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Oral lichen planus (OLP), is considered premalignant condition. This study tried to investigate the possibility of malignant transformation in OLP patients, by measuring the level of tumor suppressor protein p16INK4A, which is a product of the cyclin-dependent kinase inhibitor 2 (CDK2). CDK inhibitors may be responsible for maintenance of cell cycle. An imbalance in the cell cycle regulatory pathway involving p16/pRb may lead to unrestricted proliferation and tumorigenesis.40 patients with OLP underwent biopsy. Two control groups were included in this research, 13 healthy persons and 12 patients with oral squamous cell carcinoma (OSCC). All tissue samples were treated immunohistochemically using avidin-biotin peroxidase complex method.The number of patients with p16 positive cells was significantly higher in OLP (72.5%) in comparison to OSCC (33.33%). Although the prevalence of patients with p16 positive cells in OSCC was low, they expressed the highest percentage of p16 positive keratinocytes. Staining intensity of cytoplasm was also higher in p16 positive keratinocytes of OSCC in comparison to OLP.These results suggest that inactivation of p16 is an early detectable event in oral tumorigenesis. P16 expression could also be connected with tumor grading and may be useful marker in oral tumor progression.

Oral lichen planus (OLP) is an autoimmune skin and mucosal disorder. The range of malignant transformation in OLP varies between 0.1-3%. p53 is a tumor suppressor protein. Defective p53 could allow abnormal cells to proliferate, resulting in cancer. p53 plays an important role in cell cycle control and apoptosis and loss of p53 function has been demonstrated in about half of all human cancers. The purpose of the study was to investigate the malignant potential of OLP on the basis of p53 expression and to correlate p53 expression with clinical and histopathological features of OLP.40 patients with OLP underwent biopsy. All tissue samples were treated immunohistochemicaly using avidin-biotin peroxidase complex method.In 80% of OLP specimens the nuclei of basal and parabasal keratinocytes were p53-positive, but in low numbers. Low percentage of p53-positive cells in older and medium percentage of p53-positive cells in younger group of OLP patients were noted. Higher intensity of p53 stained keratinocytes, no matter their low number, could represent mutant and more stable form of p53 protein, and at the same time signal for monitoring of disease due to potential malignant transformation. Low percentage and weak intensity of p53-positive cells was detected mostly in OLP specimens with highly expressed civatte bodies (CB). Upregulation of apoptosis didn't correspond with the expression of CB.We believe that low percentage of p53-positive and well-marked keratinocytes in OLP represent the influence of mutant p53 protein, and that increasing expression of this protein could serve as a valuable diagnostic sign of early carcinogenesis. According to our results intensity of p53 coloration of keratinocytes could help assessing the malignant potential of OLP.