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

AIM 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 etiopathogenesis 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), its prognostic value and evaluate associated microbial, periodontal and psychosocial factors. METHODS Gingival crevicular fluid was collected in two pathological (Periodontal Pocket Depth (PPD)≥5mm) and one healthy sites (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 13-15 weeks in initial periodontal treatment. sTREM-1 and salivary cortisol levels were determined by ELISA and periodontopathogens by PCR. RESULTS Before SRP, higher crevicular sTREM-1 levels were positively associated with some increased clinical parameters (Plaque Index, tooth mobility, bleeding on probing, p<0.05), and inversely with Aggregatibacter actinomycetemcomitans abundance (p=0.03). No correlation with psychological factors nor cortisol was found with salivary sTREM-1 concentrations. After SRP, crevicular sTREM-1 levels decreased (p<0.001) and were not linked to a PPD decrease but remained higher in pathological than in healthy sites (p<0.001). Higher concentrations were also found out in unimproved sites (no change or increase in PPD) compared to improved ones (p=0.02). Higher sTREM-1 levels were associated with Porphyromonas gingivalis, Treponema denticola, Campylobacter rectus in pathological sites after SRP (p<0.05). CONCLUSION 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.

[1]  S. Vermeire,et al.  Low TREM1 expression in whole blood predicts anti-TNF response in inflammatory bowel disease , 2019, EBioMedicine.

[2]  V. Machado,et al.  Stress, salivary cortisol and periodontitis: A systematic review and meta-analysis of observational studies. , 2018, Archives of oral biology.

[3]  S. Gibot,et al.  Effects of Porphyromonas gingivalis LPS and LR12 peptide on TREM‐1 expression by monocytes , 2018, Journal of clinical periodontology.

[4]  K. Kornman,et al.  Staging and grading of periodontitis: Framework and proposal of a new classification and case definition , 2018, Journal of periodontology.

[5]  Yung-Yang Lin,et al.  Role of TREM-1 in pulmonary tuberculosis patients- analysis of serum soluble TREM-1 levels , 2018, Scientific Reports.

[6]  L. Gonzalez-Lopez,et al.  Utility of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) as biomarker to predict therapeutic response to methotrexate in rheumatoid arthritis , 2017, Innate immunity.

[7]  J. Kay,et al.  Activation of the TREM‐1 pathway in human monocytes by periodontal pathogens and oral commensal bacteria , 2017, Molecular oral microbiology.

[8]  L. Boyanova Stress hormone epinephrine (adrenaline) and norepinephrine (noradrenaline) effects on the anaerobic bacteria. , 2017, Anaerobe.

[9]  G. Seymour,et al.  Risk factors that may modify the innate and adaptive immune responses in periodontal diseases. , 2016, Periodontology 2000.

[10]  L. Su,et al.  Role of sTREM-1 in predicting mortality of infection: a systematic review and meta-analysis , 2016, BMJ Open.

[11]  P. Preshaw,et al.  Gingival crevicular fluid and saliva. , 2016, Periodontology 2000.

[12]  P. Bruneval,et al.  TREM-1 Mediates Inflammatory Injury and Cardiac Remodeling Following Myocardial Infarction. , 2015, Circulation research.

[13]  A. Teixeira,et al.  sTREM-1 predicts intensive care unit and 28-day mortality in cancer patients with severe sepsis and septic shock. , 2015, Journal of critical care.

[14]  U. Covani,et al.  Microbiological assessment of the implant-abutment interface in different connections: cross-sectional study after 5 years of functional loading. , 2015, Clinical oral implants research.

[15]  N. Bostanci,et al.  Expression and regulation of triggering receptor expressed on myeloid cells 1 in periodontal diseases , 2014, Clinical and experimental immunology.

[16]  K. Turner,et al.  Mechanisms of synergy in polymicrobial infections , 2014, Journal of Microbiology.

[17]  N. Bostanci,et al.  Elevated Oral and Systemic Levels of Soluble Triggering Receptor Expressed on Myeloid Cells-1 (sTREM-1) in Periodontitis , 2013, Journal of dental research.

[18]  F. Massin,et al.  Increased gingival crevicular fluid levels of soluble triggering receptor expressed on myeloid cells (sTREM) -1 in severe periodontitis. , 2012, Journal of clinical periodontology.

