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Review
. 2016 Mar 3;10(1-2):226-35.
doi: 10.1080/19336918.2015.1093275. Epub 2015 Sep 30.

The hydatidiform mole

Jean-Jacques Candelier  1   2
Affiliations
Review

The hydatidiform mole

Jean-Jacques Candelier. Cell Adh Migr. .

Abstract

The hydatidiform mole (HM) is a placental pathology of androgenetic origin. Placental villi have an abnormal hyperproliferation event and hydropic degeneration. Three situations can be envisaged at its origin: 1. The destruction/expulsion of the female pronucleus at the time of fertilization by 1 or 2 spermatozoa with the former being followed by an endoreplication of the male pronucleus leading to a complete hydatidiform mole (CHM) 2. A triploid zygote (fertilization by 2 spermatozoa) leading to a partial hydatidiform mole (PHM) but can also lead to haploid and diploid clones. The diploid clone may produce a normal fetus while the haploid clone after endoreplication generates a CHM 3. A nutritional defect during the differentiation of the oocytes or the deterioration of the limited oxygen pressure during the first trimester of gestation may lead to the formation of a HM. In countries with poor medical health care system, moles (mainly the CHM) can become invasive or, in rare cases, lead to gestational choriocarcinomas.

Keywords: choriocarcinoma; epigenetic; fertilization; hydatidiform mole; invasive mole; trophoblast.

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Figures

Figure 1.
Figure 1.
Macroscopic and histological aspects of HM.
Figure 2.
Figure 2.
Placenta during the first trimester and its histological description.
Figure 3.
Figure 3.
Placental development and its regulations according to pO2 variations. During the first trimester the plugging ("plug") of the arteries, generates weak pO2. The variations of pO2 induce a modification of different molecule synthesis, which supports the transition, spatially and temporally, from the proliferation phase to the differentiation phase of the trophoblast at the end of the first trimester and the remodeling of the arteries.
Figure 4.
Figure 4.
The cytogenetic origin of HM. CHM develops after monospermic (1) or dispermic (2) fertilization of an ovum whose maternal chromosomes have been lost (or destroyed) just after conception. The result is an androgenetic diploid zygote with in case of (1) an endoreplication of the paternal chromosomes. Using the hypothesis of Golubovsky (3) a normal ovum is fertilized by 2 spermatozoa and the triploid zygote is at the origin of all the types of HM including the PHM, which are generally triploid by dispermy. In rare cases (4) -some patients have recurrent CHM - the zygote has a bi- parental diploid karyotype. Genetic studies in these patients and their families have found an association with mutations in 2 genes NLRP7 and more rarely KHDC3L.
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