Changes In Bone Mass Research Articles

Effect of the material’s stiffness on stress-shielding in osseointegrated implants for bone-anchored prostheses: a numerical analysis and initial benchmark data

This study attempted to establish the link between design of implants for bone-anchored prostheses and stress-shielding, affecting the stability of the bone-implant coupling using numerical approach. The objectives were to share a numerical model capable to evaluate the long-term stability of implants and to use this model to extract data sets showing how shape and material stiffness of threaded, press-fit and modular press-fit implants affect stress-shielding intensity. Three designs were considered: threaded, press-fit and modular press-fit. The effect of shape and material stiffness of each design on stress-shielding intensity was assessed using Young's modulus (10 to 210 GPa). Furthermore, the impact of the diameter of percutaneous part (10 to 18 mm) and thickness of medullar part (5 to 1 mm) was investigated for the modular press-fit implant. The threaded design generated 4% more bone mass loss at the distal femur but an overall loss of bone mass was by 5% lower to press-fit design. The influence of Young's modulus on bone mass changes was noticeable for modular press-fit implant, depending on diameter of percutaneous or medullary part. A 20 GPa change of stiffness caused a bone mass change from 0.65% up to 2.45% and from 0.07% up to 0.32% for percutaneous parts with 18 mm and 10 mm diameter, respectively. Results suggested that threaded implant provides greater stability despite an increased bone loss at the distal femur. Altogether, this work provided an initial model that could be applied in subsequent studies on the long-term stability of current and upcoming implants.

Risk assessments for osteoporotic fracture and refracture

Osteoporosis is a metabolic bone disease characterized by decreased bone mass and degenerative changes in the microstructure of bone tissue, leading to increased bone brittleness and fracture risk. Bone fracture after osteoporosis is the most common and serious complication, which often leads to serious consequences in cases of inadequate prevention and late diagnosis. Therefore, more attention should be paid to prevention of osteoporosis and risk assessment of fracture and refracture after osteoporosis. This paper reviews the research progress in risk assessment of fracture and refracture after osteoporosis from the aspects of imaging, clinical manifestations and laboratory examination indexes. In recent years, the imaging methods have developed from dual-energy X-ray absorption, trabecular bone scoring and CT to high resolution peripheral quantitative CT; concern for their clinical manifestations has developed from independent risk factors to fracture risk assessment tools; the laboratory tests have developed from bone turnover markers and serotonin to microRNA. Although these developments have consistently increased the sensitivity of risk assessment for fracture and refracture after osteoporosis, problems still exist and need to be resolved. Key words: Osteoporotic fractures; Risk assessment; Review; Refracture

Occlusal trauma inhibits osteoblast differentiation and bone formation through IKK‐NF‐κB signaling

Occlusal trauma is an important factor promoting bone loss caused by periodontal diseases. Although there are reports of traumatic force promoting bone resorption in periodontal diseases, no studies examining the inhibition of bone formation by traumatic force and the underlying mechanism have been reported. The aim of this study was to investigate the mechanism whereby traumatic force inhibits bone formation. MC3T3-E1 cells were induced to undergo osteogenic differentiation and subjected to cyclic uniaxial compressive stress with or without stimulation with Pg. LPS. The expression of osteoblast markers and the activation of IKK-NF-κB signaling were evaluated in vitro. Then, MC3T3-E1 cells were induced to undergo osteogenic differentiation and subjected to cyclic uniaxial compressive stress with or without IKK-2 Inhibitor VI. The expression of osteoblast markers was determined. Then, the classic Wnt signaling pathway (β-catenin, Gsk3β, p-Gsk3β, and Dkk1) was further evaluated in vitro. Finally, occlusal trauma was induced in Wistar rats with or without the injection of IKK-2 Inhibitor VI, to evaluate changes in bone mass and IKK-NF-κB and Wnt/β-catenin signaling in vivo. After stimulation with Pg. LPS and traumatic force, IKK-NF-κB signaling was significantly activated in vitro. The expression of osteoblast markers and the activity of alkaline phosphatase in MC3T3-E1 cells declined after traumatic force loading and were rescued when IKK-NF-κB signaling was blocked. Wnt/β-catenin signaling was accordingly inhibited upon force loading, but this inhibition was reversed when IKK-NF-κB was antagonized in vitro. X-ray and Micro-CT analysis of the mandibles of the rats as well as HE and TRAP staining showed that bone loss induced by occlusal trauma declined after IKK-NF-κB was inhibited. The expression of p65 and IκBα was increased when occlusal trauma was induced in Wistar rats, whereas β-catenin, OCN, and Runx2 levels were decreased. After blocking IKK-NF-κB, significant upregulation of β-catenin, OCN, and Runx2 was observed in rats suffering from occlusal trauma. IKK-NF-κB signaling could be activated by traumatic force or occlusal trauma. Its activation promoted the degradation of β-catenin, ultimately inhibiting osteogenic differentiation in vitro and bone formation in vivo.

