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ation on dental books, visit our website www.jaypeebrothers.com, for detailed information on dental books, visit our website www.jaypeebrothers.cor

Anil Govindrao Ghom

Savita Anil Ghom (Lodam)

Textbook of
ORAL
MEDICINE
with FREE Book on Basic Oral Radiology

Foreword
THIRD EDITION Mahesh Verma
*
 Textbook of
Oral Medicine
 Textbook of
Oral Medicine
Third Edition

Editors
Anil Govindrao Ghom
MDS (Oral Medicine and Radiology)
Dean, Professor and Head
Department of Oral Medicine and Radiology
Maitri Dental College and Research Institute
Anjora, Durg, Chhattisgarh, India
Formerly
Rural Dental College, Loni
VSPM’s Dental College, Nagpur
Maharashtra, India
Chhattisgarh Dental College and Research Institute
Rajnandgaon, Chhattisgarh, India

Savita Anil Ghom (Lodam)

MDS (Oral Medicine and Radiology)
Senior Lecturer
Department of Oral Medicine and Radiology
Maitri Dental College and Research Institute
Anjora, Durg, Chhattisgarh, India

Foreword
Mahesh Verma

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ISBN 978 -93 -5152 -303 -1
Printed at
 Dedicated to
The loving memory of my
Mother Shantabai Ghom
and
Father Govindrao Ghom
 Contributors

Abhijeet Deoghare Anshul Khandelwal

Reader Senior Lecturer
Department of Oral Medicine and Department of Oral Medicine and
Radiology Radiology
Chhattisgarh Dental College and Maitri Dental College
Research Institute Durg, Chhattisgarh, India
Rajnandgaon, Chhattisgarh, India

Abhinav Singhal Barakha Nayak

Postgraduate Student Senior Lecturer
Department of Pedodontia Department of Oral Pathology
Maitri Dental College Maitri Dental College
Durg, Chhattisgarh, India Durg, Chhattisgarh, India

Abhishek Soni Mandeep Kaur

Reader Associate Professor
Department of Periodontia Department of Oral Medicine and
Maitri Dental College Radiology
Durg, Chhattisgarh, India Faculty of Dentistry
Jamia Millia Islamia
New Delhi, India

Ajit Mishra Manjari Gandhi (Gupta)

Senior Lecturer Postgraduate Student
Department of Oral Medicine and Department of Oral Medicine and
Radiology Radiology
Maitri Dental College Chhattisgarh Dental College and
Durg, Chhattisgarh, India Research Institute
Rajnandgaon, Chhattisgarh, India

Amina Sultan Mansi Tiwari

Associate Professor Postgraduate Student
Department of Pedodontics and Department of Oral Medicine and
Preventive Dentistry Radiology
Faculty of Dentistry Chhattisgarh Dental College and
Jamia Millia Islamia Research Institute
New Delhi, India Rajnandgaon, Chhattisgarh, India

Amit Parate Neha Dandwani

Lecturer Lecturer
Department of Oral Medicine and Department of Oral Medicine and
Radiology Radiology
Government Dental College Maitri Dental College
Nagpur, Maharashtra, India Durg, Chhattisgarh, India

Anil Ghom Pravin Lambade

Dean, Professor and Head Professor
Department of Oral Medicine and Department of Oral Surgery
Radiology Kalmegh Dental College
Maitri Dental College and Nagpur, Maharashtra, India
Research Institute
Anjora, Durg, Chhattisgarh, India
 Raghvendra Shetty Savita Ghom (Lodam)
Professor Senior Lecturer
Department of Pedodontia Department of Oral Medicine and
Chhattisgarh Dental College and Radiology
Research Institute Maitri Dental College and Research
Rajnandgaon, Chhattisgarh, India Institute
Anjora, Durg, Chhattisgarh, India

Rajkumar Diwan Shalu Rai

Senior Lecturer Professor
Department of Oral Medicine and Department of Oral Medicine and
Radiology Radiology
Maitri Dental College Institute of Dental Studies and
Durg, Chhattisgarh, India Technologies
Modinagar, Uttar Pradesh, India

Ranit Chhabra Shweta Tikekar (Singh)

Private Practitioner Senior Lecturer
Raigad, Chhattisgarh, India Department of Oral Medicine and
Radiology
New Horizon Dental College
Bilaspur, Chhattisgarh, India
Textbook of Oral Medicine

Sachin Dev Sachdeva Smriti Goswami

Head Oral Pathologist
Head and Neck Trauma Unit and Parker, Lynn, Auckland
Director, PG Medical Education and New Zealand
Research
Delhi Institute of Healthcare and Research
New Delhi, India

Sachin Manglekar Sonal Vahanwala

Professor Professor
Department of Periodontia Department of Oral Medicine and
Maitri Dental College Radiology
Durg, Chhattisgarh, India DY Patil Dental College
Mumbai, Maharashtra, India

Sarbani Deb Sikder Sukhdeep Singh

Senior Lecturer Professor
Department of Oral Medicine and Department of Pedodontics and
Radiology Preventive Dentistry
Government Dental College and Hospital School of Dental Sciences
Raipur, Chhattisgarh, India Greater Noida, Uttar Pradesh, India

Satish Chugani Vikas Mehsram

Postgraduate Student Professor
Department of Oral Medicine and Department of Oral Surgery
Radiology Kalmegh Dental College
Chhattisgarh Dental College and Nagpur, Maharashtra, India
Research Institute
Rajnandgaon, Chhattisgarh, India

viii
Virender Gombra Vivek Thombre
Assistant Professor Reader
Department of Oral Medicine and Department of Periodontia
Radiology Chhattisgarh Dental College and
Faculty of Dentistry Research Institute
Jamia Millia Islamia Rajnandgaon, Chhattisgarh, India
New Delhi, India

Vivek Lath
Senior Lecturer
Department of Prosthodontia
Maitri Dental College
Durg, Chhattisgarh, India

Contributors

ix
Prof (Dr) Mahesh Verma Maulana Azad Institute of Dental Sciences
Director–Principal MAMC Complex, Bahadur Shah Zafar Marg
New Delhi - 110002, India
Tel : 91-11-23233925
Fax : 91-11-23217061
E-mail : [email protected]
[email protected]
[email protected]
Web : www.madch.ac.in

Foreword to the Third Edition

Textbook of Oral Medicine by Dr Anil Govindrao Ghom is a comprehensive well-written text. The
strength of this book is centered in its lucid language and contemporary concepts. The same is
vigorously integrated into all the diagnostic and treatment planning of topics covered in the entire
book.
Going through the chapters, the reader could additionally focus on the ‘points to remember’
reflecting the author’s understanding of students’ need.
The extensive volume of the book is structured into 52 chapters widely covering the subject by a
group of focused teachers and researchers. All the faculty contributors have incorporated relevant
concepts very clearly pertaining to their areas of expertization.
Dr Ghom has undertaken outstanding job of editing this text into a valued resource for each
student of dentistry and oral medicine as well as dental practitioners for the professional knowledge
enhancement.
I strongly recommend this book for undergraduate and postgraduate students and clinicians.
I do congratulate Dr Anil Govindrao Ghom for bringing out the Third Edition of this book successfully.

Mahesh Verma
Director–Principal
Maulana Azad Institute of Dental Sciences
New Delhi, India
President
Indian Dental Association
 Foreword to the Second Edition
“Enthusiasm is driving force that overcome all obstacles”

It is my proud privilege to write a Foreword for Second Edition of this book by Dr Anil Govindrao
Ghom. In short time this book has become most popular among undergraduates and postgraduates
all over the country.
In the Second Edition, number of chapters have been presented in a better organized manner.
This book carries updated information of the subject in this rapidly changing world of science. New
chapter “Controversial Diseases and Terminologies” is incorporated, also there are number of new
photographs, radiographs, multiple choice questions (MCQs) and references. I am sure this new
updated Second Edition will be more beneficial for the undergraduate and postgraduate students for
reference and regular reading.

RN Mody
Professor and Head
Department of Oral Medicine and Radiology
Chhattisgarh Dental College and Research Institute
Rajnandgaon, Chhattisgarh, India
 Preface to the Third Edition
‘Always continue the climb. It is possible for you to do whatever you choose, if you first get to know who you are and
are willing to work with a power that is greater than ourselves to do it’.

This is the Third Edition of Textbook of Oral Medicine and we are gratified by the acceptance and support that the book has
received over the years from educators, students and practitioners. The purpose of Third Edition of this book is manifold. We have
evaluated and utilized suggestions from all the critical reviews and recommendations from the faculty members.
This Third Edition of book includes lot of changes. We have incorporated students-friendly points to remember, that will help
them to revise at the time of examination. Also from students’ point of view, we have included most commonly asked long answer
questions (LAQs), short answer questions (SAQs) and multiple choice questions (MCQs) at the end of each chapter.
Obviously each successive edition of this textbook finds the edition with more information. So in this edition, we have attempted
to solidify and include recent knowledge. This book also includes new chapters on halitosis, geriatric dentistry, immunomodulators,
and banned drugs in dentistry.
Again as a human being, mistakes are bound to happen. We have tried this Third Edition to best of our efforts, still there can
be shortcoming and we request readers to make note of it and we will try to rectify it in next edition.

Anil Govindrao Ghom

[email protected]
[email protected]
Savita Anil Ghom (Lodam)
 Preface to the First Edition
“You must not be discouraged if the world does not rush to you, demanding what you have;
neither must you quietly sit down to let world wonder and then seek you; you must be aggressive, you must
carry your truths to people and cause them to see them so clearly that they must accept them”

The student looked for a reference on which to build an educational foundation with regard to basic
principle. A few years ago, much of the information offered in this text was not available.
Since the principle and treatment modalities offered herein will continue to evolve, it behooves the student
to be fully informed of the state of the art to be able to critically evaluate the worthiness or applicability of any
future development.
I have endeavored to ensure that a consistent style has emerged and is in harmony, where appropriate,
with the diseases of oral region along with the differential diagnoses, which are covered in detail.
The purpose of this book is to correlate the gross and microscopic pathological features with the radiographic
appearance of oral diseases and systemic diseases manifested in the jaw.
In our increasingly litigious society, it is vital that the dentist understands the law as it relates to dentistry. The chapter on
Medicolegal Issue is an essential reading, along with the Consumer Protection Act.
Diseases can be understood best when the interpreter understands not only the disease process but also the basic science
associated with it. For this reason, I have included a separate section for basic science.
Recently, as examination pattern is changing and MCQs are getting importance, MCQs are added in a separate chapter.
I tried my best to cover all the aspects of oral diseases in this book. If this goal is achieved, then this textbook may contribute,
in a small way, to better care of patients who suffer from these diseases.

Anil Govindrao Ghom

 Acknowledgments
‘The key is to keep company only with people who uplift you, whose presence calls forth your best.

