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 CLINICAL OUTLINE OF ORAL
PATHOLOGY: DIAGNOSIS
AND TREATMENT

FOURTH EDITION

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PMPH_Eversole_FM.indd ii 1/25/2011 9:48:09 PM
 CLINICAL OUTLINE OF ORAL
PATHOLOGY: DIAGNOSIS
AND TREATMENT
FOURTH EDITION
Lewis R. Eversole

2011
PEOPLE’S MEDICAL PUBLISHING HOUSE–USA
SHELTON, CONNECTICUT

PMPH_Eversole_FM.indd iii 1/25/2011 9:48:09 PM

 People’s Medical Publishing House-USA
2 Enterprise Drive, Suite 509
Shelton, CT 06484
Tel: 203-402-0646
Fax: 203-402-0854
E-mail: [email protected]

© 2011 PMPH-USA, Ltd.

All rights reserved. Without limiting the rights under copyright reserved above, no part of this publication may be reproduced,
stored in or introduced into 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 publisher.

11 12 13 14/PMPH/9 8 7 6 5 4 3 2 1

ISBN: 978-1-60795-015-8

Printed in China by People’s Medical Publishing House

Editor: Jason Malley; Copyeditor/Typesetter: Newgen

Library of Congress Cataloging-in-Publication Data

Eversole, Lewis R.
Clinical outline of oral pathology : diagnosis and treatment / Lewis R. Eversole. — 4th ed.
p. ; cm.
ISBN 978-1-60795-015-8
1. Mouth—Diseases. 2. Teeth—Diseases. I. Title.
[DNLM: 1. Diagnosis, Oral. 2. Mouth Diseases—diagnosis. 3. Diagnosis, Differential.
4. Mouth Diseases—therapy. WU 140]
RC815.E9 2010
616.3’1—dc22
2010051383

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PMPH_Eversole_FM.indd iv 1/25/2011 9:48:09 PM

 Contents
1. THE DIAGNOSTIC PROCESS 1

Procurement of the Data Base 2 Assessment of the Findings 5

CHIEF COMPLAINT AND HISTORY OF THE Formulating a Differential
PRESENT ILLNESS 2
Diagnosis 5
MEDICAL AND DENTAL HISTORY 3
PHYSICAL EXAMINATION 4 Securing a Definitive Diagnosis 6
RADIOGRAPHIC EXAMINATION 4
CLINICAL LABORATORY TESTS 4 Formulating a Treatment Plan 7

2. WHITE LESIONS 9

Flat Plaques, Solitary 11 PROLIFERATIVE VERRUCOUS

LEUKOPLAKIA 31
FRICTIONAL BENIGN KERATOSES 11 VERRUCOUS CARCINOMA 33
LEUKOPLAKIA 12
ACTINIC CHEILITIS 14 Lacey White Lesions 34
SMOKELESS TOBACCO KERATOSES 14 LICHEN PLANUS 34
SANGUINARIA-INDUCED KERATOSES 16 LICHENOID REACTIONS 36
DYSKERATOSIS CONGENITA 17 LUPUS ERYTHEMATOSUS 37
FANCONI’S ANEMIA 18
HIV-ASSOCIATED HAIRY LEUKOPLAKIA 38
DYSPLASIA, CARCINOMA IN SITU,
SQUAMOUS CELL CARCINOMA, AND Papular Lesions 40
VERRUCOUS CARCINOMA 19
LICHEN PLANUS (HYPERTROPHIC TYPE) 21 KOPLIK SPOTS OF MEASLES 40
MUCOUS PATCHES (SECONDARY FORDYCE’S GRANULES 41
SYPHILIS) 22 DENTAL LAMINA CYSTS, BOHN’S NODULES,
EPSTEIN’S PEARLS 41
Flat Plaques, Bilateral or STOMATITIS NICOTINA 42
Multifocal 23
SPECKLED LEUKOPLAKIA 43
LEUKOEDEMA 23
GENOKERATOSES 24 Pseudomembranous Lesions 44
PLAQUE-FORM LICHEN PLANUS (SEE CHEMICAL BURNS 44
ABOVE) 30
CANDIDIASIS (MONILIASIS, THRUSH) 45
CHEEK/TONGUE BITE KERATOSIS 30
VESICULO-BULLOUS-ULCERATIVE
Verrucous/Rippled Plaques 31 DISEASES 47

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 vi Contents

3. RED AND PIGMENTED LESIONS 49

Focal Erythemas 51 Petechiae 73

NONSPECIFIC (IRRITATIONAL) SUCTION PETECHIAE 73
MUCOSITIS 51 INFECTIOUS MONONUCLEOSIS 74
MEDIAN RHOMBOID GLOSSITIS 52 THROMBOCYTE DISORDERS 75
HEMANGIOMA 53 HEREDITARY HEMORRHAGIC
VARIX 54 TELANGIECTASIA 76
ERYTHROPLAKIA 55
Focal Pigmentations 77
Diffuse and Multifocal Red Lesions 56 AMALGAM AND GRAPHITE TATTOO 77
GEOGRAPHIC TONGUE (MIGRATORY MUCOCELE 78
GLOSSITIS) 56 HEMATOMA 79
ERYTHEMA MIGRANS (MIGRATORY NEVUS 80
STOMATITIS) 57 EPHELIS, ORAL MELANOTIC MACULE 81
ATROPHIC GLOSSITIS 58
RADIATION MUCOSITIS 59
Diffuse and Multifocal
Pigmentations 82
XEROSTOMIC MUCOSITIS 60
LUPUS ERYTHEMATOSUS 61 MALIGNANT MELANOMA 82
ALLERGIC MUCOSITIS, FOREIGN BODY RACIAL PIGMENTATION 83
GINGIVITIS 63 PIGMENTED LICHEN PLANUS 84
BULLOUS/EROSIVE DISEASES 64 PEUTZ-JEGHERS SYNDROME 85
CANDIDIASIS 65 MULTIPLE NEUROFIBROMATOSIS 86
LYMPHONODULAR PHARYNGITIS 67 ADDISON’S DISEASE 87
SCARLET FEVER 67 HEMOCHROMATOSIS 88
ATROPHIC LICHEN PLANUS 68 HIV-ASSOCIATED ORAL
PIGMENTATION 89
ECCHYMOSIS AND CLOTTING FACTOR
DEFICIENCIES 70 HEAVY METAL INGESTION 90
FIELD CANCERIZATION 71 DRUG-INDUCED PIGMENTATION 91
KAPOSI’S SARCOMA 72 HAIRY TONGUE 92

4. ORAL ULCERATIONS AND FISTULAE 95

Recurrent and Multiple ACUTE NECROTIZING ULCERATIVE

GINGIVITIS 105
Ulcerations 96
ACUTE STREPTOCOCCAL/
APHTHOUS STOMATITIS 96 STAPHYLOCOCCAL STOMATITIS 106
MAJOR SCARRING APHTHOUS CHRONIC ULCERATIVE STOMATITIS 107
STOMATITIS 97 GONOCOCCAL STOMATITIS 107
BEHÇET’S SYNDROME 99 HIV PERIODONTITIS AND ORAL
GLUTEN ENTEROPATHY 100 ULCERATIONS 108
AGRANULOCYTOSIS AND
IMMUNOSUPPRESSION 100 Focal Ulcerations 109
CYCLIC NEUTROPENIA 101 TRAUMATIC ULCER 109
UREMIC STOMATITIS 102 TRAUMATIC GRANULOMA WITH STROMAL
VIRAL VESICULAR STOMATITIS 103 EOSINOPHILIA 111

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 Contents vii

ATYPICAL HISTIOCYTIC GRANULOMA 112 OROANTRAL FISTULA 122

NECROTIZING SIALOMETAPLASIA 113 SOFT TISSUE ABSCESS 123
SPECIFIC GRANULOMATOUS ULCER 114 DEVELOPMENTAL ORAL SINUSES 124
CHANCRE (PRIMARY SYPHILIS) 115 FISSURED (SCROTAL) TONGUE 125
SQUAMOUS CELL CARCINOMA 116
Perioral and Commissural Necrotic and Osseous Destructive
Lesions 126
Ulcerations and Fistulae 117
FACTITIAL INJURY AND TRAUMA 126
COMMISSURAL PITS 117
WEGENER’S GRANULOMATOSIS 127
CONGENITAL LIP PITS 118
EXTRANODAL NK/T-CELL LYMPHOMA 128
ANGULAR CHEILITIS 119
TERTIARY SYPHILIS 129
Oral Fistulae 120 OSTEORADIONECROSIS 130
PERIAPICAL ABSCESS AND MUCORMYCOSIS 131
OSTEOMYELITIS 120 ANTRAL CARCINOMA 132
PERIODONTAL ABSCESS 121 BISPHOSPHONATE-RELATED
ACTINOMYCOSIS 122 OSTEONECROSIS OF THE JAWS 133

5. VESICULOBULLOUS AND DESQUAMATIVE LESIONS 137

Febrile-Associated Vesicular BULLOUS PEMPHIGOID 151

Eruptions 139 BENIGN MUCOUS MEMBRANE
PEMPHIGOID 152
HERPETIC GINGIVOSTOMATITIS 139 BULLOUS LICHEN PLANUS 154
HERPANGINA 140 ERYTHEMA MULTIFORME 155
HAND-FOOT-AND-MOUTH DISEASE 141 STEVENS-JOHNSON SYNDROME 156
PRIMARY VARICELLA-ZOSTER PARANEOPLASTIC PEMPHIGUS 157
(CHICKENPOX) 143 ANGINA BULLOSA HEMORRHAGICA 158
SECONDARY VARICELLA-ZOSTER EPIDERMOLYSIS BULLOSA 159
(SHINGLES) 144 DERMATITIS HERPETIFORMIS (GLUTEN
Nonfebrile-Associated Vesicular ENTEROPATHY) 161
Eruptions 145 Desquamative Lesions 161
RECURRENT HERPES STOMATITIS 145 GINGIVOSIS (DESQUAMATIVE
RECURRENT HERPES LABIALIS 146 GINGIVITIS) 161
CONTACT VESICULAR STOMATITIS 148 EROSIVE LICHEN PLANUS 163
IMPETIGO 149 LICHENOID CONTACT STOMATITIS 164
CHRONIC ULCERATIVE STOMATITIS 165
Bullous Diseases 150
PYOSTOMATITIS VEGETANS 166
PEMPHIGUS VULGARIS 150 TOOTHPASTE IDIOSYNCRATIC LESIONS 168

6. INTRAORAL SOFT TISSUE SWELLINGS 171

Localized Gingival Tumefactions 173 PERIPHERAL GIANT CELL GRANULOMA 176

PERIPHERAL FIBROMA 177
PARULIS 173 GIANT CELL FIBROMA 178
PYOGENIC GRANULOMA 175 PERIPHERAL OSSIFYING FIBROMA 179

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 viii Contents

JUVENILE SPONGIOTIC GINGIVAL CHEILITIS GLANDULARIS 217

HYPERPLASIA 180 ANGIONEUROTIC EDEMA 218
RETROCUSPID PAPILLAE 181 ACTINIC PRURIGO 219
TORUS MANDIBULARIS AND INFLAMMATORY FIBROUS HYPERPLASIA 220
EXOSTOSES 181 FOREIGN BODY GRANULOMA 220
GINGIVAL CYST 183 CROHN’S DISEASE 221
ERUPTION CYST 184 TRAUMATIC FIBROMA 222
EPULIS FISSURATA 185 TRAUMATIC (AMPUTATION) NEUROMA 224
CONGENITAL EPULIS 185 MESENCHYMAL NEOPLASMS 224
MESENCHYMAL TUMORS 187 HERNIATED BUCCAL FAT PAD 225
PERIPHERAL ODONTOGENIC TUMORS 188 REACTIVE LYMPHOID HYPERPLASIA 226
SQUAMOUS CELL CARCINOMA 189 HEMANGIOMA AND VARIX 227
SARCOMAS 190 SQUAMOUS CELL CARCINOMA 229
MUCOEPIDERMOID CARCINOMA 191 MONOMORPHIC ADENOMA 230
NON-HODGKIN’S LYMPHOMA 192 OTHER SALIVARY NEOPLASMS 231
METASTATIC CARCINOMA 193
LANGERHANS CELL HISTIOCYTOSIS 194 Tongue Swellings 232

Generalized Gingival Swellings 195 MEDIAN RHOMBOID GLOSSITIS 232

ECTOPIC LINGUAL THYROID 233
FIBROMATOSIS GINGIVAE 195 THYROGLOSSAL DUCT CYST 234
DRUG INDUCED HYPERPLASIA 196 LINGUAL CYST (ENTEROCYSTOMA, GASTRIC
NONSPECIFIC HYPERPLASTIC CYST) 235
GINGIVITIS 197 HYPERPLASTIC LINGUAL TONSIL 236
WEGENER’S GRANULOMATOSIS 198 LINGUAL ABSCESS 237
TYPE I DIABETES MELLITUS 199 REACTIVE LESIONS (FIBROMA, PYOGENIC
PUBERTY/PREGNANCY GINGIVITIS 200 GRANULOMA) 237
LEUKEMIA 201 MUCOCELE 238
Swellings of the Oral Floor 202 HEMANGIOMA AND LYMPHANGIOMA 239
NEURAL SHEATH TUMORS 241
RANULA AND SIALOCYSTS 202 GRANULAR CELL TUMOR 242
DISONTOGENIC CYSTS 203 LEIOMYOMA 243
LYMPHOEPITHELIAL CYST 204 OSTEOCARTILAGINOUS CHORISTOMA 244
SIALOLITHIASIS WITH SIALADENITIS 205 ECTOMESENCHYMAL CHONDROMYXOID
SALIVARY GLAND TUMORS 207 TUMOR 245
ADENOMATOID HYPERPLASIA 207 SARCOMAS 245
MESENCHYMAL NEOPLASMS 208 AMYLOID NODULES 246
LUDWIG’S ANGINA 209 SPECIFIC GRANULOMA 247
SQUAMOUS CELL CARCINOMA 210 SQUAMOUS CELL CARCINOMA 248
Swellings of the Lips and Buccal Palatal Swellings 250
Mucosa 211 TORUS PALATINUS 250
MUCOUS RETENTION (EXTRAVASATION) CYST OF THE INCISIVE PAPILLA 251
PHENOMENON (MUCOCELE) 211 PALATAL ABSCESS 251
SIALOCYST 213 REACTIVE LESIONS OF PALATAL
MINOR GLAND SIALOLITHIASIS 214 GINGIVAL 252
NASOALVEOLAR (KLESTADT) CYST 215 ADENOMATOUS HYPERPLASIA 252
CHEILITIS GRANULOMATOSA 216 PLEOMORPHIC ADENOMA 253

