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

Abstract

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 auto-traumatization.

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 non-pregnant 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 auto-traumatization 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 non-pregnant 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.

Figures

Fig. 1

The clinical characteristics of the patients who entered the study

Fig. 2

Percentage of patients with the diagnosis of adenomyosis using limits of detection based on the thickness of the junctional zone ranging from ≥6 to ≥12 mm in the sagittal plane of the anterior or posterior wall of the uterus in 143 patients

Fig. 3

MRI scans of a 25 years old patient with extreme primary dysmenorrhea as an example for the establishment of the diagnosis of adenomyosis by ‘visualisation’. The diameter of the JZ in the mid-sagittal plane would not allow for the diagnosis of adenomyosis (a). A closer analysis of an enlargement of the JZ in the left cornual angle (b and c) revealed beginning cystic cornual angle adenomyosis (d) (arrow)

Fig. 4

Adenomyosis in a 32-year-old woman without dysmenorrhea. In the sagittal scan the hypointense area could result from an episodic neometral contraction (top). The coronal scan performed after a short lapse of time, however, reveals adenomyosis with signs of spread of the lesion in various directions (bottom)

Fig. 5

The course of a peristaltic wave of the archimyometrium as shown by a sequence of MRI scans obtained from cinematographic MRI scan in a healthy woman in the late follicular phase. Initially, the archimyometrium appears to be relaxed, indicated by a thin JZ with a less marked hypointensity (a). The peristaltic wave starts with tension of the archimyometrium in the lower half of the uterine corpus, indicated by marked hypointensity of the JZ (b). The zone of increased tension (marked hypointensity) moves in a fundal direction. A muscular package is built up, indicated by the rapid increase of the JZ as the wave moves in a fundal direction (c–e) followed by a rapid relaxation (f)

Fig. 6

Cystic coronary angle adenomyosis in an infertile woman aged 40 years with extreme primary dysmenorrhea and documented endometriosis. In the sagittal midline of the uterus, no enlarged JZ could be demonstrated

Fig. 7

Cystic cornual angle adenomyosis in an infertile woman aged 39 years with extreme primary dysmenorrhea. Laparoscopy was not performed. In addition to the cornual cysts, there is an enlargement of the JZ in the midline of the anterior uterine wall (coronary plane; bottom left)

Fig. 8

Six examples of cystic cornual angle adenomyosis. These women suffered from extreme primary dysmenorrhea

Fig. 9

The longitudinal extension of adenomyotic lesions in a percent of the cases in the upper third (a), middle third (b) and lower third (c) of the uterus. Adenomyotic lesions were localized predominantly in the upper two-thirds of the uterine corpus and extended also over the whole length of the uterine corpus (a+b+c). They rarely presented in the lower two-thirds (b+c) and never in the lower third (c)

Fig. 10

Schematic representation of the mechanism of uterine auto-traumatization by uterine peristalsis and hyperperistalsis at the fundo-cornual raphe. Green arrows direction of sperm transport. Red arrows distraction of basal stromal cells and archimyometrial myocytes at the fundo-cornual raphe by uterine peristalsis. With the development of an early adenomyotic lesion in the midline of the upper uterine corpus, a chronic process of proliferation and inflammation is established that facilitates the detachment of the basal endometrium. Fragment of detached functionalis (a) and a fragment of detached basalis (b) in menstrual blood (modified from [2, 4, 7])

Fig. 11

Recording of intrauterine pressure in an adolescent girl with extreme primary dysmenorrhea on the second day of the cycle (Courtesy L. Wildt and B. Böttcher)

Fig. 12

Schematic representation of uterine auto-traumatization by the mechanism of ‘archimetral compression due to neometral contraction’ at the onset of menstruation. N neometra; E endometrium; A archimyometrium (a). Due to the high intrauterine pressure in consequence of the contraction of the neometra, the archimyometrium ruptures in the cornual angles and fragments of basal endometrium are dislocated into the myometrial wall, where they develop into endometriotic cysts (b and c). At the same time, basal stromal cell at the fundo-cornual raphe are chronically overstretched resulting in the initiation of the TIAR mechanism and the development of an adenomyotic lesion