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Cryptorchidism, which is derived from two Greek terms: kryptos, meaning hidden, concealed; and orchis, derivatives meaning testis, has undergone a sea change regarding both social and medical consequences during the last century. Hitherto to the 20th century, the undescended testis generally lacked clinical significance. This is evidenced by the fact that among the large descriptive series of testicular maldescent from this time, usually no interventions were obtained and no documentation of testicular location and position changes were noted.
The seriousness of this condition was underscored by reports that cryptorchidism is the most frequent birth defect found during examination of sudden infant death syndrome and postmortem studies. The relationship between cryptorchidism and the incidence of germ cell tumor in the male is of sufficient epidemiologic import that international and national cancer groups now recommend surveillance of high-risk males. In addition, the treatise signature of the endocrine disrupting compounds by goods producing this condition has resulted in accelerated legislative activity by both national and international consortia.
Testicular descent is both a maturational endpoint as well as a process which is essential in the development of the normal male. Cryptorchidism arises when one or both testes fail to descend scrotally. This is strictly a disorder of boys, does not occur during adulthood, and mainly affects the neonate and young infant.
The severity of cryptorchidism is related to the location of the testes and laterality, with approximately 95% of undescended testes being found in the inguinal canal or abdomen. Cryptorchidism is a common abnormality occurring in 1 to 4% of all full-term male births, and even higher in premature boys. The likelihood of spontaneous descent drops precipitously after three months and the perceived wisdom is that the testes will be permanently undescended and will not develop normal function if they are not corrected earlier. Prompt diagnosis and treatment, as well as coexisting anomalies with other organ systems, is essential in the prevention of long-term testicular injury.
Cryptorchidism is a significant risk factor for testicular cancer, as testicular germ cell disease arises from the cell lineage that connects early gonocytes with later spermatogonia during the first year of life in males. The treatment of cryptorchidism is based on the increased risk of subfertility later in life, testicular torsion in ectopic locations, and malignant transformation of an ectopic testicle.
This has led to surgical treatment not only of descended testes, but also of cryptorchid intraabdominal and inguinal testes. However, the need for common signs of increased risk for these conditions, other than retained gonocyte maturation and test volume measurement, is not obvious. Early diagnosis may help avoid unnecessary surgery.
The congenital anomalies most associated with cryptorchidism are those of the male genitalia, such as hypospadias, bifid scrotum, and monorchism. Furthermore, cryptorchidism may be associated with an increased risk for infertility later in life, as well as long-term psychological and cosmetic effects. It also leads to human suffering related to expensive investigations and treatment.
Cryptorchidism (undescended testis) is a common developmental malformation, occurring in 1 to 2% of full-term infants and 15% of preterm infants. By the age of 8 months, more than 80% of testes have descended into the scrotum. During the first year of life, the scrotal position of the testis decreases from 4% to 25%. The greatest likelihood of spontaneous descent within the first year is when the testis is palpated at the base of the scrotum during the initial clinical examination shortly after birth.
The incidence at one year has been estimated at 30% for abdominal testes, 60% for inguinal testes, and less than 1% for absent testes. Sixty percent of incorrectly categorized vanishing testes were initially non-palpable at the base of the scrotum. Therefore, it has been suggested that some of the vanishing testes may actually be either inguinal or abdominal. The majority of vanishing testes within the first year can be explained by spontaneous descent during clinical check-ups between birth and one year of age.
This change in positioning is particularly momentous during the maturational phase for the resuming spermatogonial stem cell, a segment which also seems to be influenced by two different hormones such as anti-Müllerian hormone and testosterone. There is also an increasing number of men in whom the adverse health features of the syndrome have prompted an era of delayed fertility. We shall review the consequences of cryptorchidism on testicular development and function, and also in case with hormone insufficiency.
Constitutional testosterone insufficiency may also be accountable and germline deletions seem to be the main genetic cause of this insufficiency, which delivers evidence for the possible function of the Dachshund 1 gene in male fetal development. High grade cryptorchidism represents an extensive problem facing pediatric surgery, which might then also be consistent with failing function following the reduction or higher grade scrotal approach for closure of the internal ring and thereby potentially triggering testicular cycle alterations from its disrupted positioning during the third trimester of development.
Cryptorchidism is the failure of the testes to descend into the scrotum. However, the first weeks of testicular growth normally transpire in utero. From then on, until the second trimester of the fetal period, this descent or migration of the gonadal tissue from the intermediate mesoderm in the pelvic region to the scrotum takes place. The development of the genitofemoral nerve, the gubernaculum and the LfcR cell line or other relevant gonadogenesis-linked transcription factors seem to be likely factors to play vital modulation roles in this process.
