club foot in the horse

So-Called Club Foot in Horses
by James R. Rooney, DMV

Published in the October 1999 Issue of Anvil Magazine

Fig 1 Drawings by Lungwitz (1910).
So-called “clubfoot” has long been a vexing problem for horsemen, veterinarians, and farriers.
The term clubfoot is a misnomer for the condition in the horse and correctly refers only to a
congenital anomaly of the human foot. Lungwitz (1910) properly defined and described the
condition for the horse. There are three forms:

1. Stumpy hoof. (Figs. 1, 2) This is bockhuf, goat hoof, in German, but will be translated here as
stumpy hoof. The hoof angle is greater than normal, 60-90 degrees. The pastern is short or
appears so and is usually more or less in line with the hoof axis as seen from the side.

2. Bearfoot. (Fig.1) This is ba¨renfuss in German. The hoof angle is greater than normal, as
above, but the pastern appears longer and has a more sloping angle, “...broken strongly
forward at the coronet.” Lungwitz(1913).

3. Stiltfoot. (Fig.1) This is stelzfuss in German. It is the extreme or final case of 1. and 2. with
the foot supported only at the toe.

The major distinguishing characteristic of stumpy hoof or bearfoot — that which compels the
attention of the observer — is the consistently greater angle of one hoof as compared to the
other. The basic abnormality in all three cases is shortening of the deep flexor tendon with or
without prior or accompanying shortening of the superficial flexor and suspensory tendons.

The term “contracture,” usually used to describe these conditions, is a misnomer and will not be
used here. Tendons do not and cannot contract, either normally or pathologically. Apparent
contracture, either bilateral or unilateral, is shortening of a tendon or tendons towards the
normal rest length. The rest length is that length the tendon assumes when not under tension.

While the primary purpose of this paper is to discuss shortening of the deep flexor tendon, it is
necessary and appropriate to summarize the pathogenesis of yearling tendon shortening as well.
(The more mathematical material has been relegated to the Appendix, but that does not mean it
should be ignored.)

It must be emphasized that much of what is presented here is hypothetical and based on
gleaned experience and mechanical principles. There is no experimental data available directly
relevant to the questions examined, and it is difficult to conceive of experiments which could
reasonably be done.

Yearling Bilateral Tendon Shortening

The pathogenesis of so-called yearling contracture has been presented elsewhere (Rooney
1984, 1997). The mechanics are summarized in the Appendix. To review: with rapid weight gain,
the immature hoof is forced into a low heel, small hoof angle (as measured at the toe). This
change of hoof angle increases the tension on the deep flexor tendon by rotation of the coffin
joint. The subsequent increased tension in the deep flexor at the fetlock joint is equilibrated by
decreased tension in the suspensory and superficial flexor tendons. As the tension decreases in
these two tendons, they shorten; and, in doing so, it moves the digit into the more upright
position characteristic of yearling tendon shortening. With continuing shortening of the
superficial flexor and suspensory, the deep flexor will also shorten. While this is occurring, the
increasing body weight (weight gain), continues to force the immature hoof into a low hoof
angle.

Fig. 2 Photograph of stumpy foot of the left foot.

These changes are taking place while the tendons are still maturing, before cross-linking of the
collagen fibers has been completed. Permanent, irreparable deformity may be the result if the
shortening process is prolonged before corrective measures are taken; that is, if the tendons
become fully mature and cross-linked while in the shortened state. It is now generally
recognized that many cases of yearling tendon shortening will correct themselves if weight gain
is restricted or stopped before the process has proceeded to “knuckling-over” (stiltfoot). The
reason should be apparent from the above discussion.

The cause of bilateral tendon shortening before a year of age is due to the fact that the
immature hoof is unable to maintain a steady hoof angle while there is a rapid gain in weight.
There are, therefore, both genetic and environmental factors. The genetic factor is the rate of
maturation of the hoof wall; the environmental factor is rapid weight gain. The latter, of course,
also has a genetic component.

Unilateral or Deep Flexor (Stumpy Hoof/Club Foot) Shortening

These clinical observations are largely anecdotal from personal observation and discussions with
farriers and veterinarians.

1. The right fore foot is more often affected, about 70-80%. Both fore feet are rarely affected.
Since this condition develops in an insidious manner over time, the age of onset has been
difficult to determine, either for specific cases or in general. Most cases probably begin during
the first year of life while others may not appear until the horse is an adult. This will be further
addressed below.

2. The carpus of the affected leg is higher than the contralateral carpus.

3. The scapulohumeral angle may be smaller on the affected side.

4. The dorsal wall of the hoof may be dished.

5. The affected leg almost always stands back.

6. There may be atrophy of the musculature of the affected foreleg.

7. The breed incidence is not known. It has been reported in many (but not all) breeds, and
anecdotal evidence has suggested there may be predilection for Arabians and Arabian crosses.
Lungwitz (1910) categorically states that stumpy/bear foot is seen in all breeds and in both fore
and hind legs. I have not seen the condition in the hind legs.

