| Project/Area Number |
15591945
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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 | Ohu Unrversity |
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Principal Investigator |
YAMASAKI Akira Ohu Unrversity, dentistry, professor, 歯学部, 教授 (60110459)
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| Co-Investigator(Kenkyū-buntansha) |
ITOU Hiroshi Ohu Unrversity, dentistry, assistant professor, 歯学部, 助教授 (20184682)
SUGIURA Junko Ohu Unrversity, dentistry, lecturer, 歯学部, 講師 (80316471)
SAKURAI Yuuko Ohu Unrversity, dentistry, research assistant, 歯学部, 助手 (10306087)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2004: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2003: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | Enchondral ossification / Op mouse / Endothelial cells / MMP-9 / VEGF / Immunohistochemistry / In situ hybridization / 軟骨内骨化 / 骨端軟骨 / 大理石骨病マウス / 破(軟)骨細胞 / 電子顕微鏡 / 内軟骨性骨化 / 異所性骨化 / BMP-2 / 破骨細胞 |
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| Research Abstract |
Enchondral ossification is preceded the vascular invasion into hypertrophic chondrocyte lacunae. Although it has been described that the osteoclasts or chondroclasts are primarily responsible for the degradation or resorption of the transverse septa facing to the vascular invasion front, there are some questions to be clarified. In this study, we conducted morphological aprorch using the op mouse that has an inheritent deficiency of monocyte/macrophage lineage.
In the femoral or tibial epiphysis of the op mice appeared to be normal thickness and morphology despite the lack of both TRAP-positive osteoclasts or chondroclasts and F4/80 positive macrophages. Electron microscopically, the cells found in the vascular invasion front are only vascular endothelial cells and perivascular cells and neither osteoclasts nor macrophages were observed at all. This was also confirmed by the laminin immunohistochemistry as a marker for endothelial cell identification.
Immunohistochemistry and electron immunohistochemistry demonstrated the expression of MMP-9 protein in both cellular component and extraoellular matric at the front of the vascular invasion. The expression of MMP-9 geen also recognized in the cells located in the same region, at least some of which were vascular endothelial cells. The expression of VEGF protein, was found intensely in the metaphysic and weakly in the hypertrophic chondrocytes in the epiphyseal growth plate.
From the present study, we suggest that the vascular invasion leaded by MMP-9 and VEGF is primarily responsible for the break down of the transverse septa of hypetrophic chondrocytes lacunae and neither osteoclastic cells nor macrophages involve in this phenomenon.
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