No work is complete without the help of friends and well-wishers, and we are lucky to have them with us in this venture. We would
like to express our sincere gratitude to Dr Pravin Lambade, Dr Jitendra Sachdeo, Dr Vikas Meshram, Dr Bhaskar Patle, Dr Revant
Chole, Dr Amit Parate, Dr Sanjay Pincha, Dr Milind Chandurkar, Dr Ashok L, Dr Umaraji, Dr Tapasya Karemore, Dr Avinash Kshar,
Dr M Shimizu, Dr Fusun Yasar, Dr Iswar, Dr Bande, Dr Kadam, Dr R Kamikawa, Dr Suwas Darvekar, Dr Vijay Mohan, Dr Sonal
Gupta, Dr Shubhangi Mhaske, Dr Ambika L, Dr Ashwini Rani, Dr Mallayya Pujari, Dr Preeti Girinath, Dr Parvathi Devi, Dr Abhishek
Sinha, Dr Vijeev Vasudevan, Dr Sudhakar, Dr Sudarshan R, Dr Ajay Bhoosreddy, Dr Jaychandran, Dr Kamala Rawson, Dr Vibha
Jain, Dr B Vijay Kumar, Dr Vinay Kumar Reddy, Dr Guruprasad R, Dr Sanad K Bhuyan, G Vivekanandh Reddy, Dr Sumit Goel, Dr
Vishal Mahrotra, Dr Manu Dhillon, Dr Vijay Raghavan, Dr Prema Mathur, Dr Sreedevi, Dr Poonam Khatry, Dr Sagar Nagare, Dr
Harsha Vardhan, Dr Amit Gothwal, Dr Ravindra SV, Dr Ashok Uikey, Dr Sunitha M, Dr Stuti Bhargav, Dr Mayuri Agrawal, Dr M
Venkateshwarlu, Dr Siddharth Gupta, Dr K Anbarasi, Dr Manika Singh, Dr Vivek V, Dr Shivu M, Dr Deepankar Misra, Dr K Sridevi,
Dr Punjab Wanjari, Dr Mukta Motwani, Dr Rawlani, Dr N Kannan, Dr Manish Thadani, for their hard work and valuable input as
without their contribution, fruition of this book would have been difficult.
Special thanks to Dr Gagandeep Chawala, Dr Smriti Goswami, Dr Uma Rohra, Dr Swapnil Dewakirti, Dr Pranita Rohan, Dr
Nehal Rathore, Dr Swati Rao, and Dr Pragya Jaiswal, for their contribution in making this book enriched with colored pictures.
We extend our thanks to Dr Akash Ghosh, Dr Janhvi Verma, Dr Sunaina Shetty, for their help in completion of the book.
‘Your goals are the road maps that guide you and show you what is possible for your life.’ This is true for our teacher Dr RN
Mody, who has been a constant source of inspiration and guidance.
We would like to thank Shri Jitendar P Vij (Group Chairman), Mr Ankit Vij (Managing Director) and Mr Tarun Duneja (Director-
Publishing) of M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India, for publishing this book.
We want to express our sincere gratitude to our family whose bonding give us strength.
At last, we offer our earnest prayers to the Almighty, for endowing us the strength and confidence in accomplishing to the best
of our abilities.
 Contents

SEcTion 1: BaSicS
1. Oral Diseases—An Introduction 3
Anil Ghom

2. Neoplasm 5
Anil Ghom, Savita Ghom
Definition 5; Nomenclature 5; Normal Cell Cycle 5; Predisposing Epidemiologic Factors for the
Development of Neoplasm 5; Acquired Preneoplastic Conditions 7; Carcinogenesis 7; Biology of Tumor
Growth 9; Metastasis 11; Grading and Staging of Tumors 12

3. Infection Control in Dental Office 15

Amina Sultan, Mandeep Kaur, Sukhdeep Singh
Transmission of Infections 15; Infections that can be Transmitted in a Dental Environment (by the Oral Cavity) 15;
Standard Infection Control 16; Infection Control Protocol 16; Disinfections and Sterilization 18; Infection Control in
Radiography 20

4. Case History 22
Anil Ghom, Savita Ghom
Definition of Case History 23; Diagnostic Procedure 23; Personal Information 23; Taking and Recording
History 27; Medical History 31; Examination 32; Establishing the Diagnosis 56

5. Investigations in Dentistry 60
Anil Ghom, Savita Ghom
Diagnostic Test for Cancer Detection 60; Clinical Methods 61; Photodiagnosis 62; Histopathological
Examination 62; Molecular Methods 66; Immunofluorescence Procedure 67; Caries Activity Tests 67;
Hematological Investigation 70; Blood Chemistry 75; Radiological Investigations 77

SEcTion 2: DiSEaSES of oral STrucTurE

6. Teeth Anomalies 83
Anil Ghom, Savita Ghom
Developmental Disturbances of Teeth 83; Environmental Alteration of Tooth 105

7. Developmental Defects of Craniofacial Structures 124

Anil Ghom, Savita Ghom
Definitions 124; Developmental Disturbances of the Jaws 125

8. Keratotic and Non-keratotic Lesions 148

Anil Ghom, Savita Ghom
Normal Variation 148; Non-keratotic White Lesions 151; Candidiasis 154; Oral Genodermatoses 163

9. Oral Premalignant Lesions and Conditions 169

Anil Ghom, Savita Ghom
Concept of Precancer 169; Precancerous Lesions 169; Oral Lesions Associated with the Use of Tobacco 180;
Premalignant Conditions 182

10. Cysts of Orofacial Region 203

Anil Ghom, Savita Ghom
Definitions 203; General Diagnostic Features of Cysts 204; Theories of Cyst Enlargement 205; Classification 205;
Epithelial Developmental Odontogenic Cyst 206; Inflammatory Cysts 217; Non-odontogenic Cysts 221; Nonepithelial
Cysts 224; Cysts of Soft Tissues of the Face and Mouth 225; Syndromes Associated with Odontogenic Cysts 230;
Treatment of Cysts 231

11. Odontogenic Tumors 235

Anil Ghom, Savita Ghom
Classification 235; Benign Tumors 236; Malignant Tumor 258
 12. Benign Tumors of Orofacial Region 264
Anil Ghom, Savita Ghom
Characteristics of Benign Tumor 265; Terminology 265; Classification 265; Tumors of Epithelial Origin 265;
Tumors of Fibrous Connective Tissue Origin 269; Tumors of Cartilage Tissue Origin 274; Tumors of Adipose Tissue
Origin 275; Bone Tumors 277; Tumors of Vascular Tissue Origin 283; Tumors of Neural Tissue Origin 293;
Muscle Tumors 298; Giant Cell Neoplasm 300; Salivary Gland Tumor 303; Inflammatory Hyperplasia 303

13. Malignant Tumors of Orofacial Region 310

Anil Ghom, Savita Ghom
Oral Carcinoma 310; Epithelial Tumors 312; Tumors of Fibrous Connective Tissues 325; Tumors of Adipose
Tissues 328; Cartilage Tumors 328; Bone Tumors 330; Vascular Tumors 333; Tumors of Neural Tissues 333;
Muscle Tumors 334; Tumors of Lymphoid Tissues 335; Myeloma 344; Malignant Tumors of Salivary
Gland 346; Treatment Modalities of Oral Cancer 346

14. Vesicular, Bullous and Erosive Lesions 356

Mandeep Kaur, Virender Gombra, Sukhdeep Singh
Classification of Ulcers 356; Ulcers Associated with Trauma 358; Ulcers Associated with Infection 359; Diseases of
Unknown (Uncertain) Etiology 359; Ulcers Associated with Allergic Reactions 363; Ulcers Associated with Cutaneous
Manifestation 367

15. Orofacial Pain 384

Ajit Mishra, Savita Ghom
Types and Nature of Pain 385; Neurophysiology of Pain 385; Types of Nerve Cells 387; Sensory Receptors 387;
Pain Conduction 387; Theories of Pain 388; Measurement of Pain Intensity 389; Classification of Orofacial
Pain 390; Therapeutic Modalities of Pain Control 404
Textbook of Oral Medicine

16. Infections of Oral Cavity 409

Anil Ghom, Savita Ghom
Host Defense Mechanism 410; Oral Microflora 411; Spread of Infection 412; Diagnosis of Odontogenic
Infection 413; Pathophysiology of Infection 413; Principles of Management of Odontogenic Infection 413;
Sequelae of Pulpitis (Pulpoperiapical Abscess) 414; Radiographic Considerations 414; Etiology of Major Facial
Infection 414; Acute and Chronic Infections of Oral Cavity 415; Osteomyelitis 428; Facial Space Infections 439;
Fatal Complications of Oral Infection 445; Pulpal Infection 450; Focal Infection 451; Pits, Fistulae and Draining
Sinus of Oral Cavity 452

17. Oral Pigmentation 455

Amit Parate, Anil Ghom
Blue/Purple Vascular Lesions 457; Brown Melanotic Lesions 461; Brown Heme Associated Lesion 470;
Exogenous Pigmentation 472; Pigmentation due to Drugs and Metals 473; Summary 476; Hypopigmentation
in Oral Cavity 476

18. Dental Caries 480

Raghvendra Shetty
Etiology 481; Pathogenesis 481; Theories of Cariogenesis 481; Classification 483; Diagnosis of Dental Caries 484;
Types of Caries 487; Radiographic Differential Diagnosis of Dental Caries 496; Control of Dental Caries 498

19. Diseases of Tongue 501

Anil Ghom, Savita Ghom
Embryology and Development of Tongue 501; Anatomy of Tongue 502; Functions of Tongue 503; Specialized
Examination of the Tongue 504; Classification of Tongue Disorders 504; Congenital and Developmental
Disorders 504; Local Tongue Disorders 510; Depapillation of the Tongue 514; Neurological Disorders 516;
Premalignant Lesions and Conditions 518; Malignant Tumor 518

20. Diseases of Lip 523

Anil Ghom, Savita Ghom
Classification of Lip Disorders 523; Development of Lip 523; Anatomy 523; Developmental Disorders of
Lip 524; Cheilitis 529; Miscellaneous Disorders 535

21. Gingival and Periodontal Diseases 537

Abhishek Soni, Anil Ghom
Normal Periodontium 537; Disease of Gingiva and Periodontium 539; Gingival Diseases 539; Drug-influenced
Gingival Enlargements Dilantin Sodium 546; Non-plaque-induced Gingival Disease 550; Periodontal Diseases 554

22. Temporomandibular Joint Disorders 566

xx Anil Ghom, Savita Ghom
Anatomy of TMJ 566; Functional Movement of TMJ 569; Diagnostic Studies 569; Classification of TMJ
Disorders 569; Developmental Disorders of the TMJ 569; Degenerative Joint Diseases 574;
Inflammatory Disorders of the Joint 576; Traumatic Disorders of TMJ 580; Metabolic Disorders 591; Neoplastic
Disorders 592; Miscellaneous Disorders 593
23. Salivary Gland Disorders 600
Anil Ghom, Savita Ghom
Development of Salivary Gland 601; Classification of Salivary Glands 601; Saliva 602; Examination of Salivary
Glands 604; Diagnostic Tests of the Salivary Glands 604; Developmental Disorders of Salivary Gland 605;
Functional Disorders of Salivary Gland 607; Obstructive Disorders 609; Cysts of Salivary Gland 614; Asymptomatic
Enlargement of the Salivary Gland 617; Viral Infection 618; Bacterial Infection 619; Autoimmune Disorders 622;
Tumors of Salivary Glands 625; Benign Tumors 626; Malignant Tumors 630

24. Disorders of Maxillary Sinus 638

Anil Ghom, Shweta Tikekar (Singh)
Development of Maxillary Sinus 638; Anatomy of Maxillary Sinus 639; Functions of Maxillary Sinus 639;
Examination and Investigation of Maxillary Sinus 639; Classification of Maxillary Sinus Disorders 640; Developmental
Disorders 640; Inflammatory Disorders 641; Cysts 644; Benign Tumor 647; Malignant Tumor 648;
Traumatic Injuries to the Paranasal Sinuses 651; Calcification 654