Maternal complications during pregnancy, such as a malfunction in the endocrine or reproductive system caused by disorders associated with fluctuations in hormones, may cause cryptorchidism. Ethological studies mostly focused on pregnant women who were prescribed drugs that were either subsequently prohibited or regulated due to increased side effects connected with the use during pregnancy.
The cause of cryptorchidism is not known. The process of testicular formation and changes in fetal testosterone do not appear to be different in males with undescended testicles compared to those with normally descended testicles. The majority of cryptorchidism is nonsyndromic (meaning undescended testicle is detected alone).
However, if inversely correlated with the age of diagnosis in the individual, there is the possibility of an abnormality of hormone activity or resistance in the individual developing a syndromic condition. Despite the fact that the formation of genital abnormalities is a symptom of other problems for some of these conditions (of either severe or mild form or affecting all or a portion of the genitalia), scarcely few are associated with undescended testicle alone, not taking into account other genital irregularities, which include micropenis, hypospadias, ectopic testicle, ambiguous genitalia, etc. Scarcely few are due to mutational changes and the connected molecular causes are usually not known.
We recognize that there are significant problems with current available techniques and guidelines and that they are not able to identify those with an unnecessarily increased risk, which means that phylogenetic independent lines of thought should be the basis of evidence-based decisions to ensure that something is done.
Currently, the majority of patients undergoing orchidopexy do not have biopsies taken, as the benefits are not being recognized at this stage. However, it is essential that we continue to collect all the data that will allow us to give our patients the best care now and in the future. The significantly increased risk of testicular cancer and associated risk of hormonal/sexual development gives ample reason to continue biopsying these patients in our surveillance protocols.
We now include microlithiasia as a category of clinical relevance, as there appears to be more evidence that it may be associated with TDS. Keeping in mind that there is an association between cryptorchidism, testicular torsion, testicular trauma, and testicular cancer, this allows for a better understanding of what is normal and what is at a significant increased risk and how these boys should be monitored throughout their formative years.
When considering a patient with suspected cryptorchidism, the most pertinent questions are: Is it a testis and where is it located? These two questions determine the most appropriate clinical management strategy. To address these questions, a thorough history, physical examination, and selected investigations are typically required. Factors determining the likelihood of spontaneous descent are outlined in Table 1. There is an increased risk of associated TDS and decreased fertility in patients with undescended testes or cryptorchidism.
Cryptorchidism is associated with various forms of TDS, ranging from the silent carrier to the patient with obvious end-organ dysfunction and intersex disorder. As such, a complete and accurate diagnosis of each patient is paramount. Making the correct diagnosis will impact management decisions for the patient and their family and may also impact future fertility.
UDT is asymptomatic unless it is accompanied by complications such as testis torsion, which shows clinical signs such as abrupt onset of severe colicky groin pain and vomiting, paraesthesia is localized to the scrotal sac, radiates to groin or lower abdomen or perineal sac, the cremasteric reflex is generally sluggish, or absent. Generally, UDT is discovered and diagnosed during a routine physical examination by pediatricians, pediatric surgeons, or during formal school medical aspects such as those carried out by school doctors.
Fetal testis should already have descended to its normal anatomical position, the scrotum, by the end of the pregnancy. However, this does not occur in 3-4% of boys; one or both testes can have been retained trapped at any point in the testicle’s descental route even before or after they take place, and this is called cryptorchidism or undescended testis (UDT).
Cryptorchidism can be classified as unilateral (one testis) or bilateral UDT according to the number of testes affected. In more than 80% of cryptorchidism cases, UDT has a non-palpable status and it is intra-abdominal. A non-palpable testis is a common cause of referral to pediatric surgery and is often recognized as cryptorchidism during school medical visits. Nonetheless, pediatricians should ensure that the same checks are carried out during the neonatal period (testicular palpation during post-delivery examinations).
When looking at a child, now they are trained to find and localize the testis, which is situated in the scrotal pouch. Specifically, this is in the scrotum. The word cryptorchidism was derived from Latin, with the terms cryptus and orchis. Cryptus meaning hidden and orchis meaning testis, hence meaning cryptorchidism as the hidden testis. The normal anatomical location of the testis is inside the scrotum, as it is situated in the fetus abdomen cavity. During the last stage of gestation, the testis undergoes a maturation process before it starts to descend.
Abnormal testicular localization concerning anatomical position is what defines the congenital pathological condition called cryptorchidism. An undescended testis or a testis that has gone into the abnormal position can be diagnosed through inspection or can be the findings of radiological investigations.
