An imbalance between haemostasia and fibrinolysis, and subsequent fibrin generation within the rheumatoid joint could have a role in disease perpetuation.
To study fibrin formation at the synovial space in a model of rheumatoid arthritis, and its possible role in activating the synovial cells from inside of the cavity.
Antigen arthritis was induced by injecting ovalbumin into rabbits' knees. We looked for the appearance of fibrin in the effusion and at the inflamed tisues with immunohistochemistry, in a sequential fashion (from 24 hour to 1 week after disease induction). Morphologic changes at the intimal synovial surface in contact with fibrin matrices were studied over a long period of time by several qualitative variables. Analysis of the variables was carried out with Kruskall Wallis and Mann Whitney nonparametric tests, and linear regression was performed using the least squares method.
Fibrin aggregates appeared from the initial stages of the disease at the synovial effusion. Later on, they were localised on the synovial surface. Differentiation of the aggregates from the underlying synovial tissue was easy at the beginning, but then progressive changes were noted at the fibrin-tissue interface, ending with the invasion of the aggregates by synovial cells and their incorporation into the tissue. The process involved cross-linking of fibrin matrices with fibronectin, and synoviocyte proliferation and migration.
Fibrin aggregates generated inside the joint cavity may constitute a source of activation and acquisition of invasiveness of synovial fibroblasts, a process to explore between the perpetuating mechanisms of rheumatoid arthritis.