Chapter 33: Osteoporosis – Drug Management & Prevention

The disease pathology involves an imbalance in continuous bone remodeling, where the rate of bone resorption carried out by osteoclasts exceeds the rate of new bone formation by osteoblasts. This imbalance is often systemically regulated by hormones like parathyroid hormone (PTH) and calcitriol, and locally by factors like the RANK/RANKL/OPG system; notably, the rapid bone loss observed in postmenopausal women is linked to decreased estrogen and resulting greater osteoclast activity. Diagnosis and risk stratification rely on measuring bone mineral density (BMD) using Dual-Energy X-ray Absorptiometry (DEXA) scans to calculate T-scores (for diagnosis) and Z-scores (for age-matched comparison). Screening is recommended for all women aged 65 and men aged 70, or younger individuals possessing clinical risk factors or a history of fragility fracture. The World Health Organization's FRAX tool further assesses the patient's 10-year probability of experiencing a major osteoporotic fracture. Management includes foundational measures such as fall prevention, engaging in muscle-strengthening and weight-bearing exercises, and ensuring adequate intake of calcium and Vitamin D, which is crucial for absorption. Pharmacologic treatment is indicated for high-risk patients (T-score ≤−2.5 or high FRAX risk). Treatment options include antiresorptive agents, which slow bone breakdown, such as bisphosphonates (like alendronate), calcitonin, Selective Estrogen Receptor Modulators (SERMs, e.g., raloxifene), and RANK Ligand inhibitors (denosumab). For patients needing stimulation of new bone growth, anabolic agents are prescribed, including PTH and PTH-related protein analogs (teriparatide, abaloparatide) or the sclerostin inhibitor (romosozumab-aqqg). Effective therapy requires regular monitoring of BMD, often via DEXA every two years, and continuous assessment of patient adherence to minimize the risk of fracture-related morbidity and mortality.