Brown Jacques P, Don-Wauchope Andrew, Douville Pierre, Albert Caroline, Vasikaran Samuel D
CHU de Quebec Research Centre, Université Laval, Québec, QC, Canada.
Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada; LifeLabs, Toronto, ON, Canada.
Clin Biochem. 2022 Nov-Dec;109-110:1-10. doi: 10.1016/j.clinbiochem.2022.09.002. Epub 2022 Sep 9.
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.
成人骨骼不断进行重塑，以修复微损伤、维持骨强度和力学性能，并保持钙稳态。骨转换标志物是成骨细胞（骨形成标志物）和破骨细胞（骨吸收标志物）的产物，可对重塑（转换）进行动态评估。特异性骨吸收转换标志物通常是骨胶原分子的降解产物（N- [NTX]和I型胶原交联C端肽 [CTX]），它们释放到循环系统中并经尿液排出；或反映破骨细胞吸收的酶活性，即抗酒石酸酸性磷酸酶 [TRACP]。特异性骨形成转换标志物包括不同的成骨细胞活性：I型胶原合成（I型前胶原N端前肽 [PINP]）、成骨细胞酶（骨特异性碱性磷酸酶 [BALP]）或骨基质蛋白 [骨钙素]。在未接受骨质疏松症治疗的个体中，吸收和形成标志物紧密相关且高度相关（r = 0.6 - 0.8）。过去曾报道过显著的生物学变异性，但随着自动化检测以及对已知会影响骨转换标志物水平的分析前和分析因素的关注，这些问题已得到很大改善。骨转换标志物在骨质疏松症的诊断、个体骨丢失、骨折或罕见并发症的预测，或药物治疗的选择中并无用处。尽管在参考区间和检测方法标准化方面仍存在问题，但骨转换标志物已被证明在阐明骨质疏松症药物在临床试验中的药效学和有效性方面是有用的。作为骨密度检测的替代方法，骨转换标志物可能有助于监测骨质疏松症治疗。
