Introduction

For the purposes of this article, the definition of laminitis is:  the failure of the inner hoof wall to attach to the bone inside the hoof, called the coffin bone.  A horse has laminitis when the finger-like projections (lamellae) of the inner hoof wall no longer suspend the coffin bone.  Without proper attachment to the inner hoof wall, the weight of the horse and the forces of movement drive the coffin bone down, damaging arteries and veins and crushing the living tissues of the coronary band and sole.  This leads to unrelenting pain and a characteristic lameness.

Three Phases of Laminitis

There are generally considered to be three phases of laminitis:  developmental, acute and chronic.  The developmental phase, which actually occurs before the onset of foot pain, is when the separation of the lamellae from the coffin bone is triggered.  This may be as short as 8-12 hours when the laminitis is caused by exposure to black walnut shavings or 30-40 hours in the case of grain overload.

During the developmental phase, the horse usually experiences a problem with one or more of the following organ systems:

  • GI
  • Respiratory
  • Reproductive
  • Renal (kidney)
  • Endocrine (hormonal)
  • Musculoskeletal
  • Skin
  • Immune

It is a problem in one or more of these systems that results in the lamellae being exposed to trigger factors, which leads to separation from the coffin bone.  The exact nature of the laminitis trigger factors, apparently reaching the lamellae through the circulation, is not yet known.

Sometimes no developmental phase can be recognized:  the horse is simply discovered in the acute phase with no apparent ill health or inciting problem occurring beforehand.  This appears to be the case with grass founder, although research on grass growth suggests otherwise.  That is, under certain conditions (cold nights, sunny days) grass can manufacture high enough concentrations of sugar to cause fermentation in the horse’s gut, producing trigger factors.

The developmental phase of laminitis merges into the acute phase, which occurs from the onset of foot pain to evidence of movement of the coffin bone within the hoof.  This evidence is usually  obtained by x-rays.  After the acute phase, if the horse does not die of the disease process that caused the laminitis, it can make an apparent complete recovery or become a “sinker,”   the hallmark sign of chronic laminitis.

A “sinker” is a horse whose coffin bone has lost all attachment to the inner hoof wall and dropped to the bottom of the hoof.  The chronic phase can last indefinitely with signs ranging from persistent, mild lameness to continued severe foot pain, further breakdown of the lamellae, a deformed or even sloughed hoof wall—the horse may even go down.  It is important to realize that the process which triggered the lamellae to breakdown begins to operate during the developmental phase before the first sign of foot pain.

During the developmental phase, the specific problems of the horse often have to be attended to urgently (grain overload, tying up, retained placenta).  Unfortunately, the feet may not enter into the equation until the signs of foot pain appear.  By the time foot pain is apparent, destruction of the lamellae is under way.  In other words, foot pain is the outward sign that lamellar destruction is occurring.  To wait and see if foot pain is the sequel to another organ system’s crisis is to miss the opportunity to prevent or at least lessen lamellar damage.

The Underlying Disease Processes that Cause Laminitis

Lamellar changes

We believe that the lamellar changes of laminitis are caused by a disturbance of a normally tightly controlled process or structure in the horse’s body.  The body produces certain enzymes (MMP) in response to the stresses  and strains of normal equine life, as well as to constant growth.  When called for, enough MMP  is produced to maintain the correct shape and orientation of whatever structure is in need—bone, joint or, in this case, lamellae.  It is possible that repair of the lamellae, necessary for the hoof wall to grow past the stationary  coffin bone, is the target of the laminitis disease process.  When MMP enzymes are not inhibited, they dislodge the cells that make new lamellae from the basement membrane (a delicate tissue layer that serves as the protective barrier between the epidermis dermis).  The basement membrane then peels away in sheets.  Because the basement membrane is the key structure between the lamellae and the coffin bone, loss of the basement membrane leads to the failure of attachment between the inner hoof wall and the coffin bone that is laminitis.

Circulatory Changes

An additional component of lamellar anatomy to be affected by overproduction of MMP is the lamellar capillaries.  As the basement membrane disappears, so do the capillaries.  The loss of these capillaries may explain why resistance to blood flow was increased 3.5 times in horses during early laminitis and also why blood bypassed the capillary bed, flowing instead through the larger arteries and veins.  These two changes in circulation are what produces the “bounding digital pulses” felt in the acute phase of laminitis and are believed to occur as a result of excess MMP.

This theory of laminitis based on the triggering of MMP challenges the alternative view that laminitis develops because of circulation changes in the foot.  A current theory is that constriction of veins and high fluid pressure blocks the flow of blood through  the capillaries of the lamellae, eventually causing the lamellae to die.  However, our research has not provided any evidence that vein constriction and high fluid pressure occur.  What appears certain in the light of our research is that the disintegration of lamellae is caused by the uncontrolled release of excess MMP.

What triggers MMP release?  A factor present in cultures obtained from the gutj of the horse has been demonstrated to activate MMP and cause lamellar separation in the laboratory.  These cultures contain Streptococcus bovis, the principal bacteria responsible for fermentation of sugars during grain overload.  We are currently investigating the role of the S. bovis MMP activator in natural  cases of equine laminitis.  If it is able to cross the barrier of the gut and enter the circulation, it may be a new “cause” of laminitis.   How do the trigger factors of laminitis reach the lamellae?  There is now strong evidence that the blood vessels of the foot are dilated during the developmental phase of laminitis.  Laminitis does not occur if these blood vessels are constricted, suggesting that the trigger factors will only cause laminitis if:

  • they reach the lamellae when the blood vessels are dilated
  • they are at a high enough concentration
  • they occur over a long enough time period

Since blood vessels constrict as the temperature decreases, keeping the feet of horses that are in danger of developing laminitis as cool as possible seems logical.  Trials to determine the effect of a slurry of iced water applied to the feet of horses are underway.  Preliminary results show that horses, unlike humans, do not regard extremely cold feet as uncomfortable.

Conclusion

Laminitis, or the loss of attachment between the lamellae of the inner hoof wall and the coffin bone, occurs in three phases.  The factors thought to cause laminitis (MMP) are at work in the first phase, developmental, before foot pain is apparent.  Because these factors cannot enter the foot and cause damage unless the foot’s blood vessels are dilated, cold water should be beneficial in the prevention of laminitis.  In addition, research has shown that there are chemical agents that can block MMP and potentially aid in the prevention and management of acute laminitis.  Trials to test whether these MMP inhibitors can indeed prevent or improve laminitis are currently underway at the Australian Equine Laminitis Research Unit at the University of Queensland.

Contributed By: Christopher C. Pollitt, BVSc, PhD (AAEP)