Abstract
Recent studies strongly support the concept that gut and joint inflammation are closely related. Progress also has been made in identifying individual mechanisms that contribute to the pathogenesis of joint disease in IBD and in undifferentiated SpAs. However, the interrelationship of these mechanisms that result in chronic disease manifestations at a site distant from the initiating event remain to be elucidated. The local absence of homing molecule receptors in the gut wall combined with an expression of these receptors in target organs can be responsible for the transformation of the synovial membrane and/or the enthesis into an aberrant tertiary lymphoid organ of the gut.
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