| Your One-Stop Farrier and Hoofcare Portal - Laminitis and Founder Mon, 22 Jan 2018 22:01:23 +0000 Joomla! - Open Source Content Management en-gb Answers to Some Questions about Laminitis and Founder

LAMINITIS is the inflammation of the laminae. Laminitis is generally agreed to be due to ischemia of the laminae causing detachment of third phalanx (PIII) from the horny wall.

FOUNDER is a maritime term meaning "sinking". Founder is secondary to laminitis and is the sinking of third phalanx (PIII) in the hoof.

CHRONIC FOUNDER is an old founder that has survived by some means. The third phalanx is demineralized, with lytic areas radiographically, is badly deformed, with periodic and/or chronic lameness. Intermittent inflammation can occur in chronic founder.

ACUTE CASES occur in a short course. Active abscesses may be prevalent with inflammation to the laminae bed. These conditions must be corrected before a favorable response can be expected.

SINKER is when the bony column sinks downward, inside the hoof capsule, and 100% of the laminae die. This condition should be considered an emergency and heart bar shoes applied and a hoof resection performed. If the blood supply is destroyed, all aspects of it returning are futile, however, the horse and feet can be salvaged if a live nail bed and a live coronary plexus remain intact.

  1. What should I do if I suspect laminitis?
    • If the horse is shod, pull the shoes. A temporary first-aid measure can be provided by using a roll of gauze or carpet in the same triangular shape as the frog. This is placed directly on the frog for constant support and taped in position by using an adhesive bandage.
  2. When should I call my Veterinarian?
    • If you suspect laminitis call the veterinarian. He will administer whatever medications he deems necessary for the underlying causes. Lateral X-rays are recommended at this time.
  3. How soon do you recommend putting on heart bar shoes after the initial insult of laminitis?
    • Heart bar shoes should be applied as soon as possible to stabilize the bony column. The stabilizing effect of support of pressure on the frog seem to prevent laminae fatigue. In severe cases, where the laminae have become necrotic, the heart bar shoe should not be removed, but a hoof resection should be done. This is done to prevent pain from swollen laminae.
  4. What are the reasons for doing a hoof resection?
    • To relieve the pressure on the coronary plexus by the coronary crown of the hoof wall.
    • To debride any necrotic laminae entrapped between third phalanx (PIII) and the wall. This can be treated as an open wound. Systemic antibiotics are of very little value as there is no blood supply to carry medication to this area.
    • When pressure is applied to third phalanx via the apex of frog the anterior edge of third phalanx will have no resistance to it thus forcing the third phalanx back in a more normal position.
    • To relieve any edematous swelling which occurs between PIII and wall.
  5. Why does the Veterinarian need to run an SMA 12 or SMA 20?
    • This is done to determine any underlying causes that affect the feet. Treatment begins with an accurate diagnosis and evaluation of the primary cause.
  6. How much pressure (support) must be applied to the frog?
    • The amount of support varies with each individual case. This depends upon the amount of rotation of the PIII at the time of application and whether the sole is dropped. Stabilization of the third phalanx is calculated by measuring the amount of rotation. It is critical that the apex of the heart bar contact the frog in front of the insertion of the deep flexor tendon on the third phalanx, however, it must end at least 1 cm. palmar to the apex of the frog. The bar must not touch the sole at any point and must be sufficiently narrow to avoid applying pressure to the medial and lateral palmar digital arteries as they enter the foramen of the terminal arch deep to the digital cushion.
  7. How far forward should the bar of the heart bar shoe be placed on the frog?
    • Again, let me stress that the bar should not touch the sole in any manner. It is usually made of 1/4" X 1/2" bar stock and is "V" shaped, just like the frog. This bar, on the normal light horse of today, should extend along the frog to a point of 3/8" (6-7 mm) posterior to the apex. Problems arise if the bar is too long.
  8. Does the heart bar cause necrosis of the sensitive frog or digital cushion?
    • If the shoe is correctly applied the heart bar will not cause necrosis. Abscesses usually occur within 15 to 30 days from the first signs of laminitis, if there is edematous swelling of the laminae, sinking and/or rotation of PIII. Abscesses will normally be aseptic in these early stages. It is beneficial to use ichthammol thickly applied to the coronary band, daily or as needed, for the first 30 to 90 days of treatment. This is done to keep the coronary band soft and pliable.
  9. When do I expect abscesses to occur?
    • When more than 4 degrees of edematous swelling occurs of if sinking and/or rotation has occurred, abscesses will develop. Abscesses generally result within 15 to 30 days after the heart bar shoes have been applied. If this takes place the soles should be opened at the junction of distal laminae and the horny sole. Opening the sole at this junction helps prevent swollen solar corium and resulting exuberant tissue.
  10. How should I treat decubitus ulcers or bedsores?
    • On non-suppurating decubitus ulcers, zinc-oxide and maalox mixture (approximately one bottle of maalox to one tube of zinc-oxide) is helpful. On suppurating decubitus ulcers betadine ointment is used. These horses should be bedded on straw or shredded newspaper.
  11. How should I deal with osteomyelitis?
    • It normally will occur when there is an exposed bone and must be addressed by only those who are extremely knowledgeable in treating this problem. The severe cases result in chronic abscesses. These can be treated with sugardine but most often require surgery which involves a bone biopsy, a culture and sensitivity to determine what antibiotics are beneficial for treatment. These must be done by an experienced veterinarian.
  12. When should soaking be done and how often?
    • When there is an open wound the foot can be soaked in betadine and hot water one day, then hot epsom salt water the next. Soaking or turbulation, 10 to 15 minutes per day, when helping to clean up abscess is done until there is no more drainage or suppuration. The foot is treated with sugardine and bandaged daily. Ichthammol can be used on the coronary band to draw abscesses and to keep the coronet soft and pliable. Each case is treated individually. In the case of osteomyelitis the foot should not be turbulated.
  13. What should I do when the drainage stops?
    • Merthiolate is used when there is no more drainage. Turbulation and soaking should also be discontinued.
  14. What is happening when a severely foundered horse walks on the toe?
    • There are two possibilities:
    • An abscess has formed in the heel area. This is usually best treated by using ichthammol ointment or magna paste around the entire coronary band, to break out the infection.
    • The tendon becomes involved. If this is the case sometimes a tendon desmotomy can be done, with good results.
  15. What feed supplement have you found obtainable on today's market which stimulates rapid hoof growth?
    • In the past I used and recommended the amino acid powder, methionine, essential for epithelial cell formation. However useful it may be, many horses found it unpalatable and refused to eat it. Consequently, the internal nutrients needed to build strong hooves were lost. In the late 1970's Life Data Labs began marketing an alfalfa-based equine supplement, FARRIER FORMULA or NUTRI-TONE, which most horses like. This product contains the essential amino acid, methionine, as well as biotin and other nutrients needed to maintain healthy hooves. I have seen a visible difference in hoof growth, within weeks, using this product.
  16. How much time is involved in returning the horse to sound pasture condition or performance condition?
    • The cause of the problem must first be corrected. The severity of the problem within the hoof capsule must be evaluated before any decision can be made as to the future of the animal. Sometimes the horse will respond and return within 9 months to a year. The horse must grow a complete new hoof before any favorable commitment should be done. Again, it depends on each individual case and its severity.
  17. How often should the shoes be reset?
    • I recommend the shoes be reset every 30 days. In the early stages of treatment and shoeing the heel will out-grow the toe as much as a 4 to 1 ratio. It is essential to trim the feet on a regular basis.
  18. Do you recommend pads?
    • No. If PIII sinks inside the hoof capsule the vessels become compressed, the blood supply (arteries and vessels) can be destroyed. I use a rim pad in conjunction with the heart bar shoe. Sometimes this is necessary to clear the distal end of PIII off the ground. Pads which cover the sole cause complications because abscesses must be allowed to stay open for ventral drainage and healing.
  19. How long should I leave my horse shod with heart bar shoes?
    • Sometimes for a lifetime. Each case must be treated as an individual. It depends on the severity and condition of each individual animal.
  20. What is my responsibility, as owner, after the initial treatment?
    • A commitment must be made of time and money by the owner. It takes months for nature to restore the damaged hoof. Each case is different, but these horses do not get well overnight, therefore require good nursing and after care. I must stress the importance of after care. This care includes resetting the shoes on a frequent basis; rebandaging; exercising; and it often requires regular checkups by experienced farriers and veterinarians. Prompt resetting of the shoes, as needed, can prevent unnecessary problems caused by feet left to grow too long. Depending on the individual horse, bandaging will be needed every few days, which can sometimes last as long as several months. Exercising the horse by daily walking is beneficial in order to obtain the return of overall body mechanics and general well being. This care can be done by the owner, his agent or left in the care of a "treatment center". All of these can be time consuming and expensive.
  21. When should I use a heart bar shoe with a rolled toe?
    • In severe rotation cases the toe of the shoe should be rolled in order to take the stress of break-over off the deep flexor tendon. By rolling the toe this moves the fulcrum point posteriorly.
  22. How should I control exuberant granulation tissue?
    • In extreme cases cauterization is the best method I have found to control this tissue. This is followed by application of copper sulfate powder and continued until exuberant tissue is below the epithelial cell line.
  23. What is a "sinker" or "straight vertical displacement"?
    • A "sinker" is when the PIII is going downward in the hoof capsule. The hoof capsule moves proximally. No rotation is noticed except at the coronary band. This can be easily diagnosed by manually palpating the coronary band. If a distinct depression is noted at the coronary band from heel to heel the result is a "sinker". If the sole is intact then a heart bar shoe can be used in conjunction with a frontal hoof resection and by opening the sole at the junction of the distal laminae and the horny sole. If the horny sole has disintegrated a heart bar shoe should not be used. Instead, a heart bar device made of a thermoplastic material can be substituted.
  24. Should the foot be blocked or any kind of pain reliever be used when shoeing a horse for founder or laminitis?
    • No. The horse must be able to feel the support being applied and thus indicating if correct support has been used. The amount of pain is a significant clinical sign. If the laminae are tearing loose and the bone is likely to rotate, it is wrong to mask the signs with pain-killing drugs or nerve blocks. By using pain-killing drugs the horse continues to walk which causes more tearing of laminae hastening the separation of laminae from PIII.
  25. What are some shoes and devices that work with very little consistency?
    • The egg bar shoe has no stabilizing effect on the bony column.
    • The reverse shoe gives no stabilization to PIII.
    • The reverse wedge pad places more tension on the deep flexor tendon thus causing more rotation.
    • The hoof cast compresses the blood supply of the venous plexus of the sole, and can cause an osteothrombosis of PIII, and is dangerous for general use.
    • A bar shoe with a bar across the center of the shoe can compress the palmar digital artery, destroying the blood supply to PIII.
    • A pad with packing under it gives no stability to the bony column and frequently causes pressure on the sole, destroying its blood supply.
    • A shoe that raises the heel and takes the stress off the deep flexor tendon aligns all the laminae perpendicular to the ground, causing the bony column to sink.
Posted here with the permission of the author.]]> (Burney Chapman, Dr. George Platt) Laminitis & Founder Mon, 13 Jul 2009 05:48:15 +0000
Nonclassical Laminitis

I shall consider several forms of laminitis which are not the typical classical type: static laminitis, sickness transport laminitis, sick road founder, other anoxic situations, and road founder. There are considerable overlaps of these categories as will be apparent.