25. Traumatic Injuries of Oral Cavity 657

Anil Ghom, Savita Ghom
Traumatic Injury of Soft Tissue 657; Fracture of Teeth 663; Complications of Healing 676

26. Soft Tissue Calcifications 679

Anil Ghom, Savita Ghom
Definition 679; Classification of Calcification 679; Dystrophic Calcification 679; Idiopathic Calcification 682;
Metastatic Calcification 684

SEcTion 3: SySTEmic DiSEaSES manifESTED in Jaw

Contents
27. Bacterial Infections 691
Anil Ghom, Savita Ghom
Infections Caused by Bacteria 691

28. Viral Infections 713

Anil Ghom, Mandeep Kaur
Definition 713; Classification 713; Infections Caused by Viruses 714; Herpes Simplex Virus Infections 714;
Varicella Zoster Infections 718; Coxsackievirus Infection 723; Condyloma Acuminatum 726; Verruca Vulgaris
(Common Wart) 726

29. Fungal Infections 731

Anil Ghom, Savita Ghom
Infections Caused by Fungi 731; Protozoal Infections 738

30. Specific System Disorders 740

Anil Ghom, Savita Ghom
Basic Life Support 741; Cardiovascular Diseases 742; Respiratory Disorders 750; Renal Disorders 752; Disorders
of Gastrointestinal Tract 755; Neuromuscular Disorders 759; Granulomatous Disorders 764; Collagen Disorders 767;
Skin Disorders 769; Muscle Disorders 774; Immunological Disorders 780; Miscellaneous Conditions 781

31. Diseases of Bone Manifested in Jaw 787

Anil Ghom, Savita Ghom
Fibro-osseous Lesions 787; Fibro-osseous Lesions of Medullary Bone Origin 788;
Fibro-osseous Lesions of Periodontal Origin 799; Other Lesions of Bone 804

32. Acquired Immunodeficiency Syndrome (AIDS) 818

Anil Ghom, Savita Ghom
Definition 818; Prevalence and Epidemiology 819; Transmission 819; History of Nomenclature of
Virus 819; Characteristics of the HIV Virus 819; Mechanism of Action 820; Classification 820; AIDS-
related Complex 822; Oral Manifestations 822; Common Oral Manifestations in AIDS 823; Uncommon Oral
Manifestation in AIDS 827; Guidelines to Prevent Transmission to Dentist 828; Prevention 828; Diagnostic Tests for
AIDS 828; Management of AIDS 830

33. Endocrine Disorders 833 xxi

Anil Ghom, Savita Ghom
Functions of the Endocrine System 833; Anatomy and Physiology 833; Diseases of Pituitary Gland 835; Diseases
of Thyroid Gland 837; Diseases of Parathyroid Gland 840; Diseases of Pancreatic Gland 844; Diseases of Adrenal
Gland 848; Diseases of Gonads 850
 34. Blood Disorders 853
Anil Ghom, Savita Ghom
Physiology of Blood 854; Composition 854; Blood Coagulation 855; Blood Group 856; Diseases of Red Blood
Cells 856; Polycythemia 869; White Blood Cell Disorders 870; Quantitative Disorders 870; Qualitative Disorders
of WBC 873; Platelet Disorders 874; Hemorrhagic Disorders 879

35. Vitamins 884

Anil Ghom, Sarbani Deb Sikder
Causes of Vitamin Deficiency 884; Water Soluble Vitamins 884; Fat Soluble Vitamins 893

36. Metabolic Disorders 900

Anil Ghom, Savita Ghom
Disturbances in Protein Metabolism 900; Disturbances in Lipid Metabolism 903; Disturbances in Carbohydrate
Metabolism 906; Disturbances in Mineral Metabolism 907; Miscellaneous Disorders 910

SEcTion 4: DrugS uSED in DEnTiSTry

37. Antibiotics 915
Pravin Lambade
Antibiotics Useful for Orofacial Infections 916; Routes of Drug Administration 916; Indications for
Antibiotics 917; Principles of Prophylactic Antibiotics 917; Principles of Administration of Antibiotics 918;
Effectiveness of Antibiotics 919; Interference with Cell Membrane Structure 922; Interference with Nucleic Acid
Synthesis 922; Topical Antiseptic and Antibiotics 923; Classification of Local Antimicrobial Therapy 923
Textbook of Oral Medicine

38. Analgesic and Anti-inflammatory Drugs 927

Manjari Gandhi (Gupta)
Definition of Analgesic 927; Classification 927

39. Banned Drugs Used in Dentistry 936

Manjari Gandhi (Gupta)
Reason for Banning a Drug 936; Reason for Sale and Purchase of Banned Drug in India 936

40. Anticancer Drugs 938

Sachin Manglekar
Factors Affecting Chemotherapy 938; Kinetic Classification of Anticancer Drugs 938; Principles of Chemotherapy 939;
Use of Anticancer Drugs 939; Pharmacology 942; Principles of Treatment 942

41. Antiviral Drugs 945

Rajkumar Diwan
Classification of Antiviral Drugs 945; Antiherpes Drugs 945; Anti-hepatitis Drugs 947; Antiretroviral Drugs 947;
Anti-HIV Drugs 948

42. Corticosteroids 952

Anshul Khandelwal
Corticosteroid Action and its Regulation 952; Pharmacological Action 953; Mineralocorticoids 957

43. Immunomodulators 960

Sonal Vahanwala
Immunosuppressants 960; Immunostimulants 960

44. Drugs Used in Pregnancy 965

Mansi Tiwari
Pregnancy Trimesters 965; Pharmacokinetics in Pregnancy 965; Dental Management of Pregnant Patient 966;
FDA Categories for Drug Use in Pregnancy 966; Commonly Used Drugs and their Categories 966; Guidelines for
Prescribing Drugs in Pregnancy 968; Consideration in Lactation 968

45. Emergency Drugs Used in Dentistry 969

Vikas Meshram
Emergency Management 969; Essential Emergency Drugs 970; Additional Emergency Drugs 971; Emergency
Equipment 974; Maintenance of Emergency Kit 976

xxii 46. Antifungal Drugs 977

Abhijeet Deoghare
Classification of Antifungal Agent 977; Polyenes 977; Azoles 978; Pyrimidine Analogs 980;
Allylamines 980; Echinocandins 980; Antifungal Treatment in HIV Patients 981; Antifungal Treatment in Refractory
Mucosal Candidiasis 981; Antifungal Combinations 981
 47. Desensitizing Agents, Mouthwashes and Gum Paints 983
Vivek Thombre
Clinical Management of DH 986; Classification of Desensitizing Agents 987; Mouthwashes 989; Gum Paints 991

SEcTion 5: miScEllanEouS
48. Forensic Dentistry 995
Anil Ghom, Smriti Goswami
Scope of Forensic Odontology 995; Record Management 995; Identification 996; Age Assessment 998; Bite
Marks 998; Classification of Skin Wounds 1001; Medicolegal Aspects of Dentistry 1002 ;

49. Halitosis 1004

Sonal Vahanwala
Normal Physiologic Odor 1004; Causes of Halitosis 1005; Investigations 1006;
Treatment of Halitosis 1006

50. Controversial Diseases and Terminologies 1008

Anil Ghom, Mansi Tiwari
Bowen’s Disease 1008; Leontiasis Ossea 1009; Previous or Former Cyst 1009; Primordial Cyst 1009;
Globulomaxillary Cyst 1010; Median Mandibular Cyst 1011; Median Palatine Cyst 1011; Adenomatoid
Odontogenic Tumor 1012; Cementoma 1013; True Cementoma 1013; Gigantiform Cementoma 1013;
Reparative Giant Cell Granuloma 1013; Aneurysmal Bone Cyst 1014; Granular Cell Myoblastoma 1015;
Eagle Syndrome 1015; Hand-Schuller-Christian Disease, Letterer Siwe Disease, Eosinophilic Granuloma and
Histiocytosis X 1015; Traumatic Bone Cyst 1015; Neurilemmoma 1015

51. Syndromes of Oral Cavity 1016

Ranit Chhabra, Barakha Nayak

Contents
Etiology of Syndromes 1018; Pattern of Inheritance 1018; Syndromes Associated with Oral and
Paraoral Structures 1018

52. Geriatrics—Role of Oral Physician and Interdisciplinary Management 1030

Shalu Rai
Definition 1030; Classification 1031; Age Changes Affecting the Structures in Oral Cavity 1031; Common Diseases
Among Geriatric Patients 1031; Goal of Oral Physicians 1032

appEnDicES
Appendix 1: Causes and Classifications 1039
Vivek Lath, Abhinav Singhal

Appendix 2: Glossary 1070

Satish Chugani, Neha Dandwani

Appendix 3: Emergencies in Dental Office 1080

Sachin Dev Sachdeva

Answers Key of MCQs 1085

Index 1089

xxiii
 1
S e c t Ion

Basics
∙ Oral Diseases—An Introduction
∙ Neoplasm
∙ Infection Control in Dental Office
∙ Case History
∙ Investigations in Dentistry
 CHAPTER 1
j
o
CD
o
Oral Diseases — An Introduction LU

