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Essentials-of-Oral-Pathology-3rd-Edition by purkait

Essentials-of-Oral-Pathology-3rd-Edition by purkait

Essentials of

Oral Pathology

Essentials of

Oral Pathology


Swapan Kumar Purkait BDS (Cal) MDS (Cal)

Professor and Head
Department of Oral and Maxillofacial Pathology

Purvanchal Institute of Dental Sciences
Gorakhpur, Uttar Pradesh, India

RR Paul

Jay Gopal Ray
Tamal Kanti Pal



New Delhi • St Louis • Panama City • London

Published by
Jaypee Brothers Medical Publishers (P) Ltd

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Essentials of Oral Pathology

© 2011, Jaypee Brothers Medical Publishers

All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or
transmitted in any form or by any means: electronic, mechanical, photocopying, recording, or otherwise,
without the prior written permission of the author and the publisher.

This book has been published in good faith that the material provided by author is original. Every effort
is made to ensure accuracy of material, but the publisher, printer and author will not be held responsible
for any inadvertent error(s). In case of any dispute, all legal matters are to be settled under Delhi
jurisdiction only.

First Edition: 1999
Second Edition: 2003
Reprint: 2004, 2007, 2008
Third Edition: 2011

ISBN 978-93-5025-214-7

Typeset at JPBMP typesetting unit
Printed at Replika

My children Prithu and Pubali

and my wife Maitreyee

Foreword ...................................

Today our society needs not just a dental surgeon, but a medically competent dental surgeon.
Oral pathology is undoubtedly the most integral subject of teaching in dental curriculum
which bridges the gap between the medical and dental sciences. But the available textbooks
in this field of oral pathology are so voluminous that it becomes virtually impossible for
any dental student to gather comprehensive knowledge out of those textbooks during their
BDS course of studies. In view of this, the textbook titled Essentials of Oral Pathology written
by Dr Swapan Kumar Purkait seems to fill this lacuna admirably. I am sure this book will
be of immense importance to the general dental practitioners too.


Department of Oral Pathology
Guru Nanak Institute of Dental Sciences

Kolkata, West Bengal, India

Foreword ...................................

It gives me immense pleasure to introduce the third edition of the book on oral pathology
titled Essentials of Oral Pathology by Dr Swapan Kumar Purkait to the budding graduates of
dentistry. Oral and maxillofacial pathology is a specialty of dentistry and a very fundamental
subject for all the students contemplating to practice clinical dentistry at large.

The purpose of the latest edition of this book remains the same, i.e. to provide the reader
with a comprehensive discussion of a wide variety of diseases that affects the maxillofacial
region. The previous editions have been well accepted and so far thousands of students
were benefitted by reading the same.

The immense effort put in by the author in bringing out this edition is highly
commendable. We all trust in the basic philosophy that education brings in knowledge
with consistent effort and knowledge when properly nurtured brings in wisdom. Similarly,
this book has also grown qualitatively and refined with every new edition.

This book has twenty-three chapters, illustrations and photographs arranged
systematically to fit in with the course and curriculum for undergraduate teaching; though
much emphasis is not given on in-depth detail of molecular and biochemical aspects of
modern diagnostic pathology, since this book has been written keeping in mind the need of
undergraduate students only.

Finally, I wish Dr Purkait all success in life and my deepest regards to him for sharing
his knowledge with the students. I conclude by saying “Man is not immortal but remains
immortal through his work”. I am sure all of us will be benefitted by this book.

Jay Gopal Ray MDS (Oral Pathology)
Postgraduate Teacher and Head
Department of Oral Pathology

Dr R Ahmed Dental College and Hospital
Kolkata, West Bengal, India

Foreword to the Second Edition

There is an ongoing search for an improved approach to deliver oral healthcare to ail
human across the globe. The gap between the reality and expectations in oral healthcare
system has become wider and this disparity, however, lies with the failure of transforming
fundamental biological science into own clinical practice.

Oral pathology is one of the basic sciences in dentistry, the thorough understanding of
which can certainly bring about qualitative changes in our clinical approaches towards
amelioration of disease entity, providing both early intervention with better therapeutics
and preventions. With this mission in mind, Dr Swapan Kumar Purkait, an eminent oral
pathologist, has strived for new second edition of his book Essentials of Oral Pathology.

It is with great pleasure and profound satisfaction, I have gone through the entire edition
and found it to be very informative and useful for persuing undergraduate studies. This is
a wonderful piece of work with simple language and lucid presentation also, easy for
students to assimilate and reproduce. About 150 pages have been added to this new edition
to incorporate current contents and references and other chapters are thoroughly updated
throughout. New chapters like Syndromes Related to Oral Diseases, Classification of Oral
Diseases, and Diseases of TM Joint, will certainly enrich the readers.

The breakneck increase in information and indecent speed of expanding knowledge
have paved the way for the second edition to come out. I am sure that this book will find its
own place in dental profession and the readers shall have ready access to a comprehensive
reference that enables rapid retrieval of integrated and relevant information on the subject.

Tamal Kanti Pal
MDS, PhD, Cert Implant, New York University, USA

Head and Postgraduate Faculty
Department of Periodontics

Guru Nanak Institute of Dental Sciences
Kolkata, West Bengal, India

Preface to the Third Edition ..

The second edition of Essentials of Oral Pathology was published seven years back in the
year 2003. I am grateful to the students and teachers of oral pathology for their acceptance
and appreciation of the book. The purpose of the third edition is primarily to make
qualititative upliftment of the book and to provide the students with more elaborate
discussions on oral and orofacial diseases. Moreover, some new topics have also been
added in this version. The highlighting features of this edition are the introduction of some
special aspects of various oral lesions and the addition of several tables to pinpoint the key
features of many important diseases. This edition is also coming in multicolor version,
which I hope will be beneficial to the students in understanding the subject better.

I sincerely request the teachers and students of oral pathology to express their views and
kindly provide me with constructive suggestions as to how this book can be further improved.

Swapan Kumar Purkait

Preface to the First Edition....

Oral Pathology is an important branch of dentistry and although, there are few good
textbooks available in the subject, Essentials of Oral Pathology has been written with a view
to present the subject to the students in a more simplified but comprehensive manner.

I hope the book will fulfill the need of the students by giving them relevant guidance in
their day-to-day learning process as well as during their preparation for examination and
above all, with the book in hand, students will find the subject easy to handle.

As no one is perfect in absolute sense, I also humbly accept my limitations regarding
shortcomings in the book and therefore, I sincerely welcome the valuable suggestions from
my senior colleagues and students regarding what further should be done to improve this

Swapan Kumar Purkait

Acknowledgments ...................

This book has been accomplished with the help of many people from all over the country
and I am indebted to all of them. I wish to thank and express my sincere regards to my
teachers Dr RR Pal, Dr Amit Roy, Dr (Mrs) Kabita Chatterjee, and Dr Tamal Kanti Pal for
their constant encouragement and inspirations.

Special thanks to Dr Jay Gopal Ray for his continuous encouragement and whole hearted

Heartiest thanks are extended to Dr Alok Banerjee, Dr (Mrs) Mousumi Pal, Dr KP Das
and Dr Madhumita Bhattacharjee for providing me with some brilliant clinical photographs
for this book.

Deepest thanks to my wife Maitreyee , my daughter Pubali and Mr Suman Guha who
have done a great job in making the computer generated graphic illustrations and designing
of the tables used in the book.

I am thankful to my student Dr Sumanta Kumar Kolay (now an oral pathologist too) for
his continuous support and encouragement extended as always during the course of
writing the book.

Heartiest thanks to my seniors, friends and colleagues Dr Tushar Deb, Dr Bijoy Das,
Dr Sanjib Mitra, Dr Anjana Majumder, Dr S R Karmakar, Dr Arup Ghosh, Dr Neeta Singh,
Dr Shila Dey, Dr Narendra Singh, Dr Jayanta Chatterjee, Dr Sumit Majumder, Dr A Mamud
and Dr Sourav Bhattacharjee for their whole hearted support and encouragement.

I am fortunate to have the constant encouragement and trust of Shri Jitendar P Vij, the
Chairman and Managing Director of Jaypee Brothers Medical Publishers (P) Ltd along
with his editorial and production staff.

Last but not least, I sincerely thank the students and teachers of Oral and Maxillofacial
Pathology, who have made the 1st and 2nd edition of my book successful and this 3rd
edition would not have been possible without their acceptance and appreciation.

If someone’s name is inadvertently not included in this column of acknowledgment, I
sincerely apologize for that.

Contents ....................................

1. Developmental Anomalies of Oral and Paraoral Structures .......................... 1–63

Introduction 1 • Developmental anomalies of oral soft tissues 1 • Anomalies of lips and palate 1 • Lip pits
and fistulas 1 • Double lip 2 • Frenal tag 2 • Hereditary intestinal polyposis (Peutz-Jeghers) syndrome 3
• Oral melanotic macule (ephelis) 4 • Uvula elongata 4 • Cheilitis glandularis 5 • Cheilitis granulomatosa 6
• Anomalies of oral mucosa 7 • Fordyce’s granules 7 • Focal epithelial hyperplasia 8 • White sponge nevus 9
• Developmental defects of the gingiva 10 • Fibromatosis gingivae 10 • Retrocuspid papilla 11
• Developmental anomalies involving the jawbone 11 • Agnathia 11 • Micrognathia 11 • Macrognathia 13
• Facial hemihypertrophy 13 • Facial hemiatrophy 15 • Cleft lip and cleft palate 16 • Developmental
anomalies of the tongue 20 • Aglossia 20 • Microglossia 20 • Macroglossia 20 • Ankyloglossia 22 • Cleft
tongue 22 • Fissured tongue (scrotal tongue) 23 • Median rhomboid glossitis 23 • Lingual varices 25
• Geographic tongue 25 • Hairy tongue 27 • Lingual thyroid nodule 28 • Thyroglossal tract cyst 29
• Anomalies of oral lymphoid tissue 30 • Reactive lymphoid aggregate 30 • Lymphoepithelial cyst
(branchial cyst) 30 • Angiolymphoid hyperplasia with eosinophilia (ALHE) 31 • Anomalies of the salivary
gland 32 • Developmental anomalies involving oral hard tissues 32 • Abnormalities of teeth 32 • Disturbance
in size of teeth 32 • Microdontia 32 • Macrodontia 33 • Disturbance in number of teeth 34 • Anodontia 34
• Complete or total anodontia 34 • Partial anodontia 35 • Supernumerary teeth 36 • Disturbances in
eruption of teeth 38 • Premature eruption 38 • Delayed eruption 38 • Impacted teeth 39 • Eruption
sequestrum 41 • Disturbances in the shape of teeth 41 • Gemination (twinning) 41 • Fusion 42
• Concrescence 43 • Dilaceration 44 • Taurodontism 45 • Dens-in-dente (dens-invaginatus) 45 • Dens-
evaginatus 46 • Talon cusp 47 • Enamel pearl 47 • Disturbance in the structure of teeth 48 • Disturbance
in the structure of enamel 48 • Acquired disturbances of enamel 48 • Focal enamel hypoplasia 48
• Idiopathic enamel opacities 49 • Generalized enamel hypoplasia 49 • Effect of individual systemic
conditions on enamel hypoplasia 49 • Nutritional deficiency 49 • Congenital syphilis 49 • Hypocalcemia 50
• Exanthematous disease 50 • Birth injuries and Lowbirth weight 50 • Fluorides and mottling 51
• Hereditary disturbance of enamel formation 51 • Amelogenesis imperfecta 51 • Syndrome associated
enamel defects 53 • Disturbances in structure of dentin 54 • Dentinogenesis imperfecta (hereditary
opalescent- dentin) 54 • Dentinal abnormality due to systemic or environmental disturbances 57 • Dentin
dysplasia 58 • Regional odontodysplasia (ghost teeth) 60 • Disturbance in structure of cementum 61
• Hypercementosis 61 • Hypocementosis 62.