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 Contents ix

POLYMORPHOUS LOW-GRADE ADENOCARCINOMA, NOS 259

ADENOCARCINOMA 254 ATYPICAL LYMPHOPROLIFERATIVE
MISCELLANEOUS ADENOCARCINOMAS 255 DISEASE 259
ADENOID CYSTIC CARCINOMA 256 SQUAMOUS CELL CARCINOMA 261
MUCOEPIDERMOID CARCINOMA 258 CARCINOMA OF THE ANTRUM 262

7. PAPILLARY, PAPULAR, AND MULTIPLE POLYPOID LESIONS 265

Focal Papillary Lesions 267 PAPILLARY SQUAMOUS CELL

CARCINOMA 281
PAPILLOMA 267
VERRUCA VULGARIS 268
Diffuse Papular and Polypoid
Lesions 282
CONDYLOMA ACUMINATUM 269
VERRUCIFORM XANTHOMA 270 PAPILLARY HYPERPLASIA 282
SIALADENOMA PAPILLIFERUM 271 STOMATITIS NICOTINA 283
GIANT CELL FIBROMA 272 ACUTE LYMPHONODULAR
SQUAMOUS ACANTHOMA 273 PHARYNGITIS 284
KERATOSIS FOLLICULARIS 284
Focal and Umbilicated Papules 273 FOCAL EPITHELIAL HYPERPLASIA
(HECK’S DISEASE) 285
KERATOACANTHOMA 273
MULTIPLE HAMARTOMA (COWDEN)
WARTY DYSKERATOMA 274
SYNDROME 286
MOLLUSCUM CONTAGIOSUM 275 PYOSTOMATITIS VEGETANS 287
Diffuse and Multifocal Papillary CROHN’S DISEASE 288
Lesions 276 SPECIFIC GRANULOMATOUS
INFECTIONS 289
FOCAL DERMAL HYPOPLASIA (GOLTZ AMYLOIDOSIS 290
SYNDROME) 276 HYALINOSIS CUTIS ET MUCOSAE
NEVUS UNIUS LATERIS 277 (LIPOID PROTEINOSIS) 291
ACANTHOSIS NIGRICANS 278 HEMANGIOMA/LYMPHANGIOMA 292
ATYPICAL VERRUCOUS MULTIPLE ENDOCRINE NEOPLASIA,
LEUKOPLAKIA 278 TYPE IIB 293
VERRUCOUS CARCINOMA 280 DENTAL LAMINA CYSTS 294

8. SOFT TISSUE SWELLINGS OF THE NECK AND FACE 297

Lateral Neck Swellings 300 ACTINOMYCOSIS 306

REACTIVE PROLIFERATIONS 307
BRANCHIAL CLEFT CYST 300 SINUS HISTIOCYTOSIS 308
CERVICAL RIB AND TRANSVERSE BENIGN MESENCHYMAL TUMORS 309
PROCESS 301 CYSTIC HYGROMA (LYMPHANGIOMA) 310
NONSPECIFIC LYMPHADENITIS 301 CAROTID BODY TUMOR
INFECTIOUS MONONUCLEOSIS 303 (CHEMODECTOMA) 311
TUBERCULOUS LYMPHADENITIS METASTATIC CARCINOMA 312
(SCROFULA) 304 SARCOMAS 314
CAT-SCRATCH FEVER 305 MALIGNANT LYMPHOMA 315

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 x Contents

Unilateral Parotid and DYSGENETIC CYSTS OF THE PAROTID 338

Submandibular Swellings 316 METABOLIC SIALADENOSIS 339

ACUTE SIALADENITIS (SURGICAL Midline Neck Swellings 340

MUMPS) 316
THYROGLOSSAL TRACT CYST 340
SIALOLITHIASIS AND OBSTRUCTIVE
GOITER 341
SIALADENITIS 317
CHRONIC SIALADENITIS 318 THYROID NEOPLASIA 342
INTRAPAROTID MESENCHYMAL DERMOID CYST 343
TUMORS 319
LYMPHOMA 320
Growths and Swellings of the
Facial Skin 344
PLEOMORPHIC ADENOMA 322
PAPILLARY CYSTADENOMA NEVI 344
LYMPHOMATOSUM 323 SEBACEOUS CYST 345
ONCOCYTOMA 324 SEBORRHEIC KERATOSIS 346
MISCELLANEOUS ADENOMAS 325 ADNEXAL SKIN TUMORS 347
ADENOID CYSTIC CARCINOMA 326 BASAL CELL CARCINOMA 348
MUCOEPIDERMOID CARCINOMA 327 SQUAMOUS CELL CARCINOMA 350
ACINIC CELL CARCINOMA 329 KERATOACANTHOMA 351
ADENOCARCINOMA NOS AND MESENCHYMAL TUMORS 352
MISCELLANEOUS MALIGNANCIES 330
MALIGNANT MELANOMA 353
Bilateral Parotid and Submandibular
Swellings 332
Diffuse Facial Swellings 354
CELLULITIS AND SPACE INFECTIONS 354
ENDEMIC PAROTITIS (MUMPS) 332
SJÖGREN’S SYNDROME 333 EMPHYSEMA 355
MIKULICZ’S DISEASE 334 ANGIONEUROTIC EDEMA 356
SARCOID SIALADENITIS AND HEERFORDT’S CUSHING’S SYNDROME 357
SYNDROME 335 FACIAL HEMIHYPERTROPHY 358
TUBERCULOSIS 336 FIBROUS DYSPLASIA AND OTHER BONE
HIV SALIVARY DISEASE (DIFFUSE INFILTRATIVE LESIONS 359
LYMPHOCYTOSIS SYNDROME) 337 MASSETERIC HYPERTROPHY 360

9. RADIOLUCENT LESIONS OF THE JAWS 363

Periapical Radiolucencies 366 STATIC BONE CYST (SUBMANDIBULAR

GLAND DEPRESSION) 377
APICAL PERIODONTITIS (ABSCESS, SUBLINGUAL GLAND DEPRESSION 377
GRANULOMA, AND CYST) 366 PARADENTAL (BUCCAL INFECTED)
PERIAPICAL CEMENTAL DYSPLASIA 367 CYST 379
FOCAL CEMENTO-OSSEOUS CENTRAL GIANT CELL GRANULOMA 380
DYSPLASIA 369 MALIGNANCIES 380
FOCAL SCLEROSING OSTEOMYELITIS 371
BENIGN CEMENTOBLASTOMA 371 Interradicular Radiolucencies 383
INCISIVE CANAL CYST 372 LATERAL PERIODONTAL CYST 383
MEDIAN MANDIBULAR CYST 375 LATERALLY DISPLACED APICAL
TRAUMATIC (HEMORRHAGIC) CYST 375 PERIODONTAL CYST OR GRANULOMA 384

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 Contents xi

RESIDUAL CYST 385 Multilocular Radiolucencies 423

ODONTOGENIC KERATOCYST 386
PRIMORDIAL CYST 386 ODONTOGENIC KERATOCYST 423
CALCIFYING CYSTIC ODONTOGENIC BOTRYOID ODONTOGENIC CYST 425
TUMOR 388 GLANDULAR ODONTOGENIC CYST 425
SQUAMOUS ODONTOGENIC TUMOR 389 CHERUBISM (FAMILIAL FIBROUS
SURGICAL CILIATED CYST 391 DYSPLASIA) 427
OSTEOPOROTIC BONE MARROW CENTRAL GIANT CELL GRANULOMA 429
DEFECT 392 ANEURYSMAL BONE CYST 429
CENTRAL OSSIFYING (CEMENTIFYING) HYPERPARATHYROIDISM 431
FIBROMA 393 AMELOBLASTOMA 432
ODONTOGENIC ADENOMATOID MYXOMA 433
TUMOR 394 CENTRAL NEUROGENIC NEOPLASMS 434
ODONTOGENIC FIBROMA 396 CENTRAL ARTERIOVENOUS
CENTRAL GIANT CELL GRANULOMA 397 MALFORMATION 436
Periodontal (Alveolar) Bone Loss 398 CENTRAL (LOW FLOW) HEMANGIOMA OF
BONE 437
CHRONIC PERIODONTITIS 398 CENTRAL LEIOMYOMA 438
DIABETIC PERIODONTITIS 400 PSEUDOTUMOR OF HEMOPHILIA 439
JUVENILE PERIODONTITIS AND PAPILLON- MYOFIBROMATOSIS (DESMOPLASTIC
LEFEVRE SYNDROME 401 FIBROMA OF BONE) 440
VANISHING BONE DISEASE (MASSIVE FIBROUS DYSPLASIA 442
OSTEOLYSIS) 402 INTRAOSSEOUS MUCOEPIDERMOID
LANGERHANS CELL HISTIOCYTOSIS 403 CARCINOMA 443
CYCLIC NEUTROPENIA 405 THALASSEMIA MAJOR 443
LEUKEMIA 406
Moth-Eaten Radiolucencies 443
Widened Periodontal Ligament OSTEOMYELITIS 443
Space 407
OSTEORADIONECROSIS 445
PERIODONTIC/ENDODONTIC BISPHOSPHONATE-RELATED
INFLAMMATION 407 OSTEONECROSIS OF THE JAWS
SCLERODERMA 409 (BRONJ) 446
OSTEOGENIC SARCOMA 410 PRIMARY INTRAOSSEOUS CARCINOMA 448
CYSTOGENIC CARCINOMA 449
Pericoronal Radiolucencies 411
METASTATIC CARCINOMA 450
DENTIGEROUS CYST 411 MALIGNANT ODONTOGENIC TUMORS 452
ODONTOGENIC KERATOCYST 413 OSTEOSARCOMA AND
GLANDULAR ODONTOGENIC CYST 414 CHONDROSARCOMA 453
UNICYSTIC AMELOBLASTOMA 414 EWING’S SARCOMA 455
CALCIFYING EPITHELIAL ODONTOGENIC PRIMARY LYMPHOMA OF BONE 456
TUMOR 417 BURKITT’S LYMPHOMA 457
ODONTOGENIC ADENOMATOID FIBROGENIC AND NEUROGENIC
TUMOR 417 SARCOMA 458
AMELOBLASTIC FIBROMA 419 MELANOTIC NEUROECTODERMAL TUMOR
ODONTOGENIC FIBROMA-LIKE OF INFANCY 459
HAMARTOMA/ENAMEL HYPOPLASIA 420
CENTRAL MUCOEPIDERMOID
Multifocal Radiolucencies 461
CARCINOMA 421 BASAL CELL NEVUS SYNDROME 461

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LANGERHANS CELL HISTIOCYTOSIS 462 SENILE OSTEOPOROSIS 466

MULTIPLE MYELOMA 463 STEROID OSTEOPOROSIS 467
SICKLE CELL ANEMIA 468
Generalized Osteoporotic THALASSEMIA MAJOR 469
Lesions 465
OSTEOMALACIA 465

10. RADIOPAQUE LESIONS OF THE JAWS 473

Periapical Radiopacities 475 ANTRAL INVASIVE MYCOSES 506

FUNGUS BALL (ASPERGILLUS
PERIAPICAL CEMENTAL DYSPLASIA 475 MYCETOMA) 507
FOCAL CEMENTO-OSSEOUS DYSPLASIA 477 ALLERGIC FUNGAL SINUSITIS 508
FOCAL SCLEROSING OSTEOMYELITIS 479 DISPLACED TEETH, ROOTS, AND FOREIGN
FOCAL PERIAPICAL OSTEOSCLEROSIS 480 BODIES 509
BENIGN CEMENTOBLASTOMA 481 AUGMENTATION MATERIALS 510
ANTROLITH/RHINOLITH 511
Inter-Radicular Radiopacities 482
ODONTOGENIC TUMORS 512
RESIDUAL FOCAL OSTEITIS AND OSTEOMAS AND EXOSTOSES 513
CEMENTOMA 482 BENIGN MESENCHYMAL NEOPLASMS 515
IDIOPATHIC OSTEOSCLEROSIS 483 INVERTING PAPILLOMA 516
BISPHOSPHONATE-RELATED ANTRAL CARCINOMA 517
OSTEONECROSIS OF THE JAWS 484 ANTRAL SARCOMA 519
CALCIFYING AND KERATINIZING EPITHELIAL SILENT SINUS SYNDROME 520
ODONTOGENIC CYST/TUMOR 486
ODONTOGENIC ADENOMATOID Ground-Glass Radiopacities 521
TUMOR 486
ODONTOMA 489 FIBROUS DYSPLASIA 521
CENTRAL OSSIFYING OR CEMENTIFYING CHRONIC DIFFUSE SCLEROSING
FIBROMA 489 OSTEOMYELITIS 523
BENIGN OSTEOBLASTOMA 492 OSTEITIS DEFORMANS (PAGET’S DISEASE OF
BONE) 524
Pericoronal Radiopacities 493 HYPERPARATHYROIDISM 526
SEGMENTAL ODONTOMAXILLARY
ODONTOGENIC ADENOMATOID
DYSPLASIA 528
TUMOR 493
OSTEOPETROSIS 529
CALCIFYING EPITHELIAL ODONTOGENIC
TUMOR 494 Multifocal Confluent (Cotton-Wool)
AMELOBLASTIC FIBRODENTINOMA 496 Radiopacities 530
AMELOBLASTIC FIBRO-ODONTOMA 497
ODONTOMA 498 OSTEITIS DEFORMANS (PAGET’S DISEASE OF
ODONTOAMELOBLASTOMA 499 BONE) 530
FLORID OSSEOUS DYSPLASIA 531
Antral Opacities 500 GARDNER’S SYNDROME 533
MAXILLARY SINUSITIS 500 FAMILIAL GIGANTIFORM CEMENTOMA 534
ANTRAL POLYP 502 Cortical Redundancies (Onion-Skin
SINUS MUCOCELE 503 Patterns) 536
PERIAPICAL INFECTION WITH ANTRAL
POLYPS 504 GARRÉ’S PERIOSTITIS 536

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 Contents xiii

INFANTILE CORTICAL HYPEROSTOSIS 537 OSTEOGENIC AND CHONDROGENIC

GENERALIZED CORTICAL SARCOMA 545
HYPEROSTOSIS 538 METASTATIC CARCINOMA 546
JUXTACORTICAL OSTEOGENIC
SARCOMA 539
Superimposed Soft Tissue
Radiopacities 547
OSTEOID OSTEOMA 540
MANDIBULAR TORI AND EXOSTOSES 541 SIALOLITHIASIS 547
PHLEBOLITHIASIS 548
Irregular, Ill-Defined Expansile OSSEOUS/CARTILAGINOUS
Radiopacities 542 CHORISTOMA 549
CALCIFYING EPITHELIAL ODONTOGENIC FOREIGN BODIES 550
TUMOR 542 CALCIFIED LYMPH NODES 551
DESMOPLASTIC AMELOBLASTOMA 543 MYOSITIS OSSIFICANS 552

