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Bone sialoprotein is a specific biochemical marker of bone metabolism in postmenopausal women: a randomized 1-year study.

Accelerated bone remodeling after the menopause is associated with increased bone loss that can be abolished using hormone replacement therapy (HRT). Biochemical markers of bone metabolism are known to correlate closely with changes in bone histomorphometry and osteodensitometry. Bone sialoprotein (BSP), a major constituent of bone matrix, is almost exclusively found in mineralized tissues and therefore considered a potential marker of bone metabolism. In 82 postmenopausal women, randomly allocated to either low-dose sequential HRT or no HRT, serum BSP was measured and compared with established specific biochemical markers of bone resorption [urinary deoxypyridinoline (DPD), pyridinoline (PYD) and amino-terminal telopeptide (NTx)] and markers of bone formation [serum osteocalcin (Oc) and bone-specific alkaline phosphatase (bALP)]. Longitudinal analysis showed a marked response of BSP levels following commencement of HRT, resulting in a 52% reduction after 12 months compared with initial values. The changes of BSP levels over time were at least as strong as in conventional markers of bone formation and resorption and paralleled their changes. A moderate to close correlation was found between BSP and both markers of bone resorption (r = 0.57 for NTx; r = 0.38 for DPD) and formation (r = 0.55 for Oc; r = 0.39 for bALP; p < 0.0001, respectively). Our data demonstrate a cause and effect relationship between commencement of HRT and a change in serum BSP. In conclusion, serum BSP circumvents some of the limitations of urinary measurements and appears valuable for the quantitative monitoring of the skeletal response to HRT in healthy postmenopausal women.

Aged↗

Computer-simulated bone architecture in a simple bone-remodeling model based on a reaction-diffusion system.

Bone is a complex system with functions including those of adaptation and repair. To understand how bone cells can create a structure adapted to the mechanical environment, we propose a simple bone remodeling model based on a reaction-diffusion system influenced by mechanical stress. Two-dimensional bone models were created and subjected to mechanical loads. The conventional finite element method (FEM) was used to calculate stress distribution. A stress-reactive reaction-diffusion model was constructed and used to simulate bone remodeling under mechanical loads. When an external mechanical stress was applied, stimulated bone formation and subsequent activation of bone resorption produced an efficient adaptation of the internal shape of the model bone to a given stress, and demonstrated major structures of trabecular bone seen in the human femoral neck. The degree of adaptation could be controlled by modulating the diffusion constants of hypothetical local factors. We also tried to demonstrate the deformation of bone structure during osteoporosis by the modulation of a parameter affecting the balance between formation and resorption. This simple model gives us an insight into how bone cells can create an architecture adapted to environmental stress, and will serve as a useful tool to understand both physiological and pathological states of bone based on structural information.

Bone Remodeling↗

Effects of skeletal loading on bone mass and compensation mechanism in bone: a new insight into the "mechanostat" theory.

We have suggested that: (i) osteocalcin carboxylation is related to bone material properties (bone quality), and (ii) impairment of bone material properties could be compensated by bone mass increase. The aim of the present prospective study was to investigate whether the effects of skeletal loading on bone mass were associated with the compensation mechanism between bone mass and bone material properties. The subjects were 56 healthy female volunteers aged around 50 years. They were classified into pre- and postmenopausal groups, and each group was then subdivided into a no-exercise (control) and a vertical jumping exercise group. Bone mineral density (BMD) was measured at baseline and after the 6-month study period. Urinary gamma-carboxyglutamate (Gla), a possible parameter of osteocalcin carboxylation, was also measured at baseline. Among the premenopausal women, hip BMD in the exercise group increased significantly in comparison to the control value. Among the postmenopausal women, however, there was no significant difference in the BMD change between the control and the exercise group. In addition, the baseline urinary Gla level showed an inverse correlation with the change in whole body BMD in the premenopausal exercise group. These results suggest that: (i) estrogen plays a certain role in the high-impact exercise-induced bone gain, and (ii) the effects of skeletal loading on bone mass are involved in the compensation mechanism, i.e., bone gain due to high-impact exercise becomes greater in accordance with the degree of deterioration in bone material properties. Our concept of the compensation mechanism could provide a new insight into the understanding of the skeleton's adaptability to load-bearing.

