Cytokines and periodontitis. Part I: interleukin-1 and interleukin-1 receptor antagonist

Studies on periodontal disease pathogenesis are for years concentrating on elucidating the mechanism of immune reaction to endotoxins, exotoxins and other products of bacterial cell metabolism. The course and severity of periodontitis can be significantly affected by bacterial virulence as well as host immunity dysfunction. Periodontal tissue destruction has been proved to result from cascade of cytokines synthesized by reactive cells upon stimulation by pathogenic bacteria and lipopolysaccharides within their cell membranes. Trials are undertaken to inactivate interleukin-1 (IL-1) - the most active cytokine in the pathogenesis of periodontal disease. Much hope is placed in gene therapy, utilizing modified techniques of gene transfer into the target cells. The clinical use of genetically programmed cells, producing substances blocking IL-1, based on recombinant IL-1 antagonist, as well as cytokines activating fibroblasts and osteoblasts to regenerate the destroyed periodontal tissue could prove alternative to the conventional treatment.