Static Laminitis

This condition was first described, I believe, by clinicians at Colorado State University. Animals with severe lameness of one foreleg such as a broken bone routinely developed typical clinical and gross pathological laminitis in the other foreleg. It became apparent that this was associated with confinement to a stall. When the lame animal was allowed to move freely about a large paddock, laminitis did not develop. It appears quite clear, to me at least, that the pathogenesis was failure of adequate venous return from the foot with stagnant anoxia as the immediate cause of the laminitis.

Other Anoxic Situations

The extensive and beautiful work of Chris Pollitt on the pathophysiology of classical laminitis indicated that the basic or primary step in the pathogenesis may not be vascular. I am not completely convinced that is always the case as indicated above and elaborated below. That is not to denigrate Dr. Pollitt’s work; it is simply and without question the best work done to date on classical laminitis.

Routine gross and/or histological examination of the feet of horses dying with gastrointestinal disease (colic), postparturient metritis, severe renal disease, etc. sometimes reveals early changes in the sensitive laminae of the foot and the dermoepidermal junction of the chestnut (Rooney 1984). While these changes appear to be consistent with Pollitt’s hypothesis, they also appear to be consistent with anoxia (the inadequate perfusion of the circulatory system in these conditions).

Occasionally, mares late in pregnancy, particularly older mares, appear to develop signs of laminitis. These signs usually disappear after foaling but may recur in a later pregnancy. I know of no pathological study of such cases (they don’t die!) and suggest that this is an anoxic situation very much like both static and transport laminitis and road founder. That is, the older mare late in pregnancy moves around less than usual – is more “static.” When she does move, the feet experience greater resistance to breakover because of increased weight and, usually, because the feet have not been trimmed during the later stages of pregnancy and the toes have grown out.

Road Founder

Road founder is tearing of the tissues between the distal phalanx and the hoof wall. [This is discussed, and an illustration provided, in the essay on white line disease on this web site.] The lesion is most severe and obvious at the apex of the third phalanx, extending a variable distance toward the quarters. Histologically, there is disruption and tearing of collagen fibers with hemorrhage and edema. With time the damaged area is filled with granulation and, eventually, scar tissue.

In the old literature this was described in carriage horses, animals with heavy bodies, relatively light legs, and long toes for flashy, high “action.” These animals characteristically moved at speed on hard surfaces, for considerable distances, and pulling considerable loads. This combination of conditions is not often met with in modern times, but road founder does occur in heavier horses with long toes. It is, also, not uncommon in Shetland ponies in the Spring of the year. These animals bred for and adapted to the harsh conditions of the Shetland Islands grow long toes and put on weight with astonishing rapidity in the flush grass of early Spring. The toes are not worn down on grass pastures as they would be on the stony island ground. I do not wish to imply that every Shetland pony with clinical signs of laminitis has road founder, but it is a not insignificant cause of acute lameness in these animals.

One might think of Standardbred racehorses as candidates for road found since they move at high speed on hard surfaces. While there are undoubtedly some cases in these animals, the care given their trimming and shoeing and absence of excessive weight of animal or load, is protective.

The clinical signs with road founder can vary from slight to severe lameness of one or both front feet and in the acute stage are not readily differentiated from classical laminitis. The subsequent clinical course is less catastrophic, of course.

For those who might be interested there is information on the normal wearing of the foot on this web site.

Rooney, J R and Robertson, J L (1996) Equine Pathology. Iowa State University Press, Ames.

Rooney, J R (1984) Arteriovenous anastomoses in the digit of the horse. Journal Equine Veterinary Science 4:182-3.

]]> (James Rooney, D.V.M.) Laminitis & Founder Mon, 13 Jul 2009 05:38:27 +0000
Mechanical Treatment of Laminitis and Founder

If anyone ever figures out what exactly triggers the mechanism of the pathology we call "founder," or, better yet, figures out how to halt the process, they will be assured of wealth and fame.

Actually, the terms "founder" is often used incorrectly to describe an inflammation of the laminae. More properly, an inflammation of the laminae is called, "laminitis" and the term "founder" used to describe a detachment of the coffin bone from the hoof wall at the laminar interface.

The main attachment to the hoof capsule of the column of bones that comprise a horses lower leg is at the interface of dermal and epidermal laminae. Dermal laminae originate from the dermal corium on the dorsal surface (front) of the coffin bone. Epidermal laminae are found on the stratum internum, the most proximal (innermost) portion of the three layers which make up the hoof wall, and arise from the coronary corium.

The attachment of the laminae arising from different structures is anatomically analogous to a hook and eye attachment with one very notable exception: once laminae are separated, they will not reattach. They will not grow back together.

The coffin bone exists in precarious balance within the hoof capsule. On its dorsal side, the convoluted folds of the laminae serve to attach it to the hoof wall; simultaneously, the deep digital flexor tendon, which inserts at the semi-lunar crest ("wings") of the coffin bone, exerts constant tension on the bone and pulls the bone downward each time the foot is turned over ("flexed").

Any inflammation of the laminae, from whatever origin, is called "laminitis". As long as the laminae are well supplied with oxygenated blood, the balance between laminae and tendon is largely undisturbed; however, laminitis can disrupt the capillarial blood flow which supplies the laminae and can result in separation of the laminae at the junction of dermal and epidermal laminae (between the inner hoof wall and the top of the coffin bone). This phenomenon can have serious consequences.

Laminitis has many causes: among them, overwork, overfeeding, infections, organic toxins, shock and probably a change in the weather. All of the causes are unknown, but once laminitis occurs, the changes within the foot are fairly well-documented. Inflammation of the laminae causes blood circulation to be compromised to the middle third of the foot; with nowhere to go, this blood is immediately shunted back up the leg through the venous plexuses. Unfortunately, most of the relevant laminae are located in the middle third of the foot.

The most obvious symptoms of laminitis are distress, lying down with an unwillingness to get up, a "camped out" attitude, a reluctance to move, a pain response to hoof testers at the toe, and a pronounced digital pulse. There's a lot going on within a laminetic horse's foot and most of it's painful.

Separation at the laminar interface reduces the strength of the coffin bone's attachment to the hoof wall and laminar separation often causes bleeding within the hoof capsule.

This combination of laminar destruction and hydraulic pressure within the dorsal portion of the hoof capsule when coupled with the constant downward pull of the deep digital flexor tendon can be strong enough to pull the coffin bone downward.

Why downward? The top (proximal) portion of the coffin bone pivots at the coffin (distal interphalangeal) joint. The deep digital flexor tendon, using the navicular bone as a fulcrum, flexes that joint each time foot flexes (turns over). If the attachment of the coffin bone to the wall is compromised, when the flexor muscles pull on the tendon, instead of the foot turning over, the coffin bone is pulled away from the hoof wall. The subsequent rotation of the coffin bone is called "founder".

After coffin bone rotation has been initiated, other factors occur which can cause the phenomenon to worsen, the most important of which has to do with the incompressibility of fluids. As the laminae are torn, bleeding occurs within the hoof capsule: because the dorsal hoof wall is the least flexible portion of the wall and the coffin bone is inflexible, the hydraulic pressure exerted by this blood flow often causes more tearing, more bleeding and more coffin bone rotation. When this occurs, instead of attachment loss at the laminar interface and the pull of the deep flexor being responsible for rotation, the bone is also pushed downward by the relevant hydraulics - in severe cases, through the sole.

Laminitis and founder can be of systemic origin (as previously discussed) as well as mechanical origin. The most common mechanical origins of laminitis and founder are pawing, poor husbandry and poor farriery. Mechanical founder can sometimes occur without laminitis in the case of catastrophic insult or loss of hoof wall to disease.

These maladies most often occur in the front feet - occasionally in all four - of large equines, with all four feet being affected more often in ponies, small mules and asses. Occasionally, only one front foot is affected, but the cause of unilateral founder is always mechanical.

The third phalanx (P3) cannot rotate downward if it is stable. Once destabilized by laminitis, hydraulics, disease or injury, it will rotate downward until stability is achieved.

"Stability" is that delicate balance in which the dermal and epidermal laminae manage to maintain a hold on the hoof wall, themselves and the coffin bone while the deep digital flexor tendon (DDFT), using the navicular bone as a fulcrum, causes the articulation of the coffin (distal interphalangeal) joint. Another way of saying this is to say that if the laminae don't tear, the hoof will be turned over by those muscles high in the leg called "flexors" which transmit their energy to the foot through the associated flexor tendons. Since the foot turns over each time the horse takes a step, it follows that successful treatments for founder involve stability, support and enhanced turnover.

As an aside, medication and mechanical treatment get a lot of the credit for stabilizing horses that rightfully belongs to Nature. A great many horses destabilize, founder, then restabilize and nobody is the wiser until some farrier notices the thickened white line and asks, "When'd this horse founder?"

From a mechanical standpoint, stability of P3 is achieved by the application of some kind of mechanical pressure to the frog. (The frog lies directly below P3 and is a weight bearing structure.) But, what kind of mechanical pressure? Mechanical pressure can take several forms, including pulling the shoes and turning the horse out on sand, the application of frog pressure pads (e.g., Lily Pads) or the forging and application of shoes that apply pressure to the frog, which includes heart bars, g-bars, t-bars, and variations thereof.

Obviously, there's a thin line between stabilization and support. Mechanical support means that some mechanical device, pressure pad or pressure bar, is placing constant, direct pressure on the frog; environmental support means that the ground surface of the frog (foot shod or unshod) is in contact with the ground any time the foot is on the ground.

Assuming that the horse, for whatever reason and by whatever means, has stabilized, the most important factor becomes enhanced turnover.

