Oral Maxillofacial Surg Clin N Am 16 (2004) 399 – 408
Peripheral odontogenic tumors
Alice E. Curran, DMD, MS
University of North Carolina School of Dentistry, Department of Diagnostic Sciences,
Division of Oral and Maxillofacial Pathology, CB# 7450, Chapel Hill, NC 27599, USA
Peripheral odontogenic tumors, also referred to as
extraosseous or soft tissue odontogenic tumors, mani-
fest the histopathologic characteristics of their central
or intraosseous counterparts but arise in the soft
tissues of the maxilla or mandible, usually in gingival
tooth-bearing areas. Peripheral odontogenic lesions
are considered rare within the odontogenic tumors
classification. Clinical differential diagnosis of these
lesions infrequently includes a peripheral odontogenic
tumor, but usually favors gingival fibroma, pyogenic
granuloma, peripheral giant cell granuloma, or other
reactive hyperplasia. For the most part, it is not until
the tumor has been excised and examined histologi-
cally that the true nature of the lesion is known.
Many odontogenic tumors have been reported in
the soft tissues, including ameloblastoma, adeno-
matoid odontogenic tumor, calcifying epithelial
odontogenic tumor, odontogenic fibroma, squamous
odontogenic tumor, odontogenic myxoma odontoma,
and epithelial odontogenic ghost cell tumor.
The most commonly reported peripheral odonto-
genic tumor is the ameloblastoma. The paucity of
reports in the literature on tumors, other than periph-
eral ameloblastoma, makes it difficult to state with
certainty the biologic behavior of these lesions; there-
fore, one only can suggest the most common clini-
cal features.
The following is a summary of the most pertinent
information on the clinical and histopathologic fea-
tures of peripheral odontogenic tumors.
E-mail address: alice_curran@dentistry.unc.edu
1042-3699/04/$ – see front matter D 2004 Elsevier Inc. All rights reserved.
doi:10.1016/j.coms.2004.03.008
Peripheral ameloblastoma
The first report of peripheral ameloblastoma ap-
peared in 1949 [1]; the first completely documented
case was reported by Stanley and Krough in 1959 [2].
Peripheral ameloblastoma is defined as an odonto-
genic tumor with histologic characteristics of an intra-
osseous ameloblastoma but that occurs solely in the
soft tissues that cover the tooth-bearing areas of the
jaws [3]. This definition excludes any intraosseous
ameloblastoma that perforates the cortex to appear
extraosseous [4]. Sixty-seven percent of peripheral
odontogenic tumors are ameloblastomas and 2% to
10% of all ameloblastomas are peripheral [5 – 9].
Peripheral ameloblastomas are diagnosed most com-
monly in the fifth and sixth decades [5], with an age
range of 3 to 92 years [10,11], and a mean age of
52 years [12]. This is an older mean age than for
intraosseous ameloblastomas that have a mean age of
37 years [13]. This also is a much older mean age than
for other peripheral odontogenic tumors, in general
[12]. Peripheral ameloblastoma is more common in
men than in women [5,12]. The most common site is
the lingual aspect of the gingiva; the most common
location is the mandibular canine and premolar areas,
which is the most common sites for peripheral odon-
togenic tumors, in general [14]. When they occur on
the alveolar ridge, the patient may complain of an ill-
fitting prosthesis [10]. They have been reported in the
maxillary tuberosity [5], buccal mucosa [15], and
floor of the mouth [16]; however, some investigators
consider the latter two soft-tissue lesions in nontooth-
bearing areas to be basal cell adenoma, a benign minor
salivary gland neoplasm with columnar cellular fea-
tures that resemble ameloblastoma [17].
The clinical presentation of peripheral ameloblas-
tomas can vary; generally, they are asymptomatic,
400 A.E. Curran / Oral Maxillofacial Surg Clin N Am 16 (2004) 399–408
Fig. 1. Peripheral ameloblastoma presenting as a smooth-
surfaced nodule of the lingual gingiva. (Courtesy of Arthur
Gonty, DDS, Lexington, KY.)
exophytic, mucosal-colored, smooth or granular-
surfaced, and usually range in size from 0.5 cm to
4.5 cm. (Fig. 1) [12]. Occasionally, the surface ap-
pears verrucous or papillary (Fig. 2), which suggests
papilloma or condyloma acuminatum in the differen-
tial diagnosis [5,18]. Kahn [19] found expression of
human papillomavirus (HPV)-16 and -18 in a periph-
eral ameloblastoma; this suggested that HPV could
be a cofactor or initiator in peripheral ameloblas-
toma development.
