Magnesium in bone and the magnesium load test

ARTICLE

mrh.2011.0297

Auteur(s) : Theodor Günther

Charité, Universitlsquätsmedizin Berlin, Campus Benjamin Franklin, Institut für Molekularbiologie und Biochemie, Berlin, Germany

Correspondence. Prof. T. Günther, Waldhüterpfad 63, D 14169 Berlin, Germany

About 50% to 70% of body magnesium (Mg) is localized in bone [1, 2]. About 30% of bone Mg is exchangeable [2]. Other authors found that 1-5% of bone Mg is exchangeable with injected ²⁸Mg [3]. The exchangeable Mg fraction could occupy a site at or in the hydroxyapatite crystal surface or in the hydration layer of the apatite crystals [2].

The localization and state of the nonexchangeable bone Mg are not defined. Mg may be excluded from the apatitic lattice [4] or there may be some substitution of Mg for Ca in apatite crystals [5]. Some Mg could be present as an amorphous, nonapatitic layer, perhaps overlying the apatitic phase, or as a whitlockite phase [Ca₉Mg(HPO₄)(PO₄)₆] [2, 4, 6].

Reduction in trabecular bone Mg in osteoporotic patients or with age results in a reduced exchangeable Mg fraction with larger and more perfect apatite crystals [2, 6-8]. Thus the total apatite crystal surface must be reduced in these subjects.

To confirm the Mg state, Mg load tests were performed. In normomagnesemic patients with senile osteoporosis and in normomagnesemic diabetics, trabecular Mg content was reduced, and larger and more perfect apatite crystals were found. The intracellular Mg content was not reduced, as measured by the lymphocyte Mg content [7]. Mg retention in a parenteral Mg load test was increased in the normomagnesemic osteoporotic patients and was not changed in the normomagnesemic diabetics [7].

Almost all of the infused Mg in the Mg load test is reversibly adsorbed to the exchangeable bone Mg fraction [9], its amount depending on the total surface of the apatite crystals.

On this basis, it cannot be explained why normomagnesemic osteoporotic patients retained more Mg than controls or why normomagnesemic diabetics with the same reduction in bone Mg content and the same alteration in the bone mineral crystallinity index did not show an abnormal Mg retention [7]. Also, the inverse correlation between bone Mg content and Mg retention in normomagnesemic patients without symptoms of Mg deficiency (alcoholics, cirrhotics, diabetics, malabsorption, hip replacement therapy) [10, 11] cannot be explained by adsorption of Mg onto the exchangeable bone Mg fraction. Bone Mg content ranged from 406 to 250 mEq/kg ash [10] and from 98 to 26 mmol/kg dry substance [11]. Mg retention ranged from +28% to +92% [10] and from -100% to +62% [11]. Reductions in bone Mg content exceed the normal exchangeable bone Mg content, indicating an alteration in bone mineral state. For discussion see [9]. Are the reductions in bone Mg content and the alterations in the crystallinity of apatite crystals in normomagnesemic patients without symptoms of Mg deficiency caused by Mg deficiency or by changed activity of bone cells? Bone cells are affected by numerous bone growth factors and bone resorptive cytokines.

The diagnosis “chronic latent Mg deficiency, the most prevalent form of Mg deficiency in humans” “with a reduction in total body Mg content as measured by the Mg load test but a serum total Mg concentration within the reference interval” [12], should be re-evaluated.

References

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12. Elin RJ. Laboratory evaluation of chronic latent magnesium deficiency. In: Advances in magnesium research. Rayssiguier Y, Mazur A, Durlach J, eds. London, John Libbey 2001: 233-39.