Bisphosphonates promote apoptosis in murine osteoclasts in vitro and in vivo

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ID: 298073
1995
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Ranked #71 of 119 articles by views in journal of bone and mineral research : the official journal of the american society for bone and mineral research

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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 effect 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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openalex_W2161690532 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors D. E. Hughes, Kenneth R. Wright, Harry L. Uy, Akira Sasaki, Toshiyuki Yoneda, David Roodman, Gregory R. Mundy, Brendan F. Boyce
Journal journal of bone and mineral research : the official journal of the american society for bone and mineral research
Year 1995
DOI
10.1002/jbmr.5650101008
URL
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