Adenomyosis sits between two clinical worlds: identified frequently in routine imaging yet inconsistently linked to fertility outcomes. The lecture organises the evidence around three sequential questions: is there a plausible mechanism for an implantation effect, how should clinicians diagnose it, and when does adenomyosis actually require treatment in the ART setting?
Three phenotypes are now recognised by their anatomical relationship to the cavity: internal (junctional-zone) adenomyosis, intermediate (mid-myometrial) and external (serosal-side). Molecular drivers include altered apoptosis signalling, reduced progesterone-receptor expression with relative progesterone resistance, upregulated local aromatase activity and disrupted junctional-zone contractility. The phenotype dictates clinical consequences — only the junctional-zone variant consistently impairs implantation.
There is no single gold standard. MRI provides objective phenotype mapping but is limited by access and cost. 2D/3D ultrasound combined with the MUSA consensus criteria has comparable diagnostic accuracy and is the most widely adopted. Hysteroscopy in the «see and treat» school adds the ability to confirm and resect junctional-zone lesions in the same procedure.
Early meta-analyses suggested a uniform negative impact on live birth rates, but more recent work shows that only severe adenomyosis with junctional-zone involvement reliably impairs implantation. Studies in oocyte donation recipients confirm that the relevant pathology lies in the recipient endometrium, not in oocyte quality.
For clinically significant disease the standard algorithm combines cycle segmentation (freeze-all), PGT-A and accumulation of euploid blastocysts, GnRH agonist pretreatment of the substituted FET cycle, and selective hysteroscopic resection of visible junctional-zone lesions. Mid-luteal progesterone targets may need to be higher than the standard threshold — an extrapolation from endometriosis data. Critically, pretreatment before oocyte retrieval is not warranted, as adenomyosis does not impair oocyte quality.
Phenotyping comes first: only the junctional-zone variant warrants the full algorithm. For mild or non-junctional adenomyosis, standard IVF is the first-line approach. Documenting MUSA-based phenotype in every case allows the clinician to choose treatment intensity proportional to the actual implantation risk.
Adenomyosis and infertility: phenotype classification (internal/junctional zone, intermediate, external), current diagnostic approaches (MRI, ultrasound per MUSA criteria, hysteroscopy) and the evidence base regarding impact on ART outcomes. Management algorithm in clinically significant adenomyosis: cycle segmentation, accumulation of euploid blastocysts, GnRH agonist pretreatment before FET, selective hysteroscopic resection.
Adenomyosis and infertility: phenotype classification (internal/junctional zone, intermediate, external), current diagnostic approaches (MRI, ultrasound per MUSA criteria, hysteroscopy) and the evidence base regarding impact on ART outcomes. Management algorithm in clinically significant adenomyosis: cycle segmentation, accumulation of euploid blastocysts, GnRH agonist pretreatment before FET, selective hysteroscopic resection.
Distinguish internal/junctional, intermediate and external phenotypes — only the junctional-zone variant drives RIF.
Combine cycle segmentation, freeze-all and PGT-A accumulation for clinically significant disease.
Apply agonist priming to the substituted FET cycle, not before oocyte retrieval.
Resect visible junctional-zone lesions in patients with recurrent implantation failure.
Full Professor of Reproductive Medicine at the University of Naples Federico II and a founding member of the POSEIDON group. His research focuses on the role of LH in folliculogenesis and ovarian stimulation, endometriosis, oncofertility and reproductive endocrinology. Author of more than 100 indexed publications.
Author of the lecture "Adenomyosis and infertility"
