Stephanie Goldschmidt
BVM&S, DAVDC, DEVDC
Dr. Goldschmidt is a passionate educator in the fields of general dentistry and oral oncology and is an assistant tenure track professor in dentistry and oral surgery at the University of California, Davis. Previously, she was a clinical assistant professor at the University of Minnesota. She is currently undergoing fellowship training in both oral medicine and oromaxillofacial surgery. Her subspecialty clinical and research area is oral oncology; specifically, she is focused on improving treatment paradigms with the use of theragnostic agents. Her current projects include using fluorescence imaging to evaluate intraoperative surgical margins and lymph node status in canine oral tumors.
Read Articles Written by Stephanie GoldschmidtThe term “epulis” was first introduced in 1979 to describe common periodontal lesions in dogs. Suggested terms for common gingival lesions with similar histopathologic appearances (background stroma resembling the periodontal ligament) were acanthomatous epulis, fibromatous epulis, and ossifying epulis. However, the term “epulis” is nondescript and does not accurately characterize the biological behavior of those common odontogenic lesions. Specifically, epulis does not account for the fact that all 3 lesions are not truly benign and that they require vastly different treatments.
Updated nomenclature has been implemented and should be adopted to allow for accurate communication between pathologists, clinicians, and clients. This article describes current nomenclature, clinical and radiographic characteristics, diagnosis, and treatment for canine acanthomatous ameloblastoma (previously called acanthomatous epulis), peripheral odontogenic fibroma (POF, previously called fibromatous epulis), and POF-ossifying type (previously called ossifying epulis). Closely related lesions, including other variants of ameloblastoma and focal fibrous hyperplasia, are also briefly described.
Take-Home Points
- The term “epulis” does not convey the actual nature of the lesion or variety of recommended treatments.
- Acanthomatous epulis should be called canine acanthomatous ameloblastoma.
- Fibromatous epulis should be called peripheral odontogenic fibroma.
- Ameloblastoma and peripheral odontogenic fibroma are the most common odontogenic tumors
in dogs. - Odontogenic tumors are rare
in cats. - Ameloblastoma is invasive and requires aggressive treatment with surgery (to achieve a neoplasia-free margin) or radiation therapy.
- Peripheral odontogenic fibroma does not invade bone and can be treated solely by removing the gingival lesion in its entirety. If the client is concerned about potential local recurrence, or the lesion involves a large portion of gingiva, the tooth of origin should also be extracted.
The term “epulis” stems from the Greek words “epi” and “oulon,” which mean “on the gum.” Epulis is broadly defined as any nonspecific gingival overgrowth. The term gained common acceptance in reference to canine odontogenic tumors in 1979.1-3 In that historical publication, the authors proposed that 3 common gingival lesions be broadly categorized as “periodontal epulides” because they all share background stroma that resembles the periodontal ligament (PDL).3 Specifically, those 3 lesions were termed acanthomatous epulis, fibromatous epulis, and ossifying epulis based on distinct histopathologic features. 2-3
Epulis
Using the term “epulis” is now widely discouraged because it is nondescript and suggests that the lesion is benign. Even today, the phrase “it’s just an epulis” is used in daily practice. Yet a subset of such lesions, specifically acanthomatous epulis, can be highly invasive and must be treated. Therefore, odontogenic tumors have been reclassified on the basis of their cell of origin (i.e., epithelial, mesenchymal, or mixed), similar to the odontogenic tumor classification system used in humans. The most up-to-date classification for dogs and cats can be found in the Histological Classification of Tumors of the Alimentary System of Domestic Animals.4
Although proper nomenclature for these lesions has been controversial, the current body of literature supports canine acanthomatous ameloblastoma (CAA) as the preferred term for acanthomatous epulis, peripheral odontogenic fibroma (POF) as the preferred term for fibromatous epulis, and POF-ossifying type as the preferred term for ossifying epulis. This article describes the clinical and radiographic characteristics, diagnostic workup, and treatment for ameloblastoma, including variants other than CAA, as well as POF, including ossifying and nonossifying types.
