Gwendolyn Sowa1, Sudha Agarwal. 1. Department of Physical Medicine and Rehabilitation, Ferguson Laboratory for Orthopaedic Research, Pittsburgh, PA 15213, USA.
Abstract
OBJECTIVE: To examine the mechanisms behind the beneficial effects of motion-based therapies, the hypothesis that physiologic levels of tensile stress have a beneficial effect on annulus fibrosus cells was tested. DESIGN: To examine the roles of mechanical forces and inflammation in the intervertebral disc, changes in gene expression in response to inflammatory stimulus (IL-1 beta) and tensile stress (6% stress at 0.05 Hz) were examined in fibrochondrocytes isolated from the annulus fibrosus of Sprague-Dawley rats. RESULTS: Cells exposed to an inflammatory stimulus demonstrated an increase in catabolic gene expression, which decreased approximately 50% after exposure to both inflammatory stimulus and tensile stress. After exposure of cells to tensile stress alone, only matrix metalloprotease-13 showed a 50% decrease in expression. Collagen II showed a modest decrease in expression in response to tensile stress in the inflammatory environment. The expression of collagen I and aggrecan did not show a significant change under any of the conditions tested. CONCLUSIONS: In this in vitro model, our data demonstrate that moderate levels of tensile stress act as a protective signal by decreasing the expression of catabolic mediators under conditions of inflammation. These data suggest that motion-based therapies that create tensile stress on the annulus may exert their beneficial effects through antiinflammatory actions.
OBJECTIVE: To examine the mechanisms behind the beneficial effects of motion-based therapies, the hypothesis that physiologic levels of tensile stress have a beneficial effect on annulus fibrosus cells was tested. DESIGN: To examine the roles of mechanical forces and inflammation in the intervertebral disc, changes in gene expression in response to inflammatory stimulus (IL-1 beta) and tensile stress (6% stress at 0.05 Hz) were examined in fibrochondrocytes isolated from the annulus fibrosus of Sprague-Dawley rats. RESULTS: Cells exposed to an inflammatory stimulus demonstrated an increase in catabolic gene expression, which decreased approximately 50% after exposure to both inflammatory stimulus and tensile stress. After exposure of cells to tensile stress alone, only matrix metalloprotease-13 showed a 50% decrease in expression. Collagen II showed a modest decrease in expression in response to tensile stress in the inflammatory environment. The expression of collagen I and aggrecan did not show a significant change under any of the conditions tested. CONCLUSIONS: In this in vitro model, our data demonstrate that moderate levels of tensile stress act as a protective signal by decreasing the expression of catabolic mediators under conditions of inflammation. These data suggest that motion-based therapies that create tensile stress on the annulus may exert their beneficial effects through antiinflammatory actions.
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