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Abstract

ABSTRACT: BACKGROUND: Molecular DNA hybridization has confirmed an association of CMV infection with a variety of oral cancers. While cell mediated immunity is most important in controlling primary or reactivated CMV infection, this virus has one of most effective strategies in oral carcinogenesis via impairment of structure and function of P53 protein by interaction with viraloncoproteins. OBJECTIVE: 1.To determine the percentage of CMV-infected oral squamous cell carcinoma tissue specimens; 2. To evaluate the histopathological impact of the expression of mutated p53 tumor suppressor gene on CMV- related, as well as CMV-non-infected oral cancer; and 3.To through a light on some immunological microenvironment of OSCC,by assessing CD8-positive tumorinfiltrating cytotoxicT- lymphocytes. METHODS: This study was designed as retrospective research. A total number of seventy (70) formalin-fixed paraffin-embedded oral tissues were collected; 60 patients with oral squamous cell carcinoma, and 10 individuals with apparently-healthy oral tissues. The molecular methods for CMV DNA detection was performed by sensitive version of in situ hybridization, whereas the phenotype of cell surface antigen marker, namely CD8+ marker of tumor infiltrating lymphocytes and TP53 protein were detected via relevant immunohistochemical methods. RESULTS: Well differentiated grade constituted 81.7% of oral squamous cell carcinoma. Positive in situ hybridization reactions for CMV-DNA were observed in 43.3% of the total screened tissues. Thirtythree out of sixty (55%) oral squamous cell carcinoma showed positive immunohistochemical reactions indicating P53 over-expression, and 18.3% showed presence of CD8-positive tumor infiltrating lymphocytes. None of those control group showed positive reaction for CMV-DNA, p53, or CD8 marker. CONCLUSION: The detection of high percentage of cytomegalovirus-DNA in OSCC could mark for a parentral way of spreading of such important and well-known sexually transmitted infection among Iraqi general population.The obvious high percentage of mutated p53 over-expression indicates for an important role of such genetic events in the oral carcinogenesis.A little role for CD8-positive tumor infiltrating lymphocytes could be played in the immunological microenvironment of OSCC

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