Endometriosis can and does occur in people who have no uterus, whether the uterus was surgically removed or was never fully formed. The condition has even been documented in men. This reality upends the common assumption that endometriosis is simply “uterine lining growing in the wrong place,” because it can appear in bodies where that lining should not exist at all. The explanations for how this happens reveal that endometriosis is more biologically complex than most people realize, and they carry practical consequences for anyone managing the disease after a hysterectomy or living with a congenital uterine anomaly.
After a Hysterectomy, Endometriosis Can Come Back
The most common scenario for endometriosis without a uterus is recurrence after hysterectomy. Many people undergo hysterectomy specifically to treat severe endometriosis, and while it often helps, it does not guarantee a cure. A study tracking patients after hysterectomy for endometriosis found that whether the ovaries were left in place made a dramatic difference. Among those who kept their ovaries, about 62% experienced recurrent pain and roughly a third needed another surgery. Among those whose ovaries were also removed, about 10% had recurrent symptoms and fewer than 4% required reoperation.1PubMed. Incidence of symptom recurrence after hysterectomy for endometriosis Those numbers make it clear that removing the uterus alone does not address the root driver of the disease.
A key reason symptoms return is that microscopic endometriotic implants or deeply infiltrating lesions can be left behind during surgery. For years, surgeons assumed these remnants would simply shrivel once estrogen levels dropped. But it has never been definitively shown that endometriosis completely regresses in a low-estrogen environment, whether from surgical menopause or natural menopause.2PubMed Central. Recurrence of endometriosis after hysterectomy Recurrence tends to happen at the same location as the original disease, which strongly suggests that residual tissue is the culprit rather than brand-new disease forming from scratch.3PubMed Central. Intestinal endometriosis: Diagnostic ambiguities and surgical outcomes
Why Ovaries Matter More Than the Uterus
The six-fold higher risk of pain recurrence when ovaries are preserved tells a story about what really fuels endometriosis: estrogen.1PubMed. Incidence of symptom recurrence after hysterectomy for endometriosis Endometriotic implants behave like estrogen-responsive tissue. As long as ovaries keep producing estrogen, those implants can remain active or reactivate, regardless of whether a uterus is present. This is why the conversation around hysterectomy for endometriosis almost always involves a discussion about whether to remove the ovaries too.
Removing the ovaries forces surgical menopause, which brings its own problems: hot flashes, bone density loss, cardiovascular changes, and mood shifts, often in people far younger than the typical age of natural menopause. Hormone replacement therapy can ease those symptoms, but it introduces a dilemma. HRT after pelvic clearance for endometriosis carries a real risk of reactivating the disease.4PubMed Central. HRT in Women Undergoing Pelvic Clearance for Endometriosis—A Case Report and a National Survey One review put the rate of recurrent pelvic pain associated with HRT use after hysterectomy at about 3.5%.2PubMed Central. Recurrence of endometriosis after hysterectomy That figure may sound low, but for someone who already went through major surgery to escape debilitating pain, even a small risk of recurrence feels significant.
Endometriotic Tissue Can Make Its Own Estrogen
Here is the wrinkle that makes post-hysterectomy endometriosis especially stubborn: endometriotic implants do not always depend on the ovaries for their estrogen supply. Researchers have found that the enzyme aromatase, which converts other hormones into estrogen, is active in endometriotic tissue itself. One study detected aromatase in every endometriotic implant tested and in the uterine lining of patients with endometriosis, but not in tissue from disease-free women. In one case, the aromatase activity inside an abdominal wall endometriotic mass was four times higher than in the surrounding fat tissue.5PubMed. Aromatase expression in endometriosis Additional research has confirmed that aromatase expression is consistently elevated in endometriotic implants compared with normal tissue.6Journal of obstetrics and women’s diseases. Evaluation of aromatase expression in endometrioid heterotopias and endometria in patients with external genital endometriosis
This self-sustaining estrogen production explains why endometriosis can persist even after both the uterus and ovaries are gone and even without HRT. The implants essentially feed themselves. It also opens up a treatment avenue: aromatase inhibitors, drugs originally developed for breast cancer, can block this local estrogen production. In one reported case, a woman with persistent endometriosis pain after complete pelvic clearance found relief with the aromatase inhibitor letrozole, and she was able to take low-dose estrogen replacement for menopausal symptoms without reactivating her pain.7Obstetrics & Gynecology. Aromatase Inhibitors in the Treatment of Severe Endometriosis
Born Without a Uterus
Post-hysterectomy cases are one thing: the person once had a uterus, so the disease could have seeded itself before the surgery. More surprising are cases where the uterus never fully formed. Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome is a condition in which the uterus and upper vagina fail to develop, though the ovaries function normally. Several case reports describe confirmed endometriosis in these patients. In one case, laparoscopy revealed an endometrioma on the left ovary, and the biopsy confirmed cystic endometriosis, in a patient with only rudimentary uterine remnants.8PubMed Central. Endometriosis in a Patient with Mayer-Rokitansky-Küster-Hauser Syndrome A larger histological evaluation found endometriosis in nine MRKH patients, with endometrial remnants identifiable in several of them.9PubMed Central. Endometriosis in Patients with Mayer-Rokitansky-Küster-Hauser-Syndrome-Histological Evaluation of Uterus Remnants and Peritoneal Lesions and Comparison to Samples from Endometriosis Patients without Mullerian Anomaly
These cases initially seemed like a slam dunk for the theory that endometriosis can arise through metaplasia, meaning cells in the pelvis transform into endometrial-type tissue without ever having been shed from a uterus. But the picture is more complicated. A critical review of MRKH cases found that when biopsies were actually performed, endometriosis always appeared alongside uterine or endometrial remnants. The review argued that claims of endometriosis without any endometrial tissue were based on MRI imaging alone, which cannot rule out tiny remnants the way histology can.10Reproduction. Endometriosis in MRKH cases as a proof for the coelomic metaplasia hypothesis? In other words, these patients may not truly lack all endometrial tissue: small uterine remnants could be shedding just enough cells to seed the disease, even in a body classified as “without a uterus.”
