Bacterial quantity and interleukin-17 expression in necrotic teeth with apical periodontitis from type II diabetic patients.

Unlabelled: Diabetes 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.

Aim: To 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.

Methodology: In 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.

Results: The 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.

Conclusion: T2DM 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.