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Cyclic Tensile Stress Exerts a Protective Effect on Intervertebral Disc Cells

Sowa, Gwendolyn MD, PhD; Agarwal, Sudha PhD

American Journal of Physical Medicine & Rehabilitation: July 2008 - Volume 87 - Issue 7 - p 537-544
doi: 10.1097/PHM.0b013e31816197ee
Original Research Article: Back Pain

Sowa G, Agarwal S: Cyclic tensile stress exerts a protective effect on intervertebral disc cells. Am J Phys Med Rehabil 2008;87:537–544.

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-1β) 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.

From the Department of Physical Medicine and Rehabilitation, Ferguson Laboratory for Orthopaedic Research, Department of Orthopaedics, Pittsburgh, Pennsylvania (GS); and Biomechanics and Tissue Engineering Laboratory, The Ohio State University, Columbus, Ohio (SA).

All correspondence and requests for reprints should be addressed to Gwendolyn Sowa, MD, PhD, Department of Physical Medicine and Rehabilitation, 3471 5th Ave., Suite 202, Pittsburgh, PA 15213.

This work was supported by NIH Grant #2K12HD01097-06, Medical Rehabilitation Scientist Training Program, Association of Academic Physiatrists. Data previously presented at the Association of Academic Physiatrists Annual Meeting, Daytona, Florida, 2006 for the Electrode Store Best Paper Presentation.

© 2008 Lippincott Williams & Wilkins, Inc.