Remodeling of the navicular bone in response to exercise--a controlled study

摘要

Although navicular disease has been recognized as a cause of lameness in the horse for more than 200 years, there still remains widespread disagreement among investigators as to the pathogenesis of the disease. Predisposing factors, such as geneticpredisposition, poor conformation, a large bodyweight to hoof size ratio, and improper shoeing have been suggested. Unreliable diagnostic methods, as well as the lack of a reproducible model, have hindered progression towards full understanding of the disease. Many lesions are associated with navicular disease in the horse, including fibrocartilage erosion on the flexor surface of the bone, rarefaction and ostitis of the cortex, chronic synovitis/bursitis, and tearing of the fibers of the deep digital flexor tendon, associated with cavitation and degeneration of cancellous bone. Wright et al. described full thickness defects in the palmar surface fibrocartilage, palmar cortex erosion, medullary lysis, deep digital flexor tendon (DDFT) surface fibrillation, and DDFT core lesions and adhesions between the DDFT and the navicular bone in horses with navicular disease. These changes were not seen in age matched controls. It has been suggested that lesions associated with navicular disease are the result ofrepeated concussion of the navicular area leading to degenerative disease involving the navicular bone, navicular bursa, and the deep digital flexor tendon. Arteriosclerosis resulting in ischemia and necrosis, due to decreased blood flow to the navicular region, has also been implicated in the pathogenesis of navicular lesions; however, evidence of arteriosclerosis has been demonstrated in the navicular region of sound horses as well.