Gingival crevicular fluid biomarkers in type 1 diabetes mellitus: A case–control study

Abstract

Objective The aim of the study is to compare the levels of Gingival Crevicular Fluid (GCF) interleukin 8 (IL‐8), matrix metalloproteinase 8 (MMP‐8) and advanced glycated‐end products (AGEs) in a cohort of type 1 diabetic (T1D) subjects and healthy controls. Material and methods GCF samples and periodontal examination were assessed in 50 subjects with T1D (30 males and 20 females; mean age: 35.2 years) recruited from the Diabetology Unit of the Geneva University Hospitals and in 50 control subjects matched for gender, age and smoking status. Samples were assessed for IL‐8 and MMP‐8 using a bead array multianalyte detection system and for AGEs the ELISA. The two groups were compared using the Wilcoxon signed rank test. Results The mean HbA1c differed significantly between the groups (8.3% for the T1D group vs. 5.2% for the control group, p < 0.001). T1D subjects had significantly more plaque and gingival inflammation and presented more sites with bleeding on probing compared to the controls. The GCF levels of IL‐8, MMP‐8 and AGEs did not differ significantly between the groups. Further analysis of the GCF markers in younger (<40 years) and older (≥40 years) cohorts, revealed no significant differences between younger diabetics and controls or between older diabetics and controls. When the groups were divided according to their glycemic status (HbA1c 6.1–8, and > 8%), again no significant differences could be identified for any of the biochemical markers. Conclusions T1D subjects, particularly the younger ones, exhibited more inflammation compared to the matched healthy controls. Results on the GCF expression of IL‐8, MMP‐8 and AGEs did not differ between the groups. The diabetic population of our cohort was for the most part fairly‐controlled, with little if any complications and with presence of only mild type of periodontal disease, as 68% had gingivitis.

The use of the phrase “data not shown” in dental research

“…In open access journals advocating for more open science [ 34 , 35 ], the obscure representation of results as well as not sharing data or code should not be overlooked by the publishers or editorial teams. For instance, during the study process, we noted a study which used the raw data availability statement template without any changes: “The data that support the findings of this study are openly available in [repository name e.g., “figshare”] at http://doi.org/[doi], reference number [reference number]” [ 36 ]. Thus it seems that despite data availability statements being mandatory in some journals, the actual content of the statement does not always receive careful consideration.…”

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

“…A clinical trial that evaluated the biomarker potential of AGEs in GCF failed to detect a statistically significant difference between T1DM patients and healthy subjects. However, the main limitation of this study was the exclusion of patients with uncontrolled DM as well as those with severe periodontitis [25].…”

“…Increased RAGE and TLRs production [57] Cultured human endothelial cells and murine vasculature Increased VCAM-1 production [68] Clinical GCF Increased AGEs levels in T2DM patients [24] GCF Did not significantly increase AGEs levels between T1DM patients and healthy [25] Serum Increased AGEs levels in T2DM patients [26] Gingival tissues Increased RAGE levels in T2DM patients [46] Periodontal tissues RAGEG82S gene polymorphism as a risk factor of periodontitis [51] Saliva, serum Increased AGEs levels in periodontal patients rather than non-periodontal [53] Serum, GCF Increased TNF-α and reduced sRAGE levels [54] Gingival tissues Increased RAGE levels in DM patients [60] Gingival tissues Main location of RAGE is the basal epithelial membrane [61] Gingival tissues Anti-inflammatory effect of AGER1 [63] Gingival tissues Increased RAGE levels in gingival tissues of smokers [64] Peri…”

Salivary macrophage activation‐related chemokines and mitogen‐activated kinase kinase‐degrading proteolytic activity in type 1 diabetes mellitus

“…[13][14][15] Moreover, previous studies revealed that serum concentrations of chemokines, such as MCP-1, IP-10, and macrophage migration inhibitory factor (MIF), are elevated in T1DM patients. 16,17 However, data on the concentrations of salivary 18 and gingival crevicular fluid 19 cytokines in children with T1DM are limited, and there is still a substantial gap in the literature about the salivary concentrations of macrophage activation-related chemokines, especially in diabetic children.…”