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PubMed2004

Impact of bone lead and bone resorption on plasma and whole blood lead levels during pregnancy.

The authors tested the hypotheses that maternal bone lead burden is associated with increasing maternal whole blood and plasma lead levels over the course of pregnancy and that this association is modified by rates of maternal bone resorption. A total of 193 Mexican women were evaluated (1997-1999) in the first, second, and third trimesters of pregnancy. Whole blood lead and plasma lead levels were measured in each trimester. Urine was analyzed for cross-linked N-telopeptides (NTx) of type I collagen, a biomarker of bone resorption. Patella and tibia lead levels were measured at 4 weeks postpartum. The relation between whole blood, plasma, and bone lead and NTx was assessed using mixed models. Plasma lead concentrations followed a U-shape, while NTx levels increased significantly during pregnancy. In a multivariate model, the authors observed a significant and positive interaction between NTx and bone lead when plasma lead was used as the outcome variable. Dietary calcium intake was inversely associated with plasma lead. Results for whole blood lead were similar but less pronounced. These results confirm previous evidence that bone resorption increases during pregnancy, with a consequential significant release of lead from bone, constituting an endogenous source of prenatal exposure. They also provide a rationale for testing strategies (e.g., nutritional supplementation with calcium) aimed at decreasing prenatal lead exposure.

Adolescent↗
PubMed2006

Endostatin inhibits VEGF-A induced osteoclastic bone resorption in vitro.

BACKGROUND: Endostatin is a C-terminal fragment of collagen XVIII which is a component of basement membranes with the structural properties of both collagens and proteoglycans. Endostatin has a major role in angiogenesis which is intimately associated with bone development and remodeling. Signaling between the endothelial cells and the bone cells, for example, may have a role in recruitment of osteoclastic precursor cells. Our study aims at exploring a possibility that endostatin, either as a part of basement membrane or as a soluble molecule, may control osteoclastogenesis and osteoclastic bone resorption in vitro. METHODS: Rat pit formation assay was employed in order to examine the effect of endostatin alone or in combination with vascular endothelial growth factor-A (VEGF-A) on bone resorption in vitro. Effect of these agents on osteoclast differentiation in vitro was also tested. Osteoclastogenesis and the number of osteoclasts were followed by tartrate resistant acid phosphatase (TRACP) staining and resorption was evaluated by measuring the area of excavated pits. RESULTS: Endostatin inhibited the VEGF-A stimulated osteoclastic bone resorption, whereas endostatin alone had no effect on the basal resorption level in the absence of VEGF-A. In addition, endostatin could inhibit osteoclast differentiation in vitro independent of VEGF-A. CONCLUSION: Our in vitro data indicate that collagen XVIII/endostatin can suppress VEGF-A induced osteoclastic bone resorption to the basal level. Osteoclastogenesis is also inhibited by endostatin. The regulatory effect of endostatin, however, is not critical since endostatin alone does not modify the basal bone resorption.

Acid Phosphatase↗
PubMed1992

Role of protein kinase C (PKC) in bone resorption: effect of the specific PKC inhibitor 1-alkyl-2-methylglycerol.

The specific inhibitor of protein kinase C, 1-O-alkyl-2-O-methylglycerol (AMG), was studied for its effect on bone resorption, measured as 45Ca-release, in fetal mouse calvariae. AMG (1 to 50 microM) had no effect on basal bone resorption. AMG inhibited parathyroid hormone (40 nM) induced bone resorption in a dose-dependent manner. Resorption induced by 1,25 (OH)2-vitamin D3 (10 nM) or prostaglandin E2 (5 microM) was also inhibited by AMG. The release of beta-glucuronidase activity paralleled the course of the 45Ca-release. The production of interleukin 6, induced by parathyroid hormone, in fetal rat calvarial osteoblasts was not affected by AMG. AMG (1 to 50 microM) had no cytotoxic effects on cells or calvariae. From these results it is concluded that protein kinase C may have an important role in the regulation of bone resorption.

