What Will Er Do For Endometriosis Pain – The affiliations of editors and reviewers are current as set out in the Loop Research profile and may not reflect the current state of peer review.
Women with endometriosis, the growth of endometrial glands and stroma outside the uterus, often also develop adenomyosis, the growth of endometrial tissue within the myometrium. Each disease is associated with functional changes in the orthotopic endometrium, which often lead to pain, decreased fertility, and an increased risk of adverse pregnancy outcomes. Although the exact etiology of either disease is poorly understood, evidence suggests that the presence of endometriosis may be a contributing factor in the development of adenomyosis due to an altered systemic inflammatory response. Here, we discuss the potential role of exposure to ecotoxic agents with endocrine disrupting potential in the pathogenesis of both endometriosis and adenomyosis. The role of environmental endocrine disruptors (EDCs) in the development of endometriosis is supported by numerous epidemiological and experimental studies. However, only a few studies have investigated the potential relationship between exposure to toxic substances and the risk of adenomyosis. Nevertheless, it is relevant to discuss EDC exposure and the development of all these diseases, as women with endometriosis often also suffer from adenomyosis. We discuss possible mechanisms by which EDCs act to promote the co-occurrence of endometriosis and adenomyosis. Understanding the disease-promoting mechanisms of environmental toxins associated with endometriosis and adenomyosis is of paramount importance in developing more effective treatment and prevention strategies.
What Will Er Do For Endometriosis Pain
The co-morbid conditions endometriosis and adenomyosis, which affect millions of women of reproductive age worldwide, remain two of the least understood gynecological diseases. Endometriosis is best characterized by the growth of endometrial glands and stroma in extrauterine sites, while adenomyosis, often referred to as “internal endometriosis,” is characterized by growth within the myometrium. Defined as the presence of embedded endometrial glands and stroma. The exact etiology of both diseases is unknown, although several theories have been proposed. One of the oldest and most accepted hypotheses about endometriosis is Sampson’s theory of retrograde menstruation (Sampson, 1927). Ectopic deposition of regurgitated menstrual debris remains a plausible mechanistic explanation for the development of endometriosis, but despite the fact that the majority of circulating women experience this phenomenon, only a small percentage of circulating women develop the disease. Considering only a subset cannot explain the full incidence of the disease. disease progression (Halme et al., 1984). Other theories of endometriosis development include coelom metaplasia, stem cell activation, and intrinsic epigenetic abnormalities (Gruenwald, 1942; Baranova et al., 1999; Figueira et al., Sourial 2011). et al., 2014; Bulun et al., 2019).
Olivia Culpo Shares Struggle With Endometriosis
Figure 1. Endometriosis and adenomyosis show overlapping phenotypes. Adenomyosis is called internal endometriosis because it is histologically and phenotypically similar to endometriosis. But as the Venn diagram shows, these diseases have a lot in common, but they also have a lot of differences. Created by BioRender.com.
Several theories of the etiology of adenomyosis are also currently being proposed. One theory is that adenomyosis results from damage to the endometrial junctional zone, a steroid-dependent region between the endometrium and myometrium, resulting in myometrium in the basal region of the endometrial mucosa. It is assumed to arise from intussusception in the groin (Brosens et al., 1995; Bergeron et al., 2006; Sofic et al., 2016; Vannuccini et al., 2017; Bulun et al., 2021). The endometrial-fascial interface lacks a layer of mucosa-muscle tissue. As a result, the endometrium covers the myometrium, thereby providing an opportunity to invade the sites of weakened smooth muscle fibers in the myometrium (Uduwela et al., 2000). Another theory suggests that adenomyosis develops through de novo metaplasia of tissue derived from multipotent Müllerian ducts in the embryo (Garcia-Solares et al., 2018). Müllerian ductal tissue, composed of glands and stroma, is important for the maturation of the female genitourinary system, including the development of the fallopian tubes, cervix, uterus, and upper vagina (Wilson and Bordoni, 2021). Observations and studies of adenomyosis lesions have shown both biological and proliferative features unique to Müllerian duct tissue, including cytokeratin filaments and vimentin characteristic of Müllerian epithelium and mesenchymal tissue, respectively (Moll et al., 1983; Matsumoto et al., 1999). Another theory suggests that adenomyosis develops as a result of unavoidable mechanical stress on the uterus due to continuous remodeling activity throughout a woman’s life during the reproductive period (Leyendecker et al. 2009, 2015). As in many other tissues, mechanical stress, tissue injury, and mechanisms associated with tissue repair stimulate local estrogen production. Hyperestrogenism causes myometrial peristalsis and places a supraphysiological load on basal raphe cells (Leyendecker et al., 1998, 2004; Garavaglia et al., 2015). These events trigger tissue damage and repair systems that further increase and prolong estrogen production. This has been suggested to cause uterine dysfunction in women with membranosis (Leyendecker et al., 2009). Despite the numerous theories put forward to explain the development of adenomyosis, our current understanding of the etiology of the disease is limited. Not surprisingly, the lack of understanding of the mechanisms of this disease limits the development of treatment options for women with adenomyosis. A hysterectomy is considered a cure for adenomyosis because it is located in the uterus, but it is not an option for women who want to maintain a pregnancy. As with most women with endometriosis, fertility treatments are usually prescribed to relieve the symptoms of the disease. and are not curative.
