Cawson’s Essentials of Oral Pathology and Oral Medicine E-Book Annotations
Cawson’s Essentials of Oral Pathology and Oral Medicine E-Book TOC
3 Disorders of development
- Related chapter: 07 3 Disorders of development
Clefts of lip or palate > Cleft lip and cleft palate
- p. 45: CLEFTS OF LIP OR PALATE
- p. 45: with or without cleft palate, are genetically distinct conditions.
- p. 45: Bifid uvula
8 Infections of the jaws
- Related chapter: 12 8 Infections of the jaws
Alveolar osteitis > Treatment
- p. 120: ACUTE OSTEOMYELITIS
- p. 120: rom a focus of infectio
- p. 120: he jaws are resistant to osteomyelitis, and most patients have a predisposing cause.
Acute osteomyelitis ➔ Summary charts 5.1 and 13.1 pp. 79, 222 > Complications and resolution
- p. 122: CHRONIC OSTEOMYELITIS
Chronic osteomyelitis ➔ Summary charts 5.1 and 13.1 pp. 79, 222 > Pathology
- p. 123: DIFFUSE SCLEROSING OSTEOMYELITIS
Chronic low-grade focal osteomyelitis and sclerosing osteitis ➔ Summary charts 5.1, 13.1 and 12.2 pp. 79, 222, 203
- p. 124: computed tomography (CT). Sclerosing osteitis is a term given to a localised area of sclerosis without evidence of infection. These are probably a reaction to inflammation rather than infection and are frequently seen around the roots of non-vital teeth
- p. 124: CHRONIC LOW-GRADE FOCAL OSTEOMYELITIS AND SCLEROSING OSTEITIS
- p. 124: Focal sclerosing osteomyelitis is commoner in the young because their bone is better vascularised and produces more reactive bone deposition around the infection
9 Major infections of the mouth and face
- Related chapter: 13 9 Major infections of the mouth and face
Actinomycosis > Pathology
- p. 135: ACTINOMYCOSIS
10 Cysts in and around the jaws
- Related chapter: 14 10 Cysts in and around the jaws
Classification of cysts
- p. 139: CLASSIFICATION OF CYSTS
- p. 139: Odontogenic cysts are lined by odontogenic epithelium derived from the
- p. 139: This epithelium originates by proliferation of rests of Serres, reduced enamel epithelium or rests of Malassez.
Common features of jaw cysts
- p. 140: Hydrostatic pressure is the mechanism of cyst growth in almost all cysts. The luminal contents are under pressure for a variety of reasons. There is poor lymphatic drainage from the cavity, the wall and lining have partial properties of a semipermeable membrane and the lumen contains many degraded inflammatory proteins and dead lining cells. These and other factors produce an osmotic pressure that expands the cyst.
Odontogenic cysts > Radicular cyst ➔ Summary chart 10.1 p. 163 > Clinical features
Odontogenic cysts > Radicular cyst ➔ Summary chart 10.1 p. 163 > Radiography
- p. 143: Box 10.7 Radicular cyst: key features • Form in bone in relation to the root of a non-vital tooth • Arise by epithelial proliferation in an apical granuloma • Are usually asymptomatic unless infected or large • Diagnosis is by the combination of radiographic appearances, a non-vital tooth and appropriate histological appearances • Clinical and radiographic features are usually adequate for planning treatment • Do not recur after enucleation • Residual cysts are radicular cysts that remain after the causative tooth has been extracted • Cholesterol crystals often seen in the cyst fluid but are not specific to radicular cysts
- p. 143: Pathogenesis
Odontogenic cysts > Radicular cyst ➔ Summary chart 10.1 p. 163 > Lateral radicular cyst ➔ Summary chart 10.1 p. 163
- p. 146: DENTIGEROUS CYSTS
Odontogenic cysts > Dentigerous cysts ➔ Summary chart 10.1 p. 163 > Clinical features
- p. 147: Pathogenesis
Odontogenic cysts > Dentigerous cysts ➔ Summary chart 10.1 p. 163 > Differential diagnosis
- p. 148: ERUPTION CYST
Odontogenic cysts > Odontogenic keratocyst ➔ Summary charts 10.1 and 10.2 pp. 163, 164 > Clinical features
- p. 149: Box 10.8 Dentigerous cyst: key features • Arise in bone and contain the crown of an unerupted tooth, which is usually displaced • Are most frequently associated with unerupted third molars and canines • Clinical and radiographic features usually provide an accurate preoperative diagnosis but confirmation is histological • May be mistaken radiographically for an odontogenic keratocyst or ameloblastoma • Respond to enucleation or marsupialisation and do not recur after treatment
- p. 149: ODONTOGENIC KERATOCYST
- p. 149: The name of this cyst indicates that its epithelial lining keratinises, but this alone is not specific. Another less common cyst, the orthokeratinising odontogenic cyst, also has this feature, and minor focal keratinisation can be seen in other odontogenic cysts.
- p. 149: Definition The odontogenic keratocyst is a developmental odontogenic cyst with a tendency to recur, characterised by a histological appearance of parakeratinised lining epithelium with palisaded ameloblast-like basal cells.
