CH 30

CHAPTER 30
Odontogenic Cysts and Tumors

Eric R. Carlson, DMD, MD
Odontogenic cysts and tumors are rela- evolves into a bell shape. After forming the
tively uncommon lesions of the oral and enamel organ, the cord of dental lamina
maxillofacial region that must be consid- normally fragments and degenerates;
ered whenever examining and formulating however, small islands of the dental lami-
a differential diagnosis of an expansile na may remain after tooth formation and
process of the jaws. The clinical presenta- are believed to be responsible for the
tion, radiographic appearance, and natur- development of several of the odontogenic
al history of these lesions varies consider- cysts and tumors.
ably, such that odontogenic cysts and The enamel organ has four types of
tumors represent a diverse group of epithelium. The innermost lining is
lesions of the jaws and overlying soft tis- referred to as the inner enamel epithelium
sues. Collectively speaking, their occur- and becomes the ameloblastic layer that
rence is frequent enough to warrant a forms tooth enamel. The second layer of
thorough discussion. As a whole, these cells adjacent to the inner enamel epitheli-
pathologic entities have been studied and um is the stratum intermedium. Adjacent
reported on extensively. to this layer is the stellate reticulum, fol-
Purely defined, odontogenic refers to lowed by the outer enamel epithelium. Sur-
derivation from a tooth-related apparatus. rounding the enamel organ is loose con-
Tooth formation is a complex process that nective tissue known as the dental papilla.
involves both connective tissues and Contact with the enamel organ epithelium
epithelium. Three major tissues are induces the dental papilla to make odonto-
FIGURE 30-1 The enamel organ is seen emanat-
involved in odontogenesis including the blasts that form dentin. As the odonto-
ing from the dental lamina (hematoxylin and
enamel organ, the dental follicle, and the blasts deposit dentin, they induce the eosin; original magnification ×20) Reproduced
dental papilla. The enamel organ is an ameloblasts to begin forming enamel. with permission from Cawson RA, Eveson JW,
epithelial structure that is derived from Following the initial formation of the editors. Oral pathology and diagnosis. Color
atlas with integrated text. Philadelphia (PA):
oral ectoderm. The dental follicle and den- crown, a thin layer of the enamel organ
W.B. Saunders; 1987.
tal papilla are considered ectomesenchy- epithelium known as Hertwig’s root
mal in nature because they are in part sheath proliferates apically to provide the
derived from neural crest cells. stimulus for odontoblastic differentiation believed to be the source of epithelium for
For each tooth, odontogenesis begins in the root portion of the developing most periapical cysts but generally are not
with the apical proliferation from the oral tooth. This epithelial extension later believed to give rise to any of the odonto-
mucosa of epithelium known as the dental becomes fragmented but leaves behind genic neoplasms, with the possible excep-
lamina (Figure 30-1). The dental lamina, small nests of epithelial cells known as tion of the squamous odontogenic tumor.
in turn, gives rise to the enamel organ, a rests of Malassez in the periodontal liga- In the development of a tooth, follow-
cap-shaped structure that subsequently ment space. The rests of Malassez are ing completion of enamel formation, the
576 Part 5: Maxillofacial Pathology
enamel organ epithelium atrophies to phase, may be carried into the S phase and from the inclusion of epithelium along
form a thin flattened layer of cells that cov- perpetuated in subsequent cell divisions. embryonic lines of fusion, most jaw cysts
ers the enamel of the unerupted tooth. The G1-S checkpoint is normally regulated are lined by epithelium that is derived
This layer of epithelium is known as the by a well-coordinated and complex system from odontogenic epithelium, hence the
reduced enamel epithelium. In the normal of protein interactions whose balance and term odontogenic cysts. These cysts are sub-
sequence of events, this reduced enamel function are critical to normal cell divi- classified as developmental or inflamma-
epithelium later merges with the surface sion.1 As can be seen in Figure 30-2, once tory in nature. Although the cell type is
epithelium and forms the initial gingival genetic change occurs that encourages the often known, developmental cysts are of
crevicular epithelium of the newly erupted development of an odontogenic cyst or unknown origin; however, they do not
tooth. However, if fluid accumulates tumor, a series of events mediated by the seem to be the result of an inflammatory
between the reduced enamel epithelium odontogenic lesion occur that may pro- reaction. Inflammatory cysts, on the other
and the crown of the tooth before tooth mote proliferation. Such events support hand, are the result of inflammation
eruption, a cyst is formed that is known as the pathogenetic mechanism involved in (Table 30-1).
a dentigerous or follicular cyst. the progression of the cyst or tumor.
An understanding of the progression It is the purpose of this chapter to Dentigerous Cyst
of odontogenic cysts and tumors within review the clinically significant and more By definition, a dentigerous cyst occurs in
the oral and maxillofacial region requires a commonly encountered odontogenic cysts association with an unerupted tooth, most
thorough knowledge of the cell cycle of and tumors. In so doing, salient clinical commonly mandibular third molars.
these lesions and an appreciation of the and radiographic features are discussed, as Other common associations are with max-
concept of proliferation versus apoptosis are the pathogenetic mechanisms support- illary third molars, maxillary canines, and
(programmed cell death). Most of the ing proliferation of some of the more mandibular second premolars.2 They may
pathogenetic mechanisms of odontogenic aggressive odontogenic cysts and tumors. also occur around supernumerary teeth
cysts and tumors can be explained via the Recommendations for treatment and and in association with odontomas; how-
cell cycle (Figure 30-2). Normally cell divi- prognostic information are also offered. ever, they are only rarely associated with
sion is divided into four phases: G1 (gap primary teeth.2,3 Although dentigerous
1), S (deoxyribonucleic acid synthesis), G2 Odontogenic Cysts cysts occur over a wide age range, they are
(gap 2), and M (mitosis). A key event is the With rare exceptions, epithelium-lined most commonly seen in 10- to 30-year-
progression from G1 to the S phase. Genet- cysts in bone are seen only in the jaws.2 olds. There is a slight male predilection,
ic alterations, if unrepaired in the G1 Other than a few cysts that may result and their prevalence appears to be higher
in Whites than in Blacks. Many dentiger-
G0 ous cysts are small asymptomatic lesions
BCL2, BCLXL, that are discovered serendipitously on
others routine radiographs, although some may
BAX, P53
grow to considerable size causing bony
Apoptosis Inhibitor proteins expansion that is usually painless until sec-
M (p16, p21, p27)
ondary infection occurs.
G1 BAK, BCLXS, Radiographically, the dentigerous cyst
others presents as a well-defined unilocular radi-
olucency, often with a sclerotic border
Cell cycle pRb
(PCNA, Ki-67) E2F Proliferation (Figure 30-3). Since the epithelial lining is
(cyclins + kinases) derived from the reduced enamel epitheli-
um, this radiolucency typically and prefer-
G2
entially surrounds the crown of the tooth.
A large dentigerous cyst may give the
Growth/mitogenic
S factors
impression of a multilocular process
because of the persistence of bone trabec-
ulae within the radiolucency. However,
FIGURE 30-2 The cell cycle—a concept of proliferation versus apoptosis. PCNA = proliferating cell dentigerous cysts are grossly and
nuclear antigen. histopathologically unilocular processes
Odontogenic Cysts and Tumors 577
Table 30-1 Classification of One diagnostic dilemma for oral and

