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At least 19 recordsLinked to original sources
PubMed2006

Impact of supplement withdrawal and wheat middling inclusion on bone metabolism, bone strength, and the incidence of bone fractures occurring at slaughter in pigs.

The objective of this study was to determine if supplement withdrawal (omission of dietary vitamin and trace mineral premixes and 2/3 of inorganic P) 28-d preslaughter and the feeding of wheat middlings (dietary concentrations of 5, 15, or 30% from weaning to 16 kg, 16 to 28 kg, and 28 kg to slaughter, respectively) affect bone metabolism, bone strength, bone density, and the incidence of bone fractures at slaughter in pigs. Crossbred barrows (n = 64) were assigned to a 2 x 2 factorial arrangement of treatments (with or without supplement withdrawal, and with or without wheat middlings). Serum was collected on d 0, 14, and 27 of the preslaughter withdrawal period to determine changes in the concentrations of osteocalcin, an indicator of bone formation, and pyridinoline, an indicator of bone resorption. The serum osteocalcin and pyridinoline concentrations on d 14 and 27 were analyzed as change from the d-0 concentration. At slaughter, radiographs of the lumbar vertebrae and of the right and left femurs were taken to determine the incidence of bone fractures. Third metacarpal bones were analyzed for bone mineral density, peak load, ultimate shear stress, and percent ash. Supplement withdrawal increased (P < 0.05) serum osteocalcin and pyridinoline concentrations, indicating an increase in osteoblast activity and bone resorption. Supplement withdrawal decreased (P < 0.01) bone mineral density, peak load, ultimate shear stress, and percent ash of the metacarpal bones. Dietary wheat middling inclusion did not alter bone quality. Neither supplement withdrawal nor wheat middling inclusion affected the incidence of bone fractures at slaughter. The results of this study indicate that removing inorganic P, vitamin premix, and trace mineral premix for 28 d preslaughter increases bone turnover and decreases bone quality.

Abattoirs↗
PubMed2005

[Bone metabolism, bone density and estrogen levels in perimenopause: a prospective 2-year-study].

Bone metabolism and trabecular bone density were studied prospectively in 69 pre-, peri- and early postmenopausal women. Markers of bone resorption (OC = osteocalcin, BAP = bonespecific alkalic phosphatase) and bone formation (PYD = pyridinolin, DPD = desoxypyridnolin, NTX = N-terminal telopeptide crosslinked collagen type I, CTX = C-terminal telopeptide crosslinked collagen type I) in serum and urine were followed over a course of two years with five points of examination (0, 3, 6, 12 and 24 months). Bone density was measured at 0 and 24 months. The results of 40 hormonally untreated women who completed all examinations were compared regarding menopausal status and changes over the 2-year-period. While baseline tracecular bone density was lowest in early postmenoapusal women, perimenopausal women showed greatest bone loss (- 10,6 %) during the two year study period. Bone metabolism markers were highest in the postmenopausal group. Perimenopause was associated with a gradual rise in OC, PYD and CTX. Perimenopausal women showed the highest serum estradiol at 0 and 12 months with values exceeding those of premenopausal women. Whether the increased perimenopausal bone loss could be related to the increase in anovulatory cycles during the perimenopausal transition is subject to ongoing investigation.

Adult↗
PubMed2002

Role of endogenous regucalcin in bone metabolism: bone loss is induced in regucalcin transgenic rats.

