Highly Accessed Review

Pathogenesis of tendinopathies: inflammation or degeneration?

Michele Abate1, Karin Gravare Silbernagel2, Carl Siljeholm3, Angelo Di Iorio4, Daniele De Amicis5, Vincenzo Salini5, Suzanne Werner3 and Roberto Paganelli6*

Author affiliations

1 Postgraduate School of Physical Medicine and Rehabilitation, University G d'Annunzio, Chieti-Pescara, 66013 Chieti Scalo (CH), Italy

2 Lundberg Laboratory of Orthopaedic Research, Department of Orthopaedics, Göteborg University, Sahlgrenska University Hospital, 41345 Göteborg, Sweden

3 Stockholm Sports Trauma Research Center, Karolinska Institutet, 11486 Stockholm, Sweden

4 Section of Clinical Epidemiology and Geriatrics, Department of Medicine and Sciences of Aging, University G d'Annunzio, Chieti-Pescara, 66013 Chieti Scalo (CH), Italy

5 Postgraduate School of Orthopaedic and Traumatology, Department of Human Movement Science, University G d'Annunzio, Chieti-Pescara, 66013 Chieti Scalo (CH), Italy

6 Section of Clinical Immunology, Department of Medicine and Sciences of Aging, University G d'Annunzio, Chieti-Pescara, 66013 Chieti Scalo (CH), Italy

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Citation and License

Arthritis Research & Therapy 2009, 11:235  doi:10.1186/ar2723

Published: 30 June 2009

Abstract

The intrinsic pathogenetic mechanisms of tendinopathies are largely unknown and whether inflammation or degeneration has the prominent role is still a matter of debate. Assuming that there is a continuum from physiology to pathology, overuse may be considered as the initial disease factor; in this context, microruptures of tendon fibers occur and several molecules are expressed, some of which promote the healing process, while others, including inflammatory cytokines, act as disease mediators. Neural in-growth that accompanies the neovessels explains the occurrence of pain and triggers neurogenic-mediated inflammation. It is conceivable that inflammation and degeneration are not mutually exclusive, but work together in the pathogenesis of tendinopathies.