Sclerostin Antibody-Induced Changes in Bone Mass Are Site Specific in Developing Crania.

Sclerostin antibody (Scl-Ab) is an anabolic bone agent that has been shown to increase bone mass in clinical trials of adult diseases of low bone mass, such as osteoporosis and osteogenesis imperfecta (OI). Its use to decrease bone fragility in pediatric OI has shown efficacy in several growing mouse models, suggesting translational potential to pediatric disorders of low bone mass. However, the effects of pharmacologic inhibition of sclerostin during periods of rapid growth and development have not yet been described with respect to the cranium, where lifelong deficiency of functioning sclerostin leads to patterns of excessive bone growth, cranial compression, and facial palsy. In the present study, we undertook dimensional and volumetric measurements in the skulls of growing Brtl/+ OI mice treated with Scl-Ab to examine whether therapy-induced phenotypic changes were similar to those observed clinically in patients with sclerosteosis or Van Buchem disorder. Mice treated between 3 and 14 weeks of age with high doses of Scl-Ab show significant calvarial thickening capable of rescuing OI-induced deficiencies in skull thickness. Other changes in cranial morphology, such as lengths and distances between anatomic landmarks, intracranial volume, and suture interdigitation, showed minimal effects of Scl-Ab when compared with growth-induced differences over the treatment duration. Treatment-induced narrowing of foramina was limited to sites of vascular but not neural passage, suggesting patterns of local regulation. Together, these findings reveal a site specificity of Scl-Ab action in the calvaria with no measurable cranial nerve impingement or brainstem compression. This differentiation from the observed outcomes of lifelong sclerostin deficiency complements reports of Scl-Ab treatment efficacy at other skeletal sites with the prospect of minimal cranial secondary complications. © 2019 American Society for Bone and Mineral Research. © 2019 American Society for Bone and Mineral Research.

Longitudinal Effects of Acute Anterior Cruciate Ligament Tears on Peri-Articular Bone in Human Knees Within the First Year of Injury.

Anterior cruciate ligament (ACL) tears are common sports-related knee injuries that increase the risk of developing post-traumatic osteoarthritis. ACL tears are rarely an isolated injury but are often associated with traumatic bone marrow lesions (BMLs). While early loss of bone mass following the ACL injury has been previously described, to date, microarchitectural information has not been reported due to the limited resolution of clinical imaging systems. In this study, we provide the first evidence of detailed bone mass and microarchitectural changes in the first 10 months following an acute ACL tear, and localized to traumatic BMLs. Fifteen participants with an acute unilateral ACL tear were assessed at four-time points using dual-energy X-ray absorptiometry and high-resolution peripheral quantitative computed tomography, and traumatic BMLs were identified with magnetic resonance imaging. Loss of bone mass was localized to the injured knee (-4.6% to -15.8%, depending on bone and depth) and was accelerated immediately following the injury before suggesting a recovery phase. This loss of bone was accelerated even greater in traumatic BMLs (-18.2% to -20.6%, depending on bone). Bone loss was accompanied by microstructural degeneration of trabecular bone. For example, in the lateral femur of the injured knee, the subchondral bone plate decreased in thickness (-9.0%). This study confirmed loss of bone mass in the months following ACL tears and described the underlying bone microstructural changes. The presented bone changes were accelerated in regions of traumatic BMLs. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 37:2325-2336, 2019.

