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One of my favourite activities at these gigantic meetings is taking a couple of hours to walk and digest the headlines among the posters. It's a great time to think, spark ideas, and meet people who also can't sit still any longer in the podium talks. Here are a few key take aways from the poster-boards.
It's becoming very clear that inflammatory mechanisms differ substantially among the arthritides, buttressing the critical importance of discovery-based research for new drug targets. At FRI0009, genetic deletion of 12/15-lipoxygenase (12/15-LOX) in mice worsened age-associated and post-traumatic forms of OA. LOX seems to be needed to protect against OA-related tissue damage and expression of cartilage digesting proteases in chondrocytes. Could LOX agonists be a target in OA? #newdirections
More on the effect of metabolic derangement in OA at FRI0010. Metabolic OA was modeled in rats fed a high-fat diet, with or without a second "hit" using the femoral groove (scrape the cartilage with a needle) method of inducing OA. Eicosanoid oxidized oxylipins are products of fatty acid oxidation and an have pro- and anti-inflammatory effects. The Utrecht group identified a panel of 31 oxylipins that are increased in serum and synovial fluid in the animals given the high-fat vs normal diet. The femoral groove OA procedure caused 3 oxylipins to increase vs controls. It'sonly an association, but it lays the ground work for mechanistic studies on these molecules, which I expect will include looking to see if they account for the increased susceptibility to developing OA due to metabolic risk factors. #fatrats
Can you differentiate the undifferentiated arthritis? Maybe, if you have a mass spectrophotometer… At FRI0012, the first-ever detection of volatile organic compounds (VOCs) in synovial fluid was reported. The gas chromatography-MS method was able to discriminate OA from RA synovial fluid using four VOCs that were identified in the discovery analysis. GC-MS positively detected 100% of RA and 62% of OA samples in the testing phase. This again speaks the fundamentally different nature of chronic inflammation in OA and RA joints. #techforjoints
Synovium probably mediates the hostile joint environment that makes cartilage susceptible to OA. FRI0016 looked at proteases made by fibroblast-like synoviocytes isolated from OA synovium, including ADAMTS-17 and -12, which can break down cartilage oligomeric protein (COMP), thereby softening cartilage. It lookslike OA synoviocytes rely on Wnt signaling to increase the production of ADAMTS-7 since the Wnt inhibitor DKK1 reduced ADAMTS-7 production. This is early in vitro data and more evidence is needed linking it to tissue damage before moving to animal models . #WntMoreData
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About the Author
Dr. Tom Appleton
Dr. Appleton completed the combined MD/PhD program at Western University in Canada and is now a rheumatologist and clinician scientist at St. Joseph’s Hospital in London, Canada. In addition to his rheumatology practice, Dr. Appleton oversees a translational biology research program in early osteoarthritis.
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