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Previous Volume 351:2839-2849 December 30, 2004 Number 27 Next

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Bone is a dynamic tissue in which osteoblasts synthesize bone matrix while osteoclasts resorb bone. Therefore, bone density is dependent on the relative function of these two types of cells. Osteoclasts are multinucleated cells of hematopoietic lineage that are critical for bone remodeling; osteoblasts, in contrast, are of mesenchymal origin.¹ Osteoblasts synthesize bone matrix and in so doing lay down a microenvironment that supports osteoclast growth, maturation, and function. They also secrete macrophage colony-stimulating factor (M-CSF), granulocyte–macrophage colony-stimulating factor (GM-CSF), interleukin-1, and interleukin-6,² all of which influence the activities of osteoclasts. Direct interactions between osteoblasts or marrow stromal cells and . . . [Full Text of this Article]

Osteoclasts and Bone Resorption

Insights into the Biology of Osteoclasts

Early Differentiation Defects: PU.1 and M-CSF

Receptor Activator of Nuclear Factor-B and Related Proteins

Functional Osteoclast Defects Leading to Murine Osteopetrosis

Four Genotypes Affecting Acidification

Defects of Human Osteoclasts Associated with Osteopetrosis

Carbonic Anhydrase II Deficiency

Osteoclast Proton Pump Deficiency

Defects in the Chloride Channel

Other Genotypes Associated with Clinical Increases in Bone Density

"Acquired" Osteopetrosis

Summary

Source Information

From the Program in Blood and Marrow Transplantation, Department of Pediatrics (J.T., P.J.O.) and the Institute of Human Genetics (P.J.O.), University of Minnesota, Minneapolis; and the Department of Pathology and Immunology, Washington University, St. Louis (S.L.T.).

Address reprint requests to Dr. Orchard at 660D CCRB, MMC 366, University of Minnesota, 420 Delaware St. SE, Minneapolis, MN 55455, or at orcha001@umn.edu.

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