Prediction of bone mass changes after successful parathyroidectomy using biochemical markers of bone metabolism in primary hyperparathyroidism: is it clinically useful?

To measure type 1 serum amino-terminal propeptide procollagen (P1NP) and type 1 cross-linked C-terminal telopeptide collagen (CTX) before parathyroidectomy (PTX) in PHPT patients, correlating these measurements with bone mineral density (BMD) changes. 31 primary hyperparathyroidism (HPTP) were followed from diagnosis up to 12-18 months after surgery. Serum levels of calcium, parathyroid hormone (PTH) vitamin D, CTX, P1NP, and BMD were measured before and 1 year after surgery. One year after PTX, the mean BMD increased by 8.6%, 5.5%, 5.5%, and 2.2% in the lumbar spine, femoral neck (FN), total hip (TH), and distal third of the nondominant radius (R33%), respectively. There was a significant correlation between BMD change 1 year after the PTX and CTX (L1-L4: r = 0.614, p < 0.0003; FN: r = 0.497, p < 0.0051; TH: r = 0.595, p < 0.0005; R33%: r = 0.364, p < 0.043) and P1NP (L1-L4: r = 0,687, p < 0,0001; FN: r = 0,533, p < 0,0024; TH: r = 0,642, p < 0,0001; R33%: r = 0,467, p < 0,0079) preoperative levels. The increase in 25(OH)D levels has no correlation with BMD increase (r = -0.135; p = 0.4816). On linear regression, a minimum preoperative CTX value of 0.331 ng/mL or P1NP of 37.9 ng/mL was associated with a minimum 4% increase in L1-L4 BMD. In TH, minimum preoperative values of 0.684 ng/mL for CTX and 76.0 ng/mL for P1NP were associated with a ≥ 4% increase in BMD. PHPT patients presented a significant correlation between preoperative levels of turnover markers and BMD improvement 1 year after PTX.

The glucocorticoid receptor in osteoprogenitors regulates bone mass and marrow fat.

Excess fat within bone marrow is associated with lower bone density. Metabolic stressors such as chronic caloric restriction (CR) can exacerbate marrow adiposity, and increased glucocorticoid signaling and adrenergic signaling are implicated in this phenotype. The current study tested the role of glucocorticoid signaling in CR-induced stress by conditionally deleting the glucocorticoid receptor (GR) in bone marrow osteoprogenitors (Osx1-Cre) of mice subjected to CR and ad libitum diets. Conditional knockout of the GR (GR-CKO) reduced cortical and trabecular bone mass as compared to wildtype (WT) mice under both ad libitum and CR conditions. No interaction was detected between genotype and diet, suggesting that the GR is not required for CR-induced skeletal changes. The lower bone mass in GR-CKO mice, and the further suppression of bone by CR, resulted from suppressed bone formation. Interestingly, treatment with the -adrenergic receptor antagonist propranolol mildly but selectively improved metrics of cortical bone mass in GR-CKO mice during CR, suggesting interaction between adrenergic and glucocorticoid signaling pathways that affects cortical bone. GR-CKO mice dramatically increased marrow fat under both ad libitum and CR-fed conditions, and surprisingly propranolol treatment was unable to rescue CR-induced marrow fat in either WT or GR-CKO mice. Additionally, serum corticosterone levels were selectively elevated in GR-CKO mice with CR, suggesting the possibility of bone-hypothalamus-pituitary-adrenal crosstalk during metabolic stress. This work highlights the complexities of glucocorticoid and β-adrenergic signaling in stress-induced changes in bone mass, and the importance of GR function in suppressing marrow adipogenesis while maintaining healthy bone mass.

