Transport of intravenously-injected ferritin across the guinea-pig synovium.

Immune complexes have been found in the synovial fluid (Rawson, Abelson, and Hollander, 1965) and synovium (Kinsella, Baum, and Ziff, 1970) of patients with rheumatoid arthritis. They have also been discovered in the blood in cases of the same disease (Kunkel, Miiller-Eberhard, Fudenberg, and Tomasi, 1961) and their presence has lead to speculation on their role in the aetiology of rheumatoid disease. It is known that in conditions such as HenochSch6nlein purpura, in which circulating immune complexes are abundant, arthritis is frequent. If such circulating complexes were responsible for inflammatory arthritis, or if complexes in the joint were transported to the circulation to produce remote pathological changes, it would be of interest to know the route they follow, and the time taken for the transport ofsuch large protein particles. This primary study aims to show that such a pathway for proteinmaterial exists. A large, electron dense tracer, ferritin, was injected intravenously into guinea-pigs and its passage from the synovial blood vessel lumen to the synovial cells observed over the course of 8 days. The cellular ultrastructure of normal synovium has been well documented, but the rich vasculature of the synovium has received much less attention, even though the rapid interchange of soluble particles across the vascular endothelium has been demonstrated (Rodnan and MacLachlan, 1960) and may be of importance in some disease states. There may be some anatomical peculiarity of the synovial vasculature which induces preferential deposition of immune complexes in the synovium (rather as the kidney is frequently involved in systemic lupus erythematosus). The morphology of guinea-pig synovial vascular endothelium was therefore studied and compared with that in other sites.