Handbook of Oral Pathology and Oral

Medicine S. R. Prabhu
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Handbook of Oral Pathology and
Oral Medicine
Handbook of Oral Pathology and Oral Medicine

S. R. Prabhu BDS; MDS (Oral Path); FFDRCS (Oral Med); FDSRCS(Edin); FDSRCPS
(Glas); FDSRCS (Eng), FFGDPRCS(UK); MOMed RCS (Edin); FICD.

Honorary Associate Professor

School of Dentistry
University of Queensland
Brisbane, Australia
This edition first published 2022
© 2022 John Wiley & Sons Ltd

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Library of Congress Cataloging-­in-­Publication Data applied for

[ISBN: 9781119781127]

Cover Design: Wiley

Cover Images: Courtesy of S. R. Prabhu

Set in 9.5/12.5pt STIXTwoText by Straive, Pondicherry, India

10 9 8 7 6 5 4 3 2 1
To the victims of COVID-­19 infection and all those frontline healthcare workers who are engaged in
the fight against the disease with utmost courage and dedication.
 vii

Contents

Foreword xvii
Preface xix
Acknowledgements xxi
About the Companion Website xxiii
Nomenclature Used in The Study of Human Disease xxv
Standard Abbreviations for Prescribers xxviii

Part I Pathology of Teeth and Supporting Structures 1

1 Disorders of Tooth Development and Eruption 3

1.1 ­Anodontia, Hypodontia and Oligodontia 3
1.2 ­Hyperdontia (Supernumerary Teeth) 5
1.3 ­Microdontia and Macrodontia 6
1.4 ­Gemination, Fusion and Concrescence 7
1.5 ­Taurodontism and Dilaceration 9
1.6 ­Amelogenesis Imperfecta 11
1.7 ­Dentinogenesis Imperfecta 13
1.8 ­Dentinal Dysplasia (Dentin Dysplasia) 14
1.9 ­Regional Odontodysplasia (Ghost Teeth) 16
1.10 ­Delayed Tooth Eruption 17
1.11 ­Tooth Impaction (Impacted Teeth) 18
1.12 ­Dens Invaginatus and Dens Evaginatus 20
1.13 ­Fluorosis (Mottled Enamel) 22
1.14 ­Tetracycline-­Induced Discoloration of Teeth: Key Features 24
1.15 ­Enamel Pearl: Key Features 24
1.16 ­Talon Cusp: Key Features 25
1.17 ­Hutchinson’s Incisors and Mulberry Molars: Key Features 26
1.18 ­Tooth Ankylosis: Key Features 26
1.19 ­Supernumerary Roots: Key Features 27

2 Dental caries 29
2.1 ­Definition/Description 29
2.2 Frequency 29
viii Contents

2.3 ­ etiology/Risk Factors/Pathogenesis 29

A
2.4 ­Classification of Caries 30
2.5 ­Clinical Features 30
2.6 ­Differential Diagnosis 33
2.7 ­Diagnosis 33
2.8 ­Microsopic Features 33
2.9 ­Management 35
2.10 ­Prevention 36

3 Diseases of the Pulp and Apical Periodontal Tissues 37

3.1 ­Classification of Diseases of the Pulp and Apical Periodontal Tissues 37
3.2 ­Pulpitis 38
3.3 ­Apical Periodontitis and Periapical Granuloma 40
3.4 ­Apical Abscess (Dentoalveolar Abscess) 43
3.5 ­Condensing Osteitis 44

4 Tooth Wear, Pathological Resorption of Teeth, Hypercementosis and Cracked Tooth

Syndrome 47
4.1 ­Tooth wear: Attrition, Abrasion, Erosion, and Abfraction 47
4.2 ­Pathological Resorption of Teeth 50
4.3 ­Hypercementosis 52
4.4 ­Cracked Tooth Syndrome 53

5 Gingival and Periodontal Diseases 57

5.1 ­Classification of Gingival and Periodontal Diseases 58
5.2 ­Chronic Gingivitis 58
5.3 ­Necrotizing Periodontal Diseases 60
5.4 ­Plasma Cell Gingivitis 63
5.5 ­Foreign Body Gingivitis 64
5.6 ­Desquamative Gingivitis 65
5.7 ­Chronic Periodontitis 67
5.8 ­Aggressive Periodontitis 70
5.9 ­Fibrous Epulis (Peripheral Fibroma) 73
5.10 ­Peripheral Ossifying/Cementifying Fibroma 74
5.11 ­Peripheral Giant Cell Granuloma (Giant Cell Epulis) 76
5.12 Angiogranuloma (Pyogenic granuloma/pregnancy epulis) 77
5.13 ­Inflammatory Gingival Hyperplasia (Inflammatory Gingival Enlargement) 79
5.14 ­Generalized Gingival Hyperplasia in Pregnancy 81
5.15 ­Drug-­Induced Gingival Hyperplasia 82
5.16 ­Familial Gingival Hyperplasia 84
5.17 ­Gingival and Periodontal Abscesses 86
5.18 ­Pericoronitis/Pericoronal Abscess 89
5.19 ­Gingival Enlargement in Granulomatosis with Polyangiitis (Wegener’s
granulomatosis) 91
5.20 ­Gingival Enlargement in Leukaemia 93
5.21 ­Gingival Enlargement in Ascorbic Acid Deficiency 95
 Contents ix

