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PubMed1992

Identification of a functional mononuclear precursor of the osteoclast in chicken medullary bone marrow cultures.

Mononuclear cells were isolated from the peritrabecular bone marrow from the medullary bone of laying hens maintained on a calcium-deficient diet for 1 week. These cells were cultured for up to 7 days on devitalized bovine bone slices after removing the nonadherent fraction. The mononuclear precursors of the osteoclast that are present in such cultures adhere to bone matrix. These cells are TRAP+, express the vitronectin receptor at high levels, and also express high levels of sodium pumps and of carbonic anhydrase, enzymes that are characteristically enriched in the mature osteoclast. Finally, the most mature mononuclear precursors were found to be capable of resorbing the extracellular bone matrix before forming multinucleated osteoclasts.

Animals↗
PubMed1989

The effects of fluoride on bone and implant histomorphometry in growing rats.

The effects of fluoride at concentrations of 2.0 and 4.5 mM in drinking water on growth rate, vitamin D, water and mineral metabolism, bone histomorphometry, and osteoinduction of demineralized allogenic bone matrix (DABM) were compared in the rat. Whereas fluoride did not influence fluid intake or growth rate at the lower concentration, it increased fluid intake and inhibited growth rate at the higher concentration. Fluoride produced dose-related increases in serum fluoride and alkaline phosphatase but did not alter serum 25-hydroxyvitamin D or 1,25-dihydroxyvitamin D. Serum calcium and phosphate were reduced by fluoride at concentrations of 2.0 mM but not 4.5 mM. Cancellous bone fractional area was increased by fluoride at 2.0 mM and was reduced by fluoride at 4.5 mM. Fluoride had no effect on cancellous bone surface length or the percentage surface lined by osteoblasts and osteoclasts. Fluoride increased medullary area and decreased the endosteal bone formation rate. Fluoride increased periosteal bone formation and apposition rates at concentrations of 2.0 mM but not 4.5 mM. Fluoride inhibited mineralization in DABM implants, and at the higher concentration, fluoride increased the formation of new bone matrix. These results indicate that in the rat, fluoride increases cortical and trabecular bone at therapeutic doses and reduces trabecular bone at toxic doses. The serum concentration of fluoride at therapeutic doses in the rat is similar to that in patients with osteoporosis who are on treatment with fluoride. In the rat, there is a narrow range between toxic and therapeutic doses.

Alkaline Phosphatase↗
PubMed1985

Primary structure of bovine matrix Gla protein, a new vitamin K-dependent bone protein.

The complete amino acid sequence of bovine bone matrix Gla protein (MGP) was determined by automatic sequence analysis of the intact protein and of peptides isolated from tryptic and BNPS-skatole digests. This 79-residue, vitamin K-dependent protein contains a single disulfide bond and 4.8 gamma-carboxyglutamate (Gla) residues, one each at positions 37, 41, 48, and 52, and 0.8 Gla and 0.2 Glu at position 2. There is sufficient sequence homology between MGP and bone Gla protein (BGP) to indicate that these two bovine bone proteins arose by gene duplication and subsequent divergent evolution. Although MGP has a very low solubility in water compared to BGP, there is no hydrophobic domain in MGP which could account for its insolubility, and the overall fraction of hydrophobic residues is 32% for MGP compared to 43% for BGP. MGP is the first vitamin K-dependent protein to be discovered which has several non-gamma-carboxylated residues to the NH2-terminal side of its Gla residues. The presence of NH2-terminal Glu residues between the putative targeting domain for the gamma-carboxylase in the MGP leader sequence and the mid-molecule Gla residues suggests that the gamma-carboxylase may have additional, as yet unrecognized, specificity requirements which determine the susceptibility of Glu residues for gamma-carboxylation.

1-Carboxyglutamic Acid↗
PubMed1999

A microplate-based fluorometric assay for monitoring human cancer cell attachment to cortical bone.

