ABSTRACT
In many patients, the arthritis is characterized by exacerbations and remissions. Current theories of the pathogenesis include a genetically regulated immunologic reaction directed at an exogenous agent that localizes to the joints or an articular autoantigen. These two concepts originate from studies in experimental arthritis models, and an important breakthrough is that they are not mutally exclusive. Collagen-induced arthritis is an experimentally induced autoimmune model of chronic erosive arthritis in both rats and mice. It is produced by sensitization to native type II collagen, a major component of articular cartilage. Adjuvant arthritis is induced by intradermal administration of Freund’s complete adjuvant containing heat-killed mycobacteria. In theory, chronic joint inflammation must result from a continuous stimulus, which can be the perpetual supply of antigen from the circulation of persisting antigen in the joint. The potential relevance of common pathogenic mechanisms is illustrated in both antigen-induced arthritis and streptococcal cell wall-induced arthritis.