Odontogenic Cysts maxillofacial surgeons is distinguishing
between a dentigerous cyst and an
Developmental
enlarged dental follicle. This distinction
Dentigerous cyst
Eruption cyst
becomes clinically significant when the
Odontogenic keratocyst surgeon considers whether to submit tis-
Orthokeratinized odontogenic cyst sue removed with an impacted third molar
Gingival (alveolar cyst of the newborn) for histopathologic examination as
Gingival cyst of the adult opposed to clinical designation as a folli-
Lateral periodontal cyst cle, with simple disposal of the tissue. The
FIGURE 30-4 The biopsy of the radiolucency in
Calcifying odontogenic cyst radiographic distinction becomes some- Figure 30-3 shows an atrophic stratified squamous
Glandular odontogenic cyst what arbitrary; however, any pericoronal epithelium without significant associated inflam-
Inflammatory radiolucency that is > 4 or 5 mm is con- mation. The diagnosis is dentigerous cyst (hema-
Periapical (radicular cyst) sidered suggestive of cyst formation and toxylin and eosin; original magnification ×40).
Residual periapical (radicular cyst) should be submitted for microscopic
Buccal bifurcation cyst
examination. It is noteworthy that pathol- tooth, often without a preceding incisional
ogists also struggle with the distinction biopsy (Figure 30-5). Larger cysts that are
between dental follicles associated with treated in the operating room should prob-
and probably are never truly multilocular developing teeth and odontogenic ably undergo frozen-section diagnosis and
lesions.2 Three types of dentigerous cyst lesions.4,5 It seems that odontogenic cysts, appropriate treatment that might be dic-
have been described radiographically, odontogenic fibroma, and odontogenic tated by other diagnoses. Curettage of the
including the central variety, in which the myxoma are the lesions most often inap- cyst cavity is usually advisable at the time
radiolucency surrounds just the crown of propriately diagnosed by surgical patholo- of removal of the cyst in the event that a
the tooth, with the crown projecting into gists owing to a general unfamiliarity with more aggressive cyst is diagnosed
the cyst lumen. In the lateral variety, the the normal process of odontogenesis.4 histopathologically following removal in
cyst develops laterally along the tooth root Of perhaps even greater concern is the an office setting. Such diagnoses would
and partially surrounds the crown. The large unilocular radiolucency. Although include odontogenic keratocyst and uni-
circumferential variant of the dentigerous most commonly classified radiographically cystic ameloblastoma.
cyst exists when the cyst surrounds the as dentigerous cysts, it is incumbent upon Large dentigerous cysts may be treated
crown but also extends down along the the surgeon to section these excised speci- with marsupialization (Figure 30-6) when
root surface, as if the entire tooth were mens in the operating room and to consid- enucleation and curettage might otherwise
located within the cyst. er frozen-section analysis. In fact, some result in neurosensory dysfunction or pre-
specimens may contain a focus of unicystic dispose the patient to an increased chance
ameloblastoma and therefore require con- of pathologic fracture. Some patients who
sideration of more extensive treatment. are not candidates for general anesthesia
The histologic features of dentigerous may also be treated with a marsupialization
cysts may vary greatly depending mainly on procedure in an office setting under local
whether or not the cyst is inflamed. In the anesthesia. This permits decompression of
noninflamed dentigerous cyst, a thin epithe- the large dentigerous cyst with a resultant
lial lining may be present with the fibrous reduction in the size of the cyst and bony
connective tissue wall loosely arranged (Fig- defect. At a later date the reduced cyst can
ure 30-4). In the inflamed dentigerous cyst, be removed in a smaller-scale surgery.
the epithelium commonly demonstrates I emphasize the need for histopatho-
hyperplastic rete ridges, and the fibrous cyst logic examination of all radiolucencies that
wall shows an inflammatory infiltrate. are empirically diagnosed as dentigerous
cysts. This includes those that are enucleat-
FIGURE 30-3 This unilocular radiolucency of the
Treatment and Prognosis Most dentiger- ed as well as those that undergo marsupial-
left mandibular ramus associated with impacted
tooth no. 17 was discovered serendipitously when ous cysts are treated with enucleation of ization, during which it is important
the patient was evaluated for routine dental work. the cyst and removal of the associated to inspect the cyst lumen and submit a
Adequate diagnosis and treatment of

the odontogenic keratocyst is important
for three reasons: (1) this cyst is recog-
nized as being more aggressive than other
odontogenic cysts,10 (2) the odontogenic
keratocyst has a higher rate of recurrence
than other odontogenic cysts,11 and (3) the
association with nevoid basal cell carcino-
ma syndrome requires that the clinician
examine a patient with multiple cysts of
the jaws for physical findings that might
B diagnose this syndrome.12–14
Odontogenic keratocysts may be found
FIGURE 30-5 A, The dentigerous cyst in Figure in patients ranging in age from infancy to
30-3 is treated with enucleation and curettage of
the cyst and removal of the etiologic tooth. B, The old age; however, 60% of cases are seen in
5-year postoperative radiograph shows an people between 10 and 40 years old.15 In his
A acceptable bony fill. series of 312 cases, Brannon found a mean
age of nearly 38 years.16 The peak preva-
representative piece for histopathologic this cyst are well known; the sporadic cyst lence was in the second and third decades
examination. Support of this statement and the cyst associated with the nevoid basal of life, with only 15% occurring past the age
stems from the occasional formation of a cell carcinoma syndrome. Both variants of of 60 years. Woolgar and colleagues
squamous cell carcinoma, mucoepider- the odontogenic keratocyst are believed to reviewed 682 odontogenic keratocysts from
moid carcinoma, or ameloblastoma from be derived from remnants of the dental lam- 522 patients and found a mean age of
or in association with a dentigerous cyst.6–8 ina. This cyst shows a different growth 40 years for patients with single nonrecur-
The prognosis for most histopathologically mechanism and biologic behavior from the rent cysts and 26.2 years for patients with
diagnosed dentigerous cysts is excellent, previously described dentigerous cyst. Most multiple cysts of the nevoid basal cell carci-
with recurrence being a rare finding. authors believe that dentigerous cysts con- noma syndrome.17 A slight male predilec-
tinue to enlarge as a result of increased tion is usually seen, and 60 to 80% of cases
Odontogenic Keratocyst osmotic pressure within the lumen of the involve the mandible, particularly in the
The odontogenic keratocyst is a distinctive cyst. This mechanism does not appear to posterior body and ascending ramus.2
form of developmental odontogenic cyst hold true for odontogenic keratocysts, and Although it is rare for a dentigerous cyst to
that deserves special consideration because their growth may be related to unknown appear multilocular on radiographs, it is
of its specific histopathologic features and factors inherent in the epithelium itself of most common for odontogenic keratocysts
aggressive clinical behavior. Two variants of enzymatic activity in the fibrous wall.9 to appear multilocular (Figure 30-7). Many
A B C
FIGURE 30-6 A, This large biopsy-proven dentigerous cyst occurred in an elderly patient who had coronary artery disease. Owing to the size of the cyst and the
compromised cardiac status of the patient, a relatively noninvasive marsupialization was performed. B, An acrylic plug with a wire handle was placed in a small
surgical entrance into the cyst cavity. The cyst shrunk considerably, after which time the etiologic impacted tooth was removed with a small remnant of dentiger-
ous cyst. C, The 5-year postmarsupialization radiograph shows an excellent fill of bone.
be removed in one piece, which requires results of resection over all other thera-
acceptable access and lighting (Figure 30- peutic undertakings.20
9). As such, many patients are suitably The reported frequency of recurrence
treated in an operating room setting under of the odontogenic keratocyst ranges from
general anesthesia. This is particularly 2.5% to 62.5% in various studies.11 This
helpful when removing large cysts. It is my wide variation may be related to the total
experience and that of others that a large number of cases studied, the length of fol-
majority of sporadic odontogenic kerato- low-up periods, and the inclusion or
cysts may be effectively managed with a exclusion of orthokeratinized cysts in the
thorough enucleation and curettage study group. Several reports that include
surgery.18,19 MacIntosh has advocated the large numbers of cases indicate a recur-
resection of odontogenic keratocysts with rence rate of approximately 30%.2 Regezi
FIGURE 30-7 This multilocular radiolucency, pre- 5 mm linear margins as the preferred pri- and colleagues point out that the recur-
sent in a 54-year-old man, should suggest an
mary method of treatment, and has rence rate for solitary odontogenic kerato-
odontogenic keratocyst when formulating a differ-
ential diagnosis. reported on 37 patients with 43 lesions cysts is 10 to 30%.21 They indicate that
emphasizing the efficacy and superior approximately 5% of patients with odon-
togenic keratocysts have multiple sporadic
appear unilocular and can therefore be con- Table 30-2 Clinical Features of the jaw cysts (nonsyndromic) and that their
fused with dentigerous cysts. It is clear, Basal Cell Nevus Syndrome recurrence rate is greater than that for soli-
therefore, that the differential diagnosis of a tary lesions.21 Brannon has suggested three
≥ 50% frequency
unilocular radiolucency must include both mechanisms responsible for recurrence:
Multiple basal cell carcinomas
entities and that treatment should include (1) remnants of dental lamina within the
Odontogenic keratocysts
curettage in the event that the diagnosis is Epidermal cysts of the skin jaws not associated with the original
odontogenic keratocyst. When multiple Palmar/plantar pits odontogenic keratocyst being responsible
multilocular radiolucencies are noted on a Calcified falx cerebri for de novo cyst formation; (2) incomplete
panoramic radiograph, the clinician must Enlarged head circumference removal (persistence) of the original cyst
perform an incisional biopsy and investi- Rib anomalies (splayed, fused, partially secondary to a thin friable lining and cor-
gate the possibility of nevoid basal cell car- missing, bifid) tical perforation with adherence to adja-
cinoma syndrome (Table 30-2). Mild ocular hypertelorism cent soft tissue; and (3) remaining rests of
Histologically, the odontogenic kera- Spina bifida occulta of cervical or dental lamina and satellite cysts following
tocyst is readily recognized. A uniform thoracic vertebrae enucleation.22 Vedtofte and Praetorius
layer of stratified squamous epithelium, 15–49% frequency reviewed 72 patients with 75 odontogenic
usually six to eight cells in thickness, is Calcified ovarian fibromas keratocysts and observed remnants of
present (Figure 30-8). The parakeratotic Short fourth metacarpals dental lamina between the cyst membrane
surface is characteristically corrugated. Kyphoscoliosis or other vertebral
The wall is usually thin and friable, which anomalies
can pose problems for removal in one Pectus excavatum or carinatum
piece intraoperatively. Epithelial budding Strabismus (exotropia)
and the presence of daughter cysts may be < 15% frequency (but not random)
noted in the connective tissue wall. It is Medulloblastoma
generally advisable to ask the pathologist Meningioma
to examine the sections carefully for these Lymphomesenteric cysts
two features as they generally impart a Cardiac fibroma
more aggressive character to the cyst. Fetal rhabdomyoma
Marfanoid build
Cleft lip and/or palate
Treatment and Prognosis Like the treat-
Hypogonadism in males FIGURE 30-8 The classic histologic appearance
ment of most odontogenic cysts, the
Mental retardation of an odontogenic keratocyst from the incisional
odontogenic keratocyst may be treated biopsy of the lesion in Figure 30-7 (hematoxylin
Adapted from Gorlin FJ.14
with enucleation and curettage and must and eosin; original magnification ×40).
expression of proliferating cell nuclear 9q22.3-q31. Affected patients (Figure 30-

