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PubMed1991

Correlation between mRNA levels for bone cell proteins and bone formation in long bones of maturing rats.

This report describes the relationship between bone formation and mRNA levels for selected bone proteins. Dynamic bone histomorphometry was used to measure bone formation in tibial periosteum of male rats from weanling (3 wk) to 52 wk old. Northern blot analysis of freshly isolated periosteal cells from the long bones was used to determine steady-state mRNA levels for the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAP), the bone matrix proteins osteocalcin (BGP), and prepro-alpha-2 (I) chain of type 1 precollagen (collagen), the osteoblast marker enzyme alkaline phosphatase (AP), and the osteoblast-derived signaling factor (growth factor) transforming growth factor-beta (TGF-beta). Radial growth at the tibial diaphysis achieved a maximum value in 8-wk-old rats and decreased progressively with age thereafter. This age-related decrease in the radial growth rate was initially due to reduced osteoblast activity; however, in older rats (greater than 17 wk old) reduced osteoblast number contributed to the decrease in bone formation. There was a strong correlation between the steady-state mRNA level for collagen and the periosteal bone formation rate. In contrast, the mRNA levels for the other bone proteins were more weakly correlated (TGF-beta and AP) or not correlated (BGP). These results suggest that the decreased bone matrix synthesis by periosteal cells in long bones of maturing rats is due to decreased expression of genes for bone matrix proteins.

Aging↗
PubMed2006

[The extracellular matrix in bone tissue engineering].

OBJECTIVE: To review the research progress of osteoblast extracellular matrix (ECM) and its application in bone tissue engineering. METHODS: The recent related literatures were extensively reviewed. RESULTS: The ECM was complex in its components. The configuration of cell and cell's adhesion, migration, proliferation, and differentiation were subject to the ECM. The bioactivity of the tissue engineering products was revealed by ECM, which predicted the product's efficiency in clinic application. CONCLUSION: ECM has the potential to become the effective index in evaluating tissue engineered products.

Extracellular Matrix↗
PubMed1993

Distribution of integrin subunits on rat metaphyseal osteoclasts and osteoblasts.

A key event in bone resorption is the attachment of osteoclasts to the bone matrix. The process apparently involves integrin plasma membrane receptors for extracellular matrix proteins. In the present study the distribution of some integrin subunits among different osteoclastic and osteoblastic domains was determined using immunocytochemistry on rat metaphyseal bone. Ultrathin cryosections were incubated with polyclonal antibodies against the alpha v beta 3 integrin and against the individual integrin subunits, alpha v, beta 1, beta 3, and beta 5. Bound antibodies were detected with 10-nm colloidal gold coated with protein A. The results show that alpha v- and beta 3-subunits are enriched at the osteoclast plasma membrane facing the bone matrix, i.e., the clear zone. Furthermore, beta 1- and beta 5-subunits were somewhat enriched at the osteoblast plasma membrane facing the bone surface. The present observations corroborate and extend our previous data indicating that the alpha v beta 3 integrin mediates tight attachment of the osteoclast to the bone matrix. Moreover, a role for integrins in the attachment and interactions of the osteoblast is suggested.

Animals↗
PubMed1982

The relationship of monocytic cells to the differentiation and resorption of bone.

Osteogenesis in the developing limb is, as elsewhere, the result of two functionally integrated processes, bone matrix synthesis and matrix degradation. The latter process is a manifestation of the resorptive activity of osteoclasts (OCs), multinucleated giant cells which arise by fusion of mononuclear, blood-borne precursors. For the past several years, we have focused our efforts on several different aspects of OC development and differentiation. These efforts have included observations on patients with osteopetrosis, an analysis of monocyte (OC precursor) chemotaxis in response to bone matrix proteins, and the use of histochemical and bone grafting techniques to establish the lineage and expression of the osteoclast phenotype in the avian embryonic limb. Here, we (1) briefly review the evidence establishing the hematopoietic and probable monocytic origin of OCs, (2) present new data on the role of L-gamma-carboxyglutamic acid in osteocalcin-evoked chemotaxis and (3) describe the time course and likely developmental relationships between the appearance of circulating OC precursor cells, osteoclast differentiation, and the formation of mineralized bone matrix in the chick embryo. The results of the latter study indicate that OC differentiation is initiated by contact between precursor cells and mineralized bone, and suggest that the expression of the OC phenotype is dependent upon proteins or glycoproteins closely associated with bone mineral. We note that osteocalcin is one such protein.

