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PubMed1999

1,25-Dihydroxyvitamin D(3) and prostaglandin E(2) act directly on circulating human osteoclast precursors.

1,25-Dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) and prostaglandin E(2) (PGE(2)) are known to influence osteoclast formation indirectly through their effects on osteoblasts. To determine whether 1, 25(OH)(2)D(3) and PGE(2) also have a direct effect on circulating osteoclast precursors, these factors were added to long-term cultures of human peripheral blood mononuclear cells (PBMCs) in the presence of osteoprotegerin ligand and macrophage colony-stimulating factor (M-CSF) (+/-dexamethasone). The number of TRAP(+) and VNR(+) multinucleated cells and the area of lacunar resorption were decreased when 1,25(OH)(2)D(3) alone was added. A marked increase in resorption pit formation was noted when the combination of 1, 25(OH)(2)D(3) and dexamethasone was added to PBMC cultures. Dose-dependent inhibition of osteoclast formation and lacunar resorption was seen when PGE(2) was added to PBMC cultures in both the presence and the absence of dexamethasone. Thus, 1,25(OH)(2)D(3) and PGE(2) not only influence osteoclast formation in the presence of bone stromal cells but also act directly on circulating osteoclast precursors to influence osteoclast differentiation.

Cell Differentiation↗

PubMed2000

High extracellular calcium concentrations directly stimulate osteoclast apoptosis.

Although the inhibitory effects of high extracellular calcium concentrations ([Ca](e)) on osteoclastic bone resorption have been known for several years, the exact mechanism remains poorly understood. The present study was performed to investigate the possible effect of [Ca](e) on osteoclast apoptosis. Using highly purified rabbit osteoclasts, we have shown that calcium directly promotes apoptosis in a dose-dependent manner which correlates with the dose range of calcium for the inhibition of bone resorption. A time-course experiment of apoptotic changes of osteoclasts cultured in presence of 1.8 or 20 mM calcium showed a significant difference after as early as 8 h of culture. After 72 h of culture, we observed that 80% of the cells cultured in the presence of 20 mM calcium displayed the typical features of apoptosis compared to only 20% in the medium containing 1.8 mM calcium. Calcium channel blockers and ryanodine abrogated the effects of [Ca](e) on apoptosis while neomycin, a calcium-sensing receptor agonist, did not alter cell viability. Taken together, these results suggest that calcium influx is involved in calcium-induced osteoclast apoptosis. Our results are consistent with the concept that in the presence of high [Ca](e) generated during bone demineralization, osteoclasts are subjected to negative-feedback regulation due, at least in part, to the induction of apoptosis.

Animals↗

PubMed2000

The inhibitory effects of vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide on osteoclast formation are associated with upregulation of osteoprotegerin and downregulation of RANKL and RANK.

The presence of a network of peptidergic nerve fibers in the skeleton, expressing several neuropeptides including vasoactive intestinal peptide (VIP), has been demonstrated. This observation, together with our findings in vitro showing that VIP can regulate the activities of osteoblasts and osteoclasts as well as the recruitment of osteoclasts, has suggested the existence of a neuro-osteogenic interplay in bone metabolism. In the present study, the effects of VIP and pituitary adenylate cyclase-activating polypeptide (PACAP), two members of the VIP/secretin/glucagon superfamily, on osteoclast formation and mRNA expression of three key regulatory proteins involved in osteoclast formation have been investigated. VIP, PACAP-27, and PACAP-38, at concentrations of 10(-6) M, all significantly inhibited formation of tartrate-resistant acid phosphatase-positive multinuclear cells (TRAP + MNC) in mouse bone marrow cultures stimulated by 1, 25(OH)(2)-vitamin D3 (D3; 10(-8) M). By using semiquantitative RT-PCR, it was found that D3 upregulated the mRNA expressions of receptor activator of NF-kappaB ligand (RANKL) and receptor activator of NF-kappaB (RANK), whereas the expression of osteoprotegerin (OPG) was downregulated in mouse bone marrow cultures stimulated by D3 for 7 days. Both VIP and PACAP-38 decreased the stimulatory effects of D3 on RANKL and RANK expression, whereas the inhibitory effect of D3 on OPG expression was reversed by VIP and PACAP-38. These observations indicate that the inhibitory effects of VIP and PACAP on osteoclast recruitment are due to regulation of the expression of key proteins involved in later stages of osteoclast differentiation.