antigen (PCNA) in odontogenic cysts has 10A) may demonstrate frontal and tem-
been assessed. It is hypothesized that the poroparietal bossing, hypertelorism, and
identification of the proliferative activity in mandibular prognathism (see Table 30-
odontogenic cysts and tumors may be use- 2).14 Other frequent skeletal anomalies
ful to predict their biologic behavior. The include bifid ribs and lamellar calcification
same may be true of the Ki-67 antigen. In of the falx cerebri (Figure 30-10B).14 The
fact, two studies have been performed that
A have quantified these parameters.25,26 The
conclusion of both studies is that an
increased proliferative activity for the
odontogenic keratocyst in comparison
with the dentigerous cyst is noted consis-
tently. These results are in agreement with
the more aggressive behavior seen with the
odontogenic keratocyst.
The orthokeratinized odontogenic
cyst, once thought to be a variant of the
odontogenic keratocyst, is now generally
well accepted as being a different clinico-
B
pathologic entity from the more common
FIGURE 30-9 A, A very thin cyst lining was parakeratinized odontogenic keratocyst; it
encountered when performing the enucleation should therefore be placed in a different
and curettage of the odontogenic keratocyst in
category. These cysts usually appear as
Figure 30-7. B, The 7-year postoperative radi-
ograph shows an excellent fill of bone. A recon- unilocular radiolucencies, but occasional
struction bone plate was placed at the time of the examples have been multilocular. A major-
enucleation and curettage to prevent a patholog- A
ity of these cysts are encountered in a
ic fracture of the mandible.
lesion that appears clinically and radi-
ographically to represent a dentigerous
and overlying mucosa.23 As such, they cyst, most often involving an unerupted
advocated the excision of overlying mandibular third molar tooth. Histologi-
mucosa in conjunction with removal of cally, the epithelium is thin and orthoker-
the cyst. Williams and Connor recom- atinized, and a prominent palisaded basal
mended a primary enucleation and curet- layer, characteristic of the odontogenic
tage surgery for odontogenic keratocysts, keratocyst, is not present. Enucleation and
including the use of methylene blue as a curettage of the orthokeratinized cyst is
marking agent, followed by a 3-minute curative in most cases. The reported rate
application of Carnoy’s solution.11 They of recurrence of 2% is far lower than the
indicated that resection should be consid- previously quoted statistics for recurrence
ered for the treatment of a recurrent of the odontogenic keratocyst.2
odontogenic keratocyst, with inclusion of
appropriate bone and soft tissue margins. Nevoid Basal Cell Carcinoma Syndrome
Pathogenetically, the odontogenic ker- The nevoid basal cell carcinoma syndrome
atocyst expresses cell cycle phenomena that (basal cell nevus syndrome, Gorlin’s syn- B
support its proliferation.21 These include drome) is an autosomal-dominant inher-
the release of the cytokines interleukin 1a ited condition that exhibits high pene- FIGURE 30-10 A, This 18-year-old shows some of
trance and variable expressivity. It is the clinical features of the nevoid basal cell carci-
(IL-1a) and IL-6 as well as parathyroid noma syndrome including frontal bossing and
hormone–related protein that encourage caused by mutations in the PTCH tumor mandibular prognathism. B, The radiograph from
resorption of bone.21,24 Moreover, the suppressor gene, mapped to chromosome another patient shows a calcified falx cerebri.
most significant clinical feature is the ten- cell carcinoma syndrome can be difficult of aggressive behavior and recurrence.
dency to develop multiple basal cell carci- owing to the large number of “recur- Although it is generally accepted as being
nomas that may affect both exposed and rences” in these patients. As a matter of of odontogenic origin, it shows glandular
non–sun-exposed areas of the skin. Pitting point, I choose to refer to these as new or salivary features that seem to point to
defects on the palms and soles can be primary cysts owing to the autosomal- the pluripotentiality of odontogenic
found in nearly two-thirds of affected dominant penetrance of the syndrome epithelium as cuboidal/columnar cells,
patients (Figure 30-11). The discovery of and cyst development. It is certainly pos- mucin production, and cilia are noted in
multiple odontogenic keratocysts is usual- sible that many of these cysts are persis- these cysts. Glandular odontogenic cysts
ly the first manifestation of the syndrome tent, particularly when considering how occur most commonly in middle-aged
that leads to the diagnosis. For this reason, common it can be to retain rests of the adults, with a mean age of 49 years at the
any patient with an odontogenic kerato- dental lamina when enucleating an odon- time of diagnosis.2 Eighty percent of
cyst should be evaluated for this condi- togenic keratocyst. Whatever the mecha- cases occur in the mandible,21 and a
tion. Although the cysts in patients with nism, a resection hardly seems to be war- strong predilection for the anterior
nevoid basal cell carcinoma syndrome ranted. Marsupialization is a more region of the jaws has been reported,
cannot definitely be distinguished micro- desirable procedure (Figure 30-12) and with many mandibular lesions crossing
scopically from those not associated with has been shown to result in complete res- the midline (Figure 30-13). These cysts
the syndrome, they often demonstrate olution of the sporadic cyst, with no his- may appear either unilocular or multi-
more epithelial proliferation and daughter tologic signs of cystic remnants, daughter locular radiographically.
cyst formation in the cyst wall. cysts, or budding of the basal layer of the There is a histologic similarity between
The treatment of the odontogenic epithelium.27 Although all of the eight the glandular odontogenic cyst and the pre-
keratocyst in patients with nevoid basal cases in the series by Pogrel and Jordan dominantly cystic intraosseous mucoepi-
were sporadic cysts,27 a similar approach dermoid carcinoma. However, the epithelial
to syndrome patients with odontogenic lining of the glandular odontogenic cyst is
keratocysts that had been operated on typically thinner and does not show evi-
multiple times has been performed with dence of the more solid or microcystic
success in a small sample size.18 epithelial proliferations seen in mucoepi-
dermoid carcinoma (Figure 30-14). Wal-
Glandular Odontogenic Cyst dron and Koh reviewed the similarities
The glandular odontogenic cyst (sialo- between the two lesions and concluded that
odontogenic cyst) is a rare and recently it is entirely possible that some cases previ-
described cyst of the jaws that is capable ously diagnosed as central mucoepidermoid
A B
FIGURE 30-11 Plantar pitting can be observed

