Spondyloarthropathies are closely related to genetics and certain bacteria. The ability to study these relationships at the molecular level has revealed increasing complexity in the interplay of genetics, microbes, and the diseases. Advances have been made in the genetics at the major histocompatibility complex. The mediators of inflammation in spondyloarthropathies have begun to be elucidated. The role of bacterial pathogenesis in the joints is being better defined and implies that viable organisms are in the joints of persons with reactive arthritis at some point in the illness. Disease-prone transgenic animals have been developed that demonstrate the need for an environmental trigger. The nature of the interaction of HLA-B27 with the microbes associated with the disease is unclear. Several hypotheses are being rigorously investigated.
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