RESUMO
Actinomyces-associated lesions in the jaw, such as radicular cyst and osteomyelitis, have been reported by many authors. The lesions are caused by infection from peripheral sites and can be seen to contain Actinomyces druses on pathologic examination. To our knowledge, no previous reports have described Actinomyces-associated calcification in the jaw, although the lesions in the jaw often include druses. We report here a rare case of Actinomyces-associated calcifications in a dentigerous cyst of the mandible.
Assuntos
Actinomicose/diagnóstico , Calcinose/microbiologia , Cisto Dentígero/microbiologia , Doenças Mandibulares/microbiologia , Perda do Osso Alveolar/microbiologia , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Dente Molar/microbiologia , Dente Serotino/microbiologia , Periodontite/microbiologia , Dente Impactado/microbiologiaRESUMO
Ewing sarcoma (ES) is a primary bone malignant neoplasm and is the second most common primary malignancy of the bone found in childhood and adolescence after osteosarcoma. ES has an annual frequency in the population younger than 20 years of approximately 2.9 per million. ES occurs most frequently in the long bones of the extremities and pelvis and very rarely in the jaw. Recently, it was revealed that chromosomal translocation t(11;22)(q24;q12), which fuses the EWS gene on chromosome 22 and the FLI-1 gene on chromosome 11, occurs in most cases of ES. We report here a rare case of mandibular ES in a 10-year-old child with chromosomal translocation t(21;22)(q22;q12) in which the EWS gene is fused with the ERG gene on chromosome 21.
Assuntos
Cromossomos Humanos Par 21/genética , Cromossomos Humanos Par 22/genética , Sarcoma de Ewing/genética , Translocação Genética/genética , Criança , Terapia Combinada , Humanos , Masculino , Neoplasias Mandibulares/genética , Proteínas de Fusão Oncogênica/genética , Sarcoma de Ewing/terapia , Fatores de Transcrição/genéticaRESUMO
In the present study the significance of nuclear/cytoplasmic expression of beta-catenin (CTNNB1) and mutation of the CTNNB1 gene (CTNNB1) in odontogenic tumors was examined. Six ameloblastomas (five follicular ameloblastomas and one plexiform ameloblastoma) and three malignant odontogenic tumors (one metastasizing ameloblastoma, one ameloblastic carcinoma, and one primary intraosseous odontogenic carcinoma) were investigated for CTNNB1 expression and CTNNB1 mutation. Immunohistochemically, all follicular ameloblastomas and one primary intraosseous odontogenic carcinoma exhibited focal and moderate nuclear/cytoplasmic expression of CTNNB1, whereas the plexiform ameloblastoma and the remaining two malignant odontogenic tumors had entirely membranous expression. CTNNB1 mutation at codon 40 of exon 3 was found in one of the six follicular ameloblastomas. The other five follicular ameloblastomas, the plexiform ameloblastoma, and the three malignant odontogenic tumors did not show mutation in exon 3 of CTNNB1. These findings further confirmed that CTNNB1 mutation is not frequent in ameloblastoma and malignant odontogenic tumors, although the abnormality of Wnt signaling may be associated with some of these tumors.