Endometriosis is a disease in whichtissue similar to thelining of the uterus grows elsewhere in the body.[9] It occurs in humans and a limited number of other mammals that have a menstruation cycle, notably primates.[10] The tissue most often grows on or around theovaries andfallopian tubes, on the outside surface of the uterus, or thetissues surrounding the uterus and the ovaries.[3] It can also grow on other organs in the pelvic region like thebowels,stomach orbladder.[11] Rarely, it can also occur in other parts of the body.[3]
Symptoms can be very different from person to person, varying in range and intensity. About 25% of individuals have no symptoms,[1] while for some it can be a debilitating disease.[12] Common symptoms includepelvic pain,heavy andpainful periods, pain with bowel movements,painful urination,pain during sexual intercourse, andinfertility.[1][13] Nearly half of those affected havechronic pelvic pain, while 70% feel pain duringmenstruation.[1] Up to half of affected individuals are infertile.[1] Besides physical symptoms, endometriosis can affect a person's mental health and social life.[14]
Diagnosis is usually based on symptoms andmedical imaging;[3] however, a definitive diagnosis is made throughlaparoscopy (keyhole surgery).[3] Other causes of similar symptoms includepelvic inflammatory disease,irritable bowel syndrome,interstitial cystitis, andfibromyalgia.[1] Endometriosis is often misdiagnosed and many patients report being incorrectly told their symptoms are trivial or normal.[14] Patients with endometriosis see an average of seven physicians before receiving a correct diagnosis.[15]
Worldwide, around 10% of the female population of reproductive age (190 million women) are affected by endometriosis.[5] Asian women are more likely thanWhite women to be diagnosed with endometriosis.[16][17] The exact cause of endometriosis is not known. Possible causes include problems with menstrual period flow, genetic factors, hormones, and problems with the immune system.[3]
While there is no cure for endometriosis, several treatments may improve symptoms.[1] This includespain medication, hormonal treatments or surgery. The recommended pain medication is usually anon-steroidal anti-inflammatory drug (NSAID), such asnaproxen. Taking thebirth control pill continuously or using ahormonal IUD (coil) is another first-line treatment. Other types of hormonal treatment can be tried if the pill or IUD are not effective.[18] Surgical removal of endometriosis may be used to treat those whose symptoms are not manageable with other treatments, or to treat infertility.[19]
Endoscopic image of a ruptured endometrioma (chocolate cyst) in left ovary
Endometriosis can be subdivided into four categories:[20]
Superficial peritoneal endometriosis
Small spots of endometriosis grow on the surface layer that covers the organs inside the abdomen or pelvis (theperitoneum)
Deep infiltrating endometriosis
Lesions grow into the tissue beneath the lining of the pelvis or into the muscle layers of pelvic organs like the bowel, bladder, or ureter
Endometriomas (ovarian)
Cysts that grow in the ovaries
Extrapelvic endometriosis
Lesions outside of the pelvic regions, such as in the lungs ordiaphragm
Health care providers may call areas of endometriosis by different names, such as implants, lesions, or nodules. Larger lesions may be seen within the ovaries asendometriomas or "chocolate cysts"; "chocolate" because they contain a thick brownish fluid, mostly old blood.[21]
Endometriosis most commonly affects theovaries, thefallopian tubes between the ovaries and the womb, the outer surface of thewomb and the tissues that hold the womb in place. Less common pelvic sites are therectum,bladder,bowel,vulva,vagina andcervix[19] Deep infiltrating endometriosis occurs when endometriosis grows more than 5 mm beneath the peritoneal surface.[22] It can infiltrate the muscles around organs.[20] The prevalence of deep infiltrating endometriosis is estimated to be 1–2% in women of reproductive age.[22] Deep endometriosis often looks like nodules, and can includefibrosis andadhesions.[20]
Rarely, endometriosis appears in outside of the pelvis, such as the lungs, brain, andskin.[19] Diaphragmatic endometriosis is rare, almost always on the right hemidiaphragm, and may cause the cyclic pain of the right shoulder or neck during a menstrual period.[23] Scar endometriosis can rarely form on the abdominal wall as a complication ofsurgery, most often following aceasarean section or other pelvic surgery.[24]
Pain and infertility are common symptoms, although 20–25% of affected women are asymptomatic.[1] The presence of pain symptoms is associated with the type of endometrial lesions, as 50% of women with typical (peritoneal) lesions, 10% of women with cystic ovarian lesions, and 5% of women with deep endometriosis do not have pain.[25]
A major symptom of endometriosis is recurring pelvic pain. The pain can range from mild to severe cramping or stabbing pain that occurs on both sides of thepelvis, in the lower back and rectal area, and even down the legs. The amount of pain a person feels correlates weakly with the extent or stage (1 through 4) of endometriosis, with some individuals having little or no pain despite having extensive endometriosis or endometriosis with scarring, while others may have severe pain even though they have only a few small areas of endometriosis.[26] The most severe pain is typically associated with menstruation. Pain can also start a week before a menstrual period, during, and even a week after a menstrual period, or it can be constant. The pain can be debilitating and result in emotional stress.[27] Symptoms of endometriosis-related pain may include:
Dysmenorrhea (64%)[28] – painful, sometimes disabling cramps during the menstrual period; pain may get worse over time (progressive pain), also lower back pains linked to the pelvis
Chronic pelvic pain – typically accompanied by lower back pain or abdominal pain
Compared with patients with superficial endometriosis, those with deep disease appear to be more likely to report shooting rectal pain and a sense of their insides being pulled down.[31] Individual pain areas and intensity appear to be unrelated to the surgical diagnosis, and the area of pain is unrelated to the area of endometriosis.[31]
