Published online Sep 21, 2016. doi: 10.3748/wjg.v22.i35.7963
Peer-review started: April 4, 2016
First decision: May 30, 2016
Revised: June 29, 2016
Accepted: August 1, 2016
Article in press: August 1, 2016
Published online: September 21, 2016
Processing time: 169 Days and 15.1 Hours
Periodontal disease and inflammatory bowel disease (IBD) are both chronic inflammatory diseases. Their pathogenesis is mediated by a complex interplay between a dysbiotic microbiota and the host immune-inflammatory response, and both are influenced by genetic and environmental factors. This review aimed to provide an overview of the evidence dealing with a possible pathogenic interaction between periodontal disease and IBD. There seems to be an increased prevalence of periodontal disease in patients with IBD when compared to healthy controls, probably due to changes in the oral microbiota and a higher inflammatory response. Moreover, the induction of periodontitis seems to result in gut dysbiosis and altered gut epithelial cell barrier function, which might contribute to the pathogenesis of IBD. Considering the complexity of both periodontal disease and IBD, it is very challenging to understand the possible pathways involved in their coexistence. In conclusion, this review points to a complex pathogenic interaction between periodontal disease and IBD, in which one disease might alter the composition of the microbiota and increase the inflammatory response related to the other. However, we still need more data derived from human studies to confirm results from murine models. Thus, mechanistic studies are definitely warranted to clarify this possible bidirectional association.
Core tip: The prevalence of periodontal disease seems to be increased in patients with inflammatory bowel disease (IBD). Moreover, the induction of periodontitis seems to result in gut dysbiosis and altered gut epithelial cell barrier function. This review points to a complex pathogenic interaction between periodontal disease and IBD, in which one disease might alter the composition of the microbiota and increase the inflammatory response related to the other disease.