Abstract
BACKGROUND: Endometriosis is a common inflammatory disease characterized by the presence of endometrial cells outside of the uterine cavity. Endometriosis affects 10% of women of reproductive age and significantly reduces their quality of life as a result of chronic pelvic pain and infertility. Biologic mechanisms, including persistent inflammation, immune dysfunction, and epigenetic modifications, have been proposed as the pathogenesis of endometriosis. In addition, endometriosis can potentially be associated with an increased risk of pelvic inflammatory disease (PID). Changes in the vaginal microbiota associated with bacterial vaginosis (BV) result in PID or a severe form of abscess formation, tubo-ovarian abscess (TOA). This review aims to summarize the pathophysiology of endometriosis and PID and to discuss whether endometriosis may predispose to PID and vice versa. METHODS: Papers published between 2000 and 2022 in the PubMed and Google Scholar databases were included. RESULTS: Available evidence supports that women with endometriosis are at increased risk of comorbid PID and vice versa, supporting that endometriosis and PID are likely to coexist. There is a bidirectional relationship between endometriosis and PID that shares a similar pathophysiology, which includes the distorted anatomy favorable to bacteria proliferation, hemorrhage from endometriotic lesions, alterations to the reproductive tract microbiome, and impaired immune response modulated by aberrant epigenetic processes. However, whether endometriosis predisposes to PID or vice versa has not been identified. CONCLUSIONS: This review summarizes our current understanding of the pathogenesis of endometriosis and PID and discusses the similarities between them.