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Articular cartilage is a specialized hyaline cartilage that covers the articulating surfaces of bones within synovial joints, serving to provide a smooth, lubricated surface for low-friction movement and to distribute mechanical loads [1]. It is characterized by an extensive extracellular matrix (ECM) composed primarily of type II collagen and aggrecan, which is maintained by a sparse population of chondrocytes [2]. The tissue is unique in that it is avascular, aneural, and alymphatic, which significantly limits its capacity for spontaneous repair and complicates drug delivery [1, 4]. In degenerative conditions such as osteoarthritis, the structural integrity of the cartilage is compromised by an imbalance between anabolic and catabolic processes, leading to pain and functional impairment [3]. Therapeutic strategies targeting articular cartilage aim to either provide symptomatic relief through mechanical lubrication (viscosupplementation) or modify the disease course by stimulating chondrocyte activity and inhibiting matrix-degrading enzymes [4]. Current research focuses on overcoming the physiological barriers of the tissue to ensure sustained drug presence and effective penetration into the dense matrix [4].
Therapeutic approaches involve viscosupplementation to restore mechanical lubrication, anabolic stimulation of chondrocytes via growth factor pathways (e.g., FGF18), and inhibition of catabolic enzymes or inflammatory signaling to preserve the extracellular matrix [4].
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