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PubMed2002

Modulated bone matrix-related gene expression is associated with differences in interfacial strength of different implant surface roughness.

PURPOSE: The objective of this study was to examine the effect of implant surface topography on biomechanical strength and expression patterns of bone extracellular matrix (ECM)-related genes during implant healing. MATERIALS AND METHODS: Cylinder implants with turned or dual acid-etched (DE) surface were placed into the femurs of female Sprague-Dawley rats. At 2 and 4 weeks after the implantation, the implant push-in test was performed to measure the load-bearing strength of the bone-tissue interface. T-shaped hollow implants were separately placed and the total RNA was extracted from the ingrown tissue within the hollow chamber. The RNA was subjected to reverse transcriptase polymerase chain reaction to analyze the expression pattern of selected bone extracellular matrix-related genes. RESULTS: The push-in value of the DE implant is approximately 300% greater than that of the turned implant at weeks 2 and 4 (p=.0090). The expression of collagen II, osteocalcin and biglycan was higher in the week 2 DE implant group than the turned implant group. At week 4 the expression of collagen II and IX was 7- and 26-fold, respectively, greater in the DE implant group than in the turned implant group. CONCLUSIONS: The surface topography of implants may induce the phenotypic alteration of wound healing cells. The increased interfacial strength of the DE implant may be associated with the modulated expression of the selected set of bone extracellular matrix genes.

Acid Etching, Dental↗
PubMed1983

In vitro induction of cartilage-specific macromolecules by a bone extract.

An in vitro system has been developed to study the onset of chondrogenesis. Embryonic rat muscle mesenchymal cells, when treated in suspension culture with an extract of bovine bone matrix, synthesized cartilage-specific proteoglycan and type II collagen. The synthesis of these two macromolecules was assayed by the enzyme-linked immunosorbent assay inhibition technique. Further evidence of chondrogenesis was demonstrated by morphological changes of treated cells when cultured in firm agarose and stained for metachromatic matrix. Even with crude bone matrix extracts, the assay was sensitive at the microgram level and significant differences in cartilage macromolecules compared with controls were observed in 2-3 d. In vivo the same extract induced first cartilage and then bone.

Animals↗
PubMed1984

Bone resorption in osteogenic sarcoma--II. Resorption of the bone collagenous matrix by tumor cells, normal fibroblasts and macrophages.

Three osteogenic sarcoma cell lines of human and canine origin were compared to normal fibroblastic cells and peptone-induced murine peritoneal macrophages in terms of bone collagenous matrix (BCM) resorption capacity. The dissolution of the BCM was measured in an in vitro system consisting of the tested cells and live or killed [3H]-proline-labeled fetal mouse long bones. Experiments with osteogenic sarcoma cells revealed a paradoxical phenomenon indicating an inverse relationship between the number of tumor cells and the rate of collagen resorption from live bones. On the other hand, collagen matrix of devitalized bones, particularly those denatured by exposure to heat, is strongly resorbed by osteogenic sarcoma cells even in the presence of serum. Contrary to osteogenic sarcoma cells, normal fibroblasts do not resorb collagen from either live or killed bones, regardless of the devitalization method and culture conditions utilized. Macrophages resorb collagenous matrix from live bones, but their collagen resorption activity from devitalized bones depends greatly on choice of the incubation condition. Results have shown that osteogenic sarcoma tumor cells, when acting alone, may not have the capacity to destroy healthy bone. We suggest, therefore, that bone destruction seen in osteogenic sarcoma patients depends on the metabolic condition of the affected bone, and the interaction between the tumor and normal host cells and tissues.

Animals↗
PubMed2005

Microcracks in cortical bone: how do they affect bone biology?

Microcrack accumulation in cortical bone has been implicated in skeletal fragility and stress fractures. These cracks have also been shown to affect the mechanical and material properties of cortical bone. Their growth has been linked to osteocyte apoptosis and the initiation of the remodeling process, which also has a role in their repair. Clinically, osteoporosis is diagnosed using dual energy x-ray absorptiometry. However, evidence now indicates that bone mass alone is insufficient to satisfactorily explain the skeletal fragility of osteoporosis and consideration needs to be given to bone quality in the diagnosis and treatment of the disease. Bone quality includes parameters such as trabecular and cortical microarchitecture, morphology, bone turnover, degree of mineralization of the bone matrix, and significantly, the amount of microdamage present in the bone. Current clinical treatments concentrate on the inhibition of osteoclast activity to maintain bone mass in osteoporotic patients. However, these cells have a major role in removing existing microcracks from the bone matrix, and hence the use of bone resorption- inhibiting drugs may lead to insufficient bone repair and therefore an increase in microdamage accumulation and loss of bone quality.