Anil Ghom

The ultimate aim of entire dental education is to see how well it • Service: Service to society and healthcare professionals is the
prepares the practitioners to serve patients. To become a good objective of oral medicine. Oral medicine includes training
practitioner, it is essential to have a thorough understanding of the professional to provide current and future patient care.
the basic sciences related to dentistry. Changes in current trends in epidemiology suggest that in
Stomatology is the science of structure, function, and disease future, oral medicine professionals will have to come across
of the oral cavity. Study methods include examination of related and diagnose various different oral diseases. According to 1989
histories, evaluation of clinical signs and symptoms and use study by WHO “ trends in oral healthcare, a global perspective"
of biochemical, microscopic and radiological procedures to stated that in future, greater role is required by oral medicine
establish a diagnosis and a plan for therapeutic management. professionals.
Diagnosis is the process of evaluating patient 's health as The mouth is our primary connection to the world. It is how
well as the resulting opinions formulated by the clinician. Oral we take in water and nutrients to sustain life. Oral health is an
diagnosis is the art of using scientific knowledge to identify oral essential and integral part of overall health throughout life and is
disease processes and to distinguish one disease from another. much more than just healthy teeth. The word “oral" refers to the
whole mouth, including the teeth, gums, hard and soft palate,
History of oral medicine starts when William Gies of
linings of the mouth and throat, tongue, lips, salivary glands,
Columbia University in 1926 recommended that oral medicine
chewing muscles, and upper and lower jaws. Good oral health
topics should be covered in dental curriculum. In 1945, the
means management of tooth decay, gum disease, chronic oral
American Academy of Oral Medicine was formed. Definition of
pain conditions, oral cancer, birth defects such as cleft lip and
oral medicine was accepted in 1933 by international association
of oral medicine. It states that:
palate. Good oral health also includes the ability to carry on
the most basic human functions such as chewing, swallowing,
'Oral medicine is that area of special competence in dentistry
speaking, and smiling.
concerned with diseases involving the oral and paraoral
structures. It includes the principles of medicine that relate to
In the field of oral medicine, a basic understanding of various
diseases and their impact on oral tissue is required , so that it is
the mouth as well as research in biological, pathological, and
easy to recognize the presence of any major systemic diseases
clinical spheres. Oral medicine also includes the diagnosis and
and then accordingly make the correct diagnosis and treatment CD
medical management of diseases specific to the orofacial tissues O
and oral manifestations of systemic diseases. It further includes plan so as to do thorough justice to the sufferer.
LU
the management of behavioral disorders, the oral and dental The field of oral medicine consists chiefly of the diagnosis
and medical management of the patients with complex medical CD
treatment of medically compromised patients!
disorders involving the oral mucosa and salivary glands as
It can also be defined as ‘ diagnosis and treatment
well as orofacial pain and temporomandibular joint disorders.
of oral lesions as well as non -surgical management of
Specialists trained in oral medicine also provide dental and oral
temporomandibular joint disorders and facial pain and dental healthcare for patients with medical diseases that affect dental CD
treatment for medically compromised patients in an outpatient
treatment, including patients receiving treatment for cancer, E
sitting, or in an inpatient sitting under general anesthesia,
diabetes, cardiovascular diseases, and infectious diseases.
including specialty care in periodontics and endodontic!
Oral medicine practice provides physical and medical
The goal and objective of oral medicine are discussed evaluation, head and neck examination, laboratory analysis,
below. The goal is to provide education, research and service oral diagnosis and oral therapeutics for such conditions as:
for healthcare professionals and the public. vesiculobullous, ulcerative mucosal diseases, painful and
• Education: It consists of predoctoral , postdoctoral burning mucosa, infectious oral diseases, oral conditions arising
and continuing education training for the healthcare from medical treatment, oral manifestations of systemic diseases
professional. and salivary gland dysfunction.
• Research: It includes activities in the field of biology as it is The specialist will perform a comprehensive and / or
related to oral disease. specialized examination, provide consultation , possibly
 perform and interpret laboratory tests and perform or prescribe for patients with severe systemic disease and management of
treatments or make the appropriate referrals. the most medically complex patients is best performed in the
Dental management of medically compromised patients is hospital because of the availability of sophisticated, diagnostic
becoming a routine and increasingly important part of dental and life-sustaining equipment and the proximity of expert
practice. Several factors contribute to this phenomenon. First, consultants in all areas of healthcare.
the population continues to age. Many older patients have Most difficult and unusual problems evaluated by the dentist
multiple medical conditions. Second, as medical care becomes are seen as consultations. To handle consultations properly, the
more effective and cost issues are emphasized, many patients are dentist must be familiar with the proper method of requesting
being treated on an ambulatory basis to avoid hospitalization. and answering consultations.
Consequently, these individuals are in the community and The role of imaging in oral medicine varies greatly with the
readily seek dental care. Third, the sophistication of medical type of problem being evaluated. Certain problems, such as pain
treatment is prolonging life. And fourth, the level of and access in the orofacial region, frequently require imaging to determine
to available dental care has improved, resulting in more patients the origin of the pain. For other conditions, however, such as
(regardless of medical status) wanting dental treatment. soft-tissue lesions of the oral mucosa, imaging offers no new
Therefore, behavior disorders and diseases of the mouth as diagnostic information.
manifestations of systemic disease are seen at an increasing Thus, to conclude oral medicine expert is an important
rate, and require prompt and adequate care by experienced professional in dental and medical team of nations healthcare
specialists. scheme to public. Oral medicine personal is also expert in
Philosophically and in practice, dentistry is similar to one studying, diagnosing and treating the mouth disease.
of the various specialties of medicine and consequently, it is
imperative that the dentist understands the medical background
of patients before beginning dental therapy, which might fail Suggested Reading
because of the patient’s compromised medical status or result 1. Burden of Oral Disease-Introduction- Centers for Disease
in morbidity or death of the patients. Control, www.cdc.gov/oralhealth/publications/library/.../pdfs/
The dentist trained in oral medicine should be introduction.
philosophically atuned to the patient and have knowledge of 2. Geis WJ. Dental education in the United States and Canada:
Section 1: Basics

medically important diseases as well as of dental problems. The A report to the Carnegie Foundation for the advancement of
dentist should be well-versed in the use of rational approaches teaching. Carnegie Foundation: New York, Bulletin 19;1926.
in diagnosis, medical risk assessment and treatment. 3. Gnanasundaram N. Nine gems of the speciality and ten
commandments for specialists in oral medicine and radiology.
The hospital is frequently the setting for the most complex JIAOMR. 2006:18(4):196-201.
cases in oral medicine. Hospitalized patients are most 4. Knapp MI. Oral disease in 181,338 consecutive oral examinations.
likely to have oral or dental complications of bone marrow J Am Dent Assoc. 1971;83:1288-93.
transplantation, hematological malignancies, poorly controlled 5. Millard HD, Mason DK. Perspectives on 1988 World Workshop in
diabetes, major bleeding disorders, and advanced heart disease. Oral Medicine. Chicago: Year Book Publishers, 1989.
The hospital that wishes to provide the highest level of care for 6. Millard HD, Mason DK. Perspectives on 1993 World Workshop in
its patients must have a dental department. Oral Medicine. Ann Arbor: University of Michigan, 1995.
The hospital dental department should serve as a community 7. Pilot T. Trends in oral health care, a global perspective. World
referral center by providing the highest level of dental treatment Health Organization: Geneva, 6-23 November, 1989.

4
 c H a P t er 2
Neoplasm
Anil Ghom, Savita Ghom

ˆ Definition – Biologic Carcinogenesis

ˆ Nomenclature – Oxidative Mechanism of Carcinogenesis
ˆ Normal Cell Cycle ˆ Biology of Tumor Growth
ˆ Predisposing Epidemiologic Factors for the Development of – Induction of Malignant Changes in the Target Cell
Neoplasm (Transformation)
– Hereditary Predisposition – Growth of Transformed Cells (Kinetics of Tumor Cell Growth)
– Racial and Geographic Factors – Mechanism of Local Invasion and Distant Metastases
– Theories of Carcinogenesis
– Age
ˆ Metastasis
– Sex
– Steps of Metastasis
ˆ Acquired Preneoplastic Conditions – Routes of Metastasis
ˆ Carcinogenesis – Pattern of Metastatic Spread
– Chemical Carcinogenesis ˆ Grading and Staging of Tumors
– Physical Carcinogenesis – Grading
– Hormonal Carcinogenesis – Staging

Definition • G1 phase: After mitosis (M phase), cells spend a variable

period of resting (G1 phase) where DNA synthesis is absent
It is an abnormal mass of tissue, growth of which exceeds and but the synthesis of RNA and protein continues
is uncoordinated with that of normal tissues and persists in
• S phase: At the end of G1 phase, unknown signals
the same excessive manner, after cessation of the stimuli that
continuously institute a burst of RNA synthesis which is
evokes the changes.
followed by DNA synthesis (S phase). Then the cells undergo
Oncology is the study of neoplasm.
replication or remain polypoid and eventually die
• G2 phase: The cells cease DNA synthesis during G2 phase
Nomenclature and DNA content is fairly constant in the growing normal
There are mainly of two types of neoplasms: benign and cells. The proportion of cell population which undergoes
malignant. Benign tumors are designated by attaching ‘oma’ to active proliferation in the cycle is termed as growth fraction
cell of the organ. Malignant tumors arising from mesenchymal • G0 phase: Daughter cells may continue to remain in cell
tissues are known as ‘sarcomas’, like osteosarcoma. Malignant cycle and divide further or may undergo in resting phase
tumors of epithelial origin are called ‘carcinoma’, like of cell cycle.
adenocarcinoma and squamous cell carcinoma.
Cancer is the term for malignant tumors (Cancer stands for
Crab in Latin) because when cancer adheres to any part, seizes Predisposing Epidemiologic Factors for
it in an obstinate manner like a crab (Table 2.1). the Development of Neoplasm
Hereditary Predisposition
Normal Cell Cycle The risk of developing cancer in relatives of a known cancer
All renewing cells go through a series of events known as patient is three times higher than the control group. Genetic
cell cycle. Successive phases of progression of cell cycle are cancers comprise not more than 5% of all cancers, e.g.
described below (Fig. 2.1). retinoblastoma, familial polyposis coli, cancer of breast etc.
 Table 2.1 Differences between benign and malignant tumors
Features Benign tumors Malignant tumors
Macroscopic features
Boundaries Encapsulated or well circumscribed Poorly circumscribed and irregular
Surrounding tissues Often compressed Usually invaded
Size Usually small Often large
Growth Slow and expanding Rapid and infiltrating
Capsule Present Absent
Degeneration Rare Common
Recurrence Not common Common
Fixity Absent Present
Secondary changes Occur less often Occur more often
End of growth May come to standstill Growth rarely ceases
Microscopic features
Pattern Usually resemble tissue of origin Have poor resemblance to tissue of origin
Basal polarity Retained Lost
Pleomorphism Usually not present Often present
Nucleo-cytoplasmic ratio Normal Increased
Anisonucleosis Absent Present
Hyperchromatism Absent Often present
Mitosis May be present but always with typical mitosis Mitotic figures are increased and are generally
Section 1: Basics

atypical and abnormal

Tumor giant cells May be present but without nuclear atypia Present with nuclear atypia
Cytoplasm May show normal constituents Normal cytoplasmic elements are decreased
or lost
Function Well maintained May be retained, lost or become abnormal
Growth rate Usually slow Usually rapid
Local invasion Often compresses the surrounding tissue Infiltrates and invades the adjacent tissue
without usually invading or infiltrating
Metastasis Absent Present frequently

• Carcinoma of stomach is five times higher in Japanese than

in Americans
• Nasopharyngeal cancer is common in south East Asians.

Environmental and Cultural Factors

We are surrounded by an environment of various substances
predisposing to cancer which we eat, drink, inhale and touch.
For example:
• Cigarette smoking is the etiology of cancer of oral cavity,
pharynx, larynx, esophagus, lung, pancreas and urinary
bladder
• Alcohol causes cancer of esophagus and liver
• Alcohol and tobacco together accelerate the risk of
developing cancer of upper aerodigestive tract
• Betel nut chewing causes cancer of cheek and tongue
• Industrial and environmental materials are carcinogenic.
Fig. 2.1: Normal cell cycle—a diagrammatic representation This includes exposure to substances like arsenic, asbestos,
benzene, and naphthylamine
• Overweight individuals, deficiency of vitamin A, people
Racial and Geographic Factors consuming foods rich in animal fats and low in fiber content
Cancers are largely due to the influence of environment and have more risk of developing cancers like colonic cancer.
6 geographic differences affecting whole population such as
climate, water, diet, habit. For example: Age
• Black Africans commonly have cancers of skin, penis, cervix, Generally, it occurs in older individuals past fifth decade of life
and liver. Europeans and Americans commonly develop but, there is variation in age groups. For example, acute leukemia
malignancies of lung, breast, and colon occurs in children, neuroblastoma in infancy.
Sex carcinoma, epidermal hyperplasia, basal cell carcinoma,
It is generally more common in men except cancer of breast, and lung cancer.
gallbladder, and thyroid.
Promoters of Carcinogenesis
Certain chemical substances lacking the intrinsic carcinogenic
Points to remember for predisposing epidemiologic factors potential but helping the initiated cell to proliferate further are
for the development of neoplasm called promoter of carcinogenesis. E.g. phorbol, phenols, drugs
Hereditary predisposition, racial and geographic factors, like phenobarbital, and artificial sweetener like saccharine.
environmental and cultural factors, sex, age.
Mechanism of Action
• Binding to DNA and RNA: The great majority of chemical
Acquired Preneoplastic Conditions carcinogens are mutagens. They bind directly to DNA
and RNA or cytoplasmic proteins to specific sites within
These may be inflammatory, hyperplastic conditions or may molecule inducing miscoding error during transcription
be certain benign tumors. It includes chronic atrophic glossitis, and replication
leukoplakia of oral cavity, vulva and penis, cirrhosis of liver, • Factors affecting carcinogenicity
chronic irritation and multiple neurofibromas.
– Dose: The carcinogenicity of chemical agents is dose
dependent and multiple traditional doses have same
Carcinogenesis oncogenicity as a single comparative dose
Carcinogenesis or oncogenesis or tumorigenesis means – Administration of promoters: The carcinogenicity of
induction of tumors; agents which can induce tumors are called chemical agents can be significantly enhanced by the
carcinogens. Carcinogens are broadly divided into four groups: subsequent administration of promoters. To be effective,
• Chemical carcinogens the promoter must follow the initiator.
• Physical carcinogens (radiation)
Stage of Chemical Carcinogenesis

