ICDO code80513

Although uncommon, 75% of all cases of VC occur in the oral cavity. It is an exophytic, warty, slowly growing variant of SCC with pushing margins. It typically involves older males {950,1251,1677, 1695,2621}. Chronic smokeless tobacco use is accepted as the primary etiological factor for oral VC. Human papillomavirus subtypes 16 and 18 have been identified in up to 40% of oral VC {1927,2349}. Oral VC begins as a well-demarcated, thin white keratotic plaque which quickly thickens and develops papillary (blunted tips) or verruciform (pointed tips) surface projections. Occasional lesions present as erythaematous or pink papular masses. The colour depends on the amount of keratin produced and the degree of host inflammatory response to the tumour. This cancer almost always remains broad-based or sessile and can become quite extensive from lateral growth by the time of diagnosis. Rare fungating examples, however, may appear to be somewhat pedunculated. Smokeless tobacco ker-atosis (tobacco pouch) is often seen on adjacent mucosal surfaces in patients who chew tobacco or use snuff. Unless the tumour is infected or is encroaching on alveolar nerves in the jawbones, VC is an asymptomatic lesion. Surface ulceration and haemorrhage are not seen, unless a focus of SCC is present in the mass.

VC consists of thickened club-shaped papillae and blunt stromal invaginations of well-differentiated squamous epithelium with marked keratinization. The squamous epithelium lacks the usual cytologic criteria of malignancy, and by morphometry, the cells are larger than those seen in SCC {489}. Mitoses are rare, and observed in the basal layers; DNA synthesis (S-phase) is also limited primarily to the basal layers {737}. VC invades the stroma with a pushing, rather than infiltrating border. Dense lymphoplasmacytic host response is common. Intraepithelial microabscesses are seen, and the abundant keratin may evoke a foreign body reaction.

The surrounding mucosa shows progressive transition from hyperplasia to VC. A downward dipping of epithelium often "cups" the VC periphery, and is the ideal site for deep biopsy {174,1192}. With extensive surgical removal, and without neck dissection, the 5-year disease-free survival rate is 80-90%, although 8% of patients require at least one additional surgical procedure during that time {1870,1927}. Treatment failures usually occur in patients with the most extensive involvement or in those unable to tolerate extensive surgery because of unrelated systemic diseases. No molecular or other markers have yet shown prognostic significance for oral VC. However, one-fifth of these tumours contain a co-existing SCC which may not be identified without extensive histologic sectioning {1927}. Such hybrid tumours have a greater tendency to recur locally and a slight tendency to metastasize to the ipsilateral neck.

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