Conclusions

Endometriosis-associated implantation failure represents a complex clinical entity driven by the interaction of hormonal resistance, chronic inflammation, immune dysregulation, and persistent molecular reprogramming of the endometrium. Beyond mechanical distortion and oocyte impairment, defective endometrial receptivity emerges as a central determinant of reproductive failure in this population. Advances in reproductive immunology and molecular diagnostics have provided critical insights into the mechanisms linking endometriosis to impaired implantation. Alterations in progesterone signaling, immune cell function, cytokine networks, and epigenetic regulation collectively shape a hostile endometrial microenvironment that compromises embryo-endometrium crosstalk and placentation. While emerging biomarkers and regenerative therapies offer promising avenues for personalized intervention, current evidence emphasizes the need for cautious interpretation and selective clinical application. Integration of molecular, immune, and clinical parameters into individualized treatment algorithms represents the most rational strategy for optimizing implantation outcomes. Future progress will depend on rigorous mechanistic studies, biomarker-guided clinical trials, and multidisciplinary collaboration aimed at translating pathophysiological insights into precision reproductive medicine.