Equine Orthopedic Diseases Flashcards
What are the major components of cartilage
Proteoglycans
Water (70-80%)
Dry Weight
50% type 2 collagen
35% proteoglycans
50% of the dry weight of cartilage is
type 2 collagen
35% of the dry weight of cartilage is
proteoglycans
What are we treating with equine osteoarthritis
1) Mechanical stress
2) Inflammation
3) Decreased SF viscosity
4) Cartilage breakdown
How does synovial fluid viscosity change with osteoarthritis
it becomes more fluid (decreased viscosity)
What is the pathogenesis of equine osteoarthritis
1) Synoviocytes are subjected to trauma and inflammation
2) Release IL-1, TNF-a, Metalloporteinases, Prostaglandins
3) Act on cartilage, more inflammatory mediators
4) Chondrocytes produce more mediators like PGE2 and Metalloproteinases leading to matrix degradation
Self-sustaining process
What inflammatory mediators are produced by synoviocytes during equine osteoarthritis
IL-1
TNF-a
Metalloproteinases
Prostaglandins
What inflammatory mediators are produced by chondrocytes during equine osteoarthritis
PGE2
Metalloproteinases: Stromelysin and Collagenase
-Leads to matrix degradation
What are the stages of equine joint disease
1) Synovitis: Synovial inflammation + deteriorating joint fluid
2) Degenerative Joint Disease: cartilage changes + joint capsule fibrosis
3) Osteoarthritis: bony changes
With equine joint disease, where is the stage of no return
Once synovitis begins to develop into degenerative joint disease (cartilage changes and joint capsule fibrosis)
Inflammation of synovial and deteriorating joint fluid (more watery)
early stage of joint disease
Synovitis
cartilage changes and joint capsule fibrosis,
past the point of no return
Degenerative joint disease
bony changes seen after degenerative joint disease
osteoarthritis
How do you diagnose equine osteoarthritis
1) Lameness exam first
2) Radiographs
3) Nuclear scintigraphy- turn over of bone (remodeling areas are darker)
4) Ultrasound
5) MRI- hoof and cartilage (only distal to carpus/tarsus)
6) Exploratory arthroscopy- see cartilage lesions well that radiographs might not pick up
How do you tell what areas are undergoing active remodeling in nuclear scintigraphy
darker areas
In horses, you can only use MRI if the lesion is
distal to the carpus/tarsus
You have a 5yo QH gelding presenting for a left forelimb lameness.
Positive to distal limb flexion, all other flexions negative
Lameness improved 80% with a basisesamoid block
What imaging modality would you perform first?
Radiographs to look for bony lesions
What are goals of equine OA therapy
1) Decrease inflammation- soft tissues and cartilage
2) Alleviate pan
3) Lubricate joint
4) Restore normal environment
5) Slow down disease progression
6) Remove inciting cause
What should you consider when chooding OA therapeutic choices
1) Is it joint involved
2) Stage of OA
3) Current and intended use
4) Age
5) Regulations
6) Cost
7) Response to therapy
What do chondroprotective agents do
Support joint structure and function
1) Normalize synthesis of matrix components
2) Decrease matrix degradation
A polysulfated glycoaminoglycan used IM to systemically treat OA in horses
Adequan
What are the different systemic therapies for OA in horses
1) NSAIDs
2) Polysulfated Glycosaminoglycan (Adequan)
3) Oral, slow acting agents like Cosequin and Glycoflex
What is the mechanism of action of NSAIDS
inhibits COX’s conversion of arachidonic acid to prostaglandin
COX-1: inflammation
COX-2: Homeostatic functions- GI tract, renal tract, platelet function, macrophage differentation
What COX is responsible for inflammation
COX-2 induced