| Project/Area Number |
16390356
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
IWAI Takehisa Tokyo Medical and Dental University, Graduate school of Medical and Dentistry, Professor, 大学院・医歯学総合研究科, 教授 (90111591)
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| Co-Investigator(Kenkyū-buntansha) |
INOUE Yoshinori Tokyo Medical and Dental University, Graduate school of Medical and Dentistry, Lecturer, 大学院・医歯学総合研究科, 講師 (70280964)
ISHIKAWA Isao Tokyo Medical and Dental University, Graduate school of Medical and Dentistry, Professor, 大学院・医歯学総合研究科, 教授 (10014151)
UMEDA Makoto Tokyo Medical and Dental University, Graduate school of Medical and Dentistry, Assistant, 大学院・医歯学総合研究科, 助手 (90193937)
YOSHIDA Masayuki Tokyo Medical and Dental University, Graduate school of Medical and Dentistry, Assistant professor, 大学院・医歯学総合研究科, 助教授 (80282771)
NAKAMURA Hiroaki Saitama Medical School, Medical School, Professor, 医学部, 教授 (80073021)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥12,300,000 (Direct Cost: ¥12,300,000)
Fiscal Year 2005: ¥4,800,000 (Direct Cost: ¥4,800,000)
Fiscal Year 2004: ¥7,500,000 (Direct Cost: ¥7,500,000)
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| Keywords | Buerger disease / Smoking / Platelet engulfment / IgG antibody / periodontitis / thrombus formation / HLA / dental hygien / Treponema denticola / Porphyromanos gingivalis / PCR |
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| Research Abstract |
The cause of Buerger disease is not yet known, although many etiological factors have been suggested over the last 100 years. Last year we reported that the occluded artery of Buerger disease showed oral bacteria DNA in the arterial specimens of 13 out of 14 subjects. After that, we confirmed that smoking aggravates periodontitis, and that tobacco materials worsen arterial spastic conditions and endothelial surfaces. Periodontal bacteria, especially Porphyroinonas gingivalis (Pg), strongly activates the platelets. Because of the above- mentioned facts, the etiology of Buerger disease focused on periodontal bacteria, mainly Pg and Treponema denticola (Td). Experimental studies using an intravenous infusion of Pg showed peripheral arterial thrombus formation and positive bacterial DNA.
Oral bacteria easily reaches the venous angle, so bacteremia appears several minutes after periodontal procedures are completed. We investigated how the bacteria are transported to the vessels and heart. Ou
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r in-vitro study showed the Pg itself activates the platelets in plasma and bacteria are taken in the platelets, which are also aggregating platelets. Platelets did not demonstrate phagocytotic action within 60 minutes compared with granulocyte, in which bacteria are mostly killed. These facts were investigated with an electro-microscope. We speculated that a pretty good sized platelet lump makes an embolic action on the small arteries in Buerger disease.
Arterial thrombus formation, in which we could see micro abscesses or granulocyte infiltration, is the major pathological point. Another is well preserved arterial structures. Immuno-fluorescent microscopy detected Td bacteria itself near the internal elastic lamina and in the thrombus. Serum IgG antibodies against specific periodontal pathogens are elevated significantly in Buerger disease.
Smoking cessation and proper dental hygiene are known to decrease the incidence of Buerger disease. Now we are checking the HLA typing, which is estimated to show a strong relationship between periodontitis and Buerger disease. Less
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