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The volume of ubiquitous chemicals with estrogenic properties is on the rise and some reports relate the increase in hormonal diseases to these compounds. A morphological and immunohistochemical analysis has been performed on 42 bilateral orchiectomy specimens from adult individuals who underwent gender reassignment surgery after receiving crossed-sex hormone therapy to give insight into vascular, inflammatory and epididymal changes following long-term treatment with estrogens and antiandrogens and raise awareness of the consequences of hormone therapy. The present study confirms previously reported findings in testicular parenchyma and epididymis, such as identification of three histological patterns according to lesion severity and cell dedifferentiation, and reports for the first time vascular and inflammatory lesions (atherosclerosis and vasculitis), both on testicle and epididymis. Cross-sex hormone therapy should be provided in specialized units in order to systematize treatments and ensure adequate follow-up., (Copyright © 2020 Elsevier Inc. All rights reserved.)

The occurrence of congenital epididymal malformations with a cystic component has not been fully characterized. Most epididymal cysts occur later in life and are likely acquired. In addition, congenital malformations of the male excretory system are extremely uncommon in fetuses and neonates, and epididymal dysplastic changes have not been reported in these cases. In this study, we report 20 cases (including 19 fetal/neonatal autopsies and one surgical specimen from an older child) showing the same spectrum of histological findings in the epididymis, characterized by cystic ductal dilation with dysplastic ducts of variable diameters and irregular shapes, with ill-defined walls. Efferent ductules also showed dysplastic features. In addition, 18 cases had either renal and/or urinary tract anomalies, including renal dysplasia (eight), pelvicaliceal dilation (eight), renal agenesis (four) and hypoplasia (one), ureteral agenesis (two) and hypoplasia (one), urethra and bladder agenesis (two), prostate agenesis (two), and autosomal recessive polycystic renal disease (two). Our observations led to the recognition of a peculiar, not previously described congenital lesion of the epididymis, and we propose the term cystic dysplasia of the epididymis for this anomaly. Similar to what is observed in other male genital system anomalies (including malformations of the rete testis, vas deferens, and seminal vesicles), most lesions occurred in association with renal and/or urinary tract malformations, suggesting a spectrum of congenital malformations. The shared embryological origin of these structures may explain their simultaneous occurrence, possibly related to disrupted mesonephric duct development.

Plasma concentrations of inhibin are correlated with spermatogenetic function. Inhibin is secreted mainly by the Sertoli and Leydig cells of the testis. In the human epididymis, the location and function of inhibin are contentious. Thus, the aim of the present study was to determine the location of inhibin in the human epididymis. Investigations were performed in samples with normal testicular function at different stages of development, as well as in samples in which testicular function or the testicular-epididymal connection were altered. In fetal, newborn and infant testes, Sertoli and Leydig cells stained positive for inhibin, whereas no such staining was detected in the epididymides. Inhibin was located in both the Sertoli and Leydig cells, as well as in the epididymis, in the apical pole of mainly secretory cells in the efferent ducts. This staining pattern was not correlated with the staining pattern for macrophages. The main duct of the epididymis was negative for inhibin staining. In ischaemic atrophic testes, the few tubules in which Sertoli cells were present stained positive for inhibin, whereas the epididymides stained negative. In paediatric cryptorchidism, Sertoli and Leydig cells stained positive for inhibin, whereas the epididymides were negative. In adult cryptorchidism, Sertoli and Leydig cells stained positive for inhibin, even in tubules containing Sertoli cells only. Interestingly, inhibin was absent from the efferent ducts. In three cases undergoing hormonal treatment prior to subsequent gender change, Sertoli and Leydig cells stained positive for inhibin. In contrast, the efferent ducts were negative or only faintly positive in cases of shorter hormonal treatment. In all cases studied, the presence of inhibin in the efferent ducts was associated with its production in the testis, suggesting that the epididymis is not responsible for the production of inhibin in men. The pattern of inhibin staining does not correlate with that of macrophages, suggesting that inhibin is not degraded in the human epididymis. The data suggest that, in humans, inhibin is secreted by Sertoli cells into the seminiferous tubules and then travels towards the efferent ducts, where it is reabsorbed into the bloodstream.

