Apoptosis in endometrial glandular and stromal cells in women with and without endometriosis.
BACKGROUND
The aetiology of endometriosis is unknown. Ectopic dissemination of the endometrial cells gives origin to endometriotic lesions, but occurs in women with and without endometriosis. It has been suggested that increased ectopic cell survival facilitates their implantation. The objectives of this study were to evaluate endometrial apoptosis in women with endometriosis according to: (i) cyclic changes, (ii) glandular and stromal contribution, and (iii) stage of the disease.


METHODS
The subjects were women undergoing diagnostic laparoscopy and endometrial biopsies for suspected endometriosis. Spontaneous apoptosis was evaluated using TdT-mediated dUTP-biotin nick end-labelling (TUNEL) assay. Apoptotic cells per 10 mm(2) (apoptotic index) in an area of 10-50 mm(2) in 5 microm endometrial tissue sections were counted and location of these cells was recorded.


RESULTS
The apoptotic index in glandular epithelium was lower in endometriosis than controls (26.0 +/- 5.5 versus 51.2 +/- 9.7, P = 0.03) but not in the stroma (36.3 +/- 6.4 versus 48.4 +/- 11.3, NS). In controls, apoptosis was highest during the late secretory/menstrual and early proliferative phases and cyclic variability was apparent. In endometriosis, this cyclic variability was lost. There was a trend toward decreased apoptosis with increasing stage of the disease, but the differences lacked statistical significance.


CONCLUSIONS
Spontaneous apoptosis is decreased in the endometrial glands in women with endometriosis, especially during late secretory/menstrual and early proliferative phases of the cycle. This may indicate increased viability of endometrial cells shed during menses, facilitating their ectopic survival and implantation.
Dmowski
W P
WP
Institute for the Study and Treatment of Endometriosis, Oak Brook, IL 60523, USA. wpdmowski@oakbrookfertility.com
Ding
J
J
Shen
J
J
Rana
N
N
Fernandez
B B
BB
Braun
D P
DP
D000328:Adult; D017209:Apoptosis; D018450:Disease Progression; D004715:Endometriosis / Q000473:pathology / Q000503:physiopathology*; D004717:Endometrium / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D006801:Humans; D020287:In Situ Nick-End Labeling; D008597:Menstrual Cycle / Q000502:physiology; D012016:Reference Values; D017154:Stromal Cells / Q000502:physiology*