It is estimated that about 90% and 60% of all deaths in males and females, respectively, caused by oral cancer can be attributed to cigarette smoking. Like cancers at other sites caused by smoking, the risk of developing cancer is dose related and is related to carcinogenic aromatic hydrocarbons. The relative risks are estimated to be at least five and as high as 10-24 for patients who smoke 40 cigarettes per day and this risk increases the longer one smokes. Pipe and cigar smoking appear to result in at least as great a risk. The association of the use of smokeless ('spit') tobacco with oral carcinoma is less clear. The prevalence of oral carcinoma is low in some countries where the use of smokeless tobacco far exceeds that of cigarette smoking (La Vecchia et al., 1992; Vigneswaran et al., 1995). On the other hand, some studies have shown that smokeless tobacco users are at increased risk and that about one-half of such cancers occur at the site where the tobacco is placed (Winn et al., 1981). Another variation of topical use is seen in India and Southeast Asia where areca nut, tobacco and slaked lime are wrapped with betel leaf and chewed for long periods each day. This results in a precancerous scarring condition known as oral submucous fibrosis.
The fact that only a fraction of individuals with heavy exposure to tobacco and alcohol develop cancers of the upper aerodigestive tract suggests that there may be genetic differences between individuals that influence their susceptibility to these environmental agents. Heritable differences in head and neck cancer susceptibility have been found for nearly every step of tumorigenesis including carcinogen metabolism, DNA repair and progression as influenced by oncogenes and tumour-suppressor genes (Spitz, 1994; Khuri et al., 1997; de Andrade et al., 1998; Jahnke et al., 1999). There is also increasing evidence to suggest that some of the population variance in response to therapy is due to interindividual genetic differences (Khuri et al., 1997).
Because many heavy smokers are also heavy drinkers, it has been difficult to link alcohol use directly with oral cancer, but some investigators have estimated the relative risk at 2-6-fold. Alcohol acts synergistically with tobacco and together they increase a person's risk to 40-fold. Alcoholic beverages contain nitrosamines and hydrocarbons and, additionally, it has been proposed that contaminants or metabolites may promote malignant transformation (Blot, 1992). Malnutrition and vitamin deficiency may have a contributory role in oral cancers.
Vitamins A, B and C, are independently related to a reduced incidence of oral carcinoma and the risk of oral cancer in vitamin E users is half that of others according to one study (Gridley et al, 1992).
Cancer of the lower lip is strongly related to excessive exposure to ultraviolet light with a wavelength range of 2900-3200 A, especially in fair-skinned individuals. Actinic cheilitis, similar in name and biology to actinic keratosis of the skin, represents the premalignant clinical condition. Just as in the skin, extensive damage is done to the collagen in the lamina propria (solar elastosis), but whether or not this event has any influence on epithelial transformation is unknown. Exposure to therapeutic X-irradiation is associated with an increased risk for the development of both carcinomas and sarcomas. Evidence of infection with human papillomavirus (HPV) has been found in clinically normal oral mucosa, benign and malignant neoplasms that arise from it, and some of the metastatic tumours. About 35% of oral cavity tumours have been found to contain HPV, usually the 'high-risk' types of the virus. HPV positivity correlates with age (< 60 years) and gender (male), but not with tobacco or alcohol use (McKaig et al., 1998). Nevertheless, its exact role remains elusive.
In summary, it appears that the pathogenesis of oral carcinomas is multifactorial with suppressor genes acting in association with growth factors, viruses, chemical carcinogens and oncogenes (Scully, 1993).
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