Several studies have shown alterations in vascular anatomy and physiology in inflammatory bowel disease (IBD). These findings, together with the observed upregulation of the mediators of angiogenesis in IBD patients, suggest that angiogenesis possibly contributes to the initiation and perpetuation of IBD. There is considerable evidence of an interrelationship between the mechanisms of angiogenesis and chronic inflammation in IBD. The increased expression of endothelial junction adhesion molecules found in IBD patients indicates the presence of active angiogenesis. Evidence that angiogenesis is involved in IBD was also obtained from animal models of colitis, most notably from studies of angiogenesis inhibition. Serum levels of vascular endothelial growth factor (VEGF) correlate with disease activity in human IBD and fall with the use of steroids, thalidomide, or infliximab. Pharmacological inhibition of angiogenesis, therefore, has the potential to be a therapeutic strategy in IBD. This review outlines the evidence that the rate of angiogenesis is increased in the inflamed intestine in IBD and proposes lines for future research in this field.