Most intrascrotal masses are neoplastic in nature, however, there are a variety of tumor-like
conditions which affect the testis, adnexal structures and spermatic cord. For the purpose of
discussion, tumor-like lesions usually present as masses which clinically or macroscopically simulate a
neoplasm. There are some processes and histologic patterns that while not associated with obvious masses
may confuse the pathologist at a microscopic level. These latter conditions are also encompassed within
the umbrella of tumor-like lesions. In one series from a large general hospital, about 30% of scrotal
explorations with a suspicion of testicular or paratesticular cancer revealed non-neoplastic
disease.  A recent monograph and review article have elegantly discussed and illustrated
the wide variety of tumor-like conditions affecting the testis and paratesticular region.
This presenter's approach to classification of these diverse patterns and processes, using broad
etiologic categories is outlined in table 1.
Clearly, a complete review of this diverse list is impossible in the time constraints of this
symposium. Interested readers are encouraged to refer to the excellent reviews mentioned above. For the
purpose of this talk, I will concentrate on the inflammatory (fibroinflammatory) and hyperplastic
(proliferative) lesions which may, based on their gross and/or microscopic appearance, cause confusion
with neoplasms of the testis and paratesticular region.
Potential Tumor-like Lesions of Testis and Paratestis
Classification of Patterns and Processes
- vestigial remnants
- Mullerian (persistent Mullerian duct syndrome)
- Leydig cells
- Celes and Cysts
- cystic dysplasia of testis
- cystic dysplasia of rete testis
- mesothelial cyst
- epithelial cyst (rete, epididymis)
- epidermoid cyst
- Vascular and Ischemic
- torsion of testis/cord
- torsion of vestigial remnant
- other causes
- testicular artery aneurysm
- Inflammatory / Fibroinflammatory
- nongranulomatous – viral, bacterial, chlamydial, other
- infective – TB, syphilis, brucellosis, etc.
- idiopathic granulomatous orchitis
- meconium periorchitis
- nodular (fibromatous) periorchitis
- sperm granulomas
- sclerosing lipogranuloma
- Hyperplastic / Proliferative
- Leydig cell hyperplasia
- Sertoli cell nodules
- Pick's adenoma
- testicular feminization
- steroid cell nodules
- testicular tumor of adrenal genital syndrome (TTAGS)
- other adrenal syndromes (Nelson's, Carney's)
- hyperplasia of rete testis
- vasitis and epididymitis nodosa
- mesothelial hyperplasia
- smooth muscle hyperplasia
- inflammatory myofibroblastic tumor (proliferative funiculitis)
- tumor-like aspects of normal histology
- cribriform epididymal glands
- bizarre nuclear atypia in epithelial cells
- metanephric dysplastic hamartoma
- Rosai-Dorfman disease
- idiopathic calcification
- osseous metaplasia of epididymis
- other rare lesions
INFLAMMATORY TUMOR-LIKE LESIONS
Epididymitis, orchitis and more typically epididymo-orchitis are common conditions usually recognized
at the clinical level.
Some cases, especially longstanding examples, may give rise to a
mass and simulate a neoplasm.
Bacterial epididymitis is often secondary to Neisseria
gonorrhoeae or it may be caused by gram negative organisms, specially in prepubertal boys and older
patients. Chlamydia trachomatis is also a relatively common cause of epididymitis, especially in the
young adult males. Viral infections more typically involve the testis and while mumps is perhaps the
most well known etiology, other viruses including coxsackie and influenza viruses may be associated with
In most instances, these inflammatory conditions are clinically diagnosed and resolve with treatment
but in some cases, persistent inflammation, abscess and fibrosis leads to an enlarged firm epididymis
and/or testis leading to surgical exploration. At the microscopic level, the inflammatory nature of the
process is readily evident. In rare instances, mumps orchitis or other viral illnesses may result in
testicular enlargement and be macroscopically confused with seminoma or lymphoma. Microscopically, a
heterogeneous lymphoid infiltration is present and the tubular architecture is generally non-effaced.
Granulomatous inflammation may also involve the testis, epididymis or both. Infectious and
non-infectious forms exist. The most common type of granulomatous epididymitis is that caused by
When there is extensive involvement, secondary hydrocele and
fibrosis with adhesions may be seen. This may result in a mass lesion simulating neoplasm.