Chapter 2: Neoplasm
• Hormonal carcinogens
The phenomenon of cellular transformation by chemical
• Biologic carcinogens (virus).
carcinogenesis is a progressive process involving two different
stages. These are initiation and promotion.
Chemical Carcinogenesis
Chemical carcinogens are divided into two broad groups: Initiation
In this, initiator carcinogen interact with DNA of target cell to
Initiators of Carcinogenesis induce mutation that is more or less irreversible to transform
• Direct-acting carcinogens: These require no metabolic it into initiated cell.
conversion to become carcinogens • Metabolic activation: Only indirect acting carcinogen or
• Alkylating agents: It includes, various chemotherapeutic procarcinogens require metabolic activation chiefly by
drugs that have successfully cured, controlled or delayed mixed oxidases of cytochrome P-450 system located in
recurrence of certain types of cancers only to later evoke microsomal compounds of the endoplasmic reticulum or
a second form of cancer, usually leukemia. Various agents in the nucleus
used are cyclophosphamide, chlorambucil, busulfan, • Reactive electrophiles: They are electron deficient protons,
melphalan, nitrosourea, b-propiolactone and epoxides. which bind to electron rich portions of other molecules of
This tragic consequence is called as “Pyrrhic victory” which cell such as DNA, RNA or other protein
becomes less of a victory, when their initial use later on leads • Target molecules: The primary target is DNA, producing
to second form of cancer mutagenesis
• Initiated cell: The unrepaired damage produced in the
• Acylating agents: Substances like acetyl imidazole
DNA of the cell becomes permanent, only if the altered cell
• Indirect-acting carcinogens or procarcinogens: These are
undergoes at least one cycle of proliferation.
chemical substances requiring metabolic activation for
becoming potent initial carcinogens Promotion
• Polycyclic aromatic hydrocarbons (in tobacco, smoke, animal It does not damage the DNA but enhances the effect of direct-
foods, industrial oil, and atmospheric pollutants). Important acting carcinogen or procarcinogens. The ultimate effect is
chemical compounds included are benzanthracene, further clonal proliferation of the initiated cell. Two or more
benzapyrene, methylcholanthrene. They may cause lung initiators, i.e. chemical, oncogenic virus or radiant energy may
cancer, skin cancer, cancer of oral cavity, and sarcoma act in concert to induce malignant transformation referred to
• Aromatic amines and azo dyes: These are b-naphthylamine, as cocarcinogens.
benzidine, azo dyes used for coloring foods, and acetyl
aminofluorene. They may cause bladder cancer and Points to remember for chemical carcinogenesis
hepatocellular carcinoma Direct-acting carcinogens, Alkylating agents, Acylating agents,
• Naturally occurring product: Aflatoxin, actinomycin-D, Procarcinogens, Polycyclic aromatic hydrocarbons, Aromatic
mitomycin-C, safrole, and betel nut. It can cause amines and azo dyes, naturally occurring product, Nitroso
hepatocellular carcinoma compounds, binding to DNA and RNA, Initiation, Promotion.
• Miscellaneous: Nitroso compounds, vinyl chloride monomer, 7
asbestos, arsenical compounds, metals like nickel, lead,
chromium, and insecticides, fungicides which can cause Physical Carcinogenesis
gastric carcinoma, hemangiosarcoma of liver, bronchogenic It is divided into two groups.
 Radiation Carcinogenesis the vagina is seen with increased frequency in adolescent
• Forms of radiation: Radiation in the form of UV light from daughter of mother who had received estrogen therapy
sunlight, UV lamp, welder’s arc, or ionizing radiation like during pregnancy
X-rays, a, b and g rays, radioactive isotopes, protons and • Contraceptive hormones: There is increased risk of
neutrons are established carcinogens developing breast cancer, benign tumors of the liver and few
• Example of radiation induced cancers: Most frequent patients have developed hepatocellular carcinoma
radiation induced cancers are leukemia, cancer of thyroid, • Anabolic steroids: Consumption of anabolic steroids by
skin, breast, lung, and salivary glands. Therapeutic athletes to increase the muscle mass also increases the risk of
irradiation can also induce carcinogenesis developing benign and malignant tumor of the liver
• Facts about radiation causing cancer: Radiant energy has • Hormone-dependent tumors: It has been shown in
potential of producing mutation and even killing cells. It can experimental animals that induction of hyperfunction
affect carcinogenesis by the following facts: of adenohypophysis is associated with increased risk
– Few tumors appear only after long latent period during of developing neoplasia of the target organs following
which successive generation of clones are developed preceding functional hyperplasia.
– The radiation induced initiation is generally irreversible,
but at low dosage, it is amenable to repair Biologic Carcinogenesis
– The effect of radiation depends upon a number of factors The epidemiological studies on different types of cancer
such as type of radiation, dose, length of interval between indicate the involvement of transmissible biologic agents in
the doses, capability of cells to repair in intervals and their development, chiefly viruses. It has been estimated that
various host factors such as age, individual susceptibility, about 20% of all cancers worldwide are virus associated cancers.
immune competence, hormonal influence and type of Therefore, biological carcinogenesis is largely viral oncogenesis.
cell irradiated A large number of viruses have been proved to be oncogenic
• Mechanism: It induces cancer by following mechanism; in wide variety of animals and in certain types of cancers in
– Radiation may directly alter the cellular DNA and it may humans.
dislodge ions from water and other molecules of cell and The association of oncogenic virus with neoplasia was
result in the formation of highly reactive free radicals that observed by an Italian physician Sanarelli in 1889 who noted
Section 1: Basics

may bring about the damage association between myxomatosis of rabbit with poxvirus.
– Radiation mutation may render cell vulnerable to other Oncogenic viruses fall into 2 broad groups, i.e. those containing
carcinogenic influence, i.e. acting as co-carcinogen ribonucleic acid are termed as RNA oncogenic viruses and those
– Inhibition of cell division and inactivation of enzymes containing deoxyribonucleic acid are termed as DNA oncogenic
– Radiation might cause cell killing; permitting survivors viruses.
to proliferate and thereby, become vulnerable to
oncogenic influence. RNA Oncogenic Viruses
These are retroviruses, i.e. they contain the enzyme reverse
Non-radiation Physical Carcinogenesis transcriptase, which is required for reverse transcription of viral
Mechanical injury to tissues such as from stones in the gall RNA to synthesize viral DNA strands. Based on their activity to
bladder, stones in the urinary tract, and healed scars following transplant target cells into neoplastic cells, they all are divided
burns or trauma has been suggested as causes of increased risk into three subgroups:
of carcinoma.
• Acute transforming viruses: It includes Rous sarcoma virus in
Implants of inert materials such as plastic, glass, etc. in
chickens, leukemia-sarcoma viruses of avian, feline, bovine
prosthesis and foreign bodies like metal foils are observed to
and primate
cause tumor development in experimental animals.
• Slow transforming tumorviruses: Mouse mammary tumor
virus (MMTV) that causes breast cancer in daughter mice
Points to remember for physical carcinogenesis • Human T-cell Lymphotropic viruses (HTLV): It can cause
Radiation carcinogenesis, non-radiation physical carcinogenesis,
adult T-cell leukemia-lymphoma syndrome and AIDS.
mechanical injury, implants of inert materials.
DNA Oncogenic Viruses
Hormonal Carcinogenesis • They are divided into five groups
Carcinoma is most likely to develop in organs and tissues which • Papovavirus group: Human papilloma virus, polyoma virus,
undergo proliferation under influence of excessive hormonal SV-40 (simian vacuolating) virus
stimulation. Hormone sensitive tissues developing tumors • Herpes virus: Epstein Barr virus, Human herpes virus,
are breast, endometrium, myometrium, vagina, thyroid, liver, cytomegalovirus, Lucke’s frog virus, Marek’s disease virus
prostate, and testis. • Adenoviruses: It can cause upper respiratory infections and
• Estrogen: In experimental animals, estrogen can cause pharyngitis. In man, they are not known to be involved in
induction of breast cancer in mice. Other cancers which tumors but in hamsters they may induce sarcomas
can be induced in mice by estrogens are squamous • Poxvirus: In rabbits, it can cause myxomatosis and in
cell carcinoma of cervix, connective tissue tumor of humans, it can cause molluscum contagiosum and may
myometrium, tumor of kidney in hamsters, and benign and induce squamous cell papilloma
malignant tumors of liver in rats. In case of human women • Hepadnaviruses: Hepatitis B virus is a member of this family
8 receiving estrogen therapy and women with estrogen and it can cause acute hepatitis and is responsible for carrier
secreting granulose cell, ovary shows increased risk of state which can result in chronic hepatitis which may progress
developing endometrial carcinoma. Adenocarcinoma of to hepatic cirrhosis and further into hepatocellular carcinoma.
Mechanism of Biological Carcinogenesis
RNA viral oncogenesis
Reverse transcriptase acts as a template to synthesize a single
strand of matching viral DNA.
• Single strand of viral DNA is then copied by DNA dependent
DNA synthetase to form another strand of complementary
DNA resulting in double stranded viral DNA or provirus
• The provirus is then integrated into the DNA of the host cell
genome and may transform the cell into a neoplastic cell
• Virus replication begins after integration of provirus into
host cell genome. Integration results in transcription of
proviral genes or progenes into messenger RNA which
then forms components of the virus particle, i.e. virion core
proteins from gag gene, enveloped glycoprotein from env
gene and reverse transcriptase from pol gene
• The three components of virus particles are then assembled
at the plasma membrane of host cells and virus particles
are released by budding off from plasma membrane, thus
completing the process of replication.
DNA viral oncogenesis
• Replication: The virus may replicate in the host cell with
consequent lysis of infected cell and release of virions Fig. 2.2: Biology of tumor growth (induction phase)
• Integration: The viral DNA may integrate into the host cell
DNA. This results in neoplastic transformation of the host and specific chromosomal abnormalities predispose to
cell.

Chapter 2: Neoplasm
cancer.

