Histology
Under histology sections, Hofbauer cells have appeared with discernible amount of cytoplasm.
Hofbauer cells are oval eosinophilic histiocytes [1] with granules and vacuoles found in the placenta, which are of mesenchymal origin, in mesoderm of the chorionic villus, particularly numerous in early pregnancy.
They are named after J. Isfred Isidore Hofbauer (1871 [2] -1961), [1] a German-American gynecologist who described the cell type in his book Grundzüge einer Biologie der menschlichen Plazenta, mit besonderer Berücksichtigung der Fragen der fötalen Ernährung (Biology of the Human Placenta with a special emphasis on the question of fetal nourishment).
They are believed to be a type of macrophage [3] [4] and are most likely involved in preventing the transmission of pathogens from the mother to the fetus (so-called vertical transmission). Although there are many studies concerning placental vasculogenesis and angiogenesis, there has been a lack of evidence on the possible roles of Hofbauer cells in these processes. [5] According to a systems level single-cell transcriptomics based study of human placental cell-cell communication, Hofbauer cells produce HBEGF, an EGFR ligand, which drives differentiation of villous cytotrophoblasts (VCT) towards syncytiotrophoblasts (SCT). [6]
Under histology sections, Hofbauer cells have appeared with discernible amount of cytoplasm.
The placenta is a temporary fetal organ that begins developing from the blastocyst shortly after implantation. It plays critical roles in facilitating nutrient, gas and waste exchange between the physically separate maternal and fetal circulations, and is an important endocrine organ producing hormones that regulate both maternal and fetal physiology during pregnancy. The placenta connects to the baby via the umbilical cord, and on the opposite aspect to the maternal uterus in a species dependent manner. In humans, a thin layer of maternal decidual (endometrial) tissue comes away with the placenta when it is expelled from the uterus following birth. Placentas are a defining characteristic of placental mammals, but are also found in marsupials and some non-mammals with varying levels of development.
The chorion is the outermost fetal membrane around the embryo in mammals, birds and reptiles (amniotes). It develops from an outer fold on the surface of the yolk sac, which lies outside the zona pellucida, known as the vitelline membrane in other animals. In insects it is developed by the follicle cells while the egg is in the ovary.
Gestational hypertension or pregnancy-induced hypertension (PIH) is the development of new hypertension in a pregnant woman after 20 weeks' gestation without the presence of protein in the urine or other signs of pre-eclampsia. Gestational hypertension is defined as having a blood pressure greater than 140/90 on two occasions at least 6 hours apart.
Trophoblasts are cells that form the outer layer of a blastocyst. They are present four days post-fertilization in humans. They provide nutrients to the embryo and develop into a large part of the placenta. They form during the first stage of pregnancy and are the first cells to differentiate from the fertilized egg to become extraembryonic structures and do not directly contribute to the embryo. After gastrulation, the trophoblast is contiguous with the ectoderm of the embryo and is referred to as the trophectoderm. After the first differentiation, the cells in the human embryo lose their totipotency and are no longer totipotent stem cells because they cannot form a trophoblast. They are now pluripotent stem cells.
Syncytiotrophoblast is the epithelial covering of the highly vascular embryonic placental villi, which invades the wall of the uterus to establish nutrient circulation between the embryo and the mother. It is a multi-nucleate, terminally differentiated syncytium, extending to 13 cm.
Placenta accreta occurs when all or part of the placenta attaches abnormally to the myometrium. Three grades of abnormal placental attachment are defined according to the depth of attachment and invasion into the muscular layers of the uterus:
In biology, placentation refers to the formation, type and structure, or arrangement of the placenta. The function of placentation is to transfer nutrients, respiratory gases, and water from maternal tissue to a growing embryo, and in some instances to remove waste from the embryo. Placentation is best known in live-bearing mammals (theria), but also occurs in some fish, reptiles, amphibians, a diversity of invertebrates, and flowering plants. In vertebrates, placentas have evolved more than 100 times independently, with the majority of these instances occurring in squamate reptiles.
Chorionic villi are villi that sprout from the chorion to provide maximal contact area with maternal blood.
Placental insufficiency or utero-placental insufficiency is the failure of the placenta to deliver sufficient nutrients to the fetus during pregnancy, and is often a result of insufficient blood flow to the placenta. The term is also sometimes used to designate late decelerations of fetal heart rate as measured by cardiotocography or an NST, even if there is no other evidence of reduced blood flow to the placenta, normal uterine blood flow rate being 600mL/min.
The placenta of certain mammals contains structures known as cotyledons, which transmit fetal blood and allow exchange of oxygen and nutrients with the maternal blood.
Confined placental mosaicism (CPM) represents a discrepancy between the chromosomal makeup of the cells in the placenta and the cells in the fetus. CPM was first described by Kalousek and Dill in 1983. CPM is diagnosed when some trisomic cells are detected on chorionic villus sampling and only normal cells are found on a subsequent prenatal test, such as amniocentesis or fetal blood sampling. In theory, CPM is when the trisomic cells are found only in the placenta. CPM is detected in approximately 1-2% of ongoing pregnancies that are studied by chorionic villus sampling (CVS) at 10 to 12 weeks of pregnancy. Chorionic villus sampling is a prenatal procedure which involves a placental biopsy. Most commonly when CPM is found it represents a trisomic cell line in the placenta and a normal diploid chromosome complement in the baby. However, the fetus is involved in about 10% of cases.
Placental growth factor is a protein that in humans is encoded by the PGF gene.
A placental disease is any disease, disorder, or pathology of the placenta.
Placentitis is an inflammation of the placenta. The main forms of placentitis are:
The fetal membranes are membranes associated with the developing fetus. The two chorioamniotic membranes are the amnion and the chorion, which make up the amniotic sac that surrounds and protects the fetus. The other fetal membranes are the allantois and the secondary umbilical vesicle.
Intermediate trophoblast is a distinct subtype of trophoblastic tissue that arises from the cytotrophoblast.
Villitis of unknown etiology (VUE), also known as chronic villitis, is a placental injury. VUE is an inflammatory condition involving the chorionic villi. VUE is a recurrent condition and can be associated with intrauterine growth restriction (IUGR). IUGR involves the poor growth of the foetus, stillbirth, miscarriage, and premature delivery. VUE recurs in about 1/3 of subsequent pregnancies.
A placental infarction results from the interruption of blood supply to a part of the placenta, causing its cells to die.
Extravillous trophoblast or, abbreviated, EVT, are one form of differentiated trophoblast cells of the placenta. They are invasive mesenchymal cells which function to establish critical tissue connection in the developing placental-uterine interface. EVTs derive from progenitor cytotrophoblasts (CYT), as does the other main trophoblast subtype, syncytiotrophoblast (SYN).
Massive perivillous fibrin deposition refers to excessive deposition of fibrous tissue around the chorionic villi of the placenta. It causes reduced growth of the foetus, and leads to miscarriage in nearly 1 in 3 pregnancies affected. There are typically no symptoms, and it is rarely detected before birth. The cause is unknown, but may be autoimmune. Diagnosis is based on the histology of the placenta. There are currently no known treatments. MPFD is very rare, but recurrence is around 18% in those affected.
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