Turnover is the fourth phase of motion. At any gait, at any speed, in order to move forward, the foot must be turned over; therefore, anything that enhances turnover will lessen the inherent stress at the interface of dermal and epidermal laminae at turnover and serve to ease the pressure of the DDFT on both the navicular bone and at its insertion on P3.

How is turnover enhanced? In the main, in two ways: by increasing phalangeal angulation and/or by decreasing the effective length of the phalangeal lever. Additionally, turnover can be facilitated to a lesser degree by the farrier's choice of shoe configuration and by various forging methods.

All other things being equal, the most important factor influencing turnover is the placement of the shoe on the foot because the length of the phalangeal lever is determined by the distance from the coronary band to to the breakpoint of the shoe, not by the distance from the coronary band to the end of the hoof capsule. For this reason, the wall is not considered, other than as a limiting factor, in the placement of the shoe on the foot.

In my experience, the most effective means of mechanical treatment of founder consists of a pressure bar, set under. The problem with pressure bars is that their application must be absolutely correct; if not, they will do more harm than good. For this reason, many veterinarians are reluctant to prescribe their use and instead prescribe methods that are not as effective, but do not have the potential for damage - and litigation.

One of those stop-gap methods is the application of several wedge pads - a method that certainly increases phalangeal angulation but does not necessarily stabilize P3 angulation, with or without frog pressure. Increased angulation may negate the pull of the DDFT, but it does not necessarily stabilize P3 because other factors, especially hydraulics, can contribute to the rotation of P3.

The reader should be aware that there is no single, "best" method of mechanically treating founder. Hot (acute) founders are treated differently than chronic founders; systemic founders are treated differently than mechanical founders; however, if I were limited to only one mechanical means of treating founder, it would be a set of pressure bars, set under as far as they'd go.

Applied without drains to a stable horse; or, applied to a hot founder with pressure relief, properly applied pressure bars are unquestionably the most successful method of treating founder when mechanical treatment is indicated.

Tom Stovall is an American Farriers Association Certified Journeyman Farrier since 1983, a Member of the Texas Professional Farriers Association, and a Member of the Artists-Blacksmiths Association of North America. Thanks to him for his permission to post this article.

]]> (Tom Stovall, CJF) Laminitis & Founder Mon, 13 Jul 2009 05:30:32 +0000
Equine Laminitis Basement Membrane Pathology: Loss of Type / V Collagen, Type VII Collagen and Laminin Immunostaining


BM basement membrane Ep epidermal cells
PEL primary epidermal lamella PDL primary dermal lamella
PMNs polymorphonuclear leucocytes SDL secondary dermal lamella
SEL secondary epidermal lamella V blood vessels
TNF-a tumour necrosis factor -a TGG-b transforming growth factor -b
E erythrocytes MMP matrix metalloproteinase

Disintegration of the basement membrane (BM) of the equine hoof lamellae and failure of the BM to remain attached to the basal cells of the secondary epidermal lamellae (SEL) is one of the earliest pathological events to occur in acute laminitis. Changes in the lamellar basement membrane were investigated by immunolabelling the key structural components of the BM, type IV collagen, type VII collagen and laminin in the lamellar BM of horses 48 hours after the induction of laminitis. Lamellar tissues were harvested from 2 normal horses and 2 horses with acute laminitis. Immunostaining with antibody raised against human epitopes for lype IV collagen, type VII collagen and laminin successfully stained the basement membranes of horse hoof lamellar tissues. Vascular tissue did not immunostain with type V11 collagen antibody. Normal BM stained as a fine dark brown line and the lamellar BM was adhered to the basal cells of the SELs with no evidence of lamellar separation. At least 2 changes to the lamellar BM occurred in acute laminitis: loss of attachment of lamellar epidermal basal cells to their underlying BM and disintegration of the lamellar BM. In some sections from feet affected by acute laminitis, there was widespread separation of the SELs from their BM without loss of BM immunostaining and in others there was extensive loss of BM immunostaining. In lesions characterized by lamellar separation, the epidermal basal cells at the tips of the primary epidermal lamellae appeared to have slipped away from their BM and were an amorphous clump of epidermal cells devoid of immunostained BM. The BM from which they had separated remained in its original position in the dermis and was clearly outlined by all 3 antibodies. In other areas, however, virtually all the BM immunoreactivity at the PEL tips was absent. Only the occasional distorted SEL tip and fragments of BM retained sufficient immunostaining to allow anatomical identification. Numerous polymorphonuclear leucocytes (PMNs) invariably surrounded the tips of lamellae showing large scale loss of immunoreactivity and many PMNs had penetrated the lamellar BM and were within the epidermal compartments. PMNs were less frequent in the midlamellar region. Immunostaining of the BM of many SELs was absent in the midlamellar region. In some lamellae loss of BM immunostaining had occurred only at the bases of the SELs and fragments of immunostained BM were present in the zones of lysed BM suggesting that BM lysis was incomplete at the time of tissue fixation. In other lamellae, lysis of the BM was complete; there was no immunostained BM between SELs and the bulk of the epidermal cells of each PEL were an amorphous column of cells on either side of the central keratinised axis of the PEL. The lamellar BM which remained appeared as immunostained strands of unattached BM along the edges of the PDLs. Activation of BM degrading metalloproteinases (MMPs) occurs in acute laminitis and it seems likely that uncontrolled MMP activity is responsible for the loss and disorganization of lamellar BM demonstrated in this study.


Disintegration of the basement membrane (BM) of the hoof lamellae and failure of the BM to remain attached to the basal cells of the secondary epidermal lamellae (SEL) is one of the earliest pathological events to occur in acute laminitis (Pollitt 1996). The attenuated, distorted appearance of the BM in histochemically stained sections examined with the light microscope, led to speculation that loss of collagen and glycoprotein from the lamellar basement membrane was part of the mechanism initiating collapse of the lamellar anatomy (Pollitt 1996).

The molecular components of the BM can also be identified using immunohistochemical methods. Laminin has been identified in the equine lamellar BM as well as in adjacent dermal blood vessels using a mouse monoclonal antibody raised against human laminin (Pollitt 1994). Type IV and type VII collagen have been located in the epidermal BM of many species (Rigal et al. 1991; Germain et al. 1995; Blankenship and Given 1995) but not the horse. Immunolabelling can be used to establish changes in the amount of type IV collagen, type VII collagen and laminin in the epithelial BM. For example, immunoreactivity for laminin and type IV collagen in the BM lining the epithelium of the uterine lumen is progressively lost during implantation of the blastocyst in mice (Blankenship and Given 1995). Similarly, in a temporal study of regeneration of the epidermo-dermal junction after full thickness skin wounding in pigs, type IV collagen and laminin appear in the new BM on Day one, but the appearance of type VII collagen does not occur until Day 3 (Rigal et al. 1991). In this study the BM pathology of laminitis was investigated further, by immunolabelling type IV collagen, type VII collagen and laminin in the lamellar BM of horses 48 h after the induction of laminitis, to determine the changes that occurred in these components of the BM.

Materials & Methods

Lamellar tissues were harvested from 8 normal horses and 2 horses with acute laminitis 48 h after the administration of an alimentary carbohydrate overload. The 2 horses with acute laminitis were from another study (Pollitt and Davies 1998) which was conducted according to guidelines approved by The University of Queensland Animal Experimentation Ethics Committee. All horses under experimentation were inspected by the Animal Welfare Officer. The mid-dorsal hoof wall lamellae from 16 normal forefeet and 6 laminitis affected feet (4 fore and 2 hind) were trimmed using the method of Pollitt (1996). In some lamellar tissue hemorrhage was present at the tips of PELs. The tissue was fixed in cold (4oC) 4% phosphate buffered formaldehyde (pH7.6) for 4 h, dehydrated, cleared and embedded in paraffin. Paraffin sections of 5 lxm thickness, mounted on silanised glass slides, were deparaffinised, blocked for endogenous peroxidase with 1% hydrogen peroxide and predigested with 0.1% trypsin1 for 7 minutes using the method of Quondamatteo et al. (1994). The sections were then incubated in 10% goat serum for 30 minutes prior to overnight incubation at 4oC, in a humidity chamber, with the specific antiserum. The following antisera, diluted appropriately, were used: monoclonal mouse anti-human type IV collagen2 1:500, monoclonal mouse anti-human type VII collagent 1:200, polyclonal rabbit antihuman laminin3 1:500. Biotinylated goat anti-mouse3 or sheep anti-rabbit sera1 were diluted 1:200 and applied to the sections following overnight incubation for 30 minutes at room temperature. Immunolocalisation was shown by incubating the tissues in horseradish peroxidase and diaminobenzidine and lightly counterstaining with haematoxylin. Normal sheep serum was substituted for the primary antibody, secondary antibody and streptavidin-peroxidase complex, and diaminobenzidine was omitted from the reaction in control sections. Sections were examined with an Olympus BX-50 light microscope and photographed using Kodak T-Max 100 film.


Mouse monoclonal antibody to human type IV collagen and rabbit polyclonal antibody to human laminin clearly immunostained the lamellar BM and the BM of all the blood vessels in the surrounding dermis as a fine dark brown line (Fig lA, B). Mouse monoclonal antibody to human type VII collagen stained only the lamellar BM (Fig 1C). In the sections of lamellae from normal feet the lamellar BM was adhered to the basal cells of the SELs and there was no evidence of separation. Control sections did not stain when normal sheep serum was substituted for the primary antibody, secondary antibody and streptavidin-peroxidase complex and when diaminobenzidene was omitted from the reaction mixture.


Fig 1: Normal lamellae: type IV collagen (A), laminin (B) and collagen type VII (C) immunostaining. The basement membranes (arrowheads) of the epidermal lamellae and the blood vessels (V) of the dermal lamellae are clearly immunostained as a fine dark brown line in A and B. The blood vessels did not immunostain in C. Nuclei of the epidermal basal cells and dermal fibroblasts are. counterstained with haematozylin. The basement membrane is closely adhered to the basal cells of the lamellar epidermis and there is no evidence of separation. Bar =100 pm.


