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Query: EC:3.1.3.1 (
alkaline phosphatase
)
47,916
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The long-term effects of low concentrations of sodium fluoride (0, 1 and 5 mg/l) in drinking water on bone metabolism were examined in the growing senescence accelerated mouse (SAM-P/6) as a spontaneous experimental model of senile
osteoporosis
. In 4 and 8 months of age respectively, there were almost no differences in body weight, and serum calcium, phosphorus and
alkaline phosphatase
levels between controls and fluoride groups. Calcium contents per dry weight of femoral bone were higher in fluoride groups than in controls. The bone mass of the trabecular was not affected by the low-concentration sodium fluoride intake. However, sodium fluoride decreased the rate of bone mass loss associated with aging in the cortical bone in SAM-P/6 compared with the control. The results of this study suggest that, in growing SAM-P/6 mice, a long-term low-concentration sodium fluoride intake affects the skeletal metabolism.
...
PMID:[The effects of long-term intake of a low concentration of sodium fluoride on bone loss in the growing senescence-accelerated mouse (SAM-P/6)]. 151 55
In this study we evaluated whether the fluoride-induced increased bone formation in
osteoporosis
is mediated by stimulation of bone cell proliferation and/or differentiation. We analyzed the kinetics of DNA synthesis and the phenotypic features of osteoblastic cells isolated from the trabecular bone surface in relationship to histomorphometric indices of bone formation evaluated on the same bone biopsy in 12 osteoporotic patients treated with fluoride. Osteoblastic cells isolated from patients with a higher than normal bone formation rate, increased mean wall thickness of trabecular bone packets, and high trabecular bone volume after fluoride therapy displayed a higher than normal rate of DNA synthesis in vitro. The peak of [3H]thymidine incorporation into DNA, the maximal DNA synthesis, and the area under the growth curve of osteoblastic cells isolated from these patients were higher than the values in normal bone cells obtained from age-matched controls. By contrast, in vitro parameters of osteoblastic cell proliferation were not different from normal in fluoride-treated
osteoporosis
patients in whom bone formation was not increased, although the duration of treatment and bone fluoride content were not different. Parameters of bone cell proliferation in vitro were increased in correlation with the mean wall thickness, and the latter correlated with the trabecular bone volume, indicating that the augmentation of bone formation and bone volume induced by fluoride was paralleled by an increased proliferation of osteoblastic cells. Basal osteocalcin production (corrected for cell protein) and
alkaline phosphatase
activity in vitro were comparable, and the response to 1,25-dihydroxyvitamin D3 (10 nmol/liter, 48 h) was not different in normal osteoblastic cells and in cells from fluoride-treated
osteoporosis
patients whether they had high or normal bone formation. The results show that the fluoride-induced increased bone formation in osteoporotic patients is associated with an increased in vitro proliferative capacity of osteoblastic cells lining the trabecular bone surface, whereas parameters of osteoblast differentiation are not affected. The data also suggest that induction of a higher than normal bone cell proliferation is prerequisite for the stimulation of bone formation by fluoride.
...
PMID:Stimulation of bone formation in osteoporosis patients treated with fluoride associated with increased DNA synthesis by osteoblastic cells in vitro. 154 53
The synthesis of osteocalcin or bone gla protein by osteoblasts is markedly stimulated by 1,25-(OH)2D, a key hormone in the regulation of bone mineralization. The circulating levels of osteocalcin have been shown to reflect both the osteoid matrix production and the formation rate of mineralized bone in several metabolic bone diseases (
osteoporosis
, thyrotoxicosis, primary hyperparathyroidism) in which both mechanisms are tightly coupled because of the absence of mineralization defect. In this study, we measured in 12 patients (7 women, 5 men, 56 +/- 15 yr old) with untreated osteomalacia serum osteocalcin and vitamin D metabolites (25OHD and 1,25-(OH)2D). The results were correlated with biochemical and histomorphometric assessment of bone remodeling. Osteomalacia was due to vitamin D deficiency (5 cases), to vitamin D malabsorption (6 cases), and to hypophosphataemia in 1 case. When compared to control values, serum osteocalcin was increased in patients with osteomalacia (7.4 +/- 4 vs. 3.7 +/- 1.3 ng/mL; P less than 0.001) and was positively correlated with serum
alkaline phosphatase
(r = 0.65; P = 0.03) and negatively with 25 OHD (r = -0.61; P = 0.04). Serum osteocalcin was not correlated with 1,25-(OH)2D [r = -0.45; not significant (NS)] even after exclusion of the patient with hypophosphataemia. Serum osteocalcin was positively correlated with the osteoid volume and osteoid perimeter (r = 0.71 and 0.69 respectively; P less than 0.01) but not with any of the tetracycline-based parameter of bone mineralization at the tissue level (r ranging from -0.41 to +0.42, NS). Serum 25 OHD, but not 1,25-(OH)2D, was positively correlated with the mineralization rate (r = 0.59; P less than 0.05 and r = 0.54; NS). We conclude that in patients with osteomalacia, a condition which is characterized by an increased osteoid accumulation due to a decreased mineralization rate, the increased level of serum osteocalcin reflects the increased osteoid synthesis but not the mineralization defect. In this disease, serum osteocalcin is inversely correlated to the severity of vitamin D deficiency reflected by serum 25 OHD, but not to the serum levels of 1,25-(OH)2D.
