What drives osteoarthritis
Osteoarthritis (OA) is the most common form of arthritis. It wears away the cartilage that cushions the joint and inflames the joint lining, causing pain, stiffness and loss of movement.
OA usually begins with an injury or long-term stress on a joint. That sets off an inflammatory response carried by two groups of molecules: cytokines, which signal inflammation, and proteases, enzymes that break down proteins. In a healthy joint, proteases help clear damaged tissue. In OA they stay switched on, digesting cartilage and releasing fragments that drive more inflammation.
Several protease families are involved, including matrix metalloproteinases (MMPs), ADAMTS enzymes and cathepsins. Many past drug programs targeted one enzyme or one pathway at a time. Because OA has many drivers, we believe an effective disease-modifying treatment will need to act on several of them at once.
No treatment is currently approved to slow the structural progression of OA. A therapy that does is often called a DMOAD (disease-modifying osteoarthritis drug).
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