Page 56 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Musculoskeletal system: 1.1 A pproach to the lame horse 31

VetBooks.ir regional limb local perfusion), drainage, debride- synovium contribute to cartilage degeneration in
OA by releasing a variety of inflammatory mediators
ment and lavage, and implant removal if this is
possible.
Other complications include refracture through and degradative enzymes against both collagen and
proteoglycans. These include PGs, cytokines, such
the original fracture plane due to premature implant as IL-1 and TNF-α, and MMPs including collage-
removal or delayed healing. Implant failure during nases, stromolysins (MMP-3) and gelatinases.
anaesthetic recovery can be catastrophic and steps The exact pathogenesis of OA is still unclear
to prevent this include the use of external coaptation and it may represent a common joint response to a
such as appropriate fibreglass casts, assisting recov- number of potential causes. A single or repetitive
ery with head and tail ropes and swimming pool traumatic event may produce mechanical damage
recovery if available. Delayed healing can occur for directly to healthy cartilage, leading to the devel-
a variety of other reasons where the healing envi- opment of OA. Subsequent damage to the cartilage
ronment is less than optimal (e.g. movement at the matrix and/or cellular injury results in metabolic
fracture repair site due to inadequate fixation or release of proteolytic enzymes from chondrocytes,
immobilisation). Overloading of the opposite limb which in turn cause cartilage fibrillation and pro-
after fracture repair can lead to laminitis or suspen- teoglycan breakdown. Alternatively, the matrix of
sory ligament damage in the adult horse, which is fundamentally defective cartilage with abnormal
potentially devastating. Prevention includes as early biomechanical properties may fail under normal
a return to normal weight bearing of the repaired loading. Subchondral and epiphyseal microfracture
limb as possible (dependent on the fracture type formation from normal mechanical stresses and
and complications encountered) and the use of pro- resulting ‘stiffening’ of the subchondral bone plate
phylactic frog support bandaging. In foals, angular may lead to eventual failure of the bone–cartilage
limb deformities and hyperextension of the fetlock interface, leading to OA.
can frequently result from limb overload and, occa- Changes in the synovial fluid viscosity reflect
sionally, acquired contractural limb deformity of the joint pathology in OA. A decrease in viscos-
the carpus is seen. Prevention includes early return ity is common and is due to a depolymerisation
to normal weight bearing of the repaired limb and and reduction in concentration of the glycoprotein
application of medial acrylic hoof extensions for hyaluronan, which normally acts as a boundary
acquired carpal valgus or heel extensions for fetlock lubricant in synovial joints. Cytological and pro-
hyperextension. Limb contractures may be treated tein concentration changes are not dramatic in OA
with temporary caudally applied splints. and are not routinely used as markers of OA. A dis-
The owner must be made aware of these poten- tinction between OA in ‘high-motion’ joints and
tial complications prior to fracture repair, since they ‘low-motion’ joints has implications on clinical pre-
may lead to euthanasia on humane and/or financial sentation, pathological development and progression
grounds. and treatment. ‘High-motion’ joints include the DIP,
metacarpo/ metatarsophalangeal, antebrachiocarpal
JOINT DISEASE and mid-carpal, humeroradial, scapulohumeral,
tarsocrural, femoropatellar and coxofemoral joints,
Synovial joints are highly differentiated connective and they present with OA as above. The proximal
tissue structures composed of bone, articular carti- interphalangeal and tarsometatarsal/centrotarsal
lage, synovial membrane and periarticular soft tis- joints represent the ‘low-motion’ joints (Fig. 1.58).
sues. OA is characterised by degeneration and loss OA in these joints will not present with obvious joint
of articular cartilage. Clinically, the disease mani- effusion since the joint capsule allows less distension
fests itself as joint pain, reduction in joint move- than ‘high-motion’ joints. Subchondral bone lysis
ment, joint effusion and variable degrees of localised and sclerosis of the bones making up the articulation
inflammation. At a cellular and molecular level, contribute significantly to the overall disease process
research has shown that synoviocytes lining the joint and progression towards joint ankylosis (partial or