The mechanisms of wound healing in general have gained interest in recent years, as it has become obvious that the tightly regulated process of tissue repair and regeneration is of great importance for organ homeostasis. Insufficient as well as excessive tissue repair both impair gastrointestinal function. Formation of ulcers and fistulas on the one hand, and of fibrosis and stricture on the other, represent just two sides of one medal. So far, the physiological pathways involved in intestinal wound healing are only partially understood. During acute and chronic intestinal inflammation, macrophages and neutrophils induce local tissue damage by secreting reactive oxygen radicals and tissue-degrading enzymes. This is followed by the release of pro-inflammatory cytokines, as well as chemotactic and cell-activating peptides previously bound to the matrix. If tissue damage is severe, myofibroblasts migrate to the sites of the defect. This migratory function, the ability to contract the wound area and the production of extracellular matrix (ECM) by intestinal myofibroblast cells certainly have important roles in the physiological situation and are altered by chronic inflammation. Available treatments of intestinal strictures, fibrosis and fistulas are insufficient and unsatisfactory. New therapeutic approaches are urgently needed. Future intervention should involve stronger and more selective prevention of the continuous tissue damage and a change in wound healing by modulation of myofibroblast migration and ECM synthesis.

Severe mucosal tissue damage requiring efficient wound healing is a main feature of inflammatory bowel disease (IBD), with its two entities Crohn’s disease and ulcerative colitis. During radiation enteritis1 2 or chronic ischaemic enteritis, 3 4 the bowel wall is similarly damaged, with subsequent inflammation. Furthermore, cystic fibrosis also may lead to colonic wall thickening, fibrotic colonopathy and stricture formation. 5–10 In rare cases, recurrent diverticulitis also may cause colonic strictures. 11 12 During collagenous colitis, fibrosis typically occurs at the basement membrane directly beneath the epithelial barrier. 13–15