Bisphosphonates promote apoptosis in murine osteoclasts in vitro and in vivo (original) (raw)
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Department of Pathology, University of Texas Health Science Center at San Antonio, San Antonio, Texas
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Department of Pathology, University of Texas Health Science Center at San Antonio, San Antonio, Texas
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Audie Murphy Veterans Administration Hospital, San Antonio, Texas
Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas
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Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas
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Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas
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Audie Murphy Veterans Administration Hospital, San Antonio, Texas
Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas
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Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas
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Department of Pathology, University of Texas Health Science Center at San Antonio, San Antonio, Texas
Department of Pathology University of Texas Health Science Center at San Antonio 7703 Floyd Curl Drive San Antonio, TX 78284
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Revision received:
19 May 1995
Published:
01 October 1995
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David E. Hughes, Kenneth R. Wright, Harry L. Uy, Akira Sasaki, Toshiyuki Yoneda, David G. Roodman, Gregory R. Mundy, Brendan F. Dr. Boyce, Bisphosphonates promote apoptosis in murine osteoclasts in vitro and in vivo, Journal of Bone and Mineral Research, Volume 10, Issue 10, 1 October 1995, Pages 1478–1487, https://doi.org/10.1002/jbmr.5650101008
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Abstract
Bisphosphonates inhibit bone resorption and are therapeutically effective in diseases of increased bone turnover, such as Paget's disease and hypercalcemia of malignancy. The mechanisms by which they act remain unclear. Proposed mechanisms include inhibition of osteoclast formation from precursors and inhibitory or toxic effects on mature osteoclasts. We have developed a new in vitro model to study osteoclast survival and in this paper present in vitro and in vivo evidence that may explain both the observed reduction in osteoclast numbers and in bone resorption by mature osteoclasts, namely that bisphosphonates induce programmed cell death (apoptosis). Three bisphosphonates (risedronate, pamidronate, and clodronate) caused a 4‐ to 24‐fold increase in the proportion of osteoclasts showing the characteristic morphology of apoptosis in vitro. This observation was confirmed in vivo in normal mice, in mice with increased bone resorption, and in nude mice with osteolytic cancer metastases, with similar‐fold increases to those observed in vitro. Of the three compounds, risedronate, the most potent inhibitor of bone resorption in vivo, was the strongest inducer of osteoclast apoptosis in vitro. Osteoclast apoptosis may therefore be a major mechanism whereby bisphosphonates reduce osteoclast numbers and activity, and induction of apoptosis could be a therapeutic goal for new antiosteoclast drugs.
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