OBJECTIVE: To examine the relationship of Porphyromonas gingivalis to the presence of autoantibodies in individuals at risk of rheumatoid arthritis (RA). METHODS: Study participants included the following: 1) a cohort enriched in subjects with HLA-DR4 and 2) subjects at risk of RA by virtue of having a first-degree relative with RA. None of the study subjects satisfied the American College of Rheumatology 1987 classification criteria for RA. Autoantibodies measured included anti-citrullinated protein antibody (ACPA; by second-generation anti-cyclic citrullinated peptide antibody enzyme-linked immunosorbent assay [ELISA]) and rheumatoid factor (RF; by nephelometry or ELISA for IgA, IgM, or IgG isotype). Individuals were considered autoantibody positive (n = 113) if they had ≥1 RA-related autoantibody; individuals were further categorized as high risk (n = 38) if they had ACPA or positive findings ≥2 assays for RF. Autoantibody-negative individuals (n = 171) served as a comparator group. Antibody to P gingivalis, P intermedia, and F nucleatum were measured. Associations of bacterial antibodies with group status were examined using logistic regression. RESULTS: Anti-P gingivalis concentrations were higher in high-risk (P = 0.011) and autoantibody positive group (P = 0.010) than in the autoantibody negative group. There were no group differences in anti-P intermedia or anti-F nucleatum concentrations. After multivariable adjustment, anti-P gingivalis concentrations (but not anti-P intermedia or anti-F nucleatum) were significantly associated with autoantibody-positive and high-risk status (P < 0.05). CONCLUSION: Immunity to P gingivalis, but not P intermedia or F nucleatum, is significantly associated with the presence of RA-related autoantibodies in individuals at risk of RA. These results support the hypothesis that infection with P gingivalis may play a central role in the early loss of tolerance to self antigens that occurs in the pathogenesis of RA.
OBJECTIVE: To examine the relationship of Porphyromonas gingivalis to the presence of autoantibodies in individuals at risk of rheumatoid arthritis (RA). METHODS: Study participants included the following: 1) a cohort enriched in subjects with HLA-DR4 and 2) subjects at risk of RA by virtue of having a first-degree relative with RA. None of the study subjects satisfied the American College of Rheumatology 1987 classification criteria for RA. Autoantibodies measured included anti-citrullinated protein antibody (ACPA; by second-generation anti-cyclic citrullinated peptide antibody enzyme-linked immunosorbent assay [ELISA]) and rheumatoid factor (RF; by nephelometry or ELISA for IgA, IgM, or IgG isotype). Individuals were considered autoantibody positive (n = 113) if they had ≥1 RA-related autoantibody; individuals were further categorized as high risk (n = 38) if they had ACPA or positive findings ≥2 assays for RF. Autoantibody-negative individuals (n = 171) served as a comparator group. Antibody to P gingivalis, P intermedia, and F nucleatum were measured. Associations of bacterial antibodies with group status were examined using logistic regression. RESULTS: Anti-P gingivalis concentrations were higher in high-risk (P = 0.011) and autoantibody positive group (P = 0.010) than in the autoantibody negative group. There were no group differences in anti-P intermedia or anti-F nucleatum concentrations. After multivariable adjustment, anti-P gingivalis concentrations (but not anti-P intermedia or anti-F nucleatum) were significantly associated with autoantibody-positive and high-risk status (P < 0.05). CONCLUSION: Immunity to P gingivalis, but not P intermedia or F nucleatum, is significantly associated with the presence of RA-related autoantibodies in individuals at risk of RA. These results support the hypothesis that infection with P gingivalis may play a central role in the early loss of tolerance to self antigens that occurs in the pathogenesis of RA.
Authors: J J Bonfil; F L Dillier; P Mercier; D Reviron; B Foti; R Sambuc; J M Brodeur; C Sedarat Journal: J Clin Periodontol Date: 1999-02 Impact factor: 8.728
Authors: V R Bonagura; S E Artandi; A Davidson; I Randen; N Agostino; K Thompson; J B Natvig; S L Morrison Journal: J Immunol Date: 1993-10-01 Impact factor: 5.422
Authors: Jeffrey A Sparks; Maura D Iversen; Rachel Miller Kroouze; Taysir G Mahmoud; Nellie A Triedman; Sarah S Kalia; Michael L Atkinson; Bing Lu; Kevin D Deane; Karen H Costenbader; Robert C Green; Elizabeth W Karlson Journal: Contemp Clin Trials Date: 2014-08-20 Impact factor: 2.226
Authors: Jennifer D Kinslow; Lisa K Blum; Kevin D Deane; M Kristen Demoruelle; Yuko Okamoto; Mark C Parish; Sarah Kongpachith; Lauren J Lahey; Jill M Norris; William H Robinson; V Michael Holers Journal: Arthritis Rheumatol Date: 2016-10 Impact factor: 10.995
Authors: Michelle J Ormseth; Qiong Wu; Shilin Zhao; Ryan M Allen; Joseph Solus; Quanhu Sheng; Yan Guo; Fei Ye; Marisol Ramirez-Solano; S Louis Bridges; Jeffrey R Curtis; Kasey Vickers; C Michael Stein Journal: Ann Rheum Dis Date: 2020-09-21 Impact factor: 19.103
Authors: Ritika Khandpur; Carmelo Carmona-Rivera; Anuradha Vivekanandan-Giri; Alison Gizinski; Srilakshmi Yalavarthi; Jason S Knight; Sean Friday; Sam Li; Rajiv M Patel; Venkataraman Subramanian; Paul Thompson; Pojen Chen; David A Fox; Subramaniam Pennathur; Mariana J Kaplan Journal: Sci Transl Med Date: 2013-03-27 Impact factor: 17.956