Congenital Anomalies of the Vas Deferens and Epididymis

Kroovand, R. Lawrence; Perlmutter, Alan D.

doi:10.1007/978-94-010-3719-8_15

Cited by 12 publications

(12 citation statements)

References 42 publications

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“…Malformations of the epididymis are frequently seen in cryptorchid boys [9,24,38,40,41,49], and this supports the theory that the epididymis could be the prime mover of TD.…”

mentioning

confidence: 65%

Pathogenesis and treatment of undescended testes

Hadžiselimović¹

1982

Eur J Pediatr

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Impaired intrauterine gonadotropin secretion was the cause of cryptorchidism in 78% of cryptorchid boys studied. On the one hand, this impairment implied the underdevelopment of the epididymis and thus the cryptorchid state of the gonad. On the other hand, the histological alterations of the testis, due to impaired gonadotropin secretion were Leydig cell atrophy and an impairment in the number of the germ cells. The secondary damage, due to the unfavorable position, started during the second year of life. To avoid this damage, early treatment is highly recommended. Hormonal treatment with GnRH is the treatment of first choice. This treatment was successful in 60% of cryptorchid boys. An additional treatment of nonresponders with low doses of hCG increased the overall success rate to 80%. Six months after treatment, 14.5% of those successfully treated suffered a relapse.

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“…Malformations of the epididymis are frequently seen in cryptorchid boys [9,24,38,40,41,49], and this supports the theory that the epididymis could be the prime mover of TD.…”

mentioning

confidence: 65%

Pathogenesis and treatment of undescended testes

Hadžiselimović¹

1982

Eur J Pediatr

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“…Turek et al [5] described 6 epididymal variations that were identified in a review of 112 normally descended testes, including the variation described in our patient. Kroovand and Perlmutter [7] described 8 congenital structural abnormalities of the epididymis.…”

Section: Discussionmentioning

confidence: 98%

Torsion of the epididymis

Brisson

Feins

Patel

2005

Journal of Pediatric Surgery

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“…Clinically, failure of the human vas deferens to develop appropriately and failure of the tubules of the caput region to reach the testis, epididymal disjunction, are failures of the Wolffian duct and mesonephric tubules respectively to undergo normal morphogenesis. Interestingly, a study has shown that 30–79% of boys with an undescended testis also showed Wolffian duct abnormalities of which 25% displayed epididymal disjunction (Girgis et al, 1969; Kroovand and Perlmutter, 1981; Mehta et al, 2008; Turek et al, 1994; Zvizdic et al, 2009). Therefore, the mechanisms by which the Wolffian duct undergoes morphogenesis and the key factors that regulate this event were a focus of this study.…”

Section: Discussionmentioning

confidence: 99%

Protein tyrosine kinase 7 is essential for tubular morphogenesis of the Wolffian duct

Washington

Domeniconi

et al. 2016

Developmental Biology

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The Wolffian duct, the proximal end of the mesonephric duct, undergoes non-branching morphogenesis to achieve an optimal length and size for sperm maturation. It is important to examine the mechanisms by which the developing mouse Wolffian duct elongates and coils for without proper morphogenesis, male infertility will result. Here we show that highly proliferative epithelial cells divide in a random orientation relative to the elongation axis in the developing Wolffian duct. Convergent extension (CE)-like of cell rearrangements is required for elongating the duct while maintaining a relatively unchanged duct diameter. The Wolffian duct epithelium is planar polarized, which is characterized by oriented cell elongation, oriented cell rearrangements, and polarized activity of regulatory light chain of myosin II. Conditional deletion of protein tyrosine kinase 7 (PTK7), a regulator of planar cell polarity (PCP), from mesoderm results in loss of the PCP characteristics in the Wolffian duct epithelium. Although loss of Ptk7 does not alter cell proliferation or division orientation, it affects CE and leads to the duct with significantly shortened length, increased diameter, and reduced coiling, which eventually results in loss of sperm motility, a key component of sperm maturation. In vitro experiments utilizing inhibitors of myosin II results in reduced elongation and coiling, similar to the phenotype of Ptk7 knockout. This data suggest that PTK7 signaling through myosin II regulates PCP, which in turn ensures CE-like of cell rearrangements to drive elongation and coiling of the Wolffian duct. Therefore, PTK7 is essential for Wolffian duct morphogenesis and male fertility.

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Congenital Anomalies of the Vas Deferens and Epididymis

Cited by 12 publications

References 42 publications

Pathogenesis and treatment of undescended testes

Pathogenesis and treatment of undescended testes

Torsion of the epididymis

Protein tyrosine kinase 7 is essential for tubular morphogenesis of the Wolffian duct

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