40% of women with endometriosis suffer infertility

Endometriosis is a chronic gynecologic condition in which tissue similar to the endometrium (the lining of the uterus) is present outside the uterine cavity. It affects an estimated 6–10% of people assigned female at birth during reproductive years and is a leading cause of pelvic pain and infertility. Multiple clinical sources estimate that between 30% and 50% of women with endometriosis experience infertility; many reports commonly summarize this as approximately 40% (Mayo Clinic; Cleveland Clinic; NIH) [1–4]. This article reviews the pathophysiology, clinical features, diagnostic approach, and management of endometriosis with particular emphasis on its relationship to fertility, drawing on guidance from major medical organizations and evidence-based resources.

What is endometriosis?

Endometriosis is defined by the presence of endometrial-like glands and stroma outside the uterine cavity, most commonly on the ovaries, pelvic peritoneum, uterosacral ligaments, and rectovaginal septum. Lesions vary from superficial peritoneal implants and ovarian endometriomas (so-called “chocolate cysts”) to deep infiltrating lesions that penetrate more than 5 mm beneath the peritoneal surface. Although the ectopic tissue resembles endometrium histologically and responds to hormonal stimulation, it is not continuous with the uterine mucosa.

Endometriosis is a hormonally responsive, often estrogen-dependent disease that can cause chronic pelvic pain, dysmenorrhea (painful menses), dyspareunia (pain with intercourse), and subfertility or infertility. Symptom severity does not always correlate with extent of disease: some patients with extensive adhesions may have minimal pain, whereas others with small lesions may experience debilitating symptoms.

Epidemiology and risk factors

Prevalence: Endometriosis affects approximately 6–10% of reproductive-age women overall; among women with chronic pelvic pain or infertility, prevalence is higher (up to 50% or more) (Mayo Clinic; NIH) [1, 3].
Age: Most commonly diagnosed in women aged 25–40 years, though symptoms can begin in adolescence and, less commonly, lesions may persist into the postmenopausal period, particularly in patients on estrogen therapy.
Reproductive history: Nulliparity (never having given birth) is associated with increased risk. Some studies suggest that later age at first pregnancy or shorter durations of breastfeeding may be risk factors.
Family history: Having a first-degree relative with endometriosis increases risk, indicating a heritable component.
Other associations: Anatomical uterine abnormalities, retrograde menstruation, immune and inflammatory factors, and prior pelvic surgery (including tubal ligation in some series) have been implicated as contributors or risk modifiers.

(References: ACOG, NIH, Mayo Clinic) [1–4]

Pathophysiology: theories and mechanisms

The exact cause of endometriosis remains incompletely understood; several nonmutually exclusive mechanisms have been proposed:

Retrograde menstruation: Menstrual debris containing viable endometrial cells flows backward through the fallopian tubes into the peritoneal cavity, implanting on peritoneal surfaces. Retrograde menstruation occurs in many women, but not all develop disease, suggesting additional factors (immune dysfunction, genetic predisposition) are required.
Coelomic metaplasia: Peritoneal cells transform into endometrial-like cells under certain influences.
Lymphatic or hematogenous dissemination: Endometrial cells spread via lymphatic or blood vessels to distant sites (e.g., thorax), explaining rare extrapelvic endometriosis.
Stem cell and progenitor theories: Circulating stem/progenitor cells may differentiate into endometrial tissue at ectopic sites.
Immune and inflammatory milieu: Endometriotic lesions generate local inflammation, angiogenesis, and neurogenesis, contributing to pain and lesion persistence. Altered immune surveillance may allow ectopic tissue to implant and evade clearance.
Estrogen dependence: Endometriotic tissue is sensitive to estrogen, which promotes growth and inflammation. Local estrogen production by endometriotic lesions may perpetuate the disease.

These mechanisms help explain clinical phenomena such as lesion heterogeneity, the chronic inflammatory state, and the variable response to hormonal treatments.

Clinical presentation

Symptoms vary widely and can include:

Dysmenorrhea: Progressive, often worsening menstrual pain starting before menses and continuing during menstruation.
Chronic pelvic pain: Not confined to menses; may be constant or cyclical.
Dyspareunia: Pain associated with sexual activity, often deep pelvic pain.
Infertility or subfertility: Difficulty conceiving; endometriosis is a common finding in women evaluated for infertility.
Bowel and urinary symptoms: Painful bowel movements, constipation, diarrhea, bloating, or cyclical hematuria if urinary tract involvement occurs.
Fatigue and reduced quality of life: Chronic pain and associated symptoms can impair physical, emotional, and social functioning.
Asymptomatic disease: A significant proportion of individuals with endometriosis are asymptomatic and may be diagnosed incidentally during imaging or surgery.