Fig 2: Laminitis: type IV collagen immunostaining. Section of the tip of a primary epidermal lamella (PEL) affected by grade 3 laminitis. At the tip of the PEL the epidermal basal cells are clumped together and are devoid of BM. The immunostained BM (arrowheads) from which they have separated has remained in its original position in the dermis and has retained the outline of the secondary epidermal lamellae (SEL). The BM of blood vessels (V) in the primary dermal lamellae (PDL) are also stained and serve as positive controls. Bar =100 pm. Inset shows laminin immunostained BM of SEL, empty of epidermal cells. Bar =10 Nm


Fig 3: Laminitis: type VII collagen immunostaining. Section from the tip of a primary epidermal lamella (PEL) affected by grade 3 laminitis. The SELs are devoid of epidermal cells. The immunostained BM has remained in its original position in the dermis retaining the outline of the SEGs. Numerous PMNs (arrowheads) have already crossed the lamellar BM and are within the epidermal compartments of the SELs. The BM of dermal blood vessels did not immunostain with type VII collagen antibody. Bar = 50 pm. Inset shows, at the same magnification, laminin immunostained section cut from the same block. The BM of the blood vessels (V) as well as the lamellar BM is immunostained.

In some sections from feet affected by acute laminitis, there was widespread separation of the SELs from their BM without loss of BM immunostaining and, in others, there was extensive loss of BM immunostaining. The laminitis lesions were scored as Grade 3 using the histopathological grading system of Pollitt (1996). In lesions characterized by lamellar separation, the epidermal basal cells at the tips of the primary epidermal lamellae were clumped together and were devoid of immunostained BM (Fig 2). The BM from which they had separate (mean separation distance 13.10 gm s.e. = 2.55) appeared to have remained in its original position in the dermis and was clearly outlined by all 3 antibodies (Figs 2,3). The tubes of empty BM, derived from the tips of each SEL, had retained their normal shape and resembled the fingers of an empty glove described by Pollitt (1996). Neutrophils were numerous in the dermis surrounding the PEL tip and many had left the dermis and were located between layers of BM in what were once epidermal compartments (Fig 3).


Fig 4: Laminitis: laminin immunostaining. Sections from mid-region of single lamellae affected by laminitis. The BM of blood vessels (V) in the primary dermal lamellae (PDL) are immunostained and serve as positive controls. A. At the bases of the SELs most of the BM did not immunostain (arrowheads) suggesting that disintegration of the BM had occurred. Fragments of immunostained lamellar BM are still present in this region (arrows) suggesting that BM lysis is incomplete at this stage. The SEL tips are attenuated (compare with Fig 1) but the BM has not separated from the basal cells. B. The BM has disappeared from most of the SEL epidermal cells which are now an amorphous column of epidermal cells (Ep Cells) on either side of the central keratinised axis of the PEL. The lamellar BM hQs detached from the SEL tips and immunostains as strands along the edges of the PDLs. We propose that A and B represent stages in the progression of the laminitis lesion. Bar = 700 Nm.

Away from the PEL tip, in the mid-region of the lamellae, immunostaining of the BM of many SELs was absent. Loss of BM immunostaining was interpreted to mean that lysis of the structural elements of the BM had occurred. In some lamellae loss of BM immunostaining had occurred only at the bases of the SELs (Fig 4A). Fragments of immunostained BM were present in the zones of lysed BM suggesting that BM lysis was incomplete at the time of tissue fixation. In other lamellae, lysis of the BM was complete; there was no immunostained BM between SELs and the bulk of the epidermal cells of each PEL were an amorphous column of cells on either side of the central keratinized axis of the PEL (Fig 4B). Capillaries, normally present in the SDL, between most of the SELs (Fig 1) were no longer present at this stage. What lamellar BM remained immunostained as strands of BM along the edges of the PDLs (Fig 4B). The BM strands were, in fact, BM bilayers derived from BM originally lining the sides of each SEL tip. This was different to the separated BM from the PEL tips which retained its original shape (Fig 2). In SELs with the tapered, stretched tips, described by Pollitt (1996) a few attenuated epidermal cells were still enclosed by BM and often the BM of the SEL tip formed a dilatation (Fig 5).


Fig 5: Laminitis: type IV collagen immunostaining. Section from midregion of a single lamella affected by grade 3 laminitis. The SELs are attenuated and have tapered, stretched tips. A few distorted epidermal cells are still enclosed by BM. The BM of the SEL tips encloses dilatations (arrowheads). Fragments of immunostained BM (arrows) are occasionally present between SELs otherwise devoid of BM. The BM of blood vessels (V) is immunostained. Bar = 50 Nm. Inset at the same magnification shows occasional, very large, BM enclosed dilatations of the SEL tip, type VII collagen immunostaining.

Virtually all the BM immunoreactivity at the tips of some PELs was absent. Only the occasional distorted SEL tip and fragments of BM retained sufficient immunostaining to allow anatomical identification (Fig 6). Numerous polymorphonuclear leucocytes (PMNs) invariably surrounded the tips of lamellae showing large scale loss of immunoreactivity and many PMNs had penetrated the lamellar BM and were within the epidermal compartments (Figs 3, 6). PMNs were less frequent in the midlamellar region.


Fig 6: Laminitis: laminin immunostaining. Virtually all the immunoreactivity of the lamellar BM is absent. Only the narrow attenuated tip of an occasional SEL retains sufficient immunoreactivity to allow identification. The remainder of the BM appears to have been degraded into small fragments or has disappeared altogether. Numerous PMNs (arrowheads) either surround the disintegrating lamellar BM or are within the SEL epidermal compartments. Bar =10 pm. Many small veins and capillaries were located with no BM immunostaining for laminin and type IV collagen and many were surrounded by extravasated erythrocytes (Fig 7). Often the capillaries which did not stain, were beside capillaries which had normal staining BMs.


Fig 7: Laminitis: laminin immunostaining of dermal blood vessels. Many small veins and capillaries had lost BM immunostaining and numerous extravasated erythrocytes (E) were in the surrounding dermal connective tissue. The remains of the vessel walls (outlined with arrowheads) and fragments of immunostained vascular BM (large arrows) are still present. PMNs are in the lumen of one of the vessels and in the adjacent dermis (small arrows). Bar = 10 um.


Immunostaining with antibodies raised against human epitopes for type IV collagen, type VII collagen and laminin successfully stained the basement membranes of horse hoof lamellar tissues. Vascular tissue did not immunostain with type VII collagen antibodies. Normal basement membrane stained as a continuous dark brown line contrasting starkly against a light blue background of connective tissue and epidermis counterstained with haematoxylin. The method was superior to the histochemical methods of BM staining described by Pollitt (1996). The clear delineation of the lamellar BM in tissue sections affected by laminitis confirmed the findings of Pollitt (1996) that at least 2 changes to the lamellar BM occurred in developmental laminitis: loss of attachment of lamellar epidermal basal cells to their underlying BM and disintegration of the lamellar BM. Epidermal basal cells lost their attachment to the BM without undergoing obvious necrosis and when lamellar separation occurred the BM detached from the epidermal basal cells in intact sheets and remained attached to the dermal connective tissue. This implies that the substances causing BM lysis and separation emanate on the epidermal side of the BM and are products of the epidermal cells. Adhesion receptor molecules, called integrins, are responsible for the adhesion of epidermal basal cells to the BM. Antibody raised against (31 integrin receptors interferes with adhesion and stimulates a several fold increase in production of 92 kDa matrix metalloproteinase (type IV collagenase) in cultures of human keratinocytes (Larjava et al. 1993). Keratinocyte MMP production leads to pericellular proteolysis which is the essential first step in the detachment of keratinocytes from the BM (Salo et al. 1991) during wound healing. Triggering of lamellar keratinocyte MMP production could initiate the BM lysis and detachment of lamellar epidermal cells from BM as shown here in laminitis.

The laminitis grading system described by Pollitt (1996) was based on differences, ranging from mild to severe, of the laminitis lesions between individual horses all killed 48 h after being dosed with a laminitis inducing diet. The assumption was made that the grades of severity represented stages in the temporal progression of the laminitis disease process. Horses with Grade 3 lesions progressed through stages 1 and 2. A similar assumption, made here, enables recognition of stages of disease progression within individual horses in sections of tissues affected by laminitis. Lamellar separation and lysis of the BM appeared coincident in some sections but, in others, lysis of the BM appeared to be the first change to have occurred (Fig 4A). Lysis of the BM appears to commence between the bases of the SELs. Type IV collagen, type VII collagen and laminin, all known substrates of matrix metalloproteinases (Salamonsen 1994), disappear from the BM together. In addition to focal lysis, the BM also separates from the basal cells in intact sheets with the bulk of the lamina densa apparently intact. However, the lamina densa is attached to the plasmalemma of the basal cell by the anchoring filaments traversing the lamina lucida (Pollitt 1994) which are composed of laminin 5, a subtype of laminin. Lysis of anchoring filament laminin by MMP produced by lamellar keratinocytes could explain the wholesale detachment of lamellar BM in laminitis.

In this study, we used a panel of BM immunomarkers (laminin, type IV collagen and type V11 collagen antibodies) to establish that the loss of lamellar BM immunostaining represented a genuine structural disintegration rather than the loss of individual epitopes. The loss of an epitope could result in loss of monoclonal antibody immunostaining without necessarily implicating structural failure. Included in our panel was a polyclonal antibody to laminin and, since the BM lesions in the lamellar BM of the horses affected by laminitis were common to all 3 antibodies, we conclude that loss of immunostaining represents genuine anatomical disintegration of BM. Further, the antibodies located BM proteins of quite different structure and function: type N collagen is the structural backbone of the BM lamina densa, laminin is a glycoprotein which coats type IV collagen and type V11 collagen forms the anchoring fibrils and anchoring plaques which attach the BM to the adjacent dermis.