This debate matters beyond academic curiosity. If endometriosis in MRKH patients always requires at least some endometrial tissue, then the classic explanation of retrograde menstruation (menstrual blood flowing backward through the fallopian tubes) still holds up as the dominant pathway. If it can arise independently through metaplasia, the disease is fundamentally more unpredictable.
Endometriosis in Men
The rarest and perhaps most striking demonstration that endometriosis does not require a uterus comes from case reports in men. These are exceedingly uncommon, but they have been documented well enough to be taken seriously. A review of male endometriosis cases found that the prevailing risk factor is prolonged exposure to estrogen therapy.11PubMed Central. Endometriosis in a Man as a Rare Source of Abdominal Pain: A Case Report and Review of the Literature One case involved a 69-year-old man who developed paratesticular endometriosis after nine years of hormonal therapy for prostate cancer, with the proposed mechanism being metaplastic transformation of tissue under sustained estrogen influence.12PubMed. Paratesticular endometriosis in a man with a prolonged hormonal therapy for prostatic carcinoma Another documented case was bladder endometriosis following long-term estrogen therapy for prostate cancer.13PubMed. Bladder endometriosis developed after long-term estrogen therapy for prostate cancer
Male cases are important not because many men are at risk, but because they force a reckoning with the idea that retrograde menstruation is the only way endometriosis starts. Men do not menstruate, do not have fallopian tubes, and do not have endometrium. If endometriotic tissue can form in a male pelvis under the right hormonal conditions, other pathways must exist.
How Endometriosis Forms Without Retrograde Menstruation
The classic theory, proposed by John Sampson in the 1920s, says menstrual blood flows backward through the fallopian tubes, depositing endometrial cells on pelvic surfaces where they implant and grow. That theory explains a lot of cases, but it cannot explain them all. Several alternative mechanisms have been proposed, and the evidence suggests more than one may operate at the same time.
Coelomic metaplasia is the idea that the cells lining the pelvic cavity can, under the right conditions, transform into endometrial-type tissue. Laboratory studies have shown this is at least biologically plausible. When ovarian surface cells were cultured with estrogen in an experimental model, they formed gland-like structures with the hallmarks of endometrial tissue, including specific protein markers and structural features visible under electron microscopy.14PubMed. Coelomic metaplasia theory of endometriosis: evidence from in vivo studies and an in vitro experimental model This pathway could explain cases in men and in MRKH patients, at least in theory.
Lymphatic and blood vessel spread is another proposed route. Endometrial cells have been found inside lymphatic vessels and lymph nodes, and a comprehensive review of the evidence concluded that lymphatic dissemination likely plays a real role in how endometriosis reaches unusual locations.15Biology of Reproduction. The Role of the Lymphatic System in Endometriosis: A Comprehensive Review of the Literature A case of umbilical endometriosis without any pelvic disease provided particularly suggestive evidence for this route: the presence of endometrial-type cells in lymphovascular channels, far from the pelvis, pointed to transport through the circulatory system rather than direct spread from the pelvic cavity.16PubMed Central. Diffuse endometritis in the setting of umbilical endometriosis: a case report
A third mechanism involves bone marrow-derived stem cells. In animal studies, stem cells from bone marrow were able to travel to and incorporate into ectopic endometrial tissue. Even in hysterectomized mice, these stem cells engrafted into endometriotic implants placed in the peritoneal cavity.17PubMed. Contribution of bone marrow-derived stem cells to endometrium and endometriosis If this happens in humans, it would mean the body’s own regenerative cells could contribute to endometriosis independently of the uterus. The stem cell theory is still early-stage, but it offers a potential explanation for why the disease can persist or reappear in seemingly impossible locations.
