A histochemical study on leucinoaminopeptidase activity in the synovial membrane of patients with rheumatoid arthritis.

A joint affected with rheumatoid arthritis undergoes a number of pathological changes. The synovial membrane proliferates and begins to show round cell infiltration. Degenerative and proliferative changes are encountered in the arterioles and venules of the synovial membrane. Local necroses occur here and there in the tissue. The articular cartilage becomes thinner and spots of erosion appear in it, frequently extending up to the bone. A fluid is secreted into the joint, which differs in composition from normal synovial fluid. Since such great morphological changes are seen in the joint, it may be expected that pathological changes also occur in the metabolism of the articular tissue. It has been shown that the presence of rheumatoid disease in the synovial membrane is accompanied by a very considerable increase in oxidative metabolism (Dingle and Thomas, 1956). Synthesis of synovial mucin takes place in the lining cell tissue of both normal and rheumatoid synovial membranes (Lever and Ford, 1958). Histochemical methods have been used to demonstrate several different enzymes in the hypertrophic lining cell tissue of patients with rheumatoid arthritis. Of the glycolytic enzymes, lactico-dehydrogenase-DPNHdiaphorase has been demonstrated; of the electron transport system, DPNH diaphorase; and of the Krebs tricarboxylic acid cycle, succinic dehydrogenase (Hamerman and Blum, 1959). Cartilage erosion in rheumatoid arthritis usually first occurs at the point where the joint capsule is attached to the cartilage and pannus tissue grows over the articular surface ("chewing of cartilage"). It has been thought that enzymes secreted by the synovial pannus tissue are responsible for this cartilage degeneration (Bollet, 1963). A chondromucoprotein complex occurs in the cartilage tissue. If the cartilage is subjected to