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Orthopaedic Proceedings
Vol. 97-B, Issue SUPP_11 | Pages 22 - 22
1 Oct 2015
Morita W Dakin S Snelling S Carr A
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Introduction

Tendon healing begins with inflammation and results in an incomplete repair with fibrosis, culminating in tendon pathology along with tissue degeneration. Inflammatory mediators regulate the expression of growth factors, and members of the TGFβ superfamily including BMPs have been suggested to play a key role in the development of fibrosis. In established tendon diseases where inflammation and reparative processes persists, the cellular phenotype of tendon cells has been implied to undergo a transformation from that of normal tissue. This study investigates the inflammation-driven mechanisms of tendon pathology using an in vitro tendon cell model. We hypothesized that cells from diseased tendons will exhibit dysregulation of TGFβ superfamily members in response to inflammatory mediators when compared to cells derived from healthy tendons.

Materials and Methods

Diseased human tendon cells were isolated from patients with large to massive rotator cuff tears (n=4). Cells isolated from healthy human hamstring tendons served as control tissue (n=5). Cells were treated with human recombinant IL-1β (5ng/ml), oncostatin M (10ng/ml), IL-6 (10ng/ml), IL-10 (10ng/ml) in serum-free medium, or serum-free medium alone (control) for 24 hours. Cell viability was monitored by Alamar Blue assay, and expression of TGFB1, TGFBR1, TGFBR2, CTGF, BMP2 and BMP7 were quantified by quantitative reverse transcription polymerase chain reaction (RT-QPCR).


Orthopaedic Proceedings
Vol. 96-B, Issue SUPP_11 | Pages 260 - 260
1 Jul 2014
Dudhia J Werling N Dakin S Goodship A Smith RW
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Summary

Treatment of equine naturally occurring over-strain tendinopathy with mesenchymal stem cells suspended in bone marrow supernatant resulted in significant improvements compared to saline treated tendons in the normalisation of biomechanical, morphological, and compositional parameters with no adverse effects.

Introduction

Tendon injuries are a common age-related degenerative condition where natural repair involves scarification, resulting in a functionally inferior tissue1 that frequently re-injures. Naturally-occurring human and equine tendinopathy possess many similarities2 making the horse a good clinically-relevant model. A multitude of treatments are used but few have a strong evidence base. Regenerative approaches using mesenchymal stem cells (MSCs) to improve outcome are supported by clinical data demonstrating reduced re-injury rates in racehorses3. We therefore hypothesised that implantation of autologous MSCs into injured equine tendons would result in a tissue more closely resembling normal tendon matrix than the fibrous scar tissue formed subsequent to natural repair. The aim of this controlled experimental study was to assess the biomechanical, histological and compositional parameters following MSCs implantation into naturally injured tendons.