There are four scenarios which can be associated with the pathogenesis of stumpy/club foot.
The final pathological pathway is always abnormal shortening of the deep flexor tendon, but this
final pathway may be reached by any of four “feeder” routes or a combination thereof.

Fig.3 The moment applicable in the study of the mechanics of flexor and suspensory tendon
shortening. See the text for explanation.

1. Pain.

If the animal is unwilling to bear weight on a painful forefoot over a period of time, the F term,
the ground reaction force in equation [1] (Fig. 3, Appendix) is too small or absent. The CEc
moment, that moment produced by the common extensor tendon and the extensor branches of
the suspensory, is not large enough to equilibrate the equation and, so, DF decreases — the
tension in the deep flexor tendon decreases and that tendon shortens. When the deep flexor
tendon shortens, the heels and quarters are lifted from the shoe or surface or, at least, bear less
weight than the toe and sidewalls of the hoof. This allows the heels and quarters to grow out,
increasing the hoof angle. With increase in hoof angle, the animal will tend to “stand back” (Fig.
4). This process can be visualized in Fig. 5, which shows via the diagram how the increase of
hoof angle causes the leg to move back under the body.

Such a scenario is likely to lead to permanent stumpy foot if the process begins during the first
year of life while the tendons are still growing and maturing. (See the discussion of collagen
cross-linking with the discussion on yearling tendon shortening, above.)

Additional factors come into play with the “standing back” position of the leg, although the
effects to be described are not great. With the leg “standing back,” the coffin and fetlock joints
are both dorsiflexed, and there is less tension in the common extensor tendon and the extensor
branches of the suspensory tendon. (Rooney, 1969) This means there is less resistance to the
tension in the deep flexor tendon, and the deep flexor tendon shortens. The “standing back”
position, then, predisposes to shortening of the deep flexor tendon which in turn allows the
hoof angle to increase. Once the process has progressed far enough, the coffin joint is moved
from dorsiflexion to palmarflexion by the shortening of the deep flexor, and the lesser tension in
the common extensor and extensor branches is dependent now only upon the dorsiflexion of
the fetlock joint.

As the reciprocal process of hoof angle increases and deep flexor shortening continues, the
affected leg is less stable, and the horse may bear even less weight on that leg — allowing the
deep flexor to shorten even more. The changes in conformation of the affected leg, listed
previously, including muscle atrophy and changes of shoulder joint angle, can be ascribed to the
“standing-back” position and less weight bearing by the affected leg.

Fig 4. The usual, normal standing position of the foreleg to the left and "standing-back" position
to the right.

2. Abnormal Wear

Owen (1975) observed the development of stumpy hoof conformation in foals confined for long
periods to horse boxes during bad weather. The foals obsessively pawed the ground, wearing
away the toe and so producing the high hoof angle which allowed shortening of the deep flexor
tendon. Again, though not specifically discussed by Owen, these foals would stand back on the
large angle hoof and exacerbate the condition as described above.

Lungwitz (1910) mentions lack of attention to trimming the feet of foals running barefoot as a
causative factor. This is akin to the Owen’s cases.

3. Environmental

First, we will consider that the animal is entirely normal before the process to be described
begins, so that only environmental factors are operating.

The foot about to undergo deep flexor shortening has too small a hoof angle and the animal is
gaining weight. This is basically the same condition as for yearling tendon shortening, with the
important exception that the hoof is more mature and able to bear increasing weight without
deforming to the smaller hoof angle characteristic of yearling tendon shortening. The shortening
deep flexor, in this case, tends to lift the quarters and heels from the surface (or the shoe). This,
in turn, allows the heels to grow because of less wear, and the angle of the hoof increases — the
opposite of the yearling situation.

Increasing hoof angle means that the coffin joint is rotating, so that tension in the deep flexor
continues to decrease. That is, the deep flexor continues to shorten. The conditions which
started this process — low hoof angle and increasing weight — are now changing to high hoof
angle with less weight being borne by the affected leg. As the hoof angle increases, the leg
tends to move to the standing back posture, which exacerbates deep flexor shortening.

It is to be reiterated that increasing weight (the ground reaction force, F, of the Appendix, Fig.
3) is an important factor in the early stages of this type of tendon shortening sequence, while
decreased weight bearing is important in the latter stages.

Fig. 5 If the heel grows out (the black portion) the normal position of the leg, shown as the
dotted lines, shifts to the new, standing back position, the solid lines.The head of the horse is to
the left

4. Inherited Stumpy/Bear Foot

The stumpy/bear foot conformation can be an inherited characteristic per se. There appears to
be no hard data in the literature, but the anecdotal experience of farriers and veterinarians
suggest that there is often a genetic component: affected mares and stallions tending to have
affected offspring. Lungwitz (1910) considered both bear foot and stumpy foot to be
congenital. While it appears probable that many stumpy feet are of congenital/genetic origin,
this may not become manifest until years later if the affected foot has been carefully trimmed
and shod in the interim. By the time the condition becomes obvious, the early stages — the
conformation at birth or pain or rapid growth — have long since changed and are unlikely to be
remembered.

