Osteoporosis--a review

Osteoporosis is a major medical problem in older women. Although a variety of factors influence bone formation and resorption, ovarian failure and a reduction in adrenal androgen production are major causes of menopausal osteoporosis. The prevention of trabecular bone loss and vertebral fractures in menopausal patients is feasible. Women who are at risk, so-called "fast bone losers," can be identified by office and chemical laboratory techniques. Estrogen therapy reduces or halts osteoclastic resorption and preserves bone mass. Exercise and anabolic hormones, including progesterone, stimulate osteoblastic building of bone. The combination of estrogen and progesterone reduces the risk of uterine malignancy below that seen in patients who take estrogen alone and possibly below the incidence seen in women who take no hormones. An individual's doses of replacement hormones will vary, depending on the amount of endogenous bone-targeted hormones and the response to treatment. These doses can be determined by monitoring their effect on 24-hour hydroxyproline and calcium excretion. Another way to monitor dose effect is by observation of the FSH levels. The serum FSH levels should be reduced at least to that level considered to be diagnostic of menopause. It may be unnecessary, if not inappropriate, to strive to restore FSH levels to normal premenopausal levels. Age-associated osteoporosis is a potentially fatal disease. Osteomalacia, with the associated loss of cortical bone, is superimposed upon the trabecular bone loss due to ovarian and adrenal androgen hormone deficiencies. These hormone deficiencies continue to operate upon trabecular bone at this later stage in the continuum. In addition to estrogen therapy and progesterone replacement, patients who are fracture victims may benefit from androgen replacement to increase their bone mass. Replacing androgens using nandrolone decanoate in women may address the natural loss of their adrenal bone-targeted hormones. The identification and treatment of individuals who need vitamin D and calcium replacement will reverse this contribution to the loss of bone. Clinical experience demonstrates that monitored hormone, vitamin D, and calcium supplements reduce the frequency of fractures, especially hip fractures, which may be reduced as much as 40% to 60% over a three-year period with such treatment. Cautious fluoride supplements in addition to calcium, hormones, and appropriate amounts of vitamin D appear to reduce vertebral fracture rates. The associated suffering, disability, and death from osteoporosis-induced fractures can be dramatically altered.(ABSTRACT TRUNCATED AT 400 WORDS)