Fazzalari N L, Vernon-Roberts B, Darracott J
Clin Orthop Relat Res. 1987 Mar(216):224-33.
In contrast to the large volume of data on the cartilage and synovial fluid changes, there has been relatively little investigation of the involvement of bone in the genesis of osteoarthritis (OA). Previous researchers have hypothesized that OA follows stiffening of subchondral bone through trabecular microfractures. Although it is widely recognized that marked changes in the subchondral bone are a consistent feature of advanced OA, the nature of the changes in the bone in OA has not received significant attention. The heads of the femur from 67 patients who had joint replacement for advanced OA and 66 autopsy controls without discernible joint disease were examined microscopically to ascertain the number and distribution of trabecular microfractures in coronal slabs and to quantify the mineralization and thickness of trabecular bone in a principal compressive zone. There was a reduction in the number of trabecular microfractures in OA patients, compared with the controls, with a lack of correlation between numbers of microfractures and age in OA patients. There was no evidence for the hypothesis that increased numbers of microfractures led to the increase of bone to support the view that microfractures play a role in maintaining OA joint structure. Structural changes produced relatively sclerotic and porotic groups of OA and two subgroups of the sclerotic group.
与大量关于软骨和滑液变化的数据形成对比的是，关于骨在骨关节炎（OA）发病机制中的参与情况的研究相对较少。先前的研究人员推测，OA是通过小梁微骨折导致软骨下骨硬化而引发的。尽管人们普遍认识到软骨下骨的显著变化是晚期OA的一个一致特征，但OA中骨变化的本质尚未得到足够的关注。对67例因晚期OA接受关节置换的患者以及66例无明显关节疾病的尸检对照的股骨头部进行显微镜检查，以确定冠状切片中小梁微骨折的数量和分布，并量化主要压缩区小梁骨的矿化程度和厚度。与对照组相比，OA患者的小梁微骨折数量减少，且OA患者中微骨折数量与年龄之间缺乏相关性。没有证据支持微骨折数量增加会导致骨量增加这一假说，以支持微骨折在维持OA关节结构中起作用的观点。结构变化产生了相对硬化和疏松的OA组以及硬化组的两个亚组。
