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骨关节炎发病机制的实验研究——兔早期骨关节炎软骨中蛋白聚糖的组织学及生化改变——(作者译)

[An experimental study on the pathogenesis of osteoarthritis--histological and biochemical changes of proteoglycan in the osteoarthritic cartilage of rabbit in the early stage-- (author's transl)].

作者信息

Ida K

出版信息

Nihon Seikeigeka Gakkai Zasshi. 1979 Aug;53(8):949-62.

PMID:512433
Abstract

Osteoarthritis is generally a slowly progressive destructive disease of joints. As the disease is asymptomatic in its initial phases, it was detectable only at the later stage when radiological changes and clinical symptom had developed. The biochemical and cellular changes that had been recorded were those of the later clinically recognizable stage of the disease. Because the time of onset in not known, the initial events which might be the most important to investigate the pathogenesis of osteoarthritis, are virtually impossible to investigate except in experimentally induced models of osteoarthritis. For the purpose of investigating the pathogenesis of degenerative osteoarthritis, experimental osteoarthritic model was prepared. Section of the medial collateral and both cruciate ligaments combined with resection of the medial meniscus in adult rabbit knees showed progressive histological changes similar to those in human osteoarthritis. Therefore, qualitative and progressive alteration of the cartilage matrix proteoglycan in experimental osteoarthritis of the early stages were investigated with time. Biochemical analysis of the cartilage from experimental osteoarthritic model demonstrated a decrease in the content of glycosaminoglycan and increase in the rate of the synthesis of glycosaminoglycan as compared to the normals. The analysis of disaccharide chain revealed a decrease in the concentration of kelatan sulfate and chondroitin-6 sulfate, along with an increase in the concentration of chondroitin-4 sulfate. These findings, which were quite consistent with those in human osteoarthritis and were contrary to those in aging, indicate the attempts of cells to compensate for the proteoglycan deficiency in osteoarthritic cartilage by synthesizing large quantities of glycosaminoglycans of immature pattern. On the other hand, synthesized aggregated proteoglycans in arthritic cartilage had shown a polydispersive pattern in CsCl density gradient compared to that of normal one, which had shown a single curved pattern. Further, newly synthesized proteoglycan in osteoarthritic cartilage seemed to be polydispersive compared with control proteoglycan in molecular sizes on Sepharose 2B gel chromatography under non-aggregated dissociative condition. Large molecular size proteoglycan composed of small molecular size glycosaminoglycan on its polysaccharide chain and small molecular size proteoglycan composed of large molecular size glycosaminoglycan. This might represent the expression of repair mechanism in the damaged cartilage, or phenotypic transformation of extracellular macromolecule in osteoarthritis.

摘要

骨关节炎通常是一种关节缓慢进展的破坏性疾病。由于该疾病在初始阶段无症状,仅在后期出现放射学改变和临床症状时才能被检测到。所记录的生化和细胞变化是该疾病后期临床可识别阶段的变化。由于发病时间未知,除了在实验性诱导的骨关节炎模型中,几乎不可能研究那些可能对探究骨关节炎发病机制最为重要的初始事件。为了研究退行性骨关节炎的发病机制,制备了实验性骨关节炎模型。成年兔膝关节内侧副韧带和两条交叉韧带切断并联合内侧半月板切除显示出与人类骨关节炎相似的进行性组织学变化。因此,随着时间的推移,对实验性骨关节炎早期软骨基质蛋白聚糖的定性和进行性改变进行了研究。对实验性骨关节炎模型软骨的生化分析表明,与正常软骨相比,糖胺聚糖含量降低,糖胺聚糖合成速率增加。二糖链分析显示硫酸角质素和硫酸软骨素 - 6的浓度降低,同时硫酸软骨素 - 4的浓度增加。这些发现与人类骨关节炎的发现相当一致,与衰老的发现相反,表明细胞试图通过合成大量不成熟模式的糖胺聚糖来补偿骨关节炎软骨中的蛋白聚糖缺乏。另一方面,与正常软骨在CsCl密度梯度中呈现单一曲线模式相比,关节炎软骨中合成的聚集蛋白聚糖呈现多分散模式。此外,在非聚集解离条件下,在琼脂糖2B凝胶色谱上,与对照蛋白聚糖相比,骨关节炎软骨中新合成的蛋白聚糖在分子大小上似乎也是多分散的。大分子大小的蛋白聚糖由其多糖链上小分子大小的糖胺聚糖组成,小分子大小的蛋白聚糖由大分子大小的糖胺聚糖组成。这可能代表受损软骨修复机制的表达,或骨关节炎中细胞外大分子的表型转化。

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