314 



PHYSIOLOGY OF GONADS 



(1956j have .shown that these Ley dig cells 

 give strong histochemical reactions sug- 

 gestive of the presence of steroidal ma- 

 terials, it is presumed that the human fetal 

 testis produces androgens responsible for 

 its descent. Were this true, it would appear 

 reasonable that human chorionic gonado- 

 trophin produced throughout the pregnancy 

 could be responsible for the formation and 

 secretion of androgenic substances by the 

 fetal testis. Such an action would provide a 

 function for human chorionic gonadotrophin 

 during the last two trimesters of pregnancy. 

 However, Wells (1944) held androgens from 

 adrenal sources responsible for testicular de- 

 scent. 



The precise control of testicular descent 

 is not known. Gonadotrophins effective on 

 the Leydig cells induce rapid descent. An- 

 drogens hasten descent and estrogens in- 

 hibit it (Mussio Fournier, Estefan, Grosso 

 and Albrieux, 1947). However, Finkel 

 (1945) concluded that descent may be a 

 genetic phenomenon in the opossum, which 

 seems to be different from rodents in many 

 aspects of testicular physiology. Because 

 hormonal secretion is not detected in the 

 opossum until the 100th day and because 

 descent occurs earlier, it was doubted that 

 androgens are responsible for descent. 



The effects of cryptorchism on the histo- 

 logic appearance of the human testis have 

 been the subject of many studies. However, 

 few new observations have been made since 

 the excellent description by Cooper (1929) 

 of the normal and retained testis in man. 

 Cooper studied abdominal and scrotal testes 

 at various ages from birth to senility and 

 concluded: (1) the farther the prepubertal 

 testis descends, the more similar it is to 

 its normal scrotal mate; (2) sperm cells 

 are rare in retained testes but occasionally 

 may be found in testes held at the external 

 ring; (3) the younger the child, the more 

 normal is the retained testis; (4) the Leydig 

 cells are not affected adversely by retention, 

 nor are they more numerous, as earlier ob- 

 servers had thought. As a result of these 

 conclusions, surgical treatment of retained 

 testes in the first two years of life was ad- 

 vised. 



Rea (1939) concluded erroneously that 

 the undescended testis is normal until pu- 

 berty but stated correctly that it rapidly de- 



generates after puberty. That the retained 

 testis may not be normal before puberty and 

 is almost always abnormal after puberty 

 was confirmed by Nelson (1953), and by 

 Robinson and Engle (1954). Before the age 

 of 5 years, the scrotal testis and the crypt- 

 orchid testis are indistinguishable histologi- 

 cally; after this time, the cryptorchid tes- 

 tis is always retarded in growth and dif- 

 ferentiation. Puberty is accompanied by 

 growth of both the scrotal and the retained 

 testis, but the retained testis does not keep 

 pace with its scrotal mate. Nelson (1951) 

 pointed out that fewer spermatogonia are 

 present in the retained testis than in the 

 scrotal mate and that this difference be- 

 comes proportionally greater after puberty. 

 The testis retained for a long time becomes 

 fibrotic. The germinal epithelium (except- 

 ing the Sertoli cells) is destroyed but the 

 Leydig cells are said to be normal. How- 

 ever, Sohval (1954) found that the number 

 of Sertoli cells in the pubertal retained tes- 

 tis is less than that in the normal scrotal 

 testis. In older men, the Sertoli cells may 

 be obliterated, in which case the tubules 

 eventually become hyalinized. This is not 

 an invariable sequence in testes retained 

 for long periods. Sohval stated that a man, 

 aged 42, produced sperm from a retained 

 testis. 



The comments just presented are based 

 on the supposition that failure of descent 

 occurs in normal testes because of adhesions 

 or abnormalities of the canal, or because of 

 failure of the normal stimulus for descent. 

 However, lack of descent also may result 

 because the testis is intrinsically defective 

 (Nelson, 1953). Three boys were described 

 whose undescended testes did not contain 

 germ cells; however, the descended testes 

 also did not have germ cells, so the rela- 

 tionship between germinal aplasia and non- 

 descent is not clear. Another type of abnor- 

 nuility was described by Sohval ( 1954) and 

 referred to as "tubular dysgenesis." These 

 tubules were characterized by the absence 

 of Sertoli cells and spermatogonia. Only 

 undifferentiated cells were present. Further- 

 more, these tubules did not become fibrotic 

 after puberty. Dysgenetic tubules were ob- 

 served in about half of the cases of crypt- 

 orchism. 



Little doubt exists, therefore, that the fer- 



