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PubMed2006

Calcium supplementation trials and bone mass development in children, adolescents, and young adults.

The development of bone mass during childhood through young adulthood is an important determinant of bone health later in life, and calcium is the major building block. Most randomized, double-blind, placebo-controlled trials of calcium supplementation have been done in girls; however, calcium supplementation in boys has been investigated in recent studies. Positive short-term effects on bone measures during growth has been shown in boys and girls, particularly in weight-bearing appendicular bone, although the lifelong effect is not certain.

Adolescent↗
PubMed1990

[The development of bone mass during a lifetime].

The authors present a reminder of the methods used to evaluate the bone mass and density and, with population studies, specify the profile and significance of the physiological osteopenia in both sexes. Analysis of these studies shows that the age of onset of the bone loss and its percentage vary markedly between the various sites of the skeleton, according to the type of bone, cortical or trabecular. It seems that the "smooth" aspect of the physiological osteopenia curves obtained is women during population studies, essentially results from the disparity between the times of menopause. A general protocol of the physiological osteopenia, synthesizing all data collected with nine different methods of measurement of the mineral bone content, is presented for educational purposes.

Adult↗
PubMed1980

[Electron microscopic study on giant cell tumor of bone, based upon the development of bone in human embryo (author's transl)].

Many reports have been published about giant cell tumor of bone since its initial description in 1818 by Cooper. No theory on its histogenesis has nevertheless been unanimously admitted. The purpose of this paper is to make systemic investigation of differentiation process of osteoblast, osteocyte and osteoclast with spines of 23 human embryos mainly by means of electron microscopic observation and to compare the above results with constituent cells of giant cell tumor of bone, thus to clarify the histogenesis of the latter cells. Results. Enchondral ossification of a vertebral body takes place initially in the upper lumber spines at the beginning of the fourth embryonal month and gradually spreads cranial- and caudalwards. Almost simultaneously blood vessels accompanied by undifferentiated mesenchymal cells around them invade into the vertebral body toward ossification center. These mesenchymal cells differentiate finally into osteocytes passing through the stages of undifferentiated polygonal cell, preosteoblast, and osteoblast. Meanwhile osteoclasts appear approximately when primary marrow cavity is formed. Histogenesis of osteoclast is considered to be morphologically quite different from osteoblast, rather as being derived from macrophage or its precursor cell. The author classified stromal cells of giant cell tumor of bone into three types, of which the type 3 is similar to a giant cell and the latter to an osteoclast. From this reason, giant cell tumor of bone does not appear to be derived from osteoblast or osteocyte, but from macrophage or its precursor cell.

Adult↗
PubMed2004

Regulation of bone morphogenetic proteins in early embryonic development.

Bone morphogenetic proteins (BMPs), a large subgroup of the TGF-beta family of secreted growth factors, control fundamental events in early embryonic development, organogenesis and adult tissue homeostasis. The plethora of dose-dependent cellular processes regulated by BMP signalling demand a tight regulation of BMP activity. Over the last decade, a number of proteins have been identified that bind BMPs in the extracellular space and regulate the interaction of BMPs with their cognate receptors, including the secreted BMP antagonist Chordin. In the early vertebrate embryo, the localized secretion of BMP antagonists from the dorsal blastopore lip establishes a functional BMP signalling gradient that is required for the determination of the dorsoventral - or back to belly - body axis. In particular, inhibition of BMP activity is essential for the formation of neural tissue in the development of vertebrate and invertebrate embryos. Here we review recent studies that have provided new insight into the regulation of BMP signalling in the extracellular space. In particular, we discuss the recently identified Twisted gastrulation protein that modulates, in concert with metalloproteinases of the Tolloid family, the interaction of Chordin with BMP and a family of proteins that share structural similarities with Chordin in the respective BMP binding domains. In addition, genetic and functional studies in zebrafish and frog provide compelling evidence that the secreted protein Sizzled functionally interacts with the Chd-BMP pathway, despite being expressed ventrally in the early gastrula-stage embryo. These intriguing discoveries may have important implications, not only for our current concept of early embryonic patterning, but also for the regulation of BMP activity at later developmental stages and tissue homeostasis in the adult.

Animals↗
PubMed2004

[Progress on the related mechanism in the development of bone and joint].

The embryonic development of bone and joint involves in complicated events for vertebrate limb. It originates from determined condensation of mesenchymal cells from lateral mesoderm. These cells and the overlying ectodermal jacket form limb buds at presumptive limb levels. Then, under the control of systemic factors, mesenchymal cells aggregate and differentiate to form cartilage blastemal elements that prefigure skeletal limb components. The latter develops into skeleton through endochondral ossification. The majority of the bones of the limb form by the endochondral mechanism. The formation of synovial joint system and bone development occur simultaneously. This article reviewed the progress on the related control mechanism in the development of bone and joint recently.

