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 271 records · Page 15Linked to original sources
PubMed2006

Vanadium and bone development: putative signaling pathways.

Vanadium is a trace element present in practically all cells in plants and animals. It exerts interesting actions in living systems. At pharmacological doses, vanadium compounds display relevant biological actions such as mimicking insulin and growth factors as well as having osteogenic activity. Some vanadium compounds also show antitumoral properties. The importance of vanadium in bone arises from the studies developed to establish the essentiality of this element in animals and humans. Bone tissue, where the element seems to play an important role, accumulates great amounts of vanadium. This paper reviews the physiology of osteoblasts, the involvement of different growth factors on bone development, and the effects of vanadium derivatives on the skeletal system of animal models and bone-related cells. Two cellular lines are discussed in particular; one derived from a rat osteosarcoma (UMR106) and the other is a nontransformed osteoblast cell line (MC3T3-E1). The effects of different growth factors and their mechanisms of action in these cellular lines are reviewed. These models of osteoblasts are especially useful in understanding the intracellular signaling pathways of vanadium derivatives in hard tissues. Vanadium uses an intricate interplay of intracellular mechanisms to exert different biochemical and pharmacological actions. The effects of vanadium derivatives on some cellular signaling pathways related to insulin are compiled in this review. The comprehension of these intracellular signaling pathways may facilitate the design of vanadium compounds with promising therapeutic applications as well as the understanding of secondary side effects derived from the use of vanadium as a therapeutic agent.

Animals↗
PubMed1998

Expression of the thrombin receptor in developing bone and associated tissues.

Thrombin, a serine protease with a central role in thrombosis and hemostasis, is also a specific agonist for a variety of cellular responses in osteoblasts and stimulates bone resorption in organ culture. Cultured osteoblast-like cells express the proteolytically activated thrombin receptor, but the significance of this finding in vivo remains unknown. Immunohistochemistry was used to investigate the normal tissue distribution of the proteolytically activated thrombin receptor in developing rat bones and associated tissues. In hind limbs, the receptor was first observed on embryonic day 16 and became more abundant within the limb as gestation progressed. Thrombin receptor staining was detected on osteoblasts, macrophages, muscle cells, and endothelial cells, but not osteoclasts. Similarly, osteoblasts in developing calvariae stained positively for the thrombin receptor. The pattern of receptor expression by primary osteoblast cultures and freshly isolated macrophages and osteoclasts corresponded to that observed in vivo. The observed pattern of thrombin receptor expression in bone cells supports the hypothesis that cell-mediated thrombin-induced bone resorption is mediated by osteoblasts.

Animals↗
PubMed2005

Poor nutrition in prepubertal Japanese children at the end of World War II suppressed bone development.

OBJECTIVE: To assess the extent to which malnutrition in childhood affects bone mineral density (BMD) decades later. METHODS: BMDs were compared in healthy women (35-59 years old) who visited our hospital for annual examinations between 1992 and 1993 (group 1) and between 1999 and 2002 (group 2). RESULTS: The BMDs of 50- to 54-year-old women in group 1 averaged 0.86+/-0.15 g/cm2, which was significantly (p<0.001) lower than age-matched women in group 2 (1.02+/-0.16 g/cm2). CONCLUSION: At the end of World War II (1945) undernutrition was rampant throughout Japan, and there were unprecedented numbers of cases of malnutrition. BMD was lower in women who experienced those conditions while they were 5 years old in average, a time when rapid skeletal growth was beginning. Thus, nutrition in childhood is a particularly crucial determinant of lifelong bone health.

Adult↗
PubMed1991

Characterization of a cDNA for chicken osteopontin: expression during bone development, osteoblast differentiation, and tissue distribution.

The chicken bone phosphoprotein (approximately 66-kDa BPP) is a major noncollagenous component of bone and is the major phosphoprotein synthesized by cultured chicken embryo osteoblasts [Gotoh, Y., Gerstenfeld, L. C., & Glimcher, M. J. (1990) Eur. J. Biochem. 87, 49-58]. A cDNA clone for this protein was isolated from an expression library made from embryonic chicken bone mRNA. The complete primary protein sequence of 264 amino acids was deduced from the cDNA sequence inclusive of a 16 amino acid signal peptide sequence and terminated by 4 in-frame stop sequences. A sequence alignment indicated an approximate 35% overall similarity in protein sequence between the avian approximately 66-kDa BPP and the mammalian protein osteopontin, while at the nucleotide level 60% similarity was observed. Features of this sequence which showed the greatest similarity to mammalian osteopontin included a region in which seven of nine consecutive residues are aspartic acid, a recognition sequence for integrin-mediated cell binding (-Arg-Gly-Asp), and four possible recognition sequences for phosphorylation by casein kinase II. Hybridization analysis indicated a message of 1.5 kb found predominantly in bone and kidney. The mRNA was inducible in phorbol ester treated primary cultures of chondrocytes which show no expression under normal growth conditions. A temporal induction was seen during osteoblastic differentiation both in vivo and in vitro, thus suggesting that regulation of the approximately 66-kDa BPP is under transcriptional control during osteoblast development. In summary, both the protein's primary structure and its biological features suggest that it is the avian homologue to mammalian protein osteopontin.

