Maxillary Ameloblastic Carcinoma in a Dog

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Israel Journal of Veterinary Medicine  Vol. 69 (2)  June 2014 Aydogan, A. 98
INTRODUCTION
Ameloblastic carcinoma (AC) is a malignant odontogen-
ic epithelial tumor and combines the histologic features of
the ameloblastoma. It is a rare tumor in humans and an ex-
tremely rare entity in domestic animals (1); the tumor has
been reported in a horse and two dogs (2, 3, 4). It does not
appear in the veterinary tumor classifcation and has malig-
nant histopathological aspects such as cytologic atypia with
or without metastasis (5, 6). Although ameloblastomas are
well known and described in the literature, there is a little
known about the ameloblastic carcinoma especially in do-
mestic animals (7).
In the present case, the tumor was classifed according to
the human tumor classifcation sytem based on histopatho-
logic and immunohistochemical diagnosis. Te aim of this
report was to describe clinical, gross, microscopic, and im-
munohistochemical fndings of a maxillary ameloblastic car-
cinoma in a dog.
MATERIALS AND METHODS
A 8-year-old, mix breed, male dog was presented to the Lara
Antalya Veterinary Hospital for examination of a tumor mass
on the right maxillary region of mouth (Figure 1). Te mass
had a nodular appearance and was painful. A radiographic
examination of the chest did not show any evidence of me-
tastasis. Oral radiographs did not clearly defne the borders
of the mass. Te dog was in a good body condition and the
hematological profle was normal. Under general anesthe-
sia, the mass was excised with blunt dissection using cau-
terization. A 3 cm deep cavity appeared after dissection re-
vealing the alveolar bone of the maxilla. Two of molar teeth
were also extracted with the tumor. Severe bleeding of tumor
area was observed after dissection which was stemmed us-
ing sponges. No adequate healthy gingiva and mucosa was
available for suturing. Mouth disinfection was provided by
using glycerine-iodine 3% solution (Ulkem Gliserin Iode,
Ankara, Turkey) and broad spectrum antibiotics: Cefovecin
Maxillary Ameloblastic Carcinoma in a Dog
Aydogan, A.,
1
* Haligur, M.,
1
Ozmen, O.
1
and Esin, E.
2
1
University of Mehmet Akif Ersoy, Faculty of Veterinary Medicine, Department of Pathology, Istiklal Yerleskesi, 15030,
Burdur, Turkey.
2
Department of Surgery, Lara Antalya Veterinary Hospital, Antalya, Turkey.
* Corresponding Author: Assist. Professor Ahmet Aydogan, DVM, PhD, University of Mehmet Akif Ersoy, Faculty of Veterinary Medicine, Department of
Pathology, 15030, Istiklal Yerleskesi, Burdur-Turkey. Tel: +90 248 213 21 73, Fax: +90 248 213 20 05. E-mail: aaydogan79@gmail.com.
ABSTRACT
Ameloblastic carcinoma (AC) is a malignant odontogenic epithelial tumor and reported rarely in domestic
animals. An 8-year-old, mix breed, male dog presented to Lara Antalya Veterinary Hospital for examination
of a mass on the right molar teeth of the maxilla. Oral radiographs did not show clear borders of the
mass. Clinically and macroscopically, the mass was painful and had a nodular appearance and was reddish-
white in color. Histopathologic examination of the mass revealed irregular shaped broad islands, sheets and
nests consisting of neoplastic cells. Tese cells were immunopositive for carcinoembryonic antigen (CEA),
pancytokeratin, Ki-67 and proliferating cell nuclear antigen (PCNA). Based on gross, histopathologic and
immunohistochemical fndings, the mass was diagnosed as ameloblastic carcinoma.
Keywords: Ameloblastic Carcinoma, Pathology, Immunohistochemistry, Dog, Canine.
Israel Journal of Veterinary Medicine  Vol. 69 (2)  June 2014 99 Ameloblastic Carcinoma in a Dog
8 mg/kg (Convenia, Pfzer Animal Health, Sandwich, Kent,
UK) and Enrofoxacin 5 mg/kg (Baytril-K %5, Kansas, USA)
for 5 days.
