Placental Development Issues - Essay Example

Name Tutor Course Date Placental Development Abstract Trophoblast invasion is central to the remodeling of the various arteries of the uterine walls. Invasive trophoblasts are the cells behind the entire process of trophoblast invasion. These cells are considered unique as they emerge from the placenta to proliferate both the upper myometrium walls and the endometrium. These cells later enter in to selected uterine blood vessels where they proceed to remodel these vessels so that they can carry an increased amount of blood supply. The onset of this process has been described to be a very controversial biological phenomenon. This is with regard to the various needs of both the mother and the fetus during gestation. It emerges that while the developing fetus within the uterus requires the invasive trophoblasts to quickly penetrate in to the mother’s uterus as they remodel her blood vessels, the mother needs to protect herself against the invasive trophoblasts since they may end up subjecting her to severe hemorrhage on completely penetrating the uterus. This paper examines the process of trophoblast invasion and the subsequent remodeling of the of the spiral arteries during placental developmental with regard to the gestation period between the eighth to the twelfth week of pregnancy. Introduction During pregnancy, the uteroplacental flow of blood tends to highly increase. Abnormal pregnancies are thus highly associated with any form of alterations in the uteroplacental flow of blood. The invasion of the trophoblasts in the uteroplacental arteries causes them to increase in diameter and subsequently attain some inelasticity. This happens without the involvement of the vasomotor control of the mother. In the event of intrauterine growth restriction and subsequent resistance in the uteroplacental blood vessels, the entire remodeling of the uteroplacental arteries is disrupted. Interstitial invasion precedes any form of trophoblast invasion. If this does not occur, the trophoblast invasion process that ensues will be impaired with. The Process of Trophoblast Invasion During the eighth to about the twelfth week of pregnancy, the uteroplacental arteries are subjected to various changes. These changes include: the invasion by the trophoblasts which replaces the muscle cells of the endothelium walls. This is followed by an increase in the diameter of the blood vessels also referred to as vaso-dilation and the subsequent loss of their inelasticity. These changes occur without or against the mother’s vasomotor control that happens to be lost at this time. Various research studies indicate that the maternal blood resistance is subsequently reduced with the remodeling of the various spiral arteries (Kaufmann, Black & Huppert 3 & 4). This results in to an increase in the uteroplacental perfusion since the fetal blood requirements would have increased as from the time of fertilization to about the twelfth week. With the loss of both vasomotor control and contractility, the placenta is guarantied of an ideal blood supply from the maternal blood circulatory system. This tends to occur in spite of attempts by the maternal body system to regulate the overall blood distribution in her body. Initial research studies done by Brosens and a number of other corporate researchers indicated that reduced endovascular invasion of trophoblasts and the subsequent reduction in the remodeling of spiral arteries are precursors to the causation of Intrauterine Growth Retardation (IUGR). This condition is commonly combined with the occurrence of preclampsia. There is still a major controversy surrounding the various biochemical mechanisms that control and initiate the process of trophoblast invasion and the subsequent remodeling of the spiral arteries (Kaufmann, Black &Huppert 3 & 4). The Description of the Cells Involved in Placental Development During the process of fetal implantation in to the uterine walls that is accompanied by trophoblast invasion, there is a direct connection between the fetal trophoblast cells and both the endometrium and the myometrium that constitute the tissues of the maternal uterine system. The point at which the direct connection occurs is referred to as the matemofetal functional zone. The basal plate on the other hand forms the various sections that remained attached to the placenta after birth normally constituting the base of the intervillous space. The placental bed is composed of all the other cells remaining after the formation of the functional zone. These cells would still attach themselves on the walls of the uterus even after the birth process. The term extravillous trophoblast refers to all the various trophoblast cells that are found residing on the outer region of the placental villi. Within the basal plate, these cells tend to form proliferating stem cell clusters described as cell columns. Interstitial trophoblast is constituted by the non proliferative components of the cell columns. The endovascular trophoblast is constituted by the various extravillous trophoblasts that invade the lumens and walls of the blood arteries. The invasive pathway is thus the term that can best describe the entire route of the invasion of trophoblasts that emerges from the stem cell proliferation of the cell columns as they get in to the placental bed (Fernando & Petraglia 230-257). The Changes Occurring in the Spiral Arteries of the Uteroplacental