Equine joint disorders
The main components of a joint include the articular cartilage (hyaline) sitting on a layer of subchondral bone, coated by synovial fluid and surrounded by a synovial lining and joint capsule. The cartilage is composed of chondrocytes and an extracellular matrix of precisely arranged type II collagen and proteoglycans. This structure traps water, creating a resilient cushion in a healthy joint. Cartilage contains no vessels, no lymphatics and no nerves. Nutrition has to migrate from the synovial fluid and through the matrix. Chondrocytes have different densities and orientation depending on the distance from the articular surface. The joint capsule maintains the joint stability (prevents motion in unintended directions) while the synovium produces lubricants, manages inflammation/phagocytosis and provides nutrition.
- Type II collagen – triple helix of amino acid chains, organized in fibrils. Provides tensile strength. Produced by chondrocytes. Very limited turnover of fibrils in adults.
- Aggrecan – proteoglycan; protein strand with glycosaminoglycan chains of chondroitin sulfate and keratan sulfate attached
- Aggrecans are attached to hyaluronan strands by link proteins
- The GAGs attract water creating compressive stiffness of cartilage
Synovial fluid contains nutrients and boundary lubricants. The lubricants are necessary to minimize friction between components. The main components are hyaluronate and lubricin.
Matrix metalloproteinases (MMPs) are synthesized by synoviocytes and chondrocytes. They can digest all components of the extracellular matrix and are responsible for removing damaged components. MMPs are released in zymogen form to minimize damage. Tissue inhibitors of MMPs (TIMPS) are also synthesized by the synoviocytes and chondrocytes.
Three main pathogenic mechanisms of osteoarthritis are proposed:
- Defective cartilage – flawed matrix fails under normal loading
- Normal forces damage healthy cartilage – injured chondrocytes release enzymes which cause cartilage damage and breakdown the proteoglycan network
- Increased stiffness of subchondral bone – microfractures heal with increased bone density; this leads to limited ability to absorb shock, pushing more load onto the cartilage
Synovitis contributes. Synovial inflammation leads to increased levels of inflammatory mediators. Synovitis can develop from trauma (eg a floating osteochondral fragment or direct trauma), release of inflammatory mediators from the cartilage, and infection.
Immune related changes (rheumatoid arthritis) are not seen in horses.
- Reduced range of motion – pain, synovial effusion, synovial edema and periarticular fibrosis
- Effusion – increased levels of synovial fluid due to protein leakage
- Synovial fluid changes – high protein, low viscosity due to lower HA (hyaluronate) content
- Pain -due to synovial effusion, periosteal disruption from osteophytes, and potentially subchondral bone changes.
Cartilage helps absorb energy through creating a hydrated layer on top of the bone. Type II collagen, proteins and sugars create an environment that holds water (until it is damaged). Matrix metalloproteinases help clean up debris but create damage. Cartilage has very poor healing ability. Inflammation of the joint environment leads to arthritis – typically this is typically due to wear and tear and trauma.