| Project/Area Number |
21592328
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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 |
Morphological basic dentistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TAKATA Takashi 広島大学, 大学院・医歯薬学総合研究科, 教授 (10154783)
KITAGAWA Masae 広島大学, 病院, 助教 (10403627)
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| Co-Investigator(Renkei-kenkyūsha) |
NIIDA Syunpei 国立長寿医療研究センター, 室長 (10137630)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | γ-glutamyl transpeptidase / 慢性肝疾患 / 二次性骨粗鬆症 / 抗体治療 / 骨量減少 / 破骨細胞性骨吸収 / 骨芽細胞分化 / 歯周炎 / γ-GTP / 骨破壊 / 歯周病 / 骨粗鬆症 / 治療薬 / 抗体 / γGTP / 骨破壞 |
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| Research Abstract |
Cholestatic liver diseases often manifest the increased levels of γ- glutamyl transpeptidase(GGT) and secondary osteoporosis. GGT is known as a novel bone resorbing factor that stimulates osteoclast formation. The aim of this study was to elucidate the mechanisms by which GGT causes bone reduction.
In BDL rats with elevation of serum GGT level, bone reduction with increase of osteoclasts was evident. These changes were significantly attenuated by AGT3. In vitro study showed significant upregulation of osteoclastogenesis via osteoblasts and inhibition of osteoblast differentiation with GGT stimulation. Moreover upregulation of GGT in periodontal tissue induced alveolar bone destruction with osteoclastogenesis, whereas antibody treatment reduced it. Therefore managing the elevated GGT by AGT3 may become a novel therapeutic agent for secondary osteoporosis and periodontitis in cholestatic liver diseases.
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