Biomarkers in Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic inflammatory autoim-mune disease that leads to severe joint destruction with deformity and irremediable disability. Early diagnosis of RA and timely initiation of treatments (synthetic and/or biological disease modifying antirheumatic drugs) are both instrumental to limit joint damage and optimize the functional outcome of patients, according to the well-known concept of a " window of opportunity " to begin the treatments. New diagnosis criteria are available since 2010, thanks to the American College of Rheumatology (ACR) and the European League Against Rheumatism (EULAR) [1], which include 2 different types of biomarkers: inflammation (CRP or ESR) and immunity (autoantibodies: rheumatoid factors (RF) and anticitrullinated peptides antibodies (ACPA)). These new criteria allow better management of patients with notably the early opportunity of treatment with methotrexate. However, a significant proportion of patients with early arthritis does not fulfil these criteria for RA and are then wrongly labelled " undifferentiated " arthritis [2]. Furthermore , among the autoantibodies family, ACPA are specific for the RA disease but lack sensitivity, unlike RF which have strong sensitivity but low specificity [3]. Thus there is still a need for new diagnosis biomarkers that would allow establishing a diagnosis of RA at the very beginning of the disease continuum, importantly before the occurrence of the first joint erosions. Which type of biomarkers do we need? Several classes of markers are available: genetic polymorphisms, proteomic markers, gene-expression analysis [4], and autoantibodies. All may be used in clinical practice since their utility was demonstrated. In this special issue of " Mediators of inflammation, " novel biomarkers in RA are described. Patrice Fardellone et al. from the University of Picardy will discuss bone remodelling markers in RA, notably for bone formation (osteocalcin, serum aminoterminal propeptide of type I collagen) as well as bone resorption (C-terminal telopeptide of type 1 collagen, pyridinoline). They discuss how such bone remodelling markers allow physicians to evaluate the effect of drugs, notably biologicals that are able to reduce inflammation and also exert a protecting effect on bones. Furthermore, bone remodelling is the result of a tilted balance towards resorption or formation and involves numerous regulatory factors such as hormones, growth factors, vitamins , and cytokines, notably osteoprotegerin (OPG) and receptor activator for nuclear factor-í µí¼…B (RANK) ligand [5]. The signalling pathway OPG/RANK/RANKL maintains the balance between the activity of osteoblasts and osteoclasts. V. Milanova et al., from the Bulgarian Academy of …