Magnesium and Bone Disease

Brautbar, Nachman; Gruber, Helen E.

doi:10.1159/000183902

Cited by 15 publications

(18 citation statements)

References 55 publications

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“…Since the early 1970s, a high bone Mg content in patients with renal disease has been consistently reported by different authors (4,33,49). In 1986, Brautbar and Gruber outlined the hypothesis that increased bone Mg arises from elevated serum Mg, and that increased bone Mg plays a direct role in mineralization defects and the pathogenesis of renal osteodystrophy (60). Thus, high bone Mg content has been implicated in the pathogenesis of osteomalacic renal osteodystrophy (62,63).…”

Section: Magnesium Parathyroid Hormone and Bone Diseasementioning

confidence: 99%

Reviews: Clinical Implications of Disordered Magnesium Homeostasis in Chronic Renal Failure and Dialysis

Navarro‐González

Mora‐Fernández

García‐Pérez³

2009

Seminars in Dialysis

151

156

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Magnesium (Mg) is the fourth most abundant cation in the body, mainly located within bone and skeletal muscle. The normal total plasma Mg concentration varies in a narrow range, with approximately 60% present as free Mg ions, the biologically active form. The kidney plays a principal role in Mg balance. Approximately 70-80% of plasma Mg is ultrafilterable, and under normal circumstances, 95% of the filtered load of Mg is reabsorbed. As chronic renal failure (CRF) progresses, urinary Mg excretion may be insufficient to balance intestinal Mg absorption and dietary Mg intake becomes a major determinant of serum and total body Mg levels. Until severe reductions in glomerular filtration rate (<30 ml/min), serum Mg levels are usually normal; with lower rates of renal function, serum Mg is increased. Concerning dialysis patients, dialysate Mg plays a critical role in maintaining Mg homeostasis, with serum Mg being largely dependent on the concentration of the ion in the dialysis solution. Magnesium has been implicated in diverse consequences, both beneficial and deleterious, in patients with CRF and dialysis. Potential harmful effects of elevated Mg include altered nerve conduction velocity, increased pruritus, and alterations to osseous metabolism and parathyroid gland function (mineralization defects, contribution to osteomalacic renal osteodystrophy, and adynamic bone disease). Hypermagnesemia also may retard vascular calcification. Low Mg levels have been associated with impairment of myocardial contractility, intradialytic hemodynamic instability, and hypotension. In addition, low Mg has been also linked to carotid intima-media thickness, a marker of atherosclerotic vascular disease and a predictor of vascular events.

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Section: Magnesium Parathyroid Hormone and Bone Diseasementioning

confidence: 99%

Reviews: Clinical Implications of Disordered Magnesium Homeostasis in Chronic Renal Failure and Dialysis

Navarro‐González

Mora‐Fernández

García‐Pérez³

2009

Seminars in Dialysis

151

156

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“…The negative correlations between the V FD and Mg FD or Ca FD contents ( Table 2) may confirm the connection between the V FD accumulation and the Mg FD and Ca FD imbalance. 33,[83][84][85] Tsuboi et al 86 demonstrated that higher concentrations of Mg are maintained in the periosteal (outer) and endosteal (inner) bone surfaces, whereas Laurencin et al 87 provided direct evidence of the preferential substitution of Mg in one of the two crystallographic Ca sites of apatites, referred to as Ca(II), and suggested that incorporation of Mg in Fig. 2 However, some authors found that V did not affect the content of Mg and Ca in bone which may result from different experimental conditions used.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, it has also been reported that orthopaedic implants, if supplemented with V, might provide a source of a better model for bone formation and its turnover. [31][32][33][34][35][36][37][38][39] They also demonstrated that the long-term suboptimal Mg supply is beneficial for bone health, but long-term supplementation thereof may be deleterious. 12 In the literature, some aspects of action of V, the toxicological effects of which are well known to be dependent on many factors, 13,14 and Mg on bone under in vivo and in vitro conditions have already been described.…”

