Abstract

Purpose: OA is a whole joint disease, where breakdown of articular cartilage is considered a classical hallmark of disease pathophysiology and progression. Therefore, cartilage degeneration must be prevented or reversed in order to maintain and restore joint health. Previous studies reported the importance of Glycogen Synthase Kinase (GSK) -3 alpha and beta as key regulators in chondrocyte biology, but their roles in articular cartilage health and disease are not well understood. In this study, we examine the role of GSK-3 in knee joint OA as well as skeletal growth in cartilage-specific knock-out (KO) mice.

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