Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Bone Matrix”

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 1,783 records · Page 99Linked to original sources
PubMed2001

[The current situation and future of extracellular matrix materials for bone tissue engineering].

The requirements of ideal extracellular matrix materials for bone tissue engineering were stated, and the advantages and disadvantages of bioceramics, biodegradable synthetic polymers and natural polymers were analyzed. Based on these, we highlight a point that the ideal extracellular matrix materials for bone tissue engineering should be made up of bioceramics materials, synthetic polymers or natural polymers. These materials should possess a morphological structure of three-dimensional foam and have a self-mediated drug delivery system of bone growth factors. The design and manufacture of such compound extracellular matrix materials for bone tissue engineering is a very important and urgent challenge.

Biocompatible Materials↗
PubMed1996

Bone morphogenetic protein-induced heterotopic bone in osteopetrosis.

The objectives of the present research on the osteopetrotic mouse are to investigate the factors influencing heterotopic bone development. The osteopetrotic mutant was deficient in macrophage colony stimulating factor and failed to activate functioning monocytes, macrophages, and osteoclasts. Macrophage colony stimulating factor deficiency also caused a heretofore undescribed delay in organization and absorption of hematomas resulting from surgical operations. Surgically implanted in a heterotopic site, bone morphogenetic protein induced approximately 10% more bone in osteopetrotic than littermate+/? mice. Radiographically, the heterotopic bone was at least 50% denser than new bone. The new bone was metachromatic or slightly basophilic rather than eosinophilic and undermined with large deposits of hypercalcified hypertrophic cartilage. Bone mineral in the osteopetrotic mouse was deposited in an apatite-like form with a higher calcium/phosphorus ratio than the bone of +/? littermates. High levels of alkaline phosphatase synthesis were sustained longer in the osteopetrotic mouse than in the +/? littermate. Tartrate resistant acid phosphatase synthesis was almost nil in osteopetrotic mice during the first 4 weeks, and thereafter appeared coincidental with spontaneous remission of osteopetrosis at 6 weeks. Implants of the mineralized cortical bone matrix of the osteopetrotic mouse showed minimal if any bone morphogenetic protein activity of matrix of +/? littermate or otherwise normal mice. The cause of the remission of the bone disorder in the osteopetrotic mouse is not known but is of great interest to students studying the problem of coupling of bone formation to bone resorption.

Animals↗
PubMed1992

[Phosphate metabolism in the mineral matrix of intact bones and after single and multiple fractures].

The level of mineral matrix phosphates in unbroken bones was investigated in rats with isolated and multiple fractures. It was found out that in bones lying close to the broken one the phosphates exchange shifts were similar to the changes happening in the region of the trauma. On the resorption stage the phosphates level in the nearby intact tissue decreases, during the bone callus formation it increases, and in the process of remodelling decreases again. The authors suggest that this zone should be identified under the term "trauma field".

Animals↗
PubMed1985

Bone disease and aluminum: pathogenic considerations.

Reductions in the formation of new bone matrix are a consistent finding in both clinical and experimental studies of aluminum-associated bone disease. This adverse effect of aluminum on collagen synthesis may be mediated through reductions in either the number or the cellular activity of osteoblasts. However, diminished matrix synthesis can be dissociated from histologic evidence of defective mineralization during aluminum loading. Thus, the toxicity of aluminum on bone is probably comprised of two components, one affecting collagen synthesis and the other affecting matrix mineralization. Adynamic bone may represent the histologic consequence of primary reductions in the formation of osteoid in the absence of defective matrix calcification. In contrast, concurrent disturbances in both matrix synthesis and calcification may account for the lesion of aluminum-associated osteomalacia. Although consistent with current clinical and experimental observations, confirmation of this hypothesis will require more careful longitudinal studies of bone growth and bone histology during aluminum loading.

Aluminum↗
PubMed1989

Ultrastructural immunolocalization of a major phosphoprotein in embryonic chick bone.

