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Articular cartilage is a smooth, lubricated tissue that covers the ends of bones in synovial joints. Its unique biomechanical properties are due to a dense extracellular matrix composed primarily of collagen, proteoglycans, and water. Chondrocytes are the only cell type residing in articular cartilage, responsible for synthesis, maintenance, and repair of the matrix. The tissue is avascular (lacks blood vessels), with very poor intrinsic healing capacity. Damage or degeneration (as seen in osteoarthritis) leads to joint dysfunction and pain. While chondrocytes are essential for tissue health, neither articular cartilage nor chondrocytes constitute a molecular receptor or classic drug target; rather, therapeutics aim to protect, repair, or regenerate this tissue by modulating chondrocyte biology or applying regenerative procedures[1][2][5][8].
Drugs/procedures act indirectly by modulating chondrocyte function, proliferation, matrix synthesis, or signaling pathways regulating cartilage integrity (e.g. BMPs promote chondrogenesis and cartilage repair; FGFs regulate proliferation and hypertrophy)
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