Abstract: Surgical stabilisation of the distal phalanx (DP) is a potential therapeutic strategy for severe acute laminitis. Objective: To evaluate the effects of locking compression plate (LCP) fixation of the DP to the dorsal hoof wall. Methods: Ex vivo and in vivo experiments. Methods: A T-shaped LCP was applied to one limb per pair in six pairs of cadaver forelimbs subjected to a combination of thermally induced lamellar failure and vertical load to simulate severe acute laminitis. Standard radiographic measurements were used to compare DP displacement. The LCP was then applied to one forefoot in 12 healthy Standardbred horses either standing (n = 6) or under general anaesthesia (n = 6). Lameness was evaluated daily, then horses were euthanised (day 8) and lamellar tissue analysed using light microscopy, histomorphometery and molecular markers of apoptosis. Results: In the cadaver limb model, LCP fixation prevented the significant changes in hoof-distal phalanx distance, coronary extensor process distance and sole depth that characterised DP displacement in untreated limbs (p < 0.05). Application of the construct in vivo was well tolerated with minimal lameness (10/12 horses were sound at the trot on day 8); however, histology revealed dorsal lamellar pathology consistent with laminitis, but with extensive keratinocyte apoptosis. Adjacent to the LCP, caspase-3 positive cell counts were approximately 20-fold higher than control (p < 0.001). Conclusions: Pathology was evaluated at a single time point. Microvascular perfusion was not evaluated. Conclusions: Rigid fixation of the DP to the hoof capsule was achieved with the LCP construct in a cadaver limb laminitis model. In live horses, LCP fixation caused regional lamellar pathology with extensive apoptosis, likely due to disturbed lamellar microvascular perfusion and/or mechanostasis. Understanding these mechanisms is critical for refinement of the technique in order to avoid iatrogenic lamellar damage. Unassigned: Chirurgische Stabilisation der distalen Phalanx (DP) ist eine potenzielle therapeutische Strategie für hochgradig akute Hufrehe. Unassigned: Evaluation einer Locking Compression Plate (LCP) Fixation der DP zur dorsalen Hufwand. Methods: Ex vivo und in vivo Experiment. Methods: Eine T-förmige LCP wurde in jeweils einem Vorderfuß aus 6 Paaren von Kadaver Vorderbeinen angebracht und mit thermisch induziertem lamellarem Versagen und vertikaler Belastung ausgesetzt, um hochgradig akute Hufrehe zu simulieren. Standard radiologische Messungen wurden für den Vergleich von DP Verlagerung durchgeführt. Die LCP wurde anschließend bei 12 gesunden Standardbred Trabrennpferden in jeweils einem Vorderfuß entweder stehend (n = 6) oder unter Allgemeinanästhesie (n = 6) angebracht. Lahmheit wurde täglich beurteilt, die Pferde wurden anschließend euthanasiert (Tag 8) und das lamellare Gewebe mithilfe von Lichtmikroskopie, Histomorphometrie, und molekularer Marker für Apoptose analysiert. Unassigned: Im Kadavergliedmaßen-Modell verhinderte die Fixation mit LCP die signifikanten Veränderungen in Huf-DP Abstand, Kronrand zu Strecksehnenfortsatz Abstand und Sohlendicke welche DP Verlagerung in unbehandelten Gliedmaßen charakterisierte (p < 0.05). Applikation des Konstrukts in vivo wurde gut und mit minimaler Lahmheit toleriert (10/12 Pferde waren lahmfrei im Trab an Tag 8); indessen zeigte Histologie dorsale lamellare Pathologie vereinbar mit Hufrehe, allerdings mit umfangreicher Apoptose der Keratinozyten. Der LCP angrenzend wurde eine ca. 20-fach höhere Caspase-3 positive Zellzahl als in der Kontrollgruppe (p < 0.001) nachgewiesen. HAUPTEINSCHRÄNKUNGEN: Pathologie wurde lediglich an einem einzigen Zeitpunkt beurteilt. Mikrovaskuläre Perfusion wurde nicht beurteilt. Unassigned: Rigide Fixation der DP zur Hufkapsel wurde mithilfe des LCP-Konstrukts im Kadavergliedmaßen-Hufrehe-Modell erreicht. In lebenden Pferden verursachte die LCP Fixation regional lamellare Pathologie mit extensiver Apoptose, vermutlich durch gestörte lamellare mikrovaskuläre Perfusion und/oder Mechanostase. Verständnis dieser Mechanismen ist entscheidend für die Verbesserung der Methode um iatrogen lamellare Schäden zu verhindern.
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This study investigates the use of locking compression plate (LCP) fixation as a potential treatment for severe laminitis in horses. The research involves ex vivo and in vivo experiments on cadaver forelimbs and live horses. The results showed that the LCP fixation could effectively prevent displacement of the distal phalanx (DP) in the hoof, however, it can cause lamellar pathology and extensive apoptosis, probably due to disrupted lamellar blood supply and/or mechanostasis.
Methods
The research used a combination of ex vivo and in vivo experiments to test the effectiveness of LCP fixation in treating severe acute laminitis.
In the ex vivo experiment, the researchers subjected a T-shaped LCP to six pairs of cadaver forelimbs, inducing thermal lamellar failure and vertical load to simulate extreme acute laminitis.
In the in vivo experiments, one LCP was applied to either a standing (n=6) or an anaesthetised (n=6) forefoot in twelve healthy Standardbred horses. Daily lameness was evaluated, and lamellar tissue was analyzed posthumously using light microscopy, histomorphometry, and indicators of apoptosis.
Results
In the ex vivo model, the LCP successfully mitigated the significant changes in hoof-DP distance, coronary extensor process distance, and sole depth that characterized DP displacement in untreated limbs.
When applied in vivo, the horse subjects tolerated the LCP construct with minimal lameness. However, the histology showed dorsal lamellar pathology, indicative of laminitis, alongside widespread keratinocyte apoptosis.
Near the LCP, cell counts for caspase-3 (a sign of apoptosis) were approximately twenty times higher than the control’s.
Conclusions
The findings based on a single time point, and microvascular perfusion, were not considered in the study.
Rigid fixation of the DP to the hoof capsule was achieved with the LCP construct in a cadaver limb laminitis model.
In live horses, LCP fixation induced regional lamellar pathology and copious apoptosis, likely due to disrupted lamellar microvascular perfusion and/or mechanostasis.
Comprehending these mechanisms is crucial for refining the technique to avoid lamellar damage caused by the treatment.
Cite This Article
APA
Lean NE, Zedler ST, Van Eps AW, Engiles JB, Ford M, Stefanovski D, Walsh DM, Pollitt CC.
(2022).
Evaluation of locking compression plate fixation of the distal phalanx to the hoof wall as a potential therapy for laminitis.
Equine Vet J, 55(4), 707-716.
https://doi.org/10.1111/evj.13877
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