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  1. R J Murphy,
  2. K Kliskey,
  3. K Wheway,
  4. E B Watkins,
  5. D J Beard,
  6. A J Carr
  1. Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, UK


    Introduction In the past it has not been possible to evaluate the impact of current treatments upon tendinopathic rotator cuff tissue due to an inability to sample the tendon tissue before and after treatment. Serial tissue sampling pre- and post-intervention allows assessment of current therapies for the condition and may direct the development of novel future therapeutic options. The aim of this study was evaluate the short-term rotator cuff tendon tissue response to Glucocorticoid injection (GCI), Subacromial Decompression (SAD) and Rotator Cuff Repair (RCR).

    Methods Patients with a history of rotator cuff tendinopathy were recruited into groups defined by the treatments being undertaken and the structural integrity of the rotator cuff was assessed using ultrasound or arthroscopic diagnosis. Three groups were recruited:

    1. GCI—patients with a history of rotator cuff tendinopathy without a full thickness tear undergoing subacromial injection of glucocorticoid.

    2. SAD—patients with a history of rotator cuff tendinopathy without a full thickness tear undergoing arthroscopic subacromial decompression due to failed glucocorticoid injection therapy.

    3. RCR—patients with a full thickness rotator cuff tear undergoing rotator cuff repair surgery.

    Biopsies of the supraspinatus tendon were taken on the day of intervention, prior to treatment, and repeated at initial follow up 7-weeks post-intervention. These paired samples were then analysed to evaluate the tissue response to the intervention undertaken. Samples were taken under ultrasound guidance from the supraspinatus tendon. The tissue samples were wax embedded, sectioned and stained using the following markers: CD34 to identify vascular endothelial tissue; CD45 Leucocyte common antigen to identify white cells as a marker of inflammation; MIB-1 to identify proliferating cells; Active Caspase-3 to identify cells undergoing apoptosis.

    Slides were imaged using a Zeiss Axio Imager M1 light microscope. Analysis used computer software to calculate the cellular density from the H&E images and the proportion of positively stained tissue from the immunohistochemistry images.

    Results Table 1 details the composition of the study groups. The immunohistochemical results (figure 1 at the top of next page) show a comparison of tissue characteristics on the day of intervention (pre-) and 7-weeks post-intervention. A significant increase in vascularity is seen in the RCR group at 7-weeks post intervention. There is a significant increase in inflammatory cells post treatment in the SAD and RCR groups. Proliferation is significantly reduced post treatment in the GCI group. No difference was seen in apoptosis after any of the interventions.

    Figure 1.

    Histological analyses (*p<0.05 paired t test Pre vs Post).

    Table 1.

    Group Sizes

    Discussion This study has shown changes in tissue characteristics in response to treatment. The results show increased vascularity in the RCR group, supporting a theory of a healing response. Both surgical groups showed increased inflammation within the tissue, which may simply reflect the early post-operative sampling time point. Perhaps the most significant finding was the reduction in proliferation within the tendon tissue in response to glucocorticoid injection supporting the theory of the negative effects of steroid treatment in tendinopathy. Further work is needed to define other biomarkers of tissue response and to investigate the tissue effects of treatment at other time points post-intervention.

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