Summary. All epithelial cells in the small and large intestine are thought to originate from stem cells located towards the base of the crypts of Lieberkü hn. To-date, there are no specific intestinal stem cell markers, hence stem cell properties can only be inferred. A range of experimental techniques have been employed including cell position mapping, radiation regeneration (clonogenic) assays, chimeric and transgenic mice. This review discusses the implications of experiments performed using these techniques in order to deduce the number, location and functional properties of stem cells. Stem cell homeostasis is maintained by cell proliferation and death 'through apoptosis'. The various growth and matrix factors and genes which may control these processes, and be important for stem cell function, are discussed along with their carcinogenic and clinical implications.Keywords: stem cell, intestine, apoptosis, epithelium Proliferative organization of the intestinal epitheliumThe lumenal surface of the intestine is lined by a simple columnar epithelium. The surface of both the small and large intestine is folded into a number of deep cavities or crypts of Lieberkü hn, which are embedded in connective tissue. In the small intestine the surface area is further increased by finger-like projections, or villi, also covered by epithelium, which protrude into the gut lumen. Although the crypts are approximately 10 × smaller than the villi, they are much more numerous (7 × more in the duodenum, 4 × more in the ileum, Wright & Alison 1984). The effect of these numerous 'pits and projections' is to form a huge surface area. This surface area is further expanded by the presence of a carpet-like covering of microvilli on the apical (lumenal) surface of the columnar epithelial cells.The functional cells of the epithelium are located predominantly towards the lumenal pole of the cryptvillus axis (i.e. on the villi of the small intestine and at the top of the crypts of the large intestine). Once they have fulfilled their differentiated function (brush border enzyme secretion, mucus secretion, nutrient and water absorption) the cells senesce and are sloughed off into the lumen itself, possibly after initiating some aspects of the Int.

ObjectivesLoss of intestinal barrier function plays an important role in the pathogenesis of inflammatory bowel disease (IBD). Shedding of intestinal epithelial cells is a potential cause of barrier loss during inflammation. The objectives of the study were (1) to determine whether cell shedding and barrier loss in humans can be detected by confocal endomicroscopy and (2) whether these parameters predict relapse of IBD.MethodsConfocal endomicroscopy was performed in IBD and control patients using intravenous fluorescein to determine the relationship between cell shedding and local barrier dysfunction. A grading system based on appearances at confocal endomicroscopy in humans was devised and used to predict relapse in a prospective pilot study of 47 patients with ulcerative colitis and 11 patients with Crohn's disease.ResultsConfocal endomicroscopy in humans detected shedding epithelial cells and local barrier defects as plumes of fluorescein effluxing through the epithelium. Mouse experiments demonstrated inward flow through some leakage-associated shedding events, which was increased when luminal osmolarity was decreased. In IBD patients in clinical remission, increased cell shedding with fluorescein leakage was associated with subsequent relapse within 12 months after endomicroscopic examination (p<0.001). The sensitivity, specificity and accuracy for the grading system to predict a flare were 62.5% (95% CI 40.8% to 80.4%), 91.2% (95% CI 75.2 to 97.7) and 79% (95% CI 57.7 to 95.5), respectively.ConclusionsCell shedding and barrier loss detected by confocal endomicroscopy predicts relapse of IBD and has potential as a diagnostic tool for the management of the disease.

This document represents the first position statement produced by the British Society of Gastroenterology and Association of Upper Gastrointestinal Surgeons of Great Britain and Ireland, setting out the minimum expected standards in diagnostic upper gastrointestinal endoscopy. The need for this statement has arisen from the recognition that while technical competence can be rapidly acquired, in practice the performance of a high-quality examination is variable, with an unacceptably high rate of failure to diagnose cancer at endoscopy. The importance of detecting early neoplasia has taken on greater significance in this era of minimally invasive, organ-preserving endoscopic therapy. In this position statement we describe 38 recommendations to improve diagnostic endoscopy quality. Our goal is to emphasise practices that encourage mucosal inspection and lesion recognition, with the aim of optimising the early diagnosis of upper gastrointestinal disease and improving patient outcomes.