Disease relevance of Calcification, Physiologic

• In some patients with chronic renal failure, bone mineralization becomes defective after parathyroidectomy for secondary hyperparathyroidism [1].
• The difference in bone disease between X-linked hypophosphatemia (severe) and hypophosphatemic bone disease (mild) at comparable low serum levels of phosphate implies that 1,25-(OH)2D and phosphate may have independent roles in the pathogenesis of defective bone mineralization [2].
• Hypophosphatasia is a heritable disorder characterized by defective bone mineralization and a deficiency of liver/bone/kidney alkaline phosphatase (L/B/K ALP) activity in serum and tissues [3].
• Oncogenic osteomalacia (OOM) is associated with primitive mesenchymal tumors that secrete phosphaturic factors resulting in low serum concentrations of phosphate and calcitriol, phosphaturia, and defective bone mineralization [4].
• Abnormal vitamin B6 metabolism in alkaline phosphatase knock-out mice causes multiple abnormalities, but not the impaired bone mineralization [5].

Psychiatry related information on Calcification, Physiologic

• These metabolic changes have an impact on bone mineralization during a critical period in the development of bone mass.Recognition by physicians of the so-called 'female athlete triad', consisting of disordered eating, amenorrhea, and osteoporosis, may allow therapeutic intervention [6].

High impact information on Calcification, Physiologic

• This enzyme regulates soft-tissue calcification and bone mineralization by producing inorganic pyrophosphate, a major inhibitor of calcification [7].
• Physiological calcification occurs in bone when the soft ECM is converted into a rigid material capable of sustaining mechanical force; pathological calcification can occur in arteries and cartilage and other soft tissues [8].
• These findings indicate that the OPG/OPGL/RANK signaling pathway may play an important role in both pathological and physiological calcification processes [9].
• Serum levels of BGP corrected for alterations in renal function are superior to uncorrected S-BGP and to S-AP levels in the estimation of bone mineralization rates [10].
• Lithium chloride administration to growing rats, which resulted in circulating lithium levels of 1.4 meq/liter, was attended by significant suppression of bone mineralization and organic matrix synthesis as assessed by tetracycline labeling and histological quantitation of osteoid, respectively [11].

Chemical compound and disease context of Calcification, Physiologic

• Since 24,25-dihydroxyvitamin D3 appears to improve calcium homeostasis and bone mineralization in some patients with severe dialysis osteomalacia when administered with 1-hydroxylated vitamin D metabolites, further controlled studies are warranted [12].
• Bone tolerance studies indicate that tiludronate is a safe compound with an appreciable therapeutic margin since it can effectively inhibit bone resorption without reducing bone mineralization and strength [13].
• We conclude that inhaled beclomethasone (up to 800 micrograms/day) does not reduce bone mineralization or increase bone resorption [14].
• Thus, the estrogen which is responsible for breast cancer development, for the maintenance of bone mineralization and for the maintenance of cognitive function is not circulating estrogen but rather that which is produced locally at these specific sites within the breast, bone and brain [15].
• Even mild hypogonadism due to suboptimal testosterone replacement may result in decreased bone mineralization and osteoporosis [16].

Biological context of Calcification, Physiologic

• CONCLUSION: These data suggest that ethanol may be responsible for osteoblastic dysfunction resulting in diminished bone formation and reduced bone mineralization [17].
• These findings indicate that leptin may be of importance for osteoblastic cell growth and bone mineralization [18].
• Prominent functions of VDR-regulated genes are to promote intestinal absorption of calcium and phosphate for bone mineralization and to potentiate the hair cycle in mammals [19].
• Hypercalciuric patients also exhibit accelerated radiocalcium turnover, negative Ca balances, reduced bone density, delayed bone mineralization, fasting hypercalciuria, and increased hydroxyproline excretion, all of which reflect participation of the skeleton and presumably a more generalized acceleration of Ca transport [20].
• Calvaria were examined at 2 weeks post-implantation for changes in the bone microenvironment by histology, calcein uptake at sites of bone mineralization, and tartrate-resistant acid phosphatase staining for osteoclasts [21].

