Abstract

Endometriosis (EM) and adenomyosis (AM) are common conditions with pain and infertility as the principal symptoms. The pathophysiology of pain in EM and AM comprises sensory and somatoform pain mechanisms. Over time, these may aggravate and lead to individual complex disease patterns if not diagnosed and treated. Despite the known facts, several years often pass between the onset of symptoms and diagnosis. Chronic pain disorders with changes on a neuronal level frequently arise and are linked to depressive disorders, with the process becoming a vicious cycle. Additionally, women with EM and AM suffer from sub- and infertility. Low fecundity rates are caused by anatomical changes in combination with behavioral changes in the sexual activity of women with chronic pain as well as local proinflammatory factors that not only decrease implantation rates but also promote early abortions.

Highlights

  • The disease is described as ectopic lesions on the peritoneum of the internal genital organs

  • It has been characterized as emigration of endometriotic lesions into the myometrium

  • Typical complaints caused by EM and AM are dysmenorrhea, cyclic and acyclic lower abdominal pain, cyclic dysuria, dyschezia, dyspareunia, as well as infertility

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Summary

Pathogenesis of Endometriotic Lesions

EM is defined by endometrial tissue-like lesions that occur outside the uterine cavity. The disease is described as ectopic lesions on the peritoneum of the internal genital organs (endometriosis genitalis externa). 10–15% of all women develop EM during their reproductive phase of life [3] Other factors such as the type of cells that are translocated into the abdominal cavity, the immune system, genetic and epigenetic processes, as well as environmental factors play a role [4,5]. The first experimental data in animal models show an alteration in disease progression by epigenetic modulation, a fact that could be used as a new treatment approach [34,35] Another still-experimental aspect is the analysis of EM-specific exosomes. The clinical impact of these findings is not yet clear and needs to be further evaluated

Pathophysiologic Origin of Pain
EM-Associated Pain
Principles of Pain Development
Pathogenesis of Specific Forms of Pain
Neurogenic Inflammation
Development of Central Sensitization with Spinal Hyperalgesia
Peritoneal Lesions and Peritoneal Fluid
Endometriomas and the Ovaries
AM and Fertility
Findings
Summary
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