Bone Resorption↗
PubMed1983

Studies on the mechanisms by which 2-chloroadenosine stimulates bone resorption in tissue culture.

The effect of 2-chloroadenosine on bone resorption was studied in calvarial bones from 6-7-day-old mice in organ culture. 2-Chloroadenosine stimulated the mobilization of minerals (40Ca, 45Ca) and increased the degradation of matrix ([3H]proline) from the bones. The nucleoside also caused an increased release of beta-glucuronidase, a lysosomal enzyme. In doses above 30 microM 2-chloroadenosine was cytotoxic, as evidenced by an increased release of lactate dehydrogenase. 2-Chloroadenosine-stimulated resorption could be inhibited by calcitonin, increased concentration of phosphate in culture medium, cortisone, dexamethasone, indomethacin, naproxen, meclofenamic acid and 5,8,11,14-eicosatetraynoic acid. 2-Chloroadenosine was much more sensitive to inhibition by dexamethasone than was parathyroid hormone. The response to the maximal dose of 2-chloroadenosine could not be enhanced by parathyroid hormone, 1 alpha-hydroxyvitamin D-3 and prostaglandin E2. An exposure to 2-chloroadenosine for 12 h was not sufficient to produce prolonged resorption. The results suggest that 2-chloroadenosine stimulated bone resorption by a process which is dependent on osteoclastic activity. The possibility that the effect of 2-chloroadenosine, either directly or indirectly, is related to formation of prostaglandins is discussed in the light of the above data.

2-Chloroadenosine↗
PubMed1994

Inhibition of bone resorption in vitro by antisense RNA and DNA molecules targeted against carbonic anhydrase II or two subunits of vacuolar H(+)-ATPase.

The bone resorbing cells, osteoclasts, express high levels of carbonic anhydrase II (CA II) and vacuolar H(+)-ATPase (V-ATPase) during bone resorption. We have used antisense RNA and DNA molecules targeted against CA II, and against 16- and 60-kD subunits of vacuolar H(+)-ATPase (V-ATPase), to block the expression of these proteins in vitro. Osteoclastic bone resorption was studied in two in vitro culture systems: release of 45Calcium from prelabeled newborn mouse calvaria cultures, and resorption pit assays performed with rat osteoclasts cultured on bovine bone slices. Both antisense RNA and DNA against CA II and the V-ATPase were used to compare their specificities as regards inhibiting bone resorption in vitro. The antisense molecules inhibited the synthesis of these proteins by decreasing the amounts of mRNA in the cells in a highly specific manner. In osteoclast cultures treated with the 16-kD V-ATPase antisense RNA, acidification of an unknown population of intracellular vesicles was highly stimulated. The acidification of these vesicles was not sensitive to amiloride or bafilomycin A1. This suggests the existence of a back-up system for acidification of intracellular vesicles, when the expression of the V-ATPase is blocked. Our results further indicate that blocking the expression of CA II and V-ATPase with antisense RNA or DNA leads to decreased bone resorption.

Animals↗
PubMed1995

Osteoclast 121F antigen expression during osteoblast conditioned medium induction of osteoclast-like cells in vitro: relationship to calcitonin responsiveness, tartrate resistant acid phosphatase levels, and bone resorptive activity.

