Almost 75% of pregnancy loss that occurs before the 20th week of gestation (when the vast majority of miscarriage takes place) is due to the failure of implantation of the embryo in the uterus.

The implantation takes place approximately 6 days after conception when the blastocyst has been formed by cell division of the original cells.

The blastocyst state of the embryo is a microscopic sphere (d = 250 μ) and is composed of about 64 cells which are divided into the outer layer of the trophoblast, which will generate both the placenta and the other tissues necessary for the foetus during its inter-uterine life, and an inner mass of cells from which all the cells of the human body will develop (Figs. 18.1 and 18.2). The mechanisms through which implantation is governed and controlled are not yet perfectly understood, though it is evident that during these phases what is crucial are the strong relationships which develop between the specialized cells of the trophoblast and the cells of the endometrium taken together as epithelium, stroma and blood vessels (Fig. 18.3).

The first phase of adhesion would seem to be the simplest; however, it is premised by a series of exceptionally delicate mother–embryo interactions which can compromise the final result.

In humans, the endometrium shows maximum receptivity for embryo implantation during the mid-secretory phase, there being a precise “window of implantation” which corresponds to the 21st day of a hypothetical regular menstrual cycle of 28 days. The window is when there is the maximum level of glandular secretion, interstitial edema and optimal blood flow. These conditions of course do not explain how the adhesion of the blastocyst to the endometrium becomes stable.

In 2003, Genbacev et al. [1] discovered the protein L-selectin functioned as a type of “Velcro” allowing the outer layer trophoblast cells to adhere to the walls of the uterus, thus it is possibly one of the most important ways of mediating early stage embryo–endometrium interaction.

The outer layer of the blastocyst expresses L-selectin and the uterus expresses high quantities of glycoproteins with oligosaccharide domains which interact at a molecular level with the protein so creating “sticky” conditions between them. The blastocyst moves along the uterus sticking and unsticking to it so slowing its progress until finally it sticks to one point and there begins the embedding process. This phase is crucial for embryo development (Figs. 18.4, 18.5, 18.6, and 18.7a, b).

The body’s immune response to cell damage makes use of the process of leukocyte extravasation which needs the leukocytes to attach themselves to the vessel walls under conditions of shear stress, as is the case in the need for the blastocyst to attach itself to the uterus. These similar activities have led several scientists to propose similar mechanisms for the two events. They affirm that the molecular basis for embryo implantation must be similar to that of the transmigration process of the leukocytes through the endothelial cells of the blood vessels, which initially functions by blocking the movement of the leukocytes in the blood by molecular “stickiness” using the selectin and other proteins expressed by the leukocytes and the carbohydrate ligands on the endothelium [2].

Selectins are a C-type lectin (glycoproteins which bind to sugar molecules and require calcium for the binding) which are expressed on the surface of leukocytes, platelets and activated endothelial cells.

They are part of the linking mechanism of rolling adhesion of leukocytes and platelets onto vessel endothelium and are important for the homing of the lymphocytes to secondary lymphoid organs and for the recruiting of leukocytes to inflammation sites [3] (Fig. 18.8).

There are three types of selectins:

• 
  

  l-selectin (Fig. 18.9) expressed by all leukocytes except T-lymphocytes.

  
  
• 
  

  E-selectin (Fig. 18.10) expressed by endothelial cells activated by cytokines from transcriptional stimulation.

  
  
• 
  

  P-selectin (Fig. 18.11) expressed by platelets and activated endothelial cells where it is stored in α-granules and Weibel–Palade bodies, respectively, as pre-formed transmembrane proteins and is translocated to the plasma membrane when stimulated.

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