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

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Abstract

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.

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Most cited references 83

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Periodontal diseases

Bruce Pihlstrom, Bryan Michalowicz, Newell W. Johnson (2005)

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Interaction of lifestyle, behaviour or systemic diseases with dental caries and periodontal diseases: consensus report of group 2 of the joint EFP/ORCA workshop on the boundaries between caries and periodontal diseases.

Iain Chapple (2017)

Periodontal diseases and dental caries are the most common diseases of humans and the main cause of tooth loss. Both diseases can lead to nutritional compromise and negative impacts upon self-esteem and quality of life. As complex chronic diseases, they share common risk factors, such as a requirement for a pathogenic plaque biofilm, yet they exhibit distinct pathophysiologies. Multiple exposures contribute to their causal pathways, and susceptibility involves risk factors that are inherited (e.g. genetic variants), and those that are acquired (e.g. socio-economic factors, biofilm load or composition, smoking, carbohydrate intake). Identification of these factors is crucial in the prevention of both diseases as well as in their management.

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Periodontitis induced by Porphyromonas gingivalis drives periodontal microbiota dysbiosis and insulin resistance via an impaired adaptive immune response

Vincent Blasco-Baque, Lucile Garidou, Celine Pomie … (2016)

Objective To identify a causal mechanism responsible for the enhancement of insulin resistance and hyperglycaemia following periodontitis in mice fed a fat-enriched diet. Design We set-up a unique animal model of periodontitis in C57Bl/6 female mice by infecting the periodontal tissue with specific and alive pathogens like Porphyromonas gingivalis (Pg), Fusobacterium nucleatum and Prevotella intermedia. The mice were then fed with a diabetogenic/non-obesogenic fat-enriched diet for up to 3 months. Alveolar bone loss, periodontal microbiota dysbiosis and features of glucose metabolism were quantified. Eventually, adoptive transfer of cervical (regional) and systemic immune cells was performed to demonstrate the causal role of the cervical immune system. Results Periodontitis induced a periodontal microbiota dysbiosis without mainly affecting gut microbiota. The disease concomitantly impacted on the regional and systemic immune response impairing glucose metabolism. The transfer of cervical lymph-node cells from infected mice to naive recipients guarded against periodontitis-aggravated metabolic disease. A treatment with inactivated Pg prior to the periodontal infection induced specific antibodies against Pg and protected the mouse from periodontitis-induced dysmetabolism. Finally, a 1-month subcutaneous chronic infusion of low rates of lipopolysaccharides from Pg mimicked the impact of periodontitis on immune and metabolic parameters. Conclusions We identified that insulin resistance in the high-fat fed mouse is enhanced by pathogen-induced periodontitis. This is caused by an adaptive immune response specifically directed against pathogens and associated with a periodontal dysbiosis.