The menisci within the knee likely respond to adverse loading conditions, leading to aggravated cartilage damage and fissuring [1]. Upregulation of catabolic molecules such as interleukin-1α (IL-1α), metalloproteinases (MMPs), aggrecanases (ADAMTS-4 and -5), and cyclooxygenase-2 (COX-2), as well as release of proteoglycans [2], have been shown in vitro for meniscal explants following dynamic loading [3]. A crucial event in matrix degradation is the loss of aggrecan, caused by the ADAMTS family [4]. In osteoarthritic cartilage, IL-1 has been shown to influence COX-2 activity, leading to increased synthesis of prostaglandin E2 and subsequent proteinase activity [5].

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