There are several theories as to how endometriosis develops, but the most widely accepted one is Sampson’s theory. First hypothesized in 1927, Sampson’s theory [1] states that three elements are required to cause endometriosis: retrograde menstruation, the presence of viable cells within the retrograde menstruation, and the implantation of these viable endometrial cells, which continue to grow and form peritoneal lesions [1].

Retrograde menstruation refers to the regression of menstrual blood backwards through the fallopian tubes into the peritoneal cavity, with subsequent attachment and implantation of endometrial fragments [2]. Several studies conducted over the last six decades have suggested that retrograde menstruation occurs in most females [3–5].

According to Sampson’s theory, some part of the endometrial lining refluxes back through the fallopian tubes into the peritoneal cavity during menstruation. Here, the endometrial cells can attach to local tissues and form their own nerve endings and blood supply. Although most women of reproductive age have some amount of retrograde menstrual flow, [6] their immune systems are usually able to clear the implanted cells and prevent their growth. When this does not occur, however, the patient develops endometriosis. Up to 20 % of women diagnosed with idiopathic infertility have endometrial implants as seen via laparoscopic examination [7].

Many factors that have yet to be studied further may play a role in the development of endometriosis, such as a damaged immune system, genetics, or exogenous factors [8]. There are many points that can be argued in favor of Sampson’s theory. The site of occurrence of several observed peritoneal endometrial or endometriotic lesions corresponds to a tubal reflux pathway. Also, endometrial cells recovered post menstruation are viable and have the capacity to grow rapidly. These cells also have integrins on their surface that allows them to attach to the peritoneal cavity. In addition, the endometrium can produce certain angiogenic factors that enable the creation of neo-angiogenesis.

The oldest alternative theory to retrograde menstruation is coelomic metaplasia. Coelomic metaplasia describes the ability of normal cell derivatives of primitive parietal peritoneum to transform into endometrial tissue [9]. The metaplasia theory is used to explain endometriosis in females with absence of menstruation, such as those who are prepubescent or have a history of total abdominal hysterectomy, in premenopausal women, and in rare cases of endometriosis in males [11–13].

The theory of coelomic metaplasia is based on the fact that the ovaries and Mullerian ducts are derived from the coelomic epithelium. This epithelium may undergo metaplastic transformation to form tissue much like that of the endometrium.

The coelomic epithelium is a common ancestor to both peritoneal and endometrial cells, and it may transform into the latter by means of chronic inflammation [7]. The metaplasia theory is viable because it can explain the presence of endometriosis in the absence of menstruation, such as in men who undergo estrogen therapy for prostate cancer, pre-menarche women, and post-menopausal females [13, 14]. However, there are many points that argue against the idea. If the metaplasia theory is true, endometriosis would be possible without the presence of an endometrium, such as in women with a congenital absence of the uterus or in healthy males through the potential of peritoneal metaplasia. Coelomic metaplasia would then also be expected to occur anywhere in the body where tissue derived from the coelomic epithelium is found. Hence, most scientific institutions continue to cite the retrograde menstruation theory instead [7].