Wall Growth

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Written By Walt Friedrich

At first glance, it seems obvious – but there exists a subtle mystery of sorts at play. We know the wall is firmly attached to the coffin bone – yet it grows downward at the same time. Experts, including David Hood, Robert Bowker, Pete Ramey and others, agree that there is a paradox, and provide independent, similar explanations, while also agreeing that although we have a pretty good idea of how it all works, nobody has proved it yet. The explanations are quite plausible, but they are not etched in stone. KC LaPierre explains it well; what follows is based upon Mr. LaPierre’s work, but remember, this is just my “take” on the matter.

As you know, the components involved with the hoof wall are the coffin bone, laminar layer,  inner wall, outer wall and coronary band. We have evidence that the outer wall grows down from the coronary, as demonstrated by the downward “movement” of the scar left from a popped abscess at the coronary band. And while we can’t see it, we also know that in a healthy hoof there is a very tight attachment between all those components. The sticky part is understanding how the wall can move downward while at the same time remain locked to the coffin bone by the laminar connection.

Good question. The consensus explanation seems to be that the inner wall,
firmly attached to the coffin bone by the laminar layer, has two components: loosely packed tubules, originating from a corium at the coronary, and a thick, dense “glue” referred to as intertubular horn — an immensely strong substance that fills the inner wall, completely encapsulating its tubules. The outer wall is likewise constructed of tubules growing groundward and held together with intertubular horn, but its tubules are very densely packed.

This leads us to two important concepts: first, that intertubular horn, while very dense and tight, is actually a fluid (more on this later). One might consider the inner wall as being composed of intertubular horn with tubules embedded therein to keep that horn in place. That construction makes the inner wall extremely strong and shock-resistant. Thus a primary function of the inner wall is to provide strength for weight support as well as shock absorption for protection for everything inside and above the hoof itself. Second, the outer wall, composed mostly of tubules with enough intertubular horn to hold it together, presents an almost impenetrable shield against external damage. The ancient Greeks couldn’t have asked for a more efficient shield material, even though they did pretty well with what they had.

Back to the intertubular horn being a fluid, and enter a physics concept
called “fluid dynamics”; it says that a fluid in motion is essentially
motionless at its base, and the farther away from the base you go, the
faster it moves. It’s the way rivers work — the water’s velocity is greatest at the surface, diminishes as you go deeper. In the hoof, that property of the
intertubular horn means that while the inner wall’s base remains almost motionless, attached to the coffin bone by the laminae, its outer surface (abutting the outer wall which is moving downward) is moving right along with the outer wall, at exactly the same velocity, albeit very slowly. Intertubular horn cells initiate from the laminar layer, and grow outward, perpendicular to the wall surface and filling the inner wall’s tubular space, but as they reach the junction between inner and outer walls, they have begun to move downward, in parallel with the outer wall’s movement, thus keeping everything smoothly locked together.

Think of it: outer wall resembles a broom — stiff and strong, made of
tubules, constantly growing longer, forming an almost impenetrable shield – while inner wall performs the task of keeping everything locked to the coffin bone yet allowing the outer wall’s downward growth at the same time. The outer wall corium, located in the coronary band, has just one job, constantly generating new cells. The inner wall’s cells actually have two sources — some developing at the coronary that generate the tubules, and others developing at the laminar surface, generating the intertubular horn.

Incidentally, I’ll add an interesting side note: As long as everything is flowing smoothly and normally, the hoof will have a smooth, even outer wall — no ridges or striations. But any disturbance in the evenness of growth between the two layers will show up as a “glitch” at the outside surface – trauma to the inner layer, such as with a laminitic attack for example, or perhaps a sharp enough strike on the outer wall surface will interrupt its rate of contribution of intertubular horn to the outer wall as it grows downward, resulting in a “fold” in the outer surface, hence those rings we sometimes see running side-to-side across the toe of the hoof, and it explains why they can and do grow out. In addition, the inner wall, thanks to heavy keratinizing of the intertubular horn, is quite waterproof. But when the inner wall “thins out” due to some trauma, it loses a certain amount of its tightness against leakage, allowing some blood to find its way out, showing up eventually at the bottom of the hoof at trim time as those disheartening red areas we sometimes see. They may also indicate a trauma in the past, but do not necessarily indicate that the trauma is actually past. In addition, it’s my personal opinion that toe-first landings that send shock waves through the entire hoof are also responsible for damage to the inner wall’s intertubular horn that allows some adjacent blood vessels to rupture, the results being the blood spots we see weeks later at ground level during a trim.

