The Oral Microbiota Is Modified by Systemic Diseases

Abstract

Periodontal diseases are initiated by bacteria that accumulate in a biofilm on the tooth surface and affect the adjacent periodontal tissue. Systemic diseases such as diabetes, rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE) increase susceptibility to destructive periodontal diseases. In human studies and in animal models, these diseases have been shown to enhance inflammation in the periodontium and increase the risk or severity of periodontitis. All 3 systemic diseases are linked to a decrease in bacterial taxa associated with health and an increase in taxa associated with disease. Although there is controversy regarding the specific oral bacterial changes associated with each disease, it has been reported that diabetes increases the levels of Capnocytophaga, Porphyromonas, and Pseudomonas, while Prevotella and Selenomonas are increased in RA and Selenomonas, Leptotrichia, and Prevotella in SLE. In an animal model, diabetes increased the pathogenicity of the oral microbiome, as shown by increased inflammation, osteoclastogenesis, and periodontal bone loss when transferred to normal germ-free hosts. Moreover, in diabetic animals, the increased pathogenicity could be substantially reversed by inhibition of IL-17, indicating that host inflammation altered the microbial pathogenicity. Increased IL-17 has also been shown in SLE, RA, and leukocyte adhesion deficiency and may contribute to oral microbial changes in these diseases. Successful RA treatment with anti-inflammatory drugs partially reverses the oral microbial dysbiosis. Together, these data demonstrate that systemic diseases characterized by enhanced inflammation disturb the oral microbiota and point to IL-17 as key mediator in this process.

Keywords: bacteria; biofilm; dysbiosis; inflammation; periodontitis; periodontium.

Figure 1.

The impact of a systemic health condition on the periodontium and associated microbiota. In periodontal health there is little inflammation and gram-positive, aerobic species predominate. With a systemic inflammatory diseases associated with increased inflammation, there is a subsequent increase in periodontal inflammation, with recruitment of more inflammatory cells favoring colonization by facultative and anaerobic bacteria and gram-negative taxa. The change in bacteria may enhance inflammation.

Figure 2.

Diabetes induces microbial changes in a murine model. Diabetes increases IL-17 expression, leading to increased periodontal inflammation and a change in bacterial composition that is more pathogenic when transferred to a germ-free host as compared with a transfer from normoglycemic animals. Inhibition of IL-17 reduces the pathogenicity of the diabetic microbiota (for details, see Xiao et al. 2017).