A microplate-based fluorometric assay was developed for quantitation of cancer cell attachment to bone matrix. To evaluate this model system we used a panel of human cancer cell lines, including the human breast cancer cell line MDA-MB-231. For the assay, bovine cortical bone from the shaft of the femur was cut, turned, and sliced to 6-mm-diameter round 200-microm-thin disks and placed into the wells of a 96-well microplate. A fluorescent dye 2', 7'-bis(2-carboxyethyl-5(6)-carboxyfluorescein (BCECF-AM) and a microplate fluorometer equipped with a standard filter set for fluorescein isothiocyanate were used to detect the cells attached to the bone disks. The fluorescence was enhanced during the measurement step by using a K+ solution (pH 8.0) containing the H+/K+ ionophore nigericin, which equilibrates internal and external pH. By taking advantage of the pH sensitivity of BCECF, the fluorescence intensity in the assay was increased 2.5 times compared to cells loaded with calcein. The specificity of the assay was demonstrated with a specific immuneserum raised against the MDA-MB-231 cell line. The assay can be completed in 1 h and permits the use of a large number of samples and is therefore useful for screening potential drug candidates that could block cancer cell attachment to bone material. Moreover, the assay described can easily be used to characterize molecular structures involved in cell attachment to bone.

Animals↗
PubMed2002

Bone morphogenetic protein receptor signaling is necessary for normal murine postnatal bone formation.

Functions of bone morphogenetic proteins (BMPs) are initiated by signaling through specific type I and type II serine/threonine kinase receptors. In previous studies, we have demonstrated that the type IB BMP receptor (BMPR-IB) plays an essential and specific role in osteoblast commitment and differentiation. To determine the role of BMP receptor signaling in bone formation in vivo, we generated transgenic mice, which express a truncated dominant-negative BMPR-IB targeted to osteoblasts using the type I collagen promoter. The mice are viable and fertile. Tissue-specific expression of the truncated BMPR-IB was demonstrated. Characterization of the phenotype of these transgenic mice showed impairment of postnatal bone formation in 1-mo-old homozygous transgenic mice. Bone mineral density, bone volume, and bone formation rates were severely reduced, but osteoblast and osteoclast numbers were not significantly changed in the transgenic mice. To determine whether osteoblast differentiation is impaired, we used primary osteoblasts isolated from the transgenic mice and showed that BMP signaling is blocked and BMP2-induced mineralized bone matrix formation was inhibited. These studies show the effects of alterations in BMP receptor function targeted to the osteoblast lineage and demonstrate a necessary role of BMP receptor signaling in postnatal bone growth and bone formation in vivo.

Animals↗
PubMed2001

The molecular genetics of bone formation: implications for therapeutic interventions in bone disorders.

Skeletal biology is a complex process involving the developmental commitment and differentiation of chondrocytes and osteoblasts which produce and mineralize cartilage and bone matrix during growth and postnatal life. Several genes are involved in controlling osteogenesis by acting on target cells in a very complex manner. Manipulation of genes in mice and studies of genetic mutations affecting the skeleton in humans have enabled the assessment of the role of transcription factors, bone matrix proteins and regulatory factors involved in the control of chondrocyte and osteoblast differentiation, and have considerably improved our understanding of the bone formation process. Clinical studies and gene polymorphism analyses suggest that the variable expression of particular genes may be linked to clinical osteoporosis. A major challenge in the future will be to develop molecularly targeted approaches to stimulating bone formation and increasing bone mass. The use of mouse strain models and transgenic animals with variable bone density may be useful to identify genetic determinants of bone mass which may serve as a basis for drug discovery and development. On the other hand, the availability of gene microarrays and other emerging genomic techniques are promising tools to identify genes that are distinctly expressed in health and disease. These technologies may also serve to test the mechanisms of action of drugs aimed at increasing bone formation. Genetic studies of the molecular signaling pathways involved in normal and pathological osteogenesis may also help to identify genes that could be targeted for therapeutic intervention. Candidate approaches include selective gene transfection in target cells and the use of drugs acting on gene promoters to selectively enhance gene expression in osteoblasts. The development of these strategies is expected not only to bring new insight into the molecular mechanisms that govern bone formation in normal and pathological situations but, in the long term, may also result in the identification of novel molecular targets for therapeutic interventions for bone formation disorders.

Bone Development↗
PubMed1982

Ultrasonic measurements of deer antler, bovine tibia and tympanic bulla.

Longitudinal sonic plesio-velocity, density and mineral volume fraction of the three bone types plus bovine bone matrix are reported. The axial sonic velocity in km/s and the mineral volume fraction for each is as follows: deer antler 3.08, 0.33; bovine tibia 3.89, 0.44; tympanic bulla 4.53, 0.85; bovine matrix 1.82. A brief discussion of the deer antler and tympanic bulla histology is included.

Animals↗
PubMed1993

Effect of KTP laser ablation of endochondral bone on bone healing.