Animals↗

PubMed2001

Temporal and spatial localization of osteoclasts in colonies from embryonic stem cells.

Osteoclasts are hematopoietic cells essential for bone resorption. To understand the process of osteoclastogenesis, we have developed a culture system that employs a stromal cell line, in which differentiation of osteoclasts from single embryonic stem (ES) cells occurs. This culture, which did not require any cell passaging or other manipulations, enabled us to investigate the temporal and spatial localization of the osteoclast lineage in the colonies formed from ES cells. Cells expressing tartrate-resistant acid phosphatase, a specific marker of the osteoclast lineage, were first detected on day 8, and subsequently became localized at the periphery of colonies and matured into multinucleated cells to resorb bone. Addition of macrophage colony-stimulating factor and osteoprotegerin-ligand, which are produced by stromal cells, promoted osteoclastogenesis in whole colonies, indicating that the location and maintenance of mature osteoclasts as well as the growth and differentiation of osteoclast precursors are regulated by these two factors.

Animals↗

PubMed2001

Osteoclasts secrete the chemotactic cytokine mim-1.

Osteoclasts are terminally differentiated, multinucleated cells of monocytic origin. In this study, we report that osteoclasts secrete a 35 kD protein and that phorbol myristate acetate treatment stimulates secretion dramatically. Peptide digests of the protein were analyzed by mass spectroscopy. The protein was identified as myb induced myeloid protein-1 precursor (mim-1 protein). Mim-1 is expressed specifically by hematopoietic cells and has no known function. It is homologous with the neutrophil chemokine, chondromodulin II, which stimulates proliferation of osteoblasts and chondrocytes. Western analysis showed that osteoclasts secrete mim-1 into culture media. Immunofluorescence studies demonstrated a cytoplasmic and perinuclear distribution of mim-1 in both avian osteoclasts and human osteoclast-like cells. Expression and secretion of a chemokine-like protein by osteoclasts suggests a novel signaling pathway in the bone microenvironment that may be involved in coordinating bone remodeling.

Acetyltransferases↗

PubMed1995

Isolation and characterization of highly enriched, prefusion mouse osteoclastic cells.

This study describes the isolation and characterization of highly enriched mammalian osteoclast precursors, released by the "disintegrin" echistatin, from an osteoclast formation culture. Incubation of a 6-day coculture of mouse bone marrow cells and mouse osteoblastic cells (MB1.8) with echistatin (30 nM), an RGD-containing snake venom, for 20 min yielded an 88-95% pure population of tartrate-resistant acid phosphatase-positive cells, 1.5 x 10(5) cells per 150 cm2 culture dish. These cells were mostly mononucleated and based on the following characteristics are considered to be prefusion osteoclasts (pOC cells): (i) presence of calcitonin (CT) receptors documented by 125I-sCT autoradiography and cAMP generation in response to salmon calcitonin; (ii) expression of mRNAs for alpha v beta 3 integrin, osteopontin, 92-kDa type IV collagenase (matrix metalloproteinase 9), carbonic anhydrase II, OC-2 (an "osteoclastic" cysteine proteinase), and protein tyrosine phosphatase epsilon; and (iii) high level expression of pp60c-src protein. The pOC cells resorb bone (form "pits" on bone slices) but only in the presence of osteoblastic MB1.8 cells and 1,25(OH)2D3. Resorption was inhibited by CT. In conclusion, we describe a rapid, reproducible procedure to isolate virtually pure mammalian prefusion osteoclasts, which should help in the study of osteoclast formation, composition, and function.

Animals↗

PubMed1998

Carbonic anhydrase II plays a major role in osteoclast differentiation and bone resorption by effecting the steady state intracellular pH and Ca2+.

