Dr. Somnath Sarkar, Dr. Bruce H. Mitlak, Dr. Mayme Wong, Dr. John L. Stock, and Dr. Kristine D. Harper have financial interests in the forms of corporate appointments and stock ownership in Eli Lilly and Company. Dr. Dennis M. Black does consultant work for Eli Lilly and Company.
Relationships Between Bone Mineral Density and Incident Vertebral Fracture Risk with Raloxifene Therapy†
Article first published online: 1 JAN 2002
Copyright © 2002 ASBMR
Journal of Bone and Mineral Research
Volume 17, Issue 1, pages 1–10, January 2002
How to Cite
Sarkar, S., Mitlak, B. H., Wong, M., Stock, J. L., Black, D. M. and Harper, K. D. (2002), Relationships Between Bone Mineral Density and Incident Vertebral Fracture Risk with Raloxifene Therapy. J Bone Miner Res, 17: 1–10. doi: 10.1359/jbmr.2002.17.1.1
Portions of this work were presented in part at the meeting of the 1999 American Society for Bone and Mineral Research, 1999; the meeting of the World Congress of Osteoporosis, 2000; and the meeting of the American College of Rheumatology, 2000.
- Issue published online: 24 OCT 2009
- Article first published online: 1 JAN 2002
- Manuscript Accepted: 28 SEP 2001
- Manuscript Revised: 27 JUL 2001
- Manuscript Received: 26 FEB 2001
- bone mineral density;
- vertebral fracture;
Although low absolute values of bone mineral density (BMD) predict increased fracture risk in osteoporosis, it is not certain how well increases in BMD with antiresorptive therapy predict observed reductions in fracture risk. This work examines the relationships between changes in BMD after 1 year or 3 years of raloxifene or placebo therapy and the risk for new vertebral fractures at 3 years. In the Multiple Outcomes of Raloxifene Evaluation (MORE) trial, 7705 postmenopausal women with osteoporosis were randomized to placebo or raloxifene 60 mg/day or 120 mg/day. Relationships between baseline BMD and changes in BMD from baseline with the risk of new vertebral fractures were analyzed in this cohort using logistic regression models with the raloxifene doses pooled. As has been observed in other populations, women with the lowest baseline lumbar spine or femoral neck BMD in the MORE cohort had the greatest risk for vertebral fractures. Furthermore, for any percentage change, either increase or decrease in femoral neck or lumbar spine BMD at 1 year or 3 years, raloxifene-treated patients had a statistically significantly lower vertebral fracture risk compared with placebo-treated patients. The decrease in fracture risk with raloxifene was similar across the range of percentage change in femoral neck BMD observed at 3 years; patients receiving raloxifene had a 36% lower risk of vertebral fracture compared with those receiving placebo. At any percentage change in femoral neck and lumbar spine BMD observed at 1 year, raloxifene treatment decreased the risks of new vertebral fractures at 3 years by 38% and 41%, respectively. The logistic regression model showed that the percentage changes in BMD with raloxifene treatment accounted for 4% of the observed vertebral fracture risk reduction, and the other 96% of the risk reduction remains unexplained. The present data show that the measured BMD changes observed with raloxifene therapy are poor predictors of vertebral fracture risk reduction with raloxifene therapy.