A review of recent advances and current hypotheses on the pathogenesis of acute laminitis.

Summary

# Editorial Summary: Pathogenic Mechanisms in Acute Laminitis Katz and Bailey's 2012 review synthesises experimental evidence across multiple laminitis induction models—starch overload, oligofructose overload, black walnut extract, and hyperinsulinaemia—to establish clearer mechanistic distinctions between metabolic and inflammatory pathways in acute laminitis development. By directly comparing pathophysiological responses across these established models, the authors clarify how different triggering factors converge on lamellar dysfunction through distinct biochemical cascades, moving beyond the previous assumption that all acute laminitis shares identical aetiological pathways. A critical insight concerns pasture laminitis, which the review positions within the broader framework of metabolic dysfunction rather than purely inflammatory responses, challenging earlier clinical assumptions about seasonal disease presentation. For practitioners managing acute cases, this distinction has immediate relevance: recognising whether a laminitis episode stems from fermentable carbohydrate overload, endocrine dysregulation, or direct inflammatory insult should inform both immediate intervention and preventive strategies. Understanding these mechanistic differences enables more targeted therapeutic approaches and highlights why blanket treatment protocols may be less effective than interventions tailored to the underlying pathogenic pathway.

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Key Findings

• •Multiple experimental models (starch overload, oligofructose overload, black walnut extract, hyperinsulinaemia) produce acute laminitis through distinct pathophysiological mechanisms
• •Metabolic and inflammatory pathways represent separate mechanistic routes to laminitis development
• •Pasture laminitis mechanisms require integration with existing metabolic and inflammatory models

Conditions Studied