The molecular mechanisms leading to erosive joint damage in some, but not all, patients with rheumatoid arthritis (RA) are incompletely understood. Downstream effects of inflammatory cytokines produced by rheumatoid synovium include the induction of RANKL, a powerful osteoclast activator, the action of which is physiologically opposed by its naturally occurring antagonist osteoprotegerin (OPG).
Arthritis News
Enbrel and Humira Now Have Automated Delivery System
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Pregnancy Outcomes in Patients with Rheumatoid Arthritis and Lupus
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Risk Factors for Bisphosphonate Associated Jaw Osteonecrosis
Gastrointestinal complications, including esophageal mucosal ulceration, are the most frequent complications of bisphosphonate therapy, commonly used to treat osteoporosis, metabolic bone diseases (such as Pagets disease), multiple myeloma, and to inhibit metastatic solid tumor progression. Recent case reports have emphasized a less frequent complication of bisphosphonate therapy: osteonecrosis of the jaws. However, due to its rarity, little is know about the epidemiology of this potentially troublesome complication.
Impact of RA Disease Activity and Treatment on the Risk of Developing Lymphoma
Hematologic malignancies, particularly lymphomas, are more prevalent in RA patients. Case reports have suggested an association between RA therapeutics and the development of lymphoma, although it has been problematic using conventional epidemiologic methods to disassociate the potential for the RA disease process, presumably mediated through chronic systemic inflammation, to contribute to this risk. These concerns have limited the use of RA therapies in some patients.
Predictors of Increased Carotid Atherosclerosis in RA Patients
RA patients are at an increased risk for cardiovascular events and death from cardiovascular disease. In the general population, and in RA patients (Jane, link to ACR2005 abstract 1901), carotid atherosclerosis (defined by identification of a thickened intima-medial or plaque using ultrasound) is highly predictive of cardiovascular events. Despite this, previous studies have not identified a clear-cut increased risk for carotid plaque in individuals with RA compared to non-RA controls.