

 
Treated with chemotherapy; poor prognosis.

– A form of amyloidosis occurs in 10% of multiple myeloma patients.
–
Amyloid protein is deposited in various organs and can lead to organ dysfunction (especially kidney, heart, GI

 
 
tract, liver, and spleen).
Single organ or localized amyloidosis (may be seen in the tongue).

ODONTOGENIC CYSTS AND TUMOURS
Cysts
Classification
Odontogenic Non odontogenic Cysts of tissue of mouth, face and neck
• Developmental (NEET 2013) • Nasopalatine duct (incisive canal) • Aneurysmal bone cyst
•
•
•
• Gingival cyst of infants cyst • Dermoid and epidermoid cysts
•
•
• Odontogenic keratocyst • Nasolabial (nasoalveolar) cyst • Lymphoepithelial (branchial cleft) cyst
•

(AIPG 2009)
•
•
(primordial cyst) • Thyroglossal duct cyst

• Midpalatal raphae cyst of infants
•
• Dentigerous cyst • Anterior median lingual cyst
•
•
• Median palatine, median alveolar
•
• Eruption cyst • Cystic hygroma
•
and median mandibular cyst
•
•
• Lateral periodontal cyst • Nasopharyngeal cyst
• Globulomaxillary cyst
•
•
• Gingival cyst of adults • Thymic cyst
•
•
•
• Botryoid odontogenic cyst • Cysts of the salivary glands, mucous retention cysts,
•
•
• Glandular odontogenic (sialo ranula.
•
odontogenic) cyst • Parasitic cysts, hydatid cyst, cysticercosis cellulosae,
•
• Calcifying odontogenic cyst trichinosis.
•
• Inflammatory • Non epithelial (false cyst)
•
•
• Radicular cyst, apical and lateral • Solitary bone cyst (traumatic,
•
•
• Residual cyst simple, hemorrhagic bone cyst)
•
• Paradental cyst and mandibular
•
infected cysts
• Inflammatory collateral cysts
•

Aneurysmal Bone Cyst • Common in mandibular third molar area and in second
•
and third decades of life.
– Lesion of young persons mostly occurring in long
• More common in males
–
bones and vertebral column with history of trauma.
•
– Upon entering the lesion there is excessive bleeding, • Derived from the cells of the reduced enamel.
•
–
the blood ‘ swelling up’ from the tissue. • Develops after the crown of tooth has been formed.

•
– The tissue resembles a blood soaked sponge with large • Associated with crown of impacted embedded or
•
–
pores representing the cavernous spaces of lesion. unerupted tooth. (Kar 09 MAHE09)

(AIIMS 1993, KAR 2003) • Localized areas of “bud-like” proliferations of cystic

•
– FNAC only reveals RBCs, hence inconclusive. epithelial cells may be seen in few areas, which are
–

(AIPG 2006) known as “mural proliferations” and they indicate the

development of “ameloblastomas” from the lining of the
Odontogenic Keratocyst dentigerous cyst.
– Arises from the remnants of the dental lamina, • 17% of ameloblastomas arise within a dentigerous cyst,
–
•
– Higher tendency for recurrence. (AIPG 2008) and squamous cell carcinoma might also be seen.
–

– Develops due to the cystic degeneration of the cells • The normal follicular space is 3 -4 mm and dentigerous
–
•
of the stellate reticulum of developing tooth germ cyst can be suspected if this space is >5mm. Histologically
(before its calcification starts) the rete peg formation is absence except in cases of
– Have a more aggressive course than any other cystic secondary infection.
–
lesion of jaw and for this reason these are sometimes • The dentigerous cyst is potentially capable of becoming
•
known as “benign cystic neoplasms’:. an aggressive lesion. Cystic involvement of an unerupted
– Males> females, 2nd and 3rd decade of life, angle of mandibular third molar may result in a hollowing out of
–
mandible – 75% cases the entire ramus extending upto coronoid process and
– Bony expansion is minimum in odontogenic condyle as well as in expansion of the cortical plate due to
(NEET 2013)
–
keratocyst because in most of the cases the cyst pressure exerted by the lesion.

spreads via the medullary spaces of bones and the
remarkable bony swelling is usually absent. Nasoalveolar Cyst, Nasolabial Cyst
– Currently known as Keratocystic odontogenic
• Fissural cyst arising outside the bones at the junction of
–
tumor. (Kar 2010)
•
the globular portion of the medial nasal process, lateral

– Cholesterol crystals and hyaline bodies are found
nasal process, and maxillary process.
–
in histological analysis of OKC (AIPG 2001)
• Originally thought to arise from epithelial rests at

– Multiple odontogenic keratocysts are associated
•
embryologic junction of globular, lateral nasal, and
–
with Gorlin Goltz syndrome
maxillary processes.
Radiological Types of Keratocysts • Development from caudal end of nasolacrimal rod or
•
Replacement • When a keratocyst develops in place of duct currently favored.
•
type a developing normal tooth it is called the • Occurs near base of nostril, outside alveolar process of
replacement type. In such cases there
•
maxilla.
will be absence of a normal tooth in the
dental arch.
Envelopmental • When a cyst entirely encloses an Stafne (Static) Bone Defect

•
type impacted tooth within the bone, it is
called the extraneous type of keratocyst.
• Is due to developmental inclusions of salivary glandular
•
tissue on the lingual surface of mandible below the
Extraneous • Keratocyst develops away from the tooth
mandibular canal Diagnostic lucency of the mandible due
•
type bearing areas of the jaws
to invagination of the lingual surface of the jaw.
Collateral type • Cyst develops between the roots of a • Located in the posterior mandible below the mandibular
•
canal.
•
tooth
Traumatic Cyst
Dentigerous Cyst
• Radiolucent dead space (no epithelial lining) in the
•
 
• Odontogenic cystic lesion, which encloses the crown of an mandible of teenagers.
 
•
impacted tooth at its neck portion. • Some (not all) associated with jaw trauma.
•
430
Focal Osteoporotic Bone Marrow Defect

• Lucency in the jaw that contains hematopoietic bone marrow; often in an extraction site.
•
 
Radiological feature of Cyst

• Median anterior maxillary cyst (Nasopalatine/ • Developmental or fissural • Ovoid or heart shaped radiolucency between or
•
•
•
incisive canal cyst) (AIPG 2001) cyst above the roots of maxillary central incisors

(MAHE 2010)

• Median alveolar cyst • Odontogenic cyst • Is a rare cyst arising anterior to incisive canal
•
•
•
in the alveoli. It is a primordial cyst developing
from the supernumerary mesiodens and hence
odontogenic in origin
• Globulomaxillary cyst: (AIPG 2008) • Developmental or fissural • Inverted pear shaped radiolucent area between
•

•
•
cyst- questionable lateral incisor and cupsid

odontogenic cyst (AIPG 2014, 2007, 2012, AIIMS May 2010)
• Median mandibular cyst • Multilocular or unilocular well circumscribed
•
•
lesion in midline of mandible
• Nasolabial or naso alveolar cyst or klestadt’s • A soft tissue cyst arises from • No radiologic feature
•
•
•
cyst the junction of medial nasal,
lateral nasal and maxillary
Most Common Areas of Occurrence

Dentigerous cyst Mandibular third molar area
• Odontogenic keratocyst • Mandibular molar, angle and ramus area
•
•
• Calcifying Odontogenic cyst • Mandibular anterior region
•
•
• Lateral periodontal cyst (AIPG 2006) • Mandibular premolar area
•

•
• Globulomaxillary cyst • Maxillary lateral incisor and canine (AIPG 2007, 2012,
•
•

AIIMS May 2010)

• Globular Odontogenic cyst • Mandibular premolar area
•
•
Tumours
Classification of Odontogenic Neoplasms (Tumors)
Benign Odontogenic Neoplasms Malignant Tumors

• Neoplasms of epithelial tissue origin • Odontogenic carcinomas
•
•
– Ameloblastoma – Malignant ameloblastoma
–
–
– Squamous odontogenic tumor – Primary intra-alveolar carcinoma
–
–
– Calcifying epithelial odontogenic tumor – Malignant variants of other epithelial tissue neoplasm
–
–
– Clear cell odontogenic tumor – Malignant changes in odontogenic cysts
–
–
• Neoplasms of mixed tissue origin (Made up of both • Odontogenic sarcoma
•
•
epithelium and mesenchymal tissues) – Ameloblastic fibrosarcoma
–
– Adenomatoid odontogenic tumor (AOT) – Ameloblastic carcinosarcoma
–
–
– Ameloblastic fibroma – Ameloblastic fibrodentinosarcoma
–
–
– Ameloblastic fibro-odontoma / fibrodentinoma
–
– Odonto-ameloblastoma
–
– Complex odontoma
–
– Compound odontoma
–
– Calcifying epithelial odontogenic cyst
–
• Neoplasms of the mesenchymal tissue origin
•
– Odontogenic fibroma
–
– Odontogenic myxoma
–
– Cementoma
–
– Familial gigantiform cementoma
–
– Cementifying fibroma
–
– Benign cementoblastoma
–

Tumour Common site
• Composite compound odontoma • Anterior maxilla
•
•
• Adenomatoid odontogenic tumour
•
• Squamous odontogenic tumour
•
• Enameloma • Bifurcation and trifurcations of maxillary posterior teeth
•
•
• Composite complex odontoma • Posterior maxilla
•
•
• Ameloblastoma • Posterior mandible
•
•
• Pindborg’s tumour
•
• Metastatic carcinoma
•
• Cementoma • Mandibular incisor
•
•
• Benign cementoblastoma • Mandibular first perm. Molar
•
•
Periapical Cemental Dysplasia (Cementoma) • Radioresistant – treated by surgery
•

(AIIMS Nov 2010) • In some instances, the ameloblastic epithelium may be
•
proliferative with extension of ameloblastic epithelium
– Occurs in and around the apex of a tooth, usually
into the lumen of cystic cavity. This feature is known as
–
mandibular incisor
intraluminal proliferation
– Also known as periapical osteofibrosis, periapical
• Types:
–
cemento-osseous dysplasia, cementoma and
•
cementoblastoma • Follicular Simple and most common
•
– More common in black women over the age of 40 • Plexiform Contains ameloblast like tumour cells
–
years. (AIPG 2010)
•
arranged in irregular masses

– 3 stages: • Acanthomatous Stellate reticulum undergoes squamous
–
Initial: Radiolucent
•
metaplasia with keratin formation in central

2nd: Mixed radio-opaque and radiolucent portion of tumour islands

3rd: Completely radio opaque • Granular cell Cytoplasm of stellate reticulum cells show
•

– Tooth is vital. a very coarse granuloma eosinophilic
appearance
–
Benign Cementoblastoma: (AIPG 2002, AIIMS – Most aggressive (AIPG 2008)
–

Nov 2010) • Basal cell type Resembles basal cell carcinoma
•
– Rarest
– True cementoma because it is a true neoplasm of the
–
• Desmoplastic Found in dense collagen stroma. May
–
functional cementoblastoma
•
type appear hyalinized and hypocellular
– Common site: mandibular first permanent molar
–
– Tooth is vital Odontogenic Myxomas
–
Giagantiform Cementoma • Aggressive, intraosseous neoplasms derived from
•
– Also known as familial multiple cementoma, which embryonic odontogenic mesenchyme probably arise
from the dental papilla or follicular mesenchyme.
–
usually presents as diffuse radio opaque masses
scattered throughout the jaws. • Nearly all lesions are found in the tooth bearing areas of
•
– Involves all the four quadrants maxillary and mandibular bone.
–
Botryoid Odontogenic Cyst is a Multicystic Variant • Mandibular lesions are commonly found in the
•
premolar-molar area.
of Lateral Periodontal Cyst
• The lesions often produce multilocular radiolucency
Ameloblastoma
•
with a “soap bubble” or “honey comb” appearance in
• Term given by Churchill the bone.
•
• Defined by Robinson as usually unicentric, non • Thin and extremely delicate septa of bone are often seen
•
•
functional, intermittent in growth, anatomically benign to course through the radiolucent area and produce a
and clinically persistent. “spider-web” like or “tennis racket” like appearance
432
Ameloblastic Fibroma
• Rare benign odontogenic tumor in which both the epithelial and the mesenchymal elements are neoplastic (in ameloblastoma
•
only the epithelium is neoplastic).
• Occurs usually below the age of 20 years (average age 14 years). More often in males than females.
•
• Mandibular posterior (premolar-molar) region is the most common site, maxillary tumors are usually rare.
•
• The mesenchymal component of the tumor consists of a highly cellular, fibroblastic stroma that often resembles the dental
•
papilla of the developing tooth. When the lesion contains only dentin, it is known as ameloblastic fibrodentinoma.
Centrifugal Growth • Central cementifying
•
Pattern • Central ossifying fibroma
•
• Central cement-ossifying fibroma
•
Endo-Osteal Prolifera- • Fibrous dysplasia
•
tion • Paget’s disease
•
• Liesegang rings are found in calcifying epithelial odontogenic cyst. It is formed by amyloid like material composed of
•
conventional amyloid or immunoamyloid or APUD amyloid.
• The most distinctive microscopic feature of adenomatoid odontogenic tumour is varying number of duct like structures
•
lined by eosinophilic rim of varying thickness, which are called as hyaline ring. (AIPG 2006)

SALIVARY GLAND DISORDERS
Mucous extrava- • Recurring submucosal nodule of saliva (often bluish in color) due to escape from duct of salivary gland.
•
 
sation phenom- • Caused by traumatic severance of salivary excretory duct. (AIPG 2003)
•
 

enon • Common in lower lip (rare in upper lip) and buccal mucosa.
•
 
• Recurrence if contributing gland is not removed.
•
Mucous retention • Submucosal nodule (often bluish in color) due to blockage of salivary duct by a salivary stone (sialolith).
•
 
 
cyst • Relatively common in floor of mouth, palate, buccal mucosa, and upper lip (rare in lower lip).
•
 
• Known as ranula when occurring in floor of mouth
•
Ranula • Is a form of mucocele frequently associated with sublingual gland.
•
• Causes a swelling in the floor of mouth below the tongue. (MAHE 2011)
•

• Ranulas may be either mucous extravasation phenomena or mucous retention cysts and are most commonly
•
associated with the sublingual salivary gland duct ( MAHE 2010)

• MC cause is Trauma. Other causes include an obstructed salivary gland or a ductal aneurysm. (AIPG 2004)
•

• The lesion most commonly presents as a painless, slow growing, soft, and movable mass located in the floor of
•
the mouth, usually on one side of the lingual frenum.
Necrotizing sialo- • Chronic ulcer of the palate due to ischemic necrosis of palatal salivary glands.
•
 
metaplasia • Believed to be triggered by trauma, surgery, or local anesthesia.
•
 
• Heals in 6 to 10 weeks without treatment.
•
• Mimics carcinoma clinically and microscopically (squamous metaplasia of ducts).
•
 
Maxillary sinus • Common insignificant incidental finding in panoramic image.
•
retention cyst/ • May represent blockage of sinus salivary gland, or focal fluid accumulation of sinus mucosa.
•
pseudocyst • Lesions are asymptomatic and require no treatment.
•
Infectious sialad- • Infections of salivary glands may be acute or chronic, viral or bacterial.
•
 
enitis
Viral infections • Mumps is an acute viral infection usually of the parotid glands.
•
• Cytomegalovirus infections are chronic and may be seen in immunosuppressive states, or (rarely) in infants via
•
transplacental infection.

• Mumps
•
– Caused by polymyxovirus (RNA)
–
– Characterized by triad of pathological involvement
–
Epidemic parotitis

Orchitis–oophoritis

Pancreatitis

– Meningo-encephalitis, epididymitis and encephalitis are other complications of mumps. (AIPG 2003)
–

– When mumps involves adult males, orchitis is a great danger. Involvement of pancreas causes an increase in serum
–
lipase enzyme.
– Bilateral, rubbery or elastic salivary gland swelling, frequently elevating the ear is characteristic of mumps.
–
• Epstein Barr Virus is associated with:
•
– Nasopharyngeal carcinoma
–
– Burkitt’s lymphoma
–
– Hodgkin’s disease
–
– B cell lymphoma
–
– Oral hairy leukoplakia
–
• Coxsackie Virus
•
• Coxsackie Group A4 virus • Herpangina (AIPG 2002)
•
•

• Coxsackie virus A10 • Acute lymphonodular pharyngitis
•
•
• Coxsackie virus A16 • Hand, foot and mouth disease
•
•
Bacterial Infections
Bacterial infections usually occur when salivary flow is reduced or impeded, especially in major glands, allowing bacterial
 
overgrowth. Staphylococci and streptococci are the usual infecting agents.
Sarcoidosis
• This is predominantly a pulmonary disease, although many other organs may be affected, including salivary glands and
•
mucosa.
 
• Metabolic enlargement of major salivary glands
•
• Bilateral parotid enlargement is associated with several systemic and/or metabolic conditions. The parotids generally
•
feel soft to palpation.
• Involvement of nerve at the level of stylomastoid foramen (e.g. sarcoidosis of parotid, Melkerson Rosenthal syndrome)
•
results in facial muscle paralysis without dysguesia.
Sjogren’s Syndrome
– Chronic lymphocyte-mediated autoimmune disease affecting exocrine glands and other organ systems.
–
 
– Consists of keratoconjunctivitis sicca, xerostomia and rheumatoid arthritis.
–
– It is autoimmune in nature have sera antisalivary duct antibody.
–
– The disease is common in middle aged women. It is characterized by painless enlargement of parotid duct.
–
– The typical feature of the disease is dryness of mouth and eyes as a result of hypofunction of salivary and lacrimal
–
glands.
– They undergo malignant transformation. It is likely that benign lymphoepithelial lesion is a mild form of Sjogrens
–
syndrome.
– Thus benign lymphoepithelial lesion, Sjogrens syndrome and Mickulitz disease are related to each other.
–
– The lacrimal gland function test (sjogren’s syndrome)
–
Schemer test

BUT (break up time)

Rose Bengal

434
• Diagnosis
•
– Assessment of salivary function (usually labial salivary gland biopsy).
–
– Assessment of decrease in lacrimal function (Schirmer test).
–
– Laboratory tests for autoantibodies [rheumatoid factor (RF), antinuclear antibodies (ANA), Sjögren’s syndrome A
–
(SS-A), Sjögren’s syndrome B (SS-B)]. (AIPG 2008)

• Cause is unknown, and treatment is symptomatic.
•
• Patients are at risk for development of lymphoma.
•
• Complication of cervical caries associated with dry mouth
•
 
Primary Sjogren’s syndrome Secondary Sjogren’s syndrome
• When the disease affects only salivary and lacrimal glands • Secondary sjogren’s syndrome characteristically has xerostomia,
•
•
without other co-existing systemic autoimmune diseases, it is xerophthalmia and an associated autoimmune connective tissue
called primary Sjogren’s syndrome. disease, usually the rheumatoid arthritis, systemic sclerosis,
• Primary Sjogren’s syndrome is also referred to as “sicca primary biliary cirrhosis, periarteritis nodosa, polymyositis,
dermatomyositis or macroglobulinaemia etc
•
syndrome” in which dry mouth (xerostomia) and dry eyes
(xerophthamia or keratoconjunctivitis sicca) are the principal
features.
Benign Neoplasms of Salivary Glands

Mixed tumor (pleomor- • The term given by Wills.
phic adenoma)
•
• Most common benign tumor (major and minor glands). (AIPG 2002, 2001, 2009,2011)
•

• A mixture of more than one cell type (epithelial and connective tissue elements) in many patterns (pleo-
•
morphic).
• Arises from myoepithelial cells
•
• The majority of lesions are found in fifth and sixth decade of life.
•
• Extraorally parotid gland is the most commonly involved site. (AIPG 2006)
•

• MC for minor gland lesions - palate
•
• It is characterized by painless quiescent nodule which increases in size slowly showing intermittent growth.
•
It shows no metastasis.
• It is fixed to bone but no invasion
•
• Occasional recurrence
•
Monomorphic adeno- • Single cell type.
mas
•
• Includes basal cell adenomas, canalicular adenomas, myoepitheliomas, and oncocytic tumors (oncocytes
•
stain bright pink due to abundant mitochondrial proteins).
• Treated with surgical excision with infrequent recurrences
•
Oncocytic adenoma or • More common in women than in men.
oxyphilic adenoma or
•
• Occurs almost exclusively in elderly persons between the age of 51 and 80.
acidophilic adenoma
•
• The tumor usually measures 3 to 5 cm in diameter and appears as a discrete, encapsulated mass that is
•
sometimes nodular.
• Pain is generally absent.
•
• Histologically it has an eosinophilic cytoplasm and distinct cell membrane that tends to be arranged in
•
narrow rows or cords. The oncocytes are arranged in sheets or nests and cords.
• A variant of the oxyphilic adenoma is sometimes seen in intraoral salivary glands, particularly in the buccal
•
mucosa and upper lip – Oncocytic cystadenoma.
• In recurrent tumors, there may be marked clear cell change and these tumors may be referred to as clear-
•
cell oncocytoma.
Warthin’s tumor • Warthin’s tumor is an oncocytic tumor that also contains lymphoid
•
• Warthin’s tumour–chocolate coloured fluid
•
• It is also called as papillary cystadenoma lymphomatosum/adenolymphoma/Warthin’s tumor
•

• It is benign in nature and superficial. It is treated with partial parotidectomy by presenting the facial nerve.
•
Radial parotidectomy is done for malignant lesions.
• It is seen exclusively in parotid
•
• Higher incidence seen in smokers. EBV virus has been implicated in the etiology.
•
• Seen in men in 60-70 years age group, often bilateral in 10 percent of the cases.

•
• •
The current concept is that it arises from the parotid gland tissue entrapped in paraparotid and intraparotid
lymph nodes during development.
• It is usually superficial and arises just underneath the parotid capsule. Usually arises from the inferior pole.
•
Mickuliz’s Disease • Is also known as benign lymphoepithelial lesion.
•
• It exhibits both inflammatory and neoplastic characters. It is closely related to Sjogren’s syndrome.
•
• It is autoimmune in origin.
•
• Salivary gland and lacrimal glands are characterized by slow painless swelling of parotid and lacrimal
•
glands. It is characterized by xerostomia.
• Presence of “epimyoepithelial” islands is characteristic feature.
•
• Occasionally lesion may transform into malignant lymphoma. (MP 2006)
•

• Whereas syndrome is characterized by salivary gland enlargement, lymph node enlargement due to some
•
specific diseases like lymphoma or tuberculosis.
Malignant Tumor of Salivary Glands

Mucoepidermoid carci- • Most common salivary malignancy in both minor and major glands. (NEET 2013, AIIMS nov 2012, AIPG
•
 

noma 2001)
• Palate is the most common intraoral site.
•
• Composed of mucous and epithelial cells.
•
• Microscopic low-grade lesions rarely metastasize and have excellent prognosis.
•
 
• Microscopic high-grade lesions frequently metastasize and have fair prognosis.
•
Polymorphous low- • Second most common minor salivary gland malignancy (rare in major glands).
•
grade adenocarcinoma • Palate most common site.
•
• Polymorphous microscopic patterns.
•
• Low-grade malignancy: good prognosis following surgical excision
•
 
Adenoid cystic carci- • High-grade salivary malignancy.
•
noma • Palate most common site.
•
• Cribriform or “Swiss cheese” microscopic pattern.
•
• Spreads through perineural spaces. (AIPG 2005)
•

• Adenoid cystic carcinoma/ Cylindroma is a type of adenocarcinoma which occurs in fifth and sixth decades
•
of life. It exhibits malignant symptoms and signs like pain, fixation to underlying bone, facial nerve paralysis
if it involves parotid gland.
• Histological feature of “swiss cheese” or “honey comb” appearance is characteristic. (MAHE 2010)
•

• Majority of the tumors of palate are (Epidermoid carcinomas of the mucosa of the palate derived from the
•
minor salivary glands). (MAHE 2010)

• 5-year survival rate is 70%; 15-year survival rate is 10%.
•
 
Fluids/Secretions in Cysts
• Warthins tumor • Chocolate-coloured-fluid
•
•
• Dentigerous cyst • Clear pale, straw coloured fluid
•
•
• Odonotogenic keratocyst • Dirty, creamy white viscoid suspension
•
•
• Periodontal cysts • Clear pale yellow straw coloured fluid
•
•
• Infected cyst • Brownish fluid, seropurulent/sanguinopurulent fluid, at times paste
•
•
like or caseous consistency.
• Mucocele, ranula • Mucus
•
•
436
• Gingival cysts • Clear fluid

•
•
• Solitary bone cyst • Serous or sanguinous fluid, blood or empty cavity
•
•
• Stafne’s bone cavity • Empty cavity will filled air
•
•
• Dermoid cysts • Thick sebaceous material

•
•
• Fissural cysts • Mucoid fluid
•
•
• Vascular cyst walls • Fresh blood
•
•
• Intermedullary cavernous haemangioma • Syringe full of venous blood
•
•
• Arterial or arteriovenous malformation • Bright red blood pulsatile, pushes plunger.
•
•
Metabolic conditions associated with bilateral parotid
enlargement
– Chronic alcoholism
–
– Dietary deficiencies
–
– Obesity
–
– Sjogren’s syndrome
–
–
– Hypertension
–
– Hyperlipidemia
–
• Both benign and malignant varieties of salivary gland tumours have a strong tendency to recur due to infiltration of the
•
connective tissue capsules by neoplastic cells.The main composition of the sialolith is Ca3PO4 – 75%
• The minor salivary glands commonly affected by tumours are palatal glands
•
• Most common salivary gland tumour • Pleomorphic adenoma
•
•
• Most common parotid gland tumour • Pleomorphic adenoma
•
•
• Second most common salivary gland tumour • Warthin’s tumour (occurs almost exclusively in parotid)
•
•
• Most common malignant salivary gland tumour • Mucoepidermoid carcinoma
•
•
• Most common malignant salivary gland tumour in children • Mucoepidermoid carcinoma
•
•
• Most common salivary gland tumour in bone • Mucoepidermoid carcinoma
•
•
BACTERIAL, VIRAL AND MYCOTIC INFECTIONS
Mucosal Lesions—Physical-Chemical
Focal (frictional) hyperkera- • Common white lesion caused by chronic friction on mucosa.
•
tosis • Differentiated from idiopathic leukoplakia because cause is known.
•
Linea alba • A type of frictional hyperkeratosis that appears as a linear white line in buccal mucosa
•
Traumatic ulcer • Very common.
•
• Chronic ulcers mimic oral cancer and chronic infectious ulcers
•
Chemical burn • Usually present as ulcers.
•
• May be caused by aspirin, hydrogen peroxide, silver nitrate, phenol, etc
•
Nicotine stomatitis • White change in palate due to smoking.
•
• Red dots in the lesion are inflamed salivary duct orifices.
•
• Not considered premalignant, unless related to “reverse smoking” (lighted end in mouth)
•

Amalgam tattoo • Traumatic implantation of amalgam particles into mucosa.
•
• Most common oral pigmented lesion
•
Smoking-associated mela- • Caused by a chemical in tobacco smoke that stimulates melanin production.
•
nosis • Typically seen in the anterior gingival, and is reversible if smoking is discontinued
•
• Most common melanocytic lesion.

Melanotic macule
•
 
• May be postinflammatory, syndrome-associated [primarily Peutz Jegher’s syndrome (freckles and
•
benign intestinal polyps)], or idiopathic
Drug-induced pigmentation • Most common culprits: minocycline, chloroquine, cyclophosphamide, azidothymidine (AZT).
•
Hairy tongue • Elongation of filiform papillae, of cosmetic significance only.
•
 
• Several causes, including extended use of antibiotics, corticosteroids, hydrogen peroxide
•
Dentifrice-associated slough • Superficial chemical burn of the buccal mucosa caused by some dentifrices
•
Acrodynia (Pink disease, • Cause of the disease has been established as a mercurial toxicity reaction, either actual mercury
•
Swift’s disease) (AIIMS Nov poisoning or more likely, an idiosyncrasy to the metal.
2010) • The source of the mercury is usually a teething powder, ammoniated mercury ointment, calomel
•
lotion, or bichloride of mercury disinfectant.
• Occurs most frequently in young infants before the age of two years. Although children are
•
occasionally affected upto the age of five or six years.
• The skin, particularly of the hands, feet, nose, ears and cheeks becomes red or pink and has a cold
•
“clammy feeling”.
• The appearance has been described as resembling raw beef.
•
• The skin over the affected areas peels frequently.
•
• Severe sweating is an almost constant feature of acrodynia.
•
• Other features are a state of extreme irritability, photophobia with lacrimation, muscular weakness,
•
tachycardia, hypertension, insomnia, gastrointestinal upset and stomatitis.
• The children will frequently tear their hair out in patches”
•
Mucosal Lesions—Viral Infections
Herpes simplex • Relatively high frequency of occurrence of infections.
•
virus (HSV) • Primary disease predominantly in children. (AIPG 2001)
•

infections • Severe in immunocompromised patients.
•
• Secondary disease is reactivation of latent virus in the trigeminal ganglion.
•
 
• Reactivation is triggered by sunlight, stress, immunosuppression.
•
 
• Lesion on finger is called herpes whitlow.
•
• Intranuclear viral inclusions in epithelial cells are diagnostic when taken in clinical context.
•
Varicella (chick- • This is a self-limiting childhood disease caused by varicella-zoster virus (VZV).
•
 
enpox) • Oral lesions are uncommon
•
Herpes zoster • This disease represents reactivation of latent VZV. (KCET 2011)
•
 

• They are commonly found on the palate and other immovable mucosa.
•
• IN ITS PRIMARY FORM V–Z VIRUS CAUSES CHICKEN POX OR VARICELLA.
•

(AP 2011, COMED 2010, UPSC 01 )

• The virus remains latent in sacral ganglia and results in Herpes zoster as a secondary infection at later stage.
•

(Kar 1998, MAHE 2010)

• Inflammation of the dorsal root ganglion and vesicular eruption of the skin and mucous membrane in area supplied
•
by a sensory nerve. (AIPG 91, MAHE 2010, AIIMS 2010)

• Tzanck cells and intranuclear inclusion bodies are also present.
•
• The characteristic feature of Herpeszoster is that the vesicular eruption are unilateral(COMEDK 2009, AIPG 2007)
•

Coxsackie • Both these diseases are self-limiting childhood systemic infections, usually endemic.
•
 
infections • Sites of lesions in hand, foot, and mouth disease: hands, feet, and mouth.
•
 
(hand, foot, and • Sites of lesions in herpangina: posterior oral cavity. (AIPG 2008)
mouth disease,
•
 

herpangina)
438
Measles • This is another self-limiting childhood systemic infection caused by measles virus.
•
(rubeola) • Fever, malaise, skin rash.
•
•
•
Punctate buccal mucosa ulcers (Koplick’s spots) precede skin rash.
• Caused by paramyxovirus, an RNA virus. (Kar 2008)
•

• Portal of entry through direct contact or droplet infection or through respiratory tract.
•
• Upon entry it reaches reticuloendotelium system and there by involves skin, respiratory tract and other systems
•
along with suppression of immunity which mostly involves monocytes.
• Incubation period 8-10 days.
•
• Intraoral lesions termed as koplik spots and seen in 97% cases which disappear once the onset of rash seen. They
•
are small flecks with bright red margin with a central bluish core. (KCET 2011, AIPG 2001)

• Histopathologically Warthin-Finkeldey giant cells are seen.
•
Human papillomavirus (HPV) infections
Papillomas • Benign epithelial proliferations (pedunculated or sessile) of little significance.

•
• Term includes verruca vulgaris (wart). Warts much more prevalent in HIV+ patients.
•
 
• Most, if not all, caused by HPV.
•
Condyloma • Caused by HPV subtypes 6 and 11.
•
 
acuminatum • Oral lesions acquired by oral–genital contact.
•
(genital warts) • Broad-based verruciform lesion.
•
Focal epithe- • Most common in ethnic groups—Native Americans, Inuits, and Central Americans.
•
 
lial hyperpla- • Multiple, small, dome-shaped warts on oral mucosa.
•
 
sia (Heck’s • Caused by HPV 13 and 32.
disease)
•
Epstein–Barr (EBV) infections
Hairy leukopla- • An opportunistic infection resulting in white patch (es) of the lateral tongue.
•
kia • Almost all associated with HIV (may be a pre-AIDS sign).
•
• Infrequently seen in patients with other immunosuppressed states. Very rare in normal patients.
•
• Diagnosis is made from biopsy showing intranuclear viral inclusions.
•
• Occurrence decreasing with use of new AIDS drugs.
•
• Associated malignancies (Burkitt’s lymphoma, nasopharyngeal carcinoma). There is good evidence that EBV has an
•
etiological role in these two malignancies.
Infectious • Caused by Epstein –Barr virus. (AIPG 2004, 2007, AIIMS Nov 2010, May 2010)
•

Mononucleosis • Transmitted through deep kissing or oral exchange of saliva (for this reason, it is called as “kissing disease”
Or Glandular
•
• It is characterized by sore throat, headache lymphadenopathy, splenomegaly and hepatitis.
Fever Or Kiss-
•
ings Disease • Oral manifestation include stomatitis gingivitis and palatal petechiae.
•
(Kcet 2011) • There is increase in heterophil antibody titre. (AIPG 2003)
•

• The normal titre of agglutinins and hemolysins in human blood against sheep red blood cells does not exceed 1:8.
•
In this disease the titre raises to 1:4096, this is called positive Paul Bunnel test characteristic of this disease.

(KAR 2010)

Virus Malignancy
HSV: III or Genital herpes CA of uterine cervix
HSV: IV or Epstein Barr virus African jaw/ Burkitt’s lymphoma, nasopharyngeal CA
HSV: VII Kaposi sarcoma
Papovaviridae (Human Papilloma virus) Cervical, vulvar, penile cancers, squamous cell carcinoma
Hepadna viridae (Hepatitis B virus) Hepatocellular CA
Retroviridae (HTLV) Adult T cell leukemia

Bacterial Infections
Syphilis
– Caused by contact with patient infected with Treponema pallidum.
–
– Primary lesion (chancre), secondary lesions (oral mucous patches, condyloma latum, maculopapular rash), tertiary

–
lesions [gummas, central nervous system (CNS)/cardiovascular involvement].
– In congenital syphilis:
–
In utero infection with multiple stigmata, including Hutchinson’s triad (notched incisors, deafness, ocular

keratitis). (AIPG 2010)

Screw driver shaped incisors and mulberry/Moon’s/Fournier’s molars (irregular molars and occlusal third of

tooth is arranged in an agglomerate mass of globules) are seen. (AIPG 2004, NEET 2013)

Saddle shape nose

Underdeveloped premaxilla

ACQUIRED SYPHILIS
Primary stage Chancre at site of inoculation i.e., commonly Oral chancre is usually painless but may become painful because
occurs on penis and on the vulva of secondary infection. (AP 2010, MAHE 2010)

Secondary stage “Mucous patches” on tongue, gingival and are Painless. The serological reaction is always positive. The mucous
(develops 6 wks highly infectious. (AIPG 2003) patches on the palate and tonsil are described as “ snail – track”

after primary lesion) Split papules, condyloma latum are other ulcers. Circinate (coin –like) lesions are also characterstic

(KAR 1998, features. (MAN 2000).

AP 2002)

Tertiary stage (CNS Gumma commonly involves tongue, palate More common than primary or secondary. Causes perforation of

+ CVS are involved) (AIIMS 2004, KAR 2000, HP 2000) palate.
• Ollendor’s sign: This sign is observed in secondary syphilis. In secondary syphilis the papule is exquisitely tender to
•
the touch of a blunt probe, which is termed positive Ollendor’s sign.
• Snail track ulcers–secondary syphilis and pyostomatitis vegetans
•
• The atrophic or intestinal glossitis characteristic of syphilis–Leutic glossitis More incidence of carcinomatous
•
transformation
Tuberculosis
– Caused by inhalation of Mycobacterium tuberculosis.
–
– Oral nonhealing chronic ulcers follow lung infection.
–
 
– Incidence increasing due to overcrowding, debilitation, and AIDS.
–
– Caseating granulomas with multinucleated giant cells (Langerhans giant cells).
–
– Multidrug therapy is used to treat it (e.g., isoniazid, rifampin, ethambutol).
–
Gonorrhea
– Sexually transmitted disease caused by Neisseria gonorrhoeae.
–
 
– Oral manifestation is oral pharyngitis but is rarely seen.
–
 
Tetanus (Lock jaw)
– Acute infection of nervous system characterized by intense activity of neurons which further results in muscle spasm.
–
– Caused by clostridium tetani.
–
–
Incubation period 6–10 days

Generalized tetanus

440
Lock jaw or trismus due to spams of masseter as the first symptom.

Dysphagia, stiffness or pain in neck and shoulders

Risus sardonicus due to grimace or sneer of facial muscle.

Opisthotonous–arched back

Cephalic tetanus – trismus and facial palsy together

Local tetanus

Scarlet fever
– Systemic infection caused by some strains of group A streptococci.
–
 
– In addition to the usual “strep throat” (pharyngitis, fever, and malaise), children develop a skin rash caused by
–
 
erythrogenic toxin.
– Strawberry tongue (white coat with red, inflamed fungiform papillae).
–
 
– Treated with penicillin to prevent complications of rheumatic fever.
–
 
Fungal Infections
• Deep fungi (histoplasmosis, coccidioidomycosis, blastomycosis, cryptococcosis)
•
– Histoplasmosis is endemic to the American Midwest and coccidioidomycosis (San Joaquin Valley fever) is endemic
–
 
 
to the American West.
– Deep fungal infections of the lung may lead to oral chronic granulomatous ulcers due to oral implantation of
–
 
microorganisms.
– Oral lesions must be differentiated from oral cancer and chronic traumatic ulcers.
–
 
• Opportunistic fungi: Candidiasis (thrush, moniliasis)
•
– Candidiasis is an opportunistic fungi that is present usually in debilitated patients on prolonged antibiotic therapy,
–
corticosteroid therapy, malignant chemotherapy, drugs and diabetes mellitus etc.
– The oral lesions resemble white plaques resembling milk curds which can be wiped away with a gauze.
–
Primary Candidiasis Disease
Acute • Acute • Commonly known as thrush
•
•
pseudomembranous • It occurs in debililated immunocompromised patients or chronically ill or infants.
•
• Acute atrophic • It is characterized by soft elevated plaque, common on tongue and mucosa. It can
•
•
be wiped off with a gauze leaving a normally appearing mucosa or erythematous
area.
• Normally candidiasis is painless. This is the only type which is painful.
•
Chronic • Chronic hyperplastic • This is also called leukoplakia type having malignant potential.
•
•
• Chronic atrophic • Denture Candidiasis or denture sore mouth.
•
•
candidiasis • Angular chelitis (AIPG 2014)
•

• Chronic mucocutaneous • Median rhomboid glossitis. (AIPG 2008)
•
•

• It is characterized by involvement of skin, scalp and mucous membranes.
•
Secondary oral • Thrush is characterized by white patches on the surface of the buccal and labial
•
candidiasis mucosa, tongue and the soft palate.
• The white plaque consists of a tangled mass of fungal hyphae, blastospores,
•
bacteria, inflammatory cells, fibrin and desquamated epithelial cells
• Diagnosis may be confirmed by

•
– Culturing in cornmeal agar and Saboraud’s broth.
–
– Histological scrapings of lesion when visualized under periodic acid Schiff (PAS) reagent or methenamine silver will
–
show the presence of mycelia and hyphae.
– Fragments of plaque can be smeared on microscope under 20 percent potassium hydroxide and oxamised for the typical
–
hyphae.

• Management of oral candidiasis
•
– Traditional medication with the polyenes should be the first line of treatment and the azoles should be kept as a second
–
line of defense.

Amphotericin B: Lozenge 10 mg, 3 to 4 times a day for 2 weeks.

Nystatin: Cream 3 to 4 times per day

Oral suspension 100,000 units 4 times/day for 7 days

Clotrimazole: 1% cream

Miconazole: Oral gel

Ketoconazole: 200mg tab od or bd for 2 weeks

Fluconazole: 100mg cap od for 1-2 weeks

Itraconazole: 100mg cap od for 2 weeks

– Future strategies for management of candidal biofilms
–
Pre-coating biomaterials

Exploit quorum sensing molecules to disrupt biofilms

Probiotic agents

• Median rhomboid glossitis or posterior midline atrophic candidiasis shows male predilection in 3:1 ratio. In some cases, a
•
midline soft palate erythema may be found in areas of routine contact with the underlying tongue involvement and this is
known as kissing lesion.
• (Kissing disease: infectious Mononucleosis)
•
Botryomycosis (Bacterial Pseudomycosis)
• Chronic granulomatous bacterial infection.
•
• The principal agent is S. aureus.
•
• Also called as bacterial actinophytosis and actinobacillosis.
•
• The presence of grains and granules is a characteristic feature.
•
Sarcoidosis
• A chronic multisystem granulomatous disease (lymph nodes, salivary glands, skin and bone, etc) which resembles
•
tuberculosis in many respects.
• It is characterized by
•
– Depression of delayed type of hypersensitivity and abnormal serum immunoglobulins
–
– Oral lesions are popular nodules or “fever blisters” resembling herpetic lesions.
–
• In the oral region, parotid is often (unilaterally or bilaterally) enlarged with concomitant facial nerve paralysis.
•
Occasionally, a small nodular growth over the soft palate, gingiva, floor of the mouth or cheek may be seen.
• In rare cases, central lesions in the maxilla or mandible may occur in sarcoidosis.
•
• The microscopy reveals multiple, circumscribed noncaseating granulomas, consisting of epithelioid cells, lymphocytes
•
and multiple multinucleated giant-cells.
• The giant cells may contain star-shaped “asteroid bodies” or “schaumann bodies” (these are various inclusion bodies)
•
442
Diseases Tests

Sarcoidosis Kveim Siltzbach test (Kar 98, COMED 09, 2011, KCET 2011)

Tuberculosis Tuberculin test/ Mantoux test
Leprosy Modified Zeihl Neilson method
Cat scratch disease Demonstrable with sliver stain
Common names
• Histoplasmosis • Darlings disease
•
•
• North American Blastomycosis • Gilchrist’s disease
•
•
• South American blastomycosis • Lutz’s disease (characterized by microabscess and
•
•
pseudoepitheliomatous hyperplasia)
• Coccydomycosis • Valley fever
•
•
• Crytococcosis • Torulosis
•
•
• Candidiasis • Monialiasis/ Thrush
•
•
• Phycomycosis • Mucormycosis / Zygomycosis
•
•
PULP AND PERIAPICAL TISSUES
• Streptococcus mutans is considered to be principal etiologic agent of caries because it produces organic acids and it
•
forms gelatinous matrix.
• Pioneer bacteria in dental caries are in dentin.
•
• Orland and Fitzgerald found that animals maintained in germ free environment did not develop caries even when fed
•
on high sugar diet.
• Initiation of caries by Strept. mutans is by production by insoluble dextran and glycosyl transferase – Initiation of smooth
•
surface caries. (AIIMS Nov 11)

• Streptococcus sanguis: Another group of streptococcus to cause caries
•
• Actinomyces: Root surface caries (AIPG 2009)
•

• Liquefaction foci: Are seen in dentin in advanced cases of carious destruction. These are ovoid areas of destruction
•
parallel to dentinal tubules and are formed by focal coalescence and breakdown of few dentinal tubules.
• The first change in dental caries is loss of interprismatic substance or inter rod substance of enamel with increased
•
prominence of rods and accentuation of incremental lines of Retzius. (AIPG 2009)

• The earliest response of pulpitis is hyalinization.
•
Caries
• Sucrose is the most cariogenic sugar, because in addition to undergoing fermentation by oral bacteria, it also acts as a
•
substrate for the synthesis of both extracellular (EPS) and intracellular (IPS) polysaccharides. (AIPG 2008)

• The caries of enamel surface lead to accentuation of incremental lines of Retzius. This is an optical phenomenon due to loss
•
of minerals, which causes organic structure to appear more pronounced
Points to remember about streptococci
S. mutans Both acidogenic (acid producing) and aciduric (survives in acidic environment)
Major and most virulent caries producing organisms
Present only in dentulous mouth
S.salivarius Frequently isolated on the first day of baby’s life
S. sanguis The first colonizer of teeth during the teething process

• Vitamin suggested to be of value in termination of dental caries–synthetic vitamin K (AIPG 2011)
•

• Most severely periodontally involved tooth–Depressibility/rotatability
•
• Caries which are initiated via a lamella or organic defect in enamel and progresses rapidly through this defect to the dentin,
•
producing extensive undermining of enamel with little involvement of enamel–Penetrating caries

Widening Of Periodontal Ligament Is Seen In Obliteration Of Periodontal Ligament Space Is Seen In
• Osteosarcoma • Hypercementosis
•
•
• Scleroderma • Ankylosis
•
•
• Trauma from occlusion • Hypo function of teeth
•
•
• Paget’s disease (AIPG 2003)
•

BONE AND JOINT
Osteopetrosis or Marble Bone Disease (KAR 2008)

• Benign dominant OR Malignant recessive inherent forms.
•
• There is diffuse sclerotic process of several bones.
•
• There is normal bone formation but remodeling in absent due to lack of ribonucleic acid in osteoclasts.
•
• Development of osteomyelitis is a common complication following dental extraction.
•
• Oral Manifestations of Osteoporosis are:
•
– Medullary spaces of jaws are remarkably reduced in both forms
–
– Osteomyelitis and jaw fracture is common during tooth extraction
–
– Enamel hypoplasia, microscopic dentinal defects, and arrested root development. However this may not be the case
–
in beingn dominant form of diseases.
– Teeth are extremely prone to dental caries
–
– Retarded tooth eruption due to sclerosis of bone.
–
• Roentgenographic features
•
– Medullary cavities are replaced by bone and the cortex thickened
–
– The vertebrae are extremely diffused or show alternating bands Rugger Jersey Sign
–
– Density of bone may be such that the roots of the teeth are nearly invisible on the dental roentogram
–
– Ends of long bones are bulbous called Erlenmeyer’s flask deformity
–
– In osteopetrosis there is normal appositional bone growth but failure of physiologic root resorption
–
Achondroplasia
• Autosomal dominant
•
• There is disturbance of endochondrial bone formation resulting in characteristic form of dwarfism.
•
• Achondroplastic dwarf is short with thick muscular extermeties with brachycephalic skull and bowed legs.
•
• Arms cannot hang freely, patient can fold but cannot straighten elbow.
•
• Incongruous appearance is characteristic.
•
• Maxilla is short with relative prognathic mandible.
•
• This disease is characterized by disturbance in epiphyseal cartilage.
•
• The cartilage columns lack orderly arrangement fail to calcify not resorbed and replaced by bone in usual fashion.
•
444
Cherubism (Familial Fibrous Dysplasia of Jaw)

Characteristics • Autosomal dominant
•
••
Involves more than one quadrant
• Stabilizes after growth period (starts by 14 months 3 years )
•
• Gene 4p 16.3 affected
•
Clinical features • Cherubic look
•
• More in males
•
• Mostly bilateral (AIPG 2012, AIIMS Nov 2012)
•

• Cervical lymphadenopathy
•
• Eye to heaven appearance – a rim of sclera visible below iris
•
• Associated with Noonan’s syndrome
•
Radiographic Floating tooth syndrome
features • Ground glass appearance
•
Histologic feature Eosinophilic cuffing
Grading system • Grade I: Involvement of both mandibular ascending rami

•
for cherubism • Grade II: Involvement of maxillary tuberosities and mandibular ascending rami
•
• Grade III: Characterized by McCune- Albright syndrome with involvement of whole maxilla and mandible
•
Condylar Hyperplasia (AIIMS Nov 2012)
• More common in males and is usually discovered before the age of 20 years
•
• The condition is self limiting and tends to arrest with termination of skeletal growth
•
• Patients have a mandibular asymmetry that varies in severity depending on the degree of condylar enlargement
•
• The condyle may appear relatively normal but symmetrically enlarged, or it may be altered in shape
•
• It may be more radio-opaque because of the additional bone present.
•
Jaw abnormality Disease

Hypoplasia / Underdeveloped maxilla (Class III malocclusion) • Cleidocranial dysplasia
•
• Craniofacial dysostosis (Crouzon disease)
•
• Achondroplasia
•
• Down’s syndrome
•
• Underdeveloped mandible (Class II malocclusion)
•
• Treacher Collins syndrome
•
• Pierre Robin syndrome
•
Underdeveloped maxilla and mandible • Hypopituitarism (development of mandible is more retarded than
•
maxilla)
Enlargement of maxilla • “Leontiasis ossea” or a type of monostotic fibrous dysplasia

•
• Pagets disease of bone (common)
•
• Pituitary gigantism (rare)
•
Enlargement of mandible • Acromegaly
•
• Pagets’s disease of bone (rare)
•
• Pituitary gigantism (more common)
•
Enlargement of both maxilla and mandible • Pagets disease
•
Residual asymmetric deformity of mandible (due to cortical • Striking feature of Caffey’s disease
•
thickening)

Jaw abnormality Disease

An unusual prominence of premaxilla • Thalassemia
•
Underdeveloped premaxilla • Congenital syphilis
•
• Alkaline phosphatase levels are increased in: (AIIMS Nov 2012,2011)
•

– Pagets disease
–
– Fibrous dysplasia
–
– Caffeys dysplasia
–
– Osteogenesis imperfecta also: it is increased or normal
–
Association of Enzymes and Various Diseases
• Increased serum ALP, lactate dehydrogenase with reduced acid • Odontogenic myxoma
•
•
phosphatase and G6PD activity
• Increased serum acid phosphatase • Osteopetrosis

•
•
• Increased phosphorylase enzyme levels • Osteogenesis imperfecta
•
•
• Normal levels of serum Ca, P, and ALP • Cherubism
•
•
• Reduced serum ALP levels • Scurvy, Hypothyroidism
•
•
Paget’s Disease
• There is progressive enlargement of skull and maxilla.
•
• The patient suffers from deafness (due to compression of cochlear nerve), blindness (due to involvement of optic nerve)
•
and facial paralysis (due to pressure on facial nerve).
• Development of osteosarcoma is the most serious complication of paget’s disease. (AIIMS Nov 11)
•

• TMJ involvement is common in ‘Marie – Strumpell type’ of rheumatoid arthritis. Rh arthritis in children is called Still’s
•
disease and it results in class II division I malocclusion with anterior open bite.
• In osteosarcoma, the point where the periosteum begins to merge, an acute angle between the bone surface and the
•
periosteum is created. This is known as Codman’s triangle.
– It occurs in young person (10-25 years)
–
– Chiefly involves the femur and tibia
–
– Sunburst appearance radiographically
–
Osteoporosis
• Most common of the metabolic bone diseases i.e. disorders in which all the skeleton is involved.
•
• Loss of trabecular bone begins at an earlier age in both sexes but is probably greater in women
•
• Bone loss involves predominantly trabecular bone
•
• Bone mineral density is measured by DEXA (dual energy x ray densitometry) is an excellent predictor of future risk
•
• X ray may show cod fish vertebrae
•
Type I • In post menopausal women between 51-75 years of age
•
osteoporosis • Fracture of vertebral bodies and distal foramen are common complications
•
Type II • In women and men over age 70 years
•
osteoporosis • Associated with fracture of femoral neck, proximal humerus, proximal tibia and pelvis
•
• Osteomalacia may mimic osteoporosis but differentiated as osteomalacia presents with undetectable levels of circulating
•
25-hydroxy vitamin D and PTH with or without hypophosphatemia.
446
• In paget’s disease pure lytic radiographic features may be confused with osteoporosis but high phosphatase levels and
•
increased urinary excretion of pyridineoline crosslinks are clues to the presence of Paget’s disease.
• Causes of osteoporosis
•
Hyperthyroidism Acromegaly

Older age Multiple myeloma

Diabetes Adaptation syndrome

Renal acidosis Cushing’s syndrome

Rickets Hypo vitaminosis C

Leukemia Thalassemia

Histiocytosis Sickle cell anemia

Cyclic neutropenia Osteogenesis imperfecta

Difference Between Fibrous Dysplasia and Paget’s Disease
Fibrous dysplasia Paget’s disease
Age Youth Over 40 years
Serum No abnormality Raised alkaline Phosphatase
Radiography Homogenous density ‘ground glass’ pattern Lucent to dense depending on stage classic ‘ cotton wool’ pattern
Histology Abnormal trabeculae of immature (woven) bone in a Extensive osteoclastic and osteoblastic activity surrounding
fibrous marrow ‘mosaic’ trabeculae with vascular dilation and lymphocytic
infiltration of marrow
BLOOD DISORDERS
Hb Abnormalities
Hereditary • Hemoglobinopathies
•
– Fault in the alpha or beta chain of globin of Hb. Eg: sickle cell anemia.
–
• Thalassemias:
•
– Fault in the synthesis of alpha or beta chain. There is insufficient synthesis of the chain, but once synthesized,
–
chain is normal.
– Cooley’s Anemia – beta thalassemia. (AIPG 2014, 2011)
–

– Oral Manifestations:
–
- Unusual prominence of premaxilla results in obvious malocclusion.
-
- (Thalassemias increase haemolysis. They can produce bone marrow expansion, which can present
-
maxillary enlargement.)
- Oral mucosa exhibits characteristic anemic pallor.
-
• Porphyrias:
•
– Excess activity of enzyme ALA synthase leading to porphyrin production.
–
Acquired • Methemoglobinimia
•
• Porphyrias can also be acquired
•
Anemia
– Anemia may be the deficiency of hemoglobin in the in blood which may be caused by either too few red blood cells
–
or too little hemoglobin in the cells
– Anemias may be classified as
–
Anemia due to decrease in production of RBC e.g. iron deficiency anemia, B12 or follate deficiency anemia, bone

marrow hypoplasia/aplasia.
Anemia due to chronic blood loss e.g. chronic bleeding


Clinical features Oral manifestations
Iron deficiency • Brittle nails. • Angular chelitis
•
•
anemia •
•
Spoon shaped nails, • Glossitis
•
• Brittle hair. • Lemon tainted pallor of skin
•
•
• Atrophy of papilla in tongue and dysphagia. • Atrophy of filliform and later

•
•
• The cells are microcytic and hypochromic. (There is not enough iron fungiform papillae
•
available to form hemoglobin.hence the red cells that are produced • Loss of normal keratinization of oral
•
are smaller then normal and have too little hemoglobin. Hence mucous membrane
microcytic,hypochromic anemia).
Megaloblastic • Vitamin B12 and folic acid are essential for production of DNA, lack • Glossitis (beefy red tongue)
•
•
Anemia of either causes abnormal DNA, failure of nuclear maturation and cell • Painful and burning lingual sensation
division . So the cells become larger in size i.e. macrocytic . They can
•
• Small and shallow ulcers
carry oxygen normally but have short life because of fragility. E.g.:
•
pernicious anemia. • Atropy of papillae (bald tongue)
•
• Cabot’s rings (RBC abnormality) are seen • Oral mucosa has anemic palor
•
•
• Mucous membrane becomes
•
intolerant to dentures
Hemolytic • The no. of cells formed may be normal but they are destroyed faster
•
Anemia then formed, hence anemia results. Some of these types of anemias
may be hereditary spherocytosis, sickle cell anemia

(AIIMS Nov 2010)

Aplastic • There is lack of functioning bone marrow. Eg: a man exposed to • Petechiae purpuric spots or frank
•
•
anemia gamma ray radiation from a nuclear bomb blast is likely to sustain hematomas of oral mucosa after
complete bone marrow destruction, followed by lethal anemia haemorrhage
• Aplastic anemia and leucopenia are rare complications of • Spontaneous gingival haemorrhage
•
•
carbamezepine therapy. • Ulcerative lesions of oral mucosa /
•
pharynx
Myelophthisic • Occur in multiple myeloma, eosinophilic granuloma, osteopetrosis and

•
anaemia Osteogenesis imperfecta
(replacement
type anemia)
Polycythemia • Condition with large quantity of extra RBC’s. (AIPG 2009) • Oral mucous membrane appears
•

•
deep purplish red. (tongue and
gingiva are mainly affected)
• Secondary Polycythemia: Physiological condition, happens in • Gingiva are often engorged

•
•
condition like high altitude, cardiac failure etc. and swollen and bleed on slight
• Polycythemia Vera: A pathological condition 7-8 million/ mm3, provocation
•
hematocrit 40-45% caused by generic abnormalities in hemocytoblastic • Submucosal petechiae, ecchymoses
•
cells. In polycythemia vera total blood volume ↑ and hematomas are common.

• Viscosity ↑ may be up to 10 times of water (normal to 3 times of water). • The condition may be controlled by
•
•
• Clinical Significance: frequent bloodletting or cytotoxic
drugs.
•
–↑ Viscosity
–
–↓ Sluggish Blood
–
–↓ Venous return
–
–But blood volume ↑, So these factors balance each other→
–

↑venous return

• Colour of skin in purplish since blood flow is sluggish and large amount of
•
Hb is deoxygenated → cyanotic tint to skin.
Anaemia
• Macrocytic: Pernicious
•
• Microcytic: Anaemia due to infection and inflammation
•
• Hypochromic microcytic: Iron deficiency anaemia and thalassemia
•
• Normocytic: Anaemia due to hemorrhage, hemolysis
•
448
Adverse effects of cytotoxic drugs include

• Bone marrow depression leading to granulocytopenia, agranulocytosis thrombocytopenia, aplastic anemia
•
• Lymphocytopenia and inhibition of lymphocyte function leading to suppression of immunity
•
• Secondary cancers like leukemias, lymphomas appear frequently many years after use of cytotoxic drugs
•
WBC Type High Count Low Count

Neutrophils Bacterial infections, burns, inflammation Radiation, exposure, drug toxicity, Vit B12 def, systemic
lupus erythromatosis
Eosinophils Allergic reaction, parasitic auto immune Drug toxicity, stress

disease
Basophils Allergic reactions, leukemias, cancers, Pregnancy, ovulation, stress, hyperthyroidism

hyperthyroidism
Monocytes Viral or fungal infections, TB, some leukemias Bone marrow suppression treatment
Lymphocytes Viral infections, leukemias Prolonged illness, immuno suppressants.
Leucopenia: Granulocytopenia/Agranulocytosis
• When total count of WBCs is < 4000/ml of blood
•
• With in 2 days after bone marrow stops producing white blood cells, ulcers may appear in the mouth or colon, or person
•
develops severe respiratory infection.
• Causes:
•
– Repeated x-ray exposure
–
– Certain common medications eg. chloramphenicol (antibiotic), thiouracil (used to treat thyrotoxicosis), may cause
–
agranulocytosis.
– Nitrous oxide abuse (used in dentistry)
–
• Oral manifestations
•
– Necrotizing ulcerations of oral mucosa, tonsils and pharynx
–
– Ragged necrotic ulcers covered by a gray or even black membrane
–
– No purulent discharge
–
– Gingival haemorrhage
–
– Excessive salivation
–
• Oral surgical procedures are contraindicated
•
Leukemias
Features • Uncontrolled production of WBC’s is caused by cancerous mutation of a myelogenous or lymphogenous cell.
•
• This causes leukemia which is usually characterized by greatly increased number of abnormal WBC’s in the
•
circulatory blood.
Types of Leukemia: • Lymphogenous leukemias

•
– Caused by cancerous production of lymphoid cells, usually beginning in a lymph node or other lym-
–
phogenous tissues or then spreading to other areas of the body.
• Myelogenous leukemias
•
– It begins by cancerous production of young myelogenous cells in bone marrow and then spreads
–
throughout the body so that WBCs are produced in many extra medullary organs
Oral manifestations • Gingival hyperplasia (not seen in edentulous patients)

•
• Gingivitis, haemorrhage, petechiae and ulceration of mucosa
•
• Gingiva are boggy, edematous, deep red and bleed easily
•
• Gingival swelling ( due to leukemic infiltration)
•
• Purpuric lesions of oral mucosa
•
• Gingival haemorrhage is due to ulceration of sulcus epithelium and necrosis of underlying tissue
•
• Rapid loosening of teeth due to necrosis of PDL and destruction of alveolar bone
•

Treatment • Cytotoxic drug therapy, chemotherapy and radiotherapy.
•
• Extraction in patient with acute myeloid leukemia may lead to heamorrhage, delayed wound healing and
•
infection.
• Radiation induced mucositis and xerostomia also adds up to problems
•
• With proper precautions, extraction and minor surgical procedures can be performed without serious adverse

•
sequelae.
BLEEDING DISORDERS
• These can be classified on the basis of cause as:
•
Fault of primary hemostatic mechanism (hemostasis) Purpura
Fault of platelet (number) Thrombocytopenic purpura
Def. of quality of platelets Aspirin induced purpura

Fault of blood vessel VWD
Fault of secondary hemostasis (congenital) Factor VIII def., factor IX def.
Fault of secondary hemostasis (acquired) Liver failure
• Hemophilia: is a type of bleeding disorder in which deficiency of coagulation factor causes deficiency in intrinsic path
•
causing poor secondary hemostasis.
Types • Hemophilia A Factor VIII deficiency
•

• Hemophilia B Factor IX deficiency
•

• Hemophilia C Factor XI deficiency
•

Oral manifesta- • Bleeding is always followed by trauma
•
tions • Gingival haemorrhage (massive and prolonged)
•
• Subperiosteal bleeding with reactive new bone formation causing tumor like expansion of the bone
•
• Dental extraction or minor surgical procedure is difficult hemophillics
•
Applied • Tooth extraction by rubber bands – rubber band is placed around cervix of the tooth and is allowed to migrate
•
apically, causing exfoliation of tooth through pressure necrosis of PDL.
Characteristics of Bleeding Disorders:

Disorder PT PTT Bleeding Time
Hemophillia A Normal Prolonged (AIPG 2007) Normal

Hemophillia B Normal Prolonged Normal
Factor II def Prolonged Prolonged Normal
Factor V def. Prolonged Prolonged Normal
Factor VII def. Prolonged Prolonged Normal
Factor X def Prolonged Prolonged Normal
Factor XI def Normal Slightly Prolonged Normal
Factor I def Prolonged Prolonged Normal
Factor XII def Normal Normal Normal
450
Influence Of Haematological And Bleeding Disorders On Dental Management

• Surgical procedures
•
– Healing after surgical procedures may be compromised in patients with anaemia or white cell disorders.
–
– The timing of surgery in patients undergoing treatment for conditions such as leukaemia is important. Surgical
–
treatments should be performed during stages of remission and between chemotherapeutic regimens when the cell
count is optimal
– The management of patients taking drugs that interfere with bleeding is controversial. Following drugs have to be
–
taken care of:
Aspirin

Antiplatelet drugs such as clopidogrel and dipyridamole

Warfarin

Heparin

• Choice of anaesthesia
•
– Hamophilic patients who had received intraligamentary anaesthesia for restorative dentistry without administration
–
of Factor VIII recorded no complications related to haemorrhage or haematoma formation. Infiltration injections
should not produce significant problems.
• Medication prescribed
•
– Aspirin, diclofenac, diflunisal, ibuprofen and prolonged use of paracetamol all increase the effect of warfarin.
–
– Penicillins can increase the prothrombin time when given to patients receiving warfarin
–
– Erythromycin enhances the anticoagulant effects of both warfarin and nicoumalone by reducing the metabolism of
–
the these drugs.
– Tetracycline may enhance the anticoagulant effect of warfarin and the other coumarin anticoagulants. Miconazole
–
enhances the anti-coagulant effect of warfarin even after topical use.
• Cross-infection control
•
SKIN DISEASE
Mucocutaneous Lesions
Disease Features Etiology Management
Apthous ulcers • Recurrent painful ulcers (not preceded • Of unknown cause, but probably • Symptomatic, most
•
•
•
by vesicles). related to a focal immune defect remedies contain either
• Appear on wet (not vermilion) • May be seen in association with steroids or tetracycline
•
•
nonkeratinized oral mucosa (i.e., not some systemic diseases
hard palate or hard gingiva).
 
• Clinical Types of Aphthous Ulcers
•
– Minor Aphthous Ulcers
–
– One to several painful oval ulcers
–
<0.5 cm
– Most common type
–
 
– Duration of 7–10 days
–
– Major Aphthous Ulcers
–
– Up to 10 deep craterform ulcers
–
>0.5 cm Very painful and may
be debilitating May take several
 
weeks to heal
– Herpetiform Aphthous Ulcers
–
– Recurrent crops of minor aphthae
–
Painful, 1–2 weeks to heal. May
 
be found on any mucosal surface
Same cause as other aphthae (not
viral)

Behçet’s syndrome • Oral and genital aphthous-type • Multisystem disease believed to • Treated with corticosteroids
•
•
•
ulcers, conjunctivitis, uveitis represent immunodysfunction in and other immunosup-
(inflammation of the layers of the eye), which vasculitis is a prominent pressive drugs
arthritis, headache, and other CNS feature.
manifestations.

Erythema • Self-limiting hypersensitivity reaction • Minor form associated with • Symptomatic, steroids
•
•
•
multiforme that affects Skin and/or mucosa secondary herpes simplex controversial
hypersensitivity; major form
(Stevens-Johnson syndrome)
often triggered by drugs.
Drug reactions and • Oral lesions range from vesicular to • Potentially caused by any drug • Removal of allergen or
•
•
•
contact allergies ulcerative to erythematous to lichenoid. or foreign protein. etiology
 
 
• Acquired angioedema is a specific type • May be a hyperimmune
•
•
of allergic reaction. response or nonimmunologic
 
• Precipitated by drugs or food (shellfish, (overdose, toxicity, irritant).
•
nuts).
• Mediated by mast cell release of IgE.
•
• Results in characteristic soft, diffuse
•
swelling of lips, neck, and/or face.
 
• A rare form, hereditary angioedema, is
•
an autosomal dominant trait.
Wegener’s • Destructive granulomatous lesions • Diagnosis based on biopsy and • Treated with
•
•
•
granulomatosis with necrotizing vasculitis of unknown demonstration of antineutrophil cyclophosphamide and
 
cause. cytoplasmic antibodies corticosteroids; prognosis
• Affects upper respiratory tract, lungs, (cANCAs). good.
•
and kidneys.
Midline granuloma • Destructive necrotizing midfacial • Unknown • Good prognosis when

•
•
•
phenomenon that clinically mimics treated early with radiation.
lesions of Wegener’s granulomatosis.
• Most cases represent peripheral T-cell
•
lymphomas of the upper respiratory
tract or mouth (perforation of the hard
palate may be seen).
Lichen planus • Relatively common mucocutaneous • Clinical Features of Lichen • Responds to corticosteroids
•
•
•
 
disease (1%–2% of adults affected) Planus • Erosive form may have
•
– T-lymphocytes target (destroy) • Oral lesions typically bilateral slightly elevated risk for
–
•
basal keratinocytes; the reason in the buccal mucosa, although malignant change.
for this immunologically mediated tongue and gingival frequently
phenomenon is unknown. affected.
• Microscopically • Oral lesions exhibit white
•
•
– Hyperkeratosis. (hyperkeratotic) lines. (AIPG
–

– Lymphocyte infiltrate at the epithe- 2009,2011)
–
lial–connective tissue interface.

• Clinical types
 
– Basal zone vacuolation due to bas-
•
• Reticular: lesions consist of
–
al keratinocyte destruction.
•
– Epithelium may exhibit a “saw interlacing lines (Wickham’s
striae) (AIPG 2002)
–
tooth” pattern as it remodels fol-

lowing basal cell damage • Erosive: Ulceration also present
•
• Erythematous or atrophic:
•
Lesions are
• Predominantly red Plaque:
•
 
lesions are predominantly
plaque-like
• Cutaneous lesions
•
characteristically purple pruritic
papules on lower legs and arms
452

Lupus • Occurs in either discoid or systemic • An autoimmune disease • Treated with corticosteroids
•
•
•
erythematosus form and other drugs.
••
Discoid (chronic) type
– Affects skin
–
– Usually middle age, especially
–
women
– Lesions are erythematous; oral le-
–
sions mimic erosive lichen planus
– No systemic signs or symptoms;
–
rarely progresses to systemic form
• Systemic (acute) type
•
– Multiple organ involvement (heart,
–
kidney, joints, skin, oral).
 
– Butterfly rash over bridge of the
–
nose is classic sign. (AIPG 2007)
 

– Autoantibodies directed against
–
nuclear and cytoplasmic antigens.
 
– Serologic tests include antinuclear
–
antibodies (ANA) and lupus ery-
 
thematosus (LE) cell test
Scleroderma • Fibrosis of tissues eventually leads to • An autoimmune, multiorgan
•
•
organ dysfunction. disease of adults, especially
• Cutaneous changes include women.
•
induration and rigidity, atrophy, and • May occur concomitantly with
•
telangiectasias. other autoimmune diseases,
• Oral changes include restriction of such as lupus erythematosus,
rheumatoid arthritis,
•
orifice, uniform widening of periodontal
membrane, and bony resorption of dermatomyositis, and Sjögren’s
posterior margin of the mandibular syndrome.
ramus (best seen on a OPG).
Pemphigus • Presents as multiple, painful ulcers • An autoimmune, mucocutaneous • Treated with systemic
•
•
•
vulgaris preceded by bullae which form within disease in which antibodies are corticosteroids or
 
the epithelium. directed against desmosomal other immunosuppressive
 
• Positive Nikolsky sign may be protein (desmoglein 3). drugs.
•
present (formation of blister with
 
rubbing or pressure).
• Oral lesions precede skin lesions in
•
about half of cases.
 
• Progressive clinical course that may be
•
fatal if untreated.
 
• Tzank cells present–clumps of
•
acantholysed cells (AIPG 2006)

• Suprabasilar epithelial split
•
Mucous membrane • Affects older adults, typically over the • An autoimmune disease of • Patients are managed with
•
•
•
pemphigoid age of 50 years. mucous membranes; antibodies corticosteroids
 
• Presents as multiple, painful ulcers directed against basement
membrane antigens (Laminin 5,
•
preceded by bullae which form below
BP180, others)
 
the epithelium at the basement
 
membrane.
• Oral lesions may be found in any
•
region, especially and sometimes
exclusively in the attached gingival;
ocular lesions can lead to blindness if
untreated.
• Positive Nikolsky sign may be
•
present.
• Persistent disease.
•

Intraepithelial Bulla Sub Epithelial Bulla

• Herpes simplex • Pemphigoid
•
•
• Herpes zoster • Bullous pemphigoid
•
•
• Chicken pox • Bullous lichen planus

•
•
• Pemphigus • Dermatitis herpetiformis
•
•
• Familial benign pemphigus (Hailey- Hailey disease ) • Epidermolysis bullosa
•
•
• Epidermolysis bullosa - dystrophic recessive form • Cicatricial pemphigoid or mucous membrane pemphigoid (MMP)
•
•
• Oral lesions of erythema multiforme • Skin lesions of erythema multiforme
•
•
Immunofluorescence Techniques
Direct immunofluorescene (DIF) in cutaneous tissue (skin Indirect immunofluorescence (IIF) of serum, basement mem-

and mucosa) brane zone and/or cell surface
• Most sensitive means • The IIF test is performed on serum to detect the presence and
•
•
• It involves directly staining tissue sections for immunoglobulin amount of circulating IgG and/or IgA antibodies to epidermal/
epithelial antigens.
•
(IgG, IgM, IgA), third component of complement (C1), and
fibrinogen ••
Semiquantitative levels if antibodies are reported as titres.
• Biopsy site (perilesional)is critical and tissue specimen(s) must • Basement membrane zone antibodies
•
•
be submitted in Michel’s (or Zeus) medium.
Disease Direct Fluorescent Indirect Fluorescent

Lichen planus Globular pattern of staining – positive. Deposition of IgA, IgG in the Subepithelial deposits of fibrinogen
basement membrane zone, IgM- staining cytold bodies, usually Antigenically stainable with antifibrinogen
located in the dermal papilla or in the peribasalar area. sera
Absence of direct fluorescence with complement C1 Indirect immunofluorescence
demonstrates circulating IgA in 80%
MMP (mucous BMZ- positive – positive fluorescence for immunologically and Only 10 % of MMP patients demonstrate
membrane pemphigoid complement in the basement membrane zone in 50 to 80% of positive indirect immunofluorescence for
patients. circulating antibasement membrane zone
Specimens obtained show immunoglobulin and complement antibodies.
deposition in the intercellular substance of the prickle cell layer of
the epithellum.
DLE BMZ – deposition of immunoglobulins (e. g. IgG, IgA and IgM)in Reveals prominent circulating auto-
the basement membrane zone of the epithelium and skin, in case antibodies (ANTI NUCLEAR ANTI
of both SLE and DLE. BODIES)
Globular pattern of staining in another important finding in lupus
is that direct immunofluorescence testing of C1 in a granular
band involving the basement membrane zone and subepithelial
connective tissue.
Pemphigus vulgaris ICS – In pemphigus, immunofluorescence tests of the Antikeratinocyte antibodies against
perilesional tissue often demonstrate the deposition of specific intercellular substances that show up
immunoglobulins (IgG , IgM and IgA), and complement within the under a fluorescent microscope.
intercellular areas of epithelium Circulating auto antibodies against
Absence of ICS staining with fibrinogen. epithelial intercellular desmosomes are of
diagnostic importance
Pemphigoid BMZ shows deposition of IgG and complement along the basement Indirect immunofluorescent demonstrates
membrane as well as on the keratinocyte. antibodies that not only bind to epithelium
but to liver, heart, and bladder tissue as
well.
454
Disease Direct Fluorescent Indirect Fluorescent

Bullous pemphigoid BMZ direct immunofluorescent study of a biopsy specimen Indirect immunofluorescent study of
demonstrates deposition of IgG bound to the basement membrane serum obtained from patients with BP
demonstrates IgG antibodies bound to
the epidermal side of salt – split skin
onto antigens that have been named

BP antigens 1 and 2. This latter test is
particularly useful in distinguishing BP
from another subepithelial bullous disease
Epidermolysis bullosa Has IgG antibodies localized to the

acquisita dermal side of the salt – split skin.
Diagnostic Criteria for Diagnosis of SLE:

• Malar rash
•
• Discoid rash
•
• Scarring may occur
•
• Photosensitivity
•
• Oral ulcers
•
• Serositis
•
• Renal disorder: Proteinuria > 0.5 g/dl or 3+, or cellular casts
•
• Neurologic disorder like seizures or psychosis without other causes
•
• Hematologic disorder
•
– Hemolytic anemia or leukopenia ( < 4000 /μL) or
–
– Lymphopenia ( <1500/μL) or
–
– Thrombocytopenia ( <100,000/μL)
–
• Immunologic disorder
•
– Anti-dsDNA,
–
– Anti-Sm, and /or
–
– Anti-phospholipid
–
• Antinuclear antibodies like an abnormal titer of ANA by immunofluorescene or an equivalent assay at any point in time
•
in the absence of drugs known to induce ANAs. (MAN 1998)

Psoriasis
• Chronic disease affecting approx 2% of the population
•
• Primarily involves the skin and, to a lesser extent, the joints, nails and mucous membranes
•
• Characterized by the occurence of small, sharply delineated, dry papules, each covered by a delicate silvery scale.
•
• If the deep scales are removed, one or more tiny bleeding points are disclosed, a characteristic feature termed Auspitz
•
sign. (AIPG 2008)

DISEASE OF NERVE AND MUSCLE
Trigeminal Neuralgia (Tic Douloureux, Fothergill’s Disease) (Kar 03))

Features • > 40 yrs
•
• Occurs along the distribution of maxillary nerve
•
• Electric in character
•
• Episodic, each episode lasts 2-4 mins
•
• A pain syndrome recognizable by the patient’s history alone.
•
• The typical course is relapsing remitting over several years
•
• Development of trigeminal neuralgia in a young person suggests the possibility of multiple sclerosis.
•

Trigger points • Various triggers may commonly precipitate a pain attack.
•
• Light touch or vibration is the most provocative.
•
• Activities such as shaving, face washing, or chewing often trigger an episode.
•
••
Stimuli as mild as a light breeze may provoke pain in some patients.
• Pain provokes brief muscle spasm of the facial muscles, thus producing the tic.

•
Clinical neuro- • Mechanoceptive testing
•
sensory testing – 2 point discrimination
–
– Static light touch
–
– Directional brush stroke
–
– Vibratory sense
–
• Nociceptive testing
•
– Pain stimuli
–
– Thermal discrimination
–
Treatment • Peripheral neurectomy
•
• Injection of alcohol or boiling water into the gasserian ganglion
•
• Electro- coagulation of the same ganglion
•
• Administration of carbamazepines (drug of choice) (AIIMS Nov 2013, AIPG 2011)
•

• Baclofen is the latest drug used
•
• Percutaneous surgical procedure known as balloon compression
•
– This technique has been helpful in treating the elderly for whom surgery may not be an option due to coexist-
–
ing health conditions. Balloon compression is also the best choice for patients who have ophthalmic nerve
pain or have experienced recurrent pain after microvascular decompression.
• Glycerol injections involve injecting an alcohol-like substance into the cavern that bathes the nerve near its
•
junction. This liquid is corrosive to the nerve fibers and can mildly injure the nerve enough to hinder the errant
pain signals.
• In a radiofrequency rhizotomy, the surgeon uses an electrode to heat the selected division or divisions of the
•
nerve. Done well, this procedure can target the exact regions of the errant pain triggers and disable them with
minimal numbness.
Geniculate Neuralgia – (Lateral pterygoid followed by masseter are the two

–
muscles that are commonly involved in MPDS.
– Nervus intermedius neuralgia (AIPG 2009)

(KAR 97)
–

– Results from herpes zoster infection of geniculate

–
ganglion and nervus intermedius of facial nerve. Sphenopalatine Neuralgia is Also Called as

(AIIMS Nov 2010) Periodic Migrainous Neuralgia

Myofacial Pain Dysfunction Syndrome – This disease in due to vasoconstriction of vessels
–
– MPDS is psycho-physiologic disease seen in persons supplying nasal mucosa.
– There is ‘alarm clock’ headache occurring at the
–
with stressful situation.
–
– It results from dysfunction of entire masticatory same time of day, epiphora or watering of eyes,
blood shot eyes, sneezing, swelling of nasal mucosa
–
apparatus as well as recognition of certain psychologic
characteristics of the patient. and nasal discharge.
– There is: • Jaw winking syndrome consists of unilateral ptosis,
•
rapid elevation of ptotic eyelid on movement of
–
Unilateral pre auricular pain.
mandible to the contralateral side. (AIPG 2009)

Tenderness of muscles of mastication particularly

lateral pterygoid. – This is noted commonly when mother is feeding
–
Clicking sensation of TMJ. breast- fed babies. She notices one of the eyelid

Limitation of jaw motion. However there are no of baby shoots up while sucking (Marcus Gunn

radiologically as well as histologically abnormal phenomenon).
features.
Migraine (AIIMS May 2013, AIPG 2001)(AIPG 2009)
Migraine Cluster Headache Temporal arteritis Tension Headache
Age – females after puberty Men in 20-50 Median age – 75 yrs At all ages
Females > males Males > females (7-8 times) Female – 65% of the cases Females
456
Migraine Cluster Headache Temporal arteritis Tension Headache

Presentation – lateralized and Lateralised and periorbital Unilateral or bilateral located Bilateral frontal area
usually frontotemporal temporally in 50% patients
Pain preceded by Aura Pain (periodic attacks 1-2/day) Usually appear gradually Builds up slowly
Builds up gradually. May last for Begins without warning. Reach Occasionally it is explosive Fluctuates in severity. Persists
several hours crescendo within 5 mins. Lasts continuously for many days
for 45 mins
Usually throbbing but may be dull Excruciating deep, explosive Dull and boring in character, Headache may be episoodic or
but only rarely pulsatile seldom throbbing, pain in jaws chronic
also
Onset is after awakening and Headache is worse at night Tight band like discomfort
quietened by sleep
Associated symptoms–Nausea, Associated symptoms– Associated symptoms: Associated symptoms – Not
vomiting, diarrohea, photophobia Homolateral lacrimation Headache, fever, weight loss prominent
and visual disturbance Reddening of eye Jaw caludication Sometimes posterior neck
Parathesia with tingling and Nasal stiffness Polymyalgia rheumatica muscles are tight
numbness Ptosis ESR increase May be associated with anxiety
Other facial neurological Nausea Anaemia and depression
symptoms such as weakness Blindness due to ophthalmic artery
involvement
HEREDITARY CONDITIONS
White sponge nevus • An autosomal dominant condition due to mutation of keratin 4 and/or 13.
•
• Results in asymptomatic white, spongy-appearing buccal mucosa bilaterally
•
• Biopsy for diagnosis, no treatment necessary
•
Epidermolysis bullosa • A term that encompasses several genetic conditions and one acquired disease.
•
 
• Hereditary patterns range from autosomal dominant to autosomal recessive.
•
 
• Clinically common to all forms is the appearance of bullae from minor trauma (especially over elbows and
•
 
 
knees).
• Oral lesions (blisters, scarring, and hypoplastic teeth) are characteristically seen in severe recessive form.
•
 
Hereditary hemor- • A rare autosomal dominant condition in which telangiectatic vessels are seen in mucosa, skin, and occasionally
•
rhagic telangiectasia viscera.
• The red macules/papules (telangiectasias) are an occasional source of bleeding.
•
• Epistaxis (nose bleed) is a frequent presenting sign; oral bleeding may occur.
•
Cleidocranial dyspla- • This autosomal dominant condition is manifested by many alterations, especially of teeth and bones.
•
 
sia • The most distinctive features include: delayed tooth eruption and supernumerary teeth, hypoplastic or aplastic
•
clavicles, cranial bossing, and hypertelorism
Hereditary ectodermal • An X-linked recessive condition that results in partial or complete anodontia.
•
dysplasia (AIPG 2002) • Patients also have hypoplasia of other ectodermal structures, including hair, sweat glands, and nails.
•

(AIIMS MAY 2009)

Gardner’s syndrome • An autosomal dominant disorder
•
• Consists of intestinal polyposis, osteomas, skin lesions, impacted permanent and supernumerary teeth, and
•
 
 
odontomas.
• Intestinal polyps have a very high rate of malignant conversion to colorectal carcinoma.
•
 
IMPORTANT CHARACTERISTICS ABOUT mesoderm (AIIMS MAY 2013)

VARIOUS SYNDROMES – Presence of anti-mongoloid palpebral fissures
–
– Hypolplasia of facial bones, especially of malar bones
–
• Mandibulofacial Dysostosis (AIPG 2005) and mandible
– Malformation of external ear, middle ear and internal
•

– Also known as Treacher Collins Syndrome
–
ears
–
– Results due to failure of differentiation of maxillary – Macrostomia with abnormally high arched palate
–
–

– Facial clefts, skeletal deformities and malocclusion High refractive errors

–
– Patient has bird like or fish like face Strabismus

–
• Peutz- Jeghers Syndrome – Oral manifestations include:
–
•
– Also known as Hereditary Intestinal polyposis Hypoplastic maxilla

Angles class III occlusion
–
syndrome

– Pigmentation on fingers, toe, hands and feet, anus and Macroglossia

Scrotal/fissured tongue
–
genitalia

– Circumoral and perinasal pigmentation (1- 5 mm Protruding tongue

Anterior and posterior crossbite
–
macules) crossing vermilion border.

– Precocious puberty (Also seen in Albright’s Narrow short palate

–
Syndrome) Hypersalivation

– Gynaecomastia and growth retardation (due to Sertoli Acute necrotizing ulcerative gingivitis

–
cell tumour) • Trisomy 13 (Patau Syndrome)
•
– Facial pigmentation -------- fades with age – Cleft lip often midline
–
– Mucosal pigmentation ---- persists throughout life
–
– Flexed fingers with polydactyly
–
• MEN I ( Multiple Endocrine Neoplasia Syndrome)
–
– Ocular hypotelorism
•
– Hyperplasia of the pituitary gland with acromegaly
–
– Bulbous nose
–
– Hyperplasia of the parathyroid and adrenal cortex
–
– Low set malformed ears
–
and of pancreatic islets with increased production of
–
– Small abnormal skull
gastrin, insulin and glucagon with peptic ulcers and –
gastric hypersecretion. – Cerebral malformation especially holoprosencephaly
–
• MEN II – Microopthalmia
–
– Cardiac malformations
•
– Also known as Sipple’s Syndrome
–
– Scalp defects
–
– Hyperplasia of parathyroid gland
–
– Hypoplastic or absent ribs
–
– No tumours of pancreas.
–
– Visceral or genital anomalies
–
– No peptic ulcer
–
• Trisomy 18 (Edward syndrome)
–
– Patient may have pheochromocytomas of adrenal
•
–
medulla and medullary carcinoma of thyroid gland – Low birth weight
MEN III
–
• – Closed fists with index fingers overlapping the 3rd
•
–
– Pheochromocytomas and medullary carcinoma of digit and the 5th digit overlapping the 4th
–
thyroid gland – Narrow hips with limited abduction
–
– Oral neuromas that are common on lips, tongue and – Short sternum
–
–
buccal mucosa – Rocker bottom feet
–
– The lips are described as ‘ Bumpy Lips’ – Microcephaly
–
–
– Inherited as autosomal dominant. – Prominent occiput
–
–
– Syndrome components – Micrognathia
–
–
Oral mucosal neuromas (hamartomas). – Cardiac and renal malformations
–

Medullary carcinoma of the thyroid. – Mental retardations
–

Pheochromocytoma of the adrenal gland. – 15% cases are lethal in first year
–

 
• Down’s Syndrome • Cat’s Eye Syndrome – Partial trisomy 22
•
•
– Genetic disorder – Coloboma of iris (resembling vertical pupil of cat)
–
–
– Also known as Trisomy 21 (NEET 2013) – Downslanting palpebral fissures
–
–

– Also known as Mongolism – Hypertelorism
–
–
– Brachycephalic skull (AIPG 2004) – Anal atresia
–
–

– Short and flat bridged nose – Congenital heart disease
–
– Renal malformations
–
– Eyes
–
– Skeletal abnormalities
–
Mongoloid slant of palpebral fissures
–
• Turner’s Syndrome (45 X0): (NEET 2013)

Epicanthus
•

Dacryostenosis – Individuals with Turner’s syndrome invariably have
–

Brushfield spots of iris short stature which is probably due to the absence of

Corneal hydrops one copy of a SHOX gene, located on chromosome X

Cataracts and Y, which codes a protein that is predominantly

458
found in bone fibroblasts. – Characterized by hyperelasticity of skin
–
– The genital tract and external genitalia in Turner’s – Hyperextensibilty of joints
–
–
syndrome are female in character, since this is the – Also known as Rubber man
–
default developmental outcome in the absence of – Fragility of skin and oral mucosa
–
testes. Ovarian tissue develops normally until the – Hyperextensibility of tongue
–
third month of gestation but thereafter there is gonadal • Ramsay Hunt’s Syndrome
•
dysgenesis with accelerated degeneration of oocytes – Herpes zoster infection of geniculate ganglion
and increased ovarian stromal fibrosis, resulting in
–
– External involvement and oral mucosal involvement
‘streak ovaries’ This leads to lack of secondary sexual
–
• Fanconi’s Syndrome
characteristics. Breast and uterus are not developed
•
– Characterized by aplastic anaemia
properly.
–
– Microcephaly
– The inability of the ovarian tissue to produce oestrogen
–
– Hypogenitalism
–
results in loss of negative feedback and elevation of
–
– Microcephaly
FSH and LH concentrations.
–
– Olive brown pigmentation
– Diagnosis and management
–
• Pierre-Robin Syndrome (AIPG 2005)
–
The diagnosis of Turner’s syndrome is confirmed
•

– Cleft palate + micrognathia + glossoptosis

by karyotype analysis.
–
Prophylactic gonadectomy is recommended for – Also k/a anomaloid
–
• Melkersson Rosenthal syndrome:(Man 1997, Kar 2009,

individuals with 45XO/45XY mosaicism because
•

there is an increased risk of gonadoblastoma. Comedk 2010)

• Trotter’s Syndrome (AIIMS Nov 2010)(AIPG 2009) – Cheilitis granulomatosis
•

–
– Caused by Nasopharyngeal tumour – Facial paralysis (Bell’s palsy)
–
–
– Characterized by pain in lower jaw, tongue and side – Scrotal tongue (fissured tongue/ lingua plicata)
–
–
of head – Multiple episodes of non pitting, non inflammatory
–
– Middle ear deafness painless edema of face.
–
– Trismus of internal pterygoid ( advanced cases due to • Garderner’s Syndrome (AIPG 1993, AIIMS 1991,
•

–
involvement of mandibular nerve) 1999, AP 2001, 2003, 1999)
• Horner’s Syndrome (AIPG 2006)

– Multiple polyposis of large intestine
•

–
– Occurs due to stellate ganglion block. – Osteomas of bones
–
–
– Stellate ganglion is formed by fusion of lower cervical – Multiple epidermoid/ Sebaceous cysts
–
–
and 1st thoracic ganglion. It is blocked anterior to the – Impacted supernumerary and permanent teeth
–
tubercle of transverse process of C6 (Chassaignac – Occasional desmoid tumours
–
tubercle) vertebra. • Cleidocranial Dysostosis/ Sainton’s Disease
– Consists of
•

(AIPG 2002)
–
Miosis

– Partial or complete absence of clavicles

Ptosis
–
– Delayed closure of fontanelles

Anhydrosis over ipsilateral face and neck upto T3
–
– Wormian bones are common

Absence of pupillary dilatation on shading the eye
–
– The saggital suture is sunken, giving the skull a flat

Flushing
–
appearance

Absence of ciliospinal reflex (dilatation of pupil
– Prolonged retention of primary teeth and delayed

when skin over neck is pinched)
–
eruption of secondary teeth (AIPG 2007)
• CREST Syndrome (AIPG 2012)

– Hyoplasia of maxilla
•

– Calcinosis cutis
–
– Absence or paucity of cellular cementum on roots
–
– Raynaud’s phenomenon
–
of permanent teeth with no increased thickening of
–
– Esophageal dysfunction primary acellular cementum (KAR 2008)
–
– Sclerodactyly

– Numerous unerupted supernumerary teeth, mostly
–
– Telegiectasiasis
–
premolars and incisors. (AIIMS May 2010)
–
• Ehler’s Danlos Syndrome (AIIMS Nov 2010)(AIPG

• Myofacial pain syndrome:
•
2009,AIIMS Nov 2011)
•
– Four cardinal signs are:

–
– Connective tissue disorder Pain
–

– Autosomal Dominant trait Muscle tenderness
–


Clicking or popping noise in TMJ
• Gorlin–Goltz syndrome or Jaw Cyst Basal cell nevus or

•
Limitation of jaw motion unilaterally or bilaterally
Bifid rib syndrome

• Popliteal pterygium syndrome: – Multiple Odontogenic keratocysts (AIPG 2004)
•
–

– Polpiteal webbing (pterygia) – Basal cell CA
–
–
– Cleft lip +/-palate – Bifid rib

–
– Neurologic and ophthalmologic
–
– Genital abnormalities
–
– Sexual abnormalities.
–
– Paramedian lip pits
–
• Hand-Schuller- Christian disease:
–
– Congenital bands connecting upper and lower jaws
•
– Also known as multifocal eosinophilic granuloma.
–
(syngnathia)
–
• Archer syndrome: – Wide spread skeletal and extra skeletal lesions of
–
chronic nature.
•
– Double lip – Proliferating cell is histiocyte.
–
– Non toxic thyroid enlargement
–
– Disease is characterized by punched out multiple
–
– Blepharochalasia (recurring edema of the upper
–
lesions of the skull, exophthalmos and diabetic
–
eyelids leading to sagging of lid at the outer canthus insipidus.
of eye) – Gingivitis, loose and sore teeth with precocious
–
• SAPHO syndrome: exfoliation of teeth, failure of healing of sockets, and
•
– Synovitis loss of supporting alveolar bone mimicking advanced
periodontal disease are important oral manifestation.
–
– Acne
– Letterer- Siwe disease: Acute fulminating skeletal
–
– Pustulosis
–
and extra skeletal lesions.
–
– Hyperostosis
– Eosinophilic granulomas: Only skeletal lesions are
–
– Osteitis
–
present.
–
• Hutchinson Triad: • Hurlers Syndrome:
•
•
– Found in congenital syphilis – It is a disturbance of mucopolysaccharides
–
– Mulberry molars (MOON’s molars or FOURNIER’s
–
metabolism.
–
molars)–occlusal one third of tooth is arranged in an – Chondroitin sulfate b and Heparin sulfate are
–
agglomerate mass of globules (AIPG 1991, 1994) accumulated intracellularly.
– Hutchinson’s incisors – screw driver (AIPG 2011) – “Hurler’s cells” or “clear cells” or “Gorgyle cells” are
–
–
incisors and the mesial and distal surfaces of crown characteristic of this syndrome, which are nothing but
are tapered and incisal edge is usually notched in fibroblasts.
congenital syphilis. – Metachromatic granules or Reilly bodies are
–
• Wallenberg’s syndrome demonstrated in the cytoplasm of circulating
lymphocytes.
•
– Sensational loss on opposite side of the body due – “Claw hands”, broadening of mandible with a
–
to vascular occlusion of posterior cerebellar artery
–
wide intergonial distance, localized areas of bone
affecting V, IX and X cranial nerves. destruction, spaced dentition, gingival hyperplasia
and macroglossia are important features.
• Basal cell nevus syndrome – In addition, metachromatic granules or Reilly bodies
•
– Multiple supernumerary teeth are not found.
–
are often described in the cytoplasm of circulating
–
– Autosomal dominant: Caused by mutation of lymphocytes. (AIPG 2010, 2011)
–

patch (PCTH) – a tumor suppressor gene mapped • Melanotic Neuroectodermal Tumor (AIIMS Nov 2013)
•

by chromosome – 9q22.3-Q31. – This rare tumour occurs in the early months of life,
– It has cutaneous manifestation like basal cell
–
usually in the maxilla.
–
carcinoma, palmar and plantar keratosis, dermal
– The lesion consists of epithelial cells containing
cysts etc.
–
melanin with a fibrous stroma.
– Dental and osseous abnormalities like multiple
– Some localized bone expansion may occur.
–
odontogenic keratocyst, brachycephaly, mandibular
–
prognathism, bifid ribs. – Neural crest origin
–
– Neural abnormalities like mental retardation, dural – The condition is benign and simple excision is
–
curative.
–
calcifications, agenesis of corpus callosum.
– Sexual abnormalities like hypogonadism. – High urinary excretion of vanillyl mandelic acid
–
(AIPG 2008)
–
(VMA) is present.

