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Overview of overuse (chronic) tendinopathy

Karim Khan, MD
Alex Scott, PhD, RPT
Section Editor
Karl B Fields, MD
Deputy Editor
Jonathan Grayzel, MD, FAAEM


Tendinopathy is a clinical syndrome characterized by tendon thickening and chronic, localized tendon pain. It may result from acute trauma (eg, tendon laceration or rupture) or more commonly, from overuse. Recovery from acute tendinopathy follows more or less well-established treatment protocols, which are discussed in reviews of specific injuries.

Historically, overuse tendinopathy was commonly referred to as tendinitis. The “-itis” suffix implicated inflammation as the primary cause of pain and swelling. In fact, a classic inflammatory reaction is minimally present with overuse tendinopathy [1,2]. The pathophysiology underlying most cases, as judged by tissue analysis from a variety of commonly affected tendons, is tendinosis. Tendinosis may be broadly characterized as a failed healing response within the tendon tissue [3]. This failed healing response is associated with characteristic findings on ultrasound and magnetic resonance imaging (MRI) [4].

This topic will review the clinically relevant aspects of the pathophysiology of overuse tendinopathy. The diagnosis and management of overuse tendinopathy generally and in specific tendons is discussed separately. (See "Achilles tendinopathy and tendon rupture" and "Rotator cuff tendinopathy" and "Epicondylitis (tennis and golf elbow)" and "Overview of the management of overuse (chronic) tendinopathy".)


Our knowledge of the pathophysiology of overuse tendinopathy stems mainly from surgical biopsies taken from athletes with chronic tendon pain who have failed conservative treatment and undergone open or arthroscopic tendon debridement. Numerous histopathology and gene array studies have been performed on these tissue specimens [2,5-20].

The histopathology of a wide variety of tendons examined in this manner consistently reveals a minimal presence, of inflammatory cells. This is true of the Achilles, posterior tibial, patellar, gluteal [21], adductor [22], extensor carpi radialis brevis and longus, flexor carpi ulnaris, flexor digitorum [23], and rotator cuff tendons [7,12,18,24,25]. Gene array studies generally confirm the absence of inflammatory gene upregulation in tendinopathy [14,26]. However, the increased presence of iron-containing macrophages does indicate the likelihood of prior episodes of vascular disruption and the resulting activation of the innate immune response during the development of tendinopathy [2,20].


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Literature review current through: Sep 2016. | This topic last updated: May 11, 2015.
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