A review of denosumab for the treatment of osteoporosis.
A review of denosumab for the treatment of osteoporosis.
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DOI：
10.2147/ppa.s46192
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发表时间：
2014
影响因子：
2.2
通讯作者：
Tanaka S
中科院分区：
文献类型：
--
作者：
Miyazaki T;Tokimura F;Tanaka S
骨质疏松症是一种与年龄相关的全身性骨骼疾病，其特征在于低骨量和骨组织的微结构退化，从而导致骨脆性增加。骨重建涉及两种类型的细胞：成骨细胞和破骨细胞。核因子-κB受体激活因子配体（RANKL）是骨吸收破骨细胞形成和功能的关键调节因子，其细胞表面受体，核因子-κB受体激活因子（RANK），由破骨细胞前体和成熟破骨细胞表达。Denosumab是一种全人源单克隆抗RANKL抗体，可抑制RANKL与RANK结合，从而降低破骨细胞生成和成熟破骨细胞的骨吸收活性。尽管有许多药物可用于治疗骨质疏松症，但已证明地舒单抗对RANKL的抑制可显著影响骨代谢。地舒单抗似乎是一种有前景、高效、安全的肠外治疗，对骨质疏松症具有良好的依从性。此外，与现有替代品相比，地舒单抗可能是具有成本效益的治疗。因此，在本综述中，我们重点关注地舒单抗的研究以及这种治疗骨质疏松症的风险和获益。
Osteoporosis is an age-related systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility. Bone remodeling involves two types of cells: osteoblasts and osteoclasts. Receptor activator of nuclear factor-κB ligand (RANKL) is a key regulator of the formation and function of bone-resorbing osteoclasts, and its cell surface receptor, receptor activator of nuclear factor-κB (RANK), is expressed by both osteoclast precursors and mature osteoclasts. Denosumab is a fully human monoclonal anti-RANKL antibody that inhibits the binding of RANKL to RANK, thereby decreasing osteoclastogenesis and bone-resorbing activity of mature osteoclasts. Although there are many medications available for the treatment of osteoporosis, inhibition of RANKL by denosumab has been shown to significantly affect bone metabolism. Denosumab appears to be a promising, highly effective, and safe parenteral therapy with good adherence for osteoporosis. Moreover, denosumab may be cost-effective therapy compared with existing alternatives. Therefore, in this review, we focus on studies of denosumab and the risks and benefits identified for this type of treatment for osteoporosis.