Clinical meaning
Spermatogenesis occurs within seminiferous tubules of the testes over a 74-day cycle, regulated by the HPG axis. FSH acts on Sertoli cells to support spermatid maturation and produce inhibin B (which provides negative feedback to FSH secretion). LH stimulates Leydig cells to produce testosterone, which is essential for spermatogenesis at high intratesticular concentrations (50-100 times serum levels). Disruption at any level impairs fertility. Pre-testicular causes include hypothalamic-pituitary disorders (hypogonadotropic hypogonadism, hyperprolactinemia), exogenous testosterone or anabolic steroid use (which suppresses FSH/LH via negative feedback, ablating spermatogenesis). Testicular causes include varicocele (present in 40% of infertile men, causing testicular hyperthermia and oxidative stress), Klinefelter syndrome (47,XXY), cryptorchidism, and gonadotoxic chemotherapy. Post-testicular causes include obstructive azoospermia from vasectomy, cystic fibrosis (congenital bilateral absence of vas deferens), or ejaculatory duct obstruction.
Diagnosis & workup
Diagnostics & workup: - Semen analysis (WHO 2021): volume >= 1.5 mL, concentration >= 16 million/mL, total motility >= 42%, normal morphology >= 4% - Repeat semen analysis in 2-3 months if abnormal (one cycle of spermatogenesis = 74 days) - Hormonal panel: FSH, LH, total testosterone, prolactin - Scrotal ultrasound (varicocele detection, testicular volume assessment) - Karyotype if severe oligospermia or azoospermia (Klinefelter screening) - Post-ejaculatory urinalysis if low volume (retrograde ejaculation)