Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Feb;98(2):148-156.
doi: 10.1177/0022034518805739. Epub 2018 Oct 25.

The Oral Microbiota Is Modified by Systemic Diseases

D T Graves  1 , J D Corrêa  2 , T A Silva  2
Affiliations
Review

The Oral Microbiota Is Modified by Systemic Diseases

D T Graves et al. J Dent Res. 2019 Feb.

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.

PubMed Disclaimer

Conflict of interest statement

The authors declare no potential conflicts of interest with respect to the authorship and/or publication of this article.

Figures

Figure 1.
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.
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).
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Abusleme L, Moutsopoulos NM. 2017. IL-17: overview and role in oral immunity and microbiome. Oral Dis. 23(7):854–865. - PMC - PubMed
    1. Aemaimanan P, Amimanan P, Taweechaisupapong S. 2013. Quantification of key periodontal pathogens in insulin-dependent type 2 diabetic and non-diabetic patients with generalized chronic periodontitis. Anaerobe. 22:64–68. - PubMed
    1. Anbalagan R, Srikanth P, Mani M, Barani R, Seshadri KG, Janarthanan R. 2017. Next generation sequencing of oral microbiota in type 2 diabetes mellitus prior to and after neem stick usage and correlation with serum monocyte chemoattractant-1. Diabetes Res Clin Pract. 130:204–210. - PubMed
    1. Arimatsu K, Yamada H, Miyazawa H, Minagawa T, Nakajima M, Ryder MI, Gotoh K, Motooka D, Nakamura S, Iida T, et al. 2014. Oral pathobiont induces systemic inflammation and metabolic changes associated with alteration of gut microbiota. Sci Rep. 4:4828. - PMC - PubMed
    1. Arora T, Bäckhed F. 2016. The gut microbiota and metabolic disease: current understanding and future perspectives. J Intern Med. 280(4):339–349. - PubMed

Publication types