An overview of the regulation of bone remodelling at the cellular level
OBJECTIVES: To review the current literature on the regulation of bone remodelling at the
cellular level. DESIGN AND METHODS: The cellular activities of the cells in the basic
multicellular unit (BMU) were evaluated. RESULTS: Bone remodelling requires an intimate
cross-talk between osteoclasts and osteoblasts and is tightly coordinated by regulatory
proteins that interact through complex autocrine/paracrine mechanisms. Osteocytes, bone
lining cells, osteomacs, and vascular endothelial cells also regulate bone remodelling in the …
cellular level. DESIGN AND METHODS: The cellular activities of the cells in the basic
multicellular unit (BMU) were evaluated. RESULTS: Bone remodelling requires an intimate
cross-talk between osteoclasts and osteoblasts and is tightly coordinated by regulatory
proteins that interact through complex autocrine/paracrine mechanisms. Osteocytes, bone
lining cells, osteomacs, and vascular endothelial cells also regulate bone remodelling in the …
OBJECTIVES
To review the current literature on the regulation of bone remodelling at the cellular level.
DESIGN AND METHODS
The cellular activities of the cells in the basic multicellular unit (BMU) were evaluated.
RESULTS
Bone remodelling requires an intimate cross-talk between osteoclasts and osteoblasts and is tightly coordinated by regulatory proteins that interact through complex autocrine/paracrine mechanisms. Osteocytes, bone lining cells, osteomacs, and vascular endothelial cells also regulate bone remodelling in the BMU via cell signalling networks of ligand–receptor complexes. In addition, through secreted and membrane-bound factors in the bone microenvironment, T and B lymphocytes mediate bone homeostasis in osteoimmunology.
CONCLUSIONS
Osteoporosis and other bone diseases occur because multicellular communication within the BMU is disrupted. Understanding the cellular and molecular basis of bone remodelling and the discovery of novel paracrine or coupling factors, such as RANKL, sclerostin, EGFL6 and semaphorin 4D, will lay the foundation for drug development against bone diseases.
Elsevier