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P-117 The Subgingival Oral Microbiome in Pediatric Patients With Crohn's Disease
P-117 The Subgingival Oral Microbiome in Pediatric Patients With Crohn's Disease
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P-117 The Subgingival Oral Microbiome in Pediatric Patients With Crohn's Disease
P-117 The Subgingival Oral Microbiome in Pediatric Patients With Crohn's Disease

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P-117 The Subgingival Oral Microbiome in Pediatric Patients With Crohn's Disease
P-117 The Subgingival Oral Microbiome in Pediatric Patients With Crohn's Disease
Journal Article

P-117 The Subgingival Oral Microbiome in Pediatric Patients With Crohn's Disease

2012
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Overview
IBD is associated with a dysbiotic gut flora. As oral manifestations are commonly found in Crohn disease (CD), we hypothesized that the oral microbiome may also be dysbiotic in patients with IBD. We characterized the subgingival oral microbiota in a longitudinal cohort of pediatric patients with CD and healthy controls to determine association with disease activity.MethodsSubgingival plaque samples were obtained longitudinally from patients with CD and healthy controls at 2 time points. Samples were obtained from patients with CD prior to infliximab and at week 8 of therapy. Samples were analyzed by 16S rDNA 454 sequencing. Clinical records and diet inventories were obtained. Disease activity was measured by Pediatric Crohn Disease Activity Index (PCDAI) and fecal calprotectin (FCP).Results13 patients with CD and 13 controls were included. 85% of patients with CD demonstrated a decrease in PCDAI from severe disease, mean 37.5, to mild or quiescent disease at week 8, mean 13. There was a 77% decrease in the FCP from a mean 819, to a mean 401 at week 8. We used unweighted UniFrac to monitor changes in community membership, and found that the CD community showed greater dispersion than controls (P < 0.0001), suggestive of dysbiosis in the oral bacterial community. These alterations were observed in the absence of clinical gingivitis.Conclusion(s)This is the first study to demonstrate significant alterations in the subgingival oral microbiome in the absence of clinical gingivitis. Increased dispersion of the cohorts with CD suggests loss of regulation of the normal community. Additional analyses are underway to identify the taxa responsible for this finding. Newly diagnosed patients are being recruited to determine disease effect on the oral and gut microbiome.
Publisher
Oxford University Press