Unilateral Swelling of the Cheek

CLINICOPATHOLOGIC CONFERENCE
J Oral Maxillofac Surg
66:342-348, 2008
Unilateral Swelling of the Cheek
Fabio Costa, MD,* Roberto Cian, MD,†
Massimo Robiony, MD, FEBOMS,‡ Nicoletta Zerman, MD,§ and
Massimo Politi, MD㛳
Case Presentation
The patient had undergone orthopantomography (OPT)
and computed tomography (CT) previously (Fig 2). OPT
was negative for odontogenic or nonodontogenic mandibular or maxillary lesions. CT showed a mass anterior to the
masseteric muscle. The mass extended from the temporozygomatic fossa to left mandibular ramous and showed a
central low-density area with a peripheral thick and irregular wall.
An MRI was requested and it showed that the mass had a
masseteric intramuscular extension and present irregular
rim. The lesion showed low signal intensity on T1-weighted
images (Fig 3) and focal high signal intensity on T2weighted images to muscle with a peripherally brighter rim
(Fig 4). Fine-needle aspiration was suggested, but the patient declined. He was scheduled to undergo excisional
biopsy of the lesion under general anesthesia.
A 34-year-old man was referred to our department due to
a 4-month history of a left cheek growth. He reported a
gradual increase of the lesion. He denied fever, dysphagia,
odynophagia, difficulty breathing, and pain since 1 week
prior to visiting the department. During the last 5 days he
experienced pain, increased swelling, and reduced mouth
opening. There was no history of trauma; no other skin
lesion was present. His medical history was significant for
pericoronitis of the left lower third molar 1 year before and
previous endodontic treatment of the second left upper
molar 1 month before.
Upon initial examination, the face appeared asymmetrical
with a mass in the left cheek (Fig 1). The patient was
afebrile. A reduced mandibular opening of 2 cm was
present. The skin over the left facial region was normal.
Oropharyngeal examination showed normal findings and
good oral hygiene. No evidence of inflammation was noted
in the previous site of the left lower third molar extraction
and in the region of the second left upper molar. The oral
soft tissues were normal. Bimanual palpation showed a
diffuse, painful, mobile lesion in the left masseter muscle.
Neurologic deficits were absent. Salivary flow was normal
from the left Stenson’s duct. All hematologic parameters
were within normal limits. There were no masses or adenopathy on neck examination. The rest of the examination
was unremarkable.
Serologic tests were unremarkable except for a neutrophilia with 15,000 WBC/mL.
Differential Diagnosis
The acute 5-day evolution of a 4-month old lesion
raises the likelihood of an infectious or inflammatory
process. Associated pain gives further support to this
notion even if no elevated body temperature was
present. The limitation of mouth opening argues for a
process that either directly or indirectly involves the
muscles of mastication. The most likely causes of
acute unilateral facial infection involve teeth and salivary glands. The clinical examination and panoramic
radiograph carried out were inconclusive, and this
argues against the likelihood of an odontogenic focus.
Oral inspection disclosed normal hard and soft tissues, with good hygiene and normal salivary flow.
Bimanual palpation showed a diffuse, mobile, nontender lesion in the left masseter muscle. CT showed
the presence of a mass from the temporozygomatic
fossa to left mandibular ramous with central hypodensity, either intrinsic or extrinsic to the anterior aspect
of the masseter muscle. This is a critical juncture in
the diagnostic tree. For this reason, an MRI was requested and it showed that the mass had a masseteric
intramuscular extension with an irregular rim. The
lesion had lower signal intensity than the muscle on
T1-weighted images. On T2-weighted images, the lesion was desmogenous and hyperintense to muscle
with a peripherally brighter rim.
The presences of trismus and rim enhancement
increase the likelihood of a significant active inflamma-
*Consultant in Maxillo-Facial Surgery, Department of MaxilloFacial Surgery, University of Udine, Udine, Italy.
†Resident of Maxillo-Facial Surgery, Department of Maxillo-Facial
Surgery, University of Udine, Udine, Italy.
