Effect of Periodontal Treatment on TREM-1 Levels in Saliva

Objectives: TREM-1 is a cell-surface receptor of the immunoglobulin superfamily, involved in amplification of the innate inflammatory response to bacterial infections and may be responsible for hyper-responsiveness in generalized aggressive periodontitis (GAgP). Thus, the aim of this longitudinal study was to determine whether TREM-1 levels in saliva were altered after periodontal therapy, and correlated with the levels of key pro-inflammatory cytokines and total bacterial load.
Methods: Thirty-three patients diagnosed with GAgP (mean age: G1: 32.5±3.9, G2: 32.0±3.9) were recruited in the study and randomly assigned into either single session (G1) or quadrant-based multiple session (G2) based non-surgical periodontal therapy. Full-mouth periodontal examination was performed at baseline, and at 1, 3, 6 months. Whole saliva was also collected at these time-points. Salivary TREM-1 and Interleukin (IL)-1β were measured by ELISA and normalized against total protein levels. Total bacterial counts were determined by quantitative PCR. Statistical analysis was performed using the mixed model repeated measure Anova followed by the Tukey-Kramer post hoc test.
Results: Despite the improved clinical parameters, salivary TREM-1 remained unchanged throughout the monitoring time. After periodontal therapy, its levels slightly reduced at 1 month in both treatment groups (mean±sdev pg/mg): G1: 911.2±469.6 Vs 742.2±409.0, G2: 981.9±549.3 Vs 809.5±473.5), gradually inclined to baseline levels by 6 months (G1: 995.1±501.0 and G2: 1233±720.6) but the differences were not significant. Salivary TREM-1 levels showed positive and significant correlations with IL-1β (p< 0.0001). The total bacterial load also remained unchanged compared with that of baseline with a similar trend in both groups.
Conclusions: The present data indicate that TREM-1 is detected in saliva of patients with GAgP and remains unchanged after periodontal therapy, along with the IL-1β. This finding may implicate the sustained levels of TREM-1 in local hyper-responsive inflammation, thus rendering the host prone to further tissue destruction.