One fact that has been consistently found is that treatment of the early stage lesions of endometriosis with either surgery or medications has no significant demonstrable benefit in terms of fertility. The usual rationale for treating early stage endometriosis if it is not associated with pain (where treatment is shown to be beneficial) is that the severity of the disease usually progresses over time and is likely to develop into higher stage endometriosis if not removed. The surgical treatment of stage III (moderate) or IV (severe) endometriosis associated with infertility has been shown to be beneficial in terms of fertility. Anatomic distortions, dense pelvic adhesions or obstructive lesions caused by the chronic inflammation of endometriosis are frequently able to be treated effectively with modern surgical techniques.

There does not appear to be a single explanation for the association between endometriosis and infertility. Therefore, the infertility specialist should always consider various possible contributions from plausible links when deciding on management. These links include (but are not limited to)

• pelvic adhesions and anatomic distortions,
• implants near the site of fertilization which may produce molecular messengers that impact on fertilization
• abnormal ovarian follicular development

Massive dense pelvic adhesions resulting from the chronic irritation and inflamation of endometriosis can obliterate the cul de sac behind the uterus, distort the normal relationship between the ovaries and the fallopian tubes, destroy the delicate fimbrial ends of the fallopian tubes, completely occlude the fallopian tube so that the tube becomes fluid filled (hydrosalpinx), and cover the surface of the ovaries which may result in fibrotic deterioration. Randomized controlled studies have demonstrated a significant improvement in fertility when treating these types of changes surgically (without treatment the pregnancy rate is less than 10% and following surgery the pregnancy rates can rise to greater than 50%).

The small amount of fluid that normally exists within the pelvis is in constant contact with the adnexal organs (fallopian tubes and ovaries). It has been suggested that this fluid may contain some molecular messengers due to the presence of endometriosis that impacts on fertility. Molecular biology research in this area is active and the results are interesting. One line of research has demonstrated a reduction in both sperm motility (percentage of sperm moving) and sperm velocity in the presence of peritoneal fluid from women with endometriosis (as compared to peritoneal fluid from women without endometriosis). In rodent research, the injection of (peritoneal) fluid from women with endometriosis into hamster abdomen significantly impaired fertility when compared to the injection of (peritoneal) fluid from women without endometriosis. Another line of research has looked at the postfertilization (pre-implantation) effects of the peritoneal fluid from women with endometriosis. This research demonstrated that (mouse) embryos developing in culture (such as is done with In Vitro Fertilization) did not reach the later stages of development (blastocyst or hatching stages) as often when co-cultured with (peritoneal) fluid from women with endometriosis as compared to (peritoneal) fluid from women without endometriosis.

An association between endometriosis and poor follicular development (resulting in abnormal steroid hormone production) has been proposed. The research results in this area is often conflicting. Endometriosis is associated with an increased number of prostaglandins, macrophages, activated macrophages, and reactive oxygen groups (such as oxygen free radicals). Various groups have tried to link these molecular increases to ovarian ovulation defects including anovulation, luteal phase defects, and luteinized unruptured follicle syndrome (LUFS) with mixed results. This is presently an exciting area of research that may yield solid clinically relevant results in the near future.