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PubMed1993

High yield of osteoinductivity can be derived from demineralized bone matrix using collagenase digestion.

A bone morphogenetic protein purification method for minor quantities of bone material was developed based on collagenase splitting of bone connective tissue. Our aim was to remove and characterize the osteoinductive protein preparation in native form without using strongly dissociative agents. We started from 80 g of HCl-demineralized reindeer bone material which was treated with type I collagen splitting collagenase. The solution was dialyzed against 10 mM glycine-HCl buffer, pH 5.2. The formed precipitate was found to be osteoinductive. After fractionation of the material using HPLC gel filtration it was observed that the high-molecular-weight component of the precipitate was biologically active. Isoelectric focusing revealed that the component consisted of at least eight different protein molecules. Lower-molecular-weight components induced no bone formation. These preliminary findings suggest that in native form at least one part of BMP is in a complex form and other extracellular matrix components bound to the osteoinductive protein complex are significant for BMP action and may act synergistically or as carriers for the BMP.

Animals↗
PubMed1973

Inhibition of bone matrix formation, mineralization, and resorption in thyroparathyroidectomized rats.

In previous work we found that vitamin D-deficient and also calcium-deficient rats developed hypocalcemia and an impairment of bone formation and mineralization. The present study of thyroparathyroidectomized (TPTX) rats was undertaken to determine the effect of hypocalcemia without secondary hyperparathyroidism. TPTX rats fed a normal diet developed hypocalcemia and hyperphosphatemia in association with impairment of osteoblastic bone matrix formation and of mineralization of newly formed matrix. The serum calcium x phosphorus product was not decreased. The decreased formation was largely due to a reduction in matrix apposition indicating decreased synthetic activity of individual ostcoblasts. In contrast to the above results, when TPTX rats were fed a high-calcium diet to prevent hypocalcemia, no impairment of either formation or mineralization was found. From the results of these two experiments, it is reasonably certain that hypocalcemia was responsible for the inhibition of formation and mineralization. Moreover, based on the magnitude of the changes in serum calcium and bone parameters in TPTX rats, hypocalcemia could have accounted for the inhibition of formation and mineralization in calcium-deficient as well as vitamin D-deficient rats. In TPTX rats the mineralization defect was manifested by decreases in both the rate of osteoid maturation (indicating a delayed onset of mineralization) and the rate of mineralization. A strong correlation (r = 0.95, P < 0.001) was observed between these two rates suggesting a tight coupling of these two aspects of mineralization.TPTX rats also had lower bone resorption rates and higher serum phosphorus levels than sham-operated animals when the normal calcium diet was fed but not when the high-calcium diet was fed. Thus the inhibition of bone resorption in TPTX rats was at least partially prevented by correction of hyperphosphatemia. This is consistent with previous work showing an inverse relationship between serum phosphorus and bone resorption. Accordingly, the depression of bone resorption in TPTX rats was probably due to hyperphosphatemia as well as to hypoparathyroidism.

Animals↗
PubMed2002

Characterization of bone defect repair in young and aged rat femur induced by xenogenic demineralized bone matrix.

BACKGROUND: The osteoinductive effect of some biomaterials could be affected by those systemic conditions typical of old age. The aim of the present paper was to assess the effects of age on the healing of bone defects treated with demineralized bone matrix (DBM). METHODS: The study was conducted in young (3 month old) and aged (18 month old) rats to assess the efficacy of DBM in the treatment of osseous defects in bone with limited repair capacities. A standard bone defect was created in the distal femoral condyles of male Wistar rats: the left condyle was filled with rabbit DBM granules, while the right condyle was left empty (control). Histological and microhardness analyses were performed at 30 and 45 days after implant surgery. RESULTS: After implantation of xenogenic DBM, bone healing areas of the aged and young groups showed a significant increase in the formation of newly mineralized bone relative to controls. Measurements of trabecular thickness on day 45 revealed no differences between newly formed and preexisting bone in the young group, while control values were lower. Microhardness measurements demonstrated that newly mineralized bone, either induced by DBM or not, and preexisting bone were comparable in terms of trabecular hardness after 45 days. CONCLUSIONS: In conclusion, xenogenic DBM seems to be effective in bone defect healing, since it increases mineralized tissue volume. In both DBM-filled and empty sites, age seems to have a detrimental effect on the volume of new bone formation but no influence on bone maturation.

Aging↗
PubMed1984

Demineralized bone-matrix-induced osteogenesis.

