Abstract
Periodontitis is a multifactorial chronic inflammatory disease associated with increased secretion of several proinflammatory mediators such as Interleukin-1β (IL-1β), Interleukin-6 (IL-6), Interleukin-17 (IL-17), Tumour Necrosis Factor-α (TNF-α), Prostaglandins (PGs) in response to increased bacterial load on the tooth surface and within the gingival sulcus leading to the destruction of both hard and soft tissue of the periodontium. The Receptor for Advanced Glycation End-products (RAGE) binds multiple ligands, has a transmembrane configuration and is a part of the immunoglobulin receptor family. In healthy individuals RAGE is expressed at lower levels when compared to those with periodontitis and diabetes mellitus. Binding of RAGE to its ligands plays a key role in the inflammatory reactions that lead to disruption of a multitude of cellular processes. One such RAGE ligand involved in inducing hyperinflammatory phenotype is High Mobility Group Box 1 (HMGB1). HMGB1 is a chromatin binding protein predominantly localised in the nucleus and is associated with multiple functions such as Deoxyribonucleic Acid (DNA) repair, nuclear homeostasis, genome stability. In the presence of stressors, it migrates extracellularly and behaves like a Damage Associated Molecular Pattern (DAMP), has chemokine and cytokine activity. Extracellular HMGB1 binds to Toll Like Receptors (TLR)- 2,4 and RAGE, the HMGB1-RAGE interaction in particular has been associated with hyper inflammatory responses and currently hypothesised to be a bigger player in the pathogenesis of periodontitis as well as diabetes associated periodontitis. Therefore, understanding thoroughly the molecular mechanisms driving the tissue destruction in periodontal disease will effectively enable novel therapeutic drug based interventions based on interrupting the HMGB1-RAGE axis which in turn could mitigate the inflammation mediated tissue destruction.
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