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

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 Aβ and Aβ 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 Aβ serum levels that were maintained during the whole experiment. Aβ peptide levels peak at the end of the study. A positive strong correlation was observed between alveolar bone loss and Aβ serum levels at 7 days (r = 0.695, P = 0.012) and as well as with serum Aβ 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.