RESUMO
This article aims to describe the current status of 3-dimensional (3D) imaging in dental practice. Advances in this field have made 3D imaging far more accessible in all dental fields. This paper describes methods of imaging dental hard and soft tissues and their clinical uses. In addition, the potential advantages and disadvantages of various systems are discussed, as well as expected future developments.
Assuntos
Cefalometria/métodos , Desenho Assistido por Computador , Imageamento Tridimensional/métodos , Radiografia Dentária/métodos , Tomografia Computadorizada de Feixe Cônico/métodos , Tomada de Decisões , Implantação Dentária Endóssea/métodos , Técnica de Moldagem Odontológica , Planejamento de Prótese Dentária , Face/anatomia & histologia , Humanos , Processamento de Imagem Assistida por Computador/métodos , Mandíbula/diagnóstico por imagem , Mandíbula/cirurgia , Modelos Dentários , Procedimentos Cirúrgicos Bucais/métodos , Planejamento de Assistência ao Paciente , Educação de Pacientes como Assunto , Doenças Periodontais/diagnóstico por imagem , Intensificação de Imagem Radiográfica/métodos , Resultado do Tratamento , Interface Usuário-ComputadorRESUMO
Airway inflammation and epithelial remodeling are two key features of asthma. IL-13 and other cytokines produced during T helper type 2 cell-driven allergic inflammation contribute to airway epithelial goblet cell metaplasia and may alter epithelial-mesenchymal signaling, leading to increased subepithelial fibrosis or hyperplasia of smooth muscle. The beneficial effects of corticosteroids in asthma could relate to their ability to directly or indirectly decrease epithelial cell activation by inflammatory cells and cytokines. To identify markers of epithelial cell dysfunction and the effects of corticosteroids on epithelial cells in asthma, we studied airway epithelial cells collected from asthmatic subjects enrolled in a randomized controlled trial of inhaled corticosteroids, from healthy subjects and from smokers (disease control). By using gene expression microarrays, we found that chloride channel, calcium-activated, family member 1 (CLCA1), periostin, and serine peptidase inhibitor, clade B (ovalbumin), member 2 (serpinB2) were up-regulated in asthma but not in smokers. Corticosteroid treatment down-regulated expression of these three genes and markedly up-regulated expression of FK506-binding protein 51 (FKBP51). Whereas high baseline expression of CLCA1, periostin, and serpinB2 was associated with a good clinical response to corticosteroids, high expression of FKBP51 was associated with a poor response. By using airway epithelial cells in culture, we found that IL-13 increased expression of CLCA1, periostin, and serpinB2, an effect that was suppressed by corticosteroids. Corticosteroids also induced expression of FKBP51. Taken together, our findings show that airway epithelial cells in asthma have a distinct activation profile and identify direct and cell-autonomous effects of corticosteroid treatment on airway epithelial cells that relate to treatment responses and can now be the focus of specific mechanistic studies.