Current use of bone turnover markers in the management of osteoporosis.

Jacques P Brown, Andrew Don-Wauchope, Pierre Douville, Caroline Albert, Samuel D Vasikaran

Journal: Clinical biochemistry 2022;109-110():1-10

PMID: 36096182

Abstract

The adult bone is continuously being remodelled to repair microdamage, preserve bone strength and mechanical competence as well as maintain calcium homeostasis. Bone turnover markers are products of osteoblasts (bone formation markers) and osteoclasts (bone resorption markers) providing a dynamic assessment of remodelling (turnover). Resorption-specific bone turnover markers are typically degradation products of bone collagen molecules (N- [NTX] and C-telopeptide cross-linked type 1 collagen [CTX]), which are released into the circulation and excreted in urine; or enzymatic activities reflecting osteoclastic resorption, tartrate-resistant acid phosphatase [TRACP]. Formation-specific bone turnover markers embrace different osteoblastic activities: type 1 collagen synthesis (Procollagen type I N- propeptide [PINP]), osteoblast enzymes (bone-specific alkaline phosphatase [BALP]), or bone matrix proteins [osteocalcin]. Among individuals not receiving osteoporosis treatment, resorption and formation markers are tightly linked and highly correlated (r = 0.6-0.8). Significant biological variability was reported in the past, but these issues have been greatly improved with automated assays and attention to pre-analytical and analytical factors that are known to influence bone turnover marker levels. Bone turnover markers are not useful in the diagnosis of osteoporosis, the individual prediction of bone loss, fracture, or rare complications, or in the selection of pharmacological treatment. Despite remaining issues with reference intervals and assays harmonization, bone turnover markers have proven to be useful in elucidating the pharmacodynamics and effectiveness of osteoporosis medications in clinical trials. As an alternative to BMD testing, BTMs may be useful to monitor osteoporosis therapies.

Copyright © 2022 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.

Address: CHU de Quebec Research Centre, Université Laval, Québec, QC, Canada. Electronic address: [email protected].; Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada; LifeLabs, Toronto, ON, Canada. Electronic address: [email protected].; CHU de Quebec Research Centre, Université Laval, Québec, QC, Canada. Electronic address: [email protected].; Service de biochimie, Centre hospitalier de l'Université de Montréal, Montréal, QC, Canada. Electronic address: [email protected].; Clinical Biochemistry, PathWest-Fiona Stanley Hospital, Murdoch, WA, Australia. Electronic address: [email protected].
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