Knecht H
Beitr Pathol. 1976 Dec;159(3):249-70.
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.
许多近期的出版物表明,隐睾(以及程度较轻的下降侧睾丸)从生命的第二年起就会逐渐受到损伤。这些损伤是发生在此前一直健康的器官中,还是叠加在结构异常的睾丸上呢?为了回答这个问题,通过对连续切片进行组织学检查,比较了隐睾、下降侧睾丸和正常睾丸的部分组织。
检查了4至7个月大儿童的4个睾丸的部分组织(2个通过活检获得,2个来自尸检材料)以及1岁半儿童的4个睾丸的部分组织(2个通过活检获得,2个来自尸检材料)。活检组织用施蒂夫固定液固定。临床健康但突然死亡儿童的组织样本用4%甲醛固定。组织用石蜡包埋并连续切片;6微米厚的切片用苏木精-伊红染色。对同一小管的每个横切面和每个斜切面中的精原细胞进行计数,并将斜切面的计数调整为直径50至60微米的横切面。这种计数技术不会改变精原细胞的密度。图表展示了在所检查的小管长度上精原细胞密度的数据,并显示了小管分支和盲端情况。在生命的第一年,隐睾及其下降侧睾丸在同一小管中多次出现缺乏精原细胞的长段区域,而正常睾丸中的精原细胞分布更为均匀。在所检查的区域中隐睾的小管分支增加。在生命的第二年,隐睾及其下降侧睾丸的小管出现无生殖细胞区域、分支增加和盲端情况。隐睾还有一个完全没有精原细胞的小管。无生殖细胞的部分总是与比正常更小的小管直径相关。正常睾丸在相似长度的小管内未发现分支增加或无精原细胞区域,且精原细胞分布均匀。
隐睾中小管内精原细胞分布不同以及小管分支增加表明睾丸发育先前受到了干扰。