A Case of an Ameloblastic Fibro-Odontoma Arising from a Calcifying Odontogenic Cyst.

Oral Health Science Center, Department of Pathology, Tokyo Dental College, Chiba, Japan.
The Bulletin of Tokyo Dental College 03/2001; 42(1):51-5. DOI: 10.2209/tdcpublication.42.51
Source: PubMed


This case report describes an ameloblastic fibro-odontoma arising from a calcifying odontogenic cyst (COC) in the mandible of a twenty-three-year old male. The patient was referred to the Department of Oral Surgery, Tokyo Dental College, on March 30th, 2000, complaining of a painful swelling, which had appeared three weeks earlier on his left mandibular molar region. In a pathological view, the lesion was a round cyst the size of a chicken-egg, dark red in color, and surrounded by a thick membrane. The cyst had an epithelium of varying thickness which included many ghost cells and an enamel-like structure on the inside, and a thick wall of connective tissue with an ameloblastic fibro-odontoma on the outside. Enamel organ-like epithelial islands were structured radially in the form of strands with immature dentin. Cytokeratin 19 was strongly immunoreactive in the epithelium of the lesion; osteopontin and osteocalcin reacted in the mesenchymal cells and weakly in the epithelial element of this tumor.

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    • "En general, el FOA se caracteriza por ser una lesión asintomática , siendo el principal motivo de consulta un aumento de volumen y retraso en la erupción dentaria, sin embargo, Hu et al., 2005 y Matsuzaka et al., 2001, reportaron casos en los que se presentaba dolor como parte del cuadro clínico 7,9 . "
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    ABSTRACT: Ameloblastic fibro-odontoma (AFO) is an infrequent odontogenic tumor that affects young people of either sex and is usually located in the posterior mandibular zone. Clinically, the patient might present a delay in dental eruption with a painless increase in volume. Radiographically, it is a uni- or multilocular radiolucent lesion of variable size with radiopaque areas. Treatment varies with tumor size and the decision to conserve the adjacent teeth must be weighed carefully due to the possibility of recurrence. The case of a large AFO in a 4-year-old patient is reported. The specific histological and clinical characteristics are described and the conservative therapy and need for long-term postoperative follow-up are discussed.
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    • "They tend to form small clusters or large masses. Although characteristic of calcifying cystic odontogenic tumors (GGoT) [4], ghost cells are also found in other odontogenic lesions namely ameloblastoma [5] odontoma [6] and ameloblastic fibro-odontoma [7], and in nonodontogenic tumors such as pilomatrixoma [8], a tumor with hair matrix cell differentiation, and craniopharyngioma, a tumor of the pituitary gland [9]. Several theories of ghost cell formation have been put forth including that these cells are most likely abnormal keratinized bodies, or they might represent simple cell degeneration or a form of enamel matrix; or might be apoptotic odontogenic cells or represent different stages of normal and abnormal keratin formation resulting from metaplastic transformation of odontogenic tumors [4]. "
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    ABSTRACT: Notch signaling is an evolutionarily conserved mechanism that enables adjacent cells to adopt different fates. Ghost cells (GCs) are anucleate cells with homogeneous pale eosinophilic cytoplasm and very pale to clear central areas (previous nucleus sites). Although GCs are present in a variety of odontogenic lesions notably the calcifying cystic odontogenic tumor (CCOT), their nature and process of formation remains elusive. The aim of this study was to investigate the role of Notch signaling in the cell fate specification of GCs in CCOT. Immunohistochemical staining for four Notch receptors (Notch1, Notch2, Notch3 and Notch4) and three ligands (Jagged1, Jagged2 and Delta1) was performed on archival tissues of five CCOT cases. Level of positivity was quantified as negative (0), mild (+), moderate (2+) and strong (3+). Results revealed that GCs demonstrated overexpression for Notch1 and Jagged1 suggesting that Notch1-Jagged1 signaling might serve as the main transduction mechanism in cell fate decision for GCs in CCOT. Protein localizations were largely membranous and/or cytoplasmic. Mineralized GCs also stained positive implicating that the calcification process might be associated with upregulation of these molecules. The other Notch receptors and ligands were weak to absent in GCs and tumoral epithelium. Stromal endothelium and fibroblasts were stained variably positive.
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