Salem Valley Veterinary Clinic

Small Animal and Equine Medicine, Dentistry and Surgery

Equine Laminitis: A Revised Pathophysiology, Christopher Pollitt, BVSc, PhD.  (AAEP Meeting, 1999)

Dr. Pollitt presented his research that supports a theory that "circulating laminitis trigger factors activate lamellar enzymes which lyse the attachments between the coffin bone and the inner hoof wall. As the lamellar architecture disintegrates, the weight of the horse and the forces of locomotion drive the coffin bone down into the hoof capsule, shearing and damaging arteries and veins, crushing the corium of the sole and coronet, and causing unrelenting pain and a characteristic lameness."

Three Phases of Laminitis

Developmental Phase During this initial phase the lamellar separation is triggered by factors that reach the foot via the circulation. Disease of the gastrointestinal, respiratory, reproductive renal, endocrine, musculoskeletal integumentary or immune system can result in the release into the bloodstream of these laminitis trigger factors, the exact nature of which has yet to be elucidated. Importantly, during this phase there is no sign of foot pain.

The developmental phase merges into the Acute Phase of laminitis which lasts from the onset of clinical foot pain to the time when radiographs reveal displacement of the coffin bone within the hoof capsule.

After the acute phase, if the animal does not die from the disease which incited the laminitis, it can recover completely or enter the Chronic Phase, in which there is continued lameness due to continued degeneration of lamellar attachments and hoof wall deformation, sometimes resulting in sloughing of the hoof.

Proposed Pathophysiology

Pollitt believes that laminitis triggering factors reaching the laminae result in the release of enzymes called metalloproteinases (MMP) that weaken the connection between the hoof wall and the coffin bone. As this connection breaks down the lamellar capillaries are destroyed, resulting in resistance to blood flow and the observance of "bounding" digital pulses. This theory challenges the one that proposes that lamellar destruction is initiated by impedance of blood flow with resultant avascular necrosis of the lamellar tissues. In fact, Pollitt has strong experimental evidence to support the view that there is an increased lamellar blood flow during the developmental phase of laminitis.

A candidate for the proposed laminitis trigger factor is a factor produced by the bacteria Streptococcus bovis, the principle microorganism causing rapid fermentation in the cecum after grain overload.

Clinical Implications

Blocking the MMP enzymes that degrade the lamellar connections would provide a means to prevent and manage acute laminitis. Pollitt is presently testing several MMP inhibitors at the Australian Equine Laminitis Research Unit at the University of Queensland.

Further reading.

Last modified: September 18, 2000