2. Benign and Malignant Neoplasms of the Oral Cavity ................................. 64–174

Neoplasm (tumor) 64 • Classification of oral non-odontogenic neoplasms 65 • Neoplasms of epithelial tissue
origin 65 • Neoplasms of mesenchymal tissue origin 65 • Benign neoplasms of the epithelial tissue origin 66
• Papilloma 66 • Keratoacanthoma 68 • Pigmented cellular nevus 70 • Intradermal (intramucosal) nevus 70
• Junctional nevus 71 • Compound nevus 71 • Blue nevus 72 • Malignant neoplasms of the epithelial tissue
origin 72 • Squamous cell carcinoma 72 • Oral cancer in different intraoral locations or subsites 80
• Carcinoma of the lip 80 • Carcinoma of the tongue 81 • Carcinoma of the floor of the mouth 83 • Carcinoma
of the palate 83 • Carcinoma of the buccal mucosa 84 • Carcinoma of the gingiva/alveolar ridge 84 • Carcinoma
of the maxillary antrum 85 • Basal cell carcinoma (rodent ulcer) 94 • Verrucous carcinoma 96 • Malignant
melanoma 98 • Spindle cell carcinoma 101 • Primary intra-alveolar carcinoma 102 • Neoplasms of mesenchymal
tissue origin 103 • Benign neoplasms of fibrous connective tissue 103 • Fibroma 103 • Desmoplastic fibroma 104
• Giant-cell fibroma 105 • Myofibroma 106 • Peripheral ossifying fibroma 107 • Central ossifying fibroma 108
• Peripheral giant cell granuloma 110 • Central giant cell granuloma 113 • Benign fibrous histiocytoma 116
• Myxoma 117 • Nodular fascitis 118 • Benign neoplasm of adipose tissue origin 119 • Lipoma 119
• Benign neoplasm of vascular tissue origin 120 • Hemangioma 120 • Benign neoplasm of lymphatic vessels 124
• Lymphangioma 124 • Benign neoplasm of bone 127 • Osteoma 127 • Osteoid osteoma 129 • Osteoblastoma 129
• Benign neoplasm of cartiliage tissue 130 • Chondroma 130 • Benign chondroblastoma 131 • Benign
neoplasm of smooth muscles 131 • Leiomyoma 131 • Benign neoplasm ofstriated muscle 133 • Rhabdomyoma 133
• Granular cell myoblastoma 133 • Benign neoplasms of neural tissue 135 • Neurilemmoma (schwannoma) 135
• Neurofibroma 137 • Melanotic neuroectodermal tumor of infancy 139 • Malignant neoplasms of mesenchymal

xx Essentials of Oral Pathology

tissue 140 • Fibrosarcoma 140 • Malignant fibrous histiocytoma 143 • Liposarcoma 144
• Hemangioendothelioma 144 • Hemangiopericytoma 145 • Kaposi’s sarcoma 147 • Ewing’s sarcoma 148
• Chondrosarcoma 150 • Mesenchymal chondrosarcoma 152 • Osteosarcoma 153 • Lymphomas 157 • Non-
Hodgkin’s lymphoma (NHL) 157 • Burkitt’s lymphoma 161 • Hodgkin’s lymphoma 164 • Multiple myeloma 165
• Solitary plasmacytoma 167 • Leiomyosarcoma 168 • Rhabdomyosarcoma 169 • Neurogenic sarcoma 169
• Metastatic tumors of the jaws 171.

3. Oral Precancerous Lesions and Conditions .................................................. 175–197

Leukoplakia 175 • Oral hairy leukoplakia 182 • Leukoedema 183 • Carcinoma in situ 184 • Erythroplakia 185
• Stomatitis nicotina 186 • Oral submucous fibrosis (OSF) 187 • Sideropenic dysphagia 191 • Lichen
planus 191.

4. Diseases of the Salivary Glands ..................................................................... 198– 234

Classification of salivary gland diseases 198 • Non-neoplastic disorders 198 • Neoplastic disorders 199
• Developmental anomalies of the salivary gland 199 • Aplasia or agenesis of the salivary gland 199
• Hypoplasia of the salivary glands 199 • Ectopic salivary glands (aberrant) 200 • Atresia 200 • Accessory
ducts 200 • Diverticuli 200 • Lingual mandibular salivary glands depression 201 • Reactive lesions of the
salivary gland 201 • Salivary gland cysts 201 • Sialolithiasis 201 • Postradiation sialadenitis 205
• Chronic sclerosing sialadenitis 205 • Necrotizing sialometaplasia 206 • Infective lesions (sialadenitis) 207
• Bacterial sialadenitis 207 • Acute bacterial sialadenitis 207 • Chronic bacterial sialadenitis 208
• Recurrent parotitis 209 • Viral sialadenitis 209 • Mumps (endemic parotitis) 209 • Cytomegalic
inclusion disease 209 • Immune-mediated disease 209 • Mikulicz’s disease 209 • Sjogren’s syndrome 210
• Miscellaneous disorders of salivary gland 213 • Heerfordt’s syndrome 213 • Sialosis 213 • Ptyalism 213
• Aptyalism (xerostomia) 214 • Neoplasm of the salivary glands 215 • Pleomorphic adenoma 216
• Monomorphic adenoma 220 • Myoepithelioma 221 • Oncocytoma (oxyphilic adenoma) 222
• Adenolymphoma (warthin’s tumor) 222 • Malignant salivary gland neoplasms 224 • Malignant
pleomorphic adenoma (mixed tumor) 224 • Adenoid cystic carcinoma (cylindroma) 225 • Mucoepidermoid
tumor 229 • Acinic cell tumor 231 • Adenocarcinoma 231.

5. Odontogenic Neoplasms .................................................................................... 235–267

Classification of odontogenic tumors (modified WHO classification) 236 • Ameloblastoma 236 • Unicystic
ameloblastoma 242 • Adenomatoid odontogenic tumor (AOT) 244 • Calcifying epithelial odontogenic
tumor (CEOT) 247 • Squamous odontogenic tumor 250 • Ameloblastic fibroma 251 • Ameloblastic fibro-
odontome 253 • Odontomes 254 • Odontogenic fibroma 257 • Peripheral odontogenic fibroma 257
• Central odontogenic fibroma 258 • Odontogenic myxoma 259 • Periapical cementral dysplasia (cementoma) 261
• Familial gigantiform cementoma 262 • Cementoblastoma 262 • Malignant odontogenic neoplasms 264
• Malignant ameloblastoma 264 • Ameloblastic carcinoma 264 • Odontogenic carcinoma 265 • Odontogenic
sarcomas 265 • Clear cell odontogenic carcinoma 265 • Primary intra-alveolar carcinoma 265.

6. Cysts of the Oral Regions .................................................................................. 268–305

Classification of cysts 268 • Cysts associated with the maxillary antrum 269 • Cyst of the tissue of the
mouth, face and neck 269 • Odontogenic cysts 270 • Odontogenic keratocyst (primordial cyst) 270
• Dentigerous cyst 276 • Radicular cyst 281 • Eruption cyst 286 • Lateral periodontal cyst 287 • Dental
lamina cyst (gingival cyst) of the newborn 288 • Gingival cysts of the adult 288 • Sialo-odontogenic cysts
(glandular odontogenic cyst) 289 • Botryoid odontogenic cysts 290 • Calcifying epithelial 290 • Odontogenic
cyst (CEOC) 290 • Paradental cyst 292 • Non-odontogenic cysts 293 • Globulomaxillary cyst 293
• Nasolabial cyst (kelstadt’s cyst) 294 • Nasopalatine duct cyst (incisive canal cyst) 295 • Solitary bone
cyst (traumatic/hemorrhagic bone cyst) 297 • Aneurysmal bone cyst 298 • Cyst of the salivary gland 300
• Ranula 302 • Dermoid cyst 303 • Surgical ciliated cyst of maxilla 303.

7. Regressive Alterations of Teeth ...................................................................... 306–319

Attrition of teeth 306 • Abrasion of teeth 307 • Tooth abfraction 309 • Erosion of teeth 309 • Role of
salivary function in the prevention of dental erosion 311 • Resorption of teeth 311 • External resorption of
tooth 312 • Internal resorption of tooth 314 • Pulp calcification 315 • Hypercementosis 316 • Age changes
in teeth 317 • Cementicles 318 • Dentinal sclerosis 318.


8. Bacterial, Viral and Fungal Infections ........................................................... 320–367

Specific bacterial infections 320 • Tuberculosis 320 • Syphilis 324 • Gonorrhea 328 • Actinomycosis 329
• Scarlet fever 331 • Diphtheria 332 • Sarcoidosis 332 • Leprosy 333 • Tetanus 334 • Midline lethal
granuloma 335 • Wegener’s granulomatosis 335 • Noma (cancrum oris) 336 • Pyogenic granuloma 337
• Viral infections 339 • Acquired immunodeficiency syndrome (AIDS) 339 • Herpes virus infections 344
• Herpes simplex virus type–I infections 345 • Herpes simplex virus type-II infections 347 • Varicella-
zostervirus 348 • Infections 348 • Cytomegalovirus infection 350 • Epstein-barr virus infections 351
• Human papillomavirus infection 352 • Paramyxovirus infection 352 • Measles (rubeola) 352 • Mumps 353
• Coxsackie virus infections 353 • Herpangina 353 • Hand, foot and mouth disease 354 • Aphthous ulcers 354
• Behçet’s syndrome 357 • Reiter’s syndrome 357 • Rabies 357 • Fungal infection 358 • Candidiasis 358
• Deep fungal infections 362 • Coccidioidomycosis 362 • Histoplasmosis 362 • Cryptococcosis 363
• North american blastomycosis 364 • Mucormycosis 364.

9. Dental Caries ........................................................................................................ 368–388

Dental caries 368 • Acidogenic theory 369 • Proteolytic theory 374 • Proteolytic chelation theory 375
• Sucrose chelation theory 375 • Autoimmune theory 375 • Contributing factors in dental caries 375
• Clinical aspects of dental caries 378 • Histopathological aspect of dental caries 382 • Histology of dentinal
caries (caries in dentin) 383 • Protective responses of dentin and pulp against caries 384 • Caries activity
tests 385 • Methods of caries prevention 386 • Caries vaccine 386.

10. Diseases of Dentin-Pulp Complex and Periapical Tissues ...................... 389–413

Pulpal diseases 389 • Focal reversible pulpitis 391 • Acute pulpitis 392 • Chronic pulpitis 393
• Aerodontalgia 395 • Pulp necrosis 395 • Diseases of the periapical tissues 398 • Primary acute apical
periodontitis 398 • Periapical granuloma (Chronic apical periodontitis) 398 • Acute exacerbation of chronic
periapical granuloma (phoenix abscess) 400 • Periapical abscess (dentoalveolar abscess) 400 • Osteomyelitis 401
• Acute suppurative osteomyelitis 403 • Chronic suppurative osteomyelitis 406 • Chronic focal sclerosing
osteomyelitis (Condensing osteitis) 408 • Diffuse sclerosing osteomyelitis 409 • Chronic osteomyelitis with
proliferative periostitis (Garre’s osteomyelitis) 410 • Giant cell periostitis with hyaline change (Pulse
granuloma) 411 • Endodontic-periodontic lesions 412.

11. Spread of the Oral Infection ............................................................................. 414–425

Space infections 414 • Space infections related to maxilla 414 • Space infections related to mandible 416
• Cellulitis 419 • Ludwig’s angina 420 • Cavernous sinus thrombosis (thrombophlebitis) 421 • Maxillary
sinusitis 422 • Focal infection 423.

12. Physical and Chemical Injuries of the Oral Cavity .................................... 426–444

Physical injuries 426 • Fractures of teeth 426 • Root fracture 426 • Cemental tear 426 • Bruxism 426
• Ankylosis of teeth 428 • Submerged teeth 428 • Toothbrush injury 429 • Toothpick injury 430
• Traumatic atrophic glossitis 430 • Chronic ulcers of the tongue 430 • Traumatic ulcer 431
• Factitious injuries (self-inflicted oral wounds) 432 • Denture related injuries or lesions 433
• Electrical burns in the mouth 434 • Thermal burns in mouth 435 • Radiation injuries 435
• Various damaging effects of radiation on individual organs or tissues 436 • Osteoradionecrosis 438
• Chemical injuries 440 • Congenital porphyria 440 • Biliary atresia 440 • Erythroblastosis fetalis 440
• Fluorosis 441 • Oral manifestations of various metal poisoning 441 • Oral manifestations of
cytotoxic drug therapy 442 • Oral manifestations of tetracycline staining 442 • Angioneurotic edema 442
• Chemical burns 443 • Chemical burns due to other medicaments 443.

