Calcium phosphate deposition

In addition to the formation of scale or corrosion of metal within boilers, auxiliary equipment is also susceptible to similar damage. Attempts to prevent scale formation within a boiler can lead to makeup line deposits if the treatment chemicals are improperly ehosen. Thus, the addition of normal phosphates to an unsoftened feed water ean eause a dangerous eondition by elogging the makeup line with preeipitated calcium phosphate. Deposits in the form of calcium or magnesium stearate deposits, otherwise known as "bathtub ring" can be readily seen, and are caused by the eombination of ealcium or magnesium with negative ions of soap stearates. 

Radiographic studies show calcium-phosphate deposits in joints and/or cardiovascular system Bone biopsy of the iliac crest... 

The major effect of hyperphosphatemia is related to the development of hypocalcemia and damage resulting from calcium phosphate deposits. 

In the second stage, as the needle-like calcium phosphate deposits radially grow out of the vesicles, the surrounding collagen fibres become mineralized. 

While the standard, modem chemical treatment programs used today almost always contain a synergistic blend of polymers and other organic inhibitors, they often may not contain a specific calcium phosphate deposit control agent (as it would increase the cost of the program). This situation reinforces the need for vigilance. 

Additionally, as with risks of calcium phosphate deposition, modem trends to the reuse of wastewaters can sometimes introduce high sulfates into cooling systems via the makeup supply. 

Differential 31P 1H CPMAS technique has been applied to study mineral crystals of calcium phosphate deposited during osteoblast calcification in cell culture.198 The samples harvested after 8 days of culture represent the minerals formed at the very early stage of calcification, in... 

Similarly, supersaturation of saliva with respect to calcium phosphate salts is the driving force of calculus (i.e., mineralized dental plaque) and sialolith (i.e., salivary duct stones ) formation. In these cases, negatively charged phospholipids play a crucial role Ca + ions bind to the negative charges of such lipids, and inorganic phosphate associates with the bound calcium that forms a Ca-phosphate-phospholipid complex, which is an excellent nucleus of calcium-phosphate deposition. Salivary proteins may also play a role in this process because such complex formation occurs predominantly on lipids that are protein associated. The increase of pH facilitates these processes (13). 

The terminology used to describe conditions associated with prominent renal calcium deposits dismisses the importance of the phosphate anion. Renal parenchymal injury with prominent calcium oxalate deposition is referred to as oxalate nephropathy. Oxalate nephropathy is seen in the setting of primary hyperoxaluria or enteric hyperoxaluria secondary to fat malabsorption. Renal parenchymal injury with abundant calcium phosphate deposits is referred to as... 

In 2003, Desmeules et al. described a new pattern of renal failure resulting from the use of OSPS [29]. A 71-year-old female with a baseline creatinine of 1.0 mg/ dl presented with acute kidney injury and a creatinine of 4.5 mg/ dl two weeks following the use of OSPS. Renal biopsy revealed numerous tubular calcium phosphate deposits. Scanning electron microscopy and energy-dispersive x-ray microanalysis revealed that the calcium phosphate deposits formed crystals of hydroxyapatite. The patient s creatinine declined to 1.7 mg/dl at one year of follow-up. The authors described the process as "phosphosoda-induced nephrocalcinosis" and proposed the term "acute phosphate nephropathy". 

Autopsy revealed acute Ischemic colitis. No renal calcium phosphate deposits were noted. 

Acute phosphate nephropathy is commonly accompanied by mild to moderate interstitial inflammation composed of mainly lymphocytes. The interstitial inflammation is not associated with significant tubulitis and likely represents a response to the tubular injury and calcium phosphate deposition. Glomeruli typically appear unremarkable. Vascular disease is commonly encountered but is an expected finding given the mean age and high incidence of hypertension in patients with APhN. 

Wong L, Sissons CH, Pearce EIF, Cutress TW Calcium phosphate deposition in human dental plaque microcosm biofilms induced by a ureolytic pH-rise procedure. Arch Oral Biol 2002 47 ... 

Other signs Band keratopathy, a reflection of subepithelial calcium phosphate deposits in the cornea, is a very rare finding associated with hypercalcemia. It extends as a horizontal band across the cornea in the area that is exposed between the eyelids. 

The deposition of sparingly soluble calcium phosphates on PHEMA hydrogels, both in vitro and in vivo, can be modified by the incorporation of citric acid into the PHEMA hydrogels. In the presence of citrate anions the formation of hydroxyapatites was prevented. The calcium phosphate deposits which formed in vitro on PHEMA were mainly monocalcium phosphate monohydrate and dicalcium phosphate dihydrate. The types of deposits formed in vivo were quite different from those formed in vitro. The in vivo deposits formed on PHEMA were mostly hydroxyapatites deficient in calcium and hydroxyl ions. Citrate anions were also observed to prevent significantly the deposition in vivo of protein onto PHEMA hydrogels. 

Citrate anions are present in fresh wet bone to about 1 wt%, and they play an important role in the formation and/or dissolution of bone apatite through their adsorption onto both the reactant and the product phases (27-30,32). Thus, citric acid and its salts play important roles in calcium phosphate deposition in biological systems. 

Semi quantitative analyses of the calcium phosphate deposits were acquired using a Kratos Axis ULTRA XPS spectrometer incorporating a 165-mm hemispherical electron energy analyzer. The source of X-ray incident radiation was a monochromatic Al Ka (1486.6 eV) at 150 W (15 kV, 10 mA). Survey (wide) scans were taken at an analyzer pass energy of 160 eV. 

For complementaiy quantification of the elements present in the calcium phosphate deposits, EDS analyses were performed on carbon-coated samples using an electron energy of 15 keV and a JEOL 6460LA EDS instrument. 

Figure 2. (A) an SEM micrographs of the calcium citrate crystals formed in SBF during the first week of calcification (B) enlarged micrograph, showing the presence of calcium phosphate deposits on the citrate crystals. The concentration of citric acid released into the SBF was 0.6 mM.

The SEM micrographs shown in Figure 3 provide evidence for the proposed prevention of calcification by citrate anions. It can be seen that the calcium phosphate deposits formed on PHEMA in the presence of citric acid are much lower in amount and smaller in size (Figure 3C). In other words, under the action of citrate anions, the extent of the deposition of calcium phosphates was significantly reduced and the nature of the deposits modified. This is confirmed by the veiy low calcium contents of the calcium phosphate deposits over the whole range of calcification times (see Figure 4), as determined by XPS. It should be mentioned here that after 5 weeks of calcification time, at least one layer of calcium phosphate (with a thickness of 0.4 pm (33)) was deposited on the surface of PHEMA containing no citric acid. Thus, it is anticipated that the calcium content of the calcium phosphate deposits tends to plateau after 5 weeks in SBF solution. 

Semi-quantitative XPS analyses on the calcium phosphate deposits revealed that due to the inhibition and dissolution effects of citric acid, the calcium phosphates have Ca/P molar ratios between 0.5 and 1.2. These values are lower than the Ca/P molar ratios for the deposits formed on PHEMA containing no... 

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