CLINICAL SIGNS, SYNOVIAL FLUID CYTOLOGY
AND GROWTH FACTOR CONCENTRATIONS
AFTER INTRA-ARTICULAR PRP IN HORSES
WITH OSTEOARTHRITIS
Y. Smit
Osteoarthritis (OA) in the horse is one of the most common joint disorders
seen [1]. It has been estimated that up to 60% of lameness is related to OA
[2]. OA is frequently assosiated with lameness, poor performance and early
retirement in many equine sports [1].
OA is a chronic degenerative joint disorder that is multifactorial in origin and
characterised by destruction of the articular cartilage, subchondral bone
alterations and synovitis [3].
The pathogenesis of OA has been defined in many studies performed. It has
been classified to three fundamental mechanisms. The first mechanism being
a defective cartilage with abnormal biomechanical properties. This is when the
abnormal cartilage fails when placed under normal loading conditions. The
second mechanism involves abnormal change in the subchondral bone. For
example, in the carpus of a racehorse, considerable damage may be inflicted
directly to the articular cartilage and regions of concussion by cyclic fatigue
(as exemplified by fractures and chondral lesions un-associated with fracture)
often leading to primary damage to the subchondral bone that is presented as
subchondral sclerosis. In some cases, as described above, the bone may
increase in density to a pathological level, resulting in a stiffer or less
compliant bone-cartilage unit that is prone to failure. The third mechanism
proposed revolves around normal cartilage that is exposed to abnormal
forces, i.e. abnormal joint congruity as a result of a collateral ligament strain.
In the latter the abnormal forces will overwhelm the normal metabolic repair
mechanisms in the articular cartilage and ultimately lead to its failure [2,5].
Clinically, OA in horses manifests as varying levels of lameness, the presence
of increased synovial fluid or synovial pressure, soft tissue swelling and a pain
response to flexion.
Radiographic signs of OA includes periarticular osteophytes, joint-space
narrowing, subchondral bone sclerosis or lysis and the presence of
osteochondral fragments [5]. In horses the correlation between the clinical
signs and the disease severity is poor [5].
The current treatment strategies for OA are aimed at different complex
pathways in the disease.
There are two main goals for medical treatment of OA in the horse: firstly,
reducing the pain (lameness) and secondly, reducing or minimizing the
progression of joint deterioration [5]. The ideal therapeutic agent should be an
agent that both relieves the symptoms of lameness (symptom-modifying OA
drug, or SMOAD) as well as producing disease modifying effects (DMOAD).
Current treatments include intra-articular corticosteroids, hyaluronan (HA),
polysulfated glycosaminoglycan (PSGAG) and IL-1 receptor antagonists (IL15-‐18
February
2016
East
London
Convention
Centre,
East
London,
South
Africa
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