Testicular Anatomy | Center for Male Reproductive Medicine & Microsurgery

Anatomy of the testis

The human testis is an ovoid mass that lies within the scrotum. The average testicular volume is 20 cc in healthy young men and decreases in elderly men. In Asian men, testes tend to be smaller. Normal longitudinal length of the testis is approximately 4.5 to 5.1 cm. The testicular parenchyma is surrounded by a capsule containing blood vessels, smooth muscle fibers and nerve fibers sensitive to pressure. The functional role of the testicular capsule is unknown, but may relate to movement of fluid out through the rete testis or control of blood flow to the testis.

Testicular anatomy

The testis contains seminiferous tubules and interstitial cells. The tubules are segregated into regions by connective tissue septa. The seminiferous tubules are long V-shaped tubules, both ends of which usually terminate in the rete testis. Measurement of testicular size is critical in the evaluation of the infertile man, since seminiferous tubules (the spermatogenetic region of the testis) occupy approximately 80% of testicular volume. So, a rough estimate of spermatogenic cell capacity is provided by assessment of testicular size. Testicular consistency is also of value in determining fertility capacity. A soft testis is likely to reflect degenerating or shrunken spermatogenic components within the seminiferous tubules. The seminiferous tubules drain toward the central superior and posterior regions of the testis, the rete testis, that has a flat cuboidal epithelium. The rete coalesces in the superior portion of the testis, just anterior to the testicular vessels, to form 5-10 efferent ductules. These efferent ducts leave the testis and travel a short distance to enter the head, or caput region of the epididymis. The efferent ducts coalesce in a somewhat variable pattern within the caput epididymis to form a single epididymal tubule.

The artery to the testis is specialized in that it is highly coiled and intimately associated with a network of anastomotic veins that form the pampiniform plexus. The counterflowing vessels are separated only by the thickness of their vascular wall in some areas. This vascular arrangement facilitates the exchange of heat and small molecules, including testosterone. The transport of testosterone is a concentration-limited, passive diffusion process in men. The counter-current exchange of heat in the spermatic cord provides blood to the testis that is 2 to 4 °C lower than rectal temperature in the normal individual. A loss of the temperature differential is associated with testicular dysfunction in humans with idiopathic infertility, as well as men with varicocele or cryptorchidism. Whether elevated testicular temperature causes or is simply a reflection of testicular dysfunction is unknown. Only the association between elevated testicular temperature and seminiferous failure have been demonstrated. In the distal inguinal canal, 50% of men will have a single testicular artery identifiable under l0 x power magnification dissection of the cord, with 30% of men having two arteries and 20% with three arteries.

The venous system is somewhat unique because the spermatic veins are thin-walled, poorly muscularized, and lack effective valves except at the inflow points into the inferior vena cava or the renal vein. The right spermatic vein usually drains into the vena cava. The left spermatic vein drains into the left renal vein. The renal vein on the left side is thought to have a higher intraluminal pressure because the vein is compressed as it passes between the superior mesenteric artery and the aorta. This “nutcracker effect” may impair flow through the left renal and spermatic veins, especially in young men with limited retroperitoneal fat. The differential anatomy of the left and right spermatic veins is thought to explain, at least in part, the higher prevalence of varicoceles on the left side. The exact mechanism by which varicoceles cause infertility is unknown. In animal models, varicoceles are associated with increased blood flow to the testis and increased interstitial fluid in the testis. These two findings may impair regulation of testicular temperature and decrease intratesticular concentrations of testosterone or other local factors important for spermatogenesis.

The testicles | Canadian Cancer Society

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The testicles make sperm and male hormones. The 2 main types of cells in the testicles that perform these functions are germ cells and stromal cells.

The process of making sperm starts in germ cells, which line the seminiferous tubules. As they mature into sperm cells, germ cells move from the lining, through the maze of seminiferous tubules and to the epididymis. The epididymis stores sperm cells so they can completely mature.

Mature sperm cells travel through the vas deferens. Along the way, fluids made by the seminal vesicles and the prostate gland mix with the sperm cells to create semen. The semen is pushed out of the body through the urethra during ejaculation. Sperm in the semen can fertilize a female egg to start a pregnancy.

