title: Placental pathology in fetal growth restriction.
abstract: OBJECTIVE
  One of the causes of intrauterine fetal growth restriction (FGR) can be pathology of the placenta. The aim of this study was to compare macroscopic and microscopic changes of the placentas from intrauterine growth restricted fetuses with those from normally developed fetuses, in order to test the hypothesis that vascular damage due to decreased maternal vascular perfusion may be responsible for FGR.
  
  
  METHODS
  Between May 2007 and December 2008 we performed detailed macroscopic and histological examination of singleton placentas of 50 consecutive neonates with fetal growth restriction (FGR group) and compared them to 50 normal fetuses, born next to an FGR case, as a control group.
  
  
  RESULTS
  Gestational age, birth weight, spontaneous delivery rate, mean weight of the placenta and the fetal-placental weight ratio were all lower in the FGR group than in the control group (p<0.05). Thickening of the villous trophoblastic basal membrane, incidence of villous infarction, presence of thrombi or haematomas and the incidence of villitis were more common in the FGR group than in the controls (p<0.05). There were, however, no significant differences in perivillous fibrin deposition, stromal fibrosis and cytotrophoblast proliferation between the groups. In FGR women who smoked, intervillous haematomas and villous infarction were more common (p<0.05) than in controls.
  
  
  CONCLUSIONS
  All macroscopic and microscopic pathological changes associated with FGR were directly linked to reduction of placental blood flow. As smoking is a main risk factor for these placental abnormalities these results emphasize the need to persuade women to quit smoking not only during pregnancy, but even better long before pregnancy.
authors.affiliation: Department of Obstetrics and Gynaecology, Riga Stradins University, Riga, Latvia. natalyved@apollo.lv
authors.forename: Natalija
authors.initials: N
authors.lastname: Vedmedovska
authors.forename: Dace
authors.initials: D
authors.lastname: Rezeberga
authors.forename: Uldis
authors.initials: U
authors.lastname: Teibe
authors.forename: Ivars
authors.initials: I
authors.lastname: Melderis
authors.forename: Gilbert G G
authors.initials: GG
authors.lastname: Donders
mesh_terms: D000328:Adult; D001485:Basement Membrane / Q000473:pathology; D016022:Case-Control Studies; D049109:Cell Proliferation; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology* / Q000473:pathology* / Q000517:prevention & control; D006406:Hematoma / Q000453:epidemiology; D006801:Humans; D015994:Incidence; D007231:Infant, Newborn; D007238:Infarction / Q000453:epidemiology; D010920:Placenta / Q000098:blood supply* / Q000473:pathology*; D010922:Placenta Diseases / Q000453:epidemiology / Q000473:pathology* / Q000503:physiopathology; D021041:Placental Circulation; D011247:Pregnancy; D012907:Smoking / Q000009:adverse effects; D013927:Thrombosis / Q000453:epidemiology; D014327:Trophoblasts / Q000473:pathology; D014652:Vascular Diseases / Q000453:epidemiology / Q000473:pathology* / Q000503:physiopathology; D055815:Young Adult