Bowel infection predisposing to reactive arthritis.

Postenteric reactive arthritis is one of several syndromes in which arthritis appears to be secondary to gastrointestinal tract pathology. A wide range of microbes may trigger this type of arthritis. On the other hand, there are differences between strains in their arthritogenic potential. Two possible mechanisms, not mutually exclusive, can be forwarded to explain these findings: first, particular characteristics of the infective organisms are necessary to initiate events leading to reactive arthritis and, second, particular anatomical locations and a certain degree of mucosal involvement are needed to initiate the process. Studies on humoral and cellular immune responses have not revealed any unifying feature that could explain the pathogenesis of reactive arthritis. The HLA allele B27 plays some kind of key role. Yet the elucidation of the fine structure of B27 specificity has not led to any immediate breakthrough in the understanding of the pathogenetic pathways. Experience of reactive arthritis associated with acquired immunodeficiency syndrome suggests that helper T cells are not involved. Antigen persistence may be connected with continuation of the inflammation. Recent developments in the serology of enteric bacterial infections will provide additional tools for uncovering the triggering agents in reactive arthritis. 'Idiopathic reactive arthritis' associated with clinically silent terminal ileitis is an interesting disease entity requiring further characterization.