Animals↗
PubMed1994

Tissue segregation enhances calvarial osteogenesis in adult primates.

Calvarial defects of adult mammals have a limited potential for regeneration. Osteogenesis may be impaired by the intrusion within the defect of nonosteogenic tissues during healing, which inhibits centripetal bone deposition from the margins of the defects. Using a primate model, we evaluated bone regeneration in calvarial defects treated with demineralized bone matrix versus defects treated according to the strategy of guided tissue regeneration. Sixty-four defects, 25 mm in diameter, were prepared in 16 adult male baboons (Papio ursinus). In each animal, 2 contralateral defects were covered with a template of porous polymer, 35 mm in diameter. Templates were positioned over the calvarial margins to prevent penetration of the pericranium and the temporalis muscle within the defects, thus maintaining tissue segregation during healing. The third defect was implanted with allogeneic demineralized bone matrix, as positive control. The fourth defect was left untreated and was used as negative control. Undecalcified bone sections (7 microns thick) were prepared from the harvested specimens 3 and 6 months after surgery. Although untreated defects showed limited osteogenesis after fusion of the pericranium with the dura, defects covered with the polymeric template often showed extensive bone deposition extending centripetally from the margins of the craniotomies. Histomorphometry demonstrated that defects treated with demineralized bone matrix and defects covered with the polymeric template had greater amounts of bone and osteoid when compared with untreated defects (p < 0.01). At 6 months, greater amounts of bone formed in demineralized bone matrix-treated defects when compared with defects covered with the polymeric template (p < 0.01). The results of this study show that calvarial membranous bones of adult primates retain the potential to regenerate when segregation between the different tissue components participating in the healing of the wound is maintained. In the same model, however, implantation of allogeneic demineralized bone matrix, used as a positive control provided the most effective treatment for the defects.

Age Factors↗
PubMed1983

Panostotic fibrous dysplasia: a congenital disorder of bone with unusual facial appearance, bone fragility, hyperphosphatasemia, and hypophosphatemia.

We report a boy with unusual facial appearance, melanotic patches ("coast-of-Maine" type), myelofibrosis, recurrent femoral fractures, and widespread fibrous dysplasia of bone. Biochemical findings included raised serum alkaline phosphatase (bone isozyme) and 1,25-(OH)2 vitamin D, and low serum phosphorus levels. Elevated urinary excretion rates of total hydroxyproline, glycylproline, and gamma-carboxyglutamic acid indicated increased turnover of bone matrix. Transiliac bone biopsy showed a dearth of marrow elements, greatly increased bone turnover, and absence of normal trabecular organization. Serial radiographs showed progressive cortical thinning and loss of bony trabeculae. Calcitonin and etidronate treatments had no lasting effect on the progressive bone disease. The term "panostotic fibrous dysplasia" is suggested for this condition.

Alkaline Phosphatase↗
PubMed1991

Bone graft and bone graft substitutes: a review of current technology and applications.

The morbidity associated with autogenous bone graft harvest and the recent concern regarding the transmission of live virus through use of allografts, have been the impetus for research into a variety of materials that could take the place of these standard materials for bone grafting. The positive results reported with various ceramics and/or bone derivatives suggest the possibility of a material with osteoconductive and/or osteoinductive properties for use with or in place of bone graft. This review discusses a variety of bone graft and bone graft substitute materials. Among the osteoconductive materials outlined are the hydroxyapatite and tricalcium phosphate ceramics as well as some reportedly osteoactive polymers. While osteoconduction is a favorable quality, much interest has focussed on the use of osteoinductive or osteogenic materials such as demineralized bone matrix or bone derivatives, that is, BMP, osteogenin, etc. It is increasingly apparent that these materials require a carrier vehicle for optimal expression of osteoactivity. Therefore, the review finishes with a comparison of the various materials suggested for use as carriers.

