Mandibular Rim Excision as Treatment for
Canine Acanthomatous Ameloblastoma
Catrina Turner
Clinical Advisor: Dr. Santiago Peralta
Basic Science Advisor: Dr. John Hermanson
Senior Seminar Paper
Cornell University College of Veterinary Medicine
April 16th, 2014
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ABSTRACT
A 6 -year-old female spayed golden retriever was presented to the Cornell University
Hospital for Animals Oncology Service as a referral for recurrence of an oral mass post
marginal resection. Physical exam revealed a 1.5-cm in diameter, raised mass with
irregular margins on the buccal aspect of the caudal left mandible. Results of fine
needle aspirate of the mass were suggestive of ameloblastic fibroma. Diagnostic
workup included: complete blood count, chemistry panel, urinalysis, 3-view thoracic
radiographs, computed tomographic (CT) scan and intraoral radiographs. The latter two
procedures showed a small amount of bony lysis associated with the mass. Mandibular
rim excision was performed without complication. Histological analysis confirmed
acanthomatous ameloblastoma with clean surgical margins. This paper will use a
case-based format to discuss acanthomatous ameloblastoma, its corresponding
differential diagnosis and the indications and implications of mandibular rim excision as
compared to other types of mandibulectomy.
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INTRODUCTION
Canine Acanthomatous Ameloblastma (CAA) is a benign odontogenic tumor. It is locally
invasive, causing bone lysis and often displacing teeth.1, 2 It is generally accepted that for
malignant and benign but locally invasive oral tumors surgical excision with wide
margins is indicated. Partial to full mandibulectomy has traditionally been utilized in
most of these cases to obtain adequate margins. Another surgical technique known as
mandibular “rim excision” or alveolar ridge resection has been reported as another
potential surgical option for treatment of these masses. This procedure removes the
dorsal portion of the mandible and involved dentition while leaving the ventral cortex
intact.1, 3, 4
CASE STUDY
History
A six-year-old spayed female golden retriever was presented to the Cornell University
Hospital for Animals’ (CUHA) Oncology Service in March 2013 as a referral case from a
general practitioner for an oral mass. In February of 2013 the patients owners noticed a
quarter size oral mass on the buccal aspect of her left mandible. The mass was
marginally excised using electrocautery by their primary care veterinarian in early March
2013. Histological analysis of a biopsy obtained at the time of surgery revealed
acanthomatous ameloblastoma. Approximately two weeks after excision the patient’s
owners noticed a dime-sized mass at the same location, indicating local recurrence. At
that point the dog was referred for further diagnostic workup and possible treatment.
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Physical Exam
On presentation the patient was bright, alert, and responsive. Vital parameters were
within normal limits. The dog weighed 29.7kg and was in good body condition with a
body condition score of 5/9. On physical exam a 1.5-cm in diameter, raised mass with
irregular margins, was seen on the buccal aspect of the caudal left mandible and
moderate medial buttress of her left stifle was palpated. Otherwise her physical exam
was unremarkable.
Differential Diagnosis
Differential diagnosis for oral masses can be grouped as malignant or benign. Malignant
oral masses include melanoma, squamous cell carcinoma, fibrosarcoma,
osteosarcoma, and lymphoma. The most common benign canine oral masses are
acanthomatous ameloblastoma, odontoma, and peripheral odontogenic fibroma.
2, 4, 5
Diagnostics
Initial diagnostic staging included: fine needle aspirate of the mass for histologic
evaluation, complete blood count (CBC), serum chemistry panel, and urinalysis on free
catch urine, and three view thoracic radiographs. Results of the histologic evaluation
suggested an ameloblastic fibroma as there was roughly equal distribution of
odontogenic epithelium and mesenchymal components seen. Results of the urinalysis
and thoracic radiographs were normal. The CBC revealed a mild neutropenia of 2.6
thou/uL (2.7 – 9.4 thou/uL). The differential diagnosis for this neutropenia included:
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decreased production secondary to a myeloproliferative disease or metastatic
neoplasia, drug-induced (trimethoprim-sulfa, phenobarbital etc.), infectious causes
(ehrlichiosis, parvovirus infection), due to increased consumption secondary to
septicemia, hypoadrenocorticism, or due to normal variation. The chemistry panel
showed a mild hyperbilirubinemia of 0.3mg/dL (0.0 to 0.2mg/dL). The differential
diagnosis included prehepatic causes such as hemolytic anemia, intrahepatic causes
(cholestasis, cholangitis/cholangiohepatits), extrahepatic causes (pancreatitis,
cholelithiasis), or due to normal variation. As the patient had no clinical signs or other
supporting blood-work changes associated with the neutropenia and hyperbilirubinemia
these were deemed clinically insignificant and likely due to normal patient variation.
