What is the difference between oligospermia and azoospermia

The use of some substances, including marijuana and cocaine, may reduce sperm counts. Excessive drinking can do the same. Men who smoke cigarettes may have lower sperm counts than men who do not smoke. Being overweight or obese increases your risk for low sperm counts in several ways.

Excess weight can directly reduce how much sperm your body can make. Weight problems may also interfere with hormone production. Some men with oligospermia can still conceive despite lower sperm counts. Fertilization may be more difficult, however. It may take more attempts than couples without a fertility issue. This includes sperm motility problems.

Normal activity allows sperm to swim toward an egg for fertilization easily. The sperm may also move in an unpredictable pattern that would prevent them from reaching an egg. Timing sex to ovulation can increase your chances for conception. Some lubricants and oils can reduce sperm motility and prevent sperm from reaching an egg. If lubricant is needed, talk with your doctor about a sperm-safe option. Varicocele often require surgery. During the procedure, your doctor will close off the enlarged veins.

Based on the cause of oligospermia, Seeds of innocence determine the course of treatment suitable for the individual suffering from this medical condition. You can book an appointment with us to discuss the problem and know the best suitable treatment. A number of factors can lead to oligospermia such as ejaculation problems, medication, genetic condition, infections, steroids, stress, and hormonal imbalances.

A low sperm count is also called oligospermia, while on the other hand, a complete absence of sperm is called azoospermia. Yes, oligoasthenospermia is curable surgically. However, if the obstruction is partial, the diagnosis and the treatment may become difficult to identify.

Males with oligospermia are predisposed to genetic abnormalities, and many genetic factors like genetic mutations and polymorphisms have been identified to have a direct or indirect effect on spermatogenesis. Oligospermia cannot directly cause miscarriage, but it can lead to miscarriage if any damaged sperm fertilises an egg. Agarwal is backed by a visionary thinking, die-hard determination and industry-rich experience of more than 10 years.

Further, she received training in Embryology at the National University of Singapore. She has multiple publications in journals of national and international Journal. Hormonal imbalance : medications and hormonal replacement treatments are given to fix the hormonal imbalance. Further more if the cause is mainly male infertility due to no sperm in the ejaculate or due to low sperm count then the options of testicular sperm retrieval should be considered, where the sperms are aspirated or extracted from the testes and used in assisted reproductive techniques to fertilize an egg.

I have been married for 6 years but I do not have children. I am very disappointed. I have undergone a lot of treatment but it did not solve matter. Please help me. Your email address will not be published. Save my name, email, and website in this browser for the next time I comment.

View Lab Reports. However, in medical language it is explained as follows; Azoospermia: Azoospermia is a medical condition where there is a complete absence of sperms in the semen sample of a male, given the sample is centrifuged.

It must be recognized that small deletions in areas not covered by these STSs will not be detected, and that this method is only suitable for assessment of relatively large deletions. Pattern of amplification upper right derived from four normal males, with female DNA used as a negative control.

Products were electrophoresed on 3. Nell and Boettger-Tong, unpublished data. In a recent study by Foresta and associates, 44 using samples from subjects with well-defined forms of idiopathic testicular damage azoospermia with SCOS and oligozoospermia with hypospermatogenesis , Twenty-two percent of patients with severe oligozoospermia were also missing one or more of these STSs.

Fertile controls and the fathers or brothers of these patients did not show any abnormality, indicating that these were de novo deletions. Of the deletions observed in this highly selected group of patients, In this regard, it is noteworthy that even in this highly selected population, the vast majority Thus, either small deletions unamenable to PCR analysis in as yet unidentified genes are responsible for these phenotypes, or there are other genes not on the Y chromosome that participate in the regulation of spermatogenesis.

The latter hypothesis will be considered in the next section. Little is known about autosomal defects and infertility in humans, so much of what is known about the contribution of non-Y-chromosome genes in the control of spermatogenesis has been derived from animal models. To date, mouse mutations affecting nearly every stage of spermatogenesis have been described; this section examines a few spontaneously occurring and induced mutations that are associated with the severe impairment of fertility.

Because most infertility in humans presents as an apparently isolated condition, those animal models that have infertility as their only sequela will be discussed in the most detail. Table 1 lists a number of autosomal loci and genes that, when deleted, cause infertility. These mutations have arisen naturally e.

