Pathophysiology of adenomyosis

Abstract

Adenomyosis refers to endometrial glands and stroma located haphazardly deep within the myometrium. Similar histological alterations may be found in extrauterine locations such as the rectovaginal septum. The aetiology and pathogenic mechanism(s) responsible for adenomyosis are poorly understood. Both human and experimental studies favour the theory of endomyometrial invagination of the endometrium, although the de-novo development of adenomyosis from Mullerian rests in an extrauterine location is a possibility. The prerequisite for adenomyosis may be triggered or facilitated by either a 'weakness' of the smooth muscle tissue or an increased intrauterine pressure or both. Relatively high oestrogen concentrations and impaired immune-related growth control in ectopic endometrium may be necessary for the maintenance of adenomyosis. Smooth muscle cell hyperplasia and hypertrophy are a reflection of reactive change secondary to ectopic endometrial proliferation. Further studies are needed for insight into the precise aetiology and pathogenesis of adenomyosis. Adenomyosis is a relatively frequent endomyometrial pathology discovered in multiparous women between 40 and 50 years of age. About 2/3 of women are symptomatic with menorrhagia and dysmenorrhoea; 80% of adenomyotic cases are associated with leiomyomata uteri; and in women with endometrial adenocarcinoma, adenomyosis is relatively often seen. Definite diagnosis is made on hysterectomy specimens, although attempts are made at securing preoperative diagnosis by magnetic resonance imaging and myometrial biopsies. Definite treatment of symptomatic women is hysterectomy.