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We undertook this study to examine the independent contribution of pain centralization to the pain experience of patients with active <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A total of 263 <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content> patients with active disease underwent quantitative sensory testing (<jats:styled-content style=\"fixed-case\">QST<\/jats:styled-content>), including assessment of extraarticular pressure pain thresholds (<jats:styled-content style=\"fixed-case\">PPT<\/jats:styled-content>s), temporal summation (<jats:styled-content style=\"fixed-case\">TS<\/jats:styled-content>), and conditioned pain modulation (<jats:styled-content style=\"fixed-case\">CPM<\/jats:styled-content>). The pain experience was assessed by a pain intensity numeric rating scale and the Patient\u2010Reported Outcomes Measurement Information System pain interference computerized adaptive test. We examined associations between <jats:styled-content style=\"fixed-case\">QST<\/jats:styled-content> measures and pain intensity and pain interference. Multiple linear regression models were adjusted for demographic and clinical variables, including swollen joint count and C\u2010reactive protein level.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Patients with the lowest <jats:styled-content style=\"fixed-case\">PPT<\/jats:styled-content>s (most central dysregulation) reported higher pain intensity than patients with the highest <jats:styled-content style=\"fixed-case\">PPT<\/jats:styled-content>s (adjusted mean difference 1.02 [95% confidence interval (95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>) 0.37, 1.67]). Patients with the highest <jats:styled-content style=\"fixed-case\">TS<\/jats:styled-content> (most central dysregulation) had higher pain intensity than those with the lowest <jats:styled-content style=\"fixed-case\">TS<\/jats:styled-content> (adjusted mean difference 1.19 [95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content> 0.54, 1.84]). <jats:styled-content style=\"fixed-case\">CPM<\/jats:styled-content> was not associated with differences in pain intensity. <jats:styled-content style=\"fixed-case\">PPT<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">TS<\/jats:styled-content> were not associated with pain interference. Patients with the lowest <jats:styled-content style=\"fixed-case\">CPM<\/jats:styled-content> (most centrally dysregulated) had lower pain interference than patients with the highest <jats:styled-content style=\"fixed-case\">CPM<\/jats:styled-content> (adjusted mean difference \u22122.35 [95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content> \u22124.25, \u22120.44]).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Pain centralization, manifested by low <jats:styled-content style=\"fixed-case\">PPT<\/jats:styled-content>s and high <jats:styled-content style=\"fixed-case\">TS<\/jats:styled-content>, was associated with more intense pain. Clinicians should consider pain centralization as a contributor to pain intensity, independent of inflammation.<\/jats:p><\/jats:sec>","DOI":"10.1002\/acr.23994","type":"journal-article","created":{"date-parts":[[2019,6,4]],"date-time":"2019-06-04T13:11:13Z","timestamp":1559653873000},"page":"1122-1129","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":49,"title":["Association of Pain Centralization and Patient\u2010Reported Pain in Active Rheumatoid Arthritis"],"prefix":"10.1002","volume":"72","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3718-3886","authenticated-orcid":false,"given":"Andrew C.","family":"Heisler","sequence":"first","affiliation":[{"name":"Northwestern University  Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Song","sequence":"additional","affiliation":[{"name":"Northwestern University  Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dorothy D.","family":"Dunlop","sequence":"additional","affiliation":[{"name":"Northwestern University  Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alyssa","family":"Wohlfahrt","sequence":"additional","affiliation":[{"name":"Brigham and Women's Hospital  Boston Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"III","given":"Clifton O.","family":"Bingham","sequence":"additional","affiliation":[{"name":"Johns Hopkins University  Baltimore Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcy B.","family":"Bolster","sequence":"additional","affiliation":[{"name":"Massachusetts General Hospital  Boston"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel J.","family":"Clauw","sequence":"additional","affiliation":[{"name":"University of Michigan  Ann 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