Ameloblastoma 5

7/28/2019 Ameloblastoma 5

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Dentigerous cyst versus unicystic

ameloblastoma differential diagnosis

in routine histology

Anton Dunsche1

Ortwin Babendererde1

Jutta Luttges2

Ingo N. G. Springer1

1Department of Oral and

Maxillofacial Surgery, and2Department of Pathology,

University of Kiel,D-24105 Kiel, Germany

Correspondence to:

Dr I. Springer

Department of Oral and Maxillofacial Surgery,University of Kiel,

Arnold-Heller-Street 16,

D-24105 Kiel, Germany

Tel.: 49431 5972783

Fax: 49431 5972950

e-mail: [email protected]

Accepted for publication January 15, 2003

Copyright Blackwell Munksgaard 2003

J Oral Pathol Med . ISSN 0904-2512

Printed in Denmark . All rights reserved

Abstract

Background: Unicystic ameloblastomas (UAs) and dentiger-

ous cysts (DCs) have an identical clinical and radiographic

appearance. Some subtypes of UAs have a better prognosis

than solid or multicystic ameloblastomas, and simple enu-

cleation is the adequate treatment. The present study was

designed to test the hypothesis that UAs with small islands of

ameloblastomatous epithelium may be misdiagnosed as aDC or keratocyst if no more than two histologic sections are

examined.

Methods: A total of 101 resection specimens from 22 women

and 73 men (mean age: 46.5 years) were selected, all showing

the clinical and radiographic features of a DC. Only cysts with a

minimum diameter of 15 mm in the panoramic X-ray were con-

sidered for the present investigation. The histopathologic diag-

nosis had been routinely established by examining two sections.

For our study, the specimens were investigated by step sections

at 50 mm and by staining of 5mm thin sections with hematoxylin

and eosin (H&E) at 1 mm levels. An average of 15 slides were

evaluated per case.

Results: Microscopic examination of the step sections did not

reveal ameloblastomatous epithelium in the cyst lining epithe-

lium of the 101 cases. Thus, every primary diagnosis of a

dentigerous cyst was conrmed. In four cases, additional rather

large odentogenic cell nests were detected with palisading of

basaloid cells, while there was a lack of other signs of amelo-

blastic differentiation. All lesions were completely resected, and

no additional treatment was performed.

Conclusions: Step sectioning of larger DCs may reveal asso-

ciated odontogenic cell nests in some cases but does not lead

to the detection of formerly missed ameloblastic cells. Thus,

unicystic ameloblastomas are not misdiagnosed if only two

slides are prepared for routine diagnosis of DCs.

Key words: dentigerous cyst; odontogenic; unicystic ameloblas-toma

J Oral Pathol Med 2003: 32: 48691

An inltrative (solid or multicystic) ameloblastoma is a benign

epithelial tumor of odontogenic origin showing a strong tendency

to recurrence and local aggression (1). Intraosseus, inltrative,

peripheral, desmoplastic, or unicystic ameloblastomas are other

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subtypes of ameloblastoma (26). Unicystic ameloblastoma (UA)

is a prognostically distinct entity (4). It has a recurrence rate of

6.735.7%, and the average interval to recurrence is approximately

7 years (7).

The term `unicystic ameloblastoma' was adopted in the second

edition of the international histologic classication of odon-

togenic tumors (8). Other terms not generally used today are`mural ameloblastoma' (9) and `cystic ameloblastoma' (10). UAs

represent 522% of all ameloblastomas (5, 6). The tumor is

primarily observed during the second and third decades of

life; its preferential location is the mandible, and it can occur

inside dentigerous cysts (DCs; 2, 5, 6, 9). In most cases, UAs

are associated with tooth impaction, the mandibular third molar

being most often involved (6). There are four subtypes of UA

(2, 5, 6, 8, 11):

1. A single cystic sac lined by ameloblastomatous epithelium,

which may often be seen in focal areas (minimum criterion for

diagnosing a lesion as UA);

2. features of subtype 1 plus intraluminal proliferations;

3. features of subtype 1 plus both intraluminal and intramural

proliferations; and

4. features of subtype 1 plus intramural proliferations.

Enucleation is sufcient for tumors that have proliferated into

the lumen (types 1 and 2), whereas subtypes involving the

periphery of the brous connective tissue wall of the cyst (types

3 and 4) must be treated radically, i.e. like a solid or multicystic

ameloblastoma (2, 47, 10, 1218).

UAs and DCs are known to have a similar clinical and radio-

graphic appearance. It appears to be more difcult to differentiate

them in cases of dentigerous UAs (associated with an impacted

tooth) than in cases of non-dentigerous UAs (not associated with

an impacted tooth) (4, 7, 1921). UAs that are not associated with

an impacted tooth may mimic a residual cyst or a keratocyst (6).