Part II Pathology of Jaw Bones 99

6 Infections and Necrosis of the Jaw 101

6.1 ­Acute Suppurative Osteomyelitis 101
6.2 ­Chronic Suppurative Osteomyelitis 104
6.3 ­Sclerosing Osteomyelitis 106
6.4 ­Proliferative Periostitis (Garre’s Osteomyelitis) 108
6.5 ­Actinomycosis of the Jaw 109
6.6 ­Cervicofacial Cellulitis (Cervicofacial Fascial Space Infection) 111
6.7 ­Osteoradionecrosis of the Jaw 112
6.8 ­Medication-­Related Osteonecrosis of the Jaw 114

7 Cysts of the Jaw 117

7.1 ­Radicular, Lateral Radicular, and Residual Radicular Cysts 117
7.2 ­Dentigerous Cyst 120
7.3 ­Eruption Cyst 122
7.4 ­Odontogenic Keratocyst (Keratocystic Odontogenic Tumour) 123
7.5 ­Lateral Periodontal Cyst 126
7.6 ­Calcifying Odontogenic Cyst 127
7.7 ­Orthokeratinized Odontogenic Cyst: Key Features 130
7.8 ­Glandular Odontogenic Cyst: Key Features 130
7.9 ­Nasopalatine Duct Cyst (Incisive Canal Cyst) 130
7.10 ­Pseudocysts of the Jaw: Solitary Bone Cyst, Aneurysmal
Bone Cyst and Stafne’s bone Cyst 132
7.11 ­Nasolabial Cyst: Key Features 135

8 Odontogenic Tumours 137

8.1 ­World Health Organization Classification of Odontogenic Tumours (2017) 137
8.2 ­Ameloblastoma 138
8.3 ­Unicystic Ameloblastoma 141
8.4 ­Squamous Odontogenic Tumour 144
8.5 ­Calcifying Epithelial Odontogenic Tumour (Pindborg Tumour) 145
8.6 ­Adenomatoid Odontogenic Tumour 147
8.7 ­Ameloblastic Fibroma 149
8.8 ­Ameloblastic Fibrodentinoma and Ameloblastic Fibro-­Odontome 151
8.9 ­Odontome (Odontoma) 153
8.10 ­Dentinogenic Ghost Cell Tumour 155
8.11 ­Odontogenic Myxoma 157
8.12 ­Odontogenic Fibroma (Central Odontogenic Fibroma) 159
8.13 ­Cementoblastoma 161

9 Non-­odontogenic Benign and Malignant Tumours of the Jaw 165

9.1 ­Osteoma 165
9.2 ­Multiple Osteomas in Gardner’s Syndrome 167
9.3 ­Central Haemangioma (Intraosseous Haemangioma) 169
9.4 ­Melanotic Neuroectodermal Tumour of Infancy 171
x Contents

9.5 ­ steosarcoma 172

O
9.6 ­Chondrosarcoma: Key Features 174
9.7 ­Ewing’s Sarcoma 175
9.8 ­Myeloma (Multiple Myeloma) 177
9.9 ­Solitary Plasmacytoma 179
9.10 ­Burkitt’s Lymphoma 181

10 Fibro-­Osseous and Related Lesions of the Jaw 185

10.1 ­Ossifying Fibroma/Cemento-­Ossifying Fibroma 185
10.2 ­Cemento-­Osseous Dysplasias 187
10.3 ­Familial Gigantiform Cementoma: Key Features 190
10.4 ­Central Giant Cell Granuloma 191

11 Genetic, Metabolic, and Other Non-­neoplastic Bone Diseases 195

11.1 ­Osteogenesis Imperfecta 195
11.2 ­Cleidocranial Dysplasia 197
11.3 ­Cherubism 199
11.4 ­Gigantism and Acromegaly 201
11.5 ­Brown Tumour of Hyperparathyroidism 203
11.6 ­Paget’s Disease of Bone (Osteitis Deformans) 205
11.7 ­Fibrous Dysplasia and McCune–Albright Syndrome 207
11.8 ­Mandibular and Palatine Tori: Key Features 210
11.9 ­Focal Osteoporotic Bone Marrow Defect: Key Features 210

Part III Pathology of the Oral Mucosa 213

12 Developmental Anomalies and Anatomical Variants of Oral Soft Tissues 215

12.1 ­Fordyce Granules: Key Features 215
12.2 ­Double Lip: Key Features 215
12.3 ­Leukoedema: Key Features 216
12.4 ­Ankyloglossia: Key Features 216
12.5 ­Geographic Tongue: Key Features 217
12.6 ­Hairy Tongue: Key Features 218
12.7 ­Fissured Tongue: Key Features 218
12.8 ­Lingual Thyroid: Key Features 218
12.9 ­Microglossia and Macroglossia: Key Features 219
12.10 ­Bifid Tongue: Key Features 220
12.11 ­Bifid Uvula: Key Features 220
12.12 ­Cleft Lip: Key Features 221
12.13 ­Calibre Persistent Labial Artery: Key Features 221
12.14 ­Epstein’s Pearl and Bohn’s Nodules: Key Features 223
12.15 ­Dermoid and Epidermoid Cysts: Key Features 223
12.16 ­Oral Varicosities: Key Features 224
12.17 ­Lymphoid Aggregates: Key Features 224
12.18 ­Parotid Papilla: Key Features 225
12.19 ­Circumvallate Papillae: Key Features 226
12.20 ­Physiological Pigmentation: Key Features 226
 Contents xi

