MRC Centre for Reproductive Health, Queens Medical Research Institute, The University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.
Hum Reprod Update. 2013 Sep-Oct;19(5):558-69. doi: 10.1093/humupd/dmt024. Epub 2013 May 29.
BACKGROUND Endometriosis affects 6-10% of women of reproductive age and is associated with chronic pelvic pain, dysmenorrhoea, dyspareunia and infertility. Endometriosis is defined by the presence of endometrial tissue outside the uterus, most commonly attached to the pelvic peritoneum. The endometrium in women with endometriosis is reported to be altered and there is increasing evidence that the phenotype of the pelvic peritoneum may also play a role in the establishment and maintenance of the disease. The aim of this review is to discuss the putative role of the pelvic peritoneum in the pathophysiology of peritoneal endometriosis. METHODS A review was undertaken of the published literature on (i) the anatomy and physiology of the peritoneum and (ii) the potential roles played by peritoneal cells in the establishment and maintenance of peritoneal endometriosis. The current understanding of the biology of peritoneal endometriosis is summarized and the potential interaction of the peritoneum with ectopic endometrial cells in endometriosis is highlighted. RESULTS Several studies indicate that differential expression of peritoneal mesothelial adhesion factors occurs in women with endometriosis, providing potential ectopic endometrial cell attachment sites for the establishment of endometriosis lesions. Changes in the peritoneal mesothelial cell phenotype, including loss of tight junctions, may allow ectopic cells to bind to, or early lesions to invade into, the extracellular matrix. Epithelial-to-mesenchymal transition of peritoneal mesothelial cells may also lead to an increase in lesion invasion and formation of fibrotic tissue in and around the lesion. There is evidence that the peritoneal mesothelium may also play a role in the invasion potential of ectopic cells by production of MMPs increasing local tissue remodelling. Peritoneal immune scavenging function may be lowered in women with endometriosis; for example there is a notable increase in macrophage-derived secretion products in women with endometriosis associated with increases in cell proliferation, cell adhesion and neovascularization. CONCLUSIONS The pelvic peritoneum appears to play a key role in the development and maintenance of endometriosis.
子宫内膜异位症影响着 6-10%的育龄妇女，与慢性盆腔疼痛、痛经、性交困难和不孕有关。子宫内膜异位症的定义是子宫内膜组织出现在子宫以外的部位，最常见的是附着在盆腔腹膜上。有报道称，患有子宫内膜异位症的女性子宫内膜发生改变，越来越多的证据表明，盆腔腹膜的表型也可能在疾病的发生和维持中发挥作用。本综述的目的是讨论盆腔腹膜在腹膜子宫内膜异位症发病机制中的可能作用。方法：对已发表的关于（i）腹膜解剖和生理学和（ii）腹膜细胞在建立和维持腹膜子宫内膜异位症中可能发挥的作用的文献进行了综述。总结了目前对腹膜子宫内膜异位症生物学的认识，并强调了腹膜与异位子宫内膜细胞在子宫内膜异位症中的潜在相互作用。结果：几项研究表明，子宫内膜异位症患者腹膜间皮黏附因子的表达存在差异，为异位子宫内膜细胞建立子宫内膜异位症病灶提供了潜在的附着部位。腹膜间皮细胞表型的改变，包括紧密连接的丧失，可能使异位细胞与细胞外基质结合，或使早期病变侵入细胞外基质。腹膜间皮细胞的上皮-间充质转化也可能导致病变的侵袭性增加，并在病变周围形成纤维组织。有证据表明，腹膜间皮细胞也可能通过产生增加局部组织重塑的 MMP 来发挥作用，从而增加异位细胞的侵袭潜能。子宫内膜异位症患者的腹膜免疫清除功能可能降低；例如，子宫内膜异位症患者的巨噬细胞衍生分泌产物显著增加，与细胞增殖、细胞黏附和新生血管形成增加有关。结论：盆腔腹膜似乎在子宫内膜异位症的发生和维持中起着关键作用。
