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Oral Epithelial Tumours

Oral Epithelial Tumours. The main tumours derived from oral epithelium are:- Squamous cell papilloma(benign) Squamous cell carcinoma(malignant). Squamous cell carcinoma. Scc accounts for 90% of all oral malignant neoplasms over 90% of oral cancer occurs in pts over the age of 40 yrs

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Oral Epithelial Tumours

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  1. Oral Epithelial Tumours The main tumours derived from oral epithelium are:- • Squamous cell papilloma(benign) • Squamous cell carcinoma(malignant)

  2. Squamous cell carcinoma • Scc accounts for 90% of all oral malignant neoplasms • over 90% of oral cancer occurs in pts over the age of 40 yrs • Tongue , floor of mouth and buccal mucosa are commonest sites for scc and buccal mucosa in India.

  3. In UK, oral cancer accounts for about 1 per cent of all cancers. In the USA it accounts for about 2-4 per cent, but in parts of India it accounts for 30-40 per cent of all malignant tumours and in some regions a figure approaching 50 per cent has been reported.

  4. Aetiological factors • Tobacco Smoking • Smokless Tobacco • Betel quid and other chewing habits • Alcohol • Diet and nutrition • Dental factors

  5. Ultraviolet light • Viruses • Immunossupression • Chronic infections • Occupation

  6. Pipe and cigar smoking have been linked with carcinoma of the lip for many years, and the evidence linking cigarette smoking with intraoral carcinoma is now firmly established.

  7. Snuff-dipping is associated with a significantly increased risk for carcinoma of the gingiva and buccal mucosa, in smokeless tobacco the relative risk is about half that of smoking.

  8. Several studies have reported a link between oral cancer and liver cirrhosis, this is less striking than that seen with tobacco smoking. Histological studies suggest that alcohol and tobacco usage are associated with atrophy of oral epithelium.

  9. ONCOGENES • derived from mutated proto-onco. of normal cells • Mutation result in enhanced or inappropriate gene expression • Code for growth promoting factors • Excess or abnormal onco.product may lead to uncontrolled cell growth • Over expression of certain onco.is involved in the etiology of oral cancer

  10. Tumour-suppressor gene • Present in normal cells • Regulate cell proliferation • Mutation result in deficient protein production • Deficient or defective product may lead to uncontrolled cell growth • Mutation of the p53 gene is involved in many human cancers including oral cancer

  11. Clinical presentation Early lesion appears either as: • White patch • Small exophytic growth • Small ulcer • Area of erythroplakia • Raised swelling or crusty in lip carcinoma

  12. Advanced lesion may present as: Broad-based,exophytic mass with a rough nodular,warty,haemorrhagic,or necrotic surface,or as a deeply destructive and crater-like ulcer with raised,rolled everted edges

  13. Histopathology In well-differentiated tumours, the neoplastic epithelium is obviously squamous in type and consists of masses of prickle cells with a limiting layer of basal cells around the periphery. Intercellular bridges are readily recognizable. keratin pearls are often found within the masses of infiltrating cells, each pearl consisting of a central area of keratin surrounded by whorls of prickle cells.

  14. There is variable lymphocytic and plasma cell infiltration in the stroma supporting the invasive malignant epithelium, which probably represents a reaction by the host’s immune system to tumour antigens as well as a response to tumor necrosis and ulceration.

  15. In less well-differentiated tumours the keratin pearls are sparse or absent, and the prickle cells and their nuclei are much more pleomorphic. • Mitotic figures are usually abundant and many may be atypical.

  16. In poorly differentiate or anaplastic tumours the malignant cells are even more irregular and may hardly be recognizable as epithelial cells. In such cases, immunohistochemistry to demonstrate cytokeratins (intermediate filament proteins that characterize epithelia) is particularly valuable.

  17. PROGNOSIS The survival rate of pts with oral carcin. depends on a number of factors: • Early diagnosis • Site of the lesion • Carcinomas in females have better prog. • Age • Clinical staging system (TNM system)

  18. Carcinoma-in-situ Svere epithelial dysplasia in which the whole, or almost the whole, thickness of the epithelium is involved but the basement membrane is intact and there is no invasion of the lamina propria. usually presents clinically as leukoplakia or erythroplakia.

  19. Premalignant ( Precancerous) is defined as a morphologically altered tissue in which cancer is more likely to occur than in its normal counterpart, for example leukoplakia. That is, the lesion itself undergoes malignant transformation.

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