ArticleFrontiers in immunology2026
Hyperglycemia and systemic inflammation differentially shape immune dysregulation, tissue destruction, and microbiota in experimental periodontitis and peri-implantitis in diabetic mice.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Aim: To investigate the impact of hyperglycemia and systemic inflammation on experimental periodontitis/peri-implantitis in diabetic mice, focusing on osteoimmunological dysregulation and oral microbial alteration. Materials and methods: After implant placement, diabetic db/db mice were treated with Liraglutide, Indomethacin, or both, followed by ligature-induced experimental periodontitis/peri-implantitis. Samples were analyzed for bone loss, inflammatory cytokines, osteoclast activity, RAGE expression, IL-17-associated inflammatory responses, and Treg infiltration. The periodontal/peri-implant microbiota were examined by metagenomics and tested Results: Liraglutide, but not indomethacin, effectively reduced bone loss, immune cell infiltration, RAGE, IL-17A expression, and restored Foxp3 Conclusions: Diabetic hyperglycemia is a more predominant driver than systemic inflammation in exacerbating periodontitis/peri-implantitis tissue destruction, immune dysregulation, and eliciting a pro-inflammatory oral microbial environment. The local inflammatory response and microbial alteration around the tooth and implant were similar but not identical.
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