Histopathology of undescended testes

Hedinger, Ernst

doi:10.1007/bf00442177

Cited by 98 publications

(42 citation statements)

References 22 publications

(13 reference statements)

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“…The germ cell counts of cryptorchid testes are within normal limits during the 1st year of postnatal life. They fall below the normal range between 1 and 2 years of age, reaching the lowest level of germ cells per tubule at approximately 2 years of age (Hedinger, 1982;Huff et al, 1989;Schindler et al, 1987) ( Figure 1). The reduced fertility has been linked to the reduced number of germ cells, because the cryptorchid patients with the lowest total germ cell counts have the poorest spermiograms in adulthood .…”

Section: Increased Apoptotic Germ Cell Death In the Cryptorchid Humanmentioning

confidence: 94%

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Clinical aspects of male germ cell apoptosis during testis development and spermatogenesis

1997

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Apoptosis appears to have an essential role in the control of germ cell number in testes. During spermatogenesis germ cell deletion has been estimated to result in the loss of up to 75% of the potential number of mature sperm cells. At least three factors seem to determine the onset of apoptosis in male germ cells: (1) lack of hormones, especially gonadotropins and androgens; (2) the specific stage in the spermatogenic cycle; (3) and the developmental stage of the animal. Although male germ cell apoptosis has been well characterized in various animal models, few studies are presently available regarding germ cell apoptosis in the human testis. The first part of this review is focused on germ cell apoptosis in testes of prepubertal boys, with special emphasis on apoptosis in normal and cryptorchid testes. A higher percentage of apoptotic spermatogonia was seen in the cryptorchid testes than in the scrotal testes. The hCG-treatment increased the number of apoptotic spermatogonia. The hCG-treatmentinduced apoptosis in spermatogonia had severe long-term consequences in reproductive functions in adulthood. Increased apoptosis after hCG-treatment was associated with subnormal testis volumes, subnormal sperm density and pathologically elevated serum FSH. This finding indicates that increased apoptosis in spermatogonia in prepuberty leads to disruption of testis development. To evaluate the role of apoptosis in human adult testes, apoptosis was induced in seminiferous tubules that were incubated under serum-free conditions in the absence or presence of testosterone. Most frequently apoptosis was identified in spermatocytes. Occasionally some spermatids also showed signs of apoptosis. In short term incubations apoptosis was suppressed by testosterone. Our findings lead to the conclusion that apoptosis is a normal, hormonally controlled phenomenon in the human testis. The role of apoptosis in disorders of spermatogenesis remains to be established.

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Section: Increased Apoptotic Germ Cell Death In the Cryptorchid Humanmentioning

confidence: 94%

“…Several studies have detailed the morphometric features of cryptorchid testes during the early years of life (Hedinger, 1982;Huff et al, 1989;Schindler et al, 1987). The germ cell counts of cryptorchid testes are within normal limits during the 1st year of postnatal life.…”

Section: Increased Apoptotic Germ Cell Death In the Cryptorchid Humanmentioning

confidence: 99%

Clinical aspects of male germ cell apoptosis during testis development and spermatogenesis

1997

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“…Several previous studies have detailed the morphometric features of cryptorchid testes during the first years of life (4)(5)(6). The germ cell counts of cryptorchid testes is within normal limits during the first year of postnatal life.…”

Section: Introductionmentioning

confidence: 94%

“…The germ cell counts of cryptorchid testes is within normal limits during the first year of postnatal life. They fall below the normal range between 1 and 2 yr of age, reaching the lowest level of germ cells per tubule at ‫ف‬ 2 yr of age (4)(5)(6). The reduced fertility has been linked to the reduced number of germ cells because the cryptorchid patients with the lowest total germ cell counts have the poorest spermiograms in adulthood (7).…”

Section: Introductionmentioning

confidence: 99%

Germ cell apoptosis after treatment of cryptorchidism with human chorionic gonadotropin is associated with impaired reproductive function in the adult.

Dunkel¹,

Taskinen²,

Hovatta³

et al. 1997

J. Clin. Invest.

150

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Cryptorchidism results in impaired fertility. Reduced numbers of testicular germ cells can be shown histologically during the first years of life. The process causing germ cell loss in cryptorchid prepubertal boys is unknown, but it could be the result of a form of programmed cell death known as apoptosis. 25 adult men with a history of surgically treated cryptorchidism were studied, 15 of whom had received an unsuccessful human chorionic gonadotropin (hCG) therapy before orchidopexy. Apoptotic DNA fragmentation was assayed in testis biopsies taken during orchidopexy by endlabeling, both in extracted DNA and histochemically in situ. Only a few scattered apoptotic spermatogonias were seen by end-labeling of biopsies from patients not treated with hCG, whereas more extensive labeling of spermatogonia was seen after hCG treatment. As estimated by gel electrophoresis, the amount of low molecular weight DNA was 4.3-fold higher in the hCG-treated group when compared with the level in scrotal testis of non-hCG-treated patients ( P Ͻ 0.001). About 20 yr after the biopsy, the low molecular weight DNA fragmentation correlated negatively with the testis volume ( r ϭ Ϫ 0.84; P Ͻ 0.001) and positively with serum FSH levels ( r ϭ 0.73; P Ͻ 0.001). Findings in the semen analysis were similar between the groups. Apoptotic loss of spermatogonia after hCG treatment of cryptorchidism warrants reevaluation of the safety of this treatment. ( J. Clin. Invest.

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“…Clearly there are no human equivalents of the cellspecific AR knockouts described above but the effects of complete AR inactivation on spermatogenesis are similar in both mouse and human although the phenotype in the human may be more severe with few germ cells present and little progression into meiosis (Johnston et al, 2004;Hannema et al, 2006). In both species AR-null individuals are cryptorchid and the phenotype of AR-null testis is very similar to the cryptorchid testis (Johnston et al, 2004;Hedinger 1982). Differences between the AR-null mouse and human testis may, therefore, be at least a partial reflection of their sensitivity to elevated temperature.…”

Section: Post-natal Developmentmentioning

confidence: 99%

Role of androgen and gonadotrophins in the development and function of the Sertoli cells and Leydig cells: Data from mutant and genetically modified mice

O’Shaughnessy

Morris

Huhtaniemi

et al. 2009

Molecular and Cellular Endocrinology

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Histopathology of undescended testes

Cited by 98 publications

References 22 publications

Clinical aspects of male germ cell apoptosis during testis development and spermatogenesis

Clinical aspects of male germ cell apoptosis during testis development and spermatogenesis

Germ cell apoptosis after treatment of cryptorchidism with human chorionic gonadotropin is associated with impaired reproductive function in the adult.

Role of androgen and gonadotrophins in the development and function of the Sertoli cells and Leydig cells: Data from mutant and genetically modified mice

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