Apoptosis and Ki-67 Expression in Adenomyotic Lesions and in the Corresponding Eutopic Endometrium

Abstract

In Brief Objective To examine biologic and proliferative properties of adenomyotic lesions and to determine whether adenomyotic lesions originate in the basal layer of the eutopic endometrium. Methods We examined eutopic and ectopic endometria from 23 patients with adenomyosis. To obtain evidence for the induction of programmed cell death, apoptotic cells were identified using a modified terminal deoxynucleotidyltransferase-biotin nick end-labeling method. To evaluate cell death repressor activity, bcl-2 gene expression was examined using immunohistochemical staining. As a proliferative marker, Ki-67 expression was also examined immunohistochemically. Results In the eutopic endometrium, apoptosis was most frequently observed in epithelial cells during mid- to late secretory phases, although it was rarely found during early proliferative through early secretory phases (P < .01). In contrast, bcl-2 gene expression inversely correlated with the appearance of apoptosis. A similar tendency was observed in stromal cells. In the ectopic endometrium of adenomyosis, endometrial dating revealed that secretory change was rare, even in the secretory phase, and that induction of apoptotic cells as well as bcl-2 gene expression showed no cyclic change. In stromal cells of the ectopic endometrium, apoptosis was more frequent than was seen in the eutopic endometrium, in all menstrual phases (P < .05). Ki-67 was constantly expressed in the glandular epithelium of the ectopic endometrium, irrespective of the menstrual phases, whereas in the secretory phase it was less expressed in the eutopic endometrium of functional and basal layers (P < .01). Conclusion The induction of apoptosis seems to be regulated by hormonal changes in the eutopic endometrium and has an inverse correlation with bcl-2 gene expression. The ectopic endometrium in adenomyosis is rarely influenced by hormonal change and has different biologic and proliferative properties than events observed in the eutopic endometrium findings, which strongly suggest that the adenomyotic lesion does not originate in the basal endometrium. Ectopic endometrium in adenomyotic lesions is influenced rarely by hormonal change and has different biologic and proliferative properties than these events in the eutopic endometrium.