The role of endogenous regucalcin in the regulation of bone metabolism was investigated by using regucalcin transgenic (TG) rats. The expression of regucalcin mRNA in the femoral-diaphyseal and -metaphyseal tissues of normal (wild-type) rats was shown by using reverse transcription-polymerase chain reaction (RT-PCR) with a specific primer of regucalcin cDNA. Regucalcin protein was detected in the femoral-diaphyseal and -metaphyseal tissues of normal (wild-type) rats using Western analysis. Regucalcin levels were significantly increased in the femoral-metaphyseal tissues of regucalcin TG male rats and in the diaphyseal and metaphyseal tissues of the TG female rats. The morphologic change in the femoral-diaphyseal and -metaphyseal tissues of regucalcin TG rats was demonstrated by using a peripheral quantitative computed tomography (pQCT); morphologic change was great in the femoral tissues of female rats as compared with that of male rats. Mineral content, mineral density and polar strength strain index in the femoral-diaphyseal and -metaphyseal tissues were markedly reduced in regucalcin TG female rats. A significant decrease in cortical thickness was seen in the femoral diaphysis of regucalcin TG female rats. Calcium content in the femoral-diaphyseal and -metaphyseal tissues was significantly decreased in regucalcin TG male and female rats; a remarkable decrease was seen in female rats. Femoral-metaphyseal alkaline phosphatase activity was significantly lowered in regucalcin TG female rats. The enzyme activity was not significantly changed in the femoral-diaphyseal tissues of the TG female rats. In the diaphyseal tissue of male rats, the enzyme activity was significantly decreased in the TG rats. A significant decrease in deoxyribonucleic acid (DNA) content was seen in the metaphyseal tissue of regucalcin TG male rats and in the diaphyseal and metaphyseal tissues of the TG female rats. This study demonstrates that bone loss is induced in the femoral tissue of regucalcin transgenic rats, and that a remarkable decrease in bone morphologic index and biochemical component was seen in the female rats. Regucalcin may be involved in the regulation of bone metabolism.

Animals↗
PubMed2003

Safety profile of frequent short courses of oral glucocorticoids in acute pediatric asthma: impact on bone metabolism, bone density, and adrenal function.

OBJECTIVE: Our study was designed to establish in children with asthma the safety profile of repeated short courses of oral glucocorticoids on bone mineralization and metabolism and adrenal function. METHODS: This cross-sectional study compared the bone density, bone metabolism, and adrenal function of children who were and were not exposed to bursts of oral glucocorticoids. Children were considered exposed when, in the preceding year, they received >or=2 courses of oral glucocorticoids and were prescribed the same therapy for the index exacerbation. Children were considered unexposed when they had no exposure to oral glucocorticoids and were not prescribed any for the index exacerbation. Indices of bone metabolism were measured during the subsequent month. Cortisol responses to adrenocorticotrophic hormone stimulation and bone density were assessed 30 days after the index exacerbation. RESULTS: Eighty-three children (48 exposed, 35 unexposed) aged 2 to 17 years were enrolled. The median exposure level was 4 courses (range: 3-11) in the preceding year. Among exposed children, a transient decrease in serum osteocalcin was observed at the end of the 5-day course with a return to baseline by 30 days; no change was observed in urine pyridinoline cross-links. Mean bone density z score was similar in the exposed (-0.61 +/- 1.0 [standard deviation]) and unexposed (-0.67 +/- 0.9) groups. No cases of abnormal response to adrenocorticotrophic hormone suggestive of adrenal insufficiency were documented in the exposed (95% confidence interval: 0%-7%) or unexposed (0%-10%) groups. CONCLUSIONS: Repeated short courses of oral glucocorticoids in the treatment of asthma seem to be reasonably safe; this practice was not associated with any lasting perturbation in bone metabolism, bone mineralization, or adrenal function.

Acute Disease↗
PubMed2004

[Long-term effects of 7-year growth hormone substitution on bone metabolism, bone density, and bone quality in growth hormone-deficient adults].

BACKGROUND AND PURPOSE: Subnormal bone mineral density (BMD) and increased fracture risk are described in patients with growth hormone deficiency (GHD). Growth hormone (GH) has been reported to have beneficial effects on bone in GHD. The aim of this study was to investigate the long-term effects of GH replacement therapy on bone metabolism, BMD, and bone quality in patients with GHD. PATIENTS AND METHODS: 20 adult patients with GHD (eleven male, nine female, mean age 42.5 years) were included in the study and randomized to either GH or placebo in a dose of 0.25 U/kg body weight/week. After 6 months all patients received GH. After a 1-year double-blind, placebo-controlled study the patients were followed for another 72 months in an open study. The patients were compared to 20 age- und sex-matched healthy controls. Bone turnover was determined by ICTP (type I collagen carboxyterminal cross-linked telopeptide) as parameter of bone resorption and PICP (carboxyterminal propeptide of type I procollagen) as marker of bone formation. BMD was measured at the lumbar spine by dual-photon absorptiometry (DPA) and at the forearm by single-photon absorptiometry (SPA). Apparent phalangeal ultrasound transmission velocity (APU) was assessed as parameter of bone quality independent of BMD. RESULTS: At the beginning of the study BMD at both measuring sites was lower in patients with GHD than in healthy controls. During the 1st year of GH replacement therapy BMD decreased, followed by a continuous increase in BMD (about 12%) up to 60 months which remained unchanged thereafter, building up a plateau. After 72 months no significant difference between the patients and the healthy controls could be detected. Concerning parameters of bone turnover, first ICTP as marker of bone resorption showed a significant increase, later on the marker of bone formation increased as well. APU decreased during the first 6 months of treatment, but had returned to its baseline value after 24 months and remained unchanged throughout the rest of the study. CONCLUSION: BMD is subnormal in adults with GHD. GH replacement therapy stimulates bone turnover in patients with GHD and in the long term such stimulation results in an increased BMD. Thereby, GH shows a triphasic action on BMD: an initial decrease in BMD during the 1st year, followed by a continuous increase in BMD with buildup of a stable plateau after 60 months. The newly formed bone seems to have normal bone elasticity.