System During Trophoblast Invasion The effective growth and development of the fetal cells in the uterus is highly dependent on the remodeling of the spiral arteries of the uteroplacental system. The process of remodeling these uteroplacental arteries is accompanied by a number of changes described as physiological changes which on division on the basis of structural criteria occur in three stages. The three stages include the independent vascular changes associated with the invasion of trophoblasts and the remodeling of the spiral vascular vessels initiated by interstitial trophoblasts that are found located on the perivascular walls. The third group of changes is associated with the infiltration of the blood vessels on the uteroplacental walls with the trophoblasts (Kliman 139). If it happens that the invasion of the trophoblasts in the uteroplacental arteries is impaired with, then IUGRT ensues. In this regard, it happens that improper perfusion of the placenta is initiated by the inability of the spiral arteries to undergo the remodeling process as a result of the failure of the trophoblast invasion process to take place. It thus becomes obvious that the role played by the occurrence of the three stages of changes is vital for the remodeling of the spiral arteries to occur (Am 3&5).The adequate arterial perfusion of the placenta during the entire gestation period is only guarantied on the occurrence of the full sequence of these changes. During the initial change stages of the uteroplacental arteries, the arteries are generally pertubated alongside the endothelia basophilia accompanied with vacuolation. This is then followed by disorganized dilation of the lumen of the arteries. Changes that are induced by pregnancy tend to be independent of the entire invasion of the trophoblasts within the spiral arteries. These changes are thus highly considered to involve the activation of the rennin- angiotensin system of the local decidual artery by the maternal system. It has been demonstrated by a research study done by Craven and a group of co researchers that in the event of intrauterine pregnancy, uteroplacental arteries emerging from both the implantation and the non implantation sites exhibit various physiological changes. Spiral arteries of the walls of the endometruim happen to undergo similar physiological changes during an ectopic form of pregnancy. The second stage of changes in the process of vascular remodeling sets in after trophoblast invasion independent changes. These changes are preceded by the invasion of the uteroplacental arteries with the extravillous trophoblast. The entry of the extravillous trophoblast in to the spiral arteries is highly associated with their subsequent remodeling. These changes are highly connected with the reduction of the smooth muscle cells and the subsequent deposition of fibrinoid material that is then followed by the infiltration of the entire media with trophoblasts. This then measures the onset of the third stage of changes that is accompanied by the infiltration of the spiral arteries with trophoblasts (Jauniaux, et al 3255). The endovascular trophoblasts in this stage are quick to invade the spiral arterial walls. This subsequent invasion of the uteroplacental arteries by the endovascular trophoblasts results in to the increase in the diameter of the spiral arteries to sizes that are considered to be two times greater than the initial diameter. The loss of the elastic fibers occurs hand in hand with the invasion of the media of the smooth muscles with the trophoblasts. This invasion of the smooth muscles media with the trophoblast is an aspect that is yet to be examined for any correlation with the death of the smooth muscles or their subsequent structural differentiation. This is possibly the process responsible for the replacement of most of the endothelial cells. The Trophoblast Invasive Pathway The process of trophoblast invasion is not homogenous. Within the central region of the entire placental bed, there is a thick proliferation of the extravillous trophoblast with a thick depth along the walls of the uteroplacental arteries. This thick proliferation tends to decrease in the spiral arteries that are located along the margin of the placenta. Owing to the difficulty with which it takes to ideally examine human pregnancies in the early stages of gestation, most early pregnancy studies are done in related primates including, monkeys. Trophoblast invasion starts moments after the process of fertilization (Genbacev, et al 1670). An exact period of ten days after the process of fertilization has been associated with the onset of trophoblast invasion in a number of primates. It is important to understand that trophoblast invasion only occurs in arteries and does not spread to the veins as well. According to observations done both anatomically and through ultra sound, it has been revealed that the plugging of most of the trophoblasts in the spiral arteries and the subsequent decrease in the perfusion of the intervillous is very evident at the twelfth week of pregnancy. A study by Rodesch and co researchers postulated that it is vital to reduce the maternal supply of blood to the developing embryo during the early stages of pregnancy in an effort to shield the embryo from excess oxygen. This is more so within the initial stages of differentiation (Thornburg et al 13). A number of ultra sound observations done during the eighth and