Mucosal inflammation in spondylarthritides: past, present, and future

Curr Rheumatol Rep. 2011 Oct;13(5):409-15. doi: 10.1007/s11926-011-0198-2.


Spondylarthritides (SpA) and inflammatory bowel disease (IBD) are idiopathic, chronic inflammatory disorders. Although they are very distinct and well-defined entities, there is clinical and genetic evidence supporting some degree of overlap between the pathogenesis of the two. Subclinical gut inflammation is present in up to two thirds of all SpA patients and can evolve into IBD. This subclinical gut inflammation has been shown to be strongly associated with joint inflammation, providing a clue for a common pathophysiologic background. Despite extensive research progress in the field over the past few years, many questions remain unanswered. In this paper, we focus on the clinical, genetic, and pathophysiologic overlap of SpA and IBD. Furthermore, we discuss some of the targets that may influence therapeutic decision making.

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Antibodies, Monoclonal / therapeutic use
  • Antirheumatic Agents / therapeutic use
  • Biomarkers / metabolism
  • Cytokines / metabolism
  • Humans
  • Inflammation / drug therapy
  • Inflammation / pathology*
  • Inflammatory Bowel Diseases / drug therapy
  • Inflammatory Bowel Diseases / pathology*
  • Inflammatory Bowel Diseases / physiopathology
  • Intestinal Mucosa / drug effects
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / pathology
  • Spondylarthritis / drug therapy
  • Spondylarthritis / pathology*
  • Spondylarthritis / physiopathology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors


  • Anti-Inflammatory Agents, Non-Steroidal
  • Antibodies, Monoclonal
  • Antirheumatic Agents
  • Biomarkers
  • Cytokines
  • Tumor Necrosis Factor-alpha