Immunocytochemistry utilizing the protein A-gold technique was used to examine the ultrastructural cellular and extracellular distribution of a major phosphoprotein in chick bone. HCl-extracts of embryonic and neo-natal chick bones contain a major 66kD phosphoprotein (BPP) which was purified and used to raise polyclonal antibodies in rabbits. The mid-diaphyseal regions of 8-, 12- and 18-day embryonic chick tibiae were fixed with 1% glutaraldehyde and embedded in Epon or Lowicryl. Electron microscopy following incubation of tissue sections with the antibody and the protein A-gold complex revealed specific immunolabeling over the rER and Golgi apparatus of osteoblasts and over those areas of bone matrix containing Ca and P as determined by electron probe x-ray microanalysis. These included extracellular areas in the matrix undergoing early mineralization and electron dense patches occurring at the mineralization front and extending throughout the more mature bone regions. Biochemical analyses of bone tissue processed similarly to that used for immunocytochemistry confirmed the retention of phosphoprotein in the tissue. The spatial correlation of phosphoprotein in the extracellular matrix with Ca-P mineral deposits confirms an earlier report using 33Pi and radioautography and may indicate a role for phosphoproteins in calcification.

Animals↗
PubMed1989

A search for the osteogenic factor in dentin. Rat incisor dentin contains a factor stimulating rat muscle cells in vitro to incorporate sulfate into an altered proteoglycan.

Demineralized dentin matrix has the capacity to induce bone formation via a chondrogenic pathway when implanted into muscle, in a fashion entirely analogous to bone matrix implants. In this work we have attempted to isolate, from rat incisor dentin, the matrix factor responsible for initiating osteogenesis. Rat incisor dentin was demineralized with EDTA plus 4.0 M guanidine. HCl. The proteins in the extracts were collected and, after a CaCl2 precipitation step, fractionated on Sephacryl S-200 in 6.0 M guanidine. HCl. The primary assay for activity was the incorporation of 35S-sulfate into proteoglycan in cultures of the fibroblast-like outgrowth cells from explants of neonatal rat muscle. Two Sephacryl S-200 fractions showed enhanced sulfate incorporating activity, but only one showed enhanced incorporation without a concomitant increase in cell number. In the presence of this fraction, the cell cultures produced a larger amount of a new small proteoglycan, as compared to controls, and a significant amount of a much larger proteoglycan. The active fraction had proteins in the Mr range from 8,000 to 15,000 as the major components. These data suggest that the fraction identified may contain the factors responsible for initiating the osteogenic response to dentin matrix upon its implantation in muscle in vivo.

Animals↗
PubMed2005

[Mechanism of arterial calcification with regards to atherosclerotic calcification and medial artery calcification].

Vascular calcification is a mechanism of active process, which includes inflammation and metabolism of bone formation. There are two different types of vascular calcification; atherosclerotic calcification and medial artery calcification. As seen in bone metabolism, vascular calcification is reported to be through enchondral ossification through BMP-2-Cbfa1 signal pathway, and through intramembranous ossification through BMP-2-Msx2 signal pathway. In the tissue of vascular calcification, several proteins which are related to bone and bone matrix metabolism have been shown to be present, such as bone morphogenic protein, osteoprotegerin, matrix gla protein, and osteopontin.

Arteries↗
PubMed1999

Differential cell surface expression of the STRO-1 and alkaline phosphatase antigens on discrete developmental stages in primary cultures of human bone cells.