When the lamellar BM first separates from the lamellar basal cells it slides free of the SEL to form a dilatation at the SEL tip. When the separation process is extensive the separated BM from each SEL forms a BM bilayer with the appearance of a densely staining single strand. At intervals along the length of the single strand, and often at the tip, bifurcation of the strand reveals that the strand is in fact a bilayer. When the BM of many SELs separates and slides free, the bilayered strands form a layer of overlapping strands in the dermis on either side of the PEL. The PEL becomes an amorphous multi nucleate column of epidermal cells containing the original keratinised axis of the PEL and all the basal and suprabasal cells of the SELs, which are now without an attachment to BM. It can be assumed that the forces dragging the separated BM away from the SELs, in the direction of the distal phalanx, are those of weight bearing and locomotion (Pollitt 1996). The BM dilatations and the splits in the bilayered strands sometimes enlarge to form vacuole-like dilatations with a diameter of up to 50 lxm and far exceed the diameter of neighboring veins and capillaries. The membrane enclosing the dilatations was immunolabelled with all 3 BM antibodies used in this study. The reaction with antibodies to type VII collagen establishes unequivocally that the membrane of the dilatations is lamellar and not vascular in origin, as type V11 collagen is not present in blood vessels and the lamellar vasculature never reacted with antibodies to type V11 collagen. In the past, in sections stained by routine histochemical methods, the lamellar BM dilatations may have been confused with dilated blood vessels, giving rise to the concept that oedema was present at the lamellar dermoepidermal junction (Roberts et al. 1980). The diameter of the lumen of dermal blood vessels adjacent to the lamellar BM dilatations appeared normal and, although we can offer no explanation for the formation of the nonvascular lamellar BM dilatations, our results challenge the commonly held concept that oedema of vascular origin is involved in the pathogenesis of laminitis. Haemonhage at the tips of PELs was noted in some tissue blocks prior to fixation. Many small veins and capillaries without BM immunostaining, surrounded by extravasated erythrocytes near the tips of the PELs, were present in sections of this tissue. The haemonhage observed at the tips of PELs probably occurred because of damage to the BM of the veins and capillaries. The loss of BM immunostaining, and presumably BM lysis, in small veins and capillaries associated with the lamellar haemonhage is evidence that BM damage did occur. Microvascular endothelial cells when exposed to cytokines such as TNF-a produce MMPs capable of destroying BM structural proteins (Cornelius et al. 1995) and this may have occurred in the lamellar tissues that haemonhaged.

Virtually all the capillaries, normally present in the dermis between the SELs of each lamella were absent in the lamellar tissues affected by laminitis. Their disappearance coincided with the loss of immunostaining of the lamellar BM. There were never any capillaries with BM immunostaining in the amorphous columns of SEL epidermal cells shown in Figure 5. The loss of these capillaries may explain why resistance to blood flow was increased 3.5 times in horses during early laminitis (Allen et al. 1990) and why blood was bypassing the capillary bed through dilated arteriovenous anastomoses in the horses with acute laminitis studied by Hood et al. (1978).

Care had to be taken with the interpretation of loss of BM immunostaining. If the BM had separated and migrated then the residual basal cells would appear to have lost BM immunostaining. Therefore, loss of immunostaining was ascribed to lamellar BM only when the loss occurred in sections of BM that were continuous with BM that had retained immunoreactivity. Fragmental disintegration of the BM was identified in every section of the 6 laminitis affected feet examined. It was never present in normal controls.

By what mechanism is the lamellar BM made to lyse and separate? Many examples of loss of BM immunostaining in epithelial tissues and detachment of basal cells from BM, similar to that shown here for laminitis, have been reported in the literature. In all cases BM loss and detachment is linked to the local production of matrix metalloproteinases (MMP) or type IV collagenase. Cancers arising from keratinocytes (basal cell and squamous cell carcinomas) penetrate their underlying BM after first lysing it by the production of type N collagenase (Slade et al. 1995). As a prerequisite for wound healing keratinocytes detach from the BM and migrate to cover the exposed connective tissue. However, lysis of the BM precedes keratinocyte migration (Salo et al. 1991). Because of their ability to produce MMP keratinocytes are considered major participants in the degradation of extracellular matrix during wound healing. A strong signal for 92kDa type IV collagenase (MMP-9) is found in the basal and suprabasal epithelial cell layer of normal human oral mucosa (Salo et al. 1994). Increased quantities of MMP-9 are found in migrating basal cells, wound fluid and granulation tissue after experimental wounding. Furthermore, cultures of oral mucosal keratinocytes respond to the addition of the cytokines tumour necrosis factor -a (TNF-a), interleukin-1(3 (IL-1(3) and transforming growth factor-(31 (TGF-(31) by increasing production of MMP-9 (Salo et al. 1994).

The loss of immunostaining of the BM in lamellar tissues affected by laminitis resembled closely the pattern of BM destruction which occurs when the mouse blastocyst invades the uterine epithelium (Blankenship and Given 1995). On Day 5 of pregnancy the BM of the uterine epithelium still showed positive immunostaining for type IV collagen and laminin, but by Day 7 this had disappeared over the entire embryonic half of the uterine lining. The loss of BM immunostaining for type N collagen and laminin closely followed its anatomical disintegration and occurred adjacent to trophoblast cells, known producers of matrix metalloproteinases (Shimonovitz et al. 1994).

Increased amounts of the active forms of BM degrading enzymes (EqMMP-2 and EqMMP-9) are present in equine lamellar tissues affected by laminitis 48 h after the alimentary administration of a laminitis inducing dose of carbohydrate (Pollitt et al. 1998). This increase in MMP production by lamellar keratinocytes, possibly triggered by the arrival of cytokines via a dilated lamellar vasculature (Pollitt and Davies 1998) or by changes in glucose metabolism in lamellar tissues (Pass et al. 1998), appears to be responsible for the detachment from the lamellar BM and loss of lamellar BM demonstrated in this study. A feature of acute laminitis is the large number of PMNs found within the BM enclosed but keratinocyte free epidermal compartments of the secondary epidermal lamellae of the lamellar tips (Pollitt 1996). Equine PMNs are a potent source of Eq MMP-9 (Pollitt et al. 1998b) and the arrival and extravasation of PMNs into the lamellar tissues undoubtedly accelerates the process of lamellar BM destruction. PMNs probably gain access to the epidermal compartments of the lamellae by focal lysis of the lamellar BM.

This study contributes new information to our understanding of the mechanism causing laminitis. It demonstrates that early in acute laminitis lamellar BM is lysed and consequently disappears from many of the epidermal lamellae lining the inner hoof wall of the equine foot. It also shows that lamellar BM detaches from lamellar basal cells and forms loose strands of bilayered BM in the connective tissue adjoining the lamellae. Since the BM is the key structure bridging the epidermis of the hoof to the connective tissue of the distal phalanx, it follows that the wholesale loss and disorganization of the lamellar BM demonstrated here would lead inexorably to the failure of lamellar anatomy so characteristic of equine laminitis.


This project was funded by a grant from the Rural Industries Research and Development Corporation (RIRDC) of Australia. The authors are grateful to the Animal Health Foundation of Missouri, USA, for funds used to purchase the BX-50 Olympus microscope.

Manufacturer's Addresses

1Sigma Chemical Co. St Louis, Missouri, USA
2Zymed Laboratories Inc, San Francisco, USA
3Dako (Australia) Pty Ltd., Botany, NSW 2019, Australia


  1. Allen, D., Clark, E.S., Moore, J.M. and Prasse, K.W. (1990) Evaluation of the equine digital Starling forces and haemodynamics during early laminitis. Am. J. vet. Res. 51,1930-1934.
  2. Blankenship, T.N. and Given, R.L. (1995) Loss of laminin and type IV collagen in uterine epithelial basement membranes during blastocyst implantation in the mouse. Anat. Rec. 243, 27-36.
  3. Comelius, L.A., Nehring, L.C. Roby, J.D., Parks, W.C. and Welgus, H.G. (1995) Human dermal microvascular endothelial cells produce matrix metalloproteinases in response to angiogenic factors and migration. J. invest. Dermatol. 105, 170-176.
  4. Germain, L., Guigard, R., Rouabhia, M. and Auger, F.A. (1995) Early basement membrane formation following the grafting of cultured epidermal sheets detached with thermolysin or Dispase. Burns 21, 175-180.
  5. Hood, D.M., Amoss, M.S., Hightower, D., McDonald, D.R., McGrath. J.P., McMullan, W.C. and Scrutchfield, W.L. (1978) Equine laminitis 1: Radioisotopic analysis of the hemodynamics of the foot during the acute disease. J. equine Med. Surg. 2, 439-444.
  6. Larjava, H., Lyons, J.G., Salo, T., Makela, M., Koivisto, L., Birkedal-Hansen, H., Akiyama, S.K., Yamada, K.M. and Heino, J. (1993) Anti-integrin antibodies induce type IV collagenase expression in keratinocytes. J. Cell. Physiol.157, 190-200.
  7. Pass, M.A., Pollitt, S. and Pollitt, C.C. (1998) Decreased glucose metabolism causes separation of hoof lamellae in vitro: a trigger for laminitis? Equine vet. J., Suppl. 26, 133-138.
  8. Pollitt, C.C. (1994) The basement membrane at the hoof dermal epidermal junction. Equine vet. J. 26, 399-407.
  9. Pollitt, C.C. (1996) Basement membrane pathology: a feature of acute laminitis. Equine vet. J. 28, 38-46.
  10. Pollitt, C.C. and Davies, C.T. (1998) Equine laminitis: its development coincides with increased sublamellar blood flow. Equine vet. J., Suppl. 26, 125-132.
  11. Pollitt, C.C., Pass M.A. and Pollitt, S. (1998) Batimastat (BB-94) inhibits matrix metalloproteinases of equine laminitis. Equine vet. J., Suppl. 26, 119-125.
  12. Quondamatteo, F., Scharif, K. and Herken, R. (1994) Changes in laminin immunoreactivity as a marker for the state of liver preservation. Histochem. J. 26, 827-832.
  13. Rigal, C., Pieraggi, M-T., Vincent, C., Prost, C., Bouissou, H. and Serre, G. (1991) Healing of full-thickness cutaneous wounds in the pig. I. Immunohistochemical study of epidermo-dermal junction regeneration. J. Invest. Dermatal. 96, 777-785.
  14. Roberts, E.D., Ochoa, R. and Haynes, P.F. (1980). Correlation of dermal-epidermal laminar lesions of equine hoof with various disease conditions. Vet. Path.17, 656-666.
  15. Salamonsen, L.A. (1994) Matrix metalloproteinases and endometrial remodeling. Cell Biol. International. 18, 1139-1144.
  16. Salo, T., Lyons, J.G., Rahemtulla, F., Birkedal-Hansen, H. and Larjava, H. (1991) Transforming growth factor-beta up-regulates type IV collagenase expression in cultured human keratinocytes. J. Biol. Chem. 266, 11436-11441.
  17. Salo, T., Makela, M., Kylmanaiemi, M., Autio-Harmanen, H. And Larjava, H. (1994) Expression of matrix metalloproteinse-2 and -9 during early human wound healing. Lab. Invest. 70, 176-182.
  18. Shimonovitz, S., Hurwitz, A., Dushnik, M., Anteby, E., Geva-Eldar, T. and Yagel, S. (1994) Developmental regulation of the expression of 72 and 92 kd type IV collagenases in human trophoblasts: a possible mechanism for control of trophoblast invasion. Am. J. Obstet. Gynecol. 172, 1938-1939.
  19. Slade, N., Pavelic, J, Kruslin, B. and Pavelic, K. (1995) Type IV collagenase in squamous cell and basal cell carcinomas. Arch. Dermatol. Res. 287, 512-514.
Posted here with the permission of the authors.
First published in Equine vet. J. Suppl., (1998) 26 139-144]]> (C. C. Pollitt and M. Daradka) Laminitis & Founder Mon, 13 Jul 2009 05:10:31 +0000
What is Meant by the Term "Foundering?"

