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Department of Medicine (A.B.H.), University of Western Ontario, London, Ontario, Canada N6A 4V2; Department of Medicine, Epidemiology, and Biostatistics, Division of Medicine (D.C.B.), University of California, San Francisco, California 94105-3411; Department of Pathology (D.W.D.), Columbia University, New York, New York 10027-6902; Regional Bone Center (D.D.), Helen Hayes Hospital, West Haverstraw, New York 10993; Division of Geriatric Medicine (L.D.), University of British Columbia, Vancouver, British Columbia, Canada V6T 2B5; Division of Endocrinology and Metabolism, Department of Medicine (D.A.H.), University of Calgary, Calgary, Alberta, Canada T2N 4N1; Department of Medicine (S.T.H.), University of California, San Francisco, California 94117-3619; Department of Medicine and Endocrinology (D.L.K.), Osteoporosis Research Centre, University of British Columbia, Vancouver, British Columbia, Canada V5Z 2N6; Oregon Osteoporosis Center and Department of Medical Education (M.R.M.), Providence Portland Medical Center, Portland, Oregon 97213; Department of Medicine, University of Colorado Medical School, and Colorado Center for Bone Research (P.D.M.), Lakewood, Colorado 80227; Department of Medicine, University of Saskatchewan, and Saskatoon Osteoporosis Centre (W.P.O.), Saskatoon, Saskatchewan, Canada S7K 0H6; Department of Medicine and General Clinical Research Centre (E.O.), Oregon Health & Sciences University, Portland, Oregon 97201-3079; and Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Manitoba, and Manitoba Clinic (C.K.Y.), Winnipeg, Manitoba, Canada R3A 1M3
* To whom correspondence should be addressed. E-mail: anthony.hodsman{at}sjhc.london.on.ca.
All therapies currently recommended for the management of osteoporosis act mainly to inhibit bone resorption and reduce bone remodeling. PTH and its analog, teriparatide [recombinant human PTH(1-34)], represent a new class of anabolic therapies for the treatment of severe osteoporosis, having the potential to improve skeletal microarchitecture. Significant reductions in both vertebral and appendicular fracture rates have been demonstrated in the phase III trial of teriparatide, involving elderly women with at least one prevalent vertebral fracture before the onset of therapy. However, there is as yet no evidence that the antifracture efficacy of PTH will be superior to the bisphosphonates, whereas cost-utility estimates suggest that teriparatide is significantly more expensive.
Teriparatide should be considered as treatment for postmenopausal women and men with severe osteoporosis, as well as for patients with established glucocorticoid-induced osteoporosis who require long-term steroid treatment. Teriparatide should also be considered for the management of individuals at particularly high risk for fractures, including subjects who are younger than age 65 and who have particularly low bone mineral density measurements (T scores 
3.5). Teriparatide therapy is not recommended for more than 2 yr, based, in part, on the induction of osteosarcoma in a rat model of carcinogenicity.
Total daily calcium intake from both supplements and dietary sources should be limited to 1500 mg together with adequate vitamin D intake (1000 U/d). Monitoring of serum calcium may be safely limited to measurement after 1 month of treatment; mild hypercalcemia may be treated by withdrawing dietary calcium supplements, reducing the dosing frequency of PTH, or both. At present, concurrent therapy with antiresorptive therapy, particularly bisphosphonates, should be avoided, although sequential therapy with such agents may consolidate the beneficial effects upon the skeleton after PTH is discontinued.
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