Peritoneal, ovarian and recto-vaginal endometriosis are three distinct entities

Peritoneal endometriosis :
Vasculartization of endometriotic implants is probably one of the most important factors of growth and invasion of endometrial glands in other tissue. We have 3-dimensionally observed in red flame-like lesions an important vascular network in the lesion-peritoneum interface. The extremely rich vascular network permits further implantation in the mesothelial layers. Our hypothesis is that red lesions are the first stage of endometriosis and then progress to the so-called typical or black lesions which must be considered as enclosed implants surrounded by fibrosis.
Ovarian endometriosis:
The pathogenesis of typical ovarian endometrioses is a source of controversy. According to our histological data, the endometrioma must be considered as an invagination, but not as the result of bleeding of a superficial implant. Indeed, metaplasia of the coelomic epithelium invaginated into the ovarian cortex was proved in our study and explains the endometrioma formation. The epithelium covering the ovary, which is the mesothelium able to form any type of tissue, can invaginate into the ovarian cortex. Under the influence of so far unknown growth factors, these inclusions could be transformed into intra-ovarian endometriosis by metaplasia. Our main argument is the presence of epithelial invaginations in continuum with endometrial tissue proving the metaplasia theory. The second arguments is the capacity of the tissue to invaginate secondarily form the endometrial wall itself.
Recto-vaginal endometriosis:
Histologically, recto-vaginal endometriosis is a circumscribe nodular aggregated of smooth muscle, endometrial glands, and usually, endometrial stroma. The very similar histological descriptions to uterine adenomyosis lead us to suggest that the so-called endometriotic nodule of the recto-vaginal septum is, in fact, just like an adenomyoma or an adenomyotic nadule which can develop form Mullerian rests and consists essentially of smooth muscle with active glandular epithelium and scanty stroma. Because we observed differences between peritoneal and nodular lesions, we suggest that the nodule is not the consequence of deep-infiltrating endometriosis. Peritoneal, ovarian and recto-vaginal endometriosis are three distincts entities with a different histogenesis requiring a specific and appropriate therapy