Osteoarthritis (OA) is a disease characterized by the degeneration of articular cartilage. Disease progression is associated with the irreversible cleavage of the collagen network, surface fibrillation and loss of proteoglycans from the extracellular matrix.1, 2 These matrix changes increase surface porosity and matrix permeability, which diminish the cartilage’s ability to resist joint compressive loading. In this study, we developed an in vitro degradation model to emulate the damage that occurs in early OA in order to study how damage affects the tissue’s biomechanical function.

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