The Impact Of Smoking To Human Beta Defensin 2、3 In Gingival Crevicular Fluid And Gingival Tissue Of Patients With Chronic Periodontitis

Background and objective:β- defensins as a host defense substance, not only involved in the body’s natural immune response against the pathogen has a direct killing effect, you can also activate the acquired immune system involved in the composition of external pathogenic microorganisms resistant epithelial first line of defense. In recent years, due to the increasing number of drug-resistant strains of bacteria, and the development of new anti-infective material, a global pharmaceutical industry urgently seek a breakthrough, β- defensin antimicrobial peptides, as one of the most impressive, because of its powerful antibacterial function unique mechanism of action, bringing new hope for this study.The β-defensin 2 and 3 as endogenous antimicrobial peptides, oral mucosa major antimicrobial peptides, not only has anti-bacterial, anti-viral and other biological activity is also involved in a variety of ways the immune defenses of the oral epithelium. Periodontal disease is one of the two major oral diseases that smoking is an important risk factor for periodontal disease, the specific pathogenesis is still not clear, then smoking can affect the expression of h BD periodontal tissues, thereby affecting the periodontal development of the disease does occur, the current domestic and international research is still small.In this paper, periodontitis patients with chronic smoking and non-smoking for the study to study the impact of smoking to human beta defensin 2,3 expression in gingival crevicular fluid and gingival tissue of patients with chronic periodontitis. Methods:The research subjects were divided into healthy periodontal group, chronic periodontitis group and group of smokers with chronic periodontitis. Enzyme linked immunosorbent assay(ELISA) was used to detect the concentration of HBD2,3. Reverse transcription polymerase chain reaction(RT-PCR) was used to detect the expression of HBD2,3 m RNA and semi-quantitive analysis was performed. The SPSS17.0 software package was used to analyse the experimental data and the statistical detection level is 0.05. Results:1. In the GCF, HBD2, 3 protein was expressed, where in the concentration of expression in turn are healthy periodontal group> chronic periodontitis group> group of smokers with chronic periodontitis.2. The expression level of HBD2, 3 protein concentration in smokers with chronic periodontitis was the lowest. The difference is statistically significant(P <0.05).3. In the GCF, the expression level of HBD2 concentration of each group was higher than HBD3 concentrations. The difference is statistically significant(P <0.05).4. HBD2,3 in all the three groups has m RNA expression, while the m RNA expression level of smokers with chronic periodontitis group was significantly lower than that of healthy periodontal group and chronic periodontitis group. The difference is statistically significant(P <0.05).5. In the three groups, the m RNA expression level of HBD3 in the gingival tissues of each group was lower than that of HBD2. The difference is statistically significant(P <0.05). Conclusion:1. Smoking inhibits the expression of the HBD2, 3 protein concentration in GCF.2. Smoking can change the m RNA expression of HBD2, 3 in gingival tissues.3. The expression level of HBD 2 in GCF and gingival tissues was higher than that of HBD3.4. The results of the study suggested that smoking may have a negative effect on periodontal host immune defense system.