Reduction In Bone Mineral Content Research Articles

Alloferon-1 ameliorates estrogen deficiency-induced osteoporosis through dampening the NLRP3/caspase-1/IL-1β/IL-18 signaling pathway

Alloferon-1 is an insect polypeptide that has anti-inflammatory, antitumor and antiviral activity. This study aimed to determine the effects of alloferon-1 on estrogen deficiency-induced osteoporosis and explore the associated mechanism using a murine model of ovariectomy (OVX)-induced osteoporosis. Results showed that alloferon-1 prevented ovariectomy‑induced body weight gain, bone loss and bone mineral content reduction, affected biochemical markers of bone turnover, and restored the microstructure of bone trabeculae. Moreover, alloferon-1 suppressed the expression of the ovariectomy‑mediated inflammatory cytokines in the vertebrae bone tissues, including nucleotide-binding oligomerization domain-like-receptor family pyrin domain-containing 3 (NLRP3), cysteinyl aspartate specific proteinase-1 (Caspase-1), interleukin 1β (IL-1β) and interleukin 18 (IL-18) which were determined by immunofluorescence staining and western blot. Overall, the present study provides evidence for the effectiveness of alloferon-1 against estrogen deficiency-induced osteoporosis, suggesting an alternative drug or an auxiliary modulator for the treatment of postmenopausal osteoporosis (PMOP).

Vitamin D and Calcium Supplementation and Urolithiasis: A Controversial and Multifaceted Relationship

Patients with urolithiasis, and particularly those with hypercalciuria, frequently have a marked reduction of bone mineral content up to the levels of osteoporosis, with a significant increase in bone fracture risk. For these reasons, the indication to prescribe vitamin D and/or calcium supplementations is very frequent in such patients. On the other hand, both calcium supplementation, and even more vitamin D therapy, can worsen the risk of developing urolithiasis by increasing calcium, phosphate, and oxalate urinary excretion. Despite the clinical and practical relevance of this issue, the evidence on this topic is scarce and contradictory. Therefore, some concerns exist about how and whether to prescribe such supplements to a patient with a history of kidney stones. In this narrative review, we resume some pivotal pathophysiological concepts strictly related to the dealt topic, and we draw some considerations and personal opinions on the pros and cons of such prescriptions. Finally, we share with the reader our pragmatic algorithm for handling the urolithiasis risk in patients who have strong indications to be prescribed vitamin D and calcium supplementations.

Lactobacillus plantarum LP45 inhibits the RANKL/OPG signaling pathway and prevents glucocorticoid-induced osteoporosis.

To examine the potential effect of the probiotic strain Lactobacillus plantarum LP45 on osteoporosis and to explore the involved molecular mechanisms. A rat model of glucocorticoid-induced osteoporosis (GIO) was established, which was also orally administered with increasing doses of LP45 for 8 weeks. After the termination of the 8-week treatment, the tibia and femur bones of rats were analyzed for bone histomorphometry, bone mineral content (BMC), and bone mineral density (BMD). Femoral biomechanics were assessed. In addition, levels of osteocalcin, tartrate-resistant acid phosphatase 5 (TRAP5), osteoprotegerin (OPG), and receptor activator of nuclear factor kappa-B ligand (RANKL) in the serum and bone marrow were also measured using ELISA, Western blot, and real time-polymerase chain reaction. GIO caused obvious defects in tibia and femur bone structures, in terms of tissue/bone volume, trabecular separation, trabecular thickness, and trabecular number, which could be rescued by LP45 dose dependently. The GIO-induced reductions in BMC, BMD, osteoblast surfaces per bone surface (BS), as well as elevated osteoclast surface per BS were largely restored by LP45 administration dose-dependently. LP45 also increased femoral biomechanics of GIO rats. Importantly, LP45 dose-dependently restored the changes of osteocalcin, TRAP5, OPG, and RANKL in the serum as well as bone marrow of GIO rats. Oral LP45 administration could significantly prevent bone defects in GIO rats, suggesting its potential as a dietary supplement with beneficial effects against osteoporosis, which might involve the RANKL/OPG signaling pathway.