Acid Phosphatase↗
PubMed2005

Extracellular matrix in bone marrow can mediate drug resistance in myeloma.

Glucocorticoids such as dexamethasone, frequently used for the treatment of multiple myeloma (MM), produce a rapid reduction in tumor mass. However, despite frequent initial complete remission, prolonged dexamethasone treatment results in the appearance of chemoresistant tumor cells and most patients with MM ultimately present relapse of the underlying disease. Accumulating data suggest that bone marrow components such as cytokines, extracellular matrix (ECM) and adjacent stroma cells could cooperate to provide a sanctuary to malignant plasma cells that allow their survival after initial drug exposure. This review focuses on the two major components of the bone marrow ECM that have been identified as mediators for innate or acquired drug resistance in MM, hyaluronan and fibronectin. These two ECM molecules are thought to play a crucial role in the pathogenesis of MM, combining their protective activities to promote optimal conditions for the long life of plasma cells and contribute to de novo drug resistance. They represent promising targets for the development of innovative treatments in order to prevent interactions between tumor cells and their microenvironment and to sensitize cancer cells to chemotherapy before the emergence of acquired mechanisms of chemoresistance.

Apoptosis↗
PubMed1996

[Evaluation of the preventive role of estro-progestogens and non-hormonal therapies in postmenopausal osteoporosis].

Osteoporosis is a medical, social and economical problem for developed countries. Prevention remains the only realistic approach to reduce the burden related to this disorder. Primary prevention of osteoporosis is based on efforts to reach a maximal peak bone mass at the end of the growth period and, subsequently, at the time of menopause. No pharmacological intervention is considered at this stage. Biologically, hormone replacement therapy induces a correction of the biochemical changes observed in markers of bone remodeling at the time of the menopause. A systematic screening of asymptomatic postmenopausal women followed by the induction of hormonal replacement therapy in high risk subjects appears to be an interesting cost/benefit strategy in terms of reasonable attribution of health resources. Nasal administration of calcitonin fully prevents the trabecular bone loss observed during the first years of menopause. Notwithstanding, the exact dose of nasal calcitonin able to prevent bone loss remains to be fully elucidated. Bisphosphonates inhibit bone resorption. Tiludronate prevents trabecular postmenopausal bone loss. The use of selectif estrogen receptor modulators is based on a possible differential action of these molecules, at the level of the estrogenic receptors, depending of the tissue considered. Several direct inhibitors of osteoclastic resorption are also under development. Their main target is either to prevent the linkage of osteoclasts to the bone matrix or to prevent the acidification of bone matrix required to induce the resorption process.

Bone Density↗
PubMed2005

Bone induction by AdBMP-2/collagen implants.

BACKGROUND: Demineralized bone matrix and recombinant human bone morphogenetic protein-2 or 7 (BMP-2 or BMP-7)-containing collagenous matrix have been shown to induce new bone formation in orthotopic and heterotopic sites. We examined the ability of subcutaneous implants of collagen combined with adenoviral vector containing the BMP-2 gene (AdBMP-2) to induce bone formation in rats. We also evaluated whether targeting the AdBMP-2 vector through an alternative receptor pathway, fibroblast growth factor (FGF), would increase the vector's potency. METHODS: In a time-course study, rat subcutaneous sites were implanted with (1) AdBMP-2 in rat-bone-derived collagen or (2) rat-bone-derived collagen alone. Samples were collected three, seven, fourteen, or thirty-five days after treatment. In a dose-response study, bone induction by AdBMP-2 in collagen (AdBMP-2/collagen) or by AdBMP-2 and FGF2 Fab' anti-adenovirus knob protein antibody in collagen (FGF2-AdBMP-2/collagen) was tested at fourteen days. Viral vector doses of 1 x 10(9) PN (viral particle number), 3 x 10(9) PN, 1 x10(10) PN, 3 x 10(10) PN, or 1 x 10(11) PN per implant were used. Equal amounts of collagen (25 mg) were used to formulate all implants. Explanted tissues were evaluated histologically to determine bone formation, specific activity of alkaline phosphatase, and calcium content. RESULTS: AdBMP-2/collagen implants induced robust bone formation. New bone was formed by the fourteenth day after implantation. In contrast, little or no bone was induced by the implant containing collagen alone. FGF2-AdBMP-2/collagen implants stimulated significantly more bone formation (p < 0.05) than did AdBMP-2/collagen implants, regardless of the dose of viral particles. CONCLUSIONS: Local delivery of AdBMP-2 in a collagen matrix rapidly induces bone formation, and targeting the virus through FGF receptors enhances the osteogenic potential of AdBMP-2.

