Does the Cranial Suspensory Ligament Have a Role in Cryptorchidism?

Abstract

The cranial suspensory ligament (CSL) is a fibromuscular structure anchoring the embryonic gonad to the posterior abdominal wall in male and female mammals. Its persistence in females is believed to be responsible for retaining the ovaries within the abdomen, while its regression in males permits testis descent. Embryonic loss of the CSL in males is believed to be an androgen-dependent event, and failure of this process has been proposed as a cause of cryptorchidism. The present study demonstrates that the nuclei of mesenchymal cells in the caudal part of the CSL are immunoreactively positive for androgen receptor. We examined the effects of exposure of the non-steroidal antiandrogen flutamide during the period from gestational day 10 to birth on the development of the CSL and on testis descent. Exposure of male Albino Swiss rats to the antiandrogen flutamide during this period resulted in feminization of the external genitalia and the suppression of growth of the testes and male reproductive tracts. In adulthood, testes were found to be located in diverse positions including normal scrotal (50%), intra-abdominal (10%) and ectopic suprainguinal (40%). The CSL of the testis persisted into adulthood in all flutamide-treated males, regardless of testis location. In all cases, the ligament consisted of bundles of smooth muscle fibres in the retroperitoneal fat of the posterior abdominal wall. These findings suggest that androgen blockade during embryonic development interferes with testicular descent, but that maldescent cannot be correlated with either the persistence of the CSL of the testis or its structure.

Regional Variation in Androgen Receptor Expression and Biomechanical Properties May Contribute to Cryptorchidism Susceptibility in the LE/orl Rat

“…We found consistent AR expression in the gubernacular cord, also known as the cranial suspensory ligament (CSL). This finding is consistent with evidence from prior expression studies and from rodent models of AR deficiency in males and androgen exposure in females, which suggest that shortening of the cord is androgen dependent (7, 10, 37, 44–47). INSL3 and DHT regulate many of the same E17 gubernacular transcripts in vitro and both target WNT signaling, but the effects of DHT occur after 24 h, but not 6 h, of stimulation (38).…”

Staged rotation flap scrotoplasty and orchidopexy in a patient with inguinal ectopic scrotum

“…Testicular descent from the lumbar area to the labioscrotal folds is by a complex mechanism. The cranial suspensory ligament is a fibromuscular structure anchoring the embryonic gonad to the posterior abdominal wall; its regression permits testicular descent [ 6 ]. It is thought that loss of the cranial suspensory ligament in males is dependent on testosterone, secreted along with Müllerian inhibiting substance (MIS) by the developing testis [ 7 ].…”

GLI3 resides at the intersection of hedgehog and androgen action to promote male sex differentiation

“…The essential role of androgens in the regression of the CSL comes from animal studies that show that disturbances in androgen synthesis or action result in retained CSL [23,58]. Although it is reported that the CSL is a fibromuscular structure composed of smooth muscle fibers and abundant collagen [59], there are few details regarding the collagen content of the CSL. To our knowledge, very few studies have administered exogenous DHT to rescue failure of CSL regression [60]; our studies show that DHT was able to reduce the collagen content of the CSL suggesting an AR-mediated program in collagen degradation.…”