Absorptiometry, Photon↗
PubMed1998

Benefits of growth hormone treatment on bone metabolism, bone density and bone strength in growth hormone deficiency and osteoporosis.

Bone mass is reduced in patients with GH deficiency (GHD) leading to an increased vertebral fracture rate and clinically significant osteoporosis. Patients with GHD of juvenile onset have reduced skeletal mineralization. When substituting GH in patients with GHD, bone turnover is increased and bone mineral density initially decreases during the first year due to the increase in remodelling space. From the experience in patients with acromegaly, cortical bone mass is increased and trabecular bone mass is normal in eugonadal or decreased in the hypogonadal patients. However, bone mineral content and bone area are increased leading to a higher biomechanical competence of bone as shown in rats. In patients with GHD of juvenile onset, mineralization and bone maturation are achieved during treatment with GH in adult life after having reached final body height leading to an increase in bone mass. The GH/ IGF-I system is dysregulated in patients with post-menopausal osteoporosis. This is shown by reduced systemic IGF and IGFBP-3-levels in osteoporosis suggesting a decrease of endogenous GH-secretion or a dysregulation of the GH receptor system which is beyond the normal ageing process of the GH/IGF system, the "somatopause". A premature somatopause may be responsible for the dysregulation in some patients with osteoporosis. However, 24-h GH profiles do not differ between patients suffering from osteoporosis or osteoarthritis. Treatment of osteoporosis with GH might be beneficial due to the increased bone metabolism and improved bone geometry which occurs with GH. The substantial increase of bone remodelling achieved with GH may be helpful during late post-menopause with decreased bone turnover and impaired osteoblastic function. Using GH to prevent physiological bone loss that occurs with age seems possible, but has to be discussed on an ethical and economic basis.

Acromegaly↗
PubMed1998

Effect of long-term treatment with GH on bone metabolism, bone mineral density and bone elasticity in GH-deficient adults.

OBJECTIVE: Adults with GH deficiency (GHD) commonly have subnormal bone mineral density (BMD), and have been reported to have an increased risk of fractures. It has been suggested that GH replacement therapy may have beneficial effects on bone in such patients. The aim of this study was to investigate the effects of long-term GH replacement therapy on bone metabolism, BMD and bone elasticity in adults with GHD. DESIGN: At the start of the study, 20 adults with GHD were randomized to receive either GH, 0.25 IU/kg/week (the 'GH group') or placebo (the 'placebo group'). After 6 months, patients in the placebo group were switched to GH therapy, and all patients received GH for a further 42 months. PATIENTS: Of the 20 patients included in the study, 11 were male and nine were female. Mean age at the start of the study was 42.5 +/- 10.1 years. All patients had been GH-deficient for at least 2 years before the start of the study. MEASUREMENTS: Rates of bone resorption and formation were assessed by measuring serum levels of type I collagen carboxyterminal cross-linked telopeptide (ICTP) and carboxyterminal propeptide of type I procollagen (PICP), respectively. BMD was measured at the lumbar spine by dual-photon absorptiometry (DPA) and at the non-dominant forearm by single-photon absorptiometry (SPA). Bone elasticity was assessed by measuring apparent phalangeal ultrasound transmission velocity (APU). RESULTS: The main results in the GH group were as follows. The rate of bone resorption increased significantly during the first 6 months of treatment and remained significantly elevated above its baseline level thereafter. The rate of bone formation also rose during the first 6 months of treatment and remained elevated thereafter, but was significantly higher than at baseline only after 24 months of treatment. At both sites measured, BMD was subnormal at baseline, decreased during the first 6 months of treatment, and increased progressively for the rest of the study, eventually rising well above its baseline level. Bone elasticity decreased during the first 6 months of treatment, but had returned to its baseline level after 24 months. CONCLUSIONS: Our results support previous findings that BMD is subnormal in adults with GHD, that GH replacement therapy can stimulate bone turnover in such adults and that, in the long term, such stimulation results in a significant increase in BMD. In addition they show, for the first time, that BMD may continue to rise even after GH replacement therapy has been administered for 4 years, and indicate that bone elasticity is not adversely affected by long-term GH therapy.