Bone Transplantation↗
PubMed1994

Effects of transforming growth factor beta on bone nodule formation and expression of bone morphogenetic protein 2, osteocalcin, osteopontin, alkaline phosphatase, and type I collagen mRNA in long-term cultures of fetal rat calvarial osteoblasts.

Transforming growth factor beta (TGF-beta) is one of the most abundant of the known growth regulatory factors stored within the bone matrix. When bone is resorbed, TGF-beta is released in an active form and is a powerful bone growth stimulant. When injected into the subcutaneous tissue over the calvarial surface of rodents, it rapidly causes proliferation of the periosteal layer and accumulation of new woven bone. In this report, we describe the effects of TGF-beta 1 on first subcultures of fetal rat osteoblasts obtained from calvarial bones and cultured from confluence with ascorbic acid and beta-glycerophosphate. Under these conditions, nodules with characteristics of normal bone appear by day 8. Similar to experiments described by Antosz et al., TGF-beta added to confluent cultures inhibited the formation of bone nodules. Both the number and total area of the nodules were quantitated and shown to be completely inhibited by 2 ng/ml of TGF-beta 1. TGF-beta also impaired the expression of genes associated with bone formation, including type I collagen, alkaline phosphatase, osteopontin, and osteocalcin. TGF-beta also inhibited the expression of mRNA for the bone morphogenetic protein 2 (BMP-2). These results, showing suppression of markers representative of osteoblast differentiation, suggest that the effects of TGF-beta to stimulate bone formation in vivo are not likely a result of effects on differentiated mineralizing osteoblasts but, as suggested by previous studies, more likely are caused by effects on osteoblast precursors. These results also suggest that endogenous BMP-2 expression in fetal rat calvaria cells is important for bone cell differentiation.

Alkaline Phosphatase↗
PubMed1982

Adhesion of osteoclasts and monocytes to developing bone.

Osteoclast resorption of bone matrix during bone development is preceded by cell attachment to bone. An in vitro assay is described that measures adhesion of isolated osteoclasts and their presumed progenitor cell, the monocyte, to embryonic chick bone. Osteoclasts were isolated from day 19 chick tibia and enriched. Circulating chick hatchling monocytes were purified by Ficoll-hypaque sedimentation and attachment to plastic. Isolated cells were labeled with (32P)-KH2PO4 to quantitate cell attachment. In one series of experiments, labeled cells were inoculated into vessels containing day 19 tibias with either endosteal or periosteal bone surface exposed. Labeled cells were also inoculated into chambers containing day 6 (cartilage cores), day 12 (bone and cartilage cores), or day 19 embryonic tibias (bone). Cultures of stage 24 chick limb mesenchyme and embryonic chick skin fibroblasts served as controls. Results demonstrate that twice as many osteoclasts and monocytes adhere to bone as compared to fibroblasts and stage 24 limb mesenchymal cells. Furthermore, there does not appear to be selective adhesion to the endosteal as compared to periosteal bone surfaces. When the data is calculated on the basis of cell attachment per area of each substrate, the day 12 cores had slightly higher number of osteoclasts and monocytes attached compared to day 19 bones; day 6 cartilage cores bound few cells. These observations suggest that osteoclasts and monocytes have a high affinity to bone which seems to be influenced by the developmental age and composition of the substrate.

Animals↗
PubMed1986

Avian medullary bone in organ culture: effects of vitamin D metabolites on collagen synthesis.

A new organ culture system for the study of bone metabolism has been developed using chicken medullary bone. The presence of viable bone cells in culture was demonstrated by histological and histochemical techniques. Incorporation of 3H-proline into collagenase-digestible protein (CDP) and noncollagen protein (NCP) was determined using purified bacterial collagenase. Collagen accounted for approximately 10-15% of the total protein labeled. The addition of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) resulted in a dose-dependent inhibition of 3H-proline incorporation into CDP at doses from 10(-10)M to 10(-7)M, with maximal suppression reaching 30% of control. The effect was specific for collagen, since 3H-proline incorporation into NCP was unaffected. Hydroxyproline analysis of bone explants and culture medium revealed a 1,25(OH)2D3-induced decrease in the 3H-hydroxyproline content of the system (bone + medium), suggesting that the effect of 1,25(OH)2D3 is due to inhibition of collagen synthesis rather than enhanced collagen degradation, impaired incorporation of collagen into bone matrix, or bone resorption. Medullary bone collagen synthesis was not affected by 24,25(OH)2D3, either alone or in combination with 1,25(OH)2D3. Structure-activity studies of vitamin D metabolites showed that 1,25(OH)2D3 and 1,24,25(OH)3D3 were the most potent metabolites tested, followed by 1-alpha(OH)D3. 25(OH)D3 and 24,25(OH)2D3 had no effect at concentrations as high as 10(-7)M. These results indicate a possible role for vitamin D in the regulation of medullary bone formation during the reproductive cycle of the egg-laying hen, and suggest the potential utility of medullary bone as an in vitro model for the study of bone formation.