[19]  R. Lamont,et al.  Beyond the red complex and into more complexity: the polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology. , 2012, Molecular oral microbiology.

[20]  N. Bostanci,et al.  Doxycycline inhibits TREM-1 induction by Porphyromonas gingivalis. , 2012, FEMS immunology and medical microbiology.

[21]  K. Leung,et al.  Comparative Analysis of Single-Species and Polybacterial Wound Biofilms Using a Quantitative, In Vivo, Rabbit Ear Model , 2012, PloS one.

[22]  T. Thurnheer,et al.  Involvement of the TREM-1/DAP12 pathway in the innate immune responses to Porphyromonas gingivalis. , 2011, Molecular immunology.

[23]  B. Henderson,et al.  Aggregatibacter (Actinobacillus) actinomycetemcomitans: a triple A* periodontopathogen? , 2010, Periodontology 2000.

[24]  D. Grenier,et al.  Synergistic effects of lipopolysaccharides from periodontopathic bacteria on pro-inflammatory cytokine production in an ex vivo whole blood model. , 2010, Molecular oral microbiology.

[25]  A. Duarte-Rojo,et al.  Triggering receptor expressed on myeloid cells-1 expression on monocytes is associated with inflammation but not with infection in acute pancreatitis , 2009, Critical care.

[26]  A. Cerwenka,et al.  The TREM-1/DAP12 pathway. , 2008, Immunology letters.

[27]  M. Ornatowska,et al.  Functional genomics of silencing TREM-1 on TLR4 signaling in macrophages. , 2007, American journal of physiology. Lung cellular and molecular physiology.

[28]  M. Kemeny,et al.  Understanding the interaction between psychosocial stress and immune-related diseases: A stepwise progression , 2007, Brain, Behavior, and Immunity.

[29]  P. Eke,et al.  Case Definitions for Use in Population-Based Surveillance of Periodontitis. , 2007, Journal of periodontology.

[30]  O. Lesur,et al.  Effects of TREM-1 activation in human neutrophils: activation of signaling pathways, recruitment into lipid rafts and association with TLR4. , 2006, International immunology.

[31]  S. Zakynthinos,et al.  Does soluble triggering receptor expressed on myeloid cells‐1 play any role in the pathogenesis of septic shock? , 2005, Clinical and experimental immunology.

[32]  Shi Wei,et al.  IL-1 mediates TNF-induced osteoclastogenesis. , 2005, The Journal of clinical investigation.

[33]  J. Suvan Effectiveness of mechanical nonsurgical pocket therapy. , 2005, Periodontology 2000.

[34]  M. Béné,et al.  A Soluble Form of the Triggering Receptor Expressed on Myeloid Cells-1 Modulates the Inflammatory Response in Murine Sepsis , 2004, The Journal of experimental medicine.

[35]  S. Gibot,et al.  Soluble form of the triggering receptor expressed on myeloid cells-1 as a marker of microbial infection. , 2004, Clinical medicine & research.

[36]  C. Drisko,et al.  Nonsurgical periodontal therapy. , 2001, Periodontology 2000.

[37]  M. Colonna,et al.  Cutting Edge: Inflammatory Responses Can Be Triggered by TREM-1, a Novel Receptor Expressed on Neutrophils and Monocytes1 , 2000, The Journal of Immunology.

[38]  Y. Azuma,et al.  Tumor Necrosis Factor-α Induces Differentiation of and Bone Resorption by Osteoclasts* , 2000, The Journal of Biological Chemistry.

[39]  G. Armitage,et al.  Development of a classification system for periodontal diseases and conditions. , 1999, Annals of periodontology.

[40]  S. Socransky,et al.  Microbial complexes in subgingival plaque. , 1998, Journal of clinical periodontology.

[41]  K. Gulati,et al.  Stress, Anxiety, and Immunomodulation: A Pharmacological Analysis. , 2017, Vitamins and hormones.

[42]  N. Bostanci,et al.  Soluble triggering receptor expressed on myeloid cells 1 (sTREM-1) in gingival crevicular fluid: association with clinical and microbiologic parameters. , 2014, Journal of periodontology.

[43]  Howard C. Tenenbaum,et al.  Periodontal diseases and stress: a brief review. , 2013, Journal of oral rehabilitation.