Canonical and non-canonical pathways of osteoclast formation

Histology and Histopathology
Helen J Knowles, Nicholas A Athanasou

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 NFkappaB ligand (RANKL) and macrophage colony stimulating factor (M-CSF). Non-canonical 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, TNFalpha 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 non-canonical 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.

Citations

Jun 10, 2019·Clinical Hemorheology and Microcirculation·Rebecca RotheJens Pietzsch
Feb 25, 2021·ACS Biomaterials Science & Engineering·Sutton E WheelisDanieli C Rodrigues
Aug 27, 2021·Experimental and Therapeutic Medicine·Roxana-Maria Talpos-NiculescuLaura Cristina Rusu

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