13 Bacterial Infections of the Oral Mucosa 229

13.1 ­Scarlet Fever: Key Features 229
13.2 ­Syphilis 229
13.3 ­Gonorrhoea: Key Features 232
13.4 ­Tuberculosis 233

14 Fungal Infections of the Oral Mucosa 237

14.1 ­Candidosis (Candidiasis) 237
14.2 ­Histoplasmosis 244
14.3 ­Blastomycosis: Key Features 246

15 Viral Infections of the Oral Mucosa 247

15.1 ­Primary Herpetic Gingivostomatitis (Primary Herpes) 247
15.2 ­Herpes Labialis 250
15.3 ­Varicella (Chickenpox) 252
15.4 ­Herpes Zoster (Shingles) 253
15.5 ­Infectious Mononucleosis (Glandular Fever) 255
15.6 ­Oral Hairy Leukoplakia: Key Features 257
15.7 ­Cytomegalovirus Infection: Key Features 258
15.8 ­Herpangina: Key Features 258
15.9 ­Hand, Foot, and Mouth Disease 258
15.10 ­Squamous Papilloma 260
15.11 ­Condyloma Acuminatum: Key Features 261
15.12 ­Multifocal Epithelial Hyperplasia: Key Features 262
15.13 ­Verruca Vulgaris: Key Features 262
15.14 ­Measles: Key Features 263

16 Non-­infective Inflammatory Disorders of the Oral Mucosa 265

16.1 ­Recurrent Aphthous Stomatitis 265
16.2 ­Oral Lichen Planus 269
16.3 ­Oral Lichenoid Lesions 272
16.4 ­Pemphigus Vulgaris 273
16.5 ­Mucous Membrane Pemphigoid 276
16.6 ­Erythema Multiforme 279
16.7 ­Lupus Erythematosus: Key Features 281
16.8 ­Traumatic Ulcer: Key Features 281
16.9 ­Oral Lesions in Behcet’s Disease/Syndrome 282
16.10 ­Oral Lesions in Crohn’s Disease 283
16.11 ­Oral Lesions in Reactive Arthritis: Key Features 285
16.12 ­Uremic Stomatitis: Key Features 285
16.13 ­Chronic Ulcerative Stomatitis: Key Features 285
16.14 ­Radiation-­Induced Mucositis: Key Features 286
16.15 ­Medication-­Induced Oral Ulceration: Key Features 287
16.16 ­Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis 287

17 Non-­neoplastic Mucosal Swellings 291

17.1 ­Irritation Fibroma (Traumatic Fibroma) 291
17.2 ­Denture-­Induced Granuloma (Epulis Fissuratum) 293
xii Contents

17.3 ­ ibrous Epulis (Peripheral Fibroma): key features 294

F
17.4 ­Pyogenic Granuloma: key features 295
17.5 ­Peripheral Giant Cell Granuloma: key features 295
17.6 ­Peripheral Ossifying Fibroma: key features 295
17.7 ­Traumatic Neuroma 295
17.8 ­Squamous Papilloma: Key Features 296
17.9 ­Congenital Epulis: Key Features 297

18 Benign Neoplasms of the Oral Mucosa 299

18.1 ­Lipoma 299
18.2 ­Schwannoma (Neurilemmoma) 301
18.3 ­Granular Cell Tumour 302
18.4 ­Haemangioma 304
18.5 ­Lymphangioma 306
18.6 ­Leiomyoma (Vascular Leiomyomas): Key Features 307
18.7 ­Rhabdomyoma: Key Features 307

19 Oral Potentially Malignant Disorders 309

19.1 ­Erythroplakia 309
19.2 ­Leukoplakia 311
19.3 ­Chronic Hyperplastic Candidosis (Candidal Leukoplakia) 315
19.4 ­Palatal Lesions in Reverse Smokers 317
19.5 ­Oral Lichen Planus: Key Features 319
19.6 ­Oral Submucous Fibrosis 320
19.7 ­Oral Lichenoid Lesion 322
19.8 ­Lupus Erythematosus 324
19.9 ­Actinic Keratosis of the Lip (Actinic Cheilitis) 326
19.10 ­Graft-­Versus-­Host Disease 328
19.11 ­Dyskeratosis Congenita 330
19.12 ­Sublingual Keratosis: Key Features 331
19.13 ­Syphilitic Leukoplakia: Key Features 332
19.14 ­Darier’s Disease: Key Features 332

20 Malignant Neoplasms of the Oral Mucosa 335

20.1 ­Squamous Cell Carcinoma and Verrucous Carcinoma 335
20.2 ­Melanoma (Malignant Melanoma) 340
20.3 ­Kaposi’s Sarcoma 342
20.4 ­Fibrosarcoma: Key Features 343
20.5 ­Rhabdomyosarcoma: Key Features 344
20.6 ­Leiomyosarcoma: Key Features 344

Part IV Pathology of the Salivary Glands 347

21 Non-­neoplastic Salivary Gland Diseases 349

21.1 ­Salivary Calculi: Key Features 349
21.2 ­Mucoceles (Mucous Extravasation Cysts, Mucous Retention
Cysts and Ranula) 350
 Contents xiii

21.3 ­ jögren’s Syndrome 352

S
21.4 ­Sialadenitis: Key Features 354
21.5 ­Necrotizing Sialometaplasia: Key Features 355

