OSTEOPOROSIS - PATHOPHYSIOLOGY, PREVENTION, DIAGNOSIS, AND TREATMENT

Bone is a living tissue; throughout life, new bone formation coexists with bone resorption. Although a large number of hormones and cytokine s modulate osteoblast and osteoclast function, osteoporosis results fr om any disorder in which bone formation becomes uncoupled from bone re sorption. Many disorders are associated with the uncoupling of bone fo rmation and resorption. The most common is loss of gonadal steroid act ion on bone, as occurs in menopause or in male and female hypogonadism not associated with menopause. Other relatively common causes include primary hyperparathyroidism and endogenous or exogenous hypercortisol ism and thyrotoxicosis. A large number of other, less frequent disorde rs also cause osteoporosis. Treatment of osteoporosis consists first o f removing the cause if possible, for example, abolishing hypercortiso lism, thyrotoxicosis, or hyperparathyroidism. In menopausal women or h ypogonadal men or women, replacement of estrogens or androgens represe nts effective therapy. Estrogens and androgens given to hypogonadal su bjects strikingly reduce bone resorption. For patients with establishe d osteoporosis who either cannot take gonadal steroids or who are not hypogonadal, calcitonin decreases bone resorption and may stabilize bo ne mass. Estrogen replacement and calcitonin are approved by the Food and Drug Administration for treatment of osteoporosis. Experimental th erapies presently include 1,25-dihydroxyvitamin D (calcitriol), bispho sphonates in intermittent treatment regimes, and fluoride in lower dos ages than were used in previous studies. The use of fluoride is contro versial, and to some extent it has fallen into disrepute. Effective us e of any treatment is predicated on understanding the pathophysiology in any particular disease setting.