Amino Acid Sequence↗
PubMedDate not supplied

The role of macrophages in osteoclast neogenesis in vivo: quantitative analysis of osteoclasts and macrophages in endochondral bone development in rats treated with hydrocortisone or calcitonin.

Osteoclasts and macrophages in endochondral bone of rats were analyzed after long-term treatment with hydrocortisone (HC) or elcatonin (ECT). The growth plate-metaphysis junction ( GPMJ ) of the HC-treated bones showed increased numbers of osteoclasts, but the incidence of osteoclast profiles with ruffled borders was low and the cells had fewer nuclei. The number of macrophages in the GPMJ of HC-treated bone did not significantly differ from that in the control. In the metaphyseal trabecular (MT) region macrophages were numerous, but osteoclasts were depleted. Compared to controls the ECT-treated osteoclasts in the GPMJ had an increased number of nuclei per cell, and the incidence of osteoclast profiles with ruffled borders was reduced. There was a small increase in the number of osteoclasts and a large increase in the number of macrophages. The osteoclasts in the MT regions of ECT-treated bones were significantly larger compared to controls. The macrophages did not differ in number from the controls. This investigation supports the proposal that the GPMJ is the principal site of osteoclasts neogenesis. Discrepancies in features of osteoclasts in the GPMJ and MT regions of each treatment group were probably due to a difference in peroid when the osteoclasts were exposed to the drugs.

Animals↗
PubMed2003

Histologic examination of bone development in juvenile chimpanzees.

The purpose of this study is to determine whether histologic skeletal development in chimpanzees (Pan troglodytes) differs from that in humans. Currently, minimal quantitative data are available on the bone histology of great apes. In addition to providing baseline data on juvenile chimpanzee bone histology, the data generated by this study have potential applications for studying the comparative development between chimpanzees and humans and other primates, as well as investigating the evolution of human bone development, differences in development among limb elements, and differences in histology related to locomotor function. The study sample includes thin sections from the femoral, tibial, and fibular midshafts of 13 chimpanzees originally prepared by Kerley ([1966] Tulane Stud. Zool. 13:71-82) as part of a study on skeletal age changes in the chimpanzee. Twelve juveniles, ranging in known age from 2-15.3 years, and one adult, with a known age of 35 years, are represented. For each specimen, numbers of osteons, osteon fragments, and non-Haversian canals were counted, and percent lamellar bone was estimated. Results were compared with data extracted from Kerley ([1965] Am. J. Phys. Anthropol. 23:149-164) on a juvenile human sample. Results indicate that juvenile chimpanzees and humans exhibit similar age-related changes in histologic variables. However, age is not as strong a predictor of variation in microstructural variables in chimpanzees as it is in humans.

Animals↗
PubMed1991

Effects of dietary amino acid levels on bone development in broiler chickens.

Studies with several species suggest that dietary protein may influence bone calcification. Six pens of six male broilers in two consecutive trials were fed from 1 to 21 days either .5 or 1.0% Ca in diets with 80, 90, 100, 110, or 120% of the amino acid (AA) standards suggested by Thomas et al. in 1986 at a constant .46% nonphytate P. The BW and feed conversion rate (FCR) were determined, and bone measurements were taken. Both AA and Ca levels influenced BW with an interaction of the two factors. The Ca level, but not AA level, influenced FCR. The lower Ca level inhibited feed intake. Increasing AA levels reduced bone ash but did not affect tibia breaking strength. There was an interaction of AA and Ca on tibia ash, tibia weight, and tibia length. The higher AA levels supported normal linear growth of the tibia but decreased rate of calcification, especially in the diets with .5% Ca. In diets with marginal Ca levels, higher AA levels may reduce bone calcification.

Amino Acids↗
PubMedDate not supplied

[Structural identity of the multinuclear chondro- and osteoclasts in developing bone].

Distributional peculiarities and the ultrastructure of multinuclear elastic cells have been studied in the developed thighbone of rat and rabbit fetuses and new-borns. Multinuclear chondro- and osteoclasts exhibit no noticeable structural specificity with respect to the resorption substrate and are considered to be one and the same type of clastic cells whose main function is to resorb the mineralized tissue.

Animals↗
PubMed2006

The 'Functional Muscle-Bone Unit': probing the relevance of mechanical signals for bone development in children and adolescents.

