Cyclic loading alters biomechanical properties and secretion of PGE2 and NO from tendon explants.

Journal Article (Journal Article)

BACKGROUND: Tendon overuse injuries are a common occurrence; accounting for a large proportion of occupational and athletic injuries. The concept examined in this study is the role of load-induced intrinsic inflammation to the mechanism of these injuries. This study examined the influence of cyclical loading on the mechanical properties, cell viability, and inflammatory mediators of cultured tendon explants. METHODS: Chicken digital flexor tendon explants were isolated and separated into no-load (24 h rest), moderate load (0.25-3.0 MPa, 1 Hz, 4 h, 20 h rest), and aggressive load (0.25-12.0 MPa, 1 Hz, 24 h) treatment groups. Tissue loading was carried out with a pneumatic device under load-control. The loading regimens for each explant treatment group started at a uniform time point (day 3 from isolation, t = 0 h). Medium was collected at t = 24 and t = 48 h and analyzed for the inflammatory mediators prostaglandin E(2) and nitric oxide. Viability was evaluated at t = 48 h. FINDINGS: Biomechanical data revealed a significantly (P < 0.05) lower strength in the aggressively loaded specimens compared to the moderately loaded samples. Prostaglandin E(2) concentrations of aggressively loaded samples showed significantly higher values compared to moderately loaded samples at t = 48 h. Nitric oxide concentrations were greater in the moderately loaded samples relative to the no-load group at t = 24 h. Viability was not found to differ among the groups. INTERPRETATION: Alterations in cyclical loading of tendon may cause a change in fibroblast-mediated inflammatory mediator production in tendon. This response is of clinical significance as it may have a role in the pathology of tendon overuse injuries.

Full Text

Duke Authors

Cited Authors

  • Flick, J; Devkota, A; Tsuzaki, M; Almekinders, L; Weinhold, P

Published Date

  • January 2006

Published In

Volume / Issue

  • 21 / 1

Start / End Page

  • 99 - 106

PubMed ID

  • 16198031

International Standard Serial Number (ISSN)

  • 0268-0033

Digital Object Identifier (DOI)

  • 10.1016/j.clinbiomech.2005.08.008


  • eng

Conference Location

  • England