Int J Stomatol

Inter J Stomatol ›› 2014, Vol. 41 ›› Issue (5): 598-602.doi: 10.7518/gjkq.2014.05.023

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Molecular mechanism of peroxisomal proliferator activated receptor γ regulation in periodontitis

Chen Mingyue1,2, Wang Changning1   

  1. 1. The State Key Laboratory Breeding Base of Basic Science of Stomatology(Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan 430079, China; 2. Dept. of Stomatology, Taihe Hospital, Shiyan 422000, China
  • Received:2013-09-25 Revised:2014-01-11 Online:2014-09-01 Published:2014-09-01

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Abstract:

The study of peroxisomal proliferator activated receptor(PPAR)γ and the its molecular mechanism can reveal the relationship between periodontitis and systemic diseases. PPARγ, which is composed of six areas and four function structural domains, can regulate a variety of nucleus target genes upon being activated by its ligand. Thus, PPARγ participates in atherosclerosis, regulates the blood glucose and lipids, and improves insulin resistance. PPARγ is a transcription factor that can convert periodontal stem cells into adipocyte. It can also affect the signaling pathways in inflammatory cells and inhibit the inflammatory process. PPARγ can promote fat cell differentiation, inhibit osteoblast differentiation, and promote osteoclast differentiation through the classic and non-classic wingless-type mice mammary tumor virus integration site family and β-serial protein pathways. PPARγ exerts a protective effect on periodontitis by inhibiting the gene expression of cytokines, chemokines, and the adhesion factor in the multiple links of inflammatory transcription. Lipopolysaccharide(LPS) is the main factor in chronic progressive inflammatory alveolar bone loss. The PPARγ agonist can decrease the LPS-induced phosphorylation of protein kinase B and thus inhibits the inflammatory bone resorption of periodontitis.

Key words: peroxisomal proliferator activated receptor γ, periodontitis, bone metabolism

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  • Q 51

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