A simple analogy that we refer to as the “Seed/Soil Relationship” can help shed light on embryo implantation. Just as a successful garden needs a ”good” seed properly planted in fertile soil to produce healthy plants, successful embryo implantation requires a good seed (genetically “normal” embryo) and fertile soil (receptive uterine lining) to make a healthy baby.

One of the indicators of a receptive uterus is the thickness of the lining which causes implantation failure; the ”magic number” in stimulated IVF cycles based on our research and experience is 9mm in thickness as measured by ultrasound on the day of the hCG trigger shot. A lining thinner than this can compromise implantation potential. A secondary factor in assessing implantation potential (although less important than thickness) is a ”triple line” appearance in the lining via ultrasound. While some viable pregnancies may occur with a lining of 8-9mm, very few will occur when the endometrium measures

A “poor” endometrial lining more commonly occurs when the basal or “germinal” endometrium, from which the full endometrial layer develops, is compromised in its response to estrogen. This most commonly occurs as a result of:

1. Permanent damage to the basal endometrium:

a) Due to inflammation of the uterine lining (endometrium), i.e., endometritis (an infection occurring following a delivery, abortion or miscarriage)
b) Following repeated or over-aggressive D&C procedures
c) Following uterine surgery that causes excessive endometrial scarring.

2. Endometrial resistance to estrogen:

a) Due to overuse of clomiphene citrate
b) Developmental – as sometimes occurs following prenatal in-utero exposure to diethylstilbestrol (DES).

3. Reduced blood flow to the basal endometrium:

a) Due to multiple uterine fibroids – especially when present immediately under the endometrium (submucosal).
b) Following extensive uterine surgery
c) As a result of Adenomyosis

4. Over-exposure to ovarian testosterone:

a) Due to overgrowth of ovarian connective tissue (stromal hyperplasia) that produces testosterone in response to luteinizing Hormone (LH). This occurs more commonly in older women (beyond 40 years);
b) In poor responders to gonadotropins (especially when they are given large amounts of LH-containing gonadotropins, e.g., Repronex, Menopur)
c) In very high responders to gonadotropin stimulation, e.g., women with Polycystic Ovarian Syndrome (PCOS).

Over-exposure of endometrial cells to increased testosterone production (as might occur in all such cases, especially when high doses of LH-containing gonadotropins are administered) reduces endometrial receptivity to estrogen. This might explain why, when the same women ultimately resort to ovum donation or undergo FET’s where no ovarian stimulation with gonadotropins is undertaken, the uterine lining subsequently thickens normally following treatment with estrogen.