Human osteoblast-like cells can be readily cultured from explants of trabecular bone, reproducibly expressing the characteristics of cells belonging to the osteoblastic lineage. Dual-color fluorescence-activated cell sorting was employed to develop a model of bone cell development in primary cultures of normal human bone cells (NHBCs) based on the cell surface expression of the stromal precursor cell marker STRO-1 and the osteoblastic marker alkaline phosphatase (ALP). Cells expressing the STRO-1 antigen exclusively (STRO-1+/ALP-), were found to exhibit qualities preosteoblastic in nature both functionally by their reduced ability to form a mineralized bone matrix over time, as measured by calcium release assay, and in the lack of their expression of various bone-related markers including bone sialoprotein, osteopontin, and parathyroid hormone receptor based on reverse trancriptase polymerase chain reaction (PCR) analysis. The majority of the NHBCs which expressed the STRO-1-/ALP+ and STRO-1-/ALP- phenotypes appeared to represent fully differentiated osteoblasts, while the STRO-1+/ALP+ subset represented an intermediate preosteoblastic stage of development. All STRO-1/ALP NHBC subsets were also found to express the DNA-binding transcription factor CBFA-1, confirming that these cultures represent committed osteogenic cells. In addition, our primer sets yielded four distinct alternative splice variants of the expected PCR product for CBFA-1 in each of the STRO-1/ALP subsets, with the exception of the proposed preosteoblastic STRO-1+/ALP- subpopulation. Furthermore, upon re-culture of the four different STRO-1/ALP subsets only the STRO-1+/ALP- subpopulation was able to give rise to all of the four subsets yielding the same proportions of STRO-1/ALP expression as in the original primary cultures. The data presented in this study demonstrate a hierarchy of bone cell development in vitro and facilitate the study of bone cell differentiation and function.

Aged↗
PubMed2003

Role of RANKL-induced osteoclast formation and MMP-dependent matrix degradation in bone destruction by breast cancer metastasis.

Bone metastasis of breast cancer induces severe osteolysis with increased bone resorption. Osteoclast differentiation regulated by the receptor activator of NF-kappaB ligand (RANKL) in osteoblasts and matrix degradation induced by matrix metalloproteinases (MMPs) are thought to be involved in the process of bone resorption. When nude mice were inoculated with human breast cancer cells, MDA-MB-231(MDA-231), numerous osteoclasts resorbed bone and the degradation of the bone matrix markedly progressed in the femur and tibia with metastasis of the MDA-231 tumour. The expression of RANKL, MMP-13 and membrane-type 1-MMP mRNA was markedly elevated in bone with metastasis. When MDA-231 cells were cocultured with mouse calvaria, MDA-231 markedly induced bone resorption measured by calcium release from the calvaria, and the expression of RANKL, MMP-2 and MMP-13 was elevated in the calvaria after the coculture. The separation of MDA-231 from the calvaria using filter insert showed decreased bone resorption, suggesting that cell-to-cell interaction is essential for cancer-induced bone resorption. Adding MDA-231 cells to bone marrow cultures markedly induced osteoclast formation, and the expression of RANKL in osteoblasts was enhanced by contact with the cell surface of MDA-231 cells. These results indicate that RANKL-induced osteoclast formation and MMP-dependent matrix degradation are associated with osteolysis because of bone metastasis of breast cancer.

Animals↗
PubMed2006

Adenovirus-mediated transfer of siRNA against Runx2/Cbfa1 inhibits the formation of heterotopic ossification in animal model.

The heterotopic ossification of muscles, tendons, and ligaments is a common problem faced by orthopaedic surgeons. Runx2/Cbfa1 plays an essential role during the osteoblast differentiation and is considered as a molecular switch in osteoblast biology. RNA interference technology is a powerful tool for silencing endogenous or exogenous genes in mammalian cells. In this study, we investigated the effect of Runx2/Cbfa1-specific siRNA on osteoblast differentiation and mineralization in osteoblastic cells, and then constructed adenovirus containing siRNA against Runx2/Cbfa1 (Ad-Runx2-siRNA) to inhibit the formation of heterotopic ossification induced by BMP4, demineralized bone matrix, and trauma in animal model. Our results showed that the Runx2/Cbfa1-specific siRNA could inhibit the expression of Runx2/Cbfa1 at the level of mRNA and protein. Analysis of the expression of osteoblast maturation genes including type I collagen, osteopontin, bone sialoprotein, and osteocalcin, alkaline phosphatase activity, and matrix mineralization (von kossa) revealed that osteoblast differentiation was inhibited in cultured primary mouse osteoblasts transduced with Ad-Runx2-siRNA. Furthermore, adenovirus-mediated transfer of siRNA against Runx2/Cbfa1 could inhibit the formation of heterotopic ossification induced by BMP4, demineralized bone matrix, and trauma in animal model. It is likely that the inhibition of Runx2/Cbfa1 by RNAi could be developed as a powerful approach to prevent or treat heterotopic ossification.

