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This study was undertaken to elucidate the mechanism by which PD<\/jats:styled-content> could induce antibodies to citrullinated peptides (ACPA<\/jats:styled-content>s), by examining the antibody response to a novel citrullinated peptide of cytokeratin 13 (CK<\/jats:styled-content>\u201013) identified in gingival crevicular fluid (GCF<\/jats:styled-content>), and comparing the response to 4 other citrullinated peptides in patients with RA<\/jats:styled-content> who were well\u2010characterized for PD<\/jats:styled-content> and smoking.<\/jats:p><\/jats:sec>Methods<\/jats:title>The citrullinomes of GCF<\/jats:styled-content> and periodontal tissue from patients with PD<\/jats:styled-content> were mapped by mass spectrometry. ACPA<\/jats:styled-content>s of CK<\/jats:styled-content>13 (cCK<\/jats:styled-content>13), tenascin\u2010C (cTNC<\/jats:styled-content>5), vimentin (cVIM<\/jats:styled-content>), \u03b1\u2010enolase (CEP<\/jats:styled-content>\u20101), and fibrinogen \u03b2 (cFIB<\/jats:styled-content>\u03b2) were examined by enzyme\u2010linked immunosorbent assay in patients with RA<\/jats:styled-content> (n = 287) and patients with osteoarthritis (n = 330), and cross\u2010reactivity was assessed by inhibition assays.<\/jats:p><\/jats:sec>Results<\/jats:title>A novel citrullinated peptide cCK<\/jats:styled-content>13\u20101 (444<\/jats:sub>TSNASGR<\/jats:styled-content>\u2010Cit\u2010TSDV<\/jats:styled-content>\u2010Cit\u2010RP<\/jats:styled-content>458<\/jats:sub>) identified in GCF<\/jats:styled-content> exhibited elevated antibody responses in RA<\/jats:styled-content> patients (24%). Anti\u2013cCK<\/jats:styled-content>13\u20101 antibody levels correlated with anti\u2013cTNC<\/jats:styled-content>5 antibody levels, and absorption experiments confirmed this was not due to cross\u2010reactivity. Only anti\u2013cCK<\/jats:styled-content>13\u20101 and anti\u2010cTNC<\/jats:styled-content>5 were associated with antibodies to the periodontal pathogen Prevotella intermedia<\/jats:italic> (P<\/jats:italic> = 0.05 and P<\/jats:italic> = 0.001, respectively), but not with antibodies to Porphyromonas gingivalis<\/jats:italic> arginine gingipains. Levels of antibodies to CEP<\/jats:styled-content>\u20101, cFIB<\/jats:styled-content>\u03b2, and cVIM<\/jats:styled-content> correlated with each other, and with smoking and shared epitope risk factors in RA.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>This study identifies 2 groups of ACPA<\/jats:styled-content> fine specificities associated with different RA<\/jats:styled-content> risk factors. One is predominantly linked to smoking and shared epitope, and the other links anti\u2013cTNC<\/jats:styled-content>5 and cCK<\/jats:styled-content>13\u20101 to infection with the periodontal pathogen P intermedia<\/jats:italic>.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.40227","type":"journal-article","created":{"date-parts":[[2017,10,30]],"date-time":"2017-10-30T18:26:37Z","timestamp":1509387997000},"page":"2303-2313","source":"Crossref","is-referenced-by-count":54,"title":["Association of Distinct Fine Specificities of Anti\u2212Citrullinated Peptide Antibodies With Elevated Immune Responses to Prevotella intermedia<\/i> in a Subgroup of Patients With Rheumatoid Arthritis and Periodontitis"],"prefix":"10.1002","volume":"69","author":[{"given":"Anja","family":"Schwenzer","sequence":"first","affiliation":[{"name":"University of Oxford Oxford 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