Because symptoms can overlap with other gynecologic and gastrointestinal conditions (pelvic inflammatory disease, irritable bowel syndrome, interstitial cystitis), diagnostic evaluation often requires careful clinical assessment and targeted investigations.

Diagnostic approach

Diagnosis combines history, physical examination, imaging, and, when necessary, surgical evaluation.

Clinical evaluation

A detailed history should assess timing and pattern of pain, menstrual history, fertility goals, prior surgeries, family history, and impact on daily functioning. Pelvic examination may reveal adnexal tenderness, nodularity along the uterosacral ligaments, or fixed retroverted uterus, but is often normal, particularly in early disease.

Imaging

Transvaginal ultrasound (TVUS): First-line imaging for suspected ovarian endometriomas and to evaluate pelvic anatomy. TVUS has high sensitivity and specificity for endometriomas but limited sensitivity for superficial peritoneal disease and deep infiltrating lesions unless performed by experienced operators with dedicated protocols.
Magnetic resonance imaging (MRI): Useful for mapping deep infiltrating endometriosis and complex pelvic involvement, particularly in surgical planning. MRI provides multiplanar anatomic detail.
Computed tomography (CT): Limited role for primary diagnosis; may be used when other abdominal pathology is considered.
Specialized sonographic techniques: Transvaginal sonography with bowel preparation and dynamic assessment can improve detection of deep lesions.

(See Mayo Clinic, Cleveland Clinic for imaging guidance) [1, 2]

Surgical diagnosis

Laparoscopy with visual inspection of the pelvis is considered the gold standard for definitive diagnosis because it allows direct visualization, lesion biopsy for histologic confirmation, and simultaneous surgical treatment. Laparoscopy reveals implants, adhesions, and endometriomas; biopsy can confirm endometrial-like glands and stroma. However, given the invasiveness and cost, clinical diagnosis may be sufficient to initiate treatment, particularly when typical symptoms and imaging suggest endometriosis.

Diagnostic delays

Endometriosis is frequently underdiagnosed and underrecognized. Many patients see multiple providers and may experience delays of several years (commonly 4–8 years) between symptom onset and definitive diagnosis. This diagnostic delay has implications for pain control, fertility planning, and quality of life.

(ACOG, NIH discuss diagnostic challenges) [3, 4]

Staging and classification

The revised American Society for Reproductive Medicine (rASRM) classification stages endometriosis as I (minimal), II (mild), III (moderate), or IV (severe) based on lesion size, location, and adhesions. The rASRM score correlates poorly with pain severity but can help standardize reporting.

Deep infiltrating endometriosis (DIE), ovarian endometriomas, and extrapelvic lesions may be described separately because they have distinct clinical and surgical implications. Staging informs surgical planning and may have prognostic value for fertility outcomes, though individual variability is high.

(ACOG practice bulletins provide details on staging and implications) [3]

Endometriosis and infertility

Prevalence of infertility among women with endometriosis

Endometriosis and infertility are closely linked. Estimates indicate that 30–50% of women with endometriosis experience some degree of impaired fertility; conversely, endometriosis is found in a significant proportion of women undergoing evaluation for infertility (often cited as 20–50%) (Mayo Clinic; Cleveland Clinic; NIH) [1–4]. Because the relationship is complex and influenced by disease stage and lesion location, it is more appropriate to describe fertility impact as variable rather than uniform.

Mechanisms by which endometriosis impairs fertility

Multiple interrelated mechanisms can reduce fertility in endometriosis:

Anatomical distortion: Adhesions and scarring involving the ovaries, fallopian tubes, and pelvic organs can distort anatomy and impede oocyte capture or tubal transport.
Ovarian dysfunction: Endometriomas and surgical excision of ovarian endometriomas can reduce ovarian reserve by damaging healthy ovarian tissue and reducing follicular reserve.
Altered peritoneal environment: Inflammatory cytokines, proteases, and reactive oxygen species in peritoneal fluid can impair sperm function, fertilization, and embryo development.
Impaired ovulation or oocyte quality: Local inflammatory and hormonal effects may affect oocyte maturation and quality.
Implantation defects: Endometrial receptivity may be altered in some patients with endometriosis, reducing the likelihood of embryo implantation.
Immunologic factors: Aberrant immune cell function and autoantibodies may contribute to infertility.

These mechanisms may act singly or in combination, and the degree of fertility impairment often correlates with disease burden and lesion location. Notably, many people with minimal disease conceive without assisted reproduction, whereas those with advanced disease or ovarian endometriomas may face greater challenges.