1-Carboxyglutamic Acid↗

Changes in bone mineral and bone formation rates during pregnancy and lactation in rats.

Changes in bone chemistry, cortical bone morphometry, and periosteal and trabecular bone formation rates were determined during pregnancy and lactation in rats. Data were obtained using chemical, static morphometric, and fluorochrome-based histomorphometric methods in pregnant or lactating animals and compared with age-matched, unmated controls. There were significant increases in bone weight, ash weight, calcium content, and femoral cross-sectional area by late pregnancy and decreases in these same parameters during lactation. There were also decreases in bone mass and increases in surface:volume ratios of trabecular bone during lactation. There were increases in femoral periosteal and endosteal perimeters associated with the reproductive cycle. Bone formation and appositional rates at the periosteal and endosteal surfaces were elevated during pregnancy, particularly evident at midpregnancy. Periosteal bone formation rates declined during lactation, but trabecular bone formation rates increased. These results indicate that during pregnancy there are increases in bone formation rates contributing to the increases in skeletal mass. During lactation in rats, reductions in skeletal mass are accompanied by increases in bone turnover, particularly evident in trabecular bone.

Animals↗

Experimental evaluation of the holding power/stiffness of the self-tapping bone screws in normal and osteoporotic bone material.

OBJECTIVE: The goal of this study is to compare the holding power of the self-tapping bone screws in normal and osteoporotic bone materials. BACKGROUND: Self-tapping screws are increasingly being used in orthopaedic surgery due to their advantages over the other bone screws. METHODS: Screws were divided into five groups (six screws per group) based on the depth of insertion in the bone coupons that represented normal and osteoporotic bones. Screws were randomly inserted into the bone coupons with tips of the screws being -1 mm, 0 mm, 1 mm, 2 mm and 3 mm relative to the far cortex. Biomechanical testing was performed using an Instron 8,511 in accordance with the American Society for Testing and Materials standards for bone screws. Two-factor analysis of variance (ANOVA) was used to determine if the holding power of the screws were different with respect to insertion depths and bone materials. FINDINGS: The bone materials had a significant difference (P < 0.05) in the holding power and depths of insertion past the far cortex were significantly different from one another in holding power. The affect of the screw material on the holding power of the self-tapping screws in different bone materials was also examined. The performance of stainless steel screws was superior to that of titanium screws in the osteoporotic material. INTERPRETATION: Based on the results it can be concluded that the depth of insertion of the tip of the screw for adequate fracture fixation in normal bone is 1mm or more past the far cortex and in osteoporotic bone it is at least 2mm past the far cortex.

Bone Screws↗

Expression of bone morphogenetic proteins in normal human intramembranous and endochondral bones.

Bone morphogenetic proteins (BMPs) are growth and differentiation factors that have been purified and widely accepted to be the most important regulators in the processes of bone formation. The aim of this study was to identify the BMPs that are expressed in normal human bone, and to investigate the specific pattern of BMP2-BMP9 expression in normal human intramembranous and endochondral bone to maintain homeostasis, as well as in ex vivo primary cell culture of human osteoblasts from intramembranous and endochondral bone. Semi-quantitative RT-PCR indicated that 2 types of bone of different embryological origin have distinct patterns of BMP expression. BMP3, 4, 7 and 8 were strongly expressed in normal intramembranous bone compared to endochondral bone, whereas BMP2 and 5 were highly expressed in endochondral bone. The expression of BMP9 and BMP15 in human bone was identified for the first time. From the very similar expression patterns of BMPs in fresh normal bone and ex vivo osteoblastic cell culture, it can be proposed that the different proportions of BMPs in normal human intramembranous and endochondral bone needed to maintain normal homeostasis.

