Abstract
Objective: One of the treatment goals in type 1 diabetes and periodontitis is to address chronic inflammation to prevent the development of neurovascular complications. The aim of this study was to assess the local anti-inflammatory effects of chlorhexidine digluconate and cetylpyridine chloride on periodontal status and indicators of oxidative stress in saliva in patients with type 1 diabetes. Materials and Methods: A total of 42 subjects aged 27 (interquartile range, IQR 22–35) years, with type 1 diabetes for a duration of 12 (IQR 9–18) years, and glycated hemoglobin 8.05 (IQR 7.1–9.4)% were included. Patients were examined twice—initially, and after 14 days of using toothpaste with chlorhexidine and cetylpyridine. Clinical examination of gingival tissues was performed. Certain oxidative stress markers (TP, TEAC, TBARS, AOPP) were measured in the saliva samples. Results: There were significant changes in clinical indicators of periodontal status before and after the application of the toothpaste (API before 0.35 (0.24–0.65) vs. API after 0.265 (0.18–0.39), p = 0.03; SBI before 0.07 (0.04–0.15) vs. SBI after 0.035 (0-0.06), p = 0.002; GI before 0.88 (0.46–1) vs. GI after 0.67 (0.25–1), p = 0.0008). The concentration of saliva TBARS decreased (p = 0.00005) and TEAC increased (p = 0.09). Conclusion: Proper oral hygiene supported by antibacterial chemicals may improve the periodontal status and reduce inflammation.
Highlights
The basis of type 1 diabetes (T1D) is an autoimmune inflammation leading to destruction of the β cells of the pancreatic islets that produce insulin [1]
The metabolic control of diabetes expressed by HbA1c was not optimal as the target value for HbA1c in type 1 diabetes is below 6.5%he target may be modified in certain individuals (Table 1)
There were no differences in age, diabetes duration, C-reactive protein, total cholesterol, low-density lipoprotein (LDL)-cholesterol and high-density lipoprotein (HDL)-cholesterol between subgroups
Summary
The basis of type 1 diabetes (T1D) is an autoimmune inflammation leading to destruction of the β cells of the pancreatic islets that produce insulin [1]. Several pathogenic pathways are involved [3] These include activation of the protein kinase C pathway, formation of glycation end-products (AGEs), accumulation of sorbitol through the aldose reductase pathway, and activation of the hexosamine pathway and the polyADP-ribose polymerase (PARP) pathway, which regulates several inflammatory response gene expressions [4]. The duration of hyperglycemia, acting as a cell and extracellular matrix proliferative factor, results in the exacerbation of oxidative and nitrative stress, further inflammatory response, insulin resistance, and protein glycation [5], and it clinically manifests as micro and macrovascular dysfunction and the development of retinopathy, chronic kidney disease, neuropathy and periodontal disease [6]. A generation of reactive oxygen species (ROS) has been proposed as the essential element of different pathogenic pathways [3]. The β cells are especially sensitive to reactive oxygen species (ROS), which includes free radicals and non-radical species [7]
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