The Oral Microbiome’s Role in Promoting GI Disease

This transcript has been edited for clarity. 

Hello. I’m Dr David Johnson, professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia.

Earlier this year, I launched a series of discussions on the role of the microbiome in gastrointestinal (GI) disease. My first talk explored the esophageal microbiome. It’s available here if you haven’t had an opportunity to view it yet. Today, I want to talk about the oral microbiome, an area that I think we’re missing the boat on entirely as care providers, unless you’re a dentist. 

Why Oral Health Is Relevant to GI Health

The oral microbiome has a complex and diverse ecology. It’s made up of bacteria, fungi, viruses, and archaea. Bacterial species in the oral microbiome alone number in excess of 700. 

The oral cavity itself contains several microenvironments with distinct microbial profiles, including the lingual surface, the buccal surface, the gingiva surface, the hard and soft palate, and the hard surfaces of the tooth enamel above and below the gumline. 

Emerging data suggest that alterations in the oral pharynx may have systemic effects relevant to GI disease, which we as clinicians need to better understand. Although not the focus of this discussion, such effects in the oral microbiome have been linked to systemic diseases such as cardiovascular disease, diabetes, neurodegenerative diseases like Alzheimer’s, chronic kidney disease, cancers, and rheumatoid arthritis. 

When we think about oral health, it’s often in the form of visiting with the dentist, who reminds us that we need to brush and floss regularly. Doing so mitigates the risk for dental caries (ie, tooth decay and cavities), gingivitis, periodontal disease, and the peritonitis that causes accelerated bone resorption in later stages of severity.

It’s the association between these microbiome changes and different GI conditions that I’d like to focus on today. 

Cancer

We can go from cavities to cancer because certain bacterial organisms such as Fusobacterium nucleatum and Actinomyces odontolyticus, which are found in dental caries, are associated with GI cancers. In particular, very strong evidence has emerged showing this link in colorectal cancer (CRC). 

The proposed mechanism behind this is that gingival inflammation promotes blood flow, which in turn contributes to barrier integrity decrement. This can produce translocation of the bacteria, as well as systemic upregulation of cytokines and chemokines, which we see during systemic evaluations. 

Translocation delivers the bacteria, fungi, viruses, et cetera to another location. For example, the inflammation mediator lipopolysaccharide, which is part of the cell wall in a gram-negative bacteria, can be delivered to the tissue to mitigate processing. It’s been demonstrated that this contributes to the pathway for developing CRC via upregulation of adhesion cell-type process, activation of toll-like receptors, inductions of reactive oxygen species, and other mechanisms that ultimately result in the generation of mutation-inducing DNA changes. In this way, the association between the oropharyngeal disease state and CRC makes perfect sense. 

However, the same data would also apply for colon adenomas. In one study, the odds ratio for developing adenomas was equivalent to that of smoking. There’s also a known association between dysbiosis in the oropharynx and increased risk for gastric cancer and pancreatic cancer. 

There are also interesting new findings related to Helicobacter pylori. Not only is the prevalence of H pylori in the oral cavity concordant with the prevalence of H pylori in the gastric area, but it also appears to impact treatment response. A randomized controlled trial assessed mitigation of H pylori using a triple-therapy approach over a 10-day course, rather than the standard 14-day course. This was combined with periodontal therapy using scaling, root planing, and oral hygiene instructions. It resulted in a 12% increase in H pylori eradication.

I’m not sure that we talk about oral health in our discussions with our patients with H pylori, but it’s certainly something to consider moving forward.

Liver Disease

There is also a strong association between liver disease and inflammation arising from impairments to the oral-gut-liver axis. This has been established in longitudinal studies and is something we need to pay attention to. 

Porphyromonas gingivalis in the oropharyngeal cavity has been shown to provoke cavities and contribute to periodontal disease. Researchers have also identified the species in the brain, liver, kidney, and GI tract. A very interesting study was performed in a rabbit model that evaluated periodontal health and nonalcoholic fatty liver disease (now known as metabolic dysfunction–associated steatotic liver disease). After the rabbits were injected with P gingivalis, it accelerated inflammation and levels of gamma-glutamyl transferase, a surrogate marker for inflammatory injury. Greater fibrosis and related progression were seen. Another study in rats analyzed the injection of the same species, P gingivalis, and suggested it plays a role in disease exacerbation of nonalcoholic steatohepatitis (now known as metabolic dysfunction–associated steatohepatitis). 

These results indicate that oropharyngeal translocation risk is assuredly the real deal. It can mitigate translocation at both a local and more distant level. It may be that the products or byproducts of these bacteria in those given areas make a difference in promoting liver disease. 

Certainly, we see an incredibly high prevalence of periodontal disease among patients with cirrhosis. Dr Jasmohan Bajaj and his group at Virginia Commonwealth University published on this a few years ago. They looked at patients with cirrhosis and minimal hepatic encephalopathy, which we don’t test for very well. They were able to show that referral to a dentist to address oral hygiene and administer periodontal care resulted in marked improvement in cognitive and quality-of-life scales. 

Inflammatory Diseases

In a video from June, I highlighted two studies from Digestive Disease Week 2024 that looked at the association with oral health and dysbiosis in inflammatory bowel disease. 

The one that particularly caught my eye came from Dr Ali Keshavarzian and colleagues at Rush University Medical Center in Chicago. In assessing both oral and stool samples, they established a bidirectional effect for periodontal disease and intestinal inflammation. 

This is yet more evidence of the strong association between GI disease and the oral microbiome. 

Advising Our Patients

These data represent what I would call low-hanging fruit. Whether you’re a gastroenterologist or primary care physician, whatever your specialty or practice type, we can do better. 

Recommendations to improve dental care should begin with seeing your dentist twice a year. They’re the experts, not us. But if they’re not available owing to access or insurance-related reasons, you may be the only one to impress upon patients how important oral care and dental exams are to their health. 

Brushing twice a day, lingual brushing, dental flossing, use of antiseptics, mouthwash, toothpaste — these things are all very simple and represent good common-sense ways to promote dental health. 

When considering systemic disease and preventing its progression, maybe we should take a lead from our dental colleagues who have emphasized oral health for a long time. We can be better dental advocates, if not dental “assistants” in some regard. This isn’t about segregating out the care of our patients to other experts, but rather about recognizing how important it is to their health. 

Take a minute to synthesize these findings and prioritize them as another area of expanded care next time you see your patient. We treat so many things by essentially saying, “Take this medicine, take this injection, or take this pill.” We can act as a bridge to greater personalized care if we start to consider the relationship between GI disease and oral health.

I’m Dr David Johnson. Thanks for listening. 

David A. Johnson, MD, a regular contributor to Medscape, is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia, and a past president of the American College of Gastroenterology. His primary focus is the clinical practice of gastroenterology. He has published extensively in the internal medicine/gastroenterology literature, with principal research interests in esophageal and colon disease, and more recently in sleep and microbiome effects on gastrointestinal health and disease.