What Went Wrong?

Abstract

Arthritis is one of the most common medical problems in the world. Nearly four million Canadians are affected with arthritis and other rheumatic conditions; these numbers are expected to escalate as the population continues to age (PHAC, 2003). At present there exists only treatments for arthritis, but no cure. Osteoarthritis is a degenerative form of arthritis which occurs when the cartilaginous lining that cushions the ends of bones in joints deteriorates, leaving bones to rub against one another (Hunder, 1999). Rheumatoid Arthritis (RA), on the other hand, is not associated with wear and tear. It is thought to be an autoimmune disease in which an unidentified agent stimulates an immune response in the joint capsule (Hunder, 1999). The ensuing inflammatory response results in the thickening of the joint capsule synovium. If untreated, inflammatory mediators digest cartilage, bone, tendons and ligaments. Given the aforementioned etiology of RA, treatment regimens have focused primarily upon reducing the autoInflammatory response associated with the disease.This has led to the utilization and development of various families of anti-Inflammatory drugs one of which are the Nonsteroidal Anti-inflammatory Drugs (NSAIDs). This class of drugs, of which aspirin is a member, inhibits inflammation by interfering with an inflammatory mediator known as cyclo-oxygenase (COX). Clinical trials demonstrate that although NSAIDs are effective in alleviating symptoms associated with RA, they present a marked increase in gastrointestinal ulceration (Kremer, 2000). These findings led to the development of NSAIDs that specifically inhibit