Osteoarthritis

A network analysis of multiple therapies used in osteoarthritis found that acetaminophen (paracetamol) does not meet the minimum standard of clinical…
rheumnow.com

We've been telling patients with OA to take Paracetamol as first line pain relief medicine, because it's safe. It's even in our OA Knees treatment guidelines to General Practitioners.
Problem is, it doesn't work.
But this may be because of an overly robust placebo response. Recall the GAIT trial on glucosamine and chondroitin in OA knees: Celebrex "didn't work" either.


Objective. We aimed to examine whether the current users of specific NSAIDs have an increased risk of venous thromboembolism (VTE) among knee OA patients.
m.rheumatology.oxfordjournals.org

More bad news for OA sufferers needing pain relief medications on a regular basis. NSAIDs may relieve your pain but may well kill you in more ways than one: gastric ulcer, renal failure, heart attack, stroke, and now, deep vein thrombosis.
Naproxen seems to be the least culpable. In a separate metaanalysis, it also does not seem to increase cardiovascular risk.

Knee effusions in osteoarthritis are estimated to occur in 44% of patients, and more than half of these are painful.  Management of knee OA with effusions can be problematic given the treatment options and the high recurrence rate.
rheumnow.com

OA Knees are usually "dry". But for some patients, recurrent symptomatic effusions can be a problem.
One needs to exclude concomitant Gout and Pseudogout by imaging modalities. Yield from looking for crystals in aspirated synovial fluid is usually poor.
Colchicine, and now Spironolactone may help.
Short of addressing the underlying pathology (eg targeting inflammation or joint replacement), synovectomy can bring prolonged relief, plus histology may rarely show up other pathologies.


At the 2016 World Congress on Osteoarthritis (OARSI) meeting last week, first line results of a novel intraarticular inhibitor of the Wnt pathway (SM04690) in knee…
rheumnow.com

We are definitely moving into high gear in immunomodulation of OA here.
Intracellular Wnt signaling is involved in growth and differentiation processes in cells.
In the rat model of OA, a single intraarticular injection of the small molecule inhibitor of Wnt resulted in down regulation of inflammatory synovial cells, and allowed for chondrocyte activation to repair the damaged cartilage. Demonstrating structural regeneration is A BIG DEAL. All this without systemic spillage and side effects.
In this human study, pain relief and functional improvement were demonstrated, similarly with a single intraarticular injection. Similarly A BIG DEAL. It'll be a bigger deal if the human subjects had allowed their cartilage to be biopsied before and (some time) after the injection.
Interestingly, the subjective improvement dropped off at a much higher dose of the Wnt inhibitor. Perhaps too much inhibition will knock out the chondrocyte repair as well. As in cooking, one has to get the seasoning just right. The poison is not only in the dose, but also how and where you deliver it.

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