Department of Orthopedics, First Hospital of China Medical University, No.155 Nanjing North Street, Shenyang, China.
Health Sciences Institute, China Medical University, Shenyang 110122, China.
Biomed Pharmacother. 2023 Jul;163:114834. doi: 10.1016/j.biopha.2023.114834. Epub 2023 May 8.
Osteoporosis is becoming a major concern in the field of public health. The process of bone loss is insidious and does not directly induce obvious symptoms. Complications indicate an irreversible decrease in bone mass. The high-risk populations of osteoporosis, including postmenopausal women, elderly men, diabetic patients and obese individuals need regular bone mineral density testing and appropriate preventive treatment. However, the primary changes in these populations are different, increasing the difficulty of effective treatment of osteoporosis. Determining the core pathogenesis of osteoporosis helps improve the efficiency and efficacy of treatment among these populations. Oxidative stress is a common pathological state secondary to estrogen deficiency, aging, hyperglycemia and hyperlipemia. In this review, we divided oxidative stress into the direct effect of reactive oxygen species (ROS) and the reduction of antioxidant enzyme activity to discuss their roles in the development of osteoporosis. ROS initiated mitochondrial apoptotic signaling and suppressed osteogenic marker expression to weaken osteogenesis. MAPK and NF-κB signaling pathways mediated the positive effect of ROS on osteoclast differentiation. Antioxidant enzymes not only eliminate the negative effects of ROS, but also directly participate in the regulation of bone metabolism. Additionally, we also described the roles of proinflammatory factors and HIF-1α under the pathophysiological changes of inflammation and hypoxia, which provided a supplement of oxidative stress-induced osteoporosis. In conclusion, our review showed that oxidative stress was a common pathological state in a high-risk population for osteoporosis. Targeted oxidative stress treatment would greatly optimize the therapeutic schedule of various osteoporosis treatments.
骨质疏松症正成为公共卫生领域的一个主要关注点。骨质流失的过程是隐匿的，不会直接引起明显的症状。并发症表明骨量不可逆转地减少。骨质疏松症的高危人群，包括绝经后妇女、老年男性、糖尿病患者和肥胖者，需要定期进行骨矿物质密度测试和适当的预防治疗。然而，这些人群的主要变化不同，增加了骨质疏松症有效治疗的难度。确定骨质疏松症的核心发病机制有助于提高这些人群治疗的效率和效果。氧化应激是雌激素缺乏、衰老、高血糖和高脂血症等继发的常见病理状态。在这篇综述中，我们将氧化应激分为活性氧（ROS）的直接作用和抗氧化酶活性的降低，以讨论它们在骨质疏松症发展中的作用。ROS 启动了线粒体凋亡信号，并抑制成骨标志物的表达，从而削弱成骨作用。MAPK 和 NF-κB 信号通路介导了 ROS 对破骨细胞分化的正向作用。抗氧化酶不仅消除了 ROS 的负面影响，还直接参与了骨代谢的调节。此外，我们还描述了在炎症和缺氧的病理生理变化下，促炎因子和 HIF-1α的作用，为氧化应激诱导的骨质疏松症提供了补充。总之，我们的综述表明，氧化应激是骨质疏松症高危人群的一种常见病理状态。针对氧化应激的治疗将极大地优化各种骨质疏松症治疗的治疗方案。
