49

Chapter

Contemporary Treatment of Ameloblastoma

Deepak Kademani, David Michael Junck

A meloblastoma is the most common benign tumor of the jaws,

comprising approximately 10% of odontogenic tumors and 1%
of all cysts and tumors.1 Ameloblastoma was first described by
seventh decade in life and is rarely seen in patients less than 20 years
of age. The radiographic presentation is characterized as a multi-
locular radiolucency with a soap bubble or honeycomb appear-
Malassez in 1885.2 Due to the historically high recurrence rates and ance, although it may appear as a unilocular lesion (Fig. 49-2).
potential for local destruction and locally uncontrollable disease, a Cortical expansion, resorption of adjacent teeth roots, and associa-
thorough understanding of the pathogenesis and clinical behavior of tion with an unerupted tooth are common (Fig. 49-3). The radio-
ameloblastoma is imperative for the oral and maxillofacial surgeon. graphic margins appear irregular and scalloped, which may be seen
The treatment is based largely on the tumor biology, location, and with loss of the cortical bone margins. The histology of the solid/
extent of disease. Surgical management should primarily be focused multicystic ameloblastoma is characterized by the presence of
on a curative intent with the least degree of associated morbidity. benign proliferation of odontogenic epithelium with stellate reticu-
Surgeons have frequently struggled with this issue, due to the lack lum and varying composition of solid or cystic features. There are
of standardized treatment for ameloblastoma and the variety of several variants of solid ameloblastoma from a histologic perspec-
histologic variants described in the literature. This chapter will tive that are important to recognize; however, these have limited
review the pathogenesis, clinical presentation, histology, and treat- impact on treatment decision making presently.
ment for the contemporary management of ameloblastoma.
Follicular
CLINICAL PRESENTATION/ The follicular pattern is the most common subtype of the
solid/multicystic ameloblastoma. The tumor comprises epithelial
PATHOGENESIS islands that resemble an enamel organ in a background of fibrous
connective tissue stroma. The epithelial islands consist of a single
The ameloblastoma arises from odontogenic ectoderm.3 Malassez
outer layer of tall columnar or cuboidal cells with nuclei located on
suggested that it arose from epithelial remnants of the developing
the opposite pole to the basement membrane (reverse polarization)
root sheath.2 However, the causes of ameloblastoma are largely
and resemble ameloblasts, and there is a central zone of cells that
unknown. Ameloblastoma is classically described as a benign
resemble stellate reticulum. Areas of cyst formation are frequently
locally aggressive tumor, but it has the ability for metastasis in
observed; these areas vary from large macroscopic cystic spaces to
rare situations. Presumptive factors causing local inflammation,
microcysts that result from degeneration within epithelial islands.
such as tooth extraction, caries, infection, calculus, developing teeth,
(Fig. 49-4).
trauma, nutritional deficiencies, and viruses, have been investigated;
however, no direct causative correlation exists.4 Ameloblastoma is Plexiform
a slow-growing tumor that may take years before clinical presenta-
Plexiform ameloblastoma consists of larger sheets or long anasto-
tion. The most common presenting symptom is painless swelling of
mosing cords of odontogenic epithelium. Similar to follicular ame-
the jaws (Fig. 49-1). Other symptoms include pain, loosening of
loblastoma, the peripheral epithelial cells comprise ameloblast-like
teeth, malocclusion, and altered sensation. Many tumors are associ-
cells enclosing more loosely organized epithelial cells. Cyst forma-
ated with unerupted teeth, which are often displaced from the tumor.
tion is not common; however, if present, it is more likely due to
Root resorption of adjacent teeth is frequently seen.4 The majority
degeneration of the connective tissue stroma (Fig. 49-5).
of ameloblastomas, approximately 80%, arise in the mandible versus
20% in the maxilla.2 Most mandibular tumors arise in the third molar Granular Cell
region. There are three classic varieties of ameloblastoma: solid/
In some cases, the neoplastic epithelial cells may show transforma-
multicystic, unicystic, and peripheral. The solid/multicystic and uni-
tion to granular cells with eosinophilic granules in the cytoplasm,
cystic types have several histologic variants that can have different
which are consistent with lysosomes. The term granular cell amelo-
biologic behavior. In a review of 3677 cases, the solid/multicystic
blastoma should be reserved for those cases that show extensive
type comprises 92% of ameloblastomas, the unicystic type 6%, and
presence of granular cells. Although initially suggested as a degen-
the peripheral type accounts for 2%.5
erative change in long-standing ameloblastomas, granular cells
have been reported in younger patients and in clinically aggressive
CLASSIFICATION tumors.
SOLID/MULTICYSTIC Basal Cell
The solid/multicystic type is often termed the conventional amelo- The basal cell type contains nests of basaloid cells without central
blastoma. It can be either a solid or multicystic lesion. It occurs stellate reticulum-like cells. This is the least common type of solid/
equally in males and females. Commonly, it occurs in the third to multicystic ameloblastoma (Fig. 49-6).

