30 importance for fertility when examined in in-vitro fertilisation (IVF) populations (70,71). One theory as to the aetiology of adenomyosis, and also the pathophysiological mechanism behind its symptoms, relates to how adenomyosis affects the JZ and thereby uterine contractile function. Chronic peristaltic contractions could induce repeated (micro) trauma to the JZ, causing inflammation which in turn leads to locally increased oestrogen production, which stimulates myometrial activity and inducing a vicious cycle of chronic hyperperistalsis (61). Over a lifetime, this cycle leads to gradually worsening adenomyosis with increasing age (63). This theory has been corroborated by longitudinal studies that have reported a directly proportional relationship between JZ width, adenomyosis severity and age. (46,72–74). Several studies have investigated uterine contractility in endometriosis and adenomyosis, in an attempt to corroborate the theory that uterine contractions are abnormal in these diseases (75,76). It is theorised that with a disruption in the JZ, such as by adenomyosis, uterine contractility is likewise impaired, leading to so-called dysperistalsis (76,77) and consequently, adenomyosisrelated symptoms. Despite these studies showing promising results, the methods used to assess uterine contractility have been subjective, complex, and/or relatively user- and patient-unfriendly. If uterine contractility (in normal and abnormal uteri) could be objectively and reliably assessed, a concrete conclusion could be made regarding how, and if, uterine contractility is affected in adenomyosis patients.
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