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In the search for structure-modifying treatments for osteoarthritis (OA), could the answer lie not in preventing degradation of cartilage, but in stimulating its growth and regeneration? A
proof-of-concept study led by L. Stefan Lohmander at Lund University, Sweden, shows that intra-articular injection of a synthetic form of human fibroblast growth factor 18 (FGF18), known as
sprifermin, could reduce the cartilage loss characteristic of knee OA.
Sprifermin, which signals through FGFR3 receptors in cartilage, had previously been shown in preclinical studies to promote chondrogenesis, cartilage matrix formation and cartilage repair in
vitro, and to slow or protect joint cartilage from destruction in animal models of OA.
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