New Research in Laminitis

Newer Research
--Bear Creek Veterinary Clinic
Madalyn Ward, D.V.M.
11608 FM 1826, Austin, Texas 78737 (512) 288-0428

The American Association of Equine Practitioners met in New Orleans the end of Nov.2003. I was able to attend this meeting and it was packed with useful information. The most meaningful to me was the 4.5 hour lecture by Dr. Chris Pollitt on the pathogenesis of laminitis. Dr. Pollitt has dedicated all of his efforts to discovering the mechanism behind laminitis so it can be prevented. He works out of the Australian Equine Laminitis Unit at eh School of Veterinary Medicine at the University of Queensland.

In order to study the pathology of laminitis, Dr. Pollitt has spent a great deal of time studying the normal growth patterns of the hoof. He has discovered that the in addition to the cells of the hoof generating from the coronet, new hoof cells are also formed at the level of the tips of the primary epidural lamina in the upper portion of the hoof. There is no evidence of cell proliferation at the laminar level of the distal portion of the hoof. The fundamental problem of how the inner hoof wall lamellae remain attached to the connective tissue embedded on the surface of the stationary distal phalanx(coffin bone) while one moves over the other is unresolved.

A 20-fold decrease between the upper and lower lamellae suggests that the majority of the normal lamellae do not produce hoof wall and their main function is to suspend the distal phalanx within the hoof wall. Research suggests that in order for the new hoof wall generated at the upper part of the hoof to slide down over the stationary tissue of the lower hoof the laminar cells must be continually detaching and reattaching. The process which allows this to happen involves the controlled release of matrix metalloproteinases and their subsequent inhibition by tissue inhibitors of metalloproteinases. 

Dr. Pollitt & Mac226's research suggest that it is this normal process of continual destruction and reorganization of cells at the level of the basement membrane in the lamina that goes horribly wrong in the case of laminitis. His research suggests one mechanism for laminitis involves the ingestion of grass containing high levels of fructans. Pasture grasses produce oligofructose under certain climate conditions such as following rain or frost. Mammals have no enzymes to metabolize these fructans so they pass undigested into the caecum where they undergo rapid microbial fermentation. When this occurs, Gram positive organisms, notably Streptococcus bovis and S. equinus, proliferate and temporarily become the dominant flora. The large gram positive bacterial population could liberate toxins when they die off at the end of their growth phase or when the fructan substrate is exhausted. These toxins then penetrate the gut wall into the blood stream and trigger the release of metalloproteinases. The excess release of metalloproteinases causes widespread destruction of the laminar tissues in the hoof. 

If  Dr. Pollitt's research is correct then one of our best preventive measures for laminitis is to limit pasture access during conditions where fructans are likely to be elevated in the grasses. His research can also help us look for ways to limit the fermentation of fructans in the hindgut. Once the lamina have been destroyed treatment is often ineffective so focus on prevention of laminitis is extremely important.