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什么导致了骨关节炎?——滑膜与软骨下骨病理学。

What drives osteoarthritis?-synovial versus subchondral bone pathology.

机构信息

Osteoarthritis Research Center Basel.

Department of Rheumatology.

出版信息

Rheumatology (Oxford). 2017 Sep 1;56(9):1461-1471. doi: 10.1093/rheumatology/kew389.

Abstract

Subchondral bone and the synovium play an important role in the initiation and progression of OA. MRI often permits an early detection of synovial hypertrophy and bone marrow lesions, both of which can precede cartilage damage. Newer imaging modalities including CT osteoabsorptiometry and hybrid SPECT-CT have underlined the importance of bone in OA pathogenesis. The subchondral bone in OA undergoes an uncoupled remodelling process, which is notably characterized by macrophage infiltration and osteoclast formation. Concomitant increased osteoblast activity leads to spatial remineralization and osteosclerosis in end-stage disease. A plethora of metabolic and mechanical factors can lead to synovitis in OA. Synovial tissue is highly vascularized and thus exposed to systemic influences such as hypercholesterolaemia or low grade inflammation. This review aims to describe the current understanding of synovitis and subchondral bone pathology and their connection in OA.

摘要

软骨下骨和滑膜在 OA 的发生和进展中起着重要作用。MRI 通常可以早期发现滑膜肥大和骨髓病变,这两者都可能先于软骨损伤。包括 CT 骨吸收测量和混合 SPECT-CT 在内的新成像方式强调了骨在 OA 发病机制中的重要性。OA 中的软骨下骨经历了一种脱耦联的重塑过程,其特征是巨噬细胞浸润和破骨细胞形成。同时增加的成骨细胞活性导致终末期疾病中的空间再矿化和骨质硬化。大量代谢和机械因素可导致 OA 中的滑膜炎。滑膜组织高度血管化,因此易受全身性影响,如高胆固醇血症或低度炎症。本综述旨在描述对 OA 中滑膜炎和软骨下骨病理学及其联系的当前认识。

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