Three of the most cited long-term cohort studies demonstrated that boys operated on for undescended testes had significantly lower sperm concentrations measured on average 21, 17, and 21 years after orchiopexy compared to general populations of men. These results are very important because they show evidence that not only is there compromised fertility potential in unilaterally cryptorchid men, but that the same exposure leads to a decreased fertility potential in the contralateral descended testis as well as the operated-on testis.
Cryptorchidism is also associated with hypogonadism and testicular germ cell cancer. It has been reasoned that the testicular hypofunction and decreased sperm production may occur independently of whether the cryptorchidism is unilateral or bilateral. Beginning at puberty and continuing into middle age, a man’s total testosterone declines by 23% while his uncommitted free testosterone falls by 22%. Cryptorchid males have attenuated adult Leydig cell function, with lower basal testosterone and decreased stimulation of testosterone secretion by hCG compared with untreated cryptorchid boys.
Failure of testicular descent in early childhood results not only in such complications as infertility, testicular torsion, and testicular cancer, but also long-term effects such as decreased bone density, early onset of cardiovascular disease, and decreased life expectancy. However, the possibility that orchiopexy, which is a surgical procedure, and gonadotropin treatment, which is a relatively recent treatment, have on preventing such complications and long-term effects remains uncertain. This chapter provides valuable information derived from several studies and reports about the complications of undescended testis and the long-term effects thereof.
The optimal treatment of patients with cryptorchidism is controversial. The goals of treatment are to improve fertility, decrease the future cancer risk, and ameliorate the cosmetic appearance of the scrotum. Hormonal therapy using hCG or GnRH has been shown to be efficacious in some patients with cryptorchidism.
However, medical therapy has high degrees of variability depending on the type of therapy and the particular patient. Furthermore, surgery has high success rates when performed properly, and many of these patients would require surgery despite medical management. Autopsy, ultrasonic, and testicular fine needle aspiration cytologic examinations have been proposed as additional techniques for the evaluation of undescended testis. However, they have not found widespread use since the value of imaging is similar to that of laparoscopy.
The optimal treatment of patients with cryptorchidism is controversial. The goals of treatment are to improve fertility, decrease the future cancer risk, and improve the cosmetic appearance of the scrotum. A multitude of surgical, hormonal, and mechanical methods have been employed.
Laparoscopy provides a means of accurate diagnosis before surgical intervention. In some cases, laparoscopy provides valuable information preoperatively which prevents unnecessary inguinal exploration. The laparoscopic approach can also allow for a less invasive surgical approach. Finally, Leydig cell function can be evaluated during laparoscopy with the measurement of serum testosterone and/or hCG stimulated testosterone.
All animal experiments related to testicular descent share the mechanism, suggesting that endocrine disruptors should be strictly regulated in daily life. The estrogenic endocrine disruptor may interfere with the natural actions of estrogens during critical periods of sex-specific organization of brain, thereby affecting sex hormone-driven responses.
Maternal exposure to exogenous nonsteroidal estrogen during pregnancy resulted in avian and uterine agenesis in humans and decreased the signaling of fetal testis development. And without androgen-ball signaling, the upper phase of testicular descent was incomplete. Scientists investigated whether herbs might change mammalian sexual function and reproductive capacity between generations and whether the identified beneficial effects of medicinal plants on testis descent and sexual development could help optimize the development of gonadal function throughout mammalian life. In a larger sense, the increasing incidence of testicular dysgenesis disorders merits the search for treatments and especially prevention in the form of environmental cleanup.
Cryptorchidism often occurs in a child whose testicles would have normally descended. While debated by some experts, the prevailing view suggests that cryptorchidism is a consequence of prenatal testicular injury. Thus, the prevention of cryptorchidism should focus on the prevention of prenatal testicular atrophy.
In a general sense, the timing of hormonal exposure is crucial for the masculinization of male accessory organs and brain function and the development of male secondary sexual characteristics. Thus, the hormone environment should be regulated during fetal life to prevent cryptorchidism. The central mechanism of testicular descent is testicular secretion of testosterone, like the aforementioned regulatory control of male sexual differentiation.
The smaller hormone environments of cryptorchidism and monorchidism may lead to abnormal development that seriously affects the function of the testis. During testicular descent, Leydig cells, the testosterone-producing cells, predominate in the testis and the concentration of intratesticular testosterone increases at all stages of descent, indicating that the testis drives the inguinal phase of testicular descent through androgen signaling. Furthermore, fetal testicular androgens increase the expression of many proteins in some intra-abdominal elements, constructing the gubernaculum.
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