Thoracic endometriosis occurs when endometrium-like tissue implants in thelungs orpleura around the lungs. When it occurs in the lungs, common signs and symptoms areblood discharge from the lungs during menstruation and nodules which become bigger during menstruation. When it is found in the pleura, symptoms may be acollapsed lung during or outside of menstruation andbleeding into the pleural space. Further symptoms are a cyclical cough and cyclical shoulder pain. Most often, the endometriosis is found in the right lung.[34]
Stress may be a contributing factor or a consequence of endometriosis.[35]
Sciatic endometriosis, also called catamenial or cyclical sciatica, is a rare form where endometriosis affects the sciatic nerve. Diagnosis is usually confirmed throughMRI orCT-myelography.[39]
A 20-year study involving 12,000 women with endometriosis found that individuals under 40 are three times more likely to develop heart problems compared to their healthy peers.[40]
Endometriosis increases the risk of developing ovarian and thyroid cancers compared to women without the condition, and slightly increases the risk of breast cancer.[41]
The mortality rates associated with endometriosis are low, with unadjusted and age-standardized death rates of 0.1 and 0.0 per 100,000, respectively.[7]
"Endometriosis is associated with an elevated risk of developing depression and anxiety disorders".[42] Studies suggest this is partially due to the pelvic pain experienced by endometriosis patients.
"It has been demonstrated that pelvic pain has significant negative effects on women's mental health and quality of life; in particular, women who suffer from pelvic pain report high levels of anxiety and depression, loss of working ability, limitations in social activities and a poor quality of life"[43]
Mental health concerns like depression and anxiety can also result due to poor diagnostic procedures related to cultural norms where women's concerns are devalued or ignored, especially by medical professionals.[44][45]
Inheritance is significant but not the sole risk factor for endometriosis. Studies attribute 50% of the risk to genetics, the other 50% to environmental factors.[46] Overall, 42 differentloci (regions on a chromosome) have been associated with endometriosis risk. The genes linked to endometriosis risk help control cancer-related processes, sex-hormone signals, womb development, molecules related to inflammation and adhesions, and the growth of new blood vessels.[47]
There is significant overlap between the genetic basis of endometriosis, other pain conditions and inflammationary conditions. For instance, endometriosis shares a genetic underpinning withmigraine and neck, shoulder andback pain. Among inflammatory conditions, it shares variants withasthma andosteoarthritis.[47]
Little is known about environmental risk factors.Night work andred meat consumption seems to raise risk, as does exposure to some classes of environmental pollutants. The most studied of these areendocrine disruptors—chemicals that interfere with hormones, such as estrogen.[49] They includedioxins,phthalates,bisphenol A andpolychlorinated biphenyl. Based on epidemiological and experimental data, it is possible exposure to some of them increases the risk of endometriosis.[49][50]
Endometriosis patients show a significantly increased risk of autoimmune, autoinflammatory, and mixed-pattern psoriatic diseases, with two studies in 2025 pointing to the connection. One of the studies suggested that the chances of receiving a diagnosis of at least one of the autoimmune conditions for those with endometriosis was around twice that of a control cohort. The linked conditions include rheumatoid arthritis, multiple sclerosis, coeliac disease, osteoarthritis, and psoriasis. This reinforces the view that there is a genetic correlation between endometriosis and osteoarthritis, rheumatoid arthritis, and multiple sclerosis (MS), and a potential causal link to rheumatoid arthritis. The work suggests a shared biological basis between endometriosis on one side, and autoimmune and autoinflammatory diseases, on the other. This suggests that certain autoimmunne treatment pathways could be repurposed to provided alternative therapy options for those with endometriosis.[51][52][53]
Endometriosis is aninflammatory disease dependent onestrogen. The lesions promote local inflammation and immune system dysregulation. They also trigger the formation ofadhesions (fibrous bands that form betweentissues andorgans) andfibrosis (excess connective tissue from healing). It is not well understood how endometriosis causes infertility and pain.[20]
The main theories for the formation of the endometrium-like tissue outside the womb are backward flow of menstrual blood,metastasis via thelymphatic or thecirculatory system and local transformation of peritoneal cells into endometrial-like cells (coelomic metaplasia).[16]
Duringmenstruation, some menstrual blood, tissue, and fluid can flow backward through the fallopian tubes into the pelvic area (theperitoneal cavity). This backward flow (called retrograde menstruation) is thought to be the main reason why endometriosis develops inside the pelvic cavity. However, this explanation alone is not enough, because almost all women have some backward flow of menstrual fluid, but only some of them develop endometriosis.[2]
Evidence supporting the theory comes from retrospective epidemiological studies and DNA analysis.[54][55] Furthermore, only animals with amenstrual cycle such asrhesus monkeys andbaboons develop endometriosis. In contrast, animals likerodents andnon-human primates with anestrous cycle in which the endometrium is reabsorbed rather than shed do not develop the disease.[54]
