Definition of gastritis has its basis in histological features of the gastric mucosa. It is not erythema observed during gastroscopy, and there are no specific clinical presentations or symptoms defining it. The current classification of gastritis centers on time course (acute versus chronic), histological features, anatomic distribution, and underlying pathological mechanisms. Acute gastritis will evolve to chronic, if not treated. Helicobacter pylori (H. pylori) is the most common cause of gastritis worldwide. However, 60 to 70% of H. pylori-negative subjects with functional dyspepsia or non-erosive gastroesophageal reflux were also found to have gastritis. H. pylori-negative gastritis is a consideration when an individual fulfill all four of these criteria (i) A negative triple staining of gastric mucosal biopsies (hematoxylin and eosin, Alcian blue stain and a modified silver stain), (ii) A negative H pylori culture, (iii) A negative IgG H. pylori serology, and (iv) No self-reported history of H. pylori treatment. In these patients, the cause of gastritis may relate to tobacco smoking, consumption of alcohol, and/or the use of non-steroidal anti-inflammatory drugs (NSAIDs) or steroids.

Other causes of gastritis include:

1. Autoimmune gastritis associated with serum anti-parietal and anti-intrinsic factor antibodies; characterized by chronic atrophic gastritis limited to the corpus and fundus of the stomach that is causing marked diffuse atrophy of parietal and chief cells.
2. Gastritis causes include organisms other than H. pylori such as Mycobacterium avium intracellulare, Herpes simplex, and Cytomegalovirus.
3. Gastritis caused by acid reflux. Rare causes of gastritis include collagenous gastritis, sarcoidosis, eosinophilic gastritis, and lymphocytic gastritis.

Clinical presentation, laboratory investigations, gastroscopy, as well as the histological and microbiological examination of tissue biopsies are essential for the diagnosis of gastritis and its causes. Treatment of H. pylori-associated gastritis results in the rapid disappearance of polymorphonuclear infiltration and a reduction of chronic inflammatory infiltrate with the gradual normalization of the mucosa. Mucosal atrophy and metaplastic changes may resolve shortly, but it is not necessarily the outcome of treatment of H. pylori in all treated patients. Other types of gastritis should be treated based on their causative etiology. 

Gastritis can be acute or chronic. The causes of gastritis can be summarized as follows [1][2][3][4][5]:

1. H. pylori-associated gastritis: This is the most common cause of gastritis worldwide. 
2. H. pylori-negative gastritis: The patients should fulfill all four of these criteria (i) A negative triple staining of gastric mucosal biopsies (hematoxylin and eosin, the Alcian blue stain and a modified silver stain), (ii) A negative H. pylori culture, (iii) A negative IgG H. pylori serology, and (iv) No self-reported history of H. pylori treatment. In these patients, the cause of gastritis may relate to tobacco smoking, consumption of alcohol, and/or the use of NSAIDs or steroids.
3. Autoimmune gastritis: This is a chronic inflammatory disease characterized by chronic atrophic gastritis and associated with raised serum anti-parietal and anti-intrinsic factor antibodies. The loss of parietal cells results in a reduction of gastric acid secretion, which is necessary for the absorption of inorganic iron. Therefore, iron deficiency is commonly a finding in patients with autoimmune gastritis. Iron deficiency in these patients usually precedes vitamin B12 deficiency. The disease is common in young women.
4. Gastritis may be the result of infection by organisms other than H. pylori such as Mycobacterium avium-intracellulare, enterococcal infection, Herpes simplex, and cytomegalovirus. Parasitic gastritis may result from cryptosporidium, Strongyloides stercoralis, or anisakiasis infection.
5. Gastritis may result from bile acid reflux.
6. Radiation gastritis.
7. Crohn disease-associated gastritis: This is an uncommon cause of gastritis.
8. Collagenous gastritis: This is a rare cause of gastritis. The disease characteristically presents with marked subepithelial collagen deposition accompanying with mucosal inflammatory infiltrate. The exact etiology and pathogenesis of collagenous gastritis are still unclear.
9. Eosinophilic gastritis: This is another rare cause of gastritis. The disease could be part of the eosinophilic gastrointestinal disorders which is characterized by the absence of known causes of eosinophilia (not secondary to an infection, systematic inflammatory disease, or any other causes to explain the eosinophilia).
10. Sarcoidosis-associated gastritis: Sarcoidosis is a multisystemic disorder characterized by the presence of non-caseating granulomas. Although sarcoidosis can affect any body organ, the gastrointestinal tract, including the stomach, is rarely affected.
11. Lymphocytic gastritis: This is a rare cause of gastritis. The etiology of lymphocytic gastritis remains unestablished, but an association with H. pylori infection or celiac disease has been suggested.
12. Ischemic gastritis: This is rare and associated with high mortality.
13. Vasculitis-associated gastritis: Diseases causing systemic vasculitis can cause granulomatous infiltration of the stomach. An example is Granulomatosis with polyangiitis, formerly known as Wegner granulomatosis. 
14. Ménétrier disease: This disease is characterized by- (i) Presence of large gastric mucosal folds in the body and fundus of the stomach, (ii) Massive foveolar hyperplasia of surface and glandular mucous cells, (iii) Protein-losing gastropathy, hypoalbuminemia, and edema in 20 to 100% of patients, and (iv) reduced gastric acid secretion because of loss of parietal cells [6]. 