460
Elevated VMA is also seen in tumours of neural crest origin

•
• Ganglioneuroblastoma
•
• Retinoblastoma
•
• Neuroblastoma
•
Chronic Focal Sclerosing Osteomyelitis (Condensing Osteitis)
Chronic focal sclerosing osteomyelitis is an unusual reaction of bone to infection, occurring in instances of extremely high tissue
resistance or in case of low grade infection
Clinical features • This form of osteomyelitis arises almost exclusively in young persons before the age of 20 years
•
• The tooth most commonly involved is the mandibular first molar, which presents a large carious lesion
•
• There may be no sign and symptom of disease other than mild pain associated with infected pulp
•
Radiographic features • Circumscribed radiopaque mass of sclerotic bone surrounding and extending below the apex of one
•
or both roots
Treatment and Prognosis • May be treated endodontically or extracted since the pulp is infected and the infection has spread past
•
the immediate periapical area
• Surgical removal of the sclerotic lesions should not be attempted unless symptomatic
•
MISCELLANEOUS
Cerebral Palsy
Features • A non progressive lesion which occurs in developing brain before; during and after birth, leaving child
•
with a variety of neurological problems
• 50% children die in infancy
•
• Motor deficit is fully evident only as the child develops
•
Etiology • Decreased oxygenation to developing brain causing damage to brain
•
Classification • Based on anatomical involvement
•
• Monoplegia: Involvement of one limb only
•
• Hemiplagia: Involvement of one side of the body
•
• Paraplegia: Involvement of both legs only
•
• Quadriplegia: Involvement of all four limbs
•
• Based on neuromuscular involvement
•
– Spasticity
–
– Athetosis
–
– Ataxia
–
– Mixed
–
Dental problems • Increased caries rate than normal children
•
• Increased periodontal disease
•
• Children susceptible to trauma esp. maxillary anterior teeth
•
• Excessive drooling and difficulty in swallowing
•
• Malocclusions occur twice often than average population (commonly protrusion of teeth, excessive
•
overjet and overbite, open bite and unilateral cross-bite)
• Persistant neonatal reflexes i.e. asymmetric neck reflex, tonic labrynthine reflex and startle reflex
•
• Mental retardation may be seen with seizures, speech disorders like dysarthia
•
• Spastic palsy patients present with spastic tongue thrust, constricted mandibular and maxillary arches
•
class II div II malocclusion with unilateral cross bite
• Athetoid palsy presents with mouth breathing, tongue protruding between teeth and lips, bruxism, high
•
narrow palate and anterior open bite
• Ataxia palsy presents with staggering gait (lack of balance)
•

Lupus Vulgaris: Primary TB of Skin (AIIMS May Radiographi- • Elongated styloid process on lateral ceph

•
2009) cally and panoramic radiographs
Characteristics • Classic eagle syndrome develops after
– Commonest manifestation of cutaneous tuberculosis
•
tonsillectomy.
–
– Most frequent age group is children and young adults
• Development of scar tissue or
–
– Usually affects only exposed areas of body

•
mineralization of stylohyoid ligament
–
– Face – most common site results in cervicopharyngeal pain in the
–
– Lesion is assymetric region of cranial nerves V, VII, IX, X
–
– Lesion starts as reddish brown macule and enlarges Treatment • Surgical shortening of the styloid process
•
–
slowly over months and years to form big patch with or the mineralized ligament
well defined but irregular margin.
– Diagnostic features are: Hypophosphatasia (AIIMS Nov 2010)
–
Persistent brownish red well defined patch with
• The perinatal form is considered lethal

dermal infiltration
•
• The earliest oral manifestation of disease is loosening
Presence of apple jelly nodules
•
and premature loss of deciduous teeth, chiefly the

On healing a tissue paper like scarring is produced
incisors

in the centre
Match stick test positive: An apple jelly nodule • Dental radiographs generally reveal hypocalcification
•

has no resistace to pressure by a sharp match stick of teeth and the presence of large pulp chambers, as well
Long history expanding over years as alveolar bone loss

Tuberculin test positive • Histologically, teeth reveal decrease in Cementum,

– Military tubercles–biopsy specimen
•
which varies with the severity of the disease. This is
–
– Diagnostic test–biopsy (AIPG 2005) presumably as a result of failure of cementogenesis
–

• Both Erythema multiforme and Steven Jhonson The common factors in all forms of hypophosphatasia
•
syndrome are due to deposition of immune complexes • Reduced levels of the bone, liver and kidney isozyme of
are mediated through type III hypersensitivity reactions.
•
alkaline phosphatase
• Cancerous involvement is seen with syphilitic glossitis • Increased levels of blood and urinary phenothanolamine
•
•
• Aphthous major: periadenitis necrotica recurrens or • Bone abnormalities that resemble rickets
•
Sulton’s disease or Mikulicz’s starring aphthae.
•
• Positive pathergy is an inflammatory reaction within Four Types
•
24 hours of needle puncture, scratch or saline injection
• Perinatal
seen in Behcet’s syndrome (AIPG 2012)
•
• Infantile

•
• Childhood
Eagles Syndrome (AIPG 2008)
•
• Adult
•
Also known as • Stylohyoid syndrome
•
• Carotid artery syndrome
Keratoacanthoma: (AIPG 2009)
•
Etiology • Caused by elongated styloid process
• Self healing carcinoma, molluscum
•
or mineralized stylohyoid ligament which
•
impinges on adjacent structure pseudocarcinomatosum, Molluscum sabaceum,
• Present in 18-40% verrucoma
•
Clinical fea- • Asymptomatic mostly • It is a lesion which both clinically and histologically
•
•
tures (AIPG • Vague pain especially on swallowing, resembles epidermoid carcinoma
•
2005, 2004) turning of head or opening of mouth
• Etiology: genetic and viral factors
• Dysphagia
•
• Twice as frequently in men as in women
•
• Dysphonia
•
• Occur between 50-70 years
•
• Otalgia
•
•
• Dizziness • 90% of tumors occurred on the exposed skin, with the
•
•
• Transient syncope cheeks, nose and dorsum of the hands being most often
•
• Headache involved
•
462
• The lesion occurred on the lips in 8.1% cases, intraoral • Hyperthyroidism: Premature shedding of deciduous teeth
•
•
lesion are quite uncommon and accelerated eruption of teeth
• Treatment is surgical excision • Parulis or pus pocket is an inflammatory enlargement
•
•
seen at the terminus of fistula or sinus tract.
Keratosis Follicularis or Darier’s Disease • In osteosarcoma cumutus cloud densities from within
•
the intermedullary and soft tissue components caused by
• Genodermatome which is transmitted as autosomal
mineralizing tumour osteoid are seen.
•
dominant.
• Cancer which commonly metastasizes to oral mucosa
• It also results from deficient Vit-A metabolism.
•
and jaw bones is lung cancer in men and breast cancer in
•
• The histological picture is characterized by women.
•
hyperkeratosis, papillomatosis, acanthosis and • Common site of metastatic carcinoma in oral cavity is
•
acantholysis. mandibular molar area.
• This acantholytic cells are “corps ronds” and “grains” • According to cofactor model, the combined effects of
•
•
cells. (KAR 2008) numerous agents (herpes virus 8, HIV virus), host factors

and environmental factors encourage Kaposi sarcoma
proliferation.
Systemic Sclerosis–Hidebound Disease
• Connective tissue disorder consisting of vasomotor Common Causes of Angio or Quincke’s Edema
•
disturbances, fibrosis, and atrophy of skin, muscle, and – Allergic angioedema due to mast cell degeneration
–
internal organs. that leads to histamine release seen in IgE mediated
• Clinical features hypersensitivity reactions (AIPG 2001)

– Use of ACE inhibitors which increase the levels of
•
– Mask like appearance of face
–
bradykinin.
–
– Skin yellow, gray, ivory white waxy in nature
– Hereditary in which there is reduction of an
–
– Brown pigmentation
–
inhibitor that prevents the transformation of C1
–
– Stiff tongue
to C1 esterase that cleaves C4 + C2 and results in
–
– Microstomia
angioedema
–
– Dysphagia
– Due to presence of high levels of Ab-Ag complexes
–
– Presence of salivary gland disorder: Sjogren’s
–
(LE patients)
–
syndrome
• Coup de sabre: A linear scleroderma, a band made up of
•
furrow with elevated ridge on one side. Platybasia
• It is also found in facial hemiatrophy or Pary-Romberg • Spinal disease of a malformed relationship between
•
•
Syndrome. occipital bone and cervical spine.
• Characterized by descent of cranium onto the cervical
•
Lesions Associated with Clinically or Radiographically spine due to softened bone at the base of skull–as seen in
Missing teeth (AIIMS 1993, KAR 2000) Paget’s disease.

• Eruption cyst Ectodermal dysplasia: characterized by congenital dysplasia
of ectodermal structures manifested as hypohidrosis (partial
•
• Dentigerous cyst or complete absence of sweat glands) hypotrichosis and
•
• Gorlin cyst hypodontia. (NEET 2013)
•

• Unicystic or mural ameloblastoma • Two types:
•
•
• Adenoameloblastoma – Hypohidrotic (Christ–Siemens–Touraine Syndrome)-
•
–
• Primordial cyst common type with oral manifestations
•
– Hidrotic (Clouston syndrome)–no dental effects
–
Nikolsky’s sign is positive in (AIIMS Nov 11)

Good to Know – Pemphigus
–
– Familial benign chronic pemphigus/hailey hailey
–
• Median mandibular cyst: Multilocular or unilocular well disease
•
circumscribed lesion in the midline of mandible – Recessive dystrophic epidermolysis bullosa
–

• Epidermolysis bullosa occurs due to alteration in structure • In infectious mononucleosis the titre of agglutinin and
•
•
of type VII collagen hemolysin in blood against sheep RBC is raised from 1 : 8
• Monro’s abscesses are seen in psoriasiform of lesions, to 1: 4096 this is known as positive Paul Bunnel test.
• Gustaffon method: Age estimation based on morphology
•
which include Psoriasis, Reiter Syndrome, Benign
•
migratory glossitis and ectopic geographic tongue. and histologically changes such as attrition, resorption,
(AIPG 2005)

secondary dentin deposition etc.

• Central clearing is a feature of Tina corporis, • Parry Romberg syndrome: Facial hemiatrophy
•
investigation of choice is KOH smear
•

(AIPG 2005, 2004)

• Central scarring: Feature of Lupus vulgaris, • Ascher’s syndrome: Acquired double lip +
•
investigation of choice is biopsy
•
Blepharocholosis + non toxic thyroid enlargement
• Central crusting is seen in Leshimainasis, investigated
• LADD syndrome: Lacrimal sac inflammation +
•
by LD body demonstration
•
lacrimal gland aplasia
Also note – Auricles are deformed (cup shaped deformity of
–
• Raynaud’s phenomenon: Due to intense vasospam of ears)
– Dental: Peg shaped teeth, hypodontia and enamel
•
peripheral arteries that result in colour change of finger
–
tips as a response to cold. It is seen in scleroderma and hypoplasia
LE – Digital deformities: Clindactyly
–
• Causalgia manifests as severe pain after injury or
• Timel’s sign–earliest indication of start of nerve
•
sectioning of a peripheral sensory nerve following a
•
regeneration
difficult extraction.
• Pink spot–internal resorption (AIPG 2002)
• Involvement of chorda tympani nerve near its point
•

• Roth spot–SABE, typhoid fever
•
of origin in facial canal is accompanied by paralysis of
•
motor, gustatory and autonomic function of nerve. • Bitot spot–on conjunctiva in vitamin A deficient children
•
• Koebner’s phenomenon is seen in psoriasis
• Dick test, Scultz Charlton test–Scarlet fever
•
• FNAC is indicated to diagnose pemphigus
•
• Rosewalker test–Rh arthritis
•
•
• Kveims test–sarcoidosis
You should know
•
• Tzanck test–pemphigus, herpes simplex
• Scrofula: Tb infection of submaxillary or cervical lymph
•
• Monospot test, paul bunnel test–infectious
•
nodes
•
• Pott’s disease: Tb infection resulting in spinal curvature mononucleosis (Downey’s cells present) (AIPG 2001)
•
(Kyphosis) • Weil–Felix test–Rickettsial infection
•
• Site specificity is seen with recurrent herpes labialis
Anitschow cells ( modified epithelial cells with elongated
•
• Letterer Seiwe Disease: Is a disturbance of histiocytic •
•
nuclei and linear bar of chromatin with radiating process
•
disorder normal serum Ca level – 9-11mg %
of chromatin)–Sickle cell disease, aphthous ulcers, iron
• Casal’s necklace – formation of characteristic skin deficiency anaemia, Rh heart disease (AIIMS May 2009)
•
rash particularly in area exposed to sunlight especially • Arbiskov cells (modified monocytes)–myeloblastoma
in neck region is important feature of Niacin deficiency.
•
• Howell–Jolly bodies + Cabot’s rings–Pernicious anaemia
• Phytic acid which is found in cereals, forms insoluble Ca
•
•
phytate with ingested Ca and renders it non available. • Rushton bodies: (AIPG 2009)
•

• In amyloidosis of tongue, the amyloid is deposited in – Apical periodontal cyst
–
– Infected dentigerous cyst
•
the stromal connective tissue.
–
– Gingival cyst of newborn
• Lingua nigra or lingua villosa–another name of hairy
–
• Fessa bodies: Thalassemia
•
tongue
•
• Test tube bodies: Dilantin hyperplasia
• Idiopathic thrombocytopenia is chracterised by
•
• Saw tooth bodies: Lichen planus (AIPG 2009, 2011)
•
spontaneous hemorrhagic lesions, epistaxis, malena/
•
hematemesis and intracranial hemorrhages that results • Absence of rete pegs: OSMF
in hemiplegia. The platelet count is below 60, 000/ mm3
•
• Rhagades: Congenital syphilis
causing prolonged bleeding time.
•
• Pseudorhagades: Ectodermal dysplasia
•
464
• Regular punched out radiolucent lesions of bone: • Most median clefts of the upper lip actually represent
•
Multiple myeloma (AIPG 2008, 2007)
•
agenesis of the primary palate associated with

• Irregular punched out radiolucent lesions of bone: holoprosencephaly
•
Eosinophilic granuloma
• 2 smaller foramina carrying the nasopalatine nerves
• Punched out lesions of interdental papilla: ANUG
•
–the canals of Scarpa–are found within the incisive
•
• Stomatitis veneata: Allergic reaction due to local foramen
•
application of certain drugs • Erosion from dental exposure to gastric secretion is
• Stomatitis scarltina: Oral manifestation of scarlet fever
•
termed perimolysis
•
• Pseudohorn cysts are seen in Acanthosis nigricans • The black brown extrinsic stains on teeth are not
•

(AIPG 2002, 2010)
•
primarily of bacterial origin but are secondary to

• Tram line calcification (due to bilaminar radio opaque formation of ferric sulphide from an interaction
•
tracks) are seen in hemangioma between bacterial hydrogen sulfide and iron in the
saliva or GCF
• Greenspan lesion: Hairy leukoplakia
• A pink or red discoloration of maxillary incisors have
•
• Ghost cells are seen in odontoma and
•
been seen in lepromatous leprosy
•
craniopharyngioma, ameloblastic fibro odontoma amd
• Accessory fourth molars: Distodens or distomolars
CEOC
•
• Paramolar: Posterior supernumerary tooth situated
• Abnormal DEJ is seen in dentinogerous imperfecta and •
lingually/ bucally to a molar tooth
•
Ehler’s Danlos syndrome
• Protostylid: Analogous accessory cusp to cusp of
• Teeth commonly involved in turner’s hypoplasia–
•
Carabelli on mesio buccal cusp of mandibular molar
•
mandibular premolar > maxillary incisors
• Progeria: Condition associated with accelerated aging.

(AIPG 2009, 2011)
•
More secondary dentin is seen

• Acute adrenal cortical insufficiency–Waterhouse
• With age, pulp chambers decrease significantly in
•
Friderichsen syndrome
•
height but not width
• A periapical granuloma without cystic transformation
•
– Bay cyst
• Chronic tendon periostitis: Reactive hyperplasia of bone
• Cambium layer is seen in alveolar rhabdomyosarcoma
•
that is initiated and exacerbated by chronic overuse of
•
• Increased lateral spread of a carious lesion at the DEJ is masticatory muscles (massetor and digastrics)
•
probably due to increased amounts of organic matter in • Stratum germinativum is absent in epithelial lining of the
this region
•
cyst.
• Median anterior maxillary cyst or nasopalatine cyst–most
• Ulceration of the oropharynx and oral mucosal surface is
•
common type of developmental maxillary cyst
•
often an early sign of sensitivity to penicillin • Most common metastatising tumour in children to bones
• The routine radiographic survey may provide the initial
•
–Neuroblastoma
•
evidence of Albers-Schonberg disease primarily because • Most common malignant bone tumour in children–
the bone pattern is exceedingly dense with loss of
•
Ewing’s sarcoma
trabecular spaces.
• Hairy leukoplakia–no premalignant potential
• A subnormal temperature is common in aniline
•
• Plasintex is given for treatment of OSMF in hypertension
•
intoxication, myxedema and syncope.
•
and diabetic patients
• The most common extra oral cause of halitosis is chronic
• Blind spots in oral cavity (where carcinomatous
•
sinusitis with post nasal drip.
•
• Dryness of skin is common in ectodermal dysplasia + lesions are not visible)
•
hypothyroidism + Senile syndrome – Posterior 1/3rd of tongue
–
• Presence of Herbenden’s nodes is indicated by swelling – Retromolar trigone
–
•
of terminal finger points is most characteristic of – Gingivolabial sulcus
–
osteoarthritis • The hemangioendothelioma and hemangiopericytoma
•
• The lateral nasal processes are not involved in the are quasi malignant neoplasms of vascular endothelium
•
formation of upper lip but they rise to the alae of the nose and vascular pericytes respectively. (AIPG 2008)


• Lympho epithelioma: common site – nasopharynx • Juvenile hemangioendothelioma is believed to be in
•
mature stage of hemangioma because of excessive
•
• Rhinosporidium seebri: Fungi has predilection for cellularity and its occurrence during early life
•
blood vessels and is able to penetrate their walls and • The cementum in cemento ossifying fibroma is seen
•
produce thrombosis in H/E stain as basophilic amorphous round calcified

• Mucormycosis: Triad of structure
•
– Uncontrolled diabetes • The vitamin most commonly deficient in children who do
•
not drink milk is riboflavin
–
– Orbital infection
• Subcorneal pustular mucositis is a histologic feature of
–
– Meningoencephalitis
•
geographic tongue
–
• Toxic epidermal neurolysis (Lyell’s disease) is very serious, • Angiolymphoid hyperplasia with eosinophilia is known
•
as Kimmura’s disease
•
often fatal form of erythema multiforme
• Parakeratin plugging is a hallmark of verrucous carcinoma
• Marcus: Gunn phenomenon is characteristic of Jaw
•
• Lane tumour: Also known as spindle cell carcinoma
•
winking syndrome (AIPG 2009)
•
• Histiocytosis Y: Verruciform xanthoma

• Petechial hemorrhages at the junction of soft and hard
•
• Desquamation of epithelium is the clinical termination of
•
palate–early manifestations of infectious mononucleosis
•
scarlet fever
• Pemphigus follaceous: Also known as Brazilian wild fire • Small pox/ variola was declared eradicated by WHO on
•
•
• ‘Checker board’ histologic appearance of chromatin may 8, 1980
•
clumping is seen in plasmacytoma • Steely/Kinky hair syndrome or Menke’s syndrome is
•
associated with copper deficiency
• Bull’s eye: Radiographically is diagnostic of lingual • Trummerfled zone is seen in vitamin C deficiency
•
impaction
•
• Caffey’s disease: Infantile cortical hyperostosis
• Brachycephalic with flat occipit: Down’s syndrome
•
• Generalized cortical hyperostosis: Von Buchem
•
• Brachycephalic with narrow foramen magnum:
•
syndrome
•
achondroplasia
• Dilapidated brick wall effect: Hailey Hailey disease
• Orthodontic treatment is contraindicated in Marfan’s
•
• Duchenne is the most common form of muscular
•
syndrome patients
•
dystrophy
• Mouse eaten furrowed ulcer: Oral tb lesion
• Modified carlson crittenden cup is used to determine the
•
• Moth eaten appearance: Chronic osteomyelitis
•
rate of salivary flow
•
• Every’s syndrome: Associated with erupting 3rd molar
• Occlusal abnormalities and macroglossia may be seen in
•
• Wart (verruca vulgaris): Church spiral effect
•
myotonic dystrophy
•
• Pytriasis rosea: primary lesion – herald spot occurs • Weber cockyam syndrome: Localized EB simplex
•
•
seasonally being far more common in spring and • EB junctional: Most lethal
•
autumn than other times • EB dystrophic, recessive: Dental defects
•
• Chloasma or melasma: Hyperpigmentation of oral • Diascopy is used in hemangioma
•
•
cavity in pregnant ladies (AIPG 2010) • Joint effusion is best seen in T2 weighted MRI

•
• Most rapidly metastasing tumour: African burkitt jaw • The most common organism causing septic arthritis in
•
•
lymphoma previously normal TMJ is gonococci
• Chemodectomas are glomus tumour in aortic or carotid
•
• Amalgam tattoo: Most common oral pigmented lesion bodies
•
• Midline granuloma: Destructive necrotizing midfacial • A sudden onset of large flat painful ulcers on oral mucosa
•
and lips and latter present with black encrustation –
•
phenomenon that chronically mimics lesions of wegener’s
erythema multiforme
granulomatosis. Perforation of the hard palate may be seen
• Paradental cyst (buccal bifurcation cyst): mandibular 1st
• Cutaneous counterpart of CEOC is known as calcifying
•
molar most common in children, mandibular 3rd molar
•
epithelioma of Malherbe or pilomatrixoma most common in adults
• Connation is the union between the dentin and/or enamel • Compound odontome: Tooth like–anterior jaw
•
•
of 2 or more separate developing teeth • Complex odontome: Irregular mass–posterior jaw
•
466
Most Common in HIV/AIDS

Infection Pneumocystis carinii
Fungal infection Pneumocystis carinii

Fungal infection of oral cavity (AIIMS Nov 2012) Candida albicans

Bacterial infection Mycobacterium avium complex
Bacterial infection in India Mycobacterium tuberculosis
Malignancy Kaposi sarcoma (AIPG 2009)

Accessory Cusps
• Cusp of carabelli: Most common, palatal surface of mesiolingual cusp of maxillary molar
•
• Talon cusp: Lingual surface of maxillary incisor or canine teeth
•
• Doak’s cusp: Accessory cusp on the buccal surface of molars
•
• Dens evaginatus: Accessory cusp coming from the central groove of premolar teeth.
•
Discolorations and Pigmentations
Addisons Disease • Bronze discolorations of the oral mucosa (AIPG 2008)
•

Blue sclera(AIPG 2006) • Osteopetrosis
•
• Fetal rickets
•
• Turner syndrome
•
• Paget’s syndrome
•
• Marfan syndrome
•
• Ehler’s syndrome
•
• Normal infants
•
• Osteogenesis imperfecta
•

(AIPG 2008)

Café – au-lait spots • Neurofibromatosis
•
• Albright’s syndrome
•
• Nevoid basal cell carcinoma
•
• Cowden syndrome
•
• Tuberous sclerosis
•
• Ataxia telangiectasia
•
• Gaucher’s syndrome
•
Peutz Jegher’s syn- • Characteristic circumoral pigmentation
•
drome
Lesions
Macules • Well circumscribed, flat lesions that are inflamed or pigmented
•
Papules • Solid lesion of <1cm in diameter that are raised above skin. Seen in:
•
– Erythema multiforme
–
– Rubella
–
– LE
–
– Sarcoidosis
–
– Darier’s disease
–

Plaques • Large papules >1cm in diameter
•
Vesicles • Elevated blister like lesions that contain clear fluid and < 1cm in diameter
•
Bullae • Large vesicles that >1cm in diameter
•
Pustules • Elevated lesions containing purulent material
•
Cellulitis (Phlegmon): (AIPG 2009, 2011)
• Diffuse inflammation of the soft tissues which are not circumscribed or confined to one area, but which in contradistinction
•
to the abscess, tend to spread through tissue spaces and along fascial spaces.
• Spreading factors of Duran- Reynals
•
– Streptokinase (AIPG 02, MP 09)
–

– Hyaluronidase: (AIIMS 2K)
–

– Fibrinolysin
–
• Streptococci produce hyaluronidase and common causative organisms than the staph.
•
– Clinical appearance-Orange peel appearance.
–
Tooth Pigmentation
Yellow brown black which show fluorescences under UV light Tetracycline (AIPG 2004,2008)

Pink Internal Resorption
Yellow , green Eryhroblastosis Fetalis

Red brown Porphyria
Green stain Due to enamel cuticle or Nasmyth membrane
Orange stain By pigment producing microorganism
Mesenteric line Brown stain at cervical 3rd, in children who are immune to caries
PSEUDOMEMBRANE FORMATION IS SEEN

ANUG Pseudomembrane can be easily removable
Syphilis Pseudomembrane is undetachable
Diphtheria and Vincent’s angina Difficult to remove
Candidiasis Pseudomembrane can be removable
Erythema multiforme
Some Points on Different Types of Cells

Cell type Nature Disease
Tzanck cells Clumps of epithelial cells Pemphigus vulgaris
Herpes simplex
Angulate body cell Cell intermediate between undifferentiated Granular cell myoblastoma
mesenchymal cell and mature granular cell
Reed- sternberg cell (AIPG 2005) B–lymphocytes (or) Macrophage moncyte Hodgkins disease

derivative
Clear or Gargoyle cell (or) Hurler cell Fibroblasts Hurler’s syndrome
468
Cell type Nature Disease

Lacunar cells B –lymphocytes Nodular sclerosis type of hodgkin’s disease
LE cells Rossete of neutrophils. Pale nuclear mass Systemic lupus erythematosis

derived from lymphocyte
Strap of ribbon or racquet cells Spindle cells Rhabdomyosarcoma
Arbikosov cells Monocytes Myeloblastoma
Antischkow/cells Epithelial cells – Apthous ulcer
–
– Sickle cell disease
–
– Iron deficiency anemia
–
Ghost cells – Compound odontomas
–
– Ameloblastic fibro odontoma
–
– Craniopharyngioma
–
– Calcifying epithelial cyst
–
Hyaline cells Modifies myoepithelial cells Pleomorphic adenoma
Target cells RBC (form cells) Thalassemia
Safety pin cells Normoblasts Thalassemia
• Microcherry (Glomerules or venous like) appearance–Haemangioma

•
• Cauliflower likes–Papilloma
•
• Nicolsky’s sign
•
If non ulcerated gingiva are massaged, epithelium readily strips from connective tissue to leave raw sensitive surface, which
bleeds readily. Seen in
• Pemphigus
•
• Chronic desquamative gingivitis\
•
• Hailey-Hailey disease
•
• Epidermolysis bullosa
•
– Parrot’s beak like nose
–
Craniofacial dysostosis

Syphilis: Congenital

– Angle face: Cherubism
–
Petrified man: Generalized myositis ossificans (stiffness of organs)

Rubber man: Ehler’s-Danlos syndrome

Histological Features
Honey comb appearance (Swiss cheese and pattern): Adenoid cystic carcinoma
Pickets fence (Tomb stone) Primordial cyst, Odontogenic keratocyst
Starry sky (Macrophages scattered through tumor) Burkitt’s lymphoma. (AIPG 2001)

Cart wheel (or) Checker board pattern Multiple myeloma, pernicious anemia
C- shaped (or) Chinese character Shaped arrangement of trabeculae: Monostotic fibrous dysplasia
central ossifying fibroma of bone
Mosaic pattern of bone formation Paget’s disease (bilateral), Chronic sclerosing osteomyelitis
(unilateral) (AIPG 2009,AIPG 2011)

Jigsaw puzzle appearance of bone Resorption and formation of bone – Paget’s disease.
Saw tooth retepegs Lichen planus

Honey comb appearance (Swiss cheese and pattern): Adenoid cystic carcinoma
Micro abscess (Monr’s abscess) Psoriasiform lesions
Juxta epithelial hyalinization Oral submucous fibrosis, Ameloblastic fibroma
Microcyst formation • Acinic cell carcinoma

•
• Muco epidermoid carcinoma
•
• Neurilemmoma (antony- B type)
•
• Sq. Odontogenic tumor
•
Perineural spread • Mucoepidermoid carcinoma
•
• Kerato acanthoma
•
• Adenoid cystic carcinoma (cylindroma)
•
Haemosiderin pigment formation • Peripheral giant cell granuloma
•
• Central giant cell granuloma
•
• Aneurysmal bone cyst
•
Pseudo epitheliomatous formation • Blastomycosis
•
••
Granular Cell myeloblastosis
• DLE
•
• Sq. cell carcinoma
•
• Papillary hyperplasia
•
Keratin plugging formation • Fordyce granules
•
• Verrucous carcinoma
•
• Kerato acanthoma
•
• Verrucous xanthoma
•
• DLE
•
Stag horn pattern (AIPG 2009) • Hemangiopericytoma

•
Hemangiopericytoma
• Tumor to be derived from pericytes.
•
• Consists of numerous vascular channels with plump endothelial nuclei and a surrounding, tightly packed proliferation of
•
oval and spindle cells, hyperchromatic nuclei and a moderate amount of cytoplasm.
• The cells have indistinct cytoplasmic borders.
•
• The tumor cells do not arise from endothelial cells even though they surround irregular vascular spaces. The branching
•
vascular channels of varying sizes are often described as a Staghorn Pattern.
• Older less aggressive lesions tend to have less cellularity and may have a largely mucoid interstitial appearance, which can
•
be mistaken for myxoid lipoma or myxoid liposarcoma.
Specific bodies
• Verrucay bodies (Hyaline bodies) Neurolemmoma/ (Antony B- type schwannoma)

•
• Russel bodies immature plasma cells unable to produce Seen in chronic inflammatory diseases multiple myeloma and
•
antibodies commonly periapical granuloma
• Rushton bodies (commonly seen in odontogenic cysts of lining Indicated inflammation of cystic epithelium
•
epithelium)
• Asteroid bodies Spirotrichosis

•
• Relly bodies found in lymphocytes Hurler’s syndrome
•
• Clvatte/ hyaline or colloid bodies/ cytold bodies Lichen planus
•
470
Specific bodies
• Hinge bodies Thalassemia

•
• Negribodies Rabies (virus)
•
• Guarnier bodies Small pox

•
• Lipschultz bodies: eosinophilic ovoid, homogenous material Primary herpetic stomatitis
•
which displace nucleus and nuclear chromatin peripherally
• Howell–jolly bodies Pernicious anaemia

•
• Henderson paterson inclusions (Simply Molluscum bodies) Molluscum contagiosum
•
• Domle bodies Chediak Higashi syndrome
•
CHAPTER 11
Complete Dentures
Objectives
• Introduction • Occlusion

• Mental Attitude of Patients • Processing of Dentures

• Anatomical Landmarks in the Maxilla • Masticatory Efficiency

• Anatomical Landmarks in the Mandible • Oral Hygiene in a Complete Denture Patient

• Impression Making • Problems Associated with Complete Dentures

• Determinants of Mandibular Movements – Denture Stomatitis

– Benett Movement – Burning Mouth Syndrome (BMS)

– Chewing Cycle – Gagging

– Face-bow – Combination Syndrome

• Vertical Jaw Relation – Residual Ridge Resorption (RRR)

• Horizontal Jaw Relation • Relining

• Articulators • Tissue Conditioners

• Denture Teeth • Miscellaneous

INTRODUCTION
• Complete denture prosthodontics or Full denture prosthetics is defined as “The replacement of the natural teeth in the
•
arch and their associated parts by artificial substitutes”
– It can also be defined as “The art and science of the restoration of an edentulous mouth”.
–
– Complete denture is defined as “ A dental prosthesis which replaces the entire dentition and associated structures of
–
the maxilla and mandible”
• It can be classified as:
•
– Removable complete dentures
–
– Fixed complete dentures
–
• Parts of a Complete Denture:
•
– Denture base. – Denture flange.

– Denture border. – Denture teeth

472
• Surfaces of A Complete Denture

•
Impression surface (Intaglio That portion of the denture surface which has its contour determined by the impression
surface)
Polished surface (Cameo surface) This surface refers to the external surfaces of the lingual, buccal, labial flanges and the external
palatal surface of the denture. This surface should be well polished and smooth to avoid collection
of food debris.
Occlusal surface This surface refers to the occlusal surface of the denture teeth. It resembles the natural teeth and
usually contains cusps and sluice ways to aid in mastication.
COMPLETE DENTURES
MENTAL ATTITUDE OF PATIENTS (HOUSE’S CLASSIFICATION)

Dr. MM House in 1950 classified patient’s psychology into four types
Class I: Philosophi- • Those who have presented themselves prior to the extraction of their teeth, have had no experience in wearing
•
cal dentures, and do not anticipate any special difficulties in that regard.
• Those who have worn satisfactory dentures, are in good health, are a well-balanced type, and are in need of
•
further denture service.
• Generally they can be described as easygoing, congenial, mentally well adjusted, cooperative and confident
•
of the dentist.
• These patients have excellent prognosis
•
Class II: Exacting • Those who, while suffering from ill health, are seriously concerned about appearance and efficiency of artificial
•
dentures.
• They are reluctant to accept the advice of the physician and the dentist and are unwilling to submit to the
•
removal of their artificial teeth
• These patients are precise, above average in intelligence, concerned in their dress and appearance, usually
•
dissatisfied by their previous treatment, do not have confidence in the dentist. It is very difficult to satisfy
them. But once satisfied they become the dentist’s greatest supporter.
Class III: Hysterical • Those in bad health with long neglected pathological mouth conditions and who are positive in their minds
•
that they can never wear dentures. They are emotionally unstable and tend to complain without justification
• These patients do not want to have any treatment done. They come out of compulsion from their relatives
•
and friends.
• They have a highly negative attitude to the dentist and the treatment. They have unrealistic expectations
•
and want the dentures to be better than their natural teeth. They are the most difficult patients to manage.
They show poor prognosis.
Class IV: Indifferent • Those who are unconcerned about their appearance and feel very little or no necessity for teeth for mastication.
•
• They are, therefore uncooperative and will hardly try to become accustomed to dentures. They will not
•
maintain the dentures properly and do not appreciate the efforts and skills of the dentist.
ANATOMICAL LANDMARKS
Maxilla Manible
Limiting Structures • Labial frenum • Labial frenum.
•
•
• Labial vestibule • Labial vestibule.
•
•
• Buccal frenum • Buccal frenum.
•
•
• Buccal vestibule • Buccal vestibule.
•
•
• Hamular notch • Lingual frenum.
•
•
• Posterior palatal seal area. • Alveololingual sulcus.
•
•
• Retromolar pads.
•
• Pterygomandibular raphe.
•
Complete Dentures 473

Maxilla Manible
Supporting • Primary stress-bearing areas: – Buccal shelf area
•
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Structures – Hard palate (Jacobson and Krol) – Residual alveolar ridge
 
–
–
 
– The postero-lateral slopes of the residual alveolar
–
 
ridge
 
• Secondary stress-bearing areas:
•
 
– Rugae
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– Maxillary tuberosity, alveolar tubercle.
–
Relief Areas • Incisive papilla • Crest of the residual alveolar ridge.
•
•
• Cuspid eminence • Mental foramen.
COMPLETE DENTURES
•
•
• Mid-palatine raphe • Genial tubercles
•
•
• Fovea palatina. • Torus mandibularis.
•
 
•
Buccal Frenum • The buccal frenum separates the labial and buccal vestibule. It has attachments of the following muscles,
•
 
– Levator anguli: Attaches beneath the frenum
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– Orbicularis oris: Pulls the frenum in a forward direction.
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– Buccinator: Pulls the frenum in the backward direction.
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• These muscles influence the position of the buccal frenum hence it needs greater (wider and relatively
•
shallower) clearance on the buccal flange of the denture
Buccal Vestibule • It extends from the buccal frenum anteriorly to the hamular notch posteriorly. The size of the buccal vestibule
•
 
varies with the
– Contraction of buccinator
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– Position of the mandible
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– Amount of bone loss in the maxilla
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Posterior Palatal Seal • It is defined as “ The soft tissues at or along the junction of the hard and soft palates on which pressure within
•
Area (Postdam) the physiological limits of the tissues can be applied by a denture to aid in the retention of the denture.”-
• This is the area of the soft palate that contacts the posterior surfaces of the denture base.
•
• Functions
•
– Aids in retention by maintaining constant contact with the soft palate during functional movements like
–
speech, mastication and deglutition. (AIPG 2006)

– Reduces the tendency for gag reflex as it prevents the formation of the gap between the denture base
–
and the soft palate during functional movements.
– Prevents food accumulation between the posterior border of the denture and the soft palate.
–

(AIPG 2008)

– Compensates for polymerization shrinkage.
–
Posterior Palatal Seal
• The posterior palatal seal area can be divided into two regions based upon anatomical landmarks, namely:
•
– Pterygomaxillary seal
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– Postpalatal seal.
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• Recording the Posterior Palatal Seal
•
– The methods used to mark the postdam are:
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Conventional approach.

Fluid wax technique.

 
Arbitrary scraping of the master cast.

Extended palatal technique (Silverman proposed that the posterior border of the denture can be extended by 8 mm

for patients with class I soft palate. But, this is not accepted now).
Pterygomaxillary Seal
• This is the part of the posterior palatal seal that extends across the hamular notch and it extends 3 to 4 mm anterolaterally
•
to end in the mucogingival junction on the posterior part of the maxillary ridge.
474
• The hamular notch is located between the maxillary mucous glands. This acts as a guide to locate the posterior
border of the denture. (AIIMS Nov 11)
•
tuberosity and the hamular process of the sphenoid
 

bone. It contains loose connective tissue and few fibres • This line should lie on the soft palate. (AIPG 2012)
•

of Tensor Veli Palatini muscle covered by a thin layer of • The distal end of the denture must cover the tuberosities
•
 
mucous membrane. and extend into the hamular notches. It should end 1-2
• The position of this membrane changes with mouth mm posterior to the vibrating line. Another school of
 
•
opening hence it should be recorded accurately during thought considers the presence of two vibrating lines
impression making .The posterior extent of the denture namely:
in this region should end in the hamular notch and – Anterior vibrating line.
–
not extend over the hamular process as this can lead to – Posterior vibrating line.
–
COMPLETE DENTURES
severe pain during denture wear

Anterior vibrating line Posterior vibrating line
• It is an imaginary line lying • It is an imaginary line
Good to know
•
•
at the junction between the located at the junction of
• The posterior border of the denture should not be immovable tissues over the the soft palate that shows
•
placed over the mid-palatine raphe or the posterior hard palate and the slightly limited movement and
nasal spine. movable tissues of the soft the soft palate that shows
palate marked movement.
• If there is a palatine torus, which extends posteriorly so

(AIPG 2006) (AIPG 2008) • It also represents the
•
that it interferes with the posterior palatal seal, then the
•
• It can be located by asking junction between the
tori should be removed. (AIPG 2004) aponeurosis of the tensor
•
the patient to perform the

• The position of the fovea palatina also influences the “Valsalva” maneuver. veli palatini muscle and the
•
position of the posterior border of the denture. The muscular portion of the soft
• It can also be measured by
palate.
denture can extend 1-2 mm across the fovea palatine
•
asking the patient to say
• If a mid-palatine fissure is present, then the posterior “ah” in short vigorous bursts. • It is recorded by asking the
•
(Valsalva maneuver: the patient to say “ah’ in short
•
palatal seal should extend in to it to obtain a good patient is asked to close his but normal non- vigorous
peripheral seal. nostrils firmly and gently blow fashion. This line is usually
• In patients with thick ropy saliva, the fovea palatina through his nose). straight.
•
should be left uncovered or else the thick saliva flowing • The anterior vibrating line is
•
between the tissue and the denture can increase the cupid’s bow-shaped.
hydrostatic pressure and displace the denture.
Retro-mylohyoid Fossa
• It belongs to the posterior part of the alveololingual
Post Palatal Seal
•
sulcus. It lies posterior to the mylohyoid muscle
Class Type of soft palate Posterior palatal • This fossa is bounded:
•
 
seal – Anteriorly by the retromylohyoid curtain
–
I Soft palace is horizontal and Broad – Posterolaterally by the superior constrictor of the
extends posteriorly with minimal
–
muscular activity
pharynx
II Palatal contour is between class Medium – Posteromedially by the palatoglossus and lateral
–
I and III surface of the tongue
 
III Most acute contour usually seen Very narrow – Inferiorly by the submandibular gland.
with a high v-shaped palatal
–
vault
• Pterygomandibular raphae is the tendinous insertion
•
of superior constrictor and buccinator. It arises from the
hamular process of medial pterygoid and gets attached
Vibrating Line to the mylohyoid ridge. (AIPG 2002)

• It is an imaginary line drawn across the palate that marks
•
the beginning of motion in the soft palate, when the Also Note
individual says “ah”. • The lingual vestibule is divided into three areas; the anterior
•
• It extends from one hamular notch to the other. lingual vestibule (sublingual crescent area), the middle
•
• It passes about 2 mm in front of the fovea palatina. The vestibule, called the mylohyoid area; and the distolingual
•
fovea is formed by coalescence of the ducts of several vestibule (lateral throat from or retromylohyoid curtain).

• The distal end of the alvelo-lingual sulcus is called • The lateral throat form, also known as retromylohyoid
•
•
retromylohyoid curtain. This is a curtain of , mucous fossa, is the area situated at the distal end of the alveolingual
membrance in the floor of the mouth. It is situated between sulcus. This area is bounded anteriorly by mylohyoid ridge
and respective mylohyoid muscle palatoglossus muscle
the anterior pillar of the fauces and the pterygomandibular and medially by tongue.
fold.
• To obtain a better peripheral seal in the mandibular
• The posterolateral portion of the retromylohyoid
•
complete denture, the distolingual flange should be
•
curtain overlies the superior constrictor muscle, and the extended to include this space with proper length and
posteromedial portion covers the palatoglossal muscle. thickness. (AIPG 2001)

Muscle having dual function in relation to complete denture Masseter
COMPLETE DENTURES
Buccal frenum of maxilla contains Caninus (levator anguli oris), buccinator (pulls frenum backward),
orbicularis oris (Pulls frenum forwards)
Buccal frenum of mandible contains Triangularis (depressor anguli oris)

Buccinator
Labial frenum of mandible contains Incisive
Distobuccal flange of the mandibular denture is limited by Masseter (AIPG 2004, 2012)

Retromolar pad contains the fibres of Tempolaris
Buccinator
Superior constrictor
Pterygomandibular raphae
The lingual flange of lower denture is limited Genioglossus

• In the anterior region by Mylohyoid
•
• In the middle region by Palatoglossus and superior constrictor (AIPG 2004)

•
• In the posterior region by
•
Masseteric notch is formed due to Action of masseter on buccinator
IMPRESSION MAKING
Classification
Depending on the • Mucostatic or passive impression. (Richardson and henry Page)
•
theories of impres- – The impression is made with the oral mucous membrane and the jaws in a normal, relaxed condition.
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sion making: – Border moulding is not done here.
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– Oversized tray is used
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– Impression material of choice is impression plaster. Retention is mainly due to interfacial surface tension.
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– The mucostatic technique results in a denture, which is closely adapted to the mucosa of the denture-
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bearing area but has poor peripheral seal.
• Mucocompressive or functional impression. (Carole Jones)
•
– Records the oral tissues in a functional and displaced form.
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– The materials used for this technique include impression compound, waxes and soft liners.
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– The oral soft tissues are resilient and thus tend to return to their anatomical position once the forces are
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relieved.
– Dentures made by this technique tend to get displaced due to the tissue rebound at rest.
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– During function, the constant pressure exerted onto the soft tissues limit the blood circulation leading to
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residual ridge resorption.
• Selective pressure impression. (Boucher)
•
– The impression is made to extend over as much denture-bearing area as possible without interfering with
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the limiting structures at function and rest.
– Confines the forces acting on the denture to the stress-bearing areas.
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– This is achieved through the design of the special tray in which the nonstress-bearing areas are relieved and
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the stress-bearing areas are allowed to come in contact with the tray
– Relief is given using wax in the special tray, which should be removed before impression making.
–
476
Depending on the • Open-mouth technique.
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technique • Closed-mouth technique.
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• Hand manipulation for functional movements (Dynamic impression): Border moulding.
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Depending on the • Stock tray impression.
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type of tray • Custom tray impression.
•
Depending on the • Diagnostic impression.
•
purpose of the • Primary impression.
•
 
impression • Secondary impression.
•
COMPLETE DENTURES
Principles of Impression Making
• An impression should be made with the purpose of obtaining the following characteristics in the dentures to be
•
fabricated.
 
– Retention
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– Stability
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– Support
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– Aesthetics
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– Preservation of remaining structures
–
Retention Stability
• Retention is the ability of the denture to withstand displacement • Stability is the ability of the denture to withstand horizontal
•
•
against its path of insertion. forces. (AIPG 2005)

• The factors that affect retention can be classified as: • The various factors affecting stability are:
•
 
 
•
– Anatomical factors. – Vertical height of the residual ridge.
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– Physiological factors. – Quality of soft tissue covering the ridge.
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– Physical factors. – Quality of the impression.
–
–
 
– Mechanical factors. – Occlusal rims.
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– Muscular factors. – Arrangement of teeth.
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– Atmospheric pressure is referred to as emergency retentive – Contour of the polished surfaces
–
–
force or temporary restraining force. It is 14.7 lb/inch2. Only
effective if peripheral seal is present.
Beading and Boxing

• The main function of boxing is to preserve the integrity, extension and thickness of impression borders. The purpose of
•
the boxing is to provide a proper size base without inverting the impression. (AIPG 2006)

• The minimal height of the base is ½ in (12.5-15 mm).
•
• The master cast should preserve the exact anatomic details of the residual ridge. Hence care should be taken to preserve
•
the width and depth of the sulcus. This is achieved by beading and boxing (in some textbooks entire procedure is given as
boxing).
• In specific- Beading is done to preserve the width and height of the sulcus in the cast. Boxing is done to obtain a uniform
•
smooth well-shaped base for the cast
• Beading waxes are blue in colour while boxing waxes are white in colour.
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Separating Medium
• Cold Mould Seal: Cold mould seal is the most commonly used separating medium. It is basically an aqueous solution of
•
 
sodium alginate.

• Composition • Soluble sodium alginate reacts with calcium present in
•
•
– Sodium alginate (2% in water) the cast to form insoluble calcium alginate. Waxes or oils
remaining on the cast should be removed before applying
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– Glycerin
the separating medium. The cast should be warm but
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– Alcohol
not hot as it may break the continuity of the separating
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– Sodium phosphate medium. The separating medium should be applied with
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– Preservatives a brush using single-sided strokes.
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DETERMINANTS OF MANDIBULAR MOVEMENTS
Condylar guidance • The path of movement taken by the condyle in the glenoid fossa.
•
COMPLETE DENTURES
• The slope of the glenoid fossa is not straight, instead it is a ‘S’ bend. Hence the condyle also moves along a
•
‘S’ shaped path. This shape of the glenoid fossa, which determines the path of movement of the condyle, is
called the condylar guidance.
• The condylar guidance can be measured using a protrusive interocclusal record
•
Incisal guidance • When the mandible is brought forward (protrusion), the incisal edge of the lower anteriors slide along the slope
•
of the lingual surface of the upper anterior teeth before reaching edge to edge contact.
• The slopes of the lingual surface of the upper anterior teeth determine the path along which the mandible
•
moves during protrusive movement. In other words, the lingual surface of the maxillary anteriors guide the
mandible during protrusive movement and is called the Incisal guidance
• The angle formed between the long axis of the upper and lower anteriors is called the incisal guide angle.
•
• Absent in a completely edentulous patient. It is reproduced in the complete denture by arbitrarily setting the
•
anteriors using a standard incisal guide value and modifying them to suit the patient during aesthetic anterior
try-in.
Neuromuscular • The muscles of mastication are the most important determinants of mandibular movements
•
factors
Bennett Movement Bennett movement. (AIPG 2005)

• This shift is not associated with laterotrusion and may
• It is the bodily side shift (lateral translation) of the
•
occur before or along with laterotrusion
•
mandible which, when it occurs may be recorded in the
region of the translating condyle of the non-working • This lateral translatory motion is measured against time,
•
which is considered as the fourth dimension of mandibular
side. (AIPG 2003)
movements. Bennett movement can be classified based on

• During lateral movement, the mandible shifts (as a whole) the time at which they occur in relation to laterotrusion.
•
by 1 to 4 mm towards the working side. This shift is called
• Bennett movement is classified based on the timing of the shift in relation to the forward movement of the nonworking
•
condyle
– Immediate side shift: Lateral translation occurs before forward movement of the non-working condyle
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– Precurrent side shift: Major quotient of the lateral translation occurs during the first 2-3 mm of forward movement
–
of the non-working condyle
– Progressive side shift or Bennett side shift: Lateral translation that continues linearly after 2-3 mm of forward
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movement of the non-working condyle
• Bennet angle is formed between the path of non working • Border movement recorded in:
•
condyle and the saggital plane. It is about 7.5 – 12.80.
•
– Horizontal plane – diamond tracing
bennet angle (L) = H/8 + 12 (H = horizontal condylar
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– Sagittal plane – beak tracing
inclination)
–
– Vertical plane – shield tracing
• Bennet shift–working side condyle
–
– Combination of three – envelop of motion
•
–
• Bennet shift=2-3 mm – Chewing cycle – tear drop tracing
•
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478
Envelope of Motion
– When we combine the border movements of all the three planes, we get a three-dimensional space within which
–
mandibular movement is possible. This three-dimensional limiting space is called the envelope of motion
– It was first described by Posselt in 1952. The envelope of motion is longest and widest superiorly and narrows down to a
–
point near the maximum mouth opening (MMO) position. Hence, as the jaw separation increases, space for movement
decreases to a zero at the maximum mouth opening (MMO) position
Chewing Cycle
Preparatory phase • In this phase the tongue positions the food within the oral cavity and the mandible deviates towards the
•
 
chewing side.
COMPLETE DENTURES
Food contact • This is a phase of momentary hesitation in movement that occurs due to triggering of sensory receptors due
•
phase to food contact.
 
Crushing phase • This starts with high velocity and slows down as food gets crushed. Gibbs in 1969 observed that when
•
 
the central incisor is about 5 mm from closure, the jaw motion is stabilised at the working condyle and the
following final closing stroke is guided by this ‘braced’ condyle.
Phase of tooth • With slight change in direction without delay: Here all the reflex muscular adjustments for tooth contact are
•
contact made
Grinding phase • In this phase, there is grinding movement guided by the maxillary and mandibular occlusal tables.
•
Centric occlusion • The mandible returns to a single terminal point before it goes into the preparatory phase. (AIPG 2006)
•
 

Face-bow (Snow 1802)
Features • A caliper- like device which is used to record the relationship of the maxillae and/or the mandible to the temporomandibular
•
joints.
• The structure and functioning of the face-bow should be thoroughly learned to perform accurate orientation jaw relation.
•
Parts • U-shaped frame
•
• Condylar rods
•
• Bite fork
•
• Locking device
•
• Orbital pointer with clamp
•
Types • Arbitrary face-bow (AIPG 2008)
•

– Facia type.
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– Earpiece type
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– Hanau face-bow (Spring bow)
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– Slidematic (Denar)
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– Twirl bow
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– Whipmix
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• Kinematic or hinge bow.
•
Arbitary face-bow Kinetic face-bow
• Condyle rods are approximately located over the condyle • Accurately determines the centre of rotation axis, i.e., of the
•
•
region. condylar location.
• Attached to maxillary occlusal rim • Attached to mandibular occlusal rim

•
•
• Used in construction of complete denture • Used in construction of FPD where precision is required.
•
•

Types of Arbitrary Face-bow
Facia type • The hinge axis or the posterior reference point is 13 mm anterior to the external auditory meatus and the anterior
•
reference point is the orbitale (midpoint of the lower border of the orbit).
••
The face-bow has a pointer that can be positioned to the posterior reference point.
Earpiece Type • The posterior reference point is the external auditory meatus and the anterior reference point is the orbitale.
•
• The earpieces engage into the posterior reference points (the external auditory meatus).
•
Hanau face-bow • It is the most commonly used face-bow. A detailed description of recording the arbitrary hinge axis using a
•
Hanau face-bow has been discussed next under face-bow transfer.
• Arbitrary earpiece type, arbitrary facia type and kinematic face-bows are also available from Hanau.
•
COMPLETE DENTURES
Slidematic type • This face- bow has an electronic device, which gives the reading that can be seen in the anterior region.
•
(Denar) • This reading denotes one-half of the patient’s inter-condylar distance. These face-bows require specific
•
articulators, which accept the reading.
Twirl Bow • It is an arbitrary type of face-bow that does not require any physical attachment to the articulator. It is not commonly
•
used for CD construction. It relates the maxillary arch to the Frankort’s horizontal plane.
• A mounting guide is used to mount the transfer rod to the articulator. It is easy to manipulate because the face-
•
bow is not needed to mount the maxillary cast in the articulator
Whipmix Face-bow • These face-bows have a built-in hinge axis locator. It automatically locates the hinge axis when the earpieces
•
are placed in the external auditory meatus. It has a nasion relator assembly with a plastic nosepiece. The nasion
relator determines the anterior reference point
VERTICAL JAW RELATION
Effects of Increased vertical dimension Effects of Decreased vertical dimension

• Increased trauma to the denture-bearing area. (AIPG 2002) • Comparatively lesser trauma to the denture- bearing area.
•
•

• Increased lower-facial height. • Decreased lower-facial height.
•
•
• Cheek biting. (NEET 2013) • Angular chelitis due to folding of the corner of the mouth.
•
•

• Difficulty in swallowing and speech. (AIPG 2002) • Difficulty in swallowing.
•
•
• Pain and clicking in the temporomandibular joint. • Pain, clicking, discomfort of the temporo-mandibular joint
•
•
• Stretching of facial muscles accompanied with headache and neuralgia.
•
• Loss of lip fullness.
•
• Obstruction of the opening of the eustachian tube due to the
•
elevation of the soft palate due to elevation of the tongue/
mandible.
• Loss of muscle tone.
•
• Corners of the mouth are turned down
•
• Thinning of the vermilion borders of the lip.
•
• Decreased volume or cubical space of the oral cavity
•
Methods to Measure
Vertical dimension at rest Vertical Dimension at Occlusion

• Facial measurements after swallowing and • Mechanical methods
•
•
relaxing – Ridge relation—Distance from the incisive papilla to mandibular incisors.
–
• Tactile sense – Parallelism of ridges.
–
•
• Measurement of anatomic landmarks – Pre-extraction records
–
- Profile photographs
•
• Speech
-
- Profile silhouettes
•
• Facial expression
-
- Radiography
•
-
- Articulated casts
-
 
- Facial measurements
-
- Measurement from former dentures
-
 
480
Vertical dimension at rest Vertical Dimension at Occlusion

• Physiological Methods
•
 
– Using wax occlusal rims
–
– Physiological rest position
–
– Phonetics
–
– Aesthetics
–
 
– Swallowing threshold
–
 
– Tactile sense or neuromuscular perception
–
– Patient’s perception of comfort.
–
Closed speaking space Freeway space
COMPLETE DENTURES
Described by Silverman (Kar 2003) Described by Thompson and Niswonger

Closed speaking space measures the vertical dimension when the mandible It establishes vertical dimension when the muscles
and muscles involved in function of speech. It is the space between upper and and mandibles are in rest position.
lower teeth when sounds like eh, s, j are pronounced.
It is dynamic position established when muscles are in state of function. It is static position established when muscles are in
state of rest
It is about 1-2 mm when measured in the premolar area. It is about 2-4 mm when measured in the premolar
area.
The speaking space increases when there is small vertical dimension. The freeway space increases when there is reduced
vertical dimension.
HORIZONTAL JAW RELATION

• Relationship of the mandible to the maxilla in a horizontal plane/ anteroposterior direction.
•
• Two types:
•
– Centric relation denotes the relationship of the mandible to the maxilla when the mandible is at its posterior most
–
position.
– Eccentric relation denotes the relationship of the mandible to the maxilla when the mandible is at any position other
–
than the centric relation position.
• The centric relation has the following salient features:
•
– It is learnable, repeatable and recordable position which remains constant throughout life.
–
– It acts as a centre from which all movements can be made.
–
– If the mandible has to move from one eccentric position to another it should go to the centric relation before
–
advancing to the target eccentric position.
– Functional movements like chewing and swallowing are performed in this position
–
– It is helpful in adjusting condylar guidance in an articulator to produce balanced occlusion.
–
– It is a definite entity, so it is used as a reference point in establishing centric occlusion.
–
Methods to record centric relation
Physiological • Tactile or inter-occlusal check record method
•
methods – Pressure less method.
–
– Pressure method.
–
 
• Functional method:
•
 
- Needleshouse method: Compound occlusion rims with four metal styli placed in the maxillary occlusal
-
rim are to be used. The tracings incorporate movement in all the three planes.
– Patterson method: Wax occlusal rims are used. A trench is to be made in the mandibular rim and a mix-
–
ture of half plaster and half carborundum paste should be placed in the trench.
- Meyer’s method: Meyers used soft wax on the occlusal rims to establish a generated path. Tin foil
-
was placed over the wax and lubricated. The patient performed the functional movements to produce
a wax path. The plaster index was made on the wax path and the teeth were set to the plaster index.
– Graphic (Excursive) methods:
–
 
- Intraoral tracing (intraoral balancer, Hanau co.)
-
- Extraoral tracing (height tracer, Hanau co.)
-
Radiographic method

• Pantograph is a tracing technique
•
– It is the most accurate method of recording centric relation. It can also be used to record accentric movements. It
–
is three dimensional extraoral graphic tracer. It records mandibular movements in all three planes. Mandibular
movements are traced by a stylus.
– This is not used for complete denture and is mainly used in full mouth rehabilitation of dentulous patients
–
– A photographic tracer looks like a face bow.
–
– The surface on which tracing is done is called as FLAG. There are total six flags. Two flags on each side of the condyler
–
region are situated perpendicular to another. The remaining two are in the anterior region.
• Central bearing device in Gothic arch tracing helps in achieving actualization of pressure.
•
– Provides a central point of bearing or support between maxillary and mandibular dental arches.
COMPLETE DENTURES
–
– It is used in making intraoral or extraoral mandibular tracings. Its contacting point is attached to one dental arch
–
plate attached opposite dental arch.
– The plate provides the surface on which the bearing point rests or moves on which the tracing of mandibular
–
movements is recorded.
– This tracing is called as central arrow point tracing. The apex of the arrow tip should be sharp. If the tip of the arrow
–
is blunt it is discarded.
• The record is transferred to the articulator using indexes like nicks and notches, staple pins, etc.
•
ARTICULATORS • 1805–Garriot JB-first mechanical articulator-Garriot
•
Hinge articulator.
• Gills (1926), Boucher (1934), Kingery (1934) divided • 1830-Howarth and Ladmore, produced a most common
•
into adjustable and nonadjustable.
•
for relating casts with the help of plaster index (also called
• Back (1962) classified into suspension instrument, axis as Plaster articulators).
•
instrument and the tripod movement. • Three point articulator: Takes 3 points into
•
• Weinberg (1963)–arbitrary, positional, semi-adjustable consideration-2 guides and 1 incisal pin. Used in
•
and fully adjustable. preclinical labs for teeth setting
• Posselt (1968)–plane line, mean value and adjustable • The term ARCON was coined by Bergstrom in 1950.
•
•
• Arry (1974)–simple, hinge type, fixed guide type and • Arcon: A contraction of the words ARTICULAOTR AND
•
•
adjustable. CONDYLE used to describe an articulator containing the
• 1756–Plillip Ptaff is the first person to introduce condylar path elements within its upper member and the
•
articulators – slab articulators. condylar elements within the lower member.
Classification
Based on the theories of occlusion
Bonwill theory articulators • According to the Bonwill’s theory of occlusion the teeth move in relation to each other as guided by the
•
(WGA Bonwill) condylar and the incisal guidances
• Also known as the Theory of equilateral triangle according to which, the distance between the condyles
•
is equal to the distance between the condyle and the midpoint of the mandibular incisors (incisal point).
• An equilateral triangle is formed between the two condyles and the incisal point.
•
• Theoretically, the dimension of the equilateral triangle is 4 inches
•
• Bonwill articulators allow lateral movement and permit the movement of the mechanism (joint) only in
•
the horizontal plane.
Conical theory articulators • The conical theory of occlusion proposed that the lower teeth move over the surfaces of the upper teeth
•
(proposed by RE Hall) as over the surface of a cone, generating an angle of 45-degrees with the central axis of the cone tipped
45o to the occlusal plane
• The Hall automatic articulator designed by RE Hall follows the conical theory of occlusion
•
Spherical theory articulators • The spherical theory of occlusion proposed that lower teeth move over the surface of upper teeth as over
•
a surface of sphere with a diameter of 8 inches
• The centre of the sphere was located in the region of glabella. The surface of the sphere passed through
•
the glenoid fossa and along with the articulating eminences.
• The articulator devised by G.S. Monson operated on the spherical theory of occlusion
•
 
482
Based on the theories of occlusion

Based on the type of inter- • Class I Simple holding instrument capable of accepting a single static registration, E.g. slab
•
occlusal record used. articulators, Hinge joint, Barndor, Gysi simplex.
• Class II Instruments that permit horizontal as well as vertical motion but do not orient the motion of the
•
TMJ via face-bow transfer.
– IIA Eccentric motion permitted is based on average or arbitrary values. E.g. Mean value articulator
–
simplex
– IIB Limited accentric motion is possible based on theories of arbitrary motion. Eg: Monsons Halls
–
articulator
– IIC Limited accentric motion is possible based on engraving records obtained from the patient
–
• Class III Permit horizontal, vertical positions and also accept face-bow transfer and protrusive jaw
•
record.
COMPLETE DENTURES
– IIIA accept a static protrusive registration and they use equivalens for other types of motion. E.g.
–
Hanasu mate Dentatus, Arcon
– IIIB They accept static lateral registration also in addition to protrusive as well as face bow transfer.
–
They use equipments for other types of motion. Ney, Teledyne, kinescope, Hanau University series,
Trubyte, Panadent
• Class IV They accept 3 dimensional dynamic registration and utilize a face bow transfer.
•
– IVA The condylar path registered cannot be modified. Eg: TMJ articulator, stereograph
–
– IVB The allow customization of the condylar path. Eg Stuart instrument, gnathoscope, pantograph.
–
Based on the ability to • Arcon articulator: This instrument maintains anatomic guidelines by the use of condylar analogues
•
simulate jaw movements (condylar elements) in the mandibular element and fossae assemblies within the maxillary element
 
• Eg: Hanau series (H2, Hanau Arcon H2),
•
• Condylar articulator or non arcon type articulators (carefully note that condylar articulators are called
•
non-arcon articulators): an articulator whose condylar path components are part of the lower member
and whose condylar replica components (condylar elements) are part of the upper member.
• Eg: Hanau articulators (Hanau mate), Dentatus and Gysi.
•
Based on the adjustability of – Non-adjustable articulators: They can open and close in a fixed horizontal axis. The condylar
–
the articulator path is fixed.
– Semi Adjustable: Have adjustable horizontal condylar paths, adjustable lateral condylar paths and
–
adjustable E.g Arcon and non arcon type articulators.
– Fully adjustable: Capable of being adjustable to follow the mandibular movement in all directions.
–
Eg Stuart instrument gnathoscope (class IVB)
Disadvantages of Articulators Based on Theory of DENTURE TEETH

Occlusion
Functions of the Denture Teeth
• These articulators are based on theoretical concepts.
• Aesthetics,
•
There is no provision for variations from the theoretical
•
relationships that occur in different persons. • Mastication
•
 
• Speech
•
Classification
Based on the material Based on the morphology of the teeth:
• Acrylic teeth. • Anatomic teeth.
•
•
• Porcelain teeth. • Semi-anatomic teeth.
•
•
• Inter-penetrating polymer network resin teeth (IPN resin).
•
• Gold occlusals.
•
• Acrylic resin with amalgam stops.
•

Types of Teeth
Acrylic and Porcelain Teeth
Acrylic and porcelain teeth
Property Acrylic Porcelain
Abrasion resistance Low High
Adjustability Easy to adjust Difficult to trim
Bonding Chemical Mechanical
COMPLETE DENTURES
Staining Easily stained Does not stain
Percolation Absent if acrylic Present when acrylic
Denture base is used Denture base is used
Clicking sound Absent Present
Ease of fabrication Easy Difficult
Ease of rebasing Difficult to remove Easy to remove

Trauma to denture Less More
Bearing area
Morphology of Teeth
Anatomic Teeth • Anatomic teeth have a 33° cusp angle.
•
• Cusp angle can be defined as, “the angle made by the slopes of the cusp with a perpendicular line bisecting
•
the cusp, measured mesiodistally or buccolingually”
• Most commonly used
•
• Resemble the natural teeth
•
• Provide good aesthetics and the psychological benefit to the patient.
•
• Advantages
•
– More masticatory efficiency
–
– Balanced occlusion can be achieved in eccentric jaw positions (Protrusive, right lateral and left lateral
–
movement).
• The cusp-fossa relationship helps to guide the mandible into centric occlusion.
•
• The disadvantages of these teeth are that they magnify the horizontal forces acting on the ridge and the
•
‘teeth setting’ is very crucial to obtain proper occlusion (i.e. they should be placed in specified positions
(AIPG 2008)

Semi-anatomic Teeth • Cusp angles ranging between 0º and 30º The cusp angles are usually around 20º. They are also called
•
modified anatomic teeth.
• Victor Sears in 1922 designed the first semi- anatomic tooth, which was called the channel tooth. This
•
consisted of a mesiodistal groove in all maxillary posterior teeth and a mesiodistal ridge in all mandibular
posterior teeth. These teeth were designed for unlimited protrusive movement and limited lateral movements
Non-anatomic or 0° or • Non-anatomical teeth are defined as, “Artificial teeth with occlusal surfaces which are not anatomically formed
•
cuspless Teeth but which are designed to improve the function of mastication”
• These teeth have 0º cusp angles. (AIPG 2007)
•

• Balanced occlusion in dentures with these teeth is obtained by balancing ramps and compensatory curves.
•
• Hall in 1929 designed the first cuspless tooth and named it “inverted cusp tooth”. The occlusal surfaces of
•
these teeth were flat with concentric conical depressions producing sharp concentric ridges around a central
depression
484
Cross Bite Teeth • These teeth are used in jaw discrepancy cases leading to a posterior cross bite relationship. Here the buccal
•
cusps of the maxillary teeth are absent. Instead there is a large palatal cusp, which rests on the lower tooth.
Gysi in 1927 designed the cross bite tooth
Metal Insert Teeth (VO • Hardy designed the first metal insert tooth and he called it the “Vitallium occlusal”.
•
Posteriors) • •
Here each tooth will look like the fusion of two premolars and one molar.
• On the occlusal surface of these teeth, a Vitallium ribbon is embedded in a zigzag pattern.
•
• The Vitallium metal insert is not totally submerged into the tooth, instead it is slightly raised above the occlusal
•
surface. On occlusion, the metal-to-metal contact produces greater cutting efficiency
Selection of the Anterior Teeth

COMPLETE DENTURES
Size • Methods using Anthropological Measurements of the Patient using post- extraction records
•
– Anthropometric cephalic index by Sears: The transverse circumference of the head is measured using a
–
measuring tape at the level of the forehead. The width of the upper central incisor can be derived from this
measurement
– Width of the upper central incisor = Circumference of the head / 13
–
– The bizygomatic width can be used to determine the width of the central incisor and also the combined
–
width of the anteriors. The bizygomatic width is the distance measured between the malar prominences on
either side. This measurement is also used in Berry’s Biometric index and Pound’s formulae
• Based on the width of the nose
•
– The width of the nose is measured with a vernier calliper. This measurement is transferred to the occlusal rim.
–
The width of the nose is equal to the combined width of the anterior teeth
• Typal form theory
•
– This theory helps to determine the size and form of the anterior teeth
–
• High Lip Line gives indication of inciso-gingival length (minimal gingival display)
•
• Mark the position of the commisures of mouth with patient relaxed, mouth closed (position of distal of canines -
•
 
use the Auto-Rule to pick a corresponding mould e.g. C, D, E, F etc.)
 
• Bizygomatic width measured by facebow divided by 16= width of the central incisor; divided by 3.3 = width of
•
 
6 anterior
Shape • Tooth shape does not correspond to facial shape, but the Trubyte system can be a good starting point for
•
experimenting;
• There are proven no male/female characteristics
•
Shade • Tooth shade darkens with age, but the suggestion that there is any correlation with skin and hair colour is suspect
•
 
• Use the Portrait Shade number and not the Vita shade code when prescribing denture teeth from the Portrait
•
shade guide. (Portrait numbers begin with a “P” and are listed as the bottom-most shade code on the shade tabs)
• Anterior and posterior tooth shades are the same
•
• Shade selection for porcelain restorations should be made with the Vita shade guides (AIPG 2014)
•

Trubyte teeth for • As designed by J Leon Williams and Alfred Gysi together with a formulation of the law of harmony between faces
•
Vulcunite plates and teeth and a description of the Trubyte system of classifying face forms.
• Trubyte indicator is used to determine the facial form, size and profile and accordingly the tooth form, size (of the
•
maxillary central incisor) and profile of the anterior teeth is selected) (KAR 2006)
Blue line form • Another instrument to select anterior tooth by Ivoclar.

•
selector • It contains a caliper, facial meter with correlates with the correlation of the interalar width with the patients tooth
•
mould width.
• It also contains cards. These are helpful for selecting the tooth form (soft or bold), tooth length.
•
Phonetics in Orientation of Anterior Teeth
Labial sounds • These are b p and m
•
• They are made by passive contact at the lips
•
• Insufficient support of the lips by the teeth and denture base can cause these sounds to be defective
•

Labiodental sounds • Labiodental sounds f and v are made between the upper incisors and the labiolingual center to the posterior
•
third of the lower lip.
• Placement of maxillary anterior teeth in complete denture too far superiorly and anteriorly might result in
•
difficulty in pronouncing f and v sounds.
• If the upper anterior teeth are too short the v sound will be more like an f. If they are too long the f sound will
•
be more like a V (NEET 2013, AIPG 2004)

• Alveolar sounds t d n s and z are made with the valve formed by contact of the tip tongue with the anterior
•
part of palate (alveolous)or the lingua side of the anterior teeth.
• If the teeth are too far lingually, the t will sound like d.
•
• If the teeth are too far anteriorly, the d will sound like a t.
•
Sibilants • S Z SH ZH CH and J are called sibilants. These are also called as alveolar sounds. The upper and lower
COMPLETE DENTURES
•
incisors should approach end but not touch.
• If the gap is very narrow it results in whistling and if the gap is broad it results in lisping.
•
Dental sounds • Sounds such as Th in this, that etc. Made with the tip of the tongue extending slightly between the upper
•
and lower anterior teeth.
Palatal sounds (year, • Have no effect on dentures.
•
she, etc), velar sounds
(k,g,ng, and vowels (a,
e, I, o, u)
OCCLUSION
• Complete denture occlusion can be of three types, namely:
•
Balanced occlusion • It is defined as the simultaneous contacting of all maxillary and mandibular teeth
•
• Balanced occlusion is absent in natural dentition.
•
• For minimal occlusal balance, there should be at least three points of contract on the occlusal plane.
•
• More the number of contacts, better the balance.
•
• However Sheppard stated that Enter bolus Exit balance theory according to this statement, the balancing
•
contact is absent when food enters the oral cavity.
Monoplane or Non Bal- • It is an arrangement of teeth with form or purpose. It includes the following concepts of occlusion
•
anced Occlusion – Spherical theory
–
– Organic occlusion
–
– Occlusal balancing ramps for protrusive balance
–
– Transographics
–
• Sears also proposed occlusal pivot theory for monoplane or balanced occlusion
•
Lingualised occlusion • Gysi in 1927 gave the concept and it was modified by Payne in 1941
•
• According to this the maxillary lingual cusps are the main functional occlusal elements.
•
• This type of occlusion involves the use of a large upper palatal cusps against a wide lower central fossa
•
Neutrocentric occlu- • Proposed by Devan.
•
sion • This concept is similar to the monoplane occlusion used to set non-anatomic teeth.
•
• According to this concept, the plane of occlusion should be flat and parallel to the residual alveolar ridge.
•
• The term neutrocentric denotes an occlusion that eliminates the anteroposterior and buccolingual inclines in
•
order to direct the forces to the posterior teeth.
Types of Balanced Occlusion

Unilateral bal- • This is a type of occlusion seen on occlusal surfaces of teeth on one side when they occlude simultaneously with
•
anced occlusion a smooth, uninterrupted glide.
• This is not followed during complete denture construction. It is more pertained to fixed partial dentures.
•
Bilateral balanced • This is a type of occlusion that is seen when simultaneous contact occurs on both sides in centric and eccentric
•
occlusion positions.
• Bilateral balanced occlusion helps to distribute the occlusal load evenly across the arch and therefore helps to
•
improve stability of the denture during centric, eccentric or parafunctional movements
486
Protrusive bal- • The factors that govern protrusive balance:
•
anced occlusion – The inclination of the condylar path: This inclination recorded on the patient represents the path travelled
–
by the condyle in protrusion which is modified by the combined action of all the tissues in the temporoman-
dibular joint and the ridges covered by the recording bases.
– Angle of the incisal guidance chosen for the patient.
–
––
Angle of the plane of occlusion.
– The compensating curves chosen for orientation with the condylar path and the incisal guidance.
–
 
 
– Cuspal height and inclination of the posterior teeth.
–
 
Lateral balanced • There will be a minimal simultaneous three point contact (one anterior, two posterior) present during lateral
•
occlusion movement of the mandible.
• Lateral balanced occlusion is absent in normal dentition.
•
• When a dentulous person with canine guided occlusion moves his mandible to the right, there will be canine
COMPLETE DENTURES
•
guided disocclusion of all his teeth. That is, the canine will be the only tooth that contacts the opposing tooth. Even
the canine of the opposite side will not have contact
• The factors that govern lateral balance:
•
– Angle of inclination of the condylar path on the balancing side.
–
– Angle of inclination of the incisal guidance and cuspid lift.
–
– Angle of inclination of the plane of occlusion on the balancing side and working side.
–
– Compensating curve on the balancing side and working side.
–
– The buccal cusp heights or inclination of the teeth on the balancing side.
–
– The lingual cusp heights or inclination on the working side.
–
– The Bennett side shift on the working side.
–
Concepts Proposed to Attain Balanced Occlusion
Gysi concept (1914) • He suggested arranging 33° anatomic teeth could be used under various movements of the articulator
•
to enhance the stability of the denture.
French’s concept (1954) • He proposed lowering the lower occlusal plane to increase the stability of the dentures along with
•
balanced occlusion. He arranged upper first premolars with 5° inclination, upper second premolars with
10° inclination and upper molars with 15° inclination
Sears Concept • He proposed balanced occlusion for non-anatomical teeth using posterior balancing ramps or an
•
occlusal plane which curves anteroposteriorly and laterally.
Pleasure concept • Pleasure introduced a pleasure curve or the posterior reverse lateral curve reshaped during try in to
•
obtain balanced occlusion.
Frush concept • He advised arranging teeth in one dimensional contact relationship, which should be reshaped during
•
try in to obtain balanced occlusion.
Trapazzano concept of • He reviewed and simplified Hanau squint and proposed his Triad of Occlusion (first three).
•
occlusion
Spherical Concept of Oc- • According to this concept, the anteroposterior and mesiodistal inclines of the artificial teeth should be
•
clusion: (Monson) arranged in harmony with a spherical surface. (Refer spherical theory in articulators).
Organic Concept of Oc- • In organic or organized occlusion, the aim is to relate the occlusal surfaces of the teeth so that the teeth
•
clusion are in harmony with the muscles and joints during function.
• The muscles and joints determine the mandibular position of occlusion without any tooth guidance. In
•
function, the teeth are supposed to have a passive role and do not influence or determine the path of
mandibular movement. (In normal occlusion, tooth factors determine mandibular movements e.g. incisal
guidance).
Hanau Quint: Rudolph L Hanau proposed nine factors that govern the articulation of artificial teeth.
They are:
• Horizontal condylar inclination
•
• Protrusive incisal guidance
•
• Relative cusp height.
•
• Compensating curve
•

• Plane of orientation
•
• Buccolingual inclination of tooth axis
•
• Sagittal condylar pathway
•
• Sagittal incisal guidance
•
• Tooth alignment
•
These nine factors are called the laws of balanced articulation. Hanau later condensed these nine factors and formulated five
factors, which are commonly known as Hanau’s quint (first five).
COMPLETE DENTURES
Hanau’s Quint of Balanced Occlusion (AIPG 2006)
Condylar guidance – 1st • Only factor which can be recorded from the patient registered using protrusive registration
•
factor • Increase in the condylar guidance will increase the jaw separation during protrusion.
•
Incisal guidance – 2nd • Should be set depending upon desired overjet/overbite for the patient has more influence on the posterior
•
factor teeth than the condylar guidance.
Plane of occlusion • Established anteriorly by the height of lower canine and posteriorly by the height of retromolar and
•
Camper’s line
Compensating curve – 2 • AP curve and lateral curve

•
types • This curve should be in harmony with the mandibular movements
•
Cuspal angulation • This modifies the effect of plane of occlusion and compensating curves.
•
Factors Influencing Balanced Occlusion
• Inclination of the condylar path or condylar guidance.
•
• Incisal guidance.
•
• Orientation of the plane of occlusion or occlusal plane.
•
 
• Cuspal angulation.
•
• Compensating curves. (AIPG 2001)
•

Thielemann’s formula –
CG *IG
Balanced occlusion = CC * CI * oo
Compensating Curve
• The anteroposterior and lateral curvatures in the alignment of the occluding surfaces and incisal edges of artificial
•
teeth which are used to develop balanced occlusion
• It is determined by the inclination of the posterior teeth and their vertical relationship to the occlusal plane. The posterior
•
teeth should be arranged such that their occlusal surfaces form a curve. This curve should be in harmony with the
movements of the mandible guided posteriorly by the condylar path.
• A steep condylar path requires a steep compensatory curve to produce balanced occlusion. If a shallow compensating
•
curve is given for the same situation, there will be loss of balancing molar contacts during protrusion
Two types of compensating curves (AIPG 2012)

Anteroposterior Compen- • These are compensatory curves running in an anteroposterior direction. They compensate for the
•
sating Curves curve of Spee seen in natural dentition. If the teeth are not arranged according to this curve, there will
be disocclusion during protrusion of the mandible (Christensen’s phenomenon).
488
Lateral Compensating Curves: These curves run transversely from one side of the arch to the other. The following curves
fall in this category:
Compensating Curve for • This curve runs across the palatal and buccal cusps of the maxillary molars.
•
Monson Curve • During lateral movement the mandibular lingual cusps on the working side should slide along the
•
inner inclines of the maxillary buccal cusp.
• In the balancing side the mandibular buccal cusps should contact the inner inclines of the maxillary
•
palatal cusp. This relationship forms a balance.
Compensating Curve for • This curve runs opposite to the direction of the Monson’s curve. This curve is followed when the first
•
Anti-Monson or Wilson’s premolars are arranged. The first premolars are arranged according to this curve so that they do not
Curve produce any interference to lateral movements.
COMPLETE DENTURES
Reverse Curve • It was originally developed to improve the stability of the denture. It is explained in relation to mandibular
•
posterior teeth.
• The reverse curve was modified by Max. Pleasure to form the pleasure curve
•
Pleasure Curve • It was proposed by Max. Pleasure. He proposed this curve to balance the occlusion and increase
•
the stability of the denture.
• Here the first molar is horizontal and the second premolar is buccally tilted. The second molar
•
independently follows the anteroposterior compensating curve and lingually tilted.
• This curve runs from the palatal cusp of the first premolar to the distobuccal cusp of the second molar.
•
The second molar gives occlusal balance and the second premolar gives lever balance.
Cuspal Angulation
• The cusps on the teeth or the inclination of the cuspless teeth are important factors that modify the effect of plane of
•
occlusion and the compensating curves. The mesiodistal cusps lock the occlusion, such that repositioning of teeth does not
occur due to settling of the base
• In order to prevent the locking of occlusion, the mesiodistal cusps are reduced during occlusal reshaping. In the absence of
•
mesiodistal cusps, the buccolingual cusps are considered as a factor for balanced occlusion
• In cases with a shallow overbite, the cuspal angle should be reduced to balance the incisal guidance. This is done because
•
the jaw separation will be less in cases with decreased overbite. Teeth with steep cusps will produce occlusal interference in
these cases
• In cases with deep bite (steep incisal guidance), the jaw separation is more during protrusion. Teeth with high cuspal
•
inclines are required in these cases to produce posterior contact during protrusion
Deflective contacts Occlusal correction

Posterior teeth • Reduce fossa or marginal ridge
•
• Deflective contact is only in centric relation • Reduce both fossa and cusp
•
•
• Deflective contact is both centric and eccentric positions
•
Anterior teeth • Reduce the lower incisal edges
•
• When incisal edge of lower anteriors touching the maxillary • Deepen the lingual fossa of upper teeth and reduce the incisal
•
lingual fossa in centric relation only
•
edges of lower teeth
• Incisal edge of lower anterior touching the maxillary lingual • Bull’s law: Upper buccal cusp and lower lingual cusp are made
•
fossa both in centric and eccentric relations
•
shorter without deepening the central fossae.
• Deflective contacts occurring on working side
•
PROCESSING OF DENTURES
Denture Material • The most commonly used materials are polymers such as polymethylmethacrylate (PMMA) or acrylic
•
resins
• Polymers with chemical bonds between different chains are termed cross-linked.
•
• This process affects physical properties of the polymer. In the case of PMMA, it increases rigidity as well as
•
craze resistance, which is the tendency of resins to form minute surface cracks, and reduces the resin’s
solubility in organic solvents.

Chemical Composi- Heat-Activated PMMA
tion of Denture Base • Powder: Liquid system
•
 
Resins • Powder: Prepolymerized spheres of PMMA
•
– Initiator: Benzoyl peroxide (~0.5%)
–
– Pigments and dyed synthetic fibers
–
••
Liquid: Methyl methacrylate monomer
– Inhibitor: Hydroquinone (traces) Cross-linking agent: ethylene glycol dimethacrylate (~10%)
– Activator: NN-dimethyl-p-toluidine*
–
–
Microwave-Activated PMMA
• Powder-liquid system
•
 
• Similar to heat-activated PMMA: with slight modifications to accommodate the microwave activation
•
procedure
COMPLETE DENTURES
Light-Activated Resins
• (Single component, premixed composite sheets and ropes)
•
 
• Matrix: Urethane dimethacrylate, microfine silica
•
• Filler: Acrylic resin beads
•
• Photoinitiator: Camphoroquine-amine
•
Polymerization pro- • The polymerization process of PMMA involves the conversion of low molecular weight monomers to high
•
cess molecular weight polymers.
• Denture base resins are formed by a process of additional polymerization through the release of free radicals.
•
• The reaction passes through three stages,
•
– Activation and initiation,
–
– Propagation,
–
– Termination
–
Stages of Polymerization
Stage I - Wet sandy • During this stage no interaction occurs on a molecular level. Polymer beads remain unaltered and the
•
stage consistency of the mixture may be described as ‘coarse’ or ‘grainy’. The polymer gradually settles into the
monomer forming a fluid, incoherent mass.
 
