Abstract
Flexor tendinopathy is a common problem affecting humans and animals. Tendon healing is poorly understood and the outcomes of conservative and surgical management are often suboptimal. While often considered a localized injury, recent evidence indicates that in the short term, tendinopathic changes are distributed widely throughout the tendon, remote from the lesion itself. Whether these changes persist throughout healing is unknown. The aim of this study was to document gene expression, histopathological and biomechanical changes that occur throughout the superficial digital flexor tendon (SDFT) up to 16 weeks post-injury, using an ovine surgical model of tendinopathy. Partial tendon transection was associated with decreased gene expression for aggrecan, decorin, fibromodulin, tissue inhibitors of metalloproteinases (TIMPS 1, 2 and 3), collagen I and collagen II. Gene expression for collagen III, lumican and matrix metalloproteinase 13 (MMP13) increased locally around the lesion site. Expression of collagen III and MMP13 decreased with time, but compared to controls, collagen III, MMP13 and lumican expression remained regionally high throughout the study. An increase in TIMP3 was observed over time. Histologically, operated tendons had higher pathology scores than controls, especially around the injured region. A chondroid phenotype was observed with increased cellular rounding and marked proteoglycan accumulation which only partially improved with time. Biomechanically, partial tendon transection resulted in a localized decrease in elastic modulus (in compression) but only at 8 weeks postoperatively. This study improves our understanding of tendon healing, demonstrating an early ‘peak’ in pathology characterized by altered gene expression and notable histopathological changes. Many of these pathological changes become more localized to the region of injury during healing. Collagen III and MMP13 expression levels remained high close to the lesion throughout the study and may reflect the production of tendon tissue with suboptimal biomechanical properties. Further studies evaluating the long-term response of tendon to injury (6–12 months) are warranted to provide additional information on tendon healing and provide further understanding of the mechanisms underlying the pathology observed in this study.
Highlights
Tendon injury and tendinopathies are common in both human and veterinary medicine
The aim of this study was to identify the spatiotemporal changes in gene expression, histopathology and biomechanics that occur throughout injured tendons, using an ovine model of surgically-induced tendinopathy
The epitenon of control tendons was removed for gene expression samples, but in transected tendons it was firmly adhered to the region of the transection and required sharp dissection to remove
Summary
Tendon injury and tendinopathies are common in both human and veterinary medicine. In humans, an increased participation in sport is associated with a higher incidence of tendon injury [1,2,3,4]. In equine athletes that train or race on the flat, prevalence rates of forelimb superficial digital flexor (SDF) tendinitis have been reported to be 11.1% [11], while the prevalence of ultrasonographic evidence of pathology in the forelimb SDF tendon (SDFT) in National Hunt horses, which are required to jump obstacles while racing, was found to be 24% [12] In both humans and horses, outcomes following a diagnosis of tendinopathy are highly variable, but often suboptimal, with significant rates of re-injury and/or injury in the contralateral limb [13,14,15,16,17]. Small biopsies provide valuable information about the intratendinous environment but are limited in many respects for evaluating the healing process because the early stages of tendinopathy are often asymptomatic, the initiation of tendon healing and reconstitution is not
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