Page 71 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

46 CHAPTER 1

VetBooks.ir OSTEOCHONDROSIS Osteochondral fragments (‘joint mice’) may detach
to float free in the joint. Inflammation of the joint
Osteochondrosis (OCD) is a condition that is
term ‘osteochondritis’. Dissecting flaps of cartilage
part of a group of orthopaedic conditions affect- occurs in response to these changes, leading to the
ing young, growing horses termed developmental are specifically termed ‘osteochondritis dissecans’
orthopaedic diseases (DODs), which also includes (Fig. 1.81). Subchondral bone cysts typically occur
physitis, ALDs, flexural limb deformities and cer- at the weight-bearing portion of joints, most com-
vical vertebral malformation. OCD is defined as a monly of the distal femoral condyle, but also associ-
‘failure of normal endochondral ossification’. There ated with several other joints. While some clinicians
is a disturbance of the normal differentiation of cells regard this condition as a manifestation of OCD,
in growing cartilage at the end of the long bones in most people consider it a separate condition caused
the articular–epiphyseal growth plate; this leads to by ingress of synovial fluid into microfissures in the
retention of cartilage or dyschondroplasia. These articular surface. This results in the formation of a
microscopic changes can either repair or develop cystic lining, bone resorption and typically intermit-
into a clinical entity and lead to lameness. The mani- tent lameness.
festations of this disturbance in the horse are mul- The aetiology of OCD is not clear, but it is mul-
tiple. Necrosis of the affected cartilage may lead to tifactorial. Various trigger factors have been impli-
cartilage fibrillation and fissuring at various depths. cated. Rapid growth rate in fast growing horses such
as Thoroughbreds, Standardbreds and Warmbloods
is associated with the development of OCD, possi-
1.81 bly due to bone growth outstripping blood supply.
Recently, vascular disturbance leading to ischaemic
necrosis has been demonstrated as a cause of necrotic
cartilage in the subarticular matrix. A genetic predis-
position may also exist in these breeds and anecdotal
evidence has been shown in some breed lines. Dietary
imbalances and mismanagement are major factors. In
particular, excessive carbohydrate and protein intake
has been shown to induce OCD lesions. The exact
mechanism of these factors is not known, but excess
carbohydrate intake may influence chondrocyte
metabolism via an alteration in insulin mediation.
Excess phosphorus, calcium and zinc and insufficient
copper have been found to induce OCD. Copper
deficiency may act via lysyl oxidase dysfunction, lead-
ing to decreased collagen cross-links and subsequent
weakness of the cartilage. A recent scientific paper
reported no relationship between copper and OCD,
although it found a decreased ability of affected car-
tilage to repair if copper was low. The role of trauma
is strongly implicated as a factor (whether primary or
secondary is still controversial), although the stage of
development when the articular–epiphyseal cartilage
Fig. 1.81 Large dissecting flap lesion of the mid- complex is vulnerable to damage is unknown at the
lateral trochlear ridge of the distal femur of a 6-month- present time, and early low-grade loading may actu-
old Warmblood foal, which represents the most ally promote adaptation of immature cartilage and
common form of an OCD lesion in the stifle joint. prevent OCD lesions forming.