Osteoporosis in Women

Bone undergoes continuous remodeling through coordinated osteoclast-mediated resorption and osteoblast-mediated formation. Estrogen is a critical inhibitor of osteoclast differentiation and activity via suppression of RANKL (receptor activator of nuclear factor kappa-B ligand) on osteoblasts and promotion of osteoprotegerin (OPG), the soluble decoy receptor for RANKL. Menopausal estrogen decline removes this protective effect, dramatically increasing osteoclast activity and bone resorption. Women lose 2-3% of bone mass annually during the first 5-7 years post-menopause, with accelerated loss from trabecular-rich sites (vertebrae, distal radius). Osteoporosis is defined by DXA T-score <= -2.5 at the lumbar spine, femoral neck, or total hip. Osteopenia (T-score -1.0 to -2.5) represents intermediate risk. The FRAX tool integrates clinical risk factors with bone density to estimate 10-year fracture probability, guiding treatment thresholds. Fragility fractures (occurring from standing height or less) indicate severe osteoporosis regardless of T-score.