The Proteoglycan Metabolism of Mature Bovine Articular Cartilage Explants Superimposed to Continuously Applied Cyclic Mechanical Loading

Steinmeyer, Jürgen; Knue, Sabine

doi:10.1006/bbrc.1997.7641

Cited by 65 publications

(47 citation statements)

References 22 publications

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“…Generally, static compression suppresses cartilage metabolism in a dosedependent manner, while dynamic (sinusoidal or intermittent) loading has a stimulatory effect [12]. However, in "load-controlled" experiments (comparable to the method used in our study), both static and intermittent compression may decrease the biosynthesis and degradation of aggrecan [11,34,36,37]. Due to the viscoelastic (rate-dependent) mechanical properties of articular cartilage, the tissue does not have time to recover its original shape during load-controlled intermittent compression at physiological frequencies.…”

Section: Discussionmentioning

confidence: 93%

The effects of static and intermittent compression on nitric oxide production in articular cartilage explants

Fermor¹,

Weinberg²,

Pisetsky³

et al. 2001

Journal Orthopaedic Research

148

108

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Nitric oxide (NO) production and NO synthase (NOS) expression are increased in osteoarthritis and rheumatoid arthritis, suggesting that NO may play a role in the destruction of articular cartilage. To test the hypothesis that mechanical stress may increase NO production by chondrocytes, we measured the effects of physiological levels of static and intermittent compression on NOS activity, NO production, and NOS antigen expression by porcine articular cartilage explants. Static compression significantly increased NO production at 0.1 MPa stress for 24 h (P < 0.05). Intermittent compression at 0.5 Hz for 6 h followed by 18 h recovery also increased NO production and NOS activity at 1.0 MPa stress (P < 0.05). Intermittent compression at 0.5 Hz for 24 h at a magnitude of 0.1 or 0.5 MPa caused an increase in NO production and NOS activity (P < 0.05). Immunoblot analysis showed stress-induced upregulation of NOS2, but not NOS1 or NOS3. There was no loss in cell viability following any of the loading regimens. Addition of 2 mM 1400 W (a specific NOS2 inhibitor) reduced NO production by 51% with no loss of cell viability. These findings indicate that NO production by chondrocytes is influenced by mechanical compression in vitro and suggest that biomechanical factors may in part regulate NO production in vivo.

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Section: Discussionmentioning

confidence: 93%

The effects of static and intermittent compression on nitric oxide production in articular cartilage explants

Fermor¹,

Weinberg²,

Pisetsky³

et al. 2001

Journal Orthopaedic Research

148

108

View full text Add to dashboard Cite

show abstract

“…The organisation of the extracellular matrix components includes mechanisms transmitting tensile forces along the interfibrilar matrix. Several studies have reported that cells have the ability to produce a better organised collagen matrix modulated by cyclic load (Steinmeyer and Knue, 1997;Wang and Grood, 2000;Wang et al, 2003a;Webb et al, 2006) and this way achieve an increase in tissue stiffness (Brown et al, 1998;Lo et al, 2000). The methods used in the present study do not permit examination of such adaptation possibilities at the Achilles tendon; nevertheless, the clear changes in the tendon-aponeurosis strain-force relationship, the only regionspecific tendon hypertrophy, the increase of the tendon elastic modulus, as well as reports of other studies demonstrating an increase in human tendon stiffness and elastic modulus with no changes in the tendon's CSA (Kubo et al, 2002;Reeves et al, 2003a) provide evidence for the plasticity of the organisation of the tendon's extracellular matrix in vivo (i.e.…”

Section: Discussionmentioning

confidence: 99%

Adaptational responses of the human Achilles tendon by modulation of the applied cyclic strain magnitude

Arampatzis

Karamanidis

Albracht

2007

Journal of Experimental Biology

291

434

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SUMMARY Tendons are able to remodel their mechanical and morphological properties in response to mechanical loading. However, there is little information about the effects of controlled modulation in cyclic strain magnitude applied to the tendon on the adaptation of tendon's properties in vivo. The present study investigated whether the magnitude of the mechanical load induced as cyclic strain applied to the Achilles tendon may have a threshold in order to trigger adaptation effects on tendon mechanical and morphological properties. Twenty-one adults (experimental group, N=11; control group, N=10) participated in the study. The participants of the experimental group exercised one leg at low-magnitude tendon strain (2.85±0.99%) and the other leg at high-magnitude tendon strain (4.55±1.38%) of similar frequency and volume. After 14 weeks of exercise intervention we found a decrease in strain at a given tendon force, an increase in tendon-aponeurosis stiffness and tendon elastic modulus and a region-specific hypertrophy of the Achilles tendon only in the leg exercised at high strain magnitude. These findings provide evidence of the existence of a threshold or set-point at the applied strain magnitude at which the transduction of the mechanical stimulus may influence the tensional homeostasis of the tendons. The results further show that the mechanical load exerted on the Achilles tendon during the low-strain-magnitude exercise is not a sufficient stimulus for triggering further adaptation effects on the Achilles tendon than the stimulus provided by the mechanical load applied during daily activities.

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“…The relevance of these finding needs to be further examined. The signals elicited during acute trauma on AC may also differ among various types of loading since expression of MMPs and matrix synthesis were enhanced with cyclic loading while mechanical compression decreased proteoglycan biosynthesis [13,24]. Besides using different types and magnitude of loading, assessing gene expression at additional time points post-impact will be beneficial to determine if the expression of molecules involved in catabolism changes with time.…”

Section: Discussionmentioning

confidence: 99%

Gene expression profile of mechanically impacted bovine articular cartilage explants

Chan

Schlueter

Coussens

et al. 2005

Journal Orthopaedic Research

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Traumatic injury to a joint can initiate cartilage degradation. Blunt trauma increases matrix damage and decreases proteoglycan synthesis in in vitro models. Few studies have investigated gene expression of articular cartilage (AC) following mechanical loading. Recent advances in microarray technology allow analysis of a number of genes, and may elucidate pathways of AC degradation. In the present study, we used a bovine cDNA microarray to determine how acute trauma of cartilage explants in the absence of underlying bone alters gene expression. Results indicate that at least 19 genes were differentially expressed at 3 h after trauma. Fourteen genes were up-regulated and five genes were down-regulated relative to control explants. The up-regulated genes included cytokine and chemokine receptors, enzymes, and molecules involved in signal transduction. Genes of adhesion molecules and apoptosis were down-regulated. The results of this study highlight the potential benefits of using a bovine cDNA microarray to study cartilage metabolism.

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The Proteoglycan Metabolism of Mature Bovine Articular Cartilage Explants Superimposed to Continuously Applied Cyclic Mechanical Loading

Cited by 65 publications

References 22 publications

The effects of static and intermittent compression on nitric oxide production in articular cartilage explants

The effects of static and intermittent compression on nitric oxide production in articular cartilage explants

Adaptational responses of the human Achilles tendon by modulation of the applied cyclic strain magnitude

Gene expression profile of mechanically impacted bovine articular cartilage explants

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