Mai K T, Yazdi H M, Perkins D G, Parks W
Department of Laboratory Medicine, Ottawa Civic Hospital, Ontario, Canada.
Histopathology. 1997 May;30(5):430-42. doi: 10.1046/j.1365-2559.1997.4910725.x.
Ten cases of endometriosis of bowel, ovaries, uterine serosa and 10 cases of adenomyosis were studied. Blocks of tissue with areas of interest were submitted for serial sectioning of the entire block. Some sections were immunostained for oestrogen receptor, vimentin, Ber-EP-4 and cytokeratins. The common finding was the presence of type 1 nodules, consisting of isolated nodules of endometrial stromal cells without endometrial glands, along blood or lymphatic vessels. The stromal cells showed positive immunoreactivities for oestrogen receptor and vimentin, and negative reactivities for cytokeratins. Due to the absence of connection with adjacent endometriosis or adenomyosis, it is likely that these endometrial stromal nodules arise from the multipotential pericytes. In addition, in serosa of all cases of endometriosis, type 2 nodules, having adjacent mesothelium (Ber-EP4-) changing into epithelium (Ber-EP4+) and type 3 nodules, with non-endometrial epithelium (oestrogen receptor-) changing into endometrial gland (oestrogen receptor+) were identified. We believe that the formation of type 1 nodules from the pericytes and the transformation of the mesothelium into endometrial glands in type 2 and 3 nodules are accomplished through the process of induction by the endometrial stroma, and the proliferation is controlled by genetic, hormonal and immunological factors. Type 1, 2 and 3 nodules are likely to represent a histological continuum in the development of early endometriosis. Subsequent to the formation of endometriosis in the serosa, the pathway of development of endometriosis and adenomyosis is similar. Through the processes of induction and proliferation there is an increase in size of the stroma of type 1 nodules and that of endometrial tissue with subsequent fusion of the stroma of type 1 nodules and that of foci of adenomyosis or endometriosis. Consequently, there is enlargement of the stroma of the foci of adenomyosis or endometriosis. The 'newly enlarged stroma' serves as 'new soil' for further growth of the endometrial glands in the endometrial tissue.
对10例肠道、卵巢、子宫浆膜子宫内膜异位症患者以及10例子宫腺肌病患者进行了研究。将含有感兴趣区域的组织块进行整块连续切片。部分切片进行雌激素受体、波形蛋白、Ber-EP-4和细胞角蛋白免疫染色。常见的发现是存在1型结节,由沿血管或淋巴管分布的孤立的子宫内膜间质细胞结节组成,无子宫内膜腺体。间质细胞雌激素受体和波形蛋白免疫反应阳性,细胞角蛋白免疫反应阴性。由于与相邻的子宫内膜异位症或子宫腺肌病无联系,这些子宫内膜间质结节可能起源于多能周细胞。此外,在所有子宫内膜异位症病例的浆膜中,发现了2型结节,即相邻间皮(Ber-EP4阴性)转变为上皮(Ber-EP4阳性),以及3型结节,即非子宫内膜上皮(雌激素受体阴性)转变为子宫内膜腺体(雌激素受体阳性)。我们认为,1型结节由周细胞形成,2型和3型结节中间皮转变为子宫内膜腺体是通过子宫内膜间质的诱导过程完成的,其增殖受遗传、激素和免疫因素控制。1型、2型和3型结节可能代表早期子宫内膜异位症发展过程中的组织学连续体。浆膜中子宫内膜异位症形成后,子宫内膜异位症和子宫腺肌病的发展途径相似。通过诱导和增殖过程,1型结节的间质以及子宫内膜组织的间质增大,随后1型结节的间质与子宫腺肌病或子宫内膜异位症病灶的间质融合。因此,子宫腺肌病或子宫内膜异位症病灶的间质增大。“新增大的间质”为子宫内膜组织中子宫内膜腺体的进一步生长提供了“新土壤”。