RESUMO
OBJECTIVE: The Family with sequence similarity 5 member C (FAM5C) has been suggested to contribute in aggressive periodontitis. However, there is no data regarding its role in chronic periodontitis. The aim of this study was to evaluate the FAM5C expression in chronic periodontitis and to study association of FAM5C with key immunoinflammatory markers. MATERIAL AND METHODS: Gingival biopsies were harvested from periodontally healthy subjects (n = 10) and chronic periodontitis subjects (n = 15). The levels of mRNA of FAM5C, interleukin (IL)-17, IL-6, IL-23, IL-10, IL-4, interferon-c, toll-like receptor (TLR)-2, TLR-4, osteoprotegerin (OPG), receptor activator of NF-κB ligand (RANKL), tumor necrosis factor (TNF)-a, transforming growth factor-b, transcription factor forkhead box p3, and transcription factor orphan nuclear receptor C2 were evaluated by real-time polymerase chain reaction. RESULTS: FAM5C mRNA levels were not different between periodontally healthy and diseased tissues (P > 0.05). Gene expressions of IL-17, TNF-a, OPG, RANKL, TLR-2, and TLR-4 were higher in periodontitis, when compared to periodontally healthy sites (P < 0.05), while no differences between groups were observed for the other genes evaluated (P > 0.05). There were no correlations between the gene expression of FAM5C and the other immunoinflammatory markers (P > 0.05). CONCLUSION: Within the limits of this study, it seems that FAM5C expression does not contribute to chronic periodontitis.
Assuntos
Periodontite Crônica/genética , Periodontite Crônica/metabolismo , Citocinas/genética , Proteínas de Ligação a DNA/genética , Mediadores da Inflamação/metabolismo , Proteínas Mitocondriais/genética , Adulto , Estudos de Casos e Controles , Citocinas/biossíntese , Proteínas de Ligação a DNA/biossíntese , Feminino , Expressão Gênica , Gengiva/patologia , Humanos , Interleucinas/biossíntese , Interleucinas/genética , Masculino , Pessoa de Meia-Idade , Proteínas Mitocondriais/biossíntese , Índice Periodontal , Projetos Piloto , Ligante RANK/biossíntese , Ligante RANK/genética , RNA Mensageiro/genética , Reação em Cadeia da Polimerase em Tempo Real , Estatísticas não Paramétricas , Receptor 2 Toll-Like/biossíntese , Receptor 2 Toll-Like/genética , Receptor 4 Toll-Like/biossíntese , Receptor 4 Toll-Like/genética , Fator de Necrose Tumoral alfa/biossíntese , Fator de Necrose Tumoral alfa/genéticaRESUMO
Specific cytokines and the costimulatory protein CD40 play role in inducing immunoglobulin (Ig)A production by B cells in the humoral immune response. However, to date, the role of these mediators was not investigated in chronic periodontitis. Therefore, the aim of this study was to assess the local levels of interleukin (IL)-21, IL-21 receptor (IL-21R), IL-4, IL-10 and CD40 ligand (CD40L) on chronic periodontitis subjects and their relationship with the salivary levels of IgA. Gingival biopsies and un-stimulated saliva were collected from chronic periodontitis (n = 15) and periodontally healthy (n = 15) subjects. The mRNA levels of IL-4, IL-10, IL-21, IL-21R, CD40L in the gingival biopsies were evaluated by quantitative real-time polymerase chain reaction. The salivary levels of IgA and the levels of IL-4 and IL-10 in the gingival biopsies were analyzed by ELISA. The mean levels of IgA were significantly higher in the chronic periodontitis compared to periodontally healthy group (P < 0.05). The mRNA levels for IL-21 was higher (P < 0.05) in the chronic periodontitis when compared to the healthy group. However, the expression of IL-21R and CD40L did not differ between groups. The IL-10 was significantly elevated at mRNA and protein levels in chronic periodontitis when compared to periodontally healthy group (P < 0.05). Conversely, the mRNA levels as well as the protein amount of IL-4 were significantly lower (P < 0.05) in chronic periodontitis than healthy ones. In conclusion, the upregulation of IL-21 and IL-10 and downregulation of IL-4 in periodontitis tissues may be collectively involved in the increased levels of salivary IgA in chronic periodontitis subjects.