Stromal cells help other cells in the testicle. Different types of stromal cells do different things.

Sertoli (nurse) cells are a type of stromal cell found in the seminiferous tubules. They support the germ cells by helping make and transport sperm.

The soft connective tissue in the space between the seminiferous tubules contains specialized stromal cells called Leydig cells. They make male sex hormones, mostly testosterone. Testosterone helps germ cells make sperm. Testosterone also helps the reproductive organs develop and function. It gives men:

• sex drive (libido)
• fully developed genitals
• a deep voice
• body and facial hair
• bigger muscles and body size

• American Cancer Society
  . What Is Testicular Cancer?
  . 2018
  : https://www.cancer.org/.

• Cancer Research UK
  . About Testicular Cancer
  . Cancer Research UK
  ; 2017
  : https://www.cancerresearchuk.org/.

• Martini FH, Timmons MJ, Tallitsch RB. Human Anatomy. 7th ed. San Francisco: Pearson Benjamin Cummings; 2012.

• National Cancer Institute
  . Testicular Cancer Treatment (PDQ®) – Patient Version
  . Bethesda, MD
  : National Cancer Institute
  ; 2018
  : https://www.cancer.gov/.

• Reuter, VE
  . Anatomy and Pathology of Testis Cancer. Scardino PT, Lineham WM, Zelefsky MJ & Vogelzang NJ (eds.). Comprehensive Textbook of Genitourinary Oncology. 4th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2011: 31:532-543.

• Young B, O’Dowd G, Woodford P (eds.). Wheaters’s Functional Histology. 6th ed. Churchill Livingston; 2014.

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anatomical structure, main functions and diseases

Testicles (testes) are the male gonads. The testicles (right and left) are located in the corresponding halves of the scrotum in a man. The spermatic cords, consisting of the testicular membranes, the testicular artery, the veins of the testicular venous plexus and the vas deferens, approach the upper pole of each testicle. Along the lateral surfaces of the testicles, from the upper to the lower poles, there are appendages of the testicles, which at the lower pole of the testicle continue into the vas deferens. The testicles can be felt by hand through the skin of the scrotum in the form of rounded formations of elastic consistency. The epididymis is palpable in the form of ridges on the lateral surface of the testicles.

Anatomically, the testicle has (1) parenchyma (testicular tissue itself) and a dense and elastic (2) albuginea surrounding the parenchyma. The bulk of the parenchyma of the testis is made up of many convoluted microscopic tubules lined with spermatogenic epithelium, consisting of Sertoli cells, on which the formation and maturation of spermatozoa occurs. The tubules converge to the upper pole of the testis (a network of straight tubules), where they pass into the tubules of the epididymis. Moving along the tubules of the epididymis, the spermatozoa mature, after which they enter the vas deferens and then through the ejaculatory canals out through the urethra in the process of ejaculation. Between the tubules in the parenchyma of the testis there are Leydig cells that produce the main male sex hormone – testosterone. The regulation of testosterone concentration in the blood is carried out by the hypothalamus and pituitary gland – brain structures, due to the greater or lesser release of luteinizing hormone, which in turn stimulates Leydig cells to release testosterone. Lack of testosterone release can be caused both by poor performance of Leydig cells in case of damage to the testicle (congenital, traumatic or inflammatory changes), and by insufficient secretion of luteinizing hormone by the pituitary gland. Lack of testosterone leads to infertility, decreased libido and sometimes causes erectile dysfunction.

The testicle, initially developing in the abdominal cavity of the fetus, gradually moves downward in the process of intrauterine development and descends into the scrotum cavity by the time of birth (or immediately after them). The need to move the testicles from the abdominal cavity to the scrotum is due to the fact that the process of sperm formation requires a lower temperature than body temperature. Normally, the temperature in the scrotum is 2–4 ° C lower than body temperature.

The transfer of the testis to the scrotum leads to some peculiarities of the blood supply and the structure of the membranes. When passing from the abdominal cavity through the inguinal canal, the testicle carries along the muscles of the anterior abdominal wall and peritoneum, thus acquiring the muscular and vaginal membranes.