Thus, the simplest, undetailed answer to the question, “what makes the hoof wall grow”, may be that:

The wall is a two-layered structure: the outer wall grows downward, and consists of densely packed tubules with enough intertubular horn from the inner wall to hold the tubules together, while the inner wall grows outward, and consists of intertubular horn with just enough of its own tubules to hold the horn together. The seam between the two layers is an active place, where the descending outer wall “pulls” the outward-growing intertubular horn downward as they flow together toward the ground. Thus, as long as their coriums are functional, both inner and outer walls’ growth is guaranteed, and their functions of support and protection can exist because of the fluid characteristics of the intertubular horn. It is truly a remarkably efficient design.

Laminitis In The Equine

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Written By Dr. Kris Hiney

Earlier we posted an article on the typical causes of laminitis and some feeding strategies that may help in preventing laminitis (Feeding Horses for the Prevention and Management of Laminitis).  We also discussed how we might approach feeding a horse which has already experienced  laminitis.  This month we will begin to delve deeper into the causative factors of laminitis and how to prevent its development.

Remember that laminitis is actually a systemic disease, with just the symptoms being visualized within the hoof.  Some insult to the horse’s system creates an alteration in circulation, ultimately leading to tissue damage of the sensitive laminae.   This period of time, referred to as the development phase or prodromal phase, includes the actual insult prior to the development of symptoms.    It is thought to be due to some change within the vasculature, that leads to ischemia, or lack of blood flow to the digit.  Whether it is a lack of nutrients or oxygen due to the decreased blood flow, tissue damage or death results.  This initial insult is then followed by the acute phase of laminitis.

In the acute phase, blood flow returns to the foot, typically at an increased rate, as this is the body’s normal response to tissue injury.  Even this reperfusion response can cause tissue damage.  This is when the owner now recognizes the development of symptoms. The horse will appear very stiff and reluctant to move, and may even lie down.  A particular stance may be assumed by the horse as he appears to rock back on the hindquarters and place the forefeet forwards in order to limit weight bearing.  Due to the pain and anxiety the horse is experiencing, his heart rate and respiration rate may both be elevated.  Finally, the owner may even be able to detect an increase in temperature of the hoof wall and a bounding or throbbing digital pulse.

If permanent changes to the architecture of the foot occur, whether in PIII displacement, permanent changes to the normal lamellar architecture of hyperkeritization of the hoof wall, the horse has entered into the chronic phase. These horses are typically more susceptible to recurrent episodes of laminitis. Diet restrictions and specialized hoof care are typically required to allow the horse to lead a comfortable life (Feeding Horses for the Prevention and Management of Laminitis).
Obviously laminitis can be a devastating disease for the owner, and most would strive to prevent the disease, rather than address a symptomatic horse. If we look more closely at the causative factors in these alterations to circulation of the horse’s digit, we may be able to do a better job at identifying horses at risk.
We will begin with a review of pasture associated laminitis, which has been addressed in previous articles (Feeding Horses for the Prevention and Management of Laminitis and Carbohydrates III: Metabolic Syndrome). Remember that pastures grow more rapidly at certain times of the year, and may store their energy as different types of polysaccharides depending on the species of the plant. Frequently fructans are noted as the culprit in causing laminitis. Fructans are found in greater quantities in cool season grasses, as well as during periods where photosynthesis is favored over plant growth. As fructans contain beta bonds, which are not digested enzymatically by the equine small intestine, they pass through the tract and arrive at the large intestine where they then undergo bacterial fermentation. Other types of carbohydrates may act similarly, including sugars and starches which escape the small intestine undigested (the classic carbohydrate overload model of the horse in the grain bin), as well as other types of carbohydrates that may be rapidly fermented (pectins, resistant starches etc). (For more information on carbohydrates, please revisit Carbohydrates: Definitions and Relationship to Equine Diseases.)

In this first model of carbohydrate/rapidly fermentable fiber overload, too much of this rapidly fermentable material reaches the hindgut of the horse. These feedstuffs favor the proliferation of a particular bacterial population. These bacteria produce more lactate as their excretory waste. Excess lactate production lowers the pH of the hindgut which allows the mucosal cell wall to become permeable. In addition, too low of a pH stresses the bacteria causing them to either die or release endotoxins. Furthermore, altering the bacteria’s environment also changes their metabolism, releasing vasoactive amines into the hindgut. As the gut wall becomes more permeable, these toxins and amines are able to cross the mucosal wall and enter the bloodstream of the horse, where they then can exert their effects at the level of the hoof.