11. DENTAL DEFECTS 555

Alterations in Number: Missing EROSION 575

Teeth 558 HYPERCEMENTOSIS 576

HYPODONTIA 558 Alterations in Structure 577

INCONTINENTIA PIGMENTI 559 DENTAL CARIES 577
HYALINOSIS CUTIS ET MUCOSAE 559 ENAMEL HYPOPLASIA 579
MANDIBULO-OCULO-FACIAL CONGENITAL SYPHILIS 580
DYSCEPHALY 560
DENTAL FLUOROSIS 581
HEREDITARY ECTODERMAL DYSPLASIA 560
SNOW-CAPPED TEETH 582
CHONDROECTODERMAL DYSPLASIA 561
AMELOGENESIS IMPERFECTA, HYPOPLASTIC
Alterations in Number: TYPES 582
Supernumerary Teeth 562 AMELOGENESIS IMPERFECTA,
HYPOMATURATION/HYPOCALCIFICATION
HYPERDONTIA 562 TYPES 584
CLEIDOCRANIAL DYSPLASIA 563 SYNDROME-ASSOCIATED ENAMEL
GARDNER’S SYNDROME 564 DEFECTS 585
DENTINOGENESIS IMPERFECTA 587
Alterations in Morphology 565
OSTEOGENESIS IMPERFECTA 588
MICRODONTIA AND MACRODONTIA 565 DENTIN DYSPLASIA TYPE I 589
ACCESSORY CUSPS AND ROOTS 566 DENTIN DYSPLASIA TYPE II 590
DENTAL TRANSPOSITION 567 REGIONAL ODONTODYSPLASIA 591
ENAMEL PEARL 568 HYPOPHOSPHATASIA 593
DILACERATION 568 VITAMIN D REFRACTORY RICKETS 593
DENS INVAGINATUS (DENS IN DENTE) 570 DENTICLES AND PULP CALCIFICATION 595
TAURODONTISM 571 SEGMENTAL ODONTOMAXILLARY
GEMINATION 571 DYSPLASIA 595
FUSION 572 INTERNAL RESORPTION 597
CONCRESCENCE 573 EXTERNAL RESORPTION 598
ATTRITION 574 SUBCERVICAL RESORPTION 599
ABRASION 575 CORONAL FRACTURE 600

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Alterations in Eruption/Exfoliation BILIARY ATRESIA 604

Times 601 POSTMORTEM PINK TEETH 605
PORPHYRIA 605
PREMATURE ERUPTION 601 DENTAL FLUOROSIS 606
DELAYED ERUPTION 601 TETRACYCLINE STAINING 607
IMPACTION 602 EXTRINSIC STAINING 608
PREMATURE EXFOLIATION 603 FOCAL PIGMENTATION 609
Pigmentations 603
ERYTHROBLASTOSIS FETALIS 603

12. FACIAL PAIN AND NEUROMUSCULAR DISORDERS 611

Ophthalmic Division Pain 614 Neck and Throat Pain 638

ODONTOGENIC INFECTION 614 STYLOHYOID SYNDROME (EAGLE’S
FRONTAL/ETHMOIDAL SINUSITIS 615 SYNDROME) 638
VASCULAR OCCLUSIVE DISEASE AND HYOID SYNDROME 638
ANEURYSMS 616 GLOSSOPHARYNGEAL NEURALGIA 639
CAROTIDYNIA 640
Maxillary Division Pain 616
SUPERIOR LARYNGEAL NEURALGIA 641
ODONTOGENIC INFECTION 616 LARYNGEAL NEOPLASMS 641
MAXILLARY SINUSITIS 617
PATHOLOGIC JAWBONE CAVITIES 619 TMJ Region Pain 642
ANTRAL AND MAXILLARY NEOPLASMS 620 MYOGENIC PAIN 642
CLUSTER HEADACHE 621 TYPE I INTERNAL DERANGEMENT
TRIGEMINAL NEURALGIA 623 (REDUCING) 644
POSTHERPETIC NEURALGIA 624 TYPE II INTERNAL DERANGEMENT
COMPLEX REGIONAL PAIN SYNDROME (TRANSIENT LOCK) 646
(CAUSALGIA) 625 TYPE III INTERNAL DERANGEMENT (CLOSED
CRANIAL BASE AND CNS NEOPLASMS 626 LOCK) 647
ATYPICAL FACIAL PAIN 628 MENISCUS PERFORATION 648
OSTEOARTHRITIS (DEGENERATIVE JOINT
Mandibular Division Pain 629 DISEASE) 649
ODONTOGENIC INFECTION 629 RHEUMATOID ARTHRITIS 650
OSTEOMYELITIS 630 ACUTE INFECTIOUS ARTHRITIDES 651
TRAUMATIC NEUROMA 631 MISCELLANEOUS ARTHRITIDES 652
SUBACUTE THYROIDITIS 632 CONDYLAR FRACTURE 653
STOMATODYNIA/GLOSSOPYROSIS 633 SYNOVIAL CHONDROMATOSIS 654
CARDIOGENIC FACIAL PAIN 634 PIGMENTED VILLONODULAR
SYNOVITIS 655
Otogenic Pain 634
ACUTE OTITIS MEDIA 634
Sialogenic Pain 656

CHRONIC OTITIS MEDIA 635 SIALOLITHIASIS 656

HERPES ZOSTER OTICUS 636 ENDEMIC PAROTITIS (MUMPS) 657
MIDDLE EAR NEOPLASMS 637 ACUTE SUPPURATIVE SIALADENITIS 658

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 Contents xv

Temporal Pain 659 CONVERSION TRISMUS 671

ANKYLOSIS 671
MIGRAINE 659 HECHT-BEALS-WILSON SYNDROME 672
MYOGENIC PAIN (TENSION HEADACHE) 659 CORONOID HYPERPLASIA 673
GIANT CELL ARTERITIS 660 CONDYLAR HYPERPLASIA 673
Paresthesia 661 TMJ REGION NEOPLASMS 674
SCLERODERMA 676
MENTAL PARESTHESIA 661
ORAL SUBMUCOUS FIBROSIS 676
INFRAORBITAL PARESTHESIA 662
TETANUS 677
Localized Motor Deficits 664
Generalized Motor Function
FACIAL PARALYSIS 664 Disorders 678
HORNER’S SYNDROME 665
OPHTHALMOPLEGIA 666 AURICULOTEMPORAL SYNDROME 678
HYPOGLOSSAL PARALYSIS 667 JAW-WINKING PHENOMENON 679
SOFT PALATE PARALYSIS 668 MOTOR SYSTEM DISEASE 680
MULTIPLE SCLEROSIS 680
Limited and Deviant Mandibular MUSCULAR DYSTROPHIES 681
Opening 669 MYOTONIAS 682
MUSCLE SPLINTING 669 CONGENITAL FACIAL DIPLEGIA 683
POSTINJECTION/POSTINFECTION HEMIFACIAL ATROPHY 683
TRISMUS 670 MYASTHENIA GRAVIS 684

Appendix I 685

Appendix II 688

Appendix III 688

Appendix IV 689

Appendix V 694

Index 701

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PMPH_Eversole_FM.indd xvi 1/25/2011 9:48:11 PM
 The Diagnostic
Process 1
Procurement of the Data Base 2
CHIEF COMPLAINT AND HISTORY OF THE PRESENT ILLNESS 2
MEDICAL AND DENTAL HISTORY 3
PHYSICAL EXAMINATION 4
RADIOGRAPHIC EXAMINATION 4
CLINICAL LABORATORY TESTS 4

Assessment of the Findings 5

Formulating a Differential Diagnosis 5

Securing a Definitive Diagnosis 6

Formulating a Treatment Plan 7

PMPH_Eversole_Chapter-01.indd 1 1/17/2011 3:22:30 PM

 The diagnostic process involves four sequen-
tial steps: (1) obtainment of a comprehensive Procurement of the Data Base
overview of the patient’s past and current
health status, referred to as the historical CHIEF COMPLAINT AND
data base; (2) evaluation of all the findings HISTORY OF THE PRESENT
to correlate the chief sign or symptoms with ILLNESS
the current history, other physical findings,
and the medical history; (3) formulation of a The initial contact with the patient should be
differential diagnosis to include all disease met with concern conveying a desire to be of
processes that could conceivably account assistance. Patients are often upset, fearful,
for the collective findings; and (4) arrival at annoyed, or short-tempered when they feel
a definitive diagnosis on the basis of inter- they are ill or have something wrong with
rogation and specific clinical and laboratory them, particularly when pain is the primary
tests that exclude specific diseases and point complaint or when they have sought help
to a definite disease process. Once the diag- from other health practitioners who were
nostic process is consummated, a plan for unable to arrive at a diagnosis. Nonverbal
treatment can be generated with establish- communication such as a hand on the
ment of a follow-up assessment program. shoulder, a look of kindness, or a comment
Thorough and open communication expressing concern and determination to
between doctor and patient is a prereq- help will open the doors to trust and com-
uisite to the diagnostic process. Because munication. Once these subtle gestures have
the ultimate goal is the definitive diagno- helped to establish rapport, an assessment
sis, the doctor is charged with the duty of of the patient’s problem or chief complaint
sleuth par excellence, meaning he or she can be explored. The chief complaint usu-
must develop the communication skills to ally emerges as a symptom, a sign, or both.
become an eminent interrogator. The ques- Symptoms are subjective, represent-
tioning process is as important as having ing a definite problem expressed by the
a large knowledge base regarding disease patient. Common symptoms of oral and
processes and the skills necessary to recog- maxillofacial disease processes include the
nize tissue changes. The process of interro- following:
gation helps to exclude diseases that, on the
basis of physical appearance or symptoms Discomfort: Pain, ache, numbness (hyp-
alone, would have been included as initial esthesia), tingling (paresthesia), itching
possibilities. What questions does one ask? (pruritus), burning, rawness, tenderness,
First, the clinician must have a reasonable and clicking/popping of temporoman-
comprehensive knowledge of the possible dibular joint (TMJ).
disease entities he or she may encounter. Textural changes: Roughness, dryness
Without this knowledge base, the appro- (xerostomia, xerophthalmia), and swelling
priate line of questioning may not be obvi- (growth, enlargement).
ous. Alternatively, the examiner who is Functional changes: Difficulty with swal-
aware of the various diseases sharing com- lowing, opening, or chewing: altered bite,
mon symptoms or physical signs can ask taste, or hearing; difficulty with speech:
appropriate questions to begin the process tooth clenching or grinding: joint sounds;
of elimination (i.e., limiting the differen- loose teeth and bleeding from mouth,
tial diagnosis). As we proceed through the gingiva, or nose.
sequential steps of the diagnostic process,
emphasis is placed on the development of a Once the chief symptom is recorded,
logical approach to interrogation. questioning helps to define the problem

PMPH_Eversole_Chapter-01.indd 2 1/17/2011 3:22:30 PM

 The Diagnostic Process 3

more accurately. Interrogation revolving tissue changes that the patient observes
around the chief complaint should explore or changes that may be unknown to the
the nature of the problem, the duration, patient but have been detected during
the periodicity, the location, and associa- the course of the physical examination.
tion with factors known to the patient. For Signs should be characterized in detail by
example, if a patient complains of pain, the exploring their features and history. When
examiner should explore its nature (i.e., a patient states that he or she discovered a
sharp, dull, throbbing, etc.). How long has tissue change, the clinician should attempt
the symptom been a problem? Has it per- to uncover, through questioning, the nature
sisted for a few hours, a few days, or for of the disease from the patient’s perspec-
weeks, or months? What is the periodic- tive, the duration, the location, and any
ity of the pain? Is it constant, intermittent, associated factors. For example, a patient
only at night, only at mealtime? Where is may state that while looking in the mirror
the pain located? It is localized or does it he or she discovered a white patch on the
radiate? Can it be associated with hot liq- tongue. The examiner will want to know
uids, cold liquids, spicy foods, citrus fruits, how the patient perceives the change. Is
sugar, pressure, percussion? A similar line it sore? Can you feel its presence? How
of questioning can be pursued for other long ago did you first notice it? Is that the
subjective complaints or symptoms. only place in your mouth you’ve noticed a
Signs are objective changes that can change? Do you recall biting your tongue
be observed or detected by palpation, per- or burning it?
cussion, auscultation, or analysis of labo-
ratory data. Common signs of oral and
maxillofacial disease processes include the MEDICAL AND DENTAL
following: HISTORY
The recording of the problem—be it a
Soft-tissue changes: White, red, or pig- symptom, a sign, or both—along with the
mented spots or patches; ulcerations; history of the illness should have allowed
blisters; multiple small nodules (papules); the examiner to contemplate a partial list
nodules; papillary growths; localized of suspected disease processes. At this
swellings; and diffuse swellings. point, the chief complaint is put aside until
Hard-tissue changes (Clinical): Dental other aspects of the data base are procured.
changes in number, shape, or structure; The next step in the diagnostic process
localized or diffuse osseous swellings; is to evaluate the patient’s history of ill-
and facial asymmetry. ness. The patient’s general health status is
Hard-tissue changes (Radiographic): reviewed by determining how the patient
Dental changes, radiolucent or feels. Does he or she feel weak or febrile?
radiopaque lesions, and mixed radiolu- Any significant weight loss or loss of appe-
cent/radiopaque lesions. tite? A history of past illness according to
Neuromuscular functional changes: the body’s organ systems is reviewed; the
Paralysis or flaccidness, muscle spasm or examiner knows that certain medical prob-
hypertrophy, sensory deficits, and altera- lems require dental treatment precautions.
tion in salivation. Furthermore, many systemic diseases
manifest observable oral and facial lesions.
Not all patients relate a specific symp- Habits and medications can also affect the
tom. Often, they observe a change in the tissues of the head and neck. Previous hos-
tissues. Objective signs can be noticeable pitalizations and any complications from

