Preterm births occurs in 6-12% of all pregnancies, accounts for 75% of
neonatal death and causes significant neonatal morbidity. A large number of
preterm birth is associated with
infection (30%), because of the release of many
cytokines. In fact acute
chorioamnionitis represents the inflammatory response to extracellular microorganisms that gain access to the gestational sac. Clinical signs of
infection compare in the 12% of cases, while the prevalence of positive amniotic fluid cultures is approximately 50% in patients with preterm PROM. Despite the recent studies about the dosage of inflammatory
biomarkers in the amniotic fluid or in fetal and maternal blood, placenta histology remains the gold standard for the diagnosis of
chorioamnionitis. Histological
chorioamnionitis describes the progression of the inflammatory process. Organisms first colonise the chorioamnionic surface. Then, the neutrophils migrates to the chorion (chorionitis) and to the amnion (
chorioamnionitis) and, in the last stage, amnionic epithelial cells undergo
necrosis (necrotising
chorioamnionitis). It represents the mother inflammatory response and it differs from the fetal inflammatory response (
funisitis).
Funisitis first appears in vessels of the chorionic plate (chorionic
vasculitis) or in the umbilical vein (umbilical
phlebitis), then in the umbilical artery (umbilical
arteritis), and in the Wharton's jelly (umbilical perivasculitis). The fetal inflammatory response has been associated with inflammatory diseases of preterm infants, increasing the risk of
neonatal sepsis and
meningitis,
bronchopulmonary dysplasia and
cerebral palsy. We present our experience on the relationship between histological
chorioamnionitis,
preterm birth and inflammatory diseases of VLBW infants.