Endometriosis pathophysiology: Difference between revisions
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==Pathophysiology== | ==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: | 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: | ||
*'''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. | *'''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 also the implantation of endometrial tissue in the peritoneal cavity resulted in the disease. | **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 also the implantation of endometrial tissue in the peritoneal cavity resulted in the disease. | ||
**This theory, however, doesn't explain the disease process in premenarchal girls and new borns. | **This theory, however, doesn't explain the disease process in premenarchal girls and new borns. | ||
*'''Coelomic metaplasia theory:''' This theory postulates that endometriosis is a result of metaplasia of the cells lining the visceral and abdominal peritoneum following various hormonal, environmental, or infectious stimuli. | *'''Coelomic metaplasia theory:''' This theory postulates that endometriosis is a result of metaplasia of the cells lining the visceral and abdominal peritoneum following various hormonal, environmental, or infectious stimuli. This theory is supported by the evidence that the abdominal, pelvic, and thoracic peritoneum, the Mullerian ducts, the germinal epithelium of the ovary and the endometrium are all derived from the coelomic wall epithelium explaining the occurrence of endometriosis at these sites. | ||
*'''Embryonic rest theory:''' This theory proposes that endometrial tissue arises from the cells remaining from Mullerian duct migration during embryonic development, following estrogen stimulation. | *'''Embryonic rest theory:''' This theory proposes that endometrial tissue arises from the cells remaining from Mullerian duct migration during embryonic development, following estrogen stimulation. | ||
*'''The stem cell theory:''' This theory is based on experimental evidence explaining the fact that the endometrial stem cells from the basalis layer and the bone marrow-derived stem cells can travel via the retrograde fashion or via the lymphatic or vascular system resulting in endometriosis. | |||
====Implantation and growth of the endometrial cells==== | |||
*The presence of endometrial cells alone outside the endometrial tissue doesn't cause endometriosis. The cells must attach to the surrounding tissues and be receptive to the harmonal changes of estrogen. This is facilitated by various factors which influence the disease process: | |||
**Eutopic endometrial in endometriosis are resistant to cell mediated immunity and have increased proliferative capacity | |||
**The ectopic endometrial increased aromatase expression, leading to increased estrogen concentrations, mediated by prostaglandin E2 | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 20:56, 13 June 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
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:
- 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 also the implantation of endometrial tissue in the peritoneal cavity resulted in the disease.
- This theory, however, doesn't explain the disease process in premenarchal girls and new borns.
- Coelomic metaplasia theory: This theory postulates that endometriosis is a result of metaplasia of the cells lining the visceral and abdominal peritoneum following various hormonal, environmental, or infectious stimuli. This theory is supported by the evidence that the abdominal, pelvic, and thoracic peritoneum, the Mullerian ducts, the germinal epithelium of the ovary and the endometrium are all derived from the coelomic wall epithelium explaining the occurrence of endometriosis at these sites.
- Embryonic rest theory: This theory proposes that endometrial tissue arises from the cells remaining from Mullerian duct migration during embryonic development, following estrogen stimulation.
- The stem cell theory: This theory is based on experimental evidence explaining the fact that the endometrial stem cells from the basalis layer and the bone marrow-derived stem cells can travel via the retrograde fashion or via the lymphatic or vascular system resulting in endometriosis.
Implantation and growth of the endometrial cells
- The presence of endometrial cells alone outside the endometrial tissue doesn't cause endometriosis. The cells must attach to the surrounding tissues and be receptive to the harmonal changes of estrogen. This is facilitated by various factors which influence the disease process:
- Eutopic endometrial in endometriosis are resistant to cell mediated immunity and have increased proliferative capacity
- The ectopic endometrial increased aromatase expression, leading to increased estrogen concentrations, mediated by prostaglandin E2