title: Quantitative analysis of trophoblast invasion in preeclampsia.
abstract: BACKGROUND
  The process of physiological conversion of spiral arteries is dependent on the invasion of the interstitium and spiral arteries of the uterine wall by invasive extravillous trophoblast thereby creating a high flow-low resistance vessel. Quantitative data on restriction of trophoblast invasion and failure of spiral artery transformation are limited in preeclampsia.
  
  
  OBJECTIVE
  This study morphometrically analyzes interstitial trophoblast cells and trophoblast cells embedded in the wall of the converted spiral arteries within the decidua and myometrium of normotensive and preeclamptic Black African pregnant women.
  
  
  METHODS
  Placental bed biopsies were obtained from 25 normotensive pregnant women and 30 pregnant women complicated with hypertensive disorders. Biopsies were processed and immunostained for trophoblast cell identification, using anti-MNF 116 antibody. Image analysis of the trophoblast population within the decidua, myometrium and the spiral arteries was performed in the normotensive and in the severe proteinuric hypertensive groups.
  
  
  RESULTS
  The mean field area percentage of trophoblast cells observed in the decidua of the normotensive women was 22.79 +/- 2.1% in comparison to 18.14 +/- 1.53% in the severe hypertensive group (p < 0.01). In the myometrium, the mean field area percentage of interstitial trophoblast cells (both mononuclear and multinuclear) was 10.04 +/- 2.1% of the field area of the normotensive group compared to 2.81 +/- 0.67% in the severe hypertensive group (p < 0.001). The mean field area percentage occupied by trophoblast cells in myometrial spiral arteries was 10.15% in the normotensive group compared to none in the severe hypertensive group. The latter group displayed medial disorganization, hyperplasia and endothelial vacuolation.
  
  
  CONCLUSIONS
  This study demonstrates restricted invasion of the trophoblastic cells in preeclampsia. This inadequate invasion may influence vascular remodeling required for delivering adequate volumes of maternal blood to the placenta.
authors.affiliation: MRC Pregnancy Hypertension Research Unit, Nelson R Mandela School of Medicine, University of Natal, Congella, South Africa.
authors.forename: Thajasvarie
authors.initials: T
authors.lastname: Naicker
authors.forename: Shaun M
authors.initials: SM
authors.lastname: Khedun
authors.forename: Jagidesa
authors.initials: J
authors.lastname: Moodley
authors.forename: Robert
authors.initials: R
authors.lastname: Pijnenborg
mesh_terms: D000328:Adult; D001741:Black or African American; D001158:Arteries / Q000473:pathology / Q000503:physiopathology; D044383:Black People; D003656:Decidua / Q000098:blood supply* / Q000473:pathology* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology; D005110:Extracellular Space / Q000502:physiology; D005260:Female; D005865:Gestational Age; D006801:Humans; D009215:Myometrium / Q000098:blood supply* / Q000473:pathology* / Q000503:physiopathology; D021041:Placental Circulation / Q000502:physiology*; D011225:Pre-Eclampsia / Q000473:pathology* / Q000503:physiopathology*; D011247:Pregnancy; D011256:Pregnancy Outcome; D013019:South Africa; D014327:Trophoblasts / Q000473:pathology* / Q000502:physiology*