Preterm delivery is the leading cause of perinatal morbidity and mortality worldwide. Despite a great deal of research into this disease, we still do not understand its pathophysiology. Our treatments for this disease are only marginally effective. Biochemical markers were developed with the hope of giving us new tools to prevent preterm deliveries. Specifically the hope was that they could predict which patients were destined to have a preterm delivery. At the present time these markers perform only satisfactorily at predicting preterm labor. They are expensive and not convenient to use at present. Perhaps more importantly, though, these markers have given us insight into the complexities of preterm delivery. Preterm delivery can arise from many different etiologies. This will lead to research into new treatments as knowledge about preterm delivery is amassed. We know that any number of pathological processes may be involved in any given patient with preterm labor. Biochemical markers have the distinct advantage of being able to determine the specific pathophysiology in a given patient and may allow us to tailor therapy according to the specific problem. In the future it is likely that a careful search for specific pathophysiology will be the only way we can treat this disease effectively. For the present time the biochemical markers will be used only to predict preterm delivery. Ultrasound measurements of the cervix during the pregnancy are likely a faster and less expensive way to accomplish that goal.
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"Hence, elevated levels of IL-1b, IL-6, TNF-a, PGE2, fibronectin and a-foetoprotein in the amniotic fluid have been associated with PB, while other biomarkers such as MMPs, estriol, elastase, protease, phospholipase, prolactin myeloperoxidase and tissue inhibitor of MMP (TIMP)-1 have been evaluated but with inconclusive results. (Inglis 1997, G€ ursoy et al. 2010). Increased maternal serum levels of pro-inflammatory cytokines, such as IL-1, IL-6, IL-8 and TNF-a, have also been reported to be associated with prematurity or low birthweight (PLBW) (Greig et al. 1997, von Minckwitz et al. 2000, Turhan et al. 2000, G€ ucer et al. 2001, Hitti et al. 2001). "
[Show abstract][Hide abstract]ABSTRACT: 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.
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.
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.
Full-text · Article · Apr 2013 · Journal of Periodontology
[Show abstract][Hide abstract]ABSTRACT: The care of women with preterm labor has focused predominantly on inpatient therapy: tocolysis, antibiotics, and steroid administration. The emphasis is slowly but surely shifting to secondary prevention and outpatient therapy. Our goal should be toward primary prevention of preterm labor in all women. Then and only then will a true reduction in spontaneous prematurity rates be seen.
No preview · Article · Oct 1998 · Clinical Obstetrics and Gynecology
[Show abstract][Hide abstract]ABSTRACT: Periodontal infections, which serve as a reservoir of inflammatory mediators such as prostaglandin E(2) (PGE(2)), may pose a threat to the fetal-placental unit and cause preterm delivery. This study was conducted to estimate the levels of PGE(2) in gingival crevicular fluid (GCF) and serum to explore the possible use of the GCF-PGE(2) level as a risk predictor of preterm low birth weight (PLBW). Twenty-two pregnant female patients were selected for the study. Samples of GCF and serum were collected from each patient, and sampling was repeated at one month after parturition. The level of PGE(2) in GCF and serum was estimated using a commercially available ELISA kit (NeogenTM). The mean serum PGE(2) level was 4.4 ng/ml and 1.64 ng/ml before and after parturition, respectively, and the difference was statistically significant (P < 0.001). The mean GCF-PGE(2) level was 5.8 ng/ml and 5.5 ng/ml before and after parturition, respectively, but the difference was not significant. There was positive correlation between the serumPGE(2) and GCF-PGE(2) levels, and there was a negative correlation between PGE(2) level and gestational age. The present findings suggest that there is a weak correlation between maternal GCF-PGE(2) level and birth outcome. Further clinical trials with a larger sample size are warranted for further investigation of the association between GCF-PGE(2) level and PLBW.