Comparison of sTREM-1 and associated periodontal and bacterial factors before/after periodontal therapy, and impact of psychosocial factors.

Abstract

The immune receptor triggering receptor expressed on myeloid cell-1 (TREM-1) is responsible for an amplification of the immuno-inflammatory response in inflammatory diseases. Its role in the aetiopathogenesis of periodontitis is underexplored. The aim of this case-control and before-after study was to determine the evolution of soluble form of TREM-1 (sTREM-1) concentrations after scaling and root planing (SRP), and its prognostic value and evaluate associated microbial, periodontal and psychosocial factors. Gingival crevicular fluid was collected in two pathological sites (periodontal pocket depth (PPD)≥5mm) and one healthy site (PPD≤3mm) from thirty periodontitis patients (before/after SRP), and in one healthy site from thirty controls (patients without periodontal disease). Each patient filled-in stress/anxiety self-assessment questionnaires and provided a saliva sample. Diseased patients were followed for a total of 13-15weeks in initial periodontal treatment. sTREM-1 and salivary cortisol levels were determined by ELISA and periodontopathogens by PCR. Before SRP, higher crevicular sTREM-1 levels were positively associated with some increased clinical parameters (Plaque Index, tooth mobility, bleeding on probing, p<.05) and inversely with Aggregatibacter actinomycetemcomitans abundance (p=.03). No correlation with psychological factors nor cortisol was found with salivary sTREM-1 concentrations. After SRP, crevicular sTREM-1 levels decreased (p<.001) and were not linked to a PPD decrease but remained higher in pathological than in healthy sites (p<.001). Higher concentrations were also found out in unimproved sites (no change or increase in PPD) compared to improved ones (p=.02). Higher sTREM-1 levels were associated with Porphyromonas gingivalis, Treponema denticola and Campylobacter rectus in pathological sites after SRP (p<.05). Crevicular sTREM-1 level decreased after SRP but did not appear to be a site outcome predictive factor of periodontal healing and remained an inflammatory parameter.