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Current Trends in Tendinopathy: Consensus of the ESSKA Basic Science Committee

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Current Trends in Tendinopathy: Consensus of the ESSKA Basic Science Committee http://www.diva-portal.org This is the published version of a paper published in Journal of experimental orthopaedics. Citation for the original published paper (version of record): Abat, F., Alfredson, H., Cucchiarini, M., Madry, H., Marmotti, A. et al. (2018) Current trends in tendinopathy: consensus of the ESSKA basic science committee. Part II Journal of experimental orthopaedics, 5(38) https://doi.org/10.1186/s40634-018-0145-5 Access to the published version may require subscription. N.B. When citing this work, cite the original published paper. Permanent link to this version: http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-154642 Abat et al. Journal of Experimental Orthopaedics (2018) 5:38 Journal of https://doi.org/10.1186/s40634-018-0145-5 Experimental Orthopaedics REVIEW Open Access Current trends in tendinopathy: consensus of the ESSKA basic science committee. Part II: treatment options F. Abat1* , H. Alfredson2,3,4, M. Cucchiarini5, H. Madry6, A. Marmotti7, C. Mouton8, J. M. Oliveira9,10,11, H. Pereira9,12,13, G. M. Peretti14, C. Spang15, J. Stephen16,17, C. J. A. van Bergen18 and L. de Girolamo19 Abstract The treatment of painful chronic tendinopathy is challenging. Multiple non-invasive and tendon-invasive methods are used. When traditional non-invasive treatments fail, the injections of platelet-rich plasma autologous blood or cortisone have become increasingly favored. However, there is little scientific evidence from human studies supporting injection treatment. As the last resort, intra- or peritendinous open or endoscopic surgery are employed even though these also show varying results. This ESSKA basic science committee current concepts review follows the first part on the biology, biomechanics and anatomy of tendinopathies, to provide a comprehensive overview of the latest treatment options for tendinopathy as reported in the literature. Introduction prostaglandins, and metalloproteinases (MMPs) along The great incidence of tendon injuries in the population with tendon cell apoptosis seem to be provoked by con- as well as the failure rate of up to 25% (Lohrer et al. 2016) tinuing mechanical stimuli (Andres and Murrell, 2008; of the available conservative treatments has made this Rodriguez et al. 2015). In this context, an alternative field one of the most interesting for alternative biological anti-inflammatory and immunomodulatory approach that approaches. The study of the microenvironment of tendi- replaces the traditional anti-inflammatory modalities (i.e. nopathy is a key factor in improving tendon healing. NSAIDs) may provide another potential opportunity in There is still debate around the true role of inflammation the treatment of chronic tendinopathies. In a previous re- and of overload in the activation of the processes. They port, biology, biomechanics, anatomy and an exercise- are both factors that gradually produce degenerative based approach were discussed (Abat et al. 2017). The changes of the tendon structure due to qualitative and current concepts review here provides an overview of the quantitative alterations of tenocytes (Abate et al. 2009). some treatment options for tendinopathy as reported in Historically, tendinopathy has primarily been considered a the literature. degenerative pathological process of a non-inflammatory nature as the presence of acute inflammatory cells in chronic tendinopathy has never been confirmed. However, Treatment options thanks to the newer research tools, convincing evidence Platelet RICH plasma (PRP) that includes an increasing number of inflammatory cells The use of Platelet Rich Plasma (PRP) for the treatment in pathological tendons (Dean et al. 2016) has started to of tendinopathy is a greatly debated topic in literature. appear showing that the inflammatory response is a key The common perception that it “may” be useful in clin- component of chronic tendinopathy (Rees et al. 2014). For ical settings has led to the wide spread use of PRP to example, an increase in terms of cytokines, inflammatory treat acute and chronic tendon injuries in both Europe and the United States although conflicting evidence still exists as to its efficacy and the form in which PRP * Correspondence: [email protected] should be used. 1Department of Sports Orthopaedics, ReSport Clinic, Passeig Fabra i Puig 47, 08030 Barcelona, Spain A recent systematic review (Filardo et al. 2016)has Full list of author information is available at the end of the article highlighted the controversial results of PRP applications © The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. Abat et al. Journal of Experimental Orthopaedics (2018) 5:38 Page 2 of 17 for different pathologies. The authors affirm that, follow- subsequent regenerative response. It may also partially ing the current evidence, patellar and lateral elbow