PMPH_Eversole_Chapter-01.indd 3 1/17/2011 3:22:31 PM

 4 Chapter 1

past medical treatment can have a bear- RADIOGRAPHIC

ing on the oral and maxillofacial tissues. EXAMINATION
Finally, the dental history might have some
influence with regard to the presenting When the patient’s history and physi-
problem. cal examination suggest pain of dental or
osseous origin, salivary occlusion, asym-
metry, or osseous enlargement, appropriate
PHYSICAL EXAMINATION radiographs are obtained to characterize
dental or intraosseous disease processes.
Provided the patient has no significant med- In general, periapical and panoramic films
ical problems that would militate against are used initially. The location of the sus-
proceeding with the physical examina- pected problem dictates the use of specific
tion, the examiner should begin a system- types of radiographs (Table 1.1). New tech-
atic evaluation of the tissues. In medicine, nology is emerging rapidly in radiology;
physical diagnosis involves examination of detailed tissue imaging is possible with
the organ systems. In dentistry, the primary the use of three-dimensional computerized
emphasis is examination of the head and tomography, radioisotopic scanning, xero-
neck. Usually, prior to a detailed evaluation radiography, and nuclear magnetic reso-
of these tissues, the vital signs, including nance imaging techniques. Many of these
blood pressure, pulse, respiration, and tem- techniques are costly, yet may be extremely
perature are assessed. Subsequently, physi- valuable diagnostically as well as for deter-
cal examination should include the external mining extent of disease. In most cases,
structures of the scalp, face, exposed skin, routine radiographs and tomograms are
and hands; the oral, nasal, and laryngeal obtained initially, and special radiographs
cavities; the tympanic membrane; the sali- are obtained as needed or when indicated.
vary glands and neck; the TMJ; and the Cone beam CT has become an extremely
dentition and periodontium. During the valuable tool for dental diagnostics.
physical examination, deviations from nor- The ability of the radiologist or the cli-
mal are recorded. nician to describe the radiomorphology and
Once the physical examination has list diseases known to exhibit specific pat-
been completed, the examiner should recall terns is of major importance. Radiographic
the chief complaint and focus attention on interpretation alone is rarely diagnostic.
physical changes associated with the pre-
senting signs and symptoms. Once a lesion
has been uncovered and clinically char- CLINICAL LABORATORY
acterized, the examiner should proceed TESTS
by ordering adjunctive diagnostic tests.
Many tests are available, and they should Clinical findings may indicate the need
be used discriminantly to avoid excessive for diagnostic clinical tests conducted by
cost to the patient. In general, a differen- the pathology laboratory. These tests are
tial diagnosis is established once the data used to evaluate blood chemistries, immu-
base from the history and physical exami- nologic reactivity (serology), hematologic
nation has been completed. When signs functions, urinalysis, microbiology, and
and symptoms point to a disease process genomic assays. Specific oral signs and
in bone, however, radiographs are usually symptoms may suggest a metabolic dis-
obtained prior to formulation of a differen- ease such as hyperparathyroidism whereby
tial diagnosis. testing for serum calcium, phosphate, and

PMPH_Eversole_Chapter-01.indd 4 1/17/2011 3:22:31 PM

 The Diagnostic Process 5

TABLE 1.1 Radiographs in Oral and Maxillofacial Medicine

Area of Investigation Radiography
Dental caries Bitewing
Infections of dental origin Periapicals
Impactions Panoramic, cone beam CT
Jaw lesions Panoramic, cone beam CT
Salivary stones (submandibular) Mandibular occlusal, sonograms, cone beam CT
Salivary stones (parotid) Panoramic, sonograms, cone beam CT
Salivary occlusion, inflammation, tumors Sialogram, radioisotope scan
Sinus lesions Water’s sinus, Caldwell sinus, sinus tomograms, cone beam CT
Other paranasal sinuses Paranasal sinus tomograms, CT scans
Facial deformities CT scans, cephalometric survey
Temporomandibular joints TMJ tomograms, arthrograms, CT scans, nuclear magnetic
resonance images, cone beam CT
Facial fractures Many different radiographs are available to visualize specific
sites, cone beam CT
Jaw and facial tumors Panoramic, CT scans, radioisotope scans, nuclear magnetic
resonance images, PET scans
Vascular jaw lesions Angiography
Dental implant sites Cone beam CT

parathormone levels support or confirm a examiner’s knowledge base is comprehen-

clinical impression; serologic testing for sive, the pieces of the puzzle usually fall
antinuclear antibodies may confirm an into place readily. Occasionally, however,
autoimmune process; a blood count in a some of these puzzles are quite complex
patient with swollen, inflamed gingiva and require more sophisticated diagnostic
may disclose leukemia; a urine sample may procedures. After all the data have been
show protein indicative of renal disease; a reviewed, collated, and correlated, the clini-
culture may be obtained to identify a sus- cian should be able to list possible disease
pected fungal infection; a gene rearrange- entities that could be responsible for the
ment study may confirm lymphoma. The findings. This list of entities represents the
tests performed in the clinical laboratory differential diagnosis.
may, therefore, be the means to a definitive
diagnosis.
Formulating a Differential
Diagnosis
Assessment of the Findings The list of entities subsumed under the
Once all the preliminary data, including designation “differential diagnosis” can be
initial radiographs, is secured, the clini- quite staggering, particularly when only
cian must return to the chief complaint the presenting signs or symptoms are taken
and physical findings. All these data must into account. To the astute clinician, the
be placed in perspective by focusing on interrogative process along with the review
the problems and correlating them with of all findings should have eliminated many
the overall findings. During this process, entities from the differential diagnosis list.
new lines of interrogation may emerge. In this regard, the “differential” has already
The problems and findings represent a been limited in scope. Perhaps only two or
mosaic that must achieve the best fit in three disease processes remain worthy of
order to arrive at a diagnosis. Provided the consideration.

PMPH_Eversole_Chapter-01.indd 5 1/17/2011 3:22:31 PM

 6 Chapter 1

So far, the discussion has revolved

around principles and generalities. A spe- Securing a Definitive Diagnosis
cific example may help to clarify some Once a reasonable limited differential diag-
of these general considerations. Suppose nosis is formulated, specific tests are con-
a 40-year-old woman comes to you with ducted. These tests can further limit the
a chief complaint of painful sores in her differential by excluding some diseases
mouth. This is a presenting symptom. If (i.e., the rule out process). It is more advis-
you were to develop a differential diag- able, however, to rule in probable disease
nosis including all lesions that manifest processes. In oral medicine, the most use-
mouth sores, you would probably use up an ful diagnostic tool is biopsy. In most, yet not
entire notebook. This task might be a ter- all instances, the pathologist can provide a
rific academic exercise, but the patient is definitive diagnosis based on histologic
waiting for help. At this point, you would evaluation of the diseased tissue. Some dis-
want to obtain more history. She states that eases exhibit ambiguous or nonspecific his-
they appeared 2 weeks ago, she never had tologic changes, and clinical or laboratory
anything like this before, and they are get- findings are more germane to the process of
ting worse. Despite all this, she does not inclusion or exclusion.
feel tired or feverish. Review of her medi- Another important concept is the prin-
cal history is noncontributory, meaning she ciple of “cause and effect.” Just because two
has a clean bill of health. Furthermore, she factors occur simultaneously (i.e., they are
is not taking any medication. At this point, correlated) doesn’t mean one causes the
the long list in your differential diagnosis other. For example, an ulcer may occur on
may be somewhat shortened. the tongue adjacent to a fractured tooth
You conduct the physical examination cusp. Before concluding a cause-and-effect
and find multiple oral lesions that are red, relationship, the dentist should restore the
ulcerated, and sloughing. Furthermore, you tooth to normal contour and allow 2 weeks
discover a few large intact blisters. Being to pass. If the lesion persists, the initial
a sharp clinician, you conclude that this observation ascribing an irritational caus-
patient suffers from one of the bullous disor- ative role can no longer be substantiated. A
ders. You have now considerably shortened biopsy should then be performed, and it may
the list because less than a dozen bullous reveal an early cancerous lesion. Therefore,
diseases affect the oral tissues. Also, during a cause should be sought in all cases, and if
your examination, you failed to note any found, documentation is pursued to deter-
conjunctival, nasal, or skin lesions. What mine whether or not the observation was
you have is a limited, working differential indeed causative or merely correlative.
diagnosis. Furthermore, based on her age, In most instances, a definitive diagnosis
sex, and distribution of the oral lesions, you can be secured on a clinical, histologic, radio-
can eliminate some of the entities in the logic, and/or laboratory basis. Occasionally,
bullous disease category. a final diagnosis cannot be made because all
This example, then, helps to clarify definitive tests and criteria are ambiguous.
the process of limitation of the differen- Under these circumstances, therapeutic tri-
tial diagnosis. The final step in the diag- als may be in order. Perhaps the diagnosis is
nostic phase of the approach to the patient limited to two or three possibilities; if so, the
involves devising a plan to secure a defini- most likely disease is selected and treated
tive diagnosis. accordingly. If the treatment succeeds, then

PMPH_Eversole_Chapter-01.indd 6 1/17/2011 3:22:31 PM

 The Diagnostic Process 7

one can usually conclude, on the basis of that has a potential for recurrence should
response to treatment, that the probable be placed on periodic recall. The length and
diagnosis was correct. periodicity are determined by the behavior
and natural history of the disease process.
Formulating a Treatment Plan Some diseases never recur, and initial ther-
apy is conclusive and complete; therefore,
Once a definitive diagnosis is made, the short-term follow-up and assessment are
most efficacious treatment must be selected. adequate. Alternatively, neoplastic diseases
Depending on the disease, the following and chronic illnesses may require frequent
management strategies are considered: (1) recall assessment and retreatment.
no treatment, (2) surgical removal, (3) phar- The diagnostic process must be thor-
macologic agents, (4) palliative treatment, ough and include history procurement,
(5) behavioral or functional treatment, and physical examination, and radiologic exam-
(6) psychiatric therapy. Referral to a medical ination when indicated. All patient find-
or dental specialist may be required. One ings are integrated to synthesize a differ-
should realize that many diseases cannot ential diagnosis. The differential diagnosis
be cured, and treatment is aimed at control is pared down with selective interrogation
and alleviation of symptoms. Some diseases and specific diagnostic procedures, such as
resolve of their own accord, some require a biopsy and clinical laboratory tests. With
single curative treatment, and others require establishment of a definitive diagnosis, a
prolonged or indefinite treatment. management plan can be devised; results of
After a management strategy has been therapy should be evaluated by follow-up
formulated and implemented, a plan for assessment, and preventive measures, when
prevention of recurrence should be devised. applicable, should be instituted.
For example, a patient with leukoplakia The remainder of this text is designed
showing microscopic evidence of premalig- to aid the clinician in the attainment of
nant change (i.e., dysplasia) may have been a definitive diagnosis; each disease is
successfully treated surgically. Failure to described so that the examiner can evaluate
eliminate important etiologic factors such efficiently the signs and symptoms to arrive
as continued alcohol and tobacco use could at a definitive diagnosis. Most chapters are
result in a recurrence of the disease in the arranged according to physical findings;
same site or in a new location. The clinician the final chapter, dealing with facial pain,
should advise the patient about these poten- being subjective, is outlined according to
tially harmful habits and help the patient to presenting symptoms. The recommended
curtail them. therapy is mentioned briefly, and the reader
The final consideration, and one of may find more detail regarding manage-
paramount importance, is patient follow-up ment by referring to the current references
and assessment. Patients with a disease listed for each disease.

PMPH_Eversole_Chapter-01.indd 7 1/17/2011 3:22:31 PM

 a b

Normal mucosa Hyperkeratosis

c d

Acanthosis Lymphocytic infiltration

e f

Extrinsic coating Ulcerative pseudomembrane

White Lesions

PMPH_Eversole_Chapter-02.indd 8 1/17/2011 3:23:32 PM

 White Lesions
2
Flat Plaques, Solitary 11 Verrucous/Rippled Plaques 31
FRICTIONAL BENIGN KERATOSES 11 PROLIFERATIVE VERRUCOUS
LEUKOPLAKIA 12 LEUKOPLAKIA 31
ACTINIC CHEILITIS 14 VERRUCOUS CARCINOMA 33
SMOKELESS TOBACCO
KERATOSES 14 Lacey White Lesions 34
SANGUINARIA-INDUCED LICHEN PLANUS 34
KERATOSES 16
LICHENOID REACTIONS 36
DYSKERATOSIS CONGENITA 17
LUPUS ERYTHEMATOSUS 37
FANCONI’S ANEMIA 18
HIV-ASSOCIATED HAIRY
DYSPLASIA, CARCINOMA IN SITU, LEUKOPLAKIA 38
SQUAMOUS CELL CARCINOMA,
AND VERRUCOUS CARCINOMA 19
LICHEN PLANUS
Papular Lesions 40
(HYPERTROPHIC TYPE) 21 KOPLIK SPOTS OF MEASLES 40
MUCOUS PATCHES FORDYCE’S GRANULES 41
(SECONDARY SYPHILIS) 22 DENTAL LAMINA CYSTS, BOHN’S
NODULES, EPSTEIN’S PEARLS 41
Flat Plaques, Bilateral STOMATITIS NICOTINA 42
or Multifocal 23 SPECKLED LEUKOPLAKIA 43

LEUKOEDEMA 23
GENOKERATOSES 24
Pseudomembranous Lesions 44
PLAQUE-FORM LICHEN CHEMICAL BURNS 44
PLANUS 30 CANDIDIASIS (MONILIASIS, THRUSH) 45
CHEEK/TONGUE BITE VESICULO-BULLOUS-ULCERATIVE
KERATOSIS 30 DISEASES 47

PMPH_Eversole_Chapter-02.indd 9 1/17/2011 3:23:34 PM

 White lesions of oral mucous membranes Inflammatory lesions that may pro-
appear thus because one or more of the epi- duce thickened epithelium and/or a sur-
thelial layers is thickened or an extrinsic face pseudomembrane appear white; in
or intrinsic pseudomembrane is adherent these instances, the surface coating may be
to the surface mucosa. The white lesions rubbed away with gauze. The diagnosis of
encountered in practice may be subdivided inflammatory white lesions can be secured
into groups on the basis of pathogenesis by obtaining a thorough history, including
or etiologic factors. Developmental white questions regarding use of drugs, sexual
lesions are generally bilateral. Patients habits or promiscuity, recent contact with
relate that a familial pattern exists, because persons manifesting similar illness, or con-
most of the developmental white lesions are tact with injurious chemicals.
genetically inherited (genokeratosis). This chapter illustrates and enumer-
As a gardener’s hands become cal- ates the features of white lesions in the
loused from hours of friction from the hoe, context of clinical features as outlined ear-
so may the oral epithelium become calloused lier. The differential diagnosis for a given
or thickened in response to chronic trauma. white lesion depends on obtaining a his-
Tobacco in its many forms is also consid- tory, with primary considerations of (1) a
ered a local irritant and indeed is associated familial pattern; (2) presence or absence
with carcinomatous transformation in white of a causative agent with notations on oral
lesions of the oral mucosa. The white lesions habits, particularly tobacco use; (3) pres-
associated with physical or tobacco-product ence or absence of associated skin lesions;
irritation are grouped under the heading (4) questions relating to contact with indi-
leukoplakias, as are other white lesions of viduals showing similar lesions; (5) AIDS-
undetermined origin. Because tobacco-as- risk status; (6) presence or absence of fever;
sociated and idiopathic white lesions may and (7) exploration of the nature of the
show microscopic evidence of malignancy, white patch as to tenacity to underlying
biopsy must be performed when (1) a cause structures and ease of removal by rubbing.
cannot be detected or (2) the suspected trau- Based on responses and fi ndings regard-
matic agent is eliminated yet the lesion fails ing these considerations, a ranking of
to involute or regress. Leukoplakia of the entities in the differential diagnosis may
lateral tongue may be indicative of human ensue and, ultimately, biopsy—or in cer-
immunodeficiency virus (HIV) seropositiv- tain instances serology and blood count—
ity, particularly among patients who fall must be performed to obtain a defi nitive
into AIDS-risk categories. diagnosis.
White lesions of nonhereditary dis- The white lesions encountered most
eases may coexist with skin lesions. These frequently are (1) friction, idiopathic or
keratotic dermatoses may, however, occur tobacco-associated leukoplakias, (2) lichen
as oral lesions with skin involvement. As no planus, (3) candidiasis, and (4) Fordyce’s
etiologic agent can be discerned in oral ker- granules.
atotic dermatoses, biopsy must be under- White lesions associated with a poten-
taken to confirm the diagnostic impression tially lethal outcome include (1) premalig-
when classic clinical features of these disor- nant leukoplakias, (2) hairy leukoplakia,
ders are lacking. and (3) lupus erythematosus.

