These images are both from placentas with preterm labor at 34 week gestation with similar birth weights, one with and one without chorioamnionitis. After looking at the complete case, I diagnosed the placenta without chorioamnionitis as having advanced villous maturation for gestation. From the very limited sample above, would anyone else venture such a conclusion, and if so which image is advanced, the top or the bottom. I selected the images from comparable areas from the slides, and tried to avoid the variation that occurs with spiral artery flow in the placentone.
I often hear obstetricians state that chorioamnionitis causes preterm labor. I disagree. I don’t doubt that once a patient has chorioamnionitis, or once a monkey uterus has been injected with bacteria, that labor will progress. My concerns are that approximately a quarter of patients with preterm labor do not have chorioamnionitis, antibiotics do not have much tocolytic effect, and there is no mechanism that explains why some patients acquire chorioamnionitis.
Proposed mechanisms for developing chorioamnionitis include low grade endometritis prior to pregnancy, abnormal vaginal flora such as bacterial vaginosis, high levels of ureaplasma or even trichinosis, and acquired or genetically weakened defense mechanisms against infection ascending from the uterus. In sheep, hormonal changes can lead to cervical labor without uterine labor. An equivalent isolated cervical labor in humans might provide the vulnerability for the ascent of vaginal microorganisms.
In sheep, the lamb’s secretion of cortisol causes maturational changes and reduces the progesterone estrogen ratio in the ewe that initiates the myometrial cell cascade that leads to labor. Unfortunately, the mechanism in humans is more complex. A human mechanism that would lead to preterm labor based on fetal stress would seem to be adaptive, for example in response to utero-placental ischemia. There is some clinical basis for this as I can recall studies using low abdominal diameter to predict preterm labor. Dr. Fred Krauss made the observation some time ago that preterm labor seems to divide itself into those cases with chorioamnionitis and those with advanced maturation or ischemic changes of the villi. Certainly, just in a day to day reading of placentas this observation seems borne out. A formal study would need to have strict clinical criteria for determining gestational age, and be “blinded” to the inflammation on the slide. Then using either measurable criteria or comparison of multiple pathologists reading the “blinded” slides, the hypothesis of a maturational villous difference between types of preterm labor could be tested. The outcome would likely need to be stratified by gestation.