The continued, inflammation thus kept in existence has the effect of rendering the skin and subcutaneous tissues in the neighbourhood greatly thickened and indurated.  This in time leads to a tumour-like enlargement, and causes the structures of the coronet to greatly overhang the hoof.  At the same time the constant inflammation has made its stimulant effects noted in a great increase in the growth of the horn of the wall.

Although more abundant, however, the quality of the horn is deteriorated.  The perioplic ring has become obliterated, and the varnish-like appearance of the healthy wall destroyed.  Cracks and fissures in its surface are numerous, and sometimes deep enough to lead to exposure of the sensitive structures beneath, complicating the quittor with a sand-crack of a peculiarly objectionable type.

Pathological Anatomy of the Diseased Cartilage.—­The bulk of observers appear to agree in the statement that in quittor the necrotic cartilage is pea-green in colour, and recognise it by that characteristic.  In size the necrotic portion thus recognisable varies from the tiniest speck to a portion the size of a horse-bean.  Commonly, however, it is about as large only as a pea.  It is seen to be more or less detached from the rest of the cartilage, to which it is adherent by one of its extremities only.  In general appearance we can best liken it to the split half of a green pea, whilst others have compared it with the green sprouting of a seed.  The portions of cartilage nearest the necrotic piece are also slightly green in colour, thus indicating that here also the diseased process has commenced.  This peculiar change of colour in the affected cartilage is of great importance to the surgeon.  It enables him when operating to distinguish with some degree of certainty those portions of the cartilage which are healthy and those which are not.

(b) Necrosis of Tendon and of Ligament.—­This complication of quittor is, as we have said before, treated by other writers as a distinct form of the disease, and described by them under the heading of Tendinous Quittor.

This simply means, of course, that the diseased process has extended to either of the flexor tendons, to the tendon of the extensor pedis, or, perhaps, to the ligaments of the pedal articulation.

Of the flexor tendons, the perforans is the one commonly attacked, by reason, of course, of its more superficial position.  At times, however, especially when its aponeurotic expansion is diseased, the necrosis of the perforans spreads until the aponeurosis is eaten through and the phalangeal sheath penetrated.  Septic materials gain entrance thereto, and commence to multiply.  In this way the flexor perforatus is invaded, and comes to share in the diseased process.

The extensor pedis is usually attacked by extension of the disease from a necrotic cartilage, or results from the infliction of a severe tread in a hind-foot.  In this case the diseased structure has nothing between it and the articulation, the synovial membrane in one position actually lining its inner face.  The result is that a condition of synovitis is easily set up, and the case aggravated by that and by arthritis.