Loading…

The role of oral bacteria in inflammatory bowel disease

Over the past two decades, the importance of the microbiota in health and disease has become evident. Pathological changes to the oral bacterial microbiota, such as those occurring during periodontal disease, are associated with multiple inflammatory conditions, including inflammatory bowel disease....

Full description

Saved in:
Bibliographic Details
Published in:Nature reviews. Gastroenterology & hepatology 2021-10, Vol.18 (10), p.731-742
Main Authors: Read, Emily, Curtis, Michael A., Neves, Joana F.
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Over the past two decades, the importance of the microbiota in health and disease has become evident. Pathological changes to the oral bacterial microbiota, such as those occurring during periodontal disease, are associated with multiple inflammatory conditions, including inflammatory bowel disease. However, the degree to which this association is a consequence of elevated oral inflammation or because oral bacteria can directly drive inflammation at distal sites remains under debate. In this Perspective, we propose that in inflammatory bowel disease, oral disease-associated bacteria translocate to the intestine and directly exacerbate disease. We propose a multistage model that involves pathological changes to the microbial and immune compartments of both the oral cavity and intestine. The evidence to support this hypothesis is critically evaluated and the relevance to other diseases in which oral bacteria have been implicated (including colorectal cancer and liver disease) are discussed. This Perspective highlights an accumulating body of literature that outlines a direct role for oral-associated bacteria in inflammatory bowel disease pathogenesis. The authors propose a model by which oral-associated species might expand in the inflamed intestinal environment to exacerbate inflammation.
ISSN:1759-5045
1759-5053
DOI:10.1038/s41575-021-00488-4