Endometriosis – Pathogenesis & Complications

Described initially over three hundred years ago, Endometriosis is classically defined as the presence of endometrial glands and stroma in ectopic locations, primarily the pelvic peritoneum, ovaries, and rectovaginal septum, affecting 6-10% of women of reproductive age. The prevalence of this condition in women experiencing pain, infertility, or both is as high as 35-50%.

Pathogenesis is not fully understood; however, genetic predisposition and immunological changes have been reported to play a role.

Several hypotheses have been used to explain the various manifestations of the disease and its various locations.

1. The Retrograde Menstruation Theory

2. The Mullerian Metaplasia Theory

3. The Lymphatic Spread Theory

4. The Hematogenous Spread Theory

1. The Retrograde Menstruation Theory of Sampson Proposes that endometrial fragments shed during menstruation are transported through the fallopian tubes, then implanted and grown in growing intra-abdominal sites. (These endometrial fragments are viable and capable of producing in vivo and in vitro) Though retrograde menstruation explains the physical displacement of endometrial fragments into the peritoneal cavity, additional steps are necessary to develop endometriosis implants. Escape from immune clearance, attachment to the peritoneal epithelium, invasion of the epithelium, the establishment of local neurovascular continued growth, and survival are necessary if endometriosis is to dev develops the retrograde passage. Collectively, investigations involving the pathophysiology of endometriosis have revealed several well-supported molecular hallmarks of this disease:

• Genetic predisposition

• Estrogen dependence

• Progesterone resistance

• Inflammation

2. The Mullerian Metaplasia Theory of Meyer: Proposes that endometriosis results from the metaplastic transformation of peritoneal mesothelium to endometrium under the influence of certain unidentified stimuli.

3. The Lymphatic Spread Theory of Halban: Suggests that the lymphatics draining the uterus transport endometrial tissue to the various sites site where it grows ectopically.

4. The Haematogenous Spread Theory: Explains the presence of endometrial tissue in distant sites (lung, villa, and forehead).

Endometriosis is sensitive to ovarian hormones, and estrogen causes proliferation.

Regression of corpus luteum and removal of estrogen and progesterone causes the debris to induce a profound inflammatory response that causes significant pain and long long-terrorism—microscopical appearance depends on site, size, time since implantation and day of birth the menstrual cycle.

Colour is a good indicator and is determined by the vascularity of the lesion, the presence of fibrosis, the size of the lesions, and the presence of residual sloughed material.

It varies from red, brown, black, white and yellow.

Newer implant blood-filled active lesions.

Older lesions: Scarred with a puckered appearance.

Microscopically 2 out of 4 must be present in the biopsied specimen

1. Endometrial epithelium

2. Endometrial glands

3. Endometrial stroma

4. Hemosiderin laden macrophages

Many patients are asymptomatic. Others usually have no positive signs on examination.