This study aims to characterize the epididymis-like intratesticular structures (ELITSs), a rare lesion found in elderly men. ELITSs were identified in 6 patients from a review of 1442 autopsies and 271 surgical specimens of adult men. Bilateral lesions were seen in 5 cases. The lesion was located in the proximity of the mediastinal rete testis (6 testes) and at the testicular periphery (4 testes), and at both central and peripheral locations in 1 case. The lesion is characterized by a pseudostratified cylindrical epithelium, with a robust pankeratin and 8, 18, and 19 keratin expression, focal vimentin expression, and apical CD 10 expression, similar to what is proper of the normal human epididymidis. The epithelial layer of ELITSs was surrounded by a thin layer of smooth-muscle cells. The adjacent testicular parenchyma was atrophied and the rete testis showed some associated degenerative lesions related to arteriosclerosis. The ELITSs are distinct from atrophic seminiferous tubules with a Sertoli cell-only pattern and from the benign glandular teratomatous component of an involution of a malignant testicular germ cell tumor, the so-called burn-out germ cell tumor. Clinical and histopathological data suggest that this lesion represents a late Wolffian differentiation similar to the initial segment of the epididymal duct, which represents an unusual manifestation of the aging process.

Testicular microlithiasis is a well-defined clinical and pathologic entity easily diagnosed through testicular echography; however, its association with cancer and infertility is now under debate. Many efforts have been done in recent years to clarify the spectrum of lesions observed in testicular microlithiasis, but no published data as to the existence of a possible microlithiasis of the epididymis and the rete testis have been found. We have observed microlithiasis of the epididymis and the rete testis in surgical (8 epididymis and 6 testis) and autopsy specimens (12 cases). In decreased order of frequency, microliths of the proximal spermatic way were seen in rete testis, epididymal duct, and efferent ducts. Intraluminal, subepithelial, and interstitial microliths were localized along these segments of the spermatic way. Subepithelial microliths were the most frequently found. A granulomatous reaction around the interstitial epididymal microliths, mimicking malacoplakia, was observed in 1 case. The differential diagnosis of microliths includes corpora amilacea, Michaelis-Gutmann bodies, calcium deposits, hyaline globules, and parasites, like the giant kidney worm Dioctophyme renale. In infants and young adults, microlithiasis of the epididymis and the rete testis is frequently associated with alterations in the development of the proximal spermatic way. In elderly adults, it is related to ischemia and obstruction of the spermatic way.

Despite the knowledge and histological classification of testicular lesions, epididymal lesions associated with cryptorchidism are not well defined and only macroscopic alterations have been reported. We have evaluated the alterations in the growth of both the epithelium and muscular wall of efferent ducts and epididymis in human patients with cryptorchidism from infancy to adulthood. In addition, by cytokeratin immunostaining we have also evaluated the stage of differentiation of each segment along the human postnatal life in these patients. A decrease is shown in the size of efferent and epididymal ducts in cryptorchid children compared with normal, age-matched controls. The height of the epithelium, muscular wall, and lumen of the cryptorchid epididymis were reduced at every age studied. This decrease in all regions was seen even in the testicular quiescent period (1 to 4 years of age). In addition, the cryptorchid epididymis grows more slowly during the transition to the pubertal period. The smaller size of the cryptorchid epididymis in pubertal and adult men compared with that of normal men is due primarily to underdevelopment of the muscular wall and a reduction in epithelial height. The pattern of growth of cryptorchid efferent ducts and ductus epididymides parallels that in normal men, except that development of the lumen and muscular layer in the cauda epididymis region are delayed. Epithelial differentiation, monitored by cytokeratin expression, is minimal in efferent ducts and throughout the epididymis of the cryptorchid male, and this is already seen in children. In conclusion, our immunohistochemical and morphometric results show a reduced development of the human cryptorchid epididymis that is already evident in childhood. They indicate that cryptorchidism is a primary congenital illness of the testis and spermatic ducts, with evident lesions from the first years of life, and suggest that surgical descent would probably not be able to completely reverse these alterations.

