ABSTRACT
Rheumatoid arthritis is a chronic inflammatory disease, some characteristic features of which are inflammation within the joints, the proliferation of synovial tissue adjacent to cartilage/bone, and the proteinase-mediated destruction of cartilage/bone at these sites. In several senses the redox-related biochemistry within the rheumatoid joint is paradoxical. Within the synovial tissue, a reducing environment exists. For example, the ratio of protein -SH to -S-S-is increased compared with control synovium (1). Measurements of pO2 a nd pH within both synovial fluid and synovial tissue from rheumatoid joints are consistent with a state of chronic hypoxia and acidosis (2,3) (G.A. Ellis, S.E. Edmonds and D.R. Blake, unpublished data). Yet within the synovial fluid of the knee joint space there is evidence of oxidizing conditions, such as a decreased ratio of ascorbate to dehydroascorbate (4) and increased concentrations of markers of free radical damage to lipids and proteins. In an additional paradox, iron-loaded ferritin accumulates within the macrophage-like cells of the inflamed tissue (5), while high concentrations of ferritin molecules within the adjacent synovial fluid have low iron loading (6).
