Pathogenesis of endometriosis--current research.

Proliferative, secretory and menstrual endometrial cells of both the stroma and epithelium adhere to intact peritoneal mesothelium and mesothelial monolayers. Endometrial attachment to the mesothelium appears to occur rapidly (within 1 h) and transmesothelial invasion occurs between 1 and 18-24 h. These results demonstrate that the mesothelium is not a 'no-stick' surface and indicates that molecules present at the surface of the mesothelium are involved in the pathogenesis of the early endometriotic lesion. The inhibition of endometrial cell adherence to peritoneal mesothelium by hyaluronidase indicates that CD44-hyaluronan binding is at least one of the mechanisms involved in the pathogenesis of endometriosis. We believe that investigation of mesothelial cell adhesion molecules is central to understanding the pathogenesis of endometriosis.

Culture of menstrual endometrium with peritoneal explants and mesothelial monolayers confirms attachment to intact mesothelial cells.

BACKGROUND: To evaluate adhesion of menstrual endometrium (ME) to intact peritoneal mesothelium. METHODS: Explants of peritoneum were cultured for 1 h with ME (n = 6). Specimens were serially sectioned for haematoxylin and eosin stain and immunohistochemistry using an anti-cytokeratin antibody to label mesothelium. Confocal laser scanning microscopy (CLSM) was performed to identify an intact layer of mesothelial cells (MC) underlying sites of ME attachment. Also, ME and MC were labelled with Cell-Tracker dyes. ME was cultured with mesothelial monolayers for 1 h (n = 10). Cultures were examined with differential interference contrast and CLSM. Optical sections were taken and a three-dimensional model was constructed. RESULTS: In the peritoneal explants, ME adhered to intact mesothelium. There was no evidence of transmesothelial invasion. CLSM of sections of the explants demonstrated an intact monolayer of cytokeratin positive cells below the sites of ME implantation. Cytokeratin negative and positive ME cells adhered to mesothelial cells. Likewise, the ME attached to cultured mesothelium. Orthogonal sections and three-dimensional reconstruction confirmed an intact monolayer of mesothelium underlying ME attachment sites. CONCLUSIONS: This study confirms that ME adheres rapidly to intact peritoneal mesothelium. Further studies are needed that characterize the mechanisms of ME adhesion to, and migration through, mesothelial cells.