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GENE EXPRESSION IN TENOCYTES SUGGESTS DEGNERATIVE TENDON TEARS ATTEMPT TO HEAL
  1. A M Fearon1,2,3,
  2. J L Cook4,
  3. P Smith2,3,
  4. A Scott1
  1. 1University of British Columbia, Vancouver, Canada
  2. 2Australian National University, Canberra, Australia
  3. 3Trauma and Orthopaedic Research Unit, The Canberra Hospital, Canberra, Australia
  4. 4Monash University, Melbourne, Australia

    Abstract

    Introduction The breakdown of the extracellular matrix (ECM) is well recognised in tendinopathy and likely the cause of degenerative tendon tears. Tendinopathy and degenerative tears can be hard and expensive to treat. Understanding the cellular processes that lead to ECM breakdown will likely lead to improved treatments. With this in mind, the gene transcript profile for extracellular matrix remodelling of tendon specimens from people with greater trochanteric pain syndrome (GTPS) and associated gluteal tendon tears were compared to an age and sex matched reference group.

    Methods Tendon specimens were collected from six participants undergoing gluteal tendon reconstruction for long standing (mean duration=41 months) GTPS, and four participants from an age-matched reference group (REF) of hip OA patients asymptomatic for GTPS. Specimens were collected using sterile technique and were stored at −80°C. RNA was isolated via laser capture micro-dissection (LCM) of areas of tendon that typified tendon rather than para-tendon or vessels within the specimen—identified using light microscopy and H&E staining. Specimens were tested using the SABiosciences array (PAHS-013). Immunohistochemistry was used to confirm the site of a subset of the expressed genes.

    Results We report on gene regulation changes of at least five fold that were seen in the GTPS group compared to the REF group. Genes involved in extracellular matrix modelling were both up regulated (MMP7) and down regulated (MMP3). The following cell adhesion genes were up regulated: ITGAV, NCAM1, ITGAM, while ITG3 was down regulated. The following genes involved in ECM synthesis were up regulated (LAMC1, COL1A1, COL5A1, Col6A1), while ADMATS1, LAMB3, VTN were down regulated.

    Conclusions This paper presents a novel method of tissue specimen selection (LCM), reducing the likelihood of RNA contamination from cells other than tenocytes. Further, these results suggest that there is increased cell activity and collagen production indicating that the tendon is continuing to actively remodel despite prolonged tissue damage. This supports the role of appropriate advice regarding tendon loading and compression, exercises to strengthen the musclo-tendinous unit, and ongoing support to patients. Recovery from tendinopathy may be possible—even in longstanding cases.

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