Because of their location, peripheral ameloblasto-
mas may be exposed to local trauma and display
ulceration or keratosis. They generally occur singly.
Multicentric lesions were reported by Hernandez et al
[20] and Balfour et al [21], who stated that after se-
rial sections, no continuity between lesions could be
identified. There is no radiographic or surgical evi-
dence of bony involvement, although ‘‘cupping’’ or
‘‘saucerization’’ of the underlying bone may be seen.
This bony alteration is considered to be the result of
pressure resorption rather than neoplastic invasion
Fig. 2. Peripheral ameloblastoma presenting as a verrucous/
papillary mass on the gingiva of a 54-year-old woman.
(Courtesy of T. Morton, Jr, DDS, MSD, Seattle, WA.)
Fig. 3. Peripheral ameloblastoma with follicular pattern that
demonstrates a band of connective tissue between the tumor
and the surface; no evidence of surface involvement (2).
[12,22]. Cupping is seen in other peripheral non-
odontogenic oral lesions, such as peripheral giant cell
granuloma [3].
Peripheral ameloblastomas most likely arise from
the rests of Serres which are fragmentations of the
dental lamina that occur during the morphodifferen-
tiation stage of tooth development. Alternately, the
tumor may arise from the surface epithelium that has
the potential for production of odontogenic epithe-
lium [23].
Peripheral ameloblastomas demonstrate all of the
histopathologic patterns that are seen in their intra-
osseous counterpart (Figs. 3 and 4), although the
acanthomatous pattern that displays occasional calci-
fication or keratinization is seen more frequently in
peripheral ameloblastomas [5]. Occasionally, there is
a lymphoplasmacytic infiltrate that generally is not
seen in intraosseous lesions [3]. This may be attri-
buted to local trauma. Criteria for diagnosis as a
Fig. 4. Details of the peripheral ameloblastoma seen in
Fig. 3 (10).
 A.E. Curran / Oral Maxillofacial Surg Clin N Am 16 (2004) 399–408
peripheral ameloblastoma include that the relation-
ship of the tumor to the surface takes one of three
forms: focal continuity, suggesting development at
that site; numerous distinct areas of continuity along
a considerable length of the tumor; and a band of
connective tissue between the tumor and the surface
that suggests development from the rests of Serres
[3]. The lesion is seen in the upper layers of the
lamina propria with no extension to periosteum [21].
A subject of debate is whether the lesions that
show connection with the overlying epithelium are
demonstrating their point of origin or the ‘‘collision
tumor’’ phenomenon. The theory that peripheral
ameloblastomas arise from the surface epithelium is
supported by studies that show oral epithelium has
the potential to differentiate into odontogenic epithe-
lium [23]. Alternately, the notion that this may
represent a ‘‘collision’’ phenomenon is supported
by the fact that odontogenic epithelium, in the form
of the reduced enamel epithelium, routinely fuses with
the overlying epithelium during tooth eruption [24].
Peripheral ameloblastomas that arise from the rests of
Serres simply may have the ability to fuse with
mucosal epithelial cells when they come in contact.
Additional support for this theory comes from reports
of central ameloblastomas that erode alveolar bone
and merge with the oral mucosa [25]. Tajima et al
[26] demonstrated that the cytokeratin profile of
peripheral ameloblastoma was consistent with that
of a tooth germ and different from that of surface
epithelium; this supports the collision tumor hypothe-
sis for surface epithelial involvement [26].
The risk of malignant transformation in peripheral
ameloblastoma may be higher than for intraosseous
ameloblastoma because of the occurrence at an older
age, in addition to the chance for exposure to more
local carcinogens [14]. Malignant change of periph-
eral ameloblastomas (peripheral ameloblastic carci-
noma) is rare; only three cases have been reported
[14,27,28]. Additional cases that show epithelial dys-
plasia have been reported [22,26,29]. Bone resorption,
recurrence, and infiltration of tumor cells into the
underlying bone were noted in these cases. Baden
et al [30] reported malignant transformation to squa-
mous cell carcinoma with progression to anaplastic
carcinoma after irradiation [30]. The histopathologic
criteria for peripheral ameloblastic carcinoma are the
same as intraosseous: infiltrating growth, cytologic
atypia, high mitotic index, and perineural infiltra-
tion [27].
