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PubMed1997

Direct osteolysis induced by metastatic murine melanoma cells: role of matrix metalloproteinases.

We examined the osteolytic ability of metastatic cells and the role of tumour matrix metalloproteinases (MMPs) in bone degradation. The histomorphometry of experimental bone metastases of B16/F1 melanoma cells showed that osteolysis was associated with a 90% decrease in osteoclast number and predominance of cancer cells overlaying resorption pits. In vitro, B16/F1 cells and their conditioned medium (CM) degraded 3H-proline-labelled extracellular matrices from osteoblast-like cells and 45Ca-labelled calvariae. Using bone slices, we observed morphological evidence of degradation by B16/F1 cells. A role for tumour MMPs in bone degradation was supported by inhibition of degradation by 1,10-phenanthroline, collagen I degradation by tumour cells and the presence of TPA-inducible M(r) 90,000, 84,000 and 64,000 gelatinolytic, and 54,000 caseinolytic bands in B16/F1-CM. These studies indicate that metastatic cancer cells degrade bone matrix directly and that this is partially mediated by MMPs.

Animals↗
PubMed1994

Localization of cathepsins B, D, and L in the rat osteoclast by immuno-light and -electron microscopy.

The localization of cathepsins B, D, and L was studied in rat osteoclasts by immuno-light and -electron microscopy using the avidin-biotin-peroxidase complex (ABC) method. In cryosections prepared for light microscopy, immunoreactivity for cathepsin D was found in numerous vesicles and vacuoles but was not detected along the resorption lacunae of osteoclasts. However, immunoreactivity for cathepsins B and L occurred strongly along the lacunae, and only weak intracellular immunoreactivity was observed in the vesicles and peripheral part of the vacuoles near the ruffled border. In control sections that were not incubated with the antibody, no cathepsins were found in the osteoclasts or along the resorption lacunae of osteoclasts. At the electron microscopic level, strong intracellular reactivity of cathepsin D was found in numerous vacuoles and vesicles, while extracellular cathepsin D was only slightly detected at the base of the ruffled border but was not found in the eroded bone matrix. Most osteoclasts showed strong extracellular deposition of cathepsins B and L on the collagen fibrils and bone matrix under the ruffled border. The extracellular deposition was stronger for cathepsin L than for cathepsin B. Furthermore cathepsins B and L immunolabeled some pits and part of the ampullar extracellular spaces, appearing as vacuoles in the sections. Conversely, the intracellular reactivity for cathepsins B and L was weak: cathepsin-containing vesicles and vacuoles as primary and secondary lysosomes occurred only sparsely. These findings suggest that cathepsins B and L, unlike cathepsin D, are rapidly released into the extracellular matrix and participate in the degradation of organic bone matrix containing collagen fibrils near the tip of the ruffled border.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Age-related three-dimensional microarchitectural adaptations of subchondral bone tissues in guinea pig primary osteoarthrosis.

We explored potential mechanisms of the microarchitectural adaptations of subchondral bone tissues in a guinea pig primary osteoarthrosis (OA) model. We harvested proximal tibiae of male Dunkin-Hartley (Charles River strain) guinea pigs at 3, 6, 9, 12, and 24 months of age (10 in each group). These proximal tibiae were scanned by micro-computed tomography to quantify the three-dimensional microarchitecture of the subchondral plate, cancellous bone, and cortical bone. Subsequently, the bones were compression-tested to determine their mechanical properties. Furthermore, bone collagen, bone mineral, and bone density were determined. Mankin's score corresponded to OA grading from absent or minimal cartilage degeneration in 3-month-old to severe degeneration in 24-month-old guinea pigs. In young guinea pigs, the volume fraction and thickness of the subchondral plate markedly increased from 3 to 6 months, whereas the volume fraction of the subchondral cancellous bone displayed an initial decline followed by an increase. With age, the trabeculae increased in thickness, changed from rod-like to plate-like, and became more axially oriented. An increasing ratio of bone collagen to mineral in subchondral bone indicated undermineralized bone tissues. In subchondral cancellous bone, Young's modulus was maximal at 6 months of age, whereas ultimate stress and failure energy showed a gradual increase with age. The findings show pronounced alterations of the microarchitecture and bone matrix composition of the subchondral bone. These alterations did not appear to follow the same pattern as in normal aging and may have different influences on the resulting mechanical properties.