A telephone follow up was made at 4 and 10 months
after the surgery and the owner reported that no recurrence
had developed.
Te tumor was submitted for pathological examination to
Mehmet Akif Ersoy University, Veterinary Medicine Faculty,
Department of Pathology. Te mass was routinely fxed in
bufer formalin solution and processed in parafn-embedded
cassettes; 5 µm sections were obtained and stained with he-
matoxylin and eosin (H&E) for histopathology.
Immunohistochemical (IHC) examination was per-
formed using the routine streptavidin-biotin peroxidase
method with primary antibody against Pancytokeratin
[Mouse Monoclonal Pancytokeratin Antibody, Abbiotec,
Cat. No. 251788, San Diego, CA, USA, 1:100 dilu-
tion]; Vimentin (Mouse Monoclonal Vimentin Antibody,
Abbiotec, Cat. No. 251809, San Diego, CA, USA, 1:100 di-
lution); Carcinoembryonic antigen (CEA) (CEA Antibody,
Abbiotec, Cat. No. 250598, San Diego, CA, USA, 1:200 di-
lution); Ki67 (Rabbit Polyclonal Ki-67 Antibody, Abbiotec,
Cat. No. 250733, San Diego, CA, USA, 1:100 dilution);
Proliferating cell nuclear antigen (PCNA) (Rabbit Polyclonal
PCNA Antibody, Abbiotec, Cat. No. 250812, San Diego,
CA, USA, 1:100 dilution); Smooth muscle actin (SMA)
(Mouse Monoclonal SMA, Abbiotec, Cat. No. 251813, San
Diego, CA, USA, 1:200 dilution); S100 (Mouse Monoclonal
S-100 Antibody, Abbiotec, Cat. No. 251795, San Diego, CA,
USA; 1:100 dilution). Te reaction product was visualized by
DAB [3, 3’-diaminobenzidine chromogen (Zymed, South
San Francisco, CA, USA)) and counterstained with Harris’
hematoxylin.
RESULTS
Te tumor mass was localized in the region of the right mo-
lar teeth of the maxilla and measured 4 × 3.2 × 1 cm and
weighed 18.3 grams. It was reddish-white in color and frm
in consistency. Te cut surface of the tumor was homoge-
neous and also reddish-white in color.
Histopathological fndings revealed irregular shaped
broad islands with a variable appearance with poorly cellu-
lar collagenic tissue sheets and nests consisting of neoplastic
cell proliferations with ameloblastic diferentiation. Tese
cells were markedly pleomorphic, oval to round shaped with
large, irregular, hyperchromatic nuclei, prominent nucleoli
with moderate eosinophilic cytoplasm. Some tumor cells had
multiple nucleoli. Mitotic fgures were common and 4-6 mi-
totic fgures were seen per high power feld in the mitotically
active areas of the tumor (Figure 2). In some felds of the tu-
mor, epithelial proliferations in cords were dispersed into the
adjacent fbrous tissue. In addition, necrosis was observed in
some areas of the tumor.
Immunohistochemically, the neoplastic cells were posi-
tive for CEA (Figure 3), pancytokeratin (Figure 4), Ki-67
Figure 1: Appearance of gingival mass on the right maxillary region
of the mouth.
Figure 2: Ameloblastic carcinoma. Marked pleomorphism of the
neoplastic cells and mitotic fgures (arrows). HE, bar = 30 µm.
Case Reports
Israel Journal of Veterinary Medicine  Vol. 69 (2)  June 2014 Aydogan, A. 100
and PCNA but negative for SMA, vimentin and S100. Tese
positive cells were homogeneously distributed throughout
the tumor area.
Te localization of the tumor mass, the high mitotic
activity, pleomorphism of the cells, infltrative characteris-
tics of the tumor, presence of necrosis and immunohisto-
chemical fndings supported the diagnosis of an ameloblastic
carcinoma.
