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Although it is obvious that the heel of the horse's hoof bears weight, the traditional theory of hoof function only explains that bodyweight is transferred from P2 to P3, and from P3 to the wall by the laminae. This is an incomplete explanation, because P3 does not extend, or attach, all the way back to the heels. So, how do the heels bear weight? Obviously, in addition to P3, there is another mechanism for bearing the horse's weight. Most everywhere I look in the physiology of the horse, nature has created partially redundant (overlapping) systems. There are 2 digital extensor tendons -- and the horse can get by with either one; there are 2 digital flexor tendons -- and the horse can get by with either one; when more blood pumping capacity is needed because of exercise, muscles play a greater part in pumping the blood; 2 lungs... etc. I believe nature has also provided at least 2 partially redundant mechanisms for transferring weight to the hoof. This article explores possible additional mechanisms of weightbearing by the hoof.
The traditional theory is that the weight of the horse is transferred down the bony column of the leg through the laminar attachments of P3 to the hoof wall, period. Typically, this traditional theory simply omits any mention of any other mechanism than P3 to the hoof wall -- occasionally, it is specific: "...commonly held belief that virtually all the concussive force passing through the limb is transferred from PIII to ...the wall.... (Leach 1990)" To be valid, a theory must account for all known phenomena -- yet the traditional theory does not fully explain normal or abnormal weightbearing. We do not have to look far to see that P3 cannot be responsible for weightbearing for the whole hoof -- both old and recent findings make that very clear:
It has long been noted that the heel of the horse's hoof bears weight in relation to the hoof angle. Nearly one hundred years ago Dollar (1898, p.345) noted: "In upright hoofs the heels bear less weight than in flat hoofs." Recent research confirms that the heel and toe bear weight in direct relation to the angle of the hoof. Barrey (1990, 1991) found that at a 39 degree hoof angle 75% of the weight bears on the heels, 25% on the toe; at a 47 degree hoof angle 63% of the weight bears on the heels; and at a 55 degree hoof angle, 43% of the eight bears on the heels. The traditional theory of the weightbearing mechanism of the hoof cannot account for the effect of the hoof angle on the distribution of weight from heel to toe. If weight were transferred only from P3 to the wall, then the amount of weight borne at the heel and toe would be in proportion to the distance of the center of rotation of the distal end of P2 from toe to heel, and would not change in relation to the hoof angle. The fact weight borne at the heel and toe is related to the hoof angle, but not to the shift in position of the center of rotation, shows that, in addition to the transfer of weight from P3 to the wall, some other mechanism is involved.
Research also shows that the weight is not borne evenly across the whole bottom of the foot, but concentrated at the heels and toe, while skipping the quarters. "In all but one horse the weight (pressure) was born on the toe and heel where the bar joins the wall. Therefore, the previous view that weight is distributed equally around the wall was not supported by this study. (Leach 1990, p. 125)" How can weight be concentrated at the toe and heels if the weight is transferred only from the coffin bone to the wall, and the coffin bone ends at about the quarters? The traditional theory cannot account for this finding. This finding indicates that the mechanism which transfers weight from the bony column to the hoof wall cannot be a single path from P2 to P3 to the wall. There must be an additional weightbearing mechanism at work.
Look at figure#1. We have a problem here (Young & Novak 1991). In this case of DDF tendon laxity, only the heel -- and not the toe -- of the hoof is bearing weight. The area of ground contact of the hoof is centered around a point directly below the center of rotation of the distal end of P2. The area of weightbearing is also centered around this point (Leach 1990).
In each limb, the weight of the stationary horse is transferred from the limb to the hoof vertically down from the center of rotation of the distal end of P2. Note that in this case, P3 is not under P2. P3 is entirely in front of P2. P3 and P2 are not even in contact. Furthermore, in figure #1, the hoof directly below P3 is not in contact with the ground. Therefore, P3 cannot be supporting all -- or possibly any -- of the weight of that limb. Yet the hoof is bearing weight. There must be some other mechanism, than just the attachment of P3 to the wall, at work.
This radiograph speaks for itself (Figure #2) -- the coffin bone was removed and the hoof still bears weight. This is one of 2 similar cases (Redden 1992). Obviously, there must be something besides the coffin bone involved in transferring bodyweight to the hoof wall.
The most obvious candidate for an additional weightbearing mechanism in the hoof is the navicular bone -- after all, it is nearly half of the articular surface of the coffin joint. During the first half of the weightbearing phase of a stride, or while standing, some weight is exerted on the navicular bone -- when the DDF, and the navicular suspensory ligaments (the rest of the navicular supporting apparatus) are under little tension -- and therefore unable to support it. The only thing supporting the navicular bone at this time are the chondronavicular ligaments, and possibly the digital cushion. The chondronavicular ligaments might be able to both support the navicular bone during weightbearing and to transfer weight to the wall at the heels -- if so, they could be the missing link that explains what our current theory does not.
