Abstract
Aim
This study aimed to quantitatively and qualitatively determine the proteomic profile of apical periodontitis (AP) in Type 2 Diabetes Mellitus (T2DM) patients in comparison to systemically non-compromised patients, and to correlate the protein expression of both groups with their biological functions.
Methodology
The sample consisted of 18 patients with asymptomatic AP divided into two groups according to the presence of T2DM: diabetic group - patients with T2DM (n = 9) and control group - systemically healthy patients (n = 9). After sample collection, the root canal samples were prepared for proteomic analysis using reverse-phase liquid chromatography mass spectrometry. Label-free quantitative proteomic analysis was performed by Protein Lynx Global Service software. Differences in protein expression between groups were calculated using t-test (p < 0.05). Biological functions were analyzed using the Homo sapiens UniProt database.
Results
A total of 727 human proteins were identified in all samples. Among them, 124 proteins common to both groups were quantified, out of which 65 proteins from the diabetic group showed significant differences compared with the control: 43 up-regulated (p < 0.05) and 22 down-regulated (p < 0.05) proteins. No significant differences in protein expression were seen for the remaining 59 proteins (p > 0.05). Most proteins with differences in expression were related to immune/inflammatory response. Neutrophil gelatinase-associated lipocalin, Plastin-2, Lactotransferrin, and 13 isoforms of immunoglobulins were up-regulated. In contrast, Protein S100-A8, Protein S100-A9, Histone H2B, Neutrophil defensin 1, Neutrophil defensin 3, and Prolactin-inducible protein were down-regulated.
Conclusions
Quantitative differences were demonstrated in the expression of proteins common to diabetic and control groups, mainly related to immune response, oxidative stress, apoptosis, and proteolysis. These findings revealed biological pathways that provide the basis to support clinical findings on the relationship between AP and T2DM.
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