The patient returned 9 days later for aspirates of both mandibular lymph nodes and full
abdominal ultrasound to evaluate for signs of metastasis. A computed tomographic (CT)
scan of the skull, and intraoral radiographs were performed with the patient under
general anesthesia to obtain information for surgical planning. Findings of the
abdominal ultrasound and lymph node aspirates were unremarkable. The CT scan
revealed a small soft tissue mass in the caudal left mandible with minimal associated
bone lysis. The intraoral radiographs confirmed there was a small amount of bone lysis
associated with the mass. During recovery from anesthesia the patient regurgitated a
small amount of fluid; the endotracheal tube was in place and no secondary
complications were seen.
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Treatment
Complete surgical excision was recommended as the best treatment option. Two
surgical techniques were feasible as the mass had only invaded the dorsal portion of
the mandible and did not enter the mandibular canal: segmental mandibulectomy or
mandibular rim excision. Risks and benefits of the procedures were discussed with the
owners and surgical excision using the rim excision technique was elected.
The patient returned 12 days later for surgery. Blood was collected for a CBC and
chemistry panel; results were consistent with previously blood work. The dog was
placed under general anesthesia and the pharynx was packed with gauze to prevent
aspiration of any fluid during the procedure. To reduce the bacterial load in the mouth
before the procedure supra- and subgingival ultrasonic scaling was performed and the
mouth was rinsed with a 0.05% chlorhexidine gluconate rinse. The planned incision site
was marked with a surgical pen approximating 15mm to 20mm margins from the
surgical site, this included the left mandibular premolar 4 through the left mandibular
molar 3. An inferior alveolar nerve block was performed in the left mandibular canal.
The surgical field was created around the mouth with sterile towels. The mucosal
incision was made using a #15 blade. The mucosa on the buccal aspect was further
dissected using a P24G periosteal elevator. Osteotomy was performed using a
piezoelectric oral surgery unit while irrigating with lactated Ringer’s solution. The
osteotomy was successfully performed. The mandibular canal was exposed; the inferior
alveolar artery and nerve were preserved. The left mandibular third molar tooth and root
fragments of the left mandibular fourth premolar were luxated and extracted using 2mm
and 3mm dental luxators and Cryer’s extraction forceps. The irregular bony edges of the
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surgical site were reduced using rongeours. The area was copiously rinsed with sterile
saline and a splash block directly over the inferior alveolar nerve was performed. New
sterile drapes and instruments were used for closure. A one layer closure was
performed in a simple interrupted pattern using 25 poliglecaprone. Postoperative
radiographs were obtained confirming there were no tooth roots remaining.
The patient recovered from anesthesia uneventfully and was administered a dose of
carprofen at 1.1mg/kg subcutaneously during recovery. The dog was maintained on
intravenous fluids and fentanyl at 2µg/kg/hr for pain. Overnight the patient was
administered a 0.5mg/kg dose of dexmedetomidine and a 0.01mg/kg dose of
acepromazine intravenously to decrease anxiety in the hospital. The dog was
discharged the next morning with the following medications: tramadol (2.5mg/kg PO
BID-TID), carprofen (1.6mg/kg PO BID), and amoxicillin/clavulanic acid (17mg/kg PO
BID). The owners were instructed to feed the dog only a soft-food gruel until the recheck
appointment in 2 weeks and not allow rough play with other animals, with any toys or
other hard objects until further notice. At the 2 week recheck the site was healing well,
the sutures were still absorbing and there was minimal redness and swelling.
Histological analysis of the surgical specimen confirmed acanthomatous ameloblastoma
with clean surgical margins; 7mm margins deep and 3-5mm margins laterally were
reported.