In the western population, there is evidence of declining incidence of infectious gastritis caused by H. pylori with an increasing prevalence of autoimmune gastritis.[7] Autoimmune gastritis is more common in women and older people. The prevalence is estimated to be approximately 2% to 5%. However, available data do not have high reliability.[7][8]

Chronic gastritis remains a relatively common disease in developing countries. The prevalence of H. pylori infection in children in the western population is approximately 10% but about 50% in developing countries.[9][10] In developing countries, the overall prevalence of H. pylori varies depending on geographical region and socioeconomic conditions. It is approximately 69% in Africa, 78% in South America, and 51% in Asia.   

Socioeconomic and environmental hygiene are the essential factors in the transmission of H. pylori infection worldwide. These factors include family-bound hygiene, household density, and cooking habits. The pediatric origin of H. pylori infection is currently considered the primary determinant of H. pylori-associated gastritis in a community.[11]

H.pylori-associated gastritis transmission is via the fecal-oral route. H. pylori possess several virulence factors which facilitate cell adhesion (e.g., BabA/B, sabA, OipA), cell damage and disruption of tight junctions (e.g., Ure A/B), and evasion from the immune response (e.g. LPS). In particular, the cytotoxin-associated gene a (CagA) is considered a potent inducer of inflammation and correlate with gastric cancer development.[12]

Another factor influencing H. pylori pathogenic effects is host factors. The host susceptible factors such as polymorphism in genes coding for tall receptors or specific cytokines. The infection with H. pylori triggers IL-8, which attracts neutrophils which release oxyradicals leading to cell damages. Lymphocyte infiltration is also present in H. pylori infection.

Chronic gastritis mostly results from H. pylori infection and appears either as non-atrophic or atrophic form. These two forms are phenotypes of gastritis at different stages of the same life-long disease.[13]

The progression from acute to chronic gastritis begins in childhood as a simple chronic superficial mononuclear inflammation of gastric mucosa which progress in years or decades to atrophic gastritis characterized by loss of normal mucosal glands in the antrum, corpus, fundus or all. 

Factors that determine progression to atrophic gastritis and sequelae such as a peptic ulcer or gastric cancer are not clearly understood and unpredictable. However, Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) have been identified in gastric tumors and DNA from H. pylori, EBV, and PCR determined the presence of HCMV in biopsies from patients with gastric cancer complicating chronic gastritis.[14] Some researchers have confirmed the involvement of EBV and H. pylori in the development of gastric cancer in patients with chronic gastritis. They found no role for human papillomavirus (HPV) in gastric tumorigenesis.[15]

NSAIDs cause gastritis through inhibition of prostaglandin synthesis. Prostaglandins are responsible for the maintenance of protective mechanisms of gastric mucosa from injuries caused by hydrochloric acid.

The pathogenesis of autoimmune gastritis focuses on two theories. According to the first theory, an immune response against superimposed H. pylori antigen gets triggered, antigen cross-reacting with antigens within the proton-pump protein or the intrinsic factor, leading to a cascade of cellular changes and causing damages to the parietal cells and stopping hydrochloric acid secretion and thus these cells gradually become atrophic and not functioning. The second theory assumes that the autoimmune disorder develops irrespective of H. pylori infection, and it directs itself against the proteins of the proton-pump. As per both theories, the autoimmune gastritis is the result of a complex interaction between genetic susceptibility and environmental factors resulting in immunological dysregulation involving sensitized T lymphocytes and autoantibodies directed against parietal cells and the intrinsic factor.[16]

Histologically, gastritis definitively demonstrates by the presence of at least grade 2 neutrophils or mononuclear cells in at least one gastric biopsy site or grade 1 neutrophils or mononuclear cells in at least two sites.[17] Sampling comes from five gastric biopsy specimens from the following locations: antrum greater and lesser curvature, incisura, and corpus greater and lesser curvature. Specimens must be put into separate vials and grouped for each site of the lesion. The aim is to maximize the opportunity to identify H. pylori and hence not to miss the diagnosis.

H. pylori infection first appearance of gastritis tend to be antral. The inflammation, composing mainly of mononuclear inflammatory cells and plasma cells are superficial and mostly in the upper layers of the mucosa of the corpus (body of the stomach). The chronic inflammation of gastric mucosa is associated with neutrophilic inflammation; the effects are dependent on the cytotoxicity of the H. pylori strain. The most cytotoxic strains will result in the development of atrophic gastritis. The lost mucosal glands in atrophic gastritis become replaced with new immature glandular and epithelial cells resembling glands of intestinal tissues.

In early phases of autoimmune gastritis, lymphocytic and plasma cell infiltration of oxyntic mucosa is present with accentuation in deeper glandular portion. Hyperplasia of endocrine cells in gastric mucosa is an early feature in autoimmune gastritis. Oxyntic glands may undergo destruction, and parietal cells show pseudohypertrophy as the disease progress. In advanced disease, marked atrophy of the oxyntic glands together with diffuse lymphoblastic infiltration of the lamina propria are present. Intestinal metaplasia is present in end-stage disease.[18]