| Project/Area Number |
18592258
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Periodontal dentistry
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
NAGASAWA Toshiyuki Tokyo Medical and Dental University, Graduate school, Department of hard tissue engineering, Research associate (90262203)
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| Co-Investigator(Kenkyū-buntansha) |
NITTA Hiroshi Graduate school, Tokyo Medical and Dental University, Department of Comprehensive Oral Care, Associate Professor (70237767)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,860,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥360,000)
Fiscal Year 2007: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2006: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | OPG / RANKL / atherosclerosis / P. gingivalis / 歯周病原細菌 / 血管平滑筋細胞 / 歯肉線維芽細胞 / 歯根膜線維芽細胞 |
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| Research Abstract |
Chronic inflammation and infection play pivotal roles in the pathogenesis of abdominal aortic aneurysm (AAA). Receptor activator of nuclear factor kappa B ligand (RANKL) and osteoprotegerin (OPG) have recently been implicated as key partners of osteoimmunology and vascular diseases. Although periodontopathic bacteria were detected in AAA specimens, the role of periodontal infection in AAA pathogenesis remains unclear. This study investigated the association of periodontopathic bacteria with the expression of RANKL and OPG in AAA.
AAA and normal aorta tissues were collected from patients during surgical AAA repair. Expression of RANKL and OPG mRNA was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and localization of RANKL in AAA tissues was examined by immunohistochemistry. Periodontopathic bacteria in specimens were detected by PCR. Our results showed significantly increased RANKL, but decreased OPG, mRNA levels in AAA tissues when compared to normal aorta tissues. RANKL was localized in the intimal and medial layers and was expressed in mononuclear and vascular smooth muscle cells (VSMCs). The expression levels of RANKL, but not OPG, were positively correlated with the presence of Porphyromonas gingivalis and Treponema denticola, but not A. actinomycetemcomitans, in vessel tissues. These periodontopathic bacteria were not detected in any normal tissues. P. gingivalis lipopolysaccharide was able to upregulate RANKL expression in VSMCs. Our findings demonstrated the association between periodontopathic bacteria and RANKL upregulation in AAA, suggesting a potential role of periodontal infection in the pathogenesis of AAA, via RANKL upregulation.
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