| Project/Area Number |
16592072
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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 | Nagasaki University |
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Principal Investigator |
HARA Yoshitaka Nagasaki University, Graduate School of Biomedical Sciences, Professor, 大学院・医歯薬学総合研究科, 教授 (60159100)
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| Co-Investigator(Kenkyū-buntansha) |
ABE Tatsuya Nagasaki University, Graduate School of Biomedical Sciences, Lecturer, 大学院・医歯薬学総合研究科, 講師 (80271112)
YOSHIMURA Atsutoshi Nagasaki University, Hospital of Medicine and Dentistry, Lecturer, 医学部・歯学部附属病院, 講師 (70253680)
鵜飼 孝 長崎大学, 大学院・医歯薬学総合研究科, 助手 (20295091)
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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 |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 2004: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | B cell / Bone resorption / TNF-α / RANKL / OPG / Immunohistological study / Osteoclast / 病理組織学的研究 / Tリンパ球 / 好中球 / LPS |
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| Research Abstract |
The involvement of RANKL and OPG in lipopolysaccharide-induced bone resorption is not well understood. So in the first study, we examined changes in the number of RANKL- and OPG-expressing cells when bone resorption was increased by repeated injections of LPS and decreased by additional injection of PBS. The number of RANKL-expressing inflammatory cells increased and OPG-expressing non-inflammatory cells decreased with enhancement of bone resorption. On the other hand, the number of OPG-expressing inflammatory cells increased with decrease of bone resorption. Of the inflammatory cells assay, RANKL-expressing T cells were detected in the lesions of mice with increased bone resorption and OPG-expressing polymorphonuclear leukocytes (PMN) were detected in the lesions of mice with decreased bone resorption. These results suggested that T cells and PMNs play important roles in the regulation of inflammatory bone resorption.
The aim of the second study was to examine whether B cells truly influence inflammatory bone resorption in vivo. Alveolar bone resorption in normal mice, in SCID mice that lack both B and T cells, and in B cell-reconstituted SCID mice were compared histopathologically after repeated injections of lipopolysaccharide into mouse gingival. Furthermore, we examined whether the B cells that are stimulated by lipopolysaccharide are involved in osteoclastogenesis in vitro. As a result, the B cell-reconstituted SCID mice group showed stronger inflammatory bone resorption than the SCID mice group. Also, in vitro, lipopolysaccharide-stimulated B cells enhanced osteoclastogenesis and anti-TNF-α antibody completely blocked osteoclastogenesis induced by lipopolysaccharide-stimulated B cells. These results suggest that B cells promote inflammatory bone resorption through TNF-α.
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