Aging↗
PubMed2006

Arterial calcification in mice after freeze-thaw injury.

Vascular calcification is highly correlated with atherosclerosis and cardiovascular disease and is a significant predictor of cardiovascular morbidity and mortality. Studies in mice indicate a genetic contribution to this dystrophic extra osseous calcification. We sought to elaborate a method to induce dystrophic arterial calcification in mice and further examine the pathogenetical mechanisms involved in the phenotype. We established a method of freeze-thaw injury of the infrarenal aorta producing a limited tissue necrosis and histologically investigated the occurrence of dystrophic calcification within the aortic wall 1, 3 and 7 days after injury in C57BL/6 (a mouse strain shown to be resistant to dystrophic cardiac calcification after injury) and C3H/He (susceptible to dystrophic cardiac calcification). C57BL/6 mice exhibited no dystrophic calcification at all within the vessel wall upon injury of the infrarenal aorta (0/5 mice 1 day after injury and 0/10 animals 7 days after injury). By contrast C3H/He mice displayed a remarkable extent of calcification mainly present within the media of the infrarenal aorta which was evident as early as 24 h (three out of five animals 1 day after injury) and reached its maximum extent 7 days after injury (10 out of 10 animals at the seventh postoperative day, p<0.001 compared to C57BL/6 mice). Upon immuno-histological analysis calcification was accompanied by the occurrence of certain bone-matrix associated proteins. Osteopontin and Bone Morphogenetic Protein 2/4 expression was detected co-localized with the calcified lesions. Our results demonstrate that freeze-thaw injury of the infrarenal aorta is a sufficient method to induce dystrophic arterial calcification in mice. We present evidence that the occurrence of arterial calcification in C3H/He mice seems to be actively regulated by certain bone-matrix associated proteins.

Animals↗
PubMed1994

Long-term changes in the haversian systems following high-dose irradiation. An ultrastructural and quantitative histomorphological study.

The effects of high-dose irradiation on the morphology of haversian bone were studied, over a fifty-two-week period, in seventy-seven adult rabbits, after the administration of a single dose of radiation (therapeutic x-ray; twenty-five, fifty, or 100 gray) to one knee joint. The specimens of bone were examined with microangiography, light and transmission electron microscopy, and histomorphometry. Analysis was performed on the haversian bone in the subchondral bone plate of weight-bearing portions of the femoral condyles. Microangiography demonstrated dilatation of the microvasculature four weeks after irradiation. Beginning at twelve weeks, there was a marked decrease in vascularity; no obvious recovery of the subchondral bone had occurred by fifty-two weeks. At four weeks, morphological analysis revealed two changes in the haversian canals: simple occlusion of the haversian vessels with loss of cells in the canal, and dilatation of the capillaries with abnormal resorption of the perivascular bone matrix by osteoclasts. The abnormal bone resorption was not coupled with subsequent new-bone formation, resulting in increased porosity. Beginning at four weeks, a progressive decrease in the number of haversian vessels and in cellularity became prominent. The decrease in cellularity involved all types of cells, including endothelial cells, pericytes, perivascular mesenchymal cells, osteoblasts, osteocytes, and osteoclasts. The loss of perivascular cells was often but not always associated with occlusion of the haversian vessels. Histomorphometry revealed both time-dependent and dose-dependent decreases in capillary density (the number of intraosseous capillaries per unit area) and in the number of osteocytes in the subchondral bone plate. The porosity of the same areas showed a significant increase by four weeks (p < 0.001 after administration of twenty-five gray and p < 0.01 after administration of both fifty and 100 gray), but between twelve and fifty-two weeks, there was only a slight additional increase. Statistical analysis revealed significant correlations between capillary density and osteocyte survival (p < 0.001) and between capillary density and porosity (p < 0.001). The portion of the subchondral bone plate that was located farthest from the non-irradiated normal bone showed progressive damage and no sign of recovery at fifty-two weeks.