Peripheral ameloblastomas may resemble basal
cell carcinoma; some cases have been reported as
basal cell carcinoma of the oral cavity [15]. Occur-
rence of basal cell carcinoma on mucous membranes
401
is not accepted by some investigators [31]; thus, a
debate over whether these represent two distinct
entities or are the same lesion has appeared in the
literature [32]. Some cases of intraoral basal cell
carcinoma are considered to represent a peripheral
ameloblastoma, if found in tooth-bearing areas. Gard-
ner [3] considered peripheral ameloblastoma and
intraoral basal cell carcinoma to be the same entity.
Both arise from surface epithelium and no consistent
histopathologic features exist by which peripheral
ameloblastoma and basal cell carcinoma can be
differentiated when the classic features of ameloblas-
toma are not seen. Although both neoplasms arise
from the same cells, the innate cellular potential for
bone invasion in peripheral ameloblastoma is absent
[33]. Also, recurrences are confined to soft tissue and
no metastases have been reported [34].
It is critical for clinicians to understand that pe-
ripheral ameloblastoma manifests a different biologic
behavior than its intraosseous counterpart. Gardner
[3] suggested that the term ‘‘peripheral ameloblas-
toma’’ is ‘‘dangerous’’ because of the risk of unnec-
essary aggressive treatment if it is misunderstood
by the clinician. Peripheral ameloblastoma does not
show the invasive and destructive behavior that is
such a problem in intraosseous ameloblastoma. The
chances for recurrence of peripheral ameloblastoma
are considerably less than that of their intraosseous
counterparts, about 19% [5,12] compared with 50%
to 90% for the intraosseous counterpart, depending
on the method of treatment [33]. Gardner [4] sug-
gested that peripheral ameloblastoma has a good
prognosis because it is readily observable and, there-
fore, is treated earlier; the dense fibrous connective
tissue of the gingiva is more resistant to spread than
the delicate connective tissue of intertrabecular
spaces; and bone is an efficient barrier to invasion.
The current treatment of choice for peripheral
ameloblastoma is conservative supraperiosteal exci-
sion with adequate margins [12]. Recurrence at the
site of excision is believed to be the result of in-
complete excision [18]. Long-term clinical follow-up
is advised because of the paucity of reported cases
with long-term follow-up [19].
Peripheral odontogenic fibroma
Peripheral odontogenic fibroma is considered to
be the gingival counterpart of the central odontogenic
fibroma. The name of this neoplasm can be confused
with peripheral ossifying fibroma, a reactive lesion
that is believed to arise from periosteum that pro-
duces benign reactive osteoid and woven bone in a
402 A.E. Curran / Oral Maxillofacial Surg Clin N Am 16 (2004) 399–408
Fig. 5. Peripheral odontogenic fibroma in a 46-year-old
man with recurrent gingival lesion. This is the third
recurrence in 3 years. (Courtesy of C. Fowler, Col, USAF,
DC, Lackland AFB, TX.)
pyogenic granuloma-like proliferation of granulation
tissue, and, therefore, bears no relationship to the
ossifying fibroma. Peripheral odontogenic fibroma is
rare and accounts for 1.2% of all odontogenic cysts
and tumors [35,36].
Peripheral odontogenic fibroma typically presents
as a gingival or alveolar ridge tumor (Fig. 5) that is
characterized by an unencapsulated proliferation of
cellular fibrous or fibromyxomatous connective tissue
(Fig. 6) that exhibits variable amounts of odontogenic
epithelium (Fig. 7) and sometimes foci of calcifica-
tion in the form of dentinoid, cementicles, or bone.
Peripheral odontogenic fibroma is considered to be
ectomesenchymal in origin because the epithelium is
thought to be nonactive although it is required for
Fig. 6. Peripheral odontogenic fibroma seen in Fig. 5 show-
ing the lesion ‘‘dropping down’’ from the surface epithelium.
Fig. 7. Details of Fig. 6. Islands of odontogenic epithelium
within a cellular fibrous stroma.
diagnosis. Some investigators believe that this feature
should allow it to be considered a mixed lesion [36].
Peripheral odontogenic fibroma is considered
rare with unknown potential for recurrence. Little
follow-up is available so recurrence cannot be evalu-
ated, although a recurrence rate of 39% with a 3- to
4-year interval for recurrence was reported [36,37].
Peripheral calcifying epithelial odontogenic tumor
Calcifying epithelial odontogenic tumor (CEOT)
represents less than 1% of all odontogenic tumors. Of
all reported CEOTs, peripheral tumors account for
5% to 6% [38,39].