A histometric study of the development of the human epididymis from the fetal period to adulthood has been carried out in males without testicular or related pathology, distributed into the following groups: (I) fetuses (between the 28th and 37th week of pregnancy); (II) newborns (1-30 days of age); (III) infants (2-4 months of age); (IV) infants (5-12 months of age); (V) infants (1-4 years of age); (VI) children (5-14 years [prepubertal]); and (VII) adults (15-60 years of age). For each age group and each epididymal portion (efferent ducts, caput, corpus and cauda epididymidis) the parameters measured were (1) total surface (epithelium + muscular layer + lumen); (2) the surface occupied by the lumen; (3) the surface occupied by the muscular layer; (4) total diameter of the duct; (5) total diameter of the lumen; and (6) the height of the epithelium. The results of the present study revealed that the development of the efferent ducts and ductus epididymidis follows a biphasic pattern. A progressive development occurs from the fetal period to infants 2-4-months of age. However, this development is transient and regresses during infancy (groups IV and V). At childhood (group VI), a definitive development is initiated and completed at puberty (group VII). These changes seem to be related to the androgen-dependence of the epididymis, the different stages of testicular maturation, and the steroidogenic activity of Leydig cells.

The histological study of the testes and epididymides obtained from autopsies of 24 men with chronic renal insufficiency revealed bilateral cystic transformation of the rete testis and efferent ducts in patients who underwent hemodialysis or peritoneal dialysis, but not in patients who did not receive this treatment. The lesion was associated with an accumulation of crystalline calcium oxalate deposits in the lumen of the rete testis and efferent ducts, and in the connective tissue adjacent to these excretory ducts. The rete testis epithelium showed columnar transformation with occasional papillary proliferations. Neither atypias or mitoses were observed. In three specimens, fibrosis and giant cell reactions was also present in the rete testis at the level of crystalline deposits. In three specimens, the caput epididymidis was enlarged, and the efferent ducts showed an increase in both tubular diameter and epithelial height, irregular outline, and development of diverticula. The lesions appeared within 30 months after the onset of dialysis.

The morphology and function of the apical mitochondria-rich cells in the mammalian ductus epididymidis epithelium are revised. These cells are similar in all mammalian species studied. Apical mitochondria-rich cells are scarce (1-5 cells/100 principal cells) and are mainly found in the initial epididymal segments. Their morphology varies from slender cells that extend from the basal lamina to the epididymal lumen, to round cells that protrude into the lumen and are not in contact with the basal lamina. Their cytoplasm is more electron-dense than that of principal cells and contains more mitochondria which, in some species, are surrounded by rough endoplasmic reticulum cisternae. The adluminal cytoplasm displays a few short microvilli and contains many acid phosphatase positive vesicles. Apical mitochondria-rich cells differ from the principal cells in some histochemical features such as: (a) different lectin-staining pattern; (b) more intense reaction to the enzymatic activities: carbonic anhydrase, Ca(2+)-ATPase, peanut-agglutinin-sialidase, NADP dehydrogenase, succinate dehydrogenase, alpha-galactosidase and beta-galactosidase; (c) more intense immunoreaction to several cytokeratin types and to estradiol-related receptor protein; (d) weaker immunoreaction to epithelial membrane antigen and to retinol-binding protein. Although the function of the apical mitochondria-rich cells is still unknown, the following possible functions have been suggested: holocrine secretion; cooperation with the principal cells in epididymal reabsorption of testicular fluid; and acidification of epididymal fluid. Experimental results suggest that differentiation and maintenance of apical mitochondria-rich cells are not under androgen control and that these cells are sensitive to estrogen stimulation.

An immunohistochemical and semiquantitative study of the apical mitochondria-rich cells (AMRC) in the caput, corpus and cauda of the human epididymis from the fetal period to adulthood was performed on autopsy specimens from normal males without testicular or associated pathology. The immunohistochemical pattern of AMRC differed from that of the principal cells (PC). AMRC showed a more intense immunoreaction to several keratin types (AE1 and AE3 keratin complexes, and keratins 18 and 19) and to oestradiol-related protein receptors than did PC. In addition, immunostaining with antibodies to epithelial membrane antigen was intense in PC and weak in AMRC. Two immunohistochemical types of basal cells were observed: one was similar to the AMRC and the other to PC. PC and AMRC were already present in fetuses of 24-27 wk gestation. Basal cells were only occasionally observed at this age, but became much more numerous in the 28-33 wk fetuses. No changes in the immunohistochemical patterns of any of these cell types were found during infancy and adulthood. The numbers of PC per unit length of basement membrane were very similar in the 3 epididymal regions and at all ages studied. In all age groups, the number of AMRC decreased from caput to cauda epididymis. In the caput and corpus, the number of AMRC rose during the fetal period and the first 6 months after birth and thereafter decreased progressively during infancy and adulthood.

