Setton L A, Elliott D M, Mow V C
Department of Biomedical Engineering, Duke University, Durham, NC 27708, USA.
Osteoarthritis Cartilage. 1999 Jan;7(1):2-14. doi: 10.1053/joca.1998.0170.
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.
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.
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 transection 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.
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.
软骨力学研究旨在确定健康软骨的力学行为与组成和结构之间的基本关系，并确定与退变相关的变化机制。
综述了正常和骨关节炎（OA）人类关节软骨的力学情况。还介绍了关节不稳定的前交叉韧带横断（ACLT）模型中软骨退变的起始和发病机制研究。
在患OA的人类软骨中，拉伸、压缩和剪切行为发生了显著改变。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，与健康软骨相比，肿胀倾向增加。在OA的ACL横断模型中，也观察到了软骨力学的类似变化。此外，还发现了与人类OA一致的结构、组成和代谢变化。胶原-蛋白聚糖固体网络的退化似乎集中在关节表面，这是该模型中最早出现的软骨变化。软骨表面的初始破坏是机械力的直接结果还是软骨细胞活性改变的产物，仍有待确定。
这些数据以及使用OA实验模型进行的持续研究为我们理解OA的发病机制和病程提供了基础，并将导致开发更好的疾病干预和治疗方法。
