Laminitis: Three different paths

One cause of laminitis is physical strain on the laminae due to trauma/injury leading to the horse's weight physically tearing the laminae. This is what happened to Barbaro, his laminae gave out due to excessive weight strain. Personally I think that horseshoes can lead to chronic low-level laminitis since they force all the horse's weight on the laminae (Remember when I said the laminae aren't designed to hold up the entire horse?). I think Dr. Bowker says it best, "any weight-bearing responsibilities the laminae have should be considered their secondary role."

There are two more mechanisms that are found in laminitis that I would call chemical based, one affects the anchoring filaments and the other affects the MMPs. Both have the same result but the causation behind them and how they work is completely different. (Refer to my last post if you don't know what these are.)

Glucose overload- most people know about this cause of laminitis, a lot of them think it is the only cause for laminitis. It isn't. Glucose induced laminitis only happens to horses that are insulin resistant (IR). The horse consumes too much sugar so the body freaks out and shuts down all its sugar uptake mechanisms (similar to diabetes in humans).  Remember how I said anchoring filaments  that attach the hemidesmosomes back onto the basement membrane are made of a glycoprotein molecule? Well the body can't make any if the uptake of sugar (glucose) has been inhibited. That means that the MMPs are still doing their job of popping off the hemidesmosomes but there aren't any anchoring filaments to glue them back on, resulting in the separation of the epidermal laminae from the dermal laminae.

There is another, much more sinister, mechanism for laminitis. This one can be caused by anything that results in an inflammatory response: colic, carbohydrate overload, endotoxemia, septicemia, prolapsed uterus, retained placentas, heat cycles in mares, potomac horse fever- basically anything that ends with -itis and messes with the balance of the hindgut can cause this other kind of laminitis. This can also be referred to as SODS- single organ dysfunction syndrome. When there are bacterial toxins in the bloodstream (which often begin in the hindgut) they activate white blood cells, these toxins and white blood cells eventually migrate down to the hooves and into the lamaella, where they cause the MMPs to go haywire and start popping off the hemidesmosomes at a rate too fast and furious for the anchoring filaments to keep up with, resulting in a separation of the laminae. This action can also result in the death of the secondary epidermal laminae cells. (It's a bit more complicated than this, but I'm trying to make it easier to understand.) Unfortunately, in this case, there is usually some pretty nasty damage done to the basement membrane. 

In the case of IR, it's the failure of the anchoring filaments that lead to laminitis, in the case of SODS it's the MMPs that lead to laminitis. The important thing to remember is that even though they both have the same result they are not caused by the same thing so they cannot be treated the same way. If your horse has laminitis the first thing you need to find out is what caused it.

The hoof wall gives evidence of damage to the basement membrane. It might be the characteristic "rings" that most people think of, but it also looks like these two pictures below. In the case of founder (chronic laminitis) horses will often create a "founder ridge," a place where the hoof wall appears to bunch up. I think the cause of this is damage to the basement membrane, basically the hoof wall cannot be moved down because the foundation that it would attach to is non-functional.

References for this post include Chris Pollitt, Jim Belknap, Rustin Moore, Robert Bowker and Debra Taylor.