RESUMO
Benign fibro-osseous lesions of the maxillofacial skeleton constitute a heterogeneous group of disorders that includes developmental, reactive (dysplastic) and neoplastic lesions. Although their classification has been reviewed multiple times in the past, the most common benign fibro-osseous lesions are fibrous dysplasia, osseous dysplasia and ossifying fibroma. For the dental clinician, the challenges involve diagnosis and treatment (or lack thereof). A careful correlation of all clinical, radiologic and microscopic features is essential to establish a proper diagnosis and a clear treatment plan. This article aimed to review the clinical, radiologic and histopathologic characteristics of benign fibro-osseous lesions of the jaws, with emphasis on their differential diagnoses. With a deeper understanding of benign fibro-osseous lesions, clinicians will be better prepared to manage these lesions in their practice.
Assuntos
Cementoma , Fibroma Ossificante , Displasia Fibrosa Óssea , Neoplasias Maxilomandibulares , Cementoma/diagnóstico , Cementoma/patologia , Cementoma/terapia , Diagnóstico Diferencial , Fibroma Ossificante/diagnóstico , Fibroma Ossificante/patologia , Fibroma Ossificante/terapia , Displasia Fibrosa Óssea/diagnóstico , Displasia Fibrosa Óssea/patologia , Displasia Fibrosa Óssea/terapia , Odontologia Geral , Humanos , Neoplasias Maxilomandibulares/diagnóstico , Neoplasias Maxilomandibulares/patologia , Neoplasias Maxilomandibulares/terapiaRESUMO
Alterations of cell cycle regulatory proteins, especially those that regulate G1 to S transition, have been implicated in the pathogenesis of a wide variety of human tumors. In previous studies we showed that that there is overexpression of cyclin D1 protein predominately in the giant cell component of giant cell tumors of bone. The purpose of this study was to investigate the mechanisms that may be responsible for cyclin D1 accumulation in giant cell tumors. Giant cell tumors have high levels of cyclin D1 mRNA and the giant cell-enriched population of these tumors have significantly more mRNA and protein expression of cyclin D1 than the mononuclear cell population. The giant cells also expressed higher levels of p21 protein and more p21 bound to cyclin D1 than the mononuclear cells. It is possible that p21 may be contributing to the cyclin D1 accumulation that occurs in the giant cells and perhaps even giant cell formation in these tumors. Additional studies are required to confirm the role of p21 in the pathogenesis of these tumors.