Stage II: Early stringy • The monomer attacks the polymer by penetrating into the polymer. Some polymer chains are dispersed in the
•
stage liquid monomer. This polymer chains uncoil thereby the viscosity of the mix is increasing. The mass is ‘stringy’
or ‘sticky’ when touched or pulled apart.
Stage III: Late stringy • The strings break off at this stage when touched or pulled apart and the mass becomes dough-like
•
stage
Stage IV: Dough stage • The mass enters a dough- like stage. On a molecular level an increased number of polymer chains enter the
•
solution. Hence, a sea of monomer and dissolved polymer is formed. A large quantity of undissolved polymer
also remains.
• The mix is smooth and dough-like.
•
• The material has lost much of its tackiness and can be separated without the formation of strings.
•
 
• The material does not stick to the walls of the mixing jar and is easily mouldable.
•
Stage V: Rubbery • After the dough stage, the mixture enters a rubbery or elastic stage. Monomer is dissipated by evaporation
•
stage and by further penetration into remaining polymer beads. Clinically, the mass rebounds when compressed
or stretched. Because the mass no longer flows freely to assume the shape of its container, it cannot be
moulded by conventional compression techniques
Stage VI: Stiff stage • On standing for an extended period, the mixture becomes stiff. This may be attributed to the evaporation of
•
free monomer. Clinically, the mixture appears very dry and is resistant to mechanical deformation.
Also Note
Dough forming time The time required for the resin mixture to reach a dough-like stage is termed as ‘dough forming time’.
Working time The working time is the time elapsing between the stringy stage and the beginning of rubbery stage. The
working time is affected by temperature. Decrease in temperature increases the working time.
490
MASTICATORY EFFICIENCY
Masticatory Forces Generated
Type Forces Factor
Natural dentition 600-800 N - 60-80 kg - 120 to 180 pounds 1
Complete denture prosthesis 75-100- N - 7-10 kg - 16-22 pounds 5-6 times less
Removable partial denture 100-120 n – 10-12 kg - 22-25 pounds 4-5 times less
Fixed partial denture 250-300 N - 25-30 kg - 50-65 pounds 2-3- times less
COMPLETE DENTURES
Implant-supported complete dentures 200-400 n 4-40-kg – 10-100 pounds 1.5-2 times less
Good to know
• Maximum biting force = 640 N
•
• Maximum biting force on single tooth = 265 N (normal force on a single tooth 3-18 N)
•
• Mean sliding (freedom in centric ) = 1 mm
•
• Contact area on first molar = 15 mm; maximum stress = 20 MPa (2750-3000 cycles/day).
•
• Incisors can detect forces of 0.01 N or less, whereas the threshold for molars is 0.1 N. Force discrimination is better at
•
lower than higher levels (AIPG 2005).
• Maximum Axial forces generated during swallowing are in the range of 70 to 150 N (16-34 pounds or 7-15 kg).
•
• The highest masticatory forces are generated when the maxillary and mandibular teeth are in contact.
•
• Dr Weber worked out that 1 cm surface of perpendicular slide of any masticatory muscle can produce approximately 10
•
kilograms-force (100 N). The following surfaces were found:
– Temporalis: 8 cm2 = 80 kg = 800 N= 180 pounds
–
– Masseter: 7.5 cm2= 75kg = 750 N= 160 pounds
–
– Medial petrygoid: 4 cm2 = 40kg = 400 N= 100 pounds
–
• Thus, the total surface area of perpendicular masticatory muscles slide is about 19.5 square centimeters (3.02 sq in):= 200
•
kg = 2000 N = 440 pounds
Calculation of Occlusal Force Contacts During 24 hr Period

Contacts During Chewing
Actual chewing time per meal 450-600 sec
Four meals per day 1800-2400 sec (30-40 min)
Duration of each masticatory cycle 0.8 sec to 1 sec (60-80 cycles/min)
Duration of occlusal contact during each cycle (chewing stroke = 20- 0.25 to 0.3 sec
30% of masticatory cycle)
Total period of occlusal contact during chewing per entire day 500-600 sec (average) or 10 min
Tooth contacts during swallowing (total 600/day) 600/day
During meals
No. of deglutitions/min during chewing 3
Total No. of deglutions per day during meals 90-120
Effective swallows or deglutitions (contacts occurs only during 1/3 of 30-40

deglutition)

Duration of each swallow 1 sec
Total time of occlusal contacts by swallowing during meals per day 30-40 sec – or 1 min
Between meals
Day time – 25 /Hours (16 hours) 400 sec or 7 min

Night time – 10/hours (8 hr) 80 sec or 1.5 min
Total time of occlusal contact 18-20 min
In bruxism patients 30 – 180 minutes/day.
COMPLETE DENTURES
ORAL HYGIENE IN A COMPLETE DENTURE PATIENT
Mechanical: • Use non-abrasive cleanser (commercial pastes, dish detergents, not regular toothpaste
•
• Use soft brush with long bristles (less wear)
•
• Inner and outer surfaces must be cleaned
•
• Brush over a filled basin or face cloth (protection against damage if dropped)
•
• Brush after every meal, before bed
•
Chemical cleaners: • Efferdent, Polident etc. must be used overnight to be effective (15-30 minutes is not sufficient)
•
• Brushing is more effective (60-80% vs 20-30% plaque removal compared to soaking alone) (AIPG 2014)
•

• Combine brushing with soaking for more efficiency
•
Ultrasonic cleaners • True ultrasonic cleaners work well
•
 
• “Sonic” cleaners are not effective without chemical cleaner (brushing is more effective)
•
PROBLEMS ASSOCIATED WITH COMPLETE DENTURES
Problem Cause
Soreness on the slope of ridge Deflective occlusal contacts resulting in shifting of bases
Soreness on the crest of ridge Increased vertical dimension resulting in heavy contacts.
Generalized soreness of the basal sear area Increased vertical dimension
Fleeting painful sores Increased vertical dimension
Burning sensation in anterior palate region of a patient wearing new Inadequate relief of the incisive papilla (NEET 2013)

Numbness and tingling sensation in the anterior 1/3rd of the palate Overextension of anterior lingual border
Loosening of denture while smiling Due to inadequate relief of the buccal frenum
Loosening of upper denture while opening mouth Excessive thickness of distobuccal flange
Interference with coronoid process (AIPG 2002)

Difficulty during swallowing Due to overextension of the lingual flange into the lateral throat
form
Increased vertical dimension
Pain and soreness during chewing Deflective occlusal contacts
Mucosal irritation Overextension of the denture borders
Epulis fissuratum (AIPG 2006) (AIPG 2008) Ill-fitting or overextended dentures
492
Papillary hyperplasia Results from candidal infection and improper relief of the palatal
area in complete dentures
Small lesions are treated by curettage and large lesions are
treated by split thickness supraperiosteal excision
Clicking noise during teeth contacts Increased vertical dimension and improper retention
The dentures is tight when inserted and becomes loose during usage Errors in occlusion

(AIPG 2006) (AIPG 2008)

Cheek biting Insufficient horizontal overlap of posterior teeth
Midline Fracture of Denture

COMPLETE DENTURES
About 29% of complete denture fractures are midline fractures out of which upper dentures alone account for 60%.

(NEET 2013)

Causes
• Posterior ridge resorption
•
• Occlusion wear producing wedge effect
•
• Improper relief with medicine
•
• Absence of labial flange
•
• Deep notches to relieve the frenum
•
Due to ridge resorption, the denture flexes at the fulcrum at midline of the palate. When flexural resistance is exceeded it
starts as a small crack and on repeated stress due to fatigue fracture occurs.
In the ridge resorption, the mucosa will be compressed more (up to 100 mm permitted) than midline and if proper relief is
not provided, it fractures is midline. Remember, fractures due to sudden fall are due to low impact resistance.
Denture Stomatitis
• Pathological reaction of the palatal portion of the denture-bearing mucosa.
•
• Also known as
•
– Denture induced stomatitis
–
– Denture sore mouth
–
– Denture stomatitis
–
– Inflammatory papillary hyperplasia
–
– Chronic atrophic candidiasis
–
• Seen in 50% of the complete denture wearers.
•
• Classification (Newton)
•
Type I Localized simple infection with pinpoint hyperemia
Type II (Erythematous type) Generalized simple type presenting a more diffuse erythema involving a part or the entire denture
covered mucosa
Type III Granular type involving the central part of the hard palate and alveolar ridge. Often seen in association with type I and II
• Type I is usually trauma induced, type II and III are associated microbial plaque accumulation. Candida associated denture
•
stomatitis is often seen along with angular cheilitis (or) glossitis
• Diagnosis: presence of mycelia or pseudohyphae
•
• Predisposing Factors
•

Systemic factors Local factors
 
• Old age • Dentures:
•
•
• Diabetes mellitus – Environmental changes due to dentures
•
–
• Nutritional deficiency: Iron, folate, Vit.B12, etc. – Trauma.
–
– Denture usage, nightwear
•
• Malignancy: Acute leukemia, agranulocytosis ?etc.
–
– Denture cleanliness.
•
 
• Immune defects: Due to the use of corticosteroids and
–
• Xerostomia:
•
 
other immune suppressants.
•
– Sjögren’s syndrome
–
– Irradiation
–
– Drug therapy
–
 
• High carbohydrate diet:
•
– Increases plaque accumulation
COMPLETE DENTURES
–
• Use of broad-spectrum antibiotics: They destroy normal symbiotic
•
colonies leading to the formation of pathological colonies.
 
• Smoking tobacco: Affects oral hygiene and also produces other
•
effects.
• Management and Preventive Measures – Drug therapy

•
 
–
– Institution of efficient oral and denture hygiene Local therapy with Nystatin, Amphotericin

B, Micanazole and Clotrimazole are usually
–
habits. Correction of denture wearing habits. The
patient is advised to store the dentures in 0.2 to 2% preferred to systemic therapy.
chlorhexidine during the night. When lozenges are prescribed the patient should

– Patient is advised not to use the dentures at night or be instructed to retain the dentures during its use.
– Surgical Management: Surgical management
–
leave it exposed to air.
–
– Polishing of the external surface of the dentures includes the elimination of deep crypts in Type
III denture stomatitis. This is preferably done by
–
should be done routinely in order to facilitate denture
cleansing. cryosurgery.
Burning Mouth Syndrome (BMS)

• Characterized by burning sensation in the structures in contact with the dentures without any visible changes in the
•
mucosa
• Clinical Features
•
– No overt clinical signs or symptoms.
–
– Pain starts in the morning and aggravates during the day.
–
– Dry mouth and persistent altered taste sensation.
–
– Systemic symptoms include headache, insomnia, decreased libido and irritability or depression.
–
– More common in postmenopausal females
–
• Etiology
•
Local factors • Mechanical irritation caused by ill-fitting dentures.
•
• Prolonged period of masticatory muscle activity.
•
• Constant parafunctional movements of the tongue.
•
• Constant excessive friction on the mucosa.
•
• Candidal infections and allergic reactions can produce symptoms similar to BMS: Myofacial pain.
•
Systemic factors • Vitamin and iron deficiency
•
 
• Xerostomia
•
• Menopause
•
• Diabetes
•
• Medication
•
 
Psychogenic Factors • Anxiety
•
 
• Depression
•
 
• Treatment Depending on etiology
•
 
494
Gagging denture and the distolingual part of mandibular denture.

Gagging usually produces displacement of the denture.
• Gag reflex is normal, healthy defense mechanism, which

(AIPG 2004)
•
functions to prevent foreign bodies from entering the

trachea. • Commonly, gagging may occur due to unstable occlusal
•
conditions. E.g. increase in vertical dimension of occlusion
• It can be triggered by tactile stimulation of the soft palate,
is predisposed to gagging because the unbalanced occlusal
•
posterior part of tongue and fauces.
contacts may displace the denture and trigger gagging.
• Other stimuli like sight, smell, taste, noise, and
• Gagging can also result from other systemic conditions
•
psychological factors can produce gagging.
•
like GIT disorders, adenoids or tumors in the upper
• Persistent gagging can occur due to over-extended denture respiratory tract, alcoholism and severe smoking.
•
borders especially in the posterior part of maxillary
COMPLETE DENTURES
Treatment (NEET 2013, AIPG 2001)

Clinical techniques • Diverting the patient attention during impression making
•
• Asking patient to take long breaths
•
Prosthodontics tech- • Correction of the excess palatal thickness and overextension
•
niques • Giving the denture a neat finish instead of shiny finish
•
• Increasing he freeway space
•
• Removing the palatal extension of complete denture. The lack of retention (PPS missing) is compensated
•
by placing the intramucosal inserts or posts on remaining teeth
Pharmacologic • Injection or topical application of LA around the offending area
•
• Injection of alcohol in the area
•
• Administration of some drugs
•
– Antihistamines
–
– Sedatives
–
– Tranquilizers
–
– Parasympathetics
–
– CNS depressants
–
Physiologic • Hypnosis
•
• Behaviors therapy
•
Also • Be kind and sympathetic to the patient
•
• build patient confidence
•
• adequate reassurance to patient
•
Combination Syndrome Residual Ridge Resorption (RRR)
• First identified by Kelly in 1972, is found in patients • Chronic progressive change in the bone structure, which
•
results in severe impairment in the fit and function of the
•
wearing a complete maxillary denture, opposing a
mandibular distal extension prosthesis prosthesis.
• This complication is not seen in case of complete • Most common and important sequel of wearing complete
•
dentures.
•
dentures opposing natural mandibular posterior teeth.
• Seven characteristics – together form a syndrome • More common in women due to osteoporotic changes in
•
the bone.
•
– Flabby tissues in the anterior part of the maxillary
• There is continuous loss of bone after tooth extraction and
–
ridge with papillary hyperplasia of the maxilla.
•
– Tilting of the occlusal plane posteriorly downwards. even after the placement of a complete denture.
–
– Supraeruption of lower anteriors. • Alveolar remodeling is more important in areas with thick
•
–
– Fibrous overgrowth of tissues in maxillary cortical bone especially the buccal parts of the maxilla
–
tuberosities. and lingual parts of the mandible which are load- bearing
– Resorption in mandibular distal extension area and regions. (NEET 2013)

–
bone loss in the premaxilla region. • The mean ratio of anterior maxillary residual ridge
•
– Decreased Occlusal Vertical Dimension. resorption to anterior mandibular RRR is 1:4
–
– Facial Aesthetics often altered dramatically.
–

• Residual ridge resorption (Atwood)
•
Order I Pre-extraction-alveolus bearing tooth
Order II Post extraction-alveolus after extraction
Order III High, well rounder-high alveolar process
Order IV Knife-edge-High, narrow alveolar process
Order V Low, well-rounder-rounder flat alveolar process
Order VI Depressed-concave flat alveolar process
• Rate of RRR
COMPLETE DENTURES
•
– During the first year after extraction, the amount of RRR is about 2-3 mm in the maxilla and 4-5 mm in mandible. Later
–
the annual rate of reduction of height in mandible is 0.1 to 0.2 mm and it is four times less in the edentulous maxilla.
– The main factor that affects the rate of residual ridge remodeling is the mechanical force transferred from the denture
–
base and the tongue to the tissues.
bone resorption factor pressure
RRR ∝
bone formation factor
∝ damping factor ∝ anatomic factor
• Clinical Features
•
– The depth and width of the sulcus is reduced
–
– Muscles appear to be inserted on the crest of the ridge obliterating the sulcus.
–
– Decreased vertical dimension at occlusion.
–
– Reduction of the lower facial height (due to decreased VDO).
–
– Anterior rotation of the mandible
–
– Increase in relative prognathism.
–
– Resorption is centripetal (towards the centre) in the maxilla, and centrifugal (away from the centre) in the mandible.
–
Hence, the size of the maxillary arch will decrease with resorption and the size of the mandibular arch will increase with
resorption.
– Sharp, spiny and uneven ridge crest due to difference in rate of resorption from one place to another.
–
RELINING
Definition Process of adding base material to the tissue surface of the denture to adjust to the altered tissue contour.
Indications • Immediate dentures after 3-6 months
•
• Economical reasons where the patient cannot afford a new denture.
•
• Geriatric or chronically ill patients
•
Contraindications • When the residual ridge has resorbed excessively.
•
• Abused soft tissues due to an ill-fitting denture.
•
• Temporo-mandibular joint problems.
•
• Unsatisfactory jaw relationships in the denture.
•
• Dentures causing major speech problems.
•
• Severe osseous undercuts.
•
Advantages • Eliminates frequency of patient visits.
•
• Economical for the patient.
•
• Improves fit of the denture.
•
• A soft liner can be incorporated in this denture, if necessary
•
Disadvantages • Likelihood of altering the jaw relationship during the process.
•
• Cannot correct aesthetics, or jaw relations.
•
• Cannot correct occlusal arrangement.
•
• Cannot be used when excessive resorption has occurred. Hence it cannot be a substitute for a new
•
 
denture.
496
Rationale • Thin film is added – Relining
•
• More material – Rebasing
•
Relining Procedures • Clinical procedures:
•
• Static methods:
•
 
– Open-mouth technique.
–
 
– Closed-mouth technique
–
••
Functional methods
– Chair-side technique
–
• Laboratory procedures:
•
– Articulator method
–
COMPLETE DENTURES
– Jig method
–
– Flask method
–
Treatment • ZnOE is the material of choice. It is loaded on the tissue surface of the denture and the impression is
•
made using the denture as the special tray. After the maxillary and mandibular impressions are made
a new centric relation record is accomplished. (AIPG 2002)

• All these procedures are done in one appointment
•
TISSUE CONDITIONERS
• Highly plasticized acrylic resins
•
• Applied temporarily to the fitting surface of a denture
•
• Aid in rehabilitation of abused tissues
•
• Also used in the functional method or relining denture base
•
• Tend to harden and roughen within 4-8 weeks due to loss of plasticizer
•
Indication Contraindication
• Immediate dentures after 3-6 months where maximum residual • When the residual ridge has resorbed excessively
•
•
ridge resorption would have occurred • Abused soft tissues due to an ill denture
•
• When the adaptation of denture to the ridge is poor due to • Temporo mandibular joint problems
•
residual ridge resorption
•
• Patient dissatisfied with the appearance of the existing dentures
• Economical reasons where the patient cannot afford a new
•
• Unsatisfactory jaw relationships in the denture
•
denture
•
• Dentures causing major speech problems
• Geriatric or chronically ill patients who cannot withstand
•
• Severe osseous undercuts.
•
physical and mental stress of construction of new dentures
•
Composition
• Tissue conditioners are composed of polyethyl- methacrylate and a mixture of aromatic ester and ethyl alcohol. Tissue
•
conditioners are available as three component systems
– Polymer (Powder)
–
– Monomer (Liquid)
–
– Liquid plasticizer (Flow control)
–
• A gel is formed when these materials are mixed, with the ethyl alcohol having a greater affinity for the polymer.
•
Uses of Tissue Conditioners
• Tissue treatment
•
• Temporary obturator
•
• Baseplate stabilization
•
• To diagnose the outcome of resilient liners
•

• Liners in surgical splints
•
• Trial denture base
•
• Functional impression material
•
• Adjuncts for Tissue Healing
•
Temporary Soft Liners
• Can improve comfort, retention, occlusal vertical dimension (minor changes), and extension of denture bases (minimal).
•
• Use manufacturers recommendation for mixing, usually 1:1.5-2.0
•
• Typical composition:
•
– Powder: Polyethyl methacrylate powder/liquid.
COMPLETE DENTURES
–
– Liquid: Aromatic ester-ethanol
–
– These materials are soft and resilient and flow under pressure. - Material becomes rigid after a week - plasticizer
–
 
leeches out- Change the soft liner as necessary (usually lasts no longer than 4-6 weeks)
• The length of time required for tissue conditioning depends on the severity of irritation. A combination of treatment may
•
be necessary.
USE OF DENTURE ADHESIVES

Characteristics • Product composition should be supplied.
•
• Should not affect the integrity of the denture.
•
 
• Biologically acceptable.
•
 
• Effective function as adherent.
•
• The amount of material required for efficient retention of a denture is around 0.5 to 1.5 g.
•
 
Composition • Basic Ingredients: They swell and become viscous. E.g. Carbonyl methyl cellulose (CMC), Vegetable gums
•
• Colouring Agents: E.g. Red dye.
•
• Flavoring Agents: Menthol, peppermint, etc.
•
• Wetting Agents Preservatives Sodium borate, methyl paraffin, polyparaffin.
•
 
 
• Plasticizers: They are added to improve the handling properties of the material. E.g. polyethylene, mineral oil or
•
petrolatum.
• Dispersion Agents: They are used to prevent powders from clumping.
•
– Magnesium oxide
–
 
– Sodium phosphate
–
– Calcium stearate
–
– Calcium silicate
–
– Silicone dioxide.
–
Commonly used • Salts of Gontrez
•
are: (AIPG 2005) • Cellulose based salts
•
Indications • Improve retention and stability of the dentures
•
• To improve stability of a denture for a new or in-experienced patient.
•
• To stabilize trial bases during fabrication and insertion of the trial denture.
•
• For handicapped patients, Patients with xerostomia, Geriatric patients, Patients with poor muscle tone (such
•
as those with Parkinson’s disease, Tardive dyskinesia and Dysarthria)
 
• To provide a psychological sense of securityfor specific patients (Such as actors, teachers).
•
• To simplify the insertion for patients with tactile or movement deficiency. E.g. cerebral trauma patients.
•
 
• As an adjunct to the maxillary prosthesis.
•
Contraindications • A denture adhesive should not be used for patients with ill-fitting dentures or by patients who tend to overuse
•
denture adhesives.
• It should not to be used by patients who have medication-induced xerostomia because the adhesives require
•
ample saliva to provide retention.
498
• It should not be used for patients with worn out dentures.
•
• It should not be used as a substitute to a reliner or tissue conditioner.
•
• •
It should not be used for patients with physical inability to clean dentures.
• It should not be used in patients with temporary or immediate dentures where infection (disease) could result from
•
inadequate hygiene or adherence to dentures.
• It should not be used in patients allergic to components of adhesive. E.g. ‘Karaya’ a vegetable additive is known
•
 
to cause allergy in some patients.
MISCELLANEOUS
COMPLETE DENTURES
Modiolus is a point where eight muscles meet at the Angle of mouth

– Depressor anguli oris or triangularis
–
– Levator anguli oris or caninus
–
– Risorius
–
– Orbicularis oris
–
– Buccinator
–
– Zygomaticus major
–
– Quadrates labii superioris
–
– Quadrates labii inferioris
–
Anterior Deprogramming Devices are used in jaw relations as well as treatment of bruxism.
• Used In some patients in whom CR does not coincide with IP, protective reflexes may be encountered.
•
Snow shoe effect • This is the ability of the denture to distribute forces over wide areas due to an increase in the denture base area
•
Resiliency effect • Hanau described this factor as releaff, derived from resiliency and like effect. Soft tissues are of various densities
•
(Rosiliency and and resiliencies. Excess pressure in securing the CR must be avoided, as it causes excessive displacement of
like effects) soft tissues.
Christenson’s • The concurrent vertical changes (characteristic posterior seperation) associated with horizontal movements
•
phenomenon (anterior protrusion) of the jaws. To prevent this curve of spee is incorporated in the construction of complete
dentures.
Dentogenic con- • Teeth selection based on sex, personality and age of the patient. Also called as SPA factor.
•
cept or Dyses-
thetics (by frush
and fisher)
Balancing ramp • It is used to set non-anatomic teeth without compression curves in flat plane. The ramp is made up of acrylic or
•
amalgam distal of lower 2nd molar. Upper 2nd molar should make 3 point contact.
• Because of well-established protective reflexes that are reinforced every time the teeth come together, such patients will not
•
allow their mandible to be manipulated and hinged easily. If tooth contact can be prevented, they will forget these reflexes,
and manipulation becomes easier.
• The teeth can be kept apart with cotton rolls, a plastic leaf gauge, or a small anterior programming device made of
•
autoploymerizing acrylic resin (also known as a lucia jig).
• Deprogramming of muscles is used in the treatment of bruxism.
•
• It has been called a deprogrammer.
•
Interim immediate • Indicated when age, health or lack of time precludes more definitive treatment. Used for short time for reasons
•
denture of aesthetics, mastication or convenience, until a more definitive form of treatment can be rendered.
• It is a temporary partial denture used temporarily, during the healing period of the patient to preserve ridge
•
contour, until the permanent denture can be fabricated. They are mainly indicated in patients with periodontal
disease going in for total extraction.

Transitional denture • May be used when loss of additional teeth is inevitable teeth is inevitable but immediate extraction is not
•
advisable or desirable.
• Artificial teeth may be added to the transitional denture as and when the natural teeth are extracted.
•
• A transitional denture may become an interim denture when all of the natural teeth have been removed from
•
the dental arch
Treatment denture • To establish new occlusal relationship or vertical dimension and to condition the soft tissues that have been
•
abused by ill fitting prosthesis.
• Treatment partial denture may be used to carry tissue conditioners to abuse oral tissues and other medicaments.
•
Temporary remov- • They are used in patient where tissue changes are expected, where a permanent prosthesis cannot be
•
able partial denture fabricated till the tissues stabilize.
• They should never be used as a permanent or prolonged form of treatment because of the danger of destroying
COMPLETE DENTURES
•
the remaining oral tissues
Characteristics of Colour
Hue • It denotes a specific colour produced by a specific wavelength of light. It should be in harmony with the patient
•
skin colour.
Saturation or • It is the amount of colour per unit area of an object. It denotes the intensity of the colour
•
Chroma
Value or brilliance • It denotes the lightness or darkness of an object. It is actually the dilution of the colour with either black or
•
white to produce darker or lighter shades respectively. It is the most important aspect in selection of shade for
the restoration of match existing dentition
Translucency • Property of the object to partially allow passage of light through it. Enamel has high brilliance and translucency
•
Good to Know Points
• House gave the classification of tongue size.
•
• Wright gave the classification of tongue position
•
• Thick pasty saliva is due to reflex sympathetic stimulation of salivary glands and watery saliva is due to parasymparathetic
•
stimulation.
• Mandibular lingual tori mostly occur in the premolar region.
•
• 33% of edentulous mouths have retained root tips.
•
• Hardy’s tooth–also known as vitallium occlusal (VO) non anatomic teeth. Each tooth will look like the fusion of two PMs
•
and molars. On the occlusal surface of 3 teeth a vitallium ribbon is embedded in zigzag pattern.
• Mean denture bearing area in edentulous maxilla is 22.96cm2 and in mandible is 12.25cm2.
•
• Total available PPL area in each arch is 45cm2.
•
• Protrusive condylar path has primary influence on the distal inclines of maxillary cusps and mesial inclines of mandibular
•
cusps.
• Thickness of custom tray is 2mm
•
• The distance between incisive papilla to the labial surface • Masseteric muscle is a powerful muscle because of
•
of maxillary CI is 8mm and to the incisal edge of maxillary
•
multipennate arrangement of fibres. It has dual function
CI is 6mm. as related to complete denture.
• Number of frenii in maxilla-3 • Impression material of choice in patients with OMSF is
•
•
•
Number of frenii in mandible–4 Addition Silicone.
•
• The distal border of upper denture should extend 1-2 mm • The compact bone in combination with tightly attached
•
•
posterior to the vibrating line. dense submucosa and keratinized mucosa makes the
• The imaginary line joining the 2 Beyron points is an alveolar ridge area resistant to occlusal forces.
•
approximate hinge axis • Muscles involved in CR – temporalis and masseter
•
500
• Best esthetics for a maxillary denture is when teeth are • Will’s gauze: Measure vertical height of face
•
•
placed facial to alveolar ridge • Boley gauze: Record the measurement between the
•
• Palatal cusp of upper posterior teeth in complete denture borders of maxillary and mandibular dentures
•
patients should fall on the crest of mandibular ridge. • Osseointegration was first defined by Branemark.
•
• When noting condylar guidance, incisal pin should be out • Gnathodynamometer: An instrument for measuring the
•
of contact
•
force exerted in closing the jaws. Also called occlusometer
COMPLETE DENTURES
CHAPTER 12
Removable Partial Dentures
Objectives
• Classification of Edentulous Ridges • Secondary Impression and Master Cast for RPD
• Parts of RPD • Fabrication of RPD
• Surveying • Types of RPD
• Guiding Planes • Miscellaneous
• Principles of Design
CLASSIFICATION OF EDENTULOUS RIDGES – Unlike Cummer, Kennedy classified partially

–
edentulous arches and not the denture.
Kennedy Classification of Edentulous Arches – The classification is positional or anatomical
–
and conveys a picture of certain teeth and their
– Proposed by Dr. Edward Kennedy of New York in
relationships, but gives little information about the
–
1923.
teeth present and their positional relationships.
– Most popular classification.
–
Class I Bilateral edentulous areas located posterior to the remaining natural Mainly mucosa supported
teeth
Class II A unilateral edentulous area located posterior to the remaining natural Mainly mucosa supported
teeth
Class III A unilateral edentulous area with natural teeth remaining both anterior Mainly tooth supported
and posterior to it
Class IV A single, but bilateral (crossing the midline) edentulous area located Mucosa/teeth supported
anterior to the remaining natural teeth
Applegate’s Modification (1960)-Two more additional groups were added to Kennnedy’s Classification
Class V Edentulous area bounded anteriorly and posteriorly by natural teeth but in which the anterior abutment (e.g. lateral
incisor) is not suitable for support. It is basically a class III situation where the anterior abutment cannot be used for any
support.
Class VI Edentulous area in which the teeth adjacent to the space are capable of total support of the required prosthesis. This
denture hardly requires any tissue support. Most of the removable partial dentures are tooth tissue supported.
502
Applegate’s Rules
• Classification should follow rather than precede extractions that might alter the original classification
•
• If 3rd molar is missing and not to be replaced, it is not considered in the classification.
•
• If 3rd molar is present and is to be used as an abutment, it is considered in the classification
•
• If the second molar is missing and is not to be replaced, it is not considered in the classification.
•
REMOVABLE PARTIAL DENTURES
• The most posterior edentulous area or areas always determine the classification.
•
• Edentulous areas other than those, which determine the classification, are referred to as modification spaces and are
•
 
designated by their number.
• The extent of the modification is not considered, only the number of additional edentulous areas, i.e. the number of teeth
•
missing in the modification spaces is not considered only the number of additional edentulous spaces are considered.
• There can be no modification areas in class IV. Because any additional edentulous space will definitely be posterior to it
•
and will determine the classification.
Points to remember
• Class I arches are most common and class IV are least common. Class I and class II, long span class III and IV partial
•
dentures are tooth-tissue supported prostheses.
• Short span class III and IV are tooth supported partial dentures.
•
PARTS OF RPD
Major connector • Connects the components on one side of the arch to the components on the opposite side of the arch
•
• Largest and most important component
•
• Provide indirect retention
•
Minor connector • The connecting link between the major connector or base of a removable partial denture and other units of the
•
prosthesis, such as clasps, indirect retainers and occlusal rests
Rest • A rigid extension of a fixed or removable partial denture which contacts a remaining tooth or teeth to dissipate
 
•
vertical or horizontal forces (AIIMS Nov 2013)
• The main function of a rest is to transmit the occlusal forces acting on the denture along the long axis of the
•
abutment tooth
• Depression where the rest is fabricated to fit in is called a rest seat
•
• Functions of Rests;
•
– To direct forces along the long axis of the abutment tooth
–
– To prevent the denture base from moving cervically and impinging gingival tissue.
–
– To maintain a planned clasp-tooth relationship.
–
– To prevent extrusion of abutment teeth.
–
– To provide positive reference seats in rebasing and/or impression procedures.
–
– To serve as an indirect retainer by preventing rotation of the partial denture (Class I or II RPD’s only).
–
Direct retainer • A clasp or attachment placed on an abutment tooth for the purpose of holding a removable denture in position
•
• Most critical component for a removable partial denture.
•
Indirect retainer • A part of a removable partial denture which assists the direct retainers in preventing displacement of distal extension
•
denture bases by functioning through lever action on the opposite side of the fulcrum line
• This is not a separate component. Instead, it is a combination of the above-mentioned components, which offer
•
indirect retention
• The indirect retainer is a separate component in a distal extension denture base. It is a must and it assists the direct
•
retainer to obtain retention of the denture.
Removable Partial Dentures 503

Denture base • Artificial tooth replacement
•
• Commonly used material is
•
– Methyl methacrylate: Laboratory technique is simple, good colour stability
–
– Copolymer (Luxene): Superior toughness and strength
–
––
Styrene (Jectron): High fatigue resistance
The first five are cast in metal and the other two may be fabricated using other materials.

Function Component part Location
Support Occlusal rest Occlusal, lingual, incisal
Stability Minor connector, indirect retainer and From the marginal ridge to the junction of the middle and gingival third of
denture bases proximal surface of abutment crown
Retention, Direct retainers Retention is provided by the retentive arm of the clasp in the gingival of
stability and (clasps) buccal/lingual surface undercut.
reciprocation Stability is provided by the retentive arm of clasp at middle third of the
opposite side to that of retentive arm at junction of middle and gingival
thirds. (AIPG 2006)
Design Considerations for all Major Connectors

• The borders should be placed
•
– 6 mm away from gingival margins in the maxillary arch and 3mm in the mandible (NEET 2013)
–

– Should be rounded to avoid interference to the tongue
–
– Parallel to the gingival margins
–
– The anterior border of the maxillary major connector should end in the valley of the rugae and it should be designed
–
such that it never lies on the crest of the rugae
• The metal framework should cross the gingival margin only at right angles
•
• The part of the framework adjoining the tooth surface should be hidden in the embrasures to avoid discomfort.
•
 
• The major connector should be symmetrical and should cross the palate in a straight line
•
• It is better to avoid covering the rugae area in order to prevent any discomfort during speech.
•
• The major connector should not extend over bony prominences like tori. Relief is given for a small tori, surgical excision
•
is done for a large one
Designing steps for major connectors (AIPG 2006)

• Outline the stress bearing areas
•
• Outline the non stress bearing areas
•
• Outline the strap areas
•
• Selection of strap type
•
• Unification
•
Types of Maxillary Major Connector (AIIMS Nov 2013)
Type Important Features
Single palatal bar Derives least support from the palate. To maintain rigidity it has to be made bulky.
Palatal strap It is rigid without excessive bulk. Width increases with the path of endentulous area.
best suited for short span, tooth supported edentulous areas
504
Anteroposterior palatal bar (double palatal The most rigid palatal major connector
bar) (AIPG 2001) Derives least support from the bony palate
It is indicated in the presence of a tori that is not be removed
Anterior bar is wider than palatal bar. Anterior bar is narrower than the width of palatal strap.
Posterior bar is half oval, its width is equal to single palatal bar but less bulky
Not indicated in high narrow palatal vault and if an remaining teeth are periodontally weak.
Anteroposterior palatal strap (closed It is the best designed palatal major connector. It is indicated in almost many maxillary partial
horse shoe) denture design
Best suited for distal extension RPD

The anterior border should be located posteriorly in the valleys between the rugae crests.
U shaped or horse shoe shaped Least desirable palatal major connector. Least rigid. This is indicated only in cases of
inoperable tori extending to the posterior limit of the hard palate
Complete palate (Palatal plate) Major connector that provides greatest retention
The posterior border extends to the junction of the soft and hard palate. It is indicated when
anterior or posterior teeth are to be replaced bilaterally.
Types of Mandibular Major Connectors

Lingual Bar • Commonly used
•
• It is half pear-shaped in cross-section with the thickest portion placed inferiorly
•
• It is made from a thick (6-gauge) half pear-shaped wax pattern.
•
• There must be a minimum of 8 mm vertical clearance from the floor of mouth. The upper border of the
•
pattern should have a 3 mm clearance from the marginal gingiva to avoid any soft tissue reaction
• The minimum height of the major connector should be atleast 5 mm
•
• Lingual bar should be placed as inferior as possible so that movements of the tongue is not restricted
•
and sufficient space can be available above it.
Lingual Plate • High lingual frenum, active tissues of the floor of the mouth
•
• Long span edentulous ridges, class I or II design RPD and indirect retention in needed
•
• Anterior teeth having reduced periodontal support and need stabilization
•
Double lingual bar also k/a • Periodontal weakened tooth with spacings. Large interproximal spaces that could cause aesthetic
•
kennedy bar, lingual bar concerns by the metal display of a lingual plate.
with continuous bar, split Indications:
lingual bar Situations where the major connector must contact the natural teeth to provide bracing and Indirect retention

(AIPG 2014, AIIMS Nov and there arc open cervical embrasures whlch contraindicate the use of a lingual plate. There must be

2013) adequate space for the lingual bar portion of the major connector.
Contraindications-
• Where a lingual bar or lingual plate will suffice
•
• Any contraindication for a lingual bar.
•
• Any contraindication for a lingual plate
•
• Diastemas.
•
Labial Bar • Extreme lingual inclination of premolars and anterior teeth, inoperable large tori
•
Minor Connectors
• Are of Four Types
•
– Joining the clasp assembly to major connectors
–
– Joining the indirect retainer or auxiliary rest to the major connector.
–
– Joining the denture base to the major connector.
–
– Approach arm in bar type clasp
–
• In mandibular distal extension cases the minor connector should cover 2/3rd the length of edentulous ridge.
•
• It is available in three forms:
•
– Latticework construction.
–
– Meshwork construction.
–
– Bead, wire or nail head minor connectors.
–

Direct Retainers
• Classified as:
•
Extracoronal direct retainers (Clasps) Intracoronal direct retainers (Attachments)
• Manufactured retainers (Dalbo) • Internal attachment
•
•
• Custom-made retainers: • External attachment
•
 
•
– Occlusally approaching (Circumferential or Aker’s • Stud attachment
–
•
 
clasp) • Bar attachment
 
– Gingivally approaching (Bar or Roach’s clasp)
•
• Special attachments
–
•
Extracoronal Direct Retainers (Clasps)
Definition A part of a removable partial denture which acts as a direct retainer and/or stabilizer for the denture by
partially encircling or contacting an abutment tooth
The functional requirements of • Retention

•
 
a clasp include • Stability
•
• Support
•
• Reciprocation
•
• Encirclement
•
• Passivity
•
Clasp arms – stabilization and • Occlusal 3rd – support
•
retention • Middle 3rd – stabilization
•
• Cervical 3rd – retention
•
Bucco lingual width of the • Clasp alloys are selected based on this measurement. Alloys with greater flexibility (low modulus
•
undercut of elasticity) are used against deeper undercuts
• For a 0.010-inch undercut - cast chrome alloy is used.
•
• For a 0.015-inch undercut - gold alloy is used.
•
• For a 0.020-inch undercut - wrought wire is used.
•
Types of clasps
• Circumferential or Aker’s clasps
•
 
• Vertical projection or Bar or Roach clasps
•
• Continuous clasp
•
Types of Cast Circumferential Clasps: of 11 Different Types
Simple circlet clasp Most versatile and widely use. It Best for tooth supported partial Clasp can be adjusted only in one
approaches the undercut from the dentures direction (i.e buccolingually but not
edentulous space. It engages the occlusongingivally), Cannot be used for
undercut, located away from the distal extension cases as they engage a
edentulous space mesiobuccal undercut
Reverse circlet or re- Circlet clasp. Simple circlet clasp Usually bar clasps are preferred Poor aesthetics as the clasp runs from
verse approach clasp normally engages mesial undercut for distal extension cases. the mesial to the distal end of the facial
on the abutment tooth while reverse These clasps are used when surface
circlet usually engages a distal a bar clasp is contraindicated.
undercut on the abutment tooth E.g. if there is an undercut
located adjacent to the edentulous area in the ridge Presence of a
space. This clasp is designed in soft tissue undercut caused by
such a way that the clasp arises buccoversion of the abutment
from the mesial side and ends on tooth.
the distal undercut
506
Multiple circlet clasp A multiple clasp is simply two It is used when additional
opposing circumferential clasps retention is needed. Multiple
joined at the terminal end with two circlet clasps indicated in
minor connectors and joined by their periodontally compromised
two reciprocal arms abutments
Embrasure clasp or two simple circlets joined at their Embrasure clasp used on Embrasure clasp exhibits high
modified crib clasp bodies the side of arch where no percentage of fracture due to
edentulous space is present inadequate tooth preparation in contact
(class II or class III partial area

denture). Occasionally, a very
small edentulous space can be
closed by a modified embrasure
clasp called pontic clasp
Ring clasp Ring clasp encircles nearly all Indicated in titled molars. Difficult to adjust or repair. Increased
tooth from its origin, the ring clasp Indicated in a distal edentulous tooth surface coverage. Poor physical
needs the strength to prevent clasp condition with a distolingual qualities.
distortion due to the extreme length undercut where a reverse
of the clasp arm circlet clasp cannot be placed
(no buccal undercut)
Fishhook or hairpin It is type of simple circlet clasp, which It is used in conditions where It has poor aesthetics. It tends to trap
clasp or reverse ac- after crossing the facial surface of the undercut is near the and accumulate food debris
tion clasp the tooth loops back to engage the edentulous space. Presence of
proximal undercut beneath its point a soft tissue undercut
of origin.
Onlay clasp It is an extension of a metal crown or It is used in the occlusal As this clasp covers large structure,
onlay with buccal and lingual clasp surfaces of submerged (that are it may lead to break down of enamel
arms below the occlusal plane) so surfaces. Hence, it should be caries-
that the normal occlusal plane resistant mouth
can be restored with a onlay
Combination clasps Reciprocal arm–cast metal Used in abutment adjacent to Tedious lab procedures Easily breaks
(AIPG 2008) kennedy class I or II posterior or distorts Poor stability

Retentive arm–wrought wire edentulous areas when
It has a thin line contact which undercut is at mesio facial
collects less debris and is easy to line angle on distal abutment
maintain. It can flex in all planes tooth. It is indicated on a
abutment tooth adjacent to a
distal extension base or on a
particularly weak abutment.
(AIPG 2014)
Half and half clasp It has a retentive arm arising from This design is intended to This design produces large tooth
one direction and a reciprocal arm provide dual retention Isolated coverage
arising from another. Two minor abutment tooth if often rotated
connectors are needed for this and clasping by conventional
design means is difficult
Back-action clasp It is a modification of the ring Lack of support to the occlusal rest
clasp. Here the minor connector is reduces its function. It has both
connected to the end of the clasp biological and mechanical unsound
arm and the occlusal rest is left principles
unsupported
Grasso’s clasp or Developed by Grasso, this clasp Suitable not posterior teeth Difficult to maintain as the block out
VRHR clasp consists of a vertical reciprocal arm, with high survey lines. Does zone between the base of the reciprocal
an occlusal rest and a horizontal not require the preparation arm and the tooth tends to collect food
retentive arm, each arising of guide planes. It is a push debris.
separately from the major connector type of retention, which is
more effective than the pull
type retention provided by a
circumferential clasp

Vertical Projection or Roach or Bar Clasp (Based on the Shape of the Retentive Terminal)
T clasp • Used in a distal extension denture base with a distobuccal undercut
•
• Can also be used for a tooth supported partial denture with natural undercuts. Since the clasp is designed to
•
use the existing undercuts without creating new ones, it is referred to as clasping for convenience.
• •
Not be used on a terminal abutment tooth if undercut is located away from edentulous space.
• Should not be used over a soft tissue undercut
•
• The clasp has good aesthetics but due to the flexibility of approach arm it lacks the bracing quality

•
Modified T clasp • It is similar to T clasp but the non-retentive finger (usually the mesial terminal) of the ‘T’ terminal is removed.
•
• It is used in canines and premolar for better aesthetics.
•
• Disadvantages
•
– It does not have 180° encirclement.
–
Y clasp • Y clasp is basically a T clasp modified to suit certain abutments where height of contour is high at faciomesial
•
and faciodistal line angles but low at the center of the facial surface.
I clasp • Used on distobuccal surface of canines for aesthetics.
•
• Only the tip of the clasp (2-3 mm) contacts the tooth. Hence, stability and encirclement is decreased.
•
Infrabulge clasp or • The approach arm for the retentive terminal arises from the border of the denture base, either as an extension
•
mirror view clasp: by of a cast base or attached to the border of a resin base.
MM DeVan • There are two occlusal rests on each abutment tooth.
•
 
• The lingual aspect of the abutment may be plated (supported) or left open.
•
 
• It is more flexible because the portion of the metal base that gives rise to the approach arm has an incomplete
•
 
cut. The cut is prepared either by machining or placing a thin matrix band during casting
• The retentive arm can also be made of wrought wire, which has higher flexibility. The wire may be soldered to
•
the metal base or embedded in the resin base.
• Advantages:
•
– More aesthetic as it is placed more interproximally.
–
– Increased retention without any tipping action on the abutment.
–
– Resists distortion during handling
–
I-bar • Modified I type roach clasp introduced by Kratochvil. It has a mesial rest arising from a major connector, an
•
I-bar retentive arm and a long proximal plate.
• It is designed to reduce tooth contact.
•
• Krol in 1973, modified kratochvil’s I-bar system and introduced the RPI and RPA systems.
•
Intracoronal Direct Retainers (Attachments)
– So called because a part or the whole of the retentive components are located within the anatomical contour of the
–
abutment teeth.
– Types:
–
Internal attachment

- It is also known as precision attachment or frictional attachment or key and keyway attachment or parallel

attachment or slotted attachment.
- The matrix engages the vertical walls built into the crown of the abutment tooth to create frictional resistance

during removal
- Dr Herman ES Chayes first formulated this principle in 1906.

- Some of the commonly used internal attachments are:

* Ney-Chayes attachment.

 
* Stern Goldsmith attachment.

* Baker attachment.

External attachment

Stud attachment

Bar attachment

Special attachments

– All attachments have male and female components that are manufactured using standard measurements.
–
508
Advantages Disadvantages
Internal Attachment • Elimination of visible retentive • Preparation of abutments and castings
•
•
Used when teeth are present on both components. • Complicated clinical and lab procedures.
sides of edentulous side
•
• Elimination of visible vertical support • Wear resulting in loss of frictional resistance.
(AIPG 2001)
•
element through a rest seat.
•
• Difficult to repair and replace.

• Contraindications:
• Provides some horizontal stabilization
•
•

(AIPG 2002) • Least effective in teeth with small crowns.
•
• Stimulation of underlying tissues due to

•
– Large pulp (this limits the • Difficulty to place it completely within the
•
intermittent vertical massage

–
•
depth of the receptacle.) circumference of the abutment tooth.
– Short crowns offer lesser
–
frictional resistance.
– Cost
–
External Attachment: e.g. ASC52, • Aesthetic, • Bulky attachment requires more space within the
•
•
DALBO, CEKA, and ERA • Resilient removable partial denture.
•
• Easy to insert. • Weak and breaks easily.
•
•
• They are indicated for an anterior • Difficult to replace.
•
•
prosthesis in a young patient with a large
pulp chamber
Stud Attachment: e.g. GERBER, • More versatile • It has a tipping effect on the abutment teeth.
•
•
DALLA BONA, and ROTHERMAN • Decreased leverage • Complex design.
This attachment acts like a
•
 
•
• Can be used on malaligned abutments. • Cannot be used in cases with limited space.
stress director. They are used for
•
•
overdenture abutments • Easy to adjust and repair. • Expensive
•
•
Bar Attachment: e.g. DOLDER, • Rigid splinting • Space requirement.
•
•
HADER • Cross-arch stabilization • Needs frequent soldering.
It is used when there is bone loss
•
•
• It can be used along with other • Difficult to maintain oral hygiene
around the abutment teeth
•
•
attachments or implants for a combined
fixed-removable prosthesis.
Special Attachment
• These retainers are different from both intracoronal and extracoronal retainers and hence are classified separately.
•
• They are of two types namely:
•
– Retention based on frictional resistance.
–
– Retention based on placement of an element in the undercut.
–
• Both types have an intracoronal or an extracoronal locking device to provide retention
•
• Advantages:
•
– Highly aesthetic as the visible clasp components are absent.
–
– It reduces torque and tipping forces on the abutment.
–
• Special attachments are also classified as locking and non-locking types. The non-locking types can be used for Kennedy’s
•
class I and class II case.
• Commonly used special attachments are:
•
Neurohr spring-lock attach- It uses a tapered vertical rest within the contour of the abutment tooth. A single buccal clasp arm with
ment ball tip engages the undercut in the abutment
Neurohr-Williams shoe at- a modification of the Neurohr spring-lock attachment. Here, an additional groove is prepared on the
tachment distobuccal line angle.
Dowel rest attachment (Dr. A dimple (depression) is created on the lingual surface of the abutment. A box (projection) is fabricated
Morris.J.Thompson) on the lingual arm of the denture framework such that it fits into the dimple
Zest anchor device It has a nylon male post attached to the denture base, which fits into the female insert in the abutment.
Intracoronal magnets Magnets with opposite polarity are placed on the rest seats and the denture base. The magnetic attraction
produces retention

Hannes Anchor or IC plunger Here the male plunger fits in to a dimple on the proximal surface of the abutment. This dimple is located
below the height of contour of the abutment tooth
Servo Anchor SA or Ceka Here, the female retaining device is placed on the denture base and the male device is attached to the
abutment tooth
Bona Ball similar to Servo Anchor SA
Rotherman It has a low profile retaining device. The male component is attached to the abutment. The female

retentive clip is attached to the denture base. Compressing or spreading the retentive clips alters the
retention
Long copings They are used in cases with compromised dentition like treated cleft palate cases, cross bite, deep bite
etc. An overdenture is placed on the copings
Indirect Retainers
Types of Indirect Retainers
Auxiliary occlusal • Most frequently used.
•
rest • Located on the occlusal surface as far as possible away from the distal extension base.
•
• Placed perpendicular to the midpoint of the fulcrum line. If this perpendicular ends on the incisal area it is
•
avoided
Canine extension • In some cases a finger like extension (Lug seat) from a premolar rest is placed on the lingual slope of the
•
from the occlusal adjacent canine
rest • Used when the first premolar must also act as a primary abutment.
•
Canine rest • If the mesial marginal ridge of the first premolar is close to the fulcrum line, canine rest is used.
•
• This design can be modified by placing the minor connector anterior to the canine. The minor connector hooks
•
back into the cingular rest seat.
• This increases the efficacy of the indirect retainer (due to increase in distance from the fulcrum line).
•
Continuous bar re- • As they rest on unprepared lingual inclines of anterior teeth, they are not indirect retainers but they help to
•
tainers and linguo- provide indirect retention.
plates • They are converted to indirect retainers when they have a terminal rest.
•
• In Kennedy’s class I and class II cases, these retainers should be placed just above the middle third of the
•
anterior teeth to avoid unwanted tooth movement
SURVEYING
Survey • To examine as to condition, value, or situation; to appraise

•
Surveying is defined as • An analysis and comparison of the prominence of intraoral contours associated with the fabrication
•
of a prosthesis
Surveyor • An instrument used in the construction of a removable partial denture to locate and delineate the
•
contours and relative positions of abutment teeth and associated structure
• The surveyor is a parallelometer; an instrument used to determine the relative parallelism of surfaces
•
of teeth or other areas on a cast.
• Dr. A.J. Fortunati (1918) was the first person to use a surveyor
•
Objectives • To design a RPD such that it’s rigid and flexible components are appropriately positioned to obtain
•
good retention and bracing.
• To determine the path of insertion of a prosthesis such that there is no interference to insertion along
•
this path.
• To mark the height of contour of the area (hard or soft tissues) above the undercut.
•
• To mark the survey lines. (height of contour of a tooth)
•
 
• To mark the undesirable undercuts into which the prosthesis should not extend.
•
510
Steps in surveying (AIPG • Establish guiding planes: By altering the A P tilt of the cast
•
2006) • Establish retentive areas: Done by adjusting the lateral tilt of the cast
•
• Establish the interferences:
•
• Lingually inclined premolars and bony prominences are most common interferences
•
• Avoid them by lateral tilting of cast
•
• Establish the esthetics.
•
Types • •
The surveyors commonly used are:
– Ney surveyor (widely used)
–
– Jelenko or Will’s surveyor
–
– Willam’s surveyor
–
Uses • Surveying the diagnostic and primary casts.
•
• Tripoding the cast. (Recording the cast position).
•
 
• Transferring the tripod marks to another cast.
•
• Surveying the master cast.
•
• Contouring crowns and cast restorations.
•
• Placing internal attachments and rests.
•
• Performing mouth preparation directly on the cast to determine the outcome of treatment.
•
 
• Surveying the master cast.
•
• Surveying ceramic veneers before final glazing.
•
 
Types of surveyor
Ney Wills (Jelenko) Williams
Horizontal arm The horizontal arm is fixed The horizontal arm swivels Have revolving horizontal
horizontally around the vertical arm with a joint in the
column middle
Surveying arm Surveying arm is completely passive and is Surveying arm is spring loaded Spring mounted surveying
positioned by a locking device arm that could be locked at
any position
Level platform/surveying Universal table Universal table They have a gimbal stage
table table and are used to place
precision attachments
Vertical arm Retained by friction within a fixed bearing Spring mounted and returns to top
position when it is released
Carbon marker Circular Triangular

Undercut gauge Circular beaded A fan shaped bead with each wing
of the fan measuring different
dimensions.
Surveying Tools
Analysing rod (used • First tool to be used. It is more of a diagnostic survey tool. It helps to analyze the location of the height of
•
before survey lines are contours, the presence and absence of favourable and unfavourble is used to determine the parallelism of
marked) one surface to another. It also helps to arbitrarily determine the path of insertion
Carbon marker • The resultant line formed by the scribe (carbon marker) is known as a survey line. These survey lines help
•
us in positioning the various component parts of a removable partial denture
Undercut gauges • A gauge is a high precison instrument used to measure the linear dimension of any structure. Undercut
•
gauges are used to measure the depth and location of the undercuts on the analyzed tooth in three
dimensions.
Wax Knife • It used to eliminate or block out undersirable undercut areas with wax on the cast
•

Colour Code Index Markings on Master Cast
• Red: Denote action, rest seats (solid), recontouring (outline)
•
• Black: Survey lines
•
• Blue: Identify areas of RPD that will be made of acrylic
•
• Brown: Identify areas of RPD that will be made in metal
•
Surveying lines

Blatterfein classified survey lines as:
• Typical-Medium in the middle of tooth surface buccal
•
• Atypical-High, low and diagonal
•
High survey line passes from the occlusal It is commonly found in inclined teeth and in teeth When a high survey line is present,
third in the near zone to the occlusal third in with a larger occlusal diameter compared to its the undercut will be deep and hence a
the far zone diameter at the comentoenamel junction wrought wire clasp which is more flexible
should be used.
Medium survey line extending from the During survey, the cast should be titled such Either Aker’s or roach clasp is used for
occlusal third of a near zone to the middle third that maximum number of teeth have a medium teeth with a medium survey line. Aker’s
of the far zone survey line clasp is preferable
Low survey line is closer to the cervical third It is common teeth with marked inclination, when A modified T clasp is used for teeth with
of the tooth in both near and far. A low survey it is associated with a high survey line on the low survey lines
line arising from the gingival third of the near opposite side
zone to the gingival third of the far zone
Diagonal survey line: This survey line runs It is more common on the buccal surfaces of It can be managed by using reverse
from the occlusal third of the near zone to the canines and premolars action (hair pin) or ring type Aker’s clasp
cervical third of the far zone
GUIDING PLANES
• Guiding planes are located on proximal and axial surfaces of abutment adjacent to the edentulous area.
•
• Guiding plane preparation for distal extension RPD differs from that usually done on abutments anteriorly and posteriorly
•
to an edentulous space.
• For distal extension RPD, guiding plane should involve approximately 2/3 of vertical length of enamel crown and 1/3 the
•
buccolingual width of tooth.
• Greater the surface area contact of eath minor connector to its guiding plane, the more the horizontal distribution of
•
forces.
• Determine the path of insertion
•
• Determine the path of removal
•
• Assure predictable clasp design and retention
•
Factors determining the path of insertion and removal are:
• Guiding planes
•
• Retentive undercut areas
•
• Interference and
•
• Aesthetics
•
PRINCIPLES OF DESIGN
• There are four design concepts, which can be used to distribute the force evenly along the soft tissues and supporting tooth
•
structure. They are:
512
Conventional rigid • The denture is designed with rigid components, which act like a raft foundation to evenly distribute the forces
•
design on the supporting tissues.
• This design is used in all general cases. The only flexible component of these dentures is their retentive
•
terminal.
Stress equalization ••
Dentures with a stress breaker are also called as a broken stress partial dentures or articulated prostheses.
Physiologic basing • This technique distributes the occlusal load between the abutment teeth and the soft tissues by fabricating a
•
denture based on a functional record.
• Functional record is obtained by recording the tissues under occlusal load or by relining the denture under
•
functional stress.
• This technique involves making an impression of the soft tissues in a compressed state.
•
Broad stress distri- • According to this philosophy of design, the occlusal load acting on the denture should be distributed over a
•
bution wider soft tissue area and maximum number of teeth.
• This is achieved by increasing the number of direct retainers, indirect retainers, and rests and by increasing
•
the area of the denture base.
SECONDARY IMPRESSION AND MASTER CAST FOR RPD

• Functional Impressions
•
– McLean advocated that the tissues should be recorded in their functional form.
–
– The saddle area is recorded in functional and physiologic form and the teeth are recorded in anatomic form.
–
– The functional impression is retained in the mouth while the anatomic impression material is applied over it. So this
–
is also called as PICK UP impression as it picks up the first (functional) impression along with it.
– Functional impressions are required only to record edentulous saddles. The existing teeth do not change form
–
under load and hence they do not require a functional impression. These impressions are indicated for tooth tissue
supported partial dentures class I and class II RPD.
• Dual impression techniques are broadly of two types:
•
– Physiologial or functional dual impression
–
– Selective pressure functional dual impression
–
• The common techniques employed to record a physiological dual impression are:
•
– McLean’s technique
–
 
– Hindle’s modification of McLean’s technique
–
– Functional relining method
–
– Fluid wax.
–
FABRICATION OF RPD
• After recording the master impression, the framework is fabricated for a cast partial denture. The framework is essential
•
for other procedures like preparing occlusal rims, jaw relation, etc.
• Frame- work fabrication involves the following steps:
•
– Wax-up
–
– Duplication and preparation of refractory casts
–
– Waxing
–
– Investing
–
– Burn out
–
– Casting
–
– Finishing and polishing.
–
• Design transfer includes the following steps:
•
– Marking the height of contour
–
– Measuring the undercut
–
– Drawing the clasps
–
– Drawing the connectors.
–

• Beading is defined as, “Scoring a cast with a sharp instrument or bur in any desired area to provide a seal between the
•
finished prosthesis and the soft tissue.
– Beading is nothing but a depression created along the borders of the framework drawn on the cast so that the resultant
–
framework will have an elevation at its borders. This is done only for the maxillary cast to get a good seal.
– A spoon excavator is used to produce beading. The depth of the bead should not extend more than 1 mm and it
–
should thin down near the gingival
– The purposes of beading are:

–
To ensure intimate tissue contact of the major connector with selected palatal tissues.

To provide a visible finishing line for the casting

To transfer the major connector to the investment.

– Beading should be done in valleys of rugae and should not be more than 0.5 mm in width.
–
• Blockout of Wax is defined as Elimination of undesirable undercut areas on the cast to be used in the fabrication of the
•
removable partial denture.
• Relief: It is defined as, the procedure of placing a sheet of wax in strategic areas on the master cast to be duplicated so that
•
a refractory cast can be made.
TYPES OF RPD
Unilateral • They are used to replace single teeth or short span edentulous space.
•
Implant supported • The implant can either be used like an ordinary abutment or as an overdenture abutment depending on its
•
location
• A bar super-structure is placed over the implant with a coping screw.
•
• The bar super- structure has two parts namely, a retention bar over the implant and a cantilever bar extending
•
across the ridges from each implant
Removable partial • A root stump or a badly broken down tooth surrounded by edentulous space on both sides can be used to
overdenture
•
support the denture.
• The supporting tooth that gets covered by the denture is known as an overdenture abutment.
•
Guide plane RPD • Used in partially edentulous areas along- with periodontally weak abutments.
•
• The factors to be considered for evaluating the periodontal status of the weak teeth are:
•
 
– Protection of the teeth from continuous or intermittent movement.
–
 
– Protection of the gingiva and the interproximal tissues from food impaction.
–
– Prevention of unnecessary occlusal forces.
–
• Usually a broad stress distribution concept is used.
•
I bar RPD • I-bar is a modified direct retainer designed to minimize tooth contact. Dentures using I-bar retainers are called
•
I-bar removable partial dentures.
Swing lock • First described by Dr. Joe J. Simmons (1963).

•
• They are used in cases where the number of remaining teeth is too few to support a conventional design.
•
• They have a hinged labial arm additional to the lingual major connector, which when locked to the major
•
connector splint all the remaining teeth.
• The labial bar can be unlocked during insertion and locked after insertion. Since the labial bar moves around
•
a hinge joint these dentures are called swing lock dentures.
• The main function of the labial bar is to support the periodontally weak teeth.
•
• Indications
•
– Missing key abutments
–
– Presence of few remaining teeth
–
– Presence of unfavourable tooth contours like excessive inclination, etc.
–
– When the position of natural teeth are not conducive (facilitative) for a conventional design.
–
– Presence of unfavourable soft tissue contours like soft tissue undercuts, etc.
–
– For retention and stability of a maxillofacial prosthesis.
–
– To retain the prosthesis for patients who have lost large segments of teeth and a resorbed alveolar ridge.
–
514
Spoon dentures • These are completely mucosa borne dentures used exclusively for Kennedy’s class IV cases.
•
• They are mostly used in children.
•
• They are fabricated using acrylic resin or chrome metal or stainless steel.
•
• The denture is designed to cover a large area in the palate but the gingival margins should not be covered.
•
•
•
Atleast 3 to 4 mm gingival clearance is provided
• Design Considerations: The following points should be considered while selecting this denture
•
– Nature of mucosa: The mucosa should be firm with the presence of submucosa.
–
 
– Form of hard palate: The palatal area should be large with steep sides to provide adequate support and
–
 
indirect retention
– Closeness of occlusion
–
– Degree of overbite
–
• Advantages
•
– Easy to fabricate, requires less time.
–
– The gingiva is not affected because it is relieved.
–
 
– Since extensive tooth contact is not present, incidence of caries is considerably decreased.
–
 
Every dentures • These dentures are called so because they were first described by Every.
•
• Craddock termed them as “Precision plastic base dentures”.
•
• They are used in Kennedy’s class III cases with modifications. They are more commonly used in the maxilla.
•
• The denture is designed based on broad palatal coverage, which helps to withstand the vertical load. The
•
palatal tissues and the teeth in the anterior segment help to withstand the lateral load
• The Every denture is designed based on the following principles:
•
 
– The denture should contact the natural teeth to transfer the axiomesiodistal stress acting on the denture
–
– The proximal surfaces of the denture teeth should be convex and have a high survey line. This design
–
helps to shift the contact point with the natural abutments occlusally
– Since the contact points are placed occlusally, the gingival embrasures are widened. This produces a
–
natural look in addition to minimizing the incidence of caries and periodontal pockets.
– The posterior teeth that support the denture should be clasped to prevent backward movement of
–
teeth. The denture base is extended posteriorly to clasp the distal-most tooth
– The denture base should never extend over the gingiva.
–
– The denture gains its retention through adhesive forces and atmospheric pressure.
–
Two part dentures • Described by Lee, these dentures were designed to overcome the technical problems in using the proximal
•
undercuts in unilateral dentures.
• These dentures are constructed in 2 parts, which have different paths of insertion
•
Claspless dentures • These dentures are designed with spring-loaded nipples, which are designed to engage the proximal undercut
•
of the primary abutment. E.g. ZA anchor system.
 
• The ZA anchor system has a
•
– Nipple: The nipple is spring loaded and can be made of nylon or metal. It fits into the casing and is
–
designed to engage the proximal undercut during insertion
– Casing: The casing is a hollow cylinder with external threading, which can be screwed into the acrylic
–
denture base.. The placement of the casing is determined by processing a dummy unit, which can be
discarded later. The casing should be positioned parallel to the ridge near the undercut
• When a displacing force acts on the denture, the nipple is forced against the height of contour of the tooth
•
• The resistance offered by the spring against this compression provides retention to the denture.
•
• The entire attachment has a collar, which limits the amount of projection of the nipple from its housing
•
• Advantages
•
– This attachment is quite small; hence, it can be used even in a single tooth removable partial denture.
–
• Disadvantages
•
– Metal nipple might abrade the tooth.
–
– Nylon nipple may wear out soon
–
– Requires frequent replacement
–
Disjunct denture • Kennedy’s class I dentures with special stress breakers between the tooth- supported part and the tissue-
•
supported part of the denture.
• The stress breaker is special in that it is a bar and slot and not a conventional hinge. The bar of the stress
•
breaker is called a disjunct bar.

Immediate • They are given in cases having teeth with poor prognosis. The denture is inserted on the day of extraction.
•
• It is of two types, namely temporary immediate partial denture and permanent immediate partial denture.
•
• Advantages
•
– It is more aesthetic (improves patient psychology).
–
– Prevents supra-eruption, and drifting of the opposing and adjacent teeth respectively.
–
 
Haemorrhage and swelling is controlled because it acts like a splint over the surgical site

RPI (Rest, Proximal Plate and I-bar)
• RPI is a modified I-bar retainer system. Krol devised it in 1973. All the components of the I- bar assembly were modified
•
significantly to fulfill Krol’s design. (AIPG 2004)

• The principle of Krol’s design was “stress control with minimal tooth and gingival coverage”.
•
• The speciality of these dentures is that the direct retainer is modified such that the retentive and reciprocal units of the
•
clasp act in the mesiodistal direction (in a conventional design the retentive and reciprocal units act buccolingually).
• The advantage of adopting this design is the minimal tooth contact/coverage produced by it. Hence, these dentures are
•
easier to maintain.
• Modification of each component of the I-bar retainer required forming a RPI system.
•
Mesial Rest • The mesial rest extends only into the triangular fossa even in molar preparations. The canine rests are circular,
•
Modification concave depressions prepared on the mesial marginal ridge.
• It does not cover the entire marginal ridge
•
Proximal Plate • One of the major disadvantages of the I-bar denture was the excessive tooth contact produced by the extra long
•
Modification proximal plate. Krol introduces three modifications to the proximal plate.
• Design modification I: The proximal plate extends from the marginal ridge to the junction between the middle and
•
cervical third of the tooth.
• Design modification II: The proximal plate is extends along the entire length of the proximal surface of the abutment
•
with a minimum tissue relief. A relief is provided near the gingival margin at tooth tissue junction. This allows the
proximal plate to disengage into proximal undercut during occlusal loading
• Design modification III: Proximal plate contacts just about 1 mm of the gingival third of the guiding plane of the
•
abutment tooth. The purpose of reducing the length of the proximal plate is to improve the gingival health
I-bar Modifica- • The tip of the I-bar is modified to have a pod- shape in order to allow more tooth contact. It is placed more mesially
•
tion so that it shifts towards the mesial embrasure space under occlusal load and increases reciprocation
• The I-bar is designed to compensate for the decreased encirclement, (tooth contact), provided by the proximal plate
•
and mesial rest
RPA System (Rest, Proximal Plate and Aker’s Clasp)

• This is a modification of the RPI retainer, again devised by Krol in 1980.
•
• The I-bar in the RPI system could not be used for patients with soft tissue undercuts and high frenal attachments.
•
• In such cases the I-bar of the RPI retainer is replaced with an Aker’s (circumferential) clasp to form the RPA retainer
•
Temporary RPD
• Used for a short interval of time for aesthetics, mastication, occlusal support or convenience or to condition the patient to
•
the acceptance of an artificial substitute for missing natural teeth until more definitive prosthetic therapy can be provided
• There are three types of Temporary partial dentures.
•
– Transitional partial denture.
–
– Interim partial denture.
–
– Treatment partial denture.
–
• Transitional Partial Dentures
•
– used as a supportive therapy when the patient is expected to transit from a partially edentulous condition to a completely
–
edentulous condition due to poor periodontal prognosis of the existing teeth.
516
– Metal-based transitional dentures are preferred because they are more biocompatible.
–
• Interim Partial Denture
•
– A transitional denture may become an interim denture when all of the natural teeth have been removed from the dental
–
arch
– used as an intermediate therapy until the permanent prosthesis is fabricated.
–
– After fabricating the permanent prosthesis, these dentures are used as spare dentures.
–
– These dentures are usually fabricated using acrylic resin and do not follow sophisticated design principles to preserve
–
the health of the tissues. Since these dentures produce severe de- epithelization of the gingiva (even under normal use)
and they are known as gum strippers.
– The interim denture is fabricated using an acrylic denture base.
–
• Treatment Partial Denture
•
– used for the purpose of treating or conditioning the tissues which are called upon to support and retain a denture base
–
– Indications
–
As a vehicle to carry tissue treatment material

To increase or restore the vertical dimension on a temporary basis.

 
As a splint following oral surgical procedures.

As a night-guard to protect the teeth from trauma due to oral habits.

 
Good to know
• Draw is a term meaning the preparation possesses no undercuts
•
• A solder 580 fineness is the minimum which should be used.
•
• For greatest retention of the porcelain veneer, the coping design should be convex with no undercuts.
•
• Terminal hinge axis theory–Mc Collum
•
• The inclination of the condylar path during protrusive movement forms an average angle of 30.40 with the horizontal
•
reference plane.
• Amount of epinephrine absorbed from 2.5cm retraction cord during 5 – 15 min in gingival sulcus is 71µg.
•
• Rotary curettage (gingettage)–introduced by Amsterdam in 1954 for gingival retraction in FPD.
•
• Technique for producing wax patterns with an cusp and fossa occlusion was developed by PK Thomas.
•
• Waxing technique used for cusp marginal ridge occlusion–Payne
•
MISCELLANEOUS
• The ratio of 1.618 to 1.0 is constant that is designed as Ø (phi) also known as golden mean, golden section, golden proportion.
•
• Designing of maxillary major connecter given by Blatterfein in 1953.
•
• Porcelain jacket crown developed by Land in 1886
•
• Lingual rests used on maxillary canine–‘V’ shaped with apex incisally
•
• Incisal rests–mandibular canines–small ‘V’ shaped notch proximoincisally
•
• Extracoronal attachment first introduced by Henry R. Boos and later modified by F. Ewing Road (1908)
•
• Retentive clasp assemblies–WGA Bonwill in 1889
•
• Height of contour–Edward Kennedy in 1928
•
• Tensile strength of a wrought structure is atleast 25% greater than that of cast alloy from which it is made.
•
• Suprabulge direct retainer/Aker’s clasp–Polk E Akers
•
• Infrabulge direct retainer/ Bar clasp/ Roach Clasp–F. Ewing Roach
•
• Cast circumferential clasp design – N B Nesbit in 1916
•
• Angle formed between analyzing rod and tooth surface apical to the height of contour – angle of gingival convergence.
•

Greater is this angle greater the force required to remove retentive clasp from abutment
• Basic principles for designing a RPD–AM Schmidt in 1953

•
• A whistling sound with dentures is indicative of having a posterior dental arch form that is too narrow.
•
• Favourable throat form–square shaped soft palate with more compressibility extending 5–10 mm
•
• The linguoplate should be something that is added to, not something replacing the conventional lingual bar.
•
• The U shaped palatal major connector is probably the poorest design of all major palatal connector–lacks rigidity of other

•
types. Used only when inoperable tori extend to the posterior limit of hard palate.
• Prothero’s cone theory is the basis for clasp retention
•
• The ring clasp needs the strength of an extra strut to prevent clasp distortion due to extreme length of the clasp
•
• In class III and short span Class IV
•
– Movement of denture base towards the edentulous space is prevented by rests on abutment teeth
–
– Away from edentulous space – direct retainers
–
• In class I, II and long span IV
•
– Towards by: Accuracy and extent of denture base, supporting ridge and amount of compressible mucosa
–
– Away by: Indirect retainers
–
• Cortical bone covering relatively dense cancellous bone is the ideal residual ridge to support denture base
•
• Looseness seen in a recently delivered RPD is due to deflective occlusal contacts. Ridge soreness in denture patients may
•
be associated with occlusal disharmony.
• Continuous clasp or Kennedy bar or Double lingual bar is not a true clasp. It is a mandibular major connector.
•
• Denture base is also known as saddle.
•
• A greater angle of cervical convergence necessitates the placement of a clasp terminus nearer the height of contour than
•
if lesser angle exists
• Tightening a clasp against the tooth or loosening it away from the tooth increases or decreases the frictional resistance
•
rather than adjusting the retentive potential of the clasp.
• As a rule of thumb, proximal guiding plane surfaces should be about 2/3rds as wide as the distance between the tips of
•
buccal and lingual cusps and should extend vertically about 2/3rds the length of enamel crown, the portion of the tooth
from marginal ridge cervically.
• 20 gauze wax relief should be provided prior to duplication of the master cast beneath framework extensions onto ridge
•
areas for attachment of resin bases.
• Usually premature contact in CR are relieved by recontouring the buccal cusps of mandibular teeth and lingual cusps of
•
maxillary teeth and incisal edge of lower teeth.
• It has been estimated that the tissues covering the residual ridge are 7 to 10 times more displaceable than PDL of abutment
•
teeth
• Horizontal rotation tendencies of a class I mandibular RPD to the patient’s left are resisted in part through the denture bases
•
by the lingual slope of the left alveolar ridge and the buccalslope of the right alveolar ridge.
• Beyron’s point: 13mm anterior to posterior marking of tragus on tragus-canthus line (AIPG 2005)
•

• Retromolar pad is resistant to resorption because of insertion of the medial tendon of the temporalis muscle. Buccal shelf
•
area is also resistant to resorption since fibres of buccinator and triangularis insert into it.
• Occlusal correction is done in immediate denture after 48 hours.
•
• Lateral ceph radiograph–best method to determine amount of residual ridge undercuts with a thin mucosal covering
•
• Mouth temperature waxes:
•
– Iowa wax, white: developed by Dr Earl Smith
–
– Korecta wax No.4, orange: Dr OC Applegate
–
518
– HL Physiologic paste, yellow white: Horkings

–
– Adaptol, green: Nathan G Kaye
–
• Avery brothers: Scissors bite technique
•
• McGrane 1936: ‘Curved Cusp’ posterior tooth
•
• Hall first designed cuspless posterior teeth called them inverted cusp teeth.
•
CHAPTER 13
Fixed Partial Dentures
Objectives
• Introduction • Impression Making

• Classification • Temporization

• Parts of FPDs • Lab Procedures

• Design of FPDs • Failures in FPDs

• Types of Abutments • Maxillofacial Prosthesis

• Tooth Preparation • Miscellaneous

• Types of FPDs

INTRODUCTION
Indications for FPD
Crown Cemented extracoronal restoration that • Short span edentulous arches
covers or veneers the outer surface of the
•
 
clinical crown • Presence of sound teeth that can offer sufficient support
•
adjacent to the edentulous space.
Laminate Ve- These are prosthesis, which are made of
neers or Facial ceramic. They are used as a thin layer over • Cases with ridge resorption where a removable partial
•
Veneers the facial surface of the tooth, primarily for denture cannot be stable or retentive.
aesthetic reasons
• Patient’s preference
•
 
Inlay It is an intracoronal restoration, which is used • Mentally compromised and physically handicapped
•
for medium sized single tooth proximo-occlusal patients who cannot maintain the removable prosthesis.
and gingival lesions. They are usually made of
gold alloy or ceramic material
Onlay It is an intracoronal restoration, which is

used to restore a more extensively damaged CLASSIFICATION OF FPD
posterior tooth with a wide mesio-occluso-distal
lesion • All fixed partial dentures fall into three major classes.
•
It is any tooth, root or implant which, gives These classes are further divided into three divisions and
Abutment
attachment and support to the fixed partial the divisions are further divided into four subdivisions. It
denture. should be understood that upto 12 designs are possible in
Pontic The artificial tooth that replaces a missing tooth each single class.
in a fixed partial denture
520
Class: identifies the loca- • Class I: Posterior edentulous spaces. One or more of the posterior teeth (premolars and molars)
•
are missing
tion of the edentulous
• Class II: Anterior edentulous spaces. One or more of the anterior teeth (incisors and canines) are
•
missing
• Class III: Antero-posterior edentulous spaces. Edentulous spaces involving both the anterior and
•
posterior regions, i.e. some anterior and posterior teeth are missing
Division: gives information • Division I: Cantilever FPDs. Abutments present only on one side of the edentulous space are
•
capable of taking support
about the teeth present
adjacent to the edentulous • Division II: Conventional FPDs. Abutments that are capable of taking up occlusal load are present
•
space that are capable of on both sides of the edentulous space
FIXED PARTIAL DENTURES
taking support • Division III: Pier Abutments. A single tooth is surrounded by an edentulous space on either side
•
Sub-division: denotes the • Sub-division I: Ideal abutments. Healthy teeth, which provide good support
•
status of the tooth that is to • Sub-division II: Tilted Abutments. Either the design of the prosthesis should be modified or the tilt
•
be used as an abutment of the abutment should be corrected
• Sub-division III: Periodontally weak abutment. This abutment cannot take up occlusal load as
•
effectively as healthy abutment
• Sub-division IV: Extensively damaged abutment. The abutment has good bone support but
•
require extensive restoration e.g. inlay, onlay, dowel core.
PARTS OF FPD
Parts of FPDs are:
– Retainers
–
– Pontics
–
– Connectors
–
Retainers
– The part of a fixed partial denture which unites the abutment(s) to the remainder of the restoration
–
– Types of Retainers
–
Based on tooth coverage:

- Full veneer crowns

- Partial veneer crowns

 
- Conservative (minimal preparation) retainers

Based on the Material Being Used

- All metal retainers

- Metal ceramic retainers

- All ceramic retainers

- All acrylic retainers

Pontics
• The objective of designing a pontic includes the construction of a substitute that favourably compares with the tooth it
•
replaces. Each surface of the pontic should be designed carefully to fulfil this objective.
• There are three important factors that control the design of the pontic.
•
– Space available for the placement of the pontic.
–
– The contour of the residual alveolar ridge.
–
– Amount of occlusal load that is anticipated for that patient.
–
Classification of pontics
Based on the • With mucosal contact
•
amount of mu- – Saddle Pontic
–
cosal contact – Ridge Lap Pontic
–
– Modified Ridge Lap Pontic
–
– Ovate Pontic
–
• Without mucosal contact
•
– Bullet Pontic
–
– Hygienic or Sanitary Pontic
–
Fixed Partial Dentures 521

Based on the • Metal and Porcelain Veneered Pontic
•
type of material • Metal and Resin Veneered Pontic
•
used ••
All Metal Pontic
• All ceramic pontic
•
Based on the • Custom made pontic
•
method of • Prefabricated pontic
•
fabrication – Trupontic
–
– Interchangeable facing
–
– Sanitary Pontic
–
– Pin-facing Pontic

–
– Modified Pin-facing Pontic
–
– Reverse Pin-facing Pontic
–
– Harmony Pontic
–
– Porcelain Fused to Metal Pontic
–
– Prefabricated Custom Modified Pontic
–
Pontic Design Recommended Advantages Disadvantages Indications Contraindica- Materials
location tions
Sanitary/ Posterior mandible Good access for Poor esthetics Nonesthetic zones Where aesthetics I All metal
Hygienic oral hygiene impaired oral important. Minimal
hygiene vertical dimension

(AIPG 2005)
Saddle ridge- Not recommended Esthetic Poor esthetics Not recommended Not recommended n/a
lap
Conical Molars without Good access for Poor esthetics Posterior areas Poor oral hygiene All metal Metal
esthetic oral hygiene where aesthetics is ceramic all resin
requirements of minimal concern
Modified ridge High esthetic Good access for Moderately easy Most areas with Where minimal Metal ceramic all
lap requirements oral hygine to clean aesthetic concern aesthetic concern resin
existing

(AIPG 2008)

Ovate Maxillary incisors Superior esthetics Requires Desire for optimal Unwillingness or Metal-ceramic al
cuspids and Megligible food surgical aesthetics high surgery resin.
premolars entrapment Ease of reparation smileline
cleaning
• Preformed pontics
•
Trupontic Large gingival bulk. It cannot be used when there is reduced Recommended in maxillary posterior area
interocclusal distance due to the presence of a large gingival
bulk
Long pin facing The lingual surface of this facing is flat and consists of two
pins for retention
It can be readily modified to adapt to the ridge mucosa
Flat back or interchange It consists of a vertical slot in its lingual surface Maxillary and mandibular anterior region
able facing
Sanitary facings These resemble the sanitary pontics. The facing has a flat Mandibular posterior region
occlusal surface which is customized as needed.
Reverse pin facing Procelain denture teeth with pins can be altered to obtain the It is indicated for cases with deep bite
facing
Pontips These are used when the tissue contact of the pontic should Recommended in mandibular posterior area
be of glazed porcelain
Connectors
• The portion of a fixed partial denture that unites the retainer (s) and pontic (s)
•
• Classified as:
•
Rigid connectors • Used when the entire load on the pontic is to be transferred directly to the abutments.
•
• A rigid connection can be made by casting as part of a multiunit wax pattern or by soldering
•
522
Non-rigid connectors • Indicated in cases where a single path of insertion cannot be achieved due non-parallel abutments.
•
• These connectors allow limited movement between the retainer and pontics.
•
Types:
• Tenon-Mortise connectors: Consists of a Mortise (female) prepared within the contours of the retainer and
•
a Tenon (male) attached to the pontic
••
Loop connectors: Used when an existing diastema is to be maintained in a planned fixed prosthesis.
––
The connector consists of a loop on the lingual aspect of the prosthesis that connects adjacent retainers
and/or pontics.
– The palatal connector seen in a spring cantilever fixed partial denture is a type of loop connector
–
• Split pontic connectors: Used only with a pier abutment.
•
– Here the connector is incorporated within the pontic. The pontic is split into mesial and distal segments.
–
Each of these segments are attached to their respective retainers.
– The mesial segment is fabricated with a shoe/key. The distal segment is fabricated with a keyway to fit
–
over the shoe.
• Cross pin and wing connectors: Used for tilted abutments. A wing is attached to the distal retainer. The
•
wing should be fabricated such that it aligns with the long axis of the mesial abutment. The wing along with
the distal retainer is termed as the retainer wing component
DESIGN OF FPD
• The major factors to be considered while designing a fixed partial denture include:
•
– Primary requirement
–
– Bio-mechanical considerations
–
– Abutment selection.
–
– Residual ridge of the patient
–
– Occlusion with the opposing teeth.
–
Biomechanical Considerations
• The design of a fixed partial denture is determined by the physical factors affecting the prosthesis.
•
• The major biomechanical factors which affect the design of an FPD are:
•
– Length of the edentulous span
–
 
A long span fixed partial denture transfers excessive load to the abutment and also tends to flex to a greater extent.

Longer the span, more is the flexion of the FPD. The flexion of an FPD varies as follows: Flexion =
(Length of the fixed partial denture)3
(Occlusogingival height of the pontic)3
– Occlusogingival height of the pontic
–
– Arch curvature
–
The curvature of the arch increases the stress developed within a fixed partial denture. If the pontic lies outside

the interabutment axis, then it will behave like an arm of a lever.
In such cases forces acting on the pontic will produce torquing forces around the abutment

– The direction of forces acting on the FPD.
–
In order to resist these dislodging forces, grooves may be used on the buccal and lingual surfaces of the prepared

abutment in order to enhance resistance and structural durability of the retainer. (AIPG 2005)

Abutment Selection
• Teeth with the following characteristics are preferred abutments:
•
– Teeth adjacent to edentulous spaces.
–
– Teeth with grossly decayed crowns that can be restored with a full veneer crown.
–
– Modifications like dowel core and pin retained amalgam restorations may be needed to restore crown morphology in
–
grossly destructed teeth.

– Vital teeth are preferred, though endodontically Adequate thickness of enamel and dentin.
–

 
treated teeth can also be used. Adequate bone support

 
– Pulp capped teeth should not be used as abutments Absence of periodontal disease

 
–
because they are always under the risk of requiring Proper gingival contour

root canal treatment
• Root Configuration Types of Abutments
•
– Roots with greater labiolingual widths are preferred Cantilever • The requisites for a cantilever abutment
–

(AIPG 2005)
•
abutments are:

– Roots with irregular curvatures are preferred • More than average bone support should be

–
•
– Teeth with longer roots serve as better abutments present.
–
– Teeth with conical roots can be used for short span • Sufficient amount of tooth structure should
•
–
fixed partial dentures. be available because the final retainer
should be more retentive.
• Crown Root Ratio
• Teeth with short roots are contraindicated.
•
– Ideally the crown root ratio should be 2:3 (0.66).
•
Pier abutments • Edentulous spaces present on either
–
– Ratios up to 1:1(1.0) are acceptable
•
side. In such cases, a single prosthesis is
–
– Ratios above one (i.e. the length of the crown is longer fabricated using all three abutments.
–

than the root) are unacceptable. (AIPG 2005)

• Periodontal Ligament Area • The central (pier) abutment is subjected to
•
•
leverage and tortional forces acting on the
– The periodontal ligament area can be used as a scale different parts of the denture.
–
or measurement to determine the potency of an • In order to protect the pier abutment,
abutment.
•
specially designed fixed partial dentures
– Johnston proposed the famous Ante’s Law. using non-rigid connectors have been
–
– According to this law, “The sum of the pericemental proposed.
–
areas of abutment teeth should be equal to or surpass Tilted abut- ••
Single path of placement should be
that of the teeth being replaced”. ments planned
• Assessment of Pulpal Health • This can be accomplished either by up-
•
righting the tooth or by fabricating a partial
•
– Usually unrestored abutments are preferred veneer crown or a telescoping crown
–
Extensively • The amount of restoration for a grossly
Special Cases
•
damaged abut- destructed tooth depends upon surface
• Replacement of a Single Missing Canine ments area of the destruction
•
• By secondary retentive measures as
– A cantilever FPD is planned
•
pins, grooves, box forms and Dowel core
–
– support should be taken from both central and insertion
–
lateral incisor. Implant abut-
– complex fixed partial denture because the tooth lies ments
–
outside the inter-abutment axis and the adjacent
teeth like the lateral incisor and the first premolar Essential Factors to be Considered during Dowel Core
are very weak Preparation
– This FPD will be subjected to forces acting in an • The canal should be obturated only with gutta- percha
–
•
outward direction. and not silver cones because it is easy to remove.
• Replacement of a Single Missing Molar Removal of silver cones can lead to lateral perforation
•
– If a cantilever FPD is planned for such cases then of root.
–
support should be taken from both the premolars • The longer the dowel the greater is the retention.
•
• For proper retention, the length of the dowel core inside
•
ABUTMENTS the root should be at least 2/3rd of the length of the root
• The coronal portion of the dowel should be encircled
•
Ideal Abutments atleast by 1-2 mm of tooth structure to obtain a ‘ferrule’
effect and protect the tooth from fracture
– An ideal abutment should have the following
• An anti-rotational groove should be made on the wall
–
characteristics:
•
of the canal preparation in order to prevent the dowel
 
Ideal crown root ratio.
from rotating within the canal

 
524
• Dowels are not indicated for anterior teeth unless Greater the height of the crown, better the

retention of the restoration.
•
there is complete destruction of the coronal tooth
structure. This is because only lateral forces are present – Structural durability
–
The ability of the restoration to withstand
in relation to the long axis of these teeth and hence the

dowel will not help to withstand these forces destruction due to external forces is known as
structural durability.
• Dowel cores are of two types namely Adequate reduction during preparation is
•
– Prefabricated

mandatory to obtain adequate thickness of the
–
 
– Custom made. restoration
–
• Dowels can be parallel sided (cylindrical) or tapering. Gold alloys require 1.5 mm clearance for the
•
Dowel systems are broadly classified as passive

functional cusp and 1.0 mm clearance in the
(cemented) and active (threaded) types nonfunctional cusp.
• Threaded dowels are more retentive than cemented - Metal ceramic restorations require 1.5 to 2.0

•
dowels. mm reduction in the functional cusp (2 mm if
it is to be veneered with porcelain) and 1.0 to
1.5 mm reduction in the nonfunctional cusp.
TOOTH PREPARATION

(AIPG 2005)

- All ceramic restorations require a minimum of
• Principles

2 mm reduction throughout. (AIPG 2011)
•
– Preservation of tooth structure

- Functional Cusp Bevel: It is provided to in-
–
– Retention and resistance

crease the thickness of otherwise thin occlu-
–
 
Primary Retention
so-axial junction of the restoration

- Sleeve retention provided by the opposing ver- - Other features, which increase durability, are:

tical surfaces of the tooth preparation.

* Offset
- Wedge type retention seen in intracoronal res-

* Groove

torations.

Secondary retention: Retention obtained by * Occlusal shoulder

retentive features like pins, boxes and grooves, * Isthmus

Taper: The degree of taper is inversely proportional * Proximal box

to the retention form.

