Adenomyosis and endometriosis. Re-visiting their association and further insights into the mechanisms of auto-traumatisation. An MRI study

G. Leyendecker 0 1 2 3 A. Bilgicyildirim 0 1 2 3 M. Inacker 0 1 2 3 T. Stalf 0 1 2 3 P. Huppert 0 1 2 3 G. Mall 0 1 2 3 B. Bottcher 0 1 2 3 L. Wildt 0 1 2 3 0 G. Mall Institute of Pathology , Klinikum Darmstadt, Academic Teaching Hospital to the Universities of Frankfurt/Main and Heidelberg/ Mannheim , Grafenstr. 7, 64283 Darmstadt, Germany 1 P. Huppert Institute of Diagnostic and Interventional Radiology, Academic Teaching Hospital to the Universities of Frankfurt/Main and Heidelberg/Mannheim , Grafenstr. 7, 64283 Darmstadt, Germany 2 G. Leyendecker (&) A. Bilgicyildirim M. Inacker T. Stalf Kinderwunschzentrum (Fertility Center) Darmstadt , Bratustr. 9, 64293 Darmstadt, Germany 3 B. Bottcher L. Wildt Department of Obstetrics and Gynecology, University Clinic of Gynecological Endocrinology and Reproductive Medicine, Medical University Innsbruck , Anichstrasse 35, 6020 Innsbruck, Austria Purpose In a series of publications, we had developed the concept that uterine adenomyosis and pelvic endometriosis as well as endometriotic lesions at distant sites of the body share a common pathophysiology with endometriosis constituting a secondary phenomenon. Uterine auto-traumatization and the initiation of the mechanism of tissue injury and repair (TIAR) were considered the primary events in the disease process. The present MRI study was undertaken (1) to corroborate this concept by re-visiting, in view of discrepant results in the literature, the association of adenomyosis with endometriosis and (2) to extend our views concerning the mechanisms of uterine autotraumatization. Patients and methods MRI was performed in 143 women attending our center, in whom, on the basis of transvaginal - sonography (TVS) and historical data, such as documented endometriosis and dysmenorrhea of various degrees of severity, the presence of uterine adenomyosis was suspected. In addition to the measurement of the diameter of junctional zone (JZ) of the anterior and posterior walls in the mid-sagittal plane, the diagnosis of adenomyosis was based on visualization, in that all planes were analyzed with scrutiny. By this method of visualization all transient enlargement of the JZ, such as peristaltic waves of the archimyometrium and sporadic neometral contractions that might mimic adenomyotic lesions could be excluded. At the same time, this method allowed to lower the limit of detection in terms of thickness of the JZ for assured diagnosis of adenomyosis. Furthermore, the localizations of the individual lesions, their shapes and patterns were described. Results With the method of visualization, the diagnosis of uterine adenomyosis could be verified in 127 of the 143 patients studied. The prevalence of endometriosis in adenomyosis was 80.6 % and the prevalence of adenomyosis in endometriosis was 91.1 %. As concluded from their localization within the uterine wall, the adenomyotic lesions predominantly developed in the median region of the upper two-thirds of the uterine wall. Cystic cornual angle adenomyosis was a distinct phenomenon that was only observed in patients suffering from extreme primary dysmenorrhea. Aside from this, the majority of the patients complained of primary dysmenorrhea (80 %). On the basis of these findings and the fact that particularly extreme primary dysmenorrhea is associated with high intrauterine pressure, menstrual archimetral compression by neometral contraction has to be considered as an important cause of uterine auto-traumatization in addition to uterine peristalsis and hyperperistalsis. Both mechanical functions of the nonpregnant uterus exert their strongest power in the upper region of the uterus, which is compatible with the predominant localization of the adenomyotic lesions. Conclusions The data confirm our previous results of a high association of adenomyosis with endometriosis and vice versa. Our view of the mechanism of uterine autotraumatization by mechanical functions of the non-pregnant uterus has to be extended, in that archimetral compression by neometral contractions could be realized as the predominant cause of mechanical strain to the nonpregnant uterus. The data of this study confirm our concept of the etiology and pathophysiology of adenomyosis and endometriosis in that the process of chronic proliferation and inflammation is induced at the level of the archimetra by chronic uterine auto-traumatization. Furthermore, with respect to the diagnosis of uterine adenomyosis (and consequently endometriosis) this study shows a high degree of accordance between the findings in real-time TVS and MRI. In spite of continuous efforts, the etiology and pathophysiology of adenomyosis and endometriosis and their interrelationship are not fully understood. There is increasing evidence that adenomyosis constitutes an important factor of infertility. Therefore, the elucidation of its pathophysiology is of utmost clinical importance. In a series of reports, we had developed the view that these lesions are highly associated and are the results of uterine auto-traumatization [16]. The pathophysiological process was termed tissue injury and repair (TIAR) [79]. The present study was conducted to corroborate and extend this view. The work of Rokitansky, von Recklinghausen, Freund and Cullen [1016] laid the basis of the present understanding of adenomyosis as a benign uterine tumor derived from Mullerian duct tissue [17]. The gross and microscopic morphology, the expansion beyond the uterine confines, the occurrence at distant sites in the body and the main clinical characteristics were described in detail by these authors. With his basically correct and seminal concept of tubal dissemination of endometrial tissue into the peritoneal cavity, Sampson dealt therefore only with a segmental part of the disease [18]. Furthermore, he did not appreciate uterine adenomyosis as a significant component of the pathophysiological process. While it was well established that uterine adenomyosis resulted from a focal infiltration and/or broad expansion of Mullerian tissue into the underlying myometrium with continuity of the endometrial glandular structures [14, 19], he suggested uterine adenomyosis to result from vascular transmission [20]. Although the view that uterine adenomyosis and endometriosis constitute a nosological entity was never completely abandoned [21]; with time and enforced by the introduction of laparoscopy as a diagnostic procedure, Sampsons theory led to regard endometriosis mainly as a peritoneal disease resulting from retrograde menstruation, while uterine adenomyosis nearly fell into oblivion [8, 2224]. Until the beginning of this century much scientific effort was laid on corroborating Sampsons concept [25]. A reconsideration of the uterus as a significant determinant in the disease process was initiated, when it was shown that the non-pregnant uterus is not a quiescent organ, but rather actively involved in the early process of reproduction by mechanical func (...truncated)