Gastritis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]


Gastritis depending on the causes may be classified into acute gastritis, chronic gastritis, atrophic gastritis, and H. pylori associated gastritis. In the majority of patients with acute gastritis, the initial acute phase of gastritis is subclinical and is of short duration (about 7 to 10 days). Acute gastritis also referred to as reactive gastritis occurs as a result of the trigger by factors such as NSAIDs, stress, bile reflux, radiation, alcohol abuse, cocaine addiction, and ischemic damage. In chronic gastritis, the H. pylori infection persists leading to accumulation of large number chronic inflammatory cells leading to active chronic gastritis.


Acute gastritis


Microscopic pathology

Histological features observed includes:

Chronic gastritis

In the majority of cases, the H. pylori infection persists leading to accumulation of large number of chronic inflammatory cells leading to active chronic gastritis.


Also, these polymorphs accumulate around the pit isthmus, which is a proliferative compartment, causing lethal damage to stem cells resulting in glandular atrophy.

Microscopic pathology

Sydney system for grading of chronic gastritis[8]

Sydney system for grading of Chronic Gastritis
Feature Definition Grading guidelines
Chronic inflammation
  • Mild, moderate or severe increase in density
  • Mild: less than one-third of pits and surface infiltrated
  • Moderate: one-third to two-thirds
  • Severe: more than two-thirds
  • Mild, moderate, or severe loss
Helicobacter pylori
  • Mild colonization: scattered organisms covering less than one-third of the surface
  • Moderate colonization: intermediate numbers
  • Severe colonization: large clusters or a continuous layer over two-thirds of surface
Intestinal Metaplasia
  • Mild: less than one-third of mucosa involved
  • Moderate: one-third to two-thirds
  • Severe: more than two-thirds

Atrophic Gastritis

Atrophy of stomach is defined as loss of glandular tissue due to continuous mucosal injury. This leads to thinning of gastric mucosa.


  • The continuous mucosal injury due to long-standing H. pylori infection, leads to atrophy of stomach.
  • This continuous pathological process results in erosion or ulceration of the mucosa leading to the destruction of the glandular layer and followed by fibrous replacement.
  • The destruction of the glandular basement membrane and the sheath of supporting cells prevents orderly regeneration. This uneven regeneration follows a divergent differentiation pathway producing metaplastic glands (pseudo-pyloric appearance) which are composed of cells of the 'ulcer-associated cell lineage' (UACL).[10]

Microscopic pathology

Atrophic Gastritis, By Radioxoma (Own work) [CC BY-SA 3.0 (], via Wikimedia Commons[11]

Gross pathology

Erosive Gastritis, By Amadalvarez (Own work) [CC BY-SA 4.0 (], via Wikimedia Commons[12]


Chronic gastritis {{#ev:youtube|Wvn5TiiIB4Q}}

Atrophic gastritis {{#ev:youtube|760GB43AZqE}}


  1. Sobala GM, Crabtree JE, Dixon MF, Schorah CJ, Taylor JD, Rathbone BJ; et al. (1991). "Acute Helicobacter pylori infection: clinical features, local and systemic immune response, gastric mucosal histology, and gastric juice ascorbic acid concentrations". Gut. 32 (11): 1415–8. PMC 1379180. PMID 1752479.
  2. Slomiany BL, Piotrowski J, Slomiany A (1998). "Induction of caspase-3 and nitric oxide synthase-2 during gastric mucosal inflammatory reaction to Helicobacter pylori lipopolysaccharide". Biochem Mol Biol Int. 46 (5): 1063–70. PMID 9861460.
  3. Crabtree JE (1996). "Gastric mucosal inflammatory responses to Helicobacter pylori". Aliment Pharmacol Ther. 10 Suppl 1: 29–37. PMID 8730257.
  4. Genta RM, Hamner HW, Graham DY (1993). "Gastric lymphoid follicles in Helicobacter pylori infection: frequency, distribution, and response to triple therapy". Hum Pathol. 24 (6): 577–83. PMID 8505036.
  5. Voutilainen M, Färkkilä M, Mecklin JP, Juhola M, Sipponen P (1999). "Chronic inflammation at the gastroesophageal junction (carditis) appears to be a specific finding related to Helicobacter pylori infection and gastroesophageal reflux disease. The Central Finland Endoscopy Study Group". Am J Gastroenterol. 94 (11): 3175–80. doi:10.1111/j.1572-0241.1999.01513.x. PMID 10566710.
  6. "File:Chronic gastritis -- intermed mag.jpg - Wikimedia Commons".
  7. "File:Chronic gastritis -- very high mag.jpg - Wikimedia Commons".
  8. Dixon MF, Genta RM, Yardley JH, Correa P (1996). "Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994". Am J Surg Pathol. 20 (10): 1161–81. PMID 8827022.
  9. Neithercut WD, Milne A, Chittajallu RS, el Nujumi AM, McColl KE (1991). "Detection of Helicobacter pylori infection of the gastric mucosa by measurement of gastric aspirate ammonium and urea concentrations". Gut. 32 (9): 973–6. PMC 1379031. PMID 1916500.
  10. Pera M, Heppell J, Poulsom R, Teixeira FV, Williams J (2001). "Ulcer associated cell lineage glands expressing trefoil peptide genes are induced by chronic ulceration in ileal pouch mucosa". Gut. 48 (6): 792–6. PMC 1728308. PMID 11358897.
  11. "File:Atrophic gastritis (low zoom).jpg - Wikimedia Commons".
  12. "File:Gastritis erosiva.2278.jpg - Wikimedia Commons".

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