Effect of magnesium deficiency on bone health

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.