Endometriosis has been diagnosed in people who have never experienced menstruation including men, female fetuses, and prepubescent girls. One explanation for endometriosis in girls before puberty is coelomic metaplasia: the theory that certain cells in the peritoneum may undergometaplasia (transformation) into endometrium-like cells.Müllerian remnants, cells that normally disappear during male embryonic development, may explain rare cases of endometriosis in men.[56]Metastasis via thelymphatic or thecirculatory system may explain endometriosis outside of the pelvic region.[20]
Stem cells may play a role in the formation of endometriosis.[57] Stems cells in the basal layer of the endometrium play a role in renewing the tissue after menstruation. In women with endometriosis, more tissue is shed from this layer during menstruation, allowing more stem cells to flow back into the periteneum with retrograde menstruation, and form lesions.[58] Stem cells frombone marrow may drive the further growth of lesions, but also explain the establishment of endometriosis outside of the pelvic region.[59]
Most women with retrograde menstruation do not develop endometriosis, so other factors are needed to explain the formation.[59] For endometriosis to develop, as is done by some canceroustumors, its cells must evade the immune system, attach to a surface, and promote the formation of new blood vessels.[60] Endometriotic lesions differ in their biochemistry, hormonal response, immunology, and inflammatory response compared to the endometrium.[16]
Oestrogen is needed for the growth of endometriosis lesions. This is produced both by lesions locally and in other parts of the body.[16] Progesterone resistance in lesions make them less responsive to the hormone, and allows the lesions to grow outside of the womb.[61]
Immune dysfunction could be involved in the disease in various ways: it may lead to a decrease in clearance of endometrial cells outside the womb, a local inflammatory environment may make it more likely that the cells attach to a surface, and may reduce programmed cell death (apoptosis).[59]
Angiogenesis, the formation of new blood vessels, plays a key role in the maintenance of endometriotic lesions.[57] Gene expression around angiogenesis expressed in the endometrium of women with endometriosis are different from those without. In addition, cells in the periteneum of women with endometriosis release moregrowth factors that stimulate angiogenesis.[59]
There are multiple causes of pain. Endometriosis involves the formation of new blood vessels and nerves in a process known asneuroangiogenesis.[59] The inflammation andfibrosis around the lesions gives rise tonociceptive pain.[62] Neuropathic pain can arise from damage to nerves. In rare cases, endometriosis can infiltrate or compress nerves,[20] and damage to nerves might also occur due to surgery.[62] Estrogens can increase communication between immune cells and nerves in lesions, which may contribute to further pain.[59] Finally, there may besystemic (body-wide) inflammation, involving white blood cells. This can lead tonociplastic pain, which amplifies pain signals and reduces pain inhibition. Nociplastic pain also cause poor sleep, memory problems and fatigue.[20]
The infertility associated with endometriosis likely has multiple causes. Inflammation and hormonal dysfunction explain some instances. Theovarian reserve, the amount of viable egg cells in the ovaries, is typically lower in those with endometriosis. In particular, endometriomas may reduce ovarian reserve in affected ovaries.[59] There is contradictory evidence on whether endometriosis causes reduced ovulation. Anatomical distortions, for instance from adhesions, can explain further instances of infertility, and in severe cases, sperm or egg cells may be fully blocked. Pain during sex may lead couples to avoid it, leading to fewer opportunities for natural conception.[63]
A health history and a physical examination can lead the health care practitioner to suspect endometriosis. Symptoms in combination withultrasound orMRI imaging can lead to a presumed diagnosis of endometriosis. The gold standard for definite diagnosis is via surgery and a biopsy, but there is a shift away from requiring surgical confirmation before starting treatment to prevent delays.[20] Patients in the UK have an average delay in diagnosis of 8 years and in Norway of 6.7 years.[64] A third of women had consulted their GP six or more times before being diagnosed.[64]
Endometriosis can be classified into four different stages. The American Society of Reproductive Medicine's scale, revised in 1996, gives higher scores to deep, thick lesions or intrusions on the ovaries and dense, enveloping adhesions on the ovaries or fallopian tubes.[65]
As for deep infiltrating endometriosis, TVUS,TRUS, and MRI are the techniques of choice for non-invasive diagnosis with a high sensitivity and specificity.[66]
A trauma-informed framework is recommended for a physical examination, where the health practitioner validates pain and fosters trust. The examination focuses on assessing both general symptoms and those linked to deep endometriosis or endometriosis outside the pelvis. Risk factors are also reviewed. The physical examination can include an abdominal exam, a single digit exam of the vagina and pelvic floor, a bimanual exam and examination with aspeculum.[20]
Vaginal ultrasound can be used to diagnose endometriosis or to localize an endometrioma before surgery.[67] This can be used to identify the spread of disease in individuals with well-established clinical suspicion of endometriosis.[67] Vaginal ultrasound is inexpensive, easily accessible, has no contraindications, and requires no preparation.[67] By extending the ultrasound assessment into the posterior and anterior pelvic compartments, a sonographer can evaluate structural mobility and look for deep infiltrating endometriotic nodules.[68] Better sonographic detection of deep infiltrating endometriosis could reduce the number of diagnostic laparoscopies, as well as guide disease management and enhance patient quality of life.[68]
Ultrasounds cannot be used to exclude a diagnosis of endometriosis.[69] If a transvaginal ultrasound is not suitable or declined, an alternative is an ultrasound via the lower abdomen.[70]
Trichromatic color MRI of ovarian cysts. The bottom right cyst is endometriosis (a chocolate cyst).