Animals↗
PubMed1988

Twisted plywood architecture of collagen fibrils in human compact bone osteons.

Ultrathin sections of decalcified human compact bone, observed by transmission electron microscopy, reveal that collagen fibrils can be distributed in the form of a superimposed series of nested arcs. This characteristic pattern has never been interpreted in previous works on compact bone structure. We demonstrate, by goniometric observations at the ultrastructural level, that such series of nested arcs are a consequence of the "twisted plywood" architecture of collagen fibrils in the compact bone matrix. In the same specimens, an "orthogonal plywood" disposition of collagen fibrils is also observed; a transition exists between these two types of orders. We show that the "twisted plywood structure" accounts well for certain optical properties of osteons, observed in polarizing microscopy, described as "intermediate osteons." The particular geometry of collagen fibrils, leading to nested arcs in oblique sections, is analogous to the distribution of molecules in certain liquid crystals (called cholesteric liquid crystals). The principle of a liquid crystalline self-assembly of the collagen matrix in bone is therefore discussed.

Adult↗
PubMed1997

Specific changes of urinary excretion of cross-linked N-telopeptides of type I collagen in pre- and postmenopausal women: correlation with other markers of bone turnover.

Urinary excretion of cross-linked N-telopeptide of type I collagen (NTx) has been reported to be a specific marker of bone resorption [18]. We assessed a new immunoassay for NTx as an indicator of changes in bone resorption caused by spontaneous menopause and compared cross-sectionally the levels of urinary NTx, hydroxylysylpyridinoline (HP), lysylpyridinoline (LP), hydroxyproline (OH-Pr), other serum biochemical indices, and lumbar spine and proximal femur bone mineral density (BMD). Eighty-one Japanese women aged 22-77 participated in this study; 36 were premenopausal and 45 were postmenopausal. Urinary HP, LP, and NTx stayed at low levels in the premenopausal period and rose 21%, 30%, and 67% in the postmenopausal period, respectively. The rise in LP and NTx was statistically significant (P < 0.01), suggesting that NTx is mostly released from bone matrix when bone resorption is accelerated. When premenopausal women were divided into two age groups and postmenopausal women were divided into two groups according to years since menopause (YSM) there were significant differences in LP and NTx between women <4 YSM and women aged <40 and those women aged 41+ (P < 0.01 and P < 0.05, respectively). A significant 110% increase in urinary NTx and a 48% increase in urinary LP were observed in postmenopausal women compared with age-matched premenopausal women aged 45-55. All biochemical markers other than serum PTH correlated significantly with each other (r = 0. 243-0.858, P < 0.05-0.0001). Urinary NTx inversely correlated with lumbar spine BMD. When postmenopausal women were divided into three groups, the correlation between bone resorption and formation markers in women 0-1 YSM was greater than in women 2-10 YSM and in women 11 + YSM, indicating that resorption and formation are coupled at the early postmenopausal period. We conclude that urinary NTx is responsive to changes in bone metabolism caused by estrogen deficiency and may be a more sensitive and specific marker than HP, LP, or OH-Pr in the early postmenopausal years.

Adult↗
PubMed2005

Neurofibromin and its inactivation of Ras are prerequisites for osteoblast functioning.

