LPS-induced inflammatory response after therapy of aggressive periodontitis.

We have reported a lipopolysaccharide (LPS)-induced hyper-inflammatory response in localized aggressive periodontitis (LAP). It is unknown whether treatment is able to modulate this LPS responsiveness. Fifty-nine individuals with LAP were treated by mechanical debridement and systemic antibiotics. Clinical parameters and cyto/chemokine responsiveness of whole blood stimulated with Porphyromonas gingivalis or Escherichia coli LPS were monitored at baseline and 3, 6, and 12 months post-treatment. Overall, clinical parameters were improved following treatment. Additionally, P. gingivalis LPS induction of eotaxin, IFNγ, IL10, IL12p40, IL1β, IL6, IP10, MCP1, MIP1α, GM-CSF, and TNFα was significantly decreased (p < .05). Similarly, induction of eotaxin, INFγ, IL10, IL12p40, GM-CSF, and TNFα by E. coli LPS was also reduced post-treatment. These reductions correlated with decreases in clinical parameters. Importantly, these reductions in LPS responsiveness were most robust at 3 months, and some lost significance at 6 to 12 months post-treatment. In conclusion, LPS-induced hyper-inflammatory response in LAP can be partially modulated by periodontal therapy. Conversely, rebound in the hyper-responsiveness of some mediators, in the presence of improved clinical parameters, suggests that this phenotype could be partially influenced by a genetic trait and play a role in future disease recurrence (ClinicalTrials.gov, NCT01330719).