title: Possible roles of oxytocin receptor and vasopressin-1α receptor in the pathomechanism of dysperistalsis and dysmenorrhea in patients with adenomyosis uteri.
abstract: OBJECTIVE
  To investigate the expression of oxytocin (OTR) and/or vasopressin (VP1αR) receptor in patients with and without adenomyosis uteri.
  
  
  METHODS
  Retrospective nonrandomized study.
  
  
  METHODS
  University hospital endometriosis research center.
  
  
  METHODS
  Forty patients with histologically proven adenomyosis and 40 patients without adenomyosis who had undergone hysterectomy for dysmenorrhea, bleeding disorders, and fibroids.
  
  
  METHODS
  Immunohistochemical examination of both OTR and VP1αR expression in endometrium, myometrium, and adenomyotic lesions, and identification of smooth muscle cells using antibodies against OTR, VP1αR, and smooth muscle actin (sm-actin).
  
  
  METHODS
  The immunoreactive score (IRS) was used for expression of OTR, VP1αR, and sm-actin.
  
  
  RESULTS
  Expression of OTR in epithelial cells of adenomyotic lesions and surrounding myometrial cells was detectable. VP1αR was expressed only in myometrial cells and blood vessels. Using a specific anti-sm-actin antibody, another spindle cell population was characterized to represent smooth muscle cells which are in direct contact with the adenomyotic stroma. Compared with the unaffected myometrium, the surrounding adenomyosis-associated myometrium overexpressed OTR and showed changes in morphology. In the uteri of patients with adenomyosis, the junctional zone was often seen to be quite fissured.
  
  
  CONCLUSIONS
  In addition to the specific expression of VP1αR, OTR expression and morphologic changes in the myometrial architecture of uteri having adenomyosis support the hypothesis that dysperistalsis plays an essential role in the development of endometriosis and dysmenorrhea. In the near future, specific inhibition of this receptor might yield a promising treatment for therapy.
authors.affiliation: Endometriosis Research Center, Department of Obstetrics and Gynecology, Charité, Campus Benjamin Franklin, Berlin, Germany. sylvia.mechsner@charite.de
authors.forename: Sylvia
authors.initials: S
authors.lastname: Mechsner
authors.forename: Britta
authors.initials: B
authors.lastname: Grum
authors.forename: Christine
authors.initials: C
authors.lastname: Gericke
authors.forename: Christoph
authors.initials: C
authors.lastname: Loddenkemper
authors.forename: Joachim W
authors.initials: JW
authors.lastname: Dudenhausen
authors.forename: Andreas D
authors.initials: AD
authors.lastname: Ebert
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D004412:Dysmenorrhea / Q000150:complications / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D004715:Endometriosis / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D004717:Endometrium / Q000378:metabolism / Q000473:pathology; D005260:Female; D005767:Gastrointestinal Diseases / Q000150:complications / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008875:Middle Aged; D009215:Myometrium / Q000378:metabolism / Q000473:pathology; D010528:Peristalsis / Q000502:physiology; D017697:Premenopause / Q000378:metabolism; D018045:Receptors, Oxytocin / Q000378:metabolism / Q000502:physiology*; D017483:Receptors, Vasopressin / Q000378:metabolism / Q000502:physiology*; D012189:Retrospective Studies; D014591:Uterine Diseases / Q000150:complications* / Q000378:metabolism / Q000473:pathology
chemical_list: D018045:Receptors, Oxytocin; D017483:Receptors, Vasopressin