RESUMO
Diabetes mellitus is a common and growing global health problem leading to several complications. Among these periodontal diseases are considered as the sixth complication of diabetes mellitus. This article reviews the relationship between diabetes and oral health, particularly focusing on periodontal diseases, dental caries and xerostomia. There is a bidirectional interrelationship between diabetes and periodontal diseases. Periodontitis is more prevalent and severe in patients with diabetes than in normal population. Therapy of periodontal infection contributes to a positive glycaemic control management and enables reduction of the burden of complications of diabetes mellitus. Diabetics have an increased predisposition to the manifestation of oral diseases like candidiasis which is associated with poor glycaemic control and therapeutic dentures. This predisposition also contributes to xerostomia, which may be due to increased glucose levels in oral fluids or immune dysregulation.
Assuntos
Complicações do Diabetes/fisiopatologia , Diabetes Mellitus/fisiopatologia , Doenças da Boca/fisiopatologia , Doenças Periodontais/fisiopatologia , Idoso , Cárie Dentária/fisiopatologia , Humanos , Resistência à Insulina , Pneumopatias/etiologia , Pneumopatias/fisiopatologia , Doenças Periodontais/complicações , Fator de Necrose Tumoral alfa/fisiologiaRESUMO
We describe a general strategy for the identification of functional genes that, when downregulated, result in a selectable phenotype. This strategy is based on expression selection of cDNA fragments that counteract their cognate genes. A cDNA library containing random fragments expressed in human HepG2, A375 and CLS-354 cells was used to identify functional genes whose inhibition conferred resistance to Fas-induced apoptosis. Thirty-five clones were isolated, 28 of which were derived from unknown genes, that tagged 19 individual genes and 7 of which referred to known genes that tagged the apoptosis-related protein (APR)-1, -2 and indoleamine-pyrrole 2,3,-dioxygenase (IDO). The ability of APR-1-, -2- and IDO-derived antisense RNAs to induce resistance to Fas in HepG2, A375 and CLS-354 cells suggested that APR-1, -2 and IDO genes are involved in the machinery of Fas-mediated apoptosis. Our gene discovery strategy provides a generally applicable procedure to identify functional genes that interfere with apoptosis, and may therefore be clinically relevant for tumor therapy.
Assuntos
Apoptose/genética , Biblioteca Gênica , RNA Antissenso/genética , Anticorpos/farmacologia , Células Cultivadas , Expressão Gênica , Humanos , Indolamina-Pirrol 2,3,-Dioxigenase , Interferon gama/farmacologia , Fenótipo , RNA Antissenso/isolamento & purificação , RNA Antissenso/metabolismo , Triptofano Oxigenase/antagonistas & inibidores , Triptofano Oxigenase/genética , Triptofano Oxigenase/metabolismo , Células Tumorais Cultivadas , Receptor fas/efeitos dos fármacos , Receptor fas/imunologiaAssuntos
Fármacos Dermatológicos/uso terapêutico , Ácido Micofenólico/análogos & derivados , Ácido Micofenólico/uso terapêutico , Penfigoide Bolhoso/tratamento farmacológico , Idoso , Fármacos Dermatológicos/administração & dosagem , Fármacos Dermatológicos/efeitos adversos , Feminino , Técnica Direta de Fluorescência para Anticorpo , Técnica Indireta de Fluorescência para Anticorpo , Seguimentos , Humanos , Ácido Micofenólico/administração & dosagem , Ácido Micofenólico/efeitos adversos , Penfigoide Bolhoso/diagnóstico , Penfigoide Bolhoso/patologia , Pele/patologia , Fatores de TempoRESUMO
Porphyria cutanea tarda (PCT) is the most frequent porphyria in humans. The familial type is in contrast to the sporadic type due to an inherited defect of the uroporphyrinogen-II-decarboxylase (URO-D) and both types need additional porphyrinogens to lead to the clinical manifestation of the disease. Various factors such as xenobiotics (i.e. polycyclic aromatic hydrocarbons), alcohol, hormones and viral liver infections (hepatitis B and C) are known to induce porphyria. Cytochrome p450 enzymes play a crucial role in the metabolism of porphyrogens and therefore might have an important influence on the pathogenesis of hepatic porphyrias. Association of CYP1A2 polymorphisms with susceptibility to both types of PCT has already been described in Danish patients. We investigated 65 caucasian patients with PCT in comparison to a healthy control group concerning the tpe of PCT and the cytochrome p4501A1 polymorphisms (m1, m2 and m4) using polymerase chain reaction (PCR) and a restriction fragment length polymorphism. We found an increased incidence of the m4 polymorphism in the familial type of PCT (odds ratio 5.5, P-value 0.01), whereas the m1 and m2 mutations, might be provoked by a higher susceptibility to porphyrogens via the cytochrome p4501A1 m4 polymorphism.