Ameloblastoma
Ameloblastoma is an epithelial odontogenic tumor that is common in dogs and rare in cats.5-7 It often presents as an erythematous, cauliflower-like gingival mass closely associated with the teeth. However, if the lesion arises from an intraosseous (within the jaw) location, it may appear as a gingival swelling with bony expansion (FIGURE 1).
According to the tumor’s histopathologic features, it may be referred to as a CAA, solid/conventional ameloblastoma, or amyloid-producing ameloblastoma (TABLE 1, FIGURE 2).
CAA, which is by far the most common variant, is diagnosed by its acantholytic pattern on pathologic evaluation. In humans, there are also distinct biologic variants, which carry different prognostic and treatment implications. The presence of biologic variants has been suggested in dogs based on distinct clinical and diagnostic imaging features,8 yet that suggestion remains controversial. Currently, prognosis and treatment for all variants remain the same.
Of note, not all accept or use the term “amyloid-producing ameloblastoma”; rather, some refer to this specific variant as amyloid-producing odontogenic tumor (often called APOT).12,13 This type of tumor is relatively rare, and no large-scale clinicopathological studies have been performed in dogs or cats.
Similar to other odontogenic tumors, ameloblastomas have almost no metastatic potential. However, ameloblastomas can invade locally into the jawbone, especially when a lesion originates from an intraosseous location.10,11 The primary treatment recommendation for ameloblastomas is surgical intervention. Regardless of the variant, 10-mm surgical margins are recommended. As a result, ameloblastomas are most often treated with a maxillectomy or mandibulectomy, which usually results in long-term remission with very rarely reported (< 5%) local recurrence.14
However, if the size of the patient or tumor preclude excision with a 10-mm surgical margin, then more conservative gross margins (5 mm) are probably acceptable. One paper revealed no local recurrence of CAA even after excision with narrow (< 5 mm) and dirty pathologic margins.9 Thus, although removal of all abnormal bone is required to prevent local recurrence, a positive outcome may be achieved with only a very narrow margin of neoplastic-free bone around the tumor.14
Other reported treatment options for ameloblastomas include radiation and intralesional bleomycin. Ameloblastomas are radiosensitive, and long-term control can be achieved with a definitive radiation protocol.15 Protocols vary among institutions, but the most common protocol is 3 weeks of daily radiation therapy. The author does not recommend use of intralesional bleomycin due to the lack of large prospective studies and safety concerns for staff and clients.16
For clients who decline definitive local treatment with surgery or radiation therapy for their pet, a discussion on quality of life and palliative care is recommended. After an ameloblastoma enters the cancellous bone of the jaw, it tends to expand rapidly, causing severe bone pain. Bone pain can be controlled with a palliative radiation protocol, bisphosphonates, and/or systemic analgesics. Clients should be advised as to expectations, and a monitoring plan to evaluate pain control should be established.
In the future, BRAF inhibitors, drugs that can potentially shrink or slow the growth of tumors that have a BRAF mutation, may also be an option for medical management of canine ameloblastomas. Recent oncogenesis literature reveals that 94% of CAAs show a mutation in the HRAS gene–signaling pathway, the same pathway that is most often mutated in human ameloblastomas.17 Mutations in this pathway can activate downstream pathways that promote increased tumor growth. In humans, results of initial drug trials using BRAF inhibitors for nonsurgical cases have been promising.18
Peripheral Odontogenic Fibroma
A POF is a mesenchymal odontogenic tumor, appearing as a smooth, broad-based gingival growth, similar to a focal fibrous hyperplasia (FFH) (FIGURE 3). Histopathologic evaluation is the only way to reliably differentiate a POF from an FFH. (Historically, the term “fibromatous epulis” was often used to clinically describe FFH as well.) FFH is a benign reactive lesion that occurs in response to inflammation or trauma, which distinguishes it from neoplastic-origin POF.5
Most commonly, POFs are in the anterior maxilla (near canine and incisor teeth) of middle-aged dogs at a mean age of 8 years. There is no known sex or breed predilection, although 1 study suggests that risk among boxers is higher.5,19 Overall, POFs are benign because they do not invade bone and do not metastasize. Because of their slow expansile growth, POFs may move teeth out of their normal position. They may also create bone, in which case they are called POF-ossifying type. On radiographs, an ossifying POF shows bone proliferation but no bone lysis (FIGURE 4). Clinically, both POF and POF-ossifying type are treated the same.
