SCIENCE BEHIND HER PAIN

A quick refresher on the science behind endometriosis pain.

In endometriosis, estrogen-dependent endometriotic cells and tissues reside outside the endometrial cavity, primarily on the peritoneum, ovaries, rectovaginal septum, and uterosacral ligaments.1-4

Lesions Outside the Endometrial Cavity4,5

In endometriosis, estrogen-dependent endometriotic cells and tissues reside outside the endometrial cavity, primarily on the peritoneum, ovaries, rectovaginal septum, and uterosacral ligaments.

By promoting the proliferation of endometriotic lesions and inflammation throughout the pelvic and abdominal cavity, estrogen fuels the

3 types of endometriosis pain1,3,6-9:

  • Dysmenorrhea
  • Non-menstrual pelvic pain
  • Dyspareunia

Estradiol also specifically fuels these types of pain through its effects on the endometriotic tissue7:

  • Estradiol induces COX-2, which increases production of prostaglandin E2 (PGE2)
  • PGE2 directly causes pain and inflammation
  • PGE2 in turn leads to increased aromatase, resulting in increased local estradiol production

Thus, a positive feedback loop is created.


Estradiol specifically fuels several types of pain through its effects on the endometriotic tissue. Understand the positive loop of feedback created by it.

Given the key role estrogen plays in endometriosis pain, an effective treatment strategy may need to10:

  • Suppress menses
  • Adequately control estrogen levels throughout ovulatory cycle
Common therapeutic approaches to treating endometriosis pain.

Common Therapeutic Approaches to Treating Endometriosis Pain

LEARN MORE
Help your patients learn by downloading a “how endometriosis works” flashcard. Help your patients learn by downloading a “how endometriosis works” flashcard.

Download a How Endometriosis Works Flashcard

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See How Dr. Zev Williams Manages Endometriosis.

See how Dr. Zev Williams Manages Endometriosis

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References:

  1. Burney RO, Giudice LC. Pathogenesis and pathophysiology of endometriosis. Fertil Steril. 2012;98(3):511-519.
  2. Giudice LC. Clinical practice: endometriosis. N Engl J Med. 2010;362(25):2389-2398.
  3. Kitawaki J, Kado N, Ishihara H, Koshiba H, Kitaoka Y, Honjo H. Endometriosis: the pathophysiology as an estrogen-dependent disease. J Steroid Biochem Mol Biol. 2002;83(1-5):149-155.
  4. Hesla JS, Rock JA. Endometriosis. In: Rock JA, Jones HW III, eds. Te Linde’s Operative Gynecology. 10th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:438-477.
  5. D’Hooghe TM. Endometriosis. In: Berek JS, ed. Berek & Novak's Gynecology. 15th ed. Philadelphia, PA: Lippincott Williams & Wilkins;2012:505-556.
  6. Practice Committee of the American Society for Reproductive Medicine. Treatment of pelvic pain associated with endometriosis: a committee opinion. Fertil Steril. 2014;101(4):927-935.
  7. Bulun SE. Mechanisms of disease: endometriosis. N Engl J Med. 2009;360(3):268-279.
  8. De Graaff AA, D’Hooghe TM, Dunselman GAJ, Dirksen CD, Hummelshoj L, WERF EndoCost Consortium, Simoens S. The significant effect of endometriosis on physical, mental and social wellbeing: results from an international cross-sectional survey. Hum Reprod. 2013;28(10):2677-2685.
  9. Bourdel N, Alves J, Pickering G, Ramilo I, Roman H, Canis M. Systemic review of endometriosis pain assessment: how to choose a scale? Hum Reprod Update. 2014;21(1):136-152.
  10. Endometriosis. In: Becker K. Principles and Practice of Endocrinology & Metabolism. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001. http://ovidsp.tx.ovid.com.proxy.cc.uic.edu/sp-3.20.0b/ovidweb.cgi. Accessed August 3, 2016.