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PubMed1992

Adaptations of Goldner's Masson trichrome stain for the study of undecalcified plastic embedded bone.

Specialized adaptations for application of Goldner's Masson trichrome stain to plastic embedded undecalcified bone specimens are presented. This stain can be used successfully on methyl-glycol methacrylate, glycol methacrylate and Spurr embedded bones. The stain affords the advantage of good cellular staining due to the hematoxylin component with concomitant sharp discrimination of mature bone matrix which stains green, immature new bone matrix which stains red, and calcified cartilage which stains very pale green. Use of red filters during photomicrography aids in bone-osteoid discrimination in black and white photographs.

Azo Compounds↗
PubMed2006

The hydration characteristics of demineralized and nondemineralized allograft bone: Scientific perspectives on graft function.

Demineralized bone matrix grafts are osteoinductive due to the increase in bioavailability of bone morphogenetic proteins that occurs from demineralization. The manner by which demineralization increases their bioavailability, however, is not known with certainty. It is known that the mineral phase of bone masks the proteins of the organic matrix. Proteins depend on their interaction with water for their three-dimensional conformation, biologic activity, and stability. It is possible that demineralization allows a more complete hydration of bone matrix, changing the local environment and allowing the bone morphogenetic proteins to desorb and form a concentration gradient, signaling the appropriate cell types to begin the process of bone regeneration. Under similar test conditions, it was discovered that hydration of demineralized bone matrix powder produces a strong exotherm on the order of 14 degrees C whereas hydration of bone powder produces a smaller exotherm of about 2 degrees C. The details of the hydration reactions of demineralized bone matrix and bone were investigated by measuring the exotherm produced under varying conditions. The results suggest that bone mineral does mask, or limit, the ability of the organic matrix to interact with water. An understanding of the hydration characteristics of demineralized bone matrix can also help in the development of carrier systems that optimize osteoinductive potential.

Absorption↗
PubMed2004

Contribution of bone mineral density and bone turnover markers to the estimation of risk of osteoporotic fracture in postmenopausal women.

In osteoporosis, the main cause for concern is the increase in the risk of fractures. The level of bone mineral density (BMD) measured by various techniques has been shown to be a strong predictor of fracture risk in postmenopausal women. However, half of patients with incident fractures have BMD value above the diagnostic threshold of osteoporosis defined as a T-score of -2.5 SD or more below the average value of young healthy women. Clearly there is a need for improvement in the identification of patients at risk for fracture. Several prospective studies have shown that an increased bone resorption evaluated by specific biochemical markers was associated with increased risk of the hip, spine and non-vertebral fractures independently of BMD. The use of bone markers in individual patients may be appropriate in some situations, especially in women who are not detected at risk by BMD measurements. For example, in the OFELY study including 668 postmenopausal women followed prospectively over 9 years, we found that among the 115 incident fractures, 54 (47%) actually occurred in non-osteoporotic women. Among these women, the combination of bone markers and history of previous fracture was highly predictive of fracture risk. Thus, bone markers may be used in the assessment of fracture risk in selected cases in which BMD and clinical risk factors are not enough to take a treatment decision. Advances in our knowledge of bone matrix biochemistry, most notably of post-translational modifications in type I collagen, may allow identification of biochemical markers that reflect changes in the material property of bone, which is an important determinant of bone strength. Preliminary in vitro studies indicate that the extent of post-translational modifications of collagen--which can be reflected in vivo by the measurement of the urinary ratio between native and isomerised type I collagen--play a role in determining the mechanical competence of cortical bone, independently of BMD. Further studies in osteoporosis should explore the changes in these biochemical parameters of bone matrix as they may represent a key component of bone quality.

Biomarkers↗
PubMed1997

Increased proliferation of osteoblastic cells expressing the activating Gs alpha mutation in monostotic and polyostotic fibrous dysplasia.

We studied the osteoblastic abnormalities resulting from activating mutation of the Gs alpha gene in two patients with McCune-Albright syndrome and one patient with monostotic fibrous dysplasia. Histomorphometric analysis of dysplastic lesions showed a low number of differentiated osteoblasts along the bone surface and numerous immature alkaline phosphatase-positive mesenchymal cells actively depositing a woven bone matrix. Osteoblastic cells isolated from dysplastic bone lesions expressed a missense mutation in the Gs alpha gene in position 201 and showed increased intracellular basal cyclic adenosine 3',5'-monophosphate levels compared with normal cells isolated from a noninvolved area in the same patient. Cell proliferation evaluated by DNA synthesis was two-fold to threefold greater in osteoblastic cells expressing the mutation compared with normal cells from the same patient and was greater in cells isolated from more severe than less severe fibrotic lesions. In contrast, the synthesis of osteocalcin, a marker of mature osteoblasts, was lower in osteoblastic cells expressing the Gs alpha mutation compared with normal cells from the same patient and was lower in cells isolated from severe compared with less severe fibrotic lesions, indicating that the increased growth in mutated osteoblastic cells was associated with reduced cell differentiation. The results show that activating mutation of Gs alpha in osteoblastic cells leads to constitutive activation of adenylate cyclase, increased cell proliferation, and inappropriate cell differentiation, resulting in overproduction of a disorganized fibrotic bone matrix in polyostotic and monostotic fibrous dysplasia.

