Host and bacterial factors linking periodontitis and rheumatoid arthritis
Observations from numerous clinical, epidemiological and serological studies link periodontitis with severity and progression of rheumatoid arthritis. The strong association is observed despite totally different aetiology of these two diseases, periodontitis being driven by dysbiotic microbial flora...
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Published in | Frontiers in immunology Vol. 13; p. 980805 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Media S.A
25.08.2022
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Subjects | |
Online Access | Get full text |
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Summary: | Observations from numerous clinical, epidemiological and serological studies link periodontitis with severity and progression of rheumatoid arthritis. The strong association is observed despite totally different aetiology of these two diseases, periodontitis being driven by dysbiotic microbial flora on the tooth surface below the gum line, while rheumatoid arthritis being the autoimmune disease powered by anti-citrullinated protein antibodies (ACPAs). Here we discuss genetic and environmental risk factors underlying development of both diseases with special emphasis on bacteria implicated in pathogenicity of periodontitis. Individual periodontal pathogens and their virulence factors are argued as potentially contributing to putative causative link between periodontal infection and initiation of a chain of events leading to breakdown of immunotolerance and development of ACPAs. In this respect peptidylarginine deiminase, an enzyme unique among prokaryotes for
, is elaborated as a potential mechanistic link between this major periodontal pathogen and initiation of rheumatoid arthritis development. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 ORCID: Katarzyna Gawron, orcid.org/0000-0003-3430-6270; Jan Potempa, orcid.org/0000-0002-3600-7461 Reviewed by: Kevin Sheng-Kai Ma, University of Pennsylvania, United States; Anders Johansson, Umeå University, Sweden This article was submitted to Inflammation, a section of the journal Frontiers in Immunology Edited by: James Cheng-Chung Wei, Chung Shan Medical University Hospital, Taiwan |
ISSN: | 1664-3224 1664-3224 |
DOI: | 10.3389/fimmu.2022.980805 |