Chronic Gastritis

Proper definition, recognition and classification of chronic gastritis are fundamental for its successful therapy. Gastric inflammation based on clinical/endoscopic classification is not a pathomorphologically homogenous diagnostic group. From histopathological point of view, it seems most likely that chronic gastritis is characterized by morphological indices of chronic inflammatory changes in different parts of gastric mucosa. Chronic superficial gastritis is associated with lymphocyte and plasma cells infiltrate of the foveolar part of gastric mucosa. Chronic gastritis is associated with the inflammatory cell infiltrate predominantly consisting of lymphocyte and plasma cells in total gastric mucosa. Current classification of chronic gastritis and the worldwide accepted knowledge of the natural history of gastritis are combined in the 1994 Houston-updated Sydney System. Helicobacter pylori is by far the most important etiologic factor in chronic gastritis. Helicobacter pylori infection accompanies chronic (or chronic active) and/or superficial (or atrophic) gastritis in about 90% and the process of development of the lesions usually lasts from 20 to 40 years. Chronic gastritis, especially caused by Helicobacter pylori, is accompanied by disturbances in secretion of HCL, pepsinogen as well as gastrin and somatostatin. It has been reported that Helicobacter pylori induces increased apoptosis and hyperproliferation of gastric epithelial cells. These changes (increased apoptosis, hyperproliferation and secretion disturbances) are reduced after Helicobacter pylori eradication. It is worth mentioning that regenerative abilities of gastric mucosa glandular epithelium cells are the main mechanism determining their right functions concerning both integrity of the mucosa and normal function of its all epithelial cellular elements. In chronic atrophic gastritis, a significantly higher percentage of cells in mitotic phase is found as compared to both normal condition and chronic superficial gastritis. Moreover the proliferative activity of glandular epithelial cells is directly proportional to the increasing degree of gastric mucosa atrophy. An increase in proliferative activity of glandular epithelium in gastric mucosa was also observed in chronic, particularly atrophic, gastritis, independently of its etiology. There is strong evidence on possible progression of changes from chronic atrophic gastritis to intestinal metaplasia, dysplasia and finally adenocarcinoma. It is worth mentioning that not much attention has been drawn to the importance of the examination of regenerative activity of the gastric mucosa epithelium, neuroendocrine and immune cells for the study of chronic gastritis pathogenesis.