Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Bone Development”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed2005

Tracking of activity and sedentary behaviors in childhood: the Iowa Bone Development Study.

BACKGROUND: Physical activity tracking studies can determine when children settle into activity patterns and their risk for maintaining sedentary behaviors. This study examined the tracking of activity and sedentary behavior in relation to adiposity during middle childhood. METHODS: Activity intensities and patterns were examined during a 3-year interval in a population-based study of children using accelerometry and survey methods. Data were collected and analyzed from 1998 to 2004. Participants (n = 379) were, on average, 5.6 (standard deviation [SD] +/- 0.5) years at baseline and 8.6 (SD +/- 0.5) years at follow-up. Adiposity was measured with whole-body, dual-energy x-ray absorptiometry. Correlation coefficients and odds ratios were used to assess tracking. The association of activity with adiposity was tested using the Wilcoxon rank-sum test. RESULTS: Over the 3-year interval, Spearman rank-order correlation coefficients between baseline and follow-up activity measures were low to moderate (r = 0.18 to 0.39). Sedentary behavior was more predictable than overall activity, and tended to be more stable (r = 0.37 to 0.52), with the exception of video playing in boys (r = 0.18). Children maintaining a high degree of vigorous activity and low levels of TV viewing were less likely than peers to be in the upper quartile for adiposity at follow-up, and were less likely to gain adiposity during the study period. CONCLUSIONS: Sedentary behavior, including TV viewing, is moderately stable during middle childhood. Health promotion programs that specifically target maintaining high levels of vigorous activity and low levels of TV viewing may help reduce the increasing prevalence of childhood obesity.

Absorptiometry, Photon↗
PubMed2006

How does exercise affect bone development during growth?

It is increasingly accepted that osteoporosis is a paediatric issue. The prepubertal human skeleton is quite sensitive to the mechanical stimulation elicited by physical activity. To achieve the benefits for bone deriving from physical activity, it is not necessary to perform high volumes of exercise, since a notable osteogenic effect may be achieved with just 3 hours of participation in sports. Physical activity or participation in sport should start at prepubertal ages and should be maintained through the pubertal development to obtain the maximal peak bone mass potentially achievable. Starting physical activity prior to the pubertal growth spurt stimulates both bone and skeletal muscle hypertrophy to a greater degree than observed with normal growth in non-physically active children. High strain-eliciting sport like gymnastics, or participation in sports or weight-bearing physical activities like football or handball, are strongly recommended to increase the peak bone mass. Moreover, the increase in lean mass is the most important predictor for bone mineral mass accrual during prepubertal growth throughout the population. Since skeletal muscle is the primary component of lean mass, participation in sport could have not only a direct osteogenic effect, but also an indirect effect by increasing muscle mass and hence the tensions generated on bones during prepubertal years.

Bone Density↗
PubMed2000

The ribosomal protein QM is expressed differentially during vertebrate endochondral bone development.

Endochondral ossification is a carefully coordinated developmental process that converts the cartilaginous model of the embryonic skeleton to bone with accompanying long bone growth. To identify genes that regulate this process we performed a complementary DNA (cDNA) subtractive hybridization of fetal bovine proliferative chondrocyte cDNA from epiphyseal cartilage cDNA. The subtracted product was used to screen a fetal bovine cartilage cDNA library. Ten percent of the clones identified encoded the bovine orthologue of the human ribosomal protein "QM." Northern and western blot analysis confirmed that QM was highly expressed by cells isolated from epiphyseal cartilage as opposed to proliferative chondrocytes. In contrast, no detectable difference in the expression of mRNA for the ribosomal protein S11 was detected. Immunohistochemical analysis of fetal bovine limb sections revealed that QM was not expressed by the majority of the epiphyseal chondrocytes but only by chondrocytes in close proximity to capillaries that had invaded the epiphyseal cartilage. Strongest QM expression was seen in osteoblasts in the diaphyseal region of the bone adjoining the growth plate, within the periosteum covering the growth plate and within secondary centers of ossification. Hypertrophic chondrocytes within the growth plate adjoining the periosteum also were positive for QM as were chondrocytes in the perichondrium adjoining the periosteum. In vitro investigation of the expression of QM revealed higher QM expression in nonmineralizing osteoblast and pericyte cultures as compared with mineralizing cultures. The in vivo and in vitro expression pattern of QM suggests that this protein may have a role in cell differentiation before mineralization.

Amino Acid Sequence↗
PubMed1989

Purification and molecular cloning of a novel group of BMPs and localization of BMP mRNA in developing bone.

Using a novel purification scheme, we have characterized BMP as a 30kD fraction. After reduction, which destroys biological activity, this fraction was shown to be comprised of individual polypeptides with molecular weights of 30kD, 18kD and 16kD. Molecular cloning of these polypeptides resulted in the identification of 4 previously undescribed genes (BMP-1, BMP-2A, BMP-2B, and BMP-3) each of which is capable of directing de novo cartilage formation in vivo. While BMP-1 appears to be unrelated to other known growth factors, the derived amino acid sequence of BMP-2A, 2B, and 3 indicate that they are new members of the TGFb gene family. BMP-1, 2A and 2B are expressed in rat embryos during morphogenesis and can be localized by in situ hybridization to developing limb buds. BMP-3 localizes to neural ectoderm and later on in development to newly forming periosteum. Comparisons to other members of the TGFb family suggest that these newly identified BMPs are involved in pattern formation during early skeletal development.

Amino Acid Sequence↗
PubMed1995

Growth charts, growth velocity and bone development in childhood obesity.

