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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Bone Resorption*
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Carrier Proteins / metabolism
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Cell Differentiation
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Cell Membrane / physiology
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Cell Membrane / ultrastructure
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Glycoproteins / metabolism
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Humans
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Integrins / physiology
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Macrophage Colony-Stimulating Factor / metabolism
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Macrophages / cytology
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Macrophages / physiology
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Membrane Glycoproteins / metabolism
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Osteoclasts / cytology
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Osteoclasts / physiology*
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Osteoclasts / ultrastructure
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Osteopetrosis / genetics
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Osteopetrosis / metabolism
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Osteoprotegerin
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RANK Ligand
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Receptor Activator of Nuclear Factor-kappa B
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Receptors, Cytoplasmic and Nuclear*
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Receptors, Tumor Necrosis Factor / metabolism
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Stromal Cells / metabolism
Substances
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Carrier Proteins
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Glycoproteins
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Integrins
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Membrane Glycoproteins
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Osteoprotegerin
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RANK Ligand
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Receptor Activator of Nuclear Factor-kappa B
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Receptors, Cytoplasmic and Nuclear
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Receptors, Tumor Necrosis Factor
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TNFRSF11A protein, human
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TNFRSF11B protein, human
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TNFSF11 protein, human
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Macrophage Colony-Stimulating Factor