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Aim: Calcium silicate-based materials are hydraulic self-setting materials with physico-chemical properties suitable for endodontic surgery and good biological/clinical outcomes. The study aim was to evaluate the bio-properties (biointeractivity and apatite-forming ability) and selected physical properties (porosity, water sorption, solubility, and setting time) of Biodentine, a tricalcium silicate material for endodontics and restorative dentistry, compared to that of ProRoot MTA (Mineral Trioxide Aggregate) as gold standard material. Methods: Biodentine and ProRoot MTA pastes were prepared and analyzed for calcium release and alkalinizing activity (3 h–28 days), setting time, water sorption, porosity, solubility, surface microstructure and composition, and apatite-forming ability in simulated body fluid. Results: Biodentine showed higher calcium release, alkalinizing activity, and solubility but higher open and apparent porosity, water sorption, and a markedly shorter setting time. Calcium phosphate (CaP) deposits were noted on material surfaces after short ageing times. A CaP coating composed of spherulites was detected after 28 days. The thickness, continuity, and Ca/P ratio of the coating differed markedly between the materials. Biodentine showed a coating composed by denser but smaller spherulites, while ProRoot MTA showed large but less dense aggregates of spherulitic deposits. Conclusions: Biodentine showed a pronounced ability to release calcium and extended alkalinizing activity interlinked with its noticeable porosity, water sorption, and solubility: open porosities provide a broad wet biointeractive surface for the release of the calcium and hydroxyl ions involved in the formation of a CaP mineral. Biodentine is a biointeractive tricalcium silicate material with interesting chemical-physical properties and represents a fast-setting alternative to the conventional calcium silicate MTA-like cements.

To determine whether an “atherogenic” diet (excess of cholesterol and neutral fat) induces pathological calcification in various organs, including the kidney, and abnormal oxalate metabolism, 24 male Sprague-Dawley rats were fed either normal lab chow (controls, n=12) or the cholesterol- and fat-rich experimental diet (CH-F, n=12) for 111 ± 3 days. CH-F rats developed dyslipidemia [high blood levels of triglycerides, total, low-density lipoprotein (LDL)-, very low-density lipoprotein (VLDL)-, high-density lipoprotein (HDL)-bound cholesterol, total phospholipids], elevated serum total alkaline phosphatase and lactate dehydrogenase (LDH) levels, in the absence of changes in overall renal function, extracellular mineral homeostasis [serum protein-corrected total calcium, magnesium, parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (1,25(OH)2D)], plasma glycolate and oxalate levels. There was a redistribution of bone calcium and enhanced exchange of this within the extraosseous space, which was accompanied by significant bone calcium loss, but normal bone histomorphometry. Liver oxalate levels, if expressed per unit of defatted (DF) dry liver, were three times higher than in the controls. Urinary glycolate, oxalate, calcium and total protein excretion levels were elevated, the latter showing an excess of proteins >100 kD and a deficit of proteins >30–50 kD. Urinary calcium oxalate supersaturation was increased, and calcium phosphate supersaturation was unchanged. There were dramatically increased (by number, circumference, and area) renal calcium phosphate calcifications in the cortico-medullary region, but calcium oxalate deposits were not detectable. Electron microscopy (EM) and elemental analysis revealed intratubular calcium phosphate, apparently needle-like hydroxyapatite. Immunohistochemistry of renal tissue calcifications revealed co-localization of phospholipids and calcium phosphate. It is concluded that rats fed the CH-F diet exhibited: (1) a spectrum of metabolic abnormalities, the more prominent being dyslipidemia, hyperoxaluria, hypercalciuria, dysproteinuria, loss of bone calcium, and calcium phosphate nephrocalcinosis (NC); and (2) an interaction between calcium phosphate and phospholipids at the kidney level. The biological significance of these findings for the etiology of idiopathic calcium urolithiasis in humans is uncertain, but the presented animal model may be helpful when designing clinical studies. [ABSTRACT FROM AUTHOR]

Elevated serum phosphorus is a major risk factor for vascular calcification, which is characterized by the presence of calcium phosphate deposits, mainly hydroxyapatite crystals. In vitro studies of phosphate-induced calcification show that vascular smooth muscle cells undergo calcification with features similar to those observed in pathological vascular calcification in vivo, including the presence of hydroxyapatite crystals. Here, we describe the double-collagenase digestion method for isolating vascular smooth muscle cells from aorta, and a method for inducing calcification in vitro using high phosphate concentration.