RESUMO
The complexity of oral ulcerations poses considerable diagnostic and therapeutic challenges to oral specialists. The expert consensus was conducted to summarize the diagnostic work-up for difficult and complicated oral ulcers, based on factors such as detailed clinical medical history inquiry, histopathological examination, and ulceration-related systemic diseases screening. Not only it can provide a standardized procedure of oral ulceration, but also it can improve the diagnostic efficiency, in order to avoid misdiagnosis and missed diagnosis.
Assuntos
Humanos , Consenso , Úlceras Orais/terapiaRESUMO
OBJECTIVE: This study aimed to investigate the mechanism of cyclic stretch that promotesthe osteogenic differentiation of human periodontal ligament cells (hPDLCs) through the mediation of extracellular-signal-regulated kinase 1/2 (ERK1/2). METHODS: hPDLCs were isolated through the explant method and cultured in vitro. hPDLCs were mechanically stimulated by a multi-channel cell-stress-loading system for 1, 3, 6, 12, and 24 h. The magnitude of stretch was 10% deformation, and the frequency was 0.5 Hz. Nonloaded cells were used as control group. ERK1/2 activation was blocked by U0126, a specific ERK1/2 pathway inhibitor. Additionally, hPDLCs were transfected with adenoviral vector encoding dominant negative ERK1/2 (DN-ERK1/2) to continuouslyinhibit ERK1/2 activation. The mRNA and protein levels of target geneswere detected through real-time polymerase chain reaction and Western blot. RESULTS: Cyclic stretching promoted the expression of ERK1/2, osteocalcin (OCN) mRNA, and bone sialoprotein (BSP) mRNA. The expression of runt-related transcription factor (Runx) 2 protein and mRNA also increased at 3 and 6 h of cyclic stretching. The inhibition of ERK1/2 by U0126 and DN-ERK1/2 suppressed the expressionof Runx2 mRNA, OCN mRNA, BSP mRNA, Runx 2 protein, and p-ERK1/2 protein relative to that in stretched cells without the ERK1/2 inhibitor. CONCLUSIONS: ERK1/2 is a critical molecule in the mediation ofthe osteogenic differentiation of hPDLCs under mechanical stimulation. ERK1/2 activation induced the elevation of Runx2 protein levels, which may be involved in the stretch-induced expressions of OCN and BSP.
Assuntos
Diferenciação Celular , Osteogênese , Ligamento Periodontal , Células Cultivadas , Subunidade alfa 1 de Fator de Ligação ao Core/metabolismo , Humanos , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Ligamento Periodontal/metabolismoRESUMO
<p><b>OBJECTIVE</b>To detect the effects of human interleukin-1beta (IL-1beta) and Dexamethasone (DEX) on the expression level of keratinocyte growth factor (KGF) in cultured human fibroblasts of normal oral and oral lichen planus (OLP) mucosa.</p><p><b>METHODS</b>Three concentration gradients of IL-1beta and DEX were added to cultured fibroblasts of human normal oral and OLP mucosa respectively. 72 hours later, the supernatant was harvested for the detection of KGF concentration with enzyme linked immunosorbent assay (ELISA). Total RNA of the fibroblasts was extracted and reverse transcribed. The resulting cDNA was then amplified by polymerase chain reaction (PCR) to detect the KGF mRNA.</p><p><b>RESULTS</b>The results of the ELISA and PCR showed that the expression levels of KGF protein and mRNA were higher if the cells were treated with IL-1beta. However, the expression levels of KGF protein and mRNA were significantly reduced if the fibroblasts were treated with DEX.</p><p><b>CONCLUSION</b>IL-1beta can promote KGF expression levels of cultured normal oral and OLP fibroblasts, and it is concentration-dependent. While DEX can inhibit KGF expression of cultured normal oral and OLP fibroblasts, and it is also concentration-dependent.</p>
Assuntos
Humanos , Células Cultivadas , Dexametasona , Fator 7 de Crescimento de Fibroblastos , Fibroblastos , Interleucina-1beta , RNA MensageiroRESUMO
<p><b>OBJECTIVE</b>This study aimed at investigating effects of exogenous interleukine-10 (IL-10) on IL-6 and intercellular adhesion molecular (ICAM-1) expression in inflamed gingival tissue.</p><p><b>METHODS</b>The expression of IL-6 and ICAM-1 was examined using immunohistochemical techniques. Inflammatory gingival tissue treated with IL-10 was taken as the experimental group and the same patient's inflammatory gingival tissue without treatment of IL-10 was included into the control group.</p><p><b>RESULTS</b>IL-6 expression was found mainly in monocytes, macrophages, lymphocytes, endotheliocytes and fibroblasts. The expression of ICAM-1 was found mainly in epithelial cells, monocot-macrophages, lymphocytes, endotheliocytes and fibroblasts. The immunohistochemical optical density (IOD) of the expression of IL-6 and ICAM-1 was detected by using Image-Proplus software, and the results showed that the expression in the experimental group differed significantly from that in the control group.</p><p><b>CONCLUSION</b>The exogenous IL-10 may down-regulate IL-6 and ICAM-1 expression in inflammatory gingival tissue.</p>
Assuntos
Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Regulação para Baixo , Gengiva , Metabolismo , Gengivite , Metabolismo , Molécula 1 de Adesão Intercelular , Genética , Interleucina-10 , Farmacologia , Interleucina-6 , GenéticaRESUMO
Objective:To find the influence of the immuno-suppressive drug on the incidence and genotype of oral Candida albicans.Methods:51 patients using immuno-suppressive drug for 1 to 3 months were enrolled,the controls were 26 health subjects.Oral rinse samples from the patients and the controls were assessed for the growth of yeast.The liquid samples were plated on CHROMagar Candida.The isolates were defined to the species level and the genotypic subgroups by PCR method.PCR results were proved by sequencing.Results:The incidence of Candida albican in the patients and controls was 20% and 7.69% respectively.The genotype of the Candida albican in the controls is A subgroup,that in the patients included A,B and C subgroups.Conclusion:Long term of immuno-suppressive drug use can influence the genotype and incidence of oral Candida albican.