PMPH_Eversole_Chapter-02.indd 10 1/17/2011 3:23:35 PM

 White Lesions 11

MICROSCOPIC FEATURES
Flat Plaques, Solitary Frictional irritation may cause thickening
FRICTIONAL BENIGN of any layer or combination of layers of
the epithelium with hyperorthokeratosis,
KERATOSES
hyperparakeratosis, and/or acanthosis.
Figure 2-1 Depending on the degree of irritation,
Age: No predilection
the underlying submucosa may show an
Sex: No predilection inflammatory cell infiltrate, which is usu-
ally chronic.
CLINICAL FEATURES
DIFFERENTIAL DIAGNOSIS
Frictional keratoses represent callus forma-
tion from chronic trauma with resultant White lesions arising from chronic irritation
thickening of one of the epithelial cell lay- may be diagnosed as such when a causative
ers. The white lesions are therefore associ- agent presents itself. Providing the cause can
ated with various etiologic agents, including be eliminated or reduced (e.g., leaving ill-fit-
ill-fitting dental prostheses, chronic irrita- ting dentures out of the mouth for 2 weeks,
tional habits such as cheek- or lip-biting, smoothing irritating tooth cusps, avoiding
overzealous tooth brushing, and white cal- habits), and the white lesion regresses or
luses formed from occluding on edentulous resolves; a cause-and-effect relationship can
ridges or the retromolar pads, a condition be substantiated. Failure of a white lesion
termed oral lichen simplex chronicus. The to regress subsequent to elimination of the
individual lesions may be smooth or irregu- causative agent(s) should arouse suspicion
lar in texture, and their location and con- with regard to precancerous leukoplakia,
figuration coincide with the corresponding and biopsy is then indicated. In addition,
location of the causative agent. Frictional other diseases manifesting white lesions
keratoses may also be multifocal. may coincidentally correspond to denture-

FIGURE 2-1
Frictional keratosis due to
irritation.

PMPH_Eversole_Chapter-02.indd 11 1/17/2011 3:23:35 PM

 12 Chapter 2

bearing zones; however, diseases such as more often seen on the buccal mucosa,
lichen planus, moniliasis, or the genokera- mucobuccal fold, and oral floor. These leu-
toses are typically located in regions beyond koplakias may be smooth, ridged, rough,
the confines of a potential irritant. delineated, or diffuse. The smooth form or
planar type fails to exhibit surface irregu-
TREATMENT larity, being homogeneously white without
Elimination of the causative agent is indi- a verrucous texture, yet others may have a
cated. White lesions attributed to a chronic ridged or verrucous appearance. The term
irritant probably have a limited tendency leukoplakia is strictly clinical and has no
to undergo malignant change. Should the implications with regard to microscopy.
lesions fail to resolve after removal of the These lesions are usually benign yet may
irritant, however, a biopsy should be per- show microscopic evidence of premalig-
formed to rule out atypical cell changes that nant cellular change. Whereas leukoplakias
occur independently. as a collective group display microscopic
evidence of dysplasia, carcinoma in situ, or
squamous cell carcinoma in approximately
Additional Reading 20% of the cases, evidence suggests that
the atypical cell changes are less prevalent
Axell T, Holmstrup P, Kramer Irh, Pindborg JJ, Shear M. in the smooth planar form compared with
International seminar on oral leukoplakia and associat- the verrucous appearing lesions. Leukopla-
ed lesions related to tobacco habits. Community Dent kias of the oral floor manifest the highest
Oral Epidemiol. 1984;12:146. incidence of atypical cell change; approxi-
Cawson RA. Leukoplakia and oral cancer. Proc R Soc
Med. 1969;62:610. mately 40% harbor atypical cells.
Natarajan E, Woo SB. Benign alveolar ridge keratosis
(oral lichen simplex chronicus): a distinct clinicopatho- Microscopic features
logic entity. J Am Acad Dermatol. 2008;58(1):151-157.
Shafer WG, Hine MK, Levy BM. A Textbook of Oral The clinical extent does not necessarily pre-
Pathology. 4th ed. Philadelphia, PA: W. B. Saunders; dict the microscopic features. Idiopathic or
1983:92. tobacco-induced leukoplakias may merely
Waldron CA. In: Gorlin RJ and Goldman HM, eds. show hyperorthokeratosis, hyperparakera-
Thoma’s Oral Pathology. Vol 2. 6th ed. St Louis, MO:
C. V. Mosby; 1970:811.
tosis, acanthosis, or a combination. Alterna-
tively, and most important, cellular atypia,
dysplasia, carcinoma in situ, or frank super-
ficially invasive squamous cell carcinoma
LEUKOPLAKIA may be encountered microscopically.
Figure 2-2
Differential diagnosis
IDIOPATHIC/SMOKED TOBACCO-
ASSOCIATED LEUKOPLAKIA Idiopathic and tobacco-associated leukopla-
kia must be differentiated from frictional
Homogeneous Leukoplakia leukoplakia on the basis of history. Lichen
Age: Middle-aged and elderly adults planus, lupus erythematosus, the genokera-
Sex: Males predominantly toses, and inflammatory white lesions must
also be eliminated from consideration on
Clinical features the bases of history and biopsy findings.
White plaques of unknown etiology or
those encountered in smokers and tobacco Treatment
chewers are a common malady that may Biopsy should be performed in all instances
occur on any oral mucosal surface yet are of idiopathic or tobacco-associated leuko-

PMPH_Eversole_Chapter-02.indd 12 1/17/2011 3:23:45 PM

 White Lesions 13

FIGURE 2-2
Thickened, diffuse white
lesions representing idio-
pathic leukoplakia.

plakia to ascertain whether or not prema- managed by combined radiotherapy and

lignant cell changes exist. Benign cellular surgery.
features do not preclude future malignant
change in the same location or in a new site.
About 2% to 3% of benign leukoplakias may
progress to carcinoma, whereas 17.5% of all
Additional Reading
oral leukoplakias, including cases with and Bánóczy J, Csiba A. Comparative study of the clinical
picture and histopathologic structure of oral leukopla-
without dysplastic change, progress to car-
kia. Cancer. 1972;29:1230.
cinoma over a mean follow-up period of 7½ Holmstrup P, Vedtofte P, Reibel J, et al. Long-term
years. Most dysplasias fail to progress to car- treatment outcome of oral premalignant lesions. Oral
cinoma and many spontaneously regress. Oncol. 2006;42:461-474.
Recent studies have disclosed that benign Hsue SS, Wang WC, Chen CH, et al. Malignant trans-
formation in 1458 patients with potentially malig-
leukoplakias may progress to carcinoma nant oral mucosal disorders: a follow-up study based
over time in almost comparable numbers in a Taiwanese hospital. J Oral Pathol Med. 2007;36:
to those that are dysplastic. For these rea- 25-29.
sons, patients should be subjected to peri- Mincer HH, Coleman SA, Hopkins KP. Observations on
the clinical characteristics of oral lesions showing his-
odic follow-up with rebiopsy, particularly tologic epithelial dysplasia. Oral Surg Oral Med Oral
when a change in the clinical character of Pathol. 1972;33:389.
a lesion evolves. Lesions with a microscopic Silverman S, Jr, Gorsky M, Lozada F. Oral leukoplakia
diagnosis of dysplasia or carcinoma in situ and malignant transformation. A follow-up study of
2157 patients. Cancer. 1984;53:563.
should be surgically stripped or removed Waldron CA, Shafer WG. Leukoplakia revisited. A clini-
in toto by standard surgery, cryosurgery, or copathologic study of 3256 oral leukoplakias. Cancer.
laser surgery. Invasive carcinoma is usually 1975;36:1386.

PMPH_Eversole_Chapter-02.indd 13 1/17/2011 3:23:45 PM

 14 Chapter 2

ACTINIC CHEILITIS TREATMENT

Figure 2-3 A biopsy should be performed to deter-
mine whether or not dysplasia is present.
Age: Middle-aged and elderly adults A lack of premalignant cellular changes in
Sex: Males predominate actinic cheilitis does not preclude future
CLINICAL FEATURES evolvement. Protection from the sun with
solar protective cream containing p-amin-
Solar or ultraviolet light exposure may pre- obenzoic acid (PABA) is recommended.
dispose the vermilion border to keratotic Histologically, atypical change should be
change, and certain individuals whose managed by lip stripping with incontinuity
occupations or hobbies provide continu- wedge resection if a zone of superficial car-
ous exposure to sun are most prone to cinomatous invasion is coexistent.
develop actinic cheilitis. The lower lip If no foci of carcinoma exist, topical
is more prominent and, therefore, more application of 1% 5-fluorouracil cream twice
prone to actinic change than the upper. daily for 2 weeks will remove dysplastic epi-
The lesion is white and usually smooth thelium, allowing for regeneration of nor-
and diffuse. The borders may be sharply mal epithelium. Other effective treatments
delineated from uninvolved vermilion, or include 5% imiquimod cream and photody-
the transition may be gradual. Ulcerations namic therapy with methyl aminolevulinic
or focal zones of highly thickened keratin acid as the photosensitizer and red light at
plaque may indicate early carcinomatous 630 nm.
transformation.

MICROSCOPIC FEATURES Additional Reading

Solar cheilitis reflects a spectrum of micro- Bernier JL, Reynold MC. The relationship of senile elas-
scopic changes similar to leukoplakia. The tosis to actinic radiation and to squamous cell carci-
noma of the lip. Milit Med. 1955;117:209.
early limited changes are restricted to the
Castaño E, Comunión A, Arias D, et al. Photodynamic
keratin layer, which manifests thickening, therapy for actinic cheilitis. Actas Dermosifiliogr.
and the subjacent connective tissue zones, 2009;100:895-898.
which characteristically show clumping, Picascia DD, Robinson JK. Actinic cheilitis: a review of
fragmentation, and granulation of elastic etiology, differential diagnosis, and treatment. J Am
Acad Dermatol. 1987;17:255.
fibers known as solar or senile elastosis. Smith KJ, Germain M, Yeager J, Skelton H. Topical 5%
Progression to cytologic atypia, dysplasia, imiquimod for the therapy of actinic cheilitis. J Am
and frank invasive carcinoma can develop Acad Dermatol. 2002;47:497-501.
in actinic cheilitis. The earliest premalig- Warnock GR, Fuller RP, Jr, Pelleu GB, Jr. Evaluation of
5-fluorouracil in the treatment of actinic keratosis of
nant atypicality is represented by atrophy the lip. Oral Surg Oral Med Oral Pathol. 1981;52:501.
of the spinous cell layer, fragmentation of
the basement membrane, and mild hyper-
SMOKELESS TOBACCO
chromatism and/or pleomorphism of the
basal cells. KERATOSES
Figure 2-4
DIFFERENTIAL DIAGNOSIS
Age: No predilection
Habitual lip chewing must be differenti- Sex: No predilection
ated from actinic cheilitis. Tobacco irritants
CLINICAL FEATURES
(cigars, pipe stems, and reverse smoking)
may induce hyperkeratotic lesions of the White lesions caused by snuff and chewing
lips. tobacco usage are located under the area in

PMPH_Eversole_Chapter-02.indd 14 1/17/2011 3:23:53 PM

 White Lesions 15

FIGURE 2-3
Actinic cheilitis of the lip.

FIGURE 2-4
Corrugated white plaques attributed to smokeless tobacco (snuff dipper’s keratosis).

PMPH_Eversole_Chapter-02.indd 15 1/17/2011 3:23:53 PM

 16 Chapter 2

which these agents are habitually placed;

they are therefore encountered in the Additional Reading
mucobuccal fold region. The lesion is some- Brown RL, Suh JM, Scarborough JE, Wilkins SA, Jr,
what rough and may manifest an undulat- Smith RR. Snuff dipper’s intraoral cancer; clini-
ing or wrinkled surface. The white areas cal characteristics and response to therapy. Cancer.
are relatively well circumscribed and local- 1965;18:2.
Greer RO, Jr, Poulson TC. Oral tissue alterations asso-
ized to the area of snuff placement. Dur- ciated with the use of smokeless tobacco by teenag-
ing the 1980s and currently, the incidence ers. Part 1. Clinical findings. Oral Surg Oral Med Oral
of smokeless tobacco use by teenagers has Pathol. 1983;56:275.
increased. Rodu B, Jansson C. Smokeless tobacco and oral cancer:
A review of the risks and determinants.Crit Rev Oral
Biol Med. 2004;15:252-263.
MICROSCOPIC FEATURES
Roed-Petersen B, Pindborg JJ. A study of Danish
As with other forms of tobacco-induced snuff-induced oral leukoplakia. J Oral Pathol Med.
leukokeratosis, snuff keratosis may show 1973;2:301.
Rosenfeld L, Callaway J. Snuff dipper’s cancer. Am J
a thickening of one of the epithelial lay- Surg. 1963;106:840.
ers (i.e., hyperorthokeratosis, hyperparak-
eratosis, acanthosis), with a tendency for
“chevron”-shaped projections in the corni- SANGUINARIA-INDUCED
fied layer. Cytologic atypia is rarely seen, KERATOSES
and progression to invasive carcinoma is
Figure 2-5
rare among moist snuff users yet is signifi-
cantly more carcinogenic when dry snuff Age: no predilection
is used or when snuff is mixed with slaked Sex: no predilection
lime, a common additive in India and the
Middle East. CLINICAL FEATURES
Sanguinaria (blood root) is a chemical that
DIFFERENTIAL DIAGNOSIS has been shown to be antimicrobial and was
A white lesion in the mucobuccal fold may placed in dentifrice as well as in a mouth
represent frictional keratosis or leukoplakia rinse preparation to reduce microbial
related to tobacco products. A thorough his- plaque on tooth biofilms. A spurious find
tory will indicate whether or not the lesion among chronic and heavy users of these
is smokeless tobacco related. The “ebbing Sanguinaria products was the appearance
tide” effect on the white surface implicates of leukoplakias, particularly on the maxil-
snuff usage. lary anterior gingival and mucobuccal fold.
This localization has been attributed to the
TREATMENT physiology of mouth rinsing whereby the
All smokeless tobacco-associated white rinse is forcefully extended into the labial
lesions must be examined microscopi- compartment of pursed lips.
cally to rule out premalignancy. If atypi-
MICROSCOPIC FEATURES
cal cytologic changes are present in high
risk populations, complete excision is rec- Most biopsies from Sanguinaria-induced
ommended. Absence of cellular prema- leukoplakias exhibit benign keratosis with-
lignant changes does not preclude future out dysplasia. DNA ploidy studies, how-
evolution to cancer; therefore, the habit ever, have disclosed abnormal DNA content
should be curtailed. Tobacco-specific nit- in some of these lesions and, therefore, both
rosamines are thought to be the chief car- rinse and dentifrice have been withdrawn
cinogens in chewing tobacco and snuff. from the market.