MRI is another means of detecting lesions in a non-invasive manner.[71] MRI is not widely used due to its cost and limited availability.[71] It can reliably detect endometriomas and deep infiltrating endemetriosis. It is sometimes used for planning surgery, for instance if an ultrasound is unclear, or for diagnosis if a transvaginal ultrasound is not appropriate or is declined. The field of view is larger in an MRI compared to an ultrasound, which allows a larger part of the bowel to be assessed.[72]
Laparoscopic image of endometriotic lesions at the peritoneum of the pelvic wall
Laparoscopy (keyhole surgery) is a surgical procedure where a camera is used to look inside the abdominal cavity. Laparoscopy with a biopsy is the most accurate way to diagnose endometriosis.[20] It can be used when endometriosis is suspected, but not visible via medical imaging.[59] An alternative after negative imaging is to try out treatment and give a presumed diagnosis if that improves symptoms ('empirical treatment').[73]
Surgery for diagnosis also allows for surgical treatment of endometriosis at the same time.[74] In nearly 40% of cases, no cause for pelvic pain is discovered during laparoscopy.[59]
The lesions of superficial endometriosis often appear dark blue or black. In the earlier stages of disease, they may be white, red or yellow-brown. Ovarian cysts are typically dark brown.Adhesions are made up of fibrous scar tissue. Deep endometriosis looks like multiple distinct nodules.[59]
A biopsy may be negative even when endometriosis is present, particularly in younger women. As such, it cannot be used to exclude a diagnosis of endometriosis.[59] For confirmation, biopsy samples should show at least two of the following features:[75]
There are three staging or classification systems commonly used. Fertility is assessed with the Endometriosis Fertility Index (EFI).[59] Endometriosis can be classified as stage I–IV by the revisedAmerican Society of Reproductive Medicine (rASRM) staging system. The stages range from minimal (stage I) to severe (stage IV).[76] The scale uses a point system that assesses lesions and adhesions during surgery. The ENZIAN system focuses more on deep endometriosis compared to rASRM. The rASRM and ENZIAN systems correlate poorly with how much pain women have.[59]
TheAmerican Association of Gynecologic Laparoscopists (AAGL) endometriosis staging system, introduced in 2021, correlates well with complexity of surgery, and captures pain better than rASRM. Like rASRM, it divides endometriosis into four stages.[77]
The US Office of Women's Health states that the chance of developing endometriosis can be reduced by lowering the levels of the hormoneestrogen in the body.[19] According to theWorld Health Organization, there is no known way to prevent endometriosis.[5]
While there is no cure for endometriosis, there are treatments for pain and endometriosis-associated infertility. Pain can be treated with hormones, painkillers, or, in severe cases, surgery.[78] The goal of management is to provide pain relief, to restrict the progression of the process, and to restore or preserve fertility where needed.[16]
Treatment with medication for pain management can be initiated based on the presence of symptoms, examination, and ultrasound findings that rule out other potential causes.[79] The UKNational Institute for Health and Care Excellence recommends starting initial medication for those with suspected endometriosis, at the same time as referral for investigations such as ultrasound.[80]
In general, the diagnosis of endometriosis is confirmed during surgery, at which time removal can be performed. Further steps depend on circumstances: someone without infertility can manage symptoms with pain medication and hormonal medication that suppresses the natural cycle, while an infertile individual may be treated expectantly after surgery, with fertility medication, or within vitro fertilisation (IVF).
The hormonal coil (Mirena) is one of the treatment options for endometriosis
Progestin-only hormonal suppression (progestogen) is another first-line therapy. It come in different forms and includes thehormonal coil (intrauterine device), the oraldienogest, an injection ofmedroxyprogesterone acetate every three months or an implant under the skin.[20] Dienogest, which may better than injections,[81] is not available on its own in the US.[20] Oral progestins likely reduce overall pain and period pain compared to placebo, and may also help with pelvic pain. It is unclear how well they work compared to other hormonal therapies.[81]
Hormonal birth control pills: combined estrogren-progestin birth control pills are a first-line treatment. The recommendation is to use the pills continuously to stop periods.[20] A 2018 Cochrane systematic review found that there is insufficient evidence to make a judgement on the effectiveness of the combined oral contraceptive pill compared with placebo or other medical treatment for managing pain associated with endometriosis partly because of lack of included studies for data analysis (only two for COCP vs placebo).[82]
Aromatase inhibitors are third-line treatments and block estrogen production throughout the body. Examples of aromatase inhibitors includeanastrozole andletrozole. Common side effects are hot flashes, night sweats and functional cysts.[20][84] In premenopausal women, these should be taken with other hormones (such as the combined pill) to prevent ovarian stimulation and to prevent menopause symptoms. They can be a option for post-menopausal women who still have endometriosis symptoms, as their action is not limited to suppressing estrogen from ovaries. Evidence is limited.[20]
NSAIDs likenaproxen are anti-inflammatory medications commonly used for endometriosis pain.[86] Only a single small study has been done on it, so it has unclear effectiveness. NSAIDs can have side effects, predominantly gastrointestinal, but they are generally safe to try.[87]
Laparoscopy of the uterus and fallopian tubes. The abdomen is filled with gas so that the surgeon can see better and have space for instruments.
