Pediatric Gynecology: Assessment Strategies and Common Problems

Jane H. Kass-Wolff, RN, MS; Ellen E. Wilson, MD

Disclosures

Semin Reprod Med. 2003;21(4) 

In This Article

Normal Anatomy and Physiology

Embryonic differentiation of the normal female genital tract begins early first trimester in the presence of two normal X chromosomes and in the absence of the masculinizing Y chromosome. Development of the Müllerian ducts occurs with fusion at the midline and subsequent caudal migration of the fused ductal system to the urogenital sinus. In the female, the Wolffian duct system degenerates in the absence of testosterone.[1] At 5 to 6 weeks' gestation, the undifferentiated gonad is bipotential and is capable of differentiating into either a testis or an ovary.[2] Gonadal sex is established under the influence of the chromosomal sex. Beginning around 12 weeks' gestation the ovarian cortex begins to develop, with primordial follicles appearing at around 13½ weeks. The fetal hypothalamic-pituitary-ovarian (HPO) axis is functioning at ~12 weeks of age with unrestrained pulsatile release of embryonic hypothalamic gonadotropin-releasing hormone. There is a maturation of the HPO axis toward term with the development of a negative feedback to estradiol. At birth the female infant has ~1 to 2 million germ cells remaining.[1]

Estrogen synthesis by the fetal ovary is low at term but maternal estrogen readily crosses the placenta and estrogenizes the neonate. At birth the placental separation causes an elevation in follicle-stimulating hormone and luteinizing hormone with a brief neonatal stimulation of the ovarian axis (Fig. 1). Perinatal ovarian cysts have been described following delivery but resolve spontaneously as gonadotropin levels fall physiologically.[3] For the first year and a half or so gonadotropins will continue to cause some ovarian stimulation and endogenous estrogen production.[4] Thus, the young female has two reasons for an estrogen effect on the genital mucosa: (1) effect of high maternal estrogen levels are retained and (2) stimulation of the child's ovaries by their own gonadotropins. Beyond the first year and a half till puberty, ovarian quiescence occurs due to the exquisite pituitary and hypothalamic sensitivity to even low levels of estrogen.[1]

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