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At least 253 records · Page 14Linked to original sources
PubMed1984

[Influence of nutrition on the bone development of children].

The effect of nutrition on infant bone age was studied. Bone age was examined in children with different degrees of malnutrition using wrist X-Rays and comparing them with Greulich and Pyle Atlas. There were no differences in the socioeconomic level of the different groups. In obese children bone age was advanced, while in under-nourished, it was retarded. The more severe the undernutrition the more delayed the bone age. A positive correlation between the percentage of variation of bone age and chronological age, and percentage of height for age was found. A greater delay in bone age was detected in undernourished children who had been small for date infants.

Age Determination by Skeleton↗
PubMed2004

Atmospheric pressure as a force that fills developing bones with marrow and air.

Many theories try to explain the existence and function of paranasal sinuses. This paper is an attempt to correlate process of paranasal sinus development in human with bone pneumatization processes in animals. It is here proposed that this mechanism starts in utero and continues after birth. During endochondral development, a solid hyaline cartilage model transforms into long bones. Central chondrocytes hypertrophy and their lacunae become confluent. Dissolving of the cartilage intercellular matrix forms a primitive marrow cavity. It is soon invaded by the periostal bud. Once circulation is established in the developing bone, the dissolved hyaline matrix can be slowly washed away from the bone cavity. Circulation in the bone cavity can develop slight subatmospheric pressures, similar to negative interstitial pressures in subcutaneous tissues. The amniotic fluid conducts atmospheric pressure to the fetal body. The pressure is trying to fill enlarging bone cavities through the existing vascular openings, or to create new openings. Bone walls of developing paranasal bones are to weak to resist the pressure gradient on their walls. New openings form on the weakest spots allowing airway mucosa to form initial paranasal sinuses. The enlarging cavities of long bones that are remote from the body surface and airway also develop a slightly subatmospheric pressure that fills them with cellular elements. These elements enter bone through the feeding vessels and form bone marrow. During after birth skeletal growth, bone remodeling shapes paranasal sinuses in a process of slow evolution that do not require measurable pressure gradients. When two sinuses come in vicinity, their growth rate declines, since the remaining thin and fragile bone lamella between them does not retract anymore.

Animals↗
PubMed2002

Expression of Runx1, -2 and -3 during tooth, palate and craniofacial bone development.

We describe the expression of three Runt-related RUNX genes (previously termed AML, Cbfa, or Pebp2alpha) Runx1 and Runx3 during the development of teeth and other craniofacial tissues and compare them to Runx2 expression reported earlier. All three genes were expressed in mesenchymal condensates. Runx1 was expressed in several cartilage primordia earlier than Runx3, and Runx2 was intense in all mesenchymal condensations of bones and teeth. Only Runx1 was expressed in epithelia, and in tooth germs transcripts were detected in outer dental epithelium. Runx1 was also intensely expressed in the midline epithelium of palatal shelves. In early tooth morphogenesis Runx3 was coexpressed with Runx2 in a thin layer of mesenchymal cells underlying dental epithelium. Unlike Runx2, Runx3 was expressed in odontoblasts. However, Runx3 mutant mice did not show obvious tooth phenotype or deviations of Runx1 and Runx2 expression patterns in the tooth.

Animals↗
PubMed2003

[Rapidly developing bone destruction in a patient with type 1 Gaucher disease].

The authors report on a 25 year-old male Gaucher patient who developed rapid bone deterioration. The patient was splenectomised at age 3 and had no signs and symptoms of bone involvement for more than 20 years. In addition to the infarction in the right tibia, severe bone necrosis was detected in components of the left hip. This report suggests that bone deterioration may develop insidiously at any time in Gaucher patients, and that long-term and regular follow up is warranted.

Adult↗
PubMed2004

Bone development during GH and GnRH analog treatment.

Estrogens, GH and IGFs are essential in the development and growth of the skeleton and for the maintenance of bone mass and density. Treatment of precocious puberty with GnRH analogs (GnRHa), by reducing sex steroid levels, leads to a situation of hypoestrogenism that may theoretically have a detrimental effect on bone mass during pubertal development. A reduction in bone mineral density (BMD) during GnRHa treatment has been demonstrated, but GnRHa treatment in patients with central precocious puberty (CPP) does not seem to impair the achievement of normal peak bone mass (PBM) at final height. However, calcium supplementation is effective in improving bone densitometric levels and may promote better PBM achievement. In children and adolescents with GH deficiency (GHD), BMD assessed by dual-energy X-ray absorptiometry (DEXA) and bone turnover are significantly reduced, but they are stimulated by GH treatment. GH treatment leads to improved bone density, function of the dose and duration of treatment, and patients may require prolonged GH treatment beyond the time of growth to improve PBM. After the discontinuation of GH therapy, the more active population had higher bone mineral content (BMC) levels than patients with low physical activity. In our experience, the therapeutic association of GH and calcium also represents a valuable tool in pursuing a proper BMC in GHD patients. We concluded that nonhormonal factors, such as physical activity and nutritional factors, are important in determining bone metabolism and bone mass.

