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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 496))

Abstract

Osteoporosis is a major public health threat for millions of Americans, most of whom are women. Osteoporosis is responsible for more than one million fractures annually. Most debilitating among these are fractures of the wrist, spine, and hip. Therapeutic approaches for low bone mass or osteoporotic fracture include drugs that either suppress bone resorption or boost bone formation. Currently available therapies fall in the former category. These include estrogen/hormone replacement (e.g., conjugated estrogens), calcitonin, bisphosphonates (e.g., alendronate and risedronate), and selective estrogen receptor modulators (e.g., raloxifene). These therapies target the inhibition of osteoclastic bone resorption and reduce the rate of bone turnover. While highly efficacious in clinical trials of about 3 years duration, consequences due to longterm inhibition of bone turnover are currently unknown. Recently, long-term suppression of bone turnover in dogs was shown to lead to significant accumulation of microdamage with possibly detrimental effects on bone quality.

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Turner, C.H., Burr, D.B., Hock, J.M., Brommage, R., Sato, M. (2001). The Effects of PTH (1-34) on Bone Structure and Strength in Ovariectomized Monkeys. In: Majumdar, S., Bay, B.K. (eds) Noninvasive Assessment of Trabecular Bone Architecture and the Competence of Bone. Advances in Experimental Medicine and Biology, vol 496. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0651-5_17

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