Bone Mineral Content Estimation in People Living with HIV: Prediction and Validation of Sex-Specific Anthropometric Models.

People living with HIV (PWH) experience an accelerated reduction in bone mineral content (BMC), and a high risk of osteopenia and osteoporosis. Anthropometry is an accurate and low-cost method that can be used to monitor changes in body composition in PWH. To date, no studies have used anthropometry to estimate BMC in PWH. To propose and validate sex-specific anthropometric models to predict BMC in PWH. This cross-sectional study enrolled 104 PWH (64 males) aged >18 years at a local university hospital. BMC was measured using dual energy X-ray absorptiometry (DXA). Anthropometric measures were collected. We used linear regression analysis to generate the models. Cross-validations were conducted using the “leave one out”, from the predicted residual error sum of squares (PRESS) method. Bland–Altman plots were used to explore distributions of errors. We proposed models with high coefficient of determination and reduced standard error of estimate for males (r2 = 0.70; SEE = 199.97 g; Q2PRESS = 0.67; SEEPRESS = 208.65 g) and females (r2 = 0.65; SEE = 220.96 g; Q2PRESS = 0.62; SEEPRESS = 221.90 g). Our anthropometric predictive models for BMC are valid, practical, and a low-cost alternative to monitoring bone health in PWH.

Dynamic Effects of the Third Generation Bisphosphonate of Risedronate on Rat Osteoporotic Fractures for Clinical Usage Guidance.

ObjectiveTo better understand the risks of bisphosphonates in order to develop guidance for appropriate clinical usage, to compared femoral fracture healing at different time points and to explore the effects of Residronate on fracture healing.MethodsOsteoporosis model was achieved by ovariectomy surgery, followed by surgical incision of left femoral shaft 4 weeks after ovariectomy surgery. Three days after fracture surgery, risedronateor saline was fed by intragastric administration. X ray examination was used to check the callus formation, Bone Mineral Density (BMD), Bone Mineral Content (BMC), biomechanical, imaging and micromorphological of bone tissue as well as the trabecular bone parameters were all examined. The femoral pathology tissue of each rat was used to analyze trabecular bone parameters, including trabecular bone volume/tissue volume (Tb. BV/TV), bone surface to tissue volume ratio (BS/TV), trabecular bone mineral density (Tb. BMD), trabecular bone number (Tb. N), trabecular bone thickness (Tb. Th) and small bone Trabecular bone space (Tb. Sp).Results Via X‐ray and pathologically, risedronate treatment promoted the callus forming at the fracture site during the following 6 weeks after osteoporotic fracture by X‐ray (P < 0.01), increased the local bone mineral density (P < 0.01), and accelerated the fracture healing during the first 3 weeks (P <0.01), but delayed facture healing in the later 3 weeks (P < 0.01). Risedronate increased the bone continuity of fracture at 7th week, but this phenomenon was not found at the 10th week (P < 0.01). Delayed fracture healing occurred locally at the fracture site. At 7th week, Risedronate may promote cartilage cells proliferating at fracture site, increase the dense of bone trabeculae and the connection of bone trabeculae, thicken the bone cortex showing better fracture healing than OPF‐Saline groups (P < 0.01). However, these parameter did not continue during the 7th and 10th weeks. Comparing the first and the later 3 weeks, the rats in group Osteoporotic Fracture‐Risedronate (OPF‐RD) accelerated the local fracture healing in the first 3 weeks but not in the last 3 weeks, which is consistent for the BMD and BMC among each group (P < 0.05). Through evaluation of bone mineral density and bone mineral content, risedronate dramatically increased the BMD at the fracture site and resulted in reduction of BMC by risedronate at the fracture site (P < 0.05) among each group still exist, indicating dramatic (P < 0.05). Through load testing, Risedronate increased the structural strength and mechanical indexes of the new callus (P < 0.01).ConclusionRisedronate can improve the structural strength and mechanical index of newborn callus. Longer than 7 weeks usage of third generation bisphosphonate of risedronate does not contribute to osteoporotic fracture.

Expert consensus on clinical management of metabolic bone disease of prematurity (2021).

