Curcumin – one of the major active components of turmeric – reduced synovial hyperplasia in rheumatoid arthritis

The synovium is normally a very thin, smooth layer of cells that is closely attached to the membrane that encloses the joint and its synovial (lubricating) fluid.

In rheumatoid arthritis the synovium becomes thickened and develops finger-like projections extending out into the joint space. This thickening process is called “hyperplasia,”and typically leads to pannus formation. Pannus means “flap” – and the pannus in rhuematoid arthritis contributes to the joint destruction characteristic of that disease.

One reason the synovium may thicken is that old cells do not die as they are supposed to. So as new cells continue to be made, cells accumulate.

While it might seem strange that cell death is required to maintain health, such is often the case. This “programmed cell death” is called “apoptosis.”

The classic example of cells that do not die as they are supposed to is cancer. In cancer cells, the gene that programs for cell death (apoptosis) has somehow been turned off. So cancer cells live, and proliferate, forever.

The synovial cells in rheumatoid arthritis act like cancer cells in certain ways. They continue to reproduce and live ‘forever.’ They invade and destroy nearby tissue. And what’s ‘nearby’ is the cartilage of the joint capsule.

This, in brief, is how synovial hyperplasia leads to joint destruction. Of course preventing this hyperplasia would be a very good thing.

The publication:

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nt J Mol Med. 2007 Sep;20(3):365-72.

Curcumin induces apoptosis and inhibits prostaglandin E(2) production in synovial fibroblasts of patients with rheumatoid arthritis.

Summary of the abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disease that is characterized by hyperplasia of the synovial fibroblasts, which is partly the result of decreased apoptosis.

This study investigated the mechanisms through which curcumin, a polyphenolic compound from the rhizome of Curcuma longa, exerts its anti-proliferative action in the synovial fibroblasts obtained from patients with RA.

Exposure of the synovial fibroblasts to curcumin resulted in growth inhibition and the induction of apoptosis.

Curcumin decreased the expression levels of the cyclooxygenase (COX)-2 mRNA and protein without causing significant changes in the COX-1 levels, which was correlated with the inhibition of prostaglandin E(2) synthesis.

These results show that curcumin might help identify a new therapeutic pathway against hyperplasia of the synovial fibroblasts in RA.

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Comments:

Curcumin was found to stimulate apoptosis – the programmed cell death that is required if synovial cells are to remain as a nice smooth layer and not build up into a joint-destroying pannus.That is, it seemed to make the synovial cells behave properly.

As something of a ’side benefit’ – curcumin was found to inhibit COX-2 without affecting levels of COX-1. COX-1 is required for stomach protection. By inhibiting only COX-2 one would obtain the analgesic and anti-inflammatory benefits without the stomach-related (and kidney related) side effects common to aspirin and other NSAIDs.