by immersing the foot in povidone-iodine solu- FIGURE 30-12 The patient in Figure 30-10A had previously undergone three enucleation and curet-
tion followed by a conservative wash of the foot tage surgeries for bilateral maxillary odontogenic keratocysts. A, Development of new large cysts in
with saline. The solution is taken up in the pits this area led to additional treatment with marsupialization. B, Six months later the axial computed
present in the plantar surface of the foot. tomography shows regression of the cysts.
rence rate of approximately 30% and

therefore recommend resection.29
Calcifying Odontogenic Cyst

The calcifying odontogenic cyst (COC), or
Gorlin’s cyst, is an uncommon lesion that
demonstrates considerable histopathologic
diversity and variable clinical behavior.
A Although designated as a cyst, some investi-
gators provide evidence for subclassifica-
tion as a neoplasm as well.30,31 In addition,
the COC may be associated with other rec- A
ognized odontogenic tumors, most com-
monly the odontoma. Adenomatoid odon-
togenic tumors and ameloblastomas have
also been associated with the COC. Ghost
cell keratinization, the characteristic micro-
scopic feature of this cyst, is also a defining
feature of the cutaneous lesion known as
the calcifying epithelioma of Malherbe or
pilomatrixoma. The World Health Organi-
B
zation’s classification of odontogenic B
FIGURE 30-13 A and B, This glandular odonto- tumors groups the COC with all its variants
genic cyst presented with a unilocular radiolucen- as an odontogenic tumor rather than an FIGURE 30-15 A, The patient whose radi-
cy of the anterior mandible crossing the midline. ograph appears in Figure 30-13 underwent an
odontogenic cyst. The commentary on the enucleation and curettage of the cyst as well as
second edition by Kramer, Pindborg, and removal of the anterior mandibular teeth. B,
tumors may be reclassified as examples of Shear points out that some COCs appear to The 3-year postoperative radiograph shows
glandular odontogenic cysts.28 be non-neoplastic, but others show an infil- acceptable bony fill.
trative pattern of growth.32 They further
Treatment and Prognosis Most glandu- indicate that more experience with the COCs appear radiographically as unilocu-
lar odontogenic cysts are treated with enu- COC may provide reliable criteria for their lar well-defined lesions. The radiopaque
cleation and curettage (Figure 30-15). reclassification. The review by Hong and structures within the lesions have been
Some authors, however, point to a recur- colleagues designated 79 of 92 cases of described as either irregular calcifications
COC as cysts with the remaining 13 cases or toothlike densities.
being neoplastic in nature.30
The COC is predominantly an Treatment and Prognosis The standard
intraosseous lesion, although 13 to 30% of treatment for the COC is enucleation and
reported cases occur as peripheral lesions.2 curettage (Figure 30-16). A limited num-
Both the peripheral and central lesions ber of recurrences have been reported after
occur with about equal frequency in the such treatment. When a COC is associated
maxilla and mandible. There appears to be with another recognized odontogenic
a predilection for the incisor and canine tumor such as an ameloblastoma, the
areas. Patients range in age from infant to treatment and prognosis are likely to be
elderly, with a mean age of occurrence of the same as for the associated tumor.
about 30 years. COCs that are associated Although only a few cases have been
FIGURE 30-14 Histopathology of the lesion in with odontomas tend to occur in younger reported,31 a carcinoma arising in a COC
Figure 30-13 shows a nonkeratinized stratified
squamous epithelium with intraepithelial
patients, with a mean age of 17 years.2 The may occur. One such reported case result-
mucous cells and cilia (hematoxylin and eosin; more rare neoplastic variant of the COC ed in multiple pulmonary metastases and
original magnification ×40). appears to occur in elderly patients. Most was referred to as an odontogenic ghost
Odontogenic Tumors Table 30-3 Classification of Odontogenic

Tumors
Odontogenic tumors comprise a complex
group of lesions of great importance to oral Tumors of odontogenic epithelium
and maxillofacial surgeons. Many of these Ameloblastoma
lesions are true tumors, whereas some are • Malignant ameloblastoma
hamartomas. Like normal odontogenesis, • Ameloblastic carcinoma
odontogenic tumors demonstrate varying Calcifying epithelial odontogenic
tumor
inductive interactions between odontogenic
Squamous odontogenic tumor
epithelium and odontogenic ectomes-
Clear cell odontogenic carcinoma
enchyme. This ectomesenchyme was for- Primary intraosseous carcinoma
merly referred to as mesenchyme because it
was thought to be derived from the meso- Tumors of odontogenic epithelium with
A
odontogenic ectomesenchyme ± dental
dermal layer of the embryo. It is now accept-
hard tissue formation
ed that this tissue differentiates from the
Ameloblastic fibroma
ectodermal layer in the cephalic portion of Ameloblastic fibro-odontoma
the embryo; hence, the designation ectomes- Ameloblastic fibrosarcoma
enchyme. Odontogenic tumors are typically Odontoameloblastoma
subclassified by their tissues of origin (Table Odontoma
30-3). Tumors of odontogenic epithelium • Compound composite
are composed only of odontogenic epitheli- • Complex composite
um without any participation of the odon- Adenomatoid odontogenic tumor
togenic ectomesenchyme. Other odonto- Tumors of odontogenic ectomesenchyme
genic neoplasms, referred to as mixed ± included odontogenic epithelium
odontogenic tumors, are composed of Odontogenic fibroma
B odontogenic epithelium and ectomesenchy- Granular cell odontogenic tumor
mal elements. A third group, tumors of Odontogenic myxoma
odontogenic ectomesenchyme, includes Cementoblastoma
those tumors composed principally of
ectomesenchymal elements. Although some
odontogenic epithelium may be included odontogenic tumor. Excluding odon-
within these lesions, it does not appear to tomas, its incidence equals or exceeds the
play an essential role in their pathogenesis. combined total of all other odontogenic
The frequency of odontogenic tumors tumors. These tumors may arise from rests
seems to be geographically determined of the dental lamina, a developing enamel
C (Table 30-4). Studies from North America organ, the epithelial lining of an odonto-
seem to indicate that odontogenic tumors genic cyst, or the basal cells of the oral
FIGURE 30-16 A, This calcifying odontogenic represent approximately 1% of all acces- mucosa.2 The ameloblastoma occurs in
cyst appears as a mixed radiolucent/radiopaque
lesion on the occlusal radiograph. B, This patient sions in oral pathology laboratories,34,35 three different variants, each with specific
underwent enucleation and curettage of the whereas African studies have a much high- implications for treatment and a unique
lesion. C, The histopathology shows characteris- er incidence of odontogenic tumors.36–41 prognosis: solid or multicystic, unicystic,
tic ghost cells (hematoxylin and eosin; original
Moreover, the ameloblastoma is more and peripheral. In an analysis of the inter-
magnification ×40).
commonly encountered in African and national literature, 3,677 cases of
other underdeveloped countries than in ameloblastoma were reviewed, of which
cell carcinoma by the authors.33 It has not North America. 92% were solid or multicystic, 6% were
been demonstrated whether the malignant unicystic, and 2% were peripheral.42
COC arose from previously benign lesions Ameloblastoma
and, if so, whether that precursor was the The ameloblastoma is the most common Solid or Multicystic Ameloblastoma
cystic or neoplastic type. clinically significant and potentially lethal This variant of the ameloblastoma is
Table 30-4 Incidence of Odontogenic Tumors

