{"title":"缺镁对骨骼健康的影响","authors":"N. Diedukh, N. Grygorieva, A. Musiienko","doi":"10.15674/0030-598720234121-127","DOIUrl":null,"url":null,"abstract":"Objective. To assess the impact of magnesium deficiency on bone metabolism based on an analytical analysis of current literature, as well as to systematize data on the impact of magnesium deficiency on the development of osteoporosis, bone regeneration, and to consider it as a risk factor for fracture. Methods. The review is based on the analysis of literature sources from PubMed, Scopus, Web of Science, Cochrane Library, Google, Google Scholar, and RLNS. The search was conducted by keywords: magnesium, deficiency, magnesium and bone tissue, magnesium and osteoporosis, magnesium and fractures, magnesium and bone regeneration. Results. Magnesium is a key element in the metabolic and regulatory processes of the body. Its effects on bone tissue are direct and indirect. The direct magnesium effect on genes involved in osteogenesis is accompanied by proliferation of mesenchymal stem cells and osteoblasts, but magnesium deficiency leads to their reduction and apoptosis. In case of magnesium deficiency, the number and activity of osteoclasts increases. Magnesium regulates bone mineralization in a concentration-dependent manner. Magnesium deficiency increases bone resorption and affects osteopenia and osteoporosis, which can occur indirectly through decreased vitamin D levels, increased biosynthesis of parathyroid hormone, increased oxidative stress and biosynthesis of proinflammatory cytokines. However, data on bone mineral density at different skeletal sites in magnesium deficiency are ambiguous. Magnesium deficiency is considered a risk factor for fracture. It is of great importance for bone regeneration, affecting in various ways: it stimulates the proliferation and differentiation of mesenchymal stem cells and osteoblasts, periosteum cells, increases the movement of osteoblasts to the area of traumatic bone injury, and activates signaling pathways. At the early stage of regeneration magnesium has a positive effect on macrophages, its specificity of action is inhibition of transformation of M2 macrophages into M1 at the tissue-specific stage of regeneration. One of the mechanisms stimulating regeneration may be the effect of magnesium on axons, release and increase of calcitonin-related polypeptide α. Conclusions. Since hypomagnesemia is a potentially modifiable factor, this opens up prospects for maintaining bone health and requires further research in this area.","PeriodicalId":137495,"journal":{"name":"ORTHOPAEDICS TRAUMATOLOGY and PROSTHETICS","volume":" 10","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Effect of magnesium deficiency on bone health\",\"authors\":\"N. Diedukh, N. Grygorieva, A. Musiienko\",\"doi\":\"10.15674/0030-598720234121-127\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Objective. To assess the impact of magnesium deficiency on bone metabolism based on an analytical analysis of current literature, as well as to systematize data on the impact of magnesium deficiency on the development of osteoporosis, bone regeneration, and to consider it as a risk factor for fracture. Methods. The review is based on the analysis of literature sources from PubMed, Scopus, Web of Science, Cochrane Library, Google, Google Scholar, and RLNS. The search was conducted by keywords: magnesium, deficiency, magnesium and bone tissue, magnesium and osteoporosis, magnesium and fractures, magnesium and bone regeneration. Results. Magnesium is a key element in the metabolic and regulatory processes of the body. Its effects on bone tissue are direct and indirect. The direct magnesium effect on genes involved in osteogenesis is accompanied by proliferation of mesenchymal stem cells and osteoblasts, but magnesium deficiency leads to their reduction and apoptosis. In case of magnesium deficiency, the number and activity of osteoclasts increases. Magnesium regulates bone mineralization in a concentration-dependent manner. Magnesium deficiency increases bone resorption and affects osteopenia and osteoporosis, which can occur indirectly through decreased vitamin D levels, increased biosynthesis of parathyroid hormone, increased oxidative stress and biosynthesis of proinflammatory cytokines. However, data on bone mineral density at different skeletal sites in magnesium deficiency are ambiguous. Magnesium deficiency is considered a risk factor for