Effects of electrical physical stimuli on articular cartilage.

Articular cartilage is a hypocellular, avascular, alymphatic tissue with a dense collagen and proteoglycan matrix that provides a low-friction and highly durable wear-resistant surface1 to both shear and compressive stress. Normal maintenance of articular cartilage results from the balance between anabolic and catabolic activity. Resident chondrocytes control the extracellular matrix turnover—collagen and proteoglycans synthesis and degradation—from the tidemark to the tangential zone of the cartilage. However, little is known about the physiological processes regulating cellular turnover and cartilage homeostasis, mainly because of the large number of factors involved (mechanical load, cell density, matrix composition, growth factors, cytokines, injury, and aging) and the complexity of their interactions. Insufficient knowledge of the physiology and homeostasis of articular cartilage greatly impairs the ability to stop or slow disease progression. It is commonly accepted that articular cartilage is a tissue with little or no regenerative potential and thus undergoes degradation over time. The notion that it is impossible to prevent or reverse degeneration of articular cartilage has been challenged recently by the growing body of evidence in the literature based on basic-research findings concerning the physiology and pathophysiology of articular cartilage, so that new strategies for its maintenance and repair are emerging2. In two recent studies by Glasson et al.3 and Stanton et al.4, a knockout mouse model of osteoarthritis, a degenerative disease that eventually leads to destruction of articular cartilage, demonstrated how a single protein, ADAMTS 5, is the main aggrecanase responsible for cartilage degradation and the principal mediator of the catabolic effects of pro-inflammatory cytokines, such as interleukin-1 (IL-1). Their findings identify a rational target for therapeutic intervention to limit cartilage degradation in osteoarthritis and demonstrate that interference with a single pathway can dramatically alter the natural history of joint disease. Chondral injury rapidly results in …