Squamous intraepithelial lesions in the oral cavity and oropharynx are associated with tobacco, whether smoked, chewed or used as snuff, which seems to be the major carcinogen in this region [165, 171, 247, 298, 316, 389]. Smoking 20 or more cigarettes per day, particularly non-filtered, as well as drinking alcohol, particularly fortified wines and spirits, is an important risk for the development of oral dysplasia in the European population. Tobacco is a stronger independent risk factor for oral SILs than alcohol . The use of smokeless tobacco in the western world has a rather lower correlation with oral precancerous and cancerous lesions than south-east Asia, where chewing habits, including betel quid, strongly correlate with oral precancer and cancer development . Alcohol has been considered the second most important risk factor for oral and pharyn-geal cancer development , and its synergistic effect with tobacco is particularly evident [170, 171]. The risk of the development of oral dysplasia is increased six to 15 times in smokers and heavy drinkers compared with non-smokers and non-drinkers .
The significance of Candida albicans as a possible aetiological factor of oral leukoplakia (OL) remains disputable [24, 303], as does the role of HPV in oral carcinogenesis. The involvement of HPV in the initiation and progression of oral neoplasia is still a matter of debate. Different studies have generated conflicting results concerning the prevalence of HPV, ranging from 0 to 90% [45, 345, 386]. The discrepancy observed may be related to the varying sensitivity of the methodologies applied for HPV detection and the epidemiologic factors of the patient groups examined. A recent study on 59 oral SCCs showed that the occasional findings of HPV DNA (8.4%) may be the result of incidental HPV colonisation of the oral mucosa rather than viral infection. In the same study, HPV DNA was detected in 6.6% in the control group of healthy people who matched the subjects with oral SCCs in various clinical parameters. HPVs, therefore, probably play a limited role in the aetiopathogenesis of the majority of oral SCCs . In contrast, SCCs of the tonsil seem to be strongly aetiologically linked to the HPV infection [97, 214].
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