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PubMed1996

Bone sialoprotein stimulates in vitro bone resorption.

Bone sialoprotein (BSP) is a protein highly specific for bone, which contains an arginine-glycine-aspartic acid (RGD) cell attachment sequence involved in osteoclast adhesion to bone matrix via the vitronectin receptor. We have investigated its role in in vitro bone resorption using the well described isolated osteoclast resorption pit assay. BSP significantly stimulates bone resorption in a dose-dependent manner, increasing the overall resorbed area on ivory slices and the number of lacunae at concentrations as low as 50 nM. Neither recombinant osteopontin nor intact vitronectin has any effect on bone resorption, suggesting a specific effect of BSP. The stimulation of bone resorption induced by BSP could be partially explained by an increase in osteoclast adhesion to bone via its RGD sequence, and our results suggest another mechanism of action of BSP that might involve another region of the molecule, such as its acidic sequences. Although BSP stimulates bone resorption in a coculture system of bone marrow cells and osteoblastic cells, it dose dependently inhibits the formation of osteoclast-like cells at equivalent concentrations in this culture model. In conclusion, we provide evidence that BSP plays an important role in the bone resorption process and may regulate bone resorption as well as osteoclast formation.

Animals↗
PubMed2001

Alveolar ridge augmentation with rhBMP-2 and bone-to-implant contact in induced bone.

The objective of this study was to examine alveolar ridge augmentation following implantation of recombinant human bone morphogenetic protein (rhBMP-2) with an allogeneic freeze-dried demineralized bone matrix (DBM) mixed with autologous blood. A second objective was to evaluate bone-to-implant contact in induced bone. Bilateral surgically created supraalveolar ridge defects in five young adult beagle dogs were implanted with the rhBMP-2-DBM-blood device. Transmucosal dental implants were placed at weeks 8 and 16 postsurgery The animals were euthanized 24 weeks following ridge augmentation. Healing was uneventful in all animals. Radiographic observations indicated substantial bone formation, including regions of radiolucency, at week 8. At week 16, the radiolucencies were generally resolved, and the trabecular structure of the induced bone resembled that of the adjacent residual bone. There were no remarkable differences in radiographic observations between weeks 16 and 24 after ridge augmentation. Histologic analysis revealed dense woven and lamellar induced bone. Any residual DBM appeared remineralized, at least in part. A large portion of the dental implants (approximately 70%) were housed in induced bone with evidence of limited crestal resorption. There was no significant difference in bone density between induced and residual bone, and the levels of bone-to-implant contact were similar (approximately 55%). The rhBMP-2 construct used in this study has a potential to augment alveolar ridge defects. Also, no difference in levels of osseointegration may be expected in induced and residual bone following a two-stage procedure of rhBMP-2-induced ridge augmentation and dental implant placement.

Alveolar Process↗
PubMed1990

[Application possibilities of human bone-collagen substance as a transplant in skeletal surgery].

We present first results of our clinical trial with a demineralized-bone-matrix (DBM) not only as a transplant to fill up a defect of bone but above all to induce local osteogenesis. Indications and practical applications of the material of transplants are described. By help of the clinical progresses and the reports of laboratory examinations the biological compatibility is regarded in this paper. Roentgen morphologically fine structures of the transplants and their transplant beds are described in serial roentgenography and used as evaluation of processes of transformation and building in of bones. The in a relative good time appearing markings of trajectories of the fine structures in the sphere of the transplant as a sign of accelerated regeneration of "organic bony substance" allows the expectation on being released osteogenetic potencies by DBM for the induction of local bone regeneration.

Acetabulum↗
PubMed2006

In vitro ossification and remodeling of mineralized collagen I scaffolds.

