title: A comparison of the effects of raloxifene and estrogen on bone in postmenopausal women.
abstract: Raloxifene HCl, a selective estrogen receptor modulator, has been shown to increase bone mineral density (BMD) and decrease biochemical markers of bone turnover in postmenopausal women without stimulatory effects on the breast and uterus. However, it is not known whether the changes in BMD and bone turnover are associated with changes at the tissue level, nor how changes with raloxifene compare with estrogen. In this randomized, double blind study, we evaluated the effects of raloxifene (Evista, 60 mg/day) or conjugated equine estrogens (CEE; Premarin, 0.625 mg/day) on bone architecture, bone turnover, and BMD. Iliac crest bone biopsies were obtained at baseline and at the end of the study after double tetracycline labeling and were analyzed for standard histomorphometric indexes. Serum and urinary biochemical markers of bone turnover were measured at baseline and at 4, 10, 18, and 24 weeks of treatment. Total body, lumbar spine, and hip BMD were measured at baseline and at the end of the study by dual energy x-ray absorptiometry. Activation frequency and bone formation rate/bone volume were significantly decreased from baseline in the CEE, but not in the raloxifene, group. Bone mineralization did not change in either group. Most markers of bone resorption and formation decreased in both groups, but to a greater degree in the CEE group (P < .05). Total body and lumbar spine BMD increased from baseline in both groups, with a greater increase in the CEE group (P < 0.05). Hip BMD significantly increased from baseline in the raloxifene group, but the change was not different from that in the CEE group. These results suggest that raloxifene reduces bone turnover and increases bone density, although to a lesser extent than CEE. Thus, raloxifene is an alternative to CEE for the prevention and treatment of osteoporosis in postmenopausal women.
authors.affiliation: Center on Aging and Division of Endocrinology and Metabolism, University of Connecticut Health Center, Farmington 06030-5215, USA. prestwood@nso1.uchc.edu
authors.forename: K M
authors.initials: KM
authors.lastname: Prestwood
authors.forename: M
authors.initials: M
authors.lastname: Gunness
authors.forename: D B
authors.initials: DB
authors.lastname: Muchmore
authors.forename: Y
authors.initials: Y
authors.lastname: Lu
authors.forename: M
authors.initials: M
authors.lastname: Wong
authors.forename: L G
authors.initials: LG
authors.lastname: Raisz
mesh_terms: D000368:Aged; D000469:Alkaline Phosphatase / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001706:Biopsy; D015519:Bone Density / Q000187:drug effects*; D001842:Bone and Bones / Q000166:cytology; D002136:Calcium, Dietary; D003094:Collagen / Q000097:blood; D024042:Collagen Type I; D003404:Creatinine / Q000097:blood; D004311:Double-Blind Method; D004965:Estrogen Antagonists / Q000627:therapeutic use; D004966:Estrogens, Conjugated (USP) / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides / Q000097:blood; D017698:Postmenopause; D011347:Procollagen / Q000097:blood; D020849:Raloxifene Hydrochloride / Q000627:therapeutic use*
chemical_list: D015415:Biomarkers; D002136:Calcium, Dietary; D024042:Collagen Type I; D004965:Estrogen Antagonists; D004966:Estrogens, Conjugated (USP); D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; C042813:procollagen type I carboxy terminal peptide; D015675:Osteocalcin; D020849:Raloxifene Hydrochloride; D003094:Collagen; D003404:Creatinine; D000469:Alkaline Phosphatase