13. Biopsy and Healing of Oral Wounds .............................................................. 445–455

Biopsy 445 • Exfoliative cytology 447 • Healing of oral wounds 448 • Healing of biopsy wound 449 • Healing
of gingivectomy wound 450 • Healing of the extraction wound 450 • Dry socket (alveolar osteitis) 451
• Healing of the fractured jawbone 451 • Replantation of tooth 452 • Transplantation of teeth 453 • Healing
around osteointegrated implants 454.

xxii Essentials of Oral Pathology

14. Oral Aspects of Metabolic Disorders ............................................................. 456–478

Disturbances in mineral metabolism 456 • Calcium 456 • Phosphorus 457 • Iron 458 • Magnesium 458
• Zinc 458 • Disturbance in vitamin metabolism 458 • Vitamin D 458 • Osteoporosis 459 • Rickets 459
• Vitamin A 460 • Vitamin B complex 460 • Vitamin C (ascorbic acid) 461 • Vitamin K 462
• Disturbances in protein metabolism 462 • Amyloidosis 462 • Porphyria 463 • Disturbances in
carbohydrate metabolism 463 • Hurler’s syndrome 463 • Disturbance in lipid metabolism 464 • Hand-
schuller-christian disease 464 • Eosinophilic granuloma 465 • Letterer-siwe disease 465 • Gaucher’s
disease 466 • Niemann-pick disease 466 • Disturbance in hormone metabolism 466 • Hypopituitarism 466
• Pituitary insufficiency in adults 467 • Diabetes insipidus 467 • Hyperpituitarism 467 • Hypothyroidism 469
• Hyperthyroidism 469 • Hyperparathyroidism 470 • Hypoparathyroidism 472 • Adrenal hormones 473
• Mineralocorticoids 474 • Chronic adrenocortical insufficiency (addison’s disease) 474 • Hyperfunction
of adrenocortical hormone (cushing’s syndrome) 474 • Pancreatic hormone (insulin) 475 • Progeria 476
• Imbalance of sex hormones 476.

15. Diseases of Bone .................................................................................................. 479–501

Paget’s disease of bone (osteitis deformans) 479 • Fibrous dysplasia of bone 482 • Cherubism 486 • Osteogenesis
imperfecta 489 • Cleidocranial dysplasia 491 • Osteopetrosis (marble bone disease) 492 • Pierre robin
syndrome 494 • Gardner syndrome 494 • Marfan’s syndrome 494 • Down syndrome (trisomy 21) 495
• Infantile cortical hyperostosis (caffey’s disease) 496 • Mandibulofacial dysostosis (treacher-collins syndrome) 497
• Achondroplasia 497 • Massive osteolysis (vanishing bone disease) 498.

16. Diseases of Temporomandibular Joint .......................................................... 502–508

Developmental disorders 502 • Hypoplasia of the mandibular condyle 502 • Hyperplasia of the mandibular
condyle 502 • Traumatic disorders 502 • Luxation and subluxation 502 • Ankylosis of temporomandibular
joint 503 • Inflammatory disorders 505 • Ankylosing spondylitis 505 • Osteoarthritis 505 • Rheumatoid
arthritis 506 • Acute traumatic arthritis 506 • Myofacial pain dysfunction (MPD) syndrome 507
• Neoplasia of temporomandibular joint 507.

17. Oral Aspects of Hematological Disorders ..................................................... 509–527

Pernicious anemia 509 • Iron deficiency anemia 510 • Aplastic anemia 511 • Hemolytic anemia 512
• Thalassemias 513 • Sickle cell anemia 515 • Erythroblastosis fetalis 515 • Polycythemia vera 516
• Leukemias 517 • Agranulocytosis (granulocytopenia) 521 • Cyclic neutropenia 522 • Purpura 522
• Hemophilia 525.

18. Periodontal Disease ............................................................................................. 528–542

Gingival hyperplasia 535 • Desquamative gingivitis 537 • Acute necrotizing ulcerative gingivitis (ANUG) 538
• Lateral periodontal abscess 539 • Pericoronitis 540 • Staining of teeth 541.

19. Oral Aspects of Dermatological Disorders ................................................... 543–568

Hereditary ectodermal dysplasia 543 • Psoriasis 544 • Pityriasis rosea 545 • Incontinentia pigmenti 545
• Erythema multiforme 546 • Dermatitis herpetiformis 548 • Keratosis follicularis 549 • Acanthosis
nigricans 549 • Dyskeratosis congenita 550 • White sponge nevus 550 • Polymyositis 551 • Pemphigus 552
• Pemphigoid 555 • epidermolysis bullosa 558 • Lupus erythematosus 559 • Discoid lupus erythematosus 561
• Scleroderma 563 • Ehlers-Danlos syndrome 566.

20. Diseases of the Nerves and Muscles .............................................................. 569–576

Diseases of the nerves 569 • Trigeminal neuralgia 569 • Sphenopalatine neuralgia 571 • Glossodynia and
glossopyrosis 571 • Auriculotemporal syndrome (Frey’s syndrome) 572 • Glossopharyngeal neuralgia 572
• Bell’s palsy (facial nerve paralysis) 572 • Causalgia 574 • Eagle’s syndrome 574 • Disease of the muscles 574
• Generalized familial muscular dystrophy 574 • Myasthenia gravis 575 • Myositis ossificans 575.

21. Oral Manifestations of Generalized Diseases ............................................. 577–586

Vitamin deficiencies 577 • Important causes of lymphadenopathy 578 • Blood dyscrasias 578
• Metabolic disorders 579 • Heavy metal poisoning 580 • Endocrine disturbances 580


• Granulomatous diseases 581 • Dermatological diseases 582 • Bone diseases 582 • Acute
infective diseases 583 • Helminthic diseases 583 • Renal diseases 583 • Neural diseases 584
• Sexually transmitted diseases 584 • Cardiovascular diseases 584 • Genetic disorders 585
• Allergic conditions 585 • General manifestations of oral diseases 585.

22. Syndromes Related to Oral Diseases ............................................................. 587–597

23. Important Classifications of Oral Diseases .................................................. 598–612

White lesions of the oral cavity 598 • Red-blue lesions of the oral cavity 599 • Pigmented lesions of the oral
cavity 599 • Classification of vesiculobullous diseases 600 • Classification of ulcerative conditions 600
• Classification of discoloration of tooth 601 • Classification of cysts of the oral region 601 • Classification
of odontogenic neoplasms 602 • Classification of giant cell lesions 602 • Classification of verrucal–papillary
lesions of oral cavity 602 • Classification of diseases of salivary glands 602 • Classification of fibro-osseous
lesions 603 • Classification of vascular tissue diseases 603 • Classification of diseases of the hemopoietic
tissues and lymphoreticular system 604 • Classification of stomatitis 604 • Classification of severe infections
of the orofacial tissues 604 • Classification of chronic orofacial pain 605 • Classification of diseases of tongue 605
• Classification of gingival enlargements 606 • Classification of skin diseases 607 • Classification of taste
disorders 608 • Classification of oral swellings 608 • Classification of neck swellings 609 • Classification
of oral soft tissue 609 • Classification of yellow conditions of oral mucosa 609 • Anatomic radiolucencies of
jawbones 610 • Radiolucent lesions of the periapical region 610 • Classification of pericoronal radiolucent
lesions 610 • classification of inter-radicular radiolucent lesions 610 • Classification of multilocular
radiolucent lesions of the jaws 611 • Mixed radiolucent-radiopaque lesions associated with teeth 611
• Mixed radiolucent-radiopaque lesions not necessarily associated with teeth 611 • Multiple separate
radiopaque lesions of the jaws 611 • Generalized radiopacities of the jaws 612 • Classification of causes of
trismus 612.

Index ........................................................................................................................................613

INTRODUCTION Besides this, abnormalities in histodifferen-
tiation may cause defective formation of dental
Malformations or defects resulting from dis- hard tissues, resulting in the disturbance of tooth
turbance of growth and development are known structure.
as developmental anomalies. A large number of
such developmental anomalies, which involve the Disturbance in histodifferentiation often
body in general and oral structures in particular occurs at a later stage of tooth development as
can occur during the embryonic life. compared to the disturbance of morphodifferen-
Manifestations of such defects are evident either tiation.
at birth or sometimes after birth. These anomalies
often have some serious implications on the DEVELOPMENTAL ANOMALIES
further growth and development of the involved OF ORAL SOFT TISSUES
organ during the later stages of life.
Moreover, developmental anomalies affecting
the teeth are seen more often then any other defects LIP PITS AND FISTULAS
in the oral cavity.
Disorders of development of teeth may be due Lip pits are congenital invaginations, which can
to abnormalities in the differentiation of the dental involve either the paramedial portion of vermilion
lamina and tooth germs (abnormal morpho- border of lower and upper lips or the labial
differentiation), which results in various defects commissural area.
in the number, size and form of teeth.

Congenital anomalies Types of developmental anomalies
Hereditary developmental
anomalies The defects, which are present at birth or before birth during the
Acquired anomalies intrauterine life, are known as congenital anomalies.

Hamartomatous When certain defects are inherited by the offspring from either of the
anomalies parents, it is called hereditary anomaly. Such types of anomalies are
always transmitted through genes.
Idiopathic anomalies
Acquired anomalies develop during intrauterine life due to some
pathological environmental conditions. They are not transmitted
through genes.

A hamartoma can be defined as an excessive, focal overgrowth of
mature, normal calls and tissues, which are native to that particular
anatomic location.

Developmental abnormalities occurring due to such
hamartomatous change in the tissue are known as hamartomatous
developmental anomalies.

Developmental abnormalities of unknown cause are called idiopathic

2 Essentials of Oral Pathology

ORIGIN • In both lip and commissural pits, there are no
signs of inflammation or ulceration and both
The condition arises probably due to notching of conditions are harmless.
the lip at the early stage of labial development,
which causes fixation of tissue at the base of the TREATMENT
notch. The condition may also arise due to failure
of a complete union of the embryonic lateral sulci While commissural pits require no treatment, the
of the lip, which persist in the later life. Both lip lip pits are sometimes surgically excised for
pits and the commissural pits are developmental cosmetic reason.
malformations, which appear to be inherited as
autosomal dominant traits. DOUBLE LIP

CLINICAL FEATURES Double lip is a developmental anomaly charac-
terized by a horizontal fold of excess or redundant
Lip Pits tissue, on the mucosal side of the lip. It is usually
located on the inner aspect of upper lip, although
• The lip pit is a small depression over the lip, the lower lip can also be occasionally involved.
which can be either unilateral or bilateral and
are more commonly seen on the lower lip. CLINICAL FEATURES

• These pits can be up to 3 to 4 mm in diameter • Double lip is an oral anomaly, which can be
and may have a depth of up to 2 cm. either a congenital or an acquired one, the
aquired type occurs mostly due to trauma.
• Lip pit occur more commonly among females
and their frequency ranges from 1: 75000 to 1: • The condition clinically appears as a “cupid’s
100000 among Caucasians. bow” when the lip is tense but it is not visible
when the lip is at rest.
• Congenital lip pits may occur either as an
isolated condition or they may be associated • The defect can occur either alone or in
with cleft lip and/or cleft palate (Van der association with other anomalies.
Woude’s syndrome).
• Double lip in association with blepharochalasis
• The opening of a lip pit on the labial surface (dropping of the upper eye lid) and nontoxic
often appears as a circular or transverse slit, thyroid enlargement are known as Ascher’s
moreover a lip pit opening may be located at Syndrome.
the apex of a nipple like elevation.
• Clinically a double vermillion border is
• Mucous secretion is visible at the opening of apparent with a transverse furrow between the
those pits, which communicate with an two borders, when the patient smiles.
underlying minor underlying salivary gland.
• Since the salivary gland orifices open into these
pits, as a result saliva often exudates from them. Although, it is excised sometimes for cosmetic
However, exudation of mucus from lip pits onto reasons, double lip mostly requires no treatment.
the lower labial skin may cause embracement
to the patient.

Commissural Pits FRENAL TAG

• The commissural pits measure from 1 to 4 mm DEFINITION
in diameter, are found either bilaterally or Frenal tag is a redundant piece of mucosal
unilaterally and often they have a familial tissue, which projects from the maxillary labial
tendency. frenum.

• Commissural pits can occur in association CLINICAL FEATURES
with multiple preauricular pits. • It is a familial condition and seems to be

• Unlike lip pits, the commissural pits are more inherited as autosomal dominant trait.
frequent among males and black people are
affected more often than whites.

Developmental Anomalies of Oral and Paraoral Structures 3

• The shape and size of frenal tag varies from the oral mucosa (crosses vermillion border in
patient to patient and is clinically asympto- about 94 percent cases).
matic. • Buccal mucosa is the most frequently involved
intraoral site, followed by palate, gingiva,
• Sometimes, the condition is mistaken for a tongue and floor of the mouth, etc. Sometimes
fibrous hyperplasia caused by local injury or these macules can be seen over the hands and
irritation. feet as well.
• The skin pigmentations tend to fade away in
HISTOPATHOLOGY adult life, while the mucosal pigmentations
continue to persist.
Histologically, frenal tag consists of normal oral • Intestinal polyposis is the other very important
epithelium and connective tissue. feature of Peutz-Jegher’s syndrome besides the
melanotic pigmentations. Although the polyps
occur throughout the small intestine, colon and
No treatment is required. stomach are more commonly affected.
• Presence of these polyps can cause recurrent
HEREDITARY INTESTINAL POLYPOSIS abdominal pain (in patients younger than
(PEUTZ-JEGHERS) SYNDROME 25 years of age), unexplained rectal bleeding
and prolapse of tissue from rectum with
DEFINITION diarrhea.
• Occasionally intussusceptions and intestinal
Peutz-Jegher’s syndrome is a hereditary condition obstruction may cause even death.
characterized by gastrointestinal hamartomatous • The syndrome can also cause precocious
polyposis in association with mucocutaneous puberty, menstrual disturbances in females,
pigmentations. gynecomastia in males and development of

The disease is transmitted either through an testicular mass, etc.
autosomal dominant gene or it can occur • The polyps occur either as a hamartomatous
spontaneously. It is a developmental condition
and although pigmentation is an important growth or as an inflammatory lesion and they
feature of this disease, the primary disorder is may have a very limited neoplastic potential.
actually not of the melanocyte system. • There can be growth acceleration in few
patients due to concomitant occurrence of
Incidence rate: Approximately, one case per sertoli cell tumor.
60,000 to 300,000 populations.