384
 Contemporary Treatment of Ameloblastoma 385

Acanthomatous and acanthomatous subtypes showed a higher recurrence rate,

The term acanthomatous ameloblastoma is used for those cases that whereas the plexiform and desmoplastic patterns showed a lower
show extensive squamous metaplasia and keratin production occur- rate of recurrence.7 The desmoplastic type is the most recently iden-
ring in the central epithelial islands of the follicular ameloblastoma. tified form, first described by Eversole.8 The incidence ranges from
Caution must be used to not confuse this histologic appearance 0.9% to 12.1% and has a predilection for the anterior maxilla relative
with squamous cell carcinoma or squamous odontogenic tumor to the other types of solid/multicystic ameloblastomas.6 Radiographic
(Fig. 49-7). features are generally atypical of other ameloblastomas, being more
characteristic of fibro-osseous lesions, including an indistinct radio-
Desmoplastic graphic border with radiolucent/radiopaque appearance and periph-
Desmoplastic ameloblastoma is characterized by extensive stromal eral calcifications.9 The maxilla is often more frequently involved
collagenization (desmoplasia) with small islands and cords of tumor with greater than 50% of desmoplastic ameloblastomas.6,9 In a
cells6 (Fig. 49-8). review of 80 cases of desmoplastic ameloblastoma by Beckley et al,
Although there are many histologic subtypes of ameloblastoma, the only reports of recurrence occurred when the tumor was treated
there does not appear to be a significant difference in clinical behav- with enucleation.6 Due to the atypical radiographic appearance of
ior.4 However, Hong et al suggested that the follicular, granular cell, the desmoplastic ameloblastoma, many are treated with enucleation
initially. Upon histologic diagnosis, it is imperative that the tumor
is resected with clear margins, due to the high recurrence rate with
enucleation. There is insufficient evidence in the literature for
varying treatment algorithms based on the histologic subtype; there-
fore, all solid/multicystic ameloblastomas require similar treatment
to limit recurrence.6,9

UNICYSTIC
The clinical presentation of unicystic ameloblastomas varies from
the solid/multicystic types. Age at presentation is typically less
than for other forms of ameloblastoma, typically in the second
and third decade of life. The unicystic ameloblastoma appears

Fig. 49-1 Expansile mass of the left posterior mandible. Mucosal

changes consistent with hyperkeratosis due to the opposing dentition
are seen.

Fig. 49-2 Multilocular radiolucency of the left body of the mandible Fig. 49-3 Axial computed tomography (CT) scan image of recurrent
represents solid/multicystic ameloblastoma. Marked resorption of roots ameloblastoma. Significant expansion and disruption of the confines
of the first molar and first premolar is apparent. of the mandible are seen.

Fig. 49-4 A, Ameloblastoma (follicular variant).

Numerous neoplastic odontogenic islands featur-
ing peripheral columnar cells with reverse polar-
ization surrounding central zone of cells resembling
stellate reticulum. B, Higher magnification that
shows the reverse polarization of the peripheral
columnar cells.

A B
386 Current Therapy in Oral and Maxillofacial Surgery

Fig. 49-5 Ameloblastoma (plexiform variant). Pattern showing anas- Fig. 49-8 Ameloblastoma (desmoplastic variant). Dense connective
tomosing cords of neoplastic odontogenic epithelium. tissue surrounding thin cords and islands of ameloblastoma.

Fig. 49-9 Large unilocular radiolucency of the posterior right man-

Fig. 49-6 Ameloblastoma (basal cell variant). Neoplastic islands and dible with displacement of the third molar to the inferior border and
cords featuring hyperchromatic cells that show peripheral palisading. resorption of adjacent molar roots.

