RESUMO
The system of antimicrobial peptides (AMP) is one of the most ancient mechanisms of the macroorganism resistance to infectious pathogens invasion. The aim of the study was to determine the role of the antimicrobial peptides system and periodontal pathogenic markers in the development and progression of inflammatory periodontal diseases. Gingival pocket washes (91 samples in total) for the research were received from patients with inflammatory periodontal diseases (chronic periodontitis and gingivitis) and intact periodontium. Using ELISA, the content of antimicrobial peptides was determined: human alpha-defensin (HNP 1-3), beta-defensin (HBD 1-3) and cathelicidin (LL-37). Periodontal pathogenic markers were isolated during RT-PCR. The study revealed differences in AMP concentrations by groups: level of HBD 2 in patients with chronic periodontitis was 1,36 times higher than those in the group of patients with chronic gingivitis (p=0,023) and 2,39 times higher than those in the control group (p<0,001), the content of HNP 1-3 in the group of patients with chronic periodontitis was reduced by 1,23 times compared with the indicators of the group of patients with gingivitis (p=0,045) and by 1,97 times compared with the indicators of the control group (p<0,001). The frequency of detection of periodontal pathogenic bacteria genes was 88,0% in patients with periodontitis, 76,92% in patients with gingivitis and 33,3% in the group with intact periodontium. HBD 2 content moderately correlated with the definition of P. gingivalis (r=0,612; p=0,022), T. forsythensis (r= 0,434; p=0,015), A. actinomycetemcomitans (r=0,483; p=0,006), a moderate negative correlation was detected between the content of HNP 1-3 and the release of periodontal pathogens in associations (P. gingivalis with T. forsythensis and T. denticola) (r=-0,388; p=0,031) in the group of patients with chronic periodontitis. Thus, the revealed relationships and correlations indicate shifts in the processes of reparative regeneration of the oral cavity and the regulation of local immunity in response to microbial invasion.
