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Unilateral testicular torsion is common and leads to bilateral testicular injury. Spermiography is abnormal in 70% of patients after testicular torsion. Histological changes in the contralateral testis at the time of torsion have been previously interpreted as the consequence of a predisposing testicular pathology or a noxious effect of the twisted testis. We hypothesized that increased apoptosis in the contralateral testis in unilateral testicular torsion is a consequence of a breakdown in the blood-testis barrier of the twisted testis, which may increase the risk of infertility.A total of 17 patients 14 to 34 years old (mean age plus or minus standard deviation 20.7+/-6.1) underwent surgery to alleviate unilateral testicular torsion. Mean time from the first symptoms of torsion to surgery was 4.2+/-3.0 hours (range 0.5 to 11). Bilateral testicular biopsy was performed in all patients, and apoptosis was analyzed by terminal deoxynucleotidyl transferase mediated S-deoxyuridine triphosphate nick end labeling.Compared with controls, the incidence of apoptosis was increased in the contralateral testes in all patients. Apoptosis occurred predominantly in spermatocytes, early and late spermatids, and Sertoli's cells. In contrast, spermatogonia, peritubular connective tissue (fibroblasts and myofibroblasts) and endothelial cells seldom underwent apoptosis. Leydig cells were affected less often than spermatocytes. The extent of apoptosis and necrotic changes within the twisted testicle directly correlated with the duration of torsion.Extensive apoptosis is a phenomenon that occurs regularly in the germinal epithelium of the contralateral testis in testicular torsion. Specifically primary and secondary spermatocytes are predominantly affected. Notably spermatogonia, capillary endothelium, connective tissue and peritubular fibroblasts are rarely involved. A selection strategy has seemingly evolved that precludes the possibility of the perpetuation of genetic mutations. We hypothesize that trauma to the blood-testis barrier initiated by testicular torsion induces the release of apoptotic activating factors (cytokines), which subsequently cause extensive apoptosis in the germinal epithelium of the contralateral testis. Therefore, it is probable that repeat apoptotic episodes may explain the high incidence of infertility in these patients.

Purpose: The incidence of seminoma in men with cryptorchid testes is a contentious issue among physicians. Nevertheless, a positive correlation has been shown between the susceptibility for seminoma in patients with the oligo-asthenoteratospermia syndrome and in those with cryptorchid testes.Materials and Methods: We histologically examined 5,231 biopsies from 3,867 patients, including 1,121 men with the oligo-asthenoteratospermia syndrome, 218 men with azoospermia and 2,528 boys with cryptorchidism. Testicular tissue embedded in Epon was analyzed by light microscopy, fluorometry, electron microscopy and immunohistochemistry. Cell adhesion molecule CD44 was detected using a monoclonal antibody in all biopsies of patients suspected of having carcinoma in situ.Results: The incidence of seminoma was identical in boys with cryptorchidism and infertile men with the oligo-asthenoteratospermia syndrome but it was significantly higher than in the normal population. All biopsies were analyzed by a single i...

Secondary cryptorchidism was investigated after hernia repair in 15 patients 1 month to 7 years old. Testicular biopsy was obtained during orchiopexy. The number of spermatogonia per tubular cross section was higher in these patients than in boys with primary cryptorchidism, and the differences were significantly greater when the period of cryptorchidism was longer than 5 years. Loss of germ cells in secondary cryptorchidism was lower than in primary cryptorchidism. The spermatogonia per tubular cross section ratios were at the same low level in both groups in adolescence. These differences between primary and secondary cryptorchidism can be due to a lack of testicular exocrine function after a normal priming effect when the testes are in descended position. Collagenization of the peri-tubular connective tissue and the lack of germ cells are the only histological changes that occur in secondary cryptorchid testes when they have remained in cryptorchid position for 2 years, which is in marked contrast to primary cryptorchid testes that did not receive the priming effect in the first months of life. However, fertility is influenced minimally due to the presumably normal functioning of the contralateral testicle. Secondary cryptorchid testes demonstrate significant dysfunction after 5 years in that position. Germ cell loss occurs more slowly in secondary than in primary cryptorchidism. Despite the optimistic prognosis for fertility, we recommend early orchiopexy for secondary cryptorchidism to prevent exocrine insufficiency of the affected testicle.

In a clinical study 96 prepubertal boys with 100 testes located in the superficial inguinal pouch underwent routine orchiopexy. Of 65 patients 45 (69%) who had received hormonal treatment before the surgical procedure had a closed processus vaginalis compared with only 11 of 35 (31%) who had not (p less than 0.0002). A normal epididymis was also present significantly more often in those patients receiving hormonal treatment than in those who did not (p less than 0.039). While those testes located in the superficial inguinal pouch had significantly better histology and a greater number of germ cells than those located in a high inguinal or abdominal position (p less than 0.01), the number of germ cells per tubule was nonetheless lower than that seen in the normal controls (p less than 0.01). In conclusion, a testis located at the superficial inguinal pouch behaves as a true cryptorchid testis. Furthermore, hormonal treatment before surgery has a significant effect on epididymal development and closure of the processus vaginalis.