A hypothesis for the mode of action of anti-rheumatic drugs in a model of cartilage destruction

Abstract

Abstract We have been using as a model rats and mice with air pouches which develop lining cells closely resembling synovium (Edwards et al 1982; Sedgwick et al 1983). These pouches when sufficiently mature, i.e. 6 days, will respond to a variety of stimuli both immune and non-immune with long lasting exudates containing many migrated leucocytes (Sedgwick et al 1983, 1984a). We examined the breakdown of cartilage in both inflamed and non-inflamed pouches and have found that inflammation protected the rate of loss of proteoglycan from cartilage (Sedgwick et al 1984b. 1985; Willoughby et al 1985). Invariably the cartilage in the inflamed air pouch would float free in exudate while cartilage, in the non-inflamed pouch would adhere to the pouch wall in close proximity to the macrophages and fibroblasts of the lining cells. Unpublished findings from this department (de Brito) have shown that the presence of granulation tissue in close proximity to cartilage will speed proteoglycan loss.