Osteoarthritis (OA), also known as osteoarthrosis and degenerative joint disease, is described as the most common chronic joint disease causing large amounts of disability and pain in the community. It occurs most often in the spine, knees, hips and hands. 

Perhaps because OA is so common, nearly everyone has their own theory and ideas about what causes it and what you should do. So I'll sort through some of the facts and fiction based on evidence about what causes and worsens OA.

Definitions given to OA largely determine how this condition is treated, but recent studies indicate they are limiting the scope of what can be done to help recovery. So first let's look at how OA is defined.

Definitions

According to the American National Institutes of Health (NIH):  ‘Osteoarthritis is a joint disease that mostly affects cartilage, whereby the cartilage breaks down and wears away. This allows bones under the cartilage to rub together... (which) causes pain, swelling and loss of motion of the joint. Over time, the joint may lose its normal shape. Also, bone spurs may grow on the edges of the joint. Bits of bone or cartilage can break off and float inside the joint space, which causes more pain and damage.’

Further, according to the Australian Arthritis Foundation: ‘The older you are, the more likely you are to have some degree of primary osteoarthritis. However, not everyone gets it – not even the very old. That’s because osteoarthritis is a disease, and not part of the normal aging process. Osteoarthritis can also damage ligaments, cartilage discs (menisci) and muscles.’

A better understanding of how you load your joints is key to recovery

According to Professor of Orthopaedic Surgery at The University of Iowa, Joseph Buckwalter, prevention and treatment of OA is based on a better understanding of the primary role that mechanical forces play in the initiation and progression of joint degeneration. Professor Buckwalter states that decreasing mechanical forces to within tolerance levels on degenerated joint surfaces stimulates formation of a new biologic joint surface, so they can then begin to tolerate greater loads over time. 

OA is not "wear and tear" of the joints

One of the most entrenched beliefs about arthritis is that it is a result of “wear and tear” caused over time by repeated loading of a joint. But is this actually what happens?

Let's take the most frequently affected joint by OA - the knee. It’s easy to understand why long distance running is often thought to cause knee arthritis, since four to five times the body weight moves through a runner’s knee with every pounding of the foot against the pavement. Common sense would suggest that repeatedly applying such loads to a joint should eventually erode its protective cartilage, leading to arthritis. But this is not actually the case.

From the age of 18 through to his retirement at age 36, Robert de Castella, one of Australia's most famous marathon runners, clocked up around 250km a week, or 10,000km a year, covering a total of roughly 180,000km over his elite competitive life.

You might expect that Roberts' knees would have worn out after so many K's, but he says: ‘My knees were really good, I had very few injury problems and my knees stood up really well. It’s more in the last 5 years since I’ve been doing a lot less running that I’ve started to get knee pain’. Once Robert became more active and started running again for enjoyment his knee pains disappeared. Studies involving large numbers of runners show that Robert's knees are not unusual, at least not in this respect.

Professor Dieter Leyk, of the Institute for Physiology and Anatomy in Cologne, Germany, states that medical studies on aging have focused on biological processes, but have widely ignored the question of how much physical decline is caused by changed everyday habits (for example, a less active lifestyle). These studies have assumed that loss of performance begins around the age of 30 and is “fateful”. He says that this idea is disproved by the now available data.

One of Professor Leyk’s large cross-sectional studies involving around 75,000 runners, found “no evidence that running increases the risk of osteoarthritis, including participation in marathons.” The runners in the study, in fact, had less overall risk of developing arthritis than people who were less active, precisely and seemingly paradoxically because it involves so much running.

Cartilage thrives on cyclic loading, where a force is repeatedly applied to a joint, removed, and then applied again, such as running, walking and swimming. This type of loading stimulates cartilage cells to multiply and replenishes cartilage tissue.

Going on a slight tangent but related to ageing, another of Professor Leyk's studies examined almost a million running times and the responses to a questionnaire about sports, lifestyle, and health of 13,171 marathon and half-marathon runners aged 20 to 79.

They found no significant decline in performance before the age of 55. Average marathon and half–marathon times were nearly identical for the age groups from 20 to 49 years. And only declined moderately thereafter.

In fact, they found a quarter of the 65- to 69-year-old runners were faster than half of the 20- to 54-year-old runners. Their survey also revealed that over a quarter of the 50– to 69-year-old runners started their marathon training only in the previous 5 years.

Professor Leyk concluded that losses in performance in middle age are mainly due to a sedentary lifestyle, rather than biological aging. The results also show that, even at an advanced age, non-athletes can achieve high levels of performance through regular training.

OA is not purely a joint disease

The prevalent view that osteoarthritis is purely a joint disease, that can also damage your soft tissues, as the definition above indicates, is being challenged by recent research findings. Professor Benjamin and his team at the School of Biosciences, Cardiff University, Wales, demonstrated it’s the other way around.

