Dating the endometrial biopsy noyes
This interaction involves the embryo, with its inherent molecular programme of cell growth and differentiation, and the temporal differentiation of endometrial cells to attain uterine receptivity.Implantation itself is governed by an array of endocrine, paracrine and autocrine modulators, of embryonic and maternal origin.gene expression clusters or cytokine ‘fingerprints’) rather than single biomarkers.This strategy may be particularly relevant in the field of implantation because numerous factors are involved, many of these have multiple functions, and there is potentially a large amount of redundancy.It is clear that to improve implantation rates in stimulated cycles, it is important to find ways to pinpoint the window of implantation, ensure that the best embryo is selected and synchronize embryo transfer with the time of optimal endometrial receptivity.Importantly, ways of evaluating and enhancing endometrial receptivity and embryo quality without disrupting the delicate process of implantation itself must be identified.
This not only enables the sampling of many more potential molecular candidates, but also the identification of characteristic molecular profiles (e.g.
The endometrium is remodelled throughout the menstrual cycle, and exhibits only a short period of receptivity, known as the ‘implantation window’.
In humans, during a natural cycle, the embryo enters the uterine cavity ∼4 days after ovulation ( Croxatto , 1978 ).
Implantation in humans is controlled by a complex and sophisticated interaction between embryo and endometrium, which begins at the early stages of oocyte maturation ( Emiliani , 2005 ).
This dialogue enables synchronous development of the oocyte and maturation of the endometrium, followed by embryo orientation, apposition, adhesion and endometrial invasion by the blastocyst ( Enders , 1986 ).