Evaluation of p53 Gene Mutations in Oral Lichen Planus Lesions in a Population From Iran

Oral lichen planus (OLP) is a chronic inflammatory disorder of the oral mucosa, genetic and molecular alterations, including mutations in the p53 tumor suppressor gene, have been implicated in OLP pathogenesis. However, its molecular mechanisms are not clearly understood. This study investigates p53 gene mutations in OLP lesions.

This study analyzed 43 paraffin-embedded tissue blocks from OLP patients. Diagnosis was confirmed by two pathologists. Genomic DNA was extracted using a commercial kit, with quality and quantity assessed by spectrophotometry and agarose gel electrophoresis. PCR-sequencing was performed on exons 5-8 and part of the adjacent introns of the p53 gene. Statistical analysis was performed using SPSS version 20, with Fisher's exact test and t-test applied to assess relationships between p53 mutations and clinical parameters; significance was set at p < 0.05.

The study included 43 OLP cases (mean age 51.7  ±  13.3 years; 65.1% female). Lesions were most frequently located on the buccal mucosa (65.1%), followed by the tongue (20.9%), gingiva (19.3%), and mandible (4.7%). DNA sequencing identified 13 nucleotide changes in the p53 gene in 9 samples (20.9%), distributed across exons 5-7 and intronic regions at codons 140, 171, 185, 213, and 246, as well as at IVS4: +8(C/G), IVS7: -11(A/C), and IVS4: -18(A/T). Mutations included equal proportions of missense and silent changes, as well as transitions and transversions. Adenine mutations were most common (53.8%), followed by cytosine mutations (30.8%). No statistically significant associations were found between p53 mutations and patient gender, age, or anatomical site of sampling.

The study identified p53 gene mutations in 21% of oral lichen planus (OLP) cases, with no demographic or pathological correlations. While highlighting p53's complex role and potential as a biomarker, limited sample size necessitates larger, multi-center studies to clarify genetic/environmental influences on OLP pathogenesis and mutation predisposition.