Evidence of tendon microtears due to cyclical loading in an in vivo tendinopathy model

L H Nakama, K B King, Sven Abrahamsson, D M Rempel

Research output: Contribution to journalArticlepeer-review

82 Citations (SciVal)

Abstract

Tendon injuries at the epicondyle can occur in athletes and workers whose job functions involve repetitive, high force hand activities, but the early pathophysiologic changes of tendon are not well known. The purpose of this study was to evaluate early tendon structural changes, specifically the formation of microtears, caused by cyclical loading. The Flexor Digitorum Profundus (FDP) muscle of nine New Zealand White rabbits was stimulated to contract repetitively for 80 h of cumulative loading over 14 weeks. The contralateral limb served as a control, The tendon at the medial epicondyle insertion site was harvested, sectioned, and stained. Microtears were quantified, using image analysis software, in four regions of the tendon, two regions along the enthesis and two distal to the enthesis. The tear density (loaded: 1329 +/- 546 tears/mm(2); unloaded: 932 474 tears/mm(2)) and mean tear size (loaded: 18.3 +/- 6.1 mu m(2); unloaded: 14.0 +/- 4.8 mu m(2)) were significantly greater in the loaded limb (p < 0.0001) across all regions compared to the unloaded contralateral limb. These early microstructural changes in a repetitively loaded tendon may initiate a degenerative process that leads to tendinosis.
Original languageEnglish
Pages (from-to)1199-1205
JournalJournal of Orthopaedic Research
Volume23
Issue number5
DOIs
Publication statusPublished - 2005

Bibliographical note

The information about affiliations in this record was updated in December 2015.
The record was previously connected to the following departments: Reconstructive Surgery (013240300)

Subject classification (UKÄ)

  • Orthopedics

Keywords

  • microtears
  • tendinopathy
  • tendon
  • overuse
  • epicondylitis

Fingerprint

Dive into the research topics of 'Evidence of tendon microtears due to cyclical loading in an in vivo tendinopathy model'. Together they form a unique fingerprint.

Cite this