A promising strategy of bone tissue engineering is to repair bone defects by implanting biodegradable scaffolds that can undergo remodeling and be replaced completely by autologous bone tissue. For this purpose, it is necessary to create scaffolds that can be degraded by osteoclasts and enable osteoblasts to build new mineralized bone matrix. In order to achieve this goal a new porous material has been developed using biomimetically mineralized collagen I. These scaffolds were co-cultured with osteoclast-like cells and osteoblasts in order to characterize the capacity of these cells to remodel the material in vitro. It was possible to show the development of biologically active osteoclast- like cells that were able to invade and degrade the scaffold. They degraded the scaffold by internalizing it as intracellular vesicles, thereby making room for osteoblasts to invade and build new bone matrix. In addition, it could be shown that osteoblasts proliferated, differentiated, and produced new mineralized extracellular matrix. Hence, it could be shown that co-culture of osteoclastlike cells and osteoblasts on biomimetically mineralized collagen I is a promising approach for bone tissue engineering. In addition, it can be applied to study the process of bone remodeling in vitro.

Animals↗
PubMed1972

Collagen heterogeneity within different growth regions of long bones of rachitic and non-rachitic chicks.

The different anatomical regions involved in osteogenesis in the chick long bone have been examined for heterogeneities in collagen structure that might relate to the mechanism of ossification. Experimentally induced lathyrism was employed to enhance collagen solubility, and vitamin D deficiency to allow accumulation of osteoid, the precursor of bone matrix. The extractable lathyritic collagens of the cartilaginous and osseous regions of growing long bones from rachitic and non-rachitic chicks were examined for alpha-chain type and amino acid composition. In both groups of animals the growth plate and cartilaginous regions of the epiphysis gave collagen molecules of the constitution [alpha1(II)](3), whereas the ossifying regions contained [alpha1(I)](2) alpha2. The degree of hydroxylation of the lysine moieties was increased by approximately 50% in the alpha1(I)-chain and alpha2-chain of rachitic bone collagen. Since uncalcified osteoid is greatly enriched in rachitic bone, it is concluded that the collagen of osteoid has the configuration [alpha1(I)](2) alpha2, similar to that of bone matrix, but has an elevated hydroxylysine content. The possible relationship of this difference to the mechanism of calcification is discussed.

Amino Acids↗
PubMed2005

The effect of IL-1alpha on the expression of matrix metalloproteinases, plasminogen activators, and their inhibitors in osteoblastic ROS 17/2.8 cells.

Interleukin-1 (IL-1) plays key roles in altering bone matrix turnover. This turnover is regulated by matrix metalloproteinases (MMPs), tissue inhibitor of matrix metalloproteinases (TIMPs), and the plasminogen activation system, including tissue-type plasminogen activator (tPA), urokinase-type plasminogen activator (uPA) , and plasminogen activator inhibitor type-1 (PAI-1). In this study, we examined the effect of IL-1alpha on the expression of the MMPs, TIMPs, tPA, uPA, and PAI-1 genes in osteoblasts derived from the rat osteosarcoma cell line ROS 17/2.8. The cells were cultured in alpha-minimum essential medium containing 10% fetal bovine serum with 0 or 100 U/ml of IL-1alpha for up to 14 days. The levels of MMPs, TIMPs, uPA, tPA, and PAI-1 expression were estimated by determining the mRNA levels using real-time RT-PCR and by determining protein levels using ELISA. In IL-1alpha cultures, the expression levels of MMP-1, -2, -3, -13, and -14 exceeded that of the control through day 14 of culture, and the expression of MMPs increased markedly from the proliferative to the later stages of culture. The TIMP-1, -2, and -3 expression levels increased from the initial to the proliferative stages of culture. The expression of tPA increased greatly during the proliferative stage of culture, and uPA expression increased throughout the culture period, increasing markedly from the proliferative to the later stages of culture. In contrast, PAI-1 expression decreased in the presence of IL-1alpha through day 14. These results suggest that IL-1alpha stimulate bone matrix turnover by increasing MMPs, tPA, and uPA production and decreasing PAI-1 production by osteoblasts, and incline the turnover to the resolution.

Animals↗
PubMed2000

109Cd K x ray fluorescence measurements of tibial lead content in young adults exposed to lead in early childhood.