(ACOG and NIH discuss infertility implications) [3, 4]

Evaluation of the infertile patient with endometriosis

When evaluating infertility, clinicians should take a comprehensive approach:

Duration: Assess time attempting conception (typically 12 months for women <35 years; 6 months for women ≥35).
Semen analysis: Evaluate male partner fertility as male-factor infertility accounts for a substantial proportion of couples.
Ovulatory function: Document ovulation (basal body temperature, midluteal progesterone, cycle regularity).
Tubal patency and uterine cavity: Hysterosalpingography, saline sonohysterography, or laparoscopy as indicated to assess tubal patency and uterine anatomy.
Ovarian reserve testing: Anti-Müllerian hormone (AMH) level and antral follicle count (AFC) to assess ovarian reserve, particularly when endometriomas are present or surgery is planned.

A tailored fertility plan should account for disease severity, ovarian reserve, patient age, prior surgeries, and reproductive goals.

Management principles

Management aims to relieve pain, preserve or improve fertility when desired, and minimize treatment-related harms. Care should be individualized, balancing symptom control with reproductive planning.

Medical management for pain and disease suppression

Hormonal therapies that suppress ovulation and reduce estrogen stimulation of ectopic tissue are mainstays for pain control but generally do not restore fertility while in use. Options include:

Combined oral contraceptives (COCs): Continuous or cyclic use reduces menstrual bleeding and lesion-related pain.
Progestins: Oral progestins, medroxyprogesterone acetate, or levonorgestrel-releasing intrauterine systems (LNG-IUS) can reduce pain and lesion activity.
Gonadotropin-releasing hormone (GnRH) agonists and antagonists: Induce hypoestrogenic states that reduce lesion size and pain; limited to several months due to systemic effects. Add-back therapy may be used to mitigate hypoestrogenic side effects.
Aromatase inhibitors: Used off-label in refractory cases, often in combination with other hormonal agents.
Nonsteroidal anti-inflammatory drugs (NSAIDs): Symptomatic relief of pelvic pain and dysmenorrhea.

Importantly, while these therapies can reduce pain, they do not improve fertility during active treatment because they suppress ovulation. For patients desiring pregnancy, temporary cessation of medical suppression is necessary.

(ACOG guidance details medical options and their roles) [3]

Surgical management

Surgical intervention via laparoscopy is indicated in selected patients for both symptom relief and fertility improvement.

Laparoscopic excision or ablation: Removal of implants and adhesiolysis can reduce pain and may improve spontaneous pregnancy rates, particularly in mild-to-moderate disease.
Endometrioma management: Cystectomy (excision of ovarian endometriomas) can relieve symptoms and may improve access to follicles for assisted reproduction, but surgery can reduce ovarian reserve. The decision to operate must weigh symptom severity, cyst size, age, ovarian reserve, and desire for fertility.
Fertility-sparing surgery: Experienced surgeons aim to remove disease while preserving ovarian tissue and function. Multidisciplinary teams may be needed for complex cases (bowel, bladder involvement).
Reproductive outcomes after surgery: For minimal to moderate disease, laparoscopic ablation/excision can improve spontaneous conception rates. For advanced disease, benefits are less clear and must be individualized.

(Surgical counsel should follow standards of care and referral to specialized centers when needed) [2, 3]

Assisted reproductive technologies (ART)

When spontaneous conception is unlikely or has failed, ART may offer effective pathways to pregnancy.

Ovulation induction with timed intercourse or intrauterine insemination (IUI): May be appropriate in selected patients, particularly with minimal disease and without significant tubal dysfunction.
In vitro fertilization (IVF): IVF bypasses many pelvic factors that impede conception and is often the most effective option for those with advanced disease, tubal damage, or after failed surgical attempts. IVF success rates among women with endometriosis are generally comparable to those of other infertility diagnoses when adjusted for age and ovarian reserve, but the presence of endometriomas and diminished ovarian reserve can reduce response to ovarian stimulation.
Pre-treatment surgical considerations: Routine removal of small asymptomatic endometriomas solely to improve IVF outcomes is not universally recommended; individualized assessment is required because cystectomy may lower ovarian reserve.

(Leading fertility societies and ACOG outline indications for ART) [3]

Fertility preservation

For patients with endometriosis who plan to delay childbearing or face anticipated ovarian compromise (large endometriomas or repeated surgery), fertility preservation strategies should be considered:

Oocyte cryopreservation: Controlled ovarian stimulation and egg freezing before surgery or ovarian decline can preserve fertility potential.
Embryo cryopreservation: For patients with a partner, embryo freezing is an established option.
Considerations: Discuss timing, costs, success rates, and potential impact of endometriosis on future ART.

