Fibrosis and ossification of the heel cushion were classified as metaplasia, because these processes were considered an adaption to non-physiological strain of the heel. As the infection of the RU spreads, the tuberculum flexorium may play a central role. In advanced cases, an inflammation-related weakening of the bone tissue can lead to a pathological fracture with avulsion of the deep digital flexor tendon. Secondary infection of the distal joint may occur subsequent to any avulsion of the tendon in combination with opening of the joint cavity. More frequently, the infection is likely to have expanded from the insertion point of the joint capsule to the subchondral bone to ultimately infest the joint cavity. Changes in the bursa podotrochlearis, the common digital flexor tendon sheath and the pastern joint are assumed to develop as a consequence of arthritis in the distal joint.