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Peroxisome proliferator‐activated receptor γ plays dual roles on experimental periodontitis in rats
Author(s) -
Qiao Weiwei,
Wang Changning,
Huang Wushuang,
Hu Yingying,
Song Yaling
Publication year - 2018
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.12891
Subject(s) - periodontitis , medicine , endocrinology , agonist , bone resorption , osteoprotegerin , osteoclast , rankl , peroxisome proliferator activated receptor , inflammation , bone remodeling , dental alveolus , receptor , chemistry , dentistry , activator (genetics)
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.