Knee Arthritis Pt. 2

A few weeks ago I wrote a short blog about knee arthritis – and it sparked some interesting responses. In this blog, which might be a little heavier in terms of science talk (but bare with me), will start to elude to what might be a greater contributor to knee arthritis than just mechanical wear and tear alone.

I have to clarify, don’t get me wrong, it is inevitable the as we age, there is an element of mechanical loading that contributes to arthritis – but if we looked at a ‘pie chart’ of current thinking about OA knee’s – the pie chart is overwhelmingly dominated by the ‘wear and tear’, ‘mechanical breakdown’ mentality. All i’m saying is that this might be a smaller piece of the pie than is currently understood…

Talking about pie is a great segue actually! Metabolic syndrome is characterized by obesity, hyperglycemia (high blood sugar), hypertension (high blood pressure), insulin resistance (common with diabetics), and dyslipidemia (high levels of fat). Hang on, we’re talking about knee’s and arthritis, you say…

Yes, but this is the thing. There is emerging evidence that metabolic syndrome and even high blood pressure alone can contribute to arthritis. This is one the the heavier sentences you’ll read but i’ll do my best to translate:

“Chronic activation of innate immune responses in chondrocytes results in a robust production of pro-inflammatory cytokines and chemokines, as well as of tissue-destructive enzymes, downstream of NF-κB and MAPK (mitogen activated protein kinase) dependent pathways.”

Translation:

Cells that make cartilage can be worn down faster by inflammatory chemicals. These inflammatory chemicals can be kept hanging around at a very low level by elements of metabolic syndrome and the body’s response to the elements of metabolic syndrome.

Here is a nice, easy to understand picture of the above

Now, because we can’t be mean to humans in research, we pick on poor mice. In this study they subjected a group of poor mice to eating a high fat diet, and a group to a normal diet – both groups were then anesthetized and forced loading applied their joints (specifically their front left tibia) over a number of weeks. After 6 weeks of loading, the high fat diet mice had increased load-induced cartilage damage and also had increased blood inflammatory markers compared to normal diet mice! Both groups received the same amount of mechanical loading.

This study found that longer-chain dietary saturated fatty acids (SFA) in rats induced both metabolic syndrome and OA-like knee changes. Thus, diets containing SFA are strongly relevant to the development or prevention of both OA and metabolic syndrome.

Back to humans though – this study of over 1000 people found there was a higher frequency of obesity, hypertension, dyslipidaemia, and metabolic syndrome in people who had erosive arthritis in the hands. Now, we don’t walk on our hands – so why did those with hand OA have metabolic syndrome more often and vice versa?

Because readers, perhaps mechanical loading isn’t the only factor – perhaps there is a systemic, low level of chronic inflammation (from metabolic syndrome and its constituents) that worsens our cartilage health, that only THEN combined with mechanical loading leads to more OA.

For the clinicians out there – we know how strong the evidence base is for general exercise in improving pain with knee arthritis – as we often put this down to strengthening muscle, losing weight, lubrication of joints and gently loading cartilage, all good things of course! But perhaps, when we start our patients off on a general cardio programme, we’re also addressing metabolic syndrome and it’s individual constituents too, maybe we’re getting rid of low levels of chronic inflammation and maybe that’s the thing that helps our patients even more…