| Project/Area Number |
16390611
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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 |
Periodontal dentistry
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| Research Institution | Tohoku university |
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Principal Investigator |
SHIMAUCHI Hidetoshi Tohoku University, Graduate School of Dentistry, Professor, 大学院歯学研究科, 教授 (70187425)
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| Co-Investigator(Kenkyū-buntansha) |
KANAYA Sousuke Tohoku University, Hospital, Dentist, 病院・医員 (80375097)
ITAGAKI Yumi Tohoku University, Graduate School of Dentistry, Assistant professor, 大学院歯学研究科, 助手 (10223067)
SUGAWARA Shunji Tohoku University, Graduate School of Dentistry, Professor, 大学院歯学研究科, 教授 (10241639)
TAKAHASHI Nobuhiro Tohoku University, Graduate School of Dentistry, Professor, 大学院歯学研究科, 教授 (60183852)
SHOJI Kanako Tohoku University, Graduate School of Dentistry, Assistant professor, 大学院歯学研究科, 助手 (90302158)
根本 英二 東北大学, 大学院・歯学研究科, 助手 (40292221)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥14,400,000 (Direct Cost: ¥14,400,000)
Fiscal Year 2006: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2005: ¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2004: ¥9,700,000 (Direct Cost: ¥9,700,000)
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| Keywords | periodontitis / systemic diseases / metabolic syndrome / Porphyromonas gingivalis / immune escape / 全疫エスケープ / アディポネクチン / 血糖値 / TNF-α / TLR2 / 樹状細胞 / 実験的歯周炎モデル / P.gingivalis |
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| Research Abstract |
The purpose of this study is to explore the unidentified "missing link" to connect the relationship between periodontal and systemic diseases by molecular biological approaches. For this purpose, we focused on the most potent pathogen of chronic periodontitis, Porphyromonas gingivalis and its components, and analyzed the molecular basis of exerting virulence of this bacterium on both periodontal lesions and bodies in vivo and in vitro. Using in vivo animal models, we investigated a series of studies clarifying ; 1)the role of P.gingivalis infection on hyperlipidemia in periodontitis patients ; 2)the effect of P.gingivalis virulence factors on production of adipocytokines from adipose tissues ; 3)the molecular effects of type 2 diabetes on the healing process of periodontium. First, our in vitro study revealed that P.gingivalis LPS and fimbriae preferentially induced a unique dendritic cell subset with a weak immunostimulatory activity via TLR2-mediated signaling, finally contributing t
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o the immune escape of this bacterium in the periodontal lesion. Furthermore, in vivo studies indicated that infection of P.gingivalis is essential for up-regulation of serum triglycerides and its LPS down-regulated the serum level of adiponectin, suggesting P.gingivalis could exert its virulence after invasion into the systemic circulation. The concept of metabolic syndrome (MetS) has been evolving, that is a clustering of simple clinical measures including waist circumferences, blood pressure, triglycerides, high-density lipoproteins and glucose. This clustering appears depend on two major factors: excess body fat and metabolic susceptibility. Taken our results into this concept, invaded P.gingivalis may work as a MetS risk factor in periodontitis patients via down-regulating the serum adiponectin level. The increased risk of MetS possibly started the sequential of "Metaboic Domino" that increasing the susceptibility to diabetes and coronary heart diseases. Diabetes can delay the healing process of periodontally diseased tissue that may increase the chance of P.gigivalis invasion. In conclusion, P.gingivalis may have an adaptation system by dealing with the local immune defense that finally contributes to systemic-periodontal connection. Less
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