Fig. 49-7 Ameloblastoma (acanthomatous variant). Neoplastic

island of follicular ameloblastoma featuring central squamous
differentiation.

radiographically, similar to the more common non-neoplastic den-

tigerous cyst (Fig. 49-9). Findings such as association with a crown
of an impacted tooth, resorption of tooth roots, and cortical expan- Fig. 49-10 Axial computed tomography (CT) scan image of unicystic
sion may be seen (Fig. 49-10). In 1970, Vickers and Gorlin described ameloblastoma of a 19-year-old male. Association with unerupted
three main histologic subtypes of unicystic ameloblastoma that wisdom tooth that is displaced to the inferior border of the mandible.
have distinct clinical behavior: the luminal, intraluminal, and mural Expansion of both the medial and lateral cortices of the mandible is
types.10 Any form of unicystic ameloblastoma may arise within the seen.
 Contemporary Treatment of Ameloblastoma 387

Fig. 49-11 Unicystic ameloblastoma (luminal type). Cyst lined by

odontogenic epithelium featuring hyperchromatic basal cells with stel-
late reticulum-like overlying epithelial cells.

lining of a dentigerous cyst, therefore changing the diagnosis to a

unicystic ameloblastoma. The lining of a unicystic ameloblastoma
may not be uniform, with portions of merely a dentigerous cystic
lining to extensions of ameloblastoma beyond the confines of the
cyst wall. The unicystic variants can be difficult to histologically
differentiate from one another, unless the entire lesion can be B
evaluated.
Fig. 49-12 A, Unicystic ameloblastoma (intraluminal type). Notice
Luminal the neoplastic mass developing from the cyst lining projecting into the
lumen. B, Higher magnification of the intraluminal component.
With the luminal type of unicystic ameloblastoma, the tumor is
restricted to the luminal surface of the cyst. It contains a dense
fibrous cyst wall that encapsulates the entire cystic tumor compo-
nent, which consists of a columnar or cuboidal basal layer resem-
bling ameloblasts with overlying cells that resemble stellate
reticulum (Fig. 49-11).

Intraluminal
The intraluminal type is histologically similar to the luminal type,
except that one or more extensions or islands of ameloblastoma
project into the lumen. These extensions range from small to large
in filling the cystic space. In certain cases, the luminal tumor exten-
sions resemble the conventional plexiform ameloblastoma. These
are referred to as plexiform unicystic ameloblastoma (Fig. 49-12).

Mural
The mural type of unicystic ameloblastoma is characterized by infil-
tration of the tumor islands into the fibrous connective tissue wall
of the cyst. The ameloblastic extension could resemble both follicu- Fig. 49-13 Unicystic ameloblastoma (mural type). Cystic component
of ameloblastoma is observed along with neoplastic islands that have
lar or plexiform types of solid/multicystic ameloblastomas. The
infiltrated the connective tissue wall.
extent of infiltration into the connective tissue varies significantly,
and therefore it is necessary to obtain several sections through the
specimen so that mural invasion will not be missed (Fig. 49-13). granuloma, or peripheral odontogenic fibroma. There is typically no
radiographic evidence of bony involvement. Some lesions can cause
PERIPHERAL superficial pressure erosion of alveolar bone without invasion,
The peripheral ameloblastoma comprises 2% to 10% of ameloblas- causing the cupping or saucerization defect of the bone. The
tomas.11 The peripheral ameloblastoma is a tumor with the histologic mandible is the predominant site of occurrence, comprising approxi-
characteristics of an intraosseous ameloblastoma, yet it occurs on mately 70% of the lesions.11
the soft tissues covering the tooth-bearing aspect of the jaws.12 It Histologically, peripheral ameloblastomas feature islands of neo-
arises from epithelial rests from the periodontal ligament.11 The plastic epithelial islands within the superficial connective tissue. The
peripheral ameloblastoma is characterized by a painless, firm, exo- epithelial islands can resemble any of the histologic variants of
phytic mass with a smooth surface without ulceration or induration. solid/multicystic ameloblastomas, but the follicular and plexiform
Its location is typically the attached gingiva or alveolar mucosa.11 types are the most common. Almost half of the cases show contact
The clinical presentation may be indistinguishable from pyogenic of the neoplastic islands with the basal cell layer of the overlying
granuloma, peripheral ossifying fibroma, peripheral giant cell surface epithelium.
388 Current Therapy in Oral and Maxillofacial Surgery

