Page 844 - Adams and Stashak's Lameness in Horses, 7th Edition

810 Chapter 7

Cyclic or athletic trauma
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Inflammation of soft tissue
Loss of stability Remodeling and microfractures/ (traumatic synovitis and capsulitis)
necrosis in subchondral bone
(fractures, ligamentous tears)

Joint congruence changes Aging Osteochondrosis
(fracture,developmental defects)
Abnormal stresses
normal cartilage
Normal stresses
abnormal cartilage

Physical cell injury

Enzymatic degradation of
proteoglycans and collagen Enzymatic degradation of Decreased synthesis
Direct damage to proteoglycans and collagen of matrix components
collagen framework Decreased synthesis (direct or secondary
of matrix compounds to cytokine interation)

Secondary loss
of proteoglycans
from matrix
Morphologic breakdown of articular cartilage

Figure 7.8. Possible pathways for degradation of articular McIlwraith. Reproduced with permission of American Association
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cartilage secondary to joint trauma. Source: Redrawn from figure 4, of Equine Practitioners.

permanent fibrosis in the joint capsule, which in turn In addition to direct injury that may occur to the syno­
causes decreased motion and compromised shock vial membrane, the reaction of the synovial membrane to
absorption capabilities in that joint; and (3) prevent or articular cartilage damage or other mechanical destruction
minimize the development of OA. of intra‐articular tissues is well recognized. The presence
Synovitis and capsulitis as primary entities in athletic of cartilaginous wear particles increases the cellular pro­
horses are presumed to be associated with repeated duction of prostaglandin E , cytokines, and the neutral
2
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trauma. Severe injury to the fibrous joint capsule also metalloproteinases (collagenase, stromelysin, and gelati­
can cause instability. The synovial membrane itself is nase). It has also been shown that the proteoglycans
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mechanically weak and has no known biomechanical role, released into synovial fluid cause synovitis. 6
but it is recognized that synovial injury may have patho­ The ability of synovial membrane inflammation
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physiologic consequences in the joint. Some injuries may alone in the absence of trauma and/or instability to
affect diffusion across the synovial membrane, and others damage articular cartilage has previously been demon­
have a primary effect on the metabolism of the chondro­ strated in the horse. 66
cyte. Mechanically damaged synoviocytes may release
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degradative enzymes and cytokines, which alter the intra‐
articular environment and possibly affect articular carti­ The Importance of Synovitis
lage. It has also been suggested that high intra‐articular Synovitis (and capsulitis) is important to the horse
pressures in injured joints associated with effusion could because it produces pain, the increased synovial effusion
be sufficient to impair the flow of blood through the syno­ is uncomfortable and it eliminates the normal small
vial capillaries and potentially lead to reperfusion injury. negative pressure within the joint (therefore promoting
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Flexion of a joint with sufficient synovial effusion could micro‐instability), and it produces products that are del­
raise the intra‐articular pressure to levels of impaired eterious to joint health as a whole and articular cartilage
blood flow through the synovial capillaries. in particular. The mediators currently considered to be