Effect of mechanical stress loaded on the chondrocytes

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Although osteoarthritis is one of the popular pathway of joint deterioration results from the mechanical stress loaded on the joint tisse, the underlying mechanism has not been clarified. To elucidate this problem, we introduced Flexercell Strain Unit which enable us to load cyclic tensile stretch on the chondrocytes and investigated the alteration of chondrocytes metabolisms. Cyclic tensile stretch caused morphological change of chondrocytes and enhanced glycosaminoglycan and keratan sulfate release. DNA synthesis was significantly enhanced. On the other hand, cyclic tensile stretch clearly reduced proteoglycan synthesis and inhibitors of protein kinase C reversed stretch-induced inhibition of proteoglycan synthesis. Furthermore, pretreatment of phorbol ester abolished stress-mediated inhibition of proteoglycan synthesis. These data indicate the involvement of protein kinase C in the signal transduction of the mechanical stress loaded on the articular chondrocytes.