Simultaneous detection of periodontal pathogens in subgingival plaque and placenta of women with hypertension in pregnancy

Abstract

In cases with hypertension, periodontal pathogens are present in higher proportion in subgingival plaque and placenta.

Porphyromonas gingivalisand adverse pregnancy outcome

“…This was confirmed in vivo with a ligature model of periodontitis in rabbits that were inoculated with P. gingivalis strain A7436 or lipid phosphatase mutants that were 'locked' into producing a TLR4 agonist or antagonist [50]. In this study, all A7436 lipid A mutants altered the composition of the oral microbiota, but only TLR4 antagonist and wild-type A7436 enhanced the growth of Fusobacterium nucleatum, which is implicated in preterm delivery [53,54] and it is often found in association with P. gingivalis in placenta, amniotic fluid, and nasogastric aspirates from preterm infants [4,8]. Furthermore, the placenta is a blood-rich tissue and red blood cells contain hemin.…”

“…As a periodontal pathogen, P. gingivalis may indirectly contribute to adverse pregnancy outcomes (APO) by facilitating the release of bacterial products or inflammatory mediators into the maternal circulation that reach the maternal-fetal interface [2]. P. gingivalis could also directly promote APO via invasion and injury to utero-placental tissues; this is supported by several studies that have detected P. gingivalis DNA/antigen in the placenta, amniotic fluid, umbilical cord, and neonatal nasogastric aspirates from complicated pregnancies [3][4][5][6][7][8][9][10][11]. However, the significance of P. gingivalis as a causative agent of APO is sometimes viewed with skepticism due to several confounding factors.…”

“…Also confounding is that P. gingivalis DNA or antigen has also been detected in placentas from healthy pregnancies, albeit at a lower microbial load and lower frequency than women with preeclampsia or preterm birth [3][4][5][6][7]. It is also difficult to extrapolate the contribution P. gingivalis to APO when its detection in utero-placental tissues is usually in association with other oral bacterial species [3][4][5], or when it is not detected in placental tissues from complicated pregnancies even when other oral bacterial species are present [13].…”

“…The paradigm that the placenta is a sterile environment has been challenged by several reports that show bacterial DNA or live bacteria present in placentas obtained from normal pregnancies [3][4][5][35][36][37][38]. Interestingly, one study that used comparative 16s ribosomal DNAbased and whole-genome shotgun metagenomic analyses on 320 placental specimens reported that the placental microbiome most closely resembles supragingival plaque [35].…”

“…Monotypic infection with P. gingivalis in pregnant rodents produces lesions that disrupt the maternal-fetal barrier involving inflammation of uterine arteries and infiltration of the uterine submucosa by neutrophils [48]. These lesions could facilitate invasion of the placenta by other bacteria that gain entry into the uterus, since polymicrobial colonization/infections are more common at the maternal-fetal interface than monotypic infections [3][4][5]8,9,39].…”