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Ann Rheum Dis 72:1-2 doi:10.1136/annrheumdis-2012-202650
  • Editorial

Uncoupling of disease activity and structural damage. Does it matter clinically?

  1. Boulos Haraoui
  1. Department of Rheumatology, Université de Montréal, Montreal, Canada
  1. Correspondence to Dr Boulos Haraoui, Department of Rheumatology, University of Montreal, Institut de rhumatologie de Montréal, 1551 Ontario est, Montreal, Quebec, Canada H2L 1S6; bharaoui{at}videotron.ca
  • Accepted 25 October 2012
  • Published Online First 20 November 2012

Rheumatoid arthritis (RA) is an autoimmune disease characterised by synovial inflammation that can lead to joint damage through bone and cartilage destruction, loss of function and decreased quality of life. Fortunately, over the past few years, we have witnessed major advances in the management of RA with new agents and treatment strategies that have improved outcomes and made remission become a realistic goal. True remission has been defined as a state where there is no evidence of disease activity with complete resolution of signs and symptoms as well as arrest of joint damage and disability progression. Hence, inhibition of radiographic progression has become a major therapeutic goal given its direct relationship to patient function and quality of life.1 Clinical remission can be achieved with disease-modifying antirheumatic drugs (DMARD) alone or may need a combination of DMARDs and biologic agents. Radiographic remission is more complex as we have learned from the probability plots that the mean/median change of radiographic progression is accounted for by a minority of patients who progress radiographically. Indeed, regardless of the therapy used, approximately 50% of patients will not show radiographic progression over 2–3 years; This percentage increases up to 75–85% of patients receiving combination therapy, and those who do progress, progress less than patients on methotrexate alone.2

It has long been thought that prevention of radiographic progression was achieved through the eradication of synovial inflammation, and that antitumour necrosis factor (TNF) agents were more effective at reducing structural progression through a better control of inflammation. However, recent posthoc …