Noninvasive techniques for assessing skeletal changes in inflammatory arthritis: bone biomarkers.

摘要

PURPOSE OF REVIEW: Inflammatory arthritis diseases including rheumatoid arthritis (RA) are characterized by systemic bone loss and increased risk of osteoporosis and local joint bone erosion. Clinical and biologic parameters of disease activity and inflammation and radiologic findings are poorly sensitive for assessing skeletal changes. More specific biologic markers reflecting systemic quantitative and dynamic changes of bone turnover represent promising adjunctive tools. RECENT FINDINGS: More specific and well-characterized biochemical assays especially for type I collagen-based bone resorption markers have been recently developed. Prospective studies indicate that increased levels of some biochemical markers of bone resorption are associated with a more rapid progression of joint destruction in patients with early RA, independently of disease activity and inflammation parameters. This increased bone resorption associated with local bone erosion is likely to be mediated by changes in the balance of the OPG/RANK-L system (receptor activator of nuclear factor kappaB-ligand and osteoprotegerin) as suggested by the significant association of this ratio in serum and long-term radiologic progression. Besides their well-documented response to bisphosphonate treatment used as adjuvant therapy in patients with glucocorticoid-induced osteoporosis, bone markers may be useful to assess potential beneficial effects of new disease-modifying antirheumatic drugs on systemic bone loss and on progression of joint damage. SUMMARY: Recent evidence suggests that biochemical markers of bone resorption may be useful to predict progression of joint damage in RA. Together with new biochemical markers of cartilage turnover, they are likely to play a major role in assessing effects of treatment on joint damage. Their value in assessing systemic and local bone abnormalities should be explored in other inflammatory arthritis diseases such as ankylosing spondylarthritis.