fourth weeks of pregnancy indicated the absence of uteroplacental blood flow within this period. At the start of the twelfth week of gestation, there is a significant increase in the uteroplacental supply of blood reaching peak levels at the fourteenth week. At about the sixth and eighth week of pregnancy there is usually an intense blocking of the spiral arteries with the trophoblasts especially at the region of connection to the intervillous space. The blockage however gradually decreases as the pregnancy progress from the eighth to the twelfth week. What exactly happens during the very first trimester of pregnancy is yet to be fully accepted by many. The various controversial issues regarding this aspect have now been resolved on adopting an advanced probe for sensing oxygen levels. It has now been established that within the eighth and twelfth week of pregnancy, there is a subsequent increase in the level of anti –oxidants in line with the oxygen tension and the increase in placental perfusion. The various anti –oxidants include: glutathione peroxidase, catalase alongside superoxide dismutase. Their increased level is geared at counteracting the amounting oxidative stress that is coupled with the oxygen tension and the increased perfusion. One would thus wonder how the embryo gets its nutritional provision with these conditions. It emerges that owing to the fact that the intevillous space is usually bathed with some cellular fluid possibly filtered from the shell of the trophoblast, nutrients could possibly filter through as well. It has even been shown in a number of pregnancies that there are normally some dilated glands beneath various openings of the intervillous space. This occurrence points to the feeding mechanism of the developing embryo owing to the fact that endometrial glands as at the first trimester of pregnancy are very hyper secretive. The emerging secretions from these glands provide nourishment to the developing embryo during early stages of pregnancy. Trophoblast invasion of the spiral arteries thus exhibits two waves. The interstitial invasion that occurs during the very first trimester and the endovascular trophoblast invasion that occurs during the next trimester. The various physiological changes that come with this invasion are usually not any more a few weeks after the twelfth week. It has also been established that there exists a possibility for the interstitial trophoblasts to indirectly bring about the modification of the spiral arteries. This is bound to occur through paracrine action where the trophoblasts would simply circumvent the blood vessels. Nitric oxide has been identified as a leading precursor to the occurrence of this action. This oxide has the ability to significantly vasodilate the vessels (Kliman 836). The Regulation of the Process of Trophoblast Invasion It has not been possible to precisely elucidate the mechanism through which the entry of trophoblasts in the uterine walls from the placenta occurs. The ability to channel themselves to spiral arteries and subsequently remodel them to foster low resistance has also not be elucidated alongside the mechanism through which they are lost on delivery. With the many steps involved in their invasion, so are the processes and tools used in fostering their roles. When the trophoblasts come in contact with the deciduas, their own differentiation pathway is changed to that of anchoring trophoblast from villous trophoblasts. This occurs through contact with the extracelluar matrix of the decidua or through paracrine stimulation. Decidual cytokines have been shown to highly influence differentiation process. Among the major cytokines are; beta transforming growth factor and the leukemia inhibiting factor. Other regulators of trophoblast differentiation and invasion are colony stimulating factor-1, protein kinase C activators, Oxygen, epidermal growth factor and hepatocyte growth factor (Kliman 836). Conclusion Since not many researchers agree that trophoblast invasion is the mechanism behind the remodeling of spiral arteries, studies in this aspect have been very contradicting. Other researchers have indicated that the remodeling of spiral arteries occurs as a result of maternal decidua. Trophoblast invasion has been accepted among many researchers owing to the large volumes of research that have positively indicated their role in the remodeling of the spiral arteries. Works Cited Am, J Pathol. Uteroplacental Blood Flow. American Society for Investigative Pathology 157.6 (2000):1757-68. Fernando M., & Felice, Petraglia. Predictive Value of Hormone Measurements in Maternal and Fetal Complications of Pregnancy. The Endocrine Society 23.2 (2002): 230-257. Genbacev, et al .Regulation of Human Placental Development by Oxygen Tension. Pub Med. 277(1997):1669-1672. Jauniaux, et al. Onset of Maternal Arterial Bloodflow and Placental Oxidative Stress: A Possible Factor In Human Early Pregnancy Failure. Am J Pathol 157 (2000):3251-3262. Kaufmann P., Black S. & Huppert, B. Endovascular Trophoblast Invasion for the Pathogenesis of Intrauterine Growth Retardation and Preclampsia.Biology of Reproduction . 69(2003):1-7. Kliman, J. Trophoblast to human placenta. Knobil E Neill JD eds. Encyclopedia of Reproduction 4 (1999):834-846. Kliman, J. Trophoblast infiltration. Reproduction Med Rev. 3 (1994):137-157. Thornburg, et al. Hemodynamic changes in pregnancy. Semin Perinatol, Pub Med. 24(2000):11- 14. Read More