In studying the pathogenesis of ovarian and other forms of peritoneal endometriosis,
one must not lose sight of the important role evidently played by patency of the tubes.
At times, during menstruation, blood, carrying bits of Müllerian mucosa, escapes through
patent tubes into the peritoneal cavity. This blood may come either from the uterine
or from the tubal mucosa. Circumstantial evidence indicates that Müllerian tissue
in this blood, under favorable conditions, becomes implanted on any structure upon
which it may lodge. These early primary implants occur most frequently in close proximity
to the distal ends of the tubes, such as the lateral and under surfaces of the ovary,
the lower portions of the posterior surfaces of the uterus and broad ligaments, and
the bottom of the cul-de-sac. They may be present only on the ovary or ovaries, only
on the peritoneum, or in both situations. Some of these implants remain small and
superficial. The Müllerian mucosa in others invades its host much like implantation
carcinoma. When it invades other organs or structures than the ovary, a type of endometriosis
arises which both grossly and histologically often closely resembles a direct endometriosis
of the uterine wall.
The invasion of the ovary by Müllerian mucosa implanted on its surface and the conditions
resulting from it are in many ways similar to those arising from the invasion of the
other organs and structures by this tissue except for one very striking difference.
The ectopic endometrial cavities distended with menstrual blood in endometriosis,
in other situations than the ovary, are usually small while those in the ovary frequently
attain a large size, forming the well-known endometrial cysts of that organ. Whether
small or large these ovarian cysts often rupture and some of their contents escapes
into the peritoneal cavity frequently causing adhesions, and, under favorable conditions,
the judged peritoneal implantation of bits of the epithelial lining of the cyst which
had been cast off by menstruation. In patients with peritoneal endometriosis associated
with an endometrial cyst of the ovary, both primary implants from or through the tubes
and secondary ones from the cyst may be present.
The study of peritoneal endometriosis also indicates that menstrual blood may not
only escape from foci of endometriosis in other situations than the ovary, but adhesions
and an additional spread of the endometriosis (secondary implants) may arise from
this source. On account of the usual small size of the superficial foci of serosal
endometriosis, the results of their participation in menstruation are not as striking
as those which take place in the ovarian cysts.
If bits of Müllerian mucosa carried by menstrual blood escaping into the peritoneal
cavity are always dead, the implantation theory, as presented by me, also is dead
and should be buried and forgotten. If some of these bits are even occasionally alive,
the implantation theory also is alive.
The viability of this theory is of secondary importance to me as compared with the
pleasure and the increased knowledge of this and kindred subjects which I have gained
in these studies and the resulting more intelligent treatment of patients who have
peritoneal endometriosis. There are many other interesting unsolved problems associated
with the pathogenesis and life history of endometriosis of all types. Since it is
my desire to adhere strictly to the text which has been assigned me, I have not discussed
any of these.