Aim Gestational diabetes mellitus (GDM), gingivitis, infection with specific periodontal pathogens and systemic inflammation each increase the risk for poor pregnancy outcome. We set out to monitor the interactions of gingivitis and GDM with respect to oral infection and the systemic inflammatory burden. Materials and Methods Four case–control groups (n = 117) were recruited, (1) No gingivitis, No GDM (n = 27); (2) Gingivitis, No GDM (n = 31); (3) No gingivitis, GDM (n = 21); and (4) Gingivitis, GDM (n = 38). Oral infection with three key periodontal pathogens was determined by PCR. Systemic inflammation was determined by quantification of CRP by EIA. Results Gingivitis during pregnancy was associated with oral infection with Porphyromonas gingivalis, Filifactor alocis and Treponema denticola and combinations thereof (all p < 0.01). GDM was also associated with increased infection with individual and multiple oral pathogens (all p < 0.05). Gingivitis during pregnancy led to a 325% increase in systemic CRP (mean, 2495 versus 8116 ng/ml, p < 0.01). Conclusions Diabetes and gingivitis act in concert to increase risk biomarkers for poor pregnancy outcome.

Summary Porphyromonas gingivalis is a Gram-negative anaerobe and keystone periodontal pathogen. A mariner transposon insertion mutant library has recently been used to define 463 genes as putatively essential for the in vitro growth of P. gingivalis ATCC 33277 in planktonic culture [Library 1, (Klein et al 2012)]. We have independently generated a transposon insertion mutant library [Library 2] for the same P. gingivalis strain and herein compare genes that are putatively essential for in vitro growth in complex media, as defined by both libraries. 281 genes (61%) identified by Library 1 were common to Library 2. Many of these common genes are involved in fundamentally important metabolic pathways, notably pyrimidine cycling as well as lipopolysaccharide, peptidoglycan, pantothenate and coenzyme A biosynthesis and nicotinate and nicotinamide metabolism. Also in common are genes encoding heat shock protein homologues, sigma factors, enzymes with proteolytic activity and the majority of sec-related protein export genes. In addition to facilitating a better understanding of critical physiological processes, transposon sequencing technology has the potential to identify novel strategies for the control of P. gingivalis infections. Those genes defined as essential by two independently generated TnSeq mutant libraries are likely to represent particularly attractive therapeutic targets.

INTRODUCTIONCigarette users are more susceptible than non-smokers to periodontitis, a bacterial-induced, inflammation-driven, destructive disease of the supporting tissues of the teeth. We hypothesized that clinical periodontal findings and microbiological and/or inflammatory marker levels would be intermediate in those exposed to environmental tobacco smoke compared to active smokers and non-smokers.METHODSSixty individuals were recruited from a University periodontal clinic and assigned as non-smokers, active smokers or passive-smokers according to their self reports. Clinical periodontal measurements, comprising plaque index, probing depth (PD), clinical attachment level (CAL) and bleeding on probing, were recorded at six sites per tooth. Cotinine levels were determined in whole saliva samples by EIA. Treponema denticola and Porphyromonas gingivalis infection was determined by PCR, while matrix metalloproteinase-8 (MMP-8) and interleukin-8 (IL-8) concentrations were determined by ELISA.RESULTSStudy groups were subsequently reassigned in accordance with the cotinine data. The smoker group exhibited higher mean PD and CAL values compared to the non-smoker group (p<0.05). Passive-smokers exhibited PD and CAL values smaller than those of the active smokers and greater than those of the non-smokers, but the differences were not statistically significant. PD and CAL values correlated with cotinine concentrations (p<0.05). P. gingivalis infection was noted in most subjects, irrespective of smoking status. T. denticola infection was noted in 4/23 (17.4%) smokers, 0/16 (0%) environmentally-exposed recruits and 2/21 (9.5%) non-smokers. Salivary MMP-8 and IL-8 levels were lower in smokers compared to both non-smokers and passive-smokers but the differences were not significant (all p>0.05).CONCLUSIONSThe present clinical periodontal findings provide further support for a negative, dose-related effect of tobacco exposure on periodontal health. The tendency for a more prevalent detection of T. denticola and for a suppressed inflammatory response observed in the smokers may partly explain the increased susceptibility to periodontal tissue destruction, but needs to be verified in larger scale studies.

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