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osteoclasts; culprits in inflammatory osteolysis破骨细胞;
Available online /content/8/1/201
Review
Osteoclasts; culprits in inflammatory osteolysis
Steven L Teitelbaum
Department of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8118, St Louis,
MO 63110, USA
Corresponding author: Steven L Teitelbaum, teitelbs@
Published: 29 November 2005 Arthritis Research Therapy 2006, 8:201 (doi:10.1186/ar1857)
This article is online at /content/8/1/201
© 2005 BioMed Central Ltd
Abstract characterized by enhanced bone mass caused by a failure of
osteoclast recruitment or function. The fact that an
Periarticular osteolysis, a crippling complication of rheumatoid
arthritis, is the product of enhanced osteoclast recruitment and osteopetrotic child was cured by marrow transplantation in
activation. The osteoclast, which is a member of the monocyte/ the early 1980s established that the human osteoclast is of
macrophage family, is the exclusive bone resorptive cell, and its hematopoietic origin [6]. Subsequent studies document that
differentiation and activation are under the aegis of a variety of the resorptive cell is a member of the monocyte/macrophage
cytokines. Receptor activator of NF-κB ligand (RANKL) and
family [7] and provide the tools for generating the cell in
macrophage colony-stimulating factor are the essential osteo-
clastogenic cytokines and are increased in inflamma
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