Section: Introductionmentioning

confidence: 99%

Effects of vanadium (V) and magnesium (Mg) on rat bone tissue: mineral status and micromorphology. Consequences of V–Mg interactions

et al. 2014

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The extent to which the 12 week separate and combined administration of vanadium (as sodium metavanadate--SMV, 0.125 mg V per ml) and magnesium (as magnesium sulphate--MS, 0.06 mg Mg per ml) affects bone mineral status and micromorphology as well as the alkaline phosphatase (ALP) activity in femoral diaphysis (FD) was examined in male rats. The bone chemical composition of SMV-exposed rats was also investigated. SMV alone or in combination with MS (as SMV-MS) reduced the levels of MgFD (by 21% and 20%) and PFD (by 12% and 9%), lowered the CaFD content (by 7% and 10%), and caused a rise of the FeFD concentration (by 22.5% and 17%), compared with the control; SMV alone also reduced and enhanced the KFD and ZnFD concentrations (by 19% and 15%, respectively) but remained without significant effect on the femoral bone surface roughness (FBSR), whereas MS alone lowered the VFD, PFD, and CuFD levels (by 42%, 10%, and 20.6%), reduced FBSR, and created the regular femoral bone surface shape. The SMV-MS combination also induced a decline and rise in the levels of CuFD (by 30%) and NaFD (by 15%), respectively, compared with the control and the MS-supplemented rats; elevated ALPFD activity (by 24%, 35%, and 40%), compared with the control, SMV-exposed, and MS-supplemented animals; and increased FBSR. Relationships between the root mean square roughness (Sq) and skewness (Ssk): Sq [MS < SMV < Control < SMV-MS] ⇔ Ssk [SMV-MS > Control > SMV > MS], ALPFD and Sq: ALPFD⇔ Sq [SMV-MS > Control > SMV > MS], and between other variables were demonstrated. A partial limitation of the drop in the PFD and KFD levels and normalization of the ZnFD concentration were a consequence of the V-Mg antagonistic interaction whereas a consequence of the V-Mg synergistic interaction was the increase in the NaFD level, ALPFD activity, and FBSR. Ca10(PO4)5(SiO4)(OH) was part of the inorganic component of the bone of the SMV-exposed rats.

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“…the magnesium release and increases the availability of bone magnesium when its intake is restricted. 27 Magnesium seems to play a role in the mineralization process since a low maternal magnesium intake leads to a decrease of the number of mineralized bones in rat and mouse pups. 27 Magnesium controls bone calcification in general and crystallization processes in particular.…”

Section: Discussionmentioning

confidence: 99%

“…27 Magnesium seems to play a role in the mineralization process since a low maternal magnesium intake leads to a decrease of the number of mineralized bones in rat and mouse pups. 27 Magnesium controls bone calcification in general and crystallization processes in particular. 18 Magnesium is known to stabilize whitlockite, and an addition of magnesium to the starting powder used for ␤ whitlockite ceramic reduced the biodegradation rate of the tricalcium phosphate.…”

Section: Discussionmentioning

confidence: 99%

Influence of magnesium substitution on a collagen-apatite biomaterial on the production of a calcifying matrix by human osteoblasts

Serre

Papillard²,

Chavassieux

et al. 1998

J. Biomed. Mater. Res.

244

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The induction of a calcifying matrix is of great interest in the restoration of bone defects. In a previous in vitro study we demonstrated that a collagen sponge constituted of type I collagen fibrils, chondroitin sulfates, and hydroxyapatite crystals induces an earlier and a more abundant synthesis of a new extracellular calcifying matrix than do other biomaterials such as collagen or hydroxyapatite alone. Bone mineral contains various amounts of magnesium ions, either adsorbed at the surface of apatite crystals or incorporated inside the crystal structure. Magnesium is known to reduce the degradation rate of tricalcium phosphate ceramics and to influence the crystallization of mineral substance. Thus we evaluated two sponges modified with different substituted apatites. The substituted low magnesium-containing apatite sample decreased the osteoinductive properties of the sponge whereas the substituted high magnesium-containing apatite sample had a toxic effect on bone cells and prevented the formation of any extracellular matrix. Such a toxic effect can be explained by the presence of large numbers of magnesium ions released into the culture medium even though at physiological level magnesium is able to promote bone mineralization and to control the growth of hydroxyapatite crystals. Thus collagen sponges containing hydroxyapatite remain one of the most appropriately evaluated biomaterials used for the restoration of periodontal pockets and bone defects.

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Magnesium and Bone Disease

Cited by 15 publications

References 55 publications

Reviews: Clinical Implications of Disordered Magnesium Homeostasis in Chronic Renal Failure and Dialysis

Reviews: Clinical Implications of Disordered Magnesium Homeostasis in Chronic Renal Failure and Dialysis

Effects of vanadium (V) and magnesium (Mg) on rat bone tissue: mineral status and micromorphology. Consequences of V–Mg interactions

Influence of magnesium substitution on a collagen-apatite biomaterial on the production of a calcifying matrix by human osteoblasts

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