Osteoarthritis (OA) is a common disease of the aged. The disease is characterized by the degeneration of the articular cartilage, the tissue which covers the ends of long bones. Hemorrhage into the joint, possibly caused by trauma, may accelerate the degeneration. Bleeding disorders, such as hemophilia, display OA-like features. Aged cartilage-often shows a yellow-brown tinge, a discoloration that is suggestive of structural modifications in the tissue. In this regard, iron has been suspected to be a causative agent. Furthermore, iron has been known to be an integral component in free radical reactions, such as metal ion-catalyzed oxidation, which has been shown to modify biomolecules. Accumulation of these modified biomolecules is believed to alter the normal physiology of a tissue. Three hypotheses will be addressed: (I) That iron can produce structural changes in adhesion molecules in vitro. This hypothesis will be addressed by evaluating the antigenicity and carbonyl content of the iron-treated adhesion molecules. (2) That iron-induced structural changes alter the functional properties of adhesion molecules. (3) That these iron-induced structural changes occur in vivo. This hypothesis will be addressed by analyzing the antigenicity and carbonyl content of adhesion molecules in tissues from humans of different ages. Furthermore, the capacity of these adhesion molecules to attach cell will be investigated. These experiments will lead to a better understanding of the role of iron in aging and degenerative joint disease.
