title: No inflammatory gene-expression response to acute exercise in human Achilles tendinopathy.
abstract: Although histology data favour the view of a degenerative nature of tendinopathy, indirect support for inflammatory reactions to loading in affected tendons exists. The purpose of the present study was to elucidate whether inflammatory signalling responses after acute mechanical loading were more pronounced in tendinopathic versus healthy regions of human tendon and if treatment with non-steroidal anti-inflammatory medications (NSAID's) reduces this response. Twenty-seven tendinopathy patients (>6 months) were randomly assigned to a placebo (n = 14) or NSAID (Ibumetin NYCOMED GmbH Plant Oranienburg Germany (600 mg) × 3/day/1 week) group (n = 13) in a double-blinded-fashion. Tendon biopsies were taken from the painful and a healthy region of the same tendon 2 h after 1 h running. Gene-expression of several targets was analysed in the sampled Achilles tendon biopsies. The mRNA for TGF-β, collagen-I and collagen-III were significantly higher expressed, and decorin, CTGF, IL-6 and IL-10 were significantly lower expressed in the tendinopathic versus healthy tendon area. Only IL-10 was lower in expression in experiments with NSAID administration, while all other determined parameters were unaffected by NSAID. All ultrasonographic outcomes were unchanged in response to acute exercise and not influenced by NSAID. The signalling for collagen and TGF-beta was upregulated after acute loading in tendinopathic tendon. In contrast to the hypothesis, inflammatory signalling was not exaggerated in tendinopathic tendon 2 h after acute mechanical loading.
authors.affiliation: Department of Orthopaedic Surgery M. Bispebjerg Hospital and Center for Healthy Aging, Faculty of Health Sciences, Institute of Sports Medicine Copenhagen, University of Copenhagen, Bispebjerg Bakke 23, Copenhagen NV, Denmark. Jessica.pingel@gmx.de
authors.forename: Jessica
authors.initials: J
authors.lastname: Pingel
authors.forename: Ulrich
authors.initials: U
authors.lastname: Fredberg
authors.forename: Lone Ramer
authors.initials: LR
authors.lastname: Mikkelsen
authors.forename: Peter
authors.initials: P
authors.lastname: Schjerling
authors.forename: Katja Maria
authors.initials: KM
authors.lastname: Heinemeier
authors.forename: Michael
authors.initials: M
authors.lastname: Kjaer
authors.forename: Adrian
authors.initials: A
authors.lastname: Harisson
authors.forename: Henning
authors.initials: H
authors.lastname: Langberg
mesh_terms: D000125:Achilles Tendon / Q000000981:diagnostic imaging / Q000378:metabolism*; D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D024042:Collagen Type I / Q000235:genetics / Q000378:metabolism; D024061:Collagen Type III / Q000235:genetics / Q000378:metabolism; D055513:Connective Tissue Growth Factor / Q000235:genetics / Q000378:metabolism; D058575:Decorin / Q000235:genetics / Q000378:metabolism; D015444:Exercise; D005260:Female; D006801:Humans; D007052:Ibuprofen / Q000627:therapeutic use; D007249:Inflammation / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D052256:Tendinopathy / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism*; D014158:Transcription, Genetic; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism; D014463:Ultrasonography
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; C526317:CCN2 protein, human; D024042:Collagen Type I; D024061:Collagen Type III; C546878:DCN protein, human; D058575:Decorin; C508609:IL10 protein, human; C508600:IL6 protein, human; D015850:Interleukin-6; D016212:Transforming Growth Factor beta; D016753:Interleukin-10; D055513:Connective Tissue Growth Factor; D007052:Ibuprofen