Oral infections affect glycaemic conditions in diabetic rats and increase HbA1c levels in normoglycaemic or diabetic rats.

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Our results indicate that diabetes increases IL-17 levels in hepatic and renal tissues and also enhances IL-17 production in apical periodontitis area of rats.

Our findings indicate that diabetes may change the antioxidant status, increase the concentration of MDA and uric acid, and decrease albumin levels in the serum. In addition, AP can potentiate the effects of diabetes by reducing the levels of albumin and increasing the levels of uric acid.

Apical periodontitis and periodontal disease may potentiate the adverse effects of diabetes.

The current study aimed to investigate if a pulp lesion, which is a local inflammatory disease, can promote alterations in insulin signal and insulin sensitivity (IS). Twenty‐eight two‐month‐old (230g) Wistar male rats were randomly divided into a control group (CN) and a pulp lesion group (PL). PL group was submitted to pulp lesion induction through the opening of the coronal pulp chamber of the upper right first molars by using a dental handpiece, followed by its exposure to oral cavity, promoting bacterial contamination and chronic inflammation. Thirty days after PL induction, the following evaluations were performed: 1) pp185 (IRS‐1/IRS‐2) tyrosine phosphorylation status (pp185 P‐Tyr), after insulin stimulation, in periepididimal white adipose tissue (WAT) and gastrocnemius muscle (G) by Western Blotting analysis; 2) IS determination by intravenous insulin tolerance test. The results showed that PL promoted: 1) a significant decrease (p<0.05) in the pp185 P‐Tyr in WAT (CN=152.9±12.7 vs PL=111.3±10.2 arbitrary units/ìg of protein, n=7) and in G (CN=133.1±9.1 vs PL=103.7±7.6 arbitrary units/ìg of protein, n=7); 2) a significant difference (p<0.05) in the IS (glucose disappearance speed rate: CN=3.04±0.26 vs PL=1.97±0.25 %min, n=7). These data suggest that PL is capable of changing insulin signal in both WAT and G, and causing insulin resistance in rats. Financial Support: FAPESP (2011/04255–8).