The establishment of the experimental animal model of joint contracture, and analysis of the marker gene

本研究旨在通过观察实验模型中关节和肌肉的变化，阐明废用综合征症状之一的关节挛缩的病理学。我们制作了实验性关节挛缩动物模型。对9周龄的雄性9周龄Wister大鼠进行左侧坐骨神经的神经切断术。右侧作为对照，不进行处理。大鼠腓肠肌在神经切断后第30天出现明显萎缩，膝关节呈屈曲位，活动度降低。以制备的关节挛缩动物模型的关节软骨为材料，采用定量RT-PCR方法检测II型胶原和聚集蛋白聚糖的已知基因。失神经支配组和对照组的II型胶原基因表达水平无显著差异。聚集蛋白聚糖的基因表达水平的估计揭示了两组之间的显着差异。检测软骨细胞数量及变化 关于我们 软骨层的厚度。实验期间，两组软骨细胞的平均数量没有显示出任何增加的趋势，也没有显示出任何减少的趋势。关节软骨厚度除神经切断后第7天和第14天外，其余时间去神经组均较对照组厚。神经切断后软骨细胞数量和软骨层形态变化不大。此外，我们还探讨了MRI对失神经大鼠肌肉萎缩的定量评价。我们尝试用水和肌酸的光谱分析来估计肌肉的直径和肌肉内的扩散系数。去神经组和对照组之间的估计扩散系数没有显着差异。神经切断后8周，失神经支配组神经纤维直径明显小于对照组。这一结果与神经切断术导致肌肉萎缩的事实相一致，但差异无统计学意义。失神经组腓肠肌单位体积（体素）肌酸含量低于对照组。我们在产生神经源性关节挛缩的关节软骨中未检测到预测的未知基因。本研究通过对关节挛缩相关组织的全面评价，包括标记基因的寻找，揭示了关节挛缩发生发展过程中病理生理的复杂性。少

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 … More 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