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British medical bulletin · Dec 2019
Tendon healing in presence of chronic low-level inflammation: a systematic review.
- Emanuele Chisari, Laura Rehak, Wasim S Khan, and Nicola Maffulli.
- University of Catania, Departmento of General Surgery and Medical Specialities, Via Santa Sofia 78, Catania 95123, Italy.
- Br. Med. Bull. 2019 Dec 11; 132 (1): 97-116.
BackgroundTendinopathy is a common musculoskeletal condition affecting subjects regardless of their activity level. Multiple inflammatory molecules found in ex vivo samples of human tendons are related to the initiation or progression of tendinopathy. Their role in tendon healing is the subject of this review.Sources Of DataAn extensive review of current literature was conducted using PubMed, Embase and Cochrane Library using the term 'tendon', as well as some common terms of tendon conditions such as 'tendon injury OR (tendon damage) OR tendonitis OR tendinopathy OR (chronic tendonitis) OR tendinosis OR (chronic tendinopathy) OR enthesitis' AND 'healing' AND '(inflammation OR immune response)' as either key words or MeSH terms.Areas Of AgreementAn environment characterized by a low level of chronic inflammation, together with increased expression of inflammatory cytokines and growth factors, may influence the physiological tendon healing response after treatment.Areas Of ControversyMost studies on this topic exhibited limited scientific translational value because of their heterogeneity. The evidence associated with preclinical studies is limited.Growing PointsThe role of inflammation in tendon healing is still unclear, though it seems to affect the overall outcome. A thorough understanding of the biochemical mediators of healing and their pathway of pain could be used to target tendinopathy and possibly guide its management.Areas Timely For Developing ResearchWe require further studies with improved designs to effectively evaluate the pathogenesis and progression of tendinopathy to identify cellular and molecular targets to improve outcomes.© The Author(s) 2019. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
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