[Frontiers in Bioscience 2, e48-52, August 1, 1997]

	[Frontiers in Bioscience 2, e48-52, August 1, 1997] Reprints PubMed CAVEAT LECTOR
	ENDOMETRIOSIS: A REVIEW OF ITS PATHOGENESIS Paul J.Q. van der Linden Deventer Ziekenhuis, Department of Obstetrics and Gynecology, P.O. Box 5001, 7400 GC Deventer, The Netherlands Received 6/15/97 Accepted 7/29/97 2. INTRODUCTION At least three different forms of endometriosis must be discriminated (1). These three forms are: peritoneal, ovarian and rectovaginal. The first histological description of a lesion consistent with endometriosis was described by Von Rokitansky in 1860 (2). It was Cullen (3, 4) who, in 1896, suggested that endometriomas, or adenomyomas as he called these lesions, resembled the mucous membrane of the uterus. However to this date, the pathogenesis of this enigmatic disease is still poorly understood and remains controversial. The theories dealing with the pathogenesis of endometriosis, in particular of peritoneal endometriosis, can be divided into three main concepts. The oldest concept is that endometriosis develops in situ from the remnants of the Wolffian or Müllerian ducts, or alternatively from metaplasia of the peritoneal or ovarian tissues (5, 6). A second concept is based on the assump-tion that endometriosis results from diffe-rentation of mesenchymal cells, activated (induced) by substances released by degenerating endometrium arriving in the abdominal cavity (the induction theory) (7, 8). A third concept is based on the transplantation and subsequent implantation of endometrial tissue on the peritoneal surface (9, 10). This would include transportation of viable endometrial cells during menstruation via the fallopian tubes into the abdominal cavity, implantation of these cells onto the peritoneum and the development of these cells into the endometriotic tissue (the transplantation or implantation theory). In the following section each of these concepts is discussed.

[Frontiers in Bioscience 2, e48-52, August 1, 1997]
Reprints
PubMed
CAVEAT LECTOR

ENDOMETRIOSIS: A REVIEW OF ITS PATHOGENESIS

Paul J.Q. van der Linden

Deventer Ziekenhuis, Department of Obstetrics and Gynecology, P.O. Box 5001, 7400 GC Deventer, The Netherlands

Received 6/15/97 Accepted 7/29/97

2. INTRODUCTION

At least three different forms of endometriosis must be discriminated (1). These three forms are: peritoneal, ovarian and rectovaginal. The first histological description of a lesion consistent with endometriosis was described by Von Rokitansky in 1860 (2). It was Cullen (3, 4) who, in 1896, suggested that endometriomas, or adenomyomas as he called these lesions, resembled the mucous membrane of the uterus. However to this date, the pathogenesis of this enigmatic disease is still poorly understood and remains controversial. The theories dealing with the pathogenesis of endometriosis, in particular of peritoneal endometriosis, can be divided into three main concepts. The oldest concept is that endometriosis develops in situ from the remnants of the Wolffian or Müllerian ducts, or alternatively from metaplasia of the peritoneal or ovarian tissues (5, 6).

A second concept is based on the assump-tion that endometriosis results from diffe-rentation of mesenchymal cells, activated (induced) by substances released by degenerating endometrium arriving in the abdominal cavity (the induction theory) (7, 8).

A third concept is based on the transplantation and subsequent implantation of endometrial tissue on the peritoneal surface (9, 10). This would include transportation of viable endometrial cells during menstruation via the fallopian tubes into the abdominal cavity, implantation of these cells onto the peritoneum and the development of these cells into the endometriotic tissue (the transplantation or implantation theory). In the following section each of these concepts is discussed.