Laminitis Part 1

Published in Horses and People Magazine

 Laminitis in horses; disease & causes (part 1)

By Mariette van den Berg, BAppSc. (Hons), MSc (Equine nutrition)

Spring! Warmer temperatures and longer days trigger the growing season. Pastures become lush and store more sugars for growth. This is the time when owners of horses that are sensitive for developing laminitis are starting to worry about the well-being of their horse.

Proper nutrition and management are very important aspects that help with the preparation and maintenance of your laminitis-prone horse before Spring really hits. Although, in Spring more cases of laminitis are observed, laminitis can happen at any time of the year.

In this article the disease and the dietary, metabolic and endocrine pathways that can trigger laminitis will be explained. In part 2 of the laminitis series the nutrition and management will be covered.

What is laminitis?

Laminitis is often referred to as “founder” and is caused by a malfunction of the attachment between the distal phalanx (coffin bone) and inner hoof wall.  The laminae are responsible for this connection and transfer from hoof wall to distal phalanx, and vice versa. There are two types of laminae; the epidermal (insensitive) and dermal (sensitive) laminae. The two types of laminae have primary and secondary laminae that interlock with each other to form a bond. Each hoof contains approximately 600 primary laminae. The larger primary laminae have in turn approximately 200 smaller secondary laminae around their edges (figure 1).

The epidermal laminae form the innermost layer of the hoof wall. The cells of the epidermal laminae are keratinised and rely on the nutrient diffusion from the dermis. The primary and secondary dermal laminae are extensions of the laminar dermis. The dermis contains tough connective tissue with blood vessels and nerves. The epidermal and dermal laminae are connected by the basement membrane. Connective tissue in the dermis attaches the distal phalanx to the inner surface of the basement membrane, forming a bond with the epidermal laminae. The laminae in the foot of the horse endure significant forces as a result of weight bearing and locomotion.

The horse has laminitis when this laminae bond fails and the hoof wall separate from the distal phalanx. The weight of the horse and forces of locomotion cause the coffin bone to sink into the hoof capsule. This causes damages to important arteries and veins in the dermis and sole of the hoof. As you can imagine this is a painful process, which can cause irreversible damage to the hoof and in severe cases may lead to euthanasia for the affected horse.

Figure 1: Diagram equine foot & laminae

 The phases of laminitis

Laminitis can be divided in three phases; developmental phase, acute phase, and chronic phase.

  • Developmental phase: is the period between the initiation of factors that result in the failure of the distal phalanx to remain attached to the innermost laminae of the hoof wall. In this phase digital pulses and distal limb temperatures may be appeared, but no lameness is observed yet. Generally, pre-exciting problems with one or more of the following organ systems; gastrointestinal, endocrine, musculoskeletal, immune, respiratory, renal and reproductive are involved in the onset of laminitis. The developmental phase can go unnoticed. Many horse owners find their pony or horse already experiencing clinical signs and foot pain (acute phase), without noticing pre-exciting problems.
  • Acute phase: is the phase when the first signs of foot pain are observed. Acute laminitis can last anywhere from 24-72 hours. Depending on the severity, the horse will experience to some degree damage to the laminae tissue, foot pain and lameness and in severe cases it may go together with digital collapse (rotation and/or sinking of the distal phalanx). The clinical signs may differ per horse, some horses are lucky and only experience pain in the foot, but don’t develop distal phalanx displacement. These horses generally make a complete recovery.
  • Chronic phase: if the horse does not recovery completely and the horse experiences to some degree displacement of the distal phalanx within the hoof capsule, the horse enters the chronic phase. By radiographs you can determine if the horse developed any earlier displacements. This chronic phase may last for an extended period of time (months, years, whole lifetime) and horses may experience persistent, mild lameness, foot pain and different growth pattern of the hoof (multiple lines or rings on the hoof capsule). Chronic horses can develop further damage to the laminae attachments and displacement of the distal phalanx.

The Obel lameness grades

In 1948, a system of rating the degree of lameness resulting from laminitis was developed by the Swedish veterinarian Nils Obel. It appears that there is a good correlation between the Obel grading system and the severity of the damage to the laminae attachments.

Grade 1 horses will shift weight from one foot to the other, but the movement remains relatively freely.
Grade 2 the lameness in the horse is more obvious. The horse walks with stiff stilted gait, but still lifts one foot.
Grade 3 the horse is reluctant to move and severely resists lifting a foot.
Grade 4 the horse is immobile and often leans backwards.

