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我们能否阻止强直性脊柱炎的进展?

Can we stop progression of ankylosing spondylitis?

机构信息

Department of Internal Medicine 3, University of Erlangen-Nuremberg, Krankenhausstrasse 12, D-91054 Erlangen, Germany.

出版信息

Best Pract Res Clin Rheumatol. 2010 Jun;24(3):363-71. doi: 10.1016/j.berh.2010.01.005.

DOI:10.1016/j.berh.2010.01.005
PMID:20534370
Abstract

Ankylosing spondylitis is characterised by inflammation of the spine and the entheses followed by bone formation. Excessive bone formation in ankylosing spondylitis leads to the formation of bone spurs, such as syndesmophytes and enthesiophytes, which contribute to ankylosis of joints and poor physical function. This process is based on increased differentiation of osteoblasts from their mesenchymal precursors, which allows to rapidly build up new bone. Prostaglandins, bone morphogenic proteins and Wnt proteins play an essential role in this process. By contrast, tumour necrosis factor (TNF) does not appear to be the direct trigger for osteophyte formation in ankylosing spondylitis. The article reviews the current knowledge regarding the mechanisms and clinical role of ankylosis and explains strategies on how to prevent it in patients with ankylosing spondylitis.

摘要

强直性脊柱炎的特征是脊柱和附着点炎症,随后发生骨形成。强直性脊柱炎中过度的骨形成导致骨赘的形成,如骨桥和肌腱骨赘,这导致关节强直和身体功能不佳。这个过程是基于成骨细胞从间充质前体的过度分化,这使得快速构建新骨成为可能。前列腺素、骨形态发生蛋白和 Wnt 蛋白在这个过程中起着至关重要的作用。相比之下,肿瘤坏死因子 (TNF) 似乎不是强直性脊柱炎中骨赘形成的直接触发因素。本文综述了关于强直性脊柱炎的融合机制和临床作用的现有知识,并解释了如何在强直性脊柱炎患者中预防融合的策略。

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