BCL-2 expression in eutopic and ectopic endometrium in patients with adenomyosis and endometriosis

Abstract EN

Adenomyosis and endometriosis are common benign gynecological disorders characterized by the abnormal growth of endometrium into the myometrium or outside the uterine cavity respectively.

Despite their frequent occurrence, the precise etiology of these disorders is still unknown.

Ectopic dissemination of the endometrial cells gives origin to endometriosis lesions, but occurs in women with and without endometriosis.

Growing evidence indicates that the endometrium of women with adenomyosis or endometriosis has some fundamental differences compared with normal endometrium.

They have enhanced proliferation and increased ability to survive in ectopic location.

The inability of endometrial cells to transmit a “death” signal or their ability to avoid cell death is associated with increased expression of anti-apoptotic factors (e.g.

Bcl-2).

Ectopic endometriosis tissues are histologically similar to ectopic adenomyotic tissues and both are similar to their putative utopic precursors, yet significant biochemical differences exist between all those tissues.

The aim of this study was to investigate the BCL-2 in ectopic and ectopic endometrium in patients with endometriosis or adenomyosis and compared them with normal endometrium.

We examined a total of 37 cases; 6 were ovarian endometriosis (2 of them were Struma only), one tubal, one peritoneal, 8 adenomyosis, 12 eutopic endometria and 9 endometrial tissues obtained from patients having neither adenomyosis nor endometriosis.

In normal endometrium, Bcl-2 was detected in most cases with significant difference between proliferative and secretory endometrium (p < 0.05).

In ectopic endometrium we could detect BCL-2 in 10 out of 12 samples and the stain was stronger than that in normal cases, especially in secretory phases so, no cyclic variation could be detected(p = 0.3674).Also no significant difference was detected as regard Bcl-2 positivity or intensity between ectopic endometrium in patients with endometriosis or adenomyosis (p = 0.176).

In adenomyosis, the stain was stronger than that in ectopic endometrial glands.

The stromal expressed BCL-2 in focal and strong manner in most cases.

Both glandular and stromal staining showed no cyclic variations.

All adenomyotic samples (ovarian, tubal and peritoneal) expressed no BCL-2 stain either in the glands or the stromal.

These results strongly suggest hormone-dependent regulation of Bcl-2 expression, which could play an important role in pathogeneses of adenomyosis not endometriosis and the regulatory mechanisms involved in ovarian endometriosis, may differ from that in adenomyosis.