Osteoarthritis (OA) is a prevalent disease, afflicting 27 million people in the United States alone [1]. OA is commonly thought of as “wear and tear” of the joints caused by repeated compression and shear strains. The mechanical contribution to the onset and progression of OA is unknown; however, it is likely a result of an imbalance of cartilage homeostasis, represented by a shift in biochemical and mechanical factors that typically maintain healthy joints [2]. Cartilage homeostasis results in part from cellular mechanotransduction events, i.e. the conversion of mechanical stimuli into a biochemical response.

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