What a surprise!
"Why acute pain sometimes resolves after a few weeks or months, but becomes chronic in other people, is not entirely understood, particularly at the molecular level. A study published yesterday (May 11) in Science Translational Medicine suggests that the initial inflammatory response may be key to avoiding lasting pain.
The study authors report that pain in the lower backs of patients with elevated inflammation was more likely to resolve after three months than that of patients with a more discreet reaction. Thousands of genes, many of them related to the inflammatory response and immune cell activation, changed expression in the blood samples of those who recovered, while none seem to be altered when pain persisted. Based on mouse experiments and a database analysis of drug use and medical conditions, the team found preliminary evidence that blocking the inflammatory response with medication can prolong musculoskeletal pain.
The results challenge two decades of research indicating “that actually a proinflammatory state is accelerating the transition from acute to chronic pain,” ..."
From the abstract:
"The transition from acute to chronic pain is critically important but not well understood. Here, we investigated the pathophysiological mechanisms underlying the transition from acute to chronic low back pain (LBP) and performed transcriptome-wide analysis in peripheral immune cells of 98 participants with acute LBP, followed for 3 months. Transcriptomic changes were compared between patients whose LBP was resolved at 3 months with those whose LBP persisted. We found thousands of dynamic transcriptional changes over 3 months in LBP participants with resolved pain but none in those with persistent pain. Transient neutrophil-driven up-regulation of inflammatory responses was protective against the transition to chronic pain. In mouse pain assays, early treatment with a steroid or nonsteroidal anti-inflammatory drug (NSAID) also led to prolonged pain despite being analgesic in the short term; such a prolongation was not observed with other analgesics. Depletion of neutrophils delayed resolution of pain in mice, whereas peripheral injection of neutrophils themselves, or S100A8/A9 proteins normally released by neutrophils, prevented the development of long-lasting pain induced by an anti-inflammatory drug. Analysis of pain trajectories of human subjects reporting acute back pain in the UK Biobank identified elevated risk of pain persistence for subjects taking NSAIDs. Thus, despite analgesic efficacy at early time points, the management of acute inflammation may be counterproductive for long-term outcomes of LBP sufferers."
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