Metabolic bone disease of prematurity (MBDP) is a systemic bone disease with a reduction in bone mineral content due to disorder of calcium and phosphorus metabolism. There is still a lack of in-depth research and systematic understanding of MBDP in China, and there are many irregularities in clinical management of this disease. Based on relevant studies in China and overseas, Grading of Recommendations Assessment, Development and Evaluation was used to develop the expert consensus on the clinical management of MBDP, which provides recommendations from the following five aspects: high-risk factors, screening/diagnosis, prevention, treatment, and post-discharge follow-up of MBDP, so as to provide relevant practitioners with recommendations on the clinical management of MBDP to reduce the incidence rate of MBDP and improve its short- and long-term prognosis.

Understanding How Sex Influences the Impact of IL-10 on Bone Microarchitecture and Bone Metabolism Over Time

ObjectivesDietary interventions with pre- and probiotics favorably affect the gut-bone axis, mediated in part by the anti-inflammatory cytokine, interleukin (IL)-10. This study sought to understand how IL-10’s impact on bone metabolism and microarchitecture differs with sex and time. MethodsSix-week-old B6.129P2-Il10tm1Cgn/J (KO) and C57BL/6 (WT) mice were assigned in a 2 × 2 × 2 factorial design with strain (WT & KO), sex, and time (3 & 6 m) as factors. Mice were fed AIN-93G diet for 3 m followed by AIN-93 M for the study duration. Dual-energy x-ray absorptiometry was used to assess bone mineral content (BMC) and density (BMD). Micro-computed tomography was used to assess femur and lumbar vertebrae trabecular and cortical bone. Serum procollagen 1 intact N-terminal propeptide (P1NP) and C-terminal telopeptide of type I collagen (CTX-1), bone formation and resorption markers respectively, were assessed by ELISA. Data were analyzed using ANOVA; p < 0.05 was considered significant. ResultsReductions in BMC and BMD (P < 0.05) in KO vs WT and at 3 vs 6 m were observed; a sex effect was found with reductions in BMC in KO females compared to KO males. Femoral trabecular bone volume (BV/TV) was lower (P < 0.05) in KO vs WT, females vs males, and at 6 vs 3 m. Trabecular thickness (TbTh) decreased (P < 0.05) in KO vs WT and increased from 3 to 6 m, while decreases in trabecular number (TbN) were greater (P < 0.05) in KO mice, females, and at 6 m compared to counterparts. Cortical area and thickness were decreased (P < 0.05) in KO vs WT and in females vs males, which was greater at 6 m, while cortical bone porosity was higher in KO vs WT and increased at 6 mo. Vertebral trabecular BV/TV was lower (P < 0.05) in KO vs WT at 3 and 6 m, with KO females showing reduced BV/TV (P < 0.05) from 3 to 6 m. Reduced TbTh and TbN were observed in KO vs WT, and females had increased (P < 0.05) TbTh and trabecular separation and reduced TbN. P1NP showed a time effect (P < 0.05) with reductions in WT females and males at 6 m compared to 3 m KO females (P < 0.05). CTX-1 shows a sex effect (P < 0.05) and a trending strain effect (P = 0.059), with elevated serum CTX-1 in 3 m KO males compared to WT and KO females at 6 m (P < 0.05). ConclusionsWhile IL-10 plays an important role in maintaining both trabecular and cortical bone, it may have a more protective effect on the cortical bone of female mice over time. Funding SourcesOklahoma Agricultural Experiment Station.

The Effect of Normobaric Intermittent Hypoxia Therapy on Bone in Normal and Disuse Osteopenic Mice.

