Análise microscópica e da imunoexpressão dos marcadores de proliferação celular Ki-67 e Ciclina B1 no epitélio gengival de pacientes sob terapia com nifedipina

Abstract

Drug induced gingival overgrowth (DIGO) is an adverse effect associated with the chronic use of three main drugs: phenytoin, an anticonvulsant, cyclosporin, an immunosuppressant drug and the pharmacological agents known as calcium channel blockers (CCB). Nifedipine is a calcium channel blocker, which because of its strong vessel dilating action has become widely used in cardiotherapy, in particular for the control of arterial hypertension. The aim of this study is to evaluate the microscopic characteristics and the epithelial proliferation index of gingival tissue in patients undergoing chronic treatment with nifedipine. To do so, twenty samples of gingival tissue of patients undergoing chronic treatment with nifedipine were obtained. The majority of these patients did not present clinically detectable gingival overgrowth. For comparative purposes, nine samples of gingival tissues of healthy patients who did not use drugs associated with gingival overgrowth (control) were used. The samples were microscopically analyzed using hematoxylin-eosin staining, to determine the size of the epithelial rete pegs. To carry out the epithelial proliferation index evaluation, a cellular identification of the Ki-67 and B1 Cyclin proteins was done using the immunohistochemical technique (streptavidin-biotin-peroxidase), as well as the quantification of positive cells (+cells) in mm².The results showed that the epithelial tissue of nifedipine users has considerably longer rete pegs that of the control group (Mann-Whitney, p=0.02). However, with regard to the proliferating activity of the keratinocytes, no significant difference was observed between the two groups (Mann-Whitney, p>0.05). The findings show that the microscopic alterations observed in the epithelium of nifedipine users are not caused by the mitotic activity of the keratinocytes but taking data from the literature into consideration, it is suggested that this increase might be caused by an inhibition of apoptosis rate of these same cells.