The oral microbiome has been a topic in recent research for its potential role in systemic health. It is the second largest and most diverse microbial community in the body and contains more than 700 types of microorganisms. Dysbiosis can occur in the oral microbiome as in the gastrointestinal (GI) tract. Contributing factors may be due to certain environmental factors, genetics, stress, smoking, and antibiotic use. Recent evidence suggests that oral microbial composition and balance may be linked to certain systemic issues, including some that may lead to autoimmune activity.

Autoimmunity refers to the dysregulation of the adaptive immune system that may lead to the destruction of certain tissues or organs. Epidemiologic evidence suggests that some autoimmune issues may be increasing in prevalence.

A recently published review article by Huang and colleagues explored the potential connection between the oral microbiome and the incidence of autoimmune conditions. In the GI tract, certain microbes, such as Lactobacilli, have been shown to produce indole-3-aldehyde, which may help contribute to intestinal mucosal immune activity and the production of certain cytokines including interleukin (IL)-17 and IL-22. Oral microorganisms have been shown to induce T-helper cells in the gut-associated lymphoid tissue (GALT) in the presence of certain inflammatory conditions.

In recent laboratory studies, the potential connections between oral microbial dysbiosis and autoimmunity have been elucidated. For instance, the complement system activity associated with certain autoimmune conditions has been shown to be activated by citrullinated proteins that may be recognized by the immune system as autoimmune antigens. Porphyromonas gingivalis (P. gingivalis), a bacterium associated with the etiology of chronic periodontitis can transform arginine into citrulline in proteins. Certain other bacteria, including Aggregatibacter actinomycetemcomitans, have also been associated with periodontal health and autoimmune responses. 

The bacterium of P. gingivalis may also influence other aspects of immune function including the activity of toll-like receptors (TLRs). The main role of TLRs is to recognize potentially dangerous microbes and respond by activating signaling pathways. P. gingivalis has been shown to inhibit the protective pathway TLR2-MyD88 and activate certain harmful TLR pathways, which may in turn impair certain immune functions. P. gingivalis was found in animal studies to also disrupt gut microbial balance and increase certain markers related to the inflammatory response.

Huang and colleagues have also discussed other potential mechanisms of action associated with oral microbial balance and immune function. The authors discuss molecular mimicry; for example, Streptococcus mutans has certain structural similarities to cardiac myosin. Bacillus cereus and P. denticola may be structurally related to certain self-autoantigens. Other proposed mechanisms of action beyond the scope of this article include autoantigen overproduction, microbial translocation, and cytokine-induced amplification of autoimmunity.  

More research is needed, particularly in the clinical setting. However, evidence suggests that the balance and composition of the oral microbiome may influence certain factors related to autoimmunity. Certain micronutrients have been shown in preliminary research to help support health in the presence of an autoimmune response. In addition, some evidence suggests that certain probiotics may help support oral microbial balance.

By Dr. C Ambrose, ND, MAT