Periodontal disease and adverse pregnancy outcomes

Shub, Alexis; Swain, J.; Newnham, John P.

doi:10.1080/14767050600797749

Cited by 40 publications

(32 citation statements)

References 59 publications

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“…There are increasing reports that bacteria, specifically those from the oral cavity, are able to spread hematogenously from the maternal bloodstream to the uterine cavity (5). This is further supported by apparent associations between periodontal disease and PTB (71, 72), although this association is also contentious with numerous studies (73), including a large randomized-controlled trial (74) finding that treatment of periodontal disease during pregnancy does not reduce the rate of PTB.…”

Section: Pathways To Microbial Colonization Of the Uterine Cavitymentioning

confidence: 94%

Exploring Preterm Birth as a Polymicrobial Disease: An Overview of the Uterine Microbiome

2014

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Infection is a leading cause of preterm birth (PTB). A focus of many studies over the past decade has been to characterize microorganisms present in the uterine cavity and document any association with negative pregnancy outcome. A range of techniques have been used to achieve this, including microbiological culture and targeted polymerase chain reaction assays, and more recently, microbiome-level analyses involving either conserved, phylogenetically informative genes such as the bacterial 16S rRNA gene or whole shotgun metagenomic sequencing. These studies have contributed vast amounts of data toward characterization of the uterine microbiome, specifically that present in the amniotic fluid, fetal membranes, and placenta. However, an overwhelming emphasis has been placed on the bacterial microbiome, with far less data produced on the viral and fungal/yeast microbiomes. With numerous studies now referring to PTB as a polymicrobial condition, there is the need to investigate the role of viruses and fungi/yeasts in more detail and in particular, look for associations between colonization with these microorganisms and bacteria in the same samples. Although the major pathway by which microorganisms are believed to colonize the uterine cavity is vertical ascension from the vagina, numerous studies are now emerging suggesting hematogenous transfer of oral microbiota to the uterine cavity. Evidence of this has been produced in mouse models and although DNA-based evidence in humans appears convincing in some aspects, use of methodologies that only detect viable cells as opposed to lysed cells and extracellular DNA are needed to clarify this. Such techniques as RNA analyses and viability polymerase chain reaction are likely to play key roles in the clinical translation of future microbiome-based data, particularly in confined environments such as the uterus, as detection of viable cells plays a key role in diagnosis and treatment of infection.

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Section: Pathways To Microbial Colonization Of the Uterine Cavitymentioning

confidence: 94%

Exploring Preterm Birth as a Polymicrobial Disease: An Overview of the Uterine Microbiome

2014

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“…Bacterial vaginosis is seen in up to 30% of pregnant women [24]. In high-income countries it is estimated that about 15% of adults between 21-50 years have severe periodontitis [29]. The proportion may be even higher in low-income-countries.…”

Section: Pathways To Spontaneous Preterm Birthmentioning

confidence: 99%

Global report on preterm birth and stillbirth (2 of 7): discovery science

Gravett

Rubens

Nunes

2010

BMC Pregnancy Childbirth

172

136

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BackgroundNormal and abnormal processes of pregnancy and childbirth are poorly understood. This second article in a global report explains what is known about the etiologies of preterm births and stillbirths and identifies critical gaps in knowledge. Two important concepts emerge: the continuum of pregnancy, beginning at implantation and ending with uterine involution following birth; and the multifactorial etiologies of preterm birth and stillbirth. Improved tools and data will enable discovery scientists to identify causal pathways and cost-effective interventions.Pregnancy and parturition continuumThe biological process of pregnancy and childbirth begins with implantation and, after birth, ends with the return of the uterus to its previous state. The majority of pregnancy is characterized by rapid uterine and fetal growth without contractions. Yet most research has addressed only uterine stimulation (labor) that accounts for <0.5% of pregnancy.EtiologiesThe etiologies of preterm birth and stillbirth differ by gestational age, genetics, and environmental factors. Approximately 30% of all preterm births are indicated for either maternal or fetal complications, such as maternal illness or fetal growth restriction. Commonly recognized pathways leading to preterm birth occur most often during the gestational ages indicated: (1) inflammation caused by infection (22-32 weeks); (2) decidual hemorrhage caused by uteroplacental thrombosis (early or late preterm birth); (3) stress (32-36 weeks); and (4) uterine overdistention, often caused by multiple fetuses (32-36 weeks). Other contributors include cervical insufficiency, smoking, and systemic infections. Many stillbirths have similar causes and mechanisms. About two-thirds of late fetal deaths occur during the antepartum period; the other third occur during childbirth. Intrapartum asphyxia is a leading cause of stillbirths in low- and middle-income countries.RecommendationsUtilizing new systems biology tools, opportunities now exist for researchers to investigate various pathways important to normal and abnormal pregnancies. Improved access to quality data and biological specimens are critical to advancing discovery science. Phenotypes, standardized definitions, and uniform criteria for assessing preterm birth and stillbirth outcomes are other immediate research needs.ConclusionPreterm birth and stillbirth have multifactorial etiologies. More resources must be directed toward accelerating our understanding of these complex processes, and identifying upstream and cost-effective solutions that will improve these pregnancy outcomes.

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“…It can lead to a progressive loss of connective tissue attachment of alveolar bone. This tissue destruction is characterized by formation of periodontal pockets which act as reservoirs for bacterial colonization of the dentogingival environment [2,3].…”

Section: Introductionmentioning

confidence: 99%