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COMMENTARY |
| Crohn's disease |
Department of Medicine I, University of Erlangen-Nürnberg, Germany
Correspondence to:
Correspondence to:
Professor D Schuppan
Department of Medicine I, University of Erlangen-Nürnberg, Ulmenweg 18, 91054 Erlangen, Germany; detlef.schuppan@med1.imed.uni-erlangen.de
Keywords: fibrosis; inflammatory bowel disease; proteolysis; matrix metalloproteinases; tissue inhibitor of metalloproteinase; ulcerative colitis; vitronectin receptor; Crohns disease; fistulae
| The first 150 words of the full text of this article appear below. |
Fistulae are a common complication of Crohns disease (CD), and their most common perianal manifestation is present in 1438% of CD patients in referral populations.1 Despite advances in conservative treatment, fistulae rarely heal, while surgical resection is effective but frequently does not prevent local recurrence or fistulising disease at other sites.1 Remodelling of the extracellular matrix (ECM) is a key event in chronic bowel inflammation,2,3 especially in CD which is characterised by both active fibrogenesis (that is, ECM production and deposition), leading, for example, to stricture formation, and by enhanced fibrolyis (that is, breakdown and removal of ECM), such as occurs in fistula formation. While fibroblasts and myofibroblasts, and to a minor degree endothelial and epithelial cells, produce the intestinal ECM, many more cell types are involved in ECM breakdown by releasing a broad spectrum of enzymes that can degrade essentially every ECM component, such as the various
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