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Journal of comparative pathology2011; 145(4); 399-409; doi: 10.1016/j.jcpa.2011.02.001

Equine laminitis: comparative histopathology 48 hours after experimental induction with insulin or alimentary oligofructose in standardbred horses.

Abstract: Laminitis has many triggers and comparing the histopathology of lesions induced by different causes may help to establish whether a common mechanism or multiple pathologies are involved. The aim of this study was to describe the microscopical lesions and to quantify morphometric changes in the lamellae of horses with insulin-induced (n=4) and oligofructose (OF)-induced laminitis (n=4) compared with normal controls (n=4). Archived lamellar samples collected during two previous studies were used. Laminitis was induced within 48 h in standardbred horses with either a euglycaemic, hyperinsulinaemic clamp (EHC) technique or, in a separate experiment, with an overdose of alimentary OF. Normal tissue was obtained from control horses in the EHC experiment that received a balanced electrolyte solution intravenously for 48 h. Six measurements of lamellar length and width were recorded for each hoof. Leucocyte infiltration was assessed by immunolocalization of calprotectin. All control horses exhibited normal lamellar architecture, whereas treated horses developed clinical and histopathological changes consistent with laminitis. Laminitic samples displayed lengthening and narrowing of secondary epidermal lamellae (SELs), rounded epidermal basal cell (EBC) nuclei, mitosis and apoptosis. In the fore feet of laminitic horses, the length from the end of the keratinized axis to the axial tip of the primary epidermal lamellae (PELs) was increased (P<0.05). SELs were significantly longer (P<0.05) and narrower (P<0.05) in the treated horses compared with controls. The two treated groups did not differ from each other in SEL length or width. Calprotectin expression was absent in control horses, moderate in hyperinsulinaemic horses and marked in OF-treated horses. Laminitis induced experimentally with insulin or OF results in comparable lengthening and narrowing of the SELs and elongation of the axial end of the PELs at 48 h. Immunolocalization of calprotectin indicated that hyperinsulinaemia induces less leucocyte emigration than carbohydrate overload at 48 h. The microscopical lesion of laminitis is similar, but not identical in different forms of the disease.
Publication Date: 2011-03-22 PubMed ID: 21429503DOI: 10.1016/j.jcpa.2011.02.001Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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The researchers in this study explored the microscopic lesions and changes caused in horses by two types of laminitis, one induced by insulin and the other by oligofructose. Their findings reveal that both triggers result in comparable alterations in the structural elements (lamellae) of the horse’s hoof at 48 hours after induction, though there are differences in immune response based on the type of trigger.

Study Background

  • The main focus of this research was to identify and compare the microscopic lesions and morphometric changes resulting from insulin-induced (n=4) and oligofructose (OF)-induced laminitis (n=4) in horses, with a comparison to normal control horses (n=4).
  • Laminitis is a common and severe disease in horses, often caused by different triggers, that affects the tissues (lamellae) connecting the horse’s hoof with the underlying bone. The aim of comparison in this study was to determine whether different triggers led to different pathologies or a common disease mechanism.
  • To conduct this research, the team used archived lamellar samples from two previous studies. Two methods were used to induce laminitis: the hyperinsulinemic, euglycemic clamp (EHC) technique, and alimentary OF overload.

Findings on Lesions and Lamellar Changes

  • The research revealed that both insulin and OF-induced laminitis resulted in lengthening and narrowing of the secondary epidermal lamellae (SELs), as well as rounding of the epidermal basal cell (EBC) nuclei.
  • At the 48-hour mark post-induction, the area from the end of the keratinized axis to the tip of the primary epidermal lamellae (PELs) had significantly increased (P<0.05) in the fore feet of laminitic horses. This was consistent across both types of induced laminitis.
  • SELs in the treated horses were significantly longer and narrower compared to the controls (P<0.05). However, there were no significant differences in SEL length or width between the insulin and OF induced groups.

Findings on Immune Response

  • The study also evaluated the immune response in each case by examining the immunolocalization of calprotectin, a protein complex involved in inflammation and often associated with the migration of white blood cells (leukocytes).
  • Control horses had no calprotectin expression, hyperinsulinemic horses had moderate expression, and OF-treated horses showed marked expression.
  • This suggested that insulin triggering resulted in less leukocyte migration compared to OF triggering at the 48-hour period.

Conclusions

  • The evidence validated the hypothesis that laminitis induced by insulin or OF resulted in similar lengthening and narrowing of the lamellae at 48 h, suggesting a similar pathologic mechanism for both types of triggers.
  • However, the difference in calprotectin expression indicates that the immune response varies between triggers, suggesting that while the structural effects on the lamellae may be similar, the overall pathological processes of the disease could vary based on the trigger type. This finding proposes a need for tailored treatment methods based on the cause of the disease.

Cite This Article

APA
de Laat MA, van Eps AW, McGowan CM, Sillence MN, Pollitt CC. (2011). Equine laminitis: comparative histopathology 48 hours after experimental induction with insulin or alimentary oligofructose in standardbred horses. J Comp Pathol, 145(4), 399-409. https://doi.org/10.1016/j.jcpa.2011.02.001

Publication

ISSN: 1532-3129
NlmUniqueID: 0102444
Country: England
Language: English
Volume: 145
Issue: 4
Pages: 399-409

Researcher Affiliations

de Laat, M A
  • Australian Equine Laminitis Research Unit, School of Veterinary Science, The University of Queensland, Gatton, Queensland, Australia. m.delaat@uq.edu.au
van Eps, A W
    McGowan, C M
      Sillence, M N
        Pollitt, C C

          MeSH Terms

          • Animals
          • Apoptosis
          • Dietary Sucrose / toxicity
          • Disease Progression
          • Epidermis / pathology
          • Foot Diseases / chemically induced
          • Foot Diseases / pathology
          • Foot Diseases / veterinary
          • Glucose Clamp Technique
          • Hoof and Claw / pathology
          • Horse Diseases / chemically induced
          • Horse Diseases / pathology
          • Horses
          • Hyperinsulinism / chemically induced
          • Hyperinsulinism / complications
          • Hyperinsulinism / veterinary
          • Insulin / blood
          • Insulin / toxicity
          • Leukocyte L1 Antigen Complex / analysis
          • Oligosaccharides / toxicity
          • Random Allocation

          Citations

          This article has been cited 12 times.
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