Abstract
For the past 30 years, early arthritis clinics have been promoted as a means of improving long-term outcomes for patients, 1 the logic being that early therapy minimises structural damage (which correlates with longer-term functional loss) induced by inflammation both locally and systemically. 2 Furthermore, there is the long-held belief in the, at least theoretical, window of opportunity whereby early intervention permits a qualitatively better outcome than the same intervention applied at a later date. 1 A recent focus on individuals at risk of rheumatoid arthritis has led to the realisation that multiple pathological mechanisms are taking place before clinical signs of arthritis—eg, objective evidence of subclinical inflammation on sensitive imaging, 3 and immunological abnormalities in T-cell subset numbers.
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