Maternal Periodontitis and Prematurity. Part II: Maternal Infection and Fetal Exposure

• DOI: 10.1902/annals.2001.6.1.175
• Publication Date: 2005-02-02T10:53:45Z
• Authors: P.N. Madianos; S. Lieff; A.P. Murtha; K.A. Boggess; R.L. Auten; J.D. Beck; S. Offenbacher
• Keywords: Prevotella intermedia; Treponema denticola; Fusobacterium nucleatum

Clinical data from the first 812 deliveries a cohort study of pregnant mothers entitled Oral Conditions and Pregnancy (OCAP) demonstrate that both antepartum maternal periodontal disease incidence/progression are associated with preterm birth growth restriction after adjusting for traditional obstetric risk factors. In current we present measures infection using whole chromosomal DNA probes to identify 15 organisms within plaque sampled at delivery. addition, postpartum IgG antibody fetal exposure, as indexed by cord blood IgM level these oral pathogens, was measured bacterial immunoblots. The potential role specific 2 complexes most often periodontitis, conventionally termed “Orange” (Campylobacter rectus, Fusobacterium nucleatum, Peptostreptococcus micros, Prevotella nigrescens, intermedia) “Red” (Porphyromonas gingivalis, Bacteroides forsythus, Treponema denticola) complexes, respectively, prematurity investigated relating presence infection, IgG, IgM, comparing full‐term (gestational age <37 weeks). prevalence 8 pathogens similar among term postpartum. There 2.9‐fold higher seropositivity one or more Orange Red complex babies, compared babies (19.9% versus 6.9%, P = 0.0015, chi square). Specifically, positive C. rectus significantly neonates (20.0% 6.3%, 0.0002, well P. intermedia (8.8% 1.1%, 0.0003). A lack an increased rate odds ratio (OR) 2.2; confidence interval (CI) 1.48 3.79), consistent concept protects fetus exposure resultant prematurity. highest (66.7%) observed those without protective response coupled microbes (combined OR 10.3; <0.0001). These support in absence is systemic dissemination translocate resulting high elevated premature infants raises possibility this pathogen may serve primary infectious agent eliciting Ann Periodontol 2001;6:175‐182.