Antigen induced arthritis: antigen handling and chronicity of joint inflammation

Data are summarized on antigen handling by the joint and the relevance of antigen retention for the chronicity of joint inflammation. Antigen retention may occur at collagenous structures of the joint, when antibodies are present in these tissues or simply when the charge of an antigen favours nonimmune binding at the highly charged collagenous tissues. Antigen retention will change with alterations in antibody load and fixed charge density of these tissues. Longterm retained antigen seems not inflammatory at the retention sites, but its importance for the chronicity of joint inflammation may lie in the continuous leakage of small amounts to other compartments, where it does behave as an inflammatory stimulus, thereby rendering the joint specifically hypersensitive to antigen. Such a joint reacts to minute amounts of antigen in the circulation leading to exacerbation of smouldering joint inflammation.