Adolescent↗
PubMedDate not supplied

Perspective: cerebral palsy as a model of bone development in the absence of postnatal mechanical factors.

To ensure optimal skeletal development, mechanical loading is imperative. The consequences of the removal of, or complete absence of, mechanical loading are illustrated by the clinical condition of cerebral palsy (CP). Clinical and radiological evaluation of children with CP provides an insight into how the growing skeleton develops when mechanical loading is reduced due to non-physiological muscle function. The poor bone status or "physiologic osteopenia" that these children suffer is multifactorial compromised of both mechanical and non-mechanical effects; primarily it is the lack of normal loading from the musculature which causes the development of a bone incapable of withstanding daily activities. Fractures occur during daily activities such as dressing and handling. Increased bone resorption during periods of immobilisation after fracture or surgery, also increases bone fragility. Trials of physical, nutritional and pharmacological treatments in CP children result in increased bone mineral density. Trials that include fracture prevention as the primary end point are required in this vulnerable group of children.

Bone Development↗
PubMed2002

Human fetal bone development: histomorphometric evaluation of the proximal femoral metaphysis.

Quantitative data on metaphyseal bone histology during early human development are scarce. In the present study the proximal femoral metaphysis of 35 fetuses and newborns (gestational age 16-35 weeks) was analyzed by histomorphometry. Averaged over the entire metaphyseal area, the relative amount of bone and cartilage was higher in the third compared to the second trimester. Osteoid thickness increased with gestational age, whereas indices of bone resorption decreased. The relative amount of cartilage decreased with increasing distance from the growth plate, whereas the relative amount of bone increased. This was due to trabecular thickening, which occurred at an estimated rate of 3 microm/day in areas close to the growth plate. Despite this rapid rate of net bone gain, osteoid indices were relatively low, indicating that mineralization occurred very rapidly after bone deposition. These observations suggest that modeling, not remodeling, is the predominant mechanism responsible for the development of femoral metaphyseal cancellous bone in utero.

Analysis of Variance↗
PubMed2001

Visualizing normal and defective bone development in zebrafish embryos using the fluorescent chromophore calcein.

Zebrafish have recently become a model of choice among developmental biologists. This unique model enables both modern molecular and genetic studies to be carried out to identify genes involved in a wide variety of developmental processes. The success of the genetic approach depends largely on the application of an easy and effective screening method to identify interesting mutants. In order to develop a method for visualizing skeletal structures in zebrafish embryos that would be suitable for screening skeletal mutants, we investigated the use of the fluorescent chromophore calcein, which binds specifically to calcified skeletal structures. By using this method, we followed the development of the skeletal structures in zebrafish embryos from day 1 to day 21 postfertilization, and analyzed the effect of bone morphogenetic protein-2 (BMP2) on axial skeleton development. We found the development of the calcified skeletal structure to appear in a progressive fashion from head to tail. Calcified structures in the head (i.e., the jaw) developed first, which were then followed by the axial skeleton in the trunk. Interesting to note was that there appeared to be two domains in the calcification of vertebrae within the axial skeleton. The first three vertebrae were in the first domain; the rest being in the second domain. Compared with Alcian blue staining, we found that calcein staining indeed labels calcified skeletal structures, and, moreover, it is a more sensitive and inclusive method for visualizing skeletal structures. To determine whether calcein staining could also be used to detect abnormal bone development, we ectopically expressed BMP2 in zebrafish notochord cells. We demonstrated that ectopic expression of BMP2 in notochord cells inhibited the development of the axial skeleton. Together, these results clearly demonstrated the sensitivity of calcein staining for visualizing bone structures in developing zebrafish embryos and its effectiveness for screening for mutants that have bone structure defects.

Alcian Blue↗
PubMed1997

Collagenase-3 (MMP-13) is expressed by hypertrophic chondrocytes, periosteal cells, and osteoblasts during human fetal bone development.

Collagenase-3 (MMP-13) is a novel matrix metalloproteinase, the expression of which has so far only been documented in human breast carcinomas and osteoarthritic cartilage. In this study we have examined the expression of MMP-13 during human fetal development. Northern blot hybridizations revealed abundant expression of MMP-13 mRNAs in total RNA from fetal cartilage and calvaria at gestational age of 15 weeks. By in situ hybridization MMP-13 transcripts were detected in chondrocytes of hypertrophic cartilage in vertebrae of the spinal column and in the dorsal end of ribs undergoing ossification, as well as in osteoblasts and periosteal cells below the inner periosteal region of ossified ribs. In contrast, no expression of MMP-13 could be detected in osteoclasts. Furthermore, expression of MMP-13 mRNA was detected in osteoblasts and fibroblasts primarily on the inner side of calvarial bone of the skull at 16 weeks of gestation. Expression of MMP-13 mRNA by primary human fetal chondrocytes in culture was enhanced by transforming growth factor-beta (TGF-beta) and inhibited by bone morphogenetic protein-2 (BMP-2). No expression of MMP-13 mRNA could be noted in other fetal tissues, including the skin, lungs, neural tissue, muscle, and liver. These results suggest that MMP-13 plays an important role in the extracellular matrix remodeling during fetal bone development both via endochondral and intramembranous ossification.

