Pathogenetic mechanisms in polyarticular osteoarthritis.

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.