Dynamic aspects of endometriosis in a mouse model through analysis of implantation and progression

G Rossi, Gabriele Rossi, Edgardo Somigliana, E Somigliana, Somigliana E, Moschetta M, M Moschetta, R Santorsola, Santorsola R, Roberta Santorsola, Cozzolino S, S Cozzolino, Sabrina Cozzolino, Paola Filardo, P Filardo, Filardo P, Anita Salmaso, A Salmaso, Salmaso A, B Zingrillo, Beatrice Zingrillo, Zingrillo B
Archives of gynecology and obstetrics · 2000 · vol. 263(3) , pp. 102–107 · doi:10.1007/s004040050005 · PMID:10763836 · W2024088889
article OA: closed CC0 ⤵ 23 in-corpus citations
Full text JSON View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06+body, 2026-06-11 ⓘ

This study established an endometriosis model in immunocompetent mice, showing dynamic lesion growth and demonstrating that progression, but not implantation, of ectopic endometrium depends on ovarian function.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

This paper established a dynamic mouse model of endometriosis by surgically transplanting autologous endometrium into 30 normal immunocompetent mice and then assessing lesion initiation and growth at serial time points using histology and caliper-based lesion area measurements. Lesions were confirmed at 3 weeks and showed an initial decrease in area followed by a significant increase over the subsequent 4 weeks, indicating that implantation and progression represent different stages in disease development, with progression depending on intact ovaries (bilateral ovariectomy at the second laparotomy reduced lesion surface, unlike ovariectomy at the time of transplantation). In estrogen-supplemented mice, lesion growth appeared less evident, with only a slight non-significant increase in size. This paper is centrally about endometriosis — it characterizes implantation versus progression dynamics in a mouse model and evaluates how ovaries and estrogen modulation affect lesion development.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

The aim of this study was to use normal immunocompetent mice to set up a model for endometriosis which allowed to study the dynamic aspects involved in initiation and progression of the disease. Thirty mice were surgically transplanted with autologous endometrium and at 3 weeks showed evidence of endometriosis. Diagnosis of endometriotic lesions was histologically confirmed. Visual inspection using a caliper revealed that, after an initial decrease in size (from 33.44+/-2.33 mm2 to 24.24+/-2.37 mm2 (p<0.01)) detected at 3 weeks after transplantation, there was a significant increase of lesion area from 21.30+/-3.15 mm2 to 43.93+/-6.29 mm2 (p<0.05) in the following 4 weeks. When we compared these results to those obtained in mice which underwent bilateral annessiectomy, we observed that, when bilateral annessiectomy was performed simultaneously to endometrial transplantation, lesion surfaces were similar between mice which were or were not subjected to bilateral ovariectomy. On the other hand, when bilateral annessiectomy was performed at second laparotomy and then evaluated after 4 weeks, differently from what observed in control mice, surface values decreased from 21.24+/-2.29 mm2 to 10.58+/-3.40 mm2 (p<0.01). Finally, progression of lesions in estrogen supplemented mice seems less evident than in control mice since only a slight but not significant increase in size (from 21.32+/-3.32 mm2 to 26.18+/-6.98 mm2, p=0.32) was detected. The results presented herein demonstrate that surgically induced endometrial implants in mice are dynamic lesions and that implantation and progression of endometriosis represent different stages in the ethiopathogenesis of the disease. Moreover, we showed that progression, but not implantation, of ectopic endometrium is dependent upon the functionally and structurally integrity of the ovaries. This is a model of endometriosis established in normal immunocompetent mice, and, consequently, may represent a reliable tool for testing new immunological therapeutical approaches and studying the role of different genes using transgenic mice.
Full text 2,588 characters · extracted from oa-doi-fallback · click to expand
Abstract The aim of this study was to use normal immunocompetent mice to set up a model for endometriosis which allowed to study the dynamic aspects involved in initiation and progression of the disease. Thirty mice were surgically transplanted with autologous endometrium and at 3 weeks showed evidence of endometriosis. Diagnosis of endometriotic lesions was hystologically confimed. Visual inspection using a caliper revealed that, after an initial decrease in size (from 33.44±2.33 mm2 to 24.24±2.37 mm2 (p<0.01)) detected at 3 weeks after transplantation, there was a significant increase of lesion area from 21.30±3.15 mm2 to 43.93±6.29 mm2 (p<0.05) in the following 4 weeks. When we compared these results to those obtained in mice which underwent bilateral annessiectomy, we observed that, when bilateral annessiectomy was performed simultaneously to endometrial transplantation, lesion surfaces were similar between mice which were or were not subjected to bilateral ovariectomy. On the other hand, when bilateral annessiectomy was performed at second laparotomy and then evaluated after 4 weeks, differently from what observed in control mice, surface values decreased from 21.24±2.29 mm2 to 10.58±3.40 mm2 (p<0.01). Finally, progression of lesions in estrogen supplemented mice seems less evident than in control mice since only a slight but not significant increase in size (from 21.32±3.32 mm2 to 26.18±6.98 mm2, p=0.32) was detected. The results presented herein demonstrate that surgically induced endometrial implants in mice are dynamic lesions and that implantation and progression of endometriosis represent different stages in the ethiopathogenesis of the disease. Moreover, we showed that progression, but not implantation, of ectopic endometrium is dependent upon the functionally and structurally integrity of the ovaries. This is a model of endometriosis established in normal immunocompetent mice, and, consequently, may represent a reliable tool for testing new immunological therapeutical approaches and studying the role of different genes using transgenic mice. Similar content being viewed by others Author information Authors and Affiliations Additional information Received: 2 February 1999 / Accepted: 25 May 1999 Rights and permissions About this article Cite this article Rossi, G., Somigliana, E., Moschetta, M. et al. Dynamic aspects of endometriosis in a mouse model through analysis of implantation and progression. Arch Gynecol Obstet 263, 102–107 (2000). https://doi.org/10.1007/s004040050005 Issue date: DOI: https://doi.org/10.1007/s004040050005

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

⚙ Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback ⓘ

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

endometriosis

MeSH descriptors

Disease Models, Animal Endometriosis Peritoneal Diseases Animals Disease Progression Endometriosis Endometrium Endometrium Female Humans Mice Mice, Inbred Strains Peritoneal Diseases Peritoneum Peritoneum Transplantation, Autologous

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 (16)

Cited by (23)

Source provenance

europepmc
last seen: 2026-07-29T06:27:48.050232+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:13:41.710148+00:00
License: CC0 · commercial use OK