Osteoarthritis (OA) is a progressive joint disease that affects millions of people globally. It is characterized by the deterioration of joint tissues, most prominently the breakdown of articular cartilage. This degradation is a complex biological process that fundamentally alters the joint structure. Understanding the connection between OA and cartilage is central to grasping the disease, as the loss of this tissue drives the subsequent pain and loss of function.
The Essential Function of Healthy Cartilage
Articular cartilage is a specialized connective tissue that covers the ends of bones where they meet to form a joint. Its primary function is to provide a smooth, lubricated surface for low-friction movement and to act as a shock absorber, distributing mechanical loads across the joint.
Cartilage properties derive from its extracellular matrix, composed of Type II collagen fibers for tensile strength and proteoglycans, such as aggrecan. These proteoglycans trap water, giving the tissue its ability to resist compressive forces. Specialized cells called chondrocytes maintain this infrastructure.
How Osteoarthritis Breaks Down Cartilage
In a healthy joint, chondrocytes maintain a careful balance between the creation and breakdown of cartilage matrix components. Osteoarthritis disrupts this equilibrium, causing the joint environment to shift toward net degradation, driven by a low-grade inflammatory state.
Pro-inflammatory cytokines, notably Interleukin-1 (IL-1) and Tumor Necrosis Factor-alpha (TNF-α), stimulate chondrocytes and other cells to overexpress catabolic enzymes. The main enzymes responsible for structural damage are Matrix Metalloproteinases (MMPs) and ADAMTS. These enzymes actively dismantle the cartilage matrix, with MMPs breaking down the collagen framework and ADAMTS targeting the aggrecan proteoglycans.
This enzymatic attack causes initial structural changes, such as the loss of proteoglycans. The loss of proteoglycans reduces the cartilage’s water-retaining capacity, diminishing its shock-absorbing ability and making it vulnerable to mechanical stress. The excessive activity of these degradative enzymes ultimately overwhelms the repair mechanisms, leading to progressive cartilage erosion.
Structural Changes Caused by Cartilage Loss
As the cartilage matrix degrades, the smooth tissue begins to thin, crack, and eventually erode completely. This loss directly results in the narrowing of the joint space, which can be observed on medical imaging. When the cartilage layer is gone, the ends of the bones rub directly against one another, often described as bone-on-bone contact.
The exposed bone responds to the altered mechanical stresses and friction by undergoing structural changes. The body attempts to stabilize the joint by producing bony growths, known as osteophytes or bone spurs, typically at the joint margins. This combination of bone-on-bone friction and structural remodeling is the source of the joint pain and stiffness characteristic of the disease.
Protecting Joints and Managing Osteoarthritis
While damaged cartilage cannot be fully regenerated, management strategies focus on slowing disease progression and reducing symptoms. A significant focus is placed on non-pharmacological interventions that reduce the mechanical load on the affected joints.
Maintaining a healthy body weight is a practical step, as excess weight places substantial stress on weight-bearing joints like the knees and hips. Low-impact physical activity is also recommended to maintain joint function. Exercises such as swimming, bicycling, or walking strengthen the muscles surrounding the joint, which improves stability and provides better support.
Physical therapy can be instrumental in teaching targeted exercises to enhance flexibility and range of motion without causing undue strain. Medical treatments, including over-the-counter pain relievers and prescription anti-inflammatory medications, are used to manage the associated pain and inflammation.