[HTML][HTML] Fibroblast growth factor-18 stimulates chondrogenesis and cartilage repair in a rat model of injury-induced osteoarthritis
EE Moore, AM Bendele, DL Thompson, A Littau… - Osteoarthritis and …, 2005 - Elsevier
EE Moore, AM Bendele, DL Thompson, A Littau, KS Waggie, B Reardon, JL Ellsworth
Osteoarthritis and cartilage, 2005•ElsevierOBJECTIVE: Osteoarthritis (OA) is the most common form of arthritis and a primary cause of
disability, however, there are no treatments that can slow disease progression or repair
damaged joint cartilage. Fibroblast growth factor-18 (FGF18) has been reported to have
significant anabolic effects on cartilage. We therefore examined its effects on repair of
cartilage damage in a rat meniscal tear model of OA. DESIGN: Surgical damage to the
meniscus in rats leads to joint instability and significant damage to the articular cartilage at 3 …
disability, however, there are no treatments that can slow disease progression or repair
damaged joint cartilage. Fibroblast growth factor-18 (FGF18) has been reported to have
significant anabolic effects on cartilage. We therefore examined its effects on repair of
cartilage damage in a rat meniscal tear model of OA. DESIGN: Surgical damage to the
meniscus in rats leads to joint instability and significant damage to the articular cartilage at 3 …
OBJECTIVE
Osteoarthritis (OA) is the most common form of arthritis and a primary cause of disability, however, there are no treatments that can slow disease progression or repair damaged joint cartilage. Fibroblast growth factor-18 (FGF18) has been reported to have significant anabolic effects on cartilage. We therefore examined its effects on repair of cartilage damage in a rat meniscal tear model of OA.
DESIGN
Surgical damage to the meniscus in rats leads to joint instability and significant damage to the articular cartilage at 3 weeks post-surgery. At this time, animals received bi-weekly intra-articular injections of FGF18 for 3 weeks, and the knee joints were then harvested for histologic examination.
RESULTS
FGF18-induced dose-dependent increases in cartilage thickness of the tibial plateau, due to new cartilage formation at the articular surface and the joint periphery. The generation of new cartilage resulted in significant reductions in cartilage degeneration scores. The highest dose of FGF18 also induced an increase in chondrophyte size and increased remodeling of the subchondral bone.
CONCLUSIONS
The results of this study demonstrate that FGF18 can stimulate repair of damaged cartilage in a setting of rapidly progressive OA in rats.
Elsevier