Adenoviridae↗
PubMed2004

Evidence for a serum factor that initiates the re-calcification of demineralized bone.

The present studies show for the first time that demineralized bone re-calcifies rapidly when incubated at 37 degrees C in rat serum: re-calcification can be demonstrated by Alizarin Red and von Kossa stains, by depletion of serum calcium, and by uptake of calcium and phosphate by bone matrix. Re-calcification is specific for the type I collagen matrix structures that were calcified in the original bone, with no evidence for calcification in periosteum or cartilage. Re-calcification ceases when the amount of calcium and phosphate introduced into the matrix is comparable to that present in the original bone prior to demineralization, and the re-calcified bone is palpably hard. Re-calcified bone mineral is comparable to the original bone mineral in calcium to phosphate ratio and in Fourier transform infrared and x-ray diffraction spectra. The serum activity responsible for re-calcification is sufficiently potent that the addition of only 1.5% serum to Dulbecco's modified Eagle's medium causes bone re-calcification. This putative serum calcification factor has an apparent molecular mass of 55-150 kDa and is inactivated by trypsin or chymotrypsin. The serum calcification factor must act on bone for 12 h before re-calcification can be detected by Alizarin Red or von Kossa staining and before the subsequent growth of calcification will occur in the absence of serum. The speed, matrix-type specificity, and extent of the serum-induced re-calcification of demineralized bone suggest that the serum calcification factor identified in these studies may participate in the normal calcification of bone.

Animals↗
PubMed2002

Formation and function of the ruffled border in osteoclasts.

Osteoclasts are multinucleated hematopoietic cells specialised for bone resorption. Dissolution of the inorganic fraction of the bone matrix is mediated by acidification of the bone surface in contact with the osteoclast whereas secreted lysosomal enzymes digest organic components. Through massive exocytosis, the plasma membrane in contact with the bone surface enlarges into the ruffled border, which has unusual features more similar to endosomal/lysosomal membranes. Maintenance of the ruffled border during resorption is achieved through a balance between exocytosis and endocytosis. Inactivation of proteins necessary for the extracellular acidification or of the proteases involved in matrix degradation leads to osteopetrosis; a disease characterised by dense bones.

Animals↗
PubMed1987

Tissue specificity and developmental expression of rat osteopontin.

Osteopontin is a 44 kd phosphoprotein abundant in bone matrix. We isolated a partial length cDNA for rat osteopontin and used it to examine its tissue specificity, its expression during bone development and its hormonal regulation. Osteopontin mRNA is most abundant in bone but is also found in considerable amounts in kidney. Osteopontin mRNA is regulated by the osteotropic hormones dexamethasone and 1,25(OH)2D3. Estimates of osteopontin mRNA levels indicate that the osteopontin gene is turned on relatively late in calvarial development.

Age Factors↗
PubMed2005

Cultivation of human embryonic stem cells without the embryoid body step enhances osteogenesis in vitro.

Osteogenic cultures of embryonic stem cells (ESCs) are predominately derived from three-dimensional cell spheroids called embryoid bodies (EBs). An alternative method that has been attempted and merits further attention avoids EBs through the immediate separation of ESC colonies into single cells. However, this method has not been well characterized and the effect of omitting the EB step is unknown. Herein, we report that culturing human embryonic stem cells (hESCs) without the EB stage leads to a sevenfold greater number of osteogenic cells and to spontaneous bone nodule formation after 10-12 days. In contrast, when hESCs were differentiated as EBs for 5 days followed by plating of single cells, bone nodules formed after 4 weeks only in the presence of dexamethasone. Furthermore, regardless of the inclusion of EBs, bone matrix formed, including cement line matrix and mineralized collagen, which displayed apatitic mineral (PO4) with calcium-to-phosphorous ratios similar to those of hydroxyapatite and human bone. Together these results demonstrate that culturing hESCs without an EB step can be used to derive large quantities of functional osteogenic cells for bone tissue engineering.