Marginal integrity
- Zero degree taper is the most retentive but it is

- Poor marginal adaptation will lead to percola-

almost impossible to obtain.

tion of oral fluids (marginal leakage`) and sec-
- The sum of the degree of taper is called as de- ondary caries.

gree of convergence. - Casting shrinkage may lead to marginal dis-
- For optimum retention, 4°-10° convergence is

crepancy.

sufficient - The most accepted discrepancy is around 10 μ.
Limiting the freedom of displacement from

- The luting agent usually compensates for this

torquing and twisting forces aid to increase the

discrepancy by completing the marginal seal.
resistance of the restoration. Preservation of periodontium

Finish Lines
Finish line Indications Rotary instrument
Shoulder (90°) All ceramic crowns End cutting bur
PFM crowns
Injectable porcelains (AIPG 2006)

Shoulder with bevel (usually 135°) Proximal boxes of onlays and inlays End cutting bur
Labial finish line of metal ceramics
Occlusal shoulder of onlays
Chamfer (90° or more) (AIPG 2005) Cast metal restoration Round end tapered diamond cylinder

(AIIMS May 2010) Lingual aspect of metal ceramics Torpedo diamond (Tinker’s bur)

(AIPG 2007)


Knife edge (provides easiest fit and allows Young patients Indicated in situations where anatomy of tooth
easy burnishing of gold at margins) MOD onlays is constricted immediately cervical to the
Inaccessible areas cervical line
Finish lines in cementum
Radial shoulder (120°) Radial fissure bur or flat end tapered diamond
bur
Tooth Preparation for Special Cases

Complete cast crown

Indications Contraindications Advantages Disadvantages
• Extensive destruction from caries or trauma • Less than maximum • Strong • Removal of large amount
•
•
•
•
• Endodontically treated teeth retention necessary • High retentive of tooth structure
•
•
• Existing restoration • Aesthetics quality • Adverse effects on tissue
•
•
•
• Need for maximum retention and strength • Usually easy to • Vitality testing not readily
•
•
obtain adequate feasible
•
• To provide contours to receive a removable
resistance form • Display of metal
•
appliance
•
• Option to modify
• Other recontouring of axial surfaces (minor
•
form and occlusion
•
corrections or malinclinations)
• Corrections of occlusal plane
•
Partial Veener Crown Preparation for Posterior Teeth
Indications Contraindications Advantages Disadvantages
• Sturdy clinical crown of • Short teeth • Conserves tooth structure • Less retentive than complete
•
•
•
•
average length or longer • High caries index of tooth • Easy access to margin cast crown
•
•
• Intact buccal surface that • Extensive destruction • Less gingival involvement • Limited adjustement of the path
•
•
is not in need of contour or of withdrawl
•
•
• Bulbous teeth than with the complete cast
modification and that is well crown • Some display of metal
•
supported • Thin teeth
•
• Easy escape of cement
•
• No conflict between axial • Poor alignment
•
and good seating
•
•
relationship of tooth and
• Verification of seating is
proposed path of withdrawl of
•
simple
the FPD
• Electric vitality test feasible
•
Preparation steps Recommended armamentarium Criteria
Depth orientation grooves for Tapered carbide fissure bur or tapered round 0.8 mm on noncentric cusps and 1.3 on centric
occlusal reduction tipped diamond cusps
Occlusal reduction Round tipped diamond Clearance of 1 mm on non centric cusps and 1.5
mm on centric cusps
Depth orientation grooves for axial Chamfer depth of 0.5 mm (no more than half the
reduction width of diamond)
Axial reduction Round tipped diamond, Large Round tipped Axial reduction parallel long smooth and
Chamfer finishing diamond continuous to minimize marginal length and
facilitate finishing; distinct resistance to vertical
displacement by periodontal probe
Proximal groove Tapered carbide fissure bur Distinct resistance to lingual displacement by
probe
Parallel to path of withdrawal of restoration, 90*
angle between prepared axial wall and buccal or
lingual aspect of groove
Buccal and occlusal bevel (maxilla), Round tipped diamond Maxillary teeth: bevel extends just beyond cusp
chamfer (mandible) but remains within curvature of cusp tip
Mandibular teeth: minimum of 1mm of mandibular
clearance for cast gold in area of centric stops
Finishing Large round tipped (except diamond or All sharp internal line angles and grooves rounded
carbide) to smooth transitions
526
TYPES OF FPD
Conventional Most commonly used
Cantilever • A cantilever fixed partial denture is used when support can be obtained only from one side of the edentulous
•
space
Spring cantilever • This is a special cantilever bridge exclusively designed for replacing maxillary incisors but these dentures can
•
support only a single pontic.
• A long resilient bar connector is used to connect the posterior retainer to the anterior
•
Fixed fixed partial • The term denotes fixed partial dentures with rigid connectors.
•
denture • Conventional FPDs
•
Fixed movable partial • A fixed partial denture having one or more non-rigid connectors
•
denture • They act like stress breakers while transmitting unwanted leverage forces.
•
• The abutment is pressurized only during occlusal loading.
•
• Improves the health of the abutment
•
• Disadvantages
•
– Complex design.
–
– Prefabricated connector components are very expensive.
–
– Difficult to maintain.
–
– Movable parts tend to wear out under constant usage
–
Fixed removable • One of the major disadvantages of long span fixed partial dentures is that if one abutment fails, the entire
•
partial denture prosthesis has to be sacrificed.
• To overcome this disadvantage, fixed removable bridges were introduced.
•
• These dentures cannot be removed by the patient but can be easily removed by the dentist
•
Modified fixed • These dentures are indicated for edentulous ridges with severe vertical deficit. The prosthesis consists of a
•
removable partial fixed component and a removable component.
denture (Andrew’s • The fixed component is fabricated completely in metal and consists of two copings connected by a load-bearing
bridge system)
•
bar.
• The removable component consists of the artificial teeth and a denture flange that is designed to fit or clasp
•
the bar.
All metal FPD • These dentures are fabricated using only metal.
•
• They are indicated for replacing maxillary and mandibular posterior teeth.
•
• They are not aesthetic.
•
• They have the maximum strength and durability.
•
 
All ceramic FPD • Superior esthetics
•
• Ceramic has less fracture resistance, so alumina reinforced porcelains (Inceram) is used.
•
All acrylic FPD • Only indicated for long-term temporary or interim prostheses.
•
• Can be used for making fixed periodontal splints.
•
• Poor wear resistance.
•
• Easy to fabricate and adjust
•
• Aesthetically pleasing.
•
Veneers • Veneer is a layer of restoration placed over the labial surface of a tooth.
•
• They are primarily used as aesthetic adjuncts to discolored or fractured teeth.
•
• Can be ceramic or acrylic
•
Fixed partial denture • The primary purposes of splinting include stabilization and reorientation of forces.
•
splints • To improve form and function of teeth.
•
• To modify occlusal contact patterns.
•
• To adjust jaw relations
•
• To improve the masticatory efficiency
•
Fibre reinforced • Bridges reinforced by a bar of glass fibres over which indirect posterior composites are built.
•
composite resin • Fibre reinforced composites have two parts namely the reinforcing constituent (provides strength and stiffness)
bridges
•
and surrounding matrix (supports the reinforcement and provides workability).
• Commercially, polymer or resin matrices reinforced with glass, polyethylene or carbon fibers are available. The
•
reinforcing fibres may be unidirectional (long, continuous and parallel), braided or woven.

• Fibre reinforced composites can be classified into:
•
– Pre-impregnated (e.g. Fibrekor, Splint-it): The manufacturer impregnates them with the resin.
–
 
– Impregnation required (e.g. Ribbond, Cpost): fibre impregnation has to be done by the dentist
–
 
Resin bonded FPD • First partial dentures which are cemented onto the abutments using special resins
•
•
•
Types:
• Rochette bridge:
•
– First desgned resin bonded retainers
–
– Wing like contains conical perforations for retention.
–
– The resin exposed through the metal perforations is subjected to external stress, abrasion and marginal
–
leakage

• Maryland bridge:
•
– Developed to overcome the shortcomings of Rochette bridges
–
– Retention developed by microporosities present on the tissue surface of the retainer
–
– Microprorsities are created by etching the tissue surface of retainer
–
• Virginia bridge
•
– Uses particle roughened retainers
–
– Uses lost salt technique for creating voids that aid in retention
–
IMPRESSION MAKING
• Impression techniques can be classified based on the type of impression tray used as follows.
•
– Stock Tray/Putty-wash Impression
–
Double mix -most commonly used

 
Single mix

– Custom tray impression
–
Single mix technique.

– Closed Bite Double Arch Method or triple tray technique.
–
– Copper tube impressions.
–
Single tooth impression wherein a copper band is positioned around the prepared tooth and the impression

material is loaded into the band to record the impression.
– Post space impressions.
–
TEMPORIZATION OR PROVISIONAL RESTORATION
• After tooth preparation, a temporary protective/ functional restoration is fabricated over the prepared tooth to be used until
•
the fabrication of the final prosthesis
• Types
•
Method of • Custom made
•
fabrication • Preformed provisional restorations – limited to single tooth restorations
•
– Commonly available preformed crowns include polycarbonate, cellulose acetate, aluminium, and tin-silver.
–
Type of mate- • Resin based Provisional Restorations: The various resin-based materials used to make provisional restorations
•
rial used are:
 
– Cellulose acetate
–
 
– Polycarbonate
–
 
– Poly-methyl methacrylate: Chemically activated resin.
–
 
 
– Poly-R methacrylate: R group could be ethyl or isobutyl forms of resin. These resins have greater strength
–
 
than conventional resins.
– Microfilled composite: BisGMA (Bis- phenol A glycidyldimethacrylate).
–
– Urethane di-methylacrylate: Light cured resins. The amount of filler in these systems should have sufficient
–
filler for optimal handling or manipulation.

• Metal provisional restorations: Usually fabricated using:
•
– Aluminium
–
 
– Nickel-chromium
–
– Tin-Silver
–
Duration of • Short-term temporary: for use up to 2 weeks
•
use • Long-term temporary: for use from 2 weeks to a few months.
•
528
Technique for • Provisional restorations fabricated using direct technique.
•
 
fabrication • Provisional restorations fabricated using indirect technique.
•
 
• Provisional restorations fabricated using direct-indirect technique.
•
 
LAB PROCEDURES
Dies and Working Casts

– A die is a positive replica of the individual prepared tooth on which the margins of the wax patterns are finished.
–
– These are individual tooth replicas prepared for easier handling during wax pattern fabrication and finishing of
–
inaccessible areas of the cast.
– Types of Dies: Based on the design, die systems can be classified into:
–
 
Working cast with separate die system

 
Working cast with removable die system. Commonly used removable die systems are:

- Dowel pin system

* Straight

* Curved

- Di-lok tray system

- Pindex system

Accutrac system

Wax Pattern Fabrication
– Usually wax pattern fabrication denotes the wax pattern fabricated to cast metal or castable glass ceramics (DICOR).
–
– Wax pattern fabrication involves three major steps namely
–
Fabrication of the retainer

Fabrication of the pontic and

Fabrication of the connector.

Cementation
– Finishing and polishing
–
After ceramic firing, the restoration should be finished and polished prior to insertion.

The following procedures should be carried out during this phase.

- Surface defects can be removed using grinding stone or rubber wheel.

- Subsequently finer abrasive should be used to obtain a more effective polish.

- Only light pressure should be applied while using an abrasive.

- The polished surface will contain a microcrystalline layer known as Beilby layer.

- Superior polish can be obtained using heavy pressure against a wheel or brush coated with jeweller’s rouge at

high rotational speed.
– Luting agents
–
Luting Agents commonly used for fixed Partial dentures include

- Zinc phosphate cements – most preferred

- Zinc oxide eugenol cements

- Zinc silicophosphate cements

- Zinc polycarboxylate cements

- Glass ionomer cements

- Resin cements


FAILURES IN FPD
S No. Types Causes Management

1. Cementation failure Inadequate retainers
Partial • Short crowns Crown lengthening, make the bridge
•
• Overtapered preparation again
•
• Insufficient rigidity in casting
•
• Poor cementation technique
•
Complete • Poor cementation technique This can be prevented by ideal taper

•
• Wrong choice of materials about 5-60, use of hard gold.
Remake the bridge
•
• Contaminated materials
•
• Delay in cementation
•
2. Mechanical Breakdown • Inadequate thickness Remake Bridge
•
– Flexon, fracture of • Improper casting technique Remake bridge
–
metal Remake bridge
•
• Improper occlusion
– Solder joint failure Correct tooth preparation and remake
•
• Insufficient width and depth of the joint
–
– Pontic failure
•
–
– Failure of Bonded • Insufficient bulk of joint metal
–
•
Porcelain • Improper soldering technique
•
• Inadequate strength
•
• Faulty occlusion in lateral excursions
•
• Faulty design
•
• Incorrect occlusal preparation on teeth
•
• Inadequate strength at interproximal metal
•
3. Gingival Irritation • Plaque Retention Give correct instructions for home care
•
Gingival recession • Improper design
Remake bridge
•
• Faulty retainer margin
•
• Incorrect occlusal anatomy
•
• Overcontoured retainer
•
• Inadequate embrasure
•
4. Periodontal breakdown • Poor bridge design
•
General • Incorrect assessment of bridge strength
Local Remake
•
• Insufficient abutment selected
•
• Traumatic occlusion
•
Remake
5. Caries Conventional filling materials

Directly on the margins
Indirectly starting elsewhere
in mouth
Following cementation
failure
6. Pulpal necrosis • Improper tooth preparation technique Remove and recement/remake

•
• Increased occlusal load due to improper occlusion For anterior: apicectomy and retrograde
filling
•
For posterior: endodontic therapy
• Removing Failed Fixed Partial Denture

•
– If a permanent prosthesis fails, it can be removed by the following methods:
–
 
Using a crown remover (Back action or spring activated).

Using a straight chisel.

Using a brass ligature wire

 
530
Using a screw thread

 
Using a Richwil crown remover

Using a haemostat

Using an ultrasonic scaler tip

By cutting the retainer with a bur.

MAXILLOFACIAL PROSTHESIS
Types of Maxillary Defects
– Maxillary defects can be broadly classified as follows:

–
Congenital Acquired
• Cleft lip • Total maxillectomy
•
•
 
• Cleft palate • Partial maxillectomy
•
•
Obturators
• A prosthesis used to close a congenital or acquired tissue opening, primarily of the hard palate and/or contiguous alveolar
•
structures. Prosthetic restoration of the defect often includes use of a surgical obturator, interim obturator, and definitive
obturator (AIPG 2007)

• Types of Obturators
•
Based on the • Surgical obturator
•
phase of treat- – Immediate: Inserted at the time of surgery
–
ment – Delayed: Inserted 7–10 days after surgery
–
• Interim obturators: Several weeks or months following surgery. Usually replaces the surgical obturator
•
• Definitive obturator
•
Based on the • Metal
•
material used • Resin
•
• Silicone
•
Based on the • Palatal
•
area of restora- • Meatal: Extends upto the nasal meastus
•
tion
Extra Oral Prosthesis

– Auricular prosthesis – ear prosthesis
–
– Nasal prosthesis
–
– Ocular prosthesis
–
Treatment Prosthesis
– Mandibular guidance flange (training flange) (AIPG 2005)
–

Used for mandibulectomy patients with loss of continuity

Prevents excessive deviation of the remaining segments

The partial denture component provides retention and helps to guide the mandible into proper intercuspal position

– Radiation appliances
–
They are used to optimize the delivery of radiation while reducing the associated morbidity.

Materials used in Maxillofacial Prosthetics is
• Heat cure acrylic resin,
•
• PVC and copolymers,
•

• Polymethane elastomers,
•
• Silicones,
•
• Polyphosphazines
•
• Chlorinates polyethylene
•
MISCELLANEOUS
Svedopter

– It is used for isolating the mandibular teeth
–
– It is a metal saliva ejector attached with a tongue deflector.
–
– It is used when the patient is in a near upright position.
–
 
– Disadvantages
–
Access to the lingual surface of mandibular teeth is limited.

Since it is a metallic device, care must be taken to avoid any injury to the floor of the mouth.

Presence of mandibular tori precludes its use.

Chemical Methods of Fluid Control
– Anti-sialogogues
–
– Local Anaesthetics
–
• Anti-sialogogues: These are group of drugs that can be effectively used to control salivary flow. They are gastrointestinal
•
anti-cholinergics that inhibit the action of myoepithelial cells in the salivary glands, producing dry mouth.
 
Commonly used Anti-sialogogues
Methantheline bromide (Banthine): 50 mg 1 hr before procedure

Propantheline bromide (Pro-banthine): 15 mg 1 hr before procedure

Clonidine hydrochloride (Antihypertensive): 0.2 mg 1 hr before procedure.

– Contraindications hypersensitive patients, patients with glaucoma, asthma, obstructive conditions of congestive
–
heart failure, etc.
• Commonly used mechanical methods for gingival retraction are:

•
 
– Copper band
–
– Retraction cord
–
 
– Rubber dam
–
• Chemicals used for gingival retraction
•
– 8 per cent Racemic epinephrine
–
– Aluminium chloride
–
 
– Alum (Aluminium potassium sulphate)
–
– Aluminiumsulphate
–
 
– Ferric sulphate.
–
• A preparation on a tooth with a smaller diameter resists pivoting movements better than a preparation of equal length
•
on a tooth of larger diameter. (AIPG 2005)

• An edentulous space created by the loss of a canine and any two contiguous teeth is best restored with a RPD
•
• The amount of reduction required for a tooth for all metal crown restoration is – so that the tooth architecture interferes
•
with the arch of rotations.
• Fracture of PFM restoration occurs primarily due to:
•
– Inadequately designed metal framework
–
– Centric occlusal contacts at the porcelain metal interface
–
– Contamination of metal prior to opaque porcelain application.
–
532
• For greatest retention of the porcelain veneer, the coping design should be convex with no undercuts
•
• The inner surface of ceramic veneer is etched with 5% hydrofluoric acid
•
• Intra enamel depth preparation in porcelain laminate veneer is 0.5nm
•
• Castable ceramic–Dicor (tetrasilisicfluoromica glass ceramic)
•
• Machinable glass ceramic–Dicor MGC
•
• Shrink free ceramic–Cerestore
•
• Injection molded ceramic–IPS empress
•
• The finish line which donot have a sliding fit is shoulder.
•
• Biologically and mechanically acceptable solder joint of FPD is thin occlusogingivally and thick buccolingually and is
•
circular in form and occupies the region of contact area.
• Die spacers–Commonly used–resins–provides relief space of 25-40µs for the luting cement. It is painted 0.5 – 1 mm
•
short of the finish lines.
• In posterior hole preparation–In areas where coronal dentin has been completely lost, a small groove placed in the canal
•
can serve as an antirotational element. The groove is normally located where the roots is bulkiest usually on the lingual
aspect
• Jhonstone et al proposed the Ante’s law. Greatest pericemental area–maxillary first molar (433mm2) followed by
•
mandibular first molar (431mm2), least is mandibular central incisor (154mm2)
• The posterior tooth with least pericemental area– mandibular first premolar (180mm2)
•
• If the keyway is placed on the distal side of pier abutments the key on the mesial side of distal pontic, occlusal forces will
•
seat the key into the keyway.
• If the non rigid connector is placed at the junction of pier abutment and mesial ponticocclusal forces will unseat the key
•
from keyway.
• If the pier abutment is mobile, a rigid connecter should be used instead of a non rigid connecter
•
• A pontic as compared to the missing posterior teeth should have the same dimension Mdly but less faciolingually.
•
Approximately 2/3rd the facial lingual widths of missing tooth.
• F–L width of pontic is determined by the opposing centric stops.
•
• In FPD it is better for posterior pontic to avoid contacts in balancing side.
•
• The pontic recommended in mandibular anterior areas with extensive ridge resorption is modified ridge lap with no
•
embrasures.
• The minimum length of pontic should be 3mm
•
• Lost wax technique–Method used for fabricating cast restorations
•
• The pontic recommended in mandibular anterior areas with extensive ridge resorption is modified ridge lap with no
•
embrasures.
• The minimum length of pontic should be 3mm
•
• Lost wax technique–Method used for fabricating cast restorations
•
• Andrews bridge–Consists of 2 fixed retainers attached to their abutments and connected by a rectangular bar that follows
•
the curve of ridge under it
• Swann’s bridge: Platinum reinforced one piece porcelain bridge
•
• Davis’s crown: All porcelain crown with post and core
•
• Richmond’s crown: Porcelain facing with lingual gold portion supported by a post and band
•
• For a tooth to be selected as an abutment, it should not have tilted more than 240
•

• In metal ceramic crowns the difference of coefficient of thermal expansion should not be greater than 1 * 10-6/0C
•
• The size of wire used to reinforce platinum bridges is 14 gauzes. Sprue gauzes used for molars and premolars are 10 and 12.
•
• Relief agent provided for cementation of the retainer should not exceed 25µm.
•
• lithium carbonate added to porcelain increases the coefficient of thermal expansion from 4 to 7
•
• Palladium or platinum added to metal decreases the coefficient of thermal expansion from 14 to 7
•
• The alveolar bone around the abutment should be atleast 2/3rds the original height
•
• For gold alloys, the minimum thickness of coping should be 0.3mm
•
• For base metal alloys, the minimum thickness of coping should be 0.2mm

•
• Minimum thickness of porcelain in metal ceramic restoration should be 0.7mm
•
CHAPTER 14
Periodontics
Objectives
• Historical Background • Advances in Periodontal Diagnosis

• Anatomical Considerations • Prognosis

– Gingiva • Periodontal Treatment

– Periodontal Ligament • Periodontal Dressings

– Alveolar Process
• Healing

– Cementum

• Periodontic Endodontic Continuum

• Gingival Crevicular Fluid (GCF)

• Halitosis

• Periodontal Etiology, Immunology and

• Laser

Microbiology

• Periodontal Diseases • Periodontal Microsurgery

• Bone Destruction Patterns • Miscellaneous

HISTORICAL BACKGROUND
• Hippocrates • Father of modern medicine

• Pierre Fauchard • Father of dentistry

• John W Riggs • ‘Riggs disease’ Father of

periodontics
ANATOMICAL CONSIDERATIONS
Gingiva
• Is a masticatory mucosa and covers the alveolar process of
•
the jaw and surrounds the neck of the teeth.
– Extends from the dentogingival junction to the
–
alveolar mucosa, where it is limited by mucogingival
junction. It is subject to friction and pressure of
mastication.
– The alveolar mucosa is red and contains numerous
–
small vessels coursing close to the surface. Fig.14.1:Parts of oral mucosa
Periodontics 535

– The gingiva is normally pink but sometimes have – Produced by alternate rounded protuberance and
–
–
grayish tint. depressions in gingival sulcus.
– The stratified squamous epithelium may be – Feature of healthy gingiva
–
–
keratinized or non-keratinized but most often it is – Loss of stippling is reversible and is a common sign of
–
parakeratinized. gingival disease
• Types of gingiva: The gingival is divided into two types: – It is absent in infants and old age. (AIPG 1997)
•
–

Free or unattached or Attached gingiva – Appears in children about the age of 5 years
–
marginal gingiva • Interdental Col:
•
• Terminal edge of the • It is the continuation of the – Non keratinized
•
•
–

gingival which is usually free gingival and extends up (AIIMS Nov 2013, AIPG 2009, 2011, KAR 1999)
about 1mm wide and to the alveolar mucosa.

surrounds the teeth. – Lining is composed of non keratinized reduced
• Extends from free gingival
–
enamel epithelium, so more prone to attack by
•
• Forms one of the walls groove to mucogingival line.
•

injurious agents and less resistant to inflammatory
PERIODONTICS
of the gingival sulcus (PGI 2007, 2009)
and is separated from • Normally stippled and changes. (PGI 2002)
the attached gingival
•

keratinized – Oral hygiene accessibility is limited (AIPG 2011)
by a groove called free

(AIPG 2011,2009)
–

gingival groove. – Area for food entrapment
–
• •
Gingival sulcus:
Width of Attached Gingiva: (AIPG 2007) – V shaped shallow crevice or space that encircles the

– Greatest in incisor region:
–
tooth and presents between root and gingiva
–
Maxilla: 3.5–4.5mm

(KAR 2002)

Mandible: 3.3-3.9 mm

– Bounded by the surface of the tooth on one side and

– Least in first premolar region
–
the epithelium lining on the other side. (Mar 2011)
–

(AIPG 2010, 2011, AP 2010, AIIMS May 2010)

– In ideal conditions, depth is 0mm

Maxilla: 1.9mm
–
– Probing depth of clinically normal gingiva is 2-3 mm

Mandible: 1.8mm
–
(AIPG 2005, 2009,2004, PGI 2003, 2002, AIIMS Nov

– Increases with age and in supraerupted teeth
2010)
–

(MAHE 2008)
• The gingival epithelium: 3 types:

• Unique characteristics of attached gingiva in children are:
•
•
– The interdental clefts: Normal anatomic features – Outer or oral epithelium
–
– Sulcular epithelium
–
found in the interradicular zones underlying the
–
saddle areas – Junctional epithelium.
–
– Retrocuspid papilla: found approximately 1mm
–
below the free gingival groove on the attached gingiva
lingual to the mandibular canine. Occurs in 85% of
children and apparently decreases with age.
• Interdental papilla:
•
– Fills the space between two adjacent teeth.
–
– From oral or vestibular aspect, the surface of the
–
interdental papilla is triangular.
– The depressed part of interdental papilla is called
–
COL.
• Stippling: • Outer or oral epithelium:-The epithelium consists of the
•
following layers:
•
– Stippling is seen in attached gingiva and central core
– Stratum basale: Cuboidal cells.
–
of interdental papilla.
–

– Stratum spinosum: large polyhedral cells

(KAR 2010, Man 2002, AIPG 1995)
–

– Stratum corneum: superficial most layer,

– Absent in marginal gingiva
–

Large, wide, flat and
–
– Form of adaptive specialization or reinforcement for
lacking nucleus.
–
function.
536
PERIODONTICS
Fig. 14.3: Oral epithelium
• Sulcular epithelium: – Attached to tooth by means of an internal basal

–
lamina and to the gingival connective tissue by means
•
– Extends from the coronal area of the junctional
of external basal lamina.
–
epithelium to the free margin of the gingival.
– The internal basal lamina contains lamina densa and
– Extends from gingival margin to base of histological
–
lamina lucida to which hemidesmosomes are attached.
–
sulcus.
– Attachment to tooth is by hemidesmosomes
– Epithelium is nonkeratinized.
–

(AIPG 1997)
–
– Epithelium lacks heavy ridges and papillae.

– Basal lamina of junctional epithelium is devoid of
–
– Acts as semipermeable membrane through which
–
type IV collagen, instead type VIII is present.
–
injurious bacterial products pass into the gingiva
and tissue fluid from the gingiva seeps into the – Has a high turnover rate (AIPG 1996)
–

sulcus (AIPG 2011, AIIMS 2008) – The length of JE ranges from 0.25-1.35 mm
–

(PGI 1999)

– Sulcular epithelium has the potential to keratinize

– The distance between JE and alveolar bone remains
–
if it is reflected and exposed to the oral cavity or
–
the bacterial flora of the sulcus is totally eliminated constant–1.07-1.97 mm. (KAR 1998)

• Junctional epithelium: • Dentogingival unit:
•
•
– Cells become cuboidal after ameloblasts have finished – JE + Gingival fibres–reinforces the attachment to
–
tooth–so together known as dentogingival unit.
–
formation of enamel.

– Forms a collar around the tooth (AP 1999, 2003)

–
– Gingiva is attached to tooth by junctional epithelium
–

(AIPG 93) • Keratinization:
•

– Wider at the floor of gingival sulcus and tapers apically – Depends on functional stimulation and is age related
–
to final thickness of 3-4 cells. It consist of stratified
–
– Adaptive mechanism for masticatory forces.
–
squamous nonkeratinizing epithelium. Maximum on hard palate, followed by gingiva,
– Divided into internal and external basal lamina tongue, cheek (least keratinized)
–
Periodontics 537

Ortho Keratinization (75%) Parakeratinization (15%) Non-Keratinization (10%)
• In which the superficial cells form • In which the superficial cells retain In which the surface cells are nucleated and show
•
•
scales of keratin and lose their nuclei. pyknotic nuclei and show some signs no signs of keratinization
• A stratum granulosum is present. of being keratinized.
•

(AIPG 2002) • However, the stratum granulosum is

•
generally absent.
• Blood supply: Blood supply of gingiva is by ALVEOLAR ARTERY
•
• Three sources of Blood supply of the gingiva are as follows:
•
Supra periosteal arterioles Vessels of the periodontal ligament Arterioles from interdental septum
Along the facial and lingual surfaces of Which extend into the gingival and Which emerge from the crest of the interdental
the alveolar bone, from which capillaries anastomose with capillaries of the sulcus septa and extend parallel to the crest of the bone
extend along the sulcular epithelium and area to anastomose with vessels of the periodontal
between the rete pegs of the external ligament, with capillaries in the gingival crevicular
gingival surface. Occasional branches of areas and vessels that run over the alveolar crest
PERIODONTICS
the arteriole pass through the alveolar bone
to the periodontal ligament or run over the
crest of the alveolar bone
• Nerve supply:
•
• Cells in gingival Epithelium:
•
– Keratinocytes: comprises about 90% of the total cell production
–
– Non Keratinocytes:
–
Cells Location Function
Keratinosomes or Odland bodies Modified lysosomes present in Destruction of organelle membrane
stratum spinosum
Melanocytes (AIPG 2008) Dendritic cells located in the basal They synthesize melanin in melanosomes

and spinous layers of gingival
epithelium

(AIIMS May 2010, AIPG 2007)

Langerhans cells (COMEDK 2003) Dendritic cells located at the Phagocytic reticuloendothelial system macrophages with

suprabasal layers and are absent in possible antigenic property
JE of normal gingiva
Merkel cells Located in deep layers of epithelium Serve as tactile receptors
• Gingival connective tissue:

•
– Collagen fibre bundles 60-65%
–
– Cellular elements (fibroblasts 5%, various leukocytes, mast cells, tissue macrophages, etc 3%)
–
– Vascular elements (blood and lymph vessels), nerves and ground substance about 35%
–
538
• Gingival Fibres:
•
Name of fibre group Origin and insertion (AIPG 2003)

Principal groups
Dentogingival group Originates from cementum and spreads laterally into the lamina propria
Alveologingival group Originates from the periosteum of the alveolar crest and spreads coronally into the lamina propria
Dentoperiosteal group Originates from cementum near the cementoenamel junction into the periosteum of the alveolar crest
Circular group Originates from within the free marginal and attached gingival coronal to the alveolar crest and encircles
each tooth
Transseptal group Originates from interproximal cementum coronal to the alveolar crest and courses mesially and distally in
the interdental area into the cementum of adjacent teeth. (AIPG 2011)

PERIODONTICS
Secondary groups
Periosteogingival group Originates from the periosteum of the lateral aspect of the alveolar process and spreads into the attached
gingiva
Interpapillary group Originates from within the interdental gingiva and follows an orofacial course
Transgingival group Originates within the attached gingiva intertwining along the dental arch between and around the teeth
Intercircular group Originates from cementum on the distal surface of a tooth spreading buccally and lingually around adjacent
tooth and inserting on the mesial cementum of the next tooth
Intergingival group Originates within attached gingiva immediately subjacent to epithelial basement membrane and courses
mesiodistally
Semicircular group Originates from cementum of the mesial surface of a tooth and courses distally and inserts on the cementum
of the distal surface of the same tooth.
Periodontal ligament: (MAHE 2009, APPSC 2008, AIPG 2000, 1990, PGI 1999, AIIMS 1993)
– Specialized connective tissue that attaches a tooth to the jaw bone.
–
– Also known as
–
Periodontal membrane,

Desmodont, (AIPG 2005)

Gomphosis

Pericementum

Dental periosteum

Alveolodental ligament

– Thickness ranges from 0.15mm to 0.38mm, average 0.21mm.
–
– Periodontal ligament is hourglass shaped, being wider at ends and narrower in the middle (fulcrum of tooth)
–
• Principal Fibres
•
– Mainly composed of collagen. Collagen type I is predominant and type III is also present.
–
Transseptal fibresconsidered part • Runs between adjoining teeth • Gives interproximal support
•
•
of both periodontal and gingival • This fibre group is called as interdental • They can be regenerated after damage
•
•
fibres (AP 2004, PGI 2008) ligament.
Alveolar crest fibres • These run from cementum in apical • They prevent extrusion of the tooth.
•
•
direction to the alveolar crest movements
Oblique fibres (MAH 2011, AIPG • These run from cementum to alveolar • These are maximum in number, suspend the
•
•
1992, 1998, AIIMS 2000) bone in coronal direction tooth and resist vertical masticatory stresses
in apical direction
Horizontal fibres • Extend at right angles from cementum to • They also resist vertical displacement of the
•
•
alveolar bone teeth
Periodontics 539

Apical fibres • They arise from root ends and are absent • They resist rotation movement
•
•
in incompletely formed roots(AIPG 2008)
Interradicular fibres • They fan out cementum to the tooth in the
•
furcation area of multirooted teeth
Good to Know • Cementoblasts
•
– The cells of the dental follicle differentiate into
• The largest group of principal fibres is oblique group,
–
cementoblasts
•
extending from the cementum in a coronal direction – Once differentiated they insert cytoplasmic processes
obliquely to the bone.
–
into the unmineralised hyaline layer and begin to
• The principal fibres of PDL group that prevents deposit collagen fibrils within it at right angles to the
•
extrusion of tooth and resists lateral tooth movements root surface.
is alveolar crest group. – The cementoblasts then migrate away from the hyaline
PERIODONTICS
–
layer but continue to deposit collagen so that the fine
• Principal fibres embedded in cementum are known as
fiber bundles not only lengthen to maintain a fibrous
•
Sharpey’s fibres.
fringe on the root surface, but also thicken to form
• Principal connective tissue cells present in periodontal the fibrous matrix of acellular cementum
•

ligament are fibroblasts. These cells perform the Cementoblasts also secrete non–collagenous protein
dual function of new collagen synthesis and old such as gailprotein and osteocalcin.
collagen phagocytosis. The latter function is done • Mast Cells
•
via pseudopodia like processes that phagocytosis old – They increase in chronic inflammatory states and
–
collagen fibres and degrade them via enzyme hydrolysis. may be prevalent during the first 7 to 10 days of
• Main blood supply is from superior and inferior healing after surgery.
– They appear markedly granular with a large deeply
•
alveolar arteries.
–
staining nucleus.
• The PDL supplies nutrients to the bone and gingiva via – The cells synthesise histamine by the decarboxylation
•
blood vessels.
–
of the aminoacid histidine and may be a connective
tissue source of heparin and the sulfate.
• Indifferent fibre plexus: – Injury to the cells elicit degranulation with the release
•

–
(AIPG 2011, MAHE 2011, MP 2011) of histamine and the hydrolytic enzymes into the

– Small collagen fibres associated with large principal tissues.
–
collagen fibres. – This produces immediate hypersensitivity response.
–
– Measure around 1400 Å in diameter in SEM
Other vasoactive kinins associated with tissue injury and
–
– These course in every direction throughout the area healing are of plasma and pancreatic origins and are released
–
between bone and cementum without particular at the site of injury by the action of trypsin. Bradykinin is
orientation. They anastomose extensively with the a most important non peptide and is related to the early
principal fibres to form a continuous fibrous matrix. post surgical inflammatory process. Aprotinin, a protease
• Fibroblasts inhibitor, found to antagonize bradykinin activity.
•
– Fibroblasts are the predominant cell of connective
–
tissue • Mononuclear Macrophages
•
– Because all tissues of the tooth and its supporting – A phagocytic cell important in tissue repair
–
–
apparatus are connective, fibroblast play an important – Derived by mitosis or differentiation from the blood
–
role in the development, structure and function of the monocyte it migrates on connective tissue and
tooth. fibrinoid strands towards and into the wound.
– Fibroblasts function to form the fibers of connective – It is responsible for the phagocytosis and digestion of
–
–
tissue, that is collagen and elastin. cellular debris, bacteria, particulate exogenous matter
– They produce and maintain the ground substance in and so on
–
which they and their fibrous products are enmeshed. – Histocyte has various hydrolytic enzymes such as
–
– They exhibit contractility and motility which are acid phosphatases, collagenases, proteases, lipases,
cathepsins, it demonstrates intracytoplasmic
–
utilized in determing the structural organization of
connective tissue. inclusions of phagocytized debris.
540
• Schroeder’s Classification of cementum:

Alveolar Process
•
Acellular afibril- • Contains neither cells nor extrinsic or
• Consists of:
•
lar cementum intrinsic collagen fibres
•
– An external plate of compact bone (KAR 1998) (AAC) (Mar 2007) • Only mineralized ground substance
–

•
– Inner socket wall of thin compact bone called • Product of cementoblasts
–
•
‘alveolar bone proper’ • Found in coronal cementum
•
– Cancellous or spongy trabecular bone, in between
Acellular extrin- • Composed almost entirely of densely
–
these two compact bones. It acts as a supporting
•
sic fibre ce- packed sharpey’s fibres
bone. mentum (AEFC) • Lacks cells
• Cancellous bone is found predominantly in the inter-
•
(MAHE 2008) • Product of fibroblasts and cementoblasts
•
radicular and interdental spaces.
•
• Found in the cervical 1/3rd of the roots

(AIPG 2011, 2009, AIIMS 2006)
•
Cellular mixed • It is composed of extrinsic (Sharpey’s

• Alveolar bone proper is a thin layer of bone lining the
•
stratified cemen- fibres) and predominantly intrinsic fibres
PERIODONTICS
•
roots of the teeth and provides attachment to principal tum (CMSC) and contains cells
fibres of periodontal ligament. • Product of both fibroblasts and
•
cementoblasts
• Radiographically, this bundle bone appears as a thin
• Appears primarily in apical third of
•
radio-opaque line surrounding the roots of teeth, then
•
roots and furcation areas.
called the lamina dura.
Cellular intrinsic • Contains cells but no collagen fibres
• The alveolar bone is perforated with numerous openings
•
fibre cementum • It is formed by cementoblasts
•
by branches of intra-alveolar nerves and blood vessels
•
(CIFC) • In human it fills resorption lacunae
and therefore called cribriform plate.
•
• The distance between the crest of the alveolar bone and
• Cementum overlaps enamel in 60% cases
•
the cementoenamel junction in young adults varies
•
from 0.75 and 1.49mm. • Butt joint is seen in 30% cases
•
• Isolated areas in which the root is denuded of bone and • Cementum does not meet enamel in 10% cases – results
•
in sensitivity
•
is covered only by periosteum and overlying gingiva, is
called fenestration.
• Width of cementum (acellular) at the cervical third–20-
• When the denuded area includes marginal bone, the
•
50μm
•
defect is called dehiscence. • Width of cementum (cellular) at the apex–150-200μm
•
• Acellular cementum–forms first and before tooth reaches
Cementum
•
occlusal plane.
Acellular cemen- • First formed cementum • Most desirable cementum in regeneration–acellular
•
•
tum • Primary cementum (AP 2004) extrinsic fibre cementum.
•

• Do not contain cementocytes • Incremental lines–rest periods in cementum formation
•
•
• It is the cementum that is formed before and are more mineralized than adjacent cementum.
•
the tooth reaches the occlusal plane. It
• Fusion of cementum and alveolar bone with obliteration
covers the cervical third or half of root.
•
of periodontal ligament is knowns ankylosis.
• Thickness ranges from 30 to 230 μm
•
• Sharpey’s fibres make up most of the • Anomalies of cementum
•
•
structure of acellular cementum which
has a principal role in supporting tooth – Enamel projections: Seen in localized areas
–
• More calcified than cellular cementum
in the furcation of mandibular molars during
development.
•
Cellular cemen- • Formed after the tooth reaches the – Enamel pearls: Globules of enamel on the root
•
–
tum occlusal plane surface in the cervical area are known as enamel
• Secondary cementum (MAHE 2011) pearls.
•

• It is more irregular and contains – Hypercementosis (cemental hyperplasia)
•
–
cementocytes in lacunae – Cementicles: Globular masses of cementum
–
• Cellular cementum is more frequent on arranged in concentric lamella that may be either
•
apical half
found lying free in PDL or adhering to the root
• Thickest around the apex.
surface. They may develop from:
•
Periodontics 541

Calcified epithelial cell rests of Malassez

Small spicules of cementum that may traumatically get displaced in PDL

Calcified sharpey’s fibres

Calcified thrombosed vessels in PDL

Age Changes In Periodontium:(AIPG 2010) • Altered cell density and flattening of rete pegs
•
• Decreased number of fibroblasts • Apical migration of JE and gingival recession
•
•

(AIPG 2010, 2012, COMEDK 2007) • Coarser and denser connective tissue

•
• Decreased organic matrix production and epithelial cell • Increase in soluble to insoluble collagen, increase in
•
•
rests strength and increased denaturing
• Increased amounts of elastic fibres (COMEDK 2007) • Increased permeability to bacterial antigens and decreased
•

•
• The width of attached gingiva increases with age resistance to functional trauma
PERIODONTICS
•

(MAHE 2008)
• Decreased thickness of cementum

• Thinning and decreased keratinization of epithelium.
•
• Accumulation of resorption bays leads to increasing
•

(PGI 2008, MAN 2002)
•
surface irregularity of cementum

GINGIVAL CREVICULAR FLUID (GCF)
• An exudate; Can be harvested non-invasively. GCF is a transudate in health and an exudate in inflammation. The total
•
protein content of GCF is much less than that in serum.
• Contains rich array of cellular/biochemical mediators that reflect the metabolic status of periodontal tissues.
•
• Enzymes in GCF: – Proteinases (mammalian/bacterial)
•
–
– Acid phosphatase Cathepsin D

Elastase
–
– Alkaline phosphatase

Cathepsin G
–
– Pyrophosphatase

Plasminogen activators
–
– Beta glucuronidase

Collagenase
–
– Lysozyme

– Lactic dehydrogenase
–
– Hyaluronidase (AIPG 2011)
–
–

• The cellular immune components present in the GCF include PMNs (95-97%), monocytes (2-3%), T cells (29%) and
•
B cells (71%)
• The humoral immune components present in GCF include IgG (IgG1-IgG4), IgA, IgM and complement components.
•
• There is a gradual increase in the flow of the GCF from 6 am to 10pm and a decrease afterwards.
•
• As GCF traverses the inflammed tissue, it carries molecules involved in the destructive process which is potential to
•
be detected in advance of irreversible bone loss.
• Its close association with the site of destruction – provide more information than markers in the serum/urine.
•
• Plasma proteins, enzymes with collagenolytic activity, other microbial and host cell enzymes, inflammatory mediators à all
•
these mediators present in the crevicular fluid has been used to facilitate the diagnosis of periodontal disease.
• Methods of collecting GCF:
•
– Placing filter paper into sulcus ( intracrevicular) (MP 2006, KAR 1998)
–

– Placing paper at the entrance of sulcus (extracrevicular)
–
– Placing pre weighed twisted threads or micropipettes and crevicular washings.
–
• Periotron – used to measure GCF (KAR 2002)
•

• Glucose concentration in GCF is 3-4 times greater than in serum. (COMEDK 2007, AIPG 2005)
•

• Protein content is much less than the GCF.
•
• Amount of GCF secreted per day: 0.5-2.4ml
•
542
• Factors that increase GCF production:

•
– Circadian rhythm
–
– Sex hormones
–
– Mechanical stimulation
–
– Smoking
–
– Periodontal therapy
–
– Gingivitis
–
• GCF production is not affected by trauma from occlusion (PGI 2006)
•

GCF products can be grouped into 3 general categories
Inflammatory mediators Host derived enzymes Extra cellular components.
PERIODONTICS
and products.
• IL-1α, • Alkaline phosphatase (ALP) • May act as a predictor/marker of present/future
•
•
•
• IL-1β, • Predictor of present disease activity disease activity
•
•
• IL-6 and
•
• TNF-α
•
• Oxygen coefficient of normal gingiva–1.6 ± 0.37 (AIPG 2005)
•

• Standard probing force recommended: 25g or 0.25N or 2.5g wt
•
• Probing force that can be tolerated-75g or 0.75N or 7.5g wt
•
PERIODONTAL ETIOLOGY, IMMUNOLOGY AND MICROBIOLOGY
Plaque
• Biofilm with regular intercellular matrix consisting predominantly of micro organisms responsible for periodontitis
•

(AIPG 2008)

• The most common cause of gingivitis and periodontitis is plaque
•

(MP 2011, COMEDK 2006, AIIMS 2000,1995, AIPG 2003, 1990, MAN 2002, MAHE 1998)

• Formation of plaque occurs in following stages:
•
– Formation of pellicle
–
– Passive transport of microorganisms to the coated tooth surface by the flow of oral fluids
–
– Reversible bacterial adhesion
–
– Irreversible bacterial adhesion
–
– Coadhesion or co aggregation
–
– Multiplication of the attached micro organisms
–
– Active detachment
–
• The first formed layer after tooth brushing is pellicle (PGI 1997, 1999)
•

• Pellicle is of salivary origin and appears on tooth surfaces immediately after cleaning. It is organic in nature
•
• Pellicle formation on enamel starts with the adsorption of glycoproteins from saliva. No bacteria are present in pellicle.
•

(PGI 2003, AIIMS 2000, MP 2011, IGNOU 2011)

• It is a prerequisite for plaque formation. Bacteria progressively accumulate to form dental plaque.
•

(AIIMS 2008, AP 2004)

• The average concentration of micro organisms in saliva is approximately 750 million cells per ml (AIIMS 2006, 2009)
•

Periodontics 543

Materia Alba
– Yellow or white soft sticky deposit consisting of bacteria but does not contain the regular internal pattern.
–

(AIPG 1995, AIIMS 1992, MAN 2002,APPSC 1999, AP 2009)

– Less adherent than dental plaque
–
– Consists of microorganisms, desquamated epithelial cells, and salivary proteins – disorganized.
–
• S. mutans readily use sucrose with the help of enzyme glucosyl transferase. (PGI 2000, AIIMS 1995, AIPG 2001)
•

• Following exposure to sucrose, they produce
•
– Acid
–
– Intracellular polysaccharides (ICP), that provide a reserve source of energy for each bacterium.
–
• Extracellular polysaccharides including glucans (dextran) and fructans (levan). These help anchor the bacteria to the
PERIODONTICS
•
pellicle, as well as stabilize the plaque mass. (PGI 2000)

• The glucans and fructans are major contributors to the intercellular plaque matrix (extracellular)
•
• The interbacterial matrix accounts for 20-30% of plaque mass
•
• Glucans contribute approximately 20% of plaque dry weight, levans about 10% and bacteria the remaining 70-80%.
•
• Dextrans are sticky insoluble whereas levans are soluble and weakly adherent. (MAN 1995)
•

• Dextrans help in establishment of bacteria in plaque and plaque to tooth. (AIIMS 1999, APPSC 1999)
•

(AIPG 2010)

• Water content of plaque is about 80% (PGI 1997, 1998)
•

• The inorganic component of plaque is primarily calcium and phosphorus (KAR 1997)
•

• Maximum accumulation of plaque takes place in approximately 21 days. (AIIMS 2009, AIPG 2009, 2011)
•

Within seconds Acquired pellicle formation and bacterial adhesion (AIIMS MAY 2013, 2009, MAHE 2010)

Within 2 hours Initial plaque formation takes place, irreversible colonization of bacteria after 2 hours (AIPG 2009)

Within 6 hours Supragingival plaque is well established
Within 2 days Plaque doubles in mass
By 5-7 days Plaque maturation dominated by filamentous bacteria
By 21 days Bacterial replication slows so that plaque accumulation becomes relatively stable
By 12 weeks Well differentiated subgingival plaque is formed, dominated by gram negative
• Early supragingival plaque contains gram positive cocci and rods

•
• Mature supragingival plaque contains spirochaetes and gram negative rods e.g. Bacteroides. These cause gingivitis
•


• Subgingival tooth associated plaque contains gram positive cocci and rods, e.g. Actinomyces, which results in root
•
surface caries
• Subgingival epithelium associated plaque contains gram negative rods and filaments and causes periodontitis.
•

(MAHE 2009, PGI 2000, 2001)

• During night, the flow of saliva is less, hence the plaque growth is decreased by 50%. (AIPG 1992, 1997)
•

• Plaque preferentially forms on non-self cleaning areas. Plaque accumulates on the gingival third of tooth surface due to
•
lack of movement of food and tissue during mastication and also in cracks, pits and fissures. (AIIMS 1993)

544
Calculus (AIPG 2002)

Supragingival calculus Subgingival calculus
• Supragingival calculus is only about 30% mineralized • Subgingival calculus is about is about 60% mineralized
•
•
• White or whitish yellow • Dense, dark brown or greenish black
•
•
(AIPG 1999, 2006, 2011, AP 2007)

• Hard clay like consistency • Hard flint like consistency(AIPG 2008) (AIPG 2008)
•
•

• Mineral source is saliva, so called as salivary calculus • Mineral source is GCF and so called as cerumal calculus
•
•

(AIPG 2011)

• Hydroxyapatite and octacalcium phosphate are the major • Hydroxyapatite and magnesium whitlockite are the major
•
•
crystal forms (COMEDK 2011, AIPG 2011) crystal forms (APPSC 2008)

• More common in the upper first molar region • More common in the lower anterior region
•
•
• Can be easily detached • It is harder, thinner, and more closely adapted to tooth surface
PERIODONTICS
•
•
imperfections, subgingival calculus can be more difficult to
remove than supragingival calculus.
• Modes of attachment:
•
– By acquired pellicle or secondary dental cuticle
–
– By chemical interlocking of crystals of calculus and tooth structure
–
– By physical penetration of calculus into cementum (mechanical interlocking)
–
– Calculus attached to cementum by means of pellicle can be detached.
–
– Calculus embedded deeply into the cementum appearing morphologically as cementum is called
–
‘calculocementum’. (AIPG 1994)

Theories of Mineralization of calculus:
– Booster mechanism: suggests that the precipitation of calculus phosphate salts results from a local rise in the degree of
–
saturation of calcium and phosphate ions.
– Epitactic concept/Heterogeneous Nucleation Concept: calculus formation may be initiated through epitaxis/seeding
–
by organic complexes in the matrix.
• Dental calculus, salivary duct calculus, and calcified dental tissues are similar in inorganic composition. Only the
•
crystalline component changes.
• The ratio of calcium to phosphate is higher subgingivally, and the sodium content increases with the depth of periodontal
•
pockets.
• Micro organisms are not always essential in calculus formation because calculus occurs readily in germ free rodents
•
• Plaque has the ability to concentrate calcium at 2 to 20 times its level in saliva
•
• Calculus does not directly irritate the gingiva but it provides a fixed nidus for continued accumulation of plaque, thus acts
•
as a contributing factor. (KAR 2003)

• Subgingival calculus is highest in lower anterior region whereas supragingival calculus is highest on upper molar region.
•
• Calculus has approximately 75% to 85% inorganic content which is close to dentin (65%) as compared to enamel (96%)
•
and cementum (55%). (AP 2010)

• Filamentous organisms, diphtheroids, Bacterionema and Vellonella species have the ability to form intercellular apatite
•
crystals.
Microbiology
• Streptococcus sanguis, S.mitis, S.mutans and Actinomyces viscosus are present in plaque
•
• Streptococcus salivarius is the first organism to appear in the mouth after birth and is the predominant organism in saliva.
•
Periodontics 545

• It is not usually found in plaque. It is non-pathogenic bacterium and forms the longest chains.
•
• It is most commonly found on the tongue.
•
Plaque Hypothesis
• Both specific and non specific plaque hypothesis were proposed by Loesche (MAN 1998, KAR 1998, PGI 2007, 2009)
•

• Non specific hypothesis:
•
– States that periodontal disease results from elaboration of noxious products by the entire plaque flora.
–
– The periodontal disease can be treated by debridement (surgical or non surgical) and oral hygiene measures.
–
• Specific hypothesis:
•
– States that only certain plaque is pathogenic (AIPG 2012)
–

• Even though non-specific hypothesis is discarded, much of clinical treatment is still based on nonspecific plaque
•
hypothesis only.
PERIODONTICS
• Robert Koch developed the criteria by which a microorganism can be judged to be the causative agent in human infections.
•
These are called as ‘Koch’s postulates’
• Socransky modified the Koch postulates as related to periodontal disease. (AIIMS May 2013, Nov 2010, 2009)
•

• Sigmond Socransky criteria for judging periodontal pathogens:
•
– Be associated with disease with increase in number of organisms at diseased sites
–
– Be eliminated or decreased with treatment
–
– Demonstrate host response
–
– Demonstrate virulence factors capable of causing disease in experimental animals
–
Evidence supporting a role of A. actinomycetemcomitans and P. gingivalis as Pathogen in Periodontal Disease:
Socransky’s Criteria
Criteria A.actinomycetemcomitans P.gingivalis
Association Increased in localized aggressive periodontitis (LAP) Increased in periodontitis lesions
lesions (AIPG 2014) Found associated with crevicular epithelium

Increased in some chronic periodontitis lesions
Detected in the tissues of LAP lesions
Elimination Suppressed or eliminated in successful therapy Suppresses or eliminated in successful therapy

Found in recurrent lesions Found in recurrent lesion
Host response Increased serum and local antibody levels in LAP Increased systemic and local antibody levels in Periodontitis
Animal Studies Capable of inducing disease in gnotobiotic rats Found to be important in experimental mixed infections and in
periodontitis in the cynomolgus monkey
Virulence factors Host tissue cell invasion, leukotoxin, collagenase. Host tissue cell adherence and invasion, collegenase, trypsin-like
endotoxin (LPS), epitheliotoxin, fibroblast inhibiting enzyme, fibrinolysin, phospholipase A, phosphatase, endotoxin
factor, bone resorption-inducing factor (LPS), H2S. NH5, fatty acids, factors that affect PMN function
• Corn cob structures: • Coaggregation is the ability of different species and

•
•
– Seen in supragingival plaque towards tooth surface genera of plaque bacteria to adhere to one another. It is
predominant among gram negative organisms (AP 2004)
–
– Gram-positive cocci and short rods predominate at
• Quorum Sensing: Is the capacity of bacteria to
–
the tooth surface, whereas gram negative rods and as
•
well as spirochetes predominate in the outer surface of communicate with each other. This involves regulation
of expression of specific genes through the accumulation
the mature plaque mass.
of signaling compounds that mediate intercellular
– Highly specific cell-to-cell interactions are also communications which when reaches a threshold level
–
evident from the ‘corncob’ structures. (quorum cell density), gene expression is activated.

(KAR 2002, AP 2000, 2001, IGNOU 2011)

(KAR 2011, COMEDK 2010, MAHE 2007)

546
– Many species of bacteria use quorum sensing to that can specifically detect the signaling molecule
–
coordinate their gene expression according to the (inducer).
local density of their population. Bacteria that use • Interactions of secondary colonizers with early colonizers
•
quorum sensing constantly produce and secrete – Co aggregation of F.nucleatum with S.sanguis
–
– Co aggregation of Prevotella loeschii with A.viscosus
certain signaling molecules (called autoinducers or
–
– Co aggregation of Capnocytophaga ochracea with
pheromones). These bacteria also have a receptor
–
A.viscosus
• Nomenclature:
•
Old name New name
Actinobacillus Aggregatibacter
Bacteroides gingivalis Porphyromonas gingivalis (black pigmented bacteria)

PERIODONTICS
Bacteroides intermedius Prevotella intermedius
Bacteroides melanogenicus Prevotella melanogenius (common in Down’s syndrome)
Wollinella recta Campylobacter recta
Gingivosis Desquamative gingivitis
Periodontosis Juvenile periodontitis
Periodontal Micro-organisms: (AIIMS MAY 2009)

• Early colonizers • Naeslundii, A.viscosus
•
•
– Independent of defined complexes – Blue complex
–
– Yellow complex – Streptococcus spp
–
–
– Purple complex • Odontolyticus
–
•
• Secondary colonizers
•
– Green complexes • Corrodens, Actinobacillus actinomycetemcomitans serum a type
–
•
and Capnocytophaga species.
– Orange complexes – Fusobacterium, Prevotella, and Campylobacter spp. Actino-

–
–
bacillus actinomycetemcomitans (Aggregatibacter) serum ‘b’
type (AIPG 2014)

– Red complexes – P. gingivalis, B.forsythus, and T.denticola
–
–
Blue, yellow, purple and green sites are associated with healthy sites. Green and orange complexes include species recognized
as pathogens in periodontal and nonperiodontal sections.
• Orange and red complex consists of microbes associated with initiation and progression of the periodontal disease.
•
• The red complex is particularly important because it is associated with bleeding on probing, which is an important clinical
•
parameter of destructive periodontal disease.
• Actinobacillus actinomycetemcomitans (Aggregatibacter) serum ‘a’ type (green complex) is kind to host and Actinobacillus
•
actinomycetemcomitans (Aggregatibacter) serum ‘b’ type is more aggressive.
Periodontics 547

Periodontitis associated with some bacteria Bacterial enzyme Species
• Slow progressing • Porphyromonas gingivalis • Fibronectin degradation • P.gingivalis
•
•
periodontitis
•
•
• Prevotella intermedia enzyme • P.intermedia
•
•
• AA comitans
•
• Spirochetes • Phospholipidase A • P.intermedia
•
•
•
• Rapidly progressing • Porphyromonas gingivalis • P.melaninogenica
•
•
•
periodontitis • Prevotella intermedia
•
• Capnocytophaga Virulence Factors of A. Actinomycetemcomitans
•
• B. melanogenicus
• Factors that promote colonization and persistence in
•
• Prepubertal periodontitis • Fusobacterium
•
oral cavity:
•
•
• Campylobacter
– Adhesins
•
• Capnocytophaga
–
– Invasins
•
PERIODONTICS
• B. melanogenicus
–
– Bacteriocins
•
–
• Juvenile periodontitis • AA comitans – Antibiotic resistance
•
•

(MAN 2001, KAR 2002,
–
2010, AIPG 2006, HP • Factors that interfere with the host’s defenses:
•
2010) – Leukotoxin
–
– Chemotactic inhibitors
• Generalized Aggressive • P.intermedia
–
– Immunosuppressive proteins
•
•
periodontitis • Capnocytophaga –
•
• Pregnancy gingivitis • Prevotella intermedia
•
•

(MAHE 2009, PGI 2007, • Factors that destroy host tissues:
2009)
•
– Cytotoxins
–
– Collagenases
The Bacteria Associated with Periodontal Health are
–
– Bone resorption agents
(Protective Species)
–
– Stimulators of inflammatory mediators
• Streptococcus sanguis
–
• Factors that inhibit repair of host tissues
•
• S. mitis
•
– Inhibition of fibroblast proliferation
•
• Actinomycosis viscosus
–
– Inhibitors of bone formation
•
–
• Capnocytophaga
•
• Neisseria (AIPG 2009, 2011) Virulence Factors of P.gingivalis
•

• Veillonella
• Fimbriae
•
• Bacterial Enzymes
•
•
– Adherence to host proteins
–
Bacterial enzyme Species
– Intracellular signaling
–
– Specific receptors
• Collagenases • P.gingivalis
–
• Proteases
•

•
(AIPG 1991, 1992, • A.actinomycetemcomitans
•
20062011, AIIMS 1997, Arg-gingipain: Disruption of fibrinogen- integrin
•
–
2002, AP 2006)
–
interactions in gingival fibroblasts
• Trypsin like enzyme • P. gingivalis – Sustenins: Gingipain R degrades fibrinogen and
•
•
–
• T. denticola
activates prekallikrein directly in plasma. IL-6
•
• A.actinomycetemcomitans
induction causes bone resorption/osteoclast
•
• Aryl sulfatase • C.rectus formation.
•
•
• T. forysthus • Hemagglutinins
•
•
• P. melaninogenica
• Lipopolysaccharides
•
•
548
Influence of Host Response on Periodontal Disease • Predominant immunoglobin in saliva is IgA
•

(AIIMS 1993)

Disease aspect Host factors • The predominant cell type in GCF is the PMN. They
•
• Bacterial • Subgingivally, antibody complement account for 92% of the total leukocytes while the
•
•
colonization in GCF inhibits adherence and
mononuclear cells account for 8%.
coaggreagation of bacteria ---

potentially reduces their number by (AIPG 1991,1999, 2003,2009, 2011)

lysis • Among the mononuclear cells, 58% are B lymphocytes
•
• Bacterial • Antibody – complement –mediated and 24% are T lymphocytes
•
•
invasion lysis –decreases bacterial count • The normal T:B lymphocyte ratio in peripheral blood is
•
• Neutrophils (chemotaxis, 3:1 and value is reversed to about 1:3in GCF.
•
phagocytosis + lysis)--- decreased
bacterial counts (AIIMS 1998, MP 2010)

• Orogranulocytes are the PMNs that reach the oral cavity
PERIODONTICS
•
• Tissue • Antibody mediated hypersensitivity by migrating through the lining of the gingival sulcus.
•
•
destruction

• Cell mediated immune response (KAR 2000)
•

• Activation of tissue factors –
• Immunoglobulins are secreted by plasma cells of humoral
•
collagenase
•
immunity and get inactivated or destroyed by bacterial
• Healing and • Lymphocyte and macrophage
proteases.
•
•
fibrosis produced chemotactic factors for
fibroblasts – fibroblast activating
factors • Lysozyme present in saliva causes cell wall lysis
•
of bacteria. It is antibacterial to Vellionella and
Actinobacillus (MP 2011)

• Lactoperoxidase thiocyanate system in saliva is
•
bactericidal to Lactobacillus and Streptococcus.
Models of Periodontal Disease Activity (Socransky)

( KAR 2011)

• The term periodontal disease activity refers specifically to • Lactoferrin acts against Actinobacillus
•
•
the stage of the disease, which is characterized by loss of • Myeloperoxidase, released by leukocytes and is
attachment and alveolar bone.
•
bactericidal for Actinobacillus and also inhibits the
– Continuous Paradigm: Implies slow, continuous, and attachment of Actinomyces strain to hydroxyapatite.

–
progressive destruction of periodontal attachment (PGI 2005, 2006)

until tooth loss eventually results. • The earliest sign of gingival inflammation is bleeding
Random burst theory: Periodontal disease progression
•
– on probing. Reason is proliferation of capillaries and
–
occurs as short periods of destruction followed by increased formation of capillary loops between rete
periods of non destruction occurring randomnly with pegs or ridges.
respect to time and site within an individual.
– Synchronous multiple Burst Theory: Tissue • Neutrophils are best suited for rapid response–main
–
destruction occurs at a definite period of time in
•
defence cells in acute inflammation. They are the only cells
one’s life and then pass on to a state of remission, e.g. that can survive in the hypoxic environment of gingival
juvenile periodontitis. sulcus. They are released as a response of epithelial axis of
innate immunity to bacteria in the sulcus.
• Clinical indicators of disease activity

(AIIMS MAY 2013, AIPG 2009, 2011)
•

– Bleeding on probing • Monocytes and fixed macrophages belong to connective
–
– Exudation
•
tissue axis. Remember that lymphocytes and monocytes
–
– GCF assessment do not follow the neutrophils into gingival sulcus.
–
– Increase in gram negative anaerobic species
• Monocytes are referred as macrophages when they leave
–
– Increased sulcular temperature
•
vascular compartment and enter tissue compartment.
–
• Increased number of peripheral blood lymphocytes as a
•
Good to Know response to all bacteria is indicative of severe periodontitis.
• Predominant immunoglobin in GCF is IgG • B cells differentiate to form plasma cells in GALT in
•

•
(COMEDK 2006, KAR 2000) response to antigen exposure. Plasma cells secrete

Periodontics 549

immunoglobulins – antibodies that are glycoproteins in a • Most common cause of physiologic mesial migration is
•
nature. (AIPG 2011) failure to replace extracted 1st permanent molar.

• Antibodies are highly specific and sensitive. Specificity of • Smoking produces an immediate transient but marked
•
•
every antibody with particular antigen is due to its unique increase in GCF flow as result of blood flow changes
amino acid sequence and tertiary structure of its antibody induced by nicotine.
– combining sites. • Molecules for enzyme inhibition:
•
• Memory B cells give rise to plasma cells upon secondary – Cathepsins inhibit cysteine protease
•
–
exposure to antigen and produce high affinity antibodies. – Antileukoproteases inhibit elastase
–
– TIMP inhibits collagenases
–
• Gingivitis is known as a T cell lesion and periodontitis
Defective Neutrophil Function is Found In: (AIPG 1990)
•
is known as a B cell lesion.
• Diabetes
• IgM is released first and its levels are greater in initial
•
PERIODONTICS
• Chediak Higashi syndrome
•
stages of infection that generally decrease during later
•
stages of infection and become negligible in comparison • Juvenile syndrome
•
with those of IgG. • Papillon lefevre syndrome
•
• Cell mediated immune reactions or delayed • Neutropenia
•
hypersensitivity do not involve antibodies. They •
are based on the interaction of antigens with T • Agranulocytosis
•
lymphocytes. (AIIMS MAY 2013)
WBC Disorders That Affect Periodontium Are

• RBC lysis, ie hemolysis due to complement activation
Classified As: (AIPG 2010)
•
after Ag-Ab reaction is the basis for complement
fixation assay. Hemolysis is also the basis of colour of • Quantitative leukocyte disorders
•
subgingival calculus also known as serumal calculus. – Neutropenia
Supragingival calculus is called as salivary calculus.
–
– Agranulocytosis
–
– Leukemia
• A true pocket never forms in ankylosed teeth because
–
• Qualitative leukocyte disorders
•
apical proliferation of epithelium along root is not possible
•
– Multiple myeloma
due to ankylosis.
–
– Chediak Higashi syndrome
• Osteoclasts, formed by fusion of circulating monocytes,
–
– Leukocyte adhesion deficiency
•
–
possess elaborately developed ruffled border from which – Histiocytosis syndrome (Langerhans cell
–
hydrolytic enzymes and acids – citric acid and lactic acid histiocytosis)
are secreted.
Condition Neutrophil abnormality Chromosomal abnormality Periodontal manifestations

Neutropenia, Decreased number of neutrophils Aggressive periodontitis
agranulocytosis
Chediak–Higashi • Decreased neutrophil chemotaxis • Chromosome 1q42-43 • Aggressive periodontitis and

•
•
•
syndrome and secretion • The syndrome is caused by oral ulceration
•
• Neutrophil granules fuse to form a mututation in the lysosomal
•
characteristic giant granules called trafficking regulator gene LYST
mega bodies
Papillon LeFevre • Multiple functional neutrophil • Chromsome 11 • Severe aggressive

•
•
•
syndrome defects, including myeloperoxidase • PLS is caused by mutations in periodontal destruction at an
deficiency as well as defective early age, which may involve
•
the cathepsin C gene, located
chemotaxis and phagocytosis on chromosome 11 the primary and permanent
• Recently associated in affected dentition
•
individuals with a mutation in the
cathepsin C gene
550
Condition Neutrophil abnormality Chromosomal abnormality Periodontal manifestations

Leukocyte adhesion Defects in leukocyte function due to • Chromosome 21 • Aggressive periodontitis, at
•
•
deficiency–type I lack of integrin 32 subunit (CD18). • Mutations in the gene encoding an early age and affecting

(PGI 2006) Neutrophil defects include impaired primary and permanent
•
the β2–integrin CD18 on
migration and phagocytosis. chromosome 21 21q22.3 dentition, in individuals who
Histologically, almost no extravascular resulting in absent or markedly are homozygous for the
neutrophils are evident in periodontal reduced expression of CD11a/ defective gene.
lesions. CD18
Leukocyte adhesion Neutrophils fail to express the ligand • Chromosome 11, 19p, and 19q • Aggressive periodontitis at a
•
•
deficiency–type II (CD15) for P- and E –selectins, • Four different fucosyl young age
resulting in impaired transendothelial
•
transferases would have to be
migration in response to inflammation – affected (sle X – sialyl Lewis
defective fucose metabolism X or (CD 15s) and E and P
selectin)
PERIODONTICS
Diabetes and Periodontitis

Changes in subgingival environment • Altered microbiota
•
•
•
Change in GCF composition
Altered tissue hemostasis and wound healing • Decreased collagen production

•
• Increased matrix metalloproteinase activity
•
• Accumulation of advanced glycation end products turnover
•
Changes in host immunoinflammatory response • Decreased polymorphonucear leukocyte chemotaxis, adherence,
•
phagocytosis
• Elevated proinflammatory cytokine response from monocytes/
•
macrophages (IL-1β, PGE2, TNFα)
• Increased tissue oxidant stress
•
Role of Sex Hormones on The Periodontium – Estrogen receptors in osteoblast–like cell
–
Periosteal fibroblast
Estrogen

Scattered fibroblast of lamina propria and
– Influences the cyto differentiation of stratified

Periodontal Ligament fibroblast providing the
–
squamous epithelium and

direct action on different periodontal tissues
– Synthesis and maintenance of fibrous collagen – The inflammatory mediators may be affected by
–
–
Periodontics 551

estrogen hormone level, which may be attributed to the production of prostaglandins (PG’s) by the involvement of
estradiol and progesterone.
– Amount of circulating estradiol
–
a 1
Prevalence of periodontal disease
– Other Effects In The Periodontium Are

–
↑Amount of plaque with no increase of gingival Inflammation
�
Inhibit pro-inflammatory cytokines release by human marrow cells

↓ T-cell mediated inflammation
�
Suppressed leukocyte production from the bone marrow

Inhibit PMN chemotaxis

Stimulate PMN phagocytosis
PERIODONTICS

Progesterone:
– Play a role in coupling of bone resorption and bone formation.
–
– Action on bone
–
Directly by engaging Directly, by competing
osteoblast receptor for a
– Other effects in the periodontium are:

–
↑ Production of prostaglandins (self limiting process)
�
↑ PMN and PGEz in PGE
�
↓ Glucocorticoid anti-inflammatory effect
�
Altered collagen and non collageneous protein synthesis

Alter PDL fibroblast Metabolism

↑ Vascular permeability
�
• In relation to the elevated levels of estrogen and progesterone in pregnancy, the following changes occur:
•
– Subgingival plaque composition:
–
Anaerobic to aerobic ratio increases

Higher concentration of Prevotella intermedia (substitutes sex hormone for Vitamin K as a growth factor)

Higher concentration of Bacteroides melaninogenicus

Higher concentration of Porphyromonas gingivalis

– Increases cellular proliferation in blood vessels, increases vascular dilation, thus increases permeability (results in
–
edema and accumulation of inflammatory cells)
– Decreases keratinization
–
– Increased bleeding tendency
–
– Pregnancy gingivitis begins in the 2nd or 3rd month and increases upto 8th month and decreases during 9th month.
–
Effects of androgens on the periodontium
– Stimulates Matrix synthesis by osteoblasts and PL fibroblasts
–
– Stimulates osteoblast proliferation and differentiation
–
– IL-6 production during inflammation
–
– Inhibit PG secretion
–
– Enhance OPG Concentration
–
This suggests that overall, Androgens may protect the periodontium via a positive anabolic effect on periodontal cells, a negative
effect on the production and presence of mediators of inflammation and an inhibitory effect on osteoclastic function.
Testosterone had inhibitory effects in the cycloxygenace pathway of arachidonic acid metabolism in the gingiva and speculated

that this sex hormone may have anti-inflammatory effects on the periodontium.
552
PERIODONTAL DISEASES
Gingivitis
Stage Time Immune cells Clinical findings
I Initial lesion 2-4 days PMNs (MAN 2000) Increase in gingival flow Erythema, bleeding

(PGI 2002, KAR 2009) on probing Change in color, size, texture

II Early lesion 4-7 days Lymphocytes (AIPG 2014)

III Established (Chronic 14-21 days Plasma cells (PGI 2009,

gingivitis) (AIPG 1999) MAHE 2009, AIPG 2009, 2010,

2000, 2007, KAR 2010)
• McCall’s festoons are life preserver shaped enlargement of the marginal gingiva. Stillman’s clefts breach in the continuity
•
of marginal gingiva. Neither of them is due to trauma from occlusion.

(PGI 1999, 2002,2003, KAR 2009, MAN 1999, 2000) (AIPG 2009)
PERIODONTICS

• The two earliest signs of gingival inflammation are: (AP 2010, AIPG 1991, MAN 2000,
•

PGI 2003, AP 2005, COMEDK 2011)

– Increased GCF production rate
–
– Bleeding on probing
–
Contour changes during gingival inflammation
Gingivitis ANUG Stillman’s clefts McCall’s festoons
The margins become round, Loss of papilla leads to reverse Narrow triangular gingiva Rolled thickened margins of gingiva
rolled, and blunt. contour recession is seen seen in canine region
Acute Gingival Infections Zone 1: Bacterial zone: The most superficial,

consists of varied bacteria including a few
– NUG (necrotizing ulcerative gingivitis)
spirochetes of the small, medium and larger
–
– Primary herpetic gingivostomatitis
types. (AIPG 2009)
–
– Pericoronitis

Zone 2: Neutrophil rich zone: Contains numerous
–
• Acute necrotizing ulcerative gingivitis: (AIPG 2003)

leukocytes, preponderantly neutrophils, with
•

– NUG is an inflammatory, rapidly destructive disease
bacteria including many spirochetes of various
–
of gingiva,
– Non-communicable types, between the leukocytes.
Zone 3: Necrotic zone: Consists of disintegrated
–
– Complex etiology.

tissue cells, fibrillar material, remnants of collagen
–
– Other names: fibers and numerous spirochetes of the med and
–

(KAR 2009, COMEDK 2011, MAN 1994, AIIMS larger types with few other organisms.
1998, PGI 2001) Zone 4: Zone of spirochetal infiltration: Consists
Vincent’s infection,

of well preserved tissue infiltrated with medicum

Acute ulceromembranous gingivitis,
and larger spirochetes, without other organisms.

Trench mouth, – Spirochetes have been found as deep as 300 microns

Ulcerative gingivitis,
–
from the surface (COMEDK 2011, MAN 2002, KAR

Vincent’s stomatitis,

1998, 2000, MAHE 2010, KAR 2009)

Plant-Vincent’s stomatitis, – Psychosomatic factors: positive correlation has been

Stomatitis ulcerosa,
–
shown between stress and ANUG

Fusospirillary gingivitis,
– Characteristic lesions of NUG include:

Fetid stomatitis,
–
Punched out, crater like depression at the crest

Psuedomembraneous angina etc.

of interdental papillae, subsequently extending

– Listgarten (1965) described following 4 zones, which to the marginal gingiva and rarely to attached
–
blend with each other and may not be all present in gingiva.

every case. (AIPG 1990, 1992, 1998, 2003, 2005, 2006, AP

(COMEDK 2006, MAN 2001, MAHE 2011) 2002, PGI 2002)

Periodontics 553

Gray, psuedomembranous slough covering Contd.,

gingival craters and demarcated from rest of Stage 5: Necrosis into buccal or labial Necrotizing

gingiva by a pronounced linear erythema. mucosa (6%) ulcerative

(AIIMS 2009, AIPG 2001, 2002, COMEDK Stage 6: Necrosis exposing alveolar stomatitis

2011) bone (1%)
Red, shiny and hemorrhagic gingival margin if Stage 7: Necrosis perforating Noma

denuded of psuedomembrane covering.

cheek (0%)
Progressive destruction of gingiva and
Primary herpetic gingivostomatitis (Fever blisters, cold

periodontal structures. •
•
Spontaneous gingival hemorrhage or sores, herpes labialis) (AIPG 2002,2009)

pronounced bleeding on slightest stimulation – Etiology
Fetid odor
–
Herpes simplex virus (HSV), DNA virus - type I

Excessive salivation

Type 2 (HSV-2) usually affecting genitals and lower

PERIODONTICS

skin.
– Cogen (1990) summarized the clinical features of – Herpes virus Infections
–
ANUG as:
–
80 known herpes viruses, and eight of them are
Necessary diagnostic criteria

known to cause infection in humans:

- Interproximal necrosis and ulceration - Herpes simplex virus (HSV) 1 and 2,

(punched out crater like depressions in papil-

- Varicella-zoster virus,
lae)

- Cytomegalovirus,
- Painful gingivae

- Epstein-Barr virus, and

- Bleeding (spontaneous or on slight provoca-
- Human herpes virus 6 (HHV6).

tion)

All herpes viruses contain a deoxyribonucleic
Other

acid (DNA) nucleus and can remain latent in host

- Psuedomembrane (Fibrin, debris)
neural cells, thereby evading the host immune

- Fever, malaise, lymphadenopathy
response.

- Fetor oris.
The herpes simplex virus is composed of four

Symptoms

layers:

- Lesions are extremely sensitive to touch.
- An inner core of linear double-stranded DNA,

- Constant radiating or gnawing pain, intensi-

- A protein capsid,

fied by eating hot ‘n’ spicy food and chewing.

- A tegument, and

(PGI 2005, 2008, 2009)

- Metallic foul taste in mouth. - A lipid envelope containing glycoproteins that

is derived from the nuclear membrane of host

- Excessive amount of thick, pasty saliva.
cells.

Clinical course: Pindborg and colleagues (1966)
The two major types, HSV1 and 2 can be

have described following stages in the progress of

NUG: distinguished serologically or by restriction
- Only tip of interdental papilla is involved. endonuclease analysis of the nuclear DNA.

- Lesion extends to marginal gingiva and cause Humans are the only natural reservoir of HSV

punched-out papilla. infection, and spread occurs by direct intimate
- The attached gingiva is also affected. contact with lesions or secretions from an

- Bone is exposed. asymptomatic carrier.

Horning and Cohen (1995) extended this staging of oral The virus is transported from mucosal or

necrotizing diseases as follows: (KAR 2010, 2011, PGI 2008) cutaneous nerve endings by neurons to ganglia
where the HSV viral genome remains present in
Stage 1: Necrosis of tip of interdental papilla (93%) NUG
a nonreplicating state. During the latent phase,

Stage 2: Necrosis of entire papilla (19%) herpes DNA is detectable, but viral proteins are
Stage 3: Necrosis extending to marginal NUG/NUP not produced.” Reactivation of the latent virus
occurs when HSV switches to a replicative state.

gingiva (21%)
Clinical features: (AIPG 2001)
Stage 4: Necrosis extending to attached NUP

- The onset is abrupt

gingiva (1%)

554
-
anterior cervical lymphadenopathy, chills, fe- dency to wards bleeding make up the clinical
ver (1030 to 1050F), nausea, anorexia, irritabil- picture.
ity and sore mouth lesions. - The course of the disease is limited to 7 – 10

days scarring does not occur in the areas of
- The manifestations may vary from mild to se-
healed ulcerations.

verely debilitating Histopathology of the lesion:

- H/o previous exposure with herpetic infection - The virus targets epithelial cells which exhibit/

may be elicited. ballooning degeneration' consisting of acan-
- The affected gingiva often exhibits distinctive tholysis, nuclear cleaning and nuclear enlarge-
ment. The acantholytic cells are called Tzanck

punched-out lesions along the mid facial free
cells.
gingival margins. - Infected epithelial cells fuse, forming multinu-
- Satellite vesicles of perioral skin are fairly com-

cleated cells and intercellular edema leads to

mon. formation of intraepithelial vesicles that rup-
PERIODONTICS
- Diffuse, erythematous, shiny discoloration and ture and develop a secondary inflammatory

edematous enlargement of gingivae with a ten- response with a fibropurulent exudates.
NUG AHG
Site of ulcers Interdental papilla, Marginal gingiva Gingiva, No predilection for interdental papilla entire oral mucosa?
 
Character of ulcers • Punched out, crater like depression • Multiple vesicles that coalesce and form shallow fibrin-
•
•
covered by yellow/ white/gray slough covered regular shaped ulcers.
• Bleed readily/spontaneously • No marked tendency to bleed Non tender
•
 
•
• Painful on stimulation
•
Fever Doubtful/ slight only 38° C (or more)
Symptoms Painful gums/ dead feeling teeth Sore mouth
Duration of ulcers and Short lived (1-3 days), with appropriate More than 1 week, even with therapy
 
discomfort therapy
Etiology Interaction between host and bacteria, Specific viral etiology
most probably fusospirochetes
Age Uncommon in children More frequently in children
Contagious Non- contagious Contagious (KAR 2011)

Immunity No demonstrated immunity An acute episode results in some degree of immunity.
Chronic Desquamative Gingivitis

• The majority of patients are females (80%) and in the fourth through sixth decade of life.
•
• Prinz first used the term ‘chronic diffuse desquamative gingivitis’ in 1932. (MAHE 2010)
•

• Classification: McCarthy(1960) suggested a provisional classification based on etiologic considerations:
•
– Dermatoses
–
Lichen Planus

Mucous membrane pemphigoid

Bullous pemphigoid

Pemphigus

– Endocrine Imbalance
–
Estrogen deficiency in females following hysterectomy with oopherectomy or after menopause.

Testosterone deficiency in males.

– Aging (senile atrophic gingivitis)
–
– Metabolic disturbances
–
Nutritional deficiency (gingivosis)

Periodontics 555

– Abnormal response to irritation (modification of chronic marginal gingivitis)
–
– Idiopathic
–
– Chronic infections
–
Tuberculosis

Chronic candidiasis

Histoplasmosis

– Drug Reactions
–
Toxic–antimetabolites

Allergic–barbiturates, antibiotics etc

• Clinical Features:
•
Mild Form Moderate Form Severe Form
PERIODONTICS
• Diffuse erythema of the • Presents a patchy distribution • Characterized by scattered, irregularly shaped
•
•
•
marginal, interdental and of bright red and gray areas areas in which the gingiva is denuded and strikingly
attached gingiva involving the marginal and red in appearance.
• Usually painless attached gingiva. • Gives a speckled appearance.
•
•
• Most frequently in females • The surface is smooth and • The surface epithelium is shredded and friable and
•
shiny and the gingiva is soft in
•
•
between 17 and 23 years of age can be peeled off in small patches.
consistency.
• Surface vessels arise occasionally which rupture,
• There is slight pitting upon
•
releasing a thin, aqueous fluid and exposing an
•
pressure, and the epithelium underlying surface that is red and raw.
is not firmly adherent to the
• A blast of air directed at the gingiva causes elevation
underlying tissues.
•
of the epithelium and the consequent formation of a
• Massaging the gingiva with the bubble.
•
finger results in peeling of the
• The areas of involvement seen to shift to different
epithelium and exposure of the
•
location on the gingiva.
underlying bleeding CT surface.
This is termed ‘Nikolsky’s • The mucous membrane other than the gingiva is
•
sign’ and consists in a slipping smooth and shiny and may present a fissuring in the
or peeling of the tissue at the cheek adjacent to the line of occlusion.
dermal-epidermal junction under
slight lateral pressure.
Gingival Enlargement Systemic diseases causing gingival enlargement

- Leukemia (AP 1998, PGI 2008)
Classification: According to the etiologic factors and

- Granulomatous diseases (Wegener’s granulo-
pathologic factors:

matosis, sarcoidosis)
• Inflammatory enlargement Neoplastic enlargement (gingival tumors)
•

– Chronic - Benign tumors

–
– Acute - Malignant tumors

False enlargement
–
• Drug induced gingival enlargement

•
• Idiopathic gingival fibromatosis • Scoring of Gingival Enlargement
•
•
• Enlargements associated with systemic disease – Grade 0: No signs of gingival enlargement
–
 
– Grade I: Enlargement confined to interdental
•
Conditioned enlargement
–
papilla

(MP 2009, AIPG 2005, AP 2003)
 

– Grade II: Enlargement involves papilla and

- Pregnancy (MAN 2001)
–
marginal gingiva

- Puberty (PGI 1999) – Grade III: Enlargement covers three quarters or

- Vitamin C deficiency
–
more of the crown.

- Plasma cell gingivitis

- Nonspecific conditioned enlargement (granu- • Pyogenic Granuloma
•

lomatous pyogenicum) – Non specific conditioned gingival enlargement
–
556
– Discrete bright red or purple tumor like lesion of the interdental papilla and extends to the facial and
–
and is friable with surface ulceration and purulent lingual gingival margins (PGI 1998)

exudation, i.e. granulation tissue growth (KAR 1997) • The marginal and papillary enlargements unite and cover
•
– It is considered as an exaggerated response to minor a considerable portion of the crowns, which interfere with
–
trauma. occlusion. (BHU 2009)

• Puberty gingival enlargement • Lesion is mulberry shaped, firm, pale pink and resilient
•
•
– Conditioned gingival enlargement occurs due to with no tendency to bleed, when uncomplicated by
–
exaggerated response to local irritants inflammation
– Related to hormonal changes • Common and severe in maxillary and mandibular
–
– Microbiota seen are
•
anterior regions.
–
Capnocytophaga species
• Enlargement is chronic and slowly increases in size.

P. intermedia
•
 

P. nigresens Histological Features
PERIODONTICS

– Can be prevented with good oral hygiene • There is acanthosis of epithelium and elongation of
–
•
rete pegs. In connective tissue, there are foci of chronic
–
Pronounced inflammation of marginal gingiva
inflammatory cells particularly plasma cells and large

and interdental papilla (AIPG 2006) number of fibroblasts and new blood vessels.
Bluish red discoloration and edematous gingiva

– –
Plasma cell Gingivitis (AIPG 1989)

The gingiva appears red, friable, granular and
Drug Induced Gingival Enlargement (AIIMS MAY
bleeds easily

2013, AIPG 1996, KAR 1997, PGI 2000, 2001) It may be associated with cheilitis and glossitis

Plasma cell gingivitis is a contact hypersensitivity
– Anticonvulsant drugs associated with gingival

reaction most frequently attributed to cinnamon
–
enlargement are: Phenytoin, Phenobarbital,
Carbamazepine, Sodium Valproate, Primidone and flavored chewing gum.
Felbamate.
– Marginal gingival enlargement is seen in
– Antihypertensive drugs associated with gingival
–
Puberty
–
enlargement are: Nifedipine, Amlodipine,

Pregnancy
Nimodipine, Nicardine, Nitrendipine, Diltiazem,

Vitamin C deficiency
Felodipine and Bepridil.

Wegener’s granulomatosis (papillary type)
– Immunosuppressive drugs associated with gingival

Drug induced
–
enlargement are: Cyclosporine

– Diffuse gingival enlargement seen in
–
Clinical Features Leukemic gingivitis

• Initially the growth is painless, beadlike enlargement Idiopathic fibromatosis of gingiva

•
Pocket (AIIMS 2009, AP 1998,2000,2003, AIPG 2003, KAR 1996, 1998)
Suprabony pocket Infrabony pocket
• Relationship of the soft Base of the pocket coronal to the Base of the pocket is apical to the crest of the alveolar bone
•
 
tissue wall of the pocket level of alveolar bone Vertical Oblique
 
to the alveolar bone Follows the angular pattern of the adjacent bone. They extend from
• Pattern of bone Horizontal the cementum beneath the base of the pocket along the bone and
Normal horizontal-oblique course over the crest to join with the outer periosteum.
•
destruction
between the tooth and the bone
• Direction of
•
transseptal
fibers interproximally
 
• Direction of
•
periodontal ligament,
on facial and lingual
 
surfaces
Periodontics 557

• Pathogenesis of Pocket: Zone of semi destroyed connective tissue fibres
•
 

apical to the JE–zones 3, 4 and 5 compose the so
called plaque free zone seen in extracted teeth.
Periodontitis
• Periodontitis is an inflammatory disease of the
•
gingiva and the deeper periodontal tissues. It involves
the destruction of gingival and periodontal fibers,
resorption of alveolar bone, and proliferation of
junctional epithelium.
• The clinical feature that distinguishes gingivitis from
•
PERIODONTICS
periodontitis is the presence of clinically detectable
attachment loss.
• At the 1999 international classification workshop, the
•
different forms of periodontitis were re-classified into 3
• Correlation of clinical features and histopathologic
major forms – (COMEDK 2006)
•
features of pocket (AIPG 2006)

– Aggressive periodontitis
–
Clinical features Histopathology features –
–
Chronic periodontitis
• Bluish red colour • Circulatory stagnation – Necrotizing forms of periodontal diseases
•
•
discoloration
–
• Destruction of the connective – and into periodontal manifestations of systemic
•
• Flaccidity tissue fibres
–
diseases.
•
• Smooth shiny surface • Edema and atrophy of the
•
•
epithelium
• Edema and degeneration of Pathogenesis
• Pitting on pressure
•
the connective tissue
•
• Pink and firm gingival Fibrotic changes predominate
•
soft tissue wall over exudation and degeneration
• Bleeding elicited by Increased vascularity,
•
gentle probing engorgement of blood vessels,
and thinning and ulceration of
the sulcular epithelium
• Inner aspect of the Ulceration of the inner aspect of
•
pocket wall is painful on the pocket wall
probing
• Pus expressed on digital Suppurative inflammation of the

•
pressure inner wall of the pocket.
• Morphology of the tooth wall: Aggressive Periodontitis

•
– The following zones can be seen at the bottom of a
– Historical background
–
periodontal pocket:
–
Cementum covered by calculus: It exhibits all the Gottleib–1923: “Diffues atrophy of alveolar bone”.

root surface changes. Gottleib in 1928 gave the term “Deep

Attached plaque–It covers calculus and extends Cementopathia” and attributed it to its inhibition

apically from it to a variable degree, probably 100- of continuous cementum formation.
500μm. Wannenmacher in 1938 described the classic
Zone of unattached plaque–It surrounds attached

incisor-first molar involvement and coined the

plaque and extends apically.
Zone of attachment of junctional epithelium
term “Parodontitis marginalis progressiva”.
Orban and Weinmann – 1942: “Periodontosis”.

to the tooth–in normal sulci its extension is

more than 500μm but this is usually reduced in (AIPG 1993, PGI 2003)

periodontal pockets to less than 100μm. Chaput 1967, Butler 1969: Introduced the term

558
“Juvenile periodontitis” (AIPG 1990) The amount of destruction manifested is not

Baer in 1971 defined Juvenile periodontitis commensurate with the amount of local irritants”.

as “a disease of the periodontium occurring 1999 International Classification Workshop:

in an otherwise healthy adolescent which is renamed it as Aggressive periodontitis.
characterized by a rapid loss of alveolar bone about – Classification of Aggressive Forms of Periodontitis
–
more than 1 tooth of the permanent dentition.
Primary features (Lang 1999) Secondary features

• Non-contributory medical history • Amounts of microbial deposits inconsistent with severity of
•
•
• Rapid attachment loss and bone destruction periodontal tissue destruction
•
• Familial aggregation of cases • Elevated proportions of Aggregatibactor actinomycetemcomitans,
•
and in some far east populations, Porphyromonas gingivalis
•
• Phagocyte abnormalities
PERIODONTICS
•
• Hyper responsive macrophage phenotypes including elevated
•
productions of prostaglandin E2 and interleukin 1β in response to
bacterial endotoxins.
• Progression of attachment loss and bone loss maybe self-
•
arresting
Localized Aggressive Periodontitis (AIIMS MAY 2009) Generalized Aggressive Periodontitis

• Circumpubertal onset • Usually affecting persons under 30 years of age, but patients
•
•
• Localized first/incisor presentation with interproximal maybe older
•
attachment loss on at least two permanent teeth, one of which • Generalized interproximal attachment loss affecting atleast
•
is a first molar, and involving no more than two teeth other than three permanent teeth other than first molars and incisors
first molars and incisors. (AIPG 1990) • Pronounced episodic nature of the destruction of attachment

•
• Robust serum antibody response to infecting agents and alveolar bone
•
• The first clinical sign is tooth mobility and pathological • Poor serum antibody response to infecting agents
•
•
migration
• Bacterial etiology
•
– Localized Aggressive periodontitis: Primarily Aggregatibacter Actinomycetemcomitans (AIPG 2009, 2011)
–

– Generalized aggressive periodontitis has been frequently associated with the detection of Porphyromonas gingivalis,
–
Bacteriode forsythus and Aggregatibacter Actinomycetemcomitans.
– Aggregatibacter Actinomycetemcomitans has been shown to possess the ability to translocate across the junctional
–
epithelium and invade the underlying connective tissues.
– The enzymes produced the micro-organisms include:
–
Proteases which can digest collagen, fibrin, fibronectin etc

Arg I protease

• Inflammatory responses have been characterized by:
•
a. Intense recruitment of PMNs within the tissue and the pocket.

b. B-cells and Plasma cells, especially increased amounts of IgG producing and less IgA producing cells.

c. Depressed T-helper to T-suppressor ratio when compared to healthy gingiva and peripheral blood.

d. High levels of PGE2 IL-1α, and IL-1 βin GCF and tissues.

