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According to our guest author Marc R. Laufer, MD, the “development of the female genital tract is a complex process that is dependent upon a series of events involving cellular differentiation, migration, fusion, and canalization. Failure of any one of these processes results in a congenital anomaly.”1
In 1933, A.K. Koff coined the terms sinovaginal bulb and vaginal plate. He proposed that the upper 80% of the vagina is derived from Müllerian epithelium and the lower 20% derived from urogenital sinus epithelium.2 In 1957, D. Bulmer proposed that vaginal epithelium derives solely from urogenital sinus epithelium.3 And in 2017, Robboy et al. supported Bulmer’s proposal that human vaginal epithelium derives solely from urogenital sinus epithelium and differs from mouse vaginal development.4
Beginning at 3 weeks of embryogenesis and continuing into the second trimester of pregnancy, development of the female genital tract takes place. The sinovaginal bulbs originate in the urogenital sinus at the distal aspect of the Müllerian tubercle. At approximately 13 weeks, these two solid evaginations grow out of the pelvic part of the urogenital sinus and proliferate into the caudal end of the uterovaginal canal to become a solid vaginal plate. Degeneration of the central cells of this vaginal plate, which occur in a cephalad direction, enables creation of the lower vagina. Canalization is generally completed by 20 weeks’ gestation.
Agenesis or absence of the lower vagina is usually associated with normal development of the upper vagina, cervix, uterus, and ovaries. It is the result of abnormal development of the sinovaginal bulbs and vaginal plate.
The hymenal membrane separates the vaginal lumen from the urogenital sinus. Secondary to degeneration of the central epithelial cells, the hymen typically ruptures, leaving a thin fold of mucous membrane around the vaginal introitus. Hymenal anatomic variants include microperforate, septate, or cribriform. They occur secondary to incomplete degeneration of the central portion of the hymen.
Dr. Laufer is chief of the division of gynecology, codirector of the Center for Young Women’s Health, and director of the Boston Center for Endometriosis, all at Boston Children’s Hospital. He also is professor of obstetrics, gynecology, and reproductive biology at Harvard Medical School, Boston. Dr. Laufer is an acclaimed physician, surgeon, clinical researcher, author, and teacher, and it is truly my pleasure to welcome him to this edition of the Master Class in Gynecologic Surgery.
Dr. Miller is a clinical associate professor at the University of Illinois at Chicago and past president of the AAGL. He is a reproductive endocrinologist and minimally invasive gynecologic surgeon in metropolitan Chicago and the director of minimally invasive gynecologic surgery at Advocate Lutheran General Hospital, Park Ridge, Ill. He reported no disclosures relevant to this Master Class. Email him at pdnews@mdedge.com.
References
1. Laufer M. Congenital anomalies of the hymen and vagina. Uptodate (accessed April 2019).
2. Contrib Embryol. 1933 Sep;24(140):59-91.
3. J Anat. 1957 Oct;91(4):490-509.
4. Differentiation. 2017 Sep-Oct;97:9-22.
According to our guest author Marc R. Laufer, MD, the “development of the female genital tract is a complex process that is dependent upon a series of events involving cellular differentiation, migration, fusion, and canalization. Failure of any one of these processes results in a congenital anomaly.”1
In 1933, A.K. Koff coined the terms sinovaginal bulb and vaginal plate. He proposed that the upper 80% of the vagina is derived from Müllerian epithelium and the lower 20% derived from urogenital sinus epithelium.2 In 1957, D. Bulmer proposed that vaginal epithelium derives solely from urogenital sinus epithelium.3 And in 2017, Robboy et al. supported Bulmer’s proposal that human vaginal epithelium derives solely from urogenital sinus epithelium and differs from mouse vaginal development.4
Beginning at 3 weeks of embryogenesis and continuing into the second trimester of pregnancy, development of the female genital tract takes place. The sinovaginal bulbs originate in the urogenital sinus at the distal aspect of the Müllerian tubercle. At approximately 13 weeks, these two solid evaginations grow out of the pelvic part of the urogenital sinus and proliferate into the caudal end of the uterovaginal canal to become a solid vaginal plate. Degeneration of the central cells of this vaginal plate, which occur in a cephalad direction, enables creation of the lower vagina. Canalization is generally completed by 20 weeks’ gestation.
Agenesis or absence of the lower vagina is usually associated with normal development of the upper vagina, cervix, uterus, and ovaries. It is the result of abnormal development of the sinovaginal bulbs and vaginal plate.
