Osteoporosis is a systemic skeletal disease characterized by low bone mass and deterioration of bone microarchitecture, leading to increased fragility and fracture risk, especially in the spine, hip and wrist. It arises when bone resorption by osteoclasts chronically exceeds bone formation by osteoblasts. Age related hormonal changes, particularly the decline in estrogen after menopause, are major drivers in women. In men, age related testosterone decline and other comorbidities play important roles.

Diagnosis relies on bone mineral density (BMD) measurement, typically by dual energy X ray absorptiometry. A T score of −2.5 or lower defines osteoporosis, while values between −1.0 and −2.5 indicate osteopenia, a precursor state. However, fracture risk also depends on factors such as age, prior fractures, glucocorticoid use, smoking, alcohol intake, low body mass index, falls and certain chronic diseases. Risk prediction tools integrate these variables with BMD to estimate 10 year fracture probability.

Preventive strategies focus on achieving high peak bone mass in youth and slowing loss later in life. Adequate intake of calcium and vitamin D, regular weight bearing and muscle strengthening exercise, smoking cessation and limiting alcohol are central. Pharmacologic treatments aim to reduce fracture risk by modifying bone remodeling. Antiresorptive drugs such as bisphosphonates, denosumab and selective estrogen receptor modulators reduce bone breakdown. Anabolic agents like teriparatide and newer sclerostin inhibitors stimulate bone formation and can substantially increase BMD.

Research is exploring personalized treatment sequences, optimal therapy duration, drug holidays and combination or sequential use of anabolic and antiresorptive agents to maximize long term skeletal benefits while minimizing adverse effects.