Regeneration Following Gastric Injury
Jean Morisset, Travis E. Solomon in Growth of the Gastrointestinal Tract: Gastrointestinal Hormones and Growth Factors, 2017
The early phase of healing includes formation of granulation tissue which replaces necrotic tissue elements. The wound margins are elevated, resulting from several factors including muscle contraction, infiltration with inflammatory elements, and bulging of distorted glands. In the initial phase, both submucosal edema and cyst-like formation distort the marginal gastric glands. The gastric pits in the margin are deeper than normal and the gland lumina are often dilated. Electromicroscopic histomorphometric studies35 have revealed signs of immaturity in the epithelial cells of such glands, whereby it was not possible to establish whether the immaturity and differentiation of specialized cells were the consequence of the trauma or an indication of early repair.
Gastric Cytoprotection and Adaptation to Ethanol
Victor R. Preedy, Ronald R. Watson in Alcohol and the Gastrointestinal Tract, 2017
The gastric luminal surface and gastric pits are lined with surface mucus cells which are tall columnar, with apical portion filled with mucus granules. Mucus released from these cells along with cytomembrane-derived phospholipids (forming a hydrophobic layer) are essential for the mucosal defense barrier against digestive forces and various irritants present in the gastric lumen. Surface epithelial cells shed at the rate of half a million cells per minute. Some surface epithelial cells could be also lost by the process of apoptosis (a silent genetically programmed cell death distinct from necrosis).18 Lost cells are replaced by new cells from the glandular neck area. It usually takes 2 to 3 days to replace the whole population of surface epithelial cells.16.19 In case of massive denudation of surface epithelium the process of restitution is very rapid and effective. Within 15 min, migrating cells cover more than 90% of the mucosal surface.
The gastrointestinal system
C. Simon Herrington in Muir's Textbook of Pathology, 2020
This pattern of mucosal response is often termed ‘bile reflux gastritis’. Indeed, reflux of bile and alkaline small intestinal material is a common cause of gastric epithelial cell injury in patients with gastroduodenal motility disturbances, which may be an isolated (primary) phenomenon or may follow surgery to the pyloric region. Similar patterns of mucosal change may be seen after other chemical injuries, particularly long-term NSAID ingestion, and the term ‘chemical gastritis’ is therefore preferred. Histologically, there is marked hyperplasia in the proliferative compartment of the gastric pits (the neck cells) with oedema of the mucosa (Figure 10.24). A cellular inflammatory infiltrate is often remarkably absent or scant. H. pylori is not usually seen.
Ultra-structural study of the indomethacin-induced apoptosis and autophagy in rat gastric parietal cells
Published in Ultrastructural Pathology, 2020
Sahar M Gebril, Yuko Ito, Eman E. Abu-Dief, Mahmoud Rezk Abdelwahed Hussein, Hoda M Elsayed, Asmaa Naser Mohammad, Usama M Abdelaal, Kazuhide Higuchi
Grossly, the rat stomach is formed of two parts; fore-stomach (non-glandular part, and site of food storage), and glandular stomach (site of food digestion). As compared to the normal eating, and fasting animals, the intake of IND caused multiple superficial hemorrhagic erosive gastric mucosal lesions after 3 h that becomes deeper extending nearly all through the mucosa at 6 and 12 h. In semi-thin sections, the gastric mucosa of the normal feeding rat is intact consisting of surface mucous secreting columnar surface epithelium that invaginates to line the gastric pits. The corium contains the gastric glands with the PCs predominate underlined by thin layer of muscularis mucosa. In the fasting animals, the gastric pits and the gastric glands lumen appeared wider and the PCs containing multiple small vacuoles. In the IND-treated animals, the gastric mucosa showed superficial lesions involving mainly the PCs in the isthmic, and neck regions that became deeper after 6 and 12 hours. Some PCs contained multiple vacuoles and others shrunken with deeply stained cytoplasm having dark condensed nuclei were demonstrated. The latter cells appeared after 3 hours of IND intake and increased in number after 6 and 12 hours. These findings are shown in Figure 1(a-e).
Characteristic analysis of early gastric cancer after Helicobacter pylori eradication: a multicenter retrospective propensity score-matched study
Published in Annals of Medicine, 2023
Xinyuan Liu, Xinyu Wang, Tao Mao, Xiaoyan Yin, Zhi Wei, Jindong Fu, Jie Wu, Xiaoyu Li
Figure 2 presents the endoscopic and histopathological images of a well-differentiated adenocarcinoma in a middle-aged male patient after H. pylori eradication. A 25 × 25-mm reddish depressed lesion was observed on the anterior wall of the upper part of the gastric antrum (Figure 2(A)). The surrounding mucosa showed map-like redness. The boundary of the lesion was clear on NBI magnifying endoscopy, with grid-like microvessels and disordered surface microstructures (Figure 2(B)). The gastric mucosa around the tumor was atrophied under low magnification, showing gastric pits, decreased glandular layers, and moderate intestinal metaplasia. Some glands were more proliferative, and lymphocytes and plasma cells infiltrated the interstitium (Figure 2(C)). When properly magnifying the adenocarcinoma area, the gastric mucosa was destroyed and the glands mainly showed a thick true papillary structure. The vascular axis of the papilla was visible, and the surface was covered with atypical epithelium, showing a well-differentiated papillary adenocarcinoma. Tumors in a small part of the area expanded in the form of tube glands, with dilated and irregular lumens, and enlarged glands were observed in the deep part of the tumor (Figure 2(D)).
Oil-entrapped ranitidine HCl beads heal peptic ulcers via local and systemic mechanisms
Published in Drug Development and Industrial Pharmacy, 2019
Sayed Ismail, Mona El-Mahdy, Noura Hassan Abd Ellah, Dina Adel Abdelmalek
Rabbits of Group 2 that received indomethacin only without receiving any treatment showed several ulcerations of the mucosa (Figure 8(A)). The ulcers were deep and reached up to the basement membrane (Figure 8(B)). The average widths of the ulcers were 215.1 + 28.83 µm, 96.67 ± 14.21 µm (Figure 8(B,C)). Indomethacin has a higher ulcerogenic potential than other NSAIDs due to unclear mechanism. Indomethacin induces gastric damage through inhibition of the release of protective factors such as COX-1, prostaglandin E2, mucus, and bicarbonate; increasing acid and oxidant parameters while decreasing antioxidant parameters [36]. Moreover, severe necrosis of the mucosa and gastric pits were observed (Figure 8(D)). The gastric glands (parietal cells) had also necrosis (Figure 8(E)).
Related Knowledge Centers
- Epithelium
- Gastric Acid
- Mucus
- Parietal Cell
- Pylorus
- Stomach
- Pepsin
- Gastric Glands
- Foveolar Cell
- Hydrochloric Acid