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Program Goals
Rheumatologists should recognize that interleukin-1 (IL-1)
as well as other proinflammatory cytokines mediate
bone resorption in active RA as well as postmenopausal
and corticosteroid-induced osteoporosis.
The goal of this program is to educate practitioners
in the two types of bone loss that occur in rheumatoid
arthritis:
loss of articular structure, due to erosions and joint-space
narrowing, and osteoporosis, associated with the inflammatory
process. It is now clear that the osteoporosis in active
rheumatoid arthritis reflects the same pathophysiologic
process as in postmenopausal and steroid-induced osteopenia.
In addition to the well recognized proinflammatory cytokines,
TNF-alpha and IL-6, interleukin-1 is also important,
and appears to act synergistically in mediating bone
resorption
in these clinical situations.
Disclaimer
In weighing the benefits against the risks of
treatments discussed, physicians should be guided
by clinical judgment. Dosages, indications, and
methods for use of drugs and procedures discussed
in this monograph may reflect the clinical experience
of the authors and/or may be drawn from literature
or other clinical sources. Please consult the
prescribing information before administering
any treatments discussed.
Learning Objectives
After completing this monograph, the participant will be able to:
- Recognize that RA is a progressive disease causing joint destruction.
- Review radiographic data from randomized controlled trials (RCTs) of
newly approved treatments in rheumatoid arthritis (RA).
- Explain the need for early intervention in RA in order to effect a change
in radiographic progression of disease.
- Review the natural history and outcomes of RA from the predrug era to
the biologic age and understand the reasons for changes in the therapeutic
approach to RA in the modern era.
- Compare differences between Larsen and Sharp scoring methods when analyzing
radiographic progression in randomized controlled trials (RCTs) in active
RA.
- Recognize that data from these RCTs indicate that radiographic progression
is decreased with use of these newly developed [and approved] therapies.
- Assess the incidence of low bone mass and subsequent fracture risk in
patients with RA.
- Assess the impact of corticosteroid therapy on the incidence of low
bone mass and fracture development in RA patients.
- Describe the intercellular interactions that regulate osteoclast function.
- Discuss the role osteoclasts play in mediating bone resorption in postmenopausal,
corticosteroid-induced, and RA-associated osteoporosis.
- Recognize the strong correlation between progressive joint destruction and
increased patient morbidity and disability in RA of long-standing duration.
- Recognize that proinflammatory cytokines, including IL-1 as well as TNF-alpha
and IL-6, play a significant role in osteoclast activation and differentiation,
thereby mediating the loss of articular structure and bone mass in RA.
Faculty
Vibeke Strand, MD – Program Chairperson
Biopharmaceutical Consultant
Clinical Professor of Medicine (VCF)
Division of Immunology
Stanford University School of Medicine
Palo Alto, California
Stanley B. Cohen, MD
Clinical Associate Professor
Department of Rheumatology
University of Texas Southwestern Medical Center
Dallas, Texas
Roy M. Fleischmann, MD
Clinical Professor of Medicine
University of Texas Southwestern Medical Center
Dallas, Texas
Arthur F. Kavanaugh, MD
Associate Professor of Medicine
University of California at San Diego
San Diego, California
John T. Sharp, MD
Affiliate Professor of Medicine
University of Washington
Seattle, Washington
Lee S. Simon, MD
Associate Professor
Harvard Medical School
Associate Chief of Medicine
Beth Israel Deaconess Medical Center
Boston, Massachusetts
Michael H. Weisman, MD
Professor of Medicine
Chief, Division of Rheumatology
Cedars-Sinai Medical Center
Los Angeles, California
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