OBJECTIVE: To investigate the prevalence of Helicobacter pylori (Hp) in the oral cavity of gastritis patients and analyze the genotype similarity of Hp in the oral cavity with that in the stomach. METHODS: A total of 384 plaque samples were collected from 32 patients with chronic gastritis and chronic periodontitis, one supragingival plaque sample and one subgingival plaque sample from one tooth, totally 6 teeth having been examined for one patient. Gastric biopsy specimens were collected by gastroscopy, four pieces of specimen for one patient, to undergo rapid urease test, histopathology, and Warthin-Starry silver staining. PCR assay was conducted on each specimen with primers based on the sequences of urease C gene and cag A gene specific to Hp to amplify the 294-bp and 400-bp DNA fragments. The identity of amplified products was confirmed by restriction endonuclease digestion. Two PCR positive products (Hp urease C gene 294 bp fragments) from the dental plaque samples and one gastric biopsy specimen from one of the four patients in the same family, totalling 12 specimens, were further examined by single-strand conformation polymorphism (SSCP). RESULTS: Twenty-seven patients (84.4 %) had at least one Hp positive dental plaque sample. In total, 113 (29.4%) of the 384 tested samples were urease C gene positive and 9 (2.3%) were positive for both urease C gene and cag A gene. The Hp positive rate was significantly higher in subgingival plaque (71/192, 37%) than in supragingival plaque (42/192, 21.9 %) (P < 0.01). The Hp positive rate in dental plaque was 57.1% (48/84) at the gingiva with the probing depth (PD) >/= 4 mm, significantly higher than that at the gingiva with the PD < 4 mm (34.3%, 37/108,P < 0.05). The Hp positive rate in the specimens of gastric mucosa was 96.7% (31/32). The Hp in the 12 dental plaque specimens and gastric biopsy specimens from the 4 patients in the same family had 3 banding patterns all together. One of the patients had at least one identical banding pattern in both the plaque specimens and gastric biopsy specimens. One specific banding pattern was found in the Hp from the dental plaques of all 4 patients. In one patient, the SSCP banding pattern in the Hp from dental plaque was inconsistent with that from gastric biopsy specimens. CONCLUSION: Hp exists in the oral cavity of gastritis patients. Oral Hp infection may be an important source of gastric Hp infection. Familial clustering and oral-oral transmission of Hp infection exist.
OBJECTIVE: To investigate the prevalence of Helicobacter pylori (Hp) in the oral cavity of gastritispatients and analyze the genotype similarity of Hp in the oral cavity with that in the stomach. METHODS: A total of 384 plaque samples were collected from 32 patients with chronic gastritis and chronic periodontitis, one supragingival plaque sample and one subgingival plaque sample from one tooth, totally 6 teeth having been examined for one patient. Gastric biopsy specimens were collected by gastroscopy, four pieces of specimen for one patient, to undergo rapid urease test, histopathology, and Warthin-Starry silver staining. PCR assay was conducted on each specimen with primers based on the sequences of urease C gene and cag A gene specific to Hp to amplify the 294-bp and 400-bp DNA fragments. The identity of amplified products was confirmed by restriction endonuclease digestion. Two PCR positive products (Hp urease C gene 294 bp fragments) from the dental plaque samples and one gastric biopsy specimen from one of the four patients in the same family, totalling 12 specimens, were further examined by single-strand conformation polymorphism (SSCP). RESULTS: Twenty-seven patients (84.4 %) had at least one Hp positive dental plaque sample. In total, 113 (29.4%) of the 384 tested samples were urease C gene positive and 9 (2.3%) were positive for both urease C gene and cag A gene. The Hp positive rate was significantly higher in subgingival plaque (71/192, 37%) than in supragingival plaque (42/192, 21.9 %) (P < 0.01). The Hp positive rate in dental plaque was 57.1% (48/84) at the gingiva with the probing depth (PD) >/= 4 mm, significantly higher than that at the gingiva with the PD < 4 mm (34.3%, 37/108,P < 0.05). The Hp positive rate in the specimens of gastric mucosa was 96.7% (31/32). The Hp in the 12 dental plaque specimens and gastric biopsy specimens from the 4 patients in the same family had 3 banding patterns all together. One of the patients had at least one identical banding pattern in both the plaque specimens and gastric biopsy specimens. One specific banding pattern was found in the Hp from the dental plaques of all 4 patients. In one patient, the SSCP banding pattern in the Hp from dental plaque was inconsistent with that from gastric biopsy specimens. CONCLUSION:Hp exists in the oral cavity of gastritispatients. Oral Hp infection may be an important source of gastric Hp infection. Familial clustering and oral-oral transmission of Hp infection exist.