类风湿关节炎非甾体治疗患者的骨形成减少。
Reduced bone formation in non-steroid treated patients with rheumatoid arthritis.
作者信息
Compston J E, Vedi S, Mellish R W, Croucher P, O'Sullivan M M
机构信息
Department of Pathology, University of Wales College of Medicine, Cardiff.
出版信息
Ann Rheum Dis. 1989 Jun;48(6):483-7. doi: 10.1136/ard.48.6.483.
The cellular basis of trabecular bone loss in rheumatoid arthritis was investigated in 45 non-steroid treated patients. Mean wall thickness, an indicator of the amount of bone formed per remodelling unit, mean interstitial bone thickness, which is related to resorption depth, and the extent of trabecular surface covered by osteoid, which reflects the number of remodelling units, were assessed in iliac crest biopsy specimens. The mean wall thickness was significantly reduced in the patient group when compared with controls matched for age and sex (mean (SD) 39.8 (5.4) v 51.6 (9.7) microns). There was no significant difference between patients and controls in the mean interstitial bone thickness (51.0 (26.4) v 61.4 (31.9) microns) or osteoid surface (16.7 (11.4) v 21.0 (10.5)%). These results show that reduced bone formation at the remodelling unit level is the predominant mechanism of bone loss in rheumatoid arthritis.
在45例未接受类固醇治疗的类风湿关节炎患者中，研究了小梁骨丢失的细胞基础。在髂嵴活检标本中评估了平均壁厚度（每个重塑单元形成的骨量指标）、平均间质骨厚度（与吸收深度相关）以及类骨质覆盖的小梁表面范围（反映重塑单元数量）。与年龄和性别匹配的对照组相比，患者组的平均壁厚度显著降低（均值（标准差）39.8（5.4）微米对51.6（9.7）微米）。患者与对照组在平均间质骨厚度（51.0（26.4）微米对61.4（31.9）微米）或类骨质表面（16.7（11.4）%对21.0（10.5）%）方面无显著差异。这些结果表明，重塑单元水平的骨形成减少是类风湿关节炎骨丢失的主要机制。
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