Publication: Canonical and non-canonical pathways of osteoclast formation
Authors
Knowles, H.J. ; Athanasou, N.A.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
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.
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