Arthritis and joint pain result from inflammation. In fact the term "arthritis" literally means "joint inflammation".
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Active inflammatory processes were found to be ongoing in the subchondral bone (the bone underneath the collagen) of those with osteoarthritis.
The suggestion is offered that this ‘deeper’ inflammation may be responsible for some substantial portion of cartilage damage witnessed in osteoarthritis.
In general, genetics play a weak role in the development of osteoarthritis.
The strongest genetic association is with FRZB – also known as “frizzled-related-protein-3″ – which is associated with hip osteoarthritis in women. Why might that be?
FRZB is an antagonist to (counter balances) the effects of the WNT pathway.
When there is a slight mutation at the gene coding for FRZB, the FRZB that the body produces is slightly defective – it does not do quite so good a job at inhibiting or counter-balancing WNT. Therefore, whatever WNT does – when FRZB is defective, WNT will do more of it. Got that?
What does WNT do? One thing it does is activate NF-kB.
So defective FRZB => more WNT activity => more NF-kB activity => hip osteoarthritis in women.
I have no idea why the hip – or why women.
The role of NO as either beneficial or detrimental in the arthritic joint has long been debated. NO appears to act in a very complex manner. However, the fact that it inhibits NF-kB and therefore serves an anti-inflammatoey roles suggests that NO inhibition may have detrimental effects in osteoarthritis.
CNS regulation of peripheral inflammation, implications in fibromyalgia?
The central nervous system (CNS = brain and spinal cord) can regulate peripheral inflammation, but the pathways and mechanisms by which it does so remain unclear.
The study summarized below investigates the possibility that the neurotransmitter acetylcholine (ACh) exerts an anti-inflammatory effect via binding to a specific receptor found primarily on the synovial lining of rheumatoid arthritis and osteoarthritis joints.
That possibility is confirmed by observations of reduced pro-inflammatory cytokine activity as a result of such binding.
While the authors suggest that the receptor identified in rheumatoid arthritis and osteoarthritis joints might be a potential target for drug development, I am curious if a similar mechanism might explain the connection between observed neurotransmitter abnormalities seen in fibromyalgia and the persistence of peripheral inflammation.
Excess activation of NF-kB leads to osteoclast over-activation and increased bone destruction in arthritis.
Healthy bone metabolism requires a balance between osteoclasts (break down and re-absorb bone) and osteoblasts (make new bone.)
Osteoclasts – the bone destroying cells – are over-active in many disease conditions that include bone destruction (such as osteoarthritis.)
In the study summarized below, it was found that excess NF-kB activation led to osteoclast over-activity.
The authors note that the NF-kB inhibitor parthenolide (a major active component in the herb feverfew) has shown a beneficial therapeutic effect in reducing inflammation induced bone destruction in a mouse model.
It is noted that NF-kB over-activation and associated osteoclast over-activity is also seen in Paget’s disease of bone, and periodontitis.
Osteoarthritis has been called “wear and tear” arthritis. But that’s somewhat misleading. Osteoarthritis results not from years of use, but from years of chronic, low grade inflammation.
Yes, mechanical stress (the pounding your knee joint takes every time you walk or run) does cause mild inflammation. But that inflammation would normally resolve quickly and entirely. When it doesn’t – when your body can’t entirely turn off the inflammation – chronic inflammation results.
Chronic, mild inflammation eventually progresses to chronic severe inflammation. Osteoarthritis results when that inflammation begins causing pain.
One reason your body might have trouble turning off the inflammation is “leptin.”
Etanercept (Enbrel) inhibits NF-kB when used in the treatment of psoriatic arthritis. The immune system is extremely complex and includes many feedback loops (positive and negative) as well as much ‘cross talk’ between its various components. The relationship between NF-kB and TNF is defined (in part) by a positive feedback loop.
Americans spend approximately $1 billion each year on various forms of glucosamine supplements, primarily for the treatment of osteoarthritis. Is that money well spent, or wasted?
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.
When treated with the NF-kB inhibitor early in the course of knee inflammation, or before it begins, the result is “total prevention” of the “hyperexcitability” of the neurons – taken to be an indication of pain signaling.