Study (yr)
Specimens Regezi JA et al.34 Odukoya O36 Daley TD et al.35
(1978) (1995) (1994)
Total 54,534 1,511 40,000
Total odontogenic tumors 706 (1.3%)* 289 (19.1%)* 445 (1.1%)*
Ameloblastoma 78 (11.0%)† 169 (58.5%)† 79 (17.8%)†
Adenomatoid odontogenic tumor 22 (3.1%)† 18 (6.2%)† 14 (3.1%)†
Odontoma 473 (67.0%)† 12 (4.2%)† 204 (45.8%)†
Myxoma 20 (2.8%)† 34 (11.8%)† 24 (5.4%)†
*Percentage of total specimens in respective study.
†
Percentage of total odontogenic tumors in respective study specimens.
encountered in patients over a wide age granular eosinophilic cytoplasm; desmo-

range.43 It is rare in children in their first plastic owing to extremely dense collage- A
decade of life and relatively uncommon in nized stroma that supports the tumor; and
the second decade.44 The tumor shows a the least common basal cell variant, in
relatively equal rate of occurrence in the which nests of uniform basaloid cells are
third through seventh decades. There is present, with a strong resemblance to basal
no gender predilection, and racial cell carcinoma. In this latter tumor stellate
predilection is most controversial. About reticulum is not present in the central por-
85% of this variant of the ameloblastoma tions of the nests. One additional excep-
occur in the mandible, most commonly in tion surrounds the desmoplastic variant,
the molar/ramus region.45 About 15% of which is generally not a radiolucent tumor
multicystic ameloblastomas occur in the radiographically owing to its high content
maxilla, usually in the posterior of collagenized stroma.
regions.46–49 A painless expansion of the Pathogenetically, the proliferative
B
jaws is the most common clinical presen- capacity of ameloblastomas has been stud-
tation; neurosensory changes are uncom- ied. As might be conjectured, the recurrent FIGURE 30-17 A 17-year-old girl with obvious
mon, even with large tumors (Figure 30- ameloblastoma is associated with the high- facial expansion (A) related to a multilocular
17). Slow growth is the rule, with est number of PCNA-positive cells, fol- radiolucency of the left mandible associated
with impacted tooth no. 17 (B). Note the
untreated tumors leading to tremendous lowed by the previously unoperated advanced root resorption on teeth no. 18 and
facial disfigurement (Figure 30-18).50 ameloblastomas.26 The nuclear PCNA pos- 19, indicative of the aggressive nature of this
The most common radiographic fea- itivity of the unicystic ameloblastoma was tumor. The incisional biopsy showed solid/mul-
ticystic ameloblastoma.
ture is that of a multilocular radiolucency. notably lower than the positivity of the
Buccal and lingual cortical expansion is solid multicystic ameloblastoma.26 Other
common, frequently to the point of perfo- cell cycle features supporting the aggressive
ration. Resorption of adjacent tooth roots behavior of the ameloblastoma include the this neoplasm and how best to treat it.52 The
is common. Histologic patterns include overexpression of BCL2 and BCLX, as well literature is therefore paradoxically a source
follicular, in which the stellate reticulum is as the expression of IL-1 and IL-6.51 of both information and misinformation.
located within the center of the odonto- Conflicting opinion, extending backward in
genic island (Figure 30-19); plexiform, in Treatment and Prognosis The ameloblas- time, has served both to educate and to con-
which the stellate reticulum is located out- toma continues to be a subject of fascina- fuse, and it has been left to generations of
side of the odontogenic rest; acanthoma- tion in the international literature. Unfortu- surgeons to sift and interpret what they con-
tous, in which squamous differentiation of nately, although most agree that aggressive sider to be clinically valid. It is my strong
the odontogenic epithelium is present; treatment is essential for cure of this tumor, opinion that this neoplasm is both highly
granular cell, in which the tumor islands the fact remains that a consensus has not aggressive and curable. This notwithstand-
exhibit cells that demonstrate abundant been reached on the biologic behavior of ing, numerous methods of treatment have
FIGURE 30-18 Twenty years of undisturbed

growth of a solid/multicystic ameloblastoma led
to significant facial disfigurement (A), with an
impressive radiographic appearance (B). A seg-
mental resection of the right mandible was per-
formed (C).
A B C
been recommended, ranging from simple decades before this persistent disease ated with neoplastic transformation of
enucleation and curettage to resection.53–59 becomes clinically and radiographically evi- ameloblastomatous epithelium.65 These
The solid or multicystic ameloblastoma dent, and long after a surgeon falsely pro- histologic changes were (1) hyperchroma-
tends to infiltrate between intact cancellous claimed the patient to be cured. tism of basal cell nuclei of the epithelium
bone trabeculae at the periphery of the Owing to the highly infiltrative and lining the cystic cavities, (2) palisading and
tumor before bone resorption becomes aggressive nature of the solid or multicystic polarization of basal cell nuclei of the
radiographically evident. Therefore, the ameloblastoma, I recommend resection of epithelium lining the cystic cavities, and (3)
actual margin of the tumor often extends the tumor with 1.0 cm linear bony margins cytoplasmic vacuolization, particularly of
beyond its apparent radiographic or clinical (Figure 30-20). This linear bony margin basal cells of cystic linings. They referred to
margin.60 Attempts to remove the tumor by should be confirmed by intraoperative these changes as early histopathologic fea-
curettage, therefore, predictably leave specimen radiographs. Soft tissue margins tures of neoplasia. Unicystic ameloblastoma
behind small islands of tumor within the are best managed according to the anatom- refers to a pattern of epithelial proliferation
bone, which are later determined to be ic barrier margin principles whereby one that has been described in dentigerous cysts
recurrent disease. These must be realized as uninvolved surrounding anatomic barrier of the jaws that does not exhibit the histo-
persistent disease as the tumor was never is sacrificed on the periphery of the speci- logic criteria for ameloblastoma published
controlled from the outset. When a small men.61 When all soft and hard tissue mar- by Vickers and Gorlin.66–69 This entity
burden of tumor is left behind, it may be gins are histologically negative, the patient deserves separate consideration based on its
is likely to be cured of this neoplasm. clinical, radiographic, and pathologic fea-
Unfortunately, any less aggressive treatment tures. Moreover, in many cases it may be
modality may be fraught with inevitable treated more conservatively than the solid
persistence discovered at variable times or multicystic ameloblastoma with the
postoperatively.62 Moreover, although the same degree of cure.70
persistent and occasionally nonresectable Unicystic ameloblastomas are most
ameloblastoma is radiosensitive, once this commonly seen in young patients, with
otherwise benign tumor defies curative sur- about 50% of these tumors being diag-
gical therapy, radiation is of questionable nosed during the second decade of life.
use in salvaging these patients.63,64 The average age of patients with unicystic
ameloblastomas has been reported as
FIGURE 30-19 The incisional biopsy of the
patient in Figure 30-17 shows follicular variant
Unicystic Ameloblastoma In 1970 Vick- 22.1 years, compared with 40.2 years for
of the solid/multicystic ameloblastoma (hema- ers and Gorlin published their findings the solid or multicystic variant.42 More
toxylin and eosin; original magnification ×60). regarding the histologic alterations associ- than 90% of these tumors are found in the
the surgeon should routinely open a “cystic”

