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the treatment of osteoporosis. The four categories of available treatment options are hormone replacement, calcitonin, bisphosphonates, and raloxifene. Estrogen replacement in postmenopausal women is a cornerstone of osteoporosis and fragility fracture prevention40 . Women taking estrogen (or hormone replacement therapy combined with a progestin) have been shown to have a decreased risk of osteoporotic fractures41,42 and as much as a 25% decrease in the risk of femoral neck fractures in case-controlled studies43-46 . However, estrogen therapy causes an increased risk of breast cancer and endometrial carcinoma in women with an intact uterus as well as an increased risk of thromboembolic events47. In addition, some women cannot tolerate these exogenous hormones. Bisphosphonates are selective osteoclast inhibitors and therefore preserve bone mass48. Alendronate (Fosamax) has been studied extensively in several prospective five-year trials. Patients treated with alendronate for one year have been shown to have a 50% decrease in the risk of fragility fracture49-51. More recently, similar success has been demonstrated with risedronate38,52. A study by McClung et al.53 showed that risedronate substantially reduces the risk of hip fracture in elderly women with established osteoporosis. The most common side effect of alendronate is mild esophagitis. Some studies have shown that this side effect does not occur more often in association with alendronate than in association with placebo50. However, when alendronate is used frequently, there is clearly an increased prevalence of dyspepsia, which can be eliminated by early cessation of the drug54. Once-a-week dosing is efficacious and is associated with less esophageal irritation. Calcitonin (Miacalcin) is a hormone, commonly administered intranasally, that has been shown to have a bonepreserving effect and to be clinically efficacious for the treatment of osteoporosis55. Compared with a placebo, calcitonin has been shown to reduce the risk of osteoporotic fractures56,57 , and it is also likely to have an analgesic effect in patients who have sustained such a fracture58 . Raloxifene (Evista) is a selective estrogen-receptor agonist that activates estrogen receptors in bone tissue and inhibits bone resorption without stimulating the uterine endometrium37. In a randomized study of 7705 women, Ettinger et al.59 demonstrated that raloxifene not only inhibits bone resorption but also reduces the risk of fragility fractures in the spine. Although more long-term studies are needed, raloxifene holds promise as an effective antiosteoporotic therapy for postmenopausal women. In summary, in our series of 300 elderly men and postmenopausal women who were admitted to one of three large metropolitan medical centers because of a low-energy hip fracture between 1997 and 2000, only 6.0% of the patients were discharged with a prescription for antiresorptive therapy. Another 13.3% of the patients were discharged with a prescription for at least 1200 mg of supplemental calcium per day, a necessary but solely inadequate treatment plan following an osteoporotic fracture. The remaining 81% of the patients were discharged without medication targeting osteoporosis. However, the trends in treatment were encouraging and improved significantly over the four years of the study. The low level of treatment for osteoporosis is disturbing, but it is hoped that the treatment rates will continue to increase in the future with ongoing efforts to raise physician awareness. We present some guidelines, based on recommendations from the National Osteoporosis Foundation, for the appropriate management of this patient population. References 1. Consensus development conference: prophylaxis and treatment of osteoporosis. Am J Med. 1991;90:107-10. 2. Lane JM, Russell L, Khan SN. Osteoporosis. Clin Orthop. 2000;372: 139-50. 3. Riggs BL, Melton LJ 3rd. The prevention and treatment of osteoporosis. N Engl J Med. 1992;327:620-7. 4. Looker AC, Johnston CC Jr, Wahner HW, Dunn WL, Calvo MS, Harris TB, Heyse SP, Lindsay RL. Prevalence of low femoral bone density in older U.S. Michael J. Gardner, MD Kyle R. Flik, MD Joseph M. Lane, MD Department of Orthopaedic Surgery, The Hospital for Special Surgery, 535 East 70th Street, New York, NY 10021. E-mail address for M.J. Gardner: gardnerm@hss.edu. E-mail address for K.R. Flik: flikk@hss.edu. E-mail address for J.M. Lane: lanej@hss.edu Pekka A. Mooar, MD Department of Orthopaedic Surgery, Medical College of Pennsylvania and Hahnemann University School of Medicine, 3300 Henry Avenue, Philadelphia, PA 19129. E-mail address: pekka.mooar@drexel.edu The authors did not receive grants or outside funding in support of their research or preparation of this manuscript. They did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associate Orthopaedic surgeons and fragility fractures A SURVEY BY THE BONE AND JOINT DECADE AND THE INTERNATIONAL OSTEOPOROSIS FOUNDATION K. E. Dreinhöfer, J.-M. Féron, A. Herrera, R.
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