We tend to treat osteoarthritis as a mechanical problem to be fixed. But what if it became a cellular problem to be eradicated? Dave Duffy looks at new research that could one day change the nature of the way we approach osteoarthritis.
There’s a problem with the way we traditionally treat osteoarthritis (OA). We’ve never been able to ‘cure’ it, so all that’s left is to fix the problems it causes. That’s left orthopaedic surgeons looking rather like the medical equivalent of garage mechanics. When your car’s tyres are worn down, you get them replaced. And when your knee’s cartilage wears away, as is the case with OA, it’s time to get that replaced (or at least, resurfaced) too.
Knee replacement is extremely effective, but the Holy Grail of OA is to prevent the cartilage wearing away in the first place. We’ve seen countless potential ways of achieving that over the years and none has proved effective. But a new study involving the antidepressant paroxetine offers fresh hope for the future by switching the mechanical approach of knee replacement for a cellular approach.
How can an antidepressant prevent osteoarthritis?
The study examined the role of a protein–coupled receptor labelled GRK2, levels of which were found to be elevated in mice with OA and in damaged human cartilage. The antidepressant inhibited the GRK2 and this in turn blunted the progression of cartilage degeneration.
This is an entirely different approach to OA. It asks what’s happening at a cellular level within the knee in order for the cartilage to wear away, leaving you with exposed bone. Although this is very early days and we’re a very long way from this being a treatment, the potential is clear. If you can slow or even halt the deterioration of cartilage, you might just be able to stop OA.
And if we can do that, you’ll never need to sit on a waiting list for a knee replacement ever again.
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