Objective To assess the hypothesis that during fetal development, the external urethral sphincter changes from a concentric sphincter of undifferentiated muscle fibres to a transient ring of striated muscle which regresses caudo-cranially in the posterior urethra during the first year of life, when the sphincter assumes its omega-shaped configuration. Materials and methods The anatomy and development of the external urinary sphincter was assessed in human males and females during fetal life. Plastic-embedded sections (transverse, sagittal and frontal planes; 300-700 mm) of the pelvis of 31 females and 31 males (9 weeks of gestation to newborn) were stained with azure II/methylene blue/basic fuchsin and viewed at r 4-80. The sections of interest were taken from the bladder neck to the perineum. The sections of the membranous urethra were reconstructed three-dimensionally using a computer program. Results In both male and female an omega-shaped external sphincter was apparent in all specimens at >10 weeks of gestation. In the early fetal period (ninth week), there was undifferentiated mesenchyme; in this period the mesenchyme was more dense in the anterior part and loose in the posterior part of the urethra. In females, there was a close connection between the urethra and the anterior wall of the vagina. Conclusion The omega-shaped configuration of the external urethral sphincter was recognisable from 10 weeks of gestation in both sexes. There was no suggestion of a change from a cylindrical to an omegashaped sphincter in the fetal period to birth. Also, a transient 'tail' posterior to the sphincter was not apparent. The rectovesical septum was well developed in neonates. There is no reason to assume that the development of the septum leads to an apoptosis of muscle cells in the posterior part of the external sphincter in males after birth. The anatomical development of the external sphincter does not explain transient outlet obstruction during fetal life. The function of the muscle may change during development because of neuronal maturation.

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