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  • 11
    Electronic Resource
    Electronic Resource
    Springer
    Osteoporosis international 5 (1995), S. 283-283 
    ISSN: 1433-2965
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 12
    ISSN: 1432-0827
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 13
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 58 (1996), S. 40-44 
    ISSN: 1432-0827
    Keywords: Key words: Hyperplasia — Hypertrophy — Cell division — Morphometry.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Abstract. Phosphate administration increases both parathyroid hormone (PTH) secretion and parathyroid size in rats, but the relative contribution of hypertrophy and hyperplasia is unknown. Accordingly, we reexamined parathyroid histology in a previously published experiment [6], quantitatively rather than qualitatively. Ninety female Long-Evans rats were divided into six groups; three were given a normal diet, and three a high phosphate diet (Ca/P 1:7). One group from each arm was killed after 1, 2, and 3 months. Quantitative microscopy was performed on the parathyroid section with the largest area from each animal, without knowledge of its experimental status. Total gland area and total number of cell profiles did not change significantly in the control rats, but increased progressively in the phosphate-loaded rats. At 3 months, the difference was +194% for gland area and +151% for profile number (P 〈 0.0001), much more than could be accounted for by suppression of apoptosis. Mean nuclear profile area and mean cell profile area (including associated connective tissue as well as cytoplasm) were both significantly increased at 1 month (P 〈 0.0001). The differences persisted, but their magnitudes (about +16%) did not change further. This time course was consistent with the morphologic expression of increased PTH secretory activity. We conclude that phosphate administration to adult rats increases both size and number of parathyroid cells, the latter due to increased cell proliferation. Phosphate-stimulated parathyroid growth could be due to either hypocalcemia or decreased calcitriol production; increased cell division may also be linked to increased hormone secretion, regardless of its cause. The relative importance of these different mechanisms remains to be determined.
    Type of Medium: Electronic Resource
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  • 14
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 66 (2000), S. 425-429 
    ISSN: 1432-0827
    Keywords: Key words: Calcium infusion — Sodium excretion — Calcium excretion — Hypercalcemia — Tubular function.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Abstract. Assessment of the tubular reabsorption of calcium (Ca) by infusion is complicated by suppression of parathyroid hormone (PTH) secretion, and by activation of the serpentine Ca sensing receptor in the renal tubule, which inhibits Ca and sodium reabsorption, but little is known about the magnitude of the natriuretic effect of Ca in human subjects. Accordingly, we reanalyzed the relationship between serum Ca and urine Ca and sodium excretion expressed per unit of creatinine clearance (CaE and NaE), and per unit of time (UCa and UNa), during a standard Ca infusion, in 14 healthy volunteers and in 8 primary hyperparathyroid patients. In healthy subjects we observed a large effect of Ca infusion on NaE, which rose as high as 8 mmol/liter GFR. In patients with primary hyperparathyroidism both CaE and NaE during Ca infusion were significantly lower overall than in healthy subjects for comparable values of serum Ca (P 〈 0.05 by covariance analysis), due mainly to a decline or reversal of the slopes at the highest serum Ca levels. In both controls and primary hyperparathyroid subjects the variance of CaE as dependent variable was explained by both serum Ca and by NaE as independent variables (P 〈 0.001). We conclude that (1) The natriuretic effect of hypercalcemia was unexpected large and if maintained would lead to substantial depletion of extracellular fluid. (2) Patients with chronic hypercalcemia, including primary hyperparathyroidism, probably have mild sodium depletion, and are more susceptible to volume depletion. (3) Calcium reabsorption during Ca infusion is reduced by suppression of PTH secretion and increased by volume contraction due to sodium depletion. Discrimination between different basal levels of parathyroid function is successful because these effects usually cancel out. (4) The increase in tubular reabsorption of Ca due to volume contraction can initiate a vicious circle, of importance to the pathogenesis and treatment of severe hypercalcemia.