Consider the foal born with a bear or stumpy foot. The stumpy leg will tend to stand back. Once
again, to repeat, in this position the coffin joint is dorsiflexing, which tends to loosen the
common extensor and extensor branches of the suspensory, while the fetlock is dorsiflexed
more than in the normal standing position. This allows the extensor branches of the suspensory
to loosen. The result is decreased tension in and shortening of the common extensor and
extensor branches. For equilibrium at the coffin joint, the tension in the deep flexor must
decrease, and the deep flexor shortens. The hoof angle will gradually increase because of less
heel wear with consequent shortening of the deep flexor tendon as already described. The
loosened common extensor and extensor branches will, of course, be tightened (increased
tension) as the hoof angle increases, but this is countered by the shortening of the deep flexor
occasioned by the increasing hoof angle.

I have not encountered reports of stumpy foot in Standardbred horses. Yearling tendon
shortening does occur in Standardbreds. Since Standardbreds share genetic heritage with a
number of other breeds which do have stumpy foot, one can speculate that it is the singular
attention and care given to the feet of many of these horses which could be the protective
and/or preventive factor.

Further to that point, anecdotal evidence suggests that stumpy foot is more common in horses
used for purposes other than racing. That could be related to the more frequent trimming and
shoeing of racing horses, both Standardbred and Thoroughbred. Racing horses are exercised
and examined frequently and kept in usually thinner condition than is typical of weekend and
show horses.

Hood et al 1997, showed with force plate studies that horses over time tend to bear weight
preferentially on the left or the right side and tend to shift weight on the diagonal. They
suggested this could be related, presumably, to genetically determined “handedness.” Horses
predisposed to stumpy foot of the right fore, for example, could be bearing more weight for
more of the time on the right fore and the left hind since weight on the leg is a factor in the early
stages of the development of stumpy foot.

Appendix

If the hoof angle is decreased as by cutting down the heels, the coffin bone is rotated clockwise
(with the horse facing left), increasing tension in the deep flexor tendon. This increase of
tension will tend to push the fetlock up and forward, the pastern moving to a more upright,
vertical position.

The moment equation for the coffin joint is, (Fig.3): DFb-CEc-Fa = 0 1. where DF is the linear
tensile force in the deep flexor tendon, CE is the linear tensile force in the common extensor
tendon and extensor branches of the suspensory tendon, and F is the ground reaction force. a,
b, and c are the moment arms, the perpendicular distances from the respective linear forces to
the center of rotation in the distal end of the middle phalanx.

The moment equation for the fetlock joint is (Fig.3) given in simplified form sufficient for
present purposes:

Tr-Ff-CLEd Ò EBe = 0

2. where T is the sum of the tensile forces in the superficial and deep flexor tendons and the
suspensory tendon. r is the average moment arm of these three tendons, acting around the
center of rotation in the distal end of metacarpal

3. F is the ground reaction force and f its moment arm around the that same center of rotation.
CLEd is the moment around the fetlock produced by the common extensor and lateral extensor
tendons. EBe is the moment produced at the fetlock by the extensor branches of the suspensory
tendon. If the fetlock dorsiflexes without movement of the coffin joint, the moment EBe is
negative (-). When the coffin palmar flexes, followed or accompanied by dorsiflexion of the
fetlock, the extensor branches slide distally, so that the moment EBe becomes positive (+).

When the angle of the hoof decreases, for whatever reason, the moment arm, a, at the coffin
joint increases and the moment equation is not in equilibrium. In order to regain equilibrium, DF,
the tensile force, in the deep flexor tendon, increases. That entails an increase of T, the tensile
force acting at the fetlock since DF is part of T. Equilibrium is then lost at the fetlock and is
regained by a decrease of tension of the superficial flexor and suspensory. As the tension
decreases in these two tendons, they shorten, and the pastern becomes more upright.

The moment arm, f, of the force, F, decreases as the pastern becomes more upright, and so the
moment Ff decreases, allowing for additional decrease of T and the pastern becomes more
upright as the deep flexor, superficial flexor, and suspen-sory all shorten.

Bibliography

1. Hood, D M, Hunter, J F, Beltz, W D, Taylor, B E, Beckham A S and Pierce (1997) J R Digital
Loading Patterns in the Normal Standing Horse. Proceedings of the Hoof Project, 37-43.

2. Lungwitz, A. Trans. Adams, J.W. (1913) Horseshoeing. Facsimile edition, Oregon State
University Press, Corvallis.

3. Lungwitz, M. (1910) Leisering u. Hartmann, Der Fuss des Pferdes. 11th Ed., Schaper,
Hannover.

4. Owen J M 1975 Abnormal flexion of the corono-pedal joint of “contracted tendons” in
unweaned foals. Equine Veterinary Journal 7:40-45.

Click here Return to Home page