Stomach, Glandular Stomach - Erosion

Spontaneous occurrence of erosion of the glandular stomach is uncommon in NTP studies in mice and F344/N rats. Erosions are seen primarily in treated rats. An erosion (Figure 1 and Figure 2) is a partial thickness of epithelial loss, compared with an ulcer (see Stomach, Glandular Stomach - Ulcer ), in which the entire epithelial thickness has been lost down to or through the basement membrane and muscularis mucosa. In comparison, necrosis of epithelium is diagnosed instead of erosion if the necrotic portion of the epithelium is still present and at least partially attached to the underlying viable epithelium. Bacterial infections can occur secondary to erosion or ulceration due to local trauma from a gavage procedure or necrosis/ischemia. Indigenous bacteria in the stomach of the rat are normally found adherent to only the most luminal mucosa but not in the gastric pits. Following erosion/ulceration, bacteria can gain access to deeper portions of the mucosa and stomach wall. Compounds that produce erosions and ulcers can act via effects on mucosal blood flow, mucosal cell kinetics, mucus or acid/bicarbonate secretion, or maintenance of the mucus barrier. High-fat diets, chronic pantothenic acid deficiency, deficiency of gluconeogenic amino acids, platelet-activating factor, increased reflux of bile salts, and reduced exocrine pancreatic function are associated with ulceration but only with intact vagal innervations. The mediators of ulceration may be metabolites of the lipooxygenase pathway of arachidonic acid metabolism. Age of maternal separation of rat pups from their mothers has been reported to affect susceptibility to development of immobilization-induced gastric erosions.