Endometriosis pathophysiology: Difference between revisions

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==Overview==
==Overview==
The exact [[pathogenesis]] of [[endometriosis]] is not clear and several theories exist regarding it. The Sampson theory of retrograde [[menstruation]], the coelomic [[metaplasia]] theory, and the [[lymphatic]] and [[vascular]] dissemination theory explain the implantation and invasion of the [[Endometrium|endometrial tissue]] outside the [[uterine cavity]]. [[Immunological|Immunologic]] factors and [[genetic]] factors are also thought to play a role in the pathogenesis of [[endometriosis]].
The exact [[pathogenesis]] of [[endometriosis]] is not clear; several theories have been set forth. The Sampson theory of retrograde [[menstruation]], the coelomic [[metaplasia]] theory, and the [[lymphatic]] and [[vascular]] dissemination theory explain the implantation and invasion of the [[Endometrium|endometrial tissue]] outside the [[uterine cavity]]. [[Immunological|Immunologic]] factors and [[genetic]] factors are also thought to play a role in the pathogenesis of [[endometriosis]].


==Pathophysiology==
==Pathophysiology==
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====Invasion and growth of the endometrial cells====
====Invasion and growth of the endometrial cells====
*The [[Endometrium|endometrial]] glandular cells are involved in the process of invasion.<ref name="pmid27424048">{{cite journal| author=Smarr MM, Kannan K, Buck Louis GM| title=Endocrine disrupting chemicals and endometriosis. | journal=Fertil Steril | year= 2016 | volume= 106 | issue= 4 | pages= 959-66 | pmid=27424048 | doi=10.1016/j.fertnstert.2016.06.034 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27424048  }} </ref>
*The [[Endometrium|endometrial]] glandular cells are involved in the process of invasion.<ref name="pmid27424048">{{cite journal| author=Smarr MM, Kannan K, Buck Louis GM| title=Endocrine disrupting chemicals and endometriosis. | journal=Fertil Steril | year= 2016 | volume= 106 | issue= 4 | pages= 959-66 | pmid=27424048 | doi=10.1016/j.fertnstert.2016.06.034 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27424048  }} </ref>
*Degradation of the [[extracellular matrix]] due to the increased [[proteolytic]] activity allows the invasion of the [[Endometrium|endometrial]] cells.
*Degradation of the [[extracellular matrix]] due to the increased [[proteolytic]] activity allows for invasion of the [[Endometrium|endometrial]] cells.
*Numerous [[Proteases|metalloproteases]] and [[plasmin]] help in the degradation of the [[extracellular matrix]] and in the establishment of an endometrial [[lesion]] outside the [[uterine cavity]].
*Numerous [[Proteases|metalloproteases]] and [[plasmin]] facilitate the degradation of the [[extracellular matrix]] and the establishment of an endometrial [[lesion]] outside the [[uterine cavity]].


====Proliferation of the endometrial cells====
====Proliferation of the endometrial cells====
*The functional [[endometrium]] in the [[uterine cavity]] proliferates in response to the increase in [[estrogen]] levels. The [[estrogen]] levels are dependent on the [[aromatase]] activity which catalyzes the conversion of ovarian [[androstenedione]] into [[estrone]].<ref name="pmid28109841">{{cite journal| author=Patel S| title=Disruption of aromatase homeostasis as the cause of a multiplicity of ailments: A comprehensive review. | journal=J Steroid Biochem Mol Biol | year= 2017 | volume= 168 | issue=  | pages= 19-25 | pmid=28109841 | doi=10.1016/j.jsbmb.2017.01.009 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28109841  }} </ref>
*The functional [[endometrium]] in the [[uterine cavity]] proliferates in response to increased [[estrogen]] levels. The [[estrogen]] levels are dependent on the [[aromatase]] activity which catalyzes the conversion of ovarian [[androstenedione]] into [[estrone]].<ref name="pmid28109841">{{cite journal| author=Patel S| title=Disruption of aromatase homeostasis as the cause of a multiplicity of ailments: A comprehensive review. | journal=J Steroid Biochem Mol Biol | year= 2017 | volume= 168 | issue=  | pages= 19-25 | pmid=28109841 | doi=10.1016/j.jsbmb.2017.01.009 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28109841  }} </ref>
*[[Endometrial]] cells in patients with [[endometriosis]] have increased levels of [[aromatase]], leading to increased [[estrogen]] levels, resulting in excess proliferation.  
*[[Endometrial]] cells in patients with [[endometriosis]] have increased levels of [[aromatase]], leading to increased [[estrogen]] levels, resulting in excess proliferation.  
*[[Endometrial]] cells also have resistance to [[progesterone]] which controls the [[proliferation]] of the endometrial cells. [[Progesterone]] resistance results in uncontrolled proliferation.  
*[[Endometrial]] cells also have resistance to [[progesterone]] which controls the [[proliferation]] of the endometrial cells. [[Progesterone]] resistance results in uncontrolled proliferation.  

Latest revision as of 12:11, 17 August 2017

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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; several theories have been set forth. The Sampson theory of retrograde menstruation, the coelomic metaplasia theory, and the 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 to 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 have been put forward to explain the presence of viable and hormonally active endometrium outside the uterine cavity. These proposed theories are:[1][2][3][4][5]

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

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.