22 Salivary Gland Neoplasms 357

22.1 ­World Health Organization Histological Classification of Salivary
Gland tumours (2017) 357
22.2 ­Pleomorphic Adenoma 358
22.3 ­Warthin’s Tumour (Papillary Cystadenoma Lymphomatosum) 360
22.4 ­Mucoepidermoid Carcinoma 362
22.5 ­Adenoid Cystic Carcinoma 364

Part V Clinical Presentation of Mucosal Disease 367

23 White Lesions of the Oral Mucosa 369

23.1 ­Actinic Cheilitis: Key Features 369
23.2 ­Chemical Burn: Key Features 370
23.3 ­Chronic Hyperplastic Candidosis: Key Features 370
23.4 ­Darier’s Disease: Key Features 371
23.5 ­Dyskeratosis Congenita: Key Features 371
23.6 ­Fordyce granules: Key Features 372
23.7 ­Frictional Keratosis: Key Features 372
23.8 ­Hereditary Benign Intraepithelial Dyskeratosis: Key Features 373
23.9 ­Leukoedema: Key Features 373
23.10 ­Leukoplakia: Key Features 373
23.11 ­Oral Hairy Leukoplakia: Key Features 374
23.12 ­Oral Lichen Planus: Key Features 374
23.13 ­Oral Squamous Cell Carcinoma: Key Features 375
23.14 ­Pseudomembranous Candidosis: Key Features 375
23.15 ­Smokeless Tobacco-­Induced Keratosis: Key Features 376
23.16 ­Smoker’s Keratosis: Key Features 376
23.17 ­Sublingual Keratosis: Key Features 377
23.18 ­Syphilitic Leukoplakia: Key Features 377
23.19 ­Verrucous Carcinoma: Key Features 377
23.20 ­White Hairy Tongue: Key Features 378
23.21 ­White Sponge Nevus: Key Features 378

24 Red and Purple Lesions of the Oral Mucosa 381

24.1 ­Contact Stomatitis: Key Features 381
24.2 ­Desquamative Gingivitis: Key Features 382
24.3 ­Erythema Migrans: key features 382
24.4 ­Erythema Multiforme: Key Features 382
24.5 ­Erythematous Candidosis: Key Features 383
24.6 ­Erythroplakia: Key Features 383
24.7 ­Haemangioma: Key Features 384
24.8 ­Hereditary Haemorrhagic Telangiectasia: Key Features 384
24.9 ­Infectious Mononucleosis: Key Features 385
xiv Contents

24.10 ­ aposi’s Sarcoma: Key Features 385

K
24.11 ­Linear Gingival Erythema: Key Features 385
24.12 ­Lupus Erythematosus: Key Features 386
24.13 ­Median Rhomboid Glossitis: Key Features 386
24.14 ­Mucosal Ecchymosis, Haematoma, and Petechiae: Key Features 386
24.15 ­Plasma Cell Gingivitis: Key Features 387
24.16 ­Port-­Wine Nevus: Key Features 387
24.17 ­Radiation Mucositis: Key Features 387
24.18 ­Thermal Burn: Key Features 388

25 Blue, Black, and Brown Lesions of the Oral Mucosa 389

25.1 ­Addison’s Disease: Key Features 389
25.2 ­Amalgam Tattoo: Key Features 389
25.3 ­Black/Brown Hairy Tongue: Key Features 390
25.4 ­Drug-­Induced Pigmentation: Key Features 391
25.5 ­Heavy Metal Pigmentation: Key Features 392
25.6 ­Laugier–Hunziker Syndrome: Key Features 392
25.7 ­Melanoma: Key Features 393
25.8 ­Melanotic Macule: Key Features 393
25.9 ­Peutz–Jeghers Syndrome: Key Features 393
25.10 ­Physiological Pigmentation: Key Features 394
25.11 ­Mucosal Nevi: Key Features 394
25.12 ­Smoker’s Melanosis: Key Features 395

26 Vesiculobullous Lesions of the Oral Mucosa 397

26.1 ­Angina Bullosa Haemorrhagica: Key Features 397
26.2 ­Bullous Lichen Planus: Key Features 397
26.3 ­Dermatitis Herpetiformis: Key Features 398
26.4 ­Erythema Multiforme: Key Features 398
26.5 ­Hand, Foot and Mouth Disease: Key Features 398
26.6 ­Herpes Zoster (Shingles): Key Features 399
26.7 ­Mucous Membrane Pemphigoid: Key Features 399
26.8 ­Pemphigus Vulgaris: Key Features 400
26.9 ­Primary Herpetic Gingivostomatitis: Key Features 400
26.10 ­Herpes Labialis: Key Features 400

27 Ulcerative Lesions of the Oral Mucosa 403

27.1 ­Oral Ulcers in Agranulocytosis: Key Features 403
27.2 ­Oral Ulcers in Behçet’s Disease: Key Features 404
27.3 ­Oral Ulcers in Coeliac Disease: Key Features 404
27.4 ­Chronic Ulcerative Stomatitis: Key Features 405
27.5 ­Oral Ulcers in Crohn’s Disease: Key Features 405
27.6 ­Oral Ulcers in Cyclic Neutropenia: Key Features 406
27.7 ­Cytomegalovirus Ulcers: Key Features 406
27.8 ­Eosinophilic Ulcer: Key Features 406
27.9 ­Gangrenous Stomatitis: Key Features 406
27.10 ­Necrotizing Sialometaplasia: Key Features 407
 Contents xv