The present text deals with the relationship of muscle force and mass to bone mass and geometry in the developing skeleton of children and adolescents. Recent results of the last ten years are discussed with reflection on Harold Frost's 'mechanostat hypothesis'. Bone mass and geometry follow the development of body size and muscle force in children and adolescents. Thereby, bone is adapted to the tissue strain due to biomechanical forces. This process is modified by hormonal signals (i.e., estrogens and androgens). Therefore, the quantified relationship of muscle force to bone stability is a reasonable approach to distinguish between primary and secondary bone diseases. Primary bone diseases are characterized by a disturbed adaptation of bone to biomechanical forces. In contrast, secondary bone diseases show a correct adaptation of bone to loaded forces in combination with a decline of muscle force. Therefore, the 'Functional Muscle-Bone Unit' was introduced into the diagnostics of pediatric bone diseases. The ratio of two parameters--referred to bone strength on the one and to biomechanical forces on the other side--is a reasonable diagnostic approach to distinguish between primary and secondary bone diseases.

Adolescent↗
PubMed2004

VEGFA is necessary for chondrocyte survival during bone development.

To directly examine the role of vascular endothelial growth factor (VEGFA) in cartilage development, we conditionally knocked out Vegfa in chondrocytes, using the Col2a1 promoter to drive expression of Cre recombinase. Our study of Vegfa conditional knockout (CKO) mice provides new in-vivo evidence for two important functions of VEGFA in bone formation. First, VEGFA plays a significant role in both early and late stages of cartilage vascularization, since Vegfa CKO mice showed delayed invasion of blood vessels into primary ossification centers and delayed removal of terminal hypertrophic chondrocytes. Second, VEGFA is crucial for chondrocyte survival, since massive cell death was seen in joint and epiphyseal regions of Vegfa CKO endochondral bones. Chondrocytes in these regions were found to upregulate expression of Vegfa in wild-type mice at the time when massive cell death occurred in the Vegfa CKO mice. The expression of the VEGFA receptors Npr1 and Npr2 in epiphyseal chondrocytes and lack of blood vessel reduction in the vicinity of the cartilaginous elements in the Vegfa CKO mice raise the possibility that the observed cell death is the result of a direct involvement of VEGFA in chondrocyte survival. Interestingly, the extensive cell death seen in Vegfa CKO null bones had a striking similarity to the cell death phenotype observed when hypoxia-inducible factor 1 alpha (Hif1a) expression was abolished in developing cartilage. This similarity of cell death phenotypes and the deficient VEGFA production in Hif1a null epiphyseal chondrocytes demonstrate that HIF1 alpha and VEGFA are components of a key pathway to support chondrocyte survival during embryonic bone development.

Animals↗
PubMed2006

Physical activity augments bone mineral accrual in young children: The Iowa Bone Development study.

OBJECTIVES: This 3-year follow-up study examined associations between physical activity and bone mineral content (BMC) and whether physical activity augments BMC accrual. STUDY DESIGN: Participants were 370 children (mean age baseline 5.3 years, follow-up 8.6 years). Physical activity was measured using 4-day accelerometry. BMC was measured using dual energy x-ray absorptiometry. RESULTS: After adjustment for baseline BMC, age, and body size, mean physical activity predicted follow-up BMC at the hip, trochanter, spine, and whole body in boys and at the trochanter and whole body in girls. The variability in BMC explained by physical activity was modest (1% to 2%). However, based on a general linear model with adjustment for baseline BMC and body size, children who maintained high levels of physical activity accrued, on average, 14% more trochanteric BMC and 5% more whole-body BMC relative to peers maintaining low levels of physical activity. CONCLUSIONS: This study suggests that maintaining high levels of everyday physical activity contributes to increases in BMC in young children, particularly at the trochanter.

Bone Density↗
PubMed2001

The relative contribution of diet and genotype to bone development.

The present review addresses the relative contribution of diet and genotype to variability in human bone growth and mineralisation in the context of the aetiology of osteoporosis. Heritability studies indicate that 60-70 % of the variability in bone mineral mass or bone mineral density (BMD) can be accounted for by genetic variation. Cross-trait analyses suggest that a proportion of this variation reflects genetic influences on bone and body size, such as height and lean body mass. Candidate-gene studies have demonstrated associations between several genetic polymorphisms and bone mineral mass but, as yet, genotype determinations have proved unhelpful in identifying individuals at increased risk of osteoporosis. Variations in diet and other environmental factors contribute 30-40 % to total phenotypic variance in bone mineral mass or BMD. Correlations between intakes of individual nutrients and BMD have been reported, but these relationships are subject to confounding due to size. However, no specific dietary factor has been identified from prospective and twin studies as making a significant contribution to environmental variability in BMD or bone loss. This finding may reflect the difficulties in quantifying environmental exposures. both current and over a lifetime. In addition, the influence of diet on bone health may depend on the genotype of the individual. Optimisation of nutrition and lifestyle remains an attractive strategy for the reduction of fracture risk, but more research is required to fully define optimal dietary requirements.

Bone Density↗