Do Placental Histopathologic Characteristics Differ with Gestational Ages in Preterm and Term Deliveries?

Abstract

The study aim is to evaluate the placental histopathological characteristics and maternal risk factors in preterm and term births according to their weeks of gestation. We designed a prospective study involving a patient population (n = 355) composed of pregnant women who delivered preterm (n = 216) and term neonates (n = 139). The preterm births were divided into three groups as extremely (n = 22), moderate (n = 96) and late preterm (n = 98) births. The statistical analyses were performed using SPSS version 15 software. There was significant difference regarding maternal vascular underperfusion and inflammation in the extremely preterm group compared with the other groups (P = 0.001), but fetal vascular obstruction and villitis of unknown etiology were not found significantly different. According to our study results, the careful examination of the placenta of premature babies, particularly those of extremely preterm births, should be part of routine obstetrical management to determine the causes of preterm birth.

Correlation between placental pathology and neonatal morbidity: a case-control study

“…5,6 There is a large body of evidence that a cascade of activations of cellular components and mediators of inflammatory pathways results in onset of extremely preterm and very preterm births. [13][14][15] The current study confirms that extremely preterm and very preterm births are associated with a high incidence of chorioamnionitis, deciduitis and funisitis that represents infection-related placental and umbilical cord lesions. Most cases of histopathological chorioamnionitis represent subclinical infection.…”

“…13 Potentially, infection may develop early in gestation, before membrane fusion of the chorioamnion of the gestational sac to the opposite uterine wall at 19 -20 weeks, and then later after fusion, transmitted to the conceptus. [13][14][15] In the literature, it is found that 40 % of idiopathic preterm births placentas have chronic deciduitis. [13][14][15] Further clinical and pathological studies may improve the understanding of the implications of this entity.…”

“…[13][14][15] In the literature, it is found that 40 % of idiopathic preterm births placentas have chronic deciduitis. [13][14][15] Further clinical and pathological studies may improve the understanding of the implications of this entity. [13][14][15] The pathogenesis of preterm birth in the absence of infection may also involve activation of pathways responsible for normal onset of birth via components of the maternal and fetal hypothalamic-pituitary-adrenal axis.…”

“…[13][14][15] Further clinical and pathological studies may improve the understanding of the implications of this entity. [13][14][15] The pathogenesis of preterm birth in the absence of infection may also involve activation of pathways responsible for normal onset of birth via components of the maternal and fetal hypothalamic-pituitary-adrenal axis. 13,14 These include loss of the normally coordinated interactions and changes in systemic and local uterine balances of oxytocin levels, fetal cortisol levels, and decreasing estrogen to progesterone ratios, excessive uterine stretching, immunologically mediated processes and uterine anomalies.…”

“…13,14 These include loss of the normally coordinated interactions and changes in systemic and local uterine balances of oxytocin levels, fetal cortisol levels, and decreasing estrogen to progesterone ratios, excessive uterine stretching, immunologically mediated processes and uterine anomalies. [15][16][17] Other non-infectious triggers of preterm births are uteroplacental ischemia and oxidative stress. [13][14][15][16][17] Placental abruption is defined as the sudden separation of a significant portion of placenta from its underlying maternal blood supply prior to delivery and is important cause of acute hypoxic injury.…”