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Novel analysis of methyl mercaptan causing oral malodor as one of periodontopathic facotors.

Research Project

Project/Area Number 14571985
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Periodontal dentistry
Research InstitutionKagoshima University

Principal Investigator

SETOGUCHI Takashi  Kagoshima University, University Hospital, Faculty of Medicine and Dentistry, Assistant Professor, 医学部・歯学部附属病院, 講師 (60206646)

Co-Investigator(Kenkyū-buntansha) YAMAMOTO Matsuo  Kagoshima University, Research Center for Life Science Resources, Associate Professor, 生命科学資源開発研究センター, 助教授 (50332896)
YOTSUMOTO Yukiharu  Kagoshima University, Graduate School of Medical and Dental Sciences, Research Associate, 大学院・医歯学総合研究科, 助手 (20295265)
MACHIGASHIRA Miho  Kagoshima University, Graduate School of Medical and Dental Sciences, Research Associate, 大学院・医歯学総合研究科, 助手 (80253897)
YAEGAKI Ken  British Colombia University, Faculty of Dentistry, Clinical Professor, 歯学部, 教授
Project Period (FY) 2002 – 2003
Project Status Completed (Fiscal Year 2003)
Budget Amount *help
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2003: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2002: ¥1,500,000 (Direct Cost: ¥1,500,000)
KeywordsOral malodor / Methyl mercaptan / Periodontal disease / Cell culture / Cytotoxicity / Cell proliferation / Apoptosis / Cytokine / メチルメルカプタン / LPS / 国際情報交換 / カナダ
Research Abstract

Methyl mercaptan, one of the main causes of oral malodor, is produced in periodontal pocket and might contribute to the initiation and progression of periodontal disease.To clarify the effect of methyl mercaptan on periodontal destruction, we investigated the pathogenic effects of methyl mercaptan on the cells associated with periodontal tissues.Methyl mercaptan inhibited epithelial cell(KB cell and HSC-2 cell line)growth and proliferation and a cytotoxic effect was also noted.These effects were also shown on monocytic cells(HL-60 cell and U-937 cell line).The induction of apoptosis and necrosis by methyl mercaptan on monocytic cells was evaluated and the results showed that Methyl mercaptan induced necrosis rather than apoptosis.The production of IL-1β, IL-6, and TNF-α by monocytic cells stimulated with or without Porpyromonas gingivalis lipopolysaccharide(LPS)with or without the presence of methyl mercaptan was evaluated..Both cells produced low levels of cytokines when without LSP stimulation and methyl mercaptan had no effect on cytokine production.However, U-937 cells stimulated with LPS produced high levels of cytokines and was augmented with presence of methyl mercaptan.These results indicate that methyl mercaptan induce cytokine production by monocytic cells and related to the initiation and progression of periodontal disease.Further evaluation of the effect of methyl mercaptan as the pathologic factor is very important for investigate the mechanism of the initiation and progression of periodontal disease and establish the methods of prevention of periodontal disease.

Report

(3 results)
  • 2003 Annual Research Report   Final Research Report Summary
  • 2002 Annual Research Report
  • Research Products

    (3 results)

All Other

All Publications (3 results)

  • [Publications] T Setoguchi, M Machigashira, M Yamamoto, Y Yotsumoto, M Yoshimori, Y Izumi, K Yaegaki: "The effects of methyl mercaptan on epithelial cell growth and proliferation"International Dental Journal. 52・3. 241-246 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] T Setoguchi, M Machigashira, M Yamamoto, M Yotsumoto, M Yoshimor, Y Izumi, K Yaegaki: "The effects of methyl mercaptan on epithelial cell growth and proliferation"International Dental Journal. 52-3. 241-246 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Takashi Setoguchi: "The effects of methyl mercaptan on epithelial cell growth and proliferation"International Dental Journal. 52・3. 241-246 (2002)

    • Related Report
      2002 Annual Research Report

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Published: 2002-04-01   Modified: 2016-04-21  

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