Osteoclast differentiation from hematopoietic precursors into multinucleated cells uniquely capable of removing the organic and inorganic components of bone matrix occurs in multistep process, during which osteoclasts acquire the specialized characteristics necessary for bone resorptive activity and physiological regulation. Among those traits is a novel plasma membrane glycoprotein, reactive with the anti-osteoclast monoclonal antibody 121F, which is expressed during the course of osteoclast differentiation, shares structural and functional homologies with Mn2+/Fe2+ superoxide dismutase, and has been hypothesized to protect the osteoclast from the damaging effects of superoxide radicals generated during active bone resorption. We have reported previously that the expression of this membrane antigen is induced on multinucleated giant cells when the prefusion marrow mononuclear cells are cultured in conditioned medium from avian calvaria. The studies reported here were designed to investigate the relationship between expression of the 121F antibody-reactive osteoclast membrane antigen and tartrate resistant acid phosphatase levels, bone resorptive activity, calcitonin responsiveness, and ultrastructural features of avian bone marrow-derived multinucleated giant cells formed either in the presence or absence of diffusible osteoblast secreted factors. Parallel analyses of in vivo formed osteoclasts isolated from the same animals were performed for direct comparisons. In this report we demonstrate: (1) that the 121F monoclonal antibody-reactive osteoclast membrane antigen is stably induced in giant cells by soluble osteoblast-derived factors in a species nonrestricted but concentration- and temporal-dependent manner; (2) that osteoblast-mediated antigen induction is reflected in both increased numbers of cells and elevated expression of individual cells that are reactive with the 121F antibody, as determined by ELISA and histomorphometry; (3) that osteoblast conditioned medium, in addition to inducing this antigen in bone marrow cells, also elevates other defining osteoclast characteristics in these avian giant cells including their TRAP activity, cell retraction from the bone surface in response to calcitonin, bone resorptive function, and expression of a series of additional osteoclast antigenic markers; and (4) that secreted osteoblast products alone do not raise the levels of these traits for in vitro formed marrow giant cells to the extent associated with in vivo formed osteoclasts. Therefore, osteoblast soluble factors alone appear unable to promote the full differentiation of bone marrow cells in vitro into mature bone-resorbing osteoclasts.(ABSTRACT TRUNCATED AT 400 WORDS)

Acid Phosphatase↗
PubMed1989

A histomorphometric analysis of the alveolar bone resorption process in calcium-deficient rats.

The present study was carried out to investigate the morphological changes in the alveolar bone in rats fed a low calcium diet, in order to establish an experimental model of alveolar bone resorption. Male Wistar rats (70-85 g in body weight) were either fed a low calcium diet (0.05% Ca, 0.35% P) or a control diet (0.5% Ca, 0.35% P) by using a pair feeding technique. The rats were sacrificed at intervals of 3, 6, 9 and 20 days. No difference was found in the growth rate between the control and the low calcium group. In the low calcium group, the bone area significantly reduced at day 3 and progressively decreased to 46% of that of the controls by the end of the experiment. The bone resorption was obvious in the cancellous bone during the early period of the experiment and then the cortical bone was seen to resorb. However, the contour of bone and the rate of bone apposition did not change. At day 20, bone still remained in three regions: the alveolar bone proper that surrounds the tooth sockets, a few cancellous bones and a thin wall-like cortical bone. These results suggest that the process of alveolar bone resorption is related to the mechanical forces induced by the occlusal function of the tooth and, further, that this experimental model might be useful for investigating the mechanism of alveolar bone resorption and disorders of the alveolar bone.

Alveolar Bone Loss↗
PubMed2003

The effect of particle size and electrical charge on macrophage-osteoclast differentiation and bone resorption.

In aseptic loosening, there is commonly periprosthetic bone loss and a heavy macrophage infiltrate in response to biomaterial wear particles generated from the implant materials. Macrophages which have phagocytosed wear particles are known to be capable of differentiation into bone resorbing osteoclasts. In this investigation we determine the role of particle size and particle charge on this process. Mouse monocytes and macrophages were co-cultured with osteoblast-like UMR106 cells and 1,25 dihydroxyvitamin D3 in the presence or the absence of (i) various sizes of latex beads (0.1, 1, 10 and 100 microm) and (ii) uncharged, positively- or negatively-charged sephadex beads of uniform shape and composition. The extent of osteoclast differentiation by monocytes or foreign body macrophages was determined by the expression of the osteoclast-associated enzyme tartrate-resistant acid phosphatase and lacunar bone resorption. No significant difference in the extent of osteoclast formation and bone resorption was noted in response to particle size. Osteoclast formation was also not significantly different in the presence of positively/negatively charged and uncharged particles. These findings indicate that osteoclast formation is not significantly influenced by particle characteristics, such as particle size. They also add support to the hypothesis that macrophage involvement in periprosthetic osteolysis is not dependent on particle phagocytosis and that it may be induced by particle contact.