CLINICAL FEATURES Key points of Peutz-Jegher’s syndrome

• Peutz-Jegher’s syndrome begins in infancy • Melanin pigmentations of the vermillion border
(2nd and 3rd decade of life) and there is no sex • Multiple intestinal polyps
predilection. • Recurrent abdominal pain and obstruction
• Precocious puberty in some cases.
• Patients almost always have a positive history
of the disease in the family. HISTOPATHOLOGY
Histologic examination of the oral macular lesions
• There is multifocal melanin pigmentations in exhibits excessive accumulation of melanin
the perioral locations, which often manifest as granules in the basal cell layer.
discrete, brown to bluish-black or purpleblack
macules on the skin. DIFFERENTIAL DIAGNOSIS
• Albright syndrome
• The size of the macule varies from 1 to 5 mm in • Addison’s disease
diameter and these macules often group around • Oral melanotic macule.
the oral, nasal and orbital orifices.

• The pigmentation is most intense at the
vermilion border of the lower lip and it often
extends both to the facial skin as well as into

4 Essentials of Oral Pathology


• Pigmentation in the perioral region is unique • Microscopically, oral melanotic macule
and often diagnostic for Peutz-Jegher’s presents diffuse accumulations of melanin
syndrome. granules in the basal keratinocytes and the
lamina propria.
• Radiographic examinations can be useful for
detection of intestinal polyps. • The lesions do not evolve from proliferation of
melanocytes and there is no risk of malignant
• Genetic counseling. transformation in them .
• Familial history of the diseases also helps in
• Occasionally, melanin incontinence is observed
making diagnosis. with pigmented granules being seen in
subepithelial melanophages.
• Melanophagocytosis can also be seen.
No treatment is required for the oral and perioral
melanotic macules. However, surgical interven- DIFFERENTIAL DIAGNOSIS
tion may be required for the intestinal polyps
causing intussusceptions. • Superficial melanoma
• Blue nevi
(EPHELIS) • Addison’s disease
• Peutz-Jegher’s syndrome.
Oral melanotic macule is an idiopathic benign
pigmented lesion of oral cavity; characterized by The persistent, innocuous looking lesions do not
increased focal melanin pigmentations in the oral require any treatment, however biopsy is
mucosa. mandatory for a definitive diagnosis of the
condition as well as to rule out any possibility of
CLINICAL FEATURES malignant melanoma.

• Oral melanotic macules present small, flat, well UVULA ELONGATA
circumscribed, asymptomatic areas in the oral

• These are seen commonly on the vermilion Uvula enlongata is a developmental anomaly
border of the lip (mostly lower lip) near the characterized by abnormally long uvula, which
midline. Intraorally, the gingiva, buccal mucosa touches or hangs lower than the base of the tongue.
and the palate are the most frequently involved

• Most of the lesions are less than one centimeter • The condition is usually seen at birth and some-
in diameter or sometimes little more and their times it has a familial tendency for occurrence.
color ranges from brown or black or bluish
green, etc. • It is seen more frequently among females than
• There is no specific age group for this condi-
tion, however middle aged females are most • Although it is mostly asymptomatic, some
often affected. sensitive patients may cough or gag when the
elongated uvula touches the epiglottis or the
• The oral lesions are painless, firm in base of the tongue.
consistency and elliptical in shape.
• Acquired cases of uvula elongata, may occur
• Solitary lesion of oral melanotic macule on the as a result of chronic pharyngitis due to cola
lip is called labial melanotic macule. nut chewing.

• The conditions are asymptomatic and have no
malignant potential.

Developmental Anomalies of Oral and Paraoral Structures 5

DIFFERENTIAL DIAGNOSIS • Lower lip is involved more often than the upper
lip and the vermilion borders as well as the
Neoplasms of the uvula. labial mucosa are of normal color.

TREATMENT • However in many cases, the lip shows diffuse
keratosis with scaling of the surface.
In most of the cases, no treatment is required.
However, in symptomatic cases, astringents can • Patient sometimes complain of burning
be used which will contract the uvula. In more discomfort or a feeling of rawness in the lip.
severe cases, amputation is recommended.
• When the lip is everted due to swelling of the
CHEILITIS GLANDULARIS glands, its surface often reveals multiple pits
or fistulas representing dilated and inflamed
DEFINITION minor salivary duct openings.

Cheilitis Glandularis is an uncommon, funda- • Externalization and chronic exposure of the
mentally benign, developmental anomaly of the delicate labial mucosa often result in erosion,
lips characterized by chronic, progressive ulceration, crusting and infection, etc.
enlargement of the labial salivary glands.
• Few cases of cheilitis glandularis may undergo
Von Volkmann first introduced the term in malignant transformation and produce
1870 and described it as a clinically distinct, deep carcinoma of the lip.
suppurative, chronic inflammatory condition of
the lower lip with mucopurulent discharge. Key points of cheilitis glandularis

ETIOLOGY • Swelling of the lip due to enlargement of the

• Chronic exposure to sun (actinic damage), minor salivary glands.
wind and dust
• Lower lip involved more frequently.
• Factitial injury
• Infection, e.g. HIV • Lip is everted with multiple fistulas found on
• Neoplasm especially squamous cell carcinoma
• Use of tobacco the surface.
• Emotional stress
• Heredity. • Exudation on the lip surface with occasional

Recent investigations indicate that over- erosion, ulceration and crusting.
exposure to sun with superimposed bacterial
infection is the more likely cause of this • It is predominantly caused by sun and dust
exposure, stress and tobacco use.
• Increased risk of malignant transformation.
• Cheilitis glandularis commonly occurs among
middle aged or elderly adults and often there TYPES
is a male predilection.
Clinically cheilitis glandularis can be of three
• Inflammatory enlargement of the superficial or basic types:
deep minor salivary glands of the lip often A. The simple type
causes progressive, multinodular swelling. B. The superficial suppurative type and
C. The deep suppurative type.
• There may be secretion of clear, viscous
exudates from the minor salivary duct The simple type is the most common variant
openings on the labial mucosa. of the disease and it presents multiple, painless,
pinhead size swellings on the lip with central
• Enlargement of the labial salivary glands often depression.
cause eversion and induration of the lower
lip. The superficial suppurative type of cheilitis
glandularis presents painless swelling of the lip
with induration, areas of shallow ulcerations and

The deep suppurative type is characterized
by deep seated inflammation, abscess formation
in the lip with development of fistulas tracts. The
disease often heals by scarring.

Many believe these subtypes probably represent
a continuation of the same disease process, i.e. if

6 Essentials of Oral Pathology

the simple type of cheilitis glandularis is not believe it as a regional form of sarcoidosis or
properly treated, it becomes secondarily infected Crohn’s disease, while others suggest it as a
and progresses to the next type and then to the granulomatous lesion of allergic origin.
The disease may also occur due to hyper-
DIFFERENTIAL DIAGNOSIS sensitivity to bacterial toxins from a chronic focus
of infection in another nearby location.
• Cheilitis granulomatosa
• Crohn’s disease CLINICAL FEATURES
• Bacterial infection (Elephantiasis nostras
• Children and young adults commonly develop
verrucosa) this disease (median age 25 years) and usually
• Actinic cheilitis there is a female predominance.
• Squamous cell carcinoma
• Eczematous cheilitis • Either lower or upper or both lips show a
• Chronic factitial injury. sudden diffuse, nontendered, nodular
enlargement, which involves the entire lip.
• Generally, the lower lip is enlarged on a more
• The surface epithelium can be either normal or regular basis.
• In some rare cases, patients exhibit lip swelling
• The underlying salivary gland tissue shows along with swelling of cheeks, eyelids and
hypertrophy and inflammation with distention scalp, etc.
of acini.
• The swelling is usually painless, firm and
• Squamous metaplasia of the ductal epithelium exhibits no pitting upon pressure.
may be seen.
• There is no sign of inflammation or ulceration
• Dysplastic changes can be noted in some on the surface of involved lips in the initial stage.
cases especially in type II and type III cases
with increased risk of malignant transfor- • During the early stage, the disease is sometimes
mation. accompanied by fever, malaise and visual
disturbance, etc. Regional lymph nodes are
• Frank evidences of squamous cell carcinoma enlarged in about 50 percent cases.
are reported in about 18 to 25 percent cases in
relation to this disease. • The initial swelling subsides within few hours
or days, however with more and more attacks
TREATMENT of the disease, the swelling tends to become
larger in size and persists longer, and
Biopsy is mandatory especially in suspected eventually become permanent. Some lesions can
cases, where the lip shows excessive keratosis or even regress very slowly over the years.
• Enlarged lips often create some cosmetic
Lesions with premalignant changes should be problems due to the presence of several cracks
treated by surgical stripping of the lip without in- and fissures on the surface along with a
volving the vermillion border to save the esthetics. reddish-brown discoloration.

CHEILITIS GRANULOMATOSA • Patient may also have difficulties during
eating, drinking or talking.
Cheilitis granulomatosa is an atypical granulo-
matous disease of the lip, the origin of which is • Few lesions may exhibit scaling, fissuring and
not clearly understood. vesicle or pustule formation at the vermilion
border. The fissured lip is often painful and is
PATHOGENESIS firm, rubbery in consistency.

As mentioned above the exact cause of cheilitis • Patients sometime complain of decreased
granulomatosa is not known. Some investigators salivary secretion and loss of taste sensation.

• Cheilitis granulomatosa in association with
facial paralysis and fissured tongue
constitutes the “ Melkersson-Rosenthal

Developmental Anomalies of Oral and Paraoral Structures 7

• The facial paralysis is intermittent at first but • Generalized edema and dilated blood vessels
later on it becomes permanent in nature, the are present throughout the connective tissue.
paralysis may be unilateral or bilateral,
complete or incomplete. DIFFERENTIAL DIAGNOSIS

• Besides lip lesions, few other oral lesions can • Sarcoidosis
possibly occur in association with cheilitis • Cheilitis glandularis.
granulomatosa, these include nodular or • Angioneurotic edema
papillary tumor on the tongue, some • Leprosy
multinodular lesions and a reddish or bluish • Crohn’s disease
plaque on the buccal mucosa or palate. • Traumatic injury
• Lymphoma
Key points of cheilitis granulomatosa • Edema and cheilitis subsequent to odontogenic

• Diffuse, firm painless swelling of the lip with infections.

difficulty in eating, drinking and talking. TREATMENT

• Granulomatous inflammation or allergy is the • Intralesional injection of steroid (Triamci-
nolone) may result in reduction in the size of the
suspected underlying cause. lesion.

• Cheilitis granulomatosa, facial paralysis and • Surgical excision of the granulomas may be
effective but often there is recurrence.
scrotal tongue constitute Melkersson-Rosenthal
• Elimination of odontogenic and periodontal
syndrome. infections in the vicinity may produce reduc-
tion in the signs and symptoms of the

• Microscopically, cheilitis granulomatosa (Fig. ANOMALIES OF THE ORAL
1.1) shows granulomatous inflammation of the MUCOSA
lip with infiltration by chronic inflammatory
cells, chiefly lymphocytes, plasma cells and FORDYCE’S GRANULES
• The multinodular, noncaseating granulomas
are often located close to the blood vessels and Fordyce’s granules are ectopic collections of
these are composed of epitheloid cells and numerous sebaceous glands, generally unasso-
swirled collagen fascicles with interspersed ciated with hair follicles and are found in various
Langhans type of multinucleated giant locations within the oral cavity (Fig. 1.2).

• These noncaseating granulomas often simulate
sarcoidosis and these lesions may replace the
minor salivary glands of the lip.