lesion and look for luminal proliferation of
tumor. When able, histopathologic exami-
nation of such a process should occur with
frozen sections. This is particularly impor-
tant when dealing with large cysts. With a
histologic diagnosis of unicystic ameloblas-
toma, the surgeon should request the
pathologist to obtain multiple sections
through many levels of the specimen to
properly subclassify the variant of unicystic
ameloblastoma. When the ameloblastic ele-
A ments are confined to the lumen of the cyst
with or without intraluminal tumor exten-
sion, the enucleation has probably been
FIGURE 30-21 This unilocular radiolucency curative treatment. When the cyst wall has
associated with tooth no. 17 should generate a
been violated by the tumor as in a mural
differential diagnosis of dentigerous and other
odontogenic cysts. variant of unicystic ameloblastoma, the
most appropriate surgical management is
sists of a fibrous cyst wall with a lining quite controversial. If this diagnosis is made
that consists totally or partially of postoperatively, the surgeon may wish to
ameloblastic epithelium. The intraluminal adopt close indefinite follow-up examina-
unicystic ameloblastoma contains one or tions of the patient. If a preoperative inci-
more nodules of ameloblastoma project- sional biopsy provides a diagnosis of mural
ing from the cystic lining into the lumen unicystic ameloblastoma, the surgeon might
of the cyst. These nodules may be relative- recommend a resection of the tumor owing
ly small or largely fill the cystic lumen, to the fact that this variant of the unicystic
and are noted to show a plexiform pattern ameloblastoma has a higher rate of persis-
that resembles the plexiform pattern seen tence than do the luminal or intraluminal
B in conventional ameloblastomas. As such, unicystic ameloblastomas.
FIGURE 30-20 A, Treatment of the ameloblas- these tumors are referred to as plexiform The treatment of a luminal or intralu-
toma of the patient in Figure 30-17 required a unicystic ameloblastomas. In the third minal variant of the unicystic ameloblas-
disarticulation resection of the left mandible. B, variant, known as mural unicystic toma is enucleation and curettage (Figure
The effectiveness of the bony linear margin
should always be evaluated by intraoperative
ameloblastoma, the fibrous wall of the cyst 30-23). In a collective sense, the “recur-
specimen radiographs. is infiltrated by typical follicular or plexi- rence” rate of all unicystic ameloblastomas
form ameloblastoma. The extent and
mandible, usually in the molar/ramus depth of the ameloblastic infiltration may
region.71 A unilocular radiolucency, mim- vary considerably.
icking a dentigerous cyst, is the most com- Pathogenetically, the unicystic amelo-
mon radiographic presentation for the blastoma seems to have a proliferative
unicystic ameloblastoma (Figure 30-21). capacity between that of the odontogenic
Most, if not all, unicystic ameloblastomas keratocyst and the solid or multicystic
are unilocular radiolucencies.2 Three ameloblastoma.26
histopathologic variants of unicystic
ameloblastoma have been described that Treatment and Prognosis The clinical and
impact treatment and prognosis. In the radiographic findings in most cases of uni-
FIGURE 30-22 The histopathology of the lesion
luminal unicystic ameloblastoma, the cystic ameloblastoma suggest that the lesion
in Figure 30-21 shows luminal unicystic
tumor is confined to the luminal surface is an odontogenic cyst, most commonly a ameloblastoma (hematoxylin and eosin; original
of the cyst (Figure 30-22). The lesion con- dentigerous cyst. Under the circumstances magnification x40).
ameloblastoma is probably more aggres- (see Figure 30-24) with significant expan-
sive than the luminal and intraluminal sion such that an enucleation and curet-
variants of the unicystic ameloblastoma tage surgery would effectively result in a
owing to the presence of tumor in the cyst resection of the involved jaw.
wall and therefore closer to the surround-
ing bone. It seems logical to approach Peripheral Ameloblastoma The periph-
these tumors with a surgery similar to that eral or extraosseous ameloblastoma is the
for the solid or multicystic ameloblastoma most rare variant of the ameloblastoma.
(Figure 30-24). The final indication for This tumor probably arises from rests of
resection of a unicystic ameloblastoma is dental lamina or the basal epithelial cells
in the management of very large tumors of the surface epithelium and shows the
FIGURE 30-23 A, The luminal unicystic

ameloblastoma in Figure 30-21 is treated with
an enucleation and curettage surgery. B, The A C
5-year postoperative radiograph shows an
acceptable bony fill.
has been reported as 10 to 20% following

enucleation and curettage.70 This is signif-
icantly lower than that of enucleation and
curettage of the solid or multicystic
ameloblastoma. The question then arises
as to when to resect a unicystic ameloblas-
toma. Three instances are likely to require
such treatment. The first is the recurrent
unicystic ameloblastoma. A tumor that
recurs following a well-performed enucle- B D
ation and curettage should probably be
FIGURE 30-24 This 18-year-old presented with significant right facial expansion (A) associated with
approached with the more aggressive
the destructive radiolucency of the right mandible noted on the panoramic radiograph (B). The inci-
resection. Second is the mural ameloblas- sional biopsy documented the mural variant of unicystic ameloblastoma (hematoxylin and eosin;
toma. This variant of the unicystic original magnification ×20) (C). A disarticulation resection was performed (D).
same features of the intraosseous form of Table 30-5 Classification of

the tumor.72 Clinically, these tumors pre- Odontogenic Carcinomas
sent as nonulcerated sessile or peduncu-
Malignant (metastasizing) ameloblastoma
lated gingival lesions (Figure 30-25).
Ameloblastic carcinoma
Most examples are < 1.5 cm and usually
Primary
occur over a wide age range, with an aver-
Dedifferentiated
age reported age of 52 years. Although
Peripheral
these tumors do not infiltrate bone, they
may be seen to “cup out” bone in the jaws Primary intraosseous squamous cell
(Figure 30-26). carcinoma
Solid
Cystogenic
Treatment and Prognosis The peripheral
• Nonkeratinizing cyst
ameloblastoma is most appropriately
• Odontogenic keratocyst
treated with a wide local excision. When
Clear cell odontogenic carcinoma
surgical margins are negative for tumor,
cure is the likely consequence. Malignant Malignant epithelial odontogenic ghost
cell tumor
transformation of a peripheral ameloblas-
Adapted from Eversole LR.74
toma is very rare.73 FIGURE 30-26 A “cupped out” lesion in bone at
tooth no. 4 is noted in the patient in Figure 30-25.
Malignant Odontogenic Tumors organs.76–78 Lung metastases have some-

Malignant odontogenic tumors are very times been regarded as aspiration phe-
rare. They may arise from the epithelial nomena, yet the peripheral location of
many of these deposits supports
components of the odontogenic apparatus.
hematogenous spread. Eversole points out
The rests of Malassez, the reduced enamel
that instances of metastasis have arisen
epithelium surrounding the crown of an
from solid or multicystic ameloblastomas
impacted tooth, the rests of Serres in the
rather than unicystic tumors.74
gingiva, and the linings of odontogenic
cysts represent the precursor cells for
Ameloblastic Carcinoma Ameloblastic
malignant transformation. Odontogenic
carcinomas are malignant epithelial
carcinomas are classified in Table 30-5.74 In
odontogenic tumors that exist in the
general, all of these tumors exhibit typical
background of benign ameloblastomas.
microscopic features of malignancy, with This designation is reserved for an
A the exception of the malignant (metasta-
sizing) ameloblastoma and the clear cell
odontogenic carcinoma. Behaviorally, all of
these tumors have the potential for either
regional nodal or distant metastases.
Malignant (Metastasizing) Ameloblas-

