Cryptorchidism pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saumya Easaw, M.B.B.S.[2]

Pathophysiology

Normal Fetal Testicular Development and Descent

The testes begin as an immigration of primordial germ cells into testicular cords along the genital ridge in the abdomen of the early embryo. The interaction of several male genes organizes this developing gonad into a testis rather than an ovary by the second month of gestation. During the 3rd to 5th months, the cells in the testes differentiate into testosterone-producing Leydig cells, and anti-müllerian hormone-producing Sertoli cells. The germ cells in this environment become fetal spermatogonia. Male external genitalia during the 3rd and 4th months of gestation and the fetus continues to grow, develop, and differentiate.

The testes remain high in the abdomen until the 7th month of gestation, when they move from the abdomen through the inguinal canals into the two sides of the scrotum. It has been proposed that movement occurs in two phases, under control of somewhat different factors. The first phase, movement across the abdomen to the entrance of the inguinal canal appears controlled (or at least greatly influenced) by anti-müllerian hormone (AMH). The second phase, in which the testes move through the inguinal canal into the scrotum, is dependent on androgens (most importantly testosterone). In rodents, androgens induce the genitofemoral nerve to release calcitonin gene-related peptide(CGRP), which produces rhythmic contractions of the gubernaculum, a ligament which connects the testis to the scrotum, but a similar mechanism has not been demonstrated in humans. Maldevelopment of the gubernaculum, or deficiency or insensitivity to either AMH or androgen therefore can prevent the testes from descending into the scrotum. Some evidence suggests there may even be an additional paracrine hormone, referred to as descendin, secreted by the testes.

In many infants with inguinal testes, further descent of the testes into the scrotum occurs in the first 6 months of life. This is attributed to the postnatal surge ofgonadotropins and testosterone that normally occurs between the first and fourth months of life.

Spermatogenesis continues after birth. In the 3rd to 5th months of life, some of the fetal spermatogonia residing along the basement membrane become type A spermatogonia. More gradually, other fetal spermatogonia become type B spermatogonia and primary spermatocytes by the 5th year after birth. Spermatogenesis arrests at this stage until puberty.

Most normal-appearing undescended testis are also normal by microscopic examination, but reduced spermatogonia can be found. The tissue in undescended testes becomes more markedly abnormal ("degenerates") in microscopic appearance between 2 and 4 years after birth. There is some evidence that early orchiopexy reduces this degeneration.