Abstract
Abstract Introduction The association between smoking and periodontal diseases has been described in clinical and epidemiological studies. Objective The aim of this study was to compare the LL-37 and human β-defensin-2 (hBD-2) levels in crevicular fluid of patients with generalized periodontitis in smokers (S) and nonsmokers (NS). Material and method A total of 35 patients with generalized periodontitis stages III and IV, 15 NS (11 female, 4 male) and 20 S (7 female and 13 male), were included in the study. The evaluated clinical parameters were bleeding on probing (BOP), probing depth (PD) and clinical attachment level (CAL). Enzyme-linked immunosorbent assays were performed to quantify the LL-37 and hBD-2 levels in the gingival crevicular fluid of these patients. The results were analyzed statistically with the level of significance set at 5%. Result In relation to periodontal clinical parameters, no statistically significant difference was observed for BOP and PD between groups S and NS. There was a higher CAL in the S group than in the NS group (p = 0.0095). There was no statistically significant difference between the levels of LL-37 and hBD-2 when comparing groups S and NS (p>0.05). Conclusion It was concluded that smokers have a higher clinical attachment loss than nonsmokers, but that smoking did not influence the levels of LL-37 and hBD-2 in the gingival crevicular fluid in periodontitis.
Highlights
The association between smoking and periodontal diseases has been described in clinical and epidemiological studies
It was concluded that smokers have a higher clinical attachment loss than nonsmokers, but that smoking did not influence the levels of LL-37 and Human beta-defensins (hBDs)-2 in the gingival crevicular fluid in periodontitis
Dysbiosis results from the process of microbial succession mediated by inflammation in periodontitis, in which species associated with the disease appear temporally and spatially in the periodontal pocket[2]
Summary
The association between smoking and periodontal diseases has been described in clinical and epidemiological studies. The development and severity of periodontal disease depends on a dynamic balance between bacteria associated with plaque, the immune status of the individual, genetic and environmental factors, oral hygiene habits, smoking and alcohol. These factors can cause increased susceptibility to the disease and affect/regulate the host’s immune response to the bacteria[3]. Cigarette smoking has been demonstrated as a major risk factor in the prevalence, extent and severity of periodontal disease, and studies have suggested that smoking increases between two to six times the risk of periodontal disease[5] Environmental risk factors, such as smoking, promote alterations in the immune and inflammatory system and have a negative impact on periodontitis[6]. The secretion of antimicrobial peptides, such as defensins and cathelicidin LL-37, is an important stage of the innate defense mechanism[10]
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