In the Department of Pathology, University of Kiel, two sections

are routinely examined in case of a cystic lesion with the clinical

and radiologic features of a DC. Considering the need for exten-

sive surgical procedures in cases of type 3 and 4 UAs, we thought

it advisable to evaluate the reliability of current concepts in

routine histology. In the past, other authors had suggested thatin cases of small islands of ameloblastomatous epithelium within

the cystic epithelium of a lesion, it might be necessary to examine

the entire specimen to be sure of nding these islands (5, 6, 22).

Accordingly, we hypothesized that there was a chance that

the presence of ameloblastomatous changes in the epithelial

cyst lining may be overlooked if cysts that present like DCs

clinically are examined by preparing only two sections for routine

histology.

Patients and methods

All cystic lesions of the mandibular third molar region treated in

the Department of Oral and Maxillofacial Surgery of the Univer-

sity of Kiel, Germany, during a period of 10 years (198594) were

evaluated for the present study. All 101 lesions (95 patients)selected for the study had the typical radiographic appearance

of a DC. Therefore, only unilocular and no multilocular lesions, as

seen in the panoramic X-ray, were included. The resection speci-

mens were macroscopically bisected at their largest diameter and

embedded in parafn. A routine histologic evaluation of two slides

of the cystic lesions had conrmed the diagnosis in all cases prior

to the present study. Two sections were routinely prepared from

the parafn blocks at two different levels, one section cut from a

supercial portion of the block and one from a deeper portion

usually at 100 mm depth. Serial sectioning was only performed

during routine histology if any peculiarities were observed, such

as abnormalities of the cyst lining epithelium or a high cellularity

of the connective tissue that surrounded the cysts. All parafn

blocks were stored after routine histology and were available for

the present study.

Figure 1 shows the age distribution of 115 patients with a DC

diagnosed by panoramic X-ray and routine histology. Only 95

patients were included in the study because the parafn blocks

from 20 patients were not suitable for serial sectioning. The

maximum diameter of the cystic lesions was measured in panora-

mic radiographs and documented (Fig. 2). Cysts with a diameter

of 15 mm (approximately 10.7 mm actual diameter) or more

measured in the panoramic radiograph were included (see Dis-

cussion). In our department, a magnication of 1.4 is standard for

panoramic X-rays andmay be used to estimate the actualdiameter

of a lesion. A minimum of 15 mm was selected as a cut-off point to

exclude lesions that were unlikely to represent UAs (e.g. eruption

cysts). Ninety-ve patients, 22 females (23.2%) and 73 males

(76.8%), with 101 DCs met our criteria. The patients had a mean

age of 46.5 years (range 1182years; SD 16.8 years).

For microscopic examination, step sections were prepared, i.e.

the parafn block was completely cut into 10 mm thick sectionssaving every ftieth slide, which was cut to 5 mm and stained with

hematoxylin and eosin. This technique resulted in at least one

histologic slide per millimeter. Microscopic magnications used

were 62.5156.25. The thickness of the epithelium was evalu-

ated. Increased epithelial thickness was dened as more than six

layers. The presence of intramural islands of ameloblastoma

tissue, odontogenic cell nests with ameloblastomatous differ-

entiation and also lymphocytic inltration were evaluated. In

J Oral Pathol Med 32: 48691 487

Dentigerous cyst versus unicystic ameloblastoma


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particular, the criteria proposed by Vickers and Gorlin as indica-

tive of the development of an ameloblastoma were strictly fol-

lowed (23):

1. Basal cell palisading;

2. basal cell hyperchromatism;

3. polarization of the basal cell nuclei; and

4. vacuolation of the basal cell cytoplasm.

Results

Forty-one per cent of all cysts analyzed in this study were in

patients 4059 years of age (Fig. 1). Fifty-eight (57.4%) of the DCs

were localized in the left mandible and 43 (42.6%) in the right

mandible. The difference is not statistically signicant.

The diameters measured in the panoramic radiograph varied

from 15 mm (c. 10.7 mm calculated actual diameter) to 66 mm (c.

47.1 mm calculated actual diameter). As measured on the radio-

graph, 61 cysts (60.4%) were between 15 and 29 mm (c. 10.7

20.7 mm calculated actual diameter) in size. The average diameter

measured on the radiograph was 31.12 mm (SD 13.71 mm,

n 101); the minimum diameter was 15 mm; and the maximum

diameter was 113 mm.

