The development of novel therapeutic drug for periontitis targeting epgenetic regulation of TLR2

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K20675
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Periodontology
• Research Institution: Kyushu University
• Principal Investigator: Tanaka Urara 九州大学, 大学病院, 助教 (50734993)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: Decitabine / 歯周炎モデルマウス / DNAメチル化

Outline of Final Research Achievements

The purpose of this study was to develop a novel therapeutic drug for periodontitis targeting epigenetics.
We observed severe bone loss in the ligature induced periodontitis model in mice and Decitabine significantly inhibited the bone loss. We found that the treatment with Decitabine significantly reduced osteoclasts both in vivo and in vitro and up-regulated the anti-inflammatory cytokines (IL-10 and TGF-β) in vitro. Next, we focused on Kruppel-like Factor 2 (KLF2) which is a transcription factor regulating inflammation. As the results, Decitabine increased KLF2 and KLF2 up-regulated the transcriptional activity of CCAAT/enhancer binding protein beta (CEBPB) and the anti-inflammatory cytokines IL-10 and TGF-β. We concluded that Decitabine inhibits alveolar bone loss by limiting osteoclastogenesis in mice and shows KLF2 can regulate that. Taken together, Decitabine may have utility in treating chronic inflammatory periodontal disease in humans.

Free Research Field

歯周病学