Endometriosis
may be generated by mimicking the ontogenetic development
of the female genital tract.
Researchers at Johann Wolfgang Goethe-University
in Frankfurt, Germany, suggest that endometriosis can
arise through metaplasia
The team set out to compare the expression of genes
playing a decisive role during the embryonic development
of the female genital tract (WNT4, WNT5A, WNT7A, PAX8)
in the peritoneum of patients with endometriosis and
control patients.
An experimental study was designed using real-time
polymerase chain reaction and in situ hybridization,
and included women with and without endometriosis undergoing
surgery for benign indications. The outcome was measured
in percentage of samples positive for gene expression
by using real-time polymerase chain reaction, as well
as relative expression values compared with housekeeping
genes. Confirmation of results by in situ hybridization.
The team was able to demonstrate that expression of
WNT7A and PAX8 was found in the normal peritoneum in
approximately half of the patients with endometriosis
in contrast to the controls. In patients with endometriosis
WNT7A and PAX8 in histologically normal peritoneum (with
no evidence of endometriosis, endosalpingiosis, or other
changes) were confirmed by in situ hybridization.
The expression of these genes in the normal peritoneum
suggests that endometriosis can arise through metaplasia
and can in the process make use of the developmental
steps involved in the embryonic development of the female
genital tract.
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