fracture. It is of great importance for bone regeneration, affecting in various ways: it stimulates the proliferation and differentiation of mesenchymal stem cells and osteoblasts, periosteum cells, increases the movement of osteoblasts to the area of traumatic bone injury, and activates signaling pathways. At the early stage of regeneration magnesium has a positive effect on macrophages, its specificity of action is inhibition of transformation of M2 macrophages into M1 at the tissue-specific stage of regeneration. One of the mechanisms stimulating regeneration may be the effect of magnesium on axons, release and increase of calcitonin-related polypeptide α. Conclusions. Since hypomagnesemia is a potentially modifiable factor, this opens up prospects for maintaining bone health and requires further research in this area.\",\"PeriodicalId\":137495,\"journal\":{\"name\":\"ORTHOPAEDICS TRAUMATOLOGY and PROSTHETICS\",\"volume\":\" 10\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-01-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ORTHOPAEDICS TRAUMATOLOGY and PROSTHETICS\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.15674/0030-598720234121-127\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ORTHOPAEDICS TRAUMATOLOGY and PROSTHETICS","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15674/0030-598720234121-127","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
目的根据对现有文献的分析,评估镁缺乏对骨代谢的影响,并系统整理有关镁缺乏对骨质疏松症发展、骨再生影响的数据,并将其视为骨折的风险因素。方法。本综述基于对来自 PubMed、Scopus、Web of Science、Cochrane Library、Google、Google Scholar 和 RLNS 的文献资料的分析。搜索关键词包括:镁、缺乏、镁与骨组织、镁与骨质疏松症、镁与骨折、镁与骨再生。研究结果镁是人体新陈代谢和调节过程中的关键元素。它对骨组织的影响有直接和间接之分。镁对参与成骨的基因的直接影响伴随着间充质干细胞和成骨细胞的增殖,但缺镁会导致它们的减少和凋亡。在缺镁的情况下,破骨细胞的数量和活性会增加。镁以浓度依赖的方式调节骨矿化。缺镁会增加骨吸收,影响骨质疏松症和骨质疏松症,这可通过维生素 D 水平下降、甲状旁腺激素生物合成增加、氧化应激和促炎细胞因子生物合成增加而间接发生。然而,有关镁缺乏症不同骨骼部位骨矿密度的数据并不明确。镁缺乏症被认为是骨折的风险因素之一。镁对骨再生具有重要意义,它以多种方式对骨再生产生影响:刺激间充质干细胞和成骨细胞、骨膜细胞的增殖和分化,增加成骨细胞向创伤性骨损伤区域的移动,激活信号通路。在再生的早期阶段,镁对巨噬细胞有积极作用,其特异性作用是在再生的特定组织阶段抑制 M2 型巨噬细胞转化为 M1 型。刺激再生的机制之一可能是镁对轴突的影响、降钙素相关多肽α的释放和增加。 结论。由于低镁血症是一个潜在的可调节因素,这为维持骨骼健康开辟了前景,需要在这一领域开展进一步研究。
Objective. To assess the impact of magnesium deficiency on bone metabolism based on an analytical analysis of current literature, as well as to systematize data on the impact of magnesium deficiency on the development of osteoporosis, bone regeneration, and to consider it as a risk factor for fracture. Methods. The review is based on the analysis of literature sources from PubMed, Scopus, Web of Science, Cochrane Library, Google, Google Scholar, and RLNS. The search was conducted by keywords: magnesium, deficiency, magnesium and bone tissue, magnesium and osteoporosis, magnesium and fractures, magnesium and bone regeneration. Results. Magnesium is a key element in the metabolic and regulatory processes of the body. Its effects on bone tissue are direct and indirect. The direct magnesium effect on genes involved in osteogenesis is accompanied by proliferation of mesenchymal stem cells and osteoblasts, but magnesium deficiency leads to their reduction and apoptosis. In case of magnesium deficiency, the number and activity of osteoclasts increases. Magnesium regulates bone mineralization in a concentration-dependent manner. Magnesium deficiency increases bone resorption and affects osteopenia and osteoporosis, which can occur indirectly through decreased vitamin D levels, increased biosynthesis of parathyroid hormone, increased oxidative stress and biosynthesis of proinflammatory cytokines. However, data on bone mineral density at different skeletal sites in magnesium deficiency are ambiguous. Magnesium deficiency is considered a risk factor for fracture. It is of great importance for bone regeneration, affecting in various ways: it stimulates the proliferation and differentiation of mesenchymal stem cells and osteoblasts, periosteum cells, increases the movement of osteoblasts to the area of traumatic bone injury, and activates signaling pathways. At the early stage of regeneration magnesium has a positive effect on macrophages, its specificity of action is inhibition of transformation of M2 macrophages into M1 at the tissue-specific stage of regeneration. One of the mechanisms stimulating regeneration may be the effect of magnesium on axons, release and increase of calcitonin-related polypeptide α. Conclusions. Since hypomagnesemia is a potentially modifiable factor, this opens up prospects for maintaining bone health and requires further research in this area.