RESUMO
Rheumatoid arthritis (RA) and periodontitis (PD) are chronic inflammatory disorders that cause bone loss. PD tends to be more prevalent and severe in RA patients. Previous experimental studies demonstrated that RA triggers alveolar bone loss similarly to PD. The aim of this study was to investigate if arthritis-induced alveolar bone loss is associated with modification in the oral microbiota. Checkerboard DNA-DNA hybridization was employed to analyze forty oral bacterial species in 3 groups of C57BL/6 mice: control (n = 12; without any challenge); Y4 (n = 8; received oral inoculation of Aggregatibacter Actinomycetemcomitans strain FDC Y4) and AIA group (n = 12; chronic antigen-induced arthritis). The results showed that AIA and Y4 group exhibited similar patterns of bone loss. The AIA group exhibited higher counts of most bacterial species analyzed with predominance of Gram-negative species similarly to infection-induced PD. Prevotella nigrescens and Treponema denticola were detected only in the Y4 group whereas Campylobacter showae, Streptococcus mitis and Streptococcus oralis were only found in the AIA group. Counts of Parvimonas micra, Selenomonas Noxia and Veillonella parvula were greater in the AIA group whereas Actinomyces viscosus and Neisseira mucosa were in large proportion in Y4 group. In conclusion, AIA is associated with changes in the composition of the oral microbiota, which might account for the alveolar bone loss observed in AIA mice.
Assuntos
Perda do Osso Alveolar/microbiologia , Processo Alveolar/microbiologia , Artrite Experimental/microbiologia , Maxila/microbiologia , Microbiota/genética , Periodontite/microbiologia , Aggregatibacter actinomycetemcomitans/classificação , Aggregatibacter actinomycetemcomitans/genética , Aggregatibacter actinomycetemcomitans/isolamento & purificação , Perda do Osso Alveolar/patologia , Processo Alveolar/patologia , Animais , Artrite Experimental/patologia , Campylobacter/classificação , Campylobacter/genética , Campylobacter/isolamento & purificação , DNA Bacteriano/genética , Humanos , Masculino , Maxila/patologia , Camundongos , Camundongos Endogâmicos C57BL , Boca/microbiologia , Boca/patologia , Periodontite/patologia , Prevotella nigrescens/classificação , Prevotella nigrescens/genética , Prevotella nigrescens/isolamento & purificação , Streptococcus mitis/classificação , Streptococcus mitis/genética , Streptococcus mitis/isolamento & purificação , Streptococcus oralis/classificação , Streptococcus oralis/genética , Streptococcus oralis/isolamento & purificação , Treponema denticola/classificação , Treponema denticola/genética , Treponema denticola/isolamento & purificaçãoRESUMO
INTRODUCTION: Periodontal disease (PD) is one of the most common inflammatory diseases, affecting about 10 % of the world population. The establishment of PD is influenced by polymorphisms in genes involved with the inflammatory response. Signal Transducer and Activator of Transcription (STAT)-1 is a transcription factor that plays a key role in the intracellular signaling triggered by cytokines and, thus, its activation is critical in inflammatory diseases. AIM AND METHODS: We aim to evaluate the occurrence of association between STAT-1 (rs3771300) polymorphism and distinct clinical forms and severity of PD; we genotyped 180 subjects using realtime PCR. RESULTS AND CONCLUSION: We observed that the presence of the G allele for STAT-1 was associated with twice as high of a chance to develop aggressive periodontitis, and the most severe form of the disease.
