ORAL CAVITY AS PERMANENT RESERVOIR OF HELICOBACTER-PYLORI AND POTENTIAL SOURCE OF REINFECTION

Recent studies in developed countries showed that neither dental plaqu es 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 fr om oral cavity were not successful. This study was designed to compare the incidence of Hp in oral cavity (saliva, dental plaques and gingiv al pockets) using Campylobacter-like organism (CLO) test and culture a nd in the presence of Hp in the stomach using C-14-urea breath test (U BT), CLO-test and culture (antral biopsy specimens). Hundred dyspeptic subjects with endoscopically normal gastro-duodenal mucosa and 55 sym ptomatic patients with active duodenal peptic ulcer (DU) were tested f or 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 star t and 4 weeks after the termination of one week triple therapy (Omepra zole 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 a nd 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 cu lture, 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 tripl e 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 permanen t reservoir of Hp and that the successful Hp eradication from the stom ach by systemic therapy fails the Hp status in the oral cavity that mi ght be a potential source of gastric reinfection in these patients.