BACKGROUND: Subchorionic hematoma is a risk factor for preterm prelabor rupture of membranes and preterm birth. A small proportion of persistent subchorionic hematoma leads to a chronic abruption-oligohydramnios sequence. OBJECTIVE: To determine the mechanism by which subchorionic hematomas may damage chorioamniotic membranes. STUDY DESIGN: 1) The number and subtype of macrophages were determined by immunohistochemistry in chorioamniotic membranes from 8 subchorionic hematoma patients who delivered preterm (25.5 (24-32) weeks of gestation (median and range)) and 6 gestational age-matched control patients (25.5 (25-28) weeks of gestation (median and range)). Further, the thickness and fibrosis of the membranes were quantified. 2) We also developed an intrauterine hematoma model in pregnant mice, and the effects of hematoma on the amnion were analyzed by histology and immunofluorescence. 3) In vitro, primary human amnion mesenchymal cells were cocultured with M2-differentiated macrophages, and changes in mesenchymal cells were analyzed. RESULTS: 1) Subchorionic hematoma increased the number of iron-laden macrophages in the human amnion. These macrophages were CD206 CONCLUSION: Subchorionic hematoma induces migration of macrophages to chorioamniotic membranes which activate the transition of amnion mesenchymal cells to myofibroblasts. These myofibroblasts may contribute to fibrosis of the amnion and damage chorioamniotic membranes.