Correspondence (letter to the editor): Morphological Findings

The pathogenesis of cryptorchidism is not known and likely to be multifactorial. On one hand, the extent of testicular changes—for example, the reduced number of spermatogones per tubular cross section, the reduced diameter of the tubuli, the fibrosis of the testes—depends on the position of the gonads. Intra-abdominal testicles have the most severe lesions. On the other hand, the patients’ age at the time of the operation is important. The older the boys are at the time of their surgery the more pronounced the changes. The unphysiological position of the gonads impairs normal testicular development in adolescence and results in an increase of existing lesions. The decrease in spermatogones is crucial as it may impair fertility at a later stage.

Patients with unilateral cryptorchidism may also develop impaired fertility or even infertility. In unilateral testicular retention, the scrotal testicle will be affected by the same severe changes as the retained gonad in one third of cases.

The “increase” in spermatogones after GnRH therapy probably only seems like an increase, because these cells are stimulated by hormone therapy and are thus more clearly visible.

In so called testicular aplasia, no genuine aplasia is present; the term may be established but is erroneous. The primary embryonic gonads are subsequently partially or completely scarred, and the cause of this is usually not found.

The cause of the increased incidence of germ cell tumors in cryptorchidism remains unexplained. The presence of atypical germ cells in retained prepubertal testicles has not been confirmed as far as we are aware.