A review of the literature on bone formation induced by demineralized bone and dentin indicates that: there is considerable interest in the biology and applied science of osteoinduction; the technology has been developed, but it varies in detail from one laboratory to another because of specific and individual objectives; and the accumulated evidence supports the concept of cartilage and bone cell differentiation induced by a unique bone morphogenetic protein (BMP).

Animals↗
PubMed2002

Bone and suture regeneration in calvarial defects by e-PTFE-membranes and demineralized bone matrix and the impact on calvarial growth: an experimental study in the rat.

The aim of this study was to evaluate the effect of: guided tissue regeneration (GTR) alone, implantation of demineralized bone matrix (DBM) alone, and of the combined treatment on the healing of craniectomy defects involving the sagittal cranial suture, and to examine subsequent calvarial growth. Sixty four-week-old rats were used in the study. These animals were randomly assigned to five groups (A-E) of 12 animals. In four groups (A-D), a calvarial defect (5.0 mm) involving the sagittal suture was produced in each animal. Group A: The defect was left untreated. Group B: DBM was implanted into the defect. Group C: The cerebral and the galeal aspect of the defect was covered with an e-PTFE membrane. Group D: The defect was treated with the double membrane technique combined with implantation of DBM. Group E: The animals were sham-operated, no defect was created. In all groups, two gutta-percha points were placed to indicate the lateral borders of the parietal bones. Histological analysis 4 months following surgery showed that the untreated cranial defects (A) had healed with fibrous connective tissue in the midportion of the defect. The DBM grafted defects (B) healed either completely with bone containing DBM particles or partially with bone and connective tissue. The defects (D) treated with DBM combined with GTR healed completely with bone, while the defects (C) treated with membranes alone healed with bone but a suture-like tissue similar to the normal sagittal suture of the sham-operated controls (E) was always present in the midportion of the defect. Cephalometric radiography demonstrated that the membrane-treated (C) and the sham-operated animals (E) exhibited similar coronal growth of the cranial vault following treatment. Craniometric measurements on chemically defleshed specimens showed that sham-operated and membrane-treated animals presented significantly more biparietal width than the animals treated with DBM alone or DBM combined with GTR (P < 0.05). The results demonstrated that predictable osseous healing including the formation of a sagittal suture can be accomplished in craniectomy defects by GTR, and undisturbed cranial growth reestablished. The treatment of the defects with DBM alone or DBM combined with GTR resulted in craniosynostosis and reduced cranial growth.

Analysis of Variance↗
PubMed1993

Comparison of demineralized allogeneic bone matrix grafting (the Urist procedure) and the Ilizarov procedure in large diaphyseal defects in sheep.

The bone inductive capability of the Urist and Ilizarov procedures was compared in the repair of large diaphyseal defects in sheep. In 30 animals, a 4 cm segmental defect was created in the middle portion of the right femur and was stabilized with an external fixator. The sheep were divided into four groups according to the type of reconstruction of the defect. In group 1, a demineralized allogeneic bone matrix (DABM) cylinder was used; in group 2, DABM chips; and in group 3, gradual transport of a piece of bone detached from the proximal femoral fragment was used to fill the defect. Group 4 served as a control (the defect was left empty). New bone formation was assessed by serial radiographs until the time of death at 2 or 4 months. Postmortem specimens were analyzed with respect to bone mineral content, uptake of isotopes (45Ca and 3H-proline), and histology. The first signs of new bone formation were radiographically evident at 4 weeks. In the two groups in which reconstruction involved DABM (Urist procedures), new bone failed to form in eight of the 13 animals. Full bridging of the defect was observed at 8 weeks in one animal with a DABM cylinder and two with DABM chips. No decisive difference in bone yield could be demonstrated between the two Urist procedures. In the group treated with the Ilizarov procedure, new bone formation consistently occurred at a high rate; full bridging of the defect was observed in seven of the eight animals. Bone mineral scanning and histologic analysis essentially confirmed the radiographic results. Uptake of isotopes was selectively analyzed in two sheep from each experimental group in which new bone formation was exhibited in the defect; new bone formation was increased compared with that in the contralateral femur but was equal among the three experimental groups. Our study shows that gradual transport of a detached piece of autogeneic bone (Ilizarov procedure) is more effective than implantation of DABM (Urist procedure) in eliciting new bone formation in large diaphyseal defects in sheep. The variable bone induction by DABM may be explained by differences in host immune responses to the implants.

