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Description of the Evidence

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    Dietary changes and dietary supplements

    Several studies have shown an inverse association of fruit intake and the development of oral cancer, particularly in those who use tobacco.[9,31,34,35,36] Fiber, in the form of vegetable intake, has similarly been shown to be associated with a decreased risk of oral cancer. It is estimated that intake of fruits and vegetables may lower the risk of development of oral cancer by 30% to 50%.[34,37] The evidence is inadequate, however, of reduced oral cancer among people who have made changes in their diet.

    Dietary supplementation with alpha-tocopherol acetate (vitamin E) 50 mg per day and beta carotene 20 mg per day has been tested in a large randomized placebo-controlled 2 × 2 factorial trial of 29,133 male smokers aged 50 to 69 years.[38] After a median follow-up of 6.1 years, there were a total of 65 incident oropharyngeal cancers, with no statistically significant differences between the placebo and the active agents, whether alone or in combination. Moreover, in the same trial, beta carotene was associated with increased lung cancer incidence and mortality.

    Sun avoidance and sunscreen use

    The majority of cases of carcinoma of the lip occur on the lower lip, which has greater sun exposure than the upper lip. While tobacco has been strongly associated with lip cancer, sun exposure may be a factor as well. Sunscreen use has been associated with a lower incidence of skin cancers [39,40] and thus may lower the incidence of lip cancer. In a study of women in Los Angeles, a decreased risk of lip cancer was found to be associated with the daily use of lip protection (mostly colored lipstick).[24] Lip balm with sun protection is widely available.

    Secondary Prevention

    Agents for the reversal or prevention of recurrence of oral lesions that sometimes progress to cancer have been evaluated, with equivocal results. A randomized controlled trial (RCT) [41] found a protective effect of fenretinide against development of relapsed and new leukoplakias during 1 year of fenretinide treatment. The study had insufficient power to determine the effect on oral cancer incidence due to premature closure of the study. Other agents have been investigated for treatment of oral premalignant lesions.[42,43,44,45,46,47] None have been proven to prevent progression to oral malignancy, and none can be considered part of standard care.

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