An enzymohistochemical and immunohistochemical study of the efferent ducts was performed in normal adult men. The epithelium consists of two types of columnar cells: principal cells (PCs) and ciliated cells (CCs), and is surrounded by a lamina propria (LP) with cells arranged circularly (LPCs). Enzymohistochemical study revealed more intense activity of succinic dehydrogenase, NADP, and ATPase in the CCs than in the PCs. The LPCs also showed an intense reaction for NADP and ATPase. Acid phosphatase activity was only intense in the apical cytoplasm of PCs. Immunohistochemical study revealed that antibodies to oestradiol receptor-related protein (ER-D5) immunostained the PCs and CCs intensely and the LPCs weakly. AE1/AE3 antibodies (which stain keratins nos. 1-8 and 14, 15 and 19) immunostained the PCs intensely, but was negative in both CCs and LPCs. Antibodies to keratin Ks.4.62 (which stain keratin no. 19) immunostained PCs and CCs but not LPCs. Epithelial membrane antigen antibodies (EMA) immunostained the adluminal surface and apical cytoplasm of PCs. Anti-vimentin antibodies immunostained the cytoplasm of PCs and CCs weakly as well as isolated cells in the LP. Antibodies to desmin immunostained most LPCs. Antibodies to collagen IV immunostained the basal lamina and many extracellular spaces in the LP, mainly around the LPCs. The differences between the enzymohistochemical and immunohistochemical patterns of the efferent ducts and those of the epididymis may help to explain functional differences along the epididymis.

A quantitative immunohistochemical study was performed of the distribution of protein gene product 9.5 (PGP, a soluble protein localized in neurons and neuroendocrine cells as well as in some non-nervous cells) and ubiquitin along the rat epididymis. In the ductuli efferents, PGP immunoreaction was observed in the whole cytoplasm of some columnar cells; a smaller number of columnar cells showed ubiquitin immunoreactivity with limited apical and basal cytoplasmic localization. In the proximal caput epididymidis, the whole cytoplasm of all columnar cells showed PGP immunoreactivity, ubiquitin immunostaining was negative in this region. In the middle and distal caput epididymidis and the distal cauda, the apical cytoplasm of some columnar cells and the whole cytoplasm of some basal cells showed immunoreactivity to PGP. In these regions, immunoreactivity to ubiquitin was positive in the supranuclear cytoplasm of some columnar cells but not in the basal cells. No immunoreactivity to PGP or ubiquitin was detected in the corpus epididymis and the proximal cauda. Double immunostaining revealed that all the epididymal ubiquitin immunoreactive cells were also PGP immunoreactive, whereas most PGP immunoreactive cells did not immunoreact to ubiquitin. In ubiquitin-PGP immunoreactive cells, the site of the PGP immunoreaction differed from that of the ubiquitin immunoreaction. PGP-ubiquitin immunoreactive cells also seemed to be immunoreactive to anti-AE1/AE3 keratin antibodies. The spermatozoal heads were immunoreactive to PGP antibodies in the epididymal regions from proximal caput to distal cauda but not in the ductuli efferents. The findings suggest that non-ubiquitinated PGP immunoreactive proteins are secreted in the epididymis, mainly in the proximal caput, and attach to spermatozoa.

Our objective was to characterize epithelial cells, lamina propria, and sites of estrogen coupling in the caput, corpus, and cauda regions of the human epididymis using antibodies to cytokeratin types; epithelial membrane antigen; laminin; type IV collagen; vimentin; desmin-, and estradiol-receptor-related protein; and immuno-histochemical techniques. Principal cells immunostain by both AE1/AE3 antibodies (keratins 1-8, 10, 13-15, and 19) and anti-pan-keratin antibodies (keratin 5, 6, and 8). Immunoreactions to both anti-keratin antibodies increase from the caput to the cauda epididymis. The principal cells only immunostained by anti-keratin 19 antibodies in the cauda and showed no reaction to keratins 10 and 11. Basal cells and apical cells immunoreact to anti-AE1/AE3, antipankeratin, and antikeratin 19 antibodies, but not to antikeratin 10 and 11 antibodies, in all three epididymal regions. The principal cells immunoreact with epithelial membrane antigen antibodies in the stereocilia and subjacent cytoplasm. This immunostaining decreased from the caput to the cauda. Antivimentin antibodies stained the apical cytoplasm of principal cells and limited areas of both principal cells and basal cells. This immunoreaction decreased from the caput to cauda. Apical cells immunostained in the three regions. Immunoreaction to ER-D5 was moderate in the principal cells, basal cells, apical cells, and muscular coat cells in the cauda. The apical cells immunostained in the three regions. Antilaminin antibodies stained the epithelial basement membrane in the three regions. Type IV collagen was detected in the basement membrane as well as around the muscular coat cells in the three regions. Immunoreaction to desmin was intense in the muscular coat cells in the three regions.(ABSTRACT TRUNCATED AT 250 WORDS)

