Adenomyosis

Adenomyosis occurs when endometrial glandular tissue becomes embedded within the myometrium — the muscular wall of the uterus. The displaced tissue remains hormonally responsive, so it thickens and bleeds with each cycle. Trapped inside muscle with nowhere to drain, that bleeding drives inflammation, and the surrounding myometrium responds with hypertrophy and fibrosis. This is why the uterus enlarges and becomes boggy and tender rather than forming discrete lumps.

How the tissue crosses into the muscle is still unsettled, and three explanations are usually offered:

1. Invagination. The junctional zone between endometrium and myometrium is disrupted — by childbirth, curettage, or caesarean — letting endometrium grow down into the muscle.
2. Embryonic rests. Müllerian tissue is misplaced within the myometrium during fetal development and activates later under hormonal drive.
3. Post-inflammatory invasion. Inflammation following delivery weakens the junctional zone and permits invasion.

Estrogen sustains the process, and the lesions themselves express aromatase — they make their own estrogen locally. Progesterone resistance within the ectopic tissue compounds it. Because the whole mechanism depends on cyclical hormonal drive, adenomyosis almost always regresses after menopause, as endometriosis does.

Risk rises with age and parity: most cases are diagnosed in the forties and fifties, in women who have had children. Prior uterine surgery is the other consistent association.

Adenomyoma

An adenomyoma is a localized, well-circumscribed nodule of adenomyosis within the myometrium. It forms a discrete mass that can closely resemble a fibroid on imaging — the practical distinction is that an adenomyoma has indistinct margins and no true capsule, so it cannot be shelled out the way a fibroid can.

Diffuse Adenomyosis

Diffuse adenomyosis describes endometrial tissue spread broadly through the myometrium rather than confined to one nodule. It produces generalized, uniform enlargement and thickening of the uterine wall, often asymmetrically — the posterior wall is typically thicker than the anterior.

The classic triad is heavy menstrual bleeding, progressively worsening period pain, and a diffusely enlarged, tender uterus. Around a third of women have no symptoms at all and the condition is found incidentally.

Menorrhagia is usually the dominant complaint, and it is heavy enough in many women to produce iron-deficiency anemia — fatigue, breathlessness on exertion and pallor may be what brings them in rather than the bleeding itself. Dysmenorrhea tends to begin a few days before the period and is described as deep, dragging and cramping rather than sharp. Chronic pelvic pain between periods, deep dyspareunia, and a sensation of pelvic heaviness or bloating are common. The uterus is characteristically globular and softer than a fibroid uterus, and tender on bimanual examination — particularly just before menstruation.

Diagnosis is suggested by a diffusely enlarged, boggy, tender uterus in a woman with heavy, painful periods, and is confirmed on imaging.

Transvaginal ultrasound is the first-line investigation and is now good enough to make the diagnosis in most cases: a thickened, irregular junctional zone, myometrial cysts, asymmetric wall thickening, and linear striations radiating through the muscle. MRI is more accurate where ultrasound is equivocal, where fibroids coexist, or where surgery is being planned — a junctional zone thicker than 12 mm is the usual threshold. Histology after hysterectomy remains the definitive confirmation, but is no longer required to treat.

A full blood count is worth doing in anyone with heavy bleeding, to identify the anemia that frequently accompanies it. Endometrial sampling does not diagnose adenomyosis but is used to exclude hyperplasia or malignancy where bleeding is irregular, intermenstrual, or postmenopausal.

Adenomyosis coexists with endometriosis in a substantial proportion of women, and with uterine fibroids in up to half — the three overlap often enough that finding one is a reason to look for the others. Iron-deficiency anemia is the commonest downstream consequence. Adenomyosis is also associated with reduced fertility and with a higher rate of miscarriage and preterm birth, thought to relate to disordered junctional-zone contractility and impaired implantation.