DISCUSSION
In humans ameloblastic carcinoma is a rare odontogenic tu-
mor in comparison to its benign counterpart (1). In animals
it is a very rare tumor which has been reported to the best of
our knowledge in two dogs and a horse (2, 3, 4).
Te most
common tumor site is the mandible, but cases of maxillary
ameloblastic carcinoma have also been rarely reported in hu-
mans (8, 9, 10, 11).
In animals the maxillary location was
reported in a horse and a dog while a mandibular location
was reported in another dog (2, 3, 4).
In this case the tumor
presented at a maxillary location.
Histologic classifcation of World Health Organization
(WHO) for odontogenic tumors was updated in 2005 and
the terminology of malignant ameloblastoma was changed
to ameloblastic carcinoma (5). Evidence of ameloblastic car-
cinoma was cited as cytologic atypia with or without metas-
tasis. It should not be difcult to distinguish ameloblastic
carcinoma from ameloblastoma on routine microscopic ex-
amination owing to the cytologic atypia in ameloblastic car-
cinoma (12). In addition, ameloblastic carcinoma is destruc-
tive, grows rapidly, and invades neighboring tissues (2,13,14).
In this case, marked cytologic atypia with ameloblastic
diferentiation was seen without evidence of metastasis. Due
to the cytologic atypia, this tumor was diagnosed as amelo-
blastic carcinoma instead of ameloblastoma. In addition the
high mitotic index, local aggressive invasion of tumor and
necrosis in some areas supported the diagnosis of amelo-
blastic carcinoma.
Te most common area of distant metastasis of this tumor
is the lung, but metastasis to the skull and regional lymph
nodes has also been reported (7, 15).
In the present case, the
dog had no evidence of metastasis at the time of diagnosis.
An important feature of malignancy is increased mitotic
index in ameloblastic carcinoma (3, 4, 12).
In a case report,
mitotic fgures were determined 5 to 6 per high magnifca-
tion (4). In this case, 4-6 mitotic fgures were seen per high
power feld and this fnding was evaluated as an important
feature of malignancy.
Te tumor in the present case was tentatively diagnosed
based on the histologic characteristics of malignancy. Te di-
agnosis of AC was confrmed by immunohistochemistry. In
order to determine the origin of the tumor cells, CEA was
used as primary antibody. CEA is an important tumor mark-
er for some carcinomas and demonstrates selective epithe-
lial expression (16).
CEA positivity is used to determine the
aggressiveness of tumors showing squamous diferentiation
Figure 3: Ameloblastic carcinoma. Strong positive immunohisto-
chemical labeling for CEA stain in tumor cells. ABC method, Harris
hematoxylin counterstain, bar = 30 µm.
Figure 4: Ameloblastic carcinoma. Positive immunoreactions of
the tumor cells with pancytokeratin (arrows). ABC method, Harris
hematoxylin counterstain, bar= 30 µm.
Case Reports
Israel Journal of Veterinary Medicine  Vol. 69 (2)  June 2014 101 Ameloblastic Carcinoma in a Dog
including cases of ameloblastoma, odontogenic carcinoma,
and squamous carcinoma (17). In the present case, tumor
cells stained for CEA with strong positivity revealing the
epithelial origin and aggressiveness of the tumor.
Te vimentin negativity is generally use for ameloblastic
origin of tumors but cytokeratin positivity in this tumor is
controversial. While some authors reported positivity, other
authors reported negative staining by cytokeratin (18). In this
case, vimentin negativity revealed its ameloblastic origin and
pancytokeratin positivity revealed its epithelial origin of the
tumor cells. Ki-67 and
PCNA activity of the present case
supported malignancy of the tumor; SMA negativity showed
non-muscle origin of the tumor cells; S100 negativity ruled
out the melanocytic origin of the tumor.
Tis report regarding an rare ameloblastic carcinoma in
the dog is of importance as a contribution for the diferential
diagnosis of tumors in the oral cavity of domestic animals.
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Case Reports

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