title: Structural analysis of human placental stem and terminal villi from normal and idiopathic growth restricted pregnancies.
abstract: Studying in detail different histomorphological and pathological findings in placental stem and terminal villi of appropriate for gestational age (AGA) and idiopathic intrauterine growth restricted (IUGR) fetuses, then analyzing their correlation to the neonatal birth weight and to the some morphological features of the placenta. Fifty full-term human placentae of idiopathic IUGR and 25 of AGA pregnancies were processed for haematoxylin and eosin staining and evaluated by light microscope aided with Image Analyzer. The mean number of stem villous arteries, and the mean number of terminal villous capillaries per field are significantly lower in idiopathic IUGR group (4.63 ± 0.46, 47.09 ± 4.44, respectively) than in AGA group (12.36 ± 0.61, 73.35 ± 5.13, respectively) (p = 0.001). Both AGA and idiopathic IUGR placentae share the presence of many pathological features: (1) narrowing of stem villous arteries appears in 38 (76 %) of IUGR cases and in 9 (36 %) of AGA cases with significant difference between groups (p = 0.001); (2) cellular infiltration (villitis) of the stem villi is significantly higher in IUGR cases [24 (48 %)] than in AGA cases [2 (8 %)] (p = 0.001). The study shows significant correlation between the birth weight and different pathologic features in the stem villi as arterial number (r = 0.494; p = 0.000), arterial narrowing (r = 0.283, p = 0.004), degenerative changes (r = 0.331, p = 0.001) and villitis (r = 0.275, p = 0.005). There is also significant correlation between neonatal birth weight and terminal villous capillary number (r = 0.281, p = 0.001) but no significant correlation is found between the birth weight and terminal villous fibrotic changes (r = -0.098, p = 0.318). Histomorphological and pathological changes in the stem villi could explore the cause of idiopathic IUGR. Stem villous arterial number, arterial narrowing, degeneration and villitis could be underlying mechanisms. Further researches on the hormonal and cytokine level should be undertaken to demonstrate the precipitating factors of these changes and the possible preventing measures.
authors.affiliation: Department of Anatomy, Taibah University, Almadinah Almonawarah, Saudi Arabia.
authors.forename: Shaima M
authors.initials: SM
authors.lastname: Almasry
authors.forename: Magda A
authors.initials: MA
authors.lastname: Eldomiaty
authors.forename: Amr K
authors.initials: AK
authors.lastname: Elfayomy
authors.forename: Fawzia A
authors.initials: FA
authors.lastname: Habib
authors.forename: Maha D
authors.initials: MD
authors.lastname: Safwat
mesh_terms: D000328:Adult; D000818:Animals; D001724:Birth Weight; D002196:Capillaries / Q000473:pathology*; D002824:Chorionic Villi / Q000098:blood supply / Q000473:pathology*; D004801:Eosine Yellowish-(YS); D005260:Female; D005317:Fetal Growth Retardation / Q000473:pathology*; D005865:Gestational Age; D006416:Hematoxylin; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D011247:Pregnancy; D013194:Staining and Labeling; D014469:Umbilical Arteries / Q000098:blood supply / Q000473:pathology*
chemical_list: D004801:Eosine Yellowish-(YS); D006416:Hematoxylin