Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Department of Medicine, Fu Jen Catholic University, Hospital & Cardinal-Tien Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City, Taiwan.
Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Clin Chim Acta. 2018 Sep;484:179-191. doi: 10.1016/j.cca.2018.05.035. Epub 2018 May 18.
Osteoporosis is a systemic skeletal disorder characterized by a decrease in bone mass and microarchitectural deterioration of bone tissue. The World Health Organization has defined osteoporosis as a decrease in bone mass (50%) and bony quality (50%). Vitamin D, a steroid hormone, is crucial for skeletal health and in mineral metabolism. Its direct action on osteoblasts and osteoclasts and interaction with nonskeletal tissues help in maintaining a balance between bone turnover and bone growth. Vitamin D affects the activity of osteoblasts, osteoclasts, and osteocytes, suggesting that it affects bone formation, bone resorption, and bone quality. At physiological concentrations, active vitamin D maintains a normal rate of bone resorption and formation through the RANKL/OPG signal. However, active vitamin D at pharmacological concentration inhibits bone resorption at a higher rate than that of bone formation, which influences the bone quality and quantity. Nutritional vitamin D rather than active vitamin D activates osteoblasts and maintains serum 25(OH)D concentration. Despite many unanswered questions, much data support nutritional vitamin D use in osteoporosis patients. This article emphasizes the role of nutritional vitamin D replacement in different turnover status (high or low bone turnover disorders) of osteoporosis together with either anti-resorptive (Bisphosphonate, Denosumab et.) or anabolic (Teriparatide) agents when osteoporosis persists.
骨质疏松症是一种全身性骨骼疾病,其特征是骨量减少和骨组织微观结构恶化。世界卫生组织将骨质疏松症定义为骨量减少(50%)和骨质量减少(50%)。维生素 D 是一种类固醇激素,对骨骼健康和矿物质代谢至关重要。它对成骨细胞和破骨细胞的直接作用以及与非骨骼组织的相互作用有助于维持骨转换和骨生长之间的平衡。维生素 D 影响成骨细胞、破骨细胞和骨细胞的活性,表明它影响骨形成、骨吸收和骨质量。在生理浓度下,活性维生素 D 通过 RANKL/OPG 信号维持正常的骨吸收和形成速率。然而,药理浓度的活性维生素 D 抑制骨形成的速率高于骨吸收的速率,从而影响骨质量和数量。营养性维生素 D 而不是活性维生素 D 激活成骨细胞并维持血清 25(OH)D 浓度。尽管存在许多未解决的问题,但大量数据支持骨质疏松症患者使用营养性维生素 D。本文强调了在骨质疏松症患者中,无论骨转换状态(高转换或低转换骨代谢疾病)如何,营养性维生素 D 替代治疗与抗吸收(双膦酸盐、地舒单抗等)或合成代谢(特立帕肽)药物联合应用的作用,当骨质疏松症持续存在时。