The syncytial nature and surface location of the trophoblast layer of human placental villi positions the syncytiotrophoblast to regulate maternal-fetal exchange of molecules while also providing a barrier function. However, discontinuities in the syncytiotrophoblast breach the integrity of this interface, and deposition of fibrin type fibrinoid on the trophoblast basal lamina at the syncytial discontinuity provides a matrix for trophoblast re-epithelialization. Using the electron microscope, I tested the hypothesis that apoptosis in the syncytiotrophoblast was one process that initiated discontinuity in the trophoblast layer of term placental villi. Ultrastructural analysis of fibrin deposits on villi from six placentae from uncomplicated term pregnancies indicated the following morphological features typical of apoptosis: condensation and margination of chromatin along an intact nuclear envelop in syncytiotrophoblast nuclei associated with villous surface fibrin deposits; loss of microvilli with membrane blebbing on the surface membrane; cytoplasmic condensation; autophagocytosis of cellular debris containing nuclear fragments; absent inflammatory response. I conclude that human placental syncytiotrophoblast undergoes apoptosis, and this process is associated with breaks in the trophoblast covering of villi. The presence of trophoblastic apoptosis, and of discontinuities in the trophoblast layer of term villi, provide new insights into the pathways for maternal-fetal exchange in the human placenta.