الفهرس 
Anatomy of the spermatozoonOnly 14 pages are availabe for public view
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Abstract
Sperm motility is one of the major determinants of male fertility and is required for successful fertilization.
Unlike female infertility, the male counterpart is not, predominantly, an endocrine condition; it is a pathology affecting germ cells. Most infertile men produce spermatozoa; however, these gametes are characterized by functional deficiencies stemming from defects occurring during spermatogenesis or sperm maturation. Interest in the origins of male infertility has recently been stimulated by data indicating that spermatozoa from such patients not only suffer from an impaired capacity for fertilization but also may exhibit high rates of DNA damage to both the mitochondrial and nuclear genomes.
Sperm swimming is characterized by a rhythmic, three-dimensional and asymmetric movement of the flagellum. This unique movement is assured by the complex organization of the flagellum.
Calcium channels have been described along the plasma membrane of the entire flagellum thus suggesting the importance of calcium entry for motility.
Hyperactivation is a special type of sperm motility developed in association with the process of capacitation in the female genital tract. It is characterized by a more energetic and less symmetric flagellar beat, which helps sperm to progress through the cervical mucus, the oviduct and finally, the cumulus oophorus and zona pellucida surrounding the oocyte.
Spermatozoal ultrastructural defects, antisperm antibodies, varicoceles, partial ductal obstruction, oxidative stress, and idiopathic causes may be responsible for low sperm motility (asthenozoospermia).
Spermatozoal ultrastructural defects include dysplasia of the fibrous sheath, low membrane fluidity and mitochondrial diseases. ICSI is the treatment of choice for these diseases.
Sperm autoimmunity is an important cause of male infertility and it should be screened for routinely. Diagnosis should be made only after repeated tests demonstrating positive IBT and failure of sperm cervical mucus penetration. Patients with these characteristics are severely infertile and are unlikely to produce pregnancies without treatment with ICSI or glucocorticoids. These treatments have limited success rates and severe side effects are possible.
Despite the lack of good randomized data, many uncontrolled studies support the efficacy of varicocelectomy. Varicocelectomy remains one of the few surgical interventions available for infertility treatment, and couples will likely continue to elect to have this procedure performed if there is any chance that it will improve the possibility of conception. Our understanding of how a varicocele repair affects overall semen and hormone parameters has evolved over the past several decades. For example, correction of varicoceles has been shown to improve not only sperm motility, density and morphology but also specific functional sperm defects. Improvement in seminal parameters is demonstrated in approximately 70% of patients after surgical varicocele repair. Improvements in the sperm penetration assay, oxidant determination (ROS) and DNA fragmentation have been achieved after a varicocele repair. A varicocele repair also has been shown to improve serum follicle-stimulating hormone and testosterone levels. Ongoing clinic trials, however, continue to identify couples who would have attained pregnancy without intervention. It is for these patients that research on the controversial topic of varicocele is continued.
With the advent and increased use of high-resolutionTRUS, abnormalities of the distal ejaculatory ducts related to infertility have been well documented. Although there are no pathognomonic findings associated with ejaculatory duct obstruction, several clinical findings are highly suggestive. Partial ejaculatory duct obstruction may cause asthenozoospermia.
In select cases, TURED has resulted in marked improvement in semen parameters, and pregnancies have been achieved. As is the case with all surgical procedures, proper patient selection and surgical experience are necessary to obtain optimal results. In patients with evidence of testicular dysfunction, chances of success are minimal. In addition, extended follow-up periods are needed after TURED to examine the long-term effects of this procedure. Better understanding of the anatomy and pathology of the ejaculatory ducts will help refine diagnostic and therapeutic procedures for this disorder.
Oxidative stress is one of the major causes of defective sperm function. Free radical attacks on these cells damage the DNA in the sperm nucleus and induce lipid peroxidation in the sperm plasma membrane. As a consequence of these changes, the spermatozoa lose their capacity for fertilization and their ability to support normal embryonic development. The origins of oxidative stress include leukocytic infiltration, excess free radical generation by the spermatozoa and defects in the antioxidant protection provided to these cells during their sojourn in the male reproductive tract. Further research in this area should help to advance our understanding of the origins of oxidative stress in the male reproductive tract, and assist in the development of rational approaches towards the prevention and treatment of this condition.
Controlled, randomized, prospective studies are lacking for most of the treatment regimens for male factor infertility. Despite this problem, the experience of many experts for many years cannot be neglected. The fact that controlled studies according to the criteria of evidence-based medicine are not available in sufficient numbers does not necessarily mean that all the recommended treatment regimens are ineffective. For the time being, one can conclude that causal factors of disturbed male fertility, such as inflammatory processes, should be eliminated and/or life-style habits such as smoking be avoided.
Recommendations can be made for empiric endocrinal therapy and complementary antioxidant treatment. Both treatment modalities should be confirmed by further studies. A promising treatment option for the future may be the antiphlogistic approach, and studies of this subject are already under way. More studies based on pregnancy rate as an outcome not only on improvement of semen parameters after medical treatment of asthenozoospermia are needed. Patients with more severe male fertility disorders should be referred to methods of assisted reproduction.
ARTs are frequently indicated in idiopathic male infertility or in cases in which no therapy is available or has not effectively resulted in conception. The range of techniques varies from those that involve only manipulation of a processed sperm to more sophisticated procedures involving the manipulation of sperm, ova and/or embryos. Fertilization may occur inside the woman (in vivo) or in vitro.
Review of the literature demonstrates that open biopsy is better than FNA, even in the setting of hypospermatogenesis. Although multiple biopsies yield better results than a single random biopsy, directed biopsies may improve the yield and sacrifice less testicular tissue. Although many studies demonstrate higher success rates with microTESE, these patients are more likely to have less favorable histology (ie, Sertoli cell–only pattern). In these cases, microTESE is clearly a better choice.
Indeed, although some systemic therapies (such as oral administration of carnitine and antioxidants) have proved to be relatively efficacious, at present in vitro treatments remain the best option for the treatment of asthenozoospermia.