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Arthritis pain often persists because inflammation in affected joints can heighten the sensitivity of the nerves that carry pain signals.
To interrupt that nerve-sensitizing process, researchers used CRISPR-based epigenome editing to suppress an inflammatory receptor in nerve cells that serve the knee and jaw joints.
In lab models, the approach prevented osteoarthritis cartilage from heightening nerve sensitivity in knee-innervating neurons and substantially reduced sensitization-related responses in jaw-innervating neurons, although additional biological pathways appeared to contribute in the jaw. The findings also highlight that osteoarthritis pain is not driven by identical mechanisms across different joints.
Targeting the biological processes that amplify pain signals, rather than simply masking symptoms, may open the door to longer-lasting relief tailored to the affected joint.
𝗥𝗲𝗮𝗱 𝗺𝗼𝗿𝗲: link.springer.com/article/10.100…
𝗦𝘁𝘂𝗱𝘆: CRISPR Epigenome Editing of IL1R1 Expression of Neurons that Innervate the Temporomandibular Joint or Knee Causes Reduced Sensitization to Osteoarthritic Environment
𝗔𝘂𝘁𝗵𝗼𝗿𝘀: Joshua D. Stover, Robby D. Bowles, @Yenisel_CruzA, Robert M. Caudle, Kyle D. Allen, REJOIN Consortium Investigators, and Alejandro J. Almarza
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𝗦𝘂𝗯𝗺𝗶𝘁 𝘆𝗼𝘂𝗿 𝗺𝗮𝗻𝘂𝘀𝗰𝗿𝗶𝗽𝘁: link.springer.com/journal/10439
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