Anatomical context of Calcification, Physiologic

• Tissue-nonspecific alkaline phosphatase and plasma cell membrane glycoprotein-1 are central antagonistic regulators of bone mineralization [22].
• Because PS is thought to be important for apatite formation and bone mineralization by binding calcium and phosphate to form calcium-PS-phosphate complexes, the present data suggest that 1,25-(OH)2D3 may stimulate bone mineralization by a direct effect on osteoblasts, stimulating PS synthesis [23].
• We also demonstrate that hLMP-3 is able to induce bone mineralization and the expression of the bone-specific genes, BMP-2, OSX, RunX2, and alkaline phosphatase in human mesenchymal stem cells in a dose-dependent manner [24].
• Under high calcium/oxalate conditions, the absence of THP triggers a marked, adaptive induction in renal epithelial cells of osteopontin (OPN), a potent inhibitor of bone mineralization and vascular calcification [25].
• Concurrent administration of 1alpha,25-dihydroxycholecalciferol [1alpha,25-(OH)2-CC] to intact and thyroparathyroidectomized rats treated with ethane-1-hydroxy-1,1-diphosphonate (EHDP) prevented or reversed the EHDP-induced inhibition of bone mineralization as measured by changes in epiphyseal plate width and ash content of bone [26].

Associations of Calcification, Physiologic with chemical compounds

• Lithium inhibition of bone mineralization and osteoid formation [11].
• Abnormal bone mineralization after fluoride treatment in osteoporosis: a small-angle x-ray-scattering study [27].
• Eight of nine patients who received combined therapy with 24,25-dihydroxyvitamin D3 and calcitriol for longer than two months had clinical improvement; six patients underwent repeated bone biopsy and showed evidence of improved bone mineralization [12].
• In contrast, NE-58095 had minimal effects on bone mineralization [28].
• Bone mineralization in embryonic and postnatal bones was visualized by double staining with alcian blue and alizarin red [29].

Gene context of Calcification, Physiologic

• Our data provide evidence that TNAP and PC-1 are key regulators of the extracellular PP(i) concentrations required for controlled bone mineralization [22].
• The observed decreased mineral content in dmp1 null mice indicates a key role for dmp1 in bone mineralization [30].
• In this rare incidence of estrogen deficiency, estrogen replacement demonstrated its importance for bone mineralization and maturation and glucose metabolism in a male carrying a novel mutation in the CYP19 gene [31].
• To better define the precise role of FGF-23 in maintaining Pi balance and bone mineralization, we generated transgenic mice that express wild-type human FGF-23, under the control of the alpha1(I) collagen promoter, in cells of the osteoblastic lineage [32].
• X-linked hypophosphatemia (XLH) is phenotypically similar to OHO and results from mutations in PHEX, a putative metallopeptidase believed to process a factor(s) regulating bone mineralization and renal phosphate reabsorption [33].

Analytical, diagnostic and therapeutic context of Calcification, Physiologic

• Effects of intermittent parathyroid hormone administration on bone mineralization density in iliac crest biopsies from patients with osteoporosis: a paired study before and after treatment [34].
• CONCLUSIONS: Prepubertal children with CF do not have bone mineral deficit compared with a weight- and sex-matched control group; however, their lower vitamin D levels may portend problems with bone mineralization during adolescence and adulthood [35].
• MAIN OUTCOME MEASURE: The primary outcome was the change in bone mineralization as measured by dual-energy x-ray absorptiometry of the lumbar spine and hip before and after isotretinoin therapy [36].
• The Z scores of the lumbar spine BMD before orchidectomy were -0.8 and -3.1, confirming that patients with AIS have low BMD and that androgen plays an important role in bone mineralization in 46,XY individuals [37].
• Alendronate treatment prevented a decrease in bone mineral density and maintained bone mechanical properties after ovariectomy without impairment of bone mineralization in aged rats [38].

References