Horses which need to be restricted from pasture typically include ponies, as they are highly susceptible to laminitis.  In addition, any horse that has a history of laminitis, or has been diagnosed with PPID (pituitary pars intermedia disfunction)(Carbohydrates III: Metabolic Syndrome) should be grazed with care.  Horses with elevated insulin levels, or insulin resistant horses, also have a greater sensitivity to pasture associated laminitis, due to the influence of insulin on the vasculature of the horse.  Hyperinslulinemia increases the production of endothelin-1, and down regulates the production of nitric oxide.  A decrease in nitric oxide production has been linked to an elevation of homocysteine.  Incidentally, elevations in blood homocysteine are also linked to heart disease in humans. There has even been a suggestion, although with no scientific data to support this theory, that excessive supplementation of sulfur amino acids to horses with insulin resistance is unwarranted.  Typically sulfur amino acids (ie methionine) are included in hoof supplements, and homocysteine originates from methionine metabolism.   To further confuse the issue, it does appear that individuals are more susceptible to this disease, even if they are the same age, sex, breed and are managed the same as non-effected individuals.

Obviously preventative measures aimed at reducing carbohydrate related laminitis issues center on diet management. Certainly it is not practical or even advisable to state that all horses must be kept away from pastures. However, knowledge of which horses are susceptible to pasture associated laminitis is key. Once these individuals are identified, they should be placed on a principally harvested forage diet. The forage chosen should have very little rapidly fermentable material. However, horse’s which do not have these susceptibilities can continue to be managed with relative ease.
Next month we will continue to discuss laminitis at a more detailed tissue level, and address further strategies to limit your horse’s chances of acquiring this disease.

EQUINE THRUSH – WHAT IT IS AND HOW TO DEAL WITH IT

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Written By Walt Friedrich

It is a condition – or more precisely, an infection – in the hoof. It is not a disease. Its elimination has been the goal of massive efforts to develop the ultimate product, as witness the vast variety of thrush-busting products on tack shop shelves. All of them do sell, and each of them probably does reduce and control the infection in some hooves – but there are a couple problems: one is that a given product may clear things up for some horses, but seems ineffective for others. And secondly, many of those hooves whose thrush does get controlled end up with a re-infection a couple months later.  Right up front, the problem is not a simple one.

Just what is this elusive infection, anyway?

Well, that’s part of the problem. The term “thrush” gets hung on just about every hoof ache or pain that comes along, but it is not necessarily just one type of microbe that’s responsible. There are enough bad guys to fill a Post Office bulletin board, including yeasts, bacteria, and fungi! The most common of the “usual suspects” is a yeast named Candida albicans, a nasty little creature, and very difficult to eliminate. In addition to albicans, there are a number of other species within the genus Candida that are known to cause human and equine infections. And to add some complication, a bacterium called fusobacterium necrophorum is also commonly held responsible for many “thrush” infections, PLUS numerous fungi in the line-up as well. The invading army that causes “thrush” can have many mercenaries, and it is asking a great deal of any one treatment to go out there and kill ‘em all.

As if that’s not complex enough, yeasts and fungi exist in both “live” and spore form. Consider the spore to be an “egg”, containing the microbe, which “hatches” when environmental conditions are favorable. Killing an army of microscopic fungi may be doable, but the spores they leave behind are virtually bullet-proof; they patiently wait for those favorable conditions to return, at which time they “hatch” and re-form a brand-new army!

Tackling the problem…then back to the drawing board

So here are we, one day, observing our horse three-legged lame, perhaps, with a gooey, stinky mess exuding from a frog. “Aha,” we think, “this is thrush and I’m gonna get rid of it.” Of course, we don’t know what organism or organisms are responsible, so we ask the guy in the tack shop for the best of the thrush killers, we buy it, then take it home and have at it. Sure enough, after a few applications, things appear to getting better, the frog is healing, the goo and the smell are gone, and our horse is happy – until a few weeks later, when we see a rerun of the problem developing. The spores have hatched and have started to party again, plus some new neighbors from the stall floor have joined them, and we’re ready to return to the tack shop to look for a newer and better anti-thrush miracle cure.

