Introduction. Comparative analysis of the expression levels of a number of microRNAs (miRNAs) in placentas obtained during timely and spontaneous preterm birth (PB) will make it possible to identify those miRNAs that are involved in the genesis of spontaneous PB. MiRNAs characterized by aberrant expression in placental tissues may be promising biomarkers in the blood of pregnant women for assessing the risk of spontaneous PB. Aim. Comparative analysis of expression levels of a number of microRNAs in placental tissue in women in timely and premature birth. Materials and Methods. We performed an analysis of the expression level of a number of miRNAs in placental tissue from 30 patients with PB and perinatal losses (group 1), from 30 patients with PB without perinatal losses (group 2), from 30 maternity women with timely delivery (group 3). The expression levels of the following miRNAs were studied: 31, 100, 146, 150, 20a, 204, 221, 223, 1246, 128, let7a, 126, 451, 92a, 23a, 21, 125b, 26a, 29b, 191, and U6. For this, the material was deparaffinated step by step using mineral oil, then the RNA extraction, reverse transcription reaction, and real-time polymerase chain reaction were carried out. Results. It was found that in PB a statistically significant increase in the expression levels of miRNA-125b, miRNA-29b is observed in placental samples, and a decrease in the expression level of miRNA-451 in comparison with timely delivery placentas. In the PB with perinatal losses, a statistically significant decrease in the expression level of miRNA-150 was registered, and in the absence of perinatal losses, an increase in the expression level of miRNA-223 and miRNA-31 compared with placentas in timely delivery was revealed. In addition, in PB with perinatal losses compared to PB without perinatal losses, a statistically significantly lower level of expression of miRNA-221 and miRNA-223 is noted. Conclusion. Aberrant expression levels of miRNA-125b, miRNA-29b, and miRNA-451 in the placentas of patients with PB indicate their involvement in the pathogenesis of the latter, apparently due to dysregulation of angiogenesis, apoptosis, trophoblast invasion and glucose metabolism.