Oddly, few texts even mention these navicular to collateral cartilage ligaments. Dr. Doug Butler's (1974, p.106 1985, p.115), and Hickman Humphrey (1985) are some of the few texts that mention these chondronavicular ligaments -- however briefly. Leach (1991) mentions them, and Rooney (1991) confirms their existence. Butler (1985, p.115) notes: "The navicular ligaments suspend and support the navicular bone. ...The lateral cartilages are joined to the pastern, navicular, and coffin bones by numerous small ligaments."
It is these chondronavicular ligaments between the navicular bone and the collateral cartilages that might be the key. If they didn't exist, then the navicular bone could not bear weight and transfer it to the wall. Adams (1974), Hickman (1977), Lungwitz (1966), Stashak (1987), etc. make no mention the chondronavicular ligaments. However, the navicular bone's role in weightbearing has been described in several texts: Smythe (1972, p.177) says: "While the horse is standing erect the pressure upon the navicular bone is practically nil, but it may become very severe whenever the horse lands upon one foot, as it must do, and particularly so whenever the first foot to come to the earth is advanced well in front of the body, as happens when a hurdle is cleared at speed." Bracy Clark (1809, p.16-7) was possibly the first in this observation (though he reversed the order of weightbearing on the navicular and P3):
"The weight of the horse... passes to the foot, taking a primary bearing on the coffin bone, which it distributes over the inside of the hoof.... Next, in a secondary manner, the weight is received on a smaller bone placed in contact with, but movable upon, the coffin bone, viz. the shuttle [navicular] bone, which lying behind the former, across the more elastic parts of the foot, by its depression a share of the weight is communicated to the heels and quarters.... ...It appears therefore as though the posterior elastic parts of the horse's foot are in reality designed to receive, adjust, and balance the weight by their spring, in meeting it, whilst the front of the hoof, by its solid resistance against the ground, impels the mass when progression is required."
"One use of the navicular bone is to increase the articular surface of the [os] pedis [coffin bone]. But it is conceivable that this small articular surface of the pedis might have been increased in some other way than by the introduction of a distinct bone and other complicated apparatus, and it is evident that the value of the navicular articulation does not depend entirely on the fact that it increases the size of the joint, but that it supplies what elsewhere has been spoken of as a yielding articulation. The use of this yielding articulation is to save direct concussion. During locomotion, when the foot comes to the ground, the weight through the corona [P2] falls in the first instance largely on the navicular, which under its influence yields slightly in a downward direction; [but then he continues wrongly:] from the navicular the weight is transferred almost entirely to the pedis.... ...Briefly, then, the small dense navicular bone is enabled to form a yielding articulation in the foot, owing to the manner in which it is supported in position by the powerful perforans [DDF] tendon." However, it is clear that it is not the DDF that is supporting the navicular bone when the foot first comes to the ground. "With flat or heel first impact, the coffin joint rotates... tending to decrease tension in the deep flexor tendon (Thompson, Rooney and Petrites-Murphy 1991)." Although this decrease is counterbalanced by the opposite rotation of the fetlock joint, the tension of the DDF would not begin to increase sufficiently to bear the weight on the navicular bone until close to mid-point of the weightbearing phase -- when the fetlock stops descending. This is confirmed by Smith (1921, p.704): "If the eroded tendon of navicular disease be examined, it will be observed that the fibres are all stripped upwards, and rarely, or never downwards. This points to the greatest friction occurring, not when the bone yields under the weight, but when it returns to its place as the body, under the influence of flexor tendon, passes over the foot [i.e. breakover]."
Nor do the navicular suspensory ligaments support the navicular bone in the early support phase of the stride, or while the horse is standing. The navicular suspensory ligaments have their least tension during the first half of the weightbearing phase. They don't exert their maximum pull until just before breakover (after P2 has become vertical). Therefore, as the maximum weight is exerted on the navicular bone, neither the DDF or the navicular suspensory ligaments are in a position to support the navicular bone -- any weight thrown on the navicular bone from P2 must be supported some other way -- possibly by the navicular bone's ligamentous attachments to the collateral cartilages and hoof wall -- the chondronavicular ligaments. So while Smith assumes the navicular bone receives weight, it cannot be the DDF or navicular suspensory ligaments transferring the weight to P3 as he suggests, because they are not under tension. The navicular, if it bears weight, must transfer the weight elsewhere during the support phase of the stride.
