The gut microbiome has become famous in the last few years, but the oral microbiome is a frontier in microbiomics. First of all, the mouth is the starting point of digestion, the gateway to the rest of the body, and an integral player in our bodies’ well-being. Importantly, the oral microbiome may be an underappreciated influence in autoimmune and chronic conditions. Consequently, managing our oral microbiomes becomes essential for achieving our best possible health. This starts with proper oral hygiene, regular dental visits and attention to diet, posture and other factors. In this post, we will discuss how the oral microbiome features in overall body health.
A balanced ecosystem of microbes
As dentists or patients, we conventionally understand ‘proper oral hygiene’ as consistent brushing and flossing. However, new research on the oral microbiome suggests that a healthy mouth means maintaining balance between oral microbial species.
Plaque and the oral microbiome
For example, the first sign of an unhealthy oral microbiome is the build-up of plaque (or excess biofilm) on your teeth. We can control biofilm by brushing and flossing. However, oral disease may occur if we allow it to accumulate as plaque. This is because the biofilm thickens as more bacteria grow. At first, aerobic (oxygen-loving) microbes grow in a healthy layer of biofilm. But then, each new layer of biofilm cuts oxygen off from deeper layers. As a result, the environment shifts from high oxygen (aerobic) to low oxygen (anaerobic). Over time, this allows anaerobic pathogenic bacteria to take over and build a pathogenic biofilm. Eventually, the shifting composition of bacteria towards more pathogenic strains causes a state of imbalance known as dysbiosis. Dysbiosis represents a severe disruption in the balance of the oral microbiome, allowing disease-promoting bacteria to multiply and cause oral disease.
Disease and the oral microbiome
So, why are we concerned about dysbiosis? First, because new research shows that pathogenic oral bacteria may find their way into the bloodstream through our gum tissue. This aspect of an imbalanced oral microbiome may be a factor in chronic diseases, including autoimmune. So far, scientists have proposed three pathways linking oral infections to other diseases:
- Metastatic Infection: Bacteria from oral infections or dental procedures find their way into the bloodstream. From there, they spread through the body. Although usually eliminated within minutes or hours, some of these bacteria may find favorable conditions at a given site, settle down, and multiply.
- Metastatic Injury: Some bacteria can produce toxins that can cause damage to cells and tissues. These toxins may move from teeth and gums into the bloodstream, triggering injury elsewhere in the body.
- Metastatic Inflammation: Oral bacteria can produce molecules that react with our immune cells and antibodies, causing acute and chronic inflammatory reactions (1).
We can summarize all of these mechanisms with the term “leaky mouth.” This phrase suggests oral pathogens spreading out of the mouth through the bloodstream. Importantly, this has parallels with the notion of “leaky gut” in which undesirable bacteria, toxins or antigens enter the bloodstream through the intestinal wall. Similarly, an out-of-balance oral microbiome may trigger autoimmune disease of flares, just as gut dysbiosis may.
Periodontal disease: the result of an imbalanced oral microbiome
We can understand what a leaky mouth entails by exploring periodontal disease. When we have an imbalanced oral microbiome, our bodies respond by producing inflammation. If you haven’t flossed in a while, this is why your gums might be sensitive or bleed. This sensitivity is a symptom of periodontal disease. In its more severe form, periodontitis, periodontal disease advances to chronic inflammation leading to gum and bone loss.
As it turns out, periodontitis causes many pro-inflammatory mediators to spread through the body (2)(3). These cytokines can trigger inflammatory responses in the joints, heart, brain, etc. In the same vein, our bodies’ defensive response to periodontal disease may lead to cardiovascular disease, diabetes, obstructive pulmonary disease, and more (4)(2).
Periodontitis and Rheumatoid Arthritis
The list of negative outcomes related to periodontal disease is long. In particular, periodontitis may trigger autoimmune disease of flares. Take, for example, the connection between periodontal disease and rheumatoid arthritis (RA). How could the oral microbiome trigger an autoimmune disease? In RA the body attacks its own joint tissues. This causes damage to soft tissue, cartilage and eventually bone. While you might not think oral bacteria have any relation to this condition, research suggests otherwise. Studies show that people with periodontal disease are twice as likely to develop RA. Moreover, people with RA are twice as likely to lose teeth (5). Furthermore, studies show that treatment of periodontal disease relieves RA symptoms, while treatment of RA relieve periodontal disease.
Though the correlation between these two conditions is clear, the science is a little more complicated. In RA, like other autoimmune diseases, patients have more autoantibodies (antibodies that attack our own cells). In particular, this high level of autoantibodies contributes to the inflammatory feedback loop. Moreover, the amount of autoantibodies strongly correlates with the presence of certain strains of oral bacteria. In simpler terms, there is evidence showing that the oral bacteria worsens rheumatoid arthritis (5). It wouldn’t be too long of a shot to say that it is one of the causative factors behind its development as well.
