Publication Details
Abstract
Inflammatory processes developing in the root canal system and the periapical region represent a protective reaction of the body aimed at limiting infection and preventing its spread to surrounding tissues. The formation and progression of HAP is due to the interaction of the mechanisms of innate and adaptive immunity. Studies by various authors indicate the development of sensitization of the body, changes in immune reactivity, the formation of secondary immunodeficiency and a violation of the local immune response in patients with this disease. These changes have a significant impact on the clinical course of the pathological process, the effectiveness of therapeutic measures, the prognosis of the disease, as well as the likelihood of relapses and complications. The chronic inflammatory process leads to a rupture of the connection between cellular and humoral immunity, a weakening of phagocytic function and a decrease in the effectiveness of the immune response, which creates favorable conditions for the progression of the disease and increases the likelihood of complications. In CAP, there is increased activation of B-lymphocytes, an increase in the concentration of circulating immune complexes and pro-inflammatory cytokines, as well as an imbalance of immunoglobulins, which indicates the development of dysimmunoglobulinemia. A decrease in the intensity of oxygen-dependent metabolism of neutrophils, as well as a decrease in myeloperoxidase activity, indicate a depletion of their functional reserve and a decrease in their ability to destroy pathogenic microorganisms through oxidative killing. Studies confirm that with CAP, there is a weakening of the phagocytic activity of neutrophil granulocytes, which reflects a decrease in the effectiveness of the immune response. The production of pro-inflammatory cytokines begins at the moment of tissue damage and is a necessary component of the immune response. In response to an infectious or mechanical factor, the synthesis of IL-1b, TNF-α, IL-6 and interferon-γ is activated, which contributes to increased inflammation. In parallel, a regulatory mechanism involving anti-inflammatory factors such as TGF-β and IL-4 is triggered, which limit the inflammatory process and promote the regeneration of damaged tissues. The development of the inflammatory process in CAP is directly related to the activity of pro-inflammatory cytokines, which are produced by type 1 T-helper cells, macrophages and neutrophils. These molecules contribute to an increased inflammatory response and the destruction of bone tissue, exacerbating the course of the disease