Bromer, Frederik Duch, Mikkel Bo Brent, Michael Pedersen, Jesper Skovhus Thomsen, Annemarie Brüel, and Casper Bindzus Foldager. The effect of normobaric intermittent hypoxia therapy on bone in normal and disuse osteopenic mice. High Alt Med Biol. 22: 225-234, 2021. Background: Systemic intermittent hypoxia therapy (IHT) has been shown to elicit beneficial effects on multiple physiological systems. However, only few studies have investigated the effect of long-term normobaric IHT on bone mass and mechanical and microstructural properties. The aim of the present study was to examine the effect of IHT on bone in both healthy and osteopenic mice. Materials and Methods: Thirty mice were stratified into four groups: Ctrl, Ctrl+IHT, Botox, and Botox+IHT. Osteopenia was induced by injecting Botox into the right hindlimb of the mice causing paralysis and disuse. IHT animals were placed in a normobaric hypoxia-chamber (10% oxygen) for 1 hour twice daily 5 days/week. Animals were sacrificed after 21 days, and DEXA, micro-computed tomography, and mechanical testing were performed on the femora. Results: As expected, Botox resulted in a significant reduction of bone mineral content (-23.4%), area bone mineral density (-19.1%), femoral neck strength (Fmax: -54.7%), bone volume fraction (bone volume/tissue volume: -41.8%), and trabecular thickness (-32.4%). IHT had no measurable effect on the bone properties in either healthy or osteopenic mice. Conclusion: The study confirmed that Botox led to loss of bone mass, deterioration of trabecular microstructure, and loss of bone strength. These changes were not influenced by IHT. Notably, IHT had no detrimental effect on bone in either healthy or osteopenic mice. This indicates that IHT of ailments outside of the skeletal system may be administered without causing harm to the bone.

COMPARISON BETWEEN LOW AND HIGH DOSES OF PROPHYLACTIC VITAMIN D IN PREVENTION OF OSTEOPENIA OF PREMATURITY

Osteopenia of prematurity (OOP) is a term used to describe a reduction in bone mineral content (BMC) of the preterm infant. Its incidence has been steadily increasing with the survival of more premature neonates as a result of advances in neonatal care. The prevalence of metabolic bone disease is inversely associated with birth weight and gestational age. Up to a third of infants weighing less than one kilogram at birth are osteopenic, more so if they are breastfed.To develop normally, the skeleton of the fetus requires active materno-fetal transfer of protein, Calcium (Ca) and phosphorus (P). Bone mineralization which occurs predominantly during the third trimester will be inadequate if the fetal increased demands in Ca and P are not met. During pregnancy augmented maternal intestinal absorption and increased skeletal mobilization increase maternal Ca supply to the fetus.Factors that impede normal bone mineralization include inadequate postnatal intake of vitamin D, calcium (Ca) and phosphorus (P), extended periods of total parenteral nutrition, and also as a side effect of diuretics and corticosteroids prescribed to these infants. Poor bone mineralization is associated with common neonatal conditions. These include sepsis, bronchopulmonary dysplasia, cerebral pathology, acidosis, necrotizing enterocolitis and cholestasis.Depending on the severity of the demineralization, osteopenia can remain clinically silent or, if severe, can cause bone changes in the form of rarefaction, fraying, cupping, subperiosteal new bone formation or even fractures.

Approach to Metabolic Bone Disease of Prematurity

Neonatal metabolic bone disease (MBD), osteopenia of prematurity (OOP), neonatal rickets or rickets of prematurity, are terms used to describe a reduction in bone mineral content (BMC) of the preterm infant. Although its exact prevalence is difficult to quantify because of the various methods used for screening of infants who are at risk and also because of the difficulty in the interpretation of these results, it has been steadily increasing with the survival of more immature neonates as a result of advances in neonatal care. Pathological conditions which impair placental macro and micronutrients transfer, such as preeclampsia, intrauterine growth restriction, and chorioamnionitis are associated with an increased risk of MBD in preterm infants. There are no specific diagnostic methods for MBD of prematurity. The clinical findings appear late and sometimes the diagnosis is not carried out. Indeed, it is necessary to screen the subjects who are at risk to develop MBD. The prevalence and also the severity of OOP can be reduced by early nutritional intervention. Maintaining a sufficient supply of Ca and P for the growth of VLBW infants’ skeleton is challenging because of their relatively high physiological requirements. Because of the crucial role of mechanical forces on the development of the skeleton, daily exercises such as gentle compression and movements of the limbs are recommended in infants at risk of OOP

Longitudinal Change in Bone Density, Geometry, and Estimated Bone Strength in Older Men and Women From The Gambia: Findings From the Gambian Bone and Muscle Aging Study (GamBAS).