Adult↗

Bone marrow stem cells and biological scaffold for bone repair in aging and disease.

The loss of bone mass observed in aging enhances the risk of fractures. The process of bone repair in aging is slow and limited due to reduced activity of the osteoblasts. Bone marrow stem cells (MSCs) residing in the bone marrow are the progenitors for osteoblasts. The ability to enhance healing of bone defect in aging by MSCs can contribute in the prevention of the complications resulting from long-term immobilization that are especially fatal in old age. Our aim was to test the ability of MSCs inserted into a biological scaffold to enhance bone defect repair. Osteoprogenitor cells were selected from rat bone marrow stem cells cultured in DMEM medium supplemented with FCS, antibiotics, ascorbic acid, beta-glycerophosphate, and dexamethasone. The selected osteogenic subpopulation was identified by osteocalcin immunohistochemistry as well as Alizarin red S and von Kossa staining which are specific for bone matrix and mineral deposition. Committed osteoprogenitor cells cultured on the hydrogel scaffold were transplanted into the area of a rat tibia segmental bone defect and examined after 6 weeks. Radiology images revealed that 6 weeks post-implantaion, calcified material was present in the site of the defect, indicating new bone formation. It is concluded that committed osteogenic MSCs contained in a biocompatible scaffold can provide a promising surgical tool for enhancement of bone defect healing that will minimize the complications of bone repair in aging and disease.

Aging↗

Prednisolone alone, or in combination with estrogen or dietary calcium deficiency or immobilization, inhibits bone formation but does not induce bone loss in mature rats.

Glucocorticoid use has long been recognized as a risk factor for bone loss, resulting in an increased fracture incidence in humans. However, steroid-treated patients often present with other complications that predispose to bone loss, such as immobilization, and little is known about the interaction of these other risk factors for bone loss and glucocorticoids. In the present study, mature female rats were treated with prednisolone (Pred) or vehicle, in combination with ovariectomy (ovx), dietary calcium deficiency (LoCa), or right hind limb immobilization (IM). After 4 weeks of treatment, the rats were killed and the right tibia and tibiofibular junction were collected for quantitative histomorphometric analysis and the right femur was collected for bone mineral density (BMD) and mechanical strength determinations. As expected, ovx, LoCa, and IM decreased BMD in the distal femur and cancellous bone volume (CnBV/TV) in the proximal tibia. All Pred-treated groups responded with increases of BMD and CnBV/TV, when compared to their respective non-Pred treated groups. Mechanical strength testing of the cancellous bone of the distal femur reflected the changes in BMD and CnBV/TV. No differences in trabecular plate thickness were noted in any of the treatment groups. The Pred group showed a significant reduction in longitudinal growth rate, as well as bone formation rate (BFR/BS), in the proximal tibia when compared with their respective control groups, the latter indicated by a decrease in both mineralizing surface and mineral apposition rate. Most notably, osteoclast surface and urinary free pyridinoline, a bone resorption marker, increased significantly with each of the three risk factors. Pred treatment inhibited these increases but it did not exert significant reductions when used by itself. At the tibiofibular junction, there were no measurable changes in either total bone or cortical bone area. Endocortical BFR/BS were increased by ovx or LoCa but each was lowered by Pred treatment. Periosteal BFR/BS were increased by ovx and IM, and Pred exerted significant inhibition by itself and in combination with other risk factors. We conclude, therefore, that unlike the effects observed in humans treated with glucocorticoid, treatment of rats with prednisolone not only does not result in bone loss but may exert a protective effect on the skeleton through the inhibition of bone resorption.

Amino Acids↗

Clinical outcome of autogenous bone blocks or guided bone regeneration with e-PTFE membranes for the reconstruction of narrow edentulous ridges.

