Hormones and Inflammation: An Update on Endometriosis

Abstract

Endometriosis is a complex inflammatory, hormone-dependent disease that affects up to 10% of women in reproductive age, causing pain and infertility. Although the pathogenesis of this disease remains unknown, in the most recent decades, there has been a substantial progress toward unraveling the enigma associated with this disorder. The present chapter focuses on the influence of hormonal, immunological, and inflammatory pathways in the pathogenesis of endometriosis. The disease is characterized by an increased estrogen activity, which stimulates both eutopic and ectopic endometrial tissue proliferation; in addition, an aberrant response to progesterone, named progesterone resistance, has been shown. Stress hormones are involved in endometriosis pathogenesis. In the present chapter, the relevance of several key points in the inflammatory dysregulation contributing to endometriosis onset and progression, and related symptoms, will also be discussed. Immunological factors (cytokines, chemokines, and prostaglandins) as well as cell-mediated mechanisms play a major role in endometriosis-associated pain. Aberrant hormonal and inflammatory pathways contribute also to inflammatory comorbidities and adverse pregnancy outcome.