- p. 149: Radiography
- p. 149: Table 10.1 The two types of odontogenic cysts that keratinise
Odontogenic cysts > Odontogenic keratocyst ➔ Summary charts 10.1 and 10.2 pp. 163, 164 > Pathogenesis
- p. 150: ocysts being large at time of discovery. Pathogenesis
Odontogenic cysts > Odontogenic keratocyst ➔ Summary charts 10.1 and 10.2 pp. 163, 164 > Histopathology
- p. 151: Typical histological features of odontogenic keratocyst
Odontogenic cysts > Odontogenic keratocyst ➔ Summary charts 10.1 and 10.2 pp. 163, 164 > Basal cell naevus syndrome
- p. 153: Basal cell naevus syndrome
Odontogenic cysts > Lateral periodontal cysts > Botryoid odontogenic cysts
- p. 155: LATERAL PERIODONTAL CYSTS
Odontogenic cysts > Carcinoma arising in odontogenic cysts
- p. 157: GINGIVAL CYST OF THE NEWBORN
Odontogenic cysts > Gingival cyst of the newborn > Epstein’s pearls
- p. 158: GINGIVAL CYST OF ADULTS Gingival cysts in adults are rare and present
- p. 158: NON-ODONTOGENIC CYSTS
- p. 158: NASOPALATINE DUCT OR INCISIVE CANAL CYST
Non-odontogenic cysts > Nasolabial cyst
- p. 160: NASOLABIAL CYST
11 Odontogenic tumours and related jaw lesions
- Related chapter: 15 11 Odontogenic tumours and related jaw lesions
Benign mesenchymal tumours > Odontogenic myxoma ➔ Summary chart 10.2 p. 164 > Normal dental follicle
Fibroosseous odontogenic lesions > Malignant odontogenic tumours
- p. 183: MALIGNANT ODONTOGENIC TUMOURS
13 Genetic, metabolic and other non-neoplastic bone diseases
- Related chapter: 17 13 Genetic, metabolic and other non-neoplastic bone diseases
Fibro-osseous lesions > Polyostotic fibrous dysplasia
Bone ‘cysts’ > Solitary bone cyst ➔ Summary charts 10.1 and 10.2 pp. 163, 164 > Management
- p. 220: Aneurysmal bone ‘cyst’
15 Diseases of the oral mucosa
- Related chapter: 19 15 Diseases of the oral mucosa
Primary herpetic stomatitis ➔ Summary chart 15.2 p. 253 > Clinical features
- p. 235: HERPESVIRUS DISEASES
- p. 235: Diseases of the oral mucosa: mucosal infections
- p. 235: PRIMARY HERPETIC STOMATITIS
Primary herpetic stomatitis ➔ Summary chart 15.2 p. 253 > Pathology
- p. 236: Table 15.2 Herpesvirus diseases relevant to dentistry
Primary herpetic stomatitis ➔ Summary chart 15.2 p. 253 > Latency
- p. 238: HERPES LABIALIS
Herpes labialis ➔ Summary chart 15.2 p. 253 > Herpetic whitlow
- p. 239: HERPES ZOSTER OF THE TRIGEMINAL NERVE
Tuberculosis > Pathology
Candidosis > Thrush ➔ Summary chart 15.1 and 19.1 pp. 252, 314 > Clinical features
- p. 244: CANDIDOSIS Candidosis* is caused
- p. 244: There are various classifications of candidosis, but in reality these diseases merge into one another and can coexist. Thus, infection causes a spectrum of presentations, rather than many diseases (Box 15.5). The commonest forms are thrush, chronic hyperplastic candidosis and denture stomatitis. Chronic mucocutaneous candidosis is discussed later in this chapter and in
- p. 244: reality these diseases merge into one another and can coexist. Thus, infection causes a spectrum of presentations, rather than many diseases (Box 15.5). The commonest forms are thrush, chronic hyperplastic candidosis and denture stomatitis. Chronic mucocutaneous candidosis is discussed later in this chapter and in
- p. 244: Thrush
Candidosis > Angular cheilitis ➔ Summary chart 15.1 p. 252 > Management
18 Benign chronic white mucosal lesions
- Related chapter: 22 18 Benign chronic white mucosal lesions
Leukoplakia
- p. 291: FORDYCE SPOTS
- p. 291: Benign chronic white mucosal lesions
- p. 291: Important causes of benign mucosal white lesions
Frictional keratosis ➔ Summary charts 19.1 and 19.2 pp. 314, 315 > Diagnosis and management
Stomatitis nicotina ➔ Summary chart 19.1 p. 314 > Clinical features
- p. 293: STOMATITIS NICOTINA
Oral hairy leukoplakia ➔ Summary chart 19.2 p. 315 > Clinical features
- p. 294: ORAL HAIRY LEUKOPLAKIA
White sponge naevus ➔ Summary chart 19.2 p. 315 > Clinical features
- p. 295: WHITE SPONGE NAEVUS
White sponge naevus ➔ Summary chart 19.2 p. 315 > Management
19 Potentially malignant disorders
- Related chapter: 23 19 Potentially malignant disorders
Terminology
Lupus erythematosus
- p. 306: HPV-ASSOCIATED DYSPLASIA
Management of potentially malignant disorders > Risk assessment > Dysplasia grading
20 Oral cancer
- Related chapter: 24 20 Oral cancer
Epidemiology > Age and gender incidence