Carbonic anhydrase II (CA II) expression in characteristic for the early stage of osteoclast differentiation. To study how CA II, which is crucial in proton generation in mature osteoclasts, influences the osteoclast differentiation process we performed rat bone marrow cultures. In this model, acetazolamide, a specific CA inhibitor, decreased the 1,25 (OH)2D3-induced formation of multinucleated tartrate-resistant acid phosphatase (TRAP)-positive cells, in a dose-dependent manner. We then performed intracellular pH (pHi) and Ca2+ (Cai2+) measurements for cultured osteoclasts and noticed that addition of acetazolamide caused a rapid, transient increase of both parameters. The increase in pHi was dependent neither on the culture substrate nor on the extracellular pH (pHe) but the increase could be diminished by DIDS or by bicarbonate removal. Membrane-impermeable CA inhibitors (benzolamide and pd5000) did not have this effect. Addition of CA II antisense oligonucleotides into the cultures reduced the pHi increase significantly. CA II inhibition was also found to neutralize the intracellular vesicles at extracellular pH (pHe) of 7.4, but at less extent at pHe 7.0. In mouse calvaria cultures, bone resorption was inhibited dose dependently by acetazolamide at pHe 7.4 while inhibition was smaller at pHe 7.0. We conclude that CA II is essential not only in bone resorption but also in osteoclast differentiation. In both processes, however, the crucial role of CA II is at least partially due to the effect on the osteoclast pHi regulation.

Acetazolamide↗

PubMed1980

Lack of Fc receptors on osteoclasts.

Fc and C3 receptors, which are characteristically present on macrophages, could not be demonstrated on osteoclasts maintained in situ on their normal substrates when assayed for by use of sheep red blood cells coated with immunoglobulin (Shapiro et al. 1979). The present study tested the hypotheses that Fc receptors are present only on the osteoclast surface adjacent to bone and that Fc receptors on osteoclasts can be uncovered by enzymes or stimulated to appear. Freeze-dried, inverted osteoclasts (and osteoblasts) obtained from the endocranium of newborn rats were tested for Fc receptors using the rosette assay and examined by scanning electron microscopy. No rosettes were observed on the surfaces of the osteoclasts that had been approximal to the bone. Bone specimens were cultured for 30 min at 37 degrees C in control medium, or in medium with the addition of 10, 50 or 100 microgram/ml trypsin, 0.5 U/ml parathyroid extract (PTE), or 0.5 or IU/ml parathyroid hormone 1--34 (PTH). Additionally, two week-old rats were injected intraperitoneally with PTE (1.5 U/g body weight or 1 USP/g body weight) or with PTH (1 U/g body weight) or with vehicle alone, 6 h before sacrifice. The specimens were assayed for Fc receptors and examined by scanning electron microscopy. Macrophages were always used as controls for the assay. No rosettes were present on osteoclasts subjected to any of these treatments. Accordingly, the hypotheses were not supported.

Animals↗

PubMed1980

Effects of prostaglandin E2 on macrophages and osteoclasts in cultured fetal long bones.

Bone cultures exposed to prostaglandin E2 (PGE2) and revealed an increase in 45Ca release from bone to medium and an increase in osteoclast number compared to control bones. In addition, PGE2-treated osteoclasts contained a more extensive ruffled border region than control osteoclasts. These data suggest that PGE2 activates existing osteoclasts and causes proliferation and differentiation of osteoclast precursor cells. The existence of macrophages in resorbing fetal bone explants was documented. These macrophages contain numerous phagolysosomes and lipid vacuoles and are often located adjacent ot osteoclasts or closely apposed to calcified tissue surfaces. PGE2 caused an early increase in the number of macrophages. It is postulated that fetal bone macrophages are primarily engaged in phagocytosis and digestion of cellular debris, but also play a role in the process of bone resorption.

Animals↗

PubMed1992

Osteoclast precursors circulate in avian blood.

The osteoclast is known to be derived from a marrow-residing precursor that is a member of the mononuclear phagocyte family, but the means by which this cell moves from marrow to bone is unknown. We herein demonstrate that mononuclear progenitors capable of differentiating, in vitro, into cells exhibiting the osteoclast phenotype circulate in chickens. The mononuclear fraction was isolated on a density gradient from blood drawn from calcium-deprived laying hens and the plastic-adherent population was obtained. These cells are members of the mononuclear phagocyte family, as demonstrated by nonspecific esterase and tartrate-resistant acid phosphatase (TRAP) activities, expression of the macrophage-specific mannose receptor, and their ability to phagocytose latex particles. When cultured in the presence of devitalized bone, these cells undergo progressive multinucleation and ultimately become essentially indistinguishable from isolated osteoclasts and those generated from bone marrow precursors. Specifically, the blood-derived polykaryons are TRAP-positive, exhibit characteristic ruffled membranes, and express the osteoclast antigens 121F and 23C6. When placed on bone slices, these cells form typical resorptive "pits." Moreover, when cultured with 3H-proline-labeled bone, the blood monocyte-generated osteoclasts mobilize matrix as effectively as those derived from marrow. Thus, osteoclast precursors circulate in the blood of laying hens and can be induced to differentiate in vitro.

