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Theories of origin
 
There are several theories on the origin of endometriosis including:
 
Coelemic metaplasia This theory postulates that the cells which constitute the normal lining of your abdomen and pelvis undergo change (metaplasia) due to as-yet undetermined factors and form implants of endometriosis. This theory may explain occasional presence of endometriosis in women who do not menstruate.
 
Estrogenic Stimulation Of Muellerian Rest Cells This theory postulates that the residual cells from the time when you were an embryo in your mother's uterus remain with you throughout your life. Under certain circumstances, and with estrogen stimulation, they may develop into endometriosis.
 
Retrograde Menstruation This is the most popular theory, validated by animal experiments in which endometriosis was induced by directing menstrual flow into the abdominal cavity. The theory postulates that during menstruation, menstrual blood which contains endometrial tissue backs up through your fallopian tubes and spills into your pelvis and abdomen. There is ample evidence obtained by Laparoscopy that the overwhelming majority of women have bloody fluid (containing endometrial cells) in their pelvis during their menses. This theory sheds light on how endometrial cells find their way to your pelvis, but it does not explain why only a minority of women will actually develop significant endometriosis. Usually, endometrial cells in your abdominal cavity are regarded as an unwelcome visitor and they are sought out and destroyed by your body's immune system. If you suffer from endometriosis, this defense system does not appear to work properly. Reasons may include: your immune system is weakened or defective and is unable to either recognize or to destroy the invading cells; the endometriosis cells produce a defensive substance preventing your body from detecting or destroying them; or there are other substances or chemicals either within your body or introduced from the environment that affect the ability of your immune system to function properly.
 
Lymphatic and vascular spread This is another theory that tries to explain the presence of endometriosis in places farther away from the pelvis. Your abdominal and pelvic cavity is lined by a peritoneal lining which is not like a stainless steel covering, but rather quite permeable like a sponge. Your lymphatic system collects fluid between cells and distributes it throughout your entire body. It is quite possible that it can pickup the cells of endometriosis inside your pelvis and transfer them to more distant sites.The same principle can be applied to the vascular spread, but in this situation new vessels are grown and formed around the areas of endometriosis, so they can acquire endometrial cells quite readily and transfer them into distant parts of your body, especially areas with a significant blood supply (e.g., lungs or diaphragm).
 
Other Factors Affecting the Occurrence Of Endometriosis
 
Altered Immune Response Your body is in a state of constant vigil, trying to detect, identify, and destroy if necessary any cells or organisms which are either abnormal or wander out of their usual domains. There is ample evidence that functionality of some of the guardian cells (natural killer cells) is diminished in patients with endometriosis. There are several other conditions that seem to diminish function of the natural killer cells, including: smoking, chronic depression, major anxiety disorders, chronic illness and certain chemicals in the environment (dioxin).
 
Prolonged Menstrual Flow Prolonged and irregular menstrual flow, especially when menstrual bleeding lasts longer than seven days increases the risk of acquiring endometriosis. 
 
Congenital Defects Endometriosis may develop in young teenagers if they suffer from cervical stenosis, lack of a cervix, lack of an opening in the hymen and other congenital anomalies. These patients are unable to empty the uterus during menses such that a large amount of blood reroutes through the fallopian tubes into the pelvis, allowing endometrial cells to implant in the abdomen.
 
PHYSIOLOGIC MINIMAL ENDOMETRIOSIS AND ENDOMETRIOTIC DISEASE
 
This comprehensive theory was introduced by P.R. Koninckx . It makes a distinction between minimal superficial endometrial implants [Physiologic Minimal Endometriosis] (which are not associated with pain, inflammatory reaction, formation of adhesions, cysts or infertility) and deeply infiltrating and cystic ovarian endometriosis associated with some or all of the well known symptoms of endometriosis [Endometriotic Disease]. This theory accepts the retrograde menstruation and coelemic metaplasia as a seeding mechanism for endometrial implants in your pelvis, but as we said before, it is not enough to have these small early implants present, as most of them will be destroyed by your body's defense mechanism. These early implants may become deeply infiltrating or cystic endometriosis by interaction between multiple hormonal, immunologic, genetic and environmental factors. First they have to survive contact with your peritoneal fluid, which contains components that play an important role in destroying endometrial cells and early implants of endometriosis. The factors allowing endometrial implants to survive in your pelvis and invade its walls may include:
 
LUF SYNDROME (Luteinized Unruptured Follicle Syndrome). The ovarian follicle goes through the changes leading to ovulation, but the egg is not released from your ovary, preventing progesterone from being released from the inside of your ovary to the peritoneal fluid. LUF is associated with moderate and severe endometriosis; it is not associated with minimal endometriosis.
 
COMPARTMENTALIZATION of peritoneal fluid. Adhesions around areas of endometriosis form pockets of fluid with high concentration of "protective factors" (produced by endometriosis cells) causing shielding of these cells from immunologic attack by your body. 
 
LOCAL HORMONAL ENVIRONMENT. Concentration of estrogen and progesterone inside your ovary will reach levels of 100 times higher than level in your blood. This may play a role in stimulating growth of any endometrial cells present inside your ovary.
 
IMMUNOLOGIC FACTORS. If you have decreased cellular immunity and decreased natural killer cell activity, your peritoneal fluid may be unable to destroy early endometrial implants.
 
GENETIC FACTORS. If members of your family suffer from endometriosis you are at a higher risk for developing endometriosis yourself.