Affiliation:
1. Restorative Dental Sciences, College of Dentistry King Saud University Riyadh Saudi Arabia
2. Dental University Hospital King Saud University Riyadh Saudi Arabia
Abstract
AbstractDiabetes mellitus (DM) increases the susceptibility to infection. A plausible association between apical periodontitis (AP) and DM has been reported, but the underlying mechanism is not yet elucidated.AimTo investigate the bacterial quantity and the expression of interleukin‐17 (IL‐17) in necrotic teeth with AP in type 2 DM (T2DM), pre‐diabetic and non‐diabetic control patients.MethodologyIn all, 65 patients with necrotic pulp and AP [periapical index (PAI) scores ≥3] were included. The age, gender, medical history and medications list, including metformin and statin intake, were recorded. Glycated haemoglobin (HbA1c) was analysed, and the patients were divided into three groups: T2DM (n = 20), pre‐diabetics (n = 23) and non‐diabetic (n = 22). Bacterial samples (S1) were collected by file and paper points. Bacterial DNA was isolated and quantified using 16S ribosomal RNA gene‐targeted quantitative real‐time polymerase chain reaction (qPCR). For IL‐17 expression, (S2) samples were collected from the periapical tissue fluid using paper points passing through the apical foramen. The IL‐17 total RNA was extracted, and reverse transcription (RT‐qPCR) analysis was performed. Comparisons between the three study groups were conducted using one‐way anova and Kruskal–Wallis test to explore the relationship between bacterial cell counts and IL‐17 expression in each group.ResultsThe distributions of PAI scores were equivalent among the groups, p = .289. T2DM patients had higher bacterial counts and IL‐17 expression than other groups, but these differences were not statistically significant, p = .613 and p = .281, respectively. T2DM patients taking statin appear to have lower bacterial cell count than those who do not take statin, approaching the significance level, p = .056.ConclusionT2DM patients had a non‐significant higher bacterial quantity and IL‐17 expression compared to pre‐diabetic and healthy controls. Although these findings indicate a weak association, it may impact the clinical outcome of endodontic diseases in diabetic patients.
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