Adverse pregnancy outcomes (APOs) and periodontal disease: pathogenic mechanisms
Adverse pregnancy outcomes (APOs) and periodontal disease: pathogenic mechanisms
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不良妊娠结局（APOs）和牙周病：致病机制
DOI：
10.1902/jop.2013.1340015
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发表时间：
2013-04-01
影响因子：
6.7
通讯作者：
Offenbacher, Steven
中科院分区：
文献类型：
--
作者：
Madianos, Phoebus N.;Bobetsis, Yiorgos A.;Offenbacher, Steven
目的：评价牙周病(PD)与不良妊娠结局(APOS)之间潜在生物学途径的证据。材料与方法：对人、实验和体外研究进行评价。结果：牙周病原体/副产物可进入胎盘并扩散至胎儿循环和羊水。它们存在于胎儿胎盘间可刺激胎儿免疫/炎症反应，其特征是产生针对病原体的IgM抗体和分泌水平升高的炎症介质，这反过来可能导致流产或早产。此外，感染/炎症可能导致胎盘结构改变，导致先兆子痫和营养转运障碍，导致低出生体重。胎儿暴露还可能导致组织损伤，增加围产期死亡/发病的风险。最后，全身炎症反应可能加剧胎儿-胎盘单位的局部炎症反应，进一步增加APO的风险。结论：仍需进一步研究，以充分将基础研究成果转化为临床研究和实践。了解个体口腔微生物群和免疫反应的全身毒力潜力可能与使用帕金森病的临床症状对挑战的性质进行分类截然不同。因此，对于目前的“一刀切”干预，更个性化的靶向治疗可能是一个更具预测性的答案。目的评估关于牙周病(PD)和不良妊娠结局(APO)之间可能关联的潜在生物学途径的证据。材料与方法对人体、实验和体外研究进行评价。结果牙周病原体/副产物可进入胎盘，扩散至胎儿循环和羊水。它们存在于胎儿胎盘间可刺激胎儿免疫/炎症反应，其特征是产生针对病原体的IgM抗体和分泌水平升高的炎症介质，这反过来可能导致流产或早产。此外，感染/炎症可能导致胎盘结构改变，导致先兆子痫和营养转运障碍，导致低出生体重。胎儿暴露还可能导致组织损伤，增加围产期死亡/发病的风险。最后，引发的全身性炎症反应可能加剧胎儿胎盘单位的局部炎症反应，进一步增加APOS的风险。结论要将基础研究成果充分转化为临床研究和实践，还需要进一步的研究。了解个体口腔微生物群和免疫反应的全身毒力潜力可能与使用帕金森病的临床症状对挑战的性质进行分类截然不同。因此，更个性化的靶向治疗可能是对目前一刀切干预措施的更具预测性的回答。
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.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.