Peripheral ameloblastoma: Case report with immunohistochemical investigation

Peripheral ameloblastoma: Case report with immunohistochemical investigation

YAMAMOTO ET AL 197 J Oral Maxillof ac Surg 48:197-200.1990 Peripheral Ameloblastoma: Case Report With Immunohistochemical Investigation TETSUYA YAM...

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YAMAMOTO ET AL

197

J Oral Maxillof ac Surg 48:197-200.1990

Peripheral Ameloblastoma: Case Report With Immunohistochemical Investigation TETSUYA YAMAMOTO, DDS,· EISAKU UETA, DDS,· KAZUNORI YONEDA, DDS,t AND TOKIO OSAKI, DDS, DMD:f: Ameloblastoma is a common tumor within the odontogenic group of tumors. This tumor usually occurs intraosseously, and relatively seldom appears in the soft tissues of the alveolar process. A few cases of peripheral ameloblastoma have been reported, and its histologic characteristics have been studied in comparison with central ameloblastoma. t, 2 A common histologic pattern of peripheral ameloblastoma appears to be proliferating columnar epithelial cells resembling the tooth germ;' or basal cell carcinoma." The origin of peripheral ameloblastoma has not yet been established. Derivation from odontogenic epithelial rests" or surface epithelium" has been proposed. We report a case of peripheral ameloblastoma that developed on the lingual gingiva in the left mandibular premolar region . Lectin binding and keratins were histochemically investigated in this tumor and compared with the findings in central arneloblastomas and basal cell carcinomas. Report of a Case CLINICAL ASPECTS

A 53-year-old man was referred by his dentist for further examination of a mass on the lingual gingiva in the left mandibular premolar region . The lesion had gradually increased in size over the past 10 years, with no addi tional symptoms. The mass protruded above the gingiva, but had no sharp delineation (Fig 1). The exophytic, somewhat hard tumor measured approximately 2.0 x 1.5 x 1.0 em. The covering mucosa was slightly reddened but not inflamed. The second premolar was displaced in a

FIGURE I. Firm enlargement covered with slightly reddened mucosa is evident on the lingual side of the left mandibular.premolars.

distal direction; however, pulp tests of the teeth of the region revealed no abnormality. Dental radiographs showed alveolar bone resorption around the first premolar, but invasive resorption or enlargement of the periodontal spaces of the involved teeth was not present (Fig 2). A clinical diagnosis of fibrous epulis was made. Under infiltration anesthesia, the lesion was excised and sent for histologic examination. A diagnosis of basal cell carci-

Received from the Department of Oral Surgery, Kochi Medical School, Nankoku-City, Japan. * Staff. t Chief staff. t Professor and Chairman. Address correspondence and reprint requests to Dr Yamamoto : Department of Oral Surgery, Kochi Medical School, Kohasu Oko-cho , Nankoku-City, Kochi Prefecture, Japan . © 1990 American Association of Oral and Maxillofacial Sur-

geons 0278-2391/90/4802-0013$3.00/0

FIGURE 2. Radiograph showing alveolar bone resorption around the first premolar.

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PERIPHERAL AMELOBLASTOMA

-.

malin, and another part was frozen and stored at -70°C for future histochemical examination for keratins. After staining with hematoxylin-eosin stain, the sections were studied microscopically. The overlying mucosal epithelium was parakeratinized and slightly thickened. Below the epithelium, epithelial islands proliferated in dense connnective tissue, but continuity with the overlying epithelium could not be found (Fig 3). The tips of the islands protruded in bud shapes. The outer layers of the islands were composed of columnar and partially cuboidal cells. Stellate cells were scarce in the central areas of the islands, and many epithelial nests were composed of only basaloid cells. In some areas, metaplastic squamous cells .were observed. Nuclei were polarized away from the membrane. Mitotic figures could not be found. The stroma was dense and contained few inflammatory cells. Fibroblast nuclei were ovoid and hyperchromatic, somewhat resembling the fibroblasts of an odontogenic fibroma .