A Dynamic Model of Calcium Metabolism for Predicting the Effects of Treatments on Bone Mineral Mass in Young Growing Rats (P24-046-19)

ObjectivesQuantifying the long-term effects of nutritional or drug treatments on bone is challenging due to the delay in time between treatment and changes in bone mass. The objective of this study was to develop a dynamic (non-steady state) mathematical model of calcium metabolism in young growing rats as an analogue for human adolescents and to use that model to predict the effects of treatments on calcium mass in bone. MethodsA dynamic model of calcium metabolism was developed using kinetic data collected from Sprague-Dawley male rats (n = 54) dosed intraperitoneally with 50 μCi of 45Ca at 4 wk of age. Total calcium and 45Ca levels measured in serum and 24-h urine samples collected periodically for 45 d after treatment were analyzed by compartmental modeling using WinSAAM software. Concurrently, tracer (45Ca) and tracee (total calcium) models, together called the ‘dynamic model’, were developed. Growth of the rats was modeled using a formula based on body weight. Calcium absorption was decreased by about 50% at wk 6 to account for the reduction in bone mineral accretion in late puberty. During the first 40 d after weaning, the model included a 4-fold decrease in bone resorption and a 20-fold decrease in bone formation, consistent with previous findings of studies conducted in growing rats. Data were fitted by iterative least squares regression analysis. To mimic the effects of dietary and drug interventions during adolescence, the absorption efficiency was manipulated in terms of degree, timing, and duration and the subsequent changes in bone mass were quantified. ResultsThe dynamic model predicted that, if absorption decreased by 25% instead of 50% during growth, the rate of bone accretion would be 32% higher and the bone mineral mass at d 50 would be 24% larger, suggesting that a dietary or drug intervention that minimizes the drop in absorption, would result in a higher bone mineral mass. ConclusionsA dynamic model of calcium metabolism during growth was developed and used to predict the effect of interventions on bone mass. These predictions would be tested in future studies. Funding SourcesPurdue University Graduate School and Amgen, Inc., Thousand Oaks, CA.

Component composition of body weight in patients with non-alcoholic fatty liver disease

The issue of the relationship between the features of the component composition of body weight with the emergence and development of non-alcoholic fatty liver disease (NAFLD) is particularly relevant. The purpose of the study is to determine the features of the component composition of the body weight in patients with NAFLD compared with almost healthy people of the first mature age. A comprehensive examination and analysis of anthropometric data of 112 patients with NAFLD of the first mature age of the Podolski region was carried out in comparison with the anthropometric data of practically healthy people, which were taken from the data bank of the materials of the research center of National Pirogov Memorial Medical University. The necessary anthropometric parameters for determining the absolute amount of adipose tissue, the absolute amount of muscle tissue, the absolute amount of bone component in body weight, using the formulas of J. Matiegka. Statistical analysis of the obtained results was performed in the program “STATISTICA 8” using parametric and non-parametric methods of estimation of the obtained results. It was found that the body fat according to the Matiegka formula in men and women with NAFLD was statistically significantly higher (p&lt;0.001) than in the same sex of healthy men and women. Muscle weight and bone mass calculated by the Matiegka formula in men and women with NAFLD were statistically significantly lower (p&lt;0.05) than in the healthy sex of men and women. Moreover, muscle and bone mass in healthy and NAFLD men were statistically significantly greater (p&lt;0.05) than in the same age groups of women. Men and women with NAFLD have strong inverse correlations between muscle mass and body mass index. Also, the mean strengths of the correlation between the bone mass and body mass index were established. The obtained results, together with a known increase in body fat in NAFLD, show a significant change in muscle and bone mass toward a decrease, which allows us to identify new potential therapeutic targets.

