Project/Area Number |
14207075
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Research Category |
Grant-in-Aid for Scientific Research (A)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Morphological basic dentistry
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Research Institution | Matsumoto Dental University |
Principal Investigator |
OZAWA Hidehiro Matsumoto Dental University, Graduate school of Oral Medicine, Professor, 大学院・歯学独立研究科, 教授 (60018413)
|
Co-Investigator(Kenkyū-buntansha) |
KAWAKAMI Toshiyuki Matsumoto Dental University, Graduate school of Oral Medicine, Professor, 大学院・歯学独立研究科, 教授 (80104892)
TAKAHASHI Naoyuki Matsumoto Dental University, Graduate school of Oral Medicine, Professor, 大学院・歯学独立研究科, 教授 (90119222)
UDAGAWA Nobuyuki Matsumoto Dental University, Graduate school of Oral Medicine, Professor, 歯学部, 教授 (70245801)
KAWAGUCHI Hiroshi The University of Tokyo, Department of Orthopedics, Assistant professor, 医学部附属病院, 助教授 (40282660)
HOSOYA Akihiro Matsumoto Dental University, Department of Oral Histology, Associate professor, 歯学部, 助手 (70350824)
|
Project Period (FY) |
2002 – 2004
|
Project Status |
Completed (Fiscal Year 2004)
|
Budget Amount *help |
¥50,180,000 (Direct Cost: ¥38,600,000、Indirect Cost: ¥11,580,000)
Fiscal Year 2004: ¥8,840,000 (Direct Cost: ¥6,800,000、Indirect Cost: ¥2,040,000)
Fiscal Year 2003: ¥16,900,000 (Direct Cost: ¥13,000,000、Indirect Cost: ¥3,900,000)
Fiscal Year 2002: ¥24,440,000 (Direct Cost: ¥18,800,000、Indirect Cost: ¥5,640,000)
|
Keywords | Calcification / Bone formation / Bone resorption / Coupling factor / MyD88 / Dental pulp / Laser / EP4 agonist / BMP / OPG / EP4 / 急速凍結法 |
Research Abstract |
I. Molecular mechanisms of calcification in bone matrix formation : To identify the factor induce formation of the nuclear, we make monoclonal anti-body using matrix vesicle isolated from MLO-A5 cell in culture and clarified that the antigen localizes among the fibrae in extracellular matrix. Moreover, to estimate the effects of Mg in bone calcification, we determined the bone qualities, especially mineralization in Mg deficient rat. Loss of Mg was increased the value of Ca and had irregular crystal of hydroxyapatite in the rat. These findings indicate that the loss of Mg inhibits the crystallization of hydroxyapatite in matrix vesicle. II. Coupling mechanisms of bone metabolism : Bone formation and bone resorption were promoted in osteoprotegerin (OPG)-deficient mice. Bisphosphonate, a potential inhibitor of bone resorption, reduced both bone formation and bone resorption. Bone formation induced by bone morphogenetic protein in OPG-deficient mice did not exhibit any difference from tha
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t in wild mice. These results suggest that coupling factors activated or released by osteoclasts may be involved in the subsequent bone formation. We investigated the mechanism of osteoclastogenesis induced by lipopolysaccharide and interleukin (IL)-1. These factors induced the expression of RANKL in osteoblastic cells through MyD 88 and Ca/PKC-MEK/ERK pathways. III. Bone regeneration and reconstruction model : The subcutaneously transplanted rat dental pulp formed mineralized hard tissue possessing bone- or cementum-like characteristics, suggesting that dental pulp possesses the ability to hard tissue formation by itself. Bone formation induced laser light irradiation was shown to be caused by the odontoblast activation and the inhibition of osteoclastic bone resorption. In the study of prostaglandin E EP4 receptor agonist, the gene expression existed in odontoblast, and the bone formation activity was resulted from the decrease of adipocyte and the increase of osteoblast in bone marrow. Less
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