Magnesium to prevent kidney disease–associated vascular calcification: crystal clear?

Vascular calcification is a prognostic marker for cardiovascular mortality in chronic kidney disease (CKD) patients. In these patients, magnesium balance is disturbed, mainly due to limited ultrafiltration of this mineral, changes in dietary intake and the use of diuretics. Observational studies in dialysis patients report that a higher blood magnesium concentration is associated with reduced risk to develop vascular calcification. Magnesium prevents osteogenic vascular smooth muscle cell transdifferentiation in in vitro and in vivo models. In addition, recent studies show that magnesium prevents calciprotein particle maturation, which may be the mechanism underlying the anti-calcification properties of magnesium. Magnesium is an essential protective factor in the calcification milieu, which helps to restore the mineral-buffering system that is overwhelmed by phosphate in CKD patients. The recognition that magnesium is a modifier of calciprotein particle maturation and mineralization of the extracellular matrix renders it a promising novel clinical tool to treat vascular calcification in CKD. Consequently, the optimal serum magnesium concentration for patients with CKD may be higher than in the general population.

Enamel Subsurface Caries-Like Lesions Induced in Human Teeth By Different Solutions: A TMR Analysis

This study assessed the effectiveness of models for developing subsurface caries lesions in vitro and verified mineral changes by transverse microradiography (TMR). Enamel blocks from permanent (n=5) and deciduous teeth (n=5) were submitted to lesion induction by immersion in demineralizing solutions during 96 h, followed by pH cycles of demineralization (de) and remineralization (re) for 10 days. Two de-/re solutions were tested. Demineralizing solution “A” was composed by 2.2 mM CaCl2, 2.2 mM KH2PO4, 0.05 M acetic acid, with pH 4.4 adjusted by 1 M KOH. Demineralizing solution “B” was composed by 2.2 mM CaCl2, 2.2 mM NaH2PO4, 0.05 M acetic acid and 0.25 ppmF, with pH 4.5 adjusted by 1M KOH. Solution “A” produced cavitated lesions in permanent teeth, whereas solution “B” led to subsurface lesions in deciduous teeth. Solution “B” was then tested in enamel blocks from permanent teeth (n=5) and subsurface lesions were obtained, so that solution “B” was employed for both substrates, and the blocks were treated with slurries of a fluoride dentifrice (1450 ppm F, as NaF, n=5) or a fluoride-free dentifrice (n=5). Solution “B” produced subsurface lesions in permanent and primary teeth of an average (±SD) depth of 88.4µm (±14.3) and 89.3µm (±15.8), respectively. TMR analysis demonstrated that lesions treated with fluoride-free dentifrice had significantly greater mineral loss. This study concluded that solution “B” developed subsurface lesions after pH cycling, and that mineral changes were successfully assessed by TMR.

THE INFLUENCE OF EXOCRINE PANCREATIC INSUFFICIENCY IN THE FORMATION OF OSTEOPENIA IN PATIENTS WITH PRIMARY OSTEOARTHRITIS

The aim: Make complex study of bone density in patients with primary osteoarthritis and exocrine pancreatic insufficiency and patients with primary osteoarthritis without exocrine pancreatic insufficiency. Materials and methods: There were examined 140 patients with primary osteoarthritis without exocrine pancreatic insufficiency and combination osteoarthritis and exocrine pancreatic insufficiency. Diagnosis of osteoarthritis was based on diagnostic X-Ray criteria – according to J.H. Kellgren and J.S. Lawrence. The level of exocrine pancreatic insufficiency was based on result of Elisa test. State of mineral bone density was examined by using dual-photon densitometry. Results: It was established that there was a progressive, statistical, significant increase of mineral density of bone tissue in the 1-st group patients with osteoarthritis. Patients in the 2-nd group, with osteoarthritis in the comorbidity with exocrine pancreatic insufficiency, the densitogram rates were statistically significantly lower than in patients in the 1-st group. Conclusions: The changes of bone tissue can be explained by the formation of trophological insufficiency as a result of exocrine pancreatic insufficiency. One of the symptoms of trophic failure is bone and mineral changes, in particular, the decrease of bone density.

Chemical equilibrium of groundwater with minerals of the host rocks in Upper Jurassic sediments (Arctic regions of Western Siberia)

The results of thermodynamic calculations for a water-rock system in the Upper Jurassic deposits of the Arctic regions of Western Siberia are presented. In the area under investigation the groundwaters have been identified with mineralization up to 63.3 g/L and various chemical composition and genesis. Despite the long interaction with the rock (150-160 ma) equilibrium with endogenous minerals (albite, microcline and anorthite) is practically not observed. At the same time, groundwaters are in equilibrium with clay minerals and micas, such as: Caand Na-montmorillonites, kaolinite, paragonite, margarite, illite, muscovite and Mg-chlorite. The establishment of a balance of groundwater with primary aluminosilicate minerals is also affected by interactions with carbonate minerals. The differences in composition of groundwater in equilibrium with certain aluminosilicates and carbonates indicate that the mineral changes are formed from a solution of a strictly defined chemical composition in an appropriate geochemical environment.