Osteoporosis is a chronic skeletal disease characterized by low bone mass and deterioration of bone microarchitecture, leading to increased bone fragility and fracture risk. It arises when bone resorption by osteoclasts outpaces bone formation by osteoblasts, a process strongly influenced by aging, hormonal changes and lifestyle.

Estrogen deficiency after menopause is a major driver in women, accelerating bone loss, particularly in trabecular bone such as vertebrae. In men, age related declines in sex hormones and secondary causes, including hypogonadism, glucocorticoid therapy, alcoholism, smoking, low body weight and chronic inflammatory diseases, play important roles. Vitamin D deficiency and inadequate calcium intake impair bone mineralization and stimulate secondary hyperparathyroidism, which further increases bone resorption.

Diagnosis relies mainly on dual energy X ray absorptiometry to measure bone mineral density at the hip and spine. A T score of −2.5 or less defines osteoporosis, while values between −1.0 and −2.5 indicate osteopenia. Clinical risk factors, prior fractures and fracture risk calculators help guide decisions about treatment.

Preventive and therapeutic strategies combine lifestyle and pharmacologic measures. Weight bearing and resistance exercise, avoidance of tobacco and excessive alcohol, and adequate calcium and vitamin D intake support bone health. Pharmacologic options include antiresorptive drugs such as bisphosphonates and denosumab, and anabolic agents that stimulate bone formation, such as teriparatide, abaloparatide and newer sclerostin inhibitors. These therapies reduce vertebral and nonvertebral fractures in high risk individuals.

Research continues to explore the molecular regulation of bone remodeling, the role of inflammation and the gut microbiome, and strategies for earlier identification and personalized fracture prevention.