Epizootic ameloblastomas in Chinook salmon (Oncorhynchus tshawytscha) of the northwestern United States.

Abnormal growths were observed on the lips and in the oral cavities of 2- and 3-year-old Chinook salmon (Oncorhynchus tshawytscha) maintained in one freshwater and one saltwater captive fish-rearing facility in the Columbia River (Pacific Northwest). Initially presenting as bilaterally symmetrical, red, irregular plaques on oral mucosal surfaces, the lesions developed progressively into large, disfiguring masses. Of the 502 natural parr collected for captive broodstock, 432 (86%) displayed these tumors, whereas cohort salmon (i.e., same year classes) in these same facilities remained unaffected. Morphologically similar neoplasms were collected occasionally from adult Chinook salmon that had returned to their natal streams. Histologic features of the tumors suggested that they were derived from the portion of dental lamina destined to form tooth root sulci; therefore, these neoplasms were diagnosed as ameloblastomas. The lesions also resembled archived specimens of Chinook salmon oral tumors, which had been described decades earlier. Etiologic investigations performed during the current outbreak included bacteriologic, virologic, genetic, ultrastructural analyses, and cohabitation exposure studies. Results of these efforts did not indicate an obvious genetic basis for this syndrome, attempts to isolate potentially causative viruses or bacteria were negative, and disease transmission to naïve fish was unsuccessful. A few intracytoplasmic hexagonal structures, possibly consistent with viral particles (approximately 100 nm), were observed ultrastructurally in a tumor cell from 1 of 6 specimens submitted for transmission electron microscopy. Although the presence of these particles does not constitute sufficient evidence for causality, an infectious or multifactorial etiology seems plausible.

Human papillomavirus in ameloblastoma.

OBJECTIVE: Ameloblastomas are benign epithelial tumors of odontogenic origin, with a high recurrence rate and local aggressiveness. A few preliminary studies have demonstrated HPV presence mainly in peripheral ameloblastomas. The purpose of this study was to detect HPV-DNA in intraosseous ameloblastomas. METHODS: Eighteen cases of intraosseous ameloblastomas of different histological variants were selected. Immunohistochemistry, CISH, nested-PCR, and INNOLiPA HPV Genotyping v2 were used. RESULTS: The predominant age group was between the third and fourth decades of life. Males were more affected with 61% and females represented 39%. Of the 18 cases, 7 were solid multicystic tumors and 11 were unicystic. Of the histological variants, the plexiform represented 3 (17%) of the 18, 2 (11%) were follicular, 2 (11%) were acanthomatous, and 1 (6%) was desmoplastic. All cases were HPV negative by immunohistochemistry and CISH. HPV-DNA was detected in 6 (33%) of the cases by nested-PCR. HPV 6 was the most frequent genotype in 4 (66%) of the 6. Two cases presented a mixture of HPV 16, 33, and HPV 6, 42 respectively. Four of the unicystic ameloblastomas were HPV positive; of these, all presented koilocytic changes and were associated with dentigerous cysts, whereas only 2 positive cases corresponded to solid ameloblastomas. None of the positive cases were related to recurrence rate. CONCLUSIONS: We may conclude that HPV low and high risk was detected in our sample of intraosseous ameloblastomas. HPV positivity was observed more in the unicystic cases than solid types.

Latent infection with Epstein-Barr virus in odontogenic disorders: comparison among ameloblastoma, dentigerous cyst and odontogenic keratocyst.

In order to investigate the relationship between Epstein-Barr virus (EBV) latent infection and histogenesis of odontogenic disorders, in situ hybridization for EBV-encoded small RNA (EBER) was applied to the paraffin sections of ameloblastoma, dentigerous cyst, and odontogenic keratocyst. Eight cases (15%) of 53 ameloblastomas showed scattered signals for EBER in the parenchymal cells, whereas no reaction of EBER transcript was observed in the non-neoplastic cystic lesions. In the ameloblastoma, the follicular and plexiform types revealed the signals in the nuclei, but cystic, acanthomatous, granular, and basal cell types exhibited no reaction with EBER. The distribution of the signals without monoclonarity indicated that ameloblastoma cells may exclude EBV genomes or inactivate EBER-encoded genes. The results suggested that EBV participates as one of the transforming factors in the occurrence of ameloblastoma.

Demonstration of Epstein-Barr virus in odontogenic and nonodontogenic tumors by the polymerase chain reaction (PCR).

BACKGROUND: Although considerable insight has been gamed into Epstein-Barr virus (EBV) as an important etiologic factor in various tumors, virtually little is known about the relationship between EBV genes and oral tumors. METHOD: Thirty-two cases of nonodontogenic tumor (16 squamous cell carcinomas, 11 salivary gland tumors, 1 malignant lymphoma, 1 spindle cell sarcoma, 1 osteogenic sarcoma, 1 malignant fibrous histiocytoma and 1 verrucous carcinoma), 17 cases of odontogenic tumor (17 ameloblastomas, the most important and common type of odontogenic tumor) and 12 cases of normal oral tissue (8 normal gingival tissues and other oral mucosa) were examined for the presence of EBV-DNA, with primers specific for the BamW, BNRF1, BMLF1, BamC, IR3, BMRF1, EBNA-2A BamhY, and EBNA-2B BamhY region of the EBV genome by the polymerase chain reaction (PCR). RESULTS: Fifty-three percent (17/32) of nonodontogenic tumors, forty-eight percent (8/17) of ameloblastomas, and ninety-two percent (11/12) of normal oral tissues were positive for EBV-DNA. Of the EBV-DNA, BMLF1 demonstrated the strongest reactivity in the nonodontogenic tumors, and BamC demonstrated the strongest reactivity in the ameloblastomas and normal oral mucosae. CONCLUSIONS: Taken into account with the expression of different EBV genes in odontogenic and nonodontogenic tumors, these findings suggest that even though odontogenic tumors and nonodontogenic tumors are relatively unique, the appearance of different EBV genes seems to suggest the complicated roles that the EBV genes play.