Vessels feeding the testicle (artery and veins) originate in the upper abdomen (on the right side – from the aorta and inferior vena cava, on the left side – from the renal artery and vein) and repeat the path of the testicle to the scrotum in the retroperitoneal space and inguinal canals. Violation of the outflow through the testicular veins (occurs more often on the left) leads to the appearance of varicocele (varicose veins of the spermatic cord), which is a common cause of male infertility.

The presence of the muscular layer (cremaster muscle or muscle that lifts the testicle) leads to the possibility of pulling the testicle to the outer ring of the inguinal canal. In a vertical position, when a finger is passed over the skin along the inner surface of the thigh, the testicle begins to rise upward (cremasteric reflex).

The entrainment of the parietal (parietal) peritoneum by the testicle behind it during intrauterine movement of the testicle into the scrotum leads to the formation of the vaginal process (protrusion) of the peritoneum, which, by the time of delivery, overgrows along the spermatic cord, forming a closed serous cavity near the testicle. Non-closure of the vaginal process of the peritoneum leads to the appearance of a congenital inguinal hernia or hydrocele communicating with the abdominal cavity. The accumulation of fluid in a closed cavity inside the vaginal membranes of the testis leads to the formation of a true dropsy of the testicle – a hydrocele.

Failure of the testicle to descend into the scrotum (cryptorchidism) or stopping further progress of the testicle in the abdomen or inguinal canal often leads to significant damage to all testicular functions (infertility) and is a risk factor for the development of testicular cancer.

Penetration of the epididymis infection from the urethra through the vas deferens often leads to the development of epididymitis (inflammation of the epididymis). In sexually active men under the age of 30, acute epididymitis in 65% of cases is associated with a sexually acquired chlamydial infection. Inflammation of the epididymis can lead to male infertility due to blockage of the tubules. In addition to inflammation, a common disease of the epididymis is spermatocele (cyst of the epididymis). One of the acute diseases of the testicle is its torsion, a condition requiring emergency care. This disease is similar to inflammation of the testicle and its appendage orchiepididymitis, however, in the absence of timely assistance, it can lead to testicular necrosis. It occurs more often before the age of 20 years.

Structure and development of the boy’s reproductive system – Adolesmed

Structure of the reproductive system of boys

Male external genitalia include penis and scrotum . To internal – testicles and their appendages , vas deferens and ejaculatory ducts , seminal vesicles 9 0031 prostate gland , bulbourethral glands . Sex glands are in close functional relationship with other endocrine glands (anterior pituitary gland, adrenal cortex) and the central nervous system.

The penis consists of an anterior free part, the body, which ends with the glans, and a posterior part attached to the pubic bones. The body of the penis is covered with thin skin. The skin is mobile and hangs over the head of the penis, forming the so-called foreskin. The body of the penis consists of two cavernous bodies and one unpaired spongy one. The penis is able, when excited, to increase and acquire a significant density. This condition is called erection, which plays an important role in the performance of sexual function. With the help of the penis, spermatozoa are introduced into the woman’s vagina.

The scrotum is a musculocutaneous formation divided by a septum into two halves, each of which is a container for the testicle and epididymis, the scrotal part of the spermatic cord.

Testicle – paired male oval gonad. Its length is 4–5 cm, width 2–2.5 cm, thickness 2.5–3 cm. The mass of the testicle is on average 15–25 g. An appendage shaped like a horseshoe adjoins the posterior edge of the testicle. It consists of a head, body and tail, which passes into the vas deferens. The main function of the testicles is spermatogenesis, i.e. the formation of male sex cells. They mature at 15-16 years of age. The number of spermatozoa ejected during intercourse is large: normally, 1 ml of ejaculate contains more than 20 million of them. In addition to producing spermatozoa, the testicles synthesize male sex hormones – androgens, the main of which is testosterone.

The prostate gland plays an important role in male sexual activity . It is an unpaired glandular-muscular organ weighing 20–25 g, has a lobed structure, resembles a chestnut in shape and size. The secret of the prostate gland is part of the semen.

Above the prostate gland are located seminal vesicles – paired organs that produce a secret of gelatinous consistency, which is the main (by volume) part of the sperm, and also serves as a substrate for preserving spermatozoa.