 Other organisms such as brucellosis and rare fungal diseases such as blastomycosis and
histoplasmosis may at times involve the testis.
Additionally, conditions such as
syphilis, leprosy and toxoplasmosis may affect the testis and end up being surgically removed.
may uncommonly involve the epididymis, mostly in black patients.
The epididymal involvement may be unilateral or bilateral and may be either diffuse or nodular. When
lesions are larger, they may have a tumorous appearance. Sarcoidosis may also involve spermatic cord and
simulate a neoplasm at that particular site.  Histologic examination shows typical
non-caseating epithelioid granulomas as seen in other more common sites.
Idiopathic granulomatous orchitis
is a rare condition which in one
series accounted for 0.2% of testicular masses. This lesion generally occurs in the fifth or sixth
decades and is commonly associated with a prior history of gram negative urinary tract infection. A
history of trauma is sometimes noted. While some cases have an antecedent history of flu-like illness,
other present as a mass in the testis simulating testicular neoplasm such as seminoma and lymphoma. The
testicular enlargement may be associated with some tenderness.
The tunica albuginea is typically thickened and the testicular parenchyma is replaced by lobulated
gray, tan or white tissue. The whole surface area may be involved or a more discrete nodule may be
identified. The epididymis and spermatic cord are involved in about one-half of cases. The epididymis
on rare occasions may be the dominant or exclusive site of involvement.  Occasionally,
the epididymal disease can have a xanthogranulomatous appearance. Interestingly, Nistal et al have
described a granulomatous epididymal lesion of possible ischemic origin. 
Microscopically, there is a tubulo-centric process characterized by swollen seminiferous tubules
filled with epithelioid histiocytes usually admixed with lymphocytes and plasma cells. Langerhans-type
giant cells may also be seen. Interstitial chronic inflammation including lymphocytes, plasma cells and
eosinophils is present in most cases. The process typically has a nodular (follicular) pattern of
growth. The inflammation may extend into epididymal tubules. Important differential diagnoses include
other infective causes of granulomatous orchitis, malignant lymphoma and seminoma with a granulomatous
Malakoplakia may affect the testis alone or the testis and epididymis in about one-third of
Interestingly, the right testis is affected more commonly than the left.
Isolated epididymal involvement is uncommon. The testis is usually enlarged clinically and on gross
inspection, the testicular parenchyma is lobulated, yellow, tan or brown in coloration. The consistency
is usually soft and small abscesses may be seen. At the microscopic level, tubules and interstitium are
replaced by von Hansemann histiocytes and scattered Michaelis-Gutmann bodies are identified. In some
cases, the histiocytes may have a more spindled configuration creating some confusion with spindle cell
neoplasms. Admixed acute and chronic inflammation, fibrosis and abscess formation may be seen.
Malakoplakia may be confused with Leydig cell tumor but the latter does not involve tubules and does not
show the typical von Hansemann histiocytes. In problematic cases, immunohistochemical markers such as
inhibin A and a histiocytic marker (CD68) may be used.
There are two major forms of periorchitis, meconium periorchitis and nodular (fibromatous)
Meconium periorchitis is an uncommon condition generally associated with the clinical
presentation of a scrotal mass during the first few months of life.
Macroscopically, the tunica vaginalis shows yellow/green, granular/nodular tissue. Microscopically,
there is typically myxoid tissue with spindle cells, macrophages and foci of calcification. Squames and
rare lanugo hairs may be seen. Some accompanying mesothelial hyperplasia may be seen. Confusion with a
neoplasm is unlikely at the microscopic level since neonatal tumors are rare with the majority being
juvenile granulosa cell tumors.
Nodular (fibromatous) periorchitis also referred to as "fibrous pseudotumor" is an uncommon
condition associated with one or more fibromatous masses involving the testicular tunics.
The process is usually nodular but occasionally may be a plaque-like lesion coating the
testis. Nodular periorchitis may occur at any age and usually present as a mass sometimes associated
with hydrocele. There may be a history of infection or trauma. A rare case has been associated with
idiopathic retroperitoneal fibrosis.
Solitary or multiple, grey or white nodules and uncommonly diffuse fibrous plaques are present. They
may be discrete, confluent and in some examples completely coat the testis. Massive examples may be
seen. Rare instances of bilaterality are noted.
