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PubMed2002

[Effects of dietary calcium-deficiency on bone development in growing rats and the mechanism involved].

The effects of calcium on bone development in growing rats were studied by bone histomorphometry and the hormone changes in a model of calcium-deficient rats. Thirty growing Wistar rats were randomly allocated into three groups fed with low calcium diet, calcium-sufficient diet at libitum or pair fed with low calcium diet for 8 weeks. The calcium-deficient rats showed low bone mass, significantly decreased bone density and mineral content. The disorder of bone molding and ultrastructure at the femoral distal diaphysis of the calcium deficient rats were showed by histomorphometric parameters. The concentration of serum parathyroid hormone was significantly higher, calcitonin was significantly lower, and the content of hydroxyproline in bone was significantly lower. The results indicated that dietary calcium-deficiency might stimulate the secretion of parathyroid hormone, decrease bone mineral content and inhibit the synthesis of bone matrix, which might induce a defect on bone mineralization.

Animals↗
PubMed1991

Matrix in cartilage and bone development: current views on the function and regulation of major organic components.

Study of the growth and development of cartilage and bone has been difficult because the structure of the tissues makes biological experiments hard to conduct. Recent advances in molecular biology have offered new possibilities for studying these processes. Many cartilage and bone specific cDNAs have been cloned and characterized and consequently used to localize the corresponding mRNAs in tissue sections. Developing cartilage and bone serve as a model for the study of extracellular matrix gene regulation during the proliferation, growth and differentiation of connective tissue cells. Normal skeletal growth and development are regulated by both systemic and local factors. The effects of many systemic hormones on bone metabolism have been studied extensively, but the pathways triggered by these hormones in the target cells are less well known. Recent evidence suggests that some growth factors, such as TGF-beta, IGFs and PDGF, act as local regulators of cartilage and bone metabolism. The different extracellular matrix components, e.g. collagens, are expressed differently in distinct cell types and developmental stages during cartilage and bone development. This model, therefore, facilitates the study of relations between the production of the various extracellular matrix components and the growth factors and the proto-oncogenes which may regulate them. Existing knowledge of the expression of major cartilage and bone components and their regulation during growth, differentiation and development is reviewed. An understanding of the normal growth and development of cartilage and bone is fundamental for elucidating the mechanisms underlying the various diseases -- both hereditary and acquired -- affecting the human skeleton.

Animals↗
PubMed2003

[Sex differences over time in bone development and maintenance and their mechanisms].

There is a clear, sex-related difference in speed of bone development in favor of female infants over that of females infants, with an excess of estrogen secretion at this stage likely accounting for the difference. In this, females appear to benefit by their high level of estrogen secretion which is three times that in males. However, males are less susceptible to a drastic change in bone density even at a greater age, as they are able to develop and maintain bone mass with a much lower but constant level of estrogen than that required in females. In contrast, females undergo a drastic change in estrogen levels after menopause and are hardly able to arrest bone resorption, thus suffering a steep fall in bone mass. Thus, there is also a clear difference in bone development and maintenance over time between sexes, the reason likely being a drastic rise or fall in estrogen levels over time.

English Abstract↗
PubMed2003

Exercise training, menstrual irregularities and bone development in children and adolescents.

Weight bearing physical activity plays an important role in bone development. This is particularly important in children and adolescents since bone mineral density reaches about 90% of its peak by the end of the second decade, and because about one quarter of adult bone is accumulated during the two years surrounding the peak bone growth velocity. Recent studies suggested that the exercise-induced increase in bone mineralization is maturity dependent, and that there is a "window of opportunity" and a critical period for bone response to weight bearing exercise during early puberty and premenarchal years. This supports the idea that increase in physical activity during childhood and adolescence can prevent bone disorders (like osteoporosis) later in life. In contrast, strenuous physical activity may affect the female reproductive system and lead to "athletic amenorrhea". The prevalence of "athletic amenorrhea" is 4-20 times higher than the general population. As a consequence, bone demineralization may develop with increased risk of skeletal fragility, fractures, vertebral instability, and curvature. Menstrual abnormalities in the female athlete result from hypothalamic suppression of the spontaneous pulsatile secretion of gonadotropin releasing hormone. Recent studies suggested that reduced energy availability (increased energy expenditure with inadequate caloric intake) is the main cause of the central suppression of the hypothalamic pituitary-gonadal axis. Therefore, effort should be made to optimize the nutritional state of female athletes, and if not successful, to reduce the training load in order to prevent menstrual abnormalities, and deleterious bone effects in particular during the critical period of rapid bone growth.

Adolescent↗
PubMed1988

Effects of immobilization on fetal bone development. A morphometric study in newborns with congenital neuromuscular diseases with intrauterine onset.

