Angiogenesis, Inflammation & Therapeutics | Impact 0.1 (CiteScore) | Online ISSN  2207-872X
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Immune Dysfunction linking hyperglycemia with periodontitis in Diabetes Management

Harini Venkata Subbiah1, Polani Ramesh Babu2, Usha Subbiah1*, Daniel Rajendran T3, Vinod Kumar P3

+ Author Affiliations

Journal of Angiotherapy 5(2) 1-6 https://doi.org/10.25163/angiotherapy.52221532819191221

Submitted: 28 November 2021  Revised: 08 December 2021  Published: 19 December 2021 

This review discusses the mechanisms linking hyperglycemia with periodontitis highlights the need for comprehensive management of diabetes to improve periodontal health.

Abstract


Background: Periodontitis is a progressive inflammatory disease affecting the gums and supporting tissues, often worsened by diabetes. Its pathogenesis involves pathogenic bacteria and the host’s immune response. Hyperglycemia in diabetes elevates glucose in saliva and gingival crevicular fluid (GCF), fostering bacterial growth and periodontal tissue damage. This study investigates the mechanisms linking immune dysfunction, periodontitis, and diabetes, emphasizing advanced glycation end products (AGEs), cytokine production, and oxidative stress. Methods: We performed a comprehensive literature review to analyze the relationships among hyperglycemia, AGEs, inflammatory cytokines, oxidative stress, and periodontal damage. Data were sourced from studies examining diabetes' impact on periodontal health, focusing on AGEs and their receptor (RAGE), the RANKL/OPG system, neutrophil function, oxidative stress, hyperlipidemia, collagen synthesis, and antimicrobial peptides. Results: Persistent hyperglycemia leads to increased AGEs, which interact with RAGE to heighten inflammatory responses and oxidative stress. This interaction triggers cytokine release and disrupts the RANKL/OPG balance, enhancing osteoclast activity and bone resorption. Additionally, oxidative stress from elevated reactive oxygen species (ROS) and hyperlipidemia worsens periodontal damage. Neutrophil function in diabetic patients can be dysregulated, with either impaired or excessive activity contributing to tissue degradation. Changes in collagen synthesis and antimicrobial peptide levels further aggravate periodontal disease in diabetes. Conclusion: Hyperglycemia and periodontitis involve complex mechanisms, including AGE-induced inflammation, oxidative stress, and altered bone remodeling. Effective diabetes management is essential to mitigate its impact on periodontal health. Understanding these mechanisms can inform targeted interventions, improving treatment outcomes for patients with both conditions. Future research should focus on strategies addressing these interconnected factors for enhanced periodontal and diabetic care.

Keywords: Immune Dysfunction, Periodontitis, Diabetes Mellitus, Advanced Glycation End Products, Cytokine Production

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