Association between skeletal muscle inflammatory markers and walking pattern in people with knee osteoarthritis†
Article first published online: 29 NOV 2011
Copyright © 2011 by the American College of Rheumatology
Arthritis Care & Research
Volume 63, Issue 12, pages 1715–1721, December 2011
How to Cite
Levinger, P., Caldow, M. K., Feller, J. A., Bartlett, J. R., Bergman, N. R., McKenna, M. J., Cameron-Smith, D. and Levinger, I. (2011), Association between skeletal muscle inflammatory markers and walking pattern in people with knee osteoarthritis. Arthritis Care Res, 63: 1715–1721. doi: 10.1002/acr.20625
- Issue published online: 29 NOV 2011
- Article first published online: 29 NOV 2011
- Accepted manuscript online: 8 SEP 2011 03:39PM EST
- Manuscript Accepted: 30 AUG 2011
- Manuscript Received: 27 JUN 2011
- L. E. W. Carty Charitable Fund, Australia
- Clive and Vera Ramaciotti Foundation
- Arthritis Australia
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.
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.
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.
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.