Apigena reduz reabsorção óssea inflamatória em modelo de periodontite em camundongos

Abstract

The inflammatory process is related to increased resorption in some diseases, such as periodontitis, characterized by chronic inflammation in response to specific microorganisms that results in alveolar bone resorption (ROA) and tooth loss. Apigenin (APG), an agent found abundantly in chamomile, has received increased attention for its anti-inflammatory effects. Thus, the objective was to evaluate the antiresorptive activity of APG in experimental periodontitis in mice. For this, 48 male Swiss mice were used in ligation-induced periodontitis trials, which consists of the insertion of a cotton thread (4.0) around the lower first molars. The experimental groups consisted of: Naïve, in which periodontitis was not induced, untreated (NT) and APG, in which periodontitis was induced and received daily by gavage 10 µl/kg of TW80 and APG 1, 3 or 9 mg/ kg, respectively. After euthanasia, their mandibles were removed for analysis of ROA and attachment level (NI). Gingival tissue was also removed for quantification of IL-1β and IL-17, qRT-PCR for RANKL and OPG. Serum measurements of total alkaline phosphatase (FAT) and hepatic transaminases, analysis of renal (RI) and hepatic (HI) indices and body mass variation were performed. The ligation promoted a significant ROA, corroborated by the increase in the attachment level (NI) in the distal of the 1st molar and increase in the furcation area, as well as increasing the levels of IL-1β and IL-17 and the expression of RANKL in the gingival tissue. in NT mice compared to Naïve. On the other hand, the administration of APG (9 mg/kg) promoted a reduction in ROA, NI and the furcation area of the mandibular first molar, maintained the levels of IL-1β and IL-17 similar to those of Naïve and increased the expression of OPG Systemically, APG did not promote any significant change in the parameters evaluated. APG presented a bone protective profile, probably due to the control of disease progression through the modulation of osteoclastogenic cytokines, in addition to being systemically safe.