The study of the equine hoof

20/09/2026

20/09/2026

Today we head home to New Zealand after a fabulous week in Bali.

I so needed the rest. 🏖️

19/09/2026

It depends.

Very commonly used statement but it depends when it’s needed to be said!

Horses are biological beings and are complex. They are not clones of cells in a test tube.

It’s not always yes or no in a treatment.
It really depends..

Co robić z krzywą nogą konia?

Co robić z krzywym kopytem?

Czy powinniśmy próbować prostować krzywe stawy? Czy powinniśmy ingerować w deformacje puszki kopytowej? A jeśli tak, to co dokładnie powinniśmy robić?

Najkrótsza odpowiedź, jak zawsze, brzmi: to zależy.

Od wieku konia, rodzaju i stopnia deformacji, budowy kończyny, postawy, warunków środowiskowych, sposobu użytkowania, czy obciążeń. Lista czynników, które trzeba wziąć pod uwagę, jest oczywiście znacznie dłuższa.

O tych zagadnieniach będziemy już niedługo rozmawiać podczas konferencji HoofsCare w Salio - zarówno w teorii, jak i w praktyce.

A poniżej roczniak z deformacją stawu pęcinowego typu varus i deformacją puszki kopytowej typu II.

Jego kończyny nie będziemy już prostować. Na tym etapie jest na to po prostu za późno.

Natomiast fakt, że nie możemy wyprostować kończyny, nie oznacza, że koń musi żyć już zawsze z tak zdeformowanym kopytem, jakie miał jeszcze kilka miesięcy temu. 😊😇

Dlatego odpowiedź "to zależy” często nie jest unikaniem odpowiedzi, a najlepszym punktem wyjścia do tego, by dogłębnie zrozumieć problem z którym mamy do czynienia.

Więcej informacji o konferencji i wydarzeniu:
"HoofsCare - Salio":
https://www.facebook.com/share/p/195Jb7N8yi/

19/09/2026

The critical blood supply inside the equine foot.

This photo shows beautifully a channel (tunnel/hole) that runs through the coffin bone (P3). The channel protects a blood vessel that originated from the terminal arch deep inside the bone. Its outlet feeds the lovely red raspberry jam layer that lies against the bone. That is the laminar corium also known as laminar dermis.

A network of millions of tiny blood vessels that feed the lamellae are present in that raspberry jam layer.

The red finger like strands are the dermal lamellae and they get fed by the laminar corium. They interweave with the epidermal lamellae that arise from the inner hoof wall. They feed the epidermal lamellae simply by diffusion of glucose across a layer between dermal and epidermal lamellae.

The foot needs as much glucose as the brain.

If we radiolabelled glucose and gave it to the horse and popped it into a scanner, we would see the brain light up as well as all 4 feet.

The lamellae are highly metabolic, they work hard to suspend the coffin bone in the capsule. They are glucose hungry.

If the blood supply to the lamellae is disrupted, as in laminitis, by the catastrophic displacement of the coffin bone, then the lamina will simply die. Thus creating more laminar tissue death and necrosis.

Blood supply to the laminae (and other tissues) is simply the most important number one priority.

Restore blood supply, restore tissue healing.

Cut taken parasagittal of a normal equine foot.

©️ Lindsey Field

19/09/2026

Oh such a long time ago.
I had so much to learn.

19/09/2026

Flash back!

18/09/2026

This was a landmark study published in 2007 linking insulin to laminitis.

That wasn’t long ago, my friends, just under 20 years.

All the current internet circus that feeds misinformation is coming from folks that never set foot in a laboratory.

Some of these folk I have the greatest respect for - you know who you are….. however I must remain science focussed. If you can give me clear controlled evidence to the contrary. then I’m happy to listen.

In this paper.
The researchers wanted to answer one very important question: Could high insulin itself damage the lamellae and cause laminitis, even when blood glucose remained normal?

They used nine young, clinically healthy ponies. None had any history of laminitis or known insulin resistance. Five received insulin continuously while their blood glucose was carefully maintained within the normal range. The four control ponies received only saline.

Note the control group. That is critically important to test a hypothesis.

The results were striking. Every one of the five ponies receiving insulin developed laminitis in all four feet within 72 hours. On average, clinical laminitis developed after approximately 55 hours

Note that NONE of the control ponies developed laminitis.

Importantly, the affected ponies did not have gastrointestinal disease, hindgut disturbance or signs of systemic illness. The significant difference was their extremely high insulin concentration.

Examination of their feet also confirmed genuine structural damage within the lamellae.

This study demonstrated that prolonged, very high insulin could directly cause laminitis, even in previously healthy ponies with normal blood glucose and without carbohydrate fermentation or illness affecting the hindgut.

This was a hugely important turning point in laminitis research. It helped us understand why dietary sugar and starch can be so dangerous for horses and ponies with insulin dysregulation. It is not simply that “sugar causes inflammation” or that every case begins with fermentation in the hindgut.

In susceptible horses, sugar and starch can provoke an abnormally large and prolonged insulin response, and it is that hyperinsulinaemia that can directly damage the lamellae.

That is why recognising and controlling high insulin is so important in the prevention and management of endocrinopathic laminitis.

Despite the internet frenzy, please apply critical thinking.

18/09/2026

Equine head sagittal cut
Note size of brain!
Not the size of a walnut.

©️Lindsey Field

Processing and cut with Dr Ivana Ruddock Lange.