首页> 外文期刊>Annals of the Rheumatic Diseases: A Journal of Clinical Rheumatology and Connective Tissue Research >Repair of bone erosions in rheumatoid arthritis treated with tumour necrosis factor inhibitors is based on bone apposition at the base of the erosion
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Repair of bone erosions in rheumatoid arthritis treated with tumour necrosis factor inhibitors is based on bone apposition at the base of the erosion

机译:用肿瘤坏死因子抑制剂治疗的类风湿关节炎的骨侵蚀修复是基于骨侵蚀的基础

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Objectives: To investigate whether bone erosions in patients with rheumatoid arthritis (RA) show evidence of repair. Methods: 127 erosions were identified in metacarpophalangeal joints 2-4 of the right hands of 30 RA patients treated with tumour necrosis factor inhibitors (TNFi) and 21 sex, age and disease activity-matched patients treated with methotrexate. All erosions were assessed for their exact maximal width and depth by high-resolution μCT imaging at baseline and after 1 year. Results: All erosions detected at baseline could be visualised at follow-up after 1 year. At baseline, the mean width of bone erosions in the TNFi group was 2.0 mm;their mean depth was 2.3 mm, which was not significantly different from the methotrexate-treated group (width 2.4 mm;depth 2.4 mm). Mean depth of erosions significantly decreased after 1 year of treatment with TNFi (-0.1 mm; p=0.016), whereas their width remained unchanged. In contrast, mean depth and width of erosive lesions increased in the methotrexate-treated group. The reduction in the depth of lesions was confined to erosions showing evidence of sclerosis at the base of the lesion. Moreover, deeper lesions in the TNFi group were particularly prone to repair (-0.4 mm;p=0.02) compared with more shallow lesions. Conclusions: Bone erosions in RA patients treated with TNFi show evidence of limited repair in contrast to bone erosions in patients treated with methotrexate. Repair is associated with a decrease in the depth of lesions and sclerosis at the bases of the lesions. Repair thus emerges from the endosteal rather than periosteal bone compartment and probably involves the bone marrow.
机译:目的:探讨类风湿关节炎(RA)患者的骨侵蚀是否显示出修复的证据。方法:在30例接受肿瘤坏死因子抑制剂(TNFi)治疗的RA患者和21例性别,年龄和疾病活动相匹配的甲氨蝶呤患者的右手掌指关节2-4处发现127处糜烂。在基线和1年后通过高分辨率μCT成像评估所有侵蚀的确切最大宽度和深度。结果:在一年后的随访中可以看到在基线处检测到的所有侵蚀。基线时,TNFi组的骨侵蚀平均宽度为2.0毫米;平均深度为2.3毫米,与甲氨蝶呤治疗组(宽度为2.4毫米;深度为2.4毫米)无显着差异。用TNFi治疗1年后,平均侵蚀深度显着降低(-0.1 mm; p = 0.016),而其宽度保持不变。相反,甲氨蝶呤治疗组的糜烂病变的平均深度和宽度增加。病变深度的减少仅限于糜烂,显示病变底部硬化的迹象。此外,与较浅的病变相比,TNFi组中较深的病变尤其易于修复(-0.4 mm; p = 0.02)。结论:与甲氨蝶呤治疗的患者相比,接受TNFi治疗的RA患者的骨侵蚀显示出修复受限的证据。修复与病变深度的减少和病变底部的硬化有关。因此,修复从骨内膜而不是骨膜骨腔开始,并且可能涉及骨髓。

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