2024-03-28T16:29:06Zhttps://digitum.um.es/digitumoai/requestoai:digitum.um.es:10201/360002020-02-16T00:30:11Zcom_10201_17677com_10201_19459com_10201_3col_10201_35886
Digitum: Repositorio Institucional de la Universidad de Murcia
author
Knowles, H.J.
author
Athanasou, N.A.
2013-09-24T11:33:51Z
2013-09-24T11:33:51Z
2009
0213-3911
http://hdl.handle.net/10201/36000
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.
info:eu-repo/semantics/openAccess
Osteoclast
Osteolysis
Canonical and non-canonical pathways of osteoclast formation
info:eu-repo/semantics/article
URL
https://digitum.um.es/digitum//bitstream/10201/36000/1/Canonical%20and%20noncanonical%20pathways%20of%20osteoclast%20formation.pdf
File
MD5
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Canonical and noncanonical pathways of osteoclast formation.pdf
URL
https://digitum.um.es/digitum//bitstream/10201/36000/2/Canonical%20and%20noncanonical%20pathways%20of%20osteoclast%20formation.pdf.txt
File
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Canonical and noncanonical pathways of osteoclast formation.pdf.txt