In 2017, it was reported that 42.3% (n = 300) of women diagnosed with endometriosis also had adenomyosis (Antero et al., 2017). An additional study designed to address co-occurrence showed a significant increase in localized adenomyosis in women with endometriosis (50.2%) compared to women without endometriosis (5.4%) (Chapron et al., 2017). Using magnetic resonance imaging, Kishi et al. (2012) progressed heterogeneously with direct endometrial invasion (subtype I), ectopic endometriotic invasion (subtype II), de novo metaplasia (subtype III), and mixed phenotypes. disease (subtype IV). Interestingly, in this study, 96% of women with subtype II adenomyosis had endometriosis, whereas only 15% of women with subtype I had endometriosis (Kishi et al., 2012). In a follow-up study, the same group reported data suggesting that subtype II adenomyosis occurs as a consequence of intrapelvic endometriosis (Kishi et al., 2017). In this regard, our laboratory has identified profound adenomyosis lesions in a developmental toxicant exposure mouse model with an endometriosis-like uterine phenotype (Nayyar et al., 2007; Bruner-Tran et al., 2016). Investigating whether childhood exposure to endocrine-disrupting chemicals affects the frequency of these diseases as women’s comorbidities may provide unique insights into future treatments.
Collectively, the above studies highlight the possibility of common or overlapping diseases between endometriosis and adenomyosis. Therefore, to improve the reproductive health outcomes of patients, it is important to identify the reasons behind the development of both diseases. Many women with endometriosis and/or adenomyosis experience chronic episodes of debilitating pain, dyspareunia, dysmenorrhea, and/or infertility. Regardless of whether endometriosis and adenomyosis are two distinct entities or different manifestations of the same disease, both human and animal studies have suggested a role for inflammatory processes in their development (Jiang et al., 2016; Orazov et al., 2016; Lacheta, 2019). Vannuccini and Petraglia, 2019; Maruyama et al., 2020; Bulun et al., 2021). For example, ectopic formation of endometrial tissue is associated with induction of an inflammatory peritoneal environment that negatively affects uterine steroid sensitivity (Stilley et al., 2009; Bruner-Tran et al., 2018). ; Sharpe-Timms et al., 2020). Together, it has been suggested that the local and systemic hyperinflammatory milieu together with changes in the hormonal milieu associated with endometriosis favor the later development of adenomyosis.
Endometriosis: A Quest For Answers
Ecotoxicants are ubiquitous in the environment and may also promote disease through immune or endocrine disruption (Diamanti-Kandarakis et al., 2009; Sutton et al., 2012; Wang et al.; Street et al., 2018). Not surprisingly, environmental toxins acting as endocrine disrupting chemicals (EDCs) have been implicated in the pathogenesis of both endometriosis and adenomyosis (Bruner-Tran et al., 2016, 2017). Both diseases are estrogen-dependent, and many EDCs have been identified as estrogen mimics capable of inducing adverse effects mediated through both ER-dependent and ER-independent signaling pathways. Therefore, it is important to determine whether exposure to common EDCs is one of the triggers for endometriosis and adenomyosis. If so, how can this knowledge be used to prevent these diseases or improve patient outcomes? Pre-configure mechanisms that can facilitate
The endocrine system is an integral part of hormone-secreting tissues that facilitates interactions between hormones and their highly specific receptors to regulate vital processes such as growth and development, tissue function, metabolism, and reproduction. ). EDCs are classically defined as exogenous chemicals that disrupt the normal physiological function of the endocrine system, potentially causing adverse health effects and promoting disease (Rumph et al., 2020). Unfortunately, due to industrialization
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