Impact of smoking on protein levels of beta-defensins in periodontal disease.

Antimicrobial peptides (AMPs) are important components of the host response against invading pathogens. In addition to their direct antimicrobial activity, they can also participate in the immune system modulation. However, the role of AMPs in the etiopathogenesis of periodontal disease and the risk factors that may influence their expression in the oral cavity are not fully understood. The aim of this study was to determine the impact of smoking on beta-defensin (hBD) 1 and 2 levels analyzing samples from periodontitis patients. Fifty patients with periodontitis, 25 smokers and 25 non-smokers, and 20 periodontally healthy patients were recruited. After periodontal clinical evaluation, gingival crevicular fluid (GCF) samples were collected from healthy sites of patients without periodontal disease and from healthy and diseased sites of patients with periodontitis. Peptides quantification was performed by sandwich ELISA technique. Smokers showed reduced GCF hBD 1 levels and increased hBD 2 levels compared to non-smokers in diseased sites (p <0.05). Higher levels of hBD 1 were observed in healthy sites of patients without periodontal disease than in healthy sites of patients with periodontitis (p<0.0001). Diseased sites of non-smokers presented higher levels of hBD 2 than healthy sites (p <0.05). These results reveal that protein levels of hBDs 1 and 2 can be impaired by cigarette smoking in the presence of periodontal disease.

Gingival Crevicular Fluid Levels of Human Beta-defensin 2 and 3 in Healthy and Diseased Sites of Individuals with and without Periodontitis.

OBJECTIVE: Human beta-defensins (hBDs) play an important role in the susceptibility to periodontitis. This study aimed to evaluate the levels of hBD-2 and hBD-3 in gingival crevicular fluid (GCF) of individuals with and without periodontitis. METHODS: Twenty periodontally healthy individuals (H) and 20 with periodontitis (P) were recruited. GCF samples were collected from healthy sites (Hh; n=20) from H individuals; and from healthy sites (Ph; n=20), sites with gingival inflammation but no attachment loss (Pg; n=20) and sites with inflammation and attachment loss (Pp; n=20) from P individuals. Levels of hBDs (pg/mL) were determined using ELISA. Comparisons between individuals and among sites were performed through hierarchical linear modelling. RESULTS: GCF levels [median(Q3-Q1)] of hBD-2 were: Hh=4.80 (0.00-30.69); Ph=33.29 (28.04-38.25); Pg=27.56 (23.14-35.50); and Pp=26.20 (23.20-42.54); and of hBD-3 were: Hh=0.00 (0.00-0.00); Ph=978.44 (760.48-1268.12); Pg=938.19 (806.75- 1266.38); and Pp=613.63 (325.50-854.68). Periodontitis at the individual level was associated with higher levels of hBD-2 (p=0.023) and hBD-3 (p greater than 0.001). No influence of site phenotype was observed on hBDs levels. CONCLUSION: Individuals with periodontitis presented higher levels of hBD-2 and hBD-3 in the GCF. These levels seemed to be influenced by periodontitis at the individual level but not by periodontal site.

Impact of smoking on protein levels of beta-defensins in periodontal disease

Abstract Antimicrobial peptides (AMPs) are important components of the host response against invading pathogens. In addition to their direct antimicrobial activity, they can also participate in the immune system modulation. However, the role of AMPs in the etiopathogenesis of periodontal disease and the risk factors that may influence their expression in the oral cavity are not fully understood. The aim of this study was to determine the impact of smoking on beta-defensin (hBD) 1 and 2 levels analyzing samples from periodontitis patients. Fifty patients with periodontitis, 25 smokers and 25 non-smokers, and 20 periodontally healthy patients were recruited. After periodontal clinical evaluation, gingival crevicular fluid (GCF) samples were collected from healthy sites of patients without periodontal disease and from healthy and diseased sites of patients with periodontitis. Peptides quantification was performed by sandwich ELISA technique. Smokers showed reduced GCF hBD 1 levels and increased hBD 2 levels compared to non-smokers in diseased sites (p <0.05). Higher levels of hBD 1 were observed in healthy sites of patients without periodontal disease than in healthy sites of patients with periodontitis (p<0.0001). Diseased sites of non-smokers presented higher levels of hBD 2 than healthy sites (p <0.05). These results reveal that protein levels of hBDs 1 and 2 can be impaired by cigarette smoking in the presence of periodontal disease.

Resumo Peptídeos antimicrobianos (PAMs) são componentes importantes da resposta do hospedeiro contra patógenos invasores. Além de sua atividade antimicrobiana direta, eles também podem participar da modulação do sistema imunológico. No entanto, o papel dos PAMs na etiopatogenia da doença periodontal e os fatores de risco que podem influenciar a sua expressão na cavidade oral não são totalmente compreendidos. O objetivo deste estudo foi determinar o impacto do tabagismo nos níveis de beta-defensina (hBD) 1 e 2 analisando amostras de pacientes com periodontite. Cinquenta pacientes com periodontite, 25 fumantes e 25 não fumantes e 20 pacientes periodontalmente saudáveis foram recrutados. Após avaliação clínica periodontal, amostras de fluido crevicular gengival (FCG) foram coletadas de sítios saudáveis de pacientes sem doença periodontal e de sítios saudáveis e doentes de pacientes com periodontite. A quantificação dos peptídeos foi realizada pela técnica de ELISA sanduíche. Fumantes apresentaram níveis reduzidos de hBD 1 no FCG e níveis aumentados de hBD 2 em comparação com não fumantes em locais doentes (p <0,05). Níveis mais elevados de hBD 1 foram observados em sítios saudáveis de pacientes sem doença periodontal do que em sítios saudáveis de pacientes com periodontite (p<0,0001). Os sítios doentes de não fumantes apresentaram níveis mais elevados de hBD 2 do que os sítios saudáveis (p<0,05). Esses resultados revelam que os níveis das hBDs 1 e 2 podem ser prejudicados pelo tabagismo na presença de doença periodontal.