Estrogens, bone mass, and osteoporotic fracture
Article Abstract:
In women, bone loss usually begins at the time of menopause, when the ovaries stop making estrogen. This observation led to the hypothesis that estrogen may be required for maintaining bone mass, and that estrogen deficiency may play an important role in osteoporosis (a condition of reduced bone density). Several studies have reported that bone mass is related to ovarian function. These studies found that bone mass decreased as ovarian function decreased, either due to menopause or disease. In one study, women who had their ovaries removed three years prior to the study had lower average bone mass than women of the same age who had functional ovaries. Another study reported that ovarian failure reduces calcium absorption in the intestines and increases calcium loss from the body. Ovarian function begins to decline gradually around the age of 35, and this is accompanied by a gradual decline in bone mass. Several studies have reported that estrogen supplements can prevent the loss of bone mass that occurs when the ovaries stop functioning. In one study, spinal bone mass was 29 percent greater and bone mass in the femur was 12 percent greater in women who were treated with estrogen for 10 to 15 years than in women who had not been treated. Several shorter studies, performed over a two-year period, have produced similar results. Treatment with estrogen has been reported to reduce the risk of hip and wrist fractures by 50 percent. Maintaining an adequate dietary intake of calcium and following an exercise program may enhance the effects of estrogen therapy in preventing bone loss. One study reported that the combined use of progestogen with estrogen results in a greater increase in bone mass than either agent when used alone. However, further studies are needed to verify these findings. It is not clear whether estrogen acts directly on bone cells to prevent bone loss or it stimulates the production of other factors that inhibit bone resorption. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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Treatment of osteoporosis with sodium fluoride or parathyroid hormone
Article Abstract:
Osteoporosis, which involves a reduction in bone density, can be prevented by inhibiting the resorption (loss) of the existing bone or by stimulating the formation of new bone. Calcium, estrogen and calcitonin are agents that prevent bone resorption and they have been approved by the Food and Drug Administration for treating osteoporosis in the United States. Sodium fluoride and parathyroid hormone (PTH), on the other hand, are agents that stimulate the formation of bone. Sodium fluoride has been used in European countries to treat osteoporosis, but it has not been approved for use in the United States. Since fluoride impairs the mineralization of newly formed bone, calcium supplements are given along with fluoride therapy. Fluoride therapy has been reported to increase cancellous bone mass in the lower spines of patients with osteoporosis by 5 to 10 percent per year over a four-year period. The new bone that is formed during fluoride therapy is more crystalline, less elastic and has less tensile strength. Therefore, the increased bone mass from fluoride treatment may not greatly increase bone strength. Also, fluoride therapy has been reported to increase the rate of loss of cortical (outer layer) bone. In two studies, treatment with fluoride reduced the rate of vertebral fractures by 26 percent. However, drugs that prevent bone resorption have been reported to decrease the rate of vertebral fractures by 57 percent. Studies performed using PTH have shown that high doses of PTH increase bone resorption, while low doses increase bone mass. In women, PTH has been reported to increase bone density in the lower spine by 11 to 32 percent within 6 to 12 months, but after this period bone mass began to decrease. Also, PTH increases the loss of cortical bone mass, and this loss cannot be prevented by calcium or vitamin D. Fluoride and PTH are thus not recommended for the routine treatment of osteoporosis. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Medicine
Subject: Health care industry
ISSN: 0002-9343
Year: 1991
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