Stricture formation in Crohn's disease is a complication of an important wound healing process in the intestine. The smooth muscle cells of the intestinal musculares bear a responsibility for the repair of injured intestine, and effect this wound healing process by proliferating and laying down collagen at the site of injury. Injury in the submucosa, and chronicity of injury, are important factors in the development of stricture. The resultant accumulation of collagenous scar, thickening of the muscle layers, and contracture, all play a role in producing the critical architectural changes in the intestinal wall that impede the aboral movement of chyme. Impor-tant putative facets of intestinal smooth muscle cell biology that are involved in stricture formation include: the synthesis and secretion of procollagen; the peculiar response of these cells to cytokines, ascorbate, and corticosteroids; and changes in cell phenotype that result from chronic inflammation. Therapeutic modalities designed to ameliorate the stricturing process will need to modulate these biological activities in resident intestinal smooth muscle cells. Key Words: Crohn's disease-GI tract-Stricture-Collagen-Fibrosis-Smooth muscle cell-Intestine-Cytokine phenotype-Contracture-Wound healing.
Stricture formation is the hallmark of Crohn's disease. Its presence in a patient with chronic intestinal symptomatology confirms the suspected diagnosis and heralds the necessity for surgical intervention. Our efforts to understand the pathogenesis of this morbid problem over the last decade have led to the development of a new and fundamental conceptualization of how the bowel responds to injury and how it is this response to injury that leads to stricture. These studies have also led us to the realization that these new concepts apply not only to strictures in Crohn's disease but also to strictures in a host of common inflammatory conditions in the gastrointestinal tract.