Their MRI studies show that the earliest signs of osteoarthritis in the joints of the lower back, shoulder, knee,  and hand occur in the tendons and ligaments surrounding those joints. Cartilage defects and bone irregularities develop later. Their findings make sense because compared with your bone and cartilage, your soft tissues are more reactive to overloading so they will show the earliest signs of strain. 

The recently late, Professor Harold M. Frost, considered to be one of the most important and is one of the most cited researchers in the field of bone biology and bone medicine, stated that the greatest influence on the shape of your joints, for better or worse, after you’re born, given adequate nutrition and hormonal levels, is voluntary muscle force. Despite the widespread exclusion of muscle in the definition of osteoarthritis, muscles are of prime importance.

Muscles attach deep inside or very close to many of your joints. Early fibrotic change often forms close to these attachments because almost all of the force generated by the rest of the muscle is focused there. Fibrotic changes can restrict joint movement and can give rise to deep “joint like” pain.

Sustained loading of the muscles surrounding your joints leads to excess sustained compression of its cartilage. Many studies have found that this leads to your cartilage cells to release chemicals (enzymes) that break down cartilage, a key mechanism associated with osteoarthritis.

Whichever way you look at it, the forces generated by your muscles, particularly sustained forces, are key to understanding the loads acting on your joints and what you can do to recover new biologic cartilage. 

Your joints can regenerate

Another prevalent view is that osteoarthritis is a degenerative disease. This implies that once you have osteoarthritis it will keep degenerating and your pain will keep getting worse. Degeneration also implies that OA is irreversible. But this is not necessarily the case as Professor Graham Jones and his team at the Menzies School of Research, Tasmania, found.

In 2008, they followed the natural history of 325 knees with diagnosed arthritis. They measured defects in cartilage volume, bone size and bone spurs (osteophytes) found on X-rays at the beginning of the study.

When they remeasured two years later they found that 37% of the knees had less arthritis - these knees had regenerated. This was particularly associated with a reduction in body weight - or in other words - reduced excess compression. But there are many more common ways of unnecessarily over-compressing your joints.

Jones’s research was initially rejected by a leading arthritis journal due to the reviewers’ belief that, once destroyed, cartilage does not grow back so there must have been a mistake in their data. At that time it was widely believed that once you had arthritis there was no going back. The best you could hope for was to halt the progress or more likely slow it down. Jones's research, however, turned this idea on its head by showing that your joints have a similar potential for reversal as other tissues in your body, only perhaps a little slower.

Muscle, cartilage and bone: use it or lose it

The old adage “use it or lose it” is certainly true for your joints and surrounding muscle. Lack of mechanical stimulation results in loss of muscle mass and decreased cartilage and bone strength, which reduces your joints tolerance levels to mechanical loading. This occurs by your cells removing unused material, which is resorbed back into your system. This is part of your body's extraordinary efficiency in not wasting your precious energy on unused tissue. 

Adequate mechanical stimulation is at least as important for your bones as adequate  nutrition. A severe reduction of mechanical stimulation results in bone thinning (osteoporosis), increasing the risk of bone fracture. Osteoporosis is a major concern for astronauts, who are deprived of the effects of gravity, and also for people undergoing prolonged bed rest recovering from a severe illness. While these are extreme examples, more commonly bone thinning can result over time with an increasingly sedentary lifestyle.

Muscle wasting, or atrophy, occurs more rapidly than generally thought. It may take a few weeks or a couple of months for you to notice weakening of your muscle strength, but the underlying processes of muscle loss occur immediately.

When deprived of mechanical stimulation, the rate of bone resorption is much slower and less dramatic than for muscle. On the other hand, it takes three to four times longer to recover that bone loss.

Reduced loading results in cartilage thinning at a slightly faster rate than bone but again the rate is slower than for the changes that occur in muscle. In 2002, highly regarded arthritis researcher Dr Vanwanseele and her team at the Swiss Federal Institute of Technology in Zurich were the first team to show that progressive cartilage thinning occurs in the absence of normal joint loading and movement.

They measured the changes in the knee cartilage of spinal cord-injured patients over a two-year period. Over the first six months the cartilage thinned by about 2.5% per month. This slowed to about 1.5% per month over the next six months. So after twelve months the cartilage had thinned by about 20%. Over the next 12-month period, no further thinning occurred, showing us that, as with muscle and bone, disuse wasting stops at a certain baseline.

Conclusion

Keeping active throughout your life is key to healthy happy joints. But being in pain may significantly limit what you can do and lead to a vicious cycle of inactivity and pain. Understanding what you can do to regenerate your tissues may break this cycle of pain leading to greater mobility, strength and quality of life.