Title : Endometrial functions in recurrent pregnancy loss
Abstract:
Recurrent pregnancy loss (RPL) is a clinically challenging reproductive condition, and in a significant proportion of patients no identifiable cause is found using standard diagnostic work-up. Increasing clinical and experimental evidence suggests that endometrial dysfunction represents a key factor in the pathogenesis of RPL, independently of embryonic abnormalities or systemic maternal conditions. The endometrium plays a pivotal role in implantation and early placentation through tightly regulated processes of receptivity, decidualization, immune tolerance, and vascular remodeling.
Clinical studies have associated RPL with alterations in endometrial decidualization, dysregulated immune cell populations, impaired cytokine signaling, and defective angiogenesis. In particular, abnormalities in uterine natural killer cell activity, macrophage polarization, and T-cell–mediated immune balance may compromise embryo implantation and early placental development. Endocrine disturbances and epigenetic alterations further contribute to impaired endometrial responsiveness during the implantation window.
Current evidence highlights molecular and cellular endometrial alterations that may represent clinically relevant biomarkers of impaired receptivity in women with RPL. Moreover, emerging data suggest that endometrial inflammation, uterine microbiota imbalance, and chronic endometritis may contribute to a hostile endometrial environment, offering potential targets for diagnostic refinement and therapeutic intervention. A better integration of endometrial assessment into clinical practice may improve patient stratification and management in recurrent pregnancy loss.