Absorptiometry, Photon↗
PubMed1985

The effect of milk supplements on calcium metabolism, bone metabolism and calcium balance.

Twenty-two healthy postmenopausal women were divided into two groups, one group of 13 received milk supplementation of 24 oz per day and the other group of 9 controls received no intervention during two years of observation. Extensive inpatient metabolic balance and radiocalcium kinetic studies were performed at the beginning and at the end of one year of observation. In the milk supplement group, fractional calcium absorption (x +/- SD) decreased from .243 +/- .058 to .176 +/- .058, absorbed calcium increased from .159 +/- .052 gm/d to .248 +/- .063 gm/d, urine calcium increased from .117 +/- .034 gm/d to .146 +/- .027 gm/d, bone accretion decreased from .385 +/- .079 gm/d to .326 +/- .063 gm/d, bone resorption decreased from .446 +/- .098 gm/d to .342 +/- .106 gm/d and endogenous fecal calcium increased from .105 +/- .023 gm/d to .120 +/- .021 gm/d. All these changes were significant within the group and the mean changes were significantly different from the mean changes observed in the control group. Calcium balance in the milk supplemented group improved from -.061 +/- .056 gm/d to -.017 gm/d +/- .073 gm/d. Predicted changes in calcium and bone metabolism held true except that the suppression of bone remodeling was less than previously found using calcium carbonate supplements. We conclude that milk and milk products can be recommended as sources of calcium, that data on the effects of increasing calcium intake from other sources can be applied to milk and that milk may offer an advantage because it does not suppress bone remodeling as severely as calcium carbonate.

Aged↗
PubMed2004

Long-term changes in bone metabolism, bone mineral density, quantitative ultrasound parameters, and fracture incidence after spinal cord injury: a cross-sectional observational study in 100 paraplegic men.

To study the time course of demineralization and fracture incidence after spinal cord injury (SCI), 100 paraplegic men with complete motor loss were investigated in a cross-sectional study 3 months to 30 years after their traumatic SCI. Fracture history was assessed and verified using patients' files and X-rays. BMD of the lumbar spine (LS), femoral neck (FN), distal forearm (ultradistal part = UDR, 1/3 distal part = 1/3R), distal tibial diaphysis (TDIA), and distal tibial epiphysis (TEPI) was measured using DXA. Stiffness of the calcaneus (QUI.CALC), speed of sound of the tibia (SOS.TIB), and amplitude-dependent SOS across the proximal phalanges (adSOS.PHAL) were measured using QUS. Z-Scores of BMD and quantitative ultrasound (QUS) were plotted against time-since-injury and compared among four groups of paraplegics stratified according to time-since-injury (<1 year, stratum I; 1-9 years, stratum II; 10-19 years, stratum III; 20-29 years, stratum IV). Biochemical markers of bone turnover (deoxypyridinoline/creatinine (D-pyr/Cr), osteocalcin, alkaline phosphatase) and the main parameters of calcium phosphate metabolism were measured. Fifteen out of 98 paraplegics had sustained a total of 39 fragility fractures within 1,010 years of observation. All recorded fractures were fractures of the lower limbs, mean time to first fracture being 8.9 +/- 1.4 years. Fracture incidence increased with time-after-SCI, from 1% in the first 12 months to 4.6%/year in paraplegics since >20 years ( p<.01). The overall fracture incidence was 2.2%/year. Compared with nonfractured paraplegics, those with a fracture history had been injured for a longer time ( p<.01). Furthermore, they had lower Z-scores at FN, TEPI, and TDIA ( p<.01 to <.0001), the largest difference being observed at TDIA, compared with the nonfractured. At the lower limbs, BMD decreased with time at all sites ( r=.49 to.78, all p<.0001). At FN and TEPI, bone loss followed a log curve which leveled off between 1 to 3 years after injury. In contrast, Z-scores of TDIA continuously decreased even beyond 10 years after injury. LS BMD Z-score increased with time-since-SCI ( p<.05). Similarly to DXA, QUS allowed differentiation of early and rapid trabecular bone loss (QUI.CALC) vs slow and continuous cortical bone loss (SOS.TIB). Biochemical markers reflected a disproportion between highly elevated bone resorption and almost normal bone formation early after injury. Turnover declined following a log curve with time-after-SCI, however, D-pyr/Cr remained elevated in 30% of paraplegics injured >10 years. In paraplegic men early (trabecular) and persistent (cortical) bone loss occurs at the lower limbs and leads to an increasing fracture incidence with time-after-SCI.

