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Dr. Eric Daiter

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Dr Eric Daiter has served Monmouth and Middlesex Counties of New Jersey as an infertility expert for the past 20 years. Dr. Daiter is happy to offer second opinions (at the office or over the telephone) or new patient appointments. It is easy, just call us at 908 226 0250 to set up an appointment (leave a message with your name and number if we are unable to get to the phone and someone will call you back).


"I always try to be available for my patients since I do understand the pain and frustration associated with fertility problems or endometriosis."


"I understand that the economy is very tough and insurance companies do not cover a lot of the services that might help you. I always try to minimize your out of pocket cost while encouraging the most successful and effective treatments available."

NJ Center for Fertility and Reproductive Medicine - Infertility Tutorials

Normal Sperm Production (in Detail and Clinical Correlations)
To produce a normal semen sample upon ejaculation requires the coordination of many different events. When any one of these events is abnormal the resulting semen sample can be compromised. Two major categories of events are spermatogenesis/spermiogenesis (processes that increase the number of immature germ cells and promote the subsequent development of these primitive germ cells into mature sperm in the testes) and ejaculation (a process that includes penile erection, emission of sperm into the posterior penile urethra and ejaculation of sperm out from the penile urethra).

  1. Movement of the testes into the scrotum
  2. The testicular cells and their functions
  3. Puberty and the full maturation of sperm
  4. The course of movement for sperm upon ejaculation
  5. Ejaculation
  6. Necessary postejaculatory changes in sperm

(1) Normally testes move from the abdomen to the scrotum prior to birth.

During fetal development (inside the mother's uterus), a male normally forms testes within the abdomen and during the last trimester of pregnancy these testes descend into the scrotal sac. The testes are near the inguinal crease as they move through the inguinal canal at about 7 months gestation and the testes are normally within the scrotal sac by delivery at term.

Hormones regulate the descent of the testes, including

(a) mullerian inhibiting factor, which is primarily responsible for testicular movement from the initial location high in the abdomen to the inguinal canal and

(b) testosterone, which is primarily responsible for movement from the inguinal canal to the scrotum.

If there is failure of the testes to descend normally (called "cryptorchid testes"), the blood and nerve supply to the testes can be damaged. In this event, permanent damage to the testes can result in decreased fertility. Repair of undescended testes is ideally performed surgically (orchiopexy) within 2 years of age.

The incidence of male fetuses born at term with undescended testes may be as high as 3-4% (1 in 25-35), but since the majority of these testes go on to descend on their own within the first year of life surgery is usually delayed to allow for spontaneous recovery. The overall incidence of cryptorchidism in adult males is only 0.3-0.4% (1 in 250-350).

It has been found that males with one undescended testis usually have a decrease in semen quality compared to normal fertile men that is independent of the timing of surgical repair. This suggests that there is bilateral damage to the testes even when only one testis is undescended. However, many men with a unilateral undescended testis will be fertile despite a decrease in semen quality. Therefore, treatment for infertility in these men should follow the usual recommendations based on their semen analysis, history and physical examination.

There is a higher incidence of testicular cancer in men with undescended testes. The lifetime risk for development of invasive testicular cancers is about 0.5% (1 in 200) in the USA. This risk of invasive testicular cancer is about 5 times greater in men with a history of undescended testes. Pre-invasive testicular cancer (carcinoma in situ) can be detected by testicular biopsy. Since the incidence of carcinoma in situ in a testis that was undescended is about 5% (1 in 20) it is prudent to consider biopsy for all of these testes. Expert consultation with an experienced urologist is advised to determine appropriate follow-up in all men with a history of a cryptorchid testis.

(2) The human testes is composed of a number of cells with specific functions

* (A) germ stem cells (gonocytes)

Stem cells are cells that are not irreversibly differentiated into specialized cells, are capable of dividing (increasing their number) without limitation for the lifetime of the animal, and which divide into daughter cells that can choose to either become other stem cells or differentiate irreversibly into specialized cells. Stem cells are required to replace specialized cells (such as mature sperm cells) that cannot themselves divide.

Gonocytes continuously replenish themselves in the adult human male, which is why a man's age does not play a very important role in fertility. If there is a major insult to this stem cell population, a complete lack of sperm (azoospermia) can result. As opposed to the male situation, females are born with their entire number of eggs already present in the ovaries (they are not stem cells). This is the primary reason why a woman's age is closely related to her fertility.

