30+ things doctors wish you knew about arthritis

A device called Coolief uses specialised electrodes to send water-cooled radio waves into the tissue around your knee, which temporarily deactivate nerves. Patients reported greater, longer-lasting pain relief (up to 12 months) with Coolief than with cortisone injections.

Scientists have programmed stem cells to grow new cartilage on a 3-D template shaped like the ball of a hip joint. Using gene therapy, they have also activated the new cartilage to release anti-inflammatory molecules to fend off a return of arthritis. But the stem cell therapy offered for knee osteoarthritis in many clinics isn’t yet a proven cure.

People with low levels of vitamin D are at a higher risk for autoimmune diseases, though Dr Blum notes that low D isn’t the sole trigger for arthritis. Still, it could be one piece of the puzzle and could help explains why researchers have found that people with low blood levels of vitamin D, which boosts immune function, are at higher risk for RA. One great free source of vitamin D: sunshine.

Here are 10 ways to get your vitamins and minerals working better for you.

While there’s no way to reverse joint degeneration, getting treated as soon as possible after the onset of pain and stiffness can curb symptoms and prevent further damage. “The earlier you treat, the better,” says Dr Paula Marchetta, clinical professor of medicine at the New York University School of Medicine and president of the American College of Rheumatology. Unfortunately, a 2016 national survey found that it took people with RA four years and visits to at least three different doctors to get a proper diagnosis.

Early results from one study showed that for people with mild joint aches and high inflammation levels, one shot of rituximab cut the risk of developing rheumatoid arthritis in half. The drug, which belongs to a class of medications called monoclonal antibodies, blocks the production of compounds that trigger inflammation. “Rituximab can help put RA into remission and prevent joint damage, and most patients respond well to it,” says Dr Marchetta.

Here are 10 proven ways you can fight inflammation.

Monoclonal antibodies aren’t the only drugs for RA, notes Dr Marchetta. Disease-modifying antirheumatic drugs (DMARDs) decrease inflammation and slow the progression of RA.

“A drug may stop working after several years. Some people have to try several before they find the one that works best,” says Dr David Daikh, PhD, director of the rheumatology fellowship program at UCSF. “We don’t know why some medications stop working,” says Dr Marchetta. “There’s just an individual variation of response.”

A class of medications called biologics – drugs such as etanercept (Enbrel), golimumab (Simponi), and adalimumab (Humira) – are engineered from human genes and are usually an option if you haven’t responded to DMARDs. They work by targeting specific parts of the inflammation process rather than suppressing the immune system in general (as older DMARDs do), so they tend to have fewer side effects. One inflammatory target they zero in on is TNF or tumour necrosis factor, a chemical your body makes that drives the inflammation process in RA, says Dr Marchetta. Unfortunately, biologic drugs are also more expensive than traditional medications.

Tumour necrosis factor (TNF) is an inflammatory protein responsible for pain and cartilage degeneration in RA, and drugs called TNF inhibitors can sometimes block it. And if one TNF inhibitor – such as etanercept (Enbrel) or adalimumab (Humira) – doesn’t work, try another. In a recent study, 43 per cent of patients who didn’t respond to one type of TNF inhibitor responded positively to a different one.

“Almost every patient does better with a combination of a TNF biologic and a drug called methotrexate, says Dr Marchetta. Methotrexate is one of the most effective drugs to treat RA and is the first drug most doctors prescribe after you’re diagnosed.

You should be asking your pharmacists these questions to avoid medication errors.