Hip fractures are common causes of morbidity and mortality in older adults, with a lifetime cost for hip fractures which is a major burden in public health. Two of the most important proximal factors leading to hip fracture are low bone density (osteopenia or osteoporosis) and falls. Alcohol consumption may influence each of these factors. Although alcohol use has been associated with an increased risk for falls, leading to injury or death in a variety of populations, this relation among older adults has not been established.

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The lifetime risk for fragility fractures due to osteoporosis after the age of 50 years is about 50% in women and 20% in men. The resultant high morbidity, mortality, and economic costs for elderly people have stimulated the development of effective interventions to reduce fracture risk. Despite these advances, however, the question remains as to whether patients take their treatment as prescribed (compliance) and for the recommended duration (persistence) [1].

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That cigarette smoking is detrimental to bone is now widely acknowledged and causes are not univocal. The cellular mechanisms underlying these effects, however, are not fully understood. Two recent studies, performed in rats [1] and man [2] bring new insights into this field.

In the first study, Hapidin et al. administered nicotine to rats for 4 months. They observed that nicotine administration increased serum concentrations of IL-1 and IL-6, two interleukins known to stimulate bone resorption. Histomorphometric analysis showed that nicotine significantly decreased the trabecular bone volume, trabecular thickness, mineralizing surface, mineral appositional rate, and bone formation rate.

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