The Gut-Health Axis: Linking Periodontal Disease and IBD

Authored by: Eden Park

Art by: Lindsay Wang

Historically, researchers and professionals have treated the oral cavity and gut microbiome as mutually exclusive systems of study. The mouth has been the domain for dentists, while the gut belongs to gastroenterologists. However, emerging evidence suggests that these ecosystems have a notable connection called the oral-gut axis. Scientists increasingly describe the mouth as the “front door” to digestive and systemic health systems through microbial translocation and immune modulation. The oral-gut axis has a significant impact on human health and disease [1], such as the relationship between periodontal disease and inflammatory bowel diseases (IBD).

For background information, the mouth is filled with over 700 different types of microbiota. The oral cavity is a complex ecosystem with accumulation of microorganisms that can form dental plaque, a colorless to yellow sticky film of bacteria that forms on teeth. It develops when bacteria in the mouth feed on starchy and sugary foods and produce an acid-producting biofilm. The plaque allows for these bacteria to survive and build oral diseases like periodontal disease by producing antigens that invade the periodontal gingival mucosa and interfere with the host immune defense system [6]. Thus, with periodontal disease, invasive antigens exacerbate an inflammatory response around the gums of the teeth, which can progress to gingivitis (swollen, bleeding gums) to periodontitis (major bone and tissue loss) [4].

Key microbes that cause periodontal disease are often from the “red complex” group, which includes Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Fusobacterium nucleatum [3]. P. gingivalis is a keystone pathogen because it has the ability to disrupt the entire microbial community and host immune system. It shifts the oral microbiome into a pathogenic ecosystem, allowing microbes like Trepomena denticola and Tennella forsythia to consistently thrive, grow, and attack itself. Furthermore, P. gingivalis creates virulence factors like gingipains (proteases) that break down host tissue and release nutrients that feed other bacteria. 

Inflammatory bowel disease (IBD) is due to the repetitive episodes of inflammation of the intestinal tract, dividing into Crohn disease and ulcerative colitis [2]. Caused by an abnormal immune response to gut microflora, scientists now have discovered that one of the causes of IBD starts from the mouth. As mentioned, certain oral bacteria such as Fusobacterium nucleatum can translocate from the mouth to the gut. Once in the intestine, these microbes can disrupt the balance of the gut microbiota (dysbiosis) by outcompeting beneficial species, increasing inflammation, and attacking the gut lining.

With an inflamed host immune system, these pathogens are able to survive and move further down the gut microbiome. Specifically, Fusobacterium nucleatum is an important bridge species, meaning it connects early to later colonizing bacteria during biofilm formation with an ability to stick to other bacteria, survive in low oxygen exposure, and adhere to intestinal walls in biofilms. They have adapted mechanisms that allow them to resist gastric acidity and bile salts by activating acid-stress responses that keep their internal pH stable and pump out excess protons. Other microbes use efflux pumps to export bile. They also modify their cell envelopes to reduce damage from bile salts, and when embedded in biofilms, these structural adaptations further help buffer against the harsh conditions of intestinal transit. These processes together amplify inflammation and may trigger IBD symptoms. 

However, this is not a one-directional relationship. Research has found that people with inflammatory bowel disease are more susceptible to periodontitis. Because of an already inflamed intestinal system in both diseases, they involve symptoms such as dysbiotic microbiota, deregulation of the immune response, and chronic inflammation in genetically susceptible individuals [5]. It is important to control both periodontal and IBD diseases as they are not curable and can grow to worse health outcomes. Patients can improve their symptoms by checking up regularly with medical professionals, and alongside those directly impacted by diseases, scientists can vastly research more of the gut-health axis and understand the human body and its overlapping connections.

References:

1. Kunath, B. J., De Rudder, C., Laczny, C. C., Letellier, E., & Wilmes, P. (2024). The oral–gut microbiome axis in health and disease. Nature Reviews Microbiology, 22(12), 791–805. https://doi.org/10.1038/s41579-024-01075-5

2. McDowell, C., Farooq, U., & Haseeb, M. (2024). Inflammatory bowel disease. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK470312/

3. Mohanty, R., Asopa, S. J., Joseph, M. D., Singh, B., Rajguru, J. P., Saidath, K., & Sharma, U. (2019). Red complex: Polymicrobial conglomerate in oral flora: A review. Journal of Family Medicine and Primary Care, 8(11), 3480–3486. https://doi.org/10.4103/jfmpc.jfmpc_759_19

4. Sedghi, L. M., Bacino, M., & Kapila, Y. L. (2021). Periodontal disease: The good, the bad, and the unknown. Frontiers in Cellular and Infection Microbiology, 11, 766944. https://doi.org/10.3389/fcimb.2021.766944

5. Zhang, Y., Qiao, D., Chen, R., Zhu, F., Gong, J., & Yan, F. (2021). The association between periodontitis and inflammatory bowel disease: A systematic review and meta-analysis. BioMed Research International, 2021, 6692420. https://doi.org/10.1155/2021/6692420

6. Zhou, T., Xu, W., Wang, Q., Jiang, C., Li, H., Chao, Y., Sun, Y., & A, L. (2023). The effect of the “oral–gut” axis on periodontitis in inflammatory bowel disease: A review of microbe and immune mechanism associations. Frontiers in Cellular and Infection Microbiology, 13, 1132420. https://doi.org/10.3389/fcimb.2023.1132420