Tendinopathy—from basic science to treatment

Riley, Graham P.

doi:10.1038/ncprheum0700

Cited by 403 publications

(415 citation statements)

References 68 publications

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“…MMPs 1 and 13 were selected as they are known to be active against fibrillar collagens, including the predominant collagen type I 1, 28, 29, 30. MMP‐3 was selected as it degrades other minor proteins in tendon matrix, including collagens III, IV, IX, and X, and also proteoglycans and elastin 28, 29, 30, 31, 32, 33.…”

Section: Methodsmentioning

confidence: 99%

“…Tendinopathy is a general term for chronic tendon disease1 characterized by a combination of pain, swelling, and impaired tendon performance 2. The aetiology of this disease remains to be elucidated and is likely to be multi‐factorial.…”

mentioning

confidence: 99%

“…The aetiology of this disease remains to be elucidated and is likely to be multi‐factorial. Tendinopathy is often the result of damage accumulation during overuse, and may also involve either mechanical over‐stimulation or under‐stimulation of tenocytes and the related (imbalanced) remodeling in tendon tissue 1. Tendinopathy has often been considered a degenerative disease1 not associated with inflammation.…”

mentioning

confidence: 99%

“…Tendinopathy is often the result of damage accumulation during overuse, and may also involve either mechanical over‐stimulation or under‐stimulation of tenocytes and the related (imbalanced) remodeling in tendon tissue 1. Tendinopathy has often been considered a degenerative disease1 not associated with inflammation. However the role of inflammation within the initiation, progression, and resolution of tendinopathy remains unclear 3…”

mentioning

confidence: 99%

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Tendon extracellular matrix damage, degradation and inflammation in response to in vitro overload exercise

Spiesz

Thorpe

Chaudhry

et al. 2015

Journal Orthopaedic Research

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The role of inflammation in tendon injury is uncertain and a topic of current interest. In vitro studies of tendon accelerated overload damage can serve as a valuable source of information on the early stages of tendinopathy. Viable fascicle bundles from bovine flexor tendons were subjected to cyclic uniaxial loading from 1–10% strain. Immuno‐staining for inflammatory markers and matrix degradation markers was performed on the samples after mechanical testing. Loaded samples exhibited visible extracellular matrix damage, with disrupted collagen fibers and fiber kinks, and notable damage to the interfascicular matrix. Inflammatory markers COX‐2 and IL‐6 were only expressed in the cyclically loaded samples. Collagen degradation markers MMP‐1 and C1,2C were colocalized in many areas, with staining occurring in the interfascicular matrix or the fascicular tenocytes. These markers were present in control samples, but staining became increasingly intense with loading. Little MMP‐3 or MMP‐13 was evident in control sections. In loaded samples, some sections showed intense staining of these markers, again localized to interfascicular regions. This study suggests that inflammatory markers may be expressed rapidly after tendon overload exercise. Interestingly, both inflammation and damage‐induced matrix remodeling seem to be concentrated in, or in the vicinity of, the highly cellular interfascicular matrix. © 2015 The Authors. Journal of Orthopaedic Research Published by Wiley Periodicals, Inc. J Orthop Res 33:889–897, 2015.

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

mentioning

confidence: 99%

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Tendon extracellular matrix damage, degradation and inflammation in response to in vitro overload exercise

Spiesz

Thorpe

Chaudhry

et al. 2015

Journal Orthopaedic Research

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“…Despite its prevalence and debilitating nature, the basis for the age-associated increase in tendinopathy is unknown, although tendon injuries are thought to be preceded by changes in the underlying structure and mechanical properties (Riley 2008). We have shown that tendons stiffen considerably with age (Wood et al 2011), but the associated changes in underlying structure have not been fully elucidated.…”

Section: Introductionmentioning

confidence: 94%

Age-related changes in structure and extracellular matrix protein expression levels in rat tendons

Kostrominova

Brooks

2013

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The musculoskeletal system (muscle-tendonbone) demonstrates numerous age-related changes, with modifications in tendons the least well studied, although increased predisposition to tendinopathy and rupture have been reported. In order to gain insights into the basis of age-associated increase in tendon injuries, we compared Achilles and tibialis anterior tendons and myotendinous junctions (MTJs) from 3-to 5-and 22-to 25-month-old rats for underlying structure and composition. Significant decreases were observed by qRT-PCR for collagen I, III, and V mRNA expression in tendons of old rats, but immunostaining detected no apparent differences in collagen I and V expression on the protein level. Tendons of old compared with young rats had decreased mRNA expression levels of proteoglycan 4 (PRG4) and elastin (Eln), but no differences in the mRNA expression of connective tissue growth factor, TGF-beta 1, or stromal cell-derived factor 1. For PRG4, immunostaining showed good correlation with qRT-PCR results. This is the first study to show reductions in PRG4 in tendons and MTJs of old rats. Decreased PRG4 expression in tendons could result in increased tendon stiffness and may be associated with decreased activity in the elderly. The diminished collagen mRNA expression in combination with decreased PRG4 and Eln mRNA expression may be associated with increased risk of tendon injury with aging.

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