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Osteoclastogenesis is the multistep process by which precursor cells of hematopoietic lineage (mostly monocytes/macrophages) differentiate into osteoclasts—multinucleated cells responsible for the resorption and remodeling of bone. It is driven by key signals including receptor activator of nuclear factor κB ligand (RANKL), macrophage colony-stimulating factor (M-CSF), and various cytokines. Disruption or excessive activation of osteoclastogenesis underlies multiple skeletal diseases such as osteoporosis, bone metastases, and inflammatory skeletal disorders. While osteoclastogenesis itself is not a direct therapeutic target, inhibition or modulation of the process via key molecular regulators like RANKL, cathepsin K, V-ATPases, and sclerostin is a major area of pharmacologic intervention in bone metabolic disease
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