Molecular regulation of osteoclast activity

Rev Endocr Metab Disord. 2006 Jun;7(1-2):123-39. doi: 10.1007/s11154-006-9009-x.


Osteoclasts are multinucleated cells derived from hematopoietic precursors that are primarily responsible for the degradation of mineralized bone during bone development, homeostasis and repair. In various skeletal disorders such as osteoporosis, hypercalcemia of malignancy, tumor metastases and Paget's disease, bone resorption by osteoclasts exceeds bone formation by osteoblasts leading to decreased bone mass, skeletal fragility and bone fracture. The overall rate of osteoclastic bone resorption is regulated either at the level of differentiation of osteoclasts from their monocytic/macrophage precursor pool or through the regulation of key functional proteins whose specific activities in the mature osteoclast control its attachment, migration and resorption. Thus, reducing osteoclast numbers and/or decreasing the bone resorbing activity of osteoclasts are two common therapeutic approaches for the treatment of hyper-resorptive skeletal diseases. In this review, several of the key functional players involved in the regulation of osteoclast activity will be discussed.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Bone Resorption / genetics*
  • Cell Adhesion / physiology
  • Humans
  • Models, Biological
  • Osteoclasts / metabolism*
  • Osteoclasts / physiology
  • Receptor Activator of Nuclear Factor-kappa B / physiology
  • Receptor, Macrophage Colony-Stimulating Factor / physiology
  • Receptors, Calcitonin / physiology
  • Signal Transduction


  • Receptor Activator of Nuclear Factor-kappa B
  • Receptors, Calcitonin
  • Receptor, Macrophage Colony-Stimulating Factor