www.histopathology-india.net/GIPath.htm

The epithelial changes may become dysplastic and constitute a backround for the development of carcinoma.

30% of endoscopically normal biopsies may show chronic gastritis.

Type A : Autoimmune gastritis- Associated with pernicious anaemia. Body of the stomach is usually affected.

Type B : Environmental gastritis- Result from dietary or intraluminal factors, specially Helicobacter pylori.  Usually localized in the antrum. In severe cases, the inflammation spreads to the proximal part of the stomach.

Type C :  Chemical gastritis- Associated with ingestion of non-steroidal  anti-inflammatory drugs or bile influx

Helicobacter associated patterns of gastritis include:
(i) Antral-predominant  gastritis (principal cause of peptic ulcer)
(ii) Multifocal atrophic gastritis involving corpus, fundus and antrum ( may develop gastric ulcer and gastric carcinoma).
H pylori are  also associated with the  development of gastric lymphoma.
Cag A+strains of H. pylori (more ulcerogenic) are protective against development of gastroesophageal reflux disease.

What is Helicobacter heilmannii? IMAGE LINK (Dr Tsutsumi)

This bacteria has an elongated spiral appearance and are present only in small number of patients.
H. helmannii is a possible cause of gastric ulcer.
 

Histological responses to Helicobacter pylori infection: gastritis, atrophy and preneoplasia. Baillieres Clin Gastroenterol. 1995 Sep;9(3):467-86
 
-In the initial active phase there are features of acute gastritis characterised by neutrophil polymorphs in mucous neck region. In severe infection there is pit abscess formation.
-Cellular swelling and vacuolization, mucin loss and  desquamation of surface epithelium
-Erosion and frank ulceration.
-Degenerative and regenerative changes present.
-Regenerative changes - There are hyperplastic neck cells and elongated, distorted and tubular structures. The cells display cytoplasmic basophilia, increased mitoses and hyperchromatic nuclei, however the enlarged nuclei  show smooth regular nuclear membrane  (D/D dysplasia or ca-in situ)
- As the disease progresses there is superimposed chronic inflammation (Active chronic gastritis)
Neutrophils, eosinophils, basophils, macrophages, monocytes, plasma cells infiltrate the mucosa.
-Mucosa appears normal in thickness or slightly expanded by mononuclear cells.
-In early stage, lymphocytes and plasma cells are present in the superficial mucosa mostly along lesser curvature. (Chronic superficial gastritis)
-The inflammation extends into the glandular compartment.
- Focal epithelial cell dropout is noted.
-There is lymphoid follicle formation with or without germinal centres.  This is a marker for H pylori infection.
-Gradually develops pangastritis.
- There is glandular atrophy (Chronic atrophic gastritis) IMAGE LINK
-Intestinal metaplasia replaces the gastric glands. H pylori is markedly decreased in the late stage as  intestinal metaplasia creates an unfavourable environment for H. pylori.
- Gastric atrophy is  the end stage of chronic gastritis and is characterized by thinning of gastric mucosa in the absence of inflammation. 
Parietal and chief cells are decreased in number in the body (autoimmune gastritis). Antrum shows loss of pyloric glands (type B gastritis).
[ 2 main causes of Atrophic gastritis - i ) H.pylori associated multifocal atrophic gastritis involving corpus and antrum.
ii) Autoimmune gastritis restricted to the corpus]

Note:
Following treatment of H. pylori infection the features of chronic gastritis with lymphoid follicles may persist .
These features are gradually resolve  after few years.
Following long term therapy with proton pump inhibitors there may be pseudo hypertrophy of parietal cells. Tiny fundic glands cysts lined by parietal and chief cells may be noted.

(AFIP)IMAGE LINK ; H. pylori IMAGE LINK ; IMAGE LINK