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骨关节炎中关节破坏、疼痛及残疾的机制

Mechanisms of joint destruction, pain and disability in osteoarthritis.

作者信息

Pinals R S

机构信息

UMDNJ-Robert Wood Johnson Medical School, New Brunswick, USA.

出版信息

Drugs. 1996;52 Suppl 3:14-20. doi: 10.2165/00003495-199600523-00004.

DOI:10.2165/00003495-199600523-00004
PMID:8911795
Abstract

Osteoarthritis is characterised by progressive erosion of articular cartilage, and bony overgrowth at the joint margins. Cartilage integrity requires a balance between synthesis and degradation of matrix components, and the latter is augmented in osteoarthritis through the action of chondrocyte-derived metalloproteinases. Synthesis rates also increase but fail to keep pace with the losses. Synovial inflammation, a mild and inconstant feature of osteoarthritis, is more likely to be a consequence of cartilage breakdown than a cause, and its contribution to pain is uncertain. The origins of pain and disability are complex; pathological changes in the joint capsule and periarticular ligaments are a likely source, but nocturnal pain may be related to raised pressure in subchondral bone. In addition to structural damage in the joint, psychosocial factors, muscle weakness, and comorbidities may contribute.

摘要

骨关节炎的特征是关节软骨进行性侵蚀以及关节边缘骨质过度生长。软骨的完整性需要基质成分合成与降解之间保持平衡,而在骨关节炎中,通过软骨细胞衍生的金属蛋白酶的作用,后者会增强。合成速率也会增加,但无法跟上损失的速度。滑膜炎是骨关节炎的一个轻微且不持续的特征,它更可能是软骨破坏的结果而非原因,其对疼痛的影响尚不确定。疼痛和残疾的根源很复杂;关节囊和关节周围韧带的病理变化可能是一个来源,但夜间疼痛可能与软骨下骨压力升高有关。除了关节的结构损伤外,心理社会因素、肌肉无力和合并症也可能起作用。

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