Fig. 1.1: Photomicrograph of cheilitis granulomatosa Fig. 1.2: Fordyce’s granules

8 Essentials of Oral Pathology

CLINICAL FEATURES • These glands are located superficially, quite
• Fordyce’s granules are mostly seen in adult life close to the surface epithelium and are
composed of 1 to 5 lobules.
and there is often a male predilection. These
are rarely found in children before puberty. • They empty into a duct, which opens directly
• They commonly occur in a bilaterally onto the mucosal surface. The duct may show
symmetrical pattern over the upper lip, buccal keratin plugging.
mucosa, gingiva, anterior pillars of fauces and
occasionally over the tongue. Fordyce’s • The peripheral cells of the Fordyce’s granules
granules are seen rarely in the lower lip. are flat and darkly stained, whereas the inner
• Fordyce’s granules can also be present in many cells are lipid rich and pale in appearance.
extraoral locations such as the esophagus,
genitalia, nipples, palms and the parotid Key points of Fordyce’s granules
glands, etc.
• Normally these glands are present in the 60 to • These are ectopic collections of sebaceous
70% of adult population but their number glands in the oral cavity (normal location is skin).
varies widely between individuals.
• The number of Fordyce’s granules in the upper • Appear as multiple, yellowish, milia-like discrete
lip increases during puberty while there is an granules on the buccal mucosa (bilaterally).
increase in the number of these glands in the
buccal mucosa in the later stages of life. • Sebaceous cyst may develop from them.
• Fordyce’s granules clinically appear as multiple,
small, discrete, rice-like or milia-like yellowish- DIFFERENTIAL DIAGNOSIS
white bodies beneath the surface mucosa. They The smaller size, multiplicity and typical yellow
measure about 1 to 2 mm in diameter. color are characteristic of the Fordyce’s granules
• Those are completely asymptomatic conditions and are unlikely to be confused with any other
and in most of the cases patients are not aware mucosal lesions.
of their presence in the mouth.
• On occasions, clusters of numerous sebaceous TREATMENT
glands may form slightly raised confluent No treatment is required for this condition.
plaques with a creamy appearance. However, on rare occasions, sebaceous cysts or
HISTOPATHOLOGY adenomas may develop from the preexisting
• Histologically, Fordyce’s granules of the oral Fordyce’s granules.
mucosa are identical to those of sebaceous
glands, which are normally found in the skin, FOCAL EPITHELIAL HYPERPLASIA
except the fact that they are not associated with
hair follicles (Fig. 1.3). DEFINITION
Focal epithelial hyperplasia (commonly known
Fig. 1.3: Photomicrograph of Fordyce’s granules as Heck’s disease) is a condition characterized
by multiple papillary or sessile hyperplastic areas
in the oral mucosa.

• The disease is specifically found among

American Indians, Northern native people and
other ethnic groups in Europe and Africa.
• The exact etiology of Heck’s disease is not
known but it is probably caused by the Human
Papilloma Virus (HIV) type 13 and 32.
• Similarappearinglesionsmayalsobeencounte-
red among HIVseropositive homosexual males.

• The disease commonly occurs among children

between the ages of 3 to 18 years and there is
no sex predilection.

Developmental Anomalies of Oral and Paraoral Structures 9

• Clinically, focal epithelial hyperplasia presents WHITE SPONGE NEVUS
multiple, small, pedunculated, polypoid or
nodular soft tissue growths in the oral cavity. DEFINITION

• They also can appear as well demarcated, White sponge nevus or Cannon‘s disease is a
slightly raised plaques. congenital mucosal abnormality, which appears
to follow an autosomal dominant hereditary
• Sometimes several hyperplastic lesions may pattern and manifests as a white lesion of the oral
cluster together to produce a typical mucosa.
“Cobblestone” appearance.
• Labial and buccal mucosa are the most common
sites and lower lip is more frequently affected • This condition is transmitted as an autosomal
than the upper. However, the disease can also dominant trait with incomplete penetrance and
involve the tongue, gingiva and anterior faucial variable expressivities.
pillars, etc.
• Mutations in the genes coding for keratins 4
• Individual lesions measure about 1 to 5 mm in and 13 (the pair of keratins expressed by
diameter and are either white or pink in color. epithelial cells in the mucosa affected by the
disorder) have been identified, suggesting the
• Most of the lesions regress spontaneously after disorder as a hereditary keratin defect.
about 4 to 6 months and occasionally few
lesions can recur. • The heaping up of cells on the surface of the
epithelium also suggests the possibility of an
DIFFERENTIAL DIAGNOSIS impaired normal desquamation process of the
superficial strata of cells.
• Leukoplakia
• Keratoacanthoma
• Veruciform Xanthoma. • White sponge nevus has its onset mostly during
childhood. Some lesions are congenital and are
HISTOPATHOLOGY present at birth and few lesions may even
initiate during the adolescent period.
• Focal epithelial hyperplasia histologically
shows hyperparakeratosis of the covering • There is no sex predilection, several members
epithelium with extensive acanthosis of the same family are often affected.
(increased thickening of the spinus cell layer).
• The intraoral lesions are almost always
• The epithelial cells of the upper spinus layer bilateral and are mostly found over the buccal
show enlarged nuclei and vacuolated clear mucosa and tongue. Occasionally, the
cytoplasms (koilocytes). vestibular mucosa, palate, gingiva and floor of
the mouth, etc. are also affected.
• Deeper layer of epithelium reveals thickening,
elongation and even fusion of the retepegs. • Besides the oral mucosa, white sponge nevus
can be seen on the conjuctivital, esophageal,
• Basal cell layer of the epithelium exhibit nasal and anogenital mucosa as well.
increased mitotic activity.
• Clinically, white sponge nevus presents a thick,
• Occasionally focal areas of liquefaction bilateral, asymptomatic, deeply folded or
degeneration of the basal layer may be found. corrugated white or gray lesion on the oral
• The underlying connective tissue is loose, well
vascularized and exhibit variable infiltrates of • The surface of the lesion is soft, uneven and
lymphocytes. has a shaggy appearance with a spongy
• The lesions can be either diffuse or patchy and
Since focal epithelial hyperplasia is a harmless, have a translucent opalescence similar to that
self-regressing condition, it usually requires no of leukodema.

10 Essentials of Oral Pathology

• The disease can sometimes present ragged • Lichen planus
white areas, which can be peeled off by gentle • Candidiasis
rubbing without any ensuing bleeding. • Leukodema.

• It is a perfectly benign condition but is often TREATMENT
mistaken for leukoplakia.
No treatment is required for this disease.
• White sponge nevus histologically shows THE GINGIVAE
marked thickening of the epithelium with
mild to moderate hyperparakeratinization, FIBROMATOSIS GINGIVAE
acanthosis and spongiosis.
• Marked intracellular edema of the spinus and
parakeratinized cell layer of the epithelium is Fibromatosis gingivae are rare, benign, diffuse,
an important characteristic feature of the noninflammatory hyperplasia of the gingival
disease. tissue, which sometimes cover the entire teeth.

• The cells with intracellular edema show vacuo- It is a hereditary condition, which is trans-
lated cytoplasms and shrunken (pyknotic) mitted as an autosomal dominant trait. The
nuclei. disease is probably the result of a diffuse infilt-
rative hyperplasic proliferation of the fibroblast
• Intrestingly under microscope only the cell cells and mature collagen fibers of the gingival
walls and the pyknotic nuclei at the centers of tissue.
the cells are visible, which often gives rise to a
so called “basket weave” appearance. CLINICAL FEATURES

• Parakeratin plugging is another important • Clinically the disease is characterized by dense,
finding in white sponge nevus, which runs diffuse, smooth or nodular overgrowth of the
from the surface and extends deep into the gingival tissue.
spinus layer.
• Fibromatosis gingivae can be either genera-
• Individual cell keratinization may be seen in lized or localized in nature and it is similar in
spinus cell layer. appearance to the dilantin hyperplasia of
• The basal cells are intact and the lamina
propria shows no inflammatory changes. • The gingival enlargement mostly appears in
young children or it may be present even at
• There is no evidence that this lesion undergoes birth, however in some cases the swelling may
malignant transformation. not be noticed until the adult life.

ELECTRON MICROSCOPIC STUDY • Both sexes are equally affected in gingival
Ultra structural studies of white sponge nevus
reveal that some cells of the spinus layer • The gingiva shows multinodular enlargements
differentiate early and become enriched with especially in the interdental papilla regions.
• The gingival tissue changes become obvious
DIFFERENTIAL DIAGNOSIS soon after the eruption of the deciduous teeth.

Thick, corrugated, diffuse white lesion in the • The hyperplastic tissue is firm, painless and
mouth, with history of involvement of several retains the normal coral pink color of gingiva.
members of the same family is usually suggestive
of white sponge nevus. • Sometimes the markedly enlarged gingiva
may cover the entire crown of the erupted
However the following diseases are to be teeth. The eruption process of teeth is however
considered in the differential diagnosis of white normal.
sponge nevus.
• Leukoplakia
• Hereditary intraepithelial dyskeratosis

Developmental Anomalies of Oral and Paraoral Structures 11

• Elimination of dental plaque does not make TREATMENT
any significant reduction in the severity of the
disease. Periodic gingivectomy with placement of gingival
acrylic splints for cosmetic and functional reasons.
• Occasionally, the condition is associated with
hypertrichosis, epilepsy and mental retar- RETROCUSPID PAPILLA
dation, etc.
Retrocuspid papilla is a slightly raised area of
• Gingival fibromatosis can also be associated mandibular alveolar mucosa, which as the name
with other syndromes, e.g. Cowden’s syndrome implies, iscommonlylocatedlingualtothecuspids.
and Rutherford’s Syndrome (features of • This structure measures about 2 to 4 mm and is
individual syndrome are given in the relevant
chapter dealing with syndromes). often present bilaterally between the marginal
gingiva and the mucogingival junctions.
• Moreover, gingival fibromatosis can be a • Retrocuspid papilla is more common among
feature of “Laband Syndrome”, which is children and it has structural resemblance to
characterized by splenomegaly, enlarged nasal the incisive papilla.
and external ear soft tissue, shortened terminal • Histologically, the papilla represents a focus
phalanges, hypermobility of joints and of fibrovascular tissue with an orthokera-
hypoplasia of nails. tinized or parakeratinized surface and it
usually covers an osseous foramen of a nutrient
• Sometimes symmetrical fibrous overgrowths blood vessel.
may occur bilaterally in the maxillary
tuberosity region and few of such cases are
possibly related to gingival fibromatosis.

Histopathologically gingival fibromatosis
presents the following features: AGNATHIA
• The covering epithelium is hyperplastic and
Agnathia refers to the complete failure of
often exhibits thin elongated retepegs. development of jawbone, involving either maxilla
• The fibrous connective tissue consists mainly or mandible or even both the jaws. It is an extremely
rare condition, however, often a portion of the
of course bundles of collagen fibers with jawbone, e.g. premaxilla, condyle, or ramus, etc.
scattered mature spindle shaped fibroblasts can be developmentally missing.
few of which are multinucleated.
• Mucoid changes in the gingival connective MICROGNATHIA
tissue may occur due to the accumulation of
excessive amount of ground substances. Micrognathia is an orofacial anomaly charac-
• There are significant numbers of mast cells terized by development of jaws, which
often associated with the fibroblastic prolifera- are unusually smaller than normal (Figs 1.4
tion. to 1.8).
• Histologically, hereditary gingival fibromatosis
is indistinguishable from other forms of CAUSES
gingival enlargements including those which
are drug-induced. • Pierre-Robin syndrome
• Hallerman-Steriff syndrome
• Trisomy 18
• Phenytonin (Dilatin) sodium induced gingival • Turner syndrome
hyperplasia. • Marfan syndrome
• Progeria
• Generalized hyperplastic gingivitis.
• Leukemic infiltration of the gingiva.

History of familial involvement is extremely
important in making the diagnosis of the disease.

12 Essentials of Oral Pathology

Fig. 1.4: Micrognathia (seen from front)-I Fig. 1.6: Hemifacial microstomia (seen from side)-I

Fig. 1.5: Micrognathia (seen from side)-II Fig. 1.7: Hemifacial microstomia
(seen from front)-II
Fig. 1.8: Radiograph of hemifacial
Micrognathia can be of two types: microstomia
A. Pseudomicrognathia
B. True micrognathia

Pseudomicrognathia: It is a condition where
normal sized jawbone appears to look smaller
when compared with the opposing jaw. A
jawbone of standard size may appear smaller, if
the opposite jaw is larger than normal or if it is
positioned more posteriorly in relation to the skull.

True micrognathia: It is the condition, where the
jawbone is actually smaller than normal and it
can be either a congenital or an acquired problem.

