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Cited by 49Endometriosis Research and TreatmentGynecological conditions and treatmentsEctopic Pregnancy Diagnosis and Management

Redefining endometriosis: Endometriosis is an entity with extreme pleiomorphism

Leyendecker, G.·2000·Human Reproduction
DOI 10.1093/humrep/15.1.4
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Abstract

Endometriosis and adenomyosis have long been considered as one entity with a common, although unknown, aetiology (Meyer, 1919). After the term endometriosis was coined (Sampson, 1927), it was widely used for the intrauterine and the extrauterine variety of the disease respectively (Counseller, 1938). However, it was the theory of tubal spread of normal endometrial cells by retrograde menstruation as the cause of pelvic endometriosis (Sampson, 1927) that finally led to consideration of both localizations of ectopic endometrial growth as different entities. If Sampson's theory were correct, then infiltrative and expansive growth of endometrial glands and stroma with hyperplasia of surrounding muscular tissue into the depth of the myometrium would differ from pelvic endometriosis not only by localization but also by pathogenesis. Consequently, although the frequent association of endometriosis with adenomyosis was recognized (Emge, 1962; Pratt, 1972), it was suggested that the term `endometriosis' should be used exclusively for endometrial growth beyond the confines of the uterus and that the term `adenomyosis' should be used only for intrauterine ectopic endometrial growth (Ridley, 1968). Recently, it was suggested that there were three types of endometriotic lesions, peritoneal, ovarian and rectovaginal (Nisolle and Donnez, 1997). While peritoneal endometriosis would result from transtubal shedding and implantation of endometrial cells, ovarian endometriomata would result from metaplasia and rectovaginal endometriosis, with endometrial glands and stroma as well as muscular tissue displaying the composition of adenomyomata, would arise from Müllerian remnants. It has been suggested the existence of principally two phenotypes of endometriosis, superficial endometriosis including ovarian endometriomata and adenomyosis (Brosens, 2000). While superficial endometriosis would arise from the shedding of superficial endometrium (SE) (and the term endometriosis should be restricted to this variety), adenomyosis would result from basal endometrium (BE) and the subendometrial myometrium (junctional zone myometrium; JZM; archimyometrium) (Werth and Grusdew, 1898; Noe et al., 1999) and would preferentially present at certain locations (Cullen, 1920), particularly the uterine myometrium, the uterine ligaments and the rectovaginal septum. Superficial endometriosis would not develop into deep infiltrative endometriosis, because they both were different entities. We have recently suggested that endometriosis originates at the uterine level and constitutes primarily a disease of the archimetra (Leyendecker et al., 1998; Noe et al., 1999) since altered endometrial cells with a higher potential for growth on peritoneal surfaces gain access to the peritoneal cavity, and so adenomyosis merely constitutes a special variant of endometriosis. Meanwhile, we have extended our studies and found further evidence that pelvic endometriosis with all its phenotypes are sequelae of uterine adenomyosis or its early manifestations, and that both endometriosis and adenomyosis constitute a pathogenetic entity (Kunz et al., 2000). Several lines of evidence support this notion. Firstly, the eutopic endometrium in endometriosis shows alterations similar to those which occur in the endometriotic lesions that are not found in the endometrium of women free of disease. These alterations include signs of increased inflammatory response, such as the increased expression of monocyte-chemotactic protein-1 (MCP-1) (Jolicoeur et al., 1998) and the increased colonization with macrophages (Leiva et al., 1994), signs of increased proliferation (Wingfield et al., 1995) and of increased biochemical activity, e.g. pathological expression of P450 aromatase (Noble et al., 1996; 1997) resulting in increased tissue concentrations of oestradiol (Takahashi et al., 1989). Secondly, women with endometriosis show a significant increase in uterine peristaltic activity in comparison to women free of disease. At mid-cycle, in women with endometriosis, the peristaltic activity becomes dysperistaltic, resulting in a breakdown of directed sperm transport (Leyendecker et al., 1996). Moreover, in women with endometriosis the intrauterine pressure is increased in comparison with women without the disease (Bulletti et al., 1997; Mäkäräinen, 1988). Finally, in endovaginal sonography (EVS) and magnetic resonance imaging (MRI), women with endometriosis exhibit a significant expansion of the archimyometrium (`halo' in EVS or `junctional zone' in MRI respectively) over controls, which is similar or identical to the images obtained in adenomyosis (Leyendecker et al., 1998; Kunz et al., 2000). The depth of the archimetrial invasion was correlated with the age of the patients. Histologically, this expansion involves all components of the archimetra such as the glandular and stromal endometrium as well as the subendometrial myometrium (M.Herbertz, M.Noe, G.Kunz, G.Mall and G.Leyendecker,

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  • Early lesions usually present close to the fundo-cornual raphe of the archimyometrium.

    “Early lesions usually present close to the “fundo-cornual raphe” of the archimyometrium [3, 23, 45]”

    From The pathophysiology of endometriosis and adenomyosis, tissue injury and repair (2009) · cites this paper as [45]

  • Adenomyotic foci are usually localized in the anterior and/or posterior with preference of the posterior but only rarely in the lateral walls of the uterine corpus.

    “Adenomyotic foci are usually localized in the anterior and/or posterior with preference of the posterior but only rarely in the lateral walls of the uterine corpus.”

    From The pathophysiology of endometriosis and adenomyosis, tissue injury and repair (2009) · cites this paper as [45]

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Authors
Leyendecker, G.
Affiliations
Klinikum Darmstadt (DE)
Corresponding author
Leyendecker, G.
Venue
Human Reproduction
Publisher
Oxford University Press (OUP)
Published
2000-01
Volume
15
Issue
1
Pages
4-7
ISSN
  • 0268-1161 (ISSN-L)
  • 1460-2350
DOI
10.1093/humrep/15.1.4
OpenAlex
W2061413850
Cited by
49
References
55
Citations by year
2026: 1 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 4 · 2018: 2 · 2016: 3 · 2015: 1 · 2014: 1 · 2013: 1 · 2012: 2
FWCI
0.57
Type
journal article
Language
en
Open access
closed
Locations
  • Human Reproduction (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
  • Health Sciences › Medicine › Obstetrics and Gynecology › Gynecological conditions and treatments
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Ectopic Pregnancy Diagnosis and Management
Keywords
endometriosis, adenomyosis, endometriosis classification, superficial endometriosis, Müllerian remnants, retrograde menstruation, peritoneal endometriosis, endometrioma, rectovaginal endometriosis, endometriosis phenotypes
MeSH terms
Adult, Endometriosis, Female, Humans, Magnetic Resonance Imaging, Ultrasonography, Uterus

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