27.11 ­ ecrotizing Ulcerative Gingivitis: Key Features 407

N
27.12 ­Oral Ulcers in Reactive Arthritis: Key Features 408
27.13 ­Recurrent Aphthous Ulcers: Key Features 408
27.14 ­Squamous Cell Carcinoma Presenting as an Ulcer: Key Features 409
27.15 ­Syphilitic Ulcers: Key Features 409
27.16 ­Traumatic Ulcer: Key Features 410
27.17 ­Tuberculous Ulcer: Key Features 410
27.18 ­Oral Ulcer in Ulcerative Colitis: Key Features 411

28 Papillary Lesions of the Oral Mucosa 413

28.1 ­Condyloma Acuminatum: Key Features 413
28.2 ­Multifocal Epithelial Hyperplasia (Heck’s Disease): Key Features 413
28.3 ­Oral Proliferative Verrucous Leukoplakia: Key Features 414
28.4 ­Squamous Papilloma: Key Features 414
28.5 ­Squamous Cell Carcinoma: Key Features 414
28.6 ­Verruca Vulgaris (Oral Warts): Key Features 414
28.7 ­Verrucous Carcinoma: Key Features 415

Part VI Orofacial Pain 417

29 Orofacial Pain 419

29.1 ­Odontogenic Orofacial Pain 419
29.2 ­Neuropathic Orofacial Pain 421
29.3 ­Other Conditions with Orofacial Pain 423

Part VII Miscellaneous Topics of Clinical Relevance 427

30 Oral Manifestations of Systemic Disorders 429

30.1 ­Gastrointestinal and Liver Disorders 429
30.2 ­Cardiovascular Disease 431
30.3 ­Respiratory Disease 431
30.4 ­Kidney Diseases 432
30.5 ­Endocrine and Metabolic Disorders 434
30.6 Nervous System Disorders 435
30.7 ­Haematological Disorders 437
30.8 ­Immune System Disorders 439

31 Systemic Diseases Associated with Periodontal Infections 441

31.1 ­Cardiovascular Disease 441
31.2 ­Coronary Heart Disease (Atherosclerosis and Myocardial Infarction) 441
31.3 ­Stroke 442
31.4 ­Infective Endocarditis 442
31.5 ­Bacterial Pneumonia 442
31.6 ­Low Birth Weight 443
31.7 ­Diabetes Mellitus 443
xvi Contents

32 Other Signs and Symptoms Related to the Oral Environment 445

32.1 ­Halitosis 445
32.2 ­Taste Disorders 446
32.3 ­Dry Mouth (Xerostomia) 447
32.4 ­Sialorrhea 448
32.5 ­Trismus 449
32.6 ­COVID-­19 Infection 449

33 Outline of Diagnostic Steps and Procedures Employed in

Oral Pathology and Oral Medicine 453
33.1 ­History 453
33.2 ­Clinical Examination 454
33.3 ­Clinical Differential Diagnosis 455
33.4 ­Diagnosis 456

Index 459
 xvii

Foreword

This is an amazing work. Professor SR Prabhu has touched constructively on almost every “issue”,
every decision required, in the day-to-day practice of oral medicine and to a considerable extent,
oral/maxillofacial pathology. He has laid out the material in a very logical set of chapters. The
extensive illustrations are of uniformly high quality: many of these have been donated by col-
leagues around the world and I join in thanking them for their generosity: many have become
personal friends to us both.
I initially was hesitant to contribute this Foreword. As a quantitative scientist, I always wish to
see the evidence base for every diagnosis, test and treatment presented. This is deliberately not the
intention here - indeed it is the opposite of Prof Prabhu’s intent. As he put it in response to my
challenge “My intention is not to compete with great authors of international repute. The material
presented is truly a compilation of what is known in the scientific papers, books and case reports
that are (I might interpolate with much hard work) available. This is a humble attempt to provide
students and busy practitioners with a source that provides quick access to information”. I see the
value of this: indeed, I wish my current undergraduate and postgraduate students came to clinics
with a copy in their pockets!
Professor SR Prabhu is a remarkable professional in the autumn of a remarkable career. This has
impacted the dental profession, and particularly dental students, across the globe, for decades,
beginning with his first teaching appointment in India in 1971. We first met when he was
Commonwealth Medical Scholar in my department in London in 1974. Chronologically since then
he has taught and led teaching [including from positions as Head of Department or Dean in several
institutions] in universities in India, Kenya, Sudan, Australia, Papua New Guinea, West Indies,
Malaysia, Saudi Arabia, West Indies (again), United Arab Emirates, and several Australian univer-
sities, again. His vast knowledge reflects this.
I have learned much from his global experience and it was particularly educative for me to work
with him, as co-editor and co-author of his largest work Oral Diseases in the Tropics (Oxford University
Press 1992; Revised reprint, Jaypee Bros. 2017). Beyond that his
bibliography is extensive.
We are fortunate that he has maintained the drive and passion
to give us this valuable work at this time: one positive outcome of
Covid-2019.

Newell W Johnson, CMG

Emeritus Professor of Oral Health Sciences,
Kings’ College London, &
Dean Emeritus and Honorary Professor of Dental Research,
Griffith University, Queensland, Australia
Brisbane, June 2021
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Title: The bedbug

Its relation to public health, its habits and life history, and
methods of control

Creator: United States. Public Health Service

Release date: November 27, 2023 [eBook #72238]

Language: English

Original publication: Washington: Government Printing Office, 1924

Credits: Charlene Taylor, Donald Cummings, and the Online

Distributed Proofreading Team at https://www.pgdp.net
(This file was produced from images generously made
available by The Internet Archive/American Libraries.)

