Implantation versus Infiltration: The Sampson versus the Endometriotic Disease Theory

Koninckx PR, Philippe R. Koninckx, P R Koninckx, Barlow D, D. Barlow, Kennedy S, S Kennedy, Stephen Kennedy
Gynecologic and obstetric investigation · 1999 · vol. 47(Suppl. 1) , pp. 3–10 · doi:10.1159/000052853 · PMID:10087422 · W2017568708
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This paper proposes a new theory where endometriosis progression to disease, like benign tumors, is driven by cellular mutations and escape from peritoneal fluid regulation, rather than initial implantation or metaplasia.

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Abstract

It has been assumed that endometriosis is a progressive disease, with growth and development of lesions being inevitable once the disease has started. The implantation and the metaplasia theories describe the mechanism of initiation of endometriotic lesions, but do not explain the different clinical manifestations of endometriosis. To explain the variable expression, growth and development of lesions into severe disease, a new endometriotic disease theory is proposed. This theory suggests that progression of endometriosis to endometriotic disease is considered similar to the onset and progression of a benign tumour. In this theory, the most important factor in the development of endometriotic disease is not the initial implantation/metaplasia, but cellular changes such as mutations. According to this theory, endometriotic disease develops from endometriotic cells that have 'escaped' the influence of protective and regulatory factors in the peritoneal fluid.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Animals Endometriosis Endometriosis Endometriosis Extracellular Space Extracellular Space Female Humans Menstruation Disturbances Menstruation Disturbances Metaplasia Metaplasia Metaplasia Peritoneum Peritoneum Peritoneum

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (81)

Cited by (50)

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License: CC0 · commercial use OK