Animals↗
PubMed2003

The effect of allomatrix injectable putty on the outcome of long bone applications.

Long bone defects due to nonunion or surgical excision of benign bone tumors result in areas that require rapid regeneration of local bone. This clinical and radiographic article details the results of a commercially prepared allograft demineralized bone matrix in patients with long bone voids or gaps. Of the 76 patients included for study, 41 (54%) patients were undergoing surgical intervention for removal of benign tumors or space-occupying lesions and 35 (46%) patients had long bone nonunions. AlloMatrix Injectable Putty (Wright Medical Technology, Inc, Arlington, Tenn) was used alone in 74 (97%) patients and in combination with bone marrow aspirate in two (3%) patients with tibial nonunion. Adjunctive strut allografts were used in three patients with humeral nonunion. The average time to follow-up for the combined population was 7 months (nonunion group 6 months; benign tumor group 7 months). At the most recent follow-up, radiographic evidence of the average percent of bone healing was 85.1% for the nonunion patient group and 93% for the benign tumor patient group. From this study, AlloMatrix Injectable Putty used as a bone void filler in long bone nonunions and benign tumors shows results equal to those historically reported for autograft and other materials.

Adolescent↗
PubMed2005

Healing of a critical-sized defect in the rat femur with use of a vascularized periosteal flap, a biodegradable matrix, and bone morphogenetic protein.

BACKGROUND: The purpose of this study was to evaluate the osseous healing of a critical-sized femoral defect in a rat model with use of recombinant human bone morphogenetic protein-2 (rhBMP-2), a matrix fabricated of D,D-L,L-polylactic and hyaluronan acid (OPLA-HY), and a vascularized periosteal flap. METHODS: The carrier matrix OPLA-HY with or without rhBMP-2 was implanted in a 1-cm-long femoral defect and secured with a plate and screws. In some groups, a vascularized periosteal flap was harvested from the medial surface of the tibia. In group 1, the femoral defects in the animals were filled with the OPLA-HY matrix alone; in group 2, the OPLA-HY matrix was covered by the vascularized periosteal flap; in group 3, 20 mug of rhBMP-2 was added to the OPLA-HY matrix; and in group 4, the femoral defect containing the OPLA-HY matrix and 20 mug of rhBMP-2 was wrapped circumferentially by the vascularized periosteal flap. The presence and density of new bone formation in the femoral defect were evaluated radiographically, histologically, and with histomorphometry at four and eight weeks postoperatively. RESULTS: Groups 1 and 2, which were not treated with rhBMP-2, showed no radiographic or histologic evidence of mature bone formation at four or eight weeks. Both groups 3 and 4, which were treated with rhBMP-2, demonstrated excellent bone formation. However, with the periosteal flap, group 4 demonstrated more bone formation on histomorphometric analysis at eight weeks (43.1%) than did group 3 (28.3%) (p < 0.01). Additionally, heterotopic bone formed outside the boundaries of the defect in eight of the fifteen animals in group 3, which had no periosteal flap. CONCLUSIONS: Bone-tissue engineering with use of the OPLA-HY matrix and rhBMP-2 produced good bone formation in the rat femoral defect model. However, the addition of a vascularized periosteal flap significantly increased bone formation within the boundaries of the defect and prevented heterotopic ossification.

Animals↗
PubMed1997

Producing vascularized bone by heterotopic bone induction and guided tissue regeneration: a silicone membrane-isolated latissimus dorsi island flap in a rat model.