Musculoskeletal aging in the most resource-limited countries has not been quantified, and longitudinal data are urgently needed to inform policy. The aim of this prospective study was to describe musculoskeletal aging in Gambian adults. A total of 488 participants were recruited stratified by sex and 5-year age band (aged 40 years and older); 386 attended follow-up 1.7 years later. Outcomes were dual-energy X-ray absorptiometry (DXA) (n=383) total hip areal bone mineral density (aBMD), bone mineral content (BMC), bone area (BA); peripheral quantitative computed tomography (pQCT) diaphyseal and epiphyseal radius and tibia (n=313) total volumetric BMD (vBMD), trabecular vBMD, estimated bone strength indices (BSIc), cross-sectional area (CSA), BMC, and cortical vBMD. Mean annualized percentage change in bone outcomes was assessed in 10-year age bands and linear trends for age assessed. Bone turnover markers, parathyroid hormone (PTH), and 25-hydroxyvitamin D (25(OH)D) were explored as predictors of change in bone. Bone loss was observed at all sites, with an annual loss of total hip aBMD of 1.2% in women after age 50 years and in men at age 70 years plus. Greater loss in vBMD and BSIc was found at the radius in both men and women; strength was reduced by 4% per year in women and 3% per year in men (p trend 0.02, 0.03, respectively). At cortical sites, reductions in BMC, CSA, and vBMD were observed, being greatest in BMC in women, between 1.4% and 2.0% per annum. Higher CTX and PINP predicted greater loss of trabecular vBMD in women and BMC in men at the radius, and higher 25(OH)D with less loss of tibial trabecular vBMD and CSA in women. The magnitude of bone loss was like those reported in countries where fragility fracture rates are much higher. Given the predicted rise in fracture rates in resource-poor countries such as The Gambia, these data provide important insights into musculoskeletal health in this population. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).

Serial serum alkaline phosphatase as an early biomarker for osteopenia of prematurity.

Metabolic bone disease of prematurity is a condition characterized by reduction in bone mineral content (osteopenia). It is a problem faced by very low birth weight (VLBW) infants because of lack of fetal mineralization during the last trimester. Our aim was to assess serum alkaline phosphatase (ALP) level as an early biomarker for osteopenia in premature infants and to estimate an optimal cutoff value of serum ALP at which osteopenia is detected radiologically in premature newborns.This prospective study was conducted on a cohort of 120 newborn infants of both sex of ≤34 weeks’ gestational age and <1500 g birth weight. Two blood samples, from each infant on at least 2 consecutive weeks, were reported for calcium, phosphorus, and ALP. Evidence of osteopenia was evaluated radiologically by performing wrist/knee x-ray.Sixteen infants (13.3%) had evidence of osteopenia in x-ray, whereas 104 infants (86.7%) were nonosteopenic and all the osteopenic infants were <1000-g birth weight. Birth weight and gestational age were significantly inversely related to serum ALP levels. Both samples showed statistically significantly higher mean ALP level in osteopenic than nonosteopenics (P < 0.001, and P < 0.001 respectively). There was no constant value of serum ALP related to radiologic evidence of osteopenia. However, the optimal cutoff value of serum ALP at which osteopenia is detected is 500 IU/L with 100% sensitivity and 80.77% specificity.High levels of ALP can be considered a reliable biomarker to predict the status of bone mineralization and the need for radiological evaluation in premature infants particularly those <1000-g birth weight and <32 weeks’ gestation.

Osteopenia of prematurity: Assessment of Biochemical parameters in Very low birth weight preterm neonates

