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The Journal of Bone and Joint Surgery (American) 85:S4-S6 (2003)
© 2003 The Journal of Bone and Joint Surgery, Inc.

Cellular Mechanisms of Osteolysis

Denis Clohisy, MD

Corresponding author: Denis Clohisy, MD
Department of Orthopaedics, University of Minnesota, 420 Delaware Street S.E., Box 492, Minneapolis, MN 55455. E-mail address: clohi001@tc.umn.edu

The author did not receive grants or outside funding in support of his research or preparation of this manuscript. He did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the author is affiliated or associated.

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Over the past several years, there have been substantial advances in our understanding of the cellular and molecular events regulating osteoclast-mediated bone resorption. For decades, the coupling between bone-forming cells (osteoblasts) and bone-resorbing cells (osteoclasts) has not been well understood. Elucidation of this coupling has occurred recently with identification of the receptor/activator of NF-{kappa}B ligand (RANKL). RANKL is expressed on the cell surface of osteoblasts and bone-marrow stromal cells, and it directly stimulates the differentiation of osteoclast progenitor cells to form mature osteoclasts. RANKL-directed signaling is mediated through the receptor/activator of NF-{kappa}B (RANK), located on the cell membrane of osteoclast precursors and mature osteoclasts. By interacting with RANK, RANKL provides the coupling between bone formation and bone resorption ( Fig. 1) 1.


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