Apoptosis has been implicated in the pathogenesis of several diseases and i
s partly regulated by bcl-2, which blocks the apoptotic pathway and promote
s cell survival, Apoptosis and bcl-2 expression were examined in paired eut
opic and ectopic endometrium from women with endometriosis (n = 30 samples)
or adenomyosis (a 15 samples) and compared with control endometrium (n = 3
0 samples). Apoptotic cells were detected using the dUTP nick-end labelling
(TUNEL) assay for DNA fragmentation; bcl-2 expression was demonstrated wit
h a streptavidin-biotin peroxidase immunohistochemical technique. Apoptotic
cells were rare in eutopic, ectopic and control endometrium; there were no
significant differences between subject groups nor between eutopic and ect
opic endometrium, Stromal bcl-2 expression increased in the late secretory
phase in control and eutopic endometriun in endometriosis; double labelling
studies revealed that most stromal bcl-2+ cells were leukocytes. Stromal b
cl-2 expression in endometriotic foci was significantly increased compared
with the paired eutopic endometrium, did not vary with menstrual cycle and
included a significant population of non-leukocytic bcl-2+ stromal cells, I
n contrast, stromal bcl-2 expression in adenomyosis remained at low levels
and did not show significant cyclical variation. Glandular epithelial bcl-2
expression also varied with menstrual cycle phase and peaked in the prolif
erative phase; in contrast, surface epithelial bcl-2 expression increased i
n the late secretory phase, Elevated stromal bcl-2 expression in ovarian en
dometriotic lesions could have implications for the growth and survival of
ectopic endometrial tissue at these sites.