Endometriosis Far From the Pelvis
One of the strongest arguments that endometriosis is not just a uterine disease is where it can show up. While the pelvis is the most common location, endometriotic tissue has been found in the lungs, diaphragm, bowel wall, bladder, skin (especially surgical scars and the umbilicus), and even the brain. Thoracic endometriosis, in which implants form on the diaphragm or lung surfaces, can cause catamenial pneumothorax, a collapsed lung that recurs in sync with the menstrual cycle. One case report described a woman with endometriosis causing both bowel obstruction and catamenial pneumothorax at the same time.18PubMed Central. Thoracic endometriosis syndrome: case report and review of the literature
Critically for the “without a uterus” question, thoracic endometriosis has been documented to recur even after hysterectomy with bilateral removal of the ovaries.19PubMed Central. Catamenial pneumothorax caused by thoracic endometriosis If endometriotic implants in the chest can survive without ovaries or a uterus, the tissue’s ability to sustain itself through local estrogen production or other mechanisms becomes the most plausible explanation.
The Immune System’s Role
A normally functioning immune system should clear misplaced cells before they can establish themselves. One reason endometriosis takes hold may be that immune surveillance in the pelvic cavity is impaired. Research using single-cell analysis of peritoneal fluid from people with endometriosis has revealed immune cell dysfunction: reduced ability to engulf and destroy stray cells, decreased activity of natural killer cells, and elevated inflammatory and cell-attracting signals.20PubMed Central. Cell subtypes and immune dysfunction in peritoneal fluid of endometriosis revealed by single-cell RNA-sequencing In practical terms, the immune environment in the pelvis may be permissive: even small amounts of displaced tissue that would normally be cleared instead survive, implant, and grow.
This immune dysfunction may also help explain why removing the uterus does not always solve the problem. If the immune environment that allowed the disease to establish itself in the first place remains unchanged, residual implants face little resistance to continued growth.
Environmental Chemicals and Endometriosis
The hormonal dependence of endometriosis raises a question beyond what the body produces internally: can environmental chemicals that mimic or interfere with estrogen influence the disease? Research on endocrine-disrupting chemicals (EDCs) suggests they can. Animal studies have identified multiple synthetic chemicals capable of influencing the biological processes needed for ectopic tissue to establish itself and survive.21PubMed Central. Environmental Endocrine Disruptors and Endometriosis
A recent analysis that combined genetic data with chemical-gene interaction databases identified eight genes with strong evidence for a causal link to endometriosis risk, and several of those genes were connected to specific EDCs including perfluorooctanoic acid (found in nonstick coatings), triphenyl phosphate (a flame retardant), and bisphenol A (found in some plastics).22PubMed. Systematic analyses uncover endocrine-disrupting chemical-responsive genes linked to endometriosis This research is still evolving, and nobody is claiming that a single chemical exposure causes endometriosis. But the findings add another layer to the picture: in a body where endometriotic tissue is already present or prone to forming, environmental estrogen mimics could contribute to the tissue’s survival and growth, whether or not a uterus is in the picture.
What This Means If You Have Had a Hysterectomy
If you have undergone hysterectomy for endometriosis and symptoms return, the pain is not imaginary and it is not unrelated. Recurrence is a well-documented phenomenon, and the risk is higher when ovaries were preserved and when deep lesions were not fully excised during the original surgery.3PubMed Central. Intestinal endometriosis: Diagnostic ambiguities and surgical outcomes Because deeply infiltrating lesions can remain active even without ovarian estrogen, thorough surgical excision of all visible disease at the time of hysterectomy is now considered critical, particularly since residual deep lesions carry a small risk of malignant transformation over time.2PubMed Central. Recurrence of endometriosis after hysterectomy
For those who need HRT after surgical menopause but worry about reactivation, aromatase inhibitors represent an option worth discussing with a specialist. The evidence is still largely from case reports and small series rather than large trials, but the biological rationale is sound: blocking the implants’ ability to produce their own estrogen addresses the disease at the level that matters, rather than relying solely on systemic hormone suppression.
People living with MRKH syndrome who develop cyclic pelvic pain should know that endometriosis is a real possibility, even though they lack a typical uterus. Tiny uterine remnants, if present, can produce enough endometrial tissue to seed the disease. Diagnosis in this group is often delayed because clinicians may not think to look for endometriosis in someone without a uterus, and imaging alone can miss small implants. Laparoscopy with biopsy remains the most reliable way to confirm the diagnosis.