Snow M E, Keiver K
Food, Nutrition and Health, Faculty of Land and Food Systems, The University of British Columbia, Vancouver, Canada.
Bone. 2007 Aug;41(2):181-7. doi: 10.1016/j.bone.2007.04.182. Epub 2007 Apr 25.
Maternal ethanol intake during pregnancy results in impairments in general growth and skeletal development in the offspring. We have previously shown that ethanol retards skeletal ossification at doses lower than those that affect growth. Moreover, skeletal sites vary in their sensitivity to ethanol effects, with more severe effects occurring in bones that undergo a greater proportion of their development in utero. Taken together, these data suggest that ethanol has specific effects on bone development, and that later stages in the ossification process may be particularly affected. Such effects could have important implications for the offspring's long-term bone health, as studies suggest that the intrauterine environment can program the skeleton. The present study examined the histological stages of bone development to determine if prenatal ethanol exposure alters the morphological development of the growth plate in the fetal rat. Rats were fed a liquid diet containing ethanol (Ethanol, E group), or without ethanol (Pair-Fed, PF, or Control, C groups) for 6 weeks: 3 weeks prior to breeding and during 3 weeks of pregnancy. Fetal tibiae were fixed, decalcified and stained for histological analysis on day 21 of gestation. Maternal ethanol intake resulted in a significant decrease in fetal total bone and diaphysis lengths, compared with tibiae from PF and C fetuses. Although the lengths of the epiphyses were not affected, ethanol disrupted the organization of the histological zones within the epiphyses. Prenatal ethanol exposure decreased the length of the resting zone, but increased the length of the hypertrophic zone. Enlargement of the hypertrophic zone is consistent with an effect of ethanol on the later stages of bone development; however, ethanol's effect on the resting zone indicates that earlier stages of bone development may also be disrupted. The functional significance of these morphological changes to long-term bone health remains to be determined.
孕期母体摄入乙醇会导致后代总体生长和骨骼发育受损。我们之前已经表明,乙醇在低于影响生长剂量的情况下会延缓骨骼骨化。此外,骨骼部位对乙醇作用的敏感性各不相同,在子宫内发育比例较大的骨骼受到的影响更为严重。综合来看,这些数据表明乙醇对骨骼发育有特定影响,并且骨化过程的后期阶段可能受到特别影响。此类影响可能对后代的长期骨骼健康具有重要意义,因为研究表明子宫内环境可对骨骼产生编程作用。本研究检查了骨骼发育的组织学阶段,以确定产前乙醇暴露是否会改变胎鼠生长板的形态发育。大鼠在配种前3周及孕期3周期间喂食含乙醇的液体饲料(乙醇组,E组)或不含乙醇的液体饲料(配对喂食组,PF组,或对照组,C组),为期6周。在妊娠第21天对胎儿胫骨进行固定、脱钙并染色以进行组织学分析。与PF组和C组胎儿的胫骨相比,母体摄入乙醇导致胎儿总骨长度和骨干长度显著降低。虽然骨骺长度未受影响,但乙醇破坏了骨骺内组织学区域的组织结构。产前乙醇暴露缩短了静止区长度,但增加了肥大区长度。肥大区增大与乙醇对骨骼发育后期阶段的影响一致;然而乙醇对静止区的影响表明骨骼发育的早期阶段也可能受到破坏。这些形态学变化对长期骨骼健康的功能意义仍有待确定。