Testicular Hypoplasia Is Driven by Defective Vascular Formation.

OBJECTIVE

To determine if vanishing testis could result from a fault in embryological development as a result of an arrest in endothelial cell migration rather than secondary to just a random physical torsion/twist. A testicular nubbin or vanishing testis is considered to be secondary to a neonatal torsion and is usually associated with a hemosiderin deposit.

MATERIALS AND

METHODS

Cases of vanishing testis excision were compared with age-matched controls from cadaveric testes without known genitourinary pathology. To assess the testis microvasculature, we performed immunohistochemistry using an automated staining platform with controlled and standardized conditions and positive and negative controls. We used cluster of differentiation (CD) 34 to stain blood vessel endothelium, stem cells, and interstitium; CD31 (all endothelium); and D2-40 for lymphatic endothelium. Morphometric analysis was carried out, % of the total tissue with CD31 and CD34 positive stain was assessed, and the number of the lymphatic vessels (D2-40) per mm2 was counted.

RESULTS

Of the 10 cases, 7 had evidence of hemosiderin deposit and calcification. The % distribution of CD34 in controls was higher, 13.4 ± 3.1 (mean ± standard deviation), compared to nubbin cases, 4.5 ± 2.9 (P ≤ .001). The % distribution of CD31 was 2.8 ± 0.83 in controls compared to 1.31 ± 0.60 in cases (P ≤ .001). The lymphatic distribution was similar in both groups, cases (6.4 ± 4.3 n/mm2) and controls (6.4 ± 1.7 n/mm2) (P = .99)

CONCLUSION

This histopathological study suggests that disturbances in endothelial development may be a contributing factor leading to testicular hypoplasia and a resultant nubbin testis, independent of a physical torsion event.