Alkaline Phosphatase↗
PubMed1977

Effect of beta-aminopropionitrile on bone mechanical properties.

In vivo beta-aminopropionitrile treatment caused significant changes in the mechanical properties of rat femora. In femora treated with beta-aminopropinitrile as compared with controls, there was a 44 per cent decrease in bone stiffness and a 47 per cent increase in bone deformation to failure. Bone ash was decreased 5 per cent in the treated group. It is likely that the decrease in bone ash was secondary to impaired intermolecular bone-collagen cross-linking, which is a well established consequence of treatment with beta-aminopropionitrile. Thus, beta-aminopropionitrile influences bone mechanical properties directly by impairing collagen cross-linking and indirectly by altering bone-matrix mineralization.

Aminopropionitrile↗
PubMed1999

Cathepsin K knockout mice develop osteopetrosis due to a deficit in matrix degradation but not demineralization.

Cathepsin K is a cysteine protease expressed predominantly in osteoclasts. Activated cathepsin K cleaves key bone matrix proteins and is believed to play an important role in degrading the organic phase of bone during bone resorption. Mutations in the human cathepsin K gene have been demonstrated to be associated with a rare skeletal dysplasia, pycnodysostosis. The degree of functional activity of the mutated forms of cathepsin K in these individuals has not been elucidated, but is predicted to be low or absent. To study the role of cathepsin K in bone resorption, we have generated mice deficient in the cathepsin K gene. Histologic and radiographic analysis of the mice revealed osteopetrosis of the long bones and vertebrae, and abnormal joint morphology. X-ray microcomputerized tomography images allowed quantitation of the increase in bone volume, trabecular thickness, and trabecular number in both the primary spongiosa and the metaphysis of the proximal tibiae. Not all bones were similarly affected. Chondrocyte differentiation was normal. The mice also had abnormalities in hematopoietic compartments, particularly decreased bone marrow cellularity and splenomegaly. The heterozygous animals appeared normal. Close histologic examination of bone histology revealed fully differentiated osteoclasts apposed to small regions of demineralized bone. This strongly suggests that cathepsin K-deficient osteoclasts are capable of demineralizing the extracellular matrix but are unable to adequately remove the demineralized bone. This is entirely consistent with the proposed function of cathepsin K as a matrix-degrading proteinase in bone resorption.

Animals↗
PubMed2001

[Reorganization of the mineral matrix of the bone tissue].

Basing on experimental and clinical chronobiological investigations with an application of three different methods of estimation of osseous tissue mineral density: biochemical (phosphates content in bone tissue mineral matrix), roentgenographic densitometry and dual photon X-ray absorption, it has been shown that 4.5% of mineral matrix mass are in constant interchange with body fluids. It corresponds to the degree of fluctuations of osseous tissue mineral density (in the direction of increase or decrease) both locally and in the skeleton on the whole during the period of time amounting to about one week. This fact should be taken into consideration while evaluating the effect of drug therapy in patients with osteoporosis.

Absorptiometry, Photon↗
PubMed1995

Low-temperature heat-deproteinated compact bone to heal large bone defects.

The potential of low-temperature (400 degrees C), heat-treated bone matrix in osteorepair has been evaluated in vivo by implantation into defects artificially created in rodent tibia. Histological and ultrastructural analysis of the bone--implant interface has been carried out on samples obtained at 1 to 6 weeks from operation. The obtained data showed that calcined bone is well tolerated and does not cause acute or chronic inflammatory reactions. Osteoid tissue, tightly adhered to the implant, appears within 2 weeks of the operation, while after 6 weeks newly formed bone surrounds and infiltrates the implant. Of greater note, the detection of good adhesion between bone and implant ultrastructurally is demonstrated by the absence of fibrillar connective tissue at the interface. For these reasons, our preliminary observations suggest that low-temperature calcined bone (biological apatite or heat-deproteinated bone) may have a rightful place among the osteointegrators.

Animals↗