Program Goals
Rheumatologists should understand the role of interleukin-1 in inflammation in rheumatoid arthritis.

The goal of this program is to educate practitioners who treat rheumatoid arthritis about the role of interleukin-1 in inflammation.

Disclaimer
In weighing the benefits of treatment against the risks, physicians should be guided by clinical judgment. Dosages, indications, and methods for use of drugs and procedures referred to in this monograph may reflect the clinical experience of the authors or may be derived from the professional literature or other clinical sources. Consult complete prescribing information before administering any of the drugs discussed.

• Identify the major biological factors involved in inflammation and tissue destruction.
  
• Describe the major differences between the biological effects of interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha).
  
• Review the complex nature of matrix proteins produced by chondrocytes and the alterations in chondrocyte responses involved in cartilage matrix destruction in osteoarthritis (OA) and rheumatoid arthritis (RA).
  
• Outline candidate therapeutic targets for inhibiting cartilage destruction in RA and OA.
  
• Discuss the cellular and regulatory processes involved in the physiology of bone remodeling.
  
• Identify the cellular mechanism of bone loss in RA.
  
• Recognize the roles of IL-1, TNF-alpha, and RANK ligand (RANKL) in the pathogenesis of bone erosions in RA.
  
• Assess that, in animal models, overproduction or poor regulation of IL-1 can induce or drive all of the pathological processes associated with RA, particularly those involved in cartilage destruction and erosion.
  
• Recognize that IL-1 receptor antagonist (IL-1Ra) is an effective inhibitor of IL-1 activity in the joint and results in chondroprotection.
  
• Explain the effects of human recombinant IL-1Ra (IL-1ra) therapy on RA disease activity.
  
• Review the effects of IL-1ra therapy on radiographic progression of RA.