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Cryptorchidism (derived from the Greek ''κρυπτός'', ''kryptos'', meaning hidden ''ὄρχις'', ''orchis'', meaning testicle) is the absence of one or both testes from the scrotum. It is the most common birth defect of the male genitalia. In unique cases, cryptorchidism can develop later in life, often as late as young adulthood. About 3% of full-term and 30% of premature infant boys are born with at least one undescended testis. However, about 80% of cryptorchid testes descend by the first year of life (the majority within three months), making the true incidence of cryptorchidism around 1% overall. Cryptorchidism is distinct from monorchism, the condition of having only one testicle. A testis absent from the normal scrotal position can be found: #along the "path of descent" from high in the posterior (retroperitoneal) abdomen, just below the kidney, to the inguinal ring; #in the inguinal canal; #''ectopically'', that is, to have "wandered" from that path, usually outside the inguinal canal and sometimes even under the skin of the thigh, the perineum, the opposite scrotum, or the femoral canal; #undeveloped (''hypoplastic'') or severely abnormal (''dysgenetic''); #to have vanished (also see anorchia). About two thirds of cases without other abnormalities are unilateral; one third involve both testes. In 90% of cases an undescended testis can be felt in the inguinal canal; in a minority the testis or testes are in the abdomen or nonexistent (truly "hidden"). Undescended testes are associated with reduced fertility, increased risk of testicular germ cell tumors and psychological problems when the boy is grown. Undescended testes are also more susceptible to testicular torsion (and subsequent infarction) and inguinal hernias. Without intervention, an undescended testicle will usually descend during the first year of life, but to reduce these risks, undescended testes can be brought into the scrotum in infancy by a surgical procedure called an orchiopexy.〔The (A.D.A.M. Medical Encyclopedia )〕 Although cryptorchidism nearly always refers to ''congenital'' absence or maldescent, a testis observed in the scrotum in early infancy can occasionally "reascend" (move back up) into the inguinal canal. A testis which can readily move or be moved between the scrotum and canal is referred to as ''retractile''. ==Normal fetal testicular development and descent== The testes begin as an immigration of primordial germ cells into testicular cords along the gonadal 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 develop 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 can therefore 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 of gonadotropins 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. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「cryptorchidism」の詳細全文を読む スポンサード リンク
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