Adenomyosis is a condition in which endometrial glands and stroma — the tissue that normally lines the inside of the uterus — invade and grow within the muscular wall of the uterus (myometrium). The ectopic endometrial tissue responds to monthly hormonal cycles by proliferating and bleeding, causing the uterus to become enlarged, boggy, and painful. Adenomyosis is one of the most common and historically underdiagnosed causes of heavy menstrual bleeding and chronic pelvic pain in reproductive-age women.
Adenomyosis frequently coexists with and must be carefully distinguished from uterine fibroids — both cause heavy bleeding and uterine enlargement, but their MRI appearances are distinct and their treatment approaches differ fundamentally. Endometriosis coexists with adenomyosis in up to 50% of affected women and shares the same hormonal dependency and pelvic pain features. The heavy, painful periods of adenomyosis also overlap with those of polycystic ovarian syndrome, though PCOS typically causes irregular or absent periods rather than heavy regular bleeding. MRI is the only imaging study that can reliably establish the diagnosis of adenomyosis and simultaneously evaluate for these coexisting conditions.
Causes
Disruption of the endometrial-myometrial boundary.
The fundamental mechanism of adenomyosis involves a breakdown of the normal anatomic barrier between the endometrium and the underlying myometrium — the junctional zone, visible on MRI as a dark inner muscular layer. Several complementary theories have been proposed for how this disruption occurs. The most widely accepted is the invagination theory: endometrial glands invade downward through a weakened junctional zone into the myometrium, driven by mechanical disruption from prior uterine surgery, trauma, or abnormal endometrial-myometrial signaling. The tissue displacement theory suggests that endometrial cells are displaced into the myometrium during uterine procedures. A developmental theory posits that adenomyosis arises from Müllerian remnants within the myometrium. Most likely, adenomyosis is a heterogeneous condition with multiple contributing pathways converging on the same pathologic endpoint: ectopic endometrial glands and stroma within the myometrium, responding to estrogen and progesterone with cyclic proliferation and bleeding that cannot drain — progressively expanding and inflaming the myometrium from within.
Other contributing factors.
Prior uterine surgery — including cesarean section, dilation and curettage (D&C), hysteroscopy, and myomectomy — are the strongest modifiable risk factors, as they disrupt the junctional zone and may allow endometrial cells to gain entry into the myometrium. Multiple pregnancies (parity) are strongly associated. Prolonged unopposed estrogen exposure — through early menarche, late menopause, obesity, or tamoxifen use — promotes the growth and activity of ectopic endometrial tissue. Adenomyosis most commonly affects women between ages 35 and 50, though improved imaging has increasingly identified the condition in younger women. It frequently coexists with uterine fibroids (in approximately 50% of cases) and with endometriosis (in 20–50% of cases), often making clinical and imaging distinction essential for treatment planning.
Symptoms
The classic symptom triad of adenomyosis is heavy or prolonged menstrual bleeding (menorrhagia), severely painful periods (dysmenorrhea) that worsen progressively over time, and an enlarged, globally tender uterus. The worsening dysmenorrhea over years — rather than stable or improving period pain — is a hallmark that distinguishes adenomyosis from primary dysmenorrhea and should prompt imaging evaluation. Chronic non-cyclical pelvic pain, dyspareunia (pain with intercourse, reflecting uterine tenderness during thrusting), and a sense of pelvic heaviness or pressure are additional complaints. Iron-deficiency anemia from chronic heavy bleeding is common and may be severe. Reproductive consequences include subfertility, implantation failure in IVF cycles, and an increased rate of first-trimester miscarriage. A substantial proportion of women with adenomyosis carry a misattributed diagnosis of "bad periods" or irritable bowel syndrome for years before the correct diagnosis is established — the diagnostic delay often exceeds 5–7 years from symptom onset.
Diagnosis
Adenomyosis is suspected clinically when a woman presents with the classic symptom triad and a symmetrically enlarged, diffusely tender uterus on bimanual examination — the uterus often has a characteristic soft, boggy consistency (the "uterus feels like a bag of worms" description) distinct from the firm nodularity of a fibroid uterus. Transvaginal ultrasound may show suggestive features including myometrial heterogeneity, asymmetric wall thickening, and small anechoic cystic spaces — but the sensitivity and specificity of ultrasound for adenomyosis are significantly lower than for fibroids, and interobserver variability is high.
