APESCASSOCIAÇÃO DE PATOLOGISTAS DO ESTADO DE SANTA CATARINA

REUNIÃO DO MÊS DE JULHOVIDEIRA/TREZE TÍLIAS

CARLOS J SERAPIÃO

APRESENTAÇÃO DO CASO REG. 04-04310LAB. DE PATOLOGIA DO HOSPITAL DONA HELENAJOINVILLE

Apresentação do caso

D.P.P. , masculino, 21 anos, apresentou tumoraçãosaliente na região mentoniana, indolor, de lenta evolução.

RX - imagem cística unilocular envolvendo a coroa dedente incluso, com deslocamento e divergências de raizes.

Tratamento cirúrgico, com excisão da lesão.

DIAGNÓSTICO:

TUMOR ODONTOGÊNCIO ADENOMATÓIDE

Ghosh (1934) - AdamantinomaStefane (1948)- Cisto de desenvolvimentoCourtney (1975) - Tumor adenomatoide odontogênico

Adenomatoid odontogenic tumor: biologic profile based on 499 cases. J Oral Pathol Med 1991 Apr;20(4):149-58 Philipsen HP; Reichart PA; Zhang KH; Nikai H; Yu QX Department of Oral Medicine, Royal Dental College, Aarhus, Denmark.

Topographically, the AOT occurs in peripheral and central variants, the latter further in follicular (with embedded tooth) and extrafollicular (no embedded tooth) types. The AOT is slow growing with few or no symptoms. Tumor growth may cause displacement of teeth rather than root resorption. The follicular AOT mimics a follicular cyst, the extrafollicular a residual or "globulo-maxillary" cyst and the peripheral a gingival fibroma. All variants of AOT show identical histologic features. The central variants account for 97.2%, 73.0% of which are follicular. The follicular variant (M:F ratio 1 to 1.9) is three times as frequent as the extrafollicular. The follicular variant is diagnosed earlier in life (mean age 17 yr) than the extrafollicular (mean age 24 yr). 53.1% of all variants occur within the teens (13-19 yr). Follicular AOT is associated with one embedded tooth in 93.2%. Maxillary permanent canines account for 41.7% and all four canines for 60.1% of AOT-associated embedded teeth. Ranking four among the odontogenic tumors the AOT is not a particularly rare tumor. Conservative surgical excision is the treatment of choice. Documented recurrences have not been reported.

Adenomatoid odontogenic tumor: ultrastructural demonstration of two cell types and amyloid. Cancer 1979 Feb;43(2):505-11 Smith RR; Olson JL; Hutchins GM; Crawley WA; Levin LS

A typical adenomatoid odontogenic tumor removed from a 13-year-old female was studied by light and electron microscopy. The tumor was composed of two types of epithelial cells: Type I cells were cuboidal and occurred in nests or formed ductlike structures and Type II cells were smaller and spindle shaped. The formation of extracellular masses of amyloid was found in association with Type I epithelial cells, and amyloid formation was not observed in association with Type II cells. Results suggest that the lesion is of enamel organ origin, derived from cells of the inner enamel epithelium at the pre-ameloblastic stage, stellate reticulum and stratum intermedium. The origin of this amyloid material is unknown; however, it may be of enamel protein origin which, like amyloid, may have a beta-protein conformation.

Enamel proteins and extracellular matrix molecules are co-localized in the pseudocystic stromal space of adenomatoid odontogenic tumor. J Oral Pathol Med 2000 Nov;29(10):483-90 Murata M; Cheng J; Horino K; Hara K; Shimokawa H; Saku T Department of Pathology, Faculty of Dentistry, Niigata University, Japan.

In order to examine the functional differentiation of tumor cells of adenomatoid odontogenic tumor (AOT) as ameloblasts and to determine the participation of the extracellular matrix (ECM) in the formation of its characteristic histologic architecture, tissue samples from five cases of adenomatoid odontogenic tumor were examined by immunohistochemical staining for enamel proteins and ECM molecules. Amelogenin, enamelin, laminin, heparan sulfate proteoglycan, fibronectin, collagen type IV and type V were immunolocalized within the luminal space and along the inner rim of duct-like structures. Eosinophilic hyaline droplets within the whorled or rosette masses of tumor cells showed basically the same staining pattern as the luminal contents. High columnar tumor cells that formed duct-like structures were immunopositive for amelogenin, while the staining intensity decreased with flattening of the cells, which was a result of luminal growth. The findings suggest that the constituent cells of duct-like structures are differentiated once to ameloblasts but fail to mature further due instead to