TREATMENT 64% recurrence rate of the mural type ameloblastoma when treated
with enucleation and curettage. With marsupialization, the entire
TREATMENT OF THE SOLID/MULTICYSTIC specimen is only evaluated on subsequent enucleation of the residual
lesion. If at this time, histologic diagnosis of a mural type is made,
AMELOBLASTOMA
then it is likely that ameloblastoma within the bone may exist at the
The goals of treatment of ameloblastoma should be with curative periphery of the extent of the original lesion. The recurrences seen
intent, while minimizing functional and esthetic consequences of with enucleation are attributed to incomplete removal of the lining
ablative surgery. Historically, treatment has consisted of surgical or extension of the tumor beyond the confines of the connective
resection with 1-cm tumor-free margins, but a variety of treatments tissue capsule, which may occur with the mural type of unicystic
based on clinical presentation, histologic type, and surgeon prefer- ameloblastoma. Therefore, it can be concluded that recurrence of
ence have been described.13,14 Recurrence of ameloblastoma typi- unicystic ameloblastomas with enucleation is largely due to mural
cally occurs within a decade from the initial presentation; however, invasion and microscopic extension of ameloblastoma into the sur-
there have been reports of tumor recurrence 30 years after initial rounding cancellous bone. Unicystic ameloblastomas of the mural
treatment.15 type should be treated in the same manner as the solid/multicystic
Sehdev et al reported a 90% recurrence rate of the solid/ type. Intraluminal or luminal unicystic ameloblastomas may be
multicystic ameloblastoma of the mandible when treated with curet- adequately treated with enucleation, given that the entire specimen
tage alone.16 Marx et al showed that microscopic tumor cells can is evaluated microscopically and the mural type is excluded.
extend up to 8 mm beyond the radiographic extent of the lesion.12 Treatment of ameloblastoma in the pediatric population may
Therefore, resection with a safety margin of clinically normal- require special considerations regarding the need to obtain local
appearing bone is necessary. A review by Lau et al reported a recur- control and to balance the functional needs of the patient.
rence rate of 3.6% surgical resection; this was corroborated by Hong Ameloblastomas in young patients, typically defined as 19 years old
et al, with a recurrence rate of 4.5% when treated with resection.7,17 and younger, consist of approximately 10% to 15% of reported
Therefore, the standard treatment of solid/multicystic ameloblas- ameloblastomas, most of which are of the unicystic variant.4 In
toma is surgical resection extending a minimum of 1 cm beyond the Western countries, 76.5% were found to be unicystic in children.20
clinical extent of the tumor (Fig. 49-14). Surgical treatment should not vary significantly from the adult
patient with ameloblastoma.
UNICYSTIC AMELOBLASTOMAS
Historically, most unicystic ameloblastomas have been treated more TREATMENT OF THE PERIPHERAL
conservatively, due to a lower recurrence rate with enucleation
AMELOBLASTOMA
compared with the solid/multicystic type. Additional treatments in
conjunction with enucleation may be employed, including curettage, The peripheral ameloblastoma does not typically behave as aggres-
peripheral ostectomy, liquid nitrogen cryotherapy, and Carnoy solu- sively as its central counterpart, although rare malignant variants
tion. Lau et al reported a review of treatment of unicystic amelo- have been described.11 Treatment consists of excision with clinically
blastoma, with a 30.5% recurrence rate with enucleation alone, 25% disease-free margins. If cupping or saucerization of alveolar bone is
recurrence with marsupialization with subsequent enucleation and seen, the associated periosteum and/or bone should be excised.
curettage, and 3.6% recurrence with marginal resection.18Although Recurrence rates of 16% to 19% are reported, and long-term follow-
marsupialization has been described, it is generally not the preferred up is still imperative.11
treatment modality, because it does not allow for examination of the
entire lesion and is associated with a high risk of recurrence.
Rosenstein et al reported a series of 21 unicystic ameloblastomas SURGICAL TREATMENT AIDS AND
treated by enucleation and curettage, with a recurrence rate of 43%, ADJUNCTIVE THERAPIES
55% of which was of the mural type.19 Overall, this resulted in a
An intraoperative specimen radiograph may be used as an additional
tool to ensure uninvolved margins in the resection. If bony margins
appear close, the surgeon is able to remove additional bone imme-
diately.13 Additionally, intraoperative frozen section analysis of
medullary bone may be used to evaluate margins.13