• The abnormalities of the PMNs in LAP are:
•
– Reduced chemotaxis in 70-75% of the cases (AIPG 2009)
–

– Reduced receptor expression
–
– Reduced Phagocytosis and killing of Aa
–
– Signal transduction abnormalities
–
– Increased superoxide production
–
Periodontics 559

Refractory Periodontitis Periodontal Ab- Periapical
scess abscess
– Cases that do not respond to therapy or recur soon
Pulp vitality • Vital • Non vital
–
after adequate treatment
•
•
• Associated with • Pre existing • Deep
– Term is no longer used.
•
•
•
periodontal restoration
–
– Prominent periopathogens such as P.gingivalis, pocket, caries
–
B.forsythus, F.nucleatum, P.micros, E.corrodens or both
and S.intermedius have been found to elevated in • Clinical features • Swelling is Swelling often with
•
•
refractory periodontitis. (BHU 2009) located around a fistulous opening
the involved in the apical area.

– Often patients identified as refractory to treatment tooth and This may be
–
have other factors, particularly smoking, that may gingival margin, located away from
contribute to the disease process. seldom with a the offending tooth
fistula
PERIODONTICS
• Symptoms • Pain is dull, Pain is severe,
Prepubertal Periodontitis is Seen in
•
•
constant, throbbing and may
localized and last for days. May
– Papillon Leferve syndrome the patient can be located away
–
– Hypophatasia usually locate from the offending
–
– Down’s syndrome (AIPG 2002) the offending tooth.
tooth
–

– Chediak Higashi syndrome
–
• Pain on • Less severe More severe
– Leukemias
•
•
percussion
–
– Neutropenia
• Treatment • Drainage Endodontic
–
– Can occur before 11years of age
•
•
followed by management
–
periodontal
management
Gingival Abscess
– Localized, painful rapidly expanding lesion of BONE DESTRUCTION PATTERNS
–
sudden onset
• Horizontal defects
– It is limited to marginal gingival or interdental papilla
•
• Vertical or angular defects
–
– It is due to foreign substance carried deep into the
•
– Based on number of walls remaining, can be further
–
tissues such as a toothbrush bristle, a piece of apple
–
classified as: (AIPG 2003)
core or a lobster shell

One walled defect: one wall remaining also called
– Gingival abscess involves marginal and interdental

hemiseptum Minimum regenerative capacity
–
gingiva, whereas periodontal abscess involves Two walled defect: two walls remaining
attached gingiva (AP 2002)

Three walled defect: three walls remaining also

called intrabony defect. Maximum regenerative
Periodontal Abscess capacity (AIPG 2006,AIIMS May 2009)

– Ledges
– Defined as suppurative lesion associated with
–
– Ramps
–
periodontal breakdown and localized accumulation of
–
– Buttressing bone formation
pus within the gingival wall of a periodontal pocket.
–
– Exostosis

(AP 2001)
–

– Microbiology:
TRAUMA FROM OCCLUSION
–
Gram-negative anaerobic species are non-

fermentative and display moderate to strong
• Traumatic occlusion introduced by Stillman denotes
proteolytic activity mainly Porphyromonas
•
abnormal stresses capable of producing the injury to
gingivalis, Prevotella intermedia.
dental or periodontal structures is called occlusal trauma
Strict anaerobic, gram positive bacterial species in
• TFO refers to tissue injury that occurs when occlusal

periodontal abscesses include Peptostreptococcus
•
forces exceed the adaptive capacity of the tissues
micros, Actinomyces spp.

(MP 2011, AIPG 2001)

560
• Primary TFO occurs due to excessive abnormal occlusal • REMODELING – represents a change that occurs within
•
•
forces acting on normal periodontium the mineralized bone without a concomitant alteration of
• Changes produced by primary trauma do not alter the level the architecture of the tissue.
•
of connective tissue and do not initiate pocket formation. • Modeling and remodeling occurs throughout life to allow
•
This is probably because the supracrestal gingival fibres bone to adapt to external and internal demands
are not affected and thus prevent apical migration of the
• The alveolar bone undergoes remodeling on one side
junctional epithelium. (AIPG 1991, AP 1996, MAN 1998)
•
of the socket and modeling on the opposite side as the

• Secondary trauma from occlusion occurs when the tooth migrates at the rate of 6.7µm per day. Periodontal
•
adaptive capacity of the tissues to withstand normal ligament (PDL) width, however remain constant. Because
occlusal forces is impaired by bone loss resulting from
of this very high turnover rate, this bone is a very good
marginal inflammation. Here normal forces are causing
model to study modeling and remodeling activities.
injury in impaired periodontium.
• Remodeling of alveolar bone affects –height, contour and
• Compression of fibres, stasis of blood flow, hemorrhage,
PERIODONTICS
•
density.
•
thrombosis and necrosis of blood vessels are early signs of
trauma from occlusion BONE REMODELING CYCLE
• The necrotizing pressure areas, undergoing bone
•
resorption and endosteal bone formation are seen in
occlusal trauma. (AIPG 2001, Man 1997,

AIIMS 1992, 2000)

• Signs / Symptoms (AIIMS MAY 2013, KAR 2001)
•

– Tooth pain, sensitivity to percussion
–
– Wear facets (AIPG 2011)
–

– Increased tooth mobility (AIPG 2011, 2009, 1997,
–

1989, AIIMS 1992, MAHE 1998, COMEDK 2007)
– Cementum tears
–
– Widening of periodontal space
–
– Root resorption
–
– Thickening of lamina dura
–
– Vertical or angular bone defects (AIPG 2001)
–

• Bone Remodeling Caused By Trauma From Occlusion:
•
– TFO can produce destruction in the presence or
• Bone Coupling
–
absence of inflammation.
•
– In the absence of inflammation, the changes caused – Osteoclasts resorb organic matrix along with
–
hydroxyapatite.When collagen breaks down from
–
by TFO may vary from – compression and tension of
organic matrix it releases various organic substrates,
periodontal ligament and increased osteoclast activity which are covalently bound to collagen; Stimulates
of alveolar bone to necrosis of PDL and resorption of differentiation of osteoblasts, which deposit bone.
bone and tooth structure. These changes are reversible; – This interdependency of osteoblasts and osteoclasts is
persistant TFO, results in funnel shaped widening
–
remodeling – Coupling.
of crestal portion of PDL with resorption of alveolar • Reversal Phase
bone.
•
– Between the resorptive and formative phase is a period
– When combined with inflammation, TFO aggravates
–
termed - Reversal Phase. Its estimated that the adult
–
the bone resorption caused by inflammation and skeleton contains more then 1 million BMUs at any
results in bizarre bone pattern. time with nearly 5-fold more occuring in trabecular
bone versus cortical bone
Remodeling and Mediators of Periodontal Osseous • Bone resorption is a complex process morphologically
•
Destruction related to the:
• MODELING– represents a process that allows a change – Appearance of eroded enamel surfaces (Howship
–
lacunae).
•
in the initial bone architecture; external demands (such as
load) on bone tissue may initiate modeling. – Large, multinucleated cells(osteoclasts).
–
Periodontics 561

• Cellular events in remodeling of bone Glycosylated non-collagenous protein, found
•

– Chemotaxis: Attraction of osteoblast precursor. in high levels at areas of active mineralization
–
– Proliferation of osteoblast precursors. Though BSP is expressed in high levels by active

–
– Differentiation of mature cells capable of osteoblasts, its presence in serum reflects bone
–
synthesizing the proteins of bone. resorption rather than osteoblast activity.
– Mineralization of this matrix.
–
• In metabolic bone diseases, there are abnormalities
• Radius of action:
•
in the coordinated activity of bone forming and bone
•
resorbing cells – imbalance between precursors of bone – Range of effectiveness within which bacterial plaque
–
resorption and bone formation. can induce bone loss.
– It is postulated to be 1.5-2.5 mm. beyond that there is
–
no effect. (MP 2011, KAR 1999)
Mediators of Bone Resorption

– Angular defects can appear only in spaces that are
–
PERIODONTICS
Stimulators Inhibitors wider than 2.5mm as marrow spaces will be destroyed
completely.
• Interleukin 1 • Interferon gamma
– In periodontitis, interproximal bone typically is
•
•
• Interleukin 6 • Osteoprotegrin (OPG)
–
resorbed faster than the dense facial or lingual/palatal
•
•
• Tumour necrosis factor • Estrogens
cortical plates.
•
•
• Parathyroid hormone • Androgens
– Bony plates thinner than 1.5-2mm might be
•
•
• PTH related protein • Calcitonin
–
completely destroyed by bacterial plaque (horizontal
•
•
• Prostaglandin E2 • Cyclosporin
bone resorption), in contrast, thicker bony plates will
•
•
• Macrophage colony
develop infrabony defects.
•
stimulating factor
• Receptor activator of NFκB
Bone Destruction Caused By Systemic Disorders
•
(RANK)
• RANK ligand (RANKL) (Bone Factor Concept)
•
• 1,25 dihydroxy vitamin D3 • The concept of the role played by systemic factors has been
•
•
validated, particularly by studies of immune deficiencies
• Systemic Biochemical Markers of Bone Resorption
in severely destructive types of periodontitis.
•

(NEET 2013)
A variety of systemic conditions can affect local bone density,
– Hydroxyproline.
ultimately influencing tooth support or available bone volume
–
– Hydroxylysine glycoside.
for dental implants installation. Such diseases affecting bone
–
– Pyridinum cross: Links and related collagen
mass include osteopenia, osteoporosis and diabetes mellitus.
–
fragments ( telopeptides ).
– Bone sialoproteins (BSP). Diabetes Mellitus
–
– Hydroxyproline (OHPr): Amino acid; mainly in
• In both type 1 and type 2 diabetes, endochondral
–
fibrillar collagen; its urinary level reflects collagen
•
turnover in bone and other tissues. bone growth and bone remodeling show significant
– Hydroxylysine: Unique to collagen; reflects mainly alteration; bone formation and bone mineralization are
also decreased in type 2 DM.
–
breakdown of bone collagen.
– Collagen pyridinium crosslinks: Pyridinoline or • A proposed mechanism for adverse effects is thought
•
–
deoxypyridinoline are currently considered the most to be the contribution of advanced glycation end
promising markers of systemic bone resorption; products(AGE) to decreased ECM production and
during bone resorptive process, pyridinoline cross inhibition of osteoclast differentiation. (KAR 2011)
links are released and can be detected in the urine • AGEs à promote apoptosis of ECM producing cells;
as free aminoacid derivatives.
•
reduce the number of osteoblasts and fibrotic cells
– TRAP: An enzyme that is generally specific to available for repair of resorbed alveolar bone.
–
osteoclast; immunoassays measure TRAP in serum
as a reflection of osteoclastic activity. Cardinal Features of Osteoporosis Include:
– Bone sialoprotein(BSP): Another resorptive • Reduced Bone strength
–
marker
•
An extracellular matrix
• Reduced bone mineral density (BMD)
•

562
• Altered Macro geometry – Genetic factors.
–
•
• Prone for fracture – Certain lifestyle factors.
–
• Bone mineral density (BMD): Amount of matter per
•
The current gold standard for diagnosing osteoporosis is the
•
square centimeter of bones.
bone mineral density (BMD) test as it is the best predictor of
individuals likely to suffer fractures of the hip or spine. Bone – BMD Test: Measures density of minerals in your
–
mineral density is usually measured using a dual energy x-ray bones using a special X-ray, computed tomography
absorptiometry (DEXA) examination. scan.
– Reduced bone mineral density is the strongest
–
Buttressing Bone Formation predictor of the several risk factors for fractures.
• Tissue response to orthodontic forces:
•
• Bone formation some times occurs in an attempt to – Orthodontic tooth movement is possible because
•
buttress bony trabaculae weakened by resorption. When
–
the periodontal tissues are responsive to externally
it occurs on the external surface – peripheral buttressing applied forces.
PERIODONTICS
bone formation. Bulging of the bone contour is called – Alveolar bone is remodeled by osteoclasts inducing
LIPPING.
–
bone resorption in areas of pressure and osteoblasts
Orthodontic Tooth Movement forming bone in areas of tension.
– Moderate orthodontic force- bone remodeling and
• Its believed to result in site-specific bone remodeling in
–
repair.
•
the absence of inflammation. – Excessive force –
–
• Tensional forces stimulate formation and activity of Necrosis of Pdl and adjacent alveolar bone.

•
osteoclastic cells, whereas compressive forces promote Risk of applied root resorption.

osteoclastic activity. (AIIMS MAY 2009) • Diagnostic Potentials for Periodontal Bone Resorption
•

• Postmenopausal osteoporosis: Is a common disorder – A graduated periodontal probe–traditional
–
•
characterized by an increase in bone resorption, relative periodontal diagnosis; PD, G.Recession, CAL.
to bone formation, generally in conjunction with an – Number of factors influence.
–
increased rate of bone turnover. – Radiographs–height of alveolar bone margin.
–
• In PMO: Lack of estrogen leads to increased number – Shape and form of its outline.
–
– Sensitivity to detect early change is poor. but
•
of bone multi-cellular units and to uncoupling of bone
–
formation and bone resorption, resulting in too little bone BIOCHEMICAL MARKERS can detect changes in
laid down by osteoblasts compared with the amount of a short time.
– Sophisticated techniques–subtraction radiography
bone resorbed by osteoclasts
–
and computer-assisted image analysis detect small
• Inflammatory process in the vicinity of the skeleton changes, but have not found a place in routine clinical
•
e.g marginal and apical periodontitis, will affect the practice.
remodeling of the nearby bone tissue in such a way that,
in most patients, the amount of bone resorbed exceed that Collagenase and Related Metalloproteinases
being formed, resulting in net bone loss (inflammation- • MMPs such as-collagenases, stromelysin and elastase
•
induced osteolysis). – are found in tissues or inflammatory exudates in
• In some patients however, inflammation-induced bone periodontal lesions. Since these enzymes can specifically
•
formation exceeds bone resorption and a sclerotic lesion cleave and degrade collagen and connective tissue
will develop. matrix macromolecules they are considered as attractive
• Bone remodeling is a complex regulated by systemic and candidates as markers of periodontal destruction.
•
local factors. • Collagenase is also considered as a diagnostic marker of
•
• There are 4 possible pathways by which systemic bone periodontal bone destruction around endosseous dental
implants. Levels of collagenase, gelatinase and elastinase
•
loss may lead to more severe periodontal destruction.
around dental implants are similar to natural tooth
– Decreased BMD caused by systemic bone loss.
• But the diagnostic sensitivity and specificity values for
–
– Modified local tissue response; increased production
•
active collagenase as a predictor of attachment loss are still
–
of cytokines and inflammatory mediators.
considered low.
Periodontics 563

Extracellular Matrix Components:
Osteonectin (ON) • Is a non-collagenous calcium binding protein associated with the ECM of many tissues, especially bone
•
and is thought to play a role in remodeling and repair.
• Also known as SPARC (secreted protein acidic and rich in cysteine) and basement membrane protein.
•
• Is a single-chain polypeptide; binds strongly to hydroxy apatite.
•
••
OS is liberated from many different cell types as a heat shock protein; studies show that heat, a major
clinical sign of inflammation, induces their synthesis.
• ON in GCF, relates to inflammation in general; hence it may discriminate poorly between gingival
•
inflammation and bone resorptive disease.
Osteopontin (OPN) • Non-collagenase,Ca2 +binding, highly glycosylated extracellular protein produced by osteoblast,
•
osteoclast and macrophages with increased levels in active sites of bone metabolism.
• OPN – increases not only at the stage of matrix maturation and mineralization in osteoblast differentiation
•
but also at the site of bone resorption.
PERIODONTICS
• As its produced by both osteoblast and osteoclast, it holds a dual function in both mineralization and
•
maturation as well as bone resorption.
• Could be detected in GCF and increased OPN levels coincided with increased probing depth measures.
•
• Although additional long-time prospective studies are needed, OPN holds promise as a possible biomarker
•
of periodontal disease progression.
Osteocalcin (OCN) • Another ECM protein; associated with bone formation.

•
• Not detectable in crevicular fluid of gingivitis.
•
• It’s 200 to 500 times higher in serum of untreated periodontitis patients.
•
Glycosaminoglycans • Sulcular fluid is rich in metabolic/degradative factors of proteoglycans.
•
(GAGs) • Site specificity of various GAGs:
•
– Sulcular fluid–metabolic/degradative products of proteoglycans.
–
– Gingival Connective tissue–rich in dermatan sulfate.
–
– Alveolar bone–rich in chondroitin sulfate.
–
• 2 major GAG components–hyaluronan and chondroitin-4-sulfate.
•
• Dot blot assays and ELISA provide an accurate assessment of the GAG levels with the simplicity of a
•
“chair side” application.
ADVANCES IN PERIODONTAL DIAGNOSIS – The various manual probes designed include William’s
–
(COMEDK 2010, 2011, KAR 2011, 2008) Periodontal probe, Michigan ‘O’ probe, Glickman’s
probe, Goldman fox probe, Merritt A and B probe,
Clinical Diagnosis Premier ‘O’ probe, CPITN probe, Marquis M-1
probe, Naber’s probe, LL 20 probe etc.
• Periodontal PROBES • Pressure sensitive probes (Second generation probes):
•
•
The National Institute of Dental Research (NIDR) proposed – Vine valley probe: This is an electronic pressure
the following criteria for an ideal periodontal probe:
–
sensitive probe, which allows control of insertion
1. A precision of ± 0.1mm pressure and permits use of different types of probe

2. A range of 10 mm tips. It allows usage of pressure force within a range of

3. Constant probing force sensitivity of 5 – 100 gms.

4. Non invasive, light weight and comfortable to use – Viva care TPS probe: This is a true pressure sensitive

–
5. Able to access any location around all teeth all plastic periodontal probe with disposable probing

6. A guidance system to ensure probe angulation head which aids in detection of CEJ, calculus,

7. Complete sterilization of all portions entering the irregularities of root form and overhangs.

mouth • Automated and computerized periodontal probe (Third
•
8. No bio-hazard from material or electrical shock generation probes): Recently developed automated probes

9. Digital output commonly feature controlled force, direct computer input

• Manual probes (First generation probes): and reference landmark recognition for relative or clinical
•
– Manual probing is the most commonly used method attachment levels
–
564
• Automated Florida probe: It consists of a probe hand – Detectability of small osseous lesions compared
•
–
piece, a digital read out, a foot switch and a computer with the conventional radiographs from which the
interface and computer. It utilizes a reproducible occlusal subtraction images are produced. 5% change in
landmark or customized stent margin as a reference land mineral density can be identified.
mark and can detect a loss of attachment level of less than • Direct Digital Radiography (Radiovisiography-RVG)
•
1 mm change with a certainly of 99%. – Also called a filmless radiography, radiovisiography
–
– The Foster Miller automated probe: This utilizes CEJ uses an intra oral detector similar in concept to a
–
as its attachment level landmark and can determine miniature video camera to capture radiographic
clinical attachment levels with a repeatability of images of the diagnostic area. It depends on the
0.2mm in a vitro study of odontotype-mounted concept of Charged Couple Device (CCD) consisting
teeth. (AIPG 2006)(AIPG 2008) of pure selenium chip.

– The other electronic probes include – Advantages
–
–
The interprobe has an optical transduction Immediate image display. Thus film processing

PERIODONTICS

element and is designed to measure probing and indirect digitalizing are eliminated
depth. Contrast and brightness of image can be adjusted

Toronto probe works by constant air pressure and after image is exposed so that artifacts can be

uses the occlusal surface as its reference point to avoided
measure gingival attachment levels. 80 – 95% reduction in X-ray dose when compared

• Temperature probe: A heat sensing periodontal probe to conventional radiography using D-speed film
•
was recently developed called Periotemp. This can detect Since the image is digital it may be printed or may

temperature differences of 0.10C between core body be stored in a computer disk
temperature and that of periodontal pocket. Results are • I 125 absorptiometry
•
shown by one of the 3 light emitting diodes. – It is a non-radiographic method introduced by
–
– Green (inactive or low risk sites) Hendrickson which measures the mineral content
–
– Yellow (intermediate) of alveolar bone with a high degree of accuracy and
–
– Red (high risk sites) precision.
–
• Tooth mobility – It is based on the absorption of a low energy gamma
–
•
– This is an important clinical manifestation of an beam, originating from a radioactive source of I125 by
bone.
–
advanced periodontal disease. In practice, the extent
of tooth mobility is most often subjectively graded on – To improve the study of posterior areas mainly
–
a scale of 0 – 3. However in research situations, more furcations, photodensitometric analysis technique has
objective methods are desirable. been developed.
• Photodensitometric analysis
•
Radiographic Diagnosis – It is based on the absorption of beam of light by the
–
radiographic film, which also shows the image of an
• Conventional radiographs include
aluminium scale.
•
– Intra oral periapical radiographs, – It also has the ability to transform density reading
–
– Bitewing radiographs,
–
into millimeter of aluminium equivalent. This is
–
– Panoramic radiographs, accomplished by a microdensitometer linked to a
–
– Xeroradiographs etc., microcomputer.
–
• Radiographs are not sensitive but may be specific. • Computer Assisted Densitometric Image Analysis
•

(COMEDK 2010)
•
(CADIA)

• Subtraction radiography – This system appears to offer an objective method
•
–
– In subtraction radiography, a standardized for following alveolar bone density changes
–
radiographic image is obtained before the appearance quantitatively over time, and when compared with
of an anatomical change, such as crestal alveolar bone I125 absorptiometry and digital subtraction analysis, it
loss and is subtracted from subsequent standardized has shown a higher sensitivity and a high degree of
radiograph. reproducibility and accuracy.
– The structures that have not changed will subtract out • Nuclear Medicine Technique (Bone scanning)
–
•
and appear as neutral gray, bone loss appearing darker – It is one of the most recent advances in the assessment
gray and areas of bone gain appearing lighter gray.
–
of bone changes in bone metabolism that may precede
Periodontics 565

architectural changes. Hence it has the potential to – Advantages
–
detect the earliest stage of bone loss. Target to specific microorganism

– In this technique, a bone seeking radiopharmaceutical Rapid

Most sensitive assay
–
diphosphonate compound labeled with Technetium –

99m (99m Tc) is injected intravenously and following – Disadvantages
–
a waiting period, it allows bone uptake and clearance It requires extensive instrumentation

of radio pharmaceutical. The uptake by the bone is Reference laboratory test is needed

measured by means of a miniaturized semiconductor – Restriction Endonuclease Analysis (REA)
–
REA recognize and cleave double stranded DNA at
probe radiation detector.

specific base pair sequences. The DNA fragments
generated are separated by electrophoresis,
Microbial Diagnosis stained with ethidium bromide, and visualized
• Conventional methods: with UV light.
•
Advantages
– Dark ground microscopy
PERIODONTICS

- REA is a powerful tool for determing the
–
– Phase contrast microscopy. (AIPG 2006)

distribution of a specific pathogenic strain
–

(AIPG 2008)
throughout a population

– Bacterial cultures–gold standard - REA is also used in molecular genetic analy-
–
• Immunodiagnostic Methods:

sis of the oral bacteria like A.a, P.gingivalis,
•
– Immunodiagnostic assays utilize antibodies that P.intermedia, E.corrodens, F.nucleatum and
–
recognize specific bacterial antigens to detect T.denticola
target microorganisms. This principle is used in the - REA helps in studying the transmission pat-
following diagnostic procedures.
terns of putative periodontal pathogens among
Direct immunofluorescent microscopy assays
family members.

Indirect immunofluorescent assays
• Enzyme based Assay: B.A.N.A. (COMEDK 2010, 2011)

Latex agglutination assay
•

– The identification of black pigmented Bacteroides, as

- Evalusite: It is a membrane immunoassay.
–
it gives a positive trypsin like reaction. B.forsythus,

Used to detect Aggregatibacter actinomycet-
emcomitans, Porphyromonas gingivalis, and P.gingivalis and small spirochetes, Treponema denticola
Prevotella intermedia. and Capnocytophaga species can be identified with
ELISA
B.A.N.A. as they have in common trypsin like enzyme.
– The activity of this enzyme is measured with the

• Nucleic acid probe assays (COMEDK 2009,
–
hydrolysis of the colorless substrate N Benzoyl
•

KAR 2005, 1996) D-1 arginine-2-napthylamide (B.A.N.A.). When

– DNA probes have been developed to identify hydrolysis takes place, it releases the chromophore
–
nucleotide sequence that is specific for bacteria Betanapthylamide which turns orange and when a
believed to be of diagnostic significance including drop of fast garnet is added to the solution.
suspected periodontal pathogens. – B.A.N.A. test is not specific, since it cannot distinguish
–
– They are able to detect the presence of as few 103 cells in which of the 3 known BANA species is responsible for
–
the sample and provide information of the presence of the reaction. A commercially available BANA reagent
selected species that is as reliable as culture methods. kit is called Perioscan.
– P.gingivalis, P.intermedia, A.actinomycetem comitans, – Cannot identify Actinomycetemcomitans (KAR 2011)
–
–
E.corrodens, F.nucleatum, C.rectus, B.forsythus • Volatile Sulphur Compounds
•
and T.denticola can be detected using radioactively – P.gingivalis, P.intermedia, P.melaninogenica,
labelled probe.
–
B.forsythus, T.denticola and F.nucleatum are capable
– However DNA probes cannot provide reliable of producing toxic, volatile sulphur compounds such
–
quantitative data and are limited by the availability of as hydrogen sulphide, methyl mercaptan, dimethyl
probes. sulphide and dimethyl disulphide through their
• Polymerase chain reaction metabolic pathways.
•
– It is a nucleic acid based assay developed by Karl – Diamond probe/Perio-2000 system is an instrument
–
–
Mullis. It can detect a single microorganism and has which has the features of periodontal probe and can
therefore the greatest sensitivity of any microbiological detect volatile sulphur compounds in the periodontal
method. pocket.
566
PROGNOSIS • Mechanical plaque control
•
– Toothbrush
• Defined as the prediction of the course, duration, and
–
– Dentifrice
•
outcome of a disease and its response to treatment.
–
– Interdental cleaning aids
–
• Classification: Dental floss
•

Toothpick
Excellent • No bone loss

Interproximal brush
•
• Excellent gingival condition

– Oral irrigation
•
• Good patient cooperation
–
•
• No systemic/environmental factors
Toothbrush
•
Good One or more of the following
• Adequate remaining bone support ADA given specification Length: 1 to 1.25 inches
•
• Possibilities to control etiologic factors and • Width: 5/16 to 3/8 inches
PERIODONTICS
•
•
establish a maintainable dentition
• Surface area: 2.54 to 3.2 cm
• Adequate patient cooperation, no systemic/
•
• No. of rows: 2 to 4 rows of brushes
•
environmental factors
•
• No. of tufts: 5 to 12 per row
Fair One or more of the following
•
• Less than adequate remaining bone support • No. of bristles: 80 to 85 per tuft
•
•
• Some tooth mobility
Diameter of bristles range from: (MAHE 2011, AP 2001)
•
• Grade I furcation involvement

• Soft brushes: 0.007 inch or 0.2mm commonly preferred.
•
• Adequate maintenance possible
•

•
• Acceptable patient cooperation

•
• Presence of limited systemic/environmental • Medium brushes: 0.012 inch or 0.3mm
•
•
factors
• Hard brushes: 0.014 inch or 0.4mm
•
Poor One or more of the following:
• Moderate to advanced bone loss
• Child brush: 0.1 to 0.15mm
•
•
• Tooth mobility • Length of the bristles: 10-11mm long
•
•
• Grade 1 or 2 furcation involvemnets • Rounded bristle ends cause fewer scratch to gingiva
•
•
• Difficult to maintain areas or doubtful patient
•
cooperation
Bass Soft Brush
• Presence of systemic/environmental factors
•
• Straight handle
Hopeless One or more of the following:
•
• Advanced bone loss • Nylon bristle
•
•
• Non maintainable areas • 0.007 inch(0.2 mm) in diameter
•
•
• Extractions indicated • 0.406 inch(10.3 mm) in length
•
•
• Presence of systemic or environmental
• Rounded ends
•
factors
•
• 3 rows of tufts
•
Question- One or more of the following • 6 evenly spaced tufts per row
able • Advanced bone loss
•
• 80-86 bristles per tuft
•
• Grade I or II furcation involvements
•
•
• Tooth mobility
Powered Toothbrushes
•
• Inaccessible areas
•
• Presence of systemic/environmental factors
• Are not generally superior to manual ones
•
•
• Powered toothbrushes have been shown to improve oral
PERIODONTAL TREATMENT
•
health:
– Children and adolescents
Mechanical Plaque Control
–
– Children with physical or mental disabilities
–
• Father of oral hygiene–Fones (MAHE 2006) – Hospitalized patients
–
•
• Term oral hygiene was coined by Rhein – Patients with fixed orthodontic appliances
–
•
Periodontics 567

Ionic Tooth Brush and Its Mechanism of Action vinyl chloride, ca carbonate, ca pyrophosphate, al silicate,
diatomacious earth etc.
• Principle: that every element in nature has a positive
• Humectant: Glycerine
•
or negative charge. This is called polarity. When the
•
polarities are opposite, the two elements cling together. • Detergent: Sodium lauryl sulfate
That’s why dust sticks to your coffee table and why plaque,
•
• Fillers: Na carboxy methyl cellulose
which has a positive charge (+), clings stubbornly to your
•

negatively charged (-) teeth. (AIPG 2008, 2006)

• The Ionic Action toothbrush temporarily reverses polarity • Anti bacterial agents: Triclosan, Na lauryl sulfate
•
•
of the tooth surface from negative (-) to positive (+), • Anti caries agents: Sodium monofluro phosphate
drawing plaque towards the negatively charged Ionic
•
• Sodium fluorides, stannous flouride
Toothbrush head.
•
• Desensitizing agents: Strontium salts, NaF
•
PERIODONTICS
Tooth Brushing Techniques • Flavouring agents
•
• Horizontal brushing (scrub) • Colouring agents
•
•
• Leonard method (vertical) • Sweeteners: Saccharine
•
•
• Bass method • Anti tartar: Pyrophosphate
•
•
• Modified Bass methods Anticalculus agents: Soluble pyrophosphatase, zinc compounds
•
• Stillman method (vibratory) Embrasure form Cleansing aids
•

• Modified Stillman method (roll) TYPE–1 embrasure with
•

• Charters method tight contact zones and intact papillae Floss
•

• Methods of cleaning with powered toothbrushes TYPE–2 embrasure with
•

Dentrifice (AIIMS 2008, COMEDK 2007, KAR concave interproximal surface and Interdental or Proxa

2006,AP 2002, MAN 1999, 2001) Moderate papillary recession brush

Composition TYPE–3 embrasure with Unitufted brush

• Abrasives: silicon oxide, aluminium oxide, granular poly complete loss of papillae

•
Interdental Cleansing Agents
DESCRITPTION USES PROCEDURE SPECIAL INSTRUCTIONS

Interdental Brushes Small tapered Clean spaces between Moisten, insert at
cylindrical brush head teeth/bifurcations. an angle according
Ortho bands. to gingival contour,
Stimulation. buccolingual motion
Applying
chemotherapeutic agents.
End tuft Single/group of small Open interproximal areas. Direct interproximal

tufts Surfaces next to area, rotating motion
edentulous areas. with intermittent
Furcations. pressure, Sulcular
Fixed dental prosthesis. brushing stroke.
Interdental tip Conical, flexible Exposed bifurcations. 90-degree angle to Caution against sub gingival use.
stimulator rubber/plastic attached At/below gingival margin. long axis of tooth. DO NOT USE on patients with
to end of handle/ Open spaces. Trace gingival margin. healthy tissue.
toothbrush Stimulation. Rub against teeth as it
moves in /out of open
spaces.
568
DESCRITPTION USES PROCEDURE SPECIAL INSTRUCTIONS

Wedge cleaner/ Made of wood (balsa Interproximal areas. Moisten with saliva,
stimulator “stim-U- or birch) or plastic. Massage. using the flat part
Dent” of the triangle, it’s
placed toward the
tissue and inserted
with buccolingual
action. Change if wood
becomes splayed, this
could force splinters
into the gums.
Knitting yarn - For wide spaces where Fold double, moisten, -

floss is tool narrow to clean use same technique as
effectively flossing
PERIODONTICS
Gauze Strip - Proximal areas next to Cut about 1 inch wide -

edentulous areas or widely and 6-8 inches n
spaced teeth length. Wrap around
using a shoeshine
stroke.
Pipe Cleaner - Furcations. Check wire end to -

Exposed proximal prevent damage to
surfaces. gingiva or scratching
of cemental surfaces,
buccolingual motion.
Toothpick in holder - Interdental cleansing Moisten with saliva, Avoid subgingival insertion
Furcations trace gingival margin
Orthodontic patient with blunt end.
Plaque removed at or just
under gingival margin
Dental floss holder Needle like device with Ortho appliances -

opening on one end Under Pontics
through which floss is Areas that are too tight for
threaded floss insertion
Tongue cleaner - Smokers Use in posterior to -

Coated tongues/ deeply anterior direction
fissured
Elongated papilla (hairy
tongue)
Dental Floss increased mitotic activity in epithelium and connective

tissue
• Multifilament vs. monofilament
• Emphasizing the importance of altering or removing
•
• Twisted vs. untwisted
•
plaque rather than stimulating or thickening the
•
• Bonded vs. unbonded
keratinized surface in the plaque control program
•
• Waxed vs. unwaxed
•
• 12-18 inches for use
Chemical Plaque Control
•
• Stretch: thumb and forefinger
Classification Chemical Plaque Control Agents
•
• Up-and-down stroke
• FIRST GENERATION Eg: Antibiotics, phenol,
•
•
quarternary ammonium compounds and sanguinarine
Gingival Massage
• SECOND GENERATION Eg:
•
•
Epithelial thickening, increased keratinization, and Bisbiguanides,(chlorhexidine)
•
Periodontics 569

• THIRD GENERATION Eg: Delmopinol
•
TRICLOSAN • Phenol derivative
•
• Is synthetic and ionic
•
• Used as a topical antimicrobial agent
•
• Broad spectrum of action including both gram positive and gram negative bacterias
•
• It also includes mycobacterium spores and Candida species
•
•
•
Mechanism Of Action
––
Triclosan Act On Cytoplasmic Membrane
↓

– Induce Leakage Of Cellular Constituents
–
↓

– Bacteriolysis
–
• Triclosan is included in tooth paste to reduce plaque formation
•
PERIODONTICS
• Used along with Zinc citrate or co-polymer Gantrez to enhance its retention within the oral cavity
•
• Triclosan delay plaque formation
•
• It inhibits formation of prostaglandins and leukotrienes there by reduces the chance of inflammation
•
METALLIC IONS eg: Zn and It reduces the glycolytic activity in bacteria and delays bacterial growth
Cu ions
QUARTERNARY AMMO- • Cationic antiseptics and surface active agents

•
NIUM COMPOUNDS • Effective against gram positive organisms
•
• Positively charged molecule reacts with negatively charged cell membrane phosphates and thereby
•
disrupts the bacterial cell wall structure Eg: Benzanthonium chloride and cetylpyredinium
SANGUINARINE • It is a benzophenanthredine alkaloid

•
• It is most effective against gram –ve organisms
•
• Used in mouth rinse
•
ANTIBIOTICS • Vancomycin, erythromycin, Niddamycin and Kanamycin
•
• Due to bacterial resistance problems the use of antibiotics has been reduced
•
DELMOPINOL • Inhibits plaque growth and reduces gingivitis
•
• Mechanism of action
•
– Interfere with plaque matrix formation and also reduces bacterial adherence
–
– It causes weak binding of plaque to tooth, thus aiding in easy removal of plaque by mechanical
–
procedures
– It is therefore indicated as a pre brushing mouth rinse
–
• Adverse effect of delmopinol
•
– Staining of tooth and tongue
–
– Taste disturbances
–
– Mucosal soreness and erosion
–
Chlorhexidine (PGI 2009, 2001, AIIMS 2009,1991, AIPG 2004,1997, AP 2001, KAR 1996)
• Mechanism of Action
•
– Chlorhexidine is a potent antibacterial substance. The antiseptic binds strongly to bacterial cell membranes.
–
– It has a broad antimicrobial activity: Gram +ve and gram –ve bacteria, yeasts and some lipophillic viruses.
–

(AIIMS MAY 2009)

– Gram +ve bacteria are more susceptible. It is also a potent antifungal(Budlz – Jorgensen). At low concentration
–
results in increased permeability with leakage of intracellular conponents including potassium, hence bacteriostatic.
At high concentration chlorhexidine causes precipitation of bacterial cytoplasm and cell death, hence bactericidal.
• Commonly used concentration is 0.2% v/v (AIPG 2001)
•

570
• Side effects
•
– Reversible brown staining of teeth, tongue, restorations
–
– Transient impairment of taste
–
• It has low systemic toxicity and no teratogenicity
•
• No appreciable resistance develops in microbes.
•
Disclosing Agents (MAHE 2011, KAR 2001,MAN – Non-irritating to mucous membrane
–
 
1997) – Diffusibility - neither too thin nor too thick
–
– Astringent and antiseptic
• Disclosing agents: Disclosing solution contains a dye
–
• The various disclosing agents are
•
or other coloring substance, which imparts its color to
•
– Iodine, Iodine disclosing solution, Diluted Tincture
calculus, plaque and films on the surface of teeth, tongue
PERIODONTICS
–
of Iodine, Berwick’s solution, Buckley’s solution,
and gingiva. It is a excellent oral hygiene aids because they
can provide the patient with additional motivational tool Talbot Iodoglycerol, Metaphen, Basic fuchsin,
to improve the efficiency of plaque control procedures. It Bismarck Brown, Easlick’s solution, Bender’s solution,
also conserve operating time by making inconspicuous Mercurochrome solution, Erythrosin (FDC Red No.
deposits more evident. 3), DC yellow no. 8 fluorescein, Two tone dye (FDC
red no. 3 and FDC green no.3). Two - tone dye test
• Factors to be considered in the selection of a disclosing
uses FDC red no. 3 and FDC green no. 3 solution
•
solution are:
which stains thick accumulation of plaque as blue and
– Intensity of color
thin deposits are stained red/pink.
–
– Taste
–
Instrumentation
• Sickles with straight shanks are used for anterior teeth whereas sickle scalers with contra angled shanks adapt to
•
posterior teeth.
• Tip action of magnetostrictive ultrasonic unit is elliptical/orbital (4 active working surfaces). Piezoelectric is linear (2
•
active working surfaces)
• Scaling motion should initiate in the forearm and transmits from wrist to the hand with slight flexing of fingers
•
Comparison of area-specific (gracey) and universal curettes
Gracey Curette Universal Curete
Area of use Set of many curettes designed for specific areas and One curette designed for all areas and surfaces.
surfaces.
Cutting Edge
Use One cutting edge used work with outer edge only. Both cutting edges used: work with either outer or inner
edge.
Curvature Curved in two planes blade curves up and to the side Curved in one plane; blade curves up, not to the side.
Blade angle Offset blade; face of blade beveled at 60 degrees to Blade not offset of beveled at 90 degrees to shank.
shank.
• Gracey curette series

•
Gracey curette number Specific area of use
1/2 Anterior teeth
3/4 Anterior teeth
Periodontics 571

5 /6 Anterior teeth and premolar
7 /8 Posterior teeth, facial and lingual surfaces
9 / 10 Posterior teeth, facial and lingual surfaces
11 /12 Posterior teeth, mesial surfaces (AIPG 2005)

13 / 14 Posterior teeth, distal surfaces
• Recent additions:
•
– Number 15-16 is the modification of the standard 11-12 and is designed for mesial surfaces of posterior teeth. It
–
consists of Gracey 11-12 with acutely angled Gracey 13-14 shank.
– Number 17-18 is a modification of 13-14. It has a terminal shank elongated by 3mm and a more accentuated
PERIODONTICS
–
angulation of the shank to provide complete occlusal clearance and better access to all posterior distal surfaces.
– Extended shank curettes (After five series): The terminal shank is 3 mm longer, allowing extension into deeper
–
periodontal pockets of 5 mm or more. All standard Gracey numbers except for the no 9-10 are available in After five
series.
– Mini bladed curettes (Mini five series): Blade are half the length of standard Gracey. All except 9-10 are available
–
in this design.
– Gracey curvettes: Blade length is 50% shorter than standard Gracey
–
Sub 0 and no. 1-2: are used for anteriors and premolars

The no:11-12 is used for posterior mesial surfaces

The no: 13-14 is used for posterior distal surfaces

– Langer and mini langer curettes: Set of three curettes that combines the shank design of the standard Gracey 5-6,
–
11-12 and 13-14 curettes with a universal blade angled at 900.
Antimicrobial Therapy and only small portion of the total dose actually reaches
the subgingival microflora in the periodontal pocket.
Systemic Antimicrobial Therapy: limitations
• Adverse drug reactions are a greater concern and are more
• Systemic delivery provides a ready exposure of all
•
likely to happen if drugs are distributed via the systemic
•
periodontal sites to the antimicrobial agent, but it also route.
possesses a risk of adverse reactions to non-oral body
• Emergence of drug resistant strains also pose a problem.
sites.
•
• Local drug delivery overcomes many of the above
• The drug is dissolved by dispersal over the whole body,
•
limitations of systemic antimicrobial therapy.
•
Classification of Local Antimicrobial Agent Therapy in Periodontics
• Personally applied (In patient , home selfcare)

•
– Non-sustained subgingival drug delivery
–
(Home oral irrigation)

• Sustained subgingival drug delivery
•

(Not developed to date)

• Professionally applied (In dental office)
•
– Non -sustained subgingival drug delivery.
–
(Professional pocket irrigation)

– Sustained drug delivery system with first order kinetics and “0’’ order kinetics.
–
572
• Controlled release local delivery systems can be classified as:

•
– Reserviors without rate controlling system.
–
e.g. hollow fibers, gels , dialysis tubing.

– Reservoir with rate control system.
–
e.g. monolithic matrices, acrylic strips, ethyl cellulose strips.

Local Drug Delivery
Product Antimicrobial agent Dosage form
Actisite (KAR 1996) Tetracycline Non resorbable fibre

Arestin Minocycline Biodegradable powder
PERIODONTICS
Atridox Doxycycline Biodegradable mixture in syringe (Doxycycline gel)
Dentamycin/periocline Minocycline Biodegradable mixture in syringe – (minocycline microspheres)
Elyzol (AIPG 2006) Metronidazole Biodegradable mixture in syringe

(AIPG 2008)

Periochip Chlorhexidine Biodegradable device
Pharmacological Strategies For Treating Periodontal Bone Loss.

• Generally target–bacteria in the lesion or the host response to the bacteria.
•
Fig.14.9: Rank-rankl-opg axis
Potential therapeutic strategies to treat bone resorption: that blocks receptor activator of nuclear factor-kappa
• Agents that block the differentiation or activity of B (NF-kB) ligand (RANKL) and RANK juxtacrine
•
osteoclasts are potential therapeutic agents. interaction.
– Nonsteroidal anti-inflammatory drugs (NSAIDs) and
– Osteoprotegerin (OPG) inhibits the differentiation
–
other anti-inflammatory molecules (including p38
–
of osteoclasts through its action as a decoy receptor
Periodontics 573

mitogen-activated protein kinase inhibitors, c-jun • Low-dose tetracycline
•
N-terminal kinase inhibitors, NF-kB inhibitors, and – Tetracyclines – broadspectrum antibiotics.
the specific, high-affinity IL-1 inhibitor IL-1 [TRAP])
–
– Extensively used in management of periodontal
can inhibit the formation of hematoprogenitor cells
–
disease.
to preosteoclasts. Inhibits bacterial protein synthesis.
– Antibodies to RANKL can also block this interaction.

Blocks tissue destruction enzymes, such as MMPs.
–
MMP inhibitors reduce the protease degradation of

Chelate the cations of metalloproteinases that are
the organic matrix, and anti-integrins block the initial

required for action.
osteoclast adhesion to the matrix.
– Other non-microbial mechanisms attributed to
– Bisphosphonates and MMP inhibitors work at the
–
tetracyclines include:
–
site of the osteoclast adhesion zone to the mineralized
matrix in blocking bone resorption. – Inactivation of enzymes that activate
–
• Anti-Inflammatory Agents metalloproteinases
PERIODONTICS
•
– Agents that block cytokine production or activity are – Scavenging reactive oxygen species.
–
–
the earliest strategies to inhibit bone resorption. – Blockade of secretion of lysosomal proteinases.
–
– NSAIDs have shown promising results in slowing – Modulation of osteoclast functions and osteoblast
–
–
periodontal destruction. But their widespread use has apoptosis. (MAHE 2008)

been limited to their adverse reactions. – Low-dose tetracyclines have been shown to reduce
–
– Localized application – cut down adverse effects. collagenase activity in gingival tissue extracts and
–
– Inhibition of cycloxygenase 2(COX-2), a mediator GCF.
–
of pro-inflammatory prostaglandin activity, prevents – Long-term tetracycline therapy resulted in
alveolar bone loss in experimental animal study.
–
undesirable effects; hence CHEMICALLY
– Specifically blocking IL-1 and TNF, dramatically MODIFIED TETRACYCLINES were developed
–
reduces the loss of alveolar bone.
which – eliminate the antimicrobial properties BUT
– Blocking agents were administered by intrapapillary
maintains its activities on MMPs.
–
injection 3 times/week over a 6-week period with
significant reductions in radiographic alveolar bone – This modification produces a molecule that has no
–
loss. These types of strategies may provide future antimicrobial activity but inhibits collagenase activity
therapeutic modalities to treat periodontal bone and reduces tissue breakdown.
resorption. – Currently CMT appear to have promising therapeutic
–
• Bisphosphonates potential in the treatment of periodontitis.
Estrogen And Selective Estrogen Receptor Modulators
•
– Inhibit osteoclast formation and function. •
•
(SERMS):
–
– In high concentration its preferentially taken up by
– Estrogen deficiency à accelerated bone resorption,
–
bone tissue.
–
characteristic of postmenopausal osteoporosis.
– Bind/adhere to bone surface.
– Estrogen withdrawal à Increase in bone resorption;
–
– Inhibit resorptive activity by directly acting on
–

Enhanced osteoclast formation and
–
osteoclast; promote apoptosis of osteoclast.

reduced osteoclast apoptosis.
– Also affect protein production of osteoclast.
–
– Has inhibitory effect on both MMP-1 and – Treatment with estrogen à Inhibits bone loss
–
–
MMP-3; this blocks the initiating step in the bone and bone turnover; increases bone mineral density.
resorptive process. – A new class of drug i.e, SERMs: That exert estrogen
–
– Bisphosphonate-complexed implants results effects on various tissues has been MOA of SERMs
–
in better osteoconduction and repair in animal is same as that of estrogen – blocking production
models, suggesting that inhibition of bone resorption of cytokines that promote osteoclast differentiation
facilitates bone healing.
and by promoting osteoclast apoptosis.
– In naturally occurring periodontitis-no effect.
– Estrogen deficiency. and osteoporosis: Increased
–
– In ligature-induced periodontitis–it reduced the
–
oral bone resorption , attachment loss and bone
–
amount of attachment loss and prevented loss of
bone density. loss.
574
– Increased loss of interproximal alveolar bone Gingivoplasty and Gingivectomy

–
height: In deficiency. • Reshaping of the gingiva to create physiologic gingival
•
– IL-β level in GCF is low in estrogen sufficient contours in the absence of pockets. (AP 2003)
–

patients.
• Gingival clefts, craters and the shelf like interdental papilla
– Estrogen supplementation à decreased gingival
•
caused by ANUG are indications of gingivoplasty.
–
inflammation and decreased frequency of CAL.
(AIIMS Nov 2010, MP 2008, AIPG 2002,

2001, 1992, 1991, AP 1990)
• Osteoprotegrin (OPG):
• In gingivectomy, Kirkland knife is the first to be used for
•
– Microbial stimulation by Aa induced RANKL
•
incisions on facial and lingual surface. (PGI 1999)
–
expression on the surface of CD4+ cells and in vivo
• Orban knife is for supplemental interdental incision.
inhibition of RANKL function with the decoy
•
Merrifield knife is representative of knives commonly
receptor OPG diminished alveolar bone destruction
PERIODONTICS
used in interdental areas.

and decreased the number of osteoclasts after
microbial challenge. Rationale
– Peptides that specifically inhibit MMPs reduce MMP • Pocket elimination for root accessibility
•
–
activity and bone loss and may have therapeutic • Establish physiologic gingival contours
•
benefit with future study.
Indications Contraindications
• Suprabony pockets • An inadequate zone of keratinized tissue
•
•
• An adequate zone of keratinized tissue • Pockets that extend beyond the mucoginigival line
•
•
• Pockets greater than 3 mm • The need for osseous resection or inductive techniques
•
•
• When bone loss is horizontal and no need exists of osseous • Highly inflamed or edematous tissue
•
•
surgery • Areas of esthetic compromise
•
• Gingival enlargements • Shallow palatal vault and prominent external oblique ridges
•
•
• Areas of limited access • Treatment of intrabony pockets
•
•
• Unesthetic or asymmetric gingival topography • Patients with poor oral hygiene
•
•
• For exposure of soft tissue impaction to enhance eruption
•
• To facilitate restorative dentistry
•
• To establish physiologic and ginigival contours post – acute
•
necrotizing ulcerative gingivitis and flap procedures
Periodontal Flaps Establish physiologic architecture of hard tissues

by regeneration or resection
• Objectives of Periodontal Surgery: Augment alveolar ridge defects
•

– Access to roots and alveolar bone – Repair or regeneration of the periodontium
–
–
Enhance visibility – Pocket reduction
–
Enhance maintenance by patient and dentist

Increase the effectiveness of scaling and root

Improve long term stability

planning

– Provide acceptable soft tissue contours
Lessen tissue trauma
–
Enhance plaque control and maintenance

– Modification of osseous defects

Improve esthetics
–

• Classification of Flaps:
•
Based On Bone Exposure After • Full Thickness (Mucoperiosteal) Flaps
Reflection
•
• Partial Thickness (Mucosal) Flaps
•
Based On Flap Placement After • Non-Displaced Flaps
Surgery
•
• Displaced Flaps
•
Periodontics 575

Based On Management Of The • Conventional Flaps:
Papilla
•
– Modified widman flap
–
– Undisplaced flap
–
– Apically displaced flap
–
– Flaps for reconstructive procedures
–
• Papilla Preservation Flap
•
– Used for regenerative surgeries
–
– Preferred in areas with aesthetic concern
–

(HP 2010, AIIMS 2007, KAR 2006, AIPG 2006, 2004)

Modified Widman Flap (AIPG 2010)
• Described by Ramfjord and Nissle- 1974
•
• This difference between modified widman and original widman is that the original widman technique included:
PERIODONTICS
•
– Apical displacement of flaps
–
– Osseous recontouring
–
• Three incisions are used in this technique:
•
– Internal Bevel Incision to the alveolar crest starting 0.5-1mm away from the gingival margin parallel to long axis of
–
teeth.
– Crevicular incision is made from the bottom of the pocket to the bone, to facilitate gentle separation of the collar of
–
pocket epithelium and granulation tissue from the root surfaces
– Interdental or third incision is made after flap is reflected in a horizontal direction, close to surface of bone crest
–
separates soft tissue collar of root surfaces from bone.
Apically Displaced Flap

– Can be used for pocket elimination or widening the zone of attached gingiva.
–

(KAR 2011, AIIMS 2007, AIPG 1991, 2002)

– Has the advantage of preserving outer portion wall and transforming into attached gingiva.
–
– It increases the length of clinical crown and is not indicated for palatal pockets.
–
Resective Osseous Surgery
Osteoplasty • Vertical Grooving • Reshaping of bone without removing tooth supporting bone (COMEDK 2006)
•
•

• Radicular blending • For correction of shallow craters, bone ledges and exostoses
•
•
• Done with rotary instruments
•
Ostectomy • Flattening interproximal bone • Removal of tooth supporting bone
•
•
• Gradualising marginal bone • For correction of negative architecture one wall osseus defects
(AIPG 2004)
•
•
• Flattening interproximal bone is used in the treatment of hemisepta
•
• Ostectomy procedures are done with hand instruments
•
Furcation
Measured by Naber’s probe (AIPG 2004)(AIPG 2008)

Classification
Type of furcation Features Treatment plan

Grade I • Incipient lesion • Scaling, root planning – Odontoplasty
•
•
• Not detected by X ray • Gingivectomy for fibrous pockets (PGI 2008, PGI 1999)
•
•

• Suprabony pocket
•
• Oedematous gingiva
•
576
Grade II • Cul de sac • Moderate cases:
•
•
• Partial penetration of probe – Scaling, root planning
•
–
• May/may not be detected by X ray – GTR with bone grafts
–
•
– Osteoplasty
–
• Advanced cases:
•
– Root resection or hemisection
–
Grade III • Inter radicular bone loss • Scaling and root planning
•
•
• Through and through passage of probe • Tunneling (resection accessibility)
•
•
• Furcation is covered by gingiva • Root resection and hemisection
•
•
Grade IV • Grade III furcation with orifice • Moderate cases
•
•
uncovered by gingiva • Same as grade II with occlusal adjustment
•
• Advanced cases- extraction
PERIODONTICS
•
Root resection/ Am- • Removal of root without removal of any crown portion
•
putation • Maxillary 1st molar is most favorable for root resection
•
• Resection of distobuccal root is the choice of therapy if furcation involvement is in between buccal roots.
•
Hemisection • Surgical removal of one root and the corresponding overlying crown. The tooth is separated buccolingually
•
though the bifurcation, and the affected or diseased portion of the tooth is removed.(MP 2011, AIPG 2002)

Biscuspidisation • Molar is simply cut without removal of any part of crown or root followed by restoration as two separate units
•
• Hemisection and bicuspidation are suitable for mandibular molars
•
• Usually endodontic treatment should be done before periodontal therapy such as root resorption or
•
hemisection.
Mucogingival Surgery
• The term introduced by Friedman
•
• The 1996 World Workshop in Clinical Periodontics renamed Mucogingival surgery as Periodontal Plastic surgery- a term
•
proposed by Miller in 1993
• Periodontal plastic surgery is defined as
•
“Surgical procedures performed to correct or eliminate anatomic, developmental or traumatic deformities of the gingiva or

alveolar mucosa”
Crown Lengthening (MP 2010)
The procedure depends mainly on

• Band of attached gingiva
•
• Thickness of marginal alveolar bone (Sato 1989)
•
Periodontics 577

PERIODONTICS
Concept of Biologic Width and Its Significance
Biologic width is defined as the physiologic dimension of the junctional epithelium and connective tissue attachment. The
average width is 2.04mm; the average epithelial attachment is 0.71- 1.35 mm and the average connective tissue is 1.06-1.08mm.
Biologic width is measured from the bottom of the gingival sulcus to the alveolar crest and is maintained by homeostasis.
Impingement on the biologic width may result in
• Gingival inflammation
•
• Pocket formation
•
• Attachment loss
•
Type of Surgical Procedure
Root Coverage
• Marginal tissue recession, i.e. displacement of the soft tissue margin apical to the cemento-enamel junction with exposure
•
of the root surface is a common feature
• Indications (AIPG 2010, KAR 2001)
•

– Root hypersensitivity
–
– Esthetic concern
–
– Management of root caries, abrasion
–
– Changing the topography facilitating proper plaque control
–
• Conditions Necessary For Successful Root Coverage
•
– No loss of interdental papilla and interdental alveolar bone adjacent to gingival recession area
–
– Sufficient interdental papilla adjacent to recession area
–
– Sufficient blood supply ensured to donor tissue
–
– Root surface covered with thick donor tissue
–
– Donor tissue closely adapted to the recipient area and sutured
–
– No severe decay or abrasion on exposed root
–
Mucogingival (plastic) surgical techniques (KAR 2001)
• Techniques of increasing the width of attached ginigiva • FGG, apically displaced flap
•
•
578
Mucogingival (plastic) surgical techniques (KAR 2001)

• Techniques for coverage of denuded roots • Laterally displaced pedicle graft, coronally displaced flap, free
•
•
gingival graft
• Techniques to deepen the vestibule • Free autogenous grafts and vestibular extension procedures
•
•
• Techniques for the vestibule of frenum • Frenectomy (KAR 2006)
•
•

Tarnow technique • Semilunar coronally displaced flap (KAR 2004, AP 2000)
•

Miller’s technique • Free soft tissue autograft
•
Langer’s technique • Subepithelial connective tissue graft (KAR 2006)
•

Pouch and tunnel technique • Variant of Langer’s technique
PERIODONTICS
•
Regenerative Therapy
• Guided tissue regeneration
•
– Principle: only the periodontal ligament cells have the potential for regeneration of the attachment apparatus of the
–
tooth. Presence of any other cells retards this process (AIPG 2006)

– Consists of placing barriers to cover bone and PDL and preventing epithelial migration along the root surface
–
allowing PDL cells to directly bond to the tooth surface
– Membranes used are:
–
Non resorbable

- PTFE (Goretex membrane) removed 3-6 weeks later

Absorbable membranes:

- a second-stage surgery is not necessary because it does not require removal.

- Fewer incision line opening complications if they do occur, management is more predictable and the amount

of bone regenerated is greater than similar complications with non-resorbable materials.
- Collagen membrane.

- Polylactic/ polyglycolic acid membrane.

- Acellular dermal matrix.

– Guided Bone Regeneration: (COMEDK 2007) – The barrier membrane should be placed over a
–
–

– GBR provides many of the primary keys for bone particulate graft, rather than an empty or blood clot-
–
grafting such as: (AIPG 2006, AIIMS 2007, filled space. A blood clot, in and of itself, does not

KAR 1995) participate in bone formation under the BM. Because

Space maintenance,
a blood clot is 95% stagnant red blood cells and 5%

Protection of blood vessels,
Clot with growth factors,
platelets, the environment to grow bone is reduced, as

red blood cells lyse and reduce the pH in the region.

Graft stabilization,

Exclusion of fibrous tissue in the graft. (KAR 1999)

Bone Grafts
• Types of bone grafts(AIPG 1989, 1991, AP 1995, PGI 1996)
•

Autograft A tissue (bone) graft transferred from one position to a new position in the body of the same individual
Allograft A tissue (bone) graft transferred between individuals of same species, but of non – identical genetic disposition.
Alloplast A synthetic bone grafting material – bone graft substitute
Xenograft A tissue (bone) graft between members of different species otherwise known as Heterograft
Periodontics 579

Classification
Autogenous grafts Allogenic grafts Xenogeneic grafts Alloplastic grafts
(AIPG 2006, PGI 1994) (AIPG 1994, AP 1995)
• Corticol bone chips • Fresh frozen bone • Bovine derived • Polymers
•
•
•
•
• Osseous coagulum • Mineralised hydroxyapatite • Bioceramics
•
•
•
• Bone blend (AIPG 2010, 2011, freeze dried bone • Os purum • Tricalcium Phosphate
•
allografts (FDBA):
•

•
MAH 2008) • Boplant • Hydroxyapatite
Osteoconductive
•

•
• Bone swaging • Anorganic bone • Dense/ Non porous/ Non
• Demineralized
•
•
•
• Intraoral cancellous bone and marrow • Kiel bone resorbable
•
freeze dried bone
•
•
• Extraoral cancellous bone and marrow allografts (DFDBA): • Corallin Calcium • Porous/ Non resorbable
•
•
carbonate
•
• Have the highest osteogenic potential Osteoinductive • Resorbable
•
• Osteoconductive
•

(KAR 2005, MP 2010) • Bioactive glasses
•

(MP 2009, AP 2002)

•
Osteoconductive
PERIODONTICS
(IGNOU 2010, KAR 2003)

Mechanism of Action
Osteogenesis The viable cells present in placed graft material actively forms bone in the recipient site
Osteoinduction The placed graft by the action of factors contained in itself, such as proteins and growth factors, induces formation of
new bone
Osteoconduction The placed graft acts as a trellis or a scaffold over which new bone deposits can occur.
Cortical chips because of their relatively large size 1.559 x 1.83 mmm underwent sequestration
Sources
Osseous coagulum • Exostosis

•
• Lingual ridges of mandible
•
• Palatal excresenses
•
• Osseous tissues obtained from osteoplastic procedures.
•
Intra oral cancellous bone and marrow • Healing bony wounds
•
• Healing extraction sockets (8-12 weeks – Most productive)
•
• Edentulous ridges
•
• Mandibular retromolar areas
•
• Maxillary tuberosity
•
Extraoral cancellous bone and marrow • Anterior / Posterior iliac crest (AP 1997)
•

• Greatest osteogenic potential
•
• Risk of disease transfer in allogenic grafts
•
– Fresh frozen bone allografts one in 2 million
–
– Freeze dried bone one in 2.8 billion
–
– Creutzfeldt–Jakob disease–Risk is remote if proper exclusionary techniques are followed.
–
• Radiation sterilization must not be used to sterilize DFDBA as it was found to reduce its inductive capacity by 40%
•
• DFDBA is an osteoconductive material while demineralising FDBA exposes BMP–Osteoinductive material.
•
• Biocoral calcium carbonate obtained from natural coral genus porites. Pore size 100–200 microns. Bicoral has high
•
osteoconductive potential because no fibrous encapsulation has been reported.
580
• Bioactive glasses:
•
– Mode of action
–

CaO, Na2O, SiO2, P2O5
Exposed to tissue fluids
Covered by double layer

↓
Promotes absorption and concentration of proteins
↓
Guides and promotes osteogenesis
• Currently two forms are available
•
PERIODONTICS
– Perioglas: Particle size 90–710 microns

–
– Biogran: Particle size 300–355 microns advantageous for guiding osteogenesis.
–
• Xenogenic bone grafts
•
– Consist of deproteinized cancellous skeletal bone tissue that is harvested from one species and transferred to the
–
recipient site of another species.
– Unlimited supply of available material
–
– Has the same inherent problems as allografts, and being from different species, it may cause even more pronounced
–
immunological problems.
– Disadvantage–only osteoconductive property.
–
• Coral-derived granules • Calcium phosphates
•
•
– Natural coral exoskeleton derived from marine reefs – Similarity in composition to the bone mineral,
–
–
(madreporic corals) bioactivity, osteoconductivity and ability to form an
– Is composed of calcium carbonate. unique strong interface with bone .
–
– Has excellent mechanical properties – The major advantage of being able to readily adapt to
–
–
– The calcium carbonate of natural coral can be the shape of the bone defect.
–
converted to HA through an hydrothermal exchange – Rapidly integrate into the bone structure and are
–
process (replamine form) transformed into new bone by the action of bone cells
– The volume of porosity affects the rates of biomaterial (osteoclasts and osteoblasts) responsible for the local
bone remodeling.
–
resorption and bone formation.
– Another material Phycogene HA is derived from – Limitations-mechanical properties and slow
–
biodegradation in vivo
–
calcified marine algae.
• Alloplastic bone grafts or synthetic bone substitutes • Tricalcium Phosphate

•
•
– Synthetic materials – Similar to synthetic hydroxyl apatite ( sHA )
–
– Formulated into pastes, particles or blocks,
–
– Developed to replace human bone.
–
– Biocompatible and biodegradable.
–
– They are biocompatible and are the most common
–
– Disadvantage
–
type of graft materials utilized.
–
Unpredictable rate of bioresorption.
– Osteoconductive materials.

– Recent formulation: β-TCP (Vitoss, Orthovita,
–
– There are three types of alloplastic substances in
–
Malvern, Pa) is 3-dimensionally macroporous,
–
clinical use nowadays: CaPs; other ceramics (e.g.
containing spaces into which bone ingrowth can
Hydroxyapatite–HA), Biphasic Calcium Phosphate
occur . It also has a microporosity that is thought to
(BCP), Tricalcium Phosphate (TCP), Calcium promote diffusion of nutrients and transmission of
Sulfate and Biocompatible Composite Polymers. fluid pressures.
Periodontics 581

– Used as an processes including cell growth, differentiation and
embryonic pattern formation .
–
Osteoconductive filler
– BMPs 2, 4, 6, and 7 (also known as osteogenic protein

Bone graft extender and
–
1 [OP-1]) are thought to be the most important BMPs

A carrier of aspirated bone marrow cells .
for bone formation. Bone Morphogenetic Protein acts

as an extracellular molecule that can be classified as a
• Biphasic Calcium Phosphate morphogen as its action
•
– sHA and β-TCP. – Recapitulates embryonic bone formation.
–
–
– Recent development of BCP ceramics (HA/β- – One of the challenges in the use of BMP is in its
–
TCP), has provided materials in which bioactivity is
–
delivery to a site of action.
controlled by an association of Hydroxyapatite {Hap: – While recombinant BMP molecules are extremely
CA10 (PO4)6(OH)2} and β-ricalcium phosphate
–
potent, they are difficult to use clinically in powder
{β-TCP: Ca3(PO4)2} in adequate rations. or solution. Their handling properties and biologic
– Bioactive glasses are silico-phosphate chains activity are enhanced when BMPs are delivered with
PERIODONTICS
–
– chemically bonds with bone and are supposed to carrier materials, but the best carriers for various
–
function as small bone regenerative chambers .
surgical applications have not yet been determined
– Bioactive glasses may have osteoconductive
– More recently biodegradable gels, collagen sponges
–
properties.
–
impregnated with BMP and silica glass have been
• Calcium Sulfate used as carriers.
•
– One of the first materials investigated as a substitute • Transforming Growth Factor β
–
•
for bone graft was Plaster of Paris, the β-hemihydrate – Enhance bone healing.
form of calcium sulfate (CaSO4·1/2H2O, POP).
–
– TGF-β has been shown to participate in all phases
– It is a biological inert, osteoconductive, resorbable
–
of bone healing.
–
and high biocompatible material – During the initial inflammatory phase, TGF-β is
– Advantage
–
released from platelets andstimulates mesenchymal
–
Ease of handling, cell proliferation.

Resorption by osteoclasts and attachment and – Its chemotactic for bone forming cells,

–
deposition of osteoid by osteoblasts – Stimulates angiogenesis and
–
– Drawbacks – Limites osteoclastic activity at the revascularization
–
–
Reduced mechanical support phase

poor bioactivity. – Once bone healing enters osteogenesis,

–
faster resorption rate of the POP cement is TGF-β increases osteoblast mitoses,

too fast, which may negatively affect bone regulates osteoblast function and

regeneration. increasing bone matrix synthesis,

poor mechanical strength and low inhibits type II collagen but promoting type I

macroporosity collagen
Combinations of BMP and TGF-β, may enhance

• Osteoactive agents the osteoinductivity of an implant, while at the
same time, make it osteopromotive.
•
– An osteoactive agent is a material which has the
–
ability to stimulate the deposition of bone.
– These may be classified in three categories: Platelet-Derived Growth Factor
–
osteoinducers, osteopromoters and bioactive – Platelets are known to contain a number of different
peptides.
–
growth factors which are released into the tissue
– Urist (1965) in a classical study described ectopic after injury. These include TGF-β, PDGF, IGF and
–
bone induction in intramuscular implantation of FGF which act as differential factors on regenerating
demineralized bone matrix (DBM). periodontal tissues
– The PDGF is angiogenic and is known to stimulate
–
Bone Morphogenetic Protein the reproduction and chemotaxis of connective tissue
cells and matrix deposition.
– Osteoinductive – Platelet Rich Plasma (PRP) is one potential source
–
– BMPs belong to a group of proteins called TGF-β
–
of concentrated platelets that could be used in bone
–
superfamily that regulate many different biological regeneration
582
• Bioactive Polypeptides
•
– The last category of bioactive molecules is the polypeptide group.
–
– May act as osteoinducers or osteoenhancers
–
– Two short amino acids chain peptides that have demonstrated a bone activity are known as P-15 and OSA-117MV.
–
P-15 is reported to attract and bind osteoblasts with the bone-grafting matrix.
Stem Cell
– Human mesenchymal stem cells (MSCs), obtained from the adult bone marrow, are multipotent cells capable of
–
differentiating into various mesenchymal tissues.
– From a small volume of bone marrow, MSCs can be isolated and culture expanded into a large number due to their
–
proliferative capacity maintaining their functionality after cryopreservation. Thus, MSCs are thought to be a readily
PERIODONTICS
available and abundant source of cells for tissue engineering applications.

– MSCs can be combined with porous, biphasic calcium phosphate ceramics (hydroxyapatite/ β-tricalcium phosphate –
–
HA/TCP)
Stages in the differentiation of a stem cell. Embryonic stem cells are nearly totipotent, whereas a stem cell
in an adult tissue may be pluripotent (for example, hematopoietic stem cell) or unipotent (epithelial cell, for
example). An adult tissue may contain the stem cells and precursor cells separated from full differentiation
by one or several steps. The periodontal ligament has been shown to contain precursor cells or progenitors
to cementoblasts. The differentiated cell may also consist of subpopulations of the same cell type.
Materials For Long-Term Ridge Pres- Materials For Transitional Ridge Materials For Short-Term Ridge Preserva-
ervation. Preservation tion.
• Synthetic hydroxyapatite. • An organic bovine bone matrix. • Demineralized freeze dried bone allograft
•
•
•
• Particulate dense HA. • Resorbable calcium phosphate (DFDBA )
•
•
• Porous coralline HA. ceramics. • Autogenous bone with low-density HA,TCP
•
or ABM product in a 50:50 or 75:25 ratio.
•
• Bioactive glass. • Macroporous bioactive glass.
•
•
• Porous polymethyl methacrylate.
•
Sutures
Figure of eight suture • Given where approximation of interdental papilla is not possible (AP 2008)
•

Horizontal mattress • Indicated when multiple interdental areas are involved
•
suture • This suture is often used for the interproximal areas of diastema or for wide interdental spaces to properly
•
adapt the interproximal papilla against the bone.
• Two sutures are often necessary
•
• The horizontal mattress suture can be incorporated with continuous, independent sling sutures.
•

(KAR 2006)

Continuous sling • Indicated where the approximation of both labial and lingual flaps are tied independently
•
suture
Interdental ligation • Used when the flaps are not in close apposition because of apical flap position or non scalloped incisons
•
Closed anchor suture • Another technique to close a flap located in an edentulous area mesial or distal to a tooth
•
• Consists of tying a direct suture that closes the proximal flap, carrying one of the threads around the tooth
•
to anchor the tissue against the tooth, and then tying the two threads.
Periodontics 583

PERIODONTAL DRESSINGS
Function (MAHE 1998)
• To obtain and maintain a close adaptation of the mucosal flaps to the underlying bone especially when flap has been
•
repositioned apically to prevent coronal displacement.
• To protect the wound post surgically form irritation caused by food, air, tongue or cheek movements.
•
• To provide additional support to stabilise free gingival graft.
•
• Template for healing by preventing excessive formation of granulation tissue by filling interdental space.
•
• Facilitates healing - no curative properties.
•
• Minimises likelihood of postoperative infections and haemmorhage.
•
• Maintenance of debris free area.
•
• Protects the suture.
PERIODONTICS
•
• Splinting of mobile teeth.
•
• For the comfort of the patient.
•
• Desensitize the root surface; protect the exposed root surface from temperature changes.
•
Classification Of Periodontal Dressings
During the course of time, various periodontal dressings have been evolved.
Periodontal dressing can be mainly classified into:
• EUGENOL based periodontal dressing.
•
• NON-EUGENOL based periodontal dressing (Glickman)
•
EUGENOL based periodontal dressing NON-EUGENOL based periodontal dressing
• Wards wonder pack • Coe pak

•
•
• Orban’s pack • Perio Care
•
•
• Goldman’s pack • Peri Pak
•
•
• Kirkland’s pack • Voco Pak
•
•
• Modified Kirkland pack • Perio Putty
•
•
• Barricaid visible light curing periodontal dressing
•
• Collagen dressing
•
• Methacrylic gel dressing
•
• Cyanoacrylate dressing
•
• Powder: • TUBE – I
•
•
– Rosin – 0.52 gms. – Zinc oxide-antispetic , astringent
–
–
– Zinc oxide – 0.41 gms. – MgO-helps in setting reaction
–
–
– Bacitracin – 3000 units – Vegetable oil-plasticity
–
–
• Liquids: – Synthetic rosin-cohesiveness
•
–
– Zinc oxide – 5 % – Lorothidol-fungicide
–
• TUBE – II
–
– Hydrogenated fat – 95%
•
–
– Liquid coconut fatty acid thickened with colophony
–
– Chlorothymol: Bacteriostatic agent
–
– Modifiers: Zinc acetate,cellulose, wax
–
– Natural gums: To adjust setting time
–
HEALING
Factors Involved in Healing
• Integrins:
•
– Cell–Surface associated dimeric glycoproteins
–
– function as cell to extracellular matrix adhesion receptors
–
584
– They play key roles in: re-epithelization and granulation tissue formation
–
– Regulates a wide range of cell functions during growth, development, differentiation and immune response.
–
PERIODONTICS
Fig.14.14: Structure of integrin

• Epithelial cells can bind and also activate transforming growth β1, through γ 6.
•
α
b
• Laminin–5
•
– Found in basement membrane of skin and other epithelial tissue.
–
– It serves as a component of anchoring filaments that span through the basement membrane
–
– Laminin: 5 is also recognized by 3β1 integrin.
–
α
– Infact laminin: 5 appears to be a motility factor for keratinocytes but when proteolytically processed it starts
–
to function as the nucleator of hemidesmosomes and therefore promotes the formation of basement membrane
structures
– The role of laminin: 5 appears to be critical even for healing of the blister wounds where lamina densa remains intact.
–
Fig.14.15: Structure of Laminin
Periodontics 585

• Fibronectin: EIII Aappears to be present underneath Healing After Periodontal Therapy
•
migrating keratinocytes in vivo.
FIBRONECTIN – a critical early component of Regeneration True periodontal regeneration is the
1. Clot reformation of a functionally oriented periodontal
ligament with collagen fibres inserting in both

2. Forming granulation tissue regrown alveolar bone and reformed acellular

Cellular fibrnoectin – Produced by cementum over a previously diseased root
1. Keratinocytes surface. (MP 2011)

2. Fibroblasts Repair Process called healing by scar arrests bone

3. Macrophages destruction without necessarily increasing bone

Fibronectin vary structurally by alternative splicing of 3 height repair following periodontal therapy
regions namely occurs by the formation of
1. E III A • Long junctional epithelium
•

2. E III B (COMEDK 2010, AIIMS Nov 2010)

3. V (IIICS) • New bone with root resorption or ankylosis
PERIODONTICS
•

E III A Fibronectin → expressed by migrating keratinocytes or both.
in wound New Attach- New attachment is the embedding of new
E III B Fibronectin → expressed in embryoyonal tissue but ment periodontal ligament fibres into new cementum
not normally in adult connective tissue and the attachment of the gingival epithelium to
a tooth surface previously denuded by disease.
It is strongly upregulated during granulating tissue (AP 2009)

formation

Attachment of the ginigiva or the periodontal
• Tenascin: C are also found underneath the migrating ligament to areas of the tooth from which they
may be removed in the course of treatment or
•
keratinocytes.
during the preparation of teeth for restorations
– Function as a modulator of cell adhesion to other represents simple healing or reattachment of
–
matrix components such as fibronectin. the periodontium not new attachment.

– The reorganization of basement membrane is (AIPG 1993, 1998)

–
complete at 4 weeks at which time the localization of
all basement membrane components such as type IV • The final outcome of periodontal pocket healing
•
and VII collagens, laminin – 1 and heparan sulphate depends on the sequence of events during the healing
proteoglycan appear normal stage. (AP 2000)

– Urokinase type plasminogen activate receptor is able – If the epithelium proliferates along the tooth
–
to associated with integrins.
–
surface before the other tissues reach the area, the
• Transforming Growth Factor β
result will be a long junctional epithelium.
•
– Transforming growth factors are a family of – If the cells from gingival connective tissue are the
–
b
polypeptides that have multiple regulatory actions
–
first to populate the area, the result will be fibres
in cell growth, differentiation and developmental
parallel to the tooth surface and remodeling of the
processes.
– stimulate keratinocyte motility by switching the cells alveolar bone with no attachment to the cementum.
– If the bone cells arrive first, root resorption and
–
from the differentiating to regenerative phenotype
–
and by inducing their production of fibronectin and ankylosis may occur.
laminin – 5 – Finally only when cells from periodontal ligament
–
– In addition transforming growth factor b, other proliferates coronally is there new formation of
–
growth factors like platelet derived growth factor, cementum and new attachment.
epidermal growth factor, keratinocyte growth factor,
hepatocyte growth factor also regulate wound healing.
• Origin of wound fibroblasts Healing Following Curettage
•
Possible sources of Steps involved – Restoration and epithelialization of the sulcus
–
wound fibroblasts generally require from 2 to 7 days
– Restoration of the junctional epithelium occurs in
Surrounding connective Migration, differentiation
–
tissue
animals as early as 5 days after treatment.
– Immature collagen fibres appear within 21 days.
Pericytes Proliferation, migration
–
– Healing after curettage results in the formation
–
Bone marrow Systemic control, homing of a long thin, junctional epithelium with no new
differentiation
connective tissue attachment.
586
Healing After Gingivectomy

– The initial response is the formation of a protective surface clot;
–
– By 24 hours, there is an increase in new connective tissue cells, mainly angioblasts, just beneath the surface layer of
–
inflammation and necrosis.
– By the third day numerous young fibroblasts are located in the area
–
– After 12 to 24 hours, epithelial cells at the margins of the wound start to migrate over the granulation tissue, separating
–
it from the contaminated surface layer of the clot.
– Epithelial activity at the margins reaches a peak in 24 to 36 hours
–
– Surface epithelialization is generally complete after 5 to 14 days.
–
– Complete epithelial repair takes about one month
–
– Vasodilation and vascularity begin to decrease after the fourth day of healing and appear to be almost normal by the
–
16th day.
– Complete repair of the connective tissue takes about 7 weeks.
PERIODONTICS
–
Healing of free soft tissue grafts
The Initial Phase • In these first days of healing a thin layer of exudate is present between the graft and the recipient bed. During this
•
(From 0 To 3 period the grafted tissue survives with an avascular “plasmatic circulation” from the survival of the graft that a
Days) close contact is established to the underlying recipient bed at the time of operation.
• The epithelium of the free graft degenerates early in the initial healing phase and subsequently it becomes
•
desquamated. (AIPG 2002, 2003)

Revasculariza- • 4-5 days of healing anastomoses are established between the blood vessels of the recipient bed and those in the
•
tion Phase (From grafted tissue.
2 To 11 Days)
Tissue Matura- • During this period the number of blood vessels in the transplant becomes gradually reduced, and after approximately
•
tion Phase (From 14 days the vascular system of the graft appears normal. Also the epithelium gradually matures with the formation
11 To 42 Days) of a keratin layer during this stage of healing.
• The establishment of collateral circulation from adjacent vascular borders of the bed allows the healing phenomenon
•
of “BRIDGING”
• Another healing phenomenon frequently observed following free graft procedures is “CREEPING ATTACHMENT”,
•
i.e. a coronal migration of the soft tissue margin. This occurs as a consequence of tissue maturation during a
period of about 1 year post – treatment.
• Neovascularisation is stimulated by various growth factors.The most potent angiogenic factors are fibroblast growth factors
•
as well as TGF - a and TGF - .
b
– FGF and aFGF–stimulate endothelial proliferation
–
b
– aFGF – stimulate tubule formation
–
• Connective Tissue Repair
•
– TGF-β→ potent stimulate of fibronectin and collagen production
–
– PDGF and FGF → increases influx of fibroblasts at wound site and increase extracellular matrix production.
–
– PDGF and IGF1 → stimulates recruitment and proliferation of fibroblasts
–
– Increased collagen synthesis and maturity.
–
• Re-Epthelialization
•
– EGF and TGF- → directly increases the rate of re-epithelialisation.
–
α
– bFGF and PDGF → indirectly enhance epithelialisation by stimulating a healthy bed of new connective tissue
–
– TGF-β→ inhibits epithelial cell proliferation but stimulate their migration.
–
• Hyperbaric Oxygen Therapy
•
– Oxygen is one of the most versatile and powerful agents available to modern practitioner. The therapy used to oxygen
–
used under pressure is hyperbaric oxygen (HBO2). It assists in wound healing hyperbaric oxygen helps in
Periodontics 587

Vasoconstriction

Downregulation of inflammatory cytokines

Upregulation of growth factors

Antibacterial effect

Potential of antibiotics

– It is used successfully in hypoxic or ischemic wounds like diabetic wounds, venous stasis ulcers failing grafts and
–
flaps.
– In wound healing hypoxia prevents normal healing process. HBO2 provides the oxygen needed to stimulate and
–
supplement wound healing. It is a safe, non invasive therapy.
PERIODONTIC - ENDODONTIC CONTINUUM

Pathways of Communication Between Pulp and Periodontium
PERIODONTICS
Physiologic Pathways Non-physiologic Pathways
• Dentinal tubules • Perforations
•
•
• Lateral and accessory canals • Vertical root fracture
•
•
• Apical foramen
•
• Palatogingival groove
•
• Anatomic considerations:
•
D/D between pulpal and periodontal disease
Pulpal Periodontal
CLINICAL
1. Cause Pulp infection Periodontal infection
2. Vitality Non – Vital Vital
3. Restorative Deep or extensive Not related
4. Plaque/ Calculus Not related Primary cause
5. Inflammation Acute Chronic
6. Pockets Single narrow multiple, wide coronally
7. Trauma Primary / Secondary Contributing factor complex
Radiographically
1. Pattern Localized Generalized
2. Bone less Wider apically Wider coronally
3. Periapical vertical Radiolucent Not often related.
4. Bone Loss No Yes.
Histopathology Pulpal Periodontal

1. Junctional epithelium No apical Migration Apical Migrate
2. Granulation tissue Apical (Minima) Coronal (larger)
3. Gingival Normal Some recession
Treatment Root Canal Periodontal

Therapy Treatment
588
HALITOSIS • Halitosis is caused primarily by volatile sulfur compounds,
•
specifically hydrogen sulfide, methylmercaptan and
• Also termed as: dimethyl sulfide, which result from bacterial putrefaction
•
– Fetor ex ore of proteins containing sulfur amino acids.
–

– Fetor oris (MP 2010, COMEDK 2007)
–
– Oral malodor

• Other causes include:
–
• Are of diagnostic significance
•
– Diamines (putrescine and cadaverine)
•
• Source may be intraoral or extraoral
–
– Short chain fatty acids (butyric, valeric and propionic
•
• Common local source is food stagnation on tongue and
–
acid)
•
gingival sulcus.
• Classification (Miyazaki H 1999)
•

Classification Treatment needs Description
PERIODONTICS
• Genuine halitosis Obvious malodor, with intensity beyond socially acceptable level, is perceived.
•
– Physiologic halitosis TN-1 • Malodor arises through putrefactive process within the oral cavity. Neither
–
•
specific disease nor pathologic condition that could cause halitosis is found.
• Origin is mainly the dorsoposterior region of the tongue
•
• Temporary halitosis due to dietary factors (e.g. garlic) should be excluded.
•
– Pathologic halitosis
–
- Oral TN-1 and TN 2 • Halitosis caused by disease, pathologic condition, or malfunction of oral
-
•
tissues
• Halitosis derived from tongue coating, modified by pathologic condition (e.g.
•
periodontal disease, xerostomia), is included in this subdivision.
- Extraoral TN -1 and TN 3 • Malodor originates from nasal, paranasal, and/or laryngeal regions
-
•
• Malodor originates from pulmonary tract or upper digestive tract
•
• Malodor originates from disorders anywhere in the body whereby the odour
•
is blood borne and emitted via lungs (e.g. diabetes mellitus, hepatic cirrhosis,
uremia, internal bleeding)
• Pseudo halitosis TN-1 and TN 4 • Others do not perceive obvious malodor, although the patient complains of its
•
•
existence.
• Condition is improved by counseling (using literature support, education, and
•
explanation of examination results) and simple oral hygiene measures.
• Halitophobia TN-1 and TN 5 • After treatment for genuine halitosis or pseudohalitosis, the patient persists in
•
•
believing that he/she has halitosis
• No physical or social evidence exists to suggest that halitosis is present.
•
Description of various treatment needs
Category Description
TN -1 Explanation of halitosis and instructions for oral hygiene
TN-2 Oral prophylaxis, professional cleaning, and treatment for oral diseases, especially periodontal diseases
TN-3 Referral to a physician
TN 4 Explanation of examination data, further professional instruction, education and reassurance
TN-5 Referral to a clinical psychologist, psychiatrist, or other psychological specialist.
Periodontics 589

• Different methods of assessing the oral malodor are:
•
– Self examination
–
– Organoleptic method
–
– Gas chromatography (Oral chroma)
–
– Dark field or phase contrast microscopy
–
– Saliva incubation test
–
– Electric nose
–
• Organoleptic scoring, considered as gold standard method for oral malodor. It was introduced by Rosenberg and
•
Mcullum. (KAR 2010)

• The organisms implicated in halitosis is P.gingivalis
•
• The instrument that detects halitosis is Osmoscope (AP 2005)
•

PERIODONTICS
Extra oral sources
Breath ODOUR CONDITION

• Rotten eggs • Indicative of volatile sulfide compounds mainly responsible for
•
•
halitosis
• Sweet odour or dead mice • Liver insufficiency (KAR 2001)

•
•

• Acetone breath or rotten apples • Diabetes
•
•
• Fish odour, Musky odour • Kidney insufficiency
•
•
• Mouthrinses combining cetyl pyridinium chloride with chlorhexidine (CHX 0.05% + CPC 0.05% + zinc lactate 0.14%)
•
significantly reduces plaque and gingivitis indices as well as morning halitosis. (MP 2010)

• Halite is a tongue scraper.
•
LASER
Commercially Available Lasers
Laser Type Commercially Available
• Argon Flouride (ArF)

Excimer Laser
•
• Xenon Chloride (XeCl)
•
• Argon
•
Gas Laser • Helium Neon (He Ne)
•
• Carbon Dioxide (CO2)
•
• Indium Gallium Arsenide Phosphorous (In Ga As P)
•
Diode Laser • Gallium Aluminium Arsenide (Ga Al As)
•
• Gallium Arsenide (Ga As)
•
• Frequency doubled Alexandrite Laser
•
• Neodymium:Yag Laser (Nd:YAG)
•
• Erbium Group
Solid State Laser
•
• Erbium:YAG (Er:YAG)
•
• Erbium:YSGG (Er:YSGG)
•
• Erbium,Chromium:YSGG (Er,Chr:YSGG)
•
590
Wave Length Of Main Lasers

LASERS COLOUR WAVE LENGTH
Co2 Infra red 12.6
Neodymium Yag Infra-red 1.064
Argon Blue 0.488
Eribium-yag Infra-red 2.940
Helium neon Red 0.632
Dye Red 0.632
Krypton Green 0.504

PERIODONTICS
Ruby Green 0.531
Helium Red 0.694
Yag Infra-red 2.210
Argon fluoride Ultra –violet 0.193
Krypton fluoride Ultra-violet 0.248
PERIODONTAL MICROSURGERY
• Carl Nylen is considered the father of microsurgery.
•
Basically, there are two types of optical magnification available:
• Magnifying loupes
•
– Simple loupes
–
– Compound loupes
–
– Prism telescopic loupes
–
• Surgical microscope
•
Advantages of Periodontal Microsurgery
• Improved cosmetics
•
• Rapid healing
•
• Minimal discomfort
•
• Less invasive-As there is reduced incision size, lessened need for vertical releasing incisions and smaller surgical sites
•
 
thus, periodontal microsurgery is considered less invasive procedure
• Reduces surgical fatigue and development of spinal and occupational pathology of the operator
•
• Enhanced patient acceptance.
•
 
Advantages of Loupes Over Microscopes
• Less expensive to purchase;
•
• Easier to use
•
• Loupes tend to be less cumbersome in operating field and less likely to breech a clean operative field; and
•
 
• They are handy in free–lancing practice.
•
– Disadvantage of loupes over microscopes is that the individual light source is required for loupes.
–
 
– In periodontal surgery a magnification of × 4.5 to ×5 for loupe spectacles and ×10 to ×20 for surgical microscope
–
 
appears to be ideal.
Periodontics 591

MISCELLANEOUS • Tumour like gingival enlargement in pregnancy is not
•
a neoplasm but an inflammatory response to bacterial
• A dendritic cell is any cell that has branching processes. plaque.
•
The epithelium in addition to the keratinocytes contains • Pregnancy associated gingivitis is accompanied by
three types of resident cells of the dendritic morphology.
•
increase in steroid hormones in crevicular fluid and
These are Langerhan’s cells, Merkel cells and melanocytes dramatic increase of P.intermedia. No notable changes
• Transseptal fibres are the only fibres, which are not occur in gingiva during pregnancy in the absence of local
•
embedded into bone. They extend interproximally over irritants.
the alveolar bone crest and are embedded in cementum of
• Spirochaetes are found to penetrate necrotic tissue
adjacent teeth. Transseptal means they are always present
•
across the septum and they are a constant finding because and apparently unaffected connective tissue
they get reconstructed even after destruction of alveolar • Although the primary source of collagenase in
•
bone. (AIPG 2009) periodontal pockets is host tissue cells, bacterial
PERIODONTICS

• Passive eruption is a pathologic process of exposure of collagenases may also contribute to collagen degradation
•
teeth by apical migration of gingiva. in a similar fashion.
• Gottlieb and orban believed that active and passive • Calcification begins along the inner surface of
•
eruption occur together (AIPG 2012)
•
supragingival plaque and in the attachéd component of

• The attachment apparatus of the tooth is composed subgingival plaque adjacent to the tooth.
• Calculus does not mechanically irritate the gingiva but
•
of periodontal ligament, cementum and alveolar bone.
•
Periodontium is composed of gingiva, periodontal provides a fixed nidus for continued accumulation of
ligament, cementum and alveolar bone. plaque and retains bacterial flora and their virulence
factors in close proximity to the gingiva. Bacterial plaque
• Alveolar process is formed at the time of tooth eruption is a primary etiologic factor in periodontal diseases.
•
and disappears gradually after the tooth is lost. • Teeth least affected by periodontal disease : lower
•
• Alveolar bone proper, which is seen as lamina dura premolars and upper canines.
•
in radiographs, gives attachment to principal fibres • Composition of plaque formed on all types of restorative
•
of periodontal ligament. It is formed of partly dense materials is similar, with the exception of that formed on
lamellated bone and partly of bundle bone. silicate. The difference is in higher carbohydrate:nitrogen
• Inner wall of tooth socket, which is thin compact bone, ratio (due to reduced carbohydrate metabolism) and
lower nitrogen:calcium ratio.
•
is formed by alveolar bone proper.
• Bundle bone is the bone adjacent to periodontal
• Highest incidence of gingival infiltrative lesions
•
ligament that contains a great number of sharpey’s
•
(enlargement) is in acute monocytic leukemia (66.7%)
fibres.
> acute myelocytic – monocytic leukemia (18.7%) >
• Bone mineralization: osteoid is freshly secreted bone acute myelocytic leukemia (3.7%)
•
matrix, which is non mineralized. Mineralization
• Bleeding tendency in leukemia specially affects the
process always follows bone matrix (osteoid) formation.
•
oral cavity especially gingival sulcus. Bleeding is due to
thrombocytopenia resulting from replacement of bone
• Width of attached gingiva increases with age and eruption
marrow cells by leukemic cells.
•
of teeth, the latter phenomenon is utilized in clinical
treatment planning via ortho-perio estheitics. • True leukemic enlargement may also be seen in subacute
•
leukemia but seldom occurs in chronic leukemia.
• The width of the periodontal ligament space will decrease
• Bruxism and periodontal health/disease are
•
if the tooth is unopposed or in hypofunction.
•
independent phenomenon–no association has been
• PDL ground substance shown
•
– Glycoaminoglycans–hyaluronic acid and • Peeling of surface occurs in chronic desquamative
–
proteoglycans (chondroitin and dermatan sulfate)
•
gingivitis and drug induced gingival overgrowth
– Glycoproteins - fibronectin and laminin produces nodular surface.
–
• Actual position is the level of epithelial attachment
• Enlargement in pregnancy is usually generalized and
•
on tooth whereas apparent position is level of crest of
•
tends to be more prominent interproximally than on
gingival margin.
facial and lingual surfaces
592
by size as petechiae or ecchymoses, these lesion do not

• NUG does not lead to periodontal pocket formation
blanch when pressed.
•
because junctional epithelium is necrotic. Remember
that a viable junctional epithelium is amust for sulcus • Petechiae: Purpuric lesions 1 to 2 mm in diameter. Larger
•
deepening and pocket production. purpuric lesions are called ecchymoses.
• Pericoronitis is a incubation zone for ANUG
Nice to Know
•
• Reversed architecture is most common in maxilla. Periotron Electronic instrument used to measure
•

(MP 2010) GCF

• Maxillary premolars are least common site for furcation Peridex, perioguard Prescription solution of chlorhexidine
•
involvement. Periotemp probe Detects pocket temperature differences
• Cuneiform defect is another name for erosion. of 0.1°C from a referenced subgingival
temperature
•
• Gingivosis is associated with the deficiency of estrogen Demonstrates the periodontal disease
PERIODONTICS
•
and progesterone, because it is seen more commonly activity by measuring temperature
during menopause and perimenopause phase. changes in sulcus

(AIPG 2009) Periotriever Highly magnetized instruments designed

for retrieval of broken instruments
• The periodontal (lateral, parietal) abscess is rarely
•
associated with a fistulous tract. Periopaper Blotter paper used in measuring GCF by
electronic method
• Pus is a common feature of periodontal disease but it is
•
only a secondary sign. Presence of pus merely reflects Periochip Chlorhexidine chip placed in the pocket for
the nature of the inflammatory change in the pocket local drug delivery
wall. (AIPG 2008) Perioaid Tooth pick with handle

• Pus formation is not an indication of the depth of
Periocline 2% minocycline used in local drug delivery
•
the pocket or severity of destruction of periodontal
supporting tissues. (AIPG 2006) Periodontometer Instrument used for detecting tooth

mobility (AIPG 2009, AIIMS MAY 2009,
• Transgingival probing predicts features of the MAHE 2008, KAR 2008)
•
underlying bony topography
Periotest Test for detection of tooth mobility

(COMEDK 2008)
Few Terms to Remember

Perioscan Diagnostic kit- detection of micro-
• Macules: Well circumscribed flat lesion that are noticeable organisms in periodontal disease
•
because of their change from normal skin color
• Papule: Solid lesions raised above the skin surface that are
Iontophoresis
•
smaller than 1 cm in diameter.
• Plaque: Solid raised lesions that are over 1 cm in diam, • Also called as electrolytic medication, electromedication
•
•
they are large papules and ionic medication
• Nodules: These lesions are present deep in the dermis, • The introduction by means of electric current of ions
•
•
and of soluble salts into the tissues, usually for therapeutic
• Vesicles: Elevated blisters containing clear fluid that are purposes.
• Based on the principle of electrolysis, whereby a salt,
•
under 1 cm in diameter.
•
such as NaF, placed in the solution will undergo
• Bullae: Elevated blisterlike lesions containing clear fluid
ionization.
•
that are over 1 cm in diameter.
• The introduction of a positive electrode (anode) and
• Erosions: Moist red lesions often caused by the rupture or
•
a negative electrode (cathode) into solution, and
•
bullae as well as trauma. passing of direct current through the solution will
• Pustules: Raised lesions containing purulent material. result in concentration of fluoride at the positive pole
•
• Ulcers: A defect in the epithelium; it is a well- and sodium ions at the negative pole. When used in
dentistry, one electrode is attached to the tooth and
•
circumscribed depressed lesion over which the epidermal
layer lost. other is held in the hand.
• Purpura: Reddish to purple flat lesions caused by blood • Percentage of sodium fluoride used in iontophoresis is
•
2% (AIPG 2006)
•
vessels leaking into the subcutaneous tissue. Classified

Periodontics 593

Pigmentation
Lead line (Burtonian line) Bluish red or deep blue linear pigmentation in marginal gingiva

(AIPG 2005, MAN 1994)

Silver (Argyria) Violet marginal line
Bismuth, arsenic and mercury Black marginal line (AIPG 2005)

Mesenteric line Delicate, brown or black pigmented non cariogenic plaque found on
the enamel at the cervical margin of the tooth
PERIODONTICS
CHAPTER 15
Radiology
Objectives
• Radiation physics • Cone Beam Computed Tomography

• Biologic Effects of Radiation • Diagnostic Imaging of TMJ

• Radiation Safety and Protections • Diagnostic Imaging of Salivary Glands

• Imaging Principles and Techniques • Radiographic Interpretation

– Projection Geometry • Benign and Malignant Tumours of Jaws

– X ray Film, Intensifying Screens and Grids • Diseases of Bone Manifested in Jaws

– Processing X ray Film • Soft Tissue Calcifications and Ossification

– Digital Imaging • Characteristic Radiographic Appearances

– Panoramic Imaging • Miscellaneous

• Advanced Imaging

RADIATION PHYSICS – To ionize, an atom requires sufficient energy to
–
overcome the electrostatic force binding the electrons
You Should Know to the nucleus.
– The binding energy of an electron is related to the
• Atomic number is number of Protons. (PGI 2001)
–
atomic number of the atom and the orbital type.
•

• Atomic weight is number of protons + neutrons – Large atomic number elements (high Z) have more
•
–
• Isotopes are substances with same atomic number but protons in their nucleus and thus bind electrons in any
•
different atomic weight. (MH 2006) give orbital more tightly than do smaller-Z elements.

