Endometriosis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2]

Overview

The exact pathogenesis of endometriosis is not clear and several theories have made an attempt to describe the pathogenesis. Sampson theory of retrograde menstruation, coelomic metaplasia theory, lymphatic and vascular dissemination theory explain the implantation and invasion of the endometrial tissue outside the uterine cavity. Immunologic factors and genetic factors are also thought play a role in the pathogenesis of endometriosis.

Pathophysiology

Pathogenesis

Translocation of the endometrial cells

The exact pathogenesis of endometriosis is still unknown, however several theories were put forward to explain the the presence the of viable and hormonally active endometrium outside the uterine cavity. The theories proposed include the following:[1][2][3][4][5]

  • Sampson's theory of retrograde menstruation
    • The theory postulates that the viable endometrial tissue passes in a retrograde fashion via the fallopian tubes to reach the peritoneal cavity and subsequently implants onto the pelvic structures and organs.
    • Factors favoring the theory include the higher risk of developing endometriosis in patients with cervical stenosis and congenital outflow obstructions which result in a greater retrograde efflux, and resulting in the implantation of endometrial tissue in the peritoneal cavity.
    • This theory, however, doesn't explain the disease process in premenarchal girls and new borns.[6]
  • Coelomic metaplasia theory
  • Embryonic rest theory
  • The stem cell theory:

Implantation of the endometrial cells

Invasion and growth of the endometrial cells

Proliferation of the endometrial cells

Commonly affected sites in endometriosis

Genetics

Associated Conditions

Endometriosis is associated with an increased risk of developing ovarian cancer.[17][18]

Gross Pathology

  • The gross appearance of the lesions depend on the site, activity, day of the menstrual cycle, duration of the disease, and the presence of fibrosis.
  • On laparoscopy, endometriosis affecting the pelvic organs appears as raised dark non hemorrhagic lesions. They can also appear brown, black, white, yellow, pink or clear lesions based on the amount of blood supply.
  • Endometriosis of the ovary appears as a dark necrotic tissue and is coined as "chocolate cyst".
  • Extensive endometriosis can result in fibrosis of the pelvic structures which can be visualized on abdominal laparoscopy.

Microscopic Pathology

References

  1. Bulun, Serdar E. (2009). "Endometriosis". New England Journal of Medicine. 360 (3): 268–279. doi:10.1056/NEJMra0804690. ISSN 0028-4793.
  2. Greene AD, Lang SA, Kendziorski JA, Sroga-Rios JM, Herzog TJ, Burns KA (2016). "Endometriosis: where are we and where are we going?". Reproduction. 152 (3): R63–78. doi:10.1530/REP-16-0052. PMC 4958554. PMID 27165051.
  3. Nothnick W, Alali Z (2016). "Recent advances in the understanding of endometriosis: the role of inflammatory mediators in disease pathogenesis and treatment". F1000Res. 5. doi:10.12688/f1000research.7504.1. PMC 4760268. PMID 26949527.
  4. Begum T, Chowdhury SR (2013). "Aetiology and pathogenesis of endometriosis - a review". Mymensingh Med J. 22 (1): 218–21. PMID 23416836.
  5. Benagiano G, Habiba M, Brosens I (2012). "The pathophysiology of uterine adenomyosis: an update". Fertil Steril. 98 (3): 572–9. doi:10.1016/j.fertnstert.2012.06.044. PMID 22819188.
  6. Templeman C (2009). "Adolescent endometriosis". Obstet Gynecol Clin North Am. 36 (1): 177–85. doi:10.1016/j.ogc.2008.12.005. PMID 19344855.
  7. Smarr MM, Kannan K, Buck Louis GM (2016). "Endocrine disrupting chemicals and endometriosis". Fertil Steril. 106 (4): 959–66. doi:10.1016/j.fertnstert.2016.06.034. PMID 27424048.
  8. Patel S (2017). "Disruption of aromatase homeostasis as the cause of a multiplicity of ailments: A comprehensive review". J Steroid Biochem Mol Biol. 168: 19–25. doi:10.1016/j.jsbmb.2017.01.009. PMID 28109841.
  9. Fritel X (2007). "[Endometriosis anatomoclinical entities]". J Gynecol Obstet Biol Reprod (Paris). 36 (2): 113–8. doi:10.1016/j.jgyn.2006.12.003. PMID 17275210.
  10. Park HM, Lee SS, Eom DW, Kang GH, Yi SW, Sohn WS (2009). "Endometrioid adenocarcinoma arising from endometriosis of the uterine cervix: a case report". J Korean Med Sci. 24 (4): 767–71. doi:10.3346/jkms.2009.24.4.767. PMC 2719211. PMID 19654969.
  11. Hernández-Ramírez DA, Cravioto-Villanueva A, Barragan-Rincón A (2008). "[Rectal endometriosis: entity difficult to diagnose.]". Rev Gastroenterol Mex. 73 (3): 159–62. PMID 19671503.
  12. Collins AM, Power KT, Gaughan B, Hill AD, Kneafsey B (2009). "Abdominal wall reconstruction for a large caesarean scar endometrioma". Surgeon. 7 (4): 252–3. PMID 19736896.
  13. Chung MK, Jarnagin B (2009). "Early identification of interstitial cystitis may avoid unnecessary hysterectomy". JSLS. 13 (3): 350–7. PMC 3015962. PMID 19793476.
  14. Dirim A, Celikkaya S, Aygun C, Caylak B (2009). "Renal endometriosis presenting with a giant subcapsular hematoma: case report". Fertil Steril. 92 (1): 391.e5–7. doi:10.1016/j.fertnstert.2009.04.013. PMID 19476941.
  15. Fan W, Huang Z, Xiao Z, Li S, Ma Q (2016). "The cytochrome P4501A1 gene polymorphisms and endometriosis: a meta-analysis". J Assist Reprod Genet. 33 (10): 1373–1383. doi:10.1007/s10815-016-0783-4. PMC 5065559. PMID 27525656.
  16. Blakemore J, Naftolin F (2016). "Aromatase: Contributions to Physiology and Disease in Women and Men". Physiology (Bethesda). 31 (4): 258–69. doi:10.1152/physiol.00054.2015. PMID 27252161.
  17. Thomsen LH, Schnack TH, Buchardi K, Hummelshoj L, Missmer SA, Forman A; et al. (2017). "Risk factors of epithelial ovarian carcinomas among women with endometriosis: a systematic review". Acta Obstet Gynecol Scand. 96 (6): 761–778. doi:10.1111/aogs.13010. PMID 27565819.
  18. Lassus H, Pasanen A, Bützow R (2015). "[Is endometriosis a premalignant condition to ovarian carcinoma?]". Duodecim. 131 (19): 1777–84. PMID 26638662.