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Periodontal disease, Porphyromonas gingivalis, and rheumatoid arthritis: what triggers autoimmunity and clinical disease?

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Abstract

Rheumatoid arthritis, currently regarded as a complex multifactorial disease, was initially characterized as such at the turn of the 19th century. Ever since, multiple lines of investigation have attempted to elucidate the etiological factor(s) involved in disease incidence. Genes – including those risk alleles within HLA-DR4 – have been implicated but are insufficient to explain the vast majority of cases. Several environmental factors, therefore, are being studied. Among them, the role of periodontal disease and Porphyromonas gingivalis in the pathogenesis of rheumatoid arthritis has attracted both clinical and bench interest given supportive epidemiologic and mechanistic data.

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Abbreviations

ACPA:

Antibody to citrullinated protein antigens

DMARD:

Disease-modifying anti-rheumatic drug

PAD:

Peptydil arginine deiminase

RA:

Rheumatoid arthritis.

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Authors and Affiliations

  1. Department of Medicine, New York University School of Medicine and Hospital for Joint Diseases, 301 E17th Street, New York, NY, 10003, USA

    Jose U Scher & Steven B Abramson

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  1. Jose U Scher
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  2. Steven B Abramson
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Correspondence to Jose U Scher.

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The authors declare that they have no competing interests.

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Scher, J.U., Abramson, S.B. Periodontal disease, Porphyromonas gingivalis, and rheumatoid arthritis: what triggers autoimmunity and clinical disease?. Arthritis Res Ther 15, 122 (2013). https://doi.org/10.1186/ar4360

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