Limitations


Primed in place telomeres can be labeled for the Q-FISH techniques using a primed *in situ* (PRINS) application. The telomeric sequences on metaphase chromosomes or interphase nuclei are labeled by PRINS using fluorescently-tagged nucleotides and PCR methods with telomeric primers [93, 94].

Advantages


### Limitations


#### *2.2.5 Whole genome sequence*

Next-generation sequencing has provided the opportunity to get genetic analysis for measuring telomere length measurement [95, 96].

#### Advantages


### Limitations

• The procedure produces a lot of data.

### **3. The role of TL and prognosis of NOA**

In order to maintain genome integrity, recombination, and mitotic division, telomere length is crucial [97]. Telomere shortening has been linked to a variety of illnesses [98]. Numerous studies on male infertility with azoospermia have shown that the DNA of sperm and leucocytes from azoospermic person had shorter telomere lengths than that of males with viable sperm, indicating a potential role for telomere length in some unidentified male infertilities and azoospermia [96, 99–101]. The telomere size was evaluated in the blood leukocytes of azoospermic males [102]. In a study by Ferlin [103] on male infertility, LTL and SLT were found to be substantially associated [104–106].

### **4. Conclusion**

The absence of mature spermatozoa in the pellet examination of concentrated seminal plasma after consecutive sampling at different times is called azoospermia. The azoospermia group without obstruction or duct problems after biochemical, genetic, and physical examinations is called nonobstructive azoospermia, and it has been determined that 1% of the population and ten percent of infertile men are affected by this problem [107]. Numerous infertile males have NOA that has been linked to a variety of genetic abnormalities, such as Y chromosomal microdeletions, karyotype disorders, and missense mutations in genes important in reproductive function. However, these alterations only explain around 25% of azoospermic cases, and around 75% of cases with severe spermatogenic impairment have an idiopathic origin [108, 109]. Recent researches strongly indicate that the pathogenesis of idiopathic NOA is complex and polygenic inheritance, which may affect spermatogenic function. Whereas the molecular mechanisms leading to NOA are still far from being understood, recent developments in genetic analysis have made it possible for our knowledge to increase significantly.

Although studies on this subject continue, telomere length and telomerase activity tests to be performed between indicated NOA patients and idiopathic patients will create an important database for azoospermia without any reason. That is important to fully clarify this possibility in the NOA patient group in order to decide the diagnosis of cryptozoospermia, which is seen in approximately 25–30% of azoospermic patient group patients. More clearly and most importantly, to inform the patient about their treatment.

### **5. Future trends**

If it is possible to identify a target group with this type of telomere shortness for patients in the idiopathic NOA group, it may be possible to predict the rate of sperm finding in the posttreatment ejaculate or post-testicular operation procedure from these patient groups. However, there will be a need for studies to be carried out on this subject and the determination of target groups.

*The Hidden Factor of Azoospermia: Telomere Effect DOI: http://dx.doi.org/10.5772/intechopen.112784*