‡Associate Professor of Maxillo-Facial Surgery, Department of
Maxillo-Facial Surgery, University of Udine, Udine, Italy.
§Associate Professor of Oral Pathology, Faculty of Medicine,
University of Ferrara, Ferrara, Italy.
㛳Professor and Chairman of Maxillo-Facial Surgery, Head of Department of Maxillo-Facial Surgery, University of Udine, Udine,
Italy.
Address correspondence and reprint requests to Dr Costa:
Clinica di Chirurgia Maxillo-Facciale, Azienda Ospedaliero-Universitaria di Udine, P.le S. Maria della Misericordia, 33100 Udine, Italy;
e-mail: [email protected]
© 2008 American Association of Oral and Maxillofacial Surgeons
0278-2391/08/6602-0023$34.00/0
doi:10.1016/j.joms.2007.04.030
342
COSTA ET AL
tory component such as an abscess. The central area of
hypodensity raises concern for central necrosis.
Anatomic structures at the anterior aspect of the
masseter (buccomasseteric region) include muscles
(masseter and buccinator), the parotid duct and accessory salivary glands, the buccal fat pad, nerves,
blood vessels, and lymph nodes.1 All of these structures can present with mass lesions and are considered in light of the patient’s presentation.
Primary malignant tumors of the masseter are rare,
more frequent in childhood, and not supported by the
clinical presentation because of the 4-month history
of left cheek growth.
Both leiomyoma and leiomyosarcoma are rare in
the oral cavity. Leiomyomas arise most commonly in
the muscularis layer of the gut and in the body of the
uterus. Leiomyosarcomas arise most commonly in the
retroperitoneum, mesentery, omentum, or subcutaneous and deep tissues of the limbs. In a recent review
of the literature, 139 leiomyomas and 68 leiomyosarcomas of the oral cavity and pharynx were reported.2
Greater than 40% of leiomyomas presented as an
intraoral mass, and greater than 50% were known to
be present for longer than 1 year. About 90% of
343
FIGURE 2. Computed tomography (axial view) showing a mass
anterior to the masseteric muscle. A central low-density area with a
peripheral thick and irregular wall was present.
Costa et al. Head and Neck JXG in Adults. J Oral Maxillofac Surg
2008.
leiomyomas are symptomatic. Patients with leiomyosarcoma were much more likely to have obvious
symptoms of shorter duration, and one third presented with pain or swelling. The peak age of incidence was 40 to 49 years for benign tumors and 50 to
FIGURE 1. Patient frontal view at the initial examination showing
unilateral swelling of the left cheek.
FIGURE 3. MRI (T1-weighted image) showing the mass with its
masseteric intramuscular extension.
Costa et al. Head and Neck JXG in Adults. J Oral Maxillofac Surg
2008.
Costa et al. Head and Neck JXG in Adults. J Oral Maxillofac Surg
2008.
344
FIGURE 4. MRI (T2-weighted images) showing the mass with a focal
high signal intensity to muscle and a peripherally brighter rim.
Costa et al. Head and Neck JXG in Adults. J Oral Maxillofac Surg
2008.
59 years for malignant lesions, with the incidence in
men predominating slightly over that in women.
A malignant granular cell tumor within the masseter muscle has been reported.3 This lesion can occur
in patients of any age but is seen most commonly in
the fourth, fifth, and sixth decades of life. It is about
twice as common in women as in men.
Metastatic lesions to the masseter muscle4 are rare
and they generally present in patients older than our
patient. Adenocarcinoma is the primary tumor most
likely to metastasize to skeletal muscle, most commonly from breast, lung, and colon.
Other potential lesions occurring in striated muscle
include parasitic infections. The encysted larvae form
most commonly in the central nervous system, with
resultant neurologic symptoms, or in the globe, but
muscle and subcutaneous tissue also can be involved.5 They can remain asymptomatic for several
years, but cause pain when they die secondary to a
marked inflammatory response. The cysts can appear
radiolucent, but are more commonly calcified. This
patient does not show the calcifications or the eosinophilia typical of parasitic disease.
