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Animal reproduction science2008; 111(2-4); 261-278; doi: 10.1016/j.anireprosci.2008.03.019

The equine endometrosis: new insights into the pathogenesis.

Abstract: This paper describes the histomorphological and immunohistochemical characterisation of phenotypic variations of endometrosis as well as potential etiological factors which may influence disease progression. In total, 779 endometrial biopsies were examined. These biopsies were taken in the breeding and non-breeding season (n=509), on defined days during the estrous cycle (n=70) and before and after experimentally induced bacterial endometritis (n=200). In addition to conventional histopathology, selected biopsies were investigated using alcianblue staining as well as immunohistochemical methods for the detection of steroid hormone receptors, Ki-67-antigen, vimentin, desmin, fibronectin, smooth-muscle-alpha-actin and laminin. The equine endometrosis can be divided into a destructive and a non-destructive form. Based on the morphology of the stromal cells involved, an active or inactive state can be distinguished in fibrotic foci. In all types of endometrosis, fibrotic stromal cells show a distinctly reduced expression of steroid hormone receptors in comparison to the intact stroma, indicating their dedifferentiation. However, the steroid hormone receptor expression of involved glandular epithelia seems to depend on the activity of the fibrosis. These results suggest an independency of all fibrotic foci from the hormonal control mechanism of the uterus. The characteristical features of destructive endometrosis are a large number of smooth-muscle-alpha-actin containing myofibroblasts, a pronounced epithelial vimentin expression, excessive extracellular matrix accumulation and a progressive alteration of the basal lamina. Furthermore, the frequently seen cystic glandular dilatation and mechanical destruction of the uterine glands may occur due to the contractibility of the myofibroblasts involved. As shown in this study, a simultaneous endometritis can cause a temporary activation of fibrotic stromal cells. However, cyclic and seasonal endocrine changes seem to have no effects on progression of the disease. It can be concluded that the various types of endometrosis represent different stages in the fibrotic process, possibly leading to the destruction of the glands and subsequently resulting in the development of a stromal fibrosis.
Publication Date: 2008-03-30 PubMed ID: 18468817DOI: 10.1016/j.anireprosci.2008.03.019Google Scholar: Lookup
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  • Journal Article

Summary

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The abstract pertains to a study that investigates the different types of equine endometrosis, a fibrotic disease affecting horses’ uterine lining, and the factors promoting disease progression. From tests including histopathology, and immunohistochemical methods on 779 endometrial biopsies, the researchers found that the diseased cells show reduced hormonal control mechanism response influencing the disease’s activity. The research also identified the distinct features of a destructive form of the disease.

Research Methodology

  • The study analyzed 779 endometrial biopsies taken during breeding and non-breeding season and at specified days during the estrous cycle.
  • An additional 200 biopsies were taken before and after creating a bacterial endometritis condition.
  • Apart from conventional histopathology, immunohistochemical methods were utilized for the detection of markers indicating disease progress.

Study Findings

  • The researchers found two forms of equine endometrosis: destructive and non-destructive. Depending on the morphology of the stromal cells involved, these types can be in an active or inactive state.
  • In all types of endometrosis, fibrotic stromal cells, cells involved in forming connective tissues, exhibited reduced expression of steroid hormone receptors in comparison to healthy cells – a sign of their dedifferentiation.
  • The degree of hormone receptor expression in glandular epithelia, cells that line the glands, appear to be dependant on the fibrosis’s activity.
  • Destructive endometrosis is marked by numerous myofibroblasts (cells responsible for wound healing) containing smooth-muscle-alpha-actin, notable epithelial vimentin expression (a type of intermediate filament protein), an accumulation of extracellular matrix, and progressive changes to the basal lamina (thin layer of extracellular matrix).
  • The myofibroblasts might be causing the frequently observed cystic glandular dilatation (enlargement) and mechanical destruction of the uterine glands due to their contractibility.
  • Endometritis (inflammation of the inner layer of the uterus) can temporarily activate the fibrotic stromal cells, but cyclic and seasonal hormonal shifts do not appear to impact the disease’s progression.

Conclusions

  • The paper concludes that the different types of endometrosis represent various stages in the fibrotic process, potentially resulting in gland destruction and development of stromal fibrosis.

Cite This Article

APA
Hoffmann C, Ellenberger C, Mattos RC, Aupperle H, Dhein S, Stief B, Schoon HA. (2008). The equine endometrosis: new insights into the pathogenesis. Anim Reprod Sci, 111(2-4), 261-278. https://doi.org/10.1016/j.anireprosci.2008.03.019

Publication

ISSN: 1873-2232
NlmUniqueID: 7807205
Country: Netherlands
Language: English
Volume: 111
Issue: 2-4
Pages: 261-278

Researcher Affiliations

Hoffmann, Christine
  • Institute of Pathology, University of Leipzig, Germany. christine.hoffmann@fli.bund.de
Ellenberger, Christin
    Mattos, Rodrigo Costa
      Aupperle, Heike
        Dhein, Stefan
          Stief, Birgit
            Schoon, Heinz-Adolf

              MeSH Terms

              • Actins / metabolism
              • Animals
              • Biopsy / veterinary
              • Desmin / metabolism
              • Endometriosis / etiology
              • Endometriosis / metabolism
              • Endometriosis / pathology
              • Endometriosis / veterinary
              • Female
              • Fibronectins / metabolism
              • Horse Diseases / etiology
              • Horse Diseases / metabolism
              • Horse Diseases / pathology
              • Horses
              • Immunohistochemistry / veterinary
              • Ki-67 Antigen / metabolism
              • Laminin / metabolism
              • Receptors, Estrogen / metabolism
              • Vimentin / metabolism

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