space, the trophoblast tissue (i.e., cytotrophoblast, syncytiotrophoblast), and fetal capillaries of peripheral and stem villi. The non-parenchymal tissue is composed of the decidual and chorionic plates, intercotyledonary septa, fetal vessels, connective tissue, and fibrin deposits. The second phase of placental development, lasting from 36 weeks until term, is the maturation phase. The maturation phase of placental growth is characterized by an increase in fetal growth but without an increase in placental functional or parenchymal tissueI; only the non-parenchymal (i.e., nonfunctional) placental tissue increases. These changes are consistent with the early placental growth and development that occurs and is necessary for rapid fetal growth in the last trimester of pregnancy, when fetal weight increases from a mean of 1,000 g to 3,400 g (in the general U.S. population).
In addition to these changes, there also may be differences in placental function as a consequence of a women’s pregravid BMI. In general, obese women are more likely to have larger placentas and neonates in comparison to average-weight women. Alterations in maternal metabolic function during pregnancy are most likely mediated through placental hormone and cytokine production, which in turn affect maternal fat accretion and nutrient availability. Recently, Challier et al. (2008) reported that the placentas of obese women (pregravid BMI > 30 kg/m2) had a two- to three-fold increase in the number of macrophages in comparison with placentas of average weight (pregravid BMI < 25 kg/m2) women. There was also increased expression of the proinflammatory cytokines interleukin (IL-1), tumor necrosis factor-alpha (TNF-α), and IL-6. Hence, the chronic inflammation associated with obesity may affect placental growth and function, thereby altering maternal metabolic function and resulting in the women with pregravid obesity having decreased maternal pregravid maternal insulin resistance and decreased maternal fat accretion but increased placental and fetal growth.
The composition of the placenta varies with gestational age as well as maternal metabolic status. Approximately 88 percent of placental weight is water. In comparison, the fetus at term has approximately 80 percent water in its fat-free mass. In studies of Widdowson and Spray (1951), the composition of placentas ranging from 17 to 40 weeks’ gestation was analyzed. The mean percentage of water was 88 percent, protein 11 percent, and fat 1 percent. Garrow and Hawes (1971) similarly reported that in more than 700 placentas, the blood-free placenta had approximately 10 percent protein. In a further analysis of the effect of maternal diabetes on placental composition, Diamant et al. (1982) described increased placental mass, amount of DNA, glycogen, and lipids in the placentas of women with diabetes compared to a normal glucose-tolerant control group. The