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This chapter should be cited as follows:
Marani ML, Evangelista BC, et al, Glob. libr. women's med.,
ISSN: 1756-2228; DOI 10.3843/GLOWM.420103

The Continuous Textbook of Women’s Medicine SeriesGynecology Module

Volume 8

Gynecological endoscopy

Volume Editors: Professor Alberto Mattei, Director Maternal and Child Department, USL Toscana Centro,Italy
Federica Perelli, Obstetrics and Gynecology Unit, Ospedale Santa Maria Annunziata, USL Toscana Centro, Firenze, Italy


Endometriosis: Pathogenesis and Tailored Approach

First published: March 2024

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Endometriosis is a chronic inflammatory condition characterized by the presence of functional endometrial glands and stroma outside the uterine cavity.1 The lesions are usually located in the uterus and ovaries, but they can also be found at other multiple sites including the bowel, bladder, and diaphragm.

Endometriosis is one of the most common benign gynecological conditions; affects 10–15% of reproductive-aged women;2 associated with pain symptoms and infertility; and negatively affects social, occupational, and psychological functioning.3


Endometriotic lesions typically contains endometrial glands and stroma. Lesions are frequently surrounded by fibrous tissue and can contain blood and cysts.4

Lesion phenotypes

Endometriotic lesions can be categorized as superficial, ovarian, and deep.4,5,6

Superficial lesions: These lesions are <5 mm in depth.7 They can be visually classified as red, black, or white.

Ovarian endometrioma: It is an ovarian endometriotic cyst that is often filled with chocolate-like fluid.8

Deep lesions: The lesions extend more than 5 mm deep to the peritoneum.4,9 They commonly affect the retrocervical region, rectosigmoid colon, bladder, ureter, and vagina.10


Endometriosis is defined as the presence of endometrial tissue in ectopic locations, primarily the pelvic peritoneum, ovaries, and rectovaginal septum. Affecting 6–10% of women of reproductive age, the symptoms of endometriosis include dysmenorrhea, dyspareunia, chronic pelvic pain, irregular uterine bleeding, and/or infertility.11

Several theories have arisen to account for the disparate observations regarding pathogenesis, and these can generally be divided as those proposing that implants orginate from uterine endometrium and those proposing that implants arise from tissues other than the uterus.12

The pathogenesis of endometriosis appears to be multifactorial and includes impaired immunity, imbalanced cell proliferation and apoptosis, and genetic factors.13,14,15 Theories for the development of endometriosis include retrograde menstruation; coelomic metaplasia; and immunological, genetic, environmental, and lifestyle factors.

Retrograde menstruation

The most widely accepted theory for the development of endometriosis is retrograde menstruation.8 In this theory (Sampson’s theory), during the menstrual cycle, the endometrial cells reach the peritoneal cavity by going backward through the fallopian tubes.16

The endometrial cells then attach to the peritoneal mesothelial cells, establish a blood supply, proliferate, and produce endometrial implants. Women with endometriosis have higher volumes of refluxed menstrual blood and endometrial-tissue fragments than women without the disorder.17

Evidence supporting this comes from the observation of a higher incidence of endometriosis in girls with Müllerian abnormalities and genital tract obstructions.18,19 However, while up to 90% of women have retrograde menstruation,20,21 only 10–15% of them will develop endometriosis, suggesting that additional factors are involved.5

Several of these factors may play a role, or specific disease subtypes may be due to specific underlying biological pathways. Published studies on these mechanisms are limited.21

Coelomic metaplasia

In the 1960s, Ferguson proposed that coelomic metaplasia may also contribute to the development of endometriosis.22 This theory suggests that mesothelial cells undergo differentiation into functional endometrium.23

Another theory argues that menstrual tissue travels from the endometrial cavity through lymphatic channels and veins to distant sites, which could attribute to implants found outside the pelvic cavity.22 This theory could explain the development of endometriosis in women with amenorrhea and extrapelvic endometriosis.24


Patients with endometriosis have dysfunctional immunological responses. Impaired macrophage activation and signaling may promote survival of ectopic endometrial cells.25,26 Also, women with endometriosis may present with decreased cytotoxicity to endometrial cells secondary to defective NK-cell activity.27