Developmental Anomalies of Oral and Paraoral Structures 13

The congenital micrognathia may follow a • Paget’s disease of bone: Paget’s disease often
hereditary pattern and it often occurs in association causes increase in the size of maxilla, which is
with other congenital diseases such as Pierre-Robin directly related to the generalized overgrowth
Syndrome or congenital heart disease, etc. of the cranium.

Congenitally missing premaxilla often leads • Acromegaly: Progressive increase in the size of
to maxillary micrognathia and patients with this mandible occurs in cases of acromegally.
anomaly show retracted middle third of the face.
• Leontasis ossea: It is a form of fibrous dysplasia
Congenital mandibular micrognathia may of bone and the disease is often associated with
occur due to posterior positioning of the condyle enlargement of maxilla.
in relation to the skull.
• Hereditary causes: Mandibular prognathism
Acquired micrognathia mostly occurs due to often occurs hereditarily.
trauma or severe infections in the orofacial region Mandibular prognathism may occur due to
especially in younger age. It may cause difficulty
in feeding the child. Ankylosis of the temporo- anterior positioning of the lower jaw in relation to
mandibular joint in young individuals often the cranium, even though the exact size of the jaw
leads to mandibular micrognathia with retruded is normal.
However, there are certain factors, which cause
CLINICAL FEATURES OF MICROGNATHIA mandibular prognathism and thereby create an
appearance of mandibular macrognathia.
• Micrognathia often results in defective align-
ment of teeth, crowding and malocclusion, etc. These factors are as follows:
• Increased height of the ramus.
• Retruded chin with small face. • Increased length of the body of mandible.
• Difficulty in feeding the children. • Increased gonian angle.
• Difficulty in proper articulation and speech. • Decreased maxillary length.
• Posterior positioning of the maxilla in relation
to the cranium.
Macrognathia is a developmental anomaly • Prominent chin button.
characterized by an abnormally large jaw. The • Varying soft tissue contours.
condition can affect both the jaws at a time but more
often it involves either maxilla or mandible. CLINICAL FEATURES OF MACROGNATHIA

TYPES OF MACROGNATHIA • Mandibular protrusion (when manduibular
bone is affected).
True macrognathia: When the jawbone is abnor-
mally large in size in true sense, it is called true • Gummy smile (mostly maxillary).
macrognathia. • Ramus of mandible forms a less steep angle

Pseudomacrognathia: A normal sized jaw may with body of the mandible.
look larger when the opposing jaw is smaller than • Excessive condylar growth.
normal in size. This condition is known as • Prominent chin.
MACROGNATHIA In case of macrognathia, surgical correction
(osteotomy) of the abnormally large jaw is often
• Pituitary gigantism: It is often associated with performed for both functional and esthetic
abnormally large jawbones. Both jaws are reasons.
affected in gigantism and the bony overgrowth
is proportionate to the generalized increase in FACIAL HEMIHYPERTROPHY
the size of the skeleton.
DEFINITION (Figs 1.9 and 1.10)

Facial hemihypertrophy is a developmental
condition characterized by disproportionate

14 Essentials of Oral Pathology

Fig. 1.9: Facial hemihypertrophy (seen from front)-I appear to be vascular and neurogenic distur-
bances that cause an increased neurovascular
supply to the affected side of the face resulting in
its overgrowth. Other possible factors include the
• Hormonal imbalance
• Incomplete twining
• Chromosomal abnormality
• Defective intrauterine development (due to

asymmetric intrauterine pressure)
• Lymphatic abnormalities.


Facial hemihypertrophy clinically exhibits the
following features:
• Unilateral enlargement of the facial soft tissues,

bones and teeth.
• A positive family history is reported in many

of these cases.
• Either side of the face can be affected and there

is a slight female predilection for this condition.
• The asymmetry is more specifically noticed in

the frontal bone, maxilla, palate, mandible,
alveolar process, condyles and the associated
soft tissues.
• The skin is thick and coarse on the affected
side and also there is presence of thick and
abundant hair (hypertrichosis).

Fig. 1.10: Facial hemihypertrophy (seen from side)-II Fig. 1.11: Facial hemihypertrophy-III

unilateral enlargement of the face (Figs 1.9 and
1.10). Though the name is hemihypertrophy the
actual underlying condition is a hyperplasia.

Although most humans exhibit some degrees
of facial asymmetry only few individuals actually
develop clinically significant facial hemihyper-


Although, a number of factors have been proposed
to explain this condition, the most important ones

Developmental Anomalies of Oral and Paraoral Structures 15


Differential diagnosis of facial hemihypertrophy
includes the following:
• Neurofibromatosis
• Fibrous dysplasia is of bone
• Arteriovenous malformations of jaws.

Key points of facial hemihypertrophy

Fig. 1.12: Radiograph of facial • Unilateral enlargement of face including jaws,
hemihypertrophy teeth, alveolar bone and soft tissues.

• The sebaceous and sweat glands on the affected • Crown size of tooth and roots are larger on the
side show excessive secretions. affected side.

• The ear and eye on the affected side may also • Teeth on the affected side erupt earlier, tongue
be enlarged. is larger and malocclusion is common.

• Unilateral enlargement of the cerebral • It’s a developmental defect but hormonal
hemisphere may cause mental retardation and imbalance and lymphatic abnormality, etc. are
seizure in about 15 to 20% cases. also important predisposing factors.

• There can be an increased incidence of certain TREATMENT
systemic conditions in facial hemihypertrophy
such as Wilms, tumor of kidney, adrenocortical No treatment is usually required for facial hemi-
tumor and hepatoblastoma, etc. hypertrophy. However, selective surgical treat-
ments may be performed to improve functional
• On rare occasions, the hypertrophy may extend and cosmetic status wherever necessary.
beyond the face and include the limbs or even
the entire one side of the body. FACIAL HEMIATROPHY


• Unilateral macroglossia with an increase in the Facial hemiatrophy also known as Parry-
size of the fungiform papilla is often seen. Romberg syndrome, is a developmental anomaly
characterized by progressive decrease in the size
• Crowns and roots of teeth, especially of the of one side of the face due to atrophy of the facial
permanent teeth are often enlarged on the structures.
affected side.
• The teeth on the affected side may also erupt
prematurely. The exact etiology of the disease is not known
however certain possible factors have been
• There is often early shedding of deciduous teeth identified which can precipitate the condition.
on the affected side. These factors include the following:
• Peripheral nerve dysfunction
• The jawbone proper is larger and thicker on • Trauma
the affected side. • Heredity
• Peripheral trigeminal neuritis
• Because of the osseous and dental asymmet- • Infection
ries in facial hemihypertrophy malocclusion • Regional systematic sclerosis.
often develops.
• Because of the overgrowth of soft tissue, buccal
mucosa on the affected side appears pendulus • The condition usually begins in the first or
and velvety, and folds of tissue may hang from second decade of life. Many cases may be
there in the oral cavity. present since birth.

16 Essentials of Oral Pathology

• Initially a slightly depressed vertical furrow or lip to fuse together at the time of development.
line is noticed at the midline of the forehead This defect is more commonly seen in relation to
and eyebrow. the upper lip.

• As the condition progresses, facial tissues on Cleft palate: It is a developmental defect of palate
the affected side including the skin, subcuta- characterized by lack of complete fusion of two
neous tissue, muscle and bone, etc. become lateral halves of the palate resulting in a cleft. Cleft
atrophic, resulting in facial deformity. in the palate leads to communication between oral
and the nasal cavity.
• Usually the left side of the face is involved more
often than the right side. Cleft of the maxillofacial skeleton are quiet
common entities and these can involve many
• Affected side of the face shows hyperpig- structures of the orofacial region.
mentation of skin with loss of hair.
Congenital malformations causing
• Severe cases may often result in hollowing of clefts in the orofacial region
the cheek and depressed eye in the orbit.
• Cleft lip
• Other features associated with facial
hemiatrophy include trigeminal neuralgia, • Clefts of the primary palate
contralateral jacksonian epilepsy and ocular • Cleft of the secondary palate
and hair changes. • Mandibular cleft
• Oblique facial cleft
• The cartilage of the ear, nose and larynx, etc. • Submucosal cleft palate
may be affected. • Bifid uvula
• Pits of the lip.
• Occasionally the disease may affect other parts
of the body. These developmental defects often have very
serious impacts on the growth, development and
ORAL MANIFESTATIONS functions of the involved facial organ. Moreover,
such defects can jeopardize the appearance of the
• Intraoral tissues on the affected side exhibit an face and badly affect the personality of the patient
overall atrophy. as well.

• Delayed development of the jawbone. ETIOLOGY
• Tooth eruption on the affected side may also be
The etiology of cleft lip and cleft palate covers both
retarded. hereditary and environmental factors.
• Teeth on the affected side often have shorter
Hereditary Factors
crowns and roots.
• Development of the roots of teeth on the affected Heredity is the most important single factor in the
development of cleft lip and cleft palate. Different
side is also delayed. studies indicate that nearly 40 percent of cleft lip
cases with or without cleft palate are hereditary in
TREATMENT origin. Heredity also plays role in the development
of about 20 percent cases of isolated cleft palate.
There is no effective treatment for facial
hemiatrophy. Progression of the condition ceases Moreover research also indicates that cleft lip
after certain age and it remains static thereafter or cleft palate of hereditary origin can occur either
for the remaining part of life. due to polygenic influence or monogenic
Polygenic inheritance of cleft lip or cleft palate: If
Cleft lip and palate are the most common deve- the origin of the disease is influenced by several
lopmental defects in the head and neck region. different genes acting together, it is known as


Cleft lip: It is a developmental anomaly
characterized by a wedge-shaped defect in the
lip, which results from failure of two parts of the

Developmental Anomalies of Oral and Paraoral Structures 17

polygenic inheritance. It is presumed that every the mandibular process. Mandibular clefts are
individual carries some genetic liability for clefting mostly midline defects.
and only if the combined liabilities of both the • Cleft of the upper lip and premaxilla occur due
parents exceed a minimum threshold level, then to failure of mesodermal penetration and
clefting occurs in their offspring. subsequent obliteration of the ectodermal
grooves between the median nasal process,
Monogenic inheritance of cleft lip and cleft palate: lateral nasal process and the maxillary
When clefting is influenced by only a single gene, process, which occurs during the seventh week
it is called monogenic defect. Moreover the cleft lip of intrauterine life.
and cleft palate of monogenic origin can be
associated with numerous other syndromes. • The tongue occupies the space between two
palatal halves during the initial phase of
Environmental Factors development. However, ninth and tenth week
of intrauterine life are associated with mandi-
Several environmental factors have been identified bular enlargement and gradual downward
which probably play an accessory role in the movement of the tongue.
development of cleft lip and cleft palate.
• If the tongue does not move downwards
The factors include the following: sufficiently, the palatal shelves remain
• Nutritional factors such as deficiency of or separated and do not rotate to their horizontal
position, this causes lack of fusion between the
excess of vitamin A and deficiency of palatal shelves resulting in clefts.
• Maternal smoking (during pregnancy) is a very • Palatal fusion occurs anteroposteriorly and is
high risk factor.
• Psychogenic, emotional or traumatic stress in completed in between 11th and 12th week of
pregnant mothers.
• Relative ischemia to the area due to defective the intrauterine life.
vascular supply.
• Mechanical obstruction by enlarged tongue. • Isolated cleft of the palate develops due to the
• High dose of steroid therapy during pregnancy.
• Localized mucopolysaccharide metabolism failure of fusion between two palatal shelves
defect in the area. in the midline.
• Infections.
• Substances such as alcohol, drugs or toxins in A number of both genetic and environmental
the circulation.
• Pathological conditions like Streeter’s fetal disturbances have been isolated, which can
• Lack of inherent developmental force. cause breakdown of the normal series of

PATHOGENESIS OF CLEFT LIP AND interdependent events or steps during the
development of facial structures and result
Cleft lip and cleft palate usually develop due to
incomplete obliteration and maturation of ultimately in cleft formation.
different embryonic processes, which are
associated with the formation of normal lip and • Disturbed mesenchymal cell migration and/or
• Mandibular cleft (lower lip and/or mandi- proliferation: Failure of fusion of facial growth

bular bone) usually occurs either due to failure centers or palatal processes due to impaired
of the copula to form the mandibular arch or
due to persistence of the central groove of mosenchymal cell replacement after palatal

• Suppressed cell division in associated structures:

Reduced growth of cranial and/or Meckel’s

• Impaired intrinsic tissue function: Reduced
tongue mobility and delayed ability or inability

of palatal processes to elevate.
• Disturbance in inductive tissue interactions:

Aberrant message leading to failure of palatal

• Suppressed programmed epithelial cell death
following fusion: Incomplete palatal fusion or

reopening of fused processes.

18 Essentials of Oral Pathology

Classification of cleft lip and cleft palate

Davis and Ritchie classification • Group I: Clefts anterior to the alveolus(unilateral, median,
or bilateral CL).

