Reduced bone resorption and inflammation in apical periodontitis evoked by dietary supplementation with probiotics in rats

Aim To evaluate the relationship between systemic administration of probiotics and inflammation/resorption processes associated with apical periodontitis (AP) in a rat model. Methodology Twenty-four male Wistar rats were used. AP was induced in the mandibular left/right first molars. The animals were arranged into three groups: Control, Lactobacillus rhamnosus and L. acidophilus. Probiotics were orally administered via gavage (10(9) colony-forming units (CFU) diluted in 5 mL of water) for 30 days during the development of AP. On the 30th day, blood was collected to analyse the calcium, phosphorus and alkaline phosphatase concentrations in plasma. Then, the animals were euthanized and the jaws removed for micro-computed tomography and immune-histopathological analysis for receptor activator of NF-kappa B ligand (RANKL), osteoprotegerin (OPG) and tartrate-resistant acid phosphatase (TRAP). After the Shapiro-Wilk test of normality, the Kruskal-Wallis followed by Dunn's test was performed for nonparametric data, and analysis of variance followed by the Tukey test was performed for parametric data (P < 0.05). Results There was no significant difference in the calcium and phosphorus levels in plasma amongst the groups (P > 0.05). The level of alkaline phosphatase was significantly higher in the groups that consumed probiotics (P < 0.05). A significantly lower volume of bone resorption was observed in groups that consumed probiotics (P < 0.05). The inflammatory infiltrates and the immunolabelling for RANKL and TRAP were significantly lower in probiotic groups when compared to the control (P < 0.05). Also, the OPG was significantly more immunolabelled in the L. acidophilus group than in the L. rhamnosus and control groups (P < 0.05). Conclusion Probiotic supplementation through gavage (L. rhamnosus and L. acidophilus) had a significant effect on the reduction of inflammation and bone resorption in apical periodontitis development in rats.