Adolescent↗
PubMedDate not supplied

Biomimetic collagen scaffolds for human bone cell growth and differentiation.

Type I collagen provides a structural framework for connective tissues and plays a central role in the temporal cascade of events leading to the formation of new bone from progenitors. The aim of this study was to examine the ability of the cell-binding domain of type I collagen (P-15 peptide) to promote human bone marrow stromal cell adhesion, proliferation, and differentiation on three-dimensional scaffolds. Human bone marrow stromal cells were selected, expanded, and cultured on particulate microporous ABM ("pure" hydroxyapatite) phase adsorbed with or without P-15 under basal or osteogenic conditions. Immobilized P-15 increased alkaline phosphatase activity and bone morphogenetic protein 2 (BMP-2) gene expression after 1 and 5 days as determined by real-time polymerase chain reaction. P-15 promoted human bone marrow stromal cell attachment, spreading, and alignment on ABM as well as alkaline phosphatase-specific activity in basal and osteogenic cultures. The presence of mineralized bone matrix, extensive cell ingrowth, and cellular bridging between three-dimensional matrices adsorbed with P-15 was confirmed by confocal microscopy, scanning electron microscopy, and alizarin red staining. Negligible cell growth was observed on ABM alone. In vivo diffusion chamber studies using MF1-nu/nu mice showed bone matrix formation and organized collagen formation after 6 weeks. These studies indicate the potential of P-15 to generate appropriate biomimetic microenvironments for osteoblasts and demonstrate the potential for the exploitation of extracellular matrix cues for osteogenesis and, ultimately, bone regeneration.

Adsorption↗
PubMed1995

The anatomy of bone sialoprotein immunoreactive sites in bone as revealed by combined ultrastructural histochemistry and immunohistochemistry.

Bone sialoprotein was immunolocalized at the EM level in thin Lowicryl K4M sections of rat bone. Because of the unconventional EM morphology of the bone matrix seen in thin demineralized acrylate sections, the pattern of immunolabeling was compared with detailed structural images of demineralized bone obtained using an en bloc treatment of tissue samples with the cationic electron 'dye,' Malachite Green (MG), which provides stabilization and retention of anionic material throughout specimen processing. A system of structures corresponding to the sites of bone sialoprotein (BSP) immunoreactivity, as seen in Lowicryl K4M this sections, could be readily identified in the MG-treated, epoxy thing sections. This system includes the cement lines, and aggregates of similar material within mineralized bone and mineralizing osteoid. The virtual identity of BSP distribution with the arrangement of the MG-visualized material indicates that a BSP-enriched, noncollagenous phase can be demonstrated using different, unrelated tissue preparation and imaging protocols for EM. Besides improving our understanding of the distribution of bone sialoprotein in bone, these data assign a previously unrecognized structural dimension to noncollagenous material in the bone matrix.

Animals↗
PubMed1999

Osteopontin-deficient mice are resistant to ovariectomy-induced bone resorption.

Osteopontin is one of the major noncollagenous bone matrix proteins produced by osteoblasts and osteoclasts, bone cells that are uniquely responsible for the remodeling of mineralized tissues. Osteoclasts express the alphavbeta3 integrin, which is one of the receptors for osteopontin. Recent knockout studies revealed that noncollagenous bone matrix proteins are functionally important in regulation of bone metabolism. However, the significance of the presence of osteopontin in in vivo has not been known. We report here that osteopontin knockout mice are resistant to ovariectomy-induced bone resorption compared with wild-type mice. Microcomputed tomography analysis indicated about 60% reduction in bone volume by ovariectomy in wild-type mice, whereas the osteopontin-deficient mice exhibited only about 10% reduction in trabecular bone volume after ovariectomy. Reduction in uterine weight was observed similarly in both wild-type and osteopontin-deficient mice, indicating the specificity of the effect of osteopontin deficiency on bone metabolism. We propose that osteopontin is essential for postmenopausal osteoporosis in women. Strategies to counteract osteopontin's action may prove effective in suppressing osteoporosis.

