Regenerative strategies for engineering cartilage have recently shown promise, as they have been capable of producing tissues comparable in Young’s modulus and glycosaminoglycan (GAG) content to native cartilage [1]. The response of engineered cartilage, when implanted, relies on its ability to withstand the harsh chemical and mechanical environment of the implantation site. Mechanical stimuli, in particular, have been identified as important regulators of chondrocyte function and can induce inflammatory responses or the release of proteoglycans from cartilage explants [2–4]. The downstream effects of these responses can induce chondrocyte death as soon as a few hours after and up to 7 days post injury [5]. In cartilage explants, injury to the tissue can produce structural damage and osteoarthritic-like changes including a loss of mechanical properties, increased collagen degradation, and reduced proteoglycan synthesis [2,6]. Injurious loads have been identified as one potential mechanism leading to apoptosis and necrosis [8].

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