Parity and lactation are not associated with incident fragility fractures or radiographic vertebral fractures over 16years of follow-up: Canadian Multicentre Osteoporosis Study (CaMos).

Pregnancy and especially lactation cause loss of bone mass and microarchitectural changes, which temporarily increase fracture risk. After weaning, aBMD increases but skeletal microarchitecture may be incompletely restored. Most retrospective clinical studies found neutral or even protective associations of parity and lactation with fragility fractures, but prospective data are sparse. CaMos is a randomly selected observational cohort that includes ~ 6500 women followed prospectively for over 16years. We determined whether parity or lactation were related to incident clinical fragility fractures over 16years, radiographic (morphometric and morphologic) vertebral fractures over 10years, and aBMD change (spine, total hip, and femoral neck) over 10years. Parity and lactation duration were analyzed as continuous variables in predicting these outcomes using univariate and multivariate regression analyses. Three thousand four hundred thirty-seven women completed 16years of follow-up for incident clinical fractures, 3839 completed 10years of morphometric vertebral fracture assessment, 3788 completed 10years of morphologic vertebral fracture assessment, and 4464 completed 10years of follow-up for change in aBMD. In the multivariate analyses, parity and lactation duration showed no associations with clinical fragility fractures, radiographic vertebral fractures, or change in aBMD, except that parity associated with a probable chance finding of a slightly greater decline in femoral neck aBMD. Parity and lactation have no adverse associations with clinical fragility or radiographic vertebral fractures, or the rate of BMD decline over 10years, in this prospective, multicenter study of a randomly selected, population-based cohort of women.

Adaptive changes in micromechanical environments of cancellous and cortical bone in response to in vivo loading and disuse

The skeleton accommodates changes in mechanical environments by increasing bone mass under increased loads and decreasing bone mass under disuse. However, little is known about the adaptive changes in micromechanical behavior of cancellous and cortical tissues resulting from loading or disuse. To address this issue, in vivo tibial loading and hindlimb unloading experiments were conducted on 16-week-old female C57BL/6J mice. Changes in bone mass and tissue-level strains in the metaphyseal cancellous and midshaft cortical bone of the tibiae, resulting from loading or unloading, were determined using microCT and finite element (FE) analysis, respectively. We found that loading- and unloading-induced changes in bone mass were more pronounced in the cancellous than cortical bone. Simulated FE-loading showed that a greater proportion of elements experienced relatively lower longitudinal strains following load-induced bone adaptation, while the opposite was true in the disuse model. While the magnitudes of maximum or minimum principal strains in the metaphyseal cancellous and midshaft cortical bone were not affected by loading, strains oriented with the long axis were reduced in the load-adapted tibia suggesting that loading-induced micromechanical benefits were aligned primarily in the loading direction. Regression analyses demonstrated that bone mass was a good predictor of bone tissue strains for the cortical bone but not for the cancellous bone, which has complex microarchitecture and spatially-variant strain environments. In summary, loading-induced micromechanical benefits for cancellous and cortical tissues are received primarily in the direction of force application and cancellous bone mass may not be related to the micromechanics of cancellous bone.

Endocrine parameters in association with bone mineral accrual in young female vocational ballet dancers.