Once endometriosis develops, the immune system has also been shown to potentiate the development and increase the severity of the disease. In women with endometriosis there are increased numbers of leukocytes and macrophages in and around endometrial implants and in the peritoneal fluid. These cells secrete cytokines and growth factors (IL-1, 6 and 8, TNF, RANTES, VEGF) into the peritoneal milieu, which then recruit surrounding capillaries and leukocytes. The ultimate effect is proliferation of endometriosis implants with increased vascular supply.28,29,30

Moreover, increased inflammation and nerve fibers are involved in the genesis of endometriosis-related pain symptoms.31,32,33,34,35

Stem cells

It is presumed that de-novo development of endometrial tissue occurs from endogenous stem cells in the endometrium. Over the past decade, we have studied the possibility that bone marrow-derived cells may also differentiate into endometrial cells, and may be implicated in the development of ectopic endometrial implants.36 37 This would help explain how ectopic tissue can occur in locations outside the peritoneal cavity such as the lung and central nervous system.


For over 20 years it has been known that endometriosis has a familial tendency. Women who have a first-degree relative affected by the disease have a 7 times higher risk of developing endometriosis than women who do not have a family history of the disease.38

Müllerian embryonic rests

According to this theory, endometriosis would grow Müllerian embryonic rests, which could explain endometriosis in pre-menarche patients.39,40,41,42

The Müllerian remnants hypothesis explains endometrial-like tissue as having developed from differentiation and proliferation of embryonic cell rests that are constituted by misplaced cells of primitive endometrial tissue along the migratory pathway of Müllerian ducts.43,44

Environmental/lifestyle factors

Recent studies regarding dietary factors and lifestyle have suggested an association between these factors and susceptibility to developing endometriosis. They suggested that a diet high in fruits and vegetables and low in meat products is protective against the development of endometriosis. Additionally, women with a low body mass index are at a higher risk of developing endometriosis.45 In addition, epidemiologic studies have shown a higher risk of endometriosis in women whose mothers had a history of endometriosis, suggesting that genetic factors may be involved.46



While a large proportion of women with endometriosis may be asymptomatic, most report severe and progressive pain symptoms, including dysmenorrhea, non-cyclical chronic pelvic pain, deep dyspareunia, cyclic painful defecation, cyclic urinary pain, and other cyclic symptoms.47 However, the relationship between the severity of the condition and its symptoms has not been elucidated.

A diagnosis delay of 5–10 years is very common in healthcare settings because the symptomatology of endometriosis shows many commonalities with a wide range of diseases.48

Gynecological examination may suggest endometriosis, including focal tenderness and nodules at the uterosacral ligaments and posterior cul-de-sac, adnexal masses, and reduced mobility of the uterus. Vaginal lesions up to the mucosa can be visualized on specular examination.49,50 While physical examination findings may identify up to 80% of endometriosis compromising the retrocervical and rectosigmoid regions, the examination results can also be normal.

Imaging diagnostic

While imaging does not replace histological diagnosis, typical imaging findings make the diagnosis highly likely. In addition, imaging findings can help guide surgical planning.51,52,53,54,55,56

Transvaginal ultrasonography with bowel preparation and magnetic resonance imaging (MRI) are used to evaluate individuals with suspected endometriosis. Transvaginal ultrasonography is generally preferred because it is more readily available and costs less than MRI, although their sensitivity and specificity are comparable, particularly for rectovaginal endometriosis. However, the sensitivity and specificity of ultrasonography are dependent on the skill and experience of the sonographer.57

Biological markers

Many serum markers, including cancer antigen 125 (CA125), have been studied; however, they have poor sensitivity and specificity. Therefore, no blood test is currently available for the diagnosis of endometriosis.58

Recent studies on miRNA panels have shown promise as noninvasive diagnostic tests for endometriosis. Although an initial study reported a test sensitivity and specificity of >95%, this finding must be validated in further studies. Currently, miRNA tests are not available commercially.


