Endocrinol Metab.  2010 Dec;25(4):264-269. 10.3803/EnM.2010.25.4.264.

Molecular Understanding of Osteoclast Differentiation and Physiology

Affiliations
  • 1Department of Biomedical Laboratory Science, Soonchunhyang University College of Medical Science, Asan, Korea. nlee@sch.ac.kr

Abstract

No abstract available.


MeSH Terms

Osteoclasts

Figure

  • Fig. 1. The mechanisms of osteoclastic bone resorption. Several transport systems including the H+-ATPase proton pump, Cl/HCO3 ex-changer and chloride channel are responsible for the acidification in the osteoclastic resorption lacunae. See text for further details.

  • Fig. 2. RANKL/RANK/OPG system: the regulation of osteoclast differentiation by osteoblasts. RANKL from stromal/osteoblasts binds the RANK receptor on osteoclast precursors, thus inducing osteoclast formation whereas OPG inhibits osteoclastogenesis.

  • Fig. 3. The critical molecules affecting osteoclast differentiation and function. In the early stage, M-CSF/ M-CSF receptor and PU.1 regulate the differentiation of hematopoietic stem cells into osteoclast precursors, which form multinucleated cells by cell-cell fusion. RANKL/ RANK signaling stimulates the activation of downstream molecules, thus inducing the formation of mature osteoclast tat resorb bones.


Reference

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