OBJECTIVES: Tibia lead measurements were performed in a population of 19-29 year old people who had been highly exposed to lead in childhood to find whether lead had persisted in the bone matrix until adulthood. METHODS: (109)Cd K x ray fluorescence was used to measure the tibia lead concentrations of 262 exposed subjects and 268 age and sex matched controls. Questionnaire data allowed a years of residence index to be calculated for exposed subjects. A cumulative blood lead index was calculated from the time weighted integration of available data of blood lead. RESULTS: The mean (SEM) difference between exposed and control men was 4.51 (0.35) micrograms Pb/g bone mineral, and between exposed and control women was 3.94 (0. 61) micrograms Pb/g bone mineral. Grouped mean bone lead concentrations of exposed subjects were predicted best by age. When exposed and control subjects' data were combined, grouped mean bone lead concentrations were predicted best by cumulative blood lead index. The years of residence index was neither a good predictor of bone lead concentrations for exposed subjects nor for exposed and control subjects combined. Finally, exposed subjects had increased current blood lead concentrations that correlated significantly with bone lead values. CONCLUSION: Bone lead concentrations of exposed subjects were significantly increased compared with those of control subjects. Lead from exposure in early childhood had persisted in the bone matrix until adulthood. Exposed subjects had increased blood lead concentrations compared with controls. Some of this exposure could be related to ongoing exposure. However, some of the increase in blood lead concentration in adult exposed subjects seemed to be a result of endogenous exposure from increased bone lead stores. The endogenous exposure relation found for men was consistent with reported data, but the relation found for women was significantly lower. Further research is needed to find whether the observed differences are due to sex, or pregnancy and lactation.

Adult↗
PubMedDate not supplied

Defect repair in the rat mandible with bone morphogenic proteins and marrow cells.

OBJECTIVE: To investigate the ability of a bone growth factor mixture and bone marrow cells to repair a critical size defect of the rat mandibular body. DESIGN: Prospective, randomized controlled trial. SUBJECTS: Thirty-seven male Fischer rats. INTERVENTIONS: Critical size defects 4 mm in diameter were created in the left mandibular bodies of the rats. The defects were filled with a bone marrow cell suspension (group 1), a synthetic bone matrix consisting of bovine collagen and calcium hydroxyapatite cement (group 2), the matrix and marrow cells (group 3), the matrix with 100 micro g of bone growth factor mixture (group 4), or the matrix with bone growth factor mixture and marrow cells (group 5). Animals were killed after 8 weeks, and the nondemineralized specimens were processed histologically. Specimens from group 1 were not processed because there was no grossly appreciable bone regeneration. Stereologic techniques were used to determine and compare the volume fractions and volume estimates of mature bone, new bone, osteoid, marrow, remaining cement, and fibrous tissue in each defect. RESULTS: Volumes of mature bone, new bone, and remaining cement did not differ significantly among the groups (P =.30 for mature bone, P =.17 for new bone, and P =.34 for cement). However, group 4 and 5 specimens contained significantly more osteoid and larger marrow spaces than did the group 2 and 3 specimens (P<.001 for both). The specimens in groups 2 and 3 contained significantly more fibrous tissue ingrowth than did those in groups 4 and 5 (P<.001). CONCLUSION: The synthetic bone substitute containing bone growth factor mixture was effective in stimulating new bone and osteoid development in the rat mandibular model.

Animals↗
PubMed2004

Osteoblasts and osteocytes express MMP2 and -8 and TIMP1, -2, and -3 along with extracellular matrix molecules during appositional bone formation.

Our previous studies suggested that a part of bone extracellular matrix (ECM) molecules are degraded and remodeled during embryonic bone formation. In contrast, little is known about ECM remodeling in postnatal appositional bone formation. The present study was designed to investigate expression of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) during experimentally initiated appositional bone formation in rats. Expressions of ECM molecules, MMPs, and TIMPs were examined using in situ hybridization. Osteoblasts and osteocytes expressed MMP2 and -8, TIMP1, -2, and -3, as well as type I collagen, osteopontin, and osteocalcin in the course of the appositional bone formation, while they showed few transcripts of MMP13. The results indicated that while osteoblasts and osteocytes in the apposed bone produce ECM molecules, they degrade ECM molecules with MMPs and regulate the degradation by inhibiting the activity of MMPs using TIMPs. Osteoblasts and osteocytes may reorganize the ECM composition to mature the bone matrix in appositional bone formation.

