Pathogenetic and pharmacological problems of bone homeostasis in osteoporosis
Abstract
Osteoporosis is a systemic disease characterized by a deterioration of bone microarchitecture and a decrease in bone mass, which leads to the risk of fractures. Loss of bone mass, associated with estrogen deficiency, is often the cause of fractures in women over 50 years old. Estrogen deficiency disrupts the normal cycle of bone homeostasis by increasing the resorption activity of osteoclasts without a corresponding increase in the activity of osteoblasts, which leads to bone loss. Fractures lead to disability, deterioration of the quality of life, and increased risk of mortality. Because the risk of osteoporotic fractures increases with age, osteoporosis is a major public health problem worldwide. In this review, literature data on pathogenetic mechanisms of bone homeostasis, secondary factors affecting the development of osteoporosis and the use of pharmacological drugs to increase bone density and improve their strength are analyzed. Since osteoporosis is characterized by bone resorption that exceeds bone formation, antiresorptive drugs are one of the therapeutic options for this disease. Another therapeutic option may be the use of anabolic drugs that enhance bone formation. Hormone replacement therapy not only prevents bone loss and degradation of bone microarchitecture, but also significantly reduces the risk of fractures. In addition, calcium and vitamin D supplements remain an essential adjunct to the pharmacological treatment of osteoporosis. The review shows which pharmacological treatment options for osteoporosis are best used to reduce the risk of fractures. Literature data obtained as a result of a literature search on the PubMed platform, a Google Scholar search for clinical and pathogenetic features, diagnosis and treatment of osteoporosis were analyzed.
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