We describe an intratesticular mucinous cystadenocarcinoma in a 59-year-old man. The tumor was bilateral and appeared in the right testis and the left epididymis. The testicular tumor was a well-demarcated nodule, 3.5 cm in diameter, that extended from the lower testicular pole (close to the albuginea) to the epididymis compressing the corpus and infiltrating the cauda. The contralateral tumor, a 2.5-cm nodule located in the corpus epididymidis, compressed the ductus epididymidis. Both tumors consisted of multiple cavities varying in size, separated from one another by connective tissue septa that were incompletely lined by a columnar pseudostratified epithelium. The epithelial cells immunostained positively for carcinoembryonal antigen and comprised two cell types: cells showing a hyperchromatic nucleus, located in the basal portion of the cell, abundant rough endoplasmic reticulum, apical vacuoles, and numerous microvilli; and mucous cells. The cystic lumen showed a mucous content and sloughed epithelial cells. The differential diagnosis and histogenesis of these tumors is discussed.

An ultrastructural, enzymohistochemical, and immunohistochemical study of the ductus epididymis in normal men was undertaken to investigate the characteristics of the apical mitochondria-rich cells (AMRCs). These cells, which differ morphologically from the principal cells (PCs), appear in isolation in the caput epididymidis (5.8 +/- 1.7 cells per cross-sectional duct) and only occasionally in the corpus epididymidis. The morphologic appearance of AMRCs varies from slender cells extending from the basement membrane to the lumen to apical cells without apparent contact with the basement membrane. The former display a round pale nucleus located in the middle of the epithelium; the apical cells have a dark nucleus, which, surrounded by a narrow cytoplasmic band, protrudes into the lumen. The cytoplasm of AMRCs is electron-dense and contains numerous mitochondria surrounded by rough endoplasmic reticulum cisternae. In the apical portion, there are lysosomes, vesicles with an electron-dense granule, and vacuoles showing a variable size and content. The stereocilia are shorter and less numerous than those of the PCs. The AMRCs are similar to the PCs in the intensely positive reaction for the enzymatic activity acid phosphatase, as well as in the lack of reaction for alkaline phosphatase and phosphorylase activities. AMRCs differ from PCs in: (1) a more intense reaction to the enzymatic activities ATPase, NADP, and succinic dehydrogenease, (2) a more intense immunostaining by AE1/AE3 and Ks4.62 anti-cytokeratin antibodies, and anti-estradiol receptor protein (D5) antibodies, and (3) a lower staining affinity for epithelial membrane antigen (EMA) antibodies. No positive immunostaining for the anti-cytokeratin Ks8.6 antibodies was observed in either AMRCs or PCs.

The histological and ultrastructural study of the ductuli efferentes in epididymides from 40 adult men revealed the occurrence of multinucleate epithelial cells in all specimens. These cells appeared in the luminal protrusions of epithelial folds and correspond to either principal or ciliated cells. The ultrastructure of their cytoplasm did not differ from that of their respective mononucleate cells. Multinucleate cells contained 3-20 closely juxtaposed nuclei, thus appearing much more irregularly outlined than those of the mononucleate epithelial cells. Multinucleation four times more frequent in the principal cells than in the ciliated cells. The number of multinucleate cells increased progressively from the age of 60 years onwards. The average number of nuclei per cell increased in the fourth decade of life, was maintained up to the eighth decade, and then increased again.

This histological study of the human ductus epididymidis in autopsy or surgical specimens revealed the presence of multiple intra-epithelial cavities or pits showing a variable degree of development. In their origin, cavities were surrounded by cells with the same staining affinity and ultrastructural features as the principal cells, except for the cavity basal surfaces that were supported by lower cells. The latter cells, although otherwise like the basal cells of the ductus epididymis, displayed short microvilli in the cavity lumen. When the cavities expanded the basal cells became principal cells, while the principal cells located at the top of the cavities degenerated, creating pits that opened into the lumen of the ductus epididymidis. The surface occupied by the pitted areas increased progressively between the end portion of the caput epididymidis and the corpus-cauda transition, where it decreased abruptly. This pitted pattern was observed in all the normal adult men studied and in the children with precocious puberty but not in the normal children or in the adult men with hypogonadotrophic hypogonadism. This observation suggests that the development of pitted cavities is androgen-dependent.

