Macrophage colony-stimulating factor stimulates survival and chemotactic behavior in isolated osteoclasts.

Fuller, K.; Owens, J M; Jagger, C. J.; Wilson, Amanda; Moss, R.E.; Chambers, T.J.

doi:10.1084/jem.178.5.1733

Cited by 328 publications

(227 citation statements)

References 51 publications

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“…However, only recently osteoblasts have been recognized to play a pivotal role in osteoclastogenesis process through the production of molecular factors such as RANKL, OPG, or CSF-1 [19][20][21][22][23]. Based on this new information, it has been shown that RANKL is essential to mediate the osteoclastogenic effect of PMMA [24].…”

Section: Introductionmentioning

confidence: 99%

The influence of wear particles in the expression of osteoclastogenesis factors by osteoblasts

Pioletti

Kottelat

2004

Biomaterials

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Orthopedic implant failures are often associated with peri-implant osteolysis. Particles generated from the wear process have been suspected to play an important role in this situation. Indeed, the peri-implant osteolysis could be due to the presence of particles stimulating the osteoclastogenesis process. We hypothesize then that the presence of a low particle concentration positively influences osteoblasts to produce osteoclastogenesis factors. If true, this hypothesis would then support the idea that the particles could be at the origin of the process leading to implant loosening. To check the validity of this hypothesis, we quantified in vitro the production of different genes involved in the osteoclastogenesis process using primary isolated human osteoblasts treated or not with particles. Results showed that low concentrations of particles might have a stimulating effect on osteoblasts to produce osteoclastogenesis factors as demonstrated by the increase of RANKL and CSF-1 gene expression in the particle group. r

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Section: Introductionmentioning

confidence: 99%

The influence of wear particles in the expression of osteoclastogenesis factors by osteoblasts

Pioletti

Kottelat

2004

Biomaterials

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“…6-8 sCSF-1, released by osteoblasts and csCSF-1, through direct cell contact, stimulate the proliferation and differentiation of osteoclast progenitors and survival of osteoclasts. [9][10][11] The importance of CSF-1 in osteoclast-mediated bone remodeling and tooth eruption has been shown in osteopetrotic (op/op) mice. Absence of CSF-1 in osteoblasts/stromal cells of these mice decreases osteoclasts and leads to osteopetrosis and failure of tooth eruption.…”

Section: Introductionmentioning

confidence: 99%

Targeted expression of csCSF-1 in op/op mice ameliorates tooth defects

Werner

Gluhak-Heinrich

Woodruff

et al. 2007

Archives of Oral Biology

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Objective-The aim of this study was to characterize the tooth phenotype of CSF-1-deficient op/ op mice and determine whether expression of csCSF-1 in these mice has a role in primary tooth matrix formation.Design-Ameloblasts and odontoblasts, isolated from wt/wt frozen sections using laser capture microdissection, were analyzed for csCSF-1, sCSF-1 and CSF-1R mRNA by RT-PCR. Mandibles, excised from 8 day op/op and wt/wt littermates, were examined for tooth morphology as well as amelogenin and DMP1 expression using in situ hybridization. Op/opCS transgenic mice, expressing csCSF-1 in teeth and bone using the osteocalcin promoter, were generated. Skeletal x-rays and histomorphometry were performed; teeth were analyzed for morphology and matrix proteins.Results-Normal dental cells in vivo express both CSF-1 isoforms and CSF-1R. Compared to wt/ wt, op/op teeth prior to eruption showed altered dental cell morphology and dramatic reduction in DMP1 transcripts. Op/opCS mice showed marked resolution of osteopetrosis, tooth eruption and teeth that resembled amelogenesis imperfecta-like phenotype. At 3 weeks, op/op teeth showed severe enamel and dentin defects and barely detectable amelogenin and DMP1. In op/opCS mice, DMP1 in odontoblasts increased to near normal and dentin morphology was restored; amelogenin also increased. Enamel integrity improved in op/opCS, although it was thinner than wt enamel.Conclusions-Results demonstrate that ameloblasts and odontoblasts are a source and potential target of CSF-1 isoforms in vivo. Expression of csCSF-1 within the tooth microenvironment is essential for normal tooth morphogenesis and may provide a mechanism for coordinating the process of tooth eruption with endogenous matrix formation.

