title: Duodenal and gastric cell regenerating epithelia on margins of human duodenal ulcer and presence of H. pylori--an electron microscopic study.
abstract: Specimens from 22 cases of human duodenal ulcers obtained at surgery were studied by transmission and scanning electron microscopy. Observations were focused on the ulcer margins which always showed some evidence of healing by simple cuboidal epithelial cells migrating on the ulcer base. Two types of regenerating epithelia (RE) were found: the intestinal and the gastric cell types. The intestinal type RE originating from intestinal epithelium of the surrounding epithelium of the ulcer edge was composed of immature enterocytes, which differentiated into absorptive and goblet cells, and formed presumptive crypts and villi. The gastric type RE grew from adjacent metaplastic gastric mucosa at the edge of the ulcer and consisted of immature cells, which developed into mucous cells. Some ulcers had RE of both intestinal cell and gastric cell origin. In most margins, the RE was of only one cell type, but in others both intestinal and gastric type cells were present. In more developed regions both types formed presumptive glands. The basal lamina was frequently missing near the leading edge. This corresponded to degeneration and necrosis of RE, especially in areas of severe inflammatory foci. Helicobacter (H.) pylori colonization on gastric metaplastic epithelium was observed in about one third of the ulcer cases. In the surrounding epithelium of ulcers colonized with H. pylori there were degenerative changes, disruption of cell membranes, and massive cell exfoliation resulting in denuded lamina propria. Some gastric type RE was also colonized with H. pylori. No infection was found on intestinal epithelia. These findings suggest that H. pylori may be important in the development of duodenal ulcers as well as in the prevention or delay of ulcer healing.
authors.affiliation: Department of Surgery, Kochi Medical School, Nankoku, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Ogata
mesh_terms: D004381:Duodenal Ulcer / Q000382:microbiology* / Q000473:pathology* / Q000503:physiopathology; D004386:Duodenum / Q000382:microbiology / Q000473:pathology* / Q000503:physiopathology; D004848:Epithelium / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology* / Q000503:physiopathology; D016481:Helicobacter Infections / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology; D016480:Helicobacter pylori / Q000302:isolation & purification* / Q000472:pathogenicity / Q000648:ultrastructure; D006801:Humans; D007413:Intestinal Mucosa / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology; D008854:Microscopy, Electron; D008855:Microscopy, Electron, Scanning; D012038:Regeneration