A potential pathogenic association between periodontal disease and Crohn's disease.
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ABSTRACT:
SUBMITTER: Imai J
PROVIDER: S-EPMC8675195 | biostudies-literature | 2021 Dec
REPOSITORIES: biostudies-literature
Publications
A potential pathogenic association between periodontal disease and Crohn's disease.
Imai Jin J Ichikawa Hitoshi H Kitamoto Sho S Golob Jonathan L JL Kaneko Motoki M Nagata Junko J Takahashi Miho M Gillilland Merritt G MG Tanaka Rika R Nagao-Kitamoto Hiroko H Hayashi Atsushi A Sugihara Kohei K Bishu Shrinivas S Tsuda Shingo S Ito Hiroyuki H Kojima Seiichiro S Karakida Kazunari K Matsushima Masashi M Suzuki Takayoshi T Hozumi Katsuto K Watanabe Norihito N Giannobile William V WV Shirai Takayuki T Suzuki Hidekazu H Kamada Nobuhiko N
JCI insight 20211208 23
Oral conditions are relatively common in patients with inflammatory bowel disease (IBD). However, the contribution of oral maladies to gut inflammation remains unexplored. Here, we investigated the effect of periodontitis on disease phenotypes of patients with IBD. In all, 60 patients with IBD (42 with ulcerative colitis [UC] and 18 with Crohn's disease [CD]) and 45 healthy controls (HCs) without IBD were recruited for this clinical investigation. The effects of incipient periodontitis on the or ...[more]
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| S-EPMC10988017 | biostudies-literature
Project description:Objective To perform a meta-analysis to evaluate studies investigating the association between ATG16L1 gene polymorphism and Crohn's disease. Methods PubMed, Embase and Web of Science databases were searched for all studies focusing on the association of ATG16L1 and Crohn's disease. Combined odds ratios with 95% confidence intervals were calculated for four genetic models (allelic model: G allele versus A allele; additive model: GG versus AA; dominant model: GA?+?GG versus AA; recessive model: GG versus GA?+?AA) using either a random effects or fixed effects model. Results A total of 47 case-control studies involving 18?638 cases and 30?181 controls were included in the final meta-analysis. There was a significant association between ATG16L1 and Crohn's disease for all four genetic models. Significant associations were also shown in subgroup analyses when stratified by study design (population- or hospital-based). Conclusion In this meta-analysis, the ATG16L1 genotype was significantly associated with the risk of developing Crohn's disease.
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Project description:The course of Crohn's disease (CD) is heterogeneous, confounding effective personalized therapy. A previous analysis of differences in gene expression between patients with versus without CD groups revealed 2 subsets of patients with CD -- a group characterized by genes more highly expressed in the colon (colon-like CD) and a group with increased expression of ileum marker genes (ileum-like CD). We compared differences in microRNAs between these groups. We performed genome-wide microRNA profile analyses of colon tissues from 18 adults with CD and 12 adults without CD (controls). We performed principal component analyses to associate levels of microRNAs with CD subtypes. Colonic epithelial cells and lamina propria immune cells were isolated from intestinal tissues and levels of microRNA 31 (miR-31) were measured by real-time quantitative PCR. We validated the differential expression of miR-31 between the subtypes by measuring miR-31 levels in an independent cohort of 32 adult patients with CD and 23 controls. We generated epithelial colonoid cultures from controls and patients with CD, and measured levels of miR-31 in crypts. We performed genome-wide microRNA profile analyses of formalin-fixed paraffin-embedded colon and ileum biopsies from 76 treatment-naive pediatric patients with CD and 51 controls (234 samples) and collected data on disease features and outcomes. In comparing miRNA expression profiles between 9 patients with colon-like CD and 9 patients with ileum-like CD, we identified 19 miRNAs with significant differences in levels. We observed a 13.5-fold difference in level of miR-31-5p between tissues from patients with colon-like vs. ileum-like CD (Padj = 1.43 x 10-18). Principal component analysis found miR-31 to be the top contributor to the variance observed. Levels of miR-31 were increased 60-fold in tissues from patients with ileum-like CD compared with controls (Padj = 2.59 × 10-51). We validated the differential expression of miR-31 between the subtypes in the independent set of tissues. Colonoids derived from patients with CD had significantly higher levels of miR-31 than colonoids derived from control tissues (day 2 P=.041 and day 6 P=.0095). Levels of miR-31 were significantly increased in colon tissues from pediatric patients with CD compared with controls (~7.8-fold, P=4.64 ×10-7) and in ileum tissues from patients with CD patients vs. controls (~1.5-fold, P=9.97 × 10-7). A high level of miR-31 in index biopsies from pediatric patients with only inflammation and no other complications at time of diagnosis associated with development of fibrostenotic ileal CD. We identified differences in miR-31 levels in colon tissues from adult and pediatric patients with CD compared with controls, and in patients with ileum-like CD compared with colon-like CD. Further studies are needed to determine the mechanisms by which miR-31 might contribute to pathogenesis of this subtype of CD, or affect response to therapy.