Any acute illness with unilateral facial swelling,
pain, fever, and limitation of motion arouses concern
for inflammatory lesions of the salivary glands, such as
mumps or acute bacterial parotitis secondary to sialolithiasis. The 4-month history of swelling, hematologic examination, and imaging argue against the likelihood of an inflammatory lesion of the parotid gland.
The accessory parotid gland is salivary tissue separated from the main parotid gland and lying on mas-
HEAD AND NECK JXG IN ADULTS
seter muscle. It has a secondary duct emptying into
the Stensen’s duct. The accessory parotid gland exists
in 21% to 61% of individuals. However, the appearance of an accessory parotid tumor is rare, with a
reported frequency of 1% to 7.7% of all parotid gland
tumors.6 Pleomorphic adenoma is the most common
benign neoplasm and mucoepidermoid carcinoma
the most common malignancy.7 An asymptomatic
mass was the most common clinical presentation for
pleomorphic adenoma and this is consistent with the
patient’s first history, but falls short as a focus of
inflammation noted in the examination. Spontaneous
infarction of a pleomorphic adenoma is extremely
rare8 and there are few reports associated with necrosis in a pleomorphic adenoma of the parotid gland
after fine needle aspiration.9
Lipomas are commonly soft and superficial, but
when they are infiltrative, however, they can exist
entirely intramuscularly.10 This intramuscular type of
lipoma usually presents as painless. This falls short as
a focus of inflammation noted in the examination.
Moreover MRI excluded this diagnosis because lipomas had high signal intensity on both T1- and T2weighted images.11
Solitary neurogenic tumors, such as neurilemmoma
or neurofibroma, should be included in this discussion because they have been described in almost all
anatomic sites in the head and neck. However, the
findings on CT and MRI scan argue against this diagnosis.
Vascular lesions, such as hemangioma or lymphangioma, are not likely because they are more common in infancy and childhood, there was no primary
history, and there was no mucosal or skin discoloration.
A metastatic lymph node is also unlikely given the
age of patient, the lack of a primary lesion on head
and neck examination, and the negative medical history.
An inflamed lymph node is certainly possible in this
scenario, with an initial local infection and subsequent hyperplastic lymphadenopathy. The buccal or
facial lymph nodes12 are often the site of a reactive
hyperplastic process at the anterior border of the
masseter muscle. Lymphadenopathy may evolve into
a submasseteric abscess with the symptoms of cheek
tenderness and trismus. Submasseteric abscess is located between the masseter muscle and mandibular
ramous with different appearances as sepsis, infection, or tumor.13 Of interest, some patients may have
a partial treatment with antibiotics that may contribute to the initial absence of systemic signs and
symptoms.14 A submasseteric abscess correlated well
with the previous pericoronitis of the left lower third
molar in the medical history of the patient, the presence of trismus and pain, the central low-density area
345
COSTA ET AL
at the CT, and the high signal intensity on the T2weighted images at the MRI.
Actinomycosis has to be considered. Actinomycosis
is currently an uncommonly diagnosed human disease. However, it can still complicate trauma to the
respiratory and digestive tracts, including operative
procedures. A patient with cervicofacial actinomycosis commonly gives a history of recent dental manipulation, which usually involves extraction of a mandibular molar.15 The common initial symptoms of
infection can be absent. Infection due to actinomyces
is a well-known mimic of malignancy as clinical, radiologic, and pathologic findings and localization in
the masseter muscle have been described.16
Cat-scratch disease with subsequent acute suppurative infection may also be considered. Although it is
more common in children, cat-scratch disease also
may be present in adults. It may cause an inflammatory infection of the lymph nodes with negative serologic examination. Two to 6 weeks after the scratch,
1 or more regional lymph nodes begin to enlarge. The
nodes are tender and can get quite large. Cervicofacial
lymphadenopathy was the most common manifestation. Atypical manifestation of cat-scratch disease includes swelling of the parotid gland in 8.1% of cases.17
The age and the absence of a cat-scratch history make
this diagnosis unlikely.