The hymenal membrane separates the vaginal lumen from the urogenital sinus. Secondary to degeneration of the central epithelial cells, the hymen typically ruptures, leaving a thin fold of mucous membrane around the vaginal introitus. Hymenal anatomic variants include microperforate, septate, or cribriform. They occur secondary to incomplete degeneration of the central portion of the hymen.
Dr. Laufer is chief of the division of gynecology, codirector of the Center for Young Women’s Health, and director of the Boston Center for Endometriosis, all at Boston Children’s Hospital. He also is professor of obstetrics, gynecology, and reproductive biology at Harvard Medical School, Boston. Dr. Laufer is an acclaimed physician, surgeon, clinical researcher, author, and teacher, and it is truly my pleasure to welcome him to this edition of the Master Class in Gynecologic Surgery.
Dr. Miller is a clinical associate professor at the University of Illinois at Chicago and past president of the AAGL. He is a reproductive endocrinologist and minimally invasive gynecologic surgeon in metropolitan Chicago and the director of minimally invasive gynecologic surgery at Advocate Lutheran General Hospital, Park Ridge, Ill. He reported no disclosures relevant to this Master Class. Email him at pdnews@mdedge.com.
References
1. Laufer M. Congenital anomalies of the hymen and vagina. Uptodate (accessed April 2019).
2. Contrib Embryol. 1933 Sep;24(140):59-91.
3. J Anat. 1957 Oct;91(4):490-509.
4. Differentiation. 2017 Sep-Oct;97:9-22.
According to our guest author Marc R. Laufer, MD, the “development of the female genital tract is a complex process that is dependent upon a series of events involving cellular differentiation, migration, fusion, and canalization. Failure of any one of these processes results in a congenital anomaly.”1
In 1933, A.K. Koff coined the terms sinovaginal bulb and vaginal plate. He proposed that the upper 80% of the vagina is derived from Müllerian epithelium and the lower 20% derived from urogenital sinus epithelium.2 In 1957, D. Bulmer proposed that vaginal epithelium derives solely from urogenital sinus epithelium.3 And in 2017, Robboy et al. supported Bulmer’s proposal that human vaginal epithelium derives solely from urogenital sinus epithelium and differs from mouse vaginal development.4
Beginning at 3 weeks of embryogenesis and continuing into the second trimester of pregnancy, development of the female genital tract takes place. The sinovaginal bulbs originate in the urogenital sinus at the distal aspect of the Müllerian tubercle. At approximately 13 weeks, these two solid evaginations grow out of the pelvic part of the urogenital sinus and proliferate into the caudal end of the uterovaginal canal to become a solid vaginal plate. Degeneration of the central cells of this vaginal plate, which occur in a cephalad direction, enables creation of the lower vagina. Canalization is generally completed by 20 weeks’ gestation.
Agenesis or absence of the lower vagina is usually associated with normal development of the upper vagina, cervix, uterus, and ovaries. It is the result of abnormal development of the sinovaginal bulbs and vaginal plate.
The hymenal membrane separates the vaginal lumen from the urogenital sinus. Secondary to degeneration of the central epithelial cells, the hymen typically ruptures, leaving a thin fold of mucous membrane around the vaginal introitus. Hymenal anatomic variants include microperforate, septate, or cribriform. They occur secondary to incomplete degeneration of the central portion of the hymen.
Dr. Laufer is chief of the division of gynecology, codirector of the Center for Young Women’s Health, and director of the Boston Center for Endometriosis, all at Boston Children’s Hospital. He also is professor of obstetrics, gynecology, and reproductive biology at Harvard Medical School, Boston. Dr. Laufer is an acclaimed physician, surgeon, clinical researcher, author, and teacher, and it is truly my pleasure to welcome him to this edition of the Master Class in Gynecologic Surgery.
Dr. Miller is a clinical associate professor at the University of Illinois at Chicago and past president of the AAGL. He is a reproductive endocrinologist and minimally invasive gynecologic surgeon in metropolitan Chicago and the director of minimally invasive gynecologic surgery at Advocate Lutheran General Hospital, Park Ridge, Ill. He reported no disclosures relevant to this Master Class. Email him at pdnews@mdedge.com.
References
1. Laufer M. Congenital anomalies of the hymen and vagina. Uptodate (accessed April 2019).
2. Contrib Embryol. 1933 Sep;24(140):59-91.
3. J Anat. 1957 Oct;91(4):490-509.
4. Differentiation. 2017 Sep-Oct;97:9-22.
