Altered mechanics of cartilage with osteoarthritis: human osteoarthritis and an experimental model of joint degeneration
Altered mechanics of cartilage with osteoarthritis: human osteoarthritis and an experimental model of joint degeneration
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DOI：
10.1053/joca.1998.0170
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发表时间：
1999-01-01
影响因子：
7
通讯作者：
Mow, VC
中科院分区：
文献类型：
--
作者：
Setton, LA;Elliott, DM;Mow, VC
目的：软骨力学的研究旨在确定力学行为和健康软骨的组成和结构之间的基本关系，并确定与degeneration.Method相关的变化机制：正常和骨关节炎（OA）人类关节软骨的力学进行了审查。在前交叉韧带横断（ACLT）模型的关节不稳定性的软骨退变的启动和发病机制的研究也presented.Results：在人类软骨与OA，拉伸，压缩和剪切行为显着改变。与健康软骨相比，这些变化表现为OA软骨在拉伸、压缩和剪切载荷下的模量或刚度降低，以及膨胀倾向增加。在骨关节炎的前交叉韧带移植模型中，也观察到了类似的软骨力学变化。此外，结构、组成和as代谢的变化与人类OA一致，胶原蛋白-蛋白多糖固体网络的退化似乎集中在关节表面，是模型中最早的软骨变化。它仍然有待确定，如果最初的破坏软骨表面是一个直接的结果，机械力或产品的改变软骨细胞activity.Conclusions：这些数据和持续的研究使用实验模型的OA提供了一个基础，为我们了解的发病机制和时间过程中的事件在OA，并会导致发展更好的程序，疾病干预和治疗。
Objective: Studies of cartilage mechanics seek to determine the fundamental relationships between mechanical behavior and the composition and structure of healthy cartilage and to determine mechanisms for changes associated with degeneration.Method: The mechanics of normal and osteoarthritic (OA) human articular cartilage are reviewed. Studies of the initiation and pathogenesis of cartilage degeneration in the anterior cruciate ligament transection (ACLT) model of joint instability are also presented.Results: In human cartilage with OA, tensile, compressive and shear behaviors are dramatically altered. These changes present as decreases in the modulus or stiffness of OA cartilage in tension, compression and shear loading, and increases in the propensity to swell as compared to healthy cartilage. In the ACL transaction model of OA, similar changes in the mechanics of cartilage have been observed. In addition, changes in structure, composition, and as metabolism consistent with human OA have been found. Deterioration of the collagen-proteoglycan solid network, which appears to be focused at the articular surface, has been the earliest cartilage changes in the model. It remains to be determined if the initial disruption of the cartilage surface is a direct result of mechanical forces or a product of altered chondrocyte activity.Conclusions: These data and continued research using experimental models of OA provide a basis for our understanding of the pathogenesis and the time course of events in OA and will lead to the development of better procedures for disease intervention and treatment.