Endometriosis treatment includes hormonal therapies that aim to inhibit the growth of endometriotic implants and surgical treatment to resect endometriotic implants.59,60 Nevertheless, patient preferences and plans for fertility must be considered during treatment planning.

Medical treatment

Owing to surgery-associated risks, recovery, and cost, medical treatment is recommended as the first-line therapy for endometriosis pain management. Current medical therapies include progestogen-only contraceptives, combined estrogen–progestogen contraceptives, gonadotropin-releasing hormone (GnRH) agonists and antagonists, and aromatase inhibitors.61,62,63,64

Women with infertility associated with endometriosis should not undergo hormone treatment because it does not improve fertility. The treatment of infertility may include a combination of surgery and assisted reproductive technology, depending on the pain symptoms and ovarian reserve.65 In addition, gamete cryopreservation should be performed before surgical treatment in patients with a low ovarian reserve.

Combined and progestogen-only contraceptives are recommended as the first-line treatment, following the World Health Organization medical eligibility criteria for contraception and women’s preferences. Pain control and side effects are comparable among the currently available hormones. After 3–4 months of treatment, symptoms and lesions should be reevaluated, and women with adequate symptom control and stable lesions should continue the hormonal therapy regimen until pregnancy is desired or the average age of menopause is reached.61,62,63,64

Treatment with a GnRH analog or antagonist can be an alternative, especially in patients with myomas or adenomyosis. Because of the severe side effects, GnRH therapies are usually used for a limited time.61,62,63,64

Treatment with aromatase inhibitors is reserved for women with refractory symptoms because of severe side effects; however, data on its long-term use are limited.66,67,68,69

Laparoscopic treatment should be recommended for patients with worsening or maintenance of pain symptoms, infertility, or worsening lesions.

Surgical treatment

Laparoscopic treatment of endometriosis is recommended in patients with severe pain symptoms, infertility with failure of reproductive treatment, lesions compromising the appendix, ileum, cecum, ureter with hydronephrosis, bowel lesions with sub-occlusive symptoms, or suspected ovarian malignancy.70

The surgical procedure must include a complete inspection of the sites affected by endometriosis, staging, and complete excision of lesions, preferably in a single surgery. Surgical intervention may be conservative (maintaining the uterus and ovaries) or definitive (hysterectomy and adnexectomy), depending on the woman’s childbearing plans and age. Adjuvant hormonal treatment after surgery, usually with continuous oral contraceptives, is recommended to prevent symptom recurrence.70

Surgery is associated with the risk of bowel and urinary injuries, reduction of ovarian reserve (especially if ovarian surgery is performed), bowel and urinary fistulas, adhesions, and other common surgical risks.51,63,70


  • Women with chronic pelvic pain, dysmenorrhea, dyspareunia, urinary symptoms, intestinal symptoms, or infertility must be evaluated for endometriosis.
  • The etiology of endometriosis is still not completely understood but might involve retrograde menstruation, celomic metaplasia, immunologic alterations, Müllerian embryonic rests, and environmental factors.
  • Physical examination may reveal abnormalities according to implant location but the findings may not always be significant.
  • Transvaginal ultrasonography with bowel preparation and magnetic resonance imaging are the preferred imaging modalities. To date, no diagnostic serum biomarkers exist, and laparoscopic surgery allows for definitive diagnosis and treatment.
  • Medical therapy is the first line of treatment, starting with combined or progestogen-only contraceptives. Gonadotropin-releasing hormone analogs and aromatase inhibitors may also be used under specific circumstances.
  • Surgery allows for the removal of lesions and might be indicated due to medical treatment failure and infertility (the latter, along with assisted reproduction techniques, because these women are not candidates for hormonal suppression). Uterine and ovarian preservation must be carefully weighed based on the woman’s reproductive plan and the characteristics of the lesion.
  • Endometriotic lesions compromising the appendix, ileum, cecum, ureter with hydronephrosis, bowel lesions with sub-occlusive symptoms, or suspected ovarian malignancy should be surgically removed.


The author(s) of this chapter declare that they have no interests that conflict with the contents of the chapter.



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