Ovarian endometriosis is associated with ultrastructural features in the JZ and Cx43

Objective To study the ultrastructure of the inner and outer myometrium, in the ovarian endometriosis, especially the inner one, and meanwhile to explore the expression of Connexin 43 protein and its significance in the uterus junction zone of patients with ovarian endometriosis. Methods Multiple samples were studied using transmission electron microscopy. The SABC immunohistochemical method was used to detect the expression of Connexin 43 in the Uterine junction zone in 30 cases of EM and 30 matched normal uterine. Results In uteri with ovarian endometriosis, the myocytes exhibited cellular was not hypertrophy. The cytoplasmic myofilaments were also less abundant. Abundant intermediate filaments formed cytoplasmic aggregates. The nuclei were fusiform in shape with blunt ends, centrally placed in the myocyte, and with a irregular outline prominent nucleoli and peripherally arranged nuclear chromatin. The bands were no longer and there were fewer caveolae. The rough endoplasmic reticulum and Golgi apparatus were little more. All features were more prominent at the junctional zone. The optical density of Connexin 43 expression were significantly lower in Endometriosis with endometrium(0.0943±0.0050) and JZ(0.1540±0.0164) than in control group(P0.05), respectively. The expressions of Cx43 were significantly higher in control group of proliferative phase with endometrium(0.0943±0.0050, 0.0801± 0.0054, P0.05) and JZ(0.1540±0.0164, 0.1407±0.0179, P0.05) than secretory, but there was no significantly difference in ovarian endometriosis between proliferative phase and secretory neither with outer myometrium nor with JZ. Furthermore, the expression of Connexin 43 was no difference in outer myometrium neither in outermyometrium nor in control group(P0.05). Conclusion The myocytes of uteri harboring outer myometrium are ultrastructurally different from those of normal uteri. These ultrastructural changes suggest a possible defect in myometrial contractility. The down-regulation of CX43 in the JZ may play important roles in ovarian endometriosis, the relevant molecular mechanism requires further investigation.