Role of Innate Immunity Factors in Periodontitis Pathogenesis

Abstract

Chronic generalized periodontitis (CGP) is a disease of periodontium tissues supporting tooth induced by bacteria, that is characterized by the presence of processes of inflammation with destruction ofbone tissue. The knowledge of molecular mechanisms of CGP pathogenesis facilitates creation of the most effective methods of therapy of this disease. Bacterial infection is a primary factor in periodontitis etiology, however is not sufficient for its start and subsequent development. It is known, that bacterial factors induce a local inflammation reaction and activate the system of innate immunity through activation of Toll-like receptors (TLR), located on the surface of resident cells and leukocytes. Activation of these cells results in production of pro-inflammatory cytokines and recruitment of phagocytes and lymphocytes into the inflammation zone. In review we examined the known data regarding factors of immune protection of periodontium including cell populations and cytokines, as well as mechanisms of tissue destruction, that support the tooth. Perspectives of therapy are also discussed.

Relationship between Periodontitis and Glaucoma: A Cross-Sectional Study

“…ese cytokines activate several inflammatory pathways and recruit dedicated immune cells (macrophages, dendritic cells, eosinophils, neutrophils, T cells, and natural-killer cells) that could play significant roles in the pathogenesis of chronic periodontitis [21,22]. Glaucoma is characterized by elevated intraocular pressure; however, it is more accurately defined as a neuroinflammatory and neurodegenerative disease that results in the degeneration of the retinal ganglion cells [23].…”

Efficacy of minimally invasive therapy and laser therapy in the comprehensive treatment of endoperiodontal lesions

“…3 To date, antibiotic injections in the oral cavity are still prescribed in chronic generalized periodontitis (CGP). 4 This method of treatment contradicts all principles of antibiotic therapy, does not take into account the anatomical and physiological features of the structure of soft tissues in this area, promotes the formation of stable microflora and the development of severe complications, destabilizes the inflammatory process in the periodontium, as well as misinforms a doctor and a patient about the expected outcome of the disease. It is of general knowledge that a discharge of toxic products from the necrotic pulp into the periapical region results in its inflammation.…”

Association between pro-inflammatory cytokine interleukin-33 and periodontal disease in the elderly: A retrospective study

“…[ 9 ] Accordingly, changes in the innate and adaptive immune responses in old age may favor the development or manifestation of disease. [ 10 ] Indeed, the balance between innate immune response and acquired immune response (Th1/Th2), seems to be related to disease severity. [ 11 ] Ultimately, chronic periodontal disease activates or induces the secretion of several inflammatory proteins that promote bone resorption, resulting in loss of tooth matrix and support.…”