Animals↗
PubMed1985

The effect of aging on bone formation in rats: biochemical and histological evidence for decreased bone formation capacity.

Ectopic bone formation by subcutaneously implanted demineralized bone matrix powder (DBM) was assessed biochemically and histologically in Fischer 344 rats of different ages. The total calcium accumulated in implants was greatly depressed in older rats, as was the rate of 45Ca deposition. High alkaline phosphatase activity appeared later in the 10- and 16-month-old rats compared with 1-month-old rats, and the magnitude of the alkaline phosphatase activity was decreased in 16-month-old rats. The accumulation of the bone-specific vitamin K-dependent bone protein (bone gla protein, BGP) was decreased in the implants in older rats. Histological examination of the implants confirms the decreased ability of aged animals to produce bone in response to DBM. Measurements of total calcium, alkaline phosphatase, and BGP at the site of demineralized bone matrix implants clearly demonstrates that bone formation decreases dramatically with increasing age. Significant differences in total calcium can be detected even between 1-month-old and 3-month-old rats. Serum BGP shows a marked decrease (47%) between 1-month- and 3-month-old rats, a decrease not paralleled by a similar decrease in BGP present in calvarial or tibial bone.

Aging↗
PubMed2006

High glucose increases the expression of Cbfa1 and BMP-2 and enhances the calcification of vascular smooth muscle cells.

BACKGROUND: Vascular calcification is common in diabetes but the pathogenesis is poorly understood. METHODS: To investigate the pathogenesis, we first examined the histology of inferior epigastric arteries from diabetic and non-diabetic patients undergoing a renal transplant. To examine the role of hyperglycaemia, bovine vascular smooth muscle cells (BVSMCs) were incubated with normal (5 mM) or high glucose (25 mM) for 48 or 72 h. RESULTS: The results demonstrated that diabetic patients, compared with non-diabetic patients, had significantly greater calcification and increased expression of the bone matrix proteins osteopontin, type I collagen, bone sialoprotein and alkaline phosphatase (ALP). The in vitro studies demonstrated that high glucose increased the expression of the osteoblast transcription factor core binding factor alpha subunit 1 (Cbfa1) and its downstream protein osteocalcin by 1.9-fold and 1.8-fold, respectively, and ALP activity by 1.5-fold. These findings were blunted in the presence of an inhibitor to protein kinase C. High glucose also significantly enhanced calcification in BVSMC in a time-dependent manner (2.20 +/- 0.50 vs 1.35 +/- 0.55 micromol/mg, day 7; 5.04 +/- 1.35 vs 3.12 +/- 0.92 micromol/mg, day 14; P < 0.05). High glucose also induced the secretion of bone morphogenetic protein-2, a known osteoinductive factor, and further increased the secretion normally seen during calcification by 43% at day 7 and 57% at day 14. CONCLUSIONS: These results demonstrate that vascular calcification in patients with diabetes is a cell-mediated process characterized by a phenotypic change of VSMCs to osteoblast-like cells with increased bone matrix protein expression, and that hyperglycaemia may directly induce these changes.

Animals↗
PubMed1993

Mechanism of bone turnover.

Bone remodelling is a cellular mechanism behind the bone turnover. It renews the old bone piece by piece and thus ensures the correction of possible microdamage and enables the regulation of mineral homeostasis. The basic mechanism of bone remodelling is similar in all types of bone and includes the resorption of old bone and the formation of equal amount of new bone at the same place. Histomorphometric studies have revealed the cellular details of remodelling and have shown that it is composed by the temporally and spatially regulated action of different bone cells and their precursors. Recent in vitro studies with osteoclasts and osteoblasts have increased our knowledge of the molecular mechanisms of bone remodelling. Molecular characterization of bone matrix proteins have suggested new functions to many of them and thereby increased our possibilities of understanding the local regulation mechanisms of remodelling. Bone matrix has been shown to contain several biologically active compounds which have effects on bone forming and resorbing cells and their precursors. Details of the functional mechanism of osteoclasts are also in the process of being discovered. However, several questions concerning bone remodelling still remain open: the molecular explanation for selection of the remodelling site; the coupling of bone resorption to formation, and the interactions between different cell types during the remodelling cycle.

Bone Matrix↗
PubMed1999

A three-dimensional transport model for determining absorbed fractions of energy for electrons within cortical bone.

