In the bipotential state (6th gestational week), the external genitalia consist of a genital tubercle, a urogenital sinus, and two lateral labioscrotal swellings. Unlike the internal genitalia where both duct systems initially coexist, the external genitalia are neutral primordia able to develop into either male or female structures depending on gonadal steroid hormone signals. Normally, this differentiation is under the active influence of androgen from the Leydig cells of the testis. The genital tubercle forms the penis, labioscrotal folds fuse to form a scrotum, and folds of the urogenital sinus form the penile urethra. The testis begins androgen secretion by 8-9 weeks; masculinization of the external genitalia is manifest 1 week later and is completed by 14 weeks. To achieve this morphologic change, external genitalia target tissue cells must convert testosterone to dihydrotestosterone (DHT) by the intracellular enzyme 5a-reductase. In the male, DHT mediates the follittleing androgen events: temporal hairline recession, growth of facial and body hairs, development of acne, and development of the external genitalia and prostate.
In the absence of this androgen effect (the absence of a Y chromosome, the presence of an ovary, the absence of a gonad, abnormalities in androgen receptor or postreceptor events, or defects of the 5a-reductase enzyme), the folds of the urogenital sinus remain open, forming the labia minora, the labioscrotal folds form the labia majora, the genital tubercle forms the clitoris, and the urogenital sinus differentiates into the vagina and the urethra. Thus, the littleer vagina is formed as part of the external genitalia.

Exposure to androgens at critical time periods leads to variable masculinization.
Androgen exposure at 9-14 weeks superimposes variable external ambiguity on the basic female phenotype (clitoral hypertrophy, hypospadias, scrotalization of nonfused labia). By the same token, incompletely masculinized genitalia will result if sufficient local androgen concentration or activity is not achieved by the 12th week in the male. Because of shared common tissue origin, male-female external genital structural ambiguities reflect abnormal androgen impact: males too little, females too much.