The effects of immobilization on fetal bone development were studied through post-mortem radiographs in 11 newborns with congenital neuromuscular diseases (CNMD) of intrauterine onset. Quantitative parameters were determined in the following bones: tibia, femur, humerus, radius, 3rd lumbar vertebra, and 5th rib. Thirty stillborns or newborns of similar gestational age and deceased from causes other than neuromuscular or related diseases were used as controls. No significant differences in bone lengths were observed between both groups. However, external diameters, cortex thicknesses, and cortical areas values were significantly lower in newborns with CNMD than in the control group. In newborns with CNMD, the medullary diameter of long bones showed good correlation with gestational age. However, this diameter was greater than that expected according to the reduced external diameter. These results suggest that intrauterine immobilization induces a decrease in mechanical usage of bone, mainly influencing bone modeling and probably bone remodeling. No changes were observed in longitudinal bone growth. Bones showed osteopenia and mechanical defects and were prone to fractures. In summary, reduced immobilization in utero produces bone osteoporosis of the fetus.

Bone Development↗
PubMed1999

FGF signaling inhibits chondrocyte proliferation and regulates bone development through the STAT-1 pathway.

Several genetic forms of human dwarfism have been linked to activating mutations in FGF receptor 3, indicating that FGF signaling has a critical role in chondrocyte maturation and skeletal development. However, the mechanisms through which FGFs affect chondrocyte proliferation and differentiation remain poorly understood. We show here that activation of FGF signaling inhibits chondrocyte proliferation both in a rat chondrosarcoma (RCS) cell line and in primary murine chondrocytes. FGF treatment of RCS cells induces phosphorylation of STAT-1, its translocation to the nucleus, and an increase in the expression of the cell-cycle inhibitor p21WAF1/CIP1. We have used primary chondrocytes from STAT-1 knock-out mice to provide genetic evidence that STAT-1 function is required for the FGF mediated growth inhibition. Furthermore, FGF treatment of metatarsal rudiments from wild-type and STAT-1(-/-) murine embryos produces a drastic impairment of chondrocyte proliferation and bone development in wild-type, but not in STAT-1(-/-) rudiments. We propose that STAT-1 mediated down regulation of chondrocyte proliferation by FGF signaling is an homeostatic mechanism which ensures harmonious bone development and morphogenesis.

3T3 Cells↗
PubMed1994

Aluminum effects on blood chemistry and long bone development in the chick embryo.

Body growth, blood chemistry, and long bone development of 10- to 16-day chick embryos (Gallus gallus) treated with aluminum (Al) citrate, sodium (Na) citrate, or sodium chloride (NaCl) were investigated. Two administration protocols were used. Acutely-treated embryos received 6.0 mumol Al citrate or Na citrate on day 8 of incubation. Chronically-treated embryos received a daily dose of 1.5 mumol Al citrate or Na citrate beginning on day 8 of incubation. For both protocols, Al citrate and Na citrate had no significant influence on viability or body weight. Al citrate-treated embryos had: (a) significantly shorter mean tibia lengths by day 16 of incubation, (b) a consistently lower ratio of tibia length: body weight on all days investigated, and (c) a persistent mid-diaphyseal malformation (angulation) of the femur and tibia. Spatially correlated with the malformation was a calcification defect detected by alizarin red S staining of intact tibias and the accumulation of aluminum as demonstrated by acid solochrome azurine staining of histological sections. Aluminum was localized at the mineralization front of the osteogenic collar surrounding the cartilage core of the tibia. Aluminum citrate or Na citrate had no significant effect on serum total calcium, inorganic phosphorus, total alkaline phosphatase activity, or creatinine, except for a transitory hypercalcemia (day 10) and phosphatemia (days 10 and 12) in Al citrate-treated embryos. The concomitant localization of Al and the early calcification defect in the region of tibial malformation implicate aluminum in the pathogenesis of the skeletal abnormality.

Alkaline Phosphatase↗
PubMed2004

[Effect of selenium and zinc level in diet on bone development in rats exposed to lead].

OBJECTIVE: To explore the interaction role of selenium and zinc in diet on bone development in rats exposed to lead, and to observe the change of bone mineral content (BMC) and bone mineral density (BMD). METHODS: Wean male Wistar rats were fed with diet added with different levels of selenium, zinc and lead for 12 weeks. RESULTS: Long-term exposure to lead may inhibit the development of bone and reduce BMC and BMD, however, selenium and zinc in the diets could improve the inhibit effect of lead on weight and length, BMC and BMD of rat bone. CONCLUSION: The present study indicated that supplementing suitable amount of selenium or/and zinc could interact the side effect of lead, and increase the BMC and BMD of rat bone. The interaction mechanism of iron and zinc on bone exposed to lead in diets needs to be explore in further.

