Project/Area Number |
10470058
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Experimental pathology
|
Research Institution | Osaka University |
Principal Investigator |
NOMURA Shintaro OSAKA University Medical School, Associate Professor, 医学系研究科, 助教授 (80159087)
|
Project Period (FY) |
1998 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥11,700,000 (Direct Cost: ¥11,700,000)
Fiscal Year 1999: ¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1998: ¥9,100,000 (Direct Cost: ¥9,100,000)
|
Keywords | osteopontin / homeostasis / bone resorption / bone tissue / osteocyte / transcription / integrin / osleoclact / メカニカルストレス / 遺伝子発現 / 骨芽細胞 / 転写因子 / プロモーター |
Research Abstract |
Molecular mechanism of bone remodeling caused by mechanical stress is unknown. In this project, we identified osteopontin (Opn) as the trigger of bone remodeling. Experimental bone remodeling system developed by Waldo et al was used for the study. A 0.5mm diameter of elastic band was inserted interproximally among the upper first and second molar on both side. After 12 hours of treatment, Opn expression was detected in the osteocytes on the pressure side, and gradually spread to those on the tension side. Only 3% of the osteocytes located on the pressure side expressed Opn in the control rats. In contrast, the value was increased to 88% at 48 hoturs. Following the increased expression of Opn, a 17-fold greater number of osteoclasts compared with the control and numerous resorption pits were observed on the pressure side of the alveolar bone. Injection of RGDS-peptide strongly inhibited the increase in the number of osteoclasts. The results indicate that Opn is an important factor triggering bone remodeling caused by mechanical stress. Furthermore, Opn was identified as the crucial factor of the homeostasis of bone.
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