• Isobars are atoms having same atomic weight but different • Nonionizing radiations, such as visible light, infrared,
•
and microwave radiation, and radio waves do not have
•
atomic numbers
sufficient energy to remove bound electrons from their
• Isomers are atoms having same atomic number and orbitals.
•
atomic weight but different energy states in nucleus.
• Ionizing Radiations are:
• Ionization: When the number of electrons in an
•
– Alpha radiation (Most Ionizing) (AIPG 2010)
•
atom is equal to the number of protons in its nucleus,
–

the atom is electrically neutral. If such an atom loses – Beta radiation
–
an electron, the nucleus becomes a positive ion and the – Gamma radiation
–
free electron a negative ion. This process of forming an – X rays
–
ion pair is termed ionization. (AIIMS Nov 11) – Neutron

–
Radiology 595

• Uses:
• “Natural radiation” is derived from radioactive
•
– Cancer treatment
•
elements in the environment and cosmic rays. In
–
addition, radioactive substances have been used in – Diagnostic/imaging
–
nuclear medicine, nuclear power plants, nuclear – Measure soil density at construction sites
–
weapons, and nuclear propulsion. – Ensure proper fill levels in packing of food and drugs.
–
– Inspection of weld parts and metals for defects.
• Electromagnetic Spectrum: a bunch of types of
–
•
radiation X Rays
• Radiation is energy that travels and spreads out as it
• William Roentgen discovered X rays. (MP 2004)
•
goes
•

• Attenuation of X rays depends on “Absorption
• The difference between X-rays and visible light rays is
•
Coefficient”
•
the energy level of the individual photons.
• X rays are modified Electrons. (TN 1990)
•

Electromagnetic Radiation: (PGI 2012) • Differ from light in Energy status (AI PG 2010)
•

RADIOLOGY
• Electromagnetic radiation is the movement of energy
•
through space as a combination of electric and magnetic X ray Machine
fields. It is generated when the velocity of an electrically
charged particle is altered • •
The primary components of an x-ray machine are the
x-ray tube and its power supply
• It is classified according to frequency of waves into:
• An x-ray tube is composed of a cathode and an anode
•
– Radiowaves
•
situated within an evacuated glass envelope or tube.
–
– Microwaves
• Electrons stream from a filament in the cathode to a target
–
– Infrared radiation (PGI 2011)
•
in the anode, where they produce x rays.
–
– Visible light
•
–
– UV radiation For the x-ray tube to function, a power supply is necessary
•
–
– X rays to
–
– Gamma rays – Heat the cathode filament to generate electrons and
–
–
– Establish a high-voltage potential between the anode
Infrared rays are used in:
–
and cathode to accelerate the electrons toward the
• Placental Localization anode.
•
• Thermography
• Cathode has a tungsten filament and molybdenum
•
• Orbital Pneumography
•
focusing cup
•
• Intracerebral infarct diagnosis • The filament is the source of electrons within the x-ray
•
•
tube
Gamma Rays • The filament lies in a focusing cup, a negatively charged
•
concave reflector made of molybdenum. The parabolic
• Are electromagnetic energy shape of the focusing cup electrostatically focuses the
•
• They are emitted from nucleus of unstable (radioactive) electrons emitted by the filament into a narrow beam
directed at a small rectangular area on the anode called
•
atoms.
the focal spot
• Henry Becquerel discovered gamma rays.
• The x-ray tube is evacuated to prevent collision of the
•
• High energy ionizing radiations.
•
fast-moving electrons with gas molecules, which would
•
• Have “no mass” and “no electric charge”. significantly reduce their speed. The vacuum also
•
• Travel at speed of light prevents oxidation, “burnout,” of the filament.
•
• Cesium -137, Cobalt and Radium emit predominantly • Anode is composed of tungsten target and copper stem
•
emits gamma rays. (PGI 1988)
•
– The purpose of the target in an x-ray tube is to convert

• “Phosphorus 40” is a natural source of gamma rays.
–
the kinetic energy of the colliding electrons into x-ray
•
• “Radiation sickness” is mostly due to gamma rays. photons
•
• Have Maximum penetration power. – Because heat is generated at the anode, the
–
•

(MH 2007, AIPG 2002) requirement for a target with a high melting point is

596
clear. Tungsten also has high thermal conductivity, • Photosensitive material used in x rays is Silver bromide.
•
thus readily dissipating its heat into the copper stem. – Radioactivity: Discovered by: Curie
Finally, the low vapor pressure of tungsten at high
–

(Kerala 1988, MP 2004)
temperatures helps maintain the vacuum in the tube

at high operating temperatures. Factors that affect the Quality and Quantity of the
– The tungsten target is typically embedded in a X Ray Beam.
–
large block of copper. Copper, also a good thermal
conductor, removes heat from the tungsten, thus KVp * mAs
Radiodensity ∝
reducing the risk of the target melting. Additionally, FSFD * filtration * collimation
insulating oil between the glass envelope and the kVp • Affects both the quantity and the
housing of the tube head carries heat away from the
•
quality of the radiation beam.
copper stem. This type of anode is a stationary anode • The kVp across the X- ray tube
because it has no moving parts.
•
influences the force of attraction
experienced by an electron released
• The focal spot is the area on the target to which the by the filament as it moves towards the
RADIOLOGY
•
focusing cup directs the electrons and from which anode.
x rays are produced. The sharpness of a radiographic • Thus if the kVp is increased, then
•
image increases as the size of the focal spot decreases. the kinetic energy (E) of the electron
increases. If the kVp is doubled, then
• The heat generated per unit target area, however, the intensity increases by a factor of
•
becomes greater as the focal spot decreases in size. four.
Different methods used are: • The quality or the penetrating power
•
– Placing the target at an angle to electron beam.The of the beam increases as the kVp
increases. Quality of radiation depends
–
apparent size of the focal spot seen from a position almost entirely on the kVp.
perpendicular to the electron beam (the effective
focal spot) is smaller than the actual focal spot size. mA/mAs • Affect the quantity of radiation. It has
•
no effect on quality of beam. It has no
Typically, the target is inclined about 20 degrees to effect on quality of beam.
the central ray of the x-ray beam. This causes the
• The quantity of the X-ray beam is
effective focal spot to be approximately 11 mm, as
•
directly proportional to the mA through
opposed to the actual focal spot, which is about 13 the tube.
mm.
Filtration • Filtration affects both the quality and
– Another method of dissipating the heat from a
•
quantity of the beam. A filter is always
–
small focal spot is to use a rotating anode. In this inserted in the X-ray beam to remove
case the tungsten target is in the form of a beveled low energy photons. This removal
disk that rotates when the tube is in operation reduces the quantity, and as a result,
the meanenergy to the beam increases.
• 0.2–0.8% of cathode rays are transformed into X-rays after The beam becomes more penetrating
or harder.
•
striking the anode target
– Thicker filters reduce the quantity
• The tube current is the flow of electrons through the tube;
–
of the beam, but increases beam
•
that is, from the cathode filament, across the tube to the quality. A filter is intended to pro-
anode, and then back to the filament. tect the patient by removing these
low-energy photons.
• Tungsten is the Target metal used in x rays. (PGI 1983)
Target material • Target material with higher atomic
•

• Filters used in radiology results in “beam of greater
•
numbers increase both the quantity of
•
intensity” photons slightly and quality (energy)
of the beam. Tungsten produces a
• Use of cone results in “film of higher contrast” significantly more efficient spectrum
•
• X ray beam restrictor is a device regulating the shape and than molybdenum.
•
size of x ray beam. Source to image • The SID affects the quantity of
•
• Grid is a device used to “reduce scattered radiation.” receptor distance photons but has no effect on the
•

(AIIMS 1985) (SID) quality. The quantity is affected by the
inverse square law, which states that

• Penetrating power of x ray can be increased by the intensity (quantity) is inversely
•
increasing “frequency”. proportional to the square of the
distance.
• Contrast in x ray depends on “Kv.”
•
Radiology 597

Half value layer is the thickness of material when placed within the path of X-ray beam decreases intensity by half.
• The aluminum layer filters the low energy photons with little penetration power, and contributes to the patient exposure
•
only.
• Selective filtration of both low and high energy photons is done with intensifying screens that contain rare earth elements
•
like niobium, yttrium etc.
The Half Value Layer Depends On Voltage Of X-Ray Tube
Tube voltage in kVp mm of Al

30 to 70 1.5
71 2.1
80 2.3
90 2.5
100 2.7
RADIOLOGY
Collimation
• A collimator is a metallic barrier with an aperture in the middle used to reduce the size of the x-ray beam and thereby
•
the volume of irradiated tissue
• Round and rectangular collimators are most frequently used in dentistry.
•
• Dental x-ray beams are usually collimated to a circle 2 3/4 inches (7 cm) in diameter.
•
Bremsstrahlung Radiation
• The sudden stopping or slowing of high-speed electrons by tungsten nuclei in the target produces bremsstrahlung photons,
•
the primary source of radiation from an x-ray tube. (Bremsstrahlung means “braking radiation” in German.)
• Bremsstrahlung interactions generate x-ray photons with a continuous spectrum of energy
•
Characteristic Radiation
• Small fraction of the photons in an x-ray beam.
•
• It occurs when an incident electron ejects an inner electron from the tungsten target. When this happens, an electron
•
from an outer orbital is quickly attracted to the void in the deficient inner orbit.
• When the outer-orbital electron replaces the displaced electron, a photon is emitted with energy equivalent to the
•
difference in the two orbital binding energies.
• The energies of characteristic photons are discrete because they represent the difference of the energy levels of electron
•
orbital levels and hence are characteristic of the target atoms.
Also Note
• According to Heel effect, when cathode rays strike anode target, x rays with high intensity are found towards cathode side
•
of central ray and x rays with low intensity are found towards anode. This is due to self absorption of photons in the anode
target
• Compton scattering occurs for intermediate energy. It is the principal mechanism of absorption for gamma rays in the
•
intermediate zone of 100 kev to 10 Mev.
• Average wavelength of X rays used in dentistry is 0.6 – 1 AU
•
• Grenz rays–Soft X rays having wavelength of 2 AU
•
• Stray radiation–Radiation that is produced from tube other than focal spot
•
598
Interaction of X Rays with Matter

• The intensity of the beam is essentially uniform from the center of the beam outward. As the beam goes through the
•
patient, it is attenuated, that is, reduced in intensity. This attenuation results from interactions of individual photons in
the beam with atoms in the absorber.
• In a dental x-ray beam there are three means of beam attenuation:
•
– Thompson effect/classical scattering/coherent scattering – accounts for about 8% of total number of interactions
–
– Photoelectric absorption-accounts for about 30% of interactions
–
– Compton scattering – about 62% - major source of secondary radiation
–
– In addition, about 9% of the primary photons pass through the patient without interaction
–
– Use of collimation also improves image quality. When an x-ray beam is directed at a patient, the hard and soft tissues
–
absorb about 90% of the photons and about 10% pass through the patient and reach the film.
Dosimetry
RADIOLOGY
• Determining the quantity of radiation exposure or dose is termed dosimetry.

•
• The term dose is used to describe the amount of energy absorbed per unit of mass at a site of interest.
•
Units of Radiation
Quantity SI unit Traditional unit Conversion
Exposure Air kerma (Gy) Roentgen (R) 1 Gy = 100rad
Absorbed dose Gray (Gy) Rad 1 rad = 0.01 Gy(1cGy)
Equivalent dose Sievert (Sv) Rem 1 Sv = 100rem
Effective dose Sievert (Sv)
Radioactivity Becquerel (Bq) Curie (Ci) (AIPG 2007) 1 Bq = 2.7 ~ 10-11Ci

1 Ci = 3.7 ~ 1010Bq
• Activity is measured by: Becquerel (MP 2004)

•

• Exposure is measured by: Coulomb/cm2
•
• Absorbed dose is measured by: Gray (MAHE 2012, MP 2006)
•

• Dose equivalent: Sievert (AIPG 2014)
•

BIOLOGIC EFFECTS OF RADIATION
“Stochastic Effect” of Radiation Non Stochastic (Acute) Effects

• Stochastic effects are those that occur by chance and consist • Unlike stochastic effects, nonstochastic effects are characterized by
•
•
primarily of cancer and genetic effects. a threshold dose below which they do not occur.
• Stochastic effects often show up years after exposure. • Nonstochastic effects have a clear relationship between the
•

•
(AIIMS 2008) exposure and the effect. In addition, the magnitude of the effect is

• Stochastic effect of radiation is: “As the dose increases, the directly proportional to the size of the dose.
•
probability that effect will occur also increases.” (AIPG 2011) • Nonstochastic effects typically result when very large dosages of

•
• As the dose to an individual increases, the probability that radiation are received in a short amountof time.
•
cancer or a genetic effect will occur alsoincreases. • Examples include erythema (skin reddening), skin and tissue burns,
•
• However it can never be determined for certain that an cataract formation, sterility, radiation sickness and death
•
occurrence of cancer or genetic damage was due to a specific
exposure.
Radiology 599

Radiation Effects on Cells
• Ionizing radiation causes
•
– Chromosome breakage,
–
– Translocations, and,
–
– Less frequently, point mutations,
–
– Leading to genetic damage and carcinogenesis.
–
– UV rays induce the formation of pyrimidine dimers within DNA, leading to mutations. Therefore UV rays can give
–
rise to squamous cell carcinomas and melanomas of the skin.
• Therefore, tissues with a high rate of cell turnover, such as • Tissues with non-dividing cells, such as brain and
•
•
gonads, bone marrow, lymphoid tissue, and the mucosa of myocardium, do not suffer cell death, except at doses that
the GI tract, are extremely vulnerable to radiation, and the are so high that transcription of vital molecules is affected.
RADIOLOGY
injury is manifested early after exposure. • The dose-response curve for all mammalian cells appears
•
to have a linear-quadratic relationship.
Four important processes that occur after radiation exposure can be summarized as the “four R’s” of Radiobiology.
R-1 - Repair R-2 - reoxygenation R-3 - repopulation R-4 - redistribution
This is temperature A process whereby oxygen (and The ability of the cell population to Reflects the variability of a cell’s
dependent and is thought other nutrients) are actually continue to divide and to replace radiosensitivity over the cell
to represent the enzymatic better distributed to viable cells dying and dead cells. cycle.
mechanisms for healing following radiation injury and cell
intracellular injury killing.
Vegetative Inter Mitotic Primitive in differentiation and Most radiosensitive Eg. Cells of spermatogenic and
have high mitotic rate erythroblastic series, basal cells of oral
mucous membrane
Differentiating Intermitotic They divide regularly and Less radiosensitive than Eg. Inner enamel epithelium of developing
Cells undergo some differentiation vegetative intermitotic teeth, cells of haemopoietic series,
between divisions cells spermatocytes and oocytes
Multi Potential Connective These cells divide when there is These cells are Eg. Endothelial cells, fibroblast,
Tissue Cells a demand for more cells intermediate sensitivity mesenchymal cells
Reverting Postmitotic They divide infrequently Radioresistant Eg. Acinar, ductal, parenchymal cells of
Cells glands like liver, kidney, pancreas etc.
Fixed Postimitotic Cells Highly differentiated cells and Most resistant Eg. Neurons, striated muscle cells,
are incapable of division epithelial cells, erythrocytes
Radiosensitive Dioresponsive Radio Resistant

Sensitive to less than 2500 r Sensitive between 2500-5000 r Resistant up to 5000 r

• Germ cells • Endothelium of blood vessels • Liver
•
•
•
• Epithelium of intestine and mucosa • Salivary glands • Mature bone
•
•
•
• Bone marrow cells • Bone and cartilage • Cartilage
•
•
•
• Immature • Muscle
•
•
• Nerves and brain (AIPG 2014, 2010)
•

600
Radiosensitivities and Radioresistancies • Phase of cell cycle most sensitive to radiation: G2
•

(AIIMS 2002)

• Most radiosensitive structure in cell: DNA • Phase of cell cycle most resistant to radiation: S phase
•

(PGI 2002)
•
• The most sensitive period in humans for inducing

• Most radiosensitive cell: Lymphocyte (100 RADS)
•
developmental abnormalities is during the period of
•

(AIIMS 1993)
organogenesis (18 – 45 days of gestation)

• Radiation causes cataract of type: Posterior subcapsular
•
• Max permissible dose of Radiation should not exceed 5 Effect of Radiation on Different Organs
•
rad/year. (AIIMS MAY 2013, AIPG 1992)

• Lead aprons of size 0.5 mm are used for protection. • Temporary sterility in Testes at low doses.
•
•
• Radio resistant structure is Cartilage • Depression of hematopoiesis in Bone marrow
•
•
• Most common source of radiation originating in body: • Reversible skin effects (e.g., erythema) at low doses.
•
•
radioactive potassium. • Permanent sterility Ovaries at moderate doses.
RADIOLOGY
•
• Temporary hair loss: Skin at low doses.
• Chromosomal abnormalities due to radiation occur in:
•
• Permanent sterility Testis at high doses.
•
G1 phase
•
• Chromatid abnormalities due to radiation occur in: G2 •
•
Cataract in Lens of eye
•
phase
The Factors Effecting Tissue Damage are:
Dose The severity of deterministic damage seen in irradiated tissues or organs depends on the amount of radiation received.
Dose rate Exposure of biologic systems to a given dose at a high dose rate causes more damage than exposure to the same total
dose given at a lower dose rate. When organisms are exposed at lower dose rates, a greater opportunity exists for repair
of damage, thereby resulting in less net damage.
Oxygen The greater cell damage sustained in the presence of oxygen is related to the increased amounts of hydrogen peroxide
and hydroperoxyl free radicals formed.
Linear Ener- In general, the dose required to produce a certain biological effect is reduced as the linear energy transfer (LET) of the
gy Transfer radiation is increased.
Thus higher LET radiations (e.g., alpha particles) are more efficient in damaging biologic systems because their high
ionization density is more likely than X-rays to induce double-strand breakage in DNA.
Radiotherapy
• Radioactivity was discovered by Henry Becquerel
•
• Gamma camera in Nuclear medicine is used for: Organ imaging (AIPG 2005)
•

• Radiotherapy is based on principle of: Ionizing molecules
•
• “Karnosfky scale” is used to evaluate patient before radiotherapy.
•
• Radioactive gold is used in Malignant ascites
•
• “Mantle irradiation” is used to treat Hodgkins disease (PGI 1998)
•

• “Hyper fractionation” radiotherapy is used to treat Lung Cancer. (KERALA 2001)
•

• “Intraoperative radiotherapy” is used to treat Pancreatic cancer. (KERALA 2001)
•

• Stereotactic radiosurgery is a form of radiotherapy (AIIMS 2003)
•

• “Intensity modulated radiotherapy” is used to treat Ca prostate (PGI 2005)
•

Brachy therapy is type of radiation therapy which uses sources placed within or near tumor for therapy
• Teletherapy is type of radiation therapy which uses external beam irradiation
•
• TAT is Targeted Alpha Therapy used for control of dispersed cancers.
•
Radiology 601

• Placental localization is done with I 131
Radiation Carcinogenesis
•
• Gallium is concentrated in abscess cavities.
• Inflammatory Oncotaxis:
•
•
“Photodynamic Therapy” with Hematoporphyrins and – Is a term describing the attraction of cancer cells
light is used in treatment of:
–
to an area of tissue trauma resulting presumably
• Ovary Ca because trauma (surgery and radiation) causes
•
• Skin Ca inflammation and capillary disruption, thus
predisposing cancer cells to settle in these areas.
•
• Colon Ca (MH 2010)
For example, cutaneous metastases from colon,
•

Radiotherapy is most useful in: kidney, and cervix have been known to localize in
abdominal wall surgical incisions.
• Medulloblastoma (AIPG 2002)
•

• Small cell carcinoma lung
Stereotactic Radio Surgery: (AIIMS 2009)
•
• ALL
•
• The use of highly advanced computers to locate and
RADIOLOGY
• Germinoma
•
create a three-dimensional image of a tumor is called
•
• Leptomeningeal Rhabdomyosarcoma
stereotaxy. When used during surgery, this technique is
•
• Non Hodgkins Lymphoma
called stereotactic surgery.
•
Half life of important isotopes • •
Administered to effectively deliver high dose irradiation,
• I 131: 8 days which is precisely targeted.
• It utilizes three-dimensional mapping technique.
•
• Rn 222: 3-6 days (PGI 1988)
•
• Stereotactic radiosurgery is used as an alternative to
•

• Co 60: 5. 2 years (Delhi 1986)
•
surgery and especially used for tumors and blood vessel
•

• P 32: 14 days abnormalities of structures close to brain.
•
• Gallium: 3 days • Stereotactic surgey is done by three means:
•
• Thallium: 3 days
•
– Gamma knife using gamma rays. (Cuts tumors in
•
–
different location) (PGI 2006)
Radiation Syndromes

– Linear accelerator using high energy X-rays.
–
• In radiobiology, the latent period represent the period – Proton beam.
–
•
of time between the radiation exposure and onset of
symptoms (AIPG 2010)
Respiratory Gating

• Early symptoms of acute total-body irradiation, known
• Organ motion during the respiratory cycle is known to
•
as the Prodromal radiation syndrome, last for a limited
•
time. Clinical manifestations depend on the total body be a source of inaccuracy in treatment delivery because
dose. it leads to tumor displacement and suboptimal dose
delivery.
• Skin is the most common effected area.
• Respiratory gating is one of the latest techniques in
•
• Most common manifestation in skin is erythema
•
radiation therapy and involves matching radiation
•

(AIPG 1998) treatment to a patient’s own respiratory pattern.

• Papillary ca thyroid develops in infancy due to radiation (AIPG 2005)
•

exposure (AIPG 2003) • With respiratory gating, radiation treatment is timed to

•
• First complication after radiotherapy is mucositis an individual’s breathing pattern, targeting the tumor only
•
when it is best range.
• 2-7 Gy (200-700 rads) cause injury to hematopoietic • This approach decreases possible complications and
•
system-Hematopoietic Syndrome.
•
side effects, while using higher doses and getting better
• 7–15 Gy (700-1500rads) causes injury to GIT - outcomes.
•
Gastrointestinal syndrome • Respiratory gating involves tracking the patient’s
•
• 50 Gy and over causes injury to CVS and CNS natural breathing cycle via computer and determining
an algorithm to control radiation administration at
•
• At doses >100 Gy, death usually occurs in 24 to 48 - the optimum moments–the “gate”–to deliver dose. The
•
Cerebrovascular syndrome. computer synchronizes the beam to switch on only when
the target area is within the calculated parameters.
602
• The patient’s respiration is continuously monitored and • Patient exposure can be reduced by:
•
•
the beam switches off as the tumor moves out of the target – E speed films
range.
–
– Intensifying screens
–
– Collimation
RADIATION SAFETY AND PROTECTIONS
–
– Filtration
–
– Lead aprons
• Trace amounts of radioactive substances can be found
–
– Thyroid collars
•
in the human body.
–
– Increasing focal spot to film distance
• Maximum permissible dose for whole body for
–
– Increasing KVp and optimal exposure
•
radiation workers in 1 year is 5 Rem(for gonads and
–
bone marrow), 15rem (for skin) and in week is 0.1 Rem.
• The amount of radiation necessary to produce a
IMAGING PRINCIPLES AND TECHNIQUES -
PROJECTION GEOMETRY
•
noticeable skin reaction is called as Erythema dose. It
is 300-400 R
RADIOLOGY
• Mean exposure of radiation from 1 IOPA is 300mR. It • “Main characteristics of a dental radiograph include
•
the visual characteristics of proper film density and
•
can be reduced to as low as 1–10 mR by using improved
techniques contrast as well as the geometric characteristics of
• Mean exposure of radiation from pantamograph is sharpness (definition, details, or resolution) with minimal
•
90mR magnification and distortion.” (AIPG 2008,2007)

Density The overall degree of darkening of the exposed film is referred to as density
Radiographic contrast It is defined as the difference in densities between various region or tones on the film
Sharpness Refers to the degree to which the image reveals the differential at density boundaries. This is an inherent
property of the film itself
Definition and detail However, definition is used to denote image sharpness caused by projective geometry. Detail refers to image
unsharpness caused only by film factors. Very small details require high contrast if they are to be easily seen
Geometric Symmetry The geometric symmetry of an image depends on the position of the X-ray beam, object and film
Sharpness is increased by Sharpness is decreased/ lost by

• Finer the grain size as in slow speed films • Larger grains as in faster films
•
•
• Smaller focal spot • Sharpness is lost with intensifying screens
•
•
• Increasing the distance between the focal spot and the object • Larger the focal spot
•
•
• Reducing the distance between the object and the image • By decreasing the distance between the focal spot and the object
•
•
receptor
• Increasing the distance between the object and the image receptor
•
• Horizontal direction of beam primarily influences Paralleling Technique
•
the degree of overlapping of images of crowns and – Preferred method for making intraoral radiographs.
–
interproximal spaces – It derives its name as the result of placing the film
–
• If the central ray is more positively inclined to the parallel to the long axis of the tooth.
This procedure minimizes image distortion
•
bisector–foreshortening of image occurs –
–

– If it is more negatively inclined– elongation of image (AIPG 2008, 2010)

– The film is placed toward the middle of the oral
–
– It is perpendicular to film but not to object–
–
cavity, away from the teeth. Although this allows the
–
foreshortening of image
– If it perpendicular to object but not to film– teeth and film to be parallel, it results in some image
magnification and loss of definition by increasing
–
foreshortening of image
unsharpness.
Radiology 603

– As a consequence, the paralleling technique also uses Good to Know
–
a relatively long open-ended aiming cylinder (“long • Position and distance rule–operator should stand atleast
cone”) to increase the focal spot-to-object distance.
•
6 feet from the patient at a 900 to 1350 angle to the central
This directs only the most central and parallel rays ray beam when exposure is made
of the beam to the film and teeth and reduces image
• The horizontal angulation of beam primarily influences
magnification while increasing image sharpness and
•
the degree of overlapping of the images of the crowns at
resolution.
the interproximal spaces
Bisecting Angle Technique • Bisecting angle technique–based on CIEZYNSKI’s rule of
•
isometry (AIIMS Nov 2010,AIPG 2009)
– In this method the film is placed as close to the

–
teeth as possible without deforming it. However, • Target –focal distance (TFD) is the sum of the target-
when the film is in this position, it is not parallel to
•
object distance (TOD) and object-film distance (OFD)
the long axis of the teeth.
– This arrangement inherently causes distortion.
RADIOLOGY
–
Nevertheless, by directing the central ray The source of radiation should be as Affects sharpness
small as possible (focal spot should be
perpendicular to an imaginary plane that bisects small)
the angle between the teeth and the film, the
practitioner can make the length of the tooth’s Within limits TOD should be as long as Affects sharpness and
image on the film correspond to the actual length possible magnification
of the tooth.
– When the central ray is not perpendicular to the Within limits OFD should be as short Affects sharpness and
as possible (film should be close to the magnification
–
bisector plane, the length of the image of a projected object)
tooth changes.
If the central ray is directed at an angle that The X-ray film source and the object Affects sharpness

is more positive than perpendicular to the should be still and not moving
bisector, the image of the tooth is foreshortened.
The central X-ray should be Affects distortion
If it is inclined with more negative angulation to perpendicular (right angles) to the

the bisector, the image is elongated. object and the film
The film should be parallel to the long Affects distortion

axis of the object
Object Localization: 3 methods
Also Know
– Miller’s technique
• An indistinct image is basically a result of penumbra
–
Also called as right angle technique
•
which forms when source of radiation in the x ray tube

Similar to clarke’s rule but used in mandible.
is too close to the area being x rayed. Increasing the focal

– Cross sectional occlusal radiograph
spot to the object distance reduces the penumbra and
–
X rays are taken at right angles to each other
increases the image sharpness

Cross sectional occlusal radiograph of maxilla
• The anode to film distance commonly used for intraoral

with patient’s sagittal plane is perpendicular and
•
Ala tragus line is parallel to floor. radiograph are 8” (for bisecting technique) and 16” (for
paralleling technique)
– The next method used to identify the spatial position
–
of an object is the tube shift technique. Other names
for this procedure are the buccal object rule and X ray Film, Intensifying Screens and Grids
Clark’s rule (Clark described it in 1910). The rationale X ray film
for this procedure derives from the manner in which – Composition
the relative positions of radiographic images of two
–
Has two principle components – emulsion and

separate objects change when the projection angle at base
which the images were made is changed.(AIPG 2008) In the dental X ray film packet, there is a

protective black paper wrapping the film.

These relationships can be easily remembered
Between the wrappers in the packet there is a

by the acronym SLOB: Same Lingual, Opposite
Buccal. (AIIMS Nov 11)(AIPG 2009, 2011) thin lead foil backing with an embossed pattern

604
Base Emulsion Lead foil

Polyester • Silver Bromide + Silver Iodide • Kept on the backside of film away from the tube
•
•
polyethylene terephthalate crystals in a vehicle of gelatin • Shields the film from back scattered radiation.
•
• The function of silver iodide is to • Absorbs scattered photons and reduces the film fog, thus
•
increase the sensitivity of AgBr
•
increases image quality
crystals to X-rays.
• It also reduces the patient exposure by absorbing the residual
•
X-ray beam.
• If the film is reversed, it results in a light image with
•
characteristic HERRING BONE OR EMBOSSED pattern on
the radiograph.
Size of X-Ray Films
Size 0 22 × 35 mm For smaller children

Size 1 24 × 40 mm For anterior projections
RADIOLOGY
Size 2 32 × 41 mm Standard film size for adults

Size 3
Bite wing film
Size 0 22 × 35 mm Very small children

Size 1 24 × 40 mm Children
Size 2 32 × 41 mm Adults
Size 3 37 × 54 mm Long size bitewing film (NEET 2013)

Occlusalfilm 4 times larger than the size 2 film 52 × 76 mm
Screen films 8 × 10 inches lateral cephalograms, paranasal sinus view
5x7 inches films temporomandibular joint (TMJ) views and lateral oblique views
6x12 inches film Orthopantomography
Angulation guidelines (with occlusal plane parallel to floor)

Projection Maxilla Mandible

Incisors (primary and permanent) +40® -15®

Canine (primary and permanent) +45® -20®

Premolar/Primary molars +30® -10®

Molars +20® -5

• Types:
•
D speed film Ultraspeed provides high contrast and detail. It is the most popular film for veterinary dentistry and detection of
incipient caries (AIIMS May 2009)

E speed film Ekta speed requires 25% less exposure than D speed film with minimal loss of contrast. (NEET 2013)
F speed film Insight requires 60% less exposure than D speed and 20% less than E speed films (AIPG 2011)
G speed films Hyperspeed, 800 speed film that can halve the patient exposure without blurring the image quality
Intensifying Screens
• Screen film is sensitive to visible light because it is placed between two intensifying screens when an exposure is made
•
• Intensifying screens absorb x rays and emit visible light
•
• Reflecting layer used in IS – Titanium oxide + magnesium carbonate
•
Radiology 605

• The presence of IS creates an image receptor system that is 10 to 60 times more sensitive to x rays than the film alone –
•
thus reduced patient exposure.
• ISs are made of a base supporting material, a phosphor layer, and a protective polymeric coat
•
• In all dental applications IS are used in pairs, one on each side of the film, and they are positioned inside a cassette
•
• The purpose of a cassette is to hold each IS in contact with the x-ray film to maximize the sharpness of the image. Most
•
cassettes are rigid, but they may be flexible
• The base material of most IS is some form of polyester plastic that is about 0.25 mm thick. The base provides mechanical
•
support for the other layers.
• The phosphor layer is composed of phosphorescent crystals suspended in a polymeric binder. When the crystals absorb
•
x-ray photons, they fluoresce
• The speed and resolution of a screen depends on many factors, including the following:
•
– Phosphor type and phosphor conversion efficiency
RADIOLOGY
–
 
– Thickness of phosphor layer and coating weight (amount of phosphor/unit volume)
–
 
– Presence of reflective layer
–
 
– Presence of light-absorbing dye in phosphor binder or protective coating
–
 
– Phosphor grain size
–
• Fast screens have large phosphor crystals and efficiently convert x-ray photons to visible light but produce images with
•
lower resolution.
– As the size of the crystals or the thickness of the screen decreases, the speed of the screen also declines, but image
–
sharpness increases.
– Fast screens also have a thicker phosphor layer and a reflective layer, but these properties also decrease sharpness.
–
Grid
– A grid is a structure interposed between the subject (e.g., a tooth ) and the image receptor (i.e., the X-ray film) so as to
–
increase image sharpness (prevents fogging and increases contrast of the image) by removing scattered radiation.
– It is composed of alternate strips of a radiopaque material (usually lead), and strips of radiolucent material (often
–
plastic). Usually grid ratio is 8 or 10.
– Higher the grid ratio more effective it is in removing scattered radiation.
–
– Grids may be focused or parallel, depending on their placement in relation in the X-ray beam or moving (Called a
–
Bucky grid or Potter-Bucky diaphragm) (AIPG 99; AP2K)

Processing X Ray Film
• Film processing involves the following procedures:
•
– Immerse exposed film in developer.
–
– Rinse film in water bath.
–
– Immerse film in .
–
– Wash film in water bath.
–
– Dry film and mount for viewing.
–
Developing Solution
Developer Phenidone • Amplifies the latent image by converting silver halide crystals into metallic silver grains
•
Hydroquinone • Phenidone is the first electron donor (initiator)
•
Activator/ Na or K hydroxide • Helps in maintaining alkaline pH of 10 since developer is active at alkaline pH only
•
alkalizer which are alkaline in • Also causes gelation so that developer agents can diffuse more readily into the emulsion
nature
•
606
Preservative Sodium sulfite • Protects the developer from oxidation by atmospheric oxygen
•
• Also combines with brown oxidized developer to produce a colourless soluble compound
•
Restrainer Potassium or sodium • Reduces the development of unexposed Ag halide crystals
•
bromide • Acts as an antifog agent
•
• Fixer
•
Clearing agent Ag solution of sodium or ammonium Dissolves and removes the unexposed silver halide by forming water soluble
thiosulfate (Hypo) complexes with Ag ions
Acidifier Acetic acid pH 4 to 4.5 Inactivates the carry over developing agents and also blocks the development
of unexposed crystals
Promotes diffusion of thiosulfate complex out of the emulsion
Preservative Na or NH4 sulfite Prevents oxidation of thiosulfate clearing agent

Removes brown oxidized developer from the solution
RADIOLOGY
Hardener Aluminum salts Prevents damage to gelatin

Lessens the damage to emulsion, and limits water absorption, thus shortens
drying time
Good to know
– First intraoral radiograph was made by Edmund Kells
–
– Radiowaves used in MRI have a wavelength of 1200µm
–
– Thickness of emulsion in X ray–0.01mm
–
– Mean diameter of grains of AgBr/AgI is 0.70–0.75mm
–
• Developer replenisher
•
– In the normal course of film processing, Phenidone and hydroquinone are consumed, and bromide ions and other
–
byproducts are released into solution.
– Developer also becomes inactivated by exposure to oxygen.
–
– These actions produce a “seasoned” solution, and the film speed and contrast stabilize.
–
– The developing solution of both manual and automatic developers should be replenished with fresh solution each
–
morning to prolong the life of the seasoned developer.
– The recommended amount to be added daily is 8 ounces of fresh developer (replenisher) per gallon of developing
–
solution. This assumes the development of an average of 30 periapical or 5 panoramic films per day. Some of the used
solution may need to be removed to make room for the replenisher.
• Dark room equipment (AIPG 2007)

•

– Should be at least 4–5 feet (1.2–1.5 m)
–
– Should be light proof
–
– Safelighting is low-intensity illumination of relatively long wavelength (red) that does not rapidly affect open film but
–
permits one to see well enough to work in the area
– To minimize the fogging effect of prolonged exposure, the safelight should have a 15- watt bulb and should be mounted
–
at least 4 feet above the surface where opened films are handled. A new type of safelight uses a cluster of 20 red-emitting
diodes, thus not needing a filter.
– X-ray films are very sensitive to the blue-green region of the spectrum and are less sensitive to yellow and red wavelengths.
–
Accordingly, the red GBX-2 filter is recommended as a safelight in darkrooms where either intraoral or extraoral films
are handled because this filter transmits light only at the red end of the spectrum
– A practical size for a dental office is a master tank about 20 – 25 cm (8 – 10 inches) that can serve as a water jacket for
–
two removable inserts that fit inside. The insert tanks usually hold 3.8 L (1 gallon) of developer or fixer and are placed
within the outer, larger master tank.
Radiology 607

Problems in Film Exposure and Development
Possible causes
Character of faulty film

General Particular

Film too dark • Processing fault (overdevelopment) • Developer concentration too high
•
•
• Development time too long
•
• Developer temperature too high
• Excessive X-ray exposure
•
• Inadequate X-ray exposure
•
•
• Faculty timer on X-ray
•
• Thin patient tissue
•
• Fogged film • Light leak in darkroom
•
•
• Faulty safe lighting
•
• Old film stock
•
• Poor film storage
RADIOLOGY
•
• Light leak in cassette
•
Film too pale • Processing fault (underdevelopment) • Overdiluted developer, inadequate development time,
•
•
• Developer temperature too low, exhausted developer,
•
• Developer contaminated by fixer
• Inadequate X-ray exposure •
• Incorrect exposures setting
•
•
• Thick patient tissue
•
Inadequate or low contrast • Technique error • Film back to front
•
•
• Processing fault • Overdevelopment (plus dark films)
•
•
• Underdevelopment (plus pale films)
•
• Developer contaminated by fixer
•
• Inadequate fixation time (films opaque; milky sheen)
•
• Fogged film • Same as above
•
•
Unsharp image • Technique error • Patient movement
•
•
• Excessive bending of the film packet during exposure
•
• Poor patient positioning (in panoramic radiography)
• Cassette error
•
• Poor film/screen contact incorrect
•
•
• Intensifying screen speed
•
• Excessive X-ray exposure • Incorrect exposure setting for thin object
•
•
• Causing burn-out
•
Film marked • Handling fault • Film packet bent
•
•
• Careless handling in darkroom
•
• Processing fault • Chemical spots
•
•
• Insufficient chemicals to allow full immersion of film
•
• Automatic roller marks
•
• Patient biting too hard on the film
•
• Dirt on intensifying screens
•
Poor positioning • Film packet incorrectly positioned • Film back to front (plus pale film)
•
•
• Nor covering area of interest film used twice (plus dark film)
•
• X-ray tubehead incorrectly positioned • Too step an angle producing foreshortening
•
•
• Too shallow an angle producing elongation
•
• Patient incorrectly placed (in panoramic unit)
• Patient incorrectly positioned
•
•
608
• Management of Radiographic Wastes

When exposed to radiation, the covalent
•
– Silver may be recovered from the fixer by use of either

bonds between silicon atoms are broken,
–
the metallic replacement or electroplating methods. producing electron-hole pairs
In either case, the scrap silver can be sold to silver The number of electron-hole pairs that are
refiners and buyers.

formed is proportional to the amount of
– The lead foil is separated from the packet and collected exposure that an area receives. The electrons
–
until enough has been accumulated to sell to a scrap
are then attracted toward the most positive
metal dealer. Dental offices also should consider using
potential in the device, where they create
companies licensed to pick up waste materials. The
“charge packets.” Each packet corresponds to
names of such companies can be found in the tele-
one pixel. The charge pattern formed from the
phone directory or obtained from the state hazardous
individual pixels in the matrix represents the
waste management agency.
latent image
• Duplicating Radiographs The image is read by transferring each row of
•

– The film to be duplicated and the emulsion side of pixel charges from one pixel to the next in a
RADIOLOGY
–
the duplicating film are held in position and exposed “bucket brigade” fashion. As a charge reaches
to UV light which passes through the clear areas of the end of its row, it is transferred to a readout
the original radiograph and exposes the duplicating amplifier and transmitted as a voltage to the
film. Duplicate film gives positive image. analog-to-digital converter located within or
– Duplication typically results in images with less connected to the computer.
–
resolution and more contrast than the original Gadolinium oxybromide compounds and
radiograph
cesium iodide are used to coat the CCD surface
to increase its X-ray absorption efficiency.
Digital Imaging
– Complementary Metal Oxide Semiconductior
–
• Digitization is a process of converting graphic and CMPS technology is silicon-based, widely
•

pictorial data to digital (binary) form which can be used in the construction of computer central
directly fed and stored inside a computer. A digitizer is an processing unit chips as well as video camera
input device that does the digitization. detectors. The emulsion component of
• Computer display fundamental: Information is conventional X-ray film contains silver halide
•
graphically displayed on a computer monitor or cathode crystals, which are sensitive to X-ray and visible
ray tube (CRT). The image space on CRT is made up of light.
tiny rectangular square picture elements termed pixels, Xeroradiography: Here instead of x ray film,

arranged in a series of horizontal lines on the CRT called a thin layer of “semi conductor” is used to
raster lines. Commonly reported as the display width produce image, which is transferred to paper.
in pixels by the display height in pixels and include 640 - Xeroradiography uses photoconductive se-
by 480, 800 by 600, 1024 by 768, and 1280 by 1024. The

lenium plates instead of film
higher the resolution, the more refined the displayed - It is used in Breast cancer detection.
images appear. The entire displayed matrix of pixels is

termed a bitmap. • Flat panel detectors
• The two main technologies are:
•
– Photostimulable phosphor plate:
•
– Solid-state technology
–
The most used digital radiographic technique
–
– Photostimulable phosphor technology

uses photostimulable phosphor plate instead of
–
• Solid state Technology film. The plate is placed in a laser scanner, which
stimulates the phosphor coating into emitting
•
– Charge-coupled device (CCD)
visible light proportional to the X-ray exposure.
–
Introduced to dentistry in 1987
The light is detected and converted to grayscale

The first digital image receptor to be adapted for

intensities, creating a digital image, which is

intraoral imaging.
The CCD uses a thin wafer of silicon as the transferred to a computer and saved. Scanning
takes approximately 3 minutes. Plates are last for

basis for image recording. The silicon crystals
are formed in a picture element (pixel) matrix several thousand exposures. They are available in
cephalometric, panoramic, and intraoral sizes.
Radiology 609

The PSP material used for radiographic imaging is Improper Use of Image • Improper use of image

•
“europium- doped” barium fluorohalide. Barium Processing processing tools, such as
in combination with iodine, chlorine, or bromine filters, may result in false-
positive findings. An edge
forms a crystal lattice. enhancement filter was applied
+2) creates
The addition of europium (Eu to the panoramic image, which

imperfections in this lattice. When exposed to a produced radiolucencies at
sufficiently energetic source of radiation, valence restoration edges simulating
recurrent caries
electrons in europium can absorb energy and
move into the conduction band. These electrons Commercially available radiographic systems
migrate to nearby halogen vacancies (F-centers) in • Radio visiography
the fluorohalide lattice and may become trapped
•
there in a metastable state. • Flash Dent
•
– A number of approaches have been adopted for • Sens A Ray
•
–
“reading” the latent images on PSP plates. • Vixa
•
An approach used by Soredex in its Digora system
RADIOLOGY
• Advantages (NEET 2013, AIIMS May 2009)

Air Techniques in its ScanX system uses a rapidly
•

rotating multifaceted mirror that reflects a beam – Darkroom is not required, instant image is viewed
–
of red laser light. – The quality of image is consistent
–
As the mirror revolves, the laser light sweeps across – Signal to noise is high
–

the plate. The plate is advanced and the adjacent – Greater exposure latitude
–
line of phosphor is scanned. The direction of the – Elimination of hazards of film development
–
laser scanning the plate is termed the fast scan – Radiation dose is decreased
–
direction. The direction of plate advancement is – Capability for teletransmission
–
termed the slow scan direction.
An alternate approach to plate reading used by Panoramic Imaging

Gendex in the DenOptix system and by Kodak • Also called pantomography
in the CR 7400 system involves a rapidly rotating
•
• Is a technique for producing a single tomographic image
drum that holds the plate.
•
of the facial structures that includes both the maxillary
– Common problems in digital Imaging
and mandibular dental arches and their supporting
–
Noisy Images • PSP image degradation as a structures
•
result of excessive exposure to • This is a curvilinear variant of conventional
ambient light between image
•
acquisition and plate scanning. tomography and is also based on the principle of the
This type of noise resembles reciprocal movement of an x-ray source and an image
that of x-ray underexposure. receptor around a central point or plane, called the
Nonuniform Image • Partial exposure of PSP plates to image layer, in which the object of interest is located.
•
Density excessive ambient light prior to Objects in front of or behind this image layer are not
scanning results in nonuniform clearly captured because of their movement relative to
image density. This happens
when plates are overlapped the centers of rotation of the receptor and x-ray source.
while exposed to ambient light.
Distorted Images • Bending of PSP plates during • The principal advantages of panoramic images include
•
•
intraoral placement the following:
Double Images • PSP double image on incisor
– Broad coverage of the facial bones and teeth
•
periapical radiograph resulting
–
from incomplete erasure of – Low patient radiation dose
–
previous image of posterior – Convenience of the examination for the patient
–
periapical region and retake – Use in patients unable to open their mouths
Damaged Image recep- • Plate surface contamination
–
– Short time required to make a panoramic image,
•
tors • Scratching of receptor
–
usually in the range of 3 to 4 minutes (This includes
•
• Excessive bending of PSP plate
 
the time necessary for positioning the patient and the
•
• Malfunctioning CCD sensor
 
actual exposure cycle.)
•
resulting from rough handling
(dropped sensor). The sensor – Patients readily understand panoramic films; thus
–
produces geometric image they are also a useful visual aid in patient education
 
artifact and case presentation.
610
• The main disadvantage of panoramic radiology is that the • Based on the gyromagnetic property of proton.
•
•
image does not display the fine anatomic detail available • Soft tissues of the joint (articular disc) can be imaged with
 
on intraoral periapical radiographs.
•
MRI or arthrography.
• Image receptors • MRI produces superb images of the soft tissues in internal
•
•
– The receptor on such a machine is either an array derangement of the disc.
–
of CCDs or a film-sized PSP plate rather than film • Arthrography is invasive and has the risk of infection and
•
– Intensifying screens are used allergic reaction.
–
• The contrast medium most commonly employed is
•
gadolinium DTPA.
ADVANCED IMAGING
• Normal magnetic field used in MRI is 1500-1500 gauss
Ultrasound
•
(0.15-1.5 tesla).
• Ultra sound is sound with frequency greater than 20, 000
CT Scan
•
cycles/ second.
RADIOLOGY
• In medical use we use frequency between 1 MHz and 20

• CT scan was invented by Hounsfield.
•
MHz. (PGI 2001)
•
• Hounsfield number in CT Scanning depends on “Mass

• “Piezo electric crystal activation” principle is used in USG.
•
density” (AIIMS May 2009)
•

• Ultrasound probe is made of “Lead Zirconate titanate” • CT scan rooms are shielded by lead (AIPG 2010)
•
now a days and also Quartz previously. (MH 2000)
•

• USG is non mutagenic. Housenfield Units
•
• Contrast used is sonavist (PGI 2007)
• The Hounsfield unit (HU) scale is a linear transformation
•

• USG is non ionizing. (MRI and thermography also are
•
of the original linear attenuation coefficientmeasurement
•
non ionizing) (AIPG 2006) in one in which the radiodensity of distilled water at

• Small organisms are destroyed by USG because of standard pressure and temperature (STP)is defined as
•
“Cavitation”. zero Hounsfield units (HU), while the radiodensity of air
MRI at STP is defined as -1000 HU.
• MRI works on the principle of “Gyro magnetic property • It is the definition for CT scanners that are calibrated with
•
reference to water.
•
of proton “or Hydrogen Nucleus
• There is no radiation exposure in MRI. • Tissue CT number (HU)
•
•
• It is Non ionizing (AIPG 2006, AIIMS May 2010) – Bone 1000 (BHU 2006)
–

– Liver 40 - 60
•

• Most common contrast agent used in MRI is
–
– White matter: 20-30 HU
•
Gadolinium (DTPA, PGI 2000)
–
– Grey matter: 37-45 HU

• MRI is best for posterior cranial fossa lesions
–
– Blood 40
•
• Cardiac pacemakers, aneurysmal clips, (AIIMS 2008)
–
– Muscle 10 - 40
•

–
• Cochlear prosthesis, Ferromagnetic IVC Filters, – Kidney 30
•
–
• Ocular metallic foreign bodies, Cochlear prosthesis are – Cerebrospinal fluid 15
–
•
contraindications to use of MRI – Water 0
–
• MRI is used to detect Non ferrous objects like wood. – Fat -50--100
–
– Air -1000
•
(Concentrate) (AMU 2005)
–

• MRI rooms are shielded by continuous sheets of copper • Computed Tomography Rooms
•
or aluminum for interference from external
•
– Computed tomography rooms typically have high
• Electromagnetic radiations called Faraday cage.
–
workloads and high kilovoltage technique settings.
•
– They are shielded by Lead. (Pb)
–
– As a result, at least “1/16-Inch lead shielding” or
MRI-Nuclear Magnetic Resonance Imaging
–
equivalent is required for the walls, doors, floors,
• Described first by Bloch and Purcell but applied as ceilings, and operator’s barrier. (AIIMS 2009)

•
analytical tool by Damadian and Lautebur.
Radiology 611

– CT rooms with high workloads and with fully occupied uncontrolled space directly adjacent to the scanner may
–
need shielding that is thicker than 1/16-inch lead or 4 to 6 inches of concrete to meet the recommended NCRP.
Advantages of MRI over CT scan Disadvantages (AIPG 2012)

• Selection of any plane possible (Coronal/saggital/Oblique) • Limited slice thickness
•
•
• No ionizing radiation • Bony imaging displays marrow only
•
•
• More sensitive to tissue damage (Demyelination) • Contraindicated in:
•
•
• No bony artifacts – Patients with pace makers
•
–
– Cochlear implants
–
– Prosthetic heart valves
–
– Intraoccular metallic objects
–
– Aneurysmal clips
–
– Claustrophobia
–
RADIOLOGY
CT Scan Appearances
• Central stellate scar on CT scans in kidney indicate: Renal oncocytoma (COMED 2008)
•

• Cresentrichyperdense lesion on CT scan of skull indicates: SDH. (MH 2006)
•

• Lentigenous appearance on CT scan of brain indicates: Medulloblastoma. (TN 2006)
•

• CT scan of head with tram track appearance indicates: Sturge Weber Syndrome. (AIIMS 2001)
•

Positron Emission Tomography (PET Scan)
• PET relies on the detection of positrons emitted during the decay of a radionuclide that has been injected into a patient.
•
• The most frequently used moiety is 2-fluoro-2-deoxy-D-glucose (FDG), which is an analogue of glucose and is taken up by
•
cells competitively with 2-deoxyglucose.
• Multiple images of glucose uptake activity are formed after 45 to 60 min.
•
• Images reveal differences in regional glucose activity among normal and pathologic brain structures.
•
• FDG PET scanning has been used to assist in:
•
– Differentiating radiation necrosis from active neoplasm following therapy, AIIMS 2005
–

– In localizing temporal lobe epileptic foci,
–
– In detecting metastatic disease
–
– Determining cardiac viability.
–
– A lower activity of FDG in the parietal lobes has been associated with Alzheimer’s disease
–
CONE BEAM COMPUTED TOMOGRAPHY
• Cone-beam computed tomography (CBCT) is a recent technology initially developed for angiography in 1982 and
•
subsequently applied to maxillofacial imaging. It uses a divergent or “cone”-shaped source of ionizing radiation and a
two-dimensional area detector fixed on a rotating gantry to acquire multiple sequential projection images in one complete
scan around the area of interest (AIPG 2012)

Principles
– All CT scanners consist of an x-ray source and detector mounted on a rotating gantry. During rotation of the gantry,
–
the receptor detects x rays attenuated by the patient. These recordings constitute “raw data” that is reconstructed by a
computer algorithm to generate cross- sectional images whose component picture element (pixel) values correspond to
linear attenuation coefficients.
– CT can be divided into two categories on the basis of acquisition x-ray beam geometry, namely, fan beam and cone
–
beam
612
– Cone-beam scanners use a two-dimensional digital array providing an area detector rather than a linear detector as CT
–
does. This is combined with a three-dimensional (3D) x-ray beam with circular collimation so that the resultant beam
is in the shape of a cone, hence the name “cone beam.”
Image Acquisition
– There are four components to CBCT image acquisition:
–
X-ray generation Image detection system Image reconstruction Image display
 
• CBCT can be • Current CBCT units can be • Once the basis projection • The volumetric data set is a
•
•
•
•
performed with the divided into two groups on frames have been acquired, it is compilation of all available
patient in three the basis of detector type: necessary to process these data voxels and, for most CBCT
possible positions: image intensifier tube/ to create the volumetric data set. devices, is presented to
sitting, standing, and charge-coupled device This process is called primary the clinician on screen as
supine combination or flat- reconstruction. secondary reconstructed
• During the scan panel imager. The former • Although a single cone-beam images in three orthogonal
configuration comprises planes (axial, sagittal,
•
•
rotation, each rotation may take less than 30
RADIOLOGY
projection image is an x-ray image intensifier seconds, it produces 100 to more and coronal), usually at a
made by sequential tube coupled to a charge- than 600 individual projection thickness defaulted to the
single-image capture coupled device with a fiber frames, each with more than a native resolution
of the remnant x-ray optic coupling. Flat-panel million pixels with 12 to 16 bits of
beam by the detector. imaging consists of detection data assigned to each pixel.
of x rays with an “indirect”
• The shape of the scan • The reconstruction of these data
detector that is based on
•
•
volume can be either a is computationally complex. To
a large area solid-state
cylinder or spherical facilitate data handling, data
sensor panel coupled
are usually acquired by one
to an x-ray scintillator
computer (acquisition computer)
layer. The most common
and transferred by an Ethernet
flat-panel configuration
connection to a processing
consists of a cesium iodide
computer (workstation)
scintillator applied to a
thin film transistor made of • In contrast to conventional CT,
•
amorphous silicon. cone-beam data reconstruction is
performed by personal computer–
based rather than workstation
platforms.
• The beam projection geometry of CBCT and image reconstruction method produce three types of cone-beam–related
•
artifacts:
– Partial volume averaging
–
– Undersampling
–
 
– Cone-beam effect
–
Dual Energy X-ray Absorptiometry (DXA or DEXA)
It is an enhanced form of x-ray technology for measuring bone mineral density (BMD). It detects bone loss much earlier

than conventional X-rays. Standard X-rays cannot detect bone loss until 30% of the bone has been lost. By this time, a person
will already have osteoporosis and will be at higher risk of having painful fractures. DXA can detect as little as one percent of
bone loss and is therefore rightly termed as the gold standard for detecting osteoporosis.
• Is painless, non invasive
•
• Is accurate and detect as little as 1% of bone loss
•
• Is quick
•
• Uses a low level of radiation
•
• Can provide whole body scanning and give information about body composition including lean (muscle) and fat mass
•
• Note: measurement of lower spine and hips are most often done
•
• More portable devices that measure wrist, fingers, or heel are sometimes used for screening.
•
Radiology 613

DIAGNOSTIC IMAGING OF TMJ
Tanscranial Projection
• A sagittal view of the lateral aspects of the condyle and temporal components can be obtained.
•
• X-ray beam is directed downward from the opposite side, through the cranium and above the petrous ridge of the
•
temporal bone, at a 25-degree positive angle centered through the joint. The horizontal direction of the beam may be
individually corrected for the condylar long axis; an average 20-degree anterior angle may be used. (AIIMS May 2009)

• It includes projections of both TMJs in the closed and maxillary open positions routinely.
•
• The central and medial aspects of the joint are projected inferiorly, and only lateral joint contours are visible due to
•
positive angulation.
• Useful for identifying gross osseous changes on the lateral aspect of the lateral aspect of the joint only, displaced condylar
•
fractures, and range of motion.
RADIOLOGY
Panoramic Projection • Beam is directed from the front of the patient through the
•
ipsilateral orbit and TMJ of interest.
• Provides an overall view of the teeth and jaws, hence a
• The film cassette is placed behind the patient’s head,
•
screening projection •
• No information about condylar position or function is perpendicular to the X-ray beam.
•
provided • The patient opens maximally and protrudes the mandible,
•
• Panoramic view does not provide an adequate view thereby avoiding superimposition of the articular
•
because of superimposition by zygomatic arch and skull eminence or skull base on the condyle.
base • Very good for visualizing condylar neck fractures as entire
•
Transpharyngeal (parma) Projection mediolateral dimension of the articular eminence or skull
base on the condyle.
• It provides sagittal view of the medial pole of the • Adjuvant to diagnose degenerative changes or other
•
condyle.
•
anomalies of TMJ.
• The beam is detected superiorly at -5 degrees through A similar projection is the reverse open Towne’s projection,
•
the sigmoid notch of the opposite side and skull base which sometimes is used to image condylar neck fractures,
degrees from the anterior with maximal opening of mainly if medial displacement is suspected. (AIPG 2005)
mouth.
• The medial aspect of the condyle can be viewed because Submentovertex (Basal) Projection
•
of negative beam angulation.
• It gives a view of the skull base and condyles
• Temporal component is not imaged well.
•
superimposed on the condylar necks and mandibular
•
• Effective for visualizing erosive changes of the condyle. rami.
•
• Used to determine the angulations of the long axis of
•
the condylar head for corrected tomography. This is an
Transorbital Projection
adjuvant to find the TMJ changes in facial asymmetries,
• The patient’s head is tilted downward 10 degrees so that condylar displacement, or rotation of the mandible
•
the canthomeatal line is horizontal. in the horizontal plane associated with trauma or
orthognathic surgery.
Abnormality of TMJ Best Imaging Technique
Hard Tissues
Bony ankylosis, arthritis and joint space calcifications CT scan >conventional tomography>MRI
Developmental abnormalities CT scan >OPG >other noninvasive
Trauma: Condylar fractures Transorbital
Multiple fracture CT scan
614
Soft Tissues
Disc perforation Arthrography >MRI
Disc position MRI > arthrography
Fibrous ankylosis MRI > arthrography
Inflammatory conditions and joint effusions MRI > arthrography
Range of motion Arthrography
Neoplasm MRI >CT scan
Good to Know
• PA view with 100 tilt is called Caldwell projection
•
• Waters view/Occipitomental view: Maxillary, Sphenoid, Ethmoid sinuses (AIIMS MAY 2009)
•

• Caldwell view/ Occipito frontal view: Frontal, Ethmoid sinus
•
• Townes View: Cranial fossa
•
• Odontoid view C1 C2 vertebrae. (AIIMS 2009)
RADIOLOGY
•

• Submentovertex/ Base or full axial/Jug handle view – for viewing base of skull and fracture of the zygomatic arch
•

(AIPG 2006, 2005)

DIAGNOSTIC IMAGING OF SALIVARY GLANDS
Normal sialography “Tree limbs with bloom” or “leafless tree” AIPG 2001 There is filling of ducts and parenchyma producing image
Sialodochitis Sausage- string appearance This appearance is due to strictures
Sialadenitis Apple tree in blossom Dilation of the acini and terminal ducts
Sjogren syndrome Snow storm appearance or a “cherry blossom” or The larger ducts are elongated and smaller ducts are
“branch less fruit–laden tree” effect. disintegrated. The dye leaks out and gives this appearance.
Sialographs demonstrate the formation of punctuate,
cavitary defects
Salivary gland ‘ball–in–hand’ appearance Ducts adjacent to the lesion are curvilinearly draped and
tumors stretched around the mass, producing a characteristic
appearance
Sialography
• Radiographic procedure that is useful disgnostic adjunct for detection and monitoring of salivary gland diseases. It is
•
used to examine the ductal and acinar system of the major salivary glands
• The glands are cannulated and filled with radiographic contrast agents
•
• The contrast agents used in sialography are usually compounds with high concentration of iodine.
•
• Arcelin: Introduced sialography in 1913
•
• Jacobvisi: Introduced sialographic technique
•
• Water soluble agents result in less patient discomfort and a few foreign body reaction have been precipitated.
•
– Any residual water soluble agent in gland is rapidly absorbed by the blood and removed from the gland.
–
– These agents coat stones more adequately and allow better visualization
–
• Water soluble agents–chronic inflammatory diseases
•
• Lipid soluble agents–for tumours and masses
•
• Indications of sialography
•
– Salivary duct stones and strictures
–
– Chronic inflammation of parotid and salivary glands
–
– Tumours in parotid gland
–
Radiology 615

• Contraindication
•
– Acute sialadenitis (AIPG 2005)
–

– Contrast allergy
–
Sialography and Salivary Gland Scan
Parameter Salivary gland scan Sialography
Agent used 99
TcO4 -
Iodinated contrast media; x-ray film
Administrations i.v Retrograde pressure placement
Detector Gamma Camera; Polaroid or X-ray film Fluoroscope: X-ray film
Structures visualized • Glandular parenchyma • Ductal system

•
•
• Oral cavity • Only major salivary gland visualized at a time
•
•
• All salivary glands simultaneously
RADIOLOGY
•
• Vascular supply of gland
•
Advantage • Shows glandular function • High resolution of duct system
•
•
• B/L comparison possible • Localized controlled radiation dose
•
•
• High sensitivity • Much existing information on appearance of specific
•
•
• Lack of medical contraindications disease states
•
• Can be performed on patient with acute inflammation
•
or known tumor
Disadvantage • Lack of specificity in agent concentration • Must infer parenchymal changes by changes in
•
•
• Demonstrate little morphology ductal morphology and function
•
• Generalized higher radiation dose • Medical contraindications (allergy to iodine, known
•
tumor, acute inflammation, improper equipment)
•
• Lack of substantial baseline information on
•
appearance of specific disease states
• Can’t be performed shortly after sialogrpahy
•
Others Primarily a functional study Primarily an anatomic study
Diagnostic Imaging–Some Important Points

Structure Best view
Fracture of zygomatic arch (AIPG 2008) Submandibular /submentovertex

Base of skull Submandibular/submentovertex
Fracture of zygoma Water’s view
Maxillary sinus Water’s view

Nasal septum Water’s view (AIPG 2007)
Nasal fracture True Lateral (AIIMS May 2010,AIPG 2010)

Condylar neck fracture Reverse towne’s view
Medially displaced condylar fracture PA view
Mid mandibular ramus to condylar apex Transpharyngeal view
Coronoid process of mandible PA view of skull
Fracture of ramus of body of mandible Lateral oblique 150 (AIPG 2007)

Horizontal fracture of mandible Lateral oblique 300 (AIPG 2010)

Bony ankylosis of TMJ CT scan
Fibrous ankylosis of TMJ MRI
Lateral derangement of disk MRI

Disk perforation Arthrography
616
RADIOGRAPHIC INTERPRETATION
Age Anterior IOPA’S Posterior IOPA’S Bitewings Total films

1 – 3 years 3 - 2 4
3 – 6 years 6 4 2 12
6 – 12 years 8 4 2 14
> 12 years 8 8 4 20
Dental Caries Calculus

 
Poorly contoured or overextended restorations
– The shape of the early radiolucent lesion in the enamel

Root length and morphology and the crown-to-
–
is classically a triangle with its broad base at the tooth

root ratio
surface spreading along the enamel rods, but other
Open interproximal contacts, which may be sites
RADIOLOGY
appearances are common, such as a “notch,” a dot, a

for food impaction
band, or a thin line
 
– The classic radiographic appearance of lesions – Anatomic considerations Position of the maxillary
–
sinus in relation to a periodontal deformity
–
extending into the dentin is a broad-based, radiolucent
zone, often beneath a fissure, with little or no apparent – Missing, supernumerary, impacted, and tipped teeth
–
changes in the enamel. The deeper the occlusal lesion, – –
Pathologic considerations
the easier it is to detect on the radiograph Caries

– Low KVp increases the film contrast which is needed Periapical lesions

Root resorption
–
for demonstrating incipient caries

– Minimum dentinal destruction to get evident on – The early lesions of chronic periodontitis appear
–
radiograph is 40 microns (AIPG 2008)
–
as areas of localized erosion of the interproximal

– Various morphologic phenomena, such as pits and alveolar bone crest. The anterior regions show
–
fissures, cervical burnout, and Mach band effect, blunting of the alveolar crests and slight loss of
and dental anomalies, such as hypoplastic pits alveolar bone height. The posterior regions may also
and concavities produced by wear, can mimic the show a loss of the normally sharp angle between the
appearance of a carious lesion lamina dura and alveolar crest.
– Mach Band Effect is a simulated , false appearance – Even if only slight radiographic changes are
–
apparent, the disease process may not be of recent
–
due to the optical illusion presented from light
and dark objects (e.g., enamel and dentin) placed onset because significant loss of attachment must
next to one another. It is an optical phenomenon be present for 6 to 8 months before radiographic
in which a dark band-like radiolucency is seen in evidence of bone loss appears.
dentin at the dentinoenamel junction (DEJ) even – Also, variations in angle of projection of the x-ray
–
when no dentinal caries is present. It is due to high beam can cause a slight change in the apparent
demarcation between a darker and lighter area. The height of the alveolar bone. Small regions of bone
illusion is named after Ernst Mach. (AIPG 2008) loss on the buccal or lingual aspects of the teeth are
much more difficult to detect.

– A mild lesion does not necessarily develop into a
–
Periodontal Diseases more severe lesion later; however, if the periodontitis
progresses, the destruction of alveolar bone extends
• Radiographs are especially helpful in the evaluation of the beyond early changes in the alveolar crest and may
•
following features: induce a variety of defects in the morphology of the
– Amount of bone present alveolar crest.
–
– Condition of the alveolar crests – These patterns of bone loss have been divided into
–
–
– Bone loss in the furcation areas horizontal bone loss, vertical (angular) defects,
–
– Width of the periodontal ligament space interdental craters, buccal or lingual cortical plate
–
• Local irritating factors that increase the risk of loss, and furcation involvement of multirooted
•
periodontal disease teeth.
 
 
Radiology 617

Inflammatory and Reactive Lesions of Jaws BENIGN AND MALIGNANT TUMOURS OF
– Acute osteomyelitis: unremarkable to an ill defined JAWS
–
radiolucency
– Chronic osteomyelitis: patchy, ragged, irregular Benign Neoplasms
–
radiolucency–‘onion skinning (peeling)’
– Osteoradionecrosis (ORN): Ill defined radiolucent • Osteoma: Circumscribed sclerotic mass
•
–
areas, which may develop radiopaque zones as the • Osteoid osteoma: Well circumscribed radiolucent defect
•
dead bone separates from the residual non vital surrounded by a dense sclerotic bone.
bone. (AIPG 2012)
• Osteoblastoma: 2-10 cm diameter in size. It gives the

– Langerhans cell histiocytosis: ‘punched out
•
impression of osteosarcoma due to its ‘sunburst’ pattern.
–
radiolucencies’, ‘teeth floating in air’
• Cementoblastoma: Although the calcified mass is
•
Cysts and Cyst Like Lesions of Jaw intimately associated with the root, the root outlines are
obscured and usually surrounded by a radiolucent rim.
– Aneurysmal bone cyst: unilocular - multilocular
–
RADIOLOGY
radiolucency with a marked cortical expansion and Features of Malignant Lesion of Bone on Radiography
thinning (‘balloning or blown out distension’).
• Cortical erosion
– Simple bone cyst (traumatic bone cyst, idiopathic
•
• Cortical Destruction
–
bone cavity): well delineated radiolucent defect •
with variably defined margins, projections with • Absence of Sclerotic margin
•
scalloping between roots. • Associated soft tissue mass
– Breech of Cortex: Aneurysmal bone cyst.
•
• Irregular boundaries
–
– Fallen fragment sign: Aneurysmal bone cyst
•
• Irregular periosteal reaction
–
– Extraneous type of primordial cyst is found in
•
–
ramus
– A residual cyst has a cortical margin unless it Malignant Neoplasm of Bone
–
becomes secondarily infected. Its shape is oval or
circular. Osteosarcoma • Mixed lesion with an aggressive expansion
•
• Symmetrical widening of the PDL
•
Giant Cell Lesions • ‘sunburst’ pattern in 25% of cases
•
• Increased alkaline phosphatase
– Central giant cell granuloma: Well delineated,
•
• Codman’s triangle
–
unilocular or multilocular radiolucency (usually
•
• Highly radioresistant (AIPG 2006)
crosses the midline).
•

– Cherubism: Unilocular or more commonly
Chondrosar- • ‘sunburst’ appearance like
–
multilocular bilateral expansile radiolucencies
•
coma osteosarcoma as well as ‘ cotton wool like’
associated with multiple unerupted teeth. • Cotton wool > Sunburst
•
• Benign fibro-osseous lesions
•
Fibrosarcoma • Radiolucency associated with an
– Periapical cemental dysplasia:
•
aggressive resorption
–
Early lesion: Circumscribed periapical

radiolucency Ewing’s sar- • Primarily radiolucent with ‘onion skinning’
Mid to late: Progressive calcification surrounded
•
coma or ‘onion peel’

by a radiolucent rim.
– Focal cemento-osseous dysplasia: Well defined Multiple my- • Multiple ‘punched out’ radiolucencies
•
eloma
–
mixed lesion with irregular borders • Soap bubble appearance
•
– Florid cemento-osseous dysplasia: Multiple lobular
–
radiopaque lesions Important Points about Metastasis to Bone
– Ossifying fibroma:
• Common malignancies with bone are metastasis from
–
Well defined unilocular mixed lesion, usually
•
Breast, Bronchus, Prostate, Kidney and Thyroid

with a sclerotic border and may see downward
bowing of the inferior border of the mandible. • Axial skeleton more commonly affected
•
Juvenile ossifying fibroma: Mixed lesion with • Usually Multiple

•
fairly well defined borders.
618
Different Appearances of Bony Tumors: • Squared ver tebrae~Ankylosing • Achondroplasia
•
•
spondylitis
• Honey comb appearance: Adamantinoma
•
• Scottish dog appearance
• Soap bubble appearance, Breach of cortex:
•
•
Osteoclastoma • Spondylolesthiesis
•
• Chicken wire pattern: Chondroblastoma
X-ray Changes of Rheumatic Arthritis
•
• Linear Striations: Vertebral Hemangioma
•
• Physalipharous cells: Chondroma • Soft tissue changes
•
•
• Cuffing of bone: Peripheral giant cell granuloma • Osteoporosis
•
•
• Snow driven appearance: Pindborg tumour (CEOT) • Joint space narrowing
•
•

(AIPG 2006) • Periostitis
•

• Multiple punched out radioluciencies with regular • Bone erosions
•
•
borders: multiple myeloma (AIIMS May 2010) • Secondary osteoarthritis

•
RADIOLOGY
• Multiple punched out radioluciencies with irregular

Radiographic Features of Scurvy
•
borders: Eosinophilic granuloma
• Salt and pepper bone: Thalassemia • Metaphysealucency (Trummer field zone)
•
•
• Total disappearance of bone: Massive osteolysis/ • Metaphyseal fracture (Pelkan spur)
•
•
phantom’s vanishing bone • Radiodense metaphyseal end (Frankels white line)
•
• Drill bone/Rider’s bone/Exercise bone: Traumatic • Small epiphysis with sclerotic radiodense rim (Wimberger
•
myositis ossificans
•
sign)
• Brittle bone: Osteogenesis imperfecta • Bowing of long bones (AIIMS 2009)
•
• Wormian bone: Cleidocranial dysplasia
•

• Periosteal elevation
•
•
DISEASES OF BONE MANIFESTED IN JAWS Radiographic Features of Childhood Leukemia
• Metaphyseal translucencies
Radiographic Features of Osteomalacia
•
• Metaphyseal cortical erosions
• Loosers zone or pseudofractures
•
• Osteolytic lesions
•
• Cod fish vertebrae
•
• Periosteal reactions
•
• Rugger jersy spine
•
• Metaphyseal osteosclerosis
•
• Protrusion acetabuli
•
•
• Triradiate pelvis
Lytic Lesions
•
Radiographic Changes in Osteomyelitis • Ca bronchus,
•
• Soft tissue swelling (earliest) • Pencil in cup deformity
• Cervix,
•
• Endometrium,
•

•
(KOL 2008)

•
• Haziness • Opera glass hand • Rectum,
•
•
•
• Loss of density of effected • Ivory phalynx • Adrenal tumors,
•
•
•
bones
• Wilms Tumor
•
• Subperiosteal reaction • Psoriatic arthritis
Hyperparathyroidism
•
•
• Bone death and appearance of • Punched out skull lesions
•
•
•
(sequestrum) ~Eosinophilic granuloma/ Multiple sharply defined radioluciencies which may be
•
multiple myeloma lobulated
• Periosteal new bone formation • Champagne glass pelvis • Jaws may show ground glass appearance
•
•
•
(involcrum)
• Loss of lamina dura
•
• Squared patella ~Hemophilic • Trident hand • Osteopenia;
•
•
•
arthritis
• Spine: Vertebral compression fractures;
•
Radiology 619

• Skull: So-called salt-and-pepper skull, tiny punched – “Periventricular calcification” is most likely due
–
•
out lesions may be present in the skull, producing so to CMV infections. (PGI 1997)

called salt and pepper appearance – “Bracket calcification” in skull is seen in Corpus
–
• Phalanges: Subperiosteal resorption of digital tufts and Callosum Lipoma
– “Tram track calcification” Sturge Weber Syndrome.
•
phalanges (which is usually more marked onradial than
–
on the ulnar side of the hand) – Lemon sign Infolding of frontal bones: Neural
–
tube defects/ Arnold chiari Malformation
– Banana sign: Cerebellar deformity: Neural tube
• Brown Tumors: Occurs in severe cases; referred to as
–
defects/ Arnold chiari Malformation
•
“Giant Cell Tumor of Diaphysis”. Microscopical exam – Rice grain calcification of Brain Not Skull
revealed that it was composed of numerous osteoclasts
–
~Neurocystercosis
with stromal hemorrhage
• Soft Tissues Calcification: Bone: obilizes bone Sutural Diastasis: (AIIMS May 08)
•
and phosphate; activating and increasing number
RADIOLOGY
of osteoclasts, which destroys hydroxyapatite, thus • Is widening of cranial sutures. True sutural diastasis
•
releasing calcium and phosphate; suggest raised intracranial pressure, for eg from subdural
• Rotting fence post appearance of femur haemorrhage or hydrocephalus. Sutural diastasis on
a radiograph may also reflect deficient perisutural
•
• Pepper pot
ossification in conditions such as cleidocranial dysplasia,
•
rickets or osteogenesis imperfecta. Sutural diastasis can
Fibrous Dysplasia: 3 Basic Patterns Seen Are: occur in young patients without significant force, but in
adult patients with fused sutures it is a sign of significant
• Small unilocular or large multilocular radiolucency with
trauma and may well be associated with intracranial
•
a well circumscribed border containing a network of fine
complications.
trabeculae
• Signs of Increased Intracranial Tension in a Child in a
• Mottled appearance
•
Skull X-ray:
•
• Fibrous dysplasia: Diffuse ‘ground glass’, ‘orange peel’
– Separation of the sutures
•
radiopacity
–
– Tense anterior fontanelle
– Both variants of fibrous dysplasia show ground glass
–
– Silver beaten appearance of the bones
–
appearance
–
– Mono-ostotic fibrous dysplasia exhibits true ground • Calcification of menisci is seen in pseudogout
•
–
glass appearance, which is XO-GG (radiopaque • Calcification of Intervertebral disc is seen in
•
ground glass appearance) alkaptonuria.
– Polyostotic fibrous dysplasia exhibits pseudo ground • Calcification of interosseous membrane is seen in
–
glass appearance, which is XL – GG (radiolucent
•
skeletal flourosis
ground glass appearance)
SOFT TISSUE CALCIFICATIONS AND CHARACTERISTIC RADIOGRAPHIC

OSSIFICATION

PATTERNS
Intracranial Calcification is Seen in Sun Ray or Sunburst • Osteosarcoma (AIPG 2014)
•
Appearance • Chondrosarcoma
– Pineal calcification
•
• Osteoblastoma
–
– Dural calcification
•
–
– Cystercosis Cotton wool appearance • Paget’s disease
•
(AIPG 2005, 2004, AIIMS •
–
– “Basal ganglia calcification” is seen in Chronic sclerosing diffuse

May 2010)
•
osteomyelitis
–
Hypoparathyroidism, FAHRS Syndrome.

