Hadziselimovic F, Geneto R, Emmons L R
University Clinics, Children's Hospital, Basel, Switzerland.
J Urol. 1998 Sep;160(3 Pt 2):1158-60. doi: 10.1097/00005392-199809020-00053.
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.
单侧睾丸扭转较为常见，并会导致双侧睾丸损伤。在睾丸扭转患者中，70%的患者精子造影异常。此前，扭转时对侧睾丸的组织学变化被解释为睾丸易患病理改变的结果或扭转睾丸的有害影响。我们推测，单侧睾丸扭转时对侧睾丸中凋亡增加是扭转睾丸血睾屏障破坏的结果，这可能会增加不育风险。
共有17例年龄在14至34岁（平均年龄±标准差为20.7±6.1）的患者接受了缓解单侧睾丸扭转的手术。从扭转的首发症状到手术的平均时间为4.2±3.0小时（范围为0.5至11小时）。所有患者均进行了双侧睾丸活检，并通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法分析凋亡情况。
与对照组相比，所有患者对侧睾丸中的凋亡发生率均增加。凋亡主要发生在精母细胞、早期和晚期精子细胞以及支持细胞中。相比之下，精原细胞、睾丸间质结缔组织（成纤维细胞和肌成纤维细胞）和内皮细胞很少发生凋亡。睾丸间质细胞受影响的频率低于精母细胞。扭转睾丸内凋亡和坏死变化的程度与扭转持续时间直接相关。
广泛凋亡是睾丸扭转时对侧睾丸生精上皮中经常出现的一种现象。具体而言，初级和次级精母细胞受到的影响最为显著。值得注意的是，精原细胞、毛细血管内皮、结缔组织和睾丸间质成纤维细胞很少受累。似乎已经形成了一种选择策略，排除了基因突变延续的可能性。我们推测，睾丸扭转引发的血睾屏障损伤会诱导凋亡激活因子（细胞因子）的释放，随后导致对侧睾丸生精上皮发生广泛凋亡。因此，反复的凋亡事件可能解释了这些患者中不育的高发生率。