The advantages of using a laser to cut a hole in the ossicular chain include increased precision, decreased likelihood of disarticulation, and elimination of noise-induced threshold shift associated with conventional drills. This study was designed to determine optimal energy settings and cooling technique to minimize tissue injury. Laser ablated holes were cut in rabbit femurs with different endostat fibers at power settings of 1.6 to 5.0 watts. Comparable burr holes were cut by a high-speed drill and the animals were sacrificed at different time intervals. Specimens were evaluated microscopically for tissue injury by the amount of cell necrosis of the surrounding osteocytes, bone marrow changes, and denaturation of bone matrix. Changes in healing were assessed by the production and ossification of the granulation tissue. Laser ablated holes created with 1.6 to 2.0 watts at 2 to 7 days demonstrated thermal damage comparable to conventionally drilled holes. At 14 to 28 days these holes demonstrated advanced healing and integrated lamellar bone. In contrast, higher power (> 3.5 watts) at 2 to 7 days demonstrated Significantly more osteocyte loss, marked bone marrow fibrosis, and bone matrix denaturation. At 14 to 28 days these holes showed evidence of delayed healing and osseous plugs not integrated with the surrounding bone.

Animals↗
PubMed1998

Mechanical loading stimulates bone formation by reactivation of bone lining cells in 13-week-old rats.

The bone formation that occurs in response to mechanical stimulation is generally considered to be a means by which bone adapts to changes in its mechanical environment. We have previously shown that the expression of genes for bone matrix proteins is maximal 72 h after a single 5-minute episode of loading of tail vertebrae of 13-week-old female rats, that the predominant increase in mineralization occurs after 3 days, and that the osteogenic response to mechanical stimulation is not dependent on prior bone resorption. We have now investigated the cellular correlates of this osteogenic response. No proliferation was detected, by pulse or flash labeling, in the trabecular bone surface cells of animals killed 1 h to 10 days after the loading episode. Ultrastructural examination revealed that most of the cells covering the trabecular bone surface of control vertebrae were flat bone lining cells. After mechanical stimulation, the trabecular bone surface cells developed ultrastructural features of osteoblastic differentiation and activity, with acquisition of an increasingly cuboidal shape, rounded nuclei, and abundant rough endoplasmic reticulum. Morphometric analysis of the mean cell area, mean nuclear area, and cell and nuclear height showed that they were all maximal 48 h after loading. By 120 h after loading, the appearances of bone surface cells had reverted to those of control vertebrae. Thus, mechanical loading appears to activate lining cells, with a temporal sequence that correlates with bone matrix production.

Analysis of Variance↗
PubMed1987

Methotrexate effects on heterotopic bone in rats.

We studied the effects of high-dose methotrexate on heterotopic bone formation induced by implants of demineralized bone matrix in the abdominal wall of growing rats. Methotrexate induced an arrest in normal weight gain of the animals, more pronounced the younger the animals were. The youngest animals had reduced ash weight and decreased isotope uptake in the tibiae and teeth. However, implants from these animals, given methotrexate 10 days before implantation of bone matrix, had a 33 per cent increase in ash content. When methotrexate was given at, or 10 days after, implantation, heterotopic bone formation was reduced by 40 and 22 per cent, respectively, whereas orthotopic bone was considerably less affected in these older animals. In a second experiment, no difference in elimination rates of 45Ca between methotrexate-treated and control rats in implants, teeth, or tibiae were found. It appears that a less detrimental effect of methotrexate on new bone formation can be expected if the drug is given before, or a substantial period after, surgery requiring bone formation for healing.

Animals↗
PubMed2003

The interaction between Sillence type and BMD in osteogenesis imperfecta.

Clinical studies with bisphosphonates in children with osteogenesis imperfecta (OI) show an increase in BMD and a decrease in fracture rate. Bone strength in children with OI is not only influenced by changes in BMD but also by changes in collagen I structure of the organic bone matrix. Therefore, we studied the interaction between these two factors in a cross-sectional, single center study including 54 children. We assumed that vertebral deformities in OI represent an unbalance between load and bone strength. Body weight was considered to be a well quantifiable load on vertebral bodies. BMD served as a marker, representing the amount of bone tissue available for vertebral load bearing, and the Sillence classification, either type I or III/IV, as a marker representing the quality of the organic bone matrix. Independent associations were observed between the prevalence of vertebral deformities and (1) Sillence type (OR: 5.7, 95%Cl:1.2-26.8), (2) BMD (OR: 0.003, 95%Cl: 0-0.25) and (3) body weight (OR: 1.15, 95%Cl: 1.05-1.25). Regarding the anthropometrical differences among the different types of OI, the BMD/body weight ratio was introduced to evaluate the BMD in relation to body size. Prevalent vertebral deformities were associated with low BMD/body weight ratios (OR: 0.04, 95%Cl: 0.008-0.2) in OI type I, but no association was found in type III/IV. It was concluded that BMD and Sillence type have independent relationships with vertebral deformities. The BMD/body weight ratio correlates with vertebral deformities in children with OI type I. Its meaning in types III/IV needs further research with larger samples because of the relatively high prevalence of vertebral deformities in this group.