Animals↗
PubMed2000

The distribution of stanniocalcin 1 protein in fetal mouse tissues suggests a role in bone and muscle development.

We previously isolated a mammalian gene STC1 that encodes a glycoprotein related to stanniocalcin (STC), a fish hormone that plays a major role in calcium homeostasis. However, the mammalian STC1 gene is expressed in a variety of adult tissues in contrast to fish where STC is expressed only in one unique gland, the corpuscles of Stannius. This suggested that STC1 may have wider autocrine/paracrine functions in mammals. In the present study, using immunocytochemistry, we showed that STC1 protein is localized in the developing bone and muscle of the mouse fetus. During endochondral bone formation, STC1 is found principally in prechondrocytes and prehypertrophic chondrocytes. During intramembranous bone formation STC1 is present in the mesenchyme that is about to undergo ossification. STC1 is also found in the myocardiocytes of the developing heart and at all stages of differentiation from myoblasts to myotube formation in developing skeletal muscle. The specific localization of STC1 to chondrocytes and muscle cells suggests a role for this protein in chondrogenic and myogenic differentiation.

Animals↗
PubMed2002

Effects of caffeine and exercise on the development of bone: a densitometric and histomorphometric study in young Wistar rats.

High doses of caffeine will induce calcium loss and influence the normal development of bone, whereas the proper exercise has positive effects on bone metabolism. This study investigated the possible effects of exercise to antagonize the caffeine-induced impairment of bone development in young male Wistar rats. A total of 32 male rats (5 weeks old) were divided randomly into four groups: group 1 rats were fed caffeine; group 2 rats were prescribed an exercise program; group 3 rats were fed caffeine and prescribed an exercise program; and group 4 rats served as the control group. The caffeine was fed via the animals' dietary water and the dosage was 10 mg/100 g body weight per day, 3 days a week. The exercise program was carried out on a treadmill for 10 weeks (5 days/week, 1 h/day, 70% VO(2)max). Body weight was measured weekly. After sacrifice, the tibia length was measured and the tibia was processed for histomorphometric analysis. Bone mineral density was measured by dual-energy X-ray absorptiometer at three different sites of the tibia. In addition, the calcium content of the right femur was measured by atomic absorptiometry. The results showed that both exercise and caffeine significantly lowered the body weight gain. Rats fed with caffeine (groups 1 and 3) had a significantly longer tibia as compared with the non-caffeine-fed rats (groups 2 and 4) (p = 0.0149). The histomorphometry study showed that thickness of the growth plate in the proliferative zone, the hypertrophic zone, and total growth plate was greater in caffeine-fed groups than in non-caffeine-fed groups. The cell number in the proliferative zone was higher in the caffeine-fed groups. Area ratio of trabeculae in the primary spongiosa of rats in groups 1 and 2 were significantly greater than the control group. Caffeine feeding (groups 1 and 3) induced a lower area ratio of bone trabeculae in the secondary spongiosa, whereas exercise training (groups 2 and 3) increased the thickness of the trabeculae. The exercise program counteracted the negative effect of caffeine on the trabecular thickness, but did not correct the trabecular bone ratio. The bone mineral density (BMD) of the tibia was significantly lower in caffeine-fed rats, and the exercise program did not show any counteracting effect on the caffeine-induced BMD reduction. The calcium content assay showed that caffeine feeding decreased the weight and total calcium content of the femur. Again this exercise program did not counterbalance the negative effects of caffeine. In conclusion, high doses of caffeine seemed to stimulate the growth of long bone. However, it caused more serious negative effects on bone, including bone mineral loss, lower BMD, and lower calcium content. Exercise training at 70% VO(2)max had little antagonizing effect on caffeine-induced impairment of bone formation. Therefore, the best way to prevent caffeine-induced negative effects on bone development is to lower caffeine exposure.

Animals↗
PubMed2005

Role of IGFBP2, IGF-I and IGF-II in regulating long bone growth.

