BACKGROUND:Helicobacter pyloriis considered to be a pathogen responsible for gastritis and peptic ulcers, and a risk factor for gastric cancer. A periodontal pocket in the teeth of individuals with chronic periodontitis may function as a reservoir forH pylori.OBJECTIVE: The present study was undertaken to evaluate whether the presence ofH pyloriin the dental plaque of patients with and without periodontitis correlates with gastric involvement.METHODS: A total of 101 patients with dyspepsia were included in the present study. Subjects were divided into periodontitis and non-periodontitis groups. For the detection ofH pyloriin dental plaque, samples were collected from two teeth using a periodontal curette. Subgingival plaque was obtained by inserting two sterile paper points into periodontal pockets for 20 s. This was followed by an upper gastrointestinal endoscopy and antral biopsies.RESULTS: Sixty-five per cent of patients had dental plaque positive forH pyloriand more than 50% harboured the bacteria in their stomach. Periodontitis patients had a significantly higher percentage ofH pyloriin their dental plaque (79% versus 43%; P<0.05) and the stomach (60% versus 33%; P<0.05) than patients with no periodontitis. Additionally, 78% of patients from the periodontitis group versus only 30% from the nonperiodontitis group had a positive test result for the coexistence ofH pyloriin both dental plaque and the stomach.CONCLUSION: Patients with poor oral hygiene have a higher prevalence ofH pyloriin dental plaque and in the stomach. This finding suggests that the oral cavity may be a reservoir forH pylori,and potentially a source of transmission or reinfection.
Background Inflammatory bowel diseases (IBDs) are characterized by chronic inflammation and tissue damages in limited segments of the digestive tract. Pathogenesis in the tissue and mucosal inflammation probably differs according to disease location. Our aim was to further analyze transcriptomic profiles in different locations of IBD, differentiating ulcerative colitis (UC), colonic Crohn’s disease (CD), ileal CD, and pouchitis, with respect to normal colonic and ileal mucosa. We thus performed a meta-analysis focusing on specific transcriptomic signatures of ileal and colonic diseases. Methods We identified 5 cohorts with available transcriptomic data in ileal or colonic samples from active IBD and non-IBD control samples. The meta-analysis was performed on 1047 samples. In each cohort separately, we compared gene expression in CD ileitis and normal ileum; in CD colitis, UC, and normal colon; and finally in pouchitis and normal ileum. Results We identified specific markers of ileal (FOLH1, CA2) and colonic (REG3A) inflammation and showed that, with disease, some cells from the ileum start to express colonic markers. We confirmed by immunohistochemistry that these markers were specifically present in ileal or colonic diseases. We highlighted that, overall, colonic CD resembles UC and is distinct from ileal CD, which is in turn closer to pouchitis. Conclusions We demonstrated that ileal and colonic diseases exhibit specific signatures, independent of their initial clinical classification. This supports molecular, rather than clinical, disease stratification, and may be used to design drugs specifically targeting ileal or colonic diseases.
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