At the histologic level, one typically sees dense hyalinized collagen, sometimes associated with focal
calcification. Sometimes patchy granulation tissue or chronic inflammation is seen. Differential
diagnosis includes inflammatory myofibroblastic tumor and fibromatosis of the paratesticular soft tissue.
In some cases, nodular periorchitis may represent a late phase of inflammatory myofibroblastic tumor
involving tunics (see later section).
result when there is a granulomatous response to extravasated
sperm usually resulting in a nodule. In many cases, this finding is microscopic, however, in some
instances, clinical and macroscopic nodules may be produced. While most sperm granulomas are under 1 cm,
they have been described up to 4 cm in diameter. Sperm granulomas are usually related to prior vasectomy
but other etiologies including prior surgery other than vasectomy, trauma, infection and urinary tract
obstruction may be present. Vasitis nodosum is a common accompaniment of sperm granulomas in cases
associated with vasectomy (see later section).
At the microscopic level, the appearance of sperm granulomas varies depending on the stage of the
process. Early on, neutrophils may be seen but typically epithelioid histiocytes and occasional giant
cells may be present. Intact sperm or sperm heads are identified within histiocytes. Eventually,
calcification and fibrosis are seen. Sperm granulomas are generally not confused with other types of
granulomatous orchitis or epididymitis.
Sclerosing Lipogranuloma HYPERPLASTIC (PROLIFERATIVE) TUMOR-LIKE LESIONS
Hyperplastic (proliferative) processes may affect various histologic compartments of the testis and
paratesticular region resulting in a large number of potential neoplastic mimickers.
Non-neoplastic proliferations of sex cord-stromal cells, epithelial cells of the testicular collecting
system, mesothelium and mesenchymal tissues of testicular adnexae and spermatic cord may give rise to
mass lesions which may either clinically or macroscopically simulate a true neoplastic process.
Sclerosing lipogranulomas have been described in the testis, epididymis and spermatic cord.
They result from the injection of lipids, generally to enhance the size of the genitalia.
While in most instances, a history of exogenous lipid injection is noted, an occasional case has been
associated with trauma and rare ones are labeled idiopathic.
Microscopically, empty vacuoles demarcated by fibrous tissue are typically seen. The spaces lack an
epithelial lining. Lipid is easily identified using the fat stains. Scattered lymphocytes, plasma cells
and eosinophils may be seen. Sometimes the differential diagnosis with adenomatoid tumor is evoked,
however, the latter tend to have irregular small tubules lined by attenuated cuboidal cells. Sclerosing
lipogranuloma may be associated with scattered atypical cells with hyperchromatic nuclei dispersed in a
There are other rare examples of granulomatous disease simulating tumors including ones caused by
foreign material (glove powder) and contrast media as well as cholesterol granulomas involving the
Leydig Cell Hyperplasia
Leydig cell hyperplasia is often caused by elevated levels of luteinizing hormone or chorionic
gonadotrophin. The former may be seen in central sexual precocity and androgen insensitivity syndrome
and the latter in association with a variety of tumors, especially the germ cell neoplasms.
Gonadotrophin-independent sexual precocity may also be associated with Leydig cell hyperplasia.
 In other conditions such as Klinefelter syndrome and testicular atrophy associated with aging,
ischemic and radiation, Leydig cells may be prominent and sometimes nodular.
Leydig cell hyperplasia may occur as multiple nodules or as a diffuse intertubular process.
Occasionally, Leydig cells are even present within seminiferous tubules. Extratesticular collections of
Leydig cells may also be identified within tunica albuginea, epididymis or spermatic cord.
Perineural involvement may also be seen. In hyperplastic conditions, the Leydig cells have
essentially normal cytologic features. Distinction from Leydig cell neoplasms rests in the multiplicity
of nodules, the lack of effacement of the tubular architecture and the bland cytoarchitectural
Sertoli Cell Nodules
Sertoli cell nodules may be identified within a variety of non-neoplastic conditions.
In some situations, these represent a hamartomatous change while in others, they are truly
The Sertoli cell (Pick's) adenoma consists of a nodule of immature Sertoli cells usually in the
setting of cryptorchidism. While usually microscopic, occasional nodules may be palpable or grossly
visualized. Rounded hyaline bodies encircled by immature Sertoli cells is noted. Occasionally,
spermatogonia are present within these immature tubules. Their small size and characteristic morphology
allows distinction from the Sertoli cell neoplasms.
