Oral cavity as permanent reservoir of Helicobacter pylori and potential source of reinfection.

Recent studies in developed countries showed that neither dental plaques nor dentures are important reservoir for Helicobacter pylori (Hp), whereas studies in developing countries revealed a high prevalence of Hp in dental plaques, though elsewhere the culture of bacterium or its DNA analysis by polymerase chain reaction in the material obtained from oral cavity were not successful. This study was designed to compare the incidence of Hp in oral cavity (saliva, dental plaques and gingival pockets) using Campylobacter-like organism (CLO) test and culture and in the presence of Hp in the stomach using 14C-urea breath test (UBT), CLO-test and culture (antral biopsy specimens). Hundred dyspeptic subjects with endoscopically normal gastro-duodenal mucosa and 55 symptomatic patients with active duodenal peptic ulcer (DU) were tested for the presence of Hp. Thirty of these DU patients were also examined for presence of Hp in oral cavity and the stomach just before the start and 4 weeks after the termination of one week triple therapy (Omeprazole 20 mg bd, Clarithromycin 500 mg bd and Tinidazole 500 mg bd) when the DU was found endoscopically healed. In the group of 100 dyspeptic subjects, the Hp was detected by CLO-test in saliva, dental plaques and gingival pockets in 84%, 100% and 100% of cases and by the culture in 55%, 88% and 100%, respectively. The presence of Hp, as determined by UBT in the stomach in these subjects was 60%. Using CLO-test and culture, all (100%) out of 55 DU patients, were found to be Hp positive in the oral cavity and in 95% in the stomach. Following one week triple therapy in 30 DU patients, the Hp was still detected in oral cavity by CLO-test in all patients (100%) and by culture in 27 patients (90%), whereas in the stomach, the Hp was found by UTB and culture only in one of these patients (97% Hp eradicated). We conclude that the Polish population including dyspeptic and DU patients, the mouth is permanent reservoir of Hp and that the successful Hp eradication from the stomach by systemic therapy fails the Hp status in the oral cavity that might be a potential source of gastric reinfection in these patients.