What causes Endometriosis?
The real cause of endometriosis remains unknown. The following
theories represent current thinking of the etiology of endometriosis,
but none of them can explains all cases of endometriosis. We do
know, however, that endometriosis is not caused by anything that
the patient has done.
This theory was proposed by Dr. John Sampson of Boston in the 1920’s.
His theory that menstrual blood refluxed through the fallopian tubes
and was deposited and grew on the pelvic peritoneum and pelvic organs
remains popular, but the initial attachment of single or multiple
endometrial cells on the peritoneal surface has not been demonstrated.
Additionally, the time-related geographic spread of endometriosis
throughout the pelvis that would be predicted to occur with repeated
seeding of the peritoneum by refluxed endometrium has not been demonstrated.
The fact that 90% of women have retrograde flow but only 15 % of
women develop endometriosis further repudiate the validity of the
theory. This theory of origin also implies that older age groups
of patients with endometriosis have more disease than younger age
group and a high and progressively increasing rate of recurrence
after complete surgical resection. The literature, however, as well
as our own experience has shown that the actual rate of persistent
or recurrent disease is surprisingly low after aggressive conservative
surgical excision at laparoscopy or laparotomy, and the rate of
recurrent or persistent disease does not appear to increase with
the passage of time following excision. Because of these deficits,
Sampson’s theory is losing favor to more modern concepts.
Theory of Embryonically Patterned Metaplasia or Rests
Metaplasia means a transformation from one type of tissue to another
type of tissue. During the embryonic stage, the primitive cells
migrate and undergo differentiation to form the pelvic organs. This
embryogenesis is controlled and directed by a sophisticated, but
still incompletely understood, fetal system. This fetal developmental
control system may be the fetal analog of the adult immune system.
If a developmental or heritable defect in this controlling system
exists, then differentiation and migration of cells may be aberrant
or incomplete. Cellular morphology and functionality might be expressed
overabundantly or inadequately. Such cells or tracts of cells are
laid down in the migratory pathway of fetal organogenesis (forming
the organs) across the posterior pelvic floor, although location
anywhere might be possible, depending on the degree of aberrant
differentiation or migration. These cells may be endometrium-like
initially, or may possess the ability to undergo metaplasia into
endometriosis after puberty. Arrest of migration across the posterior
pelvis would conveniently explain the observation that endometriosis
is most commonly and predictably found in the cul-de-sac, uterosacral
ligaments, and medial broad ligaments.
Abnormalities of the fetal development control system may be preserved
into adult life, giving rise to detectable abnormalities of the
adult immune system. The degree of residual abnormality of the adult
immune system may control the aggressiveness of the endometriosis
that develops, with the result that some patients may develop invasive
disease or adhesions, while most do not. The competence of the adult
immune system might be impaired by exposure to environmental toxins
(e.g. Dioxin), with endometriosis emerging as a possible result,
as occurs in experimental laboratory primates, and endometriosis
in male bladder or prostate in later life during estrogen treatment
of advanced prostate cancer.
Hematogenous metastasis of endometriosis
This theory has been proposed to explain remote occurrence of the
disease. According to this theory , exfoliated endometrial cells
are swept into the venous drainage of the uterus, with subsequent
deposition possible anywhere in the body. Venous blood draining
from the uterus must pass through the capillary bed to the lungs.
Therefore, hematogenous spread should also result in a high rate
of secondary pulmonary endometriosis unless there exists a high
rate of occurrence of atrial or ventricular septal defects exists,
among patients with extrapelvic endometriosis. Since neither pulmonary
endometriosis nor cardiac atrial or ventricular septal defects have
been reported to be more frequent in patients with endometriosis,
hematogenous spread remains speculative.
Theory of lymphatic spread
This theory has been supported by the finding of endometriosis in
lymph nodes, although the number of reported cases is quite small
compared with the number of women with endometriosis. Endometriosis
in lymph nodes, however, could plausibly be explained equally by
a developmental process that resulted in embryonic deposition of
endometriosis in lymph nodal tissue.
Multicenter studies conducted by Stephen Kennedy, M.D. Professor
at Oxford University show that first degree relatives of women with
endometriosis are more likely to develop endometriosis. And when
there is a hereditary link, the disease tends to be worse in the
next generation. Chattanooga Women’s Laser Center is one of
the participating study centers for the genetic predisposition factors