As a Group 1 carcinogen for gastric cancer, Helicobacter pylori (H. pylori) was involved in many studies and researches focused on physiopathology and morphopathologic changes induced by this bacterium. The study included 3069 gastric endoscopies performed between January 2005 and December 2009 in "Colentina" Clinical Hospital. During upper endoscopy biopsies from antro-pyloric and corporeo-fundic region were collected. Histopathologic diagnosis of these biopsies was made using Sydney criteria. The patients were divided in two groups, based on the presence or absence of H. pylori: group A included 1414 H. pylori positive patients and group B included 1653 H. pylori negative patients. We evaluated several histopathological parameters, correlating the degree of inflammation, atrophy, metaplasia, regenerative hyperplasia and dysplasia with the presence of H. pylori infection. Our study identifies an overall tendency towards regression of premalignant lesions of gastric epithelium (regenerative epithelial hyperplasia, atrophy and intestinal metaplasia) after H. pylori eradication, as well an increasing number of patients diagnosed with early gastric cancer, thus consolidating the results of studies who foretell the significant decrease of gastric cancer mortality. These lesions are present years before becoming clinically manifest, and consequently treatable. In respect of carcinogenic mechanisms, some of our results confirm the carcinogenic cascade triggered by the H. pylori infection, as it was proposed by Correa et al. in 1975. However, we obtained data leading to the idea that the "precursor lesions" could appear (and subsequently histopathologically evaluated) independent one to the other, through other steps then Correa's model.