2003 Fiscal Year Final Research Report Summary
Mechanisms of anabolic action in low intensity pulsed ultrasound-accelerated fracture repair -synergistic effect on stretch-loading -
| Project/Area Number |
14571409
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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 |
Orthopaedic surgery
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| Research Institution | Kanagawa Dental College |
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Principal Investigator |
MIKUNI-TAKAGAKI Yuko Kanagawa Dental College, Faculty of Dentistry, Associate Professor, 歯学部, 助教授 (60050689)
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| Co-Investigator(Kenkyū-buntansha) |
ITOMAN Moritoshi Kitasato Univ., Faculty of Medicine, Professor, 医学部, 教授 (70104528)
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| Project Period (FY) |
2002 – 2003
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| Keywords | ultrasound / bone formation / mechanotransduction / fracture repair / COX2 / prostaglandin E2 / osteoblast / disuse |
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| Research Abstract |
In our previous studies, we emphasized the role of COX-2 as an amplifier of mechanical response of primary and established bone cells. With that in mind, our working hypothesis was that COX-2 sustains the anabolic effect of mechanical stimuli resulting in the amplification of the initial mechanical input. We tested COX-2 null, one-year-old mice for impaired sonic accelerated fracture repair by subjecting their fractured femur to mechanical stimulation with LIPUS, low-intensity pulsed ultrasound. Choice of older mice for experimental animals was made since the fractured femur in the COX-2 knockout mice (Dinchuk, 1995) of 10 weeks of age, healed at an almost similar rate to those in normal littermates. On the other hands, we have observed the repair process, which took much longer, was not significantly accelerated by LIPUS, in the fractured femur of one-year-old knockout mice. Whether it is due t the blockade of COX-2-related mechanotransduction pathways was investigated. Downstream target molecules such as MMP-9, MMP-13 and VEGF are suggested to be essential to the inhibitory mechanism. Not only the cartilage removal in endochondral bone formation, but the development of undifferentiated osteogenic cells are affected. Both the role of COX-2 in bone formation and the possible undesirable outcome of NSAIDs use in elderly patients during the fracture repair are discussed
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[Publications] Naruse, K., Urabe, K., Mukaida, T., Ueno, T., Migishima, F., Oikawa, A., Mikuni-Takagaki, Y., Itoman, M.: "Spontaneous Differentiatior of Mesenchymal Stem Cells Available from Fetal Rat Circulation"Bone. (in press). (2004)
Description
「研究成果報告書概要(欧文)」より
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