The IGF axis is important for long bone development, homeostasis and disease. The activities of IGF-I and IGF-II are regulated by IGF binding proteins (IGFBPs). IGF-I and IGFBP2 are co-expressed in dynamic fashions in the developing long bones of the chick wing, and we have found that IGF-II is present in the cartilage model and surrounding perichondrium, proliferative and hypertrophic chondrocytes and developing periosteum. To gain insight into endogenous roles of IGF-I, IGF-II and IGFBP2 in long bone development, we have overexpressed IGFBP2 in the developing skeletal elements of the embryonic chick wing in vivo, using an RCAS retroviral vector. IGFBP2 overexpression led to an obvious shortening of the long bones of the wing. We have investigated, at the cellular and molecular levels, the mechanism of action whereby IGFBP2 overexpression impairs long bone development in vivo. At an early stage, IGFBP2 excess dramatically inhibits proliferation by the chondrocytes of the cartilage models that prefigure the developing long bones. Later, IGFBP2 excess also reduces proliferation of the maturing chondrocytes and attenuates proliferation by the perichondrium/developing periosteum. IGFBP2 excess does not affect morphological or molecular indicators of chondrocyte maturation, osteoblast differentiation or cell/matrix turnover, such as expression of Ihh, PTHrP, type X collagen and osteopontin, or distribution and relative abundance of putative clast cells. We also have found that IGFBP2 blocks the ability of IGF-I and IGF-II to promote proliferation and matrix synthesis by wing chondrocytes in vitro. Together, our results suggest that the mechanism of action whereby IGFBP2 excess impairs long bone development is to inhibit IGF-mediated proliferation and matrix synthesis by the cartilage model; reduce the proliferation and progression to hypertrophy by the maturing chondrocytes; and attenuate proliferation and formation of the periosteal bony collar. These actions retard the growth and longitudinal expansion of the developing long bones, resulting in shortened wing skeletal elements. Our results emphasize the importance of a balance of IGF/IGFBP2 action at several stages during normal long bone development.

Animals↗
PubMed1998

Stromelysin-1 (MMP-3) and stromelysin-2 (MMP-10) expression in developing human bone: potential roles in skeletal development.

Stromelysin, a member of the matrix metalloproteinase family, demonstrates wide substrate specificity with the ability to degrade proteoglycan, fibronectin, laminin, casein, and the nonhelical region of collagen. The two forms of stromelysin (SL), types 1 (MMP-3) and 2 (MMP-10), share 82% sequence homology, but exhibit differences in cellular synthesis and inducibility by cytokines and growth factors in vitro. However, the distribution of the two isoforms in bone has not been reported. We investigated the presence of SL-1 and SL-2 in human osteophytic and neonatal rib bone using immunohistochemistry and, combined with a new method of in situ zymography, determined the activity of the immunolocalized stromelysins. Latent SL-1 was strongly expressed in the extracellular matrix in fibrous tissue surrounding areas of endochondral ossification in osteophytes, and adjacent to the periosteum of fetal rib bone. Active SL-1 expression was detected in osteocytes and the matrix surrounding osteocytic lacunae. SL-2 showed intense cell-associated staining at sites of resorption in areas of endochondral ossification and in resorptive cells at the chondro-osseous junction, which correlated with enzyme activity detected by zymography. Within the rib, active SL-2 expression was localized in chondrocytes of the growth plate, whereas only occasional SL-1 signal was evident. Vascular areas showed strong SL-2 staining with some proteolytic activity. SL-2, but not SL-1, was strongly expressed in osteoclasts and most mononuclear cells within the marrow. At sites of bone formation both isoforms were expressed by osteoblasts with SL-1 also present in osteoid. These results demonstrate, for the first time, the differential expression of SL-1 and SL-2 in developing human bone, indicating specific roles for the two isoforms. In situ zymography demonstrates that SL-2 is produced in an active form with associated degradation, whereas SL-1, in a matrix-bound proenzyme form, may act as a reservoir for later activation.

Glycoproteins↗
PubMed2003

Retinoic acid repression of bone morphogenetic protein 4 in inner ear development.

Bone morphogenetic protein 4 (BMP4) and retinoic acid are important for normal development of the inner ear, but whether they are linked mechanistically is not known. BMP4 antagonists disrupt semicircular canal formation, as does exposure to retinoic acid. We demonstrate that retinoic acid directly down-regulates BMP4 transcription in a mouse inner ear-derived cell line, and we identify a novel promoter in the second intron of the BMP4 gene that is a target of this regulation both in the cell line and in the mouse embryonic inner ear in vivo. The importance of this down-regulation is demonstrated in chicken embryos by showing that the retinoic acid effect on semicircular canal development can be overcome by exogenous BMP4.

Animals↗
PubMed2005

[Development, physiology, and cell activity of bone].