(AIPG 2007) • Fibrous dysplasia
•

– “Suprasellar calcification” is seen in • Cemento osseous dysplasia
•
–
craniopharyngioma, meningioma. (TN 1989) Onion skinning/peeling • Ewing’s sarcoma

•
– “Rail road calcification” is seen in Sturge Weber appearance (AIPG 2014) • Chronic osteomyelitis

–
•
Syndrome. • Caffey disease
•
620
Ground glass • Fibrous dysplasia – Kerly D Line: Criss crossing of Kerley A And B
•

appearance (AIPG (COMEDK 2006)
–
Lines

2006, 2007, AIIMS May • Hyperparathyroidism (osteopenia
08) – Kerly lines are a sign seen on chest radiographs with
•
in mandible and maxilla, producing
–
a fine trabecular pattern) interstitial pulmonary edema. They are thin linear
•
•
Ossifying fibroma pulmonary opacities caused by fluid or cellular
• Paget’s disease in radiolucent infiltration into the interstitium of the lungs.
•
stage – Due to pulmonary venous hypertension:
–
• Chondrosarcoma Left ventricular failure.
•

• Periapical cemental dysplsia Mitral stenosis.l
•

• Cherubism
•
Causes of “Ground • Obstructive TAPVC Radiological Signs of Fetal Death
•
Glass Pattern” on Chest • Interstitial pneumonia
Radiography • Roberts sign: Appearance of gas shadows in Heart/Great
•
• Pulmonary haemorrhage
•
vessels
•
• Alveolar proteiniosis
RADIOLOGY
• Spadlings Sign: Overlapping of cranial bones due to

•
• Pneumonia (AIPG 2001)
•
liquefaction of brain matter
•

• Collagen vascular diseases
• Balls sign: Hyperflexion of spine
•
• Silicosis
•
• Halos sign: Elevation of Pericranial fat (AIPG 2014)
•
Moth eaten appearance • Osteomyelitis – acute suppurative
•

•
(AIIMS Nov 2010, AIPG and chronic
2007,2009, 2010) • Osteosarcoma
Transposition of Great Vessels
•
• Osteoradionecrosis • Is the most common cyanotic congenital heart disease in
•
•
• Ewing’s sarcma the newborn infant (Tetralogy of Fallot is more common
•
• Langerhans cell histiocytosis – overall, but many tetralogy of Fallot cases present after
•
occasionally the newborn period).
• Hemorrhagic cyst
– Aorta arises from the right ventricle
•
• In skull – Syphilis
–
– Pulmonary artery from the left ventricle, with the
•
–
Soap/snow bubble • Ameloblastoma aorta positioned anterior and to the right of the
•
appearance • Central hemangioma pulmonary artery.
•
• Odontogenic myxoma • It is incompatible with life unless a communication
•
•
• Giant cell lesion exists between systemic and pulmonary circulation
•
• Odontogenic keratocyst (OKC) • During the newborn period, the PDA and patent
•
•
• Pindborg tumour foramen ovale (PFO) maintain this communication.
•
• Aneursymal bone cyst
• As the PDA starts to close and the PFO by itself is
•

(BHU 2008)
•
inadequate in size, the patient develops intense cyanosis,

Hair on end appearance • Thalassemia and the patient becomes tachypneic.
•
• Sickle cell anemia
• On auscultation, the second heart sound is greater in
•
•
Centrifugal growth • Cementifying fibroma intensity (UPSC 2006)

•
pattern • Ossifying fibroma • X ray shadow secondary to a small thymus, sometimes
•
•
• Cemento-ossifying giving the appearance of “Egg on side” or “Apple on a
•
Eggshell Calcification • Refers to fine calcification seen string” appearance.
•
at the periphery of a mass, and • Echocardiography confirms the Diagnosis.
•
usually relates to lymph node
calcification • The “Arterial Switch Procedure” offers the best
•
prognosis with a mortality of about 5%.
Kerly Lines
– Kerly A Line: Upper Zone (perihilar fluffy MISCELLANEOUS
–
opacities)
– Kerly B Line: Basal Zone (early change of • Supralethal dose-> 5Gy
–
pulmonary edema) (KAR 1995)
•
• In humans genetic doubling dose that results in death is

– Kerly C Line: Central Zone
•
approximately 2 Sv
–
Radiology 621

• Exostoses are common in maxilla while enostoses are • Kinking or sharp binding of an x-ray before exposure
•
more commn in mandible than maxilla
•
produces areas of low density
• High recurrence rate of Odontogenic myxoma is due to • The convex side of the dot indicates tube side of the
•
lack of encapsulation
•
film( facial aspect)
• The extent of reduced salivary flow is dose dependent and
•
reaches essentially zero at 60 Gy. (AIPG 2005) • Green film after processing is due to fil emulsion not in
•

• Film packet reversed–Herring bone pattern contact with the processing solution
•
• A film is of greatest diagnostic value when the structures • Penumbra in a processed film is related to magnification,
•
sharpness of image and detail of image. Blurring of image
•
of interest between 0.6 and 0.3 optical density units.
– penumbra effect
• The optical density of gross fog typically is 0.2 to 0.3
•
• Subclavian steal syndrome is reversal of blood flow in • The contrast medium used in arthrography is
•
•
ipsilateral vertebral artery gadolinium DTPA
• Normal magnetic field used in MRI is 1500 - 15000
RADIOLOGY
• Dyes/ Contrast agents used frequently
•
gauss
•
– Bronchography: Dianosil • Neohydiol (lipiodol) is the common contrast medium
–
– OCG: Iopanoic acid
•
in sialography
–
– Intra venous cholangiography: Biligrafin
• Zonography is a type of panoramography
–
– Lymphangiography: Lipiodal
•
• Fluoroscopy is real time radiography. It allows
–
– IVP: Conray 480
•
continuous viewing of a time varying X ray image and
–
– MRI: Gadolinium
permits live visual examination of dynamic events.
–
– Myelography (Dye used) Myodil
–
– Myelogram (Contrast used) Iohexol
• Thickness of emulsion film used for an iopa film is 0.7mm
–
•
• Le masters’ technique: Method to avoid the • Lead aprons decrease 94% of scattered radiation and
•
•
superimposition of the molar process on the roots of intensifying screens 85- 94% (AIPG 2008)

maxillary molar • Grainy leather like appearance of fine lines on dental
•
• Bitewing radiograph: Given by Riper radiographs due to extreme temperature of processing
•
• Donovan’s technique: To view impacted 3rd molars in B solution is known as reticulation
•
L phase • Adumbration refers to cervical burn out.
•
• In cephalometric radiography the distance between the
Campbell Lines seen in Occipitomental/Para Nasal View
•
subject and the source of x ray is 5 feet (60”)
(AIIMS May 2010)(AIPG 2009, 2010)
• The radioresistance of many tissues is increased when
– First line: Path from zygomatico-frontal suture to
•
irradiation is done under conditions of hypoxia
–
superior orbital margin across the glabella region
• Presence of air within the tube brings about rapid
to superior orbital margin and zygomatico-frontal
•
deterioration and eventual destruction of the filament by
suture of the other side.
oxidation.
– Second line: From zygomatico tubercle to
–
• The radiolucent portion of an x-ray film is formed continuous line of zygomatic arch till it blends
into zygomatic bone and the line continues along
•
by the silver particles. The radio opaque areas on an
x-ray film are seen as such because of removal of AgBr inferior orbital margin, across the frontal process of
crystals when it is placed in fixing solution maxilla and lateral wall of nose through septum and
then same course on the opposite side.
• Dental x-rays films are coated with emulsion on both
– Third line: From condyle across the mandibular
•
sides of the film to reduce exposure time. As x-ray beam
–
notch, coronoid process of the mandible to lateral
is divergent, the images recorded on each emulsion
wall of antrum and continuous through the medial
vary slightly with size. In general this parallax on image
wall of antrum or lateral wall of nose at the nasal
sharpness is unimportant but its effect is most apparent
floor level and the same course on the opposite side.
when the film is wet as the emulsion gets swollen with
– Fourth line: Occlusal curve of the Unilateral arches.
water and loss of image sharpness by parallax is more
–
– Fifth line: Lower border of mandible from one
evident.
–
angle to other side angle.
CHAPTER 16
Pedodontics
Objectives
• History of Pedodontics • Early Childhood Caries

• Development • Pit and Fissure Sealants

• Theories of Child Psychology • Pulp Capping

• Child Behaviour in Dental Office • Obturation Techniques

• Radiographs in Pedodontics • Stainless Steel Crowns

• Habits • Recent Trends in Pain Control

• Anatomy of Primary Teeth • Trauma

HISTORY OF PEDODONTICS Pedodontic Treatment Triangle
1763 • Joseph Hurlock published 1st book on children’s

•
dentistry
1764 • Robert Bunon ‘father of pedodontics’ reiterated the

•
importance of deciduous teeth
1920 • In India first dental college and hospital was started

•
in Calcutta by Dr Rafuddin Ahmed
• Dr Ahmed the father of dentistry is also known as Fig16.1: Pedodontic treatment triangle
•
‘The Grand Old Man of dentistry’
Modified Pedodontic Treatment Triangle
1950 • The foundation of pedodontics was laid down in
•
government dental college
1966 • Pedodontic triangle was given by Dr GZ Wright

•
1979 • Indian society of Pedodontics and Preventive
•
Dentistry was formed
1988 • Pedodontics was given independent status by DCI

•
• Dr BR Vacher is the Father of Pedodontics in India
•
Fig 16.2: Modified pedodontic treatment triangle
Pedodontics 623

DEVELOPMENT General Postnatal Changes in Neonatal Skeleton
• Behavior shaping should be started from case history • The neonate has 270 bones as compared to adult who has
•
206 bones
•
taking or even before.
• Chief complaint should be recorded in patient’s own • The ratio between the calvarial and facial portion is 8:1
•
at birth whereas it is 2.5:1 in adult female and 2:1 in male
•
words.
• Oral health is integral part of total health of child. • Skull bones in the neonate are 45 (due to incomplete
•
•
• Medical history should always be evaluated. ossification) and in the adult they are 22
•
• FDI system of teeth notation is the most accepted criterion • The frontal bone at birth is in two halves, which fuses at
•
•
for patient recording. 2 years
• Cardiovascular system starts functioning by the end of the • There are two parietal bones
•
3rd week.
•
• The occipital bone at birth consists of four pieced, which
• By the 24th day, 3 pairs of branchial arches are present
•
fuse by 3-4 years of life
PEDODONTICS
•
• By the end of 5th week, 42- 44 pairs of somites are formed • The sphenoid bone is made up of three parts (the body,
•
• Limb movements are not felt by the mother till about 17th
•
lesser and greater wings) at birth, which fuse during the
•
week first year. Sinuses do not develop in the sphenoid till 5th
• Fetal period begins at 9th week year
•
Reflexes • The ethmoid bone at birth is in three pieces (median plate
•
and a right and left labyrinth) which fuse by the 5th or 6th
• Sucking reflex: Develops by 17th to 20th weeks year of life
•
• Grasp reflex: Disappears by 12 weeks (AIPG 2005) • Each temporal bone consists of four parts which fuse by
•

•
• Moro s reflex: Disaapear by 3 months puberty
•
• Glabellar tap: Present at 32 weeks • Mastoid process is absent in neonates, thus stylomastoid
•
•
• Tonic neck reflex: Prominent between 2-4 months foramen lies superficially
•
Body Proportions
Dentistry for Kids
• The body proportions are as a result of different rates of
•
growth for cephalic and caudal ends. Massive changes in
body occur from fetal life to adulthood
• MID Point:
•
– Mid point of a two month old embryo is on chest close
–
to the chin
– At birth: The mid point at the time of the birth shifts
–
to near the umbilicus
– In adult: It is in the pubic symphysis region
–
• The length of the head doubles by adulthood but the body
•
grows even more hence at birth 22% of the area is covered
by head.
• This decreases to 13% at 12 years and only 10 % at adult.
•
Fig 16.3: Child dentistry • There is an axis of increased growth is the head towards
•
the feet. This increased growth is the cephalo-caudal
• Morning appointments are preferable in young gradient
•
patients because the child will be fresh and active at this
time. • The cephalo-caudal gradient can be observed from the
•
• The length of the appointment should be less than 30 growth of the head. In the face, the mandible which is
the farthest from the brain, grows more compared to the
•
min
maxilla, which is closer.
• The concept of four handed dentistry implies that
• In the early period of development, the cranium is larger
•
the assistant’s hands are constantly employed in the
•
treatment of child in relation to the face. Later, this proportion changes due
to increased growth of the face.
624
• In a newborn child the height is measured using a In depth the increase is somewhat smaller (approx

•

measuring tape in a lying down position and hence it is 75%)
referred to as LENGTH. The normal value of length in Increase in width is the smallest (approx 15%)

new born child is 45-50 cm The height of upper and lower face is independent.

The upper anterior face height seems to primarily
Changes In Craniofacial Complex correlated with cranial base changes. The lower
face height seems to be more dependent on
• The skeletal portion of craniofacial complex develops as muscular functions, environmental factors
•
a blend of morphogenesis of primary skull components. interfering with the air way and the posture of the
• The neurocranium: This consists of two parts: head.
•
– The desmocranium which comprises the vault of • Because of the above changes in the craniofacial complex,
•
general features of the head and the face are observed to
–
the skull or calvarium. It evolved in response to
need for protection of the brain and is formed of the be different at different ages.
PEDODONTICS
intramembranous bone. – At birth: The head circumference is around 35 cm
–
– The chondrocranium forms the base of the skull, (13.75 Inches)
–
which ossifies as an endochondral bone. – Head shape is rounded but sometimes it may get
–
• The viscerocranium is formed by the bones of facial molded during parturition as over-riding of the
•
skeleton which develop by intramembranous ossification. parietal bone takes place when the head gets engaged
This is derived from the branchial arches. in the birth canal.
– Six Months: It increases to 44 cm
• Dimensional Changes in Craniofacial Skeleton
–
– A total four inches increase takes place (2 inches first
•
–
– These changes can be appreciated even in 4 months and then 2 inches next 8 months) By the
–
intrauterine life. end of the year head circumference becomes equal to
– Third month to birth: The entire cranium becomes trunk dimension and the trunk’s may even exceed.
–
longer and wider in its relation to height. – One year onwards:
–
– At birth: – Between one to two years 4 inches increase takes
–
–
– Craniofacial skeleton undergoes changes between place.
–
30% and 60% of its total growth. – At 10 years: 95% of total head growth completes with
–
Head makes up about a greater part of the total the width of the head completed by 3 years while the

body length whereas in the adult it accounts length of the head completes by 16-18 years.
for about one-eighth of the total body height.
This change reflects the early development and Fontanelles
attainment of the final size of the head compared
with the rest of the body. • They bridge the gap between the bones that limit
The remaining dimensional increase is not
•
them. They are made up of the dura mater, the primitive

equal in all parts of the cranium. periosteum and the aponeurosis from inside outwards.
– After birth:
• Fontanelles present at Birth: (AIPG 2007)
–
While the size of the cerebral cranium will
•

– Anterior Fontanelle, between two parietal bones

increase by about 50%, the facial skeleton will
–
grow to more than twice the original size. and the frontal bone
Cranial circumference is an indicator of – Posterior Fontanelle, between two parietal bone
–
and the occipital bone

cranial volume and therefore is often used in
young infants for a rough measure of brain – Sphenoid Fontanelle, between frontal parietal,
–
development. temporal and sphenoid bone
– By 4 years: This growth is almost completed. – Mastoid Fontanelle, between the parietal, occipital
–
and Frontal bone
–
Cranial Circumference increases by 33cm(at

birth) to 50 cm by 3 years of age after which it
• Clinical Importance of Fontanelle:
increases only by 6 cm.
•
– 4th year onwards : – Enables for the fetal skull to modify the size and shape
–
as it passes through the birth canal and permits rapid
–
Facial skeleton increases in all dimensions
growth of the brain during infancy.

during Post Natal growth period, the increase
in height being the greatest (approx 200%) – Helps the physician to gauge the degree of brain
–
development by the degree of their closure
Pedodontics 625

– Anterior Fontanelle serves as a landmark for Face
–
withdrawal of blood for analysis from the superior • At birth lower third and middle third of the face are
saggital sinus
•
underdeveloped due to absence of teeth.
– Depressed level of fonatanelle indicates dehydration
• The forehead is high and bulging
–
and increased level indicates increased intracranial
•
pressure • The face of the newborn baby is round and flat
•
• The eyes dominate due to the absence of the root of the
•
• Closure Time of Fontanelle nose, appear to be widely separated
•
– Anterior fontanelle (frontal): 18-24 Months after • After the onset of puberty forehead widens and flattens,
–
•
birth lips thicken and face acquires an oval shape, mainly due to
– Posterior fontanelle (occipital): 2 Months after the growth of the jaws.
–
birth] • The child’s convex facial profile is straightened out owing
– Anterolateral fontanelle (sphenoid): 3 months
•
to the more anterior position of the jaws ‘The development
–
PEDODONTICS
after birth (paired)
of chin prominence and deeper position of the eyes
– Posterolateralfontanelle (mastoid): Begins to
through growth of the orbital ridges and the ridge of the
–
close 1-2 months after birth, closed completely by
nose enhances this impression.
12 month (paired)
Nasomaxillary Complex
Cranial Synchondroses
• Cranial synchondroses play an important role in • The maxilla develops in the membranous tissue at the
•
end of the sixth fetal week.
•
craniofacial growth.
• Sphenoccipital closes by 18-20 years • The maxilla proper is a result of a highly complex
•
growth pattern with many different components.
•
– Sphenoethmoidal closed by 2-4 years; may persist and
• The maxilla is attached to the neurocranium directly
–
fuse later in adolescence, is of little Imporatance in
•
with the frontomaxillary sutures and indirectly by
postnatal growth
means of various other facial structures such as the
– Mid sphenoid closed shortly after birth
nasal, lacrimal and ethmoid bones, nasal septum
–
• Other synchondroses
including vomer, palatine bone and zygomatic arch.
•
– Intraoccipital • Most of the structures mentioned are joined together in
–
– Sphenopetrosal
•
an edge-to-edge fashion.
–
– Petrooccipital
• During the early phase of fetal development the sagittal
–
• Craniotabes or soft skull due to paper thin bones is
•
interrelation of the jaws is characterized by mandibular
•
palpable in premature infants.
protrusion, which is gradually reversed.
• Sutures of Cranium • At birth the maxilla is placed more anteriorly giving
•
class II relationship of the jaws.
•
– Coronal suture: Between the frontal and parietal
• Later, in the course of postnatal development both
–
bones. Closes: 24 years to 35 years of age
•
maxilla and mandible with their associated soft tissues
– Sagittal suture: Between two parietal bone Closes:
grow forward and downward and establish normal class
–
22 years to 30 years of age
I relationship.
– Lambdoidal suture: Between two parietal and
• Maxillary sinuses are not well developed at birth and
–
occipital bones
•
present like slits
– Starts to close around 29 years of age.
• Development of orbital cavities is practically complete
–
– Squamous sutures and lateral anteroposterior
•
at birth
–
sutures: between the squamous portion of the
temporal bone and the parietal bone. The squamous • Nasal cavity is located between the two orbits of the
•
sutures close late in life. eyes and its floor is roughly at level with their bottoms
– Squamous sutures and lateral anteroposterior • The alveolar process can only be faintly discerned and
•
–
sutures: between the squamous portion of temporal the palate has a weak transversal curvature
bone and the parietal bone. The squamous sutures • The maxillary body is almost entirely filled with
•
close later in life. developing deciduous teeth
626
Mandible
• Although still separated by symphysis in the middle the two halves of mandibular bone fuse into a single bone by the end
•
of 1-2 years.
• At birth: The two Rami are short
•
• Condylar development is minimal
•
• A thin line of fibrocartilage and connective tissue exisits in the midline of the symphysis to separate the right and left
•
mandibular bodies
• The symphysial cartilage is replaced by bone between 4 months and end of 1 year
•
• Age Changes in Mandible
•
– The body elongates especially behind the mental foramen providing space for permanent molars.
–
– The mental foramen changes direction from anterior to posterosuperior and then almost horizontally, accommodating
–
a changing direction of the emerging mental nerve. When teeth are present, the mental foramen is located midway
PEDODONTICS
between the upper and lower borders of the mandible.

– The angle of the mandible diminishes with age.
–
– During postnatal development, growth in mandibular width is completed; this is followed by growth it length, and
–
then in height. The growth in width in eluding the dental arches completes before the adolescent growth spurt.
Gum Pad (AIPG 2004)

• The alveolar arches of an infant are called Gumpads, which are firm and pink structures with definite form
•
• Each gumpad is divided into ten segments by transverse grooves. The groove between the deciduous canine and first molar
•
segments are prominent and called the lateral sulci.
The upper Gumpad: The lower Gumpad:
• It is a horseshoe shaped and shows: • Differs from the upper.
•
•
• Gingival groove: It is the groove separating the gumpad from • It is U- Shaped, with its anterior portion everted labially
•
•
the palate • It also shows the ginigival grove that demarcates the lingual
•
• Dental groove: It originates in the incisive papilla region and extent of the gumpads
•
extends backwards to touch the gingival groove in the canine • Dental groove running from the mandible backwards, laterally to
region and then laterally to end in the molar region
•
join the gingival groove in the canine region
• Lateral sulcus: It is a deepened groove separating the canine • Lateral sulcus: a deepened groove separating the canine and
•
and deciduous first molar segments.
•
deciduous first molar segments
• Relationships of the Gumpads

•
– At rest, the gumpads are separated by the tongue lying over the lower gumpad
–
– There is no definite antero-posterior relationship of the gumpads on occlusion, but the lower gumpad being smaller
–
lies distal to that of the upper.
– There is variable overjet with contact only in the first molar segment
–
• Growth of Gumpads
Good to Know
•
– At birth the width of the gumpads are inadequate to • End of first month enamel organs are developed from
–
accommodate all the incisors
•
dental lamina
– The growth of the gumpads is rapid in the first year
• Skull bones in a neonate are 45 (due to incomplete
–
after birth
•
ossification) and in adult 22
– Growth is more in the transverse direction and in the
• Mandible: the two halves of the mandible fuse into a
–
labiolingual direction
•
single bone by the age of 1-2 years
– Due to growth the segments of each segment become
• Buccal pad of fat is also known as adiposum or Bichats
–
prominent
•
fat pad
– Eruption of deciduous teeth commences at six months
• Full swallowing and sucking is established around 32-
–
of age
•
36 weeks IU life
Pedodontics 627

• Growth of eyes is completed by 5 years.
•
• Growth of brain is completed by 10 years.
•
• Growth of heart is completed by 20 years.
•
• “Growth spurt” is sudden increase in growth.
•
• Teeth develop from the epithelial primary germ cell
•
• In humans the odontogenic epithelium which is the analogue of dentitions, can be identified in 28-30 day embryo
•
• Mineralization commences in the deciduous teeth during the 14th intrauterine week on average and begins with the
•
central incisors
• Mineralization of the permanent teeth is initiated around the time of birth on average beginning with the first permanent
•
molar
• Eruption is derived from the latin word ‘erumpere’ i.e to break through.
PEDODONTICS
•
• The mean daily eruption velocity is seen to be 71 µm/day
•
• Eruption of primary dentition usually begins in the 5th or 6th month of a childs life
•
• The first sign of root resorption is seen in the deciduous mandibular incisors and the first molars by the age of 4-5 years
•
• Resorption of the deciduous incisors take place more rapidly (lasting 1.5-2 years on average) than the canines and molars
•
(2.5-5.7 years)
• Dental age has been used for centuries as a parameter for expressing biological maturity
•
• Dental age also plays a great role in forensic odontology and pediatric endocrinopathies
•
Craniosyntosis
Oxycephaly/acrocephaly/ • Type of cephalic disorder
turricephaly (AIIMS May 08,
•
• Described as the premature fusion of all sutures (AIPG 2009, 2007)
May 10, AIPG 2011)
•

• Most severe form of craniotosis
•
Brachycephaly • Premature closure of the coronal suture expands the skull parallel to the coronal suture
•
• Resulting in short A-P diameter of skull
•
• Occurs in
•
– Apert syndrome
–
– Carpenter syndrome (AIPG 2011,2009, 2007)
–

– Cleidocranialdysostosis
–
– Chromosomal abnormalities
–
Trigonocephaly • Premature fusion of metopic suture
•
• A V shaped abnormality occurs at the front of the skull
•
• Characterized by triangular prominence of the forehead and closely set eyes
•
Dolichocephaly/scapho- • With premature closure of saggittal suture, the skull grows perpendicular to open coronal suture and
cephaly
•
appears to expand A-P in the direction of sagittal suture
• Inherited as a familial trait
•
• Seen in Crouzen’s syndrome
•
Plagiocephaly • Seen in unilateral synostosis
•
628
Growth Spurts
The timings of growth spurts are different in girls and boys.
• Just before birth

• One year after birth
• Mixed dentition growth spurt

• Boys: 8 to 11 years
– Girls: 7 to 9 years
–
• Adolescent growth spurt
•
– Boys: 14 to 16 years
–
– Girls: 11 to 13 years
PEDODONTICS
Theories of Tooth Eruption

Theory Explanation
Root elongation theory According to this theory, the crowns are pushed into the oral cavity by
virtue of root elongation
Pulpal constriction theory Growth of root dentin and the subsequent constriction of the pulp may
cause sufficient pressure to move the tooth occlusally
Growth of periodontal tissues • Pull by surrounding connective tissue

•
• Alveolar growth might push or squeeze the tooth out of its alveolus
•
Pressure from muscular action • Berten suggested that action of musculature of cheeks and lips upon
•
the alveolar process might squeeze the crown out of its alveolus.
Other theories Include:

• Resorption of the alveolar crest
•
• Hormonal theory
•
• Foreign body theory
•
• Cellular proliferation theory
•
• Vascularity theory
•
• Blood vessel thrust theory
•
• Periodontal ligament contraction theory
•
• Dental follicle theory
•
• Bony remodeling theory
•
CHRONOLOGY OF TEETH
PRIMARY DENTITION
Maxilla
Central incisor 4 months in utero 4 months 7 ½ months
Lateral incisor 4 ½ months in utero 5 months 9 months
Pedodontics 629

Canine 5 months in utero 9 months 18 months
1st molar 5 months in utero 6 months 14 months
2nd molar 6 months in utero 11 months 24 months
Mandible
Central incisor 4 ½ months in utero 4 ½ months 6 months
Lateral incisor 4 ½ months in utero 4 months 7 months
Canine 5 months in utero 9 months 16 months
PEDODONTICS
1st molar 5 months in utero 5 ½ months 12 months
2nd molar 6 months in utero 10 months 20 months
PERMANENT DENTITION
Maxilla
Central incisor 3-4 months 4-5 years 7-8 years
Lateral incisor 10-12 months 4-5 years 8-9 years
Canine 4-5 months 6-7 years 11-12 years
1st premolar 1 ½ - 1 ¾ years 5-6 years 10-11 years
2 premolar
nd
2 – 2 ¼ years 6-7 years 10-12 years
1st Molar Birth 2 ½ - 3 years 6-7 years
2nd Molar 2 ½ - 3 years 7-8 years 12-15 years
3rd Molar 7-9 years 12-16 years 17-24 years
Mandible
Central incisor 3-4 months 4-5 years 6-7 years
Lateral incisor 3-4 months 4-5 years 7-8 years
Canine 4-5 months 6-7 years 9-10 years
1st premolar 1 ½ - 2 years 5-6 years 10-11 years
2nd premolar 2 ¼ - 2 ½ years 6-7 years 11-12 years
1st Molar Birth 2 ½ - 3 years 6-7 years
2nd Molar 2 ½ - 3 years 7-8 years 11-13 years
3rd Molar 8-10 years 12-16 years 17-21 years
630
THEORIES OF CHILD PSYCHOLOGY
• Psychodynamic theories:
•
– Psychosexual theory by Freud
–
– Psychosocial theory by Eric Erikson
–
– Cognitive theory by Piaget
–
• Behavior learning theories
•
– Classical conditioning theory by Ivan Pavlov
–
– Operant conditioning theory by BF Skinner
–
– Social learning theory by Albert Bandura
–
– Hierarchy of needs by Maslow
–
Psychosexual Theory
PEDODONTICS
Freuds stages of psychosexual development

Stage Characterstics associated with fixation

Oral (birth to age2) Display many activities centredaround the mouth (excessive eating,

drinking, smoking, talking
Oral Eroticism Sucking and eating predominate, cheerful, dependent and needy, expects to be

taken care of by others
Oral Sadism Biting and chewing predominate, tends to be cynical and cruel

Anal (ages 2 to 4)

Anal retentive Excessively neat clean meticulous and obsessive

Anal expulsive Moody, sarcastic, biting and often aggressive, untidy in personal habits

Phallic (age 4 to middle childhood) Overly preoccupied with self, often vain and
arrogant, unrealistic level of self confidence and self absorption (AIPG 2005)

Latency (middle childhood) Demonstrates sexual sublimation and repression

Genital (Adoloscence through Traditional sex roles and heterosexual orientation

adulthood

Psychosocial Theory
Stage Approximate Positive outcomes Negative outcomes
age
• Trust vs Mistrust Birth – 11/2 years Feelings of trust from environment support Fear and concern regarding others
•
• Autonomy vs Shame and 1 1/12 – 3 years Self sufficiency if exploration is encouraged. Doubts about self lack of independence
•
doubt
• Initative vs Guilt 3-6 years Discovery of ways to initiate actions Guilt from actions and thoughts
•
• Industry vs Inferiority 6 – 12 years Development of sense of competence Feelings to identify appropriate roles
•
in life
• Intimacy vs Isolation Early adulthood Development of loving, sexual relationships Fear of relationships with others
•
and same sex friendships
• Generativity vs Stagnation Middle adulthood Sense of contribution to continuity of life Trivalization of one’s activities
•
• Ego integrity vs Despair Late adulthood Sense of unity in life’s accomplishments Regret over lost opportunities of life.
•
Pedodontics 631

PEDODONTICS
Fig16.4: Psychosocial theory
Theory of Cognitive Development

• Piaget’s marked four stages of cognitive growth each characterized by a different type of thinking and in each child relies
•
more upon internal stimuli.
– Sensorimotor period (birth to 2 years)
–
– Pre operational period (2 to 7 years)
–
Pre conceptual period (2 to 4 years)

Intuitive stage (4 to 7 years)

– Concrete operational period (7 to 11 years)
–
– Formal operational period (beyond 11 years)
–
Effect of Maternal Behaviour
• Bayley and Schaefer summarized the maternal attitude as:
•
Maternal behaviour Features Child’s behaviour
Overprotective • Mother gives excessive care for the child in terms Submissive, shy , anxious
•
of feeding, dressing, bathing and these conditions
continue past the usual age.
• Constantly involved with child’s daily social
•
activities and may not allow him to participate in
risk involving games.
• Excessive concern about the routine dental
•
conditions
• Infantizes the child, retards normal psychological
•
maturation
• Aggravates child demanding and expects constant
•
attention and service.
• Displays temper tantrums.
•
632
Maternal behaviour Features Child’s behaviour
Overindulgence • May be associated with overprotective or Aggressive, spoilt, demanding, shows temper
•
dominant natural trait. tantrums
• These parents give whatever the child demands
•
as far as financially possible.
• Relatively grandparents are over indulgent.
•
• Such child is spoiled and accustomed to get his
•
own way.
• His emotional development is impeded, keeping
•
him in infantile dependent state.
• He is usually incapable of amusing himself and
•
he keeps the adults around him busy.
PEDODONTICS
Under affectionate • May vary from mild detachments or indifferent to Usually well behaved, but may be unable to
•
neglect. cooperate, may cry easily.
• Mother becomes less emotionally supportive of
•
her child due to outside interests, empolyment, or
because the child is unwanted.
• Child is well behaved and appears to be well
•
adjusted.
• They are unsure of decision making capacity.
•
• Since they have not experienced love and
•
affection at home, emotional contact with is
difficult.
• They respond well to a dentist who gives them
•
affection and emotional support.
Rejecting • Acceptance vs rejection is one of the most Aggressive, overactive, disobedient

•
significant of family influences
• Maternal rejection may arrive under any
•
circumstance to which a child is unwanted.
• Rejection is usually overt
•
• Mother behaviour is characterised by neglect
•
of the child, severe punishment, nagging, and
resistant to spending time and money on the
child.
• He may show extreme anxiety and be aggressive,
•
overactive and disobedient.
• He will resort to any behaviour to gain attention.
•
• Abuse and neglect can be both physical and
•
emotional.
Authoritave • The authoritarian parent chooses technique for Evasive

•
controlling child behaviour that may be termed as
non love oriented.
• Discipline often takes the form of physical
•
punishment or verbal ridicule.
• The authoritarian mother will insist the child
•
conform to her set of norms and will expend
much effort to train the child on those lines.
• The authoritarian mother is usually the product of
•
an authoritarian upbringing.
• Child is submissive, coupled with resentment and
•
evasion.
Pedodontics 633

CHILD BEHAVIOUR IN DENTAL OFFICE
Type Rating Symbol Features

Definitely negative R a t i n g (-) • Refuses treatment
•
no. 1 – Immature behaviour: Cannot reason or cope with the situation, eg toddler, special
–
child
– Uncontrolled behaviour: Temper tantrums suggestive of extreme anxiety, eg pre-
–
schooler
– Defiant behaviour: Exhibits resistance eg spoiled, stubborn
–
• Cries forcefully: Uncontrolled behaviour eg late pre schooler or 5 years old child
•
• Extreme negative behaviour assocaited with fear
•
– Uncontrolled behaviour: Exhibited in older children with deep rooted emotional
–
problems
––
Defiant behaviour: Includes passive resistance in the individual approaching ad-
olscence
PEDODONTICS
Negative R a t i n g (-) • Reluctant to accept treatment
•
no 2 – Immature behaviour: Toddlers or pre schoolers
–
– Timid behaviour: Seen in children, who are over protected, exposed to few people
–
or dominated by strange environment.
– Influenced behaviour: Includes family and peer pressure
–
• Displays evidence of slight negativity
•
– Timid behaviour
–
– Whining behaviour
–
Positive R a t i n g (+) Accepts treatment
no 3 • Tense cooperative behaviour: Observed in all stages, follows dentists’s direction but
•
may be resistant and cautious
• Conservative behaviour: Responds harmoniously
•
• Timid behaviour: Follow dentist direction in a shy, quite manner. Can become
•
uncooperative due to any bad experience during treatment.
Definitely positive R a t i n g (++) Unique behaviour: Looks forward to understand the important preventive care and
no 4 establishes a good rapport.
Lampshire’s Classification
Cooperative Children who remain physically and emotionally relaxed and cooperative throughout the entire treatment
regardless of the treatment undertaken.
Tense cooperative Children who are tense but nevertheless cooperative
Outwardly apprehensive Child who hides behind the mother in the waiting room. Uses stalling techniques and avoids the dentists. These
patients will eventually accept the dental treatment
Fearful Children who require considerable support in order to overcome their fear of dental situation.
Stubborn/Defiant Children who passively resist or try to avoid treatment by using techniques that have been successful in other
situation
Hypermotive Children who are agitated and who adopt procedures such as screaming or kicking as defense mechanism
Handicapped Children who are physically, mentally or emotionally handicapped
Emotionally immature This category includes the young children who have not yet achieved sufficient emotional maturity to rationalize
the need for dental treatment and to cope with it.
634
Wright’s clinical classification places children in three categories”:

• Cooperative
•
• Lacking in cooperative ability
•
• Potentially cooperative
•
Classification of Behaviour Management Techniques
Psychological approach • Classical conditioning
•
– Desensitization
–
– Tell show do
–
– Voice control
–
– Verbal/non verbal communication
PEDODONTICS
–
– Distraction
–
• Operant conditioning
•
– Positive reinforcement
–
– Response extinction
–
– Behavior shaping
–
– Contingent reward management
–
– Hand over mouth exercise
–
• Observational learning
•
– Modeling
–
– Coping
–
– Audiovisual modelling
–
– Pre appointment behavior modification
–
– Hypnosis
–
Physical approach • Hand over mouth
•
• Physical restraints
•
Pharmacological • Premedication
•
• Conscious sedation
•
• General anaesthesia
•
HOME
• Introduced by Evangeline Jordan in 1920
•
• Purpose: to gain attention of the child to establish communication
•
• Indication
•
– Healthy child who can understand simple verbal commands
–
– 3-6 years old
–
• Contraindications
•
– Child below 3 years of age
–
– Physically or mentally handicapped child
–
• Technique
•
– After determining the child’s behavior, the dentist firmly places his/her hand over the child’s mouth. And expected
–
behavior is explained to the child. When the child calms down and agrees to cooperate, hand is removed and
procedure is continued
– Child’s airway should not be restricted during the procedure
–
– It should not last more than 20-30 seconds
–
Pedodontics 635

Desensitization Behavior Shaping
Used for children with preexisting fears or phobias, this The aim of this is to guide and modify the child’s responses,
involves helping the patient to relax in the dental environment, selectively reinforcing appropriate behavior, while
then constructing a hierarchy of fearful stimuli for that patient. discouraging/ignoring inappropriate behavior.
These are introduced to the child gradually, with progression Reinforcement is the strengthening of patterns of behavior,
to the next stimulus only when the child is able to cope with usually by rewarding good behavior with approval and praise,
the previous situation. If a child protests and is uncooperative during treatment, do
Modeling is useful for children with little previous dental not immediately abandon the session and return them to
experience who are apprehensive. Encourage the child to the consolation of their parent, as this could inadvertently
watch other children of similar age or siblings receiving dental reinforce the undesirable behavior, it is better to try and ensure
treatment happily. that some phase of the treatment is completed, e.g., placing a
dressing.
PEDODONTICS
Communication
Special terminology may be used for communication with the child patient like.
Slow-speed handpiece Mr Buzz/buzzy bee/bumble bee
High-speed handpiece Mr Spray/wizzy brush/tooth tickler
Handpiece and prophylaxis cup Electric toothbrush/tooth polisher
Aspirator tip Vacuum cleaner/Hoover
Rubber dam Tooth raincoat
Saliva ejector Straw
Air from 3-in-l Curly-wurly (coiled type only)
Wind
Fissure sealant Plastic coating
Etchant solution Tooth shampoo/cleaner
Lemon juice
Cotton roll Snowman
Dental light The sun/car light
Sedation
Sedation Inhalation Hypnosis General anaesthesia
Indicated for the genuinely A nitrous oxide/oxygen Hypnosis produces a state of Used only when absolutely necessary.
anxious child who wishes to mixture is used to produce altered consciousness and Alternative methods of management,
cooperate with treatment. relative analgesia (RA) relaxation, though it cannot strategies and the risks of GA must be
Oral Drugs such as and is the most popular be used to make subjects do discussed to enable parents to make an
midazolam and chloral technique for use with anything they do not wish to do. informed decision.
hydrate can be used, although children. It is effective
specialized knowledge and for reducing anxiety and
skills are required. increasing tolerance of
invasive procedures in
children who wish to
cooperate but are too
anxious to do so without
help.
636
Risks
• The risk of unexpected death of a healthy person
•
– Under GA has been estimated to be about 3 in 1 million.
–
– Under sedation has been estimated to be about 1 in 2 million
–
Choice of Anesthetic Agent
• First choice: Lidocaine 2% with 1:100,000 epinephrine.
•
• Second choice: Prilocaine 4% with 1:200,000—gives less profound anesthesia
•
RADIOGRAPHS IN PEDODONTICS
PEDODONTICS
• Size 0 is used for bitewing and periapical radiographs of small children.

•
• Panoramic radiography is used in the evaluation of traumatic injuries and dental age examination as it gives good information
•
about the eruption status of the teeth.
• Sialography is contraindicated in acute infection of the salivary glands
•
• TACT (Tuned aperture computed tomography) is used for the diagnosis of the external root resorption
•
Recommended Radiographic Examination of Children and Adolescents
• The following are types of radiographic surveys for use in a child patient
•
– Four-film survey: This series consists of maxillary and mandibular occlusal radiographs and 2 posterior bitewing
–
radiographs.
– Eight-film survey: This survey includes:
–
Maxillary and mandibular anterior occlusal graphs

4 molar periapical radiographs

2 posterior bitewing radiographs

Twelve-Film Survey

Maxillary and mandibular permanent incisors periapical radiographs

4 Primary canine periapical radiographs

HABITS
• Classification
•
– Non pressure habits
–
Mouth breathing

– Pressure habits
–
Sucking habit

- Lip sucking

- Thumb and digit sucking

Biting habit

- Nail biting

Postural

- Pillow rest

- Chin rest

Miscellaneous

- Bruxism

Pedodontics 637

Tongue Thrusting
James S Brauer and Townsend V Holt Classification of Tongue
Thrusting
Type 1 Type 2 Type 3 Type 4

Non-deforming Tongue thrust Deforming Anterior Tongue Deforming lateral tongue Deforming Anterior and lateral tongue
thrust thrust thrust
Subgroup 1: Anterior open Subgroup 1: Posterior open Subgroup 1: Anterior and Posterior
bite bite open bite
Subgroup 2: Associated Subgroup 2: Posterior cross Subgroup 2: Associated procumbency
procumbency of anterior teeth bite of anterior teeth
Subgroup 3: Associated Subgroup 3: Deep overbite Subgroup 3: Associated posterior
Posterior cross bite cross-bite
PEDODONTICS
Moyer’s classification of swallowing patterns
Type Inference
Normal infantile swallow During this swallow the tongue lies between the gum pads and mandible is
stabilized by contraction of facial muscles especially buccinators. This type
of pattern disappears on eruption of the buccal teeth of primary dentition.
Transitional swallow Intermixing of normal infantile swallow and mature swallow during primary
dentition and early mixed dentition period.
Normal mature swallow During this swallow there is very little lip and cheek activity. Mainly there is
contraction of mandibular elevators.
Simple tongue thrust swallow During this swallow there is contraction of lips, mentalis muscle and
mandibular elevators. Tongue protrudes into an open bite that has a definite
beginning and ending.
Complex tongue thrust swallow This is characteristically known as teeth apart swallow. There are marked
contraction of the lip, facial and mentalis muscles but absence of temporal
muscle contraction during swallow. Anterior open bite is also present.
Classification of Space Maintainers

According to Hitchcock According to Raymond C. Thurrow
• Removable or fixed or semi fixed • Removable
•
•
• With bands or without bands • Complete arch lingual arch and extraoral anchorage
•
•
• Functional or non functional • Individual tooth
•
•
• Active or passive
•
• Certain combinations of above
•
Distal Shoe Space Maintainer
• Advocated by Roche (AIPG 2006)
•

• Used to guide the eruption of first molar when primary second molar ha been extracted
•
• Has a distal gingival extension which must lie 1 -1.5 mm below the mesial marginal ridge of first permanent molar
•
• Distal loop which carries the gingival extension is made of 0.04 inch SS wire
•
638
Band and Loop Space Maintainers abutment tooth is intact and in the posterior segment
when single tooth is lost.
• The band and loop is a unilateral fixed appliance, indicated
• Because the loop has limited strength, this appliance must
•
tor space maintenance in the posterior segments.
•
• The simple cantilever design makes it ideal far isolated be restricted to holding the space of one tooth and is not
expected to accept functional forces of chewing
•
unilateral space maintenance. This is only indicated with
cases in period of space maintenance is short and the • Fixed, non-functional, passive space maintainer.
•
Indications: (AIIMS Nov 2013) Contraindications: Disadvantages:
• Premature loss of first deciduous • Extreme crowding and space loss • Space loss of more than one tooth
•
•
•
molars •
•
High caries activity • Non-functional
•
• When the unerupted molar is 2 yrs • Gingival slipping of loop
•
from its clinical eruption and root
•
length is less than half
PEDODONTICS
ANATOMY OF PRIMARY TEETH (WITH self-cleansing. Isthmus should not extend >1/2 intercuspal
RELEVANCE TO CAVITY DESIGN) distance. (AIPG 2005)

• Bulbous crown: Primary molars have a more bulbous
•
Primary teeth differ in several respects from permanent crown form than permanent molars, making matrix
teeth, affecting both the sequelae of dental disease and its placement more difficult.
management. • Inclination of the enamel prisms: In the cervical 1/3
•
• Thinner enamel: Enamel in primary teeth is approximately of primary molars the enamel prisms are inclined in an
•
1 mm thick, which is 1/2 that of permanent teeth. occlusal direction so there is no need to bevel the gingival
• Larger pulp horns: The pulp chamber in primary teeth floor of a proximal box.
• Cervical constriction: Is more marked in primary
•
is proportionately larger, with more accentuated pulp
•
mesiobuccal, distobuccal, and palatal. Mandibular molars, so if the base of the proximal box is extended too
first and second primary molars—four pulp horns far gingivally it will be difficult to cut an adequate floor
mesiobuccal, mesiolingual, distobuccal, and distolingual. without encroaching on the pulp.
These features mean that caries will affect the pulp sooner • Alveolar bone permeability is increased in younger
•
and there is a greater likelihood of pulp exposure during children, thus it is usually possible to achieve LA of
cavity preparation. Aim for 0.5-1.0 mm penetration of primary mandibular molars by infiltration alone, up to 6
dentin only. years of age.
• Pulpal outline: Follows the dentinoenamel junction more • Thin pulpal floor and accessory canals may explain the
•
greater incidence of interradicular involvement following
•
closely in primary teeth, therefore the cavity floor should
follow the external contour of the tooth to avoid exposure. pulp death,
• Root form Primary molars have proportionately longer
• Narrower occlusal table: Greater convergence of the
•
roots than their permanent counterparts. They are also
•
buccal and lingual walls results in a proportionately
more flared to straddle the developing premolar tooth.
narrower occlusal table. This is more pronounced in the
The roots are flattened mesiodistally, as are canals within.
first primary molar than second primary molar. Therefore,
overextension of an occlusal cavity or lock can lead to • Radicular pulp: Follows a tortuous and branching path,
•
making complete cleansing and preparation of the root
weakening of the cusps. (AIPG 2001)
canal system almost impossible, although instrumenting

• Broad contact points: Make detection of interproximal canals is often easier than suggested. In addition, as the
•
caries more difficult, and means that in primary molars roots resorb, a different approach to RCT is needed for
divergence of the buccal and lingual walls toward the the 1° dentition, pure zinc oxide and eugenol being the
proximal surface is necessary to ensure cavity margins are obturation material of choice.
Extraction Versus Restoration of Primary Teeth

• Age- the earlier the tooth is lost the greater the potential for space loss).
•
• Medical history
•
• Motivation and cooperation of parents
•
Pedodontics 639

• Caries rate in a child
•
• Pain
•
• Extent of lesion(s) in primary molars
•
• Position of tooth
•
• Presence/absence of permanent successor
•
• Malocclusion
•
EARLY CHILDHOOD CARIES
Terminologies used for ECC
• Tooth Clearing neglect: Moss (1966)
•
• Infant and early childhood dental decay: Horowitz (1998)
PEDODONTICS
•
• ECC: Davies (1998)
•
• MDSMD: Maternally derived streptococcus Mutans disease
•
Developmental Stages of ECC
Stage Clinical Stage Age Features
Stage I Initial reversible stage 10-18 Months Cervically and occasionally interproximal areas of chalky white demineralization
Stage II Damaged carious 18-24 months Lesion in maxillary anterior teeth may spread to dentin and show yellowish brown
stage discolouration
Stage III Deep lesion 24-36 months Depending on the time of eruption,cariogenicity sweetener and frequency of its use, this
stage can be reached in 10-14 months also
Molars are also affected
Frequent complaint of pain
Pulpal involvement in Maxillary incisors
Stage IV Traumatic Stage 36-48 months Teeth become so weakened by caries that small forces can fracture them
Parents may report a history of trauma
Molars are now associated with pulpal problem
Maxillary incisors become Non vital
Comparison of Caridex and Carisolv

Caridex Carisolv
Solution 1 1% NaOCl 0.5% NaOCl
Solution 2 0.1 M Aminobutyric acid glycine 0.1 M glutamic acid/ leucine/ lysine
0.1 M NaCl NaCl, NaOH
0.1 M NaOH
Dye ----- Erythrocin (pink)

pH 11 11
Physical Properties Liquid Gel
Volume needed 100 – 500 ml 0.2 – 1.0 ml
Time required 5-15 min 5-15 min
Equipment required Applicator unit None
Instruments Applicator tips Specially designed tips
Time Preparation remains active after mixing 1 hour 20 mins
640
Good to Know
• Nursing caries: Winter (1966)
•
• Nursing bottle mouth: Kroll (1967)
•
• Nursing bottle syndrome: Shelton (1977)
•
• Night bottle syndrome: Dilley (1980)
•
• Nursing bottle caries: Tsmtasorius (1986)1
•
• Baby bottle tooth decay: Min Kelly (1987)]
•
• Milk bottle syndrome: Ripa (1988)
•
PIT AND FISSURE SEALANTS AIPG 2003
PEDODONTICS
• 5 types of pits and fissures according to Nugano, 1961:

•
– V type (34%)
–
– U type (14%)
–
– I type (19%)
–
– Ik type (26%)
–
– Inverted Y type (7%)
–
• Histopathology
•
Types of Pit and Fissure Sealants
According to the chemical • MMA: Methyl methacrylate
•
structures of monomers used • TEGDM: Tri ethylene glycol dimethacrylate
•
• BPD: Bis phenol dimethacrylate
•
• Bis GMA: Reaction product of Bis phenol A and glycidyl methacrylate with a methyl methacrylate
•
monomer.
• ESPE monomer
•
• PMU: Propyl methacrylate urethane
•
Based on generations • First generation sealants: Polymerized with UV light with wavelength of 356 microns but had
•
excessive absorption and incomplete polymerization of sealant at its depth, eg Nuva lite (Caulk/
Dentsply)
• Second generation: Self cure or chemical cure resins based on accelerator catalyst system eg
•
Concise White (3M)
• Third generation sealants: Light cured with visible (blue) light of 430 – 490 microns eg Helioseal
•
• Fourth generation: Fluoride releasing sealants, eg Seal right (Pulpdent)
•
Pedodontics 641

Based on filler content: • Unfilled: Advantages include better flow and retention, but abrade easily
•
• Filled: Advantages include resistance to wear but may require occlusal adjustments
•
Based on colour • Clear: Esthetic but, difficult to detect in recall visit, eg Helioseal changes from green to white
•
• Tinted/Opaque: can be identified
•
• Coloured: Easy to see during placement and recall, eg Clinpro pink
•
Based on curing- • Autopolymerization
•
• •
Light cure
Based on ADA seal of acceptance • Alpha fluor seal II

•
• Alpha dent chemi cure
•
• Alpha dent light cure
•
• Concise light cure white cement
•
• Helioseal
PEDODONTICS
•
• Primashield
•
Properties of Pit and Fissure Sealants (NEET 2013)
Property Ideal Self cured Light cured (unfilled)
Penetration High Medium Low high
Working time Medium Short medium Medium long
Setting time Short Medium On demand

Water sorption Low High High
Thermal expansion Low High High
Wear resistance High Low Low
Ratings 100% 53% 62%
Types of Etching Patterns – (Silverstone 1975)

Type 1 There is a generalized roughening of enamel surface but with a distinct
hollowing of prism centres and relatively intact peripheral regions
Type 2 Prism peripheries appear to be damaged. Prism cores are left projecting
toward original enamel surface
Type 3 Show neither type 1 nor type 2 etching pattern but appear as generalized
surface roughening.
PULP CAPPING
Histological changes after pulp capping

• After 24 hours: Necrotic zone adjacent to Ca(OH)2 paste is separated from healthy pulp tissue by a deep staining
•
basophilic layer
• After 7 days: Increase in cellular and fibroblastic activity
•
• After 14 days: Partly calcified fibrous tissue lined by odontoblastic cells is seen below the calcium proteinate zone,
•
disappearance of necrotic zone
• After 28 years: zone of new dentin
•
642
Medications and Materials used for Pulp Capping
• Ca(OH)2: • Stimulation of reparative dentin bridge, due to a high alkalinity, which leads to enzyme
•
•
phosphatase being activated and thus releasing of inorganic phosphate from the blood (calcium
phosphate) leading to the formation of dentinal bridge.
• Also has an antibacterial action.
•
• Corticosteroids and antibiotics • Include neomysin and hydrocortisone, ledermix (Ca(OH)2 and prednisolone), penicillin or
•
•
vancomycin with Ca(OH)2.
• Inert materials: • Isobutyl cyanoacrylate and tricalcium phosphate ceramic

•
•
• Collagen fibres: • Collagen fibres influence mneralization and are less irritant than Ca(OH)2 with dentin bridge
•
•
formation in 8 weeks
PEDODONTICS
• META adhesive • The main advantage of 4 META adhesive is that it can soak into the pulp, polymerise there and
•
•
form a hybrid layer with the pulp thereby providing adequate sealing.
• Direct bonding: • Recent advances in Total etch direct bonding have evoked an interest in application for pulp
•
•
therapy.
• The advantage is that the a polygenic film can be layered over an exposure site without
•
displacing pulp tissue and onto surrounding dentin where it penetrates the tubules.
• Isobutyl cyanoacrylate: • Hemostatic agent

•
•
• Reparative dentin bridge stimulator
•
• The disadvantage of this material is that it is cytotoxic when freshly polymerized.
•
• Laser: • Andreas Meritz in 1998 evaluated the effect of laser on direct pulp capping and reported success
•
•
rate of 89%
Mineral Trioxide Aggregate (MTA): (AIPG 2004)

– Primarily of fine hydrophilic particles of tricalcium aluminate, tricalcium silicate, silicate oxide, tricalcium oxide and
–
bismuth oxide is added for radio opacity.
– Properties
–
It is biocompatible material and its sealing ability is better than that of amalgam or ZOE.

Initial pH is 10.2 and set pH is 12.5

The setting time of cement is 4 hours

The compressive strength is 70 MPA, which comparable with that of IRM.

Low cytotoxicity: It presents with minimum; inflammation if extended beyond the apex.

– Action
–
It has ability to stimulate cytokine and interleukins release from bone cells, indicating that it actively promotes

hard tissue formation.
• Bone morphogenic protien (BMP): Urist discovered BMP in 1965. He observed that demineralized bone matrix could
•
stimulate new bone formation when implanted to ectopic sites such as muscles. He also observed that demineralized dentin
also had inductive properties and it forms both bone and dentine.
– The implications for pulp therapy are immense as it is capable of inducing reparative dentin.
–
– They concluded that recombinant human osteogenic protein-1 in a collagen carrier matrix appeared to the suitable as
–
bioactive capping agent for surgically exposed dental pulp.
Pedodontics 643

Pulpotomy
Vital Pulpotomy
Types Other Names Features Examples
Devitalization Mummification It is intended to destroy or mummify the vital Single sitting

Cauterization tissue – Formocresol
–
– Electrosurgery
–
– Laser
–
Two Sitting
– GysiTriopaste
–
– Easlick’s Formaldehyde
–
– Paraform devitalizing paste
–
Preservation Minimal devitalizing, The implies maintaining the maximum vital – ZnOEugenol
–
Noninductive tissue, with no induction of reparative dentin – Glutaraldehyde
PEDODONTICS
–
– Ferric Sulphate
–
Regeneration Inductive, reparative This has formation of dentin bridge Ca(OH)2
Bone Morphogenetic protein
Mineral Trioxide aggregate
Enriched collagen
Freeze dried Bone
Osteogenic Protein
Formocresol Pulpotomy (AIPG 2001)

• Formocresol was introduced by Buckley in 1904 and since then a lot of modifications have been tried and then a lot of
•
modifications have been tried and advocated regarding the techniques of formocresol pulpotomies
• Sweet (1930): Formulated multi visit technique
•
• Doyle (1962): Advocated 2 sitting procedure (complete devitalization)
•
• Spedding (1965): Gave 5 minute protocol (partial devitalization)
•
• Venham (1967): Proposed 15 seconds procedure
•
• Current concept uses 4 minutes of application time
•
• Composition of Formocresol (Buckleys Formula)
•
– Cresol: 35% Glycerol -15% Formaldehyde -19% Water - 31%
–
– Cvek in 1978: Partial pulpotomy technique (AIPG 2006)
–

Materials used for visit pulpotomy
Gysi Triopaste Easlick’s Paraformaldehyde Paste Paraform
Tricresol Paraformaldehyde Paraformaldehyde
Cresol Procaine Base Lignocaine
Glycerin Powdered Asbestos Propylene Glycol

Paraformaldehyde Petroleum Jelly Carbowax
ZOE Carmine to colour
OBTURATION TECHNIQUES
Method Features
Endodontic pressure syringe • Developed by Greenberg and the technique was described by Spedding and Krakow in 1965. This
•
apparatus consists of a syringe barrel, threaded plunger, wrench and threaded needle.
644
Mechanical syringe • Greenberg proposed this method in 1971.
•
Tuberculin syringe • Syringe utilized by Aylord and Johnson in 1987 was a standard 26gauge, 3/8th inch needle.
•
Jiffy tubes • Material was expressed into the canal by slow finger pressure on the plunger until the canal was visibly
•
filled at the orifice. This technique was popularized by Rifficin in 1980
Incremental filling technique • First used by Gould in 1972

•
• •
Endodontic plunger corresponding to the size of canal with rubber stop is used to place a thick mix of
cement into the canal.
• Thick mix was prepared into a flame shape corresponding to size and shape of the canal and then
•
tapped gently into the apical area with the help of plugger.
Lentulospiral technique • Advocated by Kopel in 1970

•
• Lentulospiral was dipped into the mixture and then introduced into the canal to its predetermined
•
length and rotated in the canal. Additional amount of paste is added into the canal, till it is filled.
PEDODONTICS
Other techniques • Amalgam plugger by Nosonwitz (1960) and King (1984)

•
• Paper points by pedding (1973)
•
• Plugging action and wet cotton pellet by Donnenberg (19174)
•
Materials For Obturation
• Zinc oxide eugenol
•
• Calcium hydroxide
•
• Iodoform
•
• Vitapex
•
• Walkhoff paste
•
• KRI paste (AIPG 2004)
•

• Maisto paste
•
• Mineral Trioxide aggregate
•
• Endoflas
•
STAINLESS STEEL CROWNS
• First used by Hamphrey who called them chrome steel crown
•
• Used most often to restore carious primary first molar
•
• Uniform reduction of about 1 mm is done on all surfaces as tooth preparation. The margin of crown should end 0.5 -1mm
•
below gingival margin
• If the tooth to be restored is larger than the largest crown, 0.004inch SS band may be welded to the crown
•
• Indications
•
– As restoration for primary or young permanent tooth with extensive caries
–
– Hypoplastic primary or permanent teeth that cannot be restored with composite
–
– Teeth with hereditary anomaly such as dentinogenesis imperfecta or amelogenesis imperfecta
–
– After pulpotomy
–
– As an attachment for habit breaking appliances
–
– Fractured teeth
–
– For 1st primary molar when used as abutment for distal extension appliances
–
• Contraindications (AIPG 2006)
•

– Uncooperative child
–
Pedodontics 645

Classification of Stainless Steel Crowns
According to trim- • Untrimmed crowns:
ming
•
– These crowns are not trimmed nor contoured and require lot of adaptation, thus are time consuming. E.g.
–
Rocky mountain
• Pretrimmed crowns
•
– These crowns have straight, non contoured sides but are festooned to follow at line parallel to the gingival
–
crest. They still require contouring and some trimming. E.g. Unitek
• Precontoured crowns:
•
– These crowns are festooned and are also pre contoured though a minimal amount of festooning and trim-
–
ming may be required. E.g. 3M
According to com- • Stainless steel crowns–3M

position
•
• Nickel chromium crowns–Iconel
•
According to com-
PEDODONTICS
• Rocky mountain
pany names
•
• Unitek
•
• 3M
•
• Iconel
•
According to oc- • Ion: Compact occlusal anatomy
clusal anatomy
•
• Unitek: Best occlusal anatomy
•
• Rocky mountain: Occusally small
•
• Ormco: Smallest and least occlusally carved.
•
RECENT TRENDS IN PAIN CONTROL
Safety Syringes
– They minimize the risk of accidental needle stick injury occurring with contaminated needle
–
– They possess a sheath that locks over the needle when it is removed from patient’s tissues.
–
– Advantages include disposable, single use, sterile until opened and light weight.
–
– Disadvantages are more costly and may be different to use for first timers.
–
Computer Controlled Local Anesthetic Delivery System
• Introduced in dentistry in 1997
•
• Also called as the WAND system
•
• Single use disposable safety handpiece
•
• Luer-lok needle
•
• Pen like grasp allows operator to rotate handpiece during penetration and insertion.
•
• This system administers local anesthetic solution at 2 specific rates
•
– Slow rate 0.5ml/min
–
– Fast rate 1.8 ml/mi
–
• Advantages are precise control of flow rate and pressure, increased tactile sensation, non-threatening, automatic aspiration.
•
• Disadvantages are that it requires additional armamentarium and is costly
•
Comfort Control Syringe
• Introduced after WAND
•
• Electronic pre programmed delivery device
•
• Local anaesthetic is deposited more slowly and consistently.
•
• Consists of a 2 stage delivery system
•
– Injection begins at an extremely slow rate to prevent pain associated with quick delivery.
–
– After 10 seconds, comfort control syringe automatically increases speed to the pre programmed rate.
–
• Local anaesthetic with new additive
•
– Like centribucridine, Ropivacaine, Tetrodotoxin
–
646
EMLA: Eutectic Mixture of Local Anesthetic

• It is oil in water emulsion in which the oil phase is a eutectic mixture of lidocaine and prilocaine in a ratio of 1:1 by weight.
•
• Consists of a 5% cream containing 25mg/g of lidocaine and 25mg/g of prilocaine
•
• Should be applied 1 hour before procedure and the cream is covered with an occlusive dressing.
•
• Numbing occurs 1 hr after application and lasts for 1-2 hrs after removal. its use is contraindicated in infants under 6 months of age
•
because of the possibility of a metabolite of prilocaine inducing methemoglobinemia and in patients with known sensitivity to amides
• Adverse responses – transient and mild skin blanching and erythema.
•
Electronic Dental Anesthesia
• Provides pain control for administration of LA
•
• It provides excellent soft tissue anesthesia
•
• Aids in reversing local anesthetic effect. EDA when applied at its low frequency setting for a period of 10-15 minutes removes a large
•
volume of residual anaesthetic solution and thereby partially/totally reverses the anaesthetic effect
PEDODONTICS
• Used in the management of chronic pain and acute pain

•
• Contraindications are ASA IV patients, patients with cardiac pacemaker, neurological disorders, pregnancy, very young pediatric patients
•
• Advantages include no needle usage, no injection of drug, no residual anaesthetic effect at the end of the procedure.
•
• Disadvantages are cost of the unit, extensive training and the presence of intraoral electrodes.
•
Drugs In Pedodontics (NEET 2013)
Body Size-It influences the concentration of the drug attained at the site of action. The average adult dose refers to individuals
of medium built.
Newborn 3.2 0.23 12.5
• 1 Month 4.0 0,26 15
•
• 3 Months 5.5 0.32 ii 18
•
• 6 Months 7.5 0.4 22
•
• 1 Year 10 0.47 25
•
1
• 1V 14 0.62 33
•
• 3 ears
•
• 5 Years 18 0.73 40
•
• 7 Years 23 0.88 50
•
• 12 Years 37 1.25 75
•
TRAUMA
Classification of Traumatic Injuries
Rabinowich Classification (1956)
• Class I: Enamel fracture • Class II: Enamel and dentin fracture

• Class III: Enamel and dentin fracture with pulp exposure • Class IV: Root fracture
•

• Class V: Comminution • Class VI: Exarticulation
•

Ellis and Davey (1960)
• Class I: Simple fracture of crown involving only enamel with little or no dentin
•
• Class II: Extensive fracture of crown involving considerable dentin but not exposing dental pulp.
•
• Class III: Extensive fracture of crown involving considerable dentin and exposing dental pulp
•
Pedodontics 647

• Class IV: The traumatized tooth that becomes non-vital • Class IX: Traumatic injuries of primary teeth
•
•
with or without loss of crown structure
– According to Cohen: Cracked tooth
• Class V: Total tooth loss - avulsion
–
– According to Matthewson: Cyclic dislocation of tooth
•
• Class VI: Fracture of the root with or without loss of
–
•
crown structure (NEET 2013)
Root Fractures

• Class VII: Displacement of tooth with neither crown or
•
root fracture • Prevalence: <10% of injuries to permanent dentition.
Class VIII: Fracture of crown en masse and its
•
•
• 2 radiographs are required for localization of fracture.
•
displacement
•
Apical 1/3 Middle 1/3 Coronal1/3
• Usually no treatment is required • Tooth is loosened, therefore, to • Fractures in this group communicate with the gingival
•
•
•
unless mobility increases achieve repair of the fracture line with crevice, allowing ingress of bacteria into pulp.
PEDODONTICS
significantly. hard-tissue union, the tooth should – Emergency treatment consists of a choice be-
be splinted rigidly for 8-12 weeks.
–
– However, the tooth should tween either extraction of both parts of the tooth
If the coronal part is not displaced,
–
be kept under observation, or, preferably, removal of the coronal fragment,
as death of coronal 2/3 of loss of vitality is unlikely. Where root canal treatment of the remainder, and then
pulp may occur. the coronal fragment is displaced, placement of a dressing that will prevent gingi-
– Apical 1/3 usually retains reposition, splint, and, if loss of vitality val tissues overgrowing the root surface. This
occurs, perform root canal treatment
–
vitality. can be achieved by placing a temporary post-
– Prognosis is good to fracture line. Calcium hydroxide retained crown, although replacement of the
should be used as an interim dressing
–
– If extraction is required, coronal fragment using a dentin-bonding agent
to limit inflammation and resorption.
–
the apical 1/3 can be left in has been described.
situ to preserve bone. Delay in treatment diminishes good – For permanent treatment, place a post and core
prognosis. If extraction is required, –
crown. However, if fracture extends below the
consider leaving apical portion in situ. alveolar crest, you need improved access for
crown fabrication; there are two alternatives:
Ostectomy/gingivectomy Orthodontic extrusion

Gives quicker result Cervical circumference of crown

Needs post Smaller compared to

Tend to get perio pocket Contralateral tooth

Leads to reduced gingival width Better crown/root ratio

Maintain attached gingiva

Injury Features Treatment
Luxation Displacement of tooth (laterally, labially, or reposition the tooth as soon as possible, flexible splinting.
palatally). keep under observation.
Concussion Injury to supporting tissues of tooth, without Reassurance and soft diet.
displacement.
Subluxation Actually means partial displacement, but If minor, soft diet. If mobile, splint for I weeks and watch vitality.
commonly used to describe loosening of a tooth
without displacement.
Intrusion Displacement of tooth into its socket. Often Intrusion teeth with immature roots are likely to erupt and
accompanied by fracture of alveolar bone. therefore no immediate treatment is required
Teeth with closed apices have a limned potential for re-eruption
and will need orthodontic extrusion.
Extrusion Partial displacement of tooth from its socket The affected tooth should be repositioned under LA with digital
pressure and splinted for 1-2 weeks. Again, loss of vitality is
a common sequela, so the tooth should be observed for any
signs of resorption or pulp death.
648
Splinting
• Indications
•
– To stabilize a loosened tooth to promote periodontal healing and improve patient comfort. To encourage fibrous
–
rather than bony healing {ankylosis), a short splinting time with a flexible splint is recommended (avulsion = 7-10
days; luxation = <3 weeks).
– To stabilize a root fracture and encourage healing with calcified tissue. Rigid splinting for 12 weeks is generally
–
indicated.
• Methods
•
Direct Constructed on patient. An almost infinite variety of methods Indirect: This type of splint is removable, allowing an assessment of
have been described, but the following are the most popular: mobility or firmness, which is valuable in cases of reimplantation. The
• Acid-etch splint with composite resin and/or wire/orthodontic more common types are the following:
•
attachments • Upper removable appliance with cribs on maxillary first
PEDODONTICS
•
• Lone standing teeth can be supported by sling suture. permanent molars and occlusal coverage.
•
• Interdental wiring is of historical interest. • Vacuum formed thermoplastic
•
•
Factors Affecting Choice of Splint
• Type of injury and therefore length of time splint required. For example, root fracture will need 8-12 weeks of splinting,
•
therefore composite and wire splint is advisable. For a replanted tooth prolonged splinting leads to ankylosis.
• Dental status of patient, e.g., in mixed dentition and when the incisors are traumatized, a full-coverage acrylic splint is
•
needed.
• Facilities and time available
•
• Number of teeth injured and availability of uninjured adjacent teeth.
•
• Luxated or replanted teeth can be held in place with sling sutures if there are no adjacent teeth to splint to.
•
Management of the Avulsed Tooth (NEET 2013, AIPG 2011)
• Exarticulation=avulsion. Prevalence: 0-16% of injuries.
•
• Factors affecting prognosis Success depends on reestablishment of a
•
– Time from loss to reimplantation. As periodontal ligament cells rarely survive>60 min extraorally, immediate
–
replacement is treatment of choice. (AIPG 2001)

– Storage medium. Prognosis saliva > milk > water > air. (Dry storage rapidly damages periodontal cells.)(AIPG 2001)
–
– Most accepted medium is Hank’s balanced salt solution (AIPG 2014)
–

– Splinting time 7-10 days for flexible splinting. Prolonged splinting will promote ankylosis.
–
– Viability of pulp. Seepage of pulp breakdown products into PDL contributes to development of inflammatory
–
resorption. Although revascularization is possible in a tooth with an open apex that is replanted within with closed
apices and longer extra-alveolar times should be considered non vital.
Preparation of Root
Extra oral dry time less than 60 minute
Closed apex Open apex
• The root should be rinsed of debris with water or saline and • Gently rinse off debris
•
•
replanted in as gently as possible. • Soak in doxycycline for 5 minute for cover with minocycline and
•
• If closed apex is there then revascularization is not possible replant.
•
• A dry time of less than 15 to 20 minutes is considered optimal, • Revascularisation is possible which is enhanced by doxycycline
•
•
where periodontal healing is expected (1mg in 20 ml saline) for 5 minute for reimplantation.
Pedodontics 649

Extra oral dry time more than 60 minute
Closed apex Open apex
• Remove the periodontal ligament by placing in acid for 5 Replant If yes treat as a closed apex. Endodontic treatment may be
•
minutes performed out of the mouth
• Soak in 2% stannous flourideQ for 5 minutes (PGI June 2011)
•
• Emdogain (enamel matrix protein) could be beneficial for
•
extending extra oral dry time, RCT is performed extraorally
Preparation of Socket
• Socket should be left undisturbed before replantation
•
• It should be slightly aspirated if a blood clot is present
•
PEDODONTICS
Periodontal ligament (PDL) management – transitional – The remaining PDL can be removed by several
–
therapy methods: gentle scaling and root planning, soft
• When a tooth has been out of the oral cavity and in a dry pumice prophylaxis, gauze or soaking the tooth in 3%
citric acid for 3 minutes
•
environment for greater than 60 minutes, the PDL has no – This should be followed by a sodium fluoride
chance of survival
–
treatment for 20 minutes.
– If such a tooth is replanted, it is likely to undergo – The rationale for this fluoride soak is based upon
–
evidence that this procedure will delay but not prevent
–
osseous replacement resorption and over time the
ankylosis.
tooth will be ankylosed and ultimately will be lost
– Flourapatite is more resistant to ankylosis than
– To slow down this process, the remaining PDL should
–
hydroxyapatite
–
be removed because otherwise it becomes a stimulus – When teeth are soaked in fluoride before replantation,
–
of inflammation that accelerates infection related it has been shown to reduce significantly the risk of
resorption. resorption after a follow up of 5 years.
CHAPTER 17
Conservative Dentistry
Objectives
• Cariology • Amalgam Restorations

• Infection Control • Tooth Coloured Restorations

• Instrumentation – Bonding Systems

• Biomechanical Principles – Composites

• Rubber Dam – Glass Ionomer Cements

• Matricing and wedging • Bleaching

• Restorations • Miscellaneous

CARIOLOGY Microbiology
• Mutant streptococci are the most strongly associated with
Operator positions
•
the onset of caries/incipient caries/reversible caries and
Right front position (7 o’ clock) For mandibular anterior smooth surface caries.. (NEET 2013, AIPG 2008,
teeth and mandibular 2007, 2006, 2001)
posterior teeth (especially

on the right side), and • Lactobacilli are associated with active progression of
•
maxillary anterior teeth. cavitated lesions/irreversible caries.
Right position (9 o’clock) For operating on the • A.viscosus is the most likely organism to initiate root
•
facial surfaces of the caries. (AIPG 2008)
maxillary and mandibular

right posterior teeth and
occlusal surfaces of the
mandibular right posterior
teeth
Right rear position (11 o’clock) Position of choice for most
operations. The lingual and
incisal (occlusal) surfaces
of the maxillary teeth
observed in the mouth
mirror. It gives direct vision
particularly on the left side.

(KAR 2011)

Direct rear position (12 o’ clock) For lingual surfaces of
mandibular teeth
Conservative Dentistry 651

• This classification is the main basis of Minimal
•
Intervention Dentistry
Anatomic site
Site 1 Pits, fissures and enamel defects on occlusal
surfaces of posterior teeth or other smooth
surfaces
Site 2 The contact areas between any two teeth,

anteriors or posteriors.
Site 3 Cervical one third of the crown or following
CONSERVATIVE DENTISTRY
gingival recession, the exposed root.
Extent and complexity
Size 1 Minimal involvement of dentin just beyond
treatment by remineralization alone
Size 2 Moderate involvement of dentin following cavity

preparation remaining enamel is sound, well
supported by dentin and not likely to fall under
normal occlusal load. The tooth is sufficiently
strong to support restoration.
Size 3 Cavity is enlarged beyond moderate

involvement. Remaining tooth structure is
Fig.17.1: Pathogenesis of dental caries weakened that cusps or incisal edges are split
or likely to fail if exposed to occlusal load. The
cavity needs to be further enlarged so that the
Classification restoration can be designed to provide support
to the remaining tooth structure.
• GV Black’s classification of caries. (Therapeutic
•
classification) Size 4 Extensive caries and bulk loss of tooth structure
has already occurred.
Class 1 Restorations on occlusal surface of molars
and premolars
Loca- 1=Mini- 2=Moder- 3=Ad- 4=Exten-
Facial and lingual surfaces of molars
Lingual surface of maxillary incisors tion mal ate vanced sive

(AIPG 1994) Site 1: 1.1 1.2 1.3 1.4

Pits and
Class 2 Restorations on the proximal surface of
posterior teeth (MAHE 1995) fissures

Class 3 Restorations on the proximal surfaces of Site 2: 2.1 2.2 2.3 2.4
anterior teeth that donot involve incisal Proximal
angle surfaces
Class 4 (AIPG Restorations on the proximal surfaces of Site 3: 3.1 3.2 3.3 3.4
2002) anterior involving the incisal edge Cervical
Class 5 Restorations on the gingival third of the surfaces
facial or lingual surfaces of all teeth
• Chronic caries is slowly progressive and occurs in
Class 6 Restorations on the incisal edge of anterior
•
teeth or occlusal cusp heights of posterior older individuals. Chronic caries is usually open type
teeth. with depth of lesion less than the width and is usually
asymptomatic. (AIPG 1994)

– The slow rate results from periods of
Classification by Mount and Hume (1998)
–
demineralization and remineralization
• This system is designed to utilize the healing capacity of – The slow rate of caries allows time for extrinsic
•
–
enamel and dentin. It is a two numbered system. First pigmentation.
number indicates the anatomic site of caries and the – An arrested enamel lesion is brown to black, hard
–
second number indicates the extent and complexity of the and is more caries resistant than the contiguous
teeth. affected enamel. (AIIMS May 2010)

652
– An arrested lesion typically is open, dark and hard – Are seen with low caries rate which is suggestive of
–
increased fluoride exposure
–
and is termed as eburnated or sclerotic dentin.
– Believed that the increased fluoride exposure

((PGI 2009, AIPG 2007, AIIMS 2007)
–
encourages remineralization and slows down

• In contrast, acute caries occurs in young individuals
progress of the caries in the pit and fissure enamel
•
and is rapidly progressive, undermining the enamel.
while cavitation continues in dentin, and the lesions
Pain may be present.
become masked by a relatively intact enamel surface.
– It is usually in the form of many soft, light coloured – These hidden lesions are called fluoride bombs or
–
lesions in the mouth, and is infectious.
–
fluoride syndrome.
– Less time for extrinsic pigmentation explains lighter • Simple cavity–Involves one tooth surface
–
colouration.
•
• Compound cavity–Involves two surfaces
•
• Complex cavity–Involves more than two surfaces
• Forward caries: is where the caries cone in enamel is
•

(MAHE 2010)
•
larger or at least the same size as that in dentin.

Radiographic Caries Classification

(KAR 2011)

• Backward caries: when the spread of caries along the CEJ • BO-No visible radiographic lesion El-Lesion in outer one
•
•
exceeds the caries in the contiguous enamel, caries extend half of enamel
into this enamel from the junction. • •
E2-Lesion in inner one half of enamel
• Occult caries: occult or hidden caries is used to describe • D1-Lesion in outer third of dentin D2-Lesion in middle
•
•
such lesion which is not clinically diagnosed but detected third of dentin
only on radiographs. • D3-Lesion in inner third of dentin.
•
Zones of Enamel Caries
Zone 1 Translucent zone Advancing front of the lesion. It indicates a 1% loss of mineral.
Ten times more porous than sound enamel Not always present
Zone 2 Dark zone This is a thin band superficial to the translucent zone. Mineral loss is 2-4%
Usually present and thus referred as positive zone
Zone 3 Body of lesion This accounts for the bulk of the lesion. Mineral loss is upto 25%
Zone 4 Surface zone This is relatively intact layer of enamel. Mineral loss is less than 4%. Greater resistance probably due
to greater degree of mineralization and greater fluoride concentration It is less than 5 percent porous
Its radiopacity is comparable to adjacent enamel.
Zones of dentinal caries: Caries advance in dentin proceeds through three changes:
• Weak organic acids demineralizes the dentin
•
• The organic material of the dentin, particularly collagen, is degenerated and dissolved;
•
• The loss of structural integrity is followed by invasion of bacteria.
•
The Zones of Dentinal Caries Were Put Forward by Fusayama: (AIIMS May 2013)
Zone 1 Normal dentin
Zone 2 Subtransparent dentin • Zone of demineralization (by acid from caries)

•
• Damage to the odontoblastic process is evident
•
• However, no bacteria are found in the zone
•
• Stimulation of the dentin produces pain, and the dentin is capable of remineralization.
•
Zone 3 Transparent dentin • Softer than normal dentin
•
• Further loss of mineral from the intertubular area
•
• Stimulation of this region produces pain. There are no bacteria present
•
• The collagen cross linking remains intact in this zone, can serve as a template for remineralization.
•
• The intact collagen of the intertubular dentin, and thus this region remains capable of self repair,
•
provided the pulp remains vital.

