Stress deprivation simultaneously induces over-expression of interleukin-1beta, tumor necrosis factor-alpha, and transforming growth factor-beta in fibroblasts and mechanical deterioration of the tissue in the patellar tendon.

Abstract:

:To test the hypothesis that stress deprivation induces over-expression of cytokines in the patellar tendon, 40 rats were divided into the following two groups. In the stress-shielded group, we slackened the patellar tendon in the right knee by drawing the patella toward the tibial tubercle with flexible wires. In the control group, we performed a sham operation on the right knee. Animals were killed at 2 or 6 weeks for immunohistological evaluation and biomechanical examination. For IL-1beta, TNF-alpha and TGF-beta, the ratio of positively stained specimens to total specimens was significantly higher in the stress-shielded tendons than in the control tendons. The elastic modulus of the stress-shielded tendon was significantly lower than that of the control tendon, while the cross-sectional area of the stress-shielded tendon was significantly greater than that of the control tendon. Therefore, the present study indicated that stress shielding induced the over-expression of IL-1beta, TNF-alpha and TGF-beta in patellar tendon fibroblasts with mechanical deterioration of the tendon. Regarding clinical relevance, the present study suggests a possible application of an anti-IL-1beta or anti-TNF-alpha strategy for reducing the mechanical deterioration of tendons and ligaments in response to stress deprivation, although this study did not directly show that over-expression of IL-1beta or TNF-alpha in response to stress deprivation was the causation of mechanical deterioration of tendons.

journal_name

J Biomech

journal_title

Journal of biomechanics

authors

Uchida H,Tohyama H,Nagashima K,Ohba Y,Matsumoto H,Toyama Y,Yasuda K

doi

10.1016/j.jbiomech.2004.05.009

keywords:

subject

Has Abstract

pub_date

2005-04-01 00:00:00

pages

791-8

issue

4

eissn

0021-9290

issn

1873-2380

pii

S0021929004002453

journal_volume

38

pub_type

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