Relação entre citocinas, quimiocinas e maturação das células dendríticas, em indivíduos fumantes e não-fumantes, com periodontite crônica

• Ano de defesa: 2014
• Autor(a) principal: Giovanna Ribeiro Souto
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Fumo; Periodontite crônica; Quimiocinas; Citocinas; Células dendríticas; Interleucinas; Hábito de fumar/efeitos adversos; Periodontite; Doença periodontal; Células T; Células dentríticas
• Link de acesso: http://hdl.handle.net/1843/BUOS-9JVGNG

Chronic periodontitis (CP) is the most frequent form of destructive periodontal disease, and results from the interaction between bacterial biofilm and the host inflammatory response. Environmental factor as smoking is essential in determining to individual susceptibility. The present study aimed to evaluate chemokine and cytokine expressions, densities of immature and mature dendritic cells (DCs), and inflammatory infiltrate density in the gingival tissue of non-smokers (NS) and smokers (S) diagnosed with CP. The effect of smoking in chemokines, cytokines and immature and mature DCs were also evaluated. The study was approved by COEP-UFMG (423/11), and it was selected 24 NS and 21 S. Six samples of normal mucosa (NM) were used to control of chemokine and cytokine levels. It was performed periodontal examination to determine probing depth (PD), clinical attachment level (CAL), bleeding on probing (BOP). Individuals presented proximal CAL 3 mm in 2 non-adjacent teeth were diagnosed with CP. Immunohistochemistry was performed to evaluate the density (cell/mm2) of Factor XIIIa+ and CD1a+ immature DCs, and CD83+ mature DCs. Inflammatory infiltrate density was measured using hematoxylin and eosin stained sections. Chemokines (CCL2, CCL3, CCL5, CCL19, CCL20, and CXCL8) were measured using ELISA assay, whilecytokines (IL-2, IL-10, IL-4, IL-6, IFN-, TNF-, and IL-17A) were measured using CBA method, in samples of gingival tissue. The individuals were asked about the time of their smoking habit in years (SH/years) and how many cigarettes they smoked per day (C/day). CD83+ mature DCs, CCL3 and CXCL8 levels decreased in smoker group. While CCL5 levels were increased in smokers. Negative correlations between C/day and IL-17A levels and number of teeth, and between SH/years and CCL19 were observed. IL-6, CCL2, CCL20 levels were positively correlated with CD1a+ immature DCs densities. IL-2, TNF-, IFN-, IL-10, IL-17A, CCL3, CCL5, CCL19, and CXCL8 levels were increased in gingival tissue with CP when compared with NM. The percentage of sites with CAL3 mm were positively correlated with inflammatory infiltrate density, CCL3 and CXCL8 levels, and negatively correlated with CD1a+ immature DCs and IL-2 levels. In conclusion, it was observed that the smoking affect cells and inflammatory mediators of the immune response, and this can contribute for increase the susceptibility at CP in smokers. In addition, the increase of CD1a+ immature DCs was associated with higher levels of IL-6, CCL2, and CCL20. However, only IL-2, TNF-, IFN-, IL-10, IL-17A, CCL3, CCL5, CCL19, and CXCL8 levels presented increased in gingival tissues with CP. Higher density of inflammatory infiltrate, CCL3 and CXCL8 levels, as well as lower density of CD1a+ immature DCs, and IL-2 levels can result in a more severe degree of human CP.