Animals↗
PubMed1991

Treatment of nonunion by percutaneous injection of bone marrow and demineralized bone matrix. An experimental study in dogs.

Successful treatment of nonunited fractures remains a major clinical challenge. Because bone marrow and demineralized bone matrix (DBM) are capable of stimulating osteogenesis, experiments were designed to test the effectiveness of bone marrow or DBM or both when injected percutaneously into a canine nonunion model. Six-millimeter segmental defects were created in the midtibial diaphysis of 24 adult mongrel dogs and held distracted by external fixation. For comparative purposes, a 0.5-mm osteotomy was created in five dogs. Five weeks later, the 6-mm defects were injected with either saline, autogeneic marrow, DBM powder, a composite of bone marrow and DBM, or treated by open grafting techniques with autogenic cancellous bone. Healing of the defect was evaluated roentgenographically, biomechanically (three-point bending), histologically, and biochemically 13 weeks postsurgery. Marrow and DBM stimulated defect healing. However, the combination of bone marrow with DBM produced a synergistic response in the defect, which was greater than the sum of either marrow or DBM alone. Healing in the composite-grafted dogs was comparable to those treated by standard cancellous bone grafting. These data suggest that percutaneous injection of bone marrow and DBM may be a potential alternative that offers numerous advantages over standard open grafting techniques in the treatment of fractures with nonunited defects.

Animals↗
PubMed1987

Chondroosteogenetic response to crude bone matrix proteins bound to hydroxyapatite.

For the development of a new implantable biomaterial that possesses osteogenetic ability, bone matrix morphogenetic proteins were bound to hydroxyapatite (BMP-HAP). A crude protein extract including the bone morphogenetic protein (BMP) fraction was precipitated in the pores of hydroxyapatite (HAP) inside of a dialysis sac. In tissue culture, BMP-HAP or HAP was used as substratum for rat mesenchymal muscle cell explants. The BMP-HAP and HAP controls were also implanted in the muscle pouches of mice. New cartilage and/or new bone formation was observed on the exterior surface of BMP-HAP but not of HAP controls. Implantation of this HAP into bone marrow cavities of rabbit femoral and tibial condyle produced new bone formation. The deposits extended further inside BMP-HAP than HAP pores. The pore diameters of 90-200 microns produced earlier ingrowth than into larger pore sizes. BMP-HAP should be tested for clinical application as osteogenetic biomaterial for augmentation of bone regeneration.

Animals↗
PubMed1991

Osteoclast formation is related to bone matrix age.

Little is known about the relationship between the age of the skeleton and the development of multinucleated bone-resorbing cells, osteoclasts. It has been shown that mineralized bone implanted onto the chick chorioallantoic membrane (CAM) is effective in the recruitment and differentiation of osteoclast precursors. In studies reported here we used the CAM system to examine the influence of bone matrix age on osteoclast formation. Devitalized mineralized bone particles (75-250 microns) were prepared from rats of various ages (2, 4, 9, 12, and 16 months). The particles were implanted onto the chick chorioallantoic membrane and 8 days later implants were harvested and processed for morphometric or immunohistochemical analysis. Osteoclast number, cell area, nucleocytoplasmic ratio, and the presence of a distinctive osteoclast antigen, defined by the 121F monoclonal antibody, were determined. Bone particles of each age group resulted in the formation of osteoclast-like giant cells. Compared with multinucleated cells that formed in response to bone particles obtained from 2-month-old rats, matrix from the oldest age group (16 months) elicited significantly fewer and smaller cells which contained a smaller number of nuclei. These data suggest that with aging, bone undergoes qualitative and/or quantitative changes that affect the recruitment and differentiation of osteoclast precursor cells.

Aging↗
PubMed1980

[Conditions influencing bone induction after implantation of the bone matrix into mice].

In the course of implanting a decalcified bone matrix to mice intramuscularly, beneath the renal capsule and the capsule of the kidney with ligated vessels, and intramuscularly to animals with curretaged femur, bone induction was evoked in 90--100% of the cases, with no morphological differences recorded. In each series of the experiments both implants with marked bone plates full of bone marrow cells and implants with small areas of osteogenic tissue were observed. The data obtained show that the inductive process does not depend either on the degree of vascularization of the site of implantation or on the degree of calcification of adjacent tissue and may be predetermined by the presence of inducible cells sensitive to the induction stimulus.

