The present study indicates that hypermethylation may be involved in the pathogenesis of oral pre-cancerous lesions associated with betel-quid chewing in Sri Lanka.

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Betel-quid chewing, which is closely related to the high incidence of oral cancer, is prevalent in Sri Lanka. p63 has a remarkable structural similarity to p53, suggesting an aberrant expression in oral cancer. Using anti-p63 antibody and immunohistochemistry, the present study investigated the expression pattern of p63 in oral epithelial lesions, including different types of squamous cell carcinoma (SCC), different grades of epithelial dysplasia, and submucosal fibrosis associated with betel-quid chewing. Nuclear immunoreactivity for p63 was detected in all the cases, including normal oral epithelium and epithelial lesions. In normal oral epithelium, nuclear positivity for p63 was observed in some of the basal cell layers and focally in the parabasal layer. Nuclear positivity increased in the epithelial lesions. The percentage of positive nuclei in the epithelial lesions was significantly higher than in normal epithelium (P < 0.01) and was also significantly higher in oral submucosal fibrosis than in epithelial dysplasia (P < 0.05). The results indicate that the overexpression of p63 in oral precancerous lesions and SCC in betel-quid chewers in Sri Lanka may be a useful marker for oral precancerous lesions.

Human β‐defensin (hBD) 2 is an epithelial antimicrobial peptide. We studied single‐nucleotide polymorphisms in the gene of hBD‐2 in a Japanese population, and estimated the effect of a polymorphism in the promoter/enhancer region on the transcriptional activity. By sequencing the hBD‐2 gene of 50 unrelated individuals, we detected one SNP in exon 2 and nine SNPs in the promoter/enhancer region. The SNP in the coding region at the ＋1765 position is synonymous [CCC (Pre)→CCT (Pre)]. One SNP in the promoter region (－ 1029) is located at the consensus sequence for NF‐IL6 binding. By luciferase reporter assay and electrophoretic mobility shift assay, the wild‐type (G) of －1029 showed significantly lower transcriptional activity than did the variant‐type (A). The SNP at position －1029 may influence the hBD‐2 expression and cause genetic variations in susceptibility to infectious diseases.