UNLABELLED: Any radionuclide that is transported through the blood stream will also be carried through the haversian canals within cortical bone. These canals are lined with a layer of endosteum that contains radiosensitive cells. This paper introduces a new three-dimensional electron transport model for cortical bone based on Monte Carlo transport and on bone microstructural information for several cortical bone regions. METHODS: Previously published haversian cavity and bone matrix chord length distributions for cortical bone were randomly sampled to create alternating regions of bone matrix, endosteum and haversian canal tissues during the three-dimensional transport of single electrons. Electron transport was performed using the EGS4 transport code with the parameter reduced electron step transport algorithm. Electron-absorbed fractions of energy were tabulated for three adult cortical bone sites considering three source and target regions: the cortical haversian space, the cortical bone endosteum (CBE) and the cortical bone volume (CBV). RESULTS: Absorbed fractions assessed with the new model were shown to be highly energy dependent for most combinations of source-target regions in cortical bone. Although chord length data were available for three different bone sites (femur, humerus and tibia), very little variation with bone site was noted in the absorbed fraction data. CONCLUSION: International Commission on Radiation Protection (ICRP)-recommended absorbed fractions for cortical bone are given only for the CBE as target region and for the CBE and CBV as source regions. Comparisons of these recommended absorbed fractions with the absorbed fractions calculated in this study show large differences. For example, ratios of self-absorbed fractions to the CBE in this model and in the ICRP 30 model are approximately 0.25, approximately 4 and approximately 1.5 for initial electron energies of 10, 200 keV and 4 MeV, respectively. Consequently, this new transport model of electrons in cortical bone will improve the relatively energy-independent data recommended by the ICRP. This model will also allow consideration of the haversian canals as a potential radiation source.

Absorption↗
PubMed1993

Short-term oral phosphate and bone remodeling in beagles.

Attempts to increase bone volume in osteoporotic patients are still in the experimental stage. The coherence therapy, proposed by Frost, suggests that the activated bone units can remodel bone matrix in tandem. The cells (i.e., osteoclast and osteoblast which compose the remodeling units) are manipulated through specific medications timed to each of their duration of actions. The current study was to examine the effect of withdrawal of oral phosphate on bone in ovariectomized dogs. The present report demonstrates the capability of short-term oral phosphate to activate bone remodeling in the ovariectomized animal model. Results from biochemical and histomorphometric analyses confirm that remodeling units are activated following the release of parathyroid hormone. This transient scenario inflicts a shift of mineral density distribution in cancellous bone matrix of the iliac crest. Nevertheless, the bone remodeling units appear to be synchronized with each other and thus their resorptive and formative phases should be amenable to further pharmacological manipulation.

Administration, Oral↗
PubMed2001

Decreased bone mineral density in Prader-Willi syndrome: comparison with obese subjects.

Bone density, anthropometric data, and markers of bone turnover were collected on 21 subjects diagnosed with Prader-Willi syndrome (PWS) and compared with 9 subjects with obesity of unknown cause. In addition, urinary N-telopeptide levels were obtained in all subjects. N-telopeptides are the peptide fragments of type I collagen, the major bone matrix material. During periods of active bone degradation or high bone turnover, high levels of N-telopeptides are excreted in the urine. However, no significant difference was detected in the urinary N-telopeptide levels when corrected for creatinine excretion (raw or transformed data) between our subjects with obesity or PWS and the observed effect size of the between-group difference was small. Although N-telopeptide levels were higher but not significantly different in the subjects with PWS compared with obese controls, the subjects with PWS had significantly decreased total bone and spine mineral density and total bone mineral content (all P < 0.001). No differences in N-telopeptide levels or bone mineral density were observed between subjects with PWS and chromosome 15q deletion or maternal disomy. Thus, decreased bone mineral density in subjects with PWS may relate to the lack of depositing bone mineral during growth when bones are becoming more dense (e.g., during adolescence), possibly because of decreased production of sex or growth hormones and/or long-standing hypotonia. It may not be caused by loss, or active degradation, of bone matrix measurable by the methods described in this study further supporting the possible need for hormone therapy during adolescence.

Adolescent↗
PubMed2000

Activin A is an essential cofactor for osteoclast induction.

Recently, receptor activator of NF-kappaB ligand (RANKL) was shown to be necessary for osteoclast formation. We now report that activin A, a cytokine enriched in bone matrix and secreted by osteoblasts and osteoclasts, powerfully synergized with RANKL for induction of osteoclast-like cells (OCL) from bone marrow precursors depleted of stromal cells. Moreover, OCL formation in RANKL was virtually abolished by soluble type II A activin receptors (ActR-II(A)), suggesting that activin A is essential for OCL formation. Activin A was most effective when precursors were exposed to RANKL and activin A simultaneously: resistance to OCL-induction that occurs when precursors are pre-incubated in M-CSF was reduced. Incubation on bone matrix also enhanced the sensitivity of precursors to OCL-induction by RANKL; and this was prevented by soluble ActR-II(A). Thus, activin A in bone matrix, or released from osteoblastic or other cells, enhances the osteoclast-forming potential of precursors and synergizes with RANKL in inducing osteoclastic differentiation.

