Bis‑enoxacin blocks alveolar bone resorption in rats with ovariectomy‑induced osteoporosis.

Abstract:

:Postmenopausal osteoporosis is a common systemic skeletal disease that is associated with estrogen‑deficiency. Bone loss associated with bisphosphonates therapy can increase the risk of developing oral osteonecrosis. Recent studies have indicated that enoxacin may inhibit osteoclast formation and bone resorption via a different mechanism from that of bisphosphonates. Therefore, the authors hypothesized that the use of an enoxacin such as bis‑enoxacin (BE) in association with bisphosphonates may be effective in the treatment of postmenopausal osteoporosis‑associated alveolar bone resorption and reduce the risk of oral osteonecrosis by allowing the dose of bisphosphonates to be reduced. A total of 30 6‑month‑old female Sprague‑Dawley rats were randomly assigned to five groups: The Sham, Vehicle, zoledronic acid (ZOL), low concentrations of BE (BE‑L) and high concentrations of BE (BE‑H) groups. The results demonstrated that the ZOL, BE‑L and BE‑H groups had an increased bone volume/tissue volume, trabecular thickness, mineral apposition rate, mineralizing surface/bone surface and a decreased trabecular separation when compared with the Vehicle group. The microscopic evaluation of histological sections clearly supported the results of the micro‑computed tomography. The number of tartrate‑resistant acid phosphatase‑positive osteoclasts was markedly decreased in the ZOL, BE‑L and BE‑H groups, indicating that BE may inhibit osteoclast formation. The anti‑resorptive effect in the BE‑H group was close to or better than that exhibited by the ZOL group; however, this effect was poorer in the BE‑L group. In conclusion, BE has the potential to block alveolar bone resorption resulting from ovariectomy‑induced osteoporosis in rats in a dose‑dependent manner.

journal_name

Mol Med Rep

authors

Zhang X,Xu X,Liu X,Mao C,Qin A,Lu E

doi

10.3892/mmr.2017.8223

subject

Has Abstract

pub_date

2018-02-01 00:00:00

pages

3232-3238

issue

2

eissn

1791-2997

issn

1791-3004

journal_volume

17

pub_type

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