Animals↗
PubMed1991

Postmortem degradation of demineralized bone matrix osteoinductive potential. Effect of time and storage temperature.

The osteoinductive growth factors present in demineralized bone are degraded by tissue enzymes. Storage of rat limbs at low temperature (4 degrees C) before harvesting of bones preserves the osteoinductive potential of such factors. Storage at room temperature for more than 24 hours causes the recovered bone matrix to be biologically inactive, presumably as the result of biodegradation.

Alkaline Phosphatase↗
PubMed2002

Atorvastatin inhibits hypercholesterolemia-induced cellular proliferation and bone matrix production in the rabbit aortic valve.

BACKGROUND: Despite the common occurrence of aortic stenosis, the cellular causes of the disorder are unknown, in part because of the absence of experimental models. We hypothesized that atherosclerosis and early bone matrix expression in the aortic valve occurs secondary to experimental hypercholesterolemia and that treatment with atorvastatin modifies this transformation. METHODS AND RESULTS: To test this hypothesis, we developed an experimental hypercholesterolemic rabbit model. New Zealand White rabbits (n=48) were studied: group 1 (n=16), normal diet; group 2 (n=16), 1% (wt/wt) cholesterol diet; and group 3 (n=16), 1% (wt/wt) cholesterol diet plus atorvastatin (3 mg/kg per day). The aortic valves were examined with hematoxylin and eosin stain, Masson trichrome, macrophage (RAM 11), proliferation cell nuclear antigen (PCNA), and osteopontin immunostains. Cholesterol and highly sensitive C-reactive protein (hsCRP) serum levels were obtained by standard assays. Computerized morphometry and digital image analysis were performed for quantifying PCNA (% area). Electron microscopy and immunogold labeling were performed for osteopontin. Semiquantitative RT-PCR was performed for the osteoblast bone markers [alkaline phosphatase, osteopontin, and osteoblast lineage-specific transcription factor (Cbfa-1)]. There was an increase in cholesterol, hsCRP, PCNA, RAM 11, and osteopontin and osteoblast gene markers (alkaline phosphatase, osteopontin, and Cbfa-1) in the cholesterol-fed rabbits compared with control rabbits. All markers except hsCRP were reduced by atorvastatin. CONCLUSIONS: These findings of increased macrophages, PCNA levels, and bone matrix proteins in the aortic valve during experimental hypercholesterolemia provide evidence of a proliferative atherosclerosis-like process in the aortic valve associated with the transformation to an osteoblast-like phenotype that is inhibited by atorvastatin.

Alkaline Phosphatase↗
PubMed1992

Protein-S, a vitamin K-dependent protein, is a bone matrix component synthesized and secreted by osteoblasts.

Protein-S is a vitamin K (Vit K)-dependent protein synthesized by hepatocytes, megakaryocytes, and endothelial cells and plays an important role in the regulation of hemostasis. Two cases of free protein-S congenital deficiency were recently reported to be associated with osteopenia. We hypothesized that this osteopenia could be the result of a bone deficit of protein-S synthesized by bone cells. Using enzyme-linked immunoassay, immunocytochemistry, immunoblotting, and immunoprecipitation after labeling with [35S]methionine, we have shown that this protein is secreted by three human osteosarcoma cell lines and by human adult osteoblast-like cells. In addition, protein-S was present in protein extracts of human bone matrix. Protein-S secreted by MG 63 cells increased linearly from 1-7 days of culture, was biologically active, and was regulated by warfarin, as previously described for the other cell types secreting protein-S. Vit K had no direct effect on protein-S secretion or activity, but could overcome the effects of warfarin. In conclusion, in addition to osteocalcin and matrix gamma-carboxyglutamic acid (Gla) protein, osteoblasts secrete another Vit K-dependent protein, which is a constituent of the bone matrix. Our data suggest that osteopenia occurring in patients with congenital protein-S deficiency might be related to a deficiency of protein-S secretion by the osteoblasts. This finding raises the intriguing possibility that protein-S might play a role in bone turnover and bone mass.

Bone Neoplasms↗
PubMed1979

[The use of organic bone matrix as material for direct pulp capping].

The effect of bone matrix soaked in thyrocalcitonin on vitally amputated pulp was studied in beagle dogs with light and electron microscopy. All treated teeth were vital after eight weeks; the area of implantation was densely populated with cells. Formation of hard tissue differing from normal dentinogenesis had begun.

