Periodontally healthy individuals showed higher gingival crevicular fluid levels of hBD-1 when compared to individuals with chronic periodontitis. This suggests a potential protective role of hBD-1 in the susceptibility to chronic periodontitis.

Background Antimicrobial peptides are components of innate immune response that have a key role on susceptibility and resistance of the oral cavity to diseases. This study aimed to investigate the influence of smoking on cathelicidin LL‐37 and human neutrophil peptides 1 through 3 (HNP 1‒3) levels in the gingival crevicular fluid (GCF) of patients with periodontitis. The relationship between levels of these peptides with the periodontal status and selected inflammatory mediators levels in smokers and non‐smokers was also evaluated. Methods Forty patients with periodontitis, 20 smokers and 20 non‐smokers were recruited. After a full periodontal clinical assessment, GCF samples were collected from healthy (n = 5) and diseased (n = 5) sites of each patient. Peptides and inflammatory mediators in the GCF were quantitated by sandwich ELISAs and Multiplex assay, respectively. Results Diseased sites had significantly (P <0.05) higher levels of LL‐37 and lower levels of HNP 1‒3 than healthy sites in both smokers and non‐smokers. Diseased sites of smokers presented significantly lower levels of LL‐37 and HNP 1‒3 when compared with diseased sites of non‐smokers. Concentration of LL‐37 was directly correlated with the presence of proinflammatory mediators matrix metalloproteinase (MMP)‐8 and interleukin (IL)‐1β and inversely correlated with concentration of IL‐10. HNP 1‒3 concentration was positively correlated with IL‐10 and negatively correlated with concentrations of MMP‐8 and IL‐1β. Conclusions Smoking was associated with reduced levels of LL‐37 and HNP 1‒3 in GCF of patients with periodontitis. LL‐37 had a distinct expression pattern from HNP 1‒3: LL‐37 was upregulated in diseased sites, and HNP 1‒3 was increased in periodontally healthy sites.1

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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.