The Pathophysiology of Osteoarthritis - What Causes It?

The main cause of Osteoarthritis is an imbalance in the natural breakdown and repair process that occurs with cartilage. In Osteoarthritis, damaged cartilage cannot repair itself in the normal way.

It occurs when the cartilage that covers and cushions the ends of bones in your joints deteriorates over time. Cartilage is composed of water, collagen, and specific proteins. In healthy cartilage, there is a continual process of natural breaking down and repair of the cartilage in joints. This process becomes disrupted in Osteoarthritis, leading to cartilage deterioration and an abnormal repair response. The reason this normal repair process is disrupted is not known but it is likely caused by several factors.

With aging, the water content of the cartilage increases, and the protein makeup of cartilage breaks down.

Eventually, the smooth surface of the cartilage begins to deteriorate and become worn causing friction between the bones. If the Cartilage wears down completely; the result will be bone to bone contact. Repetitive use of worn joints over the years can irritate the cartilage, causing joint pain and inflammation of surrounding tissues. As pieces of cartilage break off, the bones thicken and broaden, causing inflammation. This inflammation may stimulate new bone outgrowths called spurs (also called osteophytes) to form around the joints. As the bones thicken and broaden, joints become stiff, painful, and may be difficult to move. Fluid may also build up in your joints.

An Imbalance:

An imbalance in the homeostatic process of the degradation and rebuilding phases of cartilage is believed to be the primary cause of OA. When joints engage in movement, the production of chondrocytes is stimulated in order to replace those cells lost in degradation. Prolonged disuse of joints causes changes in the makeup of the matrix of cartilage, ultimately resulting in a loss of joint function. Age-related changes in the composition of the matrix, decreased sensitivity of chondrocytes to stimulation and a loss of function of these cartilaginous cells all contribute to the development of OA in a joint.

Abnormal reparative processes and inflammation of the cartilage can lead to the formation of boney structures known as osteophytes or bone spurs, which replace normal flexible, functional cartilage. Inflammation can occur through the formation of osteophytes and through swelling that is associated with the inflammatory process, contributes to patient pain and discomfort.

Inflammation:

The most prominent inflammation, termed synovitis, presents in the form of warmth, swelling, and thickening of the fluid within the joint. Though laboratory testing has identified common signs of inflammation in some Osteoarthritic patients, not all patients with OA present with the inflammatory component of the disease.

Pain involving one or more joints is the most common complaint made by osteoarthritic patients to their physicians. The onset of pain in OA is insidious and its severity is mild to moderate. OA pain in less-advanced disease states is generally worsened with joint use and relieved by joint rest. However, patients exhibiting more advanced OA are more likely to complain of joint pain during rest and throughout the night. The degradation and loss of cartilage in the joint causes pain, as the weight-bearing joints are no longer cushioned at the junction of the two bones. The structural sources of pain include the synovial membrane, joint capsule, periarticular ligaments, periarticular muscle spasm, periosteum, and subchondral bone. The pain mechanism can be the result of one of the many abnormal features that can occur in OA. Possible mechanisms of pain in OA include: increased intracapsular pressure, pressure between bones, microfractures, effects of muscle wasting, and the structural changes within and around the joint.

Stiffness:

In addition to pain, stiffness is also a common symptom of OA. Stiffness associated with prolonged periods of immobility, as during sleep, often resolves within thirty minutes of joint use. The stiffness associated with OA is the result of abnormal joint function, and the effect that it has on the structures surrounding the joint. The duration of time for stiffness to resolve lengthens with progression of the disease. In addition to stiffness, patients may also present with crepitus, which is an often audible and palpable grinding between the bones of a joint, secondary to the increased contact between boney surfaces. Additional symptoms resulting from structural changes within the joint include a decreased range of motion in the affected joint, resulting in functional impairment.