Pathogenic Molecular Mechanisms in Periodontitis and Peri-Implantitis: Role of Advanced Glycation End Products

Advanced Glycation End Products (AGEs), the products of the non-enzymatic oxidation of proteins, nucleic acids, and lipids, are accumulated in periodontal tissues under hyperglycemic conditions such as Diabetes Mellitus (DM) and are responsible for sustained periodontal destruction. AGEs mediate their intracellular effects either directly or indirectly through receptor binding (via RAGE) in all types of periodontal ligament cells (osteocytes, gingival fibroblasts, stem cells, epithelial cells), indicating an important target for intervention. In combination with lipopolysaccharides (LPS) from Porphyromonas gingivalis (Pg), the negative impact of AGEs on periodontal tissue is further enhanced and accentuated. In addition, AGE accumulation is evident in peri-implantitis, yet through different underlying molecular mechanisms. Novel therapeutic approaches targeting the effects of AGEs in periodontal ligament cells show beneficial effects in pre-clinical studies. Herein, we provide evidence on the detrimental role of AGE accumulation in oral cavity tissues and their associated signaling pathways in periodontitis and peri-implantitis to further highlight the significance of oral or topical use of AGE blockers or inhibitors along with dental biofilms' removal and DM regulation in patients' management.

Automated summary

Advanced Glycation End Products (AGEs) accumulation in periodontal tissues under hyperglycemic conditions contributes to periodontal destruction. AGEs affect periodontal ligament cells through direct or indirect mechanisms, playing a significant role in periodontitis and peri-implantitis. Inhibition of AGEs, along with dental biofilm removal and diabetes regulation, shows promise in patient management.