Pathogenesis of tendinopathies: inflammation or degeneration?

doi:10.1186/ar2723

Arthritis Research & Therapy

Volume 11
Issue 3

Viewing options:

Abstract
Full text
PDF (285KB)

Associated material:

Related literature:

Articles citing this article
on Google Scholar
on ISI Web of Science
on PubMed Central
Other articles by authors
on Google Scholar

Abate M
Gravare Silbernagel K
Siljeholm C
Di Iorio A
De Amicis D
Salini V
Werner S
Paganelli R

on PubMed

Abate M
Gravare Silbernagel K
Siljeholm C
Di Iorio A
De Amicis D
Salini V
Werner S
Paganelli R
Related articles/pages
on Google

on Google Scholar

on PubMed

Tools:

Post to:

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

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

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

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

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

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

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

author email corresponding author email

Arthritis Research & Therapy 2009, 11:235doi: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.