Please use this identifier to cite or link to this item: http://hdl.handle.net/10201/36000

Title: Canonical and non-canonical pathways of osteoclast formation
Issue Date: 2009
Publisher: Murcia : F. Hernández
ISSN: 0213-3911
Related subjects: 616 - Patología. Medicina clínica. Oncología
Keywords: Osteoclast
Osteolysis
Abstract: Physiological 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.
Primary author: Knowles, H.J.
Athanasou, N.A.
Published in: Histology and histopathology
URI: http://hdl.handle.net/10201/36000
Document type: info:eu-repo/semantics/article
Number of pages / Extensions: 10
Rights: info:eu-repo/semantics/openAccess
Appears in Collections:Vol.24, nº3 (2009)

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