Journal Article↗
PubMed1987

Vertebral bone resorption in vitro: effects of parathyroid hormone, calcitonin, 1,25 dihydroxyvitamin D3, epidermal growth factor, prostaglandin E2, and estrogen.

We have developed and characterized a new bone resorption system to test the effect of estrogen on vertebral bone in vitro. Neonatal mouse vertebral bones prelabeled with 45Ca were maintained in stationary tissue culture for 60-108 hours at 37 degrees C in 5% CO2/air. Each vertebral bone measured approximately 1 mm X 1 mm. Hormonal treatments were added directly to the incubation medium. The morphological appearance of these bones, before and after the onset of resorption, was examined by scanning electron microscopy. Bone resorption was measured by determining the % of the bone 45Ca released into the incubation medium. Vertebral bone resorption was stimulated in a dose-dependent manner by parathyroid hormone (1-100 nM), 1,25 dihydroxyvitamin D3 (0.0325-3.25 nM), and prostaglandin E2 (3-3000 nM). Epidermal growth factor (300 ng/ml) produced a small stimulation of bone resorption which was not inhibited by indomethacin (0.5 microM). Likewise, indomethacin (0.5 microM) did not inhibit PTH-stimulated vertebral bone resorption. Calcitonin (6.6 nM) produced a 79% inhibition of bone resorption induced by PTH (10 nM), whereas estradiol (up to 3 microM) did not inhibit bone resorption. Our results demonstrate that estrogen does not have a direct effect on vertebral bone tissue in vitro. This new bone culture system is a sensitive assay for the direct effects of resorptive agents on vertebral bone.

Animals↗
PubMed2004

Inhibition of osteoclast differentiation and bone resorption by tanshinone IIA isolated from Salvia miltiorrhiza Bunge.

Osteoclasts, multinuclear cells specialized for bone resorption, differentiate from the monocyte/macrophage lineage of hematopoietic cells. Intervention in osteoclast differentiation is considered an effective therapeutic approach to the treatment of bone diseases involving osteoclasts. In this study, we found that tanshinone IIA, originating from Salvia miltiorrhiza Bunge, inhibited the differentiation of osteoclasts. Addition of tanshinone IIA to the osteoclast precursor culture caused a significant decrease in the level of calcitonin receptor, c-Src, and integrin beta3 mRNA, which are normally upregulated during the osteoclast differentiation dependent on RANKL (receptor activator of nuclear factor kappa B ligand). RANKL activated the ERK, Akt, and NF-kappaB signal transduction pathways in osteoclast precursor cells, and tanshinone IIA suppressed this activation. Tanshinone IIA also inhibited the bone resorptive activity of differentiated osteoclasts, which was accompanied with the disruption of the actin ring. Thus, tanshinone IIA has the potential to ameliorate bone-resorption diseases in vivo by reducing both the number and activity of osteoclasts.

Abietanes↗
PubMedDate not supplied

Pathogenic factors in bone resorption in cholesteatoma.

Factors present in skin appear to enhance bone resorption in chronic otitis media. These skin factors were replicated in a series of experiments using an animal model. The presence of activated granulation tissue is a universal finding in bone resorption in otitis media. Skin promotes bone resorbing connective tissue by the action of keratin as a foreign body, by the enhancement of middle ear sepsis, by stimulation and activation of inflammatory cells and most importantly through the creation of pressure.

Animals↗
PubMed1996

Activation of osteoclast-mediated bone resorption by the supernatant from a rabbit synovial cell line in response to polyethylene particles.

