Kobayashi S
Nihon Seikeigeka Gakkai Zasshi. 1982 Aug;56(8):727-38.
A qualitative and quantitative histological study of the proximal tibial condyles was performed to elucidate the features of the bone atrophy in rheumatoid arthritis. Undecalcified, methyl-methacrylate embedded sections were prepared from 21 cases of rheumatoid arthritis, 3 cases of osteoarthritis and 3 cases of non-arthritic subjects. The rheumatoid bone marrow was classified into three layers according to its morphological features. The first layer was pannus, the second was fibrofatty bone marrow and the third was fatty bone marrow. This third layer was used for this study. The characteristic finding in the rheumatoid bone marrow was their inflammatory changes observed in arterioles and venulocapillary beds. The trabecular bones were sparse and thin, and resorption surfaces associated with osteoclasts were increased, whereas osteoblastic activity on osteoid surfaces seemed to be inhibited. These findings may have consequently resulted from the inflammatory changes of vessels around the trabeculae. Inflammatory exudates from venulocapillary beds may stimulate the production of osteoclasts, while stenotic vascular change caused by arteriolitis may reduce the intramedullary blood flow, so that inhibition of osteoblastic activity and retardation of mineralizing process at osteoid surfaces may occur in rheumatoid bone.
对胫骨近端髁进行了定性和定量组织学研究,以阐明类风湿性关节炎中骨萎缩的特征。从21例类风湿性关节炎、3例骨关节炎和3例非关节炎受试者中制备了未脱钙、甲基丙烯酸甲酯包埋的切片。类风湿性骨髓根据其形态学特征分为三层。第一层是血管翳,第二层是纤维脂肪骨髓,第三层是脂肪骨髓。本研究使用的是第三层。类风湿性骨髓的特征性发现是在小动脉和微静脉毛细血管床中观察到的炎症变化。小梁骨稀疏且薄,与破骨细胞相关的吸收表面增加,而类骨质表面的成骨细胞活性似乎受到抑制。这些发现可能是由于小梁周围血管的炎症变化所致。微静脉毛细血管床的炎性渗出物可能刺激破骨细胞的产生,而小动脉炎引起的血管狭窄变化可能会减少骨髓内血流,从而导致类风湿性骨中类骨质表面的成骨细胞活性受到抑制,矿化过程延迟。