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Correspondence
Inflammation and the continuum model: time to acknowledge the molecular era of tendinopathy
  1. Neal L Millar1,
  2. Benjamin J Dean2,
  3. Stephanie G Dakin2
  1. 1 Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK
  2. 2 Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Oxford, UK
  1. Correspondence to Neal L Millar, Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences, University of Glasgow, 120 University Avenue, Glasgow G12 8QQ, UK; neal.millar{at}glasgow.ac.uk

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The original continuum theory mentioned little concerning inflammatory mechanisms in tendon disease, likely due to the lack of scientific studies at that time. Since then, we and others have clearly defined a role for inflammatory cells1 and the subsequent inflammatory/matrix crosstalk involving cytokine regulation2 in human tendinopathy. It is therefore surprising that the updated continuum model3 again fails to acknowledge the molecular role that inflammation likely plays in damage events associated with tendinopathy.

We appreciate that the term ‘inflammation’ continues to evoke divergent opinions between clinicians and scientists within the field. However, clear pathological and molecular evidence exists of its dysregulation throughout the spectrum of human tendon disease, while inflammatory change may help to explain the mismatch between pain and macroscopic tendon structure.4 The use of a quotation from a twitter feed as evidence that cytokines are biologically inert within the context of tendinopathy seems biased and inappropriate, considering the strong evidence base throughout landmark publications in the scientific literature demonstrating a key role of cytokines in musculoskeletal pathologies.5

We agree that much remains to be elucidated surrounding inflammatory mechanisms in tendinopathy and, in particular, where inflammatory mediators sit within the hierarchal pathophysiological mechanisms involved in clinical disease. However, this model has and continues to set precedent within the field, and should therefore reflect the growing molecular evidence that modulating inflammatory pathways may provide novel translational therapies to a disease for which current treatments are failing our patients.

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Footnotes

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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