The tight connection between intestinal inflammation and arthritis in spondyloarthritis (SpA) has been studied extensively. Subclinical gut inflammation, which can be considered as a model for early Crohn's disease, was shown to be strongly associated with joint inflammation. Several early mucosal abnormalities were uncovered even in the absence of histological signs of inflammation, providing clues into the pathogenesis of SpA. Nevertheless, many questions remain unanswered. In this review, we highlight recent progress on this intimate relationship between gut and joint inflammation. Emerging evidence exists favoring a role for genes beyond human leukocyte antigen B27 in the genetic predisposition of SpA and intestinal inflammation. Furthermore, the role of these predisposing genes in modulating host-pathogen interaction at mucosal surfaces and the subsequent link between gut and joint inflammation are of utmost importance in understanding the pathogenesis of SpA.