​Osteoarthritis (OA) is a leading and increasing cause of disability and has a significant impact on health-related quality of life. OA places considerable burden on the Australian  healthcare system, affecting 2.1 million Australians (ABS 2022) and costing $4.3 billion annually. 

Osteoarthritis is a structural change to the cartilage and boney surfaces in a synovial joint. Most of the joints in our skeletal system are synovial joints, which is where two opposing bones articulate in a joint capsule filled with synovial fluid. The synovial fluid is a lubricant to help the joint move, as well as a source of nutrition for the cartilage that lines the joint surfaces. The articulating surfaces in synovial joints are lined with articular cartilage, which is a smooth, glossy surface to decrease the friction in the joint (as opposed to fibrous cartilage, which is the rubbery type cartilage that plays a more structural role, found in the meniscus in knees and the rubbery part of your ribs, nose, and ears).

The fleshy parts of muscles and organs is pink because it is full of blood, which brings oxygen and nutrition, and is important for healing damage. Cartilage looks white because it doesn’t have a blood supply, so articular cartilage relies of the synovial fluid for its nutrition. This isn’t as effective as having a blood supply, so when cartilage is damaged it doesn’t heal well. Nanna damages the cartilage in her knees and it never really repairs.

Once articular cartilage is damaged, the joint tries to reinforce and repair the damaged area by laying down new tissue. It would be great if cartilage repaired itself with new cartilage cells, but the joint wants to make itself even stronger than the obviously insufficient cartilage, so it lays down a stronger building block - bone cells. So when we say that Nanna has “worn away” her knee to the point where it’s “bone on bone”, it’s not just that she’s worn away the cartilage, but actually there’s also a build up of “extra” bone, as the knee tries to make itself stronger than cartilage. Rather than being a nice smooth, glossy surface, the extra bone is now a bit rough, so we might hear and feel some gravely crunching and creaking in an osteoarthritic joint.

Osteoarthritis occurs most frequently in the knees, hips, hands, and spine and is more common the older we get. 59% of people with OA have knee OA. Osteoarthritis is diagnosed with an X-ray that shows the changes to the bony profile in the joint.

When we look at what causes osteoarthritis:

1. The biggest contributor is a previous traumatic injury that has physically damaged the cartilage. This can be a landing/twisting injury or sprain, where the trauma of knocking one bone against the other, takes a “divot” or tear in the cartilage, or bruises the cartilage and underlying bone. 
2. The second biggest cause of osteoarthritis is genetic - the way our joints age, based on our family history. Nanna had a hip replacement and so will I.
3. The third biggest contributor to osteoarthritis is BMI. Every 5 kg of weight gain, confers a 36% increase in the risk of OA. Interestingly, it isn’t the extra pressure through the joints of being heavy that causes a problem - fat people have a higher rate of hand osteoarthritis too (which are non weight-bearing joints). The problem with BMI is the systemic inflammatory effect of cytokines produced by fat tissue. Being fat causes inflammation that irritates joints, so fat people get osteoarthritis (and have heart attacks from the scarring/hardening of coronary arteries, also as a reaction to systemic inflammation caused by adipose tissue).

Osteoarthritis isn't painful most of the time. At a certain age, essentially everyone will have arthritic changes in their joints without knowing about it. When we X-ray the joint, it doesn’t look as good as it used to, but it doesn’t hurt. It’s a bit like my grey hair and wrinkles - they don’t look great anymore, and it's a sign that I’m getting older, but I don’t expect them to be painful.

If an arthritic joint is painful, it tends to go through phases of being sore and not being sore at all. It can be sore for a day, a week, a month, or a year, but then will be fine again. Whether or not it is sore is not determined by the severity of the changes we see on the X-ray. We can see nasty looking joints that have never been sore, and we see very sore joints that look fine on the X-ray. There isn’t much of a correlation. 

What determines whether or not the osteoarthritis hurts is the body’s perception of "vulnerability" in that joint - essentially whether or not it feels strong or weak. Pain is an alarm system “software”, employed to defend against damage to the "hardware”. We can have different levels of sensitivity of how easily the alarm is triggered. Very commonly, an arthritic joint starts to hurt more after a period of rest, as the body looses some fitness, muscles loose some strength, an arthritic joint gets less support from the external scaffolding of the muscles, it feels more vulnerable, and communicates that by being painful, as a way of saying “be careful”.