Little is known on bone mass development in dancers involved in vocational training. The aim of the present study was to model bone mineral content (BMC) accruals and to determine whether circulating levels of oestrogens, growth hormone (GH), and insulin-like growth factor I (IGF-1) explain differences in bone mass gains between vocational dance students and matched controls. The total of 67 vocational female dancers (VFDs) and 68 aged-matched controls (12.1 ± 1.9years and 12.7 ± 2.0years at baseline, respectively) were followed for two consecutive years (34 VFD and 31 controls remained in the study for the full duration). BMC was evaluated annually at impact [femoral neck (FN); lumbar spine (LS)] and non-impact sites (forearm) using DXA. Anthropometry, age at menarche (questionnaire), and hormone serum concentrations (immunoradiometric assays) were also assessed for the same period. VFD demonstrated consistently reduced body weight (p < 0.001) and BMC at all three anatomical sites (p < 0.001) compared to controls throughout the study period. Menarche, body weight, GH, and IGF-1 were significantly associated with bone mass changes over time (p < 0.05) but did not explain group differences in BMC gains at impact sites (p > 0.05). However, body weight did explain the differences between groups in terms of BMC gains at the forearm (non-impact site). Two consecutive years of vocational dance training revealed that young female dancers demonstrate consistently lower bone mass compared to controls at both impact and non-impact sites. The studied endocrine parameters do not seem to explain group differences in terms of bone mass gains at impact sites.

Efeitos da caminhada nórdica no perfil antropométrico e composição corporal de pessoas com doença de Parkinson: ensaio clínico randomizado

Introdução: A doença de Parkinson (DP) é caracterizada por distúrbios motores, aumentando risco de quedas e inatividade física. Objetivo: Analisar perfil antropométrico e composição corporal, antes e após um programa de treinamento de caminhada nórdica (CN) e caminhada livre (CL). Métodos: Os 33 sujeitos foram randomizados em dois grupos experimentais: CL (n = 16) e CN (n = 17) para realização das 12 sessões de treinamento. Resultados: Relação cintura/quadril reduziu (2,2%, p = 0,022) para o CL. O somatório total das dobras cutâneas reduziu em 4,3% no grupo CN (p = 0,012), e 4,7% no grupo CL (p = 0,012), sem diferença entre os grupos. O período de treinamento não promoveu alterações significativas na massa corporal (p = 0,808), IMC (p = 0,392), nas massas magra (p = 0,834), gorda (p = 0,721) e óssea (p = 0,348), bem como nos percentuais de gordura (p = 0,887). Conclusão: O treinamento promoveu melhora antropométrica efetiva para ambos os grupos.

Interaction among Calcium Diet Content, PTH (1-34) Treatment and Balance of Bone Homeostasis in Rat Model: The Trabecular Bone as Keystone.

The present study is the second step (concerning normal diet restoration) of the our previous study (concerning the calcium-free diet) to determine whether normal diet restoration, with/without concomitant PTH (1-34) administration, can influence amounts and deposition sites of the total bone mass. Histomorphometric evaluations and immunohistochemical analysis for Sclerostin expression were conducted on the vertebral bodies and femurs in the rat model. The final goals are (i) to define timing and manners of bone mass changes when calcium is restored to the diet, (ii) to analyze the different involvement of the two bony architectures having different metabolism (i.e., trabecular versus cortical bone), and (iii) to verify the eventual role of PTH (1-34) administration. Results evidenced the greater involvement of the trabecular bone with respect to the cortical bone, in response to different levels of calcium content in the diet, and the effect of PTH, mostly in the recovery of trabecular bony architecture. The main findings emerged from the present study are (i) the importance of the interplay between mineral homeostasis and skeletal homeostasis in modulating and guiding bone’s response to dietary/metabolic alterations and (ii) the evidence that the more involved bony architecture is the trabecular bone, the most susceptible to the dynamical balance of the two homeostases.

The Role of Dickkopf-1 in Thyroid Hormone-Induced Changes of Bone Remodeling in Male Mice.

