Kinderwunschzentrum (Fertility Center) Darmstadt, Bratustrasse 9, 64295, Darmstadt, Germany.
Arch Gynecol Obstet. 2009 Oct;280(4):529-38. doi: 10.1007/s00404-009-1191-0. Epub 2009 Jul 31.
This study presents a unifying concept of the pathophysiology of endometriosis and adenomyosis. In particular, a physiological model is proposed that provides a comprehensive explanation of the local production of estrogen at the level of ectopic endometrial lesions and the endometrium of women affected with the disease.
In women suffering from endometriosis and adenomyosis and in normal controls, a critical analysis of uterine morphology and function was performed using immunohistochemistry, MRI, hysterosalpingoscintigraphy, videohysterosonography, molecular biology as well as clinical aspects. The relevant molecular biologic aspects were compared to those of tissue injury and repair (TIAR) mechanisms reported in literature.
Circumstantial evidence suggests that endometriosis and adenomyosis are caused by trauma. In the spontaneously developing disease, chronic uterine peristaltic activity or phases of hyperperistalsis induce, at the endometrial-myometrial interface near the fundo-cornual raphe, microtraumatizations with the activation of the mechanism of 'tissue injury and repair' (TIAR). This results in the local production of estrogen. With ongoing peristaltic activity, such sites might increase and the increasingly produced estrogens interfere in a paracrine fashion with the ovarian control over uterine peristaltic activity, resulting in permanent hyperperistalsis and a self-perpetuation of the disease process. Overt auto-traumatization of the uterus with dislocation of fragments of basal endometrium into the peritoneal cavity and infiltration of basal endometrium into the depth of the myometrial wall ensues. In most cases of endometriosis/adenomyosis, a causal event early in the reproductive period of life must be postulated leading rapidly to uterine hyperperistalsis. In late premenopausal adenomyosis, such an event might not have occurred. However, as indicated by the high prevalence of the disease, it appears to be unavoidable that, with time, chronic normoperistalsis throughout the reproductive period of life leads to the same extent of microtraumatization. With the activation of the TIAR mechanism followed by infiltrative growth and chronic inflammation, endometriosis/adenomyosis of the younger woman and premenopausal adenomyosis share in principle the same pathophysiology. In conclusion, endometriosis and adenomyosis result from the physiological mechanism of 'tissue injury and repair' (TIAR) involving local estrogen production in an estrogen-sensitive environment normally controlled by the ovary.
本研究提出了一种关于子宫内膜异位症和子宫腺肌病病理生理学的统一概念。特别是，提出了一个生理模型，该模型全面解释了异位子宫内膜病变和患病女性子宫内膜中雌激素的局部产生。
对患有子宫内膜异位症和子宫腺肌病的女性和正常对照组进行子宫形态和功能的批判性分析，使用免疫组织化学、MRI、子宫输卵管造影、阴道超声检查、分子生物学以及临床方面。将相关的分子生物学方面与文献中报道的组织损伤和修复（TIAR）机制进行了比较。
间接证据表明，子宫内膜异位症和子宫腺肌病是由创伤引起的。在自发性疾病中，慢性子宫蠕动或蠕动过度阶段会在宫底-角部的子宫内膜-子宫肌层交界处引起微创伤，激活“组织损伤和修复”（TIAR）机制。这导致雌激素的局部产生。随着蠕动的持续进行，这样的部位可能会增加，并且越来越多的雌激素以旁分泌的方式干扰卵巢对子宫蠕动的控制，导致永久性蠕动过度，并使疾病过程自我持续。子宫会发生明显的自伤，基底子宫内膜的碎片脱落在腹腔中，基底子宫内膜渗透到子宫壁的深部。在大多数子宫内膜异位症/子宫腺肌病病例中，必须假设生殖期早期存在一个因果事件，导致子宫蠕动过度迅速发生。在晚期绝经前的子宫腺肌病中，这种情况可能没有发生。然而，正如该疾病的高患病率所表明的那样，随着时间的推移，生殖期的慢性正常蠕动会导致相同程度的微创伤，这似乎是不可避免的。随着 TIAR 机制的激活，接着是浸润性生长和慢性炎症，年轻女性的子宫内膜异位症/子宫腺肌病和绝经前的子宫腺肌病在原则上具有相同的病理生理学。总之，子宫内膜异位症和子宫腺肌病是由“组织损伤和修复”（TIAR）的生理机制引起的，该机制涉及在卵巢正常控制下的雌激素敏感环境中局部产生雌激素。
