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Several matrix metalloproteinases (MMP) have been implicated in preterm parturition.
Bacteria that have been implicated in preterm delivery include commensal bacterial species found in the vaginal tract such as genital mycoplasmas [8] [11] and Streptococcus agalactiae [12], and commensal species of the oral cavity such as Fusobacterium nucleatum [3], [13], [14].
Although HAART regimens have been implicated in preterm delivery, this does not appear to be the case for IUGR according to a French study (Briand et al., 2009).
This is consistent with the reduced rate of growth of the placenta observed with serial ultrasound scans in these cases Oxidative stress has been implicated in preterm premature rupture of the membranes, a condition associated with proteolytic degradation of the collagen fibres in the chorio-amnion.
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Elevated maternal cortisol in early pregnancy is implicated in preterm birth as a result of an earlier than expected spike in placental CRF compared to full-term pregnancies [ 9].
Several pathophysiological mechanisms have been implicated in triggering preterm birth [4].
Several metallopeptidases have been implicated in both term and preterm parturition.
A host inflammatory response has been implicated in the pathogenesis of preterm delivery [8].
Localized inflammation and increased expression of TLR4 receptors within the uterus has been implicated in the pathogenesis of preterm labor.
Systemic or local intrauterine infections have been implicated in the pathogenesis of preterm labor and delivery (for a review, see [ 23]).
*p < 0.05 vs. pregnant group, One-way ANOVA with Newman-Kuels test Localized infection-associated intrauterine recruitment/activation of neutrophils and monocytes has been implicated in the pathogenesis of preterm labor in humans (see [ 25] and references therein).
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