Abstract

BackgroundThe aim of this study was to investigate the involvement of the nitric oxide (NO) pathway in osteoarthritis (OA).Material/MethodsThe study groups consisted of 32 patients with knee OA and 31 healthy controls. In peripheral venous blood samples (from the OA patients and the controls) and in synovial fluid samples (from the OA patients), the concentrations of L-arginine (ARN), asymmetric dimethylarginine (ADMA), and symmetric dimethylarginine (SDMA) were evaluated. In plasma samples, thiobarbituric acid reactive substances (TBARS) were also measured.ResultsPlasma ARN concentrations were lower in the OA patients than in controls (53.55±16.37 vs. 70.20±25.68 μmol/l) (P<0.05), while plasma ADMA concentrations were similar. Accordingly, the ARN/ADMA ratio was lower in the OA patients than in the control group (80.85±29.58 vs. 110.51±30.48, P<0.05). Plasma SDMA and TBARS concentrations were higher in the OA patients than in controls (0.69±0.15 vs. 0.60±0.10 μmol/l, P<0.05 and 1.21±0.29 vs. 0.55±0.12, respectively) (P<0.001). In the OA patients, ADMA concentrations were significantly higher in the synovial fluid than in plasma (0.75±0.09 vs. 0.69±0.14 μmol/l, P<0.05), as were ARN concentrations (76.96±16.73 vs. 53.55±16.73 μmol/l) (P<0.00001).ConclusionsThese results indicate a poor availability of NO in the synovial fluid of the OA patients, which may contribute to the progression of OA. The decreased ARN/ADMA ratio and the increased SDMA and TBARS in the plasma of the OA patients suggest an impairment of endothelial function in these subjects.

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