Moskowitz R W, Goldberg V M
J Rheumatol. 1987 May;14 Spec No:116-8.
Osteophytes are considered characteristic manifestations of osteoarthritis (OA) but may be seen independent of structural cartilage erosive lesions. Etiopathogenic mechanisms for osteophyte formation may involve responses to synovial inflammation, stretching of the synovial membrane, general mechanical instability, and vascular metaplasia. Experimentally induced OA following partial menisectomy in rabbits demonstrates active cellular replication at the normal joint periphery. Vascular responses are seen late in parallel with osteophyte formation rather than preceding it. Osteophyte ossification is primarily endochondral. The parallel stimulatory response to perichondrium, cartilage, and bone allows speculation on the interplay of mechanical/electrical forces and chemical/hormonal transducers in the development of osteophytes.
骨赘被认为是骨关节炎（OA）的特征性表现，但也可能在无结构性软骨侵蚀性病变的情况下出现。骨赘形成的病因发病机制可能涉及对滑膜炎症的反应、滑膜膜的拉伸、一般机械不稳定以及血管化生。在兔子身上进行部分半月板切除术后实验性诱导的OA显示，在正常关节周边有活跃的细胞复制。血管反应在骨赘形成后期出现，而不是先于骨赘形成。骨赘骨化主要是软骨内骨化。对骨膜、软骨和骨骼的平行刺激反应使人推测在骨赘形成过程中机械/电力量与化学/激素转导因子之间的相互作用。