The term founder or foundering refers to a disease of the horse's foot; it is also known as laminitis and has a long history in the horse world. It dates as far back as the Greeks who referred to it as "barley disease" because they saw an association between the feeding of barley and the development of the disease. The Romans also recognized founder (laminitis) and associated it with long traveling times on hard surfaces, similar to what we now call "road founder." Other names used for the same disease include "foundid," "pumice foot," and "fever of the feet." Laminitis can be a devastating and career-ending condition for a horse and therefore has attracted great attention in efforts to both treat and prevent the disease.

When using today's common terminology of "laminitis" or "founder," there is usually a distinction made between the two with regard to how long the disease process has been occurring. Laminitis usually refers to the early stages of the disease. By definition, the word means an inflammation (-itis) of the laminar (lamin-) tissues within the foot. Inflammation is the body's response to an insult or injury. It causes the affected tissues to swell, develop heat and redness, become painful and possibly lose function. This can be compared to accidentally striking your thumb while using a hammer. There is a definite development of redness, heat, pain, swelling and possibly even temporary function loss due to this injudicious use of a hammer!

The laminar tissues within the foot are folds of tissue that connect the coffin bone, or third phalanx, to the inner hoof wall; in a sense, partly suspending the coffin bone within the hoof wall capsule. There are hundreds of tissue laminae present within the foot. When the disease is in its early stages, it involves, in part at least, these laminar tissues. The inflammation of these laminar tissues results in varying degrees of lameness (see question regarding stages of laminitis).

The terms foundering or foundered usually refer to the more chronic or long-term consequences of laminitis. In this case, the horse has already suffered from the acute stage of the disease and now has changes present within the foot that make it mechanically unstable. The horse will also show varying degrees of lameness; there can also be physical signs of hoof damage, as well as changes on x-rays (see question regarding stages of laminitis). Chronic laminitis and founder are often used to define the same phase.

First posted on the Internet in The Hoof Project Web Site.
This article has been reprinted with the permission of The Hoof Project.


]]> (Ilka Robertson, DVM and David Hood, DVM, PhD) Laminitis & Founder Wed, 13 May 2009 05:46:38 +0000


ormally the F&HRC doesn't post links to a web site or organization which sends in a request, because we receive about 100 requests a month for such links. If we posted even half of them, soon we'd be nothing but a Yellow Pages of equine sites. That's what Google is for.

There are exceptions. Katy Watts' site, SaferGrass.Org is an important resource regarding proper equine nutrition, and its relation to laminitis. Therefore, we urge everyone interested in this crucial subject to visit her site. You won't regret it.

Visit: SaferGrass.Org

]]> (Baron) Laminitis & Founder Fri, 23 Jan 2009 00:59:35 +0000
Bringing Back the Foundered Hoof

In terms of it's potential for long, drawn-out agony, laminitis is the worst malady that can strike a horse. Unless somehow the owner and vet manage to catch and reverse the process of inflammation and deterioration in the laminae -- the tissues that connect the coffin bone, or third phalanx (PIII), to the inside of the hoof wall -- early enough, the coffin bone sinks within the hoof capsule, turning laminitis into founder.

Once that happens, in some way even a horse with acute colic is luckier. But a severely foundered horse, whose coffin bone rotates out of alignment and descends, perhaps far enough that it goes through the sole, may go on and on in severe pain until his owner decides that putting the horse down is the only decent thing to do.

Even if the acute problem eventually subsides, the horse is likely to be left with a considerable residue of chronic discomfort. He may habitually stand rocked back to minimize the amount of weight he puts on sore front feet; his bones may be so misaligned that every step he takes puts some degree of unnatural stress on them; and periodically he may feel even more pain when inflammation flares up in the old trouble spots.

Within the last twenty years, however, the chances of catching laminitic deterioration in time and turning the condition around before things get that bad have greatly improved -- thanks to advances in veterinary research and in my own field of farriery, and thanks also to a growing understanding and cooperation between the two fields. We still don't fix every one of these horses, but we are fixing a lot of them that we wouldn't have twenty years ago.

In this article I'm going to tell you about some of the changes in treating, in technology, and in the thinking behind both that have enabled us to do so much better than we used to (though still not as well as we'd like). I'll also be talking about how, if laminitis strikes your horse, you can take advantage of these better treatment methods and help them work to best effect.

Heart-bar shoes and hoof-wall resections, two of the advances I mentioned earlier, are part of the reason for our improving record with victims of laminitis, and I'll be telling you about them. But besides all the insights and improvements that veterinary science and farriery have come up with, there are two other crucial factors that affect a horse's chances of surviving and returning to some degree of soundness. One is the horse himself -- how much he's suffered, how much infection is present in his feet and elsewhere in his body, and how much of a survivor he is -- how much he's willing to keep fighting. The other, as you'll see in the comeback program I sketch out, is a partnership of owner, farrier, and veterinarian committing themselves to work together to give the horse the best chance they can.

The commitment is demanding, as I try to make clear to anyone who calls in to work on a laminitic horse: It's expensive, it may need to go on for months or years--for the rest of the horse's life in some cases -- and it carries no guarantee of a positive outcome. But in the horses I've worked with that have come back, it has been a major reason for our success.


Before going into the "how" technicalities of working with a foundered horse, I want to tell you a little about the "why" -- because besides being the worst malady that can befall a horse, laminitis has long been one of the least understood.

For hundreds of years, horsemen understandably saw laminitis as a problem of the feet; when a horse foundered, they concentrated on fixing his feet. Along the way, they came up with a number of treatments--hoof casts, nailing the shoes on backward, stretching down the tendons, and so forth -- that became accepted (and were written down in books, some dating back to the 1850's or before) as "standard" because the produced relief in some cases, although they did nothing (or even did damage) in others.

Those some treatments got carried on to the next generation of books and the next. Even today some horsemen and farriers -- and some veterinarians who don't see many horses, and who don't manage to attend many continuing-education courses or come to national conventions -- regard them as appropriate for any foundered horse.

Despite such lingering misunderstanding and misinformation, however, most veterinarians, farriers, and horsemen have come to understand that in laminitis, the feet are normally the secondary problem. While some cases of are caused mechanically, by long work on hard surfaces or by trimming and shoeing that put excessive stress to the feet themselves, others -- those with the greater potential for threatening feet and life -- result from some internal problem that is causing toxic substances called endotoxins to collect in and interfere with blood supply to laminae. In these cases, until we correct that "something", we can't have a hope of correcting the laminitis.

The breakthroughs we've achieved in our understanding of laminitis have come as we've become increasingly able to observe what is going on inside the horse. For example, horsemen long thought (and every book on equine physiology used to say) that the frog pumps blood through the foot. The first researchers who said that it didn't, and that it was actually more of an arch support than anything else, nearly got run out of town. (As the late Louis L'Amour, the Western novelist, once pointed out, "Ideas are welcome as long as they do not contradict theories on which scholarly reputations have been erected.") This revised view of the frog's role gained acceptance only when researchers were able to examine blood circulation through the foot by means of scintigraphy -- visually following the progress of a small injected radioactive substance through the vascular system of the foot.

Like veterinary science, farriery has been and is still learning and revising old ideas about laminitis. The heart-bar shoe (its name comes from its shape -- a V-shaped piece of stock extends from the heels in along the frog to a point about three eighths of an inch short of the apex) has been around for years; the earliest I know of is in a book published in the 1820's, where if was called a "veterinary frog-support plate." Still, there was terrific resistance when we first started using it on laminitic horses. Now, though, there are veterinarians and farriers -- a couple on the East Coast, two or three in the Southeast, two or three in Texas, three or four on the West Coast, as well as some in Canada, Mexico, England, Scotland, and Australia (where some of the best recent work on understanding the vascular system on the foot has been done) -- who have studied it and who have had really good results using heart-bar shoes on hundreds of foundered horses. The number of successes is important because (as all the recent brouhaha about cool-temperature nuclear fusion has reminded us) research is no good unless the results can be reproduced. Enough different veterinarian-farrier teams have had success in enough cases that we believe we can say we have a standard method for working with a laminitic horse.

I'll show you how that method works, including your role as owner, for three hypothetical horses: The fellow who got into the grain bin last night and whose problems haven't progressed beyond simple laminitis; the foundered horse, in whom the coffin bone has begun to tear away from the laminae and descend; and the horse in chronic founder, whose disease is no longer active (except, perhaps, for an occasional bout of inflammation) but who's living with damaged feet. In the first two, as you'll see, our aims are threefold: to stabilize the coffin bone and prevent it from descending any farther than it already has, to relieve the pain caused by inflammation and the swelling that typically accompanies it, and to prevent the infection that might set in if problem sites were not found and treated. In the third, the deterioration is basically done; our focus is on making the horse comfortable.

(Before we go on, however, let me point out that while most veterinarians and farriers are aware of this treatment method today, not all of them have had the opportunity to work with it. And as Dr. Jim Coffman at Kansas State University once said, "Don't just draw a heart-bar shoe on a napkin, hand the napkin to your farrier, and ask him to go put a hear-bar shoe on a horse -- you'll be sorry if you do." If you have a horse with severe laminitis and your own veterinarian or farrier hasn't worked with the techniques I'm talking about, you may want to call the nearest veterinary school with a large-animal clinic, such as Texas A & M or the University of Pennsylvania's New Bolton center, for a reference. As the health consumer, you have a right and responsibility to ask questions, and if the answers you hear leave you uneasy -- if, for example, someone proposes putting a hoof cast on your horse who's newly foundered -- you should look for a second opinion.)


The evidence is clear when you arrive at the barn: Your horse is out of his stall and in the feed room, the grain-bin lid has been nosed open, and the bits of grain scattered about the floor and sticking to his muzzle seem to outnumber the few left in the open feed sack. But he's having little joy from his night of stolen delights -- he's extremely stiff, glued to the ground, and his pulse is pounding. He may seem to be trying to keep his weight back toward the rear, because his front feet (which normally carry about sixty percent of a horse's weight) feel especially tender. His insides are in an uproar, with the carbohydrate overload he's taken in working all sorts of havoc on the natural chemistry of his gut (although he probably won't be running a fever of showing signs of diarrhea or constipation).

