Mechanical and oxidative stress in osteoarthritis

抄録

Osteoarthritis (OA) is one of the most common age-related degenerative joint disorders. In addition to aging, various life-style-related factors, such as obesity and overuse of joints, have been recognized as major risk factors for OA. It has been revealed that mechanical force acting on articular cartilage induces chondrocytes to produce excess amounts of reactive oxygen species (ROS), which are known to be an OA-related catabolic factor. In addition, it has been reported that mechanical stress-induced ROS directly damage chondrocyte DNA, resulting in the downregulation of cellular activity and induction of apoptosis in osteoarthritic chondrocytes. Notably, molecular events associated with DNA oxidative damage influence the regulation of chondrocyte activity and cellular viability, supporting the notion that mechanical stress-induced oxidization of chondrocyte DNA participates in the pathogenesis of OA. Here, we review accumulating evidence supporting the involvement of mechanical and oxidative stresses in cartilage homeostasis and the pathogenesis of OA.