Effect of recent spinal cord injury on the OPG/RANKL system and its relationship with bone loss and the response to denosumab therapy

Effect of recent spinal cord injury on the OPG/RANKL system and its relationship with bone loss... Summary There is marked bone loss after spinal cord injury prospectively included. Serum OPG and RANKL levels, bone (SCI); however, its pathogenesis and clinical management re- turnover markers (PINP, bone ALP, CTX), and bone mineral main unclear. The increased circulating levels of receptor ac- density (BMD) were assessed at baseline, at 6 months of fol- tivator of nuclear factor kB ligand (RANKL) associated with low-up, prior to initiating denosumab, and 6 months after treat- bone loss shortly after SCI and the prevention of bone loss ment. The results were compared with a healthy control group. Results At baseline, SCI patients showed higher RANKL with denosumab treatment suggest a contributory role of RANKL in SCI-induced osteoporosis. levels vs. controls which were correlated with days-since-SCI Introduction Bone turnover and bone loss are markedly and total hip BMD loss at 6 months. OPG levels were similar to increased shortly after SCI. However, the pathogenesis controls at baseline. After denosumab treatment, OPG showed and clinical management of this process remain unclear, no changes, whereas RANKL levels became undetectable in especially the role of the osteoprotegerin (OPG)/RANKL 67% of patients. Patients with undetectable RANKL during system in this disorder. The aim of this study http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Osteoporosis International Springer Journals

Effect of recent spinal cord injury on the OPG/RANKL system and its relationship with bone loss and the response to denosumab therapy

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Publisher
Springer London
Copyright
Copyright © 2017 by International Osteoporosis Foundation and National Osteoporosis Foundation
Subject
Medicine & Public Health; Orthopedics; Endocrinology; Rheumatology
ISSN
0937-941X
eISSN
1433-2965
D.O.I.
10.1007/s00198-017-4090-4
Publisher site
See Article on Publisher Site

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