Efeitos da metformina na doença periodontal induzida por ligadura em ratos Wistar

Abstract

Periodontitis is a chronic disease characterized by gum inflammation, degeneration of periodontal ligaments, alveolar bone and cementum. It is considered one of the most important cause of tooth loss in adults. Experimental studies have shown pharmacological new alternatives for the treatment of periodontal disease in order to alleviate the inflammation and alveolar bone loss. The aim of this study was to evaluate the effects of Metformin (MET) on inflammation, oxidative stress and bone loss in a rat model of ligature-induced periodontitis. Male Wistar albino rats were randomly divided into 5 groups of 24 rats each and given the following treatments for 10 days: (NL) no ligation + saline, (L) ligation + saline, (MET 50) ligation + 50 mg/kg MET, (MET 100) ligation + 100 mg/kg MET, and (MET 200) ligation + 200 mg/kg MET. Periodontal tissue was analysed to determine the bone loss and histopathological characteristics. Immunohistochemical was used to examine MMP-9, COX-2, the RANK/RANKL/OPG pathway and SOD-1 and GPx. Spectroscopic UV-VIS analysis was used to examine the levels of Malonaldehyde, glutathione, IL-1β and TNF-α. Reverse transcription polymerase chain reaction was used to quantify the gene expression of AMPK, NF-кβ p65 and HMGB1. A p-value of <0.05 indicated a significant difference. Treatment with 50 mg/kg MET significantly reduced concentrations of malonaldehyde, IL-1β and TNF-α (p < 0.05); MET any of the doses statistically significant difference (p>0,05) in GSH increased compared to Group L. Weak staining for COX-2, MMP-9, RANK, RANKL and SOD-1; strong staining for GPx and OPG. Increased AMPK expression and decreased expression of NF-кB p65 and HMGB1. Metformin decreases the inflammatory response, oxidative stress and bone loss in ligature-induced periodontitis in rats.