Clinical guidelines recommend surgery when medical treatment does not work sufficiently, has unacceptable side effects or iscontraindicated. Large endometriomas can only effectively be treated with surgery. Surgery is also recommended when deep endometriosis causes problems in the bowels orurinary tract, such as obstruction. It is unclear what the effect of surgery is for pain relief in cases of superficial periteneal endometriosis.[20]
Laparoscopy (keyhole surgery) is the standard surgical approach. Treatment consists of the removal of endometriosis and the restoration of pelvic anatomy via the division ofadhesions.[88] The removal takes place viaexcision (cutting out) orelectrosurgery (coagulation or ablation/vaporisation).[89][90] With laparoscopic surgery, small instruments are inserted through incisions to remove the endometriosis tissue and adhesions. After surgery, people can usually return home the same day.[91]
Two literature reviews have compared excision to ablation. A 2017 literature review found that excision improved some outcomes over ablation for endometriosis in general. A 2021 literature review on minimal to mild endometriosis found no difference. For deep endometriosis, excision is the standard therapy, as ablation does not allow the surgeon to see if all endometriosis is removed.[92] In the United States, some specialists trained in excision for endometriosis do not accept health insurance because insurance companies do not reimburse the higher costs of this procedure over ablation.[93]
Endometriomas are usually excised (removed completely). Compared to drainage and coagulation of the cyst, excision makes it less likely the cysts and pain symptoms come back. However, excision may damage fertility, as it can affect theovarian reserve, the amount ofegg cells that can be fertilised.[59][20]
For deep endometriosis, surgery improves quality of life and pain symptoms.[94] However, the procedure can be complicated, especially if the lesions are in or near the bowel,ureter of the urinary system or the chest, and requires a interdisciplinary surgical team in those cases. For instance, forrectovaginal endometriosis, 7% of surgeries had complications.[20] Sometimes, a part of the bowel or bladder is removed.[95][96]
For women who still have significant pain after hormonal treatment and other surgery, and do not want to become pregnant, ahysterectomy (removal of the womb) can be offered. This is done in combination with removal of endometriosis lesions. Removal of the womb may be beneficial if the uterus itself is affected byadenomyosis. When the ovaries are removed too, women will experience early menopause and may needhormone replacement therapy. Removal of the ovaries comes with cardiovascular, metabolic and mental health risks.[97][20]
In an analysis with a medium follow-up of 24 months pain after surgery recurred in about 16% of women.[20] Endometriosis recurrence following surgery is estimated as 21.5% at 2 years and 40–50% at 5 years. Hormonal therapy before surgery has little effect on recurrence, but treatment afterwards reduces the risk.[59] At a median follow-up of 18 months, endometriosis recurred in 26% of women without postoperative hormonal suppression, compared with 10% of women who received it.[20] The risk of recurrence is higher in younger women and in those with a less aggressive surgery.[90]
A 2021 meta-analysis found that GnRH analogs and combined hormonal contraceptives were the best treatment for reducing dyspareunia and menstrual and non-menstrual pelvic pain.[98] A 2018 Swedish systematic review found several studies but a general lack of scientific evidence for most treatments.[67] There was only one study of sufficient quality and relevance comparing the effect of surgery and non-surgery.[99] Cohort studies indicate that surgery is effective in decreasing pain.[99] Most complications occurred in cases of low intestinal anastomosis, while the risk of fistula occurred in cases of combined abdominal or vaginal surgery, and urinary tract problems were common in intestinal surgery.[99] The evidence was found to be insufficient regarding surgical intervention.[99]
The advantages of physical therapy techniques are decreased cost, absence of major side effects, it does not interfere with fertility, and a near-universal increase in sexual function.[100] Disadvantages are that there are no large or long-term studies of its use for treating pain or infertility related to endometriosis.[100]
Assistive reproductive technology like IVF can help with fertility in endometriosis.
