Mechanical stress loaded on chondrocytes and cellular apoptosis: involvement of reactive oxygen species.

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Osteoarthrosis, a common pathway to joint deterioration, results when a physiological imbalance exists between mechanical stress on the joint tissues and the ability of those tissues to withstand that stress. Although mechanical stress is known to be an essential factor in the regulation of cartilage metabolism, the precise mechanisms involved have not yet been determined. To examine, at the cellular level, the underlying mechanisms that lead to cartilage degradation, we introduced a computerized, pressure-operated device (Flexercell Strain Unit) to induce deformation of chondrocytes. We found that while a low frequency and magnitude of cyclic tensile stretch applied to chondrocytes increased proteoglycan (PG) synthesis, a high frequency and magnitude of stress decreased its synthesis.Nitric oxide (NO) has been implicated in the pathogenesis of OA. Enhanced PG and NO synthesis were evident when cyclic tensile stretch was applied to chondrocytes. When NO production was inhibited, PG synthesis was enhanced further. These data suggest that stress-mediated alteration in PG synthesis was modulated by NO production.