PMPH_Eversole_Chapter-02.indd 16 1/17/2011 3:24:20 PM

 White Lesions 17

FIGURE 2-5
Sanguinaria-induced keratoses of the anterior maxillary gingival and vestibule.

DIFFERENTIAL DIAGNOSIS complex (DKC1, TERC, TERT, NOP10,

Sanguinaria leukoplakia may simulate idio- NHP2) or shelterin (TINF2). The syndrome
pathic leukoplakias and plaque-form lichen is characterized by atrophic nail changes,
planus. telangiectatic pigmented reticular lesions of
skin, pancytopenia, and oral white lesions
TREATMENT associated with dorsal tongue depapillation
and atrophy. Premature aging is also fea-
Discontinuing the use of the product is tured. Forty percent of oral lesions progress
required, and many months may elapse to squamous cell carcinoma before the age
before the lesions resolve. of 50.

Additional Reading MICROSCOPIC FEATURES

A nonspecific thickening of the parakeratin
Allen CL, Loudon J, Mascarenhas AK. Sanguinaria- and spinous cell layer is seen. Dysplastic
related leukoplakia: epidemiologic and clinicopatho-
logic features of a recently described entity. Gen Dent. changes, absent in pachyonychia, evolve
2001;49:608-614. and progress to squamous cell carcinoma
Eversole LR, Eversole GM, Kopcik J. Sanguinaria- in dyskeratosis congenita.
associated oral leukoplakia: comparison with other
benign and dysplastic leukoplakic lesions. Oral Surg
DIFFERENTIAL DIAGNOSIS
Oral Med Oral Pathol Oral Radiol Endod. 2000;89:455-
464. The mucosal white lesions and constellation
of other clinical findings of dyskeratosis con-
genita may be confused with pachyonychia
DYSKERATOSIS CONGENITA congenita. Fanconi’s anemia is a significant
Figure 2-6 syndrome to consider in the differential
diagnosis since it presents with bone mar-
Age: Childhood onset
row suppression and oral white lesions that
Sex: No predilection
can progress to carcinoma. Other keratoses
CLINICAL FEATURES such as white sponge nevus, HBID, and
Dyskeratosis congenita (Zinsser-Engman- lichen planus should also be considered.
Cole syndrome) is inherited as either an
autosomal recessive, X-linked or autosomal TREATMENT
dominant disorder with telomere shorten- Close clinical follow-up of oral lesions is
ing mediated by mutations in six genes that mandatory since malignant transformation
encode either components of the telomerase will occur later in life.

PMPH_Eversole_Chapter-02.indd 17 1/17/2011 3:24:20 PM

 18 Chapter 2

FIGURE 2-6
Dyskeratosis congenita. White lesions that progress to carcinoma.

deformed thumbs or agenesis. Pancytopenia

Additional Reading occurs with thrombocytopenia and neutro-
Alter BP, Giri N, Savage SA, Rosenberg PS. Cancer in penia. These events occur due to mutations
dyskeratosis congenita. Blood. 2009;113:6549-6557. in a group of core protein complexes (the FA
Armanios M. Syndromes of telomere shortening. Ann genes) whose function involves DNA repair
Rev Genomics Hum Genet. 2009;10:45-61. and antioxidant synthesis. These patients
Kirwan M, Dokal I. Dyskeratosis congenita, stem cells
and telomeres. Biochim Biophys Acta. 2009;1792(4D): may develop leukoplakias located on the
371-379. tongue or floor of the mouth that can later
Walne AJ, Dokal I. Advances in the understanding of transform to carcinoma.
dyskeratosis congenita. Br J Haematol. 2009;145:
164-172.
MICROSCOPIC FEATURES
The keratotic lesions in Fanconi’s anemia
FANCONI’S ANEMIA exhibit the same histology as those found
Figure 2-7 in idiopathic leukoplakias (i.e., benign kera-
tosis, dysplasia, carcinoma).
Age: Childhood onset
Sex: No predilection DIFFERENTIAL DIAGNOSIS
CLINICAL FEATURES The white lesions are similar to other leuko-
Fanconi’s anemia is an autosomal recessive plakias being flat plaques. The unique con-
genetic disorder involving as many as 13 stellation of syndromic characteristics usu-
genes of which mutations occur. If both par- ally allow for a straightforward diagnosis.
ents are carriers, there is a 25% risk of having
an affected child. Affected children develop TREATMENT
bone marrow suppression with erythrocyte The pancytopenia and leukemia can be
macrocytosis, and many will progress to managed by chemotherapy with greatest
acute myelogenous leukemia. Digital anom- response being seen after bone marrow
alies are characterized by anatomically transplantation. Importantly, many head

PMPH_Eversole_Chapter-02.indd 18 1/17/2011 3:24:24 PM

 White Lesions 19

DYSPLASIA, CARCINOMA
IN SITU, SQUAMOUS
CELL CARCINOMA, AND
VERRUCOUS CARCINOMA
Figure 2-8

Age: Elderly adults

Sex: Males predominate

CLINICAL FEATURES
Early cancerous change within the oral epi-
thelium may initially manifest as a white
lesion or may arise in a preexisting leuko-
plakic area. Depending on the extent of the
tumor, the white lesion may be relatively
macular or plaque-like or, in larger lesions,
associated with tumefaction and indura-
tion. Whereas oral cancer is generally local-
ized, it may, on occasion, be multifocal with
numerous isolated separate white lesions
manifesting microscopic evidence of neo-
plastic transformation. Location is highly
significant when considering the possibility
of malignancy; although malignant change
may be seen on any surface, the most com-
mon locations are oral floor, alveolar ridge
FIGURE 2-7 and vestibule, and lateral posterior tongue.
Fanconi’s anemia. Thumb anomaly, oral carcinoma. The most important contributing etio-
logic factors regarding carcinogenesis of
and neck cancers have evolved in Fanconi oral epithelium are use of tobacco and a high
patients after marrow transplantation. intake of alcohol. Patients with untreated
syphilis and the Plummer-Vinson syndrome
are also prone to develop oral or oropharyn-
Additional Reading geal cancer. Recent research indicates that
a subpopulation of patients have tumors
Auerbach AD, Rogatko A, Schroeder-Kurth TM. associated with, and probably caused by,
International Fanconi Anemia Registry: relation of
clinical symptoms to diepoxybutane sensitivity. Blood. human papillomavirus (HPV) type 16. In
1989;3:391-396. this subset, the tumors are found at the
Garcia-Higuera I, Taniguchi T, Ganesan S, et al. base of the tongue and the tonsillar pillar.
Interaction of the Fanconi anemia proteins and BRCA1 As emphasized under the section on leuko-
in a common pathway. Mol Cell. 2001;7:249-262.
Masserot C, Peffault de Latour R, Rocha V, et al. Head plakias associated with tobacco, the appar-
and neck squamous cell carcinoma in 13 patients with ent clinical innocence of white patches can
Fanconi anemia after hematopoietic stem cell trans- be misleading; the most innocuous lesion
plantation. Cancer. 2008;113:3315-3322. may be cytologically malignant. One excep-
Reinhard H, Peters I, Gottschling S, et al. Squamous
cell carcinoma of the tongue in a 13-year-old girl
tion to clinical predictability regarding
with Fanconi anemia. J Pediatr Hematol Oncol. suspicion of potential malignancy may be
2007;29:488-491. encountered in the white lesion associated

PMPH_Eversole_Chapter-02.indd 19 1/17/2011 3:24:35 PM

 20 Chapter 2

FIGURE 2-8
Dysplastic and neoplastic
white lesions. All showed
microscopic evidence of dys-
plasia or carcinoma.

with zones of erythema, so-called speckled subjacent connective tissue. Violations of

leukoplakia. Isolated mixed red and white the basement membrane integrity results
lesions should be considered malignant in superficially invasive carcinoma, which
until proven otherwise (i.e., by biopsy). then progresses to frank squamous cell
A variant form of oral squamous cell carcinoma.
carcinoma that is classically a warty-ap- Invasive squamous cell carcinoma
pearing keratotic white lesion is verrucous may contain islands and nests of tumor
carcinoma (see Chapter 6). cells that retain the characteristics of oral
epithelium by manufacturing the chief pro-
tective products of that organ, albeit dis-
MICROSCOPIC FEATURES organized, keratin and parakeratin. These
Epithelial dysplasia, carcinoma in situ, differentiated tissues are often arranged
and invasive squamous cell carcinoma are, in laminated whorls termed keratin pearls.
respectively, progressively advanced stages Tumors with this histologic morphology
of malignancy. When they are characterized are termed well-differentiated carcinomas
clinically as white lesions, they manifest and are associated with a slower course,
a thickening of the keratin or parakeratin lower metastatic potential, and thus a bet-
layer. The earliest changes, termed dysplasia, ter prognosis. A lack of, or a diminution in,
begin in the dividing cells of the basilar and keratin formation connotes a more rapidly
parabasilar layers. Initial changes include progressing lesion with a poor prognosis
nuclear hyperchromatism, pleomorphism, and is termed poorly differentiated carci-
and an increase in mitotic figures. By defi- noma. A moderately differentiated lesion
nition, all layers, top to bottom, must evince logically falls between these two extremes
atypical cell changes in carcinoma in situ; both morphologically and behaviorally.
however, the basement membrane remains Those tumors associated with HPV 16 tend
intact without evidence of invasion into the to show features that are differentiated

PMPH_Eversole_Chapter-02.indd 20 1/17/2011 3:24:41 PM

 White Lesions 21

along the lines of tonsillar crypt epithe- El-Mofty SK, Lu DW. Prevalence of high-risk human
lium; they tend to have a better prognosis papillomavirus DNA in nonkeratinizing (cylindrical
cell) carcinoma of the sinonasal tract: a distinct clini-
than non-HPV carcinomas of the head and copathologic and molecular disease entity. Am J Surg
neck. P16 is an immunohistochemical sur- Pathol. 2005;29:1367-1372.
rogate marker for HPV 16. Eversole LR. Dysplasia of the upper aerodigestive
tract squamous epithelium. Head and Neck Pathol.
2009;3:63-68.
DIFFERENTIAL DIAGNOSIS Pindborg JJ, Restrup G, Poulsen HE, et al. Studies in
oral leukoplakias. V. Clinical and histologic signs of
White lesions associated with tumefaction malignancy. Acta Odontol Scand. 1963;20:407.
and induration present no problem in the Silverman S, Jr, Gorsky M, Lozada F. Oral leukoplakia
clinical diagnosis, yet biopsy is indicated and malignant transformation. A follow-up study of
to determine the grade of malignancy (i.e., 2157 patients. Cancer. 1984;53:563.
Waldron CA, Shafer WG. Leukoplakia revisited. A clini-
differentiation of tumor cells) prior to plan- copathologic study of 3256 oral leukoplakias. Cancer.
ning therapy. Early malignant change man- 1975;36:1386.
ifesting a plaque-like white lesion must be
differentiated primarily from frictional leu-
koplakias, benign leukoplakias, and lichen LICHEN PLANUS
planus. When a causative agent cannot be (HYPERTROPHIC TYPE)
identified or eliminated, an adequate his- Figure 2-9
tory and biopsy are necessary.
Age: No predilection
Sex: No predilection
TREATMENT
Dysplasia or carcinoma in situ, if local- CLINICAL FEATURES
ized, can be managed by wide local exci- Lichen planus is described in greater detail
sion, obtaining margins free from atypical later. The disease is a delayed hypersen-
changes; margins 1 cm away from clini- sitivity reaction in which an identifiable
cally involved tissue should be adequate, antigenic stimulus is usually not evident.
yet microscopic confirmation is mandatory. The hypertrophic form is typically located
Diffuse or multifocal dysplasia or carcinoma on the dorsal tongue that is pavemented
in situ may be treated by surgery or radia- in confluent thick white plaques. These
tion therapy. Invasive carcinoma requires plaque-like lesions may also occur on the
a complete work-up with evaluation of the palate and the buccal mucosa. There may
neck, chest radiographs, and the presence of be some areas with a lacey reticulated pat-
other symptoms. As treatment may include tern, but oftentimes these typical lichenoid
a variety of therapeutic methods either figures are not present.
alone or in combination, including surgery,
laser surgery, radiation, and chemotherapy, MICROSCOPIC FEATURES
invasive squamous cell carcinoma should A chronic interface mucositis is present,
be evaluated and managed by a physician characterized by a patchy or band-like lym-
experienced in head and neck oncology. phocytic infiltrate in juxtaposition to the
basal cell layer of the overlying epithelium.
The cells are a mixture of CD4 and CD8 T
Additional Reading lymphocytes. The infiltrated basal cell layer
Bánóczy J, Csiba A. Occurrence of epithelial dysplasia
shows cytoplasmic fragmentation or liq-
in oral leukoplakia: analysis and follow-up study of 12 uefaction. Tongue cancer occurs in 0.5% to
cases. Oral Surg Oral Med Oral Pathol. 1976;42:766. 1.0% of cases, and when dysplasia is evident

PMPH_Eversole_Chapter-02.indd 21 1/17/2011 3:24:49 PM

 22 Chapter 2

FIGURE 2-9
Dorsal tongue and buccal
mucosa with plaque-form
(hypertrophic) lichen planus.

along with lichen planus features, the term MUCOUS PATCHES

lichenoid dysplasia has been used. (SECONDARY SYPHILIS)
Figure 2-10
DIFFERENTIAL DIAGNOSIS
The hypertrophic or plaque form of lichen MUCOUS PATCHES OF SYPHILIS
planus is easily confused with various Age: Adults
forms of leukoplakia. Sex: No predilection

Clinical Features
TREATMENT
Mucous patches are smooth-surfaced plaques
Close periodic follow-up is recommended
that manifest a glistening, opalescent charac-
and any zones of ulceration, redness, or
ter and are seen 6 to 8 weeks after formation
positive toluidine blue uptake should be
of the chancre. In addition to the mucosal
biopsied.
patches, split papules at the commissure
and a maculopapular rash may be present.
Additional Reading A history of promiscuous sexual activity can
usually be obtained, although some patients
Main JH, Birt BD, From L. Hypertrophic lichen planus may deny such activities. The lesions persist
of the oral mucosa. J Dent Assoc S Afr. 1992;47:216- for 1 to 3 weeks, after which they resolve.
218.
Setterfield JF, Black MM, Challacombe SJ. The man-
The lesions in this stage are infectious.
agement of oral lichen planus. Clin Exp Dermatol.
2000;25:176-182. Microscopic Features
Tan E, Malik R, Quirk CJ. Hypertrophic lichen planus
mimicking squamous cell carcinoma. Australas J Parakeratosis and fibrinous exudate over
Dermatol. 1998;39:45-47. both intact and focally ulcerated epithelium

PMPH_Eversole_Chapter-02.indd 22 1/17/2011 3:24:49 PM

 White Lesions 23

FIGURE 2-10
Secondary syphilis, mucous patches, maculopapular rash, soles of feet.

can be seen. The submucosa contains an Fiumara NJ. Oral lesions of syphilis. Med Aspects Hum
avid plasma cell infiltrate. The spirochete is Sexuality. 1972;6:68.
Fiumara NJ. Venereal disease of the oral cavity. J Oral
not visible on routine staining; a Warthin- Pathol Med. 1976;31:36.
Starry silver stain will demonstrate the Herrero-González JE, Parera Amer ME, FerranFarrés
microorganism in tissue sections. M, et al. Syphilitic mucous patches: the resurgence of
an old classic. J Dermatol. 2008;47:1281-1283.
Meyer I, Shklar G. The oral manifestations of acquired
Differential Diagnosis syphilis. Oral Surg Oral Med Oral Pathol. 1967;23:34.
Mucous patches may resemble a variety of
white lesions of the oral cavity; because they
are highly infectious, the clinician should Flat Plaques, Bilateral or
always be aware of the fact that oral white Multifocal
lesions may be luetic. The primary consid-
erations in the clinical differential diagno- LEUKOEDEMA
sis include moniliasis, plaque-form lichen Figure 2-11
planus, or leukoplakia of one type or another.
An adequate history should elicit suspicion Age: No predilection
of syphilis, and the diagnosis may be con- Sex: No predilection
firmed by fluorescent treponemal antibody
CLINICAL FEATURES
test or Venereal Disease Research Labora-
tory test. A smear with dark-field micros- Leukoedema occurs in blacks and dark-
copy will demonstrate motile spirochetes. skinned whites and is encountered so
frequently that it should be considered a
Treatment normal variation in these individuals. The
lesion is bilateral and diffuse, involving the
Treatment for syphilis is penicillin. The
buccal mucosa, and shows a filmy, mother-
patient can be referred to a dermatologist or
of-pearl appearance, often with delicate
general physician for treatment.
overlapping curtain-like mucosal folds.
When the mucosa is stretched, the white
Additional Reading appearance is diminished.

