When I was 28 years old, I was diagnosed with advanced stage osteoarthritis in my knee. I had injured it playing soccer as a teenager but, after surgery, it felt fine for years. The pain was hardly noticeable at first, just a little tenderness after a run or a long hike. But within a year or two, my knee was swelling up just from standing too long.
And I’m not alone. According to the Arthritis Foundation, about one in two people are affected by osteoarthritis at some point in life.
What has always surprised me – and what started me down the road to researching joint lubrication and arthritis – was how rapidly my condition progressed and how few treatment options were available.
For all intents and purposes, osteoarthritis is the end result of a complete breakdown of cartilage’s natural lubrication system, which ameliorates friction and protects surfaces from damage. Although cartilage uses a number of different easing processes, one of the most important is known as ‘weeping’ or ‘biphasic’ lubrication.
The structure of cartilage is rather like a water-swollen sponge made up of a dense collection of collagen micro-fibres linked into one continuous network. This three-dimensional net of fibres forms pores so small that the fluid inside cannot easily flow between them.
Every time you take a step, cartilages on opposing bones press together. The fluid trapped in the collagen fibre network becomes pressurised.
In healthy cartilage, the fluid pressure can equal as much as 99% of the pressure pushing the surfaces together, so supports 99% of the weight. The collagen fibril network, therefore, only ‘feels’ 1% of the weight. In other words, the trapped fluid takes the burden off the tissue surface and so prevents damage.
Osteoarthritis is a disease of wear of the collagen fibril network – but not all types wear are the same. Most people are familiar with abrasive wear – the sort of damage done to wood when it’s rubbed with sandpaper. This is the kind of wear associated with a related disease known as gout, the main symptoms of which, pain and inflammation, are caused by the precipitation of crystals in the joint fluid and become obvious early on.
The kind of wear associated with osteoarthritis is different and less obvious. It has the characteristics of fatigue wear, a process in which repeated compression and shear of a material produces tiny defects below the surface. In cartilage, these take the form of breakages in the links between collagen fibres and result in small ‘holes’ in the interconnected network.
When these defects are few in number, there is no obvious change in the cartilage’s properties, and the damage cannot be assessed non-invasively by a doctor. Stiffness, thickness, density and how rapidly water diffuses inside are not affected by just a few breakages. Think of a fishing net: cutting a small number of links is not going to alter its strength, nor significantly change its ability to catch fish.
But these tiny anomalies concentrate stresses in the collagen fibre network every time it’s compressed, and this gradually creates more defects in the material. Eventually, as the damage accumulates, the breakages start to merge into larger tears – a process scientists call ‘percolation.’
At this point, the now large defects begin to radically change the properties of the tissue. The cartilage softens, its surface roughens and cracks, and most importantly, the collagen fibre network no longer retains water – just like a badly torn net can no longer trap any fish.
Since the water in the tissues flows more easily, the pressure in the fluid drops significantly when you take a step and cartilage is compressed. The reduced fluid pressure shifts more of the burden onto the compromised collagen network. So instead of supporting 99% of the weight, the fluid might only support 50% – or nearly none at all in severely damaged tissue – which in turn accelerates the rate of wear.
In essence, cartilage’s main mechanism for lubrication and wear protection no longer functions effectively. Equally unfortunate is that it is typically at this point that an osteoarthritis sufferer will begin noticing pain and swelling in their joints, and treatment options are limited because the damage is already too severe.
Fortunately, there is hope. Scientists are beginning to identify chemical (rather than physical) markers that seem correlated to the beginning stages of osteoarthritis. These biomarkers – elevated or reduced levels of specific molecules – found in the blood or urine, create characteristic patterns much like a chemical fingerprint that can identify different stages of osteoarthritis progression. Although not available to doctors yet, biomarker-based early screening trials are showing promise.
I can’t help but wonder how early detection of my arthritis might have improved my quality of life not just today but years from now. How if I had started a program of disease management and lifestyle and exercise changes I might have kept the wear in my knee in check. Hopefully, the development of new diagnostic tools may one day help prevent the unnecessary suffering of millions.