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Articular cartilage synthesis is a complex biological process primarily conducted by chondrocytes to maintain the structural integrity and function of joint surfaces [4, 7, 12]. This anabolic activity involves the production of key extracellular matrix (ECM) components, specifically Type II collagen and aggrecan, which provide the compressive strength and low-friction properties essential for joint mobility [8, 9, 12]. In degenerative diseases such as osteoarthritis, an imbalance between synthesis and catabolic degradation leads to the progressive erosion of cartilage tissue [1, 5, 11]. Therapeutic strategies, categorized as disease-modifying osteoarthritis drugs (DMOADs), aim to stimulate this process through the administration of growth factors like Sprifermin (FGF-18) or Bone Morphogenetic Proteins (BMPs), or by modulating signaling pathways such as Wnt/beta-catenin to favor chondrogenesis [2, 10]. However, achieving effective synthesis remains a significant clinical challenge due to the lack of vasculature in cartilage and the risk of inducing unwanted bone formation or hypertrophic changes [5, 11].
Activation of anabolic signaling pathways, such as the FGFR3 and BMP receptor cascades, and inhibition of catabolic cytokines like IL-1 and TNF-alpha to promote the synthesis of Type II collagen and proteoglycans by chondrocytes [2, 10, 11].
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