Germ line cells produce the next generation of gametes (sperm in males, eggs in females) while somatic cells form the rest of the body. Gametes are cells that are specialized for sexual fusion resulting in an embryo.

In the human testes, the critical events that take place to form the gonocyte population are not clearly understood. This period of development has been extensively studied in male rodents (mostly rats) which is considered to be an "unproven" model for the human system. In the rat, there is an initial period of rapid proliferation (duplication of existing cells by the process of mitosis in which cells normally divide into identical daughter cells to increase their number) of gonocytes prior to birth, a subsequent arrest in proliferation until puberty, and another period of rapid proliferation of stem cells at puberty that is associated with the degeneration of a large number of these cells. The final outcome is a normal adult number of stem cells.

Clinical importance

During the quiet period between the initial expansion of cells and puberty, rat germ cells are highly sensitive to radiation. It would be important to understand whether this period in development is similarly sensitive to radiation in humans, so that we could better understand potential causes for azoospermia.

Sertoli only syndrome is a condition characterized by seminiferous tubules that are devoid of germ cells, possibly due to abnormal migration in the early male embryo. In this syndrome there is little to no peritubular hyalinization (to distinguish it from conditions like Klinefelter's syndrome where there is extensive destruction to the tubules with sclerosis and hyalinization) and only a slight decrease in size of the testes.

* (B) mature Sertoli cells

Sertoli cells are the testicular cells that ultimately control spermatogenesis.

Seminiferous tubules make up about 90% of the testicular volume and are long tubes (70 cm long, tightly coiled) lined by a single layer of Sertoli cells. At puberty, spermatogenesis is initiated by Sertoli cells within the seminiferous tubules under the influence of FSH and testosterone (as well as possibly several growth factors). After initiation, testosterone alone may maintain spermatogenesis (possibly with decreased efficiency).

Clinical importance

Sertoli cells produce a number of proteins that are critically important for normal testicular function. They produce (among other proteins) (1) mullerian inhibiting factor, which acts embryonically to cause regression of the mullerian ducts (which form the female internal genital system) and assist testicular descent to the level of the inguinal canal, (2) androgen binding protein, which remains largely in the collecting ducts and the seminiferous tubules where it concentrates testosterone in the testes at levels up to 50 fold greater than circulating levels, and (3) inhibin, which decreases circulating FSH concentrations

* (C) a blood testis barrier

Tight junctional complexes between Sertoli cells effectively create an impermeable wall that divides the seminiferous tubule into two compartments. The basal (outer) compartment is accessible to substances within the circulation (blood) whereas the adlumenal (inner) compartment is not accessible to substances in the blood. As gonocytes differentiate into specialized mature sperm cells they move across this blood testis barrier. Apparently the tight junctions transiently unzip to allow developing spermatogonia to cross.

Clinical importance

Once past the blood testis barrier the developing spermatogonia begin to develop unique surface antigens (immunoreactive components that can activate an immunologic response). If the barrier is destroyed or damaged, such as following trauma or infection, then the man's immune system can develop antibodies to the sperm (anti-sperm antibodies). The antibodies can impair sperm motility (if directed against the sperm's tail) or fertilization of an egg (if directed against the sperm's head).

* (D) mature Leydig cells

The testes produce testosterone for male sexual development and sperm maturation. Leydig cells are the testosterone producing cells in the testes. The Leydig cells reside between the seminiferous tubules within (what is called) the interstitial spaces. LH enhances testosterone production by the Leydig cells.

Clinical importance

Leydig cells are abundant prior to birth and in the neonatal period, when they produce the testosterone needed for the fetal development of male internal and external genitalia. The number of these cells then declines to very low levels in the prepubertal years when testosterone production is minimal. At puberty, there is a tremendous increase in the number of Leydig cells and their testosterone production. Pubertal testosterone is needed for spermatogenesis.

(3) At puberty, immature sperm cells (spermatogonia) develop into highly specialized mature sperm cells (spermatozoa)

* (A) the time required for spermatogenesis in humans is about 74 days.

During this time, the spermatogonia replicate (reproduce) their DNA to acquire twice the normal amount of chromosomal material and then in two steps (reduction and division) the DNA is reduced to one half the normal amount in each of 4 spermatids (immature sperm cells). In this manner, each primitive undifferentiated sperm cell (spermatogonia) gives rise to 4 chromosomally unique sperm cells (spermatids) that normally will become capable of reproduction.