CRYOTHERAPY
Application of liquid nitrogen to the bony margins, as an adjunct to
enucleation and curettage, may provide cellular devitalization within
bone21 up to 2 mm into surrounding bone. Application of liquid
nitrogen cryotherapy may be used in areas where tumor-free margins
are not easily achievable, such as the base of skull, the floor of the
orbit, or at the time of enucleation of a luminal or intraluminal
unicystic ameloblastoma.22

CHEMICAL FIXATION
The use of Carnoy solution has also been shown to be therapeuti-
cally beneficial. Based on the review by Lau et al of treatment of
unicystic ameloblastoma, only 16% of all unicystic ameloblastomas
Fig. 49-14 Specimen of resected recurrent ameloblastoma of the left recur with enucleation and application of Carnoy solution, although
mandible seen in Figure 49-3. (Courtesy Eric Dierks, DMD, MD, FACS.) that review did not differentiate the subtypes of unicystic
 Contemporary Treatment of Ameloblastoma 389

ameloblastomas.18 Use of Carnoy solution may be more effective has been efficacious for ameloblastoma. A screening examination is
than enucleation alone for luminal and intraluminal types of uni- advised for patients diagnosed with ameloblastoma and a higher
cystic ameloblastomas. index of suspicion for those with recurrent ameloblastoma and those
who develop clinical symptoms of pulmonary disease.28
Like ameloblastoma, ameloblastic carcinoma appears most
TREATMENT CONSIDERATIONS BASED frequently in the posterior mandible. Likewise, it presents most
ON ANATOMIC LOCATION commonly as swelling. Pain, rapid growth, and trismus may also
be found at presentation. The average age of presentation is appro-
The location of the occurrence of ameloblastoma varies greatly, as ximately 30 years, with a reported range of 15 to 84 years.
does the treatment and clinical behavior. Approximately 80% of The majority of ameloblastic carcinomas were of the follicular and
ameloblastomas occur in the mandible, compared with 20% in the plexiform pattern.25 In a review of 14 ameloblastic carcinomas by
maxilla.2 Of those that occur in the maxilla, most are in the posterior Hall et al, patients treated with surgical resection early in the course
maxilla. Only 2% of ameloblastomas occur in the anterior maxilla; of treatment had an improved chance for cure and the fewest number
in this location, the desmoplastic variant is the most common.6 Due of recurrences. In that series, 21.4% of the patients died of the
to the proximity of maxillary ameloblastomas to the orbit, paranasal disease.25
sinuses, nasal cavity, and skull base, the locoregional extent of the
tumor can be more difficult to control compared with the mandible.
Due to the thin cortical bone of the maxilla, compared with the
FOLLOW-UP CARE
mandible, the tumor has the ability to penetrate the surrounding bone Due to the slow-growing nature of the ameloblastoma, many recur-
with earlier soft tissue extension. The maxillary ameloblastoma is rences occur after greater than 5 years, and as long as 30 years after
more difficult to visualize clinically, and, on plain radiographs, this the initial diagnosis. Tumor surveillance in asymptomatic patients
may prohibit early detection.17 When planning treatment of amelo- should consist of clinical exams and orthopantomograms every 6
blastoma, imaging is imperative in order to view the tumor extension months for 1 year, then once per year for a minimum of 10 years.
in three dimensions and to evaluate for cortical perforation and Routine use of computed tomography (CT) scans for monitoring of
extraosseous extension of tumor. maxillary ameloblastomas is reasonable, due to anatomic overlap of
structures in this region. Due to the potential for late recurrence with
