Cooke T D
Clin Rheum Dis. 1985 Aug;11(2):203-38.
This communication has attempted to review causal processes in polyarticular osteoarthritis (poly-OA). Since mechanical features are an almost constant feature of OA joint deterioration, their interplay, both in static and dynamic form, has been stressed. Age-related polyarticular cartilage softening is expounded as an example of degeneration and atrophy--a process not to be confused with OA which is considered as an age-accelerated disorder. I have stressed the influence of genetic factors, best exemplified as a single gene aberration in the occurrence of Heberden's nodes, while a polygenetic interplay may be involved in other forms of hand GOA. These features may predispose an individual to polyarthropathy. The mechanisms by which such genetic factors promote such changes are unknown but attention is drawn to the lack of symptoms in osteoarthritic joints of many if not most poly-OA cases. This occurrence could represent a relative lack of normal proprioceptive feedback or an unusual tolerance to pain. Genetically determined influences marked by the occurrence of hand OA predispose mechanically deranged joints in that individual to deteriorate more rapidly. Mechanically abnormal joints do not inevitably deteriorate, but, in combination with other local and/or systemic factors (genetic, metabolic, hormonal or immune) may undergo accelerated degeneration to which process each additional factor may contribute. Thus in genetically predisposed poly-OA hand cases, local deformity combined with crystal deposition and laxity may provoke dramatic destruction and subluxation. Since mechanical features attend almost all OA joint disease, attention is drawn to a poorly recognized malformation of the knee denoted as dysplasia. Such deformities, well recognized at the hip and shoulder, could occur at other sites in which OA is commonly seen (i.e. DIP joints). Immune-complex deposition probably occurs from time to time in GOA joints. Such events may be associated with local inflammation and aggravate the degradation of cartilage. The available data indicate distinctive differences in the nature and form of such immunopathology to RA in which disease immune-complex deposition in cartilage may play an integral role in tissue destruction and chronic inflammation.
本交流试图回顾多关节骨关节炎（多关节OA）的病因过程。由于机械特征几乎是OA关节退变的一个恒定特征，因此强调了它们在静态和动态形式下的相互作用。与年龄相关的多关节软骨软化被阐述为退变和萎缩的一个例子——这一过程不应与被视为年龄加速性疾病的OA相混淆。我强调了遗传因素的影响，最典型的例子是在赫伯登结节发生时的单基因畸变，而多基因相互作用可能参与其他形式的手部原发性OA。这些特征可能使个体易患多关节病。此类遗传因素促进这些变化的机制尚不清楚，但值得注意的是，许多（如果不是大多数）多关节OA病例的骨关节炎关节缺乏症状。这种情况可能代表正常本体感觉反馈相对缺乏或对疼痛的异常耐受。由手部OA的发生所标志的遗传决定的影响使该个体中机械性紊乱的关节更迅速地退变。机械性异常的关节并非不可避免地退变，但与其他局部和/或全身因素（遗传、代谢、激素或免疫）结合，可能会加速退变，每个额外因素都可能促成这一过程。因此，在遗传易感性多关节OA手部病例中，局部畸形与晶体沉积和松弛相结合，可能引发严重破坏和半脱位。由于机械特征几乎见于所有OA关节疾病，因此提请注意一种未得到充分认识的膝关节畸形，即发育异常。这种畸形在髋关节和肩关节很常见，也可能发生在其他常见OA的部位（如远端指间关节）。免疫复合物沉积可能不时发生在原发性OA关节中。此类事件可能与局部炎症相关，并加重软骨降解。现有数据表明，这种免疫病理学在性质和形式上与类风湿关节炎有明显差异，在类风湿关节炎中，疾病免疫复合物在软骨中的沉积可能在组织破坏和慢性炎症中起重要作用。