* (B) "spermiogenesis" occurs

The sperm's development from the spermatid stage to the spermatozoa stage is referred to as "spermiogenesis." During this time, development includes (1) formation of the acrosome, a cap over a large area of the head of the sperm that contains a number of enzymes that are instrumental in dissolving a path through the shell of the egg (the zona pellucida) at the time of fertilization, and (2) formation of the tail of the sperm, a complex structure that contains its own energy source (called mitochondria, which are lined up in an end to end spiral) and is responsible for sperm motility.

(4) Mature spermatozoa leave the seminiferous tubules of the testes to enter a series of different ducts and tubules.

* sperm travel into the epididymis

Initially spermatozoa cross the rete testis and the efferent ducts to rapidly pass into the epididymis where they are stored.

Sperm resides in the caput or head, then the corpus or body and finally in the cauda or tail of the epididymis. As sperm traverse the epididymis they change significantly to

  1. become motile,
  2. change shape, and
  3. undergo physiologic alterations

Clinical importance

Abnormalities in the epididymis may result in abnormal sperm motility, sperm morphology (shape) or unexplained infertility.

The epididymis is formed from an embrologic structure called the Wolffian duct during the first trimester of pregnancy, under the influence of testosterone. Any genetic defect in testosterone biosynthesis will potentially result in congenital abnormalities in the epididymis.

In man, about 50% of spermatozoa are stored in the cauda (tail) of the epididymis, with the average time of storage in the epididymis between 10 and 20 days. Sperm can be damaged during epididymal storage by elevated temperature (such as in the presence of a varicocele), infection, or other hostile conditions. In some patients with persistent abnormalities in the motility and shape of sperm there is tremendous improvement in the quality of sperm with daily ejaculation to limit the time of storage in the epididymis.

(5) Ejaculation expels the sperm

* (A) erection

Penile erection is primarily a vascular event that relies on increased arterial flow with decreased venous flow (so that more blood collects into the penis to produce rigidity). The changes in blood flow are controlled by the nervous system, including the parasympathetic and sympathetic nervous system. Research suggests that some parasympathetic nerves may be able to respond to both penile tactile and psychic stimulation while other sympathetic nerves may be able to respond to predominantly psychic stimulation. Medication that affects these nerves can affect the ability to achieve an erection.

* (B) emission

Emission is the deposition of seminal fluid into the posterior urethra. This requires that the seminal fluid released from the epididymis has traversed the vas deferens into the urethra. The vas deferens is about 30cm long and initiates at the epididymis (epididymal portion), passes through the scrotum (scrotal portion) into the abdomen via the inguinal canal (inguinal portion) where it then passes through the pelvis (pelvic portion) to the posterior urethra (ampullary portion).

Emission appears to be primarily under the control of the sympathetic nervous system. Men who have had a retroperitoneal lymph node dissection (RLND) for testicular cancer occasionally will have a disruption of the sympathetic nervous system, which can result in a lack of emission and/or retrograde ejaculation into the bladder.

* (C) ejaculation

Ejaculation normally propels the seminal fluid collected in the posterior urethra out through the penis. The bladder neck's physiologic urinary sphincter is normally closed during emission and ejaculation to prevent retrograde ejaculation into the bladder. This closure of the bladder neck is predominantly controlled by the sympathetic nervous system. Men with a history of RLND may have retrograde ejaculation into the bladder due to disruption of the local sympathetic nerves.

(6) Ejaculated sperm becomes capable of fertilization hours after fertilization.

Sperm must undergo a process called "capacitation" to become capable of fertilization (allows sperm to undergo the acrosome reaction upon binding to the shell of the egg). Capacitation normally occurs during the sperm's residence in the female reproductive tract. Capacitation takes about 4-6 hours after ejaculation (whether in the female reproductive tract or artificial media) which is why sperm is not immediately used after ejaculation for insemination of retrieved eggs during IVF. If the sperm is not able to live in the pre-ovulatory cervical mucus for several hours this can result in infertility.

The acrosome reaction is a process that allows the contents of the acrosome to digest the shell of the egg (zona pellucida). The acrosome covers the top two thirds of the sperm head and as the sperm and egg meet this outer acrosomal membrane breaks down to release digestive enzymes that assist in the penetration of the egg. If an abnormal percentage of sperm have premature acrosome reactions then a problem with fertilization is possible.


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Eric Daiter, M.D. - Edison, NJ - E-Mail: - Phone: (908)226-0250

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