Magnesium, Bone Wasting, and Mineralization

Abstract

Relatively little attention has been paid to the importance of magnesium in bone metabolism, except to the degree that it affects the activity of the parathyroid glands and C cells and their secretion of parathyroid hormone (PTH) and calcitonin (CT), and the response of target organs. However, experimental magnesium deficiency causes abnormalities in skeletal structure, enzymes, and mineralization that resemble some of those seen in several clinical bone diseases. Depending on the degree and duration of the magnesium deficiency and concomitant dietary or iatrogenic imbalances (of magnesium with calcium, phosphates, vitamin D, and other calcemic agents), the pathologic skeletal findings can range from osteopenias to osteosclerosis. The effects of vitamin D, calcium, and phosphorus on magnesium requirements and on skeletal responses have been intensively studied, particularly in the 1930s, when vitamin D toxicity was the focus of much attention. Many of the results are conflicting, probably due to the dietary variations, and to species differences in requirements (i.e., of vitamin D). Only those portions of the PTH/CT/Mg data that deal directly with magnesium and bone are considered here. Much of that relating to gestational abnormalities has already been discussed. The relatively little information found on heteroionic magnesium/calcium exchange in bone, and on the magnesium interrelationships between the phosphatases that affect mineralization, alkaline phosphatase and pyrophosphatase, are brought into focus as possibly providing some insight into the conflicting and confusing data on mechanisms of pathologic skeletal processes.