Assuntos
Periodontite Agressiva/genética , Periodontite Crônica/genética , Fator de Transcrição STAT1/genética , Adolescente , Adulto , Idoso , Periodontite Agressiva/epidemiologia , Brasil/epidemiologia , Estudos de Casos e Controles , Periodontite Crônica/epidemiologia , Feminino , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , Polimorfismo Genético , Índice de Gravidade de Doença , Adulto JovemRESUMO
Periodontitis is an inflammatory disorder characterized by interactions between periodontal pathogens and host's immune response. Epigenetic may contribute to disease development and outcome by influencing the expression of genes involved in the immune response. It has been shown that Toll-like receptors (TLR) play an important role in the response to periodontopathic bacteria. The aim of study was to evaluate the methylation status and the expression of TLR2 gene in gingival samples from individuals with and without periodontitis. DNA was analyzed using the Methyl Profiler DNA Methylation qPCR assay. DNA methylation and transcript levels were evaluated by real-time polymerase chain reaction. The periodontitis group showed a hypermethylated profile and a low expression of gene. Positive correlation between the TLR2 methylation frequency and probing depth was observed. This study gives the first evidence of methylation frequency in inflamed periodontal tissues and of the possible participation of methylation in the development of periodontitis.
Assuntos
Periodontite Crônica/genética , Metilação de DNA , Receptor 2 Toll-Like/genética , Adulto , Epigênese Genética , Feminino , Gengiva/metabolismo , Humanos , Masculino , Pessoa de Meia-Idade , Transcrição GênicaRESUMO
The IL23/Th17 axis plays an important role in the pathogenesis of cell-mediated tissue damage caused either by autoimmunity or immune responses against bacterial infection. Single nucleotide polymorphisms in the IL17A, IL17F and IL23R genes have been associated with several inflammatory diseases. However, these polymorphisms have not yet been studied in periodontitis. The aim of present study was to evaluate the expression of IL17A and occurrence of the IL17A (rs2275913), IL17F (rs763780) and IL23R (rs11209026) gene polymorphisms in different clinical forms or severity of periodontitis in a sample of Brazilian individuals. Peripheral blood was obtained from 30 non-smoker individuals and analyzed by flow cytometry to determine IL-17 expression. Genomic DNA was obtained from oral swabs in 180 individuals and analyzed by Real-time PCR. The study group was composed by individuals without periodontitis (control), with aggressive periodontitis (AP) and with chronic periodontitis (CP). Higher frequency of IL17A+CD4+ T cells was observed in control group. The A+ genotype from IL17A (rs2275913) was associated with lack of disease. No association was found considering the IL17F and IL23R polymorphisms. Our data suggest that IL17A and the presence of IL17A (rs2275913) A allele are associated with the absence of periodontal disease.
Assuntos
Interleucina-17/genética , Periodontite/genética , Polimorfismo de Nucleotídeo Único , Receptores de Interleucina/genética , Adolescente , Adulto , Alelos , Brasil , Feminino , Genótipo , Humanos , Interleucina-17/metabolismo , Masculino , Pessoa de Meia-Idade , Periodontite/metabolismo , Receptores de Interleucina/metabolismo , Fumar , Adulto JovemRESUMO
A periodontite (DP) é uma doença caracterizada pela perda de tecido de suporte. O diagnóstico atual é baseado em parâmetros clínicos como profundidade de sondagem, perda de inserção, sangramento a sondagem e exames radiográficos. A meta da Periodontia é o estabelecimento de novos métodos que possibilitem o diagnóstico, a identificação precoce da doença e predizer uma futura perda de inserção. O fluido crevicular gengival (FCG) é composto de uma gama de biomarcadores celulares e moleculares. A coleta do FCG é uma técnica fácil e não invasiva, o que o torna um método diagnóstico promissor. O objetivo do presente trabalho foi realizar uma revisão da literatura crítica sobre a análise do FCG como ferramenta para o estabelecimento do diagnóstico precoce, bem como o monitoramento da evolução da doença. Na literatura é possível encontrar inúmeros estudos de possíveis biomarcadores da DP no FCG como fosfatase alcalina, citocinas, aspartato aminotransferase, oncostatina M, Rank/Rankl/OPG, catepsina B, catepsina K, osteocalcina, osteopontina, metaloproteinases e leucotrieno B4. As pesquisas apontam alguns biomarcadores promissores para o diagnóstico da DP, entretanto, não há ainda um marcador que possa predizer a futura perda de inserção ou a susceptibilidade à DP. São necessários estudos longitudinais para melhor entendimento do papel de biomarcadores do FCG.