In the testicular feminization (androgen insensitivity) syndrome,
(testes) are frequently undescended and may be found in the abdomen (pelvic brim), groin or in other
sites such as the labia majora.
These patients have a male genotype but a female habitus and external genitalia with well formed
breasts and a short blind vaginal pouch. Commonly, the gonads contain nodular collections of immature
Sertoli tubules which may on occasion simulate Sertoli cell neoplasia. In some instances, true sex
cord-stromal neoplasms and germ cell tumors may occur in this setting.
The typical gonads of testicular feminization are smaller than normal adult testes and surrounded by
thick tunica albuginea. Multiple tan nodules may be seen on the cut surface. Tightly packed immature
seminiferous tubules are identified and there is commonly Leydig cell hyperplasia as well.
Testicular Tumor of the Adrenogenital Syndrome (TTAGS)
Patients with the adrenogenital syndrome may develop masses of steroid-type cells in the testis and
While most occur in the testis proper and appear to originate
from the hilar region, others are present within tunica albuginea, epididymis or spermatic cord. The
steroid cell masses may manifest in childhood or adulthood, usually in the setting of untreated or
inadequately treated adrenogenital syndrome, most commonly the salt-losing form associated with
21-hydroxylase deficiency. These tumor-like masses may enlarge after administration of ACTH and decrease
in size when the ACTH is suppressed by corticosteroids. Surgical excision is generally not required,
however, there is a reported case of a malignant Leydig cell tumor arising in the setting of the
adrenogenital syndrome. 
These nodules grossly appear to originate from the hilar region and may reach sizes up to 10 cm in
diameter. They typically have a lobulated dark brown appearance with fibrous septae. Microscopically,
the large pink steroid cells resemble Leydig cells and may grow diffusely or in large nodules separated
by hyalinized connective tissue. The cells have abundant eosinophilic cytoplasm and rather bland round
to oval nuclei. On occasion, the nuclei may show atypical changes. The cytoplasm contains lipochrome
pigment but lacks the typical crystals of Reinke.
The clinical history of an adrenal syndrome, bilaterality and multifocality serve to separate this
tumor from the usual Leydig cell neoplasm. The latter typically has a yellow tan coloration and the
masses associated with TTAGS are usually brown. The cells tend to be larger with more abundant cytoplasm
and crystals of Reinke are not found.
Testicular and paratesticular steroid cell nodules may be found in other unusual situations such as
(rapid growth of ACTH-secreting pituitary adenoma after
bilateral adrenalectomy for Cushing syndrome) and in some examples of Carney's
Hyperplasia of Rete Testis
In atrophic testes, the rete testis may be relatively prominent resulting in an appearance which
simulates true hyperplasia. The latter condition is a more expansile nodular or diffuse proliferation,
often with a tubulopapillary (adenomatous) morphology.
In one series, 3 of 9 patients
had a grossly visible solid or cystic mass in the testicular hilum.  Hyperplasia of the
rete testis may be associated with a variety of conditions including testicular atrophy and may be seen
in patients with carcinoma of the prostate gland or breast. The pathogenesis is poorly understood but
may relate in part to estrogen excess. In one reported case, a patient received DES and androgen
blockade for prostate cancer nineteen months before a diagnosis of adenomatous hyperplasia of the rete
testis.  Rarely, rete hyperplasia may be associatead with hyaline globules causing
diagnostic confusion with yolk sac tumor.  Other rare lesions of rete testis which may
result in nodule formation include so-called nodular proliferation of calcifying connective
tissue, rete hamartoma and a variety of unusual cystic conditions including cystic
dysplasia and cystic transformation of rete testis.
Hyperplasia of the rete testis has on occasion been associated with epididymal cribriform
change (so-called "hyperplasia").
The latter is characterized by a prominent
cribriform pattern of epididymal tubules with an absence of epithelial atypia. This process usually
affects ductus epididymis but may involve efferent ductules as well.
Vasitis and Epididymitis Nodosa
Vasitis nodosa is typically identified at the time of vasovasostomy.  Grossly, it is
associated with a firm nodule at the site of prior vas disruption, and is usually palpable in the scrotum
superior to the testis. The lesions are typically small (1 cm or less) and may exude a milky fluid on
their cut surface. An analogous condition occurs in the epididymis, so-called epididymitis nodosum. 