Your first step, of course, should be a call to the veterinarian. If he arrives quickly enough, he may be able to reverse the problem with medication while it is still just a chemical one. While you're waiting for the vet to arrive, though, you can make the horse more comfortable if you apply a temporary frog support. At this point only a small percentage of laminae (if any) are likely to be damaged; if you support the frog from below now, you may prevent further tearing.

The material I recommend for this kind of first aid is indoor-outdoor carpeting. Cut it in triangular pieces the shape and size of the frog (with a little extra at the base to go up over the heels), stack enough pieces on the frog that the pile projects a quarter to three eighths of an inch beyond the bearing surface of the foot, and tape the support up around the hoof. If you don't happen to have indoor-outdoor carpeting, you can tape a roll of gauze under the frog instead; just don't use anything hard or unyielding, such as plywood, which could create additional problems by applying too much pressure. (You can buy temporary frog-support pads, but they're expensive, they're not reusable on any other horse, and I don't think they do any better job than indoor-outdoor carpet does.)

Once the veterinarian arrives, he'll administer medication to counteract the internal effects of your horse's binge; he'll instruct you to call him immediately if you see any recurring signs of discomfort. (He may warn you to be particularly watchful fifteen to thirty days after the original incident, which is the time abscesses typically take to form if a foot has any dead tissue entrapped within it.)

Unless the x-rays show a change form normal bone position -- which they probably won't if this is in fact a simple case of carbohydrate overload and you've caught it early enough -- the vet probably won't suggest having the farrier for anything particular for the foot. If there is change, he may confer with the farrier about putting heart-bar shoes (which I'll go into in more detail below, under "The Long Haul" -- because a long haul is what you'll be facing).

If you do detect a return of soreness, it's time to call the vet again. He'll open and drain any abscesses he finds (more about this below, too), and he may run blood counts to make sure no previously unsuspected infection is complicating your horse's recovery.


While a simple carbohydrate overload may not turn into founder if it's caught early enough, I regard every case of laminitis as an emergency -- because the crossover line is a very thin one, and a horse who's gone into founder is a horse in real trouble. This is where all the time and expense and potential heartbreak come in -- not so much in the initial day or two, but in the ninety to 120 days (or more) of intensive care the horse is to need to survive and come back. And this is where I try to do a lot of work up front, making people aware of the kind of commitment they're going to have to make -- in terms of time, money, and cooperation with the vet and farrier -- to have a chance of bringing back the horse to some degree of soundness.

Many of the foundered horses I get called in on are those in which the condition had progressed so far -- for any of a number of reasons, including inappropriate treatment -- that they have no hoof left at all; they're lying in the stall, covered with decubitus ulcers (bed-sores). These horses are the ones that have the least chance of being saved. I spend a lot of time with the owner of a horse like this (and with his regular veterinarian and farrier), making sure he understands that this is the horse's last chance, that it's going to expensive -- at least $12 or $15 a day in bandaging costs alone if the horse requires a hoof-wall resection, not to mention all the rest of the fees -- and that there's no guarantee of success, no matter how hard we try. All I can do is promise him that the vet and I will give it 110 percent, and that if the owner will work along with us we'll see where we are after, say, twenty days or so.

That extreme picture isn't where things start off, of course, so let's begin talking about founder at the beginning -- with a horse whose treatment begins fairly early but who has more go wrong internally than did our grain-bin raider.

A horse whose coffin bone has started tearing away from the hoof wall needs both medical and mechanical attention: from the vet, who works on identifying and correcting the underlying condition that's creating laminitis, and from the farrier, who concentrates on stabilizing the bone and keeping it from dropping and farther. If that bone is stabilized early, when maybe only fifteen or twenty percent of the laminae have been damaged, the rest of them are less subject to fatigue and tearing, and less likely to swell and shut off circulation to the rest of the foot (a major cause of tissue death or necrosis, which can actually cause the hoof to sough off).

One reason for regarding every case of laminitis as an emergency is the fact that there's no way to tell how quickly a horse may founder. I've known cases where an unsupported third phalanx has detached completely and come through through the sole, without even rotating (a condition called "sinker," which I'll tell you more about shortly), in as little as eight hours. That's why I recommend applying a temporary frog support while you're waiting for the vet to look at any horse whose feet have come up sore, and why I put heart-bar shoes on any horse who comes to me with laminitis as soon as I see the x-rays and know how much support he needs. (Given the amount of work I've done in this area and the relationship I have with the vets I work with, most of them simply give me the x-rays and say, "Burney, go and put a set of heart-bars on that horse." If either the vet or the farrier isn't so experienced in this area, the two of them would want to do more conferring beforehand.)

The Heart-Bar Shoe Fix -- Stabilizing the Bone

Each heart-bar shoe has to be built individually -- even different feeton the same horse are likely to show different degrees of the problem. If a radiograph shows that the bone is still normally positioned, even though there is some swelling of the laminae, I elevate the heart-bar portion of the shoe so that it puts no more than 1.5 to 2 millimeters (about the height of a quarter and a dime to two quarters) of support under the frog -- I don't want to run the risk of cutting off circulation and causing pressure necrosis. For the same reason, I'm careful not to let the shoe touch the sole.

The heart-bar shoe I put on a horse whose hoof wall is in tact and whose laminitis is in an early stage is made out of half-round stock with a toe turned up in front like a sled runner. That moves the fulcrum point for the foot back to where it's nearly right under the point of the third phalanx, so that when the horse moves forward, he needs less energy -- and puts less pull on the bone -- to break the foot over.

Normally the horse walks off more comfortably as soon as he's had heart-bar shoes put on. If we're lucky, that may be the end of the problem, although the owner should keep keep an eye out for soreness, and the heart-bars should be reset (and the shoes replaced if changing foot shape requires it) every thirty days for the next six months or so. Their horse should also be given plenty of chance to exercise, since exercise stimulates circulation and so brings the tissues in his feet the oxygen and other nutrients they need for repair.

I like to have the horse radiographed when I reshoe at the end of the first thirty days. I want to see whether there's been any change in the position of the bone and how I may need to change the setting on the support bar. If I see no change then, and if his condition progresses smoothly, I may not ask for new x-rays when I reshoe at the end of sixty days -- but I will want them again at the end of the third month to see if he's actually lost any bone (a problem that takes ninety to 120 days to show up). If he hasn't, his chances of coming back athletically sound are good.

Six months after the initial shoeing, I may try a horse out with half-round shoes without the rolled toe, or even normal shoes -- and let him go back to them permanently if he walks off comfortably. If he doesn't, though, he may always need the support of a heart-bar shoe -- just as some people always need arch supports in their shoes.

Abscess Drainage and Hoof-Wall Resections

Unfortunately, with a lot of horses, things don't go as smoothly as I've just described. There are many problems that can appear along the way; the sooner they're detected and corrected, the better the horse's chances.

For example:

  1. The horse walks off fine, but fifteen to thirty days later he comes up really lame in one foot. There's no need to panic; as I mentioned earlier, this is just about the time required for an abscess to form if some dead material (probably tissue crushed by the descending bone, or torn laminae too badly damaged to be repaired) is entrapped within the foot. You should call your veterinarian, who will radiograph the foot again and compare the x-ray with his earlier ones to see how much swelling is present. If there's not much, he (or the farrier, depending on the vet-farrier relationship) may simply take off the shoe, open a small hole in front at the junction of the distal laminae (the white line) and the horny sole, let the abscess drain and then put the shoe back on. (This early in the going, the abscess should be aseptic -- the serum that flows out should be just clear, pale yellow, with no odor.)
  2. The same problem may show up in the other foot at a later date; if so, the vet and farrier will probably follow the same procedure.

  3. In some cases, simply opening a small hole is not enough to relieve pressure on the laminae and clear up an abscess. The horse may need to have an anterior hoof-wall resection -- removal of part of the front hoof wall, which not only gives swollen tissue room to expand without shutting off blood supply to the laminar corium (the "nail bed") and the bone but also allows access to any necrotic tissue trapped between the coffin bone and the hoof wall. (Systemic antibiotics won't help the problem here. The whole reason you have a problem is that swelling has shut off blood flow -- so a systemic medication just isn't going to get where it needs to go.)

  4. The hoof-wall resection (again, something performed by a qualified farrier under a vet's guidance) is a serious procedure, involving a convalescence of ninety days to a year. During the first sixty to ninety days, the horse will need daily soaking and bandaging of the foot, regular exercise, diet supplementation, visits from the farrier to keep the hoof trimmed appropriately as well as to reset the shoes, and (less frequently) visits from the vet. The owners role in bringing the horse through this procedure is critical; if he doesn't follow the advice of the vet and farrier, and follow up on all the tasks they assign him, everybody's efforts are wasted.

A correctly performed hoof-wall resection is basically bloodless and painless -- it's not surgery, but more like the removal of a fingernail. (It may not look bloodless at first if, as happens in a lot of cases, there is a hematoma -- a pool of accumulated blood -- trapped between the coffin bone and the hoof wall; but once that material runs out, there should be no bleeding to speak of.) Because it is a painless procedure, and because the vet and farrier need to see whether if relieves the horse's basic discomfort, no local anesthetic should be used.

Once the hoof-wall resection is completed, the horse needs frog support so that he can begin the healing process with his hoof wall and coffin bone properly aligned. If the foot is not too painful, and if the horse has sufficient hoof wall left, I normally nail on a heart-bar shoe; if he's really sore, though, I use a glue-on shoe instead (sort of a space age spin off, and a real blessing for horses in this condition). Most glue-on shoes start out as a piece of strong polyethylene plastic, eight or ten inches square. I trace the horse's foot on the pad, then use a jigsaw or band saw to cut out the basic shape and add any configuration I need for the center, like a heart-bar, adding pieces to thicken the heart-bar insert until I have the amount of support I want. Then I weld plastic tabs to the shoe and glue them to the foot. (Another option, particularly for a horse whose foot needs more protection than the glue-on shoe alone can provide, is a glue-on adaptor rim pad that can be riveted to the bottom of a steel shoe; tabs are then welded to the pad and glued to the hoof.)

Follow-Up Care

After a hoof-wall resection, the area needs to be kept bandaged until the hoof wall has regrown. I like to use Elastikon or Vetrap for the bandaging material and cover the sole with several thicknesses of duct tape to keep the bandage from wearing through quite so fast. The bandage itself simply covers the foot, much the way an Easyboot would (but don't consider using an Easyboot instead of a bandage -- it can rub the horse's heels raw if it stays on for any length of time).