More about these nasty little critters

One of the basics we know is that we can be dealing with two entirely different entities, here – aerobes and anaerobes. Aerobes live and breathe even as do you and I, which means they need air to survive, which makes them relatively accessible to our attacks. That opens the field to most of the on-the-shelf products that we wipe on or spray on. These are the easiest to apply, and when they work, our job is easier.

The anaerobes are quite another story. They cannot live in air, consequently, when without a host, they exist in spore form, sort-of in a state of suspended animation. But those spores, along with their aerobic cousins, cover the stall floor and walls, even the very dirt we walk on, even our own shoes! It takes two things for an infection to hit a hoof: the hoof needs to be standing amid the microbes (that’s a “gimme” – if he’s in the stall, he’s standing amid them, and standing anywhere in mud or feces, it’s like he’s put out the welcome mat for infection), and the hoof needs to have some “outside doors” open – any tiny lesion on the bottom of a foot will do. Both microbes and spores get jammed into the lesion, where they get sealed in when the horse stands or walks in mud. The living microbes are already at work, and when the spores realize that there’s no air, it’s warm, it’s moist, they burst forth and join the party.

How to fight back

Now we start to see the complexity of fighting “thrush”. Topical treatments work on aerobes because we can get at them. But not so for the anaerobes. Living in an airless environment means they are buried deep in the tissues, hard for us to reach. A new approach is called for; soaking those feet in the appropriate microbe-killer long enough for the medication to soak in and do its job. A 30-minute soak in apple cider vinegar or dilute chlorine dioxide (Oxine or White Lightning, for example) will do the job on the microbes, but not their spores. For that, soaking in a product designed to kill spores is needed. There are several on the market, but the most effective may be CleanTrax, available on-line – it will kill aerobes, anaerobes, and spores.

So when you can see deterioration of the frog, and/or smell a real stink on those hooves, the “enemy” is obviously present and you can deal with it. But the real trick in dealing with it is to catch it early, before much damage has been done, and for that, some preventive measures are called for. When thoroughly cleaned, the entire bottom of the hoof is in clear view – difficult for undesirable microbes to hide. Consider forming the habit of thorough picking and wire-brushing the hoof bottom clean, a quick scrub with Dawn Detergent, every day, then spraying the entire surface with a microbe-killer; keep the foot off-ground for fifteen or twenty seconds to allow some penetration of the spray. Two very useful sprays are colloidal silver (silver ions are believed to destroy key enzyme systems in the cell membranes of these pathogens), and Usnea (a symbiosis [one organism living on another] of a fungus and an alga, used for its antibiotic and antifungal properties). Both are available on-line: consider the colloidal silver brand, “Silvetrasol”, about $20 for a spray bottle, and Usnea Tincture, about $10 for four oz., available from Essential Wholesale & Labs, among others. Mix Usnea 50-50 with water and spray daily, but Silvestrasol once a week.

Preventive medicine

Spraying is a quick and easy preventive procedure – but take it a step further and disinfect any crevices you see. For example, a healthy hoof has no crevices or clefts (the commissures don’t count), but a potential problem will show up as a cleft developing in the center of the heel of the frog. It will usually be just a slit, but if you can insert the metal tip of your hoof pick into it to any depth at all, it’s a problem in development. Left untreated, that cleft will develop into a crevice that’s as deep as your pick’s tip is long – or deeper. That means trouble is coming, and you should take countermeasures right away. Such clefts are well-protected hidey-holes for thrush-causing microbes to start their damaging work. The trick is to deposit some microbe-killer directly into the bottom of that cleft, and to do that you need a special, inexpensive, syringe (no needle). Your vet can probably provide you with one; it has a long, flexible tip that allows you to get it into tight quarters. An alternative is to buy the product, “ToMorrow”, from your local Agway, Tractor Supply, or equivalent. ToMorrow contains medication useful in treating mastitis in cow udders, hence its long, flexible tip. You can use it to deposit a pea-sized glob of medication at the very bottom of a frog cleft. You can use the mastitis treatment cream itself in frog clefts, but a better alternative is to empty the syringe, and then refill it with a 50-50 mixture of Triple Antibiotic Cream and Clotrimazole, both available on your druggist’s shelves. TA Cream is effective in combating Athlete’s Foot – a fungus infection – and Clotrimazole is a powerful treatment, especially useful in combating thrush. Added bonus is the cost for one ToMorrow syringe is only about two bucks.

