British Journal of Rheumatology 1988;27(suppl II): 116-119 PATHOPHYSIOLOGY OF CHRONIC SYNOVITIS

IT is now clear that rheumatoid arthritis ' describes a heterogeneous group of processes which lead to widespread chronic synovitis. Even within the most homogeneous group of classical cases, causality is multifactorial, with genetic, environmental and stochastic elements, each varying from person to person. It is possible that we may find an environmental agent which is necessary to the development of chronic widespread syovitis, and which can be removed without injuring health in some other way. However, it seems more likely that a wide range of endemic agents plays a part. As a clinician, I would suggest that, inasmuch as RA ' is an entity, this entity is not based on cause, but on an aspect of the consequent process which leads to a similar pattern of widespread synovitis Like an error message in a computer programme, it gives the same response to hundreds of different stimuli. In order to understand this error message we need to know why synovium acts as a target in patients with certain, as yet poorly characterized, types of immune disturbance [I] A number of explanations have been put forward. Synovial antigens have been looked for. with little success. Cartilage specific antigens exist, but their implication in tendon and bursal disease poses difficulties. Blake has championed free radicals in synovium, generated either with the help of free iron or reperfusion injury. Mast cell products, which may be released during movement, have bee