As long as there is any drainage in the area, a good topical dressing to use under the bandage is sugardine: a mixture of betadine and table sugar, and something that veterinary medicine had borrowed from human medicine. (The sugar is very compatible with new tissue, not harsh and drying like some of the things we used to apply, and it draws fluids, so it promotes drainage.) Additionally, for the first ninety days or so, it's wise to keep a thick line of ichthammol around the coronary band -- for two reasons: First, the ichthammol is a drawing agent, which will draw to a head any abscesses that can't be drained through the bottom of the foot. Second, the ointment keeps the top of the hoof capsule soft and pliable, allowing maximum blood circulation to the coronary band, which is where new hoof starts to grow.

Soaking or turbulating the foot twice a day, for ten to fifteen minutes at a time -- in hot water and betadine one time, hot water and Epsom salts the next -- will help bring any lurking abscesses to a head; it also increases circulation, and it just seems to make the horse feel better. Once the foot has stopped draining (which means you no longer run the risk of trapping inside it any material that ought to come out), you can change topical medications from sugardine to merthiolate, which speeds up the process of keratinization -- turning the new tissue to horn.

Exercise, like soaking, helps the healing process by increasing circulation and encouraging drainage. In my barn, for example, as soon as a recuperating horse's hoof wall and bone are stabilized, he goes outside and stays out as long as the weather's good; he comes in (to a box stall deeply bedded in clean straw -- which is less abrasive and less likely to ball up than shavings -- or, better yet, shredded newspaper) only if the weather's bad. If you don't have that option, you should still get your horse out of his stall and walk him at least six or seven times a day, for for five or ten minutes at a time, so that he gets a total of about an hour's exercise but gets it in small increments. (Don't hang him on a hot-walker for an hour straight -- you'll do him no good at all. Giving him short periods of work over a whole day comes much closer to what nature intended).

One element of promoting hoof growth is diet -- specifically, supplementing the regular diet with methionine and biotin. Methionine is an amino acid that's essential for hoof development, and biotin seems to act as a catalyst to methionine. Most horses don't like the taste of methionine and refuse to eat it by itself, but there are alfalfa-based methionine-biotin supplements, such as Farrier Formula or Nutri-Tone, that they find much more palatable. (Don't simply feed a supplement that's high in all amino acids; what your horse needs if he's had a hoof-wall resection is something with very high methionine levels to stimulate his hoof growth).

Reshoeing a horse that's had a hoof-wall resection presents special problems. His feet feet are likely to change shape quite a bit -- the heel, which hasn't undergone the circulation squeeze that the toe has, has been growing as much as four times faster and may have started to bend forward under the foot. The farrier needs to trim the foot regularly to keep it as close to its original shape as possible, and perhaps to back up the shoe each time he resets it.


Following a resection, the horse may be a little sore at first because the repositioning of his coffin bone puts a pull on his deep flexor tendon. Muscle soreness normally decreases as he walks more; if he continues to be sore, however, especially if he's still rocking back off his front feet when he stands, you can safely figure that you're seeing foot soreness -- and that he's still got some inflammation. Any of three things could be causing this problem: The preexisting condition that caused the laminitis in the first place may still be active, the feet may still be harboring some necrotic tissue not found in the resection, or the laminae may have sealed up before all the serum from an abscess drained.

The vet or farrier will have to attend to the horse in either of the first two cases, but in the third you may be able to correct things on your own -- so you'll want to see what you can do first. You must get the horse moving briskly (if he's reluctant, have somebody snap a towel at his hindquarters), and keep him going for several minutes. If the problem is trapped serum, there's an excellent chance that this will open up the laminae enough to get it seeping again -- and the horse will immediately move more easily. Then you can go back to your routine of soaking and sugardine until you're certain you've gotten all the fluids out.

If exercise doesn't produce results, however, your next step should be notifying the vet to come out and reassess the situation. Depending on what he finds, he may decide to reopen the sole or even (though more rarely) to do another hoof-wall resection and clean out the problem area.

Sinker -- Quick and Deadly

Once in a while a horse goes into endotoxic shock so sever that it disrupts circulation to the laminae entirely. They just die and let go so fast that the bone doesn't rotate; it simply sinks straight down -- through the sole of the foot. This is the condition called "Sinker".

This kind of horse doesn't rock back on on his feet like a foundered horse; he stands square, but he's very reluctant to move -- so he may be diagnosed as having Monday-morning sickness of myositis. One way to detect that the condition is actually sinker, however, is to run your finger down the horse's leg; if it comes to the coronary band and stops there, and you find there's a distinct depression behind the top of the hoof capsule all the way around the foot -- not just in front -- you're looking at a sinker. The horse isn't in the kind of pain normal laminitis creates -- but because there's nothing holding his feet together, he'll walk out of his hoofs in thirty days if he's not treated.

A sinker should be treated with immediate application of a heart-bar shoe (if the quarters and heel of his hoof are intact) or a glue-on heart-bar device, with a rim pad as well if more height is needed for the prolapsed bone to clear the ground. Then he should undergo a hoof-wall resection. As long as he still has circulation to the coronary plexus (the "circle" of the hoof -- just above it's top, where horn growth begins) and the circumflex artery and vein, which supply the face of the coffin bone and are one of the principal routes of blood to and from the foot, there's a chance that his foot can be saved and his hoof can grow back. Time is of the essence in this kind of case. The chances grow dimmer if circulation here had been impaired, dimmer still if the horse had begun to lose bone.


At his worst, the chronically foundered horse is the fellow you see in the books: the one with the upturned toes and the feet the always hurt to some degree. Depending on how much discomfort he feels, his radiographs may show a severely deformed or remodeled coffin bone, possibly with much of its distal (lower) end gone, way out of alignment with the two bones immediately above it (the first and second phalanx) -- which means that the deep flexor tendon is also deformed. His hoof wall may look dished, the white line may be distorted and as much as half and inch wide, and he may have "seedy toe" -- a big wedge of old laminae trapped behind the hoof wall adding to his pain. A horse with less severe pain may also have seedy toe; on x-rays, the the end of his coffin bone will probably look rough -- evidence of pedal osteitis (inflammation of the bottom of the bone).

A horse with chronic founder is like somebody who's survived polio and is living with the aftereffects. He's not in danger of dying; but depending on the damage he's sustained, he can be pretty miserable. What the vet-farrier-owner team can do for him is provide constant care to make him as comfortable as possible. Anything that gets his foot up off the ground is likely to provide him some relief (he's the one kind of horse who may feel better if somebody nails his shoe on backward). Fixing his foot means doing as much as possible to return it to normal alignment -- rasping his toe back and backing up the foot with a heart-bar shoe to give support under the frog. If the deep flexor tendon has been deformed, he may need his check ligament or even the deep flexor tendon itself cut to relieve the tension on it -- decisions in which the owner must be an active and understanding participant.

A horse with seedy toe severe enough to make him lame may need nothing more than to have his toe rasped back and and a heart-bar shoe fitted to support and help realign his foot. In a few cases the vet or farrier may need to so a resection to get all the laminar wedge -- but the horse probably won't need bandaging; in his case, what's being removed is old dead tissue (a lot like a corn in a human being).

With care, even a horse with severe chronic founder can be brought back to being pasture-sound, or even riding sound in a few cases; a horse with a milder case, though, may do yet better. In either case, though, the need for care never stops. If an owner decides after a year or two that his horse has had enough special pampering, so he stops having the feet trimmed and the shoes reset regularly, he's very soon going to have himself a lame, sorry horse.

Additional Information


In most cases, a horse's laminae begin to deteriorate and die because something has made his internal chemistry go haywire, upsetting the delicate balance that normally allows dozens of different bacteria to coexist peacefully and productively within him. The "something" may be a uterine or lymphatic infection, an infection from a puncture wound, an abscess, a hormonal imbalance, kidney failure, pancreatic malfunction, allergic reaction, gastroenteritis, carbohydrate overload (the aftermath of the classic grain-bin break-in), or perhaps some cause science hasn't yet linked with endotoxemia. Whatever the cause, the results are disruption and destruction.

When a horse breaks into the grain bin, for example, lactobacillus bacteria (which thrive on carbohydrates, and which produce lactic acid) in his gut rapidly begin multiplying. The proliferating lactobacilli increase the acidity of the gut, which heightens the activity of a second acid-producing bacterial form, streptococcus. The resulting highly acid environment wipes out a whole group of other bacteria; as these organisms die, their disintegrating cell walls release endotoxins -- internally produced poisons -- which erode the lining of the intestine and so escape into the bloodstream.

The horse's body reacts defensively to the rise of endotoxin and lactic-acid levels by releasing other chemicals, including prostoglandins -- unfortunately, in such high levels that they create damage of their own, such as constricting the smaller blood vessels and closing down some normal circulatory routes. That can set off one or more additional problems, including complete circulatory collapse (leading to shock and death), colic and all it's attendant complications and dangers, and laminitis.

The laminae are vulnerable to endotoxic damage because the blood vessels that bring oxygen and nutrients to them are so fine that a very little constriction is enough to close them down. When that happens, the laminae become damaged and die in short order. As they do, the horse's coffin bone begins to break free from them; depending on how quickly and completely that happens, the bone may either rotate out of normal alignment and gradually begin descending toward the sole of his foot (founder) or may simply drop straight down (sinker -- a condition in which all of the laminae die within a very short time, before any rotation can occur).

In the early stages, laminae being deprived of circulation become inflamed and swollen, causing pain under the hoof wall that is pinching them in. Later -- normally anywhere from two to four weeks after the problem begins -- abscesses formed around the dead laminar tissue may create additional pain, especially if the fluid-filled abscess is pressing against both the hoof wall and the wedge of dead corium. And the unsupported bone itself, out of alignment and pressing down on the sole from inside, is another source of pain.

A horse who survives his initial bout with endotoxic damage isn't necessarily out of the woods. If infection sets in (a danger greatest where the bone is actually exposed, or where an abscess remains undetected long enough that it turns purulent), there is danger of the bone itself becoming infected. If severe bone infection (osteomyelitis) sets in, the only way to save the horse may be to curette (scrape) the bone to remove dead or infected areas, or even to amputate the leg -- an option few veterinarians would recommend.

© Burney Chapman

Posted here with the permission of the author
first published in The Blood Horse Magazine

]]> (Burney Chapman) Laminitis & Founder Sun, 11 Jan 2009 07:18:51 +0000