Influência bidirecional da síndrome metabólica e periodontite apical

Abstract

The present study investigated the possible bidirectional interrelations between fructose-induced metabolic syndrome and apical periodontitis in an animal model. Twenty-eight male Wistar rats were distributed into four groups (n=7 per group): Control (C), Apical Periodontitis (AP), Fructose Consumption (FRUT), and Fructose Consumption and Apical Periodontitis (FRUT+AP). The animals received filtered water ad libitum (C and AP) or 20% fructose mixed with water to induce metabolic syndrome (FRUT and FRUT+AP). After 4 weeks of the experiment, the animals in the AP and FRUT+AP groups had the pulp of the lower right first molar exposed for 28 days to induce the formation of periapical lesions. The animals underwent inspections throughout the experiment to determine food intake, murinometric measurements, fasting blood glucose, and oral glucose tolerance test. After the 8-week experimental period, the animals were euthanized, and blood samples were collected for subsequent serum metabolomic analysis. Samples from the mandibles, livers, and kidneys were also collected and analyzed. The area and volume dimensions of periapical lesions were calculated using micro-computed tomography images. After histological processing, samples from the hemimandibles, livers, and kidneys were stained with hematoxylin and eosin for histopathological evaluation. Non-parametric data were analyzed by the Kruskal-Wallis test followed by Student Newman-Keuls or the Mann-Whitney post-tests (Wilcoxon Rank-Sum test), while parametric data used one-way ANOVA followed by Tukey's post-test or the independent t-test. The significance level was set at 5%.The groups that received fructose (FRUT and FRUT+AP) had higher liquid intakes (p<0.05) and showed significant weight gain, length, abdominal circumference, and blood glucose compared to the C and AP groups (p<0.05), indicating the development of metabolic syndrome. Significant differences were also observed in the levels of the metabolites glucose, alanine, glutamine, lipid I, valine, histidine, lactate, valerate, fatty acid, lipid III, and phenylalanine in the FRUT and FRUT+AP groups. However, there was no significant difference in the volume and area of periapical lesions in the AP and FRUT+AP groups (p=0.1048; p=0.7494, respectively), analyzed by micro-CT. All animals subjected to pulp access presented inflammatory responses in the periapical lesion areas. Inflammatory infiltrate areas were observed in the apical region of the root and small areas of necrosis and microabscess in the AP and FRUT+AP groups. Hepatic histopathological observation revealed the presence of Kupffer cells in the sinusoids in the AP group, and in the FRUT and FRUT+AP groups, microsteatosis was observed. Renal analysis showed Bowman's space dilation in the AP group, and in the FRUT+AP group, distal tubules and altered renal corpuscles were observed exhibiting Bowman's space and retracted glomeruli, compared to the C group. In conclusion, was noted that metabolic syndrome did not influence the progression of apical periodontitis in Wistar rats. However, was observed that apical periodontitis exacerbated the systemic state affected by metabolic syndrome, resulting in alterations in hepatic and renal tissues, as well as in metabolite levels.