Mucosecreting compound coiled glands including gastrin-secreting cells, unique to this anatomical region. Three to five glandular coils share the same excretory duct that opens into pits (pit-to-gland ratio: 50:50). Glandular coils reach the muscularis mucosae (mm) layer.

Scanty lamina propria (interglandular stroma) hosts only scattered resident lymphocytes.

Oxyntic simple tubular glands with short foveolar segment (pit-to-gland ratio: 25:75). Chief and parietal cells coexist in the tubular units, which include ECL cells. The deeper portion of oxyntic tubules reaches the mm.

Interglandular lamina propria is minimal and hosts rare resident lymphocytes.

Mucosecreting compound tubular glands show tortuous foveolar expansion, increased mitotic activity and decreased mucosecreting ability.

Lamina propria is oedematous, with no increased leucocyte population. Hyperplastic mm may also be present.

Under long-term PPI therapy, parietal cells show increase in cell size associated with ECL cell proliferation.

Lamina propria does not show increased leucocyte population.

Model: antral ‘reactive gastropathy’ resulting from chemical agent (eg, duodenogastric reflux; lanthanum).

Model: parietal cells hypertrophy/hyperplasia due to prolonged therapy with PPIs.

Phenotypically normal mucosecreting glands.

Lamina propria: inflammatory infiltrate of lymphocytes, plasma cells and PMNs, also intraepithelial and intraluminal.

Phenotypically normal oxyntic glands.

Lamina propria: inflammatory infiltrate of lymphocytes, plasma cells and PMNs (also intraepithelial and intraluminal).

Model: Helicobacter pylori chronic active gastritis without glandular loss.

Model: H. pylori-negative gastritis after H. pylori eradication; activity, when present, is negligible.

Model: H. pylori-negative gastritis restricted to oxyntic mucosa (non-atrophic AIG).

Loss of mucosecreting glands coexisting with inflammation. Glandular loss is replaced by fibrosis (ie, non-metaplastic atrophy) and by foci of metaplastic intestinal-type glands (multifocal IM).

Lamina propria expanded by inflammatory cells (lymphocytes, plasma cells and PMNs) with intraglandular infiltrate. The PMN component is referred to as ‘activity’.

Loss of oxyntic glands coexisting with inflammatory population. Glandular loss is replaced by fibrosis (ie, non-metaplastic atrophic) and by metaplastic pPM or IM (multifocal IM).

Lamina propria expanded by inflammatory cells (lymphocytes, plasma cells and PMNs) with intraglandular infiltrate. The PMN component is referred to as ‘activity’.

Model: H. pylori chronic active gastritis with glandular loss.

Model: AIG (with no previous/current H. pylori infection) with oxyntic gland loss. Antral mucosa is within normal limits or shows ‘reactive gastropathy’.

Loss of mucosecreting glands. Native glands are replaced by fibrosis (ie, non-metaplastic atrophic) or by foci of intestinal-type metaplastic glands (multifocal IM).

Lamina propria hosts only scattered resident lymphocytes.

Loss of oxyntic glands. Native glands are replaced by fibrosis (ie, non-metaplastic atrophy) or by foci of intestinal-type metaplastic glands (multifocal IM; pPM).

Lamina propria hosts scattered resident lymphocytes.

Model: residual gastric atrophy after successful H. pylori eradication.