The aim of this study was to analyse the clinical outcome of two different surgical methods for the reconstruction of narrow edentulous ridges before implant installation: guided bone regeneration with e-PTFE membranes and autologous bone chips or grafting of autologous bone blocks without e-PTFE membranes. Thirty partially edentulous patients, presenting insufficient bone width (less than 4 mm) in the edentulous sites for installation of screw-type titanium implants, were selected and assigned to two different treatment modalities. Fifteen patients (group 1) were treated by means of guided bone regeneration with e-PTFE membranes supported by stainless steel screws and autologous bone chips taken from intraoral sites. Fifteen patients (group 2) were treated by means of autologous bone blocks taken from intraoral or extraoral sites (anterior iliac crest and calvaria) and stabilized with titanium microscrews. Six to 8 months later, during re-entry for implant insertion, the gain of ridge width obtained was measured. In group 1 the average amount of bone gain was 2.7 mm, whereas in group 2 the value was 4.0 mm. Five to 6 months after implant placement prosthetic rehabilitation was started. The mean follow-up after prosthetic load has been 22.4 months. Success rates of implants according to Albrektsson criteria has been 93.3% in group 1, and 90.9% in group 2. Although a statistical comparison between the two treatment modalities may not be feasible, due to the bias resulting from the choice of treatment by the clinician and from the differences in donor sites and defect extension, some considerations can be made: 1) both methods are a reliable means for the correction of narrow edentulous ridges; 2) both techniques necessitate overcorrection of the defect because of interposition of connective tissue beneath the membrane in the first group and bone resorption in the second one; 3) the use of semipermeable barriers increases the costs of the surgical procedure, as compared to bone grafting without membranes; 4) guided bone regeneration presents a higher risk of infection because of wound dehiscence and membrane exposure. Therefore, in case of wide edentulous areas, reconstruction of narrow ridges should be performed with bone blocks without membranes.

Adult↗

Contribution of the periosteum to bone formation in guided bone regeneration. A study in monkeys.

The periosteum has been referred to as a protective barrier in the regeneration of bone defects. The objective of this study was to determine the contribution of periosteum as a natural barrier to bone formation in guided bone regeneration. Mucoperiosteal flaps were elevated bilaterally on the buccal aspect of the mandibular angle in 5 cynomolgus monkeys. Bleeding was induced by perforating the cortical bone. A hemispherical titanium mesh was fixed over the areas thus creating a void 5 mm in height between the mesh and the bone surface. One one side the mesh was covered with an ePTFE membrane (test side). The contralateral side did not receive further treatment (control side). After 4 month healing, histomorphometric analyses were used to determine the percentage of new bone in the void underneath the mesh, and the ratio between mineralized tissue and marrow spaces in new and old bone. The mean percentage of new bone tissue was 77.2 +/- 7.5% for the test sides and 68.6 +/- 8.4% for the control sides (P = 0.018, t-test). This new bone contained 80.0 +/- 3.6% mineralized tissue in the test group and 82.5 +/- 5.0% in the control group (P > 0.05, t-test). In both groups the newly formed bone exhibited significantly less mineralized tissue than the old bone (P < 0.05, t-test). It is concluded from this study that new bone formation was enhanced by the additional use of an ePTFE membrane under a periosteum-lined mucoperiosteal flap when space maintenance was excluded as a critical factor.

Animals↗

Bone metabolism in advanced cholestatic liver disease: analysis by bone histomorphometry.

