The Ledge – Supporting P3
This article appeared in American Farriers Journal May/June 2014 pp 68-70
There seems to be some disagreement between hoofcare professionals as to the role of the sole in weight-bearing. To suggest that the laminar attachment of P3, with transference of the horses weight to the hoof wall, is not its major means of support seems to me as absurd as suggesting the sole should take no part in weight-bearing. The consequence
of breakdown of the laminar attachment and the loss of support of P3 is very evident when a horse suffers with laminitis, and in all but the hardest of ground surfaces, when the foot sinks into the ground, the load will inevitably be spread to the sole and the frog. However, even on hard surfaces or if shod the outer edge of the sole provides support to P3. The attachment of the sole to the hoof wall, via the white line, gives the perimeter of the sole stability, and this provides a ‘ledge’ for the border of P3 to rest on. The support provided by this ‘ledge’ is reduced in a number of situations. These relate to the thickness of the sole and the integrity of the white line junction or because of abnormal forces, either to the distal hoof wall or from the tip of P3.
It was the laminitis case shown in Fig 2 that first drew my attention to the importance of this. By the time I attended this case, P3 had sunk in both front feet and the hind feet were also badly affected. For five weeks, the horse appeared to be progressing well, but at six weeks, it became severely lame on this hind foot. In the specimen, one can see that the ‘white line’ produced prior to the laminitis is intact, and still firmly attaches the perimeter of the sole to the hoof wall, but as this has grown down, the tip of P3 has ‘slipped off the ledge’ and is about to penetrate the sole. The layers of sole, that are still evident in the sole periphery, have broken away behind this, to leave a thin sole that cannot support P3.
All too frequently, one hears of a bad case of laminitis that has reportedly settled down but when the horse is turned out at 6-8weeks has ‘crashed’ and apparently had a relapse. It seems likely to me that many of these cases will not be due to a recurrence of active laminitis but due to the increased mechanical forces coinciding with the ‘ledge’ growing down or following deviation of the dorsal wall. At this point, P3 loses this extra support, and it is the mechanical effects of this that causes further breakdown of the laminae and the tip of the bone to press down directly onto unsupported sole to cause the ‘relapse’.
Although not so dramatic or acute, a loss of support of the ‘ledge’ also occurs in circumstances when the laminae are still intact. In situations where the distal hoof flares, the wall and ‘white line’ move away from P3, so that the solar border of P3 rests not on the perimeter of the sole but on the more flexible sole inside this. This part of the sole is not as well supported and is more liable to bend under the pressure from the distal border of P3, and this allows the bone to sink lower relative to the hoof wall. This is sometimes referred to as ‘distal descent’ of P3.
A similar situation can occur in an upright foot or in a club foot, when there is distal flare of the dorsal wall, and also in the foal as its initial ‘foal hoof’ grows out at three to four months. In the club foot, it is a combination of the forces on the dorsal wall that cause it to deviate and tightness of the deep digital flexor tendon increasing the pressure on the tip of P3 that can overcome the effectiveness of the ‘ledge’, with the result that the tip of the bone presses down inside the perimeter of the sole.
When the foal hoof grows out at the heel, the rest of the wall loses strength and the hoof often deviates and bends forward, so that P3 loses support from the ledge at the toe. This may explain why many cases of ‘ballerina syndrome’ occur at this stage. As the tip of P3 loses the support of the ‘ledge’, the pain caused by pressure directly on the sole may lead to deep digital flexor muscle contracture, which itself can be painful due to anoxia. This causes tightening of the tendon, so that the heel is lifted and held off the ground.
If the loss of support of the ledge occurs in these situations, when the ‘white line’ is intact, then it will be worse in cases when the white line is damaged. Although ‘white line’ produced prior to laminitis grows normally, when laminitis has progressed to a chronic stage, or possibly when a horse is insulin resistant and has low-grade laminitis, the terminal papillae become distorted and produce abnormal ‘white line’, which reduces the effectiveness of the support provided to P3. In other situations, the support provided by the ‘ledge’ may be reduced if the white line is affected by dietary imbalance or infection, as in white line disease.
In the situations that I have described, the edge of the bone will no longer be supported adequately by the ‘ledge’ and will be resting on the more flexible sole in the affected area and the horse may be lame, or if less affected will be seen to be ‘ouchy’ when walking on uneven or stony ground.
Of course, the ideal situation is for a foot to maintain a functional ‘ledge’ but in these cases described above, this support has been reduced or lost. Some people will deal with these situations with the horse barefoot and others with a variety of different hoof-wear, but whatever method is used the aim has to be to assist the structures that support and protect the solar border of P3, to reduce the forces acting on the hoof wall and to reduce the load on the tip of P3.