    Type of Medium: Electronic Resource
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  • 15
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 28 (1979), S. 1-5 
    ISSN: 1432-0827
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 16
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 29 (1979), S. 75-76 
    ISSN: 1432-0827
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 17
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 36 (1984), S. S123 
    ISSN: 1432-0827
    Keywords: Bone structure ; Resorption cavity depth ; Plate perforation ; Subendosteal cavitation ; Compensatory trabecular thickening
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary It is proposed that there are two structurally different forms of bone loss with different rates, cellular mechanisms, and biomechanical effects. Rapid bone loss is the result of excessive depth of osteoclastic resorption cavities. This leads in trabecular bone to perforation of structural elements, increased size of marrow cavities, and discontinuity of the bone structure, and in cortical bone to subendosteal cavitation and conversion of the inner third of the cortex to a trabecularlike structure, which then undergoes the same changes as the trabecular bone originally present. These structural characteristics reduce the strength of the bones to a greater extent than the reduction in the amount of bone by itself would suggest. Slow bone loss results from incomplete refilling by osteoblasts of resorption cavities of normal or reduced size. This leads to simple thinning of residual structural elements in both trabecular and cortical bone, and reduces the strength of the bones in proportion to the reduction in the amount of bone. This concept, although derived mainly from an examination of postmenopausal bone loss, may be applicable to other osteopenic states. At the same time as bone loss is occurring on the endosteal surface, rapidly or slowly, bone is being added to the periosteal surface, but much more slowly than during growth. The cellular mechanism is the converse of that causing slow bone loss, consisting of slight overfilling of shallow resorption cavities. Slow periosteal gain serves to partly offset the structural weakness resulting from endosteal loss, but is not directly compensatory. Although less well established and of uncertain frequency and magnitude, it is likely that localized bone gain also occurs on some trabecular surfaces, especially the vertical trabecular plates in the spine that are subjected to compression. In contrast to periosteal gain, this may be a compensatory response to loss of horizontal trabeculae, but the cellular mechanism is unknown.
    Type of Medium: Electronic Resource
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  • 18
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 22 (1976), S. 329-331 
    ISSN: 1432-0827
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 19
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 50 (1992), S. 97-98 
    ISSN: 1432-0827
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 20
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 53 (1993), S. S82 
    ISSN: 1432-0827
    Keywords: Bone turnover ; Osteocyte death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The most plausible purpose for bone remodeling is to prevent excessive aging of bone, which can cause osteocyte death and increase susceptibility to fatigue microdamage. The age of any particular volume of bone depends on two factors: the probability of remodeling beginning on the nearest bone surface, which is given by the local activation frequency; and the probability of a particular remodeling event penetrating to a specified distance from the surface. These two probabilities can be combined in a mathematical model. According to the model, within about 40 μm from the surface, the rate of surface remodeling is the main determinant of bone age, but beyond 40 μm, the distance from the surface becomes progressively more important. Beyond 75 μm, the bone is essentially isolated from surface remodeling. Application of the model to subjects with and without vertebral fracture indicated that the proportion of iliac cancellous bone with a mean age greater than 20 years was less than 20% in all the control subjects without fracture, but was more than 20% in about one-third of the patients with fracture. Bone age is a major determinant of the degree of mineralization, so that osteoporotic patients with prolonged bone age should have bone of higher true mineral density. Accordingly, mineral density distribution was determined by scanning electron microscopy with backscattered electron imaging, calibrated in terms of atomic number. In osteoporotic patients, the mean atomic number was lower, the proportion of bone with high values was lower, and the proportion of bone with low values was higher than in control subjects, the opposite of what would be predicted by the bone age model just described. These data, together with our failure, to date, to detect osteocyte death and fatigue microdamage in iliac cancellous bone in patients with osteoporosis, cast doubt on the role of low bone turnover and increased bone age in the pathogenesis of vertebral fracture. Although conclusive data are still lacking, bone age, osteocyte death, and fatigue failure are more likely relevant to the pathogenesis of hip fracture. Nevertheless, enhanced bone conservation as a result of modest therapeutic inhibition of remodeling activation more than offsets the hypothetical risk of increasing bone age.
    Type of Medium: Electronic Resource
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