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“…6,7 M-CSF promotes several aspects of osteoclastogenesis including the proliferation and fusion of osteoclast precursors as well as osteoclasts and the expression of the RANKL receptor by these cells. [8][9][10] The effect of M-CSF on mature osteoclast resorption activity is controversial with both a decrease and increase in lacunar resorption being reported. [11][12][13] Although bone resorption is greatly decreased in op/op mice, a few osteoclasts can still be found in skeletal tissues; op/op mice can also undergo a spontaneous age-dependent recovery of osteoclastogenesis.…”

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confidence: 99%

VEGF, FLT3 ligand, PlGF and HGF can substitute for M-CSF to induce human osteoclast formation: implications for giant cell tumour pathobiology

Taylor

Kashima

Knowles

et al. 2012

Laboratory Investigation

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Giant cell tumour of bone (GCTB) is a primary bone tumour that contains numerous very large, hyper-nucleated osteoclastic giant cells. Osteoclasts form from CD14 þ monocytes and macrophages in the presence of receptor activator of nuclear factor kappa B ligand (RANKL) and macrophage-colony stimulating factor (M-CSF). GCTB contains numerous growth factors, some of which have been reported to influence osteoclastogenesis and resorption. We investigated whether these growth factors are capable of substituting for M-CSF to support osteoclast formation from cultured human monocytes and whether they influence osteoclast cytomorphology and resorption. Vascular endothelial growth factor-A (VEGF-A), VEGF-D, FLT3 ligand (FL), placental growth factor (PlGF) and hepatocyte growth factor (HGF) supported RANKL-induced osteoclastogenesis in the absence of M-CSF, resulting in the formation of numerous TRAP þ multinucleated cells capable of lacunar resorption. Monocytes cultured in the presence of M-CSF, HGF, VEGF-A and RANKL together resulted in the formation of very large, hyper-nucleated (GCTB-like) osteoclasts that were hyper-resorptive. M-CSF and M-CSF substitute growth factors were identified immunohistochemically in GCTB tissue sections and these factors stimulated the resorption of osteoclasts derived from a subset of GCTBs. Our findings indicate that there are growth factors that are capable of substituting for M-CSF to induce human osteoclast formation and that these factors are present in GCTB where they influence osteoclast cytomorphology and have a role in osteoclast formation and resorption activity. The osteoclast is a multinucleated cell, which is formed from circulating mononuclear phagocyte precursors derived from the bone marrow. 1,2 It exhibits a number of specialised cytochemical and functional features, including the ability to carry out lacunar bone resorption. Increased osteoclast formation and activity is seen in a number of osteolytic bone and joint conditions, including notably giant cell tumour of bone (GCTB), a primary bone tumour, which contains numerous, very large, often hyper-nucleated osteoclastic giant cells that effect a considerable amount of bone resorption. 3,4 Osteoclast differentiation from monocyte or macrophage precursors requires the presence of receptor activator of nuclear factor kappa B ligand (RANKL) and macrophage-colony stimulating factor (M-CSF). 5 The importance of M-CSF in osteoclast formation is evidenced by the fact that in op/op osteopetrotic mice, which have a mutation in the M-CSF gene, very few osteoclasts are found in bone and there is markedly decreased bone resorption. 6,7 M-CSF promotes several aspects of osteoclastogenesis including the proliferation and fusion of osteoclast precursors as well as osteoclasts and the expression of the RANKL receptor by these cells. [8][9][10] The effect of M-CSF on mature osteoclast resorption activity is controversial with both a decrease and increase in lacunar resorption being reported. [11][12][13] Although bone resorption is gre...

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Macrophage colony-stimulating factor stimulates survival and chemotactic behavior in isolated osteoclasts.

Cited by 328 publications

References 51 publications

The influence of wear particles in the expression of osteoclastogenesis factors by osteoblasts

The influence of wear particles in the expression of osteoclastogenesis factors by osteoblasts

Targeted expression of csCSF-1 in op/op mice ameliorates tooth defects

VEGF, FLT3 ligand, PlGF and HGF can substitute for M-CSF to induce human osteoclast formation: implications for giant cell tumour pathobiology

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