Transformation of mesenchymal-type tissue into cartilage and bone can be induced by bone morphogenetic protein, and by its parent substratum, demineralized bone matrix. The authors were interested in transforming muscle island flaps into vascularized bone that could be used as autogeneic skeletal replacement parts. In Wistar rats, tubular latissimus dorsi muscle island flaps were created, using microsurgical techniques. The flaps were inserted by a cylinder of demineralized bone matrix (DBM) and enclosed in silicone rubber membrane tubes. The animals were followed-up for 10, 21, or 35 days. Rats with DBM implanted in muscle pouches served as controls. Quantitative radiomorphometry and qualitative histology were performed. A statistically significant linear time-related increase in radiomorphometrically-measured calcified tissue was found in the flaps with DBM from 10 days to 5 weeks. At 3 and 5 weeks, lamellar and cancellous bone with fully developed marrow was detected microscopically. There was no significant difference in bone quantity in the island flaps after 35 days, compared with the muscle pouches implanted with DBM, although the difference at 21 days was still significantly in favor of the island flaps. Using allogeneic DBM in rat muscle island flaps surrounded with a silicone membrane, it was possible to generate in vivo autogenous new bone with a good vascular supply and good mobility, allowing later transfer to another site. The experiment provided a basic technique that can be used as a standard in testing various osteoinductive substances for the production of vascular-pedicled new bone.

Animals↗
PubMed1999

Bone extracellular matrix stimulates invasiveness of estrogen-responsive human mammary MCF-7 cells.

Bone is the most frequent site of metastasis in breast cancer. This causes destructive osteolytic lesions. To achieve metastasis to bone, breast cancer cells must proliferate in a new microenvironment, arrest on extracellular matrix and invade. Breast cancer cells progress in the invasive processes only if they destroy bone with the assistance of osteoclasts. In this work, we present data suggesting that MCF-7 cells, an estradiol receptor-positive cell line that exhibits modest invasive capacity, proliferate in the presence of soluble factors secreted by the osteogenic cell line SaOS-2. The cells acquire a more aggressive phenotype when cultured on an extracellular matrix produced by the same osseous cell line. Acquisition of the invasive phenotype appears to be related to the capacity of bone extracellular matrix to induce the expression of urokinase-like plasminogen activator by MCF-7 cells, which is specific for MCF-7 cells, given that MDA-231 cells, an estradiol receptor-negative and more aggressive cell line, did not show significant changes when cultured in the presence of soluble and insoluble bone factors.

Bone Neoplasms↗
PubMed1993

Tumor necrosis factors alpha and beta can stimulate bone resorption in cultured mouse calvariae by a prostaglandin-independent mechanism.

Human recombinant tumor necrosis factors alpha and beta (TNF-alpha and TNF-beta), at and above 1 ng/ml (approximately equal to 70 pM), caused a dose- and time-dependent enhancement of 45Ca release from neonatal mouse calvarial bones in vitro. In addition, TNF-alpha and TNF-beta (3-100 ng/ml) caused a dose-dependent stimulation of prostaglandin E2 (PGE2) formation in the calvarial bones. TNF-alpha also enhanced the biosynthesis of PGI2, as assessed by analysis of the stable breakdown product 6-keto-PGF1 alpha. The stimulatory actions of TNF-alpha and TNF-beta on PGE2 formation was maximal at 12 h. Indomethacin, flurbiprofen, and meclofenamic acid, three structurally unrelated nonsteroidal antiinflammatory drugs, abolished PGE2 biosynthesis induced by TNF-alpha and TNF-beta (100 ng/ml). The 45Ca release stimulated by TNF-alpha and TNF-beta (100 ng/ml), however, was only slightly reduced by indomethacin, flurbiprofen, and meclofenamic acid. The partial inhibitory effect of indomethacin on 45Ca release was seen over a wide range of TNF-alpha concentrations, without affecting the concentration producing half-maximal stimulatory response. TNF-alpha and TNF-beta (100 ng/ml) stimulated bone matrix breakdown, as assessed by analysis of the release of 3H from bone prelabeled with [3H]proline. Also, the stimulatory effect of TNF-alpha and TNF-beta on bone matrix degradation was partially reduced by indomethacin. Hydrocortisone (1 microM) and dexamethasone (0.1 microM) abolished TNF-alpha- and TNF-beta-induced production of PGE2. In contrast to the cyclooxygenase inhibitors, the corticosteroids did not affect the stimulatory action by the cytokines on 45Ca release.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1981

A mixed packing model for bone collagen.