Cervical tuberculous lymphadenitis is a possible
diagnosis and it is still an important cause of neck
mass in many countries.18 The CT findings of cervical
tuberculous lymphadenitis were classified into 4
types. The cervical tuberculous lymphadenitis usually
shows a central low density and peripheral rim enhancement that tends to be thick and irregular compared with a malignant lymphadenopathy.
Non-Hodgkin’s lymphoma should be considered
but a non-Hodgkin’s lymphoma arising from the masticator space muscles is very rare.19
In summary, the differential diagnosis in order of
likelihood is acute infection with resultant reactive
facial lymph node necrosis contiguous with the anterior aspect of the masseter muscle; a parasitic infection with infestation in the masseter muscle; a benign
neoplastic process of accessory parotid tissue with
obstruction presenting as an infection.
Subsequent Course
The patient underwent an excision biopsy of the lesion
through an intraoral approach under general anesthesia.
The lesion was approached through a mucosal incision over
the anterior portion of the left ramous of the mandible.
Incision of the buccinator muscle was carried out. The
lesion, which arose inside the masseteric muscle, was identified (Fig 5). A complete excision of the lesion submitted
for histologic examination was followed by layered closure.
Tissue planes between the lesion and adjacent soft tissues
FIGURE 5. Intraoperative view of the lesion that arose inside the
masseteric muscle.
Costa et al. Head and Neck JXG in Adults. J Oral Maxillofac Surg
2008.
remained intact. The patient tolerated the procedure well
and was discharged from our department in excellent condition on the following day without facial nerve dysfunction. The lesion did not recur in the follow-up period of 3
years (Fig 6).
Pathologic Diagnosis
Gross examination showed a 4.5 ⫻ 2.5 ⫻ 2 cm
ovoid, fairly well demarcated but not encapsulated
specimen. The section of the mass showed a homogeneous white and yellow appearance with hemorrhagic areas. Microscopic examination showed a xanthogranuloma, which was characterized by a dense
infiltration of the fibromuscular and fat tissue by
foamy-type histiocytes (Fig 7). No Touton giant cells
were seen. Interdigitating among foamy histiocytes
were lymphocytic, neutrophil, and plasma cells with
rare multinuclear eosinophil. The lesion presents a
rich vascular congestion above all to the periphery of
the same one. Immunohistochemical studies showed
the foamy histiocytes to be reactive to CD 68 and
immunonegative for S-100 protein and CD1a.
Discussion
Juvenile xanthogranuloma (JXG) is an uncommon
non-Langerhans cell histiocytosis. JXG was first re-
346
FIGURE 6. Patient frontal view 3 years after excision of the lesion. No
recurrence was observed.
Costa et al. Head and Neck JXG in Adults. J Oral Maxillofac Surg
2008.
ported by Adamson in 1905.20 After multiple nomenclature revisions, its modern name was popularized in
1954 by Helwig and Hackney.21
Approximately 30% of cases of JXG occur at birth,
with as many as 75% of cases occurring in the first 9
months of life. The mean age at presentation is 22
months. Despite the term “juvenile” in the disease
name, 10% of cases manifest in adulthood.22 A bimodal peak is seen either before the age of 1 year or
in the fourth decade of life.23 A few cases occurring
up to the age of 50 years have been reported.22-24 A
male predilection is seen, with the gender ratio ranging from 1.5 to 4.0 male to 1.0 female.25 Caucasian
people are 10 times more commonly affected than
blacks.26 JXG can be associated with medical conditions26 that include neurofibromatosis, Niemann-Pick
disease, urticaria pigmentosa, and myelogenous leukemia.
The etiology of JXG is not known. The consensus is
that the cells of origin are dermal dendrocytes. As
postulated, JXG may be a granulomatous reaction of
histiocytes to an unidentified stimulus, possibly of
either physical or infectious etiology.27
Recent evidence from Kraus et al,28 however, suggests a possible CD4⫹ plasmacytoid monocyte origin.
HEAD AND NECK JXG IN ADULTS
Inhibition of cellular apoptosis seems to play a minor
role in the growth of xanthogranulomas.
