Embryo implantation is a critical and complex process that requires coordination between the embryo and the receptive endometrium for its success. However, a multitude of factors have the potential to contribute to implantation failure. Among these factors, bacterial infections in the uterine environment are of particular concern and are increasingly being considered as a contributing factor to implantation failure. The presence of pathogenic bacteria has been demonstrated to stimulate inflammatory responses, alter the endometrial microbiome, interfere with critical signaling pathways, and finally change the uterus microenvironments that are required for implantation. We aimed to review bacterial infection as an important potential etiology of chronic endometritis pathophysiology and its correlation with implantation failure.

Male fertility is primarily assessed using descriptive semen parameters, such as sperm concentration, motility and morphology. These conventional parameters provide an initial assessment of male reproductive health and may explain why a couple is struggling to conceive; however, they are not a direct measure of fertility potential. Growing evidence suggests that spermatozoa transmit far more than paternal DNA. Alongside the genome, spermatozoa deliver proteins, RNA and epigenetic information that are responsive to environmental and lifestyle exposures, and can influence embryo development, pregnancy outcomes and offspring health. This emerging concept challenges the view that male fertility is defined solely by successful conception. Here, we discuss evidence that spermatozoa act as carriers of environmental and lifestyle 'memories', transmitting molecular information shaped by paternal health to the next generation. We further consider the implications for assisted reproductive technologies, which select spermatozoa largely on their capacity to move while overlooking the molecular cargo they transmit. Recognising spermatozoa as vectors of environmental information reframes male fertility and highlights the need for biomarkers that assess molecular integrity alongside conventional clinical parameters.

During oocyte growth, substantial epigenetic programming occurs to establish a distinctive epigenome including appropriately patterned DNA methylation and histone modifications. Oocyte epigenetic programming must be tightly spatiotemporally regulated to ensure that a wide variety of epigenetic modifiers correctly establish their respective modifications to mediate precise control of gene expression. Furthermore, epigenetic modifications in oocytes include canonical and non-canonical genomic imprints, which are transmitted through meiosis to offspring. Significantly, disruptions in oocyte epigenetic programming can cause aberrant developmental outcomes in the next generation mediated by altered imprinting. Polycomb repressive complex 2 is an important epigenetic modifier that establishes histone 3 lysine 27 trimethylation and non-canonical imprints during mouse oogenesis, which are important for normal offspring development. While it is widely recognised that altered oocyte epigenetic programming can disrupt offspring development, mechanisms controlling maternal epigenetic inheritance remain poorly understood. The possibility remains that non-canonical imprinting exists in humans, although this requires confirmation. This review discusses mouse and human oocyte epigenetic programming including interactions between various epigenetic modifiers and modifications that form the unique oocyte epigenome. Understanding how oocyte epigenetic programming is regulated will be crucial in discerning how changes to the oocyte epigenome can disrupt epigenetic memory and alter developmental outcomes in offspring.

Endocrine-disrupting chemicals (EDCs) are ubiquitous environmental contaminants that interfere with hormone signalling and are increasingly linked to adverse reproductive outcomes. This viewpoint highlights emerging evidence that EDC exposure disrupts both endometrial and placental function, contributing to disorders including endometriosis, endometrial cancer, pre-eclampsia, fetal growth restriction and preterm birth. We discuss the biological mechanisms underpinning these associations and the growing epidemiological evidence implicating EDCs in reproductive disease. Greater awareness, improved exposure assessment and continued translational research are needed to better understand the consequences of EDC exposure on the endometrium and reproductive health in order to inform strategies that reduce disease burden.