Background and objective: Spondyloarthritis (SpA) is a well recognized extraintestinal manifestation of Inflammatory Bowel Diseases (IBDs), either Crohn's Disease(CD) or Ulcerative Colitis (UC). A much larger percentage of SpA patients have subclinical gut inflammation manifested either by endoscopic findings or by histology. The aim of the present article is to review clinical and experimental evidences regarding the immunological and genetic links between gut and joint inflammation in IBDs and SpA.
Evidence and information sources: A systematic review using PubMed database entering IBD and SpA as key words was performed.
State of the art: The association with HLA-B27 is less strong in IBD-associated SpA than in Idiopathic Ankylosing Spondylitis (AS) and there is some evidence for an association between gut inflammation in SpA and CD related CARD15 mutations. A common inflammatory pathogenic pathway has been suggested in gut and joint inflammation in IBD. Treatment of SpA associated with IBD has gained major advances in recent years with the advent of anti-TNF-alpha therapy.
Perspectives: The adaptive immune response in IBD is thought to be strictly differentiated between Th1 and Th2 in CD and UC respectively. Recent findings, however, suggest that novel effector pathways could drive tissue damage. The most important pathway now emerging is the IL-23/IL-17 axis.
Conclusions: Present and future advancements of knowledge on mechanisms of inflammation will likely lead to new therapeutic targets.