The appearance of giant cells and foamy lipid-laden
histiocytes generally occurs late and apparently is a
secondary event, possibly in response to cytokine
production by histiocytes. Both the dermal and intramuscular lesions showed similar histologic features
and consisted of diffuse infiltrates of histiocytes with
eosinophilic and foamy cytoplasm, lymphocytes, eosinophils, and Touton giant cells in varying proportions.29 Nascimento stated that the lesions of intramuscular JXG, unlike those of cutaneous JXG, tend to
be composed of a monotonous population of histiocyte-like cells, with rare, if any, foamy macrophages
or Touton-type multinucleated giant cells.30 In our
case, there were no Touton giant cells but abundant
foamy histiocytes were present.
The typical immunophenotype for JXG is CD68
(⫹), CD1a (⫺), and S-100 protein (⫾).25 Janssen and
Harms, in their clinicopathologic study of 129 patients, described that the histiocytic infiltrate showed
granular cytoplasmic staining with the macrophage
marker CD68 (8 of 8, 100%), the reaction against
CD1a was consistently negative (112 of 112, 100%),
and that the majority of cases showed a negative S-100
protein reaction (116 of 123, 94%).31 In our case, the
immunohistochemical results showed foamy histiocytes reactive to CD 68 and immunonegative for S-100
protein and CD1a.
The skin is the most commonly involved site in
cases of JXG, with a predilection primarily for the
head, neck, and the upper trunk.
Clinically, it is characterized by papule or nodule
with an erythematous to yellowish appearance; measuring less than 1 cm. Lesions are usually asymptomatic.
FIGURE 7. Hematoxylin and eosin stain (original magnification,
⫻400): histologic section of juvenile xanthogranuloma showing the
typical foamy histiocytes.
Costa et al. Head and Neck JXG in Adults. J Oral Maxillofac Surg
2008.
347
COSTA ET AL
Table 1. INTRAMUSCULAR JXG DESCRIBED IN LITERATURE
Author
Sonoda et al36
Janney et al37
White and Garen38
De Graaf et al39
Favara et al40
Yamanaka et al41
Nascimento30
Margulis et al42
Berenguer et al35
Janssen and Harms31
Present report
Location of Lesion
Age
Gender
Size (cm)
Neck
Paraspinal
Paraspinal
Paraspinal
Paraspinal
Occipital
Psoas
Paraspinal
Rectus abdominis
Chin
Latissimus dorsi
7 cases in skeletal muscle of the trunk
Masseteric
14 mo
8 mo
3 mo
2 mo
3 yr
7 mo
4 mo
6 mo
4 mo
5 mo
9 mo
*
34 yr
M
F
M
M
M
M
F
M
M
F
F
*
M
*
1.5
4
2
5
5
5
3.5
1.2
3
3
*
4
Abbreviation: JXG, juvenile xanthogranuloma.
*Data are not specified.
Costa et al. Head and Neck JXG in Adults. J Oral Maxillofac Surg 2008.
Relapsing course and spontaneous regression with
residual atrophic scar or an area of altered pigmentation are typical. The period from onset to complete
resolution ranges from months to years.26
JXG can be divided into 3 types based on the
diameter of the lesions. The papular type refers to
lesions less than 2 to 5 mm; the nodular type refers
lesions between 10 to 20 mm; and the macronodular
type or giant type refers to lesions larger than 20 mm
in diameter.22,32
Extracutaneous JXG is rare (5%) and most commonly involves the eye and periorbital region. Ocular
JXG manifests most commonly in the iris. Following
in frequency are lung and liver manifestations of JXG.
Rarely, lesions occur in the adrenal gland, appendix,
bones, bone marrow, central nervous system, gonads,
kidney, larynx, myocardium, pericardium, retroperitoneum, small and large intestines, and spleen.22,33,34
Only 50% of systemic lesions are accompanied by
cutaneous JXG, and these cutaneous lesions tend to
appear as multiple papules or nodules. The size of a
cutaneous lesion does not correlate with the presence
or absence of systemic JXG. Intramuscular JXG is
exceedingly rare.30,35 Careful review of the literature
shows 11 reported cases of intramuscular location of
JXG. Whereas most cutaneous lesions occur in the
head and neck region, intramuscular locations were
located in the trunk, commonly in the spinal muscle
of infants (Table 1).