Acid Phosphatase↗

PubMed1993

Effect of 24R,25-dihydroxyvitamin D3 on the formation and function of osteoclastic cells.

Previous reports demonstrated that the administration of large doses of 24R,25-dihydroxyvitamin D3 [24R,25(OH)2D3] to animals with normal vitamin D supply causes an increase in bone volume with reduced bone resorption and decreased osteoclast number. The present study was undertaken to clarify if 24R,25(OH)2D3 has any inhibitor effect on the formation and function of osteoclasts. The effect of 24R,25(OH)2D3 on the formation of osteoclastic cells was examined by measuring the number of tartrate-resistant acid phosphatase-positive multinucleated cells (MNCs) formed from hemopoietic progenitor cells obtained from spleens of 5-fluorouracil-treated mice. Treatment with 1,25(OH)2D3 or parathyroid hormone fragment 1-34 [PTH(1-34)] stimulated osteoclast-like MNC formation in a dose-dependent manner. Addition of 24R,25(OH)2D3 alone showed a weak stimulatory effect on MNC formation at 10(-6) M, which appeared to be due to its binding to 1,25(OH)2D3 receptors. In contrast, when 24R,25(OH)2D3 was added together with 1,25(OH)2D3 or PTH(1-34), it inhibited osteoclast-like MNC formation stimulated by these hormones. A significant inhibition of MNC formation was observed with 10(-7) M 24R,25(OH)2D3, and the stimulatory effect of 1,25(OH)2D3 or PTH(1-34) was almost completely eliminated with 10(-6) M 24R,25(OH)2D3. Neither 24S,25(OH)2D3 nor 25(OH)D3 exhibited a similar inhibitory effect. The effect of 24R,25(OH)2D3 on the resorptive function of osteoclasts was examined by measuring the formation of resorption pits by mouse bone cells on dentine slices. Treatment with 24R,25(OH)2D3 also inhibited the resorption pit formation stimulated by 1,25(OH)2D3 or PTH(1-34) with similar dose response.(ABSTRACT TRUNCATED AT 250 WORDS)

24,25-Dihydroxyvitamin D 3↗

PubMed1994

The effect of 3-amino-1-hydroxypropylidene-1,1-bisphosphonate (ADP) on the resorptive function of osteoclasts of known nuclear number.

Bisphosphonates (BP) are known to suppress osteoclastic resorption in vivo and in vitro, but doubt persists as to how, and the effect of BP on the resorptive capability of osteoclasts of known nuclear number is unknown. We aimed to find whether the addition of 3-amino-1-hydroxypropylidene-1,1- bisphosphonate (APD) changed the nuclear profile of an osteoclast population in vitro, and to measure the resorptive efficiency of individually characterized osteoclasts in the presence and absence of the BP. Prehatch chick bone cells were cultured for 24 hours on slices of dentine in medium with or without added APD at 10(-6) M or 10(-8) M, or in control medium on dentine presoaked with 10(-6) M APD for 48 hours. Total pit counts, and pit depths, areas and volumes for pits made by osteoclasts of known nuclear number, were found using confocal video-rate laser reflection microscopy and 3-D image analysis software. APD in the medium inhibited resorption and reduced the volume, area, and depth resorbed per nucleus per chick osteoclast. The nuclear number distribution did not shift significantly, suggesting that no preferential effect arose from the APD affecting one size of cell more than another. The large reduction found in pit numbers, depths, areas, and volumes in the APD dentine-pretreated group supports previous views that BP released during resorption act as metabolic inhibitors, altering protein synthesis by the cell. Larger cells made larger pits, but resorptive efficiency was similar for different cell sizes within the control or APD-treated groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

K+ and Cl- currents in freshly isolated rat osteoclasts.

