At the onset of rheumatoid arthritis (RA), a rheumatologist takes immediate steps to control the inflammation that causes severe pain, swelling and destruction of cartilage. Cartilage is not the only tissue at risk, however. Your bones can also be destroyed by the effects of inflammation, as well as from many of the drugs used to control that inflammation.

“It’s been suggested that active, systemic inflammation – the production of inflammatory cytokines – has some negative action with bone remodeling,” says Seo Young Kim, MD, a rheumatologist and researcher at Brigham and Women’s Hospital in Boston, who has studied the connection among RA, common RA drugs to fight inflammation and the loss of bone mineral density that can increase the risk of fracture.

“The bottom line is that people with RA have a high risk of osteoporotic fracture at the typical sites: the hip, forearm, pelvis,” she says. Dr. Kim estimates that if you have RA, your risk of these fractures is 25 to 30 percent higher than the average population.

“We are all losing bone mass, but some things, like RA, speed up that process,” says Michael DiMuzio, PhD, executive director of the North Shore Osteoporosis Center in Highland Park, Ill.

RA’s inflammation contributes to the damage to bone, possibly by stimulating osteoclasts, bone cells that deplete bone minerals. Prednisone, a common, inexpensive corticosteroid drug used for decades to control inflammation, is one of the notorious culprits in bone mineral density loss.

“Prednisone stops the function of bone-forming cells. When that happens, the body still needs calcium, so it takes it out of the bone, but it’s not allowing the bone-forming cells to put it back,” he says. The result: Weakened bones that boost a person’s risk for falls and painful fractures.

Corticosteroid drugs like prednisone and even disease-modifying antirheumatic drugs like methotrexate can interfere with the body’s natural process of bone remodeling – the body’s way of  putting calcium back into bone to keep it strong. Newer inflammation-fighting drugs, like the biologic class of drugs that include TNF inhibitors etanercept and adalimumab, can control inflammation without interfering with bone remodeling. 

Some early studies suggest that they may help reduce bone loss or boost bone mineral density build-up for RA patients. But experts are divided on whether the bone mineral density benefit of using these powerful – but expensive – new drugs is that they aggressively control inflammation early and, therefore, prevent bone loss, or whether the drugs themselves protect the bones apart from their inflammation-fighting power.