From 1861 to 1962, clinicopathologic research tried to explain the association of abnormal uterine bleeding with uterine enlargement. The etiology was theorized as metropathy, suggesting that myometrial dysfunction may predispose to abnormal uterine bleeding. Research reached a nadir in 1962, when a major review dismissed myometrial hypertrophy as a plausible explanation after prior rejections of the theories of chronic myometritis, fibrosis uteri, and subinvolution as causes of bleeding. Subsequent to this arose a crusade against unnecessary hysterectomies in the 1970s. Although myometrial hyperplasia was proposed in 1868, it is only in the past 25 years that tangible evidence has supported that idea. It now appears that clinically enlarged uteri are due to globoid outward bulging of the uterus, caused by increased intramural pressure—often unrelated to either uterine weight or myometrial thickness. Abnormal (dysfunctional) uterine bleeding may often be due to spontaneous rupture of thrombosed dilated endometrial vessels, due to the combined effects of obstructed venous drainage by increased intramural pressure, and Virchow’s triad. Despite a century-old known association of parity with naturally occurring outer wall myometrial scars (fibrosis uteri with elastosis), it was not previously suggested that these may reflect healing reactions to muscle tears during labor and delivery. We now suggest that smaller, similar inner wall elastotic scars in the nerve-rich inner myometrium may explain many cases of pelvic pain. This review suggests that diverse pressure-related lesions may be present in clinically abnormal uteri that have been called “normal” since the crusade against unnecessary hysterectomy.