Adenoviridae↗
PubMed1977

Transmembrane bone morphogenesis across multiple-walled diffusion chambers. New evidence for a diffusible bone morphogenetic property.

Bone generation and regeneration are associated with a bone morphogen that recruits mesenchymal cells for differentiation into bone. Experiments with particulate bone matrix gelatin implanted in multiple-walled diffusion chambers suggest that bone morphogen is a rapidly diffusible molecule, and consists of a noncollagenous bone morphogenetic protein (BMP). When particulate bone matrix gelatin is implanted inside of diffusion chambers constructed of two to five membranes, ranging from 300 to 750 cu micronm in total thickness, large deposits of bone develop on the outside. The volumes of the deposits of new bone are inversely proportional to the thickness (or distance) of transmission of the BMP. Transmission for long distances through interstitial fluid can be accounted for by a low molecular mass hydrophobic BMP, disseminated according to the laws of diffusion.

Animals↗
PubMed2002

2-methoxyestradiol induces interferon gene expression and apoptosis in osteosarcoma cells.

2-Methoxyestradiol (2-ME), a naturally occurring mammalian metabolite of 17beta-estradiol, has been implicated as a physiological inhibitor of tumor cell proliferation. In this study, the effects of 2-ME on cultured osteosarcomatous cells were investigated. Dose-dependent growth inhibition was observed in MG63 and TE85 human osteosarcoma cells exposed to 2-ME. The cell killing by 2-ME was ligand-specific; the immediate precursor (2-hydroxyestradiol), the parent compound (17beta-estradiol), and the equivalent metabolite of estrone (2-methoxyestrone) exhibited less potency and efficacy. Furthermore, 2-ME was similarly effective at killing immortalized human fetal osteoblastic cells (hFOB) with and without estrogen receptor-alpha and -beta and rat osteosarcoma cells (ROS17/2.8). The cytotoxicity of 2-ME was selective to transformed and immortalized osteoblastic cells; 2-ME (2 microm) had no effect on the proliferation of primary cultures of human osteoblasts. Co-treatment with the potent estrogen receptor ligand, ICI-182,780, did not reduce 2-ME-induced osteosarcoma cell death, implying that this action is not mediated by conventional estrogen receptors. The expression levels of bone matrix protein genes, type 1 collagen and osteonectin, were transiently reduced after 2-ME treatment, suggesting that the surviving cells are capable of producing bone matrix. The 2-ME-mediated killing of osteosarcoma cells was due to the induction of apoptosis; treatment induced expression of interferon genes within 12 h and histological evidence of apoptosis within 48 h of 2-ME treatment. Thus, our results demonstrate that 2-ME is highly cytotoxic to osteosarcoma cells but not normal osteoblasts. These findings suggest that further study of 2-ME as a potential intervention for treatment of osteosarcoma is warranted.

2-Methoxyestradiol↗
PubMed1998

[The effect of fluoride on bone extracellular matrix proteins expression in rat calvarial osteoblast in culture]

OBJECTIVE:The expression of various non-collagenous proteins and collagen protein on the rat fetal calvarial osteoblast cultured in low doses fluoride condition in vitro had been studied.METHODS:Our study applied the immunohistochemistry technique to detect the expression of bone sialoprotein, osteocalcin, osteopontin, alkaline phosphatase and type I collagen expressed in the bone matrix.RESULTS:They demonstrated that there were difference in the location and function of the collagenous and non-collagenous proteins in the development of bone matrix.CONCLUSION:The present results revealed that fluoride might enhance the proliferation activity of osteoblast precursors; simultaneously, fluoride might accelerate the phenotypic development of osteoblast and the expression of collagenous and non-collagenous proteins. As a result,low doses fluoride played a favorable role in the development of bone extracellular matrix.

Journal Article↗
PubMed2003

Constant mineralization density distribution in cancellous human bone.

