Cryptorchidism is recognized as a significant risk factor for male germ cell tumors and infertility, with a complex and multifaceted mechanism contributing to male infertility. When the testes fail to descend into the scrotum, increased local temperature and pressure lead to increased apoptosis of spermatogenic and Sertoli cells. Additionally, disruptions in the hypothalamic–pituitary–gonadal axis result in decreased testosterone levels within the testes, and abnormal secretion of follicle-stimulating hormone and luteinizing hormone, negatively impacting spermatogenesis. Cryptorchidism also induces increased oxidative stress within the testes, leading to sperm DNA damage and impairment of the sperm plasma membrane, hindering sperm–oocyte fusion. Unilateral cryptorchidism may cause injury to the ipsilateral genitofemoral nerve, further affecting the contralateral testis by increasing oxidative stress and apoptosis. Moreover, the production of antisperm antibodies can trigger autoimmune responses, potentially damaging germ cells and contributing to infertility. Damage to type A dark spermatogonia (type Ad spermatogonia) is also considered a high-risk factor for male infertility. Understanding the mechanisms by which cryptorchidism leads to male infertility may provide new avenues for enhancing fertility in affected patients.

Keywords: antisperm antibody; apoptosis; genitofemoral nerve; hypothalamic–pituitary–gonadal axis; oxidative stress; type Ad
spermatogonia