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Morphological profiles of cryptorchid XXY mouse testes
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AbstractTwo mice with an XXY karyotype and cryptorchid testes appeared spontaneously in a colony. The animals were H‐Y antigen‐positive, and had elevated serum levels of follicle‐stimulating (FSH) and luteinizing (LH) hormones. Testes of the affected mice were atrophic, containing a few solid seminiferous cords surrounded by vast amounts of compact interstitial material. The cords were delimited by a broad tunica propria in which the basal lamina was irregularly thickened and stratified into a number of alternating dense and less dense layers. Most sex cords were populated by mature Sertoli cells and small pleomorphic elements resembling monocytic‐derived macrophages. Within some cords, the macrophages aggregated into a central mass with which identifiable Sertoli cells and (PAS) periodic acid Schiff‐positive fragments of basal lamina were associated. In more severely damaged cords, the basal lamina and peripheral carpet of Sertoli cells were totally missing. Such cords were populated only by the central macrophages with fragments of basal lamina and degenerating Sertoli cells. Finally, a few collapsed remnants of cords contained compact nodules of macrophages surrounded by what appeared to be the outer part of the tunica propria. The interstitial area, as well as the outer walls of the seminiferous cords were also heavily infiltrated by macrophages. Overall, the morphological picture was one of severe immunological injury. We do not know what role, if any, the genetic constitution and/or intra‐abdominal environment may play in the expression of these bizarre pathologies. However, such severe changes have not been reported in either Klinefelter's syndrome or the undescended testes of any human or subprimate species.
Title: Morphological profiles of cryptorchid XXY mouse testes
Description:
AbstractTwo mice with an XXY karyotype and cryptorchid testes appeared spontaneously in a colony.
The animals were H‐Y antigen‐positive, and had elevated serum levels of follicle‐stimulating (FSH) and luteinizing (LH) hormones.
Testes of the affected mice were atrophic, containing a few solid seminiferous cords surrounded by vast amounts of compact interstitial material.
The cords were delimited by a broad tunica propria in which the basal lamina was irregularly thickened and stratified into a number of alternating dense and less dense layers.
Most sex cords were populated by mature Sertoli cells and small pleomorphic elements resembling monocytic‐derived macrophages.
Within some cords, the macrophages aggregated into a central mass with which identifiable Sertoli cells and (PAS) periodic acid Schiff‐positive fragments of basal lamina were associated.
In more severely damaged cords, the basal lamina and peripheral carpet of Sertoli cells were totally missing.
Such cords were populated only by the central macrophages with fragments of basal lamina and degenerating Sertoli cells.
Finally, a few collapsed remnants of cords contained compact nodules of macrophages surrounded by what appeared to be the outer part of the tunica propria.
The interstitial area, as well as the outer walls of the seminiferous cords were also heavily infiltrated by macrophages.
Overall, the morphological picture was one of severe immunological injury.
We do not know what role, if any, the genetic constitution and/or intra‐abdominal environment may play in the expression of these bizarre pathologies.
However, such severe changes have not been reported in either Klinefelter's syndrome or the undescended testes of any human or subprimate species.
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