The degree of mineralization of bone matrix is an important factor in determining the mechanical competence of bone. The remodeling and modeling activities of bone cells together with the time course of mineralization of newly formed bone matrix generate a characteristic bone mineralization density distribution (BMDD). In this study we investigated the biological variance of the BMDD at the micrometer level, applying a quantitative backscattered electron imaging (qBEI) method. We used the mean calcium concentration (Ca(Mean)), the most frequent calcium concentration (Ca(Peak)), and full width at half maximum (Ca(Width)) to characterize the BMDD. In none of the BMDD parameters were statistically significant differences found due to ethnicity (15 African-American vs. 27 Caucasian premenopausal women), skeletal site variance (20 ilium, 24 vertebral body, 13 patella, 13 femoral neck, and 13 femoral head), age (25 to 95 years), or gender. Additionally, the interindividual variance of Ca(Mean) and Ca(Peak), irrespective of biological factors, was found to be remarkably small (SD < 2.1% of means). However, there are significant changes in the BMDD in the case of bone diseases (e.g., osteomalacia) or following clinical treatment (e.g., alendronate). From the lack of intraindividual changes among different skeletal sites we conclude that diagnostic transiliac biopsies can be used to determine the BMDD variables of cancellous bone for the entire skeleton of the patient. In order to quantify deviations from normal mineralization, a reference BMDD for adult humans was calculated using bone samples from 52 individuals. Because we find the BMDD to be essentially constant in healthy adult humans, qBEI provides a sensitive means to detect even small changes in mineralization due to bone disease or therapeutic intervention.

Adult↗
PubMedDate not supplied

Histomorphometric analysis of homogenous demineralized dentin matrix as osteopromotive material in rabbit mandibles.

PURPOSE: The aim of this work was to evaluate the effectiveness of homogenous demineralized dentin matrix (HDDM) slices in surgical bone defects created in the mandibles of rabbits and occluded with a polytetrafluoroethylene (PTFE) membrane in the promotion of bone growth. MATERIALS AND METHODS: Surgical bone defects were created in 36 adult rabbits and divided into 4 groups: bone defect (control), bone defect with PTFE membrane, bone defect with HDDM, and bone defect with both HDDM and a PTFE membrane (HDDM + PTFE). The rabbits were sacrificed after 30, 60, and 90 days, and the bone defects were examined histologically and by histomorphometric analysis (analysis of variance and the Tukey test). RESULTS: The volume of newly formed bone matrix was significantly greater in the HDDM and HDDM + PTFE groups than in the control and PTFE groups. The discrete inflammatory reaction found in the HDDM and HDDM + PTFE groups did not prevent the osteopromotive activity of the dentin matrix. DISCUSSION: HDDM slices were biocompatible and were resorbed during the bone remodeling process. They stimulated the newly formed bone until 30 days after implantation. CONCLUSION: Bone repair was accelerated in the bone defects treated with HDDM in comparison to the control group.

Analysis of Variance↗
PubMed2005

Decreased collagen organization and content are associated with reduced strength of demineralized and intact bone in the SAMP6 mouse.

UNLABELLED: To examine the link between bone material properties and skeletal fragility, we analyzed the mechanical, histological, biochemical, and spectroscopic properties of bones from a murine model of skeletal fragility (SAMP6). Intact bones from SAMP6 mice are weak and brittle compared with SAMR1 controls, a defect attributed to reduced strength of the bone matrix. The matrix weakness is attributed primarily to poorer organization of collagen fibers and reduced collagen content. INTRODUCTION: The contribution of age-related changes in tissue material properties to skeletal fragility is poorly understood. We previously reported that bones from SAMP6 mice are weak and brittle versus age-matched controls. Our present objectives were to use the SAMP6 mouse to assess bone material properties in a model of skeletal fragility and to relate defects in the mechanical properties of bone to the properties of demineralized bone and to the structure and organization of collagen and mineral. MATERIALS AND METHODS: Femora from 4- and 12-month-old SAMR1 (control) and SAMP6 mice were analyzed using bending and torsional mechanical testing of intact bones, tensile testing of demineralized bone, quantitative histology (including collagen fiber orientation), collagen cross-links biochemistry, and Raman spectroscopic analysis of mineral and collagen. RESULTS: Intact bones from SAMP6 mice have normal elastic properties but inferior failure properties, with 60% lower fracture energy versus SAMR1 controls. The strength defect in SAMP6 bones was associated with a 23% reduction in demineralized bone strength, which in turn was associated with poorer collagen fiber organization, lower collagen content, and higher hydroxylysine levels. However, SAMP6 have normal levels of collagen cross-links and normal apatite mineral structure. CONCLUSIONS: Bones from SAMP6 osteoporotic mice are weak and brittle because of a defect in the strength of the bone matrix. This defect is attributed primarily to poorer organization of collagen fibers and reduced collagen content. These findings highlight the role of the collagen component of the bone matrix in influencing skeletal fragility.

Animals↗
PubMed1975

An antigenic antimorphogenetic bone hydrophobic glycopeptide (AHG).