Peripheral CEOT generally presents as a painless,
mucosal-colored to red swelling of about 6 months’
duration [40] that may produce saucerization of the
underlying bone [41]. The age range at the time of
diagnosis was reported as 12 to 48 years [42,43].
Most reported cases of peripheral CEOT are in the
anterior segments where they demonstrate a predi-
lection for incisor/premolar area, rather than the
posterior [44], which is the most common location
for intraosseous CEOT [41]. Generally, CEOTs are
asymptomatic but may produce pain, as in a reported
case with severe pain and swelling of the mandibular
third molar area that was diagnosed as periodontal
inflammation that did not respond to therapy [45].
Central CEOT is believed to be derived from the
stratum intermedium layer of the enamel organ of
the tooth germ, whereas the extraosseous CEOT is be-
lieved to arise from the dental lamina or basal layer
of oral epithelium [44]. This never has been dem-
onstrated. The peripheral CEOT shares the histo-
pathologic features of the central CEOT, including
significant cellular pleomorphism, hyperchromatism,
and rare to absent mitosis. It is composed of sheets
 A.E. Curran / Oral Maxillofacial Surg Clin N Am 16 (2004) 399–408
of polyhedral epithelial cells, amyloid-like substance
(secretion product of epithelial cells), and calcified con-
centric Liesegang rings [46]. The clear cell variant also
has been reported in the peripheral neoplasms [43].
Peripheral CEOT has a recurrence rate of up to
22% as compared with the 14% recurrence rate of
intraosseous CEOT [47]. One report described a
peripheral CEOT that was preceded by an intraos-
seous lesion. This lesion recurred as the clear-cell
variant of CEOT [48].
Peripheral adenomatoid odontogenic tumor
Adenomatoid odontogenic tumor (AOT) accounts
for 3.1% to 8.6% of odontogenic tumors [11,49]. The
central AOT accounts for 97.2% of all AOTs; periph-
eral lesions account for the remainder [50]. Yazdi and
Nowparast [51] suggested that the peripheral variant
is rarer because some lesions undergo atrophy after
eruption of the tooth. This is unlikely because in most
cases, the appearance of the lesion generally is
several years posteruption.
Peripheral AOT presents as an epulislike fibrous
swelling that can mimic periodontal disease if bone
erosion occurs. Peripheral AOT follows the same
trend as central AOT in terms of location and gen-
der [52]. The mean age for peripheral AOT is 12 to
14 years. The peripheral AOT rarely has the same
snowflake-like radiographic changes that are seen in
the intraosseous form [53]. Extraosseous and intra-
osseous AOT are more common in the maxilla where
deciduous dentition was found [53]. In most cases, it
is difficult to determine if peripheral AOTs repre-
sent superficial intraosseous AOTs that expanded
through cortex into gingival tissue. It was suggested
that peripheral lesions represent central lesions that
‘‘erupted’’ with the tooth [52], to complete their de-
velopment in the gingiva. Nevertheless, it is believed
that they all have a common origin, regardless of
location, because of consistent histopathologic find-
ings. Whether they arise from rests of Serres or from
the successional lamina that is located in the proximal
portion of the gubernacular cord, which connects the
bony crypts of the developing teeth with the lamina
propria of the gingiva, has yet to be determined [53].
There is little variation in the histopathology of a
peripheral AOT compared with an intraosseous
AOT—proliferation of odontogenic epithelium with
variable-sized ductlike structures and solid nodules of
cuboidal or columnar cells that are encapsulated by
thin connective tissue, with a vascular stroma and
diffuse calcifications [54]—although there is some
evidence to suggest that extraosseous lesions are
403
unencapsulated more frequently [55]. There is no
evidence to suggest that these peripheral neoplasms
arise from surface epithelium. Generally, at surgery,
they are not reported to be adherent to the overlying
mucosa [54].
Too few peripheral AOT cases have been reported
to draw definite conclusions on biologic behavior.
Peripheral calcifying odontogenic cyst and
epithelial odontogenic ghost cell tumor
The proper classification of the calcifying odonto-
genic cyst (COC) as a cyst versus neoplasm has been
debated since its establishment as an entity by Gorlin
et al [56]. Praetorius and colleagues [57] concluded
that COCs have a cystic and a neoplastic form. They
proposed the term ‘‘dentinogenic ghost cell tumor’’
for the neoplastic entity. Ellis and Shmookler [58]
claimed that because the ghost cells are the most
distinctive histologic feature, the term ‘‘epithelial
odontogenic ghost cell tumor’’ is preferred.