all types of ameloblastoma and the importance of long-term and
SPECIAL CONSIDERATIONS FOR vigorous follow-up, patients unable or unwilling to follow such
TREATMENT OF THE RECURRENT recommendations may be candidates for initial radical resection,
regardless of histologic variant of ameloblastoma, to minimize the
AMELOBLASTOMA risk of recurrence.
Many studies note recurrences within 5 years 50% of the time and
the remainder within 10 years, but recurrence has been seen up to
30 years after the original treatment.15 As noted, inadequate initial
CONCLUSION
surgical treatment of ameloblastoma yields a high chance of local Ameloblastoma is a benign, locally aggressive tumor with several
recurrence. Muller et al reported on 84 patients who underwent a different histologic types. Treatment is based on the histology and
total of 186 procedures for tumor clearance.23 Many patients required clinical behavior and should be with curative intent. Debate contin-
multiple operations, more extensive surgery, greater difficulty in ues in the literature regarding management of ameloblastoma. In
reconstruction, increased morbidity, and potential for mortality. general, solid/multicystic and mural unicystic variants of ameloblas-
Also, possibly there was increased chance of malignant change and toma or any recurrent tumors should be treated with surgical resec-
metastasis.24 A minimum follow-up period of 10 years is recom- tion when feasible. Other unicystic variants of ameloblastoma can
mended, especially after treatment of a recurrent ameloblastoma. be considered for conservative management, such as enucleation
Only 80% of recurrent ameloblastomas are cured with resection.16 and curettage with adjunctive therapies as first-line therapy, with the
caveat that final treatment should be based on the complete histo-
logic examination of the entire lesion. Resection must be considered
CONSIDERATIONS OF MALIGNANCY a conservative treatment approach for many patients with amelo-
There are two forms of malignant ameloblastoma. The term malig- blastoma due to the greater likelihood for cure from the initial
nant ameloblastoma refers to a lesion with histologic similarity to management and avoidance of often more complicated treatment
conventional ameloblastoma, but it has metastasized. The amelo- necessary for management of recurrent disease.
blastic carcinoma is a tumor that shows some features of ameloblas-
toma, but it has histologic features of malignancy. The ameloblastic
carcinoma is considered a more aggressive lesion than conventional
ameloblastoma.25 PEARLS AND PITFALLS
Malignant ameloblastoma is a lesion with the histologic appear-
ance of a benign ameloblastoma that has metastasized. Metastasis Initial surgical treatment of ameloblastoma gives the best chance
is likely to be to the lung or regional lymph nodes primarily, along for cure.
with reports of metastasis to liver, brain, bone, kidneys, and the Luminal and intraluminal variants of unicystic ameloblastoma
gastrointestinal system.26 The reported rate of metastasis of amelo- may be amenable to enucleation and curettage with or without
blastoma is approximately 2%. The likelihood of metastasis is adjunctive therapies.
increased with large initial tumors, delay in treatment, recurrence, Solid/multicystic and the mural type unicystic ameloblastoma
require resection with a minimum of 1-cm margins.
and primary mandibular tumors.26 The treatment of malignant
All patients with ameloblastoma should be followed for a
ameloblastoma is primarily surgical, because ameloblastoma is rela- minimum of 10 years, due to the potential for late recurrence.
tively resistant to irradiation.27 Currently, no chemotherapeutic agent
390 Current Therapy in Oral and Maxillofacial Surgery

