Early treatment of rheumatoid arthritis (RA) results in more effective disease suppression and can be key to a successful patient response. However, not all people who exhibit early synovitis develop RA; for example, in some, synovial inflammation resolves spontaneously. 1 The factors that drive RA development remain unclear and clinical tools to predict RA development are imperfect.

Tenascin-C is a proinflammatory matrix molecule that is absent from healthy joints but highly expressed in the joints of patients with RA. 2 3 We identified an immunodominant peptide in citrullinated tenascin-C, cTNC5, antibodies against which are detected in around half of the patients with RA, and can be found years before disease onset in some individuals. 4 Here, we sought to determine if anti-cTNC5 antibodies can discriminate among people with early synovial inflammation those who develop RA and those with other outcomes. Sera from 263 patients in the Birmingham early arthritis cohort were analysed. Patients were disease-modifying antirheumatic drug (DMARD) naïve with clinically apparent synovitis of≥ 1 joint and with inflammatory joint symptoms of≤ 3 months’ duration. Patients were followed for 18 months to ensure development of full disease phenotype and to allow any resolving arthritis time to resolve. At 18 months, patients were assigned to the following outcome categories: persistent RA according to the American College of Rheumatology (ACR) 2010 criteria 5(RA, n= 101), persistent non-RA arthritis (PNRA, n= 66) and resolving arthritis (no clinically apparent joint swelling, no DMARD/steroid use in the previous 3 months, n= 96). Demographic and clinical parameters were