*** START OF THE PROJECT GUTENBERG EBOOK THE

BEDBUG ***
Transcriber’s Note: New original cover art included with this eBook is
granted to the public domain.
 TREASURY DEPARTMENT
UNITED STATES PUBLIC HEALTH SERVICE
HUGH S. CUMMING, Surgeon General

THE BEDBUG
ITS RELATION TO PUBLIC HEALTH, ITS HABITS
AND LIFE HISTORY, AND METHODS OF
CONTROL

REPRINT No. 626

FROM THE

PUBLIC HEALTH REPORTS

December 10, 1920
(Pages 2964–2970)
[Revised edition, 1924]

WASHINGTON
GOVERNMENT PRINTING OFFICE
1924
 THE BEDBUG.[1]
Its Relation to Public Health, its Habits and Life History, and Methods
of Control.
[1] Reprint from the Public Health Reports, vol. 35, No. 50,
December 10, 1920, pp. 2964–2970.

The bedbug is one of the numerous insects which have been

suspected of conveying disease to man. Compared with such insect
pests as mosquitoes, lice, and fleas, however, its rôle is decidedly a
minor one. It has been claimed that the bedbug can take up the
microparasites of European relapsing fever, plague, and possibly
leprosy, along with the blood of men or animals suffering from these
diseases. It is also possible that in rare instances the bedbug may
transmit plague or European relapsing fever to man. On the other
hand, there is no convincing evidence that the bedbug is the usual
and ordinary insect transmitter of these or any other diseases at
present known to us.
If the bedbug acts as a transmitter of disease, it apparently does
so by the accidental carriage of disease elements on the mouth
parts; but this occurs only under the most favorable conditions.
These would require, first, the presence of great numbers of
microparasites on the skin or in the blood of a man or animal sick
with some disease transmissible to man by subcutaneous
inoculation; second, it would probably be necessary that there
should be many bugs biting in order that one or more of them should
bite some healthy person within a rather short space of time after
these insects had fed on the infected individual.
In actual practice these conditions would be found only in the most
filthy and insanitary surroundings and would call for drastic
measures to exterminate all vermin. It is, of course, possible that
under unsettled conditions where sick and well are crowded together
with no facilities for cleanliness, bedbugs might act as transmitters of
septicemic diseases. Experience has shown that under such grossly
insanitary conditions such insects as fleas and lice appear to be and
are far more dangerous as carriers of disease. Special measures for
their extermination should be taken. Added precautions for the
examination of bedbugs under these conditions would probably not
be justified by the results.
Notwithstanding the minor rôle which must be assigned the
bedbug as a carrier of disease, its presence is an offense against
sanitary decency. Its bites are quite poisonous to some people and
its odor is most disagreeable; and every effort should be made to
keep all dwellings, hospitals, ships, and other premises free from
these disgusting insects.
Dr. L. O. Howard, Chief of the Bureau of Entomology, United
States Department of Agriculture, and consultant United States
Public Health Service, has permitted the quotation of the following
passages from Farmer’s Bulletin No. 754, by C. L. Marlatt, which
gives an authoritative account of the habits, life history, and the
means of control of these insects.

“General Characteristics.
“The bedbug belongs to the order Hemiptera, which includes the
true bugs or piercing insects, characterized by possessing a piercing
and sucking beak. The bedbug is to man what the chinch bug is to
grains or the squash bug to cucurbs. Like nearly all the insects
parasitic on animals, however, it is degraded structurally, its parasitic
nature and the slight necessity for extensive locomotion having
resulted, after many ages doubtless, in the loss of wings and the
assumption of a comparatively simple structure. Before feeding, the
adult is much flattened, oval, and in color is rust red, with the
abdomen more or less tinged with black. When engorged, the body
becomes much bloated and elongated and brightly colored from the
ingested blood. The wings are represented by the merest rudiments,
barely recognizable pads, and the simple eyes or ocelli of most other
true bugs are lacking. The absence of wings is a most fortunate
circumstance, since otherwise there would be no safety from it even
for the most careful of housekeepers. Some slight variation in length
of wing pads has been observed, but none with wings showing any
considerable development has ever been found.

“Habits and Life History.

“The bedbug is normally nocturnal in habits and displays a certain
degree of wariness, caution, and intelligence in its efforts at
concealment during the day. Under the stress of hunger, however, it
will emerge from its place of concealment in a well-lighted room at
night, so that under such circumstances keeping the gas or electric
light burning is not a complete protection. It has been known under
similar conditions to attack human beings voraciously in broad
daylight. It usually leaves its victim as soon as it has become
engorged with blood and retires to its normal place of concealment,
either in cracks in the bedstead, especially if the latter be one of the
wooden variety, or behind wainscoting, or under loose wall paper;
and in these and similar places it manifests its gregarious habit by
collecting in masses. It thrives particularly in filthy apartments and in
old houses which are full of cracks and crevices, in which it can
conceal itself beyond easy reach. As just noted, the old-fashioned,
heavy, wooden-slatted bedsteads afford especially favorable
situations for the concealment and multiplication of this insect, and
the general use in later years of iron and brass bedsteads has very
greatly facilitated its eradication. Such beds, however, do not insure
safety, as the insects are able to find places of concealment even
about such beds, or get to them readily from their other hiding
places.
“The bedbug takes from 5 to 10 minutes to become bloated with
blood, and then retires to its place of concealment for 6 to 10 days
for the quiet digestion of its enormous meal, and for subsequent
molting, or reproduction if in the adult stage.”
“The eggs hatch in a week or 10 days in the hot weather of
midsummer, but cold may lengthen or even double this incubation
period or check development altogether. The young escape by
pushing up the lid-like top with its projecting rim. When first emerged,
they are yellowish white and nearly transparent, the brown color of
the more mature insect increasing with the later molts.”
“Unfavorable conditions of temperature and food will necessarily
result in great variation in the number of generations annually and in
the rate of multiplication, but allowing for reasonable checks on
development, there may be at least four successive broods in a year
in houses kept well heated in winter.”