Although the calcifying epithelial cyst is not a
neoplasm, it occurs peripherally with enough fre-
quency to warrant discussion here. COC makes up
less than 1% of jaw cysts; one fourth to one third of
them occur in an extraosseous location [59]. Gener-
ally, they present as hyperplastic gingival tissue that
enlarges slowly over an extended period of up to
3 years [60]. The neoplastic variant is seen in older
patients when compared with the cystic type [58].
The mean age for intraosseous COC is consistently
reported as 25 years, whereas the mean age for
extraosseous COC is 53.8 years with bimodal ranges
of 10 to 19 years and 50 to 59 years [61]. Intra-
osseous and extraosseous COCs may have different
tissues of origin, which could account for the age
difference; this has not been determined [62]. The
stimulus for either is unknown, however, gingival
irritation may stimulate peripheral growth.
As with intraosseous COC, peripheral COC dem-
onstrates no gender predilection or no jaw predilec-
tion; the location of the most lesions is anterior to the
first molar. The duration at diagnosis ranges from
8 months to 15 years. The ‘‘cupped out’’ radiographic
feature that is seen in other peripheral odontogenic
lesions can be seen and tends to be most pronounced
in lesions that have existed for longer periods of time.
The mixed radiolucent/radiopaque features that gen-
erally are seen in the central lesions also are present
in the peripheral lesions. The mean size is 1 cm but
they have been reported to be up to 4 cm [61].
There is no difference between peripheral and
intraosseous histopathologic features. They include:
404 A.E. Curran / Oral Maxillofacial Surg Clin N Am 16 (2004) 399–408
Fig. 8. Peripheral odontoma (2). (Courtesy of D. White,
DDS, MSD, Lexington, KY.)
thickened cystic epithelium, hyperchromatic basal cell
layer, eosinophilic ghost cells, stellate reticulum-like
epithelium, and dystrophic calcifications [56].
The solid form of COC, the epithelial odontogenic
ghost cell tumor (EOGCT), also occurs in the soft
tissues. The proportion of the solid neoplastic form is
higher among the peripheral form than among the
central lesions; generally, this feature is not seen when
evaluating other central versus peripheral odontogenic
tumors [61]. Peripheral EOGCT occurs in gingival
and alveolar mucosa, which engenders the clinical
differential diagnosis of fibroma, gingival cyst, muco-
cele, and peripheral giant cell granuloma. Generally,
they are described as asymptomatic, circumscribed,
and smooth-surfaced; one was reported as papillary
[63]. The mean age at diagnosis is 48, which is
younger than the age at diagnosis for peripheral
ameloblastoma. The age range has a bimodal distri-
bution with peaks in the second decade and the sixth
to eighth decades; the frequency is greater in the sixth
to eighth decades [61]. Displacement of teeth is rare.
Saucerization of the bone at surgery has been noted.
Both arches are equally affected; most tumors occur in
the incisor – premolar area [61].
The theory of histogenesis accounts for two
sources of epithelium for this tumor. Generally, the
tumor is separate from overlying epithelium which
suggests the rests of Serres as a source; however,
several cases showed connection with surface epithe-
lium. Praetorius et al [57] also suggested that the
reduced enamel epithelium may be a source; this is a
possible explanation for the development around
crowns of impacted teeth or in interproximal spaces.
Malignant transformation of central lesions has
been reported, but no cases of transformation of
peripheral EOGCT have been reported [63 – 66].
Peripheral odontoma/hamartoma
Odontomas are hamartomas of odontogenic origin
that are composed of some or all of the structures that
make up teeth. The cause of odontomas is unknown
but they may be hereditary or caused by a disturbance
in tooth development that is triggered by trauma or
infection [67]; however, evidence of this is lacking.
Evidence suggests that a mutation in the epithelial
cells of the tooth germ may change an inherent
capacity of odontogenic epithelium to go through
the bud, cap, and bell stages of tooth development
and retain its ability to stimulate the mesenchymal
differentiation that is necessary to form functional
ameloblasts and odontoblasts and lead to odontoma
formation. Depending on the stage of development
at discovery, peripheral odontomas may be radi-
opaque or have no radiographic features other than
saucerization that is seen in other peripheral odonto-
genic tumors [68].
Peripheral odontomas are asymptomatic, exo-
phytic masses of the gingiva. The differential diag-
nosis for a soft tissue odontoma is a foreign body,
soft tissue osteoma, superimposition of a calcified
mass of the adjacent soft tissue, periodontal abscess,
peripheral giant cell granuloma, or retained root tip.
