Bone is a dynamic tissue that is continuously being remodeled throughout life. Specialized cells called osteoclasts transiently break down old bone (resorption process) at multiple sites as other cells known as osteoblasts are replacing it with new tissue (bone formation). Usually, both resorption and formation processes are in balance and thereby maintain skeletal strength and integrity. This equilibrium is assured by coordinated proliferation, migration, differentiation and secretory functions of the osteoblasts which are essential both for adequate formation and resorption processes. Disturbances of this equilibrium may lead to decreased bone mass (osteoporosis), increased bone fragility and susceptibility to fracture. Epidemiological studies have provided a link associating insufficient dietary magnesium (Mg²⁺) intake in humans with low bone mass and osteoporosis. Here, we investigated the roles of Mg²⁺ and melastatin-like transient receptor potential 7 (TRPM7), a calcium and Mg²⁺ channel, in human osteoblast cell proliferation and migration induced by platelet-derived growth factor (PDGF) which has been involved in the bone remodeling process. PDGF promoted influx of Mg²⁺ in osteoblasts and stimulated the gene expression of TRPM7 channels. The stimulation of osteoblast proliferation and migration by PDGF was significantly reduced under culture conditions with low extracellular Mg²⁺ concentrations. Silencing TRPM7 expression in osteoblasts by specific siRNA prevented the induction by PDGF of Mg²⁺ influx, proliferation and migration. Our results indicate that extracellular Mg²⁺ and TRPM7 are important for PDGF-induced proliferation and migration of human osteoblasts. Thus Mg²⁺ deficiency, a common condition among the general population, may be associated to altered osteoblast functions leading to inadequate bone formation and the development of osteoporosis.