Are There Shared Mechanisms in the Pathophysiology of Different Clinical Forms of Laminitis and What Are the Implications for Prevention and Treatment?
Authors: van Eps, Burns
Journal: The Veterinary clinics of North America. Equine practice
Summary
# Editorial Summary: Shared Mechanisms in Laminitis Pathophysiology Although laminitis typically originates from distinct systemic insults—metabolic dysregulation in endocrinopathic cases, compromised blood flow in supporting limb laminitis, and overwhelming inflammation during sepsis—van Eps and Burns (2019) propose that these apparently separate pathways ultimately converge on a common final mechanism: failure of lamellar attachment through loss of epithelial cell adhesion and excessive stretch. Their review identifies growth factor signaling cascades as potential unifying mediators across all three forms, suggesting that regardless of initial cause, the acute phase involves characteristic patterns of mechanical tissue distraction, inflammatory infiltration, pain, and proliferative epithelial repair responses. This distinction between disease-specific triggers and shared downstream pathophysiology has considerable implications for clinical practice: prevention strategies can be tailored to address the unique upstream mechanisms (managing insulin resistance, ensuring adequate perfusion, controlling infection), whilst acute management protocols may be standardised around the common lamellar damage patterns observed in all presentations. Understanding these mechanistic intersections offers farriers, veterinarians and rehabilitation specialists a more nuanced framework for timing interventions and predicting tissue behaviour during the critical acute and early chronic phases of laminitis.
Read the full abstract on PubMed
Practical Takeaways
- •Identify the primary disease driver (endocrine dysfunction, ischemia, or sepsis) early, as this determines which preventive and therapeutic pathways to target
- •Recognize that despite different causes, acute laminitis shares common tissue damage patterns—address inflammation, pain management, and mechanical load strategically for all forms
- •Implement cause-specific interventions (insulin modulation, limb support/unloading, anti-inflammatory therapy) alongside general acute laminitis protocols for optimal outcomes
Key Findings
- •Three distinct pathophysiologic mechanisms drive laminitis: insulin dysregulation (endocrinopathic), ischemia (supporting limb), and inflammation (sepsis-related)
- •Disparate primary mechanisms converge through common growth factor signaling pathways to cause lamellar attachment failure via epithelial cell adhesion loss and stretch
- •Mechanical distraction, inflammation, pain, and proliferative epithelial healing response are universal features of acute laminitis regardless of initiating cause
- •Prevention and treatment strategies tailored to underlying mechanistic pathways are likely to improve clinical outcomes