Endometriosis is caused by the presence of cells which usually line the inside of the uterus being present elsewhere in the body. The major symptoms of endometriosis are pain and infertility.
Endometriosis is a condition characterised by the presence of endometrial cells (which usually line the inner surface of the uterus) outside the uterine cavity – usually within the pelvic cavity. It is estimated that 10-15% of women in the reproductive age group are affected by endometriosis.
Within the pelvic cavity lies the pelvic organs (uterus, fallopian tubes,ovaries, vagina, bladder, ureters (tubes which carry urine from the kidneys to the bladder) and rectum (bowel)):
A layer of ‘skin’ called the peritoneum covers these organs and the walls of the pelvic cavity. Endometriosis occurs by implanting within the peritoneum. Additionally, the endometriosis may subsequently penetrate into the walls of the pelvic organs. When endometrial cells are present the walls of the uterus, this is known as ‘adenomyosis’ and is usually considered to be a separate disease to endometriosis although the two often co-exist.
Despite years of research, the cause of the development of endometriosis lesions is still not clear. The most commonly accepted theory was suggested almost a century ago and suggests that during menstruation when the endometrium from the uterus is shed, instead of leaving through the vagina, a small quantity of blood and shed endometrium can pass ‘backwards’; through the fallopian tubes and into the pelvic cavity. Here, the shed endometrium implants into the pelvic cavity to form endometriosis (‘retrograde menstruation theory’). However, there is some evidence which isn’t consistent with this view and it has also been suggested that normal cells of the peritoneum (given their shared embryological origin with endometrial cells) may themselves ‘change’ into endometrial cells via mechanisms which are not known (‘coelomic metaplastic theory’). Alternatively, embryonic remains from the developing uterus as they migrate into their final position may persist in the pelvic cavity and form the basis of future endometriosis (‘Müllerian remnant theory’).
In the same way that the endometrium lining the uterus bleeds during menstruation, the abnormal endometrial cells too will bleed. The presence of these endometrial cells per se as well as this bleeding disrupts the normal pelvic anatomy and function, leading to the condition of endometriosis and associated symptoms.
The major presenting symptoms of endometriosis are i) pain and ii) infertility.
i) Pain is the most common symptom of endometriosis, occurring in around 80% of patients. The pain may be described as:
- Pelvic, lower abdominal or back pain with intermittent cramping of varying degree
- Irritable Bowel Syndrome (IBS)-like symptoms including Dyschezia (pain associated with constipation)
- Frequent urination and/or pain during urination giving cystitis-like symptoms which may be recurrent (ie. constantly subside and return)
- Dyspareunia (painful sexual intercourse)
Although pain may occur at any time during the menstrual cycle, it is often worst during menstruation (known as dysmenorrhea).
The mechanisms involved in endometriosis mediated pain are poorly understood. It is thought that the adhesions/fibrotic tissue which form in the peritoneum distort normal pelvic anatomy, resulting in the sensation of pain. In addition, endometrial cells release factors which increase the neuronal innervation of the pelvic peritoneum, and these new nerve fibres are responsible for mediating pain. Further, many cells of the immune system migrate into endometriotic lesions where they cause inflammation and release molecules which can stimulate these nerve fibres, thereby causing pain.
ii) Infertility. The link between endometriosis and infertility is well known; endometriosis is present in up to 40% of women suffering from infertility whilst up to 50% of women with endometriosis are infertile. Despite it being well known that endometriosis causes infertility, precisely how it does so is unclear. Studies have reported findings in support of a diverse range of mechanisms which act at almost every step on the road to conception, including: defective ovum (egg) development and ovulation, hindrance of sperm function, molecular changes in the normal endometrium of the uterus which hinder implantation of the fertilised ovum (perhaps via progesterone resistance) and a reduction in embryo quality. It is also worth noting that studies have shown that endometriosis not only reduces fertility by normal conception, but also reduces the success of IVF treatment.