Thyroid hormones regulate bone homeostasis, and exogenously induced hyperthyroidism and hypothyroidism in mice was recently found to be associated with an altered expression of the Wnt inhibitor Dickkopf-1 (Dkk1), a determinant of bone mass. Here, we assessed the role of Dkk1 in thyroid hormone-induced changes in bone using conditional Dkk1 knockout mice. Male mice with a global (Dkk1fl/fl;Rosa26-CreERT2) or osteocyte-specific (Dkk1fl/fl;Dmp1:Cre) deletion of Dkk1 were pharmacologically rendered hypothyroid or hyperthyroid. The bone phenotype was analyzed using micro-CT analysis, dynamic histomorphometry, and serum concentrations of bone turnover markers. Hypothyroid and hyperthyroid Cre-negative mice of either Cre line revealed the expected changes in bone volume with hypothyroid mice displaying a 40% to 60% increase in vertebral trabecular bone volume, while hyperthyroid mice lost 45% to 60% of bone volume. Similar changes were observed at the spine. Interestingly, Cre-positive mice of both lines did not gain or lose as much bone at the femur when rendered hypothyroid or hyperthyroid. While Cre-negative hypothyroid mice gained 80% to 100% bone volume, Cre-positive hypothyroid mice only increased their bone volume by 55% to 90%. Similarly, Cre-negative hyperthyroid mice lost 74% to 79% bone, while Cre-positive hyperthyroid mice merely lost 40% to 54%. Despite these site-specific differences, both global and osteocyte-specific Dkk1 knockout mice displayed similar changes in bone turnover as their Cre-negative controls in the hypothyroid and hyperthyroid states. While osteoblast and osteoclast parameters were increased in hyperthyroidism, hypothyroidism potently suppressed bone cell activities. Loss of Dkk1 is not sufficient to fully reverse thyroid hormone-induced changes in bone mass and bone turnover.

Bone Accrual in Children and Adolescent Nonelite Swimmers: A 2-Year Longitudinal Study.

To examine differences in bone mass between children and adolescents swimming competitively at nonelite levels (locally and regionally) and nonathletes and to assess changes in bone mass in these 2 groups over 24 months after taking into consideration several known confounders of bone mass. Observational prospective study. White nonelite swimmers (n = 128) and nonathletes (n = 106) 8 to 18 years of age from Memphis, Tennessee, USA. Participants underwent dual-energy x-ray absorptiometry to assess total body and hip bone mineral content (BMC) at baseline and 12 and 24 months later. At baseline, swimmers had 4.2% and 6.1% higher adjusted BMC for the total body and hip, respectively, compared with nonathletes (P values < 0.027). Averaging across assessment points, swimmers had 73.5 and 2.2 g higher BMC for the total body and hip, respectively, than nonathletes. Although there was a significant annual increase in total body and hip BMC in both groups (33.5 and 0.7 g, respectively), there was no difference in annualized bone accrual between swimmers and nonathletes for either total body BMC (swim by time effect; P = 0.213) or hip BMC (P = 0.265). Competitive swimming at nonelite levels during childhood and adolescence does not seem to compromise bone accrual.

Identification of bone mass change for individual patient of idiopathic scoliosis based on medical image data

Identification of bone mass change for individual patient of idiopathic scoliosis based on medical image data

Activity and morphologic changes in the mandible after mandibular osteotomy.

Orthognathic surgery accelerates orthodontic tooth movement, and tooth movement accelerates with demineralized bone and accelerated bone remodeling. The purpose of this study was to ascertain whether orthognathic surgery induces accelerated bone remodeling. The research design included a human model and an animal model. The levels of serum tartrate resistant acid phosphatase-5b (TRAP) and bone alkaline phosphatase (BALP) were measured in 15 patients after sagittal split ramus osteotomy. For the animal study, 18 rabbits were divided into 6 groups: a control group and 5 surgery groups. The rabbits in the surgery groups had osteotomies in the molar regions of the mandible. Changes in bone mass of the anterior mandibles were examined by microcomputed tomography, and changes in osteoblast and osteoclast numbers were analyzed by real-time polymerase chain reaction, hematoxylin and eosin staining, TRAP staining, and alkaline phosphatase staining. In the 15 patients, TRAP-5b increased from 1 to 8weeks postoperatively, and BALP increased significantly in 2weeks postoperatively. In the rabbits, the levels of mRNA expression of TRAP were increased at 3weeks, and matrix metalloproteinase 9 was increased at 4 and 8weeks, whereas mRNA expression of BALP and bone morphogenetic protein 2 were increased at 4weeks. Bone loss was detected from 1week postoperatively and reached the maximum at 3weeks; and bone mass and mechanical structure did not recoverer to preoperative levels until 8weeks postoperatively. These findings show active bone remodeling induced by osteotomy.