Animals↗
PubMed2006

Cbf beta regulates Runx2 function isoform-dependently in postnatal bone development.

Runx2 and Cbfbeta are essential for skeletal development during the embryonic stage. Runx2 has two isoforms with different N-termini. We examined the functions of the Runx2 isoforms and Cbfbeta in postnatal bone development. On luciferase and electrophoretic mobility shift assays, Runx2-I was less active than Runx2-II in the absence of Cbfb, but the two Runx2 isoforms had similar activity levels in the presence of Cbfb. We generated Runx2-I transgenic mice under the control of Col1a1 promoter and Runx2-I/Cbfb and Runx2-II/Cbfb double transgenic mice. Runx2-I transgenic mice showed less severe osteopenia and fragility than Runx2-II transgenic mice due to milder inhibition of both osteoblast maturation and transition to osteocytes, even though the former mice showed higher transgene expression. However, Runx2-I/Cbfb and Runx2-II/Cbfb double transgenic mice had enhanced inhibition of osteoblast maturation, resulting in similar severity of osteopenia and fragility, although the latter mice had less osteocytes. These findings indicate that (1) Runx2-II more strongly inhibits osteoblast maturation and transition to osteocytes than Runx2-I; (2) Cbfbeta regulates Runx2 function isoform-dependently; and (3) Runx2-I activity is highly dependent on Cbfbeta. These findings demonstrate that Runx2 isoforms exert their functions through at least partly different mechanisms and Cbfbeta regulates bone development by regulating Runx2 function isoform-dependently.

Animals↗
PubMed2002

Effects of zinc on bone development in mouse embryo in vitro.

OBJECTIVE: This study was designed to explore the effects of zinc on bone development. METHODS: Forelimbs of mice with 16 d gestation were cultured by a rotating device. RESULTS: Contents of OC and (45)Ca and activities of AKP in the bone tissues cultured at zinc-deficiency media and at media with 120 micro mol/L of Zn(2+) decreased significantly. Synthesis of OC, absorption of calcium and activities of AKP in the bone tissues cultures at media with 45 and 70 micro mol/L of Zn(2+) increased significantly. Radiograph of bone tissues showed that length of long bone cultured at zinc-deficiency media and at media with 120 micro mol/L of Zn(2+) shortened and their density reduced, and those cultured at media with 45 and 70 micro mol/L of zinc increased, as compared with self-control bone. Histological analysis showed the death of bone cells and loss of stroma in the bone tissues cultured at media with 120 micro mol/L of Zn(2+), and active proliferation and differentiation of bone cells, and secretion and synthesis of osteoid increased in the bone tissues cultured at media with 45 and 70 micro mol/L of zinc. CONCLUSIONS: Adequate supplementation of zinc could promote formation and development of bone tissues and deficiency or excess of zinc could alter their growth and development and normal metabolism.

Animals↗
PubMed2004

HDAC4: a corepressor controlling bone development.

RUNX2 is a transcription factor with a well-characterized role in bone development. In this issue of Cell, Vega and colleagues (Vega et al., 2004) show that HDAC4 interacts with RUNX2 and impacts upon chondrocyte hypertrophy and bone formation.

Animals↗
PubMed1996

Effects of caffeine on bone cells and bone development in fast-growing rats.

BACKGROUND AND METHODS: Caffeine exerts harmful effects on fetal and suckling rats. To elucidate the effects of caffeine on bone in growing rats further, dams were fed normal laboratory chow until delivery. At birth, the litters were combined and eight pups were randomly assigned to each dam. Dams with the combined litters were divided into two groups. Dams of group 1 received a 20% protein diet as a control, and dams of group 2 received the 20% protein diet supplemented with caffeine (4 mg/100 g b.w.). Pups from both groups were killed on days 11, 15, 22, and 50. Parameters studied were ultrastructure of femoral osteoblasts, osteocytes, and osteoclasts; the number of osteocytes per area of bone in femoral histological cross sections; structural remodeling and shape of the lateral tibial metaphysis as revealed by scanning electron microscopy; and plasma Cu and Zn concentrations. RESULTS: Rats in the caffeine groups had significantly fewer osteocytes per area of femoral cross section, retarded structural remodeling of the lateral tibial metaphysis, osteoblasts and osteocytes with disrupted swollen mitochondria, and decreased plasma Cu and Zn levels when compared with controls. CONCLUSIONS: These results indicate that if young, rapidly growing rats are exposed to caffeine, disruption of osteoblasts and retarded bone development occur, which could be related to the decreased plasma Cu level in the young animals.

