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

AIM: To investigate the effects of peroxisome proliferator-activated receptor γ (PPARγ) 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. PPARγ 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 8 weeks, 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 1 week, while significantly increased after 8 weeks 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. PPARγ agonist significantly reduced osteoclast counting after 1 week, while increased it after 8 weeks.

CONCLUSIONS: During periodontitis progression, PPARγ could inhibit inflammation, prevent bone resorption within a short time, while the long-term PPARγ activation would lead to increased bone resorption, and PPARγ repression by antagonist would enhance alveolar bone formation.

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