Despite the clinical importance of cholestatic osteopenia, little is known about its pathophysiologic mechanism. By tetracycline-labeled histomorphometric analysis of bone biopsies taken at the time of liver transplantation, we prospectively evaluated bone resorption and formation in 50 consecutive patients with advanced primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC). Histomorphometric analysis confirmed low bone volume parameters, consistent with the mean T-score of the lumbar spine of -1.9 by dual energy x-ray absorptiometry. Dynamic (bone formation rates, adjusted apposition rates) and static (osteoid markers, osteoblast number) parameters of bone formation were decreased in cholestatic patients with no abnormalities in mineralization. Increased osteoclast numbers and increased eroded surface areas suggested increased bone resorption, and this was supported in female patients by increased trabecular separation and decreased trabecular number. Male cholestatic patients, however, did not have significant increases in resorption parameters, although they were as osteopenic as female patients and had low bone formation markers. Bone histomorphometric changes were similar in PBC and PSC, suggesting an etiologic effect of chronic cholestasis rather than the individual diseases. Cancellous bone volume and osteoid markers correlated with bone mineral density measurements but no correlations were found between histomorphometric parameters and biochemical markers of bone metabolism. In conclusion, cholestatic osteopenia appears to result from a combination of decreased bone formation and increased resorption, especially in female patients, but the relative importance of these two abnormalities and their actual etiology remain to be elucidated.

Adult↗

Dissociation between bone resorption and bone formation in osteopenic transgenic mice.

Bone mass is maintained constant in vertebrates through bone remodeling (BR). BR is characterized by osteoclastic resorption of preexisting bone followed by de novo bone formation by osteoblasts. This sequence of events and the fact that bone mass remains constant in physiological situation lead to the assumption that resorption and formation are regulated by each other during BR. Recent evidence shows that cells of the osteoblastic lineage are involved in osteoclast differentiation. However, the existence of a functional link between the two activities, formation and resorption, has never been shown in vivo. To define the role of bone formation in the control of bone resorption, we generated an inducible osteoblast ablation mouse model. These mice developed a reversible osteopenia. Functional analyses showed that in the absence of bone formation, bone resorption continued to occur normally, leading to an osteoporosis of controllable severity, whose appearance could be prevented by an antiresorptive agent. This study establishes that bone formation and/or bone mass do not control the extent of bone resorption in vivo.

Animals↗

Polymorphisms in the low-density lipoprotein receptor-related protein 5 (LRP5) gene are associated with variation in vertebral bone mass, vertebral bone size, and stature in whites.

Stature, bone size, and bone mass are interrelated traits with high heritability, but the major genes that govern these phenotypes remain unknown. Independent genomewide quantitative-trait locus studies have suggested a locus for bone-mineral density and stature at chromosome 11q12-13, a region harboring the low-density lipoprotein receptor-related protein 5 (LRP5) gene. Mutations in the LRP5 gene were recently implicated in osteoporosis-pseudoglioma and "high-bone-mass" syndromes. To test whether polymorphisms in the LRP5 gene contribute to bone-mass determination in the general population, we studied a cross-sectional cohort of 889 healthy whites of both sexes. Significant associations were found for a missense substitution in exon 9 (c.2047G-->A) with lumbar spine (LS)-bone-mineral content (BMC) (P=.0032), with bone area (P=.0014), and with stature (P=.0062). The associations were observed mainly in adult men, in whom LRP5 polymorphisms accounted for <or=15% of the traits' variances. Results of haplotype analysis of five single-nucleotide polymorphisms in the LRP5 region suggest that additional genetic variation within the locus might also contribute to bone-mass and size determination. To confirm our results, we investigated whether LRP5 haplotypes were associated with 1-year gain in vertebral bone mass and size in 386 prepubertal children. Significant associations were observed for changes in BMC (P=.0348) and bone area (P=.0286) in males but not females, independently supporting our observations of a mostly male-specific effect, as seen in the adults. Together, these results suggest that LRP5 variants significantly contribute to LS-bone-mass and size determination in men by influencing vertebral bone growth during childhood.

Adolescent↗

Evaluation of heterotopic bone formation induced by squalane and bone morphogenetic protein composite.