Background: Osteopenia of prematurity, commonly called as metabolic bone disease (MBD), is mostly described in preterm babies (< 36weeks) with very low birth weight (VLBW). This condition is characterized by a reduction in bone mineral content (osteopenia), with or without rachitic changes, and is caused by several nutritional and biomechanical factors. Objective: To determine the incidence of osteopenia of prematurity among high risk preterm VLBW babies and also to document changes in biochemical parameters including serum calcium, serum phosphate, serum alkaline phosphate (ALP) and serum creatinine in the above cases. Material and method: This prospective observational study includes all the very low birth weight babies born fromNovember 2012 to July 2014. Present study comprised of 60 VLBW neonates of which 10 were <28weeks, 32 were 28-31week and 18 were 31-34weeks of gestation. Estimations of biochemical parameters were done at 2nd week of birth and again at 6th week to detect the incidence of osteopenia. Result: There was a significant decrease inserum calcium and serum phosphorous level where asserum ALP documented a significant increase in preterm neonates when compared to control. 14 of 60 VLBW babies developed osteopenia of prematurity at 6th week of life. Conclusion: As observed in the present study, gestational age, birth weight and ALP are considered to be significant risk factors and are associated with osteopenia. So early detection of this condition by monitoring of biochemical parameters in high-risk cases minimizes the development of osteopeniaand prevent future complications of osteopenia.

Development, validation and characterization of a novel mouse model of Adynamic Bone Disease (ABD)

The etiology of Adynamic Bone Disease (ABD) is poorly understood but the hallmark of ABD is a lack of bone turnover. ABD occurs in renal osteodystrophy (ROD) and is suspected to occur in elderly patients on long-term anti-resorptive therapy. A major clinical concern of ABD is diminished bone quality and an increased fracture risk. To our knowledge, experimental animal models for ABD other than ROD-ABD have not been developed or studied. The objectives of this study were to develop a mouse model of ABD without the complications of renal ablation, and to characterize changes in bone quality in ABD relative to controls.To re-create the adynamic bone condition, 4-month old female Col2.3Δtk mice were treated with ganciclovir to specifically ablate osteoblasts, and pamidronate was used to inhibit osteoclastic resorption. Four groups of animals were used to characterize bone quality in ABD: Normal bone controls, No Formation controls, No Resorption controls, and an Adynamic group. After a 6-week treatment period, the animals were sacrificed and the bones were harvested for analyses. Bone quality assessments were conducted using established techniques including bone histology, quantitative backscattered electron imaging (qBEI), dual energy X-ray absorptiometry (DXA), microcomputed tomography (microCT), and biomechanical testing.Histomorphometry confirmed osteoblast-related hallmarks of ABD in our mouse model. Bone formation was near complete suppression in the No Formation and Adynamic specimens. Inhibition of bone resorption in the Adynamic group was confirmed by tartrate-resistant acid phosphatase (TRAP) stain. Normal bone mineral density and architecture were maintained in the Adynamic group, whereas the No Formation group showed a reduction in bone mineral content and trabecular thickness relative to the Adynamic group. As expected, the No Formation group had a more hypomineralized profile and the Adynamic group had a higher mean mineralization profile that is similar to suppressed bone turnover in human. This data confirms successful replication of the adynamic bone condition in a mouse without the complication of renal ablation.Our approach is the first model of ABD that uses pharmacological manipulation in a transgenic mouse to mimic the bone cellular dynamics observed in the human ABD condition. We plan to use our mouse model to investigate the adynamic bone condition in aging and to study changes to bone quality and fracture risk as a consequence of over-suppressed bone turnover.

Distribution of Bone Mineral Content Is Associated with Body Weight and Exercise Capacity in Patients with Chronic Obstructive Pulmonary Disease

Background: Although low bone mineral density is highly prevalent in patients with chronic obstructive pulmonary disease (COPD), the distribution of the reduced bone mass has not been fully elucidated. Objectives: To determine regional bone mass loss in patients with COPD and investigate whether the change in distribution may be associated with body weight loss and functional capacity. Methods: Body mass index (BMI) was assessed, and height squared indices were derived for the bone mineral content index (BMCI) of the arms, legs and trunk by dual-energy X-ray absorptiometry in 45 male patients with COPD and 12 age- and sex-matched control subjects. Pulmonary function tests were performed, and maximal oxygen uptake (V·O₂max) was measured. Results: The BMCI was lower in the total bone, legs and trunk of patients with COPD than in control subjects, although the BMCI in the arms was similar between the groups. BMI correlated significantly with the BMCI in all 3 segments. Bone mineral content (BMC) in the trunk, expressed as a percentage of total BMC (BMC trunk/total BMC), correlated significantly with BMI. The BMCI in the trunk was closely related with V·O₂max but not with airflow limitation. Conclusions: There was a regional difference in BMC reduction, but a predominant reduction of bone mass in the trunk was not associated with the severity of airflow limitation but rather with body weight loss and exercise intolerance. These data suggest that body weight loss and exercise intolerance are important risk factors for vertebral fracture in patients with COPD.

