Association of Chronic Periodontitis with Helicobacter pylori Infection in Stomach or Mouth: A Systematic Review and Meta-Analysis.

Helicobacter pylori (H. pylori) infection and periodontitis are both inflammatory conditions associated with systemic diseases. Researchers have attempted to investigate the correlation between them. This systematic review and meta-analyses were conducted to investigate the association of H. pylori infection in the stomach and/or in subgingival plaque and gingival crevicular fluid with chronic periodontitis. The protocol was created according to the Preferred Reporting Items for Systematic review and Meta-Analysis Protocols (PRISMA-P) statement. The study was designed according to the Cochrane criteria. A comprehensive literature search was performed in MEDLINE, Scopus, and CENTRAL, combined with hand-searching and assessment of gray literature. The meta-analysis of the included studies was made by the Review Manager (RevMan) 5.4 software. The effect measure of the outcome was odds ratios with 95% confidence intervals. Heterogeneity was assessed by chi-square and I2. Four observational studies involving 818 subjects were included in this meta-analysis. The odds of oral H. pylori presence were higher in patients with chronic periodontitis, compared to healthy controls, with an odds ratio of 1.87 (95% confidence interval 0.85-4.10; p = 0.12). The odds of the presence of H. pylori in the stomach also were higher in patients with chronic periodontitis, with an odds ratio of 1.80 (95% confidence interval 0.82-3.95; p = 0.15). There is no evidence for an association between chronic periodontitis and the prevalence of H. pylori, detected either in subgingival plaque and gingival crevicular fluid or in the stomach.

Periodontitis and Helicobacter pylori Infection: Eradication and Periodontal Therapy Combination.

OBJECTIVES: This study was aimed to assess (1) the prevalence of salivary and gastric Helicobacter pylori (HP) infection in patients with and without periodontitis, (2) the prevalence of HP infection in patients with periodontitis according to its clinical classification, (3) the effect of periodontitis treatment in patients with or without gastric HP infection, and (4) if gastric HP eradication in combination with periodontitis treatment influences periodontitis clinical outcome. MATERIALS AND METHODS: Thirty-three adults with periodontitis treated by quadrant scaling and root planning (QSRP). The simplified plaque index (PI), bleeding on probing index (BOP), probing pocket depth (PPD), and clinical attachment level (CAL) were assessed pretreatment and 3 months of posttreatment. The patients were tested for oral and gastric HP. Gastric HP (+) patients received eradication therapy. A control group of 32 periodontically healthy volunteers was tested for oral and gastric HP. Saliva samples were evaluated by real-time polymerase chain reaction (rtPCR); gastric HP was detected by urea breath test (UBT). STATISTICAL ANALYSIS: Normality of variables assessed by the Kolmogorov-Smirnov test, while the differences of pre- and post-treatment were analyzed by paired samples t-test. Differences between subgroups were compared by a Student's t-test or a Mann-Whitney U-test. Comparisons of nominal variables were made by Pearson's Chi-square test. RESULTS: No saliva samples were positive for HP. Gastric HP was detected in six patients with periodontitis and seven controls (p > 0.05). HP infection affected patients with higher disease stages and grades. All HP (+) patients underwent successful eradication treatment. All clinical periodontitis indices improved following QSRP. HP (+) patients who received QSRP as adjunctive to eradication treatment showed improvement in BOP (p < 0.001), PI (p < 0.013), and CAL (p < 0.004) compared with HP (-) patients who received QSRP alone. CONCLUSION: Periodontitis was not associated with gastric HP infection. Saliva was not a gastric HP supply reservoir. Gastric HP infection was associated with advanced stages and grades of periodontitis. Although all periodontal clinical markers improved after QSRP, BOP, PI, and CAL, they were further improved when combined with eradication treatment. Periodontal evaluation and treatment combined with HP eradication are recommended in patients with HP gastric infection.

REDD1/Autophagy Pathway Is Associated with Neutrophil-Driven IL-1ß Inflammatory Response in Active Ulcerative Colitis.

Infiltration of neutrophils into colonic mucosa has been associated with the severity of ulcerative colitis (UC). We investigated the effect of disease microenvironment on the release of neutrophil extracellular traps (NETs) as well as the involved mechanisms in NETosis and whether certain NET proteins are correlated with disease phenotype. Peripheral blood neutrophils, sera, and colonic tissue were collected from treatment-naive and mesalazine-treated patients with active UC, treatment-naive patients with active Crohn's disease, patients suffering from infectious colitis, or healthy individuals (controls). Analysis of colonic biopsy specimens and peripheral blood neutrophils for the presence of NET-related markers using immunofluorescence confocal microscopy, ELISA, immunoblotting, flow cytometry, and quantitative PCR were performed. In vitro cell and tissue culture systems were further deployed. The local inflammatory response in colon in UC, but not Crohn's disease, is characterized by the presence of NETs carrying bioactive IL-1ß and thrombogenic tissue factor. The inflammatory environment of UC is able to induce neutrophil activation, IL-1ß expression, and NET release, as shown both ex vivo and in vitro. REDD1 expression, as a mediator linking inflammation, autophagy, and NET release, was also specifically associated with the inflammatory response of UC. We show that neutrophil expression of REDD1 in colon tissue and the presence of IL-1ß in neutrophils/NETs provide candidate biomarkers for the differential diagnosis of inflammatory colitis and possible targets for the treatment of UC, suggesting that UC shares common features with autoinflammatory disorders.

Acute motor sensory polyneuropathy (AMSAN) complicating active ulcerative colitis with a patchy distribution.

We report a case of acute motor and sensory neuropathy during a flare of ulcerative colitis. A 28-year-old male presented with a flare of distal ulcerative colitis despite treatment with mesalamine enemas and suppositories simultaneously with rapidly deteriorating weakness and needle sensation in both legs. Neurological assessment showed axonal sensorimotor polyneuropathy affecting mainly the lower limbs and to a lesser extent the upper limbs. Colonoscopy revealed moderately to severe active ulcerative colitis with a patchy distribution involving the rectum and the right colon. Vitamin and folic acid levels were normal. Virological, immunological and other laboratory tests were negative except for positive anti-ganglioside antibodies (anti-GM1). Ulcerative colitis and polyneuropathy improved when patient was treated with immunosuppressive therapy (corticosteroids, immunoglobulin and azathioprine). Peripheral polyneuropathy is a rare extraintestinal manifestation of ulcerative colitis and it is probably associated with an autoimmune pathogenetic mechanism.