The outlook is positive

And so, with all this, we’ve not yet crossed home plate – but we’re on third, waiting for the base hit that lets us score. We have a pretty good idea what causes the thrush condition. We have not yet found the silver bullet – but we’re getting closer. The thrush condition in horses is actually quite similar to the human version, and when we are able to nail it completely in humans, we should have it licked in horses, too. Meantime, we do have means to control it and make our equine partners more comfortable while we’re at it. It’s so insidious that it can slide in under the radar and our problem becomes repair rather than prevention; but to prevent takes vigilance and some effort on our part. So for our horses’ sake, keep the stalls clean, keep the floors cleared of feces, keep them clear of mud, keep that pick and wire brush close at hand and use them daily. Catch it early!

Everybody Admires a Well-Turned Leg…

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Written By Walt Friedrich
 …especially when it’s on a horse! Same goes for a pretty foot, also especially when it’s on a horse. I’m going to talk a little about horses’ legs and feet here, but I’ll refer to the feet as “hooves” for the sake of both accuracy and clarity. Know how you think of your foot as everything from the heel to the toe? If we do the same when referring to a horse, we’d be talking about fully the bottom half of an entire visible leg! (More on that a little later.) His hoof is the hard shell at the very bottom of each leg, plus its contents.
But the hoof, simple as it looks, is more than just a hard shell on the end of a horse’s leg, it’s actually a very complex system with a number of movable parts that all need to work together. And I do mean work – a feral (wild) hoof is in actual work typically twenty hours per day, seven days per week, all year long, for many years. With that kind of usage, the hoof had better be well-designed, well-built, tough, strong, and self-rejuvenating. If a horse moves twenty miles every day, and lives for twenty years, he puts 150,000 miles on each hoof over his lifetime, and even at the end most of those hooves are still functional! Only his teeth and jaws give his hooves a run for the money, so to speak, and they don’t support all that weight while they’re doing it.
Here’s a little food for thought: Enough fossilized remains have been studied that we know something of how today’s horse has evolved over the millennia. For example, vestigial bones in a horse’s leg suggest that that big old hoof is actually the equine equivalent of the last joint in your middle finger!
Let’s follow the finger analogy: his hoof is part of an “assembly” consisting of three bones, each articulating with its neighbors, and whose joints are held together with extremely strong and tough ligaments. Each of these bones moves with respect to its adjoining bone(s), controlled by tendons at the ends of muscles. Those tendons are encased in sheaths, to keep them positioned properly. You and I call this three bone assembly a “finger” – but on a horse, they’re known as the “pastern”. The last bone in the set, the bone that is encased in the hoof capsule itself, is known as the “coffin bone” – though there’s nothing at all eerie about it.
But let’s get back to that well-turned leg and examine it, top to bottom. Because they look so different, you’d never think that a horse’s foreleg and your own arm are very much alike – but they actually are, as you’ll now see. Remember the old song, “Dry Bones”? Let’s play an equine version of it — you can follow it on the adjoining sketch, and you’ll see how it relates to your own arm, step-by-step:
His shoulder blade’s connected to his upper arm bone —
 Technically, that’s his scapula connecting to his humerus – both are buried inside his body, so you can’t see them;
His arm bone’s connected to his elbow bone —
Which, finally, you can actually see (but probably have never noticed). It’s very easy to feel, though — run your hand up the back of a foreleg, and just as you get to his torso, you’ll feel a hard, round knob – that’s part of his elbow;
His elbow’s connected to his forearm bones —
Radius and ulna, that is – his forearm is the top section of his leg that’s visible to you and me;
His forearm’s connected to his wrist bones —
These are a collection of small, vestigial bones called the carpals, the “wrist” joint forming what most of us call his “knee”, because it’s in the middle of his leg and it bends forward like our own knees;
His wrist bone’s connected to his hand bone —
— by way of the one carpal bone that survived the evolutionary process to become his “lower leg”, which is actually the equine version of your hand. It’s called the Cannon bone;
His hand bone’s connected to his knuckle bone —
That joint is called his “fetlock”, the equivalent of your middle finger knuckle;
His knuckle bone’s connected to his finger bone —
Which, as we have learned, is his three-boned pastern.
Now, that’s the leg of the horse!
To help you orient yourself, that well-turned leg is vertical down to the fetlock, at which point his pastern takes an angle of 30 degrees, give or take, forward.
Let’s not omit his hind leg: the hoof is pretty much the same as those in front, right up to the fetlock. The long bone that extends from there half-way up his leg meets the joint we refer to as the “hock” – which is analogous to your heel and ankle joint! Continue upward to find his knee, which you won’t see unless you look very closely – but you can find it by running your hand up the front of his back leg, and just as you reach the torso you’ll feel the bony knob that is part of his actual knee. His thigh bone is inside his body, attaching to his hip.
