Functional cytology of the human testis.

The seminiferous tubular compartment of the human testis occupies about two thirds of the volume of the organ and is supported by loose connective tissue containing the Leydig cells. Sertoli cells extend from the basal lamina to the lumen of the seminiferous tubule and provide structural and functional support to the germ cells which proliferate and mature through the complex process of spermatogenesis, lasting for approximately 70 days. Histological examination of the human seminiferous epithelium gives the impression of a very irregular pattern of germ cell development but recent cytological, ultrastructural and computer-modelling studies have shown that the arrangement of germ cells within the seminiferous tubules is in fact highly organized into a helical pattern based upon the geometry of concentric spirals. Thus the human spermatogenic cycle is precisely regulated in accordance with the more familiar ordered arrangements of germ cells seen in most non-human primates and other mammalian species. The population of Leydig cells in the adult human testis represents the third and final phase of their developmental history, preceded by distinct neonatal and, earlier, fetal Leydig cell generations. Human Leydig cells are irregular in outline, deeply staining with basophilic dyes and exhibit a characteristic circular or ovoid nucleus. The density of their cytoplasm is attributed to extensive domains of smooth endoplasmic reticulum, characteristic of steroidogenic tissue. Mitochondria are numerous and lipid droplets and lipfuscin inclusions accumulate with advancing age. Crystals of Reinke up to 30 microns in length are often noted in the Leydig cell cytoplasm although their function remains unknown. The intertubular tissue contains small calibre lymphatic vessels, fibroblasts, collagen, blood vessels and occasional macrophages. With increasing age, declining sperm production and lowered androgen levels are correlated with decreases in the numbers of Sertoli cells and Leydig cells although the mechanisms responsible for this attrition have not been defined. Continued collaboration between morphologists and physiologists is necessary if we are to understand fully the endocrine regulation of spermatogenesis and the factors contributing to disturbances of spermatogenic function.