Canonical and non-canonical pathways of osteoclast formation

被引：2

作者：

Knowles, H. J. ^{[1
]}

Athanasou, N. A. ^{[1
]}

机构：

[1] Univ Oxford, Nuffield Orthopaed Ctr, Dept Pathol, Oxford OX3 7LD, England

来源：

HISTOLOGY AND HISTOPATHOLOGY | 2009年 / 24卷 / 03期

关键词：

Osteoclast; M-CSF; RANKL; resorption; osteolysis; COLONY-STIMULATING FACTOR; ENDOTHELIAL GROWTH-FACTOR; NECROSIS-FACTOR-ALPHA; GIANT-CELL TUMORS; OSTEOLYTIC BONE METASTASIS; HYPOXIA-INDUCIBLE FACTOR; FACTOR RECEPTOR GENE; OSTEOPROTEGERIN LIGAND; M-CSF; PHOSPHATIDYLINOSITOL; 3-KINASE;

D O I：

暂无

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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, TNF alpha 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-CSF-induced) 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.

引用

页码：337 / 346

页数：10

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