The propagation of induced tendon lesions in the equine superficial digital flexor tendon: an ex vivo study.
Authors: Bosch G, Lameris M C, van den Belt A J M, Barneveld A, van Weeren P R
Journal: Equine veterinary journal
Summary
# Editorial Summary: Propagation of Induced Tendon Lesions in the Equine SDFT The prognosis of superficial digital flexor tendon (SDFT) injuries in horses is intimately linked to lesion size, yet clinical lesions commonly enlarge substantially during the critical initial weeks post-injury through a combination of enzymatic degradation and biomechanical stress. Bosch and colleagues employed an ex vivo model using equine cadaver limbs to isolate the effects of cyclic loading on two distinct injury patterns: physically induced (mechanical) lesions and collagenase-induced (enzymatic) lesions, testing these under unloaded conditions, cyclical loading alone, and cyclical loading with immobilisation via fibreglass cast. Whilst physically induced lesions remained stable regardless of loading, enzymatically induced lesions propagated significantly when subjected to cyclic loading—a propagation that was substantially reduced by immobilisation, though casting had no effect on ultimate load at failure. These findings suggest that the synergistic interaction of enzymatic and mechanical forces drives lesion expansion, and that external support may limit this enlargement without compromising residual tendon strength. For farriers, veterinarians and rehabilitation specialists, this work provides biomechanical rationale for early aggressive immobilisation strategies in confirmed SDFT injuries, particularly where enzymatic activity is suspected; however, the authors appropriately flag that in vivo validation is essential before translating these ex vivo observations directly into clinical practice protocols.
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Practical Takeaways
- •Early immobilisation via casting may limit tendon lesion enlargement in the critical first days to weeks post-injury, potentially improving long-term prognosis
- •Lesions that involve enzymatic degradation (as in contaminated wounds or inflammatory responses) are at higher risk of propagation under normal loading and require stricter immobilisation protocols
- •Casting reduces lesion size but does not restore tendon strength, so gradual rehabilitation remains necessary despite apparent healing
Key Findings
- •Collagenase-induced lesions propagated significantly more under cyclic loading compared to unloaded controls
- •Lower limb cast immobilisation effectively reduced lesion enlargement in enzymatically-damaged tendons
- •Immobilisation reduced lesion propagation but did not improve ultimate load at failure of the tendon
- •Physical injury alone did not propagate with cyclic loading, but enzymatic damage combined with mechanical stimulation caused greatest lesion enlargement