Infertility can be treated withassistive reproductive technology (ART) such asin vitro fertilization (IVF) or surgery.[101] IVF procedures are effective in improving fertility in many individuals with endometriosis. IVF is increasingly recommended over surgery for older women or for those where there might be multiple reasons why they struggle to conceive.[102] It does not increase recurrence of endometriosis.[103] The Endometriosis Fertility Index can help guide decisions on treatment of infertility.[104] Surgery is typically not recommended before starting ART.[105]
In terms of surgery, endometriomas can be cut out (a cystectomy), or drained and destroyed (ablation). The ablation technique may be better able to preserve the number of remaining viable eggs (theovarian reserve), compared to cutting out the endometrioma.[106] On the other hand, cutting out the endometrioma may help more with pain.[102] Surgery likely also helps with infertility in the case of superficial peritoneal endometriosis.[20] Receiving hormonal suppression therapy after surgery might be help with endometriosis recurrence and pregnancy.[107] but evidence for pregancy outcomes is mixed[108] and the both NICE and theEuropean Society of Human Reproduction and Embryology recommend against hormonal suppression to improve fertility.[108][109]
Determining how many people have endometriosis is challenging because a definitive diagnosis requires surgical visualization through laparoscopic surgery.[110] Criteria that are commonly used to establish a diagnosis include pelvic pain, infertility, surgical assessment, and in some cases, magnetic resonance imaging. An ultrasound can identify large clumps of tissue as potential endometriosis lesions and ovarian cysts, but it is not effective for all patients, especially in cases with smaller, superficial lesions.[111]
Ethnic differences in endometriosis have been observed. The condition is more common in women ofEast Asian andSoutheast Asian descent than in White women.[16]
Estimates of prevalance vary. One source estimates that between 6 and 10% of the general female population have endometriosis.[1] Another estimates that between 2 and 11% of asymptomatic women are affected.[16] In addition, 11% of women in a general population have undiagnosed endometriosis that can be seen on magnetic resonance imaging (MRI).[112][110] Globally, around 176 million girls and women are effected, with roughly 22 million having a diagnosis confirmed surgically as of 2021.[113]
Endometriosis is most common in those in their thirties and forties; however, it can begin in girls as early as eight years old.[3][4] It results in few deaths with unadjusted and age-standardized death rates of 0.1 and 0.0 per 100,000.[7] Endometriosis was first determined to be a separate condition in the 1920s.[114] Before that time, endometriosis andadenomyosis were considered together.[114]
It chiefly affects adults from premenarche to postmenopause, regardless of race or ethnicity or whether or not they have had children, and is estimated to affect over 190 million women in their reproductive years.[115] Incidences of endometriosis have occurred in postmenopausal individuals,[116] and in less common cases, individuals may have had endometriosis symptoms before they even reach menarche.[117][118]
The rate of recurrence of endometriosis is estimated to be 40-50% for adults over five years.[119] The rate of recurrence has been shown to increase with time from surgery and is not associated with the stage of the disease, initial site, surgical method used, or post-surgical treatment.[119]
Endometriosis was first discovered microscopically byKarl von Rokitansky in 1860,[120] although the earliest antecedents may have stemmed from concepts published almost 4,000 years ago.[121] TheHippocratic Corpus outlines symptoms similar to endometriosis, including uterine ulcers, adhesions, and infertility.[121] Historically, women with these symptoms were treated withleeches,straitjackets,bloodletting, chemicaldouches,genital mutilation, pregnancy (as a form of treatment), hanging upside down, surgical intervention, and even killing due to suspicion ofdemonic possession.[121] Hippocratic doctors recognized and treated chronic pelvic pain as a true organic disorder 2,500 years ago, but during the Middle Ages, there was a shift into believing that women with pelvic pain were mad, immoral, imagining the pain, or simply misbehaving.[121] The symptoms of inexplicable chronic pelvic pain were often attributed to imagined madness, female weakness, promiscuity, orhysteria.[121] The historical diagnosis of hysteria, which was thought to be a psychological disease, may have indeed been endometriosis in many cases.[121] The idea that chronic pelvic pain was related to mental illness influenced modern attitudes regarding individuals with endometriosis, leading to delays in correct diagnosis and indifference to the patients' true pain throughout the 20th and into the 21st century.[121]
Hippocratic doctors believed that delaying childbearing could trigger diseases of the uterus, which caused endometriosis-like symptoms. Women with dysmenorrhea were encouraged to marry and have children at a young age.[121] The fact that Hippocratics were recommending changes in marriage practices due to an endometriosis-like illness implies that this disease was likely common.[121]
The theory of retrograde menstruation as a cause of endometriosis was first proposed byJohn A. Sampson.[122][123]
The early treatment of endometriosis wassurgical and includedoophorectomy (removal of the ovaries) and hysterectomy (removal of the uterus).[124] In the 1940s, the only available hormonal therapies for endometriosis were high-dosetestosterone andhigh-dose estrogen therapy.[125] High-dose estrogen therapy withdiethylstilbestrol for endometriosis was first reported by Karnaky in 1948 and was the mainpharmacological treatment for the condition in the early 1950s.[126][127][128]Pseudopregnancy (high-dose estrogen–progestogen therapy) for endometriosis was first described by Kistner in the late 1950s.[126][127] Pseudopregnancy, as well as progestogen monotherapy, dominated the treatment of endometriosis in the 1960s and 1970s.[128] These agents, although efficacious, were associated with intolerable side effects.Danazol was first described for endometriosis in 1971 and became the main therapy in the 1970s and 1980s.[126][127][128] In the 1980s,GnRH agonists gained prominence for the treatment of endometriosis and by the 1990s had become the most widely used therapy.[127][128] Oral GnRH antagonists such aselagolix were introduced for the treatment of endometriosis in 2018.[129]
The economic burden of endometriosis is widespread and multifaceted.[172] Endometriosis is a chronic disease that has direct and indirect costs, which include loss of work days, direct costs of treatment, symptom management, and treatment of other associated conditions such as depression or chronic pain.[172] One factor that seems to be associated with especially high costs is the delay between the onset of symptoms and diagnosis.
