Chronic generalized periodontitis is one of the most prevalent inflammatory diseases of periodontal tissues, characterized by progressive destruction of the tooth-supporting apparatus and a high rate of recurrence. A key role in its pathogenesis is played by dysbiosis of the periodontal microbiome combined with a dysregulated immune response, particularly the overproduction of pro-inflammatory cytokines, among which interleukin-1 (IL-1) is of central importance.

The aim of the study was to evaluate the effect of an IL-1 receptor antagonist (IL-1ra) Anakinra on microbial contamination of periodontal pockets in patients with chronic generalized periodontitis during combined treatment..

Materials and methods. The study included 87 patients aged 25–65 years, who were divided into three groups: basic therapy (n = 34), basic therapy with Anakinra (n = 31), and basic therapy with Cholisal gel (n = 22). Microbiological assessment was performed using quantitative PCR with identification of key periodontal pathogens.

Results. It was found that before treatment all patients exhibited a high level of microbial contamination (5.8–6.3 log10 CFU/mL), with predominance of red complex bacteria. The use of Anakinra resulted in a significantly greater reduction in bacterial load as early as 30 days (by 38.6–42.5 %, p < 0.001) compared to basic therapy and the comparison group. After 90 days, microbial reduction in this group reached 55.5–72.5 %, with levels decreasing to 2.6–3.1 log10 CFU/mL. The most pronounced reduction was observed for Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola, confirming the role of IL-1 in shaping a pathogenic microbial environment. The effect of Anakinra was shown to be indirect and mediated through modification of the inflammatory microenvironment, thereby limiting the persistence of anaerobic bacteria.

Conclusions. The obtained results demonstrated the high efficacy of IL-1ra (Anakinra) receptor antagonist in the complex treatment of periodontitis and substantiated its use as a pathogenetically targeted approach affecting both immune and microbiological mechanisms of disease progression.