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The translocation of bacteria: Inflammatory bowel disease

Dec. 22, 2022
In a meta-analysis of six eligible studies, results validated that periodontitis was significantly associated with IBD, but the mechanism was still undetermined.

Your eyes may be the window to the soul, but the mouth is the entrance to the whole body. The oral microbiome is second only to the gut microbiome in size, and all the oral bacteria can access the gut through the digestive tract. The mouth launches the regulation for our delicate ecosystem. The good news is that the gut can protect the body from invasion of oral pathogens whether through the lining of endothelial cells, stomach acid, probiotic bacteria, or immune cells. The bad news is that some pathogens still survive.

How pathogens invade and harm

Studies on mice and humans prove that oral bacteria can translocate to the gut and change its microbiota and immune defense.1 Thanks to the Human Microbiome Project, we’re learning a lot. A report in Genome Biology from the project found that oral cavity and stool bacteria overlapped in nearly half (45%) of the subjects.2

As an example, a patient with periodontal disease swallows a keystone periodontal pathogen such as Porphyromonas gingivalis (Pg), and the gram-negative beasts end up in the gut. Sadly, Pg can survive the acid in the stomach and cause significant changes in the gut microbiome.3 A host of oral bacteria has been detected in the gut, including Streptococcus species (spp), Prevotella spp, Aggregatibacter spp, Fusobacterium nucleatum, and Actinomyces spp.

Our bodies are teeming with trillions of organisms in the digestive tract. An imbalance between the good (beneficial) and bad (pathogenic) bacteria is called dysbiosis. This may bring on a small intestine bacterial overgrowth (SIBO) that can lead to a weakening of the junctions between the endothelial cells lining the gut.

This condition, called leaky gut, allows pathogens to enter the bloodstream and the rest of the body. When this happens, the immune system becomes activated to fight the foreign invaders. In a case where more and more of these foreign invaders move through the gut lining, the immune system may become hyperactive in its attempts to protect the body. A hyperactive immune system means noticeably increased inflammation. This forms the basis for autoimmune conditions such as inflammatory bowel disease (IBD). The exact cause of IBD is still unknown, but IBD is the result of a weakened immune system.4

IBD is an umbrella term that describes chronic inflammation of tissues in the digestive tract and is an immunologically mediated disease that joins a series of complex interactions such as genetics, environment, and gut microbiota. IBD affects the large and small intestines and includes Crohn's disease and ulcerative colitis. It is estimated that 3.1 million adults are stricken in the US, and IBD patients are more likely to have other chronic conditions.5 In a meta-analysis of six eligible studies, results validated that periodontitis was significantly associated with IBD, but the mechanism was still undetermined.6

Dr. Nobuhiko Kamada has studied the gut microbiome for years and notes that an overgrowth of bacteria normally found in the mouth is found in the guts of people with IBD. His research published in Cell shows two ways oral bacteria worsens gut inflammation.7

The first is periodontitis leading to an imbalance in the normally healthy microbiome found in the mouth, and an increase of bacteria that cause inflammation. Bacteria keeps moving to the gut. Mice with IBD have a weakened ability to resist the disease-causing bacteria from the mouth.

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In the second, periodontitis activates the immune system’s T cells in the mouth. These T cells travel to the gut where they exacerbate inflammation. Oral inflammation generates inflammatory T cells that migrate to the gut where—removed from their normal environment—they trigger the gut’s immune response, which worsens the disease. In a healthy gut, inflammatory and regulatory T cells work in harmony and know how to tolerate local bacteria, but the well-oiled machine is turned on its head when oral inflammation generates mostly inflammatory T cells.

How to help patients

While ulcerative colitis stays in the colon, it does have oral manifestations that can be seen as angular cheilitis, aphthous ulcers, aphthous stomatitis, dry mouth, or halitosis. Pyostomatitis vegetans is rare and usually seen in non- or ex-smokers. It’s characterized by pustules that can affect the gingiva and hard palate and are intensely red. Antibiotics are not usually beneficial, but topical treatment with corticosteroids and zinc supplementation is recommended.

