The death of one of racings all time superstars, Secretariat (left) in 1989 through a severe laminitis episode only serves to emphasize that this condition has no class or breed prejudice and can potentially strike any horse at any time. Laminitis can mean months, years, or even a lifetime of pain for horses, depending on the severity and specifics of the attack. Once a horse has suffered laminitis, they will always be susceptible and will need careful management to prevent further damage.

Though much research time and finance has been devoted to the study of laminitis, there are still relatively few answers as to the exact mechanism by which the lamellae are affected so catastrophically.

 ‘Laminitis has no class or breed prejudice
and can potentially strike any horse at any time’

Thankfully, there are now a few basic understandings that can help horse owners to be mindful of the dangers and take steps toward recognizing and preventing those situations where horses are at risk. In the majority of cases, horse owners are now so aware of laminitis that cases are usually picked up early, and with correct treatment and management, many horses can make a good recovery.

Anatomy of the Horses Foot
The equine foot is an amazing feat of engineering, designed to withstand the immense concussive forces of locomotion over rough terrain. The internal structures are highly organized to ‘buffer’ concussive forces from the hoof wall, sole and frog, through the lamellae so that by the time it gets to the pedal bone (the coffin bone, distal phalanx, 3^rd phalanx) the force is reduced by up to 90%. This comparatively tiny structure is critically organized in such a way to support the limbs and subsequent mass of the horse. By domesticating the horse and subjecting them to a diet that is far removed from that of their wild cousins, and the hooves to greater concussive stresses through ridden work, we invite a number of problems that would be devastating in the wild situation. Laminitis is one such problem.

The equine foot is surrounded by a tough outer layer: the hoof wall. The wall is incredibly strong and forms a protective waterproof barrier between the sensitive inner organs and the outside world. The tissue of the wall is like hair and nail and contains no living cells. It takes around 6-8 months for new hoof wall tissue to grow down from the coronet band to the ground, with each new section pushing the older wall downward as it grows.

The hoof wall is connected to the internal structures by numerous lamellae, a series of delicate folds of tissue that extend around the entire inner surface of the hoof wall. There are two categories of lamellae. The outer lamellae extend from the hoof wall and are folded into an accordion-like structure, with each fold bearing many smaller, secondary lamellae. Each of these folds interfold with the inner, sensitive lamellae like interlocking fingers. The inner, sensitive lamellae are in turn connected to the pedal bone and as the hoof hits the ground, the tissues of the foot are compressed and expanded to allow absorption of concussive forces and to assist in the pumping of blood from the extremities back to the heart.

The main function of the lamellae is to hold the pedal bone in place within the hoof. The folded structure of the lamellae dramatically increases the surface area of attachment, forming an incredibly strong bond between the hoof wall and the underlying structures including the pedal bone. The stability of the thin membrane that lies between the outer and inner lamellar layers is imperative to the overall stability of the internal structure of the hoof.  It is thought to be the failure of this bond which leads to the intense pain and physiological changes within the foot that are known as laminitis or founder.

 What Happens When a Horse Suffers a Laminitis Attack?
Put simply, laminitis results from the failure of the attachment between the pedal bone and the inner hoof wall i.e. the tearing apart of the inner and outer lamellar folds. It is thought that the tearing is a result of the failure of the thin basement membrane that binds the two layers, though as always with laminitis, more research is required before this can be concluded categorically.

Until recently, our knowledge of the factors that trigger this failure was limited. Australian researchers have recently elucidated a key theory as to how the breakdown is triggered. This theory implicates certain enzymes (MMP enzymes) which are naturally present in healthy hoof. The enzyme naturally breaks down the cells of the basement membrane in small areas to allow the hoof wall to slide over the inner lamellae as it grows down toward the ground. The activity of the enzyme is tightly controlled to prevent over-release and allow only tiny breakages and reattachments to happen at one time.

Careful research in this area by Dr. Chris Pollitt of the University of Queensland has led to the theory that laminitis results from a catastrophic imbalance of these enzymes and their inhibitors, leading to a partial or total breakdown of the basement membrane that separates the lamellae. During the development stage, when the membrane fails, the lamellar layers are torn apart, somewhat like tearing apart a Velcro™ strip. In the resulting gap, fluids build up; the lamellae become inflamed and the capillaries supplying the region become squeezed closed by the resulting pressure, thus depriving the lamellae of the nutrients and oxygen normally delivered in the blood. The loss of correct blood flow results in increased blood pressure as blood is diverted to the larger vessels of the foot. This increased pressure is responsible for the bounding digital pulse associated with laminitis. The extra pressure leads to the larger vessels opening wide, and is responsible for the hot feet typical of a laminitis sufferer.

 ‘Australian researchers have recently elucidated
a key theory as to how laminitis is triggered’

The pain of laminitis increases as the horse enters the acute stage of the condition. If the damage is severe, the pedal bone separates from the inner hoof wall leading to sinking or founder. The pedal bone, with its connection to the hoof wall damaged, rotates downwards or, where damage extends around the whole circumference of the hoof, simply begins to sink within the hoof – the worst possible scenario. As it descends, further tearing occurs and the underlying hoof tissues are crushed. In some cases, the pedal bone descends so far that it actually pierces the sole of the foot. Rotation or sinking can continue for days or weeks, depending on the severity of the episode, so the horse must be reevaluated often during the first month or so following the attack.

In days not so long gone, pedal bone rotation would mean only one outcome for the horse, euthanasia. Fortunately, with improvement of our understanding of the mechanics of laminitis, many horses are now able to make at least a partial recovery from this situation, and hope is not entirely lost, even when x-ray evaluation reveals a ‘sinker’.  It is important to remember that not every case of laminitis leads to founder. It is believed that many racehorses suffer from sub clinical laminitis caused by both concussion, and a grain rich diet and this may impact on performance, but has no overt symptoms.

 ‘It is important to remember
 that not every case of laminitis leads to founder’

Prior to symptoms being seen in the acute stage, a prolonged period of reduced blood supply occurs, and only when blood supply is restored, do symptoms become evident. Current work in this area by Dr. Steve Adaire from the University of Tennessee is concentrating on the blood flow to the small capillaries within the feet of horses with induced laminitis. Dr. Adaire hopes to establish the pattern of circulatory imbalance in the developmental stages of laminitis, and eventually be able to describe a treatment regime to control these circulatory changes.

In addition to the enzyme theory of laminitis, there is a theory regarding reduced glucose uptake.  Glucose uptake is regulated by a number of hormones including insulin. Laboratory models of laminitis where glucose is restricted leads to breakdown of the basement membrane and allows easy tearing of the lamellar layers. It could be that there is a hormonal influence on glucose metabolism following carbohydrate overload which is responsible for triggering MMP enzyme production.

An even more recent theory questions the basement membrane failure theory altogether. Dr David Hood and his staff at the Hoof Diagnostic and Rehabilitation Clinic at Texas A&M Universtiy have been working on an innovative new hoof biopsy technique to get a close up picture of what is going on at the cellular level when laminitis strikes. Preliminary findings suggest that damage begins on the outer surface of the hoof to bone laminar attachment and progresses inwards. It is not yet clear whether the membrane itself is merely affected, damaged or completely destroyed. Samples taken during the developmental stages showed damage to the lamellae even though the basement membrane was still intact, so challenging the idea that laminitis begins at the basement membrane.

Article reproduced courtesy of Kentucky Equine Research

Part Two
What Causes Laminitis?
Symptoms  

Part Three
Diagnosis
Current Advice on Treating Laminitis
Prevention

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