[Treatment of osteoporosis: current data and prospects]

Postmenopausal osteoporosis is characterized not only by a reduction in bone mass but also by bone microarchitecture alterations, which result in greater bone frailty and in an increased fracture risk. Many drugs have been studied to determine whether they prevent bone loss or reduce the incidence of additional fractures in patients with established osteoporosis. Primary prevention of osteoporosis rests on regular exercising and adequate intake of dietary calcium. For secondary prevention in women undergoing menopause, replacement estrogen therapy given for at least ten years is associated with substantial reductions in fractures of the radius, hip, and spine. Other drugs capable of arresting postmenopausal bone loss include parenteral, nasal or rectal calcitonin and diphosphonates. However, the long-term safety of the latter requires further evaluation. Current studies are evaluating new molecules with potential preventive efficacy, such as ipriflavone. There is no general consensus about the efficacy of treatments for established osteoporosis with fractures. To date, no controlled studies have demonstrated a reduction in the incidence of further fractures in patients given calcium alone. Studies of hydroxylated vitamin D derivatives have been disappointing, although daily administration of vitamin D3 in combination with calcium significantly reduced the incidence of nonvertebral fractures in a population of elderly institutionalized subjects. Plausible explanations for this effect include increased vitamin D levels and reduced parathyroid levels in the bloodstream. Parenteral or nasal calcitonin stabilizes or increases bone mineral content in both cancellous and cortical bone. This effect is especially marked in high-turn-over patients. Several lines of evidence suggest that calcitonin therapy has a protective effect against vertebral and hip fractures. In patients with osteoporosis, oral or intravenous diphosphonates are associated with a significant increase in cancellous bone mass with no loss of cortical bone. Etidronate may be especially beneficial in severe osteoporosis with marked loss of bone and multiple vertebral crush fractures. Fluoride stimulates the growth and synthetic activity of osteoblasts. Accurate information is needed on the optimal dosage of fluoride, on the effects of fluoride on the appendicular skeleton, and, above all, on the biomechanical properties of the bone produced under fluoride therapy. In addition to these commercially available drugs, several other agents are at various stages of the development process.(ABSTRACT TRUNCATED AT 400 WORDS)