Blotting, Northern↗
PubMed2006

A mouse model for human short-stature syndromes identifies Shox2 as an upstream regulator of Runx2 during long-bone development.

Deficiencies or mutations in the human pseudoautosomal SHOX gene are associated with a series of short-stature conditions, including Turner syndrome, Leri-Weill dyschondrosteosis, and Langer mesomelic dysplasia. Although this gene is absent from the mouse genome, the closely related paralogous gene Shox2 displays a similar expression pattern in developing limbs. Here, we report that the conditional inactivation of Shox2 in developing appendages leads to a strong phenotype, similar to the human conditions, although it affects a different proximodistal limb segment. Furthermore, using this mouse model, we establish the cellular etiology of these defects and show that Shox2 acts upstream the Runx2 gene, a key regulator of chondrogenesis.

Animals↗
PubMed1996

[Animal nutrition in veterinary medicine--actual case reports. Nutritionally related disturbences in bone development in emus and rheas].

Two cases of disturbed health and growth of the skeleton in emus and rheas caused by faults in feeding and mineral supply are reported. 13 of 37 emus developed (beginning in the 3rd week) more and more signs of perosis. The diet fed in this case was based mainly on pelleted diets for piglets and rabbits and unpelleted supplements. The ingesting behaviour (selective intake and refuse of fines and supplements) resulted in an imbalanced mineral intake. In the second case 3 of 15 young rheas showed unphysiological postures of the necks vertebral column. Disposed by an absolutely insufficient calcium supply (the real ingested diet was based on corn and white bread mainly) fractures of vertebrae were provoked by unprofessional handling. During the healing process (uncalcified) connective tissue near to fractures localization led to the abnormal posture of the neck.

Animal Feed↗
PubMed2002

[Study of the effects of zinc on bone development applying fetal mouse limbs culture].

The effects of zinc on bone metabolism is explored. A home-made rotating apparatus is used to cultivate fetal mouse front limbs at 16-day gestational age. The activity of alkaline phosphatase(AKP) and histological silce are used to analyze the effects of zinc on bone metabolism. Compared with the control group, the zinc deprived group and Zn2+ 120 mumol/L group have a lower alkaline phosphatase (AKP) activity and the contracted chromatin, membrane rupture and matrix loss are observed in bone cells. The zinc adequate group(Zn2+ concentration are 45 mumol/L and Zn2+ 70 mumol/L respectively) has a higher alkaline phosphatase(AKP) activity, more active bone generation, deeper stain of bone matrix and increased bone trabecula. It is concluded that zinc could affected the bone metabolism and growth; both zinc-deficiency and zinc-excess could alter growth and bone metabolism.

Alkaline Phosphatase↗
PubMed2004

Bone mass development and bone metabolism in juvenile idiopathic arthritis: treatment with growth hormone for 4 years.

OBJECTIVE: To study the acquisition of bone mass and changes in bone mineral density (BMD) related to age, bone age, pubertal status, and growth hormone (GH) therapy in 11 children with juvenile idiopathic arthritis (JIA) longitudinally over 4 years, in comparison to healthy children. METHODS: Bone mineral content (BMC), BMD, and vertebral area were measured by dual energy x-ray absorptiometry. Since BMC and BMD increase with size, BMD was converted to volumetric BMD (vBMD) after adjustment for vertebral size. RESULTS: At inclusion all patients (7 female, 4 male, mean age 10.3 +/- 2.1 yrs) had low BMD, with a mean z-score for area BMD (aBMD) of -2.04 +/- 0.8 SD. After adjustment for size, vBMD was 0.198 g/cm3, and after 4 years of GH treatment it increased significantly to 0.232 g/cm3 (p < 0.03), expressed as SD scores that increased from -2.97 +/- 0.81 SD to -2.83 +/- 0.67 SD. In relation to bone age, vBMD SD increased from -2.53 +/- 0.85 to -2.41 +/- 0.79. Compared to pretreatment values, bone formation and resorption markers increased significantly during treatment. CONCLUSION: Our results reflect an increase in bone turnover under GH therapy in these patients. Despite biochemical changes there was a stabilization of vBMD for age and bone age, with a percentage increase comparable to healthy children. Longterm GH treatment will be necessary to evaluate a potential positive effect of GH on bone density and metabolism in patients with JIA.

Adolescent↗