| Project/Area Number |
23593074
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Periodontal dentistry
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| Research Institution | Matsumoto Dental University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TAGUCHI Akira 松本歯科大学, 歯学部, 教授 (70243582)
NISHIDA Eisaku 愛知学院大学, 歯学部, 非常勤講師 (10512519)
MUTO Akinori 松本歯科大学, 歯学部, 講師 (50549433)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 歯周病 / 血清アミロイドA / 動脈硬化症 / Periodontal Medicine / Cardiovascular disease / Periodontal disease / Serum Amyloid A / Interleukin-6 |
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| Research Abstract |
The purpose of this study was to elucidate the onset mechanism of atherosclerosis through periodontal disease induced serum amyloid A (SAA). Both of the serum SAA protein level and the aortic lipid deposition were increased significantly in the periodontitis model mouse which injected IL-6 into periodontal tissue. And the mRNA expressions of monocyte adhesion, migration factors and the SAA-receptor TLR2 were up-regulated significantly with SAA treatment for the endothelial cells. Furthermore, the expression of TLR2 was observed at the initial disease area of the aorta immunohistochemically in the mouse model.
Therefore, these results suggest that periodontal disease induced SAA could deteriorate the atherosclerosis through TLR2, and a possibility that the onset diagnosis of arteriosclerosis could be performed according to the severity of the periodontal disease.
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