Westacott C I, Sharif M
Department of Pathology and Microbiology, University of Bristol, UK.
Semin Arthritis Rheum. 1996 Feb;25(4):254-72. doi: 10.1016/s0049-0172(96)80036-9.
The integrity of articular cartilage is maintained by the balance between cytokine-driven anabolic and catabolic processes. Unregulated or excess influences of these molecules are thought to play a part in the pathophysiology of many joint diseases. However, the role of cytokines in osteoarthritis (OA) is not well established. Our aims are twofold: firstly to consider the evidence for the contribution of cytokines to the pathophysiology of OA and secondly to evaluate their potential as markers of disease activity in OA.
Cytokine homeostasis, the role of catabolic and anabolic cytokines in maintaining cartilage integrity, and the contribution of such cytokines to destructive processes in OA were examined. Consideration was given to the interrelationship between cartilage, bone, and synovium in OA; metabolites produced by such structures were compared with cytokines as indicators of disease activity.
The evidence reviewed suggests that interleukin-1 (IL-1) and the less potent tumor necrosis factor alpha (TNF alpha) are mediators of joint damage in OA. The cytokines interleukin-6 (IL-6) and leukemia inhibitory factor (LIF) were implicted in both destructive and protective mechanisms, suggesting a dual role. Metabolites of the different components of the joint provided a better measure of disease activity than cytokines.
Experimental evidence is emerging that catabolic cytokines are mediators of joint damage in OA, although their usefulness as markers of disease activity is limited because of the need to monitor a wide range of ligands and their inhibitors simultaneously. In contrast, metabolites released from cells within bone, synovium, and cartilage related to disease activity and provided prognostic information.
细胞因子驱动的合成代谢和分解代谢过程之间的平衡维持着关节软骨的完整性。这些分子不受调控或过度的影响被认为在许多关节疾病的病理生理学中起作用。然而，细胞因子在骨关节炎（OA）中的作用尚未完全明确。我们的目标有两个：首先，考量细胞因子对OA病理生理学作用的证据；其次，评估它们作为OA疾病活动标志物的潜力。
研究细胞因子的稳态、分解代谢和合成代谢细胞因子在维持软骨完整性中的作用，以及这些细胞因子对OA破坏过程的作用。考量OA中软骨、骨和滑膜之间的相互关系；将这些结构产生的代谢产物与作为疾病活动指标的细胞因子进行比较。
综述的证据表明，白细胞介素-1（IL-1）和活性较弱的肿瘤坏死因子α（TNFα）是OA关节损伤的介质。细胞因子白细胞介素-6（IL-6）和白血病抑制因子（LIF）在破坏和保护机制中均有涉及，表明具有双重作用。关节不同成分的代谢产物比细胞因子能更好地衡量疾病活动。
越来越多的实验证据表明，分解代谢细胞因子是OA关节损伤的介质，尽管由于需要同时监测多种配体及其抑制剂，它们作为疾病活动标志物的作用有限。相比之下，从骨、滑膜和软骨中的细胞释放的代谢产物与疾病活动相关，并提供预后信息。