...
PMID:Serum osteocalcin is increased in patients with osteomalacia: correlations with biochemical and histomorphometric findings. 156 62
Intestinal disease might contribute to osteopenia. Measurements of IgA antibodies to gliadin have been established as an accepted screening procedure for detection of coeliac disease. When we applied these measurements to 92 patients with verified
osteoporosis
, 11 subjects (12%) were found to have elevated levels. This is markedly higher than the incidence in healthy subjects (3%). However, the patients with raised levels of IgA antibodies displayed no clinical symptoms and no laboratory evidence of calcium malabsorption. Thus their values for serum calcium, phosphate, parathyroid hormone (PTH),
alkaline phosphatase
and osteocalcin, as well as the fasting urinary excretion of hydroxyproline and calcium, were similar to those found in other patients with
osteoporosis
. Intestinal biopsy verified coeliac disease in three patients and was normal in another three. This gives an incidence of verified coeliac disease in this patient group that is approximately tenfold higher than that in the healthy population. Subclinical coeliac disease appears to be unusually over-represented among patients with idiopathic
osteoporosis
, and screening for gliadin antibodies might therefore be a valuable addition to the routine assessment of the osteopenic patient. The mechanisms underlying the relationship are not clear, but calcium malabsorption is not evident.
...
PMID:Screening for antibodies against gliadin in patients with osteoporosis. 158 66
Thirty seven postmenopausal women aged under 65 with densitometric
osteoporosis
defined by a bone density value below the 80th percentile of the osteoporotic population but without identifiable crush fractures, were treated and monitored for two years using clinical, laboratory and densitometric parameters. Sixteen of them were given hormonal replacement therapy combining percutaneous or transdermal 17 beta estradiol with a progestogen and the other 21 sodium fluoride at the dose of 50 mg/d combined with calcium and vitamin D. There was a significant increase in vertebral bone density in both groups: 6.3 +/- 0.9 per cent for hormone treatment and 7.1 +/- 1.5% for fluoride after 2 years, while it fell in a control group. The increase was linear with fluoride, while 2/3 of the gain was acquired by the end of the first year of hormonal therapy. Nine of the 16 patients on hormonal therapy and 9 of the 21 taking fluoride showed a significant vertebral gain at 2 years (greater than or equal to 0.043 g/cm2). There was no parameter which enabled the identification of "responders" before treatment. There was no difference in changes in femoral bone density between patients treated with fluoride and controls. From a laboratory standpoint, hormonal therapy caused a significant fall at 12 months in the urinary calcium/urinary creatinine ratio, and a non-significant fall in osteocalcin at 2 years. With fluoride, there was a marked rise in osteocalcin and a more moderate rise in
alkaline phosphatase
, reflecting stimulation of bone formation without any variation in resorption. In conclusion, this study shows the ability of both these types of treatment of increasing, by different mechanisms, the vertebral bone density of osteoporotic women. However, it does not indicate the extent to which this gain in bone density might have a positive influence on fracture risk.
...
PMID:[Comparative effects of sodium fluoride and hormonal replacement therapy on bone metabolism in osteoporotic women with high fracture risk. Results of monitoring for 2 years]. 160 21
Experimental studies in vitro indicate that insulin-like growth factor 1 (IGF-1) could be of importance for normal bone growth and remodelling, but the clinical relevance of these observations is unknown. In 12 consecutive young to middle-aged male patients (mean age (+/- SD) 46 +/- 8 years, range 30-57 years) with symptomatic idiopathic
osteoporosis
, the plasma concentrations of IGF-1 were significantly lower than in healthy subjects (0.51 +/- 0.25 vs. 0.73 +/- 0.23 U ml-1; P less than 0.01). The bone mineral densities in the spine, the femoral neck, and the forearm were significantly different between patients and control subjects. There were positive correlations between the plasma IGF-1 concentrations and the bone densities of the spine and the forearm. Three of the patients received a 5-d course of human recombinant growth hormone (GH). During this short period significant increases in plasma IGF-1 levels and in biochemical indices of bone turnover (serum bone-specific
alkaline phosphatase
, urinary calcium excretion) were recorded. These observations indicate that circulating IGF-1 could have an important role in maintaining bone mass, and suggest that impairment of IGF-1 production is involved in the pathogenesis of
osteoporosis
.
...
