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Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia
Published on: February 16, 2024
Oral cavity as a potential source of gastric reinfection by Helicobacter pylori
Elzbieta Karczewska1, Joanna E Konturek, Peter C Konturek
1Department of Physiology, Jagellonian University College of Medicine, Cracow, Poland.
Abstract:
Helicobacter pylori (Hp) is a common pathogen colonizing the a gastric mucosa, but some reports indicated that it may also be found in the oral cavity, which could serve as a reservoir of the bacteria and a source of gastric reinfection. Accordingly, we aimed to study whether the oral cavity, particularly gingival pockets, are colonized by Hp and whether it could be the source of gastric reinfection. We studied 329 patients with dyspeptic symptoms (257 with chronic gastritis, 15 with gastric ulcer, and 57 with duodenal ulcer). The [13C]urea breath test (UBT), gastroscopy, and Hp culture from gastric biopsies were carried out, and material was collected from the oral cavity (gingival pocket) for bacteriological culture and genomic DNA studies. The serum was obtained for anti-Hp IgG and anti-CagA assays and saliva for anti-Hp IgA determination using the ELISA technique. Bacteria in material from gingival pockets and biopsies from the corpus and antrum of stomach of 30 DU patients before and after Hp eradication were also examined by PCR technique, using primers specific for 16S rRNA. All Hp-positive patients (276) were subjected to one week of triple therapy (omeprazole 2 x 20 mg twice a day, clarithromycin 2 x 500 mg twice a day, and metronidazole 2 x 500 mg twice a day). The measurements described above were then repeated at four weeks and six months. Bacteriological culture showed the presence of Hp in the material from oral cavity in about 50% of patients, whereas UBT, used as a gold standard, revealed gastric Hp infection in about 84% of these patients. The eradication was successful in the majority of patients (87%), but about 13% of them were still Hp positive after four weeks and about 21% after six months. Four weeks after Hp therapy, Hp was found in culture from oral samples in 23% (P < 0.05 vs initial) and after six months in 35.1%. The IgA levels recorded in saliva were in a close agreement with UBT results. Hp DNA assessed by PCR in 30 DUs before eradication of Hp was detected in 95% of antral mucosa, 90% in corpus mucosa, and in 35% of gingival pocket material, and after eradication therapy Hp DNA values fell to 25%, 20%, and 10%, respectively. In conclusion, Hp is commonly detected in the oral cavity of patients with dyspeptic symptoms, but the gastric reinfection does not appear to occur in the patients despite oral Hp colonization.
Insights
Helicobacter pylori (Hp) is frequently found in the oral cavity of patients with dyspeptic symptoms. However, the study suggests that oral Hp colonization does not lead to gastric reinfection despite eradication therapy.
Area of Science:
- Microbiology
- Gastroenterology
- Oral Medicine
Background:
- Helicobacter pylori (Hp) commonly colonizes the gastric mucosa.
- Oral cavity colonization by Hp is suspected as a reservoir for gastric reinfection.
- Understanding the role of oral Hp is crucial for effective eradication strategies.
Purpose of the Study:
- To investigate Hp colonization in the oral cavity, specifically gingival pockets.
- To determine if oral Hp serves as a source for gastric reinfection.
- To assess the persistence of oral Hp following gastric Hp eradication therapy.
Main Methods:
- Study included 329 patients with dyspeptic symptoms undergoing gastric assessments.
- Methods included [13C]urea breath test (UBT), gastroscopy, gastric biopsies, and oral cavity sampling.
- Bacteriological culture, PCR for 16S rRNA, and serological/salivary antibody assays (ELISA) were employed.
Main Results:
- Hp was detected in oral cavities of approximately 50% of patients, while gastric infection was confirmed in 84% by UBT.
- Eradication therapy was successful in most patients, but oral Hp persisted in 23% after 4 weeks and 35.1% after 6 months.
- Hp DNA levels in gingival pockets significantly decreased post-eradication, suggesting limited gastric reinfection from the oral reservoir.
Conclusions:
- Helicobacter pylori is commonly present in the oral cavity of patients with dyspeptic symptoms.
- Despite oral colonization, gastric reinfection from the oral cavity does not appear to be a significant issue.
- Oral cavity may act as a reservoir, but its role in sustained gastric Hp infection requires further investigation.
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