Dr. Judith L. Mulholland

Endotoxin-induced microthrombosis (mini clots) in the vessels of the laminar corium are implicated as part of the laminitic process. These thrombi inhibit blood flow through the capillaries, leading to starvation of the tissues for nutrients and oxygen and accumulation of  toxins and waste products, so that inflammation, oedema, and cell death may result.

Therefore, it is now thought that the decreased perfusion of the tissues was based on studies performed while clinical laminitis was underway, and the effects observed were likely a result of the lamellar injury, rather than the cause of it. The horse tranquilliser acepromazine dilates blood vessels and appears to prevent laminitis in some cases. This effect was attributed to its inhibition of vasoconstriction or vasodilatory effects which prevents ischaemia. This drug has other metabolic effects including increasing insulin secretion, and the production of glucose by the liver, which could lead to increased use of glucose by the tissues within the hoof, which would protect them from hypoglycaemia (glucose starvation). Therefore, a new hypothesis has been put forward based on hoof glucose metabolism which combines all these factors.

Researchers at the University of Queensland, led by Professor C. Pollitt, studied blood flow to the feet of normal horses in the cold and learned that there were periods of normal blood flow, interrupted by long periods of very low flow. The hoof appeared capable of withstanding these long periods of minimal blood flow without developing laminitis. A study by the same team, using 14 horses during developmental and acute laminitis, has shown that blood flow increased prior to the development of laminitic foot pain and that those which had a raised foot temperature, indicative of vasodilatation, became laminitis positive, despite all horses in the study being equally systemically ill. The researchers found that if vasoconstriction is achieved during this phase, laminitis does not occur. It was assumed that the increased blood flow leads to a higher concentration and greater exposure to blood born trigger factors  e.g., acids and toxins. Therefore, evidence strongly suggests that laminitis is not a result of inadequate blood flow, and that this is a result of the tissue injury rather than the cause.

The hoof wall is connected to the pedal bone by connective tissue containing a row of lamellar epidermal cells. These cells are bonded to the keratinised hoof tissue on one side, and to a thin layer of specialised connective tissue, called the basement membrane, on the other. Attachment of these cells to the basement membrane is made by adhesion molecules, which act like "press studs", keeping the tissue together. These adhesion sites are called hemidesmosomes ,and are formed by several proteins and numerous submicroscopic anchoring filaments e.g., laminin-5, which are unique to hemidesmosomes.

The researchers at Queensland University led by Professor Pollitt demonstrated that if either the anchoring filaments or the hemidesmosomes are damaged and disappear, then the basement membrane separates from the basal cell. These anchoring proteins and connective filaments are substrates of connective tissue enzymes (chemical catalysts) matrix metalloproteinases (MMPs). It is thought that the greater the blood flow, the more exposure of the basal cells and hemidesmosome bonding sites to circulating blood born trigger factors which activate the MMP enzymes. This appears to be the first part of the process in the development of laminitis. The MMPs digest the bonds, and the force on the hoof due to weight-bearing then causes separation of the hoof wall from the underlying tissue, which is characteristic of laminitis. Separation of the laminae during laminitis is the specific undoing of the attachment, and not simply a tearing apart of the tissues. Therefore, separation was caused by the release of MMPs from the tissues that digested the attachment apparatus.

The researchers then blocked the activity of these enzymes, thus preventing separation of the hoof tissue. What activates the MMPs? Using small sections of hoof tissue kept alive in a special culture, they learned that inhibiting the ability of the hoof tissue to metabolise glucose caused an increase in MMP activity, and separation of the hoof. Many of the conditions which will induce laminitis involve changes in the way an animal utilises glucose. It is possible that the inciting event ,(acute disease, toxins, surgery, etc.), causes sudden glucose starvation in the hoof tissues (hgypoglycaemia) and activates the MMPs, thus weakening the attachment of the hoof to the underlying connective tissue. The force of the weight of the horse on the foot then tears the hoof attachment and tissue bleeding and cell death results. Therefore, what now seems most likely is that laminitis is mediated by the uncontrolled release of excess activated MMPs. There is also now some evidence to indicate that MMP activation is inhibited in low temperatures. Therefore, inhibiting enzyme activity by keeping the feet cold during the developmental stages of laminitis (before hoof pain occurs) shows potential as a first aid and preventive measure.

It is important to recognise that the wider veterinary knowledge of laminitis is constantly changing and that research into the biochemical pathways of the disease process and the activity of new and known chemicals and drugs in relation to laminitis may lead to new drugs or treatments which may prevent or minimise the damage done to the hoof, and shorten the recovery time if the disease is recognised and treated early. Ongoing research may lead to preventative treatments for horses at risk as well as better treatments for horses with the disease.

• Treat the primary problem e.g., colic, colitis, retained placenta, pneumonia etc.
• You do not need to wait for clinical signs to justify preventative treatment. The process leading to destruction of the bonding apparatus begins before foot pain or the first signs of laminitis are noticed.
• Discuss the risks or signs with your vet and take on board their recommendations.
• Be proactive. Get the horse on to soft bedding, keep it cool, take care with what you feed etc.

Place the feet in buckets of water with ice floating in it at all times from the moment signs are noticed e.g., increased warmth or pulse. Keep icing or hosing the feet as often as possible until the horse has shown prolonged steady improvement for its primary problem or for 24 - 48 hours.

THE  HEAVIER  THE HORSE, THE GREATER THE LOAD ON THE  LAMINAE.  A DRAUGHT HORSE HAS LESS CHANCE OF SURVIVAL THAN A SHETLAND PONY.