Absorptiometry, Photon↗
PubMed1977

Methods for the study of the glycoproteins and proteoglycans of bone using bacterial collagenase. Determination of bone sialoprotein and chondroitin sulphate.

A method has been developed for the solubilization of bone matrix using bacterial collagenase. The soluble macromolecules were separated by a column procedure on DEAE-cellulose and analysed for uronic and sialic acids. Values for the total non-collagenous fraction of bone and its content of bone sialoprotein and chondroitin sulphate were obtained. The method was compared with similar procedures using EDTA extraction and papain digestion.

Animals↗
PubMed1990

[Osteosis due to primary hyperparathyroidism. The SEM ultrastructural features of the periosteal and endosteal surfaces].

The study of four cases of osteosis caused by primary hyperparathyroidism, tree female and one male, which have undergone surgery for pathological fractures in met-epiphysis bone, allows to analyze with the help of scanning electron microscope modifications occurring in periosteal and endosteal bone matrix. The periosteal surface appears abundantly furrowed by large and deep canals, irregularly joined together. Areas of resorption, these at rest and these of osteodeposition are distributed in changeable but regular way. The bone turnover of endosteal side is particularly accentuated. This surface contains the bone trabeculae residuals and is widely marked by deep Howship's lacunae, which show intense osteoclastic activity. It seem that osteocytes cells participate actively in the process of osteolysis, widening the lacunae and small canals which appear to be surrounded by calcospherites arranged in irregular way. Osteogenetic activity, with large areas of deposition, is very intense, as a defence attempt against osteolytic resorption process.

Adult↗
PubMed1996

A bone regeneration study: transforming growth factor-beta 1 and its delivery.

Critical-sized defects (CSDs) were prepared in 60 rabbit skulls, divided evenly among five treatments and two time periods. The treatments consisted of rabbit demineralized bone matrix (DBM) and four different doses of transforming growth factor-beta 1 (TGF-beta 1) (0, 0.4, 4, and 40 micrograms) delivered in 3% carboxymethyl cellulose and Gelfilm. Quantitative assessments of bone formation in the CSDs were accomplished with computerized radiomorphometry and histomorphometry. Results indicated that rabbit DBM and 40 micrograms TGF-beta 1 promoted more new bone formation at 4 weeks than the other treatments. By 8 weeks, bone formation in the CSDs was equivalent for all but the 0-microgram dose of TGF-beta 1. The results from the study suggest a single therapeutic dose of TGF-beta 1 delivered in an appropriate carrier to a critical-sized intraosseous wound should promote bone formation.

Analysis of Variance↗
PubMedDate not supplied

New concepts in bone remodeling: an expanding role for the osteoblast.

Until recently, the prevailing view regarding the function of osteoblasts and osteoclasts was to attribute bone formation to the former and bone resorption to the latter. While the capacity of the osteoclast to degrade bone matrix remains unquestioned, there is now provocative evidence indicating that the osteoblast plays a critical role in regulating osteoclast resorptive activity as well as in contributing directly to matrix dissolution. The first of these points follows from observations indicating that the osteoblast (but not the osteoclast) 1) exhibits receptors and/or responses to resorption-promoting agents (including parathyroid hormone and vitamin D), and 2) releases agents capable of stimulating bone resorption. The second point is derived from studies demonstrating that the osteoblast produces neutral collagenase (an enzyme specialized to degrade type I collagen, the principal organic constituent of bone matrix) and an inhibitor capable of blocking collagenase activity. The synthesis of both of these proteins is, in part, regulated by parathyroid hormone and other resorption-stimulating agents and appears to involve control at the transcriptional, translational, and secretory levels. Thus, in both physiologic bone remodeling and modeling, as well as the altered bone turnover associated with some disease states, it is the osteoblast rather than the osteoclast that may hold the key to understanding the mechanism of tissue form and function.

Bone Resorption↗
PubMed2000

[Roles of magnetic resonance imaging in management of bone tumors].

