Some Ultrastructural Aspects of Chronic Gastritis

Abstract

Despite numerous observations and publications on the aethiology and pathogenesis of chronic gastritis many questions remain unanswered (1,2,3,4,6). Views on the aethiolcgy of chronic gastritis changed when in 1982 Campylobacter pyloridis (later named Campylobacter pylori CP) was first isolated in Western Australia from the stomach of patients with gastritis lesions and peptic ulceration (5).The aim of this study, carried out with cooperation with gastroenterologist, has been to investigate the ultrastructural changes in gastric surface epithelium and lamina propria in selected patients endoscopicaUy diagnosed gastritis.Observations have been carried out on 20 patients (10 men and 10 women). Biopsy material was obtained during endoscopy. In cases when the presence of bacteria has been confirmed further E M investigations have been introduced. Semithin sections for LM observations and ultrathin sections for EM were prepared according to routine EM technique.CP was found both on the airface of gastric epithelium cells, and what has not been reported so far, inside the lumen of the fundic glands (Fig. 1).

Criteria Characterizing Tumor Cells Observed in the Helicobacter Pylori- Associated-Gastric Epithelial Cells and Predicting Tumorgenesis

“…Ultrastructural changes on the surface and within the cytoplasm of mucosa cells including epithelial mucous cells were observed, indicating disturbed metabolism. Similar observation was reported by Bartel et al (1992). It is clear from this study that the ultrastructural feature induced by H. pylori in human closely resemble those described in tumor cells.…”

“…It is now well known that H. pylori infection is probably the most common bacterial infection in the world (Guisset et al, 1997). Association between H. pylori and gastric and duodenal mucosa was reported by numerous authors (Bartel et al, 1992, Noach et al, 1994Janas et al, 1995). The pathogenicity of H. pylori has recognized since 1989 in the developed world where prevalence is 20 to 40 percent (Guisset et al, 1997).…”