Study on pathological progression mechanisms of non-alcoholic steatohepatitis caused by odontogenic infection of periodontal pathogen

2015 Fiscal Year Final Research Report

• Project/Area Number: 25462855
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Morphological basic dentistry
• Research Institution: Hiroshima University
• Principal Investigator: Miyauchi Mutsumi 広島大学, 医歯薬保健学研究院(歯), 准教授 (50169265)
• Co-Investigator(Kenkyū-buntansha): Furusho Hisako 広島大学, 医歯薬保健学研究院, 助教 (00634461) ; Takata Takashi 広島大学, 医歯薬保健学研究院, 教授 (10154783) ; Inubushi Toshihiro 広島大学, 医歯薬保健学研究院, 助教 (30550941) ; Hyogo Hideyuki 広島大学, 病院(医), 病院助教 (40397930)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 歯性感染 / Porphyromonas gingivalis / Galectin-3 / 非アルコール性脂肪性肝炎 / 線維化 / 肝星細胞

Outline of Final Research Achievements

Non-alcoholic steatohepatitis (NASH) has the potential to progress to cirrhosis and hepatocellular carcinoma. Effective therapy has still not been established. In the present study, exacerbation mechanisms of inflammation and fibrosis caused by P.gingivalis　(Pg)-odontogenic infection were examined. Upregulation of TLR2 in steatotic hepatocytes (HEP) and increase of macrophages possessing TLR2 played important roles in exacerbation of inflammation through activating TLR2 pathway by Pg-LPS. On the other hand, TGFb1, which was produced by HEP/hepatic stellate cells (HSC) with Pg-infection, promoted liver fibrosis by activating HSC. Detection of Pg in liver from NASH patients were related with high serum level of hyaluronic acid (a serum maker for liver fibrosis) and advanced fibrosis. Therefore, preventing and/or eliminating P.g. infection by dental therapy may have a beneficial impact on management of NASH.

Free Research Field

口腔病理学