Executive Summary

Laminitis is not a single disease. It is a structural failure syndrome of the lamellar interface with multiple upstream drivers. Two major categories—endocrinopathic laminitis and sepsis-related laminitis—represent fundamentally different systemic pathways that converge on similar hoof pathology.

Introduction

A horse presents with acute forelimb soreness, increased digital pulses, and reluctance to turn. The clinical picture suggests laminitis. However, the deeper question is whether the laminitis is metabolic or inflammatory in origin

Endocrinopathic Laminitis: The Hyperinsulinemic Pathway

Endocrinopathic laminitis centers on insulin dysregulation. Horses may exhibit resting hyperinsulinemia or exaggerated post-prandial insulin responses. EMS is now understood as a metabolic risk phenotype defined by insulin dysregulation rather than obesity alone (Morgan et al., 2015)..

Mechanistic Insight: IGF-1 Receptor Signaling

Experimental data demonstrate that insulin can activate lamellar epithelial cells via pathways involving the insulin-like growth factor-1 receptor (IGF-1R) (Baskerville et al., 2018). This supports a direct endocrine signaling mechanism linking hyperinsulinemia to lamellar structural compromise.

Radiographic and Mechanical Patterns

Experienced farriers often report distinct mechanical patterns in chronic endocrine laminitis. Radiographs may show progressive distal phalanx rotation with lamellar stretching rather than acute catastrophic separation. Sole depth reduction is frequently gradual.

Cytokine Cascades and Vascular Dysfunction

Inflammatory laminitis involves systemic release of cytokines such as TNF-alpha and interleukins. These mediators influence vascular tone, endothelial function, and matrix metalloproteinase (MMP) activation. MMPs contribute to basement membrane degradation within the lamellar interface.

Hindgut Dysbiosis and Experimental Evidence

The oligofructose-induced laminitis model provides mechanistic insight into inflammatory laminitis. Rapid fermentable carbohydrate exposure alters hindgut microbiota composition (Milinovich et al., 2006) and can induce laminitis experimentally (van Eps & Pollitt, 2006).

Clinical Differentiation in Practice

In sepsis-related laminitis, systemic signs often precede hoof pain. Fever, diarrhea, tachycardia, depression, and dehydration may be present.

Clinical Differentiation Framework

When comparing systemic inflammation versus insulin laminitis, experienced clinicians evaluate:

Systemic context. Endocrinopathic laminitis usually presents in a metabolically predisposed but otherwise stable horse. Sepsis-related laminitis appears during systemic illness.

Conclusion

Endocrinopathic and sepsis-related laminitis are distinct systemic pathways converging on lamellar failure. Endocrinopathic laminitis is driven by insulin dysregulation and IGF-1 receptor–mediated epithelial signaling. Sepsis-related laminitis is driven by systemic inflammatory cascades often rooted in gastrointestinal barrier disruption and endotoxemia.

Frequently Asked Questions(FAQs)

Q1: How do you tell endocrinopathic laminitis from sepsis-related laminitis?

A: Systemic context is central. Endocrinopathic laminitis typically occurs in metabolically predisposed horses without systemic illness. Sepsis-related laminitis usually accompanies systemic inflammatory disease (Mitchell et al., 2014; Leise, 2021).

Q2: Are clinical signs different?

A: Hoof pain overlaps, but inflammatory laminitis often presents with fever, diarrhea, or systemic compromise, whereas metabolic laminitis may present without systemic illness.

Q3: Which horses are most at risk?

A: Horses with EMS, insulin resistance, and PPID are at higher risk for endocrinopathic laminitis. Horses experiencing colitis, endotoxemia, or severe infection are at risk for sepsis-related laminitis (Kirkwood et al., 2022).

Call to Action

When laminitis is suspected, evaluate systemic context alongside hoof findings. In metabolically predisposed horses, discuss insulin dysregulation testing and endocrine evaluation with veterinary teams. In horses recovering from gastrointestinal or inflammatory disease, maintain vigilance for early lamellar instability. Sharing evidence-based distinctions strengthens decision-making across veterinary, farriery, and breeding communities.

References 

1. Baskerville, C. L., et al. (2018). The effect of insulin on equine lamellar basal epithelial cells mediated by the insulin-like growth factor-1 receptor. PeerJ, 6, e5945.
2. de Laat, M. A., et al. (2019). Incidence and risk factors for recurrence of endocrinopathic laminitis in horses. Journal of Veterinary Internal Medicine, 33(3), 1473–1482.
3. Kirkwood, N. C., et al. (2022). Pituitary pars intermedia dysfunction in horses. Animals.
4. Leise, B. S. (2021). Laminitis updates. Veterinary Clinics of North America: Equine Practice, 37(3), 595–607.
5. Milinovich, G. J., et al. (2006). Changes in equine hindgut bacterial populations during oligofructose-induced laminitis. Environmental Microbiology, 8(5), 885–898.
6. Mitchell, C. F., et al. (2014). The management of equine acute laminitis. Veterinary Medicine: Research and Reports, 5, 177–190.
7. Morgan, R., et al. (2015). Equine metabolic syndrome. Veterinary Record, 177(7), 173–179.
8. Morgan, R. A., et al. (2016). Vascular dysfunction in horses with endocrinopathic laminitis. PLOS ONE, 11(10), e0163815.
9. Tuniyazi, M., et al. (2021). Changes of microbial and metabolome of the equine hindgut during oligofructose-induced laminitis. BMC Veterinary Research, 17, 3.

van Eps, A. W., & Pollitt, C. C. (2006). Equine laminitis induced with oligofructose. Equine Veterinary Journal, 38(3), 203–208.