Endometriosis: Scanning electron microscopic and immunohistochemical studies of pelvic endometriosis

Abstract

The pathogenesis of pelvic endometriosis has been studied by using scanning electron and light microscopy, observing the surface structure of bluish lesions obtained from 26 patients during laparotomy. Paraffin sections included another 17 tissue samples of endometriosis, based on immunohistochemical responses to epithelial membrane antigen, keratin and vimentin. Ultrastructurally, the surface epithelial cells could not be detected in 13 out of 17 pelvic peritoneal endometriosis samples. In one case in which the surface peritoneal cells were seen histologically to dip into the subperitoneal stroma, many surface peritoneal infoldings were observed, and ciliated cells were detected at the edge of these infoldings. Ovarian endometriosis was composed of three types of cells, none of which had any cilia. These findings were observed in continuity with adjacent normal mesothelial cells. No characteristic structure of the endometrial surface was observed for the bluish lesion, but the gland surface of endometriosis located in the subperitoneal stroma initially had ciliated cells. The immunoreactions in both the columnar mesothelial cells with surface peritoneal infoldings and the glands of endometriotic tissues were similar to those of normal endometrial glands, but different from those of normal mesothelial cells. Pelvic endometriosis might originate by a process of metaplasia from the pelvic peritoneum.

Coelomic Metaplasia Theory of Endometriosis: Evidence from in vivo Studies and an in vitro Experimental Model

“…We assume that a major stimulant for this metaplastic process is endometrial stroma, one of the retrograde menstrual products known to be rich in many growth factors and cytokines. Our initial morphologic observations have confirmed the findings of Nakamura and colleagues [1], namely that endometriosis may manifest as a serial change from the adjacent mesothelial cells. …”

Stereometric evaluation of peritoneal endometriosis and endometriotic nodules of the rectovaginal septum

“…The ectopic foci are more or less autonomous, not governed by the normal control mechanisms governing the uterine endometrial glands and stroma. The exact reason why a number of implants or cells do not respond to hormonal therapy is not known, but at least four hypotheses have been proposed: (i) the drug does not gain access to the endometriotic foci because fibrosis surrounding the foci prevents access locally; (ii) endometriotic cells may have their own genetic programming, while endocrine influence appears to be only secondary and dependent on the degree of differentiation of the individual cell; (iii) the lower oestrogen receptors in peritoneal ectopic endometrium and in rectovaginal nodule endometrium than in eutopic endometrium Bergqvist and Ferno, 1993;Nakamura et al, 1993;Howell et al, 1994;Nisolle et al, 1994;Bergqvist, 1995); and (iv) the different regulatory mechanisms of endometriotic steroid receptors may result in deficient endocrine dependency because the receptors, although they are present, are biologically inactive (Metzger, 1992).…”

Immune interactions in endometriosis

“…Symptomatic endometriosis is believed to occur in approximately 10% of reproductive-age women, although endometriosis is probably underdiagnosed given that confirmation of the disease requires visualization by surgeons followed by histological examination. Since first described within the medical literature more than 100 years ago [2,3], multiple hypotheses have been proposed regarding the etiology of this disease, including the retrograde menstruation (implantation) theory [4], coelomic metaplasia theory [5–8], development of ectopic growth following activation of embryonic cell rests [9,10], metastatic (hematogenic or lymphatic transport) theory [11] and the more recent adult stem cell theory [12]. Significantly, no single theory can adequately explain all presentations of this disease, including the rare cases of male endometriosis [13].…”