Animals↗
PubMed1999

Anorganic bovine bone supports osteoblastic cell attachment and proliferation.

BACKGROUND: It was the aim of these studies to examine the ability of an anorganic bovine bone matrix material as an alternative to autogenous bone grafts and demineralized cadaver bone to support the attachment, spreading, and proliferation of isolated osteoblastic cells. METHODS: Primary culture osteoblastic cells were isolated from neonatal rat calvaria by sequential collagenase digestion. In the attachment studies, cells which had been labeled with 3H-leucine were incubated with the matrix material in sterile microfuge tubes for 15, 90, or 180 minutes or 24 hours. The attached cells were released and the radioactivity measured by liquid scintillation spectrometry. In the proliferation experiments, the cells were cultured with the matrix material for 24 hours and 3H-thymidine was added during the last 2 hours of the incubation. The cells were released and the radioactivity measured by liquid scintillation spectrometry. Scanning electron microscopy (SEM) was employed to observe osteoblastic cell interaction with the anorganic bone matrix. In these studies the cells were seeded on the bone graft material, then the material was removed and processed for SEM after 30, 60 or 120 minutes, or 24 or 48 hours. RESULTS: The cells attached to the matrix material in a time-dependent manner. There were significantly (P<0.05) more cells attached after 180 minutes than after the 15 and 90 minute incubations. The matrix material also supported proliferation of the attached osteoblastic cells. Cells seeded onto 100 mg of anorganic bovine bone resulted in significantly (P<0.05) more measurable proliferation than cells seeded onto 10 mg of material. The cells appeared to be round as they attached, then flatten and spread over time. There was also evidence of cellular processes extending into the pores of the material. CONCLUSIONS: These results demonstrate that this anorganic bovine bone graft material is able to support the attachment and proliferation of osteoblastic cells.

Animals↗
PubMed1988

A monoclonal antibody against dentin phosphophoryn recognizes a bone protein(s) appearing at the beginning of ossification.

Decalcified and nondecalcified sections of fetal bovine tibia were stained immunohistochemically with a monoclonal antibody against dentin phosphophoryn. In the epiphyseal portion of the long bone, osteoblasts, osteocytes and the bone matrix were stained, but chondrocytes and the cartilage matrix were not. Similar staining was observed in the epiphyseal and diaphyseal portions of bones. These findings suggest that a protein(s) with the same epitope as phosphophoryn may be synthesized and secreted by osteoblasts at the beginning of ossification and may be involved in mineralization of bone tissue. On Western blots of proteins extracted from fetal bovine bone, the antibody reacted with two bands of molecular weights of about 71,000 and 63,000. These proteins and antibody(s) to the proteins may be useful for detection of the phenotype of osteogenesis.

Animals↗
PubMed1988

Biochemical differences between dystrophic calcification of cross-linked collagen implants and mineralization during bone induction.