Absorptiometry, Photon↗
PubMed1993

The effects of 2-year treatment with the aminobisphosphonate alendronate on bone metabolism, bone histomorphometry, and bone strength in ovariectomized nonhuman primates.

This study examined the effect of 2 yr of treatment with the aminobisphosphonate alendronate (ALN) (0.05 or 0.25 mg/kg i.v. ALN every 2 wk) on estrogen deficiency bone loss and bone strength changes in ovariectomized (OVX) baboons (n = 7 per group) and the ALN mode of action at the tissue level. Biochemical markers of bone turnover increased in OVX animals and were maintained by ALN treatment at non-OVX levels (low dose) or below (high dose). 2 yr of treatment produced no cumulative effects on bone turnover markers. Histomorphometry showed a marked increase in cancellous bone remodeling in OVX animals. Activation frequency increased from 0.48 to 0.86 per yr (L5 vertebra), and the osteoid surfaces from 9 to 13.5% (P < 0.05). No changes were observed in eroded and osteoclast surfaces. ALN treatment decreased activation frequency and indices of bone formation to control levels (low dose) or below (high dose), did not change indices of mineralization, and increased bone mineral density (BMD) in the lumbar vertebrae (L2-L4) by 15% at 0.25 mg/kg (P < 0.05), relative to vehicle-treated animals. The mean strength of cancellous bone (L4) increased by 44% (low ALN dose) and 100% (high dose), compared with vehicle. The strength of individual bones correlated with the square of the L2-L4 BMD (r = 0.91, P < 0.0034). In conclusion, ALN treatment reversed the effects of ovariectomy on cancellous bone turnover and increased bone mass and bone strength in baboons.

Acid Phosphatase↗
PubMed1998

[Effect of Kliogest on bone metabolism, bone mineral density and quality of life in postmenopausal patients].

UNLABELLED: The author investigated postmenopausal patients (with a natural menopause) (n = 32) where ammenorrhoea persisted for 1-2.2 years. They found a reduced bone mineral density (BMD) (ostoeopenia or osteoporosis) and laboratory tests revealed signs of increased bone turnover (so-called "fast losers"). Before administration of Kliogest R tablets, Novo Nordisk, Denmark, (1 tablet per day) and after 12 months the following parameters were evaluated: 1. Laboratory parameters of bone turnover: serum osteocalcin (OC) amino-terminal N-telopeptide of collagen I in 24-hour diuresis (NTx). 2. Bone mineral desnity (BMD) in lumbal vertebrae L1-L4 assessed by DXA (dual energy X-ray absorptiometry 3. By means of questionnaires climacteric symptoms were evaluated (score of climacteric symptoms). For statistical analysis of the assessed values the non-paired Wilcoxon-Wilcoxon test was used. RESULTS: After treatment the OC levels were significantly lower (alpha = 0.05, p < 0.01), the values of NTx were highly significantly lower (alpha = 0.05, p < 0.001) and the BMD values in the second lumbar vertebra (it is usually most affected by osteoporosis), expressed by the T-score, was significantly higher (alpha = 0.05, p < 0.001). When evaluating the questionnaire "Score of climacteric symptoms" after treatment the number of points characterizing the intensity of symptoms was reduced. Most frequently improvement of the following symptoms was achieved: hot flushes and noctural perspiration, weakness, fatigue, impaired sleep, nervousness, irritability, dry vagina making intercourse unpleasant. CONCLUSION: One-year use of Kliogest increased significantly the density of the bone mineral in the axial skeleton, reduced the bone turnover and improved the quality of life of postmenopausal patients.