toma Malignant ameloblastomas are
best described as neoplasms that have the
histologic features of benign ameloblas-
B toma as shown by the primary growth in
the jaws and by any metastatic growth.75
FIGURE 30-25 This lesion of the right palatal FIGURE 30-27 Histologically benign ameloblas-
The most common sites of metastatic dis-
mucosa (A) showed peripheral ameloblastoma on toma is noted in the lung. This finding satisfies the
incisional biopsy (hematoxylin and eosin; origi- ease are the lungs (Figure 30-27), followed definition of malignant ameloblastoma (hema-
nal magnification ×40)(B). by the cervical lymph nodes and visceral toxylin and eosin; original magnification ×20).
ameloblastoma that has cytologic features body region. The 5-year survival rate is Malignant Epithelial Odontogenic
of malignancy in the primary tumor (Fig- 30 to 40%.74 Squamous cell carcinomas Ghost Cell Tumor The epithelial odon-
ure 30-28), in a recurrence, or in any may also arise from the linings of odontogenic ghost cell tumor, also known as
metastatic deposit. Although ameloblas- togenic cysts. Cystogenic carcinomas are dentinogenic ghost cell tumor, is the
tic carcinomas have been reported to seen in patients > 50 years of age and solid variant of the calcifying odonto-
metastasize to the lungs and distant typically occur in the mandible. Finally, genic cyst. Both epithelial and ectomes-
organs,79,80 many cases do not metasta- dentigerous cysts can undergo glandular enchymal odontogenic elements are pre-
size. In Corio and colleagues’ series of metaplasia, and there are rare instances sent; however, only the epithelial
eight cases of ameloblastic carcinoma, of central mucoepidermoid carcinomas component shows cytologic features of
rapid growth and pain were common reported to arise from odontogenic malignancy.
symptoms.81 These symptoms are recog- cyst lining.
nized as being uncommon in patients Ameloblastic Fibroma
with benign ameloblastomas. Clear Cell Odontogenic Carcinoma The ameloblastic fibroma is considered to
Although the clear cell odontogenic carci- be a true tumor in which the epithelial
Primary Intraosseous Squamous Cell noma is of putative odontogenic origin, and mesenchymal tissues are both neo-
Carcinoma Squamous cell carcinomas histologic similarities to the developing plastic. This is in distinction to the
that are encountered in the jaws, lack any tooth germ are lacking in many ameloblastic fibro-odontoma and odon-
continuity with the oral or antral instances.74 The differential diagnosis toma that represent developmental stages
mucosa, and occur in the absence of a includes metastasis from a distant site, of the same hamartomatous lesion.82,83
primary carcinoma located elsewhere are especially the kidney. The clear cell variant The ameloblastic fibroma tends to occur
termed primary intraosseous squamous of renal cell carcinoma is the chief entity in young patients in the first two decades
cell carcinomas. These cases are assumed to consider. The clear cell odontogenic of life. The posterior mandible is affected
to arise from odontogenic epithelium. carcinoma is generally seen in elderly in 70% of cases (Figure 30-29). Radi-
They typically occur in elderly patients women, with the maxilla and mandible ographically, either a unilocular or multi-
and tend to occur in the mandibular being affected equally. locular lesion is observed.
A B C
FIGURE 30-28 A, The large destructive radiolucency

of the right mandible was present in a 22-year-old
man who complained of precipitous growth and
pain. The incisional biopsy showed benign solid/mul-
ticystic ameloblastoma. B and C, A segmental resec-
tion was performed. D and E, Final histopathology of
the resection specimen showed ameloblastic carcino-
ma in a background of benign ameloblastoma
(hematoxylin and eosin; original magnification ×20
[D] and ×100 [E]).
D E
30-30). Although recurrence is rare under with an enucleation and curettage surgery
the circumstances, resection should be (Figure 30-32). Recurrence after this
reserved for recurrent lesions. Approxi- approach is very rare. Malignant transfor-
mately 45% of ameloblastic fibrosarcomas mation of ameloblastic fibro-odontoma
develop in the setting of a recurrent has been reported but is exceedingly rare.84
ameloblastic fibroma.2
Odontoma
Ameloblastic Fibro-odontoma Odontomas are the most frequently
The ameloblastic fibro-odontoma, as previ- occurring odontogenic tumors, with
ously discussed, probably represents a prevalence exceeding that of all other
hamartoma. Moreover, some investigators odontogenic tumors combined. As stated
A
believe that this lesion is only a stage in the
development of an odontoma and does not
represent a separate entity. Slootweg points
out that when one considers the data on age,
site, and sex, it seems that the ameloblastic
fibro-odontoma is an immature complex
odontoma.82 As with ameloblastic fibromas,
the ameloblastic fibro-odontoma occurs
more frequently in the posterior regions of
the jaws. This lesion is commonly asympto-
matic and is discovered serendipitously or
B when radiographs are exposed to provide a A
diagnosis for asymmetric eruption of the
FIGURE 30-29 A, A destructive unilocular dentition in children (Figure 30-31). These
radiolucency is present in a 15-year-old boy. B,
lesions are distinctly well circumscribed
Incisional biopsy confirmed ameloblastic
fibroma (hematoxylin and eosin; original and appear as mixed radiopaque/radiolu-
magnification ×40). cent masses.
Treatment and Prognosis The ameloblas- Treatment and Prognosis The ameloblas-
tic fibroma is recognized as an indolent tic fibro-odontoma is treated effectively
tumor that is effectively treated by an enu-
cleation and curettage surgery (Figure B
FIGURE 30-31 A panoramic radiograph of a FIGURE 30-32 A, Enucleation and curettage is

9-year-old boy shows a mixed radiolucent/ performed of the lesion in Figure 30-31. The per-
FIGURE 30-30 An enucleation and curettage radiopaque lesion of the left posterior mandible. manent tooth is removed with the lesion. B and
surgery is performed in the patient in Figure 30- Ameloblastic fibro-odontoma is a likely diagno- C, The histopathology shows ameloblastic fibro-
29. The associated permanent teeth are removed sis owing to the patient’s age as well as the radi- odontoma (hematoxylin and eosin; original
with the tumor. ographic character of the lesion. magnification ×20).
previously, these lesions are generally well