Oxidative Mechanism of Carcinogenesis Growth of Transformed Cells

Active oxygen species and other free radicals have long known to
be mutagenic. Further, these agents have emerged as mediators (Kinetics of Tumor Cell Growth) (Fig. 2.3)
of the other phenotypic and genotypic changes that lead to form • Doubling: The monoclonal cancer cell (10 µm in diameter)
mutation to neoplasia. has to undergo about 30 population doublings to produce
Free radicals production is ubiquitous in all respiring 109 cells weighing approximately 1 g, which is the smallest
organisms and is enhanced by many disease states, by carcinogen clinical detectable mass. To produce a tumor of 1012 cells,
exposure and under conditions of stress. Free radicals may weighing 1 kg approximately, which is usually the maximum
therefore contribute widely to cancer development in humans. size compatible with life, the tumor cells have to undergo
Free radicals scavenging vitamins C and E have been shown 10 further population doublings. So by the time the tumor
to protect against cancer development in animal models. is clinically detectable, it has already completed a major
portion of its life cycle
• Factors affecting growth of cells: In tumor cells, there is an
Biology of Tumor Growth imbalance between cell production and cell loss, therefore,
The life cycle of malignant tumors can be divided into four the tumor grows progressively. The rate of tumor growth
phases. depends upon the growth fraction and the degree of
imbalance between cell production and cell loss.
Induction of Malignant Changes in the Target
Cell (Transformation) (Fig. 2.2) Mechanism of Local Invasion and Distant
• Effect on genes: Large number of carcinogen agents Metastases
induce neoplastic transformation of cells in vivo and in Routes of Metastasis
experimental animals. All etiologic factors ultimately affect • There are three routes through which metastases of tumor
the function of two sets of genes, one is proto-oncogenes cells occur, i.e. local invasion, via blood vessels and via
or oncogenes and another one is anti-oncogenes or cancer lymphatics
suppressor genes • Local invasion: The local invasion takes the path of least
• Binding with DNA: The majority of carcinogens are resistance and the tumor cells invade the surrounding
mutagenes which bind the DNA directly or indirectly by tissue spaces
undergoing enzymatic activation, inducing miscoding errors • Lymphatics spread: In case of oral malignancies, distant
during transcription and replication metastasis is mainly via lymphatics, either by lymphatic
• Production of growth factors: Oncogenes may code for permeation or by lymphatic embolism
growth promoting factors and as a result, the tumor cells • Blood vessels: Rarely, it spreads through blood vessels and
produce large amount of growth factors to which, only they if this occurs, the tumor cells invade the lumen of blood
can respond vessels, the tumor emboli forms, which are fragmented and
• Encoding: Oncogenes may encode a defective receptor that the tumor cells are lodged into distant tissues. 9
send stimulating signals to the cells, even in the absence of
growth factors Theories of Carcinogenesis
• Multiple mutations: Cancer is a genetic disease that results • Conheim’s theory of embryonic cell rests (1875): During the
when multiple mutations accumulate in the DNA of a cell stage of early development of embryo, islets of cells may be
 may be brought about by carcinogenic influence, i.e.
chemical, viruses, radiation or spontaneous random
mutations
– Oncogenes: Oncogenes are the transforming genes
present in many tumor cells. Closely related genes are
detected on normal animal and human cells and are
called as ‘proto-oncogenes’ or ‘cellular oncogenes’,
abbreviated as ‘c-oncs’
– ‘Cellular oncogenes’ of the host cells can transcribe
its copies in the viral genome of acute transforming
oncogenic retroviruses called as viral oncogenes or
‘v-oncs’. An alternate mechanism is by anti-oncogenes
in which, there is inactivation or deletion of genes
that normally perform the function of suppressing cell
proliferation, thus allowing them to proliferate
– Feedback deletion: According to genetic regulatory
Fig. 2.3: Biology of tumor growth (kinetics of tumor cell growth) mechanism theory, primary change in the cell consists
of a modification of repressor molecule which controls
the functions of the gene. The repressor molecules are
misplaced and may become intermingled with other tissues. either RNA or protein. The modification of repressor
These cells remain and acquire power of proliferation and molecules removes their orderly inhibitory control,
growth in later life which is responsible for normal morphogenesis and
• Hypothesis of Waldeyer and Thiersch: Under normal differentiation, and unearths the cell genetic potentiality
conditions, there is state of equilibrium or balance between for unrestricted growth. This concept of loss of growth
epithelial and connective tissues with respect to their control is described as ‘feedback deletion’
proliferative capacity. As the age advances, checking power • Virus theory of Gye and Barnand (1925): At some stage, it
Section 1: Basics

of connective tissues for this equilibrium is lost, epithelium participates in the development of cancer. The concept of
proliferates and gives rise to carcinoma mode of action of virus has taken many forms:
• Tissue tension theory of Ribbert (1911): Proliferation of cells – Act as a parasite: Virus is present as a parasite in all
is controlled or held in equilibrium by tissues tension of the tumor cells and it is transmitted from cell-to-cell and
part. Overactivity of neighboring group of cells interferes stimulates extreme hyperplasia without affecting the
with equilibrium of part. Also irritation or trauma causes genome cell
growth liberation (cells become free and attain autonomy) – Act as biologic carcinogen: It acts as a biologic carcinogen
• Theory of cellular change (Boveri): There is altered nuclear on some cellular constituents to release or activate
constitution or an abnormal chromosome complex. neoplastic potentialities normally present in cells
Metabolism of tumor cells differs from normal cell due to – Auto synthesis: Carcinogens of all kinds ultimately act
difference in character of chromosome constituents. Majority by creating some new auto-synthesizing cytoplasmic
of normal cells require oxygen for aerobic respiration; constituents, probably an auto-catalytic protein, which
whereas malignant cells exist on anerobic glycolysis can excite the cell to unlimited growth
• Hypothesis of anaplasia (Hansmann): Cells may occasionally • Immune surveillance theory: It suggests that an immune-
revert to embryonic type so that they can produce more competent host mounts an attack on developing tumor
primitive type of cells. If there is greater degree of anaplasia, cells so as to destroy them while an immune-incompetent
more chances of malignancy is reported host fails to do so. According to original immunological
• Theory of cell variation (Haddow hypothesis): Carcinogenic theory, normal cells contain specific ‘self-marker’ (identity
agents might inhibit normal cell function and tumor growth proteins) which is recognized by the normal growth
might result by process of adaption to an unfavorable regulating mechanism. These proteins serve as receptor for
environment. Carcinogen acts as enzyme poison creating chemical carcinogens (hapten) and the resulting complex is
new enzyme which gives cell a capacity for unlimited growth self-replicating. The complex (complex antigen) triggers off
• Epigenetic theory: According to this theory, the carcinogenic an immune response and the antibody (free or cell bound)
agents act on the activators or suppressors of genes and combines with the self-marker carcinogen complex and
not on the genes themselves and result in the abnormal eliminates it. The new race of cells produced is deleted with
expression of genes self-markers and goes unrecognized by growth regulatory
• Genetic theory mechanism. The high incidence of cancer in AIDS patients
– Concept: This is the most popular theory which suggests is in support of this theory
that cells become neoplastic because of alteration in • Monoclonal hypothesis: Currently, there is strong evidence
the DNA. It is suggested that, the secret of cancer lies on studies of human and experimental animals that most
within the normal cells themselves in the form of proto- of the cancers arise from single clone of transformed cell.
oncogenes (C-oncs). The mutated cells transmit their The best documentation of monoclonal origin of cancer
characters to the next progeny of cells. Inappropriate cells come from the study of G6PD in women who are
10 over expression of the gene or point mutation cause the heterozygous for its two isoenzymes A and B. It is observed
cell to produce stimulating growth factors or in some that all tumor cells in benign uterine tumor (leiomyoma)
way damages normal regulatory control. The qualitative contain either A or B genotype of G6PD—i.e. the tumor cells
and quantitative changes in the expression of genome is derived from a single progenitor cell
• Polyclonal hypothesis: Pre-neoplastic events are polyclonal, Steps of Metastasis
i.e. cell proliferation that precedes cancer tends to involve • Breaking of cells: The breaking of loose neoplastic cells from
several cell clones. Two or more cells or clones of cells the parent tumor
interact to initiate a tumor • Invasion: Invasion of the matrix (sarcoma), penetration of
• Multistep theory: According to this theory, carcinogenesis the basement membrane and invasion of connective tissue
is a multistep process which is substantiated in vitro by (carcinoma)
changes in experimental animals as well as in vivo by • Entering the blood vessels: It then entering the wall of blood
changes in human cancers. In chemical carcinogenesis, and lymphatic vessels
there are two essential features, i.e. initiation and promotion. • Survival: Survival of malignant cells in the bloodstream.
Many tumors arise from combination of activation or Survival in the compatible tissue environment and induction
growth promoting oncogenes and inactivation of growth of growth factor to stimulate new vessel formation to obtain
suppressing anti-oncogenes. In some cancers, there is initial nutrition
dysplastic change that may progress into carcinoma in situ • Emergence of cells: Emergence of the malignant cells from
and then into invasive carcinoma. the blood vessels in the form of the emboli and lodgment
in other tissues
Metastasis • Multiplication: Multiplication of neoplastic cells and growth
to form secondary neoplasm at the new site
Metastasis is defined as spread of tumor by invasion in such a way
• Control mechanism: Each of these steps is probably
that discontinuous secondary tumor mass/masses are formed at
controlled by different molecular mechanism and this may
the site of lodgment. This metastasis is the transfer of the disease
explain the differences in the behavior with reference to
from one organ or part to another not directly connected with it.
tumor metastasis. Neoplastic cells within a single tumor
If malignant cells did not metastasize, the surgical might differ in their ability to metastasize. A sub-population
removal of primary neoplasm would completely cure the of cells pre-exists within the heterogeneous primary tumor.
patient. Metastasis is fundamentally an embolic process. The The relative size of this sub-population in the primary tumor
invasiveness of malignant cells involves motility, which requires may vary with time between the neoplasms.

Chapter 2: Neoplasm
change in shape and adhesiveness and ability to degrade the
matrix in order to penetrate it. Routes of Metastasis (Fig. 2.4)
Thus, a definition of the behavior of the metastatic tumor • Lymphatics: Particularly for carcinoma and lymphosarcoma.
cells is the tendency to cross the tissue compartment/boundary For example, mouth-to-neck nodes and breast-to-axillary
and intermix with other cell types. The metastatic process can nodes
be divided into several sequential steps although these steps are • Bloodstream: Particularly veins from gut via portal
interconnected. circulation to liver, from systemic sites through right heart
Factors which control metastasis are proteolysis, cell to lung, from left heart to any systemic sites
adhesion, tumor angiogenesis, cell mediated immunity and • Cavities: Along epithelium lined cavities, e.g. respiratory
genetic factors tract, gut, urinogenital tract etc.

