Abstract
Practitioners of clinical medicine in the Western World, whether primary care providers or subspecialists, are seeing more and more patients with osteoporosis. We propose two central explanations for this reality. As stated in the introductory chapter of this text, the first reason is that low bone mineral density (BMD) and resultant skeletal fragility is becoming more prevalent in our aging society. Using only dual energy x-ray absorptiometry (DEXA) measurements of femoral BMD from the third National Health and Nutrition Examination Survey (NHANES III, 1988–1994), the prevalence of osteoporosis (defined by the [WHO] as BMD>2.5 standard deviations [SD] below the mean of young, nonhispanic white females at peak bone mass) in women 50 years and older in the United States is 13-18% of the population or 4–6 million women (1). The prevalence of osteopenia (BMD>1.0 SD below peak bone mass) ranges from 37–50% of this population or 13–17 million women in the >50 age group (1). Furthermore, the percentage of currently osteopenic patients who will develop osteoporosis is projected to increase at a rate of 2% per year well into the 21rst century (2) if we do nothing to prolong the onset of this disease.
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Adams, J.S. (1999). Genetics of Osteoporosis. In: Adams, J.S., Lukert, B.P. (eds) Osteoporosis: Genetics, Prevention and Treatment. Endocrine Updates, vol 3. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5115-7_3
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DOI: https://doi.org/10.1007/978-1-4615-5115-7_3
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