A wide variety of physical properties, including sonic velocity, dimensional changes between wet and dried stages, anisotropy of the tissue properties, density, X-ray diffraction, differential microcalorimetry, dielectric constant, and composition (water, mineral, organic content) for the mineralized and demineralized tissue was used to develop a model for the superlattice structure of bone collagen. A mixed model is suggested where the collagen molecules are in register as in SLS type of aggregation within the microfibril, and the microfibrils are staggered in D unit steps according to the Hodge-Petruska scheme. A square packing model with 4 or more molecules per microfibril best fits the HP scheme with the effective molecular diameter of the wet collagen molecule, and allows for the regular array of axial gap filling microcrystallites of 5 nm or larger diameter. It is concluded that: 1. Macroscopic dimensional changes of adult bovine bone matrix closely match molecular dimensional changes of collagen superlattice. 2. Effective molecular diameter of dry collagen is 1.09 nm and that of wet bone collagen is 1.42-1.45 nm. 3. Water layer of the wet bone collagen molecule is 0.16 nm thick. 4. Water in the bone collagen molecule is distributed in 5 regimes much like in the tendon collagen molecule. 5. "Hidden" water, 0.10 g water per dry collagen of regimes I and II, is within the triple helix. 6. "External" water incorporated in the collagen molecule provides transition between the highly structured collagen molecule and the intermolecular medium. 7. Water incorporated in the mineralized bone collagen molecule is less than in demineralized bone matrix. 8. For adult bovine cortical bone, 25% by volume is water, 32% dry organic, 43% mineral; 28% by volume of the mineral is axial gap filling, 58% radial intrafibrillar, and 14% radial extrafibrillar.

Animals↗
PubMed1987

Bone marrow matrix modulation of HL-60 phenotype.

The initiation and maintenance of cellular differentiation for a variety of cell types has been shown to be influenced by the microenvironment. To investigate the influence of bone marrow stroma on leukemic cell differentiation, HL-60 human promyelocytic leukemia cells were grown in the presence of Triton-treated extracellular matrix derived from normal human bone marrow stromal cells. This bone marrow matrix microenvironment had a dramatic impact on the phenotypic expression of this malignant line. HL-60 cellular proliferation, morphology, nonspecific esterase activity, formation of Fc rosettes, and sensitivity to induction by 12-O-tetradecanoyl-phorbol-13-acetate (TPA) were all influenced by the presence of matrix molecules. In contrast, stromal cell-conditioned media did not alter HL-60 phenotype. Thus, HL-60 cells appear to retain responsiveness to a human bone marrow stromal cell-derived matrix despite their ability to grow autonomously. Studies of the interaction of leukemic cells and marrow stroma in vitro may provide important information concerning the regulation of leukemic cell behavior.

Bone Marrow↗
PubMed2000

Higher osteoclastic demineralization and highly mineralized cement lines with osteocalcin deposition in a mandibular cortical bone of autosomal dominant osteopetrosis type II: ultrastructural and undecalcified histological investigations.

