Transcript:

[0:01]

Hi everyone, welcome back to Mad Barn Academy, and if you’re new here, welcome. We hope to earn your subscription today. If you like this video and other videos that we post, please like and subscribe. As always, we really appreciate the ongoing support. I’m Dr. Fran Row, one of the veterinary nutritionists here at Mad Barn. Today I’m covering part one of a two-part series on equine laminitis.

[0:25]

Most horse owners recognize laminitis as a serious threat to their horse’s health and well-being. Laminitis is both a common disease and a debilitating disease, which is why it really stays kind of at the top of the charts in terms of topics that interest both horse owners and researchers. Our team encounters questions about laminitis probably daily, which is why we’ve dedicated a lot of time to generating resources for horse owners on this topic. I’ve linked several of our articles about laminitis in the comment section below, so feel free to check those out after today’s video.

[1:06]

All right — without further ado, let’s get started on today’s presentation, which is an overview of laminitis. So today we’re covering part one of this two-part series. Be sure to check back for part two in the coming week or two, where I’ll be discussing endocrinopathic laminitis specifically.

[1:31]

I think we’re all familiar with the phrase “No hoof, no horse,” because it’s so true. Laminitis is the most serious disease of the equine foot, and it’s probably the second biggest killer of horses behind colic. It’s estimated that between 10–15% of horses in the United States are afflicted by laminitis at some point in their lifetime, and up to 75% of those horses eventually develop severe or chronic lameness and debilitation.

[2:11]

So, what is laminitis exactly? By definition, it’s inflammation (“-itis”) of the lamina in the foot. The lamina are these finger-like projections that arise from the coffin bone and from the internal hoof capsule, and then they link together — you can sort of think of it like Velcro. The lamina (which can also be called lamellae, just to make things extra confusing) suspend that coffin bone within the hoof capsule. This suspensory, or laminar, apparatus of the equine foot is a highly dynamic structure — it’s incredibly strong, essentially able to carry the weight of the horse — while also being incredibly flexible. It has to be able to compress and stretch and tolerate the extreme biomechanical forces applied to the foot during normal movement or accelerated movement, like exercise.

[3:30]

Here’s a graphic illustrating the basic structure of the equine hoof. There’s a lot going on in this graphic, so you might find it helpful to pause the video at this point so you can take an extra moment to study these structures and read all of the labels. For now, I simply want to highlight the lamina specifically. The dermal lamina arise from the surface of the coffin bone; the epidermal lamina arise from the innermost layer of the hoof capsule, the stratum internum. Together, they interdigitate, or link together. We can also break down the lamina into primary and secondary structures. I think of it like a bottle brush — the primary lamina are the handle, and the secondary lamina are all those bristles that extend off the brush handle. This increases the surface area of the lamina where they link together, making that bond exceptionally strong.

[4:48]

Under the microscope, this is exactly what it looks like. In this histopathology image, the darker pink tissue is the epidermal lamina, while the lighter pink tissue is the dermal lamina. The asterisk labels the primary lamina (the handle of our bottle brush), and the arrows label the secondary lamina (the bristles).

[5:27]

So now that we have a better understanding of the structure affected by laminitis — the lamina, or laminar apparatus of the foot — what happens when there’s inflammation present? Laminitis results in damage to the lamina. Inflammation weakens the bond between the hoof capsule and the coffin bone by destroying the structure and integrity of that “Velcro.” This leads to instability, which is extremely painful. The degree of damage and instability can range from mild to catastrophic and life-ending.

[6:17]

One distinction worth making is between laminitis and founder. It’s common for these terms to be used interchangeably, but technically they’re not the same thing. Founder describes displacement of the coffin bone within the hoof capsule. Not all episodes of laminitis result in coffin bone displacement, though severe or chronic laminar instability increases the likelihood. There are two types of displacement: rotation and sinking. Rotation occurs when the coffin bone is pulled away from the dorsal hoof wall by the deep digital flexor tendon. Sinking is when the coffin bone actually sinks deeper into the hoof capsule due to severe laminar breakdown around the entire foot. In catastrophic failure, the coffin bone can rupture through the sole, which is fatal.

[8:01]

In summary: laminitis is inflammation of the lamina, which results in separation between the hoof wall and coffin bone. If severe enough, the coffin bone can rotate or sink. Over time, we may also see abnormal hoof growth, widening of the white line, changes to hoof angle, and heel changes. Under the microscope, laminitis causes lamina to stretch and elongate, epithelial cell adhesion failure, and sometimes formation of a laminar wedge. Gaps from laminar separation can fill with exudate or hemorrhage, creating an environment for bacteria and secondary hoof abscesses.

[10:04]

Now, the two types of founder: in a normal hoof, the dorsal surface of the coffin bone is parallel to the dorsal hoof wall. In rotation, those lines are no longer parallel. In sinking, a cleft can form at the coronary band as the bony column sinks into the foot, pulling the coronary band down.

[11:13]

We now understand that laminitis is not a disease in itself, but rather a consequence of another systemic disease process. Researchers recognize three main mechanisms: metabolic-associated (endocrinopathic) laminitis, sepsis-induced (endotoxemic) laminitis, and mechanical overload laminitis. Endocrinopathic laminitis is linked to elevated blood insulin levels (hyperinsulinemia) from conditions such as equine metabolic syndrome or PPID (Cushing’s disease). Endotoxemic laminitis is associated with body-wide inflammation from sepsis, colitis, pneumonia, retained placenta, or even black walnut exposure. Mechanical overload laminitis comes from excessive concussion (road founder) or excessive weight bearing on one limb (support-limb laminitis).

[13:38]

We’ll be focusing on endocrinopathic laminitis from here on out for two reasons: it’s the most common cause of laminitis (believed to account for 90% or more of cases), and it’s the mechanism that can be addressed with dietary management — which we’ll cover in part two.

[14:14]

Currently, we believe there are two main ways elevated blood insulin damages the laminar bond: (1) insulin overstimulates growth factor receptors, triggering epidermal proliferation, which stretches cells and decreases structural integrity; and (2) insulin promotes vasoconstriction, narrowing blood vessels in the foot and causing tissue ischemia (lack of oxygen and nutrients). Acute hyperinsulinemia can trigger laminitis experimentally in healthy horses, but many horses with chronic insulin dysregulation develop low-grade, cumulative laminar damage over time, making them more susceptible to acute laminitis.

[16:21]

When a horse suddenly becomes acutely laminitic, we can usually identify a reason. In part two, we’ll review metabolic disease, go over clinical signs of laminitis (both acute and chronic), and discuss prevention strategies. Check back in the next week or two for that video.

[16:50]

Here are our references for today, and thanks for listening. I hope you liked this video. Please like and subscribe to our channel, and don’t forget to check out the additional resources linked in the description below. Until next time, thank you.