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首页> 外文期刊>Alcohol >A novel mouse model for the study of the inhibitory effects of chronic ethanol exposure on direct bone formation.
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A novel mouse model for the study of the inhibitory effects of chronic ethanol exposure on direct bone formation.

机译：一种新型的小鼠模型，用于研究慢性乙醇暴露对直接骨骼形成的抑制作用。

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Excessive alcohol consumption has been reported to interfere with human bone homeostasis and repair in multiple ways. Previous studies have demonstrated that chronic ethanol exposure in the rat via an intragastric dietary delivery system inhibits direct bone formation during distraction osteogenesis (DO, limb lengthening). The opportunity to extend the rat ethanol studies to mice is now possible due to the development of mouse models of DO. This study employed a novel combination of liquid ethanol diet delivery and a murine DO model to test the hypothesis that chronic ethanol exposure would result in deficits in direct bone formation during DO in contrast to the pair-fed controls. Twenty-eight 12-month-old C57BL/6 male mice were acclimated to the Lieber-DeCarli liquid control diet #710027 (Dyets Inc.) over a 1-week period. The mice were separated into two diet groups (n=14/group): pair-fed control and ethanol (diet #710260). After being on diet for 82 days, all mice underwent placement of an external fixator and osteotomy on the left tibia. Following a 6-day latency period, distraction began at a rate of 0.075 mm twice a day (b.i.d.) for 14 days. The weight changes were equivalent for both groups. The hypothesis that chronic ethanol exposure would inhibit direct bone formation and produce skeletal toxicity was supported by radiographic (P=.011) and histologic (P=.002) analyses of the % new bone formation in the DO gaps, by peripheral quantitative computed tomography analysis of the total volumetric bone mineral density of the contralateral proximal tibias (P<.001) and contralateral femoral necks (P=.012), by three-point bending on the contralateral tibias (P<.001 energy to break), by pin site bone formation measures (P<.001), and by ethanol-associated increased adipocyte area (adjacent to the gap) percentages (P<.002). We conclude that this model can be used to study the mechanisms underlying inhibition of bone formation by chronic ethanol exposure and to test preclinical interventions.
机译：据报道，过量饮酒会以多种方式干扰人体骨骼的稳态和修复。先前的研究表明，通过胃内饮食递送系统在大鼠中长期暴露于乙醇会抑制分心成骨（DO，肢体延长）过程中的直接骨形成。由于DO小鼠模型的发展，现在有可能将大鼠乙醇研究扩展到小鼠。这项研究采用了液体乙醇饮食输送和小鼠DO模型的新型组合来检验以下假设：与成对喂养的对照组相比，长期暴露于乙醇会导致DO期间直接骨骼形成的缺陷。在1周的时间内使28只12个月大的C57BL / 6雄性小鼠适应Lieber-DeCarli液体对照饮食＃710027（Dyets Inc.）。将小鼠分成两个饮食组（n ＝ 14 /组）：成对喂养的对照和乙醇（饮食＃710260）。饮食82天后，所有小鼠都接受了外固定架的放置，并在左胫骨上进行了截骨术。在为期6天的潜伏期后，开始以0.075毫米的速度开始分心，每天两次（b.i.d.），持续14天。两组的体重变化相等。放射线照相术（P = .011）和组织学检查（P = .002）对DO间隙中新骨形成的百分比进行的X线摄影（P = .011）和组织学分析（P = .002）支持了这一假设，即长期乙醇暴露会抑制直接的骨形成并产生骨骼毒性。通过对侧胫骨的三点弯曲（P <.001能量断裂），通过对侧胫骨近侧骨（P <.001）和对侧股骨颈总骨体积矿物质密度（P = .012）的分析，针部位骨形成的量度（P <.001），以及与乙醇相关的脂肪细胞面积增加（邻近间隙）的百分比（P <.002）。我们得出的结论是，该模型可用于研究慢性乙醇暴露对抑制骨形成的潜在机制，并测试临床前干预措施。

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