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 sti#ness 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.

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.