Activin Receptors, Type II↗
PubMed1977

Interaction of dichloromethylene diphosphonate and vitamin D on bone of thyroparathyroidectomized rats.

Dichloromethylene diphosphonate (Cl2MDP) antagonized the action of vitamin D on bone in thyroparathyroidectomized rats by reducing the metabolic activity of osteoblasts and osteocytes and decreasing the number of osteoclasts. Ultrastructurally, osteoblasts in Cl2MDP-treated rats were interpreted to be less active in bone matrix synthesis. Osteocytes in Cl2MDP-treated rats were interpreted ultrastructurally to be inactive; there was no evidence of bone resorption when compared to osteocytes in rats given vitamin D alone. Abnormal osmiophilic densities in the pericellular bone matrix of rats given vitamin D alone were not present in rats given vitamin D and Cl2MDP. The ultrastructure of osteoclasts was unaltered by Cl2MDT. These cellular changes were associated with a decrease in serum calcium and increase in bone ash and magnesium concentration in rats given high levels (10 mg/kg) of Cl2MDP. Bone adenosine triphosphatase and alkaline phosphatase activities were not affected by Cl2MDP. These results suggest that Cl2MDP may limit the hypercalcemia of hypervitaminosis D by directly inhibiting bone cells in addition to its physicochemical action.

Adenosine Triphosphatases↗
PubMed1977

Estrogen-induced sequential changes in avian bone metabolism.

Medullary bone was induced in male Japanese quail by administration of estradiol valerate. An increase in the organic weight of the femur was observed by 36 h after estrogen and an increase in ash weight was observed by 96 h. A complex sequence of metabolic changes in the femur occurred after estrogen treatment. A large increase in uptake of 3H-proline associated with enhanced collagen formation began 36 h after estrogen and reached a peak 3.5 times the control rate at 60 h. The onset of mineralization of the newly formed bone matrix, as determined by 45Ca uptake, began about 24 h after onset of collagen synthesis indicating that synthesis of the bone matrix and its mineralization occur sequentially. Large increases in the rates of uptake of 3H-uridine and 3H-thymidine occurred prior to the onset of medullary bone formation and appear to reflect the differentiation of osteogenic precursors to bone-forming cells.

Animals↗
PubMed1992

Primate dentine extracellular matrix induces bone differentiation in heterotopic sites of the baboon (Papio ursinus).

In rodents, demineralized dentine matrix induces local differentiation of endochondral bone. This study investigated the osteoinductive potential of primate dentine matrices when implanted extraskeletally in allogeneic recipients. Demineralized dentine cylinders prepared from adult baboon incisors and demineralized dentine matrix pulverized to a particle size of 74-420 microns were implanted into the rectus abdominis of 4 subadult male baboons (Papio ursinus). Specimens were harvested 30 and 90 d after implantation. Histological analysis on serial sections showed bone differentiation in demineralized dentine cylinders after partial resorption of the external demineralized layer, and in resorption lacunae and excavation chambers within the matrix. Implants of demineralized dentine matrix of 74-420 microns particle size showed no osteoinductive activity as determined biochemically (alkaline phosphatase activity) and histologically. The demonstration of bone induction by primate dentine prepared from fully erupted tooth matrix suggests that putative osteogenic proteins may be conserved after dentinogenesis and embryonic tooth development, and may play a role during healing after surface demineralization of exposed root surfaces during regenerative procedures in humans.

Animals↗
PubMed1982

An electron microscopic examination for the presence of acid groups in the organic matrix of mineralization nodules in foetal bone.

Several biochemical and histochemical investigations of the role of glycosaminoglycans (GAG) in bone and cartilage mineralization have been performed, but the exact relationship between GAG and mineralization is not clear. We performed an electron microscopic histochemical study of the composition of organic bone matrix at sites of beginning mineralization in mouse foetal radii, directing special attention to the presence and location of GAG. To demonstrate these substances, use was made of positive colloidal thorium dioxide and ruthenium red. The results demonstrate the presence of material containing acid groups in the young mineralization nodules. It is concluded that part of the demonstrated acid groups might be sulphate groups of glycosaminoglycans.

Animals↗