Birth weight and adult bone mass: a systematic literature review

This systematic literature review comprised 16 studies. The association of birth weight with bone parameters was much more evident for bone mineral content (BMC) rather than bone mineral density (BMD). This is an important finding since a reduction in BMC is strongly associated with an increased risk of fractures. The purpose of this study was to conduct a systematic literature review of studies that have investigated the association between birth weight (BW) and adult bone mass. The search included English language articles, indexed in MEDLINE, using the key words: ("birth size" OR "birth weight" OR birthweight) AND (osteoporosis OR "bone mass" OR "bone density" OR "bone mineral density" OR "bone mineral content" OR "bone area"). A methodological quality appraisal of the reviewed studies was performed. Sixteen articles were reviewed. Eleven of 13 studies that measured BMC verified a positive effect of BW on this parameter, and nine even after adjustment for adult body size. Among the ten studies that found an unadjusted association between BW and BMD, two reported that the significance remained after adjustment for current body size. Interaction between prenatal and postnatal variables on the determination of adult bone mass was only tested by two studies. The results must be interpreted with caution due to the existence of few papers on the issue, as well as heterogeneous sample characteristics, investigated bone sites, and implemented analysis procedures. The aspects of methodological quality that frequently fail are as follows: representativeness of the planned and actually measured sample as well as proper adjustment for confounding. Based on the amount of accumulated evidence, it is probable that BW have a positive association with adult BMC rather than BMD, which is an important finding for clinical and public health policies since a reduction in BMC is strongly associated with an increased fracture risk.

Chronic treatment with polychlorinated biphenyls (PCB) during pregnancy and lactation in the rat: Part 1: Effects on somatic growth, growth hormone-axis activity and bone mass in the offspring

Polychlorinated biphenyls (PCBs) are pollutants detected in animal tissues and breast milk. The experiments described in the present paper were aimed at evaluating whether the four PCB congeners most abundant in animal tissues (PCB-138, -153, -180 and -126), administered since fetal life till weaning, can induce long-term alterations of GH-axis activity and bone mass in the adult rat. We measured PCB accumulation in rat brain and liver, somatic growth, pituitary GH expression and plasma hormone concentrations at different ages. Finally, we studied hypothalamic somatostatin expression and bone structure in adulthood, following long-term PCB exposure. Dams were treated during pregnancy from GD15 to GD19 and during breast-feeding. A constant reduction of the growth rate in both male and female offspring from weaning to adulthood was observed in exposed animals. Long-lasting alterations on hypothalamic–pituitary GH axis were indeed observed in PCB-exposed rats in adulthood: increased somatostatin expression in hypothalamic periventricular nucleus (both males and females) and lateral arcuate nucleus (males, only) and decreased GH mRNA levels in the pituitary of male rats. Plasma IGF-1 levels were higher in PCB-exposed male and female animals as compared with controls at weaning and tended to be higher at PN60. Plasma testosterone and thyroid hormone concentrations were not significantly affected by exposure to PCBs. In adulthood, PCBs caused a significant reduction of bone mineral content and cortical bone thickness of tibiae in male rat joint to increased width of the epiphyseal cartilage disk. In conclusion, the developmental exposure to the four selected PCB compounds used in the present study induced far-reaching effects in the adult offspring, the male rats appearing more sensitive than females.

Metabolic Bone Disease in preterm newborn: an update on nutritional issues.

Osteopenia, a condition characterised by a reduction in bone mineral content, is a common disease of preterm babies between the tenth and sixteenth week of life. Prematurely born infants are deprived of the intrauterine supply of minerals affecting bone mineralization.The aetiology is multifactorial: inadequate nutrients intake (calcium, phosphorus and vitamin D), a prolonged period of total parenteral nutrition, immobilisation and the intake of some drugs.The diagnosis of metabolic bone disease is done by biochemical analysis: low serum levels of phosphorus and high levels of alkaline phosphatase are suggestive of metabolic bone disease. The disease can remain clinically silent or presents with symptoms and signs of rachitism depending on the severity of bone demineralisation.An early nutritional intervention can reduce both the prevalence and the severity of osteopenia.This article reviews the pathophysiology of foetal and neonatal bone metabolism, focuses on the nutrient requirements of premature babies and on the ways to early detect and treat osteopenia.

