The distribution of pain is variable but most often is bilateral. Local symptoms can arise from rectal, ureteral, and bladder involvement, and lower back pain can occur. Some women with extensive disease have no pain, whereas others with only minimal to mild disease may experience severe pelvic pain. All endometriosis lesion types are associated with pelvic pain, including minimal to mild endometriosis (167). Endometriomas are not associated with dysmenorrheal severity, and dysmenorrhea is less frequent in women with only ovarian endometriomas compared with other locations (168,169). Endometriomas can be considered a marker for greater severity of deeply infiltrative lesions (170). Deeply infiltrative lesions are consistently associated with pelvic pain, gastrointestinal symptoms, and painful defecation (171). The role of adhesions in pain and endometriosis is poorly understood (172).
Many studies failed to detect a correlation between the degree of pelvic pain and the severity of endometriosis (11,169,173). Some studies reported a positive correlation between endometriosis stage and endometriosis-related dysmenorrhea or chronic pelvic pain (174,175). In one study, a significant but weak correlation was observed between endometriosis stage and severity of dysmenorrhea and nonmenstrual pain, whereas a strong association was found between posterior cul-de-sac lesions and dyspareunia (176).
Possible mechanisms causing pain in patients with endometriosis include local peritoneal inﬂammation, deep infiltration with tissue damage, adhesion formation, fibrotic thickening, and collection of shed menstrual blood in endometriotic implants, resulting in painful traction with the physiologic movement of tissues (177,178). The character of pelvic pain is related to the anatomic location of deeply infiltrating endometriotic lesions (171). Severe pelvic pain and dyspareunia may be associated with deep infiltrating subperitoneal endometriosis (6,177,179). In rectovaginal endometriotic nodules, a close histologic relationship was observed between nerves and endometriotic foci and between nerves and the fibrotic component of the nodule (180). Increasing evidence suggests a close relationship between the density of innervation of endometriotic lesions and pain symptoms (176).
Subfertility Many arguments support the hypothesis that there is a causal relationship between the presence of endometriosis and subfertility (181). The following factors have been reported: 1.
Increased prevalence of endometriosis in subfertile women (33%) when compared to women of proven fertility (4%), a reduced monthly fecundity rate (MFR) in baboons with mild to severe (spontaneous or induced) endometriosis when compared to those with minimal endometriosis or a normal pelvis.
2.
Trend toward a reduced monthly fecundity rate in infertile women with minimal to mild endometriosis when compared to women with unexplained infertility.
3.
Endometriotic ovarian cysts that negatively affect the rate of spontaneous ovulation (182).
4.
Dose–effect relationship: a negative correlation between the r-AFS stage of endometriosis and the monthly fecundity rate and cumulative pregnancy rate (181,183).
5.
Reduced monthly fecundity rate and cumulative pregnancy rate after donor sperm insemination in women with minimal to mild endometriosis when compared to those with a normal pelvis.
6.
Reduced monthly fecundity rate after husband sperm insemination in women with minimal to mild endometriosis when compared to those with a normal pelvis.
7.
Reduced implantation rate per embryo after in vitro fertilization (IVF) in women with endometriosis when compared to women with tubal factor infertility (181,184).
8.