Ectopic calcification of diseased tissues or around prosthetic implants can lead to serious disability. Therefore, calcification of implants of glutaraldehyde-cross-linked collagenous tissues and reconstituted collagen was compared with mineralization induced by demineralized bone matrix (DBM). Whereas implants of DBM accumulated large amounts of calcium and a bone-specific gamma-carboxyglutamic acid protein (BGP or osteocalcin) following implantation in both young and older rats, implants of cross-linked pericardium calcified with only traces of BGP. Glutaraldehyde-cross-linked DBM failed to calcify after implantation in 8-month-old rats for 2-16 weeks. Implants of cross-linked type I collagen exhibited small calcific deposits 2 weeks postimplantation but calcium content eventually dropped to levels equal to those of soft tissues as the implants were resorbed. The calcium content of DBM implanted in 1- and 8-month-old rats reached comparable levels after 4 weeks, but the BGP content was approximately twice as high in the younger animals than in the older ones. Glutaraldehyde-cross-linked implants of DBM, tendon, and cartilage calcified significantly in young but not in old animals. This form of dystrophic calcification was associated with only trace amounts of BGP. Alkaline phosphatase activity was high in implants of DBM and undetectable in implants of cross-linked collagenous tissues. These results show that implants of glutaraldehyde-cross-linked collagenous tissues and reconstituted collagen calcify to different extents depending upon their origin and the age of the host, and that the mechanism of dystrophic calcification differs significantly from the process of mineralization associated with bone induction as reflected by alkaline phosphatase activity and BGP accumulation.

Alkaline Phosphatase↗
PubMed2002

[Vascular calcification and bone-related factors].

Bone is consisted of bone matrix proteins produced by osteoblasts and minerals, Recently, it has been reported that bone-related factors are also involved in vascular calcification. Among bone matrix proteins, osteopontin and matrix Gla protein play important roles in vascular calcification. Regulatory factors for osteoblast differentiation (BMP) and osteoclast differentiation (osteoprotegerin) are also involved in vascular calcification.

English Abstract↗
PubMed1994

Assessment of bone remodeling using biochemical indicators of type I collagen synthesis and degradation: relation to calcium kinetics.

In this study, we investigated the relation between calcium kinetic indices of bone remodeling (resorption rate, r; and formation rate, m, respectively) and two serum markers of type I collagen turnover: the pyridinoline cross-linked carboxyterminal telopeptide domains of type I collagen (S-ICTP a marker of bone matrix degradation) and the carboxyterminal propeptide of human type I procollagen (S-PICP, a marker of bone matrix formation). We studied three groups: (i) healthy controls (n = 19), (ii) a mixed group of high and low-turnover bone diseases without mineralization defects (myxedema, thyrotoxicosis and primary hyperparathyroidism n = 38), and (iii) osteoporosis (n = 52). In healthy controls, a significant regression of S-PICP on m was obtained (R = 0.53, SEE/Y = 0.44, P < 0.02). Significant regressions were also demonstrable in high- and low-turnover bone disease (R = 0.50, P < 0.001), SEE/Y = 61%) and osteoporosis (R = 0.49, P < 0.001, SEE/Y = 50%). In controls the regression coefficient for the regression of S-ICTP on r was 0.19 (NS), in high and low turnover bone disease 0.66, (SEE/Y = 59%, P < 0.001) and in the osteoporotic group 0.40 (SEE/Y = 61%, P < 0.01). We conclude that S-PICP and S-ICTP reflect whole skeletal bone formation and resorption rates in a variety of metabolic bone diseases including osteoporosis.

Adolescent↗
PubMed1991

Osteogenin (bone morphogenetic protein-3) stimulates cartilage formation by chick limb bud cells in vitro.

Osteogenin is a protein isolated from demineralized bovine bone matrix. When implanted in rats, osteogenin induces the differentiation of cartilage and formation of endochondral bone. When added to stage 24 and 25 chick limb bud mesoderm cells in culture, it stimulated synthesis of sulfated proteoglycans by over 10-fold without stimulating cell division. The increase was detected after only 2 days in culture. Morphologically, in the presence of osteogenin, all cells in the culture appeared to form cartilage, rather than the nodules of cartilage surrounded by noncartilage areas in control cultures. The distribution of type II collagen correlated with the morphological differentiation of cartilage. When nonchondrocyte and chondrocyte cell populations were separated, osteogenin stimulated sulfated proteoglycan synthesis in all populations of cells. However, the greatest stimulation (24-fold) was seen in the originally nonchondrocyte population, which apparently still had some potential to form cartilage. In this study, chick limb bud mesoderm cells in vitro responded to osteogenin, a protein derived from adult bovine bone matrix. The cells that were responsive included those that initially did not form cartilage. Osteogenin belongs to a superfamily of proteins, many of which are important in development. It is possible that osteogenin has a role in embryonic cartilage development.