Bone Density↗
PubMed2004

Immunosuppressive and postoperative effects of orthotopic liver transplantation on bone metabolism.

Bone loss occurs early after orthotopic liver transplantation (OLT) in all liver transplant recipients and leads to postoperative fractures, especially in cholestatic patients with the lowest bone mass. Little is known about the underlying changes in bone metabolism after OLT or about the etiology of these changes. Histomorphometric analysis of bone biopsies, a method that allows assessment of bone volume, resorption, and formation, has shown improved bone metabolism at 4 months after OLT. It has further suggested that accelerated posttransplant bone loss occurs in the first 1-2 months after OLT, probably by an additional insult to bone formation. This study attempts to correlate the histomorphometric bone changes in paired bone biopsies (OLT and 4 months after OLT) of 33 patients undergoing OLT for chronic cholestatic liver disease with the many clinical and biochemical changes in these patients over the same period. Cumulative steroid dosage early after OLT is shown to be important, presumably by decreasing bone formation rates. The actual effect of calcineurin inhibitors on this early phase of bone loss is less clear, although posttransplant histomorphometric findings suggest that tacrolimus-treated patients have an earlier recovery of bone metabolism and trabecular structure compared with cyclosporine patients. Other factors important in the recovery of bone metabolism after the early phase of bone loss are recovery of liver and gonadal function and better calcium balance.

Bone Density↗
PubMed2000

Interaction of the effects between vitamin D receptor polymorphism and exercise training on bone metabolism.

Bone metabolism is strongly influenced by heredity and environmental factors. To investigate interaction of the effects between vitamin D receptor polymorphism by Fok I and resistance exercise training on bone metabolism, young male subjects with FF genotype (F, n = 10) and Ff or ff genotypes (f, n = 10) followed 1 mo of weight training, and changes in bone metabolism were compared. An additional 14 subjects served as a sedentary control. Biomarkers of bone formation, bone-specific alkaline phosphatase, and osteocalcin were significantly increased by training in both F and f groups. 1, 25-Dihydroxyvitamin D(3), known to upregulate bone formation, was also increased by the training in the f but not in the F group. Bone resorption assessed by cross-linked NH(2)-terminal telopeptide of type I collagen was significantly suppressed by the training, and the decrease in F was greater and longer lasting than that in f group. In conclusion, stimulation of bone formation and suppression of bone resorption occurred within 1 mo in young men. Despite a significant increase in 1,25-dihydroxyvitamin D(3) in the f group but not in the F group, the response of bone metabolism to the training in the F was similar to or greater than that in f group, suggesting a functional difference between vitamin D receptor genotypes f and F.

Adult↗
PubMedDate not supplied

Biochemical markers of bone metabolism.

Bone metabolic homeostasis is regulated by a number of hormones and local modulators, and the study of these factors has been of major help in our understanding of bone disease. However, these parameters do not, in a strict sense reflect the metabolic and biochemical changes in the diseased bone tissue. Thus, there is a great interest in the study of biochemical specific "markers" of bone metabolic processes, namely of bone formation and bone resorption. Alkaline phosphatase, osteocalcin, osteonectin, and procollagen type I propeptides are the currently known markers of bone formation, whereas urinary hydroxyproline and hydroxylysine glycosides, plasma tartrate resistant acid phosphatase, and urinary hydroxy-pyridinium crosslinks of collagen are considered markers of bone resorption. In this paper, we review the background work on each of these markers, and subsequently give an overview of the currently available data on their usefulness in metabolic bone diseases, namely in Paget's disease of bone, primary hyperparathyroidism, osteoporosis, and renal osteodystrophy.

Biomarkers↗