ABSTRACT
This chapter deals with the mechanisms by which iron- catalyzed oxygen radical reactions may play a role in the pathogenesis of rheumatoid synovitis. The peripheral synovial joint is unique in being a mobile organ, subjected to substantial intra-articular pressure (IAP) fluxes once inflamed. The synovium, though in health a simple structure and relatively acellular, is rapidly populated with cells of the inflammatory response, becoming much thickened and prone to microbleeding, a process leading to intracellular ferritin production and iron deposition. The iron was usually deposited in siderosomes in type B synovial cells, which were the predominant cell type; and no tissue damage was observed in the vicinity of these iron-rich siderosomes. Several physiological features present within the inflamed human joint suggest that movement will provide the potential environment for hypoxic- reperfusion injury. The chapter discusses the use of an iron chelator, desferrioxamine, in an attempt to suppress iron-promoted oxygen injury.
