Equine laminitis: loss of hemidesmosomes in hoof secondary epidermal lamellae correlates to dose in an oligofructose induction model: an ultrastructural study.

This study examines the impact of different doses of oligofructose on the ultrastructure of hoof lamellae in horses, revealing a correlation between loss of hemidesmosomes and laminitis severity.

Research Objectives

• The research primarily aimed to study the ultrastructure of acute laminitis (a painful disease in the hooves) in horses. The focus was particularly on changes induced by escalating dosages of oligofructose.
• The study was driven by a need for a more precise understanding of the changes in the lamellar basement membrane zone during laminitis. The researchers believed that closer examination of laminitis-affected tissues with transmission electron microscopy could enhance the understanding of the disease’s pathogenesis and potential treatments or prevention methods.

Methods

• The study was performed on six healthy horses. They were administered varying dosages of oligofructose via nasogastric intubation – at 7.5, 10 and 12.5 g/kg body weight.
• Two days later, all six horses developed laminitis. The animals were euthanized and their forefeet processed for examination under a transmission electron microscope.
• The researchers focused on the hemidesmosome (HD) populations in the lamellar basal cells, and the distance between the cell plasmalemma and the basement membrane’s lamina densa. These parameters were compared to control tissues.

Results

• The study noted a greater loss of hemidesmosomes and more severe incidence of laminitis with increasing oligofructose dosage.
• The researchers were able to correlate the set of structural changes in horses’ hooves – characteristic basement membrane separation, cytoskeleton failure, and abnormal and rounded basal cell nuclei – to a joint failure of hemidesmosomes and anchoring filaments.

Conclusions

• The research established that when hemidesmosomes are not properly assembled, it leads to dysadhesion or loosening between the basement membrane’s lamina densa and the epidermal basal cells, underlining the critical role of hemidesmosomes in maintaining lamellar interface attachment.
• Any medical conditions that either activate lamellar matrix metalloproteinase (an enzyme that breaks down proteins) or interfere with the entry of glucose into lamellar basal cells can contribute to the failure of hemidesmosomes, thereby promoting the onset of laminitis.
• The research conclusively established a correlation between the degree of lameness in horses (laminitis severity) and progressive loss of lamellar hemidesmosomes.
• Therapeutic interventions aimed at protecting the lamellar environment from disturbances that activate matrix metalloproteinases or block glucose entry could control the development of laminitis.