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The bone remodeling process is a lifelong, cyclic sequence whereby old or damaged bone is resorbed by osteoclasts and newly formed bone is produced by osteoblasts without altering bone geometry[5][1][3]. These activities are orchestrated within the basic multicellular unit (BMU), influenced by mechanical forces, hormonal signals (such as parathyroid hormone), cytokines (such as RANKL, OPG, M-CSF), matrix proteins, and growth factors (like TGF-β and IGF-1)[1][3][5][7]. Disruptions in bone remodeling are implicated in osteoporosis, osteoarthritis, bone fragility, and other metabolic bone diseases[6][4][8]. Bone remodeling is considered an operational or physiological process and not a therapeutic target per se. However, key molecules, receptors, and enzymes participating in bone remodeling (such as RANKL, cathepsin K, sclerostin, parathyroid hormone receptor, citrate) are direct targets for several pharmacological therapies—denosumab targets RANKL, romosozumab targets sclerostin, teriparatide mimics PTH, etc.[4][6][8].
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