OBJECTIVE: Resistin is a secreted factor that is elevated in rheumatoid 
arthritis (RA) and believed to drive joint inflammation in vivo. This study was 
undertaken to determine if resistin is present in the joint following joint 
injury and to elucidate the role of resistin in cartilage degradation.
METHODS: The level of resistin was measured in paired synovial fluid (SF) and 
serum samples from patients following joint injury (anterior cruciate ligament, 
ACL or meniscus tear). Localization of resistin was visualized by 
immunohistochemistry of synovial tissue and cartilage from healthy and OA 
donors. Mouse and human cartilage cultures were used to assess the effect of 
resistin on cartilage metabolism.
RESULTS: In trauma patients, resistin levels declined with increasing time post 
injury. The resistin levels were highest in samples collected up to 1 week 
following traumatic injury (SF: 2980 pg/ml, serum: 7901 pg/ml) and lowest in 
samples collected 6-26 years post injury (SF: 686 pg/ml, serum: 5682 pg/ml). 
Resistin was shown to be expressed in macrophage-like cells in both healthy and 
OA synovial tissue. Treatment of mouse cartilage cultures with recombinant 
resistin led to a dose dependent loss of proteoglycan and induction of 
inflammatory cytokine and PGE(2) production. Recombinant resistin inhibited 
proteoglycan synthesis in human cartilage explants.
CONCLUSION: Resistin is elevated both systemically and locally in the weeks 
immediately following joint injury and has a direct effect on cartilage matrix 
turnover and cytokine production. Resistin may play a role in the early stages 
of trauma-induced OA and may represent a new therapeutic target to slow joint 
destruction in OA.