Extra cancellous bone induced by combined prostaglandin E2 and risedronate administration is maintained after their withdrawal in older female rats.
Extra cancellous bone induced by combined prostaglandin E2 and risedronate administration is maintained after their withdrawal in older female rats.
复制标题
老年雌性大鼠停药后，联合使用前列腺素 E2 和利塞膦酸盐诱导的额外松质骨得以维持。
DOI：
10.1002/jbmr.5650100618
复制
发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Ke,HZ
中科院分区：
文献类型：
--
作者：
Jee,WS;Lin,BY;Ma,YF;Ke,HZ
前列腺素E2（PGE 2）对骨的合成代谢有显著的作用，但停止PGE 2治疗后，骨增量丧失。在以前的研究中，我们在停用PGE 2治疗后给予双磷酸盐成功地维持了新骨。本研究的目的是确定PGE 2和利塞膦酸钠联合治疗停止后诱导的额外骨的命运。96只9月龄未交配雌性Sprague道利大鼠接受1或5 μg利塞膦酸盐/ kg/每周两次、6 mg PGE 2/kg/天单独给药或6 mg PGE 2/kg/天加1或5 μg利塞膦酸盐/kg/每周两次给药，持续60天（第0天），随后60天不给药（第60天）。我们已经报告了60天前治疗组的结果。本报告仅限于停药60天后各组胫骨近端干骺端继发性松质骨的组织形态计量学结果。我们发现，唯一一个在停药后保持PGE 2诱导的新骨的组是用6 mg PGE 2/kg/天加5 μg利塞膦酸钠/kg/周两次治疗的组。停止这种联合治疗会降低骨转换（基于骨的骨形成率，激活频率）和骨吸收（侵蚀周长百分比）。负责保护的组织机制来自先前沉积的利塞膦酸盐。
Prostaglandin E2(PGE2) has been recognized for its marked anabolic effect on bone, but the bone gain is lost after the cessation of PGE2treatment. In previous studies, we were successful in maintaining the new bone by administering a bisphosphonate after the withdrawal of PGE2treatment. The objective of this study was to determine the fate of the extra bone induced by a combination with PGE2and risedronate after discontinuing treatment. Ninety‐six 9‐month‐old virgin female Sprague‐Dawley rats were treated with 1 or 5 μg of risedronate/ kg/twice weekly, 6 mg of PGE2/kg/day alone or 6 mg of PGE2/kg/day plus 1 or 5 μg of risedronate/kg/twice weekly for 60 days (day 0) and followed by 60 days without treatment (day 60). We have reported the results from the groups treated for 60 days previously. This report is restricted to the histomorphometric findings on the secondary spongiosa of the proximal tibial metaphysis in the groups after withdrawal for 60 days. We found that the only group that maintained the PGE2induced new bone after withdrawal was the group treated with 6 mg of PGE2/kg/day plus 5 μg of risedronate/kg/twice a week. Withdrawal of this combined treatment depressed bone turnover (bone‐based bone formation rate, activation frequency) and bone resorption (percent eroded perimeter). The tissue mechanisms responsible for the protection drew from the previously deposited risedronate.