2005 Fiscal Year Final Research Report Summary
The establishment of the experimental animal model of joint contracture, and analysis of the marker gene
| Project/Area Number |
15300195
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Rehabilitation science/Welfare engineering
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| Research Institution | The University of Tokyo |
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Principal Investigator |
ETO Fumio The University of Tokyo, Faculty of Medicine, Professor, 医学部附属病院, 教授 (00101121)
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| Co-Investigator(Kenkyū-buntansha) |
UEMURA Toshimasa National Institute of Advanced Industrial Science and Technology・Nanotechnology research institute, chief researcher, ナノテクノロジー研究部門, 主任研究員 (60176641)
UENO Shoogo The University of Tokyo, Graduate School of Medicine, Professor, 大学院・医学系研究科, 教授 (00037988)
SEKINO Masaki The University of Tokyo, Graduate School of Medicine, Research Associate, 大学院・医学系研究科, 助手
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| Project Period (FY) |
2003 – 2005
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| Keywords | Joint contracture / Neurogenic / gene expression / Type II collagen / aggrecan / Joint cartilage / MRI / MRS |
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| Research Abstract |
This study was to examine a change of joint and muscle in the experimental model in order to elucidate the pathology of joint contracture as a symptom of disuse syndromes. We made experimental animal model of joint contracture. Neurotomy of the left sciatic nerve was performed on the male 9-week-old Wister rats of 9 weeks old. The right side as a control was not treated. A calf muscle of rat developed a remarkable atrophy at 30th day after neurotomy, and the knee joint showed a flexion position with decreased range of motion. With articular cartilage of the prepared animal model of joint contracture we evaluated the known gene of type II collagen and aggrecan by the quantitative RT-PCR. There was no significant difference in the estimated type II collagen gene expression level between the denervated group and control group. The estimated gene expression level of aggrecan revealed a significant difference between the two groups. Then we examined the number of chondrocyte and the change
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of thickness of a cartilage layer. The average number of chondrocyte did not show any tendency of increase nor tendency of decrease between the two groups during the experimental period. As for the thickness of articular cartilage, the denervated group showed thicker than the control group except for 7th and 14th day after neurotomy. The number of chondrocyte and configuration of the cartilage layer revealed little changes after neurotomy. In addition, we investigated quantitative evaluation of muscle atrophy of denervated rat using MRI. We tried to estimate the muscle diameter and diffusion coefficient inside the muscle with using the water and creatine spectral analysis. There was no significant difference in the estimated diffusion coefficient between the denervated and control groups. The estimated fiber diameter of denervated group showed smaller compared with that of the the control group at the 8th week after neurotomy. This result agreed with the fact that the neurotomy caused muscle atrophy, but the difference was not statistically significant. In denervated group, the creatine content of the gastrocnemius muscle per unit volume (voxel) was smaller than that of the control group. We could not detect the unknown gene which was predicted in the articular cartilage of produced neurogenic joint contracture. This study revealed the complexity of pathophysiology in the development of the joint contracture with having evaluated comprehensively the tissues involved in joint contracture including a search of marker gene. Less
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