Patellar tendon matrix changes associated with aging and voluntary exercise

Vailas, A. C.; Pedrini, V.; Pedrini-Mille, A.; Holloszy, J. O.

doi:10.1152/jappl.1985.58.5.1572

Cited by 61 publications

(21 citation statements)

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“…Our values for hydroxyproline content in control rats are in agreement with previous results published for tendons and other similar connective tissues (Takacs and Verzar, 1968;Vailas et al, 1985Vailas et al, , 1988. Although long term monitoring for hydroxyproline content during tendon degeneration and regeneration has never been clearly reported, we showed that the rapid loss of hydroxyproline coincides with the accumulation of PMNs and Ms, which supports the hypothesis that leukocytes phagocytose and digest collagen during the inflammatory phase.…”

Section: Effects Of Diclofenac On Tendon Inflammation and Regenerationsupporting

confidence: 92%

Nonsteroidal Anti-Inflammatory Drug Reduces Neutrophil and Macrophage Accumulation but Does Not Improve Tendon Regeneration

Marsolais

Côté

Frenette

2003

Laboratory Investigation

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SUMMARY:Whether nonsteroidal anti-inflammatory drugs have a beneficial effect on tendon regeneration is still a matter of debate. Given that inflammatory cells are thought to induce nonspecific damage following an injury, we tested the hypothesis that a 3-day treatment with diclofenac would protect tendons from inflammatory cell injury and would promote healing. Neutrophil and ED1 ϩ macrophage concentrations were determined in the paratenon and the core of the rat Achilles tendon following collagenase-induced injury. Hydroxyproline content, edema, and mechanical properties were also evaluated at 1, 3, 7, 14, and 28 days post-trauma. Collagenase injections induced a 70% decrease in the ultimate rupture point at Day 3. Diclofenac treatments (1 mg/kg bid) selectively decreased the accumulation of neutrophils and ED1 ϩ macrophages by 59% and 35%, respectively, in the paratenon, where blood vessels are numerous, but did not reduce the accumulation of neutrophils and ED1 ϩ macrophages in the core of the tendon. Edema was significantly reduced on Day 3 but persisted during the remodeling phase in the diclofenac-treated group only. The inhibition of leukocyte accumulation by diclofenac did not translate into a reduction of tissue damage or a promotion of tissue healing, because the mechanical properties of injured Achilles tendons were identical in placebo and diclofenac-treated groups. These results indicate that diclofenac reduced both edema and the accumulation of inflammatory cells within the paratenon but provided no biochemical or functional benefits for the Achilles tendon. (Lab Invest 2003, 83:991-999).

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Section: Effects Of Diclofenac On Tendon Inflammation and Regenerationsupporting

confidence: 92%

Nonsteroidal Anti-Inflammatory Drug Reduces Neutrophil and Macrophage Accumulation but Does Not Improve Tendon Regeneration

Marsolais

Côté

Frenette

2003

Laboratory Investigation

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“…Collagen content of the patellar tendon (Haut et al 1992) and tail-tendon (Vogel 1983) in animals has been shown to decrease or increase (Vailas et al 1985) with age. In humans, we recently demonstrated that collagen concentration of the patellar tendon was 34 % lower in old men compared to that in young men (Couppe et al 2009).…”

Section: Tendon Collagen Contentmentioning

confidence: 99%

Life-long endurance running is associated with reduced glycation and mechanical stress in connective tissue

