Serum markers of lipid peroxidation, antioxidant enzymatic defense, and collagen degradation in an experimental (Pond-Nuki) canine model of osteoarthritis

Background: Chondrocyte lipid peroxidation is strongly suggested to mediate collagen degradation and thus, to be involved in the pathogenesis of cartilage degradation and osteoarthritis (OA). Objectives: The objective of this study was to evaluate early changes in serum biochemical indicators of oxidative stress during the development of OA in a canine model. Methods: Experimental OA was induced in 7 dogs by transection of the anterior cruciate ligament (Pond-Nuki model). Venous blood samples were obtained prior to the operation and on postoperative days 30, 60, and 105. The activity of serum catalase (an antioxidant enzyme), malondialdehyde (MDA) concentration (a marker of lipid peroxidation), and serum C2C neoepitope concentration (a marker of collagen type II degradation) were measured. Results: A statistically significant increase in all parameters as early as the 30th postoperative day was observed, compared with preoperative values. Serum catalase activity peaked on day 60, whereas MDA and C2C concentrations increased continuously until the end of the experimental period. A significant positive correlation was found between MDA and C2C concentrations, but not between catalase activity and MDA or C2C concentrations. Conclusions: The results support the hypothesis that oxidative stress is involved in the pathogenesis of OA in the dog based on the Pond-Nuki model. The correlation between MDA and C2C concentrations suggests a possible association between oxidative stress and cartilage degeneration.