The cause of implantation defects in patients with recurrent implantation failure (RIF) and recurrent pregnancy loss (RPL) has not been clearly established. We aimed to evaluate the immunohistochemical changes in HOXA-11, β1 integrin, focal adhesion kinase (FAK), cluster of differentiation 44 (CD44), and extracellular matrix protein 1 (ECM1) molecules during the receptive endometrial period in patients with RIF and RPL. This study was retrospectively conducted at a university hospital. After the exclusion of cases with pathology that may cause a change in the level of receptors in the endometrium, biopsies performed during the receptive period were selected, and the patients were categorized into RPL (n=15), RIF (n=16), control (n=16) groups. All preparations were immunohistochemically stained for HOXA-11, β1 integrin, FAK, CD44, and ECM1. HOXA-11 and β1 Integrin expression changes were similar between the RIF and control groups. However, FAK expression was significantly increased in the RIF group (p<0.01). Additionally, ECM1 and CD44 expressions were significantly decreased in the RIF group compared with the control group (p<0.01). There was no significant difference in the endometrial staining of HOXA-11, FAK, and ECM1 in patients with a history of RPL. However, β1 Integrin and CD44 levels were significantly decreased in the RPL group compared with the control group (p<0.05). Implantation is a complex process, and altered adhesion mechanisms involved in endometrial receptivity may be related to defective implantation in patients with RIF and RPL. Among the adhesion molecules, the expression of CD44, β1 integrin, FAK, and ECM1 molecules varies in inappropriate implantation compared with the normal population.

Chronic endometritis (CE) is a localized and persistent inflammatory disorder of the endometrial lining that is most often triggered by alterations in the uterine cavity microbiota that induce low-grade inflammation. 1 Although its causal relationship with infertility remains debated, numerous studies have reported that the presence of CE can adversely affect reproductive outcomes, particularly reducing in vitro fertilization (IVF) success rates. 2 Clinical manifestations of CE are frequently subtle or absent. Although some patients may present with nonspecific symptoms such as pelvic pain, abnormal uterine bleeding, or leukorrhea, most remain asymptomatic. 3 The diagnosis of CE traditionally relies on the histopathological identification of stromal plasma cells; however, hysteroscopic diagnostic criteria have also been proposed. 4,5 Despite these developments, discrepancies between hysteroscopic findings and histopathological confirmation remain common. 3 The lack of distinctive clinical signs and standardized diagnostic criteria continues to make CE a challenging condition identify in daily practice. Given the increasing recognition of CE, particularly among women undergoing IVF, there is a growing need for rapid, inexpensive, and reliable diagnostic tools that can facilitate early detection and treatment. 6

This study aimed to evaluate the effects of astaxanthin on ovarian reserve, histopathological injury, oocyte maturation, fertilization, and early embryo development in rat models of ovarian ischemia and ischemia–reperfusion. In this randomized controlled experimental study, 48 adult female Sprague–Dawley rats were equally allocated to six groups undergoing sham surgery, ischemia, or ischemia–reperfusion, with or without intraperitoneal astaxanthin administration. Two male rats were used for in vitro fertilization. Following ovarian hyperstimulation, serum anti-Müllerian hormone (AMH) concentrations, ovarian histopathology, Caspase-3 expression, oocyte maturation, fertilization, and embryo development were evaluated. Astaxanthin significantly increased total and metaphase II oocyte counts, fertilized oocytes, and two-cell embryos in both ischemia and ischemia–reperfusion groups, as well as Grade 1 embryos in the ischemia–reperfusion group. Astaxanthin also reduced hemorrhage, edema, necrotic cell damage, inflammatory cell infiltration, and Caspase-3 expression. Furthermore, astaxanthin attenuated the injury-associated decline in serum AMH concentrations. No significant reproductive or histopathological changes were observed in astaxanthin-treated sham-operated rats. Astaxanthin administered before torsion or detorsion improved reproductive outcomes and reduced ovarian tissue injury, suggesting a protective effect that warrants further investigation before clinical translation.

Background: The cause of implantation defects in patients with recurrent implantation failure (RIF) and recurrent pregnancy loss (RPL) has not been clearly established. We aimed to evaluate the immunohistochemical changes of HOXA-11, β1 integrin, Focal Adhesion Kinase (FAK), CD44, and Extracellular Matrix Protein 1 (ECM1) in the endometrium of patients with defective implantation -RIF and RPL- in the receptive period. Methods: This retrospective case-control study was conducted in a university hospital. After the exclusion of all cases with pathology that may cause a change in the level of receptors in the endometrium, biopsies taken during the receptive period were selected, and the patients were divided into RPL (n=15), RIF (n=16), and control (n=16) groups. All preparations were immunohistochemically stained for HOXA11, β1 integrin, FAK, CD44, and ECM1. The presence or absence of staining and staining intensity were compared between groups. Results: When the RIF group was compared with the control group, there was no significant difference in HOXA-11 and β1 Integrin expression (p>0.05), FAK expression was significantly increased compared to the control group (p<0.01); ECM1 and CD44 expressions were found to be significantly decreased (p0.05); β1 Integrin and CD44 levels were significantly decreased (p<0.05). Conclusion: CD44 reduction may play a role in pathophysiology in both patient groups. In addition, decreased β1 integrin may also play a role in RPL. In RIF, the increase in FAK and decrease in ECM1 seem to be involved in the mechanisms of the disease.