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Author: Dr Delwyn Dyall-Smith, Dermatologist, 2009.
Carcinoma in situ of oral cavity is also called oral intraepithelial carcinoma. It is a common cause of oral leukoplakia. In carcinoma in situ, cancer cells are confined to the epithelium, in contrast to invasive oral cancer (squamous cell carcinoma, SCC).
Oral intraepithelial carcinoma may affect about 0.5% of the world population, although it is likely to vary with gender, geography and ethnicity.
There is a strong association with tobacco smoking (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.
It usually appears in adult life with prevalence increasing with increasing age:
Clinical features of carcinoma in situ of oral cavity
An early lesion is a slightly elevated grey-white plaque either well defined or which blends in gradually with surrounding mucosa. It can be a localised solitary lesion or multifocal and diffuse.
Two clinical forms are recognised.
1. Homogeneous – refers to homogeneous uniform colour AND texture
The surface may become leathery – smooth, wrinkled, corrugated or with shallow cracks. This form is usually asymptomatic.
2. Non-homogeneous – refers to irregularity of either the colour OR the texture
Variants of the non-homogeneous form have been described including nodular, verrucous (including proliferative verrucous) and speckled. This form may be associated with mild discomfort or localized pain.
The most common site affected is the inside cheeks (buccal mucosa) and then in decreasing order of frequency:
A large proportion of oral cancers are associated with preceding longstanding carcinoma in situ, especially the proliferative verrucous variant. Possibly 1% of all oral leukoplakias become cancer.
There may be no change in appearance or symptoms in the early stages of cancer development. Classic changes of cancer are ulceration, induration/hardness, bleeding and tumour outgrowth.
Factors reported as associated with increased risk of SCC development:
No molecular tumour markers have yet been found that can be used to predict cancer development in an individual or lesion. The role of human papillomaviruses (wart virus) has not yet been determined.
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, carcinoma in situ or invasive carcinoma. The pathology report must comment on the absence or presence of dysplasia, and the severity.
It is not known if early active treatment of in situ squamous cell carcinoma prevents the development of invasive squamous cell carcinoma. There is a high recurrence rate after treatment.
Lifelong follow-up is recommended whether or not the disorder has been treated:
Oral mucosal examination must include the floor of mouth and sides of tongue using gauze to hold tip of the tongue and pull upwards and side to side. Most oral SCC develop in the sides and undersurface of the tongue, floor of mouth and back to the soft palate and tonsillar area.
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