The most simple additional mechanism needed to explain weightbearing at the heel of the hoof is that the weight is transferred from P2 to both P3 and the navicular bone -- the navicular bone transferring its share of the load to the wall at the heels by way of the chondronavicular ligaments through the collateral cartilages; or possibly weight on the navicular bone might be transferred to the collateral cartilages by the digital cushion.
Unfortunately, it is not that simple. A cross-section of the navicular bone does not show the thickening of the bone that one would expect necessary if the bone were to bear weight.
I had the chance to investigate this simple hypothesis further -- and prove to my satisfaction that it is wrong. (Dr. Rooney had told me that it was wrong all along, but I had to see for myself.) Dave Duckett, FWCF did a hoof dissection for me specifically looking for the chondronavicular ligaments. They are difficult to find because in a standard dissection they are destroyed while working your way into the hoof. In order to find them, we had to cut the hoof in half and work our way out. In this particular specimen we found 4 chondronavicular ligaments on one side, they were threadlike, and seemed incapable of bearing much weight. However, we were surprised to find that the chondrocoronal ligament was quite short, large, and directly above the navicular bone.
Also known as the Chondrocoronalia ligament (Nomina Anatomica Veterinaria 1973), appears to be the additional weightbearing mechanism that we were looking for. It appears that the chondrocoronal ligament is what transfers most of the weight to the heels. The chondrocoronal ligament is about as big around as your little finger -- so it seems quite substantial, and may be able to handle supporting as much weight as the body. The chondrocoronal ligament joins the distal ends of P2 to the collateral cartilages, and thus can transfer weight to the heel area of the hoof, and can explain weightbearing in cases such as Dr. Redden's and Dr. Young's. This appears to be the additional mechanism that is needed.
The traditional theory that P3 is solely responsible for transferring weight from P2 to the hoof wall is incomplete. There must be one or more additional mechanisms to adequately account for weightbearing at the heels of the hoof. The navicular bone appears to be unable to support much weight through its threadlike ligament attachments to the collateral cartilages.
The digital cushion, acting as a hammock, might be able to bear some weight, however the navicular bone does not show the substance one would expect of a bone which bears weight. The navicular suspensory ligaments (now called the collateral ligament of the navicular bone), part of which attach to the collateral cartilages, might also be able to support some of the bodyweight. The chondrocoronal ligaments appear to be in a position, and strong enough, to transfer the bodyweight through the collateral cartilages, to the heels of the hoof. The chondrocoronal ligaments could well explain known phenomena of both normal and abnormal hoof weightbearing that the traditional theory cannot explain. Further research will be necessary to prove this hypothesis.
Special thanks to Dave Duckett, FWCF; Allie Hayes, Horse Sense; Gina Keesling; Randy Luikart; R. F. Redden, DVM, International Equine Podiatry Center; J. R. Rooney, DVM, University of Kentucky; and Jan Young, DVM. (Their input does not imply their complete agreement.)
Adams OR., DVM. 1974. Lameness in horses 3rd ed. Philadelphia: Lea & Febiger
Barrey E. 1990. Investigation of the vertical hoof force distribution in the equine forelimb with an instrumented horse-boot. Equine Vet J (Suppl #9) p. 35-8
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Lungwitz A. & Adams JW. 1966. A textbook of horseshoeing . Corvallis, OR: Oregon State U. Press
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Thompson KN; Rooney JR; Petrites-Murphy MB. 1991. Considerations on the pathogenesis of navicular disease. J Equine Vet Sci . 11(1):4-8
Young J. & Novak B. 1991. Neonatal flexor tendon laxity. FYI 55&56:20-21
Illustration #1 -- Dr. Young's case -- Danni (courtesy of Jan Young, DVM)
Illustration #2 -- Dr. Redden's case -- coffin bone removed (courtesy of R. F. Redden, DVM)
Illustration #3 -- Duckett's dissection, showing chondrochoronal ligament.
Illustration #4 -- Vertical cross-section of hoof, about the center of the frog, showing chondrochoronal ligaments.
Illustration #5 -- Horizontal cross-section of hoof, just below the coronary band, showing chondrochoronal ligaments.
Illustration #6 -- Anatomical drawing showing navicular suspensory ligaments and chondrocoronal ligaments. (Keesling)
Illustration #7 -- Anatomical drawing showing chondronavicular ligaments, DDF, etc. (Keesling)
"Sit down before fact as a little child, be prepared to give up every preconceived notion, follow humbly wherever and to whatever abysses Nature leads, or you shall learn nothing."
Thomas Huxley (1825-1895)