Postmenopausal osteoporosis management mandates a risk-stratified approach prioritizing bone-forming anabolic agents—teriparatide, abaloparatide, or romosozumab—in patients at very high fracture risk before transitioning to antiresorptive consolidation. Estrogen withdrawal accelerates trabecular bone loss via RANKL-mediated osteoclast activation, making early intervention critical. Anabolic therapy expands the bone modeling window and restores microarchitecture, whereas upfront bisphosphonate usage blunts subsequent anabolic efficacy. Strategic sequential therapy requires continuous long-term planning: stopping denosumab without a bisphosphonate bridge triggers catastrophic rebound resorption and multiple vertebral fractures, whereas antiresorptive therapy following anabolics preserves density gains to maximize structural fracture protection.
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