Ultrasound vs Arthritis!

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First things first: arthritis is the umbrella term for a cluster of joint diseases involving inflammation of the joints, hence “arthr-” (joint) “-itis” (suffix used to denote inflammation).

Arthritis is broadly divided into inflammatory arthritis and non-inflammatory arthritis.

Some forms, such as rheumatoid arthritis, are of the inflammatory kind. We wrote about that previously:

See: Avoiding/Managing Rheumatoid Arthritis

You may be wondering: how does one get non-inflammatory inflammation of the joints?

The answer is, in “non-inflammatory” arthritis, such as osteoarthritis, the damage comes first (by general wear-and-tear) and inflammation generally follows as part of the symptoms, rather than the cause.

We wrote about that previously, too: Avoiding/Managing Osteoarthritis

So the name can be a little confusing. In the case of osteo- and other “non-inflammatory” forms of arthritis, you definitely still want to keep your inflammation at bay as best you can; it’s just not the prime focus.

Today we’ll be looking at some new research that shows how the body can tackle this inflammation in a very different way:

Switching it up

The body has different kinds of immune response, some of it being good and necessary and some of it being misfiring. Similarly, when it comes specifically to macrophages, which are specialist white blood cells that “eat” things that need to be removed. There are two kinds, inflammatory and non-inflammatory. The former aggressively “eat” invaders. The latter are more like cellular janitors.

Specifically:

  • M1 macrophages: promote inflammation to clear damaged tissue and fight infection, but prolonged activity can damage healthy tissue.
  • M2-like macrophages: promote tissue repair, healing, and recovery.

What this most recent study found is that continuous low-intensity ultrasound encouraged macrophages to shift from the inflammatory M1 state towards the reparative M2-like state.

In particular, instead of using standard laboratory methods to trigger inflammation, they used fibronectin fragments, molecules released from damaged joint tissue, creating a model that more closely resembles what happens after a real joint injury.

The results, in few words, were:

  • Reduced biological markers associated with inflammation (this is an improvement)
  • Increased markers associated with tissue repair and M2-like macrophages (this is also an improvement)
  • Altered coordinated patterns of gene activity linked to immune responses (this is a bit complex, but the short version is that this appears to be at least a large part of what causes the other two things to happen, since the genes in question pertain to these kinds of macrophage activity)

The main advantages, of course, are that this is drug-free, non-invasive, and designed to regulate the body’s own immune response rather than suppress it with medication.

You can read the paper in full, here: Continuous low-intensity ultrasound influences the transcriptomic profile in M1 macrophages by downregulating inflammation and promoting M2-like markers

Want to learn more?

For specifically the pain management aspect, you might like to consider:

Take care!

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