Objective
The prevalence of osteoarthritis (OA) varies between joints. Cartilage in eight different joints was evaluated to elucidate the disparate susceptibilities between joints to post-traumatic OA (PTOA) and provide evidence for joint specific clinical treatments. The hypothesis was that cartilage in different joints would have varying cell death and anabolic gene expression profiles after injury.
Methods
Adult equine cartilage explants were harvested from shoulder (SH), elbow (EL), carpal (CA), metacarpophalangeal (MC), patellofemoral (FP), tarsal (TA), metatarsophalangeal (MT), and proximal interphalangeal (PP) joints, and were injured by loading with 30 MPa within 1 second. Fractional dissipated energy, cell density, cell death, and gene expression were quantified.
Results
PP had the highest fractional dissipated energy (94%, 95% confidence interval [CI] 88–101%). Cell density was most dense in superficial zone in all samples, with MC and MT having the highest peak density. Injured samples had significantly higher cell death (13.5%, 95% CI 9.1–17.9%) than non-injured samples (6.8%, 95% CI 2.5–11.1%, p=0.016); however, cell death after injury was not significantly different between joints. Gene expression was significantly different between joints. CD-RAP expression in normal cartilage was lowest in FP (Cp=21, 95% CI −80–122). After injury, the change in CD-RAP expression increased and was highest in FP (147% relative increase after injury, 95% CI 64–213).
Conclusion
Different joints have different baseline characteristics, including cell density and gene expression, and responses to injury, including energy dissipation and gene expression. These unique characteristics may explain differences in OA prevalence and suggest differences in susceptibility to PTOA.
Clinical Relevance
Understanding differences in the response to injury and potential susceptibility of OA can lead to the development of preventative or treatment strategies.