History of Periodontal Treatment and Risk for Intrauterine Growth Restriction (IUGR)

Cande V. Ananth; Howard F. Andrews; Panos N. Papapanou; Angela M. Ward; Emilie Bruzelius; Mary Lee Conicella; David A. Albert


BMC Oral Health. 2018;18(161) 

In This Article


In industrialized countries, about four-fifths of low birthweight infants are born preterm and a fifth of these preterm births are due to intrauterine growth restriction (IUGR).[1] In the absence of congenital malformations and/or chromosomal anomalies, IUGR entails two distinct processes: constitutional smallness, or pathological growth restriction.[2] The prevalence of IUGR varies substantially across populations, but prevalence rates range between 3 and 7%. The etiology of IUGR remains undetermined, but several risk factors for the condition have been identified. These include advanced maternal age, increased parity, smoking during pregnancy, low pre-pregnancy body mass index and low gestational weight gain (due to low energy intake), short maternal stature, poor maternal nutrition, maternal race/ethnicity, and low socioeconomic status being some of the important risk factors.[3] Maternal, placental and fetal infections are strongly implicated in the development of IUGR.

Periodontal diseases are associated with transient bacteremia that may facilitate dissemination of oral bacteria to the uterus, with subsequent infiltration of the amniotic fluid and the umbilical cord and invasion of the placenta. It is believed that hematogenous transport of bacteria and/or pro-inflammatory mediators from sites of periodontal infection into the placenta, fetal membranes, and amniotic cavity induces pathological processes that lead to adverse perinatal outcomes, including IUGR.[4–7] Uteroplacental infection and inflammation are thought to play key roles in the etiology of IUGR,[8] with fetal inflammatory response syndrome being characterized as the important cause of IUGR.[9] Collectively, these infections account for up to 15% of IUGR cases.[10]

Periodontal infections are associated with an increased risk for adverse pregnancy outcomes, including preterm delivery, and preeclampsia, but whether this increased risk also applies to IUGR has not been established. Since infections play an important role in IUGR, we hypothesized that: (i) maternal periodontitis is associated with an increased risk for IUGR; and (ii) treatment for periodontitis in the immediate postpartum period signifies presence of untreated periodontitis during pregnancy, and is associated with elevated risk of IUGR. Furthermore, given the increased risk of recurrence of IUGR and the temporal persistence of periodontal infections, we hypothesized that parity will be an effect modifier of the association between periodontal infection and risk of IUGR.

We tested these hypotheses by examining medical and dental insurance records in a large cohort of 32,168 women, comparing rates of IUGR among women undergoing periodontal care, other types of dental treatment, and those receiving no dental treatment, before, during and after pregnancy.