ten- sustain the positive result of PRP in chronic tendon dinopathy showed improvement from PRP treatment degeneration. while the Achilles tendon and rotator cuff do seem not The control of the inflammatory process by PRP seems to benefit from PRP application with either conservative to derive from a key element in PRP, namely the hepato- treatment or surgery. Conversely, the recent meta-ana- cyte growth factor (HGF). HGF is not simply a trophic lysis by Fitzpatrick (Fitzpatrick et al. 2017) has shown factor and an anti-fibrotic regulator. It has been previ- good clinical evidence that favors the use leukocyte-rich ously recognized as the main factor responsible for the PRP (LR-PRP) under ultrasound guidance for the treat- PRP anti-inflammatory effect on human chondrocytes ment of patellar tendinopathy, lateral epicondylitis and through inhibition of NF-kB transactivating activity Achilles and rotator cuff tendinopathy. Similarly, the (Bendinelli et al. 2010). A recent study by Zhang (Zhang study by Pandey (Pandey et al. 2016) showed a positive et al. 2013) has suggested a similar effect in rabbit and result from the application of a moderately concentrated mouse LR-PRP with a four-fold platelets concentration leukocyte-poor PRP (LP-PRP) above the repair site dur- than in whole animal blood in an in vitro rabbit teno- ing single-row arthroscopic repair of large degenerative cytes culture and in a preclinical mouse model of an cuff tears. On the other hand, a prior study by Zumstein acute Achilles tendon lesion. It is likely that HGF is not (Zumstein et al. 2016) failed to show any benefit from only delivered by the platelets but also produced by cells the application of PRP in the form of a leucocyte and following exposure to PRP. This presence of HGF may platelet-rich fibrin matrix during arthroscopic rotator partially explain the secondary reduction of the first ini- cuff repair. tial PRP-induced inflammatory phase. The fact is that there is no consensus. This is mainly A parallel and transient increased expression of trans- due to the lack of standard PRP preparation procedures forming growth factor (TGF)-beta following PRP expos- or methods of application. This, at present, suggests cau- ure has been recently described by Lyras (Lyras et al. tion in the indiscriminate first-line application of PRP in 2010) as a key factor in accelerating tendon healing. The tendon disorders. Nevertheless, basic science studies authors set up a patellar tendon defect model in rabbits may be the key to bringing the biological rationale for treated with intralesional PRP gel. TGF-beta has been PRP into safe clinical usage. Indeed, the most recent in shown to increase during the first 2 weeks, consistent vitro and preclinical studies have shown some important with an anabolic stimulus, and then decrease after this clues as to the action of PRP and the proper compos- initial phase. That likely leads to a reduction in adhesion ition to be used on tendon cells. Even if it seems that and scar formation. The same authors described this animal derived PRP has less favorable properties than PRP-driven angiogenesis during tendon healing (Lyras et human PRP, as has been observed in different settings al. 2010) as likely being driven by the expression of vas- like that of bone formation (Plachokova et al. 2009), pre- cular endothelial growth factor (VEGF) and other angio- clinical observations may give well-defined evidence of genetic factors. PRP has been shown to temporally the mechanism of PRP. increase the angiogenetic phase and subsequently lead to Firstly, the in-vitro study by Hudgens (Hudgens et al. a prompt reduction of this phenomenon, thus accelerat- 2016) with rat fibroblasts has demonstrated that one of ing the whole tendon healing process. the early responses to PRP application in rats is intermit- These different anabolic mechanisms of PRP seem to tent bouts of inflammation. They used a manually pre- be impaired by the presence of leukocytes. Indeed, the pared PRP with leukocytes and a 4-fold elevation in the recent works of Fortier and co-workers (Boswell et al. platelet concentration. Similarly to cartilage-like tissue, 2014; Cross et al. 2015; McCarrel et al. 2012) have in which the connection between a transient early in- shown that a high white blood cell concentration leads flammatory process and the expression of inflammation to a predominant expression of inflammatory and de- related NF-ĸB subunit p65 and chondrogenic differenti- gradative factors like Interleukine (IL-1) beta and ation (Caron et al. 2012; Caron et al. 2014), Hudgens MMP-9, while LP-PRP was related to a greater content (Hudgens et al. 2016) has observed the activation of in IL-6 that is associated with anti-inflammatory and re- pro-inflammatory Tumor Necrosis Factor TNF-alpha generative effects in the healing tendon. This is in ac- and NFkB pathways after PRP exposure as well as the cord with the recent study by the Andia’s group expression of genes related to cellular proliferation and (Rubio-Azpeitia et al.
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