Current concepts of the pathogenesis of endometriosis
#MMPMID29699325
Osuga Y
Reprod Med Biol
2010[Mar]; 9
(1
): 1-7
PMID29699325
show ga
Endometriosis is a disease that causes the health of women of reproductive age to
deteriorate. The implantation theory is the most widely accepted pathogenesis of
the disease, although many points remain poorly understood concerning this
theory. According to this theory, regurgitated endometrial debris has to go
through various sequential events for the disease to develop. Recent studies have
elucidated several aspects of these events. A remarkably reduced gene expression
of GnRH II and an increase in uterine contraction-induced IL-8 secretion are
suggested to be pathogenic changes in the eutopic endometrium of women with
endometriosis. An increased level of osteoprotegerin in the peritoneal fluid of
women with endometriosis is suggested to impede tumor necrosis factor
(TNF)-related apoptosis-inducing ligand (TRAIL)-induced apoptosis of
endometriotic cells. An increase in the concentration of hepatocyte growth factor
and a decrease in the concentration of interferon gamma-inducible protein-10 in
the peritoneal fluid of women with endometriosis may stimulate the angiogenesis
and development of endometriosis. Midkine, the concentration of which is very
high in the follicular fluid of the ovary, may stimulate the growth of
endometriosis at the time of ovulation. Immune cells, such as macrophages,
lymphocytes, mast cells, and neutrophils, in endometriotic lesions are suggested
to play important roles in the progression of the disease. For example, IL-4 from
Th2 cells, IL-17 from Th17 cells, tryptase from mast cells, and some serine
proteases from neutrophils have been shown to stimulate endometriotic stromal
cells, suggesting their specific roles in endometriosis. Interestingly,
adiponectin, a key factor in metabolism, also appears to be involved in the
pathogenesis of endometriosis. These novel findings sustain the current
understanding of the pathogenesis of endometriosis.
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