Fractures, especially of the hip and spine, are among the main causes of morbidity and mortality in the elderly. The term "osteoporosis" indicates increased bone porosity, resulting in low bone density, increased bone fragility and an increased risk of fracture, often from a minor trauma.

During adolescence, bone accumulation occurs rapidly, which is essential for reaching the ideal peak of bone mass, normally reached in the third decade of life. Bone mass then remains stable until the age of 40-50, when it begins to decline. Peak bone mass sets the stage for immediate and future bone health. Individuals with lower peak bone mass tend to have less optimal bone health throughout their lives, and this becomes particularly problematic in men in older age groups and in menopausal women.
The best strategy for optimizing bone health is to prevent osteoporosis from occurring in the first place. This requires attention to the factors that contribute to optimal bone health. A person's genes have a major impact on bone density, but they are not currently modifiable.
The modifiable factors are: mechanical load on the bones through physical activity, maintaining a normal body weight and adequate intake of micronutrients (such as calcium and vitamin D) and macronutrients. Medications such as glucocorticoids, which have deleterious effects on bones, should be limited as much as possible. Endocrine, gastrointestinal, renal, rheumatic and other diseases, such as cancer, known to be associated with reduced bone density and increased risk of fractures, should be treated appropriately.
Deficiency of gonadal hormones (oestrogen and testosterone) and high serum cortisol concentrations are especially harmful to bones. Hormone replacement therapy in individuals with gonadal hormone deficiency and strategies to reduce cortisol levels in individuals with hypercortisolemia are essential to prevent osteoporosis and also improve bone density over time. The same applies to the treatment of chronic forms of arthritis and diseases such as anorexia, relative energy deficiency syndrome in sport, inflammatory bowel disease, celiac disease, cystic fibrosis, chronic kidney disease and arthritis.
Once osteoporosis has set in, depending on the cause, these strategies may be insufficient to completely reverse the disease, and pharmacological therapy may be necessary to increase bone density and reduce the risk of fractures. This is particularly a problem in menopausal women and older men. In these individuals, drugs that increase bone formation or reduce bone loss may be necessary.
Bisphosphonates and denosumab are drugs that reduce bone loss; these drugs are also called "antiresorptive drugs" because they reduce bone resorption by cells called osteoclasts. Bisphosphonates (alendronate, risedronate, ibandronate, pamidronate and zoledronic acid) have a direct effect on osteoclasts, reducing their activity. Some bisphosphonates, such as alendronate and risedronate, are administered orally (daily, weekly or monthly, depending on the drug and its potency), while others, such as pamidronate and zoledronic acid, are administered intravenously: every three to four months for pamidronate, and every six to twelve months for zoledronic acid. Ibandronate is available orally and intravenously.
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