Animals↗
PubMed1999

Expression of bone matrix proteins, osteonectin and osteopontin, in salivary pleomorphic adenomas.

Osteonectin (OSN) is a glycoprotein involved in the early steps of the mineralization of skeletal tissue, while osteopontin (OPN) is a protein involved in normal and pathological calcifications. OSN and OPN are non-collageneous bone matrix proteins expressed by some epithelial tumor cells in exceptional cases. We immunohistochemically investigated the presence and the distribution of OSN and OPN in 43 pleomorphic adenomas to elucidate the production of their molecules by modified myoepithelial cells. In normal salivary glands, OSN was immunolocalized in the striated ducts, while OPN was not expressed. In pleomorphic adenomas, the inner layer of tubulo-glandular structures and modified myoepithelial cells in the myxoid areas showed moderate positivity for OSN (83.7%). OSN was expressed in all of the lacuna cells in the chondroid areas. OPN was strongly expressed in the stroma of the myxoid and hyaline areas of the pleomorphic adenomas (65.1%), but there was no expression of OPN in the chondroid area. All cases of pleomorphic adenomas expressed type IV collagen. These findings suggested that OSN was related to the production of the type IV collagen by modified myoepithelial cells, whereas OPN was involved in the stromal formation of myxoid or hyaline tissues in pleomorphic adenomas. In summary, pleomorphic adenomas expressed the bone matrix proteins OSN and OPN.

Adenoma, Pleomorphic↗
PubMed1997

Vascular endothelial growth pattern during demineralized bone matrix induced osteogenesis.

The purpose of the current study was to determine the timely ingrowth of blood vessels associated with demineralized bone matrix (DMB) induced osteogenesis. Critical-size (10 x 5mm), full thickness bony defects in rabbit parietal bone were implanted with DBM. Histological and ultrastructural changes were examined 1, 2, 3, 4, 5, 6, 7 and 14 days later. Neovascularization was assessed by immunohistochemical staining for factor VIII antigen (marker for vascular endothelium) and also confirmed by staining using pan-endothelial antibody (CD31) (a marker for endothelium). Immunohistochemical evaluation revealed a positive staining for CD31 and Factor VIII expressed by endothelial cells by day 3 post grafting. By day 4, small blood vessels were first seen budding from host bed towards the grafted DBM. Ultrastructural identification of cells in the early stages of healing revealed the presence of macrophages. The monocyte-derived macrophage appears to play a central role in the repair process using DBM. Results of this study demonstrated a rapid vascularization during the DBM induced osteogenesis. This rapid vascularization is vital to the healing and bone induction ability of the DBM.

Animals↗
PubMed1997

Bone morphogenetic protein 2 (BMP-2) enhances BMP-3, BMP-4, and bone cell differentiation marker gene expression during the induction of mineralized bone matrix formation in cultures of fetal rat calvarial osteoblasts.

Normal bone formation is a prolonged process that is carefully regulated and involves sequential expression of growth regulatory factors by osteoblasts as they proliferate and ultimately differentiate. Since this orderly sequence of gene expression by osteoblasts suggests a cascade effect, and BMP-2 is capable of initiating and maintaining this effect, we examined the effects of BMP-2 on expression of other BMPs and compared these effects with the expression pattern of bone cell differentiation marker genes in primary cultures of fetal rat calvarial (FRC) osteoblasts. To examine the gene expression profile during bone cell differentiation and bone formation, we also examined the effects of rBMP-2 on bone formation in vivo and in vitro. rBMP-2 stimulated bone formation on the periosteal surface of mice when 500 ng/day rBMP-2 was injected subctaneously. When rBMP-2 was added to primary cultures of FRC osteoblasts, it accelerated mineralized nodule formation in a time and concentration-dependent manner (10-40 ng/ml). rBMP-2 (40 ng/ml) enhanced BMP-3 and -4 mRNA expression during the mineralization phase of primary cultures of FRC osteoblasts. Enhancement of BMP-3 and -4 mRNA expression by rBMP-2 was associated with increased expression of bone cell differentiation marker genes, alkaline phosphatase (ALP), type I collagen, osteocalcin (OC), osteopontin (OP), and bone sialoprotein (BSP). These results suggest that BMP-2 enhances expression of other BMP genes during bone cell differentiation. BMP-2 may act in a paracrine fashion in concert with other BMPs it induces to stimulate bone cell differentiation and bone formation during remodeling.

Amino Acid Sequence↗