title: Association between skeletal muscle inflammatory markers and walking pattern in people with knee osteoarthritis.
abstract: OBJECTIVE
  Patients with knee osteoarthritis (OA) are characterized by increased muscle inflammation and altered gait. We investigated the association between proinflammatory mediators in the vastus lateralis and physical function and gait in patients with knee OA.
  
  
  METHODS
  Nineteen patients with knee OA underwent gait analysis, assessment of self-reported pain and physical function (Western Ontario and McMaster Universities Osteoarthritis Index [WOMAC]), and a muscle biopsy that was taken during their knee replacement surgery. Muscle was analyzed for cellular protein inflammatory mediators, interleukin-6, monocyte chemotactic protein 1 (MCP-1), p65 NF-κB, signal transducer and activator of transcription 3 (STAT-3), and JNK-1. Sagittal plane knee function, including early stance knee range of motion (ROM) and knee sagittal plane impulse, was measured using a motion analysis system. Pearson's correlation was used to assess relationships between selected variables.
  
  
  RESULTS
  Significant positive correlations were found between MCP-1 and self-perceived stiffness, physical function, and the total WOMAC score (P < 0.05). MCP-1 was also negatively correlated with early stance knee ROM (r = -0.52, P = 0.023). Reduced velocity was associated with elevated levels of p65 NF-κB and STAT-3 (P < 0.05). Knee sagittal plane impulse was negatively correlated with JNK-1 (P = 0.02), indicating reduction in knee impulse with an increased level of JNK-1.
  
  
  CONCLUSIONS
  Increased levels of several proinflammatory mediators were correlated with altered knee function during walking as well as greater physical disability and slower gait velocity. Identification of the cellular and molecular mechanisms associated with muscle inflammation is important to better understand the underlying mechanism responsible for altered gait and function in patients with knee OA.
authors: La Trobe University, Bundoora, Victoria, Australia. p.levinger@latrobe.edu.au
authors: Pazit
authors: P
authors: Levinger
authors: Marissa K
authors: MK
authors: Caldow
authors: Julian A
authors: JA
authors: Feller
authors: John R
authors: JR
authors: Bartlett
authors: Neil R
authors: NR
authors: Bergman
authors: Michael J
authors: MJ
authors: McKenna
authors: David
authors: D
authors: Cameron-Smith
authors: Itamar
authors: I
authors: Levinger
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000032:analysis; D001696:Biomechanical Phenomena; D001706:Biopsy; D018932:Chemokine CCL2 / Q000032:analysis; D003430:Cross-Sectional Studies; D004185:Disability Evaluation; D005260:Female; D005684:Gait; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D048055:Mitogen-Activated Protein Kinase 8 / Q000032:analysis; D020370:Osteoarthritis, Knee / Q000175:diagnosis / Q000276:immunology* / Q000503:physiopathology*; D010147:Pain Measurement; D052097:Quadriceps Muscle / Q000276:immunology* / Q000503:physiopathology*; D016059:Range of Motion, Articular; D050796:STAT3 Transcription Factor / Q000032:analysis; D057566:Self Report; D051996:Transcription Factor RelA / Q000032:analysis; D014739:Victoria; D016138:Walking
chemical_list: D015415:Biomarkers; C111835:CCL2 protein, human; D018932:Chemokine CCL2; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; C498143:RELA protein, human; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D051996:Transcription Factor RelA; D048055:Mitogen-Activated Protein Kinase 8