• Group II: Postalveolar clefts (CP alone, soft palate alone,soft
palate and hard palate, or submucous cleft).

Veau classification • Group I (A): Defects of the soft palate only.
• Group II (B): Defects involving the hard palate and soft

• Group III(C): Defects involving the soft palate to the alveolus,

usually involving the lip.
• Group IV (D): Complete bilateral clefts.

Kernahan and Stark symbolic • Areas 1 and 4: Lip.
classification • Areas 2 and 5: Alveolus.
• Areas 3 and 6: Palate between alveolus and the incisive

• Areas 7 and 8: Hard palate.
• Area 9: Soft palate.

International confederation of plastic • Group I: Defects of the lip or alveolus.
and reconstructive surgery classification • Group II: Clefts of the secondary palate (hard palate, soft

palate, or both).
• Group III: Any combination of clefts involving the primary

and secondary palates.

CLEFT PALATE • Pierre-Robin syndrome
• Goldenhar syndrome
Incidence varies with racial and geographic • Median cleft face syndrome
background. Incidence of cleft lip and/or • Oral facial digital syndrome
cleft palate is about 1 in 800 child births (range • Apert’s syndrome
in 1:500–1:2500). It is interesting to note • Cleidocranial dysplasia
that when a couple have their first baby born • Schenthaner-Marie-Sainton syndrome
with the defect of either cleft lip or cleft palate • Nagar syndrome
or both, their second baby will carry a 1% risk • Elashy-Waters syndrome
of having the same defect. The incidence of • Crouzon syndrome
cleft lip and cleft palate are on the rise among • Larsen syndrome.
modern population because the modern • Treacher-Collins syndrome
maxillofacial and plastic surgery can provide • Marfan syndrome
hugely improved and almost perfect esthetic • Otopalatodigital syndrome
rehabilitation to those patients who had cleft lip • Down syndrome
or cleft palate. • Edward’s syndrome.

After the perfect surgical repair, the grown up CLINICAL FEATURES OF CLEFT LIP
people do not have any problem in free social AND CLEFT PALATE
mixing. Moreover, marriages between such people, • These defects occur more commonly among
who are genetically harboring the defect may give
birth to children with even higher risk of male people.
developing cleft lip and cleft palate.

Developmental Anomalies of Oral and Paraoral Structures 19

• Mostcommontypeofcleftinbothsexescombined Fig. 1.14: Bilateral complete cleft palate
is cleft lip and palate (Fig. 1.13).
• Increased susceptibility to middle ear infections
• Most common type of isolated cleft lip only is via the auditory tube.
unilateral complete type.
• Difficulty is correct phonation and articulation
• Themildestformofcleftpalateisthecleftuvula. of speech.
• Clefting involves left side of the face more often
• There may be associated major congenital
than the right side. defects in the body including heart defects,
• As cleft palate creates a communication spina bifida and mental deficiency, etc.

between the oral and the nasal cavities, patients • Mental trauma to the child due to the unusual
appearance as well as due to the speech
often feel difficulty in taking foods and drinks problems, which often prevents them from
due to nasal reflux or regurgitation. mixing with other children freely.
• Breastfeeding is impossible to babies having
cleft lip or cleft palate, as they cannot generate • Improper or untimely surgical correction of
sufficient suction. these defects may also cause persistence of
• In case of cleft palate, upper anterior teeth may some ugly appearance and defective speech;
be misplaced, deformed or impacted. moreover improper surgical correction may also
• Bony deficiency of upper jaw may cause retru- result in an unbalanced growth of the mid face
sion of maxilla with narrow arched palate. region in future.
• Maxillary canine or premolars on the affected
side may contact in lingual occlusion to the
corresponding mandibular teeth due to
retrusion of the maxillary bone.
• Deflection of nasal tip towards the non-cleft
side and larger naris on the clefted side.
• Bilateral complete cleft is the worst situation,
where complete separation of the anterior
palate occurs (Fig. 1.14), which projects
towards the mid portion of the lip and is
attached only by the nasal septum.

Fig. 1.13: Cleft lip and palate

20 Essentials of Oral Pathology

Key points of cleft lip and cleft palate DEVELOPMENTAL ANOMALIES
• Important developmental anomaly occurring
due to failure of fusion between various embryo- AGLOSSIA
nic processes associated with development of
normal lips and palate. Aglossia is an extremely rare congenital defect
characterized complete absence of the tongue.
• Genetic abnormality is the single most This condition is usually associated with other
important cause. serious developmental defects in the body.
Sometimes it occurs in association with aglossia-
• More common in maxillary arch than mandi- adactylia syndrome characterized by congenital
bular arch. absence or severe hypoplasia of tongue with
absence of the digits.
• Maxillary cleft lip along with cleft palate occurs
due to failure of fusion between median nasal, MICROGLOSSIA
lateral nasal and maxillary processes in varying
combinations and extents. Microglossia is a rare congenital anomaly in which
only atiny or rudimentary tongue develops in the
• Two palatal halves may also fail to fuse. oral cavity. Although microglossia may develop as
• Cleft lip and palate may be unilateral or an isolated case but in most cases it occurs in
association with other congenital anomalies, e.g.
bilateral; may be complete or incomplete types. oromandibular limb hypogenesis syndrome or
• Clinically, difficulties in food intake, speech, nasal hypoglossia-hypodactylia syndrome, etc.
• Microglossia without limb deformity can occur
regurgitation of milk in children, malocclusion
and poor look, etc. are the important features. but they are also associated with some other birth
• Timely surgical intervention is required. defects such as partial anodontia, sublingual
gland hypertrophy and dextrocardia, etc.
TREATMENT • However, patients with microglossia don’t
Treatment should be aimed at achieving the have severe speech difficulties or difficulty in
following goals: taking food.
A. Restoration of feeding to the children. • Small children often have problem in sucking
B. Proper development of speech. milk.
C. Prevention of maxillary arch collapse. • Since the size of the tongue often determines
D. Cosmetic repair of the face and lips. the growth and size of the mandibular arch, in
• Cleft lip is treated surgically in the first week case of microglossia the length of the
mandibular arch is often smaller.
after birth, when the blood hemoglobin level is • Moreover, the smaller mandibular arch length
high and the kid is protected by the maternal often leads to development of severe malocclu-
antibodies. sion.
• Sometimes, the surgery may be deferred until
the baby attains 2 to 3 months of age, as by this MACROGLOSSIA
time, the infant becomes adapted to its
independent existence. Macroglossia is a relatively common condition
• Generally, cleft palates are corrected surgically characterized by an abnormally large tongue in
at the age of 18 months or immediately after the oral cavity.
that. This particular time is selected since after
this age there will be development of speech TYPES
and any further delayed in treatment will cause
abnormal speech development. Macroglossia can be either congenital or acquired
• Familial, social and psychological support is (secondary) in nature.
necessary during the protracted management.
• Obturators may be given in untreated adult
patients with palatal clefts. The appliance
helps in keeping the palatal clefts closed and
thereby helps in speech and taking food.

Developmental Anomalies of Oral and Paraoral Structures 21

Causes of macroglossia Relative Macroglossia

A. CAUSES OF CONGENITAL MACROGLOSSIA Relative macroglossia is a condition in which a
normal sized tongue appears abnormally large if
• Idiopathic muscle hypertrophy causing over- it is particularly enclosed within a small oral
development of the tongue musculature. cavity. It happens mostly in cases of maxillary
retrusion or in cases of restricated growth of
• Lysosomal storage diseases: nasopharynx.
– Hurler syndrome
– Hunter syndrome Lymphangioma restricted to the tongue or in
– MaroteauxLamy syndrome. continuity with a cystic hygroma of the neck is
the most common cause of macroglossia.
• Down syndrome
• Beckwith’s hypoglycemic syndrome. Relative macroglossia can also occur in
• Multiple endocrine neoplasia syndrome. conditions like enlarged tonsils or adenoids ,
• Lingual thyroid nodule. habitual posturing of tongue, low palate with
• Gargolysm. reduced volume of oral cavity and mandibular
• Trisomy 22. retrognathism, etc.
• Neonatal diabetes mellitus.
Apparent Macroglossia
MACROGLOSSIA Apparent macroglossia is a condition, where the
tongue appears abnormally large due to poor
Tumors in the tongue • Hemangioma muscular control of the tongue, although there is
• Lymphangioma • Carcinoma no real increase in the bulk of the tongue tissue.
• Neurofibromatosis • Metastatic tumors Apparent macroglossia is often seen in cretinism
• Plasmacytoma and in “Happy puppet” syndrome.

• Amyloidosis
• Sarcoidosis • Macroglossia causes displacement of teeth and
malocclusion as the enlarged tongue creates
Systemic conditions continuous pressure or thrust on the teeth.
• Uremia
• Iatrogenic macroglossia • It may disturb the process of speech and food
intake to some extent.
Traumatic conditions • Hemorrhage
• Surgery • Intubation injury • Some macroglossias may cause cosmetic
• Tongue biting deformity.
• Radiation injury
• The lateral margin of the tongue exhibits
Endocrine disorders • Cretinism scalloping or indentations as the tongue is
• Acromegaly • Diabetes always pressed against the teeth.
• Hypothyroidism
• Myxedema • Children with macroglossia often develop
tongue-thrusting habits, which may lead to
Obstructive lesions in the tongue malocclusion, open bite and diestema
• Lymphatic obstruction of the tongue by any formation, etc.

malignant tumor. • Macroglossia developing in adult people (as
in acromegaly or in tumors, etc.) may produce
Inflammatory conditions of tongue spacing of teeth and distortion of the
mandibular arch.
• Syphilis • Ludwig’s angina
• Blockage of the pharyngeal airway due to
• Pemphigus • Tuberculosis macroglossia may result in a condition called
“obstruction sleep apnea”, which is
• Small pox • Scurvy characterized by intermittent cessation of
respiration during sleep.
• Actinomycosis • Typhoid

• Pellagra

Cystic lesions in the tongue
• Dermoid cyst
• Epidermoid cyst

22 Essentials of Oral Pathology

• Macroglossia can also be an important compo- • Although most affected individuals can
nent of “Beckwith’s hypoglycemic syndrome, perform tongue functions almost normally,
which features—neonatal hypoglycemia, mild the restricted tongue mobility in
microcephaly, umbilical hernia, high birth ankyloglossia may sometimes cause the
weight and postnatal somatic gigantism. following problems:
It is important to note that CT scans can be – Speech disorders—patient cannot properly
pronounciate certain consonants and diph-
helpful in determining, if the tongue size is normal thongs such as L, R, T, D, N, TH, SH, Z, etc.
or there is any deviation. – Patient pronounciates the word “lemonade”
as wemonade.
TREATMENT – Infants feel difficulty in sucking breast milk.
– Deformities in dental occlusion especially
• Removal of the primary cause whenever development of open bite and mandibular
possible. prognathism, etc.
– Difficulty in swallowing food and
• Surgical reduction or trimming may be required maintaining oral hygiene.
when macroglossia disturbs the oropharyngeal – Tension in the anterior lingual gingiva in
function or is causing some major cosmetic tongue-tie may initiate some localized
problems. gingival or periodontal diseases near the
site of frenal attachment (e.g. gingival
ANKYLOGLOSSIA recession and persistent gap between lower
DEFINITION – Difficulty in kissing, licking one’s lips, eating
icecream cones and performing tongue
Ankyloglossia can be defined as a congenital tricks.
developmental condition characterized by
fixation of the tongue to the floor of the mouth; Ankyloglossia may occur sometimes in
causing restricted tongue mobility. During association with the following syndromes:
functional movements, the tip of the normal • Ankyloglossum spurious syndrome
tongue should touch the anterior palate but in • Vander Woudes syndrome
case of ankyloglossia, it fails to reach up to that • Fraser’s syndrome
limit. • Rainbow’s syndrome
• Orofacial digital syndrome, etc.
Complete ankyloglossia is an extremely rare
condition, however partial ankyloglossia, which TREATMENT
is otherwise known as “tongue-tie” is a relatively
common developmental anomaly of the tongue. Partial ankyloglossia in most of the cases does not
The tonguetie occurs either due to a short and require any treatment, however in severe cases of
thick lingual frenulum (a membrane connecting ankyloglossia, surgical correction (frenulctomy) of
the undersurface of the tongue to the floor of the the lingual frenulum is done to free the tongue.
mouth) or due to a frenulum, which attaches too Sometimes, the offending frenulum may tear
near to the tip of the tongue. spontaneously resulting in freeing of tongue.