Odontogenic cell nests with palisading of basaloid appearing

cells, but lacking other signs of ameloblastomatous differentia-

tion, were found within the cystic wall in four patients (two males

26 and 52 years of age and two females both 37years of age;

Fig. 3). In none of these patients, the tooth was displaced by the

cyst. The cysts were of average size, as measured on the radio-

graph. The two sections prepared for routine histology prior to

the present study did not dissect these palisading cells in any of

the four cases. A papillary proliferation of metaplastic squamousepithelium was found in one case after serial sectioning of the

specimen (Fig. 4), which was not detectable in the two routine

histologic slides.

In 17 cases (16.8%), no lymphocytes were found; 56 (55.4%)

showed minor inammatory inltrates, 22 (21.8%) moderate

inammatory inltrates, and 6 (5.9%) dense inammatory inl-

trates. Forty-seven (46.5%) of the DCs showed deposits of cho-

lesterol crystals. The epithelial lining appeared regular in 65 cases

Fig.1. Age distribution of patients with dentigerous cysts. Please compare to the age distribution observed in other studies (39, 40). In the present

study, DCsprimarilyoccurred between the ages of 40 and59 years. This is contrary to other studies showing that DCs primarilyoccur between the ages

of2039 years. We suppose that this isbecause of the fact that a minimum size of 15mm was required for entry into this study. The age was not regarded

as a prerequisite for entry into the study as cystic ameloblastomas occur preferably at younger age but, nevertheless, within a wide age range (29). This

gure refers to 115 patients, although 95 were examined in the study. The reason for this discrepancy is that the parafn blocks from 20 of the patients

were not suitable for serial sectioning.

Fig.2. Measurement of the diameter of the cystic lesions. Cysts with a

diameter of 15 mm or more measured in the panoramic radiograph were

included. Ninety-ve patients, 22 females (23.2%) and 73 males (76.8%),

with 101 DCs met our criteria.

488 J Oral Pathol Med 32: 48691

Dunsche et al.


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(64.4%), but the cells proliferated and the layer was thickened in

36 DCs (35.6%). The epithelium of six cysts showed elongated rete

ridges. No ameloblastomatous epithelium in the lining epithelium

of these cysts was found. In six cases, basal cell palisading was

observed, but no keratinization. Otherwise, none of the Vickers

and Gorlin criteria described in the Patients and methods section

were observed (23).

Discussion

Various contradictory theories about the development of UAs

have been proposed. While some authors suggest that UAs

develop by cystic degeneration of solid ameloblastomas, there

are certain indications that UAs may develop by mural and/orluminal ameloblastomatous change in a pre-existing cyst (1, 5, 10,

2427). It has also been shown that in UAs a coexistence of non-

neoplastic epithelium and neoplastic epithelium is possible (28).

Cystic and solid ameloblastomas are supposed to occur at a

mean age of 36 years (24, 29). UAs are thought to occur primarily

in the second and third decade of life (24). To nd denite values,

prospective studies were proposed (30). As no such prospective

study has been performed yet, we included all lesions that were

formerly diagnosed as DC in our department. The age of the

patients was disregarded, to be sure not to miss a unicystic

ameloblastoma in patients of higher age. In this context, the

minimum diameter of 15 mm measured on the panoramic X-ray

as a prerequisite for entrance into the study needs to be dis-

cussed. We suggest that two representative sections of a small

lesion are more likely to uncover small islands of proliferative

tissue in the rst place. Based on our clinical experience, we felt

that the larger the lesion the higher is the probability of aggres-

sive behaviour. Other authors found that the radiolucent area in

the panoramic X-ray tends to be smaller in cases of dentigerous

cysts than in cases of ameloblastoma (31).

All lesions studied had the typical clinical and radiographic

appearance of DCs. Only unilocular lesions were included in this

study. UAs and DCs are supposed to have a similar clinical and

radiographic appearance (4, 1921). Moreover, the histologic

distinction between UAs and certain non-neoplastic odontogenic

cysts can be difcult (20). It has been suggested that six radio-

graphic patterns for UA can be identied ranging from well-

dened unilocular to multilocular (32). This study aimed at

detecting originally misdiagnosed UAs in a group of patients with

inconspicuous radiograph and uneventful histology. Prior to this

study, all 101 cystic lesions had been diagnosedas DCs by routine

histology using two elective sections. The intraluminal epithelialproliferation in plexiform UA may closely resemble hyperplastic

odontogenic epithelium (33). In the present study, hyperplastic

odontogenic epithelium with more than six layers lined the cysts

in 35.6% of all cases. However, no signs of ameloblastomatous

differentiation were present. Also, no dysplasia was observed, and

hence these lesions were simply classied as benign DCs.

