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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Osteoporosis international 4 (1994), S. S71 
    ISSN: 1433-2965
    Keywords: Calcium ; Hip fracture ; Osteoporosis ; Vitamin D
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The two main determinants of hip fractures are falls and bone loss leading to an intrinsic femoral fragility. Substantial femoral bone loss continues throughout old age, with a continuous and exponential increase in the risk of hip fracture; thus any reduction or arrest of this loss will induce an important reduction in the incidence of hip fracture. Preventive measures may be achieved during childhood by increasing peak bone mass with calcium and exercise, by using long-term estrogen replacement therapy after menopause, but also by using vitamin D and calcium supplements for late prevention in the elderly. Vitamin D insufficiency and a deficit in calcium intake are very common in the elderly living either in institutions or at home and the cumulative response to these deficits is a negative calcium balance which stimulates parathyroid hormone secretion. This senile secondary hyperparathyroidism is one of the determinants of femoral bone loss and can be reversed by calcium and vitamin D supplements. We have shown in a 3-year controlled prospective study that the daily use of supplements (1.2 g calcium and 800 IU vitamin D3) given in a large population of 3270 elderly ambulatory women living in nursing homes reduced the number of hip fractures by 23% (intention-to-treat analysis). In parallel, serum parathyroid hormone concentrations were reduced by 28% and low baseline serum 25-hydroxy vitamin D concentration returned to normal values. After 18 months of treatment the bone density of the total proximal femoral region had increased by 2.7% in the vitamin D3-calcium group and decreased by 4.6% in the placebo group (p〈0.001). This prevention is safe and can be recommended for people living in institutions. It could also be useful in other elderly subjects at particular risk due to a low calcium intake, an absence of solar exposure, a low femoral bone density, a high serum parathyroid hormone concentration, a low serum 25-hydroxyvitamin D concentration and a previous history of falls. Prospective studies are needed for further evaluation of these risk factors.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1433-2965
    Keywords: Hormone replacement therapy ; hPTH 1–34 treatment ; Osteoporosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Twelve patients with vertebral fracture osteoporosis were recruited into a trial of treatment with hPTH 1–34 by daily injection for 1 year combined (from the 5th month) with an anti-resorptive agent (oestrogen, n=9; nandrolone, n=3). Treatment outcomes were monitored by biochemical and radiotracer measurements together with histomorphometry of transiliac biopsies before and at the end of treatment following double in vivo pre-labelling with demethylchlortetracyc-line. Indices of whole body bone formation, obtained from the analysis of85Sr data, showed substantial increases (P〈0.005) for all three indices measured) while biochemical (hydroxyproline) and kinetic measurements of bone resorption showed modest and equivocal changes only. As a result calcium balance improved. Gastrointestinal calcium absorption showed a tendency to improve, while urine calcium decreased; but these changes were statistically not significant except for radiocalcium absorption in the oestrogen treated subgroup. Histomorphometry revealed substantial increases in cancellous bone volume as reported previously with hPTH 1–34 given alone. However, iliac (as distinct from whole body) indices related to bone formation and resorption appeared to have returned towards pre-treatment values by the time of the second biopsy under the influence of the anti-resorptive agent given with the hPTH 1–34. It is confirmed that hPTH 1–34 therapy can increase iliac cancellous bone mass (as well as spinal cancellous bone mass as reported earlier) without a long-term increment in whole body bone resorption, providing the hPTH is combined with an anti-resorptive agent.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1433-2965
    Keywords: Bone histomorphometry ; Calcium-47 ; Calcium absorption ; Osteoporosis ; Vitamin D
