Because daily treatment with parathyroid hormone (PTH) increases bone mass and decreases fracture risk, physicians use this agent to treat osteoporosis. However, PTH stimulates both bone-forming and bone-resorbing cells, complicating its clinical use. New results show that, in mice, a so-called biased agonist (PTH-betaarr) that selectively activates beta-arrestin -dependent signaling leads to PTH-induced trabecular bone formation without a simultaneous increase in bone resorption. This targeted approach may pave the way for future pharmacological developments in the treatment of osteoporosis.
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