The oral microbiota is modified by systemic diseases

dc.creatorTarcília Aparecida da Silva
dc.creatorDana Graves
dc.creatorJôice Dias Corrêa
dc.date.accessioned2025-04-10T19:50:44Z
dc.date.accessioned2025-09-08T23:19:31Z
dc.date.available2025-04-10T19:50:44Z
dc.date.issued2019-02
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico
dc.format.mimetypepdf
dc.identifier.doihttps://doi.org/10.1177/0022034518805739
dc.identifier.issn1544-0591
dc.identifier.urihttps://hdl.handle.net/1843/81472
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofJournal of dental research
dc.rightsAcesso Restrito
dc.subjectBacteria
dc.subjectBiofilms
dc.subjectDysbiosis
dc.subjectInflammation
dc.subjectPeriodontitis
dc.subjectPeriodontium
dc.subjectInterleukin-17
dc.subjectDiabetes mellitus
dc.subjectOsteogenesis
dc.subject.otherBacteria
dc.subject.otherBiofilm
dc.subject.otherDysbiosis
dc.subject.otherInflammation
dc.subject.otherPeriodontitis
dc.subject.otherPeriodontium
dc.titleThe oral microbiota is modified by systemic diseases
dc.typeArtigo de periódico
local.citation.epage156
local.citation.issue2
local.citation.spage148
local.citation.volume98
local.description.resumoPeriodontal 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.
local.identifier.orcidhttps://orcid.org/0000-0001-9623-7835
local.publisher.countryBrasil
local.publisher.departmentFAO - DEPARTAMENTO DE CLÍNICA
local.publisher.initialsUFMG
local.url.externahttps://journals.sagepub.com/doi/10.1177/0022034518805739?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed

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