Written by Sharon Smith MSc SEBC(Reg) IEng BHSAPC (Top Image credit Jane Myers – Equiculture)
In this first article Equine behavior specialist Sharon discusses the common causes for Laminitis, a complex and often misunderstood condition.You can’t be around horses for very long before you hear about laminitis. The complexity of this potentially crippling condition is reflected in the variety of definitions, for example:
- ‘…a serious form of lameness in horses characterised by a hot, painful hoof, with bounding pulses that can be felt in the digital arteries…’ (University of Liverpool)
- ‘…damage to or failure of the laminae/lamellae…’ (thelaminitissite.org)
- ‘…a disease associated with ischaemia [inadequate blood supply] of digital dermal tissues, it is not primarily an inflammatory disease; hence lamin-itis is a misnomer…’ (laminitis.org)
Many owners assume the frog, sole and hoof wall spread the horse’s weight. In fact, pressure under the pedal bone in the foot actually decreases under load, so the frog and sole are not primary weight-bearing structures . Instead, weight is transferred from the pedal bone, through soft tissue, to the underside of the hoof horn/wall. A special adaptation inside the hoof wall helps to carry the huge weight. There are hundreds of thin plates of hoof horn growing into the foot. It looks like the underside of a mushroom. These plates greatly increase the surface area available for soft tissue to attach to . For clarity, I shall refer to the hard hoof plates as ‘lamellae’ and the inter-locking soft tissue folds as ‘laminae’. The all-important super-glue between the laminae and lamellae is called the ‘basement membrane’.
The importance of blood supply.
The basement membrane and laminae soft tissue are living cells and need a blood supply. Blood contains:
- red blood cells - transporting oxygen in and carbon dioxide away
- white blood cells (‘leukocytes’) - which help fight infection, release histamine (which triggers inflammation), envelop foreign bodies and assist with ‘mopping up’ fragments of damaged cells
- platelets - which stop leakage by causing clots (in veins) and scabs (on the skin)
- plasma - the liquid carrying the red and white blood cells and platelets. It also carries proteins, fats, dissolved salts, nutrients and hormones. But also carries bacteria, viruses and dissolved toxins.
Small amounts of damage to soft laminae will cause structural changes within the foot, which may lead to abnormal hoof horn growth and gait changes. This can be managed and overcome, if spotted in time. There may be serious complications with greater damage. ‘Founder’ is partial separation of the laminae/lamellae, allowing the digital flexor tendon to pull and rotate the pedal bone downwards. ‘Sinker’ is another stage on, so called because all suspension is lost. Bones sink down in the foot, against the sole, and a rotated pedal bone may even puncture the sole.
The destruction of the basement membrane (between lamellae and laminae) seems to be due to one or more of: mechanical forces; laminae inflammation or abnormal cell growth/function.
Physically breaking apart the cells of the basement membrane. A potential problem with overweight horses, severe dietary deficiency or repetitive impact on hard surfaces. Alternatively, following inflammation, cell abnormality or death (see below). It may start with minor lamellae/laminae detachment under physical stress. The platelets in the blood patch-up the damage, but they also clog up the tiny veins leaving the laminae, causing damaging back-pressure, shunt activation, loss of blood supply to the laminae and further cell death (see below).
Inflammation is the result of tissue cells signalling for more blood to enter tissue to repair damage, deal with toxins, or deal with an invasive threat, such as harmful bacteria or virus. The tissue membranes become permeable, and so weaker, to allow the plasma and blood cells in. Chronic (low-level) inflammation (eg. a result of PPID or stress) means constantly weaker tissues. Blood arrives in the horse’s heel area first . The additional nutrients used therein cause the heel area to grow quicker than the toe, and the tell-tail growth rings in the hoof. The outgoing blood is unrestricted, so pressures inside the hoof are stable and there is minimal pain, if any. The horse is still on the brink of full laminitis. One minor challenge and acute inflammation will allow more blood to flood into the laminae and swell. The solid hoof capsule stops outwards swelling. Inward swelling pushes the laminae/pedal bone away from the support of the lamellae. The forces through the pedal bone then continue to rip the basement membrane apart, separating the laminae from the lamellae. Platelets are activated by the resulting damage, restricting blood away from the foot too. All this pressure and pooling of blood in the foot causes pain, a hot hoof and a thumping pulse at the back of the fetlock. Shunts higher up will open to compensate for the increased pressure, reducing blood to the foot but eventually starving the laminae and basement membrane, so death of these structures will follow.