At the microscopic level, there is a proliferation of small gland-like structures with an irregular
(pseudoinvasive) distribution within the muscular wall of vas deferens or epididymis. Involvement of
connective tissue and nerves may cause confusion with invasive adenocarcinoma, usually secondary
The bland nature of the tubules, lack of appreciable nuclear
atypia and mitotic activity as well as the occasional presence of sperm within lumens is helpful for
differential diagnosis. Coexistent sperm granulomas are commonly seen.
Mesothelial hyperplasia may have a variety of forms.
It is commonly secondary to an
inflammatory or irritative process and may be seen in association with hernia sacs and hydroceles. Small
tubules, nests and papillae are typically entrapped in a fibroinflammatory background. Occasionally, the
hyperplasia may have a prominent papillary appearance and grow along the testicular tunics or involve a
hydrocele sac. Such mesothelial cells may show some nuclear enlargement and nucleoli. However, they do
not show complex architectural pattern, high grade atypia or tissue infiltration, the latter of which
would point to a neoplastic mesothelial proliferation.
On occasion, more nodular collections of mesothelial cells embedded within connective tissue may
invoke a differential diagnosis with metastatic adenocarcinoma.
Rosai and Dehner have
reported several cases of mesothelial hyperplasia associated with moderate degree of nuclear atypia and
occasional mitosis.  In such cases, the differential diagnosis with other tumors such as
metastatic carcinoma require the use of appropriate immunohistochemical studies.
Smooth Muscle Hyperplasia of Testicular Adnexa and Cord
Smooth muscle hyperplasia may result in a pseudoneoplastic intrascrotal mass.  Nodular
collections of hyperplastic smooth muscle may involve the epididymis or spermatic cord. Additionally,
such involvement of the tunica albuginea or vaginalis may also be seen. In one study, 16 patients
presented with palpable lesions which ranged in size from 0.6 to 7 cm. The gross appearances were either
as discrete nodules or more ill-defined fusiform masses. At the microscopic level, there is an increase
in perivascular or interstitial smooth muscle with a nodular or diffuse organization. In some instances,
the smooth muscle proliferation blends imperceptibly into the smooth muscle wall of the epididymis or vas
deferens. No significant atypia or mitotic activity is noted.
Inflammatory Myofibroblastic (Pseudo) Tumor
Inflammatory myofibroblastic tumors (IMT) affect many sites within the genitourinary tract including
urinary bladder, kidney and prostate.
Intrascrotal examples of IMT usually involve the
spermatic cord but rare examples have also been identified in the epididymis and rete testis.
Most examples of IMT of the paratestis are grossly ill-defined, gray-white nodules which may be
gelatinous or firm. Occasionally, hemorrhage and cystic change may be seen. They are generally less
than 3 cm but may measure up to 7 cm across.
The microscopic appearance depends on the histologic age of the lesion. Early lesions consist of an
irregular proliferation of delicate, stellate and spindle cells embedded in a myxomatous stroma. At
times this appearance resembles a "tissue culture". In some cases, a more fascicular morphology is seen
and in longstanding examples, areas of dense hyaline fibrosis are identified. Admixed inflammatory cells
are common and vascularity may be prominently displayed. While mitoses are commonly present, atypical
mitoses are unusual. Immuno- histochemistry shows spindle cells with a myofibroblastic
phenotype.  Focal keratin positivity may also be identified. Anaplastic lymphoma kinase
(ALK-1) staining is also present in a subset of IMT. 
The differential diagnosis includes mesenchymal malignancies such as rhabdomyosarcaoma, myxoid
leiomyosarcoma, malignant fibrous histiocytoma and liposarcoma. In some cases of testicular torsion and
infarction, one may see a rather exuberant proliferation of myofibroblastic and fibroblastic cells
resulting in an appearance similar to inflammatory myofibroblastic tumor.  As mentioned
earlier, there is some overlap between end stage IMT and nodular (fibromatous) periorchitis, and some of
the latter may represent "burnt out" IMT involving tunics. While in many cases the IMT probably
represents a reactive condition, there is evidence that a subset is clonal.
sites, a subset of IMT appears to behave in a neoplastic fashion and may give rise to recurrence. There
are overlapping morphologies among IMT, inflammatory fibrosarcoma and
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