It is unknown whether the soluble factors produced from cells activated by wear particles in the fibrous tissue around failed joint prostheses really activate osteoclastic bone resorption. In this study, the activation of osteoclast-mediated bone resorption by the products from a rabbit synovial cell line (HIG-82) stimulated by various particles was investigated using rabbit unfractionated bone cells cultured on a dentin slice. The HIG cells were challenged with the following laboratory-made particles: high-density polyethylene (PE), cobalt alloy (Co-Cr), titanium alloy (Ti6Al4V), pure titanium (Ti), and sintered hydroxyapatite (HA). The size of each particle was < 2 microns. The supernatants from HIG cells cultured with the appropriate concentration of wear particles were added to unfractionated bone cells on a dentin slice, and then resorbed areas were determined for each particle. Interestingly, resorbed areas significantly increased only when the culture medium from HIG cells with PE particles was added to unfractionated bone cells. This study demonstrates that PE particles stimulate the rabbit synovial cells to produce soluble factors that induce osteoclast-mediated bone resorption. Moreover, this experimental model is a useful method sensitively to evaluate the effects of soluble factors from the cells stimulated by particulate biomaterials from joint prostheses on osteoclastic bone resorption.

Animals↗
PubMed1987

Effect of calcitonin on the magnesium-induced bone resorption in the mouse.

This study was performed to evaluate whether Mg directly influences the activity of bone resorbing cells in vivo. Young male mice were given oral Mg supplementation (10 mM) in drinking water for 14 days. In order to inhibit bone resorption, a group of animals received 1 IU/kg/day of salmon calcitonin (CT) concurrently with Mg supplementation. The effects of CT alone were also tested separately. Skeletal changes were evaluated by histomorphometric analysis of parameters of endosteal bone resorption and formation after double tetracycline and double 3H-proline labelings. Two weeks of Mg supplementation induced a significant increase in the number of acid phosphatase-stained chondroclasts (+21.1%) and osteoclasts (+12.2%) and in the extent of osteoclastic resorbing surface (+40.5%) without change in serum mineral concentrations. Treatment with CT alone decreased the number of actively resorbing chondroclasts by 11% and decreased the osteoclastic resorbing surface by 22.4% without change in the number of active osteoclasts. Despite this 'escape' phenomenon, treatment with CT concurrent with Mg administration completely abolished the stimulatory effect of Mg on bone-resorbing cells. CT also inhibited the Mg-induced stimulation of the bone mineralization rate and produced a slight inhibition of the bone matrix apposition rate. The data indicate that Mg activates the bone resorbing cells in vivo and that CT administration blunts the Mg-induced stimulation of bone resorption.

Animals↗
PubMed1994

Interleukin-1 receptor antagonist and tumor necrosis factor binding protein decrease osteoclast formation and bone resorption in ovariectomized mice.

To investigate the contribution of IL-1, IL-6, and TNF to the increased osteoclastogenesis induced by estrogen deficiency, ovariectomized (ovx) mice were treated with either IL-1 receptor antagonist (IL-1ra), a competitive inhibitor of IL-1, TNF binding protein (TNFbp), an inhibitor of TNF, or the anti-IL-6 antibody (Ab) 20F3 for the first 2 wk after surgery. ovx increased the bone marrow cells secretion of IL-1 and TNF, but not IL-6, and the formation of TRAP-positive osteoclast-like multinucleated cells (MNCs) in bone marrow cultures treated with 1,25(OH)2D3. The increase in MNC formation induced by ovx was prevented by in vivo treatment with either 17 beta estradiol, IL-1ra, TNFbp, or anti-IL-6 Ab. However, the percent change in MNC formation induced by the anti-IL-6 Ab was similar in ovx and sham-operated animals, whereas IL-1ra and TNFbp were effective only in ovx mice. MNC formation was also decreased by in vitro treatment of bone marrow cultures with IL-1ra and TNFbp, but not with anti-IL-6 Ab. Ovx also increased bone resorption in vivo and in vitro, as assessed by the urinary excretion of pyridinoline cross links and the formation of resorption pits, respectively. IL-1ra, TNFbp and estrogen decreased bone resorption in vivo and in vitro whereas the anti-IL-6 Ab inhibited bone resorption in vitro but not in vivo. In conclusion, these data indicate that IL-1 and TNF play a direct role in mediating the effects of ovx on osteoclastogenesis and bone resorption. The data also suggest that IL-6 is not essential for increasing bone resorption in the early postovariectomy period.