So that gives us some treatment options for arthritis:

WEIGHT LOSS (Adipose)

• We know that a 5kg reduction in weight over a 10-year period decreased the likelihood of symptomatic knee OA by 50%. 
• Losing 5% of body weight has been shown to provide some pain relief, and 10% provides significant reductions in pain.

EXERCISE

• Stay as active as possible. Rest doesn’t help. Improve muscle mass and strength so the joint is more supported and feels less vulnerable.
• Both aerobic walking and quadriceps' strengthening exercises have been shown to reduce pain and disability in subjects with knee OA.

PAIN RELIEF

• Paracetamol.
• Hot packs.
• Taping.
• Sleeves.

SURGERY

• There’s a lot of research showing that “tidy up” operations, or arthroscopic surgery for osteoarthritis is no better than an exercise program. It’s the exercise you do after the surgery that provides more benefit than the surgery itself. 
• For people that never get on top of their arthritis with weight loss and exercise, the pain can get so severe that they end up needing a total joint replacement, where the bones are replaced with a metal and plastic joint. 

How do you decide when it’s time to have a joint replacement?

I suggest it’s time when you really can’t walk anymore because of the pain, and/or the pain is stopping you sleeping at night. Joint replacements last for about 25 years on average, so don’t rush into doing it too early. The rehab after surgery is 3-12 months before the leg completely feels like it’s yours. The joint replacements are good for relieving pain, but unfortunately we don’t see improvements in patients’ activity levels after surgery. Total hip replacements are easier all around than total knee replacements. 

This is a very common presentation, and having an arthroscopic debridement is a very popular decision. 75,000 knee arthroscopies are performed in Australia each year. Therefore, you would imagine there is good evidence to support having one. Unfortunately it depends on who you speak to…

A change has been in the air since a 2002 randomised controlled study allocated 180 patients with knee pain to either an arthroscopic “tidy up”, or sham surgery (where the patient was given an anaesthetic, incisions were made, but no actual “tidying up” was done) and the study concluded there was no meaningful difference in pain or function between the groups at follow up.

Since then, a number of studies have compared arthroscopic debridements and partial meniscectomy for degenerative knee injuries with exercise or doing nothing (Herrlin 2007, Kirkley 2008, Katz 2013, Sihvonen 2013, Yim 2013, Kise 2016) and the results have been unanimous.

A recent systematic review summarises: “these findings do not support the practise of arthroscopic surgery for middle aged or older patients with knee pain, with or without signs of osteoarthritis.”  

And another: “A trial of nonoperative management should be the first-line treatment for such patients.” 

“This high quality evidence dictates that meniscectomy is an ineffective treatment for symptomatic degenerative meniscal tears.”

And that…

“Arthroscopy for degenerative meniscal tears is no longer supported.” (ref)

And

“There is now overwhelming evidence that arthroscopic knee surgery offers little benefit for most patients with knee pain.” (ref)
​​

We do a lot of arthroscopes and people get better. What’s happening?

When you come and see me with degenerative knee pain and I tell you, “you need to do six to twelve weeks of strengthening exercises”, it isn't quick and easy. Understandably we want there there to be a better option. “Have surgery” doesn't sound too bad.

​After the surgery, you proceed to do six to twelve weeks of strengthening exercises, but this time you’re happier to do the work because we take surgical post-op instructions seriously.

Twelve weeks later both these two groups are a lot better. Bingo-bango, “surgery” fixed me.

Two million knee arthroscopies a year globally, costing billions of dollars.
​

A pretty typical pathway goes something like:

• Sore knee
• GP says “you’re silly to have played football”, try some pain killers
• Not much better
• GP says “we better get a scan”
• MRI shows “degenerative changes / meniscal tear” which seems like a structural injury
• Who fixes structural injuries?… Surgeons
• GP refers to surgeon
• Surgeon wants to help. What can he do? An arthroscope and a “bit of a tidy up”.

​I think we need to be careful at the MRI stage. MRIs are a lot cheaper and easier to get these days so it’s less of a big deal to get one. I was chatting to a mate with a sore knee and his MRI showed some degenerative changes. Rather than being told that it’s normal to see those sorts of things in knees as old as ours, and that it’s not necessarily the thing that’s giving him pain, he was told the knee is “bone on bone”. How can anyone ever expect to recover without surgery with that sort of imagery? Bone on bone seems definitive. Surely the only way to fix “bone on bone” is surgery?