The ejaculatory duct , leaving the scrotum, passes through the inguinal canal into the abdominal cavity and is located at the posterior lower part of the bladder, where it joins with the excretory duct of the seminal vesicle, forming the ejaculatory duct. It penetrates the prostate gland and opens into the urethra.

Development of secondary sexual characteristics

Development secondary sexual characteristics in male adolescents, on average, covers the period from 10.5 to 18 years. First of all, at the age of 10.5–11 years, the testicles increase, after 0.5–1.5 years the growth of the penis begins, pubic hair appears at the same time, after which other signs of puberty appear sequentially: voice mutation, growth of the thyroid cartilage, acne, armpit hair, face. The physique acquires typical male features – a wide shoulder girdle and relatively narrow hips.

By the age of 15.5, most adolescents have the same pubic hair as adult men. The growth of the external genitalia is usually completed by the age of 17–18, although their growth may continue until the age of 20–25. The first wet dreams (oygarhe), an important indicator of physiological maturity, occur at the age of 14 and become regular in most boys by the age of 16.

The development of secondary sexual characteristics is timed to a certain passport age and takes place in a strict sequence. Violation of this sequence indicates deviations in the normal course of development, endocrine dysfunctions, and somatic disorders. The sequence of development of secondary sexual characteristics in boys is as follows:

• the beginning of testicular enlargement – at 11-12 years;
• initial pubic hair growth – at 12-13 years old;
• the beginning of a noticeable growth of the penis – at 12-13 years;
• voice mutation – at 13-14 years old, an increase in the thyroid cartilage of the larynx – at 14-15 years old;
• The beginning of axillary hair growth is at the age of 14. The appearance of sweating with a characteristic odor;
• wet dreams – at 14-15 years old;
• the beginning of facial hair – at 14-16 years.

Major disorders in the development of the reproductive system

Already at a very early age, it is necessary to make sure that the boy’s external genital organs are correctly formed: the urethra runs along the entire length of the penis and opens on the head, the testicles are located in the scrotum, the foreskin is mobile and when it is displaced, the head of the penis is easily exposed. Any violations in the development of the external genital organs are easier to correct in early childhood.

Already in the maternity hospital, one can suspect cryptorchidism , the absence of one or both testicles in the scrotum. Untimely bringing down of the testicle can cause infertility and a malignant tumor of the testicle. Cryptorchidism leads to disruption of the development of testicular tissue and, as a consequence, to disruption of the hormonal regulation of sexual development and maturation (especially in the case of a bilateral process).

Commonly diagnosed condition – varicocele – expansion of the veins of the pampiniform plexus, mainly on the left. Most often, varicocele is associated with impaired blood outflow through the system of the internal testicular vein. In the initial stages, the disease may even be invisible to a teenager. Hence the importance of mandatory andrological preventive examinations and timely treatment of the disease. Varicocele is one of the main causes of male infertility.

One of the most common diseases of the reproductive system of boys is phimosis. This is the narrowing of the external opening of the foreskin. This disorder can be either congenital or acquired. Congenital phimosis usually disappears on its own within the first four years of life. However, the child should still be under the supervision of a pediatric urologist. There are several causes of the acquired form of the disease. These are congenital disorders in the development of connective tissue, inflammatory diseases and injuries of the foreskin. Most often, a specialist faces synechiae – adhesions between the glans penis and the foreskin.

Sometimes there is such a condition as frenulum of the penis. With this disease, the glans penis is bent downwards. During masturbation and sexual intercourse, tears and even ruptures of the frenulum occur with severe bleeding. This disease requires surgical treatment.

Some illnesses suffered by a boy can in one way or another affect his sexual development. For example, mumps sometimes complicated by inflammation of the testicles, which in turn can affect reproductive function. Moreover, the older the boy, the higher the risk of complications. In addition, the disease can proceed in different ways: in one case, inflammation of the testicles makes itself felt, in the other, it goes unnoticed. For young men who have had mumps, it is advisable to perform an assessment of the number and function of spermatozoa (spermogram).

In general, the main methods for examining children with reproductively significant diseases that determine the prognosis are: a comprehensive ultrasound examination and Doppler examination of the organs of the reproductive system, a study of the hormonal profile and spermiological examination. The latter is a universal criterion for the final reproductive prognosis.