“Food and Longevity.

“Under normal conditions the food of the common bedbug is
obtained from human beings only, and no other unforced feeding
habit has been reported. It is easily possible, however, to force the
bedbug to feed on mice, rats, birds, etc., and probably it may do so
occasionally in nature in the absence of its normal host. The
abundance of this insect in houses which have long been
untenanted may occasionally be accounted for by such other
sources of food, but probably normally such infestation can be
explained by the natural longevity of the insect and its ability to
survive for practically a year, and perhaps more, without food.”

“Influence of Temperature.
“As a messmate of human beings in dwelling houses, the bedbug
is normally protected from extreme cold and is known to be an
abundant and serious pest far north. In fact, it is often more
troublesome in north temperate latitudes than farther south. This
may be accounted for partly by the fact that the bedbug is very
sensitive to high temperatures, and a temperature of 96° to 100° F.
or more, accompanied with a fairly high degree of humidity, results in
the death of large numbers of the bugs. The mature or partly mature
bedbugs can stand comparatively low temperatures, even below
freezing, for a considerable period. The eggs and newly hatched
larvæ, however, succumb to a temperature below freezing, if this
condition is prolonged for from 15 days to a month. The feeding and
developing activity of the insect practically ceases at 60° F., the
insect remaining quiescent and in semihibernation at temperatures
below this point. The most favorable temperatures for activity are
between 60° and 98° F. The activity of the insect is controlled entirely
by temperature and food supply, and, therefore, in heated houses
the insect may remain active throughout the winter. There is some
protection in winter, therefore, in sleeping in cold bedrooms.”

“The Bite of the Bedbug.

“The bite of the bedbug is decidedly poisonous to some
individuals, resulting in a slight swelling and disagreeable
inflammation. To such persons the presence of bedbugs is sufficient
to cause the greatest uneasiness, if not to put sleep and rest entirely
out of the question. With others, however, who are less sensitive, the
presence of the bugs may not be recognized at all, and, except for
the occasional staining of the linen by a crushed individual, their
presence might be entirely overlooked. The inflammation
experienced by sensitive persons seems to result chiefly from the
puncture of the skin by the sharp piercing setæ which constitute the
puncturing element of the mouth parts, as there seems to be no
secretion of poison other than the natural fluids of the mouth.
“The biting organ of the bedbug is similar to that of other insects of
its order. It consists of a rather heavy, fleshy under lip (the only part
ordinarily seen in examining the insect), within which lie four thread-
like hard filaments or setæ which glide over one another with an
alternating motion and pierce the flesh. The blood is drawn up
through the beak, which is closely applied to the point of puncture,
and the alternating motion of the setæ in the flesh causes the blood
to flow more freely.
“To allay the irritation set up by the bite of the bedbug, peroxide of
hydrogen or dioxygen may be used with good results.
“Tincture of iodine either at ordinary or double strength is also a
good counterirritant for use in cases of flea, mosquito, bedbug, and
other insect bites, but should be used with caution on the tender skin
of small children and on those who are affected with or disposed to
eczemic disorders.”

“Natural Enemies of the Bedbug.

“Living always in houses as it does and being well concealed, the
bedbug is not normally subject to much if any control by natural
enemies. Certain other household insects, however, do occasionally
prey upon the bedbug, as, for example, the house centipede and the
common little red house ant. Such enemies, however, are of very
small importance and yield little, if any, effective control except under
very exceptional circumstances.”

