Premalignant lesions and conditions
Premalignant condition: a systemic condition that increases the changes of malignant change.
Premalignant lesion: localised areas more likely to undergo malignant change
It is beyond the scope of this article to describe in detail all premalignant oral lesions and conditions. Therefore only leukoplakia has been considered in detail.
Definition: a predominantly white lesion of the oral mucosa that can not be classified as any other lesion; associated with no other cause than tobacco.
Diagnosis: Leukoplakia is a clinical diagnosisand has no histological connotations. Clinical diagnosis is made by exclusion of all other causes.
White lesions such as leukoplakia appear white due to heaping of keratin that appears white when wet. Changes with the potential for malignancy occur in leukoplakia. Certain changes are indicators of an increased risk of malignancy.
Incidence: 1-10% depending on the part of the world and cultural smoking habits. Men and women are equally affected. Increasingly, younger people are being affected.
Presentation: the floor of the mouth and the buccal mucosa are the most common sites. Lesions affecting the floor of the mouth or the ventral of the tongue have an increased risk of malignant change.
Definition: red, velvety plaques that cannot be clinically or pathologically classified as any other condition.
Presentation: plaques can be homogenous or associated with white areas of leukoplakia (erythroplakia/speckled leukoplakia). Transformation from leukoplakia to erythroplakia is a sinister sign.
Histologically: carcinoma in situ or invasive carcinoma
Aetiology of Leukoplakia/erythroplakia
The exact aetiologyis unknown. However, several predisposing factors have been identified.
Tobacco: prevalence increases with the amount of tobacco use. In cigarette smokers, diffuse lesions occur on the cheeks, lips and tongue.
Smokeless tobacco and snuff dipping are associated with oral keratosis. Smokeless tobacco is banned in the UK.
The use of paan containing Areca nut is associated with lesions on the buccal sulcus in Asia.
Tobacco-associated keratosis can regress on cessation of the habit.
Alcohol: synergistic effects of alcohol and tobacco increase the risk of malignancy
Viruses: Human papilloma virus types 6, 16 and 18.
Epithelial atrophy: conditions that predispose to atrophy may increase the risk of leukoplakia e.g.
Tumour suppressor genes: TSG regulate cell proliferation. Mutation of gene P53 results in inactivation of the suppressor activity and uncontrolled cell proliferation resulting in dysplasia and leukoplakia.
Candida: the cause or effect role of candida is unclear. Candida has been identified in the premalignant lesion chronic hyperplastic candidosis and has been shown to thrive in tissues of altered morphology. Candida albicans can induce epithelial proliferation and can produce nitrosamines which might be carcinogenic. The plaques cannot be wiped off but may be removed by firm scraping. It is distinguishable from other leukoplakias only by biopsy.
The rate of malignant transformation is highly variable. The floor of the mouth, ventral of the tongue and the lingual aspect of the lower alveolar mucosa are most likely to undergo malignant transformation. Lesions showing dysplasia are high risk for malignant transformation. Non-homogeneous, erythroplakia and candidal-associated leukoplakia are the highest risk. However, even dysplastic lesions can regress reflecting the unpredictability of leukoplakia.
Histological indications of dysplasia:
Speckled leukoplakia and erythroplakia are the most likely to show dysplasia.
If a lesion is clinically unchanged following 3 months, the patient should be kept under 6 month review then a re-biopsy should be carried out after 3 years.
Clinical features indicating malignant transformation of leukoplakia or erythroplakia:
Size is irrelevant to the risk of malignant change. Non-smokers have the highest risk of malignant transformation.
Management of leukoplakia
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