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      Tendons – time to revisit inflammation

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          Abstract

          It is currently widely accepted among clinicians that chronic tendinopathy is caused by a degenerative process devoid of inflammation. Current treatment strategies are focused on physical treatments, peritendinous or intratendinous injections of blood or blood products and interruption of painful stimuli. Results have been at best, moderately good and at worst a failure. The evidence for non-infammatory degenerative processes alone as the cause of tendinopathy is surprisingly weak. There is convincing evidence that the inflammatory response is a key component of chronic tendinopathy. Newer anti-inflammatory modalities may provide alternative potential opportunities in treating chronic tendinopathies and should be explored further.

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          Most cited references66

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          Anti-TNF alpha therapy of rheumatoid arthritis: what have we learned?

          M Feldmann, R Maini (2001)
          Rheumatoid arthritis (RA), a systemic disease, is characterized by a chronic inflammatory reaction in the synovium of joints and is associated with degeneration of cartilage and erosion of juxta-articular bone. Many pro-inflammatory cytokines including TNF alpha, chemokines, and growth factors are expressed in diseased joints. The rationale that TNF alpha played a central role in regulating these molecules, and their pathophysiological potential, was initially provided by the demonstration that anti-TNF alpha antibodies added to in vitro cultures of a representative population of cells derived from diseased joints inhibited the spontaneous production of IL-1 and other pro-inflammatory cytokines. Systemic administration of anti-TNF alpha antibody or sTNFR fusion protein to mouse models of RA was shown to be anti-inflammatory and joint protective. Clinical investigations in which the activity of TNF alpha in RA patients was blocked with intravenously administered infliximab, a chimeric anti-TNF alpha monoclonal antibody (mAB), has provided evidence that TNF regulates IL-6, IL-8, MCP-1, and VEGF production, recruitment of immune and inflammatory cells into joints, angiogenesis, and reduction of blood levels of matrix metalloproteinases-1 and -3. Randomized, placebo-controlled, multi-center clinical trials of human TNF alpha inhibitors have demonstrated their consistent and remarkable efficacy in controlling signs and symptoms, with a favorable safety profile, in approximately two thirds of patients for up to 2 years, and their ability to retard joint damage. Infliximab (a mAB), and etanercept (a sTNF-R-Fc fusion protein) have been approved by regulatory authorities in the United States and Europe for treating RA, and they represent a significant new addition to available therapeutic options.
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            Platelet-rich plasma injection for chronic Achilles tendinopathy: a randomized controlled trial.

            Robert de Vos, Adam Weir, Hans van Schie … (2010)
            Tendon disorders comprise 30% to 50% of all activity-related injuries; chronic degenerative tendon disorders (tendinopathy) occur frequently and are difficult to treat. Tendon regeneration might be improved by injecting platelet-rich plasma (PRP), an increasingly used treatment for releasing growth factors into the degenerative tendon. To examine whether a PRP injection would improve outcome in chronic midportion Achilles tendinopathy. A stratified, block-randomized, double-blind, placebo-controlled trial at a single center (The Hague Medical Center, Leidschendam, The Netherlands) of 54 randomized patients aged 18 to 70 years with chronic tendinopathy 2 to 7 cm above the Achilles tendon insertion. The trial was conducted between August 28, 2008, and January 29, 2009, with follow-up until July 16, 2009. Eccentric exercises (usual care) with either a PRP injection (PRP group) or saline injection (placebo group). Randomization was stratified by activity level. The validated Victorian Institute of Sports Assessment-Achilles (VISA-A) questionnaire, which evaluated pain score and activity level, was completed at baseline and 6, 12, and 24 weeks. The VISA-A score ranged from 0 to 100, with higher scores corresponding with less pain and increased activity. Treatment group effects were evaluated using general linear models on the basis of intention-to-treat. After randomization into the PRP group (n = 27) or placebo group (n = 27), there was complete follow-up of all patients. The mean VISA-A score improved significantly after 24 weeks in the PRP group by 21.7 points (95% confidence interval [CI], 13.0-30.5) and in the placebo group by 20.5 points (95% CI, 11.6-29.4). The increase was not significantly different between both groups (adjusted between-group difference from baseline to 24 weeks, -0.9; 95% CI, -12.4 to 10.6). This CI did not include the predefined relevant difference of 12 points in favor of PRP treatment. Among patients with chronic Achilles tendinopathy who were treated with eccentric exercises, a PRP injection compared with a saline injection did not result in greater improvement in pain and activity. clinicaltrials.gov Identifier: NCT00761423.
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              The pathogenesis of tendinopathy. A molecular perspective.

              Lisa Riley (2004)
              Article 0 comments Cited 122 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Br J Sports Med
                Journal ID (iso-abbrev): Br J Sports Med
                Journal ID (hwp): bjsports
                Journal ID (publisher-id): bjsm
                Title: British Journal of Sports Medicine
                Publisher: BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                ISSN (Print): 0306-3674
                ISSN (Electronic): 1473-0480
                Publication date (Print): November 2014
                Publication date (Electronic): 9 March 2013
                Volume: 48
                Issue: 21
                Pages: 1553-1557
                Affiliations
                [1 ]Department of Rheumatology, Cambridge University Hospitals NHS Foundation Trust , Cambridge, UK
                [2 ]Isokinetic Medical Group, FIFA Medical Centre of Excellence , London, UK
                [3 ]Department of Physical Therapy, University of British Columbia , Vancouver, Canada
                Author notes
                [Correspondence to ] Dr Jonathan D Rees, Department of Rheumatology, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridge, CB2 0QQ, UK; j.rees@ 123456doctors.org.uk
                Article
                Publisher ID: bjsports-2012-091957
                DOI: 10.1136/bjsports-2012-091957
                PMC ID: 4215290
                PubMed ID: 23476034
                SO-VID: 1020bc5b-1718-4d09-8f5f-7ffdea8cb92a
                Copyright © Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions
                License:

                This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/3.0/

                History
                Date accepted : 13 February 2013
                Categories
                Subject: 1506
                Subject: Review
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                ScienceOpen disciplines: Sports medicine
                Keywords: immune function,immunology,tendons
                Data availability:
                ScienceOpen disciplines: Sports medicine
                Keywords: immune function, immunology, tendons

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