Membrane electrical properties of freshly isolated rat osteoclasts were studied using patch-clamp recording methods. Characterization of the passive membrane properties indicated that the osteoclast cell membrane behaved as an isopotential surface. The specific membrane capacitance was 1.2 +/- 0.3 microF/cm2 (mean +/- SD), with no difference between cells plated on glass and those adhering to a permeable collagen substrate. The current/voltage (I/V) relationship of all cells showed inward rectification and I/V curves shifted 51 mV positive per tenfold increase of [K+]out, indicating an inwardly rectifying K+ conductance. The voltage dependence of the K+ chord conductance (gK) also shifted positive along the voltage axis, and the maximum conductance increased, with elevation of [K+]out. gK for cells bathed in 4.7 mM [K+]out increased e-fold per 12 mV hyperpolarization, and half-maximal activation was at -89 mV. Approximately 18% (50 pS/pF) of the maximum gK was active at -70 mV. Inward single-channel currents were recorded in cell-attached patches at hyperpolarizing potentials. With symmetrical K+, channel conductance was 25 +/- 3 pS and reversal was close to the K+ equilibrium potential, consistent with this K+ channel underlying the whole-cell K+ currents. With both conventional whole-cell and perforated-patch recording, no voltage-activated Ca2+ current was detected. In approximately 30% of osteoclasts studied, an outwardly rectifying current was observed, which was reversibly blocked by 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS) and 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid (SITS). This DIDS- and SITS-sensitive current reversed direction at the chloride equilibrium potential. We conclude that an inwardly rectifying K+ current is present in all rat osteoclasts and that some osteoclasts also exhibit an outwardly rectifying Cl- current. Both these membrane conductances may play an important physiological role by dissipating the potential that arises from the electrogenic transport of H+ across the ruffled membrane of the osteoclast.

Animals↗

PubMed1993

Cytochalasin D reduces osteoclastic bone resorption by inhibiting development of ruffled border-clear zone complex.

The osteoclastic cytoskeleton has been demonstrated to be composed of microfilaments. Osteoclastic multinucleated cells were suspended on dentine slices and cultured for 24 hours in the presence or absence of cytochalasin D (CD), a specific and potent inhibitor of actin filament elongation to determine the role of this cytoskeleton. Cultured cells and co-cultured dentine slices were examined ultrastructurally. Unlike those in control cultures without CD, osteoclasts in CD-treated cultures became spherical in shape and lacked microvilli on their basolateral cell surfaces. Most importantly, CD treatment induced a complete disappearance of the ruffled border-clear zone complexes in osteoclasts, which resulted in loss of osteoclast-cytoplasmic polarity. Morphometric analysis of backscattered electron micrographs of co-cultured dentine slices revealed that CD treatment strongly inhibited the formation of resorption lacunae in a dose-dependent manner. These results suggest that the cytoarchitecture, as well as the bone-resorbing function, of the osteoclast is highly regulated by the F-actin-containing microfilamentous cytoskeleton in the ruffled border-clear zone complex.

Actins↗

PubMed1993

Binding of osteopontin to the osteoclast integrin alpha v beta 3.

Occupancy of the chicken osteoclast alpha v beta 3 integrin stimulates immediate cell signals. Peptides from osteopontin containing Arg-Gly-Asp and peptides from the osteopontin and bone sialoprotein sequences containing Arg-Gly-Asp stimulated immediate reductions in osteoclast cytosolic Ca2+. The changes in cytosolic Ca2+ required the Arg-Gly-Asp sequence, and were blocked by LM609, a monoclonal antibody to the alpha v beta 3 integrin. Osteoclast stimulation by the proteins through the integrin did not require immobilization since soluble peptides produced changes in cytosolic Ca2+ and inhibited osteoclast binding to bone particles and bone resorption. The decrease in cytosolic Ca2+ stimulated by osteopontin and related peptides was due to activation of a plasma membrane Ca(2+)-ATPase. Thus, the data suggest that ligand binding to the osteoclast alpha v beta 3 integrin results in a reduction in cytosolic Ca2+ which participates in regulation of osteoclast function.

