In conclusion, IL-1beta, and to a lesser extend IL-6, dysregulates enzymatic antioxidant defenses in chondrocyte. These changes could lead to a transient accumulation of H(2)O(2) in mitochondria, and consequently to mitochondria damage. These changes contribute to explain the mitochondrial dysfunction observed in osteoarthritis chondrocytes.

To address the question of whether the increased plasma concentration of interleukin 6 (IL‐6) following strenuous muscular work could be related to exercise‐induced muscle damage, 5 moderately active male volunteers underwent two isokinetic exercise sessions in the eccentric mode, separated by a period of 3 weeks during which the subjects underwent five training sessions. Before training, exercise was followed by severe muscle pain (delayed‐onset muscle soreness; DOMS), and by significant increases in plasma IL‐6 level and serum myoglobin concentration (SMb) (P < 0.001). After training, postexercise DOMS and SMb values were significantly lower than those measured before training. There was no significant difference between plasma IL‐6 levels measured at the same time points before and after training. We conclude that the hypothetical relationship between exercise‐induced muscle damage and increased postexercise levels of circulating IL‐6 is not substantiated by the present results. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 208–212, 1999

The technique Plateltex(®) makes it possible to collect the highest concentration of platelets in the smallest volume available.

Hyaluronic acid and tendon lesions by limited but encouraging short-term clinical results on pain and function. However, controlled randomised studies are still needed.