Couppé

Svensson

Grosset

et al. 2014

AGE

112

103

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Life-long regular endurance exercise is known to counteract the deterioration of cardiovascular and metabolic function and overall mortality. Yet it remains unknown if life-long regular endurance exercise can influence the connective tissue accumulation of advanced glycation endproducts (AGEs) that is associated with aging and lifestyle-related diseases. We therefore examined two groups of healthy elderly men: 15 master athletes (64±4 years) who had been engaged in life-long endurance running and 12 old untrained (66±4 years) together with two groups of healthy young men; ten young athletes matched for running distance (26±4 years), and 12 young untrained (24±3 years). AGE cross-links (pentosidine) of the patellar tendon AGE (2014) were measured biochemically, and in the skin, it was assessed by a fluorometric method. In addition, we determined mechanical properties and microstructure of the patellar tendon. Life-long regular endurance runners (master athletes) had a 21 % lower AGE cross-link density compared to old untrained. Furthermore, both master athletes and young athletes displayed a thicker patellar tendon. These cross-sectional data suggest that life-long regular endurance running can partly counteract the aging process in connective tissue by reducing age-related accumulation of AGEs. This may not only benefit skin and tendon but also other long-lived protein tissues in the body. Furthermore, it appears that endurance running yields tendon tissue hypertrophy that may serve to lower the stress on the tendon and thereby reduce the risk of injury.

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“…IL-1β is a potent pro-inflammatory cytokine produced mainly by macrophages in injured tissues and upregulates the expression of other inflammatory mediators, including COX-2, IL-6, MMP-1, and MMP-3. In fibroblasts, for example, IL-1β induces the expression of MMPs (Tewari et al, 1994;Alvares et al, 1995), which could initiate the degradation and remodeling of tissues (e.g., tendons) in response to mechanical loading (Vailas et al, 1985). COX-2 is a major marker of tissue inflammation (Gilroy et al, 1998;Lipsky, 1999) that converts arachidonic acid into prostaglandins, such as PGE 2 .…”

Section: Introductionmentioning

confidence: 99%

Repetitive mechanical stretching modulates IL-1β induced COX-2, MMP-1 expression, and PGE2 production in human patellar tendon fibroblasts

Yang

Wang

2005

Gene

246

209

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While mechanical loading is known to be essential in maintaining tendon homeostasis, repetitive mechanical loading has also been implicated in the etiology of tendon overuse injuries. The purpose of this study was to determine whether cyclic mechanical stretching regulates inflammatory responses induced by interleukin-1β (IL-1β) treatment in human patellar tendon fibroblasts (HPTFs). HPTFs were grown in microgrooved silicone dishes, where they became elongated in shape and aligned with the microgrooves, which is similar to the shape and organization of tendon fibroblasts in vivo. Cyclic uniaxial stretching was then applied to silicone culture dishes with a 4% or 8% stretch at a stretching frequency of 0.5 Hz for a duration of 4 h in the presence or absence of 10 pM IL-1β treatment. Non-stretched cells in the presence or absence of IL-1β were used for controls, respectively. The expression of cyclooxygenase-2 (COX-2), matrix metalloproteinase-1 (MMP-1), and the production of prostaglandin E 2 (PGE 2 ) were measured. In the absence of stretching, it was found that 10 pM of IL-1β markedly induced higher levels of COX-2, MMP-1 gene expression, and PGE 2 production than non-treated cells. Furthermore, cells with 4% stretching decreased the COX-2 and MMP-1 gene expression and PGE 2 production that were stimulated by IL-1β, whereas cells with 8% stretching further increased these gene products and/or expression levels in addition to the effects of IL-1β stimulation. Thus, the results suggest that repetitive, small-magnitude stretching is antiinflammatory, whereas large-magnitude stretching is pro-inflammatory. Therefore, moderate exercise may be beneficial to reducing tendon inflammation.

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Patellar tendon matrix changes associated with aging and voluntary exercise

Cited by 61 publications

References 0 publications

Nonsteroidal Anti-Inflammatory Drug Reduces Neutrophil and Macrophage Accumulation but Does Not Improve Tendon Regeneration

Nonsteroidal Anti-Inflammatory Drug Reduces Neutrophil and Macrophage Accumulation but Does Not Improve Tendon Regeneration

Life-long endurance running is associated with reduced glycation and mechanical stress in connective tissue

Repetitive mechanical stretching modulates IL-1β induced COX-2, MMP-1 expression, and PGE2 production in human patellar tendon fibroblasts

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