Osteoarthritis is a disease of the articular cartilage and underlying subchondral bone. Although the exact etiology of osteoarthritis is not known, one theory is that cartilage matrix turnover is negatively affected by degenerative forces. This disrupts the balance between cartilage synthesis and degradation. Evidence suggests that collagenase, gelatinase, and stromelysin, which are enzymes involved in cartilage degradation, are increased in osteoarthritic joints.1 The cause for this imbalance is not clear. One proposed theory is that changes to the subchondral bone instigate changes to the cartilage matrix. Radiographic evidence of subchondral bone changes is often present in patients with osteoarthritis. It is theorized that stiffening of the sub-chondral bone due to microtrauma results in an abnormal environment for the overlying cartilage. This increases cartilage turnover and leads to further degradation of the joint. However, the debate as to whether subchondral bone changes are a result or cause of cartilage degeneration is not settled.1
Also unsettled is the role of the inflammatory response in the pathogenesis of osteoarthritis. Localized inflammation has been demonstrated in certain stages of osteoarthritis, including mononuclear cell infiltrate and synovial hyperplasia. The exact role of this inflammation, be it causative or reactionary, is not clear. Markers of inflammation such as C-reactive protein (CRP) may be elevated as well.1 However, in general, systemic inflammation is not characteristic of osteoarthritis. Its presence would indicate that another pathology such as rheumatoid arthritis or gout should be considered.
■ FIGURE 13-3 CT images of Case #3 demonstrating pannus related to C1-C2 instability.
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