| Project/Area Number |
17390565
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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 |
Social dentistry
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| Research Institution | Kagoshima University |
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Principal Investigator |
OHO Takahiko Kagoshima University, Graduate School of Medical and Dental Sciences, Professor, 大学院医歯学総合研究科, 教授 (50160940)
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| Co-Investigator(Kenkyū-buntansha) |
KITADA Katsuhiro Kagoshima University, Graduate School of Medical and Dental Sciences, Research Associate, 大学院医歯学総合研究科, 助手 (90195264)
NAGATA Emi Kagoshima University, Medical and Dental Hospital, Research Associate, 医学部・歯学部附属病院, 助手 (00304816)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥14,200,000 (Direct Cost: ¥14,200,000)
Fiscal Year 2006: ¥5,600,000 (Direct Cost: ¥5,600,000)
Fiscal Year 2005: ¥8,600,000 (Direct Cost: ¥8,600,000)
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| Keywords | Dental plaque / Oral bacteria / Animal model / Endocardit is / Pneumonia / Adherence / Streptococci |
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| Research Abstract |
We examined the ability of human supragingival dental plaque to induce infective endocarditis in rats. In total, 15 out of 27 catheterized rats survived after intravenous injections with human supragingival dental plaque suspensions containing 3 x 10^6 colony forming unit of bacterial cells. In surviving rats, infected vegetations were formed in all except one rat. The microbial composition of the infected vegetations was different from that of the respective dental plaque inocula, and Streptococcus oralis comprised the majority of the isolates. In rats affected with endocarditis, the aortic sinus was filled with fibrinous vegetation containing bacteria. Inflammatory cells infiltrated the aortic valve, the aorta adjacent to the valve, and the cardiac muscles. We also examined the contribution of cell surface polysaccharides to the infectivity of Streptococcus mutans in infective endocarditis using a rat model. The polysaccharides-defective mutant of S. mutans reduced its ability to induce infective endocarditis compared to tie parental strain. The results suggest that the cell surface polysaccharides have an important role for the induction of infective endocarditis by S. mutans.
Next, we examined the ability of human dental plaque to induce pneumonia in mice. All the human dental plaque samples tested induced pneumonia in mice. In total, 12 out of 18 mice died within 3 days after inoculation with dental plaque suspension, and bacterial cells were recovered from all dead mice. Significantly larger number of bacterial cells including oral microorganisms was recovered from lungs of dead mice than that of survived ones. No characteristics were observed in the microbial composition of infected lung specimens.
These results suggest that dental plaque serves as a potent source of bacteria causing infective endocarditis and pneumonia in humans.
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