الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Osteoporosis is a common skeletal disease characterized by low bone mineral density (BMD), deterioration of bone microarchitecture and increased fracture risk. It is a complex disease with high social and economic costs. The therapeutic options currently available for the prevention of postmenopausal osteoporosis include: dietary calcium, vitamin D3 supplementation, estrogen, progestogen, and raloxifene. There are many studies approved that HRT is effective in treatment of postmenopausal osteoporosis in the form of increasing bone mineral density (BMD) and decrease fracture risk. These studies demonstrate fracture prevention in the hip, wrist and all other fractures, not just vertebral fractures. Other studies demonstrate that bone density actually increases in the first years following institution of therapy. There is a dose–response with higher doses being more effective than lower doses in increasing bone density. To reach the optimum effect of HRT the treatment must be continued for 5-10 years, but long term use of hormone replacement therapy (HRT) is associated with many risks including deep venous thrombosis, endometrial cancer and increase risk for breast cancer. Although hormone replacement therapy (HRT) relieves perimenopausal vasomotor symptoms and maintains bone density, many women discontinue therapy before the long-term skeletal benefits are fully realized. Given a decision in this issue needs to make a balance between risks and benefits of HRT as an established treatment of postmenopausal osteoporosis.