The progressive loss of bone mass that leads to osteoporosis in postmenopausal women is known to result in substantial morbidity and mortality. Underdiagnosed and undertreated, osteoporosis jeopardizes the health of an estimated 8 million American women 50 years of age or older who are at high risk for hip, vertebral, and other fractures. Because osteopenia is generally a subclinical condition that results in a lower fracture rate than osteoporosis, its potential impact is more difficult to recognize, although it is nearly three times more prevalent than osteoporosis. The question arises as to whether osteopenia should be diagnosed and treated before it transitions into osteoporosis. Because the number of postmenopausal women is projected to increase substantially in the near future and the number of postmenopausal women who will or who have discontinued their use of hormone therapy has increased sharply, the consequences of failing to identify and treat women at increased fracture risk are considerable. Moreover, the rate of bone loss in the first year after discontinuation of hormone therapy is especially rapid and similar to the rate that occurs early after menopause. Accordingly, fracture risk is substantially increased at this time in relation to the magnitude of bone loss. The goal of nonpharmacologic and pharmacologic therapy is to prevent the first fracture in any woman at risk for fracture. Initiation of antiresorptive therapy known to provide rapid efficacy can be particularly important in achieving the treatment goal in appropriate osteopenic women.
The morbidity and mortality that can result from failing to identify and treat women at increased fracture risk are considerable. This article will explore the question of whether osteopenia, a subclinical state of osteoporosis, should be diagnosed and treated before it transitions into osteoporosis.
From George Washington University, Washington, DC, and The Women's Health Research Center, Laurel, MD.
Received September 22, 2004; revised and accepted December 14, 2004.
Dr. Simon is a consultant to Abbott Laboratories; Barr Pharmaceuticals, Inc.; Berlex, Inc.; BioSante Pharmaceuticals, Inc.; Endeavor Pharmaceuticals, Inc.; Lipocine, Inc.; Merck & Co., Inc.; Novavax, Inc.; Pfizer Inc; Solvay Pharmaceuticals, Inc.; TAP Pharmaceutical Products Inc.; Warner Chilcott PLC; and Wyeth. He is a Speakers Bureau member for Aventis Pharmaceuticals; Eli Lilly and Company; Merck & Co., Inc.; Ortho-McNeil Pharmaceutical, Inc.; Pfizer Inc; and Solvay Pharmaceuticals, Inc. He has received grants and research support from Balance Pharmaceuticals, Inc.; Barr Pharmaceuticals, Inc.; Bayer; Berlex, Inc.; Besins; BioSante Pharmaceuticals, Inc.; Bristol-Myers Squibb Company; Duramed Pharmaceuticals, Inc.; Eli Lilly and Company; Endeavor Pharmaceuticals, Inc.; Merck & Co., Inc.; National Institutes of Health; Novartis Pharmaceuticals Corporation; Novavax, Inc.; Organon; Pfizer Inc; Procter & Gamble; 3M Pharmaceuticals; TAP Pharmaceutical Products Inc.; Warner Chilcott PLC; Watson Pharmaceuticals, Inc.; and Wyeth.
Address correspondence to: James A. Simon, MD, George Washington University School of Medicine, 1850 M Street, NW, Suite 450, Washington, DC 20036-5803. E-mail: email@example.com.