Department of Physical Medicine and Rehabilitation, Mackay Memorial Hospital, Taipei 104, Taiwan.
Department of Mechanical Engineering, National Yang Ming Chiao Tung University, Hsinchu 300, Taiwan.
Int J Mol Sci. 2022 Jan 25;23(3):1376. doi: 10.3390/ijms23031376.
Osteoporosis is a serious health issue among aging postmenopausal women. The majority of postmenopausal women with osteoporosis have bone loss related to estrogen deficiency. The rapid bone loss results from an increase in bone turnover with an imbalance between bone resorption and bone formation. Osteoporosis can also result from excessive glucocorticoid usage, which induces bone demineralization with significant changes of spatial heterogeneities of bone at microscale, indicating potential risk of fracture. This review is a summary of current literature about the molecular mechanisms of actions, the risk factors, and treatment of estrogen deficiency related osteoporosis (EDOP) and glucocorticoid induced osteoporosis (GIOP). Estrogen binds with estrogen receptor to promote the expression of osteoprotegerin (OPG), and to suppress the action of nuclear factor-κβ ligand (RANKL), thus inhibiting osteoclast formation and bone resorptive activity. It can also activate Wnt/β-catenin signaling to increase osteogenesis, and upregulate BMP signaling to promote mesenchymal stem cell differentiation from pre-osteoblasts to osteoblasts, rather than adipocytes. The lack of estrogen will alter the expression of estrogen target genes, increasing the secretion of IL-1, IL-6, and tumor necrosis factor (TNF). On the other hand, excessive glucocorticoids interfere the canonical BMP pathway and inhibit Wnt protein production, causing mesenchymal progenitor cells to differentiate toward adipocytes rather than osteoblasts. It can also increase RANKL/OPG ratio to promote bone resorption by enhancing the maturation and activation of osteoclast. Moreover, excess glucocorticoids are associated with osteoblast and osteocyte apoptosis, resulting in declined bone formation. The main focuses of treatment for EDOP and GIOP are somewhat different. Avoiding excessive glucocorticoid use is mandatory in patients with GIOP. In contrast, appropriate estrogen supplement is deemed the primary treatment for females with EDOP of various causes. Other pharmacological treatments include bisphosphonate, teriparatide, and RANKL inhibitors. Nevertheless, more detailed actions of EDOP and GIOP along with the safety and effectiveness of medications for treating osteoporosis warrant further investigation.
骨质疏松症是绝经后女性面临的严重健康问题。大多数患有骨质疏松症的绝经后妇女存在与雌激素缺乏相关的骨质流失。这种快速的骨质流失是由于骨转换增加导致的,其特点是骨吸收和骨形成之间的不平衡。骨质疏松症也可能由糖皮质激素的过度使用引起,这种过度使用会导致骨脱矿质,导致微观尺度上骨空间异质性发生显著变化,表明骨折的潜在风险。本文综述了目前关于雌激素缺乏相关性骨质疏松症(EDOP)和糖皮质激素诱导性骨质疏松症(GIOP)的作用机制、危险因素和治疗的文献。雌激素与雌激素受体结合,促进骨保护素(OPG)的表达,抑制核因子-κβ配体(RANKL)的作用,从而抑制破骨细胞的形成和骨吸收活性。它还可以激活 Wnt/β-catenin 信号通路,增加成骨作用,并上调 BMP 信号通路,促进间充质干细胞从前成骨细胞向成骨细胞分化,而不是向脂肪细胞分化。雌激素的缺乏会改变雌激素靶基因的表达,增加白细胞介素-1(IL-1)、白细胞介素-6(IL-6)和肿瘤坏死因子(TNF)的分泌。另一方面,过量的糖皮质激素会干扰经典的 BMP 途径,并抑制 Wnt 蛋白的产生,导致间充质祖细胞向脂肪细胞而不是成骨细胞分化。它还可以通过增强破骨细胞的成熟和激活来增加 RANKL/OPG 比值,促进骨吸收。此外,过量的糖皮质激素与成骨细胞和破骨细胞凋亡有关,导致骨形成减少。EDOP 和 GIOP 的治疗重点略有不同。在 GIOP 患者中,避免过度使用糖皮质激素是强制性的。相比之下,对于各种原因导致的 EDOP 女性患者,适当的雌激素补充被认为是主要的治疗方法。其他药物治疗包括双膦酸盐、特立帕肽和 RANKL 抑制剂。然而,EDOP 和 GIOP 的更详细作用以及治疗骨质疏松症药物的安全性和有效性需要进一步研究。