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“Bone tissue with high turnover” refers to a physiological or pathological state of the skeleton characterized by an accelerated rate of bone remodeling, where the coupled processes of osteoclastic resorption and osteoblastic formation occur more rapidly than usual; it is not a discrete molecule or receptor and therefore is not a conventional therapeutic target. High turnover can occur during life stages such as puberty and in diseases including osteoporosis, Paget’s disease, primary hyperparathyroidism, and CKD–mineral bone disorder; it is assessed using bone turnover markers such as PINP, bone ALP, osteocalcin (formation) and CTX, NTX, TRACP-5b (resorption), often alongside iPTH in relevant conditions. Therapeutic interventions that “target” high turnover act on bone cells or signaling pathways—e.g., bisphosphonates inhibit osteoclasts, RANKL inhibitors block osteoclastogenesis, SERMs/estrogen decrease resorption, and calcitonin reduces osteoclast activity—thereby lowering excessive remodeling rates and fracture risk.
Inhibition of osteoclast-mediated bone resorption (bisphosphonates); Neutralization of RANKL to block osteoclast formation and activity (RANKL inhibitors); Modulation of estrogen signaling to reduce bone resorption and improve balance of remodeling (SERMs, estrogen therapy); Direct antiresorptive effect decreasing osteoclast activity (calcitonin)
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