In rheumatoid arthritis (RA) chronic inflammation results in pain, swelling and ultimately destruction of joints. This inflammation is also related to systemic bone loss and an increased fracture risk. Glucocorticoids (GC) are widely used to suppress the symptoms of inflammation in RA. There is increasing evidence from clinical studies that GC are disease modifying, in early disease and in combination with slow acting anti-rheumatic drugs. The effects of GC on joint destruction remain a matter of debate. However, some safety issues remain to be considered for long-term treatment, related to high cumulative doses such as the dose-related risk for glucocorticoid induced osteoporosis (GIOP). Moreover, data from in vitro studies on chondrocyte cultures question the cartilage-preserving function that has been attributed to GC. Combination with bisphosphonates can be advocated as these compounds protect against GIOP and chondrocyte apoptosis. In conclusion, GC may have a disease modifying role in RA, but they have to be used in combination with other disease modifying anti-rheumatic drugs and a bisphosphonate.
Keywords: Rheumatoid arthritis, glucocorticosteroids, osteoporosis, joint destruction
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