Rheumatoid arthritis and periodontal disease: What are the similarities and differences?

  • Rongbin Li
    Center of Integrative Research The First Hospital of Qiqihaer City Qiqihaer Heilongjiang China
  • Cheng Tian
    Department of Orthopedic Surgery and BME‐Campbell Clinic University of Tennessee Health Science Center Memphis TN USA
  • Arnold Postlethwaite
    Division of Connective Tissue Diseases Department of Medicine University of Tennessee Health Science Center Memphis TN USA
  • Yan Jiao
    Department of Orthopedic Surgery and BME‐Campbell Clinic University of Tennessee Health Science Center Memphis TN USA
  • Franklin Garcia‐Godoy
    Bioscience Research Center College of Dentistry University of Tennessee Health Science Center Memphis TN USA
  • Debendra Pattanaik
    Division of Connective Tissue Diseases Department of Medicine University of Tennessee Health Science Center Memphis TN USA
  • Dongmei Wei
    Center of Integrative Research The First Hospital of Qiqihaer City Qiqihaer Heilongjiang China
  • Weikuan Gu
    Department of Orthopedic Surgery and BME‐Campbell Clinic University of Tennessee Health Science Center Memphis TN USA
  • Jianwei Li
    Center of Integrative Research The First Hospital of Qiqihaer City Qiqihaer Heilongjiang China

抄録

<jats:title>Abstract</jats:title><jats:p>Rheumatoid arthritis (<jats:styled-content style="fixed-case">RA</jats:styled-content>) and periodontal disease (<jats:styled-content style="fixed-case">PD</jats:styled-content>) are chronic inflammatory diseases that share similar osteoclasia, human leukocyte antigen‐<jats:styled-content style="fixed-case">DR</jats:styled-content>4 allelic genes and immunological profile, and characteristic cytokines. Smoking can contribute to more severe <jats:styled-content style="fixed-case">RA</jats:styled-content> and <jats:styled-content style="fixed-case">PD</jats:styled-content>; secretion of pro‐inflammatory mediators destroys the soft synovial membrane and periodontium, respectively. Anti‐citrullinated protein antibodies and anti‐α‐enolase antibody are characteristic of these two diseases. Some studies suggest that <jats:styled-content style="fixed-case">PD</jats:styled-content> may be associated with <jats:styled-content style="fixed-case">RA</jats:styled-content>. Anti<jats:italic>‐Porphyromonas gingivalis</jats:italic> (<jats:italic>P. gingivalis</jats:italic>) antibody, but no <jats:italic>P. gingivalis</jats:italic> bacterium can be detected in <jats:styled-content style="fixed-case">RA</jats:styled-content> patients’ joint fluid. Anti<jats:italic>‐P. gingivalis</jats:italic> antibody has been seen as a biomarker of <jats:styled-content style="fixed-case">RA</jats:styled-content>. Both diseases share some nosogenesis and common pathological pathways. However, there are differing views on the connection between the two diseases. Interferon‐inducible‐16 (<jats:styled-content style="fixed-case">IFI</jats:styled-content>16) is a genic marker of <jats:styled-content style="fixed-case">RA</jats:styled-content>; moreover, the association between <jats:styled-content style="fixed-case">IFI</jats:styled-content>16 and <jats:styled-content style="fixed-case">PD</jats:styled-content> is rare. Some studies suggest <jats:styled-content style="fixed-case">PD</jats:styled-content> is related to periodontal parameters and patient's pathological status rather than <jats:styled-content style="fixed-case">RA</jats:styled-content>. Disease frequency in men and women differ between these two diseases. The expression of interleukin‐17 (<jats:styled-content style="fixed-case">IL</jats:styled-content>‐17) receptor only associates with different genders in <jats:styled-content style="fixed-case">PD</jats:styled-content> (<jats:styled-content style="fixed-case">PD</jats:styled-content> of different sexes have different <jats:styled-content style="fixed-case">IL</jats:styled-content>‐17 expressions). Periodontal local treatment only affects clinical periodontal status, and it does not alter circulating levels of <jats:styled-content style="fixed-case">IL</jats:styled-content>‐6, tumor necrosis factor‐alpha or C‐reactive protein which are associated with <jats:styled-content style="fixed-case">RA</jats:styled-content>. This review examines the similarities and differences between these two diseases and explores possible interactions. Importantly, we will discuss whether <jats:styled-content style="fixed-case">PD</jats:styled-content> is a feature of <jats:styled-content style="fixed-case">RA</jats:styled-content> and whether this knowledge provides helpful information in future treatment of both diseases.</jats:p>

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