Alcian Blue↗
PubMed1990

Osteoinductive factor inhibits formation of human osteoclast-like cells.

Osteoinductive factor (OIF) is a glycoprotein in bone that induces ectopic bone formation. Implantation of OIF plus transforming growth factor beta (TGF-beta) type 1 or 2 into subcutaneous tissues of rats induces formation of bone at the implantation site. Since TGF-beta is also present in bone matrix and inhibits formation of multinucleated cells that express an osteoclast phenotype in long-term human marrow cultures, we tested the effects of OIF on formation of these osteoclast-like cells to determine the effects of OIF on cells in the osteoclast lineage. We found that OIF inhibited total multinucleated cell (MNC) formation in a dose-dependent fashion and preferentially inhibited formation of MNCs that react with monoclonal antibody 23c6 (23c6-positive MNCs), an antibody that identifies osteoclasts. In addition, low concentrations of OIF in combination with low concentrations of TGF-beta acted synergistically to inhibit 23c6-positive MNC formation. The inhibition of 23c6-positive MNC formation by OIF was not mediated by prostaglandin synthesis. These data suggest that regulatory growth factors, such as OIF or TGF-beta, that are stored within the bone matrix and released when bone is resorbed can serve as natural inhibitors of osteoclast activity by inhibiting osteoclast formation.

Alprostadil↗
PubMed2000

Healing of autogenous intramembranous bone in the presence and absence of homologous demineralized intramembranous bone.

This study was designed to examine the osteogenecity of demineralized bone matrix (DBM) prepared from intramembranous (IM) bone and to quantitatively assess the amount of new bone formed by IM autogenous bone grafts with or without DBM(IM). Forty-two defects were created in 42 New Zealand White rabbits. Twenty-one defects were grafted with IM bone alone, and the other 21 defects were grafted with composite IM-DBM(IM). Eleven rabbits, 22 defects were used as controls, where 11 defects were left empty (passive control) and the other 11 defects were filled with rabbit skin collagen (active control). Tissues were retrieved on days 1, 2, 3, 4, 5, 6, 7, and 14 for qualitative and quantitative analysis. Cells involved in the healing of composite IM and IM-DBM(IM) bone grafts were identified. No cartilage cells were detected during the healing of either grafts. Appearance of small blood vessels into the newly formed matrix was seen on day 5 in IM bone grafts and on day 4 in composite IM-DBM(IM) bone graft. Quantitative analysis was performed by means of image analysis on 100 sections of tissues retrieved after 14 days. Approximately 204% more new bone was formed in defects grafted with composite IM-DBM(IM) than in those grafted with IM bone alone (P <.0001). No bone was formed across the defects in either active or passive controls. In conclusion, DBM(IM) significantly increases the osteogenicity of IM bone grafts.

Analysis of Variance↗
PubMed2005

Treatment of segmental bone defects in rats by the stimulation of bone marrow osteo-progenitor cells with prostaglandin E2.

An alternative to bone grafting is engineered osteo-conductive material that carries osteo-progenitor cells with osteo-stimulant factors impregnated on a malleable osteo-conductive material. We used bone marrow stem cells as the source of osteo-progenitor cells and stimulated them with prostaglandin E2 using demineralised bone matrix as a carrier. We treated 35 skeletally mature male Wistar albino rats with segmentary radial bone defects using five different treatment groups. Group I received no treatment; the remaining four groups all received a mixture of bone marrow and demineralised bone matrix. In group III, a copolymer was added. In group IV, prostaglandin E2 and in group V prostaglandin E2 within a copolymer was added to the mixture. Eight weeks after the surgical procedure, the rats were sacrificed. Radiological and histological evaluation of the radial bone showed that while there was no significant healing in groups I, II and III, there was a significant healing response in groups IV and V.

Animals↗