Two incidental points of interest: one, his hind leg, from his hip down, appears longer than his foreleg, which leads us to question how he can run so smoothly. If they truly are longer, you’d expect many more steps by his forelegs than his hinds in order to keep up. But remember, his “upper arm” bone is buried inside his body so you can’t see it; furthermore, a horse has no collarbone (clavicle) to lock his scapula in place, as do you and I, so effectively he has an extra “leg bone” in his fores, which makes front and hind legs essentially of equal length. And the second point, the “cowboy tale” that you can predict the adult height of a newborn foal by measuring the distance between his “knee” and fetlock, and substituting “hands” for “inches”, turns out to have some basis in fact. It’s not an exact science, but as empirical evidence, observe a newborn standing beside his dam: his lower leg (cannon bone) will be close to the same length as his dam’s, and will grow but little more – except in girth, as it develops muscle. That makes it a fairly reliable predictor of adult height.
Whew. Congratulations, if you’ve stayed with it thus far.
Now let’s get to the hoof. We’re going to take something shaped roughly like a slip-on shoe (his hoof) and stuff it full of several interesting items, the items that make up the hoof’s “innards”.
We are all familiar with the shape of the hoof – rather like half a cone, with no top. Well, the coffin bone itself is shaped in very much the same way, attached to the leg’s bony column at an angle so its base can sit flat in the hoof capsule. It tucks neatly into the front section, and fits like a glove. The back half of the capsule contains a large wad of very tough, fibrous tissue, known as the “digital cushion” – flexible as well as tough, as it supports the horse from directly under the bony column of the leg, and it absorbs the shock when the hoof lands. The digital cushion is held firmly and tightly in place by a “belt” of even tougher material known as “lateral cartilage” – it “cups” the digital cushion from underneath, behind and both sides.
All we need to hold it all together is to sort-of glue the coffin bone to the inside of the capsule around the toe. That gets done by Velcro-like layers composed of billions of cells forming what are called “laminae”. One layer of laminae is part of the coffin bone, the other layer is part of the hoof wall; these two layers interlock like Velcro, and these form one of nature’s strongest bonds.
Finally, what’s underneath the hoof? At the very back, the wall forms two ultra-strong columns, called the “heels” – one on each side – capable of slight sideways and vertical movement to stabilize the horse when he’s moving. Between the heels and stretching toward the toe sits the “frog” — triangular-shaped, tough fibrous tissue that provides both support at the back of the hoof and stimulation for the digital cushion, immediately above it. And what’s left, covering most of the bottom of the hoof, is the “sole”. It holds everything together, and in conjunction with the wall and heels, provides the total support for the horse’s entire weight – for an average horse, that amounts to a load in the area of 200 to 300 lbs per hoof, just standing; imagine how much greater when the horse is walking, running, jumping…
Tying it all together is the blood supply. And it is RICH. It has to be – it’s the only protection the hooves have from the cold, and that protection is superb. The hoof’s components, together, are very demanding of constant, steady blood flow. They get help from what’s known as “hoof mechanism”; because of the hoof’s architecture, its blood supply is cut off for an instant with every step the horse takes, allowing a momentary pressure build in the arteries feeding the hoof and a small pressure decrease in the hoof itself. But as the hoof completes each step and raises off the ground, that blockage is released, and the built up pressure forces a spurt of blood flow through the hoof. The hoof itself also expands slightly as it takes weight with each step; that forces blood through the hoof, and when the hoof is raised, the expansion relaxes, allowing the blood pressure in the hoof to restabilize. These two actions are synchronized, with the result that each hoof is referred to as a sort-of auxiliary heart – that means five hearts working to pump blood with every step the horse takes. The laminae in the hooves especially require a strong and steady supply of rich blood, and Nature’s design provides it for them.
While the hoof and the horse date back into antiquity, you might note that the hoof is also the first four-wheel independent suspension system on the planet. The shock absorbers are the digital cushions together with the frogs, and the springs are the heels, working independently of each other. That’s why when his feet are healthy, he can stride fast across a path of rocks – each heel retracting and returning as necessary on the uneven terrain.
So you see, those four little hooves – little in comparison to the bulk and weight of the rest of the horse – actually do wonderful work, far greater than their own size and weight. But then, that sort of thing is true of the horse in general.