Bones are of crucial importance for the human body, providing skeletal support, serving as a home for the formation of haematopoietic cells, and reservoiring calcium and phosphate. Long bones develop by endochondral ossification. Flat bones develop by intramembranous ossification. Bone tissue contains hydroxyapatite and various extracellular proteins, producing bone matrix. Two biological mechanisms, determining the strength of bone, are modelling and remodelling. Modelling can change bone shape and size through bone formation by osteoblasts at some sites and through bone destruction by osteoclasts at other sites. Remodelling is bone turnover, also performed by osteoclasts and osteoblasts. The processes of modelling and remodelling are induced by mechanical loads, predominantly muscle loads. Osteoblasts develop from mesenchymal stem cells. Many stimulating factors are known to activate the differentiation. Mature osteoblasts synthesize bone matrix and may further differentiate into osteocytes. Osteocytes maintain structural bone integrity and allow bone to adapt to any mechanical and chemical stimulus. Osteoclasts derive from haematopoietic stem cells. A number of transcription and growth factors have been identified essential for osteoclast differentiation and function. Finally, there is a complex interaction between osteoblasts and osteoclasts. Bone destruction starts by attachment of osteoclasts to the bone surface. Following this, osteoclasts undergo specific morphological changes. The process of bone destruction starts by acid dissolution of hydroxyapatite. After that osteoclasts start to destruct the organic matrix.

Bone Development↗
PubMed1982

Regulatory mechanisms in the development of bone and cartilage: the use of tissue culture techniques in the study of the development of embryonic bone and cartilage: a perspective.

Tissue culture techniques were used to study a number of factors and mechanisms which are important in the development and metabolism of bone tissue. As an example of an external factor influencing bone development, the importance of the composition of the gasphase which is in equilibrium with the fluid bathing osteoblasts and hypertrophic chondrocytes, was investigated in cultured metatarsal bone rudiments. In vivo, one expects the presence of an O2 gradient in the cartilaginous epiphyses of long bones: low O2 tension between the nonhypertrophic chondrocytes, high O2 tension in periosteum and hypertrophic zone, bordering the marrow cavity. The in vitro findings correlated with these expectations. High CO2 (5%) and high O2 (40%) tensions stimulated calcification; in air, calcification was severely inhibited. On the other hand, maturing chondrocytes were damaged by high O2 tensions. An important cellular mechanism in calcification is the intracellular accumulation of calcium (and phosphate) in osteoblasts and hypertrophic chondrocytes which can be demonstrated with the GBHA stain of Kashiwa [9]. The extracellular role of alkaline phosphatase (AP) present on the cell membranes of these cells was shown to be a less decisive factor in calcification. In the presence of AP inhibitor in a concentration high enough to inhibit AP activity to a large extent, calcification was shown to proceed normally. The effects of a number of hormones known to be important for the development and metabolism of bone tissue was studied using tissue culture (calvaria) as well as culture of different isolated bone cells. The parathyroid hormone (PTH) induced rise of the intracellular cAMP level was found to originate primarily from the osteoblasts not the osteoclasts. Isolated osteoblasts showed a high cAMP response after PTH addition. Cortisol was shown to inhibit PTH induced resorption but to potentiate PTH induced cAMP response in calvaria. Various PTH fragments (desamino 1-34, 2-34, 3-34) were shown to be active as stimulators of bone resorption (although they were less active in this respect than the intact molecule 1-84), but did not stimulate cAMP production in calvaria or isolated osteoblasts. The results obtained strengthened the hypothesis that cAMP is not the (only) mediator in PTH induced bone resorption.

Alkaline Phosphatase↗
PubMed1998

Bone marrow cell development and trabecular bone dynamics after ovariectomy in ddy mice.

To clarify the relationship between the sequential changes of trabecular bone turnover and bone marrow cell development in ovariectomized (ovx) mice, bilateral tibiae of 8-week-old ddy mice were obtained. Histomorphometric analyses of the trabecular bone of the proximal tibia of ovx mice revealed increases in the bone formation rate and the osteoclast surface for the first 28 days postovariectomy. The trabecular bone volume showed a rapid decrease for the first 28 days and a steady state for the subsequent 14 days. In bone marrow cell culture experiments, the numbers of total and nonadherent bone marrow cells per tibia obtained from the ovx mice increased. The formation of osteogenic nodules and osteoclast-like multinucleated cells in the marrow cultures obtained from ovx limbs showed a significant increase on days 14 and 28 and returned to the sham-operated level by day 42. The numbers of colony forming units (fibroblastic) and colony forming units (granulocytes and macrophages) that developed from the marrow cells did not differ between the ovx and sham limbs at any time during the study period. Fluorescence-activated cell-sorter analysis revealed no population changes in the cell development of macrophages. These results demonstrate that there are two stages in the development of osteopenia after ovx. During the first 28 days after ovx, the ovariectomy enhances the developmental process from bone marrow stromal cells to osteoblasts and the terminal differentiation from osteoclast precursors to mature osteoclasts. The trabecular bone turnover also increases. In the subsequent 14 days, the changes in the osteogenic and osteoclastogenic potentials of the bone marrow cells are alleviated and the trabecular bone dynamics are in a steady state. The changes in bone marrow cell development are closely associated with those at the trabecular bone surface.

Animals↗