PERIODONTITIS FREQUENTLY AFFECTS PEOPLE WITH TYPE 1 DIABETES WITH REDUCED NEUTROPHIL ACTIVITY

Letter to the Editor

G. Varvara^*

Department of Innovative Technologies in Medicine & Dentistry, University “G. d’Annunzio” of Chieti-Pescara, Chieti, Italy.

*Correspondence to:
Giuseppe Varvara,
Department of Innovative Technologies in Medicine & Dentistry,
University “G. d’Annunzio” of Chieti-Pescara,
66100 Chieti, Italy.
e-mail: giuseppe.varvara@unich.it

Received: 29 December, 2025 Accepted: 04 February, 2026

ISSN 2279-5855 print / 2974-6345 [online] Copyright 2026 © by Biolife-publisher This publication and/or article is for individual use only and may not be further reproduced without written permission from the copyright holder. Unauthorized reproduction may result in financial and other penalties. Disclosure: All authors report no conflicts of interest relevant to this article.

KEYWORDS: Periodontitis, type 1 diabetes, diabetes mellitus, neutrophil, signal transduction pathway, receptor

INTRODUCTION

Periodontitis is chronic inflammation of the dental tissues that can affect the alveolar bone, gums, and periodontal ligament (1). Periodontal disease is a complication that frequently occurs in type 1 diabetes mellitus due to dysregulated immune responses and alterations of neutrophils (2,3). Neutrophils play a key role in the innate immune response and periodontal disease in type 1 diabetics, where these immune cells are overactive and underactive. In type 1 diabetes, periodontitis is common, very aggressive, and affects the metabolic system. This immune abnormality leads to increased vulnerability to infections and severe inflammation with the formation of microangiopathy (4). P. gingivalis may overgrow, exacerbating the disease due to ineffective neutrophil phagocytosis, with damage to periodontal tissues, including bone and ligaments.

DISCUSSION

Immune dysregulation leads to impaired coagulation and impaired tissue healing. Altered neutrophil function occurs at the systemic tissue level, contributing to the chronic inflammatory phenomenon. Neutrophils possess various surface receptors that are crucial for detecting pathogens. The most important inflammatory receptors involved in periodontal disease include Toll-like receptors (TLRs) for pathogen recognition, Fc receptors (FcγRs) for antibody-bound targets, complement receptors CR1, CR3, and CR4, and chemoattractant chemokine receptors (e.g., CXCR1/2) that drive cellular chemotaxis (5). People with type 1 diabetes have reduced neutrophil receptor activity and neutrophil counts in the bloodstream, but not in the pancreas, due to an imbalance in cell migration. Activated tissue neutrophils migrate to the site of infection and release a wide variety of molecules against microorganisms, including reactive oxygen species (ROS), leukotrienes, prostaglandins, and inflammatory cytokines, modulating inflammation (6). The inflammatory effect alters the immune response, favouring the attack of microorganisms.

Type 1 diabetes is characterized by a severe chronic increase in blood glucose levels, leading to neutrophil dysfunction. Hyperglycemia causes a severe biochemical alteration in neutrophils, with non-enzymatic glycation. High glucose levels lead to alterations in neutrophil membranes, FcγRs, and intracellular enzymes such as serine proteases, metabolic enzymes, and cationic proteins. Serine proteases in neutrophil primary granules are divided into Cathepsin G, a serine protease involved in antibacterial defence and matrix degradation, and proteinase 3, involved in inflammation and tissue remodelling (7). The secondary granules contain different enzymes. Myeloperoxidase is an enzyme composed of azurophilic granules that is essential for the production of hypochlorous acid. Lysozyme is an enzyme that attacks the cell wall of bacteria. NADPH oxidase is an enzyme complex that assembles on the membrane to produce free radicals and matrix metalloproteinase-9 is a major enzyme contained in the tertiary granules which degrades type IV collagen, facilitating neutrophil migration.

Advanced glycation end products are harmful compounds formed by the non-enzymatic bonding of sugars with proteins, lipids, or nucleic acids. They accumulate in the body due to hyperglycemia and bind to the receptor for advanced glycation end products expressed on neutrophils, activating protein kinase C (PKC), mitogen-activated protein kinase (MAPK), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), which results in the transcription of adhesion molecules and pro-inflammatory cytokines (8). Type 1 diabetes causes mitochondrial oxidative stress, causing the production of ROS, DNA damage, and oxidation of lipids and cytoskeletal membranes (9). Furthermore, elevated glucose levels alter neutrophil chemotaxis, reduce membrane fluidity, and modify chemokine receptors.

In animal models of type 1 diabetes, neutrophils, in addition to participating in inflammation, have been reported to contribute to the damage of pancreatic beta cells located in the islets of Langerhans which are responsible for insulin production (10). Pro-inflammatory substances can activate dendritic cells, increase the response of autoreactive T cells, and fuel the presentation of autoantigens.

CONCLUSIONS

In conclusion, in type 1 diabetes, neutrophil dysfunction is linked to metabolic alterations, chemotaxis, and factors that contribute to inflammation and autoimmune disease.

Conflict of interest

The author declares that they have no conflict of interest.

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