Compilato D, Amato S, Campisi G. Resurgence of syphi- MICROSCOPIC FEATURES

lis: a diagnosis based on unusual oral mucosa lesions.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. The epithelium displays acanthosis, parak-
2009;108:e45-e49. eratosis, and spongiosis.

PMPH_Eversole_Chapter-02.indd 23 1/17/2011 3:25:01 PM

Exploring the Variety of Random
Documents with Different Content
 THE SHINING CHILD 371 playthings. There was something
queer about them." But neither the children nor their mother
understood what the Count meant. THE STRANGER CHILD Soon
after these events very early one morning Fanchon and Frederic ran
off to the wood. They were feeling sad, for their mother had told
them that they must return home soon to study, so as to be ready
for the tutor that their rich cousin had promised to send them. For
the tutor was expected shortly. "Let us run and jump as much as we
can now," said Frederic, when they reached the wood, "for in a little
while we shall not be allowed to stay out here at all!" So they began
to play hide-and-seek, but everything went wrong. The wind carried
Frederic's hat into the bushes. He stumbled and fell on his nose as
he was running. Fanchon found herself hanging by her clothes on a
thorn-tree, and she banged her foot against a sharp stone so that
she shrieked with pain. In fact the children could not understand
what was the matter with them on this particular day; and they gave
up their game, and slunk dejectedly through the wood. Frederic
threw himself down under a shady tree,
 372 BOOK OF ELVES AND FAIRIES and Fanchon followed
his example. And there the two children lay gloomy and wretched,
gazing on the ground. "Ah!" said Fanchon, "if we only had our
playthings!" "Nonsense!" said Frederic, "what should we do with
them.f* I'll tell you what it is, Fanchon, Mother is right, I suspect.
The toys were good enough, but we did n't know how to play with
them. If we were as learned as our rich cousins, we should be so
wise that all our toys would now be whole; and we should know how
to play with them rightly." And at that Fanchon began to sob and cry
bitterly, and Frederic joined her; and they both howled and lamented
until the wood rang again and again: "Oh! poor, unfortunate children
that we are ! Oh ! that we were as wise as our cousins ! " But
suddenly they both stopped crying, and asked each other in
amazement : — "Do you hear anything, Fanchon?" "Do you hear
anything, Frederic?" For out of the deepest shade of the dark thicket
in front of the children, a wonderful brightness began to shine,
playing like moonlight over the leaves that trembled as if in joy.
Then through the whispering trees came a sweet musical note, like
the sound of a harp. The children lay motionless with awe. All their
sorrow passed away
 THE SHINING CHILD 373 from them, and tender, happy
tears rose into their eyes. As the radiance streamed brighter and
brighter through the bushes, and the marvellous music grew louder
and louder, the children's hearts beat high. They gazed eagerly at
the brightness. Then they saw, smiling at them from the thicket, the
most beautiful face of a child, with the sun beaming on it in
splendour. "Oh! come to us! — Come to us! — darling Shining Child!"
cried Fanchon and Frederic, stretching out their arms; and their
hearts were filled with an indescribable longing. "I am coming! I am
coming!" a sweet voice cried from the bushes. And then, as if borne
on the wings of the breeze, the Stranger Child seemed to float
hovering toward Fanchon and Frederic. HOW THE SHINING CHILD
PLAYED WITH FANCHON AND FREDERIC "What is the matter, dear
children?" asked the Stranger Child. "I heard you crying and
lamenting, and I was very sorry for you! What do you want?" "Ah!"
said Frederic, "we did not know what we wanted ; but now I see
that we wanted you — just you yourself!"
 374 BOOK OF ELVES AND FAIRIES "That's it!" chimed in
Fanchon. "Now that you are with us, we are happy again! Why were
you so long in coming?" In fact both children felt as if they had
known and played with the Stranger Child all their lives, and that
their unhappiness had been because their beloved playmate was not
with them. "You see," Frederic added, "we have no toys left, for I,
like a stupid dolt, broke all our fine things, and shied them into the
thicket." At this the Stranger Child laughed merrily, and cried: "Why,
Fanchon and Frederic, you are lying this minute among the loveliest
playthings that ever were seen!" "Where? — Where are they?"
Fanchon and Frederic both cried. "Look around you," said the
Stranger Child. Then Fanchon and Frederic saw how out of the thick
grass and moss all sorts of glorious flowers were peeping, with
bright eyes gleaming. And between them many coloured stones and
crystal shells sparkled and shone. While little golden insects danced
up and down humming gentle songs. "Now we will build a palace!"
said the Stranger Child. " Help me to get the stones together," And it
stooped down and began to pick up stones of many pretty colours.
Fanchon and Frederic helped, and the Stran 
 THE SHINING CHILD 375 ger Child placed the beautiful
stones one upon another, and soon there rose tall pillars shining in
the sun, while an airy golden roof stretched itself from pillar to pillar.
Then the Stranger Child kissed the flowers that were peeping from
the grass, and whispered to them lovingly, and they shot up higher
and higher, and, twining together, formed sweet-scented arbours
and covered walks in which the children danced about, full of delight
and gladness. The Stranger Child clapped its hands, and immediately
the golden roof, that was made of insects' golden wings, fell to
pieces with a hum, and the pillars melted away into a splashing
silver stream, on whose banks flowers grew and peeped into the
water. Then the Stranger Child plucked little blades of grass and
gathered twigs from trees, strewing them on the ground before
Fanchon and Frederic. The blades of grass turned into the prettiest
little live dolls ever seen, and the twigs became gay little huntsmen.
The dolls danced around Fanchon, and let her take them in her lap,
and they whispered in such delicate little voices: "Be kind to us! Love
us, dear Fanchon." The huntsmen shouted: "Halloa! Halloa! the
hunt's up!" and blew their horns, and bustled about. Then tiny hares
came darting out
 376 BOOK OF ELVES AND FAIRIES of the bushes, with tiny
dogs after them, and the huntsmen pursued them with shouts. This
was delightful! Then suddenly these wonders disappeared. And
Fanehon and Frederic cried out: "What has become of the dolls?
Where are the huntsmen.'^" The Stranger Child answered: "Oh,
they are always here waiting for you! They are close beside you, so
you may have them at any minute. But just now would you not
rather go with me through the wood.^^" "Oh, yes! yes!" cried
Fanehon and Frederic. The Stranger Child took hold of their hands,
crying: "Come! Come!" And with that off they went! The children felt
themselves floating along lightly and easily, through the trees; while
all the birds flew fluttering beside them, singing and warbling their
sweetest songs. Then suddenly up they soared into the air. Higher
and higher they mounted like birds, skimming above the tops of the
trees. Frederic shouted with delight, but Fanehon was frightened.
"Oh, my breath is going! I shall tumble!" she cried. And just at that
moment the Stranger Child let them down gently to the ground, and
said: "Now I shall sound my Forest-Song. Then good-bye for to-day."
 THE SHINING CHILD 377 And the Stranger Child took out a
little horn of wreathed gold, and began to sound it so beautifully
that the whole wood reechoed wondrously with its lovely music;
while a host of nightingales came flocking to the branches above the
children's heads, and sang their most melodious songs. But all at
once the music grew fainter and fainter, and only a soft whispering
seemed to come from the thicket into which the Stranger Child had
vanished. "To-morrow! To-morrow! I will come again!" the children
heard breathed gently as if from a distance. Then they sighed with
joy, for, though they could not understand it, never had they known
such happiness in all their lives. "Oh! I wish it was to-morrow, now!"
they both cried, as they hastened home to their parents. HOW THE
FOREST TALKED TO FANCHON AND FREDERIC "I should fancy that
the children had dreamed all this," said the Count to his wife, when
Fanchon and Frederic, who could think of nothing else but the
Stranger Child, and the wonderful events, and the exquisite music,
had told all that had happened. *'I should fancy that they had
 378 BOOK OF ELVES AND FAIRIES dreamed all this, if they
had not both seen the same things! I cannot get to the bottom of it
all!" "Don't bother your head about it, my dear," answered his wife.
"I think this Stranger Child was nobody but the schoolmaster's son
from the village. We must take care that he is not allowed to put any
more such nonsense into the children's heads." But the Count could
not agree with her, for he called the children to him again, to tell
how the Stranger Child was dressed and looked. Fanchon and
Frederic both agreed that its face was fair as lilies, that it had cheeks
like roses, cherry lips, bright blue eyes, and locks of gold; and that it
was more beautiful than words could tell. But what they said about
its dress sounded absurd. For Fanchon said that its dress was
wondrous beautiful, shining and gleaming, as if made of the petals
of flowers; while Frederic insisted that its garments were of sparkling
golden-green, like spring-leaves in the sunshine. And Frederic
thought that the Stranger Child was a boy; while Fanchon was sure
that it was a girl. And these contradictions confused their parents;
and the Count shook his head wonderingly. The next day, Fanchon
and Frederic hastened
 THE SHINING CHILD 379 to the wood, and found the
Stranger Child waiting for them. If their play had been glorious the
day before, it was ten times more glorious today; for the Stranger
Child did such marvellous things that Fanchon and Frederic shouted
for joyWhile they played, the Stranger Child talked sweetly to the
trees, flowers, and birds, and to the brook that ran through the
wood; and they all answered so clearly that Fanchon and Frederic
understood everything they said. "Dear children!" cried the Alder-
thicket, "why were you not here early, when my friend the Morning
Breeze came rustling over the blue hills, and brought us thousands
of greetings and kisses from the Golden Queen of the Dawn, and
plenty of wing- waf tings full of sweet perfumes!'* "Oh silence!" the
flowers broke in. "Do not mention that robber, the Morning Breeze!
Does he not steal our perfumes! Never mind the Alders, children, let
them lisp and whisper. Listen to us ! We love you so ! We dress
ourselves in the loveliest colours just for you!" "And do we not love
you, you beautiful flowers!" said the Stranger Child tenderly. But
Fanchon knelt down on the grass, and stretched out her arms, as if
she would take all the bright flowers to her heart, and cried: "Ah! J.
love you! I love you every one!"
 380 BOOK OF ELVES AND FAIRIES Then came a sighing out
of the tall dark firtrees, and they said: "We shade the flowers from
the hot sun, and shelter human children when the storm comes
rushing through the woods, but who loves us in return?" "Groan and
sigh," cried Frederic, "and murmur as much as you like, you green
giants that you are! It is then that the real woodsman's heart
rejoices in you! I love all, the green bushes, the flowers, and you
trees!" "You are quite right!" splashed the brook as it sparkled over
its stones. "Come sit down among this moss, dear children, and
listen to me. I come from afar; out of a deep, cool, dark rock I gush.
Look into my waves, and I will show you the loveliest pictures in my
clear mirror, the blue of the sky, the fleecy clouds, bushes, trees, and
blossoms; and your very selves, dear children, I draw tenderly into
my transparent bosom!" "Fanchon and Frederic," said the Stranger
Child, looking around with wondrous blissfulness. "Only listen how
they all love us! But the redness of evening is rising behind the hills,
and the nightingale is calling me home!" "Oh, but first let us fly a
little, as we did yesterday!" begged Frederic. "Yes," said Fanchon,
"but not quite so high. It makes my head giddy."
 THE SHINING CHILD 381 Then the Stranger Child took
them each by the hand again, and they went soaring up into the
golden purple of the evening sky, while the birds crowded and sang
around them. Among the shining clouds, Frederic saw, as if in
wavering flame, beautiful castles all of rubies and other precious
stones. "Look! Look! Fanchon!" he cried, full of rapture. "Look at
those splendid palaces! Let us fly along as fast as we can, and we
shall soon get to them." Fanchon, too, saw the castles, and forgot
her fear, and kept looking upward. "Those are my beloved castles-in-
the-air," the Stranger Child said. "But we must go no farther to-day!"
Fanchon and Frederic seemed to be in a dream, and could not make
out how they suddenly came to find themselves with their father and
mother. THE PALACE OF THE FAIRY QUEEN It was the next day. In
the most beautiful part of the wood beside the brook, between
whispering bushes, the Stranger Child had set up a glorious tent
made of tall slender lilies, glowing roses, and tulips of every hue.
And beneath this tent, Fanchon and Frederic were seated with the
Stranger Child, listening to the forest brook as
 382 BOOK OF ELVES AND FAIRIES it whirled, and rippled,
and sang its wonderful stories. "Tell us," said Fanchon, "darling
Shining Child, where your home is, and all about your father and
mother." The Stranger Child looked sorrowfully at the sky. "Ah, my
dear," it said with a sigh, "is it not enough that I come to you each
day? Why must you then ask about my home.f^ Though you were
to travel day after day, forever and ever, even to beyond the utmost
range of the purple hills, you could not reach it!" "Ah me!" sighed
Fanchon. "Then you must live hundreds and hundreds of miles away
from us! Is it only on a visit that you are here.^^" "Fanchon,
beloved," said the Stranger Child, "whenever you long for me with
all your heart, I am with you immediately, bringing you all those
plays and wonders. Is that not as good as being in my home.^*"
"Not at all," said Frederic, "for I believe that you live in a most
glorious place. I do not care how hard the road is to your home, I
mean to set out this minute for it." "And so you shall!" said the
Stranger Child smiling; "for when you see all this so clearly before
you, and make up your mind to be there, it is as good as done! The
land where I live, in truth, is so beautiful and glorious that I can give
 THE SHINING CHILD 383 you no description of it. It is my
mother who reigns over that land, — all glory and loveliness — as
Queen." "Ah! you are a Prince!" cried Frederic. *'Ah! you are a
Princess!" cried Fanchon. *'I certainly am," said the Stranger Child.
"My mother's palace is far more beautiful than those glittering
castles you saw in the evening clouds. For the gleaming pillars of her
palace are of the purest crystal, and they soar slender and tall into
the blue of heaven. Upon them rests a great, wide blue canopy.
Beneath the canopy sail the shining white clouds, hither and thither
on golden wings. And the red of the evening and the morning rises
and falls, and the sparkling stars dance in a singing circle around her
palace. "You have heard of the Fairies who can bring about great
wonders. My mother is Queen of the Fairies. Very often she holds a
feast for little children. It is then that the Elves, belonging to my
mother's Kingdom, fly through the air weaving shining rainbows
from one end of her palace to the other. Under these rainbows they
build my mother's diamond throne, — that in appearance and
perfume is like lilies, roses, and carnations. " My mother takes her
place upon the throne, and the Elves sing, and play on golden harps.
As soon as their music begins, everything in the
 384 BOOK OF ELVES AND FAIRIES palace and in the woods
and gardens, moves and sings. And all around there are thousands
of beautiful little children in charming dresses, shouting with delight.
*'The children chase each other among the golden trees, and throw
blossoms at each other. They climb the trees where the wind swings
and rocks them. They gather gold-glittering fruit, and they play with
tame deer and other gentle wild creatures, that come bounding up
to them and lick their hands. Then the children run up and down the
rainbows; or they ride on the backs of great Purple Birds that fly up
among the gleaming clouds. "How delightful that must be!" cried
Fanchon and Frederic, with rapture. "Oh! take us with you to your
home, beautiful Shining Child ! We want to stay there always!" "That
may not be," said the Stranger Child. And Fanchon and Frederic cast
down their eyes sadly to the ground. THE WICKED MOUCHE "Ah,"
said the Stranger Child, "you might not be so happy at my mother's
Court. Indeed, it would be a great misfortune for you to try to go to
her Kingdom. There are many children who cannot bear the singing
of the Purple Birds,
 THE SHINING CHILD 385 and, if they hear their songs, they
die. Then too, destruction might overtake you before you could
reach my mother's Court. Even I am not safe on my way thither.
"There was a time when I was safe anywhere. But now a bitter
enemy of my mother, whom she banished from her Kingdom, goes
raging about the world; and I cannot be safe from being watched,
pursued, and molested. Powerless as this bitter enemy is when I am
at home, nothing can protect me from him, when I am flying
abroad." "What sort of a hateful creature is it," asked Fanchon, "that
can do you so much harm.'*" "I have told you," said the Stranger
Child, "that my mother is the Fairy Queen. Among her many Elves
are some who hover in the sky, or dwell in the waters, and others
who serve at the Fairy Court. Once, a long while ago, there came
among those that served at Court, a stranger who called himself
Papillon. He said that he was learned in all the sciences of the world,
and could accomplish great things among us. My mother made him
prime minister. "Papillon soon showed his natural spite and
wickedness. He pretended to the Queen that he loved children and
could make them very happy. But instead of doing so, he hung
himself like a weight of lead on the tails of the Purple Birds, so that
they could not fly aloft. And when the
 386 BOOK OF ELVES AND FAIRIES children climb 3d the
rose-trees, he dragged them down by the legs. Then he knocked
their noses on the ground, and made them bleed. When the children
sang, he crammed all sorts of nasty stuff down their throats; for
sweet and happy singing he could not abide. And worst of all, he
had a way of smearing the sparkling precious stones of the palace,
and the lilies and roses, and even the shining rainbows, with a
horrible black juice, so that everything beautiful became sorrowful or
dead. "And when he had done all this, he gave a loud hissing laugh,
and said that everything was now as he wished it to be. Then,
shouting that he was greater than my mother, he went flying up into
the air, in the shape of an enormous fly with flashing eyes, and a
long snout. After which he went humming and buzzing around my
mother's throne, in a most abominable fashion. "When the Queen
my mother and her Elves saw this, they knew that he had come
among them under a false name, and that he was none other than
Mouche, the gloomy King of the Gnomes. The entire Fairy Court
thereupon rushed against him beating him with their wings, while
the Purple Birds seized him with their glittering beaks and gripped
him so tightly that he screamed with agony and rage. After which
the birds shook him violently, and threw him
 THE SHINING CHILD 387 down to the earth. He fell straight
onto the back of his old Aunt, who was a great blue toad. And she
carried him off to her hole. "But five hundred of the children in the
Fairy Court armed themselves with fly-flappers, to defend
themselves against Mouche if he should ever venture to return. Now
after he was gone, all the black juice disappeared, and everything
became as shining and glorious as before. *'So you see, dear
Children," continued the Stranger Child, "what kind of a creature I
have to fear. This horrible Mouche follows me about, and, if I did not
hide myself quickly, he would injure me. And I assure you that if I
were to take you with me to my home, Mouche would lie in wait for
us, and kill us." Fanchon wept bitterly at the danger to which the
Stranger Child was exposed. But Frederic said: "If that horrible
Mouche is nothing but a great fly, I'll soon hit him with father's big
flyflapper! And if once I give him a good crack on his nose, Aunty
Blue Toad will have a job carrying him to her hole again!" HOW
TUTOR INK ARRIVED TO TEACH THE CHILDREN Fanchon and
Frederic ran home as fast as they could, shouting as they went: —
 388 BOOK OF ELVES AND FAIRIES " Oh ! the Shining Child
is a beautiful Princess ! *' "Oh! the Shining Child is a beautiful
Prince!" They wanted, in their delight, to tell this to their parents,
but their father came to meet them with a most extraordinary man
walking by his side. This stranger kept muttering to himself : —
"What a nice pair of stupids these are! Ah! Ah!" The Count took him
by the hand, and said to the children: "This gentleman is the tutor
whom your kind Cousin has sent to teach you. So now shake hands
with him, and bid him welcome." But the children looked sidewise at
him, and could move neither hand nor foot. This was because they
had never seen such an extraordinary being. He was no taller than
Frederic. His body was round and bloated, and his little weazen legs
could hardly support its weight. His head was queer and square, and
his face too ugly for anything, for not only was his nose long and
pointed, but his little bulging eyes glittered, and his wide mouth was
opened in a ferocious way. He was clad in black from top to toe, and
his name was Tutor Ink. Now, as the children stood staring like
stone images, their mother cried out angrily: "You rude children,
what are you thinking oi? Come! come! give the tutor your hands."
 THE SHINING CHILD 389 The children, taking heart, did as
their mother bade them. But as soon as Tutor Ink took hold of their
hands, they jumped back, screaming: "Oh! Oh! It hurts!" The tutor
laughed aloud, and showed a needle, which he had hidden in his
hand to prick the children with. Fanchon was weeping; but Frederic
growled. "Just try that again, little BigBody, if you dare!" "Why did
you do that, Tutor Ink.?" asked the Count, somewhat annoyed.
"Well, it's just my way!" answered Tutor Ink; "I can't alter it!" and
with that he stuck his hands to his sides, and went on laughing until
his voice sounded like the noise of a broken rattle. Alas! after that
there was no more running about in the wood! Instead the children,
day after day, had to sit in the house, repeating after Tutor Ink
strange gibberish, not one word of which they could understand.
With what longing eyes they looked at the wood! Often they thought
they heard, amidst the happy songs of the birds and the rustling of
the trees, the voice of the Stranger Child, calling, and calling:
"Fanchon! Frederic! Are you not coming to play with me.^* Oh,
come! I have made you a palace all of flowers! We will play there,
and I will give you all sorts of
 390 BOOK OF ELVES AND FAIRIES beautiful stones! And
then we'll fly through the air, and build cloud-castles! Come! Oh,
come!" At this the children's thoughts were so drawn to the wood,
that they neither heard nor saw their tutor any longer; although he
thumped on the table with both his fists, and hummed, and growled,
and snarled. At last one day the Count perceived how pale the
children were getting, and bade Tutor Ink take them for a walk. The
Tutor did not like the idea at all. And the children did not like it
either, saying : — "What business has Tutor Ink in our darling
wood.?" WHAT HAPPENED WHEN TUTOR INK TOOK THE CHILDREN
TO THE WOOD "Well, Tutor Ink, is it not delightful here in our
wood.f*" asked Frederic. Tutor Ink made a face, and muttered:
"Stupid nonsense! All one does is to tear his stockings! One can't
hear a word because of the abominable screeching of the birds!"
"But surely you love the flowers.'" Fanchon chimed in. At this Tutor
Ink's face became a deep cherrycolour, and he beat his hands about
him, crying:
 THE SHINING CHILD 391 "Stupid nonsense! Ridiculous
nonsense! There are no decent flowers in this wood!" "But don't you
see those dear Httle Lilies-ofthe-valley peeping up at you with such
bright loving eyes?" asked Fanchon. "What! What!" the Tutor
screamed. "Flowers! — eyes? — Ha! Ha! — Nice eyes! — Useless
things!" And with that he stooped, and plucking up a handful of the
lilies, roots and all, threw them into the thicket. Fanchon could not
help shedding bitter tears, and Frederic gnashed his teeth in anger.
Just then a little Robin alighted on a branch near the Tutor's head,
and began to sing sweetly. The Tutor, picking up a stone, threw it,
and the bird fell dying to the ground. Frederic could restrain himself
no longer. "You horrible Tutor Ink!" he cried, "what did the little bird
do to you, that you should strike it dead?" And looking toward the
thicket, he called sadly: "Oh! where are you, beautiful Shining Child?
Oh, come! Only come! Let us fly far, far away! I cannot stay beside
this horrible creature any longer." And Fanchon, stretching out her
hands, sobbed and wept bitterly. "Oh, you darling Shining Child," she
cried. "Come to us! Come to us! Save us! Save us! Tutor Ink is killing
us, as he is kiUing the flowers and birds!"
 392 BOOK OF ELVES AND FAIRIES "What do you mean by
the Shining Child?' snarled Tutor Ink. But at that instant there was a
loud whispering, and a rustling, in the thicket, and a sound as of
muflfled drums tolling in the distance. Then the children saw, in a
shining cloud that floated above them, the beautiful face of the
Stranger Child, and tears like glittering pearls were rolling down its
rosy cheeks. "Ah! darling playmates!" it cried. "I cannot come to you
any more! Farewell! Farewell! The Gnome Mouche has you in his
power! Oh! you poor children, good-bye! good-bye!" And then the
Stranger Child soared up far into the clouds. And the most
marvellous thing happened! Behind the children there began a most
horrid, fearsome buzzing and humming, snarling and growling, and,
lo! Tutor Ink had changed into an enormous frightful-looking fly. And
he began to fly upward heavily, following the Stranger Child.
Fanchon and Frederic, overpowered with terror, ran out of the wood,
and did not dare to look up at the sky until they had got some
distance away. And, then, when they did so, all that they could see,
was a shining speck in the clouds, glittering like a star, and coming
nearer and downward. The star grew bigger and bigger, and the chil

