An overview of the regulation of bone remodelling at the cellular level

ObjectivesTo review the current literature on the regulation of bone remodelling at the cellular level.Design and methodsThe cellular activities of the cells in the basic multicellular unit (BMU) were evaluated.ResultsBone 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.ConclusionsOsteoporosis 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.

► Bone remodelling is a complex process involving multiple cell types.
► Cells involved produce various cytokines that have autocrine and paracrine activity.
► Multicellular communication is important for control of bone remodelling.
► Aberrant remodelling results in diseases such as osteoporosis and Paget's disease.