Cameron M, Buchgraber A, Passler H, Vogt M, Thonar E, Fu F, Evans C H
Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pennsylvania, USA.
Am J Sports Med. 1997 Nov-Dec;25(6):751-4. doi: 10.1177/036354659702500605.
Restoring knee stability through reconstruction, while providing symptomatic relief, has not been shown to decrease the incidence of degenerative changes after rupture of the anterior cruciate ligament. This suggests that posttraumatic osteoarthritis may not be purely biomechanical in origin, but also biochemical. To test this, we measured the levels of seven cytokine modulators of cartilage metabolism in knee joint synovial fluid after anterior cruciate ligament rupture. We also measured keratan sulfate, a product of articular cartilage catabolism. The sample population consisted of patients with uninjured knee joints (N = 10), and patients with acute (N = 60), subacute (N = 18), and chronic (N = 8) anterior cruciate ligament-deficient knees. Synovial fluid samples were analyzed by enzyme-linked immunosorbent assays. Normal synovial fluids contained high levels of the interleukin-1 receptor antagonist but low concentrations of other cytokines. Immediately after ligament rupture there were large increases in interleukins 6 and 8, tumor necrosis factor alpha, and keratan sulfate. Interleukin-1 levels remained low throughout the course. As the injury became subacute and then chronic, interleukin-6, tumor necrosis factor-alpha, and keratan sulfate levels fell but remained considerably elevated 3 months after injury. Concentrations of interleukin-1Ra fell dramatically. Granulocyte-macrophage colony-stimulating factor concentrations were normal acutely and subacutely but by 3 months after injury were elevated 10-fold. Our data reveal a persistent and evolving disturbance in cytokine and keratan sulfate profiles within the anterior cruciate ligament-deficient knee, suggesting an important biochemical dimension to the development of osteoarthritis there.
通过重建恢复膝关节稳定性，同时缓解症状，但尚未证明其能降低前交叉韧带断裂后退行性改变的发生率。这表明创伤后骨关节炎可能并非单纯起源于生物力学因素，还涉及生物化学因素。为验证这一点，我们测量了前交叉韧带断裂后膝关节滑液中七种软骨代谢细胞因子调节剂的水平。我们还测量了硫酸角质素，它是关节软骨分解代谢的产物。样本群体包括膝关节未受伤的患者（N = 10），以及患有急性（N = 60）、亚急性（N = 18）和慢性（N = 8）前交叉韧带损伤膝关节的患者。通过酶联免疫吸附测定法分析滑液样本。正常滑液中白细胞介素-1受体拮抗剂水平较高，但其他细胞因子浓度较低。韧带断裂后立即出现白细胞介素6和8、肿瘤坏死因子α以及硫酸角质素大幅升高。白细胞介素-1水平在整个过程中保持较低。随着损伤变为亚急性然后慢性，白细胞介素-6、肿瘤坏死因子α和硫酸角质素水平下降，但在损伤后3个月仍显著升高。白细胞介素-1Ra浓度急剧下降。粒细胞巨噬细胞集落刺激因子浓度在急性和亚急性期正常，但在损伤后3个月升高了10倍。我们的数据揭示了前交叉韧带损伤膝关节中细胞因子和硫酸角质素谱的持续且不断演变的紊乱，表明骨关节炎发展存在重要的生物化学层面因素。