Abnormal growth/function of the basement membrane
Anything that causes cells to grow too quickly or not grow in the right way, will risk laminae detaching from the lamellae. For example, a horse has a broken leg, so constantly stands on the other leg/foot. A hard floor would compress the arteries against the pedal bone, cutting off the blood supply. A lack of oxygen and nutrients to the toe area causes basement membrane cell death. Another example is where high insulin levels directly damage the basement membrane across the whole hoof, without inflammation initially. Insulin may trigger growth factors in the basement membrane , lengthening the hoof lamellae/laminae between pedal bone and hoof wall. This is structurally weaker – which is then ripe for a seemingly minor event to cause laminitis. Lamellae lengthening can be observed as a stretched ‘white line’ between the sole and hoof wall. High insulin levels and a stretched white line are associated with Equine metabolic syndrome (EMS), obesity, PPID/Equine Cushing’s disease and corticosteroids.
Triggers and risk factors
It is known that overconsumption of starch and sugars overload the foregut, causing hindgut fermentation and acidic conditions. The result is watery diarrhoea (colitis), but not laminitis in all horses. A secondary mechanism is clearly at work. One proposal is the organic acids from the overloaded hind-gut increase circulatory blood lipo-polysaccharide (LPS). LPS in sufficient quantity both induces insulin resistance and leads to chronic inflammation, including in the lamellae . Fructans in grass are often cited as triggering laminitis, but a direct link has not been found. Elevated blood sugars ARE a trigger (which can happen with sugary grass, but also starchy sweet feed and sweet hay) but these should not be such a threat if the insulin response is normal, and not resistant!
At a cellular level, there are only a few mechanisms that damage the lamellae and basement membrane. But those mechanisms can be triggered in a number of ways.
These risks are summarised in the following table:
Prevention relies on: avoiding high blood insulin levels; controlling cortisol/PPID, and appropriate hoof care.
So focus on: maintaining a healthy level of body fat; a balanced, low-carb, fibre-based diet; a low-stress but aerobically active lifestyle; avoiding fast work on hard ground and an appropriately supportive flooring/footing when not being exercised.
Read part 2 where Sharon discusses what the different treatments are trying to achieve, which may explain potentially conflicting advice.
References DYHRE‐POULSEN, P., Smedegaard, H. H., Roed, J., & Korsgaard, E. (1994). Equine hoof function investigated by pressure transducers inside the hoof and accelerometers mounted on the first phalanx. Equine veterinary journal, 26(5), 362-366.  Pollitt, C. C. (1992). Clinical anatomy and physiology of the normal equine foot. Equine Veterinary Education, 4(5), 219-224.  Katz, L. M., & Bailey, S. R. (2012). A review of recent advances and current hypotheses on the pathogenesis of acute laminitis. Equine veterinary journal, 44(6), 752-761.  Gauff, F., Patan‐Zugaj, B., & Licka, T. F. (2013). Hyperinsulinaemia increases vascular resistance and endothelin‐1 expression in the equine digit. Equine veterinary journal, 45(5), 613-618.  Wearn, J. G., Suagee, J. K., Crisman, M. V., Corl, B. A., Hulver, M. W., Hodgson, D. R., ... & McCutcheon, L. J. (2012). Effects of the insulin sensitizing drug, pioglitazone, and lipopolysaccharide administration on markers of systemic inflammation and clinical parameters in horses. Veterinary immunology and immunopathology, 145(1-2), 42-49.  Medina‐Torres, C. E., Underwood, C., Pollitt, C. C., Castro‐Olivera, E. M., Hodson, M. P., Richardson, D. W., & Eps, A. W. (2016). The effect of weightbearing and limb load cycling on equine lamellar perfusion and energy metabolism measured using tissue microdialysis. Equine veterinary journal, 48(1), 114-119.