Here is an interesting article discussing epigenetics in endometriosis. While they do assimilate epigenetics with pathogenesis of endo (since endo has been seen in fetuses, it is still more plausible that it is laid down embryonically), the incidence of epigenetics playing a role in how the disease presents itself and is influenced is interesting to consider.
Here's a tidbit:
"Endometriosis has been regarded as an ultimate hormonal disease, owing much to its estrogen-dependency and aberrations in estrogen production and metabolism (Bulun et al., 2002; Kitawaki et al., 2002; Gurates and Bulun, 2003). It also has been viewed as an immunological disease due to a myriad immunological aberration in endometriosis (Paul Dmowski and Braun, 2004; Ulukus and Arici, 2005). In addition, it has been thought of a disease caused by exposure to environmental pollution and toxins (Rier et al., 1993; Rier, 2002) although so far there are no solid human data (Guo, 2004). Finally, it has been regarded as a genetic disease (Simpson et al., 2003; Barlow and Kennedy, 2005), due, apparently, to its reported familial aggregation. Yet even the reported familial aggregation, when examined closely, may be debatable (Di and Guo, 2007), and there has been little progress regarding the identification of genetic variants that predispose women to endometriosis (Di and Guo, 2007; Falconer et al., 2007; Guo, 2009b)."
((((((NOTE: some of the references are dated- such as little progress to genetic variances when there have been such since then (2007).)))))
"Given the reported epigenetic aberrations in endometriosis, one question is whether these aberrations are the cause or merely the consequence of endometriosis. Since most, if not all, human studies reporting epigenetic aberrations in endometriosis are carried out cross-sectionally, the reported aberration may be a cause for, but also could be a consequence of, endometriosis.
"Aging (Wilson and Jones, 1983; Toyota and Issa, 1999; Richardson, 2002), diet (Jacob et al., 1998), chronic inflammation (Hsieh et al., 1998; Issa et al., 2001), prolonged transcriptional suppression (Song et al., 2002; Stirzaker et al., 2004) and even maternal care (Champagne et al., 2006). In endometriosis, it has been shown that prolonged stimulation of an endometriotic epithelial-like cell line by tumor necrosing factor (TNFα), which has been shown to have increased production in endometriosis, resulted in at least partial methylation in the PR-B promoter (Wu et al., 2008b). This provides evidence that certain phenotypic changes in endometriosis, such as increased production of proinflammatory cytokines, may also cause epigenetic aberrations, which in turn result in changes in gene expression and subsequently other phenotypic changes such as increased cellular proliferation (Wu et al., 2008a) and perhaps some phenotypic changes."