Vertebral fractures: a hidden problem of osteoporosis.

Osteoporosis is a progressive skeletal disease, which in many cases remains silent and asymptomatic until a fracture occurs. Vertebral fractures are the earliest and most common osteoporotic fractures. The prevalence of vertebral fractures increases steadily with age, ranging between 20% for 50-year-old postmenopausal women to 64.5% for older women. The majority of vertebral fractures are not connected with severe trauma, and only one in three is diagnosed clinically. Usually vertebral fractures are associated with such clinical symptoms as back pain, posture change, loss of height, functional impairment, disability, and diminished quality of live. Women with the most severe vertebral fractures are the most likely to incur further fractures, with as much as 3.4 times the risk of hip fracture, and 12.6 times the risk of new vertebral fractures. Almost 20% of women will experience another fracture within 1 year after a vertebral fracture. Vertebral fractures are accompanied by increased mortality. The relative risk of death following vertebral fracture is almost 9 times higher. The most important purpose of osteoporosis management in postmenopausal women is prevention of the first vertebral fracture. Raloxifene (Evista) is the only SERM approved by the American FDA for the treatment and prevention of osteoporosis. It is the first compound with selective estrogen agonist activity in bone and in the cardiovascular system, but with estrogen antagonist activity or no activity in reproductive tissues and breast. Raloxifene reduces the risk of positive estrogen receptor breast cancer, decreases total cholesterol and LDL cholesterol, increases HDL cholesterol, does not increase the risk of endometrial cancer or cause bleeding and spotting. After 3 years of treatment Raloxifene reduces the risk of first vertebral fracture by 55%. The fracture risk within one year is reduced by as much as 68%. Continued observation has proved its sustained efficacy in the further reduction of fracture risk by 49% in the fourth year. Raloxifene treatment does not change the physiological structure of bone quality and does not cause fibrosis, osteomalacia or other toxic effects.