Preventing Bone Erosion By Effectively Treating Rheumatoid Arthritis

Bone erosion, a common side-effect of rheumatoid arthritis, can be prevented by using a combination of close patient monitoring and individualized therapeutic regimens that include agents to block cytokines, block osteoclasts, or target abnormal cellular reactions.

Ellen Gravallese, MD, from the University of Massachusetts Medical School, discussed ways to treat rheumatoid arthritis and prevent bone erosion at the 2014 American Society of Bone and Mineral Research Conference in Houston, Texas.

In rheumatoid arthritis with hand involvement, articular erosions predict disability. These abnormalities can ultimately be seen as anatomic deformities, but they can also be identified on radiography when progression is subclinical. Parameters associated with increased risk of radiographic progression, include elevated inflammatory markers, bone erosion at presentation, genetic risk, the presence or absence of autoantibodies, and smoking.

Bone edema represents inflammation into the marrow space and the degree of edema correlates with inflammation and erosion. So, as inflammation improves with treatment, so does edema. Conversely, when inflammation worsens in the marrow space, it leads to erosion.

Dr Gravallese described how effective monitoring of patients using biochemical, radiologic, and clinical markers allows for individualized treatment. In the TICORA trial, rheumatoid arthritis patients were randomized to intensive management versus routine care. The study found that patients who were evaluated using objective instruments (such as clinical and radiographic findings) to assess joint inflammation, had improved outcomes.

Dr Gravalle also discussed the use of biomarkers in managing rheumatoid arthritis. For one study that showed dissociation between clinical remission and imaging, she said, “I would argue that it is not so important that osteoblasts go in and heal erosion sites, but healing erosions could be an important biomarker”.

There are currently three broad therapeutic classes that are being used to treat rheumatoid arthritis: agents can block cytokines, osteoclasts, or cells. Therapeutics that block cytokines include those that target IL-1, Tumor Necrosis Factor (TNF), and IL-6 (for example, tocilizumab). Therapeutic agents that have cellular targets include rituximab (B cells), abatacept (T cell co-stimulation) and tofacitinib.

Although these medications have complications, including infections and hyperlipidemia, targeted therapy against specific cytokines is a novel way of treating patients with rheumatoid arthritis. Clinical trials are currently enrolling patients who have previously been refractory to conventional treatment.