Where the stain _is_ met with in the superficial layers of horn, and is quickly pared out, then the injury has been inflicted some time before, and has not been repeated. When, as is sometimes the case, layers of horn that are stained are found alternated with layers that are healthy, then we have evidence that the cause of the corn, whatever it may be, is not in constant operation. Similar indication of the age of the injury is also afforded by the colour of the lesion. A stain that is deep red is proof that the injury is comparatively recent. A distinct yellow or greenish tinge, on the other hand, is evidence that the injury is an old one. _In the Moist Corn_ we have, in addition to the blood extravasation, the outpouring of the inflammatory exudate. In the most superficial layer of the horn this may not be noticeable. As one cuts deeper into the sole with the knife, however, it will be found that the lower layers of horn are more or less infiltrated with the discharge. This gives to the horn a soft consistence, a yellow appearance, and a touch that is moist to the fingers. With the accompanying inflammation the cells in the neighbourhood of the injury are enfeebled and their normal functions interfered with. We may thus expect a corresponding interference with the growth of horn. This is exactly what happens, and as one cuts deeper still into the horn a point is finally reached when a well-marked cavity is encountered. A pale yellow and usually watery exudate fills it. This cavity points out the exact spot where the force of the injury has been greatest, where death of certain cells of the keratogenous membrane has resulted, and where the natural formation of horn has for a time been suspended. _In the Suppurating Corn_, as in moist corn, we have pathological changes due to the tissue reaction to the injury, _plus_ the addition of pus organisms. Confined within the horny box we have a discharge that, by reason of the living and constantly multiplying elements it contains--the pus organisms--is always increasing in bulk. This must be at the expense of the softer structures of the foot. Accordingly, as the formation of pus increases, we get pressure upon and final gangrene of the sensitive sole and of the sensitive laminæ of the bars and the wall. With no outlet below, the pus formation increases until finally it finds its way out of the hoof by emerging at the coronet. This in some instances it may do by confining its necrotic influences solely to the sensitive laminæ of the wall, in which case, if a dependent orifice is quickly made at the sole, the injury to the laminæ is soon repaired by the healthy tissue remaining.