There is a strong association with tobacco smoking (leukoplakia is six times more common in smokers than non-smokers) and alcohol intake (independent of drinking pattern or beverage type). It is also associated with betel quid chewing and oral submucous fibrosis.
How is the diagnosis made?
Biopsy of clinically suspected oral leukoplakia is mandatory to: exclude recognised diseases, and to assess for the absence or presence and grade of dysplasia.
It is appropriate to wait 2 weeks after first presentation to assess clinical response to initial treatment, e.g. for candida, change in tooth brushing habit, cessation of smoking, etc
The biopsy may be incisional or excisional, single or multiple and may be done under local or general anaesthetic depending on site, number of biopsies required and type of biopsy.
Biopsies should be taken from either a symptomatic area, or if asymptomatic then from red or indurated areas.
The presence of dysplasia, carcinoma-in-situ and invasivecarcinoma cannot always be predicted clinically.
The histopathology of oral leukoplakia is not always diagnostic. Epithelial changes range from atrophy (thinned) to hyperplasia (thickened) and it may show hyperkeratosis. Dysplasia (atypical changes) may be mild, moderate, severe, carcinomain situ or invasivecarcinoma. The pathology report must comment on the absence or presence of dysplasia, and the severity.
What is the treatment of oral leukoplakia?
The treatment of oral leukoplakia depends on its cause.