Crohn’s disease affects any part of the gastrointestinal tract from the mouth to the anus. This inflammation in the digestive tract can be painful and debilitating and lead to life-threatening complications. There are two types: nonperforating and perforating or aggressive, which commonly affects women from 20 to 39 years old. Patients may experience diarrhea, fever, fatigue, weight loss, and abdominal pain. Crohn’s and ulcerative colitis are two distinct conditions and people cannot have both.

Vitamin malabsorption caused by a folic acid deficiency that is initiated by bowel inflammation can cause a red and painful tongue, glossitis, and cheilitis. Vitamin A deficiency can be revealed as hyperkeratosis of the oral mucosa, and vitamin B12 deficiency may lead to mouth ulcers. Patients may also have aphthous ulcers or deep linear ulcers in the folds between the cheek and gum, aphthous stomatitis, halitosis, oral granulomas, mucosal tags, or lip swelling.

There is no known cure, but there are therapies; however, drugs used to treat IBD can lead to dry mouth, candidiasis, hyperplasia, or a metallic taste. Steroid-based drugs used to help IBD may have an impact on bone, which could be an indication not to place implants in this population. Nonsteroidal anti-inflammatory drugs should not be prescribed as they can trigger a flare-up. It is recommended that you consult with the patient’s physician.

Gut dysbiosis occurs for many reasons—poor diet, antibiotic use, stress, poor sleep, or poor dental hygiene. We can help treat all of these areas or discuss them with our patients. IBD patients can live normal lives. When we serve as prevention strategists, we can hopefully help alleviate a small part of their burden.

Editor's note: This article appeared in the December 2022 print edition of RDH magazine. Dental hygienists in North America are eligible for a complimentary print subscription. Sign up here.


  1. Olsen I, Yamazaki K. Can oral bacteria affect the microbiome of the gut? J Oral Microbiol. 2019;11(1):1586422. doi:10.1080/20002297.2019.1586422 
  1. Segata N, Haake SK, Mannon P, et al. Composition of the adult digestive tract bacterial microbiome based on seven mouth surfaces, tonsils, throat, and stool samples. Genome Biol. 2012;13(6):R42. doi:10.1186/gb-2012-13-6-r42 
  1. Sohn J, Li L, Zhang L, et al. Porphyromonas gingivalis indirectly elicits intestinal inflammation by altering the gut microbiota and disrupting epithelial barrier function through IL9-producing CD4+T cells. Mol Oral Microbiol. 2022;37(2):42-52. doi:10.1111/omi.12359 
  1. Centers for Disease Control and Prevention. What is inflammatory bowel disease (IBD)? https://www.cdc.gov/ibd/what-is-ibd.htm Accessed 09-20-2022 
  1. People with IBD have more chronic diseases. CDC. Page last reviewed April 15, 2022. https://www.cdc.gov/ibd/features/IBD-more-chronic-diseases.html 
  1. She YY, Kong XB, Ge YP, et al. Periodontitis and inflammatory bowel disease: a meta-analysis. BMC Oral Health. 2020;20(1):67. doi:10.1186/s12903-020-1053-5 
  1. Kitamoto S, Nagao-Kitamoto H, Jiao Y, et al. The intermucosal connection between the mouth and gut in commensal pathobiont-driven colitis. Cell. 2020;182(2):447-462.e14. doi:10.1016/j.cell.2020.05.048

About the Author

Anne O. Rice, BS, RDH, CDP, FAAOSH

Anne O. Rice, BS, RDH, CDP, FAAOSH, founded Oral Systemic Seminars after almost 30 years of clinical practice and is passionate about educating the community on modifiable risk factors for dementia and their relationship to dentistry. She is a certified dementia practitioner, a longevity specialist, a fellow with AAOSH, and has consulted for Weill Cornell Alzheimer’s Prevention Clinic, FAU, and Atria Institute. Reach out to Anne at anneorice.com.

Updated May 31, 2024