4.3.1 Leukoplakia

Grading & Level of Importance: B

ICD-11

Synonyms

None.

Epidemiology

Current incidence of cancers of the oral cavity is mainly consisting of squamous cell carcinomas. It varies worldwide from less than three to seven or eight per 100,000 population. It affects mainly middle-aged and elderly people. Prevalence of oral leukoplakia is approximately 0.1% with a huge variation in different parts of the world above the age of 30-40 years. Annual risk of malignant transformation of oral leukoplakia from 2 to 3% or even much higher.

Definition

White adherent mucosal changes, reflecting increased or abnormal keratinisation of the stratified squamous (normally not keratinised) mucosal epithelium of the mouth or transitional epithelium (lips, penis).

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“A predominantly white patch or plaque that cannot be characterized clinically or pathologically as any other disorder; oral leukoplakia carries an increased risk of cancer development either in or close to the area of the leukoplakia or elsewhere in the oral cavity or the head-and-neck region” (WHO 2005 and 1978 adjustment suggestion).

Aetiology & Pathogenesis

Based on cause. Exogenous: chemical (tobacco) or mechanical irritation (abnormal teeth, dentures), also hereditary.

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Tobacco habits of different types (nitrosamines and aromatic carbohydrates such as 3,4-benzpyrene) and alcohol consumption are the most important etiologic factors (combined risk increases by 6 to 15 fold). Human papilloma virus plays a limited role in the etiology of oral cancer in contrast to its role in oropharyngeal cancer

Signs & Symptoms

Asymptomatic white plaques.

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Homogenous and inhomogenous leukoplakia. Both forms are differentin border, surface, profil, thickness and colour. Homogene Leukoplakia shows flat, thin, sharply bordered and homogenous surface pattern. Inhomogenous leukoplakia in contrast has verrucous and erosive surface as well as colour varying from white to red (erythroleukoplakia).

Localisation

Anywhere in the mouth, especially buccal or sublingual mucosa; also genital or anal mucosa.

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Mainly buccal, gingiva and lateral tongue.

Classification

Classically, two major clinical types of leukoplakia are recognized, being the homogeneous and the non-homogeneous type. The last should have a higher risk of malignant development.

Squamous intraepithelial neoplasia SIN I-III.

Laboratory & other workups

Unremarkable.

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No specific.

Dermatopathology

Epithelial hyperplasia with or without atypia.

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Oral leukoplakia histopathological findings range from hyperkeratosis without epithelial dysplasia to various degrees of epithelial dysplasia. Absence of epithelial dysplasia does not exclude oral leukoplakia as being a potentially (pre)malignant lesion. 5% invasive, 25% precursor intraepithelial.

Course

Chronic, can evolve into carcinoma.

Complications

HPV 16, 18, 31 in lesion increases risk of malignant transformation.

Diagnosis

Clinical features; if persistent or infiltrated histology is mandatory.

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Inspection and palpation followed by VELscope (Vision Enhanced Lesion Scope) and algorithm of steps incl. brush biopsy for DNA testing and regular biopsy.

Differential Diagnosis

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Frictional hyperkeratosis, lichen planus, hyperplastic type of candidiasis, restoration associated epithelial lesion, alveolar ridge keratosis. Naevus spongiosus albus mucosae.

Prevention & Therapy

Clinical follow-up, eliminating irritating factors, in some instances oral retinoids or excision.

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Prevention: avoiding risk factors as mentioned above.

Therapy: no harmonized unifying concept. Excision, cryotherapy, laser, local vitamin A acid and photodynamic therapy

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