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Science. 2000 Sep 1;289(5484):1504-8.

Bone resorption by osteoclasts.

Author information

  • Department of Pathology, Washington University School of Medicine, Barnes-Jewish Hospital North, Mailstop 90-31-649, 216 South Kingshighway, St. Louis, MO 63110, USA. teitelbs@medicine wustl.edu.

Abstract

Osteoporosis, a disease endemic in Western society, typically reflects an imbalance in skeletal turnover so that bone resorption exceeds bone formation. Bone resorption is the unique function of the osteoclast, and anti-osteoporosis therapy to date has targeted this cell. The osteoclast is a specialized macrophage polykaryon whose differentiation is principally regulated by macrophage colony-stimulating factor, RANK ligand, and osteoprotegerin. Reflecting integrin-mediated signals, the osteoclast develops a specialized cytoskeleton that permits it to establish an isolated microenvironment between itself and bone, wherein matrix degradation occurs by a process involving proton transport. Osteopetrotic mutants have provided a wealth of information about the genes that regulate the differentiation of osteoclasts and their capacity to resorb bone.

PMID:
10968780
[PubMed - indexed for MEDLINE]
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