Three cases of idiopathic hematoma are reported for the first time. The disease presented with clinical symptoms of epididymitis and was unsuccessfully treated with antibiotics. The persistence of the symptoms and the suspicion of tumor led to the removal of the lesioned epididymides. The etiology of these hematomas and their differential diagnosis in relation with other benign processes of the epididymis are discussed.

Autopsy specimens of the testes and epididymis of a 32-year-old male with Fabry's disease were studied by light and electron microscopy. The characteristic ceramide deposits (lamellar inclusions, myeloid-bodies, zebra-bodies) were found in the Leydig cells as well as in the epithelial lining of both the ductuli efferentes and the ductus of the epididymis. Similar myeloid-bodies were observed in the blood vessels, connective tissue cells and muscle cells of the testicular interstitium, tunica albuginea and epididymis. In contrast, myeloid-bodies were absent or scarce in both the seminiferous epithelium and the mediastinum testis. However, the seminiferous tubules were severely affected showing reduced diameter, thickening of the tunica propria, and a few degenerated spermatogonia and primary spermatocytes. The different degrees of involvement of the testicular structures might be related to their different functions, the absorptive and permeable structures being the most severely affected. The development of testicular alterations seems to have been slow, since the patient fathered three children.

Two cases of adenomatoid tumour of the epididymis are described. Both the histochemical and ultrastructural studied support the concept that it is of mesothelial origin. The histochemical study showed the presence of acid mucopolysaccharides in the lumen of the tubular structures. The epithelial cells presented numerous microvilli in the free surface, junction complexes, wide intercellular channels and a well-developed Golgi complex. Abundant bundles of microfilaments and intracellular spaces were observed in the cytoplasm. Lymphocytes and histiocytes were identified both in the tubular lumen and between the epithelial cells. The stroma of the tumour was made up of dense connective tissue with abundant bundles of elastic fibres. The presence of intracytoplasmic spaces in the epithelial cells and elastic fibres in the stroma had not been previously observed in this tumour.

An 18-month-old infant with recurrent congenital hydrocele presented with a mass in the caput epididymis. The tumour and several fragments of the tunica vaginalis were removed and studied by light and electron microscopy. The tumour showed the characteristic histological pattern of an adenomatoid tumour of mesothelial origin. The histological appearance of the tunica vaginalis was not uniform; some areas resembled the adenomatoid tumour to the epididymis, others exhibited histological and ultrastructural features of a haemangioma, whilst elsewhere, the two patterns were intermingled. Finally, areas of pseudofibromatous periorchitis with vascular proliferation and slit-like structures lined by mesothelial cells were recognized. These features suggest that the adenomatoid tumour originated from a localized reactive process with inflammation and vascular proliferation enclosing occasional slit-like structures originating from the mesothelial lining of the tunica vaginalis. Subsequent regression of vascular proliferation and inflammatory infiltration and continued mesothelial proliferation would give rise to the typical mesothelial pattern of adenomatoid tumour.

Mast cells are a constant cell-type in the connective tissues of the human testis and epididymis from birth to adulthood. Ultrastructural study shows that these cells are similar to those found in other connective tissues. Histometric studies revealed that the number of mast cells in the interstitium, mediastinum and albuginea of the testis as well as in the epididymal connective tissue increases slightly during infancy, decreases during childhood, and then increases again at puberty. Increases at puberty are particularly evident in both the testicular interstitium and the epididymis. During adulthood, the number of mast cells progressively decreases in all testicular and epididymal connective tissues. Changes in mast cell number may be related to changes observed in the development of testicular connective tissue which occurs primarily during infancy and puberty.

The histological study of epididymides obtained from autopsies (41 children, 7 young adults and 8 elderly men) and surgical specimens (10 young adults and 3 elderly men) revealed the presence of multiple diverticula in the cauda epididymis in all elderly men and in only 2 young adults (32 and 33 years old). The diverticula appeared as evaginations of the epithelial lining of the duct, disrupting the muscular coat and expanding into the surrounding connective tissue. The formation of epididymal diverticula seems to be an age-related process that might be caused by repeated increases in the intraluminal pressure in the cauda epididymis.