The major authors of the last century described endometriosis as ectopic endometrial lesions occurring both in the uterus and in the peritoneal cavity, and the lesions were considered as variants of the same disease process. In the 1920s a theory had been put forward that, although severely and chronically challenged, resulted in the clear cut separation of the two entities. A new understanding of the disease process, however, enables to reunify these two disease entities and to integrate them into a new nosological concept. Circumstantial evidence suggests that endometriosis and adenomyosis share a similar pathophysiology and 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, microtraumata with the activation of the basal and general mechanism of “tissue injury and repair” (TIAR). This results in the local production of estrogens. With ongoing peristaltic activity, such sites will accumulate and the increasingly produced estrogens interfere via paracrine mode of action with the endocrine 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 to uterine hyperperistalsis. In late premenopausal adenomyosis such overt 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 may result in events that accumulate to the same extent of microtraumatizations. 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 principal 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. It appears that many of the altered endometrial molecular markers described in the context of endometriosis are the consequence rather than the cause(s) of the disease.
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