2005
DOI: 10.1111/j.0105-2896.2005.00336.x
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Osteoclast precursors, RANKL/RANK, and immunology

Abstract: Rapid progress has been made in recent years in our understanding of the mechanisms regulating the formation, activation, and survival of osteoclasts, which are derived from precursor cells in the myeloid lineage. In contrast, study of the regulation of osteoclast precursors (OCPs) has been relatively slow, in part because it has been hard to accurately identify them. However, following the discovery of cell-surface markers that facilitated purification of OCPs, recent studies have demonstrated that peripheral… Show more

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Cited by 204 publications
(150 citation statements)
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“…Their precursors are formed in the marrow cavity, where they increase their proliferation and expression of c-Fms, the receptor for M-CSF, in response to cytokines such as TNF (54). OCPs circulate in the blood and are attracted to sites of inflammation, where pro-inflammatory cytokine concentrations are high (18), and to sites destined for resorption. OCPs enter resorption lacunae through blood vessels, where they appear to be separated from the adjacent marrow cells by a membrane inside which osteoclasts, osteoblasts, and other cells interact (55).…”
Section: Discussionmentioning
confidence: 99%
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“…Their precursors are formed in the marrow cavity, where they increase their proliferation and expression of c-Fms, the receptor for M-CSF, in response to cytokines such as TNF (54). OCPs circulate in the blood and are attracted to sites of inflammation, where pro-inflammatory cytokine concentrations are high (18), and to sites destined for resorption. OCPs enter resorption lacunae through blood vessels, where they appear to be separated from the adjacent marrow cells by a membrane inside which osteoclasts, osteoblasts, and other cells interact (55).…”
Section: Discussionmentioning
confidence: 99%
“…OCPs enter resorption lacunae through blood vessels, where they appear to be separated from the adjacent marrow cells by a membrane inside which osteoclasts, osteoblasts, and other cells interact (55). OCPs and osteoclasts secrete cytokines to modulate the activities of cells around them and, in that respect at least, can be considered to be immune cells at sites of inflammation in bone (8,18,56). Recent studies indicate that OCPs not only respond to osteoblasts to have their formation regulated either positively or negatively (1) but also regulate osteoblast formation both positively and negatively (30,57).…”
Section: Discussionmentioning
confidence: 99%
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“…The differentiation of monocyte/ macrophage-lineage precursor cells into mature osteoclasts is induced by the tumor necrosis factor (TNF) family cytokine receptor activator of NF-kB ligand (RANKL) together with colonystimulating factor (M-CSF), and provides an activating signal as well as survival signals to osteoclasts. (2,7) Osteoclasts are highly motile, but they firmly attach to the bone matrix in the course of bone resorption by means of a ''sealing zone,'' which is effected by an actin-rich structure, the podosome, and consists of a spatial compartment for bone resorption between the bone matrix and the osteoclast. (8) Integrin a v b 3 is important for the recognition and attachment to bone matrix by osteoclasts.…”
Section: Introductionmentioning
confidence: 99%
“…Receptor activator of NF-κB ligand (RANKL) is a key cytokine that stimulates the osteoclast precursor cells to fuse and undergo differentiation into osteoclasts (7,8). Macrophage colony-stimulating factor (M-CSF) also is an essential cytokine for osteoclastogenesis, which is important for the survival of the osteoclast lineage and the expression of RANK, the receptor for RANKL (9).…”
mentioning
confidence: 99%