REFERENCES
1. Vayvada H, et al: Surgical management of 9. Yoshimura Y, Saito H: Desmoplastic variant treatment of 21 cases. J Oral Maxillofac
ameloblastoma in the mandible: segmental of ameloblastoma: report of a case and review Surg 59(11):1311-1316, 2001; discussion
mandibulectomy and immediate recon- of the literature. J Oral Maxillofac Surg 1316-1318.
struction with free fibula or deep circumflex 48(11):1231-1235, 1990. 20. Ord RA, Blanchard RH Jr, Nikitakis NG,
iliac artery flap (evaluation of the long- 10. Vickers RA, Gorlin RJ: Ameloblastoma: Sauk JJ: Ameloblastoma in children. J Oral
term esthetic and functional results). Delineation of early histopathologic features Maxillofac Surg 60(7):762-770, 2002; discus-
J Oral Maxillofac Surg 64(10):1532-1539, of neoplasia, Cancer 26(3):699-710, 1970. sion 770-771.
2006. 11. Philipsen HP, Reichart PA, Nikai H, et al: 21. Sampson DE, Pogrel MA: Management of
2. Gorlin RJ: The pathology of ameloblastomas Peripheral ameloblastoma: biological profile mandibular ameloblastoma: the clinical basis
and its relationship to treatment. Trans Int based on 160 cases from the literature. Oral for a treatment algorithm. J Oral Maxillofac
Conf Oral Surg 230-553, 1970. Oncol 37(1):17-27, 2001. Surg 57(9):1074-1077, 1999; discussion
3. Zemann W, Feichtinger M, Kowatsch E, 12. Feinberg SE, Steinberg B: Surgical manage- 1078-1079.
Krcher H: Extensive ameloblastoma of the ment of ameloblastoma. Current status of 22. Pogrel MA: The use of liquid nitrogen cryo-
jaws: surgical management and immediate the literature. Oral Surg Oral Med Oral therapy in the management of locally aggres-
reconstruction using microvascular flaps. Pathol Oral Radiol Endod 81(4):383-388, sive bone lesions. J Oral Maxillofac Surg
Oral Surg Oral Med Oral Pathol Oral Radiol 1996. 51(3):269-273, 1993; discussion 274.
Endod 103(2):190-196, 2007. 13. Carlson ER, Marx RE: The ameloblastoma: 23. Muller H, Slootweg PJ: The ameloblastoma,
4. Kahn MA: Ameloblastoma in young persons: primary, curative surgical management. J the controversial approach to therapy. J
a clinicopathologic analysis and etiologic Oral Maxillofac Surg 64(3):484-494, 2006. Maxillofac Surg 13(2):79-84, 1985.
investigation. Oral Surg Oral Med Oral 14. Pogrel MA, Montes DM: Is there a role for 24. Adekeye EO, Lavery KM: Recurrent amelo-
Pathol 67(6):706-715, 1989. enucleation in the management of ameloblas- blastoma of the maxillo-facial region. Clinical
5. Reichart PA, Philipsen HP, Sonner S: toma? Int J Oral Maxillofac Surg 38(8):807- features and treatment. J Maxillofac Surg
Ameloblastoma: biological profile of 3677 812, 2009. 14(3):153-157, 1986.
cases. Eur J Cancer B Oral Oncol 31B(2):86- 15. Hayward JR: Recurrent ameloblastoma 30 25. Hall JM, Weathers DR, Unni KK: Ameloblastic
99, 1995. years after surgical treatment. J Oral Surg carcinoma: an analysis of 14 cases. Oral Surg
6. Beckley ML, Farhood V, Helfend LK, 31(5):368-370, 1973. Oral Med Oral Pathol Oral Radiol Endod
Alijanian A: Desmoplastic ameloblastoma of 16. Sehdev MK, Huvos AG, Strong EW, et al: 103(6):799-807, 2007.
the mandible: a case report and review of the Proceedings: ameloblastoma of maxilla and 26. Cardoso A, Lazow SK, Solomon MP, et al:
literature. J Oral Maxillofac Surg 60(2):194- mandible. Cancer 33(2):324-333, 1974. Metastatic ameloblastoma to the cervical
198, 2002. 17. Williams TP: Management of ameloblastoma: lymph nodes: a case report and review of lit-
7. Hong J, Yun PY, Chung IH, et al: Long-term a changing perspective. J Oral Maxillofac erature. J Oral Maxillofac Surg 67(6):1163-
follow up on recurrence of 305 ameloblas- Surg 51(10):1064-1070, 1993. 1166, 2009.
toma cases. Int J Oral Maxillofac Surg 18. Lau SL, Samman N: Recurrence related to 27. Goldwyn R, Constable J, Murray JE:
36(4):283-288, 2007. treatment modalities of unicystic amelobl- Ameloblastoma of the jaw. A clinical study. N
8. Eversole LR, Leider AS, Strub D: astoma: a systematic review. Int J Oral Engl J Med 269:126-129, 1963.
Radiographic characteristics of cystogenic Maxillofac Surg 35(8):681-690, 2006. 28. Witterick IJ, Parikh S, Mancer K, Gullane PJ:
ameloblastoma. Oral Surg Oral Med Oral 19. Rosenstein T, Pogrel MA, Smith RA, Regezi Malignant ameloblastoma. Am J Otolaryngol
Pathol 57(5):572-577, 1984. JA: Cystic ameloblastomabehavior and 17(2):122-126, 1996.