Joint motion and loading are required to maintain the normal composition, structure, and mechanical properties of adult articular cartilage.1,13
When the intensity or frequency of loading exceeds or falls below these necessary levels, the balance between synthesis and degradation will be altered, and changes in the composition and microstructure of cartilage will follow. Prolonged reduction of joint motion caused by rigid immobilization leads to degeneration of articular cartilage. These changes result, in part, because normal nutritive transport to cartilage from the synovial fluid by means of diffusion is diminished when the fluid does not move. In addition, the mechanical properties of articular cartilage will be compromised with immobilization. These biochemical and biomechanical changes are, at least in part, reversible if the joint is allowed tomove. A better understanding of the deleterious effects of joint immobilization has led to treatments of joint injuries that allow patients at least some joint motion while the injuries are healing. Excessive joint loading also may affect articular cartilage. Catabolic effects can be induced by a single-impact or repetitive trauma and may serve as the initiating factor for progressive degenerative changes. However, regular joint use, including running, has not been shown to cause joint damage in normal joints.14 The specific mechanisms by which joint loading influences chondrocyte functionremain unknown, although various mechanical, physicochemical, and electrical transduction mechanisms have been proposed.10,12 Matrix deformation produces fluid and ion flow, which may facilitate chondrocyte nutrition. Deformation and fluid flowlead to changes in the local charge density within the matrix, resulting in an electric potential that may serve as cellular signals.