Bone-Protective Pharmacotherapy in Endocrine Disease

Bone-protective drugs are prescribed to prevent fragility fractures, not simply to improve a bone mineral density (BMD) number. BMD matters, but a low-trauma hip or vertebral fracture already proves that bone strength has failed. A patient can also sustain a fragility fracture with a BMD above the osteoporosis range because age, falls, glucocorticoid exposure, vertebral deformity, and impaired bone architecture add risk that a scan cannot fully capture. Bone is continuously remodelled. Osteoclasts remove old bone; osteoblasts replace it. When resorption exceeds formation over years, trabeculae become thinner and disconnected, cortical bone becomes more porous, and fracture risk rises. Antiresorptive therapy slows osteoclast activity: - Bisphosphonates bind to hydroxyapatite in bone and remain there for years, continuing to suppress resorption after the drug is stopped. - Denosumab is a RANK-ligand monoclonal antibody. It blocks osteoclast formation and activity while doses continue, but it does not remain in bone. Its effect reverses quickly when injections are delayed or stopped. - Raloxifene and menopausal hormone therapy also reduce bone resorption in selected patients. Anabolic therapy is different. Teriparatide, an intermittent parathyroid hormone...