1021-P: Liraglutide Improves Periodontitis by the Anti-inflammatory Activities of GLP-1

Periodontal disease which consists of gingivitis and periodontitis is one of the diabetic complications due to the high prevalence and the severity. Periodontitis is a chronic inflammation by the infection of Gram-negative bacteria in the periodontal pocket, following the destruction of periodontal tissue. On the other hand, many researches have shown extrapancreatic functions of glucagon-like peptide-1 (GLP-1), including the anti-inflammatory action and the suppression of indirectly bone resorption. In this study, we focused on the therapeutic effects of GLP-1 on periodontitis. Experimental periodontitis was induced by placing a nylon thread ligatureat the cervical portion of the maxillary second molar in Sprague-Dawley rats. Half of the rats were administered GLP-1 receptor agonist, Liraglutide (0.4mg/kg/day). Two weeks after the ligation, periodontitis was evaluated by histological examinations (H-E staining and the immunostaining) and mRNA expressions of inflammatory cytokines. Alveolar bone loss was evaluated by the distance at maximal bone resorption site from cement-enamel junction (CEJ) to the alveolar bone crest, and the bone micro-architecture parameters, using micro-CT and analytical software. We also investigated the anti-inflammatory effects of GLP-1 on monocytes using THP-1 cells. The mRNA expressions of TNF-α, iNOS and Mac1 in gingiva and alveolar bone resorption were significantly increased in the periodontitis rats. Liraglutide significantly suppressed the periodontitis-related inflammatory cytokine expressions and alveolar bone resorption. The part of the bone micro-architecture parameters in periodontitis rats deteriorate, which was not affected by Liraglutide. In vitro study revealed that GLP-1 significantly inhibited lipopolysaccharide-induced TNF-α mRNA expression in THP-1 cells in a dose-dependent manner. In conclusion, GLP-1 may be effective in the treatment of periodontal disease mainly through the suppression of gingival inflammation. Disclosure N. Sawada: None. K. Naruse: None. T. Matsubara: None. N. Nakamura: None. M. Miyabe: None. M. Ito: None. Y. Suzuki: None. K. Adachi: None. S. Kobayashi: None. T. Kikuchi: None. A. Mitani: None. T. Toriumi: None. M. Mizutani: None. M. Honda: None.