Abstract
Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease associated with potentially debilitating joint inflammation, as well as altered skeletal bone metabolism and co-morbid conditions. Early diagnosis and aggressive treatment to control disease activity offers the highest likelihood of preserving function and preventing disability. Joint inflammation is characterized by synovitis, osteitis, and/or peri-articular osteopenia, often accompanied by development of subchondral bone erosions, as well as progressive joint space narrowing. Biochemical markers of joint cartilage and bone degradation may enable timely detection and assessment of ongoing joint damage, and their use in facilitating treatment strategies is under investigation. Early detection of joint damage may be assisted by the characterization of biochemical markers that identify patients whose joint damage is progressing rapidly and who are thus most in need of aggressive treatment, and that, alone or in combination, identify those individuals who are likely to respond best to a potential treatment, both in terms of limiting joint damage and relieving symptoms. The aims of this review are to describe currently available biochemical markers of joint metabolism in relation to the pathobiology of joint damage and systemic bone loss in RA; to assess the limitations of, and need for additional, novel biochemical markers in RA and other rheumatic diseases, and the strategies used for assay development; and to examine the feasibility of advancement of personalized health care using biochemical markers to select therapeutic agents to which a patient is most likely to respond.
Highlights
It is widely acknowledged that early diagnosis of rheumatoid arthritis (RA) and aggressive treatment to control disease activity offer the highest likelihood of preserving function and preventing disability
RA is often characterized by progressive joint damage that, if not arrested by treatment, often leads to substantial limitation of function and progressive disability
It is evident that the nature of progressive joint damage varies considerably, with some RA patients experiencing more rapid progression than others, based on underlying pathobiology, levels of response to treatment, duration and stage of disease, as well as comorbidities and concomitant medications
Summary
It is widely acknowledged that early diagnosis of rheumatoid arthritis (RA) and aggressive treatment to control disease activity offer the highest likelihood of preserving function and preventing disability. With further characterization in prospective clinical trials, the CTX-II assay may provide an example that assays for neoepitopes generated by a specific combination of enzyme and matrix molecules are potentially relevant for monitoring risk of joint damage and impact of therapy. AUC, area under the curve; BAP, bone alkaline phosphatase; COMP, cartilage oligomeric protein; CTX-I, C-terminal telopeptide of collagen type I; CTX-II, C-terminal telopeptide of collagen type II; DB, double blinded; DMARD, diseasemodifying antirheumatic drug; hsCRP, high-sensitive CRP; ICTP, type I collagen; MMP, matrix metalloproteinase; MTX, methotrexate; NTX, N-terminal telopeptide of collagen type I; OPG, osteoprotegerin; PIIANP, amino terminus propeptide of type II procollagen, splice variant A; PINP, amino terminus propeptide of type I procollagen; RA, rheumatoid arthritis; RANKL, receptor activator of NF-kB ligand; RCT, randomized controlled trial; TIMP, tissue inhibitor of metalloproteinases. The primary osteoclast driver is RANKL [78], co-stimulators such as the cytokines IL-1β, IL-6 and/or TNF-α co-stimulate osteoclasts to secrete cathepsin K into the resorption lacunae [79,80], resulting in degradation of the organic
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