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The DOI matches its Crossref record; 128 of the 128 references it cites were found in a registry or an index.

The case for periodontitis in the pathogenesis of rheumatoid arthritis

Open access
Potempa, Jan, Mydel, Piotr, Koziel, Joanna·2017·Nature Reviews Rheumatology

Abstract

Rheumatoid arthritis (RA), an autoimmune disease that affects ∼1% of the human population, is driven by autoantibodies that target modified self-epitopes, whereas ∼11% of the global adult population are affected by severe chronic periodontitis, a disease in which the commensal microflora on the tooth surface is replaced by a dysbiotic consortium of bacteria that promote the chronic inflammatory destruction of periodontal tissue. Despite differences in aetiology, RA and periodontitis are similar in terms of pathogenesis; both diseases involve chronic inflammation fuelled by pro-inflammatory cytokines, connective tissue breakdown and bone erosion. The two diseases also share risk factors such as smoking and ageing, and have strong epidemiological, serological and clinical associations. In light of the ground-breaking discovery that Porphyromonas gingivalis, a pivotal periodontal pathogen, is the only human pathogen known to express peptidylarginine deiminase, an enzyme that generates citrullinated epitopes that are recognized by anti-citrullinated protein antibodies, a new paradigm is emerging. In this Review, the clinical and experimental evidence supporting this paradigm is discussed and the potential mechanisms involved in linking periodontitis to RA are presented.

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Research works printed but not linked: 4

  1. Mankia, K. & Emery, P. Is localized autoimmunity the trigger for rheumatoid arthritis? Unravelling new targets for prevention. Discov. Med. 20, 129–135 (2015).
  2. Auger, I., Martin, M., Balandraud, N. & Roudier, J. Rheumatoid arthritis-specific autoantibodies to peptidyl arginine deiminase type 4 inhibit citrullination of fibrinogen. Arthritis Rheum. 62, 126–131 (2010). · doi:10.1002/art.27230
  3. Schwenzer, A. et al. Identification of an immunodominant peptide from citrullinated tenascin-C as a major target for autoantibodies in rheumatoid arthritis. Ann. Rheum. Dis. 75, 1876–1883 (2016). · doi:10.1136/annrheumdis-2015-208495
  4. Romero-Sanchez, C. et al. Is the treatment with biological or non-biological DMARDS a modifier of periodontal condition in patients with rheumatoid arthritis? Curr. Rheumatol. Rev. http://dx.doi.org/10.2174/1573397113666170407161520 (2017). · doi:10.2174/1573397113666170407161520

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Metadata

Authors
Potempa, J., Mydel, P., & Koziel, J.
Venue
Nature Reviews Rheumatology
Published
2017-08-24
Volume
13
Issue
10
Pages
606-620
ISSN
  • 1759-4790 (ISSN-L)
  • 1759-4804
OpenAlex
W2745725076
Cited by
437
References
128
FWCI
6.92
Type
journal article
Language
en
Open access
green
Licence
www.springer.com/tdm (tdm)

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CoChat. (2026). Citation check: The case for periodontitis in the pathogenesis of rheumatoid arthritis. https://app.cochat.ai/papers/10.1038/nrrheum.2017.132
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Potempa, J., Mydel, P., & Koziel, J. (2017). The case for periodontitis in the pathogenesis of rheumatoid arthritis. Nature Reviews Rheumatology. https://doi.org/10.1038/nrrheum.2017.132

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