The causes of female infertility can be the following:
Tubal factor. Impassibility or absence of the uterine (Fallopian tubes) where female ovum meets with male spermatozoa. In the distal sections of uterine tubes the ovum meets with spermatozoid. In the distal sections of the uterine tubes there takes place a meeting and confluence of the spermatozoa with the ovum, that is fecundation, and as a result embryo formation. The embryo moves along the tube to uterine cavity owing to muscle wall contraction. As a rule, uterine tube impassibility is the result of a blockade due to tube inflammation (salpingitis). In some cases this may be a result of female sterilization (binding or section of the uterine tubes). Absence of uterine tubes is observed after surgical tube removal, for example, due to extra-uterine pregnancy or pyosalpingitis).
Peritoneal factor. Small pelvis commissures are a result of operations, inflammatory processes and endometriosis. Commissures enclose the ovary or are placed between the tube and ovary thereby preventing ova passage into the tube. Combination of tubular and peritoneal factors is spoken of as tubular-peritoneal infertility.
1. Endocrine factor. Hormonal disturbances can be a consequence of ovary pathology (their exhaustion, polycystic ovary syndrome, etc) and pathology of other endocrine (hypothalamus, adrenals, thyroid gland) and non-endocrine organs (liver, kidneys, etc). Endocrine infertility can be caused by the metabolic disturbances, psychic stress, etc. Whatever the cause of endocrine infertility may be, the key moment is always the ovulation mechanism breakdown (anovulation).
Uterus factor. Pathology or absence of the uterus, an organ for embryo implantation and childbearing. Uterus pathology can be inbred (intrauterus septum, bifid uterus, double uterus, etc) and gained as a result of post-surgery cicatrices, myoma, endometritis, adenomyosis, polyposis, endometrium hyperplasia, etc.
Endometriosis. This disease shows itself in endometrial tissue diffusion beyond its borders. There commissures appearing among endometrial foci cause tuboperitoneal infertility.
Immunological factor. In this case female infertility is linked with the presence of antibodies to spermatozoids (antispermal antibodies).
Genetic factor. Chromosomal pathology can lead to female sterility.
Psychological factor. This infertility is considered to be a result of conscious or unconscious female non-will to have a child. Sometimes it may be a fear of pregnancy and delivery and sometimes unwillingness to have a child from a certain man, change of appearance due to pregnancy, etc.
Should a woman have any problems with conception and pregnancy, she must meet with the gynecologists-reproductologists who can assess the cause of infertility and administer her adequate treatment. It should be remembered that male infertility factor plays an essential role in the pregnancy onset. Therefore men should be examined by the urologist- andrologist. It is desirable that the couple be examined by male and female specialists for assessing general treatment tactic.
Causes of male infertility:
Anatomic-physiological abnormalities of sexual function: disturbance of the anatomical structure of male sexual organs (hypospadia, i.e. abnormal opening of the urethra not allowing sperm emission into female vagina). Erection abnormalities: erectile dysfunction, impotency. Ejaculation abnormalities: lack of ejaculate, retrograde ejaculation occurring due to impaired innervations of the urogenital organs, intake of post-operational prostate medications, etc.
Obstructive factor: impassability or a developmental lack of sperm-ejaculatory ducts. The impassability is more frequently caused by inflammatory processes in the male sexual tract and it is sometimes a result of accumulated thick secretum (at genetic disease mucoviscidosis or fibrocystosis) or post-surgical treatment such as excision of the deferent ducts (vasectomy) for contraception purpose.
Endocrine factor. Endocrine disturbances (hyper- and hypogonadotropic hypogonadism, hyperprolactinemia, etc) can lead to spermatogenesis impairments.
Secretory factor. Spermatogenic epithelium injuries, for instance, as a result of irradiation, chemotherapy, impacts of toxic substances or high temperatures, infection, scrotum trauma, hydrocele, varicocele, etc. As a result of these impacts, the production of spermatozoa in the testicles is ceased or decreased. This can be an irreversible process.
Genetic factor. Chromosomal breakdowns leading to spermatogenesis cessation.
Inflammatory factor. Inflammation of reproductive organs transmissed sexually.
Immunological factor. Formation of the autoimmune antibodies against spermatozoa.