 THE SHINING CHILD 393 dren could hear, as if it were, the
call of a trumpet; and presently they saw that the star was really a
splendid bird with shining purple plumage. It came dropping down
to the wood, clapping its mighty wings, and singing loud and clear.
"Hurrah! Hurrah!" shouted Frederic. "That is a Purple Bird from the
Fairy Court!- He will bite Tutor Ink to death! The Shining Child is
saved! — and so are we! Come, Fanchon, let us get home as fast as
we can, and tell our father about it." WHAT THE COUNT DID TO
TUTOR INK The children burst into the house where their parents
were sitting. "Hurrah! Hurrah!" Frederic shouted. "The Purple Bird
has bitten Tutor Ink to death!" "Oh, Father dear. Mother dear!" cried
Fanchon. "Tutor Ink is not Tutor Ink at all! He is really the wicked
Mouche, King of the Gnomes; a monstrous fly, but a fly with clothes
and shoes and stockings on!" "Who on earth has been putting such
nonsense into your heads.?" asked the Countess. And the parents
gazed at the children in utter amazement, while they went on to tell
about the Stranger Child whose mother was a great Fairy
 394 BOOK OF ELVES AND FAIRIES Queen, and about the
Gnome King, Mouche, and the Purple Bird. The Count grew very
grave and thoughtful. "Frederic," said he, "you are really a sensible
boy, and I must admit that Tutor Ink has always seemed to me a
strange mysterious creature. Your mother and I are by no means
satisfied with him, particularly your mother. He has such a terrible
sweet- tooth, that there's no way of keeping him from the sugar and
jams. And, then, he hums and buzzes in such a distressing manner.
But in spite of all this, my dear boy, just think calmly for a minute.
Even if there are such things as Gnomes in the world, do you really
mean to say that your Tutor has become a fly.f*" Frederic looked his
father steadily in the face with his clear blue eyes, then said: — "I
should not have believed it myself, if the Stranger Child had not said
so, and if I had not seen with my own eyes that he is only a horrible
fly, and pretends to be Tutor Ink. And then," continued Frederic,
while his father shook his head in wonder, "see what Mother says
about him. Is he not ravenous for sweet things .^^ Is that not just
like a fly? And then his hummings and buzzings." "Silence," cried the
Count. "Whatever Tutor Ink is, one thing is certain, the Purple Bird
has
 THE SHINING CHILD 395 not bitten him to death! for there
he comes out of the wood!" At this the children uttered loud
screams, and rushed behind the door. In truth, Tutor Ink was
approaching, but he was wild-looking and bewildered. He was
buzzing and humming, and springing high in the air, first to one side,
then to the other, and banging his head against the trees. He
tumbled into the house, and dashed at the milkjug, and popped his
head into it so that the milk ran over the sides. Then he gulped and
gulped, making a horrid noise of swallowing. "What ails you, Tutor
Ink?" cried the Countess. "What are you about.'*" "Are you out of
your senses? " asked the Count. "Is the foul fiend after you?" But
without making any answer. Tutor Ink, taking his mouth from the
milk-jug, threw himself down on the dish of butter, and began to lick
it with his pointed tongue. Then, with a loud buzzing, he sprang off
the table and began to stagger hither and thither about the room, as
though he was drunk. "This is pretty behaviour!" cried the Count, as
he tried to seize Tutor Ink by the coat tails; but Tutor Ink managed
to elude him deftly. Just then Frederic came running up with his
father's big fly -flapper in his hand, and gave it to the Count, crying:
—
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