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Patients with vertebral osteoporosis have a wide range of bone loss rates, bone remodelling rates and capacities for gastrointestinal (GI) calcium absorption. To test the hypothesis that variations in GI absorptive capacity determine rates of bone loss or remodelling, we have sought relationships betwen calcium absorption or vitamin D metabolite levels on the one hand and rates of cancellous and cortical bone loss (measured by serial quantiative computed tomography in the radius;n=25) or indices of bone remodelling in tetracycline-prelabelled transiliac biopsies (n=41) on the other, in a sequential untreated group. Calcium absorption (net and true) was measured in 18-day balances and by a two-isotope deconvolution method (fractional absorption and maximum absorption rate, MAR). There was no significant seasonal effect on any of these four measures of calcium absorption (variance ratio,F=0.52–1.61,p〉0.1) or on 1,25-dihydroxyvitamin D levels (F=0.13,p〉0.1; range 11–69 pg/ml), notwithstanding the expected seasonal effect on 25-hydroxyvitamin D levels (mean 18.7 ng/ml, zenith mid July, semi-amplitude 7.5 ng/ml;F=6.82,p〈0.01). Neither this metabolite nor 1,25-dihydroxyvitamin D correlated with any index of calcium absorption (p〉0.1). No measure of calcium absorption (or intake) had a significant relationship with radial cortical or cancellous bone loss (p all 〉0.1) but cancellous bone loss was associated with the rate of endogenous calcium excretion (r=0.50,p〈0.05). A positive relationship between 25-hydroxyvitamin D and unlabelled osteoid surface (a marker of reduced blast vigour) persisted after adjustment for season (Student'st=2.70,p〈0.01) but did not reflect 1,25-dihydroxyvitamin D levels. This study did not address the question of whether reduced GI calcium absorption has a uniform effect on bone remodelling in osteoporosis. However, variations in capacity for calcium absorption are unlikely to be responsible for the heterogeneity in bone loss and remodelling rates seen in vertebral osteoporosis.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1433-2965
    Keywords: Bone ; Histomorphometry ; Osteoporosis ; Osteoblasts ; Osteocalcin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To assess the bone turnover abnormalities which characterize postmenopausal osteoporosis with vertebral fractures (PMOp), a transiliac bone biopsy was performed after double labeling of the mineralizing front with tetracycline in 50 untreated PMOp patients who were compared with 13 healthy age-matched volunteer females. The analysis of bone remodeling and structure parameters demonstrated that PMOp is a disease affecting both the cancellous and the endocortical envelopes and characterized by increased resorption and by a marked decrease in the osteoblastic apposition rate due to a reduced duration of bone formation. This induces a decrease in the width of both individual osteons and trabeculae. In PMOp, the wide spectrum of bone turnover as compared with the controls, associated with the typical bimodal distribution of cancellous osteoid perimeter, allowed us to identify two subsets, one with normal turnover (NT) and one with high turnover (HT) representing 30% of the cases. When compared to NT, HT was characterized by increased osteoclast number, lower bone volume, thinner osteons, increased formation at the tissue-level and markedly decreased duration of formation. In HT the marked decrease in the duration of activity of osteoblasts and the markedly increased number of osteoclasts induced a greater decrease in bone volume, despite the increase of bone formation at the tissue level. These subsets could not be distinguished by any clinical or biochemical parameter except for serum bone gla protein (osteocalcin) which was significantly higher (as a group) in HT than in NT. The underlying cause for these two subsets is unknown. We conclude that PMOp affects the cancellous and the endocortical bone. Bone loss results from a wide spectrum of bone turnover abnormalities, with two distinct subsets, one with normal turnover and one with high turnover.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 35 (1983), S. 410-417 
    ISSN: 1432-0827
    Keywords: Bone remodeling ; Histomorphometry ; Corticosteroid therapy ; Osteoporosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary We have compared the mean wall thickness (MWT) and active formation periods (sigmaf(A)) of trabecular bone packets in iliac crest biopsies from 20 patients (7 male, 13 female) with corticosteroid-induced osteoporosis (CS-OP) and 20 age- and sex-matched controls. The trabecular bone volume (TBV) of the CS-OP patients (9.6%±2.2% [SD]) was significantly reduced compared to controls (19.3%±5.1%). The MWT of CS-OP patients (32.7±4.3 µm) was also significantly lower than the control value (48.0±6.2 µm). There was a positive correlation between MWT and TBV in both groups. The mineralization rate (M) of the CS-OP patients (0.54±0.25 µm/day) was within the normal range, and since there was no increase in osteoid seam thickness, so therefore was the osteoblastic appositional rate (OAR). The active formation period of trabecular bone packets (sigmaf(A)=MWT/M) was significantly lower in the CS-OP patients (55.9 ± 14.4 days) than in the control group (68.1 ± 9.4 days). MWT and sigmaf(A) both decreased with age in the control group, whereas in the CS-OP group they were independent of age. We conclude that corticosteroid therapy results in a reduction of the MWT of trabecular bone packets and, consequently, of TBV. In these patients, where the OAR was normal, the reduction in MWT was apparently caused by a shortening of the lifespan of the active osteoblastic population at the basic multicellular unit (BMU) level.
    Type of Medium: Electronic Resource
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