Fertility preservation counseling should occur early for patients at risk of diminished ovarian reserve.

Special populations

Adolescents

Endometriosis can present in adolescence with dysmenorrhea and chronic pelvic pain. Early recognition and management can improve quality of life and reduce delay to diagnosis. Hormonal suppression is often a first-line approach for symptom control. Surgical evaluation may be necessary in refractory cases or when diagnosis is uncertain.

Pregnancy and postmenopausal patients

Pregnancy often temporarily ameliorates symptoms due to hormonal changes, but disease may persist or recur postpartum. Endometriosis is usually estrogen-dependent and tends to regress after menopause; however, lesions may remain or become symptomatic in postmenopausal women, particularly those receiving estrogen replacement therapy. Management in these groups requires careful individualized assessment.

Long-term outcomes, complications, and quality of life

Endometriosis is a chronic condition that can lead to:

Persistent pain and decreased quality of life, including physical limitation, emotional distress, and sexual dysfunction.
Recurrent disease after conservative surgery, with rates varying by lesion type and completeness of excision.
Ovarian reserve decline following cystectomy or with progressive disease.
Rarely, malignant transformation: Ovarian endometriomas have a small risk of malignant change, but the absolute risk is low.

Comprehensive care addressing pain management, psychological support, and functional goals is essential to improve quality of life.

Multidisciplinary care and referral

Because endometriosis can involve multiple organ systems and impact fertility, a multidisciplinary approach often yields the best outcomes. Relevant specialties include:

Reproductive endocrinology and infertility (REI) for fertility assessment and ART planning.
Minimally invasive gynecologic surgeons with expertise in complex endometriosis excision.
Colorectal surgeons and urologists for deep infiltrating disease involving bowel or bladder.
Pain medicine, physical therapy, and mental health professionals for chronic pelvic pain management.
Primary care and adolescent medicine for early recognition and longitudinal care.

Referral to specialized centers should be considered for complex or recurrent disease, significant infertility, or when major reconstructive surgery is anticipated.

Counseling and patient-centered decision making

Effective counseling should include:

Explanation of the diagnosis, natural history, and uncertainty regarding progression.
Discussion of fertility implications, individualized based on age, ovarian reserve, and lesion burden.
Review of treatment options, benefits, risks, and the impact of treatments on fertility.
Consideration of timelines for conception and referral to fertility specialists when appropriate.
Attention to psychosocial impacts, including chronic pain, sexual health, and mental health.

Shared decision-making aligned with patient goals—pain control versus fertility planning—should inform therapeutic choices.

When to suspect endometriosis and when to refer

Suspect endometriosis in individuals with:

Progressive dysmenorrhea that is refractory to NSAIDs or hormonal therapy.
Chronic pelvic pain, especially with cyclical flares.
Dyspareunia or infertility without other identified cause.
Cyclical gastrointestinal or urinary symptoms.

Refer to gynecology or a specialized endometriosis center if symptoms are severe, there is suspected deep infiltrating disease, infertility is present and childbearing is desired, or prior conservative treatments have failed.

Conclusion

Endometriosis is a prevalent, often underdiagnosed gynecologic condition that can substantially affect pain, fertility, and quality of life. Approximately 30–50% of women with endometriosis experience infertility, a figure commonly summarized as around 40% in many clinical sources. Management requires individualized evaluation and may include medical suppression for pain, conservative or fertility-sparing surgery, and assisted reproductive technologies for those seeking pregnancy. Early recognition, multidisciplinary care, and informed decision-making regarding fertility preservation and reproductive planning are central to optimizing outcomes.

For current clinical guidance and patient resources, consult professional organizations and authoritative health institutions such as ACOG, the National Institutes of Health, the Mayo Clinic, and the Cleveland Clinic.

References

Mayo Clinic. Endometriosis. https://www.mayoclinic.org/diseases-conditions/endometriosis/symptoms-causes/syc-20354656 (Accessed 2026).
Cleveland Clinic. Endometriosis. https://my.clevelandclinic.org/health/diseases/15114-endometriosis (Accessed 2026).
American College of Obstetricians and Gynecologists (ACOG). Practice Bulletin and Committee Opinions on endometriosis and infertility. https://www.acog.org (search: endometriosis practice bulletin) (Accessed 2026).
National Institutes of Health (NIH) / National Institute of Child Health and Human Development (NICHD). Endometriosis information. https://www.nichd.nih.gov/health/topics/endometriosis (Accessed 2026).

(These sources provide patient-oriented and clinical information on endometriosis, its diagnosis, and management.)