Inflammatory conditions linked to poor oral health, such as severe gum infections, may worsen inflammatory bowel disease (IBD) by increasing the number of bacteria and immune cells causing gut inflammation, a study has found.
The study, “The Intermucosal Connection between the Mouth and Gut in Commensal Pathobiont-Driven Colitis,” was published in the journal Cell.
Recent studies have suggested a possible link between poor oral health and certain gastrointestinal (GI) disorders, such as IBD and colorectal cancer.
For instance, periodontitis (serious gum infection) is much more common among patients with Crohn’s disease, one of the main forms of IBD, than in people without IBD. Additionally, scientists have found that in mice with both IBD and periodontitis, the severity of inflammation in the gums tends to match that seen in the bowel.
“These observations suggest the possibility that the inflammatory processes occurring at oral and gut mucosae are somehow connected,” the investigators wrote. “However, the extent to which periodontal inflammation influences gastrointestinal diseases remains to be fully elucidated.”
To explore this possible link in more detail, researchers at the University of Michigan collaborated with colleagues at the university’s School of Dentistry to study the mechanisms by which oral infections might worsen gut inflammation associated with IBD.
In their first set of experiments, they showed that severe gum inflammation can promote the growth of several species of harmful bacteria — including Klebsiella and Enterobacter — in the mouth of a mouse model of periodontitis and IBD.
The team discovered that when ingested, these bacteria can reach the gut and activate a series of pro-inflammatory signaling cascades, ultimately resulting in gut inflammation.
To confirm these findings, the researchers placed bacteria isolated from the mouth of mice with periodontitis or healthy animals into immuno-compromised mice that lacked a functional immune system. They found that animals that received bacteria from mice with periodontitis showed signs of weight loss and increased gut inflammation, compared to those that received bacteria from healthy mice.
“This exacerbation of gut inflammation driven by oral organisms that migrate to the gut has important ramifications in emphasizing to patients the critical need to promote oral health as a part of total body health and well-being,” William Giannobile, professor of dentistry and chair of the department of periodontics and oral medicine at the University of Michigan School of Dentistry, and the study’s co-author, said in a university news story.
The team also found that in addition to promoting the shuttling of harmful bacteria from the mouth to the gut, periodontitis can lead to the formation of a subset of pro-inflammatory immune T-cells, called Th17 cells, in the animals’ mouth.
When these highly reactive immune cells are ingested, they too can cause bowel inflammation, worsening the symptoms of IBD.
“Collectively, our results provide evidence that the oral and gastrointestinal mucosae are microbiologically and immunologically connected,” the researchers wrote.
“Thus, optimal oral care (e.g., removal of pathogenic oral biofilms and reduction of periodontal inflammation) could reduce the risk of IBD by limiting the expansion of pathogenic” T-cells. Likewise, inhibiting the migration of these oral T-cells “to the gut might be an alternative strategy used to block the pathogenic mouth-gut axis in the context of IBD,” the team added.
These findings may have important implications for the development of new IBD treatments, since it suggests “that clinical outcomes in IBD may be improved by monitoring oral inflammation — an intriguing concept,” said Shrinivas Bishu, MD, co-author of the study and assistant professor of gastroenterology at the university.
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