Abstract

Lesions such as leukoplakia, dusplastic leukoplakia, erythroplakia, oral sumucious fibrosis, dysplastic lichenoid lesions, and oral lichen planus are all included in the category of oral premalignant lesions, or OPL. It has been observed that 17% of oral premalignant lesions (OPL) will progress into malignant lesions during the first seven years after diagnosis, making proper identification and treatment of OPLs crucial. Any changes to the p53 protein cause it to accumulate in the nuclei of cells; this can be important for the development of cancer, including oral premalignant lesions and oral malignant lesions. METHODS: Fifteen patients with mild to severe dysplasia oral premalignant lesions were identified both histologically and clinically. They received chemopreventive therapy for four months, consisting of betacarotene (Vit. A). Both before and after therapy, the amounts of p53 protein immunostaining were assessed. RESULTS: The average P53 optical staining density in pretreatment speciments was 59.78±10.22, while in post-treatment instances it was 39.74 ± 3.36; this indicates that the pre-treatment cases had a greater value than the the posttreatment cases. There was a 0.0003 p-value. Consequently, the difference is seen as statistically significant when compared statistically. CONCLUSION: Itis discovered that there is an inverse relationship between the expression of P53 protein in OPL and the histological and clinical responses to betacarotene supplementation.

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