Trophoblastic flatsectioning syncytial knotting Tenney Parker changes

Syncytial knotting, also called Tenney-Parker changes, is characterized by aggregated villi (Figure 10.3). Their cross-sections are covered with numerous knots of accumulated syncytial nuclei, and are connected to each other by numerous syncytial bridges again containing accumulated syncytial nuclei (Figure 10.3b-e). The intervillous space in between is particularly narrow (Figure 10.3d). As has been shown by several groups (Burton, 1986a,b; Cantle et al., 1987; Kaufmann et al., 1987; Kuestermann, 1981; for review see Benirschke and Kaufmann, 2000) the underlying structural correlates are trophoblastic flat sections due to increased branching of villi or to otherwise distorted villous surfaces (Figure 10.3a). Moreover, it has been shown that the incidence of knotting/trophoblastic flat-sectioning increases with sectional thickness due to geometric reasons (Benirschke and Kaufmann, 2000; Cantle et al., 1987). It is a rare event in ultra-thin sections (~0.1 mm) for electron microscopy (Figure 10.3b), it can be seen more often in semi-thin plastic sections (0.5-1 mm) for light microscopy (Figure 10.3c), and is a usual event in 5-10 mm paraffin

Tenney Parker Change Placenta

Figure 10.3 Tenney-Parker changes. (a) The scanning electron microscopical picture shows the densely packed and highly branched villi. (b) The electron microscopical picture reveals that the nuclei within such a flat section have the same heterogeneous chromatin distribution compared to the nucleus underneath in the syncytiotrophoblast. (c) The semi-thin section depicts the dense package of villi and the increased number of syncytial cross-sections between the villi. (d) The paraffin section reveals a high number of syncytial flat sections, the typical Tenney-Parker changes. (e) The scheme shows the seeming bridges between villi and the protrusions at the villous surfaces. They all resemble simply flat sections of a highly branched villous tree. a: x80; b: x3,100; c: x300; d: x60.

Figure 10.3 Tenney-Parker changes. (a) The scanning electron microscopical picture shows the densely packed and highly branched villi. (b) The electron microscopical picture reveals that the nuclei within such a flat section have the same heterogeneous chromatin distribution compared to the nucleus underneath in the syncytiotrophoblast. (c) The semi-thin section depicts the dense package of villi and the increased number of syncytial cross-sections between the villi. (d) The paraffin section reveals a high number of syncytial flat sections, the typical Tenney-Parker changes. (e) The scheme shows the seeming bridges between villi and the protrusions at the villous surfaces. They all resemble simply flat sections of a highly branched villous tree. a: x80; b: x3,100; c: x300; d: x60.

sections (Figure 10.3d). Accordingly, when evaluating sections one should be aware that the degree of knotting always depends on two factors, irregularity of villous surfaces and sectional thickness.

Several authors have pointed out that syncytial knotting is related to pregnancy complications such as placental ischemia and pre-eclampsia (Alvarez et al., 1969, 1970; Schuhmann and Geier, 1972; Tenney and Parker, 1940; Todros et al., 1999; for review see Benirschke and Kaufmann, 2000). It was speculated by the above authors that hypoxia is the underlying pathogenetic cause. On first glance, hypoxia is not a very likely cause for a sectional artefact. However, when bearing in mind that (a) hypoxia stimulates branching angiogenesis of villi (Kaufmann and Kingdom, 2000), and (b) that the type of angiogenesis shapes the villi since the syncytial cover behaves like a tight elastic glove around the underlying capillaries, it becomes reasonable that increased capillary coiling and branching results in increased villous branching and villous surface irregularities (Todros et al., 1999). Consequently, it is well-established that placental conditions (IUGR with preserved end-diastolic flow in the umbilical arteries — PED, with or without pre-eclampsia) resulting from low pO2 coincide with branching angiogenesis and richly branched terminal villi and increased syncytial knotting in paraffin sections (Todros et al., 1999). On the other hand, pregnancy conditions with abnormally high intraplacental pO2 (IUGR with absent or reversed end-diastolic flow in the umbilical arteries — ARED with or without pre-eclampsia) produce long filiform terminal villi with unbranched capillary loops and scarcity of syncytial knotting (Macara et al., 1996).

Taking a closer look on the morphology of the syncytial nuclei inside these flat sections, it becomes clear that neither apoptosis nor necrosis can be detected here. The nuclei show their typical irregularly shaped morphology of mature syncytiotrophoblast and an irregular distribution of heterochromatin (Figure 10.3b).

Most syncytial bridges found in histological sections are sectional artefacts as described above. However, as has been shown by Cantle et al. (1987), in rare cases also true syncytial bridges do exist. They are thought to serve as simple mechanical aids to establish junctions between neighboring villi. Langhans (1870) was the first to describe these structures. And more than 100 years later Burton (1986a, 1987) and Cantle et al. (1987) made clear that besides a huge number of artificial two-dimensional structures real syncytial bridges do exist. These bridges are very likely the result of a prolonged intimate contact of adjacent villous surfaces. First small areas of both syncytial surfaces come into contact, become bridged by desmosomes, and finally the separating apical membranes of both parts of the syncytiotrophoblast disintegrate (Benirschke and Kaufmann, 2000). Since the underlying mechanisms do not lead to changes in nuclear morphology, the nuclei in these areas show the normal characteristics of heterogeneous shapes and chromatin distribution that are typical for syncytiotrophoblast nuclei.

Was this article helpful?

0 0
Blood Pressure Health

Blood Pressure Health

Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...

Get My Free Ebook


Responses

  • Rufus
    Can tenneyparker change cause brain tumors?
    7 years ago
  • michaela
    What causes Tenney Parker changse?
    2 years ago

Post a comment