A commentary on
Role of VEGF, Nitric Oxide, and Sympathetic Neurotransmitters in the Pathogenesis of Tendinopathy: A Review of the Current Evidences
by Vasta, S., Di Martino, A., Zampogna, B., Torre, G., Papalia, R., and Denaro, V. (2016). Front. Aging Neurosci. 8:186. doi: 10.3389/fnagi.2016.00186
I read the recent systematic review which asked some interesting questions regarding the pathogenesis of tendinopathy (Vasta et al., 2016). The statement “histologic studies have demonstrated the absence of inflammatory infiltrates” is not supported by the current evidence base. Our recent systematic review on this subject demonstrated that the absence of neutrophils does not equate to the absence of inflammatory cells (Dean et al., 2016), while several recent studies have provided compelling evidence to support the hypothesis that chronic inflammation is a key factor in the pathogenesis of tendinopathy (Dakin et al., 2015; Dean et al., 2015a). In addition the search strategy does not appear to have been comprehensive. We have carried out a number of systematic reviews in this area (Dean et al., 2016; Vasta et al., 2016) which identified numerous studies which have been missed by this review (Gotoh et al., 1998; Forsgren et al., 2005; Andersson et al., 2008; Lakemeier et al., 2010; Shindle et al., 2011; Millar et al., 2012). We have also published several pieces of work related to markers such as VEGF, glutamate, various glutamate receptors, the neurokinin-1 receptor and tyrosine hydroxylase which were also not included (Dean et al., 2014, 2015a,b; Franklin et al., 2014). It is rather problematic that so many relevant studies have not been incorporated into this systematic review. It is important that readers are fully informed of the current evidence base and thus can be made aware of the role of neuro-inflammatory change in the pathogenesis of tendinopathy.
Author Contributions
The author confirms being the sole contributor of this work and approved it for publication.
Conflict of Interest Statement
The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Andersson, G., Danielson, P., Alfredson, H., and Forsgren, S. (2008). Presence of substance P and the neurokinin-1 receptor in tenocytes of the human Achilles tendon. Regul. Pept. 150, 81–87. doi: 10.1016/j.regpep.2008.02.005
Dakin, S. G., Martinez, F. O., Yapp, C., Wells, G., Oppermann, U., Dean, B. J. F., et al. (2015). Inflammation activation and resolution in human tendon disease. Sci. Transl. Med. 7, 311ra173. doi: 10.1126/scitranslmed.aac4269
Dean, B. J., Franklin, S. L., Murphy, R. J., Javaid, M. K., and Carr, A. J. (2014). Glucocorticoids induce specific ion-channel-mediated toxicity in human rotator cuff tendon: a mechanism underpinning the ultimately deleterious effect of steroid injection in tendinopathy? Br. J. Sports Med. 48, 1620–1626. doi: 10.1136/bjsports-2013-093178
Dean, B. J., Gettings, P., Dakin, S. G., and Carr, A. J. (2016). Are inflammatory cells increased in painful human tendinopathy? A systematic review. Br. J. Sports Med. 50, 216–220. doi: 10.1136/bjsports-2015-094754
Dean, B. J., Snelling, S. J., Dakin, S. G., Javaid, M. K., and Carr, A. J. (2015b). In vitro effects of glutamate and N-methyl-D-aspartate receptor (NMDAR) antagonism on human tendon derived cells. J. Orthopaed. Res. 33, 1515–1522.
Dean, B. J. F., Snelling, S. J. B., Dakin, S. G., Murphy, R. J., Javaid, M. K., and Carr, A. J. (2015a). Differences in glutamate receptors and inflammatory cell numbers are associated with the resolution of pain in human rotator cuff tendinopathy. Arthritis Res. Ther. 17:176. doi: 10.1186/s13075-015-0691-5
Forsgren, S., Danielson, P., and Alfredson, H. (2005). Vascular NK-1 receptor occurrence in normal and chronic painful Achilles and patellar tendons: studies on chemically unfixed as well as fixed specimens. Regul. Pept. 126, 173–181. doi: 10.1016/j.regpep.2004.09.008
Franklin, S. L., Dean, B. J., Wheway, K., Watkins, B., Javaid, M. K., and Carr, A. J. (2014). Up-regulation of glutamate in painful human supraspinatus tendon tears. Am. J. Sports Med. 42, 1955–1962. doi: 10.1177/0363546514532754
Gotoh, M., Hamada, K., Yamakawa, H., Inoue, A., and Fukuda, H. (1998). Increased substance P in subacromial bursa and shoulder pain in rotator cuff diseases. J. Orthopaed. Res.16, 618–621. doi: 10.1002/jor.1100160515
Lakemeier, S., Reichelt, J. J., Patzer, T., Fuchs-Winkelmann, S., Paletta, J. R., and Schofer, M. D. (2010). The association between retraction of the torn rotator cuff and increasing expression of hypoxia inducible factor 1alpha and vascular endothelial growth factor expression: an immunohistological study. BMC Musculoskelet. Disord. 11:230. doi: 10.1186/1471-2474-11-230
Millar, N. L., Reilly, J. H., Kerr, S. C., Campbell, A. L., Little, K. J., Leach, W. J., et al. (2012). Hypoxia: a critical regulator of early human tendinopathy. Ann. Rheum. Dis. 71, 302–310. doi: 10.1136/ard.2011.154229
Shindle, M. K., Chen, C. C. T., Robertson, C., DiTullio, A. E., Paulus, M. C., Clinton, C. M., et al. (2011). Full-thickness supraspinatus tears are associated with more synovial inflammation and tissue degeneration than partial-thickness tears. J. Shoul. Elbow Surg. Am. Shoul. Elbow Surg. 20, 917–927. doi: 10.1016/j.jse.2011.02.015
Vasta, S., Di Martino, A., Zampogna, B., Torre, G., Papalia, R., and Denaro, V. (2016). Role of VEGF, Nitric Oxide, and sympathetic neurotransmitters in the pathogenesis of tendinopathy: a review of the current evidences. Front. Aging Neurosci. 8:186. doi: 10.3389/fnagi.2016.00186
Benjamin J. F. Dean*
* Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Oxford, UK
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摘要
Glucocorticoids induce specific ion-channel-mediated toxicity in human rotator cuff tendon: a mechanism underpinning the ultimately deleterious effect of steroid injection in tendinopathy? Differences in glutamate receptors and inflammatory cell numbers are associated with the resolution of pain in human rotator cuff tendinopathy. The association between retraction of the torn rotator cuff and increasing expression of hypoxia inducible factor 1alpha and vascular endothelial growth factor expression: an immunohistological study.
您已经请求对我们数据库中的选定内容进行实时机器翻译。我们提供此功能的目的仅是为您提供方便,决不是为了取代人工翻译。 显示完整免责声明
无论 ProQuest 还是其授权方对此翻译均不作出任何支持或保证。翻译是“根据现状”和“根据可用性”条件自动生成的,并且不在我们的系统中保留。PROQUEST 及其授权人明确拒绝就任何明示或暗示的保证承担责任;这些保证包括但不限于任何对某一特定目的的可用性、准确性、及时性、完整性、非侵权性、可销售性或适当性的保证。您对翻译的使用需遵守您的《电子产品许可协议》(Electronic Products License Agreement) 中的所有使用限制;并且您对翻译功能的使用,表明您同意放弃任何以及所有对 ProQuest 或其授权方就您对翻译功能的使用以及任何由其生成结果带来损失的索赔。 隐藏完整免责声明