Publication Details
Abstract
Periodontal diseases are chronic inflammatory processes widespread in ¬the oral cavity, in the development and progression of which the local immune response and inflammatory mediators play a leading pathogenetic role. Pathogenic microorganisms in the microbial biofilm formed in periodontal tissues activate the innate and adaptive immune mechanisms of the host organism. In this process, biologically active substances secreted by epithelial cells, macrophages and neurophils determine the onset and duration of the inflammatory process. Bacterial components, in particular lipopolysaccharides, are recognized by cell surface receptors and cause the activation of the inflammatory cascade. As a result, the production of inflammatory mediators such as interleukins, tumor necrosis factor, prostaglandins and chemokines increases. These mediators increase vascular permeability, activate the migration of immune cells into periodontal tissues and enhance cellular infiltration in the inflammatory focus. In chronic inflammatory conditions, prolonged exposure to mediators leads to disruption of the connective tissue structure, breakdown of collagen fibers, and alveolar bone resorption. Activation of osteoclasts and excessive production of tissue enzymes are manifested by weakening of the periodontal ligaments and clinically by deepening of periodontal pockets. According to modern scientific data, periodontal diseases are considered a complex pathogenetic process associated not only with the action of microbes, but also with an imbalance of the local immune response and uncontrolled activity of inflammatory mediators. Therefore, in the prevention and treatment of periodontal diseases, it is important to deeply study the mechanisms of immune-inflammatory and their targeted regulation.