- p. 317: EPIDEMIOLOGY
Aetiology > Tobacco use > Cigarette smoking
- p. 318: Box 20.2 Possible aetiological factors for oral cancer
Pathology > Oral carcinoma histopathology
- p. 322: Table 20.2 Clinical features of oral squamous carcinoma
- p. 322: Oral carcinoma histopathology
Pathology > Local spread
- p. 323: malignancy: large and irregularly shaped nuclei, darkly stained nuclei (hyperchromatism), frequent and sometimes abnormal mitoses (Fig. 20.11). These are essentially the same cytological changes as are seen in dysplastic epithelium (Table 19.3); only invasion differentiates the two processes. Squamous carcinoma is graded according to its degree of differentiation, the degree to which the malignant cells differentiate to form prickle cells and keratin. In welldifferentiated tumours, the cells have cytoplasm that stains palely with eosin or may form concentric layers of keratin (cell nests or keratin pearls; Fig. 20.12). In poorly differentiated tumours, the cells tend to be more irregular and darkly staining and show little evidence of prickle cell differentiation or keratinisation. In the most poorly differentiated carcinomas, the cells have little cytoplasm and may not be recognisable as epithelial cells by routine microscopy (Fig. 20.13). Poorly differentiated carcinomas tend to infiltrate more widely at an early stage, are more likely to metastasise and carry a poorer prognosis. The m
Pathology > Site variation > Alveolar ridge and gingiva
- p. 326: MANAGEMENT
Management > Treatment
- p. 327: he UK patient ‘pathway’ for oral squamous carcinoma
- p. 328: Table 20.4 Tumour Node Metastasis (TNM) staging for oral carcinoma.
Management > Treatment > Management of the neck
- p. 329: Management of the neck
24 Benign mucosal swellings
- Related chapter: 28 24 Benign mucosal swellings
Papillomas ➔ Summary chart 24.1 p. 372 > Squamous cell papilloma
- p. 374: Infective warts (verruca vulgaris)
Verruciform xanthoma > Pathology
- p. 375: VERRUCIFORM XANTHOMA
26 Oral pigmented lesions
- Related chapter: 30 26 Oral pigmented lesions
Diffuse mucosal pigmentation ➔ Summary chart 26.1 p. 390
- p. 383: Oral pigmented lesions
- p. 383: DIFFUSE MUCOSAL PIGMENTATION
- p. 383: PIGMENTATION
- p. 383: Addison’s disease
- p. 383: Drugs
- p. 383: Box 26.1 Oral pigmented lesions
Localised melanin pigmentation ➔ Summary chart 26.1 p. 390 > Physiological pigmentation
- p. 384: Oral melanocytic naev
- p. 384: Acquired melanocytic naevi are otherwise known as moles. These are common developmental conditions in which melanocytes proliferate and form a mass between the epithelium and connective tissue (melanocytes outside the epithelium are called naevus cells).
- p. 384: Blue naevus
- p. 384: They are almost always on the palate of children or young adults
- p. 384: Congenital naevi cannot be distingu
- p. 384: Physiological pigmentation
- p. 384: This is the most common cause of oral pigmentation. The gingivae are particularly affected (Fig. 26.2). The inner aspect of the lips is typically spared
- p. 384: Melanotic macules
- p. 384: Gingiva, buccal mucosa and palate are the favoured sites (Fig. 26.3). The lesions are completely benign. However, as the appearance is indistinguishable from early melanoma and because they are infrequent, they are usually excised for confirmation of diagnosis unless a long history is obtained.
- p. 384: Oral melanotic macules associated with HIV infection
- p. 384: Oral and labial melanotic macules may develop in as many as 6% of patients with HIV infection, approximately twice the frequency seen in HIV-negative persons
- p. 384: Excision biopsy of melanotic macules is necessary for diagnosis. Unlike those in HIV-negative persons, these macules are more likely to enlarge and to
Localised melanin pigmentation ➔ Summary chart 26.1 p. 390 > Syndromes with oral pigmentation ➔ Summary chart 26.1 p. 390 > Peutz–Jeghers syndrome
- p. 385: Peutz–Jeghers syndrome
Localised melanin pigmentation ➔ Summary chart 26.1 p. 390 > Syndromes with oral pigmentation ➔ Summary chart 26.1 p. 390 > Other syndromes with pigmentation
- p. 386: Amalgam and other tattoos
Melanoma ➔ Summary chart 26.1 p. 390 > Clinical
- p. 388: MELANOMA
Melanoma ➔ Summary chart 26.1 p. 390 > Treatment
- p. 390: SECTION 390 Soft tissue disease Summary chart 26.1 The common causes of oral pigmented lesions.