2018-10-01 | GSE101817 | GEO
Project description:ObjectivesStudies have suggested contradictory results on the relationship between chronic obstructive pulmonary disease (COPD) and periodontal disease (PD). The aim of this study was to determine whether PD increased the risk of COPD and COPD-related clinical events.DesignA systematic review and meta-analysis.Data sourcesPubMed, Ovid EMBASE and Ovid CENTRAL were searched from inception to 22 February 2023.Eligibility criteria for studiesWe included trials and observational studies evaluating association of PD with the risk of COPD or COPD-related events (exacerbation and mortality), with statistical adjustment for smoking.Data extraction and synthesisTwo investigators independently extracted data from selected studies using a standardised Excel file. Quality of studies was evaluated using the Newcastle-Ottawa Scale. OR with 95% CI was pooled in a random-effect model with inverse variance method.Results22 observational studies with 51 704 participants were included. Pooled analysis of 18 studies suggested that PD was weakly associated with the risk of COPD (OR: 1.20, 95% CI 1.09 to 1.32). However, in stratified and subgroup analyses, with strict adjustment for smoking, PD no longer related to the risk of COPD (adjusting for smoking intensity: OR: 1.14, 95% CI 0.86 to 1.51; smokers only: OR: 1.46, 95% CI 0.92 to 2.31; never smokers only: OR: 0.93, 95% CI 0.72 to 1.21). Moreover, PD did not increase the risk of COPD-related exacerbation or mortality (OR: 1.18, 95% CI 0.71 to 1.97) in the pooled result of four studies.ConclusionsThis study demonstrates PD confers no risk for COPD and COPD-related events when strictly adjusted by smoking. Large-scale prospective cohort studies with control of potential confounding factors are warranted to validate the present findings.
| S-EPMC10410961 | biostudies-literature
Project description:Periodontal disease may be associated with increased breast cancer risk, but studies have not considered invasive breast cancer and ductal carcinoma in situ (DCIS) separately in the same population. We assessed the relationship between periodontal disease and breast cancer in a large prospective cohort study. The Sister Study followed women without prior breast cancer ages 35 to 74 years from 2003 to 2017 (N = 49,968). Baseline periodontal disease was self-reported, and incident breast cancer was ascertained over a mean follow-up of 9.3 years. We estimated hazard ratios (HR) and 95% confidence intervals (CI) using Cox proportional hazards regression, adjusting for multiple potential confounders, including smoking status. Heterogeneity in risk for invasive breast cancer versus DCIS was also estimated. About 22% of participants reported a history of periodontal disease at baseline. A total of 3,339 incident breast cancers (2,607 invasive breast cancer, 732 DCIS) were identified. There was no clear association between periodontal disease and overall breast cancer risk (HR = 1.02; 95% CI, 0.94-1.11). However, we observed a nonstatistically significant suggestive increased risk of invasive breast cancer (HR = 1.07; 95% CI, 0.97-1.17) and decreased risk of DCIS (HR = 0.86; 95% CI, 0.72-1.04) associated with periodontal disease, with evidence for heterogeneity in the risk associations (relative HR for invasive breast cancer versus DCIS = 1.24; 95% CI, 1.01-1.52). A case-only analysis for etiologic heterogeneity confirmed this difference. We observed no clear association between periodontal disease and overall breast cancer risk. The heterogeneity in risk associations for invasive breast cancer versus DCIS warrants further exploration.
| S-EPMC7718282 | biostudies-literature
Project description:BackgroundPeriodontal disease (PD) is a chronic inflammatory oral condition with potentially important systemic sequelae. We sought to determine whether the presence of PD in patients with severe carotid disease was associated with morphological features consistent with carotid plaque instability.MethodsA total of 52 dentate patients hospitalized for carotid endarterectomy (CEA) had standardized assessments of their periodontal status, including measurements of probing pocket depth (PPD), clinical attachment level (CAL) and bleeding on probing (BoP). Carotid plaque morphology was assessed by ultrasound using the gray scale median (GSM) score and by immunohistochemistry using anti-CD68 and anti-alpha-actin antibodies, markers for macrophages and smooth muscle cells (SMCs) respectively.ResultsIn total 30/52 patients (58%) had PD. Significant associations were noted between low GSM on ultrasound and each mm in PPD (p = 0.001), each mm in CAL (p = 0.002) and with a 10% increase in BoP (p = 0.009). Using the standardized PERIO definition the association remained robust (aOR = 10.4 [95% CI:2.3-46.3], p = .002). Significant associations were also observed with high macrophage accumulation and each individual PD measure (p < 0.01 for PPD, CAL and BoP) and with the PERIO definition (aOR = 15 [95% CI:1.8-127.8], p = .01). Similarly, low SMC density was also significantly associated with individual measures of PD (p < 0.05 for PPD, CAL and BoP), but not with the PERIO definition (aOR 3.4 [95% CI:0.9-12.8], p = .07).ConclusionsThe presence of PD was significantly associated with both ultrasound and immunohistochemistry features of carotid plaque instability in patients undergoing CEA.
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