Early diagnosis of violation of mineral metabolism, as a way of primary and secondary prevention of fractures Arctic army groupings

The main challenges leading to the decrease of bone mineral metabolism in the conditions of the North are covered. The presented results of a study of 29 soldiers serving in the extreme conditions of the North, to study the mineral density of bone tissue in the distal forearm. Revealed a significant decrease in bone mineral density, as well as a deficiency of essential elements in this cohort. So, when densitometric training of servicemen serving in the North, the average Z-test was 0±1,8 SD, the change in bone mass corresponded to the Z-test less than -2 SD, was determined at 31,03%. Vitamin D3 deficiency was detected in 96,5% of cases. Analysis of the bio-element state of the hair revealed a deviation of the reference interval in 100% of military personnel, a decrease in essential elements: cobalt, selenium, magnesium, vanadium and an increase in the level of barium, bromine, arsenic, as well as caesium. The interrelation of the elemental status and bone mineral density is revealed. 100% of the examined hair samples showed a significant decrease in the level of cobalt, selenium and iodine. (p0,05) a decrease in boron, magnesium, calcium, vanadium (p0,05) and a significant increase in chromium, manganese, and copper. A quantitative study of toxic elements revealed a significant (p0,05) increase in mercury, rubidium, strontium, and caesium. A correlation was established between the Z-test and the level of vitamin D3, body mass index and dynamometer. The data obtained determine the required level of trace elements in order to prevent disturbances of mineral metabolism and bone loss.

Can repeated in vivo micro-CT irradiation during adolescence alter bone microstructure, histomorphometry and longitudinal growth in a rodent model?

In vivo micro-computed tomography (micro-CT) can monitor longitudinal changes in bone mass and microstructure in small rodents but imposing high doses of radiation can damage the bone tissue. However, the effect of weekly micro-CT scanning during the adolescence on bone growth and architecture is still unknown. The right proximal tibia of male Sprague-Dawley rats randomized into three dose groups of 0.83, 1.65 and 2.47 Gy (n = 11/group) were CT scanned at weekly intervals from 4th to 12th week of age. The left tibia was used as a control and scanned only at the last time point. Bone marrow cells were investigated, bone growth rates and histomorphometric analyses were performed, and bone structural parameters were determined for both left and right tibiae. Radiation doses of 1.65 and 2.47 Gy affected bone marrow cells, heights of the proliferative and hypertrophic zones, and bone growth rates in the irradiated tibiae. For the 1.65 Gy group, irradiated tibiae resulted in lower BMD, Tb.Th, Tb.N and a higher Tb.Sp compared with the control tibiae. A decrease in BMD, BV/TV, Tb.Th, Tb.N and an increase in Tb.Sp were observed between the irradiated and control tibiae for the 2.47 Gy group. For cortical bone parameters, no effects were noticed for 1.65 and 0.83 Gy groups, but a lower Ct.Th was observed for 2.47 Gy group. Tibial bone development was adversely impacted and trabecular bone, together with bone marrow cells, were negatively affected by the 1.65 and 2.47 Gy radiation doses. Cortical bone microstructure was affected for 2.47 Gy group. However, bone development and morphometry were not affected for 0.83 Gy group. These findings can be used as a proof of concept for using the reasonable high-quality image acquisition under 0.83 Gy radiation doses during the adolescent period of rats without interfering with the bone development process.