.'

In addition to the present case , four central arneloblastomas and three basal cell carcinomas of the facial region were histochemically examined by methods described elsewhere.I-" Peroxidase-conjugated lectins such as Con A, UEA-I, and SBA were used. For keratins , an indirect immunohi stochemical staining technique, abidin-biotin complex (ABC) method was used ." Characteristics of the antibodies used are listed in Table 1.

...

, , FIGURE 3. Epithelial islands proliferate in relatively dense connective tissue. Outer layers of the islands are composed of basaloid cells which have polarized nuclei, and cuboidal and squamous cells are seen in the inner layers. (Hematoxylin-eosin stain. Original magnification, x 13_ Inset, x 200.)

noma was first made, but peripheral ameloblastoma was the final histologic diagnosis . In order to avoid recurrence, the region was completely curetted, accompanied by wide gingivectomy from canine to the second premolar and extraction of the first premolar. Healing after the operation was good, and no recurrence has been noted. HISTOLOGIC FINDINGS

The extirpated mass was solid, and its cut surface was whitish yellow. A part of the material was fixed in for-

HISTOCHEMICAL INVESTIGATION

Results

Results are shown in Table 2. In all tumors, lectin binding and keratin presence were slightly more remarkable in the inner layers than in the outer layers. However, staining intensity was almost the same in all cases examined. No clear difference could be found in either lectins or keratins among the peripheral and central ameloblastoma and basal cell carcinoma. Regarding tectins, Con A binding was the most prominent (Fig 4). Stains were positive for SBA in all tumors, but slightly weak when compared with Con A. UEA-I also was weak in its staining intensity. Total keratin, although not prominent, was also seen. However, keratins detected

Table 1. Reagents Used in This Study Lectin

Origin

Specific Sugar

Concentration
Con A

Canamlia ensiformis

150

SBA

Glycin max

Glucose Mannose N-acetyl-galactosamine Galactose

UEA-I WGA

Ulex europaeus I Triticum vulgari s

Antibody Polyclonal Total keratin Monoclonal RGE53 RKSE 60

o-t-Fucose N-acetyl-glucosamine

Molecular Weight

Dilution

30 30 30 Source

56,64 KD

1:300

Dakopatts"

45 KD 56.6 KD

1:10

1:10

Bio-Science" Bio-Science

*Dakopatts, Copenhagen, Denmark; Bio-Science, Emmenbriicke.

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YAMAMOTO ET AL

Table 2. Lectin Binding and Keratins in Ameloblastomas and Basal Cell Carcinomas SBA

Con A Case (type) Present case (basal cell) CA-l (follicular) CA-2 (follicular) CA-3 (plexiform) CA-4 (basal cell) BC-l (solid) BC-2 (solid) BC-3 (solid)

Outer

Inner

+ - t

+ - t

+ - t

t

+ - t

Outer

UEA-I Inner

Outer

Inner

+

±

±

t

±

+

±

+

t

t

±

+

±

±

+

--±

--±

+

+

+

t

±

+ - t

±

±

t

+

±

±

+

--::t

±

±

+

+ - t

+

--±

+

- - ±

±

±

:t

+

±-+

±

±

±

±

+

Inner

Outer

RGE53

TK

:t

+ - t

Outer

Inner

NO

RKSE 60 Inner

Outer

+

±

±

±

NO

"Outer" indicates outer layer cells (ameloblasts or basoloid cells), "inner," inner layer cells. Abbreviations and symbols: CA, central ameloblastoma; BC, basal cell carcinoma; -, negative; ±, traceable; +, weak; t, strong.

by monoclonal antibodies were rarely observed. When compared with the outer layers, the inner layer cells of the peripheral ameloblastoma possessed slightly more of the two keratins (Fig 5). Discussion

Peripheral ameloblastoma is extremely rare. Only 55 cases of this tumor have been reported.l'? It has been observed to occur predominantly in males, the mean age being approximately 53 years. The most prevalent site is the mandibular canine-premolar region. Some of these clinical features are contrary to those of central ameloblastoma in which a younger

