Calcium deposition in bone

Radium, similarly to calcium, deposits in bone within those areas where new bone mineral is being formed and also on all bone surfaces. Radium remains in those areas of new bone formation, but the radium deposits on bone surfaces eventually move into the depths of compact bone as new bone matrix is deposited on top of them. In this deposition process, short-lived radium-224 rapidly decays, leaving no radioactivity within bone whereas, long-lived radium-226 remains in the skeleton indefinitely (Rowland 1966). Mays et al. (1975) have demonstrated that the radon to radium ratio in bone increased with time after injection in beagles. 

Q9 The hypercalcaemia which occurs in hyperparathyroidism may be reduced by administration of a loop diuretic such as furosemide, which helps calcium excretion. Bisphosphonates, which prevent bone resorption and so reduce calcium release from bone, can be used to treat hypercalcaemia associated with malignancies. Calcitonin may also be useful in treating the hypercalcaemia associated with cancer, as it reduces calcium levels both by attenuating its renal reabsorption and by increasing calcium deposition in bone. 

A number of important biochemical reactions are promoted by the adsorption of UV-vis radiation.Vitamin D3, which regulates calcium deposition in bones, is biosynthesized in just such a photochemical reaction. This vitamin is formed when the provitamin, 7-dehydrocholesterol, is carried through fine blood capillaries just beneath the surface of the skin and exposed to sunUgJit. The amount of radiation exposure, which is critical for the regulation of the concentration of this vitamin in the blood stream, is controlled by skin pigmentation and geographic latitude. Thus, the color of human skin is an evolutionary response to control the formation of vitamin D3 via a photochemical reaction. 

Aluminium toxicity is the likely cause of three human disorders arising from long-term haemodialysis vitamin D-resistant osteomalacia, iron adequate microcytic anaemia, and dialysis dementia (Martin, 1994). The first of these conditions is consistent with interference with calcium deposition into bone, and the accumulation of aluminium in the bone matrix. 

Monomeric plutonium species deposited in the liver become concentrated in the liver ferritin, the principal iron repository (191). On analysis of plutonium deposition in bone a dichotomy becomes immediately apparent. Monomeric plutonium no longer follows an iron transport/deposition mechanism, for bone contains little or no iron complexed within the bone matrix. Calcium phosphate as a chromatographic media does, of course, retain iron. 

The radioactive isotope calcium-45 is deposited in bones and teeth as well as other plant and animal tissues. Because our bodies cannot distinguish between Ca-45 and the stable Ca-40, the radioactive isotope Ca-45 is used as a tracer to study diseased bone and tissue. At the same time, a massive overexposure to Ca-45 can displace the stable form of Ca-40 in animals and can cause radiation sickness or even death. 

Vitamin D hormone is derived from vitamin D (cholecalciferol). Vitamin D can also be produced in the body it is formed in the skin from dehydrocholesterol during irradiation with UV light. When there is lack of solar radiation, dietary intake becomes essential, cod liver oil being a rich source. Metaboli-cally active vitamin D hormone results from two successive hydroxylations in the liver at position 25 ( calcifediol) and in the kidney at position 1 ( calci-triol = vit. D hormone). 1-Hydroxylation depends on the level of calcium homeostasis and is stimulated by parathormone and a fall in plasma levels of Ca or phosphate. Vit D hormone promotes enteral absorption and renal reabsorption of Ca and phosphate. As a result of the increased Ca + and phosphate concentration in blood, there is an increased tendency for these ions to be deposited in bone in the form of hydroxyapatite crystals. In vit D deficiency, bone mineralization is inadequate (rickets, osteomalacia). Therapeutic Liillmann, Color Atlas of Pharmacology... 

The finely-powdered metal is pyrophoric. Its radioactive isotopes Sr-89 and Sr-90 emit high-energy beta radiation. They are extremely hazardous because they deposit in bones replacing calcium. Their radiation can damage bone marrow and blood-forming organs, inducing cancer. 