Only 2 cases of intramuscular JXG located in the
head and neck region were reported. The mean age of
patients presenting intramuscular JXG was 9 months
old. To our knowledge this is the first clinicopathologic report of JXG invading the muscles in the head
and neck in an adult patient. Follow-up at 3 years after
surgery showed no evidence of recurrence.
References
1. Seltzer SE, Wang A-M: Modern imaging of the masseter muscle:
Normal anatomy and pathosis on CT and MRI. Oral Surg Oral
Med Oral Pathol 63:622, 1987
2. Wertheimer-Hatch L, Hatch GF 3rd, HatchB S KF, et al: Tumors
of the oral cavity and pharynx. World J Surg 24:395, 2000
3. Nishida M, Inoue M, Yanai A, et al: Malignant granular cell
tumor of the masseter muscle: Case report. J Oral Maxillofac
Surg 58:345, 2000
4. Ahuja AT, King AD, Bradley MJ, et al: Sonographic findings in
masseter muscle metastases. J Clin Ultrasound 28:299, 2000
5. Timosca G, Gavrilita L: Cysticercosis of the maxillofacial region: A clinicopathologic study of five cases. Oral Surg Oral
Med Oral Pathol 37:390, 1974
6. Hamano T, Okami K, Sekine M, et al: A case of accessory
parotid gland tumor. Tokai J Exp Clin Med 29:131, 2004
7. Rodino W, Shaha A: Surgical management of accessory parotid
tumors. J Surg Oncol 54:153, 1993
8. Behzatoglu K, Bahadir B, Huq GE, et al: Spontaneous infarction
of a pleomorphic adenoma in parotid gland: diagnostic problems and review. Diagn Cytopathol 32:367, 2005
9. Bayramoglu H, Duzcan E, Akbulut M, et al: Infarction after fine
needle aspiration biopsy of pleomorphic adenoma of the parotid gland. Acta Cytol 45:1008, 2001
10. Califano L, Maremonti P, Arias Gallo J, et al: Infiltrating lipomas
of the face. Reporting five clinical cases. An Otorrinolaringol
Ibero Am 29:163, 2002
11. Chikui T, Yonetsu K, Yoshiura K, et al: Imaging findings of
lipomas in the orofacial region with CT, US, and MRI. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 84:88, 1997
12. Yonetsu K, Nakayama E, Yuasa K, et al: Imaging findings of
some buccomasseteric masses. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 86:755, 1998
13. Leu YS, Lee JC, Chang KC: Submasseteric abscess: Report of
two cases. Am J Otolaryngol 21:281, 2000
14. Jones KC, Silver J, Millar WS, et al: Chronic submasseteric
abscess: Anatomic, radiologic, and pathologic features. AJNR
Am J Neuroradiol 24:1159, 2003
15. Lang-Roth R, Schippers C, Eckel HE: Cervical actinomycosis. A
rare differential diagnosis of parotid tumor. HNO 46:354, 1998
16. Palonta F, Preti G, Vione N, et al: Actinomycosis of the masseter muscle: Report of a case and review of the literature.
