Abstract
Osteoclasts are primary cells for physiological and pathological bone resorption, and receptor activator of nuclear factor-kappaB ligand (RANKL) is critically involved in the differentiation, activation, and survival of these cells. Recently, therapeutics for pathological bone destruction targeting RANKL pathways has attracted a great deal of attention. Herein, we review the recent advances in the research on osteoclast biology and discuss the advantages and disadvantages of anti-RANKL therapies.
MeSH terms
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Animals
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Apoptosis
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Arthritis, Rheumatoid / etiology
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Bone Resorption / etiology*
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Bone Resorption / therapy
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Carrier Proteins / antagonists & inhibitors
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Carrier Proteins / physiology*
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Cell Differentiation
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Glycoproteins / antagonists & inhibitors*
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Glycoproteins / physiology
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Humans
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Membrane Glycoproteins / antagonists & inhibitors
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Membrane Glycoproteins / physiology*
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NF-kappa B / physiology
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Osteoclasts / cytology
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Osteoclasts / physiology
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Osteoporosis / etiology
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Osteoprotegerin
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Periodontal Diseases / etiology
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Proto-Oncogene Proteins c-bcl-2 / physiology
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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 / antagonists & inhibitors*
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Receptors, Cytoplasmic and Nuclear / physiology
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Receptors, Tumor Necrosis Factor / antagonists & inhibitors*
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Receptors, Tumor Necrosis Factor / physiology
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Signal Transduction*
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TNF Receptor-Associated Factor 6 / physiology
Substances
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Carrier Proteins
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Glycoproteins
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Membrane Glycoproteins
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NF-kappa B
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Osteoprotegerin
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Proto-Oncogene Proteins c-bcl-2
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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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TNF Receptor-Associated Factor 6
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TNFRSF11A protein, human
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TNFRSF11B protein, human
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TNFSF11 protein, human