Factors that may trigger laminitis

The primary factors that trigger laminitis are not fully understood and laminitis research is ongoing. Laminitis may be considered as a systemic disease and the mechanisms that are involved in the onset of laminitis may be the result of a variety of pre-exciting problems elsewhere in the body of the horse. The gastrointestinal tract and endocrine system are often involved and are also studied the most. Intake of excess amounts of grain or lush pasture, obesity, insulin resistance, Cushing’s syndrome and colic may all play a role in the onset laminitis.

 Figure 2: Factors that may trigger laminitis in horses

Grass & grain founder

Intensive management of horses for sport and recreation is generally associated with abrupt dietary changes, such as when pastures rapidly achieve high levels of soluble sugars and feeding excess levels of starch-containing grain, or cereal concentrates. Excessive ingestion of non-structural carbohydrates (NSC), such as simple sugars, fructan and starch,  are known risk factors for the development of digestive and metabolic disorders such as equine hindgut acidosis and laminitis.

Horses evolved primarily as grazing herbivores. To be able to gain energy from low energy, higher fibre diet of pasture, horses developed fermentation chambers in the gut (caecum and colon) to house symbiotic microbial populations (hindgut fermentation). In the horse food undergoes first digestion before it enters the hindgut and is fermented. Most of the simple sugars and starch are broken down in the small intestine and absorbed in the blood stream. Structural carbohydrates (fibre) and fructan are indigestible for the horse and ends up in the hindgut where it is fermented by microbes to products that the horse can absorb. When horses excessively ingest NSC, fructans and undigested starch end up in the hindgut where it is fermented by bacteria that rapidly proliferate when NSC are present.  The end products produced by these bacteria (gram-positive) reduce the pH in the hindgut which may lead to acidosis.  The rapid proliferation of gram-positive bacteria can cause death to large numbers of other bacteria that may release toxic substances from their cell wall which may end up in the blood stream. Other compounds that bacteria produce such as vasoactive amines may also play a role. The bacteria cascade and release of substances may both be involved in the onset of laminitis.  The low pH in the hindgut may set off secondary systems in the body that may lead to laminitis, however the exact mechanisms are not fully understood. Ingestion of high levels of NSC has also been linked to the insulin pathway which will be discussed in the next section.

Insulin resistance & obesity

The classical case of the fat pony kept on lush pasture that develops laminitis. Obesity and insulin resistance (IR) are two factors that may be involved. Excessive ingestion of NSC causes high glucose and insulin levels to circulate in the blood. When the liver and muscle cells can’t store anymore glycogen, the glucose is stored as fat. The high levels of insulin can reduce sensitivity of the insulin receptors on muscle, fat and liver cells and interfere with the glucose uptake and glycogen synthesis.  IR is that the cells become resistant to the glucose uptake action of insulin. When this happens more insulin is needed (hyperinsulinaemia) to keep blood glucose concentrations within normal limits after a starchy or high sugar meal. IR and high circulating glucose levels can impair glucose delivery to the hoof, create inflammation and damage vascular tissue, which may trigger laminitis. Research has shown that insulin can cause laminitis directly, however the mechanisms are not fully understood.

Like in humans, there is an increase in numbers of horses that can be classified as obese. Obesity can increase the chance of developing IR and hyperinsulinaemia, which have been linked to increased risk of developing laminitis. Most of the obese horses have higher intake of energy then they use, although it appears that there may also be a predisposition and breed effect. The so called “easy-keepers” are the horses that are more susceptible to obesity, IR and laminitis. They tend to have a cresty neck and greater body condition score with localised fat deposits. Not all horses with cresty neck or higher body condition score have insulin resistance and at the same time, not all horses with IR or laminitis are obese. Any horse that is given too much NSC can get digestive and metabolic problems. If your suspect your horse is at risk then it is best to research this further with your veterinarian. The next step will be proper management of your horse’s diet and exercise program if possible. Even if your horse is not diagnosed with IR, increased body weight can cause various other problems, so also for those horses it’s good to have a closer look at the diet. In part 2 the article will continue with the nutrition and management of obese, IR and laminitis-prone horses.


Asplin, K.E., Sillence, M.N., Pollitt, C.C. and McGowan, C.M. 2007. Induction of laminitis by prolonged hyperinsulinaemia in clinically normal ponies. The Veterinary Journal 174 (3) 530-535.

Carter, R.A., Treiber, K.H., Geor, R.J., Douglass, L., and Harris, P. 2009. Prediction of incipient pasture-associated laminitis from hyperinsulinemia, hyperleptinemia, and generalized and localized obesity in a cohort of ponies. Equine Veterinary Journal 41 (2) 171-178.

Pollitt, C. 1995. Color Atlas of the Horse’s Foot.

Pollitt, C. 2008. Equine laminitis – Current concepts. RIRDC Publication No 08/062.

Internet: (Australian equine Laminitis Research Unit, University of Queensland)

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