Animals↗
PubMedDate not supplied

Effect of a single botulinum toxin injection on bone development in growing rabbits.

Intramuscular injections with botulinum toxin A (BTX-A) lead to a rapid decrease in muscle mass and force, but the effect of this drug on bone development is unclear. In the present pilot study we evaluated the effect of a one-time injection of BTXA in growing rabbits. Twelve young (weight 1.5 kg) New Zealand rabbits were randomly assigned to receive either BTX-A (total dose 8 units per kg body weight) or sodium chloride 0.9% injections into the left quadriceps and gastrocnemius muscles. Both groups continued to gain weight in a similar manner following the injection. However, when the animals were sacrificed at five weeks after the injection, the group receiving BTX-A had a significant deficit (of 10%) in gastrocnemius muscle mass on the injected side, whereas no significant side-difference was found for the quadriceps. BTX-A injections did not affect the length of the tibia. Nevertheless, bone mineral content of the whole tibia, as measured by dual-energy X-ray absorptiometry, was 7% lower in the BTX-A injected side than on the contralateral side. Peripheral quantitative computed tomography showed that this bone mass deficit was larger in the metaphysis than in the epiphysis or diaphysis. In the diaphysis, the bone mass deficit was due to a reduction in cross-sectional bone dimensions, which equally affected the cross-section of the entire bone, the cortical compartment and the marrow space. BTX-A injections did not have a detectable effect on cortical bone mineral density. The bone mass deficit in the diaphysis thus appeared to be caused by a lack of periosteal bone apposition rather than increased endocortical or intracortical resorption. These preliminary data suggest that intramuscular BTX-A injections can have a deleterious effect on the development of bones that are loaded by the injected muscles.

Animals↗
PubMed1990

Effects of maternal caffeine with zinc intake during gestation and lactation on bone development in newborn rats.

On day 9 of gestation, pregnant dams were randomly divided into 3 groups. Dams of group 1 were fed a 20% protein diet as a control. Dams of group 2 were fed a 20% protein diet supplemented with caffeine. Dams of group 3 were fed a 20% protein diet supplemented with caffeine and zinc. The amount of caffeine added to the maternal diet was 2 mg/100 g body weight; the amount of zinc was 0.6 g/kg of diet. At birth, pups were mixed within each group, and 8 randomly selected pups from each group were assigned to each dam of the respective group and were continuously fed the same diet. On day 15, the pups were killed and cranial bones, mandibles and femurs removed. The bones were measured, and the mineral content of the mandibles and femurs was determined. Although there were no differences in the dimensions of the cranial bones among the groups, the measurements and mineral content of the mandibles and femurs were consistently affected by the caffeine in the diet. On the other hand, supplementation of the caffeine-added diets with zinc led to greatly improved bone development, reaching values up to or beyond control levels. Thus zinc supplementation of a caffeine diet given to the dams during gestation and lactation can favourably influence the otherwise impaired bone development of their offspring.

Animals↗
PubMed1998

Cbfa1 in bone development.

A factor fundamental to bone formation has been identified. Gene targeting shows that core-binding factor alpha 1 (Cbfa1) plays an essential role in bone formation and osteoblast differentiation. Thus, it is now possible to begin examining the molecular mechanism of bone formation--especially osteoblast differentiation.

Animals↗
PubMed1985

Developmental comparisons of boars and barrows: II. Body composition and bone development.

Differences in total carcass bone, muscle and fat, and linear measurements of the tibia and radius were evaluated in barrows at 105 kg and boars at 105, 118, 132 and 145 kg live body weight. The carcasses of five replicates were physically separated into skin, bone and soft tissues, and the linear measurements of the tibia and radius were obtained on seven replicates. At live weight of 105 kg, boars did not differ significantly in fat-free muscle, but they had 33.2% less fat, 11% greater bone weight and 14% greater skin weight than barrows. At 145 kg, boars had total carcass fat weight comparable with 105-kg barrows. Fat-free muscle, bone and skin weight of boars increased at linear rates of .41, .083 and .104 kg/kg of body weight increase from 105 to 145 kg, respectively. At 105 kg, density and length of the tibia and radius did not differ between boars and barrows. The tibia of boars were heavier than those of barrows at 105 kg, resulting in a greater ratio of tibia weight to length (indirect measure of bone thickness). As boars increased in live weight from 105 to 145 kg, total weight and length of the tibia and radius increased linearly. The ratio of weight to length of the tibia and radius increased during this 40-kg weight gain, indicating that weight of both bones increased at a greater rate than length. These results indicate that boars and barrows have the same weight of total carcass fat when boars are 40 kg heavier than the barrows. The greater bone weight of boar carcasses compared with barrows is due to greater bone thickness.

Adipose Tissue↗