Are There Shared Mechanisms in the Pathophysiology of Different Clinical Forms of Laminitis and What Are the Implications for Prevention and Treatment?

Abstract

Laminitis is a consequence of primary disease processes elsewhere in the body. The key pathophysiologic events are insulin dysregulation in endocrinopathic laminitis, ischemia in supporting limb laminitis, and inflammation in sepsis-related laminitis. These apparently disparate mechanisms converge to cause lamellar attachment failure through epithelial cell adhesion loss and stretch, possibly mediated by common growth factor signaling pathways. Tissue damage through mechanical distraction, inflammation, pain, and a proliferative epithelial healing response are features of acute laminitis regardless of the cause. Preventive and treatment strategies based on knowledge of these unique and common mechanistic events are likely to improve clinical outcomes.