Increased bone fragility after menopause is commonly associated with accelerated bone loss and aggressive osteoclastic function. This is attributed to increased RANKL production and impaired osteoprotegerin synthesis. Fast bone loss leads to trabecular perforations, dramatic diminution of bone strength, and unexpected fractures. To avoid osteoporotic fractures, elimination of fast bone loss is recommended. Antiosteoclastic drugs, apart from estrogens, are the selective estrogen receptor modulators, calcitonins, and amino-bisphosphonates. These drugs increase bone mass by 1-5%, but reduce the relative risk of a vertebral fracture by 30-70%. Long-term exposure to bisphosphonates may be related to low bone turnover. In elderly and severe osteoporosis, antiosteoclastic regimens hardly correct the depressed osteoblastic function. Intermittent teriperatide stimulates osteoblastic function, improves bone geometry, and has an additional analgesic effect. While both anticatabolic and anabolic agents increase bone mass and decrease the risk of spinal fractures and occasionally of the fracture of the femoral neck, there are differences in the mode of their action. These pathophysiological differences are tentative therapeutic tools for the prevention of osteoporotic fractures. A fast bone loss, associated with increased biochemical markers, is the main indicator for anticatabolic agents, while impaired bone geometry, normal or low bone markers, and established bone architectural changes are in favor of the anabolic agents. Strontium ranelate combines the anticatabolic effect with an additional anabolic action.
© 2010 New York Academy of Sciences.