Apoptosis in the placenta of pregnancies complicated with IUGR

Int J Gynaecol Obstet. 2001 Jun;73(3):229-35. doi: 10.1016/s0020-7292(01)00373-3.

Abstract

Objective: In this study we have investigated the presence of apoptosis in the placental tissue of pregnancies complicated with intra-uterine growth restriction (IUGR).

Method: Placental samples were obtained from 22 normal third trimester pregnancies and 20 pregnancies complicated with IUGR. The criteria for fetal growth impairment were clinical evidence of sub-optimal growth, ultrasonographic demonstration of deviation from normal percentiles of growth and birth weight under 10th percentile. Terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end labelling (TUNEL) staining was used to demonstrate the apoptotic cells in all samples. Student-t, Mann-Withney U-test, Fisher exact test and Spearman correlation were used for statistical analysis.

Results: We detected apoptosis in 10 placentas in the study group vs. none in the control group. Placentas from pregnancies complicated with IUGR demonstrated 0.12% (0.1%-0.4%) apoptotic cells. The rate of apoptotic cells in the placenta was significantly higher in pregnancies complicated with IUGR than normal uncomplicated pregnancy (P=0.0019). Apoptosis were more abundant in the trophoblasts, especially cytotrophoblasts, in the placenta. We could not find a correlation between the apoptosis in the placenta of pregnancies complicated with IUGR and birth weight, multi-parity, gestational age, birth weight percentile and mode of delivery (C/S vs. vaginal delivery).

Conclusion: We believe that the increased number of apoptosis in the placenta of pregnancies complicated with IUGR may have an important compensatory role to transmit nutrition and gas exchange easily to the fetus.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Apoptosis*
  • Birth Weight
  • Case-Control Studies
  • Delivery, Obstetric / methods
  • Female
  • Fetal Growth Retardation / etiology*
  • Fetal Growth Retardation / pathology*
  • Gestational Age
  • Humans
  • In Situ Nick-End Labeling
  • Maternal-Fetal Exchange
  • Parity
  • Placenta / pathology*
  • Pregnancy
  • Pregnancy Trimester, Third
  • Risk Factors