Ankyloglossia is almost always a congenital CLEFT TONGUE
disorder and its prevalence rate ranges from 0.04
to 6.8 percent. According to few investigators this Developmental disturbance may sometimes cause
condition may sometimes develop as a result of partial or complete cleft in the tongue. Although a
trauma. Recent study of Harris EF et al indicate complete cleft or bifid tongue is a rare congenital
that incidence of tongue tie may increase with anomaly, however a partially cleft tongue is more
maternal use of cocaine during pregnancy. frequently encountered.


• Ankyloglossia affects the males more
frequently than females (2.6:1)

Developmental Anomalies of Oral and Paraoral Structures 23

Cleft tongue usually develops due to partial or • Similar discomfort may also be felt when
complete failure of union between the two lateral fissured tongue occurs in association with
lingual swellings during embryogenesis. geographic tongue.
Incomplete cleft in the tongue develops due to
failure of mesenchymal tissue proliferation that • The fissures or groves often radiate from a
obliterates the groove. central groove on the dorsal surface in an
oblique direction.
Partial cleft tongue clinically exhibits a deep
groove in the midline, while the bifid tongue • The large and deep fissures may be inter-
shows a complete cleft along its long axis. Cleft connected and they separate the dorsum of the
tongue in most of the cases is an asymptomatic tongue into multiple lobules.
condition although sometimes irritation can be
felt due to accumulation of food debri or • The average depth of individual fissure is about
microorganisms at the bottom of the cleft. 6 millimeter.

Sometimes, cleft tongue may occur as a feature • The disease often occurs in association with
of the orofacial digital syndrome, other features of Melkersson-Rosenthal syndrome and some
this syndrome include frontal bossing, short upper investigators believe that fissured tongue can
lip with cleft, presence of thick fibrous brands in be a feature of benign migratory glossitis.
the lower anterior mucobuccal fold eliminating
the sulcus and cleft of the mandibular alveolar HISTOPATHOLOGY
process, etc. Histopathologically fissured tongue produces the
following features:
FISSURED TONGUE (SCROTAL TONGUE) • There will be loss of filliform papilla from the

Fissured tongue is a congenital developmental surface mucosa.
malformation; characterized by presence of • Neutrophilic microabscess formation within
numerous shallow or deep groves (fissures) on
the dorsal and lateral surface of the tongue. the epithelium.
• Hyperplasia of the rete-pegs and increased
thickness of the lamina propria.
The exact etiology for this condition is not known, • Mixed inflammatory cell infiltration in the
however the following factors are often suspected:
• Genetic defect (polygenic or autosomal mode connective tissue stroma.

of inheritance). TREATMENT
• Vitamin deficiency No treatment is required for fissured tongue except
• Trauma brushing of the tongue to eliminate the debris that
• It may be a normal variation of tongue irritates.


Median rhomboid glossitis is an asymptomatic,
• The overall worldwide prevalence rate of elongated, erythematous patch of atrophic
fissured tongue is about 7 percent (may be as mucosa on the middorsal surface of the tongue.
high as 21 percent), prevalence in USA is about
2 to 5 percent. ETIOPATHOGENESIS
In the past median rhomboid glossitis was thought
• Slightly more common among males. to represent a developmental defect of the tongue,
• Usually there is no clinical symptom in presumably arising as a result of persistence of
the ‘tuberculum impar’on the surface of dorsum
fissured tongue but collection of food debris of the tongue.
and microorganisms in the fissures or groves
may sometimes cause discomfort. During normal embryognesis, however the
tuberculum impar should retrude and is
overgrown by the lateral lingual swellings.

24 Essentials of Oral Pathology

In recent times, however several investigators • The color of the lesion varies from pale pink to
believe that median rhomboid glossitis occurs due bright red and occasionally there is presence
to chronic infection by Candida albicans. of a white halo.

CLINICAL FEATURES • The surface is usually smooth, flat or slightly
raised and is sometimes fissured or lobulated.
Incidence: The average frequency of median
rhomboid glossitis is about 0.2 percent among the • In many cases, the lesion exhibits an erythe-
general population. matous and nodular hyperplasia characteristic
Age: The condition is mostly seen among adults of chronic hyperplastic candidiasis.
(30–50 years) and is rarely found among children.
Sex: Median rhomboid glossitis is seen more • Some patients even develop a similar lesion on
frequently among males (M : F-3 : 1). the midline of the palate just opposite to the
Site: The lesion is located immediately anterior to tongue lesion and it occurs due to repeated
the foramen cecum and the circumvallate papillae, contact with the infected tongue surface to the
in the midline on the dorsurm of tongue (at the palate (kissing lesion).
junction of the anterior two-third and posterior
one-third areas). • Median rhomboid glossitis is usually
asymptomatic but occasionally it may cause
PRESENTATION (FIGS 1.15A AND B) slight soreness or burning sensation.

• The median rhomboid glossitis starts as a • The lesion is clinically suspicious and it is often
narrow, mildly erythematous area located along mistaken for carcinoma of the tongue. Although
the median fissure on the dorsum of the tongue dorsum of the tongue, where median rhomboid
just anterior to the circumvalate papilla.
Key points of median rhomboid glossitis
• The lesion finally appears as a diamond or
lozenge shaped area devoid papilla. • Diamond or lozenge shaped depappilated area

• Clinically, the lesion is asymptomatic and it on the mid dorsum of the tongue, anterior to the
often remains unnoticed by the patient for many
years. circumvalate papilla.

• It enlarges slowly and the fully developed • Color is erythematous and surface is generally
lesion of median rhomboid glossitis reaches to
a size of little less than 2 cm in diameter. smooth.

• Condition is asymptomatic with occasional


• Superficial candidiasis may be present

• Often mistaken for carcinoma, but it’s an

innocent developmental anomaly.

Fig. 1.15A: Median rhomboid glossitis-I Fig. 1.15B: Median rhomboid glossitis-II

Developmental Anomalies of Oral and Paraoral Structures 25

glossitis is located is not a frequent site for CLINICAL FEATURES
carcinoma of the tongue.
• In some cases the disease may regress • Varicosities can be observed in many oral
spontaneously. locations like ventral surface of tongue, floor of
the mouth, lips, buccal mucosa and the

• Squamous cell carcinoma • Among all these intraoral locations, ventral
• ‘Gumma’ of tertiary syphilis surface of tongue and floor of the mouth are the
• Granular cell myoblastoma most common sites for oral varices.
• Lingual thyroid nodule
• Tuberculous granuloma • Clinically lingual varices appear as small,
• Deep fungal infection. round, purplish nodules, lateral to the sub-
lingual vein, which is usually also deflected.
• Lingual varices are common among people
Microscopically, median rhomboid glossitis over the age of 50 years and the varices tend to
presents the following features: become more conspicuous with advancing
• Mild to severe parakeratosis of the surface age.

epithelium. • Thrombosis can occur occasionally in these
• Loss of both filliform and fungiform papilla. varicose veins, however only rarely there are
• Thinning of the supra-papillary epithelium. any clinical symptoms.
• There may be presence of acanthosis with
• In case of lingual varices, there is absence of
elongation of rete-ridges. any similar lesion in the skin and other mucosal
• The rete-ridges may either divide or locations.

anastomose. • The lesion interestingly has no bleeding
• Superficial layer of the epithelium often shows tendency either.

neutrophilic infiltration, and often there is • Presence of lingual varices before the ages of
presence of numerous candidal hyphae. 50 indicates premature ageing.
• The underlying connective tissue is usually
very vascular and is infiltrated by chronic • Lingual varices may occur in association with
inflammatory cells. leg varicosities, however there is no relation-
• Areas of irregular hyperplasia may be seen in ship established between cardiopulmonary
the epithelium as a result of chronic inflam- disorder and lingual varices.
mation in the underlying connective tissue.
• On occasions, the epithelium may show featu- • Sometimes, lingual varices can be indis-
res of dysplasia or individual cell keratini- tinguishable from hereditary hemorrhagic
zation due to the chronic fungal infection. telangiectasia.


No treatment is required for lingual varices.

No treatment is basically required for this lesion.
Antifungal agents and antiseptic gurgles are used DEFINITION
to relieve the erythema and irritation in the area.
Geographic tongue is the multifocal, patchy
LINGUAL VARICES irregular areas of depapillation of tongue
characterized by frequent remissions and


A varix is a dilated, tortuous vein which is often The exact etiology of geographic tongue is not
subjected to increased hydrostatic pressure but is known, however patients often have a positive
poorly supported by the surrounding tissue. family history of the similar problem for

26 Essentials of Oral Pathology Fig. 1.17: Geographic tongue-II
Fig. 1.18: Geographic tongue-III
generations. However, many investigators believe
that emotional stress, asthma, eczema and allergy
may also precipitate this condition.


• The condition occurs in about 1 to 2 percent of
the population.

• It can be seen among children as well as adults
and there is a slight female predilection

• Geographictongueclinicallypresentsmultiple,
irregular, well-demarcated, smooth patchy
erythematous areas on the dorsum of the
tongue with desquamation of the filliform

• At the periphery, these lesions are often
surrounded by a well-defined, slightly raised,
yellowish-white, serpigenous line on the
dorsum of the tongue.

• Although, the filliform papillae are absent in
the desquamated zone, the fungiform papillae
remain present, which appear as few red dots,
projecting from the surface.

• The lesions heal centrally and spread centri-
fugally, and they may even sometimes involve
the ventral surface of the tongue.

• Remission of the initial lesion is always follo-
wed by fresh recurrent lesion at a new location
over the tongue. Because of this tendency for
migration of the lesion from one area to the other,
it is often called “migratory glossitis” (Fig. 1.19).

• Moreover, the benign migratory glossitis lesion
mimics the continental outlines on the globe

Fig. 1.16: Geographic tongue-I Fig. 1.19: Benign migratory glossitis
(Geographic tongue-IV)

and this also makes frequent use of the term
“geographic tongue” for the condition.
• The condition is mostly painless and
asymptomatic, however on few occasions, it
may produce soreness or burning sensation

Developmental Anomalies of Oral and Paraoral Structures 27

(glossodynia) particularly during taking spicy • Chronic hyperplastic candidosis
or citrus foods. • Familiar dysautonomia.
• Soreness of the tongue may be aggravated due
to use of chemicals, e.g. chlorhexidine mouth- TREATMENT
washes or tooth whiteners, etc.
• The abnormal clinical appearance and the There is no specific treatment for geographic
persisting nature of the lesion along with the tongue. Heavy doses of vitamins may produce
associated soreness often makes the patient some results in few cases. Sometimes antihis-
cancerophoveik. taminic and local steroidal antinflammatory
• Sometimes several lesions may coalesce drugs are also used.
together to produce a typical “scalloped
pattern”. HAIRY TONGUE
• Occasionally these lesions may occur in
association with scrotal tongue or psoriasis. DEFINITION

Key points of geographic tongue Hairy tongue is an unusual condition, which
occurs due to hypertrophy of the filliform papilla
• Developmental anomaly characterized by of tongue along with loss of normal
desquamation process. The abnormal hair–like
multiple, irregular, patchy, depapillated areas growth of the papilla eventually leads to formation
of a pigmented, thick, matted layer on the tongue
on the dorsum of the tongue. surface often heavily coated with bacteria and
• The patch heals up at one location only to
Etiology of hairy tongue
reappear at a newer location; apparently
• Poor oral hygiene
exhibiting a sense of ‘migration’. • Fungal infections
• Prolonged use of antibiotics
• The lesions have irregular border and are often • Heavy smoking
• Excessive use of antiseptic mouth washes
surrounded by a white line at the periphery. • Chronic illness
• Lack of tooth brushing and consumption of soft
• Patches exhibit loss of filliform papilla but
foods with little or no roughage.
fungiform papilla are retained which appear
as elevated, red rods.
• Normally the keratinized surface layers of the
• Mostly asymptomatic but occasional burning tongue papillae are continuously desquamated
through friction of the tongue with food, rough
sensations; no treatment required. surface of the palate and the upper anterior
teeth. Following desquamation, tongue papillae
HISTOPATHOLOGY are replaced by newer epithelial cells from
• Geographic tongue microscopically shows
hyperparakeratinization of the covering • Lack of tongue movements due to local or
epithelium of tongue with loss of filliform systematic disease disturbs the regular
papilla. desquamation process of the tongue papilla;
especially the filliform papilla, which
• Intercellular edema and accumulation of lengthens considerably and produces a hairy
neutrophil polymorphs (so called spongiotic appearance on the tongue surface.
abscess) is often seen in the superficial layers
of the epithelium. • Such hypertrophied papillae are often coated
with microorganisms and become discolored
• Mild inflammatory cell infiltration is present
in the underlying connective tissue.

• The condition is histologically similar to
hyperplastic candidiasis, however candidal
hyphae are absent.


• Psoriasis
• Lichenoid reactions
• Reiter’s syndrome

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