Endometriosis Research: From Sampson to the 21st …
If Sampson’s theory was correct, endometriosis would not be possible until a girl ..
John A Sampson and the origins of Endometriosis
Endometriosis is a chronic condition that is typically diagnosed clinicallybecause of severe dysmenorrhea. Asymptomatic cases of endometriosis areoften diagnosed during peritoneal surgery. In rare cases, endometrioticgrowths are found outside the peritoneum and the reproductive tract. Sinceendometriosis develops over an extended time period, the origins of thiscondition are subject to hypothetical explanations, and no one hypothesisappears to explain all manifestations of the disease (Guarnaccia et al,2000; Evers, 1996; Cramer & Missmer, 2002). However, a diverse assortmentof clinical and animal data are consistent with the Sampson (menstrual reflux)hypothesis for explaining the origins of peritoneal endometriosis (Sampson,1927; Guarnaccia et al, 2000; Evers, 1996; Cramer & Missmer, 2002; D'Hooghe& Debrock, 2002). Sampson suggested that peritoneal endometriosis developswhen fragments of functional endometrium are released from the surface ofthe uterus during menstruation and refluxed back through the Fallopian tubesto reach the peritoneal cavity. Some endometrial fragments attach to peritonealsurfaces, growing and degenerating, cyclically, in conjunction with themenstrual cycle. These ectopic endometrial growths sometimes cause inappropriateadhesions between peritoneal tissues and organs, producing debilitatingpain. When endometrial tissues occlude the fimbriated ends of the fallopiantubes, endometriosis can cause infertility.
The pathogenesis of typical ovarian endometriosis is a source of controversy. The original paper of Sampson on this condition reported that perforation of the so-called chocolate cyst led to spillage of adhesions and the spread of peritoneal endometriosis. The findings of Hughesdon (1957) contradicted Sampson’s (1921, 1927) hypothesis and suggested that adhesions are not the consequence but the cause of endometriomas (Hughesdon, 1957). In 93 % of typical endometriomas, the pseudocyst is formed by an accumulatation of menstrual debris from the shedding and bleeding of active implants located by ovarioscopy (Brosens et al., 1994, 1995) at the site of inversion, resulting in a progressive invagination of the ovarian cortex. Some other authors (Nezhat et al., 1992, 1994) have suggested that large endometriomas may develop as a result of secondary involvement of functional ovarian cysts in the endometriotic process. According to our opinion (Donnez et al., 1993, Nisolle and Donnez,), the haemorrhagic cysts are the consequence of metaplasie of epithelial inclusions in the ovary.
The cause of endometriosis remains ..
Third, several observations in the baboon model for endometriosis (D'Hoogheet al, 1994; D'Hooghe et al, 1995; D'Hooghe et al., 1996) appear to supportthe Sampson hypothesis, and the role of out flow obstruction in the inductionof endometriosis. These observations include a demonstration of the increasedincidence of retrograde menstruation in baboons with spontaneous endometriosis(D'Hooghe et al., 1996); intrapelvic injection of menstrual endometriumcausing experimental endometriosis similar to that observed in spontaneousdisease (D'Hooghe et al, 1995); and surgically induced cervical occlusionleading to retrograde menstruation and endometriosis (D'Hooghe et al, 1994).
Epidemiological data has shown that women with early menarche, shortmenstrual cycles or longer periods of menstruation are more likely to sufferfrom endometriosis (7,8,20,22-24). These findings are consistent with theSampson reflux hypothesis for the origin of peritoneal endometriosis. Onone hand, the more frequent the challenge (i.e. in women with early onsetof menstruation and those with shorter cycles) or the larger the challenge(i.e. in women with longer periods of menstruation), the more likely itis that a woman will develop endometriosis. Some clinicians also have drawnattention to epidemiological data showing a lower incidence of endometriosisamong women who have given birth and suggested that the enlargement of thecervical opening (and corresponding reduction in resistance to menstrualoutflow) to explain this finding (Cramer & Missmer, 2002). Dysmenorrheais a strong risk factor for endometriosis, but it has generally been consideredto represent a symptom of existing disease, since it is easy to imaginethat monthly bleeding from pelvic lesions is painful. However, some datasuggest that dysmenorrhea may correlate with stronger uterine contractility(Schulman et al., 1983), and one reviewer has suggested an alternate interpretation:dysmenorrhea may be associated with some degree of outflow obstruction,caused by stronger uterine cramping, and an increased propensity to retrogrademenstruation (Cramer & Missmer, 2002).
There are different hypotheses as to what causes endometriosis
Endometriosis is characterized by the growth ofendometrial tissue outside the uterus. Endometriosis may resultfrom increased cellular proliferation or a reduction in apoptosis(). The balance betweenproliferation and apoptosis is changed in eutopic endometrium fromendometriosis. Proposed hypothetical causes of endometriosisinclude retrograde menstruation, coelomic metaplasia and embryonicrest. Sampson’s theory of retrograde menstruation hypothesizes thatthe mechanical transfer, invasive implantation and ectopic growthof endometrial tissues causes endometriosis and it remains the mostwidely accepted causal theory. However, no single theory is able tocompletely explain the origin and all aspects of this disorder(). The mechanisms responsiblefor the initial development and subsequent progression ofendometriosis are not clear.
Based on epidemiological and experimental data, itis possible to a certain extent to hypothesize that retrogrademenstruation promotes implantation and the development ofendometrial tissue, in accordance with Sampson’s hypothesis. Themechanism of the initial development and subsequent progression ofendometriosis is largely unknown. There may be at least two wavesof development of endometriosis; the first wave due to bacterialinfection and the second wave from sterile inflammation (). The initial stage of anon-specific bacterial infection, such as isbelieved to occur in the uterine endometrium and peritoneal fluid(Step 1). Oxidative stress is secondary to the influx of ironduring retrograde menstruation (Step 2). Redox-activeiron-dependent oxidative stress and PAMP/DAMP-receptor signaling(Step 3) provide the combination of antiapoptosis and persistentinflammation. The release of DAMPs from damaged cells may engendera second big wave of tissue damage during chronic processes andpotentially trigger sterile inflammation-induced antiapoptotic andoxidative stress processes. In conclusion, initial infection andsubsequent sterile inflammation are closely associated with thedevelopment of endometriosis.
History of Endometriosis - Endometriosis specialist
Nezhat's et al recent article about the history of endometriosis, ..
John A. Sampson - Wikipedia
The cause of endometriosis remains unknown, ..
John Albertson Sampson (August 17, 1873–December 23, 1946) was a gynecologist who studied endometriosis
This theory was promoted by Dr John Sampson in the 1920s.
Sampson Theory Endometriosis
Endometriosis; demonstration for the Sampson theory …
There are several sources of clinical and experimental data that supportthe Sampson hypothesis and the role that "out flow obstruction"can play in the induction of endometriosis. (figure 1)
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