Costs vary greatly between countries.[173] Two factors that contribute to the economic burden include healthcare costs and losses in productivity. A Swedish study of 400 endometriosis patients found "Absence from work was reported by 32% of the women, while 36% reported reduced time at work because of endometriosis".[174] An additional cross sectional study with Puerto Rican women, "found that endometriosis-related and coexisting symptoms disrupted all aspects of women's daily lives, including physical limitations that affected doing household chores and paid employment. The majority of women (85%) experienced a decrease in the quality of their work; 20% reported being unable to work because of pain, and over two-thirds of the sample continued to work despite their pain."[175] A study published in the UK in 2025 found that after women received a diagnosis of endometriosis in an English NHS hospital their earnings were on average £56 per month less in the four to five years after diagnosis than they were in the two years before. There was also a reduction in the proportion of women in employment.[176]
There are many barriers that those affected face in receiving a diagnosis and treatment for endometriosis. Some of these include outdated standards for laparoscopic evaluation, stigma about discussing menstruation and sex, lack of understanding of the disease, primary-care physicians' lack of knowledge, and assumptions about typical menstrual pain.[177] On average, those later diagnosed with endometriosis waited 2.3 years after the onset of symptoms before seeking treatment, and nearly three-quarters of women receive a misdiagnosis before endometriosis.[178] Self-help groups say practitioners delay making the diagnosis, often because they do not consider it a possibility. There is a typical delay of 7–12 years from symptom onset in affected individuals to professional diagnosis.[179] There is a general lack of knowledge about endometriosis among primary care physicians. Half of the general health care providers surveyed in a 2013 study could not name three symptoms of endometriosis.[180] Healthcare providers are also likely to dismiss described symptoms as normal menstruation.[181] Younger patients may also feel uncomfortable discussing symptoms with a physician. Patients are made to categorise their pain using thepain scale. However, this is not representative of endometriosis specific pain levels which impacts diagnosis and treatment.[182]
Race and ethnicity may impact how endometriosis affects one's life. Endometriosis is less thoroughly studied among Black people, and the research that has been done is outdated.[183][184]Cultural differences among ethnic groups also contribute to attitudes toward and treatment of endometriosis, especially in Hispanic or Latino communities. A study done in Puerto Rico in 2020 found that health care and interactions with friends and family related to discussing endometriosis were affected by stigma.[185] The most common finding was a referral to those expressing pain related to endometriosis as "changuería" or "changas", terms used in Puerto Rico to describe pointless whining and complaining, often directed at children.[185]
The existing stigma surrounding women's health, specifically endometriosis, can lead to patients not seeking diagnoses, lower quality of healthcare, increased barriers to care and treatment, and negative reception from members of society.[186] Additionally,menstrual stigma significantly contributes to the broader issue of endometriosis stigma, creating an interconnected challenge that extends beyond reproductive health.[187][188]Widespreadawareness campaigns, developments, and implementations aimed at multilevel anti-stigma organizational and structural changes, as well as more qualitative studies of the endometriosis stigma, help to overcome the harm of the phenomenon.[186]
A priority area of research is the search for endometriosisbiomarkers, which can help with earlier diagnoses.[189] Studies have examined potential biomarkers such asmicroRNAs,glycoproteins, and immune markers in blood, menstrual and urine samples, but none have shown the high accurarcy needed for clinical use yet.CA-125, a tumor marker, has been studied extensively. It is elevated in endometriosis, but also in many other conditions, and cannot be used on its own. MicroRNAs might be most promosing, but the high diversity in expression makes them a challenging target.[190]
Hormonal treatment is the standard way to manage endometriosis with drugs. These treatment can have undesirable side effects, and there is a search for alternative medications.Pentoxifylline, animmunomodulating agent, has been theorized to improve pain as well as improve pregnancy rates in individuals with endometriosis. There is not enough evidence to support the effectiveness or safety of either of these uses.[191]
Preliminary research on mouse models showed that monoclonal antibodies, as well as inhibitors ofMyD88 downstream signaling pathway, can reduce lesion volume. Thanks to that, clinical trials are being done on using a monoclonal antibody directed against IL-33 and usinganakinra, an IL-1 receptor antagonist.[192]
^Sarofim M, Attwell-Heap A, Trautman J, Kwok A, Still A (November 2019). "Unusual case of acute large bowel obstruction: endometriosis mimicking sigmoid malignancy".ANZ Journal of Surgery.89 (11):E542 –E543.doi:10.1111/ans.14869.PMID30277298.S2CID52902719.
^abBerlac JF, Hartwell D, Skovlund CW, Langhoff-Roos J, Lidegaard Ø (June 2017). "Endometriosis increases the risk of obstetrical and neonatal complications".Acta Obstetricia et Gynecologica Scandinavica.96 (6):751–760.doi:10.1111/aogs.13111.PMID28181672.
^Gandhi J, Wilson AL, Liang R, Weissbart SJ, Khan SA (11 November 2020). "Sciatic endometriosis: A narrative review of an unusual neurogynecologic condition".Journal of Endometriosis and Pelvic Pain Disorders.13 (1). SAGE Publications:3–9.doi:10.1177/2284026520970813.ISSN2284-0265.S2CID228834273.