But we know degenerative changes on MRI are poorly associated with symptoms, and degenerative changes are the norm in middle-aged knees (ref). 

Let’s try some strengthening. You will be surprised.
​

The people I do refer to a surgeon for cartilage surgery have suffered an acute twisting injury with mechanical “locking” symptoms (i.e., an inability to fully extend the painful knee because of a meniscus tear lodged between the articular surfaces).
​

PT Inquest, my favourite physio podcast, recently discussed this paper:

The abstract summarises:

In contrast to best practice guidelines for knee osteoarthritis (OA), findings from several different healthcare settings have identified that nonsurgical treatments are underused and Total Knee Replacement surgery is overused. Empirical evidence and qualitative observations suggest that patients’ willingness to accept nonsurgical interventions for knee OA is low.

Participants’ beliefs about knee OA and its treatment were identified. Beliefs were grouped into five belief dimensions:

• identity beliefs (what knee OA is),
• causal beliefs (what causes knee OA),
• consequence beliefs (what the consequences of knee OA are),
• timeline beliefs (how long knee OA lasts),
• treatment beliefs (how knee OA can be controlled).

The participants' beliefs are what I would guess, based on what I hear from patients everyday:

• All participants believed that their knee OA was “bone on bone” (identity beliefs).
• Most believed it was caused by “wear and tear” (causal beliefs).
• Most believed that loading the knee could further damage their “vulnerable” joint (consequence beliefs).
• All believed that their pain would deteriorate over time (timeline beliefs).
• Many believed that physiotherapy and exercise interventions would increase pain and could not replace lost knee cartilage (treatment beliefs).
• They preferred experimental and surgical treatments which they believed would replace lost cartilage and cure their knee pain (treatment beliefs).

The authors conclude: 

Common misconceptions about knee OA appear to influence patients’ acceptance of nonsurgical, evidence-based treatments such as exercise and weight loss.

Once the participants in this study had been “diagnosed” with “bone-on-bone” changes, many disregarded exercise-based interventions which they believed would damage their joint, in favor of alternative and experimental treatments, which they believed would regenerate lost knee cartilage.

​The concept of "WEAR AND TEAR" makes sense if you imagine the joint as mechanical. A cupboard's metal hinge can be opened and closed a certain number of cycles before it breaks. Metal and plastic fatigues and fails. Mechanical joints "wear out". But our joints aren't made of metal and plastic. Knees are not mechanical joints. They are biologically active joints, that adapt to what we do. 

If we do a million bicep curls, we don't expect our biceps to "wear out" - we expect to end up with bigger, stronger biceps. Similarly, the bones, cartilage, ligaments and muscles in our knees are biologically adaptive, they have regenerative ability, and adapt to what we do. Our joints get stronger with use.

Rather than "wear and tear", the more appropriate phrase should be: "use it or lose it".

Another common misconception is that running "wears out" knees.

Doctors and knee surgeons see patients complaining they have sore knees when they run. The X-ray shows some arthritis, so it's very easy to make the assumption that running causes arthritis. But we know that distance runners don't "wear out" their knees. Runners have better knees than non-runners. ​

This 2017 research comparing 2,637 runners to non-runners (matched for age, weight, mileage, injury, and other variables) concludes: There is no increased risk of symptomatic knee OA among runners compared with non-runners. In those without OA, running is not detrimental to the knees. 

This 2008 research concludes: Long-distance running among healthy older individuals was not associated with accelerated radiographic OA, and long-distance running or other routine vigorous activities should not be discouraged among healthy older adults out of concern for progression of knee OA.

This 2004 research concludes: The results of this literature review strongly suggest that regular mild-moderate impact exercise does not increase the risk of OA, and that there is some evidence that it does not increase symptoms in patients with mild-moderate OA. And: Regular running increases joint space width.

So:

• Running does not cause osteoarthritis.
• Osteoarthritis is not caused by "wear and tear".
• Most osteoarthritis should not be considered "bone on bone".
• Research supports the conservative treatment of osteoarthritis with weight loss and exercise.

A systematic review and meta-analysis published in the British Journal of Sports Medicine has concluded PRP injections for osteoarthritis of the knee reduce pain and improve function when compared with placebo injections and hyaluronic acid injections.

However the results should be regarded with caution as almost all the analysed trials included a high risk of bias.  Therefore further research is required.

Efficacy of platelet-rich plasma injections in osteoarthritis of the knee: a systematic review and meta-analysis (Laudy, 2014).