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首页> 外文期刊>Osteoarthritis and cartilage >Synovial lining macrophages mediate osteophyte formation during experimental osteoarthritis.
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Synovial lining macrophages mediate osteophyte formation during experimental osteoarthritis.

机译：滑膜衬里巨噬细胞在实验性骨关节炎期间介导骨赘形成。

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OBJECTIVE: In human osteoarthritis (OA), various forms of pathology are observed. Besides cartilage damage and fibrosis, neogenesis of bone, osteophyte formation, also occurs. Osteophytes are thought to limit joint movement and cause pain. The objective of this study was to investigate whether synovial macrophages are involved in osteophyte formation in experimental OA, and if they are, to study which mechanism may be involved. DESIGN: Experimental OA was induced by two intra-articular injections of collagenase on alternate days into murine knee joints. The role of synovial lining macrophages in this model was studied by selective removal of these cells prior to OA induction using clodronate liposomes. After 1 and 2 weeks, knee joints were dissected and examined (immuno)histologically. RESULTS: At days 7 and 14 after induction of OA, osteophyte formation and fibrosis were observed. Depletion of synovial macrophages resulted in spectacular reduction of osteophyte formation, 84% and 66%, respectively, atdays 7 and 14. Fibrosis and synovial activation, measured by MRP8/14 expression, were also ameliorated (40-60%). In addition, production of growth factors (TGFbeta, BMP-2 and BMP-4) in the lining was largely prevented but production of these growth factors in deeper layers of the synovium and the periosteum did not differ from controls. CONCLUSIONS: These results indicate the synovial macrophage to be a pivotal cell in the synovium mediating osteophyte formation and other OA-related pathology, like fibrosis, during experimental OA. Production of growth factors and induction of synovial activation by these cells may play a crucial role in this event.
机译：目的：在人类骨关节炎（OA）中，观察到各种病理形式。除了软骨损伤和纤维化，还发生骨的新生，骨赘形成。人们认为骨赘会限制关节运动并引起疼痛。这项研究的目的是调查滑膜巨噬细胞是否参与实验性OA的骨赘形成，如果涉及，则研究可能涉及的机制。设计：实验性OA是由隔天两次在鼠膝关节内两次注射胶原酶诱导的。通过使用氯膦酸盐脂质体在OA诱导之前选择性去除这些细胞，研究了滑膜衬里巨噬细胞在该模型中的作用。 1和2周后，解剖膝关节并进行组织学检查（免疫）。结果：在诱导OA后的第7和14天，观察到骨赘形成和纤维化。滑膜巨噬细胞的耗竭导致第7天和第14天骨赘形成的明显减少，分别减少了84％和66％，通过MRP8 / 14表达测量的纤维化和滑膜活化也得到了改善（40-60％）。此外，内衬中生长因子（TGFβ，BMP-2和BMP-4）的产生被大大阻止，但滑膜和骨膜较深层中这些生长因子的产生与对照没有区别。结论：这些结果表明滑膜巨噬细胞是滑膜中的关键细胞，在实验性OA中介导骨赘形成和其他与OA有关的病理，例如纤维化。在这些事件中，生长因子的产生和这些细胞对滑膜激活的诱导可能起关键作用。

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