The pathogenesis of tendinopathy. A molecular perspective

Riley, Graham P.

doi:10.1093/rheumatology/keg448

Cited by 440 publications

(398 citation statements)

References 142 publications

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“…There are 27 different collagen molecules identified to date [87]. Although Type I collagen accounts for approximately 65% to 80% of the dry mass of the tendon and represents almost 95% of the total collagen in a normal tendon [53], other collagens including collagen types II, III, IV, V, VI, IX, X, XII, and XIV have also been found in small quantities within tendon [86,107,110]. Changes in the collagen content and composition have consistently been found in tendinopathy (Table 2).…”

Section: Extracellular Matrix (Ecm)mentioning

confidence: 99%

“…Tendon injuries are common and affect a substantial portion of recreational and professional athletes and those in many occupations involving repetitive work [16,37,60,79,102]. Tendinopathy (often called tendinitis or tendinosis) is the most common tendon disorder [86,99]. It is characterized by activity-related pain, focal tendon tenderness, and decreased strength and movement in the affected area.…”

Section: Introductionmentioning

confidence: 99%

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The Basic Science of Tendinopathy

Murrell

2008

Clinical Orthopaedics &Amp; Related Research

302

254

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Tendinopathy is a common clinical problem with athletes and in many occupational settings. Tendinopathy can occur in any tendon, often near its insertion or enthesis where there is an area of stress concentration, and is directly related to the volume of repetitive load to which the tendon is exposed. Recent studies indicate tendinopathy is more likely to occur in situations that increase the ''dose'' of load to the tendon enthesis -including increased activity, weight, advancing age, and genetic factors. The cells in tendinopathic tendon are rounder, more numerous, and show evidence of oxidative damage and more apoptosis. These cells also produce a matrix that is thicker and weaker with more water, more immature and cartilage-like matrix proteins, and less organization. There is now evidence of a population of regenerating stem cells within tendon. These studies suggest prevention of tendinopathy should be directed at reducing the volume of repetitive loads to below that which induces oxidative-induced apoptosis and cartilage-like genes. The management strategies might involve agents or cells that induce tendon stem cell proliferation, repair and restoration of matrix integrity.

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Section: Extracellular Matrix (Ecm)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Basic Science of Tendinopathy

Murrell

2008

Clinical Orthopaedics &Amp; Related Research

302

254

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“…The biomechanical properties of the tendon are primarily a feature of the extracellular matrix (ECM), which is in a state of dynamic equilibrium between synthesis and degradation (4). Degradation of the ECM is principally mediated by proteinases, whose activities may be regulated at the transcriptional or the translational levels, or posttranslationally by processing or interaction with inhibitors.…”

mentioning

confidence: 99%

Expression profiling of metalloproteinases and tissue inhibitors of metalloproteinases in normal and degenerate human achilles tendon

Jones¹,

Corps²,

Pennington³

et al. 2006

Arthritis & Rheumatism

256

284

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Objective. To profile the messenger RNA (mRNA) expression for the 23 known genes of matrix metalloproteinases (MMPs), 19 genes of ADAMTS, 4 genes of tissue inhibitors of metalloproteinases (TIMPs), and ADAM genes 8, 10, 12, and 17 in normal, painful, and ruptured Achilles tendons.Methods. Tendon samples were obtained from cadavers or from patients undergoing surgical procedures to treat chronic painful tendinopathy or ruptured tendon. Total RNA was extracted and mRNA expression was analyzed by quantitative real-time reverse transcription-polymerase chain reaction, normalized to 18S ribosomal RNA.Results. In comparing expression of all genes, the normal, painful, and ruptured Achilles tendon groups each had a distinct mRNA expression signature. Three mRNA were not detected and 14 showed no significant difference in expression levels between the groups. Statistically significant (P < 0.05) differences in mRNA expression, when adjusted for age, included lower levels of MMPs 3 and 10 and TIMP-3 and higher levels of ADAM-12 and MMP-23 in painful compared with normal tendons, and lower levels of MMPs 3 and 7 and TIMPs 2, 3, and 4 and higher levels of ADAMs 8 and 12, MMPs 1, 9, 19, and 25, and TIMP-1 in ruptured compared with normal tendons.Conclusion. The distinct mRNA profile of each tendon group suggests differences in extracellular proteolytic activity, which would affect the production and remodeling of the tendon extracellular matrix. Some proteolytic activities are implicated in the maintenance of normal tendon, while chronically painful tendons and ruptured tendons are shown to be distinct groups. These data will provide a foundation for further study of the role and activity of many of these enzymes that underlie the pathologic processes in the tendon.

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“…The pathology and treatment approach to tendinopathy has recently been well discussed 16 – 18 . The cornerstone of therapy is to remove any biomechanical predispositions and treat with physiotherapy.…”

Section: Treatmentsmentioning

confidence: 99%

Enthesopathy – a personal perspective on its manifestations, implications and treatment

Cormick¹

2010

Australas J Ultrason Med

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The pathogenesis of tendinopathy. A molecular perspective

Cited by 440 publications

References 142 publications

The Basic Science of Tendinopathy

The Basic Science of Tendinopathy

Expression profiling of metalloproteinases and tissue inhibitors of metalloproteinases in normal and degenerate human achilles tendon

Enthesopathy – a personal perspective on its manifestations, implications and treatment

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