In summary, we support the hypothesis that the rheumatoid knee is subjected to repeated hypoxic reperfusion injury. Moreover, we speculate that oxidative damage induced as a consequence of hypoxic reperfusion injury leads to the synthesis of intracellular stress proteins. In certain individuals this triggers an autoimmune response which might explain the persistance of the rheumatoid disease process. This gives scope for novel therapeutic approaches in the future development of anti-inflammatory agents.