A strong association between chondrocalcinosis, resulting from calcium pyrophosphate dihydrate (CPPD) deposition, and knee osteoarthritis (OA) is firmly established. However, despite the association, a causative pathogenic role for CPPD crystals on the progression of articular degeneration in the knee has not been definitively demonstrated.

Although compelling, no clear-cut links between dietary factors and the risk of developing rheumatoid arthritis (RA) have been confirmed. Recent investigations have implicated increased consumption of red meat as a risk factor for incident inflammatory arthritis.

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).