Adverse pregnancy outcomes (APO s) and periodontal disease: pathogenic mechanisms
PN Madianos, YA Bobetsis… - Journal of clinical …, 2013 - Wiley Online Library
Journal of clinical periodontology, 2013•Wiley Online Library
Aim To evaluate the evidence on potential biological pathways underlying the possible
association between periodontal disease (PD) and adverse pregnancy outcomes (APO s).
Material & Methods Human, experimental and in vitro studies were evaluated. Results
Periodontal pathogens/byproducts may reach the placenta and spread to the foetal
circulation and amniotic fluid. Their presence in the foeto‐placental compartment can
stimulate a foetal immune/inflammatory response characterized by the production of IgM …
association between periodontal disease (PD) and adverse pregnancy outcomes (APO s).
Material & Methods Human, experimental and in vitro studies were evaluated. Results
Periodontal pathogens/byproducts may reach the placenta and spread to the foetal
circulation and amniotic fluid. Their presence in the foeto‐placental compartment can
stimulate a foetal immune/inflammatory response characterized by the production of IgM …
Aim
To evaluate the evidence on potential biological pathways underlying the possible association between periodontal disease (PD) and adverse pregnancy outcomes (APOs).
Material & Methods
Human, experimental and in vitro studies were evaluated.
Results
Periodontal pathogens/byproducts may reach the placenta and spread to the foetal circulation and amniotic fluid. Their presence in the foeto‐placental compartment can stimulate a foetal immune/inflammatory response characterized by the production of IgM antibodies against the pathogens and the secretion of elevated levels of inflammatory mediators, which in turn may cause miscarriage or premature birth. Moreover, infection/inflammation may cause placental structural changes leading to pre‐eclampsia and impaired nutrient transport causing low birthweight. Foetal exposure may also result in tissue damage, increasing the risk for perinatal mortality/morbidity. Finally, the elicited systemic inflammatory response may exacerbate local inflammatory responses at the foeto‐placental unit and further increase the risk for APOs.
Conclusions
Further investigation is still necessary to fully translate the findings of basic research into clinical studies and practice. Understanding the systemic virulence potential of the individual's oral microbiome and immune response may be a distinctly different issue from categorizing the nature of the challenge using clinical signs of PD. Therefore, a more personalized targeted therapy could be a more predictive answer to the current “one‐size‐fits‐all” interventions.
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