“Remedies.
“Undoubtedly the most efficient remedy for the bedbug is to
fumigate the infested house or rooms with hydrocyanic-acid gas.
This gas will penetrate into every crevice in the house or room where
the bedbugs conceal themselves and has an immediate
effectiveness which gives it an important recommendation,
especially when the infestation is considerable or of long standing.
This method of fumigation should be intelligently employed, as the
gas is deadly poisonous.” Five ounces of potassium cyanide per
1,000 cubic feet of space should be employed; exposure, one hour.[2]
Ten ounces per 1,000 cubic feet would be better.
[2] Creel, R. H., and Faget, F. M., Cyanide Gas for the Destruction
of Insects, with Special Reference to Mosquitoes, Fleas, Body
Lice, and Bedbugs: Public Health Reports, June 9, 1916, pp.
1464–1475; Reprint No. 343.
“The fumes of burning sulphur are also a very efficient means of
control where the conditions are such that this method can be used,
readily destroying the insect in all stages, including the egg. The
treatment is inexpensive compared with the use of hydrocyanic-acid
gas and offers much less risk of danger to human beings. There is,
however, a considerable risk of injury to household fabrics,
furnishings, and wall papers from the strong bleaching quality of
sulphur fumes. This danger will be somewhat diminished if the
fumigation can be done at a time when the room or house is
thoroughly dried out, as in winter by a furnace or other heating
system. Further precautions should be taken by removing all metallic
surfaces from the room or building, or by protecting them with a
coating of vaseline.”
Four pounds of sulphur are recommended for each 1,000 cubic
feet of space, and the building should be closed for the treatment for
at least five or six hours. “Sulphur candles may be used where
available, or the sulphurous gas or fumes can be generated by
burning the sulphur in a dish placed in the center of the room, and
for protection set within a larger vessel. Thoroughgoing precautions
must be taken to prevent accidental overflowing or the starting of a
fire, and after the fumigation the house should be given a thorough
airing.
“Other gases have been experimented with, such as formalin and
the vapors of benzine, naphthalene, and camphor, but these gases
are of little value. Similarly, insect powders are of little value, largely
from the difficulty of getting them into the crevices and other places
of concealment of the insects.
“The old-fashioned household remedies referred to below are
effective enough, though at a greater cost of time and personal
effort. They will, however, be often of much service in the case of
slight or recent infestations, or where the employment of more
poisonous and troublesome gases is objected to or is impracticable.
Of these simple methods of control perhaps the most efficient is in
very liberal applications of benzine or kerosene, or any other of the
lighter petroleum oils, introduced with small brushes or feathers, or
by injecting with syringes into all crevices of beds, furniture, or walls
where the insects may have concealed themselves. Corrosive
sublimate is also of value, and oil of turpentine may be used in the
same way. The liberal use of hot water, wherever it may be
employed without danger to furniture, etc., is also an effectual
method of destroying both eggs and active bugs.[3] A 5 per cent
solution of compound solution of cresol (liquor cresolis compositus)
in kerosene forcibly applied with a large plant sprayer is effective if
frequently applied.
[3] “A remedy for the bedbug has been devised by Mr. R. H. Pettit
(‘Notes on two insecticidal agents,’ 10th Rpt. Mich. Acad. Sci., p.
159–160, 1908) as a substitute for hydrocyanic-acid gas and
sulphur, and is reported to have proved very successful. The
preparation of this insecticide and its application are described as
follows:
“Alcohol is drawn through pyrethrum in a funnel until the powder
is well washed and a large part of the resinous principle extracted.
To do this, the powder is placed in a large funnel with filter-plate
and a layer of cotton wool at the bottom. An aspirator is attached
and the alcohol is at first slowly and later rapidly sucked through
six or eight times, during which operation it becomes highly
colored. To this liquid as a basis, are added several oils to give
permanence to the application. Both alcohol and pyrethrum
evaporate so quickly that it was thought best to carry in some
heavier volatile oils whose effects would last several days or even
weeks. The formula when completed stands as follows:
“To the extract made by washing 400 grams of pyrethrum with
2,000 c. c. of strong alcohol, are added—

50 grams gum camphor.

150 c. c. cedar wood oil.
25 grams oil citronella.
25 grams oil lavender.

“The application is best made with a large-sized atomizer, one

holding a pint or more and working with a piston instead of a
rubber bulb. * * * To obtain the best results, repeat the treatment
after about two weeks. We have tried this mixture repeatedly and
with uniformly gratifying results. Usually one application, if
thoroughly made, put a period to the complaints, about eight to
ten ounces being required in an average sleeping room. The odor
remains some little time in a room, but is not disagreeable to the
average person.
“This remedy can be readily prepared by a pharmacist in any
drug store.”
“Various bedbug remedies and mixtures are for sale, most of them
containing one or another of the ingredients mentioned, and these
are frequently of value. The great desideratum, however, in a case of
this kind, is a daily inspection of beds and bedding, particularly the
seams and tufting of mattresses, and of all crevices and locations
about the premises where these vermin may have gone for
concealment. A vigorous campaign should, in the course of a week
or so at the outside, result in the extermination of this very obnoxious
and embarrassing pest.”
“Temperature control.—The possibility of temperature control is
indicated in the discussion elsewhere of the effect of temperature on
this insect. A temperature maintained below freezing for 10 or 15
days destroys the eggs, and this temperature continued for 15 days
to a month will destroy the newly hatched young. It may be,
therefore, that if infested houses in cold climates should be opened
up and allowed to remain at a temperature well below freezing for a
considerable period, all eggs and the young, and possibly most if not
all of the adults, would be exterminated. This method of control might
perhaps be practicable at least in the case of summer houses in the
North which are left untenanted in the winter.
“The maintaining of high temperatures may be an even more
efficient method of control. The activity of the bedbug is at its
greatest between 60° and 70° to 75°. As indicated elsewhere, in a
temperature of 96° to 100° F., accompanied with a high degree of
humidity, newly hatched bedbugs perish within a few days, and, if
this temperature is raised to 113° F., in a few minutes.[4] A
temperature of 113° will also destroy the eggs, and with these higher
temperatures the item of humidity is not apparently important.”
[4] Editorial note.—An account of successful use of live steam
to eradicate bedbugs in bunkhouses, as practiced by a lumber
company in Oregon, was published in Public Health Reports, Nov.
28, 1919, pp. 2713–2714. In that instance steam pipes were
tapped, after closing all doors and windows, and a temperature of
160° F. was held for approximately 3 hours. The officials of the
company stated that 2 months after the steaming no signs of
bedbugs had been found.
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Transcriber’s Notes:
Archaic and variable spelling has been preserved.
Variations in hyphenation and compound words have been
preserved.
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