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Achilles tendinopathy – pathophysiology: state of the art
  1. Paul W Ackermann1,2,
  2. Phinit Phisitkul3,
  3. Christopher J Pearce4
  1. 1 Integrative Orthopedic Laboratory, Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
  2. 2 Department of Orthopedics and Sports Medicine, Karolinska University Hospital, Stockholm, Sweden
  3. 3 Department of Orthopedics, Sioux City, Iowa, USA
  4. 4 Department of Orthopaedic Surgery, National University Health System, Singapore, Singapore
  1. Correspondence to Dr Paul W Ackermann, Department of Orthopedics and Sports Medicine, Karolinska University Hospital, Stockholm, 17176, Sweden; paul.ackermann{at}


Achilles tendinopathy (AT), which is increasing in prevalence, continues to puzzle clinicians around the world. AT comprises insertional and non-insertional AT (NIAT). This review will deal with NIAT, which is often related to changes in activities in sports and occupation, but can also be unrelated to activities that load the Achilles tendon. Recent studies demonstrate that extrinsic risk factors such as errors in training and occupational activities and intake of drugs that interact in tendon metabolism may lead to tendinopathy. In combination with intrinsic risk factors, lower limb biomechanical abnormalities and metabolic, inflammatory conditions, for example, diabetes, hypercholesterolaemia and genetic deviations, the risk of of AT is increased. Therefore, dysregulated mechanical loading and aberrant cellular signalling due to systemic metabolic/inflammatory imbalance and local hypoxia are suggested to cause NIAT. The exact aetiology and pathophysiology of NIAT are, however, not fully known and warrant further studies. NIAT is a condition that increases with ageing and characterised by pain during activity. Recent findings demonstrate that tendinosis is characterised by a fibrotic, failed healing response associated with pathological ingrowth of blood vessels and sensory nerves into a normally aneuronal/avascular tendon proper. This pathological sensory nerve sprouting may partly explain increased pain signalling, and partly by release of neuronal mediators contribute to causing the fibrotic alterations observed in NIAT. Establishing the differential underlying risk factors of NIAT should give better preventive strategies in patient education and counselling. Unravelling the common pathophysiological processes of NIAT may provide the means for future targeted therapies using combined surgical and biological approaches.

  • ankle
  • rehabilition / physical therapy
  • tendon
  • outcome studies
  • endoscopy
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  • Contributors All authors participated in the design of the work, drafting and revising of the work, and read and approved the final manuscript. PWA focused on the conception and design of the manuscript and the first draft of the manuscript. CJP focused on drafting and revising the chapters of aetiology, anatomy and pathology. PP focused on drafting and revising the abstract, introduction and the chapter on epidemiology. All authors agree to be accountable for all aspects of the work.

  • Funding This study was supported by the Swedish National Centre for Sports Research (Project No. 2013-0039).

  • Competing interests None declared.

  • Patient consent Not required.

  • Provenance and peer review Commissioned; externally peer reviewed.

  • Data sharing statement No additional unpublished data are available relating to this article.

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