Animals↗

PubMed1984

Differential response in alveolar bone osteoclasts residing at two different bone sites.

Using a histochemical method for demonstrating acid phosphatase activity, we have studied osteoclasts residing at two different bone sites in rat incisor alveolar bone, one at the endosteum and the other at the tooth socket, and compared the response of these osteoclasts to systemic changes. After 12 days of calcium (0%) or phosphorus (0.2%) deprivation, the number of osteoclasts/cross section at the endosteum increased 463% (P less than 0.001) and 103% (P less than 0.002), respectively. After 10 days of calcium or phosphorus replenishment, the number of osteoclasts at this bone site decreased to levels not significantly different from those in the control. In contrast, the number of osteoclasts at the incisor socket remained insignificantly changed throughout the experimental period. A similar osteoclast differential response was also observed in the alveolar bone surrounding the first molar tooth. After 12 days of calcium deprivation, the number of osteoclasts/mm bone surface increased 371% (P less than 0.001) at the endosteum but remained insignificantly changed at the first molar socket. These results suggest that an osteoclast differential response exists in alveolar bone and that the response may be of significance inasmuch as the major function of alveolar bone is to support the teeth. The work described here supports the concept of local as well as systemic regulation of bone metabolism to simultaneously perform the dual functions of mineral homeostasis and mechanical support.

Animals↗

PubMed1982

Bone acid phosphatase: tartrate-resistant acid phosphatase as a marker of osteoclast function.

Organ cultures of newborn mouse calvaria were used to test the hypothesis that tartrate-resistant acid phosphatase might serve as a biochemical marker for osteoclast function. When bone resorption was stimulated in vitro with either parathyroid hormone or 1,25(OH)2D3, there was a significant increase in both tartrate-resistant and tartrate-sensitivity acid phosphatase activity in the medium relative to cultured controls. Tartrate-resistant activity was localized histochemically primarily over the osteoclast and appeared as three distinct activity bands when electrophoresed on polyacrylamide gels. The tartrate-sensitive activity was found primarily associated with bone cells other than the osteoclast using histochemical techniques, and was resolved into five bands on polyacrylamide gels. The results obtained from biochemical assays, histochemical observations, and polyacrylamide gel electrophoresis suggest that bone resorption in vitro results in the release of tartrate-resistant acid phosphatase from osteoclasts and tartrate-sensitive acid phosphatase from other bone cells as well as osteoclasts. Tartrate-resistant acid phosphatases of bone may be suitable biochemical probes for osteoclasts function, but it will be necessary to achieve further purification in order to develop analytical methods with sufficient sensitivity and specificity (e.g., immunochemical) to ensure precise localization and quantitation.

Acid Phosphatase↗

PubMed1991

Osteoclast cytomorphometry demonstrates an abnormal population in B cell malignancies but not in multiple myeloma.

Increased bone resorption in the vicinity of myeloma cells is mediated by local stimulating factors. Other malignancies of the B cell lineage are also able to produce resorbing factors responsible for increased bone resorption. We have studied three groups of subjects: 10 patients with overt multiple myeloma, 10 patients with a B cell malignancy, and 10 healthy human subjects as controls. Patients were studied at the time of diagnosis and had a transiliac bone biopsy. Osteoclasts were evident on histological sections by their acid phosphatase activity. A software was developed on an automatic image analyzer (Leitz TAS+) for measuring the maximal Feret's diameter (Oc.Le) of each osteoclast (corresponding to the osteoclast length). The histogram of Oc.Le frequency distribution was supplied in each group. In myeloma patients, the Oc.Le frequency distribution was similar to that in normal subjects and showed the histogram to be asymetric with a positive skew (maximum peak at 20-25 microns). With a graphical analysis, this distribution was shown to follow a lognormal distribution corresponding to a homogeneous osteoclast population. In other B cell malignancies, Oc.Le displayed a bimodal distribution with a peak at 20-25 microns and a lower peak at 10-15 microns. The graphical analysis showed that small (mononucleated?) osteoclasts are present in B cell malignancies with normal osteoclasts. This might reflect the secretion of different soluble factors by malignant cells of the B lymphocyte lineage.

Acid Phosphatase↗