AUTOINFLAMMATORY IN THE PATHOGENESIS OF PERIODONTITIS

Periodontitis is considered a chronic inflammatory disease in which the primary damage to periodontal tissue is caused not by the bacteria themselves, but by the destructive immune response of the host. Current scientific evidence confirms that the pathogenesis of periodontitis is underpinned by autoinflammatory mechanisms associated with hyperactivation of the innate immune system, in contrast to autoimmunity, which primarily affects the acquired immune system.

The immune response begins with the recognition of pathogen-associated molecular patterns (PAMPs) of bacteria via pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs) and NOD-like receptors (NLRs). Activation of these receptors, for example by Porphyromonas gingivalis lipid A via TLR4, triggers a cascade of signaling pathways (NF-κB), leading to the synthesis of proinflammatory cytokines. Activation of inflammasomes, particularly NLRP3, plays a key role. These inflammasomes process pro-IL-1β into its active form, which links them to the pathophysiology of chronic autoinflammatory diseases.

Key proinflammatory mediators include IL-1β, IL-6, TNF-α, and IL-17. They stimulate the production of metalloproteinases (MMPs), which destroy the extracellular matrix and bone tissue, leading to osteolysis. Studies demonstrate a significant increase in the levels of these cytokines in gingival fluid, which increases with disease severity. Anti-inflammatory cytokines (IL-4, IL-10) are designed to limit this inflammation; however, in periodontitis, their regulatory function is often impaired, exacerbating the imbalance.

Dysregulation of cellular immunity plays a significant role, specifically an imbalance between proinflammatory Th17 and anti-inflammatory Treg lymphocytes. A shift toward Th17 promotes tissue destruction. Furthermore, genetic predisposition is an important factor, such as IL-1 gene polymorphism, which is associated with an increased risk of developing severe forms of periodontitis. Thus, periodontitis is an autoinflammatory disease caused by an imbalance in the cytokine network and a dysregulated immune response. Targeted therapies aimed at correcting these immune dysfunctions offer promising treatment options.