The roles of magnetic resonance imaging (MRI) in the diagnosis and treatment of bone tumors are reviewed. Most bone tumors can be detected on plain radiography or bone scintigraphy. MRI is helpful in detecting tumors that do not destroy bone matrix or suppress reactive bone formation. Detailed analysis by plain radiography is still the most reliable method for differentiating between benign and malignant bone tumors. The T1 and T2 values, internal texture, and peritumoral edema depicted on MRI are not helpful for this differentiation. In characterizing the histologic types of bone tumors, MRI is of some advantage. For example, MRI can demonstrate cartilage matrix, hemoglobin metabolites, vascular components, and fat contents more clearly than conventional radiological techniques. MRI is now indispensable for the preoperative delineation of malignant bone tumors, because of its excellent soft tissue contrast and multiplanar imaging capability. In this article, the guidelines for evaluation of the surgical margin advocated by the JOA Musculo-skeletal Tumor Committee are introduced for radiologists. MRI monitoring of malignant bone tumors after chemotherapy or surgery can reveal change in the size of enhanced areas that may reflect viable tumors. Dynamic MRI is helpful to differentiate recurrent tumors from granulation tissue.

Bone Neoplasms↗
PubMed2002

In situ localization and in vitro expression of osteoblast/osteocyte factor 45 mRNA during bone cell differentiation.

The in situ localization of osteoblast/osteocyte factor 45 (OF45) mRNA during bone formation has been examined in the rat mandible from embryonic day 14 (E14) up to postnatal 90-day-old Wistar rats. Gene expression was also examined during cell culture not only in primary rat osteoblast-like cells but also in two clonal rat osteoblastic cell lines with different stages of differentiation, ROB-C26 (C26) and ROB-C20 (C20) using Northern blot analysis. The C26 cell is a potential osteoblast precursor cell line, whereas the C20 cell is a more differentiated osteoblastic cell line. At E15 osteoblast precursor cells differentiated into a group of osteoblasts, some of which expressed the majority of non-collagenous proteins, whereas no expression of OF45 was observed in these cells. Intercellular matrices surrounded by osteoblasts were mineralized at E16. Subsequently, the number of osteoblasts differentiated from osteoblast precursor cells was increased in association with bone formation. At E17, the first expression of OF45 mRNA was observed only in a minority of mature osteoblasts attached to the bone matrix, but not in the rest of less mature osteoblasts. At E20, concomitant with the appearance of osteocytes, OF45 mRNA expression was observed not only in more differentiated osteoblasts that were encapsulated partly by bone matrix but also in osteocytes. Subsequently, osteocytes increased progressively in number and sustained OF45 mRNA expression in up to 90-day-old rats. Northern blot analysis of the cultured cells with or without dexamethasone treatment revealed that the gene expression of OF45 correlated well with the increased cell differentiation. These results indicate that OF45 mRNA is transiently expressed by mature osteoblasts and subsequently expressed by osteocytes throughout ossification in the skeleton and this protein represents an important marker of the osteocyte phenotype and most likely participates in regulating osteocyte function.

Animals↗
PubMed1988

The distribution of lead in human hemopoietic tissue and spongy bone after lead poisoning and Ca-EDTA chelation therapy. Observations made by atomic absorption spectroscopy, laser microbeam mass analysis and electron microbeam X-ray analysis.

Two iliac crest needle biopsies were taken from a 43-year-old lead-poisoned woman during and after completion of a Ca-EDTA treatment. By atomic absorption spectroscopy the first and second biopsy were found to contain 56, respectively 41.6 micrograms lead/g wet tissue. In both biopsies 36% of the lead was extractable in 0.1 N HCl. Electron microbeam X-ray analysis proved to have too low sensitivity for quantitation of the lead in these biopsies. Laser microbeam mass analysis (LAMMA), performed only on the second biopsy, revealed a high and fairly constant residual lead concentration in all bone marrow cell nuclei (approximately 55 micrograms/g) and a low lead concentration in the cytoplasm of the same cells (4-12 micrograms/g). The extracellular bone matrix lead was greatly concentrated in the superficial 3-6 microns osteoid zone of the bony trabeculae and totally absent from deeper parts of the mineralized matrix. The LAMMA results are in good agreement with those of subcellular fractionation experiments and atomic absorption spectroscopy, provided that the relative volume fraction of nucleus and cytoplasm is accounted for. The high residual osteoid lead after completed chelation therapy indicates that lead has a stronger affinity for the organic than the mineral components of bone matrix.

Adult↗