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Periodontal diseases and adverse pregnancy outcomes: Mechanisms
Elena Figuero1, Yiping W Han2, Yasushi Furuichi3
1ETEP (Etiology and Therapy of Periodontal Diseases) Research Group, Department of Dental Clinical Specialties, Faculty of Dentistry, University Complutense of Madrid (UCM), Madrid, Spain.
Adverse pregnancy outcomes (APOs) have been defined as (a) pre-term birth, when there is a delivery before 37 completed weeks (<259 days); (b) pre-eclampsia, which is a multisystem disorder of pregnancy characterized by maternal hypertension and proteinuria after the 20th gestational week; (c) low and very low birthweight, depending on whether the weight of the baby is less of 2500 g or <1500 g and (d) the spontaneous death of the fetus with <20 weeks (miscarriage) or between 20 and 36 weeks (stillbirth). In 2012, during the Consensus Report from the Joint EFP/AAP workshop on periodontitis and systematic diseases the role of periodontal diseases on APOs was reviewed. Some years later, this evidence has grown, and an update on the literature regarding the mechanisms related to this potential association (APOs and periodontal diseases) needs to be presented. The two major pathways (direct and indirect) already accepted in 2012 are still valid nowadays. Most evidence published in the last 5 years deals with a strong and solid evidence coming from the direct pathway while there is as scarce new evidence regarding indirect pathway. In this direct pathway, the haematological dissemination of oral microorganisms and their products, would later induce an inflammatory/Immune response in the foetal-placental unit. The most plausible route for this direct pathway is the hematogenous transmission through dental bacteremia, although not many new studies dealing with bacteremia has been performed lately.
Adverse pregnancy outcomes (APOs) have been defined as (a) pre-term birth, when there is a delivery before 37 completed weeks (<259 days); (b) pre-eclampsia, which is a multisystem disorder of pregnancy characterized by maternal hypertension and proteinuria after the 20th gestational week; (c) low and very low birthweight, depending on whether the weight of the baby is less of 2500 g or <1500 g and (d) the spontaneous death of the fetus with <20 weeks (miscarriage) or between 20 and 36 weeks (stillbirth). In 2012, during the Consensus Report from the Joint EFP/AAP workshop on periodontitis and systematic diseases the role of periodontal diseases on APOs was reviewed. Some years later, this evidence has grown, and an update on the literature regarding the mechanisms related to this potential association (APOs and periodontal diseases) needs to be presented. The two major pathways (direct and indirect) already accepted in 2012 are still valid nowadays. Most evidence published in the last 5 years deals with a strong and solid evidence coming from the direct pathway while there is as scarce new evidence regarding indirect pathway. In this direct pathway, the haematological dissemination of oral microorganisms and their products, would later induce an inflammatory/Immune response in the foetal-placental unit. The most plausible route for this direct pathway is the hematogenous transmission through dental bacteremia, although not many new studies dealing with bacteremia has been performed lately.
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