Abstract
Oral lichen planus (OLP) is a chronic relapsing inflammatory disease. It involves T-lymphocyte aggression targeted to the basal layer of the oral mucosa.p53 plays a central role in the prevention of normal cells from the development of the malignant phenotype. Somatic alterations in p53 cause defects in normal p53 function. Wild type p53 plays an important role in repairable damage of the cell due to cellular stresses. Over-expression, as well as polymorphic variants of Mouse double minute 2(MDM2), have effects on p53 disturbances. In addition, degradation of p53 by E6 protein of high-risk human papillomavirus is also suggested as one of the mechanisms which attenuate p53 responses in oral carcinogenesis. Polymorphisms in p53 are anticipated to cause measurable disturbance in p53 function. Polymorphism of the codon 72 on exon 4 of the gene p53 is the first and most commonly known polymorphism of this gene. The presence of p53 has been demonstrated as an early marker of dysplasia in Oral Potentially Malignant Disorders. This review discusses about p53 polymorphism as an early indicator of genetic predisposition to neoplastic transformation in OLP.
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