[Tubular structure and germ cell distribution of cryptorchid or normal testes in early childhood (author's transl)].
Many recent publications have demonstrated that the cryptorchid testicle (and, to a lesser extent, the descended partner) are progressively injured from the second year of life onwards. Do these injuries occur in an organ which has been healthy up to this time or are they superimposed on a structurally abnormal testicle? In order to answer this, parts of cryptorchid testicles, of the descended partners, and of normal testicles were compared by histological examination of serial sections. Parts of four testes from children aged 4-7 months (2 specimens obtained by biopsy and 2 from autoptic material) and parts of four testes from children 1 1/2 years old (2 obtained by biopsy and 2 from autoptic material) were examined. The biopsies were fixed in Stieve's fixative. Tissue samples from clinically healthy children who had died suddenly were fixed in 4% formalin. The tissue was embedded in paraffin and sectioned serially; 6 mum sections were stained with HE. The spermatogonia in each cross-section and in each oblique section of a same tubule were counted and the counts of the latter were adjusted to a cross-section 50-60 mum in diameter. This counting technique did not alter the density of spermatogonia. The graphs present data on the density of spermatogonia through the lengths of the tubules examined and demonstrate tubular branching and blind ends. In the first year of life the cryptorchid testis and its descended partner showed repeated long sections lacking spermatogonia in the same tubule, whereas in normal testes the spermatogonia were more evenly distributed. The cryptorchid testis showed increased tubule branching in the areas examined. In the second year of life the tubules of the cryptorchid testis and its descended partner manifest areas free of germ cells, increased branching, and blind ends. The cryptorchid testis also had a tubule completely free of spermatogonia. The germ cell-free parts were always associated with a smaller tubule diameter than normal. The normal testes did not disclose increased branching or spermatogonium-free areas within similar lengths of tubules and showed an even distribution of spermatogonia. The different distribution of spermatogonia within the tubules and the increased branching of the tubules in cryptorchid testes indicate a previous disturbance of testis development.
[Tubular structure and germ cell distribution of cryptorchid or normal testes in early childhood (author's transl)]. Many recent publications have demonstrated that the cryptorchid testicle (and, to a lesser extent, the descended partner) are progressively injured from the second year of life onwards. Do these injuries occur in an organ which has been healthy up to this time or are they superimposed on a structurally abnormal testicle? In order to answer this, parts of cryptorchid testicles, of the descended partners, and of normal testicles were compared by histological examination of serial sections. Parts of four testes from children aged 4-7 months (2 specimens obtained by biopsy and 2 from autoptic material) and parts of four testes from children 1 1/2 years old (2 obtained by biopsy and 2 from autoptic material) were examined. The biopsies were fixed in Stieve's fixative. Tissue samples from clinically healthy children who had died suddenly were fixed in 4% formalin. The tissue was embedded in paraffin and sectioned serially; 6 mum sections were stained with HE. The spermatogonia in each cross-section and in each oblique section of a same tubule were counted and the counts of the latter were adjusted to a cross-section 50-60 mum in diameter. This counting technique did not alter the density of spermatogonia. The graphs present data on the density of spermatogonia through the lengths of the tubules examined and demonstrate tubular branching and blind ends. In the first year of life the cryptorchid testis and its descended partner showed repeated long sections lacking spermatogonia in the same tubule, whereas in normal testes the spermatogonia were more evenly distributed. The cryptorchid testis showed increased tubule branching in the areas examined. In the second year of life the tubules of the cryptorchid testis and its descended partner manifest areas free of germ cells, increased branching, and blind ends. The cryptorchid testis also had a tubule completely free of spermatogonia. The germ cell-free parts were always associated with a smaller tubule diameter than normal. The normal testes did not disclose increased branching or spermatogonium-free areas within similar lengths of tubules and showed an even distribution of spermatogonia. The different distribution of spermatogonia within the tubules and the increased branching of the tubules in cryptorchid testes indicate a previous disturbance of testis development.