Bone morphogenetic protein is an important molecule whose bioactivity depends on the carrier. Squalane is used in the formulation of various kinds of cosmetics because it is easily emulsified and has the property of spreading well. Thus, squalane might be effective as a bone morphogenetic protein delivery system. As a test for this possibility, gelatin capsules containing squalane and bone morphogenetic protein (bovine derived partially purified) composite were implanted under the hind-quarter perimuscular membrane of ddY mice. Control capsules containing only bone morphogenetic protein were used for controls. The implants were radiographically and histologically examined at 1 to 4 weeks after the operation. According to the radiographic analysis, squalane and bone morphogenetic protein composite and bone morphogenetic protein only control specimens formed widespread heterotopic bone tissues. The amount of heterotopic bone formation in the composite experimental specimens was approximately 40% greater than that in the controls. Histologic examination of experimental and control specimens revealed varying amounts of perichondral ossification by 2 weeks. By 3 and 4 weeks, the bone deposits were colonized by hematopoietic bone marrow. Squalane was effective for the slow local release of bone morphogenetic protein. Furthermore, the squalane and bone morphogenetic protein composite was a reliable osteoinductive biomaterial.

Animals↗

Do ultrasound measurements reflect bone microarchitecture rather than bone mass?: An in vitro study of the rat femur with the use of ultrasound, densitometry, and histomorphometry.

RATIONALE AND OBJECTIVES: In an experimental study in 40 rat femurs, the authors correlated the amplitude-dependent speed of bone ultrasound (Ad-SOS) with the bone mineral content and density and with the bone trabecular connectivity: trabecular bone volume, trabecular number, trabecular thickness, and trabecular separation to evaluate and compare the usefulness of the Ad-SOS to determine bone quantity and/or quality. METHODS: Bone mineral content and density were determined with dual-energy x-ray absorptiometry. Trabecular connectivity was determined with histomorphometric techniques. RESULTS: There was a strong correlation between the Ad-SOS and the other parameters studied, with a particularly high positive correlation with trabecular bone volume and trabecular thickness, and an inverse correlation with trabecular separation. The correlation was weaker with the bone mineral content and bone mineral density and with the trabecular number. For the trabecular separation, the correlation was significant in all cases, but it was negative. CONCLUSIONS: Bone ultrasound, in this case Ad-SOS, defines the quality of the bone in terms of trabecular architecture rather than bone density; however, this conclusion is valid only for the rat femur model that the authors used.

Absorptiometry, Photon↗

The significant effects of bone structure on inherent patient-specific DXA in vivo bone mineral density measurement inaccuracies.

An extended analytic exposition is developed of the effects bone structure has on the form and extent of systematic inaccuracies in planar dual-energy x-ray absorptiometry (DXA) in vivo bone mineral density (BMD) measurements. Explicit expressions for absolute and percentage BMD inaccuracies are derived and criteria governing these BMD inaccuracies delineated. It is shown that the effect of bone structure is to introduce a scale factor which modulates the sizable and unavoidable DXA in vivo/in situ BMD inaccuracies that arise directly from patient-specific anthropometric and x-ray absorptiometric disparities among the several soft tissues present within the scan region of interest of any given bone site (i.e., lean muscle tissue, interposed and admixed fat, and red/yellow marrow combinations). Different magnitudes and patterns of BMD inaccuracies are shown to pertain for bone structures that are (i) essentially wholly trabecular, (ii) wholly cortical, and (iii) those containing both cortical and trabecular bone. Over the range of soft tissue anthropometrics typical of adult patients, the overall percentage inaccuracies in DXA-measured BMD are shown to be quite sizable and to vary considerably for different bone structures. For a typical lumbar vertebral bone site, BMD inaccuracies are found to be as large as approximately 25% for normal patients, to exceed approximately 35% for osteopenics, and to approach 50% for osteoporotic individuals. For bone sites with non-negligible cortical surrounds of trabecular structures (e.g., distal radius, some segments of proximal femur, etc.), it is shown that BMD percentage inaccuracies range up to approximately 20% for normal, approximately 25% osteopenic, and approximately 35% for osteoporotic patients. The BMD % inaccuracies associated with wholly cortical bone (trabecular-free) sites (e.g., mid-shaft femur, mid-shaft radius, etc.) are comparatively small, being less than approximately 2%. Depending on bone structure, bone size and shape, and patient-specific intra- and extra-osseous soft tissue particulars of any given adult patient, DXA in vivo BMD measurements can be grossly inaccurate, and can severely under- or over-estimate the true value of BMD and mask or exaggerate true changes in BMD in ways not previously elucidated. It is concluded that in vivo DXA-measured and actual BMD cannot be considered to be synonymous, and clinical reliance upon the two being the same may readily conduce to seriously flawed and misleading diagnostic, prognostic, and prospective results.

