PURPOSE: 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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: 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
Authors: Ashok Agarwal; Reda Z Mahfouz; Rakesh K Sharma; Oli Sarkar; Devna Mangrola; Premendu P Mathur Journal: Reprod Biol Endocrinol Date: 2009-12-05 Impact factor: 5.211