FIGURE 4. Histochemical staining for Con A binding. Both peripheral ameloblastoma (A) and central ameloblastoma of follicular type (B) bind similarly to the lectin. (Original magnification, x200.)

group is affected and the lesion is usually found in the mandibular molar area. Most peripheral ameloblastomas are firm and exophytic. The overlying mucosa usually is smooth. Radiologic evidence of bone involvement generally can not be seen, but in some cases alveolar bone resorption due to pressure is exhibited.P''? The present case was typical for these features. The histologic appearance of peripheral ameloblastoma is somewhat different from central ameloblastoma.' The most common type of peripheral lesion is acanthomatous and similar to the basal cell carcinoma." Two primary origins for the histogenesis of peripheral ameloblastoma have been proposed.V' Those lesions that are entirely sepa-

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PERIPHERAL AMELOBLASTOMA

FIGURE 5. Reactivity with monoclonal antibody (histochemical staining for RGE53). Inner cells of the islands are weakly positive for this keratin in peripheral ameloblastoma (A), but negative in basal cell carcinoma (8). (Original magnification, x200.)

.' rated from the overlying surface epithelium probably arise from odontogenic remnants.V' However, the origin becomes questionable when continuity between tumor nests and mucosal epithelium is observed.'? Gardner stated that peripheral ameloblastoma and gingival basal cell carcinoma are probably the same." Greer and Hammond'" also mentioned that comparative investigation of ameloblastomas and basal cell carcinomas showed no differential features electromicroscopically between these tumor cells. With the expectation that some differences in keratin formation and lectin binding might exist between peripheral ameloblastoma and cutaneous basal cell carcinomas, we attempted histochemical examinations. However, there were no clear findings that might help distinguish the pathogenesis of peripheral ameloblastoma. References I. Buchner A. Sciubba 11: Peripheral epithelial-odontogenic tumors: A review. Oral Surg 63:688, 1987 2. Toshiyasu Y, Michihiko E, Munetaka A: Peripheral ameloblastoma: Report of two cases. Jpn J Oral MaxiIlofacSurg 33:76, 1987

3. Shiba R, Sakoda S, Yamada N: Peripheral ameloblastoma. J Oral MaxiIlofac Surg 41:460, 1983 4. Simpson HE: Basal cell carcinoma and peripheral ameloblastoma. Oral Surg Oral Med Oral Pathol 38:233, 1974 5. Stanley HR Jr, Krogh HW: Peripheral ameloblastoma. Oral Surg 12:760, 1959 6. Aisenberg MS: Histopathology of ameloblastoma. Oral Surg 6:1111,1953 7. Stoward PJ, Spicer SS, Miller RL: Histochemical reactivity of peanut lectin-horseradish peroxidase conjugate. J Histoehem Cytochern 28:979, 1980 8. Katsuyama T, Speicer SS: Histochemical differentiation of complex carbohydrate with variants of the concanavarin A horseradish peroxidase method. J Histochem Cytochem 26:233, 1978 9. Lee KW, Chin TC, Paul G: Peripheral ameloblastoma. Br J Oral Surg 8:150, 1970 10. Balfour RS, Localzo U, Sulka M: Multicentric peripheral ameloblastoma. J OralSurg 31:535, 1973 11. Richardson JF, Greer RO: Ameloblastoma of mucosal origin. Arch Otolaryngol 100:174, 1974 12. Wesley RK, Borninski ER, Mintz S: Peripheral ameloblastoma: Report of case and review of literature. J Oral Surg 35:670, 1977 13. ViIla HG: A case of ameloblastoma derived from adult oral epithelium. Oral Surg 6:1216, 1953 14. Gardner DG: Peripheral ameloblastoma. Cancer 39:1625, 1977 15. Greer RO, Hammond WS: Extraosseous ameloblastoma: Light microscopic and ultrastructural observations. J Oral Surg 36:553, 1978