Helicobacter pylori infection is an etiopathogenetic cause of chronic gastritis in more than 90% of the cases. In a proportion of infected subjects, gastritis slowly (over years or decades) progresses, for unknown reasons, into atrophic gastritis that affects antral or corpus mucosa, or both (multifocal atrophic gastritis). Some recent improvements have been made in studies of H. pylori gastritis. H. pylori gastritis has shown to associate strongly with peptic ulcer diseases and gastric cancer. The risk for ulcer (excluding the nonsteroidal anti-inflammatory drug-related ulcers) is highest in the nonatrophic forms of gastritis and the risk for gastric cancer in the severe forms of atrophic (metaplastic) gastritis. For routine histopathologic practice, the Sydney System has been developed to describe and grade the histopathologic appearances of gastritis, i.e., chronic and acute (''activity'') inflammation, atrophy (loss of normal mucosal glands), intestinal metaplasia, and H. pylori in endoscopic biopsy specimens from antrum and corpus. Different phenotypes of H. pylori gastritis can be reliably described and the risks for various gastric diseases reasonably well predicted by the System. Most recent studies from developed countries have indicated that H. pylori acquisition occurs mainly during childhood and that the infection risk is quite low in adulthood. In addition, the acquisition rate has declined in these countries during the past few decades. The observations suggest that H. pylori gastritis is a birth cohort-related phenomenon. The acquisition rate has been high and the subsequent chronic gastritis is a common disease in the cohorts (generations) born in the beginning of this century but both are much less common in cohorts born more recently.