Abstract

To report clinical findings and outcomes for 55 dogs with supraspinatus tendinopathy (ST) treated with adipose-derived progenitor cells and platelet-rich plasma (ADPC-PRP) therapy. Medical records of client-owned dogs diagnosed with ST that were treated with ADPC-PRP combination therapy were reviewed from 2006 to 2013. Data collected included signalment, medical history, limb involvement, prior treatments, physical and orthopedic examination, objective temporospatial gait analysis findings, diagnostic imaging results (radiography, magnetic resonance imaging, musculoskeletal ultrasonography), arthroscopy findings, and outcome. Following ultrasound-guided injection of ADPC-PRP, objective gait analysis was available on 25 of the 55 dogs at 90 days post ADPC-PRP therapy. Following treatment, a significant increase in total pressure index percentage (TPI%) was noted in the injured (treated) forelimb at 90 days post treatment (p = 0.036). At 90 days following treatment, 88% of cases had no significant difference in TPI% of the injured limb to the contralateral limb. The remaining 12% of cases had significantly improved (p = 0.036). Bilateral shoulder diagnostic musculoskeletal ultrasound revealed a significant reduction in tendon size (CSA) in the treated tendon at 90 days following treatment when compared to the initial CSA (p = 0.005). All cases showed significant improvement in fiber pattern of the affected supraspinatus tendon by the ultrasound shoulder pathology rating scale. These findings suggest that ADPC-PRP therapy should be considered for dogs with ST.

Highlights

  • Supraspinatus tendinopathy (ST) is a common cause of forelimb lameness in dogs

  • Medical records of client-owned dogs diagnosed with ST that were treated with adipose-derived progenitor cells (ADPC)-platelet-rich plasma (PRP) combination therapy were reviewed from 2006 to 2013

  • Medical records of 55 dogs diagnosed with unilateral ST treated with ADPC-PRP therapy were reviewed

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Summary

Introduction

Supraspinatus tendinopathy (ST) is a common cause of forelimb lameness in dogs. The etiology of ST is thought to be repeated strain activity and overuse from chronic repetitive activity, with a failure of adequate remodeling [1,2,3,4]. Tendons damaged from repeated strain demonstrate discontinuous, disorganized tendon fibers with little to no inflammation, occasional mineralization within the tendon, and bony remodeling at its insertion site in chronic cases [5, 12]. Calcification at the site of insertion has been well documented in both humans and dogs [8, 13,14,15,16]

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