Preterm Villous Maturation and Villous Hypermaturity

In 50% of placentas of preterm deliveries from the 29th to 32nd week of pregnancy and in 33% of those of preterm deliveries from the 33rd to 37th week, Schweikhart et al. (1986) found a villous maturational state that corresponded to the normal mature placenta. Becker (1981) used the term maturitas praecox placentae when the villous maturation is accelerated and reaches structurally normal term features (score 22) considerably before the 40th week. In other cases, the villi even displayed degrees of formation of terminal villi exceeding those in normal maturity, resulting in “hypermaturity” (score 34) (Salvatore, 1968). According to the results of Schweikhart et al. (1986), hypermaturity is an even more common finding in cases of preterm delivery than is maturitas praecox. Becker (1981) concluded that the prematurely matured placenta may induce labor (cf. Chapter 14).

Preterm villous maturation is characterized by normal villous features that under normal conditions would have been reached only in later stages of pregnancy. In contrast, the more severe form of this entity, hypermaturity, is struc-

Figure 15.13. Prematurely delivered placenta (37th week of pregnancy) from a pregnancy complicated by preeclampsia and IUGR. A: Scanning electron micrograph shows the typical feature of preterm maturation (or hypermaturity), with long, twisted, partly branched terminal villi that are aggregated around the hidden mature intermediate villus. The underlying pathogenesis is likely to be a severe alteration of terminal

Villous capillarization, showing local variations from nonbranching to prevailing branching angiogenesis (villous maturation score, 34). B: In a plastic section, this feature results in the appearance of numerous small cross sections of highly capillar-ized terminal villi, locally intermingled with increased trophoblastic flat sectioning. A: x125; B: x200. (Source: Part A from Kaufmann et al., 1987, with permission.)


Turally characterized by a mixture of two different types of abnormal terminal villi: (1) long, unbranched, and twisted small-diameter terminal villi, corresponding to those found in cases of postplacental hypoxia (scores 42 and rarely even 44); these terminal villi largely hide the central mature intermediate villus from which they branch (Fig. 15.13A); and (2) short, highly branched, fist-like terminal villi with increased branching angiogenesis showing increased incidence of knotting (Tenney-Parker changes) in paraffin sections. These villi resemble those displayed in preplacental hypoxia and uteroplacental hypoxia (villous maturation scores 32 or even 33). Accordingly, the features typical for hypermaturity may overlap with those found following preplacental hypoxia (e. g., maternal anemia), or they are displayed by postplacental hypoxia (IUGR with absent end-diastolic umbilical flow). Usually a mixture of both types of terminal villi, caused by mixtures of branching and nonbranching angiogenesis, is found (score 34). In histologic sections, complicated networks of narrow capillaries are accompanied in parallel by long, winding dilated capillaries. The corresponding branching patterns of the terminal villi, as seen by scanning electron microscopy (Fig.

15.13A), showed partly long winding, partly short, and multiply indented villi. Histologically, this situation results in complex pictures with partly isolated villous sections having dilated capillaries and partly net-like villous conglomerates (Fig. 15.13B).

The coexistence of these features suggests that overstimulated angiogenesis (branching or nonbranching type) is one of the underlying pathogenetic mechanisms for hypermature villous maturation. This concept agrees with the experience that these pregnancies often are complicated by hypertensive disorders as well as intrauterine growth retardation. At present it is still difficult to differentiate between cause and effect. The molecular basis of the obvious alteration of villous angiogenesis is not yet understood.

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