PURPOSE: To describe the ultrasonographic (US) appearance of fibroid calcification occurring after uterine artery embolization (UAE) and discuss its etiology and pathology. MATERIALS AND METHODS: Twenty-seven of a total of 38 patients were followed up clinically and with duplex US for longer than 6 months after UAE for uterine fibroids. At US, changes in uterine size, fibroid vascularity, and morphology have been recorded. Pathologic studies were performed by one of the authors on resected specimens from a different cohort of patients, at intervals ranging from 4 months to 1 year after UAE. RESULTS: Twenty patients reported complete resolution of symptoms. In 16 of these, a reduction in fibroid volume of 70%-85% was recorded and, at US, the development of a peripheral hyperechoic rim around an increasingly hypoechoic fibroid was noted. Computed tomography in two patients revealed it to be a rim of calcium. Histologic studies in a different cohort of patients who had undergone hysterectomy at variable intervals after UAE demonstrated early aggregation of polyvinyl alcohol (PVA) particles, an intermediate giant cell inflammatory reaction, and calcification in the periphery of the infarcted fibroid at 6-12 months. CONCLUSION: Calcification is the end stage of hyaline degeneration. However, its peripheral location is unlike that of natural fibroid involution and hyaline necrosis. Pathologic studies in resected human fibroids after embolization suggest that its development is the end result of aggregation of PVA particles in peripheral fibroid arteries.