Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Macedonia, Greece; School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Macedonia, Greece; Medical School, National and Kapodistrian University of Athens, Athens, Greece; University Hospital Zurich, University of Zurich, Zurich, Switzerland; Medical University Department, Kantonsspital Aarau, Aarau, Switzerland; 401 General Military Hospital of Athens, Athens, Greece; School of Health Sciences, International Hellenic University, Thessaloniki, Greece
aDepartment of Medicine, Second Medical Clinic, Aristotle University of Thessaloniki, Ippokration Hospital, Thessaloniki, Macedonia, Greece (Jannis Kountouras, Stergios A. Polyzos, Ioannis S. Papanikolaou, Michael Doulberis, Christos Liatsos, Elisabeth Vardaka); bFirst Laboratory of Pharmacology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Macedonia, Greece (Stergios A. Polyzos); cHepatogastroenterology Unit, Second Department of Internal Medicine-Propaedeutic, Medical School, National and Kapodistrian University of Athens, Athens, Greece (Ioannis S. Papanikolaou); dDepartment of Gastroenterology & Hepatology, University Hospital Zurich, University of Zurich, Zurich, Switzerland (Michael Doulberis); eDivision of Gastroenterology and Hepatology, Medical University Department, Kantonsspital Aarau, Aarau, Switzerland (Michael Doulberis); fDepartment of Gastroenterology, 401 General Military Hospital of Athens, Athens, Greece (Christos Liatsos); gDepartment of Nutritional Sciences and Dietetics, School of Health Sciences, International Hellenic University, Thessaloniki, Greece (Elisabeth Vardaka)
Ann Gastroenterol 2026; 39 (2): 278-279
Kouvaras et al [1] demonstrated an association between Helicobacter pylori infection (Hp-I) and the development of gastric intestinal metaplasia (IM)—complete, incomplete or mixed forms—a premalignant lesion in the Correa cascade of gastric carcinogenesis. Beyond Hp, oral Porphyromonas gingivalis (Pg) can translocate to the stomach further promoting progression along the Correa cascade [2,3].
Focusing on IM and gastric cancer (GC) associated with Hp and/or Pg, several significant findings are noteworthy:
Hp can also inhabit the oral cavity, which may serve as a main extragastric reservoir. Similarly, the oral cavity serves as a primary reservoir for Pg [2]. Pg and its virulence factors, including gingipains, appear to contribute to the aforementioned sequence of gastric carcinogenesis [4].
Among the types of IM, the incomplete type is more strongly associated with GC progression than the complete type [5].
Hp-induced inflammation, demonstrated in both mice (Houghton’s theory) and humans, triggers the migration of bone-marrow–derived stem cells to the gastric mucosa. There, these cells undergo metaplastic and dysplastic changes that can lead to GC, in line with Correa’s cascade [6].
Areas exhibiting severe inflammation, IM, atrophy, and GC also show increased mast cell density, correlated with Hp-induced gastritis [7]. The CagA and VacA cytotoxins of Hp play central roles in promoting oncogenesis, consistently with Correa’s model.
The absence of such features in cases of IM suggests a more favorable prognosis. For example, Hwang et al [8] reported that IM disappeared ≥5 years after Hp eradication. Hp eradication protects against GC in patients with IM or dysplasia (follow-up range: 2-26.5 years), and may reverse these conditions Furthermore, incomplete IM regresses within 10 years following Hp eradication [5].
Notably, radiofrequency ablation can eradicate incomplete IM [9], and endoscopic grading of IM, as a valuable surveillance tool, reduces the need for routine biopsy sampling [10].
1. Kouvaras SN, Koumarianos IG, Ekmektzoglou K, et al. Prevalence of Helicobacter pylori infection and gastric intestinal metaplasia in Greek patients. Ann Gastroenterol 2025;38:604-609.
2. Doulberis M, Tsilimpotis D, Polyzos SA, et al. Unraveling the pathogenetic overlap of Helicobacter pylori and metabolic syndrome-related Porphyromonas gingivalis:gingipains at the crossroads and as common denominator. Microbiol Res 2025;299:128255.
3. Zha T, Ding Y, Xu X, et al. The oral-gut axis in chronic atrophic gastritis:current perspectives and integrated strategies. Front Immunol 2025;16:1699501.
4. Muñoz-Medel M, Pinto MP, Goralsky L, et al. Porphyromonas gingivalis, a bridge between oral health and immune evasion in gastric cancer. Front Oncol 2024;14:1403089.
5. Wada Y, Kodama M, Mizukami K, et al. Differences in regression patterns of complete and incomplete intestinal metaplasia at ten years after Helicobacter pylori eradication. Acta Histochem Cytochem 2021;54:185-194.
6. Kountouras J, Zavos C, Chatzopoulos D, Katsinelos P. New aspects of Helicobacter pylori infection involvement in gastric oncogenesis. J Surg Res 2008;146:149-158.
7. Kazakos EI, Petinaki E, Liatsos C, Papanikolaou IS, Anastasiadou K, Kountouras J. The potential role of Helicobacter pylori-related mast cell activation in the progression from gastroesophageal reflux to Barrett's esophagus and esophageal adenocarcinoma. Microorganisms 2025;13:1883.
8. Hwang YJ, Kim N, Lee HS, et al. Reversibility of atrophic gastritis and intestinal metaplasia after Helicobacter pylori eradication - a prospective study for up to 10 years. Aliment Pharmacol Ther 2018;47:380-390.
9. Pittayanon R, Tiankanon K, Faknak N, et al. Efficacy of radiofrequency ablation as a treatment for high-risk gastric intestinal metaplasia:a randomized, self-control study. J Gastroenterol Hepatol 2025;40:891-899.
10. Lyu D, Zhao J, Jin HF, Lyu B. The role of endoscopic grading of gastric intestinal metaplasia (EGGIM) in assessing the extent and degree of gastric intestinal metaplasia. J Dig Dis 2025;26:129-134.