An MRI of the pelvis is the most accurate noninvasive diagnostic study for adenomyosis and is the imaging gold standard. The pathognomonic MRI finding is thickening of the junctional zone — the low T2-signal inner myometrial layer — to greater than 12 mm, which reflects myometrial smooth muscle hypertrophy in response to the ectopic endometrial invasion. Small T2-bright or T1-bright foci within the myometrium represent ectopic endometrial glands and hemorrhagic foci. The uterus appears globally enlarged with a diffusely heterogeneous myometrium in diffuse adenomyosis. MRI reliably distinguishes adenomyosis (diffuse, ill-defined, no pseudocapsule) from fibroids (discrete, well-defined, T2-hypointense masses with a pseudocapsule) — a distinction that determines whether the patient is a candidate for focused interventions like myomectomy and UFE, or whether hysterectomy is ultimately the appropriate treatment. MRI also evaluates for concurrent endometriosis, endometriomas, and deep infiltrating implants that may require coordinated surgical management.
Classification
Adenomyosis is classified by its distribution and morphologic pattern within the myometrium, which influences symptom severity and treatment response.
- Diffuse adenomyosis: Widespread ectopic endometrial invasion throughout the myometrium, producing global uterine enlargement and diffuse junctional zone thickening on MRI. The most common pattern and the most challenging to treat with uterus-preserving approaches.
- Focal adenomyosis (adenomyoma): A localized nodule of adenomyosis that can mimic a fibroid on ultrasound but is distinguished by its ill-defined margins, lack of pseudocapsule, and internal T2-bright foci on MRI. Can sometimes be surgically excised in fertility-preserving procedures.
- Cystic adenomyosis: Prominent T2-bright or hemorrhagic cystic spaces within the myometrium, often seen in younger women or after hormonal suppression. May have a more dramatic MRI appearance than the degree of symptom burden suggests.
- Outer myometrial (subperitoneal) adenomyosis: Ectopic tissue predominantly in the outer myometrial layer, associated more with endometriosis than with heavy bleeding — a distinct phenotype increasingly recognized with high-resolution MRI.
Treatments
Treatment is tailored to symptom severity, the extent of myometrial involvement on MRI, fertility goals, and proximity to natural menopause.
Medical management: The levonorgestrel-releasing IUD (Mirena) is the most effective medical treatment for adenomyosis-related heavy bleeding and is often first-line — local progestin delivery suppresses endometrial activity within the myometrium and reduces menstrual blood loss by up to 90% in many patients. Combined oral contraceptives and oral progestins provide symptomatic relief but less reliably than the IUD. NSAIDs reduce dysmenorrhea. GnRH agonists (leuprolide) induce a temporary menopausal state with significant symptom relief, used as a bridge to surgery, natural menopause, or to evaluate symptom response before committing to hysterectomy. GnRH antagonists (elagolix, relugolix) offer an oral, rapidly reversible alternative. Tranexamic acid reduces menstrual blood loss without hormonal effects.
Uterine artery embolization (UAE).
UAE uses the same minimally invasive approach as UFE for fibroids — occluding the uterine arteries to reduce blood supply to the adenomyotic myometrium. UAE for adenomyosis provides meaningful symptom relief in approximately 60–80% of patients, though recurrence rates at 3–5 years are higher than for fibroids because adenomyosis involves diffuse myometrial tissue that is less discretely vascularized than individual fibroid nodules. UAE is a reasonable option for women who want to preserve the uterus and avoid major surgery.
Endometrial ablation.
Thermal or radiofrequency destruction of the uterine lining reduces menstrual bleeding, but its effectiveness for adenomyosis is limited and less durable than for other causes of heavy bleeding — because the adenomyotic glands extend into the myometrium beyond the reach of surface ablation, the bleeding source is not fully addressed. Ablation is best suited for women with superficial adenomyosis without significant junctional zone thickening on MRI.
Surgical adenomyomectomy.
For focal adenomyosis (adenomyoma) in women wishing to preserve fertility, surgical excision of the discrete adenomyotic nodule — analogous to myomectomy for fibroids — can be attempted. This requires precise preoperative MRI mapping to define the lesion boundaries, as adenomyomas lack the clear cleavage plane of fibroids. Results for fertility preservation and symptom relief are variable, and recurrence is common.
Hysterectomy.
Removal of the uterus is the only definitive cure for adenomyosis and eliminates symptoms permanently. It is the appropriate treatment for women with severe, refractory symptoms who have completed childbearing. Minimally invasive approaches (laparoscopic, robotic, or vaginal) are used when feasible. The ovaries are preserved in premenopausal women unless there is an independent indication for their removal. Because adenomyosis regresses naturally at menopause, women close to natural menopause may be managed medically until they transition, avoiding surgery altogether.
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