^Low WY, Edelmann RJ, Sutton C (February 1993). "A psychological profile of endometriosis patients in comparison to patients with pelvic pain of other origins".Journal of Psychosomatic Research.37 (2):111–116.doi:10.1016/0022-3999(93)90077-S.PMID8463987.
^Culley L, Law C, Hudson N, Denny E, Mitchell H, Baumgarten M, et al. (1 November 2013). "The social and psychological impact of endometriosis on women's lives: a critical narrative review". Human Reproduction Update. 19 (6): 625–39. doi:10.1093/humupd/dmt027. hdl:2086/8845. PMID 23884896.
^Nnoaham KE, Hummelshoj L, Webster P, d'Hooghe T, de Cicco Nardone F, de Cicco Nardone C, et al. (August 2011). "Impact of endometriosis on quality of life and work productivity: a multicenter study across ten countries". Fertility and Sterility. 96 (2): 366–373.e8. doi:10.1016/j.fertnstert.2011.05.090. PMC 3679489. PMID 21718982.
^Han L, Garcia R, Busca A, Parra-Herran C (November 2023). Turashvili G, Skala SL (eds.)."Endometriosis".Pathology Outlines.Archived from the original on 7 August 2020. Retrieved18 March 2020.
^abChen I, Kives S, Zakhari A, Nguyen DB, Goldberg HR, Choudhry AJ, et al. (2025). Cochrane Central Editorial Service (ed.). "Progestagens for pain symptoms associated with endometriosis".Cochrane Database of Systematic Reviews.2025 (10): CD002122.doi:10.1002/14651858.CD002122.pub3.PMC 12509269.PMID41065045.{{cite journal}}: CS1 maint: article number as page number (link)
^abVeth VB, van de Kar MM, Duffy JM, van Wely M, Mijatovic V, Maas JW (2023). Cochrane Gynaecology and Fertility Group (ed.). "Gonadotropin-releasing hormone analogues for endometriosis".Cochrane Database of Systematic Reviews.2023 (6).doi:10.1002/14651858.CD014788.pub2.
^Garzon S, Laganà AS, Barra F, Casarin J, Cromi A, Raffaelli R, et al. (December 2020). "Aromatase inhibitors for the treatment of endometriosis: a systematic review about efficacy, safety and early clinical development".Expert Opinion on Investigational Drugs.29 (12). Informa UK Limited:1377–1388.doi:10.1080/13543784.2020.1842356.PMID33096011.S2CID225058751.
^Samy A, Taher A, Sileem SA, Abdelhakim AM, Fathi M, Haggag H, et al. (January 2021). "Medical therapy options for endometriosis-related pain, which is better? A systematic review and network meta-analysis of randomized controlled trials".Journal of Gynecology Obstetrics and Human Reproduction.50 (1) 101798. Elsevier BV.doi:10.1016/j.jogoh.2020.101798.PMID32479894.S2CID219173190.
^Batt RE, Mitwally MF (December 2003). "Endometriosis from thelarche to midteens: pathogenesis and prognosis, prevention and pedagogy".Journal of Pediatric and Adolescent Gynecology.16 (6):337–47.doi:10.1016/j.jpag.2003.09.008.PMID14642954.
^Barbieri RL (January 1992). "Hormonal therapy of endometriosis".Infertility and Reproductive Medicine Clinics of North America.3 (1):187–200.The hormonal therapy of endometriosis continues to evolve. In the 1940s and 1950s, high-dose testosterone and diethylstilbestrol regimens were the only hormonal agents available in the treatment of endometriosis. These agents, although efficacious, were associated with intolerable side effects. The current armamentarium of hormonal GnRH analogues, danazol, and synthetic progestins is efficacious and has fewer side effects.
^Barra F, Grandi G, Tantari M, Scala C, Facchinetti F, Ferrero S (April 2019). "A comprehensive review of hormonal and biological therapies for endometriosis: latest developments".Expert Opin Biol Ther.19 (4):343–360.doi:10.1080/14712598.2019.1581761.hdl:11380/1201437.PMID30763525.S2CID73455399.
^Koltermann KC, Dornquast C, Ebert AD, Reinhold T (2017). "Economic Burden of Endometriosis: A Systematic Review".Ann Reprod Med Treat.2 (2m): 1015.S2CID32839234.
^As-Sanie S, Black R, Giudice LC, Gray Valbrun T, Gupta J, Jones B, et al. (August 2019). "Assessing research gaps and unmet needs in endometriosis".American Journal of Obstetrics and Gynecology.221 (2):86–94.doi:10.1016/j.ajog.2019.02.033.PMID30790565.S2CID73480251.
^Quibel A, Puscasiu L, Marpeau L, Roman H (June 2013). "[General practitioners and the challenge of endometriosis screening and care: results of a survey]".Gynécologie, Obstétrique & Fertilité.41 (6):372–80.doi:10.1016/j.gyobfe.2012.02.024.PMID22521982.
^Agostinis C, Battista N, Costanzo M (2021). "The Search for Biomarkers in Endometriosis: a Long and Windy Road".Reproductive Sciences.28 (10):2751–2766.doi:10.1007/s43032-021-00668-2.
