intertrabecular edema and perivascular mononuclear cellular infiltration have been
identified. These lesions most likely have a different aetiopathogenesis than that of
classic navicular disease and may be acutely traumatic or inflammatory in origin.
In some other horses, fluid-filled osseous cyst-like lesions have been seen in the
distal aspect of the bone, apparently separate from synovial invaginations, and not
associated with any detectable abnormality of the flexor aspect of the bone. Such
lesions have not yet been characterised histologically and their etiology remains
speculative, but recent evidence suggest that their presence is associated with the
degenerative changes in the impar ligament. In recent post mortem studies, osseous
fragments associated with a defect in the distal margin of the navicular bone were
more common in horses with navicular disease than in age-matched controls.
Histologically, distal border fragments have variously been described as avulsion
fractures, separate centers of ossification, osseous metaplasia of the impar ligament
or synovial osteoma but pathological evidence elucidating their pathogenesis
remains elusive. More recently it was shown that the presence of these fragments
was associated with varying degrees of histopathological damage of collagen fibers
and fibroblasts in the axial third of the impar ligament.
Deep Digital Flexor Tendon
Tendinopathy of the DDFT in the foot is almost exclusively an MRI diagnosis.
Tendon damage is seen as focal signal increase within the normal contour of the
hypointense tendon lobes, on both T1- and T2-weighted sequences, variably
accompanied by enlargement of the affected lobe. There is a good correlation
between the MRI appearance of DDFT lesions and their pathological classification
into core lesions, sagittal plane splits, dorsal plane tears, insertional lesions and
dorsal abrasions.
Core lesions result in focal, circular areas of signal increase in the center or near the
dorsal border of the affected lobe, but are completely surrounded by normal ‘black’
tendon signal. Histologically they consist of various amounts of collagen necrosis,
fibroplasia and fibrocartilagenous metaplasia resulting in loss of normal fascicular
architecture. Core necrosis was seen more frequently in horses lame for less than 6
months. In horses with lameness of more than 6 months’ duration, core lesions
consisted predominantly of fibroplasia and/or fibrocartilaginous metaplasia.
Sagittal plane or oblique splits form linear hyperintensities of variable depth arising
from the dorsal surface of the tendon and progressing palmarly. Histologically,
disruption of the deep dorsal layer of the tendon by deep splits extending from the
surface can be observed9. Splits propagate mostly along septal lines, with
chondrones clustered around fibrillating tissue and around crevices but no evidence
of inflammatory cell.
Insertional lesions are limited to the distal 20 mm of the DDFT, distal to the distal
border of the navicular bone, near the tendon’s insertion on the distal phalanx. They
consist of small core lesions, sagittal plane splits or osseous changes of the insertion
site.
Severe dorsal border abrasions of the DDFT usually cause signal increase extending
from the dorsal surface towards the center of the affected lobe. Histopathologically,
dorsal DDFT fibrillations, erosions and abrasions consist of longitudinal strips of
superficial fiber damage extending the proximodistal length of the navicular bursa.
Proceedings
of
the
South
African
Equine
Veterinary
Association
Congress
2016
219