In this study we report on histological and ultrastructural investigations of the mandibular cortical bone in a case of autosomal dominant osteopetrosis type II complicated by mandibular osteomyelitis. Histologically, there was a marked increase in the number and size of osteoclasts on the inner bone surface. An undecalcified preparation showed a pair of deeply stained (highly demineralized) and stain-phobic (highly mineralized) layers on the bone surface just beneath the osteoclasts. The layers were incorporated into the bone matrix during the remodeling process as thickened cement lines. A contact microradiogram of the cortical bone revealed highly mineralized layers at the cement lines, which were closely correlated with immunohistochemical evidence of deposition of osteocalcin at the thickened cement lines. Ultrastructural examination showed that the osteoclasts had a typical clear zone, but they were deficient in ruffled border formation and had numerous lysosomal vacuoles containing dense substances. An electron-dense amorphous material layer was present on the bone surface just beneath the osteoclasts as well as at the cement lines. The layer was partly composed of a short fibrillar material, and it partially revealed the lamellar structure. Consequently, an osteoclastic malfunction might be primarily involved in the process of bone matrix resorption rather than demineralization, resulting in higher demineralization and abnormal material deposition on the bone surface and at the cement lines. Furthermore, evidence of active osteoclastic bone resorption with a brush border formation at the bone involved in the inflammatory lesion in this case suggests that the osteoclastic malfunction is influenced and recovered by a microenvironment such as inflammatory cytokines.

Bone Density↗
PubMed1983

Proteoglycan synthesis by skeletal muscle undergoing bone matrix-directed transformation into cartilage in vitro.

Myoblasts and fibroblasts of embryonic skeletal muscle reproducibly form chondrocytes when cultured on demineralized bone in vitro. The transformation occurs in 3 morphologically defined phases, with disappearance of the myoblast phenotype preceding the appearance of fibroblast-like cells and finally chondrocytes. Proteoglycan synthesis in these cultures was investigated by labeling at prechondrogenic (5 days) and postchondrogenic (6-12 days) stages with (35S)sulfate and [6-3H]glucosamine. Labeled material elutes from associative Sepharose CL-2B columns as two major included peaks, which correspond to proteoglycan monomer and a material of lower molecular size. Control cultures, cultured upon gels of type I collagen, fail to synthesize monomer-like material and contain solely a material of lower molecular size. Demineralized bone-derived monomer was rechromatographed under dissociative conditions in an attempt to detect the presence of small aggregates. Again, only a single peak of sulfate and glucosamine-labeled material appears. The data further show that the monomer resembles that of embryonic cartilage in glycosaminoglycan chain size (Mr = 8.6-12.2 X 10(3] and composition (mainly chondroitin 4-sulfate). Aggregated monomer forms a shoulder of the monomeric peak and comprises only 5% of the sulfated material. Fifteen to thirty-four per cent of the monomer elutes as aggregate after addition of rooster comb hyaluronic acid (HA). Failure to aggregate appears to be related to endogenous synthesis of short chain HA. Synthesis of long chain HA may constitute a rate-limiting step in chondrogenesis. Material of lower molecular size, from cultures grown on demineralized bone, bind to exogenous HA, whereas the elution pattern of sulfated material from control cultures remains essentially unchanged. These latter data suggest that proteoglycans of low hydrodynamic size may participate in the early formation of proteoglycan aggregate.

Animals↗
PubMed1996

Healing of a tibial double osteotomy is modified by clodronate administration.

We studied the healing of tibial double osteotomies in rats during clodronate administration 10 mg/kg daily subcutaneously for 6 weeks. Clodronate treatment did not inhibit the endochondral bone formation in callus or in the epiphyseal plate. The differentiation of osteoblasts into mature osteocytes was disturbed, and the bone structure around the osteocytes was not normal. In the clodronate-treated group, the amount of newly formed bone matrix seemed increased, but mineralization of the bone matrix was delayed. The bundle bone trabeculae in callus were not so spatially well organized as in the controls. No delay in the union of the bone segment by new bone was seen during clodronate administration.

Administration, Cutaneous↗
PubMed2006

Effect of recombinant human tissue inhibitor of matrix metalloproteinase-1 in rabbit mandibular distraction osteogenesis: a histological and immunohistochemical study.