Absorptiometry, Photon↗

Bone markers and bone mineral density during growth hormone treatment in children with growth hormone deficiency.

Growth hormone (GH) has a positive impact on muscle mass, growth and bone formation. It is known to interact with the bone-forming unit, with well-documented increases in markers of bone formation and bone resorption within weeks of the start of GH therapy. These changes relate significantly to short-term growth rate, but it is not evident that they predict long-term response to GH therapy. The consequences of GH deficiency (GHD) and GH replacement therapy on bone mineral density (BMD) have been difficult to interpret in children because of the dependency of areal BMD on height and weight. Some studies have tried to overcome this problem by calculating volumetric BMD, but results are conflicting. The attainment of a normal peak bone mass in an individual is considered important for the future prevention of osteoporosis. From the limited data available, it appears difficult to normalize bone mass totally in GH-deficient individuals, despite GH treatment for long periods. Studies to date examining the interaction between GH and bone have included only small numbers of individuals, making it difficult to interpret the study findings. It is hoped that these issues can be clarified in future research by the direct measurement of bone density (using quantitative computer tomography). Mineralization is only one facet of bone strength, however; other important components (e.g. bone structure and geometry) should be addressed in future paediatric studies. Future studies could also address the importance of the degree of GHD in childhood; how GH dose and insulin-like growth factor-I levels achieved during therapy relate to the final outcome; whether or not the continuation of GH therapy after the attainment of final height may further enhance bone mass; whether the timing and dose of other treatments (e.g. sex hormone replacement therapy) are critical to the outcome; and whether GHD in childhood is associated with an increased risk of fracture.

Biomarkers↗

Assessment of bone mineral content and bone mass by non-invasive radiologic methods.

Methods for quantitative determination of bone mineral and bone mass in normal subjects and in patients with metabolic bone disorders can be measured by the Compton scattering technique, the neutron activation analysis, by measurement of metacarpal bone mass, by single and dual photon absorptiometry, and by quantitative computed tomography. Measurement on metacarpal bone (radiogrammetry) seems to be able to distinguish between resorption and/or new bone formation at the periosteal and/or endosteal surface. The intraindividual observer variation on combined cortical thickness (D-d), cortical area (D2-d2), metacarpal bone mass (D2-d2)/D2-varies from 0.7 to 2.5 per cent and the interindividual observer variation from 1.0 to 5.8 per cent. Single photon absorptiometry measures bone mineral content in the forearm with great precision. The reproducibility using repeated measurements and automatic selection of the measuring area is about one per cent and can be used to follow changes in mineral content with time in patients with metabolic bone diseases. The dual photon absorptiometry may be used for measurements of bone mineral content in lumbar spine, in the femoral neck and measurement of total body calcium with an accuracy of less than 6 per cent and a precision below 3 per cent. Quantitative computed tomography has the ability to measure trabecular and cortical bone both centrally and peripherally. Using CT scanning, scanner related changes with time (day-to-day variation +/- 4%), patient repositioning (less than 1.5%), and fat concentration (residual uncertainty of approximately 1/6 of the biologic variation) are important factors influencing the accuracy and reproducibility of the values of the measured bone mineral content.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone Diseases, Metabolic↗