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Canonical and non-canonical pathways of osteoclast formation

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dc.contributor.authorKnowles, H.J.es
dc.contributor.authorAthanasou, N.A.es
dc.date.accessioned2013-09-24T11:33:51Z
dc.date.available2013-09-24T11:33:51Z
dc.date.issued2009
dc.description.abstractPhysiological and pathological bone resorption is mediated by osteoclasts, multinucleated cells which are formed by the fusion of monocyte / macrophage precursors. The canonical pathway of osteoclast formation requires the presence of the receptor activator for NFkB ligand (RANKL) and macrophage colony stimulating factor (M-CSF). Noncanonical pathways of osteoclast formation have been described in which cytokines / growth factors can substitute for RANKL or M-CSF to induce osteoclast formation. Substitutes for RANKL include LIGHT, TNFa and interleukins 6, 11 and 8. M-CSF substitutes include vascular endothelial growth factor (VEGF), placental growth factor (PlGF), FLt-3 ligand and hepatocyte growth factor (HGF). These growth factors can also influence canonical (RANKL / M-CSFinduced) osteoclast formation. Both canonical and noncanonical pathways of osteoclast formation play a role in the formation of osteolytic lesions where there is increased osteoclast formation and activity, such as in giant cell tumour of bone.es
dc.formatapplication/pdfes
dc.format.extent10es
dc.identifier.issn0213-3911es
dc.identifier.urihttp://hdl.handle.net/10201/36000
dc.languageenges
dc.publisherMurcia : F. Hernándezes
dc.relation.ispartofHistology and histopathologyes
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectOsteoclastes
dc.subjectOsteolysises
dc.subject.other616 - Patología. Medicina clínica. Oncologíaes
dc.titleCanonical and non-canonical pathways of osteoclast formationes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.24, nº3 (2009)