Oral Cavity and Oropharynx

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 [165]. 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 [298]. Alcohol has been considered the second most important risk factor for oral and pharyn-geal cancer development [247], 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 [371].

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 [186]. In contrast, SCCs of the tonsil seem to be strongly aetiologically linked to the HPV infection [97, 214].

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