Many attempts have been made to establish specic immu-

nohistochemical markers for ameloblastomas (20, 3437). For

Fig.4. Papillary proliferation of metaplastic squamous epithelium. A

papillary proliferation of metaplastic squamous epithelium (P) is seen

in this specimen. The two sections prepared for routine histology had not

dissected this lesion. Epithelial lining of the cyst (arrow), brous capsule

of thecyst (F). This picture illustrates ourhypothesis. If this specimen was

cut along the two lines (L), this proliferation of metaplastic epithelium (P)

would not be visible. Microscopic magnication: 100.

Fig.3. Large odentogenic cell nest exhibiting some palisading of the

outer cell layer (left side, large arrow) but without clear ameloblastic

differentiation (A). This nding did not become apparent in the course of

routine histology. While this nding does not have clinical consequences,

it demonstrates that two elective sections may miss certain histologic

elements in some cases. Microscopic magnication: 250.




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example, it has been suggested that differences in the expression

of cell surface carbohydrates with blood group specicity may

distinguish ameloblastomas from odontogenic cysts (34),although

this hypothesis was not conrmed by other authors (33). Another

approach aimed at the evaluation of proliferating cell nuclear

antigen (PCNA) in the cystic tumor lining of UA and found

signicantly more PCNA-positive cells in UA than in dentigerouscyst linings (37). Recently, it has been suggested that calretinin is

a specic immunohistochemical marker for neoplastic ameloblas-

tic epithelium and may serve as a diagnostic tool for differentiat-

ing cystic odontogenic lesions from ameloblastic tumors (20).

However, up to date, no general recommendations exist.

Odontogenic cell nests are a frequent nding in the connective

tissue that is associated with odontogenic cysts (38). Some of

them may show palisading of basaloid cells located at the outer

circumference while other signs of true ameloblastic differentia-

tion are lacking, such as basal cell hyperchromatism, polarization

of the basal cell nuclei, or vacuolation of the basal cell cytoplasm

(23). In our study, extensive step sectioning revealed rather large

odontogenic cell nests in four out of 101 cases (3.96%). They,

however, lacked further criteria of ameloblastic differentiation. As

these cell nests were in the close vicinity of the cysts and did not

reach the margins of the specimens, it could be assumed that they

were completely resected. In particular, as there was no true

ameloblastic differentiation, the patients were not treated further

and special follow-up was not thought to be required. We suggest

that at present a histologic examination is the most sensitive tool

for differentiating between odontogenic cysts and UAs. However,

both clinical and radiologic ndings contribute to the diagnosis.

Based on a series of 33 cases of the dentigerous variant of UA, it

was suggested that the involved tooth crown is displaced by the

cystic tumor rather than being projected into the cyst lumen (7).

Because certain types of UA require radical resection (2, 46,

10, 1214), we saw a need to test the reliability of the current

practices in routine histology. Our results showed that step

sectioning of 101 specimens failed to reveal any case of UA not

detected with conventional methods. Therefore, we suggest that

step sectioning will not improve the reliability of the differential

diagnosis of UA versus DC signicantly. In future, the use ofspecic immunohistochemical markers for UA might be a valu-

able tool in the differential diagnosis of DC versus UA (20, 3335).

After all, if only two sections are examined in cases of cystic

lesions that appear to be DCs, certain minor ndings might be

missed, as demonstrated in this study: one case with papillary

proliferation of metaplastic squamous epithelium (Fig. 4) and four

cases with odontogenic islands within the cystic wall (Fig. 3).

None of these ndings were visible in the two elective sections

examined in the course of routine histology; however, none of

these ndings would have had an impact on the prognosis or the

course of therapy.

The patients included in this study were between 11 and

82 years of age (mean 46.5 years, SD 16.8 years). This differs

from the data of other authors, who have reported that DCs

occurred primarily between the ages of 20 and 39 years (39, 40;Fig. 1). We suggest that this may be because of the fact that a

minimum size of 15 mm was required for entry into our study.

In cases of both DC and UA, inammatory inltrates are a

common nding, whereas conventional ameloblastomas rarely

develop inammatory inltrates (25). In our study, 68.3% of all

cystic lesions showed inammatory inltrates. These consisted of

a small number of lymphocytes and a few plasma cells, but did not

lead to clinical symptoms. Inammation is not a feature of DCs,

but it frequently occurs when there is a connection to the oral

cavity, which then leads to secondary inammation.

According to our results, the examination of two sections of

cystic lesions with the clinical and radiographic appearance of a

DC seems to be appropriate because no unicystic amleoblastomas

have been misdiagnosed.

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Acknowledgements

We gratefully acknowledge the nancial support of the Department of Oral

and Maxillofacial Surgery and the Department of Pathology of the Uni-

versity of Kiel. We would like to thank Prof. Dr. F. Harle for his constant

support to our work.



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