The molecular signalling pathways, the ultrastructural changes governing endometrial receptivity are only partially known. Asynchronous development of the endometrium in some subfertile women may account for the failure of the embryo to implant during the highly controlled implantation window. An abnormal hormonal milieu, such as the one resulting from controlled ovarian hyperstimulation or an underlying disease like endometriosis, may alter the mechanisms involved in implantation and early pregnancy. Endometriosis, one of the most common causes of infertility and chronic pelvic pain, affects about 10% of women in the reproductive-age group, with this number increasing to 30% in patients with infertility and up to 45% in patients with chronic pelvic pain. It is defined as the extrauterine growth of endometrial glandular epithelial and stromal cells, with the lesions developing on pelvic peritoneal and visceral surfaces. The mechanisms by which endometriosis impairs fertility are varied, from distortion of pelvic anatomy to negative effects on implantation. Postulated mediating factors include local paracrine action of cytokines, alteration in inflammatory responses and/or autoimmune influences. Owing to the increased prevalence of endometriosis in subfertile women, many studies have focused on the development, growth and structure of these lesions. But, to date, little is known about the structural changes that might be present in the eutopic endometrium of women with this disease. Here, we describe the current literature pertaining to such anomalies and also describe findings from our own recently published investigations on endometrial ultrastructure and glycosylation in women with endometriosis.