Abstract
The diagnosis of rheumatoid arthritis and osteoarthritis remains primarily clinical. Available diagnostic criteria represent minimum requirements and cannot adequately describe the broad areas of variability in clinical manifestations, natural history, and severity, nor the probable heterogeneity in etiology and pathogenesis. Host factors that determine clinical course and response to treatment are poorly defined and often not considered in therapeutic trials. Traditionally, treatments have developed empirically, and only later have efforts been made to account for mechanisms of action. The modern approach, however, involves the screening of a large number of promising agents and their analogues, using both animal models and in vitro systems. In osteoarthritis, pain relief has been the primary target; additional measures have aimed at reducing the impact of mechanical stress. The increasing realization that inflammation may contribute to the disruption of cartilage in osteoarthritis has raised questions about the importance of anti-inflammatory activity in therapeutic agents. These effects are also important in rheumatoid arthritis, but the extraordinary complexity of its pathogenesis confounds therapeutic efforts since it is unclear which facet or aspect of the process is most relevant. Thus, the approaches to therapy include classic anti-inflammatory agents, pheresis, chemical and radioactive cytotoxicity, and immunomodulation. The risks and benefits of these efforts are demonstrable in relatively short-term trials, but the ultimate goal of disease modification over a period of years is still elusive and difficult to document.
Published Version
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