Figure 4. Radiographic appearance of an ossifying peripheral odontogenic fibroma at the left mandibular second premolar (306) (white arrows). Note the proliferative bone but lack of bone lysis.
Although POFs do not invade bone, surgical treatment is still recommended because potential pseudopocketing around teeth predisposes the patient to periodontal disease. As the size of the mass increases, the patient may traumatize the lesion. Treatment is focused on removal of the entire lesion. Preventing recurrence does not require leaving a surgical margin of normal tissue. Historically, extracting the tooth of origin has also been recommended because many believe the origin of a POF to be the PDL. Under this belief, tooth extraction is required to effectively remove the entire lesion. However, the true origin of POFs has not been definitively determined. Germinal cells in the gingiva, surface epithelium, alveolar bone, or PDL are speculative origins. In humans, POFs have been noted in edentulous regions, making gingiva the likely source of origin.20 Consequently, a conservative approach with removal of the gingival lesion down to the periosteum, without tooth extraction, is probably appropriate.
However, if removal of a POF causes a large gingival defect, tooth extraction or another advanced periodontal procedure may be necessary (FIGURE 5). As a reminder, to be periodontally sound, all teeth require a minimum of 2 mm of gingiva. Furthermore, if the lesion is not completely removed, there is a risk for local recurrence. A thorough discussion with clients about risks associated with more conservative treatment without tooth extraction is essential. The exact risk for recurrence without tooth extraction has not been quantified; in the author’s experience, it is rare. In addition, POFs have never been reported to malignantly transform (i.e., become a fibrosarcoma or malignant odontogenic tumor) with recurrence of the mass.
Summary
Common odontogenic tumors were historically referred to as an “epulis.” However, this term is nondescript and is now highly discouraged. The most common “epulides” have been relabeled as ameloblastoma and POF. Ameloblastomas are invasive and should be treated with either surgery or radiation. POFs can cause local irritation and pseudopocketing but do not invade bone. Treatment includes removal of the entire gingival lesion; a surgical margin of normal tissue is not required. With treatment, odontogenic tumors carry an excellent prognosis.
References
- Soukup JW, Bell CM. Nomenclature and classification of odontogenic tumors – part I: historical review. J Vet Dent. 2014;31(4):228-232. doi:10.1177/089875641403100402
- Bell CM, Soukup JW. Nomenclature and classification of odontogenic tumors – part II: clarification of specific nomenclature. J Vet Dent. 2014;31(4):234-243. doi:10.1177/089875641403100403
- Dubielzig RR, Goldschmidt MH, Brodey RS. The nomenclature of periodontal epulides in dogs. Vet Path. 1979;16(2):209-214. doi:10.1177/030098587901600206
- Head KW, Cullen JM, Dubielzig RR, et al. Histologic classification of tumors of odontogenic origin of domestic animals. In: Head KW, Cullen JM, Dubielzig RR, et al., eds. Histological Classification of Tumors of the Alimentary System of Domestic Animals. Armed Forces Institute of Pathology; 2003:46-57.