J Craniofac Surg 14:915, 2003
17. Ridder GJ, Boedeker CC, Technau-Ihling K, et al: Cat-scratch
disease: Otolaryngologic manifestations and management. Otolaryngol Head Neck Surg 132:353, 2005
348
18. Lee Y, Park KS, Chung SY: Cervical tuberculous lymphadenitis:
CT findings. J Comput Assist Tomogr 18:370, 1994
19. Connor SE, Chavda SV, West R: Recurrence of non-Hodgkin’s
lymphoma isolated to the right masticator and left psoas muscles. Eur Radiol 10:841, 2000
20. Adamson HG: Society intelligence: The Dermatological Society
of London. Br J Dermatol 17:222, 1905
21. Helwig EB, Hackney VC: Juvenile xanthogranuloma (nevoxantho-endothelioma). Am J Pathol 30:625, 1954
22. Shapiro NL, Malis DJ, Charon CC, et al: Giant juvenile xanthogranuloma of the tongue. Am J Otolaryngol 20:241, 1999
23. Tanyeri H, Weisenberg E, Friedman M: Juvenile xanthogranuloma of the tongue. Otolaryngol Head Neck Surg 123:641, 2000
24. Tahan SR, Pastel-Levy C, Bhan AK, et al: Juvenile xanthogranuloma. Clinical and pathologic characterization. Arch Pathol
Lab Med 113:1057, 1989
25. Flaitz C, Allen C, Neville B, et al: Juvenile xanthogranuloma of
the oral cavity in children: A clinicopathologic study. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 94:345, 2002
26. Iwuagwu FC, Rigby HS, Payne F, et al: Juvenile xanthogranuloma variant: A clinicopathological case report and review of
the literature. Br J Plast Surg 52:591, 1999
27. Fang TJ, Lin CZ, Li HY: Juvenile xanthogranuloma of the nasal
cavity. Int J Pediatr Otorhinolaryngol 67:297, 2003
28. Kraus MD, Haley JC, Ruiz R, et al: “Juvenile” xanthogranuloma:
An immunophenotypic study with a reappraisal of histogenesis. Am J Dermatopathol 23:104, 2001
29. Kuo FY, Eng HL, Chen SH, et al: Intramuscular juvenile xanthogranuloma in an adult: A case report with immunohistochemical study. Arch Pathol Lab Med 129:31, 2005
30. Nascimento AG: A clinicopathologic and immunohistochemical comparative study of cutaneous and intramuscular forms of
juvenile xanthogranuloma. Am J Surg Pathol 21:645, 1997
HEAD AND NECK JXG IN ADULTS
31. Janssen D, Harms D: Juvenile xanthogranuloma in childhood
and adolescence: A clinicopathologic study of 129 patients
from the Kiel pediatric tumor registry. Am J Surg Pathol 29:21,
2005
32. Magana M, Vazquez R, Fernandez-Diez J, et al: Giant congenital
juvenile xanthogranuloma. Pediatr Dermatol 11:227, 1994
33. Patel AV, Meechan JG, Soames JV: Juvenile xanthogranuloma of
the oral cavity: A case report. Int J Paediatr Dent 3:43, 1993
34. Freyer DR, Kennedy R, Bostrom BC, et al: Juvenile xanthogranuloma: Forms of systemic disease and their clinical implications. J Pediatr 129:227, 1996
35. Berenguer B, Gonzalez B, Marin M, et al: Intramuscular juvenile
xanthogranuloma. Cir Pediatr 17:49, 2004
36. Sonoda T, Hashimoto H, Enjoji M: Juvenile xanthogranuloma.
Clinicopathologic analysis and immunohistochemical study of
57 patients. Cancer 56:2280, 1985
37. Janney CG, Hurt MA, Santa Cruz DJ: Deep juvenile xanthogranuloma. Subcutaneous and intramuscular forms. Am J Surg
Pathol 15:150, 1991
38. White W, Garen P: Deep juvenile xanthogranuloma. Subcutaneous and intramuscular forms. Am J Surg Pathol 15:150, 1991
39. De Graaf JH, Timens W, Tamminga RY, et al: Deep juvenile
xanthogranuloma: A lesion related to dermal indeterminate
cells. Hum Pathol 23:905, 1992
40. Favara BE, Caldwell S, Steele A, et al: Atypical juvenile xanthogranuloma. Pediatr Pathol Lab Med 15:169, 1995
41. Yamanaka K, Suita S, Kakumori S, et al: Juvenile xanthogranuloma of the pelvic origin: A case report. Eur J Pediatr Surg
5:246, 1995
42. Margulis A, Melin-Aldana H, Bauer BS: Juvenile xanthogranuloma invading the muscles in the head and neck: Clinicopathological case report. Ann Plast Surg 50:425, 2003

Download Report