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骨关节炎为何会引起疼痛?局部和中枢疼痛处理的证据。

What makes osteoarthritis painful? The evidence for local and central pain processing.

机构信息

Department of Biomedical Sciences, St George's University of London, London, UK.

出版信息

Rheumatology (Oxford). 2011 Dec;50(12):2157-65. doi: 10.1093/rheumatology/ker283. Epub 2011 Sep 27.

DOI:10.1093/rheumatology/ker283
PMID:21954151
Abstract

OA is a chronic arthritic disease characterized by pain, local tissue damage and attempts at tissue repair. Historically, cartilage damage was believed to be the hallmark of OA. However, since cartilage is an avascular, aneural tissue, the mechanisms of pain are likely to be complex and influenced by non-cartilaginous structures in the joint including the synovium, bone and soft tissue. Imaging studies reveal the presence of synovitis and bone marrow lesions that may mediate pain. The presence of local joint inflammation and altered cartilage and bone turnover in OA implicates a potential role for a range of molecular mediators in OA pain. Mechanisms of pain perception may include the activation and release of local pro-inflammatory mediators such as prostaglandins and cytokines accompanied by the destruction of tissue, which is mediated by proteases. However, clinically, there is often disparity between the degree of pain perception and the extent of joint changes in subjects with OA. Such observations have prompted work to investigate the mechanisms of central pain perception in OA. Functional MRI has identified multiple areas of the brain that are involved in OA pain processing. These data demonstrate that pain perception in OA is complex in being influenced by local factors and activation of central pain-processing pathways. In this review, we will discuss current concepts underlying the pathophysiology of pain perception in OA and suggest possible directions for the future management of pain in this condition based on recent clinical studies.

摘要

OA 是一种慢性关节炎疾病,其特征为疼痛、局部组织损伤和组织修复尝试。历史上,软骨损伤被认为是 OA 的标志。然而,由于软骨是一种无血管、无神经的组织,疼痛的机制可能很复杂,并受到关节中非软骨结构的影响,包括滑膜、骨骼和软组织。影像学研究显示存在滑膜炎和骨髓病变,这些可能介导疼痛。OA 中存在局部关节炎症和软骨及骨代谢改变,表明一系列分子介质在 OA 疼痛中可能发挥作用。疼痛感知机制可能包括局部促炎介质(如前列腺素和细胞因子)的激活和释放,同时伴随着组织破坏,这由蛋白酶介导。然而,临床上,OA 患者的疼痛感知程度与关节变化程度之间常常存在差异。这些观察结果促使人们研究 OA 中中枢疼痛感知的机制。功能性 MRI 已经确定了大脑中多个参与 OA 疼痛处理的区域。这些数据表明,OA 中的疼痛感知很复杂,受到局部因素和中枢疼痛处理途径激活的影响。在这篇综述中,我们将讨论 OA 中疼痛感知的病理生理学的现有概念,并根据最近的临床研究,为该疾病的疼痛管理提出可能的方向。

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