Effects of Restricted Calcium Intake on Bone and Maxillofacial Growth

To investigate the effects of a low calcium diet on maxillofacial development by evaluating Bone Mineral Content (BMC) in the lower alveolar bones, femurs, and tibias and by performing cephalometry on growing rats. Thirty 5-week-old male Wistar rats were randomly divided into 3 groups; the control group (n = 10) was given standard diet for 6 weeks, the low calcium/standard diet group (n = 10) was given a calcium-restricted diet for the first 4 weeks, and then a standard diet for the following 2 weeks, and the low calcium diet group (n = 10) was given the calcium-restricted diet for 6 weeks. After the rats were euthanized, heads and legs were fixed and cephalometry was performed. Next, mandibles, femurs and tibias were digitally photographed and the BMC was evaluated using our newly developed software. The BMC was decreased in all of the bone samples from the two groups that received restricted calcium. In the low calcium/standard diet group, the BMC recovered the most in the tibias and least in the lower alveolar bones. Development of the mandibles in the anterior-posterior direction was accelerated, while that in the superior-inferior direction was inhibited in those rats. The BMC reduction following calcium deficiency in the lower alveolar bone hardly recovers, so prevention is important. Development of the mandible in a superior-inferior direction is inhibited while that in an anterior-posterior direction is accelerated due to a calcium-restricted diet.

Experimental studies on the bone metabolism of male rats chronically exposed to cadmium intoxication using dual-energy X-ray absorptiometry

Cadmium (Cd) has been identified as the etiologic agent of itai-itai disease. The purpose of this study was to investigate whether chronic Cd exposure affects bone metabolism in a male rat model and to estimate the bone mineral density (BMD) differences in lumbar and femoral bone because of Cd exposure. Six-week-old male Hos Donryu rats were used in this experiment. Cadmium was administered at a dose of 200 ppm to rats in the diet to produce experimental chronic Cd poisoning. Bone mineral density was measured using dual-energy X-ray absorptiometry (DEXA) with a high-resolution scan collimator (0.25 mm diameter) (Hologic QDR-2000). The Cd content in renal tissue reached a critical concentration of 128.42 +/- 14.38 microg/g 10 months after the administration of the element (Table 3). The average blood urea nitrogen (BUN) value was increased throughout the period of the experiment, and the serum creatinine value of the experimental group showed an increase after 2 months of Cd administration (0.46 +/- 0.09 mg/dL). The concentration of urinary calcium changed in the experimental group after exposure to Cd for 12 months (15.4 +/- 0.13 mg/dL). DEXA showed a greater reduction in the bone mineral density of the 5th vertebral body (L5) in rats that had ingested Cd for 4 months (0.359 +/- 0.013 g/cm2) than in control rats (0.372 +/- 0.012 g/cm2, P < 0.01). On the contrary, the difference in bone mineral content between rats ingesting Cd for 6-8 months and control rats was not significant. However, significant reductions in bone mineral content were again noted in rats that had ingested Cd for 12 months (0.339 +/- 0.023 g/cm2) compared with the control group (0.385 +/- 0.012 g/cm2, P < 0.01). The bone mineral density of the right femoral bone in control rats was 0.328 +/- 0.018 g/cm2 and that in experimental rats was 0.306 +/- 0.012 g/cm2, and a meaningful difference was recognized (P < 0.05). Histological examination of the rats exposed to Cd for 12 months showed that the 5th lumbar vertebral body (L5) exhibited osteomalacia. The results of our studies show that Cd stimulated a loss of bone mineral at an early stage to a great extent in male rats. In the examination of male rats, bone injury and renal functional disorder were encountered simultaneously. This study suggested that osteomalacia was induced by a direct action of Cd on the bone through abnormal calcium homeostasis at an early stage in male rats.