Prenatal ethanol exposure has differential effects on fetal growth and skeletal ossification

Simpson, M.E.; Duggal, Shalu; Keiver, Kathy

doi:10.1016/j.bone.2004.11.011

Cited by 41 publications

(70 citation statements)

References 56 publications

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“…These data suggest that ethanol affects bone development at multiple stages. Moreover, ethanol's effects on the hypertrophic zone are consistent with the hypothesis that ethanol has specific effects on the later stages of bone development [32].…”

Section: Discussionsupporting

confidence: 85%

“…Although it is difficult to separate effects on general growth from those on skeletal development, we have shown that prenatal ethanol delays fetal skeletal ossification at doses below those that affect body weight and length [32]. In addition, the skeletal elements differed in their sensitivity to ethanol's effects, with more severe effects occurring in the bones that undergo a greater proportion of their development in utero [32].…”

Section: Introductionmentioning

confidence: 81%

“…Two fetuses from each litter were selected in a blinded fashion (and without reference to sex) and the left tibiae dissected free from soft tissue under a Zeiss dissecting microscope. All fetuses in each litter were not examined because ethanol's effects have been shown to be consistent among fetuses in a litter [11] and previous work in our lab has demonstrated that coefficients of variation for ossification measures among littermates in the E group are similar to those of PF and C groups [32]. The tibia was chosen for analysis as this bone is consistently highly affected by prenatal ethanol exposure [15,17, and 32].…”

Section: Methodsmentioning

confidence: 99%

“…In addition, the skeletal elements differed in their sensitivity to ethanol's effects, with more severe effects occurring in the bones that undergo a greater proportion of their development in utero [32]. These data suggest that ethanol's effects on bone are not limited to decreasing longitudinal growth, and that more subtle effects may occur at levels of maternal drinking below those associated with growth retardation.…”

Section: Introductionmentioning

confidence: 91%

“…To maximize the ability to detect potential effects, we chose to use a dose of ethanol (36% ethanol derived calories [EDC]) that consistently results in delayed ossification of fetal bone in the rat model. This dose of ethanol produces blood ethanol levels that are slightly higher than the legal limits for drunk driving (50-100 mg/dL) in Canada and the United States [32], and are well within the range that has been reported in human alcoholics [36]. Fetal Alcohol Spectrum Disorder has a high prevalence, with estimates approximating 1% of live births in the United States [22 and 30].…”

Section: Introductionmentioning

confidence: 99%

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Prenatal ethanol exposure disrupts the histological stages of fetal bone development

Snow

Keiver

2007

Bone

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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 indicate 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.

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Section: Discussionsupporting

confidence: 85%

Section: Introductionmentioning

confidence: 81%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

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Prenatal ethanol exposure disrupts the histological stages of fetal bone development

Snow

Keiver

2007

Bone

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Abnormal growth and morphogenesis of placenta at term is linked to adverse fetal development after perigestational alcohol consumption up to early gestation in mouse

Gualdoni

Pérez-Tito

Barril

et al. 2022

Birth Defects Research

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Background: Gestation alcohol consumption produces fetal growth restriction and malformations by affecting the embryo-fetal development. Recently a relationship between abnormal placentation and fetal malformation and intrauterine growth retardation has been suggested. However, the effects of perigestational alcohol ingestion up to early pregnancy on the placenta at term and its association with fetal abnormalities are little known. Methods: In female mice, ethanol 10% in water was administered for 15 days previous and up to days 4 (D4), 8 (D8), or 10 (D10) of gestation (TF), and gestation continues without ethanol exposure. Control females (CF) received ethanol-free water. At day 18, feto-placental units and implantation sites were studied.Results: TF had increased resorptions and only fetuses from D8-TF and D10-TF had significantly increased weights versus CF. D4 and D10-TFplacentas had significantly reduced weights. All TF had increased junctional zone (JZ) and reduced labyrinth (Lab) areas (PAS-histology and morphometry) compared with CF. Fetuses with mainly with craniofacial abnormalities and skeletal defects (Alizarin red staining), significantly increase; while the fetal bone density (alizarin color intensity, ImageJ) was reduced in D4, D8 and D10-TF versus CF. Although all TF-placentas were histo-structural affected, TF-abnormal fetuses had the most severe placental anomalies, with junctional abundant glycogenic cells into the labyrinth, disorganized labyrinthine vascularization with signs of leukocyte infiltrates and feto-maternal blood mix. Conclusions: Perigestational alcohol consumption up to early gestation induces at term fetal growth alterations, dysmorphology and defective skeleton, linked to deficient growth and abnormal morphogenesis of placenta, highlighting insight into the prenatal etiology of FASD.

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High doses of alcohol during pregnancy cause DNA damages in osteoblasts of newborns rats

Carvalho

Dutra

Andrade

et al. 2015

Birth Defects Research

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Prenatal ethanol exposure has differential effects on fetal growth and skeletal ossification

Cited by 41 publications

References 56 publications

Prenatal ethanol exposure disrupts the histological stages of fetal bone development

Prenatal ethanol exposure disrupts the histological stages of fetal bone development

Abnormal growth and morphogenesis of placenta at term is linked to adverse fetal development after perigestational alcohol consumption up to early gestation in mouse

High doses of alcohol during pregnancy cause DNA damages in osteoblasts of newborns rats

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