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Michael R. McClung, MD; Javier San Martin, MD; Paul D. Miller, MD; Roberto Civitelli, MD; Francisco Bandeira, MD; Molly Omizo, MD; David W. Donley, PhD; Gail P. Dalsky, PhD; Erik F. Eriksen, MD

Arch Intern Med. 2005;165:1762-1768.

Background  Antiresorptive agents for the treatment of osteoporosis suppress bone remodeling and reestablish bone turnover at a lower rate to reduce bone loss. Recombinant teriparatide (human parathyroid hormone 1-34) stimulates bone formation, increases bone mass, and improves bone microarchitecture. We contrasted the effects of once-daily doses of 20 µg of teriparatide and 10 mg of alendronate sodium on bone mineral density (BMD) and markers of bone turnover.

Methods  Markers of bone turnover and areal BMD were assessed in 203 postmenopausal women with osteoporosis in an 18-month randomized parallel double-blind study; volumetric BMD was measured in a subset of women.

Results  Teriparatide significantly increased markers of bone turnover that peaked at 6 months (serum procollagen type I N-terminal propeptide, 218%, and urinary N-telopeptide corrected for creatinine, 58%; P<.001); alendronate significantly decreased the markers at 6 months (–67% and –72%, respectively; P<.001). At 18 months, areal and volumetric spine BMDs were significantly higher with teriparatide than with alendronate (10.3% vs 5.5% [P<.001] and 19.0% vs 3.8% [P<.01], respectively). Areal femoral neck BMD was significantly higher than baseline in the teriparatide and alendronate groups (3.9% and 3.5%, respectively). There were no significant differences in trabecular femoral neck BMD between the teriparatide and alendronate groups (4.9% and 2.2%, respectively). Cortical volumetric femoral neck BMD was significantly different between the teriparatide and alendronate groups (–1.2% and 7.7%, respectively; P = .05).

Conclusion  Two distinct options for the management of osteoporosis lead to increases in BMD by opposite mechanisms of action on bone remodeling.

Author Affiliations: Oregon Osteoporosis Center, Providence Portland Medical Center, Portland (Drs McClung and Omizo); Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, Ind (Drs San Martin, Donley, Dalsky, and Eriksen); Colorado Center for Bone Research, Lakewood (Dr Miller); Barnes-Jewish Hospital, Washington University School of Medicine, St Louis, Mo (Dr Civitelli); and Osteoporosis Center, University of Pernambuco, and Hospital Agamenon Magalhaes, Recife, Brazil (Dr Bandeira).

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