3. Changes in the Tendon. - The effect of these calcareous deposits on the under surface of the bone is to produce a certain amount of roughness. Seeing that with every movement of the foot the perforans tendon is called upon to glide over this surface, it is clear that a secondary effect must be that of inducing erosion and destruction of the tendon. The point at which this usually commences is at the bottom of the depression that accommodates the ridge on the bone. With erosion of the cartilage and of the tendon at points exactly opposite each other, we have two surfaces come together that are prone to readily unite, and fibrous tissue adhesions often take place between the bone and the tendon. In some measure this accounts for the torn and ragged appearance of the tendon. Adhesions take place, and, under some small strain, are broken down. This may happen more than once or twice, and with each breaking of the adhesion between the bone and tendon, fibres from the latter are lacerated and torn from their place (see Fig. 162).

4. Changes in the Bone. - The changes occurring in the bone are essentially those of a rarefactive ostitis. These changes are described by many writers, and, whether originating primarily in the bone or not, it seems certain that extensive changes may have occurred within the bone, with but little or nothing to be noted on its outer surface. It would seem that the first change is one of congestion of the vessels of the bone's cancellous tissue. With the cause, whatever it may be, in constant operation, the congestion persists until a low type of inflammation is set up, interfering, not only with the flow of synovia in the adjoining bursa, but with the nutrition of the bone itself. As the disease progresses, there is softening and enlarging of the cancellated tissue towards the centre of the bone. The cells break up, and absorption takes place. This goes on until a large portion of the interior of the bone is in a state of dry necrosis, with, in many cases, but slight signs of mischief on the exterior of the bone.

In other cases, however, the changes in the interior of the bone are accompanied by well-marked lesions on its gliding or postero-inferior surface, and by evidences of an osteoplastic periostitis along its edges.

That an osteoplastic periostitis has been in existence is witnessed by the appearance along the edges of the bone of numerous outgrowths of bone, termed osteophytes (see Fig. 163).

Fig. 162.   A Foot With The Seat Of Navicular Disease Exposed

Fig. 162. - A Foot With The Seat Of Navicular Disease Exposed. On The Anterior Surface Of The Perforans Fibres Of The Tendon Are Seen To Be Torn Away From Their Abnormal Adhesion With The Navicular Bone, While Others Are Seen To Be Still Attached Thereto. The Surface Of The Navicular Bone Itself Exhibits Small Defects In The Bony Substance, Which Have Been Brought About By A Rarefactive Ostitis. A, The Perforans Tendon Cut Through And Reflected; B, The Sole.

The interosseous and postero-lateral ligaments of the articulation often participate in the inflammatory changes, and in many cases become completely ossified. The true articulatory surface of the bone, that articulating with the os pedis and with the os coronae, is never affected.

Causes. - In enumerating the causes of navicular disease, we shall follow the example of Colonel Smith and classify them under certain headings - namely, (1) Hereditary Predisposition; (2) Compression; (3) Concussion; (4) A Weak Navicular Bone; (5) A Defective or Irregular Blood-supply to the Bone; and (6) Senile Decay.

Fig. 163.   The Navicular Bone From A Case Of Long Standing Navicular Disease

Fig. 163. - The Navicular Bone From A Case Of Long-Standing Navicular Disease. The Erosion Of The Cartilage On Its Central Ridge Is Most Marked, And The Porous Appearance Of The Bone Thus Uncovered Points To The Existence Within It Of A Rarefactive Ostitis. Along Its Edges Large Osteophytic Outgrowths Speak Of The Effects Of An Osteoplastic Periostitis.

1. Hereditary Predisposition. - That navicular disease is hereditary is a fact that has for a long time been insisted on, and has come to be so generally admitted that we do not intend to dwell on it here. As we have said before, it is found in the lighter breeds of horses (and, according to Zundel, especially in the English breeds), and is there seen to be frequently transmitted from parent to offspring.

2. Compression. - By this is meant the compression of the navicular bone between the os pedis and the os coronae in front, and the perforans tendon behind.

In order to appreciate this explanation of the causation of navicular disease at its true value, it will be well to consider briefly the physiology of the parts in question.

The navicular bone is what we may term a complement of the os pedis. It exists, in fact, simply in order that the os coronae may have a sufficiently large articulatory surface to play upon. One wonders at first that Nature did not arrive at this by originally placing a larger bone below. Colonel Smith explains this by suggesting that this would in all probability have meant its fracture. In progression the hind part of the foot comes to the ground first, and upon the hinder portion of the articulation would fall the first effects of concussion, together with the greater part of the body-weight. A yielding joint was in this position necessary, and that formed by the navicular bone fills all requirements.

In this connection one next considers the part played by the front limbs during progression. As Zundel expresses it, they are columns of support rather than of impulsion, and, as the body-weight is thrown forward by the hind-limbs, it is the duty of the fore-limbs to receive it. The shock or concussion of the body-weight thus thrown forwards is first received by the muscles uniting the limb to the trunk, and a great part of it there minimized by their sling-like attachment. It is further absorbed by the shoulder-joint, and from there passed on to the almost vertical bony column represented by the radius and ulna, the knee, and the metacarpus. On reaching the first phalanx, a portion of the remaining force is passed on to the front of the phalanges and loses itself in front of the hoof, while the other portion is transmitted to the flexor tendons, finally to the perforans, and to the posterior parts of the foot. During progression, therefore, the navicular bone is constantly pushed downwards and backwards by the bony column, and is just as constantly pushed forwards and upwards by the resistance of the perforans tendon. This means, of course, that the navicular bone is more or less constantly subject to compression, and constant pressure, as we know full well, is a pretty sure factor in bringing about malnutrition of the parts, with atrophy or chronic inflammatory changes as an end result.

Even with the limb at rest the pressure on both sides of the navicular bone is still constant. The only circumstances under which we can conceive of it being entirely absent, in fact, are when the tension on the tendon is relaxed, and the body-weight altogether removed by the animal adopting the recumbent position.

The compression theory as to the causation of navicular disease was, we believe, first originated by Colonel Smith. He, at any rate, has laid much stress on it in his writings. If we accept it, and we see every reason that we should, then we must, with the author, admit the possibility of navicular disease arising from long standing in one position.