PMID:Low plasma levels of insulin-like growth factor 1 (IGF-1) in male patients with idiopathic osteoporosis. 164 Jan 93
Study was undertaken to identify polypeptide factors in the commercially available ossein-mineral-compound and to see if they are present in a biologically relevant quantity. Using the guanidine-EDTA extraction, 35.7 +/- 0.1 mg proteins were obtained from 1 g of the ossein-mineral-compound. At concentration 1 micrograms/ml, guanidine-EDTA-extractable proteins stimulated the incorporation of thymidine into DNA by human bone cells to 581 +/- 122% (p less than 0.001) of that by bovine serum albumin-treated control cells, decreasing thereafter. Similarly, it stimulated the activity of
alkaline phosphatase
in the human bone cells. Growth factors IGF-I, IGF-II, and TGF-beta were identified in the ossein-mineral-compound. This leads to speculation regarding possible role of growth factors in explaining the beneficial effects of the compound in retarding bone loss in patients with
osteoporosis
.
...
PMID:Quantitation of growth factors in ossein-mineral-compound. 165 84
1. We studied the mechanism of action of the anabolic steroid, stanozolol, in 23 patients with
osteoporosis
, using a combination of biochemical and histomorphometric techniques. 2. Treatment with stanozolol (5 mg/day) for 1 year was associated with a marked and significant decrease in the fasting urinary excretion of calcium (P less than 0.01) but not with changes in the serum concentrations of calcium and phosphate, the serum activity of
alkaline phosphatase
, the renal tubular reabsorption of calcium or the urinary excretion of hydroxyproline. 3. Histological examination of trabecular bone showed an increase in bone turnover and the bone formation rate increased twofold (P less than 0.02). There were no significant changes in bone volume or wall thickness after treatment. Tetracycline labelling was used to discriminate bone structural units completed before and during treatment. Measurements of the wall thickness of those bone structural units formed during treatment showed no significant change. 4. Measurements made on the endocortical surface also showed an increase in bone turnover, but in contrast to trabecular bone, the bone structural units formed at endocortical sites during treatment had a significantly greater wall thickness than those formed before treatment (P less than 0.05). 5. We conclude that stanozolol increases the turnover of trabecular bone and increases the endocortical apposition of bone.
...
PMID:Stanozolol stimulates remodelling of trabecular bone and net formation of bone at the endocortical surface. 165 3
Protective effects of ipriflavone, an isoflavone derivative, in
osteoporosis
are believed to be caused by the inhibitory action on bone resorption. A direct effect of ipriflavone on bone formation is as yet unknown. Ipriflavone and four of its metabolites (I, II, III, and V) were examined for their effects on parathyroid hormone response, collagen synthesis,
alkaline phosphatase
activity, and cell proliferation in a clonal cell population of rat osteoblastic cells. Pretreatment of osteoblasts with high concentrations of ipriflavone for 48 h significantly inhibited the cAMP response to parathyroid hormone, producing a shift in the dose-response curve; at lower concentrations metabolites II and III potentiated the cAMP accumulation induced by low doses of parathyroid hormone. The 48 h treatment with metabolite V at the 1 nM dose significantly stimulated collagen synthesis in osteoblastic cells. Ipriflavone and metabolite I showed a biphasic stimulatory action on the
alkaline phosphatase
activity of osteoblasts, with a maximal effect at the 0.1 and 1 nM doses, respectively. A similar biphasic response was observed with ipriflavone and metabolite I on osteoblastic cell growth, with a maximal effect at the 0.1 nM concentration. These results suggest a direct role of ipriflavone in modulating the synthetic and growth properties of osteoblast-like cells.
...
PMID:Effects of ipriflavone and its metabolites on a clonal osteoblastic cell line. 166 5
For assessing the risk of adverse complications of surgery the group of 130 patients with post-operational hypoparathyroidism was analysed. Surgical hypoparathyroidism has been diagnosed in 51% of operated on thyroid gland patients. Laryngeal nerves have been damaged in 46.6% of patients. The injury to laryngeal nerves has been irreversible in 2/3 of patients, and reversible in the remaining 1/3. Cataract, nephrolithiasis and vitamin D3 intoxication have been observed in some cases before surgery. Their incidence increased in severe surgical hypoparathyroidism.
Osteoporosis
of the spine has been diagnosed in 49% of patients including some with vertebral fractures. No correlation between the degree of spine
osteoporosis
and diagnosis before surgery, number of operations on thyroid gland, and type of therapy has been noted. The symptoms of hypercalcemia have been diagnosed in 5 patients out of which hypercalcemia has been transient in 2 patients, and lasted for 1-5 months in the remaining 3 patients. The results of 7,873 analyses of mineral metabolism have been assessed. Hypocalcemia has been found in 38.4%, hypercalcemia in 1.6%, hypomagnesemia in 25.7%, hyperphosphatemia in 41.5%, decreased
alkaline phosphatase
serum activity in 28.7%, and hypercalciuria in 22.4% of cases. Surgical hypoparathyroidism is frequently accompanied by surgical hypothyroidism and injury to the recurrent laryngeal nerves.
...
PMID:[Postoperative hypoparathyroidism: risk of complications]. 166 68
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