Skeletal problems and osteoporosis occur in up to 50% affected neurofibromatosis type 1 (NF1) humans. Inactivation of neurofibromin results in deregulation of Ras signal transduction. Little is known of bone biology in humans with NF1. The goal of our work was to determine if loss-of-function of Nf1 gene was associated with altered bone homeostasis and Ras signal transduction. Because homozygous Nf1 mice are embryonically lethal, heterozygote Nf1 (Nf1+/-) male mice were used to investigate skeletal phenotypes and osteoprogenitor functions, using standard in vivo and in vitro assays. We found that bone mass and geometry of Nf1+/- mice did not differ from wild type controls, despite a trend to less bone formation. Nf1+/- committed osteoprogenitors from femur metaphysis exhibited premature apoptosis and higher proliferation. Ras signaling was activated in primary Nf1+/- bone marrow-inducible osteoprogenitors. Inducible osteoprogenitors exhibited lower induction of osteoblast differentiation, assessed as alkaline phosphatase positive CFU-f. A screen of osteoblast marker genes showed a selective increase in osteopontin (OPN) mRNA and protein expression in these cells. OPN protein was increased in Nf1+/- bone, especially in cortical bone matrix. Because bone cell abnormalities in Nf1 haploinsufficiency were detected in vitro, redundant pathways must compensate for the deregulation of Ras signaling in vivo to maintain normal bone mass and function in vivo. Our in vitro data revealed that neurofibromin and its control of Ras signaling are required for osteoprogenitor homeostasis.

Animals↗
PubMed2006

A new approach to repairing cleft palate and acquired palatal defects with distraction osteogenesis.

Cleft palate (CP) is one of the most common human congenital deformities, and acquired palate defects after trauma or tumour resection are also common. In this study, distraction osteogenesis (DO) for CP and other palatal bone defects was evaluated. Twenty cats were assigned randomly to 3 groups of (1) 15, (2) 3 and (3) 2 cats. In groups 1 and 2, a rectangular ostectomy, in the posterior of the palatal bone shelf, was performed in the sagittal axis to establish the CP defect model. At the same time, a pure titanium intraoral distractor was fixed to molar teeth with brackets and to the palatal bone shelf across the defect with titanium miniscrews bilaterally. Four weeks later, a secondary transport disc (TD) osteotomy was performed, and gradual DO treatment started at 0.4mm twice a day, after 6 days of latency. DO was performed until the TD reached the opposite margin over the gap in 5-6 days. Three cats each of group 1 were killed at 2, 4, 6, 8 and 12 weeks after completion of DO. In group 2, the bone and soft-tissue defects were untreated until death 6 weeks later. Group 3 cats (control) were killed after 6 weeks. The TD successfully recombined with the opposite palatal bone stump, and proportional expansion of the overlay mucoperiosteal flap was achieved. Intramembranous bone formation was revealed: parallel collagen bundles gradually deposited on new bone trabeculae while the proliferative osteoblasts produced bone matrix. The bone defect was finally reconstructed by de novo osteogenesis. The control group was observed to have no spontaneous repairing. These results suggest that the CP defect was reconstructed by osteogenesis in situ, and the soft tissues expanded simultaneously to achieve functional correction. The intraoral distractor provided both effective distraction and stability.

Animals↗
PubMed2003

The reaction of osteoclasts when releasing osteocytes from osteocytic lacunae in the bone during bone modeling.

Osteocytes are released from the osteocytic lacunae when osteoclasts resorb the bone matrix during bone modeling and remodeling. It remains unknown how osteoclasts react when releasing osteocytes during bone modeling, and the fate of these released osteocytes is also unclear. Femoral mid-shafts of 2-day-old kittens were sectioned into serial 0.5 microm-thick semithin or 0.1 microm-thick ultrathin sections, and examined by light microscopy (LM) and transmission electron microscopy (TEM). The sections showed many osteoclasts at the endosteum but there were no osteoblasts. There were many half-released, fully released, half-exposed, and fully exposed osteocytes on the bone surfaces. Many cell-like structures were seen in the cell bodies of osteoclasts by LM, and some semithin sections were re-sectioned into ultrathin sections for re-observation by TEM. By TEM, these were determinated to be mononuclear cells. The serial ultrathin sections showed that the mononuclear cells appeared to be engulfed in osteoclasts on one section but that the cell was connected with the bone surface of the osteocytic lacuna on another section. These results show that the mononuclear cells in the osteoclasts were osteocytes. The present study suggests that osteoclasts engulf some osteocytes but do not engulf others when releasing osteocytes during bone modeling.

