How to fix joint pain

At first, Agnieszka Ozieblo refused to let the pain in her right knee slow her down. The office worker, now 56, carried on with her favourite activities: brisk walks near her home in Warsaw, Poland, and longer hikes along mountain trails whenever she could. But about 15 years ago, her knee screamed in protest just walking around town. She went from doctor to doctor. X-rays revealed her diagnosis: osteoarthritis (OA), often simply called arthritis, the most common of joint disorders.

If you’ve ever eaten a chicken leg, that rubbery gristle you see covering the ball and socket where the bones meet is actually cartilage, much like our own. And it’s what gets damaged in OA, usually after decades of wear and tear, or through injury. It typically starts in the cartilage, but OA doesn’t necessarily stop there.

“I was scared that I would be immobilised for good”

“Once you get damage to cartilage, the bone that supports it starts to get damaged,” says Philip Conaghan, professor of musclo-skeletal medicine at the University of Leeds and medical advisor to Arthritis Research UK. Because cartilage is slow to grow back, the bone grows instead, attempting to fill the gap. This “repair” makes the problem worse.

As if this weren’t bad enough, it “isn’t the only source and cause of osteoarthritis”, says Dr Eric Strauss of NYU-Hospital for Joint Diseases in New York. “It’s that, combined with the production of inflammatory enzymes in the joint.” Those enzymes rush to the scene of the injury, where they break down more cartilage. The cycle keeps repeating itself, causing more disability as it progresses.

Although OA can affect almost any joint, it most commonly occurs in the knees, hips, hands and spine. The condition is especially prevalent in people older than 50—and about half of everyone older than 65 has it to some degree. But it can also occur in younger people, especially those who carry a bit too much weight and thus overload their joints. Losing weight can’t stop OA, but it often reduces the aching of over-taxed joints.

Genes play a role in OA. Gender does as well: women are more susceptible. And the joint injuries you suffer in sport can set you up for OA years later.

Although exercise might seem to be the last thing you’d want to do with tender joints, it can reduce the pain of OA-affected knees and make it easier to get around. And, counter-intuitively, exercise can also be anti-inflammatory. Of course, if you have a painful joint, you should only start an exercise programme under the supervision of a physiotherapist. And although we often hear that walking is great exercise, in OA, explains Professor Conaghan, it might not be your best choice because “it doesn’t build muscle that well”.

He does, however, suggest “walking laps in a swimming pool”, as that, unlike strolling or hiking, builds muscle. Other exercises that might help include non-weight-bearing activities such as riding an exercise or road bike, or using gym equipment such as a cross-trainer or glider.

A 2011 analysis of previous studies found that while physiotherapy can improve symptoms, there was no evidence that it could stop the progression of OA. Even so, says Stefan Lohmander, professor of orthopedic surgery at Lund University in Sweden, it might help you delay the need for more aggressive treatments.

Physiotherapy did help to reduce Agnieszka’s knee pain at first. But eventually, OA’s progression outpaced exercise’s benefits. About five years ago, Agnieszka’s left knee began to hurt too. “I was scared that I would be immobilised for good,” she says.

Fortunately for her, newer treatments held promise for better results. Her doctor performed arthroscopic surgery on her knee in an attempt to repair damaged cartilage. But it brought her “no relief”.

Then, in 2012, Agnieszka heard of a promising new OA treatment: platelet-rich-plasma (PRP) injections. Cartilage doesn’t heal itself readily, and one major reason is because it lacks a blood supply. The platelets in blood are necessary to healing. PRP treatments are autologous, meaning that the patient’s own blood is used. Doctors separate out the platelets and plasma in a centrifuge, then inject the resulting PRP into the arthritic joint.

Agnieszka had PRP injections in January 2012. While they may not work for every patient, she, at long last, found sweet relief. For more than six months, “I didn’t feel any pain.” Although her symptoms gradually returned, Agnieszka doesn’t feel discouraged. She’s considering having PRP treatment again.

When Marja-Liisa Tapaninen's right knee began to ache, she didn’t change her active routine. But soon after, OA struck her left knee as well. By 2007 both knees had become so painful she had to give up her evening walks.

Physiotherapy didn’t bring much relief. “I took hyaluronan injections in both knees, but to no avail,” says Marja-Liisa. Injections of this natural component of joint fluid, or of corticosteroids, are often recommended by doctors. While each person responds differently, steroid injections typically reduce symptoms for about a month or two, while hyaluronan’s effects may last longer.

In November 2011, she had both knees replaced. Now retired, she takes long walks, skis, goes dancing with her husband and even takes Zumba lessons. Again doing physiotherapy to keep her muscles strong, Marja-Liisa says she’s extremely happy. “I’m living the time of my life. And I can exercise as much as I wish.”

As with PRP, cells are taken from the person’s body, typically from bone marrow or fat tissue. In studies these cells appear to “slow down the body’s inflammatory reaction”, says Dr Strauss. “They also have the potential both to block further damage and regenerate new cartilage.”

But Professor Lohmander cautions that unscrupulous practitioners are already advertising untested treatments using stem cells. “The evidence for these treatments being effective is essentially non-existent,” he says. The dangers of infection or complications at unregulated facilities, however, are very real.

“I envision a time when we don’t replace a total joint,” says Dr McClelland. Instead, he sees surgeons in the not-too-distant future transplanting new cartilage that’s grown in a lab using the patient’s own cells.

Although no one has yet perfected bioengineered cartilage that can both adhere to the natural bone and with stand the stress we place on our joints, several research facilities are working to develop it.

Dr Strauss’s research in this area focuses on preventing OA from developing after an injury to a ligament—the tough band of tissue that holds together a joint. Even when the ligament is successfully treated, “ten to 20 years later, about 60 to 70 percent will develop arthritis”, says Dr Strauss.

If there’s any imbalance in the cocktail of enzymes that the body rushes to the injury, it can damage cartilage. The imbalance might be different in each patient, but once identified, he says, doctors should be able to correct it and stop OA before it starts.

The older we get, the greater the risk we’ll get osteoarthritis. But people with OA have a number of good treatment options available today—and even better ones might be just around the corner.