accepted as representing hamartomas.
Odontomas present centrally within the
jaws in one of two forms: compound, in
which multiple small toothlike structures
exist; and complex, in which irregular
masses of dentin and enamel are present
with no anatomic resemblance to a tooth.
Compound odontomas are predominant-
A
ly seen in the anterior maxilla (Figure 30-
33), whereas complex odontomas are typ-
ically seen in the posterior maxilla or
mandible (Figure 30-34).
FIGURE 30-34 A complex odontoma of the left
Treatment and Prognosis Odontomas posterior mandible.
are treated with simple enucleation and
curettage and are not known to recur.
enchyme and histologically resembles the
Odontogenic Myxoma dental papilla of the developing tooth.
The odontogenic myxoma is an uncom- These tumors are slow growing with a
mon benign neoplasm of the jaws that is potential for aggressive behavior and a
thought to be derived from ectomes- high recurrence rate after subtherapeutic B
removal.85 They occur over a wide age
FIGURE 30-35 A large soft tissue mass of the left
range but seem to occur most commonly posterior mandibular gingiva (A) associated
in the third decade of life. Although the with an underlying radiolucent lesion of the
tumor can occur anywhere in the jaws, the mandible (B).
posterior mandible is most common loca-
tion (Figure 30-35). Histologically, the pression of antiapoptotic cytokines BCL2
tumor is composed of haphazardly and BCLX.51
arranged stellate, spindle-shaped, and
round cells in an abundant loose myxoid Treatment and Prognosis Odontogenic
stroma that contains only a few collagen myxomas should be treated with resection
A
fibrils (Figure 30-36). Radiographically, with 1.0 cm bony linear margins as con-
the odontogenic myxoma appears as a firmed with a specimen radiograph (Figure
unilocular or multilocular radiolucency
that may displace or cause root resorption
of teeth in the area of the tumor. Although
not pathognomonic of the odontogenic
myxoma, the radiolucent defect may con-
tain thin wispy trabeculae of residual
bone, which are often arranged at right
angles to one another in a “stepladder”
pattern (see Figures 30-35B and 30-37). In
some patients the tumor may have a
B greater tendency to form collagen fibers;
such lesions are designated fibromyxomas.
FIGURE 30-33 A, An expansile lesion of the
Pathogenetically, the proliferation FIGURE 30-36 The odontogenic myxoma shows
right maxilla. B, Multiple small toothlike calci- a loose myxoid stroma, in this case, eroding into
fied structures are removed that represent com- and aggressive behavior of the odonto- the cementum of a tooth root (hematoxylin and
pound odontoma. genic myxoma may be related to overex- eosin; original magnification ×40).
30-37). These tumors are not encapsulated genic tumor among a collective series of
and tend to infiltrate the surrounding bone 1,440 odontogenic tumors. Fewer than
such that complete removal by curettage is 200 cases have been reported in the inter-
nearly impossible. Resection of the tumor national literature. Although this tumor
with a normal surrounding margin of has been reported over a wide age range,
bone and soft tissue that shows negative it is most often encountered in patients
margins should be curative. between 30 and 50 years of age. 86
Approximately two-thirds of these neo-
Calcifying Epithelial plasms occur in the mandible.87 A pain-
Odontogenic Tumor less slow-growing mass is the most com-
The calcifying epithelial odontogenic mon presenting sign. Radiographically,
tumor, also known as the Pindborg the most common presentation is a A
tumor, is an uncommon lesion that mixed radiopaque/radiolucent lesion,
accounts for < 1% of all odontogenic frequently associated with an impacted
tumors. It is particularly noteworthy that tooth (Figure 30-38).
the three studies depicted in Table 30-4 Histologically, the Pindborg tumor is
reported only 15 cases of this odonto- quite unique. Discrete islands, strands, or
sheets of polyhedral epithelial cells in a
fibrous stroma are noted. Large areas of
amorphous eosinophilic hyalinized
(amyloid-like) material are also present.
Calcifications, which are a distinctive fea-
ture of the tumor, develop within the amy-
loid-like material and form concentric
rings, known as Liesegang rings (Figure B
30-39). The precise nature of the amyloid-
like material is unknown. The material
does stain as amyloid when stained with
Congo red or thioflavine T. After Congo
red staining, the amyloid exhibits apple-
A green birefringence when viewed with
polarized light. It has been illustrated that
the amyloid-like material may actually
represent amelogenins or other enamel
proteins secreted by the tumor cells.88
Treatment and Prognosis Although

C
slow growing, the Pindborg tumor is
highly infiltrative and destructive and is FIGURE 30-38 A 40-year-old woman with a
capable of aggressive behavior.88,89 Owing 5-year history of an expansile mass of the left max-
illa (A). The panoramic radiograph (B) and the
to the small number of reported cases and coronal computed tomography scan (C) show a
B lack of consistent follow-up, evidence- mixed radiolucent/radiopaque lesion of the left pos-
based recommendations for treatment are terior maxilla.
FIGURE 30-37 A, The patient in Figure 30-35
underwent a segmental resection of his odonto- not available. Nonetheless, the tumor is
genic myxoma. B, As with the ameloblastoma, generally recommended to be treated
specimen radiographs should be obtained when identically to the ameloblastoma and ure 30-40). When this treatment was
resecting an odontogenic myxoma to verify the
bony linear margin. A better depiction of the
odontogenic myxoma, with 1.0 cm bony undertaken for Franklin and Pindborg’s
“stepladder” pattern of the odontogenic myxoma linear margins and the appropriate atten- series of tumors, only one patient under-
is noted on this specimen radiograph. tion to soft tissue anatomic barriers (Fig- going resection experienced recurrence.87
patients, and two-thirds of all cases are diag-

nosed in the second decade.92–95 The tumor is
extremely uncommon in patients > 30 years.
It has a predilection for the anterior region
of the jaws and is found twice as often in the
maxilla than in the mandible. Females are
affected about twice as often as males. Most
adenomatoid odontogenic tumors are A
small, rarely exceeding 3 cm in diameter. In
about 75% of cases, the lesion appears as a
FIGURE 30-39 Incisional biopsy of the patient well-circumscribed unilocular radiolucency
in Figure 30-38 shows signs indicative of the that involves the crown of an erupted tooth,
Pindborg tumor including discrete islands of frequently a canine.
odontogenic epithelium, calcification (Liesegang Histologically, the adenomatoid
rings), and hyalinized material suggestive of
amyloid (hematoxylin and eosin; original mag- odontogenic tumor is a well-defined
nification ×40). lesion that is usually surrounded by a
thick fibrous capsule (Figure 30-42).
Adenomatoid When the lesion is bisected, the central B
Odontogenic Tumor portion of the tumor may be essentially
FIGURE 30-42 Incisional biopsy of the lesion in
solid or may show varying degrees of cys- Figure 30-41 shows a well-encapsulated lesion
The adenomatoid odontogenic tumor,
tic change with intraluminal prolifera- (hematoxylin and eosin; original magnification
regarded by many as a hamartoma, is an
tion of tissue. The lesion is composed of ×10) (A) with duct-like structures and rosettes
uncommon odontogenic lesion, accounting (hematoxylin and eosin; original magnification
for 3 to 7% of all odontogenic tumors. This ×40) (B). These findings are indicative of the
lesion was once believed to be a variant of adenomatoid odontogenic tumor
ameloblastoma and was previously desig-
nated adenoameloblastoma.90,91 Its clinical
spindle-shaped epithelial cells that form
features and biologic behavior permit dis-
sheets, strands, or whorled masses of
tinction from the ameloblastoma (Figure
cells in a scant fibrous stroma. The
30-41). These lesions are limited to young
epithelial cells may form rosette-like
structures about a central space that may
be empty or contain small amounts of
A eosinophilic material that may stain for
amyloid.96–98 Tubular or duct-like struc-
tures are characteristic for the adenoma-
toid odontogenic tumor (see Figure 30-
42). These consist of a central space
surrounded by a layer of columnar or
cuboidal epithelial cells whose nuclei
exhibit reverse polarization.
Treatment and Prognosis Owing to this

lesion being encapsulated, it separates eas-
ily from the surrounding bone. As such, an
enucleation and curettage surgery is cura-
B tive (Figure 30-43). Of the 499 cases of
FIGURE 30-41 An expansile lesion of the lingual
adenomatoid odontogenic tumor report-
FIGURE 30-40 The patient with the Pindborg
tumor in Figure 30-38 is treated with hemimax- aspect of the left mandible (A) associated with a ed in the literature, only 1 acceptable case
illectomy. unilocular radiolucency of the left mandible (B). of recurrence has been documented.99
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CHAPTER 30

Odontogenic Cysts and Tumors

Table 30-1 Classification of One diagnostic dilemma for oral and

Adequate diagnosis and treatment of

expression of proliferating cell nuclear 9q22.3-q31. Affected patients (Figure 30-

FIGURE 30-11 Plantar pitting can be observed

rence rate of approximately 30% and

Calcifying Odontogenic Cyst

Odontogenic Tumors Table 30-3 Classification of Odontogenic

Table 30-4 Incidence of Odontogenic Tumors

encountered in patients over a wide age granular eosinophilic cytoplasm; desmo-

FIGURE 30-18 Twenty years of undisturbed

the surgeon should routinely open a “cystic”

FIGURE 30-23 A, The luminal unicystic

has been reported as 10 to 20% following

same features of the intraosseous form of Table 30-5 Classification of

Malignant Odontogenic Tumors organs.76–78 Lung metastases have some-

Malignant (Metastasizing) Ameloblas-

FIGURE 30-28 A, The large destructive radiolucency

FIGURE 30-31 A panoramic radiograph of a FIGURE 30-32 A, Enucleation and curettage is

previously, these lesions are generally well

Treatment and Prognosis Although

patients, and two-thirds of all cases are diag-

Treatment and Prognosis Owing to this

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