Peroxisome proliferator-activated receptor γ plays dual roles on experimental periodontitis in rats

Aim: To investigate the effects of peroxisome proliferator-activated receptor (PPAR) on inflammation control and bone remodelling in experimental periodontitis in rats. Materials and methods: Experimental periodontitis was induced in rats by thread ligation around cervixes of mandibular first molars. PPAR agonist, antagonist and vehicle were intraperitoneally administrated, respectively, into rats. Ninety-six male SD rats were randomly divided into control, ligation+vehicle, ligation+agonist and ligation+antagonist groups. After 1, 4 and 8weeks, alveolar bone loss was assessed by Micro-CT and HE staining. Inflammation and bone metabolism factors were evaluated by ELISA and immunohistochemical examination. Osteoclasts were quantified by tartrate-resistant acid phosphatase (TRAP) staining. Results: Alveolar bone loss was significantly reduced after 1week, while significantly increased after 8weeks in agonist group, but antagonist group showed the opposite trend. Agonist decreased some inflammatory cytokines expression after 1 and 4 weeks, downregulated OPG, RUNX2, BMP-2 and upregulated RANKL after 8 weeks, but antagonist brought the opposite effect. PPAR agonist significantly reduced osteoclast counting after 1 week, while increased it after 8weeks. Conclusions: During periodontitis progression, PPAR could inhibit inflammation, prevent bone resorption within a short time, while the long-term PPAR activation would lead to increased bone resorption, and PPAR repression by antagonist would enhance alveolar bone formation.