OBJECTIVE: To compare the growth charts of obese subjects (4-18 years) with the Tanner's growth curves and to analyze the growth velocities and bone age of obese children in prepuberty and adolescence. Moreover to compare the relationship between the serum insulinemic and glycemic levels and height standard deviation score (HSDS). DESIGN: Growth charts: this study included 1250 obese subjects (669 males, 581 females) observed between 1981 and 1993 and divided into seven age categories (4-6, 7-8, 9-10, 11-12, 13-14, 15-16, 17-18 years). Growth velocities: yearly growth velocities of 579 obese subjects (325 males, 254 females) were compared to growth velocities of 473 controlled children of the same sex, chronological age and pubertal stage. Bone age (BA) of 846 obese subjects (470 males, 376 females) was estimated. Blood analysis: insulin secretion of 70 obese children was considered and compared to 70 lean controls of equal chronological age and sex. MEASUREMENTS: Growth rate, standardized height and other physical characteristics of the children were measured by trained examiners. All subjects were evaluated singularly for at least 4 years with a follow-up every 6 months. BA was estimated by radiograph of the left hand and wrist using the Tanner-Whitehouse II system by a single observer. For the insulin secretion study and glycemic levels oral glucose tolerance test (OGTT) was performed using a glucose load of 1.75 g/kg per body weight. Plasma insulin was assessed by a double antibody radioimmunoassay. RESULTS: In adipose children the growth charts, referred to 97th centile, 50th centile and 3rd centile, were superior to those of the normal population up to the age of 13 and 12.5 years for male and for female respectively; growth decreases at the above age in both sexes. The obese subjects were equal in height to the non obese subjects as they reached their 18th birthday. The growth velocity (cm/yr) of the obese child, in the age range considered here, does not show differences when compared with the lean child in the prepubertal status (P not significant) but decreases during Tanner's stage II, III IV in boys and girls (P < 0.0001). BA is more advanced over chronological age (delta BA-CA) in both sexes. The increase of BA over CA does not show a remarkable difference during pubertal maturation in boys (P not significant); whereas in girls the delta BA-CA decreases with advancing sexual maturation (P < 0.0001). Our obese subjects have significantly higher plasma insulinemic levels compared with the lean controls (P < 0.0001). Moreover there is a positive correlation between plasma insulinemic levels and HSDS (r = 0.881, P < 0.0001). We did not observe a correlation between serum glycemic levels and HSDS. CONCLUSION: Our data demonstrate that the growth increase in an obese child starts in the first years of life. The statural advantage acquired in the first years of life would be exploited and maintained up to the beginning of puberty and with a growth velocity equal to that of the lean subject. Skeletal maturation is strongly increased in both sexes. Bone age remained advanced during the entire period of pubertal development. During puberty obese subjects demonstrate a less notable growth spurt when compared with lean subjects. The growth advantage gradually decreases and final adult height of obese and normal subjects is equal.

Adolescent↗
PubMed1992

Long bone development in extrinsic fetal akinesia: an experimental study in rat fetuses subjected to oligohydramnios.

The transverse growth of long bones during intrauterine development was studied in rat fetuses subjected to experimental oligohydramnios in order to determine whether the skeletal changes, if any, in extrinsic fetal akinesia were similar to those observed in curarized rat fetuses with the fetal akinesia deformation sequence. Oligohydramnios was induced by daily extraction of amniotic fluid from day 17 of gestation until term. Experimental fetuses were compared with a sham-operated control group. The total area and perimeter, the absolute and relative amount of periosteum and bone trabeculae, the major and minor axes, and the elongation factor were measured in histological cross sections of the femoral metaphysis and diaphysis with an IBAS 1 image analysis system. Rat fetuses in the experimental group showed multiple articular contractures, redundant skin, and lung hypoplasia, a phenotype consistent with the oligohydramnios sequence. No alterations in femoral shape and transverse growth of the metaphysis and diaphysis were noted in these fetuses. These results suggest that the main mechanical factor related to fetal bone modeling is muscular strength, while motion would be mainly involved in fetal joint development.

Animals↗
PubMed1999

Ablation of the PTHrP gene or the PTH/PTHrP receptor gene leads to distinct abnormalities in bone development.

Parathyroid hormone (PTH) and parathyroid hormone-related peptide (PTHrP) bind to and activate the same PTH/PTHrP receptor. Deletion of either the PTHrP gene or the PTH/PTHrP receptor gene leads to acceleration of differentiation of growth plate chondrocytes. To explore further the functional relationships of PTHrP and the PTH/PTHrP receptor, bones of knockout mice were analyzed early in development, and the phenotypes of double-knockout mice were characterized. One early phenotype is shared by both knockouts. Normally, the first chondrocytes to become hypertrophic are located in the centers of long bones; this polarity is greatly diminished in both these knockouts. The PTH/PTHrP receptor-deficient (PTH/PTHrP-R(-/-)) mice exhibited 2 unique phenotypes not shared by the PTHrP(-/-) mice. During intramembranous bone formation in the shafts of long bones, only the PTH/PTHrP-R(-/-) bones exhibit a striking increase in osteoblast number and matrix accumulation. Furthermore, the PTH/PTHrP-R(-/-) mice showed a dramatic decrease in trabecular bone formation in the primary spongiosa and a delay in vascular invasion of the early cartilage model. In the double-homozygous knockout mice, the delay in vascular invasion did not occur. Thus, PTHrP must slow vascular invasion by a mechanism independent of the PTH/PTHrP receptor.

Animals↗