title: Differential expression of mitogen activating protein kinases in periodontitis.
abstract: OBJECTIVE
  Following toll-like receptor (TLR) engagement, lipopolysaccharide (LPS) can stimulate the expression of pro-inflammatory cytokines thus activating the innate immune response. The production of inflammatory cytokines results, in part, from the activation of kinase-induced signalling cascades and transcriptional factors. Of the four distinct classes of mitogen-activated protein kinases (MAPK) described in mammals, p38, c-Jun N-terminal activated kinases (JNK1-3) and extracellular activated kinases (ERK1,2) are the best studied. Previous data have established that p38 MAPK signalling is required for inflammation and bone loss in periodontal disease pre-clinical animal models.
  
  
  METHODS
  In this study, we obtained healthy and diseased periodontal tissues along with clinical parameters and microbiological parameters. Excised fixed tissues were immunostained with total and phospho-specific antibodies against p38, JNK and ERK kinases.
  
  
  RESULTS
  Intensity scoring from immunostained tissues was correlated with clinical periodontal parameters. Rank correlations with clinical indices were statistically significantly positive (p-value < 0.05) for total p38 (correlations ranging 0.49-0.68), phospho-p38 (range 0.44-0.56), and total ERK (range 0.52-0.59) levels, and correlations with JNK levels also supported association (range 0.42-0.59). Phospho-JNK and phospho-ERK showed no significant positive correlation with clinical parameters of disease.
  
  
  CONCLUSIONS
  These data strongly implicate p38 MAPK as a major MAPK involved in human periodontal inflammation and severity.
authors.affiliation: Department of Periodontics and Oral Medicine, School of Dentistry, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Suncica
authors.initials: S
authors.lastname: Travan
authors.forename: Fei
authors.initials: F
authors.lastname: Li
authors.forename: Nisha J
authors.initials: NJ
authors.lastname: D'Silva
authors.forename: Elizabeth H
authors.initials: EH
authors.lastname: Slate
authors.forename: Keith L
authors.initials: KL
authors.lastname: Kirkwood
mesh_terms: D001439:Bacteroides / Q000302:isolation & purification; D055113:Chronic Periodontitis / Q000201:enzymology* / Q000276:immunology / Q000382:microbiology; D003774:Dental Plaque Index; D005260:Female; D005884:Gingival Hemorrhage / Q000201:enzymology / Q000276:immunology / Q000382:microbiology; D005889:Gingival Recession / Q000201:enzymology / Q000276:immunology / Q000382:microbiology; D006801:Humans; D008214:Lymphocytes / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000032:analysis; D048057:Mitogen-Activated Protein Kinase 10 / Q000032:analysis; D048052:Mitogen-Activated Protein Kinase 3 / Q000032:analysis; D048055:Mitogen-Activated Protein Kinase 8 / Q000032:analysis; D048056:Mitogen-Activated Protein Kinase 9 / Q000032:analysis; D020928:Mitogen-Activated Protein Kinases / Q000032:analysis*; D017622:Periodontal Attachment Loss / Q000201:enzymology / Q000276:immunology / Q000382:microbiology; D010512:Periodontal Index; D010514:Periodontal Pocket / Q000201:enzymology / Q000276:immunology / Q000382:microbiology; D010519:Periodontium / Q000201:enzymology; D010950:Plasma Cells / Q000276:immunology; D016966:Porphyromonas gingivalis / Q000302:isolation & purification; D048373:Treponema denticola / Q000302:isolation & purification; D048051:p38 Mitogen-Activated Protein Kinases / Q000032:analysis
chemical_list: D048057:Mitogen-Activated Protein Kinase 10; D048056:Mitogen-Activated Protein Kinase 9; C535150:MAPK1 protein, human; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D048055:Mitogen-Activated Protein Kinase 8; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases
keywords: cell signalling; inflammation; mitogen activating protein kinases; periodontitis