They also may be found in the opercula of unerupted
teeth [69].
Histopathologically, peripheral odontomas appear
as small, opaque, white masses that contain dentin,
cementum, and pulplike material but little odonto-
genic epithelium or enamel matrix (Figs. 8 – 10). All
Fig. 9. Details of Fig. 8 showing lobules of ectomesenchy-
mal tissue that resembles dental papilla (10).
 A.E. Curran / Oral Maxillofacial Surg Clin N Am 16 (2004) 399–408
Fig. 10. Peripheral odontoma showing island of odonto-
genic epithelium with calcified tissue (40).
peripheral odontomas are of the compound type.
Multinucleated giant cells have been identified. These
lesions differ from eruption sequestrum in that they
represent vital odontogenic tissue rather than nonvital
tissue [70]. Onishi et al [69] found hamartomas in
more than half of opercula from teeth that failed to
erupt on schedule. The investigators questioned if an
odontoma would have developed if the lesions had
been left alone. The teeth in question were removed
because of failed eruption. Therefore, the age range is
younger than that reported for most odontogenic
tumors, although one case that involved a 39-year-
old man was reported [68].
Intraosseous odontomas have been known to erupt
[71] but these lesions are excluded from the discus-
sion of peripheral odontoma. Also excluded are
extraosseous odontomas that have been reported in
some unusual locations, including the midpalate [72]
and the middle ear [73].
Odontomas can occur with other odontogenic
lesions, such as COC, so cases of odontoma may
be reported with other tumors [74,75]. There are no
reports of peripheral odontomas erupting and no
reports of recurrence following excision.
Peripheral odontogenic myxoma
Several cases of peripheral odontogenic myxoma
have been reported [76 – 81]. Most of the lesions were
on the gingiva and were described as having the same
histopathologic features as central odontogenic myx-
oma. The investigators reported lesions with and with-
out bone resorption. It is difficult to determine from
the cases that reported bone involvement whether
they represent central lesions that perforated alveolar
405
bone. Lesions without bone involvement suggest that
the peripheral odontogenic myxoma is a distinct en-
tity; however, it also was suggested that these le-
sions may not be odontogenic in origin and that the
presence of odontogenic epithelium may not be
conclusive evidence that they arise from cells of the
odontogenic apparatus [81].
The age range for peripheral odontogenic myxoma
has been reported from 15 to 97 years; most cases
occur in the fourth to sixth decades [81]. No cases
with recurrence after excision have been reported.
Peripheral ameloblastic fibroma
Ameloblastic fibroma is a true mixed odonto-
genic tumor that is made up of epithelial and
ectomesenchymal neoplastic elements. Two reported
cases in the English literature include a 40-year-old
Japanese woman who had a lesion of the gingival
swelling in the mandibular premolar regions [82]
and a congenital lesion of the mandible that was
removed from a 3-year-old [83]. The photomicro-
graphs of the lesion that was removed from the
3-year-old do not show the classic features of ame-
loblastic fibroma, however. These investigators specu-
lated that the lesion had been a congenital epulis of
the newborn that transformed to an ameloblastic fi-
broma. Absolutely no evidence supports this theory.
In a review of peripheral odontogenic tumors in 1987,
Buckner and Scuibba [5] reported no peripheral ame-
loblastic fibromas.
Peripheral squamous odontogenic tumor
There is only one reported case of a peripheral
squamous odontogenic tumor occurring as a nod-
ule on the maxillary gingiva of a 74-year-old man
[84]. The age range for intraosseous lesions is 11 to
74 years with a peak in the third decade. There is
equal distribution of the central lesions between
maxillary anterior areas and the mandibular premolar
areas. Six cases with multiple site involvement have
been reported [85,86]. Central lesions are believed to
arise from rests of Malassez. These rests are not
present in gingival tissues so peripheral lesions may
arise from the rests of Serres. The single report of a
peripheral lesion showed ‘‘dropping off’’ from over-
lying epithelium so the investigators suggested that it
may have arisen from surface epithelium. No recur-
rence was reported at 15 months [84].
406 A.E. Curran / Oral Maxillofacial Surg Clin N Am 16 (2004) 399–408
Summary
In the clinical setting, most peripheral odonto-
genic tumors resemble benign reactive lesions. All
benign-appearing hyperplastic lesions of the gingiva
should be examined histopathologically to ascertain
their true diagnosis, to reassure the patient, and to
provide the practitioner with information in regard to
the recurrence potential and the type of follow-up
treatment that is necessary.
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