Thus, the jsd mutation, which effects stem-cell renewal, is considered first. From a clinical point of view, because these genes are autosomal, fertility problems are likely only in the homozygous state. However, as infertility in these animals arises in the context of only one genetic mutation in the presence of an intact Y chromosome, it is clear that these autosomal genes play a role in spermatogenesis for which Y genes cannot substitute. Table 1. Autosomal loci and genes that cause infertility when deleted.

Spontaneously occurring mutations that result in infertility are, by definition, selected against during evolution. If, however, the heterozygote condition has no effect on fertility and if only one sex is affected by the homozygote condition, this would be an ideal model for the study of an autosomal gene involved in spermatogenesis.

Some spontaneously occurring mouse mutations fulfill the aforementioned criteria and, significantly, show no other phenotypic effects in other organ systems.

Of these, jsd is of particular interest because the phenotype of homozygous mutant animals is reminiscent of human Sertoli-cell-only conditions. The jsd mutation, reported in by Beamer and colleagues, 45 defines a locus affecting postnatal proliferation of spermatogonial cells.

The phenotype in these animals was apparent only after puberty, when a single round of apparently normal spermatogenesis occurred; thereafter, mature sperm were not produced. Histologic analysis of the seminiferous tubules in postpubertal 9-week-old animals indicated seminiferous tubules devoid of spermatogenesis; these tubules were small in diameter and populated by Sertoli cells and the occasional type A spermatogonia.

The authors thus proposed that the defect was due to a failure of spermatogonial stem-cell renewal, resulting in insufficient numbers of stem cells for normal spermatogenesis to occur.

Reminiscent of many types of testicular failure in humans, serum FSH levels in these animals were significantly elevated in comparison to their heterozygote littermates. The latter histologic sample resembles the histologic sample of a Sertoli-cell-only human testis see Fig. Beamer and colleagues 45 mapped the jsd locus to mouse chromosome 1; Rohozinski and Bishop 52 and Bradley et al.

The mUtp14b gene was retrotransposed from a ubiquitously expressed gene located on the X chromosome, apparently acquiring a germ cell specific function. Additional studies by Rohozinski et al. Note the absence of spermatogenesis in the seminiferous tubules of the mutant, with Sertoli cells and an occasional spermatogonia present.

In , Zhao and co-workers 46 reported that the generation of mice with a targeted mutation in bone morphogenetic protein 8B Bmp8b resulted in male germ-cell deficiency and infertility. BMPs belong to the transforming growth factor-B superfamily of secreted signaling molecules. A number of BMPs have been identified, with diverse functions centered around the regulation of embryonic development. Bmp8b is expressed in the placenta during embryogenesis and in male germ cells during postnatal development; early postnatal expression of Bmp8b is seen in spermatogonia and primary spermatocytes.

In the Bmp8b homozygous mutant mouse, two testis-specific abnormalities are apparent: the first influences germ-cell proliferation, and the second affects pachytene spermatocyte survival. In the study by Zhao and Hogan, 55 homozygous mutant males had much smaller testicles and partial to nearly complete germ-cell depletion. Sertoli and Leydig cells were apparently normal.

Although two of the mutant males sired litters, they later became sterile. Thus, the authors suggested that Bmp8b is required for both the normal mitotic proliferation and differentiation of germ cells and for the survival of pachytene spermatocytes. The contribution of the human homologue of this gene to the control of spermatogenesis has yet to be established. In the mouse, the homologue of the human Y chromosome gene DAZ is located on an autosome and has been named Dazla.

Targeted disruption of Dazla results in male and female infertility due to an early loss of germ cells. Fertility impairment caused by Dazla mutation in both sexes is in contrast to the male-specific infertility phenotype resulting from mutation of the Drosophila homologue boule.

These data support the notion that DAZ participates in spermatogenesis but indicates that, in the mouse, an autosomal DAZ is sufficient for the maintenance of fertility. It has long been known that vitamin A is required for normal testicular function. A report by Kastner and associates, 47 indicating a male-sterility phenotype in mice with a mutation of retinoid X receptor b Rxr b , provides new insight into the role of retinoids in spermatogenesis. However, it is of interest for two reasons:.

The authors suggested that the defect is in the Sertoli cells, based on the normal expression pattern of Rxr b unique to Sertoli cells and the histology of the mutant testis. Homozygotes were characterized by early and progressive accumulation of lipids in the Sertoli cells, which preceded a failure of spermatid maturation and release.

It is of note that accumulation of lipids has been seen in the Sertoli cells of some infertile men.