I can't help but wonder if the reported increase in heart disease associated with active RA is really due to increased inflammation affecting plaque formation or the effects of NSAIDs that have been widely used in the past as background therapy for DMARDs. Another condition for whuch we have little therapy and is possibly related to inflammatory OA is CPPD disease. All we really have is steroids for pseudogout even though colchicine and DMARDs are used in desperation, not to mention Plaquenil. I appreciate your concise reports.