Periodontitis and Cardiovascular Disease
In addition to RA, we have also identified periodontitis as a risk factor for cardiovascular disease (CVD). Though we don’t fully understand the mechanism, the spread of oral pathogens through the bloodstream likely plays a major role. For example, studies show that people who have experienced heart failure tend to have higher rates of periodontitis (6).
When looking at CVDs, we should also consider the role of inflammatory mediators in response to oral infection. These cytokines trigger immune responses throughout the body. Sometimes the immune response produce negative effects. For example, studies show that P. gingivalis may cause blood-clotting factors to accumulate and obstruct blood flow. In relation to the heart, these mediators may cause the accumulation of arterial plaque. This has clear implications for cardiovascular health because The build-up of plaque is one of the early stages of atherosclerosis (7).
Periodontitis and Chronic Obstructive Pulmonary Disease
The oral cavity’s close proximity to the respiratory tract is reason enough to explore the relationship between oral and respiratory health. In fact, recent studies show that people with periodontal disease have an increased risk of chronic obstructive pulmonary disease (COPD)
Recent research identifies two primary pathways by which oral disease may cause lung disease. Firstly, the inhalation of oral pathogens into the lungs can trigger infection or damage. Secondly, the increased adhesion of respiratory pathogens in the lungs may enable chronic infection or a chronic immune response.
Periodontitis and Cancer
Next, does periodontal disease have anything to do with cancer? Turns out, a recent follow-up study (over the course of 10 years) conducted on 68,273 adults, explored the connection between periodontal disease and cancer (9). The results showed that periodontal disease is a risk factor for higher cancer mortality (specifically in pancreatic cancer).
Though research on this topic is still in the early stages, the basis on which it stands traces back to periodontal disease and an imbalanced oral microbiome.
The bottom line: take care of your oral microbiome
In conclusion, as our understanding of the oral microbiome begins to change, our understanding of “oral health” must change as well. In addition to our daily hygiene habits, we also must consider the balance of our bacterial friends. Managing your oral microbiome is essential if you have an autoimmune disease. These bacterial populations have significant effects on the overall well-being of our bodies. Although there is still much for us to explore, there is one thing we are certain of:
Taking care of your teeth and gums is just as important as taking care of the rest of your body.
Written by: Bonnie Feldman, DDS MBA, Anthony Tung, Ellen M. Martin
References:
- Masthan M. K, Anitha N, Jacobina J. J, Babu N. A. Oral Infections Causing Systemic Diseases. Biomed Pharmacol J. 2016;9(2).
- Kim J, Amar S. Periodontal disease and systemic conditions: a bidirectional relationship. Odontology. 2006;94(1):10–21. doi:10.1007/s10266-006-0060-6
- Nair S, Faizuddin M, Dharmapalan J. Role of autoimmune responses in periodontal disease. Autoimmune Dis. 2014;2014:596824. doi:10.1155/2014/596824
- Minty, M., Canceil, T., Serino, M. et al. Oral microbiota-induced periodontitis: a new risk factor of metabolic diseases. Rev Endocr Metab Disord 20, 449–459 (2019). https://doi.org/10.1007/s11154-019-09526-8
- Marines du TE, et al., Talk to your gut: the oral-gut microbiome axis and its immunomodulatory role in the etiology of rheumatoid arthritis. FEMS Microbiology Reviews. 2019;43(1):1-18 https://doi.org/10.1093/femsre/fuy035
- Licardo D, Cannavo A, et al. Periodontal Disease: A Risk Factor for Diabetes and Cardiovascular Disease. Int. J. Mol. Sci. 2019;20(6):1414 https://doi.org/10.3390/ijms20061414
- Bingham, Clifton O., and Malini Moni. Periodontal Disease and Rheumatoid Arthritis: the Evidence Accumulates for Complex Pathobiologic Interactions. Current Opinion in Rheumatology. 2013;25(3):345–353. doi:10.1097/BOR.0b013e32835fb8ec.
- Ramesh A, et al. Chronic Obstructive Pulmonary Disease and Periodontitis – Unwinding Their Linking Mechanisms. Journal of Oral Biosciences. 2016:58(1):23-26 doi:10.1016/j.job.2015.09.001.
- Heikkilä P.,, et al. Periodontitis and Cancer Mortality: Register‐Based Cohort Study of 68,273 Adults in 10‐Year Follow‐Up. International Journal of Cancer. 2018;142(11):2244-2253. doi:10.1002/ijc.31254.