- Fiani N, Verstraete FJM, Kass P, Cox DP. Clinicopathologic characterization of odontogenic tumors and focal fibrous hyperplasia in dogs: 152 cases (1995-2005). JAVMA. 2011;238(4):495-500. doi:10.2460/javma.238.4.495
- Wingo K. Histopathologic diagnoses from biopsies of the oral cavity in 403 dogs and 73 cats. J Vet Dent. 2018;35(1):7-17. doi:10.1177/0898756418759760
- Casazza K, Gracis M, Cavicchioli L, Di Giancamillo M. Feline ameloblastoma: literature review and description of a new case. Veterinaria. 2010;24(5):45–54.
- Tjepkema J, Bell CM, Soukup JW. Presentation, diagnostic imaging, and clinical outcome of conventional ameloblastoma in dogs. J Vet Dent. 2020;37(1):6-13. doi:10.1177/0898756420924847
- Goldschmidt SL, Bell CM, Hetzel S, Soukup J. Clinical characterization of canine acanthomatous ameloblastoma (CAA) in 263 dogs and the influence of postsurgical histopathological margin on local recurrence. J Vet Dent. 2017;34(4):241-247. doi:10.1177/0898756417734312
- Goldschmidt SL, Bell CM, Waller K, Hetzel S, Soukup J. Biological behavior of canine acanthomatous ameloblastoma assessed with computed tomography and histopathology: a comparative study. J Vet Dent. 2020;37(3):126-132. doi:10.1177/0898756420969869
- Amory JT, Reetz JA, Sanchez MD, et al. Computed tomographic characteristics of odontogenic neoplasms in dogs. Vet Radiol Ultrasound. 2014;55(2):147-158. doi:10.1111/vru.12101
- Masoud NS, Iwaide S, Itoh Y, Hisada M, Harada T, Murakami THT. Identification of ameloblastin as an amyloid precursor protein of amyloid-producing ameloblastoma in dogs and cats. Vet Sci. 2023;10(2):166. doi:10.3390/vetsci10020166
- Blackford Winders C, Bell CM, Goldschmidt S. Case report: amyloid-producing odontogenic tumor with pulmonary metastasis in a Spinone Italiano—proof of malignant potential. Front Vet Sci. 2020;7:576376. doi:10.3389/fvets.2020.576376
- Goldschmidt SL. Surgical margins for ameloblastoma in dogs: a review with an emphasis on the future. Front Vet Sci. 2022;9:830258. doi:10.3389/fvets.2022.830258
- Mayer M, Anthony J. Radiation therapy for oral tumors: canine acanthomatous ameloblastoma. Can Vet J. 2007;48(1):99-101.
- Kelly JM, Belding BA, Schaefer AK. Acanthomatous ameloblastoma in dogs treated with intralesional bleomycin. Vet Comp Oncol. 2010;8(2):81-86. doi:10.1111/j.1476-5829.2010.00208.x
- Peralta S, McCleary-Wheeler AL, Duhamel GE, Heikinheimo K, Grenier JK. Ultra-frequent HRAS p.Q61R somatic mutation in canine acanthomatous ameloblastoma reveals pathogenic similarities with human ameloblastoma. Vet Comp Oncol. 2019;17(3):439-445. doi:10.1111/vco.12487
- Fernandes GS, Girardi DM, Bernardes JPG, Fonseca FP, Fregnani ER. Clinical benefit and radiological response with BRAF inhibitor in a patient with recurrent ameloblastoma harboring V600E mutation. BMC Cancer. 2018;18(1):887. doi:10.1186/s12885-018-4802-y
- Ambridge JT, Ambridge EM, Jahns H, McKay JS, Riccardi E, Kelly PA. Clinicopathological features of peripheral odontogenic fibromas in dogs and risk factors for their laboratory diagnosis. J Small Anim Pract. 2023;64(5):343-349. doi:10.1111/jsap.13586
- Ritwik P, Brannon RB. Peripheral odontogenic fibroma: a clinicopathologic study of 151 cases and review of the literature with special emphasis on recurrence. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2010;110(3):357-363. doi:10.1016/j.tripleo.2010.04.018