BACKGROUND: Bone matrix metalloproteinases are capable of degrading bone matrix during the remodelling, and their degradation activities can be down regulated by the tissue inhibitors of matrix metalloproteinases. This study evaluated the influence of exogenous tissue inhibitor of matrix metalloproteinase-1 on the expression of matrix metalloproteinases and endogenous tissue inhibitor of matrix metalloproteinases in mandibular distraction osteogenesis. MATERIAL AND METHODS: Fifteen New Zealand white rabbits were assigned to three groups: a negative control; a sham control group implanted with a collagen sheet; and an experimental group implanted with recombinant human tissue inhibitor of matrix metalloproteinase-1 impregnated in a collagen sheet. Rabbits were sacrificed at 6 weeks, 12 weeks and 24 weeks of consolidation. RESULTS: Major expression of matrix metalloproteinases and tissue inhibitors of matrix metalloproteinases was observed at the early stage of consolidation, only positive signals of tissue inhibitors of matrix metalloproteinases were observed at 24 weeks. The addition of recombinant human tissue inhibitor of matrix metalloproteinases-1 did not affect bone maturation and remodelling. CONCLUSIONS: An equilibrium of bone formation and resorption was reached at 24 weeks of consolidation in the rabbit mandible. No obvious influence of recombinant human tissue inhibitor of matrix metalloproteinase-1 on bone remodelling of mandibular distraction osteogenesis was noted.

Animals↗
PubMed1993

Ultrastructural immunolocalization of noncollagenous (osteopontin and osteocalcin) and plasma (albumin and alpha 2HS-glycoprotein) proteins in rat bone.

The high-resolution, postembedding protein A-gold immunocytochemical technique was used to visualize the distribution of two noncollagenous bone proteins, osteopontin (OPN) and osteocalcin (OC), and two plasma proteins, alpha 2HS-glycoprotein (alpha 2HS-GP) and albumin (ALB), in sections of Lowicryl K4M-embedded rat tibial and alveolar bone. In the primary spongiosa of the metaphysis, a seam of organic material (lamina limitans) that labeled intensely with OPN and OC antibodies was observed at the bone/calcified cartilage interface just below the zone of vascular invasion of the growth plate. With deposition of bone matrix proper by osteoblasts in this region and its subsequent mineralization, extensive areas of bone were heavily labeled with anti-OPN, anti-OC, and anti-alpha 2HS-GP antibodies, where the majority of gold particles were associated with amorphous, electron-dense patches of organic material throughout the mineralized bone. In the unmineralized osteoid, substantially less labeling was observed, and where occasional mineralization loci were dispersed throughout the osteoid layer, these sometimes showed a concentration of gold particles. ALB labeling, on the other hand, was moderate and generally diffuse throughout the mineralized bone matrix and the osteoid. In alveolar bone, labeling patterns were generally similar to those found in tibial bone. Particularly striking in alveolar bone, however, was an intense anti-OPN labeling of (1) the lamina limitans at cell-lined bone surfaces, including that surrounding cell processes and osteocytes, (2) cement (reversal, resting) lines, and (3) the perilacumar matrix of some osteocytes. In summary, these data suggest that certain plasma proteins, such as alpha 2HS-GP, interact with bone matrix proteins, such as OPN and OC, at sites of tissue mineralization and that the presence of OPN in mineralized bone and at bone surfaces (lamina limitans) and cement lines has a multifunctional role, including regulation of mineralization and mediation of cell dynamics during endochondral and intramembranous bone modeling and remodeling.

Animals↗
PubMed1991

Bone morphogenetic protein: a review.

The osteogenic potential of bone and bone matrix has been characterised only by its biological effects and the parameters influencing it. Recently, the osteoinductive ability of bone matrix had been defined chemically by the description of a bone morphogenetic protein (BMP), and the parameters of osteogenic factors from different species have now been recognised. The current state of isolation, purification and characterisation of these factors is summarised in this review. General aspects of the isolation and testing of BMP preparations, and the results of orthotopic application of BMP implants, including clinical cases, are reported.

Animals↗