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Inflammatory cells do not decrease the ultimate tensile strength of intact tendons in vivo and in vitro: protective
David Marsolais1, Elise Duchesne, Claude H Côté
1Centre de Recherche du Centre Hospitalier Universitaire de Québec, Quebec City, Quebec, Canada.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|August 19, 2006
Summary
Acute inflammation does not damage mechanically stressed collagen fibers. Mechanical loading protects tendons from inflammatory cell degradation, highlighting intrinsic resistance to proteolytic activity.
Area of Science:
- Biochemistry
- Histology
- Biomechanics
- Cell Biology
Background:
- Inflammatory cells contribute to various pathological processes.
- The role of inflammation in tendon dysfunction remains under-investigated.
- Investigating inflammation's impact on tendons requires understanding its interaction with mechanical stress.
Purpose of the Study:
- To determine if acute inflammation, without mechanical trauma, damages intact collagen fibers.
- To analyze the biochemical, histological, and biomechanical effects of leukocyte invasion on tendons.
- To assess if mechanical loading protects collagen from inflammatory cell-induced damage.
Main Methods:
- Carrageenan injection induced leukocyte accumulation in rat Achilles tendons.
- Assessed matrix metalloproteinase (MMP) and tissue inhibitor of matrix metalloproteinase (TIMP) levels.
- Analyzed hydroxyproline content, load to failure, and in vitro mechanical stress effects on collagen bundles.
Main Results:
- Leukocyte accumulation increased MMP activity and decreased TIMP content.
- No significant changes were observed in hydroxyproline content or load to failure.
- In vitro mechanical stress protected collagen bundles from inflammatory cell degradation.
Conclusions:
- Acute inflammation does not damage intact, mechanically stressed collagen fibers.
- Mechanically loaded collagen exhibits intrinsic resistance to proteolytic degradation.
- This protective effect is independent of increased TIMP levels.
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