Acid Phosphatase↗
PubMed1990

A method for continual monitoring of bone resorption in rats: evidence for a diurnal rhythm.

A method has been developed to monitor bone resorption (BR) based on the urinary excretion of [3H]tetracycline ([3H]TC) from chronically prelabeled rats. This is possible because the [3H]TC released from bone has been found to be in a form that is not or only poorly bound to apatite and thus not reincorporated into newly formed bone. When BR was increased by means of dietary calcium restriction, parathyroid hormone (PTH) infusion, or retinoid injections, urinary [3H]TC doubled. When BR was inhibited by feeding calcium supplements or administration of dichloromethylenebisphosphonate, [3H]TC excretion dropped by two-thirds. Thyroparathyroidectomy inhibited [3H]TC excretion by one-third. The results obtained with this technique are therefore similar to those obtained with other methods such as 45Ca kinetics. The effect of dietary manipulations on BR was detected within 6 h of changing diet. Furthermore, a strong diet-dependent but PTH- and calcitonin-independent diurnal rhythm in BR was found. By use of this technique, bone resorption can be assessed continuously over long periods, and the acute regulation of bone resorption can be studied for the first time.

Animals↗
PubMed1976

Tooth eruption and bone resorption: experimental investigation of the ia (osteopetrotic) rat as a model for studying their relationships.

The osteopetrotic (ia) rat was examined as an experimental model for studying the dependence of tooth eruption on bone resorption. In ia rats eruption of incisors and first molars was rare and eruption of second and third molars was reduced and delayed. Autoradiographic studies of 3H-proline incorporation showed that delayed eruption was not due to reduced tooth formation. Microscopic study revealed distortion and failure of posterior growth of the apical ends of incisors, unresorbed bone blocking the eruption pathway for molars, and ankylosis of incisors and first molars to alveolar bone. A reduction in bone resorption, known to be the primary cause of the disease in ia rats, is presumed to be the cause of the delayed or unerupted dentition. The effectiveness of attempts to increase bone resorption in ia rats at an early age by injection of vitamin A and/or parathyroid extract or by parabiotic union with a normal littermate was determined by measuring their effect on the relative size of the tibial marrow cavity. Only parabiosis had a beneficial effect on bone resorption but surgical union could not be performed in animals young enough to affect eruption of incisors and first molars in ia parabionts. These results suggest that parabiotic union of neonatal rats should allow resorption to begin early enough to test the presumed dependence of tooth eruption on bone resorption.

Animals↗
PubMed2003

Interleukin-8 stimulation of osteoclastogenesis and bone resorption is a mechanism for the increased osteolysis of metastatic bone disease.

Interleukin 8 (IL-8) is a member of the alpha chemokine family of cytokines originally identified as a neutrophil chemoattractant. Recently, we reported that elevated levels of IL-8, but not parathyroid hormone-related protein (PTHrP), correlated with increased bone metastasis in a population of human breast cancer cells. We hypothesized that IL-8 expression by breast cancer cells would either indirectly influence osteoclastogenesis via nearby stromal cells or directly influence osteoclast differentiation and activity. In the present study, we investigated the role of IL-8 in the process of osteoclast formation and bone resorption, which is associated with metastatic breast cancer. The addition of recombinant human (rh) IL-8 (10 ng/ml) to cultures of stromal osteoblastic cells stimulated both RANKL mRNA expression and protein production, with no effect on the expression of osteoprotegerin. In addition, rhIL-8 also directly stimulated the differentiation of human peripheral blood mononuclear cells into bone-resorbing osteoclasts. In these cultures, IL-8 was able to stimulate human osteoclast formation even in the presence of excess (200 ng/ml) RANK-Fc. The effect of IL-8 on osteoclasts and their progenitors was associated with the cell surface expression of the IL-8-specific receptor (CXCR1) on the cells. These results demonstrate a direct effect of IL-8 on osteoclast differentiation and activity. Together, these data implicate IL-8 in the osteolysis associated with metastatic breast cancer.

Animals↗