| Project/Area Number |
16591882
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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 |
Pathobiological dentistry/Dental radiology
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| Research Institution | Tohoku University |
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Principal Investigator |
SHOJI Noriaki Tohoku University, Hospital, Lecturer, 病院, 講師 (70250800)
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| Co-Investigator(Kenkyū-buntansha) |
SASANO Takashi Tohoku University, Graduate School of Dentistry, Professor, 大学院・歯学研究科, 教授 (10125560)
IIKUBO Masahiro Tohoku University, Hospital, Lecturer, 病院・講師 (80302157)
SUGAWARA Syunji Tohoku University, Graduate School of Dentistry, Professor, 大学院・歯学研究科, 教授 (10241639)
KOSEKI Kenyoshi Tohoku University, Graduate School of Dentistry, Professor, 大学院・歯学研究科, 教授 (80291128)
SAKAMOTO Maya Tohoku University, Hospital, Lecturer, 病院・講師 (90157686)
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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 |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2004: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | IL-10 / Apical Periodontitis / Inflammatory bone resorption / Transgenic mice / Cytokine |
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| Research Abstract |
Periapical bone resorption occurs following infection of the dental pulp. Bone destruction has been linked to excessive expression of inflammatory cytokines, particularly interleukin (IL)-1. IL-10 is an anti-inflammatory cytokine, produced by various immune cells including macrophages and T2 cells, that we previously found was a key endogeneous inhibitor of infection-stimulated peripheral bone resorption in vivo, likely acting via IL-1 inhibition. More recently, we have shown that IL-10^<-/-> mice are also extremely susceptible Porphyromonas gingivalis (Pg)-stimulated periodontal bone loss, without an increase in gingival IL-1 levels. In contrast, no significant bone loss is induced by the Pg infection in corresponding wild-type (WT) mice. In the present study, we will employ the IL-10^<+/+> mice model, a ‘reverse‘ model of IL-10^<-/-> mice, to test the hypothesis that induction and progression of apical periodontitis can be ameliorated by modulating IL-10, IL-10 receptors their signaling, and cytokine network that IL-10 regulates. The dental pulps of the first molars were exposed and infected with a mixture of four common endodontic pathogens, and bone destruction was determined by micro-computed tomography at sacrifice on day 21. The results demonstrate that IL-10^<+/+> mice model had no significantly greater infection-stimulated bone resorption in vivo compared with wild-type mice, although IL-10 in alveolar bone of them was over-expressed compared with that of wild-type mice.
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