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Over the last decade, the outlook for patients with rheumatoid arthritis (RA) has improved, but there is growing interest in preventing RA by treating individuals in pre-arthritic phases of disease. Although clinical trials in people at increased risk of RA have shown promising initial results, complete prevention of RA is not yet possible and several questions remain unanswered. Just as RA is a heterogeneous disease, consisting of at least autoantibody-positive and autoantibody-negative subsets, and perhaps additional subsets within this dichotomy, the pre-RA phase also appears heterogeneous. A range of different genetic and environmental risk factors (including smoking and professional dust) have been implicated. Clinical phenotypes in the pre-arthritis phases vary, with some people experiencing significant symptoms for prolonged periods of time, in some cases associated with imaging evidence of tenosynovitis and synovitis, while in other people clinically apparent arthritis develops without a prolonged clinical prodrome. However, not everyone with risk factors and symptoms of clinically suspect arthralgia (CSA) actually develops RA. The development of RA, at least in most people, occurs over years, with various processes occurring sequentially and the risk of RA gradually increasing over time. Yet, all observational studies and clinical trials show that a large proportion of people at risk ultimately do not develop clinically apparent synovial inflammation. Understanding which processes are at play at which points during the pre-RA phase is an important step towards precision prevention, where the goal is to alter the deleterious environmental events or to administer the right medication to the right patient at the right time in the at-risk setting, thereby reducing symptom burden in the at-risk phase and/or preventing RA or modifying the trajectory of the RA that does eventually develop so that its articular and extra-articular impacts are lessened.