<b>Evaluation of periodontal pathogens in amniotic fluid and the role of periodontal disease in pre-term birth and low birth weight</b>

Ercan, Esra; Eratalay, Kenan; Deren, Özgür; Gür, Deniz; Özyüncü, Özgür; Altun, Belgin; Kanli, Ceyda; Özdemir, Pınar Gökmirza; Akincibay, Hakan

doi:10.3109/00016357.2012.697576

Cited by 64 publications

(73 citation statements)

References 27 publications

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“…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.…”

Section: Introductionmentioning

confidence: 63%

“…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.…”

Section: Introductionmentioning

confidence: 92%

“…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].…”

Section: Introductionmentioning

confidence: 99%

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Porphyromonas gingivalisand adverse pregnancy outcome

Reyes

Phillips

Wolfe

et al. 2017

Journal of Oral Microbiology

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Porphyromonas gingivalis is a Gram-negative, anaerobic bacterium considered to be an important pathogen of periodontal disease that is also implicated in adverse pregnancy outcome (APO). Until recently, our understanding of the role of P. gingivalis in APO has been limited and sometimes contradictory. The purpose of this review is to provide an overview of past and current research on P. gingivalis that addresses some of the controversies concerning the role of this organism in the pathogenesis of APO.ARTICLE HISTORY

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Section: Introductionmentioning

confidence: 63%

Section: Introductionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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Porphyromonas gingivalisand adverse pregnancy outcome

Reyes

Phillips

Wolfe

et al. 2017

Journal of Oral Microbiology

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“…Nevertheless, this does not mean that oral bacteria are not implicated in the process leading to preterm birth as several studies have confirmed the dissemination of periodontal pathogens to extraoral sites in pregnancy [32,33]. Aagaard et al have also reported a very close similarity between placental and oral microbiomes [34].…”

Section: Page 6 Ofmentioning

confidence: 83%

Microbiologic and Inflammatory Markers of Periodontitis are Different to those of Preterm Birth

M¹,

Gayet-Ageron²,

Roux‐Lombard³

et al. 2017

Gynecol Obstet

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Citation: Lumbreras Areta M, Gayet-Ageron A, Roux-Lombard P, Schrenzel J, AbstractBackground: Comparing microbiologic and inflammatory markers of periodontitis with those of preterm birth (PTB).Methods: Secondary analysis of a prior prospective case-control study done at the Geneva University Hospitals. Cases were women delivering at 22-34 6/7 weeks (early PTB, n=30) and controls were women delivering at ≥ 37 weeks (term delivery, n=87). We collected dental plaque during labour to quantify RNA levels from Aggregatibacter actinomycetemcomitans (Aa), Tannerella forsythia (Tf), Porphyromonas gingivalis (Pg) and Treponema denticola (Td). We also collected cord blood for cultures and cytokine quantification (IL-1Ra, IL-6, IL-8, IL-10, IL-17, TNF-α, MCP-1 and RANTES). Periodontal status was evaluated at the immediate postpartum using the American Consensus definition. Data was analysed by univariate and multivariate logistic regression.Results: Levels of Pg and Td were significantly higher in dental plaque of women with severe and moderate periodontitis. Microbiologic composition of dental plaque was not different between preterm and term delivery groups. There were no differences in cord blood cultures between groups. Cord TNF-α ≥ 8 pg/ml and IL-10 ≥ 1.3 pg/ml were associated with a higher risk of periodontitis (OR 2.78, 95% CI: 1.09-7.13, P=0.033; OR 2.78, 95% CI: 1.09-7.08, P=0.032 respectively), but differences were not significant at multivariate analysis. Cord MCP-1 ≥ 350 pg/ml was associated with a higher risk of PTB at both univariate (OR 40.25, P<0.001) and multivariate analysis (OR 53.71, P<0.001). Conclusion:In labour, microbiologic markers and inflammatory responses associated with periodontitis and PTB are different. The mechanisms linking periodontitis and PTB therefore still need to be elucidated. Page 2 of 9Citation: Lumbreras Areta M, Gayet-Ageron A, Roux-Lombard P, Schrenzel J, 2.38, 95% CI: 1.36-4.14, P=0.002) [20]. In this secondary analysis, we aim to compare the type of bacteria (in dental plaque and cord blood) and cytokines/chemokines (in cord blood) in women with severe periodontitis with those in women with early PTB. The objective is to determine if the microbiological and/or inflammatory pathways in periodontitis are the same as those involved in early PTB. A shared molecular pathway would explain the aetiology of the association between periodontitis and increased risk of PTB that was observed in our previous study. Methods Study designThis is a planned secondary analysis of women included in a prior prospective case-control (1:4) study performed between 09 November, 2007 and 18 March, 2010 at the maternity unit of the Geneva University Hospitals, Switzerland [20]. Briefly, the study evaluated the association of periodontitis in cases (women delivering spontaneously between 22 and 34, 6/7 weeks of gestation) compared to controls (women delivering as term [≥ 37 weeks]). The study was approved by the Ethics Committee of Geneva (study number 07-008, approved 28 March 2007). All partic...

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“…Periodontal diseases may increase the systemic inflammatory challenge, due to hematogenous spread of bacteria and their products as a result of ulceration of epithelial cells in periodontal pockets [240,241]. P. gingivalis and T. denticola were found at a significantly higher level among the pregnant women with periodontitis [221].…”

Section: Periodontal Diseases and Gdmmentioning

confidence: 99%

Porphyromonas gingivalis infection in gestational diabetes mellitus and survival in tobacco smokers.

Gogeneni¹

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Evaluation of periodontal pathogens in amniotic fluid and the role of periodontal disease in pre-term birth and low birth weight

Cited by 64 publications

References 27 publications

Porphyromonas gingivalisand adverse pregnancy outcome

Porphyromonas gingivalisand adverse pregnancy outcome

Microbiologic and Inflammatory Markers of Periodontitis are Different to those of Preterm Birth

Porphyromonas gingivalis infection in gestational diabetes mellitus and survival in tobacco smokers.

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