Yamamoto K
Department of Orthopaedic Surgery, Tokyo Medical College, Japan.
Nihon Seikeigeka Gakkai Zasshi. 1990 Jul;64(7):648-65.
In order to clarify the cause and mechanism of joint degeneration in osteoarthritis (OA), a histopathological study and ultrastructural-histochemical analysis were performed on the articular cartilage of the C57 Black mouse, a model of spontaneous osteoarthritis. Using transmission electron microscopy (TEM), in all stages of light microscopically recognized OA, we found that Golgi apparatus++ were poorly developed, intracellular microfilaments markedly increased, proteoglycan granules decreased and collagen networks broken. Observing histologically normal models of different ages by TEM, we found Golgi apparatus++ and other organelles to be well developed regardless of age. Many proteoglycan granules were seen, mainly consisting of keratan sulphate in the later months. Collagen networks were maintained. These results suggest that disturbed protein transport and sugar synthesis in chondrocytes due to the deficient development of Golgi apparatus++ caused the degenerative change in articular cartilage and that, with aging, the structure and function of the matrix were maintained mainly due to the continued presence of keratan sulphate.
为了阐明骨关节炎(OA)中关节退变的原因和机制,对自发性骨关节炎模型C57黑小鼠的关节软骨进行了组织病理学研究和超微结构 - 组织化学分析。使用透射电子显微镜(TEM),在光镜下识别出的OA的所有阶段,我们发现高尔基体++发育不良,细胞内微丝明显增加,蛋白聚糖颗粒减少,胶原网络断裂。通过TEM观察不同年龄的组织学正常模型,我们发现无论年龄大小,高尔基体++和其他细胞器都发育良好。可见许多蛋白聚糖颗粒,在后期主要由硫酸角质素组成。胶原网络得以维持。这些结果表明,高尔基体++发育不足导致软骨细胞中蛋白质运输和糖合成紊乱,从而引起关节软骨的退行性改变,并且随着年龄增长,基质的结构和功能主要由于硫酸角质素的持续存在而得以维持。