A Critical Review of Endometriosis Pathology

Brittany Lauren Cureton
In: Theses and Dissertations · 2013 · W142429543
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This review examines the etiology, development, and treatment of endometriosis, exploring theories on its cause, contributing factors like angiogenesis and immune dysfunction, and animal models used in research.

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This 2013 master’s thesis critically reviews the literature on endometriosis pathology, focusing on etiology, development, and treatment. It summarizes how endometriosis—ectopic endometrial tissue causing pain and infertility—has been approached through multiple theories including angiogenesis, immune dysfunction and immune evasion, and possible contributions from environmental toxicants, diet, and genetic polymorphisms, while noting that no single genotype consistently confers increased risk across populations. The thesis also discusses staging systems, the role of upregulated angiogenic factors in lesions, decreased T-cell cytotoxicity as an observed immune abnormality, and the use and limitations of rodent and non-human primate animal models. This paper is centrally about endometriosis — it reviews endometriosis pathology, including immune/angiogenic mechanisms and how etiology and treatments have been studied.

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Abstract

Endometriosis is a complex, multifactorial, reproductive disorder present in approximately 10-15% of adult women between the ages of 25-35. This disorder occurs when endometrial glands and stroma grow ectopically on the surface of the ovaries, pelvic peritoneum, fallopian tubes, and the uterus. Endometriosis causes varying degrees of painful symptoms and infertility in infected individuals. Three main theories of endometrial accumulation attempt to explain the etiology of this elusive disease. There have been various staging of endometriosis symptoms that attempt to standardize classification as well as predict pain and infertility. Angiogenesis, necessary to the survival of endometrial tissue, along with immune dysfunction and evasion have been examined as possible contributing factors to the development of endometriosis. Certain angiogenic factors are upregulated in ectopic endometrial tissue and endometriotic lesions, while decreased cytotoxicity of T cells is shown to be an abnormal immune process observed in individuals with this disorder. Other factors including exposure to environmental toxicants, diet, and population specific polymorphisms have also been examined for their role in this disease. While various genetic variations have been identified as increased risk factors of endometriosis in certain populations, there has not been a specific genotype that demonstrates increased risk for this disease in all populations. Two endometriosis-induced animal models, which include rodents and non-human primates, are primarily responsible for the advancement of our understanding of this disease. Although limitations exist for animal models, they have been an important contributor to current research. There is no cure for endometriosis, but various treatment options exist for both pain and infertility. The purpose of this thesis is to review current literature relevant to the etiology, development, and treatment of endometriosis.
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Date of Award 1-1-2013 Document Type Open Access Thesis Department Biological Sciences First Advisor Holly A LaVoie Abstract Endometriosis is a complex, multifactorial, reproductive disorder present in approximately 10-15% of adult women between the ages of 25-35. This disorder occurs when endometrial glands and stroma grow ectopically on the surface of the ovaries, pelvic peritoneum, fallopian tubes, and the uterus. Endometriosis causes varying degrees of painful symptoms and infertility in infected individuals. Three main theories of endometrial accumulation attempt to explain the etiology of this elusive disease. There have been various staging of endometriosis symptoms that attempt to standardize classification as well as predict pain and infertility. Angiogenesis, necessary to the survival of endometrial tissue, along with immune dysfunction and evasion have been examined as possible contributing factors to the development of endometriosis. Certain angiogenic factors are upregulated in ectopic endometrial tissue and endometriotic lesions, while decreased cytotoxicity of T cells is shown to be an abnormal immune process observed in individuals with this disorder. Other factors including exposure to environmental toxicants, diet, and population specific polymorphisms have also been examined for their role in this disease. While various genetic variations have been identified as increased risk factors of endometriosis in certain populations, there has not been a specific genotype that demonstrates increased risk for this disease in all populations. Two endometriosis-induced animal models, which include rodents and non-human primates, are primarily responsible for the advancement of our understanding of this disease. Although limitations exist for animal models, they have been an important contributor to current research. There is no cure for endometriosis, but various treatment options exist for both pain and infertility. The purpose of this thesis is to review current literature relevant to the etiology, development, and treatment of endometriosis. Rights © 2013, Brittany Lauren Cureton Recommended Citation Cureton, B. L.(2013). A Critical Review of Endometriosis Pathology. (Master's thesis). Retrieved from https://scholarcommons.sc.edu/etd/489 Included in Life Sciences Commons, Medicine and Health Sciences Commons, Physical Sciences and Mathematics Commons

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