The amount of calcium deposited tit bone at any moment may be determined from experiments with radioactive calcium. In grow ing individuals, it exceeds the amount removed by bone destruction. In adults, it is about the same as the amount removed. Such individuals arc considered to be in "zero" calcium balance. In older persons. Ihe amount deposited is less than the amount removed. 

Vitamin D is used in the maintenance of plasma calcium ion concentrations. The normal level of free calcium ions in the plasma ranges from 1,0 to 1.5 mM. This concentration is needed to support a rxormal rate of deposit of calcium In bone during growth and during bone turnover. Apparently, vitamin D has no direct effect on the deposit of calcium ions in bone. It seems to act only indirectly and in maintaining plasma calcium at a level required to support bone mineralization. Note, however, that there remains interest in the possibility that vitamin D does have a direct effect on the cells that synthesize bone. A few details on bone formation and structure and on the vitamin D-dependent process of bone resorption are presented here. 

The distribution of the element is similar to that of calcium which means that 99% of the body burden is deposited in bone [44]. Within the dialysis population, bone strontium levels were found to be significantly higher in subjects with osteomalacia as compared to this presenting the other types of renal osteodystrophy [45]. A causal, dose-dependent role of strontium in the development of this bone disease has been established in a chronic renal failure ratmodel [46,47]. Moreover the bone osteomalacic lesions were found to be reversible after withdrawal of strontium [9,48]. 

Calcium absorption can be measured by the double-isotope technique. In this technique a meal containing caldum-45 is consumed and the radioactivity in the urine measured. The measurement of urinary Ca alone cannot provide the fractional absorption, because some of the Ca absorbed is taken up by cells, deposited in bone, or excreted in the bile. A second isotope of calcium, Ca, is used to correct for the fates of absorbed calcium, other than excretion in the urine. The use of the Ca is intended to eliminate cell uptake, bone deposit, and biliary losses as variables in the study of the absorption of the dose of cdcium-45. 

Rey G, Shimizu M, GoUins B, Glimcher MJ (1990) Resolution-enhanced Fourier transform infrared spectroscopy study of the environment of phosphate ion in the early deposits of a solid phase of calcium phosphate in bone and enamel and their evolution with age. 1. Investigations in the V4-PO domain. Galcif Tissue Int 46 384-394... 

Use Research aid for studying water purification, calcium exchange in clays, detergency, surface wetting and other surface phenomena, calcium uptake and deposition in bone, soil characteristics as related to soil utilization of fertilizer and crop yield, diffusion of calcium in glass, etc. 

The answer is b. (Murray, pp 505-626. Scriver, pp 4029-4240. Sack, pp 121—138. Wilson, pp 287-320.) Calcium ions and calcium deposits are virtually universal in the structure and function of living things. In humans, calcium ions are required lor the activity of many enzymes. Calcium is taken up Irom the gut in the presence ol lorms of vitamin D, such as cholecalciferol. Calcium is also primarily excreted through the intestine. When soluble, it is present as a divalent cation. When insoluble, it is found as hydroxyapatite (calcium phosphate) in bone. It is required by muscle cells for contraction and is sequestered into the sarcoplasmic reticulum during relaxation. It is actively transported by a calcium-ATPase across the sarcoplasmic reticulum. 

In addition to an increase in serum urea and creatinine levels, uric acid and inorganic phosphate levels also increase in chronic renal failure. The increase in serum inorganic phosphate leads to deposition of calcium phosphate in bones, causing hypocalcemia. In the early stages of chronic renal failure, calcium levels are restored by the stimulation of parathyroid hormone. However, as the renal disease progresses, the ability of the kidney to hydroxylate vitamin D and thus convert it to the active form decreases, thereby affecting the uptake of calcium by the gut and thus perpetuating hypocalcemia. Serum alkaline phosphatase levels increase due to disordered bone metabolism. Loss of bicarbonate is seen in some patients with increased parathyroid hormone activity. 

Tetracyclines bind to calcium and then become deposited in bone, causing damage to developing bone and teeth. Intravenous administration of tetracyclines has been observed to cause venous thrombosis. 

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