Zone 4 Turbid dentin • Turbid dentin is the zone of bacterial invasion

•
(KAR 2009) • Widening and distortion of the dentinal tubules which are filled with bacteria

•
• There is very little mineral present and collagen in this zone is irreversibly denatured
•
• The dentin in this zone will not self repair
•
• This zone cannot be remineralized and must be removed prior to restoration
•
Zone 5 Infected dentin • The outermost zone, infected dentin, consists of decomposed dentin that is teeming with bacteria
•
• There is no recognizable structure in dentin
•
•
•
Absence of collagen and mineral content
• Great numbers of bacteria are dispersed in this granular material
•
• Removal of infected dentin is essential to sound, successful restorative procedures as well as
•
prevention of spread of the infection.
Affected dentin Infected dentin

• Softened demineralized dentin that is not yet invaded by • Both softened and contaminated with bacteria
•
•
bacteria • Zones 4 and 5
•
• Zones 2 and 3 • Collagen is irreversibly remineralized and has to be removed
•
•
• The collagen is reversibly denatured and remineralizable • It can be selectively stained in vivo by 1% acid red 52 (acid
•
•
• It is dark brown in colour, hard in texture and should not be rhodamine B or food red 106) in 0.2% propylene glycol. This
•
excavated. solution stains the irreversibly denatured collagen in the outer
carious layer but not the reversibly denatured collagen in the inner
carious layer. (AIPG 2005)

Arrested Caries The three most common microorganisms considered to
• Lesion that may have formed earlier and then stopped. be associated with recurrent caries are:
•
• Presents as a large open cavity which no longer retains – Streptococcus mutans
•
–
food and becomes self-cleansing. – Lactobacilli
–
 
• Commonly seen on lingual and labial aspects of teeth and – Actinomyces viscosus.
•
less commonly interproximally.
–
• These have been associated with caries because of their
•
• In arrested caries, superficially softened and decalcified ability to grow and produce acid at low pH.
•
dentin is gradually burnished away due to mastication
until it takes on a brown stained, polished appearance • Tooth remineralization can take place if the pH of the
which is hard. This type of dentin is referred as “eburnation
•
environment adjacent to the tooth is high due to:
dentin”.
– Lesser number of cariogenic bacteria
–
First Stage • The acids produced by bacteria dissolve – Availability of fluoride
•
the mineral in the surrounding intertubular
–
dentin.
– Lack of substrate for bacterial metabolism
–
• The tubule fluid becomes saturated with
– Elevated secretion rate of saliva
–
– Strong buffering capacity of saliva
•
calcium magnesium and phosphate ions.
–
• If less acid is produced then the second – Presence of inorganic ions in saliva
–
•
stage can occur. – Quick washing of retained food
 
–
Second • Large crystals of tricalcium phosphate are
Enamel Prism
•
Stage formed by precipitation of saturated crystals.
Third Stage • The odontoblast process secretes collagen

• The structural components of the enamel prism are
•
millions of small, elongated apatite crystallites. The
•
into the dentin tubule.
• Hydroxyapatite crystals accumulate and crystallites are tightly packed in a distinct pattern of
orientation that gives strength and structural identity
•
block the tubule. Also the growth of crystals
takes place in the intertubular dentin. This to the enamel prisms. The long axis of the apatite
 
concept of activity affects directly on
management of caries because active
crystallites within the central region of the head (body)
is aligned almost parallel to the rod’s long axis
 
lesions require active management.
654
• The crystallites incline with increasing angles (upto Etiology • The microflora responsible for root
•
•
65 degree) to the prism axis in the tail region. The caries consists of Streptococcus mutans,
Lactobacillus and Actinobacillus.
susceptibility of these crystallites to acid, either from

(AIPG 2011)
an etching procedure or caries appears to be correlated

• The rate of demineralization of root occur
with their orientation, whereas the dissolution process
•
at higher pH and is much faster than that
occurs in the head regions of the rod, the tail regions of enamel because the root has much less
and the periphery of the head regions are relatively mineral content (55%) than that of enamel
(99%).
resistant to acid attack.
Contributing • Xerostomia.
•
Factors • Low salivary buffer capacity.
Secondary Caries
•
• Poor oral hygiene.
•
• Espelid and Tveit (1991) classified secondary caries as: • Periodontal disease and periodontal
•
surgery.
•
– S-1: Initial carious lesion characterized by • Gingival recession.
–
discoloration only
•
• Radiation therapy.
– S-2: Lesions characterized by softness in enamel
•
• Limited exposure to fluoridated water
–
– S-3: Lesions with cavitation on the root surfaces
•
–
• Diagnosis of secondary caries is a usually difficult because Diagnosis (AIPG • Clinical examination is best carried out
•
•
of: 2006) with an explorer.
• Accurate radiographs
– Diagnosis of recurrent caries lacks consistency.
•
• Special dyes can be useful for detecting
–
– Small size of the initial lesion.
•
root caries, these dyes stain the infected
–
– Color change that is dusty white to brownish is dentin and thus allow the clinician to
–
difficult to interpret in amalgam restorations. detect caries.
– It is difficult to examine wall lesion clinically unless
Recent Advances in Caries Diagnosis
–
there is adequate demineralization, which is seen
through the overlying enamel. Diagnodent • A variant of Quantitative Laser or Light
– Stains at the margins of tooth-colored restorations are
•
Induced Fluorescence system. Light

(AIIMS May
–
difficult to differentiate from recurrent caries. 2013) source – diode laser red light 655nm
– Catch formed while probing tooth restoration • Red light is transported via an angulated
•
tip with central fibre. Reflected light is
–
interface may not be carious, though it appears to be. eliminated by and taken up by the photo-
 
– Two-dimensional radiographic picture. diode and processed and presented on
–
– Radiopacity of restoration obstruct the lesion. display as 0-99
–
– The burnout at the cervical margin may • 5-25 initial lesions in enamel
–
make interpretation difficult.
•
• 25-35 initial dentinal caries
 
 
•
Root Caries • >35 advanced dentinal lesion
•
Dye–Enhanced • It had higher sensitivity than laser auto
•
Features of • Root surface caries are initiated when fluorescence alone.
laser Fluores-
•
Root Caries there is periodontal attachment loss • Dyes used are:
cence
exposing the root surface to the oral
•

environment.
(PGI 1995) – Pyromethane 556
–
– Sodium flurescin
• Root caries is a soft, irregular, progressive
–
• A blue light (400-500nm) is used to excite
•
lesion occurring at or apical to the CEJ. Endoscope
•
fluorescence with in the tooth.
• An area where root caries has taken place
• Advantage: 5-10 fold magnification
•
may appear as round or oval in shape
•
which then may spread radially and join • For caries enamel
Dye penetration
other areas of root caries.
•
methods –Procion: disadvantage – irreversible
• These areas appear as white or discolored
–
as dye reacts with nitrogen and hy-
•
having irregular outline, with or without a droxyl groups of enamel
cavity at an exposed root surface. – Calcein: Complexes with calcium
–
• Root caries are more common in males – Flourescent: i. Brilliant blue, ii. Zyg-
•
–
than females. toZX -22
• Most commonly they are seen in • For caries dentin
•
•
mandibular molars, followed by – 0.5% basic fuschin in propylene gly-
–
premolars, canines and incisors. This col
order is reversed in the maxilla. – 1% acid red in propylene glycol
–

Other new Diagnostic modalities for caries lesion Xylitol
• Multi photon imaging
• Xylitol is a five-carbon sugar alcohol derived primarily
•
• Terahertz imaging
•
from forest and agricultural materials with the taste
•
• Transversal wavelength independent microradiography almost identical to that of table sugar.
•
• Infrared thermography or infrared fluorescence • It is nonfermentable, noncariogenic sugar and has
•
• Frequency domain photothermal radiometry
•
anticaries effects.
•
• Frequency domain luminescence • Anticariogenic effects of xylitol:
•
•
• Fibre optic transillumination (AIPG 2004) – Xylitol reduces plaque formation
•

–
– It reduces bacterial adherence
Phosphor Imaging System
–
– It inhibits enamel demineralization
–
• Imaging using a photo stimulable phosphor can also be – It has a direct inhibitory effect on S.mutans
–
– Increases salivary flow
•
called as an indirect digital imaging technique.
–
• The image is captured on a phosphor plate as analogue – It is nonfermentable
–
– It increases concentration of amino acids which
•
information and is converted into a digital format when
–
the plate is processed. neutralize the plaque acidity.
• Two sizes of phosphor plates, similar in size to • Xylitol chewing gums or lozenges used four times are
•
effective anticaries therapeutic measures. Also because
•
conventional intraoral film packets are provided. They
have to be placed in plastic light-tight bags, before of Xylitol’s anticaries effects, it is recommended for
being used in the mouth. They are then positioned pregnant mothers. Studies have shown that mothers
in the same manner as film packets, using holders, using xylitol gum during the first two years of their
incorporating beam-aiming devices, and are exposed child’s age show much lower caries in the children later
using conventional dental X-ray equipment.
• The image is displayed and manipulated. A hard copy
•
can be obtained if necessary. Cheese
• Advantages • Cheese is considered responsible for:
•
•
– Low radiation dose (90% reduction). – Increasing the salivary flow
–
–
– Almost instant image (20-30 seconds). – Increasing the pH
–
–
– Wide exposure latitude (almost impossible to burn – Promoting the clearance of sugar
–
–
out information).
– Same size receptor as films. Remineralizing Approaches
–
– X-ray source can be remote from PC. • Commonly used agents are calcium glycerophosphate
–
– Image manipulation facilities.
•
and calcium lactate, dicalcium phosphate dihydrate
–
(DCPD), and calcium carbonate. Recently, Casein
phosphopeptide (CPP), amorphous calcium-phosphate
Prevention of Dental Caries
(ACP) complexes have also been considered as agents
Methods to reduce • Dietary measures for remineralization. Because of high solubility and
•
demineralizing • Methods to improve oral hygiene ability to rapidly hydrolyze to form apatite, Amorphous
factors
•
• Chemical measures Calcium Phosphate Agents (ACPs) come under good
•
Methods to increase • Methods to improve flow, quantity and source for tooth remineralization
•
protective factors quality of saliva
• Mechanism of action CPP-ACP
• Chemicals altering the tooth surface
•
– CPP stabilize calcium phosphate in solution and
•
or tooth structure:
–
– Fluorides increases the level of calcium phosphate. Thus CPP-
ACP nanocomplexes act as a reservoir of calcium
–
 
– Iodides
–
 
– Zinc chloride and phosphate ions so as to have supersaturation
–
– Silver nitrate state with respect to tooth enamel and buffer plaque
–
– Bisbiguanides
pH.
–
• Application of remineralizing agents
– Provide ions for tooth remineralization.
•
• Use of pit and fissure sealants
–
– CPP-ACP inhibit caries by concentrating ACP in
•
• Sugar substitutes:
–
dental plaque, preventing demineralization and
•
– Xylitol
increasing remineralization.
–
– Sorbitol
 
–
656
Genetic Modalities in Caries Prevention

New strains of S. mutans The genes for enzyme glycosyl transferase were decoded, resulting new strains of S. mutans which
lacked the capability to produce lactic acid responsible for caries.
Genetically Modified Foods Modified fruits and vegetables are being developed by incorporating antagonist peptides to work
against glycosyl transferase.
Genetically Modified Organisms A new strain of S.mutans has been created which lacks lactodehydrogenase gene, thus unable to
produce lactic acid. Lactobacillus zeae: Researches have been conducted to find a good bacteria
 
called lactobacillus zeae. These are genetically modified bacteria which produce antibodies so as to
attach to surface of S. mutans resulting in their death.
Probiotic approach In this approach, S. mutans strain is modified to increase the production of enzyme urease. This
urease converts urea into ammonia which helps in remineralization of enamel.
Rationale of Caries Vaccine

– Rationale for caries vaccine is that immunization with S. mutans should induce an immune response so as to prevent
–
organisms from colonizing the tooth surface and thus prevent carious decay.
– General public should be well exposed to vaccine.
–
– Vaccine should be given before eruption of deciduous teeth so as to achieve maximum benefits.
–
 
• Problems in Development of Caries Vaccine
•
– Since complete etiology of caries is not known, 100% effectiveness of vaccine is not possible.
–
– Due to variation in number of etiological microorganisms, infective dose also varies.
–
– Even with same level and type of S. mutans, variation in severity of disease occur due to other factors.
–
– Cross reactivity of S. mutans cell antigens is seen with heart muscles.
–
– Lack of immunological competence can result in lack of response to S. mutans.
–
– There is non-availability of human models to study immunological response.
–
 
• Three routes have been tried to achieve caries immunity in animal studies:
•
– Systemic immunization
–
– Mucosal immunization
–
 
– Passive immunization.
–
Chemochemical Caries Removal (CMCR) Method
Caridex Carisolv
Composition • Solution I containing sodium hypochlorite and • In 1998, carisolv was introduced.
•
•
• Solution II containing glycine, aminobutyric acid, • It is available in two syringes, one containing the sodium
•
•
sodium chloride and sodium hydroxide. hypochlorite and other a pink viscous gel consisting of
 
• The two solutions are mixed immediately before lysine, leucine and glutamic acid, amino acids, together with
carboxymethyl- cellulose to make it viscous and erythrocin to
•
use. The solution is applied to the carious lesion by
means of applicator. Application is done until the make it readily visible in use.
sound dentin comes. • The contents of the two syringes are mixed together
•
immediately before use. The gel is applied to the carious
lesion with hand instruments and after 30 seconds, carious
dentin can be gently removed. Another application may be
required until no more carious dentin remains. (AIPG 2010)
Advantages • No need for local anaesthesia • Volume required is less.
•
•
• Suited for treatment of anxious and pediatric patients • Does not require heating or a delivery system.
•
•
• Indicated in medically compromised • Since it involves gel not liquid, it is much easier to use than
•
•
patients Conservation of sound tooth structure caridex
 
• Reduced risk of pulp exposure. • Better contact with the carious lesion.
•
•
Disadvantages • Instruments may still be needed for the removal of • Use of rotary instruments may still be required for some
•
•
caries or material cavities.
• It leaves a surface with many overhangs and
•
undercuts • Large volumes of solution are needed •
 
Procedure is slow • It is ineffective in the removal of
 
hard eburnated parts of the lesion
 
• Unpleasant taste
•

Ozone Treatment of Dental Caries applied to the demineralized tooth surface. Tooth is
restored with glass ionomer cement.
• The introduction of Aero-therapeutic ozone therapy to
– Carving and finishing of glass ionomer cement is
•
completely eliminate bacteria at and below the preparation
–
done.
surface enhances the success of treatment. Ozone is a
– Over it, after confirming remineralization, place
proven antimicrobial agent that a 10 second application
–
composite restoration.
eliminates more than 99% of the microorganisms found
in dental biofilm. Good to Know
• Mechanism of Action: • In carious enamel and dentin, fluoride content is 139
•
•
– Ozone occurs naturally when molecular oxygen ppm and 223 ppm, whereas in sound enamel and dentin
(O2) is photodissociated into activated ions (O–)
–
it is 410 ppm and 873 ppm, respectively.
which further combines with other oxygen molecules • Stephan showed the relationship between changes in
(O2) to form transient radical anions (O3). Ozone
•
plaque pH over a period of time following a glucose
ultimately decomposes to a hydroxyl radical which rinse in form of a graph. This graph is called a Stephen
is a powerful oxidant. It oxidizes biomolecules like curve’ (Stephan and Miller 1943) (AIPG 2008, 2006)
cysteine, methionine, and histidine resulting in cell

• The critical pH value for demineralization usually
death.
•
ranges between 5.2 and 5.5
– Just 20 to 40 second exposure of ozone kills all oral
• The earliest manifestation of incipient caries of enamel
–
microbes and their protective biofilm environment. •
Because of this change in microenvironment, the is seen beneath dental plaque as areas of decalcification
remineralization of enamel and dentin can be (white spots). As caries progresses it appears bluish
accomplished. It has been shown that when GIC is white in colour.
placed in direct contact with the demineralized tooth • Transillumination takes advantage of the opacity of a
•
surface, it acts as a brilliant source of ions for tooth demineralized tooth surface over a more translucent
remineralization. healthy structures. The decalcified area will not let the
• Technique of using Ozone Therapy light pass through as much as it does in ahealthy area
•
– Carious lesion is diagnosed visually, tactily and/or generating a shadow corresponding to decay
–
radiographically. Entry through the enamel is made • Cervical burnout is an apparent radiolucency found just
•
with airotor. Disposable sterile cup on the Ozone is below the CEJ on the root due to anatomical variation
used to form a seal around the prepared tooth. (concave root formation posteriorly) or a gap between
– Once the seal is obvious, ozone is delivered, and the enamel and bone covering the root (anteriorly)
–
refreshed 300 times per second, for 40 seconds. mimicking root caries. Posteriorly this radiolucency
Healozone remineralizing solution which contains disaapears when the radiograph is taken at a different
xylitol, fluoride, calcium, phosphate and zinc, is angulation.
INFECTION CONTROL
Aerosols • Invisible particles ranging from 50 μm to 5μm that can remain suspended in the air and breathed for hours
•
Mists • Become visible in a beam of light, consist of droplets estimated to approach or exceed 50μm.
•
Splatter • Consists of particles generally larger than 50μm and even visible splashes. Spatter has a distinct trajectory, usually falling
•
within 3 feet of the patient’s mouth, thus having the potential for coating the face and outer garments of the attending
personnel.
• US Congress passed the occupational safety and health act in the year 1970.
•
• Nitrile latex utility gloves are preferred for cleaning and sorting of sharp instruments.
•
• Masks with highest filtration are rectangular folded types.
•
• The ultrasonic scaling cleaning is found to be 9 times effective than the hand cleaning of instruments.
•
658
• The medical, surgical and dental instruments are classified into:

•
Critical instruments Semi critical instruments Non-Critical Instruments
These are instruments that contact or Items that touch mucosa but do not cut or These are the environmental surfaces such as
cut tissues or penetrate tissues and are penetrate the tissue. Sterilization should be chairs, benches, floors, walls, and supporting
considered to be critical items and always considered but if instruments are sensitive equipment of the dental unit that are not
require thorough cleaning and sterilization then high-level disinfection should be ordinarily touched during treatments. They come
for reuse. E.g. endodontic file, scalpel bur, carried out. (KAR 2011) in contact with intact skin. Intermediate or low

extraction forceps. level of disinfection should be followed. Surface
disinfection is adequate.
Hand Piece Sterilization (AIPG 2010) Heat Treatment of Materials

• Autoclave: Has been found to be better than dry heat • For gaining maximum benefits from instruments made
•
from carbon or stainless steel, they are subjected to
•
which causes turbine wear.
two heat treatments—hardening and tempering heat
• Chemicals cause rusting and loss of torque
treatment.
•
• In autoclave, the steam primarily has an effect on
– Hardening heat treatment: In this, instrument is
•
fiberoptic handpiece in the sense that the fiber may
–
heated to 815°C in oxygen free environment and then
become dulled with repeated cycles due to oil residues
quenched in a solution of oil. By hardening treatment,
and debris baked on the ends of optical fibres.
the alloy becomes brittle.
• Glass bead sterilizer uses table salt which consists – Tempering heat treatment: In this, instrument is
•
approximately of 1 percent sodium silicoaluminate, –
heated at 176°C and then quenched in solutions of oil,
sodium carbonate or magnesium carbonate. Salt can acid or mercury. Tempering heat treatment is done to
be replaced by glass beads. The instruments can be relieve the strains and increase the toughness of alloy
sterilized in 5 to 15 seconds at a temperature of 437 to • Nomenclature for the Instruments: Dr GV Black has
4650 F (2600 C) even when inoculated with spores.
•
given a way to describe instruments for their easier
• The specific disadvantage of these sterilizers is that the identification similar to biological classification.
•
 
handle portion is not sterilized and therefore these – Order: Function or purpose of the instrument, e.g.
articles are not entirely ‘sterile’.
–
excavator, condenser.
• Handpiece must be first cleaned and then sterilized – Suborder: Position, mode or manner of use, e.g. push,
•
–
after each patient. Cleaning can be done by using water pull.
and detergent or wiping the handpiece using a suitable – Class: Design or form of the working end, e.g. hatchet,
–
disinfectant like alcohol. Lubricate the handpiece prior spoon excavator.
to sterilization and finally sterilize it by autoclaving. – Subclass: Shape of the shank, e.g. binangle, contra-
–
angle.
INSTRUMENTATION These names are combined to give a complete description
of the instrument. Naming of an instrument generally moves
• Carbon steel or stainless steel are most commonly used from 4 to 1. Sometimes, the suborder is omitted due to
•
for manufacturing of cutting instruments. variable and nonspecific use of the instrument. For example,
The Carbon Steel Stainless Steel
the instrument will be named according to the classification as
biangle enamel hatchet or biangle spoon excavator.
• Carbon steel alloy contains • Stainless steel alloy contains
•
•
0.5 to 1.5% carbon in iron. 72 to 85 percent iron, 15 to 25
• Instruments made from percent chromium and 1 to 2 Instrument’s Formula
percent carbon. GV Black established an instrument formula for describing
•
carbon steel are known
for their hardness and • Instruments made from dimensions of blade, nib or head of the instrument and angles
•
sharpness. stainless steel remain shiny
bright because of deposition
present in the shank of the instrument.
• But disadvantages with
of chromium oxide layer
•
these instruments are First Width of the blade or the primary cutting edge
their susceptibility to on the surface of the metal in tenths of a millimeter.
and chromium reduces the number
corrosion and the fracture
of instrument if dropped. tendency to tarnish and Second Angle formed by the primary cutting edge and long axis
corrosion. number of the instrument handle in clockwise centigrade.
• They are of two types:
• Problem with stainless steel
•
– Soft steel: It con- Third Length of the blade in millimeters that is from the shank
•
instruments is that they tend
–
tains < 0.5% carbon number to the cutting edge.
to lose their sharpness with
– Hard steel: It con-
repeated use, so they need to Fourth Angle which the blade forms with long axis of the handle
–
tains 0.5-1.5% car-
sharpened again and again. number or the plane of the instrument in clockwise centigrade
bon

• Manufacture’s number: This number is found on the handle of the instrument. This number is used when ordering the
•
instrument and indicates the instrument’s placement in a set of instruments.
• Examples of three number formula instruments are chisels, hatchets and hoes
•
• Examples of four number formula instruments are angle formers, and gingival marginal trimmers. (AIPG 2006)
•

• Angle formers is a type of excavator which is monoangled with the cutting edge sharpened at angle to the long axis of the
•
blade. Angle is between 80 to 85 degrees. It is used with a push or pull motion for accentuating line and point angles, to
establish retention form in direct filling gold restoration.
• Gingival margin trimmer (GMT) is a modified hatchet which has working ends with opposite curvatures and bevels.
•
Distal gingival margin trimmer is used for the distal surface and mesial GMT is used for mesial surface. If 2nd number in
GMT is 75 to 85, it is mesial GMT, if it 95 to 100 it is distal GMT. It is used for planning of the gingival cavosurface margin
and to bevel axiopulpal angle in Class II tooth preparation.
• Single bevel instruments have single bevel that forms the primary cutting edge. These can be right or left bevel and mesial
•
and distal bevel instruments.
• Beveled instrument has two additional cutting edges which extend from the primary cutting edge.
•
• In triple beveled instrument, three additional cutting edges extend from the primary cutting edge.
•
• Shephard’s crook or curved explorer has semilunar shaped working tip perpendicular to the handle. This is used for
•
examining occlusal surfaces.
• In straight chisel, the cutting edge of the chisel makes a 90° angle to the plane of the instrument. It is used for gingival
•
restoration of the anterior teeth.
• In the angled chisel, the primary cutting edge is in plane perpendicular to the long axis of the shaft and may have either a
•
mesial or distal bevel. It is used with a push or pull motion for anterior proximal restorations, smoothening proximal walls
and gingival walls for full coverage restorations.
Bur Designs
Bur blade Blade is a projection on the bur head which forms a cutting edge. Blade has two surfaces:
• Blade face/Rake face: It is the surface of bur blade on the leading edge.
•
• Clearance face: It is the surface of bur blade on the trailing edge.
•
Rake angle This is angle between the rake face and the radial line
– Positive rake angle: When rake face trails the radial line.
–
 
– Negative rake angle: When rake face is a head of radial line.
–
 
– Zero rake angle: When rake face and radial line coincide each other
–
 
Radial line It is the line connecting center of the bur and the blade.
Land It is the plane surface immediately following the cutting edge

 
Clearance angle This is the angle between the clearance face and the work
 
Clearance angle provides a stop to prevent the bur edge from digging into the tooth and provides adequate chip
space for clearing debris.
Blade angle It is the angle between the rake face and the clearance face
Concentricity It is a direct measurement of symmetry of the bur head
Run out It measures the accuracy with which all the tip of blades pass through a single point when bur is moving. It
measures the maximum displacement of bur head from its center of rotation. In case, there is trembling of bur
during rotation, this effect of run out is directly proportional to length of bur shank. Run out occurs if:
• Bur head is off center on axis of the bur.
•
• If bur neck is bent.
•
 
• If bur is not held straight in handpiece chuck.
•
Run out causes:
• Increase in vibration during cutting.
•
• Causes excessive removal of tooth structure.
•
660
Factors Affecting Cutting Efficiency of Bur • Visual contact with bur head: For efficient tooth cutting,
•
it is mandatory to maintain visual contact with bur head
• Clearance angle, rake angle and blade angle: Clearance while working.
•
angle reduces the friction between cutting edge and the • Design of flute ends: There are two types of flute ends
work. It also prevents the bur from digging excessively
•
– Star cut design: Here the flutes come together in a
into the tooth structure. But an increase in rake angle
–
common point at the axis of bur.
decreases the blade angle which in turn decreases the – Revelation design: Here the flutes come together at
–
bulk of bur blade. Positive rake angle increases cutting two junctions near diametrical cutting edge. It has
efficiency of bur, but increase in rake angle causes decrease better efficiency in direct cutting.
 
in bulk of bur blade and clogging of flute space because of
Recent Advances In Rotary Instruments
 
production of larger chips.
• End cutting or side cutting bur: According to particular

• Fissurotomy burs.
•
task, choice of bur can be end cutting, side cutting or
•
combination of both. For example, it is preferred to make • Smart Prep Burs
•
entry to enamel by end cutting bur, while for making • Chemical Vapor Deposition (CVD) Diamond Burs
•
 
preparation outline, use side cutting bur. • Fiberoptic handpiece.
•
• Neck diameter of bur: If neck diameter of bur is large, – Now-a-days to avoid shadow or visibility problem
–
•
it may interfere with accessibility and visibility. But if associated with external lightening, handpiece
diameter is too short, it will make bur unable to resist the with a built in optics have been made available.
lateral forces. This fiberoptic delivers a high beam of light to the
handpiece head directly on working site.
• Spiral angle: Burs with smaller spiral angle have shown
•
better efficiency at high speeds.
Smart Prep Burs
• Linear surface speed: Within the limit, faster the speed of
• Smart prep instrument is also known as polymer bur or
•
cutting instrument, faster is the abrasive action and more
•
smart bur.
efficient is the tooth cutting instrument. Bur speed should
• This type of instrument is made from polymer that safely
be increased in limits because with ultra high speed,
•
and effectively remove decayed dentin without affecting
centrifugal force comes into the play. the healthy dentin.
• Application of load: Load is force exerted by a operator • Smart prep bur has property of self-limiting, this means it
•
on tool head. Normally for high speed instruments, load
•
will not cut the healthy dentin. It cuts dentin only when
should range between 60-120 gm and for low rotational large amount of force is applied.
speeds, it should range between 1000-1500 gm. Cutting • Availability
•
efficiency decreases when load is applied, there is increase – Sizes 2, 4, 6.
–
in temperature at work face which results in greater wear • Used with slow speed handpiece (500-800rpm).
•
and tear of handpiece bearings. • Single patient use.
•
 
• Concentricity and run out: The average clinically
Advantages Disadvantages
•
acceptable run out is 0.023 mm. Increase in run out causes
• Used for deep caries removal • Technique sensitive.
increase in vibrations of the bur and excessive removal of
•
•
in direct capping procedure. • This instrument leaves
tooth structure.
•
• Chances of iatrogenic pulp large amount of decayed
•
• Lubrication: Lubricant/coolant applied to tooth and exposure are less. portion unexcavated.
•
bur during cutting increases the cutting efficiency and • Minimum removal of tooth • Costly.
•
•
structure. • Chances of damage of
decreases the rise in temperature during cutting. Absence
•
bur are more if, touches
of coolant can result in increase in surface temperature the enamel or sound
which may produce deleterious effects on pulp. dentin during and after the
procedure.
• Heat treatment of bur: Heat treatment of bur preserve
•
the cutting edges and increases shelf life of the bur. Chemical Vapor Deposition (CVD) Diamond
• Number of blades: Usually a bur has 6-8 number of Burs
•
blades. Decrease in number of blades reduces the cutting • In 1996, CVD diamond burs attached to an ultrasonic
•
efficiency but causes faster clearance of debris because of handpiece were introduced to eliminate problems faced
larger chip space with diamond burs.

– These diamond burs are obtained by chemical – Disadvantages
–
Should be used with suitable restorative materials
–
 
vapor deposition of diamond film over a

Costly.
molybdenum substrate.

 
– These tips are made in a reactor in which mixture of
–
methane and hydrogen gas results in the formation BIOMECHANICAL PRINCIPLES (AIIMS 2011,
of artificial diamond layer over the molybdenum 2008, 1993, HP 2010, AIPG 1992)
substrate.
 
– These tips require only slight touch to promote Tooth Preparation
–
tooth grinding. If too much pressure and force is
• Black gave following guidelines for tooth preparation:
 
applied during cutting, the effects would be:
•
Excessive heat generation. – Providing definite mechanical retention in
–

Decrease in cutting efficiency. the preparation.
 

Excessive noise production. – Extension of preparation in adjacent pits and
–

Pain. fissures for prevention of recurrent caries.
 

Fracture of the molybdenum substrate. – Removal of infected and affected dentin from
–

 
– Advantages all surfaces.
 
–
Less noise – Removal of even healthy tooth structure to gain
–

 
Greater durability access and good visibility
 
 

 
Better access and visibility • Nowadays because of change in following conditions,
•

 
Better cooling design of the tooth preparation has become most

 
Effective tooth preparation conservative.

 
Improved proximal access • Tooth preparation is divided into two stages, each

 
•
Reduced risk of metal contamination consisting of many steps. Though each step should be

Preservation of tooth structure and also done to perfection, but sometimes modifications can be

minimal damage to gingival tissues. made in steps.
– Disadvantages
Stage I: Initial tooth Stage II: Final tooth preparation
–
Technique sensitive
 
preparation steps steps

Very costly.
 
• Outline form and • Removal of any remaining enamel

•
•
initial depth. pit or fissure, infected dentin and/or
Fissurotomy Burs • Primary resistance old restorative material, if indicated.
•
form: permits • Pulp protection, if indicated.
– New instrument for ultraconservative dental
•
restoration to • Secondary resistance and
–
treatment. withstand occlusal
•
retention form.
– As the name indicates, these are specially designed for forces (AIPG 2006)
• Procedures for finishing the external

–
• Primary retention
•
pit and fissure lesions. walls of the tooth preparation.
•
form: prevents
 
– Available in three different shapes and sizes: displacement of
• Final procedures: cleaning,
•
–
inspecting and sealing. ?Under
Original fissurotomy. restoration
 
special conditions these

Original fissurotomy micro STF. • Convenience form sequences are changed.

•
Original fissurotomy micro NTF.
• The following factors affect the outline form and

– Original fissurotomy and fissurotomy micro NTF has
•
initial depth form of tooth preparation:
–
head length of 2.5 mm while fissurotomy micro STF
has head length of 1.5 mm. – Extension of carious lesion.
–
– Fissurotomy micro STF is suitable for deciduous – Proximity of the lesion to other deep structural
–
surface defects.
–
teeth, adult premolars, enameloplasty, etc.
 
– Relationship with adjacent and opposing teeth.
– Fissurotomy bur is mainly indicated for small caries
–
– Caries index of the patient
–
and enlarging the fissure
–
– Need for aesthetics
– Advantages
–
– Restorative material to be used.
–
Minimum heat build up and vibration
–

Conservation of tooth structure • Extension for prevention means the placing the margins
•

 
Increased patient comfort of preparations at areas that would be cleaned by the

662
excursions of food during chewing. It is done with the Advancements in restorative materials

objective of preventing the recurrence of caries at the Modifications in tooth preparations designs

margins of fillings where the recurrence of decay is most • Features for establishing a proper outline form are:
commonly seen. His concept also included extending
•
– Preserving cuspal strength.
preparations through enamel fissures to allow cavosurface
–
– Preserving strength of marginal ridge.
margins to be placed on nonfissured enamel.
–
– Minimizing the buccolingual extensions.

(AIPG 2002)
–
– If distance between two faults is less than 0.5

– For this:
–
mm, connect them.
–
 
Margins of the restoration are placed on line – Limiting the depth of preparation 0.2-0.8 mm

–
angles of the tooth into dentin.
 
Occlusal surface is extended through pits and – Using enameloplasty wherever indicated.

–
fissures
Proximal line angles extended buccally and • Enameloplasty
•

lingually through embrasures and cervically – Enameloplasty is the careful removal of sharp and
–
below the gingival margin irregular enamel margins of the enamel surface by
 
– Advantages ‘rounding’ or ‘saucering’ it and converting it into a
–
 
Prevents recurrence of decay in the tooth surface smooth groove making it self-cleansable, finishable

adjoining restoration and allowing conservative placement of margins.
Results in self-cleaning embrasure areas – Enameloplasty is done when caries are present only
–

– Contraindications in the superficial part of the enamel or a fissure is
present in less than one-third thickness of the enamel.
–
Natural remineralization (via calcium and
The enameloplasty does not extend the outline form,

phosphate from saliva)
Fluoride induced remineralization
also the use of enameloplasty often confines the
preparation to one surface and restoration is not done

Advancements in instrumentation
in the recontoured area.

Retention Form
Retention is increased in restorations by the following
Amalgam • Providing occlusal convergence (about 2 to 5%) the dentinal walls towards the tooth surface.
•
 
• Giving slight undercut in dentin near the pulpal wall.
•
 
• Conserving the marginal ridges.
•
• Providing occlusal dovetail
•
• For secondary retention – threaded pins (AIPG 2003)
•

Cast metals • Close parallelism of the opposing walls with slight occlusal divergence of two to five degrees
•
 
• Making occlusal dovetail to prevent tilting of restoration in class II preparations.
•
• Use of secondary retention in the form of coves, skirts and dentin slot.
•
• Give reverse bevel in class I compound, class II, and MOD preparations to prevent tipping movements.
•
Composites • Micromechanical bonding between the etched and primed prepared tooth structure and the composite resin.
•
 
• Providing enamel bevels
•
Direct filling gold • Elastic compression of dentin and starting point in dentin provide retention in direct gold fillings by proper
•
condensation.
Tooth preparation Location of retention grooves

• Class II • Buccoaxial + linguoaxial line angles
•
•
• Class III • Axiogingival line angle
•
•
• Class V (AIPG 2002) • Occlusaloaxial + gingiva axial line angle
•

•

Pulp Protection is Achieved using Liners, Varnishes and Bases Depending Upon
• The amount of remaining dentin thickness (RDT) (NEET 2013)
•

– In human teeth, dentin is approximately 3 mm thick
–
 
– Dentin permeability increases with decreasing RDT
–
 
– RDT of 2 mm or more effectively precludes restorative Damage to the pulp
–
 
– At RDT of 0.75 mm, effects of bacterial invasion are seen
–
– When RDT is 0.25 mm, odontoblastic cell death is seen
–
• Type of the restorative material used.
•
– Liners and varnishes are used where preparation depth is shallow and remaining dentin thickness is more than 2 mm.
–
They provide:
Barrier to protect remaining dentin and pulp

Galvanic and thermal insulation. (AIPG 2005)

– Bases are the cements used on pulpal and axial walls in thickness of about 0.5 to 2 mm beneath the permanent
–
restorations. They provide thermal, galvanic, chemical and mechanical protection to the pulp.
– Commonly used restorative materials as base are zinc phosphate cements, glass ionomers, polycarboxylate cements,
–
zinc oxide eugenol, and calcium hydroxide cement.
Good to Know Points About Biomechanical Preparation • Commonly seen locations of pit and fissure in teeth
•
• Primary determinant of the outline form is the extension are:
•
of the caries. – Palatal pits of maxillary incisors
–
• External shape is related to the contour of the marginal – Palatal grooves and pits of maxillary molars
–
– Occlusal surfaces of posterior teeth
•
gingiva
–
– Facial grooves and pits of mandibular molars
• The axial wall is slightly deeper at the incisal wall, where
–
– Pits occurring in teeth because of irregularities in
•
there is more enamel (1-1.25 mm) than at the gingival
–
the enamel formation.
wall, where there may be little or no enamel (0.75–1 mm)
 
• The direction of mesial and distal walls follows the • The junction of a prepared tooth surface wall and external
•
surface of the tooth forms-Cavosurface angle. The
•
direction of enamel rods, i.e. MD walls diverging, OG
walls diverging (AIPG 2002) acute junction is referred to as preparartion margin or
cavosurface margin.

• All the walls are perpendicular to the external surface and
• High copper amalgam alloys (that include occlusal
•
usually diverge facially
•
dovetail) does not require locks in preparation as they
• Retention grooves placed at the axioincisal and exhibit less creep.
•
axiogingival line angles or 4 retention coves are placed in
• Coves are small conical depressions prepared in healthy
each of the four axial point angles to provide the retention
•
dentin to provide additional retention.
forms. The retention grooves are placed with No. ¼ bur
with 0.2mm into the DEJ and 0.3 to 0.5mm inside the • Slots or internal boxes are 1.0 mm deep box like grooves
•
prepared in dentin to increase the surface area. These are
cemental cavosurface margin. The depth of the grooves
prepared in occlusal box, buccoaxial, linguo axial and
should be half the diameter of the bur head (i.e. 0.25mm).
gingival walls.
• The axial wall is convex mesiodistally following the
• Skirts are prepared on one to all four sides of the
•
external contour of the tooth.
•
preparation depending upon the required retention.
• Direct filling gold is ideal restorative material for class V • Amalgam pins are vertical posts of amalgam anchored
•
cavities.
•
in dentin. Dentin chamber is prepared by using inverted
• The mesial and distal walls will be divergent outwards, cone bur on gingival floor 0.5mm in dentin with 1 mm to
•
allowing maximum tooth bulk for protection of axial line 2mm depth and 0.5 to 1mm width.
angles. If the both class II and V cavities are present, first • Air abrasion technique (advanced particle beam
prepare and restore class V cavity. (AIPG 2011)
•
technology or microabrasion) involves high energy

664
sandblasting of tooth surface. Basically in this technique, Usually they contact at axial line angles. Clamps can also
the abrasion particles are emitted in a well defined sharply be used to retract gingiva. They are tied with dental floss
focused beam to the target. Commonly used particle size approximately of 12 inches before carrying into mouth to
is 25um to 30um with 60 to 120 pounds per square inch prevent accidental swallowing or aspiration.(AIPG 1994)

pressure. • Distance between 2 adjacent holes – ¼ inch or 6.3mm
•

(AIPG 2006)

RUBBER DAM – When more distance is present – wrinkling or folding
–
of rubber dam sheet
• Introduced by SC Barnum in 1864 – When distance is less – stretching of rubber dam sheet
–
• 1st hole to be punched
•

(KAR 2007, PGI 2009)
•

• The dam material is available in 5X5 inches and 6X6 – Maxilla–CI
–
– Mandible: Posterior anchor teeth
•
inches.
–
• For maxillary central incisors, hole lies 1 inch from the
• The thickness or weights available are:
•
superior border of dam
•

(AIPG 2007, MP 2010)
• Isolation of minimum 3 teeth is recommended except in

– Thin (0.006 inches {0.15mm}) (AIPG 2007)
•
cases of RCT (AIPG 2006)
–

– Medium (0.008 inches {0.2 mm})

• For cervical restorations
–
– Heavy (0.01 inches {0.25 mm}) •
–
– Extra heavy (0.12 inches {0.3 mm}) – Thicker dam material is used to aid in gingival
–
–
– Special heavy (0.14 inches {0.35 mm}) retraction
– Hole distance between adjacent holes increases
–
–
• Clasp is an anchoring device for rubber dam. marginally
• When thinner dam is used, holes should be smaller
•
• Clasps with four point contact blades are used for newly
•
• Rubber dam compresses the gingiva but not the clamp.
•
erupting teeth and are also used in single tooth isolation.
•
• Recent Modifications in the Designs of Rubber Dam
•
Insti-Dam • It is recently introduced rubber dam for quick, convenient rubber dam isolation.
•
• Salient Features of Insti-Dam
•
– It is natural latex dam with pre-punched hole and built- in white frame.
–
– Its compact design is just the right size to fit outside the patient’s lips.
–
– It is made up of stretchable and tear-resistant, medium gauge latex material.
–
• Radiographs may be taken without removing the dam.
•
• Built-in flexible nylon frame eliminates bulky frames and sterilization.
•
 
• Off-center, prepunched hole customizes fit to any quadrant—add more holes if desired.
•
 
 
Handi Dam • This is preframed rubber dam, eliminates the need for traditional frame.
•
• Handi dam is easy to place and saves time of both patient as well as doctor. It allows easy access to oral cavity during
•
the procedure.
Dry Dam • Does not require a frame
•
 
Optra dam • It is recently introduced dam in which no metal clamps are required, resulting in fast and easy placement by one
•
person and patient comfort. Both arches are fully exposed and a completely dry field is achieved simultaneously.
Opti dam • It is anatomically designed frame and dam which provide better access and visibility. Because of preshaped dam and
•
frame, the time consuming procedure of conventional rubber dam application is saved. Assembly and placement are
easy and quick.
• Throat shield is especially important when the maxillary prior to procedure. But since it has autonomic effects,
•
tooth is being treated. In this, an unfolded gauze sponge is atropine is contraindicated for nursing mothers and
stretched over the tongue and posterior part of the mouth. patients with glaucoma.
It is useful in recovering a restoration (inlay or crown), if it • Rotary curettage (Gingettage) is troughing technique
•
is dropped in the oral cavity. which is used to remove minimal amounts of gingival
epithelium during placement of restorative margins
• Occasionally, atropine is the drug which is used in subgingivally. This is usually done with a high speed hand
•
restorative dentistry in a dose of 0.3 to 1.0mg, 1-2 hours piece and chamfer diamond bur.

MATRICING AND WEDGING
Parts of ••
Retainer: It holds a band in desired position and shape.
Matrix • Band: It is a piece of metal or polymeric material, intended to give support and form to the restoration during its
•
insertion and setting. Commonly used materials for bands are:
– Stainless steel
–
– Polyacetate
–
– Cellulose acetate
–
– Cellulose nitrate.
–
 
Size and • Matrices range in width from 6.35 mm (1/ 4”) to 9.525 mm (3/8”) for permanent teeth and 3.175 mm (1/8”) to 7.9375
•
mm (5/16”) for deciduous teeth.
placement
• Their thickness may range between 0.0381 mm (0.0015”) to 0.0508 mm (0.002”). (AIPG 2001)
•

• Matrix band should extend 2 mm above the marginal ridge height and 1 mm below gingival margin of the
•
preparation.
Functions • To confine the restoration during setting
•
 
• To provide proper proximal contact and contour
•
• To provide optimal surface texture for restoration
•
• To prevent gingival overhangs.
•
Methods of Tooth Separation
Slow or delayed separation Rapid or immediate separation
• Separating rubber ring/bands • Traction principle
•
•
• Rubber dam sheet • Wedge principle.
•
 
•
• Ligature wire/copper wire
•
 
• Gutta-percha stick
•
• Oversized temporary crowns
•
• Fixed orthodontic appliances.
•
• Traction principle used for separation: This type of the contact area of teeth, which in turn, produce the
•
principle always uses mechanical devices which engages separation. This is usually accomplished by 2 means:
 
the proximal area of the tooth with holding arms. These – Elliot separator
–
holding arms are moved apart to create the separation – Wedges
–
between the contacting teeth. • Elliot separator
•
– Ferrier double bow separator – Also known as ‘Crabclaw’ separator because of its
–
design.
–
Non-interfering true separator.
– Mechanical device consisting of:

Ferrier double bow separator: As the name
–
Bow

indicates, it has 2 bows.

Two holding jaws
Each bow engages the proximal contact area of

Tightening screw.

tooth just gingival to contact area of tooth.

Two holding jaws are positioned gingival
A ‘Wrench’ System is used for turning the threaded

to contact area without damaging the

bars, this helps in causing separation.
 
interproximal area.
Advantages
 
– Clockwise rotation of tightening screw moves

- Stabilization of the separation throughout op-
–
the contacting teeth apart.

 
eration. – These should not be more than thickness of
–
 
- Separation is achieved at expense of both con- periodontal ligament, i.e. 0.2-0.5 mm.

 
tacting teeth rather than one tooth. – Uses: Used for examination and final polishing of
–
Uses: Tooth preparation and during finishing and proximal restoration

polishing of class III direct gold restoration. • Types of wedges:
•
 
• Wedge principle used for rapid separation: A pointed, – Wooden wedges
•
 
–
wedge shaped mechanical device is inserted beneath – Plastic wedges
–
 
666
Wooden wedges • These are most commonly used and preferred as they can be easily trimmed and can be fitted in gingival
•
embrasure
• Adapt well in the gingival embrasure
•
• Easy to use
•
• Wooden wedges absorb water, thus increase the interproximal retention
•
 
• Provide stabilization to matrix band
•
•
•
Available in 2 shapes:
––
Triangular
– Round
–
Triangular wedge • Most commonly used
•
• It has two positions—apex and the base
•
• Apex of the wedge usually lies in gingival portion of the contact area
•
• Base lies in contact with gingiva. This helps in stabilization and retraction of gingiva
•
• Used in tooth preparations with deep gingival margins.
•
Round wedge • Not so commonly used
•
• Made from wooden tooth picks by trimming the apical portion
•
 
• It has uniform shape
•
• Used in class II tooth preparation.
•
Plastic wedges • Though commercially available but they are not much preferred because:
•
• Trimming is difficult
•
• Adaptability is difficult in some cases.
•
Light transmitting wedge • As the name indicates this type of wedge transmits 90-95% of incident light
•
• It is a type of plastic wedge
•
• Transparent in nature
•
• Designed for use in cervical area of class II composite resin restoration.
•
 
• Advantages of light transmitting wedges over other wedges in composite restorations:?
•
 
– Helps in reducing the polymerization shrinkage as it transmits light?
–
 
 
– Better adaptability.
–
• Modified wedging techniques
•
Double wedging • Two wedges are used: One is inserted from buccal embrasure and another is inserted from lingual
•
embrasure. (AIPG 2012)

• This technique is indicated in following cases:
•
– Spacing between adjacent teeth where single wedge is not sufficient
–
 
– Widening of proximal box in buccolingual dimension.
–
– it is trimmed to fit 1mm beyond the preparation margins.
–
• In double wedging technique, two wedges are used, one is inserted from buccal embrasure and another is
•
inserted from lingual embrasure. It is done when single wedge is not sufficient
Wedge wedging • In wedge wedging technique, two wedges are used. One wedge is inserted from lingual embrasure areas while
•
another is inserted between the wedge and matrix band at right angle to the first wedge. It is mainly indicated
while treating mesial aspect of maxillary first premolar.
Piggy back wedging • In this technique two wedges are used.

•
• One (larger) wedge is inserted as used normally, while the other smaller wedge (Piggyback) is inserted above
•
 
 
the larger one.
• It is indicated in cases of shallow proximal box with gingival recession.
•
 
• This technique provides closer adaptation and contour of the matrix band.
•
 

Good to Know the presence of shallow ditching around an amalgam
restoration is not an indication for replacement.
• Tofflemeire universal matrix band retainer was
•
designed by Dr BF Tofflemeire. It is well known as • Intermediary restoration/provisional restorations
•
‘universal matrix’ because it can be used in all types are used in the interim between tooth preparation and
of tooth preparations of posterior teeth, though it fitting a definite restoration. They protect the pulp by
is preferred for class II and compound amalgam sealing and insulating the prepared tooth from the
restorations. oral environment and maintain the tooth position and
• Omni matrix is modified pre-assembled disposable prevent occlusal changes.
•
tofflemeire retainer. It is less time to use. • Zinc oxide eugenol cement is one of the oldest used
•
• Retainerless automatrix system can be adjusted cement. Though other cements are also used for
•
according to tooth shape and size. The matrix is adapted temporization, but zinc oxide eugenol cement is used
over the tooth with the clip on the buccal aspect. To most commonly because it is only mild irritant to the
tighten the band, an automated mechanical device is pulp, less soluble in oral fluids and produce better
used. Once the restoration is complete, the band is cut marginal seal than zinc phosphate.
with the help of cutting pliers.
• In EBA (orthoexthoxybenzoic acid) cement, EBA
• S shaped matrix band is used for restoring distal part of
•
chelates with zinc forming zinc benzoate. Addition of
•
canine and premolar. In this, stainless steel matrix band EBA results in increase in compressive strength and
is taken and twisted like S with the help of a mouth decrease in setting time.
mirror handle.
• In polymer reinforced zinc oxide eugenol cement, resin
• Precontoured matrix/palodent bitine system consists
•
helps in improving strength, smoothness of the mix
•
of precontoured matrices made up of soft metal. In this, and decreasing flow, solubility and brittleness of the
the wedge is used to separate the teeth and hold the cement. Olive oil acts as plasticizer and mask irritating
sectional matrix in position. properties of eugenol.
• Transparent crown forms matrices are ‘stock’ plastic
• The liquid of zinc phosphate cement is phosphoric acid
•
crowns which can be contoured according to tooth
•
and water in the 2:1 ratio.
shape and size. These are specially used for bilateral
class IV preparations. After selecting the appropriate • Repeated opening of the bottle containing the cement
•
crown form. liquid or early dispensing of the liquid prior to mixing
should be avoided because evaporation of liquid can
result in decrease in pH and an increase in viscosity of
Some Indications for Replacing Restorations are as the mixed cement.
Follows • For making temporary restorations, self cure acrylic
•
• Marginal void, especially in the gingival one third, that restorations have been used successfully. When used
with direct technique, free monomer and the heat
•
cannot be repaired.
produced during exothermic reaction can harm pulp
• Poor proximal contour or a gingival overhang that
and the gingival tissues. To avoid this, indirect method
•
contributes to periodontal breakdown.
is used.
• A marginal ridge discrepancy that contributes to food
•
impaction.
Indirect tooth-colored restorations include:
• Overcontour of a facial or lingual surface resulting in
• Processed composite: Although processed composite
•
plaque gingival to the height of contour and result in
•
inflammation of gingiva overprotected from the rubbing- restorations possess improved wear resistance over direct
cleansing action of a food bolus or toothbrush. composites, they are indicated primarily for conservative
Class I and Class II preparations in low to moderate stress
• Poor proximal contact that is either open (resulting
 
areas
•
in interproximal food impaction and inflammation of
impacted gingival papilla) or improper in location or size. • Feldspathic porcelain: Feldspathic porcelain inlays and
•
 
onlays for Class I and II restorations are highly esthetic
• Recurrent caries that cannot be adequately treated by a
but suffer from a relatively high incidence of fracture,
•
repair restoration.
especially if subjected to heavy occlusal forces. Porcelain
• Ditching deeper than 0.5 mm of the occlusal amalgam restorations also have the potential to wear opposing
•
margin that is judged carious or caries-prone. By itself, tooth structure.
668
• Cast ceramic: Cast ceramic inlays and onlays for Class – Tooth preparation.
–
 
•
I and Class II preparations offer excellent marginal fit, – 90-degree cavosurface margins. (AIPG 2007)
–

low abrasion to opposing tooth structure, and superior – Thickness of amalgam (1–2 mm).
–
strength compared to processed composite or feldspathic – Mechanical retention form.
–
 
porcelain. They offer an excellent esthetic alternative to – Seal tubules.
–
cast metal restorations. – Good condensation (including lateral condensation).
–
• Computer-generated [computer-aided design (CAD)/ – Appropriate development of contours and contacts.
•
–
computer-assisted machined (CAM)] inlays and onlays-
Good to Know About Amalgam
Because these restorations are fabricated chairside
[Chairside Economical Restorations of Esthetic Ceramics • In pre amalgamated alloys, mercury 3 percent is used
(CERECTM) system], only one appointment is required
•
which react more rapidly when mixed mercury.
for placement as compared to the two appointments
• Lathe cut is made by cutting fillings of alloy from a pre
required for the other types of indirectly fabricated
•
tooth-colored restorations. Computer-generated ceramic homogenized ingot which was treated at 4200 C for
many hours. The fillings are then reheated at 1000 C for
 
restorations for Class I and Class II preparations possess
high strength and low abrasiveness and are highly esthetic 1 hour for aging of the alloy.
because of the intrinsic coloration and highly polishable • Spherical (spheroidal) alloy is formed when molten
•
nature of the material. alloy is sprayed into a column filled with inert gas, this
molten metal solidifies as fine droplets of alloy.
AMALGAM RESTORATIONS
• Presence of zinc can result in delayed expansion after 3
•
• M Taveau gave the first form of silver mercury mixture in to 5 days of restoration, if during manipulation, zinc
•
1826 at Paris. containing amalgam comes in contact with moisture or
• Dental amalgam is an alloy of mercury with silver, tin saliva. This occurs due to formation of zinc oxide and
•
and varying amounts of copper, zinc and other minor hydrogen gas when zinc react with water. This expansion
constituents. can result in extrusion of restoration beyond preparation
• Types margins and pulpal pain.
•
– Low copper—generally inferior • According to ADA specification no. 1, amalgam should
•
have minimum 1 hour compressive strength of 11,600psi
–
– High copper
–
 
Spherical. (80MPa). Amalgam has higher compressive strength

Greater leakage. (7times) than tensile or shear strength making it brittle
Greater postoperative sensitivity. material.
Admix
• Creep is the time dependent response of an already

• Properties
•
set material to stress. This response is in form of plastic
•
 
– The linear coefficient of thermal expansion (LCTE) of
deformation. By ADA specification no 1, creep is
–
amalgam is greater than that of tooth structure.
limited to 3 percent in a set amalgam.
 
– The compressive strength of high-copper amalgam is
–
similar to tooth structure. • In amalgam, corrosion causes decrease in strength of a
•
 
– The tensile strength of high-copper amalgam is lower restoration, the advantageous fact of corrosion is that
–
than tooth structure. the byproducts that form, seal the preparation margin,
 
– Amalgams are brittle and have low edge strength. resulting in self sealing property of amalgam.
–
– High-copper amalgams exhibit no clinically relevant • In low copper amalgams, the most corrosion prone
–
•
creep or flow. phase is gamma 2 (Sn7-8 Hg3) phase. In these alloys,
 
– Amalgam is a high thermal conductor. corrosion products are tin oxides and tin chlorides.
–
• Clinical performance Here the corrosion proceeds from outer surface to
•
– Marginal fracture. interior of restoration making it porous and spongy.
–
– Bulk fracture. • In high copper amalgam, corrosion amalgam, corrosion
–
 
– Secondary caries.
•
products are similar to that of low copper alloys, in
–
• Necessary factors for a successful amalgam restoration addition there is formation of copper chloride which
•
 
– Appropriately indicated clinical situation. corrode slower than low copper amalgams.
–
– High-copper material.
–

• High copper alloys corrode slower because they • Post carve burnishing is done after completion of
•
•
contain little or none of gamma 2 phase. Also the carving with the help of small sized burnishers using
corrosion is not of penetrating type as in low copper light strokes. It helps in producing denser amalgam at
alloys. margins, improves marginal seal and increases surface
• Microleakage occurs when there is 2 to 20 micron wide hardness.
• Finishing and polishing of the amalgam restoration
•
gap between the amalgam and tooth structure.
•
should be done atleast 24 hours after the placement
• In the bonded amalgam technique, a dentin bonding of the amalgam. Premature finishing and polishing
•
system is used along with a viscous resin liner which interferes with the crystalline structure of the hardening
physically mixes with the amalgam and forms a amalgam. The result will be a weakened restorations
micromechanical union to increase amalgam’s retention with high copper alloys because they have a tendency
to tooth structure. of self polishing.
• For this monomer molecule having hydrophilic and • Scrap amalgam during insertion and condensation
•
•
hydrophobic ends of 4 methoxy ethyl trimellitic anhydride should be carefully collected and stored under water,
(4 META) based systems are used. glycerin or spent X ray fixer solution in tightly capped
• Handling of gallium alloys is difficult because they have jar.
•
tendency to stick to the instruments. This sticking problem • Spent X ray fixer is preferred for storage of amalgam
•
can be reduced by adding a drop of absolute alcohol to scrap because it is source of both silver and sulfide ions,
mix before trituration. Alcohol slowly evaporates and thus which react with mercury present in scrap amalgam to
does not adversely affect the properties of the amalgam. form solid product and decrease the mercury, vapour
• Reverse curve is given in the teeth with broader contacts, pressure.
•
to both widen the box yet remove less tooth structure. It • The accepted threshold limit for exposure to mercury
•
is given to the proximal walls by curving them inwards vapour for 40 hour per week is 50ug/m2 (given by
towards the contact area. OSHA)
• If the excessive flare is given in these teeth, proximal walls • Spherical amalgams (which contain less Hg) are condensed
•
will end past the axial angle of tooth through the cusps
•
with light pressure produce adequate strength.
resulting in weakening of tooth structure and fracture of
• High condensation pressures are required to minimize
restoration.
•
porosity and to expel mercury from lathe cut amalgams.
• Eames preferred 1:1 ratio of alloy/ mercury for best • Methyl Hg is the most toxic form and is absorbed 90 –
•
results. Generally 5:8 or 5:7, if mercury content is more
•
95% from the gut
than required amount, resultant mix will be weaker, but
if it less, it might not sufficiently wet the alloy particles. • Maximum level of occupational exposure that is
•
considered safe is 50µg of Hg/mm3.
• Lathe cut amalgam alloys require more mercury (45%)
• Hg is 14 times denser than H2O
•
to wet than spherical alloys (40%)
•
• Purpose of trituration is to remove oxide layers from • About 65-85% of inhaled Hg vapour is retained in the
•
•
the alloy particles so as to coat each alloy particle body.
with mercury resulting in a homogenous mass for • Half life of Hg is 55days
condensation.
•
• 15µg/ml of Hg in urine and 4ng/ml of Hg in blood is the
• Signs of good trituration are
•
acceptable normal level.
•
– Amalgam is shiny, homogenous mass that adheres • The lower blood Hg level at which earliest nonspecific
–
together.
•
symptoms starts is 35ng/ml and 30µg/ml in urine.
• Undertrituration results in a crumbly mix that is very
Levels of Hg Toxicity
•
weak.
• Mulling is done so that all alloy particles are properly • At level of 4μg: This level is attributed as the upper
•
limit in urine when extensive restoration of amalgam is
•
coated with mercury. In other words it is the
continuation of trituration. present in patient’s month
• Precarve burnishing is done after condensation so as • At level 0-25 μg: No known health hazards are detected
•
•
to improve marginal adaptability of the restoration and • At level 25-100 μg: Decreased response on tests done
•
remove excess mercury from over packed amalgam. for brain conduction. Decreased response related

(AIPG 2012) to verbal skills

 
670
• 100-500 μg: Mild-to-moderate effects can be seen: a. Pin Restorations

•
 
Irritability b. Memory loss c. Depression d. Tremors e. • A pin retained restoration is defined as any restoration
•
 
Nervous system disturbances which requires the placement of pin/pins in the dentin in
order to provide sufficient retention and resistance form
• 500-1,000 μg: Pronounced symptoms
to the restoration.
•
• Inflammation of kidney • Types of Pins
•
•
 
• Tremors and pronounced nervous system disturbances – Direct pins/nonparallel pins.
•
–
– Indirect pins/parallel pins.
–
 
Direct pins Indirect pins
• Are generally made of stainless steel and inserted into • Are made smaller in size when compared to their pinholes and they
•
 
•
dentin after this restoration is placed directly over them. constitute an integral part of a cast restoration. These pins are also known
Pins can also be made from other materials like silver, as the parallel pins because the these pins are placed parallel to each
titanium, stainless steel with gold plating, etc. other and also to the path of insertion of the restoration.
– These pins are also called as the nonparallel pins • Two types of pins are used in the parallel pin technique.
–
•
because they can be inserted directly into the tooth – Cast gold pins: These pins have a smooth surface. For making res-
structure and need not be parallel.
–
toration using parallel pins, place nylon bristles or plastic pins in the
– Direct pins are generally made of stainless steel and pinholes, over this build rest of the restoration in the conventional
–
inserted into dentin after this restoration is placed di- form with a blue inlay wax. Invest whole assembly and cast it with
rectly over them pins forming an integral part of the cast restoration.
– Types of direct pins: – Wrought precious metal pins: Surface of these pins has been
–
- Cemented pins
–
roughened by means of threaded or knurled patterns. Commonly
-
 
- Self-threading pins used pins are alloys of gold, platinum, palladium or platinum-indium.
-
- Friction locked pins In this pins are placed in the pinholes and included in the wax pat-
-
tern. These pins are 20-30% more retentive than smooth cast pins.
• Types of pin sizes
•
Minuta Minikin Minim pins Regular
Smallest of size Minikin pin is considered as the pin of This pin is also preferred in some cases, Regular is largest diameter pin
among these self- choice in grossly decayed posterior depending upon the availability of dentin. among Thread Mate System pins.
 
threaded pins. teeth. This pin causes: • It provides less dentinal crazing as It is rarely used because of its
 
•
It is too small to • Less risk of dentin crazing compared to regular pins. following disadvantages:
•
 
 
provide retention in • Good retention • It is used in cases where pinholes • Great amount of stress and
•
the tooth crazing among pins.
•
•
• Less chances of pulpal retention for minikin was over-prepared or
 
threads strip during pin placement. • More chances of perforation in
•
• Less chances of potential
 
•
pulp chamber.
•
perforation
• Pin Design: All of above mentioned pins are available in the following designs:
•
 
– Standard
–
– Self-shearing
–
– Two-in-one
–
– Link series
–
– Link plus series.
–
• Number of Pins: simple rule should be followed for use of number of pins, i.e. one pin per missing cusp and one pin for
•
each missing axial line angle.
• Pin amalgam restoration is more conservative than tooth preparation for cast restoration. Pins increase the resistance and
•
retention of the restoration
• Pins are contraindicated in patients with occlusal problem, when esthetics is concerned and when direct restoration is not
•
possible because of functional or anatomical considerations.
• Placing pins close to each other (minimum interpin distance 2mm) increases retention. At distances lesser than 2 mm pin
•
retention is reduced because of the less amount of material present between the pins and increase in residual stresses in
dentin. (AIPG 2011, 2007)


• Stresses are seen maximum with use of friction locked and threaded pins in dentin. Stresses are developed since pins
•
are inserted into channels 0.001 to 0.004 mm smaller than the diameter of the pins. If the stresses exceed dentin’s plastic
limit, craze lines or cracks are seen. These fracture lines can cause pulpal involvement. (AIPG 2010)

• Cemented pins are shown to induce the least stresses, threaded pins induce intermediate stresses and friction locked pins
•
the maximum stress.
• Stress tolerance of different types of dentin in a decreasing order is: secondary dentin> sclerosed dentin> tertiary dentin>
•
calcific barrier.
• Cemented pins are therefore the only preferred pins in endodontically treated nonvital teeth.
•
• Concept of amalgam pins was given by Shavell in 1980 to allow amalgam to act as retentive pins. Amalgam pins are
•
vertical posts of amalgam anchored in dentin.
Inlay and Onlay Restorations

• Circumferential Tie
•
– Refers to the design of cavosurface margin of an inlay tooth preparation.
–
– This junction between tooth cement inlay is the weakest part of the cast metal restoration.
–
– For the success of restoration, the margins of restoration should be designed so as to achieve its maximum adaptation
–
to tooth structure.
– Cavosurface margins of an inlay preparation can be of two types:
–
Bevels

Flares.

Bevels
• Inclination that one surface makes with another when not at right angles
•
– Objective of bevel is to form a metal wedge of 30o to 35°, thus enhancing the chance to achieve closure at the interface
–
of cast gold and tooth.
– By beveling, a strong enamel margin with an angle of 140° to 150° can be produced.
–
– Bevels are the flexible extensions, i.e. they allow inclusion of faults, wear facets, etc. without overextending the
–
preparation margins.
– Gingival margins become finishable and cleanasable because of gingival bevels. (AIPG 2011, 2009)
–

– Counter bevel increases the resistance form to remaining tooth structure.
–
– Because of beveling, the gingival margin has a lap sliding fit which provides better fit at this region.
–
• Types of bevel:
•
Ultrashort or partial • Beveling of less than two-third of the total enamel thickness.
•
bevel • Used to trim the enamel rods from preparation margins.
•
• Used in type I casting alloys.
•
Short bevel • Beveling of full thickness of enamel wall but not dentin.
•
• Used mostly for restorations with type I and II casting alloys
•
Long bevel • Includes full thickness of enamel and half or less than half thickness of dentin.
•
 
• Preserves the internal ‘boxed up’ resistance and retention features of the preparations.
•
 
• Used in types I, II and III of cast gold alloys.
•
Full bevel • Includes full enamel and dentinal wall.
•
• It deprives the preparation of its internal resistance
•
• Full bevel should be avoided except in cases where it is a must.
•
 
Hollow ground (con- • Hollow ground is concave in shape and not a bevel in true sense.
•
cave) bevel • It is rarely used.
•
672
Counter bevel • Used when capping of the cusps is done to protect and support them.
•
• It is opposite to an axial wall of the preparation on the facial or lingual surface of the tooth.
•
• It has a gingival inclination facially or lingually.
•
Reverse or inverted • It is beveling in the reverse or inverted shape given on the gingival seat in the axial wall toward the root in
•
bevel in anterior anterior teeth.
teeth:
Reverse or inverted • In posterior teeth (in MOD preparations for full cast metal restorations), it is used to prevent tipping of cast
•
bevel in posterior restoration in the directions shown with the arrows and to increase the resistance and retention.
 
teeth
Flares
– Flares are concave or flat peripheral portions of the facial or lingual proximal walls.
–
– Types:
–
Primary flare Secondary flare
• It is basic part of circumferential tie. It is like a long bevel and is • It is a flat plane superimposed peripherally to the primary flare
•
•
always directed 45° to the inner dentinal wall proper •
•
It may have different angulations, involvement and extent
• Primary flare is indicated when normal contacts are present. depending upon requirement.
•
• When there is minimal extension of caries in buccolingual • Secondary flare is not given in the areas where aesthetics is more
•
•
direction important.
• Functions: • Indications of secondary flares:
•
•
– Weak enamel is removed. – When broad contact area is present
–
–
– Improves junctional relationship between the restorative – To include the faults present on facial and lingual walls be-
–
 
–
 
material and tooth. yond primary flare
– Maintains the marginal seal. – When caries are widely extended in buccolingual direction.
–
–
 
– Brings the facial and lingual margins to cleansable – To include the undercuts present at cervical aspect of facial
–
–
 
and finishable areas. and lingual walls. Advantages of secondary flare:
 
 
– Secondary flare encourages self-cleansing margins because
–
it is extended into the embrasures.
TOOTH COLOURED RESTORATIONS
• Adhesion or bonding: The forces or energies between atoms or molecules at an interface that hold two phases together.
•
• Adherend: The surface or substrate that is adhered
•
• Adhesive/adherent: A material that can join substances together, resist separation and transmit loads across the bond
•
• Adhesive failure: The bond that fails at the interface between the two substrates.
•
• Cohesive failure: The bond fails within one of the substrates, but not at the interface.
•
• Adhesion can occur by
•
– Chemical means
–
– Physical means
–
 
– Mechanical means
–
Reasons for better bonding in moist dentin
• The acetone trails water and improves penetration of the monomers into the dentin for better micromechanical bonding.
•
• Water keeps collagen fibrils from collapsing, thus helping in better penetration and bonding between resin and dentin.
•
Dental Bonding
• Advantages of bonding to the tooth structure
•
– Less microleakage.
–
– Less marginal staining.
–

– Less recurrent caries.
–
– Less pulpal sensitivity.
–
– More conservative tooth preparation.
–
– Improved retention.
–
– Reinforcement of remaining tooth structure.
–
– Reduced sensitivity in cervical erosion/abrasion lesions.
–
– More conservative treatment of root surface carious lesions.
–
• Status of bonding to tooth structure
•
Enamel bonding: (30%–40% phosphoric acid) Dentin bonding
• 15-second etch is sufficient. • Penetration of adhesive monomers into the collagen fibers left
•
 
•
• Is fast, reliable, predictable, and strong. exposed by acid etching
•
• Microleakage is virtually nonexistent at etched enamel margins. – Is slower, less reliable, not as predictable.
–
– May have some microleakage.
•
• Resists polymerization shrinkage forces of composite.
–
– May have similar or higher bond strengths than enamel.
•
 
–
– May not resist polymerization shrinkage forces.
–
• Factors that affect the ability to bond to dentin
•
– Microstructural features of dentin
–
Composition

- Enamel: 90% mineral (hydroxyapatite).

- Dentin: Much less mineral, more organic (type I collagen), and more water.

 
– Structural variations
–
Enamel prisms and interprismatic areas—all etched and bondable

– Dentin-tubules: Peritubular, intratubular, intertubular channels
–
Tubules from pulp to DEJ.

Contain the odontoblastic extensions and fluid.

 
Much larger (2.4 μm) and numerous (45 K/mm2) near pulp than near the DEJ (0.6 μm, 20 K/mm2).

 
 
Fluid movement inside that is dictated by pulpal pressure

 
Sclerosis: Dentin that is aging, below a carious lesion, or exposed to oral fluids exhibit increased mineral content

and is much more resistant to acid-etching and therefore the penetration of dentin adhesive is limited.
Smear layer: This is the debris left on surface after cutting and consists of hydroxyapatite and altered denatured

collagen and fills the orifices of the tubules (forming smear plugs), decreasing dentin permeability by 86%.
Etching that removes the smear layer results in greater fluid flow onto the dentinal surface which may interfere
with adhesion.
Linear coefficient of thermal expansion: For dentin, is altered four times less than the composite material when

subjected to thermal changes.
Dentin Conditioning
• Chemical
•
– Removal of the smear layer by the use of acids and calcium chelators
–
– Acid conditioners:
–
Include phosphoric acid, maleic acid, citric acid, nitric acid, oxalic acid, pyruvic acid and hydrochloric acid.

10% phosphoric acid appears better than 37% concentration as dentin conditioner

Maleic acid removes the smear layer but not the smear plugs.

– Chelators
–
Removes smear layer without significant physical changes or decalcification of the underlying dentin

Usually known as EDTA (pH 7.4)

• Thermal conditioning
•
– Lasers are used as they can cause recrystallization of dentin resulting in fungiform appearance that contributes to
–
increased micro retention.
674

Dentin Bonding Agent

First Generation Dentin Bonding • The first step to achieve bonding to dentin was anticipated by application of coupling
•
Systems agent such as glycerol- phosphoric acid dimethacrylate as a primer and N-2- hydroxy-3-
methacryloxypropyl and N-phenyl phenyl glycine (NPG-GMA) and silane coupling agents.
• Cervident (SS White Co, King of Prussia, PA)-first dentin bonding agent
•
• Low bond strength, in the order of 2 to 3 MPa insufficient to retain the restorative material
•
 
for extended periods of time.
 
• Loss in bond strength overtime.
•
• Lack of stability of individual components during storage.
•
 
 
Second Generation Dentin Bonding • Introduced in late 1970s.
•
Systems • These leave the smear layer intact
•
• Bond strengths ranging from about 4.5 to 6 MPa.
•
• Three types of second generation products were made available:
•
– Etched tubule dentin bonding agents: Etching the tubules with 25% citric acid and
–
then making use of ethylmethacrylate to mechanically interlock with the etched tubules.
– Phosphate ester dentin bonding agents: These bonding agents used analogs of Bis-
–
GMA with attached phosphate esters. The phosphate group bonded with calcium pres-
ent in the tooth structure while the methacrylate end of the molecule bonded to the
composite resin. These bonding agents showed 10 to 30% increase in bond strength.
– Polyurethane dentin bonding agents: These bonding agents were based on the iso-
–
cyanate group of the polyurethane polymer which bonds to different groups present in
dentin like carboxyl, amino and hydroxyl groups.
• Most of these agents used diisocyanates which simultaneously bonded to both the dentin and
•
composite resin.
• Problems with second generation bonding agents:
•
– Low bond strength
–
 
– Unstable interface between dentin and resin because of the insufficient knowledge about
–
the smear layer
Third Generation Dentin Bonding • Advantages

•
Systems – Higher bond strengths (8to15MPa)
–
– Reduced microleakage
–
– Form strong bond to both sclerotic and moist dentin
–
– Reduced need for retention for minimal tooth preparation
–
– Can be used for porcelain and composite repairs
–
– Erosion, abrasion and abfraction lesions can be treated with minimal tooth preparation.
–
 
Fourth Generation Dentin Bonding • Mechanism of bonding:
•
Agents – Characterized by the process of hybridization at the interface of the dentin and the com-
–
posite resin.
– Hybridization is the phenomenon of replacement of the hydroxyapatite and the water
–
in the surface dentin by resin. This resin, in combination with the collagen fibers, forms
a hybrid layer. In other words, hybridization is the process of resin interlocking in the
demineralized dentin surface
– This concept was given by Nakabayashi in 1982.
–
• The fourth generation adhesives consist of:
•
 
– Conditioner (Etchant): Commonly used acids are 37% phosphoric acid, nitric acid, ma-
–
leic acid, oxalic acid, pyruvic acid, hydrochloric acid, citric acid or a chelating agent, e.g.
EDTA. Use of conditioner/etchant causes removal or modification of smear layer, demin-
 
eralizes peritubular and intertubular dentin and exposure of collagen fibrils.

(AIIMS Nov 2010)

– Primer: Primers consist of monomers like HEMA (2-Hydroxyethyl methacrylate) and
–
4-META (4-Metha cryloxyethyl trimellitate anhydride) dissolved in acetone or ethanol.
Thus, they have both hydrophilic as well as hydrophobic ends which have affinity for
the exposed collagen and resin respectively.(AIIMS nov 2013) Use of primer increases
wettability of the dentin surface, bonding between the dentin and resin and encourages
monomer infiltration of demineralized peritubular and intertubular dentin. (AIPG 2009)

– Adhesive: The adhesive resin is a low viscosity, semi filled or unfilled resin which flows
–
easily and matches the composite resin. Adhesive combines with the monomers to form
a resin reinforced hybrid layer and resin tags to seal the dentin tubules.

• Examples:
•
– All bond-2 (Bisco)
–
 
– Scotch bond multipurpose (3M)
–
– Optibond FL (Kerr)
–
 
– Clearfil liner bond 2 (Kuraray).
–
• Advantages
•
– Ability to form strong bond to both enamel and dentin.
–
– High bond strength to dentin (17to25MPa)
–
– Ability to bond strongly to moist dentin
–
– Can also be used for bonding to substrates such as porcelain and alloys (including amal-
–
gam).
Fifth Generation Dentin Bonding • Also known as “one-bottle” or “one- component” bonding agents.
•
Agents • The first product in this category was Prime and Bond.
•
• The basic differences between the fourth and fifth generation dentin bonding agents is the
•
number of basic components of bottles.
• Advantages
•
– High bond strength, almost equal to that of fourth generation adhesives, i.e. 20 to 25
–
MPa.
– Easy to use and predictable.
–
 
– Little technique sensitivity
–
 
– Reduced number of steps
–
 
– Bonding agent is applied directly to the prepared tooth surface
–
– Reduced postoperative sensitivity.
–
• Disadvantages: Lesser bond strength than fourth generation bonding agents.
•
• Fifth generation systems in the market.
•
 
– Prime and Bond (Dentsply)
–
 
– OptiBond Solo (Kerr)
–
 
– Single Bond (3M)
–
Sixth generation dentin bonding • Further of two types:
•
agents • Self etching primer and adhesive
•
• Available in two bottles:
•
– Primer
–
– Adhesive
–
• Mechanism of bonding:
•
– In these agents as soon as the decalcification process starts, infiltration of the empty
–
spaces by dentin bonding agent is initiated
• Advantages of self etching primers:
•
– Comparable adhesion and bond strengths to enamel and dentin.
–
– Reduce post operative sensitivity because they etch and prime simultaneously.
–
– They etch the dentin less aggressively than total etch products.
–
– The demineralized dentin is infiltrated by resin during the etching process.
–
– Since these do not remove the smear layer, the tubules remain sealed, resulting in less
–
sensitivity.
– They form relatively thinner hybrid layer than traditional product which results in com-
–
plete infiltration of the demineralized dentin by the resin monomers.
– This results in increased bond strength.
–
– Much faster and simpler technique.
–
– Less technique sensitive as fewer number of steps are involved for the self etch system
–
 
• Disadvantages of self etching primers:
•
– pH is inadequate to etch enamel, hence bond to enamel is weaker as compared to
–
dentin.
– Bond to dentin is 18 to 23 MPa.
–
 
– Since they consist of an acidic solution, they cannot be stored and have to be refreshed.
–
– May require refrigeration
–
– High hydrophilicity due to acidic primers
–
– Promote water sorption
–
 
– Limited clinical data.
–
• Total etch technique
•
– Total etch technique involves the complete removal of the smear layer by simultaneous
–
acid etching of enamel and dentin.
676
– According to this, smear layer is considered hurdle to adhesion because of its low cohe-
–
sive strength and its weak attachment to tooth structure.
– After total etching, primer and adhesive resin are applied separately or together.
–
– Acid removes the dentin smear layer, raises surface energy and modifies the dentin sub-
–
strate so that it can be infiltrated by subsequently placed primers and resins.
Seventh Generation Bonding • They achieve the same objective as the 6th generation except that they simplified the multiple
•
Agents sixth generation materials into a single component, single bottle system, thus avoiding any
mistake in mixing.
• They provide the bond strength of 18 to 25 MPa.
•
• Both the sixth and seventh generation adhesives are self etching, self priming adhesives
•
which are minimum technique sensitive. The seventh generation DBAs have shown very little
or no postoperative sensitivity. Example of seventh generation bonding agent is ‘i Bond’
• Nanofilled Bonding Agents

•
– These bonding agents contain extremely small filler particles. Bonding agents under this type are Prime and Bond
–
NT (Dentsply/Caulk)
– Prime and Bond NT contains 7-nanometer fillers, greater concentration of resin and a smaller molecular weight
–
resin.
– Advantages of Using Small Fillers
–
Small fillers make the bonding agent tougher and stronger.

Covers dentin in one application

It has shown that they penetrate dentin better

Provide improved marginal integrity

Allow film thickness

Satisfactory bonding to sclerotic and aged dentin

• Smear layer is apparently responsible for:
•
– Physical barrier for bacteria and bacterial products
–
– Restricting the surface area available for diffusion of both small and large molecules.
–
 
– Resistance to fluid movement. In vital teeth, the smear layer restricts the dentinal fluid from flushing the dentin surface.
–
 
It also hinders the chemical process that produces marginal seal
– In nonvital teeth, marginal seal is improved because of the lack of moisture within dentinal tubules.
–
– The initial sealing process occurring under amalgam restorations may be compromised because of inability of the smear
–
layer and its penchant for leaching under amalgam.
– This leaching process will produce a widening of amalgam tooth microcrevice and ultimately weaken the sealing
–
mechanism.
• Agents for Smear Layer Removal
•
– Citric acid: Acid etching dentin for 60 sec with 6% citric acid removed nearly all of the smear layer as well as the
–
surface peritubular dentin of the tubules.
– Polyacrylic acid: It is used in combination with glass ionomer cement. An application of not more than 5 sec followed
–
by a copious water rinse results in cleaner surface.
– Chelating agent, EDTA: The use of chelating agents soften the smear layer allowing its successful removal. Although
–
it is not bacteriocidal, but it is considered to be antibacterial to the extent since it eliminates the bacteria contaminated
smear layer.
– Maleic acid: Maleic acid has been in use as acid conditioner in some adhesive systems.
–
Composite Resins have been Classified in Different Ways:
According to Skin- • Traditional or conventional composite—8-12 μm
•
ner • Small particle filled composites—1-5 μm
•
 
• Microfilled composites—0.4-0.9 μm
•
 
• Hybrid composites—0.6-1 μm
•

Philips and Lutz • Macrofiller composites (particles from 0.1-100 μ)
•
classification ac- • Microfiller composites (0.04 μ particles)
•
cording to filler • Hybrid composites (fillers of different sizes).
particle size
•
According to the •
•
Traditional composite resins
mean particles size • Hybrid composite resins
•
of the major fillers • Homogeneous microfilled composites—if the composite simply consists of fillers and uncured matrix
 
•
 
 
material, it is classified as homogeneous
• Heterogeneous microfilled composites—if it includes procured composites and other unusual filler, it is called
•
 
as heterogeneous.
Classification ac- • Megafill
•
cording to Bayne • Macrofill
•
and Heyman • Midifill
•
• Minifill
•
• Microfill
•
• Nanofill
•
Classification ac- • BIS-GMA
•
 
cording to matrix • UDMA
•
compositions
“Smart” Composite
• In smart composites the micron size sensor particles are embedded during manufacturing process into composite. These
•
sensors interact with resin matrix and generate quantifiable anions. This type of composites was introduced in 1998
under the name Ariston pHc (Vivadent).
• It releases fluoride, hydroxyl and calcium ions if the pH falls in the vicinity of the restoration. The fall in pH value is
•
attributed to the deposition of plaque in that area. Smart composites work based on the recently introduced alkaline
glass fillers which inhibit the bacterial growth and thereby reduce formation of secondary caries. The paste of smart
composites contain Barium, Aluminium Fluoride and Silicate glass fillers with Silicon dioxide, Ytterbium trifluoride and
Calcium silicate glass in dimethacrylate monomers. Filler content in these composites is 80% by weight.
• The fluoride release from smart composites is higher than that of compomers but less than conventional glass ionomers.
•
Fiber Reinforced Composite
• In this, silane treated glass fiber or plasma treated polyethylene are added to resin matrix during the manufacturing process.
•
• Advantages of addition of polyethylene fibers are that they strengthen the restoration and increase its toughness.
•
• Vectris (Ivoclar Williams, Amherst, Ny) is recent material which has been built from fiber reinforced technology.
•
• Advantages of Fiber Reinforced Composites
•
 
– High flexure strength
–
 
– Increased compressive strength
–
Ceromers (Ceramic Optimized Polymer)
• It is advanced type of composite material, which also utilized the properties of ceramic fillers (metal oxides).
•
• Introduced by Ivoclar who termed it Tetric ceram
•
• Properties similar to composites
•
• Fluoride release less than conventional GIC or compomer
•
• Composition: CEROMERs consist of fine particle ceramic fillers, which are closely packed and embedded in advanced
•
 
organic polymer matrix. This material consists of paste containing barium glass, ytterbium trifluoride and silicon dioxide
in dimethacrylate monomers.
678
• Advantages:
•
 
– Ease of final adjustment.
–
– Excellent polishability.
–
– Low degree of brittleness, hence less chances of fracture.
–
– Good abrasion resistance.
–
– Optimum aesthetic properties.
–
• Indications
•
– Shallow lesions.
–
– Deep lesion with minimal occlusal access.
–
– Large cervical defects.
–
– Pulp capping.
–
– Splinting.
–
Ormocers – organically modified ceramics
• Composed of a polymer of multifunctional urethane and thioether acrylate alkoxysilanes.
•
• The silanes provide for rigid 3D structure and methacrylate groups available for photochemical polymerization.
•
• Supplied in tube
•
• Filler particle – 1 – 15u, filler volume- 61%
•
• Properties (as compared to composites)
•
– Increased hardness and strength
–
– Increased abrasion resistance
–
– Decreased polymerization shrinkage
–
– CTE close to that of tooth – less thermal expansion
–
– Biocompatible
–
– More protective against caries
–
• Giomers–Pre reacted GIC with composite
•
• Compomer–Polyacid modified composite
•
Polymerization Shrinkage
• It accounts for 1.67–5.68 percent of the total volume.
•
• In light cured composites, about 60% polymerization occurs within 60 seconds, further 10% in next 48 hours; remaining
•
resin does not polymerize.
• Since the material nearest to the light sets first. Shrinkage in light cured composites occurs in the direction of light
•
• For chemical cured composites shrinkage occurs slowly and uniformly towards the center of restoration
•
• Polymerization shrinkage can result in:
•
– Postoperative sensitivity
–
 
– Recurrent caries
–
 
– Failure of interfacial bonding
–
 
– Fracture of restoration and tooth
–
• Polymerization shrinkage can be reduced by:
•
– Decreasing monomer level
–
– Increasing monomer molecular weight
–
– Improving composite placement technique: Placing successive layers of wedge-shaped composite (1–1.5 mm)
–
 
decreases polymerization shrinkage
• Polymerization rate:“soft-start” polymerization reduces polymerization shrinkage
•

Configuration or “C-factor”
• The cavity configuration or C-factor was introduced by Prof Carol Davidson and his colleagues in 1980s. The configuration
•
factor (C-factor) is the ratio of bonded surface of the restoration to the unbonded surfaces. The higher the value of ‘C’-
factor, the greater is the polymerization shrinkage (AIPG 2012)

C factor = Bonded surface
Unbonded surface
Microleakage and Nanoleakage
Microleakage Nanoleakage
• Passage of fluid and bacteria in microgaps (6–10 m) between • It is passage of fluid/dissolved species in nanosized (9–10 m)
•
•
 
restoration and tooth. It can result in damage to the pulp. gaps. These nanosized porosities occur within hybrid layer.
Microleakage can occur due to: These can occur because of: – Inadequate polymerization of
 
 
– Polymerization shrinkage of composites primer before application of bonding agent. – Incomplete resin
 
 
infiltration.
–
– Poor adhesion and wetting
 
• Polymerization shrinkage of maturing primer resin. Nanoleakage
–
– Thermal stresses
•
 
can result in sensitivity during occlusal and thermal stresses.
–
– Mechanical loading
–
 
• Microleakage can result in bacterial leakage which can further
•
cause discoloration, recurrent caries and pulpal infection.
Curing Lamps
Several techniques have been used for curing of light cure composite resins. The various types of light used in curing of composite
are: (AIPG 2010)

 
• Tungsten-Quartz halogen curing unit (TQH)
•
 
• Plasma arc curing unit (PAC)
•
 
• Light emitting diode unit (LED)
•
 
• Argon laser curing unit.
•
Tungsten-quartz Halogen • Conventional and most commonly used curing light for composite resins.
Curing Unit (TQH)
•
• It is incandescent lamp which uses visible light in the wavelength in the range of 410-500 nm.
•

(AIPG 2005)

• Disadvantages of this technique are:
•
– Limited bulb life, i.e. 100 hours.
–
– Intensity of bulb decreases with time.
–
– Time consuming.
–
Plasma Arc Curing Unit • In late 1990’s, this system has been introduced as a means of rapid light curing.
(PAC)
•
• Mechanism: In this, high frequency electrical field is generated using high voltage. This field ionizes
•
the xenon gas into a mixture of ions, electrons and molecules, thereby releasing energy in the form of
plasma.
• Light guide helps in filtering the light to spectrum of visible light (450-500 nm) for peak absorption of
•
camphoroquinone. PAC produces high intensity light more than 1800 mW/cm2 curing cycle in PAC is
6-9 seconds
• Disadvantages of this technique are:
•
– Expensive.
–
– Large size.
–
680
Light Emitting Diode Unit Light emitting diode unit usually have long life and emits powerful blue light. This light falls in narrow
(LED) wavelength range of 400-500 nm which is in the range of camphoroquinone photoinitiator found in most of
composite resins.
Advantages
• Low power consumption.
•
• Can be used with batteries also.
•
• Does not require filter.
•
 
• Long life, i.e. 10,000 hours (approximately).
•
• Minimal changes in light output over time.
•
Disadvantage
Only suitable for camphoroquinone based composites (because it has limited wavelength spectrum).
Argon Laser Curing Unit Argon laser light has a wavelength of 470 nm which is monochromatic in nature. It produces intensity of
200–300 mW.
Advantages
• Polymerization is uniform, not affected by distance.
•
• Greater depth of curing achieved with this light.
•
• Degree of polymerization is higher with dark shades as compared to conventional halogen lights.
•
 
Disadvantages
• May affect adjacent restorations.
•
• Chances of damage to pulp can occur due to rise in ?temperature.
•
 
Glass Ionomer Cements
Classification Of Glass Ionomer Cements
According to their use Type I—For luting cements
Type II—For restorations
Type III—Liners and bases
Type IV—Fissure sealants
Type V—Orthodontic cements
Type VI—Core buildup
Generation Of Glass Ionomers

ASPA I Discovery of the glass ionomer cement resulted as a hybrid of silicate cements and zinc polycarboxylates. But these initial
cement pastes were impracticable, with slow setting and hydrolytically unstablity. There was less reactivity of the glass
powder towards the polymer. Wilson and Kent in 1972 produced first glass that was high in fluoride, content called as
ASPA. However, ASPA I showed slow setting, susceptible to moisture and low translucency.
ASPA II Wilson and Crisp in 1972 added d-tartaric acid to extend the working time and promote a snap set by helping ion extraction
from the glass particles. The use of tartaric acid allowed the use of lower fluoride containing glasses, which are less opaque.
This modification of ASPA I was called as ASPA II.
ASPA III In ASPA II cement, polyacrylic acid was used as liquid which has a tendency to gel with time because of increase in
intermolecular hydrogen bonds. In ASPA III cement, methyl alcohol was added to polyacrylic acid solutions because methyl
alcohol inhibits the ordering of structures in solution and thereby gelation.
ASPA IV Since copolymers of acrylic acids are less regular than polyacrylic acid, they are less liable to form intermolecular hydrogen
bonds. To improve stability of cement, in ASPA IV cements, copolymer of acrylic and itaconic acid was made, which showed
more stability
Fluoride releasing ability of glass ionomers also depends on following factors:

• Hand mixed glass ionomers release less fluoride than mechanically mixed glass ionomers.
•
 
• On addition of resin monomers to its composition, fluoride release decreases significantly.
•
 
• Covering of GIC restoration with a sealant reduces fluoride release.
•
 

BLEACHING
• Stains caused by different metals
•
– Copper dust—green stain.
–
– Iron dust—brown stain.
–
– Mercury—greenish black stain.
–
– Nickel—green stain.
–
– Silver—black stain.
–
Classification of Extrinsic Stains (Nathoo in 1997)
• N1 type dental stain (Direct dental stain)—Here colored materials bind to the tooth surface to cause discoloration. Tooth
•
has same color, as that of chromogen.
• N2 type dental stain (direct dental stain)—Here chromogen changes color after binding to the tooth.
•
• N3 type dental stain (Indirect dental stain)—In this type prechromogen (colorless) binds to the tooth and undergoes a
•
 
chemical reaction to cause a stain.
Constituents of Bleaching Gels

• Carbamide Peroxide (CH6N2O3) • It is a bi functional derivative of carbonic acid.
•
•
• It is available as:
•
– Home bleaching - 5%, 10%, 15%, 20% carbamide peroxide
–
 
– In office bleaching - 35 percent solution or gel of carbamide peroxide.
–
 
• Hydrogen Peroxide (H2O2) H2O2 breaks down to water and nascent oxygen. It also forms free radical perhydroxyl (HO2) which
•
is responsible for bleaching action
• Sodium Perborate • It comes as monohydrate, trihydrate or tetrahydrate. It contains 95 percent perborate, providing
•
•
10 percent available oxygen.
• Thickening Agents • Carbopol (Carboxy polymethylene): Addition of cabopol in bleaching gels causes:
•
•
– Slow release of oxygen.
–
– Increased viscosity of bleaching material, which further helps in longer retention of material
–
in tray and need of less material.
– Delayed effervescence–thicker products stay on the teeth for longer time to provide neces-
–
sary time for the carbamide peroxide to diffuse into the tooth.
 
– The slow diffusion into enamel may also allow tooth to be bleached more effectively
–
• Urea • It is added in bleaching solutions to:
•
•
– Stabilize the H2O2
–
 
– Elevate the pH of solution.
–
– Anticariogenic effects.
–
• Surfactants • Surfactant acts as surface wetting agent which allows the hydrogen peroxide to pass across
•
•
gel tooth boundary.
• Preservatives • Commonly used preservatives are phosphoric acids, citric acid or sodium stannate. They
•
•
sequestrate metals such as Fe, Cu, Mg accelerate breakdown of H2O2 and give gels better
durability and stability.
• Vehicle • Glycerine: It is used to increase viscosity of preparation and ease of manipulation.

•
•
• Dentifrice
•
• Flavors • They are added to improve patient acceptability
•
•
• Fluoride and 3% Potassium They are added to prevent sensitivity of teeth after bleaching.
•
Nitrate
682
Mechanism of Bleaching
Mechanism of bleaching is mainly linked to degradation of high molecular weight complex organic molecules that reflect a
specific wavelength of light that is responsible for color of stain. The resulting degradation products are of lower molecular
weight and composed of less complex molecules that reflect less light, resulting in a reduction or elimination of discoloration.
Rate of color change is affected by

• Frequency with which solutions are to be changed. • Amount of time, the bleach is in

contact with tooth.
• Viscosity of material. • Rate of oxygen release.

• Original shade and condition of the tooth. • Location and depth of discoloration.

• Degradation rate of material.

Bleaching Technique
For vital teeth For nonvital teeth
• Home bleaching technique/Night guard vital • Thermocatalytic in-office bleaching.
•
•
bleaching. – Superoxol is placed in pulp chamber and heated to produce
–
– 16-25% carbamide peroxide (AIPG 2012) oxidative radicals (AIPG 2006)
–
 

• In-office bleaching – Increased incidence of external cervical root resorption
•
 
–
– Thermocatalytic • Walking bleach/Intracoronal bleaching
•
–
- 30 – 35% H2O2 (superoxol ) is used. – Uses sodium perborate mixed in water/normal saline or sodium
-
–
– Non-thermocatalytic perborate mixed with 30% H2O2
–
– Microbrasion. – Advantages are less chair time required
–
–
• Inside/outside bleaching
•
 
• Closed chamber bleaching/Extracoronal bleaching.
•
• Ultraviolet Photo oxidation
•
– Superoxol is placed in pulp chamber followed by exposure to UV
–
light for 2 mins
• Laser assisted bleaching.
•
Softening of the restoration: Using the Knoop hardness test, Hannin and colleagues reported a significant decrease in the
surface hardness of bleached composite resins, not only on superficial surfaces, but in the deeper layers of the filling materials
as well. Similarly, another research study concluded that bleaching with different peroxide concentrations significantly
decreased the surface microhardness of a microfilled composite resin. These results were related to the high oxidation and
degradation of the resinous matrix in the composites.
• Decrease in tensile strength.
•
• Increased microleakage.
•
• Surface roughening. (NEET 2013)
•

MISCELLANEOUS
Micro and Macro Abrasion (AIPG 2004)
Microabrasion • Involves surface dissolution of the enamel by hydrochloric acid along with abrasiveness of the pumice to remove
•
superficial stains or debris
• In newer products
•
– 11% HCl concentration
–
– Silicon carbide is used instead of pumice
–
• Stains and discolorations are removed by physical removal of tooth structure. There is no bleaching action
•
involvement.

• Indications
•
– Stains limited to most superficial layer of enamel with depth no more than 0.2 -0.3mm
–
– Fluorosis stains
–
••
Immediately following treatment, topical fluoride is applied to the teeth to enhance mineralization.
• It has the advantage of ensuring better control of removal of tooth structure
•
• More recommended in children than macroabrasion
•
Macroabrasion • Uses 12 fluted composite finishing bur or a fine grit finishing diamond in a high speed handpiece to remove the
•
defect
• Air water spray is recommended both as a coolant and to maintain a hydrated state to facilitate assessment of
•
defect removal.
McInnes Microab- • A solution of sparts 30% H2O2, Sparts 36% HCl and 1 part diethylether is applied directly to the desired area for
•
sion Technique 1-2 minutes.
• A 30 fluted composite finishing bur is used to remove any facets or striations at the treatment. Final polishing is
•
done with abrasive and rubber point.
• It is technique sensitive and can have catastrophic results if the clinician fails to use extreme caution.
•
• Faster and doesn’t require the use of rubber dam
•
Good to Know
• Gallium alloys was introduced by Puttkamer in 1928.
•
• Disadvantage of Gallium alloys
•
– Surface roughness
–
– Expansion leads to tooth fracture
–
– Marginal discoloration
–
– Difficult manipulation
–
• The percentage of unconsumed alloy in low copper amalgam is 8.8%
•
• The most frequent complaint of patients shortly after amalgam restoration is placed is cold sensitivity.
•
• Pin retained amalgam is not used in hypoplastic teeth
•
Difference between class II amalgam and cast restoration is mainly bevels.
Type of cavity I II III V MOD
Point angle 4 6 3 4 8
Line angle 8 11 6 8 14
Proximal cavity walls - 4 4 - 8
• Cohesion of gold occurs by cold welding or metallic bond between increments of gold under the pressure of compaction.
•
• Electra alloy is electrolytic precipitate of gold, alloyed with calcium. The calcium content of the finished product is about
•
0.1%. its purpose is to produce stronger restorations by dispersion strengthening.
Types of Gold Use
• Mat gold • Bulk filler

•
•
• Gold foil • For external surface veneering
•
•
• Mat foil • Veneering
•
•
• Electralloy • Core and finishing
•
•
• Photopolymerization stress build up can be reduced by soft start polymerization.
•
• Concentration above 50% H3PO4 results in the formation of monocalcium phosphate monohydrates which prevents
•
dissolution. Concentration below 30% results in dicalcium phosphate dehydrate that cannot be easily removed.
684
• Sprue gauze for inlay – 8-12

•
• Sprue gauze for onlay – 10-14
•
• Class II inlay: Preparation feature that prevent proximal displacement – occlusal dovetail and proximal grooves
•
– Preparation feature that occlusal displacement – parallel facial and lingual proximal walls
–
• Water quenching of investment after casting helps in cracking of investment resulting in easy removal of gold casting –
•
particularly used for gypsum bonded investments used for gold alloys.
• The sprue should be positioned in the thickest portion of the pattern. It should also be attached at the least anatomical area
•
ie an area of no grooves, cuspal anatomy, fossa or ridges.
• The ideal position is near the proximal surface or just below the non functional cusp. The next choice is marginal ridge.
•
• Chisel with shank and blade slightly curved – Wedelsaedt chisel

•
• Horning machine is used to hold silver points
•
• The number of blades or teeth in a bur is usually 6-8 (always even). Increasing the blade number decreases the amount
•
of material engaged by each blade, resulting in less cutting, clogging and smooth finish. Burs used for finishing and
polishing have upto 40 blades.

(AIPG 2003)

• Beilby layer is a synonym for molecular disorganized surface on a highly polished metal. (AIPG 2010)
•

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REVIEW OF

ALL DENTAL SUBJECTS

The Health Sciences Publisher

Review of All Dental Subjects

From the Publisher’s Desk

Eyes Corneal Keratocyte

Myofibroblast Fibroblast Fibrocyte

Arch Skeletal element Nerve Muscle

Skull is composed of 22 bones. (AP 2003, 1999)

Lambda Junction of sagittal and lambdoid sutures

Pterion (AIPG 2006, Man 2000)

Saddle joint (Sellar) Thumb, sternoclavicular calcaneocuboidal, incudo-

Ball and socket Shoulder, hip, incus- stapedial joint

They are called joints of ‘yes’ or “positive” expression

Lesser palatine foramen Transmits middle and posterior palatine nerves.

Palatovaginal canal transmits • Pharynegeal branch from pterygopalatine ganglion.

Canalis innominatus Tansmits lesser petrosal nerve.

Foramen magnum • Through wider posterior part

Jugular foramen (AIPG 2003) Through anterior part;

Typmpanic canailculus Transmits tympanic branch of glossopharyngeal nerve to middle ear.

Optic canal transmits Optic nerve and ophthalmic artery

Good to know points

Facial expressions Muscles involved

Sadness Levator labli superioris and levator anguli oris

Grief Depressor anguli oris

Anger Dilator naris and depressor septi

Frowning (KAR 2000) Corrugator supercilii and procerus

Functional groups of facial muscles

Nostrils Compressor naris • Dilator naris.

The posterior branches are small and unnamed.

Superficial temporal artery Transverse facial is a small branch of superficial temporal.

Dangerous area of Face

- Deep layer: Into the upper part of the ramus

* Lower head: Arises from the • Articular disc of

• Medial pterygoid: It is a thick Raises the mandible

Protrusion (PGI 2001) Lateral and medial pterygoid

• The daily secretion of saliva: 500 and 1500 milliliters.

• Hyoglossus • Lateral side of tongue • Hypoglossal • Depression of tongue

• Chondroglossus: • Into the musculature of tongue • Hypoglossal • Aids hyoglossus

• Styloglossus: • It blends with the musculature • Hypoglossal • Upward and backward

• Verticalis: Flattens and broadens the

The longitudinal muscle coat consists of: Hypopharyngeal diverticula

Inferior meatus (largest) Nasolacrimal duct

• Posterior ethmoidal air sinus opens into: (COMEDK 2012)

• The lateral wall and the floor are completed

Blood, Nerve Supply and Lymphatic Drainage

• Internal and external carotid systems.

Anterior Triangles (AIPG 2003)

Submental triangle Submental lymph nodes

Digastric triangle ANTERIOR PART

Muscular triangle INFRAHYOID MUSCLE

Posterior Triangles Important contents

Action a. When one muscle contracts:

• The different folds of dura mater are

Falx cerbelli Sickle shaped, encloses occipital sinus

Diaphragm sellae Forms the roof of hypophyseal fossa

• Venous sinuses of dura mater are:

1,2,3 Primary sensory cortex; lies in the postcentral gyrus

White Matter of Cerebral Hemispheres

Part Descending fibres Ascending fibres

Genus Cortico nuclear Anterior part of superior thalamic radiation

• Main functional areas of cerebral cortex

Fleeing, Feeding and sex.

Hypothalamus “Head ganglion of the autonomic nervous system”

Carries preganglionic fibres of superior salivary