Animals↗
PubMed2003

Requirement of calcium and phosphate ions in expression of sodium-dependent vitamin C transporter 2 and osteopontin in MC3T3-E1 osteoblastic cells.

Osteoclasts dissolve mineralized bone matrix at bone resorption sites and release large amounts of calcium (Ca(2+)) and phosphate (PO(4)(3-)) ions into the extracellular fluid. However, the exact nature of Ca(2+) and PO(4)(3-) on osteoblasts remains unclear. We proposed that Ca(2+) and PO(4)(3-) ions are required for the expression of sodium-dependent vitamin C transporter (SVCT) 2 and a differentiation marker, osteopontin (OPN), in osteoblasts as a response to the osteoclastic degradation. Results from Northern blotting indicated that a deficiency of Ca(2+) or PO(4)(3-) inhibited both SVCT2 and OPN expression in a time-dependent manner, whereas elevated Ca(2+) (1 to 4 mM) or PO(4)(3-) (1 to 4 mM) dose-dependently induced SVCT2, OPN expression and OPN promoter activity. In addition, the L-type calcium channel blocker, nifedipine (5 to 20 micro M) and the phosphate transporter inhibitor, foscarnet (0.15 to 0.6 mM), dose-dependently abolished Ca(2+)- and PO(4)(3-)-induced SVCT2, OPN expression and OPN promoter activity. Furthermore, the results from L-ascorbic acid uptake assay and Western blotting indicated that the stimulatory effect of Ca(2+) and PO(4)(3-) on functional SVCT2 protein expression. These findings suggested that Ca(2+) and PO(4)(3-) regulate osteoblastic phenotype by entering into cells to stimulate SVCT2 and OPN expression.

Animals↗
PubMed2003

Upregulation of osteoclast alpha2beta1 integrin compensates for lack of alphavbeta3 vitronectin receptor in Iraqi-Jewish-type Glanzmann thrombasthenia.

Osteoclasts utilize alphavbeta3 integrin adhesion to bone matrix during bone resorption. We have generated osteoclasts from the peripheral blood of Iraqi-Jewish patients with Glanzmann thrombasthenia (GT) who are completely deficient in beta3 integrin and exhibit a haemorrhagic diathesis resulting from the absence of platelet alphaIIbbeta3. We show that, in contrast to osteoclasts generated from normal subjects or patients with alphaIIb integrin deficiency, GT osteoclasts lack alphavbeta3. These osteoclasts exhibited a two- to fourfold increase in alpha2 and beta1 integrin expression, whereas other alphav integrins, including alphavbeta5, were not significantly affected. An accompanying decrease in bone resorption was observed, with 44% and 59% declines in pit number and depth, respectively, and resorption lacunae showed abnormal morphology on scanning electron microscopy. However, osteoclasts from GT developed in similar numbers to controls and exhibited an otherwise 'normal' phenotype. We conclude that the observed rise in alpha2beta1 expression compensates for the chronic genetic deficiency of alphavbeta3 in osteoclasts from patients with GT and is sufficient to enable bone resorption to proceed, albeit to a submaximal extent. This explains why Iraqi-Jewish patients with GT do not have osteopetrosis.

Adolescent↗
PubMed1989

Stimulation of the expression of osteogenic and chondrogenic phenotypes in vitro by osteogenin.

Osteogenin was recently purified and the amino acid sequences of tryptic peptides were determined. Osteogenin in conjunction with insoluble collagenous bone matrix induces cartilage and bone formation in vivo. To understand the mechanism of action of osteogenin, we examined its influence on periosteal cells, osteoblasts, fibroblasts, chondrocytes, and bone marrow stromal cells in vitro. Osteogenin stimulated alkaline phosphatase activity and collagen synthesis in periosteal cells. The cAMP response to parathyroid hormone in periosteal cells was increased by osteogenin. In primary cultures of calvarial osteoblasts, osteogenin stimulated alkaline phosphatase activity, the cAMP response to parathyroid hormone, and the synthesis of collagenous and noncollagenous proteins; however, cell proliferation was not affected. Osteogenin increased the production of sulfated proteoglycans in fetal rat chondroblasts and in rabbit articular chondrocytes. The present experiments demonstrate the significant influence of osteogenin in the stimulation of osteogenic and chondrogenic phenotypes in vitro.

Alkaline Phosphatase↗