title: Are periodontal bacterial profiles and placental inflammatory infiltrate in pregnancy related to birth outcomes?
abstract: BACKGROUND
  The aim of this study is to determine whether periodontal clinical parameters, periodontal bacterial profiles, and inflammatory infiltrate in placental chorionic villi are associated with adverse pregnancy results.
  
  
  METHODS
  The authors designed an observational case-control study in 244 postpartum females: mothers with preterm/low-birth weight newborns (n = 91 cases) and mothers with full-term, normal-weight infants (n = 153 controls). Sociodemographic, gynecologic, and periodontal variables were gathered for all participants. Data on placental inflammatory infiltrate in biopsies from 68 cases and 65 controls and the gingival bacterial profile in mothers with periodontitis were gathered, detecting associations with bivariate analyses and constructing a multiple logistic regression model with the number of positive inflammatory cells as the dependent variable.
  
  
  RESULTS
  Periodontal values were significantly worse in cases versus controls. Numbers of leukocyte subsets per square millimeters in maternal and fetal vascular spaces were similar between cases and controls. CD45 in maternal placental space was related to the presence of periodontitis (P = 0.029) but not to case or control group (P = 0.264). The anaerobic and commensal bacterial profile in mothers with periodontitis was similar between the groups.
  
  
  CONCLUSIONS
  Periodontal disease was more severe and a periodontitis diagnosis more frequent in mothers with preterm or low-birth weight versus normal delivery. No differences in anaerobic or commensal bacterial profile were found between mothers with periodontitis in the two groups. Local placental factors, such as the nature of the inflammatory infiltrate and slightly higher expression of cyclooxygenase-2 in the females with these adverse pregnancy outcomes, may be related to a subclinical proinflammatory status that could contribute to triggering premature labor.
authors.affiliation: Periodontology Department, School of Dentistry, University of Granada, Granada, Spain. fmesa@ugr.es
authors.forename: Francisco
authors.initials: F
authors.lastname: Mesa
authors.forename: Elena
authors.initials: E
authors.lastname: Pozo
authors.forename: Vanessa
authors.initials: V
authors.lastname: Blanc
authors.forename: Alberto
authors.initials: A
authors.lastname: Puertas
authors.forename: Manuel
authors.initials: M
authors.lastname: Bravo
authors.forename: Francisco
authors.initials: F
authors.lastname: O'Valle
mesh_terms: D000328:Adult; D001419:Bacteria / Q000145:classification; D058491:Bacterial Load; D001706:Biopsy; D001724:Birth Weight; D016022:Case-Control Studies; D002824:Chorionic Villi / Q000276:immunology; D051546:Cyclooxygenase 2 / Q000032:analysis; D005260:Female; D052776:Female Urogenital Diseases / Q000150:complications; D005322:Premature Rupture of Fetal Membranes / Q000276:immunology / Q000382:microbiology; D005881:Gingiva / Q000382:microbiology; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D007234:Infant, Premature; D018836:Inflammation Mediators / Q000032:analysis*; D017493:Leukocyte Common Antigens / Q000032:analysis; D007962:Leukocytes / Q000145:classification; D010518:Periodontitis / Q000382:microbiology*; D010920:Placenta / Q000276:immunology*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000382:microbiology*; D011256:Pregnancy Outcome; D047928:Premature Birth / Q000276:immunology / Q000382:microbiology; D012959:Socioeconomic Factors
chemical_list: D018836:Inflammation Mediators; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D017493:Leukocyte Common Antigens; C516769:PTPRC protein, human