A hydrophobic glycopeptide, isolated from fresh marrow-free cortical bone of the rat, extinguished the bone morphogenetic response of insoluble bone matrix gelatin which otherwise invariably produces new bone from migrating mesenchymal cells after implantation in muscle of the rat. Incubation of the 10 to 100 mug of the glycopeptide per milligram of bone gelatin in phosphate or Tris-HCl buffer, pH = 7.4, for 24 hours recombines the hydrophobic polypeptide and gelatin. Incubated with doses of 50 to 100 mug, implants of gelatin in Sprague-Dawley recipients are rapidly resorbed by a lymphocyte-plasma cell-macrophage infiltrate without developing any new bone. With 10 to 20 mug, infiltrate appears and bone develops inversely in proportion to the dose. Bone develops at all dose levels only when bone matrix gelatin and glycopeptide were prepared from an inbred strain of Lewis rats and recipients were of the same strain, and thereby suggests that only allogeneic AHG, produces an antigenic antimorphogenetic resonse. The glycopeptide was isolated from bone together with lipids and other hydrophobic proteins or polypeptides by chloroform-methanol (1:1) extraction and further purified by chromatography on ion-exchange columns and molecular sieves. The molecular weight established by Sephadex G-100 filtration and by calibrated dialysis is about 5000 daltons. Analysis of the biologically active fraction shows 75% of proteinaceous material and close to 25% carbohydrate with trace amounts of hexosamines and sialic acid. Amino acid analysis shows high levels of alanine, valine and leucine in comparison to other chloroform-methanol extractable but immunogenically relatively-inactive fractions.

Amino Acids↗
PubMed1988

Effects of bone associated growth factors on DNA, collagen and osteocalcin synthesis in cultured fetal rat calvariae.

Studies in bone and bone cell cultures have shown that osteocalcin synthesis is dependent on the maturity of the osteoblast and the presence of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3. The bone matrix is a rich source of growth factors that play a role in bone formation, but their effects on osteocalcin synthesis and their interactions with 1,25(OH)2D3 have not been examined. Insulin-like growth factor I (IGF I), basic and acidic fibroblast growth factor (bFGF and aFGF), platelet-derived growth factor (PDGF) and transforming growth factor beta (TGF beta), are growth factors associated with the bone matrix. These factors were shown to stimulate [3H]thymidine incorporation into DNA in 24 h cultures of fetal rat calvariae, and their effect was not modified by 1,25(OH)2D3. IGF I and TGF beta stimulated [3H]proline incorporation into calvarial collagen while the other growth factors studied did not; 1,25(OH)2D3 inhibited collagen synthesis in control as well as in IGF I and TGF beta treated calvariae. IGF I, bFGF and aFGF stimulated osteocalcin synthesis 1.5 to 2.5 fold but only IGF I was synergistic with the stimulatory effect of 1,25(OH)2D3. PDGF and TGF beta had no effect on osteocalcin synthesis. In conclusion, bone matrix-associated factors have important mitogenic effects in bone cultures, but only IGF I and FGFs stimulate osteocalcin synthesis, an effect that is of small magnitude when compared to that of 1,25(OH)2D3.

Animals↗
PubMed2005

Promises and pitfalls of stem cell therapy for promotion of bone healing.

UNLABELLED: There is promise in combining stem cells with allogeneic bone matrix to promote bone healing. Murine bone marrow, peripheral blood, and compact bone cells were transplanted ectopically under the kidney capsule in mice, alone or in combination with allogeneic matrix products: powder and putty to determine their bone forming potential in comparison to transplanted femoral bone fragments and long-term cultured bone marrow cells. The end point was the amount of bone formed as determined by quantitative histology. Mononuclear cells from marrow, peripheral blood, or bone alone transplanted under the kidney capsule did not form bone. Mononuclear cell populations did not combine readily with matrix products and there was in vivo migration of the transplanted combinations. Kidney subcapsular transplanted cultured bone marrow cells formed bone in proportion to the culture period, but after 9 weeks, the extent was only 20% by area of that of similarly transplanted femoral bone fragments. An inductive stimulus for bone formation seemed necessary. Osteoprogenitor cells were not detected in significant numbers in blood unless high doses of cytokines were administered. A better definition of the optimal cell populations and manipulations required for promotion of bone healing is needed along with new (transplant) models that allow for cell tracking. Much work remains to overcome current pitfalls in the use of stem cells to promote allograft integration and bone healing. LEVEL OF EVIDENCE: Therapeutic study, Level V (expert opinion). See the Guidelines for Authors for a complete description of levels of evidence.

Animals↗