Maintenance of gastric mucosal structure depends on a dynamic balance between cell loss and cell renewal. The surface epithelial cells exfoliate at a rapid rate (usually in response to luminal contents) and are entirely replaced within 3–5 days. The loss of parietal, chief, and endocrine cells is much slower, but there is little information concerning the morphologic aspects of this process. Because in other tissues cells are physiologically eliminated through a process of apoptosis—genetically programmed cell self-destruction and loss—we studied whether this process occurs in normal gastric mucosa and in the mucosa of recently healed gastric ulcers in the rat. Degeneration and loss of the surface epithelial cells into the gastric lumen occurs in normal oxyntic mucosa, and more extensive desquamation of poorly differentiated mucous cells in the dilated gastric glands takes place within mucosal scars of grossly healed gastric ulcers. Apoptosis of parietal, chief, and endocrine cells in normal oxyntic mucosa and apoptosis of poorly differentiated cells lining dilated glands in mucosal scar were assessed and characterized by electron microscopy. Apoptosis affects single glandular cells and involves a rapid initial condensation of both nucleus and cytoplasm, with subsequent fragmentation. Finally, the cell is converted into a cluster of membrane-bound apoptotic bodies, which usually are engulfed by adjacent cells or disposed into a glandular lumen. Desquamation of surface epithelium and apoptotic self-destruction of glandular epithelium stimulate a constant cell renewal and thus contribute to the maintenance of the ulcer healing process. Rapid and “excessive” proliferation of regenerating gastric epithelium enables reepithelization of ulcer crater. This is not a final process, however, and is followed by remodeling and slow differentiation of the scar, with some cell loss (by desquamation and apoptosis).