Prognosis
The prognosis for patients with complete surgical excision of CAA is considered
excellent. If 1-cm margins are obtained the surgery is often considered curative. One
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study reports 100% survival rate 1 year post wide surgical excision in 25 dogs. 7 Another
study, using the mandibular rim excision technique in 7 dogs with CAA, had a follow-up
time ranging from 3 month to 5 years and there was no evidence of tumor recurrence
seen.1
DISCUSSION
In domestic animals there are only 2 commonly occurring odontogenic tumors; CAA and
peripheral odontogenic fibroma.2, 5 CAA has various names in the literature as it has
changed through the years along with the advancement of research. Historically, CAA
was referred to as acanthomatous epulis which was replaced by peripheral
ameloblastoma and later changed to CAA.4 It is widely accepted that CAA arises from
remnants of the odontogenic epithelium in the future tooth bearing regions of the
gingiva. There are reports, however, that it is possible that CAA arises intraosseously
and breaks out of the bone.4,6 What makes CAA different from other odontogenic tumors
is that it tends to invade the underlying cancellous bone and has a high rate of
recurrence after marginal resection.1,2,4 Clinically, it appears as a gingival mass usually
having an irregular surface. It may be ulcerated and sometimes displaces surrounding
teeth. It has been diagnosed in a wide age range of dogs but the mean age of
occurrence is 7.5 to 10.5 years.2 In the dog there has been no reports of metastasis.1,4
Histologically CAA appears as islands and cords of squamous epithelium
irregularly dispersed through a connective tissue stroma. Many basal cells are
columnar and palisading, some having reverse nuclear polarization and cytoplasmic
vacuolation.2, 4, 6
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Due to its tendency to recur after marginal resection wide surgical excision is usually the
recommended treatment option for CAA though radiation therapy is also sometimes
used. Wide local excision has commonly been accomplished by used of a partial
mandibulectomy or maxillectomy but in recent years the rim excision procedure has
come into play as another potential treatment option.1,4 This procedure has been used in
humans with oral neoplasms since 1987 with comparable success as segmental
mandibulectomy.3 As previously discussed, this procedure removes the dorsal portion of
the segment of the mandible containing the mass and the involved dentition, leaving the
ventral cortex containing the mandibular canal intact. The mandibular canal contains the
inferior alveolar artery, vein, and nerve, along with loose connective tissue, and fat.
Preservation of these structures and the ventral cortex, which is the strongest portion of
the bone does offer several benefits. It is important to point out that any tumor invasion
of the mandibular canal would automatically eliminate the rim excision procedure as a
treatment option.1, 3, 4
The most common postoperative complication seen with the segmental
mandibulectomy is “mandibular drift” where the remaining rostral portion of the mandible
on the affected side drifts medially causing a traumatic malocclusion. Here lies the main
benefit of the rim excision procedure, due to the preservation of the ventral cortex this
mandibular drift does not occur. Another benefit of the rim excision procedure is that
there is a preservation in some jaw stability as the ventral cortex of the mandible is the
strongest portion of the bone.1,3,4 Studies have shown that bony remodeling occurs in
the mandibular defect eventually giving many patients a full return to normal function.
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There is a risk of jaw fracture at the site, especially during the few months after
surgery.3
REFERENCES:
1. Murray, R. L., Aitken, M. L., Gottfried, S. D. The Use of Rim Excision as a Treatment
for Canine Acanthomatous Ameloblastoma. Journal of American Animal Hospital
Association, 2010; 46:91-96
2. Gardner D.G. Canine acanthomatous epulis; The only common spontaneous
ameloblastoma in animals. Oral surgery, Oral medicine, Oral pathology, 1995; 79: 612615
3. Arzi, B., Verstraete, F. Mandibular Rim Excision in Seven Dogs. Veterinary Surgery,
2010; 39: 226-231
4. Verstraete F., Lommer M. Oral and Maxillofacial Surgery in Dogs and Cats. Saunders
publishing. 2012. 403-409, 467-478
5. Gardner D.G., An Orderly Approach to the Study of Odontogenic Tumours in
Animals. Journal of Comparative Pathology, 1992; 107, 427-438
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6. Garder D.G., Baker D.C. The relationship of canine acanthomatous epulis to
ameloblastoma. Journal of Comparative Pathology, 1993; 108:47-55
7. White RA, Gorman NT. Wide local excision of acanthomatous epulides in the dog.
Veterinary Surgery, 1989; 12-14
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