Gökhan Açikgoz1, Inci Devrim, Sükrü Ozdamar. 1. University of Ondokuz Mayis, Faculty of Dentistry, Department of Periodontology, Samsun, Turkey. gacikgoz@omu.edu.tr
Abstract
BACKGROUND: Keratinocytes are chiefly cells of the epidermis but also constitute 90% of the gingival cells. The molecular mechanisms of proliferative activity in keratinization whereby diabetes alters periodontal physiology have not been elucidated. In this study, we aimed to investigate the role of gingival keratinocytes in hyperglycemic subjects by examining their mitotic activities. METHODS: We tested 30 patients with periodontitis, of whom 15 were type II diabetics and the remainder systemically healthy. Biopsies were obtained from the bottom of the deepest pocket in each subject by reverse beveled incision. Formalin-fixed and paraffin-embedded specimens were then processed for periodic acid-Schiff (PAS)-diastase histochemistry and proliferating cell nuclear antigen (PCNA) (P10). Immunohistochemical studies were employed to determine the presence of PCNA and were used to detect the proliferating potential of keratinocytes needed in synthesizing DNA. The expression of PCNA was evaluated using an immunoperoxidase technique and PC10 monoclonal antibody to PCNA. Mitotic index was calculated from basal cells. Statistical analysis employed the chi-square test. RESULTS: No significant difference between the diabetic and non-diabetic patients was found in the mitotic index of the oral-gingival epithelium. CONCLUSION: Although the mitotic index in patients with diabetes was slightly lower, keratinization in the gingival tissues for both groups was essentially identical.
BACKGROUND: Keratinocytes are chiefly cells of the epidermis but also constitute 90% of the gingival cells. The molecular mechanisms of proliferative activity in keratinization whereby diabetes alters periodontal physiology have not been elucidated. In this study, we aimed to investigate the role of gingival keratinocytes in hyperglycemic subjects by examining their mitotic activities. METHODS: We tested 30 patients with periodontitis, of whom 15 were type II diabetics and the remainder systemically healthy. Biopsies were obtained from the bottom of the deepest pocket in each subject by reverse beveled incision. Formalin-fixed and paraffin-embedded specimens were then processed for periodic acid-Schiff (PAS)-diastase histochemistry and proliferating cell nuclear antigen (PCNA) (P10). Immunohistochemical studies were employed to determine the presence of PCNA and were used to detect the proliferating potential of keratinocytes needed in synthesizing DNA. The expression of PCNA was evaluated using an immunoperoxidase technique and PC10 monoclonal antibody to PCNA. Mitotic index was calculated from basal cells. Statistical analysis employed the chi-square test. RESULTS: No significant difference between the diabetic and non-diabeticpatients was found in the mitotic index of the oral-gingival epithelium. CONCLUSION: Although the mitotic index in patients with diabetes was slightly lower, keratinization in the gingival tissues for both groups was essentially identical.