Porphyromonas gingivalis lipopolysaccharide-induced periodontitis and serum amyloid-beta peptides

Abstract

Objective The aim of this investigation was to determine the circulating levels of amyloid beta (Aβ) peptides using the Porphyromonas gingivalis (Pg) lipopolysaccharide (LPS) model to induce periodontitis. Methods Experimental periodontitis was induced in 6 male Sprague-Dawley rats. Alveolar bone loss was measure by micro computed tomography. Serum concentrations of Aβ1–40 and Aβ1–42 prior to periodontal induction, at 24 h, 7, 14, and 21 days the last injection of Pg-LPS. Results The distance between the cemento-enamel junction and the bone crest (i.e., alveolar bone loss) was significantly higher at the end of periodontal induction compared to baseline (2.92 ± 0.29 mm vs. 3.8 ± 0.28 mm, P < 0.001). Periodontitis evoked a slight acute elevation of Aβ1–40 serum levels that were maintained during the whole experiment. Aβ1–42 peptide levels peak at the end of the study. A positive strong correlation was observed between alveolar bone loss and Aβ1–40 serum levels at 7 days (r = 0.695, P = 0.012) and as well as with serum Aβ1–42 concentrations at 21 days (r = 0.968, P = 0.002). Conclusions Periodontitis induced Pg-LPS produced increased serum levels of Aβ peptides. Further studies are needed to confirm our results and to investigate the mechanisms by which periodontitis could be associated with an overexpression of Aβ