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实验性诱导骨关节炎中犬软骨的生物力学和生化特性

Biomechanical and biochemical properties of dog cartilage in experimentally induced osteoarthritis.

作者信息

Altman R D, Tenenbaum J, Latta L, Riskin W, Blanco L N, Howell D S

出版信息

Ann Rheum Dis. 1984 Feb;43(1):83-90. doi: 10.1136/ard.43.1.83.

Abstract

The finding of other investigators that increased water content is often associated with signs of a torn collagen network in human osteoarthritic (OA) cartilage led to this study. In the Pond-Nuki model of post-traumatic OA experimental but not control femoral condylar cartilage showed evidence of breakdown and stiffening of collagen network as assessed by measurement of swelling properties and indentation behaviour respectively. These changes in the unstable knees occurred despite lack of erosion of that surface cartilage ascertained from carbon black mapping and history. The stiffening rather than softening change was therefore attributed to cartilage oedema of the middle and deep certilagenous zones, wherein breakdown of collagen network has been postulated to occur. Because of insignificant reduction of total hexuronate in these cartilages, a proteoglycan (PG) profile of sedimentation coefficients for aggregate (PGA) and subunit species (PGS) was analysed to see if collagen network changes in the dog preceded PG alteration. Despite minimal histological changes our results confirmed previous findings in the tibial plateau cartilage in this model, that PGA was reduced in size and PGS increased in amount. Slight enzymatic breakdown of PGs, or altered synthesis due to cellular responses to either the injury directly or to synovial inflammation, seems necessary to explain such changes in the absence of cartilage erosion.

摘要

其他研究人员发现,在人类骨关节炎(OA)软骨中,水分含量增加往往与胶原蛋白网络撕裂的迹象相关,这引发了本研究。在创伤后骨关节炎的Pond-Nuki模型中,通过分别测量肿胀特性和压痕行为评估,实验性股骨髁软骨而非对照股骨髁软骨显示出胶原蛋白网络的破坏和硬化迹象。尽管通过炭黑映射和病史确定该表面软骨没有侵蚀,但不稳定膝关节仍出现了这些变化。因此,这种硬化而非软化的变化归因于中深层软骨区的软骨水肿,据推测胶原蛋白网络在此处发生了破坏。由于这些软骨中总己糖醛酸减少不显著,分析了聚集物(PGA)和亚基种类(PGS)沉降系数的蛋白聚糖(PG)谱,以查看狗的胶原蛋白网络变化是否先于PG改变。尽管组织学变化极小,但我们的结果证实了该模型中胫骨平台软骨先前的发现,即PGA尺寸减小,PGS数量增加。在没有软骨侵蚀的情况下,PG的轻微酶解或由于细胞对直接损伤或滑膜炎症的反应导致的合成改变,似乎是解释这些变化所必需的。

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