11

Fig. 2.4: Different routes of metastasis in the human body

 • Others: Transcelomic spread, cerebrospinal fluid, tissue • Intermediate grade: In it, the cells are somewhere between
planes and through nerve sheath. the high and the low grades. These cancer cells are called
‘moderately-differentiated.
Pattern of Metastatic Spread
• Mechanistic theory: The capillary bed of the first organ
Broder’s Classification System (Fig. 2.5)
• Grade I—(Well-differentiated, i.e. less than 25% anaplastic
which encounter viable neoplastic cells is the preferred site
cells): It is characterized by the presence of relatively mature
of metastasis
cell with few nuclear aberration and with the presence of
• Seed and soil hypothesis: It suggests that availability of fertile
keratin pearls and individual cell keratinization
environment (the soil) in which compatible tumor cells (the
• Grade II—(Moderately differentiated, i.e. 25 to 50%
seed) can grow is important. Ewing suggested that varying
anaplastic cells): It is characterized by the presence of tumor
pattern of metastasis is due to fact that different tumor cells
cells exhibiting a wide range of differentiation, keratinization
thrive in certain biological sites (soils) but not in the other sites
is occasionally present, and nuclear aberrations are
• Cell interaction: Interaction between cell surface protein of
moderately abundant. Usually, the invasion is poorly
malignant cells and organ specific protein, e.g. fibronectin
delineated from the stroma
receptor.
• Grade III—(Moderately differentiated, i.e. 50 to 75%
anaplastic cells): It is characterized by disorderly and poorly
Grading and Staging of Tumors differentiated cells with no tendency toward keratinization.
Grading and staging of tumours are important because of their Nuclear aberrations are abundant
clinical relevance and so that different clinicians know how to • Grade IV—(Poorly differentiated, i.e. more than 75%
standardize, plan and organize patient’s treatment. anaplastic cells): In this, the cells are so poorly differentiated
that they cannot be identified as of epithelial origin on the
Grading basis of histology alone. Nuclear aberrations are abundant
Grade: grade of a tumor is determined by how abnormal the and no keratinization is found.
cancer cells appear when examined under a microscope. The
grading features are those which are indicative of proliferation CIN Grading
Section 1: Basics

and differentiation. It is defined as, ‘macroscopic and microscopic Alternative classification for grading of dysplasia and carcinoma
degree of differentiation of tumor’. Grading depends mainly on in situ together is cervical intraepithelial neoplasia (CIN).
two histologic features; the degree of anaplasia and the rate of According to this grading, the criteria are as follows:
growth. Tumor grading is a system used to classify cancer cells in • CIN I: It represents less than 1/3rd involvement of the
terms of how abnormal they look under a microscope and how thickness of the epithelium
quickly the tumor is likely to grow and spread. • CIN II: In this, there is 1/3rd to 2/3rd involvement
• CIN III: There is full thickness involvement. Or equivalent to
Types carcinoma in situ.
Depending upon how the tumor looks under a microscope,
cancer may be given one of the three grades. Warren’s Grading
• Low grade: In it cancer cell looks very much like a normal • Grade I: 1–2 abnormal mitosis/HP field
cells, with only slight, abnormal changes. These cancer cells • Grade II: 3–5 abnormal mitotic figures/HP field
are called ‘well-differentiated’ • Grade III: 6 or more abnormal mitotic figures/HP field.
• High grade: In it, cells look very abnormal and shows little
or no resemblance to normal tissue. These cancer cells are Staging
called ‘poorly-differentiated’ It is the extent of spread of tumor within patients.

12

Fig. 2.5: Broder’s classification (Grading system)—a diagrammatic representation

Assessment • Distant metastasis (M)
It is assessed by following ways: – Mx: Distant metastasis cannot be assessed
• Clinical examination: Staging can be assessed clinically by – M0: No distant metastasis
the size and extent of primary lesion – M1: Distant metastasis
• Investigations: Investigations like radiology, sonography can – Category M1 may be further specified according to the
lead to staging of disease notation
• Pathological examination: This is very important part - Pulmonary—PUL
while staging of neoplastic process is done. Mainly biopsy, - Osseous—OSS
cytology are used - Hepatic—HEP
• Infiltration: Degree of infiltration of primary lesion should - Brain—BRA
be carried out - Lymph nodes—LYM
• Metastasis: It includes presence or absence of metastasis - Bone marrow—MAR
to regional lymph nodes, presence and absence of distant - Pleura—PLE
metastasis, involvement of contralateral or ipsilateral node - Peritoneum—PER
and whether node are fixed or not. - Skin—SKI
- Other—OTH
Objectives
AJC (American Joint Committee) Staging
• Treatment planning: It aids the clinician in the planning of
It divides all cancers into stage 0 to 4, and takes into account all
treatment.
three previous TNM systems.
• Prognosis: To give some indication of prognosis
• Stage 0: T0 N0 M0
• Evaluation of treatment: To assist in evaluation of the result • Stage 1: T1 N0 M0
of treatment • Stage 2: T2 N0 M0
• Exchange of information: To facilitate the exchange of • Stage 3: T3 N0 M0, T1 N1 M0, T2 N1 M0, and T3 N1 M0
information between treatment centers • Stage 4A: T4 N0 M0, T4 N1 M0, any T N2 M0

Chapter 2: Neoplasm
• Investigations: To contribute to the continuing investigations • Stage 4 B: Any T N3 M0
of human cancer. • Stage 4 C: Any T, Any N, M1

TNM Staging Dukes ABC Staging

The tumor-node-metastasis (TNM) staging system was first It is used in cancers of bowel
reported by Pierre Denoix in the 1940s. It is universally accepted • Stage A—when tumor is confined to submucosa and muscle
system which is developed by UICC (Union Internationale and cure rate is 100%.
Centre of Cancer). • Stage B—tumor penetrates the entire thickness of bowel
• Primary tumor (T): Local extent is major factor contributing wall into pericolic or perirectal tissues and cure rate is 70%.
to prognosis • Stage C—it is characterized by lymph node metastasis and
– Tx: Primary tumor cannot be assessed reduces the cure rate to 30%.
– T0: No evidence of primary tumor
STNMP Staging System
– Tis: Carcinoma in situ
• S—site of primary tumor
– T1: Tumor 2 cm or less in diameter – S1: Lip and skin
– T2: Tumor 2 to 4 cm in diameter – S2: Lip mucosa
– T3: Tumor more than 4 cm in greatest diameter – S3: Tongue
– T4: Tumor of any size in which tumor invades adjacent – S4: Cheek
structure (e.g. cortical bone, inferior alveolar nerve, floor – S5: Palate
of mouth, skin of face, etc.) – S6: Floor of mouth
• Regional lymph nodes (N) – S7: Alveolar process
– Nx: Regional lymph node cannot be assessed – S8: Antrum
– N0: No regional lymph node metastasis – S9: Central carcinoma of bone
– N1: Metastasis in single ipsilateral lymph node less than • Size of tumor—it is denoted by T
3 cm in diameter – T1: Less than 2 cm in diameter
- N1a: Nodes considered not contain to tumor growth – T2: Between 2 cm and 4 cm in diameter
- N1b: Nodes considered to contain growth – T3: Between 4 cm and 6 cm in diameter and extending
beyond the primary region and extending through
– N2: Single lymph node, no more than 6 cm in greatest
adjacent periosteum
dimension, of bilateral/contralateral lymph node, no
– T4: Greater than 6 cm in diameter and extending to
more than 6 cm
involve adjacent structures
- N2a: Single ipsilateral lymph node more than 3 but
• Regional nodes were grouped as
less than 6 cm
– N0: No palpable nodes
- N2b: Multiple ipsilateral lymph nodes less than 6 cm. – N1: Equifocal node enlargement
- N2c: Bilateral or contralateral lymph node less than – N2: Clinically palpable homolateral regional nodes,
6 cm in greatest dimension not fixed 13
• N3: Metastasis in lymph node more than 6 cm and it is fixed. – N3: Same as N2 but fixed
– N3a: Ipsilateral nodes at least one greater than 6 cm – N4: Clinically palpable contralateral or bilateral nodes,
– N3b: Bilateral nodes greater than 6 cm not fixed
– N3c: Contralateral nodes at least one greater than 6 cm – N5: Same as N4 but fixed
 • Metastasis 4. Following are the initiators of carcinogenesis except:
– M0: No distant metastasis. (a) Chlorambucil (b) Benzidine
– M1: Clinical evidence of distant metastasis without (c) Phenols (d) Methylcholanthrene
definite histological or radiographic conformation. 5. The chemical substances which require metabolic activation for
becoming potent initial carcinogens are called as:
– M2: Proven evidence of metastasis beyond regional
(a) Promoters of carcinogenesis
nodes
(b) Indirect-acting carcinogens
• Pathology of lesion
(c) Direct-acting carcinogens
– P0: Hyperkeratotic lesion showing atypia (d) Acylating agents
– P1: Carcinoma in situ
6. In case of biologic carcinogenesis, following are the DNA onco-
– P2: Basal cell carcinoma genic viruses except:
– P3: Verrucous carcinoma (a) Adenoviruses
– Well differentiated squanuous cell carcinoma (b) Herpes virus
– Moderately differentiated squanuous cell carcinoma (c) Human T-cell Lymphotropic viruses
– Poorly differentiated squanuous cell carcinoma. (d) Pox virus
7. Following are the theories of carcinogenesis except:
Suggested Reading (a) Epigenetic theory
(b) Virus theory
1. Franks LM, Teich NM. Introduction to the Cellular and Molecular (c) Immune surveillance theory
Biology of Cancer (3rd edn), Oxford University Press; 1997.
(d) Multiclonal theory
2. Howaldt HP, Kainz M, et al. Proposal for modification the TNM
8. Following are the route of metastasis except:
staging classification for caner of the oral cavity: DOSAK. J
(a) Lymphatics (b) Blood stream
Craniomaxillofac Surg. 1999;27:275-88.
(c) Cavities (d) Salivary
3. Khalili M, et al: Grading of oral cancer: Comparision of different
systems with respect to lymph node matastasis in tongue SCC, 9. In Broder’s classification system of grading and staging of tumors,
Iran. J Oral Pathol Med. 18(8)432. grading is done as:
(a) Stage A, B and C
Section 1: Basics

4. Underwood JCE. General and Systematic Pathology (3rd edn),

(b) Grade I, II, III and IV
Churchill Livingstone, 2000
(c) CIN I, II and III
(d) Mild, moderate and sever
10. In TNM staging, stage to means:
Multiple Choice Questions (a) T0 N0 M0 (b) T2 N0 M0
1. Malignant tumors arising from mesenchymal tissues are known (c) T1 N0 M0 (d) Any T N3 M0
as
(a) Carcinomas (b) Sarcomas Long Answer Questions
(c) Lipomas (d) Osteomas
2. Following are the acquired preneoplastic conditions except 1. What is carcinogenesis? Write types of carcinogenesis and write
(a) Leukoplakia of the oral cavity in detail about chemical carcinogenesis.
(b) Chirrhosis of liver 2. Define metastasis? describe in detail about routes, steps & pat-
(c) Chronic irritation tern of metastasis.
(d) Benign migratory glossitis
3. Carcinogens are broadly divided into which 4 groups: Short Answer Questions
(a) Chemical, Mecanical, Hormonal, Biologic
(b) Chemical, Physical, Hormonal, Biologic 1. Mechanism of biologic carcinogenesis.
(c) Psychological, Physical, Hormonal, Biologic 2. Theories of carcinogenesis.
(d) Chemical, Physical, Psychological, Mecanical 3. TNM staging of tumor grading.

