Definition. - Chronic inflammatory changes occurring in connection with the navicular bursa, affecting variously the bursa itself, the perforans tendon, or the navicular bone, and characterized by changes in the form of the hoof and persisting lameness. The disease is commonly noticed in thoroughbreds or in horses of the lighter breeds, and is but seldom observed in heavy cart animals. Usually it is met with in one or both fore-feet. Although of extremely rare occurrence, it has been noticed in the hind.

History. - To English veterinarians appears to belong the credit of discovering navicular disease. As early as 1752 we find one, Jeremiah Bridges, in 'No Foot, No Horse,' drawing attention to 'coffin-joint lameness,' and advocating for its treatment setoning of the frog. It appears, too, that Moorcroft, prior to his departure for India in 1808, was acquainted with what was then known as coffin-joint[A] lameness, having drawn attention to it in 1804 in a letter to Sir Edward Codrington.[B] In 1819 Moorcroft made it even plainer still that he was fully acquainted with what we now know as navicular disease. This we learn from a letter written by him to Sewell, in which he laid claim to being the originator of neurectomy. In this letter he says:

[Footnote A: The coffin-joint at this time included the navicular bursa.]

[Footnote B: Percival's 'Hippopathology,' vol. iv., p. 132.]

'On dissecting feet affected with these lamenesses, the flexor tendon was now and then observed to have been broken, partially or entirely, but more commonly to have been bruised and inflamed in its course under the navicular or shuttle bone, or at its insertion into the bone of the foot. Sometimes, although seldom, the navicular bone itself has been found to have been fractured; at others its surface has been deprived of its usual coating, and studded with projecting points or ridges of new growth, or exhibiting superficial excavations more or less extensive.'[A]

[Footnote A: Ibid.]

Pathology and Point of Commencement of the Disease. - The exact position in which the diseased process starts has for a long time been a subject of discussion, and even now it is doubtful whether the point has been definitely settled. To mention but a few among many: We find Mr. Broad, of Bath, strenuously insisting on the fact that the disease commences in the interior of the navicular bone. Just as strenuously we find the editor of the journal in which the matter is being discussed, the late Mr. Fleming, asserting that the disease commences in the bursa.[A] Others, too, hold that the disease commences primarily in the tendon. Wedded to this view was the discoverer, Mr. Turner, of Croydon; while Percival commits himself to the statement that it is either the central ridge or the postero-inferior surface of the navicular bone, or the opposed concavity in the perforans tendon, that shows the earliest signs of the disease. The observations made by Dr. Brauell, the first Continental writer to fully describe the disease, led him to the statement that neither the bone nor the bursa was the invariable starting-point of the trouble, but that usually it commenced in inflammation of the bursa itself.

[Footnote A: Percival's 'Hippopathology,' vol. iv., p. 132.]

Without, therefore, committing ourselves to an expression of opinion as to the precise starting-point of the affection, we shall describe the pathological changes occurring in navicular disease as noted in (1) the bursa, (2) the cartilage, (3) the tendon, and (4) the bone.

1. Changes in the Bursa. - Upon the internal surface of the bursal membrane is first noticed a slight inflammatory hyperaemia, accompanied by more or less swelling and tumefaction, owing to its infiltration with inflammatory exudate. The portion covering the hyaline cartilage of the navicular bone has lost its peculiar pearl-blue shimmer, and become a dirty yellow.

Remembering that the bursal membrane is a synovia-secreting one, and bearing in mind what happens in ordinary synovitis and arthritis (with which, of course, this may be very closely compared), we shall first expect changes in the bursal contents. It is highly probable, though difficult of proof, that in the very early stages the chronic inflammatory stimulus has the effect of increasing the flow of synovia. In every case, however, where it can with any certainty be said that navicular disease exists, it is too late to meet with this condition. The disease has then progressed until destruction of the secreting layer of the bursal membrane has been seriously interfered with, and in this case we find a distinct deficiency in the quantity of synovia in the bursa. In advanced cases it is even found that the bursa is absolutely dry.

2. Changes in the Cartilage. - Directly that portion of the bursal membrane covering the cartilage is the subject of inflammatory change, the cartilage itself, by reason of its low vitality, soon suffers.

Under a process, which we may term 'dry ulcerative,' the cartilage covering the ridge on the lower surface of the bone commences to become eroded, and in appearance has been likened, both by English and Continental writers, to a piece of wood that has been worm-eaten (see Fig. 161).

Fig. 161.   Navicular Bone (Postero Inferior Surface) Showing The 'Worm Eaten' Appearance Caused By Erosion Of The Hyaline Cartilage, And Commencing Rarefactive Arthritis

Fig. 161. - Navicular Bone (Postero-Inferior Surface) Showing The 'Worm-Eaten' Appearance Caused By Erosion Of The Hyaline Cartilage, And Commencing Rarefactive Arthritis.

'At this stage, or much earlier' - we are quoting Colonel Smith, A.V.D. - 'may be found calcareous deposits in the fibro-cartilage and the bone. They are scattered like fine sand here and there, generally across the inferior half of the face of the bone; they are sometimes numerous, frequently scanty, occasionally entirely absent. The amount of calcareous degeneration depends upon the lesions present. If much destruction of bone exists, there will be but few calcareous deposits; whilst if there are many calcareous deposits, there may be but slight ulceration of bone tissue, and perhaps none at all. In fact, I have held the opinion, and see no reason to modify it, that calcareous deposits are safeguards against caries.'[A]

[Footnote A: Journal of Comparative Pathology and Therapeutics, vol. vi., p. 195.]