14
 c H a P t er 3
Infection Control in Dental Office
Amina Sultan, Mandeep Kaur, Sukhdeep Singh

ˆ Transmission of Infections ˆ Disinfections and Sterilization

Infections
ˆˆˆ that can be Transmitted in a Dental Environment – Sanitization
(by the Oral Cavity) – Disinfection
ˆ Standard Infection Control
– Sterilization
– Rationale of Infection Control
– Classification of Surfaces for Infection Control – Proper Disposal of Dental Waste
ˆ Infection Control Protocol – Formal Education and Training
– Dental Unit Design – Immunization
– Patient Evaluation – Waterlines and Water Quality
– Personal Protection and Barrier Protectio – Use of Mouth rinses
– Hand Hygiene (e.g. Handwashing, Hand Antisepsis, or
ˆ Infection Control in Radiography
Surgical Hand Antisepsis)

The battle between man and microbe begins much before the
patient even sits on the dental chair. Considering the diversity
of the oral microbial pathogens, the risk of infection is a high
priority issue for the patient as well for the dental healthcare
provider. With the world becoming a big global village, pathogens
are not localized to particular geographic area especially with
viral pathogens such as herpes, hepatitis and HIV.
The dental clinics as well as the staff should be well versed
with the use of standard precautions for infection control so as
to insure the safety of the patients and the clinician.

Transmission of Infections
Fig. 3.1: Different routes of infection transmission
The transmission of any disease or infection (cross infection)
between the patient and the staff within a clinical environment
requires: Infections that can be Transmitted in a
• Source of the Infectious agent (bacteria, virus, fungi, etc.) It
is the person with the infection (index case). The sources of Dental Environment (by the Oral Cavity)
infection in clinical dentistry are mainly human with overt • Viral hepatitis: It includes mainly hepatitis B and C. The
infections or people in prodromal stage of certain infections incidence of hepatitis B has increased significantly during
and healthy carriers of pathogens. the past 20 years. Nearly all body fluids carry the virus, but
• Modes of transmission: It is the vehicle by which the infective only blood, saliva, semen and vaginal fluids have been
agent is transmitted. It can be transmitted by direct contact, shown to be infectious. Two percent of the populations are
indirect contact (fomite, vector) and airborne known carriers of HBV which can be transmitted by saliva.
• Routes of entry of pathogen in new host: It can be done by High risk in HBV infection can be related to variety of factors,
inhalation, ingestion, skin abrasion, and mucous membrane including occupation, place of residence, lifestyle, and
(Fig. 3.1). parenteral drug abuse. Healthcare personnel are included
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littp://www.arcliive.org/details/celebratedjumpinOOtwai
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REFERENCE ■^'d S533888 etA 

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. THE CELEBRATED JUMPING FROG OF CAIATEKAS

COUNTY,, By JAauk Twain. EDITED BY JOHN PAUL. C. H. W:ES3i,
^uhUsher, //.9 & /5/ JS'ASS^U ST. AMERICAN NEWS CO., AGENTS.
1869.
The text on this page is estimated to be only 16.04%
accurate

Entered, according to Act of Congress, in the yecr ISGT, by

C. II. WEBB, In tlie Clerk's Office of the District Court of the United
States for the Southern District of New-York. JOHN A . G K AY &. G
11 E K N , 16 AND IS Jacob St., N«w-Yokk
The text on this page is estimated to be only 20.70%
accurate

TO John Smith, WnOlI I HAVE KNOWN IN DIVERS AND

SUNDRY PLACES ABOUT THE WORLD, AND WHOSE MANY AND
MANIFOLD VIRTUES DID ALWAYS COMMAND MY ESTEEM, I It is
said that the man to whom a volume is dedicated, always buys a
copy. If this prove true in the present instance, a princely affluence
is about to burst upon rMJ7 :4.UriI01i.
 ADYEETISEMEI^T. " Mark Twain " is too well known to tlie
public to require a formal introduction at my hands. By his story of
the Frog, he scaled the heights of popularity at a single jump, and
won for himself the sobriquet of The Wild Humorist of the Pacific
Slope. He is also known to fame as The Moralist of the Main ; and it
is not unlikely that as such he will go down to posterity. It is in his
secondary character, as humorist, however, rather than in the primal
one of moralist, that I aim to present him in the present volume.
And here a ready explanation will be found for the somewhat
fragmentary character of many of these sketches ; for it was
necessary to snatch threads of humor wherever they could be found
— very often detaching them from serious articles and moral essays
with which they were woven and entangled. Originally written for
newspaper publication, many of the articles referred to events of the
day, the interest of which has now passed away, and contained local
allusions, which the general reader would fail to understand; in such
cases excision became imperative. Further than this, remark or
comment is unnecessary. Mark Twain never resorts to tricks of
spelling nor rhetorical buffoonery for the purpose of provoking a
laugh ; the vein of his humor runs too rich and deep to make
surface-gilding necessary. But there are few who can resist the
quaint similes, keen satire, and hard good sense which form the
staple of his writings. J. P.
 coi^te:^ts. PaG3 The Celebrated Jumping Frog of
Calaveras County, 7 Aurelia's Unfortunate Young Man, 20 A
Complaint about Correspondents, dated in San Francisco, ... 26
Answers to Correspondents, 34 Among the Fenians, 58 The Story of
the Bad Little Boy who Didn't Come to Grief, . . 60 Curing a Cold, CT
An Inquiry about Insurances, 76 Literature in the Dry Diggings, 82
"After" Jenkins 85 Lucretia Smith's Soldier, 89 The Killing of Julius
Csesar " Localized," 99 An Item which the Editor Himself could not
Understand, .... 110 Among the Spirits, 116 Brief Biographical Sketch
of George Washington, , 127 A Touching Story of George
Washington's Boyhood, 132 A Page from a Californian Almanac,
........ 141 Information for the Million, 144 The Launch of the
Steamer Capital, 153 Origin of Illustrious Men, 163 Advice for Good
Little Girls, 164 Concerning Chambermaids, 167 Remarkable
Instances of Presence of Mind, . 172 Honored as a Curiosity in
Honolulu, j , 176 The Steed " Oahu," 179 A Strange Dream, 182
Short and Singular Rations, , 194
 THE CELEBRATED JUMPING EEOG rALAYERAS LOUNTY ? N"
compliance with tlie request of a friend of mine, wlio wrote me from
tlie East, I called on good-natured, garrulous old Simon Wlieeler, and
inquired after my friend' s friend, Leonidas W. Smiley, as requested
to do, and I hereunto append the result. I have a lurking suspicion
that Leonidas W, Smiley is a myth ; that my friend never knew such
a personage ; and that he only conjectured that, if I asked old
Wheeler ahout him, it would remind him of his infamous Jim Smiley,
and he would go to work and l)ore me
 8 THE JUMPING FBOO. nearly to death with some infernal
reminiscence of him as long and tedious as it should Ibe useless to
me. If that was the design, it certainly succeeded. I found Simon
Wheeler dozing comfortably by the bar-room stove of the old,
dilapidated tavern in the ancient mining camp of Angel' s, and I
noticed that he was fat and bald-headed, and had an expression of
winning gentleness and simplicity upon his tranquil countenance. He
roused up and gave me good-day. I told him a friend of mine had
commissioned me to make some inquiries about a cherished
companion of his boyhood named Leonidas W. Smiley— Hev.
Leonidas W. Smiley — a young minister of the Gospel, who he had
heard was at one time a resident of Angel' s Camp. I added that, if
Mr. Wheeler could tell me any thing about this Kev. Leonidas W.
Smiley, I would feel under many obligations to him. Simon Wheeler
backed me into a corner and blockaded me there with his chair, and
then sat me down and reeled off the monotonous narrative which
follows this paragraph. He never smiled, he never frowned, he never
changed his voice from the gentle-flowing key to which he
 TUE JUMPING FROG. 9 tuned tlie initial sentence, lie never
Ibetrayed the slightest suspicion of enthusiasm ; but all through the
interminable narrative there ran a vein of impressive earnestness
and sincerity, which showed me plainly that, so far from his
imagining that there was any thing ridiculous or funny about his
story, he regarded' it as a really important matter, and admired its
two heroes as men of transcendent genius m finesse. To me, the
spectacle of a man drifting serenely along through such a queer yarn
without ever smiling, was exquisitely absurd. As I said before, I
asked him to tell me what he knew of Rev. Leonidas W. Smiley, and
he replied as follows. I let him go on in his own way, and never
interrupted him once : There was a feller here once by the name of
Jim Smiley, in the winter of '49 — or may be it was the spring of '50
— I don't recollect exactly, somehow, though what makes me think it
was one or the other is because I remember the big flume wasn't
finished when he first came to the camp ; but any way, he was the
curiosest man about always betting on any thing that turned up you
ever see, if he could get any body to
 10 THE JUMPING FROG. "bet on the other side ; and if he
couldn't, he'd change sides. Any way that suited the other man
would suit him — any way just so's he goi a "bet, Tie was satisfied.
But still he was lucky, uncommon lucky; he most always come ont
winner. He was always ready and laying for a chance ; there couldn't
be no solitry thing mentioned l)ut that feller' d offer to bet on it, and
take any side you please, as I was just telling you. If there was a
horse-race, you'd find him flush, or you'd find him busted at the end
of it ; if there was a dog-fight, he'd bet on it ; if there was a cat-
fight, he'd bet on it: if there was a chicken-fight, he' d bet on it ;
why, if there was two birds setting on a fence, he would bet you
which one would fly first ; or if there was a camp-meeting, he would
be there reg'lar, to bet on Parson Walker, which he judged to be the
best exhorter about here, and so he was, too, and a good man. If he
even seen a straddle-bug start to go anywheres, he would bet you
how long it would take him to get wherever he was going to, and if
you took him up, he would f oiler that straddle-bug to Mexico but
what he would find out where he was bound for and how long he
was on the road. Lots of
 THE juMPma FBoa. 11 tlie boys liere lias seen tliat Smiley,
and can tell you about him. Wliy, it never made no difference to Mm
— lie would bet on any tiling — tlie dangdest feller. Parson Walker's
wife laid very sick once, for a good while, and it seemed as if they
warn't going to save her ; but one morning he come in, and Smiley
asked how she was, and he said she was considerable better —
thank the Lord for his inf 'nit mercy — and coming on so smart that,
with the blessing of Prov'dence, she'd get well yet ; and Smiley,
before he thought, says, ''Well, I'll risk twoand-a-half that she don't,
any way." Thish-yer Smiley had a mare — the boys called her the
fifteen-minute nag, but that was only in fun, you know, because, of
course, she was faster than that — and he used to win money on
that horse, for all she was so slow and always had the asthma, or
the distemper, or the consumption, or something of that kind. They
used to give her two or three hundred yards start, and then pass her
under way ; but always at the fag-end of the race she'd get excited
and desperate-like, and come cavorting and straddling up, and
scattering her legs around limber, sometimes in the air, and some 
 12 THE JUMPING FROG. times out to one side amongst tlie
fences, and kicking up m-o-r-e dust, and raising m-o-r-e racket witli
lier coughing and sneezing and blowing lier nose — and always fetch
np at the stand just about a neck ahead, as near as you could cipher
it down. And he had a little small bull pup, that to look at him you'd
think he wan't worth a cent, but to set around and look ornery, and
lay for a chance to steal something. But as soon as money was ujd
on him, he was a different dog ; his under-jaw'd begin to stick out
like the fo' castle of a steamboat, and his teeth would uncover, and
shine savage like the furnaces. And a dog might tackle him, and
bully-rag him, and bite him, and throw him over his shoulder two or
three times, and Andrew Jackson— which w^as the name of the
pup — Andrew Jackson would never let on but what Tie was
satisfied, and hadn't expected nothing else — and the bets being
doubled and doubled on the other side all the time, till the money
was all up ; and then all of a sudden he would grab that other dog
jest by the j'int of his hind leg and freeze to it^ — not chaw, you
understand, but only jest grip and hang on till they throwed up
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